Medical Exams Questions Bank

g. Guillain Barre Syndrome

Check your hypothesis against the clinical signs:

Remember FVC monitoring in GBS.

a. Brain Metastases

A difficult question because of the volume of data to interpret.

List everything that is pathological:

1. Seizure
2. Low Sodium at 129 mmol/l
3. Hypertension
4. Ill defined lesion in left mid zone on CXR

1. The seizure may be idiopathic/ relate to a structural/ drug/ metabolic disturbance.
2. The sodium isn’t particularly low enough to provoke a seizure (Once the Na+ gets <120 and more seriously <110 the risk of seizure is greatly increased. As such the sodium on its own is not a strong risk factor for a seizure). Causes: drugs (he is on none/ SIADH of any cause)
3. The hypertension is most likely to be idiopathic: there are no clues to an underlying endocrine cause
4. The ill defined chest X-ray lesion could represent a malignancy (1^o/ 2^o)/ infection (bacterial/ viral/ tuberculosis etc)

c. Pancreatic cancer

No marks for anything other than this: the famous Courvoisier’s law:

In the presence of a palpable gallbladder (GB) in painless jaundice the diagnosis is unlikely to be gallstones.

Why?

Gallstones cause chronic GB fibrosis. A distended GB suggests a more acute obstruction

Why not PBC or alcohol?

The LFT’s show an “obstructive picture (high Alk Phos/ GGT/ Bili + reasonably low ALT). Alcohol would not do this or give the distended GB. PBC could give the obstructive picture but you’d be less likely to find the palpable GB.

d. It can be used to discharge patients based on their underlying estimated clinical risk score

D-dimer test can be used to exclude DVT in patients who are assessed to be in the category of “low clinical risk” of DVT.

An individuals pre-test risk can be estimated using a “Wells score”. A patient who is clinically “low risk” with a negative D dimmer can be reassured.

The Wells score is shown below.

The Wells score and an example of its clinical application in terms of planning investigations into a DVT

Although you clearly cant memorise a wells score its clear from the score itself that patients with numerous risk factors (e.g a man with lung cancer with a swollen right leg with pitting oedema) that a negative D-dimer is not sensitive enough to rule the diagnosis out.

D-dimer is still of some use in patients with a low pre-test probability score.

b. Contraindicated drug

The trick here is the penicillin allergy which means penicillin and its derivatives are all essentially contraindicated until a further allergy history is taken, i.e:

• Ampicillin
• Amoxicillin (formerly amoxycillin)
• Flucloxacillin
• Piperacillin (Tazocin ®)
• Cephalosporins

Cephalosporins (e.g. cefuroxime, cefotaxime, cefalexin) also have a cross reactivity in penicillin allergy that may approach 10%. Therefore for exam purposes I would also consider these drugs contraindicated (e.g. cefuroxime). The true incidence of anaphylaxis with cephalosporins seems to be much lower.

For exam purposes in these instances senior support or microbiological advice is often suggested if no alternative is obvious.
Alternative drugs in patients with a penicillin allergy include quinolones (e.g. ciprofloxacin), macrolides (e.g. clarithromycin), tetracyclines (e.g. doxycycline), aminoglycosides (e.g. gentamycin), metronidazole, vancomycin, and teicoplanin.

Although co-amoxiclav is normally given 3 times a day, 4 times a day is still within a reasonable dose range. This is an easy way to "outfox" a student with a more important error.

d. None of the above

The key question is "what is the explanation for his symptoms", not "what is the effect of antibiotics on warfarin"

His INR is stable. This therefore does NOT explain his symptoms over the past 5 weeks and an alternative cause should be sought. The INR represents one measurement of the clotting cascade, but represents only one aspect of clotting.

His INR level does not explain his bruising, therefore there must be another explanation.

There is a simple way of remembering drugs that effect the metabolism of warfarin, and the oral contraceptive pill.

The full list of enzyme inducers and enzyme inhibitors regarding hepatic metabolism can be remembered from the following two acronyms:

PCBRAS and ODEVICES…

For example: a patient taking warfarin may well have a higher than expected INR if he is put onto trimethoprim, and the opposite if he is put onto carbamazepine.

a. Beta HCG
c. AFP (alfa fetoprotein)
f. PSA (prostate specific antigen)

The other tests are not specifically designed as "screening tests" for patients. For example a man losing weight should not simply have a CEA, CA19-9 and Ca 125(!) checked as:

• there is no replacement for clinical examination and planned investigations
• "negative results" do not negate the need for further investigation
• "positive results" do not necessarily infer any diagnostic specificity.

A careful history, examination, investigations and clinical assessment is much more important than just requesting lots of tests.

