RHEUMATOLOGY

RA
• Rheumatoid arthritis is a multisystem inflammatory disease primarily affecting the synovium
and adjacent tissues.

• RA is an autoimmune condition characterised by chronic inflam- mation, granuloma formation

and joint destruction.

• The earliest change is swelling and congestion of the synovial membrane and the underlying
connective tissues, which become infiltrated with lymphocytes, plasma cells and macrophages.

• TNF plays a central role in triggering local inflammation and regulating cytokines responsible for
the systemic effects of RA.

Etiology
Immunogenic factors :

• The combination of conserved amino acid sequence In the third hypervariable region of HLA-
DRB1 with positive rheumatoid factor identifies individuals at 13 times greater risk of developing
bony erosions at 1 year.
Other factors :

(a) Hormonal factors – Incidence of RA In women is greater before menopause and remission of RA
during pregnancy is well known.

(b) Oral contraceptive pill

(c) Low economic status is associated with a worse disease outcome in RA.

Clinical features
• The most common presentation is with a gradual onset of symmetrical arthralgia and synovitis
of small joints of the hands, feet and wrists.

• Sometimes RA has a very acute onset with florid morning stiffness, polyarthritis and pitting
oedema. This occurs more commonly in old age.

• Occasionally, the onset is palindromic, with relapsing and remitting episodes of pain, stiffness
and swelling that last for only a few hours or days.

• Extra-articular features : Anorexia, weight loss and fatigue are common and may occur
throughout the disease course. Common in patients with long-standing seropositive erosive
disease but may occur at presentation especially in men.
 • Rheumatoid nodules occur in seropositive patients usually at sites of pressure such as the
extensor surfaces of the forearm, achilles tendon and toes.

• The most common ocular symptom is dry eyes (keratoconjunctivitis sicca, secondary Sjogren’s
syndrome).

• Painless episcleritis may cause intense redness but sight is unimpaired. Scleritis is more serious
and potentially sight-threatening, the eye is red and painful, and vision is impaired.

Grading
Grade I : No handicap

Can carry on all daily activities

Grade II : Moderate restriction of activities but independent

Grade III : Marked restriction of activities mostly limited to self care

Needs assistance
Grade IV : Bed or chair bound

Incapacitated & independent

Pathogenesis
Foreign antigen

CD4+ T-cells

Activation of B-cells & T-cells Activation of macrophages Activation of endothelial cells

Initiates hyper immune Initiation & recruitment of Leads to increased expression of

responses in the blood pro-inflammatory cytokines adhesion molecule

Formation of immune TNF-α, IL-1β, IL-NF-kβ Inflammatory cells begin to

complexes accumulate

Plannus formation

RA
Diagnosis
• The clinical criteria for the disease must have been present for at least 6 weeks. The joints feel
hot and swollen and are usually tender to touch, and generalized lymphadenopathy may also be
present.

• Laboratory: Abnormal investigations may include:

o Increased WBC count
o Thrombocytosis
o Mild normocytic anemia

o High ESR or acute phase reaction

o Positive rheumatoid factor
o Positive anti-CCP antibody

o Arthrocentesis of synovial fluid shows it to be strawcolored with increased neutrophils

Joint involvement in RA
• Joints commonly involved are metacarpophalangeal, proximal interphalangeal joints, the wrists
and the knees.

• In early stages joints are warm, swollen and tender. Weakening of the joint capsule and tendon
along with ligament damage lead to joint instability, subluxation or dislocation and so produces
characteristic deformities of RA. Eventually severe joint damage may lead to fibrous or bony
ankylosis or secondary degenerative changes.

INVESTIGATIONS
1. Tests for inflammation :

Raised ESR, C-reactive protein and plasma viscosity. Other laboratory tests to support inflammatory
disease – Normochromic, normocytic anemia (with low iron levels and iron-binding capacity),
thrombocytosis, elevated hepatic alkaline phosphatase, polyclonal gammopathy, and elevation of acute
phase proteins, e.g. ferritin.

2. Immunological tests :

Rheumatoid factor – RF is an autoantibody directed against the Fc fragment of immunoglobulin G (IgG).

The commonly used Rose Waller Latex agglutination tests detect only the IgM type of RF, because IgM is
a multivalent immunoglobulin and hence a better agglutinator. Either 1 in 80 dilution or 80IU/ml is
taken as positive for diagnosis of RA.
3. Radiology : Sequence of changes

(a) Periarticular osteopenia with soft tissue swelling

(b) Erosions at junction of synovium, subchondral bone and articular cartilage

(c) Loss of joint space

(d) Deformity such as subluxation or complete dislocation of affected joints

4. Special investigations :

(a) Synovial biopsy – Rheumatoid pattern (villus formation with thickening of synovial layer and
infiltration with abnormal cells) in RA (also in Still’s disease, SLE).

(b) Synovial fluid – Not helpful in differential diagnosis.

(c) Arthroscopy – will not distinguish RA from various inflammatory seronegative arthritides. In acute RA
synovium is oedematous, diffusely erythematous and friable. In more chronic conditions, it becomes
thickened, polypoid.

(d) Renal biopsy – if reduced glomerular or tubular function.

(e) Pulmonary biopsy – to distinguish rheumatic nodules from carcinoma or to establish diagnosis of
fibrosing alveolitis.

Management
General Measures
Education – Provides information on the disease and its therapies. It also emphasizes the role of
patients in caring for and controlling their own disease.
Exercise – Much of the pain and stiffness in RA arises from periarticular tissues such as muscles and
tendons and patients should perform a general (range of motion).
Physiotherapy/occupational therapy – Physiotherapeutic modalities such as electric therapy
(ultrasound or interferential), heat or cold. Joint protection in form of splinting to prevent deformity
during episodes of acute pain. Dietary advice includes weight reduction and the addition of fish oil or
evening primrose oil.

Pharmacotherapy – Once the diagnosis of RA has been confirmed, treatment with drugs that retard
joint destruction and reduce disability.

NSAIDs – NSAIDs are derived from various chemical classes with a common mechanism of action –
reduction of prostaglandin synthesis.

Treatment
• There is no cure for rheumatoid arthritis. But clinical studies indicate that remission of
symptoms is more likely when treatment begins early with medications known as disease-
modifying antirheumatic drugs (DMARDs).

(a) NSAIDs : Can relieve pain and reduce inflammation. Over-the-counter NSAIDs include ibuprofen
(Advil, Motrin IB) and naproxen sodium (Aleve). Side effects may include stomach irritation, heart
problems and kidney damage.
(b) Steroids : Corticosteroid medications, such as prednisone, reduce inflammation and pain and slow
joint damage. Side effects may include thinning of bones, weight gain and diabetes.
(c) Conventional DMARDs : These drugs can slow the progression of rheumatoid arthritis and save the
joints and other tissues from permanent damage. Side effects vary but may include liver damage and
severe lung infections.
(d) Biologic DMARDs : Usually most effective when paired with a conventional DMARD, such as
methotrexate. This type of drug also increases the risk of infections.
(e) Targeted synthetic DMARDs : May be used if conventional DMARDs and biologics haven’t been
effective. Higher doses of tofacitinib can increase the risk of blood clots in the lungs, serious heart
related events and cancer.

(f) Surgery : If medications fail to prevent or slow joint damage, Surgery may help restore your ability to
use your joint. It can also reduce pain and improve function.

Rheumatoid arthritis surgery may involve one or more of the following procedures :

Synovectomy : Surgery to remove the inflamed lining of the joint (synovium) can help reduce pain and
improve the joint’s flexibility.

Tendon repair : Inflammation and joint damage may cause tendons around your joint to loosen or
rupture. Your surgeon may be able to repair the tendons around your joint.

Joint fusion : Surgically fusing a joint may be recommended to stabilize or realign a joint and for pain
relief when a joint replacement isn’t an option.
Total joint replacement : During joint replacement surgery, your surgeon removes the damaged parts of
your joint and inserts a prosthesis made of metal and plastic.

ANKYLOSING SPONDYLITIS
• Ankylosing spondylitis is an inflammatory dz that cause some of the small bones in spine to fuse.
This fusing makes the spine less flexible and can result in a hunched forward posture.

Etiology
(a) Sex – More common in men than in women. Women tend to have more peripheral joint
involvement, men have more spinal disease.

(b) Genetic factors – HLA-B27 and HLA-DR1 confer susceptibility to the spondyloarthropathies.

(c) Environmental triggers of the disease remain unknown.

Pathogenesis
Macrophages infiltration

Synovitis

Myxoid appearing bone marrow

Proliferating fibroblasts, neovascularization and over expression of TNF, IL-1, VEGF

Infiltrating cells include CD4+ & CD8+ lymphocytes T-cells

Pannus and granulation tissue

Bone resorption and proteoglycan breakdown

Bone eroded by osteoclast

Heals by endochondral ossification

Bone ankylosis

Clinical Features

• Back pain and stiffness—insidious onset, duration >3 months. Association with morning
stiffness. Improvement with exercise

• Extraaxial arthritis—hip and shoulders 25–35%

• Chest pain—from involvement of thoracic skeleton and muscular insertions

• Extra/juxtaarticular pain—due to “enthesitis

• Constitutional symptoms—fever, fatigue, weight loss may occur

• Ankylosing spondylitis does not burn out, it continues to be active. Fatigue is a major
component. No system in the body is unaffected.
 • Sacroiliac joints and spine – Early sign is evidence of sacroiliac joint arthritis. Examination of
spine may reveal muscle spasm and loss of normal lordosis with positive Schober test (a useful
clinical measure of flexion of the lumbar spine performed during examination).

Investigations
Radiology – demonstrates sacroiliitis. Early change in Lumbar spine is manifested as squaring of the
superior and inferior margins of vertebral body. Later change results in bamboo spine.

Laboratory tests – (i) ESR is elevated in 50% (ii) Serum IgA may be elevated (iii) Serum creatinine
phosphokinase and alkaline phosphatase may be slightly raised (iv) HLA-B27 is present in 95%

Management
(a) Physiotherapy has a major role in long-term management

(b) Pharmacotherapy as in treatment of RA.

(c) DMARDs – Sulfasalazine and methotrexate appear to have an effect only in patients with peripheral
joint involvement
(d) Bisphosphonates may act on both the underlying osteoporosis and inflammatory disease itself.

(e) Surgery is most often used in patients with advanced hip involvement.

OA
• Osteoarthritis is an abnormality of synovial joints characterized by softening, splitting and
fragmentation (fibrillation) of articular cartilage not attributable to direct contact with
inflammatory tissue. This is usually accompanied by subchondral sclerosis and bone cysts, joints
space narrowing and bony overgrowths at tissue joint margins (osteophytes).

Etiology
a. Age is a major risk factor

b. Race – Hip OA is less common in Chinese and Asians than in those of Western origin, whereas knee
osteoarthritis is more common in Afro-Carribbeans.
c. Genetic predisposition – Heberden’s nodes are more common in sisters of affected women than in
the general population. 20% of individuals with osteoarthritis have a positive family history. There is
greater concordance in identical twins at several joint sites

d. Gender and hormonal factors – Below 45 years, the disease is in men, in whom it usually involves one
or two joints. Above 55 years, it is more common in women, usually involving several joints (particularly
interphalangeals, first metacarpal and knees).

e. Obesity – The relationship is stronger in women than in men and is strongest at the knee.
f. Other systemic factors – In women a significant association between hand disease and elevated serum
cholesterol levels. Hypertension has been associated with generalized osteoarthritis in men and knee
osteoarthritis in non-obese women.

Pathogenesis
• The pathogenesis of OA involves enzymatic degradation of aggrecan and collagen within the
articular cartilage, with fissuring and thinning of the cartilage surface.

• Cysts develop within the subchondral bone, possibly due to osteonecrosis resulting from
increased pressure on the bone as the cartilage fails.

• At the joint margins, new fibrocartilage grows and then ossifies, forming osteophytes. Bone
remodelling and cartilage thinning gradually alter the shape of the OA joint.

• This is accompanied by wasting of the surrounding muscles, synovial hyperplasia and thickening
of the joint capsule.

Clinical features
• OA is characterised by gradual development of joint pain, stiffness, limitation of movement and
swelling, which may be caused by synovitis with effusion or from osteophyte formation (as in
Heberden’s nodes)

• Pain and functional restriction

• Insidious onset over months or years

• Pain worsened by movement and relieved by rest

• Only brief (< 15 mins) morning stiffness and brief ‘gelling’ after rest (in contrast to inflammatory
arthritis)

• Usually only one or a few painful joints

• The bony enlargement that accompanies osteophyte formation may lead to joint deformity

Examination
• Generalized OA refers to involvement of at least three joints or a group of joints (e.g.
interphalangeal joints).

• There are two types nodal and non-nodal – Features Heberden’s nodes of the interphalangeal
joints, predominates in women and exhibits a strong tendency to familial transmission.

• Hands – Limitations of activity that require dexterity (e.g. dressing, feeding) are affected.

• Hip disease – First sign is usually pain or restriction of internal rotation followed by pain on
flexion.
 • Knee – Tibiofemoral arthritis is usually bilateral and is associated with early morning stiffness
and pain on weight bearing particularly on climbing stairs. Night pain is a sign of severe disease.
In elderly patients, knee effusions and crepitus are common.

• Severe OA of the knee joints leads to valgus deformity of the joints.

Investigations
• Plain X-rays may reveal joint space narrowing, subchondral sclerosis, osteophytes and bone
cysts.

• However, correlation between radiographic changes, symptoms and disability is variable.

• MRI is indicated if nerve root compression is suspected. Routine blood tests are normal in OA.

Management
Non-surgical treatment
Pharmacological
• Analgesics and anti-inflammatory treatment – Simple analgesics the appropriate first-line treatment
for uncomplicated osteoarthritis e.g. paracetamol 4g/day.

• Intraarticular therapies – Intraarticular glucocorticoids are used in treatment of knee osteoarthritis.

When pain and swelling persist despite drugs such as NSAIDs, and may temporarily relieve symptoms.
• Chondroprotective agents – Glucosamine and chondroitin have been shown to modify symptoms to a
degree equivalent to anti-inflammatory agents.

Non-pharmacological
• Self-management programmes

• Weight reduction

• Physiotherapy

• Occupational therapy
• Aids (e.g. shoe wedges, patella-taping, cushioned training shoes, stick)

Surgery
• Arthroplasty is successful in both hip and knee disease.

• Osteotomy relieves pain and can stimulate fibrocartilaginous healing of the joints. Nowadays
total knee replacement is a preferred modality.
REACTIVE ARTHRITIS
• Reactive arthritis is joint pain and swelling triggered by an infection in another part of body most
often intestines, genitals or urinary tract.

Causes
• Numerous bacteria can cause reactive arthritis. Some are transmitted sexually, and others are
food borne.
• Reactive arthritis isn’t contagious. However, the bacteria that cause it can be transmitted
sexually or in contaminated food.
• Only a few of the people who are exposed to these bacteria develop reactive arthritis.The most
common ones include:
o Chlamydia
o Salmonella
o Shigella
o Yersinia
o Campylobacter

Symptoms
The signs and symptoms of reactive arthritis generally start one to four weeks after exposure to a
triggering infection. They might include:
o Pain and stiffness : The joint pain associated with reactive arthritis most commonly occurs in
your knees, ankles and feet. You also might have pain in your heels, low back or buttocks.
o Eye inflammation : Many people who have reactive arthritis also develop eye inflammation
(conjunctivitis).
o Urinary problems : Increased frequency and discomfort during urination may occur, as can
inflammation of the prostate gland or cervix.
o Inflammation of soft tissue where it enters bone (enthesitis) : This might include muscles,
tendons and ligaments.
o Swollen toes or fingers : In some cases, your toes or fingers might become so swollen that they
resemble sausages.
o Skin problems : Reactive arthritis can affect your skin a variety of ways, including a rash on your
soles and palms and mouth sores.
o Low back pain : The pain tends to be worse at night or in the morning.

Risk factors
Age : Reactive arthritis occurs most frequently in adults between the ages of 20 and 40.
Sex : Women and men are equally likely to develop reactive arthritis in response to food borne
infections.
Hereditary factors : A specific genetic marker has been linked to reactive arthritis. But many people who
have this marker never develop the condition.
Diagnosis
During the physical exam is likely to check joints for signs and symptoms of inflammation, such as
swelling, warmth and tenderness, and test range of motion in spine and affected joints and check eyes
for inflammation and skin for rashes.

Blood tests / Joint fluid tests

White blood cell count : An increased number of white blood cells might indicate inflammation or an
infection.

Infections : Bacteria in your joint fluid might indicate septic arthritis, which can result in severe joint
damage.

Crystals : Uric acid crystals in your joint fluid might indicate gout. This very painful type of arthritis often
affects the big toe.

X- rays : Low back, pelvis and joints can indicate whether there is any characteristic signs of reactive
arthritis.

Prevention
• Make sure food is stored at proper temperatures and is cooked properly to help you avoid the
many foodborne bacteria that can cause reactive arthritis, including salmonella, Shigella,
Yersinia and campylobacter.
• Some sexually transmitted infections can trigger reactive arthritis. Using condoms might lower
your risk.

Treatment
Medications
o Nonsteroidal anti-inflammatory drugs (NSAIDs) : Prescription NSAIDs, such as indomethacin
(Indocin), can relieve the inflammation and pain of reactive arthritis.

o Corticosteroids : Injection of a corticosteroid into affected joints can reduce inflammation and
allow you to return to your normal activity level.

o Topical steroids : These might be used for skin rashes caused by reactive arthritis.

o Rheumatoid arthritis drugs : Limited evidence suggests that medications such as sulfasalazine,
methotrexate or etanercept can relieve pain and stiffness for some people with reactive
arthritis.
Physical therapy
• A physical therapist can provide targeted exercises for joints and muscles. Strengthening
exercises develop the muscles around affected joints, which increase the joints support. Range-
of-motion exercises can increase joints flexibility and reduce stiffness.

INFECTIOUS ARTHRITIS
• It is the external struggle between microbes and human being ever since the down of
mankind on mother Earth

1. Septic arthritis
• Common in children, immune-compromised individual

• Hip & knee joint commonly affected with abrupt of pain & swelling

• Joint movement restricted

• Shaking chill can occur sign of acute inflammation are minimal or typical in elderly and those
with co-existent joint disease, steroid intake, immunosuppressor.

• Dissemination from osteomyelitis

• Lymphatic spread from soft tissue infection

• Iatrogenic

• Penetrating trauma

o Sepsis sets in inflammation which in turn causes synovial fluid proliferation, effusion,
increases joint pressure and enzymatic degeneration of cartilage

Investigations
• Demonstration of infective organism by gram stain or culture of synovial fluid

• Synovial fluid - Leukocytosis : Total WBC : 50,000 to 100000 per mm, Presence of infection
Radiography - joint space narrow, erosion

• CT scan

• Prosthetic joint infection

• Causative organism : staphylo, strepto

• Organism colonize on foreign surface of prosthesis

Treatment
• Oral antibiotic : Pencillin resistance vancomycin for gram+
 • Aminoglycoside for gram negative

• Gonococcal arthritis

• Disseminated gonococcal infection

• Migratory polyarthrologia

• Tenosynovitis

• Mono or oligoarthritis

• Skin : painless, maculopapular, vesicular or necrotic lesion

Rx
• Cefriaxone 1-2 gram per day

• Doxycycline 100mg

• pencillin with 10 to 20 million unit per day

• Amoxicillin 500mg
• Erythromycin

2. Brucellosis
• Caused by small aerobic, non-motile gram negative, coccobacilli transmitted from infected
animal and injection of dairy product and milk

Clinical features
• Sacrolitis

• Spondylitis

• Peripheral oligoarthritis

• Osteomyelitis

• Bursitis

Rx
• Doxycycline 100mg

• Rifampicine 15mg

• Tubercular arthritis

• M. tuberculosis infection of bone and joint

• Extrapulmonary TB and often seen in children and younger

Types
• Pott’s spine

• Pancet’s disease

• Peripheral arthritis

• Tenosynovitis and bursitis

• Dacylitis and osteomyelitis

Psoriatic arthritis
• Define as arthritis associated with psoriasis and usually negative for rheumatoid factor. 7%
to 42% of patient reported.

Etiopathogenesis
1. Hormonal factor

2. Immunological mechanism
3. Genetic factor

T-cell mediated disease

There is up-regulation of leukocyte homing receptor in synovium

Results in leucocyte infiltration of synovium

Cytokines are secreted by leucocytes which meditate arthritis

Clinical features
• Joint pain - swelling presentation

1. Distal interphalangeal joint disease- uncommon, mainly affecting men, it targets finger distal IPJ
& surrounding tissue with nail dystrophy.
2. Arthritis mutilans : Deformity, destructive arthritis involving the small joint of hands and feet.

3. Peripheral oligoarthritis or polyarthritis : Asymmetrical pattern of joint involvement initially

some of whom progress to a more symmetrical disease

4. Spondylitis mainly in males, Spinal involvement, Cervical spine involvement

 Skin : Plague – silvery scales underneath the breast, navel, scalp, behind the ears, extensor aspect of
knees, elbows and back

Investigations
• ESR, CRP raised

• RF & CCP negative

• Xray show erosion change with joint space narrowing

• Sterile synovial fluid with moderate increases in neutrophils

D/D
• Reactive arthritis

• Gout

• Osteoarthritis

• SLE

Management
• Therapy with NSAIDs and analgesics

• MARDS

• Anti TNF alpha therapy improves peripheral arthritis, skin lesions

• Other agents : Retinoic acid & Psorrten plus

GOUT
• Gout is the term used to describe the constellation of clinical features that result from
deposition of microcrystals of sodium urate monohydrate or uric acid from hyperuricemic body
fluids. These include acute arthritis, tenosynovitis, bursitis or cellulitis, tophaceous deposits,
renal disease and urolithiasis.

• Gout is a “king of diz” or “diz of king”.

Etiology
1. Idiopathic

o Hereditary family members have hyperuricemia without gout

o Race: Whites> Blacks

o Sex: Males >Females

 o Age : 2nd to 4 decade common at 40 years

2. Adrenal cortex insufficiency : an adequate amount of corticosteroids counteracts the gouty attack

3. Disturbed electrolyte equilibrium : Marked diuresis that preceeds acute attacks of gout

Pathogenesis
• In all populations, serum urate concentration is the major determinant of risk of developing
gout.

• Uric acid is the end product of purine metabolism in humans, who lack the enzyme uricase
(which degrades uric acid to allantoin in most animals).

• The miscible body pool of urate in normal individuals is about 1 g, and about 60% of this is
replenished daily from catabolism of newly synthesized and dietary proteins.

• Two-third of urate formed each day is excreted by the kidneys and one-third from GI tract.

• Genetic and environmental factors lead to gout and hyperuricemia by reducing excretion of uric
acid (90%) and/or increased production of uric acid (10%) .

• The inherent metabolic aberration in gout is hyper-uricemia which is defined as an elevation in

serum urate (SUA) level ≥ 6.8 mg/dL.

Classification
1. Primary gout

o Common type (95%)

o Idiopathic
o Due to under excretion or overproduction of monosodium urate (MSU)
2. Secondary gout

o Comprises 5%
o Prolonged hyperuricaemia
o Administration of diuretics
o Renal failure

Clinical features
The natural history of gout has four stages:

1. Asymptomatic hyperuricemia
2. Acute gout – may be precipitated by many factors
o Trauma
 o Unusual physical exercise

o Surgery
o Severe systemic illness
o Severe dieting

o Alcohol
o Drugs

• First attack occurs commonly in men aged 30–60 years, usually monoarticular, the
metatarsophalangeal joint of the great toe is the first joint affected in 70%.

• Acute Gouty arthritis can occur in ankles, knees, wrists, elbows and small joints of hands and
feet, it seldom occurs in axial skeleton or large joints such as the hip and shoulder.

• The initial attack may be sudden. The affected joint becomes hot, red and swollen with shiny
overlying skin and is extremely painful and tender.

• First attacks are seldom associated with residual disability, but recurrent attacks are followed by
progressive cartilage and bone erosion, deposition of tophi, secondary OA and disability
associated with permanent restriction of joint function.
3. Intercritical gout

4. Chronic tophaceous gout : Tophus formation is related to serum uric acid and to local factors. Tophi
seldom develop in individuals with asymptomatic hyperuricemia.

Diagnosis
Diagnosis is supported by :

• Raised serum uric acid

• Characteristic radiological changes (soft tissue swelling with patchy calcification, cortical erosions of
phalanges, punched-out erosions and secondary degenerative changes) in patients who have had
recurrent attacks.
Diagnosis is established by :

• Demonstration of needle-shaped, negatively birefringent crystals of monosodium urate in

synovial fluid neutrophils by polarizing light microscopy.

• Serum uric acid levels can be normal or low at the time of an acute attack.

Differential diagnosis
• Infective arthritis

• Bursitis, cellulitis, Tenosynovitis

 • Sarcoid Arthritis

• Pseudogout caused by calcium pyrophosphate

• Rheumatic fever

• Haemarthrosis

Management
Acute Attack
NSAIDs – Any can be used but aspirin should be avoided because it causes uric acid retention unless
given in very large doses.

Selective COX-2 inhibitors e.g. Etoricoxib 120 mg o.d. or Valdecoxib 20–40 mg b.d. Advantage is low risk
of GI toxicity.

Colchicine 0.5 mg p.o. every 2 hours, up to 4-6 mg/day is now reserved for patients without renal,
hepatic or bone marrow disease, in whom the more effective NSAIDs are contraindicated or poorly
tolerated.

Corticosteroids – In patients with acute microcrystalline synovitis in whom neither NSAID nor colchicine
are recommended, e.g. elderly people and those with renal insufficiency, hepatic dysfunction, cardiac
failure, peptic ulcer disease.

Long-term
Management with drugs that lower serum urate : Indications –

• Recurrent attacks

• Evidence of tophi or chronic gouty arthritis

• Associated renal disease

• Young patient with high serum uric acid and family history of renal or heart disease

• Normal levels of serum uric acid cannot be achieved by lifestyle modifications (gradual weight loss,
and restriction of alcohol and food with high purine content)

Allopurinol – is the drug of choice. It lowers serum uric acid by inhibiting xanthine oxidase, which is
responsible for conversion of xanthine and hypoxanthine to uric acid. Kidney function should be checked
before the drug is started.

Uricosuric agents – Probenecid or sulfinpyrazone as an alternative to allopurinol with colchicine if renal

function is not impaired. Contraindications:

(a) Gout with overproduction of uric acid and gross uricosuria

(b) Patients with kidney failure

(c) Presence of urate urolithiasis.

Benzbromarone – 100 mg daily in those with moderate renal impairment when other uricosuric agents
are ineffective and there is allopurinol hypersensitivity.

SLE
• Systemic lupus erythematosus is a multisystem autoimmune disease with protean clinical
manifestations that may affect any organ or system.

• The disease is characterized by flares, remissions and autoantibodies directed against several
intracellular and cell-surface antigens.

• Prevalence is 0.2% in Afro-Caribbeans and 0.03% in Caucasians. Several autoantibodies are

associated with SLE.

Clinical features
Fever, weight loss and mild lymphadenopathy occur during flares of disease activity, fatigue, malaise
and fibromyalgia like symptoms are not particularly associated with active disease.

Arthritis : This is a common symptom occurring in 90% of patients and often associated with early
morning stiffness. Tenosynovitis may also be a feature but clinically apparent synovitis with joint
swelling is rare.
Raynaud’s phenomenon : Arthralgia or arthritis in combination with Raynaud’s phenomenon is the
most common presentation of SLE.

Skin : Three types of rash are characteristic : ● The classic butterfly (malar) facial rash ● The subacute
cutaneous lupus erythematosus (SCLE) rash ● The discoid lupus rash

Kidney : The typical renal lesion is a proliferative glomerulonephritis characterised by haematuria,

proteinuria.

Cardiovascular : Pericarditis is the most common feature. Myocarditis and Libman–Sacks endocarditis
also occur.
Lung : Pleurisy can cause pleuritic chest pain, a rub or a pleural effusion.

Neurological : Cerebral lupus causes visual hallucinations, chorea, organic psychosis, transverse myelitis
and lymphocytic meningitis.
GI : Oral ulcers are common.

Investigations
• Blood should be sent for haematology, biochemistry, ANA, antibodies to extractable nuclear
antigens, and complement levels.

• Patients with active SLE almost always test positive for ANA, but ANA-negative.

• Patients with active disease tend to have low C3 and C4 but this may reflect inherited
complement deficiency that predisposes to SLE.
 • A raised ESR, leucopenia and lymphopenia are typical of active SLE as are anaemia, haemolytic
anaemia and thrombocytopenia.

• CRP is often normal in active SLE except in the presence of serositis, elevated CRP suggests
coexisting infection.

Management
• Patients should avoid sun exposure and should apply high-factor sun blocks.

• Mild disease : Disease restricted to skin and joints may require only analgesics, NSAIDs and
hydroxychloroquine. Short courses of oral prednisolone may be needed for flares of disease
(e.g. synovitis, pleuro-pericarditis).
• Life-threatening disease (e.g. renal, cerebral, cardiac) : This requires high-dose corticosteroids
(IV methylprednisolone) in combination with IV cyclophosphamide, repeated at intervals of 2–3
wks. Haemorrhagic cystitis and Pneumocystis pneumonia are important complications of this
treatment.

• Maintenance therapy : Azathioprine, methotrexate and MMF are used for maintenance.
Patients with thrombosis and the antiphospholipid syndrome require lifelong warfarin.

OSTEOPOROSIS
• Osteoporosis causes bones to become weak and brittle, so brittle that a fall or even mild
stresses such as bending over or coughing can cause a fracture. Osteoporosis -related fractures
most commonly occur in the hip, wrist or spine.

• There typically are no symptoms in the early stages of bone loss.

Classification
1. Primary osteoporosis
• This is the most common type of osteoporosis and occurs more in women than men. Peak bone
density (mass) is reached between the ages of 25 and 30. With increased bone loss, the rate of
bone generation will also decrease.

• The chances of developing osteoporosis depend on the density of one’s bones earlier in life.
Diet, health and physical exercise will also determine bone density (to a degree) throughout
life.

2. Secondary osteoporosis
• Secondary osteoporosis occurs as a result of certain medical conditions such as leukaemia,
hyperthyroidism or hyperparathyroidism.
 • This type of osteoporosis may also result from taking certain medications that lead to the
breakdown of bones, these include high-dose inhaled or oral corticosteroids that have been
used for longer than six months. Secondary osteoporosis can affect anyone at any age.

3. Osteogenesis imperfect
• This is an extremely rare type of osteoporosis that causes the bones to fracture with no logical
reason. Osteogenesis imperfecta is seen at birth.
4. Idiopathic juvenile osteoporosis
• This type of osteoporosis is also very rare and affects children who are between eight and 14
years old (a time of rapid growth in a child’s life).
Pathogenesis
Age 51-70 yrs

Estrogen deficiency Other factor

Increases bone loss

Decrease PTH secretion

Decrease 125 (OH)2 D3 production

Decrease calcium absorption

Clinical features

• Osteoporosis is asymptomatic until a fracture occurs. The most common sites are the forearm
(Colles fracture), spine (vertebral fractures causing back pain, height loss and kyphosis) and
femur (hip fracture)

• Back pain, caused by a fractured or collapsed vertebra

• Loss of height over time

• A stooped posture

• A bone that breaks much more easily than expected

Risk factors
• Sex hormones : Lowered sex hormone levels tend to weaken bone. The fall in estrogen levels in
women at menopause is one of the strongest risk factors for developing osteoporosis.
Treatments for prostate cancer that reduce testosterone levels in men and treatments for
breast cancer that reduce estrogen levels in women are likely to accelerate bone loss.

• Thyroid problems : Too much thyroid hormone can cause bone loss.

• Other glands : Osteoporosis has also been associated with overactive parathyroid and adrenal
glands.

• Low calcium intake

• Eating disorders

• Gastrointestinal surgery

• Long-term use of oral or injected corticosteroid medications

• Seizures

• Gastric reflux

• Cancer

• Transplant rejection

Investigations
• BMD is measured using dual energy X-ray absorptiometry (DEXA) of the lumbar spine and hip.
DEXA should be performed in patients sustaining low trauma fractures or other features of
osteoporosis.

• The T-score measures by how many standard deviations the patient’s BMD value differs from
that of a young healthy control.

• The Z-score measures by how many standard deviations the BMD deviates from that of an age-
matched control. Osteoporosis is diagnosed when the T-score value falls to −2.5 or below.

• T-scores between −1.0 and −2.5 indicate osteopenia, and values above −1.0 are regarded as
normal.

• If osteoporosis is confirmed by bone densitometry, any predispos- ing factors should be sought.
Relevant blood tests include: ● U&Es, calcium, phosphate ● TFTs ● Immunoglobulins ● ESR ●
Anti-tissue transglutaminase (for coeliac disease) ● 25(OH) vitamin D ● PTH ● Sex hormone and
gonadotrophin levels
Management
• Patients with osteopenia should be given lifestyle advice :

• Cessation of smoking

• Limitation of alcohol intake

• Adequate dietary calcium intake (1500 mg daily)

• Regular exercise

• Osteopenic patients should be offered a repeat BMD measurement in 2–3 yrs

• Pharmacological treatment is indicated in those with T-scores below −2.5, steroid-treated

patients with T-scores between −2.5 and −1.5, and patients with non-traumatic vertebral
fractures

• Bisphosphonates are first-line drugs in the treatment of osteoporosis

• Calcium (500 mg daily) and vitamin D supplements (800 U daily) are used as an adjunct to other
treatments. They do not reduce fracture risk in osteoporosis when given as monotherapy

• Strontium ranelate inhibits bone resorption and increases BMD. It is effective in secondary
prevention of vertebral and non-vertebral fractures in post-menopausal women but can cause
diarrhoea and thrombosis

• HRT with oestrogen and progestogens prevents post-menopausal bone loss and reduces
vertebral and non-vertebral osteoporotic fractures. It is mainly used to prevent osteoporosis in
women with an early menopause

OSTEOMALACIA
• Osteomalacia means "soft bones."

• Osteomalacia is a disease that weakens bones and can cause them to break more easily. It is a
disorder of decreased mineralization, which results in bone breaking down faster than it can re-
form. It is a condition that occurs in adults.

Causes
• Deficiency of vitamin D or defects in vitamin D metabolism

• Hypophosphataemia

• Drug-induced inhibition of bone mineralization

• Certain surgeries

• Celiac disease
 • Kidney or liver disorders

Pathophysiology
• Reduced activated vitamin D

• Reduced intestinal absorption of calcium and excessive loss of calcium from the body

• Low serum calcium and phosphate

• Demineralisation of bone (calcium resorption) with softening, weakening, deformity, fracture

• Muscle weakness

Clinical features
• Diffuse joint and bone pain (especially of spine, pelvis, and legs)
• Muscle weakness

• Difficulty walking, often with waddling gait

• Hypocalcemia (+ve Chvostek sign)

• Compressed vertebrae and diminished stature

• Pelvic flattening
• Weak, soft bones

• Easy fracturing

• Bending of bones

• Proximal muscles are weak, and there is difficulty in climbing up stairs and getting up from a
squatting position
• Physical signs include deformities like triradiate pelvis and lordosis. The patient has a typical
“waddling” gait

Risk Factors
• Malnutrition

• Malabsorption / Postgastrectomy

• Renal defects

• Decreased solar exposure

• Darker skin more susceptible

• Geriatric patients Medications
Diagnosis
1. Biochemistry

(a) Plasma calcium low or normal

(b) Serum phosphate raised

(c) Raised alkaline phosphatase

2. Radiography – Looser’s zones, linear areas of defective mineralization especially in long bones, pelvis
and ribs

3. Therapeutic trial – Response to vitamin D or one of its active metabolites.

Management
• Rickets and osteomalacia caused by vitamin D deficiency respond rapidly to oral vitamin D and
calcium supplementation. Higher doses may be required in patients with malabsorption.
• Osteomalacia due to renal failure and vitamin D-resistant rickets type I requires treatment with
active vitamin D metabolites (1-α-(OH)D3 or 1,25(OH)2D3) since these bypass the defect in 1-α-
hydroxylation of 25(OH)D3.
• Serum calcium and alkaline phosphatase should be mon- itored to assess response to
treatment.

RICKETS
• Rickets is the softening weakening of bones in children, usually because of an extreme and
prolonged vitamin D deficiency.

Etiology
Age – From 4 months to 2 years, also in prematures.
Diet – Less common in breastfed infants, may develop if mother’s diet is poor.
Growth – Rickets will only develop if growth is taking place, marasmic infants are seldom rachitic, but as
soon as the infant begins to put on weight rickets is likely to develop. Dark-skinned infants more prone,
lack of adequate exposure to sunlight.

Classification
• Dietary deficiency of vitamin D (inadequate intake of Calcium, vitamin D exposure to sunlight).
• Secondary rickets: due to malabsorption, e.g. coeliac disease.
• Resistant rickets: Resistance to therapeutic doses of Vitamin D, e.g. familial hypophosphatemia rickets
or Vitamin D dependent rickets.
• Renal rickets (Poor conversion of 25 OH-D3 to 1.25-dihydroxy D3 – active principle of vitamin D3) in
Chronic kidney failure.
• Malignancy – Tumour-based rickets.Hereditary forms – (i) Vitamin D-dependent rickets (VDDR) –
deficiency of 1-hydroxylase enzyme, autosomal recessive, low calcium type. (ii) Vitamin D Resistant
Rickets (VDRR) – Primary defect is phosphorus wasting by proximal tubule (low phosphorus type).
Clinical Features
1. Head
• Apparently larger than normal in horizontal diameters, forehead prominent (frontal bosses) and
occiput and vault flattened out, hot-cross bun appearance, posterior portion of the skull in the
first year may have demonstrable softening on pressure (ping-pong resilience, craniotabes).
• Face appears small
• Upper jaw being narrow, temporary teeth usually appear late. Excessive sweating over
forehead.

2. Thorax
• Beading of ribs at the junction of ribs with costal cartilages, best developed in the 4 th, 5th and 6th
ribs just external to the nipple – rachitic rosary. Sternum unduly prominent producing a “pigeon
breast”.
• The diaphragm below which there is a flaring of the ribs (Harrison’s groove), occasionally funnel
shaped depression of lower part of sternum.
3. Spinal column
• Kyphosis due to weakness of muscles, which disappears if child is suspended from armpits.
4. Extremities
• Metaphyseal enlargement at wrists and ankles; knock-knee and bow legs; coxa vara, curving of
bones of forearm outwards.Multiple Greenstick fractures in severe rickets.
5. Ligaments and muscles
• Relaxed and weak, hence deformity of spine, late standing and walking and over extension of
knee joints – “acrobatic rickets”.
6. Digestive system
• Pot-belly due to weakness of abdominal muscles, and ptosis of liver and spleen.
7. Nervous symptoms
• Restlessness at night with rocking of head on the pillow. Predisposition to tetanic convulsions.
8. Respiratory system
• Adenoid and tonsillar hypertrophy, rhinitis, pharyngitis, bronchitis and bronchopneumonia
common.

Diagnosis
Early signs of rickets
(a) Restlessness and irritability
(b) Sweating of head
(c) Head rolling
(d) Craniotabes.
(e) Beading of ribs
(f) Anterior fontanelle noticeably big
(g) Enlargement of metaphyses at the wrists
(h) Delay in dentition
1. Radiology
• Loss of zone of provisional calcification and widened growth plate
• Fraying of metaphysis – metaphyseal margins tend to be blurred and indistinct
• Splaying (widening of the metaphysis) and cortical spurs
• Cupping of the metaphysis
• Rachitic rosary
• Bowing of tibia (in long standing cases)
2. Laboratory
• Increased alkaline phosphatase in plasma earliest change.
• Low concentration of phosphorus except in late renal osteodystrophy where it may be high
• Calcium level may also fall in tetany though it is usually normal, low in VDDR, can fall with
infections, high phosphorus diet, alkali administration, administration of low doses of vitamin D
• Generalized aminoaciduria except in VDDR.

Management
1. Administration of vitamin D
(A) Ordinary case of rickets – 1200–2000 units per day.
1. Fish oils – Fish liver oils contain Vitamin D3. The fat of the oil is a valuable addition to the diet.
(a) Cod liver oil – 1 teaspoonful (containing about 400 units of vitamin D3) three times a day. (b) Halibut
liver oil – 10 times more potent than cod liver oil.
2. Vitamin D milk
(a) Fortified milk
(ii) Irradiated milk standardised to contain 400 IV of Vitamin D3 per quart.
(c) Fortified fish oils – Calciferol has been added to fish oils to enrich their Vitamin D content.
(d) Exposure to sunlight daily for at least 1–2 hours.
(e) Massive doses of vitamin D (Stoss regime) – 600,000 IU of Vitamin D (15 mg calciferol) in oil solution
intramuscularly or by mouth.
(B) Refractory rickets – Vitamin D dependent rickets – 40,000 units daily. Vitamin D resistant
(hypophosphataemic) rickets – 400,000 units daily.
2. Calcium : Not usually necessary except in tetany. In acute convulsions 2 ml/kg calcium gluconate
10% IV.
3. Use of cereals : In diet should be restricted because phytate of cereal combines with calcium to
form an insoluble compound which is passed out in the faeces.
 SKIN
PSORIASIS

• A chronic, recurrent, inflammatory disease of the skin of unknown origin, characterized by well-
circumscribed erythematous, dry plaques of various sizes, covered with mica-like scales.

Etiology
Genetic factors
• Identical twins have a concordance rate of 50–70%. There is a strong association of the disease
with HLA-Cw6, and weaker associations with HLA B13, B17 and DR7.

• Both HLA associations and a family history of psoriasis are more common in patients who
develop the disease before 40 years of age.

Environmental factors
• Attacks of psoriasis can be precipitated or aggravated by stress, infection (streptococcal, HIV),
pregnancy, trauma, drugs (chloroquine/antimalarials, lithium), alcohol, tobacco smoking,
sunlight.

Pathogenesis
• Psoriasis results from a polygenic genetic disposition and an environmental trigger.

• Key components of the pathogenesis are potential therapeutic targets.

(a) Activated T lymphocytes – appear to be important in all phases of the disease process (initiation,
maintenance and resolution). Patients with psoriasis who undergo bone marrow transplantation from a
healthy donor sometimes experience long-term remission.

