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Yr 4 - CCC > Corrections - Cardiology > Flashcards

Corrections - Cardiology Flashcards

1
Q

1st line treatment of PE?

A

DOACs

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2
Q

1st line treatment of massive PE with circulatory failure (e.g. hypotension)?

A

Thrombolysis

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3
Q

Describe the pain in aortic dissection

A

‘Tearing’, radiates into back

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4
Q

What may be seen in a CXR in aortic dissection?

A

Widened mediastinum

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5
Q

Features of pericarditis?

A
  • chest pain: may be pleuritic. Is often relieved by sitting forwards
  • other symptoms include a non-productive cough, dyspnoea and flu-like symptoms
    pericardial rub
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6
Q

What ECG changes are seen in pericarditis?

A

The changes in pericarditis are often global/widespread, as opposed to the ‘territories’ seen in ischaemic events

1) ‘saddle-shaped’ ST elevation
2) PR depression: most specific ECG marker for pericarditis

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7
Q

What is the most specific ECG marker for pericarditis?

A

PR depression

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8
Q

Major cardiac complicaton of Kawasaki disease?

What investigation can be used to screen for this?

A

Coronary artery aneurysm –> echocardiogram

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9
Q

What is B-type natriuretic peptide (BNP)?

A

a hormone produced mainly by the left ventricular myocardium in response to strain

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10
Q

Give some causes of an increased BNP

A
  • LV hypertrophy
  • Ischaemia
  • Tachycardia
  • RV overload
  • Hypoxaemia (including PE)
  • GFR <60 ml/min
  • Sepsis
  • COPD
  • Diabetes
  • Age >70
  • Liver cirrhosis
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11
Q

Give some causes of an decreased BNP

A
  • Obesity
  • Diuretics
  • ACEi
  • Beta blockers
  • Angiotensin 2 receptor blockers
  • Aldosterone antagonists
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12
Q

What is indicated in patients with clinical signs of heart failure and raised BNP greater than 400 pg/ml?

A

Urgent (within 2 weeks) specialist review and echocardiogram

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13
Q

What should be given in addition to aspirin to all NSTEMI patients unless high bleeding risk?

A

Fondaparinux

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14
Q

Classic CXR signs in pulmonary oedema?

A
  • Kerley lines
  • Bilateral peri-hilar shadowing (‘bat wing appearance’)
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15
Q

What are 2 respiratory causes of erythema nodosum?

A

1) TB
2) sarcoidosis

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16
Q

What is TURP syndrome?

A

A rare and life threatening complication of transurethral resection of the prostate surgery.

Caused by venous destruction and absorption of the irrigation fluid.

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17
Q

Symptoms of TURP syndrome?

A

typically presents with CNS, respiratory and systemic symptoms

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18
Q

Risk factors for developing TURP syndrome?

A

surgical time > 1 hr
height of bag > 70cm
resected > 60g
large blood loss
perforation
large amount of fluid used
poorly controlled CHF

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19
Q

Give some causes of RBBB

A

1) normal variant - more common with increasing age
2) right ventricular hypertrophy
3) chronically increased right ventricular pressure - e.g. cor pulmonale
4) pulmonary embolism
5) myocardial infarction
6) atrial septal defect (ostium secundum)
7) cardiomyopathy or myocarditis

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20
Q

ECG features in LBBB vs RBBB

A

in LBBB there is a ‘W’ in V1 and a ‘M’ in V6

in RBBB there is a ‘M’ in V1 and a ‘W’ in V6

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21
Q

What investigation is used to capture episodic arrhythmias?

A

Holter monitoring (24 hours)

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22
Q

Cardiac features of thyrotoxicosis?

A

1) palpitations, tachycardia
2) AF
3) high output HF

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23
Q

Give some symptoms of acute mitral regurgitation

A

Acute mitral regurgitation can lead to flash pulmonary oedema:
- acute onset shortness of breath
- bibasal crackles
- hypotension
- systolic murmur

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24
Q

Damage to what muscle can cause acute mitral regurg after MI?

A

Papillary muscles (leads to loss of competency of the mitral valve)

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25
Q

Main monitoring parameters in:

a) statins
b) ACEi
c) amiodarone

A

a) LFTs
b) U&Es
c) TFTs, LFTs

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26
Q

Main monitoring parameters in:

a) methotrexate
b) azathioprine

A

a) FBC, LFTs, U&Es
b)FBCs, LFTs

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27
Q

Main monitoring parameters in:

a) lithium
b) sodium valproate

A

a) lithium level, TFTs, U&Es
b) LFTs

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28
Q

Main monitoring parameters in glitazones/

A

LFTs

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29
Q

NSTEMI (managed with PCI) antiplatelet choice:

a) if taking an oral anticoagulant
b) if the patient is not taking an oral anticoagulant

A

a) clopidogrel
b) prasugrel or ticagrelor

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30
Q

What 2 things should be measured when starting an ACEi?

A

1) serum creatinine
2) potassium levels

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31
Q

What rise in creatinine and potassium is acceptable after starting an ACEi?

A

1) increase in serum creatinine up to 30% from baseline

2) increase in K+ up to 5.5 mmol/L

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32
Q

If a patient is having persistent myocardial ischaemia following thrombolysis (fibrinolysis), what should you do?

A

Transfer patient for PCI

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33
Q

In a suspected PE, if the CTPA is negative what is the next investigation?

A

Consider proximal leg US if DVT is suspected

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34
Q

Bradycardia can be a complication of an MI.

Which type of MI (i.e. which aspect of the heart) is most likely to cause bradycardia? Why?

A

Inferior MI (affect RCA) - can cause ischaemia of AV node causing AV block

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35
Q

If a patient presents with sudden HF: bibasal crackles, raised JVP, pulsus paradoxus, muffled heart sounds etc, what complication of MI is most likely?

A

LV free wall rupture

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36
Q

What investigations should be done in all new cases of hyperkalaemia?

A

ECG

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37
Q

At what K+ level should treatment be immediately offered?

A

> /= 6.5 mmol/L

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38
Q

What electrolyte abnormalities can cause a long QT interval?

A

Hypokalaemia
Hypomagnesaemia
Hypocalcaemia

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39
Q

An ECG shows progressive prolongation of the PR interval until a dropped beat occurs.

What heart block is this?

A

Second degree heart block (Mobitz I)

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40
Q

Describe the murmur in mitral stenosis

A

mid-late diastolic murmur, ‘rumbling’ in character

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41
Q

Most likely infective organism in infective endocarditis in patients with no medical history?

A

S. aureus

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42
Q

Mechanism of thiazide diuretics?

A

inhibits sodium reabsorption by blocking the Na+-Cl− symporter at the beginning of the distal convoluted tubule

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43
Q

New LBBB is always pathological. Causes of LBBB?

A

1) Myocardial infarction (especially if new LBBB)

2) HTN

3) Aortic stenosis

4) Cardiomyopathy

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44
Q

Causes of RBBB?

A

normal variant - more common with increasing age

right ventricular hypertrophy

chronically increased right ventricular pressure - e.g. cor pulmonale

pulmonary embolism

myocardial infarction

atrial septal defect (ostium secundum)

cardiomyopathy or myocarditis

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45
Q

How can amiodarone affect QT interval?

A

Can lengthen it

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46
Q

Kidneys in HIV-associated nephropathy vs CKD?

A

HIV-associated: bilateral large or normal sized kidneys on US

CKD: bilateral small kidneys

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47
Q

Give 4 causes of enlarged kidneys on US

A

1) autosomal dominant polycystic kidney disease

2) Chronic HIV-associated nephropathy

3) amyloidosis

4) diabetic nephropathy

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48
Q

What is a normal cardiac variant in atheletes?

