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CARDIOLOGY > PPT > Flashcards

PPT Flashcards

1
Q

Outline the stepwise approach to drug treatment of hypertension?

A

<55 and not African or Caribbean origin
1: ACE or ARB
2: add CBB
3: add thiazide-like diuretic
4: spironolactone

> 55 or African or Caribbean origin
1: CCB
2: add ARB (or ACEi)
3: add thiazide-like diuretic
4: spironolactone

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2
Q

How long should you leave Antihypertensive drug therapy to check for therapeutic effect?

A

Allow 1 month before emulating therapeutic effect
!!! Unless treating hypertensive crisis!

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3
Q

Whats the blood pressure level aims when on Antihypertensive drug therapy?

A

If <80
<140/90mmHg in clinic
<135/85mmHg (home bp measurement)

If >80
<150/90 in clinic
<145/85 at home

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4
Q

Why should you not use ACEi and ARBs together?

A

Particular risk of hyperkalaemia

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5
Q

What proportion of pt on ACEi will get a dry cough?

A

~10%

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6
Q

Why dont ARBs cause a dry cough like ACEi?

A

ACE inhibitors cause cough by increasing bradykinin levels
ARBs have minimal effect on bradykinin

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7
Q

What are the important cautions of ACEi?

A

First dose hypotension - take first dose before bed because of this
Agranulocytosis - very rare
Anaphylactoid reactions - also very rare
Risk of hyperkalaemia if taken with diabetes however these drugs are still given despite this

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8
Q

What are contraindications of ACEi?

A

Angioedema (hereditary or idiopathic)
Taking with aliskiren with eGFR or diabetes
Pregnancy and breast feeding
Aortic stenosis
Hyperkalaemia >= 5.0mmol/L
Renovascular disease

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9
Q

What do ACEi interact with?

A

Aliskiren (direct renin inhibitor) - significant increased risk of renal impairment and hyperkalaemia
Allopurinol - higher risk of hypersensitivity and haematological reactions e.g. Stevens-Johnson syndrome
Azathioprine - increased risk of anaemia and leukopenia
Everolimus (a protein kinase inhibitor for neuroendocrine tumours of GIT/pancreas) - increased risk of angioedema
Lithium (ACEi increase its concentration and increase risk of toxicity)
High-dose diuretic therapy e.g. >80mg furosemide - significantly increases risk of hypotension

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10
Q

What is Stevens-Johnson syndrome?

A

a severe systemic reaction affecting the skin and mucosa that is almost always caused by a drug reaction

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11
Q

What drugs cause Stevens-Johnson syndrome?

A

penicillin
sulphonamides
lamotrigine, carbamazepine, phenytoin
allopurinol
NSAIDs
oral contraceptive pill

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12
Q

What are features of Stevens-Johnson syndrome?

A

Maculopapular rash with target lesions that may develop into vesicles or Bullae
Mucosal involvement
Systemic symptoms - fever, arthralgia

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13
Q

What are the common + important SE of ACEi?

A

Dry cough
Dizziness
Headaches
Diarrhoea and vomiting
Blurry vision
Angioedema
Hyperkalaemia
First dose hypotension

Rare but important - agranulocytosis, liver dysfunction, kidney disease

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14
Q

Who is most likely to experience first-dose hypotension when taking ACEi?

A

Pt taking diuretics

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15
Q

What are the sick day rules for ACEi?

A

Consider temporarily stopping if experiencing D+V as the dehydration can increase the risk of AKI and enhance the drug effects - may experience more dizziness/falls etc

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16
Q

What monitoring is done for ACEi?

A

U&Es should be checked before treatment is initiated and after increasing the dose

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17
Q

How much of an effect can lifestyle changes have on cholesterol levels?

A

It can only really reduce cholesterol by 10% compared to statins which can have an effect of up to 50% reduction!

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18
Q

Whats the moa of ACEi?

A

inhibit the conversion angiotensin I to angiotensin II. Decreased production of angiotensin II means less coronary blood vessel constriction which reduces vascular resistance and vascular smooth muscle cell proliferation
Increased levels of bradykinin also causes vasodilation g effects

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19
Q

When should you treat stage 1 hypertension?

A

treat if < 80 years of age AND any of the following apply; target organ damage, established cardiovascular disease, renal disease, diabetes or a 10-year cardiovascular risk equivalent to 10% or greater

Suggestion… consider antihypertensive drug treatment in addition to lifestyle advice for adults aged under 60 with stage 1 hypertension and an estimated 10-year risk below 10%.

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20
Q

Which CCB are used for treating hypertension?

A

Verapamil
Diltiazem
Nifedipine
Amlodipine
Felodipine

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21
Q

Why should verapamil not be given with beta blockers?

A

It can cause heart block

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22
Q

Whats the MOA of calcium-channel blockers?

A

They interfere with the inward displacement of Ca2+ though the slow channels of the active cell membranes which influences the myocardial cells anc cells of vascular smooth muscle
Thus, myocardial contractility may be reduced, the formation/propagation of electrical impulses within the heart may be depressed, and coronary or systemic vascular tone may be diminished

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23
Q

What are cautions for CCB?

A

Elderly - STOPP criteria
Known hypersensitivity - contraindication
Heart failure - except amlodipine
Cautions in cardiac outflow obstruction, diabetes, AV block, unstable angina or MI within 1 month
Cautions with hepatic and renal impairment
Pregnancy and breastfeeding - avoid

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24
Q

What are SE for CCB?

A

Abdominal pain
Dizziness and drowsiness
Flushing
Headache
Nausea and vomiting
Palpitations
Peripheral enema
Skin reactions
Tachycardia

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25
Q

Whats the MOA of statins?

A

They inhibit HMG CoA reductase which reduces intracellular cholesterol levels - this activates a protease which causes upregulation of expression of the LDL receptor gene = increased receptor-mediated endocytosis of LDL = reduces serum LDL

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26
Q

Why is it suggested that Simvastatin is taken at night?

A

Because of the diurnal variation of HMG-CoA reductase
The enzyme is more active at nigh so more LDL is synthesised at night
Simvastatin has a much shorter half life than atorvastatin so its best taken at night

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27
Q

What metabolises statins?

A

CYP3A4 in the liver

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28
Q

What are the SE of statins?

A

Myopathy
Liver impairment
GI discomfort
Headache
Sleep disorders
Thrombocytopenia

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29
Q

What can interact with statins?

A

CYP3A4 inhibitors:
Grapefruit juice
HIV protease inhibitors
Macrolide antibiotics
Azole antifungal
CCB - diltiazem and verapamil

CYP3A4 inducers:
St John’s wort
Glucocorticoids
Antiepielptics
Rifampicin

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30
Q

What are monitoring requirements for statins?

A

Before starting - full lipid profile, TSH, renal function, CK, LFTs
LFTs- repeat at 3 and 12 months (stop if serum transaminases raised >3 times upper limit of reference range)
HbA1c if at risk of diabetes mellitus and repeat after 3 months

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31
Q

Whats the moa of fibrates?

A

Agonist of PPAR-alpha
They decrease triglyceride levels and increase HDL

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32
Q

Who are fibrates contraindicated in?

A

Gallbladder disease
Hypoalbuminaemia
Nephrotic syndrome
Severe hepatic impairment
Pregnancy and breast feeding
Hypersensitivity

Caution with renal impairment as may increase Cr, and may interact significantly with anticoagulants therapy

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33
Q

What monitoring should be done for fibrates?

A

Monitor LFTs
Before starting check TFTs and if hypothyroidism correct this first
Monitor CK if using alongside statins

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34
Q

What are the SE of fibrates?

A

Tend to be mild - GI disturbances and headache
Pruritus and rashes have also been reproyted

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35
Q

Whats the moa of ezetimibe?

A

Inhibits intestinal absorption of cholesterol

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36
Q

What are SE of ezetimibe?

A

GI discomfort and fatigue
Myopathy particularly if used alongside statins/niacin, can damage pancreas and liver
Allergic reactions

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37
Q

Whats the moa of bile acid sequestrants?

A

Binds to bile acids and prevents their reabsorption = promotes hepatic conversion of cholesterol into bile acids = increased LDL receptor activity = increased clearance of LDL from plasma

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38
Q

Who are bile acid sequestrants contraindicated in?

A

Complete biliary obstruction - not likely to be effective

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39
Q

What are SE of bile acid sequestrants?

A

GI upset and headache
May interfere with absorption of fat-soluble vitamine - ADEK and folic acid

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40
Q

What are examples of bile acid sequestrants?

A

colestyramine, colestipol, colesevelam.

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41
Q

Whats the thiazide-like diuretic suggested by NICE?

