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Final review for Step 2 Ck > Renal > Flashcards

Renal Flashcards

1
Q

Renal artery stenosis in a young woman from fibromuscular dysplasia is treated how? HY

A

Treat fibromuscular dysplasia with a STENT, not surgery. use surgery if stent fails (Angioplasty with stent)

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2
Q

What is a sign of uremia in labs?

A

uremia sign is high BUN and look for asterixis

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3
Q

BUN correlates to what indication for dialysis

A

BUN elevation can show uremia which is an indication for dialysis

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4
Q

What are signs of uremia (high BUN )

A

Asterixis with encephalopathy and pericarditis/bleeding

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5
Q

What are uremia signs of dialysis

A

Dialyze with uremia (high BUN) and pericarditis, bleeding or ecephalopathy

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6
Q

When is an acidosis indication for dialysis

A

Dialysis when pH

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7
Q

When is dialysis used for eletrolyctes

A

Refractory K+ >6.5 or EKG changes and ventricular arrythmia

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8
Q

When is dialysis used for volume overload

A

Dialysis is used for volume overload refractory to diuretics

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9
Q

How is hypernatremia treated?

A

The MCC of hypernatremia is volume status. First assess volume status and if volume is low then give NS if symptomatic and D5W 1/2NS if asymptomatic

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10
Q

What happens if you replace and lower hypernatremia to fast?

A

Lower hypernatremia too fast you get cerebral EDEMA

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11
Q

Labs of dehydration?

A

Increased Cr and BUN, increased HCT from hemoconcetration and dry mucuous membranes, common in elderly

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12
Q

When is hypertonic saline used

A

use hypertonic saline when severe hyponatremia exists with s/s present (3%) is hypertonic and use until Na is back to 120 and s/s are gone

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13
Q

What happens if hyponatremia is corrected to quick?

A

Central pontine myelinolysis results when hyponatremia is corrected to quickly

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14
Q

How is mild SIADH treated

A

Mild SIADH causes hyponatremia, without syx they can just get fluid restriction

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15
Q

how is moderate wiht syx SIADH treated

A

syx hyponatremia with SIADH = 3% hypertonic saline until Na >120 and syx are gone

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16
Q

First step in hyper K diagnosis

A

first step in hyper K diagnosis i EKG which determines treatment

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17
Q

what two things determine treatment in hyper K

A

Hyperk Tx is determiend by K > 7 or changes on EKG

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18
Q

Preferred tx for no EKG changes and K

A

IV furosemide, or hemodialysis. First line is IV loop diuretics.

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19
Q

EKG hyperK signs?

A

Long PR and QRS and peaked T

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20
Q

what do peaked T tell you

A

peaked T tell you there is hyper K

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21
Q

When do you see long PR QRS, peaked T and low P?

A

Peaked T and long PR and QRS with low P is hyperK

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22
Q

When do you see sine wave

A

Sine wave is hyper K

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23
Q

How does albuterol affect K

A

Albuterol nebulizer causes K+ to move into the cells it is B2 agonism

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24
Q

what electrolyte does TMPSMX affect

A

TMP SMX affects K+

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25
Q

Peaked T =

A

hyperkalemia

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26
Q

Why is Cl low in vomiting

A

KCl and HCl loss causing hypovolemia and hypochloridia; alkalotic due to H+ loss and aldosteorne release and reabosrption of HCO3-

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27
Q

Classic sign on labs of diarrhea

A

Acidosis with hypokalemia

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28
Q

why is there acidosis in diarrhea

A

metabolic acidosis occurs in diarrhea as HCO3 is wasted in stool with potassium

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29
Q

What is the cutoff for oliguira

A

less than 250mL in 12 hours

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30
Q

First step in oliguira?

A

First step in oliguira is actually bed side bladder either followed by cath if retention or figuring out underlying cause

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31
Q

Oliguria workup postop

A

Bladder scan is first step; inconclusive = cath, retention = cath. No retention = run labs and find cause.

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32
Q

What are common AE of trypitylines? (TCAs_

A

TCAs are anticholinergs = dry mouth, urinary retention, delirium, pinpoint pupils, orthostatic hypoTN

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33
Q

In ADPKD why is the right kidney easier to palpate?

A

it lies lower due to the liver, you may not always feel both kidneys, but suspect in historyof b/l kidney masses and HTN and h/o kidney cysts

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34
Q

Someone gets AKI due to furosemide IV in cor pulmonale and has kidney failure, why AKi and why a metabolic anion gap acidosis?

A

Furosemide used for CHF exac/ cor pulmonale IV can cause hypovolemia and lead to AKI, the resultant increase in uremia is a foreign body that leads to anion gap metabolic acidosis

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35
Q

In persons with renal failure, why do you see metabolic acidosis?

A

uremia and/or lactic acidosis or bicarbonate loss from incompetent responding kidneys

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36
Q

what pH precipitates uric acid stones

A

uric acid stones are precipitated by low pH

37
Q

uric acid stones are precipitated by low pH, how can they be treated?

A

Potassium citrate is alkaline and urine excreted, if you alkalanize the urine, you raise urinary pH and prevent crystallization of low pH compounds in the urine

38
Q

Does lupus drop complement?

A

yes, lupus cause IC3 complex deposition and low complement

39
Q

how can lupus kidney failure be distinguished from other causes in the absence of systemic syx by just basic labs?

A

Lupus causes low WBC/anemia/low plt as well as proteinuira and RBC casts and low complement

40
Q

what kidney dysfuncitons (2) is SLE assoc with?

A

Diffuse proliferative GN (wire LOOPus-ing) and membranous nephropathy (black people (AA) in membranes (spike and dome) playing sports

41
Q

What does drug induced interstitial nephritis show

A

eosinophilia with WBC

42
Q

what are signs of acute interstitial nephritis?

A

Develops 7-10d after ingestion fo the toxin/medicine and causes rash, eosinophilia, pyuria

43
Q

what are causes of secondary amyloidosis

A

secondary amyloidosis is due to deposition of b2 microglobulin (AA = bTWO (2)), lipoprotein and transytheritin and may cause kidney disease and other end-organ failure

44
Q

when do you see b2 microglobulin

A

AA (secondary) amyloidosis from systemic inflammation like RA, SLE, IBD and chronic disease of TB

45
Q

When do you see AL (light chain) primary amyloidosis

A

MM and Waldenstrom – lambda light chains = primary AL

46
Q

MCC of AA amyloidosis?

A

RA

47
Q

tx of hyeprcalcemia fo malginancy?

A

IV hydration + bisphosph long term

48
Q

first step in hyperlcacemia

A

IV hydration

49
Q

what is long term treatment in hypercalcemia of granulomatous disease

A

steroids (1ahydroxylase in M0)

50
Q

What is a way to tell methanol toxicity?

A

Do optho exama nd look for disc hyperemia (damages eyes) and metabolic gap acidosis due to foreign body

51
Q

What type of acid base disorder does salicyclates cause?

A

They cause a respiratory alkalosis and a metabolic acidosis

52
Q

What are the causes of anion gap metabolic acidosis?

A

MUDPILES- methanol, uremia, DKA (NOT diarrhea), phenol, INH/iron, lactic acidosis, ethanol, salicyclates

53
Q

RAA system causes excretion of what ion and retention of what ion?

A

RAA excretes K+ and retains HCO3-

54
Q

What is type 4 RTA due to

A

It is due to failure of aldostorone response or secretion

55
Q

why does RTA 4 causes acidosis

A

loss of bicarb, cannot be absorbed due ot failure of aldosterone

56
Q

How does uremia affect the platelets

A

Blood counts are normal (plt, PTT and aPTT) but the PLT fxn, is not (count is ok) = uremia just affects platelet function

57
Q

why is there metabolic acidosis in ESRD

A

no HCO3 retention + foreign body uremia and foreign body lactic acdisosi

58
Q

Cause of anemia in ESRD?

