NSG2HPB EXAM

● Part 1 - 30 Minutes; 25 Multiple Choice Questions - 25 Marks

● Part 2 - 30 minutes; 25 multiple choice Questions - 25 Marks
● Part 3 - 20 Minutes ; 15 case study based multiple choice questions (3 case studies
comprising 5 multiple choice questions) - 15 Marks
● Part 4 - 40 minutes; 4 x short answer questions total of maximum 400 words: 100 words
per main question (each short answer question is broken into smaller sub-questions; not
in essay style and not referenced) - 35 Marks

Cancer and chronic pain

1. Describe the pathway from one normal cell all the way to a metastatic
cancer. What makes a normal cell change to a cancer cell and what
makes a cancer cell grow to invade tissues and organs?

Metastasis is the movement of cancer cells from their primary location to

another region of the body. Cancer cells can spreay through the bloodstream
(hematogenous) , the lymphatic vessels or locally through the body wall
(transcolemic) and can do so because chemicals that ordinarily keep cells
where they belong in the body are absent. Healthy cells turns cancerous when
they experience a genetic change instead of undergoing regular cellular death,
they become immortal.

2. Define Apoptosis and differentiation (in relation to cancer cells)

Apoptosis is programmed cell death. Cancer cells do not die. Cancer

differentiation refers to the graded classification of tumors.Well differentiated,
Grade 1 - Mostly resembles normal tissue and usually has a good prognosis
Moderately differentiated, Grade 2-Intermediate forms of tumour with both
good and bad prognosis, Badly differentiated, Grade 3 and undifferentiated,
 Grade 4- Tumours spread easier than other tumours, and their prognosis is a
little worse than for others,

3. Compare and contrast the anti-neoplastic medication classes

(described in the Oncology medication Lecture and the readings or
pages 402-3 of your Pearson med Surg textbook.)

Alkylating agents are a class of antineoplastic or ● Nitrogen mustards (eg,

anticancer drugs which act by inhibiting the
Alkylating Agents transcription of DNA into RNA and thereby stopping bendamustine, chlorambucil,
the protein synthesis.
cyclophosphamide, ifosfamide,
mechlorethamine, melphalan)
● Nitrosoureas (eg, carmustine,
lomustine, streptozocin)
● Alkyl sulfonates (eg, busulfan)

Antimetabolites An antimetabolite is a chemical that inhibits the use ● Folic acid antagonist:
of a metabolite, which is another chemical that is part Methotrexate.
of normal metabolism. ● Pyrimidine antagonist:
5-Fluorouracil, Foxuridine,
Cytarabine, Capecitabine, and
Gemcitabine.

Anthracyclines Anthracyclines are a class of drugs used in cancer

chemotherapy that are extracted from Streptomyces
bacterium.

Antibiotics Antibiotics are special and unique type Doxorubicin, mitoxantrone, and
of chemotherapeutics agents obtained bleomycin
from living organisms such as bacteria
or fungi

Miotic Inhibitors A mitotic inhibitor is a drug that inhibits mitosis, or docetaxel, estramustine, paclitaxel,
 cell division. These drugs disrupt microtubules, which and vinblastine.
are structures that pull the chromosomes apart when
a cell divides.

Hormonal Agents It involves the manipulation of the endocrine ● Aromatase inhibitors (AIs), such as
system through exogenous or external
administration of specific hormones, particularly anastrozole, exemestane, and
steroid hormones, or drugs which inhibit the letrozole
production or activity of such hormones (hormone
antagonists). Because steroid hormones are ● Selective estrogen receptor
powerful drivers of gene expression in certain
cancer cells, changing the levels or activity of modulators (SERMs), such as
certain hormones can cause certain cancers to tamoxifen and raloxifene
cease growing, or even undergo cell death.
● Estrogen receptor antagonists,
such as fulvestrant and toremifene

4. Define chronic pain, why do some people get it and what are the
effective treatments?

Chronic pain is pain that lasts more than several months (variously defined as 3 to 6
months, but longer than “normal healing”)Sometimes chronic pain has an obvious
cause. You may have a long-lasting illness such as arthritis or cancer that can cause
The best treatment plans use a variety of strategies,
ongoing pain.
including medications, lifestyle changes and therapies.

GIT

1. Describe Gastro-oesophageal Reflux Disease and the main

treatments.

A chronic digestive disease where the liquid content of the stomach refluxes into the oesophagus,
the tube connecting the mouth and stomach. Treatments include: antacids that neturalize stomach
acid, medications such as histamine blockers that reduce acid production, medications such as
proton pump inhibtiors that block acid production and allow for the esophaguys tissue to heal.

2. How would you know if your patient had GORD or peptic ulcer disease?
 Endoscopy

3. What are the differences in treatment between these conditions?

GORD Peptic ulcer disease

● Lifestyle modifications - avoiding ● Cessation of NSAIDS and

large meals and waiting hours smoking/vaping
before lying down after eating. ● Drugs that reduce acid secretion
● Avoidance of acidic food. (histamine h2-receptor
● Antacids for mild symptoms. antagonists and proton pump
● Histamine blockers to reduce inhibtiors)
acid productions ● Some antibiotics
● Proton pump hinhibitors that
block acid production and allow
for the esophagus to heal

4. Compare and contrast the pathophysiology of the conditions in the

lectures. Describe the mainstays of treatment for both conditions.

GORD Peptic ulcer disease

● A key factor in the development of A peptic ulcer is characterised by a mucosal

GORD is believed to be lower
oesophageal sphincter (LOS)
dysfunction , such that there is a failure
of tonic LOS contraction. The sphincter
becomes incompetent, allowing the
regurgitation of gastric contents into the
oesophagus
erosive injury about 5 mm or more in depth
(see Figure 35.4). The damage exposes the
underlying smooth muscle, blood vessels and
sensory nerves to the gastrointestinal contents
within the lumen.

5. What is a colonoscopy? What is its purpose and how far does it

extend?
A colonoscopy (koe-lun-OS-kuh-pee) is an exam used to look for changes — such as
swollen, irritated tissues, polyps or cancer — in the large intestine (colon) and
rectum.The colonoscope is a long flexible tube-like device that can
reach about 170-180 cm. Sometimes, the entire length of the
colonoscope goes inside your bowels.

6. Discuss the difference between polyps and adenomas

The key difference between adenoma and polyp is that adenoma is a type of
polyp that shows a higher probability of turning into cancer, whereas polyp is
benign and has the least probability of developing into cancer. Adenoma and
polyp are types of abnormal growths in the body.

7. What are the risk factors for, and the pathophysiology of, Colon
cancer?

Risk factors: age, with a peak incidence at 60-70 yrs old, the presence of large
numbers of adenomas, especially in the familial adenomatous polyposis, and
the presence of inherited hereditary non-polposis colon cancer (HNPCC)
genes. Other risks include people who have ulcerative colitis.

Pathophysiology: Colon cancer includes tumoursthat arise in the porximal

colon that grow along one wall. However if it grows in the distal colon, it
constrict bowel movements and penetrate th router surface spreading to
blood and lymph nodes. Most colon cancers produce carincoembryonic
antigen (CEA). This is a protein involved in cell adhesion that is produced in
the fetus but is not usually found in adults. The production of CEA may simply
reflect disorder in the internal regulation of tumor cells rather than an adaption
to their circumstances….. It is a marker for the recurrence of colon cancer.

8. Do you know the drugs in the lecture - the indications and mechanisms
of action?
 Renal

1. What is the pathophysiology of AKI (this is not widely covered just know
the overview of AKI and the three main types) and CKD (CKD is covered in
much more detail on the exam than AKI).

Aki: acute kidney injury

When the kidneys are injured, the kidney has ‘excess capacity’ and a
considerable proportion of nephrons (80-90%) may be lost. When the kidney
function is imp[aired the volume of urine, will fall and blood will retain water,
potassium (K+) ions and hydrogen (H+) ions and nitrogenous wastes, such as
urea, measured in the laboratory as blood urea nitrogen (BUN) and creatinine.
Aki is classified as prerenal, intrarenal and postrenal. Prerenal AKI develops
upstream of the kidneys, and is usually due to disruptions in renal blood supply. Intrarenal AKI
develops when the insult occurs within the kidney tissue. Postrenal AKI is due to obstructions of
urine flow distal of the kidneys.

