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Block 6 - Renal > Palmer Clin Med > Flashcards

Flashcards in Palmer Clin Med Deck (47):
1

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

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

2

What are the histologic findings of lead nephropathy?

early PROXIMAL tubule injury
intranuclear inclusion bodies of lead-protein complex

3

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

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

4

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

Type 1 RTA
nephrogenic DI

5

What is the definition of CKD?

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

6

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

stage 1 CKD

7

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

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

8

How are diuretics used in management of CKD?

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

9

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

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

10

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

Kayexalate = sodium polystyrene sulfonate - K binding resin
give with bowel cathartic to prevent constipation - but not one with Mg (risk of hyperMg with CKD)

11

How is metabolic acidosis involved in CKD?

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

12

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

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

13

What metabolic bone diseases are present in CKD?

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

14

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

iron deficiency
osteitis fibrosa cystica
Al overload

15

What are the cardiovascular manifestations of uremia?

pericarditis
volume overload
HTN
Accelerated atherosclerosis

16

What are the skin manifestations of uremia?

pruritis
skin pigmentation

17

What are the neurologic manifestations of uremia?

encephalopathy
seizures
peripheral neuropathy

18

What are the GI manifestations of uremia?

nausea, vomiting
gastritis, colitis

19

What are the pulmonary manifestations of uremia?

pleuritis
pneumonitis

20

What are the endocrine manifestations of uremia?

menstrual disturbance, anovulation
decrease in testosterone and spermatogenesis

21

What are the indications for hemodialysis in CKD?

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

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

intrarenal vasoconstriction, ischemic tubular injury, interstitial fibrosis

23

What kind of acidosis can indicate post renal obstruction?

Type IV RTA

24

What is the cardinal feature of pre renal azotemia?

decreased EABV

25

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

pre renal: normal, hyaline casts
ATN: granular muddy brown casts, RBC casts, WBC casts

26

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

because the tubules are functioning normally

27

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

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

28

What is the basic pathogenesis of pre renal renal failure?

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

29

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

adrenal insufficiency
renal salt wasting
diuretics

30

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

nonreabsorbable anions
bicarbonaturia
ketoacids
penicillins

31

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

increased urine ammonia - chronic diarrhea

32

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

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

33

What are typical features of ATN?

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

34

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

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

35

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

oliguric - ischemic injury or rhabdo
nonoliguric - nephrotoxic

36

How do NSAIDs cause NSAID induced ATN?

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

What is the primary source of renal artery emboli?

mural thrombi

38

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

2 hrs
shorter can cause ATN

39

What are the clinical manifestations of renal artery thrombi?

can be asymptomatic
nausea, vomiting, flank pain, fever

40

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

high serum LDH with little or no elevation in serum transaminase

41

What are the manifestations of cholesterol crystal emboli?

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

When do renal vein thrombi tend to form?

nephrotic syndrome

43

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

PE

44

In what condition is RVT most common?

membranous GN

45

How do ARBs or ACEIs induce renal dysfunction?

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

46

Who should you absolutely not give ACEIs or ARBs to?

patients with bilateral renal artery stenosis

47

What might you see on imaging of RVT?

ureteral notching, asymmetry in kidney size