A

1) 1st degree heart block

2) 2nd degree heart block mobitz type 1 (Wenckebach phenomenon)

3) sinus bradycardia

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49
Q

All patients with suspect ACS should be given aspirin 300mg, but further drug management depends on the type of ACS and proposed intervention.

What else should be given if the patient is to receive PCI?

A

Dual antiplatelet therapy:
1) Aspirin and prasugrel (if the patient does not take an oral anticoagulant)

2) Spirin and clopidogren (if they do take an oral anticoagulant)

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50
Q

All patients with suspect ACS should be given aspirin 300mg, but further drug management depends on the type of ACS and proposed intervention.

What else is offered to patients with unstable angina or an NSTEMI who do not have a high bleeding risk?

A

Fondaparinux

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51
Q

In an obese patient with a generalised headache, blurred vision, papilloedema and nausea/vomiting, what is msot likely?

A

idiopathic intracranial hypertension

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52
Q

What triad is seen in Boerhaave syndrome?

A

1) vomiting
2) thoracic pain
3) SC emphysema

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53
Q

What are the anterior ECG leads?

A

V1-V4

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54
Q

What are the inferior ECG leads?

A

II, III, aVF

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55
Q

What is a dangerous complication of fluid resuscitation in patients with diabetic ketoacidosis?

A

Cerebral oedema

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56
Q

Symptoms of cerebral oedema?

A

1) deteriorating mental status/ level of consciousness

2) incontinence

3) abnormal neurogenic respiratory pattern (e.g. grunting, abnormal tachypnoea, apnoea)

4) vomiting

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57
Q

Pain in pericarditis vs myocarditis?

A

Pericarditis - burning, pleuritic, relieved by sitting forward

Myocarditis - stabbing, not relieved by sitting forward

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58
Q

Contraindication of nitrates?

A

Hypotension (<90 mmHg)

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59
Q

Adverse effects of PPIs?

A

1) hyponatraemia, hypomagnasaemia

2) osteoporosis –> increased risk of fractures

3) microscopic colitis

4) increased risk of C. difficile infections

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60
Q

A LV aneurysm can develop post-MI. What signs may be seen?

A

1) Persistent ST elevation
2) LV failure e.g. SOB, bibasal crackles, raised JVP, peripheral oedema

This is due to the ischaemic damage sustained weakening the myocardium resulting in aneurysm formation.

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61
Q

Once a STEMI has been confirmed the first step is to immediately assess eligibility for coronary reperfusion therapy.

There are two types of coronary reperfusion therapy. What are they?

A

1) PCI (percutaneous coronary intervention)

2) fibrinolysis

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62
Q

When can PCI be offered in a STEMI?

A

Should be offered if the presentation is within 12 hours of the onset of symptoms AND PCI can be delivered within 120 minutes of the time when fibrinolysis could have been given

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63
Q

When should fibrinolysis be offered in a STEMI?

A

should be offered within 12 hours of the onset of symptoms if primary PCI cannot be delivered within 120 minutes of the time when fibrinolysis could have been given

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64
Q

If patients having a STEMI are indicated to have PCI, what must they have before?

A

Dual antiplatelet therapy (i.e. aspirin + 1 more)

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65
Q

In dual antiplatelet therapy before PCI, what should the 2nd antipplatelet be in patients not taking an oral anticoagulant?

A

Prasugrel

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66
Q

In dual antiplatelet therapy before PCI, what should the 2nd antiplatelet be in patients who are taking an oral anticoagulant?

A

clopidogrel

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67
Q

Patients with a STEMI undergoing fibrinolysis must be given what prior?

A

Antithrombin drug e.g. fondaparinux

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68
Q

Patients with a STEMI undergoing fibrinolysis, how can the success be monitored?

What are the next steps?

A

An ECG should be repeated after 60-90 minutes to see if the ECG changes have resolved.

If patients have persistent myocardial ischaemia following fibrinolysis then PCI should be considered.

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69
Q

1st line management of NSTEMI/unstable angina?

A

Aspirin 300mg + fondaparinux (if no bleeding risk) if no immediate PCI planned

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70
Q

After initial management with aspirin and fondaparinux in NSTEMI/unstable angina, what is next done?

A

Use GRACE score to establish 6 month mortality

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71
Q

If a patient having an NSTEMI/unstable angina has a Grace score of </= 3% (i.e. low), what is next step?

A

Conservative management –> give ticagrelor

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72
Q

If a patient having an NSTEMI/unstable angina has a Grace score of > 3% (i.e. high), what is next step?

A

Consider PCI:
a) immediately if clinically unstable
b) within 72 hours if stable

73
Q

Give some differentials for chest pain

A

1) MI
2) Pneumothorax
3) Pericarditis
4) Myocarditis
5) PE
6) Dissecting aortic aneurysm
7) GORD
8) Pleural effusion
9) MSK pain
10) Pneumonia
11) Shingles
12) Boerhaaves syndrome
13) Perforated peptic ulcer

74
Q

Describe pain in dissecting aortic aneurysm

A

‘Tearing’ chest pain radiating through to the back

75
Q

Potential exam finding in dissecting aortic aneurysm?

A

Unequal upper limb blood pressure

76
Q

Why should metformin be stopped in patients having an MI?

A

Due to risk of lactic acidosis

77
Q

When are antihypertensives offered?

A

a) age <80 y/o
AND
b) ambulatory BP of >/= 135/85 mmHg
AND
c) one or more of; target organ damage, established CVS disease, renal disease, diabetes and/or QRISK 10% or more

78
Q

AV block can occur following an MI affecting which part of hear?

A

Inferior

79
Q

Features of hypernatraemic dehydration?

A
  • jittery movements
  • increased muscle tone
  • hyperreflexia
  • confulsions
  • drowsiness or coma
80
Q

In patient with HTN who is already taking ACEi and has a history of gout, what is next step?

A

Add CCB e.g. nifedipine (history of gout favours CCB over thiazide like diuretic)

81
Q

Signs and symptoms of malignant HTN?

A

1) bilteral retinal haemorhages
2) papilloedema (must be present before a diagnosis of malignant HTN can be made)
3) increased cranial pressure (headache, N&V)
4) nosebleeds
5) haematuria due to kidney failure

82
Q

If a patient has a BP of >/= 180/120 mmHg and no worrying signs, what is next step?

A

Urgent investigation for end-organ damage

83
Q

If a patient having a STEMI suddently develops worsening SOB and a new pan-systolic murmur, what is most likely cause of SOB?

A

Flash pulmonary oedema 2ary to acute mitral valve regurg.

Features:
1) widespread systolic murmur
2) hypotension
3) pulmonary oedema

This is most likely due to rupture of the papillary muscle during MI.

84
Q

Side effects of adenosine?

A
  • Flushing
  • Chest discomfort
  • SOB
  • Headache
  • Sense of impending doom
85
Q

In a patient with a PE, what is the strongest indication for thrombolysis?

A

Massive PE + hypotension –> thrombolyse

86
Q

How does a posterior MI typically present on an ECG?

A

Tall R waves V1-2

87
Q

What Abx should be avoided in pregnancy?

A

1) tetracyclines e.g. doxycycline
2) aminoglycosides e.g. gentamicin
3) trimethoprim
4) quinolones e.g. ciprofloxacin

88
Q

What drugs should be avoided in pregnancy?

A

1) ACEi
2) ARBs
3) Statins
4) Warfarin
5) Sulfonylureas
6) Retinoids (including topical)
7) Cytotoxic agents
8) Lithium (weigh up)

The majority of antiepileptics including valproate, carbamazepine and phenytoin are known to be potentially harmful.

89
Q

In what trimester are ACEi contraindicated?

A

2nd and 3rd

90
Q

Persistent ST elevation following recent MI with no chest pain and SOB indicates what?

