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RACP Written 2018 > Cardiology - Miscellaneous > Flashcards

Cardiology - Miscellaneous Flashcards

1
Q

Effect of diabetes on cardiac?

A
  • higher CAD risk
  • abnormal LV systolic and diastolic dysfunction
  • coronary MICROVASCULAR disease
  • endothelial dysfunction
  • autonomic dysfunction
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2
Q

Thiamine deficiency (Beri Beri) effects of cardiac system?

A

High output failure

Dilated cardiomyopathy

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3
Q

Hyperhomocysteinaemia effects on cardiac system?

A

Premature atherosclerosis

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4
Q

Obesity effects on cardiac system?

A
  • LVH

- Excessive LV filling presure on exertion

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5
Q

HypERthyroidism effect on cardiac system?

A

SVT
HTN
AF (in 15%)
Means-Lerman Scratch: systolic pleuropericardial rub at left 2nd ICS on EXPIRATION

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6
Q

Means-Lerman Scratch

A

= systolic pleuropericardial rub at left 2nd ICS on EXPIRATION

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7
Q

Hypothyroidism effects on cardiac disease

A
  • decreased cardiac output
  • decreased stroke volume
  • decreased HR
  • decreased pulse pressure
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8
Q

Cardiac Tumours:

What is the most common cancer to metastasise to the heart?

A

Metastatic melanoma

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9
Q

Cardiac Tumours:

What is Carney Complex?

A 
Carney Complex: mutation in tumour suppressor PRKAR1A
Autosomal Dominant
Blue naevi
Myxoma
Endocrine overactivity
- Cushing's
- Testicular tumor
- Pituitary adenoma
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10
Q

Cardiac Tumours:

What mutation is seen in Carney Complex?

A

Mutation in tumour suppressor gene PRKAR1A

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11
Q

What clinical features would represent an atrial myxoma?

A
  • AF
  • Mid-diastolic murmur with ‘tumour plop’
  • Embolism
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12
Q

What murmur do you hear with an atrial myoxoma?

A

Mid-diastolic murmur with ‘tumour plop’

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13
Q

If a Carney Complex atrial myxoma what is the problem with surgical resection?

A

Carney complex myxoma often recur.

Normal myxoma recurrence in 5-15% after resection

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14
Q

What is Loeffler’s Endocarditis?

A

Eosinophilic endocardial disease

Associated with restrictive cardiomyopathy

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15
Q

What is Fabry’s Disease and how is it related to the heart?

A

X linked recessive deficiency of alpha-galactosidase A.

Associated with restrictive cardiomyopathy

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16
Q

What is Kaussmaul’s sign?

A

INCREASE in JVP on inspiration

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17
Q

Is carotid sinus hypersensitivity more common in males or females?
Which age group?

A

Males more common
Increased age

Also more commonly right-sided hypersensitivity

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18
Q

On carotid massage when is it diagnostic for carotid sinus hypersensitivity?

A

Reproducible on massage and if:

  • Asystole >3 seconds (indicates cardioinhibitory CSH)
  • Decrease in SBP of >50mmHg independent of HR (indicates vasodepressor CSH)
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19
Q

When would you do a pacemaker in carotid sinus hypersensitivity?

A

If it is cardioinhibitory (ie carotid sinus massage reproduces symptoms and has asystole >3 seconds)

or if mixed carotid sinus hypersensitivity

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20
Q

A patient has syncope/dizziness/falls on turning their head or tight fitted collars….what do you think of?

A

Carotid sinus hypersensitivity

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21
Q

How does DIGOXIN work? (5 ways)

A

1) Cardiac Glycoside: direct VASOCONSTRICTION in smooth muscle (arterial and venous)

2) POSITIVE Inotrope:
Direct inhibition of membrane bound NaK-ATPas –> increases intracellular Ca
- associated increase in slow inward Ca current during action potential

3) SLOWED conduction
4) INCREASED REFRACTORY PERIOD by stimulation of vagal tone
5) PARASYMPATHETIC PROPERTIES: hypersensitises carotid baroreceptor and stimulates central vagal nuclei

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22
Q

Causes of supratherapeutic digoxin level:

A

1) renal impairment
2) MI and acidosis –> suppression of Na/K ATPase
3) Hypothyroidism –> decreased renal excretion
4) Drugs

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23
Q

Drugs that INCREASE digoxin level

A

Verapamil/Diltiazem
Erythromycin
Tetracyclines
Paroxetine

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24
Q

Drugs that DECREASE digoxin level

25
Q

Visual changes in digoxin toxicity

A 
Yellow-green distortion
Xanthopsia (yellow halo around eyes)
Transient scotoma
Decreased acuity
Photophobia
26
Q

GIT complications of digoxin toxicity

A

General (anorexia / n+v / diarrhoea)

Mesenteric ischaemia after rapid IV infusion

27
Q

Cardiac complications of digoxin toxicity

A

palpitations
syncope
peripheral oedema
bradycardia + hypotension

28
Q

Neuro complications of digoxin toxicity

A 
drowsiness/fatigue/confusion
neuralgia and headache
paraesthesia and neuropathic pain
hallucinations
seizures
29
Q

ECG findings of digoxin toxicity

A 
AV block
Sinus bradycardia
Torsades
ST reverse tick
Short QT
Flattened/inverted T waves
30
Q

Dialysis of digoxin?

A

DON’T DIALYSE DIGOXIN TOXICITY!!! (minimal clearance)

31
Q

Treatment of digoxin toxicity?

