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phase 2 cardiovascular and respiratory block > week 2 > Flashcards

week 2 Flashcards

1
Q

risk factors for atherosclerosis

A 
age
male gender
family history
smoking 
hypertension
hyperlipidaemia 
diabetes
obesity
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2
Q

causes of chest pain

A 
cardiac
respiratory 
gastrointestinal
musculoskeletal
other
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3
Q

most common cardiac causes of chest pain seen in clinical practice

A

cardiac ischaemia
aortic dissection
pulmonary embolism

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4
Q

types of cardiac ischaemia

A

troponin positive and troponin negative

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5
Q

causes of troponin positive (cardiac)

A

type I and type II MI
coronary spasm
spontaneous coronary artery dissection (SCAD)

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6
Q

causes of troponin negative (cardiac)

A

angina

coronary artery spasm

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7
Q

where does cardiac pain typically radiate to

A

left arm, neck and jaw

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8
Q

typical cardiac pain

A

site - central
radiation - arm, jaw, other
character - tight pressure
precipitating and relieving factors - exercise/rest
severity - variable but usually severe
duration - prolonged
associated symptoms - breathlessness, pallor, sweating, nausea and vomiting

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9
Q

investigation of chest pain

A 
layered history
observations
lab tests
ECG
serial ECG
CXR
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10
Q

invasive coronary angiogram

A

insert plastic tube through radial artery (or femoral) and take pictures of coronary arteries
can cause dissections, arhythmic events and can induce an MI

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11
Q

tests for cardiac chest pain

A 
exercise stress test
stress echo
myocardial perfusion scan
CT coronary angiogram
stress perfusion cMR
invasive coronary agiogram
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12
Q

how can you tell there is significant occlusion in a blood vessel

A

ST depression during exercise

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13
Q

anti-anginal drug action

A 
reduce cardiac workload:
slow heart rate
reduce force of contraction
reduce pre-load/after-load
improve blood supply:
coronary artery vasodilation
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14
Q

types of drugs for angina

A 
beta-blockers
calcium antagonists
nitrates
K+ channel activator
If blocker
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15
Q

risk factors for atherosclerotic disease

A 
age
family history
sex
ethnicity
cigarette smoking
diabetes mellitus
hyperlipidemia
hypertension
obesity
physical inactivity
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16
Q

acute coronary syndromes

A

unstable angina (comes on at rest)
NSTEMI - non ST elevation MI
STEMI (more heart muscle damage)

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17
Q

unstable angina

A

unstable plaque without myocardial necrosis

critical coronary disease

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18
Q

NSTEMI

A

plaque rupture/thrombus without total vessel occlusion

ST depression

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19
Q

treatment of type I MI (NSTEMI)

A

dual platelet therapy to stop platelets sticking
statin
ACE inhibitor
Beta-blocker

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20
Q

treatment of type I MI (STEMI)

A

primary percutaneous coronary intervention

systemic thrombolysis - dissolving clot

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21
Q

STEMI

A

complete vessel occlusion

ST elevation

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22
Q

complications of acute MI

A 
pericarditis
RV infarct
mural thrombus
heart failure
mechanical ventricular septal defect
aneurysm 
ischemia
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23
Q

treatment of coronary artery disease

A 
no cure
primary prevention
anti-anginal drugs
anti-platlet drugs
thrombolytic drugs
angioplasty and stents
CABG surgery
secondary prevention
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24
Q

two types of risk factors

A

non-modifiable

modifiable - cannot be changed

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25
Q

how can you use risk

A 
inform or educate the public and patients
modify behaviour 
selection for interventions
measure effectiveness of interventions
deliver health/public health services
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26
Q

risk measurements

A 
absolute risk
relative risk
odds ratio
attributable risk
population attributable risk
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27
Q

what is absolute risk

A

the incidence of disease in a population
population could be the general pop, a subgroup of a pop, those with a risk factor
it is the number of new cases per population over specified time - so x new cases per x population per x years

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28
Q

what is relative risk

A

if having a risk factor/exposure is related to the outcome

compare two populations: one with exposure/RF and one without

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29
Q

working out incidence

A

number with disease/total population

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30
Q

working out relative risk

A

incidence in exposed/incidence in not exposed

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31
Q

if RR = 1

A

risk in exposed = risk in not exposed

so no association

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32
Q

if RR > 1

A

risk in exposed > risk in not exposed
positive association
risk may be a cause of outcome

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33
Q

if RR < 1

A

risk in exposed < risk in not exposed
negative association
exposure/risk may be protective