A

left ventricular aneurysm

91
Q

Indapamide vs bendroflumethiazide?

A

Indapamide is a thiazide-like diuretic and bendroflumethiazide is a thiazide.

Only thiazide-like diuretics are recommended in HTN.

92
Q

For a STEMI, in the absence of contraindications, what should patients be given?

A

1) Aspirin

2) P2Y12-receptor antagonist e.g. clopidogrel, ticareglor, prasugrel

3) Unfractionated heparin (alternative is warfarin) –> usually given for patients who’re are going to have a PCI.

93
Q

Threshold for transfusion of RBCs in patients with ACS?

A

Hb level of <80 g/L

94
Q

What is most common cause of acute pericarditis?

A

Viral infection (patient may have had flu-like symptoms)

95
Q

ECG findings in acute pericarditis?

A

1) Widespread ‘saddle shaped’ ST elevation
2) PR depression

96
Q

Is risk of falls sufficient reasoning to withold anticoagulation in AF?

A

No

97
Q

In AF, there is a subgroup of patients for whom a rhythm control strategy should be tried first (before rate control).

What are these exceptions?

A

1) Coexistent HF
2) First onset AF
3) Where there is an obvious reversible cause.

98
Q

When can new onset AF be considered for electrical cardioversion?

A

If within 48 hours of presentation

99
Q

In cases of ischaemic stroke and atrial fibrillation, what is pharmacological management?

A

2 weeks of aspirin 300mg OD before consideration of lifelong anticoagulation.

100
Q

Common contraindication of beta blockers in AF?

A

Asthma

101
Q

What is the most likely cause of an irregular broad complex tachycardia in a stable patient?

A

Atrial fibrillation with bundle branch block

102
Q

If a patient has been in AF for more than 48 hours then anticoagulation should be given for at least 3 weeks prior to cardioversion.

What is an alternative?

A

An alternative strategy is to perform a transoesophageal echo (TOE) to exclude a left atrial appendage (LAA) thrombus

103
Q

If a patient has a new BP >= 180/120 mmHg AND retinal haemorrhage or papilloedema, what is next step?

A

Admit for specialist assessment

104
Q

What score is used to assess the bleeding risk of anticoagulation?

A

ORBIT score

105
Q

1st line investigation in marked tachycardia?

A

ECG

106
Q

Overdose of tricyclic antidepressants is a common presentation to emergency departments.

What 2 are particularly dangerous in overdose?

A

Amitryptiline & dosulepin (dothiepin)

107
Q

Early features of TCA overdose?

A

relate to anticholinergic properties: dry mouth, dilated pupils, agitation, sinus tachycardia, blurred vision.

108
Q

Features of severe TCA overdose?

A
  • arrhythmias
  • seizures
  • metabolic acidosis
  • coma
109
Q

ECG changes seen in TCA overdose?

A
  • sinus tachycardia
  • widening of QRS
  • prolongation of QT interval
110
Q

What is widening of QRS interval associated with?

A

1) QRS > 100ms is associated with an increased risk of seizures

2) QRS > 160ms is associated with ventricular arrhythmias

111
Q

1st line management of TCA overdose?

A

IV bicarbonate (indications include widening of the QRS interval >100 msec or a ventricular arrhythmia)

112
Q

What should be avoided in TCA overdose?

A

1) class Ic antiarrhythmics (e.g. Flecainide)

2) class III drugs (e.g. amiodarone) should also be avoided as they prolong the QT interval

113
Q

Why is amiodarone contraindicated in TCA overdose?

A

As it prolongs QT interval

114
Q

What is the most common heart lesion associated with Duchenne muscular dystrophy?

A

Dilated cardiomyopathy

115
Q

Driving rules surrounding hypoglycaemia?

A

Patient with diabetes who have had two hypoglycaemic episodes requiring help needs to surrender their driving licence

116
Q

Wht is spontaneous intracranial hypotension?