A

Low EPO

59
Q

What does EPO cause as AE

A

high hct resulting in HTN

60
Q

What must be monitored before EPO admin

A

Before EPO admin administer iron

61
Q

what is prerenal AKI

A

hypoperfusion (low vol, heart failure, IV diuresesis overload)

62
Q

Postvoid > 50mL means?

A

urinary retention.

63
Q

When does injury due to contrast spike Cr levels

A

within 24 hours there is a spike in Cr for contrast injury that falls in 5-7d and is prevented by IV hydration and isotonic bicarb or acetylcysteine

64
Q

Which has low C3, IgA nephro or PSGN

A

PSGN occurs later AND has a drop in C3 versus IgA nephropathy which does NOT have low C3 like Lupus and PSGN do.

65
Q

What are findings in HTN kidney

A

intimal thickening with sclerosis and small kdineys and luminal narrowing

66
Q

what are findings in DM nephropathy

A

large kidneys wiht mesangial expansion and kimmelstein wils nodular sclerosis along with icnreased ECM

67
Q

When is U/S needed for nephrolithiasis

A

use U/S instead of CT for nephrolithiasis when the patient is pregnant

68
Q

Gold standard for nephrolithiasis

A

CT, unless pregant = U/S

69
Q

Who gets MCD and how is ti treated?

A

MCD is treated withotu biopsy with stseorids and is common in lympoma in kids and MCC of nephroapthy in kids
Focal

70
Q

what kidney disease does HIV get

A

HIV patients and heroine users get focal segmental

71
Q

who gets focal segmental glmoerulo

A

AA wih HIV/iV drugs andobese

72
Q

who gets membranous nephropathy

A

membranous = remember HBV

73
Q

other than HBV who gets membranous nephropathy

A

other than HBV membranous happens in SLE and HBV with solid tumors

74
Q

Prevention of calcium stones

A

hydrate and HCTZ diuretics

75
Q

what diruretics prevent calcium stones

A

HCTZ increase reabsorption of calcium

76
Q

What is MC stone

A

oxalate

77
Q

what is a common cause of oxalate stones

A

calcium malabsorption (I.E IBD)

78
Q

What crystals result from ethylene glycol

A

calcium oxalate

79
Q

why do struvite stones form

A

urine alkalinization and precipitation of struvite due to proteus, klebsiella, morganzlel, pseudo, ureasplams

80
Q

how is uric acid stone treated

A

alkalinize urine (low pH) with cistrate

81
Q

diagnosis of polycystic kidney disease?

A

Just use U/S to look for bilateral cysts

82
Q

What lab abn is common in RCC?

A

many have increased EPO and Hct in RCC resulting in polycythemia

83
Q

How is RCC diagnosed

A

RCC is diagnosed by going right to CT do not get a U/S

84
Q

When you have an acid base disorder with COPD patient and a GI bleed + BUN/Cr issue, how can you confirm what the cause is?

A

you HAVE to check ANION GAP every time you see an acidosis that is metabolic

85
Q

How is uremic platelet dysfunction treated?

A

DDAVP to realese VIII and vWF – (plt not working right give them more to grab onto)

86
Q

What are hyperkalemia EKG findings

A

Everything stretches due to slowing of conduciton with peaked t waves, long QRS and long PR interval

87
Q

How does pyschogenic polydipsia present

A

very dilute urine with very dilute Na. the body’s ability to excrete the Na is overwhelmed and this drops Na and causes maximally dilute urine

88
Q

When should you suspect cyanide toxicity in a patient

A

when a patient is treated with nitroprusside and get CNS changes or skin flushing and a metabolic acidosis due to CN- foreign body

89
Q

Is serum C3 normal in IgA nephro or PSGN?

A

igA nephro has NORMAL C3

Final review for Step 2 Ck (12 decks)

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