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year 1 > CARDIO PHARMACOLOGY > Flashcards

CARDIO PHARMACOLOGY Flashcards

1
Q

what receptors do adrenaline and noradrenaline act on in the heart

A

b1

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2
Q

what kind of receptor is B1

A

g protein coupled receptor

Gs protein

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3
Q

what happens when B1 receptors are stimulated

A

Gs coupled protein stimulates adenylyl cyclase to increase intracellular cAMP

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4
Q

what does increased intracellular cAMP do in monocytes

A

stimulates pKA

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5
Q

what does increased intracellular cAMP do to pacemaker cells

A

increases the slope of the PMP and so increases heart rate

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6
Q

what receptor does ACh act on in the heart

A

M2

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7
Q

what kind of receptor is M2

A

G-protein coupled receptor

Gi protein

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8
Q

what happens when M2 receptors are stimulated

A

Gi coupled protein decreases the activity of adenylyl cyclase to decrease intracellular cAMP and opens K+ channels to hyper polarise the SA node

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9
Q

what is the effect of M2 receptor stimulation in the heart

A

decreased slope of PMP and so decreased heart rate

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10
Q

what is Bachmann’s bundle

A

anterior interatrial myocardial band - pathway going to LA from SAN

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11
Q

what is the funny current

A

inwards current of the PMP

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12
Q

what is the funny current stimulated by

A

hyperpolarisation and cAMP

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13
Q

what are HCN channels

A

hyperpolarisation-activated cyclone nucleotide gated channels

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14
Q

what does the blockage of HCN channels do

A

decreases the PMP slope

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15
Q

give an example of a selective HCN channel blocker

A

ivabradine

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16
Q

true / false

sympathetic stimulation decreases the cardiac efficiency with respect to O2 consumption

A

true

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17
Q

what happens to the frank starling curve in heart failure

A

the curve fails as force not able to match the VR

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18
Q

what is the frank starling law

A

the more the myocardium is stretched the greater the force it exerts upon contraction i.e. the greater the VR the greater the stroke volume

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19
Q

increased skeletal muscle activity
increased venomotor tone
increased respiratory pump

all do what to the VR

A

increase VR

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20
Q

how do APs reach the ventricular muscle cells

A

t tubules

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21
Q

how is depolarisation of ventricular muscle cell initiated

A

fast Na+ influx

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22
Q

what does the fast Na+ influx do to the T tubule membranes

A

Voltage-gated L-type Ca2+ channels located in the T tubule membrane are opened by depolarisation and let a small amount of Ca2+ in

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23
Q

what does the small Ca2+ influx cause

A

activation of RyR (ryanodine) receptors

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24
Q

what does the stimulation of RyR receptors cause

A

CICR - release of large amounts of intracellular calcium within the SR into the cell

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25
Q

for contraction to occur within the ventricular muscle cell what must the calcium do

A

activate myofilaments

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26
Q

how is the calcium removed from the cytoplasm back into the SR

A

Ca ATPase (SERCA)

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27
Q

how is the calcium removed from the cytoplasm out of the cell

A

sarcolemma Na+/Ca2+ exchanger

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28
Q

how is relaxation achieved

A

decreased intracellular Ca2+

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29
Q

what are 4 sites of PKA phosphorylation action

A

Ryanodine receptors
L-type calcium channels on T tubule membrane
PLB
troponin

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30
Q

what does phosphorylation of RyR cause

A

increases the size of calcium transient i.e. the amount leaving the SR causing increased force of contraction

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31
Q

what does phosphorylation of LTCC cause

A

increases trigger calcium so increases CICR causing increased force of contraction

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32
Q

what does phosphorylation of PLB cause

A

increases uptake by SERCA so accelerates relaxation (makes contraction shorter) and increases SR calcium content

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33
Q

what does phosphorylation of troponin cause

A

reduces affinity for calcium - minor reduction in contraction which accelerates relaxation

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34
Q

what is the principle determinant of calcium binding to troponin C to cause contraction

A

rate calcium diffuses from the SR (i.e. phosphorylation of RyR)

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35
Q

what is the principle determinant of the unbinding of calcium once a contraction has occurred

A

phosphorylation of troponin

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36
Q

what do thyroid hormones do to the HR

A

increase HR

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37
Q

what 2 ways can intracellular [Ca2+] be increased in vascular smooth muscle cells

A

influx of Ca2+ across membrane gradient (conc or electric)

released from intracellular stores

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38
Q

what does calcium do to initiate contraction in a smooth muscle cell

A

calcium binds to calmodulin to form a calcium-calmodulin complex

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39
Q

what does the calcium-calmodulin complex do

A

activates myosin light chain kinase MLCK which phosphorylates myosin light chain

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40
Q

what does the phosphorylated myosin light chain do

A

forms cross bridges and allows myosin and actin to slide over each other and contract

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41
Q

how does cGMP initiate smooth muscle relaxation

A

activates myosin-LC-phosphotase

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42
Q

what does myosin-lc-phosphatase do

A

strips a phosphate from the phosphorylated (active) Myosin-LC converting it to inactive myosin-LC
this causes the bridges to break and relaxation to occur

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43
Q

what does NO do to the HR

A

increases HR

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44
Q

how does NO signal

A

paracrine

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45
Q

true / false

bradykinin, ANP and serotonin are vasodilators that work through NO

A

true

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46
Q

what does NO do within vascular smooth muscle

A

activates guanylate cyclase - converts GTP to cGMP which initiates the relaxation pathway
activates calcium-dependent potassium channels - causes potassium to leave the cell causing repolarisation - closes VGCC and causes relaxation

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47
Q

how do calcium dependent potassium channels become active

A

NO or depolarisation

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48
Q

what do NO, NPs and sheer stress do to the production of endothelin

A

down regulate endothelin production

49
Q

what is the long term effect of AT II

A

promotes cell growth

50
Q

where is ACE found

A

bound to membrane of endothelial cells

51
Q

what 2 things does ACE do

A

converts AT I to AT II

inactivated bradykinin

52
Q

what is better for variant angina - BB or CCBs? and why?

A

CCBs - variant angina is caused by episodic coronary spasms so calcium antagonists work well by not allowing the cell to obtain the calcium required for a spasm

53
Q

what is the function of lipoproteins

A

transport non-polar lipids in blood

54
Q

what makes up the hydrophobic core of a lipoprotein

A

esterified cholesterol and triglycerides

55
Q

what makes up the hydrophilic coat of a lipoprotein

A

monolayer of amphipathic cholesterol, phospholipids and one or more apoprotein

56
Q

what is the apoprotein of HDL

A

ApoA1

ApoA2

57
Q

what is the apoprotein of LDL

A

ApoB-100

58
Q

what is the apoprotein of VLDL

A

ApoB-100

59
Q

what is the apoprotein of chylomicrons

A

apoB-48

60
Q

what lipoprotein has the largest diameter

A

chylomicrons

61
Q

where are chylomicrons formed

A

intestinal cells

62
Q

where is VLDL formed

A

liver hepatocytes

63
Q

what is VLDL assembled from

A

free fatty acids from adipose tissue and denovo synthesis

64
Q

what is the function of apoB-containing lipoproteins

A

deliver triglycerides to muscle for ATP and adipocytes for storage

65
Q

what are the 3 phases of ApoB containing lipoproteins

A

assembly
intravascular metabolism
receptor mediated clearance

66
Q

what does intravascular metabolism of ApoB containing lipoproteins involve

A

hydrolysis of triglyceride core

67
Q

how is a chylomicron formed

A

1) triglyceride broken down into monoglyceride and free fatty acids
2) absorbed by intestine
3) triglyceride resynthesised in the enterocyte
4) forms a droplet with apoB-48 inside
5) lipidation
6) cholesterol esters added
7) chylomicron leaves by exocytosis
8) goes to lymphatic system

68
Q

how are chylomicrons and VLDL activated

A

transfer of apoC2 from HDL particles - activated to target triglyceride delivery to adipose and muscle tissue

69
Q

what does apoC2 facilitate once transferred to the VLDL/chylomicron

A

binding to lipoprotein lipase

70
Q

what is LPL associated with

A

endothelium of capillaries in adipose and muscle tissue

71
Q

what is the function of LPL

A

hydrolyses the lipoprotein core triglycerides to free fatty acids and glycerol which enter tissues

72
Q

what makes up the chylomicron/VLDL remnants

A

lipoprotein particles containing cholesteryl esters (depleted of triglycerides)

73
Q

true / false

the chylomicrons and VLDL then dissociated from LPL

A

true

74
Q

what is ApoC2 exchanged for when transferred back to HDL

A

apoE

75
Q

what does ApoE cause

A

remnants to return to liver

76
Q

what is the fate of the remnants once in the liver

A

metabolised by hepatic lipase
all apoB48 and 1/2 apoB100 containing remnants are cleared by receptor mediated endocytosis into hepatocytes
the other 1/2 of apoB100 lose further triglycerides through hepatic lipase so become smaller and more enriched in cholesteryl ester - become IDL then LDL

77
Q

what does receptor mediated clearance of ApoB containing lipoproteins involve

A

attachment of lipoprotein to a receptor, endocytosis into the cell and removal
depends on the expression of LDL receptor expressed by liver and other tissues

