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Z MD1 Cardiac physiology > Cardiac histology and pathology > Flashcards

Cardiac histology and pathology Flashcards

1
Q

Cytokines that cause increased adhesion molecules on endothelial cells during atheroma formation

A

IL-1 and MCP-1

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2
Q

potential consequences of emboli

A

transient ischaemia

infarction

acute respiratory compromise

death

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2
Q

definition of hyperplasia

A

an increase in number of cells

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3
Q

function of tunica adventitia

A

anchors BV to surrounding tissue

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3
Q

definition of embolus

A

intravascular solid, liquid or gaseous mass carried in the blood stream to some site remote from its origin or point of entrance into the blood stream

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3
Q

cytokines that attract macrophages and T cells during atheroma formation

A

IL-1 and MCP-1

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4
Q

potential complications of thrombus

A

obstruction to blood flow embolism

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4
Q

Which type of T cells are involved in the formation of atheroma and what do they do

A

Th1 cells

provide IL-2 to help monocytes differentiate into macrophages

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5
Q

Function of intercalated dics

A

Anchor actin filaments in one cells sarcomere to the sarcomere in the other via fascia adherens

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6
Q

what is the importance of venules

A

preferred site of diapedesis of leukocytes

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6
Q

What is ischaemia?

A

a deficiency, real or relative, of oxygen blood in a tissue causing a shortage of oxygen and impaired aerobic respiration

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6
Q

types of aneurysms

A

saccular - focal dilation fusiform - entire circumference dilated false aneurysm - blood goes into the extravascular CT surrounding the BV

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6
Q

potential causes of infarction

A

arterial occlusion venous occlusion systemic reduction in tissue perfusion compartment syndrome

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6
Q

haematoma definition

A

collection of blood outside the blood vessel

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6
Q

timescale of morphological (macroscopic) changes after infarct

A
  • see nothing for hours - by 1-2 days, pale, creamy area - when older - fibrous tissue - old infarct - whiter, no haemorrhage around it and the wall is often thinnger
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8
Q

endocardium of the heart composed of

A

endothelial squamous epithelium, subendocardial CT

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9
Q

where are elastic arteries found?

A

close to the heart where there is the highest BP fluctuations

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10
Q

structure of veins

A

media thinner than arteries adventitia thicker than veins valves (assissted by skeletal muscle contractions)

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11
Q

function of tunica media

A

constricts the lumen of the BVs, –> increasing resistance –> increase in BP

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11
Q

why does hypertophy occur

A

due to an increased functional demand or stimulation by hormonal or growth factors

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12
Q

Cytokines produced by macrophages that recruit SM cells from media and precursors from blood in atheroma formation

A

TGF-beta and PDGF

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13
Q

non modifiable risk factors for atherosclerosis

A

age - >45 in men and post menopausal in women gender - male>female (?oestrogen protection) genetic

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13
Q

causes of aneurysms?

A

atherosclerosis congenital weakness in the wall systemic hypertension infection in the artery wall

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13
Q

why does hyperplasia occur

A

due to stimulation by hormones or growth factors

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13
Q

Microscopic changes at 10 days after MI

A
  • most necrotic tissue has gone - infarcted area largely occupied by residual macrophages, lymphocytes and plasma cells in loose oedematous mesh in which few capillaries and fibroblasts herald earliest signs of granulation tissue
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14
Q

tunica media composed of

A

smooth muscle arranged concentrically

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14
Q

the meta arteriole is characterised by

A

incomplete smooth muscle coat

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14
Q

classifications of gangrene

A

primary secondary - wet and dry

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15
Q

what is a thrombus?

A

a clotted mass of blood that forms within the cardiovascular system during life

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16
Q

how does diabetes mellitus increase your risk for atherosclerosis?

A

causes chronic hyperglycaemia which cause AGE –> leads to oxidate stress and endothelial alterations Altered balance of LDL and HDL and have smaller denser LDL (more atherogenic)

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16
Q

haemorrhagic infarct normally due to

A
  • venous occlusion and resulting significant congestion - arterial occlusion and then collateral supply congestion - reperfusion
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17
Q

most cells in the body are within what distance of a capillary

A

50 microns

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19
Q

structural features of medium to large veins

A

subendothelial CT well developed adventitia enlarged (often at the expense of media)

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20
Q

what causes venuous infarcts?

A

venous occlusion arterial occlusion - then colateral supply congestion reperfusion

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21
Q

histology of muscular arteries

A

little elastin in the media - it is concentrated in the internal and external elastic laminae

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22
Q

What causes an aneurysm?

A

loss of muscle and elastin from the media causes weakening of the vessel wall, predisposing to a localised area of dilatation

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23
Q

what are the two possible mechanisms for sudden cardiac death?

A
  • arrhythmic - most common - mechanical - tamponade
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25
Q

epicardium of the heart composed of

A

simple squamous epithelium, subepicardial CT with BVs, fat, and nervous tissue within

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25
Q

what is arteriosclerosis

A

thickening and hardening of walls of arteries - generally via fibrosis and deposition of ECM non-specific term - includes atherosclerosis and age related changes

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25
Q

what features influence the development and size of an infarct?

A
  • the size of the artery occluded - the duration of occlusion - the vulnerability of the cells involved - whether the artery is carrying oxygenated or deoxygenated blood - the nature of the arterial supply - the oxygen content of the blood - the st
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26
Q

how many layers of smooth muscle do arterioles have

A

1-3

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26
Q

macroscopic look of arterial thrombus and venous thrombus

A

arterial - dense and composed mainly of aggregated platelets and fibrin venous - resembled clotted blood containing masses of WBC and RBC

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28
Q

What causes the lipid rich core of atherosclerosis?

A

The entry of LDLs into the intima (due to endothelial dysfunction), which are phagocytosed by macrophages (recruited by chemokines), which are then degraded over time to release the lipid which associate with cholesterol crystals

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30
Q

tunica intima composed of

A

simple squamous epithelium lying on a basal lamina, supported by a thin, subendothelial CT layer

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31
Q

how does the medial layer thin during atheroma formation

A
  • loss of supporting elastic tissue - atrophy of smooth muscle - progressive medial fibrosis
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32
Q

histological signs of atherosclerosis (7)

A

fibrous cap around lumen lipid rich core ECM in intima chronic inflammatory cells foam cells calcification cholesterol clefts

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32
Q

which area (in general) of the heart does the right coronary artery supply

A

POSTERIOR (inferior part of LV, part of the RV, 1/3 of IV septum)

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33
Q

which area (in general) of the heart does the circumflex branch suppy

A

LATERAL side of LV

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33
Q

definition of atrophy

A

when cells decrease in size and activity

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33
Q

definition of involution

A

physiological atrophy involving apoptosis

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34
Q

what are the causes of hypoxia?

A

ischaemia impaired respiratory function decrease in oxygen carrying capacity of the blood

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35
Q

what causes arteriolosclerosis

A

endotheilal stress - walls become leaky - deposition of plasma proteins and increased collagen in the wall. Causes the wall to become thickened by homogenous eosinophilic glassy materia - narrowing the lumen

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35
Q

How are smooth muscle cells recruited to the intima during atheroma formation

A

Via TGF-B and PDGF released by macrophages

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36
Q

Where is the elastin concentrated in elastic and muscular arteries?

A

elastic - in the media muscular - in the intima

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38
Q

what kind of plaque is most susceptible to rupture

A

plaques with thin fibrous caps

39
Q

what causes the lines of Zahn

A

successive deposition of a number of layers of thrombus

40
Q

steps in the healing of inarction

A
  1. coagulative necrosis 2. acute inflammation 3. organization 4. scarring
41
Q

what alters oxygen supply to the myocardium?

A

oxygen content of blood myocardial blood flow

42
Q

what alters myocardial oxygen demand

A

ventricular wall stress heart rate contractility

43
Q

levels of creatinine kinase in the blood after infarction?

A
  • levels go up at about 3-4 hours - peaks after 24 hours - gone by 4 days
44
Q

function of muscular arteries

A

distribute blood to the tissues and regulate BP

45
Q

different collagen types in the media and adventitia

A

media - collagen III adventitia - collagen I

46
Q

fates of a thrombus

A
  1. embolisation 2. fibrinolysis 3. organisation 4. persistence
46
Q

definition of hypertrohy

A

an increase in size of existing cells (no cell division)

48
Q

What is hypoxia?

A

Deficiency of oxygen in the tissues

48
Q

when does wet gangrene occur?

A

complicates acute apendicitis or cholecystectomy or infarction of the small wall

50
Q

function of arterioles

A

distribute blood to capillaries contribute most to BP

51
Q

potential causes of infarction

A

arterial occlusion venous occlusion systemic reduction in tissue perfusion compartment syndrome

52
Q

function of elastic arteries

A

passive contraction of the BV means blood flow is continuous, but pulsatile

53
Q

how is the tunica media CT made?

A

the smooth muscle cells themselves secrete the CT in which it is embedded

55
Q

CT of tunica adventitia

A

collage type 1 and elastin, plus ground substance

56
Q

causes of cardiac valve disease

A
  • congential - prolapse mitral valve -degenerative (calcification)
57
Q

definition of sudden cardiac death

A

unexpected fatal event occurring within 1hour of the beginning of symptoms or one whose disease was not so severe as to predict such an outcome

59
Q

what is ischaemia due to?

A

increased demand for oxygen that isn’t met local vascular narrowing/occlusion systemic reduction in tissue perfusion

60
Q

what is an embolus?

A

an intravascular solid, liquid or gas mass carried in the bloodstream to some site remote from its origin or point of entrance into the blood stream

62
Q

where to pale infarcts mainly occur

A

spleen, kidney and heart

63
Q

What is a mural thrombis

A

Thrombus n the heart or major artery that covers part of the luminal wall as a plaque like structure

64
Q

levels of troponin in the blood after infarction?

A
  • elevated at about 3 hours after - peak at about 36 hours - back to normal after 10-14 days
65
Q

What is atherosclerosis?

A

accumulation of lipid and fibrous CT in the INTIMA of medium and large arteries caused by endothelial dysfunction and chronic inflammation

66
Q

timescale of histological changes after infarct?

A
  • 1 day - dead muscle tends to be more eosinophilic with wavy fibres with few netrophils - 2 days - more neutrophils, nuclei start to fade (coagulative necrosis) - 1-2 weeks - granulation tissue (no nuclei) - months - fibrous scar
66
Q

microscopic changes at 12 hours after MI (starts at 4 hours)

A
  • patchy loss or blurring of cross-striations - become more intensely stained by eosin - may have early neutrophil infiltrate, interstitial oedea and capillary engorgement as part of the acute inflammatory response
68
Q

what is a mycotic aneurysm?

A

an aneurysm due to an infection in the wall

69
Q

Microscopic changes over weeks after MI

A

granulation tissue

71
Q

examples of chronic ischaemia

A

1) claudication in the legs 2) chronic ischaemia in the heart due to severe atherosclerosis of coronary arteries –> subendocardial scarring and LV failure –> heart failure

72
Q

how long before myocytes die?

A

20-40 minutes

73
Q

structure of capillaries

A

a single endothelial cell rolled into a tube, sealed with a tight junction, lying on a basal lamina Sometimes associated with a pericyte surrounded by only a few collagen fibres (adventitia)

74
Q

acute ischaemia is frequently due to what

A

an increased demand for oxygen that is not met

76
Q

pathogenesis of thrombus (3)

A

1) arterial thrombi - mostly caused by atherosclerosis or aneurysm 2) cardiac thrombi - following infarction or in LV aneurysms, AF, inflammation of valves 3) venous thrombi - slowing of blood, hypercoagulability

77
Q

what are the age related changes of the BVs

A

aortic arteriosclerosis arteriolosclerosis

78
Q

role of endothelium in BVs

A
  • actively inhibit clotting - prime underlying subendothelial CT with VW factor (activates clotting) - release vasoactive substances
80
Q

what type of CT in tunica media

A

collage type 3 (reticulin), elastin and ground substance

81
Q

common complications of myocardial infarction

A
  • fatal arrythmia - acute cardiac failure - pulmonary oedmea (due to LV failure) - thrombus forms in LV - embolise - stroke - pericarditis -rupture of papillary muscle - valvular incompetence - rupture of free wall of LV - cardiac tamponade - infa
83
Q

potential causes of infarction (4)

A

1) Arterial occlusion - most common (usually thrombotic) 2) venous occlusion - generally thrombotic or twisting of veins 3) systemic reduction in tissue perfusion 4) other: eg. compartment syndrome

85
Q

what is vasa vasorum

A

blood supply to the tunica adventitia

86
Q

How do cholesterol clefts form

A

Formed from foam cell reak down liberating free lipid - forming cholesterol clefts

88
Q

What is difference about a dissecting aneurysm?

A

The blood goes into the medial layer - wall does not balloon out

89
Q

What is the earliest sign of atherosclerosis on a blood vessel?

A

fatty streaks

90
Q

what is primary gangrene

A

gas gangrene - due to anaerobic bacteria that metabolises dead tissue and produces gas

90
Q

Cytokine from Th1 cells that mature monocytes into macrophages during atheroma formation

A

IL-2

92
Q

3 layers of a blood vessel

A

tunica intima tunica media tunica adventitia

94
Q

when does dry gangrene occur?

A

with infarction of toes/feet/leg - usually associated with altered altered Hb and atherosclerotic vessels

95
Q

which area (in general) of the heart does the left anterior descending artery supply

A

ANTERIOR (anterior part of LV, anterior part of RV and anterior 2/3 or interventricular septum)

96
Q

Which adhesion molecules do monocytes use to enter the intima of endothelial cells during the formation of an atheroma

A

ICAM-1 and VCAM-1

97
Q

why is the adventitia thicker in veins than arteries

A

to help withstand hydrostatic pressure

98
Q

what are Purkinje cells

A

modified cardiac muscle cells - now larger - no longer specialised for contraction - full of glycogen (less pink) - form bundles in subendocardium

99
Q

complications of atherosclerosis

A

ischaemia infarction aneurysm

101
Q

order of the normal thickeness of the 3 layers of the heart

A

myocardium - thickest epicardium endocardium

102
Q

how long after MI do you see this

A

2-3 days

103
Q

how long after MI is this seen?

A

weeks

104
Q

consequences of myocardial infarction

A
  • predisponse to infectiveendocarditis - incompetence of the valve - stenosis of the valve - AF - thrombi formation in the LA - stroke
105
Q

Microscopic changes seen at 2-3 days after MI

A
  • acute inflammatory response is marked with massive infiltration of neutrophils and oedemous interstititum - necrotic myocardium undergoes autolysis and fragmentation - infarcted fibres more intensely eosinophilic and most have lost their nuclei
107
Q

LDL and HDL roles in atherosclerosis as risk factors

A

higher LDL –> increased risk HDL - prevents oxidation of LDL and removes cholesterol from the circulation –> decreased risk

108
Q

important sites for atherosclerosis (5)

A

aortic aorta carotid arteries femoral arteries renal artery small bowel

109
Q

what size are arterioles

A
111
Q

what is an infarct?

A

an area of necrosis caused by ACUTE ISCHAEMIA

113
Q

how do you determine a lymphatic vessel on histology

A

looks like a vein but don’t have RBCs in them

115
Q

what is sudden cardiac death normally due to

A

coronary atherosclerosis

116
Q

definition of metaplasia

A

adaptive cellular change in cell differentiation

117
Q

role of Purkinje fibres

A

to co-ordinate contraction of different chambers (as gap junctions only co-ordinate on local scale)

118
Q

what is metaplasia due to

A
  • long standing change in environmental conditions - cytokine or GF driven reprogramming of the line of differentiation of adult/somatic stem cells
119
Q

How long after MI do you see this?

A

10 days

121
Q

myocardium of the heart composed of

A

myocytes and abundant capillaries

122
Q

what determines whether a cell undergoes hypertrophy or hyperplasia

A

if a cell is labile, stable or permanent (in the cell cycle)

123
Q

what causes the fibrous CT in atherosclerosis

A

migration of smooth muscle cells from the intima (due to GFs released by endothelium) which proliferate and make ECM

124
Q

how long after MI is this seen

A

12 hours

125
Q

common predisposing factor for arterial thrombus and venous thrombus

A

arterial - turbulent flow Venous - stasis

126
Q

predisposing factors for thrombus

A

1) endothelial dysfunction or injury 2) hypercoagulability of the blood 3) changes in blood flow

128
Q

what determines the size of an infarct? (6)

A

1) size of the artery occluded 2) the duration of the occlusion and vulnerability of those cells to ischaemia 3) whether the artery is carrying oxygenated or deoxygenated blood 4) the nature of the arterial supply (end artery, dual supply, collateral circulation 5) oxygen content of blood 6) the state of the systemic circulation

129
Q

what is arteriosclerosis

A

medial elastic tissue degeneration and fibrosis - causing loss of elasticity and dilatation

130
Q

what are pale infarcts usually due to

A

the blockage of end arteries

131
Q

What causes ischaemia?

A

increased demand for oxygen that isn’t met local vascular narrowing/occlusion systemic reduction in tissue perfusion

132
Q

pathological causes of atrophy

A
  • inadequate nutrition - diminished blood supply -denervation -disuse -loss of endocrine stimulation - pressure
133
Q

microscopic changes after months after MI

A

Scar - densely collagenous, pale pink stained

134
Q

modifiable risk factors for atherosclerosis (8)

A

hypertension diabetes mellitus smoking lipoproteins obesity and the metabolic syndrome physical inactivity proteinuria type A personality

135
Q

3 layers of the heart

A

epicardium myocardium endocardium

Z MD1 Cardiac physiology (13 decks)

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