Palmer Clin Med Flashcards

1
Q

What are findings that can point to analgesic nephropathy considering the nonspecific renal picture?

A

most patients women between 30-70
Hx of headaches or back pain leading to use
other somatic complaints - malaise, weakness
ulcer like symptoms or hx of PUD

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2
Q

What are the histologic findings of lead nephropathy?

A

early PROXIMAL tubule injury

intranuclear inclusion bodies of lead-protein complex

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3
Q

What finding is present in lead nephropathy that is different than most other syndromes with similar symptoms?

A

increased uric acid in blood
lots present with gout too
use chelation test to diagnose

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4
Q

What two other syndromes are commonly present in patients with Sjogrens syndrome presenting with chronic TIN?

A

Type 1 RTA

nephrogenic DI

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5
Q

What is the definition of CKD?

A

GFR <60 or evidence of kidney damage for more than 3 months

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6
Q

What does persistent proteinuria in the setting of normal or increased GFR indicate?

A

stage 1 CKD

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7
Q

What happens with sodium and water imbalance in CKD and how should it be managed?

A

limited range for excretion
monitor salt intake - be careful of patients weight, give more if losing, give less if gaining
GFR <20 needs diuretics too
Follow Na and adjust water intake if necessary

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8
Q

How are diuretics used in management of CKD?

A

thiazides and K sparing not potent enough
K sparing can cause hyperkalemia
use loops - furosemide! - high doses due to decreased delivery - can add metolozone

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9
Q

What kind of potassium imbalances are present in CKD and how should they be managed?

A

normal until GFR <10
hyperkalemia at later stages suggests TIN or RAAS disturbance
low K diet, then admin of loop diuretic (increases distal Na delivery)
if acidotic - admin bicarb - increases distal Na and causes K to shift into cells

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10
Q

If K is still high after all the initial therapies, what may have to be given?

A

Kayexalate = sodium polystyrene sulfonate - K binding resin

give with bowel cathartic to prevent constipation - but not one with Mg (risk of hyperMg with CKD)

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11
Q

How is metabolic acidosis involved in CKD?

A

can’t regenerate bicarb, decreased ammonium, decreased H+ excretion
non gap early, anion gap later
can lead to bone resorption and protein catabolism
sodium bicarb tablets - monitor for volume overload

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12
Q

What management is available for maintaining phosphate levels at normal in CKD?

A

low phosphate diet
phosphate binders - high CaPhosphate product use non Ca binder, low use calcium containing binder
then normalize calcium
then look at PTH

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13
Q

What metabolic bone diseases are present in CKD?

A

osteitis fibrosis cystica (high PTH) - high bone turnover, Brown tumors
osteomalacia - increased unmineralized osteoid - usually accompanied by high turnover dz = mixed osteodystrophy
adynamic bone dz - stage 5 CKD, low turnover, can happen with any therapies aimed at decreasing PTH

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14
Q

If a patient’s anemia is not responsive to admin of Epo, what other causes should be considered?

A

iron deficiency
osteitis fibrosa cystica
Al overload

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15
Q

What are the cardiovascular manifestations of uremia?

A

pericarditis
volume overload
HTN
Accelerated atherosclerosis

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16
Q

What are the skin manifestations of uremia?

A

pruritis

skin pigmentation

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17
Q

What are the neurologic manifestations of uremia?

A

encephalopathy
seizures
peripheral neuropathy

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18
Q

What are the GI manifestations of uremia?

A

nausea, vomiting

gastritis, colitis

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19
Q

What are the pulmonary manifestations of uremia?

A

pleuritis

pneumonitis

20
Q

What are the endocrine manifestations of uremia?

A

menstrual disturbance, anovulation

decrease in testosterone and spermatogenesis

21
Q

What are the indications for hemodialysis in CKD?

A

Fluid and electrolyte disturbances refractory to
medical therapy
Pericarditis
Encephalopathy, seizure, neuropathy
Uremic symptoms: nausea, vomiting, anorexia,
altered food taste, disturbance in sleep wake cycle
Evidence of malnutrition: decreased BUN/Cr,
hypoalbuminemia

22
Q

What damages does a post renal obstruction cause to the kidney?

A

intrarenal vasoconstriction, ischemic tubular injury, interstitial fibrosis

23
Q

What kind of acidosis can indicate post renal obstruction?

A

Type IV RTA

24
Q

What is the cardinal feature of pre renal azotemia?

A

decreased EABV

25
Q

What is seen in the sediment of pre renal vs. ATN?

A

pre renal: normal, hyaline casts

ATN: granular muddy brown casts, RBC casts, WBC casts

26
Q

Why is the electrolyte composition and osmolality of the urine normal in pre renal states?

A

because the tubules are functioning normally

27
Q

What constitutes evidence for a patient with pre renal failure due to vomiting?

A

azotemia, high bicarb, low plasma Cl with symptoms and signs of volume depletion
also hx of vomiting - causes metabolic alkalosis

28
Q

What is the basic pathogenesis of pre renal renal failure?

A

decreased EABV triggers kidney to conserve Na and water at expense of retaining nitrogenous wastes
kidney is structurally normal - just give fluids!

29
Q

What are causes of high urine sodium and high urine chlorine in volume depletion?

A

adrenal insufficiency
renal salt wasting
diuretics

30
Q

What are the causes of a high urine sodium and low urine chlorine in volume depletion?

A

nonreabsorbable anions
bicarbonaturia
ketoacids
penicillins

31
Q

What causes a low urine sodium and high urine chlorine in volume depletion?

A

increased urine ammonia - chronic diarrhea

32
Q

What leads to the reduction in GFR and azotemia seen in ATN?

A

tubule obstruction from dead sloughed cells, renal vasoconstriction, and backleak of filtered solutes

33
Q

What are typical features of ATN?

A

hyponatremia, metabolic acidosis, hyperkalemia, hyperphosphatemia, hypocalcemia, marked azotemia

34
Q

What is the difference between oliguric ATN and non-oliguric ATN?

A

oliguric - urine flow <400 ml/day - more injury, azotemia, and volume overload
non - only uremic complications require dialysis, better prognosis

35
Q

What are the main causes of oliguric vs. nonoliguric ATN?

A

oliguric - ischemic injury or rhabdo

nonoliguric - nephrotoxic

36
Q

How do NSAIDs cause NSAID induced ATN?

A

prostaglandins normally dampen effects of AII, catechols, ADH and symp nerves - renal function maintained normal even though circulation is clamped down
NSAIDs inhibit prostaglandin production - exaggerated renal vasoconstriction and magnified antidiuretic and antinatriuretic effects

37
Q

What is the primary source of renal artery emboli?

A

mural thrombi

38
Q

How long does an occlussion need to be present to cause an infarct in the kidney?

A

2 hrs

shorter can cause ATN

39
Q

What are the clinical manifestations of renal artery thrombi?

A

can be asymptomatic

nausea, vomiting, flank pain, fever

40
Q

What lab finding is the only one highly suggestive of renal infarction?

A

high serum LDH with little or no elevation in serum transaminase

41
Q

What are the manifestations of cholesterol crystal emboli?

A

usually after coronary angiography or aortic surg
can see skin (levido reticularis) or retinal artery emboli (hollenhorst plaque)
rising serum Cr with bland urine sediment

42
Q

When do renal vein thrombi tend to form?

A

nephrotic syndrome

43
Q

With slow onset RVT, what may be the only clue to diagnosis?

A

PE

44
Q

In what condition is RVT most common?

A

membranous GN

45
Q

How do ARBs or ACEIs induce renal dysfunction?

A

block AII mediated constriction of efferent arteriole so GFR drops rather than being maintained during times of low flow or afferent constriction

46
Q

Who should you absolutely not give ACEIs or ARBs to?

A

patients with bilateral renal artery stenosis

47
Q

What might you see on imaging of RVT?

A

ureteral notching, asymmetry in kidney size