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2002 FRACP paper one

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Question 1 Download PDF

A 35 year old man has undergone surgical repair of a transposition of the great arteries 30 years previously. His ECG in sinus rhythm is shown:

Which one of the following correctly defines the QRS abnormality?

  Right Bundle Branch Block Right Ventricular Hypertrophy Axis
A Yes No +140 o
B No Yes +140 o
C Yes Yes +240 o
D Yes Yes +140 o
E No Yes +240 o

Answer: C

To answer this question, you need to know:

a) How to recognize a RBBB
  • Usually RSR pattern (“M”) in V1 and “W” pattern in V6 (MarroW)
  • Inverted T waves in V1 (and occasionally V2 and V3)
  • Deep slurred S wave in V6
  • QRS complex usually > 120ms (RV and LV not contracting at the same time -> takes longer)
  • Prevalence increases with age (slow progressive degenerative process)
  • No association with risk factors for IHD/ ACS or myocardial death
  • Independent predictor of all-cause-mortality in suspected or proven coronary artery disease (not significant for incomplete RBBB)
  • RBBB in ACS is associated with increased mortality rate
  • Long term prognosis good if no underlying heart disease
  • Does not need PPM unless syncope (especially if other conduction defects present
  • Structural heart disease: chronic RV strain (eg cor pulmonale), acute RV strain (eg PE), acute coronary syndrome or myocarditis
  • Iatrogenic: eg secondary to Swan Ganz
  • Functional: eg rate related
  • Pseudo: related to primary ventricular arrhythmias eg Brugada
b) How to recognize RVH
  • Increase in RV mass and size, seen best in V1
  • Right axis deviation
  • f RV larger, the LV loses its dominant effect on the shape of the QRS ie height of R > depth of S
  • Peaked P waves (right atrial hypertrophy)
  • If severe: T wave inversion V1-V2

c) How to calculate the cardiac axis (Normal axis -30o to +900)
  • Axis points towards any lead where R > S
  • Axis points away from any lead when S > R
d) Previous transposition of great arteries
  • Commonest congenital cyanotic heart disease (still rare)
  • Isolated defect in 90% ie no syndromes/ extra-cardiac defects
  • 1/3 have coronary arterial anomalies
  • Systemic and pulmonary circulation run parallel rather than in series
  • Incompatible with life unless mixing of oxygenated and deoxygenated blood occurs: ASD/ VSD/ PDA
  • No mention of ECG abnormalities but any changes should reflect that of the surgery rather than the primary problem
  • 2 surgical options
    1. Atrial switch/ venous switch (Mustard or Senning procedure) ie creates a tunnel between the 2 atria (artificial ASD)
    2. Arterial switch ie relocating aorta and pulmonary artery in rightful place

Topic

Cardiology: Cardiology Investigations

Question 2 top

Question 3 top

Question 4 top Download PDF

A 37 yo woman on no medications presents with a 6/12 Hx of intermittent episodes of headache, sweating and confusion, which are relieved by eating. After 12 hours of fasting, she experiences similar symptoms and at that time, a series of investigations are performed.

Which combination of test is most suggestive of a diagnosis of an insulinoma?

  Serum glucose
(mmol/L)
[3.5 – 6.0]

Serum insulin
(Mu/L)
[5-12]

Serum C peptide
(pmol/L)
[250-700]
Urinary Sulphonylurea screen
A 3.5 3 260 Negative
B 2.0 18 800 Negative
C 2.0 18 130 Negative
D 2.0 18 130 Negatie
E 2.0 18 800 Positive

Answer: B

The symptoms sound characteristic of hypoglycaemia:
  • When lessthan3 mmol/L :(sympathoadrenal symptoms) restlessness, tremor, sweating and hunger
  • When less than 2.8 mmol/L: (neuroglycopenic symptoms) confusion, drowsiness, loss of consciousness and seizures
  • These thresholds may vary within individuals
  • All hormonal responses should normally begin well before onset of any symptoms
Hierarchy of physiological responses to hypoglycaemia:
Plasma Glucose level Hormone
less than 4.4
less than 3.6 - 3.9
3.3 - 3.6
less than 3.3
decrease insulin secretion
increase glucagon + adrenalin
increase growth hormone
increase cortisol

 

  1. In normal person and new T1DM: the predominant counter-regulatory hormone released is GLUCAGON
  2. However, when hypoglycaemia is prolonged, catecholamines, growth hormone and cortisol become important
  3. In those with longer-standing T1DM, the glucagons secretatory response becomes deficient but ADRENALIN plays a compensatory role so T1DM become dependant on it for counter-regulation
  4. In those with autonomic neuropathy, this compensatory mechanism becomes deficient -> incidence of severe hypoglycaemia increases
  5. May also be altered thresholds or deficiencies in counter-regulatory hormone secretion

