Documente Academic
Documente Profesional
Documente Cultură
2015
Compiled by Joshua Loke and edited by Joel Zhou
UNSW Med VI 2015
Page 1 of 67
Table of Contents
Pharmacology.................................................................................................................... 3
Pharmacology 1- DVT...................................................................................................... 3
Pharmacology 2- Inflammatory Bowel Disease...............................................................8
Pharmacology 3- Major depression...............................................................................12
Anatomy.......................................................................................................................... 17
Anatomy 1- Pneumothorax........................................................................................... 17
Anatomy 2- Larynx........................................................................................................ 20
Anatomy 3- Inguinal hernia...........................................................................................23
Pathology......................................................................................................................... 26
Pathology 1- COPD........................................................................................................ 26
Pathology 2- Primary hyperparathyroidism...................................................................31
Pathology 3- Nephrotic syndrome.................................................................................34
Pathology 4- DKA.......................................................................................................... 38
Pathology 5 - Lymphoma...............................................................................................42
Diagnostics...................................................................................................................... 46
Diagnostics 1- Urinary tract infection............................................................................46
Diagnostics 2- meningitis..............................................................................................51
Diagnostics 3- Infective endocarditis............................................................................55
Page 2 of 67
Pharmacology
Pharmacology 1- DVT
A 65-year-old woman presents with unilateral leg pain and swelling of 5 days' duration.
There is a history of hypertension, mild CHF, and recent hospitalisation for pneumonia.
She had been recuperating at home but on beginning to mobilise and walk, the right leg
became painful, tender, and swollen. On examination, the right calf is 4 cm greater in
circumference than the left when measured 10 cm below the tibial tuberosity. Superficial
veins in the leg are more dilated on the right foot and the right leg is slightly redder than
the left. There is some tenderness on palpation in the popliteal fossa behind the knee.
Vital signs
Heart rate (b/min) 80
Blood pressure (mmHg)
128/85
Respiratory rate (/min) 12
Temperature (0C)
36.8
Page 3 of 67
- Negative result plus a low pretest clinical probability score (as determined
by Wells criteria) excludes DVT
- Positive result can be raised in infection, pregnancy, malignancy, post-op;
do U/S
FBC Leukocytosis if cellulitis. Platelet count (prior to anticoagulation)
UEC prior to anticoagulation
Coags APTT, INR (prior to anticoagulation).
LFTs baseline.
If suspicious of PE
- ABG - low PO2
- ECG tachycardia, RBBB, RV strain (S1Q3T3)
- CXR paucity of vascular markings, peripheral wedge opacity, basal
collapse
- V/Q scan (use with caution in patients with renal impairment)
- CTPA (gold standard) - Use Wells criteria to assess for PE
Thrombophilia tests before commencing anticoagulants if there are no
predisposing factors, recurrent DVT or if there is a family history of DVT
Page 4 of 67
P Mentions Wells score but is not clear what are its
(70m) constituents.
Mentions a good variety of investigations but is
not able to organise them.
Talks about Doppler ultrasound, CTPA
Does not know what are the important
investigations.
P+ Mentions Wells score:
(90m) o Understands what makes up the Wells
score.
o Knows cut offs for further investigation
o Understands the value of the D-dimer
assay when there is a low pretest
probability of DVT
Is able to organise investigations into bedside,
blood and imaging studies, mentioning the most
important tests first.
Is able to state situations where V/Q scan is
favoured over CTPA
3)What pharmacological management will you prescribe for this patient and
what are their mechanisms of action and side effects?
Anticoagulation:
Low molecular weight heparin (LMWH) enoxaparin 1.5mg/kg SC daily or
1mg/kg SC bd
o MOA:
Potentiates effects of antithrombin III inactivation of thrombin
(IIa) & Xa.
Note: inactivates thrombin (IIa) to a lesser extent than UFH because
smaller molecules(2000-6000 vs. 5000-30,000) and therefore
cannot bind to both thrombin and antithrombinsimultaneously.
o S/E:
Heparin induced thrombocytopenic thrombotic syndrome (HITTs)
(ASK MECHANISM of HITTS):
More likely with heparin
Occurs after 5-7 days on heparin with 50% fall from platelet
baseline, cease heparin & administer danaparoid (Orgaran)
Mechanism of HITTS: Heparin binds to platelet factor
4 (PF4) exposes a previously unmasked epitope
increases production of IgG antibody IgG binds to
hepain-PF4 complex forms immune complex that
binds to platelets platelets activated
hypercoagulable state and thrombocytopenia.
Bleeding
Long term side effect- osteoporosis
o Other facts that candidate may mention:
Twice daily dosing preferred for patients at high risk of bleeding or
of thrombus extension e.g. older, obese, malignancy.
Advantages of LMWH over UFH: Longer duration of action
(once/twice daily dosing), response more predictable, no routine lab
monitoring, outpatient management.
Page 5 of 67
Dose adjustment required in the presence of renal impairment
(eGFR<30)
Warfarin:
o Orally, daily (dose according to initiation protocol) then daily dosing
adjusted to an INR of 23
o MOA:
Warfarin inhibits Vitamin K epoxide reductase and quinine
reductase therefore blocking the -carboxylation of glutamic acid
residues therefore production of factors II, VII, IX, X, protein C, S
and Z.
o S/E:
Common (>1%): bleeding
Rare (<0.1%): skin necrosis, purple discolouration of toes, alopecia,
fever, rash, nausea, vomiting, diarrhoea, hepatic dysfunction,
allergic reactions, eg hypersensitivity
4) How will you start and monitor warfarin? What is the benefit of LMWH over
UFH?
Starting:
o Exact dosage depends on age and INR. But usually a dose of 5mg would
be given.
o Patients routinely receive doses at 4.00pm during titration protocol, blood
samples for INR obtained 8.00-10.00am (16 hours after previous dose).
Page 6 of 67
o Commence on same day as LMWH: High recurrence of VTE if
commenced alone because warfarin initially prothrombotic
(depletes C&S before factor II, VII, IX, X)
Monitor:
o INR daily until 2 consecutive readings are above INR of 2
o Then weekly for 1 month
o Then 4-6 weeks while stable
Duration of anticoagulation depends on risk of recurrent VTE & bleeding:
o 3 months if DVT provoked by transient major risk factor (eg post-op)
o 3 months if DVT unprovoked, and distal
o 6 months if first unprovoked proximal DVT or PE
o Indefinite if first unprovoked proximal VTE plus active cancer, multiple
thrombophilias, anti-phospholipid antibody syndrome; or recurrent
unprovoked VTE.
