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BM4 Part 1 > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

Affinity

A

The extent to which a drug binds to its receptor at a given concentration.

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2
Q

Intrinsic Activity

A

Same as efficacy. The ability of a drug to illicit a pharmacological effect (full agonist = 1, antagonist = 0).

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3
Q

What is the function of spare receptors?

A

To improve the speed of response.

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4
Q

What are the 4 processes of pharmacokinetics?

A

Absorption
Distribution
Metabolism
Excretion

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5
Q

Enteral

A

Passing through the gut.

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6
Q

Parenteral

A

Occurring outside of the gut.

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7
Q

Volume of Distribution

A

The volume of body fluids into which a drug appears to have been distributed.

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8
Q

Absorption

A

The movement of a drug into the blood following administration.

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9
Q

Distribution

A

The postabsorptive reversible transfer of a drug from the systemic circulation to other compartments of the body.

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10
Q

First Pass Hepatic Metabolism

A

Metabolism of a drug in the liver before reaching general circulation, due to passage from the gut to through the hepatic portal vein.

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11
Q

What are the 3 most common parenteral administration routes?

A

Intravenous, intramuscular and subcutaneous.

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12
Q

What is the function of ACE?

A

Angiotensin Converting Enzyme - converts angiotensin I to angiotensin II.

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13
Q

What is the main effect of angiotensin II?

A

Fast acting vasoconstriction, therefore increases BP.
Also increases the release of aldosterone (slow acting BP increase).

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14
Q

What is the effect of aldosterone?

A

Increases renal salt and water reabsorption thereby increasing blood volume and BP (slow acting).

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15
Q

How does noradrenaline affect blood vessel diameters?

A

Vasoconstriction and vesoconstriction.

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16
Q

How does ADH control BP?

A

Anti-Diuretic = against excessive urine production.
Increases water retention, therefore increasing blood volume (increasing BP).
Vasopressin = vasoconstriction (also increases BP).

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17
Q

What is the neurotransmitter for muscarinic receptors?

A

Acetylcholine.

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18
Q

What is the neurotransmitter for nicotinic receptors?

A

Acetylcholine.

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19
Q

What is the neurotransmitter for adrenergic receptors?

A

Noradrenaline or adrenaline.

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20
Q

What receptors are present in the parasympathetic nervous system?

A

Nicotonic (ganglia) and muscarinic (target muscle).

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21
Q

What receptors are mainly present in the sympathetic nervous system?

A

Nicotonic (ganglia) and adrenergic (target tissue).

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22
Q

What are the exceptions to the adrenergic receptors of the sympathetic nervous system?

A

Sweat glands (muscarinic receptors) and adrenal gland (preganglionic neuron synapses with the adrenal gland at a nicotinic receptor - i.e. no postganglionic neuron).

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23
Q

Where are beta-1-adrenoreceptors primarily found?

A

The heart, kidneys and fat cells.

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24
Q

Where are beta-2-adrenoreceptors primarily found?

A

Lungs (bronchodilation), gastrointestinal, bladder, uterus (relaxation of all 3).

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25
Q

Where are alpha-1-adrenoreceptors primarily found?

A

Vascular smooth muscle (vasoconstriction).

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26
Q

Where are alpha-2-adrenoreceptors primarily found?

A

On pre-synaptic cells and inhibit the release of neurotransmitter.

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27
Q

What adrenoreceptors causing pupil dilation?

A

Alpha adrenoreceptors.

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28
Q

What group of people can beta-blockers not be given to?

A

Asthmatics as this will prevent asthmatic rescue medication from working (blocks beta receptors that asthmatic medication stimulates).

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29
Q

What are the main uses of beta-antagonists?

A

Beta-blockers to treat hypertension; B1-antagonists for angina pectoris or regulation of dysrhythmias.
Beta-blockers (e.g. propranolol) have also been used as anxiolytics.

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30
Q

What are the common side effects of beta-antagonists?

A

Bradycardia, hypoglycaemia, fatigue, cold extremities, bronchoconstriction.

