Pathology Chapter 1: Cell Injury

Front 1

Inadequate oxygenation of tissue

Back 1

hypoxia

Front 2

Decreased PaO2

Back 2

Hypoxemia

Front 3

Impaired oxygen delivery to alveoli

Back 3

Ventilation Defect

Front 4

Absence of blood flow to alveoli

Back 4

Perfusion Defect

Front 5

Why does inadequate oxygen decrease production of ATP?

Back 5

Because Oxygen is the final electron acceptor in the ETC which produces ATP.

Front 6

Which compound improves oxygen delivery to tissues by stabilizing hemoglobin in the taut form, which decreases O2 affinity and fascilitates its movement from Hb into tissues?

Back 6

2,3 BPG

Front 7

What effect does a perfusion decrease have on dead space?

Back 7

It increases dead space.

Front 8

Decrease O2 diffusion through the alveolar-capillary interface

Back 8

Diffusion Defect

Front 9

Decreases Hb concentration

Back 9

Anemia

Front 10

Hb with oxidized heme groups

Back 10

methemoglobin

Front 11

Causes chocolate colored blood and cyanosis caused by an increase in deoxyhemoglobin

Back 11

methemoglobinemia

Front 12

Which two compounds inhibit cytochrome oxidase in the ETC?

Back 12

CO and Cyanide

Front 13

Name two watershed areas where the blood supply is vulnerable to hypoxia.

Back 13

Cerebral vessels and mesenteric arteries

Front 14

Which cardiac tissue receives the least amount of O2?

Back 14

Subendocardial Tissue

Front 15

What does a depressed S-T segment on an ECG suggest?

Back 15

Subendocardial ischemia

Front 16

What is the most adversely affected cell in tissue hypoxia?

Back 16

Neurons

Front 17

Unstable chemical compounds with a single unpaired electron in their outer orbital:

Back 17

Free Radical

Front 18

Damage membranes and DNA

Back 18

Free Radicals

Front 19

What is the most destructive type of free radical? How are they formed?

Back 19

Hydroxyl FRs - produced by ionizing radiation and high concentration of O2

Front 20

What four compounds neutralize free radicals?

Back 20

Superoxide Dismutase (SOD), Glutathione Peroxidase (GSH), Vitamin E and Vitamin C

Front 21

What is the best neutralizer of Hydroxy FRs?

Back 21

Vitamin C

Front 22

How do you treat FRs created by acetaminophen?

Back 22

With N-acetylcysteine which generates GSH

Front 23

How does reperfusion injury occur?

Back 23

Superoxide FRs and increased cytosolic calcium.

Front 24

What is the effect of the relase of cytochrome c from damaged mitochondria?

Back 24

Initiates apoptosis by activating caspases in the cytosol.

Front 25

A rare inherited condition in which there is a defect in post-translational modification of lysosomal enzymes in the golgi membrane:

Back 25

I-Cell disease

Front 26

Caused by a deficiency in glucocerebroside which causes an accumulation of glucocerebrosides in the lysosome.

Back 26

Gaucher's Disease

Front 27

Disease characterized by giant lysosomal ganules caused by a defect in formation of phagolysosomes:

Back 27

CHS (Chediak-Higasi Syndome)

Front 28

A defect in tubulin synthesis in the G2 phase of the cell - associated with which two drugs?

Back 28

Etoposide and Bleomycin

Front 29

Mitotic Spindle defects are caused by which three compounds:

Back 29

Vinca alkaloids, colchicine, and paclitaxel.

Front 30

Stress protein that binds to damaged intermediate filaments and marks them for degradation inproteosomes and lysosomes in the cytosol-

Back 30

Ubiquitin- intermediate filament degradation

Front 31

Damaged cytokeratin intermediate filaments in hepatocytes in alcoholic liver disease

Back 31

Mallory Bodies

Front 32

Damaged neurofilaments in idiopathic parkinson's:

Back 32

Lewy Bodies

Front 33

Name two causes of fatty liver:

Back 33

Increased TG synthesis, Decreased TG secretion

Front 34

What is the chemical cause of fatty liver? How does this relate to alcohol use?

Back 34

Occurs from increased conversion of DHAP to G3-P. Increased production of NADH from alcohol metabolism accelerates conversion of DHAP to G3-P.

Front 35

Fatty changes in cardiac muscle can be caused by which two things?

Back 35

Anemia and Diptheria

Front 36

Major soluble iron storage protein:

Back 36

Ferritin

Front 37

Feritin degradation product:

Back 37

Hemosiderin

Front 38

Deposition of calcium phosphate in necrotic tissue:

Back 38

Dystrophic calcification

Front 39

In which conditions is dystrophic calcification commonky seen?

