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Nephrology 2 Flashcards

1
Q

What is urea osmotic diuresis?

A

Following AKI, high BUN leads to high urea in urea, which creates osmotic diuresis, leading to hypernatremia

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2
Q

preeclampsia clinical features

A
  • new-onset HTN + proteinuria *occurs after 20 weeks of pregnancy
  • new onset end-organ damage (liver, kidney, pulmonary edema, cerebral or visual symptoms, thrombocytopenia are also diagnostic)
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3
Q

What is eclampsia?

A

Presence of generalized tonic-clonic seizures in women with preeclampsia

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4
Q

anemia features in HELLP

A

Microangiopathic hemolytic anemia (thus, must have elevated bilirubin level and schistocytes on peripheral smear)

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5
Q

Composition of kidney stones in patient taking topamax

A

Calcium phosphate

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6
Q

Evidence for sodium bicarbonate in CKD

A

Thought to slow CKD progression and reduce mortality

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7
Q

When bicarb should be started in CKD

A

Serum bicarb chronically less than 22 (below reference range)

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8
Q

Most common reason for patients to have recurrent kidney stones

A

Hypercalciuria (not hypercalcemia), which is often idiopathic and commonly familial

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9
Q

Why thiazides are used to treat recurrent kidney stones

A

Thiazides cause calcium reabsorption, thus decreasing calcium content in urine

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10
Q

Milk alkali syndrome cause + clinical features

A
  • ingestion of large amounts of calcium and absorbable alkali (eg calcium carbonate)
  • hypercalcemia + metabolic alkalosis + AKI
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11
Q

When does pseudohyperkalemia occur?

A

Extremely high levels of leukocytes or platelets (caused by intracellular release of potassium by leukocytes in specimen)

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12
Q

Management of edema in nephrotic syndrome refractory to loop diuretic

A
  • add thiazide (metolazone typically) and or potassium-sparing diuretic
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13
Q

Definition of high and low urine chloride

A

Low is less than 5

High is greater than 15

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14
Q

How albumin challenge works

A
  • no improvement in creatinine with albumin administration suggests hepatorenal syndrome
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15
Q

Gestational hypertension vs chronic hypertension

A 
chronic = hypertension starting before pregnancy or before 20 weeks of gestation (suggesting it preceded pregnancy)
gestational = hypertension developing later on in pregnancy, after 20 weeks (blood pressure typically declines in first 2 trimesters and then rises in 3rd trimester)
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16
Q

Pathogen responsible for infection-related glomerulonephritis in which patient develops glomerulonephritis during infection

A

staph aureus

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17
Q

infection-related glomerulonephritis vs. post-streptococcal glomerulonephritis

A

infection-related glomerulonephritis = AKI in the setting of infection
post-streptococcal glomerulonephritis = Latent period between resolution of infection and acute onset of nephritic syndrome. pathogen is typically streptococcal

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18
Q

Pathogen responsible for most post streptococcal glomerulonephritis

A

Group A strep or strep pyogenes

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19
Q

What is monoclonal gammopathy of renal significance?

A
  • patients who would otherwise be MGUS but have an abnormal UA and AKI
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20
Q

Management of patient with MGUS and AKI

A

Kidney biopsy for MGRS (demonstrating presence of monoclonal immunoglobulin deposition in the kidney)

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21
Q

tacrolimus mechanism of action

A

calcineurin inhibitor

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22
Q

Classic bone disease resulting from CKD or dialysis

A

Osteitis fibrosa cystica

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23
Q

Bone disease in CKD/ESRD patients but with normal labs –PTH/vitamin d/calcium

A

Adynamic bone disease

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24
Q

Osteitis fibrosa cystica pathophys and labs

A
  • High PTH leads to increased bone turnover and alk phos levels
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25
Q

Term for mineral bone disease associated with vitamin D deficiency

A

osteomalacia

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26
Q

Most common cause of membranoproliferative glomerulonephritis

A

Hep C

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27
Q

what is the definition of hypertension per ACC/AHA guidelines?

A

SBP greater than 130 or DBP greater than 80 (SBP between 120-129 is defined as elevated blood pressure)

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28
Q

Kidney disorder in patients from balkans + clinical features

A
  • Balkan endemic nephropathy

- urothelial cancers

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29
Q

Management of Balkan endemic nephropathy

A

cystoscopy + upper urinary tract imaging

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30
Q

goal percent sat in CKD

A

30%

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31
Q

Management of ACEi/ARBs when small bump in Creatinine

A

continue

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32
Q

GFR cutoff for SGLT2 inhibitors

A

GFR over 30

*continue if only small bump

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33
Q

Statins okay in CKD?