(b) T-helper lymphocytes migrate from blood vessels into the skin, where they interact with antigen-
presenting cells and then become activated into a T-helper type 1 phenotype, proliferate and release
various cytokines and chemokines which attract and activate T-cytotoxic lymphocytes.
(c) Interferon-α and tumour necrosis factor (TNFα) are released by immune cells, further promoting
inflammation and development of psoriatic lesions.

(d) Epidermal cells overlying the inflammatory process proliferate and turn over at four times the
normal rate, resulting in thickening of the epidermis with overlying scales. In the upper epidermis
proliferation of vessels occurs.
Classification
1. Plaque psoriasis :
• It is the most common type of psoriasis. It is also known as psoriasis vulgaris. It appear as a
raised, inflammed, red skin covered by silvery patches or scales.

• Sites : Elbows, Knees, sacrum, Scalp, lower back, hands and feet.

2. Guttate psoriasis (Latin Gutta-drop)

• Characterized by eruption of small (0.5 to 1.5 cm in diameter) papules over the upper trunk and
proximal extremities.

• Manifests at an early age. Streptococcal throat infection frequently precedes or is concomitant

with the onset or flare.

3. Pustular psoriasis
• It is usually uncommon but mostly appear in adult. It appear as pus filled lesion surrounded by
red skin.

• It appear mostly at hands and feet. It is the serious condition so immediate medical attention is
required.

Erythrodermic psoriasis
• The disease affects all body sites. Erythema is the most prominent feature with superficial
scaling / peeling that may appear like burning.

• Causes : sun burn, allergic Reaction, strong coal Product use

Clinical manifestation
o The patches of skin dry, swollen and inflamed covered with silver white flakes Raised and thick
skin.
o Pain, itching and burning
o Restricted joint motion or pain Cracked and bleeding skin

o Dandruff on scalp
o Pus filled blisters
o Genital lesions in males

o Pitting, small depression on the Surface of the nail Yellow, dicsolored nail
o Koebner phenomenon
o Arthritis
Diagnostic Investigations
• Collect history

• Physical examinations

• Skin biopsy under local anesthesia

• Blood and radiography test was done to rule out psoriatic arthritis (ESR. C- ReactiveProtein)

Management
I. Topical therapies
1. Topical corticosteroids – Potent category (e.g. clobetasol) applied BD to localised lesions. Overnight or
occlusive therapy will initiate involution in most cases. Hydrocolloid dermatological patches can be
applied over steroids on localised psoriatic plaques for 2 to 7 days.

2. Topical Vitamin D analogues – Calcipotriol ointment, cream or lotion is applied BD. Dose should not
exceed 100 g/week because of risk of hypocalcemia and kidney stones.

3. Topical tazarotene gel and cream (0.05% and 0.1%) to minimise irritation – (i) Tazarotene should be
applied to the affected skin only at bedtime, with protection of normal skin with vaseline. (ii) Apply a
mid to high potency steroid in morning.

4. Coal tar therapy (3–6% crude coal tar) can be combined or alternated with topical corticosteroids. The
patient should apply a corticosteroid cream with or without occlusion during the day tar overnight, and
UVA exposure in morning.
6. Exposure to sunlight or UVB from the point of mild erythema and induce flattening or clearing of
many lesions.

Treatment of Severe or Widespread Involvement

1. Aggressive UVB pototherapy 5 times a week or daily most effective single agent therapy.

2. Photochemotherapy – Psoralen plus PUVA – 10 to 20 treatments are required.

3. Combined therapy for clearing resistant and wide spread disease twice weekly UVB with one weekly
methotrexate for 8 week.

II. Oral systemic agents

1. Acitretin – A synthetic vitamin A is effective in pustular, guttate and erythrodermic psoriasis. Dose 10–
20 g/day with maximum 50 mg/day.
2. Antimetabolite therapy

(i) Methotrexate oral or IM Dose – Initial 7.5 mg/week with increase of 2.5 g/week as tolerated

(ii) Cyclosporine 3.5 g/kg/day

Other agents – (i) Mycophenolate mofetil 500 mg QDS

Scalp care:

(i) Mild case – Tar shampoo (10%) or steroid containing shampoo

(ii) Severe case – Removal of scales and application of keratolytic gel and then covered with occlusive
plastic shower cap for several hours or overnight.

Nail care :

(i) Removal of subungual debris and application of corticosteroids under occlusion

(ii) Injection of triamcinolone (0.1 mL of 3 mg/mL) into the nail bed at 2–3 week intervals.

Special Groups
Psoriasis in childhood : Topical corticosteroids should be avoided. Phototherapy is effective, but
exposure to ultraviolet light is kept to a minimum. Retinoids or cyclosporine are the systemic agents of
choice.
Psoriasis in pregnancy : Retinoids are best discontinued in female patients after puberty because of the
risk of teratogenicity. Pregnancy should be avoided within 2 years of taking acitretin.

Eczema
• Dermatitis is a group of inflammatory skin dz provoked by wide variety of stimuli including direct
injury from toxic chemicals, mechanical trauma & immunological reactions.
• Eczema – Greek word (eczein : to boil over and effervescence)

• The term dermatitis and eczema are often used as synonyms but the term eczema is preferably
used for exudative dermatitis.

Etiology
1. Predisposing factors

o Idiosyncrasy
o Familial predisposition
2. Extreme heat and cold

o Trauma
o Warm humid condition
o Infection

o Psychogenic

Stages
1. Acute eczema
 o Wet dermatitis

o Intense pruritus, erythema, oedema, papules, vesicles, oozing, crusting

o Blister formation
2. Subacute eczema

o Diffuse erythema, oedema & scaling

o In this stage, oedema, vesiculation & oozing components come down

3. Chronic eczema

o Severe itching
o Hyperkeratosis & lichenification

Classification
Endogenous Exogenous
Cause : Problem arise from pts inherent Cause : Is result of exposure of pts skin to
constitutional factor rather than environment. environmental noxious agent

Atopic dermatitis Contact dermatitis : Irritant & Allergic

Seborrhoeic “ Photo “ : Phototoxic & Photoallergic

Nummular “ Infectious : Eczematoid dermatitis

Asteatotic “
Stasis “
Juveline & lichen simplex “

ATOPIC DERMATITIS
• Atopic dermatitis (atopic eczema) is a common endogenous form of dermatitis and usually
begins in childhood. It is an itchy, chronic and relapsing dermatitis.

Pathogenesis
• Atopic dermatitis depends on a complex interaction between genes and environment.

• Genetic studies have shown linkage in three loci, but the environment in early life also has a
profound influence on the immune over-activity that develops in this condition.

• An ‘imbalance’ in the immune system with preferential activation of Th2 CD4 lymphocytes
seems to be a crucial step in the development of atophy.

Clinical features
 • Acute dermatitis : Red, wet, weepy vesicles

• Subacute dermatitis : Red, dry, scaly

• Chronic dermatitis : Dry, thickened excoriated

Distribution : In infants eczematous lesions are often present on exposed areas such as the cheeks, or
outer aspects of forearms. In older child, eczema usually affects flexural sites such as the front of the
elbows and popliteal fossa.

Variants : Follicular eczema may occur, especially in dark skin. Discoid eczema is a morphologically
variant seen in all racial groups. It presents as itchy, well-circumscribed, crusted lesions, often on the
limbs.

Diagnostic criteria
• An itchy skin condition (or parenteral report of scratching or rubbing in a child)

• Onset in infancy

• History of skin creases involvement (including cheeks) in children under 10 years

• History of generally dry skin in the past year

• Other atopic features (or history of any atopic disease in a first-degree relative in children under
4 years)

• Visible flexural dermatitis (or dermatitis of cheeks/forehead and outer limbs in children under 4
years).

Investigations
• These may reveal peripheral eosinophilia, raised serum IgE to a variety of common
environmental agents (detected by radioallergosorbent tests or skin-prick tests).

Management
1. Avoiding irritants and allergens : Use of cotton clothes and bedding covers. Families should be advised
not to keep cats or dogs. Swimming can worsen dermatitis because of irritant effect of chlorine.

2. Dietary manipulation : Standard dermatitis therapies usually control the dermatitis without the need
for dietary change.

3. Emollients and washing : Regular bathing to remove skin debris and crusts. Soaps should be avoided;
bath oil and soap substitutes such as aqueous cream prevent the skin drying out.

4. Corticosteroids : On inflamed skin only. Mild corticosteroids on face and under the nappy, and
moderate strength on body.
5. Non-steroidal topical therapies : These drugs inhibitor production of the proinflammatory cyclin
interleukin-2 (IL-2), reduce lymphocyte proliferation and activation, down-regulate high-affinity IgE
receptor expression on Langerhans cells, and reduce IgE-induced mediator release from mast cells and
basophils.

6. Adjunct therapies

a. Antibiotics for infected dermatitis. Recurrent infections may be treated with antiseptic bath oil and
emollients. For eczema herpeticum oral acyclovir can be given IV if child is unwell.

b. Antihistamine do not help because the itch of eczema is not histamine-mediated.

7. Systemic therapies are used because atopic dermatitis can prevent sleep, disrupt social and
educational development and cause growth retardation.
8. Complementary therapies – Psychotherapy, hypnotherapy and acupuncture can help patients relax,
and may assist in breaking the itch-scratch cycle in some.

COMPLICATIONS
• Bacterial infection because bacteria adhere well to scaly, inflamed skin. It is usually not
associated with pyrexia and malaise.

• Eczema herpeticum describes a widespread herpes simplex virus infection of atopic skin with
swinging pyrexia, malaise and occasionally severe morbidity.

• It presents with clusters of vesicles particularly on face, but can occur anywhere.

SEBORRHOEIC DERMATITIS
• Is common chronic inflammatory disorder characterized by a greasy scales overlying
erythematous macules, papules, patches or plaques with characteristic distribution of
lesions in areas rich in sebaeous glands.

Causes
• Yeast : Malasseria further
• Bimodal occurrence : manifest in early infancy & adult life

• Pityriasis capitis (dandruff) - mildest form of the disease

• In adults - red scaly areas associated with whitish / yellowish fine greasy scales

• Area of involvement : Scalp, eyebrows, nasolabial folds, pre-sternal area of chest, axilla,
groins

• Pruritis is common

Management
• Dandruff treatment with shampoo containing selenium sulfide, zinc pyrithione
 • Treatment of mild to moderate cases - topical steroids, tropical antifungal agent

INFANTILE ECZEMA/DERMATITIS
• Rash starts on the cheeks but may occur on any part of the body. Generally the nappy area is
spared. Initial lesions are oedematous, erythematous papules which may become confluent.

• They are often markedly excoriated with exudation and crusting. When the dermatitis flares,
intermittent morbilliform erythema may appear on the trunk.

• Secondary infection and lymphadenopathy often occur.

Other patterns of eczema

o Infantile seborrhoeic dermatitis

o Pityriasis alba

o Lip-licking dermatitis

o Juvenile plantar dermatosis

o Napkin dermatitis (Napkin rash)

o Stasis dermatitis

Treatment : Emollients occ 1% hydrocortisone ointment

CONTACT DERMATITIS
• Contact dermatitis is an eczematous eruption caused by external agents.

• Contact dermatitis often exacerbates pre-existing endogenous eczema.

• Causes can be broadly divided into irritant substances that have a direct effect on the skin and
allergic chemicals with which dermatitis follows delayed type IV cell-mediated hypersensitivity
reactions.

1. Irritant contact dermatitis

• Any physical or chemical agent that is capable of producing, if applied for sufficient time and in
sufficient concentration can lead to irritant dermatitis.

• Dermatitis occurs when the repair capacity of the skin is exhausted or when the penetration of
chemicals excites an inflammatory response.

• It is often occupational in origin, the most common industries are those in which workers
engage in wet-work (e.g. hair dressing, cleaning, metal engineering, food processing, fishing).
 • Pre-existing dermatitis (particularly of the hands) of an atopic nature is a strong risk factor for
developing irritant contact dermatitis. Common irritants include :

o Solvents

o Rubbing alcohol

o Shampoos, Permanent wave solutions

o Saw dust or Wool dust

o Fertilizers and Pesticides

Diagnosis
• Sharp demarcation in the distribution of the dermatitis.

• Definite history

• Patch-testing : The allergens are applied on day 1, left on for 48 hours and then removed;
readings are taken at 48 and 96 hours. Care must be taken to ensure that the allergens do not
cause false-positive irritant reactions.

Management
(a) Elimination of causative factors.

(b) Topical corticosteroids with emollients and soap substitutes when appropriate

(c) Immunosuppressant (cyclosporine, azathioprine) for very resistant cases.

2. Allergic contact dermatitis

• It is type IV / delayed type hypersensitivity reaction mediated by T- lymphocytes against certain
chemicals coming in contact with the skin.
o Metals (chrome, Nickel)
o Plants (Grass)
o Rubber chemicals

o Hair dyes
o Fragnance
o Medication – Topical corticosteroids & Lanolin

o Anti bacterial agents (Neomycin, Nitrofurazone)

o Direct or Airborne contact
o Cosmetics
Mechanism
Simple chemicals with are allergen or haptens

Hapten confine with epidermal cell protein

Fall allergens

(Epidermal carrier protein complex)

Epidermal Langerhans cell progress allergen and present it to T lymphocyte

Release IL-1

IL-2/ T-cell

IL-2 promote proliferation & activation of T-cell

Re-exposure of same allergen in sensitized person

Activated T-cell migrate to skin

React with allergens

Release lymphokinase

Cause inflammatory response

Allergic contact dermatitis

Clinical features
Acute : Redness, swelling with ill-defined margins

Papules, vesicles, large blister

Exudation & cracking & Scaling

Chronic : Present above all features less vesicular and exudative

Lichenification : Dry leathery thickening with increased skin marking

P/H or F/H : Atopy, Food allergy

Asthma, Allergic Rhinitis

Investigations
• Patch test – Allergic dermatitis

• IgE – Atopic dermatitis to determine specific environmental allergens

Eg : Horse hair, House dust mite, Pollens & food

• Prick test – Atopic

• Bacterial & Viral culture – useful in secondary infection

Management
• Explanation, Reassurance, Encouragement

• Avoidance of contact dermatitis

• Regular use of greasy emollients

• Appropriate use of topical corticosteroids

• Sedative Antihistamine, Systemic corticosteroids

Prevention
• Avoid contact

• Maintain strict hygiene

• Avoid scratching

• Cut nails
SCABIES
• A contagious disease caused by a mite Sarcoptes scabiei is spread through contact with infected
individuals or rarely through contact with infected clothes, bed linen or towels.

• Scabies is contagious and can spread quickly through close physical contact in a family, child
care group, school, class or nursing home.

Life Cycle
• The fertilized female excavates a sloping tunnel (burrow) in the stratum corneum depositing
eggs and then dying in the burrow.

• The larvae emerge from the eggs after 3–7 days wander to the skin surface and form shallow
pockets in the horn of the original or a new host and reach maturity 14–17 days after the eggs
were laid.

• Copulation occurs in the pocket and the female excavates her burrow while the male soon dies.
In children palmar involvement is common. Total number of mites is 10–15 ovigerous females.

Pathophysiology
• The symptoms are caused by an allergic reaction of the host’s body to mite proteins not exactly
known.

• The mite proteins are also present from the gut, in mite feces, which are deposited under the
skin.

• The allergic reaction is both of the delayed (cell-mediated) & immediate (antibodymediated)
type, & involves IgE presumed to mediate the very rapid symptoms on reinfection.

• The allergy-type symptoms (itching) continue for some days, and even several weeks, after all
mites are killed.

• New lesions may appear for a few days After mites are eradicated. Nodular lesions from scabies
may continue to be symptomatic for weeks after the mites have been killed.

Clinical Features
Pruritus : The sole complaint is severe itching worse at night. Itching starts two to four weeks after the
contagion, this time lag being required for the development of lesions other than the burrow.

Burrow : It is the diagnostic sign of scabies. It is a slightly elevated greyish tortuous or dotted line in the
skin ridge. It represents a tunnel made by the female mite in the horny layer of the skin in which to lay
her eggs. Burrows are best seen in the soft parts of the skin, such as the hands, feet, penis and scrotum.
Scratching destroys the roofs of the barrows and mites, keeping the population under control.
Rash : During the initial phase of infection, the host is asymptomatic but after 4–6 weeks a
hypersensitivity response to mite antigen occurs and an itchy rash develops. The rash comprises tiny
inflammatory papules which occur predominantly in the interdigital folds of hand, around the axillae, in
the periareolar regions, on the abdomen (particularly the periumbilical region) and on the buttocks and
medial aspects of thighs, legs and feet. In males inflammatory papules on penis and scrotum, which are
pathognomonic of scabies.

Complications
1. Eczematization : It is common in infants and young children. Involved areas of the extremities and
trunk show erythema, oedema, vesiculation, oozing and crusting.

2. Secondary infection : Secondary bacterial infection (Strepto or staphylococcal) may occur in case of
untreated scabies. The existing lesions turn into pustules and even bullae which when they burst are
covered with yellowish crusts. Scratching results in excoriations.

3. Id eruption

4. Urticaria
5. Contact dermatitis to antiscabietic drugs.

Variants of Scabies
1. Scabies in the clean – These have fewer lesions, some of which are at atypical sites, but cause severe
itching.
2. Scabies incognito – occurs in persons treated with steroids.

3. Nodular scabies –Red pruritic nodules are often found on the genitals. Scabietic nodules often do not
contain mites.
4. Genital scabies – In males there are inflammatory papules on the penis and scrotum which are
pathognomonic of scabies.

5. Norwegian (crusted) scabies–The crusts and psoriasis form scales, loaded with scabies mite affect the
hands, scalp, face and trunk. Itching may be minimal. Susceptible individuals are only marginally
immunosuppressed and may simply be elderly, or pregnant.
6. Scabies in AIDS is more severe and extensive with involvement of face and scalp.

7. Paraphimosis may be a complication in children.

Diagnosis
History of similar illness in other members of the family. Characteristic distribution pattern of lesions.
Itching worse at night.

Diagnosis is made by de-roofing a burrow with an oil-coated needle and examining scrapings for mites
and their ova microscopically.
Management
• All the family members should be treated at the same time.

• The clothes, bed linen and towels should be disinfected.

• Secondary infection should be treated first.

• Specific therapy – The patient must bathe and scrub the body with a brush to lay open the
burrows. After the bath, the skin is dried and the scabicide applied from neck to toes.

• Treatment of infants – If benzyl benozoate is used, it should be diluted with 2 or 3 parts water to
reduce its irritancy. Permethrin dermal cream can be used on the necks and hand area.

• Treatment of crusted scabies is as for ordinary scabies, but several applications of scabicide are
necessary. Oral Ivermectin may be useful in resistant cases.

URTICARIA
• Urticaria (nettle rash, hives) presents with short-lived, itchy wheals which may be pale or pink in
the centre, surrounded by a red flare.

• Urticaria is divided into acute less than 6 weeks, and Chronic forms for more than 6 weeks.

• Deeper swellings of the skin or submucosa are termed ‘angio-oedema’. They are usually in the
mouth, on the eyelids or on the genitals, but may occur anywhere on the skin.

Causes
• Drugs : Penicillin, sulphonamides, aspirin, etc.

• Foods : Milk, moong dal, masoor dal, eggs, peas, fish.

• Physical causes : Dermographism, pressure urticaria, cold or heat or solar urticaria.

• Inhalants : Pollens, fungi, insecticides, house dust.

• Infections and infestations : Chronic septic focus, UTI, virus infection, candida infection,
protozoal and helminthic infections.

• Food additives : Yeasts, citric acid, azo dyes, benzoic derivatives.

Pathogenesis
• Urticaria is caused by transient leakage of plasma through small blood vessels, usually as a result
of release of histamine through skin mast cells.
 • There are many causes of this including type I hypersensitivity reactions. Histamine also causes
itch, by stimulating nerve receptors.

• Other mediators causing vasopermeability include kinins in hereditary angioedema, and

leukotrienes in pseudoallergic reactions caused by aspirin and NSAIDs.

TYPE INVESTIGATIONS

Ordinary urticaria Skin prick test / RAST

Acute (< 6 weeks) Autologous serum skin test
Chronic (>6 weeks)

Physical urticaria Ice / overheating / skin stroking

Cold / Cholinergic / Dermographism Sustained local pressure
Delayed pressure

Contact urticaria Skin prick test / RAST

Immunological Skin rechallenge

Non-Immunological

Urticarial vasculitis Skin biopsy, serum C3,C4

Angio-oedema without wheals C1 esterase inhibitor, C4

Idiopathic
C1inhibitor deficiency
Drug-induced (angiotensin converting enzyme
inhibitors, aspirin)

Clinical features
• Various itchy and swelled hives may combine to form one big rash

• Batches on face, arms legs or shoulder

• Burning sensation around the cheeks hands, eye, lips, feet and genitals

• Welts of different sizes

• Tightness in chest

• Difficulty in bathing

• Tongue or throat swelling

Management
Histamine-mediated urticaria
1. Remove identifiable cause

2. Non-drug therapy
o Explanation and information

o Cooling lotions (e.g. calamine, 0.5% menthol in aqueous cream)

o Avoid aspirin, NSAIDs, codeine, ACEHs

o Minimize stress, over-eating, alcohol

o Exclusion diet when indicated by history

3. Pharmacological therapy

First line – All patients

o Non or low-sedating antihistamine (cetirizine or loratadine 10 mg/day)

o If little or no response, add sedating H1 antihistamine at night

o If little or no response add H2 antagonist (e.g. ranitidine)

Second line – special indications

o Prednisolone 0.5 mg/kg stat or a tapering regimen over 1–2 weeks (in severe or delayed
pressure urticaria) for short-term use

o Adrenaline 0.5–1 mL of 1:1000 Im or SC in severe throat angio-oedema

Third-line – specialist use only

o Immunotherapies – plasmapheresis or IV immunoglobulin, or cyclosporine (if severe refractory

autoimmune urticaria)

Immune complex mediated urticaria

o Antihistamines are often ineffective in urticarial vasculitis.

o Corticosteroid-sparing drugs to minimize or replace long term oral corticosteroid exposure –

dapsone 75–150 mg/day, indomethacin 25–50 mg t.d.s., hydroxychloroquine 200–400 mg/day,
azathioprine 2–2.5 mg/kg/day, and colchicine 0.5–2 mg/day.

o Management of chronic urticaria is removal of identifiable cause followed by non-drug therapy

or pharmacological therapy.
 • Urticaria pigmentosa is a skin disease in which clinical features are due to a pathological
increase in dermal mast cell numbers.

• Childhood urticaria pigmentosa presents with number of brownish dermal papules and plaques
widely distributed over the body, when rubbed these become urticated (Darier’s sign). Pruritus
is common and in severe cases wheezing, diarrhoea and syncope. Lesions may become bullous.

• Adult urticaria pigmentosa presents with an insidious onset of monomorphic pigmented

maculopapular lesions, sometimes with prominent telangiectasia on trunk and limbs. Systemic
symptoms include weight loss, bone pain, abdominal pain. Palms and soles are usually spared.
Episodes of flushing may occur after rubbing the skin or following intake of alcohol.

Investigations : Skin biopsies may not be diagnostic unless special tests for mast cells are performed.

Treatment : Avoidance of trigger factors including drugs like morphine and codeine and alcohol.
Administration of H1 , H2 antihistamines is helpful.

DERMATOPHYTOSIS (RINGWORM)
• Dermatophytes are cutaneous fungi which infect only the keratinized tissues by liberting
keratinase enzyme which helps them to invade into keratinized tissue like stratum corneum
layer of skin, hair and mail.

• There are three genera of dermatophytes : Trichophyton, Microsporum and Epidermophyton.

They are grouped according to their natural habitat as geophilic (soil), zoophilic (animals), and
anthrophilic (humans).

• Transmission may be indirect (via desquamated epithelium) or direct through bodily contact.

• Predisposing factors – Warm, humid climate, poor nutrition and hygiene, obesity, diabetes
mellitus and debilitating illness.

Pathogenesis
Dermatophytes

Spores from soil/ animal/man

Enter stratum corneum

Release keratinase

Inflammatory reaction (Redness, swelling,

Heat, Alopecia)
 Movement away from the site of infection

Central healing with classical ringed lesion

Clinical types
1. Tinea Capitis
A. Non-inflammatory type –

o Partial or complete round or oval shape areas

o Black dot patch – Scaly areas of alopecia with black dots due to broken off hair from endothrix
infection
o Grey patch, dull grey hairs with scaly alopecia patch
o Seborrhoeic dermatitis type with dry scaling

B. Inflammatory type –

o Kerion due to zoophilic fungi. Boggy painful inflammatory swelling with exudative
folliculopapules, with fallen off or easily pluckable hair.
o Favus – Circular yellow crusts (scutula) around hair follicles. Patients have a “mousy” odour.

2. Tinea Barbae
• Is usually found in adult males. It is acquired from a barber’s instruments or from animals. They
commonly are observed on the chin, neck and maxillary areas.

• Hair in the affected areas can be easily pulled out. Resolution leaves behind scarring and
alopecia.
o Superficial or sycosiform type – Diffuse erythema with perifollicular papules and pustules.
Anthropophilic organisms (T. rubrum and T. violaceum) invading the endothrix are the cause.

o Circinate or spreading type – with a vesiculopustular spreading border, spreading peripherally

and clearing in the centre.
o Non-inflammatory type – starts as a small erythematous papule surrounding a hairy shaft, later
on these patches of partial alopecia, circular or oval in shape, showing numerous broken off
hair, dull grey or lustreless.
o Inflammatory type – Lesions are nodular and boggy, often associated with seropurulent
discharge.

• Treatment – Systemic antifungal (e.g. griseofulvin 500–1000 mg/d). Topical antifungals, wet
compresses and debridement of crusted lesions.
3. Tinea Faciei
• Annular, shiny lesion due to lack of scaling

4. Tinea Corporis
• Ringworm of the glabrous skin can occur anywhere on the body. It is caused most often by
Trichophyton species.

• The lesion starts as a papule which spreads ring-like peripherally with central clearing. The
lesions are usually circinate with an active border consisting of vesicles and scaling.

• Waistline, axillae, buttocks, other parts of the trunk and extremities but not palms, soles and
groins.

5. Tinea cruris
• Ringworm of the groins and upper and inner parts of the thighs. Obesity, moisture, warmth and
friction are the important factors for its existence. It spreads to the buttocks and lower
abdomen.

6. Tinea Pedis
• It is very pruritic, may be vesicobullous in nature and occurs on the instep and plantar surface of
the foot.

• The fungus is acquired from the flooring, shoes and socks or communal baths. Sometimes the
only evidence is a chronic, hyperkeratotic scaling eruption with minimal infiltration.
Four types with overlap:

• Chronic intertriginous type

• Chronic papulosquamous pattern – Inflammatory and patchy or diffuse moccasin-like scaling over
soles

• Vesicular type near instep and mid-anterior plantar surface

• Acute ulcerative variant with maceration

Tinea manuum
• It affects the hands, is usually caused by T. rubrum. Inflammation is often minimal. The palm
becomes dry with mild scaling which is most obvious in the palmar creases.

Tinea Unguium
• Is a dermatophyte infection of the nail plate with brittleness, friability and thickening of the nail.
The infection usually starts at the free margin and lateral border of the nails and progresses
towards the nail fold. There may be a tinea infection on other parts of the body.
Acne Vulgaris
• Acne vulgaris is a disease in which the pilosebaceous follicle becomes oversensitive to normal
levels of testosterone.

• Acne is chronic inflammation of the pilosebaceous units. It is extremely common generally starts
during puberty and has been estimated to affect over 90% of adolescents.

• It is usually most severe in the late teenage years but can persist into the thirties and fortes,
particularly in females

Exacerbating factors
• Acne worsens with stress and in premenstrual period. In patients with aggressive or recalcitrant
acne, underlying cause may be a virilising syndrome in women, acromegaly, occupational
exposure to acnegenic agents.

• Drugs that worsen acne are steroids, hormones (androgen and progesterone), anti-epileptic
drugs, iodides; can follow facial massage.

• Genetic and hormonal factors also play a role.

Grading of severity
➢ Mild disease : Open (black heads) and closed (white heads) comedones with sparse
inflammatory lesions. Some comedones are deep seated (submarine comedones).
➢ Moderate : Numerous papules and pustules

➢ Severe : Polymorphic eruption with comedones, papules, pustules, nodules and cysts.

Pathogenesis
• The key components are increased sebum production : colonisation of pilosabaceous ducts by
Propionibacterium acnes which in turn causes inflammation, and hypercomnification and
occlusion of pilosebaceous ducts.

• Severity of acne is associated with sebum excretion rate, which increases at puberty. Both
androgens and progestogens increase sebum excretion and destrogens reduce it but most
patients with acne have normal hormone profiles.

• There may be a positive family history and there is high concordarice in monozygotic twins.
indicating that genetic factors are important but the candidate gones are poorly defined.

Clinical features
• Acne usually affects the face and often the trunk. Greasiness of the skin may be obvious
(seborrhea).
 • The hallmarks is the comedone [open comedones (blackhead) are dilated keratin-filled follicles,
which appear at black papules due to the keratin debris, closed comedones (whiteheads usually
have no visible follicular opening and are caused by accumulation of sebum and keratin deeper
in the pilosebaceous duct.

• Inflammatory papules, nodules and cysts occur and may arise from comedones. Scaring may
follow deep-seated or superficial acne and may be keloidal. There are also distinct clinical
variants:

1. Acne conglobate : Characterised by comedones, nodules, abscesses, sinuses and cysts, usually with
marked scarring. It is rare, usually affecting adult males, and most commonly occurs on trunk and upper
limbs.

2. Acne fulminans : Rare but severe presentation of acne associated with fever, arthralgias and systemic
inflammation with raised neutrophil count and plasma viscosity. It is usually found on the trunk in
adolescent males. Costochondritis can occur.

3. Acne excoriee : Self-inflicted excoriations due to compulsive picking of pre-existing or magined acne
lesions. It usually affects teenage girls and underlying psychological problems are common.
4. Secondary acne : comedonal acne can be caused by greasy cosmetics or occupational exposure to
oils, tars or chlorinated aromatic hydrocarbons. Predominantly pustular acne can occur in patients using
systemic or topical glucocorticoids, oral contraceptives, anticonvulsants um or antineoplastic drugs, such
as the epidermal growth factor receptor (EGFR) inhibitors.

Investigations
• Investigations are not required in typical acne vulgaris. Secondary causes and suspected
underlying endocrine disease or virilisation should be investigated.

Management
1. Topical therapies are the mainstay of treatment for mild acne.

o Benzoyl peroxide 5% has antibacterial and keratolytic properties. It treats both inflamed and
non inflamed lesions effectively, but can cause irritation and bleaching. Bacterial resistance is
reduced when used in combination with antibiotics.

o Topical antibiotics are useful in reducing inflammatory lesions. Patients with greasy skin may
tolerate clindamycin 1% and erythromycin 2% because of the alcoholic base.

o Clindamycin lotion is less irritating to dry, scaly skin.

o Topical retinoids are particularly useful in non inflamed lesions.

2. Systemic therapy antibiotics reduce inflammatory mediators and have to be used for 3–6 months.
Higher doses may be required in patients with marked seborrhoea.

o Adjunctive therapy – Intralesional steroids for neurocystic lesions. Comedone extraction,

chemical peels, dermabrasion, laser and light therapy.
 o Hormonal therapy is useful because androgen hormones mediate sebum production.
Cyproterone acetate 2 mg with ethinyloestradiol 35 µg is effective if given for 3–6 months.

Management of scarring
(a) Punch excision, elevation : In depressed scars, punch elevation followed by full-thickness graft of
normal skin. For superficial ice-pick scars punch elevation to raise level flush with surrounding skin.

(b) Intralesional triamcinolone or cryotherapy for hypertrophic and keloid scars.

(c) Dermabrasion : The skin is planed using a deep-wire brush.

(d) Laser therapy – CO2 ultrapulse and YAG lasers have been used successfully.

Leucoderma (Vitiligo)
• Leucoderma is a skin disease that causes loss of skin pigmentation (melanin) that leads to skin
whitening. The white patches on the skin are termed as leukoderma. Also known as vitiligo.

• When the condition gets severe, the spots cover almost all parts of the body including scalp,
face and the genitals.

Causes
• The exact cause of vitiligo is unknown
• It is believed to be due to genetic susceptibility

• That triggered by an environmental factor

• Autoimmune disease which result in the destruction of Skin pigment cells

Pathology
1. Immune hypothesis

Associated with immune response against melanocytes

2. Neural hypothesis
Neurochemical mediators mediators destroyed melanocyte or inhibit melanin production

3. Self destruction

Melanocyte destruction is due to an intermediate product of melanin synthesis

4. Genetic hypothesis
Genetic defect in metabolism of toxic intermediates, melanocyte signal
Pathogenesis
Genetic defect in metabolism In keratinocyte

of toxic intermediates melanocyte signal

Abnormal (accumulation of toxic) metabolites

Destruction of vulnerable melanocyte

Release of melanocyte antigens

Recruitment of langherhans cells

Formation of melanocyte antibodies

T cell sensitization

Destruction of melanocytes

Risk factors

Family history of autoimmune diseases such as

• Hyperthyroidism

• Alopecia areata

Classification
There are two types of leukoderma :

• Segmental Leukoderma - The symptoms of segmental leukoderma start showing up at an early

stage while affecting one side or segment of the body. This type progresses only for a few years.

• Non-Segmental Leukoderma - Starting with a short-lived burst of discolouration, this type

affects both sides of the body and expands with new cycles of pigment loss throughout the life.
There are following five types : Generalised, Universal, Focal, Acrofacial, Mucosal vitiligo
Symptoms
o Milky white patches on the skin

o Premature greying of hair (eyelashes, beard and eyebrow)

o Loss of colour in the mucous membranes (tissues that line the inside of the mouth)
o Change in colour of retina

o Though leukoderma can affect any part of the body, pigmentation usually occurs first on sun
exposed areas of the body

Differential diagnosis
Chemical leucoderma is a similar condition due to multiple exposure to chemical. Vitiligo however is a
risk factor, triggers may includes
o Inflammatory skin conditions
o Burns

o Intralesional steroid injection

o Abrasions
o Other conditions with similar symptoms includes the following : Pityriasis alba, Tunerculoid
leprosy, Tinea versicolor, Post inflammatory hypopigmentation, Albinism, Idiopathic Guttate
Hypomelanosis, Piebaldism.

Treatment
• Since there is no permanent leukoderma treatment available, the primary goal of the doctors
during the treatment is to improve the appearance of the affected area.

o Medication - To help re-pigment the skin, doctors advise topical creams that control
inflammation or affect the immune system.
o Light Therapy - Repeated light therapy sessions have proved fruitful in restoring some colour of
the affected area. Narrow-band UVB (311) phototherapy and PUVA therapy are the two types of
light therapy used in leucoderma treatment. PUVA has a more powerful effect on pigment cells
as compared to Narrow-band UVB (311) phototherapy.

o Cosmetics - Application of skin tanners or makeup on the affected area remains the safest
option for those with minor patches of leukoderma.
o Surgery - Pigmented skin is removed from the affected area using skin and blister grafting
techniques that are then attached to the affected areas.
LICHEN PLANUS
• It is an inflammatory disorder of the skin and mucous membrane of unknown origin. The term
lichenoid is applied to eruptions that clinically resemble or have a similar histology in particular,
a heavy lymphocytic infiltrate immediately under the epidermis, the basal layer of which suffers
the most damage.
• Lichenoid eruptions may be caused by drugs or may occur as a part of chronic graft-versus-host
disease.

• Shiny, flat-topped, violaceous, polygonal papules of varying size, clustered around on the wrists.
Irregularly linear or reticulate white striae (Wickham’s) are often seen in the papules.

• The lesions are usually itchy sometimes intensely so but are occasionally asymptomatic. The
inflammation usually subsides within 2 years and is commonly followed by post-inflammatory
pigmentation.
• Mucosal lichen planus is in form of whitish papular lesions, linearly disposed, may criss -cross to
form a lacy pattern, coalescence of papules may result in plaque formation. It accompanies
cutaneous disease in about 50% of patients, and is common alone.

• Usually flexor areas are more affected. In males the genitals may also be involved in about 10%
of patients.

Pathogenesis
• The disease probably has an autoimmune basis since there is an association with inflammatory
bowel disease, primary biliary cirrhosis, autoimmune hepatitis, hepatitis B and C. alopecia
areata, myasthenia gravis and thymoma.

• There are also similarities with graft-versus-host disease. Lichen planus can occasionally occur in
families and possible HLA associations have been reported but there is no clear inheritance
pattern.

• On skin biopsy, characteristic histological changes include hyperkeratosis, basal cell

degeneration and a heavy, band like T-lymphocyte infiltrate in the papillary dermis, with affinity
for the epidermis (epidermotropism).

• The dermo-epidermal junction has a ‘sawtooth’ appearance.

Variants
o Persistent hypertrophic lesions, usually on the lower legs
o Scalp lesions may cause scarring alopecia
o Bullous lichen planus – Blistering tends to occur within typical lesions in lower legs

o Erosive disease may affect the gingiva, vagina and vulvar vestibule (vulvo-vaginal-gingival
syndrome of Hewitt and Pelisse).
Clinical features
• Lichen planus occurs in both sexes and at any age, although usually between 30 and 60 years. It
generally presents on the distal limbs, most commonly on the flexural aspects of the wrists and
forearms and on the lower back.

• It is intensely itchy and lesions are violaceous, shiny, flat-topped, polygonal papules, with a
characteristic fine lacy, white network on the surface (Wickham’s striae).

• New lesions may appear at sites of skin trauma (Köbner phenomenon) and the rash may
become generalised. Individual lesions may last for many months and can become hypertrophic
and modified by scratching, particularly on the lower legs.

• The eruption usually remits over months but can become chronic, particularly with hypertrophic
disease. Post-inflammatory pigmentary change is common, particularly in darker skin types.

• Genital and other mucosal surfaces can also be affected. Nail involvement occurs in about 10%
and can range from longitudinal ridging to a destructive nail dystrophy, scarring (pterygium) and
nail loss. Scalp involvement usually presents as an inflammatory scarring alopecia, often with
tufting of residual hairs.

• The classical presentation of lichen planus is unmistakable, but less common atypical variants,
which include annular, atrophic, actinic, linear, bullous, follicular, pigmented and ulcerative
types, can be a diagnostic challenge.

Investigations
• A skin biopsy should be performed if there is diagnostic doubt. A careful drug history must be
taken, as although the classical presentation of lichen planus is usually idiopathic, the main
differential is a drug-induced lichenoid reaction.

Management
• The condition is usually self-limiting, although rarely it may persist for years, particularly oral
lichen planus.

• Treatment is symptomatic and potent local glucocorticoids (topical, with occlusion or by

injection for hypertrophic disease, or as oral rinse for oral involvement) may help the intense
itch, short courses of systemic glucocorticoids are sometimes required for extensive disease.

• UVB, PUVA or UVA1 can be beneficial and, for recalcitrant disease, retinoids or
immunosuppressants, such as ciclosporin or methotrexate may be needed.

• A low but significant risk of malignant transformation exists with persistent oral and genital
disease, so active treatment, surveillance and smoking cessation are important.
Treatment
• Milder cases may require no treatment. For localized itchy lesions strong topical steroid (e.g.
clobetasol propionate).

• Systemic therapy – If distressing itch, extensive eruption, destructive nail involvement, or

erosive mucosal lesions. Prednisolone 20 mg/day reducing according to response and
cyclosporine 5 mg/kg/day usually for several weeks.

• The retinoid acitretin produces a slower response but is a safer drug when long-term control is
required. Dapsone may also be given.

• Patients with severe, especially erosive mucosal lichen planus should be followed up for early
detection of carcinoma.

• Lichenoid drug eruption – It may be caused by thiazides, antimalarials, gold, NSAIDs, β-blockers
and captopril. Lichen planus of the mouth may be drug-induced or be a reaction to dental
materials.

• Graft-versus-host disease : About 10% of patients with allogenic bone marrow transplants
develop chronic graft-versus-host disease. The earliest skin manifestations are usually lichenoid.

INFECTION
DENGUE

• Dengue is viral infection transmitted by mosquitoes. Dengue viruses are flaviviruses related to
yellow fever virus and Japanese encephalitis virus.
TRANSMISSION
• Transmission is from infected to susceptible individuals by day-biting Aedes aegypti
mosquitoes. It is not transmitted directly between humans.
• The virus passes from the mosquito’s intestinal tract to salivary glands after an extrinsic
incubation period of about 10 days. Mosquito bites after this result in infection.
• In the skin, dengue virus infects immature dendritic cells which mature and migrate to local or
regional lymph nodes where they present viral antigen to T cells.
Pathophysiology
• DENVs produce several syndromes depending on age and immunological status of the host:
(a) During initial infections most children have subclinical reaction or mild febrile syndromes
(b) During secondary infection, pathophysiology of the disease changes dramatically, such infections can
result in acute vascular permeability syndrome leading to dengue shock syndrome (DSS).
• Predisposing factors for life-threatening dengue infection : Individuals with asthma, diabetes
and chronic diseases. Most factors include female sex, HLA class 1 alleles and AB blood group.
Clinical features
 • Subclinical infection may be present as undifferentiated febrile disease, often with
maculopapular rash, particularly in infants and young children.
Dengue Fever (DF)
• A benign febrile illness begins abruptly with fever 5-8 days after a bite from an infected mosquito.
• Fever is often accompanied by severe headache, retro-orbital pain, and intense myalgia and
arthralgia (break bone fever).
• A rash, macular or scarlatiniform starts on hands and legs and then becomes generalised sparing
the face. The fever usually lasts 4-7 days and is followed by complete recovery.

