High yield (cell injury) Flashcards

1
Q

If the oxygen partial pressure (in the plasma) is decreased, the oxygen saturation (on Hb) MUST also decrease.

A

Thrombosis in a muscular artery is the most common cause of ischemia

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2
Q

Hypoxemia (decrease oxygen partial pressure) is a cause of hypoxia

A

Respiratory acidosis => CO2 inc => pO2 dec (and vice versa).

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3
Q

Hypoxemic patient that gets 100% oxygen and his pO2 didn’t increase => shunt => ventilation defect (ARDS, hyaline membrane disease).

A

Perfusion defect (PE) => inc dead space (100% O2 will get the pO2 up)

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4
Q

Diffusion defect (sarcoidosis, pulmonary edema)

A

J reflex innervated by the Kent nerve, cause dyspnea (fluid in lung interstitium irritating the J receptors).

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5
Q

Anemia (Hb related problem) => pO2 normal, saturation normal, Hb decreased => exertional dyspnea.

A

House fire produces tissue hypoxia in 2 ways: CO poisoning (saturation dec, give 100% oxygen) and CN poisoning. Both inhibit cytochrome oxidase.

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6
Q

Cyanosis is the clinical evidence of decreased saturation. Red pigment hides the cyanosis in CO poisoning (most frequent symptom is headache).

A

MetHb => saturation decreased because the Hb is Fe3 and not Fe2 (chocolate color blood) => 100% oxygen doesn’t improve cyanosis. Treatment is IV methylene blue, vitmamin C (also but not main)

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7
Q

Sulfa and nitro drugs (oxidizing agent): 1. produce MetHb. 2. Hemolytic anemia, G6PD deficiency.

A

MetHb common in HIV, because we use sulfa drugs to treat pneumocystis carinii

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8
Q

Right shift curve: 2,3BPG inc, high altitude, acidosis, fever.

A

Left shift curve: CO, MetHb, HbF, 2,3BPG dec, alkalosis.

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9
Q

Uncoupling agents (mitochondrial membrane permeable to protons): dinitrophenol (wood preserving), alcohol, salicylates. To compensate, NADH, FAD producing systems (which produce protons) increase => hyperthermia (alcoholics are more susceptible to heatstroke).

A

Respiratory acidodis = Hb normal, Saturation dec, pO2 dec

Anemia = Hb decrease, saturation normal, pO2 normal

CO + MetHb = Hb normal, saturation dec, pO2 normal

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10
Q

Anaerobic glycolysis => lactate acidosis => denature proteins + enzymes (can’t even
auto digest itself) => coagulation necrosis => infarct.

A

Anaerobic glycolysis => ATP pump malfunction, decrease ATP => Na enters cells => water follows ! cellular swelling (reversible!).

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11
Q

Irreversible cell damage: ATP decrease => Ca ATPase dec => intracellular Ca inc => activates nuclear enzymes ( => pyknosis), phosphlipase (=> cell membrane damage)
=> pancreatitis.

A

Cell death: CK, GOT, GLT, amylase increase.

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12
Q

Lipofuscin (wear and tear pigment) is a brown pigment in atrophic organs in elderly. It cannot be digested. Hemosiderin or bilirubin can also produce a brown pigment.

A

Reperfusion injury (oxygen radicals) can be caused after giving TPA for coronary thrombosis, then oxygenated blood go to the injured cardiac muscle.

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13
Q

IRDS: retinopathy of prematurity (oxygen radicals destroying the retina, blindness) and bronchopulmonary dysplasia (fibrosis)

A

Most common cancer of radiation is Leukemia

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14
Q

Iron overload cause free radicals => cirrhosis, restrictive cardiomyopathy, pancreas failure => malabsorption + diabetes

A

Acetoaminaphen (Tylenol) is the #1 cause of drug induced fulminant hepatitis (damage around central vein). Treatment: N-acetyl cystein (inc glutathione)

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15
Q

Neutralization of superoxide is by superoxide dismutase (turns into peroxide).

A

PPP generates Glutathione and NADPH.

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16
Q

CCL4 can also be converted to a free radial (CCL3) ! fulminant hepatitis.

A

Acetoaminaphen (radicals) + Aspirin (dec PG) => kidney damage (renal medulla)

17
Q

Di-george syndrome: absence of thymus, cause tetany.

A

Councilman body in Hepatitis: apoptotic eosinophilic cell with no nucleus

18
Q

Coagulation necrosis - Pale infarct: Heart, kidney, spleen, liver

Hemorrhagic infarct: Bowel, testicle (torsion), lungs.

A

Vegetation of acute rheumatic fever rarely embolize. Infective endocarditis does.

19
Q

Mitral stenosis can cause thrombi in left atrium => atrial fibrillation

A

The arrhythmia most associated with systemic emboli is atrial fibrillation

20
Q

Most common cause of non traumatic amputation is diabetes (inc ATH of popliteal
artery)

A

Most common cause of bowel infarction: #1: adhesions of previous surgery, #2: piece of small bowel trapped in an indirect inguinal hernia.

21
Q

Liquefactive necrosis is related to an infection where neutrophils are involved (acute inflammation, lung/brain abscess, cellulites by strep.) and also related to brain infarct.

A

Granulmatose necrosis: caseous – mycobacteria or systemic fungal infection. Non caseous – sarcoidosis.

22
Q

Epigastric distress with pain radiating to the back => pancreatitis (retroperitonea

A

Enzymatic fat necrosis (pancreas) or traumatic fat necrosis (breast, adipose) ca both calcify (look like cancer on X-ray) but it’s painful unlike cancer.

23
Q
  • Calcium bound to fatty acid = saponification (chalky white areas on X-ray).
  • Bluish discoloration on histologic sections is calcium (dystrophic calcification).
  • Fibrinoid necrosis (looks like fibrin but isn’t): immunological diseases (rhematic fever,
    rheumatic arthritis, glomerulonephritis, SLE, vasculitis).
  • Palpable purpura: small vessel vasculitis, hypersensitivity type 3. Conditions that present with palpable purpura include: Henoch-Schönlein purpura, subacute bacterial endocarditis and Rocky Mountain spotted fever.
A
  • Immune complex => activate alternative complement system=>! C5a => chemotaxis of neutrophils that cause the actual damage.
  • Yellow fever (Arbovirus) damages the liver zone 2 (mid-zone necrosis)
24
Q
  • Alcoholics have fasting hypoglycemia, lactic acidosis (inc NADH shift pyruvate to lactate so there is no substrate for GNG), keto-acidosis (B-hydroxybutyrate).
  • Restriciting CH will reduce the synthesis of VLDL (Glycolysis provides glycerol 3 phosphate, which is the backbone of TAG which is incorporated into VLDL).
  • Kwashiorkor: reduce protein intake => no apo-proteins => huge fatty liver: Reduce protein intake => no oncotic pressure => Ascites.
  • Ferritin (soluble iron storage) is a marker for diagnosing iron deficiency anemia or hemosiderosis, hemochromatosis: Hemosiderin (insoluble iron storage), stored in MP and BM. Stained with Prussian blue.
A
  • Dystrophic calcification: damaged tissue gets calcified (fat necrosis, ATH, aortic
    stenosis, hemolytic anemia), normal serum calcium.
  • Metastatic calcification: hypercalcemia or hyperphosphatemia => calcium deposits in
    normal tissue.
  • Congenital bicuspid aortic valve is the most common cause of aortic stenosis.
  • Spectrin is needed to keep a bi-concave disc, if it’s defective => spherocytosis.
  • Ubiquination - Mallory bodies = alcoholic hepatitis
  • Neurofibrillaty tangles (tau protein) = Alzheimer, Creutzfeldt-Jakov disease.
  • Lewy body = Parkinson (substantia nigra, dopamine)
25
Q
  • Labile cells = division is via stem cells (BM, skin, intestinal crypts), in cell cycle.
  • Cell cycle specific or non specific drugs => BM suppression, diarrhea, rash.
  • Stable cells = mostly in G0, but can be stimulated to divide (liver, spleen, kidney, smooth muscle, endometrium)
  • Permanent cells = can’t get into the cell cycle (striated and cardiac muscles, neurons), can go through hypertrophy.
  • Hyperplasia = increase in number, hypertrophy = increase in size.
  • The length of the cell cycle is decided by the length of the G1 stage.
  • Glucagon is a phosphorylator, insulin is a dephosphorylator.
A
  • Rb (chr.13) prevents the cell from going into S phase. When phosphorylated by CDK, it’s inactive. p53 (chr.19) induces a CDK inhibitor, gives time to detect and correct defects before entry to S phase.
  • HPV E6 suppresses p53, HPV E8 suppresses Rb.
  • No Rb protein => Retinoblastoma, osteogenic sarcoma, breast cancer.
  • Codman’s triangle seen in: osteosarcoma, Ewing sarcoma, subperiosteal abscess.
  • Vinca Alkaloids (periwinkle plant), Paclitaxel (chemotherapy, yew tree), Colchicine, Griseofulvin (M phase), Etoposide (G2 phase), MTX, Bleomycin (S phase)
  • MTX, used in rheumatoid arthritis, inhibits DHF reductase => can cause macrocytic anemia.
26
Q
  • Atrophy = decrease in tissue mass, decrease cell size, less mitochondria.
  • Hydronephrosis is mostly caused by renal stones => increase pressure => ischemia => atrophy of renal tubules.
  • ATH, Alzheimer (B-amyloid protein, layers 3,5,6 destroyed), ALS => brain atrophy, neuron degeneration.
  • Hypopituitarism => adrenal gland atrophy (zona reticularis and fasiculata ONLY)
  • Oral thyroid => thyroid atrophy.
  • CF (Chr.7) => block lumen => pancreas atrophy
  • Renal vascular hypertension => kidney atrophy, other kidney hypertrophy (inc renin)
  • If you block G2 phase, you have 4n chromosomes (no mitosis)
  • Hyperplasia left unchecked is predisposing for cancer (EXCEPT prostate)
  • Unopposed estrogen (no progesterone) causes endometrial hyperplasia => atypical hyperplasia => cancer.
  • Gravid uterus (after delivery): 50% hypertrophy, 50% hyperplasia.
  • RBC hyperplasia in BM may be caused by COPD
A
  • Erythropoetin is made in the endothelial cells of the peri-tubular capillary.
  • Psoriasis is an unregulated proliferation of squamus cells in the skin (hyperplasia). Treatment: MTX (works on the basal cells).
  • All hormone stimulated glands go through hyperplasia, not hypertrophy.
  • Urinary bladder goes through hypertrophy of smooth muscle cells related to afterload caused by urethra narrowing.
  • H. Pylori is the most common cause of adenocarcinoma of the stomach.
  • Clonorchis Sinensis (Chinese liver fluke) is associated with cholangiocarcinoma
  • Schistosome Haematubium causes squamus metaplasia (instead of transitional) in the
    urinary bladder => SCC.
  • Dysplasia = atypical hyperplasia, precursor for cancer.
  • Actinic (solar) keratosis is premalignant to SCC of the skin, related to chronic sun exposure and excess keratin. If off, it grows back.
  • No premalignant lesion to basal cell carcinoma. It is more common.