Medical questions 2 Flashcards

1
Q

How do you classify the severity of aortic stenosis?

A

1) Using aortic valve area - the normal aortic valve orifice is 3-4cm2. Mild AS is >1.5cm2, moderate is 1.5-1.0 and severe is 50mmHg.

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2
Q

What are the clinical signs of severe aortic stenosis?

A

Low volume pulse
Slow rising pulse
Narrow pulse pressure
Heaving apex
Systolic thrill
Reversed splitting of the second heart sound
Soft or absent aortic component of the second heart sound
Fourth heart sound
Late systolic peaking of a long murmur
Signs of pulmonary hypertension
Signs of pulmonary congestion or heart failure

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3
Q

What are the differential diagnoses for an ejection systolic murmur?

A
Aortic stenosis
Hypertrophic obstructive cardiomyopathy
Supravalvular aortic stenosis
ASD
VSD
Flow murmur
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4
Q

What are the causes of aortic stenosis?

A

Common: bicuspid aortic valve (65), rheumatic valve disease, congenital

Rarer: infective endocarditis, hyperuricaemia, alkaptonuria, Paget’s disease of the bone

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5
Q

What do you understand of the term ejection-systolic murmur?

A

It is a crescendo-decrescendo murmur after the first heart sound, or after an ejection click.

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6
Q

How would you manage a patient with aortic stenosis who is asymptomatic?

A

Advise endocarditis prophylaxis - good dental hygiene
Report symptoms of angina, palpitations, syncope and breathlessness
Patients with severe aortic stenosis should be regularly screen for these symptoms. Sudden death predominantly occurs in symptomatic patients, and such patients warrant aortic valve replacement.

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7
Q

What is the prognosis for symptomatic aortic stenosis?

A

Angina - 5 years
Syncope - 3 years
Dyspnoea - 2 years

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8
Q

What is the mechanism of syncope in aortic stenosis?

A

Aortic stenosis results in a low cardiac output state. There may be a transient electro-mechanical dissociation, where the left ventricle is unable to contract against a stenosed valve. During exercise, peripheral dilatation is not accompanied by an increase in cardiac output. Arrhythmias may also co-exist.

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9
Q

What are the indications for aortic valve replacement for aortic stenosis?

A

Symptomatic patients - symptomatic severe AS

Asymptomatic patients - those with moderate/severe AS undergoing other cardiac surgery e.g. bypass, and those with severe aortic stenosis and any of the following - LV systolic dysfunction, abnormal BP response to exercise, VT or valve area <0.6cm2.

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10
Q

How would you investigate a patient with aortic stenosis?

A

1) ECG - LVH, left ventricular strain, left atrial hypertrophy/dilatation, left axis deviation, conduction abnormalities
2) CXR - post-stenotic dilatation of proximal ascending aorta, calcification of aortic valve, cardiomegaly, pulmonary congestion, prominent pulmonary arteries
3) Echocardiogram
4) Coronary angiography - to exclude coronary artery disease as a cause of symptoms. All patients having valve replacement should have coronary angiography to exclude stenoses which would require bypass grafting at the time of valve replacement

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11
Q

What are the different kinds of prosthetic valves?

A

Mechanical prostheses
- Starr-Edwards/ ball and cage
- Tilting disc valve
- bjork-Shiley valve - a single tilting disc valve with laminar flow
St-Judes valve - a bileaflet, double tilting disc valve

Xenografts - porcine or pericardial valve

Homografts - cadaveric aortic or pulmonary valves

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12
Q

Which patients should receive a bioprosthetic valve?

A

In patients where anticoagulation would be contraindicated

Where life expectancy is shorter than the predicted lifespan of prosthesis

Patient age >70, as the rate of degeneration is slow in these patients.

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13
Q

What are the complications of prosthetic valves?

A

Thromboembolism
Complications of anti-coagulaiton e.g. bleeding
Valve dysfunction i.e. leakage, dehiscence, obstruction due to thrombosis, fibrosis and clogging
Endocarditis
Haemolysis

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14
Q

What are the causes of anaemia in a patient with a prosthetic valve?

A

Blood loss secondary to anticoagulation
Haemolysis (commonly aortic prostheses)
Endocarditis

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15
Q

What are the causes of mitral regurgitation?

A

Chronic - mitral valve prolapse, rheumatic fever, infective endocarditis, functional secondary to ventricular dilatation, connective tissue disorders e.g. Marfan’s, inflammatory conditions e.g. rheumatoid arthritis and SLE, papillary muscle dysfunction e.g. secondary to ischaemia, mitral annular calcification, cardiomyopathies

Acute - infective endocarditis, rupture of the chordae tendinae, trauma

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16
Q

What are the clinical signs of severe mitral regurgitation?

A
Soft first heart sound
Third heart sound
Fourth heart sound (if in sinus rhythm)
Displaced apex beat
Precordial thrill
Mid-diastolic flow murmur
Widely split second heart sound
Signs of pulmonary hypertension/congestion
17
Q

How would you manage a patient with mitral regurgitation?

A

Asymptomatic patients - endocarditis prophylaxis and annual echocardiography to assess progression of mitral regurgitation

Management of AF if present

Management of heart failure

18
Q

What are the indications for mitral valve surgery?

A

Patients who are symptomatic i.e. NYHA functional class II or IV, despite optimum medical therapy

Asymptomatic patients should be followed up every 6 moths with echocardiography or radionuclide assessment of LV size and function. When the LVEF falls to 60% or left ventricular end-systolic diameter is greater than 45mm, mitral valve surgery should be considered.

19
Q

What is the pathophysiology of HHS?

