Imported: Pathoma Chapter 1

Front 1

Atrophy means...

Back 1

a decrease in size AND number

hypertrophy means only size

Front 2

mechanism of decrease in cell size during atrophy

Back 2

ubiquitin-proteosome pathway

autophagy by lysosomal enzymes fusing with cellular components packages in vacuoles

Front 3

Epithelium-- 3 broad categories

Back 3

Squamous Cell Epithelium
--> keratinizing/non-keratinizing

Columnar Epithelium
--> ciliated?

Transitional
--> really only the bladder lined with this

Front 4

normal esophageal lining?

Back 4

nonkeratinizing squamous epithelium

Front 5

barrett's esophagus

Back 5

nonkeratinizing squamous epithelium metaplasia to

nonciliated, mucin producing columnar cells

Front 6

Metaplasia is

reversible? irreversible?

Back 6

reversible

Front 7

What type of metaplasia does not increase risk of breast cancer

Back 7

Apocrine metaplasia of the breast

Front 8

What symptoms does Vitamin A deficiency present with?

Back 8

Vitamin A necessary for differentiation of specialized epithelial surfaces such as the conjunctiva covering the eye, thus deficiency can lead to

keratomalacia or stratified keratinizing squamous epithelium

Front 9

What can happen after trauma to muscle?

Back 9

Myositis ossificans
metaplasia of muscle to bone during healing after trauma

Front 10

fibromuscular dysplasia

Back 10

Most commonly affects renal artery and carotid artery

Front 11

Most common cause of Budd-Chiari syndrome

Back 11

Polycythemia Vera

Front 12

Causes of Ischemia

Back 12

Decreased arterial perfusion, blocked venous drainage, Shock--generalized hypotension resulting in poor perfusion

Front 13

Describe the path of oxygen to tissue using lab values

Back 13

FiO2 --> PAO2 --> PaO2 --> SaO2

pressure of oxygen in air --> pressure of oxygen in alveoli --> pressure of oxygen in blood --> saturation of hemoglobin

Front 14

Lab values in hypoventilation

Back 14

Increased CO2 causes decreased O2 which means O2 sats go down

Front 15

Lab values in diffusion defect

Back 15

PAO2, that is alveolar PO2 normal but it can't diffuse across membrane, so PaO2 goes down, and SaO2 goes down

Front 16

Cherry red appearance of skin, headache

Back 16

CO poisoning, causes a leftward shift in the curve, making oxygen harder to unload. Also

reduces SaO2
PaO2 normal

Also inhibits Cytochromes in electron transport.

Front 17

Chocolate colored blood with cyanosis. lab values? treatment?

Back 17

Methemoglobinemia
PaO2 normal
SaO2 decreased
Iron oxidized to Fe+3 and cannot bind oxygen. Seen with OXIDANT STRESS such as nitryl or sulfa drugs.

TREATMENT: Methylene blue, which catalyzes natural reduction of methemoglobin reductase by offering an electron acceptor

Front 18

Describe pathophys of low ATP

Back 18

1.) disruption of ATP pump leads to Na+ influx into cell
2.) Ca+2 pump needs ATP so influx of Ca+2 as well
3.) Ca+2 activates enzymes
4.) Anaerobic glycolysis causes lactic acid buildup which lowers pH and precipitates DNA

Front 19

Hallmark of reversible injury and what it leads to

Back 19

Cellular Swelling
1.) loss of microvilli
2.) cellular blebbing
3.) ribosomes fall off rough ER causing decreased protein synthesis

Front 20

Hallmark of irreversible damage is?

what is leads to...

Back 20

Membrane damage

1.) allows enzymes to leak into the serum(cardiac troponin after MI/necrosis)
2.) more calcium enters cell
3.) mitochondrial membrane damage breaks electron transport
4.) that same mitochondrial membrane damage allows cytochrome c to leak out which activates apoptosis
5.) lysosomal membrane damage allows hydrolytic enzymes to leak into cell and wreak havoc

Front 21

Coagulative necrosis

Back 21

loss of nucleus but cell shape and organ structures are preserved by coagulation of proteins. In other words, necrotic tissue that remains firm.

Front 22

What are the macrophages of the CNS

Back 22

microglial cells

Front 23

Acute inflammation can be caused by...

Back 23

infection OR necrosis

neutrophil count will increase in both

Front 24

Which organs have white infarcts?

Back 24

Heart, Kidney, Spleen

Front 25

Which organs have red infarcts?

Back 25

lungs, liver, testes, ovaries, gut

Front 26

most common necrosis in lower limb ischemia

Back 26

gangrenous. if superimposed infection occurs can be liquefactive as well(wet gangrene)

Front 27

necrosis associated with Pancreatitis

Back 27

liquefactive necrosis in pancreas parenchyma and fat necrosis in peripancreatic fat

Front 28

Dystrophic calcification

Back 28

[Ca+2] normal

example: psammoma bodies. Bicuspid aortic valves have dystrophic calcification

Front 29

Metastatic calcification

Back 29

[Ca+2] increased, PTH increased, [PO4-3] increased

Front 30

what is fibrinoid necrosis

Back 30

necrotic damage to blood vessel wall causes leaking of proteins into vessel wall(including fibrin)

Front 31

necrosis associated with hypertension or vasculitis

Back 31

fibrinoid necrosis

common example is fibrinoid necrosis of placenta secondary to high Bp due to pre-eclampsia

Front 32

Malignant hypertension can cause what?

Back 32

fibrinoid necrosis of blood vessels

Front 33

Apoptosis activation -- intrinsic mitochondrial pathway

Back 33

cellular or DNA damage or loss of hormonal stimulation can cause inactivation of Bcl2

Inactivation of Bcl2 --> leakage of cytochrome c from inner mitochondrial membrane into cytoplasm --> cytochrome c activates caspases in cytoplasm --> caspases activate proteases that wreak havoc, in an orderly fashion

Front 34

Apoptosis activation -- extrinsic receptor-ligand pathway

Back 34

FAS ligand binds FAS death receptor(CD95) on target cell, activating caspases
example: negative T-cell selection in Thymus

ORRRRR
TNF binds TNF receptor on target cell activating caspases

Front 35

What receptor is the FAS death receptor?

Back 35

CD95

Front 36

Apoptosis activation -- Cytotoxic CD8+ T-cell mediated pathway

Back 36

Perforins secreted by CD8 make pores in membrane
Granzyme enters pores and activates caspase

example: CD8+ kills virally infected cells

Front 37

Which is the worst free radical? How is it made?

Back 37

Hydroxyl free radical

it is created by IONIZING radiation

Front 38

Describe pathway of bleach creation

Back 38

O2 --> O2- free radical --> H2O2 --> HOCl

Oxygen is turned into a free radical by NADPH oxidase. Called oxidative burst!
Oxygen free radical is reduces to hydrogen peroxide by superoxide dismutase
Hydrogen peroxide is turned into bleach, HOCl, by myeloperoxidase

Front 39

Chronic Granulomatous Disease

Back 39

deficiency in NADPH oxidase. However if extrinsic hydrogen peroxide provided, MPO can make bleach and be bacterial. Thus catalase positive organisms are particularly dangerous to these people.

Front 40

NBT dye is for what?

Back 40

oxidative burst! or...
O2 --> O2 free radical
catalyzed by NADPH oxidase

Front 41

MPO deficiency

Back 41

These people will respond to NBT dye test. But they cannot make HOCl(bleach) because of defective MPO and thus are susceptible to chronic infection.