A

Indapamide

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42
Q

What are contraindications for thiazide-like diuretics?

A

Refractory hypokalaemia.
Hyponatraemia.
Hypercalcaemia.
Addison’s disease.
Symptomatic hyperuricaemia.
Severe liver disease.
Severe renal impairment
Pregnant women

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43
Q

What are adverse effects of thiazide-type diuretics?

A

dehydration
postural hypotension
hyponatraemia, hypokalaemia, hypercalcaemia*
gout
impaired glucose tolerance
impotence

Rare- thrombocytopenia, agranulocytosis, photosensitivity rash, pancreatitis

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44
Q

What are side efefcts of beta blockers?

A

bronchospasm
cold peripheries
fatigue
sleep disturbances, including nightmares
erectile dysfunction

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45
Q

What are contraindications of beta blockers?

A

uncontrolled heart failure
asthma
sick sinus syndrome
concurrent verapamil use: may precipitate severe bradycardia

46
Q

What is a drug eluting stent?

A

A stent coated in anti-proliferating agents to prevent the endothelium regrowing over the stent - i.e. prevents formation of new clots

47
Q

Why do dihydropyridines cause ankle swelling?

A

As they have a vasodilators effect

48
Q

What is tachyphylaxis?

A

the appearance of progressive decrease in response to a given dose after repetitive administration of a pharmacologically or physiologically active substance
This is why we give nitrates with assymetric dosing

49
Q

Why should you avoid giving oxygen in ACS unless sats are <90%?

A

Because it may increase the number of free radicals or cause coronary artery spasm

50
Q

Why should you avoid morphine in ACS unless pain is unacceptable?

A

Because of the risk of respiratory depression

51
Q

What are examples of classes of antiplatelet drugs?

A

COX inhibitors - aspirin
Phosphodiesterase inhibitors - dipyridamole
Adenosine diphosphate receptor antagonists - clopidogrel or ticagrelor
Glycoprotein IIb/IIIa receptor antagonists - abciximab and tirofiban

52
Q

How does the dose of aspirin affect the pharmacodynamics?

A

Low doses - inhibition of COX1 which inhibits platelet generation of thromboxane A2 = antithrombotic effect
Intermediate doses - inhibiton of COX1 and COX2 = blocks prostaglandin production = analgesic and antipyretic
High dose - anti-inflammatory mechanism for use in rheumatic disorders. Limited usefulness due to toxicity

53
Q

What are the contraindications of aspirin?

A

Active peptic ulcers or previous peptic ulceration
Bleeding disorders
Children <16 due to risk of Reye’s syndrome
Haemophilia
Severe cardiac failure
Hypersensitivity to aspirin or any NSAIDs

54
Q

What are SE of aspirin?

A

Dyspepsia
Bleeding
PUD
Bronchospasm - dyspnoea
Hyperuricaemia

55
Q

What are the main features of salicylate poisoning?

A

hyperventilation, tinnitus, deafness, vasodilatation, and sweating. Coma is uncommon but indicates very severe poisoning.

56
Q

What are examples of adenosine diphosphate receptor antagonists?

A

Clopidogrel
Ticagrelor
(P2Y12 antagonist)

57
Q

Whats the moa of clopidogrel and ticagrelor?

A

They antagonize P2Y12 platelet receptors and therefore prevent the binding of ADP to the P2Y12 receptor. = a decrease in aggregation of platelets = inhibits thrombus formation.
Clopidogrel is an irreversible inhibitor whereas ticagrelor binds to a different site on the receptor and produces reversible inhibition

58
Q

What are the main differences between clopidogrel and ticagrelor?

A

Clopidogrel has a slow onset of action of about 5 days for the full effect without a loading dose
Ticagrelor has a more predictable platelet inhibiting action and a more rapid onset of action wit a shorter half life

59
Q

Whats the moa of dipyridamole?

A

It’s a Phosphodiesterase inhibitor - inhibits the cellular reuptake of adenosine which increases its plasma concentration = leads to inhibitionopf expression of cell surface GPIIb/IIa receptors = inhibits platelet aggregation

60
Q

What are examples of glycoprotein IIb/IIIa receptor antagonists?

A

Abciximab and tirofiban

61
Q

What are examples of glycoprotein IIb/IIIa receptor antagonists?

A

Abciximab and tirofiban

62
Q

What are the 2 main mechanisms of angina?

