Brainscape's Knowledge GenomeTM

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


See full index

Y1 Cardiovascular > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

Muscle contraction mechanism

A
  1. L type Ca2+ channels open (due to depolarisation), allowing Ca2+ influx
  2. Ca2+ binds to troponin C and cause troponin-tropomyosin complex to move away from myosin binding site on actin
  3. allows troponin-tropomyosin complex to bind to actin and cause muscle contraction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Muscle relaxation mechanism

A
  1. L type Ca2+ channels close
  2. Ca2+ actively transported out of the cell via NCXR
  3. Ca2+ actively transported back into SR via SERCA
  4. reduction in Ca2+ causes troponin-tropomyosin to block myosin binding site, preventing myosin from binding -> muscle relaxation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Examples of beta adrenoceptor agonists

A

Adrenaline
Noradrenaline
Dobutamine

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

What type of adrenoceptor are adrenaline and noradrenaline

A

Mixed adrenoceptor - acts on beta and alpha adrenergic receptors

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

Which adrenergic receptor is adrenaline more effective

A

beta adrenergic

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

Which adrenergic receptor is noradrenaline more effective in

A

alpha adrenergic

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

What type of adrenergic receptor is dobutamine selective for

A

beta 1

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

Effects of beta adrenergic agonists

A
  1. positive chronotropic
  2. positive inotropic
  3. positive dromotropic
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is the overall effect of beta adrenergic receptor agonists

A

Increases HR and force of contraction (contractility) hence increases cardiac output
Increases O2 consumption of the heart muscle

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

Use of adrenaline

A

cardiac arrest

anaphylactic shock

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

What are the additional effects of adrenaline except from positive chronotropic and inotropic effects

A

Acts on alpha 1 adrenergic receptors - Constriction of arterioles in skin / gut / mucosa to redirect more blood to the heart

Acts on beta 2 adrenergic receptors - Dilatation of coronary arteries to increase blood flow

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

What is cardiac arrest

A

When the heart suddenly stops pumping, can be due to coronary artery disease blocking the coronary arteries

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

Side effects of adrenaline

A

tremor
arrhythmias
headache

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

Why does adrenaline have additional effects

A

because it is a non-selective beta agonists and it can also bind to alpha adrenergic receptorss

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

Uses of dobutamine

A

Acute heart failure

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

What is acute heart failure

A

Weakening of heart’s ability to contract

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

Side effects of dobutamine

A

Tachycardia
headache
palpitations

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

Examples of non-selective beta blockers

A

propanalol
nadalol
pindolol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Examples of selective beta blockers

A

atenolol
bisoprolol
metoprolol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What does the effect of beta blockers depend on

A

the degree of sympathetic stimulation because beta adrenergic receptors are used only during sympathetic stimulation (when not used, blocking it has no effect bc it is not producing an effect anyways)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Effect of beta blockers

A

Decreases HR and force of contraction hence cardiac output

Decreases O2 consumption

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Uses of beta blockers

A

Angina - first line treatment apart from CCB
Arrhythmias - supraventricular tachycardia and AF - first line treatment
Compensated heart failure
Post MI management

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

How does beta blockers help with arrhythmias

A

Decreases excessive sympathetic activity and conduction velocity through AV node

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What should you be aware of in using beta blockers for compensated heart failure

A

Use low doses only

Because some patients may have compensated heart failure by using sympathetic drive

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Which beta blocker is used in heart failure

A

carvedilol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Side effects of beta blockers

A 
bronchospasm 
aggravation of heart failure 
bradycardia 
hypoglycaemia 
fatigue
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Why may beta blockers cause hypoglycaemia

A

Because B2 recepors in liver controls the release of glucose

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Effects of muscarinic antagonists

A

No effect on force of contraction

Increases HR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What type of drug is atropine

A

muscarinic antagonist

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Use of muscarinic antagonist

A

First line treatment for bradycardia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Contraindications for beta blockers

A

Asthma

Use of verapamil

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Side effect of ACE inhibitors

A

hyperkalaemia
cough
angio-oedema
first dose hypotension

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Example of thiazide diuretic

A

hydrochlorothiazide
indapamide
Bendrofluazide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Which conditions contraindicate the use of thiazide diuretics

A

Hypokalaemia
Hypercalcaemia
Hyponatraemia
Addison’s disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Mechanism of action of diuretics

A

Increases urination hence loss of fluid, including Na+ -> loss of plasma volume -> lower blood pressure

Decreases excretion of Ca2+

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

What conditions do thiazide diuretics treat

A

heart failure - to relief resistant oedema

resistant hypertension - last line of treatment for hypertension

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Side effects of diuretics

A

dehydration
postural hypotension
gout (painful form of arthritis)
impotence

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Which medication is used to treat digoxin toxicity

A

Digibind

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Example of angiotensin receptor blocker

A

candesartan

Losartan

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Mechanism of action of cardiac glycoside

A

Blocks Na+/K+ channel so there is no Na+ gradient for NCXR hence Ca2+ cannot be moved out of cell

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Inotropic drugs

A

Cardiac glycoside
PDE inhbitors
Levosimendan

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Mechanism of PDE inhibitors

A

PDE deactivates adenylyl cyclase which lowers cAMP

Inhibit PDE -> more cAMP -> more Ca2+

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Effect of PDE inhibitors

A

Positive inotropic

Vasodilation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Use of digoxin

A

Last line of treatment for Acute and chronic heart failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Side effects of digoxin

A 
Heart block 
Arrhythmia
disturbs colour vision 
diarrhea 
nausea
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Anti hypertensive drugs

A

ACE inhibitors
Calcium Channel Blockers
Diuretics
beta blockers (not used anymore unless present with other comorbidities)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Effect of ACE inhibitors

A

Venous dilatation -> decrease in preload
Vasodilation -> decrease in SVR -> decrease in BP
Decrease in release of aldosterone -> less Na+ and water reabsorption -> lower BP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Examples of ACE inhibitors

A

Ramipril
Lisinopril
enalapril

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Uses of ACE inhibitors

A 
Hypertension - first line treatment for those with type 2 diabetes
Heart failure (left ventrircular systole dysfunction) - first line treatment
Post MI managemnet
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Side effects of ACE inhibitors

A 
Dry cough (most common) 
Hyperkalaemia 
hyponatraemia 
Initial dosage hypotension 
Angio-oedema (life threatening)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

What drug can be used if ACE inhibitors are not well tolerated

A

Angiotensin Receptor blocker

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

What conditions contraindicates the use of ACE inhibitors

A

Chronic kidney disease
Severe valve disease
Pregnancy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

What type of drug is Losartan and Candesartan

A

Angiotensin receptor inhibitor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

What causes dry cough when using ACE inhibitors

A

bradykinin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

Effect of Calcium channel blockers

A

Negative inotropic
Negative chronotropic (bc phase 0 of nodal action potential depends on L type Ca2+ channels)
Vasodilation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

Why is calcium channel blockers used against hypertension

A

Blocks L type Ca2+ channels on vascular smooth muscle
less Ca2+ influx -> less CICR -> less Ca2+ binds with CaM -> less activation of myosin LCK -> less phosphorylation of myosin LC -> less muscle contraction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

Examples of CCB

A

Verapamil - selective for cardiac L type Ca2+ channels
Amlodipine - selective for smooth muscle L type Ca2+ channels
Dilitiazem - intermediate selectivit.y

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

Use of CCB

A

Hypertension (amlodipine) - first line treatment
Angina (verapamil) - used with GTN when beta blockers are contraindicated
Arrhythmia (verapamil / dilitiazem)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

Drugs for angina

A

Beta blockers - first line
CCB - if beta blocker not tolerated
Nitrates - if beta blocker not tolerated
ACE inhibitors - for patients with diabetes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

