Pathology

Question 1

Apoptosis

Answer 1

Programmed cell death (requires ATP) that utilizes caspases to mediate cellular breakdown. No inflammation. Characterized by eosinophilic cytoplasm, cell shrinkage, PKK, membrane blebbing, and consumption by macrophages.

Question 2

DNA Laddering to detect apoptosis

Answer 2

DNA laddering detects apoptosis because during karyorrhexis, endonucleases cleave to yield 180 BP fragments.

Question 3

Intrinsic pathway

Answer 3

Involved in tissue remodeling during embryogenesis and occurs when a regulatory factor is withdrawn or exposure to toxin. Increased mitochondrial permeability and cytochrome c release. BAX and BAK are pro-apoptotic. BCL2 is anti-apoptotic.

Question 4

How does BCL-2 Work?

Answer 4

Stabilizes mitochondrial membrane by inhibiting APAF1 (which induces caspase activation). BCL2 is overexpressed in follicular lymphoma.

Question 5

Extrinsic pathway

Answer 5

Fas ligand and FAS death receptor (CD95). This occurs in thymic t-cell selection. Binding of FasL to Fas causes death domain induction.

Question 6

How do CD8 T cells induce response?

Answer 6

They release perforin which cuts holes in cells, and granzyme which activates caspases.

Question 7

Coagulative necrosis

Answer 7

During ischemia (except in brain). Tissue is firm with structure preserved.

Question 8

Liquefactive necrosis

Answer 8

Occurs in pancreas, brain, and abscesses. Enzymes dissolve tissue leading to liquification.

Question 9

Caseous necrosis

Answer 9

Seen in TB and fungal infections (like liquefactive + coagulative)

Question 10

Fibrinoid Necrosis

Answer 10

Happens in blood vessels due to protein deposition in the wall. Occurs during malignant hypertension and vasculitides and preeclampsia. Highlighter pink appearance on histology

Question 11

Gangrenous necrosis

Answer 11

Happens in patients with diabetes (looks like mummified foot), or can be wet if superimposed infection. Common in limbs or GI tract.

Question 12

Hallmark of reversible injury

Answer 12

Cell swelling (due to decreased Na-K ATPase)

Question 13

Hallmark of irreversible injury

Answer 13

Pyknosis (nuclear shrinking), karyorrhexis (breaking up), karyolysis (dissolving).

Question 14

Hallmark of reversible injury

Answer 14

Cell swelling (due to decreased Na-K ATPase). Ribosomes pop off and protein synthesis is down.

Question 15

Hallmark of irreversible injury

Answer 15

Membrane damage. Pyknosis (nuclear shrinking), karyorrhexis (breaking up), karyolysis (dissolving). Amorphous densities in mitochondria, leakage of cyt c, and activation of caspases.

Question 16

Red infarcts

Answer 16

Received dual blood flow and are loosely organized (testicle, lung, liver, intestine)

Question 17

White infarcts

Answer 17

Receive single blood flow and are dense (spleen, heart, kidney).

Question 18

Distributive shock

Answer 18

High output cardiac failure (increased co increased venous return, decreased resistance). Decreased PCWP, vasodilation, failure to increase BP with fluids.

SEPSIS, anaphylaxis

Question 19

Hypovolemic/cardiogenic shock

Answer 19

Low output failure (decreased CO, increased TPR) increased PCWP in cardiogenic, decreased PCWP in hypovolemic. Blood pressure restored with fluids

Question 20

Where does increased vascular permeability happen in acute inflammation

Answer 20

In post capillary venule.

Question 21

Chromatolysis

Answer 21

A process that can be seen in a damaged neuron that increases protein synthesis in order to heal. Marked by cellular swelling, displacement of the nucleus to the periphery, and dispersion of nissl substance.

Question 22

How do free-radicals damage cells?

Answer 22

Via lipid peroxidation (membranes) and oxidation of DNA.

Question 23

How is O2- neutralized?
How about H2O2?
How about OH-?

Answer 23

SOD to H2O2
H2O2 via catalase, to h2o and o2
Via glutathione peroxidase.

Question 24

Fenton reaction

Answer 24

Fe3+ creates OH-

Question 25

Neutrophil oxidative burst

Answer 25

O2 to O2- via NADPH oxidase.

Question 26

Neutrophil oxidative burst

Answer 26

O2 to O2- via NADPH oxidase.

Question 27

How does CCL4 cause free radical injury?

Answer 27

Creates CCL3 which is a free radical, causes cell to swell, ribosomes pop off, decreased protein synthesis, decreased apolipoproteins, fatty change of liver.

Dry cleaning chemical.

Question 28

Hypertrophic scars vs keloid

Answer 28

Keloid has markedly increased collagen synthesis with disorganization. In hypertrophic scars, the collagen is arranged in parallel. Hypertrophic scars may not recur following resection but keloids frequently do.

Question 29

First collagen at wound?

Answer 29

Type III later replaced by type I which increases tensile strength.

Question 30

Percent of tensile strength regained 3 months after a wound?

Answer 30

70-80%.

Question 31

Granuloma formation

Answer 31

TH1 cells secrete gamma interferon which activates macrophages. They secrete TNF alpha which induces granuloma formation.

Question 32

Exudate vs transudate

Answer 32

Exudate is thick, cellular, and protein rich.

Transudate is thin, acellular, and protein poor. Low specific gravity.

Question 33

Things that decrease ESR

Answer 33

Polycythemia vera, sickle cell anemia

Question 34

Familial Mediterranean fever

Answer 34

Dysfunction of neutrophils so increased inflammation. Causes fever and serositis (appendicitis, MI, etc). Lots of inflammation leads to secondary amyloidosis: SAA and AA deposition.

Question 35

Where does dialysis-related amyloid deposition occur?

Answer 35

B2 microglobulin (component of MHC class I) doesn’t get removed during dialysis so builds up. Deposits as amyloid in joints and can cause carpal tunnel syndrome.

Question 36

Where does dialysis-related amyloid deposition occur?

Answer 36

B2 microglobulin (component of MHC class I) doesn’t get removed during dialysis so builds up. Deposits as amyloid in joints and can cause carpal tunnel syndrome.