CKD: Chronic kidney disease

Developed in long-standing disease sthat affect the kidney, such as chronic glomerular disease,
chronic pyelonephritis also associated with diabetes mellitus and hypertension as well as polycystic
kidney diseases. CKD is characterized by a progressive loss in nephron function, most readily
measured in reductions of the GFR The affected person’s kidneys have a significant capacity to
adapt to the loss of nephrons. Clinical manifestations of renal impairment— such as changes in
nitrogenous wastes, fluid, sodium and potassium— are not apparent until renal function is reduced
by 70– 75% of normal. Progressive structural and functional changes in the glomerulus (i.e.
glomerular hypertension , hyperfiltration and glomerosclerosis ), tubulointerstitial inflammation and
 renal fibrosis are the hallmarks of the pathophysiological process. Proteinuria is an important clinical
sign in CKD. The proportion of the blood protein albumin in total protein is usually increased in
proteinuria, and its measurement is considered an important laboratory test in CKD. It is usually
measured as albumin/creatinine ratio , and normal excretion is higher in women (3.5 mg/mmol
versus 2.5 mg/mmol for men). Microalbuminuria is defined as 3.5– 35 mg/mmol for women and 2.5–
25 mg/mmol for men), while macroalbuminuria is classified as values above the upper limit for
microalbuminuria..End-stage kidney disease (ESKD) is the end-point of CKD, and occurs when the
GFR falls below 60 ml/min/1.73m 2 and persists for greater than three months. It manifests clinically
when more than 90% of nephron function is lost. Unlike the outlook in AKI, there is no possibility of
recovery of nephron function. People with end-stage kidney disease require regular dialysis for the
rest of their lives, or a kidney transplant.

2. Describe creatinine and urea, why they increase in kidney disease.

Creatine - is a waste product filtered by gloreular and further secreted into

urine by the distal tubule. If creatine increases, the kidney function is reduced
as the waste is not being removed. (normal range is 60-120micromol/L)

Urea is filtered then 50% is reabsorbed ( inhibits water reabsorption). Urea is a

waste product of protein ,elevated levels indicate that the kidneys are unable
to excrete it.

3. How would I know whether my patient had hypo or hyperkalaemia?

HYPERKALAEMIA > 6.5mmol/L HYPOKALEMIA <2.5 mmol/L

ECG CHANGES: ECG CHANGES:

1) Small P wave 1) Small/inverted T wave
2) Broad QRS 2) U wave
3) Tall tented T wave 3) Non-specific ST depression
4) Prolonged PR 4) Prolonged PR
5) Arrthymias 5) TDP
6) Arrhythmias
Elevated levels of potassium (K+) Low levels of potassium (K+)

CAUSES: CAUSES:
Kidney failure Emesis, diarrhea, medications..

Symptoms: Symptoms:

shortness of breath, chest pain, fatigue, constipation, muscle

nausea, vomiting, heart palpitations weakness and spasms constipation,
tingling and numbess

4. In general, how should we treat a patient with hyperkalemia?

 ● Medicines will be given to remove potassium from your body. This will
lower your potassium levels. This medicine may be given as a pill or an
enema.
● Most likely would be treated with calcium
● Dialysis may be needed if other treatments do not work. Dialysis uses a
machine to remove waste products and toxins from your blood. Ask your
healthcare provider for more information about dialysis.

6. At the cellular level – what happens for someone to get peripheral

oedema?

Edema occurs when an excessive volume of fluid accumulates in the tissues, either
within cells (cellular edema) or within the collagen-mucopolysaccharide matrix
distributed in the interstitial spaces (interstitial edema)

Accumulation of fluid in the interstitial space that occurs as the capillary filtration
exceeds the limits of lympthatic damage

Haematological

Particularly review the following sections and think of the following

questions:

1. What is anaemia and what are the general types

Anaemia is defined strictly as a lack of erythrocytes (a: meaning no or low;

aemia: pertaining to blood) but the medical definition encompasses both a
reduction in functional erythrocytes and a decrease in quality and quantity of
haemoglobin.

Anaemia commonly results from defective production of erythrocytes, iron

deficiency or blood loss.

Anaemia is defined by level of haemoglobin:

 ● <120 g/L for people ages 12-14 years and females aged over 15 who
are not pregnant
● <130 g/L for males over 15
● <110 g/L for pregnant women

Microcytic - hypochromic Normocytic - Macrocytic -

Normochromic normochromic

Small and pale Normal shape and colour Large normal colour

Iron deficiency Haemorrhage Lack of vitamin b12

anaemia Insufficient production Folate deficiency
haemolysis

2. How would anaemia be treated?

Treatment includes : diet or supplements

Or blood transform in severe cases

3. What are the risk factors for leukaemia?

Leukaemia is the cancer of cells in the bone marrow.

