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Cardio Week 2 Flashcards

1
Q

where are phrenic nerves located

A

descending across lateral borders of pericardium

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2
Q

the fibrous pericardium is lined internally by what

A

parietal serous pericardium

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3
Q

what covers the anterior surface of heart

A

epicardium (same thing as visceral pericardium) that excretes pericardial fluid

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4
Q

where is the pericardial cavity located

A

between the 2 layers of serous pericardium

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5
Q

what is cardiac tamponade

A

when pericardial cavity fills with blood and pressure around heart prevents it from contraction

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6
Q

what is pericardiocentesis

A

drainage of fluid from pericardial cavity - needle inserted via infrasternal angle and directed superioposteriorly

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7
Q

what is the transverse pericardial sinus

A

space within pericardial cavity (lies posterior to ascending aorta and pulmonary trunk) and surgeons use this to identify and isolate great vessels

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8
Q

what is the only artery that carries deoxygenated blood

A

pulmonary artery

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9
Q

what is the only vein that carries oxygenated blood

A

pulmonary vein

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10
Q

what is the coronary sinus

A

short venous conduit (in AV groove posteriorly) which receives deoxygenated blood from most of cardiac veins and drains into right atrium

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11
Q

what is the first branch of the aorta

A

coronary arteries as they come off ascending aorta

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12
Q

where do coronary arteries course

A

just deep to epicardium - usually embedded in adipose tissue

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13
Q

where is the right coronary arteries situated

A

right atrioventricular groove

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14
Q

where is the left (main stem) coronary artery situated

A

left AV groove between pulmonary trunk and left auricle

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15
Q

are left and right coronary arteries connected

A

yes - via anastomoses

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16
Q

what is the consequence of a septal defect

A

hole (mixes arterial and venous blood) - reduces O2 content of systemic arterial blood in aorta - hypoxaemia

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17
Q

where is mitral valve located

A

between left atrium and left ventricle

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18
Q

where is tricuspid valve located

A

between right atrium and right ventricle

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19
Q

what are examples of organic nitrates

A

glyceryl trinitrate (GTN), isosorbide mononitrate, isosorbide denigrate, erythrityl tetranitrate, pentaerythriol tetranitrate

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20
Q

when are organic nitrates used

A

angina - decreased myocardial O2 requirement via decreased preload, after load and improved perfusion

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21
Q

how do organic nitrates work

A

metabolised to release NO - elevates cGMP (vasodilation)

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22
Q

what are examples of ACE inhibitors

A

captopril and enalopril

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23
Q

when are ACE inhibitors used

A

chronic heart failure and hypertension

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24
Q

how do ACE inhibitors work

A

block conversion to angiotensin II (blocks sympathetic response) and promotes diuresis since it is blocking hormones that cause renal Na+ and water retention

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25
Q

give examples of angiotensin II receptor blocker (ARB)

A

losartan and valartan

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26
Q

how do ARBs work

A

selectively inhibit effect of angiotensin II without affecting bradykinin levels

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27
Q

what side effect is present in ACE inhibitors but not ARBs

A

chronic cough - ACE metabolises bradykinin and substance P whereas ARB does not

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28
Q

what can ACEI and ARB cause in pregnancy

A

renovascular disease and aortic stenosis

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29
Q

what are examples of calcium antagonists

A

verapamil, amiodipine and diltiazem

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30
Q

when are calcium antagonists used

A

hypertension (first line) angina (in combo with GTN) and in dysrhythmias

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31
Q

how do calcium antagonists work

A

prevent opening of L type Ca++ channels so limit increasing Ca2+ - reduced rate of conduction through AVN as well as reducing force of contraction

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32
Q

what is the adverse effects of calcium antagonists

A

excessive vasodilation - hypotension, dizziness and ankle oedema

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33
Q

give examples of potassium channel openers (K+ATP openers)

A

minoxidil and nicrorandil

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34
Q

when are potassium channel openers used

A

minoxidil - last resort hypertension but cause reflex tachycardia and salt and water retention, treat hair lossnicrorandil - NO donor activity, used in angina (side effect - mouth ulcers)

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35
Q

how do potassium channel openers work

A

open channels which causes hyper polarisation which switches off L type Ca2+ channels - less calcium causes vasodilation etc

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36
Q

what are examples of a1 adrenoceptors

A

prazosin and doxazosin

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37
Q

when are a1 adrenoceptors used

A

hypertension

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38
Q

how do a1 adrenoceptors work

A

vasodilation by blocking a1 adrenoceptors - decreases MABP

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39
Q

what are examples of diuretics

A

furosemide, bumetanide, torasemide and ethacrynic acid

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40
Q

what are the two different kinds of diuretics

A

thiazide (inhibit reabsorption in distal tube) and loop diuretics (inhibit reabsorption in thick ascending limb of the loop of hernie)

