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Pathology > Cellular Response To Stress > Flashcards

Cellular Response To Stress Flashcards

1
Q

Name the two patterns of reversible cell injury?

A
  1. Cellular swelling
  2. Fatty change
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2
Q

Fragmentation into nucleosome-sized fragments occurs in which type of cell death?

A

Apoptosis

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3
Q

The brain is special in that it undergoes what type of necrosis when ischemic ?

A

Liquefactive necrosis

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4
Q

What is the most common form of metaplasia ? What is its cause?

A

Squamous metaplasia specifically columnar to squamous metaplasia from cigarette smoking and vitamin A deficiency.

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5
Q

What do you call the mediators of the apoptotic pathway?

A

Caspases - a unique family of cysteine proteases. Caspases are also inactive form of zymogens.

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6
Q

What do you call the sand like lamellated calcifactions seen in papillary cancers?

A

Psammoma bodies

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7
Q

What finding is seen when there are multiple collections of triglycerides in lamina propia of the gallbladder?

A

Strawberry gallbladder

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8
Q

What is the only endogenous brown-black pigment?

A

Melanin

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9
Q

Increase in size of cells resulting in increased size of organ; cellular adaptation of non-dividing cells eg. Myocardial cells.

A

Hypertrophy

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10
Q

Increase in the number of cells?

A

Hyperplasia

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11
Q

Reduction in cell size and number resulting in decreased sizeof organ.

A

Atrophy

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12
Q

A reversible change wherein one differentiated cell type is is replaced by another cell type.

A

Metaplasia

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13
Q

55/M with long standing history of hypertension eventually expired from myocardial infarction. Autopsy shows increased thickness of the left ventricular wall with a large infarct. What is the cellular adaptation seen in this case?

A

Left ventricular hypertrophy; Pathologic Hypertrophy

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14
Q

47 G0 with adult granulosa cell tumor presented with menorrhagia. UTZ shows thickened endometrium. Patient underwent diagnostic curettage. Biopsy shows back to back endometrial glands with nuclear atypia. What is the diagnosis (for the endometrium), and what is the cellular adaptation seen in this case?

A

Atypical hyperplasia ( Endometrial Intraepithelial Neoplasia); Pathologic hyperplasia

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15
Q

35/ M with history of poliomyelitis presented with disproportionately thinner right lower extremities. Muscle biopsy shows decrease in size of skeletal myocytes. What is the cellular adaptation seen in this case?

A

Denervation atrophy; Pathologic atrophy

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16
Q

39/F with history of heart burn and water brash. Endoscopy shows multiple pinkish tan area at the GEJ. Biopsy shows fragments with simple columnar epithelium with goblet cells. What is the diagnosis, and what is the cellular adaptation seen in this case?

A

Barett esophagus; Intestinal Metaplasia

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17
Q

The first manifestation of almost all forms of injury to cells ; changes is due to influx of ions ( and consequently, water) due to failure of energy-dependent ion pumps ( Na,K, ATPase)

A

Cellular Swelling

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18
Q

Appearance of lipid vacuoles in the cytoplasm, often seen in cells participating in fat metabolism (liver, heart)

A

Steatosis

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19
Q

Type of cell death that results from a pathologic cell injury.

A

Necrosis

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20
Q

Type of cell death that is energy dependent , tightly regulated and associated with normal cellular functions; programmed cell death”.

A

Apoptosis

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21
Q

Components cells are dead but the basic tissue architecture is preserved ( acidophilic tombstone) often seen in ischemic injury to most solid organs ( heart, spleen, kidney) except the brain.

A

Coagulative necrosis

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22
Q

Digestion of dead cells resulting in transformation of the tissue into a viscous liquid mass; often seen in infections (pus) and in hypoxic death of cells within CNS.

A

Liquefactive necrosis

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23
Q

The term reserved for ischemic coagulative necrosis of the limbs (dry) , may have superimposed bacterial infection with liquefactive necrosis (wet).

A

Gangrenous necrosis

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24
Q

Cheese-like gross appearance of necrotic areas; often seen in tuberculous infections; tissue architecture is not preserved.

A

Caseous necrosis

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25
Q

Focal areas of fat destruction typically seen in acute pancreatitis , foci of necrosis contain shadowy outlines of necrotic fat cells with basophilic calcium deposists ( saponification) surrounded by an inflammatory reaction.

A

Enzymatic fat necrosis

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26
Q

What Pathway shows inactivation of anti-apoptotic BCL2 protein that leads to activation of BAX/ BAK channel, allowing cytochrome C to leak out of the mitochondria , activating apoptosis?

A

Intrinsic (mitochondrial) pathway

27
Q

Seen in immune reactions , involving blood vessels , deposits of immune complexes together with fibrin that have leaked out of vessels result in bright pink and amorphous appearance.

A

Fibrinoid necrosis

28
Q

Calcium deposits occurring in dead tissues in the absence of calcium metabolic derangements eg. Psamomma bodies in cancers with papillary architecture and meningioma.

A

Dystrophic calcification

29
Q

Calcium deposition in normal tissues occurring in the setting of hypercalcemia eg. Calcinosis.

A

Metastatic calcification

30
Q

Among the following, which is not an electron microscope finding of reversible cell injury?
a. Plasma membrane blebs
b. Myelin figures
c. Dilation of endoplasmic reticulum
d. Karyolysis

A

Karyolysis

31
Q

Nuclear shrinkage

A

Pyknosis

(na ipit - ipitnosis)

32
Q

Nuclear fragmentation

A

Karyorrhexis

(fRRRagmentation - kaRyoRRhexis)

33
Q

Dissolution of nucleus.

A

Karyolysis

Karyo (nucleus) lysis (dissolution)

34
Q

73 Male with ischemic stroke. What is the expected pattern of necrosis?

A

Liquefactive (brain - ischemic stroke)

35
Q

Patient with malignancy in the para-aortic nodes was given chemotherapeutic agents which cause marked regression in the size of the lesions.

36
Q

Which conditions shows scattered loss of individual cells with karyorrhexis and cell fragmentation but with intact tissue structure.

A

Apoptosis

No inflammation in apoptosis due to intact cell membrane structure.

37
Q

Elderly male complaining of difficulty in urination with DRE findings of prostate gland twice its normal size wherein TURP is done and microscopy revealed nodules of glands with intervening stroma.

A

Hyperplasia

38
Q

Biopsy showed hyperemic mucosa which showed columnar epithelium with goblet cells in the esophagus. What cell change describes this finding?

A

Metaplasia

Normal epithelial lining of esophagus is stratified squamous.

39
Q

Cell alteration that explains the decrease in the size of calf muscles after 6 weeks of immobilization?

40
Q

Examples of Metabolic alkalosis? (3)

A

Hyperaldosteronism
Vomiting
Thiazide & Loop Diuretics use

41
Q

Respiratory Alkalosis examples? (5)

A

Pneumonia
Pulmonary embolus
High altitude
Psychogenic
Salicylate intoxication

42
Q

Apoptosis results from the activation of what proteases?

43
Q

Are proteases that contains cysteine in their active site and cleave proteins after aspartic residues which activates apoptosis?

44
Q

Controls the release of pro-apoptotic proteins?

A

BCL2 Family

45
Q

Anti-apoptotic proteins from BCL-2 Family? (3)

A

BCL2
BCL-XL
MCL-1

( 2 XL si MC Lhoyd )

46
Q

Pro-apoptotic proteins in BCL2 Family? (2)

A

BAX and BAK

47
Q

Regulated apoptosis initiators, that can initiate apoptosis when upregulated and activated? (6)

A

BAD
BIM
BID
Puma
Noxa

( Puma eat BAD BI BImbab and Nauseated)

48
Q

Nuclear changes which shows basophilia of chromatin may fade?

A

Karyolysis

49
Q

H& E stains of necrotic tissue shows?

A

Increased eosinophilia

50
Q

Extrinsic / Death Receptor Initiated Pathway of Apoptosis is controlled by what receptors? (2)

A

TNFR1 and Fas (CD95)

51
Q

Free radicals (6)

A
  1. Superoxide anion (O2-)
  2. Hydrogen peroxide (H2O2)
  3. Hydroxyl radicals (OH)
  4. CCL3
  5. Peroxynitrite anion (ONOO-)
  6. NO2 and NO3
52
Q

Biochemical pathways involved in muscle hypertrophy? (2)

A
  1. Phospoinositide-3-kinase ( PI3K) / AKT Pathway: most important physiologic hypertrophy
  2. Signaling downstream G-protein coupled receptors: more important in pathologic hypertrophy.
53
Q

Most common cause of steatosis in the liver? (2)

A

Alcohol abuse and NAFLD

54
Q

Most common cause of steatosis in the liver? (2)

A

Alcohol abuse and NAFLD

55
Q

Exogenous pigments? (2)

A
  1. Carbon coal dust in anthracosis and coal worker’s pneumoconiosis.
  2. Tattoing : pigments inoculated are phagocytosed by dermal macrophages
56
Q

Exogenous pigments? (2)

A
  1. Carbon coal dust in anthracosis and coal worker’s pneumoconiosis.
  2. Tattoing : pigments inoculated are phagocytosed by dermal macrophages
57
Q

Endogenous pigments (3)

A
  1. Melanin
  2. Lipofuschin / Lipochrome/ Wear-and-tear pigment
  3. Hemosiderin
58
Q

Syndrome which shows premature aging, and the defective gene is a DNA Helicase.

A

Werner Syndrome

59
Q

Syndromes caused by mutated genes that encodes proteins involved in repairing double strand breaks in DNA. (2)

A
  1. Bloom syndrome
  2. Ataxia-telangiectasia
60
Q

Involves progressive shortening of telomeres which ultimately results in cell cycle arrest.

A

Cellular Senescence

61
Q

Process where eating less increases longevity by caloric restriction attenuation of IGF-1 signaling leads to lower rates of cell growth and metabolism and possible reduced cellular damage.

A

Dysregulated Nutrient Sensing

62
Q

Diet which increase sirtuins which promote the expression of several genes whose products inhibit metabolic activity, reduce apoptosis, stimulate protein folding and counteract harmful effects of oxygen free radicals, thereby increasing longevity.

A

Caloric restriction diet

63
Q

Drink that activates sirtuins and thus increase lifespan.

Pathology (23 decks)

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