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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
PaO2, SaO2, OBC, and Cytochrome oxidase in Methemoglobinemia
PaO2=Normal SaO2=Decreased OBC=Left-Shifted Cytochrome oxidase=Normal
26
PaO2, SaO2, OBC, and Cytochrome oxidase in CN poisoning
PaO2=Normal SaO2=Normal OBC=Normal Cytochrome oxidase=Inhibited
27
Examples of uncoupling agents and MOA
Alcohol, Dinitrophenol, and Salicylates Uncouple proton gradient across inner mitochondrial membrane (any rxn that makes NADH or FADH2 revs up --> hyperthermia)
28
Ischemic colitis
Watershed infarct at splenic flexure at junction of SMA/IMA
29
ST-segment depression ECG
Subendocardial ischemia
30
Nephron locations susceptible to hypoxia
Proximal tubule | Thick ascending limb
31
What are the most adversely affected cell in tissue hypoxia?
Neurons (irreversible damage after 5 mins)
32
What hepatocytes are most susceptible to hypoxia?
Zone III hepatocytes (drain into venules, furthest from portal triad)
33
What is the primary source of ATP in hypoxia?
``` Anaerobic glycolysis (lactic acidosis) ```
34
Consequences of increased intracellular lactate
low pH denatures structural/enzymatic proteins
35
What is the mechanism of cellular swelling in tissue hypoxia?
Na/K pump impaired (H2O enters cell)
36
What occurs in irreversible cell injury due to hypoxia?
Ca ATPase pump impaired | ~cannot pump Ca out of cytosol
37
Effects of increased Ca in cytosol
``` Activates phospholipase (increases cell and membrane permeability) Activates proteases (damage cytoskeleton) Activate endonucleases (karyolysis) Activates caspases (induce apoptosis) ```
38
Effects of increased Ca in mitochondria
Increased permeability to cytochrome c | Apoptosis
39
Definition of free radical
single unpaired electron in outer orbital
40
What are the primary targets of free radicals?
Membranes and Nucleic acids
41
What transitional metals generate hydroxyl free radicals?
Fe and Cu (Fenton reaction)
42
Which free radical is the most destructive?
Hydroxyl
43
Oxidized LDL
Free radical important in atherogenesis
44
Super-Oxide Dismutase
Neutralizes superoxide free radicals
45
Glutathione peroxidase
Neutralizes H2O2, OH, and NAPQ1 (acetaminophen) free radicals
46
Catalase
Neutralizes H2O2
47
Vitamin E as an antioxidant
Prevents free radical injury to cell membranes
48
Vitamin C as an antioxidant
Best neutralizer of hydroxyl free radicals
49
Why do smokers have decreased vitamin C?
Vit. C used up neutralizing free radicals generated from cigarette smoke
50
Acetaminophen poisoning
Diffuse chemical hepatitis due to NAPQ1
51
How does how is acetaminophen toxicity potentiated in alcoholics?
Alcohol induces CYP2E1 which forms NAPQ1
52
What is the treatment for acetaminophen poisoning?
N-Acetylcysteine Provides cysteine for glutathione synthesis
53
Acetaminophen and NSAIDs free radical damage to kidneys
Renal papillary necrosis
54
CCL4 as a free radical
Solvent in dry-cleaning industry CypP450 converts to free radical Causes liver necrosis with fatty change
55
Retinopathy of prematurity
Destruction of retinal cells by superoxide free radicals after Oxygen treatment of RDS
56
Iron overload free radicals
Intracellular Fe generates OH free radicals via Fenton reaction Results in cirrhosis and pancreas dysfunction
57
Copper overload free radicals (ie Wilson's disease)
Copper excess in hepatocytes generates OH free radicals | Results in cirrhosis and damage to lenticular nuclei in brain
58
What causes megamitochondria in hepatocytes?
Salicylates and alcohol
59
Phenobarbital toxicity
Alcohol inhibits CYP2B2 (which inactivates Phenobarbital) | If both are consumed in large amounts toxicity occurs
60
Phenytoin effect on CYPs
Induces CYP3A4 | Results in increased metabolism of antiepileptic agents (including itself)
61
What effect does P450 induction have on the SER?
Hyperplasia Increased drug metabolism Decreased drug effectiveness
62
Inhibitors of P450s
Omeprazole H2-blockers (cimetidine) Decreased drug metabolism Increased drug toxicity
63
I-Cell Disease
``` 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
Chediak-Higashi Syndrome (CHS)
Giant lysosomal granules (fusion defect) Defect in formation of phagolysosomes Susceptible to S. aureus infections
65
What drugs inhibit the synthesis of tubulin and in what phase of the cell cycle?
Etoposide and Bleomycin | G2 phase
66
What drugs act on mitotic spindle?
Vinca alkaloids (inhibit assembly) Colchicine (inhibit assembly) Paclitaxel (inhibit disassembly)
67
Ubiquitin
Marker for damaged intermediate filaments (tags for destruction)
68
Mallory bodies
Ubiquitinated intermediate filaments in hepatocytes in alcoholic liver disease Eosinophilic inclusion bodies in hepatocytes
69
Lewy bodies
Ubiquitinated neurofilaments that are present in Parkinson's
70
Fatty liver formation in Kwashiorkor
Increased intake of carbs - no protein | Increased DHAP --> more TGs
71
How does alcohol consumption lead to fatty liver?
1) Increased NADH from alcohol metabolism Accelerates conversion of DHAP to G3-P --> TG 2) Increased fatty acids
72
Ferratin
Fe-binding protein in macrophages and hepatocytes
73
Ferratin
Fe-binding protein in serum Decreased in iron deficiency anemia
74
Hemosiderin
Ferritin degradation product | Stains with Prussian blue
75
Dystrophic calcification
Calcification of necrotic tissue Serum calcium and phosphate are normal (Ca enters cells and binds phosphate released from damaged membranes)
76
Metastatic calcification
Calcification of normal tissue | Increased serum Ca or PO4
77
Nephrocalcinosis
Metastatic calcification of collecting ducts | Produces diabetes insipidus

Evan's Step 1 Prep Material (72 decks)

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