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34
Q

case control study

A

compare 2 groups of people defined by their outcome eg. people with disease and people without
compare two groups on whether they report having had the exposure/risk

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35
Q

relative risk or odds ratio

A

RR can only be obtained from cohort studies

OR used for case control and cross sectional studies

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36
Q

what is attributable risk

A

incidence of cases among those exposed that are due to the exposure/risk factor
= incidence of disease in exposed - incidence of disease in un-exposed

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37
Q

attributable risk percent

A

percentage of cases among those exposed that are due to the exposure/risk factor
= AR x 100 / incidence of disease in exposed

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38
Q

population attributable risk (PAR)

A

incidence of cases among whole population that are due to exposure
= AR x prevalence of exposure

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39
Q

prevalence of exposure

A

= total exposed/total population

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40
Q

population attributable rise percent

A

percentage of cases in the whole population that are due to the exposure/RF
= PAR x 100 / incidence of disease in population

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41
Q

modifiable risk factors for acute MI risk

A 
smoking
hypertension
lipids
abdominal obesity
diabetes
fruit and veg
alcohol
exercise
psychosocial
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42
Q

primary prevention strategies for MI

A

single risk factor strategy eg treat bp in individuals with hypertension
population health strategy eg lower bp in whole population
high baseline risk strategy eg treat bp and other risk factors in individuals with high overall risk

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43
Q

primary prevention

A

reducing risk of getting the disease

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44
Q

secondary prevention

A

reducing the risks associated with having the disease

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45
Q

haemostasis

A

functions to limit blood loss following vascular damage

does not compromise the fluidity of blood

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46
Q

thrombosis

A

occlusion of blood vessel by an intravascular blood clot or platelet clump

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47
Q

describe platelets

A

cell fragments produced from megakaryocytes in bone marrow
no nucleus so cannot produce new proteins
danger of haemorrhage if there is a deficiency

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48
Q

how is intravascular blood coagulation and platelet activation normally supressed

A

non-thrombrogenic surface of endothelium
production by endothelium of prostacyclin (PGI2) and nitric oxide which inhibit platelet aggregation - nitric oxide also inhibits adhesion of platelets to vascular wall
presence of natural anticoagulants in plasma
NO increases cGMP which has an anti-platelet effect

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49
Q

how are platelets and the coagulation cascade activated

A

platelets adhere to exposed sub-endothelial collagen and become activated
coagulation initiated by exposure of blood to tissue factor (f3) and is facilitated by exposure of pro-coagulant phospholipid on platelet surface

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50
Q

role of platelets in coagulation

A

platelets release agents which promote vasoconstriction and aggregation ie. thromboxane A2, 5-HT and ADP

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51
Q

stages in platelet activation

A

vessel is cut or atherosclerotic plaque ruptures leading to activation of platelets by sub-endothelial collagen
platelet surface integrin (glycoprotein (GPIb) permits adhesion to collagen in vessel wall via von Willebrand factor bridge
platelets change shape from discoid to spherical with development of pseudopodia
activated platelets expose another cell-surface integrin (GPIIb/IIIa)
platelets aggregate - fibrinogen cross-links GPIIb/IIIa receptors on adjacent platelets
arachidonic acid metabolism initiated forming thromboxane A2 - activates adjacent platelets and promotes vasoconstriction
platelets degranulate releasing stored ADP and 5-HT to activate adjacent platelets and promote vasoconstriction
exposure of pro-coagulant phospholipid on platelet surface activates the coagulation cascade (intrinsic pathway)

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52
Q

which factor catalyses the formation of thrombin

A

10a

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53
Q

von willebrand disease

A

deficiency of von willebrand factor

binds to and stabilises factor VII and binds platelets to collagen

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54
Q

blood clotting disorders

A

von willebrand disease

haemophilia A, B and C

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55
Q

haemophilia A

A

deficiency of factor VIII

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56
Q

haemophilia B

A

deficiency of factor IX

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57
Q

haemophilia C

A

deficiency of factor XI

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58
Q

fibrinolytic system

A

physiological repair system for removing blood clots

plasminogen bound to fibrin is converted to plasmin by tissue plasminogen activator

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59
Q

venous thrombosis

A

intravascular blood clot forms in deep veins, particularly of the legs when flow is sluggish
fragment may bud off (embolus) and block blood vessel, often pulmonary artery
anticoagulant drugs such as warfarin and heparin used to treat