A

a very rare cause of headaches that results from a CSF leak

117
Q

Key features of headache in spontaneous intracranial hypotension?

A

Strong postural relationship with the headache generally much worse when upright. Patients may, therefore, be bed-bound

118
Q

Major risk factor for spontaneous intracranial hypotension?

A

Connective tissue disorders such as Marfan’s syndrome.

119
Q

What is a sudden collapse occurring soon after a rupture of membranes suggestive of?

A

amniotic fluid embolism.

120
Q

What is the Cushing reflex?

A

a physiological nervous system response to increased intracranial pressure (ICP) that results in hypertension and bradycardia

121
Q

Describe HR and BP in increased ICP?

A

1) HTN with wide pulse pressure
2) Bradycardia

122
Q

What is Cushing’s triad in raised ICP?

A

1) HTN with wide pulse pressure

2) Bradycardia

3) Irregular breathing

123
Q

1st line for treating atrioventricular nodal re-entry tachycardia (AVNRT)?

A

Adenosine

124
Q

Adverse effects of adenosine?

A
  • Feeling of doom
  • Chest pain
  • Bronchospasm
  • Transient flushing
125
Q

What is hypertrophic obstructive cardiomyopathy (HOCM)?

A

An autosomal dominant disorder of muscle tissue caused by defects in the genes encoding contractile proteins.

126
Q

What is the most common cause of sudden cardiac death in the young?

A

hypertrophic obstructive cardiomyopathy (HOCM)

127
Q

Pathophysiology of HOCM?

A

1) mutation in the gene encoding β-myosin heavy chain protein or myosin-binding protein C

2) results in predominantly diastolic dysfunction: left ventricle hypertrophy –> decreased compliance –> decreased cardiac output

128
Q

Most common cause of sudden death in HOCM?

A

Ventricular arrhythmias

129
Q

Features of HOCM?

A
  • often asymptomatic
  • exertional dyspnoea
  • angina
  • syncope (typically following exercise)
  • sudden death
  • jerky pulse, large ‘a’ waves, double apex beat
  • systolic murmurs (ejection systolic murmur, pansystolic)
130
Q

If a patient’s AF has been going on for >48 hours, what is most appropriate action?

A

1) control rate with bisoprolol (unless contraindicated)

2) anticoagulate for at least 3 weeks

3) after this period, electrical cardioversion would be safe

131
Q

What is the indication for immediate electrical cardioversion in AF?

A

Acute presentation of atrial fibrillation plus signs of haemodynamic instability (e.g. hypotension, heart failure)

132
Q

What ECG sign is considered pathognomic for cardiac tamponade?

A

Electrical alternans

133
Q

What triad of symptoms is seen in cardiac tamponade?

A

1) hypotension
2) raised JVP
3) muffled heart sounds

134
Q

What post-MI complication is typically associated with persistent ST elevation and left ventricular failure?

A

Left ventricular aneurysm

135
Q

What is Takotsubo cardiomyopathy?

A

A type of non-ischaemic cardiomyopathy associated with a transient, apical ballooning of the myocardium.

It may be triggered by stress.

136
Q

Features of Takotsubo cardiomyopathy?

A
  • chest pain
  • features of heart failure
  • ECG: ST-elevation
  • normal coronary angiogram
137
Q

Management of Takotsubo cardiomyopathy?

A

Supportive

138
Q

What is idiopathic intracranial hypertension?

A

a condition classically seen in young, overweight females.

139
Q

Risk factors for idiopathic intracranial hypertension?

A
  • obesity
  • female sex
  • pregnancy
  • drugs: COCP, steroids, tetracyclines, retinoids (isotretinoin, tretinoin) / vitamin A), lithium
140
Q

Features of idiopathic intracranial hypertension?

A
  • headache
  • blurred vision
  • papilloedema (usually present)
  • enlarged blind spot
  • sixth nerve palsy may be present (bilateral)
141
Q

Do patients who’ve had a catheter ablation for atrial fibrillation still require long-term anticoagulation?