Dengue Haemorrhagic Fever/dengue Shock Syndrome (DDS)

Pathogenesis :
• Pre-circulating antidengue antibody is the predominant risk factor in DHF/DSS. This may have
been acquired from previous infection with a different serotype or in infants from transplacental
transfer of maternal antibody.
• The major pathophysiological abnormality differentiating DF from DHF is the plasma leakage
syndrome (haemoconcentration, hypoproteinemia and/or serous effusion).
Clinical features :
• DHF/DSS is usually clinically indistinguishable from dengue fever during the initial phase of
illness.
• After 2-7 days, more serious manifestations of disease become apparent, reflecting disordered
haemostasis and increased permeability.
• The capillary leak explains the rise in haematocrit, peripheral oedema, pleural effusion and
ascites.
• Encephalopathy, GBS and acute transverse myelitis have also been associated with dengue virus
infection.
Prognostic factors :
• BP- 90/60, haematocrit-50%, platelet count < 50000, bleeding other than petechiae e.g.
ecchymoses, haematemesis or epistaxis.
• Grading of severity of DHF :
I - Positive tourniquet test and/or easy bruising
II - Spontaneous bleeding
III - Early signs of circulatory failure
IV - Profound shock
Diagnosis :
(a) Dengue antigen (NS1) detection test - NS1 Ag and Ab combicard - Rapid visual test for detection of
dengue NS1Ag and IgM and IgG antibodies in human serum/plasma/whole blood.
(b) Combination of both dengue antibody IgG and IgM with NS1 antigen is essential for diagnosis of early
dengue fever and differentiate between primary and secondary dengue infection. NS1 is a glycoprotein
produced by all Flaviviruses and is essential for viral replication.

Management : There is no specific antiviral therapy.

Treatment:

• For shock - Crystalloids like Dextrose normal saline or Ringer’s lactate 10-20 ml/kg over 30
minutes, then every hr till pulse, BP, CVP and urine output normalise.
 • In profound shock initially colloids like hetastarch or haemaccel. Platelet transfusion for
symptomatic thrombocytopenia.

• Dengue fever - Paracetamol. Avoid aspirin because of increased bleeding tendency and risk of
developing Reye’s syndrome.

VIRAL HAEMORRHAGIC FEVERS

• Viral haemorrhagic fevers are acute illnesses characterized by fever and in most severe cases
shock and bleeding.
Transmission :
• Person to person transmission to bodyfluids and secretions or excreta. Major viral haemorrhagic
fevers. Lassa virus – The host is the rat Mastomys natalensis which excretes large amounts of
virus in its urine.
Clinical features :
• Insidious onset with influenza like symptoms. Abdominal pain, diarrhoea and vomiting may
occur.
• Common physical signs are fever, pharyngitis and conjunctival injection. In severe cases bleeding
begins towards end of first week.
• Hypotension and shock, encephalopathy and ARDS is seen in very severe cases.
Investigations :
• Specific diagnosis of these infections is by demonstrating the virus, antigen, IgM antibody or a
fourfold rise in IgG antibody in blood.
Treatment :
• Ribavirin reduces mortality if given in first week in Lassa fever Dose: 30 mg/kg iv loading
dose,then 16 mg/kg IV 6-hrly for 4 days, then 8 mg/kg IV 8-hrly for 6 days (total duration of
treatment 10 days).
Yellow fever
• The prototype of viral haemorrhagic fever is an acute infection characterized by renal failure,
cardiovascular collapse and bleeding.
Causative agent : Mosquito borne RNA virus belonging to the family Flaviviridae.
Transmission : A zoonosis transmitted between treehole-breeding mosquitoes and monkeys in forests of
Africa and South America.
Clinical features : Spectrum of illness in yellow fever is variable, it ranges from nonspecific febrile
disease which cannot be diagnosed without virological tests, to a severe infection characterised by liver
and kidney failure, shock and haemorrhage.
Lab. findings : Neutropenia and thrombocytopenia, proteinuria elevated serum aminotransferases, and
elevated bilirubin and creatinine, prolonged prothrombin time and partial thromboplastin time.
Investigation : Detection of virus in serum by ELISA or PCR. Virus can also be cultured from serum.
Management : is supportive.

LEPROSY
• A chronic infectious disease caused by Mycobacterium leprae with a predilection for cooler,
superficial regions of the body, namely skin, mucous membrane, and peripheral nerves.
Epidemiology
M. leprae is a slowly multiplying organism which has been grown in the footpads of mice and in the
armadillo.
Transmission : Lepromatous individuals discharge bacilli from the nose. Infection occurs through the
nose followed by haematogenous spread to skin and nerve.
Pathogenesis
• M. leprae has a predilection for Schwann cells and skin macrophages. The patient’s immune
response determines the features of the disease, the two poles are tuberculoid (paucibacillary)
and lepromatous (multibacillary) leprosy.
• At the tuberculoid pole, cell-mediated immunity and delayed hypersensitivity control bacillary
multiplication.
• In the lepromatous form, there is cellular anaergy towards M. leprae resulting in abundant
bacillary multiplication.
• Between these two is a continuum varying from moderate cell-mediated immunity (borderline
tuberculoid) through true borderline, to little cellular response (borderline lepromatous).
Clinical features
• Skin lesions consistent with leprosy with definite sensory loss, with or without thickened nerves
• Skin smears positive for acid fast bacilli
• A person presenting with skin lesions or symptoms suggestive of nerve damage in whom
cardinal signs are absent or doubtful should be labelled as a suspected case
Skin lesions
• Can be single (TT) or multiple (LL)
• Usually hypopigmented, though may be erythematous
• Usually macules or papules, in BL or LL papules or nodules may be seen
• May be well defined (TT, BT), or poorly defined (BL, LL), when nodules of BL and LL subside there
may be dermal atrophy
• Absent hair and sweating are more conspicuous in TT and BT. Hence these lesions may appear
dry
• Anaesthesia/hypoanaesthesia : Anaesthetic lesions in TT, BT, BB, BL hypoaesthetic,
neuroaesthetic in LL. First sensation to be affected is temperature and pain.
Lepra reaction
(a) Type 1 lepra reaction :
• Can occur in borderline leprosy and is characterised by swelling and redness of skin lesions accompanied
by pain and swelling in one or more nerves.
• Oedema of face, hands and feet often occur. Skin lesions may break down, and nerve damage from
cellular reaction and oedema may lead to facial palsy, claw hand, or footdrop.
(b) Type 2 lepra reaction (Erythema nodosum leprosum) :
• An antigen-antibody reaction in lepromatous leprosy.
• Characterised by transient erythematous nodes and patches occurring in crops in any part of the skin but
particularly on face, arms and thighs, usually fading in a few days and being replaced by fresh lesions but
sometimes becoming necrotic and ulcerating.
• Other manifestations include fever, neuritis, swollen joints, painful tibiae, swelling and tenderness of one
or more lymph glands, epistaxis, epididymoorchitis, iridocyclitis and proteinuria.
Diagnosis
1. Slit smear stained by modified Ziehl-Neelsen method. The number of bacilli seen are estimated as the bacillary
index which is useful for classification.
2. Histopathology : Characteristic features are
(a) Granuloma : (i) At the tuberculoid end of the spectrum, the granuloma is made of epithelioid cells, giant cells
and lymphocytes. (ii) At the lepromatous end of the spectrum, the granuloma is ill defined and full of foamy
macrophages and AFB.
(b) Lepromin test : If positive, it indicates good immunity to M. leprae and that the patient has been able to
contain the infection i.e he has tuberculoid or borderline tuberculoid leprosy.
Management
A. Chemotherapy
B. Acute reactions : (a) Rest and sedatives (b) Anti-leprosy drug should be stopped
C. Surgical treatment : (a) Excision of small lesions. Large nodules touched with strong carbolic or nitric acid.
Removal of necrosed bones and splitting of nerve sheath if a nerve is constricted by dense fibrous tissue.
(b) For persistent localised severe nerve trunk pain, infiltration of the thickened nerve sheath or the nerve itself
with 10 ml 1% procaine, or with the latter solution to which 25 mg of hydrocortisone and 1,500 units
hyaluronidase have been added.
(c) Reconstructive surgery is required for paralysed fingers, foot-drop, and hammer toe, and plastic surgery can
correct facial disfigurement caused by loss of eyebrows, facial palsy, saddle-nose deformity, ectropion, pendulous
ear lobes.
Prevention : Child contacts may be given BCG vaccination, especially infants born in leprous families.

AIDS
• HIV-1 and HIV-2 are members of the lentivirus family of retroviruses.
• HIV-1 is probably a cross-species transmission to humans from chimpanzee virus (SIVcpz),
whereas HIV-2 probably arose separately from sooty mangabey virus (SIVsm). A CD4 count <
200/μL in and HIV infected individual is defined as AIDS.
• HIV is an enveloped RNA retrovirus and consists of :
o Outer envelope - Bilipid membrane in which the viral antigens are embedded.
o Inner core bounded by a protein coat containing 3 viral enzymes (Reverse transcriptase,
Integrase, Protease).
TRANSMISSION
1. Sexual
Homosexual : Most HIV infections occur in homosexual and bisexual men who have a large number
ofsexual partners.
Heterosexual : Multiple heterosexual contacts, often prostitutes.
2. Blood and tissue fluids
Contaminated blood
Blood products e.g. factor VIII
3. Contaminated needles and syringes
Injecting drug use
Needle stick injuries
Inadequately sterilized medical equipment.
4. Organ and tissue donations
Semen
Kidney, skin, cornea
Bone marrow
5. Mother to child
In utero
At birth
Breast milk
Pathogenesis
• HIV virus infects target cells (CD4 + T cells, monocytes, macrophages and dendrite cells) through
CD4 receptors.
 • On entering T cells, the virus integrates its RNA genome into the host cell genome by first
transcribing this genome into DNA (HIV provirus) with the help of enzyme reverse transcriptase.
• Provirus is then transcribed and translated along with the host cell DNA to synthesize specific
viral components, which eventually assemble to produce complete virus particles.
• At this time patient is seronegative i.e. antibodies against the virus are not present. But patient
is
• highly infectious. This period is labelled window period.
• Although some virions are killed, HIV continues to multiply infecting increasing number of CD4
cells.
Clinical Features
• Primary HIV infection : Clinical illness is usually self-limiting and several manifestations can occur
including a glandular fever-like illness, meningoencephalitis and peripheral neuropathy.
Seroconversion time (defined as the time from infection to detection of specific antibodies) is 8
days to 10 weeks after onset of acute illness.

• Early manifestations of HIV infection : Individuals may be asymptomatic or have enlarged

lymphnodes with or without minor symptoms e.g. tiredness, lethargy, excessive sweating, and
pains in muscles or joints.

• Later manifestations : In addition to AIDS, other manifestations that indicate a serious prognosis
: 1. Constitutional symptoms or unexplained diarrhoea, fever (> 38°C) for > 1 month or
unexplained weight loss of > 10% body weight. 2. Neurological problems (e.g. neuropathy,
myelopathy). 3. Recurrent Salmonella bacteraemia, extensive herpes zoster, recurrent oral
candidosis and oral hairy leukoplakia.

Laboratory diagnosis
Screening tests : Screening antibodies against HIV in patient suspected of being HIV infected. They are
also used for screening blood and blood products and have a high sensitivity and positivity.

1. ELISA or EIA useful test can be modified frequently to quantify the result (number of viral copies/mL).
Time required 60–90 min.
2. Rapid tests are useful in emergency clinics, causalities and trauma. Time required < 30 min.

Supplemental tests are used to confirm positive results of screening tests. These tests are false negative
in early stage of infection as they are not so sensitive.

Western block (WB) is a specific test for detecting antibodies to different HIV antigens.
Immunoblot (IB) test also allows differentiation between HIV-1 and HIV-2 infections.

Indirect immunofluorescent antibody assay is an expensive test and results are same as Western block.
Confirmatory tests are to confirm presence of virus in the person who is either positive or has equivocal
results to HIV-specific antibodies.
Newborn : Done by one or more combinations of detection of IgA and/or IgM anti-HIV antibodies,
estimation of p24 antigen, PCR, or in vitro antibody production assay, in vitro isolation of virus from
blood or tissues and indirect indicators of HIV infection.

MALARIA
Acute febrile illness characterised by paroxysms of fever as a result of asexual reproduction of plasmodia within
the red cells. Plasmodium vivax, P. ovale and P. malariae are associated with morbidity but no major mortality,
P.falciparum and also are the parasites responsible for some potentially fatal malaria.
Transmission
(a) Presence of suitable anopheline mosquito
(b) Reservoir of malaria infection in the area
(c) Suitable non-immune or partly immune hosts
(d) An environmental temperature with suitable humidity
• Infection is normally transmitted to man by the bite of a mosquito, rarely it may occur across the
placenta, or as a result of blood transfusion or syringe transmitted.
• Infection is initiated by sporozoites from the bite of a female Anopheles mosquito. The sporozoites
multiply within hepatocytes giving rise to thousands of merozoites which invade RBCs.
• In the RBCs the small ring forms grow through the trophozoite stage to the schizont form which ruptures
and releases further merozoites.
Pathogenesis
• Clinical symptoms and signs are caused by the asexual forms of the parasite which invade and
destroy RBCs, localise in tissues and organs by binding to endothelial cells (cytoadherence) and
induce release of many pro-inflammatory cytokines [e.g. tumour necrosis factor-α (TNF-α)].
• The initiating step in pathogenesis is when merozoites invade RBCs. Once inside the cell, the ring
matures via the trophozoite to the schizont stage, which binds specifically to endothelial cells in
post capillary venules in organs such as the brain.
• Cytoadherent parasites probably cause microvascular obstruction. Cytoadherence may also
localize the effect of putative parasite ‘toxins’, which leads to endothelial cell activation and, or
damage as a result of cytokine release.
• The mature parasite is also capable of resetting process in which RBCs containing the more
mature stages of parasite bind uninfected RBCs to the surface.
Clinical Features
Onset : Lassitude, anorexia, headache, chilliness for several days before actual attack.
Paroxysm – 3 clinical stages :
(a) Cold stage – Patient shivers from head to foot, his teeth chatter and he covers himself with blankets.
Temperature goes on rising. The stage lasts for about half hour.
(b) Hot stage – Shivering abates and gives place to a feeling of intense heat, the patient throwing off the
blankets. Flushed face, headache, vomiting, dry and burning skin. Temperature rises to 40°C or more.
The stage lasts for 3-4 hours.
(c) Sweating stage – Patient breaks into profuse perspiration and the temperature rapidly declines with
feeling of relief.
Diagnosis
1. Clinical : Periodic fever with rigour, sweating, anaemia and perhaps enlarged spleen.
2. Blood film : Identification of the parasites in thick and thin blood film. Common microscopic
characters of falciparum malaria are – high concentration of parasites, predominance of thin ring-
shaped trophozoites. Quantitative buffy coat analysis.
3. Malarial antigen spot test using parasite LDH – P. falciparum antigens e.g. histidine-rich protein2
(PfHRP2), LDH in blood from finger prick. These tests use monoclonal antibodies to capture the parasite
antigens and are read out as coloured bands.
4. Immunofluorescent microscopy and PCR.
Management
General Management
• Admission to ICU
• Measurement of glucose and if possible lactate and arterial blood gases
• Fluid balance because both dehydration and overhydration can occur as a result of disease or
treatment
• Treatment of convulsions with diazepam
• Attention to hypoglycemia and hyponatremia
• Blood for cross-matching and coagulation studies
• Parameters for monitoring treatment include twice daily parasite counts, regular pH and blood
gas measurements and when appropriate, measurement of glucose (during iv quinine therapy),
lactate, CRP and kidney function
Management of Specific Complications
• Cerebral malaria – Antimalarial drugs
• Hypoglycemia – Dextrose IV Acute renal failure – Dialysis or haemofiltration.
• Acidosis – Adequate fluid replacement. Transfusion if Hb falls below 7.5 g/dl.
• Bacterial superinfection – Antimicrobial drugs should be given.
• Jaundice – Mild jaundice is mainly caused by haemolysis.
• Malaria in pregnancy : Rapid therapy with an effective antimalarial is the key to good
management.
Complications
• In severe malaria are seen as either sequestration related such as cerebral malaria or non-
sequestration related in P. vivax infection such as anaemia and thrombocytopenia.
• Severe manifestations include cerebral malaria, hepatic and kidney dysfunction, ARDS, severe
anaemia, pulmonary oedema and haemoglobinuria.
• Late Complications Tropical splenomegaly syndrome (TSS) – is seen in endemic falciparum
malaria.

TYPHOID FEVER
• Typhoid fever is an acute illness associated with fever caused by the Salmonella typhi bacteria. It
can also be caused by Salmonella paratyphi, a related bacterium that usually causes a less
severe illness.
• Food-water borne disease.
• Enteric fever also known as typhoid fever.
Epidemiology
• Causative organism : Gram-negative bacillus Salmonella typhi, a human pathogen which
depends on man-to-man transfer for continued existence, and can survive for many weeks in
sewage.
• Transmission – Main source of transmission in contamination of food and water with faeces
from infected patients and carriers.
Pathogenesis
 • After ingestion and passage through gastric acid barrier, the organisms attach to small intestinal
mucosa, penetrate it and are transported by the lymphatics to the mesenteric lymph nodes.
• Following multiplication, they enter the blood stream via thoracic duct, then spread to bone
marrow, spleen and liver, where they multiply.
• Secondary invasion of the blood and re-invasion of the bowel via infected bile then occurs.
• A particularly strong inflammatory response occurs in the ileal Payer’s patches, and may lead to
necrosis, ulceration, bleeding and occasionally perforation.
• Incubation period – 10-15 days.
Clinical Features
• Classically there is gradual onset of fever in the first week, remittent in second week and falling
in third week.
• Patients complain of headache, anorexia, vague abdominal pain, constipation or diarrhoea, and
dry cough. Rigors are uncommon.
• Occasional features include sore throat, epistaxis, coated tongue (typhoid V tongue) and relative
bradycardia.
• In the second week tender hepatomegaly, (typhoid hepatitis) and palpable spleen, and signs of
bronchitis.
• Meningism may occur. Rose spots are scanty pink macules, usually on the trunk, that blanch on
pressure are seen from second week onwards.
• In the third and fourth weeks of illness gastrointestinal bleeding and intestinal perforation
occur; both are life-threatening and require immediate fluid resuscitation and surgical
intervention.
• Untreated patients can become toxic, mentally stuporose and dehydrated, and may develop
ileal perforation, GI haemorrhage, coma, shock, pneumonia, nephritis and acute psychosis.
Laboratory Diagnosis
o Blood culture
o Specific serologic test : Identify salmonella antibodies/antigens & Widal test and ELISA
o Urine & stool culture (2 & 3 week)
o Marrow culture : 90% sensitive unless until after 5 days commencement of antibiotic
o Punch-biopsy samples of rose spots culture : 63% sensitive
o Clot culture : may be obtained from CSF, peritoneal fluid. Gallbladder, tonsils, abscess, bone
Differential Diagnosis
• Paratyphoid fever – Wider remissions of temperature, Eruption more profuse, Less toxaemia
• Short fever – A fever lasting for 8 to 10 days
• Amoebic liver abscess
• Viral hepatitis
• Tuberculous meningitis
• Heat fever – Fever may be continuous or touch normal for some
• hours every day
• Malaria
• Kala-azar
Management
Antibiotic
o Chloramphenicol 500mg qd
o Ampicillin 750mg qd
o Co-trimorazole 2 tablets/iv bds
o Treatment should be continued for 14 days.
General care
1. Fluid and electrolyte replacement. Inotropic support in shock.
2. Diet – To provide about 3,000 calories per day. Advantages are – increases patient’s resistance,
haemorrhage and perforation less likely, prevents rapid emaciation. Articles of diet given – milk, lactose,
toast, butter, mashed potatoes, lightly boiled egg, boiled chicken or fish, corn flour or well-boiled rice
pudding, and custard, bananas and apples. Feeds 2 hourly.
Symptomatic management and management of
complications
(a) Abdominal distension – (i) Omit sugar (ii) Reduce amount of milk (iii) Flatus tube
(b) Diarrhoea – may be due to disease itself or sometimes the drug (i) Reduce quantity of milk or dilute it
further. Give butter-milk and sago kanji or rice kanji in water, apple juice or pomegranate juice (ii) Omit
sugar (iii) If intractable stop milk and give albumen water or whey for few days.
(c) Hyperpyrexia – (i) Tepid sponge (ii) Ice bag to head (iii) Sponging with ice-water (iv) Ice water enema
(d) Haemorrhage – Most episodes of GI bleeding are selflimiting, and only a few patients require
transfusion
(e) Perforation – (i) Slow perforation – Gastric suction and IV fluids. Broad spectrum Gram-negative
agent (eg. cefotaxime with metronidazole) (ii) Acute perforation– Laparotomy
Relapse comprises a second episode of fever, usually milder than the first, occurring 1 or 2 weeks after
recovery from the episode. It is managed as in the initial episode.
Treatment of carriers – 4 week course of fluoroquinolone gives best results.

PLAGUE
• Plaque is an infectious disease spread by rats that causes swellings on the body, a very high
temperature and often results in death.
Epidemiology
• Causative organism – Gram negative bacilli Yersinia pestis.
• Transmission – It is normally transferred from rodent to rodent (in whom it is enzootic) by fleas
(Xenopsylla cheopis). Man can be infected through the infected flea or occasionally by louse or
bedbug, and sometimes from droplet infection from cases of pneumonic plague. Permanent
immunity results from an attack.
• Incubation period – 2-4 days.
Clinical features
1. Bubonic plague
(a) Stage of invasion :
o Bodyache, mental confusion. Bubo appears on second or third day, usually in groin. Very tender
and associated with cellulitis of surrounding tissues.
(b) Febrile stage :
o Onset may be with high fever without prodromata. The temperature continues as a high
remittent fever for 2-5 days and then falls suddenly or gradually after 3-4 days, synchronous
with the full development of the buboes.
 o It may rise again if and when the buboes suppurate. Congested eyes, speech dull resembling
alcoholic intoxication.
o Marked prostration, delirium, vomiting and oliguria, retention of urine, coma and convulsions
may occur.
o Thready pulse, dilatation of heart and perhaps haemorrhages in later stages. Spleen and liver
enlarged. Death may occur on third or fifth day.
(c) Stage of recovery :
o Constitutional symptoms abate usually on 10th day with fall of temperature and perspiration.
Bubo continues to enlarge and may burst or suppuration may not occur.
2. Primary pneumonic :
o Rigour, malaise, vomiting, fever, and prostration. Chest pain, dry cough, dyspnoea and cyanosis
with profuse, watery, blood-tinged sputum. Haemorrhages frequent. Unilateral to begin with,
later might progress to bilaterally.
3. Septicemic :
o Systemic dissemination via blood stream with involvement of many organs. Haematogenous
invasion of lungs results in secondary pneumonic plague. It can occur prior to lymph node
involvement, persons older than >40 years are at increased risk.
LABORATORY DIAGNOSIS
• White cell count – Leucocytosis with absolute predominance of neutrophils.
• Detection of Y. pestis – which is easily recovered from bubo aspirates, blood or sputum on
culture media such as blood agar or MacConkey’s agar, where it grows aerobically Y. pestis is a
Gram negative bacillus with bipolar beading that gives it a ‘safety-pin’ appearance.
• Serology – Haem-agglutinating antibodies to F1 antigen appear within one week of onset of
illness and specific IgM and IgG can be demonstrated by ELISA techniques.
MANAGEMENT
• Specific – (a) Streptomycin 30 mg/kg/day IM in 2 divided doses for 10 days to prevent relapse.
(b) Tetracycline if allergy to streptomycin. 2-4 g/day in 4 divided doses for 10 days. (c)
Chloramphenicol – for patients with meningitis 25 mg/kg loading dose IV followed by 60 mg/kg
in 4 divided doses and after clinical improvement continued orally for 10 days. (d) Levofloxacin
500 mg OD is also approved for treatment and prophylaxis of plague
• Local – In early stages buboes painted with iodine or glycerine and belladona, or treated with
infra-red rays. Opened only when they point, allowed to drain, and dressed with antibacterial
powder.
• General – Good nursing. Sedatives for pain and restlessness. Pneumonic plague patients must
be strictly isolated to prevent droplet infection.
• Immunisation : Vaccine containing 2,000 million killed organisms per ml. 0.5 followed by 1 ml
after 7-10 days. Immunity lasts for 6-12 months.
• Protection of contacts – Tetracycline 500 mg 6-hourly for 7 days for close contacts of plague
patients or those believed to be incubating the disease. Doxycycline 200 mg/day and
levofloxacin, as mentioned above, also used for prophylaxis.

CHIKUNGUNIYA
• Chikungunya fever is a viral disease transmitted by the bite of infected Aedes aegypti mosquito.
• The term is derived from Kungunyala meaning to become contorte or more specifically as ‘that
which bends up’.
• This refers to the stooped posture adopted by the patient as a result of arthritic symptoms. The
disease is almost always self-limited and rarely fatal.
Clinical features
• After incubation period of usually 3-12 days, there is sudden onset of flu-like symptoms
including severe headache, chills, fever (>40°C, 104°F), arthralgia or arthritis, conjunctival
suffusion, mild photophobia, nausea and vomiting.
• Joints of the extremities in particular become swollen and painful to touch. In some, joint pain is
incapacitating and arthritis may last for weeks and months.
• Dermatological manifestations include a petechial or maculopapular rash on the limbs.
• Other features observed have been lichenoid eruption and hyperpigmentation in
photodistributed areas, aphthous like ulcers over scrotum, crural areas and axilla,
vesiculobullous lesions in infants and subungual haemorrhage.
• Acute chikungunya fever typically lasts a few days but as with dengue and other arboviral fevers,
some patients have fatigue lasting several weeks.
Diagnostic tests
• Detection of antigen and antibody in blood by ELISA test.
• An IgM capture ELISA is necessary to distinguish the disease.
• Elevated levels of aspartate aminotransferases and C-reactive protein is seen.

Management
• Treatment is symptomatic with relief of pain with ibuprofen, naproxen, aceclofenac or
paracetamol.
• Aspirin should be avoided.
• Chloroquine phosphate 250mg/day has been found useful.
Chikungunya and pregnancy
• There have been cases of mother-to-foetus infection between 2 and 4.5 months into pregnancy.
IgG that is produced around day 15 passes through the placenta and confers immunity to the
foetus.
• However, there is a possibility of risk of infection at birth if the virus is present in the mother’s
blood. Such infection in the foetus is rarely serious and majority recover quickly without
sequelae.

MUMPS
Also known as epidermis parotitis is an acute communicable dz caused by paramyxovirus with
predilection for glandular & nervous tissue.
Etiology
• Age – Majority in children under 15
• Causative agent – Paramyxoma virus
• Portal of entry – Upper respiratory tract; it spreads through blood stream and has tendency to
multiply in glandular structures. Spreads from human reservoir by direct contact, airborne
droplet nuclei or fomites contaminated by infected saliva.
• Incubation period – 16–21 days.
Clinical features
Onset :
(i) Moderate fever, sore throat, drawing or puckering feeling at angle of jaw
(ii) Swelling of face may be the first to draw attention
(iii) Onset with rigor or convulsion
(iv) With meningeal reaction – “cerebral mumps”
Early signs :
(i) Pain or tenderness on pressure beneath angle of lower jaw
(ii) Reddening of parotid duct orifice
Parotid glands :
o Usually one gland affected followed by the other after a varying interval; or only one gland
affected throughout; or simultaneous enlargement of both.
o The swelling reaches its maximum in about 3 days, remains at its peak for about 2 days and then
slowly recedes.
o The lobe of the ear is in the centre of the swelling which is tender on pressure.
Fever : May rise to 40°C after appearance of parotitis, remittent, or intermittent, falls by lysis in 3–7
days.
Other symptoms :
o Diminished salivation, furred tongue and foul breath
o Marked enlargement of parotid may cause trismus and deafness
o Submaxillary and less frequently sublingual glands may enlarge, ovaries, pancreas, thyroid and
breasts may be affected.

Diagnosis
(a) Viral isolation – from saliva or nasopharynx in acute illness or from CSF in mumps meningitis
(b) Antibody titre – Four-fold rise 1–2 weeks after infection
Differential diagnosis
1. Infection and inflammation
(a) Acute suppurative parotitis
(b) Recurrent parotitis
(c) Chronic parotitis
2. Obstruction of major salivary ducts usually by salivary calculi, rarely by injury or tumour
3. Drug reactions : Hypersensitivity to phenothiazines, thiouracil, iodides, thiocyanate, isoprenaline,
copper, lead and mercury.
4. Neoplasms – So-called mixed tumour.
5. Associated with systemic disease
(a) Sialosis
(b) Sarcoidosis
(c) Sjögren's syndrome
Management
1. Diet – Liquids or semisolids depending on patient's ability to chew
2. Oral hygiene – Frequent mouth wash
3. Paracetamol – for pain and fever
4. Management of orchitis – Complete bed rest, ice compress to scrotum, sling support for testicle.
Prednisolone if swelling very severe 15 mg qds for 4 days and then gradually tapered. If pain severe,
incision of tunica vaginalis or injection of spermatic cord at the external inguinal ring with 10–20 mL of
1% procaine solution.
5. Mumps vaccine is not recommended over 6 years of age because reactions are more common in
older children. Risk of vaccination (brain damage) can be reduced if vaccine is not given to infants
with brain injury, CNS damage, personal or immediate family history of fits, or previous reaction to
vaccine.
Complications
• Orchitis and epididymitis
• Meningitis
• Oophoritis
• Acute pancreatitis
• Meningoencephalitis
• Cranial nerve involvement
• Polyneuritis
• Arthritis
• Mastitis
• Thyroiditis
• Nephritis
• Foetal endocardial fibroelastosis

Influenza
• Influenza is a highly contagious viral infection of the nose, throat and lungs that occurs most
often in the late fall, winter and early spring.
• Influenza viruses are small RNA-containing enveloped viruses. There are three types – A, B and
C. Influenza A viruses are further classified according to the properties of their surface proteins,
haemagglutinin (HA) and neuraminidase (NA) found on the surfaces of influenza viruses.
• The typical seasonal influenza viruses exhibit frequent point mutations that lead to gradual
shifts in their genomes. This process is known as antigenic drift and it is the reason that new
influenza vaccines must be prepared each year.
• Poultry are the natural reservoirs of type A viruses. Influenza B viruses are only found in humans
and have caused epidemics in the past but never pandemics.
• Influenza C virus causes only mild illness in adults.
• Incubation period – 1 to 3 days.
Clinical Features
Clinical features of influenza A and B illness
• Onset – Sudden with fever, chilly sensations, and prostration, catarrhal symptoms, headache,
pains and dry cough.
• Sometimes erythematous rash.
Clinical Types
1. Febrile type :
• Fever, malaise, headache, severe bodyache, catarrhal, congestion of eyes and throat, rapid
prostration.
• Dry cough with few or no signs in chest. Fever lasts for 4 to 6 days, there may be relative
bradycardia.
2. Respiratory type :
(a) Bronchitis and bronchopneumonia
(b) Pleurisy, empyema not uncommon
(c) Pneumonia
(i) Fulminating rapidly fatal form in which pneumonia is present from the onset
(ii) Progressive form in which on the 2nd or 4th day signs of pneumonia begin to develop with copious
fine crepitations usually basal. The sputum may be pinkish, frothy and copious or tenacious mucus of
several hues
(iii) Late form in which often after apparent recovery from the primary influenza, pneumonia suddenly
supervenes on the 4th to 10th day after the onset.
3. GI type – Temperature rarely above 37.5°C, severe anorexia and vomiting, abdominal discomfort and
general prostration. Tympanitis, diarrhoea and continued fever may simulate typhoid fever.
4. Malignant type – Severe toxaemia, cyanosis and rapid cardiac failure.
5. Nervous type – Headache sometimes very severe, delirium, intense depression which may continue
after the acute illness. A true meningitis may occur.
Diagnosis
• The Genexpert system can perform rapid and accurate determination of Flu A and Flu B
infection along with identification of the H1N1 novel influenza virus strain.
• The assay results are obtained in 2 hours which is important in starting appropriate therapy and
maximizing infection control measures.
Complications
• Bacterial bronchopneumonia or lobar pneumonia, less often pure viral pneumonia
• Post-influenzal psychoses, insomnia, irritability, polyneuritis, neurasthenia, meningitis and
haemorrhagic encephalitis.
• Cardiac dilatation, irregularities, pericarditis, endocarditis
• Otitis media, mastoiditis, sinusitis
• Thrombophlebitis, arthritis, orchitis, myositis, nephritis, intestinal hemorrhage
Management
1. Analgesics and sedatives
2. Cough suppressive such as codeine
3. Antibiotics for secondary infections such as otitis media and pneumonia
4. Antiviral drug – Neuraminidase inhibitors – act on viral neuraminidase, and prevent release of virus
particles from infected cells and can be given oral or by inhalation
Prevention
(a) Vaccines – Haemophilus influenzae type B conjugate vaccine 1 mL subcutaneously or 0.1-0.2 mL
intradermally given 1–2 weeks apart gives moderate temporary protection against current strains.
(b) Anti-viral agents –Ribavirin 100–200 mg is effective as vaccination against Influenza A strains and
may be started at the same time as vaccination to provide protection until immunity develops.

LEPTOSPIROSIS
• An acute infectious disease caused by Leptospira interrogans, highly motile, tightly coiled
thin organisms with hooked ends.
• It is characterised by a broad spectrum of clinical manifestations, from unapparent
symptoms to fulminating and fatal infection.
EPIDEMIOLOGY
(a) Animal hosts : Rats and small rodents are the most important reservoirs. Dogs, pigs, cattle, goats,
wolves, foxes and other wild animals can also carry the organisms.
(b) Transmission : Human infection results from contact with tissues of an infected animal or
indirectly from contaminated water or soil.
 (c) Routes of infection : Moist or abraded skin, intact mucous membrane (nasopharynx,
conjunctivae, vagina).
(d) Individuals at risk – include sewer workers, abattoir workers, coal miners, farmers, fish workers
and those employed on canals, docks and river drainage.
Laboratory workers are at risk from handling animals.
Incubation period 5-30 days 2-10 days
Pathophysiology
Causative agent
(Contact with soil, water or plants that have been contaminated by animal urine)

Enters human body through abraded skin or through m.m

Leptospirosis enters the bloodstream Causes damage to inner lining of blood vessels

Spread to all organs of the body

Ishaemic damage to kidney, liver, muscles, meninges

Leptospirosis
Clinical features
Febrile illness (first week)
(a) Septicemic phase : Fever, headache, skin rash and myalgia simulate influenza and leptospirae
appear in blood and CSF. Mild proteinuria to kidney failure in severe leptospirosis. Jaundice may be
present. This stage lasts for 4 to 7
days followed within 48 hours by:
(b) Immune phase (second week) : lasts 4-30 days. Leptospirae disappear from all tissues except
kidney and aqueous humuor in parallel with rise in circulating antibodies. Symptoms may include
rash and secondary fever, meningeal symptoms, uveitis; hepatic and renal manifestations of febrile
phase remain and may be more severe in some patients. The following clinical spectrum can be seen
in the second phase:
(i) Haemorrhagic fever with renal syndrome : Renal manifestations include an oliguric renal failure
due to acute tubular necrosis or tubular interstitial damage leading to non-oliguric renal failure, high
excretion of potassium and hypokalaemia, which can cause hyporeflexic paralysis.
(ii) Atypical pneumonia syndrome : Delayed resolution, small nodular densities and confluent areas
of consolidation are radiological findings. Leptospirosis should be suspected
in rapidly developing pneumonia with myalgia.
(iii) Neurological : Aseptic meningoencephalitis, Myocarditis, Cardiac dilatation, atrial fibrillation,
cardiac failure and sudden death have been recorded.
Investigations
1. Biochemical laboratory features
(a) Leucocytosis with neutrophilia
(b) Thrombocytopenia
 (c) Urinanalysis – Cellular elements, granular and pigmented casts and mild proteinuria
(d) Other tests done to confirm diagnosis are PCR, Indirect haem-agglutination test assay (IHA) and
IgM ELISA. IgM antibodies become positive by 5th day. MAT does not have any diagnostic
significance in 1st week and peaks about 3rd week
(e) CSF may show aseptic meningitis like picture.
2. Chest X-ray : often shows dense confluent shadows suggestive of pulmonary haemorrhage
3. Serology : Microscopic agglutination test (MAT) is the gold standard with either a fourfold rise in
titres or a single titre of > 1:800 being diagnostic.
4. PCR assay : Positive in acute infection. Suggests antigenimia. Positive before antibodies appear in
blood.
Management
(a) Antibiotics – Mild leptospirosis – Doxycycline 100 mg po bd, Amoxicillin 500 mg po bd
Moderate/severe leptospirosis – Inj. Ceftriaxone 1g/day IM or by IV slow infusion for 7days.
Signs and symptoms may include rigours, high fever, low BP, headache and myalgias.
(b) Dialysis – for kidney failure.
(c) Blood transfusions or platelet transfusions may be necessary
Chemoprophylaxis – Doxycycline 200 mg once a week, Azithromycin 250 mg once or twice week.

FILIARASIS
• Filarial infections are caused by parasitic, tissue-dwelling, filarial nematode worms, which are
transmitted by biting insects. Two main types of filariasis are :
1. Lymphatic filariasis transmitted by mosquitoes
2. Subcutaneous filariasis (onchocerciasis and loiasis) transmitted by biting flies.
Life cycle
• Adult female worms situated in various tissues in the human host produce embryonic
microfilariae which are sucked up by mosquitoes or biting flies during a blood meal.
• Microfilariae develop to their larval stage in the insect vector and are passed on to a new human
host in which the final maturation to adult worms takes place.
• Periodicity of microfilariae – In most endemic areas the microfilariae of W. bancrofti appear in
greatest numbers in peripheral blood in the night between 10 pm and 2 am, during the day they
return to the pulmonary capillaries.
• Microfilariae of B. malayi exhibit either nocturnal periodicity or diurnal periodicity with a peak in
the early evenings.
Lymphatic filariasis can be caused by
o Wuchereria bancrofti transmitted by Anopheles, Culex and Aedes mosquitoes.
o Brugia malayi transmitted by Mansonia and Anopheles mosquitoes.
o Brugia timori transmitted by Anopheles barbirostris.
Clinical features : Two syndromes
(a) Lymphatic filariasis caused by adult or developing adult worms, producing episodic inflammation of
lymphatic vessels, followed by obstructive lymphatic lesions
(b) Syndrome caused by immune hyper-responsiveness of human host against microfilaria, producing
occult filariasis (circulating filarial antigens or microfilaraemia)
Acute C/F
1. Filarial fever – Attacks of fever with rigors, headache and malaise, lasting 3-7 days, recurring at
intervals, and sometimes associated with an attack of filarial adenolymphangitis
2. Filarial lymphangitis and lymphadenitis – (a) Acute lymphangitis – in extremities with fever with
rigours and toxaemia. The tender inflamed lymphatics are seen as red streaks. Lymphatics anywhere in
the body may be involved, those of spermatic cord and testis are especially susceptible.
(b) Lymphadenitis – occurs episodically most often in inguinal area. Other sites are medial aspect of leg,
axilla or medial side of arm.
Chronic C/F
1. Hydrocele – is common with W. bancrofti
2. Lymphoedema – is most common in lower limbs but also occurs in the upper limb or the breast
3. Elephantiasis – results from further progression with dermatosclerotic and papillomatous changes
superimposed
4. Rupture of lymphatic varices – into renal pelvis or bladder gives rise to chyluria (when the lymph
vessel is draining the intestine) or lymphuria (when it is not)
5. Tropical eosinophilic syndrome – A hypersensitive reaction to lymphatic-dwelling parasites and char-
acterised by chronic cough, wheezing and persistent eosinophilic count which may reach more than
50,000/µl
Diagnosis
(a) Simple parasitological confirmation depends on finding the characteristic sheathed microfilariae in a
thick blood film taken at the peak of periodicity of the strain (usually midnight) and stained with Mayer’s
haemalum.
(b) Enzyme-linked immunosorbent assay card test detects circulating W. bancrofti antigens, and W.
malayi DNA can be detected using PCR analysis.
Management
1. Drugs :
• Diethylcarbamazine citrate (DEC) kills the microfilariae and a proportion of the adult worms of
the lymphatic-dwelling filariae.
• A single dose of 6 mg/ kg given annually is effective in the long-term killing of microfilariae and
adult worms. It is usually given in mass campaign to reduce transmission, along with an annual
dose of albendazole 400 mg which supplements its antifilarial action.
• Simple hygiene effective in preventing infection in secondary collateral lymph channels which
can re- establish lymph flow.
2. Palliative treatment :
(a) Acute lymphangitis –
o Rest, elevation of limb, hot fomentations, infra-red rays or short wave diathermy
o Analgesics for relief of pain. Broad spectrum antibiotics to control infection
(b) Chyluria – Treated surgically
(c) Elephantiasis –
(i) Twice daily washing of affected parts with soap and water
(ii) Raising the limb at night
(iii) Working the foot up and down to promote lymph flow
(iv) Keeping the nails clean, wear shoes
(v) Use of antiseptic or antibiotic creams to treat small wounds or abrasions
o Long-term low-dose DEC may also help to reverse chronic lymphoedema and elephantiasis.
o For resistant case lymphnodovenous shunt operation, followed by surgical removal of excess
tissue.

Onchocerciasis
 • It is a chronic filarial disease caused by Onchocerca volvulosus and transmitted by black flies of
the genus Simulium. In mild infections there is pruritus with papulourticarial dermatitis.
Generalised onchocerciasis presents with involvement of skin, eyes and lymphnodes.
Diagnosis – confirmed by demonstration of microfilariae in skin snips, or cornea or anterior chamber
(using slit lamp), or of adult worms in subcutaneous nodules.
Treatment – Suramin kills adult worms also DEC or ivermectin.

CHICKEN POX
• A highly contagious viral infection which causes an itchy, blister like rash on the skin. It is caused
by varicella-zoster virus.
Epidemiology
Age : Primarily children, uncommon in adults
Causative agent : Virus is identical to virus of herpes zoster and hence designated varicella zoster virus
(V-Z virus)
Transmission : Droplet discharges from air passages. May be direct skin contact or by recently
contaminated utensils
Incubation period : 14 to 15 days
Period of infectivity : Patients are infectious 48 hrs before onset of the vesicular rash during the period
of vesicle formation (which generally lasts 4–5 days) and until all vesicles are crusted.
Clinical Features
Stage of Invasion or Prodromata : Not constant. Headache, sore throat and fever for 24 hours.
Prodromal rashes : Erythematous, scarlatiniform, morbilliform or urticarial. Rarely haemorrhagic.
Stage of Eruption
Exanthem : Earliest lesions on buccal and pharyngeal mucosa
(a) Evolution – in crops, at first back then chest, abdomen, face, and lastly limbs
(b) Character – At first macule in few hours dark pink papule which soon turns into vesicle
(i) superficial in the skin (glass pox)
(ii) elliptical or oval (tear drop vesicles) with axis parallel to ribs
(iii) unilocular hence collapse if pierced with a needle. Vesicles turn into pustules in 24 hours. Scabs in 2
to 5 days
(c) Distribution – centripetal, i.e. more on upper arms and thighs and upper part of face
(d) Cropping – Rash matures very quickly and most spots dry up within 48 hours of appearance
Other symptoms :
Pruritus of varying degree
Generalized lymphadenopathy may occur and enlargement of suboccipital and posterior cervical lymph
nodes from secondarily infected scalp lesions
Unusual Forms :
1. Varicella hemorrhagica
2. Varicella bullosa
3. Varicella gangrenosa
4. Congenital and Neonatal chickenpox – Virus may pass through the placenta and the baby is born with
chickenpox or develops it in neonatal period.
Laboratory Diagnosis
A Tzazk smear performed by scraping the base of an acute lesion and staining with Giemsa’s or
Papanicolaou’s stain, may demonstrate multinucleated giant cells containing intranuclear inclusions.
Other tests include fluorescent antibody against membrane antigen, immuno-adherence
haemagglutination and enzyme-linked immunoabsorbent assay.
Differential Diagnosis
Papular urticaria
Infected scabies – Lesions never occur in mouth, face not affected except occasionally in children,
Impetigo contagiosa
Herpes zoster
Insect bites
Dermatitis herpetiformis
Rickettsial pox
Bullous impetigo, pemphigus, and bullous form of erythema multiforme
Management
1. No need to confine patient to bed unless symptoms are severe.
2. For pruritus : Calamine lotion with or without phenol (0.4%) and sedative antihistaminics by mouth. If
there is much scabbing, gauze soaked in 1 in 5,000 solution of potassium permanganate which is
changed every 4 hours may be applied to areas most affected.
3. For secondary infection : Antibiotics
4. For true varicella pneumonia : Oxygen
5. For encephalitis : Oxygen and corticosteroids
6. Paracetamol for fever. Aspirin is contraindicated because of the association with Reye’s syndrome. 7.
Oral acyclovir initiated within 24h of rash results in a decrease in the duration and magnitude of the
fever, and in the number and duration of skin lesions.
Complications
• Bacterial infection of skin causing impetigo, cellulitis and post inflammatory scarring.
Other uncommon complications :
• The most common extracutaneous site of involvement in children is the CNS.
• The syndrome of acute cerebellar ataxia and meningeal inflammation generally appears 21 days
after onset of the rash and rarely develops in the pre-eruptive phase.
• Others are otitis media, pneumonia, cerebellar ataxia, Reye’s syndrome and aseptic meningitis.
Prevention
(1) Varicella zoster immunoglobulin
Indications :
(a) Following significant exposure to chickenpox in immunocompromised and susceptible children
(b) Susceptible adolescents and adults, particularly pregnant women
(c) Newborn infants whose mothers have chickenpox within 5 days before delivery or within 48 hours
after delivery
(d) Premature infants of less than 28 weeks gestation
(e) Premature infants whose mothers do not have a history of chickenpox. Dose – 125 units (1.25
mL)/10 kg body wt. IM within 48 hours and preferably not later than 96h after exposure. Maximum
suggested dose is 625 units.
(2) Vaccine – Live attenuated varicella vaccine
Safe and highly protective in both healthy and immunocompromised children.
Adverse effects : Minor rash often accompanied by fever.
Dose : In children 2–12 years who have not had chickenpox, two doses recommended the first at 12–15
months of age second at 4–6 years of age.
AMERICAN TRYPANOSOMIASIS (CHAGA’S DISEASE)
• It is caused by T. cruzi and usually transmitted to vertebrates by blood-sucking triatomine bugs.
Also through blood transfusion and congenital.
Clinical Features
Acute phase :
• Local reaction at site of inoculation, often presenting as orbital oedema (Romana’s sign) with
local lymphadenopathy.
• After about 2 weeks a toxaemic phase may follow with fever, hepatosplenomegaly. Death in this
phase results from cardiac involvement.
Chronic phase : Gradual development of serious complications
(a) Heart – Amastigotes form pseudocysts in myocardial tissue causing cardiomyopathy, arrhythmia and
cardiac failure
(b) Intestinal tract – Dilatation of intestinal organs (mega-oesophagus, mega-colon)
Diagnosis
(a) Direct methods for acute Chaga’s disease - Demonstration of trypanosomal parasites or DNA
(b) Indirect methods for chronic Chaga’s disease - Demonstration of specific antibodies
Management
(a) Nifurtimox 8-10 mg/kg/day in 3 divided doses for 30-120 days
(b) Benznidazole 5-10 mg/kg/day in 2 divided doses for 30-60 days, more effective than nifurtimox and
well tolerated.

Anaphylaxis
• Anaphylaxis is a sudden, severe allergic reaction that can be life-threatening It is a medical
emergency case. It can occur within seconds or minutes of exposure to something someone is
allergic to.

• Anaphylaxis is under hypersensitivity type 1

Etiology
• Our immune system produces antibodies that defend against foreign substances. This is good
when a foreign substance is harmful (such as certain bacteria or viruses).

• But some people’s immune systems overreact to substances that shouldn’t cause an allergic
reaction. When this occurs the immune system sets off a chemical chain reaction leading to
allergy symptoms.

• Normally, allergy symptoms are not life-threatening. But some people have a severe allergic
reaction that can lead to anaphylaxis.

The most common causes of anaphylactic shock are :

o Certain medications, especially penicillin

o Foods, such as peanuts, tree nuts (walnuts, pecans), fish, shellfish, milk and eggs
o Insect stings from bees, yellow jackets, wasps, homets and fire ants
Less common causes of anaphylaxis include:

o Exercise, often after eating certain foods

• Anaphylaxis usually happens within minutes of exposure and almost always within two hours.

Pathophysiology
• Anaphylaxis is a severe allergic reaction of rapid onset affecting many body systems.

• It is due to the release of inflammatory mediators and cytokines from mast cells and basophils
typically due to an immunologic reaction but sometimes non immunologic mechanism.

Risk factors
There aren’t many known risk factors for anaphylaxis but some things that may increase your risk
include :

• A personal history of anaphylaxis : If experienced anaphylaxis once, risk of having this serious
reaction is increased. Future reactions may be more severe than the first reaction.

• Allergies or asthma : People who have either condition are at increased risk of having
anaphylaxis

• A family history : If family members who have experienced exercised-induced anaphylaxis

Sign & Symptoms

Skin reactions including hives along with itching, flushed or pale skin (almost always present with
anaphylaxis)

• A feeling of warmth

• Sensation of a lump in throat

• Constriction of the airways

• Swollen tongue or throat which can cause wheezing and trouble breathing

• A feeling of impending doom, Anxiety, confusion

• Weak and rapid pulse

• Nausea, vomiting or diarrhea

• Dizziness or fainting, Hypotension

• Abdominal cramps

Investigation
• Allergy testing is ordered to help in determining the trigger.
 • Skin allergy testing (such as patch testing) is available for certain foods and venoms.

• Blood testing for specific IgE can be useful to confirm milk, egg, peanut, tree nut and fish
allergies.

Diagnosis
• Anaphylaxis is diagnosed based on clinical criteria. When any one of the following three occurs
within minutes/hours of exposure to an allergen there is a high likelihood of anaphylaxis:

1. Involvement of the skin or mucosal tissue plus either respiratory difficulty or hypotension.

2. Two or more of the following symptoms : Involvement of the skin or mucosa, Respiratory difficulties,
Low blood pressure, Gastrointestinal

• During an attack, blood tests for tryptase or histamine (released from mast cells) might be useful
in diagnosing anaphylaxis due to insect stings or medications. However these tests are of limited
utility if the cause is food or they are not specific for the diagnosis.

Treatment
During an anaphylactic attack, an emergency medical team may perform cardiopulmonary resuscita tion
(CPR) if the patient stops breathing or his heart stops beating. Medications given :

• Epinephrine (adrenaline) to reduce the body’s allergic response

• Oxygen to help compensate for restricted breathing

• Intravenous (IV) anthistamines and cortisone to reduce inflammation of a passages and improve
breathing

• A beta agonist (such as albuterol) to relieve breathing symptoms

Complication
• Airway blockage

• Cardiac arrest (no effective heartbeat)

• Respiratory arrest (no breathing)

• Shock
CEREBRAL MALARIA
• Manifestation of severe plasmodium falciparum malaria

• Unarousable coma more than 30 mts with a glasgow coma scale <7/15 with evidence of acute
falciparum infection (asexual form is peripheral blood smear)

Pathogenesis
Mechanical hypothesis

Sequestration of RBC in the brain by cytoadherence / resetting

Toxin/cytokine hypothesis

Malarial toxin induced cytokines

Stimulating excessive Nitric oxide
Production
MECHANICAL HYPOTHESIS
Cytoadherence

• Parasite after invading RBC membrane, 12/15 hrs later protuberances appear on the
erythrocyte’s surface.

• These “knob” extrude a high molecular weight, antgenically variant, strain specific erythrocyte
membrane adhesive protien (pEMPI) that mediates attachment to receptors on venular and
capillary endothelium. This eventually black capillaries and venules.

Rosetting

• Binding of 2 or more uninfected RBC’s to an infected RBCs.

Agglutination

• The binding of 2/more infected RBC’s.

TOXIN/CYTOKINE HYPOTHESIS
• Glycolipid material released on merozite rupture initiates cytokine cascade from macrophages
and monocyte series and endothelium with release of interleukin-1, TN alpha, interleukin-6 and
interleukin-8

• Evidence of positive correlation cytokine levels and prognosis

• TNF alpha>100pg/ml associated with cerebral pathology and death

 HUMORAL HYPOTHESIS
Malarial toxin macrophage activation
TNF alpha & IL-6

Uncontrolled nitric oxide

Production

Nitric oxide diffuse blood brain barrier

impairs synaptic transmission

(like general anesthetics/ethnol)

Coma

Clinical features

Onset :

o Acute following seizures

o Gradual
Consciousness :

o Drowsiness, confusion
o Disorientation, delirum and agitation

Seizures :

o Repeated generalised convulsions > 2/24 hrs

o Papilloedema in <1%
o Retinal hemorrhages-15%
o Pupils and corneal reflex-normal

o Transient dysconjugate a gaze – no paresis

o Jaw jerk may be brisk
o Forced jaw closure/Bruxism

Motor system :

o Decorticate rigidity
 o Decerebrate rigidity

o Tone may be increased decreased or normal

o Cremasteric and Abdominal reflex normal
o DTR and Plantar reflex variable

• Very high fever

• Hypoglycemia

• Hyponatremia

• Severe anemia

Investigations
• Microscopic examination of blood film is gold standard for diagnosis of malaria

• Thick blood film : Species specific and inexpensive

• Thin blood fim : Rapid, species specific and inexpensive

• PRP2 dipstick card test : Rapid and sensitive, Detects only p. falciparum

• Role of PCR : Most sensitive and specific

Results only after 24hrs

Treatment
• Medical emergency requires ICU care

• Ventilatory support, cardiac monitoring

• Connection of fluids, electrolytes and acid base balance

• Blood transfusion

• Artesunate is drug of choice - 2.4mg/kg (2vails) IV at 0hr and 24hrs then daily till pt can take
orally

• Quinine in case of first trimester of pregnanacy - 20mg/kg in 5% dextrose saline in 4 hrs then 8
hrly orally to complete 7 days

• Doxycycline - 3.5mg/day for 7 days

• Tetracycline/clindamycin (children and pregnancy)

• ACT - combination therapy

FEVER
• Fever is an elevation of body temperature that exceeds normally daily variation and occurs in
conjunction with an increase in the hypothalamic set point for e.g. 37°C 39°C.

Causes
• Hot environment

• Excessive exercise

• Neurogenic factors like injury to hypothalamus

• As an undesired side effect of a therapeutic drug

• Chemical substances e.g caffeine and cocaine directly injected into the bloodstream

• Infectious disease and inflammation

• Severe hemorrhage

Classification or patterns
1. Intermittent fever : Temperature returns to acceptable value at least once in 24 hours. The
temperature curve returns to normal during the day and reaches its peak in the evening. Eg. in
septicemia.
2. Remittent fever : Fever spikes & falls without a return to the normal temperature levels. The
temperature fluctuates but does not return to normal. Eg. TB, viral diseases, bacterial infections
3. Sustained fever : The temperature remains continuously elevated above 38 degree Celsius &
demonstrates little fluctuation.
4. Relapsing fever : Periods of febrile periods interspersed with acceptable temperature values i.e
periods of fever are interspersed with periods of normal temperature.
Grades
1. Low grade fever : 37.1 - 38.2 C (98.8 - 100.6 F)
2. High grade fever : 38.2 – 40.5 C (100.6 - 104.9 F)
3. Hyperpyrexia : >40.5 C (104.9 F)

Signs & symptoms

• Flushed face

• Hot dry skin

• Headache

• Nausea and sometimes vomiting

• Constipation and sometimes diarrhea

 • Body aches

• Scanty highly colored urine

• Anorexia

• Increased heart rate, respiratory rate

• Shivering, pale cold skin

• Cyanotic nail beds

Hyperthermia
• It is an elevated body temperature due to failed thermoregulation that occurs when a body
produces or absorbs more heat than it dissipates.

• Temperature ranges - >37.5 - 38.3 degree C (99.5 - 100.9 degree F)

Causes
1. Heat stroke :

Prolonged exposure to sun or high environmental temperatures. These condition causes heat stroke – a
dangerous heat emergency with a high mortality rate.
o Anxiety, confusion
o Skin Hot & Dry

o Impaired sweating
o Listlessness
o Seizures, Delirium, Coma
o Increasing Body temperature

2. Drug induced hyperthermia :

Due to increased use of psychotropic drugs eg. Monoamine oxidizes inhibitors, phencyclidine, selective
serotonin uptake inhibitors(SSRI), MAO’s( Serotonin Syndrome), use of narcoleptic agents like
haloperidol (NMS).
3. Endocrinopathy :

Thyrotoxicosis and pheochromocytoma can lead to increased thermogenesis

4. Central nervous system damage :

Cerebral hemorrhage, status epileptics, hypothalamic injury can cause hyperthermia

Management
• Acetaminophen : Adult : 325-650 mg PO q 4-6 hrs. Children : 10-15mg/kg body weight q 4-6 hrs.
 • Ibuprofen (NSAID) : Adult : 200-400mg PO q 6hrs. Children : 5mg/kg body wt for temp. <102.5
to mg/kg body wt. for temp 102.5F (not to exceed 40 mg/kg/day).

• Indomethacin and naproxen (NSAID)

• Aspirin : Adult 325-650 mg PO q 6hrs. Children 10-20 mg q 6hrs.

• Glucocorticosteroid : Potent antipyretic inhibit PGE2 synthesis.

• Mepridine, morphine sulphate, chlorpromarine used in severe hyperthermia pt’s.

Management of fever and hyperthermia

• Provide adequate nutrition and fluids to meet the increased metabolic demands and prevent
dehydration.

• Reduce physical activity to limit heat production especially during the flush stage.

• Provide a tepid sponge bath to increase heat loss through conduction.

• Provide dry clothing and bed linens.

• Remove excess blankets when the patient feels warm but provide extra warmth when pt feels
chilled.

• Administer antibiotics as ordered.

PYREXIA OF UNKNOWN ORIGIN

• The term Pyrexia of Unknown Origin (PUO) may be used to describe the condition of a patient
who has
o An oral temperature of 38°C on at least two occasions
o More for longer than 3 weeks
o No known immunocompromised state
Causes
• Infections
• Neoplasms
• Collagen vascular / Hypersensitivity diseases
• Miscellaneous conditions
• Inherited & metabolic diseases
• Thermoregulatory disorders
Diagnosis
• Physical examinations
• Blood investigations – Tumour markers, PPD for TB, Serological studies, Peripheral smears
• X-ray
• Bone marrow biopsy, Liver biopsy
• CT-scan, MRI, Ultrasonography
Treatment
• Continuous observation and examination.
 • Do not start with immediate antibiotic therapy as it delineate the cause of PUO.
• The debilitating symptoms are treated by NSAIDs & glucocorticoids.
• If neutropenia & vital sign instability are present then empirical therapy with fluroquinolone &
piperacillin is given.
• When no underlying source of infection is found even after 6 months the prognosis is generally
good.

INFECTIOUS MONONUCLEOSIS (glandular fever)

• Is an acute self limiting febrile illness caused by EBV (primary infection). Epstein barr virus

Mode of transmission :

• Virus particles are present in pharynx and saliva during acute attack

• Transmission occurs by closed contact (eg. Kissing, sharing, eating, utensils)

Incubation period : 30 to 45 days

Causes
• HIV

• EBV infection

• CMV

• Human herpes virus

• Adenovirus

• Hepatitis A virus

• Influenza A and B virus

• Rubella virus

Clinical features
• Anxiety

• Palate petechiae

• Fever temperature - high and last one to two weeks

• Lymphadenopathy - Anterior and Posterior cervical chains

• Prodromal symptoms : Malaise, anorexia, fatigue, headache, fever

• Symptoms : Peak 7 days after onset and dissipate over next one to three weeks

• Spleen enlargement is common

 • Less common : Upper airway obstruction, abdominal pain, hepatomegaly, jaundice, eyelid
oedema

Investigations
• Haematology : WBC increases, Increases mononuclear cells

• Serology : Non-specific heterophile antibody is a present (40 % of pts during first week, 60%
second week, 80% third week)

Management
• Mainly symptomatic

• Initial period of bed rest : 2 to 3 weeks

• Gargles with soluble Aspirin helpful for relieving sore throat

• Antibiotic : Erythromycin if secondary infection

• Corticosteroids if severe pharyngitis

• Ampicillin should be avoided as it produces a rash

Complications
• Autoimmune hemolytic anaemia

• Neurological : Encephalitis, Meningitis, Bell’s palsy

• Others : Cardiac non-specific ECG changes, Pericarditis

FOOD POISONING
• Food poisoning suggests a foodborne disease outbreaks where more than two individuals
develop similar symptoms following the ingestion of common food.

• Most common form of food poisoning is gastroenteritis following consumption of food

containing performed toxins or organisms that produce toxins in the gut.

Causes
(A) Infective
I. Toxin-induced

1. Preformed toxins : Staphylococcus aureus & Bacillus cereus

2. Enterotoxins produced in intestine : Vibrio Cholera, E.coli, Clostridium perfringens, Clostridium

difficile
II. Changes in mucosa
1. Mucosal alteration without invasion - Rotavirus

2. Invasion of mucosa with destruction – Shillega, E.coli, Yersinia, Salmonella and Entaamoeba
histolytica, Bacillus anthracis

(B) Noninfective

1. Allergic – Shellfish, Strawberries

2. Non allergic – Scrombrotoxin (fish), Ciguotoxin (tropical fish), fungi, arsenic poisoning

Clinical features
• Vomiting & Diarrhoea within 48 hours of consumption of contaminated food or drink
• Stools may be bloody

• Crampy abdominal pain

• Fever

• History of simultaneous occurrence of symptoms in more than one member of house or

institution

Investigations
• Identification of pathogen by culture of patients stool vomitus of blood

Treatment
• IV fluid & Electrolyte

• Codeine phosphate or loperamide for controlling diarrhoea

• Antibiotic therapy
 GIT
INFLAMMATORY BOWEL DISEASE
• IBD is commonly used to include two idiopathic bowel dz having many similarity but condition
usually have distinctive morphological appearance.

1. ULCERATIVE COLITIS
• Ulcerative colitis is an inflammatory disorder of the colonic mucosa characterized by relapses
and remissions.
• The rectal mucosa is always involved, occasionally by microscopic inflammation alone and the
disease extends proximally.
• UC is classified into severity in two ways : According to extent of involvement or according to
symptoms.
• If the disease is limited to only the rectum (proctitis) and limited to rectum and sigmoid colon
(proctosigmoiditis). Left sided UC involves descending colon, sigmoid colon and rectum.
• The term pancolitis suggests involvement of the whole colon or most of the colon. Sometimes
ileum gets involved called as Backwash ileitis .
Pathogenesis
Genetically susceptible individual

An abnormal host response

Inflammation of intestine
Bacteria antigen taken up by specialized M cells

Enter the lamina propria through ulcerated mucosa

Type 1 T helper cells by antigen presenting cell in lamina propria

T cell mediated cytokine response

TNF alpha secretion

Further amplification of T cells

Release of other cytokine like IL-23, 6, 1, TNF

Damage tissue of rectum, sigmoid colon, whole colon (Pancolitis)

Long lasting pancolitis

Bowel shortened & pseudopolyps develop

Dyplasia Colon ulcer

Clinical Features
• Onset is usually gradual.
• Bloody diarrhoea is the hallmark of the disease, though proctitis may present with rectal
bleeding and constipation.
• Urgency and crampy abdominal discomfort before defecation.
• Stool frequency is related to the severity of the disease.
• Tenesmus
• Anorexia
• Weight loss
• Anemia
• Fever
• Tachycardia
• Abdominal tenderness
Investigations
1. Sigmoidoscopy & rectal biopsy : The appearances can be graded as
(a) Mild : Hyperaemia and oedema
(b) Moderate : Granular mucosa with contact bleeding
(c) Severe : Ulceration, spontaneous bleeding
Characteristic microscopic features are a chronic inflammatory infiltrate, glandular distortion, goblet cell
depletion and crypt abscesses.

2. Plain abdominal radiography in only severe disease to assess faecal distribution.

3. Colonoscopy vs barium enema : Colonoscopy is always preferable in initial investigation of bloody

diarrhoea, because it provides better mucosal definition and allows biopsies.
4. CT abdomen can also define active colitis and its proximal extent.
5. Stool examination to exclude pathogens such as E. histolytica, Clostridium, E. coli

6. Full blood count, ESR or CRP to evaluate severity

7. Liver function investigation once in remission

Differential Diagnosis
• Infection : Other causes of bloody diarrhoea include Clostridium, E. coli

• Crohn’s colitis

• Ischemic colitis : Usually sudden onset, rectum not affected

• Microscopic colitis : Causes watery, not bloody diarrhoea

• Lymphocytic colitis : Diagnosis is made by finding chronic inflammatory infiltrate

• Radiation colitis : History of pelvic or abdominal node irradiation with mucosal telangiectasia

• Toxic megacolon is defined as a severe attack of colitis with total or segmental dilatation of
colon
 • Rectal mucosal prolapse (solitary rectal ulcer syndrome)

Management
• If initial response to corticosteroids and relapse with reduction of dose to 15 mg/day or within 6
weeks of stopping corticosteroids

• Azathioprine 1.5–2.5 mg/kg/day

• Monitoring full blood count every 4–6 weeks

• If tolerated the drug is continued for 3–5 years to prevent relapse

• Methotrexate if no response to azathioprine

• Cyclosporine IV in severe UC refractory to steroids

• Mycophenolate mofetil is effective in maintaining remission as also Infliximab

• Tofacitinib an oral inhibitor of janus kinases 1, 3 is effective in moderate to severe UC in clinical

trials

Indications for Surgery

(a) Emergency surgery for severe disease, toxic dilatation of colon, perforation, severe hemorrhage

(b) Elective surgery : Acute disease that fails to respond to medical treatment, frequent relapses in spite
of adequate treatment, chronic disease with permanently damaged bowels, strictures, total bowel
involvement with activity extending over more than 10 years. Colectomy with temporary ileostomy and
ileoanal pouch construction is operation of choice.

2. CROHN’S DISEASE
• A non-specific granulomatous inflammation involving sharply demarcated single or multiple
areas of the intestine and probably a non-specific pathological response to a variety of exciting
agents.
• It is an idiopathic, chronic, transmural inflammatory process of the bowel that can affect any
part of the GIT from the mouth to the anus.
• It can affect any part of the GI tract but most commonly affects the terminal ileum or the
ileocaecal region.
Etiology
Genetic factors : About 15–20% of patients with Crohn’s disease have one or more family members with
either Crohn’s disease or ulcerative colitis. Mutations in the CARD15 (NOD2) gene on chromosome 16
have been found in about one-third of patients with Crohn’s disease and are particularly associated with
ileal disease. Genes within the HLA region appear to influence colonic involvement and the presence of
extraintestinal manifestations.
Smoking : Smokers are more likely to develop the disease than non-smokers.
Infective organisms : Mycobacterium paratuberculosis has been found in tissue of a small number of
patients with Crohn’s disease.
Diet : High intake of refined sugar and low intake of fibre from fruits and vegetables have been reported
in patients with Crohn’s disease.
Immune mechanisms : There is evidence that the normal mechanisms for down-regulating mucosal
immune response are impaired in patients with Crohn’s disease.
Pathogenesis
Antigenic stimulation
Microbial / dietary antigen

Intestinal mucosa Gut immune system

Physiological inflammation

Genetic predisposition
Normal host Susceptible host Environmental factors

Limited inflammation Uncontrolled inflammation

Healing with no tissue injury Extensive tissue injury

Crohn’s dz
Clinical Features
• Abdominal pain, Flatulence, Bloating
• Diarrhoea, Perianal discomfort
• People who have had surgery often end up with short bowel syndrome of the GIT
• Dysphagia
• Fever
• Mouth sores (Aphthous ulcers)
• Reduced appetite & weight loss
• More than 20 bowel movements per day and may need to awaken at night to defecate
• Fistula
Investigations
1. Stool examination to exclude known pathogens
2. Sigmoidoscopy and rectal biopsy : Patients with small bowel involvement may show histological
evidence of
rectal inflammation.
3. Imaging :
(a) Small bowel enema (enteroclysis) and an air-contrast barium enema
(b) Indium 111-labelled or 99 technetium – HMPAO labelled leucocyte scans may also be helpful in
demonstrating extent of inflammation if barium radiology is equivocal.
(c) Ultrasonography may be helpful in patients with a palpable abdominal mass in order to differentiate
an inflammatory mass from an abscess.
(d) CT is often more useful and may show thickened loops of affected intestine.
(e) MRI is the procedure of choice for investigating complex perianal disease.
Differential Diagnosis
Small intestinal disease :
(a) Tuberculosis : Colonoscopy with multiple biopsy may be helpful and laparotomy may detect serosal
tubercles. (b) Microscopic colitis is characterised by chronic watery diarrhea. Collagenous and
lymphocytic colitis are the two common forms of microscopic colitis.
(c) Other conditions include intestinal lymphoma, carcinoid, α-chain disease, actinomycosis, amyloidosis,
Behcet’s disease and carcinoma.
Management
1. General measures
• Well-balanced diet with high fibre content. Low-fat, low-residue diet if steatorrhoea or
strictures.
• Vitamin supplements.
• Rest in bed during acute phase with liquid diet.
• If anemia, iron by injection or B12 and folic acid if megaloblastic anaemia.
• Codeine sulphate, diphenoxylate or loperamide helps to reduce bowel looseness.
2. Drug treatment
• Aminosalicylates—Sulphasalazine 1g tds orally in active colonic disease.
• Mesalazine delayed release 400mg tds for maintenance therapy.
• Corticosteroids are beneficial in active disease :
(a) Local therapy : Hydrocortisone suppositories for disease of rectosigmoid colon, foam or liquid enema
for more proximal disease od or bd × 3–6 weeks. Prednisolon 0.25–0.75 mg/kg to maximum of 60 mg
for 4 months.
(b) Systemic treatment : Parenteral corticosteroids e.g. Hydrocortisone 100 mg. IV 8-hourly useful for
inducing remission in severely ill patients with acute Crohn’s colitis.
• Metronidazole 400 mg t.d.s. if associated sepsis
• Immunosuppressive agents—Azathioprine 2.5 mg/kg/day or 6-mercaptopurine 1.5 mg/kg/day
may be used if other therapy has failed and surgical treatment is inappropriate.
• Immunotherapy : Infliximab Single infusion of 5mg / kg IV
3. Surgical
Indications:
• Intestinal obstruction
• Perforation
• Failure to respond to medical therapy
• Complications such as fistulas and perianal disease. Limited resections, stricturoplasty or end-to-
end anastomosis as necessary.
• Split ileostomy to isolate colon in case of fistulas and perianal disease.
Complications
• Strictures : More common in small intestine. May cause obstructive symptoms.
• Fistulas : May develop between loops of bowel adjacent to the bladder or vagina. Pneumaturia
and recurrent urinary infections indicate fistula into the bladder. Passage of flatus or feculent
vaginal discharge signifies a vaginal fistula.
• Perianal disease : Fissures, fistulas and abscesses
• Carcinoma of intestine
• Secondary amyloidosis in long standing cases
PEPTIC ULCER
• The term peptic ulcer applies to mucosal ulceration near the acid bearing regions of the
gastrointestinal tract. Most ulcers occur in the stomach or proximal duodenum but they may
also occur in the oesophagus (due to acid reflux), in jejunum (at site of gastrointestinal
anastomosis) and rarely in relation to ectopic gastric mucosa (near a Meckel’s diverticulum).
Causes
• Bacteria : Helicobacter. Pylori
• Certain pain relievers
• Smoking cigarettes & drinking alcohol
• Stomach cancer
• Radiation therapy
Types
Gastric ulcers : Ulcers that develop inside the stomach
Oesophageal ulcers : Ulcers that develop inside the oesophagus
Duodenal ulcers : Ulcers that developin the upper section of the small intestines, called the duodenum
ETIOPATHOGENESIS OF PEPTIC ULCER
1. Heredity and strong family history
2. Peptic ulceration results from digestion of the mucosa with acid and pepsin of gastric juice. Acid
secretion is
more important in etiology of duodenal ulcer than gastric ulcer.
3. Mucosal resistance (Gastric mucosal barrier). Mechanism:
(a) Secretion of bicarbonate by surface epithelial cells under the influence of mucosal prostaglandins.
These cells also secrete mucus that impedes diffusion of ions and molecules such as pepsin.
(b) The tight intercellular junctions and surface lipoprotein level provide a mechanical barrier.
(c) The submucosal area provides micronutrients and oxygen while removing toxic metabolic products of
gastric epithelial cells.
(d) Factors reducing mucosal resistance – Drugs like aspirin, NSAIDs, H. pylori infection, reflux of bile and
intestinal contents into stomach due to poorly functioning pyloric sphincter.
SIGNS & SYMPTOMS
• Abdominal discomfort usually occurs in epigastric area radiating to the back
• Dull gnawing pain comes and goes for several days
• Pain may increase when the stomach is empty at night or half to three hours after meal
• Fatigue
• Bloating, blurping
• Chest pain
• Nausea and anorexia
• Vomiting(relieves episodes of pain)
• Emergency symptoms : Sharp sudden persistent pain
Bloody or black stools
Blood vomit or look like coffee grounds
• Tenderness : Deep tenderness to the right of the middle in epigastrium. Localised over the site
of lesion on deep palpation. Superficial tenderness may be present.
• Muscle guarding or rigidity : may be present with active ulcer or deeply penetrating ulcer.
 • Peristaltic waves may be observed in presence of obstruction. Gastric splash may suggest gastric
retention due to duodenal ulcer near pylorus.
• Occult blood in stools
INVESTIGATIONS
Endoscopy is the ideal method of diagnosing duodenal ulcer. The ulcer often appears like a severe
aphthous ulcer with a creamy base.
Barium meal
Acute stage
• Ulcer crater. Persistent pool of barium.
• Ulcer niche. Crater jutting beyond margins, shown to be on anterior or posterior wall on rolling
the patient.
• Irritable duodenal cap seen as spasticity of the cap or a hurry of the barium as it passes through
the cap.
Healing stage
• Radiating folds. Mucosal folds radiating away from the ulcer.
• Scarred and deformed duodenal cap (trifoliate deformity) with multiple ulcers and healing.
Radiographic criteria for benign gastric ulcer
Ulcer crater extending beyond gastric wall
Gastric folds radiating into base of ulcer
Thick radiolucent collar of oedema (Hampton’s line) surrounding ulcer base.
Smooth, regular, round or oval ulcer crater
3. Gastroscopy
4. Tests for H. pylori
5. Fasting plasma gastrin concentration—Elevated in Z-E syndrome. Fasting gastrin levels are usually
<150 pg/mL.
6. Hb and MCV—To exclude anemia of iron deficiency
Management
1. Life style modification
• Discontinue NSAIDS
• Smoking cessation & Alcohol cessation
• Stress reduction
2. Hyposecretory drugs
• Proton-pump inhibitors : suppress acid production
• H2 receptor antagonists : Block histamine stimulated gastric secretions
• Antacids : neutralizes acid and prevent formation of pepsin. Give 2hrs after meals and at
bedtime
• Mucosal barrier fortifiers : forms a protective coat
3. H.pylori eradication therapy
• Proton pump inhibitor
• Two Antibiotics : Metronidazole + Clarithromycin, Clarithromycin + Amoxicillin
4. Surgical
• Failure of medical treatment
• High level of gastric secretion and combined duodenal and gastric ulcer
• Surgical procedures : Gastroenterostomy, Vagotomy, Pyloroplasty
Complications
1. Bleeding—Most common
2. Perforation—Acute or chronic perforation into surrounding organs – pancreas, liver, bile duct, colon
3. Pyloric stenosis
4. Malignancy at site of ulcer
5. Pancreatitis due to posterior penetration of ulcer

ACUTE PANCREATITIS
• Acute pancreatitis is characterized by sudden, severe abdominal pain and a varying degree of
systemic upset.
• It is reversible pancreatic parenchymal injury associated wwith inflammation.
• Severe pancreatitis manifest as organ failure and local complication such as necrosis, abscess or
pseudocyst.
Causes
• Mechanical : Gallstones, trauma blunt and penetrating
• Alcohol, Scorpion sting
• Drugs : Tetracyclines, oestrogens, azathioprine, thiazides, valproic acid, corticosteroids,
organophosphorus poisoning
• Infections: Viral hepatitis, mumps, toxoplasmosis, roundworms
• Iatrogenic : ERCP
• Metabolic conditions : Hypertriglyceridemia, kidney failure, post-kidney transplantation,
hypercalcemia, acute fatty liver of pregnancy
• Hereditary : Mutation in cationic trypsinogen & trypsin inhibitor gene
• Idiopathic
Pathology
• Pancreas show oedema, necrosis of acinar & dust cell & infiltration with inflammation.
• It extends to surrounding area & it produce H’ge. (Release of enzyme lead to fat necrosis)
• Pancreatic secretion may collect to form one or more pseudocyst which may have not epithelial
lining & have granulation tissue. Pancreatic abscess may form when pseudocyst or inflammatory
mass become infected.
Clinical Features
• Pain – usually epigastric radiating to the back
• Vomiting
• Dehydration
• Epigastric tenderness
• Confusion (due to hypoxia)
• Jaundice (10–20%)
• Hypotension
• Discoloration of flanks (Grey-Turner sign)
• Discoloration of periumbilical area (Cullen’s sign) : Both these signs indicate severe necrotizing
pancreatitis.
Pathogenesis
Duct obstruction Acinar cell injury Defective intracellular transport

Interstitial oedema Release intracellular proenzyme Delivery of proenzyme to

& lysosomal hydrolase lysosomal compartment

Impaired blood flow

Ischaemia Activation of enzyme Intracellular activation of enzyme

Interstitial inflammation Protease Fat necrosis H’ge

Oedema

Proteolysis

Acute pancreatitis
Investigations
• LFTs in first 24 hours indicate a likely biliary cause (raised transaminases or bilirubin)
• Abdominal ultrasonography reveals any stones in GB.
• CT may be helpful when there is doubt about the diagnosis, but it is preferable to wait 7–10
days after onset of symptoms for detection of pancreatic necrosis.
Diagnosis
(a) Point-of-care urine Trypsinogen - 2 test. Good sensitivity and specificity and can be used at the bed
side.
(b) In such cases CT should be performed to confirm the diagnosis.
Serum amylase and serum lipase elevated three fold or more. Serum amylase value tends to be normal
in 3–7 days even in continuous presence of pancreatitis while serum lipase takes 7–14 days.
Differential diagnosis
• Acute cholecystitis
• Splenic rupture
• Appendicitis
• Renal colic
• Peptic ulcer
• Intestinal obstruction
Management
• Immediate treatment : Patient must be fitted with a face mask and given oxygen until there is
no danger of organ failure. Simultaneously fluid replacement with a mixture of crystalloid and
colloid to restore circulating volume and maintain urine output.
• Nutritional management : Enteral therapy is started after 2–3 days of admission.
 • Treatment to remove the cause: ERCP for gallstones within 48–72 hours of admission to
hospital. Endoscopic sphincterotomy should be performed in all patients undergoing ERCP.
• If secondary to alcohol consumption or medication (valproate, pentamidine, azathioprine,
oestrogens, corticosteroids) patient should avoid these agents in future.
• Early enteronutrition is safe and preferred to parenteral nutrition.
• Prophylactic antibiotics in patients with predicted severe pancreatitis including evidence of
pancreatic necrosis.
• Surgical treatment may be necessary for complications such as pancreatic necrosis or
pseudocyst.
Complications
• Pseudocysts
• Necrosis
• H’ge
• Duodenal obstruction
• Pericardial effusion
• ARDs
• ARF
• DIC
• Internal fistulas
Conservative treatment
P : Pain relief, Protease inhibitor
A : Antibiotic, Anticholinergic
N : Nasogastric aspiration, Nutritional support
C : Calcium, Calcitonin
R : Rehydration, Respiratory support, Ranitidine, Resuscitation
E : Entrachal intubation (electrolytes management)
A : Antacids
S : Somatostatin

CHRONIC PANCREATITIS
• Chronic pancreatitis is a progressive, irreversible inflammatory disease. The dominant symptom
is usually upper abdominal pain which can be incapacitating. As the disease progresses, exocrine
insufficiency (manifested as weight loss and steatorrhoea) or endocrine insufficiency (diabetes
mellitus) become more common.
Etiology
1. Chronic calcifying pancreatitis (CCP)
Alcohol is the major cause, the risk related to duration of drinking and amount consumed. CCP is more
likely
to develop in individuals with a high-fat, high-protein diet. Patients with hyperlipidaemia or
hyperparathyroidism commonly present with acute pancreatitis, but some develop CCP.
2. Chronic obstructive pancreatitis is less common than CCP :
o Tumors of ampulla and pancreas (mostly malignant)
o Cystic lesions—Most inflammatory, few congenital or neoplastic
Pancreatic duct damage due to acute pancreatitis, resolution of cyst or pseudocyst or trauma
o Ampullary stenosis or associated diverticulum.
o Cholelithiasis usually causes acute pancreatitis but some patients have chronic disease.
Pathogenesis
Four major theories :
1. Toxic metabolic proposes that alcohol directly toxic to acinar cells through changes in cellular
metabolism.
2. Oxidative stress theory proposes overactivity of hepatic mixed function oxidase as a cause.
3. Stone & Duct obstruction

Increases lithgenecity of pancreatic fluid

Leading to formation of plug & stone

Chronic contact with stone

In pancreatic ductal produce ulceration & scarring

Obstruction, stasis

Further stone formation

4. Necrosis & Fibrosis

Recurrent acute pancreatitis

Chronic pancreatitis
Clinical Features
• Severe episodic upper abdominal pain radiates to the back. It lasts for hours or days and may be
relieved by bending forwards or vomiting.
• Some patients particularly with idiopathic CCP experience no pain.
• Steatorrhea
• Diarrhoea
• Fat-soluble vitamin deficiency such as bleeding, osteopenia and osteoporosis
• Endocrine insufficiency - diabetes mellitus
• Jaundice or Cholangitis
• Rarely upper GI bleed
Investigations
• Plain abdominal radiograph may show pancreatic calcification.
• Ultrasonography shows changes in pancreatic size, shape, echotexture and calcification.
Endoscopic ultrasonography allows detailed investigation of difficult cases (notably cystic or mass
lesions).
• CT scan : It shows diffuse calcification, dilated ducts and atrophic pancreas.
 • ERCP is the ‘gold standard’ investigation.
• Pancreatography demonstrates stenosis or disruption of pancreatic duct, variant duct anatomy
and connections to cystic lesions.
• Cholangiography shows choledocholithiasis and ampullary or common bile duct stenosis.
• Magnetic resonance cholangiopancreatography provides information about ductal and vascular
structure
• and function.
• Biochemical investigations—There is no reliable biochemical test for chronic pancreatitis.
• Serum enzymes amylase, isoamylase, trypsin and lipase levels may be elevated.
• Endocrine function test: Oral glucose tolerance test is impaired.
• Pancreatic biopsy : It is used to determine the nature of pancreatic mass lesions.
Management
Control of Pain : Nonsteroidal analgesics are preferred but most patients with severe pain require oral
narcotic analgesics.
Steatorrhoea : Pancreatic enzyme supplements enteric coated. A few patients also require H2 receptor
antagonists
or dietary fat restriction.
Diabetes : may be controlled using diet or oral hypoglycaemic agents. Patients who require insulin are
prone
to hypoglycaemic episodes.
Endoscopic therapy and ERCP : Patients who are suitable for endotherapy are first subjected to intensive
ESWL sessions for stone pulverization followed by ERCP and stone clearance.
Antioxidant therapy : Micronutrient supplementation with selenium, methionine and vitamins A, C and
E since evidence suggests that oxidative stress is an important factor in pathogenesis of pancreatitis.
Surgery : Patients who have a complete distal pathology in the head, have an inflammatory head mass,
those who have predominantly tail stones and those who have an atrophied gland with severe pain are
most suitable for surgical intervention (Head coring, bypass or resection).
AUTOIMMUNE PANCREATITIS
• It is disorder with autoimmune pathology and characteristic laboratory, histological and morphological
features. It is associated with other disorders of presumed autoimmune etiology and this has been termed
IgG4 systemic disease.
Types
Type1 : Pancreas is involved as part of systemic IgG4 disease. On histopathology, there is
lymphoplasmacytic infiltration with IgG4 positive cells.
Type2 : It is without IgG4 positive cells and systemic involvement.
Clinical Features
• Abdominal pain
• Weight loss
• New onset diabetes
• Steatorrhoea
• Associated systemic IgG4 diseases- Sjogren’s syndrome, RA, cholangitis, Mikulicz’s disease,
autoimmune thyroiditis, ulcerative colitis, tubulointerstitial nephritis.
Investigations
• Alkaline phosphates elevated out of proportion to minimally elevated aminotransferase
• Elevated IgG4 levels
• Autoantibodies seen like ANA, rheumatoid factor
 • CT scan reveals focal enlargement, diffuse enlargement and distinct enlargement of pancreatic
head
• ERCP or MRCP reveal diffuse irregular narrowing of pancreatic duct
Treatment
• These patients respond well to systemic steroids.
• Prednisone is started at the dose of 40 mg/day for 2–4 weeks then as per patient response it is tapered 5
mg/week.
• Response is monitored with clinical improvement, decrease in alkaline phosphatase level and IgG4 levels
and serial changes in imaging.
• Type 1 patients tend to relapse in those patients use of azathioprine has shown improvement.
• Other agents like rituximab, cyclophosphamide, cyclosporine have been successful in small group of
patients.

CIRRHOSIS OF LIVER
• The term cirrhosis is applied to chronic diffuse liver disease of varied etiology and characterised
by hepatic cell
• necrosis, proliferation of connective tissue and nodular regeneration or in other words
abnormal reconstruction
• of lobular architecture and disturbed hepatic circulation.
Pathological classification
1. Micronodular cirrhosis (portal or alcoholic cirrhosis) : Characterised by thick, regular bands of
connective tissue, by regenerating small nodules of almost same size and involvement of every lobule of
the organ.
2. Micronodular coarse cirrhosis (post-necrotic) : Liver reduced in size. Nodules of regenerating liver
cells of different sizes intersected by fibrous bands of varying thickness containing proliferating bile
ducts.
3. Mixed micronodular and macronodular : Following bile duct stricture and minimal liver cell failure and
portal hypertension.
Etiology
• Viral hepatitis B & C
• Alcoholic cirrhosis
• Cryptogenic cirrhosis
• Biliary obstruction
• Budd chiari syndrome
• Congestive heart failure
• Drugs
• Wilson’s dz
Pathogenesis
Liver injury

Kuppfer cell & hepatocytes produces cytokines

Cytokines activate stellate cells which are multifunctional

 Transformation of stellate cells into myofibroblast

Myofibroblast cells are capable of producing collagen, pro-inflammatory cytokines & mediators

Hepatocellular damage tissue’s fibrosis

Clinical features
• Vague with anorexia, dyspepsia, weight loss, malaise and loss of libido
• Haematemesis
• Asymptomatic with hepatomegaly
• Hepatomegaly : Liver may be palpable, non-tender, shrinks as disease advances.
• Jaundice : Uncommon, when present it may be due to hepatocellular failure or intrahepatic
cholestasis.
• Ascites : Water retention due to cirrhosis
Decreased plasma colloid pressure due to reduced albumin synthesis in liver
Portal hypertention
Increased hepatic lymph production due to obstruction
• Haematological : Purpura, Anaemia
• Dermatological & MSS : Alopecia
Arterial spiders (Spider naevi)
Palmar erythema (Liver palms)
• Endocrine : Male—Gynecomastia, testicular atrophy, feminization, impotence
Female—Lowered libido and usually atrophy of the breasts
• Neurological : Porto-systemic encephalopathy
Peripheral neuropathy
• Miscellaneous : Swelling of ankles, diarrhoea, low grade fever
Investigations
1. Blood
(a) Anaemia—Normocytic, normochromic
(b) Low white cell count or reduced platelets due to hypersplenism
(c) Raised ESR from abnormal serum protein
2. Liver function tests
May be normal in patients with compensated cirrhosis. Usually slight increase in aminotransferase and
immunoglobulin levels and fall in serum albumin.
3. Radiology : Barium swallow—Oesophageal and gastric varices.
4. Imaging : Ultrasound
(i) In cirrhosis may cause a ‘bright liver’ (also in fatty infiltration and chronic hepatitis) and nodules may
be seen
(ii) In portal hypertension a large congested spleen is seen with dilatation of splenic and portal veins
(iii) Can also detect very small amounts of ascites
• CT scan
• Trans-splenic portal venography
• Liver biopsy
Differential diagnosis
 • Hepatomegaly
• Haematemesis
• Splenomegaly
• Jaundice
• Ascites
• Encephalopathy
Management
Management is palliative
• Rest in bed to maximize treatment of any reversible element of underlying liver disease and to
improve renal perfusion.
• Correction of any etiological factor e.g. abstinence from alcohol, prednisolone for chronic
hepatitis, antiviral agents for viral hepatitis.
• Diet : Low salt. Total daily intake of 2000 calories with protein intake of 120 gm.
• Drugs :
(a) Corticosteroids may help patient with active post-hepatitis cirrhosis. Prednisolone 10 mg daily for
many months.
(b) Immunosuppressive agents – Azathioprine dose 50–75 mg daily.
• Symptomatic treatment :
(a) Anaemia : Oral iron preparations or blood transfusion.
(b) Restlessness : Sedative drugs like Oxazepam or lorazepam
(c) Ascites : Low sodium diet—Sodium intake up to 500 mg daily. Diuretics : First 4 days—Bed rest.
Complications
1. Due to portal hypertension : Haematemesis, thrombosis of portal vein
2. Due to liver cell dysfunction : Portasystemic encephalopathy
3. Due to formation of regeneration nodules : Hepatoma
4. Mechanical due to ascites : Hernia
5. Due to infection : Spontaneous bacterial peritonitis, Secondary bacterial peritonitis, Tuberculous
peritonitis.
6. Hypersplenism
7. Chronic kidney failure

ACUTE LIVER FAILURE

• Acute liver failure is a rare, life threatening clinical syndrome, resulting in loss of hepatic
metabolic & immunological function, in a person with no prior history of liver dz.
Classification
1. Hyper-acute—Jaundice (Illness) for <7 days before onset of encephalopathy (e.g. paracetamol
poisoning)
2. Acute—Jaundice (Illness) for 8–28 days (7–21 days) before onset
3. Subacute—Jaundice (Illness) for 4–12 weeks (21 days to 26 weeks) before onset
Causes
• Drugs : Acetaminophen, Antibiotics, NSAIDs
• Toxin : CCI4, Mushroom poisoning
• Metabolic : Wilson dz
• Pregnancy
• Sepsis, Malignant infiltration
Pathophysiology
• Loss of normal function of hepatic tissue which occurs over a short period of time.
• It results in the loss of the metabolic, secretory & regulatory effects of the liver cells.
• This results in the rapid accumulation of toxic substances, when then manifests in the pt as an
altered sensorium, cerebral oedema, hemodynamic abnormalities & even multiorgan failure.
Clinical features
• Pain and tenderness in upper right side of stomach
• Hepatic encephalopathy
• Flappy tremor
• Mild drowsiness to complete unresponsiveness. Fetor is usually absent.
• Hypertension (with cerebral oedema)
• Hypotension
• Tachyarrhythmias
• Bradycardia
• Fever
• Melena & hematemesis
• Ascites
• Kidney failure—Early with paracetamol overdose
• Respiratory failure—Mainly due to infection, fluid overload and adult respiratory distress
syndrome Coagulopathy—May manifest as bleeding from puncture sites and urinary and GI
tracts
Investigations
• Tests for infection—Blood screened for acute hepatitis A and B by testing for anti-HAV IgM and
anti-HBc IgM respectively.
• Ultrasonography and CT—For patency of hepatic veins, malignant infiltration and estimate of
liver volume.
• Prothrombin time and serum bilirubin, aminotransferase levels, serum albumin, serum
creatinine, electrolyte levels.
Management
Drugs
(a) N-acetylcysteine is the only drug with a proven role. Its metabolism produces glutathione which
detoxifies the toxic molecule.
(b) Sucralfate to reduce bleeding from gastric erosions.
(c) Vitamin K parenterally to patients who have been jaundiced for more than 2 weeks.
Inotropic support—Combination of noradrenalin or dopamine with N-acetylcysteine or prostacyclin.
Treatment of complications :
Liver transplantation—It has a survival rate of more than 60%. Auxiliary liver transplantation for a
subgroup of patients who have the capacity to regain normal function in the native liver.
Other techniques—Extracorporeal circuits incorporating viable hepatocytes to offer artificial liver
support. These devices aid recovery by acting as a bridge to transplantation with or without a
preliminary hepatectomy which often temporarily stabilises critically ill patients.

ASCITES
• Ascites is defined as the accumulation of free fluid in the peritoneal cavity.
Causes
1. Normal peritoneum
Hypoalbuminemia : Nephrotic syndrome
Protein-losing enteropathy
Severe malnutrition with anasarca
Miscellaneous conditions : Chylous ascites
Pancreatic ascites
Nephrogenic ascites
Meig’s syndrome
2. Disease of peritoneum
Infections : Tuberculous peritonitis
Spontaneous bacterial peritonitis
Fungal – Candida, histoplasma
Parasitic – Schistosoma, enterobius
Viral – Acute severe hepatitis
Neoplasms : Primary mesothelioma
Secondary carcinomatosis
Pseudomyxoma peritonei
Familial paroxysmal peritonitis
Miscellaneous : Vasculitis
Granulomatous peritonitis
Pathogenesis
Cirrhosis

Portal hypertension

Splanchnic arterial vasodilatation

Reduced effective arterial blood volume

Stimulation of antiatriuretic / vasoconstrictor systems

Increased tubular sodium reabsorption

Sodium & fluid retention

Ascites
Investigations
Ascitic Fluid Analysis
 o Clear—usually occurs in congestive heart failure, hypoalbuminemia, cirrhosis, inferior vena cava
obstruction, Budd-Chiari syndrome, Meigs’ syndrome and vasculitis.
o Turbid is common in tuberculous peritonitis, peritoneal malignancy, bacterial peritonitis,
pancreatic ascites, and myxoedema.
o Haemorrhagic—Tuberculosis, acute haemorrhagic pancreatitis, mesenteric artery thrombosis,
malignancy involving peritoneum or liver surface, benign hepatic adenoma or spontaneous
bleeding from intra-abdominal portal-systemic collaterals.
o Chylous (milky)—Trauma to thoracic duct, filariasis, congenital.
• Protein content seldom exceeds 1.5 g/dL. Higher values indicate infection, hepatic venous
obstruction or malignancy.
• Serum-ascites albumin gradient : SAAG is more useful than total protein concentration of ascitic
fluid.
• Ascitic amylase high in pancreatic ascites.
• SBP in patient with cirrhosis and ascites has high mortality.
• Ultrasonography can detect as little as 100 ml of abdominal fluid and may suggest the cause.
• Liver biopsy of value in cirrhosis or malignancy of liver.
• Liver function tests to confirm cirrhosis.
• Liver scan for space occupying lesions of the liver.
• Laparoscopy useful for (i) paracentesis (ii) direct visualization of abdominal viscera (iii) biopsy of
liver
• Selective arteriography of the hepatic and splenic arteries with delayed films to visualise the
portal vein may be helpful in ascites of obscure cause.
• Needle Biopsy of peritoneum for diagnosis of tuberculous and malignant peritonitis.
• CT scan
Physical examination
1. General appearance : Spider man—thin limbs with protuberant abdomen.
2. Free fluid in peritoneal cavity—Generalised abdominal distension, bulging in the flanks, umbilicus
transversely stretched or everted.
3. Increased intra-abdominal pressure—Abdominal wall hernias (umbilical or inguinal), divarication of
recti, increased inferior vena cava pressure causing lower limb oedema.
4. Causative condition
(a) Portal hypertension—Splenomegaly, portal-systemic venous collaterals.
(b) Chronic liver disease—Peripheral stigmas of chronic liver disease, or cholestasis, hepatic
encephalopathy.
(c) Evidence of tuberculosis elsewhere in tuberculous peritonitis.
5. Rectal examination for hemorrhoids, malignant lesion in pelvis or fluid in pouch of Douglas.
Management
Of the cause :
• Digitalis for cardiac failure, anti-tuberculous drugs for tuberculous peritonitis, pericardiolysis for
constrictive pericarditis, Vitamin B1 for beriberi.
Of ascites itself :
1. Bed rest improves renal perfusion.
2. Diet—Low sodium diet if fluid non-inflammatory. Restrict fluid to 1 litre/day.
3. Diuretics—Spironolactone 100 mg, if no response, add frusemide 40 mg. Aim is to achieve weight loss
of 300–500 g/day in ascitic patients with peripheral oedema.
4. Therapeutic paracentesis : Technique
 • Ask patient to empty his bladder and prop him up in bed. Paracentesis is usually performed in
the right iliac fossa avoiding inferior epigastric vessels, visible venous collaterals and scars of
previous operations.
• The skin is cleansed and local anaesthetic infiltrated through to the peritoneum. To minimize
chances of subsequent leakage of ascitic fluid, a thin bore needle (21–23 gauge) attached to a
20ml syringe is used.
• The aspiration needle is inserted through the skin which is then pulled sideways and the needle
pushed through the abdominal wall, muscle and peritoneum. The fluid is drained slowly.
• An abdominal binder or many-tailed bandage is placed round the abdomen and it is tightened as
required.
• Paracentesis can also be performed with special needle with side holes, attached to low grade
suction.
Complications
• Fainting
• Acute peritonitis
• Perforation of viscus
• Acute liver failure
• Depletion of proteins
• Peritoneovenous shunt

JAUNDICE
• It is a symptom complex characterized by yellowish pigmentation of skin (increase of bile
pigments in body fluids and tissues).
• Jaundice is perceptible only when the level of bilirubin and its conjugates exceeds 1.5 mg per
100 mL plasma.
• In its mildest form it is recognized by yellow discolouration of sclera. With deeper jaundice the
skin and mucous membrane are also stained.
Classification
Based upon derangement of bilirubin metabolism
1. Unconjugated Jaundice : Causes
• Increased bilirubin production : i. Haemolysis ii. Ineffective erythropoiesis iii. Reabsorption of
hematoma
• Impaired hepatic uptake : i. Drugs ii. Sepsis
• Decreased conjugation : i. Neonatal jaundice ii. Crigler-Najjar syndrome iii. Gilbert’s syndrome
2. Conjugated Jaundice : Causes
(a) In most cases of acquired liver disease whether acute hepatitis or cirrhosis, jaundice is predominantly
conjugated and accompanied by dark urine.
(b) In most cases cholestasis is the most common pattern of drug-induced jaundice. Common causes of
extrahepatic cholestasis are bile duct stones and malignant bile duct obstruction (e.g. pancreatic
cancer).
Based upon pathological mechanism
1. Hemolytic jaundice : Results from increased destruction of RBCs or their precursors in the marrow,
causing increased bilirubin production.
Causes : Sperocytes
Sickle cell anaemia
Thalassemia
 G6PD deficiency
Malaria
2. Hepatocellular jaundice : Its results from inability of the liver to transport bilirubin into thr bile
occurring as a consequence of parenchymal dz. Bilirubin transport across the hepatocytes may be
impaired at any point between uptake of conjugated bilirubin into the canaculi.
Causes : Viral hepatitis
Alcoholic “
Chronic “
Cirrhosis
3. Cholestatic (obstructive) jaundice :
Causes : Failure of hepatocytes
Obstruction of bile duct
Obstruction of bile flow in extrahepatic bile ducts between porta hepatis & papilla of vater
Signs & Symptoms
• Anaemia
• Jaundice usually mild and of a lemon yellow tint. No pruritus.
• Pigmented gallstones may be associated with features of chronic cholecystitis
• Splenomegaly in chronic forms
• Ulcers or pigmentation from healed ulcers usually over the malleoli in some cases
• Stools : Dark in colour due to increased stercobilinogen
• Urine : Urobilinogen increased
• Haemoglobinuria
• Pruritus
• Abdominal pain
• Xanthelasma on eyelids, tendons (lipid deposit)
• Hepatomegaly
• Secondary biliary cirrhosis
• Bone pains
Investigations
Treatment
Complications

HEMETEMESIS
• Hematemesis indicates a site of bleeding proximal to duodenal - jejunal junction, because blood
entering the gut distal to this point seldom returns to the stomach.
• The colour of the blood depends on whether the blood has been in the stomach, a large volume
of bright red blood suggests a rapid and sizable hemorrhage, whereas a small amount of dark
blood (coffee grounds) is more suggestive of a smaller bleed that has been altered by contact
with gastric acid.
Causes
1. Oesophagus
• Mallory-Weiss tear
• Oesophageal carcinoma & varices
• Reflux oesophagitis
• Foreign body
2. Stomach
• Peptic ulcer
• Erosive gastritis
• Portal hypertensive gastropathy
• Gastric carcinoma
• Lymphoma
• Leiomyoma
• Angiodysplasia
3. Duodenum/jejunum
• Peptic ulcer
• Erosions/duodenitis
• Vascular anomalies (AVMs)
• Hemophilia
• Polyps
Clinical features
• Dizziness , feeling faint
• Confusion
• Enlarged pupils
• Weakness
• Rapid, shallow breathing
• Reduced urine production
• Cool, clammy, pale skin
• Anxiety
Investigations
History
• Vomiting or retching
• Heart burn and regurgitation : Reflux oesophagitis
• Dysphagia and weight loss : Oesophageal malignancy
• History of peptic ulcer or abdominal pain
• Drugs : Intake of aspirin or NSAIDs
• Alcohol intake
• Haematemesis with melena—Indicates that the source of bleeding must be proximal to the
jejunum.
Blood tests
• Hemoglobin concentration : Low Hb
• Urea and electrolytes : Elevated blood urea suggests severe bleeding
• Liver function tests
• Prothrombin time
• Angiography/CT angiography does not detect bleeding at rates below 1mL/min, but occasionally
reveals underlying vascular abnormalities.
Examination
• Does the patient look pale or shocked?
• Pulse rate and BP
• Postural hypotension
• Presence of purpura or petechiae
 • Splenomegaly, dilated abdominal veins or ascites : Signs of portal hypertension in patients
bleeding from gastric or oesophageal varices.
• Presence of jaundice
Management
Primary care (before hospital admission)
• IV access with infusion of normal saline
• Oxygen
• Early hospitalization
Hospital management
Resuscitation : Insertion of large bore cannula into a substantial vein. If pulse rate > 100/min or systolic
BP falls below 100 mm Hg – infusion of crystalloids such as normal saline is started.
If blood transfusion is required, 2–4 units of whole cross-matched blood. Aim is to maintain Hb
concentration of 10g/dL.
After resuscitation : Endoscopy must be done within 24 hours and is necessary for diagnosis in order to
plan treatment.

DYSPHAGIA
• Dysphagia indicates a delay in the passage of solids or liquids from the mouth to the stomach.
• In general, mechanical causes lead to dysphagia for solid foods whereas patients with motility
disorders tend to complain of non-progressive dysphagia for both liquids and solids from the
onset.
CAUSES OF DYSPHAGIA
1. Oropharyngeal
• Myasthenia gravis
• Multiple sclerosis
• Bulbar palsy
• Polyneuropathy
• Candida
• Herpes
• Aortic aneurysm
• Mucosal mass
• Thyroid enlargement
• Globus hystericus
2. Oesophageal
• Achalasia
• Diffuse oesophageal spasm
• Oesophagitis
• Oesophagus CA & stricture
Investigations
1. Laryngoscopy—Ulceration or growth of larynx
2. Barium swallow—Cardiospasm, stricture, growth
3. Barium meal—For hiatus hernia or peptic ulceration
4. X-ray chest—Mediastinal tumour, aneurysm, mitral valve disease.
5. Endoscopy is the best way to determine the cause of dysphagia because of high diagnostic accuracy
and opportunity to take biopsies
History
 • Children : Cleft palate, foreign body or diphtheritic paralysis.
• Young females : Hysterical spasm, Menopause, Sideropaenic dysphagia
• Males : Above 50 Carcinoma oesophagus
• Oropharyngeal dysphagia is usually distinguished from oesophageal dysphagia by the patient’s
awareness of inability to initiate swallowing properly and occurrence of nasopharyngeal
regurgitation, there may also be aspiration of swallowed fluid into the airway.
P/H : Swallowing corrosives or of instrumentation, globus hystericus, cholecystitis or peptic ulcer
Physical examination
1. Mouth and throat : For stomatitis, malignancy tongue and abnormalities of pharynx
2. Neck : Enlarged lymph glands, goitre, malignancy of thyroid
3. Chest : For evidence of aneurysm, mediastinal tumour, pericarditis, marked cardiac hypertrophy,
empyema, and pulmonary abscess
4. Skin : scleroderma or mucocutaneous diseases such as pemphigoid and epidermolysis bullosa
Symptoms
1. Dysphagia
(a) Onset : Acute in foreign body, encephalitis, thrombosis of cerebellar artery or hysterical.
(b) Type of distress
(i) Difficulty in swallowing both liquids and solids
(ii) Difficulty in transferring bolus of food from mouth to gullet
(iii) Sensation of food sticking retrosternally
(c) Progress : Long history with intermittent symptoms in achalasia.
(e) Deglutition with strangulation or cough
2. Pain
(i) Burning, substernal contact pain is felt when hot, acid, spicy or alcoholic material passes through
the inflamed oesophagus.
(ii) A prolonged history of heartburn
(iii) Impact pain : When a bolus ‘impacts’ above a narrowed oesophagus.
(iv) Spasm pain : Oesophageal pain
3. Regurgitation
4. Hematemesis
5. Nasal twang and nasal regurgitation
6. Hoarseness of voice
Management
(a) If symptomatic the disease must be treated. Gastric lavage if there is pathological retention of food
in the stomach.
(b) Diet – Appetizing food. No sweets between meals. No hurry.
(c) Exercise and fresh air
(d) Avoidance of excessive smoking and alcohol
(e) Appetizers – Cyproheptadine hydrochloride dose of 2–4 mg according to age as tablets or syrup bd.
(g) Anabolic steroid – Norethandrolone 50 mg daily by mouth or 25 mg IM once a week.

GERD
• Gastro-oesophageal reflux disease (GERD) is caused by recurrent reflux of gastric contents into
the distal oesophagus.
• The pathophysiology is multifactorial, but dysfunction of the lower oesophageal sphincter (LOS)
has a primary role.
 • Motility disorders of the distal oesophagus (e.g. reduced peristaltic amplitude, decreased
velocity and increased duration of peristaltic contractions) cause prolonged exposure of the
oesophagus to refluxed gastric contents.
Causes
GERD is caused by frequent acid reflux.
Hiatus hernia
Ascites
Obesity
Alcohol, smoking

Pathophysiology
Reflux of gastric contents occurs through a relaxed or hypotonic sphincter

LOS relaxation swallow mediated

During period if gastric distention

Lead to spontaneous relax LOS

Impaired oesophageal motor function

Inadequate volume clearance occurs in oesophagitis

Reflux (gastric content remain inside)

SYMPTOMS
• Typical symptoms : Heartburn, acid regurgitation
• Atypical symptoms : Dysphagia, globus sensation, noncardiac chest pain, dyspepsia or
abdominal pain
• Extraesophageal symptoms : Hoarseness or sore throat or both, sinusitis, otitis media, chronic
cough, laryngitis or polyps on the vocal cords or both, dental erosions, non-atopic asthma,
recurrent aspiration or pulmonary fibrosis, or both.
• Sleep related GER can present with multiple awakenings. Substernal burning and chest
discomfort, indigestion or heartburn. Other symptoms include a sour or bitter taste in the
mouth, water brash, coughing or choking.
• Malignancy : Oesophageal adenocarcinoma, head and neck cancer.
Barrett’s oesophagus is found in 10–20% of patients with reflux oesophagitis, the squamous epithelium
is injured by chronic gastro-oesophageal reflux and repair is effected by columnar instead of squamous
cells Upper GI scopy can be diagnostic assisted by biopsy. This columnar epithelium may undergo
malignant transformation.
Investigations
Barium swallow with fluoroscopy :
• Upper oesophageal sphincter disorders Defective opening of pharyngo-oesophageal segment
Airway aspiration.
Body motility
Non-propulsive (tertiary contractions) Uncoordinated or weak post-swallow contractions. Identification
of hiatus hernia, mucosal ulceration, stricture, oesophageal dilatation.
Upper oesophageal endoscopy : Indications :
• GI bleeding, iron deficiency anemia, progressive unintentional weight loss, progressive difficulty
swallowing, persistent vomiting, epigastric mass on palpation, suspicious barium meal result or
other suspicious imaging result.
Manometry
Oesophageal pH testing
• Acid reflux time
• Number and duration of reflux episodes
• Symptom index
Scintigraphy : This technique can demonstrate reflux as well as provide quantitative measure of its
presence.
MANAGEMENT
1. Conservative measures
• Abstain from eating within 2 hours of bed time
• Elevate head of bed by 6 inches
• Sleep in left lateral decubitus position
• Avoid caffeine, nicotine, alcohol, chocolate, mints, carbonated beverages, high-fat foods,
• tomato or citrus - based products.
• Anticholinergic, theophylline, prostaglandin, calcium channel blockers, alendronate.
• Rabeprazole, esmoprazole provide superior gastric acid suppression.
2. Acid suppression
(a) Proton pump inhibitors
(b) Prokinetic agents
3. If no response or relapse : Test and treat for H. pylori.
4. Surgery
• If persistent non-acid reflux. Antireflux surgery augments the reflux barrier by a full or partial
wrap of the gastric fundus (fundoplication) around the lower oesophagus.

GI BLEEDING
• GI bleeding is a potentially life threatening problem.GI bleeding is a symptom of a disorder in
digestive tract.
1. Acute upper GI bleeding
History & physical examination
• Episode of bleeding
• Illness : Peptic ulcers, liver cirrhosis, Bleeding disorders
Etiology
• NSAIDs
• Prior surgery for peptic ulcer
• Acute variceal H’ge
• H. pylori infection
• Erosive gastropathy
• Oesophageal varices
2. Acute lower GI bleeding
History
 • Passage of blood either separately or coating the stool
• Bloody diarrhea
• Weight loss
• Recent change in bowel habits
Causes
• Haemorrhoids
• Anal fissure
• Mucosal prolapse
• Meckel’s diverticulum
• Juvenile polyps
• IBD
• Carcinoma
• Diverticular disease
• Angiodysplasia
• Ischemic colitis
Clinical features
H/O : Dyspepsia, alcoholism, NSAIDs, weight loss
Black or tarry stool
Bright red blood in vomit
Cramps in the abdomen
Dizziness or faintness
Paleness
Shortness of breath
P/R examination : Prolapsed piles, Mass polyp, Ulcer, Fissures
Investigations
• May be planned after resuscitation.
• Digital anorectal examination and proctosigmoidoscopy. Upper GI endoscopy if a local cause is
not found. Capsule endoscopy is useful in detection of small bowel lesions in Crohn’s disease,
non-steroidal anti-inflammatory drug enteropathies.
• CT angiography may be helpful in locating bleeder
Occult GI bleeding
• Bleeding that is not visible and is manifested by positive faecal occult blood (FOB) testing or iron
deficiency anemia.
• Physical examination findings which might provide a clue about the source or bleeding :
• Facial or oral telangiectasia can suggest hereditary telangiectasia.
• Acanthosis nigricans in axilla suggest possible malignancy.
• Perioral pigment spots are associated with Peutz-Jeghers syndrome.
• False positive FOB can result from pseudoperoxidase in various foods e.g. red meat, raw
broccoli, turnips, cauliflower, radishes.
Management
1. Hospitalization if suspicion of significant bleed.
2. Correction of hypovolemia with plasma expanders followed by blood transfusion. Central venous
pressure or Swann-Ganz monitoring helps prevent over transfusion in the elderly and is a sensitive
indicator of continued or recurrent bleeding.
3. Blood for Hb, clotting screen and urea and electrolyte estimation.
PORTAL HYPERTENSION
• Portal hypertension is a condition characterized by prolonged elevation of portal venous
pressure .
• It is defined as hepatic venous pressure gradient more than 5mmHg . HVPG >10 mmHg define
portal HTN.
• Normal portal venous pressure is 10-15 cm saline or 5-6 mm Hg.
Causes
Pre-hepatic : Portal vein thrombosis & Splenic vein thrombosis
Intra-hepatic : Primary biliary cirrhosis, Sarcoidosis, TB, Wilson’s dz, Haemochromatosis
Extra-hepatic : Hepatic vein thrombosis, Chronic constructive pericarditis
Pathogenesis
1. Portal venous pressure
• Portal blood flow
• Portal vascular resisance
2. Increased portal vascular resistance lead to
• Reduction in the portal blood flow to liver
• Development of collateral vessels allowing portal blood to bypass the liver and enter systemic
circulations.
3. Collateral circulation occurs particularly in oesophagus, stomach, rectum, anterior abdominal wall and
in renal, lumbar, ovarian & testicular vasculature.
4. With the development of collateral vessels, initially portal blood & later almost all of the entire portal
blood is stunted directly to the systemic circulation, bypassing the liver.
Clinical features
• Hematemesis & melena
• Abdominal wall veins are often prominent and rarely they may form a caput medusae around
the umbilicus.
• Murmurs—A venous hum may be heard over the collaterals radiating occasionally to the
precordium or over liver (Cruveilhier-Baumgarten syndrome).
• The paraxiphoid umbilical veins indicate intrahepatic portal venous hypertension.
• Spleen—Enlarges progressively, the edge is firm.
• Liver—High pressures are more often associated with a small, fibrotic liver. A soft liver suggests
extrahepatic portal venous obstruction, a firm liver cirrhosis.
• Ascites—Portal hypertension raises capillary filtration pressure and increases quantity of ascitic
fluid.
Investigations
• Ultrasonography and Echo-Doppler : Ultrasonography should exclude an obvious space-
occupying lesion and establish patency of the portal and hepatic veins.
• Retrograde CO2 portography or splanchnic arteriography may be necessary to visualize the
portal vein.
• Portal venography demonstrates the site and often the cause of portal venous obstruction and
is performed prior to surgery. A typical ‘spider web’ appearance on hepatic venography is
diagnostic of Budd-Chiari syndrome.
• Portal venous pressure measurements are seldom needed but can be used to confirm portal
hypertension.
Management
• Non selective beta-blockers (propanolol & nadolol) produces vasodilatation of both splenic
arterial bed & portal venous system along with reduced cardiac output.
• Nitrates (nitroglycerine & isosorbide dinitrate) reduce venous return & post-sinusoidal
resistance & are useful in combination with beta-blockers.
• Beta-blockers with or without nitrates are used for primary prophylaxis of variceal bleed.

HIATUS HERNIA
• Is the herniation of stomach into the thorax through oesophageal hiatus in the diaphragm.
• Protrusion of the stomach above the diaphragm.

Etiology
• Most common in middle-aged, obese females.
• It may be congenital
• Due to conditions which raise intra-abdominal pressure eg. obesity, pregnancy, ascites or
abdominal tumours.
Types
1. Type I Sliding—Commonest variety. Simple upward slide of fundus of stomach with oesophago-gastric
junction through the hiatus into the chest.
2. Type II Rolling (Paraesophageal)—The oesophagogastric junction is within the abdominal cavity but
part of the gastric fundus protrudes through the hiatus into the thoracic cavity.
3. Type III—Combined sliding and paraesophageal hernia.
4 Type IV—viscera other than the stomach herniate into the mediastinum most commonly the colon.
Clinical features
1. Asymptomatic
2. Symptoms due to reflux
(a) Retrosternal chest pain or discomfort especially on stooping or lying down soon after meals
(b) Heart burn or regurgitation of acid fluid, or food on bending or stooping. Nocturnal regurgitation
may cause choking attacks and aspiration pneumonia
(c) Dysphagia due to oesophageal muscle spasm, oesophagitis
3. Symptoms due to pressure
(a) From pressure on mediastinum – Dyspnoea, palpitation, cough, anginal pain
(b) From pressure on diaphragm – Hiccup, spasmodic pain.
4. Symptoms due to hemorrhage
Iron deficiency anemia due to massive hematemesis or oozing from oesophageal ulcers.
5. Symptoms due to associated diseases : Peptic ulcer at level of diaphragmatic hiatus, cholecystitis,
ischemic heart disease.
Investigations
1. Radiology
(a) X-ray chest : If a sliding hernia is large, it may be seen as retrocardiac shadow with fluid level.
(b) Barium swallow to assess hernia size and development of complications.
2. Endoscopy and biopsy
Mainly of value in assessment of oesophagitis and of consequent bleeding, ulceration and stricture
formation.
3. Manometry is the only sensitive method, as in absence of dilation, barium meal may be reported as
normal.
Management
A. Medical
1. To minimise gastro-oesophageal reflux
(a) Elevate bed head by 20 cm
(b) Avoid posture precipitating reflux, e.g. bending or stooping forwards, sitting in a low chair
(c) Avoid large meals
(d) No food or drink for 3–4 hours before bedtime
(e) Reduce weight if obese. Stop non-steroidal anti-inflammatory drugs
(f) Avoid foods which provoke symptoms, e.g. pastries, coffee
2. Reduce gastric acidity and pepsin secretion – with ranitidine or famotidine or antacids.
B. Surgical : Surgical correction in resistant cases.

WILSON’S DISEASE
• Wilson’s disease is an inherited disorder of hepatic copper deposition caused by mutations in
the gene ATP7B on chromosome 13, pattern of inheritance is autosomal recessive.
Pathophysiology
• In Wilson’s disease copper is not incorporated into ceruloplasmin within hepatocytes and is not
excreted into bile.
• The level of ceruloplasmin is lower than normal and because ceruloplasmin contains most of the
copper in blood, serum copper levels are low.
• In addition because copper is not excreted from the liver via the bile, it accumulates in
hepatocytes.
• When hepatocellular storage capacity is exceeded, free copper is liberated into the blood and
deposited in various organs, notably the brain, eyes and kidneys. Rarely massive release of
copper occurs, leading to acute liver failure, extensive intravascular haemolysis and renal
dysfunction.
Clinical Features
• Difficulty speaking & swallowing
• Tremors
• Rigid muscles
• Depression, Anxiety, Mood swings
• Jaundice
• Swelling or pain in abdomen
• Vomiting blood
• Fatigue
Diagnosis
• Primary test : Ceruloplasmin <10 mg/L
• Supportive test : Urine/serum copper >80 mg/24 h
• Definitive test : Liver biopsy with quantitative copper >200 μg/g dry weight
• Blood tests & urine tests
• Liver biopsy
• Eye exam
Management
 • Treatment is life-long
• Avoidance of alcohol and major sources of dietary copper
Drugs
• D-penicillamine : About one-third of patients have to change to a different chelator because of
side effects including skin disorders, protein-losing nephropathy, lupus-like systemic
inflammatory conditions and bone marrow suppression.
• Trientine is an alternative to penicillamine, it has fewer adverse effects.
• Zinc 50 mg tds depletes total body copper stores by inducing enterocyte metallothionein, which
binds copper avidly.
• The anticopper effects of trientine and penicillamine can be monitored by following 24-h “free”
serum copper levels.
Liver transplantation is indicated in patients with fulminant hepatic failure or liver disease unresponsive
to standard treatment.

MAL-ABSORPTION DISORDER
• Mal-absorption is a failure of normal absorption of nutrients across the GIT.
Types
1. Generalized malabsorption affects all classes of nutrients. It usually results from small intestinal
disease or conditions in other organs. When severe it is manifested by one or more clinical features of
mal-absorptive stage. Because fat absorption is most affected, excess undigested fat in the stool
(steatorrhoea) is strong evidence of generalized malabsorption.
2. Specific malabsorption is a failure of the processes governing absorption of one class or type of
nutrients eg. genetic or acquired failure to absorb disaccharide sugars (eg. lactase or vitamin B12m
deficiency).
Causes
• Diarrhoea and weight loss
• Family history may suggest coeliac disease, Crohn’s disease or familial pancreatitis
• Previous surgery may lead to short gut syndrome
• Immunodeficiency may lead to frequent infections
• Radiation treatment may cause radiation enteritis
• Obvious heavy steatorrhoea (oily stools) may indicate pancreatic insufficiency
• Abdominal pain though uncommon, suggests a diagnosis of pancreatitis, intestinal strictures or
small intestinal ischemia
Pathogenesis
• Easier to understand the physiology of intestinal handling of fluid electrolyte and various
nutrient.

• Content of upper small bowel have a variable molarity with high potassium content and
those of the rest of the small bowel and large bowel are mostly isotonic.

• Terminal ileum is capable of absorption all the nutrients like electrolyte and water,
magnesium and zinc that are normally absorbed by the proximal small bowel.

Malabsorption result from abnormality of three processes :

1.Intraluminal mal-digestion
 • Defective pancreatic secretion

• Chronic pancreatitis

• Pancreatic cancer

• Cystic fibrosis

2. Mucosal mal-absorption

• Results from small bowel resection or condition which damage the small intestinal
epithelium

3. Post mucosal lymphatic obstruction

• Prevents the uptake and transport of of absorbed lipids into lymphatic vessels

Symptoms
Diarrhea often steatorrhea
Weight loss
Growth retardation
Swelling or oedema
Anaemia
Muscle cramps & bleeding tendencies
Investigations
Tests for Evidence of Malabsorption :
• Full blood count
• Mean cell volume, mean corpuscular hemoglobin
• Serum iron/total iron-binding capacity (or ferritin)
• Vitamin B12
• Serum (or RBC) folate
• Prothrombin time
• Plasma proteins
Tests for Cause of Malabsorption
• C-reactive protein, ESR
• Immunoglobulins (hypogammaglobulinemia)
• Endomysial and antigliadin antibodies (coeliac disease)
• Small intestinal biopsy at endoscopy with punch biopsy
• Capsule endoscopy as alternative to biopsy of small intestine to detect villous atrophy in
patients suspected of coeliac disease.
Radiology : Barium Meal follow through
• Delayed transit time
• Abnormal small intestinal pattern :
(a) Smooth appearance of margins of barium-filled intestine.
(b) Clumping of barium or transformation of a normal feathery appearance to a ladder pattern
resembling a stack of coins.
(c) Radiological anatomical abnormality in stagnant loop syndromes, small intestinal resection, Crohn’s
disease, systemic sclerosis.
(d) Nodular lymphoid hyperplasia suggests immunoglobulin deficiency and possibility of an enteric
infection such as giardiasis.
Management
• Replacement of nutrients, electrolytes & fluid may be necessary.
• In severe deficiency, hospital admission may be required for parenteral administration.
• Pancreatic enzymes are supplemented orally in pancreatic insuffiency.
• Dietary modification is important in some conditions :
o Gluten free diet in celiac dz.
o Lactose avoidance in lactose intolerance.
• Antibiotic therapy will treat small bowel bacterial overgrowth.

DYSENTRY
• The term dysentery is used to mean diarrhoea with abdominal cramps tenesmus causes of
mucus in stool

Types
1. Bacillary dysentery : Acute infection by shigella species. S dysentery, S flexneri S. sonneri
Epidemiology
• Spread may occur via contaminated food or flies but transmission by unwashed hands after
defecation.

Pathology
• Grossly : Lesion found in colon occ. in ileum.

• Superficial transverse ulceration of mucosa of bowel occur in region of lymphoid follicles.

• Mucosa : Hyperemic

• Oedematous

• Microscopically : Mucosa overlying lymphoid follicle is necrosed.

• Surrounding mucosa : Congestion

• Oedema and infiltration by neutrophils and lymphocyte

• Mucosa : Covered by greyish yellow pseudo membrane

Clinical features
• Usually insidious

• Moderately severe illness

• Diarrhoea

• Colicky abdominal pain

 • Tenesmus

• Stool small after few evacuation contain blood

• Purulent exudate with little fecal material

• Fever

• Dehydration

• Weakness with tenderness over colon

Complications
• Hemorrhage

• Perforation

• Stenosis

• Polyarthritis

Investigations
• Stool : Bright red colour over 10 days

Management
• Plenty of water / fluid are given

• Oral rehydration therapy

• Severe diarrhoea IV (replacement of water and electrolytes)

• Antibiotics : Ciprofloxacin 500 mg

• Anti diarrhoea medication should be avoided

Prevention
• Prevention of faecal contamination of food, milk

• Hand washing

• Isolation of case

2. Amoebic dysentery
• Infection by E. histolytica

• More prevalent in tropical countries & primarily affect large intestine

Pathology
• Grossly : Early intestinal lesion appear as small area of elevation of an mucosal surface
 • Typical flask shaped ulcer : Narrow neck & broad base

• Microscopically : Ulcerated area shows chronic inflammatory reaction

Trophozoites of of entamoeba

Infection occur from ingestion of parasite

Cyst wall dissolved in small intestine from where liberated amoeba

Large intestine

They invade epithelium of mucosa

Reach submucosa

Produce characteristic flask shaped ulcer

Clinical features

• Incubation period ranges from 2 weeks to many years

• Diarrhea alternating with constipation common as if mucus sometime with streaks of blood

• Offensive stool

• Tenesmus

• Tenderness along line of colon, caecum and pelvic colon

• Acute bowel symptoms with very frequent motion and passage of mucus blood & mucus

Complications
• Amoebic liver abscess

• Amoebic hepatitis

• Perforation

• Hemorrhage
• Tumor like mass
Diagnosis
Stool examination : Microscopic appearance

• Stool : Copius, semi liquid, brownish black, 6 to 8 per day

• Offensive

• Acid in action

Sigmodoscopy : Reveal typical flask shaped ulcers.

Management
• Rest

• Liquid diet

• Quickly respond to oral metronidazole, Tinidazole

Prevention
• Personal precautions

• Not eating fresh, cooked vegetables, drinking on purified water

DIARRHOEA
• Decreases in consistency or increases liquidity of stools.
• It is usually due to faeco-oral transmission of bacterial toxins, virus, bacteria or protozoal
organism.