PSA, HCG and AFP are different as a result of their sensitivity and specificity and relative prevalences of each of the conditions they act as "markers" for namely: prostate cancer, Choriocarcinoma and hepatoma.

The other tests are not validated as ‘cancer screening’ tools and should not be used in this way.

Commonly cited tumour markers:

e. Skin Pigmentation

Most of the symptoms of adrenal insufficiency (e.g. hypotension, weight loss) result from low cortisol levels and therefore do not distinguish between adrenal or pituitary failure.

This question tests your understanding of the hypothalamic-pituitary-adrenal axis. This is another example where negative feedback is used to control hormone release.

ACTH is released from the pituitary gland. It acts on the adrenal glands stimulating cortisol release.

In primary adrenal failure (Addison’s disease), there is destruction of the adrenal glands and therefore they do not produce cortisol. In an attempt to stimulate the failed adrenal glands, the pituitary gland secretes high levels of ACTH.

ACTH is synthesised within the anterior pituitary gland from pro-opiomelanocortin (POMC). The cleavage of the POMC molecule results in the production of ACTH as well as a number of molecules including forms of MSH (melanocyte stimulating hormone). In fact, alpha-MSH is identical to the start of the ACTH molecule.

High levels of circulating ACTH act as MSH causing increased pigmentation.

Look in the buccal mucosa and at the palmar creases.

If the cause of hypoadrenalism is from pituitary failure, neither ACTH nor MSH will be released, hence there’s no increase in pigmentation.

a. Benign Intracranial Hypertension

The pressure is very high! The CT was normal essentially excluding raised intracranial pressure secondary to an obstructive hydrocephalus (e.g. meningioma obstructing the 4^th ventricle draining CSF). The red cells are high in the first sample of CSF but as further CSF is tapped off, this clears. This supports a slightly “traumatic” tap. Xanthochromia testing in the sample is negative, providing no evidence of a prior bleed into the CSF which has then been broken down into xanthochromia.

To diagnose a S.A.H. you have to have either blood or altered blood in the CSF. As a rule of thumb you should have "no" red cells in the CSF if its not a traumatic tap and there is no other pathological processes.

The diagnosis is BIH. This is reasonably common in young people and is not benign: untreated it can threaten sight. Treatment is via means to reduce CSF pressure e.g. repeated lumbar punctures.

a. Post infective glomerulonephritis

Penicillin is the standard treatment for guttate psorias: treat the streptococci infection. S Its likely that its a type III (antigen antibody complexes getting stuck in the kidney) hypersensitivity reaction, although the steptococci may also produce toxins which result in direct renal injury. The haematuria in posrt strep GN may be "frank" or microscopic.

So the history is is classical of post streptococcal Glomerulonephritis!

In this situation he has had a recent streptococcus infection causing guttate psoriasis. For an exam: post streptococcal: think post strep GN.

Urinalysis would probably show blood and protein (e.g. Blood 3+ Protein3+) The management is generally supportive without the use of prednisolone or a renal biopsy, unless there is renal impairment etc.

Although interstitial nephritis could occur and present like this, its less likely than the classic association of post strep GN. Interstitial nephritis is commonly caused by drugs(NSAIDs and others, hypersensitivity) and presents with malaise/ eosinophillia/ renal impairment. They usually have no/ minimal proteinuria as its a disease of the renal tubules, not the glomeruli.

Glomerular injury (in glomerulonephritis) damages the capillaries and/ or glomerular basement membrane. This renal damage allows red blood cells and larger plasma proteins to "leak" through the glomeruli and into the proximal convoluted tubule and out in the urine.

THIS IS WHY blood and protein in the urine is such an important finding on urinalysis, and why a urinalysis is such a helpful test/ marker of renal disease.

• 3+ blood 3+ protein on urinalysis? think: Infection (UTI)? Glomerulonephritis

b. Warfarin

Based on NICE Guidance 36 (AF) and the CHADS 2 scoring system.

The CHADS2 score is an excellent aide memoir to anticoagulation in AF. It is based on:

SCORE
2 or over=Warfarin
1= Warfarin or aspirin
0=aspirin

This means our chap here will score:

1 for being >75
1 for being hypertensive

This means he should be treated with warfarin (assuming he has no contraindications)

A link to the original publication citation in circulation is available here.(link will open in a new window)

d. Observation initially

The pneumothorax is small. Its likely to resolve with no treatment. You can simply repeat the CXR after a period (e.g. 24-48 hours)Aspiration may be successful but is risky in such small effusions.

The British Thoracic Society suggest for a larger pneumothorax:

• Aspirate effusions >2cm in diameter

• Then repeat the CXR

• If unsuccessful: consider either repeat aspiration or chest drain.

In essence this means that in anyone with a spontaneous pneumothorax of >2cm you should consider an aspiration first.

