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Internal Medicine: PGY-1 > Nephrology > Flashcards

Nephrology Flashcards

1
Q

Name a few causes of low vs. high BUN

A

High
- high protein diet
- antianabolic meds (steroids, tetracyclines)
- catabolic process (fever, infection)
- low effective arterial blood volume
- UGIB

Low
- low protein diet
- malnutrition
- impaired hepatic function

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2
Q

What is the expected rise in serum creatinine in 24h-period in average patient with anuric AKI? When can it be expected to be worse?

A
  • 88-176mmol/L per day
  • extreme catabolic state, rhabdo
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3
Q

Risk factors for developing AKI?

A
  • prior CKD
  • age
  • diabetes
  • black race
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4
Q

What are the symptoms of AKI?

A
  • Asymptomatic
  • Decreased urine output
  • Peripheral edema
  • Gross hematuria
  • SOB
  • Uremia symptoms: fatigue, weak, N/V, low appetite, pruritus, asterixis, paresthesia, anemia, pericarditis
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5
Q

When should you consider RRT in patients with AKI?

A
  • anuria >6h
  • severe oliguria (<200ml x12h)
  • severe hyperK (>6.5)
  • severe metabolic acidosis (pH<7.2 with normal PaCO2)
  • hypervolemia (esp. if pulm. edema present)
  • severe azotemia
  • uremia sequelae (eg., pericarditis)
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6
Q

Definition of CKD?

A
  • presence of kidney damage (albuminuria), or
  • decreased kidney function (GFR <60) >3 months
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7
Q

Structures affected in AKI:
1. prerenal
2. intrarenal
3. postrenal

A
  • structures: up to and including afferent arterioles
  • renal parenchyma: glomeruli, interstitium, tubules, blood vessels
  • any: process obstructing urine flow
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8
Q

Biocemical lab to suggest prerenal AKI? Intrarenal?

A

BUN:creat
- pre: >20:1 (caused by increased urea reabsorption in PCT 2/2 low effective arterial blood volume
- intra: <15:1

FENa
- pre: <1% or <35% (if on diuretics)
- intra: >1-2% or >35%

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9
Q

Urine sediments:
- prerenal
- intrarenal
- postrenal

A

Prerenal
- Bland, hyaline casts

Intrarenal
- ATN: granular, “muddy”, pigmented; tubular epithelial cells
- AIN: WBC casts
- GN: RBC casts
- Nephrotic: Fatty casts

Postrenal
- Hematuria (stones, bladder Ca, clots)
- Absent (neurogenic bladder)

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10
Q

How does hyperCa2+ cause AKI?

A

Causes:
- a reduction in glomerular filtration related to afferent arteriolar contriction
- renal salt wasting –> hypovolemia

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11
Q

HRS 1 vs 2: main difference?

A

HRS 1
- Rapid, doubling creatinine in <2wks
- commonly associated with MOF
- Oliguria more common

HRS 2
- Indolent
- Stable course often associated with refractory ascites

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12
Q

What are the general categories of intrarenal AKI?

A
  • Vascular
  • GN
  • ATN
  • AIN
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13
Q

Which type of vasculitis can involve the renal artery? Associated with intrarenal AKI?

A

Renal Artery
- Medium: PAN, Kawasaki
- Large: GCA, Takaysu

Intrarenal AKI
- Small: GPA, eGPA, Churg-Strauss Syndrome, microscopic polyangiitis, HSP (often cause GN)

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14
Q

What are the lab features of atheroembolic renal disease? (intrarenal AKI)

A
  • peripheral + urinary eosinophilia
  • serum hypocomplementation
  • other labs can indicate other organ involvement: hepatocellular injury (etc.)
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15
Q

What is the mechanism of AKI in ATN?

A

Tubular dysfunction 2/2 tubular epithelial cell injury (ischemic vs. toxic)

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16
Q

What is the timing + prognosis of contrast-induced nephropathy?

A
  • CIN develops 24-48h after contrast exposure
  • Recovery usually within 7-10 days
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17
Q

Common meds associated with ATN?

A
  • NSAIDS
  • Vancomycin
  • Aminoglycosides
  • Polymyxins
  • Pentamidine
  • Ampho B
  • Foscarnet
  • Tenofovir
  • Cisplatin
  • MTX
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18
Q

Why pigment and contrast-induced nephropathies can sometimes be associated with FENa <1%?

