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MEDI > CR IV MEDI Renal > Flashcards

CR IV MEDI Renal Flashcards

1
Q

In AKI presently, what will you see in labs?

A

High urine osm
U[Na] < 10
FEna < 1

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2
Q

What must a patient be off of for 24 hours prior to obtaining urine to diagnose pre-renal AKI?

A

Diuretics

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3
Q

If muddy brown casts are seen, what type of AKI is it?

A

Acute tubular necrosis

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4
Q

What is the most common cause of acute tubular necrosis?

A

Ischemia from hypovolemia

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5
Q

What is the definition of AKI?

A

Abrupt decline in GFR or [Cr]>.3 increase in 48 hours

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6
Q

What should be removed immediately in AKI?

A

ACEI or ARB

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7
Q

Is there a drug to treat AKI? What are some corrective measures?

A

No drug to cure it
If volume depleted, give NaCl
If in sepsis - give NaCl and vasopressors

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8
Q

When should dialysis be used to treat AKI?

A

Last resort - If uremic, K >6.5, pulmonary edema, or metabolic acidosis

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9
Q

Does Cr equal GFR in older people? Why or why not?

A

No because it does not rise like it should due to decreased mobility and muscle mass

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10
Q

What three things are older people at increased risk for due to their aging kidney?

A

Anemia
Vit D deficiency -> fractures
Insulin clearance impairment -> susceptible to diabetes

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11
Q

Why are older women slightly more protected from aging kidney than men?

A

Due to lack of testosterone

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12
Q

What precedes hypertension and diabetes in obese individuals?

A

Renal disease

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13
Q

What is the most important predisposing factor for insulin resistance?

A

Central obesity

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14
Q

What is seen in presentation/pathology in kidneys of obese individuals?

A

Glomerulomegaly

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15
Q

What does thiazolidendiones do?

A

Improves insulin sensitivity

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16
Q

What are the 5 types of Cardiorenal syndrome?

A

Type I - Acute CHF - Acute AKI - most common
Type II - Chronic CHF -> CKD
Type III - Acute/worsening kidney -> acute cardiac
Type IV - Primary CKD -> cardiac dysfunction
Type V - systemic -> cardiac and renal dysfunction

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17
Q

What is the major cause of Cardiorenal syndrome?

A

Reduced renal perfusion

VOlume overload and venous congestion

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18
Q

How do you treat Cardiorenal syndrome?

A

Loop diuretics
ACEI/ARB
Etc.

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19
Q

What does hepatorenal syndrome resemble? However, what does it not respond to?

A

Pre-renal azotemia

However, does not respond to volume

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20
Q

How does portal hypertension cause renal dysfunction?

A

Portal hypertension -> vasodilator splanchnic -> reduced systemic VR -> constriction at kidney = decreased perfusion

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21
Q

What is needed for diagnosis of hepatorenal syndrome?

A

Cr > 1.5 or GFR <40
AND
Chronic/active liver disease

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22
Q

What are the two types of hepatorenal syndrome? Which is worse? What can cause one to convert to the other?

A

Type I - rapid renal decline, in hosp. Pts usually >90% death in 3 months
Type II - less severe, slow, life exp. > 6 months
Triggers for II to I - bacterial peritonitis, hypovolemia, NSAIDs, ACEI, ARB

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23
Q

What is seen in a urinalysis of a hepatorenal patient?

A

<500 ml urine
Na < 10 (lowest you will see!)
Serum Na also low

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24
Q

Is treatment for Heptorenal syndrome easy? What can be done?

A

Albumin and terlipressin
Antibiotic (if needed)
Paracentesis
IV steroids - if septic and renal failure

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25
Q

What is toxic in rhabdo? What is the most common cause? Others?

A

Myoglobin
Trauma
Others: spin class, propefol, quail, statin + gemfibrozil, surgery

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26
Q

What color will the urine be in rhabdo? What will not be found?

A

Urine - red-brown, NO RBC, +4 on dipstick

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27
Q

What is the treatment for Rhabdomyolysis? What can be used to reduce uric acid?

A

Aggressive saline and maintain urine flow
Allopurinol - reduce uric acid
Stop statins and fimbrates

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28
Q

When does Cr rise in contrast nephropathy?

