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Renal 2 > PostMT, AKI > Flashcards

PostMT, AKI Flashcards

1
Q

Cr levels in AKI.

What affects Cr levels?

A

Elevated by 50% of normal (if known) or by 0.5 - 1.0mg/dL.

Muscle mass affects Cr levels.

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2
Q

BUN levels in AKI.

What is this called?

A

Elevated BUN.

Called azotemia.

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3
Q

BUN elevation + confusion = ?

A

Uremia

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4
Q

What is the physiological cause of pre-renal? Due to what disease?

A

Common cause is Effective Volume Depletion!

Due to possible renovascular disease, such as EARLY Renal Artery stenosis.

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5
Q

Fractional Excretion of Sodium in pre-renal cause of AKI

A

less than 1.0

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6
Q

What does pre-renal suggest about the origin of the AKI?

A

Although affected/damaged, tubules and glomeruli were not the origin/initial location of pathology.

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7
Q

FeNa equation and how do you obtain samples?

A

Urine sample around same time as blood draw.

((Una x Pcr) / (Pna x Ucr)) x 100

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8
Q

Factors that suggest a chronic disease.

A

Anemia - decreased EPO
Underlying hx of conditions like HTN or DM.
Known prior hx of kidney problems.

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9
Q

What is effective volume depletion?

What does body perceive systemic conditions as?

A

When perfusion to the kidney is decreased, due to a variety of reasons like third spacing, vomiting&raquo_space; dehydration, hypotension.

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10
Q

What can cause effective volume depletion?

A

Pancreatitis!
Heart failure - decreased CO (i.e. post-MI) so kidney perceives decreased perfusion.
Vasomotor dilation - During SEPSIS, have high CO, but pooling in periphery instead of maintaining organ perfusion.

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11
Q

Is CT or abdominal ultrasound better for AKI diagnostic test?
What setting do you use this?

A

CT has better details in setting of pancreatitis, but iodinated would further compromise kidneys.

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12
Q

Treatment basics for AKI (2).

A

Maintain optimal renal perfusion.

Maintain optimal intravascular volume.

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13
Q

Treatments for pre-renal.

A

Treat hypovolemia with fluid replacement IV.

Treat the underlying cause!

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14
Q

Renal lithiasis

A

Most common in summer months when it is compounded by dehydration. Stones can lodge anywhere in Urinary Tract.

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15
Q

Diagnostic testing for renal lithiasis.

What is NOT indicated for renal lithiasis?

A 
Urinalysis with microscopic.
BMP v. CMP
Mg
CBC
Abdominal series for radiolucent stones.
Ultrasound for dilation of structures proximal to obstruction and shows kidney size.

CT is NOT indicated at this time.

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16
Q

Urine dipstick shows what?

Urine microscopic shows what?

A

Dipstick shows specific gravity ([urine]), pH, screens fo rblood, protein, leukocyte esterase, nitrites, urobilinogen, glucose, ketones.
Microscopic verifies dipstick and shows RBC, WBC, bacteria, presence of any crystal and cast formation.

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17
Q

BMP v. CMP

A

BMP: electrolytes plus BUN and Cr
CMP: BMP plus liver enzymes, protein, calcium

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18
Q

What are complications of Acute Renal Failure?

What compound is important to avoid?

A

Intravascular volume overload.
HyperK, hypoNa.
Metabolic acidosis.
Avoid Mg.

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19
Q

A person with Acute Kidney Failure is unresponsive to conservative measures. When should temporary hemodialysis be considered?

A 
Volume overload refractory to diuretics.
Hyperkalemia
Encephalopathy otherwise unexplained.
Percarditis, pleuritis, etc >> HEART
Severe metabolic acidosis compromising respiratory or circulatory function.
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20
Q

Possible causes of pre-renal (5)?

A
  1. Hypovolemia: dehydration, viral syndromes, acute pancreatitis, diuretics
  2. Low CO - CHF
  3. Altered Renal/SVR ration: sepsis, cirrhosis
  4. Renal hypoperfusion with impaired autoregulation - NSAIDS
  5. Hyperviscosity Syndrome (rare) - Myeloma
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21
Q

What can cause intrinsic renal failure (6)?

A
  1. Renovascular obstruction: Renal artery OBSTRUCTION due to embolism, dissecting aortic aneurysm
  2. Disease of glomeruli or microvascular: accelerated HTN
  3. Acute Tubular Necrosis: Iodinated contrast dye (used for CT’s, vascular studies, IntraVenous Pyelograms)
  4. Interstitial Nephritis: acute pyelonephritis, NSAIDS, can also be contrast dye or drug induced
  5. Intratubular deposition and obstruction: Myeloma
  6. Renal graft rejection.
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22
Q

Possible causes of post-renal (3)?

A
  1. Ureteric blockage - calculi (stones), blood clot, sloughed papilla, cancer, external compression (tumor, retroperitoneal fibrosis)
  2. Bladder neck blockage - Neurogenic bladder, prostatic hypertrophy, calculi, cancer, blood clot
  3. Urethra blockage - stricture, congenital valve, phimosis
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23
Q

Definition of CKD

A

Long standing, irreversible impairment of renal function.

UREMIA - clinical symptoms resulting from profound loss of renal function.

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24
Q

How is GFR measured (2 ways).

A
  1. 24 hour urine Creatinine clearance.

2. Inulin, but must be given IV and assay not available in most labs.

25
Q

Cockcroft -Gault Equation (male and female) for GFR calcultion

A

Male = [(140-age) x wt (in kg)] / (SCr x 72); Female = 0.85 x Male CrClearance

26
Q

Five stages of CKD.

A

Based on decrease in GFR

  1. Kidney damage with normal or increased GFR. Greater than or equal to 90.
  2. Mild decrease in GFR. 60-90
  3. Moderate decrease in GFR. 30-60
  4. Severe decrease in GFR. 15-30.
  5. Kidney failure/ESRD. Less than 15 or on dialysis.
27
Q

Characteristics of early stage CKD.

A

Usually symptom free. Overall function intact. RESERVE FUNCTION diminished. BUN/Cr may even be in normlal range.

28
Q

Later stages of CKD.

A

Azotemia and accompanying symptoms and signs.
Reserve decreased sufficiently so sudden stress can induce further compromise. Infection, urinary obstruction, dehydration, nephrotoxic drugs.

29
Q

Systemic effects of uremic toxins on cellular function.

How are these corrected/reversed?

A

Reduction of transmembrane voltage - increased intracellular Na, decreased intracellular K, inhibition of Ca flux.
Reversed with dialysis.

30
Q

Systemic effects of uremic toxins on whole body composition.

A

Osmotically induced OVERhydration of cells.
Increased extracellular volume.
Malaise, anorexia, N/V/D due to: protein and calorie malnutrition, negative nitrogen balance, or profound loss of lean body mass and fat deposits.

31
Q

Effects of uremic toxins on metabolism.

A

Hypothermia (decreased active sodium transport).
Intracellular deficits of potassium.
Metabolic acidosis.

32
Q

Effects of uremic toxins on nitrogen and lipids.

A

Protein intolerance - increased catabolism of urea and decreased elimination.
Hypertriglyceridemia, decreased HDL, normal cholesterol - decreased removal by lipoprotein lipase, increased lipogenesis, possibly increased production by liver and intestine.

33
Q

Effects of uremic toxins on sodium and volume homeostasis.

A

In stable CKD - total Na and water increased modestly.
Excessive salt ingestion can lead to CHF, HTN, ascites, edema.
Excessive water ingestion can lead to hyponatremia, weight gain.

34
Q

What is the recommended fluid intake pre-dialysis?

A

The recommended urine output + 500mL/day

35
Q

Potassium effects on CRD.

A

Normal to late stages: adaptation of DT and colon (both sites where aldosterone enhances K+ secretion).

36
Q

Increased K+ makes a person at risk for?

A

cardiac arrhythmias

37
Q

Drugs that can increase serum potassium.

A 
Antikaliuretic drugs (spirolactone, triamterene, amiloride, trmethoprim, pentamidine).
Others - ACE-1, Beta blockers
38
Q

V/D/Fever result in what that also contributes to CKD?

A

Extrarenal fluid loss, resulting in fluid depletion.

39
Q

What is the most common complication of ESRD?

What are chronic dialysis patients also at risk for?

A

HTN

Chronic dialysis patients also at risk for accelerated atherosclerosis.