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60
Q

arterial thrombosis

A

platelets aggregate usually at the site of a ruptured atherosclerotic plaque, then encapsulated by clot
common at CAs leading to an MI or cerebral arteries leading to a thrombotic stroke
immediate therapy - dissolve existing clots with fibrinolytics
long term therapy - anti-platelet drugs (antithrombotics) such as aspirin

61
Q

anticoagulants used in vitro (when blood is being stored)

A

heparin - sulphated glycosaminoglycans of variable chain length - polyanionic meaning multiple negative charges on chain
calcium chelators - remove calcium which is required in coagulation cascade - would not use in vivo

62
Q

anticoagulants used in vivo

A

heparin or low molecular weight heparin (LMWH)

oral anticoagulants - vitamin K antagonists and newer agents such as thrombin inhibitors and factor Xa inhibitors

63
Q

mechanism of action of heparin

A

heparin binds to and enhances the action of endogenous anticoagulant, antithrombin III
the heparin-antithrombrin III complex binds to and inhibits the action of clotting factors IIa, IXa, Xa, XIa, XIIa
immediate inhibition of clotting
low MW heparins inhibit factor Xa predominantly

64
Q

difference between aspirin and heparin

A

heparin is an anticoagulant so prevents blood clot formation

aspirin is an anti-inflammatory drug that reduces platelet aggregation and so reduces blood clotting

65
Q

differences between un-fractionated (standard) heparin and LMWH

A

both can inhibit action of Xa by binding to antithrombin
in order to inactivate thrombin (IIa), heparin molecule must be long enough to bind to both antithrombin and thrombin - < half od chains of LMWH are long enough

66
Q

advantages of LMWH

A

high bioavailability of subcutaneous route
lower incidence of HIT (heparin induced thrombocytopenia - abnormally low levels of platelets)
no need to monitor PTT
ideal during pregnancy (SC route)

67
Q

disadvantages of LMWH

A

requires dosage adjustment in renal sufficiency - renal function monitoring required
cannot be used in patients with HIT once it develops
longer half life may prolong risk of bleeding
only partially reversed with protamine
expensive
bruising at injection site

68
Q

administering heparin and LMWH

A

not orally active
IV or subcutaneously
does not cross placenta or blood-brain barrier

69
Q

uses of heparin and LMWH

A

deep venous thrombosis
safe for pre-eclampsia of pregnancy - warfarin not safe
in vitro anticoagulant

70
Q

side effects of heparin

A

allergic reactions
haemorrhage - heparin causes more bleeding if already bleeding
heparin induced thrombocytopaenia (HIT)

71
Q

how to reverse side effects of heparin

A

protamine is a heparin antagonist

a polycationic protein that binds and inactivates heparin

72
Q

oral anticoagulant

A

warfarin

blocks synthesis of coagulation factors

73
Q

mechanism of action of warfarin

A

reduced vitamin K is essential for post ribosomal gamma-carboxylation of glutamic acid residues at N-terminals of factors II, VII, IX and X
warfarin blocks vit.K reductase so blocking carboxylation
no gamma-carboxyglutamate therefore no Ca2+ binding therefore no coagulation

74
Q

uses of warfarin

A

venous thrombosis
prevention of pulmonary embolism
prevention of embolism in patients with atrial fibrillation
prophylaxis of thrombosis after insertion of prosthetic heart valves etc

75
Q

activity of warfarin

A

active in vivo not vitro

effect delayed 1-3 days - existing pool of functional clotting factors need to be replaced by the dysfunctional ones)

76
Q

administration of warfarin

A

oral
99% bound to plasma albumin
aspirin displaces warfarin from binding sites on albumin, increasing plasma [warfarin] - aspirin also inhibits platelet function

77
Q

side effects of warfarin

A

haemorrhage

crosses placenta and blood brain barrier - haemorrhage in foetus

78
Q

reversal of side effects

A

transfuse with plasma or coagulation factor concentrates

oral vitamin K - slow

79
Q

what is INR

A

INR stands for international normalized ratio and is measured with a blood test called PT-INR. PT stands for prothrombin time. The test measures how much time it takes for your blood to clot and will determine if you’re receiving the right dose of warfarin

80
Q

how is INR derived

A

from the ratio of a patients prothrombin time to a control sample
INR target range on warfarin is 2-3
high INR increases risk of haemorrhage
low INR decreases risk of thrombosis