Hypoglycaemia is rare in the absence of treatment for diabetes

Ddx (in otherwise well person)
  1. Facetitious (insulin or OHAs)
  2. Insulinoma
  3. Islet cell hyperthrophy/ nesidioblastosis (very rare)
  4. Intense exercise
  5. Ketotic hypoglycaemia
  6. Other predisposing drugs: salicylates/ quinine/ pentamidine

In a sick person, can often multi-factorial and part of underlying disease

Insulinoma
  • characteristic clinical manifestation: fasting hypoglyacemia with symptoms
  • up to 10% misdiagnosed with epilepsy/ peuso-seizures/ depression
  • mainly due to decreased hepatic glucose output rather than increased peripheral glucose utilization
  • mechanism that high insulin levels are maintained in low glucose levels unknown (? mutated insulin mRNA with autonomy)
  • rare (approx 4/1000 000/ year)
  • female more than male (slightly)
  • mean age 47
  • those with multiple associated with MEN1 syndrome (10%) thus need to be screened
Diagnosis (all interpreted in setting of hypoglyceamia)
Test Insulinoma
BSL less than 3

Plasma insulin 3 indicating excessively high insulin levels with hypogycaemia

Unfortunately some overlap: some with insulinoma can maintain BSL greater than 3 and some normal subjects can have BSL less than 2.8

 

Plasma C-peptide

  • no known biological function
  • surrogate marker for acute insulin secretion
  • often plasma levels higher than insulin due to longer half life (30minutes) and decreased hepatic clearance
    Ddx between endogenous and exogenous hyperinsulinaemia

When BSL less than 2.5 likely insulinoma if c-peptide greater than 0.2nmol/L

Plasma proinsulin

B cells of pancreas secrete pre-proinsulin becomes proinsulin beocmes insulin + c-peptide


Elevated more than 5x in insulinomas during hypoglycaemia
Plasma B hydroxy-butyrate

Decreased

  • high insulin thus less ketogenesis
  • used when borderline values of insulin and c-peptides

IM glucagon test

  • insulin is anti-glycogenolytic and thus encourages glycogen storage in the liver
  • in hyperinsulineamia, when glucagons is injected there should be a counter-regulatory release of glucose
  • normal subjects would have almost exhausted all glycogen by the end of 72 hours fast

Positive with raised BSL of > 1.4 mmol/L

Ddx of insulinoma
  • Familial persistant hyperinsulinaemia hypoglycaemia: genetic cause
  • Primary islet cell hypertrophy (niseroblastosis)
  • Noninsulinoma pancreatogenous hypoglycemia (post prandial)
  • Paraneoplastic syndrome with IGF secretion
  • Massive metastatic cancer burden with high metabolic needs
  • ACTH deficiency
Treament
  • surgical excision (dependant on location/ single vs multiple)
  • medical therapy directed towards decreasing insulin secretion (diazoxide/ octreotide) or chemotherapy
Topic

Endrocrinology:



Question 5 Download PDF

In patients with cirrhosis and oesophageal varices, the strongest predictor of variceal bleeding is:

  1. Prothrombin time
  2. Platelet count
  3. Child- Pugh’s class
  4. Portal venous pressure
  5. Systemic blood pressure

 

Answer:

Portal hypertension

  • Portal pressure = Portal flow volume x resistance to outflow from portal vein
  • Defined as > 5mmHg
  • Obstruction to portal venous outflow
    • Pre-sinusoidal (postal vein thrombosis, portal fibrosis, infiltrative lesions)
    • Sinusoidal (hepatic cirrhosis)
    • Post-sinusoidal (veno-occlusive disease, Budd-Chiari)
  • Splanchnic vasodilation -> relative renal hypoperfusion -> activates renin-angiotensin-aldosterone system -> salt and fluid retention
  • Oesophageal varices form when difference between portal veins and hepatic veins > 12mmHg
  • Meta-analysis of 12 studies showed that ß in hepatic venous pressure gradient HVPG < 12 mmHg -> significant ß in variceal bleeding and mortality
    • HPVG = WHVP – FHVP
      • WHVP: Wedged hepatic venous pressure (approximates sinusoidal pressures)
      • FHVP: Free hepatic venous pressure
  • Portal HT -> oesophageal varices, haemorrhoids, ascites, splenomegaly (+/- pancytopenia from sequestration)

Variceal bleeding:

  • Each bleed 30% risk of death
  • If survive 1st bleed, risk of rebleeding in 1 year is 70%
  • 90% of those with cirrhosis will develop varices
  • 20% with small varices progress to large varices in 1 year

Risk classification of predicting bleeds:

  • Child Pugh’s class
Classification of severity of liver disease

Class A: Score 5-6 (well compensated), 1 year survival 100%
Class B: Score 7-9 (significant functional compromise), 1 year survival 80%
Class C: Score 10-15 (decompensated), 1 year survival 45%

