Cardiac histology and pathology Flashcards
(135 cards)
1
Q
Cytokines that cause increased adhesion molecules on endothelial cells during atheroma formation
A
IL-1 and MCP-1
2
Q
potential consequences of emboli
A
transient ischaemia
infarction
acute respiratory compromise
death
2
Q
definition of hyperplasia
A
an increase in number of cells
3
Q
function of tunica adventitia
A
anchors BV to surrounding tissue
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
3
Q
cytokines that attract macrophages and T cells during atheroma formation
A
IL-1 and MCP-1
4
Q
potential complications of thrombus
A
obstruction to blood flow embolism
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
5
Q
Function of intercalated dics
A
Anchor actin filaments in one cells sarcomere to the sarcomere in the other via fascia adherens
6
Q
what is the importance of venules
A
preferred site of diapedesis of leukocytes
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
6
Q
types of aneurysms
A
saccular - focal dilation fusiform - entire circumference dilated false aneurysm - blood goes into the extravascular CT surrounding the BV
6
Q
potential causes of infarction
A
arterial occlusion venous occlusion systemic reduction in tissue perfusion compartment syndrome
6
Q
haematoma definition
A
collection of blood outside the blood vessel
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
8
Q
endocardium of the heart composed of
A
endothelial squamous epithelium, subendocardial CT
9
Q
where are elastic arteries found?
A
close to the heart where there is the highest BP fluctuations
10
Q
structure of veins
A
media thinner than arteries adventitia thicker than veins valves (assissted by skeletal muscle contractions)
11
Q
function of tunica media
A
constricts the lumen of the BVs, –> increasing resistance –> increase in BP
11
Q
why does hypertophy occur
A
due to an increased functional demand or stimulation by hormonal or growth factors
12
Q
Cytokines produced by macrophages that recruit SM cells from media and precursors from blood in atheroma formation
A
TGF-beta and PDGF
13
Q
non modifiable risk factors for atherosclerosis
A
age - >45 in men and post menopausal in women gender - male>female (?oestrogen protection) genetic
13
Q
causes of aneurysms?
A
atherosclerosis congenital weakness in the wall systemic hypertension infection in the artery wall
13
Q
why does hyperplasia occur
A
due to stimulation by hormones or growth factors
13
Microscopic changes at 10 days after MI
- 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
14
tunica media composed of
smooth muscle arranged concentrically
14
the meta arteriole is characterised by
incomplete smooth muscle coat
14
classifications of gangrene
primary secondary - wet and dry
15
what is a thrombus?
a clotted mass of blood that forms within the cardiovascular system during life
16
how does diabetes mellitus increase your risk for atherosclerosis?
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)
16
haemorrhagic infarct normally due to
- venous occlusion and resulting significant congestion - arterial occlusion and then collateral supply congestion - reperfusion
17
most cells in the body are within what distance of a capillary
50 microns
19
structural features of medium to large veins
subendothelial CT well developed adventitia enlarged (often at the expense of media)
20
what causes venuous infarcts?
venous occlusion arterial occlusion - then colateral supply congestion reperfusion
21
histology of muscular arteries
little elastin in the media - it is concentrated in the internal and external elastic laminae
22
What causes an aneurysm?
loss of muscle and elastin from the media causes weakening of the vessel wall, predisposing to a localised area of dilatation
23
what are the two possible mechanisms for sudden cardiac death?
- arrhythmic - most common - mechanical - tamponade
25
epicardium of the heart composed of
simple squamous epithelium, subepicardial CT with BVs, fat, and nervous tissue within
25
what is arteriosclerosis
thickening and hardening of walls of arteries - generally via fibrosis and deposition of ECM non-specific term - includes atherosclerosis and age related changes
25
what features influence the development and size of an infarct?
- 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
26
how many layers of smooth muscle do arterioles have
1-3
26
macroscopic look of arterial thrombus and venous thrombus
arterial - dense and composed mainly of aggregated platelets and fibrin venous - resembled clotted blood containing masses of WBC and RBC
28
What causes the lipid rich core of atherosclerosis?
