Clinical Medicine 9/20/16--Kirila Flashcards

1
Q

Acute Kidney Injury

A
  • increase in serum creatinine +/- decrease in urine output over hours to days
  • electrolyte disturbances, acid-base disturbances (metabolic acidosis), inability to excrete nitrogenous waste, intravascular volume overload
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2
Q

Orthostatic hypotension

A
  • volume contraction or ECV depletion (dehydration)

- due to fluid losses from nausea and vomiting

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3
Q

Fractional excretion of sodium

A
  • calculated using a random urine sample close to time of the blood draw–helps sort between pre-renal and intrinsic renal
  • (Una/Pna)/(Ucr/Pcr)x100
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4
Q

FeNa less than 1% means

A

tubules intact and are sodium avid i.e. retaining sodium as would be expected in dehydration

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5
Q

FeNa greater than 1-2% means

A

tubular function not intact

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6
Q

Pre-renal origin suggests

A

-that the tubules and glomeruli were not the initial location of pathology, though they will eventually become affected and possibly permanently

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7
Q

BUN/Creatinine in AKI

A
  • elevation in serum Creatinine by 50% or by 0.5-1.0mg/dL (affected by muscle mass available to generate creatinine)
  • BUN also elevated due to retention of nitrogenous wastes
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8
Q

Elevated BUN=

A

azotemia

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9
Q

Elevated BUN plus confusion=

A

uremia

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10
Q

eGFR=

A

175x (serum creatinine)^-1.154x(age)x0.742 [if female] x 1.22 [if black]

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11
Q

Pre renal causes of acute kidney injury

A
  • anything that compromises renal perfusion
  • hypovolemia: dehydration, viral syndromes, acute pancreatitis, diuretics
  • low cardiac output: CHF
  • altered renal/SVR ratio: sepsis, cirrhosis
  • renal hypo perfusion with impaired autoregulation: NSAIDS
  • hyperviscosity syndrome (rare): myeloma
  • not something that started in the kidney! Something before you got to the kidney
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12
Q

Effective Volume depletion

A
  • 3rd space

- results in decreased kidney perfusion as seen in pre-renal disease

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13
Q

Pre renal treatment

A
  • hypovolema: fluid replacement IV; treat underlying cause
  • even with effective volume depletion such as pancreatitis, large quantities of IV fluids are indicated, with close monitoring for systemic volume overload
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14
Q

Intrinsic renal failure

A
  • renovascular obstruction: renal artery obstruction e.g. embolism, dissecting aortic aneurysm (can be pre renal or intrinsic renal)
  • disease of glomeruli or microvasculature: accelerated HTN
  • acute tubular necrosis: iodinated contrast dye–used with CTs, vascular studies, IVP’s, etc
  • interstitial nephritis: acute pyelonephritis, NSAIDs, also can be contrast dye induced, other drugs
  • intratubular deposition and obstruction: myeloma
  • renal allograft rejection
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15
Q

Post renal AKI

A

-blockage

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16
Q

Ureteric blockage

A

-calculi (stones), blood clot, sloughed papilla, cancer, external compression (tumor, retroperitoneal fibrosis)

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17
Q

Bladder neck blockage

A

-neurogenic bladder, prostatic hypertrophy, calculi, cancer, blood clots

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18
Q

Urethra blockage

A

-stricture, congenital valve, phimosis

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19
Q

If AKI unresponsive to conservative measures,

A
  • consider temporary hemodialysis in the following:
  • volume overload refractory to diuretics
  • hyperkalemia
  • encephalopathy otherwise unexplained
  • pericarditis, pleuritis
  • severe metabolic acidosis comprising respiratory or circulator function
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20
Q

Chronic Kidney disease

A
  • long-standing, irreversible impairment of renal function

- uremia: clinical syndrome resulting from profound loss of renal function

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21
Q

Glomerular filtration rate

A
  • Creatinine clearance: 24 hour urine sample measured for creatinine in addition to obtaining serum creatinine
  • can use inulin as substance to measure, but has to be given IV and assay for inulin not available in most labs
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22
Q