  • Variceal size
  • Independent risk factor for bleed (LaPlace’s law – small increase radius -> big increase in wall tension -> increase rupture risk)
  • Need to insufflate the oesophagus with air for accuracy
    • F1: small and straight varices
    • F2: enlarged and tortuous, occupy < 1/3 lumen
    • F3: large coiled shaped, occupy > 1/3 lumen

 

  • Variceal appearance
  • Presence of red wale markings is increase risk
  • Continued ETOH abuse

 

Primary prevention:

  • B-blockers
    • Propanolol or nadolol
    • ß bleeding rates in large varices but no clear mortality benefit
    • No ß bleeding rate/ mortality benefit in small varices
  • Variceal band ligation
    • ß bleeding rates at both 1st and 2nd year
    • Mortality benefit significant at 2nd year
    • Banding better than B blocker but costly
  • Useless: sclerotherapy, nitrates

 

Secondary prevention:

  • B blockers
    • ß rebleeding and mortality
  • B blockers + endoscopic banding vs B blocker alone
    • < rebleeding but no mortality difference
    • Cease B blocker when varices eradicated
    • Banding better than sclerotherapy

 

Acute variceal bleed:

  • Non aggressive resuscitation
    • Aim systolic BP 90mmHg sufficient
  • Evidence for:
    • Octreotide (somatostatin analogue)
    • Terlipressin (vasopressin analogue: more sustained effect compared octreotide)
    • Vasopressin (direct vasoconstrictor of mesenteric arterioles thus ß portal venous inflow – only marginal effects in early rebleeding bleed and no mortality benefit in acute bleed) + nitrates (to counteract effect of systemic vasoconstriction)
    • Endoscopic Rx with banding +/- sclerotherapy OR balloon tamponade (only for short term)
  • Some evidence for prophylactic antibiotics (ß overall mortality and ß infectious complications)
  • Debatable: use of B blockers

 

Causes of acute GIT bleed

  • Peptic ulceration
  • Gastritis/ erosions
  • Oesophageal variceal bleeding
  • AV malformations
  • MW tears

Rarely:

  • Tumours
  • Dieulafoy lesions (dilated aberrant submucosal vessel 1-3mm that erodes overlying epithelium)
  • Gastric antral vascular ectasia (GAVE/ watermelon stomach: ectatic and sacculated mucosal vessels in cirrhosis or systemic sclerosis or idiopathic)
  • Haemosuccus pancreatitis (bleeding from pancreatic duct with cancer, pseudocyst or chronic pancreatitis eroding into vessel)
  • Aorto-enteric fistula (D3 or D4, followed by jejunum and ileum; from atherosclerotic AAA, syphilis or TB, AAA vascular graft)
  • Cameron lesions (erosions or ulcers in sac of hiatal hernia)

Topic

Gastroenterology:CLD complications cirrhosis: ascites, encephalopathy, portal hypertension/varices.

 

Question 6 top Download PDF

For an 82 year old nursing home resident who experiences recurrent falls, which one of the following is least likely to prevent hip fractures?

  1. Oestrogen replacement therapy
  2. Bisphosphonates
  3. Calcium supplements
  4. Balance and strengthening exercises
  5. Hip protectors

 

Answer: C

Falls

  • 50% age >80 fall every year, 6th leading cause of death
  • Balance assessment
    • Postural blood pressure
    • Visual testing
    • Test of balance
      • Static balance
      • Dynamic balance
        • Self generated (functional reach)
        • Externally generated (sternal push)
    • No routine Ix

Fractures

  • Hip fractures: leading cause of delirium
  • To increase fracture risk (think treatment of osteoporosis)
    • Bisphosphononates
    • Strontium
    • Oestrogens (no longer recommended as increase risk AMI, breast and ovarian cancer, thrombo-embolic events)
    • SERMS (decrease vertebral but not hip, decrease risk breast cancer, no menopausal Sx)
    • Calcium (> 1200mg) +/- Vit D (> 800 units) daily as prevention
  • Non-pharmacological:
    • Hip protectors but only in Ý risk and compliant

 

Other possible falls question:
1) Which of the following has been shown to be a risk factor for falls in the elderly?

  1. Alcohol consumption
  2. Visual contrast sensitivity
  3. Reduced vestibular function
  4. Postural hypotension
  5. Home hazards

Answer: B
Strong evidence, developed in Melbourne – essentially measuring threshold for detecting 2 shades of grey. No evidence backing up the rest even though it’s intuitive.

2) Which of the following single intervention strategies has not been proven effective in fall prevention in the elderly?

  1. Strength and balance training
  2. Optometry assessment and refraction correction
  3. Cataract removal
  4. Reduction of psychotropic medication
  5. Vitamin D and calcium supplementation

Answer: B
Another Australian study (published 2007). Falls surprisingly more common in the treatment group.

Topic

Geriatrics: Falls

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