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Unused archive Spring 2014 > Pathology: Test 1: 04-05 Cellular and Tissue Accumulations I II > Flashcards

Pathology: Test 1: 04-05 Cellular and Tissue Accumulations I II Flashcards

1
Q
  1. What are cellular adaptations and what causes them? <br></br>Give 4 kinds of cellular adaptation and briefly describe what each one does
A

a. Cellular adaptations are reversible functional/structural responses to sever physiological stress/pathological stimuli
<br></br>i. Hypertrophy: increase in size/functional activity of cell
<br></br>ii. hyperplasia: increase in # of cells
<br></br>iii. atrophy: decrease in size/metabolic activity of cells
<br></br>iv. metaplasia: change in cell phenotype

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2
Q
  1. When does cell injury occur? What are the stages of progressive impairment of the cell?
A

When limits of adaptive response to stimulus are exceeded
<br></br>Adaptation, reversible injury, and cell death represent stages of progressive impairment of cell’s normal function/structure

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3
Q
  1. What are the two patterns of cell death and how are they different from each other? Give an example of each
A

Necrosis: cell death after abnormal stresses (i.e. ischemia/chemical injury), always pathological
<br></br>Apoptosis: cell death occurring because of internally controlled suicide pattern (i.e. embryogenesis; withdrawal of hormones.

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4
Q
  1. What kind of cell process does nutrient deprivation trigger?
A

Autophagy (self-eating)

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5
Q
  1. What may cause subcellular alterations in a cell?
A

Cells exposed to sublethal or chronic stimuli.

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6
Q
  1. What are intracellular accumulations due to?
A

Metabolic derangements.

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7
Q
  1. Give and briefly describe two forms of metabolic (subcellular alterations) accumulations/deposits
A

(Intracellular accumulations due to metabolic derangements, depositing of i.e. proteins, lipids, carbohydrates)
<br></br>Pathological calcification: Ca deposits at site of cell death
<br></br>Cell aging: cells show morphological and functional changes

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8
Q
  1. What are physiological adaptations?
A

Responses to normal stimulation by hormones or endogenous chemical mediators (breast, lactation)

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9
Q
  1. How is pathological adaptations different/same than physiological adaptations?
A

Pathological adaptations share the same underlying mechanism, but they allow modulation of environment and ideally escape injury.

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10
Q
  1. What happens to cells in hypertrophy? Is it physiologic or pathologic? Caused by? Can occur in conjunction with? Most common stimulus for hypertrophy is?
A

<br></br>No new cells, just BIGGER cells, happens in non-dividing cells
<br></br>Can be both
<br></br>Caused by increased functional demand or specific hormone
<br></br>Can occur alone or with hyperplasia (increased # cells), if cells are able to divide
<br></br>Most common stimulus is increased workload

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11
Q
  1. What causes the physiological enlargement of the uterus?
A

Both hypertrophy of existing smooth muscle cells and hyperplasia of smooth muscle

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12
Q
  1. Give two examples of pathological hypertrophy occurring in the heart

What enlarges? When does it happen?

A

Cardiac enlargement that occurs with hypertension or aortic valve disease

Enlargement of individual cardiac fibers following an myocardial infarction (MI, heart attack) with death of surrounding myocytes (makes up for dead cells)

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13
Q
  1. How do striated muscle cells divide in the heart and skeletal muscle? Undergo what cellular adaption?
A

Cannot divide and make more cells, thus only hypertrophy

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14
Q
  1. What hypertrophies in the heart?

<br></br> when does this happen after?

A

Enlargement of individual cardiac fibers following an myocardial infarction (MI, heart attack) with death of surrounding myocytes

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15
Q
  1. In chronic cardiac overload, what genes are expressed? What does contractile proteins switch to?
A

Genes normally in neonatal heart reactivate <br></br>

Contractile proteins switch to fetal isoforms (contract slower)

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16
Q
  1. What is hyperplasia and what it result in? What does its occurrence depend on?
A

Hyperplasia: Increase in # of cells, leads to increased organ size and weight.<br></br>
Occurs if cell synthesize/mitosis

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17
Q
  1. What are the two kinds of physiologic hyperplasia?
A 
Hormonal hyperplasia (increase function) e.g. lactating breast, pregnant uterus<br>
Compensatory hyperplasia e.g. liver grows to make up for lost cells
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18
Q
  1. Pathologic hyperplasia usually results from?
A

Excessive hormones/growth factors

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19
Q
  1. Describe the pathological hyperplasia’s role in menstruation
A

Imbalance between estrogen and progesterone endometrial hyperplasia can occur (abnormal menstrual bleeding)

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20
Q
  1. What induces benign prostatic hyperplasia?
A

Androgens

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21
Q
  1. How are hormonal/growth factor stimulation and cancer different?
A

When hormonal/growth factor ceases, then stimulation ceases.<br></br>
In cancer however, cells continue to grow.