A

Yes - as per their CHA2DS2-VASc score

142
Q

Which CCB is used in rate control AF (e.g. if beta blocker is contraindicated)?

A

Verapamil

N.B. Amlodipine is not a rate-limiting calcium channel blocker, and therefore unsuitable for AF

143
Q

Why must patients with AF either be a) anticoagulated for 3 weeks, or b) have had symptoms for < 48 hours before cardioversion?

A

To reduce risk of stroke

144
Q

How often should BP be checked in patients with clinic BP <140/90 mmHg?

A

Every 5 years (more often if closer to 140/90)

145
Q

Management of patient with clinic BP of 140/90 to 179/119 mmHg?

A

1) Offer ABPM (or HBPM if ABPM declined or not tolerated).

2) Investigate for target organ damage: U&Es, urine dip (haematuria), urinary ACR, fundoscopy, ECG

3) Assess QRISK

146
Q

What to discuss when initiating ACEi in HTN:

A

1) Side effects: cough (can come on years down line)

2) Safety net: angioedema

3) 1st dose: can cause postural hypotension so take sitting down

4) U&Es required 2 weeks after starting

5) Monitor BP 4 weeks after starting

6) Explain may need to be titrated up to achieve desired target

147
Q

Management of patient with clinic BP of 180/120 or more?

A

1) Assess for target organ damage ASAP.

2) Consider starting drug treatment immediately without ABPM if target organ damage.

3) Repeat clinic BP in 7 days if no target organ damage.

148
Q

what indicates the need for a same day review in patients with a clinic BP of 180/120 mmHg or more?

A

1) retinal haemorrhage or papilloedema (accelerated HTN) or;

2) life-threatening symptoms or;

3) suspected pheochromocytoma

149
Q

Management options for patients with stage 1 HTN (135/85 to 149/94 mmHg)?

A

1) Offer lifestyle advice

2) Age >80 y/o with clinic BP >150/90 mmHg –> consider drug treatment

3) Age <80 y/o with target organ damage, CVD, renal disease, diabetes or QRISK >/= 10%

4) Age <60 y/o with QRISK <10%

5) Age <40 y/o need specialist evaluation of 2ary causes

150
Q

When to consider drug treatment in patients <80 y/o with BP 135/85 to 149/94?

A

a) diabetes

b) CVS disease

c) renal disease

4) QRISK >/= 10%

5) target organ damage

151
Q

Management of patients with stage 2 HTN (>/= 150/95 mmHg)?

A

Lifestyle AND drug treatment

152
Q

What is base target for postural hypotension based on?

A

Standing BP

153
Q

Does furosemide improve outcomes in HF?

A

No - symptomatic management

154
Q

Management of HF with preserved EF?

A

1) Treat symptoms (e.g. loop diuretic)

2) If unsuccessful, refer to specialist

155
Q

Acute management of HF exacerbation?

A

1) IV loop diuretic: furosemide/bumetanide

Possible additional treatments:

2) Oxygen

3) Vasodilators e.g. nitrates

156
Q

When are vasodilators indicated in acute HF management?

A

Should NOT be given routinely.

May be indicated if concomitant myocardial ischaemia, severe HTN or regurgitant aortic or mitral valve disease.

157
Q

What is the major side effect/contraindication of nitrates in acute HF management?

A

Hypotension

158
Q

What is considered as 3rd line therapy for HF management in Afro-Caribbean patients (i.e. not responding to ACE-inhibitor, beta-blocker and aldosterone antagonist therapy)?

A

Hydralazine and nitrate

159
Q

What is a systemic complication of acute pancreatitis?

A

Acute respiratory distress syndrome (high mortality rate - around 20%)

160
Q

Which drug is indicated as 3rd line therapy in management of HF if there is coexistent atrial fibrillation?

