Renal Assessment Ex 3 Flashcards
Dr Morderca
How is osmolar homeostasis maintained?
What are 3 functions?
-Osmolar homeostasis mainly mediated by osmolality-sensors in anterior hypothalamus
-Cause pituitary release of ADH
-stimulate thirst
-Cardiac atria releases ANP→act on kidney to ↑Na+/H20 reabsorption
How does the juxtaglomerular apparatus mediate volume homeostasis?
It senses changes in volume and triggers RAAS to reabsorb Na and water
Interstitial fluid makes up __ of ECF
Plasma makes up ___ of ECF
3/4
1/4
ecf is more immediatly altered by kidneys
Which Na+ level do you correct prior to elective surgery?
less than 125 and >155!!
What are some causes of hypovolemic hyponatremia?
What are some causes of euvolemic hyponatremia?
hypovolemic: diuretics, gi loss, burns, trauma
euvolemic: Salt resitriction, endocrine related like hypothyroidism & SIADH (holding on to H2O and Na)
What are some causes of hypervolemic hyponatremia?
ARF, CKD, heart failure
Why are 15% of hospitalized patients hyponetremic?
-The are over fluid resiscuitated
-They have high levels of endogenous vasopression (inc H20 reabsorption)
S/S of Na 130-135
asymptomatic, H/A, N/V, fatigue, confusion, muscle cramps, depressed reflexes
Whare are s/s of Na 120-130?
120-130: HA, NV, fatigue, confusion, muscle cramps, malaise, unsteadiness
What is the treatment of hyponatremia?
Correction should not exceed what?
How fast do you infuse 3% NS?
treat underlying cause (volume status), REPLACE (electrolye drinks, NS), diuretics, hypertonic Saline
***should not exceed correction of 1.5 meq/lL/hr *
3% NS @ 80 mL/hr for 15 hr & check Na level q4h
What can happen if you correct Na+ too fast?
What is the treatment for hyponatremic seizures?
rapid correction (>6 meq/L in 24 hr) can cause** osmotic demyelination syndrome **and result in permanent neuro damage
3-5 mL/kg 3% NS over 20 min! until seizures resolve.
What are common causes of hypernatremia?
Hypovolemic-Renal or GI loss
Euvolemic- DI, insensible loss (skin, respiratory)
Hypervolemic- ↑Na+ intake( IV), hyperaldosteronism, Cushings
-overcorrection of hyponatremia, excessive sodium bicarb when treating acidosis
What are s/s of hypernatremia?
What is the treatment?
-orthostasis, restleness, lethargy, tremor, muscle twitching, seizures, death
-Assess volume status (US, UOP, turgor, cvp)
hypovolemic: NS
euvolemic: water replacement; or D5W
hypervolemic: diuretic
Goal for treatment for hypernatremia ?
- want reduction rate of <0.5 mmol/L/hr and <10 mmol/L/day to avoid cerebral edema seizures, neuro damage
Serum K+ reflects more ____ K+ regulation than total body K+.
Aldosterone causes the distal nephron to ____ K+ and ____ Na+
- Serum K+ reflects transmembrane K+ regulation more than total body K+
secrete k+ and reabsorb Na
<1.5% of K in ECF
What are common causes of hypokalemia?
- Low PO Intake
- Renal loss- Diuretics, Hyperaldosteronism
- GI loss – N/V/D, malabsorption
- Intracellular shift- Alkalosis, beta agonists, Insulin
- DKA (osmotic diuresis)
- HCTZ (in BP meds)
- Excessive licorice
3 categories- renal loss, GI loss, trancellular shift
What are symptoms of hypokalemia?
What is the treatment?
muscle weakness/ cramps, ileus, U waves
-PO, or 10-20 meq/L/hr
-each 10 meq rises K by 0.1 mmol/L
Avoid excessive insulin, B agonists, hyperventilation and diuretics
What are causes of hyperkalemia? (8)
- Hypoaldosteronism
- Renal failure
- Drugs that inhibit RAAS- Aldosterone inhibitors
- Drugs that inhibit K+ excretion
- Depolarizing NMB (Succs)
- Acidosis
- Cell death (trauma, tourniquet)~ cell rupture
- Massive blood transfusion
Succ increases serum K+ by 0.5-1 mEq/L
Symptoms of hyperkalemia?
- Skeletal muscle paralysis,↓fine motor
Cardiac dysrhythmias: - peaked T wave ; first sign
- P wave disappearance
- prolonged QRS complex
- sine waves
- asystole
Chronic intially minimal symptomatic (malaise, GI upset)
What is treatment for hyperkalemia?
-Dialyze~ 24 hr before surgery
-Ca+ (First)
-Hyperventilation- inc pH by 0.1 and lowers K by 0.4-1.5 mmOl/L
-10 u insulin and 25g D50 (works in 10-20 min)
-bicarb, loop diurettics, Kayexalate
avoid succ, hypoventilation, LR
Only 1% of Ca+ is in ___; 99% is stored in ___
60% of plasma Ca+ is ___ bound.
Ionized Ca+ level is affected by ___ levels and ___
ECF; stored in bone
protein bound
albumin levels and pH- high pH= low iCa+
Only ionized Ca+ is active
normal Ca= 1.2-1.38
What hormones regulate Ca+? (3)
- Parathyroid hormone: ↑’s GI , renal, and bone absorption
- Vitamin D: augments intestinal absorption
- Calcitonin: inhibits bone resorption
What are some causes for hypocalcemia? (6)
-Low PTH secretion (thyroid complication)
-parathyroidectomy* common complication is laryngospasm*
-Mg deficiency (Mg required for PTH production)
-Low Vit D
-Renal failure
-massive blood tranfusion
citrate preservative binds to Ca+, check iCa+ after 4 pRBC
Majority of pt’s w/ hypercalcemia have _____ or _____
hyper-parathyroid or cancer
Hyperparathyroid serum Ca++ <11
Cancer serum Ca++ >13
Less common causes of hypercalcemia
Vit D intoxication
Milk-alkali syndrome (excessive GI Ca++ absorption)
Granulomatous diseases (sarcoidosis)
S/S of hypercalcemia
confusion, lethargy, hypotonia, drop in DTR, abd pain, D/V, short QT.
Chronic: high Ca+–>hypercalcicurla and nephrolithiasis
s/s of hypocalcemia
paresthesias, irritability, HTN, seizures, myocardial depression, prolonged QT
Post-Parathyroidectomy-hypocalcemia-induced laryngospasm (life threatening complication)
What are s/s of hypomagnesia
Treatment?
Muscle weakness or excitation
seizures
Ventricular dysrhythmia (Polymorphic V-tack/Torsades De Pointes)
Slower infusions for less severe
Torsade’s/seizures→ 2g Mag Sulfate
What are the symptoms for Mag of 4-5 meq/L?
>6 MEQ?
>10?
What are treatments for hypermagnesium?
- 4-5 mEq/L: Lethargy, N/V, Flushing
- > 6 mEq/L: hypotension, ↓DTR
- > 10 mEq/L: Paralysis, apnea, heart blocks, cardiac arrest
-Treatment: diuresis, IV calcium, dialysis
common causes: preclampsia, or pheochromocytoma
What part of the kidney recieves 85-90% of RBF?
What part is vulnerable for developing necrosis in response to hypotension?
cortex
loop of henle
What is AKI?
What are the causes?
- AKI: Failure to excrete nitrogenous waste products or maintain fluid/electrolyte homeostasis
Caused by hypotension, hypovolemia, nephrotoxins
AKI affects 20% hospitalized pt and 50% ICU pt
What are AKI diagnostic criteria? (4)
-inc Cr by 0.3 mg/dL in 48 hr
-inc Cr by 50% in 7 days
-decrease creatinine clearence by 50%
-obrupt oliguria
normal CR: 0.6-1.3 mg/dL; Creatinine clearence: 110-140 mL/min
What is azotemia?
Azotemia: hallmark of AKI; buildup of nitrogenous products like urea and creatnine
AKI w/ MODS has 50% mortality rate :(
What are causes of prerenal azotemia?
What is the treatment?
hemorrhage, GI fluid loss, trauma, surgery, burns, cardiogenic shock, aortic clamping, thromboembolism (low renal perfusion)—-usually a volume issue and reverseable; can turn into renal azotemia
-Tx: Restore RBF: fluids, mannitol, diuretics, maintain MAP, pressors if needed.
BUN:CR >20:1;
What are causes of renal azotemia? (7)
nephron injury/ intrinsic
-acute glomerulonephritis, vasculitis, interstitial nephritis, ATN, contrast, nephrotoxic drugs, myoglobinuria
most difficult to reverse
Common labs in renal azotemia
-high serum Cr (d/t low filtration)
-low urea reabsorption –>low BUN
-BUN:CR <15:1
low GFR usually a late symptom
What are causes of postrenal azotemia? (4)
Tx?
nephrolithiasis, BPH, clot retention, bladder CA. due to obstruction!! causes high nephron tubular hydrostatic pressure
Tx: Remove the obstruction!
easiest to treat!
What are neurological complications of AKI? 7
R/t protein/ amino acids buildup,
uremic encephalopathy,
mobility disorders, neuropathies, myopathies, seizures, stroke
CV complications of AKI?
HTN, LV hypertrophy, pulmonary edema, CHF, uremic cardiomyopathy, arrythmias
- In order of incidence HTN→ LVH→ CHF→ischemic heart disease→ anemic heart failure→ rhythm disturbances→pericarditis & effusion→ cardiac tamponade, uremic cardiomyopathy
What are hematological compliations of AKI?
anemia (d/t low epo production, low RBC production and low RBC survival), platelet dysfunction, and vWF disrupted by uremia
ddabp to improve vWF and Factor VIII and improve coagulation
What are metabolic complications of AKI?
hyperkalemia, water and Na imbalances, hypoalbuminemia (kidneys allowing it to escape)
metabolic acidosis, malnutrition, hyperparathyroidism (parathyroid in overdrive to stimulate kidney to reabsorb Ca+)
What to consider when giving anesthesia to AKI patients?
- Correct fluid, electrolyte, acid/base status
= Volume; NS preferred for renal (no K+) - Careful w/colloids
- MAP maintained (20% of baseline)
- Vasopressors? (Vasopressin, Alpha-agonists)
- Prophylactic sodium bicarb
vasopressin constricts efferent arteriole and this inc RBF
Why give sodium bicarb to AKI patients
Sodium bicarb decreases formation of free-radicals
Prevents ATN from causing renal failure
CKD stages~ irreversible and progressive
What is the GFR in each stage of CKD?
Stage 1:
Stage 2:
1: normal or increased GFR >90
2: mildly decreased GFR, 60-89
GFR decreases by 10 per decade starting from age 20 :(
What is the GFR in each stage of CKD?
Stage 3
Stage 4
Stage 5
3: moderately dec GFR 30-59
4: severely decreased GFR 15-29 (HD)
5: kidney failure! GFR <15
Why are ACE and ARBs used in CKD?
Do you continue them day of surgery
↓systemic BP and glomerular pressure
↓proteinuria by reducing glomerular hyperfiltration
↓glomerulosclerosis
hold day of surgery cause they cause risk of profound hypotension!
What 5 complications indicate need for dialysis
- Volume overload during surgery (maybe surgery took longer than expected)
- Severe hyperkalemia
- Metabolic acidosis
- Symptomatic uremia
- Failure to clear medications
K should be what range on elective surgery?
HD should be dialyzed within ___ of elective procedure
K <5.5 MEQ/L
within 24 hr
Active metabolite of demerol is _____
What is the half life?
What are the 4 signs of neurotoxicity?
Normeperidine.
half life is 15-30 hours, as compared to demerol which is 2-4 hr
nervousness, tremors, muscle twitches, seizures
How much of morphine is cleared in urine? What is the active metabolite?
40% cleared through urine.
morphine-6 glucuronide which can cause life threatening resp depression
Failure to clear leads to active metabolites
normal range for GFR? and why it matters
125 - 140 mL/min
best measure of renal fxn over time
normal range for creat clearance?
why it matters?
110 - 140 mL/min
most reliable measure of GFR
24 hr urine test
serum creat normal range?
why does it matter?
0.6 - 1.3 mg/dL
inversely r/t GFR, acute doubling of serum creat can mean a drop in GFR by 50%
normal range for BUN?
why it matters?
10-20 mg/dL
urea is reabsorbed to concentrate our urine and hold more volume
low BUN = volume diluted or malnourished
high BUN = high protein diet, dehydrated, GI bleed, muscle wasting
normal BUN:creat ratio?
why it matters?
10:1
good measure of hydration status
whats the normal value of protein in our urine?
why is this impt?
what does proteinuria look like?
< 150 mg/dL
> 750 mg/day could mean glomerular injury or UTI
frothy urine!!
normal range of urine specific gravity?
why it matters?
1.001 - 1.035
measures nephron’s ability to conc urine
what does a drop in urine output suggest?
a LATE SIGN of volume loss
normal UOP range?
0.5 - 1 mL/kg/hr; 30 mL/hr
how can we measure volume status using US?
assess IVC
>50% collapse indicates fluid deficit
other ways: CVP, RAP, LAP, PCWP, PAP, SVV
what’s an easy way to determine fluid responsiveness?
passive leg raise
Which non-depolarizing muscle relaxer is not dependent on renal elimination that would be best for renal pts? based on her ppt
cisatracurium (nimbex), but rmbr its slow-ish onset
how much does GFR decrease per decade starting from age 20?
decreases by 10 :(
What’s the 1st line treatment for patients w/ CKD?
thiazide diuretics
What drugs do we need to HOLD on day of surgery (that a CKD pt is likely on)?
ACE-I and ARBs
to reduce the risk of profound hypotension!
Whats our target Hgb for a CKD patient?
10
- may need to transfuse and/or give some exogenous EPO if pt anemic
What are some risks with transfusing an anemic CKD patient?
- excessive Hgb leads to sluggish circulation
- acidosis and hyperkalemia also assoc w/ blood transfusions
what type of dialysis is more efficient?
HD > PD
what type of dialysis may be more suitable for a renal pt with poor cardiac function?
PD - slower, so less dramatic volume shifts
What do we need to give the renal pt if we’re expecting them to bleed a lot during surgery?
desmopressin (DDAVP) to help them produce more vWF and improve coagulation
tachyphylaxis risk tho
peaks 2-4h and lasts 6-8h
What NMBD is best for aspiration precaution patients especially in DM?
high dose roc, no succ
What are s/s of Na <120
<120: H/a, restleness, lethargy, seizures, brain stem herniation, respiratory arrest, death, coma
How are lipid insoluble drugs eliminated?
What are some examples she mentioned
Unchanged thru urine, use renal dosing. They will have a prolonged duration
o Thiazide diuretics
o Loop diuretics
o Digoxin
o Many antibiotics
