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Pharmacology > Cardiovascular therapeutics > Flashcards

Cardiovascular therapeutics Flashcards

1
Q

Describe the action of beta-blockers and name their uses

A

They are the first choice for prevention of angina and treat CHF/AF/MI/hypertension

They block beta-adrenoceptors ;

Negative inotropic and chronotropic effects - weaken the heart’s contractions and slow the heart rate

Coronary blood flow only occurs during diastole ;

beta-blockers slow down the heart , increasing the diastolic period so more time for coronary blood flow

Also anti-arrhythmic effects

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2
Q

Calcium channel blockers When are they used What is they mode of action

A

treat hypertensions/angina ; All cause vasodilatation and improve coronary blood flow

Some are rate limiting agents - decreases force of hearts contraction and slows down HR

Verapamil also is anti-arrhythmic; most end in -dipine

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3
Q

K+ channel activators

A

Targets ATP-sensitive K+-channel (KATP)

they promote potassium efflux, hyperpolarize the cell membrane, thus preventing influx of calcium through the voltage-dependent calcium channels = vasodilation via relaxation of smooth muscle

treats hypertension and angina

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4
Q

Statins

Describe their use and mode of action

A

Inhibit cholesterol synthesis in liver

this leads to increased LDL uptake

reduces cardiovascular risk and reduces high cholesterol

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5
Q

Statin interactions

A

Macrolides (type of antibiotic e.g erythromycin and clarithromycin)

grapefruit juice

calcium channel blockers

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6
Q

Beta blockers + rate limiting Ca2+ blocker =

A

Fatal (dihydropyradine is the only exception)

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7
Q

ACEIs should be given to treat …

A

Hypertension

type 2 diabetes and diabetic nephropathy

non-black patients with <55years of age that pose a significant cardiovascular risk or secondary prevention post MI CHF

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8
Q

CCI(calcium channel inhibitors) are used to treat…

A

Patients that are >55years or black with significant cardiovascular risk

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9
Q

diagnosis of angina

A

History

ECG - ST segment depression

angiography of coronary arteries (x-ray of blood vessels)

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10
Q

Treatment of angina

A

Coronary artery bypass grafting

angioplasty + stenting

nitrates to cause veno/coronarydilation ; glyceryl trinitrate, or GTN. It comes as a mouth spray or tablets that dissolve under your tongue. beta-blockers and CCI are used to prevent angina

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11
Q

What is a CABG (coronary artery bypass graft)?

A

involves taking a blood vessel from another part of the body (usually the chest, leg or arm) and attaching it to the coronary artery above and below the narrowed area or blockage.

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12
Q

Describe how angioplasty and stenting work

A

Catheter with balloon and stent on the end inserted into the coronary arteries via a vessel in the arm

ballon is inflated to insert the stent then removed leaving the stent behind

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13
Q

Treatment given post MI

A

Beta-blocker

ACEI

statin

antiplatelet drugs

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14
Q

what is cardiomegaly?

A

enlarged heart

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15
Q

how is cardiomegaly detected on a chest X-ray?

A

cardiothoracic ratio (CTR) >0.5 ; ratio of max heart diameter to max thoracic diameter

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16
Q

histological consequences of hypertensive arteriosclerosis

A

Hypertrophy of media (middle layer)
Firboelastic thickening of intima
Elastic lamina reduplication
Reduction in size of lumen

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17
Q

Consequences of hypertensive vascular changes

A

Reduction in lumen = reduced flow - ischaemia
Increased rigidity of vessel wall = loss of elasticity and contractikuyt - unresponsive to vasodilators/constrictors

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18
Q

Atheroma occur in

A

High pressure systems (large and medium arteries)

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19
Q

What is an ulcer ?

