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ACP Cardi and Respi system > L8 Pathology of vessels > Flashcards

L8 Pathology of vessels Flashcards

1
Q

Clinical presentations of atherosclerosis depend on the end-organ ischemia. Which of the following are possible clinical presentations of atherosclerosis?

A. Claudication (pain on exertion)
B. Cold dry skin
C. Toe gangrene
D. Pulseless
E. Bruit
A

All of the above,

also with acute persistent pain e.g. acute myocardial infection.

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2
Q

What are the changeable risk factors for atherosclerosis? (4)

A

三高一吸

  1. Hyperglycemia
  2. Hyperlidpidemia
  3. Hypertension
  4. Smoking
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3
Q

Atherosclerotic plague complications? (3)

A
  1. Significant stenosis (80%) > symptoms
  2. Thrombotic occlusion > infarcts
  3. Aneurysmal mural thrombosis > embolism
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4
Q

What is the definition of atherosclerosis?

A

Focal accumulation of lipid (1) and proliferation of smooth muscle cells (1) within tunica intima (1) of arteries

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5
Q

Risk factors of atherosclerosis can be divided into non-modifiable and modifiable risk factors. Name a few non-modifiable risk factors.

A
  1. Fx
  2. Age
  3. Male and post-menopausal F
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6
Q

What are the 3 different stages of morphology/ types of atherosclerotic plaques?

A
  1. Fatty streaks
  2. Atheroma (atheromatous plaque)
  3. Complicated atheroma
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7
Q

Fatty streaks are foamy ____________(Cell type) that can be presented as slightly raised yellow deposits within the tunica intima (TI).
There are formed in virtually all children > 10 years old and develops into atheroma progressively.

A

macrophages

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8
Q

What is an atheroma/ atheromatous plaque?

What are the components? (memorise!)

A

Fibrous cap + Necrotic center

  • Fibrous cap: smooth muscle cells, macrophages, foam cells, collagen..
  • Necrotic center: cell debris, cholesterol crystals, foam cells

Components:

  1. Cells: smooth muscle cell, foam cells (lipid-laden macrophages + SMC)
  2. Extracellular matrix (ECM): collagen + elastic fibers
  3. Lipids: cholesterol cleft/crystal + calcification if old enough
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9
Q

What are the most common sites for atheroma to deposit onto? (4) List them in descending order.

A
  1. Infra-renal abdominal aorta
  2. Coronary arteries
  3. Popliteal arteries
  4. Internal carotid arteries
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10
Q

Complicated atheroma is the latest stage of morphology of atherosclerosis. What is it?

A

Unstable plagues

- with thinner fibrous cap, larger lipid core, more inflammation

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11
Q

What will complicated atheroma cause? (3As!)

A
  1. Acute plague changes
    - rupture/ ulceration/fissuring: expose underlying necrotic centre (thrombogenic subendothelial basement membrane) to endothelial surface > induce thrombus formation > occlusion > ischemia, infarction
  • Hemorrhage into a plague: plaque volume expansion
    2. Atheroembolism: ruptured plague discharges debris into blood - micro emboli
    3. Aneurysm: atherosclerosis-induced pressure or ischemic atrophy of tunica-media (TM) > loss of elastic tissue and structural weakening > aneurysmal dilation and rupture
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12
Q

Pathogenesis of atherosclerosis?

A
  1. Chronic endothelial injury (e.g. HTN, hypercholesterolemia) + Accumulation of lipoproteins (e.g. oxidised LDL and cholesterol crystals) in vessel wall
    • Monocytes (become tissue macrophage) and other inflammatory cells migrate to subendothelial space
    • Platelets adhere to endothelium
  3. Release cytokines and growth factors
  4. SMC proliferates and migrates to tunica intima from tunica media***
  5. Foam cells are formed as cholesterol enters SMC and macrophages
  6. SMC and macrophages release cytokines > produce Extra-cellular matrix
    * ** SMC proliferation and ECM deposition are irreversible process converting fatty streak into atheroma
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13
Q

Hypertension can be essential or secondary.
How many of each type of hypertension is benign?
What is the significance of defining benign/malignant?

A

Essential: 90% benign, 10% malignant
Secondary: 80% benign, 20% malignant

  • Benign: gradual increase in BP
  • Malignant: rapid elevation of BP, associated with direct end-organ damage
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14
Q

What end organ damage can malignant hypertension cause (can be seen in PE)? (2)

A
  1. Papilloedema
  2. Retinal hemorrhage (& exudate)
    * Fundoscopy can reflect severity of malignant hypertension
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15
Q

Type of atherosclerosis in elastic and large vessels?

What are the 2 main complications

A

Hypertensive atherosclerosis
1. Aneurysm: HT more commonly associated with aortic aneurysm

  1. Acute dissection (due to acute tearing off of the intima) - in long standing HT
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16
Q

Tunica media hyperplasia and hypertrophy occurs in _________ blood vessels. Fibroelastic hyperplasia is the reduplicate of internal elastic lamina + fibrous thickening of tunica media.

A

Muscular

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17
Q

Arteriole hypertension causes __________ arteriosclerosis in benign hypertension and _____________ arteriosclerosis in malignant hypertension.

A

Hyaline;

Hyperplastic

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18
Q

What is hyaline arteriosclerosis?

A
  • caused by benign hypertension
  • arterioles hardening due to subendothelial deposits of the glassy pink materials (exudative materials including fibrin), also found in ageing and DM
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19
Q

What does hyperplastic arteriosclerosis look like?

A

Onion-skin like;
concentric muscular thickening (tunica media) +/- wall thickening (tunica intima)

  • Fibrinoid necrosis: increased permeability of small vessels to fibrinogen
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20
Q

What is the type of kidney disease caused by hypertension?

