Medical questions Flashcards

1
Q

What are the causes of cirrhosis?

A

The commonest causes of cirrhosis are probably alcohol-related liver disease, NASH and viral hepatitis.

Other causes include autoimmune conditions such as PBC, PSC and autoimmune hepatitis and metabolic disorders such as haemochromatosis and Wilson’s disease. Cirrhosis can also be due to drugs such as methotrexate and amiodarone.

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2
Q

What factors can lead to decompensation of chronic liver failure?

A

Any stress on the system, for example infection, spontaneous bacterial peritonitis, hypokalaemia (which decreases renal ammonia clearance), GI bleeding, sedatives and HCC.

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3
Q

How would you manage this patient with liver failure?

A

After ABC, the strategy would be three-fold:

1) Treat the underlying cause
2) Preventing further damage to the liver e.g. stopping alcohol, vaccination against Hep A and Hep B
3) Preventing complications - monitoring for hepatoma through ultrasound and AFP, and endoscopy to look for oesophageal varices. Patients with varices should be treated with non-selective beta-blockers. Following an episode of SBP, prophylactic antibiotics are indicated.

If all else fails, the patient may be considered for a liver transplant.

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4
Q

What are the commonest causes of ascites in developed countries?

A

Cirrhosis
Congestive heart failure
Cancer

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5
Q

What investigations would you request to determine the aetiology of the ascites?

A

I would request a diagnostic paracentesis to look at the fluid and ultrasound the abdomen to look for any masses, splenomegaly (portal hypertension) or thrombosis in the hepatic vein. I would also do blood tests to assess liver function - LFT and PT, and FBC to look for hypersplenism and portal hypertension.

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6
Q

What are the major causes of chronic kidney disease in developed countries?

A
Diabetes
Hypertension
Glomerulonephritis
Polycystic kidney disease
Drugs
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7
Q

How would you treat someone with chronic renal disease?

A

I would approach this patient in three ways. I would treat the underlying cause if it was reversible. Then I would try and slow disease progression by treating their hypertension and cardiovascular risk factors, and then treat the complications of renal disease.

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8
Q

What problems can occur with haemodialysis?

A

Haemodialysis can cause haemodynamic instability. It can also lead to infection or bacteraemia, especially with tunnelled or non-tunnelled venous catheters. Bleeding can also occur due to the use of heparin as an anticoagulant during haemodialysis. Additionally, because there is decreased clearance of beta-microglobulin, the build up of protein can lead to amyloidosis.

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9
Q

What problems can occur with peritoneal dialysis?

A

Bacterial peritonitis - occurs once every patient year.
There can also be ultrafiltration failure as a consequence of peritoneal sclerosis, diabetes from systemic absorption of glucose from the dialysate and local complications such as hernias from the raised intra-abdominal pressure.

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10
Q

What are some inherited conditions predisposing to colorectal cancer?

A

Hereditary Nonpolyposis Colorectal Cancer (HNPCC) - autosomal dominant disorder with high penetrance caused by mutations in DNA repair genes.
Familial Adenomatous Polyposis - autosomal dominant condition caused by mutation in the APC gene. Patients are also at risk of other GI cancers, follicular or papillary thyroid cancer and CNS tumours. Diagnosis is based on the presene of more than 100 adenomatous polyps in the colon.
Peutz-Jegher syndrome - AD, characterised by multiple hamartomatous polyps in the small intestine, colon and stomach.

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11
Q

How do you screen for ADPKD?

A

Ultrasound screening for those with a family history after age 20.

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12
Q

At what level of the spine should you insert a needle during an adult LP? What are the surface anatomy landmarks? What structures do you pass through as you perform an LP?

A

The spinal cord in adults ends at L1/L2, with peripheral nerves extending beyond that as a loose bundle of fibres (cauda equina). A safe place to insert the needle is at or below L3/L4. This can be found by tracing a line between the posterior superior iliac crests (Tuffier’s line) which marks the L4/L5 space.

The following structures are sequentially traversed: skin, subcutis, supraspinous ligament, interspinous ligament, ligamentum flavum (first give), dura (second give) arachnoid space.

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13
Q

What are the relative contraindications for an LP?

A

Raised intracranial pressure due to a SOL, as the sudden drop in pressure can cause brainstem herniation. If there is any doubt, imaging should be performed first.
Increased bleeding tendency
Infection at prospective site of puncture
Cardiorespiratory compromise

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14
Q

What are the risks of an LP?

A

Headache - 30% due to intracranial hypotension
Nerve root pain - 10% due to irritation by the needle of one of the nerves forming the cauda equina
Infection at site of puncture

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15
Q

What are the possible causes for raised intracranial pressure?

