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CBRC > Renal Disorders > Flashcards

Renal Disorders Flashcards

1
Q

The Kidney

A

Recieves 20-25% Cardiac Output

Cleans blood to maintain homestasis

Regulation of Erythropoietin and Renin/Angiotensin

Vit D Activation

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2
Q

How Does the Kidney Maintain Homesostasis

A

Maintain Blood Volume-Excrete excess

Selective Re-Absorption (Na, K, etc)

Excretion of waste products

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3
Q

Why are Kidney’s Important to RTs

A

Blood volume increases may cause pulmonary edema

Electrolyte disturbanced may manifest in cardiopulmonary symptons (ex. arrhythmias)

Metabolic acidosis

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4
Q

Classification of Renal Disorders

A

Acute Kidney Failure

Chronic Kidney Failure

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5
Q

Acute Kidney Failure

A

State of acute impairment of renal function

Often reversible

Prerenal, renal, and post renal causes

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6
Q

Chronic Kidney Failure

A

Often irreversible

Divided into 5 stages

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7
Q

Normal BUN Levels

A

7-20

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8
Q

Normal Creatine

A

Men <1.4

Women <1.2

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9
Q

Acute Renal Failure Stages

A

Stage 1: Glomerular Filtration Rate will remain normal for a long time and only start to increase as entering into stage 2

Stage 2: GFR decrease and there is an abnormal increase in BUN

Stage 3: GFR will continue to decrease and BUN will continue to increase

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10
Q

Prerenal Etiology

A

Any disease that leads to inadequate perfusion of the kidney where tubular and glomerular function remain normal

Shock

Heart Failure

Hypotension

Sepsis

Atherosclerosis of renal artery

Rhabdomyolysis

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11
Q

Renal (Intrinsic) Etiology

A

Any disease that leads to actual damage of the nephron of the kidney

Acute tubular necrosis

Acute Glomerulonephritis

Acute Interstitial Nephritis

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12
Q

Acute Tubular Necrosis

A

Direct damage to the kidney tissue, especially the tubule

Ischemic or cytotoxic in origin

A cmomon cause of kidney failure in hospitalized pt

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13
Q

Acute Tubular Necrosis Causes

A

Blood Transfusion

Low perfusion for >30 min

Major surgery

Septic shock

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14
Q

Acute Glomerulonephritis

A

Vascular in origin

The glomerulus become inflamed and damaged

Often due to auto-immune response or infection

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15
Q

Acute Interstitial Nephritis

A

Inflammation of the kidney

Often caused by a medicine

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16
Q

Postrenal Etiology

A

Mechanical obstruction of the urinary collecting system (ureter, bladder, urethra. Will increase tubular pressure and the decrease filtration driving force

Stone disease

Tumor

Stricture

Thrombosis

Compressive hematoma

Enlarge prostate

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17
Q

Acute Clinical Manifestations Clinical Manifestations

A

Can vary widely depending on etiology

  • General Commonalities
    • Impact on urine output (oliguria or anuria)
    • Fluid overload-Leading to pulmonary edema
    • Electroyte imbalance
    • Weakness due to electrolyte abnormalities
    • Nausea and vomitting
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18
Q

Oliguria

A

Failure to produce adequate urine

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19
Q

Anuria

A

Total failure to produce urine

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20
Q

Acute Renal Failure Pathophysiology

A

Initial kidney insult-Decrease urine output where the other kidney will try to compensate

Retention of nitrogen wastes leading to fluid overload and increased extra cellular fluid

Renal acidosis

Electroylte imbalances

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21
Q

Acute Renal Failure

Nitrogen Waste

A

Urea, uric acid, and creatinine

22
Q

Acute Renal Failure

Renal acidosis

A

Kidneys cannot excrete fixed acid

Acid/base dsyfunction

23
Q

Acute Renal Failure

Electrolyte Imbalance

A

Common

Hypernatremia, Hyperkalemia, hyperchloremia

24
Q

Normal Urine Lab Findings

A

Yellow to Amber in color

Specific Gravity 1.010-1.025

pH 4.6-4.8

Rarely showing RBC, WBC, epithelial cells, and casts

25
Q

Pathological Urine Lab Findings

A

Increased BUN or Creatine

Urinanalysis may reveal sedimentation, WBC, and RBC

26
Q

Acute Renal Failure Management

A
  • Treat cause
    • Restore circulation with volume expanders, vasopressors, blood volume
    • restore circulation to kidney remove neoplasms, clear obstructions
  • Monitor for fluid overload
  • Monitor electroyltes particularly K+ level
  • Monitor for anemia-Kidney produce erythopoetin whic commands stem cell in marrow to form RBC
  • Beware inefficent drug elimination
    • Medication cleared by kidney will linger longer
27
Q