81
Q

newly introduced oral anticoagulants

A

potential to replace warfarin but expense restricts
dabigatran exilate - direct thrombin (factor IIa) inhibitor
rivaroxaban - direct Xa inhibitor
active immediately
do not require monitoring

82
Q

mechanism of action of low dose aspirin

A

irreversibly inhibits cyclooxygenase (COX) - acetylation of terminal serine530
inhibits synthesis of platelet TXA2 - this cannot recover since platelets have no nucleus
also inhibits endothelial production of prostacyclin but this recovers through synthesis of new COX
LDA prevents re-infarction

83
Q

mechanism of dipyridamole

A

inhibits cyclic nucleotide phosphodiesterases
increases cAMP and increases cGMP
so inhibits platelet activation

84
Q

epoprostenol

A

must be given IV
short duration of action
used during haemodialysis - prevents extra activation of platelets

85
Q

clopidogrel

A

blocks platelet ADP receptors preventing GPIIb/IIIa receptor exposure
widely used to prevent re-infarction
used in combination with aspirin

86
Q

abciximab

A

blocks GPIIa/IIIa receptors exposed by any pathway
used during surgical exploration/clearing of intravascular blockage
antigenic - can only be used once

87
Q

fibrinolytic agents

A

tPA and streptokinase

88
Q

tPA

A

enzyme produced by vascular endothelium

activates only plasmin bound to fibrin

89
Q

streptokinase

A

isolated from group c haemolytic streptococci
activates plasminogen systemically - high incidence of haemorrhage
not an enzyme - binds to plasminogen and activates it by conformational change
antigenic and so ineffective after recent streptococcal infection - antibodies present

90
Q

uses of fibrinolytics

A

venous thrombosis
MI or thrombotic stroke to re-open occluded arteries (given with aspirin to inhibit platelets)
never in haemorrhagic stroke
haemorrhage treated with tranexamic acid an inhibitor of plasminogen activation

91
Q

side effects of fibrinolytics

A

allergy and haemorrhage

92
Q

what are lipids

A

a group of substances soluble in organic solvent and virtually insoluble in water

93
Q

3 main classes of lipids

A

cholesterol
triglycerides
phospholipids

94
Q

cholesterol uses

A

component of all cell membranes
synthesis of bile acids - allows absorption of fat soluble vitamins
precursor for endogenous vit d production
precursor for steroid hormones

95
Q

uses of triglycerides

A

used as an energy source in tissues

used for energy storage in adipose tissue

96
Q

function of lipoprotein system

A

transports fats in the aqueous environment of plasma

97
Q

structure of a lipoprotein

A

complex spherical structure
central core of hydrophobic lipids (triglycerides and cholesterol esters)
surface layer of polar components - phospholipids, free cholesterol, proteins, apoliopoproteins

98
Q

main lipoproteins in order of density (least to most dense)

A

chylomicron
very low density lipoprotein
low density lipoprotein
high density lipoprotein

99
Q

chylomicron function

A

synthesised in gut after a meal

main carrier of dietary triglyceride

100
Q

very low density lipoprotein function

A

synthesised in the liver

main carrier of endogenously produced triglyceride

101
Q

low density lipoprotein function

A

generated from VLDL in the circulation

main carrier of cholesterol

102
Q

high density lipoprotein function

A

returns cholesterol from extrahepatic tissues to the liver for excretion

103
Q

structure of apolipoproteins

A

they are amphiphilic compounds
hydrophobic region interacting with lipid core which provides structure to the lipoprotein
hydrophilic region interacting with the aqueous environment

104
Q

functions of apolipoproteins in lipid metabolism

A

guiding the formation of lipoproteins
acting as ligands for lipoprotein receptors
serving as activators or inhibitors of enzymes involved in the metabolism of lipoproteins

105
Q

exogenous cycle of lipoprotein metabolism

A

Dietary cholesterol and fatty acids are absorbed.
Triglycerides are formed in the intestinal cell from free fatty acids and glycerol and cholesterol is esterified.
Triglycerides and cholesterol combine to form chylomicrons.
Chylomicrons enter the circulation and travel to peripheral sites.
In peripheral tissues, chylomicrons are metabolised by lipoprotein lipase, releasing free fatty acids from the chylomicrons to be used as energy, converted to triglyceride or stored in adipose.
Remnants are used in the formation of HDL.

106
Q

endogenous cycle of lipoprotein metabolism

A

VLDL is formed in the liver from triglycerides and cholesterol esters.
These can be hydrolysed by lipoprotein lipase to form IDL or VLDL remnants.
VLDL remnants are cleared from the circulation or incorporated into LDL.
LDL particles contain a core of cholesterol esters and a smaller amount of triglyceride.
LDL is internalised by hepatic and non-hepatic tissues.
In the liver, LDL is converted into bile acids and secreted into the intestines.
In non hepatic tissues, LDL is used in hormone production, cell membrane synthesis, or stored.
LDL is also taken up by macrophages and other cells which can lead to excess accumulation and the formation of foam cells which are important in plaque formation.

107
Q

cardiovascular disease due to circulation problems

A

ischaemic heart disease and MIs

108
Q

non-modifiable risk factors for CVD

A 
sex - male
age - advancing
family history of premature CVD
ethnicity
comorbidites
109
Q

modifiable risk factors for CVD

A 
hypertension
high blood triglycerides
high LDL
low HDL
psychosocial issues
smoking
alcohol
high body weight
bad diet
lack of exercise
hypercholesterolaemia/dyslipidaemia
110
Q

individuals known to be at high risk of CVD

A

those diagnosed with CVD
chronic kidney disease (stage 3+)
diabetics aged >40 years or with >20 years of disease or with evidence of diabetes-related organ damage (ie. eyes - retinopathy)
those with familial hypercholesterolaemia

111
Q

risk calculators for CVD

A

ASSIGN risk calculator

Qrisk3

112
Q

the reverse cholesterol transport pathway

A

HDL particles act as cholesterol ester shuttles which help remove the sterol from peripheral tissues and return it to the liver, either directly or via other lipoproteins
this is thought to be anti-atherogenic, with an elevated HDL conferring a decreased risk of CHD

113
Q

if cholesterol levels fall..

A

LDL receptors are upregulated and more cholesterol is taken up by the cell
leads to lower blood concentrations

114
Q

where are the four main lipoproteins synthesised

A

chylomicron - gut after eating
HDL - mainly liver
LDL - generated from VLDL in circulation
VLDL - liver

115
Q

what happens if the fatty acids attached to the cholesterol in LDL become oxidised

A

LDL particles are not taken up by the normal LDL receptor on the liver
they are taken up by scavenger receptors on macrophages at a faster uncontrolled rate and amount
leads to the formation of cholesterol-laden foam cells which can develop into fatty streaks and athermatous plaques which cause narrowing of the arteries

116
Q

why is HDL important

A

it carries cholesterol from tissues back to the liver where it is excreted
it clears cholesterol from the blood stream

117
Q

how does saturated fat alter blood cholesterol levels

A

increases total cholesterol, LDL cholesterol and HDL cholesterol
increase in chylomicrons and triglycerides which are thought to be harmful to the arteries

118
Q

how does monounsaturated fat alter blood cholesterol levels

A

decreases total cholesterol and LDL cholesterol
increases HDL cholesterol
increase in chylomicrons and triglycerides which are thought to be harmful to the arteries but these levels fall quicker than in saturated fats

119
Q

how does polyunsaturated fat alter blood cholesterol levels

A

decreases total cholesterol and LDL cholesterol

varied effect on HDL

120
Q

how do fats influence formation of LDL

A

saturated fats increase LDL formation in plasma by decreasing turnover as they decrease LDLR activity and protein
unsaturated fats increase hepatic LDLR number and LDL turnover

121
Q

target levels of cholesterol for primary prevention of CVD (no prior CVD)

A

<5mmol/L for total cholesterol
>1 for men, >1.2 for women - HDL
<3 for LDL

122
Q

target levels of cholesterol for secondary prevention of CVD (established CVD)

A

<3mmol/L for total cholesterol
>1 for men, >1.2 for women - HDL
<1.8 - LDL

123
Q

normal lipid profile

A

Total Cholesterol - Below 5.2 mmol/L
LDL - less than 2.6 mmol/L
HDL - Above 1.5 mmol/L
Triglycerides - Below 1.7 mmol/L

124
Q

effects of exercise on heart

A

increased CO
heart rate can increase to 190-200 bpm
increase in SV
filling time decreased ~33%

125
Q

how does dynamic exercise effect BP

A

increase in systolic pressure
decrease in diastolic pressure - dilated arteries in skeletal muscles and lungs
mean BP stays roughly the same

126
Q

bruce test/protocol

A

test is based on step increases in intensity of exercise on a treadmill
7 stages of 3 minutes each
completion of 9-12 minutes of exercise or reaching 85% of the maximum predicted heart rate is usually satisfactory
used to diagnose CVD

