Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Emma III > Pathology (all) > Flashcards

Pathology (all) Flashcards

1
Q

definition of edema

A

Swelling.
Excessive fluid accumulation in tissues or body cavities.
Capillary/lymphatic leak.

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

severe generalized edema

A

anasarca

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

intraalveolar fluid

A

pulmonary edema

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

fluid accumulation in pleural space

A

pleural effusion/ hydrothorax

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

fluid accumulation in peritoneal cavity

A

ascites

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

transudate (associated with ?, appearance, specific gravity, glucose levels)

A 
associated with increased hydrostatic pressure.
Clear, sterile, few cells.
Low specific gravity.
Low protein content.
Glucose content near serum levels.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

exudate (associated with ?, appearance, specific gravity, glucose levels)

A 
associated with malignancy/inflammation.
Turbid/bloody/opaque.
Many cells.
High specific gravity.
High protein content.
Low glucose levels (cells consume it)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

acute pulmonary congestion

A

SUDDEN pulmonary capillary engorgement/dilation.
Leakage of fluids –> alveolar edema.
Seen in sudden cardiac/ventricular arrhythmia with left ventricular insufficiency

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

chronic pulmonary congestion

A

Chronic capillary engorgement –> slow leakage of fluid edema into alveolar spaces.
Hemosiderin-laden macrophages (ingested RBCs) = heart failure cells.
Seen in long-standing left ventricular insufficiency.

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

hemosiderin-laden macrophages

A

Ingested RBCs.
Heart failure cells.
Seen in chronic pulmonary congestion.

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

petechiae

A

small punctuate bleedings from capillaries

thrombocytopenia

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

purpura

A

Small bleedings larger than petechiae.

Associated with blood extravasation from small arterioles, vasculitis.

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

ecchymoses

A

Larger cutaneous bleedings. (basically normal bruises)
Due to trauma.
Seen in the elderly.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

myocardial ischemia

A

symptom: angina pectoris
Coronary blood flow does not meet myocardial oxygen demand.
Most frequent cause: coronary artery stenosis.

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

cerebral ischemia

A

Symptom: TIA
Short, temporary dysfunction of brain (neurological deficit)
Most frequent cause: decreased arterial supply due to arterial occlusion.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

lower extremity ischemia

A

Symptom: claudicatio intermittens.

Decreased blood flow to lower extremities.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

ischemia can lead to _____

A

Ischemia can lead to INFARCT.
Ischemic necrosis of tissue.
Caused by occlusion of arterial supply or venous drainage (thrombosis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

hemostasis definition

A

response to vascular injury resulting in formation of a hemostatic plug

No hemorrhage.
Blood still flows.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

endothelium produces:

A

procoagulant, and anticoagulant factors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

platelets cause ______ by production of __________

A

Platelets cause AGGREGATION (of platelets) by production of ADP/ATP, epinephrine, serotonin, fibrinogen, von Willebrand Factor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

basic steps of hemostatic plug formation

A

platelet activation/adhesion, secretion, aggregation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

end result of coagulation cascade

A

Fibrin formed (fibrinogen cleaved by thrombin)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

fibirin

A

Large, insoluble, forms clot.

Product of coagulation cascade.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

thrombosis

A

Pathologic activation of clotting mechanism with formation of a thrombus.

In UNINJURED vasculature.
Results in VASCULAR OCCLUSION.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

hemostasis vs thrombosis

A

hemostasis: physiologic; does not block blood flow; in injured vasculature
thrombosis: pathologic; blocks blood flow; in uninjured vasculature

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

virchow’s triad

A

three factors involved in thrombus formation:

1) endothelial injury
2) abnormal blood flow
3) hypercoagulability/thrombophilia

27
Q

endothelial injury (virchow’s triad)

A

Exposed ECM leads to platelet activation, coagulation cascade.

Could also be caused by dysfunctional endothelium (DM, smoking, hypercholesterolemia)

28
Q

abnormal blood flow (virchows triad)

A

Turbulence esp. at bifurcation sites, areas of atherosclerotic plaques.

Stasis: slowing of blood

Hyperviscosity: increased cellular elements of blood.

29
Q

hypercoagulability/thrombophilia

A

Disorder in coagulation pathway.

30
Q

fates of thrombi

A

1) thrombolysis (clot removed by fibrinolytic system)
2) organization (remodeling, recanalization)
3) embolization

31
Q

paradoxical embolism

A

Emboli that cross from venous to arterial circulation via septal heart defects (ex: patent foramen ovale)

32
Q

arterial thromboembolism

A

Emboli that originate within arterial circulation (bacterial growth/clot formation in heart valve/chambers, vegetation on valves due to metastatic cancer/treatment)

33
Q

types of emboli

A

Amniotic fluid emboli.
Septic emboli (cardiac valve vegetations).
Air emobli.
Fat emboli

34
Q

suspect thrombophilia if:

A

<60 years old.
Family history.
Spontaneous/massive DVT/VTE

35
Q

Risk factors for acquired thrombophilia

A 
Immobilization.
Major surgery/fracture/burns.
Malignancy.
MI.
Heparin.
Pregnancy/estrogen.
Smoking.
36
Q

types of hereditary thrombophilia

A 
Mutation in factor V Leiden.
Prothrombia gene mutation.
Antithrombin III deficiency.
Protein C deficiency.
Protein S deficiency.
Hyperhomocystinemia.
37
Q

arteriosclerosis

A

Umbrella term.
Hardening of the arteries.

