Pathology-Alaa > Atherosclerosis > Flashcards

Atherosclerosis Flashcards

(46 cards)

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1
Q

what is this finding called?

A

corneal arcus

White, grey, or blue opaque ring in the corneal margin as a result of hypercholesterolemia.

Arcus senilis can be confused with the limbus sign, which reflects calcium rather than lipid deposits.

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2
Q

what is menhoraggia?

A

excessive heavy periods

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3
Q

(patient’s elbow.)

What is present?

How do these appear microscopically?

What condition is the patient likely to have?

What does this condition mean for the patient?

A
  • Xanthelasma
  • plaques or nodules composed of lipid laden histiocytes (macrophages) in the skin (expecially in eyelids) (Xanthelasma)
  • Familial Hypercholesterolemia
  • Increase risk of atherosclerosis.
  • due to high
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4
Q

what is this called?

A

xanthelasma

signs of Hyperlipidemia

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5
Q

Define Atherosclerosis

A

is the accumulation of intracellular and extracellular lipid in the intima and media of large and medium sized arteries

or

the thickening and hardening of arteries due to an atheroma!

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6
Q

Define Aretrioscelrosis

A

hardening of the walls of the arteries and arterioles usually as a result of hypertension or diabetes

(no due to atheroma)

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7
Q

**atherosclerosis does NOT effect veins and cappillaries

A

ok

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8
Q

what does an atheromatus plaque consist of?

roughly, how thick is it usually?

A

raised lesion w/ soft and yellow, grumous core of lipid (mainly cholestrol and CE) covered by a fibrous plaque!

1-2mm thick

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9
Q

what is an atheroma? what does it consist of?

A

the necrotic core of the atherosclerotic plaque!

  • dead cells
  • debris
  • cholstrol crystals

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10
Q

what r the 3 macroscopic feautures of atherosclerosis?

A
  • fatty streak
  • simple plaque
  • complicated plaque
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11
Q

Describe the appearence of a fatty streak

A
  • Lipid deposits in intima, yellowy and slightly raised
  • composed of foam cells.
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12
Q

flow through a stenosed tube or artery is not significantly affected until the lumen is reduced by_______%.

A

70-80%.

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13
Q

where does atheroscleosis occur?

where is it nost commonly seen?

A

elastic arteries= aorta, carotid, iliac

medium Muscular= coronory, popliteal

It is commoner in the abdominal aorta rather than the thoracic aorta.

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14
Q

what is Monkeyberg’s disease?

A

an uncommon disease where there is calcification of the Media of large arteries

monkey likes taking pics of calsified arteries!

🐒+📸

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15
Q

Arteriosclerosis

Atheroscleosis

Areterioloscleroisis

A
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16
Q

“athere” is Greek for porridge

A

why do u do this to me why?

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17
Q

what type of plaque is this?

describe its macroscopic feauture

A

Simple plaque

  • raised white and yellow
  • widely distributed
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18
Q

what type of plaque is this?

describe its macroscopic feauture

A

complicated plaque

there has been:

  • thrombosis into plaque
  • hemmorhage
  • aneurysm
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19
Q

describe the structure of the epithelium starting from inwards to out

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A

(theres elastic tissue in the media as well, and depending on where the artery is, that will determine the amount of elastin there is) ex nearer the heart> the more there is, aorta)

20
Q

Arteriosclerosis

Atheroscleosis

Areterioloscleroisis

monkeybergs disease

21
Q

the plaque is the basic lesion of atheroscelrosis.

what r the 3 basic components of it?

Study These Flashcards
A

Come Eat Lipids!

  • Cells= leucocytes, SMC
  • ECM= collagen, peptidoglycan, elastin
  • Lipids

22
Q

what is the earliest lesion in atherosclerosis?

how do they appear microscopiclaly

Study These Flashcards
A

-fatty streak!

  • Lipid deposits in intima, yellowy and slightly raised
  • composed of foam cells, SMC, Extracellular lipid

(these r FLAT, bs there is no disturbance of BF yet)

23
Q

after the fatty streak has formed, what comes after that?

describe what there is miscroscopicallY?

Study These Flashcards
A

fatty streaks grow to become plaques!

they impinge in the lumen of the artery and r partially circumfrential.

there is fibrosis, necrosis, cholestrol clefts, extension into media & growth on small vessel from adventitia

24
Q

what r some of the plaque complications?

