Brainscape's Knowledge GenomeTM

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


See full index

Pathology > Chapter 1 > Flashcards

Chapter 1 Flashcards

1
Q

Pathology

A

study of disease

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

sign

A

observed by doctor

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

symptom

A

reported by patient

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

Cervical lymphadenopathy

A

swollen lymph nodes

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

streptococcal phayrngitis

A

strep throat

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

URTI

A

Upper respiratory tract infection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

etiology

A

origin of disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

pathogensis

A

steps in development, how etiologic factors caused cellular change

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

metaplasia

A

cell becomes stressed to the point of becoming another one-EX cells of throat from smoking

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

phenotype

A

observable characteristics or traits

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

steatosis

A

fat accumulation

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

Karyolysis

A

nuclear fading-chromatin dissolution

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

pyknosis

A

nuclear shrinkage-DNA condenses

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

karyorrhexis

A

nuclear fragmentation-nuclei membrane ruptures

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

necrosis

A

cell swells and dies, is accompanied by inflammation, and is irreversible

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

apoptosis

A

cell shrinks, not accompanied by inflammation, and plasma membrane remains intact, programmed cell death

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

coagulative necrosis (ischemic necrosis)

A

vascular occlusion leads to cell death. tissue structure is preserved and is firm. denatures proteolytic enzymes

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

gangrenous necrosis

A

coagulative necrosis in an extremity

examples of causes: diabetes, PVD, atherosclerosis

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

dry gangrene

A

has a dry flaky apperance

20
Q

wet gangrene

A

appears to be wet to the touch

21
Q

gas gangrene

A

appears swollen and puffy

22
Q

liquefactive necrosis

A

dead cells are completely digested by WBC’s whose enzymes then produce a liquid viscous mass

Can be a result from infections of CNS ischemia/hypoxia

23
Q

Caseous necrosis

A

has a “cheese-like” appearance and is enclosed within a distinctive border

typical of TB infections, chronic lung infections

24
Q

Fat necrosis

A

localized fat destruction in which fat is saponified (turned into soap)

can be from trauma to the breasts or from acute pancreatitis

25
Q

fibrinoid necrosis

A

autoimmune reactions, immune complexes and fibrin are deposited into arterial walls and is Eosinophilic when under microscope

leads to weakened vessels walls posing a risk for an aneurysm

requires a histological evaluation via light microscopy

26
Q

Apoptosis

A

programmed cell death in which no inflammation is caused and membranes are left in tact

activated by caspases

27
Q

Mitochondrial pathway (intrinsic)

A

decreased GF, DNA damage, misfolded proteins, increased membrane permeability

caspase 9

28
Q

death receptor pathway (extrinsic)

A

binding with surface molecules

eliminates self reactive lympocytes or virus infected cells

caspase 8

29
Q

Autophagy

A

“self eating”

survival mech during nutrient deprivation

rids misfolded proteins

30
Q

depletion of ATP

A

decreased oxidative phosphorylation, hypoxia, nutritional deficiency, mitochondria damage, toxins

31
Q

mitochondrial damage

A

disrupted membranes and increased ROS production, hypoxia, toxins, irradiation

32
Q

influx of calcium

A

ischemia and toxins which activates enzymes

33
Q

oxidative stress

A

accumulation of ROS, ischemia-reperfusion, toxins, irradiation, cellular aging, inflammation

34
Q

defects in membrane permeability

A

decreased production and increased breakdown of phospholipids

35
Q

DNA & protein damage

A

severe irreparable damage from oxidative stress, irradiation, and abnormal protein folding

36
Q

Ischemia and hypoxic injury

A

produces acute cellular injury and impacts both aerobic and anaerobic metabolisms

restoration of blood flow can reverse damage

37
Q

ischemia reperfusion

A

temporary ischemia with a restoration of flow possibly causing injury

38
Q

chemical injury

A

direct-cell absorbs and stores toxins which inhibts ATP or damages membranes

indirectly-conversion of molecule produces reactive metabolite

39
Q

intracellular accumulations

A

abnormal metabolism, defective protein folding/transport, defective or absent enzymes, ingestion of indigestible materials

40
Q

Fatty change (steatosis)

A

abnormal accumulation of fat

41
Q

anthracosis

A

carbon pigments

42
Q

lipofuscin

A

wear and tear pigments in elderly

43
Q

hemosiderin

A

excessive iron, hemosiderosis

44
Q

dystrophic calcification

A

accumulation of Ca in damaged tissues

45
Q

metastatic calcification

A

accumulation of Ca in normal tissues

46
Q

Cellular aging

A

reduced functional capacity of cells due to accumulation of cellular/molecular damage

Pathology (3 decks)

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