Benefit of LMWH over UFH
o Greater bioavailability than unfractionated heparin
o Extensive clinical experience with subcutaneous administration, often
facilitating outpatient treatment
o Longer duration of the anticoagulant effect, permitting administration only
once or twice daily and administration in the outpatient setting
o Better correlation between dose and anticoagulant response, permitting
administration of a fixed dose without laboratory monitoring
o Lower risk of heparin-induced thrombocytopenia
o Lower incidence of osteoporosis
Page 7 of 67
is based on risk of thrombus formation.
Understands all the benefits of LMWH over UF
Heparin
Page 8 of 67
Pharmacology 2- Inflammatory Bowel Disease
A 27-year-old woman presented to the Emergency Department with severe bloody
diarrhoea. The diarrhoea commenced 6 weeks earlier and has gradually worsened. She
was passing up to 6 stools a day containing mucus and blood, and is associated with
crampy abdominal pain. She does not have any similar previous episodes of diarrhoea
but has stated that she had recently returned from Bali about 2 months ago.
On examination, she was pale and dehydrated with generalised tenderness to the left
lower quadrant. Bowel sounds were increased. Digital rectal examination revealed no
masses but dark red blood and mucus were present on the glove.
Vital signs
Heart rate (b/min)
112
Blood pressure (mmHg)
110/70
Respiratory rate (/min) 18
Temperature (0C)
37.8
Page 9 of 67
o C. difficile toxin test: exclude pseudomembranous colitis if recent antibiotic
use
Blood tests:
FBC:
o Anaemia (IBD chronic disease OR blood loss OR malabsorption of iron,
folate, B12)
CRP & ESR:
o in inflammation
EUC:
o Na& K from diarrhoea (unlikely to have metabolic acidosis from
hypoperfusion)
LFT:
o ALP & bilirubin from Primary Sclerosing Cholangitis (associated with UC),
baseline
Albumin:
o (chronic diarrhoea/malabsorption)
Blood cultures:
o -ve, exclude bacteraemia and infectious diarrhoea when this sick + fever
Serologic testing for IBD:
o IgA and IgG antibodies to anti-Saccharomyces cerevisiae (ASCA) for
Crohns disease
o p-ANCA for UC
TFTs: TSH &T4 = hyperthyroidism (if diarrhoea was not bloody)
Test for Coeliac disease:
o IgA
o Anti- endomysial
o Anti-transglutaminase
o Anti-endomysial antibody
Imaging:
CXR: exclude perforation
AXR: UC no faecal shadows, colonic dilation, mucosal thickening. Skip lesions
(think Crohns). Ensure not toxic megacolon >6cm (risk of perforation)
Barium Enema (not during attack):
o UC: loss of haustra, granular mucosa, shortened colon
o Crohns: cobblestoning, rose thorn ulcers, colon strictures with rectal
sparing
Colonoscopy (not if toxic megacolon perforation risk)
Page 10 of 67
o IgA and IgG antibodies to anti-
Saccharomyces cerevisiae (ASCA)
o p-ANCA
Page 11 of 67
(corticoster steroid-receptor complex enters CUSHINGOID:
oid) nucleus andeffects gene Cataracts
transcription annexin-1 (protein) Ulcers
(& COX-2 directly) Skin: striae, thinning,
phospholipaseA2 COX2 bruising
PG, LT, PAF Hypertension/ Hirsutism/
Hyperglycemia
Infections
Necrosis, avascular necrosis
of the femoral head
Glycosuria
Osteoporosis, obesity
Immunosuppression
Diabetes
Sulfasalasin A combination of 5-aminosalicylic Vomiting, Oligospermia, Mild
e acid (an anti-inflammatory) and haemolysis
sulfapyridine (an antibacterial).
Toxicity to lymphocytes > other
cells and immunoregulation
reduced T cell mediated
inflammation.
Mesalazine 5-aminosalicylic acid (5-ASA) which Common (>1%): nausea,
has an anti-inflammatory action on rash, headache, diarrhoea
colonic mucosa. Infrequent (0.11%):
Toxicity to lymphocytes > other interstitial nephritis
cells and immunoregulation Rare (<0.1%): blood
reduced T cell mediated dyscrasias, pancreatitis
inflammation. (reversible), hepatitis
Azathioprin Metabolised to mercaptopurine Myelosuppression, Alopecia,
e altered purine synthesis impairs Diarrhoea, Mouth ulcers,
cellularimmunity, cell Oesophagitis
proliferation, inhibited inflammatory
response
Methotrexat Competitive dihydrofolate Nausea, Mouth ulcers,
e (+ Folic reductase inhibitor AST/ALT (esp with
Acid) Inhibit DNA synthesis and cell leflunomide),
replication by inhibiting folic acid Myelosuppression,
conversion cytotoxic, Pneumonitis/fibrosis. NB:
immunosuppressive and anti- SE with folic acid
inflammatory action supplementation
FOR UNRESPONSIVE UC (Cyclosporin and Infliximab)
Cyclosporin Calcineurin inhibitor Gingival hyperplasia &
Cyclosporin forms complexes with hirsutism
cyclophilin which then blocks the
action of calcineurin in activated T
cells preventproduction of IL-2 &
other cytokines T cell
stimulation & proliferation
Infliximab TNF antagonist Delayed hypersensitivity,
Binds to TNF alpha (cytokine from Serum sickness (Type 3
macrophages for inflammatory & hypersensitivity reaction to
immune responses) foreign protein/serum)
Page 12 of 67
Grade Content Remarks
F Is not able to state other possible drugs used
(30m) Unclear about the mechanism of action and S/E
of the medications (e.g. N/V/D)
P- Is able to list 2 other drugs
(50m) Briefly describes their mechanisms of action
Unclear about the S/E of these drugs
P Is able to >2 other drugs
(70m) Describes in detail their mechanisms of action
and S/E
P+ Is able to >2 other drugs
(90m) Describes in detail their mechanisms of action
and S/E
Is able to state the indications of the drugs used
Page 13 of 67
Pharmacology 3- Major depression
A 32 year-old single mother with 2 children under age 5 comes to see you, her GP,
complaining about headaches and lack of energy. She is unemployed and divorced 6
months ago. On further questioning, she reveals that she has had little appetite and has
lost 5kg in the last two months. She struggles to fall asleep, often wakes up in the middle
of the night and finds it hard to get back to sleep. She has lost interest in doing things
that she used to enjoy, like walking and gardening, as well as worrying about her
parenting. She finds herself losing her temper easily and yells at her children, leading
her to believe that she is a bad mother. She often feels like crying for no apparent
reason.
