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RCS > L28- CVS Pathology VI > Flashcards

L28- CVS Pathology VI Flashcards

1
Q

pericardial diseases usually result from (1) or (2)

A

1- effusions and hemopericardium
2- inflammations (pericarditis)

-mostly secondary to cardiac or systemic diseases

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2
Q

(1) is the distension of the pericardial sac due to fluid accumulation. The fluid can be (2), (3), (4), or (5).

A

1- pericardial effusion and hemopericardium

2- serous (CHF, hypoalbuminemia)
3- serosanguineous- some blood (trauma, malignanvy)
4- chylous- lymph, fatty (mediastinal lymphatic obstruction)
5- blood = hemopericardium (cardiac tamponade via aortic dissection, MI, penetrating trauma)

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3
Q

Pericardial effusion effects are dependent on (1). The pericardium is able to hold up to (2) amount of fluid. Rapid accumulation of (3) amount of fluid can cause (4).

A

1- speed / rate of accumulation
2- 1L (pericardium is able to stretch if slow accumulation, normally holds 30-50 mL)
3- 250mL
4- tamponade

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4
Q

(Primary/Secondary) pericarditis is more common. Primary pericarditis is caused by (2). Secondary pericarditis is caused by (3).

A

1- secondary (primary is uncommon)
2- usually infectious, mostly viral
3- uremia** (most common, CKD), MI, cardiac surgery, radiation induced, rheumatic fever, SLE, malignancies

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5
Q

list the 4 types of pericarditis (include common causes)

A
  • Fibrinous: ‘bread and butter’, irregular and shaggy; seen in rheumatic disease, uremia, post-MI, post-viral
  • Fibrous and Hemorrhagic: malignancies
  • Fibrinopurulent / suppurative: bacterial pericarditis
  • Caseous: Tb
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6
Q

list the clinical features of acute pericarditis (minus cardiac tamponade signs)

A
  • atypical chest pain: no relation to exertion, worsens with reclining, relieved by leaning forward
  • high-pitched friction rub
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7
Q

list the signs of Cardiac Tamponade

A
  • faint distant (muffled) heart sounds
  • distended neck veins
  • declining CO
  • shock
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8
Q

what are the 3 outcomes of pericarditis

A

1) resolution, no clinical sequalae
2) immeadiate hemodynamic complications with large enough effusion
3) progress to chronic fibrosing: following caseous (Tb) or suppurative (bacterial) –> chronic constrictive pericarditis

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9
Q

Chronic percarditis produces a combination of (1) and (2) signs, similar to (3).

It usually has (4) present within pericardial space, and in severe/extreme cases (5) can be evident.

A

1- R sided venous distension
2- low CO
3- restrictive CM
4- delicate adhesions to dense, fibrotic scars that obliterate pericardial space
5- heart is completely encased with dense scar tissue, not allowing heart expansion –> constrictive pericarditis

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10
Q

define constrictive pericarditis

A
  • a result of chronic percarditis
  • pericardium is entirely dense scar tissue, encasing the heart
  • this doesn’t allow the heart to expand
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11
Q

what are the layers of arteries

A

Intima- endothelial cells

Media- smooth muscle cells

Adventitia- CT

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12
Q

what are the 2 principle mechanisms of blood vessel disease

A

-Narrowing or Complete Obstruction of lumen: i) progressive due to atherosclerosis; ii) suddenly due to thrombosis

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13
Q

what are the ‘other’ diseases of blood vessels

A
  • HTN
  • inflammation disorders / vasculitis
  • congentital malformation
  • neoplasms
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14
Q

define arteriosclerosis

A
  • hardening of arteries

- generic term for arterial wall thickening and loss of elasticity

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15
Q

list the types of arteriosclerosis

A

1) arteriolosclerosis: small arteries, arterioles; hyperplastic or hyaline
2) Monckeberg medial sclerosis: tunica media calicification in muscular arteries (never encroach vessel lumen, age 50 yrs and not clinically significant)
3) atherosclerosis

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16
Q

list the Non-Modifiable Major risk factors for atherosclerosis

A
  • age
  • gender
  • genetic predisposition
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17
Q

list the Modifiable Major risk factors for atherosclerosis

A
  • hyperlipidemia
  • HTN
  • DM
  • cigarette smoking
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18
Q

list the additional / uncertain risk factors for atherosclerosis (note- exhaustive list)

A
  • hyperhomocystinemia
  • lipoprotein-a
  • fibrinolysis inhibitors
  • elevated PA-1 inhibitors
  • CRP
  • lack of exercise (sedentary life-style)
  • post-menopausal estrogen deficienct
  • ‘type A’ personality
  • obesity
  • unsaturated fat intake
  • high carb diet
  • chlamydia pneumoniae
19
Q

how is age and atherosclerosis related

A
  • risk starts in childhood and progresses / increases with age
  • 40-60 y/o have 5x inc incidence in MIs
20
Q

define atherosclerosis

A

(atheros in greek = soft gruel or porridge like)

  • hardening of arteries
  • chronic inflammatory disorder of intima of large arteries
  • characterized by formation of fibro-fatty plaques, atheroma
21
Q

Atherosclerosis is more common in (male/females). Therefore it is uncommon in (2) people and those who are on (3).

A

1- males
2- premenopausal
3- postmenopausal women on hormone replacement therapy

22
Q

how do genetics affect atherosclerosis

A
  • familial clustering (aggregation of trait, behaviors, disorders in a family) of ‘other risk factors’
  • familial hypercholesterolemia
23
Q

In the relationship between hyperlipidemia and atherosclerosis, (1) is most important. Therefore it has a direct correlation to (2) and inverse relationship to (3). If in combination with (4), premature and severe atherosclerosis will result.