A

Decreases oxygen supply - reduced coronary blood flow
Increased oxygen demand - due to raised HR, myocardial contractility and ventricular wall tension

63
Q

How do beta blockers help in angina?

A

They decrease HR, reduce the force of cardiac contraction and lower bp = reduces myocardial oxygen demand

64
Q

How do beta blockers help in angina?

A

They decrease HR, reduce the force of cardiac contraction and lower bp = reduced myocardial oxygen demand

65
Q

What are examples of cardio selective beta blockers?

A

beta-1-blockers
atenolol, betaxolol, bisoprolol, esmolol, acebutolol, metoprolol, and nebivolol.

66
Q

What are the main SE of beta blockers?

A

bronchospasm
cold peripheries
fatigue
sleep disturbances, including nightmares
erectile dysfunction
Bradycardia + hypotension - i.e. falls
May worsen PVD

67
Q

What are the main contraindications of beta blockers?

A

uncontrolled heart failure
asthma
sick sinus syndrome
concurrent verapamil use: may precipitate severe bradycardia

68
Q

What are the features of beta blocker overdose?

A

bradycardia
hypotension
heart failure
syncope

69
Q

How do we manage beta blockers overdose?

A

if bradycardic then atropine
in resistant cases glucagon may be used

70
Q

How do CCBs help in angina?

A

Dihydropyridines - peripheral arterial dilation, coronary artery dilation
Non-dihydropyridines - negative chronograph effect and reduce cardiac contractility

= overall effect is too reduce myocardial oxygen demand

71
Q

Why do dihydropyridines selectively bind to Ca2+ channels in vascular smooth muscle?

A

As they preferentially bind to L-type calcium channels in its inactivated state and more of these channels are in their inactive state in relaxed vascular smooth muscle than cardiac muscle
This explains their relative vascular selectivity and why non-dihydropyridines are used as antiarrythmics

72
Q

What are the main SE of calcium channel blockers?

A

Flushing
Headache
Ankle swelling

73
Q

What are indications for dihydropyridines CCB?

A

Hypertension
Angina
Raynauds

74
Q

What are indications for dihydropyridines CCV?

A

Angina
Hypertension
Arrhythmias

75
Q

What are contraindications for CCB?

A

Acute porphyrias
Atrial flutter or atrial fibrillation associated with accessory conducting pathways
Bradycardia
Hypotension
Second and third degree AV block
Sick sinus syndrome
Sino-atrial block
Cardiogenic shock
HF
Impaired LV function

76
Q

Which type of CCB can result in reflex tachycardia?

A

Dihydropyridines - they can peripheral vasodialtion

77
Q

Whats the MOA of nurtartes?

A

nitrates cause the release of nitric oxide in smooth muscle, activating guanylate cyclase which then converts GTP to cGMP, which in turn leads to a fall in intracellular calcium levels
in angina they both dilate the coronary arteries and also reduce venous return which in turn reduces left ventricular work, reducing myocardial oxygen demand

78
Q

What are SE of nitrates?

A

hypotension
tachycardia
headaches
flushing

79
Q

Which nitrates dont cause tachyphylaxis?

A

Isosorbide mononitrate

80
Q

How can nitrate tolerance be avoided?

A

Assymetric dosing - take second dose of the day after 8 hours so that you have a 10-14 hour nitrate-free period = allows blood-nitrate levels to fall for 4 hours and maintain the effectiveness

81
Q

Whats the moa of nicorandil?

A

A potassium channel opener in vascular smooth muscle cells = vasodilation in systemic and coronary arteries
Lowers bp and reduces myocardial oxygen demand

82
Q

Whats the moa of ivabradine?

A

Specific inhibitor of If current = slows the rate of firing of the SAN
(Works best at higher heart rates as efficacy increases with the frequency of channel opening)

83
Q

Whats the moa of ranolazine?

A

A late sodium current inhibitor and reduces Ca2+ accumulation and lowers wall tension in ventricles = reduces myocardial oxygen demand and reduces compression of small intramyocardial coronary vessels = improving myocardial perfusion in diastole

84
Q

What drugs are used for acute pulmonary oedema?

A

Loop diuretics

(CPAP and balloon pumps may be used??)

85
Q

What does ‘high ceiling diuretic’ mean?

