THERAPY FINAL QUESTIONS AND ANSWERS 2012

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1) Rheumatic fever
a) Definition
systemic immune disease due to pharyngeal infection with group A beta-hemolytic streptococci involves the
heart, joints, CNS, skin, subcutaneous tissue
b) Epidemiology
- 3% with streptococcal sore throats develop rheumatic fever
- 5-15 years old
- Mortality decline (antimicrobial therapy)
c) Classification
1. According to clinical variant
- Acute
- Recurrent
2. According to clinical signs
a. Major manifestation - Raised ESR or C-reactive protein
- Carditis - Arthralgia
- Erythema marginatum - Previous rheumatic fever
- Polyarthritis - Leukocytosis
- Subcutaneous nodules - 1st or 2nd degree AV block (prolonged
- Chorea PR)
b. Minor manifestations - Mitral/aortic regurgitation
- Fever - preceding streptococcal infection
3. According to outcome
- Recovery
- Chronic rheumatic heart disease with or without valve involvement
4. According to stages of heart failure
Senior’s
1. According to changes in heart
a. Active phase
- Rheumocarditis without valve disease
- Relapsing rheumocarditis (at places of old valve disorders)
- Rheumatic fever without heart changes
b. Non active phase
- Myocardiosclerosis
- Valve disorders
- Changes in other organs (chorea, nephritis, hepatitis, changes in skin, encephalitis, meningitis)
2. According to duration
- Acute –attack duration before 2 months, exudates, good effect from treatment
- Subacute – slow attack, 3-6 months, has exudation, no absolute effect from treatment
- Relapsing -attack acute (6-12 months), has exudation, not good effect from treatment
- Long – slow attack, (6-12 months), no exudation, some effects from treatment
- Latent –has valve disorders,
d) Etiology (role of hemolytic streptococcus). Pathogenesis
Etiology
- Group A streptococci (streptococcal sore throat)- pharyngeal route
- Causes rheumatic fever recurrence
- acute stage – increased antibodies titers to streptococcal antigens
- virulence properties
1. serotypic surface M protein
2. hyaluronic acid capsules
Pathogenesis
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- ―Molecular mimicry‖ type of autoimmunity
- streptococcal antibodies higher in patients with acute rheumatic fever
- Latent period – 1-5 weeks after acute pharyngeal streptococcal infection
- several streptococcal antigens – cross-reactivity with cardiac & other tissues
- non-type-spesific peptides of M protein - cross-reactive immunologically with myosin, keratin, other
coiled proteins found in cardiac tissues
- Hyaluronic acid of group A streptococcal capsules & hyaluronic acid of human host tissue - chemically
identical
Factors that lead to Strepto attack:
1. Strepto infection
2. weak immunity
3. chronic (Strepto Ag ↑ by time to time)
4. Ag irritates humoral immunity
5. Sensibilization
Pathogenesis
Streptococcus produce streptolysin, streptokinase, hyalurinidase which acts on joints, connective
tissue ,nerves or cvs and cause degradation.
In streptokinase infection decrease immunity; disorders of basophils occur; inflammatory mediators are
secreted; generalized inflammatory response occur; hyperergic reaction to streptococcus; autoimmune
process develop and cause lesion and degradation of connective tissue, cvs, cns, and joints.

e) Morphological stages of rheumatic disease

- Lesions of rheumatic fever - dissemination throughout body
- affect connective tissues
- Focal inflammatory lesions around small blood vessels
- Myocardial Achoff body – submiliary granuloma (pathognomonic)
Aschoff body lying between muscle bundles & surrounding vessels
- Fibrinoid collagen degeneration
- Phases:
1. Mucoid swelling
2. Fibrinoid changes
3. Granulomatosis
4. Sclerosis
- Stage 1 : Period of exudation -From time of infection till 2 months. Absent of clinical features. Difficult
to diagnose.
- Stage 2 : Cells infiltration - 3-6 months. Develop clinical signs and features. Develop generalized
inflammatory response.
- Stage 3 : Sclerotic organic changes - Deformation of organs. Forms granulomas by Aschoff Nodular.

f) DUKKET-JONES CRITERIA
1. Major manifestation - Raised ESR or C-reactive protein
- Carditis - Arthralgia
- Erythema marginatum - Previous rheumatic fever
- Polyarthritis - Leukocytosis
- Subcutaneous nodules - 1st or 2nd degree AV block (prolonged PR)
- Chorea - Echocardiography – mitral / aortic
2. Minor manifestations regurgitation (>10-14 days)
- Fever
Minor manifestation plus preceding streptococcal infection: recent scarlet fever, raised antistreptolysin O or
other streptococcal antibody titer, positive throat culture
Evidence of recent streptococcal infection is particularly important if there is only 1 major manifestation
(2 major/1 major + 2 minor manifestations)
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- Carditis: tachycardia, murmur
- Arthritis: migratory, affect large joints
- Subcutaneous nodules: small, mobile painless on extensor surface of joint and spine.
- Erythema marginatum: geographical rash with red raised edges and clear centre on trunk, thighs, arm
- Sydenham;s chorea : unilateral or bilateral involuntary semi-purposeful movement. May be preceded by
emotional lability and uncharacteristic behaviour.

g) Clinical picture: symptoms of primary and recurrent rheumocarditis

- Sudden onset (2-3 weeks after acute - Major clinical manifestations
pharyngeal streptococcal infection) with 1. migratory polyarthritis
1. Fever (38-39°C) 2. carditis
2. Sweating 3. Sydenham‘s chorea
3. Joints pain 4. subcutaneous nodules
4. Malaise 5. erythema marginatum
5. Loss of appetite - No single symptom, sign or laboratory test –
- Prevalence – childhood & adolescence age several combinations
group - Rule: 2 major or 1 major + 2 minor
- Peak - between ages 5-15, rare - before 4, after manifestations
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Senior’s
1. Rheumocarditis
- changes in endocardium (valve disorders) & b. Dilatation of heart chambers
myocardium c. heart failure
- Myocarditis d. Pericardial effusion → pericarditis devmt
a. soft heart tones e. Inflmtory edema
b. enlarged heart borders - Thickening of cusps & slight scarring
c. systolic murmur above mitral valve - Valves Firstly
d. gallop rhythm a. formation of commissures (1st time)
e. heart insufficiency – dyspnea, fatigue, b. 2nd time – dev incompetence (shrinking &
edema coalescence)
- Signs of rheumocarditis c. Aortic & other valve D – after many
a. Heart murmurs recurrent attacks
2. Arthritis
- In young ppl, polyarthritis, large joints (knees, elbow, ankles), visible charac of inflmtn (defiguration,
edematous, skin pink & hot, pain (upon palpation or spontaneous)
- May dev rapidly & has migrating character, respond to treatmt
- In adult, normally is arthralgia
3. Chorea 5. Kidneys
- For young ppl - 2‘ glomerulonephritis
- Can‘t control mimic mm & extremities - (hematuria, proteinuria)
- Hyperkinetic activity of joints 6. Liver – reactive hepatitis
- Responds to treatmt 7. Changes in eyes
4. Skin changes – in young (allergy) 8. Meningitis, encephalitis
h) Results of laboratory investigations
- Throat swab culture for streptococcal infection
- Antibody tests for preceeding streptococcal infection:
1. Antistreptolysin O increased titers
2. antihyaluronidase
3. Antistreptozyme test - hemagglutination reaction to concentrate of extracellular streptococcal
antigens absorbed to RBC
- Raised ESR
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- Increased C-reactive protein in serum
- Leukocytosis
- Increased mucoproteins, alpha-2, gamma globulins
- Anemia (suppression of erythropoeisis)
Biochemical-dysproteinemia, absent or decrease antistreptolysin
Urine analysis- decrease specific gravity, present red cells, leukocytes protein casts.
i) Differential diagnosis of bacterial endocarditis
Rheumatic fever – endocarditis manifestations
- Diminished S1
- mitral & aortic regurgitation
- left ventricular dilatation
j) Treatment: antibiotics, NSAIDs, indications to corticosteroid therapy
1. Etiological therapy – on streptococcus antibiotics with bactericidal action e.g. penicillin
- Within 2 weeks e.g. amoxicillin
- Prevent long time antibiotic therapy
- Every 2-3 weeks injection long acting antibiotics
2. Pathogenic therapy – antinflammatory drug (NSAID, corticosteroids)
- Corticosteroid indicated to severe carditis with heart failure or diffuse carditis
- Immunodepressant
Senior’s
Antibiotics- penicillin, erythromycin 60-120mg 4 times daily
NSAID- i) Orthrofan 0.25mg 3 times daily
ii) buthodine , brofine, Indomethacin, ibuprofen, Ketoprofen, Reopirin
corticosteroids- glucocorticosteroids (prednisolone 20-30mg/day in very acute process)
- indications: 2 or 3 degree with vasculitis, chorea
k) Prophylaxis
- Local streptococcal infection treatment e.g. pharyngitis and tonsillitis by AB minimum 5-7 days.
- Antibiotic therapy – long acting penicillin every 3 weeks during minimal 5 years
- Seasonal prophylaxis – spring + autumn when immunity is decreased- use anti inflmtory remedies for 1
mth to avoid inflmtory rXn - Annual prophylactic in 3-5 years
- If recurrent – can be long life antibiotic therapy
- NSAID – selective; non selective (aspirin, inhibitor SOX-II – meloxican)
- 5 years - rheumatic fever without carditis
- >5 years (or all life) - rheumatic fever with carditis
1. Management:
- Bed rest till CRP normal for 2 weeks- 3 months
- Analgesia for carditis/arthritis: aspirin for 6 weeks, monitor salicylates level. Alternative: NSAIDs
- Steroids improve symptoms
- Immobilize joints in severe arthritis
- Haloperidol or diazepam for chorea
2. Secondary prophylaxis:
- Penicillin till no longer at risk. Alternative : suldadiazine. give antibiotics prophylaxis for dental and
other surgery.

2) Infective endocarditis
a) Etiology
- Microbial infection of a heart valve
- bacterium, rickettsia (Coxiella burnetti - Q fever endocarditis), chlamydia or fungus
- Streptococcal - viridans, enterococci
- Staph aureus
- Gram-negative bacilli, Haemophilus
- Gram –ve Klebsiella, E-Coli, Viruses.
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b) Pathogenesis
- presence of organisms in the bloodstream and abnormal cardiac endothelium facilitating their adherence
and growth.
- may occur due to patient- (poor dental hygiene, intravenous drug use) or be associated with procedures
(dental treatment, intravascular cannulae, cardiac surgery, or permanent pacemakers).
- Damaged endocardium promotes platelet and fibrin deposition allows organisms to adhere and grow.
Valvular lesions may create non-laminar flow, and jet lesions from septal defects or a patent ductus
arteriosus result in abnormal vascular endothelium.
- Aortic and mitral valves are most commonly involved in infective endocarditis apart from intravenous
drug users in whom right sided lesions are more common.
c) Clinical picture
Infective endocarditis may occur as an acute, fulminating, chronic or subacute illness with low-grade fever.
High clinical suspicion:
a. Regurgitant-murmur
b. embolic event
c. sepsis
d. haematuria, glomerulonephritis and suspected renal infarction
e. ‗fever‘ plus:
- prosthetic material inside the heart
- other high predisposition for infective endocarditis, e.g. i.v. drug abuse
- newly developed ventricular arrhythmias or conduction disturbances
- first manifestation of congestive cardiac failure
- blood cultures (with typical organism)
- cutaneous (Osler, Janeway) or ophthalmic (Roth) manifestations
- peripheral abscesses (renal, splenic, spine)
- recent diagnostic / therapeutic interventions result in bacteraemia.
Low clinical suspicion. Fever only

Senior’s
1. Acute:
- increased perspiration, weakness, anorexia, sleeplessness, ↑ temperature > 39 degrees, lose weight.
muscle dystrophy, hypovolemia with tachycardia, anemia, damage of valve, wide spread abscess,
thromboembolism
2. Subacute :
- Onset : Cold, weakness, malaise, headache, sweat, subfebrile 1-2months.
- After 2-3weeks, like in acute: ↑ temperature then drop to subfebrile level, lose weight, colour skin change
- clubbed fingers, splenomegaly, liver cirrhosis, disease of blood.
- inspiratory dyspnoe, palpitation, enlarged heart shape, sstolic & diastolic murmur.
- Vascular patho : Embolism & toxical vasculitis, myocarditis (enlarged heart by edema), pericarditis (pain)
exarcebate heart failure, embolism to coronary vessels.
- Petechial; spots HR in sclera & conjuctiva.
- Systemic immune vasculitis : Causes glomerularnephritis & HT. Hematuria.
- vasculitis on skin : Osler‘s Nodules in palm, soles. painful, red colour, protruded.
- Systemic vasculitis in liver with toxic effect & hepatitis - hepatomegaly.
- thrombosis of pulmonary artery with necrosis, infarction of lung. pneumonitis.
- Toxicity with depression of bone marrow: hyporegenerative anemia, lymphopenia, plasmocytosis.

1. syndrome of inflammatory changes and septicaemia

- fever, chill, hemorrhagic rash, leucocytosis shift to left, accelerated ESR, high fibrinogen and α2
globulin contents, positive bl cultures
2. intoxication syndrome
- weakness, hyperhidrosis, headache, myalgia and arthralgia, poor appetite, pallor with icteric blue
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3. syndrome of thromboembolic complication
- focal nephritis, MI, Infarction of spleen and intestine, Cerebral thrombo embolism
- Embolism of retina and vessels of lower extremities
4. syndrome of valvular lesions
- involvement of aortic and mitral valves
5. syndrome of immune disorders
- immune complexes in circulating blood
6. syndrome of immune lesions of organs and systems
- diffuse glomerulonephritis, myocarditis, hepatitis, vasculitis

d) Investigation
1. Microbiology
- Blood cultures - positive.
- Serological tests (i.e. Coxiella, Bartonella, Legionella and Chlamydia).
2. Other laboratory tests
- Full blood count. anaemia and leucocytosis. Thrombocytopenia or thrombocytosis.
- Urea and electrolytes. Renal dysfunction in sepsis.
- Liver biochemistry. Serum alkaline phosphatase may be increased.
- Inflammatory markers. C-reactive protein (CRP) and ESR are increased.
- Urine. Proteinuria and haematuria.
- PCR in culture-negative infective endocarditis.
3. ECG
- New atrioventricular block.
4. Chest X-ray
- heart failure or, in right-sided endocarditis, multiple pulmonary emboli and/oral abscesses.
5. Echocardiography
- valvular dysfunction, aortic root abscesses.
Senior’s
1. Blood :
- Aneosinophilia symptomatic for whole period of disease.
- Plasmacytosis appear in blood.
2. Biochemical :
- Dysproteinaemia : alpha2-globulinaemia.
- transient azotemia
- serum Ig are increase, total complement and C3 complement are decreased
3. Urine :
- Proteinuria, hematuria, leucocyturia, cylinduria: Toxic kidney/glomerulonephritis.
- Presence bacteria in blood : Not sterile.
4. Instrumental :
- US : Show bacteria situated in valve. shows vegetations & cond of chambers (size,etc).
- US of spleen (enlarged), kidney.

e) Treatment (role of antibiotics)

- combination of antibiotics
- Blood cultures should be taken prior to empirical antibiotic therapy (4–6 weeks)
- Serum levels of gentamicin and vancomycin monitored to ensure adequate therapy and prevent toxicity.
- penicillin allergy, glycopeptide antibiotics, vancomycin or teicoplanin, can be used.
Senior’s
1. Antibacterial/Antiinfective Remedy :
- Penicillin. If mix flora, combination therapy with A‘glycoside (Gentamycin/Tobramycin).
- Monolactam AB : Tionam. last gen Penicillin : beta lactam, Amoxycoclaf. plus
Vancomycin/Cephalosporins of 3rd – 4th gen & Lincomycin.
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- Enterococci : Vancomycin + Cephalosporins.
- Ampicillin; Pepericillin; Vancomycin; Tobramycin.
- Gram –ve : Cephalosporins (3rd & 4th gen), A‘glycoside last gen, Monolactam AB.
2. Remedy for immunity : Cephalosporins with A‘glycosides or Quinolones.
- Fungi : Diflucan, Ketokenazole, Fungisone.
- Antivirus : Cicloferon, Foskarnet.
- AB Fluoroquinolone before minor surgery.

- staphylococcal – vancomycin; gentamycin

- streptococcal – penicillin, gentamycin
- enterococcal – ampicillin / amoxicillin; gentamycin

3) Mitral stenosis
a) Etiology
- due to rheumatic heart disease. common in women.
- Other causes include:
1. Lutembacher‘s syndrome, combination of acquired mitral stenosis and an atrial septal defect
2. congenital mitral stenosis
3. in the elderly, calcification and fibrosis of the valve, valve ring and chordate tendineae
4. carcinoid tumours metastasizing to the lung, or primary bronchial carcinoid.
b) Hemodynamics abnormalities
The pathological process results after some years in valve thickening, cusp fusion, calcium deposition, a
narrowed (stenotic) valve orifice and progressive immobility of the valve cusps.
Senior’s
- Normal mitral valve orifice is 4.5-6cm²
- When mitral valve becomes stenosed, the l flow frm the left atrium into the left ventricle decreases and
cardiac output thus drops
- When mitral valve orifice is reduced the press in the left atrium increases to help ejection of bl
- The press rise in the left atrium causes hypertension in the pulmonary veins and capillaries
- Venous hypertension thus develops
- In response to the progressively increasing press in the left atrium and in pulm vein, an active spasm of
pulmonary arterioles dev (Kitaev‘s reflex)
- The press in pulmonary artery does not correlate with the increasing press in the left atrium
- So called active/arterial pulmonary hypertension develops
- Press in the pulmonary artery rises in response to this spasm and can be 2-3 times higher than in aorta
- Pronounced hypertrophy of right ventricle develops in response to considerable rise in the pressure in the
pulmonary artery
- As the contractile activity of right ventricle later decreases, congestion in greater circulation develops
- Left ventricle slightly reduces in size due to the lesser amount of blood entering it & so, lesser activity.
c) Clinical picture
Symptoms
- no symptoms until the valve orifice is moderately stenosed (2 cm2).
- Because of pulmonary venous hypertension and recurrent bronchitis, severe dyspnoea develops. A cough
productive of blood-tinged, frothy sputum, and frank haemoptysis.
- pulmonary hypertension leads to right heart failure and symptoms of weakness, fatigue and abdominal or
lower limb swelling - edema.
- left atrium atrial fibrillation, palpitations. systemic emboli to the cerebral vessels, mesenteric, renal and
peripheral. pulmonary embolism.
Signs
1. Face--mitral facies or malar flush. bilateral, cyanotic or dusky pink discoloration the upper cheeks
2. Pulse--small-volume pulse, atrial fibrillation resulting irregular pulse.
3. Jugular veins--If right heart failure develops, there is obvious distension of the jugular veins.
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Palpation--tapping impulse felt parasternally on the left side. diastolic thrill
percussion - displacement of upper border of relative dullness
4. Auscultation--loud first heart sound if the mitral valve is pliable, but not in calcific mitral stenosis.
‗opening snap‘. low-pitched ‗rumbling‘, mid-diastolic murmur at apex, murmur louder at end of diastole.
5. In pulmonary hpt
- accentuated S2 over the pulmonary artery
- diastolic murmur at the left side of the sternum (Grahm‘s Steel‘s murmur)
Senior’s
- chest pain, ascites
- Ortner‘s sign (hoarseness): Recurrent laryngeal nerve compression by dilated left atrium.
- epigastric pulsation due to hypertophy of right ventricle.
- right ventricular failure - hepatic enlargement, engorgement of the neck vein, edema of the legs

d) Investigation (ECG, Ultrasound, X-ray)

1. Chest X-ray
- small heart with an enlarged left atrium. Late of the disease a calcified mitral valve seen on lateral view.
signs of pulmonary oedema or pulmonary hypertension may be apparent when the disease is severe.
2. Electrocardiogram
- sinus rhythm, bifid P wave owing to delayed left atrial activation. atrial fibrillation. right ventricular
hypertrophy (tall R waves in V1).
Senior’s
1. ECG :
- P-Mitrale (left atrial hypertrophy).
- Right ventricular hypertrophy. In pulmonary hypertension : tall peaked P waves in lead II & upright in
V1, right ventricular hypertrophy.
2. US :
- estimate transvalvular gradient & mitral orifice size, the presence & severity of disease.
- the extend of restriction of valve leaflets, thickness, degree of distortion of subvalvular apparatus.
- assess size of cardiac chambers (left AV orifice will be decreased)& left ventricular function.
3. X-Ray :
- prominence pulmonary arteries, dilatation of upper lobe of pulmonary veins & backward displacement
of the esophagus by an enlarged left atrium.
- In severe stenosis, all chambers & vessels upstream to the narrowed valve are prominent.
- Kerley B lines are fine, dense, opaque, horizontal lines that are prominent in lower & midlung fields.

e) Indications for surgical treatment

- If pulmonary hypertension develops or the symptoms of pulmonary congestion persist.
Senior’s
- severe narrowing of the mitral valve.
- develops complications such as severe atrial fibrillation, systemic embolization, right ventricular failure,
tricuspid regurgitation, uncontrollable pulm edema, limiting dyspnea, pulm HT, RV HT
Contraindication:
- Asymptomatic Patient, CHF, Arrythmias

4) Mitral regurgitation
a) Etiology
rheumatic heart disease and a prolapsing mitral valve. Other causes include:
- aortic valve disease - ischaemic heart disease
- acute rheumatic fever - infective endocarditis –destruction of the
- myocarditis mitral valve leaflets
- dilated cardiomyopathy - left ventricular contraction is disorganized
- hypertensive heart disease - systemic lupus erythematosus (SLE)
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- collagen abnormalities – Marfan‘s syndrome - rupture of the chordae tendineae
and Ehlers–Danlos syndrome - Drugs, e.g. fenfluramine; dopamine agonists.
- degeneration of the valve cusps or mitral - Atherosclerosis
annular calcification
b) Hemodynamic abnormalities
- Incomplete closure of the valve leaflets results in regurgitation of the bl frm the LV to LA during
ventricular systole
- A large volume of bl thus accumulated in LA and it is dilated
- The LV also filled with excess amount of bl which also causes its dilation and compensatory hypertrophy
- Excess distension of atrium increases the blood press inside it and stimulates hypertrophy of myocardium
- Later, as the contractile power of LV decreases, press in LA increases and this press transmitted
retrogradely to pulmonic vein, capillaries and arterioles
- As press in lesser circulation increases and dystrophy develops in myocardium, its contractile power
decreases and congestion in greater circulation develops
- increased pressure in pulmonary veins → spasm of arterioles in lesser circulation( Kitaev‘s reflex) →
increased pressure in pulmonary artery→ intensify load in RV → RV hypertrophy.

c) Clinical picture
Symptoms
- The increased stroke volume is sensed as a ‗palpitation‘.
- Dyspnoea and orthopnoea. Fatigue and lethargy.
- late stages, symptoms of right heart failure lead to congestive cardiac failure. subacute infective
endocarditis.
Signs
- laterally displaced apex beat and a systolic thrill (if severe)
- soft first heart sound, pansystolic murmur, prominent third heart sound, (sometimes a short mid-diastolic
flow murmur may follow the third heart sound).
- signs related to atrial fibrillation, pulmonary hypertension, and left and right heart failure develop later.
Senior’s
- Pulse is of high volume & tachycardic & in later stages might be irregular pulse due to atrial fibrillation.
Jugular veins are dilated. later might develop right heart failure with edema & ascites development.
- cough either dry or with sputum containing traces of blood
- Heart pain can be boring, stabbing and pressing
- Hepatic congestion, Central cyanosis/peripheral cyanosis, facies mitralis
- Systolic thrill palpate at cardiac apex
- Epigastric pulsation
Percussion: upper border shifted up
- Lateral displacement of the hearts borders due to dilation of LV

d) Investigation (ECG, Ultrasound, X-ray)

1. Chest X-ray
- left atrial and left ventricular enlargement. mitral valve calcification may seen.
2. Electrocardiogram
- left atrial delay (bifid P waves) and left ventricular hypertrophy - tall R waves in leads I and V6, and deep
S waves in leads V1 and V2. Atrial fibrillation may be present. hypertrophy of LA - P wave elongates
Senior’s
X ray- later stages can see enlarged right side due to right ventricular hypertrophy.
Ultrasound - shows dilated LA and LV, specific features of chordal/ papillary mitral rupture

e) Prognosis
- in case of adequate treatment, it is good
- in case of rheumatic, it is dangerous
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- better than in mitral stenosis

5) Stenosis of aortic valve

a) Etiology
- turbulent blood flow through congenitally abnormal aortic valves in men.
- Rheumatic fever. rheumatic heart disease
- Calcific valvular disease in the elderly.
- Arteriosclerosis, infective endocarditis.
b) Hemodynamics abnormalities
Calcific valvular disease in the elderly is an inflammatory process involving macrophages and T
lymphocytes with initially thickening of the subendothelium with adjacent fibrosis. The lesions contain
lipoproteins which calcify, increasing leaflet stiffness and reducing systolic opening
Senior’s
- During systole, LV is not emptied completely because portion of blood fails to pass the narrowed aortic
valve into the aorta.
- When a new normal portion of blood is delivered into LV during diastole from LA it is mixed with the
residual volume & ventricle thus becomes overfilled.
- The pressure in inside LV thus rises. This cause intensification of LV work thus it hypertrophies as a
compensatory mechanism. Thus diminished compliance of the hypertrophied LV wall
- hypertrophied LV muscle mass elevates myocardial O2 requirementsmay be interference with coronary
blood flowischemia
c) Clinical picture
Symptoms
- no symptoms until aortic orifice is reduced to one-third of its normal size. At this stage, exercise-induced
syncope, angina pain and dyspnoea develop. death within 2–3 years if no surgical intervention.
Signs
1. Pulse -The carotid pulse is of small volume
2. Precordial palpation
- pulsation is sustained and obvious.
- systolic thrill in the aortic area.
3. Auscultation
- ejection systolic murmur (crescendo–decrescendo) in the aortic area. It radiates into the carotid arteries.
- systolic ejection click, unless the valve has become immobile and calcified
- soft or inaudible aortic second heart sound when the aortic valve becomes immobile
- splitting on expiration
- prominent fourth heart sound
Senior’s
- Aortic face-pale.
- Giddiness, headache, tendency to faint (exertional syncope)
- acute pulmonary edema.
- peripheral cyanosis, orthopnea, severe pulmonary HT leading to RV failure and systemic venous HT,
hepatomegaly, AF, and TR in severe AS
d) Investigation
1. Chest X-ray - small heart with dilated ascending aorta. aortic configuration of heart with LV hypertrophy
2. ECG - left ventricular hypertrophy and left atrial delay. depressed ST segments and T wave inversion.
3. Echocardiogram--thickened, calcified and immobile aortic valve cusps. Left ventricular hypertrophy.
- Cardiac catheterization-to document the systolic pressure gradient between the aorta and the left ventricle
and assess left ventricular function. Coronary angiography is necessary before recommending surgery.
Senior’s
1. ECG- signs of coronary insufficiency. LBBB.
2. US- in US we measure the diameter of the aortic valve orifice.
- In soft degree it‘s 1.2-2cm2,
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 - moderate it‘s 0.75-1.2 cm2
- severe is less than 0.75 cm2.

6) Aortic valve regurgitation

a) Etiology
rheumatic fever and infective endocarditis. congenitally abnormal valve (e.g. a bicuspid valve).
1. Acquired—trauma, aortic dilatation (Marfan‘s syndrome, syphilis, aneurysm)
2. Congenital--bicuspid valve or disproportionate cusps
b) Hemodynamics abnormalities
- reflux of blood from the aorta thorugh aortic valve in to the left ventricle during diastole and blood is
also delivered in to left ventricle from atrium at the same time, this lead to overfills and distend the left
ventricle during diastole. during systole left ventricle has to contract with greater force to expell large
amount of blood into the aorta. intensified work of left ventricle cause its hypertrophy and increase
systolic volume in aorta cause dilation. There is a marked variation of BP in aorta during systole &
diastole. Increased blood vol in aorta at systole ↑es systolic P & part of blood returned to vent at diastole
causes diastolic P to↓.
c) Clinical picture
Symptoms
- symptoms occur late. ‗pounding of the heart‘ because increased left ventricular size and its vigorous
pulsation. Angina pectoris is a complaint.
- Paroxysmal nocturnal dyspnoe, Tachycardia, dyspnea, weakness, Giddiness-deranged b/supply to brain
- Pallid skin, Aortic face
Signs
- The pulse is bounding or collapsing. hyperdynamic circulation:
1. Quincke‘s sign – capillary pulsation in the nail beds
2. De Musset‘s sign – head nodding with each heart beat
3. Duroziez,s sign –murmur on femoral artery is auscultated with pressure applied
4. pistol shot femorals –sharp bang on auscultation over the femoral arteries with each heart beat.
- high-pitched early diastolic murmur at the left sternal in expiration. ejection systolic flow murmur.
d) Investigation
1. Chest X-ray--left ventricular enlargement and dilatation of the ascending aorta.
2. ECG--left ventricular hypertrophy– tall R waves and deeply inverted T waves in left-sided chest leads,
and deep S waves in the right-sided leads. Normally, sinus rhythm is present.
3. Echocardiogram- vigorous cardiac contraction and a dilated left ventricle. aortic root enlarged. Diastolic
fluttering of the mitral leaflets or septum (Austin Flint murmur).
4. Cardiac catheterization--injection contrast into the aorta outline aortic valvular abnormalities and assess
degree of regurgitation.
Senior’s
1. Palpation- shifting apex beat to the left & inferiorly
2. Percussion- cardiac dulless- shifted to left
3. Auscultatn- Soft both heart sounds.
- diastolic murmur at Botkin Erb point (in deep breathing)
- Austin Flint murmur- soft mid-diastolic murmur present
- 3rd & 4th sound may appear.
- Traube double sound heard over femoral aa
4. Pulse- fast , full & ↑.

7) Tricuspid valve regurgitation

a) Etiology
- Functional tricuspid regurgitation in right ventricle dilates, e.g. in cor pulmonale, MI or pulmo hpt.
- Organic tricuspid regurgitation in rheumatic heart disease, infective endocarditis, congenitally
malpositioned tricuspid valve and congenital abnormalities of atrioventricular valves.
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b) Hemodynamics abnormalities
- incomplete closure of the tricuspid valve during right ventricle systole.blood regurgitate into right atrium
and mix with blood fro vena cava. It lead to distension of right atrium and cause hypertrophy
- during diastole large volume of blood is pumped into right ventricle and lead to right ventricle
hypertrophy. right atrium and ventricle intensify their activity as a compensatory mechanism. Exhaustion
and failure of compensatory mechanism lead to congestion of blood in greater circulation.
c) Clinical picture
- symptoms of right heart failure.
- large jugular venous ‗cv‘ wave and pulsation of liver in systole. right ventricular impulse at the left
sternal edge, blowing pansystolic murmur on inspiration at lower left sternal edge. Atrial fibrillation
- Feeling of heaviness
- Pain in the right hypochondrium
- Edema, ascites
- Skin cyanotic.
- positive venous pulse.
d) Investigation
1. Inspection- pulsation in region of RV
2. Palpation- rolling movements when place one hand on liver & the other on RV region.
- apex beat not pronounced bcoz displaced postly by hypertrophified RV.
3. Percussion- marked displacement of the heart border to the right
4. Auscultation- at base of xiphoid process- diminished 1st sound
- Systolic murmur at xiphoid process & at 3rd &4th interspace, to R of sternum- murmur increase
when patient keep his breath at height of inspiration
- Diminished 2nd sound over pulmo trunk .
5. ECG : hypertrophy of RV (electrical axis shift to R).
- reveal signs of hypertrophy
- P wave is high
- deep S wave in left chest lead
- high R wave in right chest lead.
1. X ray: hypertrophy of right chambers.
2. Echocardiography-reveal paradoxical movements of interventricular septum.
3. Phonocardiography-records systolic murmur at base of xiphoid process and 3rd, 4th interspaces to right
sternum.
4. Phlebogram-phlebogram of jugular vein records high positive a wave.