CKD Stage 1

A

-kidney damage with normal or increased GFR>or = 90

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23
Q

CKD Stage 2

A

-mild decrease in GFR

60-89

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24
Q

CKD Stage 3

A

moderate decrease in GFR

-30-59

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25
Q

CKD Stage 4

A

Severe decrease in GFR

-15-29

26
Q

CKD Stage 5

A

kidney failure (aka ESRD)

27
Q

Early stage of CKD

A
  • usually symptom free
  • overall function intact
  • reserve function diminished
  • BUN/Cr may even be in normal range
28
Q

Later stages of CKD

A
  • azotemia and accompanying symptoms/signs
  • reserve decrease sufficiently so sudden stress can induce further compromise: infection, urinary obstruction, dehydration, nephrotoxic drugs
29
Q

Effects of Uremic Toxins on Cellular Function

A
  • reduction in transmembrane voltage
  • increased intracellular Na+
  • decreased intracellular K+
  • inhibition of Ca+ flux
  • uremia and its effects are largely reversible with dialysis
  • normal erythrocytes incubated in uremic serum demonstrates similar changes
30
Q

Effects of Uremic Toxins on Whole Body Composition

A
  • osmotically induced over hydration of cells
  • increased extracellular volume
  • malaise, anorexia, N/V/D
  • protein and calorie malnutrition
  • negative nitrogen balance
  • profound loss of lean body mass and fat deposits
31
Q

Effects of Uremic Toxins on Metabolism

A
  • hypothermia (decreased Active Na+ transport)
  • intracellular deficits of K+
  • metabolic acidosis
32
Q

Effects of Uremic Toxins on Nitrogen and Lipids

A
  • protein intolerance
  • increased catabolism in uremia
  • decreased elimination
  • hypertrigliceridemia, 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
  • total body content of Na+ and water are increased modestly–in stable CKD
  • excessive salt ingestion can lead to: CHF, hypertension, ascites, edema
  • excessive water ingestion: hyponatremia; weight gain
  • recommended fluid intake pre-dialysis: urine output plus 500ml/day
34
Q

Potassium effects in chronic renal disease

A
  • normal until late stages: adaptation in renal distal tubule and colon=sites where aldosterone enhances K+ secretion
  • increased K+–cardiac arrhythmias
35
Q

Drugs that can increase serum potassium

A
  • antikaliuretic drugs: spironolactone, triamterene, amiloride, trimethoprim, pentamidine
  • others: ACE inhibitor, beta blockers
36
Q

Extra renal Fluid loss also contributes to CKD

A
  • impaired renal mechanism to conserve Na+ and water in CKD
  • vomiting, diarrhea, fever
  • –volume depletion: dry mucous membranes, dizziness, syncope; tachycardia, decreased JVP; orthostasis; cardiovascular collapse
37
Q

The most common complication of ESRD

A
  • hypertesion as a result of primary renal disease or effects on kidney from systemic disease
  • chronic dialysis patients also have a higher incidence of accelerated atherosclerosis which contributes to the HTN
38
Q

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

A
  • salt wasting form of renal disease causing CKD: polycystic or medullary cystic disease; chronic tubulointerstitial disease; papillary necrosis
  • volume depletion
  • on antihypertensive therapy at the time
39
Q

Associated conditions with CKD: pulmonary congestion

A
  • unique form–even in absence of volume overload
  • normal or mildly elevated intracardiac or pulmonary capillary wedge pressures
  • CXR: butterfly wing distribution (peripheral vascular congestion)
  • increased permeability of alveolar capillary membranes
40
Q

Associated conditions with CKD: pericarditis

A
  • less frequent with early dialysis–thought secondary to metabolic toxins
  • if occurs in well dialyzed, likely viral infection or systemic disease
  • effusion often hemorrhagic
  • treatment: pericardiocentiusis, pericardiectomy
41
Q

Associated Conditions with CKD: hematologic–abnormal hemostasis

A
  • prolonged bleeding time
  • decreased platelet factor III activity
  • abnormal platelet aggregation and adhesiveness
  • impaired prothrombin consumption
42
Q

