Brainscape's Knowledge GenomeTM

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


See full index

Concepts in Pathology and Tissue Morphology > Pathology > Flashcards

Pathology Flashcards

1
Q

define “signs” of abnormal clinical findings, and what are some examples

A
  • something that can be detected by a clinician even if patient is unconscious
  • swelling
  • redness
  • fever
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

define “symptoms” and what are some examples

A
  • something that the patient must tell you
  • chest pain
  • SOB
  • nausea
  • HA
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

some underlying etiology causes cell damage, which leads to tissue changes and then pathogenesis. At which point in this process could changes be detected through testing?

A

at the level of tissue change, morphologic changes can be seen on biopsy and molecular changes can be detected in blood

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

hypertorophy

A

increase in cell size due to increase in stress

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

hyperplasia

A

increase in number of cells due to increase in stress

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

mechanism of hypertrophy

A

gene activation, protein synthesis and production of organelles

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

mechanism of hyperplasia

A

proliferation of mature cells and in some cases, increased output of new cells from stem cells

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

hyperplasia and hypertrophy often occur together (eg uterus during pregnancy). What is an exception to this rule

A

permanent tissues cannot undergo hyperplasia and therefore will only undergo hypertrophy
•cardiac muscle, skeletal muscle, nerve

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

uterus hypertrophy/hyperplasia during pregnancy is an example of a physiologic process. Contrast this with pathologic hyperplasia

A

eg endometrial hyperplasia

in the pathologic process, hyperplasia can progress to dysplasia and eventually cancer

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

benign prostatic hyperplasia (BPH) is a pathologic process, but is unique in that

A

unlike other pathologic hyperplasia, it does not increase the risk of prostate cancer

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

atrophy

A

decrease in number and size of cells due to a decrease in stress

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

mechanism of decreased number of cells in atrophy

A

apoptosis and autophagy

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

metaplasia

A

a change in cell type due to a change in stress on an organ

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

most common cell types involved in metaplasia

A

one type of surface epithelium to another (squamous, cuboidal, columnar)

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

mechanism of metaplasia

A

reversible reprogramming of stem cells -> production of new cell type

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

dysplasia

A

disordered cellular growth, most often refers to proliferation of precancerous cells

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

dysplasia often arises from longstanding pathologic ___ or ___

A

hyperplasia or metaplasia

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

dysplasia is reversible with alleviation of inciting stress. If stress persists however, it progresses to

A

carcinoma, which is irreversible

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

aplasia

A

failure of cell production during embryogenesis (eg unilateral renal agenesis)

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

hypoplasia

A

decrease in cell production during embryogenesis, resulting in relatively small organ (ie streak ovary in turner syndrome)

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

what is a common cause of pathologic hyperplasia

A

excessive or inappropriate actions of hormone or growth factors

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

mechanism of decreased size of cells in atrophy

A
  • protein synthesis decreased b/c reduced metabolic or nervous activity
  • ubiquitin-proteosome degradation of cytoskeleton and autophagy of cellular components
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

what are 2 features of reversible cell injury that can be recognized under light microscopy?

A

cellular swelling and fatty change

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

when does cellular swelling occur

A

•when cells are incapable of maintaining ionic and fluid homeostasis

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

cause of cellular swelling

A
  • failure of energy-depending ion pumps in plasma membrane

* ie decreased ATP -> decreased Na/K pump activity

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

when does fatty change occur

A

hypoxic injury and various forms of toxic or metabolic injury

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

what cells is fatty change usually seen in

A
  • cells involved in and dependent on fat metabolism

* ie hepatocytes and myocardial cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

ATP depletion is a mechanism of cell injury. What happens here?

A

failure of energy-dependent functions -> reversible injury -> necrosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Mitochondrial damage is a mechanism of cell injury. What happens here?

A

ATP depletions -> failure of energy-dependent fxns -> ultimately necrosis; under some conditions leakage of mitochondrial proteins can trigger apoptosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Influx of calcium is a mechanism of cell injury. What happens here?

A

activation of enzymes that damage cellular components and may also trigger apoptosis

31
Q

accumulation of reactive oxygen species is a mechanism of cell injury. What happens here?

A

covalent modification of cellular proteins, lipids, nucleic acids

32
Q

increased permeability of cellular membranes is a mechanism of cell injury. What happens here?

A

may affect plasma membrane, lysosomal membranes, mitochondrial membranes -> typically causes necrosis

33
Q

accumulation of damaged DNA and misfolded proteins is a mechanism of cell injury. What happens here?

A

triggers apoptosis

34
Q

morphologic appearance of necrosis is the result of

A

denaturation of intracellular proteins and enzymatic digestion

35
Q

what happens in irreversible cell injury (cell death)?

A
  • karyolysis
  • pump failure, leakage of enzymes
  • profound disturbances in membrane function
36
Q

what happens to the cytoplasm (histologically) in cell death

A
  • becomes more eosinophilic

* loss of basophilia that was normally imparted by the RNA in cytoplasm

37
Q

what is karyolysis

A
  • breakdown of nucleus due to DNase activity

* basophilia of chromatin fades

38
Q

What is pyknosis

A

nuclear shrinkage -> increased basophilia

39
Q

what is karyorrhexis

A

when the DNA condenses into a solid shrunken mass

40
Q

most common kind of necrosis is

A

coagulative, liquefactive may be second

41
Q

coagulative necrosis can occur in all organs except what

A

the brain

42
Q

histologic appearance of coagulative necrosis

A

eosinophilic, anucleate cells may persist for days to weeks, then ultimately removed by phagocytosis

43
Q

what is a localized area of coagulative necrosis called?