8) Chronic heart failure

a) Etiology
- Ischaemic heart disease
- Cardiomyopathy
- Hypertension
- Valvular heart disease
- Congenital heart disease (ASD, VSD)
- Alcohol and drugs (inotropic effect,Ca blocker,hypotensive drugs,vasodilators, chemotherapy)
- Right heart failure (pulmonary hypertension, pulmonary embolism, cor pulmonale (COPD))
- Arrhythmias (atrial fibrillation)
- Pericardial disease (constrictive pericarditis, pericardial effusion)
- Infections (Chagas‘ disease)
- kidney pathology:acute glomerular nephritis,renal failure
- vitaminosis,bad nutrition,stress,associated disease:pneumonia,anemia
b) Pathogenesis
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heart fails, Small cardiac output, ↓ contractility of cardiac muscle, compensatory mech to maintain cardiac
output and peripheral perfusion such as
- Ventricular dilatation
- Myocyte hypertrophy
- Increased collagen synthesis
- Altered myosin gene expression
- Increased ANP (Atrial natriuretic peptide) secretion (vasodilator)
- Salt and water retention (renin–angiotensin–aldosterone system)
- Sympathetic stimulation
- Peripheral vasoconstriction
However, as heart failure progresses, these mechanisms become pathophysiological causes cardiac
decompensation. Factors involved are venous return, outflow resistance, contractility of the myocardium, and
salt and water retention.
late course causes accumulation of edema
c) Classification
1. NYHA heart failure classification
2. Functional class
d) Clinical sign according to stages
Stages of CHF
e) Treatment: Glycosides, diuretics, vasodilators, ACE-inhibitors
1. Cardiac glycosides
- Digoxin 0.125–0.25 mg daily (reduce dose in elderly or renal impairment), is indicated in patients in
atrial fibrillation with heart failure
- Digitoxin, Strophantin
2. Diuretics
a. Furosemide 20–40 mg daily/max. 250–500 mg daily
b. Bumetanide 0.5–1.0 mg daily/max. 5–10 mg daily
c. Bendroflumethiazide 2.5 mg daily/max. 10 mg daily
d. Metolazone 2.5 mg daily/max. 10 mg daily
- Loop diuretics (e.g. furosemide and bumetanide) and thiazide diuretics (e.g. bendroflumethiazide,
hydrochlorothiazide) -relief of dyspnoea and improve exercise tolerance, relieve fluid retention,reduce
edema and jugular venous distention
a. Thiazides
- Hypothiazides ( 25-100mg/d )
- Cyclomethiazines ( 0.5-1.5mg/d )
b. Spironolactone
- Veroshspirone ( 0.25mg 1 tablet with combination to other drugs )
- Triamterine ( 50mg ), Amiloride ( 5 mg )
3. Vasodilators and nitrates
a. Isosorbide dinitrate 20–40 mg × 3 daily
b. Hydralazine 37.5–75 mg × 3 daily
4. Angiotensin-converting enzyme inhibitors ACEI
a. Captopril 6.25 mg × 3 daily/25–50 mg × 3 daily
b. Enalapril 2.5 mg daily/10 mg × 2 daily
c. Ramipril 1.25–2.5 mg daily/2.5–5 mg × 2 daily
d. Candesartan 4 mg daily/32 mg daily
e. Valsartan 80 mg daily/320 mg daily
f. Losartan 50 mg daily/100 mg daily
- symptomatic improvement.

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- The main adverse effects are cough, hypotension, hyperkalaemia and renal dysfunction. The
contraindications include renal artery stenosis, pregnancy and previous angioedema.

9) Acute heart failure

a) Etiology
- Primary causes → IHD, MI, Myocarditis, Sclerosis
- aortic valve insufficiency & mitral valve insufficiency
- stenosis of the aorta, arterial HPT (1° & 2°)
- Q8.
- Pulmonary diseases- acute pneumonia, acute cor pulmonale, thromboembolism of pulmonary artery.
- Brain insult or trauma
- Toxicity
b) Types
- Right & left
- Systolic & diastolic
- Low output & high output
- Forwards & backward
c) Pathogenesis
- Small cardiac output due to ↓ contractility of the cardiac muscle
- Activation of sympathetic nervous system
 Spasm of a.a & v.v
 Tachycardia development
- Small bf in the kidney (ischemia)
- Activation of the renin angiotensin converting system → spasm of a.a & v.v
- Aldosteron system activation
 Improve reabsorption of Na+ & H2O
 a.a.r enlargement circulation blood. Blood stagnation
- Dilatation chambers of the heart
- ↓ contractility of the cardiac muscle. Decrease cardiac output
- Heart failure develop.

d) Clinical symptoms
1. left sided heart failure:
a. interstitial edema
- fatigue, dizziness, inspiratory dyspnea, orthopnea, dry cough at onset, foamy pinkish sputum
- peripheral cyanosis, cold sweat, pale grayish skin.
- weak cardiac activity, tachycardia, poor pulse,
- auscultation - crepitation and moist rales in lower part of lungs, weak cardiac sound, gallop
rhythm, and systolic murmur
- percussion reveal dilated left ventricle.
b. alveolar edema
- more intensive dyspnea, cough with pink foamy sputum, tachypnea
- central diffuse cyanosis, skin is pale grayish, cold skin
- auscultation- diffuse intensive moist rales, bronchial breathing, gallop rhythm
- percussion – dilated left ventricle
2. right sided heart failure
- headache, nausea, vomiting, dyspnea, dizziness, fatigue, discomfort in chest
- dilation of neck veins, epigastric pulsation.
- hepatomegaly with positive plesh sign
- ascities, hydrothorax, tachycardia, cough with bloody sputum
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 - central cyanosis in face and chest
- oliguria
- encephalopathy, loss memory.
- auscultation- gallop rhythm
- percussion- dilated right ventricle.
- edema of legs
- fluid in pericardium
- anasarca (edema appears in evening and disappears in morning)
- urine: presence of protein, leucocyte and erythrocyte, increase density
- gastritis, colitis, cachexia
e) Emergency care
- Admit ICU and oxygen therapy.
- patient is to sit and not to lie down
- evaluation of blood
- veins tourniquet for depletion blood in vein of leg
- IV morphine
- Diuretics i.e. furosemide 60mg IV
- Vasodilators i.e nitrous (sublingual) i.e. nitroglyceride, nitrosorbides
- Dexamethasone (4-8mg) depending on he arterial pressure and mass of patient
- Cardioglycosides
- In ↑ arterial pressure : nitroprusside
- In ↓ arterial pressure : prednisolone, mesathone
- beta blockers
- symptomatic treatment

10) Atherosclerosis
a) Epidemiology
Risk to atherosclerosis to IHD
- in developed countries - stressful life style.
- western Europe > eastern and asian coutries.
- age > 40- 60
- males
- BP 160/90-95 or higher
b) Etiology – modifying & non modifying risk factors
Modifying: 8. Stressful life
1. elevated level of BP 9. Hyper- & dyslipidemia
2. high cathecholamine 10. dyslipoproteinemia
3. Smoking Non modifying risk factors:
4. DM type II 1. Age >40-60
5. Hypodynamia 2. sex- males
6. Obesity 3. genetics- familial hypercholesterolemia,
7. Alcohol abuse polygenic
c) Role of dyslipoproteinemia
Forms: free fatty acids, cholesterol, triglycerides, esthers, phospholipids
Dyslipoproteidemia dev due to:
1. ↑ absorption fr GIT
2. Changes of receptor activity/ sensitivity
3. Transport systems affected
4. When cholesterol is not evacuated properly
Mech:
15
 5. lipoprotiens play important role in regulation cholesterol level in blood and excretion of cholesterol.
6. LDL play important role in transport of cholesterol from liver to peripheral tissues while HDL play
role in transport of cholesterol from peripheral tissues to liver which later excreted in bile.
7. dyslipoproteinemia lead to disbalance of lipoprotein in circulation and cause accumulation of
cholesterol in circulation which cause development of atherosceloris.
1. Initial damage to blood vessel
2. Inhibition by lipids
3. Damage of cells
4. Stimulation of smooth muscles cells
5. Formation of atherous cap containing atherosclerotic debris
8. Receptors in dyslipoproteinemia is reset due to changes in permeability & metabolism
9. Lipid is not metabolized & deposited on membrane. This block ions & energy exchange & push
organelles to aside
10. Cells that filled with lipid cannot function normally, thus cell is atrophied
d) Types according to fredrikson’s classification
Primary dysproteinemia
1. Hyperlipoproteinemia type I (lipoprotein-lipase deficicency) -↑ chylomicrons
2. Hypercholesterolemia types IIA and IIB
 IIA – only LDL↑
 IIB – ↑ LDL and VLDL
3. Dysbetalipoproteinemia - ↑IDL
4. Hypertriglyceridemia - ↑ VLDL
5. Hyperprelipoproteinemia - ↑ chylomicrons and ↑ VLDL
Secondary dysproteinemia
1. DM, hypothyroidism
2. primary biliary cirrhosis of liver
3. nephritic syndrome
4. kidney insufficiency with uremia dev
5. alcohol, drug
e) Pathogenesis
Dysplipoproteinemia→ lipids absorbed on endothelial cells of blood vessels→ primary injury to cells→
change in permeability→ receptors activity ↓→ cholesterol becomes depot in cell, block other cell activities
e.g. metabolism→ dystrophy→ intima of blood vessel disappear→ basement membrane exposed→
thrombosis covers defect, ↑ activity of smooth muscle cells (localized hypertrophy)→ intimal thickening→
formation of atherous cap containing atherosclerotic debris
chronic endothelial injury:
11. endothelial dysfunction- increase permeability cause migration and adhesion of leukocytes and
monocytes.
12. Smooth muscles migration from media to intima. Macrophages and smooth muscles engulf lipid. Lipid
accumulation.
13. Smooth muscle proliferation and collagen and other extracellular material deposition take place. Lipid
plagues are formed. Atherosclerosis develop.
Major theory of atherosclerosis
1. injury theory - hypertension, high CO2, CO
2. Infective theory - Chlamydia pneumoniae, herpes, cytomegalovirus
f) Morphological stages of atheroma formation
1. Fatty streaks – adhesion of intima by extralipids causing formation of fatty streaks. Intimal thickening
(reversible)
2. accummulation of lipid (lipoidosis) & fibrous tissue (fibrosis)

16
 3. Migration of smooth muscle cells from tunica media to intima & smooth muscle cells elaborate
extracellular matrix - leads to diffuse thickening of intima (intima is convered by fibrous cap -
atheroma formation), may occlude lumen (reversible / irreversible)
4. Complication: Total scarring – unstable plaque, stress, physical activity, break fibrous cap, contents
rush out cause stimulation of thrombocytes and form large thrombus→ infarction, stroke of vessels
→ growth of collagenic fibres→ shrinking→ calcification (irreversible)
g) Clinical symptoms of aorta, brain & peripheral arteries atherosclerosis
1. Aorta atherosclerosis
Acute: Cause thromboembolism, leads to turbulent blood flow & thrombus formation, IHD
Chronic:Wall of aorta is calcified, loss elasticity, thicked. Aorta atherosclerosis leads to aneurysm &
aortic valve stenosis
- symptoms of suphenic papav- rise of murmur when raise the trunk.
- auscultation of organic murmur over aorta
- accentuation of S2 at aorta.
2. Brain athesosclerosis - Decreased blood flow to brain & infraction of brain. Manifest as stroke, vertigo,
headache, encephalitis
3. Peripheral atherosclerosis
Acute: bilateral gangrene of both extremities
Chronic: intermittent claudication
- pale and cold skin
- pain during exercise or movement of affected body part.
- weakness
- decrease sensation
h) Treatment: diet, medicaments
Diet
1. reduce total fat intake
2. reduce dietary cholesterol intake
3. increase intake of fibre
4. reduce alcohol consumption
Medicaments
1. statins: lovastatin, prastatin, simvastatin,fluvastatin (↓ CLTRL synthesis)
2. sequesters of bile acid: cholestyramine & colestipol ( block absorption of fats fr food by GIT)
3. nicotinic acid (niacin) – (increasing lipid metabolism)
4. fibrates: clofibrate, gemfibrozil ( ↑ HDL)
5. probucol (block synthesis and CLTRL absorption)
6. Combination therapy
i) Prognosis
associated with risk of myocardial infarction, cerebrovascular disease and death from vascular causes;
reduction risk factors - useful therapy
1. Reversible changes of the lumen and compensatory form of plaque can be treated easily and the
prognosis is very good.
2. irreversible changes of lumen, decompensated form of plaque, difficult to treat. Prognosis is poor.

11) Ischemic heart disease

a) Definition - occurs when there is an imbal. btwn supply of O2 & myocardial demand
b) Epidemiology
Men: Women= 4:1
Peak incidence men age 50 – 60 years, female age 60 – 70 years.
It‘s the most common, serious, chronic, life-threatening illness in USA. causes > deaths & disability

17
c) Etiology
1. atherosclerosis of the coronary arteries
2. Obstruction : atheroma,thrombosis,spasm,embolus,coronary stenosis,coronary arteritis in SLE
3. ↓ O2 blood to myocardium: anemia, ↓ coronary perfusion, carboxyhaemoglobulinaemia
4. ↑ demand O2 due to ↑ cardiac output ( thyrotoxicosis)/ myocardial hypertrophy (aortic stenosis/HPT)
5. Abnorm constriction/failure of norm dilation of coronary resistance vessels
6. changes in the blood coagulating and anticoagulating systems.
Risk factors :
- age, - gout, - hereditary predisposition
- male sex, - contraceptive pills, - heightened coagulability of
- hyperlipidaemia, - homocysteinaemia, the blood
- hypertension, - ↑LDL,↓HDL, - diabetes mellitus
- excessive alcohol intake, - smoking - familial
- obesity, - fatty food, stress, hypercholesterolemia
- lack exercise, - endocrine disturbance
d) Pathogenesis
1. narrowing of coronary arteries by plaque formation (atherosclerosis) → fissuring, thrombosis →
obstrucn, coronary b.flow ↓ → reduces myocardial perfusion → myocardial ischemia
2. Disturbances of vascular endothelium func (local ctrl of vascular tone, maintenance of a/coagulant
surf, defense against inflamn cells) causes inappropriate constricn, luminal clot formation ,abnorm
interacn wit monocytes & platelets
3. ↓ in luminal diameter of arteries causes hemodynamically significant stenosis → smaller distal
intramyocardial arteries & arterioles are max dilated → any ↑ in myocardial O2 demand provokes
ischemia
e) Classification
1. Acute : Angina pectoris, Myocardial infarction, Sudden coronary death
Chronic : Diffuse /post-infarct cardiosclerosis, Arrythmia, Heart failure (CHF)
2. Acc to location : Ant, Post, Lat, Interventricular wall, large(diffuse)
3. Acc to involvement of heart m : Subendocardial, transmural, intramural
4. Acc to duration : Transient ischemia(angina pectoris), Prolonged ischemia ( myocardial necrosis &
scarring)
AP – new onset, stable (I, II, III, IV), progressive exertional, variant / stable, unstable
MI - transmural, non transmural.
f) Primary prophylaxis
- Exercise
- Stop smoking
- Diet: low cholesterol, sugar, unsaturated fat, low salt
- Adequate rest and avoid chronic stress
- Stop using of contraceptive pill
- Stop alcohol consumption
- Always check blood pressure, glucose test. (medical check up frequently)
Treatment of risk factor / disease eg: oral hypoglycemic agent for DM

12) Acute coronary death

- Acute coronary death due to changes of heart - ischaemic heart disease.
- Acute coronary death is within 6 hours of onset of symptoms without absolute reason.
Etiology:
1. cardiac causes
a. coronary- acute MI, chronic IHD, congenital anomality of coronary arteries
b. non-coronary- hypertrophic cardiomyopathy, valvular heart disease, ventricular fibrillation.
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 2. extracardiac causes- asphyxia, hypoxia, hypercapnea, metabolic and electrolytes disorders,
intoxication.
Common signs and symptoms:
- tachycardia, pacemaker everywhere, heart rate >300, ECG abnormality, dizziness, cardiac region pain.
Treatment:
i. cardiac resuction
ii. Drugs – lidocaine, amiodarone.
a) Asystole
absent of cardiac systole and referred as death arrhythmias.
Asystole is a direct plane of ECG
Rate none
P wave may be seen
QRS none
Conduction none
Rhythm none
Asystole occurs following termination of atrial, ventricular tachycardias. This pause is usually insignificant.
Asystole of longer duration in the presence of acute MI and CAD is fatal.
Etiology:
- changes of pacemaker, MI near SA node, deep ischemia, recurrent MI, thrombosis of main left
coronary artery.
Clinical pictures:
- loss of consciousness, pale skin, absent of heart rate, BP, pulse
Treatment:
i) Antiarrythmic drugs- lidocaine
ii) Defibrillation therapy
iii) Direct or indirect cardiac massage.
- CPR, 100% oxygen, IV infusion, intubation
- epinephrine 1.0 mg., IV push, q3-5 minutes, atropine
Prognosis: bad
b) Fibrillation
- fibrilatory changes of cardia due to ischemic process.
- Ventricular fibrillation is very rapid & irregular ventricular activation.
- Clinical picture: no pulse, unconscious, respiration ceases (cardiac arrest)
Stages of ventricular fibrillation:
Stages Heart rate (beats/min) Amplitude Duration
I 300 High 2 sec
II 600 High 1 min
III >1000 Low 3 mins
IV (atonic) <400 Very low 1-2 mins
Mechanism:
- acute ischemic changes due to spasm or thrombosis. lead to alteration of Na-K ATPase activity and cause
leakage of K. and increase excitability. It cause non specific irritation and tachyarrythmias which lead to
ventricular fibrillation
Clinical picture:
- loss of consciousness, pale skin, absent pulse, decrease Bp and heart rate, apex beat absent.
- ECG- wide and deformed T, low complexes and irregular R-R intervals.
1. sudden development
2. within 15 seconds, patient in laying position
3. in 40 seconds, 1 time muscles contraction
4. in 1 min 30 seconds, maximum dilatation of pupil
19
 5. > 2 mins, rhythm stop, coronary death, heart stop pumping, but patient still breathing (clinical death)
Treatment:
1. defibrillation therapy
2. antiarrythmic drugs
3. heart massage.
4. reanimation
5. artificial lung ventilation
6. CPR
c) Tamponade of the heart
- compression of the heart due to accumulation of effusion in pericardium, thus produce disturbances in
circulation by preventing ventricular filling
Mechanism: pericardial fluid collects and cause increase pericardial pressure. Heart cannot fill normally and
cause stop of pumping activity.
Causes:
- pericarditis, cardiac trauma, MI, neoplastic disease, idiopathic pericardiac disease, uremia
- less common cause- hemopericardium result in cardiac operation or trauma, lung or breast cancer.
Clinical pictures:
- increase CVP, systemic vascular resistance, jugular venous pulse
- decrease cardiac output, BP, pulse.
- limitation of ventricular filling
- dyspnea, orthopnea
- muffled heart sound, kusmaul sign (dilatation of neck veins during insp.)
ECG- alteration of P and T wave
X-Ray- globular heart, convex or straight heart border
Treatment:
- pericardiocentesis, surgical drainage
- antiarrythmic drugs
d) Emergency care
Tamponade: Puncture/pericardiocentesis & conventional surgical approach
- CPR
- O2 therapy
- ECG monitoring
- Systemic infusion therapy
- CVP monitoring

13) Angina pectoris

a) Definition
chest pain that is the product of transient myocardial ischemia.
Etiology – artherosclerotic (narrow artery), hypercoagulation, supply of O2 & myocardial demand imbalance.
b) Pathogenesis
Ischemia happens when there is demand and supply disbalance
1. When only demand is  ( dynamic changes )
2. Supply is impaired, demand not 
3. Demand increase and supply decrease
4. Demand & supply both ↑ - Heart effects & bad regulation. Bad factor accompany with each other.
Main mechanism due to spasm of artery and transient hypercoagulation
1. Spasm
a. hyperactivity of  receptor in large and middle sized coronary artery cause general spasm of coronary
system. spasm of these large trunk cause  in blood and O2 supply
b. Disbalance of  and  receptor -  receptor dilate coronary system in stress condition
20
 c. Atherosclerotic plaque  damage endothelium
2. Hypercoagulation - coagulation of artery depend on thrombocyte activation
c) Classification
1. Stable
- occlusion caused by atheroma ( not spasm )
- 4 grades acc to tolerance to physical activity ( Canadian Cardiology Society )
- characterized by stereotypic characteristics, pain arises after a particular level of physical exertion is
relieved by specific NG.
Grade 1 Pain in physical activity in higher than normal activity due to  demand
Grade 2 Common attacks of angina which is walking 100- 500m , climbing > 1 floor, walking
against frozen cold wind
Prominent angina when > 2 vessel affected , change in the lumen , stereotypic
Grade 3 Pain at rest, at night  angina starts during REM sleep ( ↑ SNS  ↑ demand )
Grade 4 Few patient survive till here , pain when walk < 100m , can‘t carry up themselves , can‘t
do anything simple, typical rest angina attack
Decubitus variant and nocturnal
20-50 attacks /day may occur
- Decubitus angina – Due to changes of posture, increase preload to heart, attack.
- Noctural angina – This group is loss because majority of them dies.
2. Unstable angina (Due to destabilizations of arthrosclerosis plug)
- due to dynamic spasm characterized by absence of stereotype-prolonged pain, severe, can occur in rest,
decreased physical activities, need more tablets to relieve the pain.
a. Progressive exertional / accelerated angina
- patient > stable
- duration of attack/ year: 15-20
- tolerance to physical activity very short
- NG not so effective
b. New onset angina
- suddenly appear
- can‘t predict the outcome
c. Variant/ Prinzmetal angina
- appear only at rest and physical activity don‘t provoke it
- angina > prolonged
- > severe pain
- no absolute effect of NG
d) Clinic of coronary pain syndrome
- Pain when low blood supply (energetic disbalance)
- In heart no pain receptor, only specific receptor baroreceptor, chemoreceptor, mechanoreceptor
- In ischemic zone, overactivity of receptor   electrical function to brain  reach thalamus and irradiate
to cortex
- pain is transient
- Pain localised in the chest , substernal area
- Duration: never exceed 20-30 min normally 5-10 min, Duration of pain is >1 min & <20 min, pain less
than 5 minutes is not angina pain
- Physical activity like walking, climbing, carrying heavy things, stress, ↑ eating volume cause  SNS
- Nitroglycerin sublingual relieve pain in < 5 min at rest
- Irradiation to central part of the chest, left shoulder, scapula region, neck, jaw, arm, hand till 4th & 5th
- Character of pain: struggling, heaviness, squeezing, burning, sharp, and localised pain which can be
shown by finger, Pressing, aching.

21
- Associated symptoms: headache, dizziness, inspiratory dyspnea, arrhythmic pulse, nausea, cold sweat,
palpitation, weakness, fear of death
e) Pharmacological & stress testing: indication, c/i & evaluation of result
Pharmacological test 
1. Positive effect
a. Nitroglycerin
b. Β-blockers - propranolol, metoprolol, atenolol, nadolol, and timolol.
c. Calcium antagonists
2. Negative effect
- Diperidamole and Curantile. Injection intravenously. - It will cause attack.
3. Cardiac catheterization with coronary arteriography - for direct visualization of the coronary arteries by
injection radiographic contrast. used for coronary artery disease.
4. Cardioscintigraphy - thalium is injected into peripheral venous blood
5. Pharmacological stress - injection of vasodilator - normal vessels are dilated. Abnormal vessels show
ischemia.they cannot dilate.
6. Indications
- Angina refractory to medical therapy. - to put diagnosis
- Strongly positive exercise test. - to know grades of angina
- Angina occurring after myocardial - checking of therapy effectiveness
infarction. - to check ability of patient with M.I
- When the diagnosis of angina is uncertain.
7. Contraindications
- Myocardial infarction, fresh in 2 weeks - Allergy for drug.
- Transmural. - ↑ BP (180/110), tachycardia
- Unstable angina(new onset, stable, - Stroke and surgical operation of brain.
Prinzmetal) - any varaiant of acute fresh inflammation
- Acute/ chronic resp failure - aneurysm of the heart
- Acute/chronic cardiac failure - serious arrythmia
- Stenosis of aortic valve, fever, disease of - diseases of the joint
joint - episodes of thrombophlebitis
Stress test (provocation test)
- don‘t need to wait demand supply disbalance
- e.g. step test, ergometry (walking, cycling), treadmill
- Provocation  BP X HR at moment of investigation
Age Watt ( bpm )
20-30 170
30-40 150
40-50 150
50-60 140
- physical work done step by step in 2 variants
a. non stop – increasing in mechanical load
b. 1 min of rest after each step for old people
- record ECG in next few minutes 2,3,4,5,10
- some people can reach submax level without changes in ECG
- inflammatory changes / dystrophy process in the heart check in ECG and clinical signs
1. Indication
- give artificial condition to test the heart function before angina occurs
2. Contraindication
- stress test for people > 60 yrs old not done
- no leg, weakness
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3. Evaluation of results of stress test
Clinical prove of angina :
- if patient stop before or have sudden chest pain provoked by testing
- if BP < 25-30% stop test and if BP > 220/110 stop the test
- sensitivity of stress test, may be false and patient don‘t show problem in test
During stress test
a. direct signs of ischemia-classical pain episode, dyspnea, dizziness, cold sweat, decrease blood pressure
b. ECG
- ST depression
- abnormal shape of QRS complex
- appearance of transient pathological Q wave
- episode of transient ventricular arrhythmia
Stress echocardiography - based on principles as stress radionuclide ventriculography but an echocardiograph
is used to produce the images of wall motion abnormalities.
f) General management of angina pectoris
1. Nitrates – sublingual/IV
- nitroglycerin sublingual
- Dinitrate isosorbide – tablet
- NG in IV
- glyceryl trinitrate (GTN) spray /sublingual tabs, oral nitrate e.g. isosorbide mononitrate
2. β blockers
- Propanolol
- selective group, Atenolol
- Nebivalol
3. Ca channel blocker
- Verapamil, Diltiazem
- Ca antagonists: amlodipine
- Alteration of life style: stop smoking, encourage exercise, weight loss.
- Modify risk factors: diabetes, hypertension.
- Aspirin
- adding a K+ channel activator, e.g. nicorandil per os.
g) Indication of surgical treatment
- 3rd class angina pectoris
- stenosis of > 75% of 3 coronary vessel
- no effect on drug
- patients who remain symptomatic despite optimal medical therapy & whose disease is not suitable for
percutaneous transluminal coronary angioplasty
h) Prognosis
1st and 2nd grade angina pectoris have good prognosis but 3rd and 4th grade bad prognosis
If recent onset exertional angina:
- Up to 1/3 experience symptom remission.
- Annual mortality is 2-3%.
- There is a 90% 8 year survival when angina is mild & stable.
Unstable angina has a worse prognosis, 30% suffering myocardial infarction /death within 3 months.
i) Unstable angina pectoris (progressive exertional type)
- acute transitory vasospasm occurs in damaged vessel
- a change in status occurs (e.g., new-onset angina: angina of increasing severity, duration, frequency; or at
rest for the first time).
- close observation and intensive therapy required.
- may be immediate precursor of MI.
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Pathogenesis
- Non occlusive thrombus –platelet plug – overlying a fissured atherosclerotic plaque.
- Dynamic obstruction –spasm of coronary artery.
- Severe, organic luminal narrowing
- Arterial inflammation leading to thrombosis
- Increase in myocardial O2 demand caused by tachycardia, fever & thyrotoxicosis.
Clinical picture
1. Low risk
- Increased chest pain frequency, severity, duration.
- Chest pain provoked at lower threshold.
- New onset angina, <2 months.
2. Intermediate risk
- Rest angina.
- Nocturnal chest pain.
- New onset angina, <2 weeks.
3. High risk
- Prolonged rest angina.
- Cardiac failure, S3, new systolic murmur, hypotension.
Tactic of management
- hospitalization
- monitoring of BP
- stop pain, by oral NG / opiode IV / NG IV under BP control
- Metabolic therapy
- stable condition, send to ward with aspirin, give β blocker, (Metaprolol, Athenolol) and tablets NG
- Concomitant conditions (tachycardia, hypertension, diabetes mellitus) treated.
- Glyceryl trinitrate - overcome superimposed coronary artery spasm.
- Low molecular weight heparin - combination of heparin & aspirin
- Beta-blockers
- Calcium antagonist. (verapamil)
- Discharge after 10 days
- strict bed rest until stabilization of coronary blood flow and oxygen
j) Stable angina pectoris
Classification of the grades – page 21
Clinical symptoms
- pain in constant situation
- Chest discomfort, heaviness, pressure, squeezing
- Radiate to the left shoulder & to both arms, ulnar surfaces & hand.
- It can also radiate to the back, neck, jaw, teeth & epigastrium.
Treatment according to grades of the angina
1. Grade 1 2. Grade 2
- only nitroglycerin before physical exertion - antianginal therapy.
- Nitroglycerin-sublingual,shortacting - β blockers, nitrate, Ca channels blockers with
- prevent the further atherosclerosis:-aspirin aspirin to diminish coagulation.
therapy, regular diet - beta blockers-proparanol and athenolol
- decrease cholesterol level: - aspirin-75-80/daily
Statins-levastatin, lovastatin - drugs that decrease cholesterol
Derivatives of fibric acids-clofibrate - Ca channel blockers
Probucal - prolonged nitrates
Nicothinic acid 3. Grade 3
Bile acid sequestrants
24
- Combined therapy (β-blockers & Ca) and 3 - change lifestyle
groups together (β-blockers, Ca & sublingual 4. Grade 4
nitroglycerin). - combination of nitrates + beta blockers + Ca
- If condition is worst, surgical treatment -tube channel blockers
catheter,ballon catheter,bypass surgery - Metabolic therapy (mexidole). riboxin
- aspirin - surgical treatment
- drugs that decrease cholesterol - rest
- metabolic drugs-riboxin
k) Spontaneous angina
-normally it occurs at rest and is not a result of myocardial demands.
Pathogenesis
- focal spasm of coronary arteries.
- also atherosclerotic coronary artery obstruction.
Clinical picture
- Chest pain at rest at night and early morning.
- pain is over 30 minute, <45 min.
- Pain is more intensive and prolonged than classical angina
- accompanied by dyspnoea & / palpitations.
- triggered by exertion.
Investigation
- transient ST-segment elevation, resolve spontaneously / with nitroglycerin.
- ECG - arrythmias, fibrillations
Treatment
- Nifedipine & nitrates
- Coronary stent
- opiodes may be given
- Ca2+ channel blockers
l) Differential diagnosis of stable & unstable types
Differential diagnosis of stable
- Ischemic heart disease.
- Myocardial infarction.
Differential diagnosis of unstable
- Percarditis - Aortic dissection
- Myocarditis - Pulmonary embolism
- MI - Esophageal spasm/reflux
- Angina
Characteristics Stable Unstable
Occurrence Pain after/during phy exertion Pain at rest
Duration Pain 5-10 min Pain 45 min
Drug NTG effective NTG no effect
Place of pain Mainly L part & apex of cardia d substernal area Other part but larger place
Irradiation of pain Irradiate to L shoulder, shoulder,neck, jaw Other place of irradiation
Character After treatment pain stops Pain do not stop
pressing, heaviness, burning, squeezing

