Renal 4 Flashcards

1
Q

What syndrome may be a complication of SLE or other autoimmune disorders?

A

> SLE patients have antiphospholipid antibodies, so they are at risk of developing a hypercoagulable state by activating phospholipid-dependent coagulation pathways.
Antiphospholipid Antibody Syndrome occurs in the setting of venous/arterial thromboembolism and/or recurrent pregnancy loss.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is Tumor lysis syndrome?

A

When tumors are treated w/ chemotherapy, they can lyse and release intracellular ions (K, PO4, uric acid). Urate can precipitate in the acid environment of the distal tubules and collecting ducts, thus obstructing these segments w/ urate crystals, possibly causing Acute renal failure.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are the 3 main causes of Metabolic Alkalosis?

A

1) Vomiting, Nasogastric suctioning: H+ and Cl- losses increases serum alkali. – hypotensive, low urine Cl.
2) Thiazide, Loop diuretics: volume depletion causes aldosterone secretion, loss of H+ and K+ – hypovolemic, high urine Cl.
3) Inc. Mineralocorticoid: inc. Na reabsorption, inc. H+ and K+ losses, relative inc. serum HCO3 – HTN, high urine Cl.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What parts of the kidney is most susceptible to reflux-induced damaged in pyelonephritis?

A

The compound papillae at the upper and lower poles are always open, so they are more commonly damaged by reflux. They appear as dilated calyces along w/ cortical scarring from ongoing injury.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What 2 factors should be determined to identify the cause of metabolic alkalosis?

A

> Volume status (hypo/hypervolemic)

>Urine Cl- concentration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

How can hypovolemia (vomiting, diarrhea) result in Acute kidney injury?

A

Hypovolemia results in dec. RPF and GFR. The subsequent inc. ATII leads to efferent arteriolar constriction, thus inc. FF and maintaining GFR at near normal levels. As RPF continues to decline w/ vomiting and diarrhea, the inc. glomerular oncotic pressure will overwhelm the compensatory inc. hydrostatic pressure. This will cause super dec. GFR and thus renal failure.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

How does IgA nephropathy (Berger disease) present? What is a common associated syndrome?

A

> Painless hematuria ff. a URT infection. Hematuria will last days before temporarily subsiding, then it will return every few months or w/ another URI.
If w/ accompanying extrarenal ssx (abd. pain, purpura, arthralgia), the syndrome is HSP.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is diagnostic for Nodular glomerulosclerosis seen in Diabetic nephropathy?

A

Kimmelstiel-Wilson nodules
>progressive expansion of mesangium
>(+)PAS, eosinophilic and H and E stain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What side effects can Foscarnet toxicity cause?

A

Forscarnet is sometimes used for ganciclovir-resistant CMV infections. It can chelate Ca and promote nephrotoxic renal Mg wasting, leading to Hypocalcemia and Hypomagnesemia, w/c can cause seizures.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

How does renal osteodystrophy become a complication for CKD?

A

CKD causes hyperphosphatemia due to dec. PO4 clearance, and PO4 can bind to free Ca, causing hypocalcemia. Loss of normal renal parenchyma dec. active Vit D synthesis, so there’s dec. Ca absorption. To compensate, inc. PTH prodn causes bone resorption to surpass formation, resulting in osteopenia or osteomalacia.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is the pathogenesis of HSP?

A

HSP is the MC small vessel vasculitis in kids, often ff. URI. An antigen stimulates IgA prodn, and IgA-containing immune complexes deposit on vessel walls, inducing an inflammatory rxn in many organs.
>Abd. pain in GIT, Berger dse, purpura on buttocks, arthralgias.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

3 Stages of Acute Tubular Necrosis

A

1) Initiation: ischemic injury to renal tubules.
2) Maintenance: oliguric stage; dec. UO, fluid overload, inc. BUN/Crea; Hyperkalemia (potential for Vtach).
3) Recovery: gradual inc. UO w/ high-volume diuresis; possible hypokalemia due to slow recovery of tubular fxn.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly