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Pathoma > Ch 1 - Growth Adaptations, Cell Injury, Cell Death > Flashcards

Ch 1 - Growth Adaptations, Cell Injury, Cell Death Flashcards

1
Q

Permanent cells: hyperplasia or hypertrophy

A

HYPERTROPHY ONLY - cardiac muscle, skeletal muscle and nerve cannot make new cells

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2
Q

Example of hyperplasia that does NOT progress to DYSPLASIA and eventual CA

A

BPH

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3
Q

Ubiquitin-proteosome degradation

A

Decreases the cell SIZE; intermediate filaments of the cytoskeleton are tagged with ubiquitin and destroyed by proteosomes

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4
Q

Is METAPLASIA reversible? If so, how?

A

Metaplasia is REVERSIBLE with removal of the driving stessor

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5
Q

Example of METAPLASIA that does NOT progress to DYSPLASIA and eventual CA

A

Apocrine metaplasia of the breast

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6
Q

Vitamin deficiency that results in metaplasia

A

Vitamin A deficiency- KERATOMALACIA -THIN SQUAMOUS lining of the conjunctive undergoes metaplasia into STRATIFIED KERATINIZING SQUAMOUS epithelium

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7
Q

Barrett Esophagus cell change

A

NONKERATINIZED SQUAMOUS –> NON-CILIATED MUCINOUS COLUMNAR

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8
Q

Example of METAPLASIA in mesenchymal (connective) tissues

A

MYOSITIS OSSIFICANS - muscle tissue changes to bone during healing after trauma

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9
Q

DYSPLASIA and CARCINOMA - reversible or irreversible?

A

DYSPLASIA is REVERSIBLE but if stress persists it progresses to CARCINOMA which is IRREVERSIBLE

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10
Q

Aplasia

A

FAILURE of cell production during embryogenesis - Ex: unilateral renal agenesis

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11
Q

Hypoplasia

A

DECREASE in cell production during embryogenesis resulting in relatively small organ - Ex: streak ovary in Turner syndrome

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12
Q

Acute Myeloid Leukemia (AML) Pathophys

A

t(15, 17) involving retinoic acid receptor (vit A receptor) –> cells remain in blast state –> accumulation/AML

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13
Q

Budd-Chiari Syndrome Pathophys

A

Thrombosis of hepatic vein –> decrease of fresh blood to liver –> decreased O2 (ischemia)

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14
Q

MC cause of Budd-Chiari

A

Polycythemia Vera - increased # of RBCs –> increases viscosity of blood

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15
Q

PaO2 and SaO2 in Anemia

A

PaO2 and SaO2 both NORMAL

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16
Q

Carbon Monoxide Poisoning Pathophys; PaO2 and SaO2 levels

A

CO binds Hgb ~100x more avidly than O2; PaO2 is NORMAL, SaO2 is DECREASED

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17
Q

Common sources of Carbon Monoxide

A

Smoke from fires and exhaust from cars or GAS HEATERS

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18
Q

Early sign of exposure to Carbon Monoxide

A

HEADACHE

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19
Q

Hallmark of REVERSIBLE injury

A

CELLULAR SWELLING –> loss of microvilli, membrane blebbing, swelling of the rER causing dissociation of ribosomes and decreased protein synthesis

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20
Q

HYPOXIA –> Cell damage

A

Hypoxia impairs oxidative phosphorylation resulting in decreased ATP; Low ATP disrupts: 1) Na-K pump –> Na & H2O buildup in cell (swelling); 2) Ca2+ pump –> Ca2+buildup in cytosol –> activates enzymes; 3) Switch to anaerobic glycolysis –> lactic acid buildup –> low pH denatures proteins and precipitates DNA

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21
Q

Hallmark of IRREVERSIBLE injury

A

MEMBRANE damage - plasma membrane, mitochondrial membrane, and lysosome membrane

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22
Q

Irreversible injury post-MI

A

Plasma membrane damage –> cardiac troponin leaking into the serum

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23
Q

Specific location of e- transport chain

A

INNER MITOCHONDRIAL MEMBRANE

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24
Q

Irreversible injury –> apoptosis activation

A

Mitochondrial membrane damage –> CYTOCHROME C leaks into cytosol –> activates CASPASES