A

Continue statins in CKD

NEVER start when on dialysis (okay to continue)

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34
Q

Dysmorphic RBCs think

A

nephritic disease

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35
Q

know kimmelstein wilson nodule

A

see photo online

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36
Q

Which GN is associated with a resistance to African Sleeping Sickness?

A

FSGS (this is why it’s more common in blacks)

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37
Q

Only patient population in which FeNa is indicated?

A

Oliguric patients

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38
Q

Other causes of low FeNa

A
  • contrast induced nephropathy
  • rhabdo
  • GN
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39
Q

Major SE of vaptans

A
  • liver failure
40
Q

management of renal stones greater than 10mm without clinical improvement

A

shock wave lithotripsy

41
Q

Treatment of chronic kidney stones

A
  • Decrease sodium intake
  • normal to increased dietary calcium
    IF urine citrate is low – potassium citrate
    IF urine calcium high – thiazide
42
Q

Ingredient in APAP that causes pyroglutamic acidosis

A

5-oxoproline

43
Q

Type 1 vs type 2 RTA

A

Type 1 = stone forming

Type 2 = no stones

44
Q

GFR cutoff for starting SGLT2

A

GFR greater than 30

45
Q

calciphylaxis treatment

A

sodium thiosulfate

46
Q

Sirolimus and everolimus mechanism

A

MTOR inhibitors

47
Q

Clinical use of urine anion gap + interpretation generally

A

Differentiating non gap acidosis
Positive = distal RTA, chronic respiratory alkalosis
negative = diarrhea

48
Q

drugs that are most common causes of AIN

A

antibiotics
*PPIs
NSAIDS

49
Q

AIN clinical features + lab features

A
  • rash, fever, eosinophilia
  • pyuria, hematuria, *white blood cell casts, varying degrees of proteinuria
  • may or may not have urinary eosinophils, not very useful
  • patients rarely have all 3
50
Q

Treatment of AIN

A
  • discontinue offending drug

- systemic steroids

51
Q

lab features of immune complex or post streptococcal GN

A

proteinuria + RBC casts

52
Q

Interpretation of Weber test

A

IF sensorineural hearing loss –> lateralization to unaffected ear
IF conductive hearing loss –> lateralization to affected ear (ambient noise dampens sensitivity on unaffected side)

53
Q

Management of acute sensorineural hearing loss

A

audiometry + MRI

54
Q

Causes of conductive hearing loss

A

Any cause that limits sound from gaining access to the inner ear (otitis externa or *media, cholesteatoma, trauma, cerumen, *tympanic membrane perforation)

55
Q

Management of moderate to severe exacerbation of COPD

A

Trial BPAP (unless contraindicated)

56
Q

Other contraindications to BiPaP

A
  • severe acidosis (pH less than 7.1)
  • inability to clear secretions
  • ARDS
  • uncooperative or agitated
  • upper airway obstruction
  • facial surgery or trauma
57
Q

Next step in young patient with pseudogout

A

Test for secondary cause (serum iron for hemochromatosis, hypothyroidism, hyperparathyroidism)

58
Q

X-ray findings in pseudogout

A
  • linear calcifications of menisci and articular cartilage

- chondrocalcinosis

59
Q

Presentation of crystal-induced AKI

A
  • acute flank pain + dysuria (presents similarly to nephrolithiasis but is bilateral) (drug precipitates in the tubules)
  • AKI shortly after starting a drug
60
Q

Treatment of crystal-induced AKI

A
  • hydration
  • alkalinize urine to pH greater than 7.15
  • diuretic
  • stop drug
61
Q

Meds associated with crystal-induced AKI

A
  • acyclovir
  • sulfonamides
  • MTX
  • ethylene glycol
  • protease inhibitors
  • uric acid (TLS)
62
Q

Diagnosis of crystal-induced AKI

A
  • urine sediment analysis for crystals
63
Q

Treatment of recurrent uric acid stones

A

Potassium citrate (which alkalinizes urine, and uric acid stones are highly soluble in alkaline urine) + hydration

64
Q

Results of water deprivation test in primary polydypsia and nephrogenic and central DI

A
  • water deprivation test = no change
  • nephrogenic DI = no change
  • central DI = increased urine osmolality
65
Q

When eGFR is valid

A
  • stable, steady-state clinical setting
  • most accurate for CKD patients
    *tend to underestimate actual
    GFR
    *less accurate for patients with a normal GFR and young patients
66
Q

