Brainscape's Knowledge GenomeTM

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


See full index

CVR 2 > Drug Treatment of Angina > Flashcards

Drug Treatment of Angina Flashcards

1
Q

what is angina?

A

check pain due to myocardial ischaemia
build up of metabolites [(eg adenosine, CO2 which dissolves in fluids) and lowers pH, lactate, K+ ions] activates sensory nerves
not a disease itself, it is symptoms

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

How does ischaemia (aninadequateblood supply to an organ or part of the body, especially the heart muscles.) develop?

A

An increase in myocardial oxygen demand which is not met

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

what are the 3 types of angina?

A

stable angina
unstable angina
variant angina

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

what is stable angina?

A

most common
attacks are predictable, eg exercise, stress
myocardial O2 demand not met
involvement of chronic occlusive coronary artery disease, i.e. atherosclerosis (use of cholesterol lowering drugs-statins)

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

what is unstable angina?

A

-attacks are unpredictable
-coronory artery occlusion due to platelet adhesion to ruptured atherosclerotic plaque (use of anti-platelet drugs)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what is variant angina?

A

least common
-attacks unpredictable
-coronory artery occlusion by vasospasm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is the effect of dilation of coronary arteries in treating angina? What are the benefits and negatives?

A
  • May be valuable in variant angina
  • Dangerous in stable and unstable angina - may cause coronary steal (where dilatation can occur, this sends more blood to already well perfused areas, but where dilatation cannot occur, less blood is delivered because of the fall in input pressure)\The arteries distal to the occlusion are maximally dilated, which means these vessels can’t dilate any more, but the normal coronary vessels elsewhere will dilate and “steal” blood away from where it is needed
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

how do beta-1 blockers work?

A
  • β1-adrenoceptor blockers – competitive reversible antagonists of adrenaline and noradrenaline at cardiac β1-adrenoceptor
  • reduced heart rate and force leading to reduced myocardial work
  • reduced myocardial O2 demand
    -used in all forms of angina
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

what are some examples of B-1 blockers?

A

propranolol (B1 and B2)
atenolol (B1 selective)

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

what are some adverse effects of beta -1 blockers?

A
  • Exacerbate asthma (block of β2-adrenoceptors in bronchi - avoid by use of alternative drug class)
  • Intolerance to exercise
  • Hypoglycaemia = deficiency of glucose in the bloodstream
  • Blockade of β-adrenoceptors may uncover α1-mediated constriction in coronaries
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

how do funny channel blockers work?

A
  • Not first line intervention
  • Recently introduced to treat angina (all forms)
  • Blocks If (Na+) current that contributes to SA node depolarisation towards threshold
  • Decreases heart rate but not force by slowing the signals of the sinus node
  • This is beneficial if there are other conditions/drugs that the patient is on that reduce inotropy
  • Leading to reduced myocardial O2 demand
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

what is an example of a funny channel blocker?

A

ivabradine

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

what is pre load?

A

amount of blood that comes back to the heart

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what is after load?

A

the force the heart has to contract against to open the aortic and pulmonary valves

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

how is the dilation of arteries changed by vasodilator drugs?

A

-decreased after load
-decreased myocardial work
-myocardial O2 demand

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

how is the dilation of veins changed by vasodilator drugs?

A

-decreased pre load

17
Q

how is the dilation of venous changed by vasodilator drugs?

A

-decreased venous return
-decreased pre load
-decreased stretch of ventricle + atria
-decreased strength of contraction
-decreased myocardial work
-decreased myocardial O2 demand

18
Q

what is the Bainbridge reflex?

A

If pre-load increases, you will get both the Starling and the Bainbridge reflex

19
Q

what are nitrovasodilators?

A
  • Particularly used for prophylaxis and immediate relief
  • Most commonly used anti-anginal
  • The primary therapeutic effect of nitrates is on the veins. At high doses you see arterial dilatation, which can lead to side effects like throbbing headache. You also get tolerance.
20
Q

what is GTN?

A

GTN (nitroglycerine, 10% in inert lactose base)

  • taken as sub-lingual tablet or spray
  • not orally active (destroyed by first-pass metabolism)
  • rapidly absorbed → rich blood supply
21
Q

what is amyl nitrate?

A

Amyl nitrite (volatile liquid)

  • vials opened and inhaled
  • not now used clinically but has become drug of abuse (poppers)

Both drugs rapid in onset, but action short-lived

22
Q

what are Isosorbide dinitrate/mononitrate?