Back 39

Chronic pancreatitis, atheroscerotic plaques, and congenital CMV infection

Front 40

Deposition of calcium phosphate in normal tissue:

Back 40

Metastatic Calcification

Front 41

Causes of hypercalcemia leading to metastatic calcification:

Back 41

Primary hyperparathyroidism, malignancy induced

Front 42

Causes of hyperphosphatemia leading to metastatic calcification:

Back 42

Renal failure, primary hypoparathyroidism

Front 43

Decrease in size and weight of a tissue or organ

Back 43

Atrophy

Front 44

Tissue discoloration resulting from lysosomal accumulation of lipofuscin - also known as wear and tear pigment

Back 44

Brown Atrophy

Front 45

Increase in cell size

Back 45

Hypertrophy

Front 46

Increase in the number of normal cells-

Back 46

Hyperplasia

Front 47

Name five common causes of hyperplasia:

Back 47

Hormone stimulation, chronic irritation, chemical imbalance, antibodies, and viral infections

Front 48

Replacement of one fully differentiated cell type by another:

Back 48

Metaplasia

Front 49

Distal esophagus epithelium shows an increase in goblet cells and mucus secreting cells in response to acid reflux:

Back 49

Barrett's Esophagus- glandular metaplasia

Front 50

Disordered cell growth:

Back 50

Dysplasia

Front 51

Death of groups of cells, often accompanied by an inflammatory infiltrate

Back 51

Necrosis- always pathologic

Front 52

Type of necrosis that preserves the structural outline of dead cells:

Back 52

Coagulation Necrosis- caused by denaturation of enzymes and structural proteins

Front 53

Gross manifestation of coagulation necrosis secondary to the sudden occlusion of a vessel- pale and hemorrhagic types

Back 53

Infarction

Front 54

Type of necrosis that occurs when increased density of tissue prevents RBCs from diffusing through necrotic tissue:

Back 54

Pale Infarction

Front 55

Cisatracurium
Dosing--card

Back 55

Ind. 0.1mg/kg (0.1-0.15)
Inf. 1-2mcg/kg/min

Front 56

Necrotic degradation of tissue that softens and becomes liquefied:

Back 56

Liquefaction necrosis- seen in wet gangrene

Front 57

Cerebral infarction causes which type of necrosis?

Back 57

Liquefaction- not coagulative

Front 58

Variant of coagulation necrosis, associated with acellular, cheese-like (caseous) material

Back 58

Caseous Necrosis- Seen in TB

Front 59

Most common cause of caseous necrosis:

Back 59

Tuberculosis

Front 60

Most common cause of Enzymatic Fat Necrosis:

Back 60

Acute Pancreatitis

Front 61

Occurs in fatty tissue as a result of trauma and is not enzyme mediated:

Back 61

Traumatic Fat Necrosis

Front 62

Necrosis of immune mediated disease- limited to small muscular arteries, venules, and glomerular capillaries

Back 62

Fibrinoid Necrosis

Front 63

Programmed, enzyme-mediated cell death

Back 63

Apoptosis

Front 64

Involves binding of tumor necrosis factor (TNF) to its receptor and eventual activation of caspases:

Back 64

Extrinsic pathway of apoptosis

Front 65

Involves mitochondrial leakage of cytochrome C into cytosol and eventual activation of caspases:

Back 65

Intrinsic pathway of apoptosis

Front 66

Gene family located on chromosome 18 that inhibit apoptosis by preventing mitochondrial leakage of cytochrome c

Back 66

BCL2 Gene Family

Front 67

Gene that temporarily arrests the cell in G1 to repair DNA and promotes apoptosis if DNA damage is too great:

Back 67

TP53 supressor gene

Front 68

Gene that activates apoptosis by inactivating BCL2 gene

Back 68

BAX

Front 69

Group of cysteinr proteases whose activation induces apoptosis; must be activated by the intrinsic or extrinsic system

Back 69

Caspases

Front 70

Marked by deeply eosinophilic cytoplasm and pyknotic nucleus

Back 70

Apoptosis

Front 71

Marker of diffuse liver cell necrosis, mitochondrial enzyme preferentially increased in alcohol-induced liver disease

Back 71

Aspartate Aminotransferase (AST)

Front 72

Marker of diffuse liver cell necrosis, more specific for liver cell necrosis than AST

Back 72

Alanine Aminotransferase

Front 73

Isoenzyme increased in acute MI or myocarditis

Back 73

Creatine Kinase MB (CK-MB)

Front 74

Marker enzymes for acute pancreatitis

Back 74

Amylase and Lipase

Front 75

Which (amylase or lipase) is more specific for pancreatitis?

Back 75

Lipase