On discussing the situation with this woman, you believe that she is suffering from major
depression. You discuss options for therapy, including CBT and pharmacotherapy. She
does not feel she can commit to CBT at the present time.
1) What features of depression does this woman exhibit? How severe is her
depression? What other differential diagnoses would you consider?
DDx:
Organic causes:
Alcohol abuse
Illicit drug use
Hypothyroidism
Vit B12/Folate deficiency
Addisons disease
Medication (Antihypertensives [beta blockers; methyldopa]; steroids; H2 blockers
[ranitidine]; benzoz; muscle relaxants; appetite suppressants; chemotherapy
agents)
Infections (Lyme disease; Infective mononucleosis; HIV encephalopathy; Syphillis)
Inflammatory conditions (SLE)
Page 14 of 67
Premenstrual dysphoric disorder (PMDD)
Grief reaction
Anxiety disorders
2) What classes of anti-depressant drugs are available, and which would you
prescribe in this case? Justify your answer.
Antidepressant drugs:
The commonest two pharmacological types of anti-depressants are:
Selective serotonin reuptake inhibitors (SSRIs)
Tricyclic antidepressants (TCAs)
Others:
Serotonin-noradrenaline (norepinephrine) reuptake inhibitor (SNRI)
5-HT2 receptor antagonist (mirtazapine)
Bupropion (dopamine re-uptake inhibitor)- NOT used in Australia.
Which would I prescribe?
The choice of medication should be based on:
Patient preference, tolerability
Past evidence of effectiveness in the patient or in a family member (but
this is a NEW patient).
According to the evidence, the best therapy for this patient is:
Psychotic Major depression Minor depression
depression
1st line -ECT Antidepressant + Antidepressant or
-Antidepressant + psychotherapy psychotherapy
psychotherapy
If 1st -ECT Change antidepressant Change antidepressant
line -Antidepressant + regimen: regimen:
fails psychotherapy 1) TCA 1) TCA
+ 2) SSRI/SNRI + mirtazapine 2) SSRI/SNRI +
-Antipsychotic mirtazapine
3) ? Adding atypical
antipsychotic
Page 15 of 67
(50m)
P Mentions SSRI + TCA + SNRIs and mirtazapine
(70m)
P+ Mentions SSRI + TCA + SNRIs and mirtazapine
(90m) Knows that SSRIs are the most commonly used
antidepressant
Takes into account patient preference, tolerability
and previous evidence of
3) Describe the mechanism of action and side effects of SSRIs and other drugs
that can be used to treat depression.
Dru Mechanism of Example S/E Comments
g action s
SSRI Inhibit the reuptake Citalopra -S/E resemble a hangover- -Cause less
of the monoamine m N+V, headache, diarrhea and S/E compared
serotonin (5-HT) Escitalopr dry mouth. to tricyclics
within the synapse. am -Insomnia and paradoxical e.g. SSRIs do
Fluvoxami agitation can occur when not cause sig.
ne first starting the drugs. weight-gain
Fluoxetine -SEROTONIN syndrome when -Long half-life
Paroxetine ingesting 2 drugs e.g. (possible to
Sertraline SSRI+ MAOI or dopaminergic give OD). Easy
drugs (e.g. selegiline) or a to comply.
TCA. Therefore
-SEROTONIN syndrome SSRIs are first-
(remember HARMED): line treatment.
Hyperthermia
Autonomic instability
Rigidity
Myoclonus
Encephalopathy
Diaphoresis
Page 16 of 67
Is -SNRI. e -Nausea
Mirtazapine Mirtazapin -Hypertension at high doses
-5-HT2 and 5-HT3 e Mirtazapine:
receptor antagonist Raboxetin -Sedating at low doses
-a potent 2- e -Weight gain
adrenergic blocker. -Agranulocytosis (rare)
( NA and selective Raboxetine
serotonin -Dry mouth
transmission). -Insomnia
Reboxetine -Constipation
-Selective -Urinary hesitancy
noradrenaline -Tachycardia
reuptake inhibitor.
MAO Irreversibly Phenelzin - appetite MAOIs should
I inhibiting the e -Weight gain not be given
intracellular -Erectile dysfunction within 2 weeks
enzymes -Insomnia of a SSRI
monoamine oxidase
A and B, of
noradrenaline,
dopamine and 5-
hydroxytryptamine
in the brain
Page 17 of 67
4) What information would you give this woman regarding potential drug-drug
interactions?
SSRI:
SEROTONIN syndrome when ingesting 2 drugs e.g. SSRI+ MAOI or
dopaminergic drugs (e.g. selegiline) or a TCA.
SEROTONIN syndrome (remember HARMED):
Hyperthermia
Autonomic instability
Rigidity
Myoclonus
Encephalopathy
Diaphoresis
MAOI:
o Produce a severe and dangerous hypertensive reaction with foods
containing tyramine or dopamine and therefore a restricted diet is
prescribed.
o Tyramine: present in cheese, pickled herrings, yeast extracts, certain red
wines, and any food, such as game, that has undergone partial
decomposition.
o Dopamine: present in broad beans.
o MAOIs interact with drugs such as pethidine and can also occasionally
cause liver damage.
o MAOIs should not normally be given within 2 weeks of a serotonin reuptake
inhibitor, depending on half-lives.
Page 18 of 67
Anatomy
Anatomy 1- Pneumothorax
A 20-year-old man was brought in by ambulance to the emergency department after a
motor vehicle accident with complaints of right-sided chest pain and shortness of breath.
He states that these symptoms began suddenly. He has no significant past medical
history but has smoked cigarettes since the age of 16 years.
The following are his vital signs:
Vital signs
Heart rate (b/min)
140
Blood pressure (mmHg)
90/65
Respiratory rate (/min) 24
Temperature (0C)
36.8
1) A Pan Scan was performed. Describe the following CT scan, name the
labelled structures and from the scan, determine the cause for this mans
shortness of breath.
Page 19 of 67
F
A
C E
This is an axial CT scan taken at T5-6with lung windows. The labelled structures
are:
o A- Ascending aorta
o B- Descending aorta
o C- Left pulmonary artery
o D- Superior vena cava
o E- Pulmonary trunk
o F- Right ventricle
o G- Azygos vein
Page 20 of 67
Mentions that he/she is given an axial CT scan
with lung windows
Is able to identify the approximate level in which
the CT scan is taken
Page 21 of 67
Therefore, if a communication develops between an alveolus and the pleural
space or between the atmosphere and the pleural space, gases will follow the
pressure gradient and flow into the pleural space.
This flow will continue until the pressure gradient no longer exists or the abnormal
communication has been sealed.