A

infarct

44
Q

where does liquefactive necrosis predominantly occur?

A

brain/CNS

45
Q

hypoxic death of cells within CNS often manifests as

A

liquefactive necrosis

46
Q

what is liquefactive necrosis characterized by

A
  • digestion of dead cells -> transformation of tissue into liquid viscous mass
  • necrotic material often creamy yellow because of dead leukocytes (pus)
47
Q

where does fat necrosis commonly occur

A

in the peripancreatic fat due to release of activated pancreatic lipases into pancreas and peritoneal cavity

48
Q

histologic appearance of fat necrosis

A

foci of shadowy outlines of necrotic fat cells with basophilic calcium deposits, surrounded by an inflammatory reaction (foamy macrophages)

49
Q

what is a common site of caseous necrosis

A

lung

50
Q

what is usually the underlying cause of caseous necrosis

A

infection with mycobacterium (ie TB) or fungal infections

51
Q

histologic appearance of caseous necrosis

A
  • necrotic area appears as a structureless collection of fragmented or lysed cells and amorphous granular debris enclosed w/in a distinctive inflammatory border -> granuloma
  • key is presence of multinucleated cells
52
Q

where does fibrinoid necrosis occur

A

in blood vessels

53
Q

what typically causes fibrinoid necrosis

A

deposition of antigen-antibody complexes in walls of arteries

54
Q

histologic appearance of fibrinoid necrosis

A

deposits of “immune complexes” with fibrin that has leaked out of vessels -> bright pink and amorphous appearance in HandE stains

55
Q

what is dry gangrene

A

common in lower limbs of diabetics. it is histologically a coagulative necrosis

56
Q

what is wet gangrene

A

necrosis caused by loss of blood supply (coagulative) with a concurrent bacterial infection causing pus formation (liquefactive)
*not as common as dry gangrene

57
Q

what is apoptosis

A

a regulated mechanism of cell death -> eliminated unwanted and irreparably damaged cells with LEAST possible host reaction

58
Q

apoptosis is characterized by enzymatic degradation of proteins and DNA followed by recognition and removal of dead cells by phagocytes. What initiates it

A

caspases

59
Q

what are the 2 major pathways of apoptosis

A
  • mitochondrial pathway (INTRINSIC)

* death receptor pathway (EXTRINSIC)

60
Q

physiologic apoptosis, such as that which occurs in embryogenesis follows which pathway

A

intrinsic (mitochondrial) pathway

61
Q

examples of physiologic apoptosis

A
  • embryogenesis
  • involution (endometrium, lactating breast, thymus)
  • proliferating populations (intestinal crypts)
62
Q

examples of pathologic apoptosis

A
  • DNA damage (chemotherapy)
  • misfolded proteins (neurodegenerative disease)
  • infections (viral)
  • pathologic atrophy in parenchymal organs after duct obstruction, such as occurs in pancreas, parotid gland, and kidney
63
Q

contrast cell size in necrosis and apoptosis

A
  • in necrosis, cells become enlarged -> burst

* in apoptosis cells shrink

64
Q

contrast what happens to the nuclei in necrosis and apoptosis

A
  • necrosis: pyknosis -> karyorrhexis -> karyolysis

* apoptosis: cut into nucleosome-sized fragments

65
Q

contrast what happens to plasma membranes in necrosis and apoptosis

A
  • necrosis: membranes disrupted

* apoptosis: intact; but altered structure, esp. orientation of lipids

66
Q

contrast adjacent inflammation in necrosis and apoptosis

A
  • necrosis: frequent adjacent inflammation

* apoptosis: never

67
Q

Ca2+ is normally mainly extracellular. If some injurious agent allows excessive Ca2+ influx cellular enzymes can be activated that cause cellular damage. What types of damage can increased cytosolic Ca2+ cause

A
  • phosopholipase and proteases can lead to MEMBRANE DAMAGE
  • endonucleases can lead to NUCLEAR DAMAGE
  • INCREASED MITOCHONDRIAL PERMEABILITY -> DECREASED ATP
68
Q

Autophagy is a survival mechanism in times of nutrient deprivation; starved cell eats its own contents and recycles -> provided nutrients and energy. What is the process of autophagy

A

lysosomal digestion of cell’s own components

69
Q

bulk autophagy is nonselective, and can be contrasted with selective autophagy, which involved

A

ubiquitin tagging

70
Q

atuophagy is involved in the clearance of _____.

Therefore defective autophagy may a cause of _____

A

misfolded proteins; neuronal death induced by accumulation of the misfolded proteins -> neurodegenerative disease

71
Q

3 major causes of hypoxia

A
  • ischemia
  • hypoxemia
  • decreased O2 carrying capacity of blood
72
Q

what is saponification?

A
  • occurs when fatty acids released by trauma or lipase join with calcium
  • this is part of the process of fat necrosis
73
Q

caspaces are the mediators of apoptosis. What do they do?

A
  • activate proteases (break down cytoskeleton)

* activate endonucleases (break down DNA)

74
Q

what is the key mediator of the intrinsic (mitochondrial) pathway of apoptosis?

A

cytochrome C (which is located in the mitochondrial membrane)

Concepts in Pathology and Tissue Morphology (10 decks)

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