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25
Q

Morphologic hallmark of CELL DEATH

A

Loss of the nucleus - pyknosis, karyorrhexis, & karyolysis

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26
Q

Pyknosis

A

Nuclear condensation

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27
Q

Karyorrhexis

A

Nuclear fragmentation

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28
Q

Karyolysis

A

Nuclear dissolution

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29
Q

Necrosis involving firm, wedge-shaped and pale necrotic tissue with cell shape and organ structure preservation

A

COAGULATIVE necrosis; wedge-shaped necrosis points to occulsion site

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30
Q

Liquefactive necrosis in brain infarction

A

Proteolytic enzymes from MICROGLIAL CELLS

31
Q

Liquefactive necrosis in abscess

A

Proteolytic enzymes from NEUTROPHILS

32
Q

Liquefactive necrosis in pancreatitis

A

Proteolytic enzymes from PANCREAS liquefy PARENCHYMA

33
Q

Necrosis in PANCREATITIS

A

LIQUEFACTIVE (parenchyma) and FAT NECROSIS

34
Q

Ischemia of lower limb is classic presentation of which type of necrosis?

A

GANGRENOUS necrosis

35
Q

Examples of CASEOUS necrosis

A

TB and fungal infections

36
Q

FAT Necrosis Pathophys and Appearance

A

Necrotic adipose tissue with chalky-white appearance due to deposition of Ca2+ joining with fatty acids (SAPONIFICATION)

37
Q

2 examples of FAT Necrosis

A

Trauma to fat (ex: breast) and pancreatitis

38
Q

DYSTROPHIC Calcification

A

Necrotic tissue acts as a nidus for calcification in setting of NORMAL serum Ca and phosphate (Ex: saponification in fat necrosis)

39
Q

METASTATIC calcification

A

HIGH serum Ca or phosphate levels lead to Ca deposition in normal tissues

40
Q

Necrotic damage to BLOOD VESEEL WALL

A

FIBRINOID necrosis - leaking of proteins (including fibrin) into vessel –> bright pink staining of wall

41
Q

FIBRINOID necrosis is characteristic of:

A

Malignant HTN and Vasculitis

42
Q

Apoptosis Morphology (“falling of leaves”)

A

Dying cell shrinks –> cytoplasm becomes more eosinophilic; Nucleus condenses (pyknosis) and fragments (karryorhexis); APOPTOTIC BODIES fall from cell and are REMOVED BY MACROPHAGES; NOT followed by inflammation

43
Q

What mediates Apoptosis?

A

Mediated by CASPASES which activate proteases (cytoskeleton breakdown) and endonucleases (DNA breakdown)

44
Q

INTRINSIC Mitochondrial Pathway Activation of Apoptosis

A

Cell injury, DNA damage or loss of homronal stimulation –> INACTIVATION OF BCL-2 –> CYTOCHROME C LEAKS into cytoplasm –> ACTIVATES CASPASES

45
Q

When would a 30yo female present with MALIGNANT HYPERTENSION?

A

PRE-ECLAMPSIA - presents in 3rd trimester with PROTEINURIA and INCREASED BP; FIBRINOID NECROSIS of placental blood vessels

46
Q

EXTRINSIC Recptor-ligand pathway activation of apoptosis

A

FAS ligand binds FAS death receptor (CD95) on the target cell –> activates caspases

47
Q

NEGATIVE Selection of thymocytes in thymus would activate apoptosis via which pathway?