127
Q

effects of static exercise eg wall sit

A

increase in HR

increase in systolic and diastolic BP so mean BP increases

128
Q

what is angina pectoris

A

chest pain due to myocardial ischemia - ischaemia due to an increase in myocardial O2 demand which is not met
when demand is not met there is a build up of metabolites eg adenosine, CO2, lactate, K+ ions which activate sensory nerves - pain signals to brain
can be due to atherosclerosis

129
Q

3 types of angina

A

stable
unstable
variant

130
Q

stable angina

A

narrowing of one or more CAs
attacks are predictable - exercise, stress
myocardial demand not met
involvement of chronic occlusive coronary artery disease - atherosclerosis

131
Q

unstable angina

A

attacks unpredictable

coronary artery occlusion due to platelet adhesion to ruptured atherosclerotic plaque

132
Q

varient angina

A

attacks unpredictable

coronary artery occlusion due to vasospasm - reduces artery diameter

133
Q

coronary steal

A

dilates areas that do not need to be dilated
sends more blood to already perfused areas and where dilation cannot occur, less blood is delivered because of the fall in input pressure

134
Q

coronary vasodilators in angina

A

problematic as blood flow increased to areas that do not need it

135
Q

reducing myocardial O2 demand

A

B1-adrenoceptor blockers - competitive reversible antagonists of adrenaline and noradrenaline at cardiac B1-adrenoceptor
this decreases HR and force which decrease myocardial O2 demand
used in all forms of angina

136
Q

adverse effects of b-adrenoceptor blockers in angina

A

exacerbates asthma
intolerance to exercise
hypoglycaemia
may uncover a1-mediated constriction in coronaries

137
Q

ivabradine

A

recently introduced to treat angina
blocks Na+ current that contributes to SA node depolarisation towards threshold
decreases HR but not force
decreases O2 demand

138
Q

vasodilator drugs in angina

A

dilation of arteries:
decrease in afterload which decrease myocardial work and O2 demand
dilation of veins:
decreases preload
venous dilation:
decreases venous return, decreases preload, decreases stretch of ventricle and atria, decreases strength of contraction which decreases myocardial work and O2 demand

139
Q

bainbridge reflex

A

a sympathetic reflex initiated by increased blood in the atria
causes stimulation of the SA node
stimulated baroreceptors in the atria causing increased SNS stimulation

140
Q

nitrovasodilators

A

GTN - taken as sub-lingual tablet or spray - would be destroyed if taken orally
amyl nitrate - vials opened and inhaled - not used now – these are poppers
both have rapid onset but short lived
uses:
prophylaxis in stable angina
rapid relief of ongoing anginal attack

141
Q

mechanism of nitrovasodilators

A

lipophilic so readily enter SMCs and are reduced to NO
mimic action of endothelium-derived NO:
NO activates soluble guanylate cyclase
sGC is a cytoplasmic soluble enzyme
receptor on sGC contains and ferrous (Fe2+) haem moiety
NO binds to haem receptor causing enzyme activation, GTP converted to cGMP, increase in cGMP leads to vasodilation

142
Q

problems with nitrovasodilators

A

headache - dilation of cerebral arteries

tolerance on prolonged use

143
Q

locations of voltage gated Ca2+ channels

A

Smooth muscle, cardiac muscle, pacemakers, neurons

different types in different locations

144
Q

function of voltage gated Ca2+ channels

A

open upon membrane depolarisation

reduced Ca2+ entry results in coronary and peripheral arterial vasodilation

145
Q

classes of voltage gated Ca2+ channels

A

L = long lasting current
T = transient current
N
P/Q = positive potentials

146
Q

mechanism of l-type channel block

A

allosteric modulators bind at allosteric site and reduce probability of channel opening at a given voltage
also dilate arteries which decreases TPR

147
Q

uses of L-type blockers

A

anti-hypertensives
anti-anginals
anti-dysrhythmic agents

148
Q

nicorandil

A

K+ channel activator
only drug in this class approved for angina
no tolerance
hybrid compound - nicotinamide vitamin group with an organic nitrate
nitrate like action - increased level of cyclic guanosine monophosphate, decrease in cytosolic calcium (opening of K+ channels), vascular smooth muscle relaxation

149
Q

initial anti-anginal drug treatment for stable angina

A

offer beta blocker or calcium channel blocker
then consider switching to the other option or using both
consider adding a third anti-anginal drug if these options have not worked

phase 2 cardiovascular and respiratory block (5 decks)

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