Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Cardiovascular System > SIHD & Angina - Therapy > Flashcards

SIHD & Angina - Therapy Flashcards

(52 cards)

Start Studying
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 _______.

Study These Flashcards
A

tone
vasodilatation
afterload

22
Q

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

Study These Flashcards
A

heart rate

contractility

23
Q

CCBS may also produce coronary __________ but of little importance.

Study These Flashcards
A

vasodilatation

24
Q

What are the contraindications to CCBs?

Study These Flashcards
A

nifedipine:

  • never use immediate release
  • reflex tachycardia
  • risk of acute MI/stroke
25
What are some adverse drug reactions that occur with CCBs? | 4
- ankle oedema (no response to diuretics) - headache - flushing - palpitations
26
How do nitrates work? What are the different types? (3)
- vasodilators - short acting - sustained release
27
Give examples of nitrates that may be used in treating angina. State how they act. (3)
- glyceryl trinitrate (GTN): short acting - isosorbide mononitrate: long acting - ivabradine (new drug)
28
Briefly outline how nitrovasodilators work. | 5
- relax smooth muscle - releases NO - stimulates release of cGMP - reduced preload/afterload - reduced O2 consumption
29
How do vasonitrates relieve angina, in terms of reducing afterload? (3)
- arterial dilation - reduced afterload - reduced myocardial O2 consumption - reduced O2 demand
30
How do vasonitrates relieve angina, in terms of reducing preload? (3)
- peripheral venodilation - reducing venous return - reduced preload - reduced myocardial workload
31
Why is GTN spray often administered sublingually?
to avoid first pass metabolism
32
Which nitrates tend to be given orally? | 2
- sustained release, long acting nitrates | - used for prophylaxis
33
When might nitrates be administered intravenously?
- unstable angina | - in combination LMWH (e.g. enoxaparin)
34
What is a problem associated with overuse of nitrates? How is this overcome?
- tolerance built up | - giving asymmetric dose, sustained release formulation
35
What are some adverse drug reactions that occur with nitrates? (2)
- headache | - hypotension (GTN syncope)
36
Which CCB tends to increase vasodilation?
amlodipine
37
Which CCBs tends to reduce contractility and heart rate?
verapamil | diltiazem
38
Advances in understanding of myocardial ischaemia have prompted evaluation of a number of new antianginal strategies, including: Ischaemic preconditioning with _________.
nicorandil
39
Advances in understanding of myocardial ischaemia have prompted evaluation of a number of new antianginal strategies, including: Sinus node inhibition with _______.
ivabradine
40
Advances in understanding of myocardial ischaemia have prompted evaluation of a number of new antianginal strategies, including: Late Na+ current inhibition with __________.
ranolazine
41
- 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?
nicorandil
42
- Nicorandil acts as a pharmacological ___________ agent. | - It has a ___________ effect.
preconditioning | cardioprotective
43
- 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?
Ivabradine
44
- inhibits persistent or late inward sodium current (INa) in heart muscle in a variety of voltage gated sodium channels.  - inhibiting that current leads to reductions in intracellular calcium levels. Which drug is this describing?
Ranolazine
45
________ is a potent inhibitor of platelet thromboxane production.
Aspirin
46
Thromboxane stimulates ______________ and ____________.
platelet aggregation | vasoconstriction
47
Aspirin Use for the symptomatic treatment of chronic stable angina in adults with normal sinus rhythm and heart rate _____ bpm.
≥ 70
48
- 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?
clopidogrel | aspirin
49
What type of drugs are cholesterol lowering agents? Give examples. (3)
statins atorvastatin simvastatin pravastatin
50
What is the treatment regime for stable angina? Give examples of drugs. (10)
- 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
What are the NICE guidlines, in terms of the order in which drugs should be prescribed for anginal patients?
1. beta-blocker (+GTN) 2. CCB 3. combination, or other therapy
52
What drugs should be taken as secondary preventors pf further ACS/MI? Give dosage. (4)
- 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.
© 2025 Bold Learning Solutions. Terms and Conditions