Renal Flashcards
What are the kidneys dominant role?
filtration
* regulate concentration solutes extracellular fluid
* remove metabolic waste
Renal blood flow route
Renal Art
Afferent arterioles
Glom
Vasa reca/caps
Venous
Nephron
functional unit of the kidney
composed of glomerulus, bowmans capsule, p/d convoluted tubule, collecting ducts
Where is renin released?
What is the action?
Distal tubule
Senses fluid volume and acts to regulate BP
Kidney functions (5)
- eliminate waste
- BP regultion
- erythrocyte production
- vitamin d activation
- acid/base balance
If kidneys loose function what are two conditions you may see (r/t functions)
anemia
calcium deficiency
Glomerular Filtration RAte
Rate of filtrate (pee) is formed
dependent on blood flow
pressure in bowman’s capsule and oncotic pressure
GFR autoregulation
Afferent arterioles adjust diameter to maintain BP
GFR values
<100 is decrease in function
<15 is kidney failure
Fluid balance components
Intra = 40%
Extra =
Intravascular 5%
Interstital 15%
Normal serum plasma
275 to 295
Isotonic
equal concentration as plasma
indicated in hypotension
1. 0.9 NaCl
2. Lactated ringer (K+!)
Hypertonic
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)
Hypotonic
lower concentration than plasma (decreased CVP/Wedge)
1. 0.25% NaCl(Quarter Normal Saline)
1. 0.45% NaCl(Half-Normal Saline)
Colloid
high molecular weight subtances
(do not usually cross capillary membrane)
* Fluid into intravascular
* (Albumin/Blood)
Free H20 solutions
Do not stay in intravascular space (contraindicated when intravascular replacements are required)
seen in hypernatremia
*Dextrose
5%, 10%, 50%
one leter D5W is 170kcal
Acute Kidney Injury Definintion
- decline in gfr
- retention of products in the blood normal excreted
- electrolyte imbalances
- acid/base abnormalities
- fluid volume disruptions
Acute Kidney Injury Diagnostics
Increased BUN
Increased CR
Oliguria (<400ml/day)
Blood Urea Nitrogen
end product of protein metabolism
10-20mg/dl
influenced by protein intake, blood in GI, cell catabolism and diluted by fluid administration
Creatinine
end product protein metabolism
indicator or renal function
0.7-1.4mg/dl
Pre-Renal AKI causes
- decrease CO (HF)
- Hemorrhage
- Vasodilation
- Thrombosis
decrease BF to kidneys
Pre-Renal AKI assessment
hypoperfusion
AEB hypotension, tachycardia, low CVP/Wedge, BUN/Cr, H+H, sodium levels
Intra-Renal AKI causes
produces ischemic/toxic insult to nephron
* Renal ischemia
* Exogenous (contrat)
* Endogenous (rhabdomyolysis) (elderly down)
* Infection
Intra-Renal assessment
- UOP
- BUN/Cr elevation
- PMH
- Use of contrast
- Infection
Post-Renal AKI causes
hinders urine flow after filtration
* kidney stone
* cath block
* tumor
monitor for anuria <100 ml/24hr
Nursing assessment AKI
- Weights
- I/O
- med check
- monitor BUN/Cr
- hemodynamics
Acute Tubular Necrosis
hospital aquired
(intrarenal)
* ischemic results from prolong hypoperfusion (pre-renal)
Nephrotoxic ATN
concentration of dye/med cases necrosis of tubular cells
1. Amniglycosides (cins)
2. Vanco
3. Zosyn
4. Contrast
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
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
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
ATN - Oliguric/Anuric Electrolytes
- Hyperkalemia
- Hyponatremia
- Hyperphosphatemia
- Hypocalcemic (most common)
ATN - Diuretic phase
increase in GFR
* Polyuria 2-4L/day
* hypotension
ATN - Diuretic Electrolytes
- Hypokalemia
- Hypernatremia
ATN - Recovery phase
kidney function slowly returns to normal
* increase urine out
* GFR back to normal within 1-2 years
Potassium
regulate nerve impulse conduction, cardiac and muscle contraction
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
Hypokalemia
- ECG changes (INVERTED T)
- Dysrhythmia
- Hypotension
Treat via
Potassium replacement
diuretic phase
Sodium
135-145
major cation, predictor of serum osmolality (movement H20 in body)
low = overhydration
high = dehydration
Hyponatremia
- weakness
- lethargy
- headache
- confusion
- tremor/convulsions
- seizure
- risk for respiratory arrest
treat via
fluid restriction
diuretics
renal replacement therapy
oliguric
Hypernatremia
- dehydration
- tachycardia
- hypotension
- neuro changes (muscle irritability, restless, agitation, decrease LOC)
Treat via
IVF hypotonic (0.45% NS) admin slowly
diuretic
Calcium
absorption from small intestine under influence of vitamin D
regulated by parathyroid hormone
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
Hypercalcemia
- weakness
- drowsiness
- ECG –> QT shortened, heart block
Treatment via
Calcitonin therapy
diuretics
dietary modification
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
Hyperphosphatemia
- hypocalemia
- hyperreflexia
- muscle weakness
- pruritus
treat via
Calcium carbonate
Tums, PhosLo,RenaGel
oliguric
Phosphate rich foods
- dairy
- processed meats
- nuts
- carbonated beverages
Hypophosphatemia
- muscle weakness
- respiratory function
- tissue hypoxia
- decreased reflexes
- bone pain
treat via
phosphate replacement
Magnesium
responsible for transmission of sodium and potassium across cell membrane
decrease=decrease calcium and potassium
Hypomagnesaemia
- Dysrhythmia (PVC)
- VTACH/VFIB
Treat via
Replacement therapy
replace mag before potassum
Bicarbonate
anion regulated by the kidneys (takes 48-72 hours)
produced in distal
resorption in proximal
AKI results in metabolic ____
acidisosis
hydrogen into cell and potassium out
AKI treatments
Early detection
Treat cause
restore and maintain fluid balance
Restore electrolyte imbalances
restore preserve renal function
RRT/ hemodialysis
Renal replacement therapy
Dialysis
hemodialysis and continuous renal replacement therapy
Dialysis
Works by circulating blood outside the body (synthetic tubing)
Ultrafiltration
remove fluid
* positive hydrostatic pressure applied to the blood
* negative pressure applied to the dialsate bath
* pressures pull blood drained into the machine
Renal Replacement Therapy
indicators for use of therapy
- bun >90
- hyperkalemia
- drug toxicity
- fluid overload
- acidosis
- pericarditis
- GI bleeding
- changes in mentation
Contraindication of hemodialysis
- Hemodynamic instability
- inability to anticoagulate
- lack of access to circulation
- (vascular cath)
- (av fistula)
Continuous Renal Replacement Therapy
- hemodyanmic stability is maintained d/t longer filtration time
- helps when pt’s are hypotensive
Capillary Leak Syndrome “third spacing”
fluid shift from intravascular to interstitial space
Occurs by diffusion (hydrostatic/oncotic pressure)
involve loss and reabsorption phase
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
CLS - Loss phase assessment findings
- decreased CVP/wedge
- hypotension
- tachycardia
- increased osmolality
- decrease urine output (increase CR/BUN)
CLS interventions (loss phase)
Administration of hypertonic or colloids
*pull back fluid into vasculature
CLS - Reabsorption phase
fluid back into intravascular space from interstitial
* trauma/inflammation subside
* cap repairs/nromal permeability
* lymph blockage decreases
plasma protein returns!!
CLS - Reabsorption phase clinical findings
- Increased wedge / CVP
- assess for fluid overload
- hemodynamic return to baseline
CLS - Reabsorption interventions
- decrease IVF administration
- diuretics
Antidiuretic Hormone
secreted post pit
* controls extracellular volume
↑ osmolality =
ADH released =
circulated to nephrons =
reabsorption of H20 =
decreases osmolality
Syndrome of Inappropriate ADH
excessive amounts of ADH secreted into osmolality
SIADH
Causes
- pit tumor
- bronchogenic
- mech ventilation (decreases blood to right side of the heart dropping BP=dropping ADH)
SIADH
pathophysiology
increase adh =
increased water absorption=
excess extracellular compartment=
hyponatremia
SIADH
assessment
- water rention/toxicity
- Na+ under 125
- slight weight gain
- mental confusion
- seizures
- decrease LOC
- coma/death
SIADH
interventions
- fluid restriction
- slow sodium replacement
- furosemide
- demeclocycline(ADH)
How fast do you replace sodium?
no faster than 1-2 mEq/L/hour
Diabetes Insipidus
deficiency of antidiuretic hormone resulting in dehydration
Central DI
posterior pit fails to release
* CNS head trauma
* neurosurgery
* ↑ icp
Nephrogenic DI
inability of kidneys to respond to ADH
DI
clinical manifestations
- polyuria (3-20L/day)
- ↓ urine specific gravity
- polydipsia
- weight loss
- dehydration
DI interventions
prevent dehydration
* Free water intake
* hypertonic IVF when serum sodium >145
Central DI intervention
Vasopressin
Nephrogenic DI intervention
Hydrochlorothiazide
