Cardiovascular therapeutics Flashcards

1
Q

What occurs in coronary artery disease?

A

narrowing of the lumen of blood vessels due to the formation of atheromas plaques in the intima
Symptoms occur when thrombosis and plaque rupture take place

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2
Q

How is CAD treated?

A

not possible to offer treatment to those suffering consequences therefore preventative measures are vitally important

  • leading causes of death in the developed world
  • majority deaths due to MI occur outside of hospital
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3
Q

What are the 2 key lifestyle factors used to prevent/reduce CAD?

A

smoking cessation and dietary changes

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4
Q

What is the main treatment for smoking cessation?

A

NRT - must have parenteral or topical application due to poor GIT absorption + additional support and counseling

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5
Q

What are the side effects of NRT?

A

Nausea, cramps, cough and insomnia

Caution must be taken in severe CVD as risk of coronary artery spasm

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6
Q

What is an alternative treatment to NRT for smoking cessation?

A

bupropion - non-selective dopamine reuptake inhibitor

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7
Q

What are the side effects of bupropion?

A

mood and eating disorders
seizures and CNS tumors
alcohol and benzodiazepine withdrawal
additional care must also be take in liver and renal disease

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8
Q

What is a very important RF for CAD?

A

Hypertension

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9
Q

What is the current NICE guidelines advice for when to start treating hypertension?

A

> 160/100 or >140/90 in certain circumstances, such as organ damage, high CVD risk and diabetes

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10
Q

What is the gold standard for diagnosing hypertension?

A

24 ABPM - avoids life long treatment of white coat hypertension
however if initial BP is >185/110 then ABPM is not undertaken and treatment is started immediately

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11
Q

What do the treatment options for hypertension depend on?

A

age and ethnicity (due to ascot trial)

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12
Q

What treatments are first line for those = 55 ?

A

ACE inhibitors or AT2 R blockers

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13
Q

What treatments are first line for those >55 or of afrocaribbean/african ethnicity ?

A

initially treated with calcium channel blockers

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14
Q

What happens if hypertension persists after one of the treatments?

A

2 classes of drugs are combined before adding a thiazide diuretic and then the final date is the addition of a beta blocker

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15
Q

Other than hypertension what else are calcium channel blockers used for?

A

angina and dysrhythmias (diltiazem)

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16
Q

What are the 3 forms of calcium channel blockers?

A

1) phenylalkalines (verapamil)
2) dihydropyradines (nifedipine)
3) benzothiazepines (diltiazam)

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17
Q

How do calcium channel blockers work?

A

relax smooth muscle and cardiac muscle by preventing calcium entry (through L type channels) = AV block to slow heart (phenylalkalines and benzothiazepines)
= vasodilation in terms of dihydropyradines

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18
Q

What are the side effects of calcium channel blockers?

A

flushing, headache, ankle swelling, constipation, heart block, exacerbation of HF

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19
Q

What are thiazide diuretics used to treat and how do they work?

A

mild HF and hypertension

  • act at the Na/Cl pump of the DCT preventing cotransport and therefore leading to the loss of Na, Cl and K in the urine
  • loss of theses salts lowers water retention and leads to vasodilation
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20
Q

What are the adverse effects of thiazide diuretics?

A

diuresis, hyponatraemia and hypokalemia, erectile dysfunction, gout and an association with diabetes

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21
Q

Other than hypertension what other conditions do drugs that act on the RAS treat?

A

HF, diabetic neuropathy, renal insufficient, ischemia heart disease and after MI (esp. with ventricular damage)

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22
Q

What are the different types of RAS drugs?

A

1) renin inhibitors (aliskiren) - rarely used due to safety concerns
2) ACE inhibitors - ramipril, enalapril
3) AT2 receptor blockers (candesartan)

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23
Q

What are the side effects of RAS drugs?

A

hypotension, angioedema, bilateral renal artery stenosis (therefore kidney function must be checked regularly)

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24
Q

What is the most common side effect of ACE inhibitors and why does it occur?

A

persistent dry cough - inhibition of the kinase enzyme, causing build up of bradykinin

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25
Q

Which group of people are beta-blockers not used for HF and hypertension?

A

young women due to risk of teratogenicity

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26
Q

What is the additional benefit of carvedilol?

A

beta blocker + also had alpha-1 blocking activity

27
Q

What is the additional benefit of nebivolol?

A

selective beta blocker with additional activity causing NO release

28
Q

What group of patients is beta-blockers contraindicated in?

A

asthmatics - due to risk of bronchoconstriction

29
Q

What are the other adverse effects of beta-blockers?

A

bradycardia, hypoglycemia, fatigue, cold extremities

30
Q

What types of cholesterol are bad?

A

increased plasma LDL and total cholesterol positively correlate with incidence of cardiovascular disease whereas increased HDL cholesterol has a negative correlation
- less strong positive correlation between CVD and plasma triglyceride levels

31
Q

What are statins used for and how do they work?

A

commonly prescribed for primary and secondary prevention of strokes, TIAs, MI and angina

up regulate LDL receptor expression on hepatocytes as well as inhibiting the LDL producing enzyme HMG-CoA reductase

32
Q

What are the risks of statins?

A

well tolerated but risk of myositis

very rare cases the proteins released in the breakdown of muscle can lead to rhabdomyolysis and renal failure

33
Q

Other than statins, what are another type of lipid lowering drugs?

A

fibrates = benzafibrate, fenofibrate - less powerful at reducing cholesterol levels but increase HDL and lower triglycerides - actions stem from increasing LDL uptake at the liver

34
Q

What are the side effects of fibrates?

A

myositis

contraindicated in those with liver problems

35
Q

What is ezetimibe?

A

cholesterol lowering drug - inhibits cholesterol absorption from the gut
rarely used and increases risk of rhabdomyolysis if used in conjunction with a statin

36
Q

What have anti-coagulants been shown to be beneficial against?

A

reduce risk of death in MI and stroke patients

most commonly used = aspirin (anti-platelet)

37
Q

What is aspirin mainly used in?

A

secondary prevention but also been suggested to have a cancer preventative effect

38
Q

How does aspirin work?

A

irreversible COX inhibitor preventing production of thromboxane in platelets
also temporarily reduces production of platelet aggregating inhibitor PG12, but endothelial cells that produce PG12 are able to synthesize more enzyme

39
Q

What are the side effects of aspirin?

A

mostly GIT bleeding and dyspepsia

overdose- tinnitus, vertigo and decreased hearing

40
Q

Why is aspirin contraindicated in children and who else?

A

due to risk of reye’s syndrome - encephalopathy and liver failure
can’t be used alongside warfarin (bleeding risk) or uricostatic agents (due to risk of gout)

41
Q

Other than aspirin what are some other anti-platelet drugs?

A

IIb/IIIa receptor inhibitors as well as ADP blockers (clopidogrel and prasugrel)

42
Q

How do ADP blockers work?

A

irreversibly inhibit ADP induced platelet aggregation causing an additive effect with aspirin due to different pathways

43
Q

What is prasugrel?

A

not a prodrug therefore can be used in patients with low levels of liver enzyme cyp2c19

44
Q

What is ticagrelor?

A

reversible ADP blocker

45
Q

What are examples of anti-coagulants that function at the coagulation cascade?

A

warfarin - blocks vit K - needs close monitoring - can be reversed by giving vit K

Dabigatran blocks thrombin

Apixaban - blocks activated factor X

46
Q

What is prescribed in patients that have a STEMI?

A

Prasugrel or ticagrelor are prescribed after having had percutaneous coronary intervention (PCI)

47
Q

What is prescribed for non-STEMIs?

A

aspirin and clopidogrel

Aspirin also given after TIA

48
Q

When are IIb/IIIa inhibitors?

A

only used during cardiac catheter procedures if clots are visibly forming

49
Q

What drugs are typically used to treat angina?

A

vasodilators such as calcium channel inhibitors and nitrates
nitrates work through release of NO = ventricular relaxation, venorelaxation to lower preload, coronary vasodilator and arterial vasodilation= lower after load

50
Q

What is the major issue with nitrates?

A

tolerance - leading to postural hypotension and headaches

51
Q

What are examples of short and long acting nitrates?

A

acute attacks use GTN

longer acting preps oral isosorbide mononitrate

52
Q

When are intravenous nitrates used?

A

acute coronary syndrome and acute HF

53
Q

Other than vasodilators what else is used in angina?

A

beta blockers to slow heart rate to reduce cardiac work

Ca channel blockers are also used

54
Q

What are the key first things that need to be done for an MI?

A

pain relief and re-open occluded vessels

determine whether its an NSTEMI or STEMI on ECG

55
Q

What constitutes a STEMI?

A

ST elevation with initial T wave inversion and later Q wave inversion

56
Q

How is a NSTEMI differentiated from angina?

A

based on troponin T levels

57
Q

What are the treatments for MI?

A

Diamorphine - pain
Metoclopramide - nausea
aspirin, heparin and clopidogrel - thin blood
PCI and thrombolysis must be performed

58
Q

How does thrombolysis work?

A

drugs activate plasminogen, degrading fibrin to break up thrombi
Streptokinase was the dominant treatment for past but has now been replaced by alteplase

59
Q

How is a NSTEMI treated?

A

angiography before treatment plan is formed whereas all STEMIs have PCI

60
Q

What is HF?

A

End stage of CVD - had incredibly poor prognosis but treatment is available to treat symptoms and improve QoL

61
Q

What are the aims of the treatments for HF?

A

Reduce fluid load and edema using loop directions (furosemide) = blocks Na/K/2Cl in ascending loop of hence

62
Q

What are at the adverse effects of loop diuretics (furosemide)?

A

hypovolemia, hypotension, hypokalemia and hypomagnesemia and hyperuricaemia

63
Q

Other than loop diuretics what other treatments help to treat HF?

A
ACE inhibitors (ramipril) 
spironolactone = aldosterone antagonist = promotes Na loss and increase k retention aiding fluid loss 
Low dose Beta blockers