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High Acuity > Renal > Flashcards

Renal Flashcards

1
Q

Explain blood flow through the nephron

A

Aorta

Renal artery

Afferent arteriole

Highly vascular

glomeluar/bowmann’s capsule filters blood

efferent arteriole brings filtered blood into renal vein

Unfiltered blood/filtrate continue into tubule where it will be
- reabsorbed ito peritubular capillary
- secreted into tubule

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2
Q

Main Functions of Kidneys (7)

A
  1. Urine formation/regulation of fluid components through filtration, reabsorption, secretion, and excretion
  2. Acid base balance
  3. fluid and electrolyte balance
  4. remove metabolic waste from body
  5. EPO production: control production of RBC by bone marrow
  6. Blood pressure regulation through renin release
  7. Produces most active form of vitamin D: regulates bone density
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3
Q

Explain RAAS system

A
  1. Kidneys sense drop in BP and fluid volume
  2. Release renin which acticates angiotensinogen to angiotensin I
  3. This is converted from angiotensin II by ACE
  4. This acts on adrenal gland to release aldosterone
  5. aldosterone acts on kidney’s to resorb sodium and constrict blood vessels
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4
Q

Normal BUN

A

2.9-8.2

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5
Q

What does BUN reflect

A

GFR and urine concentrating capacity

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6
Q

What effects BUN

A

hydration status, level of catabolism, protein intake, and GI bleeding

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7
Q

BUN increases as GFR _______

A

decreases

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8
Q

Why is BUN not the most reliable measure of GFR?

A

Because it is resorbed back into the blood from tubule to peritubular capillary

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9
Q

Normal creatinine

A

50-110

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10
Q

What is creatinine?

A

End-product of muscle metabolism

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11
Q

Why is creatinine the most reliable indicator of renal health?

A

Released back into blood at constant rate

Elimiinated at a rate related to renal function

Not resorbed back into blood

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12
Q

What occurs in the body when kidneys fail?

A

Less waste is removed, inability to regulate fluid, electrolytes, and pH, creatinine and BUN build in blood

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13
Q

Define AKI and what 3 things does it lead to

A

Abrupt decrease in kidney function leading to:
1. failure to regulate F/E/A/B
2. rapid decrease in urine output
3. Decreased GFR (elevated BUN/creatinine) leading to azotemia

Rapid, progressive, reversible

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14
Q

Define prerenal AKI

A

decrease in blood flow to kidney (inadequate perfusion)

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15
Q

Define intrarenal AKI

A

something that happens to the structures in the kidney (i.e. infection such as acute glomerulonephritis, drug toxicity, etc.)

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16
Q

Define postrenal AKI

A

obstruction to urine outflow (i.e. kidney stone, prostate cancer, etc.)

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17
Q

Causes of prerenal AKI

A

Decreased kidney perfusion

  1. Decreased volume
    - hemorrhage
    - burns
    -diaphoresis
    - vomiting/diarrhea
    - polyuria (DKA/diuretics)
    - decreased CO (HF, MI, cirrhosis)
    - shock states
  2. arterial occlusion/emboli
  3. drugs that alter renal perfusion/nephrotoxic
    - ACE/ARBS
    - NSAIDS
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18
Q

What lab value characterizes prenal AKI

A

Increased BUN

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19
Q

Causes of intrarenal AKI

A

Direct damage to renal parenchyma

  • acute tubular necrosis (ischemia, necrosis)
  • vascular problems (hypertension)
  • Glomerulonephritis and other infections
  • nephrotoxic drugs
  • rhabdomyolysis clogging up glomeruli causing dark urine
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20
Q

Nephrotoxic drugs

A

ACEs/ARBs
NSAIDs
CT contrast***
Chemo
Antibiotics (aminoglycosides, gentamycin, cephalosporins, PipTaz, Vanco)

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21
Q

Management of rhabdo to prevent AKI

A

Massive breakdown of skeletal muscle (trauma)- release of myoglobin (plugs glomeruli- damages lining in tubules)
Dark urine
Monitor CK levels, give fluids

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22
Q

What lab values characterize intra renal AKI

A

Increased BUN and creatinine

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23
Q

Cause of post renal AKI

A

Caused by an obstruction to the outflow of urine from the kidneys (bladder, ureters, urethra)
- kidney stone
- prostate cancer
- BPH
- catheter obstruction

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24
Q

What lab values characterize post renal AKI

A

Increased creatinine

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25
Q

What are the risk factors for AKI?