A

In addition to toxicity of renal tubules, they can induce afferent arteriole constriction = prerenal physiology

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19
Q

What is AIN? Classic triad?

A
  • Inflammation + edema within renal interstitium
  • Triad: fever, maculopapular rash, peripheral eosinophilia (all 3 present only 10-15% of cases)
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20
Q

Meds associated with AIN?

A

Most common:
- NSAID + antibiotics
- PCN, cephalosporins, cipro, rifampin, sulfa, vanco

Others:
- Allopurinol, acyclovir, famotidine, lasix, PPI, phenytoin

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21
Q

When does AIN usually develop in relation to exposure to medication?

A
  • 7-10 days
  • sooner possible, especially if repeat exposure to culprit drug
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22
Q

AIN etiology typically meds, infection, autoimmune, and tubulointerstitial nephritis uveitis (rare). Which infection more commonly associated with AIN? Autoimmune? Which population typically affected by TINU?

A

Infection
- bacterial: brucella, campylobacter, e. coli, legionella, salmonella, strep, staphy, yersinia
- viral: CMV, EBV, HIV, hantavirus

Autoimmune
- SLE, sarcoidosis, sjorgren

TINU
- young women
- S&S: uveitis, TIN, constitutional symptoms

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23
Q

Which malignancies are typically associated with renal obstruction?

A
  • RCC
  • bladder
  • prostate
  • TCC of collecting system
  • MM
  • mets
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24
Q

Most common primary cause of glomerular disease?

A

IgA Nephropathy

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25
Q

Nephrotic vs Nephritic syndromes: urinary findings

A

Nephrotic
- proteinuria >3.5g/d
- fatty casts: frothy urine
- microscopic hematuria
- sediment: bland

Nephritic
- sediment: dysmorphic RBC, RBC casts +/- WBC
- varying proteinuria <3.5g/d
- hematuria
- sterile pyuria

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26
Q

DDx: Nephrotic vs. Nephritic; BONUS - most common causes of nephritic-nephrotic syndrome?

A

Nephrotic
- MCD
- FSGS
- Membranous nephropathy
- Diabetes
- Amyloi light chain, amyloidosis, light chain deposition
- Lupus nephritis

Nephritic
- PSGN
- IgA nephropathy (Berger)
- GPA, eGPA (Wegener)
- Goodpasture
- Alport
- RPGN
- Lupus nephritis

Nephritic-nephrotic syndrome
- Membranoproliferative GN
- Diffuse proliferative GN

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27
Q

Nephrotic syndrome: what are the [1] symptoms, [2] exam findings?

A

Symptoms
- swelling, weight gain (nephrotic)
- fatigue
- dyspnea
- foamy urine

Exam
- HTN
- peripheral edema
- ascites
- pleural effusions
- less common: Muehrcke’s lines [nails], eruptive xanthoma, xanthelesma

28
Q

General lab features of nephrotic syndrome?

A
  • proteinuria >3.5g/d
  • albumin <2.5g/dL
  • hyperlipidemia
  • creatinine variable
29
Q

Common sites of theombosis in nephrotic syndrome?

A
  • renal veins
  • lower extremity veins
30
Q

Agents available to treat nephrotic syndrome?

A

ACEi

31
Q

Which primary cause of nephrotic syndrome associated with thromboembolism more?

A

membranous nephropathy

32
Q

Meds associated with nephrotic syndrome?

A
  • NSAIDs
  • lithium
  • gold
  • penicillamine
  • captopril
  • tamoxifen
33
Q

What infections are associated with nephrotic syndrome?

A
  • Bacterial: IE, vDRL
  • Viral: HIVm HBV, HCV
  • Protozoal: malaria, toxoplasmosis
  • Helminthic: schistosomiasis, filariasis
34
Q

Most common malignancies associated with nephrotic syndrome?

A
  • MM
  • lymphoma
  • lung
  • RCC
35
Q

In addition to amyloidosis as secondary cause of nephrotic syndrome, what other disease associated with fibrillar deposits in mesangium or GBM?

A
  • fibrillary GN (more common)
  • immunotactoid glomerulopathy
36
Q

Nephritic syndrome: symptoms and exam findings?

A

Symptoms
- hematuria, oliguria (AKI)
- CP, dyspnea (uremic pericarditis)
- peripheral edema (low albumin)
- headache (HTN)

Exam
- HTN
- Skin: palpable purpura (small-vessel vasculitis)
- pericardial friction rub (uremic pericarditis)

37
Q

What type of dysmorphic RBC is most specific for GN?

