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Medical Studies 1 > CVS week 1 > Flashcards

CVS week 1 Flashcards

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1
Q

what are the surfaces of the heart

A

right pulmonary surface

anterior surface

posterior surface

left pulmonary surface

diaphragmatic surface

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2
Q

describe the chambers of the heart in relation to the heart surfaces

A

the right atrium is along the right pulmonary surface and posterior surface

the left atrium is along the posterior surface

the right ventricle is along the anterior surface and diaphragmatic surface

the left ventricle is along the anterior surface and diaphragmatic surface

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3
Q

describe the chambers of the heart in relation to the cardiac borders

A

the right border forms the right atrium

the left border forms the left ventricle

the inferior border forms the right ventricle

the superior border forms the right and left atria

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4
Q

describe the fibrous cardiac skeleton of the heart

A

dense fibrous connective tissue forming the ‘skeleton’ of the heart to allow attachment of the valves and electrical isolation in terms of cardiac conduction

contains the fibrous coronet (aortic and pulmonary valves) and fibrous rings (mitral and tricuspid valves)

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5
Q

describe the function of the right atrium

A

receives deoxygenated blood from the body via the IVC and SVC

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6
Q

describe the function of the right ventricle

A

receives deoxygenated blood from the right atrium via the right atrioventricular opening, which is then pumped into the pulmonary circulatory system via the pulmonary artery

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7
Q

describe the function of the left atrium

A

receives oxygenated blood from the lungs via the 4 pulmonary veins

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8
Q

describe the function of the left ventricle

A

receives oxygenated blood from the left atrium via the left atrioventricular opening, which is then pumped into the systemic circulatory system via the aorta

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9
Q

describe the function of the atrioventricular (AV) valves

A

the tricuspid valve prevents back flow of blood into the right atrium from the right ventricle

the mitral valve prevents the back flow of blood into the left atrium from the left ventricle

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10
Q

how is eversion of the AV valves prevented

A

both AV valves are connected to papillary muscles via cordae tendinae, preventing the valves from collapsing in on themselves

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11
Q

describe the function of the semilunar (SL) valves

A

the aortic valve prevents back flow into the left ventricle from the aorta

the pulmonary valve prevents back flow into the right ventricle from the pulmonary trunk

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12
Q

why do cardiomyocytes have a high cell to capillary ratio

A

they have a high oxygen demand

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13
Q

where are the orifices of the coronary arteries located

A

above the aortic valve

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14
Q

the source of the posterior interventricular artery and posterior left ventricular artery determines…

A

whether the coronary circulation has a balanced distribution, left coronary dominance or right coronary dominance

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15
Q

describe the left coronary artery

A

ostium in left coronary sinus

runs b/w posterior part of pulmonary trunk and left auricle

gives rise to the LAD and left circumflex

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16
Q

describe the left anterior descending (LAD) artery

A

anastomoses w posterior interventricular artery

supplies 2/3 of interventricular septum

supplies adjacent left and right ventricles

gives off lateral branch

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17
Q

describe the left circumflex artery

A

runs along the coronary sulcus

gives off left marginal branch (supplies LV)

occasionally posterior left ventricular branch

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18
Q

describe the right coronary artery

A

ostium in right coronary sinus

runs along sulcus b/w right side pulmonary trunk and right auricle

gives rise to right marginal branch, AV nodal branch, posterior interventricular branch

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19
Q

what does the right marginal branch supply

A

adjacent right ventricle

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20
Q

what does the AV nodal branch supply

A

AV node

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21
Q

what does the posterior interventricular branch supply

A

1/3 of posterior interventricular septum

adjacent left and right ventricles

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22
Q

in a normal balanced distribution of the coronary circulation, what does the LEFT coronary artery supply

A

LV
LA
part of RV
2/3 interventricular septum
AV bundle
SA node (in 40% of ppl)

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23
Q

in a normal balanced distribution of the coronary circulation, what does the RIGHT coronary artery supply

A

most of RV
RA
diaphragmatic part of LV
1/3 interventricular septum
AV node (80% of ppl)
SA node (60% of ppl)

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24
Q

when is coronary perfusion at its highest

A

during diastole

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25
Q

what factors regulate vascular diameter

A

autoregulation
metabolic factors
endocrine molecules
autonomic innervation
physical factors
endothelial factors

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26
Q

what is autoregulation of vascular diameter

A

maintenance of blood flow in response to different perfusion pressures

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27
Q

what are examples of endothelial factors affecting vascular diameter

A

NO
PGI2
EDHF
ET

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28
Q

outline sympathetic innervation of coronary arteries

A

innervation of conduction system, coronary arteries, cardiomyocytes

pre-ganglionic fibres from lateral horn of spinal cord

post-ganglionic fibres from 3 cervical ganglia and sympathetic chain

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29
Q

outline parasympathetic innervation of coronary arteries

A

innervation of conduction system and coronary arteries

pre-ganglionic fibres w cell bodies in vagal nuclei of brainstem and travel w vagus nerve

post-ganglionic fibres from neurons of cardiac plexus

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30
Q

what two factors impact blood flow through a vessel

A

pressure gradient (difference in pressure b/w two ends of a vessel)

vascular resistance (impediment to flow through a vessel)

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31
Q

what is Ohm’s law

A

flow = pressure gradient / resistance

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32
Q

what are the two types of blood flow typically observed

A

laminar flow

turbulent flow

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33
Q

what is laminar blood flow

A

blood flows in streamlines with each layer remaining the same distance from the vessel wall

highest velocity in centre of vessel

lowest velocity along vessel wall

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34
Q

what is turbulent blood flow

A

blood flow is disorderly, flowing crosswise in the vessel

increases resistance and energy required to maintain flow

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35
Q

when does flow become turbulent

A

rate of flow too high

blood passes an obstruction or makes sharp turn

blood passes over a rough surface

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36
Q

what is reynold’s number

A

tendency for turbulence to occur

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37
Q

how is reynold’s number calculated

A

(velocity x diameter x density) / viscosity

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38
Q

what are 5 factors affecting vascular resistance

A

vessel diameter

vessel length

organisation of vascular network

characteristics of blood

extravascular mechanical forces

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39
Q

what is vascular conductance

A

measure of blood flow through a blood vessel for a given pressure gradient

it is proportional to the fourth power of the diameter

it is highly sensitive to variations in vessel diameter

increases in resistance will reduce vascular conductance (vice versa)

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40
Q

how is vascular conductance calculated

A

conductance = 1 / resistance

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41
Q

what does poiseuille’s equation illustrate and what is the equation

A

it basically highlights that pressure, vessel radius, blood viscosity, and vessel length are all key factors that influence blood flow

flow = (pi x pressure gradient x fourth power radius) / (8 x viscosity x length)

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42
Q

What are 3 features of the coronary circulation

A

High O2 consumption

High resting O2 extraction

Limited anaerobic capacity

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43
Q

Adjustments to supply of O2 to the cardiac muscle is primarily governed by changes in…

A

Coronary vasomotor tone

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44
Q

What is the influence of PO2 in terms of coronary blood flow

A

Venous PO2 acts as an estimate for myocardial tissue PO2

Hence, a greater O2 demand would potentially decrease coronary venous PO2

A decreased PO2 results in an increase in CBF

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45
Q

What are 5 metabolic vasodilatory influences released during periods of high cardiac metabolic demand

A

PCO2

H+

K+

Adenosine

PO2

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46
Q

What is the effect of adrenergic alpha receptors and where are they located

A

They have a vasoconstrictory effect

Located mostly in larger, upstream epicardial vessels

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47
Q

What is the effect of adrenergic beta receptors and where are they located

A

They have a vasodilatory effect

Located mostly within small, intramuscular vessels

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48
Q

What is the effect of endothelial NO on coronary blood flow

A

NO production is stimulated by endothelial shear stress

It results in a vasodilatory effect

Its effect is greatest under conditions of reduced perfusion pressure e.g ischemia

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49
Q

Describe regulation of coronary blood flow under physiological stress

A

Parallel mechanisms act to increase CBF

This means that no single mechanism is mandatory but they can also work in conjunction to produce larger effects and can also have a compensatory effect when one mechanism is blocked/inhibited

