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Med Study > Nephrology > Flashcards

Nephrology Flashcards

1
Q

Bartter syndrome Normotensive

A

Hypokalemia / Hypercalciuria / Polydepsia / Polyuria

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2
Q

Hemolytic-uremic syndrome

A
  • Hemolytic anemia (anemia caused by destruction of red blood cells)
  • Acute kidney failure (uremia)
  • Low platelet count (thrombocytopenia)

Clinical Dx / Supportive therapy HD

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3
Q

Thrombotic thrombocytopenic purpura

A
  • Microangiopathic hemolytic anemia (anemia, jaundice and a blood film featuring evidence of mechanical fragmentation of red blood cells)
  • Kidney failure
  • Thrombocytopenia (low platelet count), leading to bruising or purpura
  • Neurologic symptoms (fluctuating), such as hallucinations, bizarre behavior, altered mental status, stroke or headaches
  • Fever
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4
Q

FSGS / Focal segmental glomerulosclerosis / Nephrotic Syndrome

A
  • Intravenous drug abuse - HIV infection * - Malignancy - HTN* - Obesity * - African-American *
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5
Q

Hypocomplementemia in Renal Disease

A

• Membranoproliferative GN • Atheroemboli • Lupus • Cryoglobulinemia • Post-infectious GN

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6
Q

Membranoproliferative Glomerulonephritis:

A

• Low complement, hematuria, HTN / Tram traks • Tumors and CLL • Infections — endocarditis, hepatitis B/C • Mixed essential cryoglobulinemia • Systemic lupus erythematosus

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7
Q

Henoch-Schb’nlein purpura

A
  • Purpura, arthritis and abdominal pain are known as the “classic triad” - Crescentic Glomerulonephritis – C3 and IgA
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8
Q

Behcet’s syndrome

A
  • Complex of recurrent oral aphthous ulcers, genital ulcers, and uveitis - Crescentic Glomerulonephritis
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9
Q

Alport Syndrome

A
  • Type IV collagen defect - X linked - Kidney / EYE / EAR
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10
Q

Nephronophthisis-MCD Complex Medullary CYSTIC kidney vs MEDULLARY SPONGE KIDNEY

A

• Polyuria, polydipsia, anemia, FTT, retinitispigmentosa, * NORMAL U/A • Medullary CYSTIC kidney - progressiveto ESRD * MEDULLARY SPONGE KIDNEY * - “Paintbrush” pattern / Nephrolithiasis, hematuria - Urinary tract infections / Decreased concentrating ability - *** Good prognosis

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11
Q

von Hippel-Lindau (Cystic dz)

A
  • AD - RCC (in 40-70%) * - Retinal angiomas, CNS hemangioblastomas (pancreatic and renal) cysts, pheo
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12
Q

Name the Diuretics that work on these section of CT. Proxima CT: diuretics Loop: diuretics Distal CT: diuretics

A

Proxima CT: diuretics Acetazolamide / AE:Metabolic acidosis Loop: diuretics furosemide Like “Bartter’s” AE: Hearing loss if > 500 mg a day Distal CT: diuretics thiazides Like “Gittleman’s” A/E HypoNa, hypergly, hyperCa, bone marrow suppression

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13
Q

Increased BUN

A
  • Steroids - Gl bleeding - High protein intake (TPN) - Severe cardiomyopathy - Catabolic states (burns, sepsis, etc.)
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14
Q

Prerenal - Hepatorenal syndrome *

A
  • FENa less than 1% - Urine Na < 10 mOsm/L / Urine osmolality > 500 mOsm/L - “End-stage” liver disease / Euvolemia: unresponsive to IVF * - Exclude other etio for ARF (sepsis, hypotension, etc.) - Often precipitated by bacterial peritonitis or over-aggressive paracentesis
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15
Q

Prerenal Azotemia (~ 70%)

A
  • Dx: volume depletion or decreased effective circulatory volume - U/A: hyaline casts, FENa < 1 %, SG > 1.018 - Studies: Pul-Artery catheter, response to restoration of renal perfusion
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16
Q

Acute Tubular Necrosis

A

• associated with ischemia and/or nephrotoxins - < 500 mL/day or < 20 mUhr/ Diuretics do NOT change prognosis * - Prototypically runs a 3-week course Acute Tubular Necrosis: Ischemic - U/A: muddy brown granular casts, * RTEs, FENa>1%