14) Myocardial infarction

a) Epidemiology. Risk factors. Pathogenesis
- necrosis or irreversible damage of the myofibril caused by a prolonged ischemia, occlusion of coronary
artery due to thrombosis.
Epidemiology :
25
- more than a million cases in US, Russia.
- Mortality is more than 15% (primary infarction); if secondary (re-occur disease) up to 30%.
- more in men
- 1-5 million cases are reported each year
- 1 of every 25 patients who survives the initial hospitalization dies in the 1st yr after acute attack.
- survival is reduced in elderly patients (over age 75).
Risk Factors :
- Familial hypercholesterolaemia - alcoholism.
- Smoking - Surgical manipulations
- Stress - previous history of AP
- Family history of MI - Age – male (45-55 yrs); female (55 and
- Hypercoagulability of blood above ).
- Hypodynamia - Sex – male (mostly); female (after menopause).
- High intake of fatty food - Hyperlipidemia.
- hypertension, - Estrogen-progesterone containing drugs.
- diabetes, - triggering factors : physical exhaustion and
- obesity, mental stress.
Pathogenesis :
- coronary thrombosis/ stenotic coronary sclerosis spasm/ disruption of atherosclerotic plaque, vasospasm,
platelet aggregation leading to coronary artery occlusion.
- no blood supply to the myocardium, necrosis of the myocardium.
- 1st period: Moderate ischemia-activity decreased, slow.
- 2nd period(After 30 minutes): Deep ischemia-no activity. Cells don‘t function.
- 3rd period: Damage of myofibrils-Necrotic mass. Irreversible pathological stage.
b) Classification
- Acc investigation of ECG: ST elevation, Non-ST elevation
1. Acc etiology :
- caused by atherosclerosis
- caused by other reasons such as trauma, embolism, atheritis
2. Acc Clinical Pic
- Typical
- Atypical : Asthmatic form, Abdominal form, Cerebral form, Arrythmic form, Painless/Silent form
3. Location: Anterior, Posterior, Lateral, apex, septum
4. Stages: Acutus, Acute, Subacute, Chronic
5. Morphological: Transmural, Subendocardial
6. Acc to square: Transmural, Q MI, Non Q MI
c) Typical clinical picture
- Pain - heavy, crushing, pressing, squeezing, & exarcebate in time. impossible to overcome pain. Next day,
pain disappears because of damage of all tissue.
- Pain is located in the substernal area.
- Pain prolonged more than ½ hour till next day. patient may fall to shock.
- Irradiation to left shoulder, neck, jaw, left arm & sometimes right shoulder.
- Pain more severe from hour to hour.
- Affect of nitroglycerine is absent. sit flat calmly not useful.
- restless.
- Associated symptoms:
Fear of death. Anxiety Weakness
Cold sweat Bad mood
Short dyspnoea Discomfort in chest.
Palpitations Fever (38)
26
Sinus tachycardia Rapid weak pulse
d) Clinic of atypical variants
1. Asthmatic Type :
- Pain is absent; attack of symptom like cardiac asthma.
- tachypnoe, cold sweat, palpitation, fear of death, weakness, orthopnoe, apnoea & rales.
- inspiratory dyspnea, tachycardia, dizziness, peripheral cyanosis, intestitial edema
- 1st Group: Old people 65-70 years, with cardioclerosis
- 2nd Group: Previous MI. Secondary infarction
2. Arrythmic Type :
- without pain. In some case, Accompanied by pain at rest
- Presence of palpitation, dizziness, fast & irregular pulse.
- Often in patient more than 40 years old.
- sudden attack, ventricular arrhythmia, tachycardia, extrabeats, transient arrythmias.
- predispose to fibrillation
3. Central/Brain Dependant Type :
- like stroke; loss of consciousness, weakness, dizziness, vomiting, vertigo, nausea, headache.
- Impaired movement extremities one side; impaired feeling of skin, paresis of muscle.
- When infarction area is big, cause hypoxaemia
4. Silent Infarction :
- No symptoms showing heart disorder
- Might have discomfort in chest, pain in the teeth or tip of finger.
- necrosis isn‘t so large.
- sudden weakness, soft vertigo, diminish activity of heart
- normally for pt with nerve insensitivity eg; DM
5. Abdominal variant:
- Abdominal(epigastric pain). GIT dysfunctions (meteorism, diarrhea, nausea, vomiting).
- Bradycardia. Paralysis of bowel.
- Irritation of phrenic/vagus nerve
- associated with irritation of intestine dyspepsia (belching, distention, flatulence)
- palpation in upper abdomen is painful.
e) Investigation
1. Lab Test :
- creatine phosphokinase (MB fraction). after pain appear at the 1st 6 hours & peak for the next 24hours.
Next day, enzyme is absent.
- AST, ALT. It increases gradually in 1st 6 hours & peak next day till 3rd-4th day; then disappears.
- LDH. Max 5th-7th day after onset of infarction & disappear after 2weeks.
- Troponins are elevated at end of 1st & 2nd day.
- Leucocytosis Reactive – Max 1-2days; disappears at end of 1st week. ESR ↑ in 1st week, slowly
disappears during 10-14 days. ↑ band leucocytes (in 1st 1-3days).
- C-rective proteins increases till 1 week
- transmural infarction: Aneosinophilia in 1st/2nd after infarction, it reappears again. ↑ myoglobin in
blood. transient hyperglycaemia;
2. ECG
Transmural Type: ↑ ST
a. Acutus: 6 hours, increase ST with T wave
b. Acute: 6 hours to 5th/7th day
- R disappears.
- ST elevation presence.
- QS complex/syndrome.
- Elevated T-wave.
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 c. Subacute: QS, prominent –ve T
d. Chronic: QS wave, ST normalizes (after 8th week), +ve T
Non Transmural Type :
- Subendocardial & intramural.
- It can stay 2 days after onset of infarction.
- Change in ST & T-wave only; Q-wave don‘t exist. (Last more than 30 minutes)
- Comes quick, 2nd/3rd day S may disappear. (-T) till 8th week.
- After 8 weeks, there is no trace of any changes.
- So if it is transmural, after 8th week, we will not see (-T)
non-Q wave MI - no ST elevation and no Q wave.
Q wave MI - ST elevation, and evolve Q wave
3. Ultrasound :
- discoordination of myofibrils. No contraction
- aneurysm of heart, dyskinesis or akinesis of myofibrils.
4. Imaging methods :
- many changes in MI. using contrast
- echocardiography: abnormality of wall motion, estimation of Left Ventricle function.
- angiography abt the coronary vessels.
5. Auscultation: S3, S4, Open-snap phenomenon. S2 Accentuation. Low S1.
f) Differential diagnosis of unstable angina
AP MI
Pain synd Present Absent
NTG Effective Not effective
ECG Changes disappears after NTG Present changes.
Enzyme No changes Changes present
g) Main principles of tactic
reduce the chest pain: Thrombolytic treatment / Fibrolytics:
- Nitrates - Streptokinase.
- beta blockers (Metoprolol/Esmolol) - Urokinase
- morphine sulfate - Tissue type plasminogen activator
To stop pain: antiplatelet /antiaggregant agents: Aspirin
- Analgesic – Analgine anticoagulating / antithrombin agents:
- Sublingual Nitroglycerin - Heparin (unfractioned heparin)
- Narcotics: Morphine - Enoxaparin (Lovenox).
- Neuropeptic drug: Doperidole + Fentanyl - Dalteparin (Fragmin)
h) Treatment of pain syndrome (tachi- & bradiarrhythmias)
1. Treatment of pain syndrome.
a. morphine
b. nitroglycerin
c. beta blockers -metoprolol
d. Opioid(synthetic alkaloid)+Neuroleptic Neuroleptanalgesia Fentanyl or Droperidol
2. Treatment of arrhythmic syndrome
a. sustained ventricular tachycardia - Lidocaine
b. ventricular fibrillation
- prompt defibrillation (200-360 J)
- -recurrences treated with lidocaine infusion
c. atrial fibrillation -IV digoxin or IV amiodarone, verapamil, cloradole
d. sinus bradycardia - IV atropine,
3. To treat arrhythmia :
- Quinidine
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 - Amiodarone/Sotalol
- Ca-channel antagonist: Verapamil (for supraventricular arrhythmia)
- Beta-blockers: reduce chance of ventricular arrhythmia, reinfarction. Supraventricular arrhythmia.
Propanol, Metaprolol
- AV Block – Atropine, Euphiline or Prednisolone
i) Anticoagulant & fibrinolytic therapy
Anticoagulant Therapy: Heparin, Warfarin
- Unfractioned heparin - initial dose is i/v 10000, then 5000 or 2500 unit acc to weight of the pt.
- low molecular weight heparin (LMWH).
Fibrinolytic therapy:
- tPA, streptokinase, tenecteplase, reteplase, alteplase, urokinase, prourokinase.
- -converts plasminogen to plasmin and lysis the thrombi.
- side effects like allergy, hemorrhage, arrhythmias, relapsing of the thrombosis.
- Contraindications:
Active internal bleeding
Aortic dissection
Previous hemorrhagic shock
Intracranial neoplasm
j) Complications of early period. Causes
- Rupture of myocardium. Tamponade. Heart does not relax.
- Intraventricular rupture. right overdilated. right-sided failure
- Rupture papillary muscle in left ventricle
- Dysfunction of mitral valve. Regurgitation to aorta and back to atrium. Edema (irreversible). Death
- Ventricular septal defect
- Aneurysm (Acute, subacute)
- Unstable coronary blood flow, Prolonged infarction
- Exacerbation of thrombosis in 1st/2nd day
Post myocardial infarction syndrome:
- -Fever, chest pain
- -Due to autoimmune pericarditis, pleuritis, pneumonitis.
Systemic embolization
- acute coronary failure, edema of the lung, cardiogenic shock, rupture of the aneurysm, arrhythmias,
thromboembolism of pulmonary, acute LV insuff, acute pericardiatis
k) Clinical symptoms & diagnosis
1. Cardiogenic shock
Symptom : - S1 very soft, and S3 may be audible.
- pale with cyanosis skin. Diagnosis :
- very low Bp. - blood analysis- leucocytosis
- pulse is weak and rapid. increase BUN and creatinine.
- severe bradycardia - ECG
- oliguria - echocardiography with color Doppler
- tachypnea, Cheyne-stokes resp, and jugular - chest Xray
vein distension.
2. Pulmonary edema
symptom : dyspnea at rest. Tachypnea, tachycardia, wheezing, HT
Diagnosis :
- Xray- diffuse haziness, and Kerley B lines of interstitial edema.
- echocardiography – to diff betw cardiogenic or noncardiogenic cause.
- ballon flotation catheter – measures diff betw high and normal pressure causes of pulmonary edema.
3. Pulmonary embolism:
29
Symptom : dyspnea, chest pain, hemoptysis, cough
Diagnosis :
- blood test- polymorphonuclear leucocytosis, elevated ESR, increase LDH
- chest X-ray—raised hemidiaphgram, previous infarct seen as opaque linear scars.
- pulmonary angiography – can detect emboli
4. Acute cardiac failure:
Symptom : dyspnea, orthopnea, edema, tachycardia, memory, emotional disturbances
Diagnosis : chest X-ray, ECG, Echo, blood test , ventriculagraphy, cathetarization chamber of the heart, US
l) Cardiogenic shock. Types. Pathogenesis. Criteria
- Cardiogenic shock crisis of microcirculation due to the spread of infarction
- systemic hypoperfusion, depression of the cardiac index, systolic hypotension.
4 types :
- True cardiogenic shock .
- Reflex cardiogenic shock.
- In permanent ventricular/fibrillation
- Areactive shock
Pathogenesis :
- Decreased ejection due to blocking in MI/spasm of peripheral vessels.
- reduced coronary perfusion, hypoxemia and lactic acidosis develop
- blood decrease in brain, kidney.
- blood move slow, stagnate in peripheral area, decreased preload, liquid blood come out to the interstitial
system.
- After 6-12hrs, organ start to die – Reduced liver activity, etc.
- After 12hrs, it changes to irreversible organ type of shock.
Criteria of shock
- pale, cold extremities, diffused acro-cyanosisle - pulse is weak and rapid
- spoor/stupor, Acute renal failure. - severe bradycardia
- Systolic BP less than 60; diastolic less than 40 - tachypnea, Cheyne-stokes resp, and jugular
- psychosis vein distension.
- low cardiac output - S1 very soft, and S3 may be audible.
- poor cerebral function
m) Emergency care. Rehabilitation. Secondary prophylaxis. Prognosis
Emergency care:
- complete rest
- continuous oxygen therapy
- venous dilators - glyceryl trinitrate or sodium nitroprusside IVly
- cardiac inotropes - epinephrine, dobutamine
- infusion therapy of vasopressors ( dopamine, dobutamine )
- ballon aortic contrapulsation
- analgesic ( Analgine or Morphine), aspirin
- NTG
- Arrhythmic: vent extrabeat – Lidocaine
 supravent – verapamil, beta blockers
 AV block –atropine, euphiline
atrial fibrillation – verapamil, cloradole
- Thrombolytics: Streptokinase
Rehabilitation:
- after infarct or post-infarct
- exercise test. conducted with progressive exercise in the hosp and after discharge. Education.
- 3 weeks – when there is non-complicated MI
30
- 5 weeks – when complicated MI present.
Secondary prophylaxis
- to stop progression of the disease.
- long term - antiplatelet ( aspirin ) or clopidogrel
- ACEI for heart failure.
- routine of oral beta blockers
- warfarin for at risk of embolism.
- Statins( lipid-lowering therapy )
- Amiodarone/Sotalol (Tachyarrhythmias)
- Heparin, Anticoagulants (For thromboembolism)
Prognosis.
- Young patients, adequate treatment and with secondary prophylaxis, good prognosis.
- most patient can resume working after abt 1 month after rehabilitation

15) Essential hypertension and secondary hypertension

Essential hypertension
a) Definition
- elevated arterial pressure (sys: >140, diastolic> 90).
b) Epidemiology
- > 50%
- prevalence in man
- Highest in Germany
- After 50 years of age, more than 50% have hypertension.
- 20-30% of adult population.
- black Africans among which 40-45% of adults are affected.
c) Etiology
- Genetic - Stress.
- Diet- high salt, alcohol - Dyslipidemia
- Obesity - Smoking
- Racial: African American - Diabetus mellitus
d) Pathogenesis
1. Abnormal cardiac and peripheral hemodynamics - elevation in cardiac output, total peripheral resistance,
or both.
2. Impaired pressure natriuresis - In normal, elevation in blood pressure leads to alteration intrarenal
hemodynamics and physical forces results in natriuresis, causes diuresis, decrease total extracellular
volume, and fall in blood pressure. In hypertension, kidney fails, natriuresis is impaired.
3. Baroreceptor in carotid arteries and aorta to ―reset‖ higher pressures toward lower blood pressure.
4. Abnormal sodium transport - sympathetic simulation, proliferation of smooth muscle of myocardium and
vessels
5. Stimulation of sympathetic nervous system - increase in cardiac output and minute volume
6. Action of renin-angiotensin system – stimulates sympathetic activity, increase in aldosterone production,
sodium retention, vasoconstriction, increase in peripheral resistance
7. Deficiency of vasodilator substance
8. Endothelial dysbalance between vasoconstrictor and vasodilator substances
Vasoconstrictors: endothelin, angiotensin II, thromboxane, prostaglandin F and norepinephine
Vasodilators: nitrous oxide, postacyin, bradykinin, arial natriuretic peptide and prostaglandin E2
Pressor: SNS, Ag-renin system, Aldosterone, endothelin
Counter: Kalikrein-kinin system, Prostaglandin, Prostacyclin E, Baroreflex system
e) Classification
- degree, stages and stratification
31
 - Primary (essential) hypertension is hypertension that has no known cause
- Secondary hpt is diagnosable disease and accounts for the remainder of cases of hypertension.
f) Clinical picture according to stages
1. Stage 1
- Head –headache occiput, diffuse or temporal; vertigo
- Heart –tachycardia, extrabeats, pain
2. Stage 2: got changes in organ target (Hypertrophy of LV, changes in heart, microalbunemia fr kidney,
hypertrophy- angiopathy from brain, albuminuria, spasm of artery and enlargement of vein in brain)
All previous complaints, plus decreased eyesight due to angiopathy of retina and enlarged left heart
border
3. Stage 3: Complication from organ target
- Brain: encephalopathy insult, stroke
- Heart: Ischemic heart disease, M.I, HF
- Kidney: kidney insufficiency, Kidney failure
All stages possible plus paralysis, decreased mental function. Severe Chest pain, arrhythmia. Oedema,
pulmonary congestion, peripheral cyanosis, fatigue, weakness. Renal oedema
g) Investigation
1. Obj : measure BP
2. Percussion of heart: enlargement of Left heart borders
3. Aus: systolic murmur at apex, accentuation of S2 above aorta
4. Blood analysis : K, Ca, Na, cholesterol, creatinine, protein, sugar level
5. biochem changes - Na+, K+, Ca2+, cholesterol, creatinine, protein
6. Urine analysis: creatine. Sugar level
7. ECG: LV hypertrophy
8. X ray- LV hypertrophy, heart enlargement
9. Echocardiography
10. Specific tests:
- Brain- rheography (cerebral vessels), encephalography, electroencephalogram
- Kidney- Zimnitsky test, Nichiparenko, US, contrast angiography, contrast urography, biopsy
- Consult neuropathologist, ophthalmologist
- Hormone levels – thyroid, glucocoticoids, cathecolamines
h) Complications
1. CNS - Stroke, encephalopathy, Subarachnoid HR, Brain vessels spasm and enlarged veins of brain.
2. Retina:
- Grade 1: Mild arteriolar narrowing
- Grade 2: >marked narrowing + appearance of arterio-venous nipping when thickened retinal aa pass
over retina
- Grade 3: grade 2 + flame-shaped HR & soft cotton wool exudates
- Grade 4: G3 + papiloedema
3. Heart: LV hypertrophy, IHD, heart failure, Coronary artery disease
4. Kidney: Proteinuria, renal failure, microalbuminuria
i) Prophylaxis of complications
- Treatment by pharmalogical & non pharmalogical to maintain the level of arterial Pressure.
- Dietary: low salt, sugar, fat and cholesterol
- Adequate water intake, rest
- Lifestyle: Low stress, no smoking, exercise.
j) Treatment according to stages & pathogenetic
To reduce the diastolic blood pressure < 90 mm Hg and the systolic blood pressure <150 mm Hg.
Non pharmaco:
- Sodium < 2 g/day. Diet- diet no 10- low sodium, low fat and low water.
32
- Physical- running and swimming are good. Contraindicated heavy or stressful activities.
- Weight reduction in obese patients
- Limitation of alcohol consumption. no smoking

Pharmaco
According to the stages.
- Stage I: β blockers or diuretics.
- Stage II: β blockers + diuretics
- Stage III: β blockers + diuretics + calcium antagonist
- Stage IV: Diuretics + β blockers + calcium antagonist + ACE inhibitor
1. no risk factor
I - Life-style change only
II and III stage - Life style change and medication
2. Have at least 1 risk factor excluding DM
I – life style change only (medication in consideration)
II, III – life style change and medication
3. Have DM with / w/o target organ damage and existing heart disease
I, II, III – life style change and medication
According to pathogenesis
- If patient has tachycardia, high systolic, emotional activity- β blockers
- If hyporenin form of hypertension- diuretics
- If high diastolic arterial pressure- calcium channel blockers
- renal (activated renin-Ag activity) – ACE inhibitor : lozartan
Pharmacologic measures.
1. Diuretic
- Thiazide diuretics (hydrochlorothiazide, chlorothiazide, metolazone)
- loop diuretics (furosemide, bumetanide, torsem ide, ethacrynic acid).
- Potassium-sparing diuretics (amiloride, triamterene)
- Spironolactone
2. β blockers: Propranolol, nadolol, metoprolol, atenolol, timolol, betaxolol, carteolol, pindolol, carvedilol,
acebutolol, and Labetalol
3. Centrally acting adrenergic antagonists: Methyldopa, clonidine, guanabenz, and guanfacine, clofillin
4. Peripherally acting sympathetic antagonist: reserpine and guanethicine.
5. Calcium channel antagonists: dihydropyridines (nifedipine, nicardipine, isradipine, felodipine,
nimodipine, amlodipine, nitrendipine), diltiazem, and verapamil
6. Direct vasodilators: l-hydralazine and rhinoxidil
7. ACE inhibitor : Captopril, enalapril, fosinopril, benazepril, quinapril, ramipril, and Eosinopril
8. α blockers (Prazosin)
k) Prognosis
- If treatment is adequate- prognosis is good
- If development of crisis & no treatment- prognosis is bad
- 1st and 2nd stages, adequate treatment and stop of risk factors, prognosis for life is positive and prognosis
for work is good or moderately decreased depending on degree.
- 3rd stage, prognosis for life is moderate and prognosis for work is poor.

Secondary hypertension
a) Definition - arterial P rises as a symptom of some other disease.
b) Etiological group of causes
1. Central/ cerebral - trauma, tumors, infection: meningitis, encephalitis, focal ischemic lesions
2. Hemodynamics art HPT
33
- aortic insufficiency
- artherosclerosis of aorta
- congenital disorders ( coarctation of aorta, AV block, aortic disorder )
- Stenosed carotid and vertebral arteries
3. Drug art HPT
- ephedrine containing drugs
- narcotics
- Coffee, tea (Caffeine containing drugs or food)
- Contraceptives: oestrogen, progesterone containing
- Glucocorticoids
4. Endocrine HPT
- Hyperthyroidism, hypothyroidism
- Acromegaly- Tumor in hypophysis
- Cushing‘s disease/ syndrome – suprarenal tumors
- Conn‘s syndrome – results of tumor wh produce aldosterone
- Pheochromocytoma
5. Renal HPT
- Parenchymal : Glomerulonephritis, Interstitial nephritis, Amyloidosis, Pyelonephritis, polycystosis,
Nephrolithiasis, hydronephrosis, TB, tumors, rheumatic disorders: nodulus periarteritis.
hypoplastic/dystopic kidney, abnormal renal arteries, Lithiasis
- Renovascular : stenosis, fistules, muscular dysplasia, aneurysm, atherosclerotic, fibromuscular disposing,
thromboembolism, congenital disorder of vessels, tumor near vessels, aorta arteritis.
c) Properties of clinic
- Very high artery Pressure
- No effect of antihypertensive Tx . (need to treat primary disease)
- High arterial press: Headache, Vertigo, Spots before the eyes, tinnitus, Pain in the heart
- Stable arterial HT: Hypertrophy of LV, Accentuated S2 over aorta, Changes in optic fundus
- General clinical symptoms as in essential hypertension.
- In addition specific symptoms associated to the etiology.
Endocrine - Thyrotoxicosis, Hypercorticism, Signs of acromegalia
Renal - Pitting oedema, Acites, Pain and tenderness over the lumbar region, Changes in urine quality.
Neurological - Stupor, sopor or coma. Meningeal signs, Phantom smells in case of tumour
Haemodynamic - Changes in heart sounds, Tachycardia
d) Investigation
Same as primary hypertension
e) Differential diagnosis from essential type
Primary Secondary
No causes has a visible cause:
- coarctation of heart, valve disorders,
- Kidney disorders- face edema, urine changes
- CNS- trauma, brain inflammation
In anamnesis : got ↑ BP In anamnesis : no ↑ BP
↑ level of both sys & diast bp Only ↑ of systolic usually
Secondary:
- pt normally in young age
- pt with family history
- crisis are typical
- treatment give +ve result

16) Cardiomyopathies
34
Classification
Clinical classification - Obstructive
a. Dilated: L and/or R ventricular enlargement, impaired systolic function of the left and/or right ventricle,
CHF, arrhythmias, emboli. no abnormal loading conditions eg HT, valve diseases
b. restrictive: endomyocardial scarring or myocardial infiltration resulting in restriction to L and/or R
ventricular filling
c. Hypertrophic: disproportionate L ventricular hypertrophy, typically involving septum more than free wall,
with or without an intraventricular systolic pressure gradient; usually nondilated L ventricular cavity.
disorganization of cardiac myocytes and myofibrils occur
Primary myocardial involvement
- idiopathic (dilated, restrictive, hypertrophic)
- familial (dilated, restrictive, hypertrophic)
- eosinophilic endomyocardial disease (restrictive)
- endomyocardial fibrosis (restrictive)
Secondary myocardial involvement
a. Infective (dilated) - systemic lupus erythematosus
- viral myocarditis - polyarteritis nodosa
- bacterial myocarditis - rheumatoid arthritis
- fungal myocarditis - progressive systemic sclerosis
- protozoal myocarditis - dermatomyositis
- metazoal myocarditis f. Infiltrations and granulomas (restrictive,
- spirochetal dilated)
- rickettsial - amyloidosis
b. Metabolic (dilated) - sarcoidosis
c. Familial storage disease (dilated, restrictive) - malignancy
- glycogen storage disease g. Neuromuscular (dilated)
- mucopolysaccharidoses - muscular dystrophy
- hemochromatosis - myotonic dystrophy
- Fabry‘s disease - Friedreich‘s ataxia (hypertrophic, dilated)
d. Deficiency (dilated) h. Sensitivity and toxic reactions (dilated)
- electrolytes - alcohol, radiation, drugs
- nutritional i. Peripartum heart disease (dilated)
e. Connective tissue disorders (dilated)

Obstructive Hypertrophic cardiomyopathy

a) Pathogenesis
- Characterized by variable myocardial hypertrophy, involving the interventricular septum &
disorganization of cardiac myocytes & myofibrils.
- hypertrophy, systolic anterior motion of the anterior mitral valve leaflet & rapid ventricular ejection
causing dynamic left ventricular outflow tract obstruction
- May also due to familial, autosomal dominant & mutations in the genes encoding sarcometric proteins.
b) Clinical symptoms
- Usually asymptomatic or mild
- Chest pain, dyspnoea, syncope / presyncope (with exertion), cardiac arrhythmias & sudden death
- Fatigue, left ventricular emptying is impaired, compounded by outflow obstruction.
- Systolic good until progressive dilatation occur.
- Atrial fibrillation
- Double or triple apical precordial impulse, a rapidly rising carotid arterial pulse, and a 4th heart sound
- systolic murmur, harsh, diamond-shaped, after 1st heart sound. at lower L sternal border & apex
- Pansystolic murmur at mitral regurgitation
35
c) Investigation
- ECG - left ventricular hypertrophy, ST & T wave changes. Widespread, deep, broad Q waves suggest old
MI. Many have both atrial and ventricular arrhythmias.
- Echocardiogram - asymmetric left ventricular hypertrophy, systolic anterior motion of the mitral valve,
vigorously contracting ventricle, Septum with unusual ―ground-glass‖ appearance. LV cavity is small,
vigorous posterior wall motion, reduced septal excursion
- Pedigree analysis - autosomal dominant inheritance
- Exercise test & ECG ambulatory recording
- CXR: mild to moderate increase in cardiac silhouette
- Radionuclide scintigraphy with thalium 201: reveal myocardial perfusion defects
d) Treatment
- Beta blockers, verapamil (to treat chest pain)
- disopyramide for obstruction, to reduce LV contractility and outflow pressure gradient
- amiodarone: reducing frequency of supraventricular & life-threatening ventricular arrhythmias
- verapamil and diltiazem - reduce stiffness of ventricle, reduce the elevated diastolic pressures, increase
exercise tolerance, and reduce severity of outflow tract pressure gradients
- combination beta blockers and calcium antagonists used with caution
- dehydration avoided, diuretics used with caution
- AVOID vasodilators, nifedipine
- Resection of septal myocardium
- Implantable defibrillators
- strenuous activity should be prohibited
e) Complications
- Hyperthrophy in diff portion of L ventricle
- Ventricular septum thickness disproportionally increased
- Disproportion of apex or L vent free wall
- Disarrangement cardiac muscle cell
f) Prognosis
- improvement of symptoms with time
- LV systolic impairment, wall thinning, and chamber enlargement occurs over time
- predictors of sudden death include age less than 30 yrs, ventricular tachycardia on ambulatory monitoring,
marked ventricular hypertrophy, syncope (esp in children), genetic mutations associated with an
increased risk, and a family history of sudden death

Dilated cardiomyopathy
a) Pathogenesis
- majority no cause is found - ‗idiopathic‘; familial inheritance is usually autosomal dominant; probably
myocardial damage produced by toxic, metabolic, or infectious agents, & late sequel of acute viral
myocarditis mediated through an immunologic mechanism
- So, L or R ventricular systolic function is impaired, progressive cardiac enlargement, remodeling process
produce symptoms of CHF. mural thrombi may be present in the LV apex
- reversible form may be with alcohol abuse, pregnancy, selenium deficiency, hypophosphatemia,
hypocalcemia, thyroid disease, cocaine use, and chronic uncontrolled tachycardia
b) Clinical symptoms
- Presentation of congestive heart failure
- Initial presentation is with sudden cardiac death.
- Syncope, dyspnea during slight physical extertion/rest, Suffocation and cardiac pain
- Borders of heart displaced to right, upwards and left
- Heart sounds at apex dulled, 2nd sound over pulmo trunk is accentuated, gallop rhythm, systolic murmur
- Pulse is small and fast
36
- Arterial pressure decreased (usually)

c) Investigation
- Chest X-ray - enlargement of cardiac silhouette due to LV enlargement; lung fields: pulmonary venous
HT and interstitial or alveolar edema
- ECG - diffuse non-specific ST segment & T wave changes. Sinus tachycardia, conduction abnormalities
& arrhythmias. atrial fibrillation, ventricular arrhythmias, L atrial abnormality,
- Echocardiography and radionuclide ventriculography - LV dilatation, normal or minimally thickened or
thinned walls, and systolic dysfunction (reduced ejection fraction)
- angiography: dilated, diffusely hypokinetic LV, some degree of mitral regurgitation
d) Treatment
- salt restriction, ACEI, diuretics (not be used in isolation), and digitalis
- beta-adrenergic blocker prevent arrhythmias
- myocardial inflammation treated with immunosuppressive therapy
- alcohol should be avoided
- insertion of an implantable cardioverter-defibrillator in patients with malignant arrhythmias
- cardiac transplantation considered in ptts with advanced disease
e) Complications
- Congestive heart failure.
- Sudden cardiac death.
- Ventricular tachy or bradyarrhytmia
f) Prognosis - Positive because improvement of symptoms with time

Restrictive cardiomyopathy
a) Pathogenesis
- restricted ventricular filling, resulting in symptoms & signs of heart failure.
- Dilatation of the atria & thrombus formation occur.
- associated with amyloidosis, Loeffler‘s endocarditis, endomyocardial fibrosis, hemochromatosis,
glycogen deposition, sarcoidosis, Fabry‘s disease, the eosinophilias, and scleroderma
- The idiopathic form may be familial.
- due to abnormal diastolic function; ventricular walls excessively rigid and impede ventricular filling,
transplanted heart; and in neoplastic infiltration and myocardial fibrosis
- myocardial fibrosis, hypertrophy, or infiltration
b) Clinical symptoms
- Dyspnoea, fatigue & embolic symptoms
- Restriction to ventricular filling - elevated venous pressures, hepatic enlargement, ascites & dependant
oedema
- exercise intolerance
- enlarged, tender and pulsatile liver
- jugular venous pressure elevated or may rise with inspiration (Kussmaul‘s sign)
- heart sounds may be distant, S3 and S4 are common
- apex impulse easily palpable
- mitral regurgitation
- Friedreich‘s sign (high jugular venous pressure with diastolic collapse)
c) Investigation
- Chest X-ray: show pulmonary venous congestion. The cardiac silhouette can be normal / show
cardiomegaly & / atrial enlargement.
- Echocardiogram: symmetrical myocardial thickening & normal systolic ejection fraction, impaired
ventricular filling.
- Endomyocardial biopsy permit specific diagnosis such as amyloidosis to be made.
37
- ECG: low voltage, nonspecific ST-T wave changes and various arrhythmias
- Xray: pericardial calcification is absent
- Doppler recordings: accentuated early diastolic filling
- cardiac catheterization: decreased cardiac output, elevation of R and L ventricular end-diastolic pressures,
and a dip-and-plateau configuration of the diastolic portion of the ventricular pressure pulse. Helps
distinct from constrictive pericarditis
d) Treatment
- no specific treatment.
- Cardiac failure & embolic manifestations is treated.
- Cardiac transplantation considered in severe cases, especially the idiopathic variety.
- In primary amyloidosis, combination therapy with melpalan + prednisolone with / without colchicines
- hemochromatosis (desferoxamine has been helpful in reducing myocardial iron content)
- chronic anticoagulation to reduce the risk of embolization from the heart
e) Complications
- Cardiac enlargement.
- Congestive heart failure.
- Mural thrombi.
- Myocyte necrosis.
- Cellular infiltration.
f) Prognosis - Restrictive cardiomyopathy have a worse prognosis