A

Acute: charcoal within 6-8 hours

Treat K abnormality BUT DON’T USE CALCIUM (delays depolarisation and precipitates VT)

Treat hypoMg

Digibind

(if unavailable then use phenytoin or lidocaine –> dissociates inotrope and dysrhythmic action of digoxin)

Arrythmias: DON’T USE CCBs!!!! (as these increase digoxin levels)

32
Q

Classic ECG findings of hypokalaemia

A 
U waves
Small or absent T waves
Prolonged PR
ST depression
Long QT

** “in hypokalaemia U have no Pot and no T, but a long PR and a long QT” ***

33
Q

Classic ECG findings of hypothermia:

A 
Bradycardia
J waves
1st degree HB
Long QT
Atrial and ventricular arrythmias
34
Q

JVP Physiology:

what are ‘a’ waves and what abnormalities might you see?

A

‘a’ waves = atrial contraction
(first bump on the JVP)

LARGE: due to atrial pressure (ie tricuspid or pulmonary stenosis, or pulmonary HTN)

ABSENT: AF

CANNON: due to atrial contractions against CLOSED tricuspid in:

  • complete HB
  • ventricular tachycardias/ectopics
  • single chamber pacing
35
Q

JVP Physiology:

When might you see ‘cannon’ a waves and why do they occur?

A

CANNON: due to atrial contractions against CLOSED tricuspid in:

  • complete HB
  • ventricular tachycardias/ectopics
  • single chamber pacing
36
Q

JVP Physiology:

What is the ‘c’ wave?

A

= closure of tricuspid valve
NOT usually seen

(2nd little bump after the ‘a’ wave on the JVP)

37
Q

JVP Physiology:

What is the ‘v’ wave?

A

= passive filling of blood into atrium against closed tricuspid valve
(3rd bump)

GIANT: tricuspid regurg / RHF

38
Q

JVP Physiology:

What is the ‘x’ descent?

A

= fall in atrial pressure during ventricular systole

2nd ‘trough’

39
Q

JVP Physiology:

What is the ‘y’ descent?

A

= opening of tricuspid valve

final downward bit of the JVP

40
Q

JVP Physiology:

What part of the JVP represents atrial contraction?

A

‘a’ wave

41
Q

JVP Physiology:

What part of the JVP represents closure of the tricuspid valve?

A

‘c’ wave (not usually seen)

42
Q

JVP Physiology:

What part of the JVP represents passive filling of blood into the atrium against a closed tricuspid valve?

A

‘v’ wave

43
Q

JVP Physiology:

What part of the JVP represents fall in atrial pressure during ventricular systole?

A

‘x’ descent

44
Q

JVP Physiology:

What part of the JVP represents opening of the tricuspid valve?

A

‘y’ descent

45
Q

Who does fibromuscular dysplasia tend to affect?

A

Women in childbearing years

46
Q

Which arteries does fibromuscular dysplasia affect?

A

Medium sized arteries

47
Q

How does fibromuscular dysplasia present?

A

Usually asymptomatic

RENAL: involved in 60 - 70%
–> renovascular hypertension

CNS: in 25-30%

  • -> stroke
  • -> sudden onset exposive headache and neck stiffness suggests FMD-associated aneurysm
  • -> predisposing factor in 15% of spontaneous carotid cervical dissections

VISCERAL: abdo pains or ischaemic bowel

LIMBS: intermittent claudication

48
Q

How do you diagnose fibromuscular dysplasia?

49
Q

Management of fibromuscular dysplasia?

A

Nil treatment if asymptomatic
Antiplatelets
Surgery if RENAL FMD

50
Q

When is the onset of radiation cardiotoxicity?

A

5-20 years

51
Q

With which cancer is pericardial effusion associated with radiation cardiotoxicity?

A

Oesophageal cancer

52
Q

Which valves are associated with valvular disease relating to radiation cardiotoxicity?

A

Left sided valves more affected.

Increased risk if also using anthracycline

53
Q

With what chemotherapy agent is short term chemo cardiotoxicity associated?

A

5-Fluorouaracil is associated with high incidence of chest pain and ECG changes (death in 2-8%)

Usually resolve within 7 days

54
Q

With which chemo agents are associated with long term chemo cardiotoxicity?

A

Anthracyclines
Trastuzumab
Kinase inhibitors

55
Q

Important facts about trastuzumab-induced chemo cardiotoxicity?

A
  • increased risk of >50 YEARS OLD or if PREVIOUS ANTHRACYCLINES
  • REVERSIBLE
  • NOT dose related (so can rechallenge later)
56
Q

When and what is affected in anthracycline-induced chemo cardiotoxicity?

A
  • symptoms usually occur within a few months, but can occur up to 20 years later
  • subclinical decline in systolic and diastolic dysfunction
57
Q

What are the risk factors for anthracycline-induced chemo cardiotoxicity?

A
  • Cumulative dose (STRONGEST RF)
  • -> Incidence <1% if cumulative <400)
  • age at treatment
  • concomitant therapy with other cardiac toxics
  • chest radiation
  • pre-existing cardiac disease
58
Q

How can you modify the response to anthracyclines in anthracycline-induced chemo cardiotoxicity?

A
  • liposome encapsulation
  • infusion rather than bolus
  • structural analogues (epirubicin / mitoxantrone)
  • adjunctive cardioprotective agents (ie: dexrazoxone = EDTA chelator which reduces risk)

RACP Written 2018 (167 decks)

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