Brainscape's Knowledge GenomeTM

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


See full index

Pathology > Cellular Adapt & accumulations II > Flashcards

Cellular Adapt & accumulations II Flashcards

1
Q

What are subcellular reponses to injury?

A

Distinctive alterations involving subcellular organelles and cytosolic proteins

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

What are lysosomes filled with?

A

Hydrolytic enzymes

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

What are primary lysosomes?

A

Small membrane-bound vesicles budding from the Golgi

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

Primary lysosomes form secondary ones how?

A

By fusing with pinocytotic or phagocytic vesicles derived from invaginated plasma membrane (phagolysosomes)

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

What is heterophagy?

A

Materials from extracellular environment taken up through endocytosis

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

What is autophagy?

A

Lysosomal digestion of cells own components

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

What are residual bodies formed from in cells?

A

indigestible material resulting from intracellular free radical lipid peroxidation

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

Hereditary lysosomal storage diseases result in what?

A

Abnormal accumulation of intermediate metabolites

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

What happens to the sER during increased chemical intake? What is the consequence of this?

A

Hypertrophy to increase p450 enzymes

This may lead to the production of more ROS

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

EtOH abuse leads to what mitochondrial changes in the liver?

A

Enlarged and abnormal shapes

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

What are mitochondrial myopathies?

A

Mitochondrial alterations (like MEERF, MELAS, Leber’s Hereditary optic neuropathy)

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

What comprises the cytoskeleton (3)?

A

Thin filaments
Microtubules
Intermediate filaments

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

Abnormalities in the cytoskeleton reflects what?

A

Defects in cell function or intracelluarl accumulation of fibrillar material

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

What are the thin filaments?

A

Actin, myosin, movement, phagocytosis

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

What are microfilaments used for?

A

Motility, phagocytosis mitotic spindles

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

What are intermediate filaments used for?

A

Intracellular scaffold maintain cellular architecture

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

What are cytoskeletal elements’ role in signal transduction?

A

Linked to cellular receptors to transduce signals

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

Intracellular accumulation are the result of what?

A

Metabolic derangements

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

What are the three categories of intracellular accumulations?

A
  1. Normal endogenous substance produced at normal or increased rate, but metabolism cannot remove it
  2. Normal or abnormal endogenous substance accumulates
  3. Abnormal exogenous substances is deposited
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What are four mechanisms of intracellular accumulations?

A
  1. Abnormal metabolism
  2. Alterations in proteins folding and transport
  3. Deficiency of critical enzymes
  4. Inability to degrade phagocytosed particles
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What happens in intracellular accumulations?

A

Normal substances are produced at normal or increased rates, but metabolism cannot keep up

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

What is steatosis? What is this usually caused by?

A

Abnormal accumulations of triglycerides within cells

DM or EtOH use

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

What are the causes of steatosis?

A

Toxins
Protein mutations
Malnutrition
EtOH

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

The significance of steatosis depends on what?

A

Cause and severity

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

FAs accumulate as what?

A

Triglycerides

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

FAs are usually metabolized to what? (3)

A

Phospholipids
Cholesterol esters
Ketones

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

What are xanthomas?

A

Macrophages accumulate cholesterol underneath the skin

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

What is cholesterolosis?

A

Gallstones

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

What is atherosclerosis?

A

Abnormal accumulation of cholesterol/esters in the tunica intima of arteries

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

What are foam cells? What happen if these rupture?

A

Macrophages that accumulate lipids.

If rupture = cholesterol clefts form

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What are atheroma?

A

Aggregates of cholesterol macrophages

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What is the MOA of atherosclerosis?

A

Accumulation of foam cells on vessel walls

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Strawberry gallbladder is d/t what?

A

Cholesterolosis of gallbladder

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What are the histological features of cholesterolosis?

A

Foam cells in gallbladder

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What causes proteins to accumulate within a cell?

A

Misfolding

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

What is hyaline?

A

Pink material in the cytoplasm

37
Q

What are the causes or protein accumulations?

A

Reabsorption
Increased synthesis
Defect in folding

38
Q

What does protein accumulation appear like histologically (e.g. in the renal tubules)?

A

Vacuoles accumulation of pink hyaline

39
Q

What are Russell bodies? Is this pathogenic

A

Immunoglobulins packing into b (plasma) cells–abnormal

40
Q

What are Mallory bodies?

A

alcoholic hyalin (structural protein) accumulations in the liver

41
Q

Hyaline is eosinophilic or basophilic?

A

Eosinophilic

42
Q

How can protein misfolding lead to accumulations?

A

Partially folded intermediates vulnerable to aggregate

43
Q

What are chaperones used for?

A

Aid in protein folding and transport repair misfolded proteins

44
Q

What is ubiquitin?