A

HEMODYNAMIC CHANGES RESULTING IN DECREASED FLOW TO KIDNEYS

  • HTN
  • Trauma
  • diabetes
  • nephrotoxic agents
  • exposure to heavy metals
  • recent hypotensive episode
  • tumor/vascular obstruction
  • infection/sepsis
  • age
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26
Q

What urinary output changes occur in AKI

A

Changes in amount and concentration depending on injury

Usually oliguria, which causes fluid to buildup in body

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27
Q

What respiratory changes occur in AKI

A

Pulmonary edema with fluid buildup

Increased RR as body tries to compensate for metabolic acidosis

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28
Q

What A/B changes occur in AKI and why?

A

Metabolic Acidosis

decreased excretion of nonvolatile acids via urination and decreased renal synthesis of bicarbonates

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29
Q

What electrolyte changes occur in AKI?

A
  • Potassium excess (high)
  • Sodium imbalance (normal, high or low)
  • Calcium deficit (low)
  • Phosphate excess (high)
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30
Q

What hematological disorders occur in AKI?

A
  • Anemia (EPO production)
  • Urea decreases clot formation
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31
Q

What neurological changes occur in AKI?

A

Related to increased ICP (excess fluids), or increases uremia (build up of nitrogenous waste)

Symptoms: Headache, confusion, irritability, seizure, asterixis (hand tremor)

32
Q

What CV changes occur as result of AKI?

A

Fluid overload/HTN

MI - clotting with hypocalcemia

33
Q

What integument changes occur as a result of AKI?

A

Uremic frost; dry itchy pale skin – buildup of urea

34
Q

What GI symptoms can occur as a result of AKI?

A

N/V secondary to acidosis

malnutrition

ulcers (urea is irritating)

35
Q

How does hypoproteinemia occur is AKI? What is the result?

A

The glomerular damages leads to incresed permeability across membrane, leading to proteinuria

The decrease proteins in the blood decreases oncotic pressuure so fluids leak into interstitial spaces causing edema

36
Q

Normal urine output and at what value is there concern?

A

1500/2000ml/day ; 1-2ml/kg/hr

0.5ml/kg/hr

37
Q

Normal BUN:Creatinine and value indicative of AKI

A

Normally BUN and Creatinine ratio ~ 10:1 or 15:1
* A 20:1 ratio of BUN / Creatinine may indicate AKI

  • BUN/Cr ratio can be used to diagnose
38
Q

When is creatinine elevated?

A

Creatinine is not elevated until ~25% of the nephrons are not functioning

39
Q

A decrease in CCR indicates a:

A

A decrease in creatinine clearance rate indicates a decrease in glomerular function

40
Q

Doubling of serum creatinine means:

A

a decrease in GFR of about 50%

41
Q

Normal GFR

A

Kidneys control own filtration rate dependent upon fluid volumes and BP
Normal = 125 ml/min

42
Q

What will be seen in the urinalysis and 24 hour Urine of AKI/how in urine osmolality altered?

A

When renal function is altered:
Urine osmolality increases and urine specific gravity increases
* How much stuff and how heavy the urine is (how concentrated the urine is)

43
Q

How is serum osmolality altered in AKI?

A

Serum (blood) osmolality may stay the same
* Electrolytes (serum & urine)
Give insight into what is being filtered or not

44
Q

Priorities of Treatment for AKI (9)

A
  1. restore perfusion
  2. fluid overload
  3. electrolyte imbalance
  4. infection prevention
  5. acid-base imbalance
  6. Impaired gas exchange
  7. acute confusion
  8. coagulopathies
  9. diet challenges
45
Q

How is fluid overload managed in AKI?

