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BDS2 BAMS Cardiovascular > Cardiovascular Pathology > Flashcards

Cardiovascular Pathology Flashcards

1
Q

what is arteriosclerosis

A

arteriosclerosis is the hardening and thickening of the wall of the arteries, occurs typically in old age and can happen due to inflammation

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2
Q

what is atherosclerosis

A

happens due to the deposition of cholesterol in the blood vessel wall

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3
Q

what is the most important risk factor in atherosclerosis

A

hyperlipidemia

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4
Q

how does an atheroma occur

A

there is chronic inflammation due to cholesterol deposition, there will also be a healing response but there is actually no healing and it is these processes that result in atheroma

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5
Q

what is the vascular pathology that happens due to atherosclerosis

A

either stenosis or obstruction or weakening of the walls leading to dilation/rupture

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6
Q

what are the non-modifiable risk factors for atherosclerosis

A

age
gender
genes

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7
Q

what is the gene that can affect risk factors for atherosclerosis

A

family hypercholesterolemia is mutation of the LDL receptor gene

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8
Q

what happens if there is a mutation of the LDL receptor gene

A

there is not as much cholesterol uptake meaning there is more circulating cholesterol which puts the person at higher risk of atherosclerosis from a young age
any lifestyle factors will also increase the risk

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9
Q

describe endothelial cells in the basal state

A

normal when BP is within a normal range

cells will be smooth and non adhesive

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10
Q

what factors can cause endothelial cells to change

A

lifestyle factors - smoke, lipid products etc

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11
Q

describe endothelial cells in the activated state

A

turbulent flow
change in the cells due to cytokine productions
encouragement of pro coagulation
can produce cytokines and growth factors which can cause a lot of different changes in the blood vessel

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12
Q

what are the two phases in the formation of an atheroma

A

chronic inflammatory phase

healing response phase

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13
Q

what is the chronic inflammatory response due to in the chronic inflammatory phase

A

response to lipoproteins

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14
Q

what happens in the chronic inflammation phase

A

endothelial cells change surface cell receptors and become more permeable to lipids
change cell adhesion molecules for monocytes so attach to endothelium and move into blood vessel walls

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15
Q

what are the monocytes in the chronic inflammatory phase

A

monocytes include macrophages and t cells

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16
Q

what level of the blood vessel wall do the lipids pass into

A

intima - first level

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17
Q

why do the macrophages do

A

they ingest lipid that is deposited into the wall and become big and pale colored - foam cells

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18
Q

what happens to the lipid that the macrophages ingest

A

it stays in the macrophages until death

as the macrophages die the lipid returns into the circulation

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19
Q

what is the healing response phase

A

there is proliferation of smooth muscle cells
fibrous tissue formation
growth factor production
fibro fatty plaque is formed with a central mass of lipid and necrotic tissue
neovascularisation may be seen at the periphery of the plaque
a hemorrhage can occur in the plaque
calcification of the lipid and necrotic tissue may sometimes occur

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20
Q

describe the 5 stages of the formation of an atheroma

A

1, chronic endothelial cell injury (may be genetic mutation, inherited, hypertension)

  1. permeability increases, lipid deposited in the intimal layers
  2. macrophages move in and become foam cells. fatty streaks form
  3. smooth muscle proliferation. macrophages produce IL-1 which activates T-cells. more cytokines, chemokine, ROS activate more inflammatory cells
  4. (healing phase). fibrous tissue formation, over the lipid and a fibre fatty atheroma is formed (plaque). dystrophic calcification may occur at late stages.
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21
Q

what are the effects of atherosclerosis

A

decreased blood supply to tissue/organ (ischemia)
complete occlusion of the blood vessel leads to infarction
thrombosis
embolism

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22
Q

how does thrombosis occur because of atherosclerosis

A

there is release of thrombogenic factors
coagulative process occurs
formation of blood cut on top of atheroma and completely cuts off blood supply

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23
Q

what happens in peripheral vascular disease

A

you can get ischemia which results in claudication

ischemia can cause gangrene (form of coagulative necrosis) and infection

24
Q

what is an aneurysm

A

abnormal dilation

25
Q

where can aneurysm occur

A

blood vessel or in the cardiac wall

26
Q

what are the causes of aneurysm

A

can be factors such as developmental, degenerative or traumatic

27
Q

what is an abdominal aortic aneurysm

A

commonest and results from atherosclerosis

28
Q

how does aneurysm play a role in peripheral vascular disease

A

it is associated with macrophages in the blood vessel wall
MMP can breakdown fibres in the blood vessel wall widening it and can weaken the structure and this can happen in the cardiac wall as well

29
Q

what are acute coronary conditions

A

angina pectoris

myocardial infarction

30
Q

what happens in myocardial infection

A

loss of blood supply, oxygen nutrients ect
results in coagulation necrosis of the myocardial muscle
it cannot survive on anaerobic respiration
healing is by granulation tissue and this affects heart function as the new tissue does not have the same function as the myocardial tissue

31
Q

what happens to the cells in coagulation necrosis

A 
cell retain outline so can be identified
cytoplasm becomes darker
remains of nuclei 
striations lost 
neutrophils come into the tissue first and then macrophages come after
granulation tissue is formed
32
Q

how is granulation tissue formed

A

fibroblasts produce collagen
capillaries are formed to bring blood to rapidly dividing cells
gradually overtime the number of blood vessels decrease, inflammation decreases

33
Q

what does congestive heart failure follow from

A

usually follows on from ischemic heart disease, hypertension or valvular heart disease

34
Q

what does congestive heart failure result in

A

ventricular hypertrophy
edema
chronic venous congestion of lungs and liver

35
Q

what is the pathophysiology of congestive heart failure

A

hypertrophy of myocyte (adaptation)
capillaries do not increase in number
increased metabolic demands can result in ischemia and this causes injury to the myocyte
the end result can be necrosis and heart failure

36
Q

what are the different types of tumors of the blood vessels

A

hamartomas
kaposi sarcoma
angiosarcoma: rare, aggressive

37
Q

what is a hemangioma

A

it is a hartoma
rapid growth during the first weeks of life
usually regress over the first 10 years

38
Q

what are vascular malformations

A

common
present at birth and persist during life
may be more noticeable in the elderly as the mucosa becomes thinner

39
Q

what are the types of vascular malformations

A

capillary
cavernous
sturge weber syndrome

40
Q

what happens in sturge weber syndrome

A

the haemangion extend to the midline and the distribution follow the distribution of nerves
this person may have extensive haemangioma intra orally and they may also have hemangioma in their jaw bone - must be treated for invasive dentistry in hospital

41
Q

what is the cause of kaposi sarcoma

A

herpes virus 8

42
Q

what is kaposi sarcoma

A

multi-focal low grade sarcoma of lymphatics and blood vessels

43
Q

what is the common patient with oral KS

A

HIV infected patients

44
Q

what is the importance of kaposi sarcoma

A

with treatment, 90% of cases are controlled

the virus has the ability to produce this malignancy in those who are immune suppressed

45
Q

what does immune deficiency have a role in

A

carcinogenesis

46
Q

how common are cardiac tumors

A

rare

47
Q

what are the benign cardiac tumors

A

myxoma

lipoma

48
Q

what are the malignant cardiac tumors

A

angiosarcoma

49
Q

what is valvular heart disease

A

congenital or acquired

50
Q

if valvular heart disease is acquired what is it most likely because of

A

a result of other cardiac diseases such as ventricular hypertrophy

51
Q

what can valvular heart disease pathology result in

A

stenosis (injury to valve)
insufficiency - closing of the valve will be impaired so there will be a regurgitation of blood back into the chamber
vegetations - growths of lumps upon cusps of valve

52
Q

what is calcific aortic stenosis

A

commonest of all valvular conditions
dystrophic calcium deposits happen as a result of tissue inflammation
results in the narrowing of the valvular orifice and makes the valve stiff and hard to open
may require valve replacement

53
Q

what should be kept in mind if a patient has a valve replacement

A

that they are on anticoagulants

54
Q

what is rheumatic heart disease

A

results from rheumatic fever
mainly affects valves
host immune reaction against streptococcus A antigens that cross react with host proteins
damage is caused by a combination of type 2 and type 4 reactions

55
Q

describe the pathology of rheatmic heart disease

A

inflammation of endocardium and valves results in fibroid necrosis
vegetations formed along the lines of closure
thickening and fusion results in the calcification of valves
can result in aortic dilation, atrial fibrillation, thrombi formed on the wall of the atrium
susceptible to developing infective endocarditis

56
Q

what is infective endocarditis

A

microbial infection of heart valves
damaged or prosthetic valves are particaruly susceptible
oral pathogens may be implicated: s. viridens and s. aureus
vegetations formed on cusps contain fibrin, inflammatory cells, and infective pathogens
can cause infective emboli

BDS2 BAMS Cardiovascular (6 decks)

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