Types: atherosclerosis, monckeberg medial calcific stenosis, arteriolosclerosis

38
Q

atherosclerosis

A

Formation of lipid rich fibrous plaques in intima.

Affects ELASTIc/MUSCULAR arteries

39
Q

monckeberg medial calcific stenosis

A

No clinical significance.

Calcification in tunica media.

40
Q

arteriolosclerosis

A

Disease of small arteries/arterioles.
Associated with DIABETES MELLITUS/HYPERTENSION.
Most often in KIDNEYS.

41
Q

hyperplastic arteriolosclerosis

A

hyperplasia of smooth muscle
onion skin appearance

Most often in kidneys with malignant hypertension.

42
Q

hyaline arteriolosclerosis

A

Leakage of plasma proteins, excess ECM production –> narrowed lumen

Associated with hypertension/diabetes

43
Q

epidemiologic significance of atherosclerosis

A

Leading COD in US for both males and females.

More prevalent among developed nations.

44
Q

non-modifiable major risk factors of atherosclerosis

A 
age
sex
men > women (estrogen is protective)
family history
genetic abnormalities
45
Q

modifiable major risk factors of atherosclerosis

A 
hyperlipidemia
hypertension
smoking
diabetes
CRP
46
Q

minor risk factors of atherosclerosis

A 
obesity
physical inactivity
stress
homocysteine
post menopause
alcohol
lipoprotein a
unsaturated fat intake
47
Q

fatty streak

A

Lipid filled foam cells.
T lymphocytes.
Extra cellular lipids.

Precursor to atheromatous plaque

48
Q

intimal thickening

A

White, thickened areas at branch points.
Smooth muscle cells, CT (no lipids)

Precursor to atheromatous plaque

49
Q

atheromatous plaque

A

Smooth muscle cells, macrophages, leukocytes.
CT, ECM.
Intracellular and Extracellular lipid deposits.

50
Q

progression of atherosclerotic lesions

A

1) initial lesion/dysfunction
2) isolated/few macrophages
3) fatty streaks, intimal thickening, intracellular lipid accumulation
4) increase in extracellular lipid
5) atheroma (plaque)
6) fibroatheroma (fibrous plaque)
7) complex lesion

51
Q

a complex lesion can lead to

A

1) aneurysm and rupture
2) occlusion by thrombosis
3) critical stenosis

52
Q

vasculitis (general)

A

Inflammation of vessel wall due to infection or other causes (immune complex rxn)
May affect any vessel, but most commonly small vessels.

Types: giant cell arteritis, polerarteritis nodosa, thromboangitis obliterans

53
Q

giant cell (temporal) arteritis

A

Giant cells and lymphocytes.
Intimal fibrosis.
Unknown cause (immune??)
Blindness if opthalmic artery involvement.
Sx: pain/tenderness over temporal head, jaw pain
Tx: prednisone

54
Q

polyarteritis nodosa

A

Systemic and segmental involvement of SMALL and MEDIUM arteries.
Causes necrotizing inflammation, swarms of lymphocytes.
30% have HEPATITIS B in system.
Young adults, mostly males.

55
Q

thromboangiitis obliterans (Buerger’s Disease)

A

Small and intermediate arteries, sometimes veins, of EXTREMITIES.
Untreated leads to gangrene, autoamputation.
Associated with heavy cigarette smoking.

56
Q

aneurysm definition and risks

A

dilatation due to weakened vascular wall

Risks: rupture, thrombosis & embolism, erosion of adjacent structures

57
Q

abdominal aortic aneurysm

A

Intrinsic/acquired defect in wall
>65 years
Usually below renal arteries and above iliac bifurcation

58
Q

risk factors for AAA

A

atherosclerosis
smoking
family history of AAA

Risk of rupture increases with size

59
Q

rupture triad (symptoms of AAA rupture)

A

1) severe, sudden back pain
2) hypotension
3) pulsatile abdominal mass

60
Q

berry aneurysms

A

At bifurcations of circle of willis.

etiology:
genetic, SMOKING, HTN, PCKD

61
Q

aortic dissection (definition, symptoms, most common cause)

A

entry of blood into wall of aorta through tear in tunica media, subsequent pushing apart of wall layers (tunica media)

Sx: abrupt onset severe chest /back pain, “tearing pain”

Most common cause: chronic HTN
Associated with CT disorders (Marfans, Ehler-Danlos, coarctation, bicuspid aortic valve)

62
Q

sequelae of AAA

A

1) rupture into surrounding soft tissues
2) rupture into pericardial space
3) rupture into pleural space
4) re-entry into aortic lumen
5) compression of branch ostia

63
Q

hemangioma

A

benign vascular tumors with increased number of normal and abnormal vessels.

usually in head/neck, sometimes internal organs

Present at birth and SPONTANEOUSLY regress over time (no treatment/surgery)

64
Q

angiosarcoma

A

Rare malignant neoplasm arising from endothelial cells of blood vessels.

Soft tissue, skin, breast, bone, liver, spleen

Can develop after radiation Tx for another cancer

Emma III (28 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions