Clues From Heather Flashcards

1
Q

Corticosteroid (= prednisone) therapy can increase which type of WBC?

A

Neutrophils

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2
Q

Steps for Granuloma formation

A

Pathogen (= TB) triggers CD4+ T cells to release IFN gamma

IFN gamma activates macrophages

Macrophages differentiate into epithelioid histiocytes

Epithelioid histiocytes join with horseshoe-shaped, multinucleated Langhans giant cells to form granuloma

(Langhans giant cells = fused, activated macrophages)

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3
Q

What interleukin is produced by CD4, CD8, and NK cells?

A

IL-2

Strong pro-inflammatory & some anti-inflammatory
High-dose IL-2 used in treatment of advanced renal cell carcinoma & metastatic melanoma.
-> can lead to long-lasting remission d/t increased cytotoxic activity of NK cells against the tumor

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4
Q

PTH function in bones

A

Indirect activation of osteoclasts
-> increase bone resorption

Releases Ca and phosphorus

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5
Q

PTH function in kidneys

A

Decr reabsorption of phosphate in PCT
Incr reabsorption of calcium in DCT and CD

Upregulates 1-alpha-hydroxylase => more active vit D (1,25-hydroxyvitamin D)

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6
Q

Causes of Relative erythrocytosis
(Normal RBC mass)

A

Dehydration
Excessive diuresis

(Incr total RBC mass indicates absolute erythrocytosis)

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7
Q

Causes of Absolute erythrocytosis
(True increase in RBC mass)

A

Polycythemia Vera
- all 3 cell lines increase

Secondary erythrocytosis
- only RBC increases, but platelets and WBCs are normal
- d/t hypoxia or EPO-producing tumors

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8
Q

Kinesin
- what is it?
- function?
- example?

A

Microtubule-associated ATP-powered motor protein

Facilitates anterograde transport towards “plus” end of microtubules

EX: NT-containing secretory vesicles down axons to synaptic terminals

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9
Q

Alternative Dx, presenting with:
- solitary brain lesions
- HIV/AIDS or immunocompromised
- low CD4+ count
- high viral load

A

Primary CNS lymphoma (= non-Hodgkin lymphoma)
- most common for all S&Sx listed

Others:
Bacterial abscess
Cerebral toxoplasmosis
Primary brain tumors (= glioblastoma)
Metastatic lesions

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10
Q

5 Steps of urea cycle

A

1) entry into urea cycle
- create carbamoyl phosphate
- substrates = HCO3 & NH3
- product = carbamoyl phosphate

2) carbamoyl phosphate + ornithine => citrulline

3) citrulline + Aspartate => arginosuccinate

4) hydrolysis of arginosuccinate => arginine + fumarate

5) hydrolysis of arginine => urea + ornithine

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11
Q

5 Enzymes and locations for urea cycle

A

1) carbamoyl phosphate synthetase 1
(in mitochondria of liver)

2) ornithine carbamoyltransferase
(Mitochondria)

3) argininosuccinate synthetase
(Cytosol)

4) arginosuccinase
(Cytosol)

5) arginase
(Cytosol)

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12
Q

Vit D deficiency

A

Decr intestinal Ca absorption
Hypocalcemia
Incr PTH secretion
Incr PTH-mediated bone resorption

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13
Q

Wiskott-Aldrich syndrome triad

A

Thrombocytopenia (from birth)
Eczema (develop around 6 to 12 months of age)
Combined B and T cell deficiency (develop around 6 to 12 months of age)

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14
Q

Acid-base for salicylate poisoning

A

Primary respiratory alkalosis
Primary anion gap metabolic acidosis

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15
Q

Electrolytes levels in Fanconi syndrome

A

d/t generalized PCT dysfunction

Urinary loss of:
- glucose
- phosphate
- potassium
- water
- amino acids

Serum chloride rises to maintain electronegative balance from bicarb loss
Serum glucose remains normal d/t counterregulatory mechanisms.

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16
Q

Type 2 RTA

A

Unable to reabsorb bicarb in PCT
Commonly a part of Fanconi syndrome

17
Q

Fanconi syndrome

A

Generalized resorption dysfunction (= tubular damage) affecting PCT

  • decr HCO3 -> metabolic acidosis
  • incr serum Cl
  • serum glucose remains normal
  • low serum phosphate -> rickets
  • low serum potassium -> muscle weakness
  • aminoaciduria
  • growth failure (d/t chronic acidosis, hypophosphatemia, hypokalemia)