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Y1 CARDIOLOGY > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

Adrenaline activates B2 adrenoceptors in the heart to cause increased heart rate. True/False?

A

False

Acts on B1 adrenoceptors

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2
Q

Which muscarinic receptor does ACh act on in the heart to cause decreased heart rate?

A

M2 receptors

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3
Q

What does adenylyl cyclase do?

A

Increases production of cAMP

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4
Q

Which channels, when blocked, decrease the slope of the SA node action potential?

A

HCN channels

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5
Q

Name a drug that is a selective blocker of HCN channels and for what heart condition it is mainly used

A

Ivabradine

Used for angina

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6
Q

Sympathetic stimulation decreases AV nodal delay. True/False?

A

True

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7
Q

Sympathetic stimulation causes increased automaticity. What is this?

A

Increased tendency for non-nodal regions to acquire spontaneous conduction activity

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8
Q

Sympathetic stimulation causes a decrease in the duration of systole. True/False?

A

True

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9
Q

What factors increase venous return?

A

Increased skeletal muscle activity
Adrenergic effects on blood vessels
Increased depth + frequency of respiration

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10
Q

What is the function of ryanodine receptors with regards to calcium action + action potentials?

A

Enable release of Ca++ from sarcoplasmic reticulum through the process of calcium-induced calcium release

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11
Q

What is the function of SERCA with regards to calcium action + action potentials?

A

Removes Ca++ from the cytoplasm to bring about relaxation

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12
Q

What happens when phosphalamban is phosphorylated with regards to calcium action + action potentials?

A

This increases Ca++ storage in the SR and also activates SERCA to promote relaxation

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13
Q

What happens when troponin I is phosphorylated with regards to calcium action + action potentials?

A

Decreases affinity of troponin C for calcium, thus accelerating relaxation

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14
Q

Name a B1 agonist drug used sometimes in heart failure

A

Dobutamine

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15
Q

Propranolol is a selective B2 receptor antagonist. True/False? Give one special use of this drug

A

False
It is non-selective
Thyrotoxicosis

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16
Q

Name a selective B1 antagonist drug

A

Atenolol

Metoprolol

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17
Q

Give some clinical uses of B-blockers

A

Arrhythmias
Hypertension
Angina
Heart failure (low-dose)

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18
Q

Give some adverse effects of B-blockers

A 
Bronchospasm (aggravate asthma) 
Hypoglycaemia (especially in diabetes)
Cold extremities
Bradycardia
Fatigue
Acute heart failure
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19
Q

Which class of drug is atropine?

A

Non-selective muscarinic antagonist

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20
Q

Name the main clinical use of atropine

A

Reverse bradycardia modestly

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21
Q

What are the dangers of digoxin?

A

It has a low therapeutic ratio and is thus toxic, especially in hypokalaemia
Can cause heart block, arrhythmias, nausea, vomiting, diarrhoea and disturb colour vision

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22
Q

What is an indirect effect of digoxin?

A

Slows AV node conduction to increase refractory period (good in heart failure and AF - increase cardiac output)

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23
Q

In the smooth muscle cell, calcium binds with _____, which undergoes a conformation change. The __-__ complex then interacts with _____ to activate it. The active ____ then phosphorylates ___-__ which, when phosphorylated, ultimately causes contraction.

A

In the smooth muscle cell, calcium binds with calmodulin, which undergoes a conformation change. The Ca-CaM complex then interacts with MLCK to activate it. The active MLCK then phosphorylates myosin-LC which, when phosphorylated, ultimately causes contraction.

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24
Q

In the endothelial cell, Ca-CaM complex activates ___ which binds _-____ and __ to form NO, which rapidly diffuses into the smooth muscle cell (to ultimately cause relaxation).

A

In the endothelial cell, Ca-CaM complex activates eNOS which binds l-arginine and O2 to form NO, which rapidly diffuses into the smooth muscle cell (to ultimately cause relaxation).

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25
Q

In the smooth muscle cell, NO does 2 things:
1] activates ___ ____ which synthesises cGMP from ___. cGMP activates protein kinase _ which ultimately causes relaxation.
2] keeps Ca-dependent _ channel open, allowing _ to efflux, leaving _ve charge in the cell which causes membrane potential to ______ so we get relaxation.

