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Critical Care > Renal > Flashcards

Renal Flashcards

1
Q

What are the kidneys dominant role?

A

filtration
* regulate concentration solutes extracellular fluid
* remove metabolic waste

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2
Q

Renal blood flow route

A

Renal Art
Afferent arterioles
Glom
Vasa reca/caps
Venous

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3
Q

Nephron

A

functional unit of the kidney
composed of glomerulus, bowmans capsule, p/d convoluted tubule, collecting ducts

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4
Q

Where is renin released?
What is the action?

A

Distal tubule
Senses fluid volume and acts to regulate BP

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5
Q

Kidney functions (5)

A
  1. eliminate waste
  2. BP regultion
  3. erythrocyte production
  4. vitamin d activation
  5. acid/base balance
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6
Q

If kidneys loose function what are two conditions you may see (r/t functions)

A

anemia
calcium deficiency

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7
Q

Glomerular Filtration RAte

A

Rate of filtrate (pee) is formed
dependent on blood flow
pressure in bowman’s capsule and oncotic pressure

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8
Q

GFR autoregulation

A

Afferent arterioles adjust diameter to maintain BP

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9
Q

GFR values

A

<100 is decrease in function
<15 is kidney failure

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10
Q

Fluid balance components

A

Intra = 40%
Extra =
Intravascular 5%
Interstital 15%

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11
Q

Normal serum plasma

A

275 to 295

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12
Q

Isotonic

A

equal concentration as plasma
indicated in hypotension
1. 0.9 NaCl
2. Lactated ringer (K+!)

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13
Q

Hypertonic

A

greater concentration than plasma
(increased CVP/Wedge)
1. 3% NaCl
2. D5 NaCl(D5 Normal)
3. D5 in Lactated Ringer’s(D5LR)
4. D5 0.45% NaCl(D5- Half Normal)

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14
Q

Hypotonic

A

lower concentration than plasma (decreased CVP/Wedge)
1. 0.25% NaCl(Quarter Normal Saline)
1. 0.45% NaCl(Half-Normal Saline)

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15
Q

Colloid

A

high molecular weight subtances
(do not usually cross capillary membrane)
* Fluid into intravascular
* (Albumin/Blood)

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16
Q

Free H20 solutions

A

Do not stay in intravascular space (contraindicated when intravascular replacements are required)
seen in hypernatremia
*Dextrose
5%, 10%, 50%
one leter D5W is 170kcal

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17
Q

Acute Kidney Injury Definintion

A
  • decline in gfr
  • retention of products in the blood normal excreted
  • electrolyte imbalances
  • acid/base abnormalities
  • fluid volume disruptions
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18
Q

Acute Kidney Injury Diagnostics

A

Increased BUN
Increased CR
Oliguria (<400ml/day)

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19
Q

Blood Urea Nitrogen

A

end product of protein metabolism
10-20mg/dl
influenced by protein intake, blood in GI, cell catabolism and diluted by fluid administration

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20
Q

Creatinine

A

end product protein metabolism
indicator or renal function
0.7-1.4mg/dl

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21
Q

Pre-Renal AKI causes

A
  • decrease CO (HF)
  • Hemorrhage
  • Vasodilation
  • Thrombosis

decrease BF to kidneys

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22
Q

Pre-Renal AKI assessment

A

hypoperfusion
AEB hypotension, tachycardia, low CVP/Wedge, BUN/Cr, H+H, sodium levels

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23
Q

Intra-Renal AKI causes

A

produces ischemic/toxic insult to nephron
* Renal ischemia
* Exogenous (contrat)
* Endogenous (rhabdomyolysis) (elderly down)
* Infection

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24
Q

Intra-Renal assessment

A
  • UOP
  • BUN/Cr elevation
  • PMH
  • Use of contrast
  • Infection
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25
Q

Post-Renal AKI causes

A

hinders urine flow after filtration
* kidney stone
* cath block
* tumor
monitor for anuria <100 ml/24hr

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26
Q

Nursing assessment AKI

A
  • Weights
  • I/O
  • med check
  • monitor BUN/Cr
  • hemodynamics
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27
Q

Acute Tubular Necrosis

A

hospital aquired
(intrarenal)
* ischemic results from prolong hypoperfusion (pre-renal)

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28
Q

Nephrotoxic ATN

A

concentration of dye/med cases necrosis of tubular cells
1. Amniglycosides (cins)
2. Vanco
3. Zosyn
4. Contrast