Associated Conditions with CKD: anemia

A
  • normocytic, normochromic anemia
  • hemolysis–uremic patients
  • GI, chronic dialyzer blood loss
  • hypersplenism–occasional
43
Q

Associated Conditions with CKD: enhanced susceptibility to infection

A
  • lymphocytopenia
  • atrophy of lymphoid structures
  • neutrophil production relatively unimpaired
  • uremia impairs function of all leukocytes
44
Q

Bone changes with uremia

A
  • renal rickets–widened osteoid seams at growth margins
  • osteitis fibrosis cystica–due to secondary hyperparathyroidism: stochastic bone resorption; subperiosteal erosions; terminal phalanges
  • osteosclerosis
45
Q

Bone Changes in Long Term Dialysis

A
  • adynamic or aplastic bone disease
  • aluminum-induced osteomalacia
  • dialysis-related amyloidosis (DRA)
  • -carpal tunnel syndrome; tenosynovitis of hands; shoulder arthropathy; bone cysts; cervical spondyloarthropathy; cervical pseudo tumors
46
Q

FSGS

A
  • progresses to CKD in 5-10 years

- no proven therapy–may see trial of steroid +/- cytotoxic agent

47
Q

Signs and symptoms of CKD

A
  • severity depends on: magnitude of loss in renal function
  • rapidity of loss
  • anorexia
  • weight loss
  • dyspnea
  • fatigue
  • pruritis
  • sleep and taste disturbance
  • confusion, possibly other forms of encephalopathy
48
Q

CKD Physical Exam findings

A
  • hypertension
  • JVD
  • pericardial +/or pleural friction rub
  • muscle wasting
  • asterixis
  • excoriations and ecchymoses
49
Q

CKD Lab findings

A
  • potassium, phosphate, uric acid all high
  • calcium, albumin, hemoglobin all low
  • metabolic acidosis
50
Q

Conservative Treatment for CKD

A
  • aggressive control of hypertension
  • eliminate volume overload (diuretics, volume intake restriction)
  • EPO (rHuEPO)–recombinant human erythropoietin
  • phosphate binders–Ca carbonate or acetate
  • restrict dietary potassium
  • sodium polystyrene sulfonate binds potassium
  • Ace inhibitors: diabetes significant protein uria (>1 gm/day)
  • 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
  • needs for fluids/drugs also a consideration
52
Q

Dialysis methods

A

-Peritoneal dialysis cycler vs dwell time then drain

53
Q

Intermittent hemodialysis

A
  • most common type used for AKI

- many CKD patients maintained on 3x/week

54
Q

Night time dialysis

A
  • in-center hemodyalisis

- in-home hemodialysis

55
Q

CRRT (Continuous renal replacement therapy)

A
  • if intolerant to intermittent hemodialysis

- may see in extremely unstable ICU patients

56
Q

Peritoneal Dialysis Complications

A
  • peritonitis
  • hyperglycemia
  • hypertriglyceridemia
  • obesity
  • hypoproteinuria
  • dialysis-related amyloidosis
  • insufficient clearance due to vascular disease or other factors
57
Q

Hemodialysis complications

A
  • hypotension
  • accelarated vascular disease
  • rapid loss of residual renal function
  • access thrombosis
  • access or catheter related sepsis
  • dialysis-related amyloidosis
  • protein-calorie malnutrition
  • hemorrhage
  • dyspnea/hypoxemia
  • leukopenia
58
Q

Renal Transplant ABSOLUTE Contraindications

A
  • active glomerulonephritis
  • active bacterial or other infection
  • active or very recent malignancy
  • HIV
  • Heb B surface antigenemia
  • Severe comorbidity (vascular disease)
59
Q

Renal Transplant RELATIVE Contraindications

A
  • age>70 years
  • severe psychiatric disease
  • moderately severe degrees of comorbidity
  • Hep C with chronic hepatitis or cirrhosis
  • noncompliance with dialysis or other treatment
  • primary renal diseases: primary focal sclerosis with prior recurrence in transplant; multiple myeloma; amyloid; oxalosis
60
Q

Renal Transplant Complications

A
  • rejection

- immunosuppression: infection, neoplasm