A

Digoxin

161
Q

Medical management of angina?

A

1) All patients should be on. aspirin, statins & GTN spray (as long as no contraindications)

2) 1st line: Beta blocker or CCB

3) Increased (2) to max dose tolerated

4) Add beta blocker/CCB (whichever haven’t used)

5) If a patient is on monotherapy and cannot tolerate the addition of a CCB:
- a long-acting nitrate
- ivabradine
- nicorandil
- ranolazine

162
Q

Which CCB should be used in the management of angina?

A

1) if monotherapy: a rate-limiting one such as verapamil or diltiazem should be used

2) if used in combination with a beta-blocker then use a longer-acting dihydropyridine CCB (e.g. amlodipine, modified-release nifedipine)

163
Q

What is rapid drainage of a pneumothorax a risk factor for?

A

Developing re-expansion pulmonary oedema

Risk factors:
- Large pneumothorax
- History of diabetes

164
Q

In patients with HF who have not responded to an ACE-inhibitor, beta-blocker and aldosterone antagonist therapy, what are next options to consider?

A
  • ivabradine
  • sacubitril-valsartan
  • digoxin
  • hydralazine in combination with nitrate
  • cardiac resynchronisation therapy
165
Q

Criteria for ivabradine in 4th line HF?

A

sinus rhythm > 75/min and a left ventricular fraction < 35%

166
Q

How can 1ary and 2ary aldosteronism be differentiated?

A

Look at renin levels:

If renin low: 1ary cause more likely
If renin high: 2ary cause more likely

167
Q

Most common cause of renal artery stenosis?

A

Atherosclerosis

168
Q

Features of renal artery stenosis (secondary to atherosclerosis)?

A
  • HTN
  • CKD
  • ‘Flash pulmonary oedema’
169
Q

How can renal artery stenosis result in 2ary hyperaldosteronism?

A

ACEi can worsen stenosis, resulting in a drop in eGFR, activating RAAS.

170
Q

2nd line therapy in HF?

A

1) aldosterone antagonist

2) SGLT-2 inhibitors e.g. dapagliflozin

171
Q

What is Charcot joint?

A

A Charcot joint is also commonly referred to as a neuropathic joint. It describes a joint which has become badly disrupted and damaged secondary to a loss of sensation.

172
Q

Causes of Charcot joint?

A
  • Diabetic neuropathy
  • Alcoholic neuropathy
  • Syphilis
  • Cerebral palsy
173
Q

Features of Charcot joint?

A
  • Non-tender, swollen, erythematous and hot foot
  • Xray findings: osteolysis and joint dislocation
174
Q

In patients with acute HF and respiratory failure, management option?

A

CPAP

175
Q

Management option of acute HF in patients with hypotension (e.g. <85 mmHg)/cardiogenic shock?

A

This can be a difficult scenario to manage -
some of the treatments typically used for acute heart failure (e.g. loop diuretics and nitrates) may exacerbate the hypotension.

1) Inotropic agents e.g. dobutamine (considered for patients with severe left ventricular dysfunction who have potentially reversible cardiogenic shock)

2) Vasopressor agents e.g. norepinephrine (normally only used if insufficient response to inotropes and evidence of end-organ hypoperfusion)

3) Mechanical circulatory assistance

176
Q

How does liver feel in RHF?

A

Firm, smooth, tender and pulsatile liver edge

177
Q

Causes of hypoglycaemia?

Mneumonic: EXPLAIN

A

E - Exogenous drugs (typically sulfonylureas or insulin)

P - Pituitary insufficiency

L - Liver failure

A - Addison’s disease

I - Islet cell tumours (insulinomas)

N - Non-pancreatic neoplasms

178
Q

What condition can thiazide diuretics (e.g. bendroflumethiazide) exacerbate?

A

Gout: by increasing serum uric acid levels (thiazides reduce renal uric acid excretion)

179
Q
A

Yr 4 - CCC (54 decks)

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