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31
Q

What are the two phases of metabolism?

A

Inactivation of drug.
Conjugation of drug.

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32
Q

What are CYP450 enzymes?

A

Cytochrome P450 family of isoenzymes.
Membrane-bound haemoproteins that bind and directly catalyse inactivation reactions (e.g. oxidation, reduction, hydrolysis etc.).

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33
Q

What are the main CYP450 enzymes?

A

CYP1A, CYP2A, CYP2C, CYP2D, CYP2E, CYP3A (70-80% of phase I metabolism).

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34
Q

Where are CYP450 enzymes found?

A

Mainly in the SER of hepatocytes.

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35
Q

Where does Phase I and Phase II metabolism occur?

A

I - SER of hepatocytes.
II - cytoplasm.

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36
Q

What are examples of reactions that occur as part of Phase II metabolism?

A

Glutathione conjugation, amino acid conjugation, glucuronidation, acetylation, sulphation, methylation.

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37
Q

What are examples of zero-order drugs?

A

Alcohol, aspirin, heparin, warfarin, fluoxetine.

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38
Q

How is clearance calculated?

A

Total Clearance (CL) (L/H) = rate of elimination of drug from body (mg/h) / plasma concentration (CP) (mg/L).

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39
Q

What is steady state?

A

When the rate of administration equals the rate of elimination so that a constant plasma concentration is maintained.

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40
Q

What does a Vd < 5 L mean?

A

Drug is plasma protein bound and confined to plasma water.

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41
Q

What does a Vd of 10-15 L mean?

A

Large water soluble drug confined to extracellular water (interstitial and plasma).

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42
Q

What does a Vd of 40-45 L mean?

A

Small water soluble and lipid soluble drug confined to total body water (interstitial, plasma and intracellular).

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43
Q

What does a Vd of 60-100 L mean?

A

Lipid soluble drug confined to adipose tissue where it has been absorbed and sequestered.

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44
Q

Grade 1 Hypertension

A

140-159 and/or 90-99

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45
Q

Grade 2 Hypertension

A

160-179 and/or 100-109

46
Q

Grade 3 Hypertension

A

> 179 and/or > 109

47
Q

Factors contributing to hypertension

A

Obesity
Alcohol
Exercise
Smoking
Age
Genetics
High Dietary Salt
Stress

48
Q

Effects of Angiotensin II

A

Increases sympathetic activity
Vasoconstriction
Pituitary ADH (water retention)
Aldosterone (salt and water retention)

49
Q

Mechanism of ACE Inhibitors

A

Inhibit ACE, blocking synthesis of Angiotensin II

50
Q

Side effects of ACE inhibitors

A

Cough
Angioedemia
Pregnancy problems
Taste changes
Other (rash, fatigue)
Proteinuria
Renal insufficiency
Increased potassium
Low blood pressure

51
Q

Examples of ACE inhibitors

A

Captopril
Enalapril
Ramipril

52
Q

Mechanism of ARB/ARA

A

Block Angiotensin II receptors (AT1) on heart, vessels, kidney, adrenal cortex, lung and brain

53
Q

Examples of ARB/ARA

A

Candesartan
Losartan

54
Q

Side effects of ARB/ARA

A

Low BP
Other (fatigue, headache, dizziness)
Swelling
Allergic reaction
Raised potassium
Teratogenic
Acute kidney injury
Nasal congestion

55
Q

Mechanism of beta blockers

A

Blocks B1 receptors on the heart (reduces heart rate)
Blocks B1 receptors on the kidneys (reduces release of renin)

56
Q

Examples of beta blockers

A

Atenolol, bisoprolol, metoprolol

57
Q

Side effects of beta blockers

A

Bronchoconstriction
Erectile dysfunction
Temperature (cold extremities)
Animated dreams (vivid nightmares)
Bradycardia
Low sugar (hypoglycaemia)
Orthostatic hypotension
heart bloCK