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41
Q

when are diuretics used

A

chronic heart failure and hypertension

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42
Q

how do diuretics work

A

act on kidney to increase excretion of Na, Cl and H2O and exert additional relaxant effects on vasculature

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43
Q

what are examples of class I drugs

A

disopyramide, lignocaine and flecainide (respective IA, IB and IC)

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44
Q

how do class I drugs work

A

block voltage gated Na+ channels

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45
Q

characteristics of IA drugs

A

associate and dissociate moderately - slow rise of AP and prolong refectory periodused in ventricular arrhythmias

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46
Q

characteristics of IB drugs

A

associate and dissociate rapidly - prevents premature beatsused in ventricular arrhythmias after MI

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47
Q

characteristics of IC drugs

A

associate and dissociate really slowly and depress conduction used for prophylaxis of paroxysmal atrial fibrillation

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48
Q

give example of class II drugs

A

metoprolol

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49
Q

how do class II drugs work

A

block b-adrenoceptor - decrease rate of depolarisation in SA and AV nodes

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50
Q

give examples of class III drugs

A

amiodarone and sotolol

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51
Q

how do class III drugs work

A

block voltage activated K+ channels - prolong AP duration increased refractory period

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52
Q

give examples of class IV drugs

A

verapamil, dilitazem

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53
Q

how do class IV drugs work

A

block voltage activated Ca2+ channels - slow conduction in SA and AV nodes - decrease force of contraction

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54
Q

what classes of drugs act on atria (rate control of supra ventricular tachycardia)

A

IC (flecainide) and III (amiodarone, sotolol)

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55
Q

what classes of drugs act on ventricles

A

IA, IB and II

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56
Q

what classes of drugs act on the AV node (rhythm control of SVT)

A

adenosine, digoxin, classes II (metoprolol) and IV (verapamil)

57
Q

what classes of drugs act on atria and ventricles AV accessory pathways

A

amiodarone, sotalol, classes IA and IC

58
Q

what are the four main types of SVT (supra ventricular tachycardia)

A

atrial fibrillation, paroxysmal supra ventricular tachycardia (PSVT), atrial flutter and Wolff Parkinson white syndrome

59
Q

what is the inner layer

A

tunica intima (single layer of squamous epithelium - endothelium)

60
Q

what is middle layer

A

tunica media (smooth muscle, thickness varies)

61
Q

what is outer layer

A

tunica adventitia (supporting connective tissue)

62
Q

what separates tunica intima from tunica media

A

internal elastic membrane (external elastic separates TM and TA)

63
Q

largest arteries have their own vascular supply; what is this called

A

vasa vasorum

64
Q

what are capillaries composed of

A

endothelial cells and basal lamina - often have pericytes (connective tissue with contractile properties)

65
Q

where are continuous capillaries found

A

muscle, connective tissue, lung, skin and nerve

66
Q

where are fenestrated capillaries found

A

mucosa of gut, endocrine glands, glomeruli of kidney

67
Q

where are sinusoidal (discontinuous) capillaries found

A

liver, spleen and bone marrow - lack basal lamina and have large gaps

68
Q

what is components of vein

A

tunica intima, thin but continuous tunica media (vena cava/HPV has thick tunica adventitia)

69
Q

what veins have valves

A

small to medium sized veins - valves are inward extensions of tunica intima

70
Q

what is the role of endocardium

A

lines entire surface of heart including valves

71
Q

what is the structure of endocardium

A

endothelium, basal lamina, thin layer of collagen fibres, layer of denser connective tissuesome areas has subendocardium of loose connective tissue containing small vessels and nerves

72
Q

what is the role of myocardium

A

thick middle layer

73
Q

what is structure of myocardium

A

bundles and layers of contractile cardiac muscle cells, individual muscle fibres surrounded by delicate, continuous connective tissue with rich capillary network

74
Q

what is the role of intercalated discs in myocardium

A

attach muscle cells and allow spread of electrical activity

75
Q

what is role of epicardium

A

outer layer of heart

76
Q

what is structure of epicardium

A

on surface: single layer of flattened epithelium (mesothelium)contains basal lamina, fibroelastic connective tissue and in some places adipose tissue

77
Q

what are the two parts of pericardium

A

fibrous pericardium (sac of tough fibrocollagenous connective tissue)serous pericardium (simple squamous epithelium backed by basal lamina and connective tissue)

78
Q

what is the two layers of serous pericardium

A

parietal serous pericardium - inner surface of fibrous visceral serous pericardium - covers surface of heart