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22
Q
  1. What is responsible for hyperplasia’s healing ability? Give an example
A

Growth factors stimulated by viral infections, warts/papillomaviruses, etc.

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23
Q
  1. What are two stimuli for hyperplasia?
A

Increased growth factor, increased new cells from tissue stem cells

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24
Q
  1. Is atrophy physiological or pathological? Give an example
A

Both, physiological (embryonic structures) or pathological (atherosclerotic brain atrophy)

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25
Q
  1. Give 6 causes of atrophy
A

i. decreased workload<br></br>
ii. loss of innervation<br></br>
iii. decreased blood supply (senile atrophy)<br></br>
iv. inadequate nutrition<br></br>
v. loss of endocrine stimulation<br></br>
vi. pressure

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26
Q
  1. What does the decrease in cell size and organelles in atrophy reduce? Why?
A

Metabolic needs; permit survival

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27
Q
  1. The structural components of the cell reduced in number are because of what two reasos?

The structural components of the cell, are reduced in number due to?

A

Due to decreased protein synthesis<br></br> increase protein degradation

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28
Q
  1. What are autophagic vacuoles?
A

Accompanies atrophy and are fused lysosomes and intracellular organelles

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29
Q
  1. What happens to cell debris that resist digestion?
A

May persist as membrane-bound residual bodies (i.e. lipofuscin)

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30
Q
  1. What is metaplasia and why does it occur?
A

Reversible change in cell type to another. Cells stressed are replaced by cells types better able to withstand (columnar -> squamous, as in resp. tract)

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31
Q
  1. Metaplasia arises by?
A

Genetic reprogramming of epithelial stem cells or undifferentiated mesenchymal cells

32
Q
  1. Most common epithelial metaplasia?
A

Columnar -> squamous e.g. resp. tract of trachea and bronchi

33
Q
  1. In the epithelial metaplasia of the respiratory tract, what happens as an negative side effect?
A

Important protective mechanisms are lost e.g. mucus secretion and cilliary clearance

34
Q
  1. If metaplasia is persistent, what may occur?
A

metaplastic transformation may induce cancer transformation in the metaplastic epithelium

35
Q
  1. Metaplasia in CT causes the formation of what that is usually not found here? Example?
A

Cartilage, bone, or adipose tissue (mesenchymal tissues)

e.g. myositis ossificans

36
Q
  1. Subcellular responses to injury are associated with alterations only to?
A

Subcellular organelles and cytosolic proteins

37
Q
  1. What lysosomes are involved in lysosomal catabolism?
A

Primary lysosomes fuse with membrane bound vacuoles containing material for digestion to form secondary lysosomes or phagolysosomes

38
Q
  1. Secondary lysosomes/phagolysosomes are involved in?
A

Breakdown of ingested material in heterophagy or autophagy

39
Q
  1. Define heterophagy, phagocytosis, and pinocytosis
A

Heterophagy: external materials taken up<br></br>
Phagocytosis: take up of larger materials<br></br>
Pinocytosis: uptake of smaller soluble material
<br></br>

40
Q
  1. How are endocytosed vacuoles degraded?
A

Comine with lysosomes, insides degraded

41
Q
  1. Metabolism of cholesterol and cholesterol esters are tightly regulated for synthesis of cell membrane. Give intracellular accumulation in 3 different processes with specific example for 2 out of 3 of these
A 
Atherosclerosis
<br>
Xanthomas (acquired &amp; hereditary hyperlipidemic states)
<br>
Cholesterolosis (gallbladder)
42
Q
  1. What are mallory bodies composed of? Histologically stains? Give an example of where mallory bodies are found
A

Eosinophilic intracytoplasmic inclusions composed of cytoskeletal filaments in damaged liver cells

43
Q
  1. What are 3 categories of substances that can be intracellular accumulated?
A

Excessive cell parts <br></br>
Abnormal substances<br></br>
Pigments

44
Q
  1. What are four general mechanisms cells get abnormal intracellular accumulations?
A

i. abnormal metabolism <br></br>
<br></br>ii. alterations in protein folding and transport
<br></br>iii. deficiency of critical enzymes
<br></br>iv. inability to degrade phagocytosed particles

45
Q
  1. What classes of lipids can be accumulated?
A

All major classes, triglycerides, cholesterol, cholesterol esters, and phospholipids