A
  • Diuretics
  • Fluid restriction as prescribed
  • HR, BP, lungs, heart, ECG
  • STRICT Intake and output
  • Daily weights
  • Watch for electrolyte imbalances
  • Monitor for evidence of heart failure with fluid overload that has been happening; has heart been able to compensate?
46
Q

What electrolytes are you most concerned about in AKI

A

Potassium: acidosis and decreased excretion causing hyper
- arrhythmias (wide QRS)

Sodium: dependent on fluid status
hypo: early due to lack of reabsorption because of lack of healthy nephrons to resorb
hyper: later on which causes cellular dehydration

47
Q

Why is there increase risk for infection with AKI?

A

toxin buildup alters inflammatory response
* Changes in leukocyte function
* Altered immune response and function
* Diminished inflammatory response
* Protective mechanisms lost

48
Q

Why does acid-base imbalance occur in AKI? What is the typical ABG?

A

Kidneys unable to excrete acid load; defective regeneration and absorption of HCO3
* Metabolic Acidosis

49
Q

Why is gas exchange impaired in AKI?

A

Pulmonary edema

50
Q

Why does acute confusion/decreased cognition occur in AKI?

A
  • Increased ICP in fluid overload (hyponatremia)
  • Toxic effects of azotemia
51
Q

Why doe coagulopathies occur in AKI?

A
  • Bleeding (EPO deficiency)
  • Toxic buildup reduces platelet adhesion
52
Q

What diet challenges occur in AKI?

A
  • High state of catabolism (breaking proteins down into amino acids)
  • Therefore: high calorie, low protein, AVOID K, Na
  • Lack appetite
53
Q

What 5 reasons would dialysis by used in AKI?

A
  • Refractory acidosis (not responsive to correction)
  • Electrolytes (refractory; severe increased K+)
  • Acute intoxication on salicylic acid, lithium, magnesium laxatives, ethylene glycol
  • Overload with fluid (pulls fluid off without having to administer diuretics that may be damaging to kidneys)
  • Uremic complications (pericarditis, platelet dysfunction leading to bleeding)
54
Q

Define CKD

A

Slow, progressive, irreversible loss of renal function, affecting nearly all organ systems

55
Q

What does CKD result from?

A
  • Primary renal condition (polycystic kidney disease, glomerulonephritis)
  • Other diseases that produce a long-term renal insult (diabetes, hypertension)
56
Q

Risk factors for CKD

A
  1. diabetes
  2. HTN
  3. proteinuria
  4. family history
  5. increasing age/wear out over time
57
Q

Why is diabetes a risk factor for CKD?

A
  • Excess glucose stiffens efferent arteriole causing it to stiffen and narrow so blood cannot leave glomerulus
  • Leads to hyperfiltration and increased glomerular pressure, expanding size and stiffness of glomerular
58
Q

Why is HTN a risk factor for CKD?

A
  • Narrowed lumen and thickened walls mean less blood and oxygen delivered to the kidney causing ischemic injury
59
Q

Symptoms of CKD

A

Sodium/Water Imbalance
- HTN
- increased vascular volume/edema
- HF
Impaired Potassium Balance
-Hyperkalemia
Impaired nitrogenous waste elimination/uremia
- coagulopathies (urea increases bleed rx)
- pericarditis
- impaired immune function
- skin disorders
- GI manifestations
- neuro manifestations
- sexual dysfunction
Decreased EPO production
- anemia
A/B imbalance
- acidosis
Lack of Vit D activation/phosphorous elimination
- hypocalcemia
- hyperPTH
- osteodystrophies

60
Q

Explain the roles of phosphorous and calcium in the development of osteodystrophies in AKI

A
  1. Phospohate
    - is retained
    - binds to calcium, decreasing serum levels
  2. Calcium
    - decreased production of active vit D
    - decreased absorption, decreasing serum levels

Both of these things cause PTH release

PTH release releases calcium stored in bones (bone demineralization and density loss)

Serum caclium increases

Phosphate binds again (hyperphosphatemia in AKI) which furthers metastatic calcifications that can lodge in organs in vessels

61
Q

What are the various sources of anemia in CKD?