A

Marker for degradation by a proteosome

45
Q

What are the four cellular responses to increased misfolded proteins?

A
  1. Increase chaperones
  2. Decrease translation
  3. Increase degradation
  4. Apoptosis
46
Q

What is ER stress? What does this lead to?

A

Demand for proteins is greater the capacity to produce

Leads to misfolded response

47
Q

What is alpha-1-antitrypsin deficiency? What does this lead to?

A

Build up of proteases d/t misfolded antiprotease (alpha 1 antitrypsin)

Leads to tissues damage (cirrhosis/ COPD etc)

48
Q

True or false: there is a balance of proteases and antiproteases

A

True

49
Q

What are the histological features of alpha-1-antitrypsin def?

A

Red globules with PAS stain in the liver

50
Q

What are the histological features of amyloidosis?

A

Orange-red stain on Congo red stain

51
Q

What is amyloidosis?

A

Build up of amyloid in issue

52
Q

What is a hyaline change?

A

A non-specific morpholiogical change; pink homogenous appearance on H&E staining

53
Q

Hyaline change can be seen in intracellular or extracellular aggregations?

A

Both

54
Q

Hyaline change in the walls of arterioles occur in what disease?

A

DM and HTN

55
Q

Glycogen appears like what histologically? (with H&E)

A

Clear cytoplasmic vaculoes

56
Q

In DM, glycogen can be seen in what?

A

Cytoplasm of renal tubular epithelium via glycosylation of proteins

57
Q

What are the two types of diseases where glycogen is accumulated?

A

DM

GSDs

58
Q

How do GSDs appear histologically (with H&E)?

A

empty vacuoles

59
Q

Pompe’s disease = ?

A

Type II GSD

60
Q

Pigments are endogenous or exogenous?

A

Both

61
Q

What is the most common exogenous pigment?

A

Carbon

62
Q

What happens to carbon inhaled?

A

Picked up by macrophages and transported to lymph nodes

63
Q

What is anthracosis? What can this lead to in severe conditions?

A

Macrophage accumulation of carbon.

May lead to fibrosis if too large and pneumoconiosis

64
Q

What is the MOA of tattooing?

A

Localized exogenous pigmentations of skin d/t dermal macrophages

65
Q

What is lipofuscin?

A

Brown pigment resulting from lipochrome (lipids and phospholipids)

66
Q

Where does lipofuscin accumulate?

A

Heart, liver, brain

67
Q

Lipofusin is a marker of what?

A

Past free radiacal injury

68
Q

How does lipofusin appear grossly?

A

Brown

69
Q

What is melanin? What cells produce it?

A

Normal pigment in basal epithelial cells produced by melanocytes (via oxidation of Y by tyrosinase)

70
Q

Melanin accumulates where?

A

Keratinocytes in skin or dermal macrophages

71
Q

What is spitz nevus?

A

Benign melanin mole found in children

72
Q

What is hemosiderin?

A

Hb derived gold-yellow/brown pigment in which Fe is stored

73
Q

Excess Ferritin forms what in the body?

A

Hemosiderin granules that accumulate into micelles in cells

74
Q

Hemosiderin pigments represents what?

A

Aggregates of ferritin micelles

75
Q

Excesses of Fe build up leads to what?

A

Hemosiderosis

76
Q

What are the causes of hemosiderosis? (4)

A

Increase Fe intake
Impaired use of iron
Hemolytic disease
Transfusions

77
Q

Hemochromatosis = ?

A

Accumulation of Fe, in the liver d/t protein absorption in the gut that causes it to absorb more

78
Q

What is the stain for Fe?

A

Prussian blue

79
Q

Hemochromatosis leads to what?

A

Liver damage

80
Q

What is bilirubin?

A

Hb, NOT Fe

81
Q

What is dystrophic calcification?

A

Local processes where normal serum Ca leads accumulation organ dysfunction

82
Q

What is metastatic calcification?

A

Increased serum calcium (hypercalcemia) leading to increase deposition in tissues

83
Q

What are the three major ways that hypercalcemia is brought about?

A
  1. CA in bone
  2. High PTH levels
  3. Vit D disorder
84
Q

What is the ultimate end product of dystrophic calcification? Metastatic?

A

Calcium phosphate for dystrophic, leading to tissue destruction

Thin Ca layer without dysfunction of tissue

85
Q

What do protein inclusions look like histologically?

A

Dark, eosinophilic inclusions in cells

86
Q

Hemosiderin-laden macrophages indicate what disease process?

A

Heart failure

87
Q

Where is Fe stored in the body?

A

Macrophages in the bone marrow

88
Q

Apoprotein + triglyceride = ?

A

Lipoproteins

89
Q

What is the main secondary structure associated with Amyloid? What does this stain?

A

Beta pleated sheets that stain with congo red, and fluoresces

Pathology (32 decks)

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