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AY Cardiovascular > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

What are lipids used for in the body?

A 
Membrane biogenesis 
Membrane integrity 
Energy source 
Precursors for hormones 
Signalling
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2
Q

How are non-polar lipids transported in the blood?

A

Within lipoproteins (e.g. HDL & LDL)

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3
Q

What is the basic structure of a lipoprotein?

A 
Hydrophobic core (contains triglycerides) 
Hydrophilic coat (contains cholesterol, phospholipids, apoproteins)
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4
Q

What are the 4 main lipoproteins?

A

HDL
LDL
VLDL
Chylomicrons

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5
Q

What apoproteins do HDL particles contain?

A

apoA1 & apoA2

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6
Q

What apoproteins do LDL particles contain

A

apoB-100

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7
Q

What apoproteins do VLDL particles contain?

A

apoB-100

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8
Q

What apoproteins do chylomicrons contain?

A

apoB-48

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9
Q

What is the role of ApoB-containing lipoproteins?

A

Deliver triglycerides to:

(i) muscle for ATP biogenesis
(ii) adipocytes for storage

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10
Q

Where are chylomicrons formed?

A

Intestinal cells

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11
Q

What do chylomicrons transport?

A

Dietary triglycerides

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12
Q

What pathway do chylomicrons use to transport triglycerides?

A

Exogenous pathway

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13
Q

Where area VLDL particles formed?

A

Liver cells

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14
Q

What do VLDL particles transport?

A

Triglycerides synthesised in that organ

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15
Q

What pathway do VLDL particles use to transport triglycerides?

A

Endogenous pathway

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16
Q

What are the steps in the ‘life cycle’ of an ApoB-containing liposome?

A

Assembly
Intraday ulnar metabolism
Receptor mediated clearance

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17
Q

What does Lipoprotein lipase (LPL) do?

A

Hydrolyses core triglycerides to free fatty acids and glycerol which enter tissues

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18
Q

Where does clearance of apoB-containing lipoproteins occur?

A

The liver

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19
Q

What is HMG Co-A reductase?

A

Rate limiting enzyme in de novo cholesterol synthesis

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20
Q

Which organ has the capacity to eliminate cholesterol from the body?

A 
The liver 
(Secreted into bike or used to synthesise bile salts)
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21
Q

What is the difference between primary and secondary dislipidaemia?

A

Primary - caused by diet & genetic factors

Secondary - consequence of other disease

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22
Q

What is the mechanism of action of statins?

A

Competitive inhibitor of HMG-CoA reductase

Rate limiting step in cholestrol synthesis in hepatocytes

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23
Q

How does inhibiting HMG-CoA reductase lower cholestrol?

A

Decreased cholestrol synthesis

Increase in LDL receptor expression

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24
Q

Benefits of statins?

A 
Lower cholesterol 
Decrease inflammation 
Reverse endothelial dysfunction 
Decreased thrombosis 
Stabilisation of atherosclerotic plaques
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25
Q

How are statins administered and at what time of day?

A

Orally at night

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26
Q

Adverse effects of statins?

A 
Myositis
Rhabdomyolosis (more likely if combined with a fibrate)
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27
Q

In what patients are fibrates first line treatment?

A

Patients with very high triglyceride levels

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28
Q

What is the mechanism of action of fibrates?

A

Agonists of PPAR alpha to enhance transcription of LPL encoding gene

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29
Q

Adverse effects of fibrates

A

Myositis
Rhabdomyolosis
(Best avoided in alcoholics)
Incidence for other adverse effects is greater than for statins

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30
Q

Example of bile acid binding resins?

A

Colestyramine
Cholestrol
Closevelam

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31
Q

What is the mechanism of action of bike acid binding resins?

A

Cause the excretion of bile salts resulting in more cholestrol being converted to bile salts

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32
Q

Adverse effect of bile resins?

A

G.I. tract irritation

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33
Q

What does ezetimibe do?

A

Reduces cholestrol absorption by inhibiting NPC1L1

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34
Q

Adverse effects of ezetimibe

A

Diarrhoea
Abdominal pain
Headache

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35
Q

In what patients is ezetimibe contraindicated?

A

Breast feeding females

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36
Q

Are lipids soluble in water?

37
Q

What is haemostasis?

A

Arrest of blood loss from a damaged blood vessel

38
Q

What are the actions in haemostasis?

A

Local vasoconstriction
Adhesion and activation of platelets at site of injury
Formation of fibrin (blood coagulation)

39
Q

What is thrombosis?

A

Pathological haemostasis

A haematological plug in the absence of bleeding

40
Q

What is Virchow’s triad?

A

Injury to vessel wall
Abnormal blood flow
Increased coagulability of the blood

41
Q

What colour is an arterial thrombus?

42
Q

What colour is a venous thrombus?

43
Q

Where do arterial thrombus’ normally lodge?

A

Artery in the brain or other organ

44
Q

Where does a venous thrombus normally lodge?

A

Lungs (PE)

45
Q

What is clotting factor II also known as?

A

Prothrombin

46
Q

How is vitamin K involved in blood clotting?

A

It mediates the enzyme which converts clotting factors (precursors) to active factors

47
Q

In what conditions are anticoagulants used?

A

DVT
Prevention of post-operative thrombosis
Patients with artificial heart valves
AF

48
Q

What is the major risk when prescribing warfarin?

A

Haemorrhage

49
Q

What is the mechanism of action of warfarin?

A

Competes with vitamin K for binding to hepatic vitamin K reductase preventing the conversion to the active hydroquinone

50
Q

How is warfarin admimistered?

51
Q

How long is the onset of warfarin?

52
Q

Factors that potentials warfarin action?

A 
Liver disease (decreased clotting factors)
High metabolic rate 
Drug interactions
53
Q

Factors that lessen warfarin action

A

Pregnancy
Hypothyroidism
Vitamin K consumption
Drug interactions

54
Q

How is overdose of warfarin treated?

A

Administer vitamin K or concentrate of plasma clotting factors

55
Q

What does antithrombin III do?

A

Inhibits coagulation by neutralising serine protease factors by binding to their active site

56
Q

What is the action of heparin?

A

Binds to antithrombin III, increasing its affinity for serine protease clotting factors particularly Xa and IIa (thrombin)

57
Q

Examples of LMWHs?

A

Enoxaparin

Dalteparin

58
Q

What is the difference between heparin and LMWHs?

A

LMWHs inhibit facto Xa not thrombin (IIa)

59
Q

What order of kinetics does heparin exhibit?

A

Zero order kinetics

60
Q

What order of kinetics do LMWHs exhibit?

A

First order kinetics

61
Q

Adverse effects of heparin and LMWHs?

A

Haemorrhage
Osteoporosis
Hypoaldosteroidnism
Hypersensitivity reactions

62
Q

How do platelets adhere to subendothelial molecules?

A

GPlb receptor

vWF (acts as bridge)

64
Q

What does the exposure of acidic phospholipids on platelet surfaces cause?

A

Promotes thrombin formation which stimulates further aggregation stabilised by formation of fibrin from fibrinogen

65
Q

Are anti-platelets mainly used in arterial or venous thrombosis?

66
Q

Are anti-coagulants mainly used in arterial or venous thrombosis?

67
Q

Example of anti-platelet drugs?

A

Aspirin
Clopidogrel
Tirofiban

68
Q

What is the mechanism of action of aspirin?

A

Blocks COX in platelets preventing TXA2 synthesis but also COX in endothelial cells inhibiting production of antithrombotic prostaglandin I2 (PGI2)

69
Q

What does TXA2 do?

A

Drive platelet aggregation

70
Q

Main side effect of aspirin

A

GI bleeding and ulceration

71
Q

What is the mechanism of action of clopidogrel?

A

Links to P2Y12 receptor by a disulphide bond producing irreversible inhibition

72
Q

What does P2Y12 do?

A

Helps secrete ADP which drives platelet aggregation

73
Q

When is clopidogrel most commonly used?

A

When patients are intolerant of aspirin

74
Q

When is Tirofiban used?

A

Given IV in short term management to prevent MI in high risk patients with unstable angina (with aspirin & heparin)

75
Q

What happens in the fibrinolytic cascade?

A

Plasminogen is converted to plasmid by tPA
Plans in converts fibrin to fibrin fragments
Fibrin fragments lyse clots

76
Q

What are fibrinolytics principally used in?

A

Reopen occluded arteries in MI or stroke

Less frequently in venous thrombosis

77
Q

Examples of fibrinolytic drugs?

A

Streptokinase
Alteplase
Duteplase

78
Q

What patients should streptokinase not be given in?

A

Patients who’ve had recent streptococcal infections

79
Q

Side effect of fibrinolytics

A

Haemorrhage

80
Q

How is haemorrhage induced by fibrinolytics controlled?

A

Tranexamic acid - inhibits plasminogen activation

81
Q

What do platelets adhere to after vascular damage?

A

Subendothelial molecules

82
Q

What substances drive platelet aggregation?

A

ADP, 5-HT and coagulation factors from storage granules

TXA2 synthesis via the enzyme COX

83
Q

Mechanism of action of spironolactone

A

Aldosterone receptor antagonist

84
Q

Side effects of spironolactone

A

Hyperkalaemia
Renal dysfunction
Gynaecomastia

85
Q

What does ivabradine do?

A

Slow heart rate

86
Q

When is ivabradine used?

A

If HR is fast despite beta blockers

87
Q

Side effects of digoxin

A 
Yellow vision 
Nausea 
Vomiting 
Bradycardia 
Heart block 
Arrhthymia's
88
Q

What is digoxins mechanism of action?

89
Q

What is the immediate therapy for acute LVF?

A
  1. Sit up
  2. Oxygen (beware COPD)
  3. IV furosemide
  4. IV diamorphine (not in COPD)

AY Cardiovascular (28 decks)

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