Because the thoracic cavity is normally below its resting volume, and the lung is
above its resting volume, the thoracic cavity enlarges and the lung becomes
smaller when a pneumothorax develops.
A tension pneumothorax is a medical emergency and occurs when the
intrapleural pressure exceeds atmospheric pressure, especially during
expiration, and results from a ball valve mechanism that promotes inspiratory
accumulation of pleural gases.
The build-up of pressure within the pleural space eventually results in
hypoxaemia and respiratory failure from compression of the lung.
5) How do you insert a chest tube? (Extra question that the examiners might
ask)
Triangle of safety (Mid axillary line; Border of pectoralis major; 5 th intercostal
space)
Drape and prep the area as appropriate
Use local anaesthetic (1% Lignocaine), inject over the area
Incision is made above the rib to avoid the neurovascular bundle
Blunt dissection using finger until the pleural surface is reached
Make an incision and use finger to feel around the area to ensure in right direction
Insert drain with a clamp
Connect to underwater seal
Suture
Page 22 of 67
Anatomy 2- Larynx
A 57-year-old man presents with a 6-month history of hoarseness. Over the past week he
has noted progressive difficulty breathing. He also has otalgia, dysphagia, odynophagia
(painful swallowing), and a 9-kg weight loss. He has an 80-pack-year tobacco history and
drinks 8 beers per day. Neck examination demonstrates a right-sided mass that is firm
and fixed. There is mild biphasic stridor with deep inspiration and expiration, but the
patient has no increased work of breathing at rest, and breath sounds are clear.
1) What is your provisional diagnosis for this patient and other differential
diagnoses for hoarseness?
PDx: Laryngeal cancer (must rule out, especially if >2 weeks)
DDx:
o Infection:
Laryngitis
Epiglottitis
o Inflammation:
Toxic
Fumes
Reflux
Smoking
o Functional
o Overuse:
Singers nodules
o Neurological
Central strokes, tumours, MS
Peripheral laryngeal nerves
o Infiltrative causes:
Sarcoidosis
o Autoimmune:
Wegener's granulomatosis: Patients may present with nasal
congestion, nasal crusting, cough and difficulty breathing, and
haematuria.
Page 23 of 67
B- hypoid cartilage (C2)
C- corniculate cartilage
D- arytenoid cartilage
E- thyroid cartilage (C4)
F- cricoid cartilage (C6, usually at the
sternal notch)
G- trachea
H- false cord
I- ventricle of morgani or laryngeal
ventricle
J- vocal cord
3) Can you describe the intrinsic musculature of the larynx and their effects on
the vocal ligaments?
Abduction:posterior crico-arytenoid muscles
Adduction:Transverse and oblique arytenoid muscles
Slackening: vocalis and thyroarytenoid muscles
Tensing: cricothyroid muscles
Page 24 of 67
Grade Content Remarks
F Is not able to answer the question
(30m)
P- Mentions 2 muscles
(50m)
P Mentions 3-5 muscles
(70m)
P+ Mentions all 6 structures
(90m) Is able to express answer in a manner that
demonstrates understanding of the function of
each muscle
Page 25 of 67
o They pass posteromedially to the thyroid along the tracheooesophageal
groove to supply all the muscles of the larynx except the cricothyroid
Cricothyroid muscle is the only laryngeal muscle supplied by the branch of the
vagus nerve known as the EXTERNAL BRANCH OF THE SUPERIOR
LARYNGEAL NERVE (rather than the recurrent laryngeal nerve).
Page 26 of 67
He denies any other significant past medical or surgical history. On physical examination,
a bulge is present when standing that disappears when supine.
2) What types of inguinal hernias do you know? How would you differentiate
them(based on anatomical landmarks)?
Direct:
o Hernia sac comes through the inguinal floor medial to the inferior
epigastric artery and the deep inguinal ring.
o Comes through Hesselbach's triangle:
Medial border- Lateral margin of the rectus sheath, also called linea
semilunaris
Superolateral border- inferior epigastric vessels
Inferior border- inguinal ligament (Poupart's ligament)
Page 27 of 67
Indirect:
o Hernia sac comes through the internal (deep) inguinal ring, lateral to the
epigastric artery.
Pantaloon hernia: ipsilateral, concurrent direct + indirect inguinal hernias.
Sliding hernia:
o Important subclassification of indirect hernia
o Bowel fused to the peritoneum comes through the internal inguinal ring.
Strangulated:
o Blood supply of the hernia contents is compromised ischaemia
gangrene and perforation of the affected bowel segment.
o A strangulated hernia can also contain omentum or other viscera, such as
bladder.
Page 28 of 67
Grade Content Remarks
F Unable to answer
(30m)
P- Mentions 2-3 anatomical structures of the
(50m) inguinal canal
P Mentions 4-6 anatomical structures of the
(70m) inguinal canal
P+ Mentions 8 anatomical structures of the
(90m) inguinal canal
4) What are the contents of the spermatic cord? What is the purpose of the
pampiniform plexus?What are the layers of the testes?
Contents of Spermatic Cord:
3 Arteries:
o 1. Testicular
o 2. Cremasteric
o 3. Artery of Ductus Deferens
3 other vessels:
o 1. Pampiniform (L: vines wrapping) plexus
o 2. Cremasteric vein
o 3. Lymphatics
3 Nerves:
o 1. Genital branch of genitofemoral nerve (NB: ilioinguinal n is in the canal
not the cord)
o 2. Testicular sympathetic nerve
o 3. Autonomic plexus of ductus deferens
Grade Content Remarks
F Unable to answer
(30m)
P- Mentions 2-3 constituents of the spermatic cord
(50m) Mentions 2-3 layers of the testes
P Mentions 4-6 constituents of the spermatic cord
(70m) Mentions 4-6 layers of the testes
P+ Mentions 7 constituents of the spermatic cord
(90m) Mentions all the layers of the testes
Understands the purpose of the pampiniform
plexus
Page 29 of 67
Pathology
Pathology 1- COPD
Vital signs
Heart rate (b/min)
106
Blood pressure (mmHg)
Page 30 of 67
140/70
Respiratory rate (/min) 26
Temperature (0C)
37.5
Page 31 of 67
Grade Content Remarks
F Unable to read ABG at all
(30m)
P- Is able to deduce that this is a respiratory
(50m) acidosis
Unable to determine the nature of compensation
P Is able to deduce that this is a respiratory
(70m) acidosis
Is able to determine that there is adequate
metabolic compensation
P+ Is able to deduce that this is a chronic
(90m) respiratory acidosis
Is able to determine that there is adequate
metabolic compensation
3) How will this patients ABG affect his management (especially with regards
to oxygen therapy)?