A

In the smooth muscle cell, NO does 2 things:
1] activates guanylate cyclase which synthesises cGMP from GTP. cGMP activates protein kinase A which ultimately causes relaxation.
2] keeps Ca-dependent K channel open, allowing K to efflux, leaving -ve charge in the cell which causes membrane potential to hyperpolarise so we get relaxation.

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26
Q

How do organic nitrates (GTN) work in the smooth muscle cell?

A

Combines with SH groups to liberate NO, which then acts like endogenous NO in signalling pathways

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27
Q

Nitrates cause arteriolar dilation at low doses. True/False?

A

False

Mainly cause venorelaxation, but can cause arteriolar dilation at high doses

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28
Q

How do nitrates help in angina?

A

Decrease preload + afterload

Improve perfusion to ischaemic zone (dilates collateral vessels) - INCREASE CORONARY BLOOD FLOW

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29
Q

Name 2 examples of organic nitrates used clinically

A 
GTN tablet/spray (short acting)
Isosorbide mononitrate (long acting)
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30
Q

Why is it important to have nitrate-low periods? List some other side effects of nitrates

A

Repeated use can develop tolerance and reduce efficacy

Postural hypotension, headaches

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31
Q

Endothelin-1 causes vasodilation. True/False?

A

False

Causes vasoconstriction

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32
Q

Which substances cause upregulation of endothelin production?

A

Adrenaline
Angiotensin II
ADH

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33
Q

Which substances cause downregulation of endothelin production?

A

Nitric oxide

ANP

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34
Q

Name a renin inhibitor

A

Aliskiren

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35
Q

Renin inhibitors (aliskiren) can be used in conjunction with an ARB or ACEi. True/False?

A

False

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36
Q

What are the effects of ACE?

A

Converts AT I to AT II

Inactivates bradykinin

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37
Q

Name an ACEi used in Tayside

A

Lisinopril

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38
Q

Name an ARB used in Tayside

A

Losartan

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39
Q

What are the main differences between ACEi and ARBs?

A

ARBs do not inhibit bradykinin and do not produce dry cough - block AT II from working on receptor

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40
Q

How do calcium antagonists work?

A

Prevent opening of Ca channels to limit intracellular Ca++ to reduce heart rate and force of contraction

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41
Q

Verapamil is selective for cardiac L-type channels. True/False?

A

True

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42
Q

Amlodipine is selective for which L-type channels?

A

Smooth muscle L-type channels

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43
Q

Amlodipine is preferred to verapamil - why?

A

Minimises unwanted effects on cardiac muscle, e.g. heart block

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44
Q

Why is verapamil useful in arrhythmias?

A

Slows conduction of AV node, can help reduce AF

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45
Q

K+ channel openers act primarily on arterial smooth muscle. True/False?

A

True

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46
Q

Name two K+ channel opener drugs. What are they used in?

A

Minoxidil
Nicorandil

Severe hypertension

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47
Q

Name two alpha blockers. What is their action? What are they used in? List one side effect.

A 
Prazosin
Doxazosin
Block alpha adrenoceptors causing vasodilatation
Hypertension (and BPH)
Postural hypotension
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48
Q

What is the main/overall action of diuretics?

A

Increase Na, Cl and water excretion from the kidneys

Indirectly relax vasculature

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49
Q

What is the undesirable effect of diuretics?

A

Loss of K+

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50
Q

Name a thiazide diuretic, give its action and conditions it is used in

A

Bendroflumethazide
Inhibit NaCl reabsorption in distal tubule
Mild heart failure, hypertension

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51
Q

Name a loop diuretic, give its action and conditions it is used in

A

Furosemide
Inhibit NaCl reabsorption in the Loop of Henle
Chronic heart failure, acute pulmonary oedema

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52
Q

What are some side effects of diuretics?

A 
Hypokalaemia
Arrhythmias
Hyperglycaemia
Gout
Impotence
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53
Q

What is the main side effect of dihydropyridine Ca antagonists? Give an example

A

Ankle oedema

Amlodipine

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54
Q

Name conditions in which amlodipine can be used

A

Hypertension

Angina

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55
Q

In addition to hypertension and angina, verapamil can be used for what? Give one side effect

A 
SVT arrhythmias (AF, VT) but NOT alongside B blockers
Heart block
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56
Q

ACEi and ARBs are safe in pregnancy. True/False?

A

False

NEVER use in pregnancy

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57
Q

Name conditions in which nitrates can be used

A

Angina

Acute heart failure

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58
Q

Name some antiplatelet agents. What is their mode of action? List a major side effect.

A

Aspirin
Clopidogrel
Prevent new thrombus getting bigger
Haemorrhage

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59
Q

Name some anticoagulants. What is their mode of action? List a major side effect.

A

Heparin (IV)
Warfarin (oral)
Prevent new thrombus getting bigger
Haemorrhage

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60
Q

What do fibrinolytics simply do?

A

Dissolve formed clots

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61
Q

Name two commonly used fibrinolytics. List a major side effect

A

Streptokinase
Tissue plasminogen activator (tPa)
Haemorrhage

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62
Q

CV disease is associated with low LDL and HDL. True/False?

A

False

High LDL and/or low HDL causes CV disease

63
Q

The bigger the HDL:LDL ratio, the better (in terms of health). True/False?

A

True

64
Q

What are the components of a lipoprotein?

A

Hydrophobic core + hydrophilic coat

65
Q

What makes up the hydrophobic core of a lipoprotein?

A

Esterified cholesterol

Triglycerides

66
Q

What makes up the hydrophilic coat of a lipoprotein?

A

Amphipathic cholesterol
Phospholipids
Apoproteins

67
Q

Name the major lipoproteins

A

HDL
LDL
VLDL
Chylomicrons

68
Q

What does HDL contain?

A

apoA1 and apoA2

69
Q

What does LDL contain?

A

apoB100

70
Q

What does VLDL contain?

A

apoB100

71
Q

What do chylomicrons contain?

A

apoB48

72
Q

What is the function of apoB lipoproteins (LDL, VLDL, chylomicrons)?

A

Deliver triglycerides to muscle for ATP genesis + to adipocytes for storage

73
Q

Chylomicrons are formed in liver cells and transport triglycerides formed in the liver. True/False?

A

False

VLDL is formed in the liver and takes part in the endogenous pathway

74
Q

What is the exogenous pathway of triglyceride transport?

A

Chylomicrons formed in intestinal cells to transport dietary triglycerides

75
Q

What are the three stages of the life cycle of apoB lipoproteins?

A

Assembly
Metabolism [hydrolysis]
Clearance

76
Q

Which enzyme breaks down triglyceride into 2 fatty acids and monoglycerol?

A

Pancreatic lipase

77
Q

Why does the triglyceride molecule need to be broken down?

A

It is insoluble and cannot be absorbed into the enterocyte

78
Q

What happens when monoglyceride and 2 fatty acids are in the enterocyte?

A

Combine to reform triglyceride

79
Q

Which receptor enables amphipathic cholesterol to enter the enterocyte?

A

NPC1L1 protein

80
Q

What needs to be added to the chylomicron to allow its export from the enterocyte?

A

apoA1

81
Q

Exported chylomicron enters the blood and is deposited into the venous system. True/False?

A

False

Deposited into lymphatics and then the venous system

82
Q

Where and how is VLDL assembled?

A

Liver cells, from free fatty acids derived de novo + from adipose tissue

83
Q

Before chylomicron and VLDL can offload their contents, they need to be activated. How does this happen?

A

HDL transfers apoCII to VLDL and chylomicrons which facilitates their binding

84
Q

Which enzyme hydrolyses apoB lipoprotein (chylomicron, VLDL, LDL)?

A

Lipoprotein lipase (LPL)

85
Q

What facilitates binding of chylomicrons and VLDL to LPL?

A

apoCII (that was transferred from HDL)

86
Q

What does LPL do to apoB lipoproteins?

A

Attacks and hydrolyses core triglycerides to fatty acids and glycerol which can be absorbed

87
Q

What are chylomicron and VLDL remnants?

