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Evan's Step 1 Prep Material > Ch2 Cell Injury EC > Flashcards

Ch2 Cell Injury EC Flashcards

1
Q

Pulse oximetry use and limitation

A

Measures oxygen saturation (SaO2)

Falsely increased SaO2 in metHb and COHb

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2
Q

What can be used to measure SaO2 with metHb or COHb?

A

Co-oximeter (not pulse ox)

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3
Q

What are the clinical findings in hypoxia?

A

Cyanosis
Confusion
Cognitive impairment
Lethargy

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4
Q

Ischemia

A

Decreased arterial blood inflow and/or venous outflow

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5
Q

What are the consequences of ischemia?

A

Atrophy
Infarction
Dysfunction

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6
Q

Hypoxemia

A

Decrease PaO2

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7
Q

If PACO2 increases, what happens to PAO2

A

It must decrease in order for the sum of partial pressures to remain equal (assuming N2 is constant)

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8
Q

What are the causes of hypoxia?

A

Ischemia (MCC, ie thrombus)

Hypoxemia (

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9
Q

What are the causes of hypoxemia?

A 
Respiratory acidosis (increased CO2 means O2 must go down)
Ventilation defects (ie respiratory distress syndrome)
Perfusion defects (ie PE)
Diffusion defect (ie sarcoidosis)
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10
Q

Define anemia

A

Decrease [Hb] (and thus O2 content)

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11
Q

What happens to pO2 levels and O2 saturation in anemia?

A

NOTHING!

There is no hypoxemia in anemia

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12
Q

Describe the conversion of methemoglobin to the ferrous state.

A

NADH reductase system

Electrons from NADH transferred to CYTOCHROME B5 then to metHb by CYTOCHROME B5 REDUCTASE yielding FE2+

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13
Q

What are the causes of methemoglobinemia?

A 
Oxidant stress (drugs, sepsis)
Congenital deficiency of cytochrome B5 reductase
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14
Q

How does methylene blue treat methemoglobinemia?

A

Accelerates the enzymatic reduction of MetHb by NADPH methemoglobin reductase (in PPP)

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15
Q

Clinical findings in methemoglobinemia

A

Cyanosis UNRESPONSIVE to O2

Chocolate-colored blood

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16
Q

What drugs commonly cause methemoglobinemia?

A 
(same as for hemolytic anemia in G6PD)
Dapsone
Primaquine 
Nitroglycerine/Nitroprusside
TMP-SMX 
~common to see methemoglobinemia in AIDS b/c on TMP-SMX prophylaxis for PCP
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17
Q

Clinical findings in CO poisoning

A

Headache (most common symptom)
Cherry red discoloration
Dizziness
Seizures/Coma

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18
Q

Why don’t you see cyanosis in CO poisoning?

A

Masked by cherry red discoloration

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19
Q

Treatment for CO poisoning

A

100% oxygen

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20
Q

Response to high altitude

A

Hypoxemia stimulates peripheral chemoreceptors which leads to hyperventilation
Respiratory alkalosis increases intracellular pH which activates PFK (increasing glycolysis)
Increased production of of 2,3DPG by mutase reaction
OBC shifts to R

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21
Q

What is the function of the BCL-2 gene?

A

Prevents cytochrome C from leaving the ETC by maintaining the integrity of the mitochondrial membrane.
(If cytochrome C enters the cytosol, caspases are activated –> apoptosis)

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22
Q

How do CO and CN affect the ETC?

A

Inhibit CYTOCHROME OXIDASE in complex IV (cannot consume O2)

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23
Q

PaO2, SaO2, OBC, and Cytochrome oxidase in Anemia

A

PaO2=Normal
SaO2=Normal
OBC=Normal
Cytochrome Oxidase=Normal

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24
Q

PaO2, SaO2, OBC, and Cytochrome oxidase in CO poisoning

A

PaO2=Normal
SaO2=Decreased
OBC=Left-shifted
Cytochrome oxidase=Inhibited

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25
Q

PaO2, SaO2, OBC, and Cytochrome oxidase in Methemoglobinemia

A

PaO2=Normal
SaO2=Decreased
OBC=Left-Shifted
Cytochrome oxidase=Normal

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26
Q

PaO2, SaO2, OBC, and Cytochrome oxidase in CN poisoning

A

PaO2=Normal
SaO2=Normal
OBC=Normal
Cytochrome oxidase=Inhibited

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27
Q

Examples of uncoupling agents and MOA

A

Alcohol, Dinitrophenol, and Salicylates

Uncouple proton gradient across inner mitochondrial membrane (any rxn that makes NADH or FADH2 revs up –> hyperthermia)

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28
Q

Ischemic colitis

A

Watershed infarct at splenic flexure at junction of SMA/IMA

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29
Q

ST-segment depression ECG

A

Subendocardial ischemia

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30
Q

Nephron locations susceptible to hypoxia

A

Proximal tubule

Thick ascending limb

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31
Q

What are the most adversely affected cell in tissue hypoxia?

A

Neurons (irreversible damage after 5 mins)

32
Q

What hepatocytes are most susceptible to hypoxia?

A

Zone III hepatocytes (drain into venules, furthest from portal triad)

33
Q

What is the primary source of ATP in hypoxia?

A 
Anaerobic glycolysis
(lactic acidosis)
34
Q

Consequences of increased intracellular lactate

A

low pH denatures structural/enzymatic proteins

35
Q

What is the mechanism of cellular swelling in tissue hypoxia?