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29
Q

ATN pathophysiology

A

tube obstruction which blocks interworking
* results in inflammation = cell injury and death
* decrease UOP
* continues till perfusion is restored or complete loss of nephrons
* Ischemic cause more damage to cells than nephrotoxic injury

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30
Q

ATN - Onset phase

A

ischemic injury is evolving
* GFR decreases d/t ischemic/nephrotoxin
* cell death starts
* treatment and early rec can prevent irreversible damage
remove toxic agent and maintain hemodynamics

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31
Q

ATN - Oliguric/Anuric phase

A

necrotic cellular debris blocks formation of urine and removal of waste
* oliguria occurs
* muddy brown cast in urine
* increased fluid overload (respiratory failure/edema)
* BUN/Cr rapid increase
* metabolic acidosis

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32
Q

ATN - Oliguric/Anuric Electrolytes

A
  • Hyperkalemia
  • Hyponatremia
  • Hyperphosphatemia
  • Hypocalcemic (most common)
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33
Q

ATN - Diuretic phase

A

increase in GFR
* Polyuria 2-4L/day
* hypotension

34
Q

ATN - Diuretic Electrolytes

A
  • Hypokalemia
  • Hypernatremia
35
Q

ATN - Recovery phase

A

kidney function slowly returns to normal
* increase urine out
* GFR back to normal within 1-2 years

36
Q

Potassium

A

regulate nerve impulse conduction, cardiac and muscle contraction

37
Q

Hyperkalemia

A
  • Muscle weakness
  • flaccid paralysis
  • ECG changes –> lethal dysrhythmia
    Treat via

diuretics
IV insulin / glucse (K cocktail)
Sodium polystyrene (kayexalate)

PEAK T WAVE

>6.0 and above

38
Q

Hypokalemia

A
  • ECG changes (INVERTED T)
  • Dysrhythmia
  • Hypotension
    Treat via
    Potassium replacement

diuretic phase

39
Q

Sodium

A

135-145
major cation, predictor of serum osmolality (movement H20 in body)
low = overhydration
high = dehydration

40
Q

Hyponatremia

A
  • weakness
  • lethargy
  • headache
  • confusion
  • tremor/convulsions
  • seizure
  • risk for respiratory arrest
    treat via
    fluid restriction
    diuretics
    renal replacement therapy

oliguric

41
Q

Hypernatremia

A
  • dehydration
  • tachycardia
  • hypotension
  • neuro changes (muscle irritability, restless, agitation, decrease LOC)
    Treat via
    IVF hypotonic (0.45% NS) admin slowly

diuretic

42
Q

Calcium

A

absorption from small intestine under influence of vitamin D

regulated by parathyroid hormone

43
Q

Hypocalcemia

A
  • decrease CO/contraction
  • hypotension
  • Dysrhytmias
  • muscle spasms
  • positive chvostek (facial nerve)
  • Trousseau’s sign (finger contract)
    Treat via
    Calcium replacement
    Diet low in phosphorus

oliguric

44
Q

Hypercalcemia

A
  • weakness
  • drowsiness
  • ECG –> QT shortened, heart block
    Treatment via
    Calcitonin therapy
    diuretics
    dietary modification
45
Q

Phosphorus

A

source of ATP
muscle contraction and nerve impulses
regulate parathyroid

PTH helps calcium resorbed back into bloodstream and excrete phosphorus into urine

INVERSE RELATIONSHIP TO CALCIUM

46
Q

Hyperphosphatemia

A
  • hypocalemia
  • hyperreflexia
  • muscle weakness
  • pruritus
    treat via
    Calcium carbonate
    Tums, PhosLo,RenaGel

oliguric

47
Q

Phosphate rich foods

A
  1. dairy
  2. processed meats
  3. nuts
  4. carbonated beverages
48
Q

Hypophosphatemia

A
  • muscle weakness
  • respiratory function
  • tissue hypoxia
  • decreased reflexes
  • bone pain
    treat via
    phosphate replacement
49
Q

Magnesium

A

responsible for transmission of sodium and potassium across cell membrane
decrease=decrease calcium and potassium

50
Q

Hypomagnesaemia

A
  • Dysrhythmia (PVC)
  • VTACH/VFIB
    Treat via
    Replacement therapy
    replace mag before potassum
51
Q

Bicarbonate

A

anion regulated by the kidneys (takes 48-72 hours)

produced in distal
resorption in proximal

52
Q

AKI results in metabolic ____

A

acidisosis

hydrogen into cell and potassium out

53
Q

AKI treatments

A

Early detection
Treat cause
restore and maintain fluid balance
Restore electrolyte imbalances
restore preserve renal function
RRT/ hemodialysis

54
Q

Renal replacement therapy

A

Dialysis
hemodialysis and continuous renal replacement therapy

55
Q

Dialysis

A

Works by circulating blood outside the body (synthetic tubing)

56
Q

Ultrafiltration

A

remove fluid
* positive hydrostatic pressure applied to the blood
* negative pressure applied to the dialsate bath
* pressures pull blood drained into the machine

57
Q

Renal Replacement Therapy

indicators for use of therapy

A
  • bun >90
  • hyperkalemia
  • drug toxicity
  • fluid overload
  • acidosis
  • pericarditis
  • GI bleeding
  • changes in mentation
58
Q

Contraindication of hemodialysis

A
  • Hemodynamic instability
  • inability to anticoagulate
  • lack of access to circulation
  • (vascular cath)
  • (av fistula)
59
Q

Continuous Renal Replacement Therapy

A
  • hemodyanmic stability is maintained d/t longer filtration time
  • helps when pt’s are hypotensive
60
Q

Capillary Leak Syndrome “third spacing”

A

fluid shift from intravascular to interstitial space
Occurs by diffusion (hydrostatic/oncotic pressure)
involve loss and reabsorption phase

61
Q

CLS - Loss phase

A

dehydrated intravascular vessel
* loss of plasma proteins (albumin)
* decreases oncotic pressure in blood vessel
* increased capillary permeability (sepsis/lymphatic blockage)
intravascular fluid moves to interstitial spacce

62
Q

CLS - Loss phase assessment findings

A
  • decreased CVP/wedge
  • hypotension
  • tachycardia
  • increased osmolality
  • decrease urine output (increase CR/BUN)
63
Q

CLS interventions (loss phase)

A

Administration of hypertonic or colloids

*pull back fluid into vasculature

64
Q

CLS - Reabsorption phase

A

fluid back into intravascular space from interstitial
* trauma/inflammation subside
* cap repairs/nromal permeability
* lymph blockage decreases
plasma protein returns!!

65
Q

CLS - Reabsorption phase clinical findings

A
  • Increased wedge / CVP
  • assess for fluid overload
  • hemodynamic return to baseline
66
Q

CLS - Reabsorption interventions

A
  • decrease IVF administration
  • diuretics
67
Q

Antidiuretic Hormone

A

secreted post pit
* controls extracellular volume
↑ osmolality =
ADH released =
circulated to nephrons =
reabsorption of H20 =
decreases osmolality

68
Q

Syndrome of Inappropriate ADH

A

excessive amounts of ADH secreted into osmolality

69
Q

SIADH

Causes

A
  • pit tumor
  • bronchogenic
  • mech ventilation (decreases blood to right side of the heart dropping BP=dropping ADH)
70
Q

SIADH

pathophysiology

A

increase adh =
increased water absorption=
excess extracellular compartment=
hyponatremia

71
Q

SIADH

assessment

A
  • water rention/toxicity
  • Na+ under 125
  • slight weight gain
  • mental confusion
  • seizures
  • decrease LOC
  • coma/death
72
Q

SIADH

interventions

A
  • fluid restriction
  • slow sodium replacement
  • furosemide
  • demeclocycline(ADH)
73
Q

How fast do you replace sodium?

A

no faster than 1-2 mEq/L/hour

74
Q

Diabetes Insipidus

A

deficiency of antidiuretic hormone resulting in dehydration

75
Q

Central DI

A

posterior pit fails to release
* CNS head trauma
* neurosurgery
* ↑ icp

76
Q

Nephrogenic DI

A

inability of kidneys to respond to ADH

77
Q

DI

clinical manifestations

A
  • polyuria (3-20L/day)
  • ↓ urine specific gravity
  • polydipsia
  • weight loss
  • dehydration
78
Q

DI interventions

A

prevent dehydration
* Free water intake
* hypertonic IVF when serum sodium >145

79
Q

Central DI intervention

A

Vasopressin

80
Q

Nephrogenic DI intervention

A

Hydrochlorothiazide

Critical Care (9 decks)

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