Brainscape's Knowledge GenomeTM

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


See full index

Pathology > Cell Injury & Death > Flashcards

Cell Injury & Death Flashcards

1
Q

Define etiology

A

Cause of disease

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

Define pathogenesis

A

Mechanism of development

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

Define molecular or morphogenic changes

A

Biochemical and structural alterations

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

Define clinical manifestations

A

Functional consequences of disease or dysfunction

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

What are the (2) circumstances that lead to cell injury?

A
  • exceeding limits of adaptation

- adaptive resources unavailable when needed

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

What is the difference between symptoms and signs?

A

Symptoms = what a pt feels

Signs = what is observed during exam

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

Define edema

A

Accumulation of fluid in body tissues and cavities

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

What are protooncogenes?

A

Genes of differentiation

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

Define atrophy

A

Shrinkage of cells or organs

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

What is the most common cause of pathologic atrophy?

A

Hypoxia

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

What are less common causes of pathologic atrophy?

A
  • disuse
  • pressure
  • denervation
  • endocrine deficiency (target organ experiences atrophy)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Define hypertrophy

A

Enlargement of existing cells - especially permanent, non-dividing cells - due to increased work load or hormonal action

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

Define hyperplasia

A

Enlargement of tissue due to proliferation of cells - only in mitotic cell populations

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

Define metaplasia

A

Substitution of one type of mature cell with another cell type

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

What is Barrett’s Esophagus?

A

Columnar cell metaplasia of lower esophagus

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

Define dysplasia

A

Atypical metaplasia - bad growth

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

What is a prominent example of dysplasia and what does it lead to?

A

Uterine cervix dysplasia as seen with HPV, usually leads to cancer

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

What usually regulates hyperplasia?

A

Growth factors & inhibitors

Cytokines

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

What is are examples of nonpathological hyperplasia?

A
  • compensatory response to partial loss of tissue
  • pregnancy & nursing (uterine & breast tissue hyperplasia)
  • wound repair
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is ischemia?

A

Injury due to decreased blood flow - can be local or systemic

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

What is hypoxemia?

A

Decreased blood oxygen due to decreased available oxygen or hemoglobin issues

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

What is the first cellular problem during hypoxic injury?

A

Depletion of ATP stopping cellular activity, especially of NA/K pumps

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

What are the enzymes activated by increased intracellular calcium, that can lead to cell injury and death?

A
  • phospholipases
  • proteases
  • ATPases
  • endonucleases
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

How are free radicals removed or degraded?

A
  • spontaneous decay
  • action of enzymes
  • antioxidant action (like vit A and C)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What is the consequence of mitochondrial injury?

A

Cell death

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

What are the (4) characteristics of fatty change seen in reversibly injured cells?

A
  • Cell swelling & cloudiness
  • mitochondria & ER swelling
  • dispersed ribosomes
  • formation of blebs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What change to cell membranes usually leads to cell death?

A

Degradation of membrane phospholipids reducing membrane integrity

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

What serum marker is considered to be a sign of cell injury and death?

A

Increased serum enzymes

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

Define pkynosis

A

Condensation - nuclear shrinkage

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

Define karyorrhexis

A

Fragmentation and breakdown of nucleus

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

Define karyolysis

A

Dissolution of nucleus

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

Coagulation necrosis is common in what types of tissue?

A

Solid organs - heart, kidney, muscle, adrenals

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

What is coagulation necrosis?

A

Denaturation of cytoplasmic proteins

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

What is liquefaction necrosis?

A

Tissues are lysed by enzymes from injured cells - a fluid filled cavity (cyst) forms

35
Q

What is a common cause of liquefaction necrosis?

A

Infarcts of soft tissue (stroke!)

36
Q

What is caseous necrosis?

A

Necrotic tissue has cheesy appearance - thought to be a combination of coagulation and liquefaction

37
Q

What are common causes of caseous necrosis?

A

TB and leprosy

38
Q

What is fat necrosis?

A

Hydrolysis of lipid deposits present in adipose -

Resulting fatty acids interact with calcium to form chalky soap deposits

39
Q

What are examples of fat necrosis?

A

Acute pancreatitis

Liver saponification

40
Q

What is gummatous necrosis?

A

Chronic, nodular fibrotic deposits

41
Q

What disease causes gummatous necrosis?

A

Syphilis

42
Q

What is gangrene?

A

Coagulation necrosis often with putrefaction from bacterial activity

43
Q

What is dry gangrene and what body parts are most often affected?

A

Mummification - coagulation happens and the affected tissue dries out before bacteria activity

Happens in the digits and superficial structures

44
Q

What are 2 common causes of dry gangrene?

A
  • frostbite

- infarctions

45
Q

What is wet gangrene and what are common body parts affected?

A

Necrosis with bacterial infection leading to liquefaction

Intestinal infarcts
Acute appendicitis

46
Q

What is gas, or infectious, gangrene?

A

Occurs in deep, blood deprived wounds with anaerobic bacteria that destroy tissues and release gas bubbles

47
Q

Does apoptosis cause inflammation?