In terms of oxygen therapy:
o Try to give patient O2 via nasal prongs (1-2L/min) so that he can blow off
CO2.
o If known CO2 retainer, titrate oxygen to SaO2 88-92%, use of venturi
mask if necessary for precise oxygen delivery.
High flow O2 will compromise their respiratory drive. For the normal person,
breathing is driven by increased CO2 levels. In COPD patients however, their
respiratory centres have been dulled by chronic increased CO 2 levels therefore
hypoxia is driving their respiration. High flow O2 will dull this respiratory drive.
4) What are the two major clinical syndromes that are classified as chronic
obstructive pulmonary disease? How do they differ? (Abbreviated question:
What is the pathophysiology of COPD ?)
Definition:
1. COPD is an intentionally imprecise term used to denote a process
characterised by the presence of chronic bronchitis or emphysema that
may lead to the development of fixed airway obstruction.
2. The hallmark of COPD is chronic inflammation that affects central airways,
peripheral airways, lung parenchyma and alveoli, and pulmonary
vasculature.
Page 32 of 67
3. The main components of these changes are narrowing and remodelling of
airways, increased number of goblet cells, enlargement of mucus-secreting
glands of the central airways, and, finally, subsequent vascular bed
changes leading to pulmonary hypertension.
Chronic bronchitis and emphysema are frequently encountered together in the
same patient.
Chronic bronchitis:
1. Clinical history of productive cough for 3 months of the year for 2
consecutive years.
2. Dyspnoea and airway obstruction, often with an element of reversibility,
are intermittently to continuously present.
3. Cigarette smoking is by far the leading cause of this disease, although
other inhaled irritants may induce the same process.
4. Pathologic events:
Inflammation in larger airways
Ciliary dysfunction
Mucosal thickening
Mucus hypersecretion- goblet cell size and number
N.B.: It is the inflammation in smaller bronchioles that is the
principal site of increased airflow obstruction.
Pulmonary emphysema:
1. Irreversible enlargement of the airspaces distal to the terminal bronchioles
2. Destruction of the walls of the terminal bronchioles, most often without
obvious fibrosis.
3. In the respiratory unit walls, there is elastin breakdown. This results in a
loss of appropriate recoil tension to support distal airways during
expiration.
4. Progressive dyspnoea and non-reversible obstruction accompany the
airspace destruction without mucus hypersecretion and productive
cough.
5. The loss of alveolar surface area and the accompanying capillary bed for
gas exchange contribute to the progressive hypoxia and dyspnoea.
ABCs of ABG:
1. Look at pH: is it acidosis or alkylosis?
2. Does the amount of CO2 explain the pH?
a. Yes? Primary respiratory
b. No? Primary metabolic
3. If primary respiratory acidosis, for every in 10 of CO2, is HCO3 by 2, 4 or
something else?
Page 33 of 67
a. by 2mmHg acute resp. acid. with metabolic compensation
b. by 4mmHg chronic resp. acid. With metabolic compensation
c. None of the above mixed picture or no compensation
4. If primary respiratory alkylosis, for every in 10 of CO2, is HCO3 by 2.5?
a. Yes adequate metabolic compensation
b. No no compensation or mixed picture
5. If Primary metabolic acidosis or alkylosis, is the CO2 within 5mmHg of the last 2
digits of pH?
a. Yes adequate respiratory compensation
b. No mixed picture
Examples:
Page 34 of 67
Page 35 of 67
Pathology 2- Primary hyperparathyroidism
1) ASK FOR WHITE BOOK (spend at most 2mins on this segment): Test
examined: ______________________
Select one anatomical cut up the candidate observed. Please discuss the
pathological processes that contributed to the specimen you saw.
Select a morgue case.Have the candidate to describe the process of dissecting
the corpse.
Clinical biochemistry
Sodium (mmol/L) 138 135-
145
Potassium (mmol/L) 3.7 3.5-5.0
Chloride (mmol/L) 105 95-107
Calcium (mmol/L) 3.7 2.10-2.55
Phosphate (mmol/L) 0.4 0.8-1.5
25-hydroxy vitamin D (nmol/L) 120 50-
140
Alkaline phosphatase (U/L) 110 36-126
Page 36 of 67
Urea (mmol/L) 6.0 3.0-
8.0
Creatinine (mol/L) 87 60-110
Parathyroid hormone (pmol/L) 185 1.1-
6.9
A radionucleotide scan was also performed for this patient. The image is shown below:
1) What is your provisional diagnosis? What are your differential diagnoses for
hypercalcaemia?
PDx:
Primary hyperparathyroidism:
o Accounts for most cases of hypercalcemia
o Given the chronic nature of this womans Sx and the Hx of recurrent renal
stones, this is the most likely diagnosis.
Most likely due to a parathyroid adenoma or carcinoma (rare):
o Elevated PTH levels in presence of normal renal function and Vitamin D
DDx:
Primary hyperparathyroidism
Hyperthyroidism
Adrenal insufficiency
Medication-related hypercalcaemia
Granulomatous disease (TB or sarcoidosis)
Phaeochromocytoma
Medications: particularly lithium and thiazide diuretics
Grade Content Remarks
F Unable to offer a PDx or DDx
(30m)
P- Is able to get to the PDx with lots of prompting
(50m) from the examiner
P Mentions PDx and 2 DDx
(70m)
P+ Mentions PDx and 4 DDx
(90m)
Page 37 of 67
Reabsorb calcium
Stimulates 25 (OH)-1- hydroxylase conversionof 25-
hydroxyvitamin D3 to its more active form of 1,25-dihydroxyvitamin
D3. This active vitamin D is responsible for the GI absorption of
calcium.
o Complications of hypercalcaemia (stones, bones, groans and psychiatric
overtones):
Stones- renal or biliary stones
Bones- Bone pain, osteitis fibrosa cystica
Groans- GI disturbance (LOA, nausea, constipation), acute
pancreatitis, peptic ulcers
Psychiatric overtones- Neuropsychiatric changes (e.g., mood
disturbance, fatigue, confusion, stupor, and coma)
Others: polyuria and polydipsia, short QT, bradycardia, AV block,
cardiac arrest
Page 38 of 67
Thyrotoxicosis
Chronic or acute leukaemia
Milk-alkali syndrome: patients usually have a history of excessive intake of
antacids
Thiazide diuretic
Grade Content Remarks
F Unable to answer even with much prompting
(30m) from the examiner
P- States 1-2 causes
(50m)
P States 4-5 causes
(70m)
P+ States 6 causes
(90m)
1) ASK FOR WHITE BOOK (spend at most 2mins on this segment): Test
examined: ______________________
Select one anatomical cut up the candidate observed. Please discuss the
pathological processes that contributed to the specimen you saw.