A

Acanthocytes, ring-shaped RBCs with vesicle-shaped protrusions (“mickey Mouse ears”)

38
Q

What are the subcategories of GN based on serology?

A
  • ANCA+
  • Anti-GBM+
  • Low C3/4
  • Other
39
Q

What does “ANCA” refer to?

A

Antineutrophil cytoplasmic antibodies: group of antibodies against proteins found in the cytoplasm of neutrophils (eg., PR3, MPO)

40
Q

When patients are ANCA positive, what are the 2 distinct patterns seen on immunofluorescence microscopy?

A
  • c-ANCA: antibodies to PR3
  • p-ANCA: antibodies to MPO
41
Q

What causes of GN are associated with low complement levels?

A
  • PSGN (low c3, normal c4)
  • Membranoproliferative GN (low c3, normal c4)
  • SLE (both low, but C3<C4)
  • IE (low c3, normal c4)
  • Cryoglobulinemia (low C4 ++, N-low C3)
42
Q

DDx of renal injury in the setting of IE?

A
  • renal infarction 2/2 septic emboli
  • AIN 2/2 meds
  • ATN 2/2 septicemia or abx
43
Q

Typical clinical features of IgA nephropathy? % of which will progress to ESRD?

A

Typically 2nd/3rd decades
More common white/asian men
2 presentations:
1. macroscopic hematuria usually ~5 days s/p URTI (more common in <40yo), or
2. asymptomatic with abn urine sediment + proteinuria (more common in older)

40%!!!

44
Q

What 2 causes of GN are histologically the same? How are the differentiated?

A
  • HSP and IgA nephropathy
  • Extrarenal manifestations: palpable purpura is universally present in HSP
45
Q

Symptoms of hyperK+?

A
  • cardiac arrhythmia, palpitations
  • weakness, paralysis, paresthesia
  • N/V, diarrhea
  • reduced DTR
46
Q

ECG changes of hyperK+?

A
47
Q

What [1] conduction abnormalities and [2] dysrhythmias are assocaited with hyperK+?

A

Conduction
- BBB
- bifascicular block
- AV block

Dysrhythmia
- sinus brady
- asystole
- idioventricular rhythms (VT, VF)

48
Q

DDx: Hematuria (4 main categories)

A

1) Pigments
- beets, myoglobin, hemoglobin, porphyrin, rifampin, food colouring

2) Transient:
- menstruation, UTI, fever, exercise, trauma, endometriosis, renal vein thrombosis

3) Glomerular
- nephritic: MPGN II, RPGN, IgA
- hereditary: Alport’s, thin BM disease, Loin pain hematuria syndrome

4) Extra-glomerular
- tumor: kidneys, ureter, bladder, urethra
- stones
- cystic kidney disease: PCKD, medullary cystic kidney disease, medullary sponge kidney

49
Q

Hematuria: glomerular vs. extra-glomerular

A

Glomerular
- cola urine
- proteinuria
- dysmorphic RBC (acanthocytes)
- RBC casts
- no clots

Extra-glomerular
- bright red urine
- no proteinuria
- no dysmorphic RBC, clots, RBC casts

50
Q

DDx: Proteinuria (4 main categories)

A

1) Functional [<1g/d]
- infection, fever, exercise, orthostatic

2) Tubular [0.5-1g/d]
- interstitial nephritis, ATN

3) Glomerular [1-3g/d, usually >3g/d]
- nephrotic/nephritic syndrome, early diabetes

4) Overflow [any amount, usually >1g/d]
- MM

51
Q

Proteinuria: test which detects all proteins?

A

Sulfosalicylic acid test

52
Q

Which medication can cause “pseudo-renal failure”?

