Jeef First Aid Pathology Part 1

Front 1

1. Is energy required for Apoptosis?

Back 1

a. Yes, requires ATP.

Front 2

2. Intrinsic pathway of apoptosis?

Back 2

a. Occurs during:
1. Embryogenesis
2. Hormone induction (e.g., menstruation)
3. Atrophy (endometrial lining during menopause)
4. As a result of injurious stimuli (e.g., radiation, toxins, hypoxia).

Front 3

3. Pathophys of intrinsic pathway of apoptosis?

Back 3

a. Changes in the levels of anti- and pro-apoptotic factors lead to ↑ mitochondrial permeability and release of cytochrome c.

Front 4

4. Extrinsic pathway of apoptosis?

Back 4

a. Occurs w/ligand-receptors interactions (e.g., Fas ligand binding to Fas [CD95] or immune cell Tkiller release of perforin and granzymes B.

Front 5

5. What do both the intrinsic and extrinsic apoptotic pathways lead to?

Back 5

a. Activation of cytosolic caspases that mediate cellular breakdown.

Front 6

6. Key features of apoptosis to memorize.

Back 6

a. Cell shrinkage
b. Nuclear shrinkage and basophilia (pyknosis)
c. Membrane blebbing
d. Pyknotic nuclear fragmentation (karyorrhexis)
e. Nuclear fading (karyolysis)
f. Formation f apoptotic bodies, which are then phagocytosed.
g. No significant inflammation.

Front 7

7. Necrosis?

Back 7

a. Enzymatic degradation and protein denaturation of a cell resulting from exogenous injury.
b. Intracellular components extravasate.
c. Inflammatory process (unlike apoptosis).

Front 8

8. Where does Coagulative necrosis occur?

Back 8

a. Heart, liver, kidney.

Front 9

9. Where does Liquefactive necrosis occur?

Back 9

a. Brain, bacterial abscesses, pleural effusion

Front 10

10. When does caseous necrosis occur?

Back 10

a. TB
b. Systemic fungi.

Front 11

11. Where does fatty necrosis occur?

Back 11

a. Pancreas (saponification)

Front 12

12. Where does Fibrinoid necrosis occur?

Back 12

a. Blood vessels

Front 13

13. Where does Gangrenous necrosis occur?

Back 13

a. Dry (ischaemic coagulative) or
b. Wet (w/bacteria)
c. Common in limbs and GI tract

Front 14

14. Gene changes in Intrinsic apoptotic pathway

Back 14

a. ↑ BAX (pro-apoptotic)
b. ↓ BCL-2 (anti-apoptotic)

Front 15

15. Reversible cell injury (w/O2)?

Back 15

a. ↓ ATP synthesis
b. Cellular swelling (no ATP > impaired Na/K pump)
c. Nuclear chromatin clumping
d. ↓Glycogen
e. Fatty change
f. Ribosomal detachment (↓protein synthesis)

Front 16

16. Irreversible cell injury?

Back 16

a. Nuclear pyknosis, karyolysis, karyorrhexis.
b. Ca2+ influx -> caspase activation
c. Plasma membrane damaged
d. Lysosomal rupture.
e. Mitochondrial permeability

Front 17

17. Red (haemorrhagic infarcts)/

Back 17

a. Occur in loose tissues w/collaterals, such as liver, lungs, or intestines
b. Or following reperfusion.
c. “REd= REperfusion”.
d. Reperfusion injury is due to free radicals.

Front 18

18. Pale infarcts?

Back 18

a. Occur in solid tissues w/single blood supply, such as heart, kidney, and spleen.

Front 19

19. Steps in leukocyte extravasation?

Back 19

1. Rolling
2. Tight binding
3. Diapedesis
4. Migration
5. (Phagocytosis)

Front 20

20. Step 1 of neutrophil extravasation?

Back 20

a. Rolling
b. Mediated by E-selectin and P-selectin on vasculature/stroma.
c. Sialyl Lewis X = Important component of E and P selectin- Deficient in “Leukocyte Adhesion Deficiency-2”.

Front 21

21. Step 2 of neutrophil extravasation?

Back 21

a. Tight binding,.
b. Mediated by ICAM-1.
c. LFA-1 “Integrin” important.

Front 22

22. Step 3 of neutrophil extravasation?

Back 22

a. Diapedesis- Leukocyte travels between endothelial cells and exits blood vessel.
b. Mediated by PECAM-1

Front 23

23. Step 4 of neutrophil extravasation?

Back 23

a. Migration- leukocyte travels through interstitium to site of injury or infection guided by chemotactic signals.
b. Chemotactic signals involved in migration- Bacterial products and “CILK”:
1. C5a
2. IL-8
3. LTB4
4. Kallikrein

Front 24

24. How is free radical injury initiated?

Back 24

a. Radiation exposure
b. Metabolism of drugs (phase I)
c. Redox reaction
d. Nitric oxide
e. Transition metals
f. Leukocyte oxidative burst.

Front 25

25. 8 Granulomatous diseases?

Back 25

1. TB
2. Fungal infections (e.g. hist)
3. Syphilis
4. Leprosy
5. Cat scratch fever
6. Sarcoidosis
7. Crohn’s disease
8. Berylliosis.

Front 26

26. Mechanism of granuloma formation?

Back 26

a. Th1 cells secrete γ-interferon, activating macs.
b. TNF-α from macs induces and maintains granuloma formation.
c. Anti-TNF drugs can break down granulomas, leading to disseminated disease.
d. T cells secrete TNF-α contributing to granuloma formation.

Front 27

27. Transudate?

Back 27

a. Hypocellular
b. Protein poor
c. Specific gravity <1.012
d. Due to: ↑Hydrostatic pressure, ↓oncotic pressure, or Na retention.

Front 28

28. Exudate?

Back 28

a. Cellular
b. Protein rich
c. Specific gravity > 1.020
d. Due to:
1. Lymphatic obstruction
2. Inflammation.