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
30
tunica intima composed of
simple squamous epithelium lying on a basal lamina, supported by a thin, subendothelial CT layer
31
how does the medial layer thin during atheroma formation
- loss of supporting elastic tissue - atrophy of smooth muscle - progressive medial fibrosis
32
histological signs of atherosclerosis (7)
fibrous cap around lumen lipid rich core ECM in intima chronic inflammatory cells foam cells calcification cholesterol clefts
32
which area (in general) of the heart does the right coronary artery supply
POSTERIOR (inferior part of LV, part of the RV, 1/3 of IV septum)
33
which area (in general) of the heart does the circumflex branch suppy
LATERAL side of LV
33
definition of atrophy
when cells decrease in size and activity
33
definition of involution
physiological atrophy involving apoptosis
34
what are the causes of hypoxia?
ischaemia impaired respiratory function decrease in oxygen carrying capacity of the blood
35
what causes arteriolosclerosis
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
35
How are smooth muscle cells recruited to the intima during atheroma formation
Via TGF-B and PDGF released by macrophages
36
Where is the elastin concentrated in elastic and muscular arteries?
elastic - in the media muscular - in the intima
38
what kind of plaque is most susceptible to rupture
plaques with thin fibrous caps
39
what causes the lines of Zahn
successive deposition of a number of layers of thrombus
40
steps in the healing of inarction
1. coagulative necrosis 2. acute inflammation 3. organization 4. scarring
41
what alters oxygen supply to the myocardium?
oxygen content of blood myocardial blood flow
42
what alters myocardial oxygen demand
ventricular wall stress heart rate contractility
43
levels of creatinine kinase in the blood after infarction?
- levels go up at about 3-4 hours - peaks after 24 hours - gone by 4 days
44
function of muscular arteries
distribute blood to the tissues and regulate BP
45
different collagen types in the media and adventitia
media - collagen III adventitia - collagen I
46
fates of a thrombus
1. embolisation 2. fibrinolysis 3. organisation 4. persistence
46
definition of hypertrohy
an increase in size of existing cells (no cell division)
48
What is hypoxia?
Deficiency of oxygen in the tissues
48
when does wet gangrene occur?
complicates acute apendicitis or cholecystectomy or infarction of the small wall
50
function of arterioles
distribute blood to capillaries contribute most to BP
51
potential causes of infarction
arterial occlusion venous occlusion systemic reduction in tissue perfusion compartment syndrome
52
function of elastic arteries
passive contraction of the BV means blood flow is continuous, but pulsatile
53
how is the tunica media CT made?
the smooth muscle cells themselves secrete the CT in which it is embedded
55
CT of tunica adventitia
collage type 1 and elastin, plus ground substance
56
causes of cardiac valve disease
- congential - prolapse mitral valve -degenerative (calcification)
57
definition of sudden cardiac death
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
what is ischaemia due to?
increased demand for oxygen that isn't met local vascular narrowing/occlusion systemic reduction in tissue perfusion
60
what is an embolus?
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
where to pale infarcts mainly occur
spleen, kidney and heart
63
What is a mural thrombis
Thrombus n the heart or major artery that covers part of the luminal wall as a plaque like structure
64
levels of troponin in the blood after infarction?
- elevated at about 3 hours after - peak at about 36 hours - back to normal after 10-14 days
65
What is atherosclerosis?
accumulation of lipid and fibrous CT in the INTIMA of medium and large arteries caused by endothelial dysfunction and chronic inflammation
66
timescale of histological changes after infarct?
- 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
microscopic changes at 12 hours after MI (starts at 4 hours)
- 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
what is a mycotic aneurysm?
an aneurysm due to an infection in the wall
69
Microscopic changes over weeks after MI
granulation tissue
71
examples of chronic ischaemia
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
how long before myocytes die?
20-40 minutes
73
structure of capillaries
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
acute ischaemia is frequently due to what
an increased demand for oxygen that is not met
76
pathogenesis of thrombus (3)
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
what are the age related changes of the BVs
aortic arteriosclerosis arteriolosclerosis
78
role of endothelium in BVs
- actively inhibit clotting - prime underlying subendothelial CT with VW factor (activates clotting) - release vasoactive substances
80
what type of CT in tunica media
collage type 3 (reticulin), elastin and ground substance
81
common complications of myocardial infarction
- 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
potential causes of infarction (4)
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
what is vasa vasorum
blood supply to the tunica adventitia
86
How do cholesterol clefts form
Formed from foam cell reak down liberating free lipid - forming cholesterol clefts
88
What is difference about a dissecting aneurysm?
