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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

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2
Q

What are lysosomes filled with?

A

Hydrolytic enzymes

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3
Q

What are primary lysosomes?

A

Small membrane-bound vesicles budding from the Golgi

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4
Q

Primary lysosomes form secondary ones how?

A

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

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5
Q

What is heterophagy?

A

Materials from extracellular environment taken up through endocytosis

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6
Q

What is autophagy?

A

Lysosomal digestion of cells own components

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7
Q

What are residual bodies formed from in cells?

A

indigestible material resulting from intracellular free radical lipid peroxidation

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8
Q

Hereditary lysosomal storage diseases result in what?

A

Abnormal accumulation of intermediate metabolites

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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

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10
Q

EtOH abuse leads to what mitochondrial changes in the liver?

A

Enlarged and abnormal shapes

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11
Q

What are mitochondrial myopathies?

A

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

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12
Q

What comprises the cytoskeleton (3)?

A

Thin filaments
Microtubules
Intermediate filaments

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13
Q

Abnormalities in the cytoskeleton reflects what?

A

Defects in cell function or intracelluarl accumulation of fibrillar material

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14
Q

What are the thin filaments?

A

Actin, myosin, movement, phagocytosis

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15
Q

What are microfilaments used for?

A

Motility, phagocytosis mitotic spindles

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16
Q

What are intermediate filaments used for?

A

Intracellular scaffold maintain cellular architecture

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17
Q

What are cytoskeletal elements’ role in signal transduction?

A

Linked to cellular receptors to transduce signals

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18
Q

Intracellular accumulation are the result of what?

A

Metabolic derangements

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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
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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
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21
Q

What happens in intracellular accumulations?

A

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

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22
Q

What is steatosis? What is this usually caused by?

A

Abnormal accumulations of triglycerides within cells

DM or EtOH use

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23
Q

What are the causes of steatosis?

A

Toxins
Protein mutations
Malnutrition
EtOH

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24
Q

The significance of steatosis depends on what?

A

Cause and severity

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25
Q

FAs accumulate as what?

A

Triglycerides

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26
Q

FAs are usually metabolized to what? (3)

A

Phospholipids
Cholesterol esters
Ketones

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27
Q

What are xanthomas?

A

Macrophages accumulate cholesterol underneath the skin

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28
Q

What is cholesterolosis?

A

Gallstones

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29
Q

What is atherosclerosis?

A

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

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30
Q

What are foam cells? What happen if these rupture?

A

Macrophages that accumulate lipids.

If rupture = cholesterol clefts form

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31
Q

What are atheroma?

A

Aggregates of cholesterol macrophages

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32
Q

What is the MOA of atherosclerosis?

A

Accumulation of foam cells on vessel walls

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33
Q

Strawberry gallbladder is d/t what?

A

Cholesterolosis of gallbladder

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34
Q

What are the histological features of cholesterolosis?

A

Foam cells in gallbladder

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35
Q

What causes proteins to accumulate within a cell?

A

Misfolding

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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

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?

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?

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?

61
Q

What is the most common exogenous pigment?

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?

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)

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