 ● Exposure to radiation
● Chemotherapy medications
● Smoking
● Certainblood dirodres
● Certain genetic disorders

4. What are the similarities and differences between the leukaemias? -

Review workshop 4

Acute myeloid Leukaemia Acute Lymphocytic Chronic Myeloid Chronic Lymphocytic

(AML) leukaemia (ALL) Leukaemia (CML) Leukaemia (CLL)

Mainly affects older people Mainly affects children Mainly affects older people Mainly affects older people
(60+) (60+) (60+)

Grows quickly Grows quickly Grows slowly Grows slowly

Caused by a change in Caused when bone marrow Caused by a spontaneous Exact cause not know.
DNA in the blood forming produces immature white genetic effect due to a Attributed to genetic
cells in bone marrow blood cells due to a gene process called mutations.
defect. chromosomal
translocation

Symptoms: fever, fatigue, Symptoms: bruising fever Symptoms: easy bleeding, Symptoms: painless
and easy bruising of the and bone pain weight loss, pale skin, enlarged lymph nodes,
body fatigue, night sweats fatigue and fever.

5. Describe how the leukamias can increase a person’s susceptibility for

infection? What would you expect to find on a Full Blood Count?

In leukemia, abnormal white blood cells (WBCs) grow and divide uncontrollably,
replacing typical WBCs. This can have wide-reaching effects on the body.

FBC;
 ● Reduced haemoglobin normochromic, normocytic anaemia.
● WBC <1.0x10⁹/l to >200x10⁹/l, neutropena and f blast cells
● Thrombocytopenia <10x10⁹/l

6. What does it mean if the values on a full blood count are too low/ too high?
(i.e WCC, neutrophils, platelets, Haematocrit, haemoglobin)

Too high Too low

White Blood Cell Count A high white blood cell count usually indicates: An A low white blood cell count usually means
increased production of white blood cells to fight your body isn't making enough white blood
an infection cells. It can increase your risk of all sorts of
infections.

Neutrophils a high neutrophil count is commonly associated
with an active bacterial infection in the body.
Platelets If the platelet count is high, it would indicate
thrombocythemia or thrombocytosis.
A drop in neutrophil blood levels
typically occurs when the body uses
immune cells faster than it produces
them or the bone marrow is not
producing them correctly.
Thrombocytopenia A low platelet count means
that your blood is lacking the small cells it needs
to form clots

Haematocrit A high hematocrit is mean that a person isn’t getting A low hematocrit level means the are too few red
enough oxygen, suffers from dehydration, or is at blood cells in the body. In these cases, a person
risk of heart disease. may experience symptoms that signal anemia

Haemoglobin Polycythemia - makes your blood thick and Anemia

is cancer of the blood as it overporduces red
blood cells

7. What is thrombocytopaenia? How does a patient get it?

A condition where abnormally low level of platelets are observed.

● Enough platelets are not made in the bone marrow

● Increased breakdown of platelets in the bloodstream
● Increased breakdown of platelets in the spleen or liver

Caused by an existing bone disorder or an effect of taking medications

 8. Differentiate between the different types of severe transfusion reaction
(Flippin’ Blood Chart on LMS)
Fever 38°C and rise ≥ 1°C from
baseline within 15 minutes
of starting transfusion or ≥
39°C
Dsypnoea Hypotension, fever,
with/without tachycardia.
Potentially l
Do not restart transfusion.
• Investigate to exclude
other serious or severe
reactions with sepsis and
incompatible blood
work-ups. Consider
haemolysis and DIC
work-ups.
Provide cardiovascular
and airway support; give
oxygen and ventilation as
necessary; diuretics are
not beneficial and may
worsen this reaction. •
 Notify Lifeblood to ensure
quarantine and testing of
components from the
same donation

Urticaria or rash Over more than 2/3 of the Over more than 2/3 of the
body, within 45 minutes of body, within 45 minutes of
starting transfusion starting transfusion
(majority within 5 minutes (majority within 5 minutes

9. Do you know the drugs in the lecture - the indications and mechanisms of
action of Warfarin/TpA/Heparin/PGy12 Inhibitors etc

Indications MOA Adverse Effects

Heparin Anticoagulant therapy. Works by activating Haemorrhage,

Good for use in bypass or antithrombin Thombrocytopaenia,
dialysis circuits, where the Allergy, Watch use with
blood is traveling through Gingko Biloba. Antidote on
an artificial membrane. hand.

Warfarin Anticoagulant therapy. Works by inhibiting the Regular INR tests. Bleeding
Regular APTT tests 4/24. synthesis of vitamin gums, nose bleeds.
Use if Hx of PE,DVT,AF. K-depedent clotting
factors/

Aspirin Anti-inflammatory, Inhibits the conversion of Epigastric discomfort and

anti-pyretic, anti-platelet
arachidonic acid to the bleeding, tinnitus, renal
prostagladndins (thus dysfunction
inhibits cyclo-oxygenase -
needed for thromboxane
synthesis)

PGy12 Inhibitors Anti-platelet drugs act as antagonists of the Diarhhea, itching, nausea.
platelet adenosine
 diphosphate receptor P 2 Y
12, thereby inhibiting
platelet aggregation.

Fibrinolytic drugs
Potent plasminogen Binds to plasminogen and
activator acts on all other
plasminogen molecules.
Clot specific. Very
expensive.
May have anaphylactic
reaction. Fever. Cardiac
monitoring essential.
Cannot give any other
anticoagulation.

Dipyridamole Phosphodiestraase Increases the Headache, Fever. Hot flush.

inhibtior concentration of cAMP in
the platelets, therefore
decreasing adhesiveness.
Also has vasodilator
properties. Works better
with other anti-coagulant
(warfarin, heparin…)

Ticlopidine (Also same as
Clopidogrel)
PGy12 Inhibitors Inhibits the role of Neutropenia, BUT is
adenosine diphosphate reversible.
(ADP) in platerlet
aggrgration ( not
prostaglandin synthesis)

10. Mechanism by which vaccines work

Vaccines contain weakened or inactive parts of a particular organism (antigen) that

triggers an immune response within the body. Newer vaccines contain the blueprint for
producing antigens rather than the antigen itself. Regardless of whether the vaccine is
made up of the antigen itself or the blueprint so that the body will produce the antigen,
this weakened version will not cause the disease in the person receiving the vaccine,
but it will prompt their immune system to respond much as it would have on its first
reaction to the actual pathogen.
 Musculoskeletal

1. Describe the pathophysiology of osteomyelitis and osteoporosis

Osteomyelitis Osteoporosis

Osteomyelitis is an infection of the Osteoporsis is a metabolic bone

bone. It can be acute or chronic. The
most common pathogen is
Staphylococcus aureus. In acute OM,
inflammatory tissue responses are
induced by the invading pathogens. In
chronic OM, necrosis is evident. There
are three phases of OM… 1) Initial
Infection 2) Acute 3) Chronic.
disorder characterised by a significant
loss of bone mineral density and a loss
of microstructure. Bones become brittle
and fragile leading to an increased risk
of fractures. Underlying the condition is
a change in the balance between bone
formation and resportion. This balance
is controlled by two population of bone
cells arranged on bone surfaces.
Osteoclasts, which are derived from
bone marrow cells that differentiate
along the granulocyte -monocyte
pathway, break down bone tissue and
facilitate its resportion. Osteoblasts,
which are specialised fibroblast cells,
form new bone.

2. What are the differences between osteoarthritis and rheumatoid arthritis?

Osteoarthritis Rheumatoid Arthritis

Degenerative disease. Breakdown of Autoimmune disease. The immune

cartilage, which is the cushion between system attacks itself.
joints.

Joint stiffnes, pain, decreased range of Joint pain, swelling, stiffness, fever,
motion fatigue, loss of energy
Middle aged to older adults Between 30 and 50 years

Common in weight bearing joints, like Occurs in joint pairs, hand, ankles, etc.
hips knees and neck

3. List the common medications to treat these diseases and some common
drug interactions and adverse effects.
Corticosteroids can interact with herbal and NSAID medications
- An injection of a corticosteroid (sometimes combined with a local anesthetic) directly into an individual joint
can reduce inflammation and pain due to arthritis.

4. Compartment syndrome – what is the pathophysiology and what are you

looking for in your patient?

Compartment syndrome is a condition occurring as result of excessive

pressure within a muscle compartment. Compartments group muscles, which
are covered by a strong membrane called fascia. Normally, the fascia are
responsible for maintaining structural shape and keeping the tissues in place
and therefore, fascia does not stretch or expand easily.
Pathophysiology: inflammation/bleeding into a muscle compartment creates
a build up of pressure within the compartment. Due to the nature of fascia, inc
pressure is directed inwards, resulting in compression of capillaries, nerves
and myocytes. Ischemia can then develop (-o2 & nutrients, failure to clear
toxic waste) This can further damage cells within the compartment.