A

A local loss of epithelium and sometimes deeper tissue in skin or mucous membrane

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20
Q

Describe the possible complications of atheroma symptoms:

A

Expansion of intima = reduction of lumen size = ischaemia

Ulceration of atheromatous intima = predisposition ot thrombus formation = vessel occlusion

Plaque fissure formation and haemorrhage

Replacement of muscle and elastic fibres in media = loss of elasticity = thinning and stretching = aneurysm

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21
Q

Ischaemia of coronary arteries causes

A

Angina (chest pain)

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22
Q

Ischaemia in the leg arteries can cause

A

Intermittent claudication (leg pain)

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23
Q

Ischaemia in the mesenteric arteries results in

A

Ischaemic colitis (inflammation of large intestine

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24
Q

Describe the formation of aneurysm

A

Aneuryms = abnormal permant focal dilation of an artery

Enlarging intimate atheroma plaque leads to atrophy of media

Muscle and elastic fibres in media replaced by collagen

Collagen strong but neither contractile nor capable of elastic recoil = with each heart beat the wal stretches and thins

Most common in abdominal aortas

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25
Q

What are the 3 common aneurysm*

A 
Atheromatous aortic aneurysm (most likely to occur in abdominal area)
Aortic dissection (when there is a tear in the innermost layer wall of the aorta) 
Cerebral berry
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26
Q

Common treatments for chronic heart failure

A

ACEIs
Diuretics
Beta blockers or CCIs
Digoxin

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27
Q

Treatment for hypertension

A

ACEIs
Ca2+ channel inhibitors (used instead of beta-blockers for asthmatics )

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28
Q

How is stable angina represented on an ECG

A

ST-segment depression

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29
Q

Management of stable angina

A

Lifestyle changes
Coronary artery bypass grafting
Balloon angioplasty and stenting

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30
Q

Describe percutaneous transluminal coronary angioplasty (PTCA)

A

Balloon inflated at site of plaque and inserts stent
Drug in stent prevent regrowth of blood vessel

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31
Q

Pharmacological management of stable angina

A

Nitrate such as glyceryl trinitrate (GTN)

Results in release of NO which leads to venodilatation (decreased preload anf reduction in cardiac work) ; coronary vasodilation also occurs (but minor effect)

Nitrate tolerance can occur upon prolonged exposure

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32
Q

Chronic heart failure (aka congestive heart failure) What is it?

A

Due to failure of heart muscle or failure of the heart valves

failure can occur in LV or RV or both

Chronic or acute (post MI)

Often secondary : most commonly (ischaemic heart disease), hypertension, cardiomyopathies (alcohol/viral)

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33
Q

CHF is precipitated (made worse) by …

A

Pregnancy
Anaemia
Hyper/hypothyroidism
Fluid retaining drugs (glucocorticoids and NSAIDs)

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34
Q

explain the neurohormonal adaptation of the body in CHF

A

Neurohormonal adaptation to compensate for circulatory failure

  • activation of SNS, RAAS + release of ADH, ANP(atrial natriuretic peptide)
  • Release of ANP is the only good effect ;
  • the other the effects causes afterload/preload/resistance(from vasoconstriction) to increase and blood pressure to decrease (in the short term cardiac output increases but long-term heart failure is exacerbated due to cardiac remodelling)
  • vicious cycle occurs; impaired renal function=more water/salt retention=further activation of RAAS(also due to decreased BP due to action of SNS/ADH)
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35
Q

Effect of ANP

A

Acts on kidneys causing increased K+ excretion this results in:

reduction of extracellular fluid (ECF) volume,
improved cardiac ejection fraction with resultant improved organ perfusion, decreased blood pressure,

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36
Q

Describe left-sided failure

A

Often secondary to hypertension

poor output of LV = increase in left atrial/pulmonary venous pressure and pulmonary oedema (breathlessness)

37
Q

Signs and symptoms of CHF

A

Fatigue

Poor exercise tolerance (determines grade)

Cold peripheries

Low blood pressure

Reduced urine flow

Weight loss

Echocardiogram - ejection fraction <45%

BNP levels abnormal

chest X-ray to check for cardiomegaly

38
Q

Signs and symptoms of LV failure

A

Pulmonary oedema

Breathlessness – sensation of drowning. ‘Cardiac asthma’

wet cough

Orthopnoea – breathless on lying which is relieved by sitting up. Nocturnal problem(paxosysmal nocturnal dyspnoea)

Inspiratory crepitations

39
Q

Signs and symptoms of RV failure

A

Raised venous pressure

Increased JVP - jugular venous pressure

Enlarged liver

Oedema – ankles; if lying down rises to thighs/abdomen

40
Q

Describe RV failure

A

RV output fails

causes:

  • often due to lung disease such as COPD (cor pulmonale)
    • pulmonary hypertension as an adaptation to prolonged hypoxia = increased preload = increase pressure on RHS of heart
  • pulmonary valvular stenosis
    • due to congenital or rheumatic heart disease
  • secondary to left sided heart failure
    • increased pressure in pulmonary vasculature due to backward flow of blood from dysfunctional LV/LA
41
Q

Biventricular failure

A

When both chambers fail

can be secondary to LVF due to pulmonary congestion or due to disease that affects both ventricles (such as ischaemic heart disease)

42
Q

What are the 2 most important drugs for treating CHF?

A

ACE inhibitors (they have -pril at the end) and beta-blockers (vasoprilol and very low dose)

43
Q

Side effects of ACEIs

A

Hyperkalaemia

May cause severe hypotension ; treatment withdrawn for a few days

cause deterioration of renal function in pre-existing renal disease

cough

44
Q

Explain the mechanism of action for ACEIs

describe how counselling for them would work

A

ACE inhibitors prevent an enzyme in the body from producing angiotensin II, a substance that narrows blood vessels

This reduces afterload/preload

reduce salt/water retention

inhibits RAAS

also used to treat hypertension

start low go slow ; monitor eGFR and K+ before and during treatment

45
Q

when should ACEIs be contraindicated ?

A

stenosis of renal arteries ;

reduced blood flow to kidneys = xs renin secreted = renal function dependant on RAAS ; as ACEIs block this compensatory method they can cause renal failure in these patients

46
Q

Effect of ACEIs on K+ levels

A

Aldosterone is a sodium retaining K+ losing enzyme

ACEIs cause K+ retention so plasma [K+] increase

47
Q

Describe the alternative drugs to ACEIs

A

AT1 Receptor antagonists - block the action of AII ; inhibits vasoconstriction ; less likely to cause cough so can be given to people who experience severe coughing with ACEIs

48
Q

uses of beta-blockers

A

Often used in COPD treatment

reduce sympathetic stimulation/heart rate/O2 consumption/anti-arrhythmic/oppose neurohormonal activation during CHF (especially ischaemic heart failure)

start with low dose for CHF ; symptoms may get worse at first

49
Q

describe the mechanism of action of diuretics

A

Loop diuretics used to treat CHF such as furosemide

reduce circulating volume/pre-load/oedema

some may cause hypokalaemia

50
Q

Describe the action of digoxin

A

+ve inotrope - increases force of heart contraction ; inhibits Na+/K+ ATPase = accumulation of Na+ in myocyte which is exchanged with Ca2+ = more intracellular [Ca2+]

51
Q

What is the major use of digoxin

A

To treat AF/CHF in elderly patients

positive ionotropic (increased contractility but slowed down SAN conduction = slower HR); while also inhibiting SNS and RAAS

rarely used now - reserved for HF with AF or when ACEIs/diuretics fails

its effects are enhances by ACEIs

52
Q

What are the negative effects of cardiac remodelling

A

Myocyte apoptosis

changed expression of contractile proteins

remodelling of matrix

dilatation

53
Q

Pulmonary oedema histology

A

Alveolar walls are congested by fluid

54
Q

Right ventricular failure results in ….

A

Raised end diastolic pressure

raised atrial and JVP

raised central venous pressure

liver distension(abdominal discomfort) and peripheral oedema

55
Q

Why does CHF cause oedema

A

Heart failure diminishes blood flow and in response, your body tends to retain fluid in an effort to maintain adequate blood volume. But a failing heart is unable to accommodate this extra fluid, so it is transferred out of your blood vessels and into your tissues – usually in those body parts that are lower than others.

also increased venous pressure opposes re absorption of fluid

56
Q

Why are creatinine levels monitored?

A

Abnormal creatinine levels indicate impaired renal function

If there is a problem with your kidneys, creatinine can build up in the blood and less will be released in urine

57
Q

Why are NSAIDs/glucocorticoids contraindicated with CHF?

A

They are fluid retaining so can exacerbate CHF?

58
Q

Counselling for furosemide

A

Take in morning to prevent sleep disturbance

may cause falls due to dizziness side effect - be careful

omit dose when patient has diarrhoea or vomiting

furosemide dosing is interrupted as few days before administering beta-blockers

59
Q

Does CHF cause renal impairment ?

A

Yes;

When the heart is no longer pumping efficiently it becomes congested with blood, causing pressure to build up in the main vein connected to the kidneys and leading to congestion of blood in the kidneys, too. The kidneys also suffer from the reduced supply of oxygenated blood.

60
Q

How does heart failure cause elevated BNP ?

A

Symptom of failing ventricles ; BNP primarily is secreted by the ventricles in the heart as a response to left ventricular stretching or wall tension ; only released after prolonged volume overload

61
Q

Counselling for ACEIs

A

Purpose - to treat heart failure

expect blood presssure to go lower

take at night to reduce the effects of low blood pressure

62
Q

Effects of ACEIs and Furosemide on [K+]

A

ACEI can cause hyperkalaemia because aldosterone causes K+ excretion so reduced aldosterone release = increased K+ retention

Furosemide can cause hypokalemia as its a diuretic (loss of all electrolytes in blood)

63
Q

When are DOACs contraindicated?

A

in patients with mechanical heart valve replacements

64
Q

Why is cardiac hypertrophy problematic ?

A

It increases the work of the heart whilst also lessening the ejection fraction

65
Q

Congested liver histology

A

Dark areas - centrolobular congestion

pale areas - periportal fatty change

66
Q

Causes of RVHF

A

lung disease

thromboemboli

Pulmonary valve stenosis

67
Q

How does lung disease cause RVF

A

emphysema destroys alveolar walls and capillaries

hypoxia constricts pulmonary arteries

pulmonary hypertension

68
Q

what is a normal creatinine clearance?

A

100 mL/min

69
Q

Most common cause of haemorrhagic stroke

A

most caused by ontracerebral haemorrhage

some caused by subarachnoid haemorrhage

70
Q

Define infarct and describe the types

A

Area of ischaemic necrosis due to abrupt cessation of arterial supply (arterial infarction) OR venous drainage (venous Infarction)

arterial infarction is the most common

pale or white infarct occur in solid organs such as the heart and spleen (due to lack of blood flow)

red or haemorrhagic infarcts occur in loose spongy tissue rich in blood supply or has dual blood supply (ischemia results in vessels bursting)

causes - septic (due to vegetation of sub acute bacterial endocarditis )

71
Q

factors affecting the development of an infarction

A

Vascular occlusion - degree of obstruction

rate of development of occlusion - is it abrupt or gradual

nature of vascular supply - is there dual blood supply or just one artery to that organ/tissue

type of tissue - neurones can only survive minutes without oxygen, myocardium can survive 20-40 mins, fibroblasts can survive many hours

72
Q

Describe the cellular morphology of iscaemic coagulative necrosis

A

Wedge shapes infarct - apex at occluded artery

occurs in all organs except the brain

inflammatory response (tissue turns red from pale) followed by reparative response and scar tissue formation

73
Q

What are the cardiac muscle injury markers ?