58
Q

Mechanism of dihydropyridine CCBs

A

Blocks voltage-operated L-type slow Ca2+ channels in peripheral arteriolar smooth muscle cells

59
Q

Mechanism of non-dihydropyridine CCBs

A

Blocks voltage-operated L-type slow Ca2+ channels in peripheral arteriolar and cardiac smooth muscle

60
Q

Examples of dihydropyridine CCBs

A

Nifedipine, amlodipine

61
Q

Examples of non-dihydropyridine CCBs

A

Verapamil, diltiazem

62
Q

Side effects of CCBs

A

Hypotension
Bradycardia (mainly NDHP)
Heart block (mainly NDHP)
Headache
Abdominal discomfort
Peripheral oedema (mainly DHP)

63
Q

Examples of thiazides

A

Bendroflumethiazide, metolazone

64
Q

Mechanism of thiazide

A

Inhibits Na/Cl co-transporter in the distal convoluted tubule

65
Q

Side effects of thiazides

A

Metabolic alkalosis
Hypokalaemia
Hypercalcaemia
Hyperglycaemia
Hyperlipidaemia
Hyperuricaemia

66
Q

Examples of loop diuretics

A

Furosemide, bumetanide

67
Q

Mechanism of loop diuretics

A

Significantly reduces Na+ reabsorption by inhibiting the Na/K/Cl transporter in the thick ascending limb of the loop of Henle

68
Q

Side effects of loop diuretics

A

Hyponataemia
Hypokalaemia
Hypocalcaemia
Hypomagnesaemia
Ototoxicity
Hyperglycaemia
Hyperlipidaemia
Hyperurecaemia

69
Q

Examples of K+ sparing diuretics

A

Amiloride
Triamterene
Eplerenone
Spironolactone

70
Q

Mechanism of K sparing diuretics

A

Inhibiting the exchange of sodium and potassium in the collecting duct
(spironolactone and eplerenone are both mineralocorticoid receptor antagonists)

71
Q

Side effects of K sparing diuretics

A

Hyperkalaemia (cardiac arrhythmias)
Metabolic acidosis
Gynecomastia (males)
Breast tenderness (females)

72
Q

Mechanism of spironolactone

A

Inhibits aldosterone
Aldosterone increases reabsorption of Sodium and Chloride and increases excretion of Potassium

73
Q

Aterial vs Venous thrombi

A

Arterial = platelets predominate
Venous = fibrin predominates

74
Q

3 steps of platelet in coagulation

A

Adhesion
Activation
Aggregation

75
Q

What initiates adhesion of platelets

A

Vessel wall injury exposing sub-endothelial collagen

76
Q

Clopidogrel

A

Irreversibly blocks P2Y12 ADP receptor, increasing cAMP within the platelet and preventing aggregation.

77
Q

cAMP role in platelet activation

A

cAMP stimulates Ca/Mg dependent ATPase to lower cytoplasmic Ca levels. Therefore when inhibited by activation of P2Y12, intracellular levels of Ca2+ increase.

78
Q

Dipyridamole mechanism

A

Increases intracellular cAMP by inhibiting phosphodiesterase

79
Q

Side effects of clopidogrel

A

Haemorrhage
GI upset
Dyspnoea (ticagrelor)

80
Q

Synthetic PGI2

A

E.g. epoprostenol
Increases cAMP via prostacyclin receptor (IP)
Mimics anti-aggregatory effect of prostacyclin

81
Q

Eptifibatide

A

Synthetic peptide that binds reversibly to GPIIb/GPIIIa receptor and blocks binding of fibrinogen
Mainly used in angioplasty procedures to prevent thrombosis (with heparin and aspirin)
Given IV

82
Q

Tirofiban

A

Non-peptide antagonist of GPIIb/GPIIIa
Mainly used in angioplasty procedures to prevent thrombosis (with heparin and aspirin)
Given IV

83
Q

COX-1 role in coagulation

A

COX-1 catalyses the production of Thromboxane A2 in platelet cells.
COX-1 catalyses the production of prostacyclin in endothelial cells.

84
Q

Mechanism of aspirin as an antiplatelet

A

Irreversibly acetylates COX-1 in platelets and endothelium.
Endothelium regenerates within hours, whereas platelets take 5-9 days.
Therefore anti-aggregatory effects of PGI2 outweighs pro-aggregatory effects of Thromboxane A2.

85
Q

Intrinsic clotting cascade

A

Vessel endothelium ruptures exposing underlying tissue (e.g. collagen). Platelets cling and their surface provides sites for mobilisation of factors.

86
Q

Extrinsic clotting cascade

A

Tissue cell trauma causes release of tissue factor

87
Q

Mechanism of warfarin

A

Inhibition of Vitamin K epoxide reductase to prevent the recycling of vitamin K for synthesising vitamin K dependent coagulation factors

88
Q

Vitamin K dependent coagulation factors

A

II, VII, IX, X

89
Q

Warfarin cautions

A

Narrow therapeutic index
Metabolism of warfarin in the liver is highly variable
Lots of drug interactions
Pregnancy (Foetal Warfarin Syndrome)

90
Q

Heparin mechanism

A

Anti-thrombin III enhancer

91
Q

Anti-thrombin III role

A

Inhibits thrombin and Factor Xa to prevent uncontrolled coagulation. But has a slow onset time.

92
Q

Examples of LMWH

A

Dalteparin, enoxaparin

93
Q

Fondaparinux

A

New class of selective anti-thrombin-dependent Factor Xa inhibitors
No antidote

94
Q

Main groups of DOACs

A

Direct Oral AntiCoagulants
1. Direct Thrombin Inhibitors
2. Direct Factor Xa Inhibitors

95
Q

Examples of Direct Thrombin Inhibitors

A

Bivalirudin
Dabigatran (gatrans)

96
Q

Examples of Direct Factor Xa Inhibitors

A

Rivaroxaban (xabans)

97
Q

Mechanism of nitrates

A

Binds and activates guanylate cyclase and increasing intracellular levels of cGMP which leads to vasodilation.
General peripheral vasodilation, reducing preload and afterload

98
Q

Glyceryl Trinitrate

A

Short Acting Nitrate
Rapid onset
SE = orthostatic hypertension, reflex tachycardia, headaches

99
Q

Isosorbide mononitrate/dinitrate

A

Long Acting Nitrate
Used prophylactically (but not first line)

100
Q

Cardioselective Beta Blockers

A

Bisoprolol, atenolol

101
Q

Angina Treatment

A

Nitrate (GTN or isosorbide)
Beta blocker (bisoprolol)
CCB (NDHP - diltiazem/verapamil)

102
Q

What activates natural tissue plasminogen activator (tPA)?

A

Thrombin - to limit clotting

103
Q

Plasminogen Activators

A

Streptokinase (risk of anaphylaxis)
rt-PA (e.g. alteplase, reteplase, tenecteplase)

104
Q

Timeframe of plasminogen activators

A

Within 12 hours of MI - preferably within first hour

105
Q

PCI

A

Percutaneous Coronary Intervention

106
Q

Early Management of Acute MI

A

Morphine (+ anti-emetic)
Oxygen
Nitrate (GTN)
Aspirin

PCI/Fibrinolysis if applicable
rtPA if applicable

107
Q

When is PCI offered?

A

If presenting within 12 hours of symptoms and PCI can be delivered within 120 mins

108
Q

When is fibrinolysis offered?

A

If presenting within 12 hours of symptoms, but PCI cannot be delivered within 120 mins

109
Q

Examples of statins

A

Simvastatin, atorvastatin, pravastatin, fluvastatin

110
Q

Mechanism of statins

A

Reduce cholesterol synthesis by inhibiting HMG-CoA reductase in hepatocytes

111
Q

Long-term Management of MI

A

Beta blocker/ACE Inhibitor
Statins
Aspirin
Lifestyle changes

BM4 Part 1 (11 decks)

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