A

1-3 days after dye use

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29
Q

What are two risk factors for contrast nephropathy?

A

Renal insufficiency

Diabetes

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30
Q

How can contrast induced nephropathy be prevented?

A

Hydration (saline before if in hospital)

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31
Q

When does renal function decline in Contrast nephropathy? What does it usually improve by?

A

Function decreased days 3-5

Returns - day 10

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32
Q

When does nephrogenic systemic fibrosis occur?

A

When gadolinium is given for and MRI in pts with kidney disease

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33
Q

What is the most common cause of primary tubulointerstitial nephritis?

A

Drug induced - long term antibiotics

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34
Q

What is found in the urine of someone with tubulointerstitial nephritis?

A

Sterile pyuria
No protein or albumin
Unable to concentrate urine

35
Q

What three symptoms point you towards tubulointerstitial nephritis?

A

Fever, rash, eosinophilia

36
Q

What is the gold standard for diagnosing someone with tubulointerstitial nephritis?

A

Renal biopsy

37
Q

What is the treatment for tubulointerstitial nephritis?

A

Steroids only if caught in first 7-14 days

38
Q

What must be ordered if you suspect glomerular disease?

A

Microalbumin

39
Q

Should you get a 24 hour urine in someone with mild proteinuria? When do you treat? When do you recheck?

A

Mild - <1g/day - Do not get 24 hour urine
If asymptomative, reassess at 6-12 months
If protein has gone up, get biopsy
If protein has not gone up, reassess at 6-12 months

40
Q

What is the most common cause of glomerular hematuria?

A

IgA nephropathy our Thin Basement membrane nephropathy

41
Q

What are differences between nephrotic and nephritic syndrome?

A

Nephrotic - slow developing asymptomatic, symptoms at flare ups include edema, hyperlipidemia, hypoproteinemia. Thrombolitic disease

Nephritic - acute onset, lots of blood, Increase in BP and JVD, no edema because no time. RBC casts

42
Q

What is the most common nephrotic syndrome? Nephritic?

A

Nephrotic - membranous nephropathy or focal segmental glomerulosclerosis
Nephritic - Cresenteric, IgA, proliferating

43
Q

How does Alport syndrome differ from IgA Nephropathy?

A

Alport Syndrome will always have microscopic hematuria in between episodes of gross hematuria

44
Q

What is the most common nephrotic syndrome in children?

A

Minimal change disease

45
Q

What is the clinical presentation of minimal change disease?

A

Abrupt nephrotic
Normal Cr, low albumin
Effacement of podocytes

46
Q

What is the treatment for Minimal change disease? If recurrent, what can you treat with? What do you use to reduce triglycerides?

A

Prednisone
Cyclosporine 1-2 years
Statins to reduce triglycerides

47
Q

How does focal segment glomerulosclerosis differ from Minimal Change disease?

A

It does not respond to steroids

48
Q

Which primary glomerulonephritis is aggressive in coming back in transplant kidneys? Which doesn’t usually come back?

A

Focal Segmental - aggressive in transplant kidneys

IgA glomerular nephropathy - does not usually come back in transplant kidneys

49
Q

What is the most common GN leading to ESRD? What population is it more common in? What is seen clinically?

A

Focal Segmental Glomerulosclerosis
African Americans
Proteinuria, hematuria (>50%), renal failure (>33%), hypertensive

50
Q

What is the most common primary GN in adults? Where is the autoimmune antibody deposited? How is it treated?

A

Membranous Nephropathy
Subepithelial deposits destroy basement membrane
Month 1,3,5 - Solumedrol for 3 days, prednisone for 27
Months 2,4,6 - Oral cyclophosphamide

51
Q

What are the two types of MPGN? Which is worse? What is associated with each? What is the hallmark seen histologically?

A

Type I - Hep C - deposits all over
Type II - worse - C3 nephritic factor
Thickened capillary loops - “tram track”

52
Q

What is the histological hallmark of rapidly progressive glomerulonephritis? What is the treatment?

A

Crescent formation

IV solumedrol, prednisone, cytoxan - be aggressive!

53
Q

What is the most common GN in the world? What is deposited where?

A

IgA glomerular nephropathy

IgA in mesangium

54
Q

What is seem simultaneously to IgA nephropathy? Is serum IgA helpful?

