Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Cardiovascular System > SIHD & Angina - Therapy > Flashcards

SIHD & Angina - Therapy Flashcards

1
Q

Coronary artery disease happens as an interaction between both ______________________ risk factors.

A

modifiable and non-modifiable

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

How would you describe the interaction between risk factors leading to ACS/stable angina?

A

synergistic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Outline some modifiable risk factors.

A 
smoking
alcohol
stress
sleep
diet/Na intake
exercise
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Outline some non-modifiable risk factors.

A

age
sex
Fx

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are the risk factors for SIHD/angina?

6

A 
smoking
hypertension
hyperlipidaemia
hyperglycaemic
male
post-menopausal female
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Myocardial ischaemia can result from both supply ischaemia and demand ischaemia.

What are the determinants of demand ischaemia?

A
  • HR
  • contractility
  • systolic BP
  • myocardial wall stress
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Myocardial ischaemia can result from both supply ischaemia and demand ischaemia.

What are the determinants of supply ischaemia?

A
  • coronary artery diameter/tone
  • collateral flow
  • perfusion pressure
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Most change in atherosclerosis are in which layer of the blood vessels?

Which cell types accumulate?

A

intima

macrophages (foamy macrophages), monocytes, lymphocytes, connective tissue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are the aims of drug therapy in treating SIHN/angina?

What are some of the mechanisms behind drugs used? (3)

A

reduce O2 demand/increase O2 supply

reduce HR
reduce contractility
reduce afterload

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What drug classes may be used in treating angina (give examples)?

(8)

A
  • short acting nitrates (GTN)
  • long acting nitrates (isosorbide mononitrate)
  • beta blockers (bisoprolol)
  • CCB (amlodipine)
  • potassium channel openers (nicorandil)
  • new drugs (ranolazine, ivabradine)
  • antiplatelets (aspirin, clopidogrel)
  • statins (atorvastatin)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Which drugs work by increasing blood/O2 supply?

How?

A
  • nitrates (vasodilation)

- CCBs (vasodilation)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Which drugs work by reducing blood/O2 demand?

How?

A
  • beta blockers (reduce HR)

- CCBs (reduce contractility)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Outline briefly how beta blocker work?

A
  • antagonists of B1 and B2 receptors
  • block the SNS
  • reduce HR/contractility
  • reduce CO/BP
  • protect myocytes from O2 free radicals
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What beta blockers may be used in treating angina?

A

bisoprolol

atenolol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is the rebound phenomena?

A
  • sudden cessation of beta blocker use may precipitate MI
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are the contraindications to beta blockers?

5

A 
asthma
peripheral vascular disease
Raynaud's phenomena
bradycardia/heart block
HF
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What are some adverse drug reactions that occur with beta blockers?

(3)

A

impotence
bradycardia (heart block)
bronchospasm (asthma)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What issues can arise from drug-drug interactions with beta blockers, and which drugs are the cause?

(2)

A
  • hypotension (other antihypertensives/NSAIDs)

- bradycardia (CCBs e.g. verapamil/diltiazem)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Outline briefly how calcium channel blockers (CCBs) work?

A
  • Prevent Ca2+ influx into myocytes and smooth muscle lining arteries and atrerioles by blocking the L-Type calcium channel.
  • rate limiting (reduced HR/contractility)
  • vasodilation (reflex tachycardia?)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What calcium channel blockers may be used in treating angina?

(4)

A

amlodipine/nifedipine
verapamil (rate limiting)
diltiazem (rate limiting)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

CCBs reduce vascular ____ and produce __________ and reduce _______.

A

tone
vasodilatation
afterload

22
Q

Rate limiting CCBs reduce the _______ and the force of myocardial ________.

A

heart rate

contractility

23
Q

CCBS may also produce coronary __________ but of little importance.

A

vasodilatation

24
Q

What are the contraindications to CCBs?

A

nifedipine:

  • never use immediate release
  • reflex tachycardia
  • risk of acute MI/stroke
25
Q

What are some adverse drug reactions that occur with CCBs?

4

A
  • ankle oedema (no response to diuretics)
  • headache
  • flushing
  • palpitations
26
Q

How do nitrates work?

What are the different types?

(3)

A
  • vasodilators
  • short acting
  • sustained release
27
Q

Give examples of nitrates that may be used in treating angina.

State how they act.

(3)

A
  • glyceryl trinitrate (GTN): short acting
  • isosorbide mononitrate: long acting
  • ivabradine (new drug)
28
Q

Briefly outline how nitrovasodilators work.