A

Cimetidine, trimethoprim
- can reduce tubular secretion of creatinine causing small but significant increase in creat w/o change in GFR

53
Q

Contrast-Induced Nephropathy:
- Timing: onset, peak, recovery
- Risk factors
- Prevention

A

Timing
- immediately after exposure
- peaks: 48-72h
- recovery: same as ATN

Risk Factors
- CKD, MM, Dm, HTN, volume deplete, HF, nephrotoxins, procedures (dye load)

Prevention
- use low-dose dye (if possible)
- IVF:
1. NS0.45% 1ml/kg/h 12h before/after dye, or
2. NS or NaHCO3 at 3ml/kg/h 1h prior/6h post dye, or
3. NAC 150mg/kg in 500mL NS 30min before contrast then 50mg/kg 4h after

54
Q

GN terms:
- Focal
- Diffuse
- Segmental
- Global

A

Area of glomerulus affected:
- Focal: <50%
- Diffuse: >50%
- Segmental: segment of glomerulus
- Global: entire glomerulus

55
Q

GN: proliferative vs. non-proliferative

A

Non-proliferative
- lack of cell proliferation in glomerulus, usually nephrotic

Proliferative
- increased cells # in glomerulus; usually nephritic

56
Q

DDx: non-proliferative vs. proliferative GN

A

Non-Proliferative (nephrotic)
- MCD
- FSGS
- Membranous
- Other (amyloidosis/MGRS, Dm)

Proliferative (nephritic)
- MPGN
- ANCA: GPA, eGPA
- RPGN (linear, immune, pauci immune)

57
Q

Causes (primary/secondary) of Nephrotic syndromes?

A

1) MCD
- Cancer: T-cell lymphoma/Hodgkins, leukemias
- Drugs: NSAIDs, Li, COX2i
- Infx (rare): HIV, EBV, TB

2) FSGS (more severe form of MCD)
- Drugs: Li, heroin, pamidronate, ‘roids
- Hyperfiltration: obesity, single kidney, reflux nephropathy, HTN, SCD
- Infx: HIV, parvo, EBV

3) Membranous
- SLE
- Cancer: solid tumors, CLL
- Drugs: gold, penacillamine, NSAID, anti-TNFs
- Infx: HBV, HCV, HIV, syphilis

58
Q

DDx + Tx: RPGN:
1) linear
2) immune
3) pauci immune

A

1) Linear
- anti-GBM disease (syndrome if lung involved)
- Tx: PLEX + pulse steroids + Cyclo; if no improvement at 3 months, taper off

2) Immune
- SLE: low C3/4; hydroxychloroquine + steroids
- PSGN: low C3; resolves 3-4 weeks
- IgA: normal C3/4; ACEi + steroids + Cyclo/Azathio
- MPGN: low C3/4 - HCV, cryo, CLL) ; steroids + Cyclo

3) Pauci Immune
- ANCA: GPA/Wegener (c-anca), microscopic polyangiitis, eGPA (p-anca), churg-strauss; steroids + Cyclo (if RPGS, if not, use Ritux)

59
Q

DDx - CKD

A
  • any causes of acute AKI
  • renovascular: atherosclerosis, HTN, glomerulosclerosis (with age)
  • diabetes
  • GNs
  • PCKD
  • MM
  • nephrotoxins
60
Q

Risk factors for progression of CKD?

A
  • hypertension
  • age
  • proteinuria
  • dyslipidemia
  • high protein diet (unclear)
61
Q

S&S Uremia

A
  • Constitutional: tired, weak
  • Neuro: poor concentration, slow speech, myotonic jerks, altered taste/smell, restless leg
  • GI: N/V, anorexia
  • Heme: anemia, platelets dysfunction
  • MSK: bone disorders, cramps
  • Derm: pruritus
  • Sex: amenorrhea, sex dysfunction
62
Q

CKD-MBD - targets for PO4, Ca2+, PTH?

A
  • Ca2+: normal
  • PO4: <1.5mmol/L
  • PTH: <2-3x normal
63
Q

Criteria for dialysis in CKD?

A
  • any acute (AEIOU) indications
  • GFR <10
  • albumin <35
  • uremic symptoms
64
Q

How do ACEi help in CKD? Should be started in which patients? When should it be discontinued?

A

Benefits
- ACEi cause efferent arteriole vasodilation > decrease intraglomerular pressure > decreased long term remodeling/stress > slow progression of CKD
- lowers BP, proteinuria, and mediators of glomerular tubule hypertrophy/fibrosis

Should START
- in all CKD +/- HTN +/- proteinuria

Shoudl STOP
- if >30% rise in creatinine after starting

65
Q

RTA type I, II, IV (III extremely rare)
- Patho
- Serum K+
- Serum HCO3
- Urine pH
- Urine AG (urine net charge; UNC)
- Tx

A

Internal Medicine: PGY-1 (17 decks)

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