The blood goes into the medial layer - wall does not balloon out
89
What is the earliest sign of atherosclerosis on a blood vessel?
fatty streaks
90
what is primary gangrene
gas gangrene - due to anaerobic bacteria that metabolises dead tissue and produces gas
90
Cytokine from Th1 cells that mature monocytes into macrophages during atheroma formation
IL-2
92
3 layers of a blood vessel
tunica intima tunica media tunica adventitia
94
when does dry gangrene occur?
with infarction of toes/feet/leg - usually associated with altered altered Hb and atherosclerotic vessels
95
which area (in general) of the heart does the left anterior descending artery supply
ANTERIOR (anterior part of LV, anterior part of RV and anterior 2/3 or interventricular septum)
96
Which adhesion molecules do monocytes use to enter the intima of endothelial cells during the formation of an atheroma
ICAM-1 and VCAM-1
97
why is the adventitia thicker in veins than arteries
to help withstand hydrostatic pressure
98
what are Purkinje cells
modified cardiac muscle cells - now larger - no longer specialised for contraction - full of glycogen (less pink) - form bundles in subendocardium
99
complications of atherosclerosis
ischaemia infarction aneurysm
101
order of the normal thickeness of the 3 layers of the heart
myocardium - thickest epicardium endocardium
102
how long after MI do you see this
2-3 days
103
how long after MI is this seen?
weeks
104
consequences of myocardial infarction
- predisponse to infectiveendocarditis - incompetence of the valve - stenosis of the valve - AF - thrombi formation in the LA - stroke
105
Microscopic changes seen at 2-3 days after MI
- 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
LDL and HDL roles in atherosclerosis as risk factors
higher LDL --\> increased risk HDL - prevents oxidation of LDL and removes cholesterol from the circulation --\> decreased risk
108
important sites for atherosclerosis (5)
aortic aorta carotid arteries femoral arteries renal artery small bowel
109
what size are arterioles
111
what is an infarct?
an area of necrosis caused by ACUTE ISCHAEMIA
113
how do you determine a lymphatic vessel on histology
looks like a vein but don't have RBCs in them
115
what is sudden cardiac death normally due to
coronary atherosclerosis
116
definition of metaplasia
adaptive cellular change in cell differentiation
117
role of Purkinje fibres
to co-ordinate contraction of different chambers (as gap junctions only co-ordinate on local scale)
118
what is metaplasia due to
- long standing change in environmental conditions - cytokine or GF driven reprogramming of the line of differentiation of adult/somatic stem cells
119
How long after MI do you see this?
10 days
121
myocardium of the heart composed of
myocytes and abundant capillaries
122
what determines whether a cell undergoes hypertrophy or hyperplasia
if a cell is labile, stable or permanent (in the cell cycle)
123
what causes the fibrous CT in atherosclerosis
migration of smooth muscle cells from the intima (due to GFs released by endothelium) which proliferate and make ECM
124
how long after MI is this seen
12 hours
125
common predisposing factor for arterial thrombus and venous thrombus
arterial - turbulent flow Venous - stasis
126
predisposing factors for thrombus
1) endothelial dysfunction or injury 2) hypercoagulability of the blood 3) changes in blood flow
128
what determines the size of an infarct? (6)
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
what is arteriosclerosis
medial elastic tissue degeneration and fibrosis - causing loss of elasticity and dilatation
130
what are pale infarcts usually due to
the blockage of end arteries
131
What causes ischaemia?
increased demand for oxygen that isn't met local vascular narrowing/occlusion systemic reduction in tissue perfusion
132
pathological causes of atrophy
- inadequate nutrition - diminished blood supply -denervation -disuse -loss of endocrine stimulation - pressure
133
microscopic changes after months after MI
Scar - densely collagenous, pale pink stained
134
modifiable risk factors for atherosclerosis (8)
hypertension diabetes mellitus smoking lipoproteins obesity and the metabolic syndrome physical inactivity proteinuria type A personality
135
3 layers of the heart
epicardium myocardium endocardium