A
  • taken orally
  • slower in onset and more prolonged in duration than GTN
  • used for sustained prophylaxis in all forms of angina
23
Q

what are the uses of nitrates?

A
  • prophylaxis in stable angina (i.e. taken immediately before exercise)
  • rapid relief of ongoing anginal attack (all forms)
24
Q

what are the mechanisms of action of nitrates?

A

All nitrovasodilators are pro-drugs

  • lipophilic - readily enter smooth muscle cells and are reduced to nitric oxide (NO)
  • they are termed “NO donors”
  • mimic action of endothelium-derived NO
25
Q

how do nitric oxides activate soluble granulate cyclase (sGC)?

A
  • cytoplasmic (soluble) enzyme
  • receptor on soluble guanylate cyclase contains a ferrous (Fe2+) haem moiety (like O2 binding site of haemoglobin)
  • NO binds to haem receptor leading to enzyme activation which converts GTP to cGMP
  • This results in an increase of cGMP, therefore vasodilatation
26
Q

what are the side effects of nitrovasodilators?

A
  • headache (dilatation of cerebral arteries) - particularly if you are naive to nitrates
  • tolerance on prolonged use – need drug free “washout” period to restore efficacy
27
Q

what are the classes of voltage gated Ca2+ channels and their location?

A

L (long lasting current - smooth muscles, cardiac muscles and pacemakers
T (transient current) - cardiac pacemakers and smooth muscle
N - neurones (Ca2+ for exocytosis)
P/Q (positive potentials) -neurones

28
Q

what does reduced Ca2+ entry result in?

A

coronory and peripheral arterial vasodilation

29
Q

what are some examples of L type calcium channel blockers?

A

-open channel block -cork in bottle
-phenylalkylelamines (verapamil
-benzothiazepines (diltiazem)

30
Q

What is the mechanism of action of the different L-type channel blockers?

A

-allosteric modulators bind at allosteric site and reduce probability of channel opening at a given voltage

31
Q

what is an example of a dihydropyridine antagonist?

A

nifedipine
increase probability of channel opening at a given voltage

32
Q

What are the different tissue selectivities of L-type Ca++ channel blockers?

A

smooth muscle - nifedipine>diltiazem>verapamil
cardiac muscle - verapamil- diltiazem > nifedipine

also have N-, L- and T-type VOCs in the ZG of the adrenal cortex- blocking may reduce biosynthesis of aldosterone

33
Q

What are the vascular actions of L-type Ca++ channel blockers?

A

Dilate arteries (little effect on veins) →↓Total peripheral resistance (TPR)

34
Q

what are the uses of L-type blockers?

A
  • anti-hypertensives (dihydropyridines preferred due to rebound tachycardia)
    • ↓ TPR plus ↓ C.O. due to ↓HR and ↓ SV
  • anti-anginals (drugs with more “cardiac” effects preferred due to less reflex tachycardia)
    • ↓ TPR → ↓ after-load and ↓ C.O → ↓myocardial Odemand
  • anti-dysrhythmic agents (Class IV)
  • verapamil > diltiazem > nifedipine
35
Q

what are the anti-anginal effects of Ca+ channel blockers?

A
  • dilate arteries (little effect on veins) therefore reduced after-load
  • Reduced myocardial O2 demand
  • Reduced heart rate and reduced force therefore reduced myocardial O2 demand
  • useful in all forms of angina
  • dilatation of coronary arteries valuable in variant angina (vasospasm) but may cause coronary steal in stable and unstable angina
  • nifedipine leads to coronary steal in 10% of patients
  • Other uses of L-type blockers:
    • anti-hypertensive agents (reduced TPR; reduced HR and reduced SV leading to reduced C.O.)
    • anti-dysrhythmic agents (Class IV)
36
Q

what are the limitations of beta-blockers, CCBs and nitrates?

A

-beta blockers-absolute or relative contradcation in asthma, COPD and peripheral vascular disease
-CCBs, heart failure in patients with poor LVEF, ineffective in preventing no reflow phenomenon, ADRs (flushing & peripheral oedema)
-nitrates, long term use associated with tolerance

37
Q

what is nicroandil?

A

K+ channel activation -> relaxation
-cardioprotective action is good
-key advantages- no tolerance, comparable efficiency and tolerability to existing agents, potent cardio protective action

38
Q

what is a hybrid compound?

A

-comprised of nicotinamide vitamin group and an organic nitrate
-mechanism of action like action increased level of cyclic guanosine monophosphate, decrease in cytosolic calcium, vascular smooth muscle relaxation dilation of coronory epicardial arteries

CVR 2 (9 decks)

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