Acute diarrhea
Cause
• Infections : Rota virus

Herpus simplex virus

E. coli

Salmonella, Shigella

E. Histolytica
Giardia

• Food poisoning / Toxins : Bacillus cereus

Salmonella

Staphylo
 Vibrio

• Drugs : Antiblotics – amoxicillin

Anti-Hypertensive – angiotensin converting enzyme inbihitors

Anti-neoplastic drugs

Anti- depressants

Cholesterol lowering drugs

• Poorly absorbed Sugars : Fructose, mannitol, sorbitol

• Non infectious : Acute diverculitis

Pelvic inflammatory dcz

Bowel malignancy

Pathophysiology

1. Partially compensated by ability of colon to reabsorb fluid however when this capacity

is either over

Affected by action of enterotoxin

Results

In severe diarrhoea
2. Certain pathogens (Virus, protozoa, bacteria, parasites)

Invade mucosa of small intestine

Significant inflammation or ulceration

Inhibition of iron absorption in small intestinal villi

Watery diarrhea
Investigations
• Stool specimen : Occult blood

• Ova, cyst, parasites

• Blood tests : CBC & differential

• Urea electrolytes

• ESR & CRP

• Blood culture

• Rigid sigmoidoscopy

• Plain abdomen radiograph

Management
• Rest

• Fluid replacement
• IV fluid therapy

• RL solution

• Oral rehydration therapy

• Anti mobility agent

• Diphenoxylate

• V cholerate - deoxycycline (antibiotics)

Chronic diarrhoea
Causes
• Same as acute diarrhoea
• Lactose intolerance

• Malabsorption

• Chronic pancreatitis

• Inflammatory bowel disease

• Radiation colitis

• Neoplasms

• Collagenous colitis
 • Endocrine disorder – DM, hyperthyroidism, hypoadrenalism

• Purgative use - anorectal surgery

Investigations
History

• Age : Early age : Parasitic dysentery, Abdominal TB, Genetic or biochemical abnormalities

• Middle age : Colonic carcinoma, IBD, Pancreatic disease, Laxative abuse

• History of allergy

• Family history of allergy

Signs & Symptoms

• Chronic bloody diarrhoea

• Weight loss

• Abdominal pain

• Abdominal distension

• Rectal tenesmus

• Sense of urgency

• Abdominal tenderness - diffuse in intestinal TB

• Abdominal bruit may be heard

• Mass carcinoma, tumor or diverticulitis

• Anal abnormalities – fissures, perianal or ischiorectal abscess and fistula may present as
complication
• Type of faeces : Mucus and blood - amoebic and bacillary dysentery

• Profuse purulent discharge : Chronic UC

• Mucus : IBS, chronic constipation following injection of strong purgatives

• Fatty stool : Steatorrhoea

• Frequent soft, non fatty stool : Diarrhoea of gastric origin

• Watery stool : Emotional diarrhea

VIRAL HEPATITIS
 • It is an inflammation of liver characterized by presence of inflammatory cells due to infection
with various hepatrophic viruses.

Causes
A. Main cause : Hepatotrophic viruses

1. Hepatits A virus
2. Hepatits B virus

3. Hepatits C virus

4. Hepatits D virus
5. Hepatits E virus

B. Less common causes :

a) Epstein- Barr (EB) virus

b) Cytomegalo virus (CMV)

c) herpes simplex virus (HSV)

1. Hepatitis A
Transmission : Faeco oral, Blood transfusion, Through illicit use of injectable drugs, Sexual contact
Incubation period : 15-50 days
Clinical features
Prodomal symptoms :
Malaise, Loss of appetite, Nausea, Vomitting, Fever
Onset of dark urine (1st indication ) followed by jaundice and pale stools.
Normal colour of urine and stool return after 2-3 weeks.
Investigations
• S- bilirubin
• S- albumin
• ALT levels indicate severity of hepatocytc lysis
• Presence of urine urobilinogen may be the first syp. even before jaundice
• Positive IgG anti-HAV

Treatment

• Bed rest
• Intake in form of fruit juices, sugar cane juices
• Avoidance of physical exertion and of alcohol

Prophylaxis
 • Passive immune prophylaxis with human immunoglobulin has been replaced by vaccine for
active immunization which provides long lasting immunity.

Complications

• Cholestatic hepatitis with itching and jaundice lasting upto

• Relapsing course with a second hepatitis flare 30-90 days later

2. Hepatitis B
Transmission : In babies born to HBV infected mothers, after transmission of blood (vertical
transmission ), IV drug use, Sexual contact, Blood transmission
Incubation period : 45-180 days

HBV
1. Acute HBV infection

• In week before icterus appear, some patients develop a serum sickness like syndrome including
Arthralgia, Fever, Urticaria, Rarely fulminant hepatitis

• Patient recover within 1-2 months

2. Chronic HBV infection

• Hbe positive virus infection : Virus replicates and encodes infected liver cells to synthesize and
secrete HB antigen (HBeAg).

• Hbe negative virus infected : Variant for HBV can lead to produce viral infection without secretion
of HBeAG.

Stages of infection in HBe +ve virus infection

Second stage
First stage Inflammatory Third stage Fourth stage
Inflammatory process become Patient Viremia &
decreases of sufficiently continue to hepatitis in
hypatocytes intense for lysis of produce HBeAg absence of
with viremia infected because of HbeAg
& HBeAG in hepatocytes, integrated antigens.
serum =+ve clearance of sequence of
HBeAG and viral DNA with
development of in host cell DNA
anti HBe. Cirrhosis
may develop
Clinical features
1. Incidental presentation : Asymptomatic
2. Symptomatic presentation :

• Malaise
• Fatigue
• Arthragia
• Hypochondrial discomfort
• Patient may present with acute flares hepatitis

Treatment
• Lomirudine 100 mg/d/po (mg per day by mouth )

• Adefovil dipivoxil 10 mg/d/po

Prevention : Hepatitis B immunization

Complication :
• Cirrhosis and its complications ending in encephalopalty and death
• Hepatocellular Ca

3. Hepatitis C
Individual at risk :

• Injecting drug users

• Health care workers

• Individuals on hemodialysis

• High risk sexual partner

• Unsafe injection
• Use of blood comntaminated implements for surgery
• Acupuncture
• Tattooing, ear piercing
• Mother infant transmission

HCV
1. Acute Hepatitis C

• Infection is clinically mild.

• Only 25 % are icteric

2. Chronic Hepatitis C
 • S. aminatransferace level remain abnormal after 12 month in 60-85% of patients with HCV.

Incubation period : 14-180 days

Investigations : Hepatitis C RNA level in serum or liver tissue is positive
Treatment
Acute Hepatitis C : INF alpha 3-6 MU, 3 time /wk for 12 months

Chronic Hepatitis C : Combination therapy, INF alpha 2b (3MU) 3 times /wk + Ribavirin 1000-2000 mg po

Hepatitis D
Transmission : Via parenteral route
Incubation period : 42-180 days
Clinical features
• HDV depends on HBV for replication and expression. Thus it is found only in points with
Hepatitis B Infection.

• Chronic infection is more severe and has more high morality than other type.

• Cirrhosis occurs in 60-80% patient.

4. Hepatitis D
Transmission : Faeco oral route
Incubation period : 21-55 days
Clinical features
• Self limiting and there is no clinical biological evidence of chronic dz.

• Resolution of hyperbilirubinemia and abnormal salt within 3 wks.

Prophylaxis : Depends primarily on clean drinking water and improved sanitation.

AUTOIMMUNE HEPATITIS
Autoimmune hepatitis is an unresolving inflammation of liver cause that is characterized by

• Hypergammaglobulinemia

• Auto antibodies in serum

• H/O other autoimmune disorder

Clinical features
A. Type 1

• Annerxia, nausea, malaise and fatigue

• Palmar erythema

• Spider naevi

• Moon face

• Buffalo hump

• Abdominal obesity

• Mild to moderate raise in S transminases

Associated condition :

• Keratoconjunctivitis sisca
• Renal tubular acidosis
• Peripheral neuropathy
• Graves disease
• Ulcerative colitis
• RA
B. Type 2

• Occurs in children

• Acute/fulminant type progression to severe liver disease and cirrhosis

Associated with

• Autoimmune thyroid disease

• Insulin dependent DM

• Vitiligo

C. TYPE 3 (similar to type 1)

Diagnosis (Ix)

• Liver biopsy
• Transominases

• Serological testing for anti LKM and anti SLA/LP is important

PEPTIC ULCER
• Peptic ulcer are the areas of degeneration & nerosis of GI muosa exposed to peptic secretion.
They can our commonly in proximal duodenum in stomach & also occur in lower end of
oesophagus, meckel’s diverticulum or at site of gastro jejunum anastomosis.

• Male:Female ratio for duodenal ulcer varies from 5:1 to 2:1 & Gastric ulcer 2:1.

Types
1. Gastric ulcer

2. Duodenal ulcer

Etiology
Gastric ulcer Duodenal ulcer
H.puloric infection, NSAIDS, Neoplasm, Stress NSAIDs, H.pyloric infection ,Hypercalcaemia,
ulcer, Crohnls dz, Neoplasm- lymphoma, Infection-CMV, TB,
Infection(herpes,simlex,cytomegalovirus), Herpes simplex
Mucosal trauma, Local ischemia, Antral stasis,
Spicy food, Anxiety, Alcohol, smoking, Burn
,trauma, shock

Pathology
Gastric ulcer Duodenal ulcer

Acute : Any where in stomach Acute :

5:1-ulcer are oval circular in shape
2:1-they are shallow punched out and usually do
no invade the muscular coat
Chronic :
Duodenal ulcer extremely uncommon
Chronic :
Duodenal ulcer are usually smaller than the
chronic gastric ulcers

It is larger, tends to penetrate deeply and Ulcer are vary in shape – circular, oval, cresentri,
associated with greater degree of fibrosis pear-shaped or (triangular)

When felt ulcerated area will be hard fibrotic

and button like

Pathogenesis
1. Gastric ulcer
• Pathogenesis mainly explained on basis of impaired gastric mucosal defense against pepsin
secretion.
 • Hyper acidity may occur in gastric ulcer due to increase serum gastrin level in response to
ingested food in an atonic stomach .

• Normally protective gastric mucus barrier against acid-pepsin deranged in gastric wall & formed
ulcer.

2. Duodenal ulcer
Conclusive evidence of that role of high acid secretion cause(duodenal ulcer )

Generally hypersecretion of gastric acid into stomach at night take place influence of vegal stimulation.
There is high basal as well as maximal acid output in response to various stimuli.

Antral inflammation

Lead to
Reduced somatostatin production

Result in

(Beacuse is has negative feedback effect on gastric production)

Hypergastrinemia

Gastrin acts on parietal wall

Result in

High stimulated acid production

o Increases duodenal acid load

o Formation of protective gastric metaplasia in duodenum.

o H. pylori cannot colonize normal duodenum but can colonize gastric metaplasia causing

Inflammation & ulceration

Clinical features

Chronic gastric ulcer Chronic duodenal ulcer

Age : middle age Young adult 25 to up year

Sex : more common in male Male dominating through not as much as gastric
ulcer
Constitution : pt thin &anaemic with J shaped Pt healthy males with steer horn stomach
Hypotonic stomach

Periodicity : periodicity less mark Periodicity well marked

Epigastic Pain : Boring & pricking in nature More severe and spasmodic in nature

It occurs almost immediately after eating It occur 2 to 3 hrs after eating

Pain is not felt in empty stomach Pain is very much felt in empty stomach
Food not relieved pain Food relived pain

Not felt in night Felt in night

Vomiting : vomiting occurs after food and which Rare

relieve pain

Appetite : good Quite good

Cannot eat because it initiate pain Frequently eats to avoid pain

Diet : avoid fried and spicy food Does not avoid anything.

Weight : loss of weight Weight gain

Haemetemesis more common H’ge more common

Signs
• Tenderness : Deep tenderness to Rt of middle in epigastrium. Superficial tenderness may be
present.

• MS rigidity : present with active ulcer and deeply penetrating ulcer

• Peristaltic waves : may be observed in presence of obstruction

• Blood : in stool

D/D
• Chronic gastric ulcer
• Gastric carcinoma
• Chronic gastritis
• Duodenitis
• Ca of duodenum
• Chronic cholecystiris
• IBS
• Nervous dyspepsia
• Hiatus hernia
Investigations
• Examination of blood : low Hb, ESR raised
• Examination of stool : blood in stool
• Gastric function test
• Radiological Ix : Barium meal x-ray
• Endoscopy

Management
• Rest

Indication for hospitalization:

• Tarry stool

• Constatnt pain replacing previous ulcer rhythm

• Gastric retention

• Uncontrollable nightpain
Diet :

• Balanced diet

• 3 hourly feed throughout the day small, digestible but of adequate caloric value

Pharmacotherapy :

• H2 receptor antagonists
Antacids :

• Magneshium hydroxide

• Aluminium hydroxide
Mucoprotective drugs :

• Prostaglandin analogues

• Eradication of H.pylori

• Anti-cholinergics

Relief from anxiety & mental stress :

• Psychotherapy

• Anti-depressant
Avoidance of gastric irritants & stimulans

• Tobacco, alcohol, coffee, tea

• Sour fruits

• Meat extracts, ulcerogenic drugs

Complications
• Bleeding
• Perforation
• Pyloricstenasis
• Malignancy

IRRITABLE BOWEL SYNDROME (IBS)

• IBS consist of group of GI symptom particularly associated with lower bowel in absence of
demonstrable organic pathlogy. In which abdominal pain is associated with defecation or
changes in bowel habit.
• Functional gastrointestinal disorder are extremely common & defined by absence of structural
pathology. Young women more commonly affect.

Criteria for delta of IBS

At least 3 month continuous or recurrent symptoms of abdominal pain, associated with

• Relief by defection

• Change in stool frequency

• Change in stool consistency

Symptom support the delta

• Altered stool frequency

• Altered stool form

• Altered stool passage

• Passage of mucus

• Abdominal bloating

Epidemiology : Approximately 20% general population fulfill criteria for IBS

Etiology/pathophysioloy
1. Psychosocial factor :
 • Anxiety

• Depression

• Neurosis

• Panic attack common

• Acute psychological stress

• Marital difficulties

2. Altered gastrointestinal motility :

• If pt come with diarrhea as predominant symptom increases number of fast & propograted
colonic contraction

• Those pt who are constipated decreases number of high amptitude propogated colonic
induced

3. Abnormal visceral perception :

• IBS associated with increases sensitivity to intestinal distention induced by infection of ballons in
ileum, colon, rectum, a consequence of altered CNS processing of visceral sensation.
• More common in female & diarrhea predominant IBS

4. Luminal factors :

• Gastroenteritis
• Common in young women
• Intolerance of specific dietary
• Components : Lactose, wheat
• Abnormalities of microflora leading to increases fermentation & gas production - Minimal
inflammation

5. Infection & allergy :

• Inflammatory cell produces histamine

6. Post- infective /post- inflammatory causes

Clinical features
• Pain : Recurrent pain

Localized to periumbilical region or lower abdomen left side

> by defaection
Colicky or crampy pain

• Abdominal bloating
 • Diarrhea- frequent defection, produce low volume stool

• Passage of mucus - common

• Dyspepsia indigestion

• Heartburn

Extra-intestinal symptoms

• Dymenorrhoea

• Dyspareunia

• Headache

• Urinary frequency

Investigations
• CBC, ESR

• Sigmoidoscopy

• Double contrast barium enema or colonoscopy

• Rectal biopsy

• Routine stool examination

Management
• Explanation & reassurance : Regarding absence of organic diease

• Specific therapy : Dietary fiber with supplementation with bulking agent

• Excusion diets : Lactose – free diet

• Drug therapy :

• Anti-spasmodics

• Anti-diarrheal agent – Loperamide & Diphenoxylate

• Anti-depressants

• Non-drug tx :
o Eliminate diet when diarrhea is predominant
o Relaxation for stress

o Psychotherapy
GASTRITIS
• Gastritis is acute or chronic inflammation of the stomach and is most often diffuse.

• It is usually diagnosed on upper gastrointestinal endoscopy and classified histologically by

performing gastric biopsy.

Classification
Types Etiology
Non-atropine H.pylori
Atrophic

-autoimmune Autoimmunity

-multifocal atrophic H.pylori + environmental insults NSAIDs, Bile,

Alcohol
Chemical
Radiation injury
Radiation
Granulomatosis
Non-infectious granulomatous Eosinophilic
Food sensitivity
Other infections
Bacteria other than H. pylori, viruses

1. Acute gastritis
• Acute gastritis is a transient acute inflammatory involvement of the stomach, mainly mucosa.

Etiopathogenesis
• Diet and personal habits : Highly spiced food, Excessive alcohol consumption, Malnutrition,
Heavy smoking

• Infections : H.pylori, Diphtheria, Salmonellosis, Staphylo, Food poisoning, Viral hepatitis,

Influenza, Infections mononucleosis

• Drugs : NSAIDs, Aspirin, Cortisone, Chemotherapy agents

• Chemical and physical agents : Intake of corrosive chemicals (caustic soda, phenol), Gastric
irradiation, Freezing
• Severe stress : Emotional factors – Shock, Anger, resentment

Pathophysiology
The mucosal lining of the stomach normally protects it from the action of gastric acid. This mucosal
barrier is composed of prostaglandins.
 Due to any cause

This barrier is penetrated

HCL comes into contact with the mucosa

Injury to small vessels

Oedema, Haemorrhage & possible ulcer formation

Clinical features

• Epigastric discomfort

• Abdominal tenderness

• Cramping

• Belching

• Reflux

• Severe nausea & vomiting

• Hemetamesis

• Sometimes GI bleeding

Diagnosis
• Diagnosis is based on detailed H/O food intake, medications taken & any disorder related to
gastritis.

• Histological examination by biopsy of sample.

Treatment
• Omission of offending agent

• Acid suppressive agent : H2 receptor

Antagonist

Proton pump inhibitors

Prostaglandins
2. Chronic gastritis
• Chronic gastritis is the commonest histological change observed in biopsies from the stomach.

• Condition occurs more frequently with advancing age being 45 years which corresponds well
with the age incidence of gastric ulcer.

Etiopathogenesis
• Recurrent attacks of acute gastritis may result in chronic gastritis

• Reflux of duodenal contents into the stomach

• Infection with H.pylori

• Associated disease of stomach and duodenum

• Immunological factors

• Autoantibodies to gastric parietal cells

• Autoantibodies against intrinsic factor

Pathophysiology
The stomach lining first becomes thickened & erythematous & then becomes thin & atrophic

Continued deterioration & atrophy

Loss of function of the parietal cells

Acid secretion decreases

Inability to absorb vitamin B12

Development of pernicious anaemia

Classification of Chronic gastritis

A. Type A gastritis (autoimmune gastritis)

• Involve body fundic mucosa

• Due to presence of circular antibodies

• Antibodies against parietal cells and intrinsic factor

 • Depletion of parietal cells and impaired secretion of intrinsic factor
B. Type B gastritis (H.pylori related)

• Involve region of antral mucosa

• Hypersecretory gastritis due to excessive secretion of acid

• Due to infection with H.pylori

C. Type AB gastritis (Mixed gastritis, chronic altrophic gastritis, environmental gastritis)

• Involve body fundic and antral mucosa

• Number of unidentified environmental factors have been implicated in its
etiopathogenesis

Histologically
• Chronic superficial gastritis : Inflammatory infiltrate – in the superficial layer of the gastric
mucosa.
• Chronic atrophic gastritis : There is inflammatory cell infiltrate in the deeper layer of the
mucosa and atrophy of the epithelial elements including destruction of the glands.
• Gastric atrophy : Thinning of the gastric mucosa with loss of glands but no inflammation.
• Chronic Hypertrophic gastritis : Thickening of gastric rugal folds.

Symptoms
• Upper abdominal pain
• Indigestion
• Bloating
• Nausea
• Vomiting – coffee ground material
• Belching
• Loss of appetite
• Weight loss
• Burning feeling in stomach
• Hiccough
• Black tarry stools

Risk Factors
• High fat diet
• High salt diet
• Smoking

Investigations
• Upper endoscopy
 • Blood tests – for pernicious anemia
• Faecal occult blood test (stool test)
• Endoscopic biopsy
• Culture of micro organism
• Histological examination – for identification of microorganism
• Serologic tests

Treatment
• Antacids
• Other drugs : Proton pump inhibitors
• Avoid hot and spicy foods
• Antibiotics
• Acid Blocking drug : Proton pump inhibitors & H2 receptor antagonist
• If patient have pernicious anaemia - Vit.B12 shots given
• Eliminating irritating foods from diet

STOMATITIS
Stomatitis Causes C/F Treatment
1.Catarrhal Local : Excessive Red m.m with increases Elimination of cause
tobacco, Alcohol, exudate Hexidine mouth wash
Spices, Antibiotics Vit.B complex
Systemic : Debility
2. Recurrent apthous Positive F/H/O Tiny shallow ulcers on Steroids by mouth
stomatitis Stress erythematous base Mouth wash NAD
Local trauma covered with grayish Antiseptics :
Food allegy white exudate Chlorhexidine
Analgesics :
Benzydamine
3. Infection :
A. Bacterial vincent’s Preexisting gingivitis on Ulcer Metronidazole 200mg
angina local trauma pseudomembranous TDS , Oral hygiene
Tobacco use slough Surgical correction of
Increased salivation, distorted gingivae
foetid odour
Gingival bleeding. Fever
Lymphadenopathy

B. Viral Herpes simplex Severe ulceration of Bed rest

oral m.m with fever, Mouth wash
malaise
Lymphadenopathy
C. Fungal Candidosis White slighty raised Oral suspension mouth
patches rinse
4. Spirochatae Secondary Syphilis Circular mucous Treatment of syphilis
patches
5. Drug induced Hypersensitivity Ulceration of buccal, Symptomatic tx
Cytotoxic drugs labial, palatal mucosa
6. Vitamin deficiency Nicotinic acid deficiency Raw red tongue Tx Vit.B complex

HYPERLIPIDEMIA
• Hyperlipidemia, hyperlipoproteinemia involves abnormally elevated levels of any or all
lipids and lipoproteins in the blood.
• It is the most common form of dyslipidemia (which also includes any decreased lipid levels).
Causes
1. Primary (genetic)
2. Secondary : Diet rich in saturated fat
Sedentary lifestyle
Alcoholism
Diabetes mellitus
Hypothyroidism
Nephrotic syndrome
Cushing’s syndrome
Liver disease (obstructive)
Drugs (steroids, thiazide diuretics, oestrogens)
Pathophysiology
• Hypercholesterolemia develops as a consequence of abnormal lipoprotein metabolism,
mainly reduction of LDL receptor expression or activity and consequently diminishing
hepatic LDL clearance from the plasma.
• It is a major predisposing risk factor for the development of atherosclerosis. This mechanism
is classically seen in familial hypercholesterolemia and when excess saturated fat or
cholesterol is ingested.
• In addition, excessive production of VLDL by the liver as seen in familial combined
hyperlipidemia and insulin resistance states such as abdominal obesity and type 2 Diabetes
can also induce hypercholesterolemia or mixed dyslipidemia.
Clinical features
• Hyperlipidemia usually does not cause symptoms.
• Very high levels of lipids or triglycerides can cause :
o Fat deposits in the skin or tendons (Xanthelasma and Xanthoma )
o Pain, enlargement or swelling of organs such as the liver, spleen, or pancreas ( Pancreatitis)
o Obstruction of blood vessels in heart and brain
• If not treated, high lipids can cause : Heart Attack & Stroke
• Atherosclerosis (hardening of the arteries)
• Lipemia retinalis
• The presence of tendon xanthomas along with xanthelasma indicates familial
hypercholesterolaemia.
Diagnosis
• This condition is diagnosed with blood tests. These tests measure the levels of lipids in the
blood.
• The National Cholesterol Education Program advises that you have your lipids checked at least
once every five years, starting at age 20.
• Also, the American Academy of Pediatrics recommends lipid screening for children at risk (eg, a
family history of hyperlipidemia).
• Testing may consist of a fasting blood test for:
o Total cholesterol
o LDL (bad cholesterol)
o HDL (good cholesterol)
o Triglycerides

Management
• Young primary hypercholesterolaemia, hypertriglyceridaemic patients especially if there is
family history of early onset cardiovascular disease.
• All hypertriglyceridaemic patients with levels in excess of 1000 mg/dL to prevent
pancreatitis.
• Diet : Calorie restriction and exercise in overweight patient. Reduction of saturated fats and
replacement with unsaturated fats (vegetable) oils. Increase in carbohydrate content to
about 55% of total calories.
• Weight reduction
• Exercise helpful in lowering triglyceride and cholesterol levels.
• Discontinuation of drugs such as thiazide diuretics and beta-blockers can lead to reduction
of cholesterol and LDL levels.

GALL STONE
• Gall stones are small, pebble like substances that develop in the gallbladder.
• Inflammation of GB mucosa can lead to excessive absorption of water and bile salts leaving
cholesterol in higher concentration.
• The cholesterol the precipitates in many small crystals which may progress to large crystals.
Types
1. Cholesterol : made of hardened cholesterol (yellow-green)
2. Pigment (brown/black) : made of bilirubin
3. Mixed stones
Pathogenesis
Physiochemical Factors
• Increased hepatic cholesterol secretion and chronic supersaturation of bile
• Enhanced cholesterol crystal nucleation in gallbladder bile
Motility Defects
• Gallbladder motility defects
• Gallbladder stasis
• Intestinal motility defects. Prolonged intestinal transit, longer migrating motor cycles and
disrupted motilin release
Pathophysiology
Decreased bile acid synthesis

Increased cholesterol synthesis in the liver

Super saturation of bile with cholesterol

Formation of precipitates

Gall stones (Cholelithiasis)

Clinical features
In the gallbladder
1. No symptoms (Silent gallstones)
2. Biliary colic—Due to contraction of gallbladder against a stone impacted in common bile duct. This
gives rise to midline or right hypochondrial pain, at times associated with vomiting but generally without
fever or systemic upset.
3. Acute cholecystitis
Symptoms :
• Pain type : Peritoneal pain with overlying skin tenderness and muscle rigidity in right
hypochondrium. Referred pain radiating to right scapular region. Digestive tract pain causing
abdominal colic, nausea and flatulence without vomiting.
Signs :
• Include fever with often chills at onset and tachycardia.
• Tenderness and muscle guarding in right upper quadrant.
• Palpable mass – of globular shape below right costal margin and moving on inspiration may be
felt.
• Murphy’s sign – Patient complains of pain on taking a deep breath while the examiner’s hand is
pressed below the right costal margin.
• Boas sign – Area of hyperaesthesia over right subscapular region.
• A palpable, non-tender gall bladder (Courvoisier’s sign).

Investigations :
1. Leucocyte count raised with increased polymorphs
2. Radiograph—Plain film of the abdomen may reveal radio-opaque gallstones or soft tissue mass in
region of GB.
3. Ultrasonography is the most commonly used method of detecting stones. Stones must be greater
than 1–2 mm in diameter to be seen.
4. Oral cholecystography identifies radiolucent stones
5. CT is more sensitive in identifying gallstone calcification than plain radiology
Management:
1. Diet : Nothing by mouth for first 24 hours or till nausea and vomiting have abated
2. Broad spectrum antibiotics : Parenterally to prevent peritonitis, cholangitis and septicaemia
3. Special measures :
(a) Local heat to abdomen
(b) 5% glucose saline intravenously
(c) TPR 2 hourly
(d) Examine abdomen every 2 hours to follow changes in tenderness, rigidity, and character of any
palpable mass.
4. Surgery : Cholecystectomy within 2—3 days of the onset of symptoms shortens total hospital stay and
avoids incidence of repeated attacks of waiting period of delayed ‘cold’ cholecystectomy.
In bile ducts
1. Biliary colic with transient jaundice : Due to migration of small stones into the common bile duct and
ejection through the papilla of Vater.
2. Acute pancreatitis : Due to probably reflux of bile into pancreatic duct through a common channel in
ampulla of Vater.
3. Obstructive jaundice : From impaction of stone in common bile duct.
4. Cholangitis
Management
Surgical treatment : Laparoscopic or open cholecystectomy is the only radical procedure for
symptomatic gall- stones.
Non-surgical treatment
1. Oral litholytic treatment : Bile acids Chenodeoxycholic acid 10–12 mg/kg/day and Ursodeoxycholic
acid 10–12 mg/kg/day alone or in combination (using one half of the dose of each) is suitable for
radiolucent small stones (<10 mm in diameter).
2. Contact dissolution treatment : Percutaneous transhepatic gallbladder puncture followed by
application of methyl-butyl ether directly to the stones.
3. Extracorporeal shockwave lithotripsy (ESWL) : The procedure is suitable for patients with up to three
stones of diameter 10–30 mm.
Complications
• In the gallbladder : Biliary colic
Acute cholecystitis

Chronic cholecystitis

Empyema of the gall bladder

• In the bile ducts : Biliary obstruction

Acute cholangitis

Acute pancreatitis

• In the intestine : Intestinal obstruction (gallstone ileus)

Cholecystitis
• The inflammatory condition of gall bladder is called as cholecystitis.
1. Acute cholecystitis
• Acute bacterial inflammation of gall bladder with or without stone.
Types
1. Calculous : It is the obstructive cholecystitis due to gall stones having the most common variety in
which around 90% of people having gall stones suffers. Majority of cases of calculous cholecystitis are
due to organism such as E. coli, Streptococci, Salmonella, Klebsiella, etc
2. Acalculous : It is the non-obstructive type which is common in person suffering from major illness like
never sepsis, burns, DM, dehydration, multiple injury etc.

3. Acute Emphysematous Cholecystitis

Pathology
• Inflammation
• Perforation
• Obstruction
• Gangrene
Pathogenesis
Stone

Outlet obstruction Mucosal erosion

Stasis Destruction of cells by toxic bile salts

Bacterial proliferation

Necrosis & Perforation

Signs & Symptoms

Pain
• Distension pain giving rise to a deep, central poorly localised pain
• Peritoneal pain with overlying skin tenderness and muscle rigidity in right hypochondrium
• Referred pain radiating to right scapular region.
• Digestive tract pain causing abdominal colic, nausea and flatulence without vomiting
General : Include fever with often chills at onset and tachycardia
Local :
(a) Tenderness and muscle guarding in right upper quadrant.
(b) Palpable mass of globular shape below right costal margin and moving on inspiration may be felt.
(c) Murphy’s sign – Patient complains of pain on taking a deep breath while the examiner’s hand is
pressed below the right costal margin.
(d) Abdominal distension – may occur and if marked simulates intestinal obstruction.
(e) Boas sign – Area of hyperaesthesia over right subscapular region.
Investigations
• Leucocyte count raised with increased polymorphs.
• Radiograph—Plain film of the abdomen may reveal radio-opaque gallstones or soft tissue
mass in region of GB.
• Ultrasonography is the most commonly used method of detecting stones. Stones must be
greater than 1–2 mm in diameter to be seen. It is unable to distinguish between cholesterol
and calcified stones.
• Oral cholecystography identifies radiolucent stones.
• CT scan : Not only detect gallstones but also detects perforation. Used when USG findings
are not clear.
Differential Diagnosis
• Perforated Peptic Ulcer
• Acute Pancreatitis
• High Retroceacal Appendicitis
• Amoebic Liver Abscess
• Lobar Pneumonia

Treatment
1. Conservative (60-70%)

• Admission
• Aspiration of HCL with Ryle’s Tube
• Antispasmodics : Inj Morpine 8-10 mg IM along with Inj Atropine 06 mg to relieve spasm
• Antibiotics : Cefazoline or Amikacin
• Pt is kept for 2-3 days. During this period IV fluids are given

2. Early Cholecystectomy : This can be done from 2 to 7 days of admission as there’s proved of having
complications of inflamed GB prior to these the conditions like OM, HTN etc should be made corrected.

3. Emergency Cholecystostomy : About 10% pt needs emergency cholecysostomy. The deciding factors
to be considered are High Grade Fever, Septic Shock, etc.
4. Prophylactic Cholecystectomy : It means complete removal of GB with stones & without symptoms.

URINARY SYSTEM
ACUTE RENAL FAILURE (ARF)
• Acute renal failure is a sudden reduction in kidney function that results in nitrogenous wastes
accumulating in the blood.
• The substances normally eliminated in the urine accumulate in the body fluids as a result of
impaired renal excretion leading to a disruption in endocrine and metabolic functions as well as
fluid, electrolyte and acid-base disturbances.
Etiology
• Hypovolemia
• Renal hypoperfusion
• Hypotension
• Hepatic cirrhosis
• Nephrotic syndrome
• Tubular injury
• Vasculitis
• Post-renal

1. Intrinsic :

o Intra-luminal – Stone, blood clot, papillary necrosis

o Intra-mural – Urethral stricture, prostatic hypertrophy or
2. Extrinsic :

o Pelvic malignancy
o Retroperitoneal fibrosis

Pathophysiology
• Pre-renal ARF is an appropriate physiological response to effective or true hypovolaemia
resulting in intense renal conservation of sodium and water at the expense of decreased GRF.
• Renal function returns rapidly to normal once the underlying cause is corrected. Reduction in
renal arterial perfusion pressure below the level at which autoregulation of GRF occurs is an
important contributor.
• However, in hypovolaemic or septic patients, pre-renal ARF may still occur as a result of intra-
renal vasoconstriction.
• Acute tubular necrosis (ATN) results from the insults that cause pre-renal ARF but lasting long
enough to cause Ischaemic injury to renal tubules. This results in long-lasting reduction in GFR.
This is caused by a combination of :
• Persistent, intense intra-renal vasoconstriction caused by endothelin, other autocrine mediators
and increased intracellular calcium.
• Loss of polarity of tubular cells leading to loss of function
• Formation of tubular casts, blocking the lumen and preventing urine flow
• Back-leak of tubular filtrate as a result of loss of tubular viability and obstructing casts
• Post-renal ARF : Increased pressure within the renal collecting systems results in reduced GRF,
reduced tubular reabsorption of sodium and water and acquired renal tubular acidosis,
phosphaturia and other abnormalities of tubular function. Obstruction is not rapidly relieved.

Clinical features : Stages

1. Early or pre-oliguric stage
 • This is overshadowed by symptoms of the primary cause. Symptoms like lethargy, nausea,
headache, are indicative of overhydration and should arouse suspicion of impending renal
insufficiency.

2. Oliguric stage

A. Oliguria (less than 400 mL urine in 24 hours in adults) sets in majority within 24–48 hours. The
duration varies, average being 4–10 days.

B. Gastrointestinal : Anorexia, nausea, vomiting at times diarrhoea, mouth ulceration, dynamic ileus or
pseudo-peritonitis if these are related to uncontrolled uraemia, they disappear after dialysis.

C. Circulatory : Hypertension is common in acute glomerulonephritis, renal infarct and cortical necrosis
D. Respiratory : Dyspnoea is related to metabolic acidosis, to pulmonary infection or oedema.

E. Neuromuscular : Drowsiness, confusion and agitation occur in advanced uraemia and may indicate
water or drug intoxication.

F. Infection : Secondary sepsis is a major risk in patients with ARF.

3. Diuretic stage

• This phase of the disease is ushered in by increase in urinary output to about 1000 ml in 24
hours, this may progress to polyuria. Febrile reaction is common and uraemic symptoms may be
aggravated and lead to coma.

Investigations
• Urinalysis : Suggests a renal inflammatory process. Red cell casts diagnostic in
glomerulonephritis
• Biochemistry (Creatinine, electrolytes metabolic, serum bicarbonate, CRP, Serum
immunoglobulins, Serum protein and Electrophoresis, Bence-Jones proteinuria) : Markedly
elevated creatine kinase and myoglobinuria suggests non-specific marker of infection or
inflammation.
• Haematology : Eosinophilia may be present in acute interstitial nephritis, cholesterol or
vasculitis. Thrombocytopenia red cell fragments suggest thrombotic Disseminated intravascular
coagulation associated with sepsis.
• Immunology [Antinuclear antibody (ANA), Antineutrophil cytoplasmic antibody (ANCA)] : ANA
positive in SLE and other autoimmune disorders.

Management
A. Early Management

1. Restoration of fluid and electrolyte balance –There are two good physical signs of volume depletion
(a) Low jugular venous pressure

(b) Postural drop in BP

2. Intravascular volume depletion should be corrected rapidly. If large veins in forearms or antecubital
fossa are not available, access should be established through Femoral vein.
B. Other measures

If oliguria persists after adequate circulation is established in order to increase renal tubular flow and
promote glomerular vasodilatation.

Fluids restricted to previous 24-hr urine volume plus other losses. Sodium and potassium restricted to
<80 mmol/day and 60 mmol/day respectively:

(a) Mannitol : 100–150 ml of 10% solution or 50 ml of 20% solution (maximal dose 50 g/24 hours) after
Shock and/or fluid depletion has been treated and urinary obstruction excluded. If urine flow exceeds 50
ml/hour, further doses should be given 3 or 4 hours later to maintain an output of about 100 ml/hour.
Mannitol can also be used to determine whether renal failure is due to dehydration.
(b) Frusemide : in large doses is equally effective. Shock, hypotension or fluid depletion must be
excluded or corrected first. A first dose of 100–200 mg IV (or 250–500 mg by mouth) is followed every
3–4 hours by equal doses if urine flow increases. Urinary losses of water, electrolytes must be replaced
by 5% dextrose containing 4–6 g/litre.
(c) Dopamine : 2.5 µg/kg/minute, if oliguria persists after adequate circulation has been established.

Management of Diuretic Phase

• Fluid and electrolyte replacement during this stage must be based more on clinical observation
such as general condition, pulse, blood pressure and thirst, and biochemical observations rather
than on quantitative and qualitative loss of water and electrolytes in urine.
• Intravenous therapy is stopped and the patient encouraged to take a high potassium, high salt
diet and liberal intake of water (about 3000 ml). Infection remains a problem during this phase.
Dialysis should be continued until there is a spontaneous drop in creatinine and urea.

CHRONIC KIDNEY DISEASE (CKD)

• Structural or functional abnormalities of the kidneys for > 3months as manifested by kidney
damage with or without decreased GFR.
• GFR < 60ml/min/1.73 m3 with or without kidney damage.

Stages
Stage 1 : > 90 mL/min → Kidney damage with N or ↑ GFR

Stage 2 : 60–89 mL/min → Kidney damage with mild ↓ GFR

Stage : 30–59 mL/min (Moderate) ↓ GFR

Stage : 15–29 mL/min (Severe) ↓ GFR

Stage : 15 mL/min – Dialysis required

Causes
• Glomerulonephritis

• Diabetic nephropathy

• Hypertensive renal disease

• Renovascular disease (especially in elderly)

• Acute interstitial nephritis and other drug reactions

• Vasculitis in the kidney (e.g. Wegener’s granulomatosis, microscopic polyangiitis)

• Obstructive uropathy

Pathogenesis
Diabetes Hypertension

Increased RBF
Sodium retention

Glomerular hyperfiltration

Increased tubular reabsorption

Increased oxygen consumption

Decreased nitric oxide Tubulointerstitial injury

Increased RAS Tissue hypoxia Microvascular rarefaction

Insufficient HIF activation Glomerulosclerosis

Decreased AMPK
CKD

Clinical features
Urinary : Poyuria, Oliguria, Anuria

GI : Anorexia, Nausea/Vomiting
Cardiac : HTN, Heartfailure, Pericarditis, CAD

Skin : Pruritis, Pallor

Neurological : Seizures, Coma, Muscle twitching, Encephalopathy

Haematologic : Anaemia, Altered immune response and function

Pulmonary : Tachypnea, Pneumonitis

Reproductive : Amennorrhea, Infertilty

MSS : Bone fractures, Muscle cramps, Foot drop

Diagnosis

• Urine test : Albumin is present in the urine when kidneys are damaged.

• Kidney scans

• Kidney biopsy : An analysis of kidney tissue makes it easier to make a precise diagnosis of kidney
disease.

• Chest X-ray : The aim is to check for pulmonary edema which is fluid retained in the lungs.

• GFR : GFR is a test that measures the levels of waste products in the person’s blood and how
many milliliters of waste the kidneys can filter per minute (ml/min).

Management
• Diet : A person should regulate their salt intake carefully to control hypertension. A person may
also need to limit potassium and phosphorus as these can be dangerous for people with chronic
kidney disease.

• NSAIDs People with chronic kidney disease should avoid NSAIDs such as ibuprofen, certain
antibiotics.

• Control blood sugar if diabetes. Keep a healthy blood pressure

• Exercise at least 30 minutes on most days of the week.
• Do not smoke or use tobacco. Limit alcohol.
• Injections of erythropoiesis-stimulating agents (ESAs) are the most common treatment for
chronic kidney disease and anemia.

• People with vitamin D deficiency may require supplementation.

 • People with chronic kidney disease need to be careful with their fluid intake and restrict how
much salt they consume.

End-stage treatment

Kidney dialysis : Dialysis is the mechanical removal of waste products and excessive fluids from the
blood when the kidneys cannot do properly anymore.There are two main types of kidney dialysis.
1. Hemodialysis : A dialyzer (an artificial kidney) machine pumps blood out of the person’s body.

2. Peritoneal dialysis : The person’s abdomen filters the blood.

Kidney transplant : A kidney transplant is a better option than dialysis for those with no other health
conditions apart from kidney failure.

HEMATURIA
• Hematuria is the presence of red blood cells in the urine. It can be either

o Visible haematuria (VH) also called macroscopic haematuria or gross haematuria.

o Non-visible haematuria (NVH) also called microscopic haematuria or dipstick-positive

haematuria.

Causes
• Infection : cystitis, tuberculosis, prostatitis, urethritis

• Tumour: renal carcinoma, Wilms' tumour, carcinoma of the bladder

• Renal tract trauma due to accidents

• Glomerulonephritis

• Haematological: sickle cell disease, coagulation disorders

• Surgery: invasive procedures to the prostate gland or bladder

• Toxins: sulfonamides, cyclophosphamide, NSAIDs

• Others: genital bleeding, including child abuse, menstruation

Pathophysiology
• The origin of hematuria may be traced back to the kidneys (glomeruli, convoluted tubules,
collecting tubules, interstitium) or the urinary tract (the collecting system, ureter, urinary
bladder, and urethra).

• When RBCs are of glomerular origin they enter the capillary lumen after crossing the glomerular
endothelial–epithelial barrier.
 • Hence glomerular hematuria is accompanied by deformed RBCs (acanthocytes), RBC casts and
proteinuria.

• The presence of leukocytes in urine and renal tubular epithelial casts suggests that the
hematuria originated within convoluted tubules or collecting tubules.

• Possible explanations for hematuria in hypercalciuria are irritation of uroepithelium by micro

calculi and microscopic nephrocalcinosis.

• Non-renal conditions such as high fever and heavy physical exercise can produce transient
hematuria by altering renal hemodynamics.