Management of abrupt onset severe psoriasis

A

test for HIV (common in patients with HIV infection and may be initial manifestation of disease)

67
Q

Other factors that can precipitate psoriasis

A
  • streptococcal infections (guttate psoriasis)
  • smoking, drinking
  • withdrawal from systemic steroids
68
Q

association of explosive onset multiple itchy SKs

A

GI malignancy

69
Q

association of recurrent herpes zoster

A

HIV infection

70
Q

associations of multiple skin tags

A
  • insulin resistance
  • pregnancy
  • Crohn’s
71
Q

Management of suspected thoracic aortic dissection in patient with renal insufficiency

A

TEE

72
Q

How to test for pseudohyperkalemia

A

redraw arterial blood with care to prevent hemolysis (no tourniquet or shaking, stored on ice, analyzed promptly)

73
Q

Diagnosis of BK polyoma virus

A
  • renal biopsy + IHC using antibodies against BK virus
74
Q

specific finding of BK polyoma virus

A

Intranuclear inclusions

75
Q

why are calcimemetics (cinacalcet) used to treat CKD patients with secondary hyperPTH and hyperphosphatemia?

A
  • decrease frequency of fractures and reduce rate of parathyroidectomy
  • also reduce cardiovascular disease in older patients
76
Q

First step in management of hyperphosphatemia in CKD patients

A

reduce dietary phos

77
Q

Second step in management of hyperphosphatemia in CKD patients

A

IF serum calcium low – calcium carbonate or acetate

IF serum calcium high – sevelamer

78
Q

management of secondary hyperPTH in CKD patients

A

IF serum phos high – start cinacalcet

IF serum phos low – add vitamin D analog

79
Q

MOA of calcimemetics

A
  • increase calcium sensitivity of calcium-sensing receptors on PTH glands and reduce serum PTH, calcium and phos levels
80
Q

Clinical features of ADPKD

A
  • hepatic + pancreatic cysts
  • cardiac valvular disease (mitral or aortic regurg)
  • intracerebral aneurysms (may say family history of CVA)
  • multiple unilateral or bilateral kidney cysts (can be asymptomatic otherwise)
81
Q

Presentation of scurvy

A

alcoholic or malnourished patient with petechiae + bruising + bleeding gums and dental caries + impaired wound healing

82
Q

treatment of scurvy

A

oral or injectable vitamin C

83
Q

Luekocytoclastic vasculitis clinical features

A

petechiae and or palpable purpura 7-10 days after starting a new drug (eg penicillin) OR new infection

84
Q

Definition of nephrotic range proteinuria

A

Greater than 3 g/24 hour period

85
Q

orthostatic proteinuria clinical features

A

young adult + healthy otherwise + (generally less than 1 g/day but may surpass 3 g/day in select patients)
*proteinuria in the upright position but minimal to no proteinuria in the supine position.

86
Q

When patients have transient proteinuria

A

Fever and after exercise

87
Q

When dialysis access is needed

A
  • typically when GFR is 15-20
  • AV fistula’s are preemptive placed if hemodialysis is antiquated (maturation of a fistula takes up to 3 months)
  • waiting until dialysis is emergently required places patients at high risk for complications
88
Q

Correlation of uremia with bleeding risk in CKD

A
  • no correlation with bleeding risk
89
Q

Labs in uremic coagulopathy in CKD patients

A
  • normal coags
  • platelet count normal
  • prolonged bleeding time
90
Q

How does conjugated estrogen treat bleeding coagulopathy?

A

Thought to be from increased platelet reactivity

91
Q

How does DDAVP treat bleeding coagulopathy?

A
  • increases release of Factor VIII and von willebrand factor polymers from endothelial storage sites
92
Q

Dysmorphic RBCS in the urine suggest what?

A

Glomerular disease

93
Q

Presentation of IgA nephropathy

A
  • one or more episodes of gross hematuria + typically following a URI
  • proteinuria
  • IgA immune complex
94
Q

IgA nephropathy vs. Infectious GN in terms of physiology

A

IgA nephropathy = immune complex, IgA mediated (HSP is a subtype)
Infection-related GN = immune complex but not IgA

95
Q

Next step after patient presenting with hematuria following URI

A

Quantify proteinuria

96
Q

Relationship between creatinine and GFR and implication for interpreting Cr

A
  • non-linear (exponential) - very time GFR halves, serum creatinine doubles
  • so when GFR is normal, large decreases in GFR result in only small increases in creatinine
  • and thus when GFR is significantly decreased, small decrements in GFR produce relatively large changes in serum creatinine

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