A

SOL e.g. tumour, haematoma, abscess or cyst
Cerebral oedema
Increased blood pressure in the CNS e.g due to vasodilator drugs, malignant hypertension, hypercapnic vasodilation, venous sinus thrombosis or SVCO
Hydrocephalus

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16
Q

Define delirium.

A

Delirium is defined as a transient, usually reversible, cause of cerebral dysfunction and manifests clinically with a wide range of neuropsychiatric abnormalities.

The Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5) diagnostic criteria for delirium is as follows[3] :

Disturbance in attention (ie, reduced ability to direct, focus, sustain, and shift attention) and awareness.
Change in cognition (eg, memory deficit, disorientation, language disturbance, perceptual disturbance) that is not better accounted for by a preexisting, established, or evolving dementia.
The disturbance develops over a short period (usually hours to days) and tends to fluctuate during the course of the day.
There is evidence from the history, physical examination, or laboratory findings that the disturbance is caused by a direct physiologic consequence of a general medical condition, an intoxicating substance, medication use, or more than one cause.
17
Q

What treatment would you give someone presenting with confusion and a history of alcohol abuse and why?

A

All such patients should be given thiamine as prophylaxis for Wenicke’s encephalopathy. This classically presents as a triad of confusion, ataxia and ophthalmoplegia and is potentially reversible in the early stages. Failure to do so results in irreversible damage, knnown as Korsakoff’s syndrome, characterised by amnesia and confabulation.

18
Q

What is a Stoke-Adams attack? How are they treated?

A

A Stoke-Adams attack is a sudden transient loss of consciousness induced by a slow or absent pulse with a subsequent loss of cardiac output. The underlying problem is either complete heart block or sinoatrial disease. After the attack, the patient becomes flushed as the well-oxygenated blood in the pulmonary capillaries during circulatory arrest is pumped around. It is synonymous with cardiogenic syncope or syncope due to cardiac arrhythmia.

Stoke-Adams attacks are treated with a pacemaker.

19
Q

What should you, by law, advise patients with an episode of LOC about driving?

A

The DVLA have clear guidance on this matter. For cars and motorcycles:
- If it was a simple faint with prodromal symptoms and a provoking factor can be identified that is unlikely to recur whilst sitting, there are no restrictions and no need to advise the DVLA.
- If LOC was due to syncope with a low risk of recurrence, the patient can drive 4 weeks after the event.
- If LOC was likely syncope with a high risk of recurrence, the patient can drive after 4 weeks providing the cause is identified and treated, or 6 months if not identified and treated.
- If LOC is unexplained and there are no suggestions that it was a seizure, the patient cannot drive for 6 months.
- If LOC was associated with seizure markers, the patient cannot drive for one seizure-free year.
If someone with epilepsy has been on anti-epileptic medication and wants to stop, they cannot drive until 6 seizure-free months have passed.

20
Q

What are the main side effects of sodium valproate?

A
Weight gain
Hair loss and curling
Nausea
Rash
Drowsiness
Tremor
Drug-induced hepatitis
21
Q

What are the main side effects of lamotrigine?

A
Rash (SJS)
Headaches
Dizziness
Insomnia
Vivid dreams
22
Q

What are the main side effects of carbamazepine?

A
Rash
Nausea
Ataxia
Diplopia
Agranulocytosis
Hyponatraemia
23
Q

What are the main side effects of phenytoin?

A
Acne
Rash
Ataxia
Ophthalmoparesis
Sedation
Gingival hyperplasia
24
Q

What are the potential complications of thyroidectomy?

A

Specific complications:

1) Recurrent laryngeal nerve injury - 1:100. Unilateral damage = hoarse voice; bilateral damage = breathing difficulties
2) Injury to superior laryngeal nerve - 1:20 - difficulties adjusting the pitch of phonation
3) Transient voice changes in the absence of nerve injury - 1:10
4) Transient hypocalcaemia due to bruising of parathyroid gland
5) Hypoparathyroidism
6) Hyperthyroid storm if hyperthyroid patients are not adequately medicated prior to surgery
7) Post-operative haemorrhage and airway compromise

General complications: infection hypertrophic or keloid scarring, thromboembolism and anaesthetic complications

25
Q

How does the tachycardia seen with hyperthyroidism differ from the tachycardia seen in generalised anxiety states?

A

Often associated with AF, especially in older patients
Tachycardia due to hyperthyroidism will persist while the patient is sleeping, while tachycardia due to anxiety should disappear.

26
Q

What are the risk factors for oesophageal cancer?

A

There are two main types of oesophageal cancer - squamous cell carcinoma and adenocarcinoma.

The risk factors for SCC: alcohol, smoking , dietary nitrosamines, aflatoxins, achalasia, Plummer-Vinson syndrome, coeliac disease

Risk factors for adenocarcinoma - Barrett’s oesophagus (hence any factor that predisposes to reflux oesophagitis). Smoking and alcohol appear not as important.