Side effects of amlodipine

A

hypotension
dizziness
swollen ankles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

How does Nitric Oxide affect the vasculature

A

It diffuses into smooth muscle from endothelium, activating cGMP to inhibit myosin LCK and stimulate myosin phosphatase

62
Q

Mechanism of organic nitrates

A

at low dose - venodilation

at high dose - vasodilation

63
Q

Effect of organic nitrates

A

1) decreased preload
2) decreased afterload
3) vasodilation of collateral arteries in patients with angina

64
Q

Why are organic nitrates used in angina

A

In angina patients, collateral vessels develop between healthy and diseased vessels. Nitrates cause vasodilation of those collateral vessels so redirect blood flow to ischaemic area

65
Q

Uses of organic nitrate

A

Angina - if beta blockers not tolerated

Acute MI

66
Q

How do patients with angina benefit from using nitrates

A

1) increased blood flow to ischaemic area

2) decrease preload and afterload so lower O2 requirement

67
Q

Side effects of Nitrates

A

Headaches
Hypotension
Fainting

68
Q

Examples of nitrates

A

GTN

Isosorbide mononitrate - prophylaxis for angina

69
Q

Drugs for heart failure (first line)

A

Diuretics
Beta blockers
ACE inhibitors
AT inhibitors if ACE inhibitors not tolerated

70
Q

What is haemastasis

A

Arrest of blood loss from injury

71
Q

List the 3 main steps of blood clot

A

1) injury / damage to the vessel
2) Primary haemastasis - local vasoconstriction and formation of soft plug
3) Activation of coagulation cascade and formation of solid clot

72
Q

Describe primary haemastasis

A

1) damage to the blood vessel exposes collagen (at connective tissue layer) and thromboplastin
2) Platelets bind to collagen and becomes activated
3) Activated platelets release TXA2
4) TXA2 causes local vasoconstriction
4) TXA2 binds to TXA2 receptors (TP receptors) on platelets, causing platelets to release 5-HT and ADP
5) ADP binds to P2Y12 receptors to cause
- attract more platelets
- increased expression of GP receptors so binds more fibrinogen between platelets -> forms soft plug
- exposes acidic phospholipids that stimulate coagulation cascade
5) 5-HT binds to HT receptors to cause local vasoconstriction

73
Q

Describe coagulation cascade

A

Inactive factor X -> Active Xa by tenase
Active Xa and Va is part of prothrombin
Inactive factor II -> Active IIa by prothrombin = thrombin
Thrombin converts fibrinogen to fibrin = solid blood clot

74
Q

Where are P2Y12 receptors found

A

On platelets

75
Q

What is thrombosis

A

Pathological haemastasis

76
Q

Pathology of thrombosis

A

Virchow’s trial

  • abnormal blood flow
  • increased coagulability of blood
  • injury to vessel
77
Q

What conditions can cause abnormal blood flow

A

Atrial fibrillation / HF -> slow blood flow

Slow blood flow more likely to clot

78
Q

What conditions causes increased coagulability of blood

A 
Pregnancy
Physical inactivity 
dehydration 
prolonged bed rest / long flight 
smoking
alcohol 
obesity
79
Q

What is thrombophilia

A

Inherited or acquired condition that makes the blood more likely to clot

80
Q

Difference between arterial and venous thrombus

A

Arterial - platelets enriched ; white

Venous - red ; fibrin and erythrocytes enriched

81
Q

In which type of thrombus is anticoagulants normally used in?

A

Venous thrombus

82
Q

What type of drug is used for arterial thrombus

A

Antiplatelets because it is enriched with platelets

83
Q

Types of anticoagulants

A

Warfarin
Heparin
LMWH
DOAC

84
Q

Mechanism of action of warfarin

A

Blocks Vitamin K+ reductase (competes with vitamin K).