17) Diseases of pericardium. Dry effusion and constrictive pericarditis

a) Pathogenesis
- pericarditis dev in the presence of rheumatism or tuberculosis
- rheumatic and tuberculous pericard are manifestations of infectious allergic process.
- some, tuberculous pericard depends on the spread of infection from lungs and tracheobronchial lymph
nodes to the pericardium.
- pericarditis develop in other infections as well eg scarlet fever, measles, influenza, or sepsis
- sometimes it dev due to transition of inflammation from the adjacent organs in pleurisy, pneumonia, MI,
and injuries to heart and uraemia.
Constrictive pericarditis
- without accumulation of effusion .
- promote lesion of the valvular apparatus
- thickening of pericardium and calcification produce a rigid membrane around the heart
- scar affect the orifice of the vena cave and the fibrous membrane of the liver
- ventricles are quickly filled with blood at the beginning of diastole .
- end of diastole the blood flow in to the right ventricles becomes abruptly upset.
- so blood pressure drops in jugular vein during ventricular filling and end diastolic pressure increase .
- bp increase in the vein of the greater circulation causing enlargement of the liver, ascites and edema
b) Clinical picture
Dry pericarditis:
- Chest pain that is
- Pericardial friction rub (cardinal sign),
Dry effusion
- 1st stage -heart pain - substernal and sharp, increase body temperature, dyspnoea
pain at heart apex, bottom of sternum, radiate to neck, left shoulder, epigastrium
intensive during respiration and in sitting position
- 2nd stage - friction rub heard at lower left sternum, leathery triphasic sound has 3 component
1st heard before 1st heart sound
2nd during systole
38
 3rd at the beginning and middle of diastole
Pericardial effusion:
- Pressing sensation in chest and pain in heart
- Dyspnea and dysphagia
- Fever
- edematous, skin cyanotic and pallied
- Neck veins are swollen
- Orthopnea
- soft heart sounds
- Enlargement of cardiac dullness
Constrictive pericarditis:
- ascites, edema, hepatomegaly, jugular venous distension, breathlessness, pulmonary distension, sinus
tachycardia
- Signs of impaired ventricular filling (Kussmaul‘s sign)
- Friedreich‘s sign
- Pulsus paradoxus
- Fatigue and exercise intolerance
- Atrial fibrillation and loud 3rd sound
c) Investigation
Dry pericarditis:
- ECG -During 1st few weeks, ST elevation. AVR, V1 show ST depression. Later ST segment normalize
and T wave inversion present. sinus tachycardia.
- Blood analysis: Leucocytosis - lymphocytosis, increase of cardiac enzymes
- Chest x-ray - large globular or pear shaped heart
- Doppler sound-increase flow in tricuspid and pulmonary valves and decrease in mitral flow during
inspiration
Pericardial effusion:
- ECG shows low voltages
- Chest x ray - large globular or pear shaped heart
- EchoCG - demonstrating effusion and right ventricular collapse during late diastole
- Doppler - increased flow through tricuspid and pulmo valves
- MRI – detect hemopericardium
Constrictive pericarditis:
- Chest x-ray: small heart with obvious calcification of pericardium on lateral film
- ECG: low QRS voltage and T wave inversion, high R in 2nd lead and P in v1 is similar to p-mitrale
- EchoCG: thickened pericardium with calcification over right heart, ventricular cavities are small and
dilated atria
- Cardiac catheterization and MRI: diastolic pressure equal in all 4 chamber.
d) Treatment
Dry pericarditis:
- Anti-inflammatory drugs (aspirin)
- Indometacin, ibuprofen for symptom relief.
- corticosteroids eg prednisalone
- Azathioprine, colchicines in cases of corticort-resistance
- pericardiocentesis when malignant, tuberculosis or a purulent pericarditis is suspected.
Pericardial effusion:
- Pericardiocentesis
- In cases of reaccumulation, pericardial fenestration via balloon pericardiotomy under local anesthesia or
by conventional surgical approach
Constrictive pericarditis: Surgical removal of thickened pericardium.
39
18) Pneumonia
a) Classification
Pneumonia is acute inflammatory process of infectious origin affecting the pulmonary acinus.
1. International - mixed
- Community acquired pneumonia / typical 5. According to severity:
- Hospital acquired (nosocomial) - mild.
pneumonia - moderate.
- Aspiration pneumonia - severe.
- Pneumonia in immunocompromised 6. According to morphological stage:
host(including AIDS) - congestion.
- Atypical pneumonia - hepatization.
2. according to pathogenesis: - resolution.
- primary- due to primary etiology such as 7. According to etiology:
bacteria & virus. (typical , atypical) - typical : pneumococcal
- secondary- at height of chronic bronchitis. - atypical : mycoplasma, legionella,
after operations & ventilation. chlamydiae, coxiella burnetti, ricketsia
complication of other disease CVS , - viral and Q fever
disease of blood , metabolic , superimpose - parasitic.
chronic disease of respiratory system - fungal.
3. According to localization: - atypical microbes.
- 1 sided- can be total, lobal, segemental, - aspiration.
sublobular & central. - Immune deficiency.
- 2 sided. - Radiotherapy
- localized (whole of one or more lobes) - Allergic mechanism
- diffuse ( lobules) - chemical and physical factors
4. according clinico morphological signs 8. According to course
- parenchymatous ( lobe, lobular) - acute
- interstitial - prolonged
b) Main syndromes
1. Syndrome of infiltration of lung tissue.
- Lung tissue is infiltrated by cells & exudates.
- Percussion- dull tympanic sound.
- X ray - white homogenous shadow.
2. Syndrome of intoxication.
- Fever. Weakness. Athralgia & myalgia. Headache, Dyspnea, Palpitation, Sleeplessness
3. Consolidation syndrome
4. General inflammation - Increase temperature, Chill, Leucocytosis
5. Acute respiratory insufficiency
6. Respiratory failure – Dyspnea
7. Affection of the other organs / In atypical causes
a. Liver Syndrome.
- Short duration of icterus.
- Pain in liver palpation.
- Increased ALT & ALT.
b. Kidney syndrome.
- toxic renal affection.
- proteins, RBC & leucocytes in urine.
c. GIT syndrome. - Diarrhea, nausea & vomiting.
d. Brain syndrome. - Encephalopathy. Psycosis.
e. Heart syndrome. - Myocardial dystrophy, myocarditis & pericarditis.
40
c) Diagnostic criteria
1. Blood 3. X-ray
- Leukocytosis Shift to the left - Infiltration of lung
- Increase neutrophil - Decrease transparency on affected area
- Disproteinemia - Moderate consolidation
- Increase C protein - Physiological emphysema
- Increase fibrinogen 4. ECG
2. Urine - Moderate cor pulmonale
- Hypovolemia - Tachycardia
- Proteinuria - Enlargement of heart
- Microerythrocyturia 5. Sputum
- Increase specific gravity - Rusty with blood
- Indirect jaundice (3rd-4th days)
d) Differential diagnosis of pulmonary infiltration
- Part of lung enlargement of volume
- Decrease perfusion
- X ray decrease transparency with 1 lobe or 2
- Sometimes homogenous but less patchy
- Border line of infiltration is cloudy
- Root of pneumonia is enlarge

Primary pneumonia
a) Epidemiology
- community acquired or hospital acquired - AIDS over 50%
- Incidence: 1-3/1000 population - Male > female 50-55%
- Mortality: 10% (patients admitted to - Age > 50-55%
hospital) - Season of the year and geographic
- 10,000 people 7-14 cases location are other predictor of etiology
- 5 years – 10%
b) Etiology
- bacteria & viruses.
- Bacteria: gram –ve & +ve.-. E. coli, S. pneumonia. Pneumococcus, Hemophilus influenza,
Legionella, Klebsiella
- Viruses - influenza, parainfluenza & measles.
- Weather, occupational
c) Pathogenesis
- pathogen reach lower respiratory tract in sufficient numbers or virulence.
- Possible routes - aspiration, microaspiration, aerosolization, hematogenous or direct spread
- Microaspiration - colonization bacteria at oropharyngeal, secretion aspirated into lungs. Aspiration -
in postoperative or coma patients. Hematogenous spread by endocarditis & infections.
- virulent factors overcome the host defense causes pneumonia. common when the patient immune
system is decreased.
d) Clinical picture of lobular pneumonia
- Lobular pneumonia same as - Moderate hyperemia of the face; cyanosis
bronchopneumonia. of the lips.
- Cough with sputum - Tachypnoea (25-30 per min).
- Pain in the chest - vocal fremitus – increased
- Fever remittent, irregular (subfebrile). - dull percussion sound
- Dyspnoea - decrease vesicular breathing
- vesiculobronchial or bronchial breathing,
41
 - dry / consonating moist rales, crepitation - More patchy alveolar consolidation
associated with bronchial and bronchiolar
inflammation
e) Investigations
- Blood test: mild leucocytosis, moderately increased ESR.
- Sputum: mucopurulent; leucocytes, macrophages and columnar epithelium. Bacterial flora
- X-ray: focal consolidations at least 1-2 cm in diameter

Lobar pneumonia.
Homogeneous consolidation of one ore more lobes, associated with pleural inflammation
a) Symptoms according to different pathomorphological periods
1. Congestion.
- hyperaemia of lung tissue, exudation, obstruction of capillary & stasis of blood.
- shaking chills or rigor with fever ( 39-40 C ).
- Pleuritic pain on the affected side.
- Dyspnoea. Cough is dry.
- Severe headache & pain in limbs in atypical form.
- condition is grave, confused or delirious in alcoholics, convulsions.
- fascies pneumonica- hyperaemea of cheeks on affected side, nostrils breathing, herpes nasalis &
labialis & cyanosis.
- lagging of affected side, Vocal fremitus is increased. dull tympanic sound, weak vesicular breathing,
crepitation indux & increased bronchophony.
- It lasts from 12 hours to 3 days
2. Hepatization. - Height of the disease
- Gen inspection - lagging of affected side, tachypnoea. tachycardia
- Cough & a rusty sputum in the beginning of red hepatization stage.
- In palpation there‘s increased vocal fremitus. In percussion absolute dull sound. In auscultation -
bronchiol breathing & in pleuritis - pleural friction rub. There‘s increased bronchophony, egophony.
a. Red hepatization
- Massive confluent exudation with RBC, neutrophils & fibrin filling the alveolar spaces. Lobe
appears red, firm & airless with liver like consistency
- The lobe now appears distinctly red, firm, and airless with a liver like consistency.
- Continues from 1 to 3 days
b. Gray hepatization
- progressive disintegration of RBC. Alveoli containing fibrin becomes filled with leucocytes.
- persistence of fibrosupurative exudates giving gross appearance of grayish brown & dry surface.
- Lasts from 2 to 6 days
3. Resolution
- Consolidated exudates within alveolar spaces undergoes enzymic digestion produce granular
semifluid debris that is resorbed, ingested by macrophages or coughed up.
- Cough with mucopurulent sputum, dyspnoea decreased & condition improves.
- Palpation decreased vocal fremitus. Percussion gives dulled tympanic sound.
- Auscultation weak vesicular breathing, crepitation redux & small moist bubbling rales.
b) Complications
1. Lung type - Parapneumonia or metapneumonic
- Obstruction effusion
- Pleuritis - Post pneumonia
- Acute respiratory insufficiency - Emphysema of pleura
- acute respiratory distress syndrome - empyema,
- Pleurisy - lobar collapse,
42
 - pneumothorax - Toxic hepatitis
- lung abscess - Meningoencephalopathy
2. extrapulmonary complication - septicemia,
- Infectional intoxicational shock - renal failure, nephritis
- Bacterial endocarditis - multi organ failure,
- Infection endocarditis - ectopic abscess,
- Cor pulmonale - pericarditis, myocarditis
- Cardiodystrophy - intoxication psychosis
- Meningitis

c) Etiological & pathogenetic treatment of primary pneumonia

1. etiology treatment
- antibiotic combined w sulpha drug eg: sulphadimethoxine
- penicillin.
- Groups of cephalosporins. combination with alcohol is not good.
- Aminoglycosides. Contraindication in pregnancy.
- Macrolides
- Tetracycline.
- Metronidazole.
- Florquinolone. Contraindication in young children & pregnancy.
- Chloramphenical..
- nitrofuran, furazolin.
- In resolution stage use physiotherapy.
2. pathogenic treatment
- immunomodulation preparation (interferon, levamisol, zymosan)
- patient with viral pneumonia give anti influenza n globuli
- passive immunization w hyperimmune anti-staphylococcal plasma/staphylococcal antitoxin to
patient of staphylococcal pneumonia
- Vit C,E,B n biogenic stimulant to restore nonspecific body resistance
- Broncholytic (euphyline, ephedrine)
d) Principles of antibiotic therapy
- Give antibiotics in the 1st hour.
- By the 3rd day must have positive effect. decreased intoxication, condition improves, decreased
fever & normalization of peripheral blood otherwise change antibiotics.
- If successful, duration of antibiotics given for 2 weeks.
- Unknown etiology:
penicillin + aminoglycoside
aminoglycoside + cephalosporin
e) Prognosis
Good if the treatment given is appropriate and in time.
moderate & mild pneumonia w localized inflammation ends in complete cure in 3-4weeks

Nosocomial pneumonia.
a) Etiology (klebsiella, staphylococcus)
- new episode of pneumonia occurring at least 2 days after admission to hospital.
- Etiology such as gram –ve microbes. E.g. klebsiella, staphylococcus, E. coli and proteus.
- Severe underlying disease, immunosuppression, prolonged antibiotic therapy, invasive access device
eg: intravascular catheter, pt on mechanical ventilation (at risk)
b) Pathogenesis

43
- immune system is decreased reduced by corticoid treatment in any underlying diseases, malignancy,
DM, disordered mucociliary clearance in anaestehtic & in post operative period. Presence of
endotracheal tube, nasogastric tube & mechanically ventilation.
- aspiration of nasopharyngeal, vomiting cause introduction of bacteria into respiratory tract.
- bacteremia - primary bloodstream infections, those associated with intravascular devices, infections in
medical and surgical intensive care units (ICUs) and infections by antimicrobial-resistant pathogens
- infections become manifest after 48 h.
c) Properties of clinical picture
- Klebsiella- in chronic alcoholism, DM & cirhossis. Acute beginning of symptoms with severe
intoxication syndrome & respiratory insufficiency. In CXR -changes in apex in 1 side & abscess.
- Staphylococcus- acute beginning, intoxication with high fever & lung changes. Changes in skin, joints
& brain. CXR - polysegmental infiltration with focal destruction, destroyed lung tissue causes
pyopneumothorax. In blood - leucocytosis left shift, toxic changes in neutrophils & maybe sepsis.
- Bloody jelly foul sputum, fever
- pulmonary infiltrates, purulent tracheobronchial secretions
- breathlessness
- cough
d) Complications
- lung abscess - myocarditis
- empyema - pneumothorax
- respiratory failure - empyema
- pleural effusion - pleural effusion
- septicaemia - lung collapse
- gangrene of lung - heart and lung failure
- lung bleeding - lung abscess
- pericarditis - pulm infarction
e) Treatment
- aminoglycoside IV + antipseudomonal penicillin IV or 3rd generation cephalosporin IV
- antibiotic
- vancomycin
- quinupristin-dalfopristin and linezolid
- broad spectrum antimicrobial therapy
f) Prognosis
- Prognosis is good if treatment is correct and adequate

Atypical pneumonia.
a) Etiology (chlamidia, legionella, mycoplasma, viruses)
- atypical courses which are not bacterial e.g. mycoplasma, chlamidius, virus & legionare.
- Disease of upper airways
- Malnutrition
- Alcoholism
b) Properties of clinical picture
- In atypical forms clinical picture are predominated by non lung changes.
- Chlamidia- risk factor contact with birds children in school. It has acute beginning, non productive
cough, laryngitis & pharyngitis.
- Mycoplasma- in winter & autumn & in schools. It has slow beginning, laryngitis, pharyngitis, myalgia,
hemorrhagic anemia, leucopenia & myocarditis. In CXR - lung pattern more defined.
- Legionares- risk factor contact with contaminated water. severe acute beginning & duration with
intoxication syndrome, diarrhea, Cough, Abdomen pain, Vomiting, Hypernatremia, increased liver size,

44
 icterus, increased ALT, AST, changes in urine & encephalopathy. CXR -changes in lower lung &
pleural oxidation.
- Viral- epidemic of influenza. Viral intoxication syndrome in beginning & after 3 days develop
pneumonia. leucopenia & increased lymphocytes. myocarditis & hemorrhagic pneumonia, rhinitis,
myalgia, headache. In CXR - lung is net like picture.
c) Differential diagnosis from typical form
- Typical forms caused by bacterial forms. Also clinical picture are predominated by lung signs while
atypical forms clinical picture are predominated by nonlung changes
- Sudden onset of fever, cough with purulent sputum, shortness of breath, in some cases pleuritic chest
pain; signs of pulmonary consolidation (dullness, increased fremitus, egophony, bronchial breath
sounds, and rales), radiographic abnormality.
d) Treatment
- Chlamydia- macrolides (erythromycin) & tetracycline (doxicyclin).
- Mycoplasma- no effect from penicillin & cephalosporin, so use macrolides & tetracycline.
- Legionares- absent effect from penicillin so use other antibiotics.
- Same as other type of pneumonia + antiviral (acyclovir, interferon)

19) Chronic bronchitis

a) Etiology
- Smoking
- Chemical agent
- Congenital disorders: deficiency ά1- antitrypsin, deficiency serum elastase inhibitors
- Infection: Gram (+) and (-), virus, mycoplasma, influenza
- Air pollution
- Environmental - changes of weather
- Climate: autumn and spring
- dysfunction of cilia transport, chronic inflammation with sclerosis
b) Pathogenesis
1. Problem with mucociliary transport
2. Infection develop
- infiltration of cells
- hyperproduction of mucous
- sclerotic changes in parabronchial tissue
- inflammation develops, edema, atrophy of epithelium
3. Obstruction syndrome
- Functional component –result of spasm, edema & high mucous production
- Organic component – sclerotic changes
4. development of emphysema - present problem with gas metabolism in lung
- develop increased arterial pressure in pulmonary system
- development of hypertrophy and enlargement of right atrium and ventricle of heart leading to Cor
Pulmonale
c) Classification
1. Acc to character of sputum - Distal – aseptic, obstructive with pus
- Mucous : catarrhal/ simple bronchitis - Proximal - with/without pus purulent
- Purulent : purulent bronchitis - simple, superficial
- Catarr-purulent: mixed form / 3. Acc to obstructive syndrome:
mucopurulent - Obstructive bronchitis
- Hemorrhage - Non-obstructive bronchitis
- Fibrinogen form 4. Acc to phase:
2. Acc to localization: - Relapsing
45
 - Remission - Bleeding
5. Acc to complication: - Pulmo insufficiency, hpt
- Emphysema - Bronchiectasis (secondary)
- Pneumosclerosis - Cor pulmonale
- Chronic respi failure
d) Main syndromes
1. Obstructive syndrome
- Dry cough, dry rales, expiratory dyspnea
2. Intoxication syndrome
- fever ( <38°C ), myalgia, athralgia, Loss of appetite
3. Sign of inflammation: increase temperature, leukocytosis, fibrinogen, increase ESR&CRP
e) Investigation
1. General blood analysis: leucocytosis shift to the left, ↑ ESR, erythrocytosis
2. Biochemical blood analysis: increase C protein, serous mucoid, fibrinogen
3. Sputum examination: vol, character, colour, epithelium & neutrophiles in sputum
- clinical: serum, serum-purulent, purulent
- microbial: pneumococcus, hemophilic influenze, staphylococcus
4. X-ray
- enlargement root of the lung & diffusion pneumosclerosis
- if develop emphysema, present features of emphysema
- increase transparency
5. Fibrobronchoscopy: differential diagnosis in cancer & bronchoectatic disease
6. U/S : changes in right heart in case of lung hypertension
7. ECG: right ventricle, atrium hypertrophy, R wave II,III >7mm, parodoxal S wave in V5 and V6
8. Pnemotocography: registration of rapid phase of expiration and inspiration
9. Spirometry: registration of constant volume in breathing
10. radionuclide isotope: see lung perfusion, reduction of pulm system
f) Treatment
1. Antibiotics - penicillin, cephalosporin, - IV detoxication therapy: glucose, Ringer‘s
erythromycin solution
2+
2. Correction of immune system - T-activin, 7. Ca antagonist
deucifrom 8. O2 inhalation
3. Broncholytics - xanthines: theophylline, 9. Diuretics
euphyline, methylxanthines, salbutamol, 10. Cardioglycosides
albuterol (atropine) 11. immunocorrection drugs – Thimollin
4. M-cholinoblockers, Adrenomimetics 12. α-antitripsin
5. Mucoregulators - bromixin, bronhexin 13. expectorants: mucolytics-acetylcysteine,
6. Detoxification therapy trypsin
- drink alkalines: hydration of sputum ( eg: 14. heparin
mineral water ) 15. stabilise immunity: anabol,tactirin
g) Prognosis
- Prognosis is good after adequate treatment
- Prognosis is bad only in severe cases and complications

Small airways disease

a) Etiology
- viral infection (bronchiolitis)
- cigarette smoking
- climate and air pollution
- professional factors
46
b) Pathogenesis
- bronchi are inflamed and pus is seen in the lumen
- infiltration of the walls of the bronchi and bronchioles with acute and chronic inflammatory cells
- epithelial layers become ulcerated and when the ulcers heal, squamous epithelium may replace the
columnar cells
- the inflammation leads to widespread narrowing in the small airways
- small airways affected early in the disease, initially without significant breathlessness & is
reversible
- progression leads to squamous cell metaplasia, and fibrosis of the bronchial walls
- physiological consequences in development of airflow limitation
c) Clinical symptoms of obstructive syndrome
- cough w/o sputum
- dry rales
- expiratory dyspnea
d) Investigation
1. General blood analysis - Leucocytosis shift to the left, ↑ ESR, Hemoglobin elevated
2. Blood gases - in advanced cases there is evidence of hypoxaemia and hypercapnia
3. Sputum - Present epithelium & neutrophiles in sputum
4. Sensitivity to microbe test
5. ECG - Hypertrophy of the right atrium & ventricle
6. X-Ray
- Enlargement root of the lung
- Diffusion pneumosclerosis
- If dev emphysema, present features of emphysema
- presence of bullae, severe over-inflation of the lungs with low, flattened diaphragms, and large
retrosternal air space on the lateral film. Deficiency of blood vessels in the peripheral half of the
lung fields compared with relatively easily visible proximal vessels
7. Fibrobronchoscopy - differential diagnosis with cancer & bronchoectatic disease
8. Lung functional tests - shows evidence of airflow limitation
e) Treatment
1. Antibiotics - Penicillin & cephalosporin – - IV detoxication therapy ( Glucose,
Cefaclor, Cefixime Ringer‘s solution )
2. Correction of immune system - T-activin, 9. Ca2+ antagonist
deuxiform 10. O2 inhalation
3. Broncholytics - Xanthines 11. Diuretics, cardioglycosides
4. M-cholinoblockers 12. Bronchodilators - Salbutamol, Ipratropium
5. Adrenomimetics bromide, Oxytropium bromide
6. Mucolytics - Trysin 13. Corticosteroids - prednisolone
7. Mucoregulators - Bromixin 14. α1-antitrypsin replacement
8. Detoxification therapy 15. vaccines
- Drink Alkalines ( hydration of sputum )

Copd: 2 types
Q20 f, Page 49 (first table)
1. blue bloaters: - gas exchange abnormal
- Bluish as central cyanosis, - blue,hypoxemia, carbon dioxide retention
- smoker, - secondary polycythaemia cor pulmonale:
- obstructive bronchitis since young, sclerosed lung
- barrel chest due to emphysema, 2. pink puffer:
- cough due to upper part of lung affected, - pink and puffing
47
 - Due to alpha1 antitrypsin, - no parabronchial sclerosis, no cor
- speak with puffing lips, pulmonale
- intolerance to exercise-not trained, - suffering from emphysema with little
- hypoxemia, bronchitis

20) Emphysema of the lungs

a) Etiology
- smoking
- air pollution
- hyperresponsive airways
- infections
- Primary emphysema- congenital: α1 antitrypsin deficiency, Serum elastase inhibitor deficiency
- Secondary emphysema- due to other lung pathology: chronic bronchitis, obstructive bronchus,
chronic pneumonia, chronic asthma, heavy exercise
b) Pathogenesis
1st stage : destruction of alveoli due to distension in bronchus
2nd stage : diffuse destruction and alveolar loss it elasticity
c) Classification
1. Acc to anatomy:
- Centrilobular
- Pan-acinar
- Distal
2. Acc to pathology:
- Only enlargement of air spaces
- Destroyed walls of alveolar spaces
3. According to enlargement
- Develops due to bronchial obstruction e.g. in tumours
- Develops due to changes in respiratory bronchioles.
4. According to mechanism
- Involutive emphysema of lungs- doesn‘t involve reduction of vessels (normal physiological process)
- Recurrent emphysema of the lung (compensative emphysema)- after removal of a lung or a lobe of
lung, remaining pulmonary tissue becomes emphysematous.
- Mac Cloude‘s lung- congenital emphysema of one lung
5. According to development
- Primary- due to α1 antitrypsin deficiency, deficiency of serum elastase inhibitors
- Secondary- caused by obstructive process in the lungs- 1st stage- dilatation of the alveoli
2nd stage- reduction of vessels
6. type A (pink puffer/primary) and type B (blue bloater/secondary)
7. destructive form are divided into diffuse and local
d) Clinical symptoms
Subjective
- Long history of exertional dyspnoea.
- Minimal cough and very slightly productive with mucoid sputum.
Objective
1. Inspection
- asthenic,
- Patient distressed with use of accessory muscles in respiration.
- Tachypnoea, prolonged expiration pursed lips begun with grunting sound.
- chest wall moves forward on inspiration.
- Orthopnoea position.
48
 - Neck veins dilated during expiration but quickly collapse with inspiration.
- Lower intercostal spaces retract with each inspiration.
- chest barrel form, face swell and redness of cheeks
2. Palpation
- right ventricular impulse in the subxiphoid region.
- ↑ chest rigidity
- Wide ICS
- ↓ Vocal fremitus (palpation)
- ↓ elasticity of thorax
3. Percussion
- hyperresonant. Band box sound
- Cardiac dullness is absent or diminished.
- ↑ kroenig‘s isthmus
- Increased sound in apex, decreased motility and decreased traube‘s space
4. Auscultation
- breathing sounds faint, high pitched ronchi, towards the end of expiration.
- Presystolic gallop accentuated during inspiration. Weak vesicular breathing
e) Investigation
1.Chest X-ray
- presence of bullae
- overinflation of lungs (↑ lung field)
- flattened diaphragms or lowered
- ↓ diaphragm mobility
- transparent lung field increased
- more horizontal position of the ribs
- wide ICS
2.Sputum examination
3.Lung function test
4.ECG - Cor Pulmonale ( taller P wave, Right bundle branch block )
5.CT scan, bronchoscopy and radio isotope scan
6.Respiratory function tests- spirometry- total lung capacity and respiratory volume are increased, vital
capacity is low, maximal expiratory flow rate is low.
f) Properties of type a & b
Type A Type B
( Pink Puffers ) ( Blue bloaters )
Age 60 ± 50 ±
Dyspnea severe mild
Cough After dyspnea Before dyspnea
Sputum Scanty, mucoid ( little ) Copious, purulent
Bronchial infections Less frequent More frequent
Res insuff episodes Often terminal episodes
Hyperinflation, bullae changes, ↑ bronchovesicular marking,
X-ray
small heart large heart
Chronic PCO2 35-40 50-60
Chronic PO2 65-75 45-60
Ht 35-45 50-55
Constitution Asthenia Hypersthenic
Cyanosis Absent Present

49
 Rales Absent ( no changes in bronchi ) Present ( changes in bronchi )
Erythrocytosis absent present
O2 level Normal or ↓ in physical exertion ↑
Normal because no changes in
Ht present
erythrocytes

Criteria Type A (primary emphysema) Type B (secondary

pink puffer emphysema) blue blotter
Constitution Asthenic Hypersthenic
Mass Decreased Increased
Breathing character Weak vesicular breathing Harsh breathing with rales
Tidal volume Small Large
Physical activity More severely decreased Less decreased
elastic recoils decreased increased
Hypoxia Only on exersion At rest also
Complications e.g. heart Develop later Develop early
decompensation, cor pulmonale

21) Bronchial asthma

chronic aseptic relapsing diffuse inflammatory of small airways characterized by reversible air flow
limitation and bronchial obstruction due to hyperresponsiveness of tracheobronchial tree to intrinsic and
extrinsic stimuli.
a) Epidemiology
- affect 10-15% of population
- in adult 2-5% both sex
- in children 5-10% with ratio male to female 1:2
- occurs before age 10 and 1/3 of cases before age 40
b) Etiology
1. Allergens - Drugs (beta antagonist, ACEI‘s, grps
- Home (all kinds of cosmetics, perfume) of prozevin)
- Epidermal (cats, dogs, birds) 2. Pharmacological stimuli
- Insects 3. Environmental and air pollution
- Fungal 4. Occupational factors
- Microbes and virus 5. Infections
- Food (orange, chicken eggs, seafood) 6. Exercise
7. Emotional stress
Predisposing:
- Genetic factors
- allergic factors eg vasomotor rhinitis, Quincke‘s edema, migraine, increase IgE
- Increase level of eosinophils
c) Classification
1. according origin - immunological
- extrinsic - non immunological
- intrinsic 4. International
2. according to phase a. Primary allergic asthma
- exacerbation - allergic bronchus asthma
- aggravating - allergic rhinitis
- remission - atopic asthma
3. according forms: - exogenous allergic asthma

50
 - pallen dependent variant - status asthmaticus
b. non-allergic asthma 5. according severity
- latrogenic asthma - mild
- endogenic- hormonal dependent - moderate
- mixed - severe
- asthma of unknown cause
d) Different pathogenetic variants
According to Gell Coombs, 3 take part in BA:
- IgE mediated (Anaphylactic)
- Immune complex mediated
- Delayed hypersensitivity
1. Atopic/ immunological variant:
a. immune stage
- exposure to allergens, cause formation Ig E against antigen on mast cells. It cause disbalance of
immune system and decrease Ts activity. Sensitization of bronchi occurs.
b. Biochemical stage
- exposure to allergen again cause formation of Ag-Ab mast cell complex and release of preformed
mediators histamine and serotonin.
c. Pathphysiological stage
i. immediate type
- anaphylactic Ag-Ab reaction due to release of histamine and serotonin.
- this cause immediate bronchoconstriction
ii. delayed reaction
- develop due to synthesis and release of mediators from other cells
- activation of eosinophils will cause release of bioactive substances:
lipid mediatory
oxygen radicals
granules - kinins, leukotrines, eosinophil.
- activation of these bioactive substances cause:
epithelial shedding
increase permeability and microvascular leakage lead to congestion of vessels and exudation.
T lymphocyte activation
- inflammatory mediators cause:
congestion of blood vessels
exudation of plasma into lumen
contributing of mucous plugging
decrease mucociliary clearance
release of kinins and increase vascular permeability
edema of wall facilitates epithelial damage.
2. Non atopic variant:
a. nervous mechanism
- vagal hypertonia. Absolute vagotonia of bronchus and disbalance of autonomic nervous system
- relative hypertonia with relative changes in vagal system or decrease sympathetic nervous activity.
- disbalance of nervous system cause dryness of bronchial wall and trigger intensive activity of
smooth muscles. It lead to increase production of mucus and spasm of smooth muscles wall.
b. Dyshormonal mechanism
i. syndrome of adrenergic disbalance
- increase production of glucocorticosteroids.
- increase reactivity of alpha receptors and decrease activity of beta receptors.
ii. syndrome of primary dyshormonal disbalance
51
 - increase glucocorticosteroids production
- increase production of PGF2alpha
- it lead to hypersensitivity of receptors of bronchoconstriction.
iii. thyroid hormone
- increase of thyroid hormone production
- increase production of alpha receptor mediators and cause spasm of bronchial wall smooth muscles.

Bronchial asthma attack

a) Clinical symptoms
- Attack in second half of night. 1. Beginning/Initial
- Sudden attack of asphyxia and expiratory - Nasal raining
dyspnea. - Emotional changes
- Non productive cough, headache, - Cough
dizziness. - Itching
- Maximum respiration with hyperinflated - Changes of smell/taste
chest. 2. During attack
- Use of accessory respiratory muscles. - Expiratory dyspnea
- Respiratory acidosis - Orthopnea/Tripod posture
- Tachypnea, tachycardia, increase BP - Central cyanosis
- Pale color of skin - Distant rales
- Polyphonic wheezes 3. Stop of attack:
- Percussion- decrease vocal fremitus, band - Big sputum volume
box sound - Stop of dyspnea
- Auscultation- decrease vesicular breathing, - Weakness
dry rales - Sleepy
b) Emergency care
- Inhalation short activating beta-2 symphatomimetics
- 10 ml, 2.4% solution theophylline
- IV glucorticoid eg prednisalone
- Inhalation glucocorticoid
- Oxygen therapy
- Inhalation of beta agonist- salbutonol, xanthinine derivatives
- systemic corticosteroids
- 5% glucose infusion 500ml- 1L
- monitoring of arterial blood gases.