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50
Q

What are 2 determinants of coronary blood flow

A

Coronary perfusion pressure

Coronary vasomotor tone

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51
Q

Outline how extravascular influences impact coronary blood flow

A

Compressive forces generated during LV contraction reduces CBF, more so in the endocardium than the epicardium, resulting in an increased CBF during diastole compared to systole

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52
Q

what are the 3 general stages of plaque formation in atherosclerosis

A
  1. initiation of atherosclerosis - inflammation
  2. mid stage atherosclerosis - switch from acute to chronic inflammation
  3. late stage atherosclerosis - less of an impact of vascular inflammation
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53
Q

what are 5 triggers of endothelial injury

A

physical injury or stress

turbulent blood flow

circulating reactive oxygen species (free radicals)

hyperlipidaemia

chronically elevated blood sugar levels

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54
Q

what happens during the initiation stage of atherosclerosis

A

damage to endothelium which leads to the upregulation of adhesion molecules such as selectins, chemokines, VCAM-1 and ICAM-1

then, LDLs to enter the intimal layer

then, the LDLs are oxidised into ox-LDL

then, due to the selectins, chemokines, integrins and CAMs, monocytes are attracted to the site of endothelial injury

then, the chemokines allow the monocytes to enter the intimal layer too via endothelial transmigration

then, the monocytes differentiate into macrophages

then, the macrophages phagocytose the ox-LDL

then, they continue to take up ox-LDL which leads to the formation of foam cells

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55
Q

what happens during the mid stage atherosclerosis

A

macrophages continue to take up LDL in unregulated manner which leads to apoptosis of themselves

then, macrophages secrete pro-inflammatory cytokines (e.g interleukins and chemokines) and sets up a chronic inflammation process

then, smooth muscle cells migrate from the vessel wall into the plaque

then, these SMCs secrete collagen in an effort to form a fibrous cap on the developing plaque to stabilise it

then, neovessels start to invade the plaque

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56
Q

what happens during late stage atherosclerosis

A

the size of the lipid core grows continually

then, the fibrous cap becomes unstable, mainly at their shoulder regions

then, there is increased BP at this site due to increased plaque size, which can trigger the plaque to rupture

then, the contents of the plaque are released into the blood stream which can lead to MI or stroke

then, a thrombus forms, which further occludes the vessel

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57
Q

what are selectins

A

family of 3 C-type lectins expressed exclusively on bone marrow-derived cells and endothelial cells

membrane-bound proteins

58
Q

what are 3 types of selectins

A

L (leukocyte)

E (endothelial)

P (platelet + endothelial)

59
Q

what is the main role of selectins

A

mediate monocyte adhesion under flow. ie tether or capture

60
Q

what are 3 key selectin ligands that monocytes can use to bind to the endothelium

A

PSGL1

ESL1

CD44

61
Q

what are integrins

A

membrane-bound proteins

must be activated in order to bind their ligands

adherence is weak when activated by selectins

adherence is strong and allows interactions with ICAM and VCAM when activated by chemokines

62
Q

what are 4 examples of integrins

A

alpha-L-beta-2

VLA-1

alpha-4-beta-1

LFA-1

63
Q

what are CAMs

A

cell adhesion molecules

transmembrane proteins

64
Q

what is VCAM-1

A

vascular CAM

induced by inflammatory stimuli

binds to VLA-1 and alpha-4-beta-1 integrins

predominantly expressed on endothelial cells but is also present on SMCs

65
Q

what is ICAM-1

A

intercellular CAM

induced by inflammation but more constitutively expressed

binds to LFA-1

expressed on endothelial cells and also on leukocytes including neutrophils and monocytes

66
Q

what are chemokines

A

chemoattractant cytokines

function through 7 transmembrane g-protein-coupled receptors

4 major families

67
Q

what is the fatty streak

A

early stage atherosclerosis

precursor lesions of complex atheroma as they lack features like fibrosis, thrombosis, calcification

68
Q

is plaque progression linear

A

no, bursts of growth may occur during life history of plaque prompted by episodes of plaque disruption with thrombosis