A

Na/K pump impaired (H2O enters cell)

36
Q

What occurs in irreversible cell injury due to hypoxia?

A

Ca ATPase pump impaired

~cannot pump Ca out of cytosol

37
Q

Effects of increased Ca in cytosol

A 
Activates phospholipase (increases cell and membrane permeability)
Activates proteases (damage cytoskeleton)
Activate endonucleases (karyolysis)
Activates caspases (induce apoptosis)
38
Q

Effects of increased Ca in mitochondria

A

Increased permeability to cytochrome c

Apoptosis

39
Q

Definition of free radical

A

single unpaired electron in outer orbital

40
Q

What are the primary targets of free radicals?

A

Membranes and Nucleic acids

41
Q

What transitional metals generate hydroxyl free radicals?

A

Fe and Cu (Fenton reaction)

42
Q

Which free radical is the most destructive?

A

Hydroxyl

43
Q

Oxidized LDL

A

Free radical important in atherogenesis

44
Q

Super-Oxide Dismutase

A

Neutralizes superoxide free radicals

45
Q

Glutathione peroxidase

A

Neutralizes H2O2, OH, and NAPQ1 (acetaminophen) free radicals

46
Q

Catalase

A

Neutralizes H2O2

47
Q

Vitamin E as an antioxidant

A

Prevents free radical injury to cell membranes

48
Q

Vitamin C as an antioxidant

A

Best neutralizer of hydroxyl free radicals

49
Q

Why do smokers have decreased vitamin C?

A

Vit. C used up neutralizing free radicals generated from cigarette smoke

50
Q

Acetaminophen poisoning

A

Diffuse chemical hepatitis due to NAPQ1

51
Q

How does how is acetaminophen toxicity potentiated in alcoholics?

A

Alcohol induces CYP2E1 which forms NAPQ1

52
Q

What is the treatment for acetaminophen poisoning?

A

N-Acetylcysteine

Provides cysteine for glutathione synthesis

53
Q

Acetaminophen and NSAIDs free radical damage to kidneys

A

Renal papillary necrosis

54
Q

CCL4 as a free radical

A

Solvent in dry-cleaning industry
CypP450 converts to free radical
Causes liver necrosis with fatty change

55
Q

Retinopathy of prematurity

A

Destruction of retinal cells by superoxide free radicals after Oxygen treatment of RDS

56
Q

Iron overload free radicals

A

Intracellular Fe generates OH free radicals via Fenton reaction
Results in cirrhosis and pancreas dysfunction

57
Q

Copper overload free radicals (ie Wilson’s disease)

A

Copper excess in hepatocytes generates OH free radicals

Results in cirrhosis and damage to lenticular nuclei in brain

58
Q

What causes megamitochondria in hepatocytes?

A

Salicylates and alcohol

59
Q

Phenobarbital toxicity

A

Alcohol inhibits CYP2B2 (which inactivates Phenobarbital)

If both are consumed in large amounts toxicity occurs

60
Q

Phenytoin effect on CYPs

A

Induces CYP3A4

Results in increased metabolism of antiepileptic agents (including itself)

61
Q

What effect does P450 induction have on the SER?

A

Hyperplasia
Increased drug metabolism
Decreased drug effectiveness

62
Q

Inhibitors of P450s

A

Omeprazole
H2-blockers (cimetidine)

Decreased drug metabolism
Increased drug toxicity

63
Q

I-Cell Disease

A 
Defect in posttranslational modification of lysosomal enzymes in Golgi
PHOSPHOTRANSFERASE DEFICIENCY (Mannose residues not phosphorylated)
Without mannose-6-P, lysosomal enzymes dumped into blood
64
Q

Chediak-Higashi Syndrome (CHS)

A

Giant lysosomal granules (fusion defect)
Defect in formation of phagolysosomes
Susceptible to S. aureus infections

65
Q

What drugs inhibit the synthesis of tubulin and in what phase of the cell cycle?

A

Etoposide and Bleomycin

G2 phase

66
Q

What drugs act on mitotic spindle?

A

Vinca alkaloids (inhibit assembly)
Colchicine (inhibit assembly)
Paclitaxel (inhibit disassembly)

67
Q

Ubiquitin

A

Marker for damaged intermediate filaments (tags for destruction)

68
Q

Mallory bodies

A

Ubiquitinated intermediate filaments in hepatocytes in alcoholic liver disease
Eosinophilic inclusion bodies in hepatocytes

69
Q

Lewy bodies

A

Ubiquitinated neurofilaments that are present in Parkinson’s

70
Q

Fatty liver formation in Kwashiorkor

A

Increased intake of carbs - no protein

Increased DHAP –> more TGs

71
Q

How does alcohol consumption lead to fatty liver?

A

1) Increased NADH from alcohol metabolism
Accelerates conversion of DHAP to G3-P –> TG

2) Increased fatty acids

72
Q

Ferratin

A

Fe-binding protein in macrophages and hepatocytes

73
Q

Ferratin

A

Fe-binding protein in serum

Decreased in iron deficiency anemia

74
Q

Hemosiderin

A

Ferritin degradation product

Stains with Prussian blue

75
Q

Dystrophic calcification

A

Calcification of necrotic tissue
Serum calcium and phosphate are normal
(Ca enters cells and binds phosphate released from damaged membranes)

76
Q

Metastatic calcification

A

Calcification of normal tissue

Increased serum Ca or PO4

77
Q

Nephrocalcinosis

A

Metastatic calcification of collecting ducts

Produces diabetes insipidus

Evan's Step 1 Prep Material (72 decks)

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