Brainscape's Knowledge GenomeTM

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


See full index

s2 - Embryo, Cardio, Endo, GI, Neuro, Pharm > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

Give 2 ways you can regulate HR/decrease SAN frequency

e.g. to treat angina, HF, arrythmias

A
  • VGCa2+C blockers aka CCB to slow the phase 0 upstroke

- Block the If channels to increase phase 4 reducing myocardial O2 demand

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

Dihydropyridines are an example of which type of Calcium Channel Blocker?

A

Vascular Selective

e.g. Amlodipine

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

Diphenylalkamines are an example of which type of Calcium Channel Blocker?

A

Cardiac Selective

e.g. Verapamil

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

Benzothiazepines are an example of which type of Calcium Channel Blocker?

A

Vascular AND Cardiac selective

e.g. Diltazem

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

How can CCBs worsen HF and cause heart block?

A
  • They can block cardiac myocyte action impairing contraction
  • they can block conduction at the AV node
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Ivabradine is an example of what type of drug?

A

If Channel Blocker

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

What action does Ach have on the autonomic control of SAN?

A
  • Acts at M2 recptors via Gai
  • decreased PKA, decreases If activiity
  • reduced HR (parasympathetic)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What effect B-blockers have?

A

e.g Atenolol

Reduce sympathetic effect on SAN so HR slows reducing work and o2 demands on heart

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

When should you not use B-blockers?

A 
Asthmatics
With CCBs (both may lead to bradycardia)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

How do Muscarinic Receptor Blockers stabilise CO?

A

e.g. Atropine

reduce vagal parasympathetic action on SAN so remove inhibitory vagal tone on HR, (HR increases)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Name 3 categories of ionotropic of agents and an example of each.

A

GaS Agonists e.g. Adrenaline. Dobutamine

PDE Inhibitors e.g. Amirone PDE 3i (heart specific)

Cardiac Glycosides e.g. Digoxin

Calcium Sensitisers e.g. Levosimedan, Omecamtiv

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

Why might a HF patient be given a GaS agonist such as glucagon in stead of Adrenaline/doputamine?

A

If the patient is taking B-blocker medication they will be given glucagon as the others will be innefective

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

How does the ionotropic agent, PDE3 inhibitor Amirone work?

A

causes c.AMP to build up, activates PKA
so more VGCaC and Ca influx
More CICR, TnC and contraction

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

How does digoxin increase contractility?

effect on HR?….

A

Inhibits the Na/K ATPase so Na+ builds up in the cell and there is less of a gradient for Ca2+ extrusion via the Na/Ca exchanger.
More Ca uptake into stores leading to more CICR

…it increases vagus activity so decreases HR

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

What is the advantage of calcium sensitisers over GaS agonist in increasing ionotropy?

A

GaS agonists are proarrythmyogenic as they increase HR. Also the Ca2+ rise they induce requires more Ca2+ ATPase activity/more 02 consumption
vs
Calcium sensitisers only increases the sensitivity of the contractile apparatus (not pro-arrythmyogenic)

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

How does the calcium sensitiser Levosimedan act?

A

Binds to TnC and increases binding of calcium to TnC

17
Q

How does the calcium sensitiser Omecamtiv act?

A

Increases actin-myosin interactions in absence of Ca2+ rise

18
Q

Give 2 reasons of giving a B-blocker in chronic HF.

A
  • prevent overworking by slowing HR and increasing coronary perfusion
  • reduce contractility so decrease 02 demand for more efficient functioning
19
Q

Decreasing BP can increases SV/CO.

Give 2 examples of drug types that do this?

A

Diuretics-via decrease blood vol, and CVP

AngRB-via blocking v.constriction so v.dilation results hence reduced TPR. Also less aldosterone so less water reabsorption, lower blood vol
ACEi

20
Q

L-Arginine with endothelium NO Synthase —> NO
NO causes vasodilation.
Give and example of a drug that mimics this process and what is it used for.

A

The nitrate donor GTN

Used to dilate coronary arteries during cardiac pain

21
Q

How does Sildenafil act?

A
  • it inhibits phosphodiesterase 5 which means less c.GMP is degraded
  • hence more NO release and vasodilation to maintain blood flow
22
Q

Name 2 pharmacological vasoconstrictor agents and their mechanism of action.

A

Norad - acts on a1 VSMC to increase TPR and BP and is cardiac protective
Adrenaline - in high conc is given to act at a1 VSMC as well as B1 receptors on heart to increase BP and HR

23
Q 
Pharmacological vasodilator agents block/inhibit
-ARB
-ACE 
-a1
-ETA 
give an example of each
A
  • ARB - Losartan
  • ACEi - Enalapril
  • a1-antagonist - Prazposin
  • ETA antagonist - Bosentan
24
Q

Where does the pharmacological vasodlilator agent, ‘Nicrorandil’ act?

A
  • at K+ channels opening them

- hyperpolarisation

25
Q

From what level is the sympathetic outflow?

NT used?

A

T1-L2 Thoracolumbar

Ach on Nic at pre. NA on a/B at post.

26
Q

From where is the parasympathetic outflow?

NT used?

A

CNIII, VII, IX, X and S2, S3, S4 - craniosacral

Ach on Nic at pre and at post-ganglionic fibres

27
Q

From what amino acid does DA, NA and A originate?

A

Tyrosine

28
Q

Dopamine is converted into NA by dopamine hyroxylase. What happens to the NA?

A

It is released from the nerve

In the adrenal medulla, PNMT can convert it to Adrenaline

29
Q

What effect does reserpine have on Adrenergic transmission?

A
  • prevents NA storage in vesicles
  • NA is broken down by MAO in cytoplasm
  • less NA released/decreased symp. activity
30
Q

What effect does tyramine have on Adrenergic transmission?

A
  • facilitates release by displacing NA from vesicles into cleft
  • increased symp. activity
31
Q

What causes the fusion of Ach vesicles with the pre-membrane?

A

Ca2+ entering the bouton

32
Q

Where is Ach broken down and by what?

A

In the synaptic cleft

By acetylcholinesterase

33
Q

How does botulism toxin affect cholinergic transmission?

A
  • degrades Ach vesicles so inhibits cholinergic motor activity
  • > dry mouth, blurred, muscle paralysis
34
Q

How does the Nic. Agonist, ‘Suxamethonium’ cause muscle relaxation?

A
  • stays at Nic receptor due to poor dissociation
  • sustained EJP leads to Na+ channels inactivating
  • prevents APs. This is ‘depolarising block’
35
Q

How is bradycardia brought about via parasympathetic system?

A
  • Vagus releases Ach, this acts at M2 receptors on SAN

- decreased frequency of pacemaker potentials

36
Q

How does stimulation of the pre-synaptic a2 receptor by excess NT (e.g. NA) cause decrease NT release?

A

Gai - PKA decreases, less Ca2+ activity as less channels phosphorylated
So less vesicles fuse

37
Q

Where does NA preferentially act?

A 
alpha receptors
(coronary/skeletal muscle = v.rich in B receptors so get vasodilation here instead)

s2 - Embryo, Cardio, Endo, GI, Neuro, Pharm (6 decks)

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