Study These Flashcards
A
  • -u think studying atheromas comes easy? Haha*
  • -ulceration*
  • -thrombosis*
  • -spasm*
  • -Aneurysm*
  • -Calcification*
  • -Embolism*
  • -Rupture of atherosclerotic artery*
25
Clinical effects of atherosclerosis?
**-Heart\>**\> ***IHD***, Arryhtmia, MI, angina, cardiac failure, chronic ischemic heart disease **-brain\>**\> TIA, cerbral infarction, mutli-infarct dementia **-Kidney\>**\> Hypertension, renal failure **-Legs\>\>** gangrene, peripheral vascular disease **-Bowel\>\>**bowel ischemia
26
Risk factors of atheroscelrosis? | (modifiable and nonmodifiable)
(for more detail look at handout!) *_nonmodifiable_* **Age** **Gender** -common in men than in women (*but increases after* the *menopause as oestogen is protective,)* **Genetic predisposition** *_modifiable_* **Hyperlipidaemia** **Hypertension** **Cigarette smoking** **Geography** **Obesity** **Infection**
27
what is an Aneurysm?
dilations of the artery due to weaking of the arterial wall! *(they r almost always secondary to atherosclerosis!)*
28
describe the different shapes of aneurysms!
- Saccular\> shaped like a sac! - Fusiform\> shaped like a spindle!
29
where do u usually find saccular aneuryms?
in the abdominal aorta!
30
dilation of the arteries r called? veins?
aneurysm Varices
31
\*\*genetic variations in the apopolipoprotein \_\_\_, r asscoaited with changes in LDL levels!
E
32
how can cigarrette smoking increase risk of atheroscleross?
- inflammation - dmage to BV =increased predisobositon of thrombis -Oxidation of lipids! (OxLDL) REduced PG12 -nicotine makes platelets sticky
33
how can hypertension cause atherosclerosis?
high pressure causes endothelial damage!
34
apparently small amounts of alchohol can have protective effects from atherosclerosis -.-
wtf
35
what types of infections can contribute to atherosclerisis?
*  Chlamydia pneumoniae *  Helicobacter pylori *  Cytomegalovirus
36
significance of Apo E lipoprotein
**LDLrecepto**r on hepatocytes **binds apoE & chylomicron** remnant taken up by receptor mediated endocytosis
37
Name and explain the 4 possible theories for the possible mechanisms of atherosclerosis!
*  **Thrombogenic theory**\> plaques formed by repeated thrombi, lipid core dervied from thrombi *  **Insudation theory\>** endothelial injury, inflammation,  increased permeability to lipid from plasma * ** Monoclonal hypothesis\>** * ** Reaction to injury hypothesis \>** atheroscelrosis is a chronic inflammatory response of the arterial wall initiated by injury ***T**hrombosis **i**s **R**ed **m**ess*
38
what r the Cells Involved in atherosclerosis process?
*  Endothelial cells * SMC * *Platelets* * * Macrophages* * * Lymphocytes* * * Neutrophils*
39
what is the role of SMC in atherosclerosis?
1) Take up LDL and other lipid to become foam cells 2)Form the roof of the plaque (fibrous cap) w/ synthesis of collagen and proteoglycans and ECM in it.
40
role of macrophages in atherosclerosis
*  Oxidise LDL by releasing FR * eat lipids to become foam cells *  Secrete proteases which modify matrix *  Stimulate proliferation and migration of smooth muscle cells
41
role of lymphocytes
*  **TNF** may affect lipoprotein metabolism *  Stimulate proliferation and migration of smooth muscle cell
42
role of neutrophils in atherosclerosis
 Secrete proteases leading to continued local damage and inflammation
43
when do atherosclerosis symptoms appear?
atherosclerosis is a totally silent disease. Symptoms eventually arise when plaques become complicated.
44
Prevention of atherosclerosis
* No smoking * Reduce fat intake * Treat hypertension * Not too much alcohol *  Regular exercise/weight control *  Stop smoking *  Modify diet *  Treat hypertension *  Treat diabetes *  Lipid lowering drugs -statins, and aspirin prophylaxis, * Anti-oxidants, such as vitamin E, may be protective.
45
examples of lipid lowering drugs?
statins and anaphylaxis lowring drugs
46
What do these holes indicate?
In the final step of atherosclerosis, the cells in the centre of the plaque DIE and necrosis. these dead cells release cholestrol and cholestrol crytal appear, these crystals r removed suring tissue section and leave behind these hole **Cholestrol clefts!**
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