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Renal > Day 3 5/14/15 > Flashcards

Day 3 5/14/15 Flashcards

1
Q

Normal Na Level

A

140 mEq/L

-low suggests avid tubular sodium reabsorption ( 40 mEq/L)

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2
Q

Normal K Level

A

4.5 mEq/L

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3
Q

Normal Cl Level

A

104 mEq/L

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4
Q

Normal Total CO2

A

27 mEq/L

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5
Q

Normal Glucose Level (Fasting)

A

90 +/- 30 mg/dL

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6
Q

Normal Creatinine Level

A

1.0 mg/dL

-usually viewed in concert with plasma creatinine; a UCr/PCr value greater than 20 suggests avid tubular water reabsorption, a value less than 10
suggests less avid water reabsorption

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7
Q

Normal BUN Level

A

12 +/- 4 mg/dL

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8
Q

Normal Phosphorous Level

A

4 mg/dL

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9
Q

Normal Ca Level

A

9.5 mg/dL

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10
Q

Normal Cholesterol Level

A

140-200 mg/dL

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11
Q

Normal Osmolality Level

A

285 mosm/kg

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12
Q

Acute Kidney Injury

A
  • rapid reduction in glomerular filtration rate manifested by a rise in plasma creatinine (Pcr) concentration and urea
  • results in reduced clearance of waste products
  • produces state called azotemia
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13
Q

3 Types of Acute Kidney Injury

A
  1. pre-renal azotemia- dec. in GFR due to dec. in renal plasma flow and/or renal perfusion pressure
  2. post-renal azotemia or obstructive neuropathy- dec. in GFR due to obstruction of urine flow
  3. intrinsic renal disease- dec. in GFR due to direct injury to kidneys
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14
Q

Uremia and Sx

A
  • signs and sx of multiple organ dysfunction caused by retention of uremic toxins and lack of renal hormones due to acute or chronic kidney injury
  • sx: nausea, vomiting, abdominal pain, diarrhea, weakness and fatigue
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15
Q

Azotemia

A

-buildup of nitrogenous wastes in blood, ex. BUN and creatinine

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16
Q

Oliguria

A

-urine volume

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17
Q

Anuria

A

-urine volume

18
Q

___________ is the most common cause of an abrupt call in GFR in a hospitalized pt.

A

-prerenal azotemia

19
Q

Causes of Pre Renal Azotemia

A

Dec. ECF Volume

  • renal losses
  • third space losses
  • GI losses
  • hemorrhage

Inc. ECF Volume

  • dec. cardiac output: CHF, MI, valvular disease, pericardial tamponade
  • systemic arterial vasodilation: cirrhosis, sepsis, medication, autonomic neuropathy
20
Q

Causes of Post Renal Azotemia

A
  • obstruction of ureters
  • bladder outlet obstruction
  • urethral obstruction
21
Q

Intrinsic Renal Diseases That Cause AKI

A
  • vascular diseases: cholesterol emboli, renal vein thrombosis
  • glomerular diseases: acute glomerulonephritis, hemolytic uremic syndrome
  • interstitial diseases: acute interstitial nephritis, infection, myeloma kidney
  • tubular diseases: ischemic or nephrotoxic acute tubular necrosis (ATN)
22
Q

Pre Renal Signs and Symptoms

A
  • intravascular volume depletion
  • dec. weight
  • flat neck veins
  • postural changes in BP/pulse
  • cardiac dysfunction
  • edema
  • pulmonary rales
  • S3 gallop
23
Q

Signs and Sx of Intrinsic Renal Disease

A
  • hx of exposure to renal insults associated with ATN
  • hypotension
  • surgery w/ large blood loss
  • transfusion rxns
  • exposure to radiocontrast dye
24
Q

Signs and Sx of Post Renal Disease

A

-anuria, intermittent anuria, large swings in urine flow rate

25
Q

In general, a ____ FEN suggests prerenal azotemia.

A

low

26
Q

Common Causes of Death in Acute Tubular Nephritis

A
  • infections

- gastrointestinal bleeding

27
Q

Nephrotic Syndrome Management

A
  • low salt diet
  • diuretics
  • BP control
  • cholesterol lowering drugs
  • ACE inhibitors to dec. proteinuria
  • Vit D replacement
  • normal or slightly low protein diet
28
Q

Nephrotic Syndrome Classification

A
  • proteinuria (>3.5 g/d)
  • hypoalbuminemia
  • edema (even around eyes)
  • hyperlipidemia
  • lipiduria
29
Q

Causes of Idiopathic Nephrotic Syndrome

A
  • minimal change disease (most common in children)
  • focal glomerular sclerosis
  • membranous nephropathy
  • membranoproliferative GN
  • other proliferative GN
  • also diabetes, amyloid and light chain disease, SLE
30
Q

Minimal Change Disease

  • presentation
  • lab
  • associations
  • phathophys
A

• Presentation:

  • Peak Incidence 2-6 years old
  • Male-female 2-1
  • Edema, ascites
  • Hypertension (20%)

• Lab:

  • Renal function normal or slightly depressed
  • Urinalysis: 4 + protein, hyaline casts, microscopic hematuria rare
  • Normal Light Microscopy
  • Negative Immunofluorescence
  • EM with foot process fusion

• Associations:

  • History of allergy/atopy
  • Hodgkin’s lymphoma
  • Nonsteroidal drugs (idiosyncratic reaction)

• Pathophys:
- ? T cell disorder
- Loss of charge barrier


31
Q

Focal and Segmental Glomerulosclerosis

A

• Presentation:

  • most common cause of nephrotic syndrome in young adults and AAs
  • proteinuria
  • hypertension
  • urinary sediment often with RBCs
  • may be idiopathic or related to previous minimal change disease
  • IV heroin, HIV, etc.
  • Lab:
  • Associations:
  • usually idiopathic
  • may occur in subjects w/ HIV

• Pathophys:

  • not mediated by immune complexes
  • may be due to circulating factor (suPAR)
  • pathology factor APO lipoprotein L1

• Tx: steroids (for 6 months); relapse is high.

32
Q

Membranous Nephropathy

A

• Presentation:
-presents w/ nephrotic syndrome

• Lab:
-histology looks like “burning bush”

• Associations:

  • idiopathic 2/3 cases (due to antibodies to phopholipase A2 on podocyte)
  • hep B
  • drugs (gold, mercury)
  • SLE
  • cancer

• Pathophys:
-up to 50% progress to chronic kidney disease if not tx

33
Q

Membranoproliferative GN

A

• Presentation:
-two types

• Lab:

  • light microscopy: mesangial proliferation and GBM thickening
  • IF type 1: granular deposits IgG, C3, +/- C4
  • IF type 2: granular deposits C3
  • EM type 1: subendothelial deposits
  • EM type 2: dense intramembranous depsits

• Associations:

  • type 1: hep C infection
  • type 2: complement disorder

• Pathophys:
-Hep C type 1: 70% response to interferon

34
Q

Clinical Classification of Nephritic Syndrome

A
  • dec. renal function
  • hypertension
  • RBC casts
  • edema
  • proteinuria (
35
Q

Complications of Nephrotic Syndrome

A
  • inc. coagulation factors leads to hypercoagulable state

- inc. risk bacterial infections

36
Q

Clinical Features of Glomerulonephritis

A
  • inflammatory injury of glomeruli
  • infiltration leukocytes
  • deposition of immune proteins
  • disturbed function of affected tissue
  • rapidly progressive
  • nephritic
  • pulmonary-renal syndrome
  • crescentic GN
37
Q

Mechanisms of Injury in Glomerulonephritis

A
  1. deposited immune complexes
  2. antibodies specific for renal antigens
  3. other causes of inflammation within glomeruli
    - GN is usually caused by immune-mediated glomerular injury
38
Q

Algorithm for Dx Glomerulonephritis

A
  • definitive dx require kidney biopsy
  • blood tests
  • urinalysis
39
Q

Tx for Glomerulonephritis

A
  • immunosuppressive drugs: prednisone, cyclophosphamide, rituxumab, etc
  • plasma exchange
40
Q

4 Causes of Glomerulonephritis

A
  • IgA nephropathy
  • lupus nephritis
  • anti-GBM disease
  • ANCA associated vasculitis

Renal (14 decks)

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