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Medical terms > Cardiology block > Flashcards

Cardiology block Flashcards

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USMLE® Step 1 flashcards
1
Q

What type of drug is propranolol?

A

beta blocker

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2
Q

What leads show ST elevation in an anterior STEMI?

A

V3 and V4

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3
Q

Which leads show ST elevation in an inferior STEMI?

A

aVF, II, III

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4
Q

What is a common side effect of taking statins?

A

Myalgia- muscle pain

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5
Q

What are rare side effects of taking statins?

A

Angio-odema (rapid swelling under the skin) and rhabdomyolysis (break down of damaged skeletal muscle releasing myoglobin into the bloodstream)

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6
Q

What does afebrile mean?

A

not feverish

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7
Q

What is cardiac output? (definition and maths)

A

The amount of blood the heart pumps out in one minute i.e. Heart rate x stroke volume

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8
Q

How do you calculate ejection fraction?

A

(Stroke volume/ End diastolic volume) x 100

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9
Q

What does ejection fraction tell you about heart failure?

A

40% or below ejection fraction indicates systolic heart failure

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10
Q

Does diastolic heart failure affect the ejection fraction?

A

No because both stroke volume and total volume have decreased

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11
Q

What is preload?

A

Vol of blood in ventricle before it contracts a.k.a end diastolic volume

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12
Q

What is afterload?

A

The pressure the heart has to work against to eject blood during systole

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13
Q

What does the frank starling mechanism show?

A

Increasing ventricular filling during diastole increases stroke volume during systole (heart stretches more in diastole so it contracts with greater pressure in systole)

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14
Q

What type of drug are losartan and valsartan?

A

ARBs (angiotensin receptor blockers). All drugs ending in ‘-sartan’ are ARBs.

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15
Q

Common side effect of ACE inhibitors?

A

dry cough

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16
Q

In which chamber of the heart is the fossa ovalis located?

A

right atrium

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17
Q

What is an aneurysm?

A

Bulge in blood vessel bc of weakened blood vessel wall (can cause haemorrhage)

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18
Q

What is central venous pressure?

A

Blood pressure within the vena cavae. Increased central venous pressure = increased venous return

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19
Q

What 4 factors affect stroke volume?

A

cardiac contractility, cardiac size, preload and afterload

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20
Q

What’s contralateral hemiparesis?

A

Weakness on the opposite side of injury

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21
Q

What do you use CHA2DS2-VASc score for?

A

To the risk of stroke and/or systemic emboli in people with atrial fibrillation

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22
Q

What is the mitral valve between? And what’s another name for it?

A

The left atrium and the left ventricle.

Bicuspid valve

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23
Q

What is the aortic valve between?

A

The left ventricle and the aorta

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24
Q

What’s the pulmonary valve between?

A

The right ventricle and the pulmonary trunk

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25
Q

What is Virchow’s triad?

A

The three factors needed for venous thrombosis:
-hypercoagulability
-stasis
-vessel wall injury
one or more of these factors being present will put you at risk of VTE (PE or DVT)

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26
Q

What is the different between infarction and ischemia?

A

Infarction is tissue death whilst ischemia is reduced oxygen supply to tissues (this is due to reduced blood supply).
So ischemia can lead to infarction.

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27
Q

long term; what condition does infective endocarditis increase the risk of?

A

Stroke- infective endocarditis increases the risk of emboli

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28
Q

What are the layers of the walls of the heart (superficial to deep)?

A
  • pericardium (envelopes the heart and has two layers- parietal and visceral/epicardium)
  • myocardium
  • endocardium
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29
Q

What type of drug is amlodipine?

A

CCB (calcium channel blocker)

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30
Q

What is thrombocytopenia?

A

Abnormally low platelet levels

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31
Q

What is a pulmonary embolism?

A

blockage of a pulmonary artery in your lungs due to blood clot

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32
Q

What’s QRISK score used for?

A

calculating a person’s risk of developing a heart attack or stroke in the next ten years

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33
Q

What is endothelin?

A

A vasoconstrictor and bronchoconstrictor

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34
Q

What is the role of atrial and ventricular natriuretic peptides?

A

They decrease systemic vascular resistance and increase the excretion of sodium

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35
Q

How do thiazide diuretics work?

A

They inhibit sodium and chloride reabsorption in the distal convoluted tubules

36
Q

What are the side effects of thiazide diuretics?

A

hypokalaemia and hyponatraemia

37
Q

What is the mechanism of action of statins?

A

They decrease LDLs in the blood by working as HMG- CoA reductase inhibitors in the liver

38
Q

Which one is water soluble, conjugated or unconjugated bilrubin?