A

EXTRINSIC receptor-ligand pathway (FAS ligand)

48
Q

CYTOTOXIC CD8+ T-cell mediated pathway activation of apoptosis

A

CD8+ T cell secretes PERFORINS to create pores in membrane of target cell; GRANZYME from CD8+ T cell then enters pores and activates caspases

49
Q

Most DAMAGING FREE RADICAL

A

*OH radical

50
Q

Free radical(s) generated with IONIZING RADIATION

A

*OH radical

51
Q

Free radical(s) generated with INFLAMMATION

A

*O2 (superoxide) - generated by NADPH oxidase during oxygen-dependent killing by neutrophils

52
Q

Enzyme that mediates O2 –> *O2 (superoxide)

A

NADPH oxidase

53
Q

Free radical(s) generated with excess METALS (Cu & Fe)

A

*OH radical via Fenton reaction

54
Q

Underlying mechanism of tissue damage in Wilson’s disease and Hemochromatosis

A

Tissue damage from *OH radical generated from excess metals

55
Q

Antioxidants used to eliminate free radicals

A

Glutathione and Vitamins A, C, E

56
Q

Superoxide dismutase

A

Eliminates *O2 by converting it to H2O2

57
Q

Glutathione peroxidase

A

Primary method of *OH radical

58
Q

Catalase

A

Eliminates H2O2 by converting it to O2 and H2O

59
Q

Cell injury resulting from CCl4

A

Converted to CCl3 free radical by P450 system of hepatocytes –> swelling of rER –> ribosomes detach –> lack of protein synthesis –> decreased apolipoproteins –> FATTY CHANGE IN LIVER

60
Q

REPERFUSION injury

A

Return of blood to ischemic tissue –> production of O2 derived free radicals –> further tissue damage

61
Q

Why do cardiac enzymes continue to rise after reperfusion of infarcted myocardial tissue?

A

O2 derived free radicals produced by return of blood to ischemic tissue cause more damage to damaged tissue and continued release of cardiace enzymes

62
Q

PRIMARY AMYLOIDOSIS

A

Plasma cell dyscrasias (ex: multiple myeloma) –> overproduction of Ig light chain –> SYSTEMIC deposition of AL amyloid

63
Q

SECONDARY AMYLOIDOSIS

A

Chronic inflammatory states, malignancy, Familial Mediterranean Fever –> increased serum amyloid-associated protein (SAA) –> SYSTEMIC deposition of AA amlyoid

64
Q

Examples of conditions that may produce SECONDARY AMYLOIDOSIS

A

Chronic inflammatory states - Crohn’s, UC, chronic osteomyelitis, Autoimmune including SLE or RA

65
Q

Familial Mediterranean Fever (FMF)

A

Presents with episodes of FEVER and acute SEROSAL INFLAMM - can mimic appendicits, arthritis, or MI - high SAA deposits –> secondary amyloidosis (AA amyloid)

66
Q

MC organ involved with SYSTEMIC AMYLOIDOSIS

A

KIDNEY - Nephrotic syndrome

67
Q

SENILE CARDIAC AMYLOIDOSIS

A

LOCALIZED amyloidosis; NON-MUTATED SERUM TRANSTHYRETIN deposits in the heart; usually ASYMPTOMATIC, >80yo

68
Q

FAMILIAL AMYLOID CARDIOMYOPATHY

A

LOCALIZED amyloidosis; MUTATED SERUM TRANSTHYRETIN deposits –> restrictive cardiomyopathy –> heart failure

69
Q

Amyloid deposits in Type II Diabetes

A

AMYLIN in ISLETS of pancreas; amylin is derived from insulin

70
Q

Amyloid deposits in ALZHEIMER DISEASE

A

A_ amyloid –> amyloid plaques in brain

71
Q

Alzhemier Disease and Down Syndrome association

A

A_ amyloid derived from _-amyloid precursor protein whose gene is on chromosome 21; pts with Down syndrome (trisomy 21) develop Alzheimer by age of 40

72
Q

DIALYSIS-associated AMYLOIDOSIS

A

_2-MICROGLOBULIN deposits in JOINTS; _2M is structural component that helps expression of MHC Class I molecules on surface of cells and dialysis pts cannot filter _2M well from blood

73
Q

Amyloid deposits in MEDULLARY CARCINOMA of the THYROID

A

CALCITONIN deposits within the tumor (TUMOR CELLS IN AMYLOID BACKGROUND); calcitonin is produced by C-cells

Pathoma (3 decks)

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