Dialysis Types

A

Peritoneal

CRRT

Hemodialysis

28
Q

Peritoneal Dialysis

A

Tube inserted into the abdomen and a dialysis is exchanged

29
Q

Dialysis-Continuous Renal Replacement Therapy

A

An extracorpeal purification therapy to substitute for impaired renal function over an extended period of time

“Slow” dialysis that has less dramtic swings in fluid balance-better suited for the ICU patient

30
Q

Hemodialysis

A

Usually 3 weeks

A vascular acess is created usually in a foremen A-V fistula (shunt)

Inpatients or outpatients

31
Q

Loop Diuretics

A

Eg. Lasix

32
Q

Potassium-Sparing Diuretics

A

Aldactone

33
Q

Carbonic Anhydrase Inhibitors

A

Diamox

34
Q

Thiazide Diuretics

A

Names that end in zide

Hydrochlorothiazide (microzide)

35
Q

Osmotic Diuretics

A

Mannitol which is very powerful

36
Q

Definition of Chronic Renal Disease

A

Kidney disease lasting longer than 3 months

37
Q

Chronic Renal Failure Etiology

A

Most commonly due to-Diabetes (type 1 and 2) and hypertension

Other causes- Auto-immune diseases, multiple episodes of kidney failure, inflammation, polycystic kidney disease, congenital defects, drugs and toxins

38
Q

Chronic Renal Failure Pathophysiology

A

Will be categorized into 5 stges based on

  • Amount of kidney function remaining
  • Symptons
  • Estimated glomerular filtration rate (GFR)
39
Q

Chronic Kidney Disease

Stage 5

A

End stage renal disease with severe impairment and starting to not be able to keep the pt alive

<15 ml/min GFR

<15 % kidney function

Symptons include poor sleepin, difficultly breathing, itichness, vomitting

High levels of creatine and urea are present

Start replacement therapy, dialysis, or transplant

40
Q

Chronic Kidney Disease

Stage 4

A

Kideny damage has become so severe and function is so poor that the body struggle to keep the person alive

15-29 ml/min GFR

15-29 % kidney function

Symptons include tiredness, poor appetite, and itching

plan for dialysis and assessment for transplate

41
Q

Chronic Kidney Disease

Stage 3

A

Even worse kidney damage with less funcion

30-59 ml/min GFR

30-59 % kidney function

Early symptons such as tiredness, poor appetite, and itching

Creatine levels rise and excess urea is present, and anemia may begin to occur

Treatment is totry to slow the disease and discuss further treatment options

42
Q

Chronic Kidney Disease

Stage 2

A

Worsening kidney damage with reduce function

60-89 ml/min GFR

60-89% kidney function

No symptons observed

Urea and creatine levels are normal or mildly elevated

Treatment is to monitor creatine levels, BP, and general health

43
Q

Chronic Kidney Disease

Stage 1

A

Early kidney damage with normal or even increased function

90% kidney function

No symptons observed

Urea and creatine levels are normal

90 ml/min GFR

Treatment is to identify the cause and try to reverse it

44
Q

Chronic Renal Failure Clinical Manifestation

A

May not have symptons until considerable often irreparable damage has occured

Tiredness

Poor appetite

Itiching

High creatine and BUN levels

Anemia

Poor sleep/dyspnea

Frequent vomitting

45
Q

Chronic Renal Failure Management

A

Depends on stage of CRF

Identify cause and try to stop it

Monitor cretaine, BP, and General health

Pt Education

Dualysis (including creation of access site)

Transplant

46
Q

PPV and Renal System

A

PPV can reduce urinary output

Associated with reduction in renal blood flow, glomerular filtration rate, Na and K excretion

Decrease mean arterial pressure

PPV also has a marked afect on Na and water retaining hormonal system

47
Q

PPV and ADH

A

ADH is release and is affected by intrathoracic pressure (PPV enhances ADH release)

48
Q

PPV and Atrial Natriuretic Factor

A

PPV reduces atrial filling pressure (decrease atrial strech) causing decreased secretion of ANP

49
Q

PPV and Renin Angiotension/Aldosterone

A

Renin angiotensin/aldosterone activation leading to increased sodium and water retention

50
Q

Renal System and Decreased CO

A

Increased intrathoracic pressure will decrease thoracic venous return and in turn decrease CO

This will both increase sympathetic activity (which causes vasoconstriction) and decreases renal blood flow

Ultimate result is a decrease glomerular filtration rate and increased soldium and water retention

51
Q

Affect of decreased renal blood flow

A

Increase vasopressin release

RAAS activation

Both of the above will decrease GFR and increase NA and water retention

CBRC (20 decks)

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