A

It is characterised by severe hyperglycaemia in the absence of any ketosis. The hyperglycaemia causes fluid shifts under osmosis from the extravascular compartment to the intravascular compartment, causing cellular dehydration. There is then osmotic diruesis, resulting in hypovolaemia. If this becomes severe, patients become vulnerable to shock, thrombosis and neurological impairment.

20
Q

What are the sick day rules for insulin?

A

Never stop taking insulin even if not eating.
There may be a need to increase the dose.
Test blood glucose more often (at least 4 times a day)
Drink lots of fluids to prevent dehydration
Replace normal meals with carbohydrate drinks if necessary
Test urine for ketones
Seek medical advice if you develop vomiting or are unsure what to do.

21
Q

What are the features of a basal cell carcinoma?

A

A pearly nodule with rolled telangiectatic edge on the face. Metastases are very rare.

Lesions on the trunk can appear as red scaly plaques with a raised smooth edge.

22
Q

What are the treatments for BCC?

A

Excision, radiotherapy if a big lesion. Cryotherapy and currettage if in a non-critical site. Consider imiquimod if superficial.

23
Q

What are the features of a squamous cell skin cancer?

A

A persistently ulcerated or crusted firm irregular lesion often on sun-exposed sites. Also related to smoking, chronic inflammation e.g. venous leg ulcers, and HPV.

24
Q

What are the treatments for SCC?

A

Excision.
Topical imiquimod or 5FU if superficial.

Metastasis is rare, although commoner in places like ears.

25
Q

What investigations should be done for suspected pneumonia?

A

Aim to establish diagnosis, identify pathogens and assess severity.

  • CXR
  • Assess oxygenation - ABG if necessary
  • Bloods - FBC, U&E, LFT, CRP, blood culture
  • Sputum microscopy and culture

In severe cases, check for legionella (sputum culture and urine antigen), atypical organisms/viral serology (complement fixation tests and paired serology), check for pneumococcal antigen in urine and pleural fluid may be aspirated for culture.

Consider bronchoscopy or bronchoalveolar lavage if patient is immunocompromised or on ITU.

26
Q

What are the potential complications of pneumonia?

A
Pleural effusion
Empyema
Lung abscess
Respiratory failure
Septicaemia
Brain abscess
Pericarditis
Myocarditis
Cholestatic jaundice
27
Q

Can you explain the features of Brown-Sequard syndrome anatomically?

A

Each half of the spinal cord contains upper motor neurons innervating the ipsilateral side of the body, dorsal column neurons innervating the ipsilateral side of the body and spinothalamic neurons innervating the contralateral side of the body.

Thus, section of half of the spinal cord results in loss of power and loss of vibration, proprioception and fine touch on the same side of the body below the lesion, but loss of pain and temperature on the opposite side of the body.

28
Q

What are the causes of SIADH?

A

Lung disease: infection, tumours, mechanical ventilation
CNS: lesion (tumour, abscess, haematoma), inflammation (encephalitis, meningitis, SLE), Guillain Barre, trauma (e.g. to posterior pituitary)
Iatrogenic: nicotine, tricyclics, ecstasy, desmopressin
Tumours: pancreas, uterus, leukaemia
Others: pain, opiates, barbiturates, nausea

29
Q

What causes a raised osmolar gap (>10)?

A

Ethanol
Methanol
ethylene glycol

(Presence of an osmotically active substance not included in osmolality calculation)

30
Q

What is the calculation for plasma osmolality?

A

2 (Na + K) + urea + glucose

31
Q

What is the criteria for SIADH?

A

Hyponatraemia, low plasma osmolality
Urine osmolality inappropriately high
Euvolaemia - no oedema
Normal renal, adrenal and thyroid function
Urinary sodium loss > 20 mmol/L. Not conserved despite hyponatraemia
Clinical response to fluid restriction

32
Q

How do you treat SIADH?

A

Fluid restriction.
Demeclocycline, raptans (antagonise ADH)
Correct at the same speed as onset otherwise risk of central pontine myelinolysis

33
Q

How do you treat hypernatraemia?

A

Hypotonic fluids (dextrose saline, dextrose)
Identify and remove the cause
Correct at the same speed as onset.

34
Q

What are the causes of diabetes insipidus?

A

Central: pituitary surgery, pituitary infiltration e.g. sarcoid, head injury

Nephrogenic: familial, metabolic (hypercalcaemia, hypokalaemia), RTA, PKD, amyloid, drugs (lithium, demeclocycline)

35
Q

What are the causes of hypokalaemia?

A
  1. Reduced uptake (dietary or replacement)
  2. Increased renal loss, diuretics, hyperaldosteronism, drugs e.g. theophyllines, aminoglycosides
  3. Increased gut loss - diarrhoea, laxatives, vomiting, villous adenoma, enterocutaneous fistula
  4. Cutaneous loss - sweating
  5. Transcellular movement e.g. insulin, salbutamol, rapid cell proliferation, alkalosis
36
Q

Which ECG changes are associated with hypokalaemia?

A
Arrhythmias
ST depression
T wave inversion/flattening
U wave
Prolonged PR interval
37
Q

What are the causes of hyperkalaemia?

A

Artefact
Excessive intake
Transcellular movement e.g. tissue damage, tumour lysis, acidosis, reduced insulin
Parenteral infusion
Reduced excretion e.g. AKI, chronic kidney disease, mineralocorticoid deficiency

38
Q

What ECG changes are associated with hyperkalaemia?

A
Tented T wave
Broad QRS
Flattened P wave
Sine wave
VF
39
Q

How do you manage hypokalaemia?

A

Ensure that patient is not hypomagnesaemic

Give potassium

  • Dietary
  • SandoK (12 mmol) - 3 tablets TDS
  • IV