A

Nope. Cells shrink, nucleus undergoes karyorrhexis and karyolysis - then consumed by phagocytes

48
Q

What are (4) non pathological causes of apoptosis?

A
  • programmed tissue remodeling
  • scheduled involution of tissues (thymus, post-lactating breast)
  • regulated cell turn over of proliferating cells (dermis)
  • programmed destruction of activation inflammatory cells (neutrophils) at the end of inflammation
49
Q

What are pathological causes of apoptosis?

A
  • radiation
  • toxins / viruses
  • autoimmunity
  • neuron loss (Alzheimer’s)
50
Q

Where does lipofuscin come from and what does it make?

A

From the accumulation of lipid products

Can make residual bodies

51
Q

What is lipid accumulation or fatty metamorphosis?

A

Accumulation of lipids in parenchymal cells, especially common in the liver

52
Q

What happens in the liver as a result of fatty metamorphosis?

A

Enlargement
Softening
Yellowing
Blunted margins

53
Q

What leads to fatty liver?

A
  • overloading the system with fatty acids

- failure to secrete lipoproteins

54
Q

When can the heart experience fatty metamorphosis?

A
  • chronic hypoxia, as in anemia

- profound hypoxia

55
Q

What is the tigered effect?

A

Alternating yellow fat and red muscle bands in heart muscle.

AKA thrust breast

56
Q

What is a xanthoma, and what causes it?

A

Cluster of lipids, often in macrophages, often in the dermis and tendons

Caused by hyperlipidemia

57
Q

What are foam cells and what disorders are they associated with?

A

Cells that have accumulated metabolites due to deficiency of specific lysosomal enzymes

Associated with lysosomal storage disorders

58
Q

What kind of disorder is Tay-Sachs disease, and what is it’s most common symptom?

A

A lysosomal storage disorder - hexosaminidase is deficient

Main symptom = macular cherry red spot (retina)

59
Q

What kind of disorder is Neimann-Pick disease, and what is it’s distinguishing symptom?

A

Lysosomal storage disorder - sphingomyelinase is deficient

Fovea cherry red spot

60
Q

What is deficient in Gaucher’s disease?

A

Glucocerebrosidase

61
Q

What are Russell bodies?

A

Accumulated immunoglobulins - part of a hyaline storage disorder because they stain pink

62
Q

What are Mallory bodies?

A

Alcoholic hyaline - accumulation of fibrils and ubiquitin in hepatocytes

63
Q

What are Lewy bodies?

A

Hyaline deposits in Parkinson’s

64
Q

Which diseases have neurofibrillary tangles of hyaline deposits?

A

Alzheimer’s

Huntington’s

65
Q

What are chaperonins?

A

Proteins that participate in protein folding in normal cells - minimizes injury

66
Q

What are ubiquitins?

A

Proteins that appear after injury to refold denatured proteins

67
Q

What is an amyloid?

A

Starch-like deposit of fibrils in organs or tissues

68
Q

What conditions are associated with AAP (amyloid associated proteins)?

A

Chronic inflammation: Chron’s or RA

Infections conditions: TB or leprosy

69
Q

Excess abnormal amyloids are associated with which degenerative condition?

A

Alzheimer’s

70
Q

What is deficient in von Gierke’s disease?

A

Glucose-6-phosphatase (type 1 glycogen storage disorder)

71
Q

What is Pompe’s disorder?

A

A type II glycogen storage disorder, affecting the heart, resulting from a defect in alpha glucosidase

72
Q

What is albinism?

A

Congenital lack of melanin

73
Q

What is vitiligo?

A

Patchy areas of skin depigmentation - acquired

74
Q

What is alkaptonuria?

A

Accumulation of homogenistic acid, giving urine a black color

75
Q

What is ochronosis?

A

Tissue discoloration resulting from accumulated homogenistic acid

76
Q

What is hemochromatosis?

A

Accumulation of iron, usually through excess absorption, that can cause organ damage

May cause crystal formation in joints

77
Q

What is the classic triad of manifestations of hemochromatosis?

A

Cirrhosis
Pancreatic fibrosis
Bronzed skin

78
Q

What is lipofuscin and where is it found?

A

Undigestible lipid derivatives - usually brown

Found in ear wax

79
Q

Plumbism is the absorption of what material? Where does it manifest in the body?

A

Lead.

Lead-sulfide line at gingival margin (gums)

Effects on CNS development in children

80
Q

What disease is related to the accumulation of copper? Where does it deposit in the body?

A

Wilson’s disease

Deposits in liver, basal ganglia, and eyes

81
Q

What are examples of extracellular calcifications?

A

Hematomas
Phleboliths
Tunica media of arteries
Uterine fibroids

82
Q

What is a lithopedion?

A

A stone child - a calcified unaborted fetus

83
Q

What is the Hayflick phenomenon?

A

Limitations in doubling:

The finite potential of a cell to duplicate - implication that all organisms are programmed to wear out and die.

84
Q

What is the standard expectation for fibroblast doubling in normal adults?

A

50

Pathology (4 decks)

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