Pathology - Blood Vessles Flashcards

0
Q

List the vasoconstrictors that determine vascular resistance.

A
Angiotensin II
Catecholamines
Thromboxane
Leukotrienes
Endothelin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
1
Q

Define hypertension.

A

Clinically defined hypertension is a sustained diastolic pressures >89mmHg or systolic pressures >139mmHg.

Malignant hypertension is characterised by a systolic >200mmHg, diastolic >120mmHg, retinal haemorrhage and renal failure.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

List the vasodilators that determine vascular resistance.

A

Kinins
Prostaglandins
Nitric oxide
Adenosine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Blood volume is affected by:

A

Sodium load
Mineralocorticoids
Natriuretic factors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Hypertension is associated with which 2 forms of small arteriolar disease?

A

Hyaline arteriosclerosis:
Increased SMC synthesis with pink hyaline arteriolar wall thickening.

Hyperplastic arteriosclerosis:
Concentric laminated thickening. Necrotising arteriolitis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are the 3 patterns of arteriosclerosis?

A

Arteriolosclerosis: S-M sized vessels

Monckeberg medial sclerosis: Medial calcification in muscular arteries occurring after the age of 50. Doesn’t cause ischaemia by itself!

Atherosclerosis:
Most frequent and clinically important.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Major classic RF for cardiovascular disease?

A
Family history
Smoking
Diabetes
Hypercholesterolaemia
Hypertension
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Apart from the major RF, what are 5 additional contributing factors to cardiovascular events?

A
Inflammation
Hyperhomocysteinuria
Metabolic syndrome 
Lipoprotein a
Haemostatic markers
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Describe the pathogenesis of atherosclerosis:

A
  1. Endothelial injury or dysfunction
  2. Monocyte and platelet adhesion
  3. GF release and SM recruitment
  4. SMC and ECM proliferation
  5. M➰ and SMC take up cholesterol
  6. Necrosis of fatty core.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

How do lipids worsen EC dysfunction?

A

Increased circulating lipids encourage formation of local oxygen free radical formation, which worsens EC and SMC dysfunction.

Moreover, oxidised LDLs are ingested by M➰ creating pro-inflammatory foam cells.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Complicated plaques include plaques which exhibit:

A

Calcification
Haemorrhage
Fissuring
Ulceration.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Most cases of MI are associated with critical or subcritical stenoses?

A

Sub critical!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Unstable plaques are characterised by:

A

Large, deformable lipid cores
Thin fibrous caps
Increased inflammatory content.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What are the 3 pathological changes underlying aneurysmal disease?

A
  1. Poor intrinsic quality of the matrix. Marfans, scurvy etc.
  2. Imbalance of matrix synthesis and degradation. For example in vasculitides or inflammation.
  3. Loss of SMC in the media or a change in SMC matrix synthesis via ischaemia or degeneration.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

AAA rupture rate when 5-6 cm?

A

11% per annum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

AAA rupture rate when >6cm?

A

25% per annum

16
Q

AAA operative mortality when electively versus emergently performed?

A

5% elective. 50% emergent.

17
Q

Classification of Aortic Dissection?

A

Type A: Involve ascending aorta.
Type B: Distal lesions, usually distal to subclavian.

Type A is worse and requires operative management.

18
Q

What is MPO-ANCA?

A.K.A p-ANCA

A

Anti myeloperoxidase ANCA. Directed against lysosomal constituents in neutrophils. Associated with microscopic polyangiitis and Churg-Strauss syndrome.

19
Q

What is PR3-ANCA?

A.K.A c-ANCA

A

ANCA directed against neutrophil azurophilic granule constituent. Associated with Wegener’s granulomatosis.

20
Q

Which vasculitides are thought to involve T-cell mediated hypersensitivity?

A

Giant Cell Arteritis (Takayasu…)
Kawasaki disease
Wegener’s granulomatosis
Beurger disease.

21
Q

Characteristics of juvenile haemangiomas?

A

Present at birth ~1/200
Grows rapidly for a few months
Begins regressing at 1-3 years
Most disappear by the age of 7.

22
Q

Where might cavernous haemangiomas form?

A

Skin, liver, CNS, other viscera.

23
Q

Cavernous haemangiomas in the cerebellum, brainstem, and eyes associated with angiomatous or cystic lesions in the pancreas and liver suggest…

A

von Hippel Lindau disease.

24
Q

What is Bacillary angiomatosis?

A

A vascular proliferation resulting from opportunistic infection in immune-compromised host caused by gram negative Bartonella.

25
Q

Angiosarcomas are associated with what aetiological causes?

A

Ipsilateral radical mastectomy
Radiation
Foreign bodies!

26
Q

Patency of GSV for bypass vessel at 10 years?

A

50%

27
Q

Patency of internal thoracic artery for bypass vessel at 10 years?

A

90%

28
Q

AA-type Amyloid is associated with what disease states?

A

Chronic inflammatory states; Crohn’s, RA.

29
Q

Which type of Amyloidosis is associate with MM?

A

Primary type Amyloidosis. Occurs in 5-15% of patients with MM