Extrinsic bronchial asthma

- known as atopic or allergic type of asthma
a) Etiology
- hypersensitivity of airway to various allergens.
- exposure to home dust with various fungal spores, bacteria
- contact with domestic animals- fur and feaces
- specific food intake- fish, egg, milk, wheat
- specific drugs- aspirin
- exposure to occupational dusts and chemicals
- pollen grains
- pseudoallergic variant
b) Immunologic mechanism
Q21 d, page 51– Atopic/ immunological variant
c) Clinical picture
52
 - Page 52, subQ a – left column
- attack occurs immediately after exposure to allergen
- edematic face
- Forced posture of body with hands on the edge of bed and shoulders are fixed.
d) Investigation
1. Blood test- eosinophilia, lymphocytosis
2. serological test- increase level of Ig E
3. X-ray of chest- normal transparency with signs of hyperinflation and signs of pneumothorax
4. sputum analysis- eosinophils, chancat Leydon crystals, and Churshman spirals
5. spirogram- alteration of PEFR, FEV, VC of respiration
6. Arterial blood gases analysis- decrease in PO2 and PCO2
7. skin allergy test- positive result
8. ECG- cor pulmonale

Intrinsic bronchial asthma

- late onset of asthma, allergens don‘t play role, occur at any age in non- atopic individuals
a) Etiology
1. respiratory infections
2. emotional overstrain
3. exposure to cold air
4. environmental or occupational factors
b) Pathogenesis
Q21 d, page 51 – non-atopic type
c) Clinical picture
- same as extrinsic, but attack develop gradually not sudden attack
- Page 52, subQ a – left column
d) Investigation
- same as in extrinsic but negative skin allergy test.
Extrinsic Intrinsic
Age Young pts(<5) Older pts (>45)
Specific attacks Present Absent
Changes btw attacks Absent Present
Hyposensibilization Effective Not effective
reaction
Disorders Migraine, vasomotor rhinitis, Chronic disease of resp sys
Quincke‘s edema e.g. chronic bronchitis, relapsing
pneumonia, viral infections, rhinitis
with relapsing
Prognosis Better because stop allergen Worse because mech of dev of disease
contact, stop disease stay in pt all time

Differential diagnosis of bronchial & cardiac asthma

Character Bronchial Asthma
Definition Dyspnea episodes accompanied by
wheezing resulting fr Narrowing of
bronchi due to bronchospasmas a result
of hyperresponsiveness of bronchial
smooth muscle. Wheezes are distant
History Previous periodic attacks of asthma-
53
Cardiac Asthma
Dyspnea episodes accompanied or not by
wheezing occurring in associated with
pulm congestion/edema
Etio: Various heart disease- congenital
heart disease, valvular disease, rheumatic
disease, thromboembolism
Cardiac risk factors (diabetes, HT,
 family history of allergic diseases
smoking)-previous history of angina. MI
(eczema, rhinitis, urticaria) or valvular heart disease- infectious
endocarditis
Time of Usually in early morning Usually in middle of night (orthopnea
onset/Age Middle aged/ young people and paroxysmal nocturnal dyspnea)
Middle aged, elderly-maybe in young
(congenital)
Symptoms Expiratory dyspnea and cough with Exp and insp dyspnea and cough with
expec of small sticky, stringy sputum expectoration of foamy, watery frothy
secretion, maybe blood stained
Signs Tripod posture Orthopnea (forced posture), normal chest,
Chest barrel shaped or pigeon asphyxia
Only prolonged exp Prolonged both in insp and exp (half
sitting position
Chest shape Barrel chest Normal chest
Ausc Wheezing > prominent than crepitation Crepitation (base of lung) > prominent
than wheezing
CVS exam no cardiomegaly (except advanced Cardiomegaly with heaving apex beat-
stages with RV failure-dt pulm HT cor raised JVP, pedal edema, gallop rhythm,
pulmonale) murmur, decreased S1 and BP,
tachycardia
If affection of chambers, valves give
murmurs (org/func)
Chest X ray Normal or hyperinflation Cardiomegaly with prominent pulm
artery shadow
ECG Sinus tachycardia LV hypertrophy
P-pulmonale LA hypertrophy
RV hypertrophy MI
EchoCG Normal/enlarged RV Systolic/diastolic dysfunc/congenital or
valvular lesions
Pulm func Obstructive pattern
test
Response to Best to bronchodilators Nitrates, diuretics, ACE-I‘s
treament

Basic treatment according to steps

1. 1st: Stop contact with origin, and use inhalants of beta-2 agonists (ventalin) and NSAIDS (intal, keto)
2. 2nd: Inhalation beta-2 agonists (short acting) every day and anti-inflammatory drugs eg intal, tyled
3. 3rd: All drugs in 2nd step + inhalation of glucocorticosteroids 200-300microgramms eg becodisk +
bronchodilators (long activating) eg salmetarol
4. 4th: All drugs in 3rd step + inhalation of glucocorticosteroids 800-1200microgramms + bronchodilators
(long activating) + systemic/parallel glucocorticoids.

Complications
- Pneumodiastinum - Acute respiratory failure
- Emphysema - Status asthmaticus
- Pneumopericardium - Pneumothorax , acute emphysema
- Subarachnoid hemorrhage - Thromboembolism of pulmonary artery
- Cor pulmonale, acute right heart failure - Associated lung infections

54
 - Exhaustion and dehydration- shock - Growth retardation in children

Metabolic & anaphylactic types of severe asthma

- Anaphylactic- short, acute term
- Metabolic (anaphylactoid) – long term
a) Pathogenesis
There are 3 stages of immune reaction:
1. 1st: sensitization (involves primary exposure of Ag and production of Atb)
2. 2nd : pathochemical (involves 2ndary exposure of Ag and release of mediators)
3. 3rd: pathophysiological (result of mediator actions on resp system)
Mediators:
- Leucotrienes
- Protein mediators (that increase vascular perm)
- PGD2 (bronchoconst, vasodilators)
- Eosinophilic chemotaxic factors
- Platlet activiating factors
- Histamine
3 main mechanisms to airflow obs in BA:
- Edema of wall of respiratory system
- Bronchospasm
- Mucous oversecretion
b) Diagnostic criteria
- Blood picture (eosinophilia, leucocytosis)
- Sputum (has eosinophils, Kurshmann‘s spirals, Charcot-Leyden crystals)
- Spirometry (decreased FVC, FEV:FVC decrease) - signs of broncho obstruction
- X-ray (wide IC spaces, horizontal ribs)
- Arterial blood gas (decrease CO2 tension < 36mmHg)
- Immune system test (inhalation/injection with allergens cause local reddish skin, edema, rash)
c) Diff diagnosis of severe asthma (status asthmaticus) & common attack of dyspnea
Stages of status asthmaticus
1. I stage (relative compensation).
Severe cough. Orthopnea. Tachypnea. Inability to speak in sentences. Added muscles are involved.
Distant wheezes. Cyanosis. Bandbox sound. Ausc.: no sound over the low lobes, hash breathing over
the upper parts. Tachycardia(120/min.). Nerve excitation, hallucinations.
2. II stage (decompensation, silent lung).
Severe dyspnea. Inability to speak. Superficial respiration. Orthopnea. Tachypnea. Pale-grayish skin.
Bandbox sound. Ausc.: no sound over the hole lobes, small amount of rales over the small part of the
lungs. Tachycardia (140/min). Pulsus paradoxus. Hypotension. Mental status changes (confusion).
3. III stage (hypercapnia coma).
Patient is unconscious. Diffuse cyanosis. Superficial respiration. Chain- Stock's breathing. Ausc.: no
sound over the hole lobes (―silent chest‖). Tachycardia(140/min.). Pulsus filliformis. Arrhythmia.
Hypotension. Gallop rhythm.
Criteria Status asthmaticus Common dyspnea attack
1. onset of attack Anytime Second half of night
2. sputum No Present
expectoration
3. alteration of Block of bronchi Temporary narrowing
bronchi
4. dyspnea > than few hours Temporary expiratory
dyspnea
55
 5. coma Hypoxemic coma Absent
6. CNS disorder Present Absent
7. Drug effect No effectiveness of beta stimulator, Effective
bronchodilators and Xanthanine
d) Emergency care & intensive therapy
- Rehydration eg glucose solution 3-4L daily
- Correction of electrolyte balance
- Heparin: improve rheological blood and sputum
- Euphyllines 6mg/kg
- Glucocorticoids: depending on stages 1mg/kg
- Oxygen therapy
- In 2nd stage, do artificial lung ventilation with bronchial lavage
e) Prognosis
Dangerous situation for life. Constant medication needed during attacks and hospitalization if effect of
medication absent. Not treatable and will present for life.

22) Chronic respiratory failure

Respiratory insufficiency
a) Definition
- Condition with abnormal gas composition of the blood, or this abnormality is compensated for by
intense work of external respiratory apparatus & higher load of the heart.
- Occurs when pulm gas exchange is sufficiently impaired to cause hypoxemia with or without
hypercapnia.
- Present when PaO2 < 8 kPa (60mmHg) or the PaCO2 > 7 kPa (55mmHg)
b) Pathogenesis
Arises during uneven distribution of air in the lungs when a part of the lung is not ventilated (in pneumonia
atelectasis) with preservation of blood circulation. Part of venous blood is not oxygentd before it enters
pulm vv & the L heart chambers. Vascular shunting (fr R to L) during which part of the venous blood fr the
pulm artery syst enters directly the pulm vv (bypassing the capillaries) to mix with oxygenated arterial
blood. Oxygenation of blood in lungs is thus upset but hypercapnia may be present but to compensatory
intensification of ventilation in the intact parts of the lungs. This is partial respi insufficiency (different fr
total respi insufficiency where hypoxemia & hypercapnia are present).

c) Classification
1. Type IA Respiratory failure (Acute Hypoxemic RI)
- PaCO2 is normal (35-40mmHg) or low but PaO2 is reduced (80-100 mmHg).
- Hypoxia with respiratory alkalosis.
- marked V/Q abnormality (V – ventilation, P – perfusion) & intrapulmonary shunting
- Occurs aar of pulmonary restriction in diffuse PN, pulmonary edema, ARDS, pulmonary embolism &
fibrosing alveolitis
2. Type IIB Respiratory insufficiency (Ventilatory failure)
- PaCO2 is elevated & PaO2 is reduced i.e. hypoxemia & hypercapnia – ventilatory failure
- both V/Q imbalance & inadequate alveolar ventilation
- Occurs in COPD, chronic bronchitis, emphysema, acute obstructive lung disease, asthma &
intrinsically by narcotics & sedatives, due to general bronchial obstruction

d) Clinical symptoms according to stages

These grades of respiratory failures:
Grade 1 2 3

56
Charac Dyspnea & mild hypoxemia Dyspnea, cyanosis & Dyspnea, cyanosis & severe
with strenuous, prolonged inadequate hypoxemia hypoxemia with minimal
exertion with ordinary physical physical activity or even at
No signs of RF at rest activity rest
PaO2 50-85 mmHg 30-50 mmHg <30 mmHg
PaCO2 45-50 mmHg 50-80 mmHg >80 mmHg
e) Subjective examination
- Dyspnea
- ↓ed tolerance level of physical activity
- Early: dyspnea, cyanosis, inadequate changes in ventilation (rapid & deep breathing at slight physical
exertion)
- Later : cardiac failure (edema), tachypnea, tachycardia & signs of intensified work of respiratory mm,
involvement of accessory mm during light exercise & at rest,
f) Objective examination
- Dyspnea at either significant physical load/light exercise/rest – rapid changes of resp, rapid & deep
breathing, intensified work of resp mm., ↑ resp rate, paradoxical respiration (abdominal & thoracic
compartments move in different direction)
- Cyanosis – Pink puffers (hypoxemia w/o hypercapnia) & blue blotter –edematous cyanotic ptts with
ventilatory failure (hypoxia & hypercapnia)
- Disorderred orientation, flaring of nostrils, pursed-lip breathing, use of accessory muscles of respiration
- Heart failure (edema)
- Tachycardia
g) Investigation of respiratory function
1. Pulmonary function test (spirometry) – rise resp rate, tidal volume measurement, vital capacity
2. Arterial blood gas
3. ECG
4. Chest X ray
5. JVP, physical examination
h) Obstructive type
- Characterized by difficult passage of air through the bronchi (bronchospasm) & compression/contractn
of large bronchi & trachea. Obstruction of air passage increases load on resp mm. The ability of resp.
apparatus to perform additional functional load decreases : fast inspiration & expiration, & rapid
breathing becomes impossible. The 1‘ obstructive ventilatory defects are :
COPD, Chronic bronchitis, Pulmonary emphysema, Bronchial asthma, Cystic fibrosis
i) Restrictive type
- Occurs in limited ability of lungs to expand & to collapse. limited depth of maximum inspiration.
Vital capacity of lungs ↓ but dynamics of resp is not affected & breathing rate is normal. The 1‘
restrictive ventilatory defects are :
1. Parenchymal disorders - Pneumothorax
- Alveolar & interstitial procs (edema, - Fibrothorax
fibrosis, infection) 4. Neuromuscular diseases
- Large space occupying tissue - Guillian-Barre syndrome (resp mm.
- Atelectasis weakness)
- Resection of pulm tissue - Diaphragmatic weakness: pleural nerve
2. Chest wall disease palsy
- Obesity - Spinal cord injury, Poliomyelitis
- Kyphoscoliosis - Disorders of respiratory center (drug
- Ankylosing spondilytis intoxicant, vascular disorders, trauma,
3. Pleural diseases infection)
- Effusion - Disorders of impulse transmission
57
 Test Obstructive lung Restrictive lung
FEV1 Markedly ↓ ↓
Vital capacity (VC) ↓ / Normal ↓
FEV1/VC (80%) the difference ↓ to 70-75% Normal >75%
index
j) Treatment
1. Initial management – establish adequate oxygenation (endotracheal tube + mechanical ventilation)
2. Depends on the etiology
- removing excess secretion by suction
- treating infections – AB
- suppress inflmtn – anti inflmtory/immunosuppressive drugs
- treat obstruction – bronchodilators
- Dissolving blood clots – anticoagulants or thrombolytics
- lung transplantation
k) Prognosis
- Younger patients hace better survival rate
- Good prognosis with adequate treatment

23) Lung bleeding

a) Etiology
Pulmonary hemosiderosis - lung disorder which bleeding (hemorrhage) leads to accumulation of iron,
anemia and lung damage. There are pulmo hemorrhage with autoimmune, immune & non immune disease.
1. unilateral reasons - diffuse periarthritis nodusa
- TB in lung apex. - deficiency vitamin C
- pneumosclerosis - cardiac failure- 4th functional grade
- tumor of lung - valve disease- bacterial endocarditis,
- bronchiectasis rheumatic disease
- staphylococcal, fungal , viral pneumonia - trauma of chest
- lung abcesses - primary hypertension
- Aspergillosis - hemorrhagic diathesis- Randi Osler
2. bilateral reasons disease
- hemophilia - Good posture syndrome.
- diffused pneumosclerosis
b) Diagnosis
If symptoms suggest hemosiderosis, blood test for iron and chest x-ray help confirm the diagnosis. A
tube inserted into the lungs and tissue tested for iron build-up.
c) Clinical symptoms
- hemoptysis, iron deficiency anemia, and lung tissue changes.
- If hemosiderosis comes slowly, symptoms develop such as chronic fatigue, poor growth in children,
cough, and persistent runny nose.
1. subjective 2. objective
- discomfort in throat - bloody sputum
- heaviness and squeezing in substernal area. - blood is foamy, scarlet red
- salty taste - paleness, cold sweat
- can smell blood even without blood - hypotonia
expectoration. - tachycardia
- dry cough - dull percussion
- suffocation in breathing. - cripitation, moist rales
- dizziness - diminished vesicular breathing

58
d) Emergency care
- If lung bleeding - respiratory therapy, oxygen, immunosuppression, and blood transfusion.
- Milk sensitivity treated by removing all milk and milk products from the diet
- If hemosiderosis due to another disorder, treating the underlying condition.
- bed rest
- monitor respiratory rate, pulse and BP.
- stimulate coagulation - fibrinogen, platlet, coagulative factor
- replenish blood loss - polyglucine, ringer solution, plasma
- artificial pneumothorax

24) Abscess of the lung

a) Definition
local suppurative necrosis in lung associated with cavity formation containing necrotic debris/fluid.
b) Etiology
1. Bacteria - Pseudomonas aeruginosa, Klebsiella PN, Staphylococcus aureus, Streptococcal PN,
Nocardia spp, Haemophilus influenza.
2. Nonbacterial pathogens e.g. parasites (Paragonimus, Entamoeba), fungi (e.g. Aspergillus,
Cryptococcus, Histoplasma, Blastomyces) & Mycobacterium
3. Decrease immunized patients,alcoholic.
4. As an outcome of pneumonia and complicated bronchiectasis, septic embolism
5. wounds to the chest, aspiration of foreign bodies and after operation on the upper airwys.
6. lung infarction or presence tumour.
7. Way of spreading - lymphogenic, hematogenic and contact
c) Classification
1. Acc to localization – L/R lung/both sides
2. Acc to etiology :
- 1‘ abscess – infectious origin, caused by aspiration of pneumonia in healthy host
- 2‘ caused by preexisting conditn (e.g. obstructn), spread fr extrapulm site, bronchiectasis
immunocompromised state.
3. Acc to duration :
- Acute: < 6 mths, abscess has thin wall
- Chronic: > 6 months, has capsule with pyogenic membrane and fluid
4. Periods:
- formation of abscess; it continues 10-12 days
- opening of the purulent abscess into the bronchus
Criteria for 1‘ & 2‘:
- devmt of destruction of lung tissue – intoxication syndrome
- no (+ve) dynamics in clinical pic
- no effects from treatment
d) Pathogenesis
- immune insufficiency patient
- aspirated material settles in distal bronchial system and develops localized pneumonitis
- Within 24-48 hours, a large area of inflammation results, consisting of exudate, blood, and necrotic
lung tissue. The abscess frequently connects with a bronchus and partially empties
- After pyogenic pneumonitis develops, liquefactive necrosis occur secondary to bacterial proliferation
and inflammatory reaction to produce acute abscess
- As the liquefied necrotic material empties through the draining bronchus, a necrotic cavity contain air-
fluid level is created
- infection may extend into pleural space and produce an empyema without rupture of the abscess cavity
- infectious process can extend to the hilar and mediastinal lymph nodes, and may become purulent.
59
e) Clinical picture
1. Formation of abscess (10-12 days)
- Intoxication syndrome, Pain syndrome
- Cough with little or no sputum
- Infiltration of lung tissue, Dyspnea, General indisposition
Objective examination
- Vocal fremitus increase at the place of infection
- Infiltration syndrome – bronchial breathing
- diminished vesicular or bronchial breathing, harsh with dry rales (superficial)
- In deep abscess or small size, results of objective examination not changed
2. Opening of purulent abscess into bronchus
- ↓ Intoxication syndrome (↓ T‘C & chills, ↓ weakness, arthralgia, myalgia↓)
- Ptt‘s condition improve. slight dyspnea, Pain in the chest
- Infiltration of lung tissue syndrome
- full mouthed sputum (~ 500ml) – depends on size of abscess
- Severe cough with offensive purulent sputum (―full mouth‖): on standing separates into 3 layers:
mucous, serous and purulent (from 200 ml to 1-2 L/day)
Objective examination
- dull tympanic sound
- Auscultation: if drainage of abscess (road) & cavity > 3 cm (large abscess) – amphoric breathing
- Additional sounds: small bubbling rales – inflammatory changes/pneumonia
- Unilateral thoracic lagging(affected side)
- VF – increased
- Percussion: tympanic / metallic sound; crackled - pot sound
- Auscultn: bronchial (amphoric / cavernous) breathing; resonant moist rales; gutta cadens (falling –
drop sound)

1. Infiltration Syndrome - myalgia

- asymmetrical movement of chest in - arthralgia
respiration - loss weight
- dull sound on percussion 3. Evacuation Syndrome
2. Intoxication Syndrome - decrease in temperature
- fever - absent arthralgia/myalgia
- low appetite - normal appetite
- weakness - improvement of condition of patient
f) Investigation
1. Blood cultures – neurophilic leucocytosis, shift to the left, increased ESR,
2. Biochemical
- increase protein inflammation (C-reactive protein, seromucous)
- decrease albumin
3. Sputum exam :
- 1st stage – not specific
- 2nd stage – presence of 3 layers (mucous, serous, purulent), Elastic fibers, Leucocytes and
erythrocytes. Dittrich‘s plugs
4. Chest Xray
- 1st stage – signs of infiltration, > intensive in central part & < intensive in periphery
- 2nd stage – cavity with air-fluid level
5. Bronchoscopy : differential Dx with tumor, TB. may evacuate fluid if abscess is near large bronchi.
bronchitis detection
6. CT scan –abscess walls well defined margin, localization, size, form
60
7. Specimen obtained by transtracheal aspiration, bronchoscopy or percutaneous transthoracic aspiration
with ultrasound guidance.
g) Treatment
1. 1st stage : intensive antibiotic therapy – combi of 3 AB
- Penicillins/Cephalosporins for G(+)
- Metronidazole
- Aminoglycosides, fluoroquinolones.
Symptomatic treatment - expectorants and broncholytics.
Detoxification therapy by infusion therapy- glucose, Ringer‘s solution, Vits B1, 6, C,
2. 2nd stage
- mucolytics, expectorants
- increase drainage – intensive Atbs & detoxification.
Not based on stage:
- Immunocorrection therapy
- Bed rest
- Antibiotics and sulpha drugs – penicillin, streptomycin given with tetracycline.
- Adequate draining, emptying of the cavity.
- Surgical treatment given in a month.
h) Indications for surgical treatment
- Destruction of wall of abscess with massive hemorrhage
- Septicemia
- Multiple abscesses
- Absent effect from antibiotic therapy
- wide spread development of process
- Conditions lead to amyloidosis of other internal oragans e.g. kidneys

25) Cor pulmonale

a) Etiology
1. pulmonary vascular disorder 3. musculoskeletal disorder (causing chronic
- acute pulmonary thromboembolism underventilation)
- primary pulmonary HT - kyposcoliosis
- multiple pulmonary stenosis - poliomyelitis
- recurrent pulmonary embolism - myasthenia gravis
2. disease lung and parenchyma 4. disturbance of respiratory control
- COPD - cerevascular disorder
- Asthma - obstructive sleep apnoe
- Bronchiectasis 5. left heart disorder
- Pulmonary fibrosis - mitral stenosis
- Lung resection - Left atrium myxoma
- LVF
Disease primarily affecting the lung and alveoli; excursion of the chest; pulmonary vessels
1. disease affecting primarily bronchopulmonary apparatus
- chronic bronchitis and pneumonia
- lung emphysema
- fibrosis and granulomatosis
- tuberculosis and occupational lung disease
2. disease primarily affecting the lung ventilation due to pathological excursion of the chest
- kyphosis, scoliosis, costal pathology, disease of the diaphragm, Bekhterer‘s disease, obesity
3. thromboembolism of pulmonary disease
- vasculitis
61
 - primary pulmonary hypertension
- atherosclerosis
4. left heart disorder, mitral stenosis, left atrial myoxma, LV failure
5. appetite suppressant drugs
b) Pathogenesis
Alveolar hypoxia causes releasing of biogenic amines (histamines, serotonin) which attended by edema
of capillary endometrium. This leads to narrowing of pulmonary vessel, hence increases the pressure in
pulmonary artery. Subsequently, pulmonary hypertension develops which in turn causes hypertrophy in
the right heart chamber: 1st RV then RA. When RV failure develops, decompensated cor pulmonale
established.
c) Stages
1. Acute – stage of pulmonary embolism
- sign in heart, cyanosis upper part of body, distension jugular vein, liver enlargement
- thrombus in systemic veins.
- Clots formed, local injury or compression of the vein and hypercoagulable state.
2. Subacute
3. Chronic
- in chronic obstructive pulmonary disease
- enlargement of the right ventricle because of increase in afterload due to disease of the thorax, lung
and pulmonary circulation.
Divided in to compensated and decompensated.
Decompensated cor pulmonale
- central cyanosis
- peripheral edema
- neck vein distension
- +ve jugular +ve jugular pulse
- Enlargement of liver,+ve plesh sign (hepatojugular reflex)
- Ascitis
- Hydrothorax
- Hydropericardium
d) Clinical picture
- Pallor, sweating, hypotension, rapid pulse of small amplitude
- Pleuritic chest pain
- Exertional dyspnea
- Syncope, fatique
- The neck veins are distended, swelling and prominent v waves
- The liver pulsatile, distended, and tender. enlarged, painful to palpate
- systolic murmur of tricuspid regurgitation accompanied by gallop sound.
- Arterial blood gas shows reduced PaO2 and low Pa CO2
- epigastric pulsation, ascites, shifting of R atrium, pulm-trunk, P-pulmonale, deep S in V4-V6,
complete/ incomplete RB block
- Sudden onset
- Respiration rate increase but expiration not elongate
- Haemoptysis (present only when infarction has occurred)
- Do not respond to bronchodilation preparation
- work capacity decreases, drowsiness and headache
- general cyanosis, Acrocyanosis
- Fingers and hand became cold to touch
- Shins became puffy and entire lower extremities are edematous
- Permanent tachycardia
62
e) Investigation
1. Chest X-ray
- diaphragm well rounded
- cardiac silhoute enlarged
- pulmonary arteries more prominent
- linear atelectasis /blunting of costophrenic angle
- translucency of an underperfused distal zone is seen
- RV enlargement and right artrial dilatation
- Pulmonary trunk and hilar vessels enlarged, descending right pulmonary artery embolism
2. ECG
- Increase P wave in 3rd and AVF leads ( p – pulmonale)
- Increase R wave in V1-2
- Increase S in V5-6
- Right limb block in Hiss bundle in V1
- T wave inversion in right precordial lead
3. Echocardiography
- Shows vigorously contracting LV and a clot in RV outflow tract
- Hypertrophy and dilation of RV
- Tricuspid regurgitation
4. Spiral CT scan - IV contrast show good sensitivity & specificity for medium sized pulmonary emboli
5. Ultrasound - increase size in RV
6. Pulmonary angiography, MRI
7. Blood test
- if infraction occurred polymorphonuclear leucocytosis
- Elevated ESR
- Increase lactate dehydrogenase level in serum
8. Blood gases - Shows hypoxia and hypocapnia
9. Ophthalmologic examination – papilloedema
f) Treatment
1. For acute management
- high –flow oxygen (60-100%)
- Diuretics for RV failure
- bed rest and analgesics
- Severe cases IV fluid and inotropic agents to improve pumping of right heart
- Prevention of further emboli
a. IV 10000 units of unfractionated heparin
b. Oral anticoagulants
c. Insertion filter in the inferior vena cavae right above level of renal vein
- Dissolution of thrombus – fibrinolytic therapy (streptokinase IV)
- Surgery – embolectomy
- Management – treat underlying causes eg: COPD and pulmonary infection
- Treat resp failure
2. chronic management
- determined by condition underlying pulmonary HT, used Diuretic
- hypoxia use oxygen therapy

26) Bronchiectasis
a) Definition
It is a permanent dilatation of the bronchus due to destruction of muscle and elastic tissue

63
b) Etiology
- Primary infections – Staphylococcus aureus, Klebsiella, Mycobacterium tuberculosis, Mycoplasma
pneumoniae, viral, Mycobacterium avium complex
- Bronchial obstruction – endobronchial tumours, stenosis, broncholithiasis, foreign body aspiration
- Cystic fibrosis
- Congenital - Young disease, primary ciliary dyskinesia,
- Congenital dysgenesis – bronchopulmonary sequestration, yellow-nail syndrome, Williams-Campbell
syndrome (congenital cartilage deficiency)
- Allergic bronchopulmonary aspergillosis
- Immunodeficiency states – hypogammaglobulinemia, agammmaglobulinemia
- Autoimmune diseases – rheumatic disease
- α1-antitrypsin deficiency
- Diseases of upper airways
c) Pathogenesis
- Main pathogenic mechanism is obstruction and chronic dilatation of bronchial tree and chronic
persistent infection. inflammation & destruction of bronchial wall is irreversible
- infections release toxins damage the respiratory epithelium & impairs mucociliary clearance. Frequent
bacterial infection add in
- bronchodilation occur, while host immune response & mediators from neutrophiles causing epithelial
injury. This condition permit reinfection in dilated airways
- Therefore vicious cycle is formed, impaire clearance of secretions causes recurrent infection back to
bronchial damage.
- obstruction of large bronchi is by compression of collapsed or congenitally inadequate bronchi &/
prolonged obstruction of the bronchi with a dense mucoid plug in acute resp infections
- bronchodilatating forces (high intrabronchial pressure during cough, bronchial distension due to
accumulated secretion) promotes persistent dilatation of the bronchi
- bronchial dilatation and retention of bronchial secretion, promotes development of inflammation
d) Morphological types
- Saccular – ulceration with bronchial neovascularization and a resultant ballooned appearance that may
have air-fluid levels.
- Cylindrical – diffuse mucosal edema, with resultant bronchi dilated minimally but have straight, regular
outlines
- Fusiform – bulbous appearance with a dilated bronchus and interspersed sites of relative constriction
and, potentially, obstructive scarring.
- Mixed – a combination of 2 or more
e) Clinical symptoms
2 phases: Relapsing, Remission
3 stages:
1. Mild - relapse 1-2x and btw them condition is satisfactory
2. Moderate - sputum < 100ml, & moderate disturbance
3. Severe - volume of sputum > 200ml, short remission & fever
Early stage:
- Persistent or recurrent cough - Fever, malaise
- Purulent sputum production. In severe - On auscultation – crackles, rhonchi,
cases, continous production of thick, foul- wheezing
smelling sputum - Chronic hypoxia
- Hemoptysis - Possible weight loss
- May be severe pneumonia - finger clubbing
- Dyspnea – wheezing - breathlessness
In late stages, signs similar to cor pulmonale appear (page 62)
64
f) Clinical picture
- cough with purulent sputum - fever if relapsing > 38 C, in remission normal
- if relapsing full mouth sputum < 37.3
- in remission have 2 level of sputum - has syndrome of obstruction
- haemoptysis - malaise
- dyspnoe - clubbing
- pain in the chest if near pleura pleuritis
g) Investigation
1. Objective examination
- dull sound/ band box sound
- respiration - rash , moist rales, medium bubbling rales which increase and decrease after cough
2. Blood – leucocystosis, toxic changes in neutrophil, increase ESR, anemia
3. Biochemical picture – increased inflammatory proteins, decreased globulins
4. serum immunoglobulins
5. sputum has 2 level
- Mucous / serous
- Died neutrophil
- colour according to infectious agent, yellow in relapse, white in remission, mucous, presence of
leukocytes
- stap aureus, pseudomonas aeruginosa, H. influenza and anaerobes
6. X-ray
- no specific changes
- maybe foci of inflammation
- sign of coarse deformation of lung pattern, in lower segment or the middle lobe of the right lung
7. Bronchography
- if the diagnosis is in doubt
- morphological signs of bronchiectasis seen
- localized changes, widespread bulging
8. Pulmonary function test – to determine degree of obstruction if present
9. CT scanning – differentiation between morphological types
10. bronchokinetography – reveal bronchiectasis with movable and rigid walls and to differentiate
deforming bronchitis frm bronchiestasis
11. bronchial arteriography – reveal blood shunting thru pathologically dilatated bronchopulmonary
anastomoses
12. lung scanning – reveal marked disturbances in capillary circulation
h) Treatment
1. Conservative treatment
- Antibiotics – penicillin, ampicillin, amoxicillin. eg Ceftazidine
a. mild cases – intermitten chemotherapy with cefaclor / aprofloxacin
b. flucloxacillin if stap. Aureus is isolated
c. if p. aeruginosa, chemotherapy ceftazidime, ciprofloxacin
- Immunocorrection – respective globulin infusion
- Disintoxication
- Mucolytics – acetylcysteine (aerosol), bromhexine
- Bronchodilators – isoprenaline, salbutamol, theophylline
- Anti-inflammatory drugs – corticosteroids. Inhaled/oral steroids
- Immunization – influenza, pneumococcal pneumonia
- Pneumatic compression vest & nebulization with saline solution
- NSAIDS
- Broncholytics
65
 - To increase immunity - Timolin, Timogen, T-activin
- postural drainage - uppermost lobe, 3 times daily for 10-20 min
2. Surgical
- Surgical resection to correct localized form of bronchiectasis without complications
- Lung transplantation
- Bronchial arterial embolization
i) Indication for surgery
- complication present
- positive result if operate - result of narcosis

