Sodium (renal III) Flashcards

1
Q

Major physiologic trigger for release of ADH? Sensed by what?

A

plasma osmolality (VERY low E

sensed by hypothalamus

released by posterior pituitary

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2
Q

Symptoms of hyponatremia?

A

malaise, stupor, coma, nausea

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3
Q

What are situations that you may see high serum osmolality along with hyponatremia?

A

hyperglycemia or mannitol

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4
Q

What are situations that you may see hyponatremia with normal serum osmolality? ?

A

hyperlipidemia

hyperproteinemia (multiple myeloma)

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5
Q

common causes of SIADH?

A

drug induced (carbamazepine, cyclophosphamide)

paraneoplastic (small cell lung cancer)

CNS

pulmonary disease

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6
Q

Special treatment of SIADH?

A

demeclocycline

(tetracycline antibiotic) - ADH antagonist

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7
Q

Symptoms of hypernatremia?

A

irritability, stupor, coma

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8
Q

Common causes hypernatremia?

A
  • water loss
  • diabetes insipidus
    • acquired: hypercalcemia, hypokalemia, lithium, amphoteracin B
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9
Q

Treatments for nephrogenic DI?

A

thiazide diuretics (incrase proximal Na/H20 reabsorption)

NSAIDS (inhibit prostaglandins, which are ADH antag)

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10
Q

“ultrafiltrate” is composed of what substance?

A

water, electrolytes, glucose, amino acids

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11
Q

The epithelium in the glomerulus is composed of what cell type?

A

podocyte

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12
Q

What are filtration layers to the glomerulus?

A
  • Endothelium (fenestrated)
    • only small molecules (<40nm) can pass through
    • repels RBC, WBC, platelets
  • basement membrane
    • negatively charged (type IV collagen wrapped in heparan sulfate)
    • repels (-) charged molecules like albumin
  • epithelium (podocytes)
    • food processes that wrap around capillaries
    • slitsbetween foot processes filter - further size barrier
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13
Q

General difference between nephritic & nephrotic syndromes?

A
  • nephritic
    • RBC casts
    • mild proteinuria (< 3.5)
    • renal failure
  • nephrotic syndrome
    • massive proteinuria
    • hyperlipidemia
    • protein in urine (< 3.5)
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14
Q

What are the two mechanisms that lead to edema in nephrotic syndrome?

A

decreased plasma oncotic pressure d/t loss of albumin

the decrease in ECV causes a decrease in GFR which stimulates the RAAS and leads to Na/H20 retention

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15
Q

why do you see hyperlipidemia in patients with nephrotic syndrome? This leads to what?

A

the loss of albumin causes the liver to become to be active as it tries to replace it (but it cannot)

however, b/c the increased liver metabolic activity, you will see hyper lipidemia (high levels total cholesterol & HDL)

fatty casts & oval fat bodies in the urine (maltese cross)

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16
Q

Why can patients with nephrotic syndrome develop a pulmonary embolism?

A

losing anti-thrombin III in the urine

causes a hypercoaguable state that predisposes patients thrombosis

17
Q

Why do patients with nephritic syndrome excrete less protein in their urine than patients with nephrotic syndrome?

A

Nephritic syndrome decreases GFR, which decreases the amout of protein they are able to excete per day

this is also why you see an increase in the BUN/Cr ratio, oliguria, and increased hydrostatic pressure (which can cause hypertension & edema)

18
Q

What is the condtion that is basically IgA nephropath with extrarenal involvement?

A

Henich-Schonlein Purpura

MC childhood systemic vasculitis

19
Q

Focal segmental glomerulosclerosis is associated with what conditions?

A

HIV

Sickle Cell Patients

Heroin users

massive obesity

pts. on interferon treatment

20
Q

What are the respective findings in renal biopsy of membranous nephropathy for each of the following methods:

light microscopy

electron microscopy

immunofluorescence

A
  • light microscopy
    • capillary / BM thickening
  • electron microscopy
    • subepithelial deposits
  • immunofluorescence
    • granular IgG/C3
21
Q

What are the 3 secondary causes of membranous nephritis?

A

tumor

hepatitis

rheumatoid arthritis

22
Q

MPGN type 1 is associated with what conditions?

A

hepatitis C & B

23
Q

What antibody is commonly seen in patients with MPGN type II?

A

C3 nephritic factor

C3 convertase (activates alternative pathway) stabilizing antibody