A

1- elevated cholesterol (hypercholesterolemia)
2- LDL levels
3- HDL levels
4- DM, nephrotic syndrome, hypothyroidism

24
Q

HTN is most important in terms of causing atherosclerosis after (1).

  • there is a 5x more risk of developing IHD with (2) BP compared to (3) BP
  • antihypertensives help reduce the risk of (4)
A

1- 45 y/o
2- 169/95
3- 140/90
4- (atheroclerosis causing…) stroke, IHD

25
Q

how does smoking related to atherosclerosis

A
  • 1 or more packs per day for several years => double the rate of death
  • dec HDL => inc atherosclerosis
26
Q

DM is a cause of atherosclerosis because of its (1) property. There is also an increased for (2), (3), and (4).

A

1- predisposition for elevated cholesterol
2- 100x inc risk for Atherosclerosis induced gangrene of lower extremities
3- strokes
4- MIs

27
Q

Patients with (1) will have premature vascular disease (atherosclerosis). Low levels of (2) can also cause high levels of (3- related to (1)).

A

1- homocystinuria (high plasma homocysteine)
2- folate (B9), cobalamin (B12)
3- plasma homocysteine

28
Q

(1) is an altered form of LDL, where its risk for causing atherosclerosis is independent of (2). Elevated (1) levels are associated with higher risk of (3).

A

1- Lipoprotein a, Lp(a)
2- cholesterol or LDL levels
3- coronary and cerebrovascular disease

29
Q

lower levels or less the of the following 6 parameters are great factors for preventing atherosclerosis

A
  • blood sugar
  • BP
  • BMI
  • LDL
  • stress
  • No. cigarettes
30
Q

(1) is the key player in the role of atherosclerosis development. Its activation will lead to (2) and (3). (4) and (5) are the common causes of (1).

A

1- endothelial injury
2- inc permeability
3- inc expression of adhesion molecules + inc leukocyte adhesion
4- hemodynamic factors: inc frequency of lesions at branch points / ostia of vessels
5- hypercholesterolemia

31
Q

(1) are considered cytotoxic to endothelial cells and will result in the increase of (2) production. (3) will accumulate in intima and generate (4)- b/c of (2). (4) will be ingested to form (5), it will stimulate the release of (6- include result), and it will inhibit (7).

A

1- lipids
2- local free radical production
3- lipoproteins
4- oxidized / modified lipids (LDL, => atherogenic properties)
5- foam cells (macrophage ingestion)
6- CKs –> chemotaxis for circulating monocytes
7- inhibits motility of local macrophages

32
Q

Smooth muscle proliferation is involved in atherosclerosis pathogenesis by….

A

converting fatty streaks into fibrofatty atheromas

33
Q

Macrophages play a role in atherosclerosis by engulfing (1), which triggers (2) production in order to increase the amount of (1). They also produce (3) and (4), (4) will lead to proliferation of (5).

A 
1- oxidized lipids (LDL)
2- free radicals
3- CKs: TNF, IL-1
4- GFs
5- smooth muscle cell proliferation
34
Q

(1) are isolated macrophage foam cells described as (2) in structure / morphology

A

fatty dots: multiple yellow flat spots, <1mm in diameter

35
Q

(1) are the precursor lesions to atherosclerotic plaques, defined as (2) in comparison to fatty dots. It is composed of (3). It will present in all people older than (4).

A

1- fatty streaks
2- coalesced fatty dots into a streak 1 cm or longer
3- lipid laden macrophages, some extracellular lipids
4- 10 y/o

36
Q

Define atherosclerotic plaque and its 3 components

A

-key feature is intimal thickening and lipid accumulation

1) Cells: SM cells, macrophages, T cells
2) ECM: collagen, elastin, proteoglycans
3) intracellular and extracellular lipid deposits

37
Q

describe the structure of an unstable plaque

A
  • thin fibrous cap
  • more lipids, T cells, macrophages
  • less smooth muscle cells
  • slender fragile neovascularization (–> hemorrhage into plaque spontaneously or b/c vasospasm)
  • ‘shoulder’ more susceptible
38
Q

list the 4 main systems affected by the clinical manifestations of atherosclerosis

A
  • CHD
  • cerebral vascular disease
  • abdominal aortic aneursym
  • peripheral vascular disease
39
Q

what are the CHDs seen as a result of atherosclerosis

A
  • acute MI
  • angina: stable, unstable
  • chronic IHD –> CHF
  • SCD
40
Q

what are the cerebral vascular diseases seen as a result of atherosclerosis

A
  • stroke / CVA
  • TIA
  • chronic ischemic encephalopathy
41
Q

what are the peripheral vascular diseases seen as a result of atherosclerosis

A
  • claudication (intermittent leg cramping/spasms)
  • ischemic bowel disease (mesenteric occlusion)
  • gangrene
42
Q

what are the 4 local complications that can arise from an atherosclerotic plaque

A

1) calcification (patchy or massive)
2) rupture, ulceration, or both –> thrombus formation –> cholesterol emboli / athero-emboli
3) hemorrhage: secondary to cap rupture, rupture of new BVs due to weak wall (role of vasospasm)
4) aneurysmal dilatation: atrophy of underlying media

43
Q

list the primary and secondary preventions measures for atherosclerosis

A

Primary: stop smoking, exercise, weight loss, HTN control, lower LDL and high HDL via diet, statins

Secondary: ASA (anti-platelet), statins, β-blockers, CABG, carotid endarterectomy

RCS (29 decks)

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