27) Pleurisy
a) Dry & effusion types
Pleurisy - inflammation of the pleura, secondary to disease of the lung
- Effusion type - pleural space lies between the lung and chest wall and normally contains a very thin
layer of fluid. Present when there is an excess quantity of fluid in the pleural space
inflammatory effusion – serous, serofibrous, purulent, Hemorrhagic
- Dry type - Pleurisy characterized by a fibrinous exudation, resulting in adhesion between the surfaces
of the pleura. Also called adhesive pleurisy, fibrinous pleurisy, plastic pleurisy.
b) Etiology
- In serous and serofibrinous pleurisy: TB, Pneumonia, Certain infection, Rheumatism
- In purulent: pneumococci, streptococci, staphylococci
- in Hemorrhagic type :
a. TB of pleura
b. Bronchogenic cancer of the lung with the involvement of the pleura and injury to the chest
Dry pleurisy
- complications of respiratory tract infections, such as pneumonia, viral infections, and tuberculosis.
- tumor or an injury
- gastrointestinal tract diseases (liver and pancreas) which inflame the diaphragm and the portions of the
pleurae that cover the diaphragm.
c) Pathogenesis
- In serous pleurisy - due to allergic reaction
- In purulent type - complication of bronchopneumonia (inflammation to pleura turn to abscess and open
to pleural cavity). inflammation of the pleura attended by increase permeability of the wall of the
affected capillary of the pulmonary pleura
1. Effusion due to heart failure - -LV failure: increased amounts of fluid in the lung interstitial spaces exit
in part across the visceral pleura, lymphatics can‘t remove adequately
2. Hepatic hydrothorax - cirrhosis and ascites: direct movement of peritoneal fluid through small holes in
the diaphragm into the pleural space
3. Parapneumonic effusion - associated with bacterial pneumonia, lung abscess, or brochiectasis
4. Effusion secondary to malignancy (lung carcinoma, breast carcinoma and lymphoma) - secondary to
metastatic disease
5. primary malignant mesothelioma - arise from the mesothelial cells that line the pleural cavities related
to asbestos exposure
6. Effusion secondary to pulmonary embolization - transudative or exudative
7. Tuberculous Pleuritis - due to a hypersensitivity reaction to tuberculous protein in the pleural space
8. Effusion secondary to viral infection - AIDS: common cause is Kaposi‘s sarcoma, followed by
parapneumonic effusion
9. Chylothorax - thoracic duct is disrupted and chyle accumulates in the pleural space caused by trauma,
tumors in the mediastinum
10. Hemothorax - result of trauma; rupture of a blood vessel or tumor
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- In dry pleurisy - thickening of the pleura and deposition of fibrin, pleural membrane become dull and
hyperemic commisure and adherence develop
- pleurisy with effusion - presence of exudate in the pleural cavity
- after inflammation - effusion usually resolves but pleura remain thick, membrane adhere to one another
d) Clinical symptoms
In dry pleurisy:
- cough is usually dry
- weakness and subfebrile
- respiration is superficial (deep breathing cause pain due to friction)
- lying on the affected side lessen the pain
- Sharp, stabbing pain towards the side and lower part of the chest. Radiate to shoulders, neck and
abdomen. breathing or coughing, will aggravate the pain, shortness of breath
In pleurisy with effusion:
- fever
- pain and feeling of heaviness in the affected side
- dyspnea, mild cough
- gen condition - grave in purulent pleurisy - increase T, chills and sign of general toxicosis
- mostly are asymptomatic and discovered during physical examination or on chest x-ray.
e) Investigation
In dry pleurisy :
- Inspection : unilateral thoracic lagging during respiration
- Percussion : decrease mobility of the lung on the affected side
- Auscultation : pleural friction rub on the affected site
- X-ray : limited mobility of the diaphragm
- Blood: moderate leucocytosis .
In pleurisy with effusion :
- Inspection : asymmetry of the chest due to enlargement of the affected side.
- Palpation: Vocal fremitus not transmitted at the area of fluid accumulation
- Percussion : over the of fluid are dull sound
a. transudate > freely press the lung and Damoisseau curve not determined
b. Garland triangle on affected side and has dull tympanic sound
c. Rauchfuss –Grocoo triangle on the healthy side

1. Thoracentesis: Fluid may be clear yellow (serous), milky (chylous), blood-tinged (serosanguineous),
grossly bloody (sanguineous), or translucent or opaque and thick (purulent). Specimens should be taken
for chemical, bacteriologic, and cytologic examination.
2. lateral decubitus radiograph
3. thoracoscopy
4. needle biopsy of the pleura; open pleural biopsy
5. CT scans: evaluating the underlying lung parenchyma in pleural disease; lung abscess, pneumonia, or
bronchogenic carcinoma beneath loculated pleural effusion; lung abscess differentiated from empyema
with a bronchopleural fistula and an air-fluid level; Pleural plaques differentiated from parenchymal
lesions; pleural densities of mesothelioma are readily identified.
6. perfusion lung scanning and / or pulmonary arteriography

f) Different variants of exudate

Feature Transudative Exudative
Appearance Clear, thin, non clotting Cloudy, viscous
LDH Normal Increase
Protein < 30 g/l >30g/l
67
 Relative density 1.006- 1.012 1.018-1.022
Rivalto’s reaction Negative Positive
WBC Absent / few Large num , RBC
Fluid/ serum LDH ration < 0.6 > 0.6
Fluid / serum protein ration <0.5 > 0.5
- transudative: LVF, pulmonary embolism and cirrhosis
- exudative: bacterial pneumonia, malignancy, viral infection, and pulmonary embolism
- transudative pleural effusion occurs when systemic factors that influence the formation and absorption
of pleural fluid are altered
- exudative pleural effusion occurs when local factors that influence the formation and absorption of
pleural fluid are altered
g) Role of x-ray
In dry pleurisy : Limited movement of diaphragm
In pleurisy with effusion : Homogenous density over the area of dullness
- precise way to confirm physical findings and demonstrate the presence of pleural fluid.
- upper border of the fluid is meniscus-shaped.
- patient upright, the minimum amount of detectable fluid ranges from 200 to 500 mL.
- in lateral decubitus view, < 100 mL of fluid is detectable.
- Large pleural effusions result in complete opacification of the hemithorax and in mediastinal shift to
the contralateral side.
- Adhesions between visceral and parietal pleurae may result in atypical loculated collections.
- Loculations in the horizontal or oblique fissure may be confused with an intrapulmonary tumor and are
called "vanishing tumors."
- Obliteration of the costophrenic angle usually denotes a fibrosing and healing reaction and may remain
after healing is complete.
- Pleural plaques due to asbestos exposure present as localized areas of pleural thickening, sometimes
calcified, and usually in the lower 2/3 of the thorax.
h) Treatment
- in rheumatism : salicylate, amidopyrine, corticosterone
- in pneumonia : sulpha drug, antibiotics
- TB : streptomycin
- Symptomatic Tx: vitamin
- Evacuation of fluid, 0.5- 1L of effusion is removed and antibiotic injected into the pleural cavity
- Give diuretics

In pleural effusion
- Thoracentesis relieves dyspnea
- antibiotic therapy. Pleural fluid is usually reabsorbed spontaneously.
- Empyema is treated with high doses of parenteral antibiotics and drainage - water-sealed tube
thoracostomy preferable; open drainage; surgical decortication
- if due to malignant pleural implants - pleurodesis: The lung is reexpanded by tube thoracostomy,
followed by instillation of a sclerosing agent (asbestos-free talc) given in a slurry, or doxycycline. The
result is an intense pleuritis that obliterates the pleural space so that fluid cannot reaccumulate.
- For hemothorax, water-sealed tube drainage is generally sufficient. Fibrinolytic enzymes
(streptokinase-streptodornase or urokinase) instilled through an intercostal drainage tube to lyse
fibrinous adhesions if the effusion becomes loculated. thoracotomy and decortication may be necessary
to expand the lung and obliterate the pleural space.
- Treatment of chylothorax is directed at the underlying cause of ductal damage.

68
In dry pleurisy
- treat the underlying infection or disease, often with antibiotics.
- resting.
- Strapping the chest firmly with an adhesive elastic bandage.
- Painkillers
- Anti-inflammatory medications, cortisone drugs in relieving the inflammation and pain
i) Complications
- Heart failure
- Pneumothorax may complicate thoracentesis if the visceral pleura is punctured or if air leaks into the
pleural space as a result of a break in the continuity of the thoracentesis system.

28) Chronic gastritis

a) Definition
Chronic inflamn of gastric mucosa, changing mucous secretion, charac. of gastric juice, structural alteration
of glandular compartments. Atrophy and metaplasia of mucosa wall and development of secretory,
evacuatory, motility and metabolic insufficiency.
b) Type A
Atrophic gastritis, Diffuse corporal atrophic gastritis, Pernicious anemia gastritis, Metaplastic atrophic
gastritis, Atrophic pan gastritis
Etio: Autoimmune
Patho: associated with Hashimoto‘s thyroidits, Hyperthyroidism, Hypothyroidism.
- Non-bacterial. Involvemt of autoIM response (↑incidence pernicious anemia in relatives )
- atypical changes of mucosa as a result of protein struc changes affecting body of stomach & severely
impairs acid secretion
- gastric secretion ↓ (hyposecretion)
- older ppl ( 50-55y.o)
- erosion & ulceration rare, dev B12 def anemia
- absent malignization
Clinical pic:
- Pain not typical. Dullness,heaviness, hardness in epigastric w/o irradiation
- discomfort after meal
- gastric dyspepsia : vomiting with bile, nausea (not specific)
- intestinal dyspepsia : diarrhea
- Loos of appetite, loss of weight
- Dev symptoms of pernicious anemia(weakness, changes of hair,skin,red tongue)
- severe weakness
- during palpation can reveal pain in pyloric region, dull, no radiation, no tenderness
c) Type B
Non-atrophic gastritis, superficial gastritis, Diffuse antral gastritis with H.pylori, Interstitial-follicular non-
atrophic gastritis
Etio: Helicobacter pylori, Camphylobacter
Patho: H.pylori infects 1‘ the antrum & adheres to gastric epithelial cells→it produces proteases,
phospholipase, urease→ inflamn →host response includes addition of inflammatory infiltrate (T&B cells,
lymphocytes) in the lamina propria & epithelium
- gastric secretion ↑(hypersecretion)
- affect younger ppl ( 25-55y.o)
- obvious erosion & ulceration
- dev Ferum deficient anemia
- present malignization
Clinical pic:
69
- Pain in epigastric aft eating. Food ↓pain but ↑aft ½ hr.Wit or w/o irradiation.> intensive
- Gastric dyspepsia : heartburn( ↑acid), nausea, vomiting, eructation wit acid taste
- Intestinal dyspepsia : Constipation
- ↑ appetite at early onset of disease, aft prolongation : ↑ weakness & heartburn
- White tongue
- local pain in epigastric on palpation
syndrome Type A Type B
I. asthenic Vertigo, weakness, inactive Vertigo, weakness, inactive
II. pain Low secretin level As in gastroduodenitis
-discomfort in epigastric region -same clinical pictures in peptic ulcer
-loosing of appetite -spastic pain
-dull pain
III. dyspeptic Stomach: spoiled egg smell Stomach: burning, acidic, nausea &
Intestininal: diarrhoea vomiting with acidic taste
Intestinal: constipation
IV. secretin Stomach: low Stomach: high
level Serum: high Serum: low
d) Investigation
1. Blood analysis : anemia (type A), ↓ albumin & cell count
- vitamin B & iron deficiency anemia (↓ RBC, ↓ Hb, ↓ CI -<0.85, microspehrocyte)
2. fibrogastroduedenoscopy –presence of bile refluxes
3. x-ray –thickening of fold of stomach
4. biopsy -see changes in stomach mucosa
5. gastroscopy –hyperproduction of gastric juice
e) Role of x-ray, gastroscopy & biopsy in diagnostic of chronic gastritis
X-ray:
- Enlargement of fluid vol (↑secretion)
- examination of motor disorder ( ↓peristalsis, disorder of motor func)
- shape,size,position& mobility of stomach
- direction& shape of mucosa folds,thickness,continuity( A-folds ↓, B-folds ↑)
Fibrogastroduodenoscopy :
- Location,size,shape
- condition of gastric mucosa( ∆ in colour,surface,growths)
- presence of bile in gastric juice ( if reflux present)
- height,width,density of folds
- reveal tumor/ulcers
- A- thin mucosa,diffuse paleness; B- hyperemia,erosions,hypertrophy
Biopsy.
- Removal of polyps
- A - atrophic B- dystrophic
- Gastroscopy & biopsy: true diagnosis of gastritis
- Inflammatory changes must be found in minimum 3, maximum 7 parts of stomach mucosa in order
to put diagnosis
f) Evaluation of stomach secretary function
acid secretion is ↓ in Type A & ↑ in Type B
Hyposecretion :
- Gastric juice excreted ,30ml/hr on fasting stomach
- Achlorhydria ( absent HCl)
- Achylia ( absent pepsin )
- pH metry : 3.0-5.0 ( norm 2.5 )
70
Hypersecretion :
- Gastric juice excreted >60ml/hr on fasting stomach
- pH metry : 0.9-1.3 ( norm 2.5 )
serum gastrin level r elevated substantially in patient with pernicious anemia
Substances for stimulation secretion: pepsin, gastrin, pentagastrin
- high secretion: high initial secretin
- low secretion: increase secretin level, causes stomach to secrete more secreatin (compesative
mechanism)
- In atrophic: no effect on stimulation
g) Treatment: diet, medicaments
Diet:
- diet no 1
- min 4-6x daily food ( freq wit small proportion)
- avoid gas containing, very hot,very cold,fatty,acidic food
Medications:
- Antibiotics: Metranidazole, penicillin (Amoxicillin), cephalosporine, Macrolides ( Clarithromycin )
- antacid
a. non water soluble: almagen, phospogen
b. water soluble: sodium bicarbonate, calcium bicarbonate, magnesium hydroxide
- H2 histamine blocker: nizatidine, Famotidine,Ranitidine,Cimetidine
- Proton pump inhibitors ( Omeprazole, Lansoprazole)
- Mucosal protective: Bismuth, De-nol
- in case of reflux: cerucol, metachlorpromide (to improve motoric function of GIT)
- specific treatment for pernicious anemia
- vitamin b12 administration
- Pain syndrome : Spasmolytics- Atropine,Perenzipine (↓gastic secretion)
- symptomatic: spasmolytic: baralgin, plantaglycin, papaverin
- sodium carbinosolium- ↑ b.flow in stomach mucosa
- calcium channel blokers -decrease production of hcl acid
- cholinergic receptor blocker, perezipine
- sodium carboxalon

29) Peptic ulcer

a) Definition
Chronic relapsing disease with the lost of part of mucosa of epithelium cells of any portion of GIT
(stomach, duodenum) exposed to aggravation action of gastric juice.
b) Classification
- Type→ 10 , 20
- Sites→ stomach (<curv, antrum, body), duodenum
- Duration→ mild(relapse <2x/year), moderate(relapse 2x/yr), severe (>2x/yr)
- Size→ small (<0.5cm), large (> 1 cm), very large : stom (<3cm), duo (> 3cm)
- Layers → superficially (< 0.5cm), deeply (> 0.5cm)
c) Risk factors
- Genetic predisposition - Male
a. ↑ parietal cells so ↑ HCL, pepsinogen - 1st degree relative with duodenal ulcer
& gastrin secretion. - GIT disorder
b. Blood group O - Alcohol, smoking
c. Astenic constitution - drugs: aspirin & other NSAID
- Stress - dietary regime
d) Etiology
71
Endogenic factor : - Arteriosclerotic vessels
- hyperpepsinogenaemia, α-antitrypsin - psychoemotional stress
deficiency and hyperfunction of G- cells Exogenic factor:
- ZE syndrome (tumor of pancreas) - diet, alcohol, smoking,
- Acute stress ulcer - H.pylori
- Cushing syndrome - NSAID, cortocosteroids
e) Pathogenesis
1. psychoemotional theory
Stress→ ↑ SNS & PNS→ results problem in innervation of stomach →↓ prod of gastric juice→ ↑
motor activity of GIT→ spasm of vessel (with trophic damage)→ dev of PU
2. Infection ( Campylobacter pylori )
- camplylobacter is situated btw folds→releases uric acid→ acid present in region of neutralization &
it not destroyed by gastric juice. (must give Atb)
- decrease somatostatin in duodenum, increased secretion of H
3. Imbalance between the defensive & aggressive factors. ( ↓ defense, ↑ aggressive )
a. Defense Factor b. Aggressive Factor
- production of mucous - campylobacter pylori
- high regeneration - acid & pepsin
- prostaglandin production - bile reflux
- intensive blood flow ( mucosal ) - peptic activity, impaired inhibition of
- bicarbonate secretion acid-pepsin secretion
- neurohormonal reg: somatostatin, secretin, - duodenal reflux; exogenous: smoking,
enterogastrin NSAIDs
f) Clinical picture
1. Pain syndrome- epigastric region
- dull, cramping
- Pain stops after meals, milk (buffer), antacids, spasmolytics (pain ↓)
- early→ after 30 mins after meal (upper stomach)
- late→ after 2 hours after meals, hungry after 7 hrs after meal, 2-5 hrs of night pain(lower stomach
& duodenum)
Trigger factor after pain:
- food stimulating secretion ( spastic contain, alcohol, acidic, hot)
- heavy physical exercise
- emotional stress
2. Dyspeptic Syndrome (Gastric)
- Vomiting, nausea, heartburn (due to reflux, hyperacidity), sour eructatn, acid taste
3. Intestinal Dyspepsia
- Constipation (due to hyperacidity, motor disorders)
g) Gastric ulcer
- Early type of pain syndrome - 15-20min after meal
- Food intake may cause pain.
- Antacid & milk – relieving factor
- Tyical radiation to the back (5th lung vbrae)
- Pain: in epigastric region, and b4 food intake, patients afraid to eat
- dyspeptic syndrome : nausea, vomiting
h) Duodenal ulcer
- Late pain syndrome (hunger pain at night)
- Does not irradiate.
- Relieved after eating.
- Stereotype pain- appear at same localization & constant
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- pain in epigastric region
- Dyspeptic syndrome: heart burn.
i) Properties of peptic ulcer. Clinical symptoms acc to localization (cardia, pylorus, below duodenal)
1. Cardia- when pain is in epigastric region (near xiphoid process)
- early pain syndrome
- Males > 45 years old
- Radiate to L and chest
- Not intensive
- Heartburn typical
- Associate with hiatus hernia
- Typical complication - bleeding
2. lesser curv- common place
- males (middle age), females (>50)
- epigastric pain
- acidity normal
- heartburn present
3. greater curv- rare
- males
- associate with normal & hypoacidity
- 50% in malignization
4. antrum- young male typical
- typical late hunger/ night pain
- dangerous for malignizatn
- typical compli- bleeding
5. pylorus - occur in men and occurs with decreasing of HCl secretion.
6. duodenum bulb- male <40
- mainly on ant wall
- seasonal character
- night hunger late pain is typical
- typical compli – perforatn
7. Below duodenum: men, 40-60 years old. primary complication is bleeding due to hypersecretion of
HCL and heart burn.
j) Investigation
1. Fibrogastroduodenoscopy- used in primary description of PU
2. Gastroscopy with biopsy
3. Secretion investigation
4. X-ray with barium meal
- direct ( niche,crater)
- indirect (one mobile point, fast evacuation,finger pointing on opp side)
- determine its localization,deformation and complication.
- ―De Ker Ver‖ syndrome present in PU
5. Blood analysis - ↓ Hb, RBC & C.I., erythrocytosis, anemia (Iron deficiency)
6. Corpological analysis - feaces on blood occult - Greger Sand Webber rxn
7. Biochemical - urease activity
k) Role of x-ray & gastroscopy in investigation
X ray: to identify the type, size, shape, localization, radiation of ulcerous process.
- To make accurate diagnosis with help of barium meal.
- To determine the severity of disease acc to layers affected (superficial, deep)
- detect cancer ( as differential diagnostic )
- present of fluid in ulcer
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Gastroscopy- helps to make diagnosis & to take biopsies:
- It also can help detect cause & source of HR if present.
- to observe the mucosal surface of PU
- to perform rapid urease test, culture of biopsy, histology of gastric mucosa
l) Treatment: antacids, h2-receptor antagonist, anticholinergic drugs, bithmus
Dietary regime- 5-6x daily in small portions.
- Exclude coffee, alcohol, smoking
- Include fish, milk production, porridge, juices
1. Antacids- neutralization of HCL & peptic juice. (NaCO3, CaCO3, Aluminium OH)
2. H2 receptor antagonists
- cimethidine, ranithidine, famothidine, nizathidine
- ↓ prod of HCL & ↓ night secretion
3. Anticholinergic drug
- Proton Pump Inhibitors
- omeprazole, lansoprazole, rabeprazole and pantoprazole
- inhibit all phases of gastric secretion
4. bismuth chelate eg. tripotassium dicitratobismuthate
- can binds to the ulcer crater and stimulate prostaglandin secretion, ↑ b/flow, protect mucosa
- effective against H. pylori
m) Complications of peptic ulcer: penetration, perforation, gastric outlet obstruction
1. Penetration
- Invasion to nearest organs
- posterior wall of stomach involve pancreas, post wall of duodenum.
- Constant pain irradiatn to back, pancreas digest itself (autolysis)- gen inflammatory effect.
- May find silent puncture if omentum closes defect.
- investigation - xrays, endoscopy, laparoscopy, US, MRI, amylase.
- operation - relief pain, prevent any exocrine & endocrine insufficiency
2. Perforation
- Acute destruction of stomach wall.
- Young pt (19-45), more typical in DU.
- pain syndrome (knife stab)
- Peritonitis syndrome- flat abd, lose consciousness, no liver dullness-tympanic sound
- X-ray - gas below liver.
a. massive
- < 3 hours : sign of acute abdomen - rebound tenderness, high temperature, pale skin,decreased liver
dullness,decreased of peristastic sound.
- 3-6 hours : decreased sign of acute abdomen as peritoneum secrete fluids and cover pain. high
temperature and paralytics ileus occurs.
- 6 hours : detectable fluids amounts.
b. slow
- perforation sealed by the greater omentum.
- analgesic, infusion to treat dehydration and also shock, nasogastric tube, catherization, prophylaxis
antibiotic and CVS monitoring. Operation repair of perforation and for duodenal ulcer.
3. Gastric Outlet obstruction
- hardness after food intake, bad appetite, foul smell from mouth, nausea, vomiting after meals
- splash sound, shifting of lower border of stomach lower than umbilicus.
- X ray after barium. compensative (<6hrs), subcompensative(6-24 hrs), decompensative(>24 hrs)
a. functional
- present during exacerbation only, due to edema & spasm
- located near antrum or sphincter.
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b. Organic
- deformation & stenosis due to scar formation - necrotic
- with exacerbation & remission. sign and symptoms occurs at any time
- surgical treatment
4. Malignization
- Ulcer like tumor variant.
- exam pt after & before treatment (If cancer, no effect of Tx, pain present at all times)
- Cachexia (loss mass), no appetite.

Gatrointestinal bleeding
a) Causes
- Duodenal, gasric ulcer - Crohn‘s ulcerative infective colitis
- Hemorrhagic gastropathy & erosions - Haemorrhoids
- Mallory-Weiss syndrome - Anal fissure
- Gastric varices - Solitary ulcer in rectum
- reflux oesophagitis - Meckel‘s diverticulum
- ischemic colitis - Carcinoma of ceacum
- polyps - Angiodysplasia
- diverticula
b) Clinical picture
- constipation, melena, vomiting with coffee ground mass
- After bleeding, pain disspear bcoz of its alkaline rXn neutralizes stomach‘s acid.
- weakness, vertigo, pale skin, tachycardia, dyspnea, low arterial pressure
c) Emergency care
- monitor bp & pulse, ice per os & on epigastric, cold food (ice-cream), drugs (vicasol-vitamin K), statin-
after 3 days, thrombocyte aggregant (Dixinom)
- Instrumental: embolization, tamponade, infusion of fluid (glucose, ringer, NaCl 0.9%, albumin, plasma,
RBC. If still x stop: surgery (Billroth 1 or 2/ gastroectomy)
d) Investigation
- systolic murmur at apex
- blood analysis (Hb & Ht, coagulation)
- endoscopy- to detect cause & localization of Hemorrhage.
- rectal examination ( eg. carcinoma )
- proctoscopy ( eg. haemorrhoids )
- sigmoidoscopy ( eg. inflammatory bowel disease )
- barium enema – ischemic colitis
- colonoscopy – for any mucosal lesion and removal of polyps
- angiography – vascular abN ( eg. angiodysplasia)
e) Tactic
- Place cold compression on GI region or per os (ice)
- Transfusion of crystalloids, colloids RBC mass
- Stop bleeding – vicasol (vit K), Dixinom (aggregation of thrombocyte), epsilone amino caproic acid.
- Fibrogastroduodenoscopy
- Surgical - coagulated vessel, temponate PU, resection part of stomach, Bilorth I or II, Gastrectomy,
gastrostomy

30) Chronic enterocolitis

a) Definition
Chronic polyetiological, inflammatory disease of small bowel and colon wit functl & strucl disorders /
damage of the GIT mucosa characterized by the appearance of maldigestion, disorders of motor function,
75
secretion and finally synd of malabsorbtion. Inflamn & atrophy of mucosa, dysbacteriosis & 2‘ metabolic
disorders
b) Etiology
- Infectn ( Salmonella,Typhoid,Dysentery,Staphylococcal,Streptococcal, Shigella, Amoebiasis, TB,
Entamoeba Histolica, parasite - helminthes, protozoa )
- Alimentary factor – Irregular meals (spicy, hot, fat, cold, gas), overeating of poorly digestable food,
chronic constipation
- Alcohol, toxic chem. (arsenic, phosphorus, mercury), drug induced (NSAIDs, AB & cytostatics)
- Allergy, Stress
- Ischaemic (systemic/local AT) - (Ischemic colitis)
- 2‘ affection due to othr GIT disorders : stomach, pancreas, hepatobiliary system
- Radiation therapy
- Congenital enzymopathy (↓enz for absorpn - gluten and lactase)
- Acute enteritis
- Dysbacteriosis: upset microbial equilibrium in intestine
- Endocrine factor (diarrhea in thyrotoxicosis)
c) Pathogenesis
1. Inflamn & infiltration of mucosa
- etiologic lesion damages epithelial cells of bowel, mucin secreting cells & ↓ the ability for
reparations.
- Neutrophilic infiltration & oedema of lamina propria
- Progression destruction of mucosa: erosion, ulceration, submucosal inf
- Decrease epithelial cell nutrition
- Decrease act of enzyme
- Decrease absorption - motor dysfunction
2. Atrophy of mucosa-↓ functl ability & enz production
3. Probs wit absorpn of protein, CHO, fats. Insuff. in vits
- diarrhea → loss of water (↓ vol of circulating H2O)
- Progressive destructn → erosions,ulceration,digestion&motor disorders
4. allergic r-Rx : ↑sensitivity to diff subs
5. dysbacteriosis : secrete harmful subs.
6. Motor hyperfunction of small intestine, ingested food not process sufficiently before enter large
intestine → irritates its mucosa
7. Long standing kinetic disorder, Persistent constipation, Renal dysfunction, Autoinfection → cause
development of colitis
8. Release m/o and their toxin. Toxic products circulate in body in cases with upset metabolism
d) Classification
1. Acc to location 4. Acc to severity: Mild, moderate, severe
- small bowel (proximal colitis) - Jejunum, 5. Specific, Non-specific
ileum 6. primary
- large bowel (distal colitis) - sigmoid, asc, - Parasitic: helminthic, protozoa
des, transverse - Toxic: exogenous, endogenous
2. Atrophy (superficial/deep), w/o atrophy - Alimentary
3. Acc to stages: Exacerbation (mild, moderate, 7. Symptomatic / secondary
severe), remission
e) Investigation
1. Bld analysis: decreased RBC, increase ESR, thrombocytopenia, B12/ iron anemia, leukocytosis
2. Biochemical changes: low electrolyte, Na,K, Ca, decrease protein
3. Coprological: stetorrhea, amylorhea, creatorrhea
4. fibrocolonoscopy: can find atrophic mucosa, could be pale/inflamed wit visible vessels
76
 - presence of oedema & mucus covering the mucosa, polyps, ulcers, erosions, diverticula
- take specimens of intestinal mucosa
- diagnose cancer tumor
5. X-ray: distension of bowel, abnorm position of plica, fast/slow evacuation of barium, spasm, signs
of hypotonia, feather-like pattern of mucosa, presence of gas&liquid, info abt motor func, length,
position, shape, tone, haustration. Atypical: distention of bowel, ulcers, Cobblestone
6. rectosigmoidoscopy and colonoscopy - Biopsy w histological examination
f) Main clinical & lab syndrome. Proximal & distal variants
Proximal (Enteritis)
1. Pain syndrome- superficially in the umbilical region/central.
- Aching pain – due to stretching of bowel by gases (meteorism)
- Colic/spastic pain- due to motor disorder - spasm of bowel
- Deep dull pain- affectn of mesenteric lymph vessels & nodes
2. Dyspeptic syndrome
- Intestinal dyspepsia - diarrhea, steatorrhea, creatorrhea, amylorrhea, constipation & meteorism
- Gastric dyspepsia: nausea,vomiting & eructation
3. Syndrome of maldigestion & malabsorpn
- insuff enz, abnorm digestion of protein, CHO, fats & vits insufficiency, dysbacteriosis
- hypoproteinaemia - Loss of weight, weakness, Immune system ↓, oedema, ↓ production of enzyme
- moderate hypoglycaemia
- hypolipidaemia – polyhypovitaminosis, osteoporosis, B12 & iron def anemia, trophic changes in
skin & nails, progressive atrophy of muscle, cachexia, polyneuritis, night blindness
- electrolyte disorders - ↓Na,K,Ca – paraesthesia of fingers & tongue, weakness, tachycardia &
arrhythmias
- Dehydration (loss of H20 & electrolytes)
4. Syndrome of polyglandular insuff
5. asthenic syndrome - Loss of weight, skin pale & dry, brittle nails, anemia, weakness, decrease ability
to work, restless
Distal ( Colitis )
1. Pain syndrome in L and lower part of abdmn
- Dull, aching or colic
- ↓ after defecation (↓ stretching of wall)
- Defecation may ↑ pain if inflamn intensive/rectal inflmn
2. Dyspepsia syndrome
- Intestinal dyspepsia : Diarrhea, constipation & meteorism
- Gastric dyspepsia – Loss of appetite, nausea, vomiting
- feeling of incomplete evacuation aft defecation
- tenesmus (oedema of mucosa)
3. Dehydration (loss of H20 & electrolytes)
4. asthenic syndrome
g) Management
Diet: adequate nutrition (fruits, vege, prot, CHO). Diet No. 4
Drugs:
1. AB-Biceptol, Doxycylin, metronidazole, Tetracycline-levamasitine, Sulfonamide-Stalsol
2. Enzyme: pancreatin, abomin, pansinorm, festal
3. Improve motor func – cerucal, Metoclopramide (a/emetic activity)
4. Pain syndrome – Bismuth (mucosa protective &↓ pain), spasmolytics in colic pain- atropine,
pirenzepine
5. stop diarrhea- loperamide, pectin, diphenoxylate, Immodeium
6. Long standing diarrhea- antacids-almagel & pratop (salts-hydroxide of Al & Mg),
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 7. Maldigestion, dehydration
- IV glucose, protein, hormones; Nitrates (↑absorpn of H2O) - relaxn of vessels
8. non-specific therapy
- Vit & iron therapy depends on deficiency
- Normalization mass of body-anabolic steroid. parental nutrition
- Good sanitary. Eubiotics