A

Synpharyngitic macroscopic hematuria

Serum IgA not helpful

55
Q

What are three symptoms of IgA nephropathy? What are mild and progressive treated?

A

Hypertension, proteinuria, blood
Mild - ACEI or ARB
Moderate - ACEI or ARB and 6 month steroid
Progressive - cytotoxans

56
Q

What is cANCA pathoneumonic for?

A

Wegner’s syndrome

57
Q

What is the classic Wegner’s patient?

A

Older white male puking blood, cutaneous purpura

58
Q

What is the treatment for Wegner’s?

A

Predinsone and cytoxan

Plasmaphoresis last resort

59
Q

What is seen clinically/labs for Good pastures?

A

Circulating anti-GBM antibodies, widespread crescents, monophonic lesions

60
Q

What is the treatment for Goodpastures?

A

Plasma exchange - to remove antibodies
Steroids - for inflammation control
Cyclophosphamide - stop formation of new antibodies

61
Q

How is diabetic nephropathy diagnosed?

A

Persistent proteinuria > 300mg at least twice separated by 3-6 months

62
Q

What are hallmarks of diabetic nephropathy?

A

Hypertension
Progressive proteinuria
Progressive GFR decline

63
Q

What must always be requested when ordering a urinalysis and suspecting diabetic nephropathy? How often should it be screened/checked?

A

Microalbumin

Every 6 months

64
Q

For diabetic nephropathy, what test must be done? What is used to treat if GFR > 30? GFR <30? Two additional treatments?

A

24 hour urine
SGLT-2 inhibitors (lower HbA1c, decrease weight and BP)
Use DPP-4 inhibitor if GFR <30
Antihypertensives and Statins

65
Q

Do ACEI work prophalactically to prevent diabetic nephropathy?

A

No

66
Q

What are family CV disease and hypertension risk factors for?

A

Diabetic nephropathy

67
Q

Parental hypertension is a risk factor for which two things?

A

Diabetic nephropathy

IgA nephropathy

68
Q

What is seen on labs in chronic renal failure?

A

Increased BUN and Cr

Uremia in advanced CKD

69
Q

What is the best hemodialysis? 2nd? Third?

A

1st - artery to vein
2nd - graft
3rd - catheter (WORST)

70
Q

What clinical manifestation of CKD is the last function to lose?

A

Potassium regulation

71
Q

What is high in CRF that causes sexual dysfunction in men and infertility in women?

A

Prolactin

72
Q

What is the most common cause or uremic anemia? What do you need to diagnose it?

A

Dysfunction of vWF

Diagnose using bleed time only! (Because platelets are still there)

73
Q

What is used to treat renal osteodystrophy?

A

REstrict phosphate, use phosphate binders, supplement vit. D

74
Q

What is the most common kidney stone?

A

Calcium stones

75
Q

What is the gold standard for diagnosis of kidney stones? What can be used to avoid radiation?

A

Non-contrast helical CT - gold standard

Ultrasound

76
Q

How do you treat all kidney stones?

A

Allow to pass - pain control, hydration, strain urine

Consult urology - lithotripsy

77
Q

What is the most common metabolic abnormality causing kidney stones?
What is seen in plasma and urine?

A

Idiopathic hypercalciuria

Hypercalciuria w/o hypercalciuria

78
Q

How do you treat hyperoxaluria?

A

Increased dietary Ca to decrease oxalate absorption

79
Q

How do you treat hyperuricosuria stones? What population is it often seen in?

A

Allopurinol

Cancer pts - pre treat them with allopurinol

80
Q

Which population is more susceptible to struggle stones? DO they usually pass on their own?

A

Women

No

81
Q

What causes cysteine stones? What is used to diagnose them? What do you treat them with if hypertension is also present?

A

Defect in AA transport in kidney
Diagnose using Na nitroprusside test
Treat with catopril

82
Q

What test is used to diagnose benign positional vertigo? What is used to treat?

A

Dix-Hallpike - diagnose

Epley - treat

83
Q

What are the three types of syncope?

A

Neurally-mediated - increased parasympathetic, decreased sympathetic
Orthostatic hypotension - sympathetic should fire but they don’t
Cardiogenic - collapse and tachycardia

MEDI (11 decks)

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