A

A diuretic where the higher the dose, the greater the effect

86
Q

Whats an example of:
- IV loop diuretic
- oral loop diuretic

A

IV - furosemide
Oral - furosemide or bumetanide

87
Q

What drugs are used in chronic HF?

A

Loop diuretics
ACEi/ARBs
Aldosterone antagonists
Beta blockers

88
Q

Which chronic HF drugs are used for symptom improvement?

A

Loop diuretics

89
Q

Which chronic HF drugs are used for morbidity/mortality reduction?

A

ACEi/ARB
Aldosterone antagonist
Beta blocker

90
Q

Whats the moa of loop diuretics?

A

Inhibit the Na+/K+/Cl- cotransporter in the thick ascending limb of the loop of Henle = reduces the absorption of NaCl

91
Q

Why may pt with poor renal function need escalating doses of loop diuretics?

A

As loop diuretics work on the apical membrane so they must first be filtered into the tubules by the glomerulus before they can have an effect = larger doses will be needed to ensure a sufficient concentration is achieved within the tubules

92
Q

What are indications of loop diuretics?

A

HF
Resistant hypertension, particularly in pt with renal impairment

93
Q

What are adverse effects of loop diuretics?

A

Hypotension - dizziness
Hyponatraemia, Hypokalaemia, Hypomagnesaemia, Hypocalcaemia
Ototoxicity- tinnitus or deafness (more common in renal impairment)
Hypochloraemic alkalosis
Renal impairment
Hyperglycaemia
Gout
Muscle spasms
Nausea

94
Q

What are contraindications for loop diuretics?

A

Anuria
Comatose and precomatose states associated with liver cirrhosis
Renal failure due to nephrotoxic or hepatotoxic drugs
Severe hypokalaemia
Severe hyponatraemia

95
Q

What are examples of mineralocorticoid receptor antagonists used for managing chronic HF?

A

Spironolactone
Eplerenone

96
Q

What monitoring is needed for aldosterone antagonists?

A

K+ monitoring (especially if used alongside ACEi as both cause hyperkalaemia)

97
Q

What are examples of SGLT2 inhibitors used for managing HF?

A

canagliflozin, dapagliflozin and empagliflozin

98
Q

What are contraindications of mineralocorticoid receptor antagonists?

A

Hyperkalaemia

99
Q

What are SE of mineralocorticoid receptor antagonists?

A

Hyperkalaemia and other electrolyte abnormalities
Renal impairment
Arrhythmias
Constipation or diarrhoea
Dizziness
Dyslipidaemia
Gynaecomastia (at higehr doses than are used for managing HF)
Muscle spasms
Nausea and vomiting

100
Q

What drugs are used for managing AF?

A

Beta blockers
Digoxin
Non-dihydropyridine CCB

Anticoagulants!

101
Q

What are class 3 antiarrhthmics on Vaughn Williams classification?

A

Amiodarone
Sotalol

102
Q

What drugs are given in CPR?

A

Adrenaline and amiodarone

103
Q

What drugs can be given for tachycardias?

A

Amiodarone - broad QRS i.e. most likely VT
Adenosine - regular narrow QRS

104
Q

What drug can be given for bradycardia?

A

Atropine

105
Q

Whats the indications for adenosine?

A

Terminating supraventricular tachycardias

106
Q

Whats the moa of adenosine?

A

Causes transient heart block in the AV node - agonist of the A1 receptor in the AVN which inhibits adenylyl class thus reducing cAMP and causing hyperpolarisation by increasing outward K+ flux

107
Q

Whats the half life of adenosine?

A

8-10 seconds

108
Q

Whats the moa of amiodarone?

A

blocking potassium channels which inhibits repolarisation and hence prolongs the action potential. Amiodarone also has other actions such as blocking sodium channels (a class I effect)

109
Q

Whats the half life of amiodarone?

A

20-100 days - loading doses are frequently used because of this extremely long half life

110
Q

What is antimicrobial synergy? And what is a good example of it?

A

Where the combined activity of 2 antimicrobial agents is greater than the sum of their activities when used individually
In bacterial endocarditis when we use penicllin combined with gentamicin

111
Q

What is antimicrobial synergy and what is a good example of it?

A

When the combined activity of 2 antimicrobial agents is greater than the sum of their activities when used individually
E.g. in bacterial endocarditis when we use penicillin combined with an aminoglycosdie (usually gentamicin)

112
Q

F

A

F

CARDIOLOGY (19 decks)

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