A

Nephrosclerosis

- sclerosis of small renal arteries and arterioles that is strongly associated with hypertension

21
Q

Pathogenesis of benign nephrosclerosis?

A
  • Hyaline atherosclerosis of renal arterioles > ischemia > necrosis, fibrosis and sclerosis of glomeruli > symmetrically renal atrophy + finely granular cortical surface with retention cysts
22
Q

Malignant nephrosclerosis:

  1. Fibrinoid necrosis of arterioles causing ____________
  2. Hyperplastic arteriolosclerosis: “onion skin” lesion
A

petechiae hemorrhage

23
Q

__________ is a localised, permanent dilatation of artery/vein.

A

Aneurysm

24
Q

What is true and pseudo aneurysm?

A

True: involves all 3 layers of the artery (intima, media, adventitia)

Pseudoaneurysm (false aneurysm): involves only tunica media and adventitia with ruptured vessel wall creating a collection of blood bounded externally by adherent extravascular tissues

25
Q

Atherosclerosis can cause abdominal aortic aneurysms.

Syphillis can cause infection of the ________________ of ascending aorta > immune response > obliterative end arteritis - reduces blood flow to tunica media > ischemic damage to media > weakness and subsequent dilatation of ascending aorta

A

vaso vasorum

26
Q

What is the most common cause for mycotic aneurysm? = caused by infection

A

Infective endocarditis
- mostly affect cerebral arteries

Pathogenesis: septic embolus, extension of suppuration or direct infection into arterial wall

27
Q

Berry aneurysm is a congenital fibrous replacement of tunica media, typically found in? what complication?

A

Circle of Willis

- SAH if ruptured

28
Q

_________________ is associated with DM and HT, it is the segmental weakening and dilatation of vessel wall, especially in lenticular-striae artery of MCA.
It is the precursor of primary hypertensive intracerebral hemorrhage.

A

Capillary micro-aneurysm

29
Q

What are the 2 main forms of aneurysms classified by shape?

A
  1. Fusiform - spindle dilatations

2. Saccular - large spherical outpouching

30
Q

Biggest risk factor of AAA?

A

atherosclerosis

31
Q

Biggest risk factor of ascending aorta aneurysm?

A

hypertension

32
Q

Weakening of the vessel wall can be due to vasculitis, trauma or congenital.

Name a congenital cause and briefly explain.

A

Marfan’s syndrome

- abnormal connective tissue synthesis

33
Q

Weakening of the vessel walls may can be due to excessive ECM degradation.
Proteolytic enzymes are released from macrophages in atherosclerotic lesions > fragmentation of elastic fibres thus weakening of? (layer of blood vessel)

A

tunica media

34
Q

Other than excessive ECM, weakening of blood vessel wall is also due to the loss of? Why is there such a loss?

A

Smooth muscle cell;
ischemia due to increased diffusion distance (thickening of arterial wall due to atherosclerosis)
/ narrowing of aortic vasa vasorum (HT)

35
Q

Which of the following is true about aortic aneurysm?
A. Located mostly infrarenal
B. Pulsatile mass is detected
C. Causes fatal hemorrhage if rupture
D. May cause vascular occlusion due to atheroma
E. Can impinge on adjacent structures, e.g. ureter/ vertebra

A

All of the above

36
Q

What is the definition of aortic dissection?

A

Tear of the aortic intima and blood dissects to tunica media

37
Q

Aortic dissection is commonly presented in? (2)

A
  1. male, aged 40-60 with HT

2. young patients with connective tissue disorder e.g. MFS

38
Q

Pathology of aortic dissection?

A

Cystic medial degeneration/necrosis: degradation of ECM and SMC in tunica media

39
Q

Intimal tear of aortic dissection mostly occurs proximal to? (2)

A

within 10cm of aortic valve
- retrograde dissection into aortic root: disruption of aortic valve and compression of coronary arteries

  • extend distally to great arteries > obstruction
40
Q

How is aortic dissection classified?

A

Type A:
- ascending aorta +/- descending aorta

Type B:
- descending aorta (Beyond subclavian artery)

41
Q

What is the clinical feature of type A aortic dissection?

A
  • Absent radial pulse

- retrograde dissection into aortic root

42
Q

Prognosis and treatment of 2 types of aortic dissection?

A
  1. Type A
    - 75% mortality
    - surgery + intensive antihypertensive (beta-blockers)
  2. Type B
    - 25% mortality
    - conservative management e.g. antihypertensive
43
Q

Complications of aortic dissection?

A
  1. Rupture: massive hemorrhage in cavities (pericardial, pleural, peritoneal cavities)
  2. Cardiac tamponade due to retrograde extension of dissection
  3. Ischemia due to extension of dissection into various great vessels
44
Q

Name the blood vessels down the abdominal aorta.

*Answer thoracic/ infra-renal abdominal aorta in exams!

A
  1. Celiac trunk
  2. SMA
  3. Left and right renal arteries
  4. IMA
45
Q

Virchow’s triad?

A
  1. Endothelial injury
  2. Stasis of blood flow
  3. Hyper coagulability
46
Q

What are the clinical features of abdominal aortic aneurysms? (3)
Complications? (3)

A
  1. Pulsatile
  2. Expansile mass
  3. Bruit +++

Complications

  1. Mural thrombosis > emboli
  2. Rupture risk = diameter
  3. Fistula > shock
47
Q

Causes of thoracic aortic aneurysms?

A
  1. Syphilis
  2. Marfan syndrome
  3. Takayasu arteritis
48
Q

Clinical features of thoracic aortic aneurysms?

A
  • AR murmur
  • Chest mass
  • left heart failure (volume overload)

ACP Cardi and Respi system (5 decks)

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