85
Q

Why is vitamin reductase needed in clotting

A

Vitamin reductase converts oxidised form of vitK into reduced form
Reduced form of vitK is needed in gamma carboxylation which converts inactive factors X, II, IV, VII to active form

86
Q

Uses of anticoagulants

A

prevention of venous thrombosis and embolism

87
Q

Features of warfarin

A

Slow onset of action (2-3 days)

Long half life

88
Q

Risk of using warfarin

A

Haemorrhage
low therapeutic ratio
conditions that increases risk of haemorrhage

89
Q

What does low therapeutic ratio mean

A

The therapeutic window is small; dose that gives therapeutic effects is close to dose that cause toxicity

90
Q

What factors potentiate effects of warfarin (increase risk of haemorrhage)

A 
liver disease
increased metabolism of clotting factors
Drugs
- aspirin 
- NSAID
- drugs that reduce vitamin K
91
Q

Why shouldn’t aspirin be used with warfarin

A

It inhibits platelet functions which potentiates the effect of warfarin and increases risk of haemorrhage

92
Q

What measures the time it takes for blood to clot

A

INR

93
Q

How should the use of warfarin be monitored

A

By monitoring INR

94
Q

Contraindications for warfarin

A

third / late trimesters of pregnancy

patients that are due to have surgery

95
Q

How to manage overdose of warfarin

A

Give vitamin K (as phytomenadione)

Give plasma clotting factors

96
Q

Mechanism of action of heparin

A

binds to antithrombin IIIa and increases its affinity for active factors Xa and IIa
Antithrombin IIIa inactivates those factors

97
Q

Administration of warfarin

A

Orally

98
Q

Use of warfarin (except for prevention of venous thrombosis and embolism)

A

arterial thrombosis in patients with synthetic valves / atrial fibrillation

99
Q

Use of LMWH (except for prevention of venous thrombosis and embolism)

A

ACS; patients with NSTEMI that need immediate angiography

100
Q

Administration of heparin

A

IV - for immediate effect

SC - delayed an hour

101
Q

Side effects of heparin and LMWH

A

Haemorrhage
Osteoporosis
Hypoaldosteronism - hyperkalaemia
Hypersensitivity reactions

102
Q

Difference between heparin and LMWH

A

LMWH does not inactivate factor IIa

Lower risk of haemorrhage, osteoporosis, HIT

103
Q

What is HIT

A

heparin induced thrombocytopenia - increases risk of thrombosis; a side effect of heparin and less commonly LMWH

104
Q

Administration of LMWH

A

IV

105
Q

Example of LMWH

A

enoxaparin

dalteparin

106
Q

Why is heparin more preferred in renal failure

A

Because LMWH requires renal excretion

107
Q

Examples of DOAC - direct inhibition of thrombin

A

Dabigatran

108
Q

Examples of DOAC - direct inhibition of Xa

A

Rivaroxiban
Apixaban
fondaparinux

109
Q

Examples of antiplatelets

A

Aspirin
Clopidogrel
Prasugrel
Ticagrelor

110
Q

Mechanism of action of aspirin

A

Irreversibly blocks COX which synthesizes TXA2

Only start producing TXA2 again when affected platelets are replaced

111
Q

Use of aspirin

A

Prevention of arterial thrombosis and embolism
Acute coronary syndrome
Treatment for acute ischaemic attack

112
Q

Administration of aspirin

A

Orally

113
Q

Side effects of aspirin

A

GI bleeding and ulceration

Reye’s syndrome - more common in children

114
Q

Contraindications for aspirin

A

Children

Previous GI ulceration history

115
Q

Mechanism of action of clopidogrel

A

Blocks P2Y12, prevents ADP from binding

116
Q

Use of clopidogrel

A

Prevention of arterial thrombosis and embolism

Acute coronary syndrome

117
Q

Mechanism of action of fibrinolytics

A

Activates plasminogen which converts into plasmin that breaks down fibrin hence lyses the blood clot

118
Q

Use of fibrinolytics

A

Used when PCI is not available promptly

To reopen occluded arteries in MI / stroke

119
Q

Examples of fibrinolytics

A

Streptokinase
Duteplase
Alteplase

120
Q

What to do if haemorrhage occurs while using anticoagulants

A

Stop anticoagulant and reverse effect
Heparin - protamine
Warfarin - vitamin K (phynometadione) / plasma of clotting factors

121
Q

What is atherosclerosis associated to

A

Increased LDL, decreased HDL

122
Q

Why is LDL the bad cholesterol

A

Involved in formation of atherosclerotic plaque

123
Q

Why is HDL the good cholesterol

A

HDL can accept excess cholesterol and transport it back to liver to use it in bile

124
Q

Mechanism of action of statins

A

HMG CoA reductase inhibitors

125
Q

Effects of statins

A 
Decrease LDL
Decrease TAG 
Increase HDL 
Decrease thrombosis, inflammation
Reverse dysfunction of endothelium
Stabilize atherosclerotic plaque
126
Q

Examples of statins

A

Atorvastatin
Simvastatin
Prevastatin
Fluvastatin

127
Q

When should fluvastatin be used

A

When you don’t know if the patient can tolerate statin or not

128
Q

Why should fluvastatin be used in patients with unknown tolerance of statin

A

Because it has lowest efficacy

129
Q

Uses of statin

A

First line prevention if the patient has high cholesterol

130
Q

Why is statin prescribed at night

A

Because HMG CoA reductase has highest activity at night

131
Q

Side effects of statin

A 
Diarrhea 
Myopathy (rhabdomyolysis) 
Drug induced liver injury
dizziness 
Headache
132
Q

What life threatening myopathy can statin cause

A

rhabdomyolysis

133
Q

What rare side effect may atorvastatin cause

A

angio-oedema

134
Q

Mechanism of action of fibrates

A

Agonists of PPAR to induce transcription of genes that encode LPL

135
Q

Examples of fibrates

A

Fenofibrate
Bezafibrate
Gemfibrozil

136
Q

Why are fibrates worse than statin

A

Better than statin at increasing HDL and decreasing TAG but worse than statin at decreasing LDL

137
Q

Side effects of fibrates

A

Diarrhea
Nausea
GI upset

138
Q

When are fibrates used

A

when the patient has hypertriacylglyceridemia and low HDL

139
Q

Mechanism of bile acid binding resin

A

Blocks reabsorption of bile acid so forces the body to use more cholesterol to produce bile

Lower cholesterol -> more LDL receptors -> more LDL clearance

140
Q

Is atropine a selective or non-selective muscarinic antagonist

A

Non-selective

141
Q

Where are M2 receptors found and what does blocking them do

A

Heart; positive chronotropic effect

142
Q

Where are M3 receptors found

A

Smooth muscles - vessels / bronchi
Endocrine glands
Exocrine glands

143
Q

What decreases the effect of ACE inhibitors and what may occur

A

NSAIDs such as ibuprofen

this causes blood pressures to still be high despite taking ACE inhibitors

144
Q

Example of 5-HT antagonist to treat leg claudication

A

Naftidrofuryl

145
Q

Mechanism of action of adenosine

A

Adenosine receptor agonist; binds to A1 receptor in AV node, inhibit adenylyl cyclase

146
Q

Treatment for recurrent DVT or PE despite adequate anticoagulation

A

Insert inferior vena cava filter

147
Q

What receptors do ACh released from preganglionic neurone act on

A

Nicotinic receptors

M1 receptors

148
Q

Side effect of bile acid sequestrants

A 
Vitamin deficiency 
Constipation
Indigestion
Abdominal cramps 
Bloating
149
Q

What causes vitamin deficiency when using bile acid sequestrants

A

malabsorption of fat due to less micelles formed (caused by less bile acid) = malabsorption of fat soluble vitamins

150
Q

What type of vitamin deficiency causes excessive bleeding

A

Vitamin K

Y1 Cardiovascular (6 decks)

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