Select a morgue case.Have the candidate to describe the process of dissecting
the corpse.
Page 39 of 67
was ankle swelling extending up to her mid shin and, for the first few hours of the day,
some swelling around her eyes. She has also noticed foamy urine.
2) What is the likely diagnosis? How could you support this diagnosis?
PDx: Nephrotic syndrome:
o Facial and dependent oedema (peri-orbital oedema is the classical finding)
o Proteinuria (foamy urine)
o B/G of T1DM.
How would I support this diagnosis?
Serum albumin and cholesterol measurement.
Proteinuria:
o 24hr urine collection: The normal amount of protein is <150 mg/day.
o Patients excreting >3.5 g/day (or >3 g/day) are considered to have
nephrotic-range proteinuria.
o Total urine protein-to-creatinine ratio (mg/mg) on a random urine specimen
(first morning is preferred)
Normal urine protein-to-creatinine ratio is <0.2 mg/mg.
Ratios >3.5 mg/mg = nephrotic range for proteinuria.
Investigations:
o FBC, EUC, LFT (albumin), lipids, coags, BSL
o Urinalysis, MCS, PCR
o CXR, renal US
3) Describe the main features and function of the glomerular filtration barrier.
Page 40 of 67
made of nephrin. The podocytes have a negatively charged coat that repels
negatively charged stuff e.g. albumin.
Filtration of plasma water and solutes is extracellular and occurs through the
endothelial fenestrae and filtration slits. Cells, proteins and other macromolecules
are generally not able to pass through the glomerular filtration barrier.
ESL is the endothelial surface layer, which restricts plasma flow, can exclude
RBCs and some macromolecular solutes
Layers of the GBM:
o Lamina rara externa- adjacent to podocyte process, comprises heparin
sulphate and blocks by charge
o Lamina densa- dark central zone- comprises type 4 collagen & laminin &
blocks by size (MW>5800kDa)
o Lamina rara interna- adjacent to endothelial cells- comprises heparin
sulphate & blocks by charge
Grade Content Remarks
F Unable to answer question
(30m)
P- Mentions that it functions as a sift
(50m)
P Mentions several layers of the glomerular
(70m) filtration barrier:
o Fenestrated endothelium
o Glomerular basement membrane
o Podocytes
o Filtration slits made of nephrin
o ESL
P+ Mentions all layers of the glomerular filtration
(90m) barrier:
o Fenestrated endothelium
o Glomerular basement membrane
o Podocytes
o Filtration slits made of nephrin
o ESL
Understands that the podocytes have a
negatively charged
Layers of the GBM:
o Lamina rara externa
o Lamina densa
o Lamina rara interna
Page 41 of 67
o Antithrombin III
o Vitamin D binding protein,
o Immunoglobulin (in particular IgG)
o Transferrin
o Albumin
o Lipoprotein
5) Explain the pathophysiology of this womans oedema and her lipid changes.
What other complications can occur in this disease?
An increase in glomerular permeability albuminuria and hypoalbuminemia:
o In turn, hypoalbuminemia lowers the plasma colloid osmotic pressure,
causing greater transcapillary filtration of water throughout the body and
thus the development of oedema (Starlings equation)
In the nephrotic syndrome, levels of serum lipids are usually elevated.
o This can occur via:
Hypoproteinemia that stimulates protein, including lipoprotein,
synthesis by the liver.
Diminution of lipid catabolism caused by plasma levels of
lipoprotein lipase
Other complications
o DVT, PE : loss of antithrombin III and other anticoagulant proteins
o Immune deficiency: loss of Ig
o Malnutrition: catabolic state from protein losses
o Hypocalcaemia: loss of vit D binding protein
o CVD: hyperlipidaemia + thrombotic state
Page 42 of 67
(90m) albuminuria and hypoalbuminemia
Understand that this affects starling forces
oedema
Mentions that hypoproteinemia protein
synthesis especially hepatic lipoprotein synthesis
hyperlipidaemia
Mentions at least 3 other complications
Page 43 of 67
Pathology 4- DKA
1) ASK FOR WHITE BOOK (spend at most 2mins on this segment): Test
examined: ______________________
Select one anatomical cut up the candidate observed. Please discuss the
pathological processes that contributed to the specimen you saw.
Select a morgue case.Have the candidate to describe the process of dissecting
the corpse.
Vital signs
Heart rate (b/min)
123
Blood pressure (mmHg)
106/67
Respiratory rate (/min) 32
Temperature (0C)
37.1
Page 44 of 67
1) How would you interpret the history and physical findings? What is the likely
diagnosis? What are your differential diagnoses?
PDx:
DKA- first presentation
DDx:
Hyperosmolar hyperglycaemic state (HHS)
Lactic acidosis
Starvation ketosis
Alcoholic ketoacidosis
Salicylate poisoning
Ethylene glycol/methanol intoxication
Uraemic acidosis
Grade Content Remarks
F No PDx or DDx offered
(30m)
P- Mentions only PDx
(50m)
P Mentions PDx and 1 DDx
(70m)
P+ Mentions PDx and 3 DDx
(90m)
Page 45 of 67
HCO3: 1.9 24-34
Base access: -27.9 -3<BE<3
Page 46 of 67
F Is not able to give an answer even after much
(30m) prompting
P- Brief description of the pathogenesis of polyuria
(50m) and polydipsia and ketoacidosis in DKA
P Recognises that there is absolute insulin
(70m) deficiency in T1DM
Describes in detail the pathophysiology of
polyuria and polydipsia
P+ Items in P PLUS:
(90m) Mentions the TCA cycle.
Identifies both ketone bodies responsible for
acidosis- acetoacetate & -hydroxybutyric acid
Page 47 of 67
(50m) Classifies them into macro- and micro-vascular
complications
P Mentions AGEs
(70m) Describes their effects on the endothelium and
basement membrane
P+ Items in P PLUS:
(90m) Describes how hyperglycaemia causes
disturbances in polyol pathway
Describes how the activation of intracellular
protein kinase C causes LT complications of T1DM
Page 48 of 67
Pathology 5 - Lymphoma
1) ASK FOR WHITE BOOK (spend at most 2mins on this segment): Test
examined: ______________________
Select one anatomical cut up the candidate observed. Please discuss the
pathological processes that contributed to the specimen you saw.
Select a morgue case.Have the candidate to describe the process of dissecting
the corpse.
Page 49 of 67
o Primary lymphoma, leukaemia
o Secondary
Infective:
o Bacterial Strep, Staph, TB
o Viral EBV, HIV, CMV
o Protozoa - toxoplasmosis
o Fungal - histoplasmosis
Other:
o Autoimmune SLE, RA
o Drugs phenytoin
o Sarcoidosis
Grade Content Remarks
F No DDx offered
(30m)
P- Mentions 1-3 DDx
(50m)
P Mentions 4-5 DDx
(70m)
P+ Mentions 5 DDx
(90m) Is able to categorise DDx
Page 50 of 67
Bone marrow aspirate and trephine biopsy (bone marrow involvement, explain
paenias). Only if hot spot on PET.
3) Biopsy of the cervical lymph node showed the following that patient had
diffuse large B-cell lymphoma. Describe a staging system used for lymphoma.
In this case, what is the stage?
The MODIFIED Ann Arbor classification" if you add the A,B,X,S,E symptoms
o Stage 1: Single lymph node group
o Stage 2: Multiple lymph node groups on same side of diaphragm
o Stage 3: Multiple lymph node groups on both sides of diaphragm (above
and below)
o Stage 4: Multiple extranodal sites or lymph nodes and extranodal disease
(e.g. liver and lung)
A = no systemic symptoms (or no B symptoms)
B = presence of symptoms (weight loss >10% in 6months, fever >38C,
drenching night sweats)
X = bulky disease (>1/3 widening of mediastinum at T5/T6, or >10 cm nodal
mass)
S = spleen involved
E = involvement of a single contiguous nodal site
This patient has oropharyngeal and cervical lymphoid tissue involvement and
spleen involvement he is at Stage IIIBof the disease
Page 51 of 67
(30m)
P- Vaguely describes the Ann Arbor classification
(50m) Unclear about the classification details
P Mentions the Ann Arbor classification
(70m) Provides the details of each stage
States the stage of the disease but not the
modifier (i.e. A, B, X, S and E)
P+ Items in P and:
(90m) Knows the modifiers to the Ann Arbor
classification (i.e. mentions the A, B, X, S and E)
Is able to accurately identify the stage and
modifier
Page 52 of 67
Diagnostics
Diagnostics 1- Urinary tract infection
1) ASK FOR WHITE BOOK (spend only 2mins on this segment): Test examined:
_______________________
Ask about 1 lab test
Grade Content Remarks
F Has not prepared for the test at all
(30m)
P- Poorly knowledge of the test
(50m)
P States the indication for the test
(70m) Detailed step-by-step explanation of how the
process of processing the sample
P+ Opens with the history of the patient and how the
(90m) test specimen was obtained
States the indication for the test
Detailed step-by-step explanation of how the
process of processing the sample
Understands the clinical relevance/implications of
the results
Is able to relate findings back to the case
Is able to answer the examiners questions
regarding the tests
Page 53 of 67
Bedside:
Urine dipstick: nitrites ++, leukocytes ++
If +ve for nitrites and leukocytes then treat empirically. If ve then consider these:
Urine microscopy (UA): leukocytes and or bacteria, note: epithelial cells =
contamination
MSU:
o Urine Culture & Sensitivity: >105 colony forming units per mL or 108CFU/L
o Urine Gram stain: if +ve = 93% sensitive & 95% specific
gram ve rods = e. coli, klebsiella, enterobacteria, pseudomonas
gram +ve cocci = staphylococcus saphrophyticus
Blood:
EUC: check renal function
FBC
CRP
Blood cultures: if systemically unwell
Imaging:
Bladder Ultrasound: stone, tumour. Consider more in men, children, UTI not
responding to therapy, pyelonephritis or haematuria found
Renal US & KUB X-ray
Cystoscopy: if no answers still
Page 54 of 67
(50m) (poor understanding of the process)
P Describes most of the above-mentioned steps
(70m)
P+ Describes all the above-mentioned steps
(90m) Mentions measures to avoid false positives when
the sample cannot be sent immediately to the
laboratory (e.g. freezing sample).
4a) A MSU specimen was collected from the patient. Interpret the results.
Would you treat this patient?
Allow the candidates to recognise that this is a contaminated specimen. If not prompt as
required
MSU 1 - Contaminated specimen
Result Units Ref Interval
Urine White Blood Cells >100 x10E6/L (<10)
Urine Red Blood Cells <10 x10E6/L (<10)
Urine Squamous Epithelial cells >100 x10E6/L (<10)
Organism 1 (Gram -ve Rods) >100 x10E6/L
Organism 2 (Gram +ve Coccus) >100 x10E6/L
Upon recognition of contaminated specimen,
4b) A second MSU was collected from this patient. Interpret the results. Would
you treat this patient? What is the causative organism in this case?
Page 55 of 67
P Able to identify contaminated specimen and
(70m) specimen with UTI but unable to identify e.coli
Understands that one organism needs to be >108
for UTI to be diagnosed
Understands that if there are two organisms from
the culture, only 1 can be >108
P+ Correctly identifies contaminated specimen and
(90m) specimen with UTI. Able to identify e.coli as
causative organism.
Understands that if there are two organisms from
the culture, only 1 can be >108
Knows when the sample is contaminated
5) What organisms can cause a UTI and what organisms can contaminate the
MSU?
Common UTI organisms:
1. E. coli = 70-95% (gram ve bacillus aerobic and facultative anaerobic)
2. Staph saprophyticus = 5-20% (gram +ve cocci facultative anaerobe)
3. Proteus mirabilis = ~1% (gram ve facultative anaerobe)
4. Klebsiella (men, children)
5. Pseudomonas aeruginosa (instituitionalised/IDUC)
6. Enterococci
7.