40
Q

If no HTN on clinical exam of ESRD patient, consider what additional factors?

A

Salt wasting form of renal disease causing CKD (polycystic or medullary diseae, chronic tubulointerstitial disease, papillary necrosis).
Volume depletion.
That the patient may be on antihypertensive therapy at the time.

41
Q

Conditions associated with CKD (4).

A 
Pulmonary Congestion
Pericarditis
Hematologic Anemia
Hematologic-Abnormal Hemostasis
Enhanced susceptibility to infection
**See ppt for additional info - slides 54-57
42
Q

Bone changes with uremia (3).

A

Renal rickets
Osteitis fibrosis cystica
Osteosclerosis

43
Q

Renal rickets.

A

Due to uremia.

Widened osteoid seams at growth margins.

44
Q

Osteitis fibrosis cystic

A

Due to secondary hyperparathyroidism.

osteoclastic bone resorption, subperiosteal erosions, terminal phalanges, long bones, and distal clavicles.

45
Q

Bone changes in long term dialysis.

A

Adynamic or aplastic bone diseaes
Aluminum induced osteomalacia
Dialysis related amyloidosis (carpal tunnel, tenosynovitis of hands, shoulder arthropathy, bone cysts, cervical spondyloarthropathy, cervical pseudotumors)

46
Q

FSGS - progression and therapy

A

Progresses to CKD in 5-10 years.

No proven therapy

47
Q

Signs and symptoms of Chronic Renal Failure.

A

Anorexia, weight loss, dyspnea fatigue, pruritis, sleep and taste disturbance, confusion possible other forms of encephalopathy.

48
Q

What do you see on PE of CKD?

A

HTN, JVD, pericardial and or pleural friction rub, muscle wasting, asterixis, excoriations and ecchymoses.

49
Q

CKD labs

A

Elevated potassium, phosphate, uric acid
Low calcium, albumen, hemoglobin
Metabolic acidosis

50
Q

Conservative treatment of CKD.

A

Aggressive HTN control.
Eliminate volume overload with diuretics and volume intake restriction.
EPO
Phosphate binders
restrict dietary potassium
Sodium polystyrene sulfonate (Kayexalate) binds potassium
AC inhibitors (diabetes and significant proteinuria - >1gm/d)
Dietary protein restriction

51
Q

Indications for dialysis.

A

Unresponsive to conservative measures.
Volume overload refractory to diuretics.
Hyperkalemia
Encephalopathy otherwise unexplained
Pericarditis, pleuritis
Severe metabolic acidosis compromising respiratory or circulatory function.
Need for fluids/drugs also a consideration.

52
Q

Dialysis methods

A

PD
Intermittent HD (most common type for AKI, many 3x/week)
Night time dialysis (in-center HD, In-home HD)
CRRT - continuous renal replacement therapy used if intolerant to IHD, unstable ICU patients

53
Q

Complications of PD

A

Peritonitis, hyperglycemia, hypertriglyceridemia, obesity, hypoproteinemia, dialysis-related amyloidosis, insufficient clearance due to vascular disease or other factors.

54
Q

Types of fistulas

A

AV fistula

AV graft

55
Q

Complications of HD

A

Hypotension, accelerated vascular disease, rapid loss of residual renal function, access thrombosis, access or catheter sepsis.
Dialysis-related amyloidosis, protein-calorie malnutrition, hemorrhage, dyspnea/hypoxemia, leukopenia.

56
Q

ABSOLUTE contraindications of Renal Transplant.

A 
Active glomerulonephritis.
Active bacterial or other infection.
Active or very recent malignancy.
HIV
Hep B surface antigenemia.
Severe comorbidity (vascular disease)
57
Q

RELATIVE contraindications of Renal Transplant

A 
70+yo
Severe psychiatric disease
Moderately severe degrees of comorbidity
Hep C with chronic hep or cirrhosis
Noncompliance with dialysis or other tx.
Primary renal diseases - primary focal sclerosis with prior recurrence in transplant, multiple myeloma, amyloid, oxalosis
58
Q

Complications of renal transplant.

A

Rejection

Immunosuppression - infection, neoplasm

59
Q

Definition of AKI

A

Rapid decline in GFR. Hours to weeks. Can result in disturbances in ECF volume, electrolytes, and acid base balance.

Renal 2 (12 decks)

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