Extra- basics

Question 1

Acute inflammation signs & causes?

Major cell type?

Answer 1

1. Rubor (redness): vasodilation via SM relax from histamin, bradykinin, PG
2. Calor (heat) ^ same
3. Tumor (swell): post capillary venule leak via histamine and tissue damage (disrupt endo)
4. Dolar (pain): PGE2 and bradykinin
5. Fever: pyrogens (MO-> IL-1, TNF -> ↑ COX to ↑ PGE2 set point)
6. Loss of function

Neutrophils

Question 2

Activators of neutrophils?

Answer 2

1. IL-8
2. LTE-B4 (chemotaxis and adhesion as well)
3. C5A
4. Bacteria (exogenous)- specifically N-formylmethionine terminal AA in some lipids (GPCR)

*then activate Rac/Rho/cdc42 pathway

Question 3

Cells involved in each:

Acute Asthma

Chronic Asthma

Chronic atherosclerosis

Answer 3

Acute and Chronic Asthma: Eosinophil, IgE

Chronic atherosclerosis: macrophage, lymphocytes

Question 4

Exudate vs Transudate

Answer 4

Exudate: inflammatory, increase in vascular permeability

• Component: high protein, blood, fluid
• Causes: infection, malignancy

Transudate: no change in permeability

• Components: low protein (main albumin), no cell debris, low specific gravity (ultrafil plasma)
• Causes: ↓osmotic (low albumin) or ↑hydrostatic pressure (HF)

Question 5

What factors increase vascular permeability?

Answer 5

histamine

bradykinin

leukotrienes

Question 6

Lymphangitis vs Lymphadenitis

Answer 6

Lymphangitis: vessels inflam, red streak around wound

Lymphadenitis: nodes (hyperplasia, ↑ immune cells)

Question 7

What initiates leukocyte rolling?

Answer 7

TNF and IL-1 from MO act on endothelial cells of post-cap venules to express E-selectin and ligands for L-selectin within 1-2 hrs

Question 8

What factors accomplish leukocyte rolling?

Answer 8

Selectins:

L: on leukocytes

E: on endothelium

P: on endothelium and plts

Question 9

What stimulates P-selectin? Where is it released from?

Answer 9

Thrombin and histamine stimulate Weibel palade bodies to redistribute P-selectin

Question 10

What protein accomplishes leukocyte transmigration (diapedesis)?

Answer 10

CD31 (PECAM-1)

Question 11

3 types of Reactive Nitrogen Species? Which is most important in infections?

Answer 11

1. eNOS (endothelial)
2. nNOS (neuronal)
3. iNOS (inducible) <– microbes, IFN-y = kill microbes

Question 12

What stimulates and inhibits phospholipase A2?

Answer 12

Stimulate: increase cytoplasmic Ca, external kinases

Inhibit: steroids

Question 13

What degrades bradykinin? Clinical application?

Answer 13

ACE: ACE inhibitors can ↑ level = angioedema

C1 inhibitors: deficiency –> hereditary angioedema

Bradykinin: vasodilates, ↑ permeability, pain

Question 14

What is an inflammasome?

Answer 14

multiprotein complex develops in cyto in response to damage of infection.

Contains NLR which bind to components of dying/necrotic cells

activators: uric acid, EC ATP, free DNA

Produces IL-1

Question 16

Physiologic examples of hypertrophy

Answer 16

1. body builders (increase muscle <- increase workload)
2. uterus in pregnancy (increase hormones)

Question 17

Physiologic example of hypertrophy

Answer 17

LVH/Cardiomegaly: increase in hemodynamic load (htn)

Question 18

Hypertrophy:

Characteristics?

Pathyways involved?

Causes?

Answer 18

Characteristics: ↑ protein synthesis

Pathyways involved: PI3k/AKT -> GATA4, NFAT, MEF2

Causes: ↑ functional demand, change in hormone

Question 19

Hyperplasia

Characteristics?

Causes?

Answer 19

Characteristics: ↑ cell #, DNA, protein, mito

Causes: excess hormone stimulation or GF to increase function capacity or in damaged/resected tissues

Question 20

Examples of Physiologic Hyperplasia?

Answer 20

• Breast growth @ puberty and pregnancy (glandular epi)
• Liver regeneration (hepatocytes or intrahepatic stem cells)
• Bone marrow (EPO <- Anemia)

Question 21

Pathologic Hyperplasia?

Stimulation?

Answer 21

Stimulation: virus, excess/inappropriate hormone action or GF

1. Endometrial hyperplasia: ↑ estrogen from adipocytes
2. Prostatic hyperplasia (↑androgen, DHT)
3. HPV

Maligancy can develop from uncontrolled growth

Question 22

Hypertrophy vs Hyperplasia

Answer 22

Hypertrophy: premanant/non-dividing cells, G0 state

• heart, skeletal m, nerves

Hyperplasia: cells capable of division

• epithelial (GI, breast, skin)

Question 23

Physiologic Atrophy

Answer 23

• Embryonic structures (notochord)
• Uterus following birth (loss of hormone stimulation)
• breast/uterus/vagina at menopause (↓endocrine stimulation)

Question 24

Characteristics of Atrophy

Causes?

Answer 24

Character: autophagy, ↓ protein synthesis

Causes: ↓ intracellular organelles, ↓ hormone stimulus

Question 25

Pathologic Atrophy

Answer 25

• Unused skeletal m: ↓ workload (bed rest, travel, immobile), ubiquination
• Cachexia: poor nutrition (marasmus)
• ↓ Blood Supply: senile atrophy of brain (atherosclerosis)
• Loss of innervation (neuromuscular disorder), disrupt fxn and metabolism of skeletal m

Question 26

Atrophy in cancer caused by?

Answer 26

muscle wasting

TNF suppresses appetite and depletes lipid stores

Question 27

atrophy mechanisms

Answer 27

1. ubiquinatin-proteasome path
2. autophagy

Question 28

Metaplasia mechanism

Answer 28

Change in cell PRODUCTION to adapt by changing cell type of epithelial cells, NO CHANGE in phenotype.

Question 29

Clinical Examples of Metaplasia

Answer 29

• Resp tract (colum->squam) <- smolking
• Barretts esophagus (squam->colum) <- acid
• Myositis Ossificans (muscle to bone) <-trauma
• Vit A Def: upper resp (to keratinizing squam), Xeropthalmia (eye to keratinizing squam)
• Apocrine: fibrocystic in breast to lobular