27
Q

What is the pathophysiology of achalasia?

A

Achalasia is caused by an absence of ganglion cells in the myenteric plexus (Auerbach’s plexus) of the oesophagus, resulting in a failure of relaxation of the lower oesophageal sphincter and aperistalsis in the oesophageal body. The underlying cause is unknown. Chagas disease results in an identical pathophysiology and infiltrating carcinoma can also produce similar effects through invasion of the myenteric plexus.

28
Q

A dysphagic patient presents with a hoarse voice and a bovine cough. What could account for all these symptoms?

A

Hoarse voice and bovine cough are characteristic of recurrent laryngeal nerve palsy. There are two main ways in which this can be connected with dysphagia.

1) Infiltration of the nerve by a malignancy which is causing dysphagia
2) Ortner’s syndrome - the recurrent lyarngeal nerve is compmressed by the cardiovascular system, most commonly left atrial dilatation secondary to mitral stenosis.

29
Q

What are the common complications after an oesophagectomy?

A

1) Breakdown of the anastomosis
2) Pneumonia due to poor ventilation secondary to pain
3) Cardiac arrhythmia - manipulation of the tissue near the heart predisposes patients to intraoperative and post-operative cardiac arrhythmias

30
Q

Why is a recurrent laryngeal nerve palsy more common on the left than the right?

A

The left branch of the RLN loops around the archo of the aorta and thus has a longer intrathoracic course (and hence is more likely to be affected by chest pathology. The right RLN loops around the right subclavian artery.

31
Q

What is the doctrine of double effect?

A

The doctrine of double effect applies when a treatment has two (or more) effects. The primary (intended ) effect is to relieve the symptoms. The secondary effect, which is foreseen but not intended, in some way hastens death. In legal terms, although the treatment is bringing about mortality, as its primary effect is beneficial it is viewed as distinct from euthanasia.

32
Q

What investigations should you request for a patient with new onset angina?

A

1) Exercise tolerance test - ST depression of >=2mm, typical symptoms of exertional angina or ST elevation >-1mm usually indicate stenosis of the coronary arteries. A fall in BP is a poor prognostic sign.
2) Stress echocardiogram - the patient is given dobutamine to simulate stress while their cardiac function is assessed by echocardiogram. A normal heart shows increased motility when stressed, whereas stressed ischaemic myocardium is hypokinetic.
3) Myoview scan - patients are injected with radioactive thallium and a picture is taken with gamma camera. Pictures are compared at rest and after exercise. Areas of the myocardium with good perfusion appear as warm spots.
4) Angiography/angioplasty.

33
Q

Describe the progression of ECG changes you would expect to see over 7 days in a patient presenting with acute STEMI.

A

1) Tented T waves (due to localised hyperkalaemia following myocyte ischaemia)
2) ST elevation in the affected leads with ST depression in reciprocal leads, lasting 24-48 hours
3) T wave inversion, developing in 1-2 days and persisting for weeks/months
4) Q waves, developing within days and remaining permanently.

34
Q

What is the basis for Q waves?

A

Old infarcts are visible on ECGs as the infarcted tissue no longer conducts electrical impulses. If they are full thickness, they can be thought of as a window. Thus, an electrode positioned next to an area of full thickness infarct will look through the window of infarcted tissue and pick up the electrical impulses passing through the myocardium on the other side of the heart.

35
Q

When is mastectomy preferred over breast-conserving surgery?

A

Wide local excision followed by radiotherapy has been shown to produce long-term survival equal to mastectomy, with only a slight increase in the rates of local recurrence. However, not all patients are suitable for WLE. Mastectomy may be necessary to achieve tumour clearance if the tumour is large relative to the breast, a tumour that occupies a central position within the breast, multifocal tumours, recurrent tumours or patient preference. Mastectomy is also indicated for the treatment of male breast cancer.

36
Q

What components of the clotting cascade does warfarin interfere with? What additional drug should all patients starting warfarin be placed on and why?

A

Warfarin is a competitive antagonist of vitamin K, the cofactor used to synthesise factors II, VII, IX and X, protein C and protein S. Warfarin can take a few days to have an effect on clotting because the factors take a few days to become depleted. Additionally, it can cause an initial paradoxical increase in clotting because of the depletion of protein C and protein S (anticoagulant) before the depletion of the procoagulant factors. Therefore, patients are started on LMWH for up to 5 days or until the INR>2 for two consecutive days.

37
Q

Which diseases and drugs produce a pro-thrombotic state?

A

Congenital mutations: Factor V Leiden, Prothromin mutation, Antithrombin III deficiency, Protein C deficiency, Protein S deficiency

Disease: any malignancy, antiphospholipid syndrome, DIC, polycythaemia

Drugs: COCP, HRT, heparin-induced thrombocytopenia