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17
Q

Acute Tubular Necrosis: Management / timing

A

• Aminoglycoside-induced renal failure — time lag 7-10 days • Amphotericin B - K/Mg waste, dRTA, concentration defect • Cisplatin: Mg wasting • Contrast-induced renal failure / Mgmt: need to establish euvolemia

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18
Q

Indications for Dialysis

A
  1. Unresponsive hypervolemia 2. Unresponsive hyperkalemia 3. Unresponsive acidosis 4. Uremic pericarditis or symptomatology 5. Undesirable poisonings CAN NOT HD DIGOXIN
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19
Q

Contraindications to Transplant

A

• Active infection • Uncontrollable malignancy • Anti-GBM antibodies • ABO incompatibility • Antilymphocyte antibodies against donor

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20
Q

Renal Transplantation * DZ that cause loss of a transplanted kidney

A
  1. Focal segmental glomerulosclerosis 2. Membranoproliferative glomerulonephritis 3. Thrombotic thrombocytopenic purpura (TTP) and/or hemolytic uremic syndrome (HUS) 4. IgA nephropathy (graft loss less common than histologic presence) • Mean half-life cadaveric = 15 years • Mean half-life LRD = ~ 20 years
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21
Q

Major Transplant Drugs Groups

A

• Corticosteroids • Purine analogs / Azathioprine (Imuran) / Mycophenolate mofetil (CellCept) • Calcineurin Inhibitors/ Cyclosporine (Neoral, Sandimmune,Gengraf) / Tacrolimus (Prograf) • Antiproliferatives / Sirolimus (Rapamune)

22
Q

A/E - Calcineurin Inhibitors/ Cyclosporine (Neoral, Sandimmune,Gengraf) / Tacrolimus (Prograf)

A
  • nephrotoxicity * - Interstitial fibrosis - Gingival hyperplasia * / Change group - Hypertrichosis * - Diabetes mellitus* Monitor for CP450 inhibition and inducing
23
Q

A/E – Corticosteroids

A
  • opportunistic infections, HTN, edema, Gl effects, glucose intolerance, accelerated atherosclerosis, cataracts, glaucoma, weight gain
24
Q

A/E – Antiproliferatives

A

anemia, thrombocytopenia, leukopenia, hepatoxicity, infections, posttransplant malignancy, Gl toxicities

25
Q

Major Medical Complications Post-Transplant

A
  1. Cardiovascular events 2. Malignancies: skin and lymphoma 3. Infections: CMV, EBV, hepatitis
26
Q

Causes of CKD

A
  • 40% DM
  • 25% HTN
  • 11% GN
  • 4% Interstitial Nephritis
27
Q

Uremic Bleeding

A
  • Decreased Factor III
  • Abnormal platelet aggregation
  • Increased prostacyclin
  • Abnormal vWF-VIII complex production
  • Tx:- Desmopressin (DDAVP®) — acute / Cryoprecipitate & FFP / PRBCs - Estrogen — chronic therapy - Dialysis if uremic
28
Q

Renal Osteodystrophy

A
  • Vitamin D and calcium
  • Phosphate control: binders and diet
  • Calcimimetics (cinacalcet)
  • Monitor secondary hyperparathyroidism(target iPTH 150-300)
29
Q

Acidosis

A
  • Usually GFR < 30 mL/min / Treatment - Sodium bicarbonate
30
Q

Recommendations for Prevention of Progression CKD

A

• BP < 130/80 / Use an ACEI/ARB, or anything that works! • Diabetes mellitus: • Correct anemia - Check iron stores quarterly: give iV Fe / erythropoietin • Serial estimation of renal function • Microalbuminuria screening yearly in all diabetics - Spot urine albumin to creatinine ratio: • > 30 mg/g is 80% DN risk • < 30 is 4% DN risk • Dipstick NOT adequate for screening

31
Q

Nephrolithiasis

A

• 75-80% contain calcium Indinavir causes Crystals Uric acid stones: typically not visible on x-ray Rx: alkalinization, allopurinol, increasing fluid intake, and a low purine diet

32
Q

Staghorn calculi

A
  • Uric acid stones (Coffin shape) - Struvite - Cystine (hexagon shape)
33
Q

Cystinuria and cystine kidney stones *

A
  • Cystinuria: inherited disorder, excessive “COAL” Cystine Ornithine Arginine, Lysine
34
Q

Nephrolithiasis and RTA 1

A
  • Untreated Type renal tubular acidosis is associated with hypercalciuria, hyperphosphaturia, nephrolithiasis, hypocitraturia, and nephrocalcinosis
35
Q

Pregnancy-Induced HTN: Preeclampsia

A

• HTN and proteinuria (Edema no longer part of the definition) • Typically 20 wks gestation/ If before 20 wks, suspect underlying chronic renal disease • Preeclampsia is typically associated with hyperuricemia • Pregnancy-induced HTN associated with low uteroplacental flow; avoid lasix Tx HTN & pregnancy methyldopa, hydralazine, and metoprolol (probably CBB)

36
Q

Severe Preeclampsia with HELLP Syndrome

A

• Haemolysis \ Abnormal peripheral smear \ Bilirubin > 1.2 \ LDH > 600 • Elevated LFT’s \ AST > 70 • Low Platelets: < 100,000

37
Q

Acute Fatty Liver of Pregnancy

A

• fever, abdominal pain, nausea, and vomiting after 35th week • Exam: jaundice, hypertension, edema, abdominal pain • Lab: hyperbilirubinemia, mild elevation of transaminases, hepatic/renal failure • Treatment: termination of pregnancy

38
Q

Idiopathic Postpartum Renal Failure

A

• Clinical Features: - Microangiopathic hemolytic anemia - Renal thrombotic microangiopathy - Acute renal failure - Malignant hypertension - Thrombocytopenia • Begins days to weeks following a normal pregnancy • Treatment: usually plasma exchange

39
Q

HTN in End-Stage Renal Disease and Transplantation

A

• Volume-dependent hypertension • Cyclosporin and tacrolimus * • Renal artery stenosis * (especially if rising creatinine and worsening HTN)

40
Q

Pheochromocytoma

A

• The classic triad: headaches, sweating, and tachycardia • Orthostatic BP changes • Screen: 24-hour urine metanephrine measurement, could also measure a 24-hour urine VMA * • Falsely elevated levels of urinary metanephrine due to Sympathetic drugs / Monoamine oxidase inhibitors / Labetalol • Localization: CT scan (MBIG is rarely used)

41
Q

High serum or urine aldosterone + urinary K+loss of > 30 mEq/day + HTN + low renin =

A
  • Primary hyperaldosteronism Aldosterone:renin ratio > 20 is suggestive of primary hyperaldosteronism.
42
Q

HTN + low K+ + low urinary K+ loss =

A
  • Previous diuretic therapy and/or Gl loss of K+
43
Q

HTN + high renin + high urinary K+ loss =

A

Renovascular

44
Q

HTN + low renin + low aldosterone + high urinary K+ loss + low K+ =

A
  • Ingestion of exogenous mineralocorticoid or licorice
45
Q

What is Liddle syndrome?

A
  • HTN, hypokalemia, metab alk. Rx amiloride/triamterene. Due to chronically open Na channels.
46
Q

SIDE EFFECTS ACEI / ARB / CCB / Clonidine / Beta-blockers / Diuretics / minoxidil, etc.

A

• ACEI: cough, hyperkalemia • ARB: hyperkalemia • CCB: constipation, pedal edema, AV block • Clonidine: sedation, dry mouth, rebound • Beta-blockers: fatigue, bronchospasm • Diuretics • Hydralazine, minoxidil, etc.

47
Q

autosomal dominant polycystic kidney disease (ADPKD) infected Cysts

A

Ciprofloxacin

48
Q

Prevent tumor lysis syndrom / Tx

A

Manifestations include acute kidney injury and arrhythmias resulting from the release of potassium, phosphorus, and uric acid from cells. Increase IVF Avoid Sodium Bicarb as it may cause CaPO4 parcipitation hence renal injury

49
Q

Rasburicase

A

Rasburicase directly breaks down uric acid and minimizes xanthine accumulation

50
Q

proliferative lupus nephriti

A

24-hour urine protein excretion greater than 500 mg/24 h UA > 10 erythrocytes/hpf UCx -ve with erythrocyte or leukocyte casts in a sterile urine sample Or kidney biops

51
Q
A

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