69
Q

what can be used to visualise proliferating macrophages in plaque

A

BrdU

this binds to replicated DNA of macrophages so that proliferating macrophages can be seen in flow cytometry or immunofluorescence

70
Q

what is atherosclerotic plaque neovascularisation

A

inflammatory process that occurs in late stage plaques

initially driven by hypoxia as plaque becomes larger

vessels deliver inflammatory cells that secrete growth factors that promote further neovascularisation

plaque neovessles are fragile and permeable, which contributes to its instability

71
Q

what 6 things can make plaque unstable or vulnerable

A

thin fibrous cap

large lipid core

abundant inflammatory cells

punctate or spotty calcification

few SMCs

increased neovascularisation

72
Q

what are 2 types of plaque destabilisation

A

plaque rupture

superficial erosion

73
Q

what is superficial erosion

A

lipid poor plaque

proteoglycan rich

high triglycerides

female predominance

endothelial cell apoptosis

74
Q

what are 7 key cell types in atherosclerosis

A

neutrophils

monocytes

macrophages

smooth muscle cells

platelets

dendritic cells

T cells

75
Q

what is the role of platelet and monocyte interactions in the initiation of atherosclerosis

A

activated platelets exacerbate atherosclerosis

they release chemokines

increase inflammation

76
Q

what is the role of macrophage and SMCs interaction in initiation of atherosclerosis

A

they move towards top of plaque, secrete collagen and form a cap

they contribute to plaque expansion by releasing inflammatory chemokines

they anchor monocytes into the plaque

macrophages trigger SMC apoptosis causing further instability

77
Q

describe differentiation of macrophages into dendritic cells that leave the plaque

A

when exposed to a regressive environment, the macrophages can leave the plaque by increasing their expression of CCR7 which allows them to acquire a macrophage-dendritic dual phenotype so that they can leave via the lymphatic system

78
Q

what are 4 key determinants of blood pressure

A

intravascular volume

autonomic NS

RAAS

local vascular factors

79
Q

what are the 4 types of adrenergic receptors (adrenoreceptors)

A

alpha 1

alpha 2

beta 1

beta 2

80
Q

what are the two generic types of hypertension

A

primary (90-95% of cases)

secondary

81
Q

what are 5 causes of secondary hypertension

A

metabolic syndrome

renal e.g parenchymal or vascular disease or phaeochromocytoma

adrenal e.g cushing’s syndrome or hyperaldosteronism

other endocrinopathies e.g thyroid issues, increase PTH

medications and non-prescribed drugs

82
Q

what are 7 complications of hypertension

A

left ventricular hypertrophy

coronary heart disease

heart failure

stroke

renal failure

peripheral vascular disease

retinopathy

83
Q

describe the prevalence of hypertension in men globally

A

34% of men have hypertension

51% of men w hypertension are not even diagnosed

out of all the men w diagnosed hypertension, only 18% are both treated and controlled

84
Q

describe the prevalence of hypertension in women globally

A

32% of women have hypertension

41% of women w hypertension are not even diagnosed

out of all the women w diagnosed hypertension, 23% are both treated and controlled

85
Q

describe the prevalence of hypertension in australia

A

33.7% of the population has hypertension

36% of men have hypertension

31.4% of women have hypertension

86
Q

what classifies as normal BP

A

<130 systolic

AND

<85 diastolic

87
Q

what classifies as high-normal BP

A

130-139 systolic

AND/OR

85-89 diastolic

88
Q

what classifies as grade 1 hypertension

A

140-159 systolic

AND/OR

90-99 diastolic

89
Q

what classifies as grade 2 hypertension

A

> = 160 systolic

AND/OR

> = 100 diastolic

90
Q

what are the 3 ‘types’ of severe hypertension

A

severely elevated BP without symptoms

hypertensive urgency

hypertensive emergency

91
Q

describe severely elevated BP without symptoms

A

180/110 or higher

no symptoms

no end organ damage

no immediate threat to life

1-2 days timeframe to achieve initial BP reduction

92
Q

describe hypertensive urgency

A

180/110 or higher

symptoms present

acute end organ damage is not present but moderate nonacute damage may be present

no immediate threat to life

few hours timeframe to achieve initial BP reduction

93
Q

describe hypertensive emergency

A

usually 220/140 or higher

symptoms present

significant acute end organ damage

immediate threat to life

few minutes timeframe to achieve initial BP reduction

94
Q

what are clinical features of hypertension

A

for the most part, patients may be asymptomatic

however, very high BP can present w headaches, epistaxis, arrythmia, chest pain, dyspnoea, visual issues, and confusion

in terms of end organ damage, coronary heart disease, stroke, renal impairment and retinopathy may be present

95
Q

what is the difference between primary and secondary hypertension

A

primary hypertension does not have a definitive cause whereas secondary hypertension has a known cause

96
Q

describe the pathophysiology behind secondary hypertension caused by CKD

A

reduced renal function leads to sodium and fluid retention, which increases intravascular volume, hence an increased BP

97
Q

describe the pathophysiology behind secondary hypertension caused by RENOVASCULAR HYPERTENSION

A

stenosis of renal arteries reduces blood flow to kidneys, activating the RAAS

98
Q

describe the pathophysiology behind secondary hypertension caused by HYPERALDOSTERONISM

A

excess aldosterone causes sodium retention and potassium secretion

99
Q

describe the pathophysiology behind secondary hypertension caused by PHAEOCHROMOCYTOMA

A

adrenal tumours secrete catecholamines which increases heart rate and vascular resistance

100
Q

describe the pathophysiology behind secondary hypertension caused by CUSHINGS SYNDROME

A

excess cortisol increases blood volume and vascular sensitivity to catecholamines

101
Q

describe the pathophysiology behind secondary hypertension caused by HYPER/HYPOTHYROIDISM

A

imbalances in thyroid hormones affect cardiac output and vascular resistance

102
Q

describe the pathophysiology behind secondary hypertension caused by COARCTATION OF THE AORTA

A

narrowing of the aorta increases resistance to blood flow

103
Q

how can primary hypertension be diagnosed and investigated

A

BP measurements

history and physical exams

basic tests e.g blood tests, urinalysis, ECG

104
Q

how can secondary hypertension be diagnosed and investigated

A

renal function tests

imaging

hormonal assays

105
Q

What are 5 different types of chest imaging

A

CXR

Chest CT

Chest MRI

Ultrasound

Digital subtraction angiography

106
Q

What are 5 types of chest CT

A

High resolution CT chest (HRCT)

Standard post contrast CT chest

CT aortogram (CTA)

CT pulmonary angiogram (CTPA)

CT coronary angiogram (CTCA)

107
Q

What angle is a standard CXR done at

A

Posteroanterior

Can also do a lateral view

108
Q

What densities can an X-ray depict

A

Air

Fat

Fluid/soft tissue

Bone

Metal

109
Q

What are X rays good for

A

Looking at bones and distinguishing air-filled structures from fluid filled/soft tissue

110
Q

What is a limitation of X-ray

A

Adjacent tissues of the same density cannot be distinguished from each other meaning it does not distinguish different types of soft tissue e.g heart muscle and blood look the same

111
Q

Describe a PA standard X-ray

A

X-ray beam traverses from patient posterior to anterior

Upright in full inspiration

Beam is horizontal

X ray tube is 6 feet away from film

Patient is close to the film which reduces magnification and increases sharpness

112
Q

Describe a lateral film in a standard X ray

A

Left side of chest against X ray cassette

Also taken at 6 feet

Left hemidiaphragm is not differentiated from the heart anteriorly as they are of same density

Right sided nodule will appear larger than an identical left sided nodule due to increased magnification

113
Q

Describe an anteroposterior film in a standard X-ray

A

Usually portable film for adult patients too sick to tolerate normal PA view

Children are viewed using AP

May be supine or sitting

Taken at shorter distance from film therefore greater magnification and less sharp images

Cardiomediastinal contour is augmented

Lung markings may appear crowded

114
Q

Describe a lordotic view of standard X-ray

A

Patient leans slightly back so that clavicles are raised and projected above the lungs

