Pathology Flashcards

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1
Q

What happens during ischemia

A

Na pump slows.

In flux calcium, efflux of potassium.

Anerobic increase

low glycogen ,increase. lactic acid, low pH

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2
Q

Mechanisms of irreversible injury

A

Low ATP

Mitochondrial damage

Membrane damage (calcium influx)

Increased ROS damage to lipids , proteins, and NA

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3
Q

Reversable vs irreversible

A

Reverse: swelling of ER and mitochondria, goes back down.

Irr: Breakage of PM , organelles , and nucleus leakage.

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4
Q

Morphology of irreversible damage

A

Hypereosinophilia (RNA loss-pink)

Mitochondrial swelling nad amorphous densities.

Nuclear pynknosis (chromatin condensation), fragmentation, and dissolution.

Intracytopladmic myelin figures.

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5
Q

Loss of O2 in cell

A

decrease in phospholipids

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6
Q

Effect of increased cytosolic calcium

A

Lipid break down (due to phospholipase and protease activation).

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7
Q

Examples of liquefaction

A

brain infarct , abscess

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8
Q

Examples of fat necrosis

A

pancreatitis , pancreatic trauma

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9
Q

Example of caseous necrosis

A

TB, histoplasmosis.

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10
Q

Example of fibrinoid necrosis

A

nectorotic tissue due to immunological reaction.

Usually seen in blood vessels with deposition of complement and antibodies in vessels wall.

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11
Q

Physiological apoptosis

A

embryogenesis , menstrual cycle, lactating breast

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12
Q

Pathologic apoptosis

A

viral, injuring agents, anticancer drugs, radiation.

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13
Q

Apoptosis mechanisms

A

Endonuclease activation

Cytoskeleton disruption by protease

Cytoplasmic protein cross linking by transglutaminase

Cell surface changes leading to phagocytosis

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14
Q

Apoptotic morphology

A

shinrkage

chromatin condense

bleb (apoptotic bodies)

phagocytosis

lack of inflammatory reaction

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15
Q

Intrinsic pathway (mitochondrial)

A

**cytochrome C

Due to DNA damage or protein misfolding

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16
Q

Extrinsic pathway

A

Receptor ligand interaction

Fas , TNF receptor

caspase activation

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17
Q

Intrinsic pathway

A

cytochrome C

caspase -9 activated,

process inhibited by BCL2

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18
Q

Extrinsic pathway

A

occurs in special cases

remove self reactive T-cells and kill infected cells, etc

also lead to caspase activity that breaks nucleus and cytoplasmic structure

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19
Q

Hyperplasia

A

Physiologic: hormone induce

Pathologic: viral, papillomavirus. BPH -excessive stimulation.

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20
Q

Hypertrophy

A

Physiologic: hormonal stimulaiton.

Pathologic: LVH, due to HTN, or valve stenosis-heart works very hard. The myocytes cannot divide, so only option is to increase in size.

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21
Q

Metaplasia

A

Reversible change
One type to another
-ciliated columnar to squamous (which is not functional in bronchi) can lead to squamous cell carcinoma.

If stimulus such as smoking persist, it can progress to displasia (cancer growth).

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22
Q

Hemosiderosis

A

iron overload in phagocytic cells (WBCs) no tissue damage

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23
Q

Hemochromatosis

A

iron overload in parenchymal cells

there is tissue damage

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24
Q

Causes of metastatic calcification

A

hyperparathyroidism

bone breakdown (cancer)

Increased vitamin D or sarcoidosis

Renal failure

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25
Q

Dystrophic calcification

A

deposition of calcium salts in necrotic/ injured tissues.

hereptrophic bone may form with time.

26
Q

3 signs of chronic inflammation

A

Angiogenesis

Mononuclear cell infiltrate

Fibrosis

27
Q

Inducible nitric oxide production

A

Macrohages

28
Q

ROS is rapidly induced by assembly of phagocyte oxidase (respiratory burst)

A

Neutrophil

29
Q

Low levels of NO

A

Neutrophil

30
Q

High protein content , may contain white and red cells

A

Exudate

31
Q

Vascular reactions

A
  1. Increased blood flow
  2. Leakage of plasma proteins —>Edema
  3. Neutrophil emigration
32
Q

When proteins leak out of the vessel wall

A

exudate

33
Q

Decreased colloidal osmotic pressure (liver is not making enough protein to maintain osmotic pressure. Fluid leakage. Low pressure pushing down to keep fluid in.

A

Transudate - low protein content, few cells.

Can occur in liver and kidney disease.

34
Q

When you see pink fibrin. . think . . .

A

exudate

35
Q

WBC move toward

A

LPS, C5a

Leukotriene B4 (arachidonic acid derivative)
Cytokines -IL-8
36
Q

6-24 hours

A

Neutrophills

37
Q

24-48 hours

A

monocytes/macrophages

38
Q

Opsonins

A

Fc-gragment of IgG antibodies

C3b

39
Q

Primary granules in Neutrophils contains MPO which

A

H2O2——MPO—–> OCl- (bleach)

40
Q

Mast cells, basophils, and platelets secrete

A

histamine

41
Q

platelets secrete

A

serotonin

42
Q

neutrophils and macrophages secrete

A

lysosomal enzymes

43
Q

Vasodilation

A

histamine and prostaglandins

44
Q

Increased vascular permeability

A

histamine, C3a and C5a

Leukotrienes C4, D4, and E4

45
Q

Chemotaxis ans leukocyte recruitment and activation

A

TNF, IL-1
C3a , C5a
Leukotriene B4

46
Q

Fever

A

IL-1 , TNF

Prostaglandins

47
Q

Pain

A

prostaglandins

Brady kinin

48
Q

Tissue damage

A

Lysosomal enzymes of leukocytes

ROS

49
Q

Steroids inhibits

A

phospholipase

50
Q

Blister in thermal burn

A

serous
- Occurs with low cellular content in the exudate.

Micropgraph: look for separation with low cellular volume.

51
Q

uremic pericarditis , viral/chemical pneumonitis , idiopathic

A

Fibrinous

Micrograpth: shows abundant pink fibrin.

52
Q

Meningococcal meningitis

A

purulent

Micropgraph: pus + neutrophils. **Abundant neutrophils.

53
Q

IgE mediated, -asthma and parasitic infection

A

Eiosinophilic

54
Q

Rickettsial

A

Hemorrhagic

55
Q

Diptheria and pseudomembranous enterocolitis

A

Pseudomembranous

*Pseudomembrane formed due to disruption of the tissue.

** Micropgraph shows : dead tracheal epithelial cells, dead inflammatory cells, and fibrin exudate.

56
Q

Chronic inflammation micrograph

A

lots of blue-full of DNA

Pink – fibrotic tissue

57
Q

Inflammation and tissue injury

A

ROS
Protease, cytokines , etc,

Coagulation factors,

AA metabolites

58
Q

Repair

A

GF
Fibrogenic cytokines
Angiogenic factors
Remodeling collagenesis

59
Q

Granulomatous inflammation

A

Inflammation involving activated macrophages with an epithelioid appearance.

Few lymphocytes and plasma cells.

60
Q

Granuloma

A

Aggregation of epithelioid macrophages surrounded by a collar of lymphocytes and occasional plasma cells.

May have a rim of fibrous connective tissue.

61
Q

M2 macrophages produce cytokines and growth factors

A

FGF-2 and TGF-b (these help synthesize collagen)