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M103 T3 > M103 T3 L14 > Flashcards

M103 T3 L14 Flashcards

1
Q

What are the two ways in which drugs are designed to treat hypercholesterolaemia?

A

to inhibit cholesterol uptake from GI tract

to reduce cholesterol production in liver

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2
Q

Where is cholesterol produced?

A

85% - liver

15% - food eaten

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3
Q

What are two examples of statins? (SIMulATOR)

A

SIMvastatin

ATORvastatin

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4
Q

What is the role of HMG CoA reductase?

A

used to synthesise CLSR in the liver

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5
Q

What is the effect of inhibiting HMG CoA reductase?

A

reduces the amount of cholesterol produced by the liver

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6
Q

What happens when the amount of cholesterol produced by the liver is reduced?

A

genes that produce the LDL receptor are activated
LDL particles bind to the LDL receptor on liver cells
LDL particles become internalised

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7
Q

Where are the LDL receptors expressed?

A

on the surfaces of cells that require CLSR - this is usually liver cells

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8
Q

When do cholesterol particles do the most harm?

A

when they are outside of cells in the bloodstream

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9
Q

When do cholesterol particles do the least harm?

A

when they are inside of cells

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10
Q

What are two examples of antiplatelet agents?

A

AsPiriN
cloPidogrEL

ANtiPlatELet

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11
Q

What is an example of an ACE Inhibitor?

A

rAmIpril

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12
Q

What are three examples of an ARB? (LOve VAlour CANDor)

A

LOS-artan
VALS-artan
CANDES-artan

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13
Q

What is the end goal of an ARB?

A

to decrease the workload of the heart

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14
Q

What three conditions does stable angina digress into?

A

unstable angina

NSTEMI, STEMI

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15
Q

How is stable angina treated?

A

(Bonk & CoNk)

β-blockers
CCBs
Nitrates

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16
Q

How is unstable angina treated?

A

stable angina treatment (Bonk & CoNk) + ANTIPLATELETS

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17
Q

Why are antiplatelets added when treating unstable angina?

A

bc the atherosclerotic plaques are more likely to rupture and form a thrombus in unstable angina

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18
Q

What are the antiplatelet drugs used to treat unstable angina?

A

aspirin

clopidogrel

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19
Q

G What are two alternatives to clopidogrel?

A

prasugrel

ticagrelor

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20
Q

What are the two phases platelets have to go through before agglutination can occur?

A

activation

aggregation

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21
Q

When do platelets begin to be activated?

A

when endothelial cells are damaged

when the plaque ruptures

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22
Q

Why are platelets activated when the plaque ruptures?

A

lots of substances under the endothelium drive their activation, e.g. ADP, collagen & COX

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23
Q

Which two substances are key to platelet activation?

A

ADP & TXA2

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24
Q

By what process does TXA2 further activate platelets?

A

positive feedback

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25
Q

How does aspirin work as an AntiplAtelet Agent?

A

it inhibits COX irreversibly
it prevents the production of TXA2
reduces platelet activation

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26
Q

What are three examples of ATP receptor antagonists?

A

(PCT)

clopidogrel
prasugrel & ticagrelor alternatives

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27
Q

What is the effect of ATP receptor antagonists?

A

they prevent platelet aggregation

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28
Q

Why is the prevention of platelet aggregation beneficial?

A

in a patient with unstable angina

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29
Q

How does platelet aggregation cause pain?

A

platelets sticking together block coronary arteries

cause the pain that’s associated with an ischaemic event

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30
Q

What is special about clopidogrel?

A

it was the first P2 Y12 receptor antagonist to be developed

it’s a prodrug

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31
Q

What activates clopidogrel?

A

CYP2C19

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32
Q

How does prasugrel work?

A

it undergoes hydrolysis by an esterase to form an intermediate compound, then an active compound

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33
Q

What is a disadvantage of both prasugrel and clopidogrel?

A

they both are irreversible

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34
Q

What is a consequence of the irreversibility of prasugrel and clopidogrel?

A

if bleeding occurs, it’s very difficult to reverse the effects of the drugs quickly

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35
Q

Which P2 Y12 receptor antagonist is reversible?

A

ticagrelor

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36
Q

What is the pathway of ticagrelor?

A

it’s absorbed from the gut
some gets metabolised
some is absorbed as the active ingredient
binds to the ATP receptor

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37
Q

What symptoms are used to diagnose a heart attack?

A

pain that does not go away with rest
sweating
tachycardia
cold clammy skin

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38
Q

What do the symptoms of a heart attack indicate about the NS?

A

that there is a problem with the sympathetic NS

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39
Q

What causes the symptoms of a heart attack?

A

heart has becomed damaged
cardiac output is impaired
bp drops and is detected by baroreceptors
they send signals to the medulla oblongata
activates the sympathetic system

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40
Q

What is the treatment for a heart attack?

A

pain relief, oxygen
aspirin / GTN
fibrinolytics

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41
Q

What is an example of a pain relief drug for treating a heart attack?

A

diamorphine

42
Q

What is an example of a clot busting drug?

A

tenecteplase

43
Q

What is the number one option for heart attack treatment?

A

pain relief

44
Q

What is the specific type pain common in patients who have had a heart attack?

A

a pain radiating through the shoulder and down the the arm

45
Q

What is the main reason for giving painkillers to patients with the radiating pain down the arm?

A

most people will think this pain is due to actively having a heart attack thanks to the media
this will cause anxiety

46
Q

What is the effect of anxiety on a patient who’s recently had a heart attack?

A

anxiety drives the sympathetic NS
it will make the heart work harder
the muscle cells are being asked to contract to relax much more forcibly and frequently than they would do normally
can cause ischaemia in the tissues - more likely to die bc they can’t get the neccessary oxygen supply for this activity

47
Q

What is the effect of diamorphine?

A

it decreases pain, anxiety & sympathetic activity

it increases vasodilation in the coronary arteries

48
Q

Why is oxygen administered to patients who have had a heart attack?

A

so that any blood that bypasses the blockage is maximally oxygenated
therefore it’s helping the tissue downstream of that blockage as best it can to to survive

49
Q

Why is GTN administered to patients who have had a heart attack?

A

it dilates coronary blood vessels

it reduces the workload of the heart

50
Q

Why is aspirin administered to patients who have had a heart attack?

A

to prevent any more thrombi from forming

51
Q

What is the effect of tenecteplase?

A

acts as a fibrinolytic - degrades clots

produces plasmin which breaks down fibrin

52
Q

What three types of drug are used to treat heart attacks? (Anti B.ACE)

A

Anticoagulant
Beta blockers
ACE inhibitors

53
Q

What is the effect of beta blockers?

A

they decrease cardiac workload

they prevent arrhythmias

54
Q

Why is metoprolol used in the hospital as a short term solution?

A

the hospital can adjust the dose very carefully bc of its short half life

55
Q

What is the effect of anticoagulants for patients in long term bed rest?

A

prevents thrombus formation

56
Q

What are examples of anticoagulants? (WAR.DabiL)

A 
warfarin
apixaban
rivaroxaban
dabigatran
LMWHs
57
Q

What is the effect of beta blockers against adrenaline?

A

they try to prevent adrenaline affecting the damaged heart muscle cells

58
Q

What is an example of a LMWH?

A

TINZAparin

59
Q

How does digoxin work?

A

it binds to the Na+/K+ ATPase and inhibits its action
this increases Na+ levels in the cardiomyocytes
AAR the Na+/Ca2+ exchanger is inhibited
build up of Ca2+ inside the muscle cell
leads to a stronger contraction

60
Q

What is digoxin used to treat?

A

HF that may develop from a heart attack

61
Q

What is the effect of digoxin?

A

it will ics the force of contraction of the heart

ics cardiac output

62
Q

What drug is used to treat dysrhythmias?

A

Amiodarone

63
Q

What type of drug is amiodarone?

A

a K+ channel blocker drug

64
Q

How does amiodarone work to reduce arrhythmias?

A

blocks some of the K+ channels
the actpts last longer - so the refractory period of ventricular myocytes is increased
can terminate arrhythmias

65
Q

What is heroin otherwise known as?

A

diamorphine

66
Q

What are ARBs otherwise known as?

A

Angiotensin receptor blockers

Ang II receptor antagonists

67
Q

What are ARBs used to treat?

A

high bp and HF

chronic kidney disease

68
Q

What medication is prescribed following a heart attack?

A

Angiotensin receptor blockers - ARBs

69
Q

Google How is unstable angina treated?

A

(antiplatelet agents) clopidogrel + aspirin (up to 12 months) + an ACE inhibitor

70
Q

For how long is unstable angina treated using clopidogrel + aspirin?

