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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
Morphologic hallmark of CELL DEATH
Loss of the nucleus - pyknosis, karyorrhexis, & karyolysis
26
Pyknosis
Nuclear condensation
27
Karyorrhexis
Nuclear fragmentation
28
Karyolysis
Nuclear dissolution
29
Necrosis involving firm, wedge-shaped and pale necrotic tissue with cell shape and organ structure preservation
COAGULATIVE necrosis; wedge-shaped necrosis points to occulsion site
30
Liquefactive necrosis in brain infarction
Proteolytic enzymes from MICROGLIAL CELLS
31
Liquefactive necrosis in abscess
Proteolytic enzymes from NEUTROPHILS
32
Liquefactive necrosis in pancreatitis
Proteolytic enzymes from PANCREAS liquefy PARENCHYMA
33
Necrosis in PANCREATITIS
LIQUEFACTIVE (parenchyma) and FAT NECROSIS
34
Ischemia of lower limb is classic presentation of which type of necrosis?
GANGRENOUS necrosis
35
Examples of CASEOUS necrosis
TB and fungal infections
36
FAT Necrosis Pathophys and Appearance
Necrotic adipose tissue with chalky-white appearance due to deposition of Ca2+ joining with fatty acids (SAPONIFICATION)
37
2 examples of FAT Necrosis
Trauma to fat (ex: breast) and pancreatitis
38
DYSTROPHIC Calcification
Necrotic tissue acts as a nidus for calcification in setting of NORMAL serum Ca and phosphate (Ex: saponification in fat necrosis)
39
METASTATIC calcification
HIGH serum Ca or phosphate levels lead to Ca deposition in normal tissues
40
Necrotic damage to BLOOD VESEEL WALL
FIBRINOID necrosis - leaking of proteins (including fibrin) into vessel --> bright pink staining of wall
41
FIBRINOID necrosis is characteristic of:
Malignant HTN and Vasculitis
42
Apoptosis Morphology ("falling of leaves")
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
What mediates Apoptosis?
Mediated by CASPASES which activate proteases (cytoskeleton breakdown) and endonucleases (DNA breakdown)
44
INTRINSIC Mitochondrial Pathway Activation of Apoptosis
Cell injury, DNA damage or loss of homronal stimulation --> INACTIVATION OF BCL-2 --> CYTOCHROME C LEAKS into cytoplasm --> ACTIVATES CASPASES
45
When would a 30yo female present with MALIGNANT HYPERTENSION?
PRE-ECLAMPSIA - presents in 3rd trimester with PROTEINURIA and INCREASED BP; FIBRINOID NECROSIS of placental blood vessels
46
EXTRINSIC Recptor-ligand pathway activation of apoptosis
FAS ligand binds FAS death receptor (CD95) on the target cell --> activates caspases
47
NEGATIVE Selection of thymocytes in thymus would activate apoptosis via which pathway?
EXTRINSIC receptor-ligand pathway (FAS ligand)
48
CYTOTOXIC CD8+ T-cell mediated pathway activation of apoptosis
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
Most DAMAGING FREE RADICAL
*OH radical
50
Free radical(s) generated with IONIZING RADIATION
*OH radical
51
Free radical(s) generated with INFLAMMATION
*O2 (superoxide) - generated by NADPH oxidase during oxygen-dependent killing by neutrophils
52
Enzyme that mediates O2 --> *O2 (superoxide)
NADPH oxidase
53
Free radical(s) generated with excess METALS (Cu & Fe)
*OH radical via Fenton reaction
54
Underlying mechanism of tissue damage in Wilson's disease and Hemochromatosis
Tissue damage from *OH radical generated from excess metals
55
Antioxidants used to eliminate free radicals
Glutathione and Vitamins A, C, E
56
Superoxide dismutase
Eliminates *O2 by converting it to H2O2
57
Glutathione peroxidase
Primary method of *OH radical
58
Catalase
Eliminates H2O2 by converting it to O2 and H2O
59
Cell injury resulting from CCl4
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
REPERFUSION injury
Return of blood to ischemic tissue --> production of O2 derived free radicals --> further tissue damage
61
Why do cardiac enzymes continue to rise after reperfusion of infarcted myocardial tissue?
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
PRIMARY AMYLOIDOSIS
Plasma cell dyscrasias (ex: multiple myeloma) --> overproduction of Ig light chain --> SYSTEMIC deposition of AL amyloid
63
SECONDARY AMYLOIDOSIS
Chronic inflammatory states, malignancy, Familial Mediterranean Fever --> increased serum amyloid-associated protein (SAA) --> SYSTEMIC deposition of AA amlyoid
64
Examples of conditions that may produce SECONDARY AMYLOIDOSIS
Chronic inflammatory states - Crohn's, UC, chronic osteomyelitis, Autoimmune including SLE or RA
65
Familial Mediterranean Fever (FMF)
Presents with episodes of FEVER and acute SEROSAL INFLAMM - can mimic appendicits, arthritis, or MI - high SAA deposits --> secondary amyloidosis (AA amyloid)
66
MC organ involved with SYSTEMIC AMYLOIDOSIS
KIDNEY - Nephrotic syndrome
67
SENILE CARDIAC AMYLOIDOSIS
LOCALIZED amyloidosis; NON-MUTATED SERUM TRANSTHYRETIN deposits in the heart; usually ASYMPTOMATIC, >80yo
68
FAMILIAL AMYLOID CARDIOMYOPATHY
LOCALIZED amyloidosis; MUTATED SERUM TRANSTHYRETIN deposits --> restrictive cardiomyopathy --> heart failure
69
Amyloid deposits in Type II Diabetes
AMYLIN in ISLETS of pancreas; amylin is derived from insulin
70
Amyloid deposits in ALZHEIMER DISEASE
A_ amyloid --> amyloid plaques in brain
71
Alzhemier Disease and Down Syndrome association
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
DIALYSIS-associated AMYLOIDOSIS
_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
Amyloid deposits in MEDULLARY CARCINOMA of the THYROID
CALCITONIN deposits within the tumor (TUMOR CELLS IN AMYLOID BACKGROUND); calcitonin is produced by C-cells

Pathoma (3 decks)

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