A

hemolysis, bone marrow suppression, decreased erythropoietin and iron

Decreased platelets - bleedings

62
Q

Nursing care of CKD

A
  1. Dialysis
  2. HTN management
  3. Nutrition
  4. hypoxia
  5. infection risk
  6. metabolic acidosis
  7. drugs to treat
    * Hyperkalemia
    * HTN
    * CKD-mineral and bone disorder
    * Anemia
    * Dyslipidemia
63
Q

Diet for CKD

A
  • Low protein diet, sodium, potassium, phosphate restrictions
64
Q

Why does hypoxia occur in CKD

A

associated with anemia with decreased RBC carrying capacity

65
Q

Why is infection risk high in CKD

A

Buildup of nitro waste, azotemia effecting response

66
Q

When is RRT required

A

when kidneys are functioning at < 10-15% of their normal rateT

67
Q

True or false dialysis is a cure

A
  • Doesn’t cure kidney disease or make kidneys well
  • Doesn’t fully replace kidney function
  • (CKD) must continue to have dialysis for rest of life (unless transplant)
68
Q

2 Types of RRT

A
  • Hemodialysis (AKI, CKD) 2 types:
  • Intermittent (generally 3 x 4hr “runs” per week)
  • Continuous renal replacement therapy (CRRT) – AKI patients
  • Peritoneal dialysis (CKD)
69
Q

How does dialysis work

A
  • Dissolved particles are transfused across a semipermeable membrane from one fluid compartment to another
  • Corrects fluid, electrolyte and acid-base imbalances, and removes waste products
70
Q

What is a dialysate?

A
  • Used in both types of dialysis
  • Uses osmosis & oncotic pressure to transfer fluids/particles back and forth across the semi-permeable membrane
  • Specific solution prescribed based on patient’s current bloodwork to facilitate diffusionA
71
Q

Advantages of peritoneal dialysis

A

Can be done on a regular basis so that fluid and electrolyte shift is less dramatic
Can be done at home (don’t need to be in hospital)
Relieves uremic symptoms
Greater flexibility with treatment (can do other activities/work while dialysis happens; can travel)

72
Q

Disadvantages of peritoneal dialysis

A

Considerable infection risk (peritonitis)
Permanent catheter in abdomen
Can’t get wet (no swimming)
Dialysis a daily part of life
Slow (slower than hemo)
Abdominal discomfort

73
Q

Describe the hemodialysis system

A
  • Blood Compartment
  • Contains electrolytes, wastes, toxins, excess water
  • Exerts oncotic and hydrostatic pressure
  • Dialysate Compartment
  • Contains electrolytes similar to plasma
  • Circulates on the outside of the tubing system
  • Has a semi-permeable membrane; forces movement of waste from blood into dialysate
  • Adjustable
74
Q

How to assess arm of fistula for hemodialysis

A
  • High risk!! Clots, bleeds, infection
  • DO NOT take BP or blood work on the arm of a fistula!
  • Inspect the AV fistula for redness, bruising, pustules, swelling, bulging
  • Palpate for a thrill (should have)
75
Q

Advantages of hemodialysis

A

Relieves uremic symptoms
Quick and efficient
Requires min. 3 treatments/week (4-8hrs)
Most individuals have suitable vessels to establish an access site

76
Q

Diadvantages of hemodialysis

A

New medications, restricted intake of fluids
Requires vascular access each time and anticoagulation
Must plan around hemodialysis schedule
Travel to dialysis unit
Restricts activity level

77
Q

Who is CRRT used for?

A
  • For patients who are hemodynamically unstable
  • Has less hemodynamic side effects than intermittent hemodialysis
  • Useful in AKI
  • Allows for more gradual removal of excess electrolytes/fluid
  • Critical care setting ONLY
  • Uses different methods to clear excess fluids, fluids and solutes, electrolytes, creatinine, and urea.

High Acuity (20 decks)

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