31) Chronic pancreatitis

a) Definition
Chronic relapsing, aggressive, polyetiological inflammatory destructive disease manifested with obstructn
of ducts, sclerosis, irreversible loss of exocrine & endocrine func & deterioration of pancreatic struc.
b) Etiology
1. Alcohol intoxication
2. Prob. Wit flow of bile
- Disease of biliary tract and liver: infection in lymphatic tracts, cholelithiasis, tumors, parasites,
cholecystitis: regurgitation of bile to pancrease and activate enzyme and digest parencyme
- Disease of duodenum: Duodeno-pancreatatic reflux, oedema, duodenal ulcer, duodenitis, peptic
ulcer below duodenal capillary
3. Obstruction pancreatic duct (stenosis, stones, carcinoma)
4. Alimentary factors – Vit insuff & ↓protein in meals, chronic disease of gastrointestinal tract
5. Drugs – Corticosteroids, Sulfanamides, NSAIDs, diuretics, cytostatics, glucocorticosteroids,
immunosuppressive, a/coagulants, indomethacin, paracetamol, estrogens, tetracyclines
6. Trauma of the pancreas
7. Toxic chem. – mercury, arsenic
8. Infectn – herpes, measles, parasites of GIT
9. Allergy – food allergy
10. Hormonal disorder- calcification due to ↑Ca (hyperparathyroidism)
11. Hereditary -insuff of alpha-antitripsin, metabolic disorders in Wilson disease
12. Hyperlipidemia, hypertriglyceride (deposition of fat under glands)
13. Idiopathic
c) Pathogenesis
1. Obstruction pancreatic duct - spasm in sphincter Odi (↓bicarbonate secretion, ↑protein concentration)
- Protein precipitation in tissue of pancreas leads to prob of flow of enz thus obstrucn of small
ducts→ ↑P in pancreatic duct→oedema of pancreas→autodigestion by enz→fibrosis
2. ↓ inhibitory enz → Activation of enz in pancreas production → autodigestion
- abn production of juice - H2O , HCO3 , proton , lipase , tripsin , amylase
- abnormal drainage through lymph – edema of pancrease
3. Alcohol consumption
- prodn of pancreatic enz. cause deposition of protein plugs
- Obstrucn of small ducts→ ↑pressure in pancreatic duct→oedema of pancreas→autodigestion
- Decrease proteins and increase enzyme juice concentration, enzyme start digesting pancreas
4. Biliary tract disease → temporary gallstone → obstructn of Sphincter Odi/ ↑pancreatic duct P →
inflamn → sclerosis-fibrosis
5. Common bile duct - increase pressure in common bile duct - disturbance in the flow of juice of panc -
stagnation of the enz containing juice cause destruction of panc tissue – autolysis - place of destruction,
appear sclerosis and fibrosis development.
6. Duodenitis/dystrophy or atrophy of duodenal mucosa → ↑secretin, cholecystokinin, pancreozitin prodn
→ ↑duodenum P → spasm of Sphincter Odi→↑P pancreatic duct →c-on of pancreatic juice→
deposition of prot plug formn → sclerosis-fibrosis
d) Classification
78
1. acc to clinical stage : Relapsing, Algesia(pain), - chronic relapsing pancreatitis
Latent - chronic pancreatitis with permanent pain
2. acc to phase: Recurrent/relapse, Remission (algesia) syndrome
3. acc. to dev : - chronic latent pancreatitis
- 1st stage- no prob in endo&exocrine func - pseudotumour of the pancreas
- 2nd stage – present endo&exocrine - Sclerotic
dysfunc 8. Acc etiology
- 3rd stage- Diarrhea, LOW, Vit insuff Primary:
4. Rome classification - alcohol
- Chronic calcifying pancreatitis (alcohol - chronic obstruction of main pancreatic
intoxication) duct (stenosis,stones,carcinoma)
- Chronic obstructive pancreatitis (obstrucn - infection
of bile duct) - drug-induced
- Chronic fibrous in duration - idiopathic
- Fibrotic-sclerotic - hereditary
- Chronic cystosis & pseudocystosis - Trophic - result of Kwashiorkor
5. According to pathophysiology: Secondary:
- Chr obstructive pancreatitis - diseases of biliary tract
- Chr calcifying pancreatitis - hyperparathyroidism
- Infiltrative fibrotic /inflammatory - chronic disease of gastrointestinal tract
- Fibrotic sclerotic form - hyperlipidemia, hypertriglyceride
- Cyst type 9. Acc morphology
- Retrograde flow - obstructive
6. Primary / secondary - sclerotic arounds glands (calcified,
- Primary – inflammation of the panc tissue alcoholic)
- Secondary – result of other GIT diseases. - atrophic (parenchymatous, inflammatory)
7. according clinical form and pancreatic - Oedematous, Fibrous, Pseudo-cystic
function
e) Main syndrome
1. Pain
- epigastric region, sharp spastic pain, belt like pain, 30-40 min after meal, hrs to days
- trigger factor - fatty food, alcohol, ice-cream, stress, physical exhaustion, when lie flat
- relieving factor - lie on R side wit leg pulled towards abdmn, avoid eating, cold application on
epigastric region, spasmolytics, antacids, cholinolytics
2. Dyspeptic
- Gastric dyspepsia: nausea, vomiting, hypersalivation, belching, weight loss
- Intestinal dyspepsia: Diarrhea, constipation, meteorism, loss of apptte & weight, jaundice, dry skin
3. Inflammatory – Fever, lymphadenopathy, arthalgia, vasculitis
4. Asthenic – weakness,↓activity to work, restless, malaise
5. Malabsorpn (Q30 f, page 77)
- Hypoproteinaemia, hypoglycaemia, hypolipidaemia, electrolyte disorders, dehydration
- disturbed digestion by panc juice
6. Endocrinal insuff- hyperglycemia, glucose intolerance
7. Exocrine insufficiency (destructn of pancreatic cells, obstructn of ducts)
- Pancreatic triad (Calcification, Steatorrhea, Exocrine pancreatic insuff)
8. Jaundice
f) Investigation
Objective examination
- Skin grey, dry, dirty color, red spot; enlarged nails, loss weight, muscle guarding, coated tongue,
painful palpation on epigastric, weakness and fear of eating.
79
 - Mayo-Robson‘s sign – Tenderness at L costovertebral triangle
- Kach‘s sign – Tenderness at L rectus abdominis, 5cm above umbilicus
- Shaffar zone (Degarden‘s point)
- Kerte‘s sign – muscular resistance of epigastric area.
Laboratory
- Blood – Leucocytosis L shift, ↑ESR, Normochromatic / hypochromic anemia, ↑enz in blood and urine:
amylase, tripsin, lipase; ↑transaminase & urine amylase, hypercalcemia, glucosuria, bilirubin in blood
- Corprology : Steatorrhea, Amylorrhea, Creatorrhea
- Pancreatic juice examination
- Biochem - C-Reactive protein increase with mucoid, dysproteinemia
Instrumental:
1. U/sound - enlargement, form, density, edematous, fibrosis, cyst(stones) in the panc duct
2. X-ray:
- Enlargement/deformed duodenum, ↑duodenal papilla, dislocation
- calcification (stones) in pancreas
- ↑ retrogastric space
- dilated ducts, central loop of small bowel, dilatation of transverse colon
- In contrast, double line seen.
3. Fibroduodenogastroscopy – stones, changes in Sphincter Odi, large papilla sphincter in tumor
4. Endoscopic-pancreato-cholangiography- stones, stenosis of tracts
5. Angiography- deformn+dilatation of arteries, abnorm distribution, disappearance of small arteries
6. CT scan- size of organ, edema, calcification of pancreas, cyst, fibrosis, obstructn of biliary tract: stones,
dilated vessels, differentiate wit tumor
7. retrograde cholangiography
8. ECG- tachycardia
9. laproscopy and laparotomy – acute pancreatitis
g) Treatment
1. Diet N.5, no triggering food (hot, cold, spicy, gassy, alcohol, fatty)
2. Pain
Spasmolytics – Analgin, Baralgin , Noshpa, Atropine, Papaverin
Analgesics –Pramidol, Meperidine
Lidocaine/Novocaine
Cold compression
Cytostatic eg. 5-uracil
3. Treatment of maldigestion & malabsorpn - avoid eating 2-3 days
4. insulin therapy
5. substitution therapy to restore normal flow of bowel
6. Etiological: due to infectn- A/biotics: Penicillin, cephalosporin, erythromycin, amoxicillin
7. Pathogenetic:
- Antacids: almagel & pratop (salts-hydroxide of Al & Mg); phosphotical
- H2-antagonists: Famotidine,Ranitidine,Cimetidine - ↓ gastric & pancreatic secretion
- Proton pump inhibitor: Omeprazole
- M-cholinorcp blocker: atropine
8. Enzyme: (contains trypsin: Pancreatin, pancreamexin, Mezim, pancitrate, Festal); (lipase containing –
Krion) - pancreatine, pancreatoazemine
9. enzyme inhibitors: Contrical, Gardox, Tricivil, Aprotinin, Trasilol
10. Diuretics
11. Cytostatics to stop secretion
12. Hormones: glucocorticoids
13. Antitoxic therapy – ringer
80
14. correction of exocrine - krion, Mizhil
15. Surgical treatment - in acute phase, present complication, organic duodenal stasis
h) Complications
- Jaundice - Ascites
- GIT (bleeding, enterocolitis, cholangitis, - Abscess, cyst, stone
hepatitis, 2‘ peptic ulcer) - HR pleurisy, polyarthritis, relaxation of L
- DM dome of diaphragm, hypotonic state
- Malignization - Thrombosis of spleen veins
- stenosis of diff levels of tract - stone in duodenal
- local steato-necrosis in bones
i) Prognosis
Bad because have to ctrl diet and if not, present relapse & need drug treatment whole life & high risk of
developing othr complications that may be fatal for life

32) Chronic cholecystitis

a) Definition
Chronic, polyetiological, inflammatory, non-calculus gallbladder associate wit dyskinesia of the bile tract
& changes composition of bile (dyscholia). Duration : >6mths
b) Etiology
- infectn: Gram –ve & +ve, E.coli, Strep, Staph, - trauma
Enterococcus, mycoplasma, Fungi, Virus Predisposing factors :
hepatitis, Parasites ( Ascaris, Lamblia) - obesity
- Duodenobiliary & duodenogastric reflux - Pregnancy
- Allergic reaction - Chronic stress
- GIT patho - gallstone in cystic duct, tumor of - trigger fatty food
pancreas / liver, enteritis, pancreatitis / - Dysbacteriosis of intestine
cholangitis - Immunodeficient
- ↓blood supply to GB - Bile stasis
- Acute cholecystitis - Congenital, family history
- Gallbladder sludge - metabolic disease -diabetes,gout
- Alcoholic - female, fertile, forties, fat, fair
c) Pathogenesis
1. Infectn
a. Enterogenic (intestine) / ascending - due to transient sepsis, reflux of sphincter Odi, disturbances in
motor func of bowels
b. Hematogenic- frm infectn of URTI (pharyngitis, otitis, sinusitis, tonsillitis). Occur due to ↓ immunity &
hypersensitivity to infectious agent causing allergy. Hyperergic agent ↑ permeability of blood vessels of
GB & colonizes mucosa to cause inflamn
c. lymphogenic
2. Bile stasis – GB stones formed due to hypokinesias in obese ppl, high levels of TG, VLDL, cholesterol
in blood causes ↑ prodn in bile & causes prolonged stagnation in GB. As a result, protein coagulates,
mineral precipitation & form stones
3. Infectn+bile stasis
Infection → bile reflux→neuroendocrine disorders→hypotonia of GB →neurodystrophy of GB wall→
bile stasis→ Inflamn & thickening of GB wall→ cholecystitis
d) Clinical picture
1. Pain syndrome:
- Spastic pain in right hypochondrium radiate to R shoulder, clavicle, scapular, chest, back. 2-3 days
- Increase pain with deep breathing & emotional stress; heavy work; alcohol; spicy, hot or cold, fatty,
gassy food, egg yolk. Pain disappear aft application of hot water bottle / spasmolytics
81
2. Dyspeptic syndrome
a. Gastric dyspepsia- nausea, vomiting, belching+bitter taste
b. Intestinal dyspepsia- Diarrhea+constipation, meteorism, jaundice
3. Inflammatory syndrome- weakness, malaise, restlessness, fever
4. Neurotic syndrome – depression, anxiety, neurosis, with vegetative signs - vascular tone changes:
disorder in GIT regulation,tachycardia
5. Cardiac syndrome
a. Angina like pain - spastic pain in precordial region, irradiate to the L part, assoct wit arrhythmic
syndrome (supraventricular fibrillation) & physical activity
b. Cardialgia- pain in the apex, indefinate duration, spontaneous charac, not assct wit physical activity
6. Mech. Jaundice- Yellow skin & eyes
7. Dyskinetic syndrome
a. Hyperkinetic- acute spastic pain due to trigger factors, nausea,vomiting, acute periodic episodes due
to spasm of isthmus, distension causes pain; relaxation by myolitics
b. Hypokinetic – Dull permanent pain w/o signs of inflamn due to stasis of bile, distension causes pain;
need analgesics
8. Solaric plexus syndrome
9. Asthenic syndrome- decreased appetite, weakness, decreased activity
10. Allergic syndrome- skin itching
11. rigid abd
12. Murphy, Courvoiser, Kehr, grekov–ortner, Rashbar‘s, Kaikar‘s, Musy‘s signs
e) Investigation
Ortner‘s, Kalk‘s, Ker‘s, Murphy‘s, Mussi-Georgievsky‘s, Razba‘s, Shotkin Blumberg‘s, & Kurvuasie‘s
signs are positive
If jaundice- yellow color of skin, painful palpation & muscle guarding on right side
Lab:
1. Blood analysis – L shift leucocytosis, ↑ESR, ↑α2 & γ-globulin, ↑fibrinogen, ↑bilirubin, if present liver
prob: changes in ALT, AST
2. Bile aspiration frm duodenum, GB, & bile duct
Bile in GB - leucocytosis, mucus, cylinder epithelium, cholesterol crystals, pathological no of bact.,
spec. pigmented cells, changes in bile pigments, large volume.
3. liver function test
4. blood culture
Instrumental:
1. U/sound : thickening of GB wall >3cm
- Shape, size, stones, dislocation, deformation, ↓mobility, crystals of cholesterol, density of contents
2. X-ray: retrograde pancreato-cholangiography, percutaneous transhepatic cholangiography
- change of bile duct (widening of ducts, fragment of duct due to sclerosis narrowing)
- shadow of bladder is not seen, absence of GB
- stone seen if present
- functional disorder (emptying)
3. CT
4. Thermography
5. Endoscopy if stones are in the papulla.
6. Radioisotopic examination if cancer is suspected.
7. hepatobiliary scintigraphy - imaging of liver, bile duct, gallbladder and upper part of small intestine
8. laparoscopy
9. fibroduodenoscopy
10. cholecystography
f) Treatment
82
1. Diet N5. No triggering food. Including boiled and steamed food and increase protein
2. Choleretics
- increase bile acid (true choleretics): cholagol, decholic, Alahol, Decharin, Oxaphenamide
- increase bile water component (Hydroretics): sodium salicylate Sodium salicylates, cholekinetics.
3. Cholekinetics
- ↑tone of GB, ↓ tone of bile tracts – Sarbite, Mannite, Xylite
- Relaxation of GB & bile tract- nitroglycerin, atropine ,euphylinne, platyphilline, spasmolytic
4. antibiotics
1st choice- ampicillin, erythromycin, lincomycin, rifampicin
2nd choice- Tetracycline
3rd choice- quinollones, cephalosporins, nitrofuran
5. Pain syndrome:
- Spasmolytics – Baralgin, Noshpa, Atropine, Papaverin, nitroglycerine
- Analgesics –Pramidol
6. Prevent stones formn- dehydrocholic acid - Cholagin
7. Improve immunity – vit & anabolics
8. Detoxification therapy - Ringer
9. Etiologic: bacterial - antibiotics
10. Pathogenetic: choleretics, cholekinetics
11. anti-inflammatory drugs if inflammation present
12. symptomatic – drug for dyspeptic syndrome
13. dissolution of gallstone – methyl ter-butyl ether, bile acids, chenodeoxycholic acid
14. Surgical treatment: Indicated in complications and obstruction by stone.
g) Complication
- Rupture, gangrene of GB - abscess
- Sepsis - Fistulas in the intestine, perforation
- Peritonitis, cholangitis, enterocolitis - Malabsorption of lipids leading to
- Malignization metabolic disorders
- Stenosis of bile tract - Intestinal dyskinesia.
- GIT bleeding - empyema and hydrops
- Jaundice - gallstones ileus
- DM - limely bile and porcelain gallbladder
h) Prognosis
- Prognosis for life is good but complete recovery is doubtful.
- Prognosis for work is also good or moderate depending on severity.
- Overall it is favourable but exarcebation period triggered by wrong intake of food & complications.

Bile tract dyskinesia

Functional disorders of the biliary tract.
a) Etiology
- chronic stress after viral infection
- dysfunc of the CNS
- Vegetative nervous system disorder.
- Chronic cholecystitis.
b) Pathogenesis
- Hyperkinetic - due to trigger factors, spasm of isthmus, distension causes pain (retention of bile)
- Hypokinetic – > SNS, ↓vagus nerve→spasm of Sphincter Odi. Due to bile stasis, distension causes pain
- Vegetative nervous system disorder (stress) causes hyper or hypotonia of the gall bladder and bile ducts.
- In hypertonia, the spasmic contraction of the bile duct obstructs the lumen, stop bile from flowing out,
resulting in bile retention.
83
- In the hypotonic bile duct, wave contractions of the bile duct which usually causes the excretion of bile
are absent, therefore bile retention occurs too.
- Chronic cholecystitis can cause spasmic contractions resulting the same condition.
c) Hyper- & hypotonic types
Criteria Hypotonic Hypertonic
1. Pain syndrome Dull, permanent, discomfort, Colicy, spastic, periodic, intensive
↑ after food intake
2. Dyspeptic syndrome ↓pain aft vomiting Often ↑ aft vomiting
3. Bile portion Large volume Rapid evacuation, x enlarged
4. X-ray GB enlarged & round. GB not enlarged, tonic condition, small
Evacuation of bile is slow. diameter, rapid evacuation or bile.
5. Treatment Spasmolytics Choleretics
d) Differential diagnosis
Cholangitis Bile tract dyskinesia
High fever, constant spastic pain in the - No organic changes in GB
right, jaundice, vena portal thrombosis - disturbances in emotional
& infection, leukocytosis - disturbances of motor evacuation func.(X-ray)
- no inflamn symptoms (x fever,x chills)
- 2 diff forms: hypo&hyper-tonic
- Pancreatitis- pain is in epigastric region, belt like.
- Cholecystitis- pain syndrome, dyspeptic syndrome, cardiovascular syndrome, solaric syndrome,
asthenic syndrome, allergic syndrome, jaundice syndrome, inflammatory syndrome.
e) Treatment - Cholekinetics:
Hypotonic –↑bile flow e.g. xylite, sarbite, mannite
Hypertonic – Relaxation wit spasmolytics (Papaverin, Baralgin, Noshpa, euphillyn) nitroglycerine, atropine,
platyphilline

33) Chronic hepatitis

a) Definition: chronic polyetiological inflammatory process of the liver parenchyma which lasts > 6 mths
b) Etiology
1. Viral infections
2. Toxicochemical – heavy metal & chemical agents.
3. Toxicoallergic agents – NSAIDs, tetracycline, diuretics, steroids, TB, aminoglycosides, hormones
4. Alcohol
5. Autoimmune diseases
6. Hereditary - α1 antitrypsin deficiency, Wilson-Kanovalov‘s Disease, Hemochromatosis
7. Mushroom poisoning
8. inflmtory bowel disease (ulcerative colitis)
9. Idiopathic
10. Non specific reactive hepatitis
11. Secondary biliary hepatitis superimposed upon extrahepatic cholestasis.
c) Types
1. Viral hep A
- Epidemical hepatitis/ infectional jaundice/ Botkin‘s disease.
- benign acute, self lmited disorder tht does x lead to chronic/ carrier state.
- water-borne, fecal oral transmission, short incubation / latent period
- Cytolysis w/out persistence of virus in cells.
- diff morphological structures
- no serological markers
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 - acute hep with healing w/out complicatns of cirrhosis.
2. Viral hep B
- parenteral route, sexual contact, downwards transmission fr mother to fetus
- relapsing, progressive, sometimes no remissions, leads to liver failure (chronization)
- chronization (acute to chronic Hep B) :
a. if asso with Hep D (delta)
b. if alcoholic & b4 has acute/chronic alcoholic hepatitis
- Markers: (HBs Ag- surface Ag), (HBc Ag, Hbe Ag- core Ag)
3. Viral hep C
- parenteral, sexual intercourse, downwards transmission from mother to fetus
- Progressive, leads to liver failure, cirrhosis, hepatocellular carcinoma, death
- Has direct hepatotoxic activity
- Not constant structure, mobile, < active clinical pic during the years
- After appearance of 1st sign → fast progression → death
- silent killer (non visible in progression)
4. Viral hep D
- Causes coinfection & superinfection.
- Superinfectn occurs in person with HBV & may manifest as acute exacerbation of chronic hep B.
- Direct hepatotoxic effect
- Ability for replication only with viral hep B or C
- By direct contact, blood transfusion
- Stimulates fibrotic septa formation (fast & irreversible → transformation into cirrhosis)
5. Viral hep E
- Sporadic & epidemic forms of acute hep.
- water-borne, fecal oral transmission & no risk of subsequent chronic liver disease.
d) Pathogenesis
1. Persistent hepatitis :
- Parenchymal: dystrophic changes, Mesenchymal: inflmtory changes
Inflmtn of periportal areas (interstitial, reticuloendothelial tissue, bile ducts, vssls of portal syst, arteries)
- Affection → infiltration of lymphocytes & monocytes → produce enzymes → inflmtn (effusion, edema,
infiltration, immune response) but no sclerosis
- Serous effusion is slight (liver enlargemt 3-5 mm) → no affection of metabolic funct of liver → may
persists for years without changes of liver (benign form of disease)
- May ↓ after treatment /↓ of etiological factor
2. Aggressive hepatitis
- ↓ metabolic activity, ↓ synthetic function, ↓detoxification functn
- Acute attack of virus → stay long time in organism (in DNA) → virus disturb funct of m‘brane → cell
dystrophy (direct degradation & necrotic changes) → virus activated by DNA polymerase →
replication of virus → affected cells secreting special Ag (liver specific lipoproteins) → organism
produce Ab → delayed hypersensitivity → macrophages infiltrate into lobule → produce enz → cell
affectd
- Later if hyperactivity of lymphocytes → affection of whole liver
- Cell damage is due to infiltration & autoAb causes necrotic changes → free spaces occupied by
collagenic tissues → liver fibrosis → Imbalance btw parenchyma & fibrotic tissues → sclerosis
3. Lupoid type of hepatitis (Autoimmunological)
- If T lymphocytes ↓ → autoimmune rxn against liver specific lipoproteins → auto Abs against liver
structure
4. Biliary hepatitis

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- Bile tract pathology → stasis of bile btw lobules → transudation of bile from duct to periportal spaces
→ bile acids affect periportal spaces → inflmtn, edema, increased permeability, infiltration → necrotic
changes (lobules are affected later)
5. Alcoholic hepatitis
- Direct toxic effect
- Indirect - ↓ parenchymal activity; inactivation of cytochrome P450; hyperuricemia; block Vit B12
absorption; hyperlactermia in bowels
e) Classification
1. acc to activity - Wilson-Kanovalov disease
- Mild – ↑ed ALT <3X 4. Acc to etiology – viral hep A,B,C,D,E,F,G
- Moderate – ↑ed ALT 3-10X 5. Acc to morpho changes
- Severe – ↑ed ALT >10X - Hep with 1‘ affection in periportal area
2. acc to duration - Hep with affection of lobules
- active phase – mild, moderate, severe (hepatocytes)
- non active phase - Mixed
- acute & chronic 6. Acc to clinical form
3. Los Angeles classification - Persistent hepatitis (alcoholic, drugs)
- Chronic hepatitis B - Aggressive hepatitis: viral; autoimmune;
- Chronic hepatitis C non viral non autoimmune
- Chronic hepatitis D - Lobular (mix)
- Autoimmune hepatitis - Autoimmune
- Drug hepatitis 7. Acc to biliary affection (biliary hepatitis)
- Insufficiency of α1 antitrypsin - Persistent: asso with periportal tract
- 1‘ biliary hepatitis - Aggressive: total involvemt of periportal
- 1‘ sclerotic cholangitis & lobules
f) Main clinical & lab syndromes
1. Pain syndrome
- Discomfort, dull pain & heavy feeling in projection of the liver
- Prolonged for hours, mild & moderate, no radiation.
- Trigger factors: eating, catch cold, stress, physical activity, drugs, alcohol.
2. Dyspeptic syndrome
- Stomach dyspepsia: nausea, vomiting, LOA,
- Intestinal dyspepsia meteorism, flatulence, belching, unstable stool, LOW
- epigastric discomfort and regurgitation and constipation
- Laboratory signs: low counts and changed function of thrombocyte, decreased synthesis of blood
coagulating factors II, V and VII
3. Asthenic syndrome
- Weakness, malaise, ↓ working ability, restlessness, oss of interest in everything
4. Immunoinflammatory syndrome
Clinically: - Specific Ab against nucleus, mitochondria
- Arthralgia & sm mm
- Fever - Increased leukocytes
- Vasculitis - Decreased albumins
- Lymphadenopathy - Decreased reaction of leucocyte migration
- Spleen enlargement inhibition
Lab: - If it‘s alcoholic liver, ↑ lupoid (LE) cells
- High γ-globulins marker
- ↑ ESR, ↑ed Ig M, A, G
5. Cholestasis syndrome
Clinically:
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 - Itching (bile acids accum in skin) – can‘t sleep
- Icterus, dark urine, pale stool
- skin pigmentation, xanthelasmas, fever
- To evacuate bile, antidote is used :
a. non specific enterosorbance: enterogel, interstopan
b. specific: bile acid sequestrants
Laboratory signs: high level of conjugated bilirubin, cholesterol, γ glutamate transpeptide, ↑ alkaline
phosphatase (cholestasis)
6. Hemorrhagic syndrome
- Epistaxis (nasal bleeding), Gingival bleeding, Metrorrhagia, petecchiae/ecchymosis after injectn
Lab:
- ↓ production of coagulative factors, Vit K defic – prothrombin & fibrinogen ↓
- low level of thrombocytes, high spleen activity
7. Cytolysis syndrome
Weight loss, fever, jaundice, hemorrhagic diathesis, changes in CNS, extrahepatic signs.
Laboratory signs:
- low albumin, prothrombin, cholesterol, cholinesterase and factors V and VII
- ↑ AST, ALT (transaminases), LDH5, alkaline phosphatase
- ↑ glutamate transpeptidase / γ-glutamine transpeptidase
- ↑ bilirubin (conjugated)
8. Splenomegaly syndrome
9. Hepatomegaly syndrome
10. Hypersplenism syndrome
- ↑ function of spleen/liver activity – destruction of all blood cells (pancytopenia)
- thrombocytopenia → hemorrhagic syndrome
- leukocytopenia → infections ↑
- anemia
11. Abnormal pigments syndrome
- Jaundice with or w/o cholestasis- xanthelasma
- Skin icterus, itching, dark urine, light feces color
- ↑ CNS disturbances → ↑ toxicity → sleeplessness
12. Hepatodepression syndrome
- ↓ albumins & ↑ γglobulins → dysproteinemia
- ↓bromsulfurin
13. Portal hypertension syndrome – meteorism, splenomegaly, hepatomegaly, varicose esophagus vein,
caput medusa, ascitis
14. Non liver/small liver Signs
- Liver hand - hyperemia of thenar & hypothenar, clubbing, palmar erythema, pale nail
- Vascular stars - zone by Dekolte (neck, upper part of chest), small dots which disappear after pressing
- Trophic disorders (syndrome of dirty grey skin) lipid & CLTRL metab disorder→ accumulation in skin
- Teleangioectasia, gynecomastia, red tongue, xanthoma, xanthelasma
Lab
- ↓Albumin production
- ↓ prothrombin, fibrinogen
- ↓ Cholesterol, cholinesterase
- ↓ bilirubin, ↑ toxins in blood
- ↓ V, VII clotting factors (HRgic syndrome)
- ↑ γ globulin
g) Morphological properties of different types
1. Chronic active
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 - necrosis w periportal connective tissue septa extending to liver lobule.
- bridging necrosis (connect 2 central vv, 2 portal tracts or a central vein with a portal tract) &
fibrosis are present in > severe forms & most likely to involve many lobules with progressive liver
destruction which lead to cirrhosis, chronic liver failure & death.
2. Chronic persistent
- infl is localized within the portal tracts. There‘s minimal necrosis & usually benign course.
- inflmtn & infiltratn at portal tracts but no necrosis of hepatocytes.
- lobular architecture is preserved (normal), periportal tracts intact
- No extension of necroinflmtn into liver lobule
- Fibrosis is minimal/absent, inflmtn is often reversible
3. Chronic lobular - portal infl within portal tract plus foci of necrosis & inflammation in the liver lobule
4. Alcoholic cirrhosis
- liver is fatty & enlarged, with a smooth, yellow tan, greasy surface - micronodular pattern
- fibrosis increases with time, fat content decreases & liver becomes blowner.
- regeneration of liver cells cause scattered larger nodules may be up to 1 cm in diameter.
- early micronodular stage, fibrous septa & bridging cause lobules to be encapsulated. The scarring &
regeneration distort the normal lobular architecture. A lymphocytic infiltrate & reactive bile duct
proliferation sometimes present within the scarring.
- the final irreversible form of alcoholic liver disease evolves slowly.

Chronic persistent hepatitis

a) Etiology - Alcoholic/drug induced – metronidazole, isoniazide, nitrofurane
b) Clinical symptoms
Mild or asymptomatic - Ascites, jaundice
- Pain in hypochondrium Syndromes
- Hepatomegaly, nausea, anorexia - Asthenic
(dyspepsia) - Dyspeptic
- Hepatic signs (spider nevi and stars on - Pain syndrome
skin upper part of chest, upper extremities, - syndrome of hepatic signs
face) - Hepatomegaly
- Palmar erythema, strawberry tongue, - Jaundice
gynecomastia, hair loss - Cytolysis syndrome
- Splenomegaly, fatigue, LOA - hepatodepression syndrome
c) Investigation
1. Liver function test
Increase ALT, AST, hyperbilirubinemia, dysproteinemia, hyper-γ-globulinemia, hypoglobulinemia,
glutamine transpeptidase, electrolytes, and alkalinephosphatase
2. Gen blood analysis:
Leukocytosis, increase cholesterol, ↑ bleeding times
3. Blood screening – exclude viral hepatitis, hemochromatosis, carcinoma, biliary disease
4. Electrolyte tests – hypophosphatemia, hypomagnesemia, alcoholic acidosis, respiratory alkalosis
5. Immunology
- high Ig M, A, G
- specific cells – lupoid (LE) cells
6. U/S
- diffused parenchyma, hyperechogenic structures without nodules
- liver enlargement, spleen enlargement
- Changes of tissue density (initial stage of cirrhosis)
- Changes of bile ducts
7. gastroscopy – stomach acid
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8. Liver biopsy – lymphocytes in portal tract, dystrophic changes, fibrosis, cell membrane destruction,
leukocytes infiltration, necrotic changes
d) Treatment
1. Diet No. 5 – no fatty food, spices, alcohol. high-protein, vit & mineral diet
2. Antiviral drugs, interferon (reaferon) drugs (↑ level of immune syst)
3. Hepatoprotectors – Riboxin, acid glutaminic acid, Vipamic; colchicine, asensal, catechin
4. Immunodepression drugs – Prednisolone
5. Vitamins; Myolytics; Cholinergic
6. Liver transplantation
e) Prognosis
- In mild/early onset of hepatitis, prognosis is usually good w complete recovery if treatment is
adequate, complete withdrawal from alcohol or drug and monitoring of diet
- In late stages, liver cirrhosis develops, extrahepatic complications appear such as encephalopathy,
coagulopathy, ascites, portal hypertension, iron overload

Chronic active virus hepatitis

a) Etiology - Viral Hepatitis B commonly associated with Viral Hep D.
b) Pathogenesis - Page 85 - Aggressive hepatitis
c) Clinical picture
- Dull pain, arthralgia, LOW, xanthomas, vasculitis, hyperpigmttn
- hepatomegaly, splenomegaly, Hypersplenism, red nose, club fingers (AV shunt)
- small liver syndrome, hemangioma (small red spots)
- Red lips, jaundice, spider nevi, palmar erythema, gynecomastia, raspberry tongue.
- Cytolysis, immunoinflmtory, Cholestasis, Hepatodepression, Hemorrhagic syndromes
- Mesenchymal inflammation – arthralgia, myalgia, enlarged lymph nodes, vasculitis, fever,
dysproteinemia, ↓ albumins
- nausea, anorexia, urine dark and stools pale
d) Symptoms & signs
- 3-5 yrs after acute viral infection
- Hepatomegaly, jaundice
- Pain – boring, aching, intensive, increased after physical exertion
- Ascites, edema
- Fatigue, weakness, bad mood, dyspepsia
- hepatodepression, cytolysis, Hemorrhagic syndrome, mesenchymal inflmtn
- hypersplenism – pancytopenia
- hepatic signs – stars erythema
- progressive period (virus replicatn): nephritis, carditis, ↑AST & ALT, Liver failure, Death
Investigation
- Liver biopsy –bridging necrosis, infl infiltrate, fibrosis
- US – hepatomegaly & splenomegaly
- Lab: +ve serological test for respective virus, ↓prothrombin, ↓cholinesterase, ↓cholesterol, ↓fibrinogen,
↑toxins, ↑ALT, AST, conjugated bilirubin
- liver biochemistry – bilirubinuria and increased urinary urobilinogen. Increased AST and ALT
- Haematological tests – leucopenia with lymphocytosis.
- Viral markers: antibodies to HAV
e) Etiological diagnostics
Hep B immunological Dx (viral serological markers Abs to virus B, C, D)
- HBsAg & HBV DNA with HBE Ag found in serum
- HBs Ag – may be seen as ground glass, appearance in cytoplasm on H & E stain
- HBc Ag seen in hepatocytes by immunohistochem staining
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 - Hepatitis B – HbsAg, IgG anti-HBc, HBeAg, HBV DNA
- Hepatitis C – anti-HCV, HCV RNA
- Hepatitis D – anti-HDV, HDV RNA, HBsAg, IgG anti-HBc
f) Treatment
1. Diet No. 5 – no fatty food, spices, alcohol, rest, balanced diet
2. Etiological Tx
Antiviral drugs - interferon, acyclotin, virocides, Lamivudine, Adeforvir, Dipivoxil, Interferogens,
Exogenous interferons (interferon-α)
3. Pathogenetic Tx
- Hepatoprotectors – Riboxin, acid glutaminic acid, Vipamic, Legalon, lipoic acid, phospholipids
- Glucocorticoids
4. Symptomatic Tx
- Diuretics – for ascites
- Liver funct improvemt: vitamins B, C & PP
- prednisolone, contra-cholerectics & cholekines
g) Prognosis
- prognosis is excellent with complete recovery.
- Prognosis is usually poor w liver cirrhosis development in last stages within 10 years after infection.
- complications associated w cirrhosis such as acsites, esophageal varices, encephalopathy
- Prognosis is worse if Hep B + D

Chronic active autoimmune hepatitis

a) Etiology
- Actual causative factor unknown 3 types of autoimmune hepatitis (acc to Abs):
- hepatotropic viruses - anti- smooth mm – common
- metabolic / genetic derangements - antinuclear Ab – in children & old ppl
- hepatototoxic drugs - cellular liver & kidney – for old people
- known to mainly affect women
b) Pathogenesis
- If T lymphocytes ↓ → autoimmunological rXn against liver specific lipoproteins → auto Abs against
own liver structure
- Viral dependent changes & autoimmunological changes present together in practice → hepatocellular
necrosis, inflmtn, fibrosis of liver (intralobular necrosis) → leads to cirrhosis & liver failure
- Progressive disease, recovery is impossible

- When body exposed to triggering factor, it actives host cell-mediated immune response.
- HLA on the surface of hepatocytes causes immune response to form antibodies against it.
- The antibodies then cause T-cytotoxic cell & plasma cells to infiltrate healthy tissue, release cytokines
and destroy the tissue
c) Clinical picture
Symptoms
- Abdmnl, chest pain, severe acne, joint affection, cessation of menses, diarrhea, fever, large abdomen,
hepatic signs, ascites, edema, polyserositis, myocarditis and echymosis.
- asymptomatic, fatigue, anorexia, dark colour of urine, jaundice, hepatomegaly, itching
Syndromes
- Asthenic - Cytolysis
- Hepato-splenomegaly, hypersplenism - Hepatodepression
- Extrahepatic signs – liver hand, vascular - Mesenchymal inflammation
stasis, trophic disorders - systemic inflmtn (leucopenia, increased ESR,
- Hemorrhagic syndrome anemia, fever)
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d) Investigation
1. Gen blood analysis
- Pancytopenia - mild leucopenia w eosinophilia,
- ↑ bleeding time & high prothrombin time - thrombocytopenia
- normochromic normocystic anemia, - ↑ESR
2. Biochemical of blood
- changes in γ globulins - increased serum bilirubun
- electrolyte tests - increased alkaline phosphotase
- increased ALT, AST - hypoalbuminemia
3. Immunology
- high level Ig G
- viral markers in blood dependent on phase of activity of viruses
- specific cells – Lupus Erythematosus Test (LE cells) – positive
- Absence of viral serological markers
- Serum protein electrophoresis – presence of IgG
4. U/S - Changes of tissue density, bile ducts, diameter of liver
5. Liver biopsy – piece-meal necrosis, bridging necrosis, fibrosis, lobular collapse,
e) Treatment
1. Diet No. 5 – no fatty food, spices, alcohol. High calorie diet ( protein rich)
2. Antiviral drugs
3. Drugs that ↑ level of immune syst –interferon (reaferon)
4. Hepatoprotectors – Riboxin, acid glutaminic acid, Vipamic
5. vitamins
6. Immunodepression drugs – Prednisolone, cytostatics, corticosteroids
7. liver transplantation if liver cirrhosis - prednisolone with azathioprine given daily for 2 weeks
f) Prognosis
- Good prognosis if there is adequate treatment and management; spontaneous remission
- Prognosis is very poor if patient develops liver cirrhosis & if patient suffers from multiple relapses
& inability to gain remission

Differential diagnosis of persistent & active chronic hepatitis

Persistent chronic hepatitis Active chronic hepatitis
Etiology alcohol, drugs viral, autoimmune
Morphology portal thrombosis, less fibrosis liver lobule extends, fibrosis of septa
Progressive X progressive Progressive
Hepatomegaly Severe Severe
Splenomegaly  
Pancytopenia  
Symptom (+ve) (-ve)
Complaints < (mild) > (edema, ascites) (severe)
Morphology Morphological necrosis Piece meat & bridging necrosis
Outcome benign, good recovery. liver failure and liver cirrhosis.
- Persistent - pain, dyspepsia, cytolytic syndrome, asymptomatic, fatigue, moderate level of
aminotransferase, slight hyper bilirubinemia
- Active - cytolytic syndrome, fatigue, amenorrhea, jaundice, high activity of transaminase,
mesencyhmal inflammation, hemorrhagic syndrome, hypersplenomegaly.

34) Cirrhosis of the liver

a) Definition
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Liver cirrhosis is polyetiological irreversible fibrosis with total destruction of liver with appearance of false
lobules (changes of architectonics of liver tissue), blocking normal filtration of hepatocytes, loss of
function and formation of macro/ micronodules with portal hypertension development.
b) Etiology
1. Alcohol 6. biliary duct disease- intra and extrahepatic
2. Infections: 7. autoimmune disorders
- Virus (hepatitis B,C,D, E,F,G) 8. Autoimmune hepatitis
- Parasites – Giardia lambia etc 9. Hereditary haemochromatosis
- Bacterial 10. Hepatic venous congestion
- fungal 11. Budd-Chiari - syndrome
3. Hepatotoxic chemicals: tetracyclines, 12. hereditary disorders- Wilson disease, alpha-1
mushroom poisoning (amonitine), anabolic antitrypsin deficiency
hormones (contraceptives, estrogens etc), 13. metabolic and electrolytes disorders- iron and
heavy metals copper.
4. secondary hepatitis → peptic ulcer and 14. alimentary disorders
cholecystitis 15. cryptogenic
5. Biliary cirrhosis. Biliary diseases of liver
c) Pathogenesis
Etiological factor cause irritation of hepatocytes, there is constant inflammation and infiltration of
immune cells to liver parenchyme, necrosis as a result of ischemia due to abnormal circulation resulting
in formation of nodules, release of growth factors and cytokines which stimulate fibroblast
development and fibrosis development→ scarring and eventually cirrhosis
(Chronic injury to liver: inflammation, necrosis, fibrosis, scarring and eventually cirrhosis)
d) Classification
1. Anatomically / Morphologically : - Remission
- Micronodular – <3mm, common cause is 4. Stages
alcohol - Compensation – liver functions
- Macronodular – >3mm, common cause is compensated by healthy hepatocytes, only
viral hepatitis morphological changes can be seen.
- Mixed - Subcompensation
- Incomplete septal fibrosis/cirrhosis - Decompensation – liver insufficiency and
2. Clinical picture: failure
- Quick progressing 5. By etiologically
- Slow progressing - Alcoholic cirrhosis
- Latent - Viral cirrhosis
- Not progressive - Biliary cirrhosis – primary (autoimmune)
3. Phase: and secondary (disturbed bile flow)
- Active
e) Main clinical & laboratory syndromes
1. Pain syndrome
- Dull and heavy in projection of liver
- Prolonged for hours
- No radiation
- Triggering factors include – eating, stress, physical activity, drugs and alcohol.
2. Dyspeptic syndrome
- Gastric : nausea, vomiting, loss appetite, bitter taste of mouth and dryness
- Intestinal : meteorism and flatulence, unstable stool, bleeding
3. Asthenic syndrome
4. Mesenchymal inflammatory syndrome
- Fever, arthralgia, lymphoadenopathy, splenomegaly, vasculitits, myocarditis etc.
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 - Labs : ↑ ESR, ↑ WBC ↑ C-reactive proteins
5. Syndrome of cytolysis
6. Edematous syndrome – Ascitis, ↓ Urine output
7. Hemorrhagic syndrome
8. Cholestatic syndrome
9. Liver insufficiency syndrome
- ↓ albumin, bilirubin, prothrombin, cholesterol, coagulating factors (V, VIII), Fibrinogen
- In late stage → dev encephalopathy or coma
10. Non -liver signs syndrome
- Liver hands – palmar erythema
- Clubbing of fingers
- Zone by Decholte – presence of spider nevi in chest and neck
11. Syndrome of dirty grey skin - disorder of metabolism of lipids and cholesterol
12. Portal hypertension syndrome
a. 1st stage: - Collaterals visible
- Pressure 150 mmHg - No ascitis
- No splenomegaly, no caput medusa, c. 3rd stage
no collaterals, no ascitis - 300 – 700mmHg
b. 2nd stage: - Splenomegaly, all collaterals
- 160-300mmHg pronounced even with complications
- Splenomegaly like bleeding
- Osophageal vein varicose absent with - Ascites
caput medusa
f) Prognosis
- Very poor prognosis in cirrhosis as in many cases it is indicated as irreversible pathology and
develop many complications. Patient may have good prognosis in case of effectiveness of
symptomatic treatment and liver transplantation.
- Alcoholic cirrhosis – poor prognosis because often die from bleeding
- Biliary cirrhosis has long duration of development but may have many problems
- Viral cirrhosis – bad prognosis because always relapse of hepatitis and progression of cirrhosis.

Biliary disease of the liver

a) Etiology
- Primary biliary cirrhosis– intrahepatic idiopathic, intrahepatic cholestasis, possibly autoimmune
- Secondary biliary cirrhosis– extrahepatic bile duct obstruction: biliary atresia, gallstones, stricture,
carcinoma of pancreatic head, extrahepatic cholestasis,
b) Pathogenesis
1. Primary biliary cirrhosis – chronic, progressive cholestatic liver disease, characterized by destruction of
intrahepatic bile ducts, portal inflammation and scarring, and eventual cirrhosis and liver failure
2. Secondary biliary cirrhosis
Extrahepatic bile duct obstruction → Cholestasis (bile stasis) → inflammation with neutrophilic
infiltration→ necrosis→ periportal fibrosis→ hepatic scarring and nodule formation→ cirrhosis
3. Autoimmune mechanism - (expression of MHC class II on bile duct epithelial cells and accumulation
autoreactive T- cells around bile ducts) →production of antimitochondrial and antinuclear antibodies→
non suppurative inflammation (lymphocytic infiltration) →destruction of medium sized intrahepatic
bile ducts→ necrosis→ portal tract scarring and bridging fibrosis → cirrhosis
c) Clinical picture
Primary biliary cirrhosis - slower onset; Secondary billiary cirrhosis
- asymptomatic - Neuritis and neuralgia
- Dyspeptic syndrome - Osteoporosis
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- pain in bones- spines and ribs - Diarrhea, steatorrhea
- Bleeding tendency - Sicca syndrome (dry eyes and dry mouth)
- Ascities - Xanthoma, drumstick finger, spider
- hepatosplenogmegaly angiomata
- portal hypertension - CREST syndrome (Calcinosis, Raynaud‘s
- pruritus, fatigue. phenomenon, esophageal dysmotility,
- jaundice. sclerodactyly, telangiectasia)
d) Investigation
1. Blood test - leukocytosis, increase ESR
2. Biochemical test
- increase alkaline phosphatase, beta globulin, gamma glutamate transpeptidase, transaminase,
antimitochondrial antibodies, bilirubin, IgG, IgM in blood
- Increase lipids, phospholipids, cholesterol and lipoproteins in blood.
3. X-ray - deformation of vertebrae, varicose dilation of esophageal veins
4. Esophagogastroscopy - dilation of gastric and esophageal veins.
5. US, coeliography and gastroduodenoscopy - obstruction of biliary duct, tumor, cholestasis
6. Biopsy
- necrosis, infiltration and fibrosis revealed.
- destructive changes of bile ducts.

Micronodular liver cirrhosis

a) Etiology
Alcoholic liver disease, liver injury, biliary tract disease, vitamin-protein deficiency
b) Pathogenesis
Chronic alcohol intake→ direct toxicity to hepatocytes/ develop alcohol proteins (Mallory bodies)
leading to autoimmune reaction→ inflammation→ massive necrosis of hepatocytes → release of
cytokines and growth factors by hepatocytes and immune cells→ irreversible scarring and fibrosis→
appearance of false lobules (weblike septa of connective tissue) and change of liver tissue architecture,
replacement of healthy hepatocytes with fibrous tissue→formation of micronodules → cirrhosis and
portal hypertension development
c) Clinical picture
- mayb clinically silent, symptoms usually insidious in onset
- Anorexia and malnutrition lead to weight loss
- easy brusing, increasing weakness, and fatigue.
- jaundice, bleeding fr gastroesophageal varices, ascites, and encephalophathy.
- liver enlarged, normal, or decreased in size.
- spider angiomas, parotid and lacrimal gland enlargement, clubbing fingers, splenomegaly, muscle
wasting, and ascites with or without peripheral edema. extrahepatic signs (palmar erythema, spider nevi)
- Asthenic, dyspepsia
- discomfort and pain in right hypochondrium
- enlargement of abdomen, nasal bleeding, deranged sleep, irritability
- white and plain nails, myopathy, polyneuritis, anemia
- umbilical hernia, splenomegaly, avitaminosis
- Men may have decreased body hair, gynecomastia and testicular atrophy.
- Women - signs of menstrual irregularities.
d) Investigation
1. General blood analysis:
- Folic acid & Vit B 12 Anemia
- Serum prothrombin time prolonged
- Serum albumin depressed, serum globulin are increased.
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2. Biochemical studies:
- hyperproteinemia, hypoalbunemia, hyper gamma globulinemia, increase bilirubin level, low
cholesterol and prothrombin.
3. Immunological test - Ig A increase markedly
4. X-ray - reveal varicose dilated veins of esophagus
5. Radionucleide scanning of liver
- portal cirrhosis characterized by low contrast
- uneven distribution of radioactive preparation and almost completely absent in peripheral part of
organs. Mostly accumulate in spleen.
6. Laproscopy and liver biopsy
- hepatic enlargement
- fatty atrophy of hepatocytes, micronodular lesions, hepatocellular fibrosis.

Macronodular liver cirrhosis

a) Etiology - Viral hepatitis - HBV infection.
b) Pathogenesis
Viral hepatitis infection→ chronic inflammation → production of inflammatory cytokines and growth
factors → irreversible fibrosis→ appearance of false lobules and change of liver tissue architecture,
replacement of healthy hepatocytes with fibrous tissue→formation of macronodules→ cirrhosis and portal
hypertension development
c) Clinical picture (page 92, 93)
- Icterus
- Dyspeptic syndrome
- Mesenchymal inflammatory syndrome
- Hemorrhagic syndrome
- Non -liver signs syndrome
- Portal hypertension syndrome
d) Investigation
1. Blood test - anemia, thrombocytopenia, leucopenia
2. Biochemical test - dysproteinemia, hypoalbunemia, hyper gamma globulinemia, increase bilirubin level,
low cholesterol and low prothrombin, high level of transaminase.
3. immunoflorocent test - surface antigen for hepatitis
4. X-ray - reveal varicose dilated veins of esophagus
5. Radionuclide test
- diffuse reduction of isotope
- uniformity in isotope distribution and active accumulation of isotope in spleen.
6. Laproscopy and biopsy of liver
- macronodular lesions of liver
- formation of necrotic foci
- nodular regeneration and hydrotropic dystrophy.

e) Differential diagnosis of active hepatitis & cirrhosis of the liver

Active hepatitis Cirrhosis
Potal hypertension and its signs Absent Present
(ascites, collateral circulation,
caput medusa etc)
Pathomorphology Inflammation of liver parenchyma Inflammation, necrosis, fibrosis
without necrosis or fibrosis and and scarring
scarring of liver tissue
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Objective exam Enlarged liver with normal liver Liver decreased in size, may
shape palpate nodules and change in
liver shape
clinical picture More quick to appear and severe at Less quick, progressively severe
onset
f) Treatment: diet, medicaments
Diet No.5, don‘t eat fat, spices and substances which stimulate liver, stop alcohol, reduce salt intake,
aspirin and NSAIDS should be avoid. Low protein diet
Drugs:
- Antiviral- interferon alpha, lamivudine and ribavarin; reverse transcriptase inhibitors, acyclovir
- Hepatoprotectors – carcil, ligalone, acid glutamidase, riboxin, vitamins and Phospholipids, interferon,
carbile, lipamid
- Diuretics, aldosterone antagonist, vasopressin to stop ascites
- Symptomatic treatment – antidyspeptic drugs, immune regulators
- Detoxication - 5% glucose IV infusion
- liver metabolism improver- glucocorticosteroids
- immunosuppressive agents - Corticosteroids – prednisolone, triamcinolon, dexamethasone
- infusion theraphy of plasma and albumin in case of catabolic syndrome.
g) Indications of immunosuppression
- Predisposition to infection
- Pancytopenia esply with decrease in leukocyte, lymphocyte and monocyte counts
- Cirrhosis caused by autoimmune disorder - autoimmune hepatitis or idiopathic (non-viral hepatitis)
- Serum antimitochondrial or self antibodies in blood investigation.
h) Complications
- Portal hypertension complications – - detoxicating syndrome- hepatic coma
variceal bleeding, hepatic encephalopathy, - liver insufficiency
ascites - gastro-esophageal bleeding
- Hepatocellular carcinoma - haemorrhagic problems- coagulopathy,
- Progressive liver failure→death anemia, hemophilia
- Cirrhosis, liver decompensation. - hepatopulmonary syndrome
- jaundice - spontaneous bacterial peritonitis
- inflammatory syndrome - Hepatic encephalopathy.

Metabolic hepatic coma & portocaval hepatic coma

- Metabolic hepatic coma – due to destruction of liver tissue: acute viruses, chemical necrosis, mushroom
poisoning, usually leading to death
- Portocaval coma - develop as a result of portocaval anastomosis which arises from different types of
cirrhosis
a) Pathogenesis
Metabolic hepatic coma
- Fulminant hepatic failure due to viruses, toxins, chemical necrosis, mushrooms, drugs → ↑ toxins in
circulating blood → intoxication of brain→ encephalopathy develop under 2 weeks → coma
Portocaval coma – mechanism is unknown but have factors playing part.
- Liver cirrhosis → blood bypass liver via collaterals and toxic metabolites pass directly to brain esply
ammonia→ encephalopathy→coma
b) Clinical picture
Metabolic hepatic coma
- Jaundice, small liver, encephalopathy, deterioration of conscious ness from drowsiness, confusion and
disorientation to unresponsive coma with convulsations, fetor hepaticus, spasticity and extension of

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 arms and legs, plantar response remain flexed, cerebral oedema, infections, GIT bleeding, respiratory
arrest, renal failure and pancreatitis
Portocaval coma
- Increasingly drowsy and comatose, fetor hepaticus, constructional apraxia (can‘t draw or write),
decreased mental function, convulsions, nausea, vomiting and weakness, hyperreflexia and ↑ tone,
asterixis, rigidity, hyperreflexia, alterations in personality, mood disturbances, deterioration of self-care.
c) Treatment
Metabolic hepatic coma Portocaval coma
- reanimation room - reanimation room
- remove possible cause e.g. drugs, protein diet, - Evacuation of bowels, restrict protein intake
infections etc. - remove possible precipitating cause
- Bleeding – vit K, platelets, blood, fresh frozen - Give purgation and enemas to empty bowels
plasma from nitrogenous substances
- Infection – antibiotics - Infusion therapy – correct electrolyte
- Respiratory failure – artificial respiration imbalance and detoxification
- Renal failure – hemodialysis - Give antibiotics
- Infusion therapy - correct electrolyte - Ammonia absorbtion - Lactulose or neomycin
imbalance and detoxification - vegetable protein

Portal hypertension
Pressure in portal vein is 70 – 150 mm of water columns in normal but in portal hypertension ↑ 400-600
mm of H2O columns.
a) 3 groups of causes
1. Prehepatic / presinusoidal - Congenital hepatic fibrosis
- Portal vein thrombosis. - Myelosclerosis (extramedullary
- Compression by tumors haemopoiesis)
2. Intrahepatic / sinusoidal: due to distortion of - Granulomata
liver 3. Posthepatic / post sinusoidal: due to blockage
- Cirrhosis of vein outside the liver
- Hepatitis (alcoholic) - Budd-Chiari syndrome
- Idiopathic non-cirrhotic portal HT - Veno-occlusive disease.
- Schistosomiasis - Right heart failure (rare)
- Partial nodular transformation - Constrictive pericarditis.
b) Pathogenesis
Portal vascular resistance is increased in case of obstruction of veins or chronic liver disease. Stellate cells
are activated and transform into myofibroblasts. Under influence of mediators (endothelin, prostaglandins
or nitric oxide) the contraction of the activated cells contributes to abnormal blood flow patterns and
increase resistance to blood flow. In addition the balance of fibrogenic and fibrolytic factors is shifted to
fibrogenesis and blockage of veins developed. Finally portal hypertension occured and opening of
portosystemic anastomoses develop.
c) Signs
- Meteorism - Varicose distension of veins in esophagus,
- Dyspepsia hemorrhoids and subcutaneous veins and
- Splenomegaly, hepatomegaly caput medusa
- Hypersplenism - Ascities
- Collateral circulation- portocaval shunt - Encephalopathy
- Bleeding - hematemesis or melaena
d) Complications of portal hypertension
- Mucosal edema, malabsorption syndromes, exudative enteropathy, melaena, ascites, bleeding of
gastro-esophageal varices / trauma
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 - Hepatic failure, bacteremia, bacterial peritonitis, endotoxinemia, deranged detoxification function,
hepatic encephalopathy and hepatic coma

Jaundice
a) Different types
1. True jaundice:
- Hemolytic jaundice (pre hepatic jaundice)
- Hepatocellular (parenchymatous) jaundice
- Post hepatic or obstructive jaundice, cholestatic jaundice
2. False jaundice: due to hypercarotinemia, increase intake of carrot or mango, DM.
b) Pathogenesis
1. Hemolytic jaundice (prehepatic jaundice)
↑ destruction of RBC (intra or extra vascular hemolysis) by spleen or ↑ destruction of RBC in bone
marrow (ineffective erythropoiesis) causing excess bilirubin production to blood.
2. Hepatocellular jaundice
Hepatitis, cirrhosis, liver tumor causing rupture of bile canaliculi, necrosis of hepatic cells and ↑ hepatic
cell permeability. Impaired excretion conjugated bilirubin into hepatobiliary system. Hence, increased
accumulation of conjugated bilirubin in hepatocytes and secondarily diffusion into plasma.
May be due to impaired bilirubin conjugation as in Gilbert‘s syndrome or due to ↓ glucuronyl
transferase which may be hereditary or acquired.
3. Post hepatic jaundice
Complete obstruction of extrahepatic bile duct by stones, tumor or strictures of common bile duct or
sphincter Oddi
4. Cholestatic jaundice
Extrahepatic cholestasis - bile outflow is impaired due to complete obstruction of common bile duct by
stone, tumor, or strictures; Intrahepatic cholestasis (failure of bile secretion).
c) Clinic
1. Cytolytic syndrome 9. Hepatic encephalopathy syndrome - ↓
2. Mesenchymal inflammatory syndrome alertness, poor concentration, progressive
3. Cholestatic syndrome restlessness, aggressive outbursts, drowsiness,
4. Asthenic syndrome confusion, slurred speech, convulsions, coma,
5. Dyspeptic syndrome 10. Hepatorenal syndrome - Oligouria, with ↑
6. Hemorrhagic syndrome blood urea nitrogen and creatinine
7. Hypersplenism syndrome 11. Hepatopulmonary syndrome - Hypoxic state,
8. Portal hypertension syndrome clubbing fingers.
d) Investigation
1. Viral markers for HAV, HBV and HCV.
2. US examination (to exclude extrahepatic obstruction)
3. Liver biochemistry confirm the diagnosis.
- In hepatitis, serum AST or ALT tends to be high early in disease with only small rise in serum ALP.
- In Extrahepatic obstruction, ALP is high with a smaller rise in aminotransferase.
- Protrombin time and serum albumin is low in chronic liver disease.
4. Haematological test.
- Bilirubin raised and liver biochemistry is normal in hemolytic jaundice.
- Raised in WBC indicate infection
- Leucopenia occurs in viral hepatitis

Investigation accoding to types of jaundice:

1. Hemolytic jaundice
- pathology of bone marrow (ineffective erythropoiesis) or spleen
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 - yellow discolorization of skin, sclera and mucosa, splenomegaly, hepatomegaly, ascities
- absence itching
- urine and stool is dark brown
- Unconjugated hyperbilirubinemia
- increase level of circulating bilirubin
- Bilirubin absent in urine
- ↑ urobilinogen in urine
- ↑ stercobinogen in stool
- RBC↓ Hb, Ht↓
- Normal C.I.
- Reticulocytosis
- ↓ RBC survival rate
2. Hepatic jaundice (impaired conjugation)
- yellow discolorization of skin, sclera and mucosa,anemia, splenomegaly, hepatomegaly, ascities
- absence itching
- Unconjugated hyperbilirubinemia
- ↓ urobilinogen in urine
- ↓ stercobilinogen in feces
- No bilirubin in urine
- AST and ALT and Alkaline phosphatase are normal
- decrease level of UDP-glucuronosyl transferase
3. Hepatic hepatocellular jaundice
- yellow discolorization of skin, sclera and mucosa,anemia, splenomegaly, hepatomegaly, ascities
- mild itching present
- dark urine, pale stool
- Mixed hyperbilirubinemia (conjated, unconjugated)
- Bilirubinuria
- ↑ urobilinogen in urine
- ↓ stercobilinogen in stool (pale, clay like)
- ↑AST and ALT, Alkaline phosphatase
- Ultrasound reveal destruction of liver, tumor or cirrhosis
- Liver biopsy reveal hepatic necrosis.
4. Cholestatic jaundice
- skin pigmentation, xanthomas (in elbow and knee), pruritus, xantholomas (in eyelid), bone pain.
- dark urine , pale stool.
- Hepatomegaly, splenomegaly, ascities, hemorrhagic syndrome
- Hyperbilinurinemia mixed but predominantly conjugated bilirubin
- Bilirubinuria
- ↓ level of urobilinogen in urine
- ↓ level of stercobilinogen in stool
- ↑ Alkalin phosphatase
- ↑ cholesterol and bile acids
- Decrease vitamin A, D, E, K levels.
- US/MRI reveal cirrhosis, tumor, or biliary rupture/ damage
5. Post hepatic jaundice
- itching more severe, skin pigmentation, xanthomas, pruritus, xantholomas, bone pain.
- dark urine , clay stool.
- Hepatomegaly, splenomegaly, ascities
- Conjugated hyperbilirubinemia
- ↑ AP level
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 - Bilirubinuria (dark brown urine)
- Absence of urobilinogen in urine
- Absence of stercobilinogen in stool
- US/MRI reveal extrahepatic obstruction due to stone, tumor, or edema

35) Disease of esophagus

a) Diverticulum
Local enlargement of the walls. Outpouching of the wall of esophagus, regurgitation of saliva & food
Etiology:
- Traction frm old adhesion
- motor abnormality
- trauma
- infection
- Congenital disease
Types:
1. Zenker‘s diverticulum: appears in natural zone of weakness in post hypopharyngeal wall (Killian‘s
triangle) & causes regurgitation of saliva & food particles. When it becomes large & filled wit food, it
compresses esophagus & cause dysphagia/ complete obstruction
2. Midesophageal diverticulum: caused by traction from old adhesions or by propulsion.
3. Epiphrenic diverticulum: caused by achalasia of cardia.
4. Diffuse intramural diverticulosis: caused by dilation of the deep esophageal glands.
Features:
- Pain syndrome - acid regurgitation
- Inflamn syndrome - heart burn
- Dyspeptic syndrome - painful swallowing
- dysphagia - weight loss
Investigation:
- contrast X-ray barium swallow and meal & fibrogastroduodenoscopy
- chest X-ray
- esophagoscopy
- Manometry: shows aperistalsis of the esophagus
- CT-scan
Treatment:
- Zenker‘s diverticulum: Treated by cricopharyngeal myotomy with or without diverticulectomy.
- Large symptomatic esophageal diverticula removed surgically.
- When they are associated with motor abnormalities, distal myotomy is performed.
- Strictures associated with diffuse intramural diverticulosis are treated with rubber dilators.
b) Achalasia of the cardia
failure of atonic muscle of cardia to relax, disturbed peristaltic activity of the esophagus, deranged reflex
opening of the cardia on swallowing & impaired passage of food into the stomach & dilatation of the
esophagus due to retention of food
Etiology:
- motor abnormalities
- idiopathic etiology
Pathogenesis:
- Degenerative lesions in vagus and ↓ ganglionic cells in myenteric nerve plexus of esophageal wall.
- Nitric oxide-containing neurons are affected more than cholinergic nerves thus relaxation of the
sphincter is impaired
Clinical pic: Severe Retrosternal chest pain, dysphagia & regurgitation of food, weight loss
- Pain – paroxysmal attacks occur at night associated wit empty/overdistended esophagus
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 - Dysphagia- during swallowing. Emotional stress exarcebates.
- Regurgitation – food mass regurgitated when person bends dwn wit esophagus overfilled/during
night sleep. The mass may be aspired causing recurrent aspiration pneumonia
- Vomiting & nausea
Investigation:
1. Contrast X-ray
- dilatation & elongation of esophagus, upset peristalsis, stomach empty
- cardial segment of esophagus narrowed, barium meal retained in esophagus.
- gastric air bubble absent
2. fibrogastroduodenoscopy
3. Esophagoscopy, CT-scan: exclude carcinoma
4. Manometry: aperistalsis of the esophagus and relaxation failure of the lower esophageal sphincter.
Treatment:
- cerucal- normalization of motor func
- cardiodilatation/balloon dilatation
- endoscopic dilatation of the lower esophageal sphincter using a pneumatic bag.
- Endoscopic injection of botulinum toxin into the lower esophageal sphincter.
- surgical division of muscle at lower end of esophagus (Cardiomyotomy) laparoscopically.
- In older patients, nifedipine (20mg sublingually) or sildenafil tried initially to treat aperistalsis.
c) Stenosis of esophagus
Narrowing space of esophagus. Problem with movement of food
Etiology: congenital disorder, chem. Influence, trauma, cancer of esophagus
Clinical syndrome: Pain (in substernal area), Dyspeptic (heart burn), Prob wit taking meals (solid)
Investigation:
- Blood count (if cancer- ↑ESR & anemia)
- Contrast x-ray (stenosis of esophagus) & Fibrogastroduodenoscopy (changes in mucosa)
Treatment:
- Limitation in diet, > fluid intake.
- H2 histamine blockers (lower level of secretion)
- Dilatation of esophagus & plastic of esophagus

1. Upper esophageal stenosis

- Plummer-Vinson syndrome
- unknown etio and patho
- Clinical pic: dysphagia, iron deficiency anaemia, glossitis, angular stomatitis.
- Investigation: esophagoscopy, Chest X-ray
- Treatment: Dilatation of the web/ ring; Iron for iron deficiency anemia
2. Cricopharyngeal dysfunction
- Etio and patho: poor relaxation of the cricopharyngeal muscle during swallowing
- Clinical pic: dysphagia, odynophagia
- Investigation: barium swallow, chest X-ray, CT-scan
- Treatment: dilatation; surgical myotomy
3. Lower esophageal (Schatzki ring)
- etio and patho: narrowing lower end of esophagus due to ridge of mucosa or a fibrous membrane.
- Cli pic: asymptomatic; dysphagia after swallowing a large bolus of bread or meat.
- Investigation: barium swallow
- Treatment: dietary advice,
d) Esophagitis
Inflamn of esophagus. (acute & chronic)
Etiology:
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1. achalasia & stenosis
2. reflux esophagitis (reflux of gastric juice)
3. peptic ulcer, cholelithiasis (spastic contraction of pylorus/gastric hypertonia &↑ intragastric P )
4. pregnancy & large growths of abdml cavity due to ↑intra abdml P
5. Infectious esophagitis
- Viral - Herpes simplex virus, Varicella-zoster virus
- Bacterial - Lactobacillus and β-hemolytic streptococci
- Fungal - Cryptosporidium or Pneumocystis carinii, Mycobacterium tuberculosis
- Parasitic
6. 2‘ to infectious (scarlet fever, diphtheria, sepsis, acute pharyngitis/gastritis)
7. Radiation esophagitis (radiation treatment for thoracic cancers)
8. Corrosive esophagitis (ingestion of hot food/drinks / strong alkali or acid)
9. Drugs esophagitis (antibiotics, NSAIDS, potassium chloride, ferrous sulfate)
Pathology: irritation of the mucosa by thermal, chem., toxic, peptic, allergic, bacterial
Clinical pic:
- pain on swallowing (odynophagia) - chest pain, discomfort
- dysphagia - nausea
- HR esophagitis- haematemesis,maleana - vomiting
- Heartburn - ulcerations
- retrosternal discomfort-intensifies when
person lying dwn/bends
Investigation:
- Esophagoscopy – assess degree of inflamn, extension & charac.
- endoscopy and biopsy of ulcer
- immunohistology with monoclonal antibodies to the causative agents
- barium swallow
Treatment:
1. fasting
2. A/biotics if bacteria present
3. Astringents (bismuth nitrate/silver nitrate)
4. Sleeping in semi-reclining position
5. viral esophagitis - acyclovir, ganciclovir
6. candida esophagitis – fluconazole, amphotericin B
7. radiation esophagitis - viscous lidocaine, indomethacin
8. Corrosive esophagitis - dilatation with dilators passed over a guide wire though the stricture.

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