5

A
  • relax smooth muscle
  • releases NO
  • stimulates release of cGMP
  • reduced preload/afterload
  • reduced O2 consumption
29
Q

How do vasonitrates relieve angina, in terms of reducing afterload?

(3)

A
  • arterial dilation
  • reduced afterload
  • reduced myocardial O2 consumption
  • reduced O2 demand
30
Q

How do vasonitrates relieve angina, in terms of reducing preload?

(3)

A
  • peripheral venodilation
  • reducing venous return
  • reduced preload
  • reduced myocardial workload
31
Q

Why is GTN spray often administered sublingually?

A

to avoid first pass metabolism

32
Q

Which nitrates tend to be given orally?

2

A
  • sustained release, long acting nitrates

- used for prophylaxis

33
Q

When might nitrates be administered intravenously?

A
  • unstable angina

- in combination LMWH (e.g. enoxaparin)

34
Q

What is a problem associated with overuse of nitrates?

How is this overcome?

A
  • tolerance built up

- giving asymmetric dose, sustained release formulation

35
Q

What are some adverse drug reactions that occur with nitrates?

(2)

A
  • headache

- hypotension (GTN syncope)

36
Q

Which CCB tends to increase vasodilation?

A

amlodipine

37
Q

Which CCBs tends to reduce contractility and heart rate?

A

verapamil

diltiazem

38
Q

Advances in understanding of myocardial ischaemia have prompted evaluation of a number of new antianginal strategies, including:

Ischaemic preconditioning with _________.

A

nicorandil

39
Q

Advances in understanding of myocardial ischaemia have prompted evaluation of a number of new antianginal strategies, including:

Sinus node inhibition with _______.

A

ivabradine

40
Q

Advances in understanding of myocardial ischaemia have prompted evaluation of a number of new antianginal strategies, including:

Late Na+ current inhibition with __________.

A

ranolazine

41
Q
  • Activate “ATP sensitive potassium channels.
  • K+ entry into cardiac myocytes inhibits Ca2+ influx and so has a negative inotropic action.

Which drug is this describing?

A

nicorandil

42
Q
  • Nicorandil acts as a pharmacological ___________ agent.

- It has a ___________ effect.

A

preconditioning

cardioprotective

43
Q
  • a selective sinus node channel inhibitor.
  • slows the diastolic depolarisation slope of the SA-node.
  • results in a reduction in heart rate.

What drug is this describing?

A

Ivabradine

44
Q
  • inhibits persistent or late inward sodium current (INa) in heart musclein a variety of voltage gated sodium channels.
  • inhibiting that current leads to reductions in intracellular calcium levels.

Which drug is this describing?

A

Ranolazine

45
Q

________ is a potent inhibitor of platelet thromboxane production.

A

Aspirin

46
Q

Thromboxane stimulates ______________ and ____________.

A

platelet aggregation

vasoconstriction

47
Q

Aspirin

Use for the symptomatic treatment of chronic stable angina in adults with normal sinus rhythm and heart rate _____ bpm.

A

≥ 70

48
Q
  • inhibits ADP receptor activated platelet aggregation.
  • prevention of atherosclerotic events in PVD.
  • same incidence of bleeding as _______ but possibly lower GI bleeding.

Which drug is this prescribing?

What is the blank?

A

clopidogrel

aspirin

49
Q

What type of drugs are cholesterol lowering agents?

Give examples. (3)

A

statins

atorvastatin
simvastatin
pravastatin

50
Q

What is the treatment regime for stable angina? Give examples of drugs.

(10)

A
  • short acting nitrate (GTN)
  • beta-blocker (bisoprolol)
  • rate limiting CCB (verapamil, diltiazem)
  • dihydropiridine CCB (amlodipine)
  • long acting nitrate (isosorbide mononitrate)
  • new drugs (Ivabradine/ Ranolazine)
  • K channel activator (nicorandil)

Secondary preventors:

  • statin (atorvastatin)
  • antiplatelet (aspirin, clopidogrel)
  • ACE inhibitor
51
Q

What are the NICE guidlines, in terms of the order in which drugs should be prescribed for anginal patients?

A
  1. beta-blocker (+GTN)
  2. CCB
  3. combination, or other therapy
52
Q

What drugs should be taken as secondary preventors pf further ACS/MI? Give dosage.

(4)

A
  • aspirin (75mg/day)
  • atorvastatin (80mg/day)
  • ACE inhibitor
  • antihypertensives/beta-blocker

Cardiovascular System (37 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions