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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
How are statins administered and at what time of day?
Orally at night
26
Adverse effects of statins?
``` Myositis Rhabdomyolosis (more likely if combined with a fibrate) ```
27
In what patients are fibrates first line treatment?
Patients with very high triglyceride levels
28
What is the mechanism of action of fibrates?
Agonists of PPAR alpha to enhance transcription of LPL encoding gene
29
Adverse effects of fibrates
Myositis Rhabdomyolosis (Best avoided in alcoholics) Incidence for other adverse effects is greater than for statins
30
Example of bile acid binding resins?
Colestyramine Cholestrol Closevelam
31
What is the mechanism of action of bike acid binding resins?
Cause the excretion of bile salts resulting in more cholestrol being converted to bile salts
32
Adverse effect of bile resins?
G.I. tract irritation
33
What does ezetimibe do?
Reduces cholestrol absorption by inhibiting NPC1L1
34
Adverse effects of ezetimibe
Diarrhoea Abdominal pain Headache
35
In what patients is ezetimibe contraindicated?
Breast feeding females
36
Are lipids soluble in water?
No
37
What is haemostasis?
Arrest of blood loss from a damaged blood vessel
38
What are the actions in haemostasis?
Local vasoconstriction Adhesion and activation of platelets at site of injury Formation of fibrin (blood coagulation)
39
What is thrombosis?
Pathological haemostasis | A haematological plug in the absence of bleeding
40
What is Virchow's triad?
Injury to vessel wall Abnormal blood flow Increased coagulability of the blood
41
What colour is an arterial thrombus?
White
42
What colour is a venous thrombus?
Red
43
Where do arterial thrombus' normally lodge?
Artery in the brain or other organ
44
Where does a venous thrombus normally lodge?
Lungs (PE)
45
What is clotting factor II also known as?
Prothrombin
46
How is vitamin K involved in blood clotting?
It mediates the enzyme which converts clotting factors (precursors) to active factors
47
In what conditions are anticoagulants used?
DVT Prevention of post-operative thrombosis Patients with artificial heart valves AF
48
What is the major risk when prescribing warfarin?
Haemorrhage
49
What is the mechanism of action of warfarin?
Competes with vitamin K for binding to hepatic vitamin K reductase preventing the conversion to the active hydroquinone
50
How is warfarin admimistered?
Orally
51
How long is the onset of warfarin?
2-3 days
52
Factors that potentials warfarin action?
``` Liver disease (decreased clotting factors) High metabolic rate Drug interactions ```
53
Factors that lessen warfarin action
Pregnancy Hypothyroidism Vitamin K consumption Drug interactions
54
How is overdose of warfarin treated?
Administer vitamin K or concentrate of plasma clotting factors
55
What does antithrombin III do?
Inhibits coagulation by neutralising serine protease factors by binding to their active site
56
What is the action of heparin?
Binds to antithrombin III, increasing its affinity for serine protease clotting factors particularly Xa and IIa (thrombin)
57
Examples of LMWHs?
Enoxaparin | Dalteparin
58
What is the difference between heparin and LMWHs?
LMWHs inhibit facto Xa not thrombin (IIa)
59
What order of kinetics does heparin exhibit?
Zero order kinetics
60
What order of kinetics do LMWHs exhibit?
First order kinetics
61
Adverse effects of heparin and LMWHs?
Haemorrhage Osteoporosis Hypoaldosteroidnism Hypersensitivity reactions
62
How do platelets adhere to subendothelial molecules?
GPlb receptor | vWF (acts as bridge)
64
What does the exposure of acidic phospholipids on platelet surfaces cause?
Promotes thrombin formation which stimulates further aggregation stabilised by formation of fibrin from fibrinogen
65
Are anti-platelets mainly used in arterial or venous thrombosis?
Arterial
66
Are anti-coagulants mainly used in arterial or venous thrombosis?
Venous
67
Example of anti-platelet drugs?
Aspirin Clopidogrel Tirofiban
68
What is the mechanism of action of aspirin?
Blocks COX in platelets preventing TXA2 synthesis but also COX in endothelial cells inhibiting production of antithrombotic prostaglandin I2 (PGI2)
69
What does TXA2 do?
Drive platelet aggregation
70
Main side effect of aspirin
GI bleeding and ulceration
71
What is the mechanism of action of clopidogrel?
Links to P2Y12 receptor by a disulphide bond producing irreversible inhibition
72
What does P2Y12 do?
Helps secrete ADP which drives platelet aggregation
73
When is clopidogrel most commonly used?
When patients are intolerant of aspirin
74
When is Tirofiban used?
Given IV in short term management to prevent MI in high risk patients with unstable angina (with aspirin & heparin)
75
What happens in the fibrinolytic cascade?
Plasminogen is converted to plasmid by tPA Plans in converts fibrin to fibrin fragments Fibrin fragments lyse clots
76
What are fibrinolytics principally used in?
Reopen occluded arteries in MI or stroke | Less frequently in venous thrombosis
77
Examples of fibrinolytic drugs?
Streptokinase Alteplase Duteplase
78
What patients should streptokinase not be given in?
Patients who've had recent streptococcal infections
79
Side effect of fibrinolytics
Haemorrhage
80
How is haemorrhage induced by fibrinolytics controlled?
Tranexamic acid - inhibits plasminogen activation
81
What do platelets adhere to after vascular damage?
Subendothelial molecules
82
What substances drive platelet aggregation?
ADP, 5-HT and coagulation factors from storage granules | TXA2 synthesis via the enzyme COX
83
Mechanism of action of spironolactone
Aldosterone receptor antagonist
84
Side effects of spironolactone
Hyperkalaemia Renal dysfunction Gynaecomastia
85
What does ivabradine do?
Slow heart rate
86
When is ivabradine used?
If HR is fast despite beta blockers
87
Side effects of digoxin
``` Yellow vision Nausea Vomiting Bradycardia Heart block Arrhthymia's ```
88
What is digoxins mechanism of action?
A-V block
89
What is the immediate therapy for acute LVF?
1. Sit up 2. Oxygen (beware COPD) 3. IV furosemide 4. IV diamorphine (not in COPD)

AY Cardiovascular (28 decks)

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