Clinical features
• Hematuria of the upper urinary tract origin : brown, cola- or tea-colored or burgundy urine

• Hematuria of the lower urinary tract origin : bright-red or pink-colored urine

• Hematuria of the lower urinary tract origin : terminal hematuria, blood clots, normal
morphology of urinary RBCs and absent or minimal proteinuria

• Persistent urge to urinate

• Pain

• Burning with urination

• Extremely strong-smelling urine

Investigations
Plasma creatinine and estimated glomerular filtration rate (eGFR)

Measure proteinuria

Measurement of blood pressure

FBC (anaemia) and clotting screen

Urine red cell morphology : dysmorphic erythrocytes suggest a renal origin

Urine culture : Checks for an infection

Urine cytology : Checks for any abnormal appearing cells

Cystoscopy : A test that uses a device called a cystoscope to look at the inside of the bladder and
urethra

Computed tomography (CT) scan : A test that uses X-rays and computers to make cross-sectional
images of the abdomen and pelvis

Differential diagnosis
 • Haemoglobinuria : dipstick-positive but no red cells on microscopy

• Myoglobinuria

• Food : eg beetroot

• Drugs : eg rifampicin, nitrofurantoin, senna

• Porphyria : urine darkens on standing

• Bilirubinuria : obstructive biliary disease

Treatment

• If an infection such as a UTI prescribe antibiotics to kill the bacteria causing the infection.

• Hematuria caused by large kidney stones can be painful if left untreated. Prescription
medications and treatments can help you pass stones using a procedure called extracorporeal
shock wave lithotripsy (ESWL) to break up the stones.

• If an enlarged prostate prescribe medication such as alpha blockers or 5-alpha reductase

inhibitors. In some cases, surgery may be an option.

• To prevent infections, drink plenty of water daily, urinate immediately after sexual intercourse
and practice good hygiene.

• To prevent stones, drink plenty of water and avoid excess salt and certain foods like spinach and
rhubarb.

• To prevent bladder cancer, refrain from smoking, limit your exposure to chemicals, and drink
plenty of water.

ACUTE GLOMERULONEPHRITIS
• A disease most common in children characterised pathologically by diffuse inflammatory
changes in the glomeruli and clinically by usually abrupt onset of macroscopic hematuria,
proteinuria (usually moderate), oedema, hypertension and impaired kidney function with or
without oliguria. Not all features may be present at the same time.
Etiology
• Poststreptococcal glomeruinephritis

• Infective endocariditis

• Syphilis

• Mumps, Measles, Hepatitis B, Malaria

• SLE

• Good pasture’s syndrome

• Glomerulonephritis

• Miscellaneous : Malignancy, Eclampsia, Penicillamine

Pathogenesis
Two chief pathogenesis are recognized :

o Deposition of antigen-antibody complexes in glomeruli

o Deposition of an antibody in glomerular basement membrane which then reacts with antigen in
the basement membrane

• Immune complexes are removed through hosts reticuloendothelial system

o Impaired ability of the same results in deposition in glomerular capillary walls

• Immune complex and antibody against glomerular antigen trigger injury by following
mechanism
o Complement activation
o Fibrin deposition
o Platelet aggregation
o Lease of cytokines and free orygen radical

Clinical Features
Modes of onset

(a) Oedema – puffiness of face

(b) Urinary symptoms – Scanty and smoky or frank bloody urine

(c) Symptoms of acute infection – Fever, bodyache, vomiting

(d) Cerebral symptoms – Headache, convulsions

(e) Insidious onset – Weakness, pallor, loss of appetite

Symptoms and Signs

1. Oedema – may come on suddenly or gradually. Puffiness of face and whitish pallor constitute
“nephritic facies”, swelling of face usually in morning. Generalized anasarca may occur.

2. Hypertension – occurs in majority ofcases, the diastolic pressure being 90 to 120 mm usually and as a
rule persists for at least one week, returning to normal a few days after patient has had diuresis. Renal
retention of salt and water is responsible for the circulatory disturbance.

3. Impaired renal function – Oliguria

Laboratory Tests
1. Urine – Volume reduced, dark in colour or smoky when fresh, tea-coloured after haemolysis.
Proteinuria variable rarely more than 2.5 g per day.

2. Evidence of streptococcal infection – in post streptococcal GN

3. Haematology – Polymorphonuclear leucocytosis, raised ESR

4. Osmolality – of diagnostic help because osmolality of urine is often appreciably higher than that of
plasma in acute nephritis in contrast to other forms of acute renal failure.

5. Renal biopsy – Indications : (i) Unusually protracted course, especially if accompanied by kidney
failure. (ii) Suspicion of multisystem disease. (iii) Transition to nephrotic phase. (iv) Persistent
hypocomplementaemia.

Management
1. Rest in bed – diminishes risk of pulmonary oedema and hypertensive crises.

2. Restricted fluids – (Fruit juices contain potassium and should be used with caution in oliguric
patients). First 24–28 hours only 500 ml of water and glucose or barley water. After that if urine volume
in 24 hours is less than 400 ml treat as for acute renal failure.

3. Diet – Low protein diet.

4. Antibiotics – Benzathine penicillin G 500,000 units IM 6-hourly to destroy any residual haemolytic
streptococci. Erythromycin 250 mg qds if penicillin is not tolerated.

5. Management of complications

(i) Convulsions – IV Diazepam 10 mg slowly, if fits recur phenytoin sodium 100 mg bd IM

(ii) Hypertension – ACE inhibitors or angiotensin II receptor antagonists

(iii) Acute renal failure

6. Dialysis
7. Transplantation for those who progress to ESKF

Complications
• Pulmonary edema

• Hypertensive encephalopathy

• Renal failure

NEPHROTIC SYNDROME
• Manifestation of glomerular disease characterized by nephrotic range proteinuria and a triad of
clinical findings associated with large urinary losses of protein : hypoalbuminaemia, edema and
hyperlipidemia.

Causes
1. Primary glomerular diseases
Minimal change nephropathy
Mesangioproliferative glomerulonephritis
Membranous nephropathy
2. Idiopathic
3. Secondary to other diseases
Infections : Malaria, hepatitis B, herpes zoster
Drugs : NSAlDs
Heavy metals such as gold, anticonvulsants, penicillamine, ACE inhibitors
Malignancy : Hodgkin’s disease and other lymphomas
Systemic diseases : Diabetes mellitus, amyloidosis, SLE
Pathophysiology
Hypoalbuminemia

Reduced intravascular osmotic pressure

Loss of fluid into the interstitial space

Increased albumin production &

Lipoprotein synthesis Reduced plasma volume

Increased serum triglycerides & low density Increased aldosterone secretion &
Lipoproteins Decreased renal function

Lipiduria Salt & Water retention

Oedema
Clinical Features
1. Oedema : Is peripheral involving the limbs, particularly lower limbs.
In children, oedema may be more obvious in the face and abdomen.
Usually massive generalized anasarca, the patient almost weighing double his true weight.
2. GI symptoms : Anorexia causes severe malnutrition.
Diarrhoea and vomiting due to oedema of intestinal wall
3. General symptoms : Prolonged protein loss causes anorexia, lethargy, tiredness, frequent infections
and muscle wasting
4. Dyspnoea may occur if there is fluid in the pleural cavity
5. Hypertension
Laboratory investigations
1. Urine
(i) Oliguria while oedema is forming, diuresis or normal amount of urine during period of subsidence of
oedema
(ii) Proteinuria : Massive, usually more than 5 g/day though variable from time to time. Daily loss of
protein may be 20–50 g
(iii) Red blood cells absent or few
(iv) Casts : Fatty casts, tubular cells, oval fat bodies, doubly refractile bodies
2. Blood
(i) Anaemia – Slight, normochromic
(ii) Hypoalbuminaemia – Serum albumin usually less than 3 g/100 mL
(iii) Hyperlipoproteinaemia (LDL level in particular) and hyperfibrinogenaemia (contributing to raised
ESR)
3. Renal biopsy – is normal on light microscopy but electron microscopy shows typical abnormalities
(effacement of epithelial cell foot processes)
Management
1. Corticosteroids produce rapid and complete remission with clearing of proteinuria in 90% cases.
Dose : Prednisolone 1 mg/kg/day, maximum 80 mg/day.
Remission usually occurs between 7 and 14 days though some patients need up to 16 weeks
therapy to achieve complete remission.
After disappearance of proteinuria or one week after remission, prednisolone dose is reduced to
0.5 mg/kg/day and then tapered slowly.
2. Immunosuppressive drugs : In steroid-resistant patients or in those in whom remission can only be
maintained by heavy doses of steroids, cyclophosphamide 1.5–2 mg/kg/day for 8-12 weeks with
concomitant prednisolone 7.5–15 mg/day.
The neutrophil count must be checked every 2 weeks and cyclophosphamide stopped if it falls below 2 ×
103/mm3.
Cyclosporine 3–5 mg/kg/day is effective in some corticosteroid resistant or dependent patients.
Prednisolone 7.5–15 mg/day is also given.
Levamisole : In corticosteroid dependent children 2.5 mg/kg to maximum 150 mg on alternate days is
useful in maintenance of remission.
Complications
1. Protein malnutrition – Wasting, striae, osteoporosis, poor wound healing
2. Hypercoagulability – Spontaneous venous and arterial thrombosis due to rise of many clotting factors
in plasma
3. Impaired resistance to infection – Cellulitis, primary peritonitis with pneumococci, UTI
4. Acute hypovolaemia
5. Hyperlipidaemia

UTI
• An infection in any part of the urinary system, kidneys, bladder or urethra.
• UTI is the presence of microbial pathogens in the normally sterile urinary tract.
• In females, vaginitis is another syndrome which commonly overlaps.

Etiology
Uncomplicated urinary tract infection
• Bacterial virulence
• Host defence – Colonization of vagina and mucosa
• Anti-microbials (loss of commensal population)
• Sexual intercourse
• Ageing (post-menopausal oestrogen decrease, loss of detrusor power)
Complicated urinary tract infection
• Outflow obstruction
• Urethral stricture
• Stone/tumours
• Renal cysts
• Diabetes mellitus
• Alcoholism
• Pregnancy
Pathophysiology
• Bacterial virulence factors : Critical to the pathogenesis of bacteria is adherence to the
uroepithelium as infections ascend from the urethral orifice to the bladder and to the kidney in
pyelonephritis.

• E. coli have special fimbriae (also called pili) which permit adhesion.

• Other virulence factors include flagellae (to permit mobility), production of enzymes such as
haemolysin (E. coli and Proteus) which induces pore formation in cell membranes. E. coli also
inhibits phagocytosis.

• Urease is produced by some organisms (e.g. Proteus), it hydrolyses urea and increases
ammonia, which facilitates bacterial adherence.

• Host predisposing factors include any functional or anatomical abnormality of the urinary tract
such as urinary stasis, reflux or stones.

• Other important risk factors include sexual intercourse, diabetes mellitus, immunosuppression,
instrumentation (including catheterisation) and pregnancy.

• Urine itself is inhibitory to the growth of normal urinary flora (non-haemolytic Streptococcus
corynebacteria, Staphylococcus) through its pH and chemical content.
 Clinical features
1. Urethritis:

• Discomfort in voiding

• Dysuria

• Urgency, frequency

2. Cystitis :

• Dysuria, urgency and frequency urination

• Pelvic discomfort

• Abdominal pain

• Pyuria

3. Hemorrhagic cystitis :

• Visible blood in urine

• Irritating voiding symptoms

4. Babies and infants :

• Failure to thrive

• Fever

• Apathy

• Diarrhoea

4. Children :

• Dysuria, urgency, frequency

• Haematuria

• Acute abdominal pain

• Vomiting

5. Adults :
• Lower UTI- frequency, urgency, Dysuria, Haematuria

• Upper UTI- fever, rigor and loin pain and symptoms of lower UTI

Diagnosis
• Microscopic examination of urine : Uncontaminated, midstream urine sample used
 • Urinalysis : Presence of pus, white blood cells, red blood cells

• Urine culture : For pyelonephritis

Not a rapid diagnostic tool

Differential leukocyte count increased neutrophils

• Imaging techniques – CT scan and MRI

• Intravenous pyelography

• Voiding cystourethrography

• Cystoscopy

Management
• Urethritis : Ceftriaxone 250 mg IM plus either Azithromycin 1g po once or Doxycycline 100 mg
po bd for 7 days.

• Cystitis : First-line treatment of uncomplicated cystitis is nitrofurantoin 100 mg po bd for 3 days

(it is contraindicated if creatinine dearance iz<60 mL/min) Trimethoprim/sulfamethoxazole
(TMP/SMX) 160/800 mg po bid for 3 days.

• Acute pyelonephritis : Antibioties are required. Outpatient treatment with oral antibiotics is
possible if patients are expected to be adherent, immunocompetent, have no nausea or
vomiting or evidence of volume depletion or septicemia. Ciprofloxacin 500 mg po bid for 7 days.

• Do not treat non pregnant women (of any age) with asymptomatic bacteriuria with an
antibiotic.

• Treat non-pregnant women of any age with symptoms or signs of acute LUTI with a three day
course of trimethoprim or nitrofurantoin.

• Particular care should be taken when prescribing nitrofurantuin in the elderly who may be at
increased risk of toxicity.

WILM’S TUMOUR
Wilm’s Tumor is also known as Nephroblastoma. It is a highly malignant embryonal neoplasm.

It may involve one or both kidney

The exact cause of tumor is unknown but it has been identified that tumor suppressor gene acts to
promote normal kidney development. This gene may be absent or missing in wilm’s tumor.
Pathophysiology
Mostly wilm’s tumor is unilateral but it can be bilateral in 5% of cases

Nephroblastoma are generally large and rapidly growing

Tumor generally start growing in renal parenchyma or at the tip of kidney

It causes suppression of normal tissue remaining

Majority of tumors present a as single encapsulated mass that separates the normal kidney and tumor

Although the tumor is encapsulated but the membrane may be very thin and get easily torn

Rupture of tumor put patient at the risk of hemmorhage and dissemination of tumor

Clinical features
• Presence of abdominal mass

• Pain if tumor is enlarging

• Anoreria

• Hematuria

• Nausea and vomiting

• Urinary tract infection

Stages
Stage I (43 cases) – Tumor limited to kidney and completely resectable

Stage II (23% cases) – Tumor extend beyond kidney into nearty fatty tissue but resectable

Stage III (23% cases) – Non hematogenous spread in abdomen like spread to fymph nodes in abdomen
and pelvis but this stage tumor is not completely resectable
Stage IV (10% cases) – Hematogenous metastatis to lungs and liver

Stage V (5% cases) – Bilateral renal involvement

Diagnosis
• History : The child may have positive family history

• Physical examination reveals presence of abdominal mass

• Urinanalysis reveals presence of blood in urine

• Abdominal ray

• Ultrasound

• Chest X-ray to detect metastasis to lungs

• Increased Blood urea nitrogen creatinine values

Management
The management of children with wilm’s tumor include :

1. Radiation Therapy

• Wilm’s tumor may be bilateral or large in size.

• May be inoperable for such cases radiation therapy may be used to reduce the size of tumor so
that surgery can be performed.
2. Chemotherapy

• The objective of chemotherapy is to treat any metastatic lesions that may exist and destroy any
cells in blood stream before they get implanted.

• The drugs used for chemotherapy are Actinomycin D, Doxorubicin and Vincristine.

3. Surgical

• Partial or complete nephrectomy is done for unilateral and for bilateral partial nephrectomy is
done.

• After surgical management chemotherapy and radiation therapy is given if indicated.

Treatment
Treatment for wilm’s tumor is based mainly on the stages of the cancer :

Stage 1 – These tumors are still only in the kidney. Standard treatment starts with surgery to remove the
part of kidney containing tumor. The chemotherapy is given for 18 weeks.

Stage 3 – Treatment is usually surgery followed try radiation therapy to the abdomen over several days.
This is followed by chemotherapy for about 6 months.

Stage 4 – These tumors are already spread to distant parts of the body at the time of diagnosis so
standard treatment is surgery followed by radiation and chemotherapy.
Stage 5 – In this stage usually tumor is bilaterally present, standard treatment involves surgery.
Radiation and chemotheracy repeatedly until normal kidney tissue left behind. In case if not enough
kidney tissue is left after surgery that child may need to place on dialysis. If there is no evidence of any
cancer after year or two, a donor kidney transplant may be done.

RS
ACUTE BRONCHITIS
• Acute infection of mucous membrane of trachea and bronchi produced by viruses, bacteria or
external irritants.

Causes : Precipitating causes

(i) Infection – Either bacterial or viral or descending infection from nasal sinuses or throat

(ii) Complicating other diseases – e.g. measles, whooping cough

(iii) Physical and chemical irritants – Inhaled dust, steam, gases like SO2 , ether
(iv) Allergic bronchitis – following inhalation of pollens or organic dusts

Pathophysiology
Irritation of airways due to any etiological stimulant

Infiltration of neutrophils in the lung tissue

Release of inflammatory substance by neutrophils

Hypersecretion of goblet cells Hyperemic and oedematous Diminished bronchial mucociliary

mucus lining function

Clogging of air passages

Acute bronchitis with predominant cough

Symptoms

• Toxaemic– Malaise, fever, palpitation, sweating, etc

 • Irritative – Cough with expectoration, at first scanty viscid sputum, later more copious and
mucopurulent, substernal pain or raw sensation under the sternum

• Obstructive – Choked up feeling, paroxysms of dyspnoea particularly following spells of

coughing relieved with expectoration

• Shortness of breath

• Chest pain

• Wheezing

• Inflammation or swelling of the bronchi

Diagnosis
History collection

Physical examination

Chest x-rays
Sputum cultures

Pulmonary function test

Spirometer excercises
Bronchoscopy

Treatment
• Antibiotics : Effective for bacterial infections but not for viral infections. They may also prevent
secondary infections.

• Cough medicine : one must be careful not to completely suppress the cough, for it is an
important way to bring up mucus and remove irritants from the lungs.

• Mucolytics : Thin or loosen mucus in the airways making it easier to cough up sputum
• Anti-inflammatory medicines and glucocorticoid steroids

• Pulmonary rehabilitation program : Includes work with a respiratory therapist to help breathing

• Appropriate antibiotic therapy eg: Amoxicillin, Cephalosporin or Clarithromycin

• Bronchodilators in patients with chronic airflow limitation

CHRONIC BRONCHITIS
• A clinical disorder characterised by productive cough due to excessive mucus secretion in the
bronchial tree not caused by local bronchopulmonary disease, on most of the days for at least 3
months of the year for at least two consecutive years.
 • Chronic simple bronchitis is characterised by mucoid sputum production, chronic mucopurulent
bronchitis by persistent or recurrent purulent sputum production in absence of bronchiectasis
and chronic asthmatic bronchitis in patients who experience severe dyspnoea and wheezing
during acute respiratory infections or following inhaled irritants.

Causes
1. Infection

(a) Result of acute bronchitis

(b) Infective focus in upper respiratory tract, the nasal sinuses, tonsils or lungs (eg: bronchiectasis,
fibrosis, or tuberculosis)
2. Smoking – particularly of cigarettes

3. Air pollution – due to industrial fumes and dust

4. General illness – which favour infections, eg: obesity, alcoholism, and chronic kidney disease

Pathogenesis
Etiologic factor

Phagocyte migration, proinflammatory mediators releasing (cytokines, enzymes),

their storage in mucous membrane

Respiratory tract mucous membrane direct impairment Vessel reaction

Vasodilation

Increased permeability of vessel wall

Exudation

Mucous membrane edema

Bronchial hypersecretion due to irritation and dilation of goblet cells
Symptoms
• Cough – Constant paroxysmal, worse in winter or on exposure to cold winds or sudden change
of temperature

• Expectoration – Variable may be little, thin and mucoid or thick or frothy, mucoid and sticky.
May become mucopurulent during attacks of acute bronchitis in winter

• Dyspnoea – In advanced cases, breathing becomes quick and wheezing present even at rest

• Fever – Absent except in acute exacerbation

• Haemoptysis – Usually in the form of streaks of blood

Signs
(a) Build – usually short and stock

(b) Cyanosis – rarely with clubbing

(c) Signs of airway obstruction – Prolonged expiration, pursing of lips during expiration, contraction of
expiratory muscles of respiration. Widespread wheezes of variable pitch usually most marked in
expiration. Crackles at lung bases in patients with excessive bronchial secretions. Both wheezing and
crackles may be altered in character by coughing

Investigations
• Ventilatory indices – Reduced PEF and VC

• Chest radiography may be normal. Infected episodes may produce patchy shadows of irregular
distribution due to pneumonic consolidation and small linear fibrotic scarring may result.

• Chest X-ray

• Sputum (mucus coughed up from the lungs, to be tested on analyzing presence of bacteria

• Pulmonary Function Test (checks for signs of asthma of emphysema by measuring how well
you’re able to breathe • CT scan, high resolution X-rays of the body from various angles

Diggerential diagnosis
Bronchiectasis

Purulent bronchitis
Bronchiolitis
Lung abscess
Management
1. To remove the cause if possible – Air pollution, smoking. Elimination of aerosol sprays such as deo-
dorants, insecticides and hair sprays.

2. To prevent acute exacerbations – By avoiding overheated rooms, damp and foggy places, stuffy
clothing, overfeeding, smoking and too much alcohol.
3. To try and arrest the progress of the chronic disease by : Increasing patient’s power of resistance,
Regular exercises in fresh air and within limits of tolerance, Encouraging deep breathing and efficient
clearance, coughing should follow a full inspiration.

4. To give the patient as much comfort as possible

(a) Antitussives such as linctus codeine if dry cough

(b) Mucolytics and inhalation of medicated steam

(c) Expectorants (i) Ammonium salts, bromhexine or ambroxol in mixture form (ii) Hot alkaline drink

(d) Bronchodilators

(e) Antibiotics – Clarithromycin or Co-amoxiclav for 7–14 days

BRONCHIECTASIS
• Bronchus – Airways. Ectasia - Dilation

• Bronchiectasis is a destructive lung disease characterized by chronic (permanent/irreversible)

dilatation of the bronchi associated with persistent though variable inflammatory process in the
lungs.

• These changes may involve any area but are predominantly found in the lung bases and can be
divided into localized and diffuse forms.

Pathology
The diagnostic feature of bronchiectasis is dilated bronchi. The Reid classification differentiates between
pathological and radiological appearances of bronchiectasis.

Cylindrical bronchiectasis – Bronchial dilatation is mild and the bronchi retain their regular relatively
straight outline.

Varicose bronchiectasis – Bronchial dilatation is greater and local constrictions are present, giving the
airway an irregular appearance.

Saccular/cystic bronchiectasis is the most severe form and is characterized by large areas of distal
‘grape-like’ bronchial dilatation and loss of bronchial subdivision.

Atelectatic bronchiectasis is a localized form related to proximal bronchial distortion or occlusion.

Pathogenesis
Pathogens activate toll like receptors on the surface of many cells like macrophages, neutrophils,
lymphocytes which initiate the inflammatory process

Stimulation of mucus secreting glands

Increased mucus production

Repeated episodes of infections

Lead to transmural inflammation in the airways which causes thickening & fibrosis of walls

Cilia are damaged leading to impaired mucociliary clearance

Destruction of the cartilage in the walls of the proximal airways

Damage of supporting structures

Bronchi get dilated

Clinical features : Types

1. Bronchitic – Attacks of recurrent bronchitis more common in winter. Clubbing of fingers diagnostic

2. Haemorrhagic (bronchiectasis sicca) – Recurrent haemoptysis with good health in-between or attacks
of bronchitis
3. Suppurative – Chronic cough, copious purulent expectoration, general toxaemia, clubbing of fingers
vary- ing from slight parrot beak curvature of finger nails to bulbous drum stick enlargement (pulmonary
osteoarthropathy).
Pleuritic chest pain is caused by distended peripheral airways and inflammation adjacent to the visceral
pleura. Pyrexia is rare during exacerbations if it is present, pneumonia should be excluded.
4. With relatively rapid onset – Symptoms developing with comparative suddenness as a sequel to
partial bronchial obstruction by a foreign body or after anaesthesia

There may be signs of bronchitis, fibrosis, consolidation, collapse or cavitation.

Early stages – Fine crackles or sticky rhonchi and slight alteration in character of breath sounds
Late stages – Bronchial breathing, coarse crepts and perhaps signs of a cavity
Investigations
• Sputum : To exclude diagnosis of underlying pulmonary tuberculosis

• Sinus radiographs – for chronic sinusitis

• Chest radiography – for changes suggestive or associated with the diagnosis : Collapse
(segmental or lobar), Crowding of pulmonary vessels, indicating area of damage or consolidation
that may become infected, Tramline shadows suggesting bronchial wall oedema

• HRCT : High-resolution CT has replaced bronchography and is the preferred investigation

• CT findings include the following : The ‘signet ring’ sign (end-on dilated bronchi that are larger
than the accompanying pulmonary artery) is seen in all form of bronchiectasis

• Immunoglobulins – Raised plasma concentrations of immunoglobulins (especially IgA)

• Barium studies – For gastrooesophageal reflux, since association of basal bronchiectasis is well
recognised.

Differential diagnosis
• Cavitated bronchial carcinoma – Elderly patient. Pain in chest, cough and dyspnoea. Cancer cells
in sputum.

• Purulent bronchitis – Long history. No elastic tissue in sputum

• Caseating tuberculosis – Positive sputum

• Infected lung cyst – Particularly bronchogenic and hydatid, difficult to differentiate unless
previous X-ray shows uninfected cyst or cysts in other parts of the

• Pulmonary infarction – Postoperative or antecedent cardiovascular disease

• Empyema with bronchopleural fistula – Fistula can be demonstrated by injectin

Management
1. Postural drainage – Deep breathing or coughing, assisted by percussion of the affected part (clapping)
helps to dislodge the secretions. It should be carried out at least twice daily for 15–20 minutes at a time.
Expectoration is facilitated by cough mixtures or better inhalation of nebulized bronchodilator
isoproterenol.
2. Antibiotic therapy – Antibiotics can delay progression in patients with cystic fibrosis. β-lactam
antibiotics (e.g. amoxicillin 500 mg t.d.s. for 10–14 days) remain the first line therapy. Nebulized
antibiotics allow maximal concentrations of antibiotics in the airways with reduced systemic effects.
Amoxicillin 500 mg b.d., gentamicin 80 mg b.d., and tobramycin solution for inhalation 300 mg b.d. can
be used.
3. Prophylactic therapy – One guideline for therapy is when there are exacerbations every 2 months that
prevent participation in normal activities of 2 weeks or more during the exacerbation. Continuous
therapy is considered in patients who persistently expectorate purulent sputum.

4. Intravenous immunoglobulin replacement is thought to be effective in panhypogammaglobulinemia

but is given only to patients with established widespread lung damage.
4. Alpha-antitrypsin replacement therapy by inhaled route has the potential to neutralize damaging
processes that are released as part of the airways inflammatory response.

5. General supportive treatment :

(a) Adequate nutrition

(b) Eradication of chronic nocturnal post-nasal discharge and treatment of sinusitis

(c) Avoidance of smoking

(d) Adequate hydration

Complications
• Pulmonary – recurrent pneumonia, lung abscess, haemoptysis

• Pleural – pleurisy, pleural effusion or empyema

• Corpulmonale

• Cerebral abscess

• Amyloidosis

• Seronegative arthropathy

BRONCHIAL ASTHMA
• Asthma is a syndrome of variable airflow obstruction. It is characterized pathologically by
bronchial inflammation with prominent eosinophil infiltration, physiologically by bronchial
hyper-reactivity and clinically by variable cough, chest tightness and wheeze.

• Atopy is the principal associate of asthma in individuals aged 5–30 years. It is a state of
disordered immunity in which predominant T-helper lymphocyte type 2 (TH2) immune
mechanisms drive production of IgE on exposure to common environmental antigens or
allergens.

Classification
1. Extrinsic asthma – applies to those who produce excessive IgE in response to allergens (atopic).

2. Intrinsic asthma – refers to those cases in which excessive IgE production cannot be demonstrated
(non- atopic).
3. Mixed forms

Triggers
1. Infections – Recurrent bouts of significant airflow limitation in constitutionally small airways may
result from viral infection.

2. Cigarette smoke – If parents smoke during the first two years of their child’s life, the child is likely to
develop asthma.

3. Allergens – The influence of both genetic and environmental factors is important and asthma is a
complex response to a variety of stimuli, making it difficult to identify specific factors.

(a) Aero-allergens (inhalants) – Such as house dust, mite allergens, tree pollens, feathers, paint, smoke,
animal dander, moulds.

(b) Ingestants – Milk, eggs, nuts, chocolates, fish, shell-fish, strawberries, etc.
4. Induced by gastro-oesophageal reflux

5. Cough variant asthma

Pathophysiology
Susceptible Person

Release of substance from mast cell, basophils, esinophills, neutrophils, macrophages

Response to asthmatic stimuli

Release of lipid mediators derived from arachidonic acid, such as leukotrienes and prostaglandins

Inflammation of airway, edema and desquamation of bronchial epithilium and hypertrophy of bronchial
smooth muscles

Airway obstruction
 Trigger Factor

Airway Inflammation

Hypersecretion of Mucus Airway Muscle Constriction Swelling bronchial membranes

Narrowing breathing passages

Wheezing, Cough, Shortness of Breath, Tightness in Chest

Clinical features
• Wheezing

• Dyspnea and cough

• Variable - both spontaneously and with therapy

• Tenaceous mucus production

• Symptoms worse at night

• Nonproductive cough

• Limitation of activity

Signs
• Increased respiratory rate with use of accessory muscles

• Hyper resonant percussion note

• Expiratory rhonchi, expiration > inspiration

• During very severe attacks, airflow may be insufficient to produce rhonchi →silent chest

• No findings when asthma is under control or b/w attacks

Investigations
1. Chest radiograph may be normal or show signs of segmental or lobar collapse.

2. Full blood count – Eosinophilia

3. Sputum – Eosinophils, Charcot-Leyden crystals and at times Curschmann’s spirals may appear
purulent (due to eosinophilic leucocytes) in absence of infection.
4. Skin tests – may confirm allergens suggested by history.

5. Lung function test – Spirometry shows reduction in FEV1, FEV1/FVC ratio and peak expiratory flow
(PEF). Reversibility, which is one of characteristic feature of asthma, is shown by >12% or 200 ml
increase in FEV1 15 minutes after inhaled short acting β2 agonist or 2–4 weeks trial of oral
corticosteroids.
6. Provocation (challenge) tests – Exercise challenge tests useful in young adults and can be used to
confirm diagnosis of asthma, since fall in FEV1 or PEFR occurs after 5–7 minutes of vigorous exercise in
most patients with asthma.

7. IgE and IgE specific test – Elevation of total serum IgE supports diagnosis of atopy, and measurement
of fractions of IgE specific to one allergen.

Differential diagnosis
• Other causes of paroxysmal dyspnoea

• Chronic obstructive pulmonary disease

• Tropical eosinophilia

• Obstruction in upper respiratory tract, trachea or primary bronchus

• Allergic lung disease

• Constrictive bronchiolitis

• Cryptogenic organizing pneumonia

Management
• Mild intermittent asthma : Use of inhaled short-acting β-agonist as required for symptom relief
is acceptable
• (Mild persistent) Regular preventer therapy : Add inhaled low dose corticosteroid
(beclomethasone or equivalent) 200–400 µg/day (usually 400 µg/day)
• (Moderate persistent) Add-on therapy : Add long-acting β2-agonist assess control of asthma by
following means :
• Good response to long-acting β2-agonist – continue
• Benefit from long-acting β2-agonist but control remains inadequate – continue and increase
inhaled corticosteroid to 800 µg/day
• No response to long-acting β2-agonist – stop and increase inhaled corticosteroid to 800 µg/day
• (Severe persistent) Persistent poor control : Increase inhaled corticosteroid to 2000 µg/day. Add
a fourth drug (e.g. leukotriene receptor antagonist, theophylline, β2-agonist tablet)
• (Very severe persistent) Continuous or frequent use of oral corticosteroids : Maintain high dose
inhaled corticosteroid 2000 µg/day
• Bronchodilators - rapid relief by relaxation of airway smooth muscle

• Controllers-inhibit the inflammatory process

• Anticholinergie agents : Prevent cholinergie nerve induced bronchoconstriction

COMPLICATIONS
• Bronchiectasis

• Spontaneous pneumothorax

• Cystic degeneration of lungs

• Recurrent bronchitis and pneumonia

• Dysrhythmias from hypoxia and stress of asthma

• Myocardial infarction rarely in acute severe asthma

• Hypokalemia : Due to high-dose corticosteroids, high dose β-agonists

COPD
• COPD is defined by the Global Initiative for Obstructive Lung Disease (GOLD) as a disease
characterized by air- flow limitation that is not fully reversible. The airflow limitation is usually
both progressive and associated with an abnormal inflammatory response of the lungs to
noxious particles or gases.

Causes
• Genes

• Exposure to particles : Tobacco smoke, Indoor air pollution from heating and cooking with
biomass fuel in poorly ventilated homes

• Occupational dusts :
o Coal mining, cement and textile mill manufacturing, auto-mobile drivers and vehicular
mechanics, chlorinated organic compounds, dyes, rubber products, grain dust and fungi in
farmers, leather manufacturing.
o Exposure to crystalline silica : Cement industry, brick manufacturing, pottery and ceramic work,
silica, sand, iron and steel, gold mining and iron and steel founding.

• Outdoor air pollution

• Old age (physiological obstruction)

• Low socio-economic status

Risk Factors
• Passive smoking

• Occupational exposure

• Ambient air pollution

 • Genetic abnormalities including a deficiency of Alpha1-antitrypsin enzyme

Pathophysiology
1. Elastin proteolysis results in reduction in elastic recoil pressure in the lungs. Also the damage to the
elastin results in significant airway narrowing.

2. Fibrotic remodelling of airways results in fixed airway narrowing causing increased air resistance that
does not fully revert with bronchodilators.
3. Histological feature such as emphysema which also reduces lung elastic recoil pressure which leads to
reduced pressure for expiratory and physiological features such as decreased surface area of alveoli for
gaseous exchange and ventilation-circulation (V/C) mismatch.

4. Lung hyperinflation or air tapping is hall mark of COPD and is the primary cause of dyspnoea, poor
quality of life and disease prognosis. The barrel shaped chest in COPD is attributed to hyperinflation of
the lungs

Noxious particles and gases

Host factors
Lung inflammation

Antioxidants Antiproteinases
Oxidative stress Proteinases

Repair mechanism

COPD

Symptoms

COPD is characterized by three primary symptoms :

1. Cough

2. Sputum production
3. Dyspnea on exertion (DOE)

Dyspnea may be severe and often interferes with the patient’s activities. Weight loss is common
because dyspnea interferes with eating.

Diagnosis
• History collection (The nurse should obtain a thorough health history for a patient with known
or potential COPD)
 • Pulmonary function studies are used to help confirm the diagnosis of COPD, determine disease
severity, and follow disease progression.

• Spirometry is used to evaluate airflow obstruction

• Arterial blood gas (ABGs) measurements may also be obtained to assess baseline oxygenation
and gas exchange.

• Chest x-ray

• Alpha1-antitrypsin deficiency screening may be performed for patients under age 45 or for
those with a strong family history of COPD.

Management
The main objective of COPD management are following :

• Relieve symptoms

• Prevent disease progression

• Reduce mortality & improve exercise tolerance

• Prevent and treat complications

Medical Management

• Risk reduction : Smoking cessation is the single most effective intervention to prevent COPD or
slow its progression.

Pharmacologic therapy

• Bronchodilators relieve bronchospasm and reduce airway obstruction by allowing increased

oxygen distribution throughout the lungs and improving alveolar ventilation. These medications
are delivered through a metered-dose inhaler (MDI) by nebulization or via the oral route in pill
or liquid form.

• A metered-dose inhaler (MDI) is a pressurized device containing an aerosolized powder of

medication.

• Inhaled and systemic Corticosteroids (oral or intravenous) may also be used in COPD but are
used more frequently in asthma.

• Oxygen therapy can be administered as long term continuous therapy, during exercise or to
prevent acute dyspnea. Long-term oxygen therapy has been shown to improve the patient’s
quality of life and survival.

Surgical management

• Bullectomy : Bullae are enlarged airspaces that do not contribute to ventillation but occupy
space in the thorax, these areas may be surgically excised
 • Lung volume reduction surgery : It involves the removal of a portion of the diseased lung
parenchyma. This allows the functional tissue to expand.

• Lung transplantation

Complications
• Respiratory insufficiency

• Pneumonia & respiratory infection

• Right-sided heart failure

• Pulmonary hypertension

• Pneumothorax

• Skeletal muscle dysfunction

• Depression and anxiety disorders

PNEUMONIA
• Pneumonia is an accumulation of secretions and inflammatory cells in the alveolar spaces of the
lungs caused by infection. The infecting organism, the inflammatory response and the
disturbances of gas exchange caused by alveolar involvement are responsible for the clinical
manifestations.

Etiology
• Bacteria, viruses, mycoplasmas, fungal agents & protozoa
• Aspiration of food, fluids

• Inhalation of toxic/caustic chemicals, smoke, dusts/gases

• Influenza

Risk Factors
• Advanced age

• History of smoking

• Upper respiratory infection

• Tracheal intubation

• Malnutrition

• Dehydration
 • Cigarette smoking

Classification
Epidemiological :

1. Community-acquired pneumonia (CAP)

2. Nosocomial or hospital acquired (HAP, VAP, HCAP)

3. Pneumonia in elderly

4. Ventilator associated pneumonias

5. Pneumonia in immunocompromised host

Anatomical :

1. Lobar pneumonia occurs due to acute bacterial infection of a part of a lobe or complete lobe
commonly Staph. Pneumoniae, Staph. Aureus, β Haemolytic streptococci are responsible.

2. Bronchopneumonia : Acute bacterial infection of terminal bronchioles characterized by purulent

exudation which extends into surrounding alveoli through endobronchial route resulting in patchy
consolidation. It is usually seen in extremes of age and in association with chronic debilitatory
conditions.

3. Interstitial pneumonia : Patchy inflammatory changes caused by viral or mycoplasma infection mostly
confined to the interstitial tissue of the lung without alveolar exudates. Commonly mycoplasma
Pneumoniae, Influenza virus, Adenoviruses, CMV.

Pathology
1. Congestion

• Presence of a proteinaceous exudates often of bacteria in the alveoli

2. Red hepatization

• Presence of erythrocytes in the cellular intra-alveolar exudates

• Neutrophils are also present

• Bacteria are occasionally seen in cultures of alveolar specimens collected

3. Gray hepatization

• No new erythrocytes are extravasating, and those already present have been lysed and
degraded

• Neutrophil is the predominant cell

• Fibrin disposition is abundant

• Bacteria have disappeared

 • Corresponds with successful containment of the infection and improvement in gas exchange
4. Resolution

• Macrophage is the dominant cell type in the alveolar space

• Debris of neutrophils, bacteria, and fibrin has been cleared

Pathophysiology
Offending organism/agent

Inflammatory pulmonary response

Lose defense mechanisms of the lungs

Allow organisms to penetrate the sterile LRT

Develop inflammation

Disruption of the mechanical defenses (cough & ciliary motility)

Colonization of the lungs

Inflamed & fluid-filled alveolar sacs

Alveolar exudates tends to consolidate

Difficult to expectorate

Clinical features

1. General symptoms : Malaise, fever, rigors, and night sweats, vomiting in the elderly confusion and
disorientation
2. Pulmonary symptoms : Dyspnoea, cough and sputum which is often blood-stained or rusty and
difficult to expectorate
3. Pleural symptoms : Pain aggravated by cough, deep breath or movement usually localised to site of
inflammation

Signs
1. General : Patient appears ill with tachycardia, rapid respiratory rate, high fever, flushed dry skin,
herpes labialis, confusion, hypotension
2. Pulmonary

(a) Early signs – Slight impairment of percussion note over the affected area with weakness of breath
sounds or possibly harshness with prolonged expiration and fine crackles on deep inspiration or after
cough
(b) Signs of consolidation on second or third day

(c) Resolution : Most signs disappear by end of second week but fine crackles and impairment of
percussion note may be found longer. At times there may not be typical signs of consolidation

Investigations
• WBC count : If raised points to bacterial infection

• Chest auscultation

• Sputum culture analysis & sensitivity / serologic testing

• Fiber optic bronchoscopy / Transcutaneous needle aspiration / biopsy

• Skin tests

• Blood & urine cultures

• Transcutaneous oxygen measurements

• Chest X-ray examination

Management
• Specific antibiotic therapy: Broad spectrum antibiotics
• Respiratory support :
o Administer oxygen
o Bronchodilator medications
o Postural drainage
o Chest physiotherapy
o Tracheal suctioning
o Nutritional support
o Fluid & electrolyte management

PULMONARY TUBERCULOSIS
 • Pulmonary tuberculosis (TB) is a contagious bacterial infection that mainly involves the lungs,
but may spread to other organs caused by the Mycobacterium tuberculosis and Mycobacterium
bovis.

Etiology
• Mycobacterium tuberculosis
• Droplet Nuclei (coughing, sneezing, laughing)
• Exposure to TB

Risk factors
• Close contact with sputum-smear positive individual.
• Environmental factors that lower resistance – Malnutrition, poor and overcrowded housing,
alcoholism and/ or drug addiction, heavy smoking, corticosteroid therapy.
• Relation to other disease – Not uncommon after influenza, whooping cough. More common
with diabetes mellitus, cirrhosis of liver, pneumoconiosis, and following partial gastrectomy.
• Immunosuppression (including drugs and autoimmune deficiency syndrome)
• HIV infection/AIDS
• Other risk factors – Kidney failure, diabetes, silicosis, family history, IV drug abuser.
• Route of infection – In majority by inhalation of air-bone infected droplet nuclei derived from
sputum of an adult with cavitary pulmonary tuberculosis.
Clinical types
1. Primary pulmonary tuberculosis – Primary tuberculosis refers to events following invasion by
tubercle bacillus infection, being commonly caused by inhalation (rarely through skin or ingestion) of the
bacilli into the lungs.
Primary complex– Inhaled bacilli are deposited in the alveoli where a sub-pleural inflammatory lesion
occurs. When they reach the regional lymph nodes, these also become infected. The tuberculin test
becomes positive within 6 weeks of the infection.
2. Post-primary tuberculosis – Reactivation
a. As a progressive primary lesion
b. As result of reactivation of dormant/primary lesion
c. Haematogenous spread to the lungs
I. Acute pulmonary tuberculosis
1. Pneumonic tuberculosis– affects usually upper lobe, rarely whole lung. Symptoms like acute lobar
pneumonia, but irregular temperature, rapid breathing, sweats, signs of cavitation. Leucopenia and
failure to respond to antibiotics.
2. Bronchopneumonic tuberculosis– Abrupt onset at times following influenza, or in children measles or
whooping cough, or as a sequel of haemoptysis with aspiration of tuberculous matter into bronchi.
3. Miliary tuberculosis – Types
i. Acute miliary TB
• Onset gradual with vague ill-health, loss of weight and fever
• Fever irregular, wide variation between morning and evening
• Hepatosplenomegaly in 20–30% of cases
• Dyspnoea and cyanosis out of proportion to signs in chest. Slight dry cough, scattered wheeze
 • Headache common, often severe. Signs of meningeal irritation in early stages
• Tachycardia
• Miliary lesions of skin rarely as macules, papules or purpuric lesions
ii. Cryptic (obscure) miliary TB
• Occurs in elderly patients with prolonged low grade fever, hepatosplenomegaly may occur.
• Chest radiograph is usually normal, miliary mottling may appear months later. Tuberculin test is
usually negative.
iii. Acute disseminated haematogenous tuberculosis
• Pyrexia of unknown origin lasting over few weeks with sudden deterioration especially in
immuno-compromised patients
• Sputum absent or scanty, ARDS, Tachypnoea
II. Chronic pulmonary tuberculosis
• Symptom-free – Diagnosis on routine radiography.
• Insidious – Malaise, undue fatigue, loss of weight, evening rise of temperature and cough.
• Persistent cough or “smoker’s cough”
• Unexplained loss of weight
• Pyrexia of unknown origin
• Catarrhal or influenzal
• Haemoptysis
• Non-resolving pneumonia
• Hoarseness of voice due to laryngeal tuberculosis
Pathophysiology
Initial infection or primary infection

Entry of microorganism through droplet nuclei

↓
Bacteria is transmitted to alveoli through airways

Deposition and multiplication of bacteria

↓
Bacilli are also transported to other parts of the body through blood stream and phagocytosis by
neutrophils and macrophages

Accumulation of exudate in alveoli

↓

Broncho pnemonia
↓
 New tissue masses of live and dead bacilli are surrounded by macrophages which form a protective
mass around granulomas
↓

Granulomas then transforms to fibrous katral tissue mass andtral portion of which is called ghon
tubercle [the material (bacteria and macrophages) becomes necrotic forming cheesy mass]

↓
Mass becomes calcified and becomes colagendus scar

Ghon tubercle ulcerates and beleasing cheesy material into bronche

↓
Ulcerated tubercle heals and recomes scar tissue

↓
Infected lung become inflammed

Further development of pneumonia and tubercle formation

Clinical features
Constitutional symptoms

• Anorexia
• Low grade fever
• Night sweats
• Fatigue
• Weight loss

Pulmonary symptoms

• Dyspnea
• Non resolving bronchopneumonia
• Chest tightness
• Non productive cough
• Mucopurulent sputum with hemoptysis
• Chest pain

Extrapulmonary symptoms

• Pain
• Inflammation
Diagnosis
• History collection
• Physical examination
• Clubbing of the fingers or toes in people with advanced diseases
• Swollen or tender lymph nodes in the neck or other areas
• Fluid around a lung (pleural effusion)
• Unusual breath sounds (crackles)

If miliary TB

• A physical exam may show: Swollen liver, lymph nodes, spleen

Tests may include:

• Biopsy of the affected tissue (rare)

• Bronchoscopy
• Chest CT scan
• Chest x-ray
• Sputum examination and cultures
• Thoracentesis
• Quantiferon gold test : Gold test measures interferon-gamma in the testee’s blood after
incubating the blood with specific antigens from M. Tuberculosis proteins
• Tuberculin skin test (also called a PPD test)

0.1 ml of ppd is injected forearm (sc)

After 48-72 hrs check for induration at the site

If induration is equal to and more than 10mm Positive

Management
• Pulmonary TB is treated primarily with anti-tuberculosis agents for 6 to 12 months

Pharmacological management :

First line anti-tubercular medication

• Streptomycin 15mg/kg Isoniazide INH(Nydrarid) 5 mg/kg 300 mg max per day)
• Rifampin 10 mg/kg
• Pyrazinamide 15-30 mg/kg
• Ethambutol (Myambutol) 15-25 mpkg daily for weeks and continuing for up to 4 to 7 months

Second line medications

• Capreomycin 12-15 mg/kg

 • Ethionamide 15mg/kg
• Paraaminosalycilate sodium 200-300 mg/kg
• Cycloserine 15 mg/kg
• Vitamin b(pyridoxine) usually adminstered with INH

Third line drugs

• Other drugs that may be useful, but are not on the WHO list of SLDs :
• Rifabutin
• Macrolides eg. Clarithromycin (CLR)
• Linezolid(LZD)
• Thioacetazone(T)
• Thioridazine
• Arginine

PNEUMOTHORAX
• Pneumothorax is air in the pleural cavity. Air may enter the pleural cavity through the chest wall,
mediastinum, or diaphragm or from a puncture of the visceral pleura covering the lung.
• Primary spontaneous pneumothorax occurs in patients without clinical evidence of lung disease.
• Secondary spontaneous pneumothorax is related to parenchymal lung disease.
Causes
Spontaneous Pneumothorax
1. Primary spontaneous pneumothorax
• Due to rupture of apical subpleural bleb (benign spontaneous pneumothorax)
• Most common in young men
• Exclusively seen in smokers
2. Secondary spontaneous pneumothorax
• Rupture of Subpleural TB focus
• Congenital cysts and bullae
• Honeycomb lung
• Bacterial pneumonia, lung abscess
• Sarcoidosis, Pneumoconiosis
• Asthma
• Cystic fibrosis
Traumatic Pneumothorax
a.Penetrating trauma – e.g. stab wounds, gunshot wounds, primarily by injuring the peripheral lung.
b.Blunt trauma can lead to rib fracture and cause increased intra-thoracic pressure and bronchial
rupture manifested by ‘fallen lung sign (ptotic lung sign)’ hilum of lung is below expected level within
chest cavity.
c. Pulmonary barotrauma – at high altitude of 3050 m or in scuba divers.
Symptoms
Vary depending on
(a) amount of air in the pleural sac
(b)rapidity of its accumulation
(c) condition of the lungs
1. Insidious onset – Vague discomfort in chest, later shortness of breath on exertion. In tuberculous
spontaneous pneumothorax the onset is not always sudden as the condition commonly occurs in
patients suffering from advanced pulmonary TB which has already cut down their normal activities.
Patient may complain of more breathlessness or may have chest pain or the pneumothorax may be
latent and detected by routine chest examination.
2. Sudden onset – Feeling of something snapping in the chest, severe pain, shock, increasing shortness
of breath. Blood streaked sputum, cyanosis, restlessness and collapse.
3. If hydropneumothorax – Splash of fluid in the chest when he jumps may be the first intimation to the
patient.
Signs
Hyper-resonance with silence
1. Closed pneumothorax
• The opening in the lung is very small and rapidly heals, thus allowing the lung to re-expand.
• Inspection – Diminished expansion on affected side, Bulging on the side of pneumothorax,
Displacement of apex beat towards sound side
• Palpation – Trachea may be displaced
• Percussion – Hyperresonance, If on the left side abolition of cardiac dullness
• Auscultation – VR absent, Breath sounds diminished or absent, Crunching sound
2. Open pneumothorax
The opening remains patent and the pressure in the pleural space remains equal to that of the
atmosphere.
(i) Cracked pot sound may be heard on percussion
(ii) On auscultation air can be heard passing to and fro through the opening
(iii) Voice sounds and cough heard with metallic echo
3. Tension pneumothorax
• The opening is valvular and air can enter into the pleural space during inspiration but cannot
escape during expiration so that a positive pressure occurs in the pleural cavity. Tension
treatment, blocked or displaced chest drains.
Investigations
• Chest Radiograph
• Chest CT scanning : A CT scan is more sensitive than a chest radiograph in evaluation of small
pneumothorax and and pneumomediastinum. It is the gold standard for diagnosing occult
traumatic pneumothorax not apparent on supine chest radiograph.
• 3.Ultrasonography : Ultrasonic features include absence of lung sliding. M mode imaging
demonstrates an alternating pattern of absent lung sliding with normal lung sliding. This occurs
at the boundary of pneumothorax where during inspiration the lung is seen to slide transiently
and during expiration the sliding is abolished. This phenomenon known as the ‘lung point’ is
100% specific for pneumothorax and can be used to determine the size of the pneumothorax.
Differential Diagnosis
Emphysematous bulla of large size
Pulmonary emphysema
Obstructive emphysema
Congenital large cyst
Hernia of stomach or colon through diaphragm
Subphrenic abscess
Management
Medical
1. No treatment
• Only observation if small pneumothorax (occupying less than 20% of the hemithorax) as the air
usually gets absorbed within a few days.
• The exception is the patient with severe lung disease who cannot tolerate even a small
pneumothorax and air has to be removed.
• Anti-tuberculous therapy if evidence of tubercle
2. Simple aspiration
Indications
• Significant dyspnoea
• Traumatic (minor)
Technique
• Aspiration can be performed with a 16-guage IV cannula attached to a 50 ml syringe and a
three-way tap.
• An intercostal space is selected from chest radiographs and after sterilizing the skin over the
intercostal space, it is anaesthetised with lignocaine down to parietal pleura.
• The cannula is then inserted through the intercostal space and pneumothorax aspirated into the
syringe, and expelled via the three-way tap.
• As a precaution, a plastic tubing is attached to the exit arm of the three-way tap and its end
placed in a bottle of sterile water.
• This will ensure that with each turn of the tap, air is being drawn from the pneumothorax.
• Aspiration is discontinued when gentle suction yields no more air from the pneumothorax,
suggesting that the lung has fully re-expanded or earlier if patient shows signs of distress.
• If more than 2 litres of air are aspirated, a chest radiograph should be repeated to judge the
volume of re-expansion.
• Disadvantage : Chances of subcutaneous emphysema
3. Intercostal tube drainage
A. Tube drainage – Initial use of small tubes (10–14 F) in most cases:
Indications :
• Aspiration fails to resolve
• Tension pneumothorax
• Air space more than 50% of pneumothorax
• Traumatic (major)
• Ventilated (barotrauma)
Procedure : 2nd intercostal space in mid-clavicular line or sixth space in mid-axillary line. For women a
basal drain is preferred to avoid an anterior chest scar. Chest radiographs should be used as a guide
together with ultrasound if necessary.
B. Indwelling catheter drainage
Indications same as for large-bore tube drainage
C. Chemical pleurodesis via an intercostal drain
Surgical treatment
1. Surgical closure of bronchopleural fistula
2. Thoracoscopy/thoracotomy and cauterization of the breach in the pleura or excision of the bulla and
oversewing of the defect.
3. Pleurectomy – Bullectomy and partial apical pleurectomy is surgical treatment of choice. Re-
expansion of the lung then leads to obliteration of the pleural space.
4. Decortication – Stripping off of fibrin from affected visceral pleura.
Video-assisted thoracic surgery (VATS) is a technique that causes less operative pain allows earlier
discharge. However it is often unsuitable for a patient with chronic lung disease.

PLEURAL EFFUSION
• Pleural effusion is an accumulation of fluid in the pleural space as a result of excessive
transudation or exudation from pleural surfaces.
• Pleural cavity normally contains less than 20 ml of fluid.
Mechanisms of Pleural Fluid Formation
• Increased pulmonary capillary pressure
• Decreased tissue oncotic pressure (e.g. hypoproteinemia)
• Decreased negative intrapleural pressure (e.g. atelec- tasis)
• Increased permeability of pleural membrane (e.g. pleurisy, malignancy)
• Obstruction of lymphatic flow (e.g. mediastinal nodal metastases)
• Transdiaphragmatic fluid flow from peritoneum (e.g. ascites from hepatic cirrhosis)
Causes
• Hypothyroidism
• Nephrotic syndrome
• Mitral stenosis
• Pulmonary embolism
• Pneumonia
• TB
• Pulmonary infarction
• Hypoproteinaemia
• Myxoedema
• Meig’s syndrome
Symptoms
(i) Acute with attack of pleuritic pain or pyrexia of unknown origin, later with pain
(ii) Subacute
(iii) Insidious with ill-defined health followed by dyspnoea
• Pain in early stage due to dry pleurisy replaced by dull ache
• Dyspnoea depends on rate of collection of fluid
• Cough usually dry
• Loss of weight
• Symptoms of toxaemia : Malaise, fever, anorexia
Signs
About 500 ml of fluid is required to produce physical signs.
Inspection
Tachypnea
Sternomastoid sign (Trail’s sign) : Sternomastoid muscle on side of mediastinal displacement may be
prominent
Palpation
Decreased expansion
Percussion
Absolute dullness
Skodaic resonance or boxy note just above the effusion
Auscultation
Diminished or absent breath sounds
Crackles may be heard at the base of the opposite lung due to congestion
Investigations
• Chest radiograph – Obliteration of costophrenic sinus on affected side with an opacity extending
up the chest wall concave towards the lung on PA film in presence of about 200 ml. Smaller
effusions (50 ml) can be detected if radiograph is taken with patient in lateral decubitus
position.
• Ultrasonography is more accurate than plain chest radiography for estimating pleural fluid
volume and also aids thoracentesis when effusion is small or localized. It is also useful in
demonstrating fibrinous loculation, and differentiates fluid and pleural thickening.
• CT can detect pleural abnormalities more readily.
• Examination of pleural fluid
• pH : Low pleural fluid pH usually defined as <7.2, represents a substantial accumulation of
hydrogen ions (normal pleural pH is about 7.6 because of accumulation of bicarbonate).
• Differential cell counts have a minor role in assessment of a pleural effusion.
• Pleural lymphocytosis is seen in tuberculous effusions and malignancy and eosinophilic pleural
effusion are often not benign.
• Rheumatoid factor in rheumatoid effusion
• Antinuclear factor in connective tissue diseases
• Complement level may be low in rheumatoid or SLE effusions but also in malignancy and
infection.
• Toracoscopy is used when less invasive techniques have failed.
Differential Diagnosis
• Pleural effusion
• Empyema
• Hydrothorax
• Lobar pneumonia
• Fibrosis of lung
• Bronchial carcinoma
• Hydatid cyst of lung
• Liver abscess
Management
I. General – Rest in bed till fluid gets absorbed, nourish- ing diet, vitamins.
II. Chemotherapy
a.Tuberculous effusion – Antituberculous therapy
b. Malignant effusion – After complete aspiration, injection of Tetracycline hydrochloride 500 mg in 20
ml saline into pleural cavity via intercostal drain followed by further 20 ml saline.
III. Management of the fluid itself – Certain disadvantages may result from allowing the fluid to remain
in the pleural cavity for any length of time – fibrin is deposited, the pleurae become thickened, re-
expansion of the lung is hampered and the process may eventually lead to immobility of the thorax with
loss of functional efficiency (frozen chest).
Complications
1. High negative intrapleural pressure – The lung is unable to expand fully as indicated by increased pull
on the syringe plunger. Patient feels tightness in the chest accompanied by coughing.
2. Pleural shock – due to vagal inhibition.
3. Air embolism
4. Pulmonary oedema
6. Rupture of intercostal vessel – rare
7. Pneumothorax or haemoptysis – if lung is punctured
8. Empyema – due to introduction of infection into the pleural space

EMPYEMA
• An accumulation of thick, purulent fluid within the pleural space, often with fibrin development

Etiology
• Lung diseases : Pneumonia, Lung abscess
• Subphrenic abscess
• Post traumatic
• Post-operative
• Blood spread (post PE)
• Iatrogenic

Risk factor
• Alcoholism
• Drug use
• HIV infection
• Neoplasm
• Pre-existent pulmonary disease

Pathophysiology
Presence of Parapneumonic Effusion

↓
Release of inflammatory mediators

Increased permeability of the capillaries

↓
Attracts WBCs to the site

Escape of albumin & other protein from the capillaries

 ↓

Increased Pleural fluid

↓

Presence of free-flowing, protein rich pleural fluid (Stage I)

Inflammation worsens
↓

Attracts more WBCs to the site

↓

Extensive purulent exudate production

↓

Initiation of fibroblastic (collagen and other proteins) activity (Stage II)

Adherence of the two pleural membranes (Stage III)

↓

Formation of a “Peel”

1. Acute Empyema
Symptoms
1. Those of primary disease – Imperfect recovery in pneumonic cases, or sudden increase in fever
perhaps with rigors.
2. Those due to mechanical effect – Pleuritic chest pain in early stage, dyspnoea, cough and sputum.
3. Those due to toxaemia– Malaise, anorexia, sweats and loss of weight.
Signs
a. Same as effusion with sometimes oedema of chest wall.
b. Finger clubbing may develop within 2–3 weeks of the onset.
Investigations
• Chest radiograph : Uniform opacity free in pleural space or localized by adhesions. Fluid level if
bronchopleural fistula.
• Leucocyte count : 15,000–20,000 per cmm.
• Culture of fluid for causative organism. Lack of bacterial growth suggests tuberculosis.
• CT scan
Complications
• Bronchopleural fistula
• Empyema necessitans : Untreated, an empyema may present as an abscess of the chest wall
commonly in relation to costochondral junction of the rib.
• Pyopneumothorax
Management
Objectives of therapy – Control of infection, evacuation of pus, obliteration of pleural space, re-
expansion of lung, and restoration of normal pulmonary function.
1. Aspiration – Pus is usually thin and should be aspirated with syringe every second or third day.
Continuous drainage to a water seal may be necessary if fluid re-accumulates very rapidly.
2. Antibiotics – Penicillin 1 million units 6-hourly IM. Also intrapleurally 500,000 units at each aspiration
in 5 to 10 ml of normal saline. If organism insensitive to penicillin other suitable broad spectrum
antibiotic and metronidazole 400 mg tds.
3. Intercostal drainage – if no definite improvement after about 10 days and in severely ill children.
Indications for removal of drainage tube
(a) No fever suggesting control of infection
(b) Less than 100 ml fluid drainage in 24 hours
(c) Complete lung expansion
(d) Bronchopleural fistula if present gets closed
4. Breathing exercises – as soon as signs of general toxicity disappear
2. Chronic Empyema
Empyema of more than 3 months duration is considered chronic emphyema
Causes
• Ineffective drainage or failure to diagnose acute empyema
• Chronic infection : Tuberculosis, lung abscess, bronchiectasis, actinomycosis
• Carcinoma lung with pleural involvement
• Bronchopleural fistula due to lung abscess, lung trauma or rupture of infected lung cysts
• Foreign body in pleural cavity eg. drainage tube, rib sequestrum
• Inadequate drainage of subphrenic abscess
Symptoms and Signs
• Recurrent symptoms of chest pain and fever
• Loss of weight and anaemia
• Clubbing of fingers
• Chest wall deformity from fibrosis
• Chronic sinus tracts into the skin or lungs may develop
• When bronchopleural fistula is present, air can be heard (or felt) blowing through a patent sinus
during coughing
Diagnosis
• Demonstration of presence of bacteria in pleural space by culture or staining
• Culture negative pleural fluid with pH < 7 and glucose content < 40 mg/dL
• Chest radiograph – Dense pleural opacity, crowding of ribs and elevation of diaphragm on
affected side
Management
• Intercostal drainage with instillation of appropriate antibiotics, streptokinase or rib resection
and open drainage.
• When this fails, thoracotomy with excision of empyema sac allowing the lung to re-expand and
obliterate the dead space.

LUNG ABCESS
• Circumscribed suppurative inflammation of lung by pyogenic organisms leading to cavitation
and necrosis.
Causes
1. Aspiration abscess – Aspiration of infected material –
(a) From upper respiratory tract – Oral or pharyngeal sepsis, oesophageal obstruction, trachea-
oesophageal fistula, drowning
(b) Bronchiectasis
2. Specific abscesses
(a) Lobar pneumonia particularly Klebsiella, Staphylococcal or haemolytic streptococcal pneumonia
(b) Tuberculosis
(c) Fungal infection, e.g. actinomycosis.
3. Infected cysts or bullae – Congenital or acquired
4. Extension from neighbouring organs – Diaphragm eg. amoebic infection, vertebral column
5. Other – Wegener’s granulomatosis, pneumoconiosis (silicosis, coal)
Pathophysiology
Lung infection
↓

Inflammatory response
↓

Cavity extend to bronchus

Promotion of abscess into encapsulated

↓
Tissue necrosis

↓
Increased production of sputum

↓
Sputum discharge

Symptoms
• Mild general toxaemia – with slight fever. No symp- toms referable to respiratory tract.
• Sudden onset – with high fever, pleuritic chest pain, cough and later copious expectoration.
• Symptoms of subacute or chronic respiratory disease – cough, foetid breath, expectoration and
general toxaemia. Haemoptysis may occur, or pain due to associated pleurisy.
Signs
Depend on situation and size of abscess and surrounding infiltration.
1. In early stages – Pleural rub, local area of dullness and weak breath sounds or signs of consolidation.
2. After evacuation of pus – Signs of cavitation or signs of localized consolidation with amphoric or
cavernous breath sounds and crackles of the resonating variety.
3. Signs of effusion – may overshadow those of the lung lesion.
4. Clubbing of fingers
Investigations
Leucocyte count – 20,000 to 30,000 cells per c.mm.
Sputum – Pus cells, organisms and necrotic lung tissue.
Chest radiograph – In acute phase dark shadow, later cavity with fluid level.
Bronchoscopy – to exclude foreign body or carcinoma
CT scan
Differential diagnosis
• Bronchiectasis
• Cavitated bronchial carcinoma
• Purulent bronchitis
• Caseating tuberculosis
• Infected lung cyst
• Pulmonary infarction
• Pulmonary haematoma
• Wegener’s granulomatosis
Complication
• Haemoptysis
• Extension of inflammation to other parts of lung
• Cerebral abscess
• Rupture into pleural cavity
Management
1. General
(a) Rest in bed. Ambulation as soon as signs of toxicity disappear
(b) High caloric, high protein diet with additional vitamins
(c) Transfusions as indicated
(d) Deep breathing exercises to encourage drainage
2. MECHANICAL PROCEDURES
(a) Postural drainage – Percussion therapy or “clapping” over the site of the abscess with the patient in
the postural drainage position is often effective in dislodging and expelling secretions from the cavity.
(b) Bronchoscopy – Suction is applied to the orifices of the bronchi leading to segments presumed to be
involved in the process in hope of initiating or promoting drainage.
3. Chemotherapy
Penicillin is the most useful antibiotic in the common forms of lung abscess. Amoxicillin 1g tds po +
Metronidazole 400 mg tds po or Co-amoxiclav 500 mg tds or Clarithromycin 250–500 mg tds
4. Bronchoscopy – may be needed to remove particulate matter or to exclude bronchial obstruction.
5. Surgical resection
If at end of 3 weeks, there is no clinical and radiological improvement, segmental resection of lung,
lobectomy or pneumonectomy. Also if localized malignancy or massive haemoptysis.
Prognosis
Following factors indicate poor prognosis :
1. Age > 60 years
2. Sepsis at presentation
3. Abscess size > 6 cm
4. Aerobic growth on culture
5. Symptoms longer than 8 weeks
HAEMOPTYSIS
• Haemoptysis is the expectoration of blood or blood stained sputum that originates below the
vocal cords from tracheobronchial tree or pulmonary parenchyma.
• A spectrum that varies from blood streaking of sputum to coughing up of large amounts of pure
blood.

Classification
• Mild haemoptysis is < 20 ml of blood in 24 hrs
• Moderate haemoptysis is 20-200 ml in 24 hrs
• Severe haemoptysis is 200- 500 ml in 24 hrs
• Massive haemoptysis is any amount of blood loss more than 600 ml in 24 hrs

Causes
• Bronchiectasis
• TB
• Pneumoconiosis
• Lung abscess
• Wegener’s granulomatosis
• Pneumonia
• Leukemia
• DIC
Pathophysiology
Active or chronically inflamed lung

Opening of Bronchopulmonary shunts with dilatation of bronchial and non bronchial collaterals

Rupture of the small fragile vessels in the inflamed tissue due to erosion or when they are
exposed to the systemic arterial pressure
↓
Haemoptysis

Symptoms

• Blood in mucus that lasts longer than a week, is severe or getting worse or comes
and goes overtime
 • Chest pain
• Weight loss
• Soaking sweats at night
• Fever higher than 101 degrees
• Shortness of breath
Diagnosis
• Sputum : For tubercle bacilli and malignant cells. Rarely spirochetes, or ova of lung fluke.
• X-ray chest – For diagnosis of pulmonary TB, hilar mass suggestive of carcinoma, pneumonia or
pulmonary infarct.
• Blood : Red blood cell count and haemoglobin, bleeding, coagulation and prothrombin time.
• Renal function tests and urinalysis is done in suspected patients with pulmonary-renal
syndrome. If urinalysis shows red blood cells or casts testing of patient serum for antiglomerular
basement membrane antibody, antineutrophil cytoplasmic antibody and antinuclear antibody
should be considered.
• Bronchoscopy : To exclude foreign body and malignant growth and for diagnosis of
bronchiectasis.
• Bronchography : To establish presence of localised bronchiectasis if sputum repeatedly negative
and plain X-ray inconclusive.
• Needle aspiration biopsy : If chest X-ray shows localised intrapulmonary lesion.
• Pulmonary angiography : May show anomaly of vascular structure of lung, eg. haemangioma or
distribution of aberrant vessels to pulmonary A-V fistula.
• CT scan : Useful in diagnosis of pulmonary infarction, lung carcinoma, cavitary diseases like
tuberculosis, bronchiectasis.
Management
• Hospitalization in ICU if massive haemoptysis. Sedation with diazepam or its equivalent.
Pethidine or morphine is seldom necessary and a depression of the cough reflex is not desirable.
Reassurance.
• Posture : If site of bleeding is located, patient must be put in a semi-reclining dependent
position (bleeding lung should be in dependent position)
• Fluids : Colloids or crystalloids. Blood transfusion if profuse bleeding.
• Antitussives : If cough exhausting or troublesome, small repeated doses of codeine or other
cough suppressive.
• Antibiotics : Useful in preventing secondary infection. Patients with active tuberculosis must be
given anti- tuberculous drugs if not already in use.
• Balloon tamponade for 24–48 h. If there is no bleeding on deflating the balloon and for 6–8 h
subsequently, balloon can be removed.

ARDS
• ARDS is a sudden, progressive form of respiratory failure characterized by severe dyspnea,
refractory hypoxemia, and diffuse bilateral infiltrates.

Phases
1. Exudative Stage (0-6 Days)
 • Characterized by accumulation of excessive fluid in the lungs due to exudation (leaking of fluids)
and acute injury.
• Hypoxemia is usually most severe during this phase of acute injury, as is injury to the
endothelium (lining membrane) and epithelium (surface layer of cells).
• Some individuals quickly recover from this first stage; many others progress after about a week
into the second stage.
2. Proliferative Stage (7-10 Days)

• Connective tissue and other structural elements in the lungs proliferate in response to the initial
injury. Including development of fibroblasts. The terms “stiff lung” and “shock lung” frequently
used to characterize this stage.
• Abnormally enlarged air spaces and fibrotic tissue (scarring) are increasingly apparent.
3. Fibrotic Stage (>10-14 Days)

• Inflammation resolves.
• Oxygenation improves and Extubation becomes possible.
• Lung function may continue to improve for as long as 6 to 12 months after onset of respiratory
failure, depending on the precipitating condition and severity of the initial injury.
• Varying levels of pulmonary fibrotic changes are possible.

Etiology
• Pneumonia
• Aspiration
• Pulmonary embolism
• Chest trauma with lung contusion
• Near-drowning
• Sepsis
• Blood transfusions with transfusion-related acute lung Injury (TRALI)
• Acute pancreatitis
• Toxic ingestions, e.g.. aspirin, tricyclic antidepressants

Pathogenesis
• ARDS is a consequence of an alveolar injury which produces diffuse alveolar damage. The injury
causes the release of pro-inflammatory “cytokines”.
• Cytokines recruit neutrophils to the lungs, where they become activated and release toxic
mediators (eg, reactive oxygen species and proteases) that damage the capillary endothelium
and alveolar epithelium.
• Damage to the capillary endothelium and alveolar epithelium allows protein to escape from the
vascular space.
• The oncotic gradient that favors resorption of fluid is lost and fluid pours into the interstitium,
overwhelming the lymphatic system.
 • Breakdown of the alveolar epithelial barrier allows the air spaces to fill with bloody,
proteinaceous edema fluid and debris from degenerating cells. In addition, functional surfactant
is lost, resulting in alveolar collapse.
• Healthy lungs regulate the movement of fluid to maintain a small amount of interstitial fluid and
dry alveoli.
• Lung injury interrupts this balance causing excess fluid in both the interstitium and alveoli.
• Results of the excess fluid include impaired gas exchange. Decreased compliance, and increased
pulmonary arterial pressure.

Symptoms
• Latent period between time of initial insult and onset of respiratory symptoms 4–24 hours
• Dyspnoea : acute in onset or developing over several hours. Dry cough
• Cyanosis may not be apparent, despite marked hypoxemia.
• Tachypnoea leads to hypocapnia causing superficial vasoconstriction and a pale, waxy
complexion.
• However patients with established ARDS due to sepsis may have hyperdynamic circulation due
to increased basal metabolism with warm peripheries.
Signs
• Initially normal but within 24 hours non-specific signs appear including widespread crackles and
wheezes and diminished basal breath sounds.
• With progression :
(a) Sepsis
(b) Failure of other organs : Abnormal haematological indices (reduced platelet count, increased
fibrinogen degradation products), shock, kidney failure, liver failure, ileus, CNS depression and metabolic
derangements.
Course : ARDS tends to reach its maximal initial severity over the next 24–48 hours and may be rapidly
fatal if severe and untreated.
Investigations
1. Chest radiograph – Initially normal but within 24–48 hours diffuse ill-defined patchy shadowing of
non-specific appearance is seen.
The early changes of interstitial oedema rapidly become confluent (snowstorm or whiteout
appearance).
2. Arterial blood gas analysis – PaO2 reduced and may be as low as 4–5 kPa despite FiO2 of 0.4–0.6 (40–
60%) or more.
3. Tests for presence of other organ dysfunction – Renal, hepatic, haematological parameters.
4. Bacteriology – Blood culture, culture of tracheal aspirate and culture of bronchoalveolar lavage in
patients with nosocomial pneumonia.
Management
1. Removal of underlying cause if possible eg. broad spectrum antibiotics for sepsis, drainage of infected
fluid collections, removal of necrotic tissue.
2. Support of the injured lung by restoration and maintenance of adequate tissue oxygen delivery. Most
patients require ventilatory support.
o Indications – Severe respiratory failure, fatigue, tachypnoea, or evidence of circulatory
inadequacy (e.g. lactic acidosis, poor tissue perfusion, hypotension).
 o The purpose of respiratory support is to achieve adequate arterial oxygenation without
exacerbating the underlying lung injury.
o The usual aims are low respiratory rate (< 10–14/minute), low tidal volume (6–8 mL/ kg),
relatively high positive end-expiratory pressure (5–20 cm H2 O).
3. Additional measures
o Prone positioning is most effective in early exudative phase of lung injury when it allows
recruitment of alveoli, improving ventilation/perfusion matching. There are also cardiovascular
benefits.
o Inverse ratio ventilation : In this method inspiratory time is increased so that it is longer than
expiratory time. With decreased time to exhale, dynamic hyperinflation leads to increased and
expiratory pressure which is similar to ventilator provided PEEP
o High-frequency ventilation (HFV) : entails ventilating at extremely high respiratory rates (5–20
cycles per second) and low VTs (1–2 ml/kg).
o Use of partial liquid ventilation (PLV) with perfluorocarbon (inert, high density liquid that easily
solubilizes oxygen and carbon) has shown improvement in pulmonary function of ARDS patients
with no survival benefit.
o Lung-replacement therapy with extracorporeal membrane oxygenation (ECMO) which provides
a clear survival benefit in neonatal respiratory distress syndrome, may also have utility in
selected adult patients with ARDS.
o Corticosteroids : may be beneficial in ARDS caused by inflammation (e.g. acute pancreatitis)
rather than sepsis. They may also hasten recovery and improve outcome in those with severe
pulmonary fibrosis or persistent ARDS.
Complications
1. Early
(a) Due to anaesthesia and muscle paralysis necessary for intubation
(b) Aspiration due to loss of protective laryngeal reflexes
(c) Reduction in cardiac output due to decreased venous return as a result of initial positive pressure
breaths
(d) Barotrauma and pneumothorax from positive intrapulmonary pressure
2. Later complications
(a) Local trauma from endotracheal tube
(b) Damage to lungs and fibrosis due to high O2 concentration
(c) Barotrauma may occur when stiff lungs require high inflation pressures to achieve adequate
ventilation or if emphysematous bullae are present
(d) Intrinsic positive end expiratory pressure (PEEP) – During lung deflation, relatively proximal
ENDOCRINE
Hypothyroidism
• Hypothyroidism is a common endocrine disorder resulting from deficiency of thyroid hormone.
Usually a primary process, thyroid gland is unable to produce sufficient amounts of thyroid
hormone.

• Can be secondary, the thyroid gland is normal but it receives insufficient stimulation because of
low secretion of thyrotropin (i.e thyroid-stimulating hormone [TSH]) from the pituitary gland.

• Clinical condition resulting from lack of effects of thyroid hormones on body tissues or from ↓es
circulating levels of T3 or T4 by the thyroid gland irrespective of cause. Women than men,
between 40-50 yrs of age

Causes
1. Primary Hypothyroidism

With goitre : Hashimoto’s thyroiditis

Iodine deficiency disorder

Drug induced Anti-Thyroid

With goitre gland : Atrophic thyroiditis

Thyroid dysplasia

2. Transient primary hypothyroidism

o After thyroiditis : Silent, Subacute or post -partum thyroiditis

3. Secondary hypothyroidism
o Due to TSH deficiency
o Pitutary / Hypothalamus dz – tumour
o Granulomatous dz
o TSH receptor defects

Pathophysiology
Thyroid gland needs lodine to secrete thyroid hormone

Production of thyroid depends upon the TSH, lodine intake and also protein intake
 Enlargement of thyroid gland results goitre form increased secretin of pituitary gland

TSH stimulates the thyroid to secrete more level of T4

In the blood, T4 levels are low, the thyroid gland will be more large and compress then neck and also the
chest

Causing in respiratory manifestation

Clinical features
• Onset gradually develop

• ↓ed appetite

• Tiredness

• Somnolence

• Weight gain

• Cold intolerance

• Goitre

• Hyperlipidemia

• Pale & cool skin

• Coarse dry skin

• ↓es metabolic rate : deposition of glucosammoglycans Boggy & non-pitting oedema

• Puffiness of face

• Minimal sweating

• Alopecia

• Vitiligo

• CVS : Bradycardia, Angina, Pericardial effusion, HTN

• GIT : Constipation, Ascites

• Slow Physical & mental Functions

• Lethargy & bodyaches

• Madness (Depression)
 • Diminished Libido

• Failure of ovulation

• Polymenorrhoea

• Menorrhagia

• Infertility/ impotence

• IDA

• Congenital Hypothyroidism

• Feeding difficulty in child

• During infancy : Delay in eruption of deciduous teeth & reaching physical & mental milestone,
Growth & Mental retardation, Delayed puberty

Diagnostic Investigations
• Thyroid Function Test
o Reduction in free & total T4
o Rise in Serum TSH

o Elevated S. TSH & normal Serum T4 -- Subclinical Hypothyrodism

o Elevated – anti TPo (Thyroide peroxidase antibodies)

• Serum cholesterol elevated in primary thyroid failure

• Anti-thyroid antibodies detection

• Nuclear Scintigraphy

• FNAC : Procedure of choice for evaluating suspicious nodules

• CBC may show anemia

• Electrolytes may show dilutional hyponatremia

• Lipid levels may be elevated

• Creatinine may be elevated (reversible)

• Liver function and creatinine kinase elevations have been found

• US used to detect nodules and infiltrative disease

Differential diagnosis
• Anemia
 • Autoimmune thyroid disease

• Myxedema

• Thyroid lymphoma

• Addison’s disease

• Constipation

Management
• T4 levothyroxine, T3 Liothyroxine, T3 & T4 Thyroglobulin liotrix are used to treat hypothyroidism
and suppress non toxic goitre.

• Sodium levothyroxine is administered parentally to restore T4 level.

• Replacement therapy is used to myxedema disappear and normal metabolic activity.

• Fluids are administered cautiously because of the danger of water intoxification.

Treatment
• Treat any underlying disorder

• Thyroid replacement (levothyroxine)

o For most cases of mild to moderate hypothyroidism, a starting levothyroxine dosage of 50-75
µg/day
o For elderly or if known ischemic heart disease

- Start at ¼ th to 1/2 of the expected dosage

- Adjust in small increments after no less than 4-6 weeks

• Clinical benefits begin in 3-5 days and level off after 4-6 weeks

• After dosage stabilization, monitored q 6 months or annually

• If central (i.e pituitary or hypothalamic) hypothyroidism

• Use T4 levels, not TSH levels to guide treatment

• Monitor the patients clinical status

Hashimoto’s Thyroiditis (Diffuse lymphocytic

thyroiditis)
An auto-immune disorder is characterised by 3 principle feature :

o Diffuse (Goitres enlargement) of thyroid

 o (Lymphocytic infiltration) of thyroid gland
o Occurrence of (thyroid auto-antibodies)

Etiopathogenesis
Hashimoto’s thyroiditis is an auto immune disease

↓
1. Other auto-immune disease association (grave’s dz, SLE, RA, pernicious anaemia, type1 DM)

2. Immune destruction of thyroid cells (helper)

Initial infiltration of (CD4 + T cells)

↓
Induced infiltration of (CD8 + T cytotoxic cells) in thyroid parenchyma

Active B cells to from autoantibodies immune destruction of thyroid parenchyma

(It is characterised by intra-thyroid lymphocytes infiltration with germinal centre formation, follicular
damage or destruction & fibrosis)

3. Detection of auto antibodies

↓
In sera of most pt with Hashimoto’s thyroiditis

- Thyroid microsomal autoantibodies

- Thyroglobulin autoantibodies
- TSH receptor autoantibodies

4. Inhibitory TSH – Receptor antibodies

5. Genetic Basis : Higher incidence in first degree relatives of affected pt

o Immunogenetical predisposition : Exposure to excess iodine. Seen more with HLADR3 & HLADR5

Pathology
• Extensive infiltration of gland by (lymphocytes, macrophage)
• Decreased number of thyroid follicles
• Follicular epithelial cells are transformed into their degenerated state
• Slight fibrous thickening of septa separating the thyroid lobules

Clinical features
 • Painless, firm, moderate, goitres enlargement of thyroid gland

• Many of the symptoms associated with thyroid hormone deficiency

• Fatigue

• Difficulty with learning

• Dry brittle hair and nails

• Dry itchy skin

• Putty face

• Constipation

• Weight gain

• Heavy menstrual flow

• Increased frequency of miscarriages

• Increased sensitivity to many medications

Diagnosis
• TSH test - ultrasensitive test is usually the first test performed it detects even tiny TSH in blood
TSH reading above normal mean person has hypothyroidism

• T4 test measure actual amount of thyroid hormone circulating in blood level of T4 in blood is
lowered than normal

• Anti-thyroid antibody for the presence of thyroid autoantibody

• Ultrasound, CT scan

Treatment
• Synthetic hormones - levothyroxine

• Monitoring dosage - a tablet taken keeps hormone level normal

• Low level laser therapy - low level infrared therapy proven effective

• Gluten free diet may reduce autoimmune response for thyroid degeneration

Complication
• Goiter

• Heart problem

• Mental health issues

 • Myxedema

• Birth defects

Myxedema
• The adult onset of severe hypothyroidism causes myxedema.
• The term myxedema non-pitting oedema due to accumulation of hydrophilic mucopoly
saccharide in ground substance of dermis & other tissues.
• T3, T4 Low, TSH elevated

Etiology
• Autoimmune thyroiditis
• Endemic or sporadic goiter
• Hypothalamic-pitutary lesion
• Thyroid cancer
• Prolonged administer of anti-thyroid drugs

Clinical features
• Cold intolerance
• Mental & physical lethargy
• Constipation
• Slowing of speech & intellectual function
• Pufffness of face
• Loss of hair
• Altered texture of skin
• Weakness
• Depressed mood
• Goiter
• Enlarged tongue
• Husky voice

MYXEDEMA COMA
Myxedema coma is a rare life-threatening condition. It is the decompensated state of severe
hypothyroidism in which the patient is hypothermic and unconscious. The condition occurs most often
among elderly women in the winter months and appears to be precipitated by cold.

Pathophysiology
Hypothyroidism and precipitating factor
 Low serum T4 and intracellular T3

Fluid retention Decreased inotropism and chronotropism Hypothermia Stupor

Hyponatremia Cardiogenic shock Respiratory failure Worsening mental status

Coma

Clinical features

• Decreased breathing (respiratory depression)

• Lower than normal blood sodium levels
• Hypothermia (low body temperature)
• Confusion or mental slowness
• Shock
• Low blood oxygen levels
• High blood carbon dioxide levels
• Coma
• Seizures

Investigations
• TFTS - TSH (0.4-4mU/L) is elevated and fT3 & fT4 is low
• A low or normal TSH level with low levels of free T4(0.7-1.9ng/dl) and free T3 (80-18ong/dl) may
indicate that the disorder is due to pituitary or hypothalamic dysfunction
• Other tests : Serum osmolality (hyponatremia), serum creatinine (because of decreased renal
perfusion), CBC (infection), serum cortisol
• CXR (signs of Pulmonary edema, Cardiomegaly, CHF, Pericardia effusion)
• ECG (sinus bradycardia, low-amplitude QRS complexes, prolonged QT interval, flattened or
inverted T waves or arrhythmias)

Management
• Levothyroxine sodium-lifelong therapy
• Myxedema Coma
• Maintain a patent airway
• Oxygen administration
• I/V fluids
• Vital signs to be monitored
• Correct hypothermia
 • Vasopressor for tissue perfusion
• Levothyroxine sodium with I/V glucose, corticosteroids

Differential diagnosis
• Hypothermia
• Septic shock
• Psychiatric disorders
• Dementia (including Alzheimer’s disease), Depression
• Encephalitis and meningitis
• Hepatic encephalopathy
• Cerebrovascular disease