A

Particles depleted of triglyceride but still containing cholesterol ester

88
Q

apoCII is returned to HDL in exchange for which apoprotein? How does this facilitate clearance of apoB lipoprotein?

A

apoCII is returned to HDL in exchange for apoE, a high affinity ligand for receptor-mediated clearance

89
Q

All apoB100 and apoB48 remnants are cleared via receptor-mediated clearance. True/False?

A

False

Only 50% of apoB100 remnants are cleared this way

90
Q

What happens to the remaining apoB100 remnants?

A

Eventually become LDL

91
Q

Which receptor is vital for LDL clearance? Where is it importantly located?

A

LDL receptor in liver

92
Q

How does cholesterol release from LDL influence cholesterol release by hepatocytes?

A

The more cholesterol returning to the liver (in LDL), the less liver is synthesised by hepatocytes

93
Q

How does cholesterol release inhibit cholesterol synthesis by hepatocytes?

A

Inhibits HMG CoA reductase

Downregulates LDL receptor expression

94
Q

Why is LDL “bad” cholesterol?

A

Uptake during endothelial injury causes LDL oxidation to atherogenic OXLDL
Macrophages uptake OXLDL, converting cholesterol into foam cells, forming a fatty streak and ultimately a plaque

95
Q

Why is HDL “good” cholesterol?

A

Accepts excess cholesterol and delivers it to the liver (reverse cholesterol transport)
It then interacts with scavenger receptors that enable uptake of cholesterol into hepatocytes

96
Q

What are the drugs of choice for reducing LDL (and moderately increasing HDL)? Give examples

A

Statins - simvastatin, atorvastatin

97
Q

How do statins work?

A

Inhibit HMG CoA reducatase, causing decrease in de novo cholesterol synthesis + increase in LDL receptor expression to enhance cholesterol clearance

98
Q

When and how are statins administered?

A

Orally at night

99
Q

What other drugs can be used for decreasing triglycerides?

A

Fibrates - bezafibrate, gemfibrozil

100
Q

How do fibrates work?

A

Inhibit PPAR-alpha to enhance LPL production

101
Q

What do bile acid binding resins do?

A

Cause excretion of bile salts, causing more cholesterol to be converted into bile salts

102
Q

Name some bile acid binding resin drugs and a notable side effect

A

Colestyramine
Colestipol
Can cause GI irritation

103
Q

What does Ezetimibe do?

A

Inhibits NPC1L1 protein to reduce cholesterol absorption by enterocytes, ultimately causing decrease in LDL

104
Q

What are the 3 components of Virchow’s triad? What do they predispose to?

A

Abnormal blood flow
Vessel wall injury
Increased coagulability of blood
These predispose to thrombosis

105
Q

An arterial thrombus is a white thrombus. True/False?

A

True

106
Q

What colour is a venous thrombus?

A

Red

107
Q

Where do white thrombi commonly lodge?

A

Brain (detached embolus from left heart)

108
Q

Where do red thrombi commonly lodge?

A

Lung (detached embolus from right heart)

109
Q

What do VIIa, XIa and XIIa do downstream in the blood coagulation pathway?

A

Activate X to Xa

110
Q

What does Xa do downstream in the blood coagulation pathway?

A

Activates II to IIa[prothrombin to thrombin]

111
Q

What does IIa (thrombin) do downstream in the blood coagulation pathway?

A

Activates fibrinogen to fibrin, the component of fibrin clots

112
Q

What happens in response to endothelial damage in terms of platelets?

A

Adhere to site of injury and become activated, attracting other platelets, causing aggregation

113
Q

What mediators do activated platelets secrete/synthesize? What do they do?

A

ADP, 5-HT, TXA2

Enhance platelet aggregation

114
Q

Name the inactive precursors of the main clotting factors involved in coagulation

A

II, VII, IX, X

115
Q

What do the inactive precursors of clotting factors require initially in order to be able to become activated?

A

Gamma-carboxylation

116
Q

What does the enzyme which carries out gamma-carboxylation of clotting factor precursors require?

A

Vitamin K

[in its reduced, hydroquinone form]

117
Q

What are the two forms of Vitamin K that exist?

A

K1 from diet

K2 from bacteria in intestine

118
Q

How does warfarin work?

A

Competitively binds to vitamin K reductase, causing inhibition and thus reducing hydroquinone VK [ultimately inactivating clotting factor precursors]

119
Q

How is warfarin administered? How fast is its onset of action?

A

Oral

2-3 days

120
Q

What is the main risk with anticoagulant drugs?

A

Risk of haemmorhage

121
Q

How does liver disease potentiate activity of warfarin?

A

Decreased clotting factors

122
Q

How does a high metabolic rate potentiate the activity of warfarin?

A

Increased clearance of clotting factors

123
Q

How does pregnancy decrease the effect of warfarin?

A

Increased synthesis of clotting factors

124
Q

How might a warfarin overdose be treated?

A

Vitamin K/clotting factor infusion

125
Q

What does Antithrombin III (ATIII) do?

A

Inhibits IIa and Xa to inhibit coagulation

126
Q

How does heparin cause anticoagulation?

A

Accelerates inhibition of IIa and Xa through ATIII - increases affinity of the latter for the former

127
Q

Heparin must bind to ATIII and IIa in order to inhibit IIa. True/False?

A

True

128
Q

Heparin must bind to ATIII and Xa in order to inhibit Xa. True/False?

A

False

Only needs to bind to ATIII

129
Q

LMWH inhibits IIa but not Xa. True/False?

A

False

Inhibits Xa but not IIa

130
Q

Give examples of LMWHs

A

Enoxaparin

Dalteparin

131
Q

How is heparin administered?

A

Intravenously or subcutaenously

132
Q

How is LMWH administered?

A

Subcutaneously

133
Q

Name an oral active inhibitor of thrombin

A

Dabigatran etexilate

134
Q

Name an oral active inhibitor of Xa

A

Rivaroxaban

135
Q

What is the role of vWF in platelet pathway?

A

Acts as a bridge to help platelets adhere to damaged endothelium

136
Q

Which enzyme aids platelet synthesis of TXA2?

A

COX

137
Q

Which receptor does ADP bind with to enhance platelet aggregation? Which drug blocks this receptor?

A

P2Y12 receptor

Clopidogrel blocks this

138
Q

Which platelet receptors does fibrinogen bind with to enhance platelet aggregation?Which drug blocks this?

A

GPIIb/IIIa receptorsTirofiban

139
Q

Which drug blocks the synthesis of TXA2 through inhibiting COX enzyme? What is it’s adverse effect?

A

Aspirin

GI bleeding and ulceration (give with PPI)

140
Q

How is aspirin administered?

A

Oral

141
Q

How is clopidogrel administered? What is it’s action?

A

Oral

Binds to P2Y12 receptor via a disulphide bond causing irreversible inhibition

142
Q

What is the role of plasmin in the coagulation cascade?

A

Enforces fibrin degradation to form fibrin fragments (clot lysis)

143
Q

How do fibrinolytic drugs work?

A

Activate plasminogen to form plasmin to cause clot lysis

144
Q

Give examples of fibrinolytic drugs

A

Streptokinase
Aleplase
Duteplase

145
Q

How are fibrinolytic drugs administered?

A

Intravenously

146
Q

What is the ‘funny current’?

A

Influx of sodium and potassium inwards during sinus rhythm

147
Q

What are some uses of ACEi and ARBs?

A

Hypertension

Heart failure

148
Q

List the side effects of ACEi

A

Dry cough
Hypotension
Renal dysfunction
Angioneurotic oedema

149
Q

In what situation, must you avoid ACEi and ARB? In what situation are they useful in.

A

Pregnancy
Bilateral renal artery stenosis

Diabetic nephropathy

150
Q

What is used to control warfarin dosing?

A

International normalised ratio (INR)

151
Q

Give some side effects of statins and fibrates

A

Mysositis

Rhabdomyolosis

152
Q

What are some considerations when prescribing streptokinase?

A

Action blocked after 4 days by Ig generation

Be careful of allergic reactions in recent streptococcal infections

153
Q

Give one side effect of tPa

A

Haemorrhage

Y1 CARDIOLOGY (16 decks)

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