46
Q
  1. What is the term for fatty change and what does it refer to? Is it reversible itself? Often seen? Causes?
A

Steatosis
<br></br>Any abnormal accumulation of triglycerides within parenchymal cells
<br></br>Reversible
<br></br>Seen around necrotic cells or liver
<br></br>Causes: toxins, protein malnutrition, diabetes mellitus, obesity, and anoxia. Though alcohol and diabetes most common in industrialized nations

47
Q
  1. What is the significance of fatty change?
A 
Mild = no impairment of cellular function<br>
Sever= impair cellular function and cell death
48
Q
  1. What does CCl4 and protein malnutrition do?
    Anoxia?<br></br>
    Starvation?<br></br>
A

i. Decrease synthesis of protein<br></br>
ii. Decreased fatty acid oxidation<br></br>
iii. Increased fatty acid mobilization from stores

49
Q
  1. Fatty accumulation appears as what in parenchymal cells? What happens if there is a lot of fat?
A

Clear vacuoles <br></br>

Organ enlarges and yellowed

50
Q
  1. What are five ways phagocytic cells become overloaded with lipid?
A

i. Atherosclerosis<br></br>
ii. Hyperlipidemic syndromes<br></br>
iii. Inflammation and necrosis<br></br>
iv. Gallbladder as in cholesterolosis <br></br>
v. Niemann-Pick disease

51
Q
  1. In atherosclerosis, what cells are in plaques, where, and what are they filled with? Appearance? What happens when these rupture?
A

Smooth cells and macrophages in intimal layer<br></br>
Filled with lipid vacuoles of cholesterol and cholesterol esters <br></br>
Foam cells with yellowy appearance <br></br>
Lipids released then cholesterol esters crystallize into cholesterol clefts

52
Q
  1. Where does hyperlipidemic syndrome occur? What forms?
A 
Foamy macrophages in subepithelial tissues in CT<br>
Forms xanthomas (foam masses)
53
Q
  1. What type of disease is Niemann-Pick disease? What happens in Niemann-Pick disease?
A

Type C (lysosomal storage disease), cholesterol accumulation

54
Q
  1. How do protein accumulations appear?
A

Pink, hyaline droplets, vacuoles, cytoplasmic aggregates

55
Q
  1. Give two examples of protein accumulation
A

i. Resorption droplets in renal disease<br></br>

ii. Synthesis of excess protein such in plasma cells synthesizing immunoglobulins (in eosinophilic Russell bodies)

56
Q
  1. What cell injuries accumulate intracellular proteins?
A

Alcohol disease may cause mallory body or alcohol hyaline (eosinophilic)

57
Q
  1. What proteins in cells are vulnerable to form aggregates/entanglements?
A

Partially folder chains (intermediates)

58
Q
  1. What stabilizes partially folded chains? When are they produced? What other process do chaperones do? Give a heat-shock protein and its role?
A

i. Chaperones <br></br>
ii. Constitutively or by stress<br></br>
iii. Facilitation of chaperones successfully folder proteins are degraded<br></br>
iv. Ubiquitin, marks abnormal protein for degradation by proteasome

59
Q
  1. What are three mechanisms of protein folding defects that cause intracellular accumulations?
A

i. Defective intracellular transport<br></br>
ii. ER stress from unfolded/misfolded proteins <br></br>
iii. Abnormal protein aggregation<br></br>

60
Q
  1. Give an example of defective intracellular transport and secretion of critical protein
A

α1-antitrypsin deficiency = buildup of partially folded <br></br>intermediates which aggregate and can’t be secreted -> deficiency of enzyme (emphysema)

61
Q
  1. What do unfolded protein response cause?
A

i. Decreased unfolded proteins though an<br></br>

ii. Increase in chaperones and slowdown of protein translation

62
Q
  1. What enzyme is concurrently activated and lead to cell death?
A

Carpases

63
Q
  1. Give four diseases that are associated with aggregation of abnormally folded proteins?
A

Alzheimer’s, Huntington’s, Parkinsons, maybe type II diabetes

64
Q
  1. What are disorders of aggregation of abnormal proteins that interfere with normal tissue function called? Example?
A

Proteinopathies/protein-aggregation disease, i.e. amyloidosis

65
Q
  1. Excessive intracellular deposits can be seen in what disorders/cells? (give 5)
A

i. Diabetes mellitus<br></br>
ii. Renal tubular epithelium<br></br>
iii. Cardiac myocytes <br></br>
iv. β cells of the islets of Langerhans<br></br>
v. glycogen storage diseases
<br></br>