Allows for assessment of apical pathology that may be obscured on a frontal film

115
Q

Describe a lateral decubitus view of a standard X-ray

A

Patient lays down on their side

Intrapleural fluid layers differentiate

Intrapleural air rises

If air-trapping is present, there is no physiological collapse of the lungs

116
Q

Describe an expiration view of a standard X ray

A

Less air in lungs so they appear denser and the lung markings are more crowded

Heart is elevated and appears large

Can be used to detect focal air trapping (obstructed lung will appear blacker)

May accentuate a small pneumothorax (the fixed amount of Intrapleural air is relatively larger)

117
Q

Describe a systemic approach in interpreting a CXR

A

Go inside out:

Heart

Mediastinum

Hilar

Lungs

Pleural reflections

Upper abdomen

Bones

Soft tissues

118
Q

Describe computed tomography (CT) scans

A

2D images in the axial plane but can be reconstructed in multiple 2D planes and in 3D

Greater contrast resolution than CXR

Can be given contrast to improve resolution

Images can be manipulated (windowed) post acquisition to accentuate different tissue densities

119
Q

What are CT scans good for

A

Ability to locate lesions in 3D space

Allows differentiation between different soft tissues

120
Q

What are two other post processing techniques of CT scans

A

MPR - multiplanar reconstructions

MIP - maximum intensity projection

121
Q

What are hounsfiled units

A

Standardised unit, relative to water, reflecting attenuation or density

122
Q

What is the hounsfield unit of air

A

-1000

123
Q

What is the hounsfield unit of fat

A

-120 to -90

124
Q

What is the hounsfield unit of water

A

0

125
Q

What is the hounsfield unit of organs

A

20 to 60

126
Q

What is the hounsfield unit of bone

A

2000

127
Q

What is the hounsfield unit of metal

A

3000

128
Q

What can standard CT chest indicate

A

Pneumonia

Malignancy

Pleural disease

129
Q

What can HRCT indicate

A

Parenchymal disease e.g interstitial lung disease

130
Q

What can CTA indicate

A

Aortic pathology

131
Q

What can CTPA indicate

A

Pulmonary embolism

132
Q

What can CTCA indicate

A

Coronary artery disease

133
Q

Describe standard CT chest

A

Performed post contrast

Triggered at ~20 seconds when the contrast is in the arterial system

Also includes upper abdomen (liver)

134
Q

Describe HRCT

A

Non contrast

Thin slices obtained

Excellent detail of lung parenchyma

Sometimes additionally performed in expiration (to look for air trapping)

Sometimes additionally performed prone (to differentiate b/w dependent change and true pathology)

135
Q

Describe CTA

A

More rapid injection of contrast

Maximise enhancement of aorta

Can be ‘gated’ to minimise pulsation artefact (scan is triggered to a particular point in the cardiac cycle using ECG)

Usually mid to end diastolic phase

136
Q

Describe CTPA

A

Contrast injected at rapid rate

Timed for peak contrast enhancement in the pulmonary arteries

Apices to diaphragm only

137
Q

Describe CTCA

A

Uses high contrast flow rate

Timed for peak opacification of coronary arteries

Medications sometimes used to lower heart rate, avoid arrhythmia and dilate coronary arteries e.g beta blockers

ECG gated

Post processing - curved reconstructions, MPR, MIP

138
Q

Describe MRI

A

Limited use cases

Superior soft tissue resolution

Can acquire 4D imaging

139
Q

What can MRI be used for

A

Cardiac MRI

Chest wall pathology

Mediastinal pathology

140
Q

Describe DSA

A

Better visualisation of inside of vessels

Limited info about surrounding tissues

Allows angiographic interventions e.g angioplasty and stenting

141
Q

What makes up the mediastinal borders on a frontal CXR

A

Brachiocephalic vein

SVC

RA

IVC

Left subclavian artery

Aortic knob

Main pulmonary artery

Left atrial appendage

LV

142
Q

Describe the position of the cardiac valves in a lateral X-ray

A

Imaginary line from carina to cardiac apex:
P and A valves above
T and M valves below

Imaginary horizontal line bisect cardiac silhouette:
A valve upper
M valve lower
T valve anterior
P valve posterior

Medical Studies 1 (16 decks)

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