Common organisms that can contaminate the MSU are from the normal flora of the
periurethral and urethral regions:
Lactobacilli
Coagulase-negative staphylococci
Corynebacteria
Streptococci
Page 56 of 67
Grade Content Remarks
F Lists 1-2 antibiotics
(30m)
P- Lists 3-4 antibiotics
(50m)
P Lists 3-4 antibiotics
(70m) Understands how severe infection can be treated
Mentions pharmacological and non-pharmacological
methods of treatment
P+ Lists 3-4 antibiotics
(90m) Understands how severe infection can be treated
Appreciates the potential that this woman may become
pregnant and alters management accordingly
Mentions pharmacological and non-pharmacological
methods of treatment
Page 57 of 67
Grade Content Remarks
F Is unclear how this is performed
(30m)
P- Very brief description of CDS
(50m)
P Describes the above-mentioned steps (in the
(70m) picture)
States the types of antibiotic discs used
P+ Describes the above-mentioned steps (in the
(90m) picture)
States the types of antibiotic discs used
Mentions the need to measure the zone of
inhibition and that this is smaller for vancomycin
Page 58 of 67
Diagnostics 2- meningitis
Vital signs
Heart rate (b/min)
100
Blood pressure (mmHg)
95/60
Respiratory rate (/min) 18
Temperature (0C)
39.0
Page 59 of 67
o Neisseria meningitidis
o S pneumoniae
o Haemophillus influenza type B (if not immunised)
Newborns <3 months (the most common pathogens are those to which the infant
is exposed in the maternal genitourinary canal) remember GEL:
o GBS
o E coli
o Listeria monocytogenes
o Other gram-negative bacilli
Grade Content Remarks
F Is able to get the PDx but not the aetiological agents
(30m)
P- Mentions PDx
(50m) Is able to give some aetiological agents
P Mentions PDx
(70m) Is able to give most of the abovementioned aetiological
agents basedon age
P+ Mentions PDx
(90m) Mention that meningitis can be cause by fungal and viral
infections
Is able to give most of the abovementioned aetiological
agents based on age
Mention that the patient most likely has a bacterial
meningitis
Page 60 of 67
o Opening pressure: 7-18cm = N, >40 = likely meningitis, 14-30 = typical in
meningitis
o Appearance
o CSF gram stain: +ve for causative organisms in 50-90% (bacterial), -ve
(viral)
o CSF cell count: turbid, neutrophils ++ (bacterial), lymphocytes ++ (viral).
o CSF protein: elevated (bacterial/viral)
o CSF glucose: low (bacterial/viral use glucose for energy)
o CSF culture: positive (bacterial), -ve (viral)
o Antigen detection for CSF: N. meningitidis capsular LPS antigen
Imaging:
CXR: pneumonia (s. pneumoniae is a common cause of meningitis)
Grade Content Remarks
F No mention of relevant investigations
(30m)
P- Mentions non-appropriate investigations
(50m)
P Mentions a good variety of investigations but is
(70m) not able to organise them.
Provides the rationale for the proposed
investigations.
P+ Items in P and:
(90m) Is able to organise investigations into bedside,
blood and imaging studies, mentioning the most
important tests first.
Volunteers further tests for LP
Knows contraindications for LP
Page 61 of 67
o Vancomycin 1.5grams IV 12-hourly AND ciprofloxacin 400mg IV, 12-hourly.
Note Vanc: adjust for renal function, monitor blood concentrations
o OR Moxifloxacin 400mg IV, daily
N.B.:
Antibiotics should be started immediately, without waiting for imaging study or
lumbar puncture if delay is anticipated in these procedures.
The use of corticosteroids has been shown to decrease the risk of sensorineural
hearing loss among children with H influenzae meningitis and mortality among
adults with pneumococcal meningitis.
The benefit of adjuvant corticosteroids for other types of meningitis is unproven.
5) What is the pathogenesis of this mans presentation? What factors aid the
colonisation and spread of the bacteria?
Colonisation of the hosts nasopharynx local invasion of the mucosal epithelium
bacteraemia cerebral endothelial cell injury follows BBB permeability,
facilitating meningeal invasion.
The resultant inflammatory response in the subarachnoid space causes cerebral
oedema, vasculitis, and infarction CSF, hydrocephalus, worsening cerebral
oedema, ICP, and cerebral blood flow.
Page 62 of 67
complement-mediated bactericidal activity, enhancing bacterial survival and
replication.
Grade Content Remarks
F Offers no answers
(30m)
P- Briefly describes the pathogenesis of N.
(50m) meningitides meningitis
P Is able to in great detail describe the
(70m) pathogenesis of N. meningitides meningitis
P+ Is able to in great detail describe the
(90m) pathogenesis of N. meningitides meningitis
Is able to state 1-2 virulence factors
Page 63 of 67
Diagnostics 3- Infective endocarditis
A 55-year-old man who recently emigrated from China presents to the emergency
department with fever. He has had recurring fevers over the past 3 weeks, associated
with chills, night sweats, and malaise. He admits to infrequent intravenous heroin use
and has a 10-pack-year smoking history.
Ophthalmoscopic examination is remarkable for retinal haemorrhages. Cardiac
examination is notable for a grade 3/6 pansystolic murmur heard loudest at the left lower
sternal border.
Vital signs
Heart rate (b/min)
108
Blood pressure (mmHg)
120/80
Respiratory rate (/min) 16
Temperature (0C)
38.5
Oxygen saturations
97% on RA
Page 64 of 67
Bloods:
FBC: leucocytosis and neutrophilia, normocytic anaemia
Blood Cultures: +ve in 2/3 sets
ECG:
o Can have conduction problems e.g. prolonged PR
o New AV block is suggestive of abscess formation
ESR: non-specific but indicates inflammation rather than bleeding disorder
Imaging:
Echocardiogram:
o Valvular vegetations
CXR:
o Cardiomegaly
o CXR: evidence of heart failure and multiple pulmonary infiltrates (in right-
sided endocarditis)
Grade Content Remarks
F No mention of relevant investigations
(30m)
P- Mentions non-appropriate investigations
(50m)
P Mentions a good variety of investigations but is
(70m) not able to organise them.
Provides rationale for the proposed
investigations.
P+ Items in P and:
(90m) Is able to organise investigations into bedside,
blood and imaging studies, mentioning the most
important tests first (blood cultures and echo).
Page 65 of 67
P Describes most of the above-mentioned steps
(70m)
P+ Describes all the above-mentioned steps
(90m) Mentions that blood cultures should be taken
BEFORE antibiotics are given but in situations
when empirical antibiotics must be given
emergently, blood cultures can be taken ASAP
afterwards.
Page 66 of 67
minor criteria
5) What are the common causative agents?If the patient is not responding to
initial antibiotic therapy, what organisms should you be considering?
IVDU (SSEG): staph aureus, streptococci, enterococci, gram ve bacilli
Native valve (SVC): staph aureus, viridians (oral) group streptococci (strep
sanguis, oralis), coagulase negative staphylococci
Prosthetic valve endocarditis (SSE): staph aureus, staph epidermidis, enterococci
Viridans Group Streptococcus (s. sanguis, oralis, salivarius) = commensal flora of
the mouth and GIT
o Gram +ve cocci, coagulase negative, alpha (green) haemolytic
o Typically produce a greenish (viridians) discoloration on blood agar
o Leading cause of subacute bacterial endocarditis (SBE)
If the patient is not responding to initial antibiotic therapy, consider the HACEK group of
organisms:
Usually culture-negative
Haemophilus species
Actinobacillus actinomycetemcomitans
Cardiobacterium hominis
Eikenella corrodens
Kingella
Page 67 of 67