Brainscape's Knowledge GenomeTM

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


See full index

Pharmacology > Pharm 8 - SNS Antagonists > Flashcards

Pharm 8 - SNS Antagonists Flashcards

1
Q

Describe the effects of Alpha 1 adrenoceptors.

A

Vasoconstriction

GI tract relaxation

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

Describe the effects of Alpha 2 adrenoceptors.

A

Inhibition of transmitter release

contraction of vascular smooth muscle

CNS actions

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

Describe the effects of beta 1 adrenoceptors.

A

Heart - increased heart rate + contractility
Kidneys - increased renin release
GI tract relaxation

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

Describe the effects of Beta 2 adrenoceptors.

A

Bronchodilation
Vasodilation
Relaxation of visceral smooth muscle
Hepatic glycogenolysis

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

Describe the effects of Beta 3 adrenoceptors.

A

Lipolysis

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

State 5 adrenoceptors antagonists and the receptors they block.

A 
Labetalol = alpha 1 + beta 1 (more beta 1 (4:1))
Phentolamine = alpha 1 + alpha 2
Prazosin = alpha 1
Propranolol = beta 1 + beta 2
Atenolol = beta 1
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

State 4 main clinical uses of SNS antagonists.

A

Hypertension
Angina
Arrhythmia
Glaucoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is defined as hypertension?

A

Sustained diastolic blood pressure greater than 90mmHg

or greater than 140/90

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

State the 3 things which contribute to hypertension.

A

Blood volume
Cardiac output
Peripheral vascular tone

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

What is the main control of blood pressure?

A

Sympathetic drive to the kidneys via beta 1

this triggers renin release from the kidneys causing increase in angiotensin II and aldosterone

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

Blockade of which receptors cause the positive and negative effects of beta blockers.

A

blockade of b1 = positive effects

blockade of b2 = negative effects

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

What effect is responsible for most of the anti-hypertensive effect of beta blockers?

A

b1 blockade in the kidneys leading to reduced renin release

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

What effect does beta 1 blockade have on the heart?

A

decrease in heart rate

decrease in cardiac output

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

How does the effect of beta blockers on the heart change with prolonged treatment?

A

reduced efficacy as heart begins to reset itself

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

What is the effect of presynaptic beta 1 receptors?

A

have a positive facilitation effect on the synthesis and release of a neurotransmitter

so blockade of this adds to the antihypertensive effect

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

State 4 conditions in which you would not give a patient a beta blocker.

A

1) Asthma - blockade of beta 2 will cause bronchoconstriction
2) Cardiac failure - rely on SNS input to have adequate cardiac output
3) COPD - bronchoconstriction via beta 2 blockade
4) Diabetes - masks the symptoms of hypoglycaemia + inhibits hepatic glycogenolysis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

State 2 side effects of beta blockers.

A

Fatigue

Cold extremities

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

Why would you still not give a cardioselective beta blocker to an asthmatic?

A

selectivity is based on concentration

19
Q

What are the effects of labetalol?

A

acts more on beta 1 than alpha 1
lowers blood pressure by reducing TPR via alpha 1

reduces heart rate and contractility via b1 blockade

20
Q

What is the main mediator of TPR?

A

Alpha 1 mediated vasoconstriction

21
Q

What are the effects of an alpha blocker?

A

vasodilation causing a fall in TPR and hence a fall in blood pressure

22
Q

What is the main side effect of alpha blockers?

A

Postural hypotension

reflex tachycardia via baroreceptors

23
Q

State some of the problems with non-selective alpha blockers ?

A

alpha 1 blockade will cause vasodilation and decrease in TPR

blockade of alpha 2 will cause INCREASE in transmitter release, so more noradrenaline released

this would enhance reflex tachycardia

24
Q

What are the effects of prazosin - alpha 1 antagonist?

A

leads to vasodilation and fall in TPR

get less tachycardia as not losing inhibitory alpha 2

25
Q

Describe the mechanism of action of methyldopa.

A

Methyldopa is taken up by noradrenergic neurones and is decarboxylated and hydroxylated for form alpha-methyl noradrenaline This is not deaminated by MAO so accumulates more than noradrenaline in the synapse Alpha-methyl noradrenaline displaces NA from the synaptic vesicles It is less effective than NA on alpha 1 receptors so does not cause as much vasoconstriction It is more effective than NA on alpha 2 receptors thus reducing noradrenaline release

26
Q

What are arrhythmias caused by and why?

A

Myocardial ischaemia

27
Q

What controls the pacemaker current in the heart?

A

Sympathetic drive

28
Q

What can precipitate or aggravate arrhythmias?

A

increase in sympathetic drive to the heart via b1

29
Q

What part of the heart’s electrical circuit depend on the sympathetic drive?

A

AV conductance

30
Q

What effect do beta antagonists have on the refractory period of the AV node?

A

increases the refractory period

slows down ventricular rate

31
Q

What class of drugs are beta blockers?

A

Class II anti-arrhythmics

32
Q

What is propanolol particularly effective at treating?

A

arrythmias causes by exercise or mental stress

33
Q

Define angina.

A

chest pain that occurs when oxygen supply to myocardium is insufficient for its needs.

34
Q

Describe the 3 different types of angina.

A

Stable - pain due to fixed narrowing

Unstable - pain with less and less exertion

Variable - occurs at rest, caused by coronary artery spasm

35
Q

What is the mechanism of unstable angina?

A

atheromatous plaque begins to rupture
Platelet fibrin thrombus associated with the ruptured plaque

high risk of infarction

36
Q

Describe how beta blockers can help prevent angina attacks.

A

decrease heart rate, contractility and systolic pressure

less oxygen demand on the heart

so less chance of reaching angina

37
Q

State some adverse side effects of beta blockers.

A 
Fatigue
Insomnia
Dizziness
Sexual dysfunction
Bronchospasm
Bradycardia
Heart block
Hypotension
Decreased myocardial contractility
38
Q

State some other circumstances in which you would not give a beta blocker?

A

hypotension
bradycardia
congestive heart failure
bronchospasm

39
Q

Where is aqueous humour produced?

A

ciliary body via carbonic anhydrase

40
Q

What dictate the amount of humour produced?

A

Blood flow in ciliary body

41
Q

Where does the humour drain into?

A

Trabecular meshwork in the canals of Schlemm

42
Q

How can adrenaline affect intraocular pressure?

A

can act on alpha 1 receptors to cause vasoconstriction and reduce blood flow through ciliary body

43
Q

Describe the use of beta antagonists in treating glaucoma.

A

Reduce the rate of aqueous humour produced by blocking receptors on ciliary body

44
Q

State some other used of beta antagonists.

A

Anxiety
Migraine
Benign tumours

Pharmacology (10 decks)

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