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CLIN MED II, Nephro > Acute / Chronic Renal Failure > Flashcards

Acute / Chronic Renal Failure Flashcards

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1
Q

a designation for a heterogeneous group of conditions that share common diagnostic features: specifically, an increase in the blood urea nitrogen (BUN) concentration and/or an increase in the plasma or serum creatinine (SCr) concentration, often associated with a reduction in urine volume

A

Acute Kidney Injury (acute renal failure)

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2
Q

True or false: its possible to have AKI without injury to the kidney parenchyma

A

TRUE

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3
Q

Some causes of community-acquired AKI

A

Volume depletion

Medications

Urinary Tract Obstruction

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4
Q

Some causes of hospital-acquired AKI

A

Sepsis

Major surgical procedures

Heart/Liver failure

IV iodinated contrast

Medication

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5
Q

3 categories of AKI

A

Prerenal Azotemia, Intrinsic, Postrenal

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6
Q

Most common form (broad) of AKI

A

Prerenal Azotemia

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7
Q

A rise in SCr or BUN concentration due to inadequate renal plasma flow and intraglomerular hydrostatic pressure to support normal glomerular filtration.

A

Prerenal Azotemia

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8
Q

Main causes of pre renal azotemia

A

Hypovolemia

Decreased cardiac output

Liver failure
- low protein = low osmotic pressure

NSAIDs, ACE-I / ARB, Cyclosporine (mess w renal autoregulation)

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9
Q

What might prolonged periods of renal azotemia lead to?

A

Ischemic injury (acute tubular necrosis)

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10
Q

True or false: pre renal azotemia is reversible

A

TRUE - reversible once hemodynamics restored

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11
Q

Urinalysis in prerenal azotemia

A

Essentially normal, maybe a few hyaline casts

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12
Q

Urinalysis in postrenal failure

A

Essentially normal, maybe a few hyaline casts

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13
Q

Urinalysis in intrinsic renal failure

A

granular casts, WBC casts, RBC casts, proteinuria, tubular epithelial cells

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14
Q

General symptoms of AKI

A 
N/V/D
Pruritis
drowsiness / dizzy
hiccups
SOB
anorexia
hematochezia
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15
Q

A distended bladder, costovertebral angle tenderness, or enlarged prostate indicate which cause of AKI

A

Postrenal

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16
Q

Evidence of volume depletion

A

Tachycardia
Hypotension (absolute or postural)
Low JVP
Dry mucous membranes

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17
Q

Elevated BUN/Cr Ratio - above 20:1

Urine sodium < 20 mEq/L

FeNa <1%

Hyaline casts in urine sediment, possible

A

Prerenal azotemia

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18
Q

Decreased BUN/Cr Ratio < 15:1

Increased Urine sodium > 40

FeNa > 1-2%

A

Intrinsic renal causes

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19
Q

When short term dialysis is indicated for AKI

A

When SrCr > 5-10 mg/dL

Unresponsive acidosis

Electrolyte disorders

Fluid overload

Uremic complications

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20
Q

Most common causes of Intrinsic AKI

A

Sepsis
Ischemia
Nephrotoxins (endogenous / exo)