A

Troponin, myoglobin CK MB

74
Q

Describe the appearance of myocardium 12-24 post MI

A

Coagulative necrosis occurring

nuclei are breaking down and streaks in muscle (mottling)

75
Q

Describe the appearance of myocardium 3-14 days post MI

A

Macrophagic removal of debris and vascular granulation tissue formation

area of necrosis is pale and still soft

hyperaemic(excess blood) border around area of necrosis

76
Q

Morphological changes in myocardium 3 week + post MI

A

fibrous granulation tissue becomes tough scar tissue

77
Q

Describe the early and late complication of MI

A

Early :

sudden death due to dysrhythmia,

rupture of myocardium during healing stage = heart fills with blood (haemopericardium) and cardiac tamponade,

rupture of papillary muscle = acute valve failure = LVF,

mural thrombus (blood clot form on wall on heart/vessel where the infarct has occurred ) = embolism elsewhere

fibrinous pericarditis = pericardium becomes rough, granular, and has many fibrous adhesions

late :

CHF

ventricular aneurysm - loss of flexibility of ventricular wall

78
Q

Describe renal infarcts

A

Usually caused by emboli from the L side of heart

wedge shaped

pale area with surrounding hyperaemia

heals by scar formation

79
Q

Describe cerbral infarcts (aka ischaemic stroke)

A

Liquedative necrosis due to the lack of CT in the brain; Brain cells have a large amount of digestive enzymes (hydrolases). These enzymes cause the neural tissue to become soft and liquefy.

results in hypoperfusion and microembolism

heals by astrocytic gliosis (perforation of glial cells) - loss of cells

80
Q

describe gangrene

A

Arterial infarction in extremities or bowel

Complication of necrosis caused by ischaemia following Injury or infection

common in diabetics

tissue becomes black (bacteria break down dead tissue to form black iron sulfate) and smells bad

dry gangrene occurs when the arterial blood supply is occluded but the venous drainage is intact

wet gangrene occurs when the venous drainage is occluded plus putrefaction; can also be caused by bacterial infection (without the need of ischaemia)

81
Q

Describe venous infarctions and give some common examples

A

Occur when venous drainage from an organ or tissue is and remains completely obstructed

tissues become congested with blood and capillaries/venules may rupture ; arterial blood cannot enter as venous pressure>arterial pressure = hypoxia

bowel infarction - volvulus(bowel twists on itself), hernial strangulation

torsion in testes and ovaries

82
Q

pros and cons of LMWH

A

usually administered subcutaneously so unpleasant for patient; unsuitable for renal failure; short acting and good intial treatment

83
Q

pros and cons of vit K antagonists

A

pros - only needs to be take once daily ; several reversal agents ; cheaper cons; requires close INR monitoring, many drug/food interactions, variable dosing

84
Q

pros and cons of DOACs

A

pros - no monitoring required; lower risk of haemorrhage; cons - reversible agents less available; may need to be taken twice a day, more expensive

85
Q

A patient appears to be hypertensive and their blood pressure continue to increase, which three tests should you order and why

A

eGFR - to guide which medication to give ; long term hypertension can also cause a decline in eGFR

glucose later haemoglobin (HbA1c) to test for diabetes (hypertensive diabetics have higher risk of stroke and MI) or hypertension can be a symptom of diabetes

plasma potassium levels - low potassium can be a cause of hypertension (symptom of overactivation of the RAAS)

86
Q

NICE guidlines for antihypertensive drugs : what are the first line antihypertensive choices for a) type 2 diabetic hypertensive patients b) >55 or black at any age c)<55 and non-black

A

a) ACEIs or ARB (AT1 Receptor Blockers) b) CCI c) CCI (you start adding one drug at a time if hypertension persists)

87
Q

NSAIDs can exacerbate hypertension

true or false

A

True

88
Q

Main differences between right sided and left sided heart failure

A
89
Q

How do ischaemic and haemorrhagic stroke arise?

A

Ischaemic stroke - when a thrombus or embolus gets stuck in the cerebral vessels → necrosis of neurons → release of hydrolyses → inflammation

haemorrhagic stroke : stress up brain tissue → vessel rupture → infarction

2 types : intracerebral (bleeding inside brain) due to hypertension or XS use of anticoagulants/thrombolytics and subarachnoid due to head injury or cerebral aneurysm

Pharmacology (13 decks)

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