79
Q

what is the fibrous skeleton

A

formed by thick bands of connective tussle around heart valves which supports the valves but also provides attachment for cardiac muscle fibres

80
Q

what is the structure of valves

A

have outer endothelial layer with basal lamina with layer of collagen and elastin fibreshave a core of dense connective tissue called lamina fibrosa in continuity with fibrous skeleton

81
Q

the leaflets of the valves separating atria from ventricles are anchored to papillary muscles in wall of ventricles by what

A

chord tendineae (which merge with lamina fibrosa)

82
Q

what is the structure of pacemaker cells

A

smaller than myocytes and embedded in more connective tissueappear pale because of paucity of organelles few myofibrils, little glycogen and no proper T tubule system

83
Q

what is the structure of purkinje fibres

A

larger than myocytes, found in subendocardial layer, abundant glycogen, no T tubules, no intercalated discsappear pale and very pale/clear centre

84
Q

what is the structure of lymphatic vessels

A

no central pump but smooth muscle in walls, hydrostatic pressure in tissue and the compression of vessels by voluntary muscle combined with valves in vessels, produce flow

85
Q

how do sympathetic signals reach organs

A

exit spinal cord at one of T1-L2/3 and then travel either superiorly or inferiorly in sympathetic chain to another ganglion and synapse

86
Q

what are the cardiopulmonary splanchnic nerves

A

postsynaptic fibres from cervical and upper thoracic sympathetic chainssympathetic nerves to heart and lungs

87
Q

how do parasympathetic signals reach organs

A

via cranial nerves III (oculomotor nerves) VII (facial nerves), IX (glossopharyngeal nerves) and X

88
Q

what is the role of CN V (vagus nerve) in parasympathetic signals

A

presynaptic parasympathetic fibres in vagus nerves then synapse onto postsynaptic neurones

89
Q

AP’s arriving at postcentral gyrus of parietal lobe (somatosensory) bring what sensations into consciousness

A

body wall (somatic)

90
Q

AP’s arriving at pre central gyrus of frontal lobe (somatomotor) bring what sensations into consciousness

A

contractions of body wall (somatic) skeletal muscle

91
Q

what is the source of sharp central chest pain by herpes zoster (shingles)

A

patient with shingles developing in T4/T5 - pain precedes blisters

92
Q

what could be the source of sharp central chest pain by muscle, joints or bones

A

pectorals major or intercostal muscle strain, dislocated costochondrial joint, costovertebral joint inflammation, slipped thoracic disc

93
Q

what could be the source of sharp central chest pain by parietal pleura and fibrous pericardium

A

pleurisy and pericarditis

94
Q

what would be the source of dull central chest pain by the trachea

A

tracheitis

95
Q

what would be the source of dull central chest pain by aorta

A

ruptured aneurysm of aortic arch

96
Q

what would be the source of dull central chest pain of the abdominal viscerae

A

gastritis, cholecystitis, pancreatitis, hepatitis

97
Q

what would be the source of dull central chest pain of the heart

A

angina and myocardial infarction

98
Q

how do pain signals from organs reach brain

A

visceral afferent APs pass bilaterally to thalamus and hypothalamus then diffuse areas of the cortex

99
Q

what is an example of pain signals from organs reaching brain

A

ischaemic chest pain: cardiopulmonary splanchnic nerves plus visceral afferents from chest organs

100
Q

if pain is originating in a somatic structure then where is the radiation felt

A

along the affected dermatome

101
Q

is the pain is originating in the heart then where is the radiation felt

A

the dermatome supplied by the spinal cord at levels which the cardiac visceral afferents enter sympathetic chain

102
Q

what is referred pain due to

A

afferent (sensory) fibres from soma and afferent (sensory) fibres from viscera (visceral afferents) entering spinal cord at same levels brain chooses to believe pain from organ is actually coming from soma

103
Q

where is cardiac pain referred to

A

upper limbs (esp left) or from back, neck or jaw

104
Q

what are the common sites of coronary atherosclerosis

A

anterior inter ventricular branch (LAD) of LCA, RCA, circumflex branch of LCA, left main stem coronary artery

105
Q

what happens in coronary artery bypass grafting

A

grafts anastomosed proximally to ascending aorta

106
Q

what is the main artery used for grafting

A

left internal thoracic (mammary artery) used - not disconnected from patient but instead cut distally and attached to coronary artery

107
Q

what is the other arteries used for grafting

A

bilateral internal thoracic artery, gastroepiploic and radial arteries

108
Q

what is shock

A

an abnormality of the circulatory system resulting in inadequate tissue perfusion and oxygenation

109
Q

how does hypovolaemic shock (also known as haemorrhage shock) occur

A

loss of blood volume - decreased venous return - decreased EDV - decreased SV - decreased CO and BP.- inadequate tissue perfusion

