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Flashcards in First Aid: Pathology + Pharm Deck (25):
1

What are two absolute requirements for apoptosis to occur?

ATP and Caspases

2

Bcl 2 and BAX are key factors involved in the intrinsic apoptosis pathway. What would occur if either were overexpressed? What is the key step leading to apoptosis in this pathway?

Changes in pro/anti-apoptotic factors can lead to INCR MT permeability and cytochrome c release --> activates caspases

INCR Bcl2--> Apaf 1 over inhibitition, DECR. caspase activation --> tumorigenesis (e.g. follicular lymphoma)
INCR BAX (BAK) --> Pro-apoptotic

3

What are the two pathways of the extrinsic apoptosis pathway? What happens if there is a defect in one of these?

1. Ligand receptor interactions (FasL binding to Fas [CD95] --> crosslinking --> coalesce --> death domain binding site --> FADD --> activates caspases)

2. Immune cell (cytotoxic T-cell release of perforin and granzyme B)

A defect especially in Fas-FasL binding --> autoimmune disorders (this process responsible for thymic negative selection)

4

Match the type of necrosis with main associated characteristics and/or pathologies/locations:
1. Coagulative
2. Liquefactive
3. Caseous
4. Fatty
5. Fibrinoid
6. Gangrenous

1. Heart, liver, kidney (protein denaturation then enzymatic degradation)
2. Brain (CNS), bacterial abscess (lysosomal enzyme release)
3. TB, systemic fungi, Nocardia
4. Enzymatic (pancreatitis-saponification) or nonenzymatic (breast trauma)
5. Vasculitides, malignant HTN
6. Dry (ischemic coagulative) and wet (infection); limbs and GI tract

5

A cell is swollen and also exhibits MT swelling. You also notice nuclear chromatin clumping and fatty change on gross specimen. Are these changes reversible? When would they not be reversible?

Yes, with proper oxygenation

Irreversible - PLasma membrane damage, lysosomal rupture, MT peremeability

6

Match the Organ with areas of ischemic susceptibility:
1. Brain
2. Heart
3. Kidney
4. Liver
5. Colon

1. ACA/MCA/PCA boundary areas
2. Subendocardium (LV)
3. Medulla: Straight segment of proximal tubule and thick ascending limb
4. Area around central vein (zone III)
5. Splenic flexure, rectum

7

Where would you see red infarcts? Pale infarcts?

Red - areas w/ lots of blood supplies and loose tissue --> Lungs, liver, intestine

Pale - solid tissue --> Heart, kidney, spleen

8

A patient presents with tachycardia, low BP, and warm dry skin. you determine they are in a state of shock and have high cardiac output. What type of shock could this be and would IV fluids help increase the BP?

Septic, neurogenic or anaphylactic shock

-IV fluids would not increase BP
Could give Epi

9

What mediates acute inflammation and how long does this last? What about chronic inflammation? What are the outcomes of each?

Acute - PMNs, eosinophils and antibodies (rapid onset in seconds/minutes, can last minutes/days)
outcome - complete resolution or abscess formation

Chronic - Mononuclear cell (lymphocyte, monocyte, macrophages) and fibroblast mediated (onset in 2-3 days, can last long time)
outcome - granuloma, scarring and amyloidosis

10

What characteristics define a granuloma?

Epithelioid Histiocytes

Giant cells and rim of lymphocytes can also be present, but may not be

11

What is chromatolysis?

Process involving cell body after axonal injury --> Round cell swelling, displace nuclease to periphery, dispersion of Nissl substance in cytoplasm

12

What is chromatolysis?

Process involving cell body after axonal injury --> Round cell swelling, displace nuclease to periphery, dispersion of Nissl substance in cytoplasm

13

What is dystrophic calcification and where is it seen? What would serum calcium levels reveal?

Calcium deposition secondary to necrosis

Localized (e.g. heart valves) - TB (lungs/pericardium), liquefactive necrosis of chronic abscesses, fat necrosis, infarcts, thrombi, schistosomiasis, Monckeberg arteriolosclerosis, congenital CMV + toxoplasmosis, psammoma bodies

Normocalcemic in serum test

14

What is metastatic calcification and where is it seen? What would you see on serum exam?

Widespread deposition secondary to hypercalcemia (primary hyperparathyroidism, sarcoidosis, hypervitaminosis D) or high calcium-phosphate product (e.g. chronic renal failure + 2nd hyperPTH, long term dialysis, calciphylaxis, warfarin)

Calcium mainly in interstitial tissues of kidney, lungs and gastric mucosa (high pH favors deposits)

High serum calcium

15

What is metastatic calcification and where is it seen? What would you see on serum exam?

Widespread deposition secondary to hypercalcemia (primary hyperparathyroidism, sarcoidosis, hypervitaminosis D) or high calcium-phosphate product (e.g. chronic renal failure + 2nd hyperPTH, long term dialysis, calciphylaxis, warfarin)

Calcium mainly in interstitial tissues of kidney, lungs and gastric mucosa (high pH favors deposits)

High serum calcium

16

What are the 4 key steps to leukocyte extravasation and what are the factors involved on the cell and endothelium? Where does this process occur?

Extravasation is at POSTCAPILLARY VENULES

1. Margination and rolling - Vasodilation allows for margination, E-selectin P-selectin GlyCAM-1/CD34 on vasculature bind Sialyl-LewisX and L-selectin on leukocyte
2. Tight biding - ICAM1/VCAM on vasc. to CD11/18 integrins and VLA4 INTEGRINS on leukocyte.
3. Diapedesis - travel between endothelial cells, PECAM1 on both
4. Migration - travel to site of injury via chemotactic products

17

What are some important chemotactic products that can draw a leukocyte to the site of injury or infection?

Bacterial products, C5a, IL8, LTB4, kallikrein, platelet-activating factor

18

Which key factors enhance phagocytosis by PMNs?

C3b and IgG

19

What are three key ways free radicals can incite cell damage?

membrane lipid peroxidation

protein modification

DNA breakage

20

What are some ways free radicals can be eliminated in the cell?

1. Enzymes - catalase, superoxide dismutase, glutathione peroxidase
2. Spontaneous decay
3. Antioxidants - e.g. Vitamins A, C, E

21

Name some key free radical pathologies:

1. Retinopathy/prematurity
2. Bronchopulmonary dysplasia
3. Carbon tetrachloride --> liver necrosis (fatty change)
4. Acetaminophen overdose --> fulminant hepatits, renal papillary necrosis
5. Iron overload --> hemochromatosis
6. Reperfusion injury (e.g. superoxide), like after thrombolytic therapy

22

How does granulomatous disease occur?

Th1 cells secrete gamma-interferon activating macrophages

Macrophages release TNF-alpha

TNF-alpha induce and maintain granuloma

23

What is one of the leading causes of death from toxic agents in children? How does this lead to death? Symptoms?

Iron poisoning --> Cell death from peroxidation of membrane lipids

Acute sx --> N/V, gastric bleed, lethargy
Chronic sx --> Met Acidosis, Scarring --> GI obstruction

24

What does lipofuscin staining indicate?

Normal aging (Yellow-brown intracellular "wear and tear" pigment)

25

Name the CYP 450 live enzyme inducers and inhibitors:

INDUCERS: Chronic Alcohol abuse, Carbamazepine, Phenobarbitol, Phenytoin, Rifampin, Griseofulvin

INHIBITORS: Acute alcohol abuse, Cimetidine, Ciprofloxacin, Erythromycin, Azole antifungals, Grapefruit juice, Isoniazid, and Ritonavir (protease inhibitors)