A

up to 12 months - most benefit occurs during the first 3 months

71
Q

G What are alternatives to clopidogrel in certain patients? (PT)

A

prasugrel or ticagrelor

72
Q

NHS What substance is used to treat stable angina?

A

GTN

73
Q

NHS What is the most common type of angina?

A

stable angina

74
Q

NHS How is GTN administered?

A

tablets (sublingual administration)

GTN mouth spray

75
Q

NHS What is the NHS advice for people having an angina attack?

A

Stop what you’re doing and rest.
Use your GTN medicine.
Take another dose after 5 minutes if the first one does not help.
Call 999 if you still have symptoms 5 minutes after taking the 2nd dose

76
Q

NHS When can GTN be used by patients at risk of angina attacks?

A

prophylactically before e.g. exercise

77
Q

NHS What might patients experience soon after using GTN prophylactically?

A

headache, flushing or dizziness

78
Q

NHS What is the difference between sublingual and buccal administration?

A

sublingual - drug placed under tongue to dissolve and absorb into the bloodstream through the tissue there
buccal - drug placed between gums and cheek, where it also dissolves and is absorbed into the bloodstream

79
Q

NHS When do GTN tablets expire?

A

about 8 wks after the packet is opened

80
Q

NHS When do GTN spray expire?

A

3 years

81
Q

What is the chemoreceptor of ADP?

A

P2Y12 receptors

82
Q

What happens when endothelial cells are damaged?

A

platelet activation: ADP < P2Y12 receptors (on platelets) < GPIIb/IIIa receptors expressed
fibrinogen binds to these GPIIb/IIIa receptors to crosslink different platelets

83
Q

How does ADP activate platelets?

A

it acts on P2Y12 receptors on the platelets, stimulating the expression of GPIIb/IIIa receptors

84
Q

Where are P2Y12 and glycoprotein IIb/IIIa receptors located?

A

on platelets

85
Q

How does COX indirectly activate platelets?

A

it produces TXA2

86
Q

By what processes are platelets activated?

A

ADP *pathway

COX *pathway

87
Q

What substance does aspirin inhibit?

A

COX, irreversibly

88
Q

How does clopidogrel and prasugrel work as ADP antagonists?

A

by blocking ADP’s receptors on platelets, P2Y12 receptors

89
Q

What does the expression of GPIIb/IIIa receptors on platelet surfaces allow for?

A

agglutination via these GPIIb/IIIa receptors
fibrinogen and blood proteins bind to the receptors on two different platelets, causing them to stick together [crosslink]

90
Q

What is clopidogrel’s relationship with CYP2C19?

A

it needs CYP2C19 to activate it

but the CYP2C19 has lots of polymorphisms, most of which reduce the activity of clopidogrel

91
Q

What is a consequence of the polymorphisms in CYP2C19 on the dosage / effectiveness of clopidogrel?

A

for a given dose of clopidogrel, the amount of the active compound in the bloodstream is far less than the prodrug dose initially given

92
Q

Why was prasugrel developed after clopidogrel was made available?

A

bc of the polymorphisms in CYP2C19 which activate clopidogrel, it needs a much higher dosage than it should
prasugrel works by a different pathway that doesn’t involve CYP2C19

93
Q

What is the difference between stable and unstable angina?

A

stable: angina symptoms during moderate+ physical activity, which go away with rest and/or medication
unstable: angina symptoms while doing very little or resting

94
Q

How do beta blockers work?

A

they block the release of the adr + noradr in certain parts of the body

95
Q

What happens to b-adrenergic receptors signalling pathways AAR of HF?

A

they undergo several adaptive and sometimes maladaptive regulatory changes

96
Q

What activities are beta-adrenergic receptors responsible for when activated?

A

modulating the heart rate and myocardial contractility

97
Q

What is the difference between arrhythmia and dysrhythmia?

A

nothing - they’re the same

98
Q

What is TXA2 produced by?

A

activated platelets during haemostasis that produce COX-1 isoform (from which TXA2 is synthesised)

99
Q

What is the role of TXA2?

A

has prothrombotic properties - it stimulates activation of new platelets and increases platelet aggregation via Glycoprotein (GP) IIb/IIIa receptors

100
Q

What is the difference between agglutination and aggregation?

A

agglutination - the joining of platelets only, without other cells and debris
aggregation - platelets, cells and debris clumping all together

M103 T3 (21 decks)

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