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21
Q

Exogenous nephrotoxins

A

Aminoglycosides
Cisplatin
Amphotercin

Iodinated Contrast

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22
Q

Endogenous nephrotoxins

A

Hemolysis
Rhabdomyelosis
Myeloma
Intratubular crystals

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23
Q

Intrinsic AKI - Vascular causes

A

Vasculitis

Malignant HTN

TTP-HUS

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24
Q

Cardiac output and O2 consumption of kidneys

A

20% of cardiac output

10% of resting O2 consumption

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25
Ischemia associated AKI
Systemic hypotension, coupled with risk factors: - sepsis - limited renal reserve (CKD, older age)
26
Urine sediment with granular casts, renal tubule epithelial cells
Ischemia associated AKI (ATN) Nephrotixic tubular injury
27
Common causes of post renal / obstructive AKI
Bladder neck obstruction (prostatitis, neurogenic bladder, anticholinergics) Obstructed foley catheters Clots Calculi Urethral strictures
28
Diagnostic definition of AKI
a rise from baseline of at least 0.3 mg/dL within 48 h or at least 50% higher than baseline within 1 week, or a reduction in urine output to less than 0.5 mL/kg per hour for longer than 6 h. ** Serial blood tests showing continued substantial rise of SCr represents clear evidence of AKI **
29
Radiologic studies that indicate CKD (as opposed to AKI)
Small, shrunken kidneys with cortical thinning on renal ultrasound Evidence of renal osteodystrophy
30
Laboratory studies that indicate CKD (as opposed to AKI)
Normocytic anemia in the absence of blood loss Secondary hyperparathyroidism with hyperphosphatemia and hypocalcemia
31
A history of prostatic disease, nephrolithiasis, or pelvic or paraaortic malignancy would suggest the possibility of
Postrenal AKI
32
Physical signs of orthostatic hypotension, tachycardia, reduced jugular venous pressure, decreased skin turgor, and dry mucous membranes are often present in
Prerenal AKI
33
_____ should be suspected in the setting of vomiting, diarrhea, glycosuria causing polyuria, and several medications including diuretics, NSAIDs, ACE inhibitors, and ARBs.
Prerenal AKI
34
Colicky flank pain radiating to the groin suggests
Acute ureteric obstruction
35
Nocturia and urinary frequency or hesitancy can be seen in
Prostatic disease
36
Abdominal fullness and suprapubic pain can accompany
Massive bladder enlargement
37
Definitive diagnosis of obstruction requires
Radiologic investigations
38
Idiosyncratic reactions to a wide variety of medications can lead to
Allergic interstitial nephritis
39
Allergic interstitial nephritis may be accompanied by
fever, arthralgias, and a pruritic erythematous rash.
40
AKI accompanied by palpable purpura, pulmonary hemorrhage, or sinusitis raises the possibility of
Systemic vasculitis with glomerulonephritis
41
Complete anuria early in the course of AKI is uncommon except in the following situations:
complete urinary tract obstruction, renal artery occlusion, overwhelming septic shock, severe ischemia (often with cortical necrosis) severe proliferative glomerulonephritis vasculitis
42
Extremely heavy proteinuria (“nephrotic range,” >3.5 g/d) can occasionally be seen in
glomerulonephritis, vasculitis, or interstitial nephritis (particularly from NSAIDs)
43
If the dipstick is positive for hemoglobin but few red blood cells are evident in the urine sediment,
Rhabdomyelosis, hemolysis
44
AKI from ATN due to ischemic injury, sepsis, or certain nephrotoxins has characteristic urine sediment findings:
pigmented “muddy brown” granular casts and tubular epithelial cell casts. These findings may be absent in more than 20% of cases, however
45
Electrolyte imbalances seen in AKI
Hyperkalemia Hyperphosphatemia Hypocalcemia
46
Anion gap is ____ in uremia
often increased - due to retention of anions such as phosphate, hippurate, sulfate, and urate
47
Low anion gap may provide a clue to the diagnosis of
Mulitple myeloma (presence of unmeasured cationic proteins)
48
Laboratory blood tests helpful for the diagnosis of glomerulonephritis and vasculitis include
depressed complement levels high titers of antinuclear antibodies (ANAs) (SLE)? antineutrophilic cytoplasmic antibodies (ANCAs) (Vasculitis) antiglomerular basement membrane (AGBM) antibodies (Goodpastures) cryoglobulins.
49
Enlarged kidneys in a patient with AKI suggests the possibility of
Acute interstitial nephritis
50
Kidney biopsy considered when
the cause of AKI is not apparent based on the clinical context, physical examination, laboratory studies, and radiologic evaluation Most often used when glomerulonephritis, vasculitis, interstitial nephritis, myeloma kidney, HUS and TTP, and allograft dysfunction suspected
51
Administration of excessive hypotonic crystalloid or isotonic dextrose solutions can result in
Hypoosmolality, hyponatremia >> neurologica abnormalities / seizures
52
Marked hyperkalemia is particularly common in
rhabdomyelosis, hemolysis, tumor lysis - muscle weakness - cardiac arrhythmias
53
Major cardiac complications of AKI
Arrhythmias Pericarditis Pericardial effusion
54
Survivors of an episode of AKI requiring temporary dialysis are at high risk for
progressive CKD, and up to 10% may develop end-stage renal disease.
55
A spectrum of different pathophysiologic processes associated with abnormal kidney function and a progressive decline in glomerular filtration rate (GFR
CKD
56
Stages of CKD are stratified by
Estimated GFR Degree of Albuminuria
57
Accumulation of toxins, fluid, and electrolytes normally excreted by the kidneys results in
Uremic Syndrome Requires dialysis or kidney transplant
58
Most common inherited form of CKD
Autosomal Dominant Polycystic Kidney Disease
59
Clinical and laboratory complications in CKD become more prominent in what stages?
CKD Stage 3 and 4
60
Some of the most evident complications of CKD include
anemia and associated easy fatigability decreased appetite with progressive malnutrition abnormalities in calcium, phosphorus, and mineral-regulating hormones, such as D3 (calcitriol), parathyroid hormone (PTH), and fibroblast growth factor 23 (FGF-23) abnormalities in sodium, potassium, water, and acid-base homeostasis
61
Normal GFR in elderly
GFR values can be compatible with CKD stage 2 or 3, but most will show no further deterioration of kidney function
62
The most frequent cause of CKD in North America and Europe is
Diabetic nephropathy (mostly TIIDM)
63
When no overt evidence for a primary glomerular or tubulointerstitial kidney disease process is present, CKD is often attributed to
HTN
64
Major causes of CKD
- Diabetic nephropathy - Glomerulonephritis - Hypertension - associated CKD (includes vascular and ischemic kidneydisease and primary glomerular disease with associated hypertension) - Autosomal Dominant Polycystic Kidney Disease - Other cystic and tubulointerstitial nephropathy
65
Uremic syndrome can be divided into manifestations in three spheres of dysfunction
(1) those consequent to the accumulation of toxins that normally undergo renal excretion, including products of protein metabolism (2) those consequent to the loss of other kidney functions, such as fluid and electrolyte homeostasis and hormone regulation (3) progressive systemic inflammation and its vascular and nutritional consequences
66
GFR which is diagnostic of CKD
a GFR < 60, and/or presence of kidney damage (proteinuria) for > 3 months
67
Stage 1 CKD
Kidney damage with normal GFR >90 Persistant albuminuria * Asymptomatic, SrCr/BUN normal, * Acid-base compensated to normal (via increase in remaining nephron function)
68
Stage 2 CKD
Kidney damage with mild decrease in GFR, 60-89 * Asymptomatic, SrCr/BUN normal, * Acid-base compensated to normal (via increase in remaining nephron function)
69
Stage 3 CKD
Moderate decrease in GFR, 30-59 * May still be symptomatic, but SrCr/BUN increase * PTH, EPO, D3 become abnormal
70
Stage 4 CKD
Severe decrease in GFR 15-29 *Symptomatic - with anemia, acidosis, hyperkalemia, hypocalcemia, hyperphosphatemia
71
Stage 5 CKD
Kidney failure with GFR < 15
72
Seen almost exclusively in patients with CKD, livedo reticularis and advances to patches of ischemic necrosis, especially on the legs, thighs, abdomen, and breasts
Calciphylaxis something to do w calcium imbalance and/or warfarin
73
Leading cause of morbidity and mortality in patients at all stages of CKD
Cardiovascular disease (10-200 fold increased risk of developing CVD if you have CKD) - Ischemic CVD - Cardiac troponin levels are frequently elevated in CKD without evidence of acute ischemia. - HF - HTN, LVH
74
HTN med of choose for CKD
ACE-I or ARB - esp w proteinuric patients
75
Comorbidity Tx goals in CKD
BP < 130/80 A1C 6.5 - 7.5% LDL < 100 HDL > 50 Trigly < 150 Tobacco cessation Weight los
76
Hemostasis Tx in CKD
EPO Iron supps Antiplatelet therapy

CLIN MED II, Nephro (3 decks)

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