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Renal Flashcards

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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
Post-Renal AKI causes
hinders urine flow after filtration * kidney stone * cath block * tumor monitor for anuria <100 ml/24hr
26
Nursing assessment AKI
* Weights * I/O * med check * monitor BUN/Cr * hemodynamics
27
Acute Tubular Necrosis
hospital aquired (intrarenal) * ischemic results from prolong hypoperfusion (pre-renal)
28
Nephrotoxic ATN
concentration of dye/med cases necrosis of tubular cells 1. Amniglycosides (cins) 2. Vanco 3. Zosyn 4. Contrast
29
ATN pathophysiology
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
30
ATN - Onset phase
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**
31
ATN - Oliguric/Anuric phase
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
32
ATN - Oliguric/Anuric Electrolytes
* Hyperkalemia * Hyponatremia * Hyperphosphatemia * Hypocalcemic (most common)
33
ATN - Diuretic phase
increase in GFR * Polyuria 2-4L/day * hypotension
34
ATN - Diuretic Electrolytes
* Hypokalemia * Hypernatremia
35
ATN - Recovery phase
kidney function slowly returns to normal * increase urine out * GFR back to normal within 1-2 years
36
Potassium
regulate nerve impulse conduction, cardiac and muscle contraction
37
Hyperkalemia
* 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
Hypokalemia
* ECG changes (INVERTED T) * Dysrhythmia * Hypotension Treat via **Potassium replacement** | diuretic phase
39
Sodium
135-145 major cation, predictor of serum osmolality (movement H20 in body) low = overhydration high = dehydration
40
Hyponatremia
* weakness * lethargy * headache * confusion * tremor/convulsions * seizure * risk for respiratory arrest treat via **fluid restriction diuretics renal replacement therapy** | oliguric
41
Hypernatremia
* dehydration * tachycardia * hypotension * neuro changes (muscle irritability, restless, agitation, decrease LOC) Treat via **IVF hypotonic (0.45% NS) admin slowly** | diuretic
42
Calcium
absorption from small intestine under influence of vitamin D regulated by parathyroid hormone
43
Hypocalcemia
* 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
Hypercalcemia
* weakness * drowsiness * ECG --> QT shortened, heart block Treatment via **Calcitonin therapy diuretics dietary modification**
45
Phosphorus
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
Hyperphosphatemia
* hypocalemia * hyperreflexia * muscle weakness * pruritus treat via **Calcium carbonate Tums, PhosLo,RenaGel** | oliguric
47
Phosphate rich foods
1. dairy 2. processed meats 3. nuts 4. carbonated beverages
48
Hypophosphatemia
* muscle weakness * respiratory function * tissue hypoxia * decreased reflexes * bone pain treat via **phosphate replacement**
49
Magnesium
responsible for transmission of sodium and potassium across cell membrane decrease=decrease calcium and potassium
50
Hypomagnesaemia
* Dysrhythmia (PVC) * VTACH/VFIB Treat via **Replacement therapy replace mag before potassum**
51
Bicarbonate
anion regulated by the kidneys (takes 48-72 hours) produced in distal resorption in proximal
52
AKI results in metabolic ____
acidisosis hydrogen into cell and potassium out
53
AKI treatments
Early detection Treat cause restore and maintain fluid balance Restore electrolyte imbalances restore preserve renal function RRT/ hemodialysis
54
Renal replacement therapy
Dialysis hemodialysis and continuous renal replacement therapy
55
Dialysis
Works by circulating blood outside the body (synthetic tubing)
56
Ultrafiltration
remove fluid * positive hydrostatic pressure applied to the blood * negative pressure applied to the dialsate bath * pressures pull blood drained into the machine
57
Renal Replacement Therapy | indicators for use of therapy
* bun >90 * hyperkalemia * drug toxicity * fluid overload * acidosis * pericarditis * GI bleeding * changes in mentation
58
Contraindication of hemodialysis
* Hemodynamic instability * inability to anticoagulate * lack of access to circulation * (vascular cath) * (av fistula)
59
Continuous Renal Replacement Therapy
* hemodyanmic stability is maintained d/t longer filtration time * helps when pt's are hypotensive
60
Capillary Leak Syndrome "third spacing"
fluid shift from intravascular to interstitial space Occurs by diffusion (hydrostatic/oncotic pressure) involve loss and reabsorption phase
61
CLS - Loss phase
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
CLS - Loss phase assessment findings
* decreased CVP/wedge * hypotension * tachycardia * increased osmolality * decrease urine output (increase CR/BUN)
63
CLS interventions (loss phase)
Administration of hypertonic or colloids *pull back fluid into vasculature
64
CLS - Reabsorption phase
fluid back into intravascular space from interstitial * trauma/inflammation subside * cap repairs/nromal permeability * lymph blockage decreases **plasma protein returns!!**
65
CLS - Reabsorption phase clinical findings
* Increased wedge / CVP * assess for fluid overload * hemodynamic return to baseline
66
CLS - Reabsorption interventions
* decrease IVF administration * diuretics
67
Antidiuretic Hormone
secreted post pit * controls extracellular volume ↑ osmolality = ADH released = circulated to nephrons = reabsorption of H20 = decreases osmolality
68
Syndrome of Inappropriate ADH
excessive amounts of ADH secreted into osmolality
69
SIADH | Causes
* pit tumor * bronchogenic * mech ventilation (decreases blood to right side of the heart dropping BP=dropping ADH)
70
SIADH | pathophysiology
increase adh = increased water absorption= excess extracellular compartment= hyponatremia
71
SIADH | assessment
* water rention/toxicity * Na+ under 125 * slight weight gain * mental confusion * seizures * decrease LOC * coma/death
72
SIADH | interventions
* fluid restriction * slow sodium replacement * furosemide * demeclocycline(ADH)
73
How fast do you replace sodium?
no faster than 1-2 mEq/L/hour
74
Diabetes Insipidus
deficiency of antidiuretic hormone resulting in dehydration
75
Central DI
posterior pit fails to release * CNS head trauma * neurosurgery * ↑ icp
76
Nephrogenic DI
inability of kidneys to respond to ADH
77
DI | clinical manifestations
* polyuria (3-20L/day) * ↓ urine specific gravity * polydipsia * weight loss * dehydration
78
DI interventions
prevent dehydration * Free water intake * hypertonic IVF when serum sodium >145
79
Central DI intervention
Vasopressin
80
Nephrogenic DI intervention
Hydrochlorothiazide

Critical Care (9 decks)

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