The full British Thoracic Society (BTS) guidelines for pneumothorax are available by clicking the link here .

d. Ramsay Hunt Syndrome

Firstly this is a lower motor neuron (LMN) facial (CN VII) palsy: facial weakness of the whole of the face.*

Bell’s is a lower motor neurone lesion which is idiopathic in nature.

The aetiology is probably thought to be a herpes virus and there is some evidence to support the use of short course oral corticosteroids and aciclovir.

• about 50% of people will get better with no treatment
• steroids for approximately 1 week seem to help 50% of cases
• the benefit of aciclovir remains controversial

However: Ramsay Hunt is a facial nerve palsy caused by associated herpes zoster infection (as manifested in this case by the vesicles). When a patient presents with a CNVII weakness, this is one of the key reasons to perform otoscopy, as otherwise you may miss the vesicles.

*Remember in UMN lesions the upper half of the face is spared as there is bilateral UMN innervation. You would not expect this in Ramsay hunt as its a LMN lesion.

• Delusions: A belief firmly held despite evidence to the contrary. Must be inappropriate in terms of cultural beliefs. For example if believing in reincarnation is culturally appropriate, it is not a delusion.

^{"I think I can fly"}

• Hallucinations are sensory perceptions (e.g. visual auditory) occurring in the absence of an external stimulus: in contrast to illusions which are misperceptions of external stimuli

^{"I can see cats running up and down the walls"}

• Compulsions are repetitive and behaviours with a degree of apparent purpose, and are therefore associated with obsessional behaviour which comprises of thoughts that enter the mind. People often try to (unsuccessfully) resist obsessions.

• Overvalued ideas are thoughts which can then lead to changes in behaviour or actions which are neither obsessional nor delusional. Praying an unusually large amount of time is an example: the praying may be consistent with the religious belief but not the extent which its being taken.

^{"I need to pray 14 times a day to satisfy my religious belief. However it is beginning to affect the way I bring up my children and the time I spend with them"}

• Mood disorders encompass the usual depression anxiety and other more normal emotions of elation irritability, emotional lability etc.

^{"Every day at work I shout at my junior doctors at the drop of a hat if even the simplest and most insignificant thing is out of place or not how I like it. I have subsequently been suspended"}

• Illusion: misperception of a “real” external stimulus e.g. seeing the a car travelling with no wheels (although the car is there). Differentiated from a hallucination by the fact it is a "misperception" of a real physical stimulus.

^{"The car over there driving down the street has no wheels" (whilst looking at a car driving normally down the street)}

e. 0.85

Fill out the tables below

Sensitivity is therefore 600/ (600+100)= 600/700 = 6/7 =0.85 [85%]

b. Rheumatoid arthritis

Symmetrical disease?
Erosions?
This is classical of RA X-ray changes that include

1. Erosions
2. Reduced joint space
3. Peri-articular osteoporosis
4. Nodules

So from the initial history of disease [small joints, both hands], the likely diagnoses would be

• RA
• PsA
• (less likely) gout.

Erosive changes are not specific to RA however but the findings were symmetrical

• both gout and PsA tend to be asymmetrical

Don’t be put off by the fact he’s male, although RA is roughly 3x commoner in women. You cont get a mention of which joints are affected here: RA has a penchant for the wrists and MCP joints. Erosions of the ulnar styloid are very common.

Common x-ray changes of the different arthritides are shown below.

This system of hypersensitivity was devised by Messrs Gell and Coombs in the 1960’s, and is a helpful way of thinking about immunological reactions

b. The chance of transmission of hepatitis C is around 3%

The chances of transmission are as follows:

The risk is higher with hollow bore needles than with normal needles (e.g. suturing). This data varies widely across specialities. Individuals vaccinated against Hepatitis B have a lower risk of transmission following a needle stick.

The prevalence of needle stick injuries has been estimated to be as high as 33% in a 6 month period for healthcare workers.³

Hep B is the most transmissible of all 3 conditions. As a healthcare professional with a transmittable disease it may preclude you from working in certain specialities e.g. some surgical specialities.

Remember the prevalence of Hepatitis B, HIV and Hepatitis C in the UK is still low (<1% for each).

1. The risk of Hep C transmission rate varies from 3-5%. If a person is exposed, the usual practice is to PCR the blood for the hepatits C virus .
^{MS Sulkowski et al. Needlestick transmission of hepatitis C. JAMA 2002 287: 2406-2413.}

2. A study of 75 medical students and interns in New York
^{F Resnic, MA Noerdlinger. Occupational exposure among medical students and house staff at a New York City medical center. Archives of Internal Medicine 1995 155: 75-80.}

A good review can be read from Bandolier here