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Extra Y2 > Pharm Term 2a > Flashcards

Pharm Term 2a Flashcards

1
Q

Give a drug that only blocks If current (funny current)

A

ivabradine

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2
Q

Two classes of CCB

A

TWO CLASSES:
Rate slowing (Cardiac and smooth muscle actions)
Phenylalkylamines (e.g. Verapamil)
Benzothiazepines (e.g. Diltiazem)

Non-rate slowing (smooth muscle actions – more potent)
Dihydropyridines (e.g. amlodipine)

Non rate slowing Calcium antagonists have pretty much No effect on the heart. However, Profound vasodilation can lead to reflex tachycardia

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3
Q

What are the side effects of verapamil?

A
  • Bradycardia and AV block (too much Ca2+ channel block, this happens when you take it chronically and their effects can build up)
  • Constipation (blocked Gut Ca2+ channels,=reduced motility)
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4
Q

Give an example of ARB

A

Lorsartan

‘sartan’ = ARBs

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5
Q

Give an example of ACE inhibitor

A

enalapril, ramipril

‘pril’= ACE inhibitors

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6
Q

give an examples of dihydropyridines (non rate limiting CCB)

A

Nitrendipine
Amlodipine
Nisoldipine

Nitrendipine and nisoldipine are from first year

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7
Q

a1 blocker example

A

prazosin

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8
Q

What are the side effects of verapamil?

A
  • Bradycardia and AV block (too much Ca2+ channel block, this happens when you take it chronically and their effects can build up)
  • Constipation (blocked Gut Ca2+ channels,=reduced motility)
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9
Q

What are the side effects of dihydropyridines?

A
  • Ankle oedema - vasodilation allows more blood into capillary beds and so increased hydrostatic pressure
  • Headaches/flushing - vasodilation in brain and peripheral vasodilation causes flush
  • Palpitations- baroreceptor reflex due to reduced TPR
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10
Q

how does adenosine work

A

VSMC:
Bind to A2 (adenosine 2) receptors and stimulates cAMP to cause relaxation. (B2 also uses cAMP to cause relaxation)

SAN and AVN:
Bind to A1, decreases cAMP and slows the heart down. Nb this is the same mechanism as M2 receptors for para NS. Ach from vagus binds to M2 receptors which reduces cAMP. See notes for more details

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11
Q

What is the target of cardiac glycosides like digoxin?

A

Na+/K+ ATPase

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12
Q

side effects of amiodarone

A

Amiodarone accumulates in the body (t½ 10 - 100days)
Has a number of important adverse effects including:
- photosensitive skin rashes
- hypo- or hyper-thyroidism
- pulmonary fibrosis

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13
Q 
Uses of:
adenosine
verapamil 
amiodarone
digoxin
A

adenosine: terminate supraventricular tachyarrhythmias
verapamil: Reduction of ventricular responsiveness to atrial arrythmias
amiodarone: supraventricular and ventricular tachyarrhythmias/ re-entry circuit problems
digoxin: atrial fibrillation and flutter

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14
Q

most potent cannabinoid

A

delta 9 THC

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15
Q

what is the potent metabolite from the breakdown of the cannabinoid THC

A

11-OH-THC

more potent than delta 9 THC

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16
Q

name an endogenous cannabinoid

A

anandamide

we have CB1 and CB2 receptors for a reason

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17
Q

Cannabinoid receptor location

A

CB1 - brain

CB2 immune cells

18
Q

which area in the brain does cannabis interact with which causes the psychotic/schizophrenic effects? What is this area involved in?

A

anterior cingulate cortex
-Involved in error detection
eg GREEN (this is grey)
-Involved with performance monitoring with behavioural adjustment in order to avoid losses (eg you are talking + driving on an easy road then theres a slope and you need to focus so u stop talking- example of performance monitoring and adjustment )
long term cannabis users = hypoactivity in ACC

19
Q

What are the two main groups of neurones that are involved in stimulating appetite?

A

MCH (melanin concentrating hormone) neurones

Orexin neurones

20
Q

how does cannabis increase hunger

A

Cannabis inhibits the inhibitory effect of GABA on MCH neurones, thus leading to increased MCH firing
Cannabis also directly stimulates orexin production
This leads to hunger

21
Q

How does cannabis cause tachycardia and vasodilation

A

act on TRPV1 receptor rather than CB receptors

vasodilation common in conjunctivae hence blood shot eyes

22
Q

State 4 drugs that are either cannabinoid agonists or antagonists.

A 
Agonists:
Dronabinol - act like Delta-9-THC 
Nabilone - act like Delta-9-THC 
Sativex -  act like Delta-9-THC + cannabidiol 
Antagonists:
Rimonabant – CB1 antagonist
23
Q

how does cannabis cause memory loss

A

inhibits production of BDNF(brain derived neurotrophic factor) which is involved in memory formation in hippocampus

24
Q

What is sativex used for

A

Treatment for symptom improvement in adult patients with moderate to severe spasticity due to multiple sclerosis

25
Q

What can Rimonabant be used for?

A

Anti-obesity medication (it was removed from the market because it was shown to cause depression and suicidal thoughts)
weed makes you hungry

26
Q

cocaine half life

A

20-90mins v quick

27
Q

where is cocaine metabolised

A

liver and plasma hence very short half life

to ecognine methyl ester + benzoylecognine

28
Q

half life of nicotine

A

1-4 hours

29
Q

2 side effects of cocaine

A

CVS (myocardial infarction)

Hyperthermia

30
Q

where is nicotine broken down and what is it broken down into

A

liver

into cotinine which is excreted via urine

31
Q

Name a drug used in alcohol aversion therapy

A

disulfiram
aldehyde dehydrogenase inhibitor, leads to increase in acetaldehyde and hence the person will feel ill after drinking alcohol as acetalddehye is toxic

32
Q

2 enzymes that convert alcohol to aldehyde in the liver and 1 enzyme that converts aldehyde to acetic acid

A

alcohol dehydrogenase and mixed function oxidase

then aldehyde dehydrogenase

33
Q

What does dabigatran block

A

It is an anticoagulant involved in blocking factor 2a during the initiation stages of coagulation.

34
Q

What does rivaroxaban block

A

factor 10a inhibitor (part of the prothrombinase complex)

35
Q

Drug that increase antithrombin activity?

A

Heparin, 2 types:

heparin and low molecular weight heparin eg Dalteparin

36
Q

3 stages of coagulation (sohag structure)

A

initiation- activation of thrombin by prothrombinase complex
amplification- thrombin then activates platelets which makes them sticky and aggregate
Propagation- Now we have activated platelets plus a lot of thrombin as well. Thrombin converts fibrinogen to fibrin

37
Q

summarise amplification stage

A

F2a binds to PAR receptor which leads to ADP release from platelets. ADP bind to P2Y12 receptor via autocrine signalling.

PAR and P2y12 activation lead to COX activation, which produces Thromboxane A2. Thromboxane A2 allows Gp2b/3a production which allows platelets to stick together

38
Q

name an irreversible COX1 inhibitor

A

aspirin

39
Q

name a P2y12 receptor antagonist (ADP receptor antagonist)

A

Clopidogrel

40
Q

Name a Gp2b/3a receptor antagonist

A

abciximab

41
Q

name a thrombolytic

A

alteplase - recombinant tPA

Extra Y2 (16 decks)

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