A

conjugated bilirubin

39
Q

How is bilirubin formed? And how does it become conjugated?

A

Bilirubin is produced from the break down of haem within red blood cells by macrophages. It binds to albumin (a protein found in the blood) and is transported to the liver where it combines with glucuronic acid to form conjugated bilirubin.

40
Q

What type of drug is doxazosin?

A

alpha blocker

41
Q

What is Raynaud’s disease?

A

When your fingers and toes change colour due to reduced blood flow to those areas when you’re cold or anxious.

42
Q

Does angiotensin 2 increase or decrease blood pressure?

A

Increase

43
Q

Does aldosterone increase or decrease blood pressure?

A

Increase

44
Q

How does the renin-angiotensin-aldosterone system work? Include where each hormone is produced.

A

1) Liver produces angiotensinogen
2) In response to step 1, the kidneys produce renin
3) Renin converts angiotensinogen into angiotensin 1
4) ACE in the lungs converts angiotensin 1 to angiotensin 2
5) Angiotensin 2 increases blood pressure by increasing:
- sympathetic nervous system activity
- vasoconstriction (increases SVR)
- aldosterone production
6) Aldosterone is produced by the adrenal cortex (of the adrenal glands) and acts on the kidneys so more water and sodium goes into the blood stream -> increases blood volume -> increases blood pressure

45
Q

What is mean arterial pressure (MAP)? What factors affect it? How is it calculated?

A

average pressure in a patient’s arteries in one cardiac cycle.
affected by:
-cardiac output
-systemic vascular resistance (SVR)
-central venous pressure (CVP)
Note: CVP is almost 0 so MAP is calculated as;
MAP = CO (HR X SV) X SVR

46
Q

What is blood pressure?

A

force exerted by blood against the walls of blood vessels

47
Q

How do noradrenaline and adrenaline affect blood pressure?

A

Both increase it by;

1) binding to alpha 1 receptors on the smooth muscle surrounding blood vessels -> smooth muscle contracts -> lumen narrows (vasoconstriction) => BP increases
2) a) binding to beta 1 receptors on pacemaker cells in the heart -> increases heart rate => increases blood pressure
b) binding to beta 1 receptors on cardiac myocytes -> increases force of cardiac contraction -> increases CO -> increases bp
3) binding to beta 2 receptors outside of the heart e.g. on vascular smooth muscle => bronchoconstriction and peripheral vasoconstriction

48
Q

What do alpha 1 receptor blockers do?

A
  • lower blood pressure by blocking noradrenaline/adrenaline binding to alpha 1 receptors on smooth muscle surrounding blood vessels
  • decrease total cholesterol in the body
49
Q

What is the difference between cardiac selective and non-selective beta blockers?

A

Non-selective beta blockers act on beta 1 and beta 2 receptors whilst selective beta blockers only act on beta 1 receptors (beta 1 receptors are more prevalent in the heart than beta 2 receptors)

50
Q

What type of receptors are alpha and beta receptors?

A

Adrenergic- they are activated by adrenaline/noradrenaline

51
Q

Are binding sites present on actin or myosin? What is usually present on these binding sites and how does that change when calcium binds to troponin?

A

Binding sites are found on actin. When myosin is not bound to actin, a troponin is on the binding sites and is attached to tropomyosin. When calcium binds to troponin C, troponin moves tropomyosin away from actin binding sites so myosin can bind to actin.

52
Q

What are the three types of diuretic and which one is strongest?

A

-Loop
-thiazide
-potassium sparing
Loop diuretics are the strongest

53
Q

How do loop diuretics act work?

A

They inhibit the Na-K-2Cl transporter in the ascending limb of the loop of Henlé

54
Q

How do thiazide diuretics work?

A

They inhibit the Na-Cl transporter in the distal convoluted tubule

55
Q

How do potassium sparing diuretics work? (What are the two types and where do they work?)

A

They can inhibit epithelial Sodium channels (ENaC) e.g.amiloride or be aldosterone receptor antagonists in the distal convoluted tubule/collecting duct e.g. spironolactone

56
Q

What cardiovascular drugs are associated with sexual dysfunction?

A

Thiazide diuretics

57
Q

What effect does NSAIDs have on ACE inhibitors?

A

Reduces anti-hypertensive effect

58
Q

Who doesn’t get ACE inhibitors as first line for hypertension? What do they get instead?

A

Over 55s and african/carribean people get CCBs as first line for hypertension and ARBs are used in people who don’t tolerate ACE inhibitors well.

59
Q

What effect does antacids have on ACE inhibitors?

A

reduces ACE inhibitor absorption

60
Q

What are the last 3 steps in the clotting cascade for both intrinsic and extrinsic clotting cascade?