78
Q

what is receptor mediated endocytosis

A

uptake of LDL particles by hepatocytes

79
Q

what happens once the LDL has been taken up by the hepatocyte

A

cholesterol is released from the cholesterol ester by hydrolysis

80
Q

what does cholesterol released from LDL cause

A

inhibition of HMG CoA reductase
down regulation of LDL receptor expression
storage of cholesterol as an ester

81
Q

what is HMG CoA reductase

A

rate limiting enzyme in de novo endogenous cholesterol synthesis

82
Q

how do statins work

A

competitively inhibit HMG CoA reductase
–> decrease in hepatocyte cholesterol synthesis –> decreased [cholesterol] in hepatocyte –> increased LDL receptor expression –> enhanced LDL clearance

83
Q

how is cholesterol absorbed by enterocyte

A

transport protein NPC1L1

84
Q

how does HDL reduce cholesterol levels in the body

A

transports excess cholesterol from cells to liver where it is removed from the body - synthesised to make bile salts or secreted in bile

85
Q

true / false

HDL reaching liver interacts with receptor that allows transfer of cholesterol and cholesteryl esters into hepatocytes

A

true

86
Q

true / false

CETP mediates the transfer of cholesterol from LDL and VLDL to HDL in plasma

A

false
CETP mediates the transfer of cholesterol from HDL to LDL and VLDL in the plasma, indirectly returning cholesterol to the liver

87
Q

what occurs in familial hypercholesterolaemia

A

homozygous

LDL receptors lacking

88
Q

what does thrombin IIa do

A

converts fibrinogen to fibrin

89
Q

how are clotting factors activated

A

proteolytic cleavage

90
Q

what does activated clotting factor Xa do

A

activated prothrombin II

91
Q

what are the 2 pathways factor X can be activated

A

in vivo pathway

contact pathway

92
Q

true/false

factors XIa and XIIa are in vivo pathway factors

A

false

contact pathway factors

93
Q

true/false

factor VIIa and tissue factor are in vivo pathway factors

A

true

94
Q

what are 2 pre-formed aggregation factors released from activated platelets

A

ADP

5-HT

95
Q

what is an aggregation factor synthesised on demand by activated platelets

A

TXA2

96
Q

what do aggregation factors do

A

act on cell surface receptor of platelets to cause aggregation and cross linking via fibrinogen

97
Q

how do platelets help the coagulation cascade

A

provide surfaces which bring clotting factors together

98
Q

before a clotting factor can attach to the negative phospholipid on the platelet surface what must occur

A

gamma-carboxylation of glutamate residues of the clotting factor

99
Q

what is hydroquinone

A

reduced vitamin k

100
Q

what is epoxide

A

oxidised vitamin K

101
Q

what does carboxylase enzyme that mediates gamma-carboxylation of glutamate residues of clotting factors require

A

vitamin K cofactor in reduced form - vit K becomes oxidised in the process

102
Q

what is the purpose of vitamin K reductase

A

converts oxidised vitamin K into reduced vitamin K

103
Q

how does warfarin work

A

blocks vitamin K reductase –> prevents formation of reduced vitamin K –> prevents gamma-carboxylation of glutamate residues of clotting factors

104
Q

what is haemostasis

A

preventing blood loss from a damaged vessel

105
Q

what is an example of pathological haemostasis

A

thrombosis - a haematological plug formed in the absence of bleeding

106
Q

what are the 3 aspects of virchows triad

A

increased coagulability of blood
injury to vessel wall
abnormal blood flow

107
Q

a thrombus is white, mainly platelets and fibrin mesh and produces emboli which lodge in systemic arteries
is it arterial or venous

A

arterial

108
Q

a thrombus has a white head with a jelly like red tail, is rich in blood cells and fibrin and produces emboli which lodge in the pulmonary arteries
is it arterial or venous

A

venous

109
Q

what are arterial thrombi treated with

A

antiplatelets

110
Q

what are venous thrombi treated with

A

anticoagulants

111
Q

what is antithrombin III

A

clotting factor inhibitor

binds to clotting factors rendering them inactive

112
Q

what is Von Willebrand factor

A

allows platelets to adhere to endothelium

113
Q

what cascade opposes the coagulation cascade

A

fibrinolytic

114
Q

what occurs in the fibrinolytic cascade

A

plasminogen is converted to plasmin which breaks down the fibrin into fibrin fragments causing clot lysis

115
Q

what order of kinetics is this

“2mg are eliminated per unit time”

A

zero order

same amount of drug is eliminated per unit time regardless of plasma conc

116
Q

what order of kinetics is this

“2% of available drug is eliminated per unit time”

A

first order

same proportion of drug is eliminated per unit of time - variable amount eliminated based on plasma conc

117
Q

what order of elimination is heparin

A

zero order

118
Q

what order of elimination is LMWH

A

first order

year 1 (45 decks)

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