66
Q
  1. What is the most common exogenous pigment? How is it processed in body? What is it called when heavily accumulated? Give two examples
A

Carbon<br></br>
Inhaled, phagocytosed, transported to tracheobronchial lymph nodes<br></br>
Anthracosis<br></br>
Emphysema and coal worker’s pneumoconiosis

67
Q
  1. a. Give an endogenous pigment and describe its appearance.
    <br></br>b. What is it a marker for?
    <br></br>c. What does it consist of and what is this derived from?
    <br></br>d. Seen most often in what kind of patients?
A

<br></br>a) Lipofuscin (lipochrome) aka wear/tear pigment. Appears yellow-brown intracytoplasmic granules microscopically.
<br></br>b) Marker for past free radical injury
<br></br>c) Consist of lipid-protein complexes derived from free radical catalyzed peroxidation of polyunsaturated lipids of subcellular membranes
<br></br>d) Most often seen in aging patients or ones with malnutrition/cancer cachexia

68
Q
  1. a. What kind of pigment is melanin?
    <br></br>b. What is it derived/formed from?
    <br></br>c. What is unique about melanin?
    <br></br>d. Protects against what and accumulates where?
A

<br></br>a. Endogenous
<br></br>b. non-Hb derived pigment formed from tyrosinase catalyzing oxidation of tyrosine to dihydroxyphenylalanine.
<br></br>c. Only normal endogenous brown-black pigment
<br></br>d. UV radiation and can accumulate in basal keratinocytes in skin or dermal macrophages

69
Q
  1. a. Hemosiderin is an endogenous pigment derived from?
    <br></br>b. Appearance?
    <br></br>c. Occurs when?
    <br></br>d. Hemosiderin pigments are aggregates of?
    <br></br>e. ID with?
A

<br></br>a) yellow-to-brown granular pigment
<br></br>b) Occurs when excess of iron, ferritin forms hemosiderin granules
<br></br>c) Hemosiderin pigment represent aggregates of ferritin micelles
<br></br>d) ID’ed with Prussian blue iron stain

70
Q
  1. a. Local hemosiderin can result from?

<br></br>b. What do macrophages produce when they take up Hb?

A

a. Hb-derived golden, yellow-to-brown granular pigment

<br></br>b. lysosomal enzymes convert Hb and convert to hemosiderin, a ferritin containing pigment

71
Q
  1. When does hemosiderosis occur?
A

i. systemic overload of iron occurs in setting of increased absorption of dietary iron
<br></br>ii. impaired use of iron
<br></br>iii. hemolytic anemias (excess RBC breakdown)
<br></br>iv. Transfusions (increase exogenous load of iron)

72
Q
  1. a. What is progressive accumulation also known as and what does it injure?
    <br></br>b. What else can occur and what can it injure?
A

<br></br>. Hemochromatosis can injure liver, pancreas, heart, and endocrine organs
<br></br>b. Liver fibrosis, heart failure, diabetes mellitus

73
Q
  1. a. Bilirubin is the major pigment found in?
    <br></br>b. What is jaundice caused by?
    <br></br>c. Bilirubin is derived from? Without what element?
A

a. bile<br></br>
b. excess bilirubin pigment<br></br>
c. Hb-derived, contains no iron <br></br>

74
Q
  1. a. What is pathologic calcification?
    <br></br>b. What does it contain?
    <br></br>c. Two main types?
A

a. Abnormal deposition of Ca salts <br></br>
b. Calcium salts with smaller amounts of iron, magnesium, and other mineral salts<br></br>
c. Dystrophic and metastatic <br></br>

75
Q
  1. Dystrophic calcification is seen in?
    <br></br>Commonly seen on?
    <br></br>Grossly appears?
    <br></br>Histologically calcium salts appear?
A

a. Areas of injury & necrosis, atheromas of atherosclerosis<br></br>
b. Damaged heart valves<br></br>
c. Fine, white granules/clumps<br></br>
d. Basophilic (blue/purple)

76
Q
  1. Metastatic calcification occurs when? <br></br>
    What are the four main causes of hypercalcemia?<br></br>
    Primarily affects?<br></br>
    What organ dysfunction is caused by metastatic calcification?
A

a. Normal tissues with hypercalcemia <br></br>
b. Four main causes:<br></br>
i. Increased secretion of PTH<br></br>
ii. Destruction of bone<br></br>
iii. Vitamin D disorders<br></br>
iv. Renal failure<br></br>
c. Primarily affects interstitial tissues of the gastric mucosa, kidneys, lungs, systemic arteries, and pulmonary veins <br></br>
d. Usually none, occasionally lung and renal

Unused archive Spring 2014 (1 decks)

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