110
Q

what is the causes of hypovolaemic shock

A

haemorrhage (trauma, surgery, GI)vomiting, diarrhoea, excessive sweating results in decreased ECFV thus decreased blood

111
Q

what is cardiogenic shock

A

sustained hypotension caused by decreased cardiac contractility

112
Q

how does cardiogenic shock occur

A

decreased contractility - decreased SV - decreased CO and BP - inadequate tissue perfusion

113
Q

how does tension pneumothorax (obstructive shock) occur

A

increased intrathoracic pressure - decreased venous return - decreased EDV - decreased SV - decreased CO and BP - inadequate tissue perfusion

114
Q

how does neurogenic shock occur

A

loss of sympathetic tone - massive venous and arterial dilation - decreased venous return and SVR - decreased CO and BP - inadequate tissue perfusion

115
Q

how does vasoactive shock occur

A

release of vasoactive mediators - venous and arterial vasodilation and increased capillary permeability - decreased venous return and decreased SVR - decreased CO and BP - inadequate tissue perfusion

116
Q

what is the treatment for shock

A

ABCDE, high flow O2, volume replacement, inotropes for cardiogenic shock, immediate chest train for pneumothorax, adrenaline for anaphylactic shock, vasopressors for septic shock

117
Q

what is an example of HDL

A

apoA1 and apoA2

118
Q

what is an example of LDL/VLDL

A

apoB-100

119
Q

what is example of chylomicrons

A

apoB-48

120
Q

what is the role of ApoB containing lipoproteins

A

deliver triglycerides to muscle for ATP biogenesis and adipocytes for storage

121
Q

where are chylomicrons formed and what is their role

A

intestinal cells and transport dietary triglycerides - carried in lymph to systemic circulation (subclavian vein) via thoracic duct - exogenous pathway

122
Q

where are VLDL formed and what is their role

A

formed in liver cells from free fatty acids derived from adipose tissue (during fasting) and de novo synthesis and transport triglycerides synthesised in that organ - endogenous pathway

123
Q

what is lipoprotein lipase (LPL)

A

lipolytic enzyme associated with endothelium capillaries in adipose and muscle tissueIt hydrolyses core triglycerides to free fatty acids and glycerol which enters tissues

124
Q

what facilitates the binding of chylomicrons and VLDL particles to LPL

A

ApoCII

125
Q

what are examples of statins

A

simvastatin and atorvastatin

126
Q

when are statins used

A

drug of choice to reduce LDL - reduce LDL by 60% and triglycerides by 40%, also increase HDL by 10%other benefits: decreased inflammation, thrombosis and stabilisation of plaquesorally at night

127
Q

how do statins work

A

competitive inhibitors of HMG-CoA reductase - rate limiting step in cholesterol synthesis decrease in cholesterol causes increase in LDL receptor thus enhances its clearance

128
Q

give examples of fibrates

A

bexafibrate and gemfibrozil

129
Q

when are fibrates used

A

pronounced decrease in triglycerides (first line drugs in patient with very high triglycerides)

130
Q

how do fibrates work

A

act as agonists of nuclear receptor (PPARa) to enhance transcription of genes, including encoding LPL

131
Q

what are adverse effects of fibrates

A

myositis, best avoided in alcoholics who are predisposed to hypertriglyceridaemias but also rhabdomyolysis other effects (GI symptoms, pruritus and rash) greater than for statins

132
Q

give examples of drugs that inhibit cholesterol absorption

A

colestyramine, colestipol and colsevelam

133
Q

how do drugs that inhibit cholesterol absorption work

A

bind to bile acid and cause excretion of bile salts resulting in more cholesterol to be converted to bile salt by interrupting enterohepatic recycling ingested orally, not absorbed from GI tract which prevents reabsorption of bile saltsalso causes decreased absorption of triglycerides and increased LDL receptor expression

134
Q

what is adverse effects of drugs which inhibit cholesterol absorption

A

GI tract irritation

135
Q

what is a drug which inhibits the transport of cholesterol

A

ezetimible

136
Q

who do drugs which inhibit the transport of cholesterol work

A

act to inhibit NPC1L1 transport protein in enterocytes of duodenum, reducing the transport of cholesterol decrease in LDL with little change in HDL

137
Q

when is drugs in inhibit transport of cholesterol work

A

used in combination with statins when latter alone does not achieve sufficient response orally - metabolised to activate metabolite that undergoes enterohepatic recycling that contributes to long half life (22hr)

138
Q

what are adverse effects of drugs that inhibit transport of cholesterol

A

diarrhoea, abdominal pain and headache contradicted in breast feeding females

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