A
  • > Factor X is activated (Xa)
  • > prothrombin is converted to thrombin
  • > fibrinogen is converted to fibrin
61
Q

What clotting factors are in the intrinsic clotting cascade and which ones are in the extrinsic clotting cascade?

A

intrinsic clotting cascade: factor i, ii, ix, x, xi, xii

extrinsic clotting cascade: factor i, ii, vii, x

62
Q

How do direct oral anticoagulants such as Rivaroxiban work?

A

They are factor Xa inhibitors and factor Xa is used to activate thrombin.

63
Q

What are the main side effects of anticoagulants?

A

bleeding (heparin can also cause thrombocytopenia)

64
Q

What type of drug is fondaparinux?

A

Direct oral anticoagulant- factor Xa inhibitor

65
Q

Which clotting factors does warfarin act on?

A

The vitamin K dependent ones i.e.

1972- factors X, iX, Vii, ii (prothrombin)

66
Q

What’s the mechanism of action for nitrates?

A

They decrease intracellular calcium => smooth muscle relaxation

67
Q

What’s the mechanism of action for nitric oxide?

A

Nitric oxide :
1) activates guanylyl cyclase to form cGMP -> cGMP inhibits calcium entry into the cell -> smooth muscle relaxation
2) activates K+ channels
3) Activates phosphatase
All of these lead to smooth muscle relaxation

68
Q

What is the mechanism of action of statins?

A

They decrease LDLs in the blood by inhibiting HMG-CoA reductase in the liver

69
Q

What’s the mechanism of hydralazine?

A

It increases cGMP levels -> this inhibits calcium entry into the cell => smooth muscle relaxation

70
Q

Which type of anti-hypertensive drug exacerbates symptoms of peripheral vascular disease?

A

Beta blockers

71
Q

What type of drug is diypridamole?

A

It is a non-phosphodiesterase inhibitor and decreases uptake of adenosine into cells

72
Q

Where do you auscultate to hear each valve sound?

A
  • > right second intercostal space- aortic valve
  • > left second intercostal space- pulmonary valve
  • > left fourth intercostal space- tricuspid valve
  • > left fifth intercostal space in the mid clavicular line- mitral/bicuspid valve
73
Q

What does the first heart sound represent? i.e. what valves are closing and when does this happen?

A

S1- when the atrioventricular valves close
This happens at the beginning of systole when ventricular pressure exceeds atrial pressure to prevent backflow of blood into the atria

74
Q

What does the second heart sound represent? i.e. what valves are closing and when does this happen?

A

S2- when the semi lunar valves close because pressure in the aorta and pulmonary artery is greater than pressure in the ventricles. This happens at the beginning of diastole/the end of systole.

75
Q

What do the S3 and S4 heart sounds indicate?

A

S3 is a subtle heart sound heard after S2. In younger patients it generally indicates rapid ventricular filling and is coming from the chordae tendinae but in older patients it can indicate heart failure and ventricular stiffness/weakness.
S4 is after S3 and is always abnormal. it indicates turbulent blood flow from the atria to the ventricles due to stiff or hypertrophic ventricles. This happens during ventricular filling and coincides with the P wave on an ECG.

76
Q

Where do the heart sounds radiate to in aortic stenosis and mitral regurgitation?

A
  • aortic stenosis radiates to the carotids

- mitral regurgitation radiates to the axilla

77
Q

Young fit person esp. young athletes with sudden cardiac death, what is the most likely cause?

A

HOCM- hypertrophic obstructive cardiomyopathy

78
Q

What is ischemic heart disease? And what is the main cause?

A

Reduction of blood flow to the myocardium (a.k.a coronary heart disease). Main cause is atherosclerosis.

79
Q

Which coronary artery supplies which area of the heart?

A
  • The left coronary artery supplies the left atrium
  • The right coronary artery supplies the SA node, AV node and the right ventricle
  • The left marginal artery and the left anterior descending artery supplies the left ventricle
80
Q

What valvular disease can present with pulsatile hepatomegaly?

A

Tricuspid regurgitation

81
Q

What are the two main risk factors in CHAD VASC score?

A

CHA2D VAS2C
age over 75 years
stroke or TIA previously

82
Q

What is the most common causative organism for infective endocarditis in patients with a prosthetic valve?

A

staph epidermis

83
Q

What type of antibiotics can lead to torsades de pointes?

A

macrolides e.g. Clarithromycin

84
Q

What’s a general rule for bundle branch blocks?

A

They all cause wide QRS complex

85
Q

What do natriuretic peptides do?

A

The decrease atrial blood pressure by decreasing blood volume and systemic vascular resistance

Medical terms (6 decks)

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