Pathology Flashcards

(61 cards)

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Mechanisms of irreversible injury

A

Low ATP

Mitochondrial damage

Membrane damage (calcium influx)

Increased ROS damage to lipids , proteins, and NA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Reversable vs irreversible

A

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

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Loss of O2 in cell

A

decrease in phospholipids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Effect of increased cytosolic calcium

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Examples of liquefaction

A

brain infarct , abscess

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Examples of fat necrosis

A

pancreatitis , pancreatic trauma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Example of caseous necrosis

A

TB, histoplasmosis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Physiological apoptosis

A

embryogenesis , menstrual cycle, lactating breast

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Pathologic apoptosis

A

viral, injuring agents, anticancer drugs, radiation.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Apoptosis mechanisms

A

Endonuclease activation

Cytoskeleton disruption by protease

Cytoplasmic protein cross linking by transglutaminase

Cell surface changes leading to phagocytosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Apoptotic morphology

A

shinrkage

chromatin condense

bleb (apoptotic bodies)

phagocytosis

lack of inflammatory reaction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Intrinsic pathway (mitochondrial)

A

**cytochrome C

Due to DNA damage or protein misfolding

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Extrinsic pathway

A

Receptor ligand interaction

Fas , TNF receptor

caspase activation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Intrinsic pathway

A

cytochrome C

caspase -9 activated,

process inhibited by BCL2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Hyperplasia

A

Physiologic: hormone induce

Pathologic: viral, papillomavirus. BPH -excessive stimulation.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Hemosiderosis

A

iron overload in phagocytic cells (WBCs) no tissue damage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Hemochromatosis

A

iron overload in parenchymal cells

there is tissue damage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Causes of metastatic calcification

A

hyperparathyroidism

bone breakdown (cancer)

Increased vitamin D or sarcoidosis

Renal failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Dystrophic calcification
deposition of calcium salts in necrotic/ injured tissues. hereptrophic bone may form with time.
26
3 signs of chronic inflammation
Angiogenesis Mononuclear cell infiltrate Fibrosis
27
Inducible nitric oxide production
Macrohages
28
ROS is rapidly induced by assembly of phagocyte oxidase (respiratory burst)
Neutrophil
29
Low levels of NO
Neutrophil
30
High protein content , may contain white and red cells
Exudate
31
Vascular reactions
1. Increased blood flow 2. Leakage of plasma proteins --->Edema 3. Neutrophil emigration
32
When proteins leak out of the vessel wall
exudate
33
Decreased colloidal osmotic pressure (liver is not making enough protein to maintain osmotic pressure. Fluid leakage. Low pressure pushing down to keep fluid in.
Transudate - low protein content, few cells. Can occur in liver and kidney disease.
34
When you see pink fibrin. . think . . .
exudate
35
WBC move toward
LPS, C5a ``` Leukotriene B4 (arachidonic acid derivative) Cytokines -IL-8 ```
36
6-24 hours
Neutrophills
37
24-48 hours
monocytes/macrophages
38
Opsonins
Fc-gragment of IgG antibodies C3b
39
Primary granules in Neutrophils contains MPO which
H2O2------MPO-----> OCl- (bleach)
40
Mast cells, basophils, and platelets secrete
histamine
41
platelets secrete
serotonin
42
neutrophils and macrophages secrete
lysosomal enzymes
43
Vasodilation
histamine and prostaglandins
44
Increased vascular permeability
histamine, C3a and C5a Leukotrienes C4, D4, and E4
45
Chemotaxis ans leukocyte recruitment and activation
TNF, IL-1 C3a , C5a Leukotriene B4
46
Fever
IL-1 , TNF Prostaglandins
47
Pain
prostaglandins | Brady kinin
48
Tissue damage
Lysosomal enzymes of leukocytes | ROS
49
Steroids inhibits
phospholipase
50
Blister in thermal burn
serous - Occurs with low cellular content in the exudate. Micropgraph: look for separation with low cellular volume.
51
uremic pericarditis , viral/chemical pneumonitis , idiopathic
Fibrinous Micrograpth: shows abundant pink fibrin.
52
Meningococcal meningitis
purulent *Micropgraph: pus + neutrophils. ***Abundant neutrophils.
53
IgE mediated, -asthma and parasitic infection
Eiosinophilic
54
Rickettsial
Hemorrhagic
55
Diptheria and pseudomembranous enterocolitis
Pseudomembranous *Pseudomembrane formed due to disruption of the tissue. ** Micropgraph shows : dead tracheal epithelial cells, dead inflammatory cells, and fibrin exudate.
56
Chronic inflammation micrograph
lots of blue-full of DNA Pink -- fibrotic tissue
57
Inflammation and tissue injury
ROS Protease, cytokines , etc, Coagulation factors, AA metabolites
58
Repair
GF Fibrogenic cytokines Angiogenic factors Remodeling collagenesis
59
Granulomatous inflammation
Inflammation involving activated macrophages with an epithelioid appearance. Few lymphocytes and plasma cells.
60
Granuloma
Aggregation of epithelioid macrophages surrounded by a collar of lymphocytes and occasional plasma cells. May have a rim of fibrous connective tissue.
61
M2 macrophages produce cytokines and growth factors
FGF-2 and TGF-b (these help synthesize collagen)