Can develop after severe injury (crash injury, severe haematoma, fracture).
Iatrogenic injury can be caused when health professionals apply bandage,
splint, cast too tight - this can result in CS. Exercise induced CS occurs after
excessive inc circulation to a muscle, exceeding capacity of fascia to absorb
inc pressure. Exercise induced CS resolves quickly when activity is ceased.

Looking for in patient: Intense pain, paresthesia and/or paralysis, peripheral

limb digits cold/discolored, evidence of trauma or gross deformity

5. Describe the pathophysiology and treatment of back pain

Mechanical: injury to spine, intervertebral discs, soft tissues. Fractures can be

acute or chronic process. Lumago is acute or a strain to quadratus lumborum
muscle or paraspinal muscle. Disc herniation & pregnancy.

Degenerative: Osteoarthritis of spine includes facet joint OA, sacroiliac joint

OA, spinal stenosis, degenerative disc disease.

Inflammatory: Inflammatory spondyloarthropathies - ankylosing spondylitis.

Sacroiliitis is most common. Pathophysiology depends on etiology - most
often, may be part of an acute inflammatory process.

Oncologic: Lytic lesions to spine, cancer of marrow, compressive nerve

phenomena from adjacent space-occupying lesions.

Infectious: Infection of spine, discs, epidural abscesses, muscular/soft tissue

abscesses.
 Treatment: Acupuncture, massage, electrical nerve stimulation, NSAIDs,
Cortisone injections, radiofrequency ablation, implanted nerve stimulators,
surgery.

7. Do you know the drugs in the lecture - the indications and mechanisms of
action of the classes of COX-1 & COX- 2 inhibitors, anti-rheumatic drugs &
anti osteoporosis drugs and treatments.

indications moa

COX-1 Management of chronic generates prostaglandins that

pain, helps line the are involved in the protection
of gastrointestinal mucosa,
stomach (used for chemo
to help sensitivity on
stomach)

COX-2 Chronic pain (helps reduce generates prostaglandins that

inflammation) mediate inflammation and pain
in sites throughout the body.

Anti-rheumatic Helps with rheutmaotoid

arthritis

Anti-osteoporsois Helps with ostoeporsosis

Part D study.
https://www.meddean.luc.edu/lumen/meded/mech/cases/case24/answers1.htm#q1

51 y/o male
pruritis (itchy skin) lethargy (tiredness, low energy), ankle oedema

Possible diagnoses: uremia (renal disease)..

Hx; Unwell for 2 weeks, increasing oedema, cough, malaise(discomfort), lethargy and
pruritis(ithcy skin)

MED HX: • Hypertension(high bp) • Atrial Fibrillation(irregular heartbeat) • Type 2 Diabetes •

Hyperlipidaemia (high levels of fat/cholestrol in blood) • Chronic Kidney Disease • Obesity • Low
back pain • Osteoarthritis (B) knees and (R) ankle

SURG HX: • Complete melanoma excision 20 years ago (skin cancer removal) • Wisdom teeth
extraction as a child

MEDICATIONS • Frusemide (dieuretic used to treat fluid build up) • Atenolol (beta blocker used
to treat high blood pressure) • Metformin (used to control the amount of glucose in ur blood) •
Warfarin (prevents blood clots, anticoagualant)

FAMILY HX: • Adopted -nil known

SOCIAL HX • Works as a plumber • Active social life • Hobbies- socialising, fishing • No

programmed exercise

ALCOHOL TOBACCO AND OTHER DRUGS: • smoked for 20 years currently -gave up in his
30s • Drinks around a bottle of wine a week (approx. 1 standard drink a day). • Denies other
drug use

PHYSICAL EXAMINATION: Vital Signs • RR – 20; SpO2 97%; HR 84; BP 160/94; T: 36.8

CNS • Lethargic, Oriented to place and time Resp system • Crackles in bases of both lungs on
Auscultation – persistent cough

CVS Bounding peripheral pulses palpable in upper limbs Pitting oedema to 3 cm above ankles
in both legs

UGS No Urine output since arriving Bladder scan shows 100ml

Integ Dry broken skin on arms and legs

MSK Reflexes normal in upper and lower limbs Strength normal