EXAM 2 NEPHROLOGY Flashcards
Fluid and electrolytes homeostasis First step = ◦ RBF depends on
production of glomerular filtrate from the renal plasma systolic BP and circulating BV
◦ GFR depends on
RBF
Kidneys receive _______CO over wide range of
20-30%; BP via auto-regulation
◦ Best perfused organ per gram of weight is the ______
Kidney
Renal hormones of autoregulation ◦ Vasodilators: PIND
prostaglandins E and I2, dopamine, nitric oxide
◦ Vasoconstrictors: ATEA
angiotensin II, thromboxane, adrenergic stimulation, endothelin
Nitrous oxide
increase GMP
Too much blood flow
Trauma There is delicate low pressure
RBF + GFR ______during the first
Double in first 2 weeks of post natal life
GFR estimated based on
Cr and height
GFR =
Height(cm) x k /serum creatinine
Better for function is ______but _____gives a close estimate
Creatinine Clearance; GFR
the K constant is dependent on
Age
◦ Kidneys regulate total body Na+ balance and maintains (2) Filters _______mEq Na per day but excretes ___due to
normal extracellular and circulating volumes 25000; 1% efficient resorption
The Proximal tubule resorbs ____-____% and Ascending limb of loop of henle _____% and distal tubule____% (____think PAD)(great to least)
50-70%, ascending limb of loop of Henle 25%, distal tubule 10%
Serum OsmolaLity controlled by (what hormone) Stimulated by ______(HINVOIS)
ADH, Increasing in plasma osmolaLIty , Hypotension, NV, opioids, inflammation and surgery
Normal serum osmolarity
275-295 mosm/kg
Osmolarity Osmolality
L/mosm Kg/mmosm
Potassium Regulation depends on_______ ◦ Binds to receptors in → ______
aldosterone distal nephron; ↑ K+ excretion
◦ Neonates cannot regulate or do this efficiently_______, they normally have ______ Normal K+ 0-1months; 1month - 2 years
- Potassium regulation (neonates less efficient at excreting potassium loads) - ↑ K+ 4-6 4-5.5
Secrete Potassium: Name of the cells
Principal cells
Hyperkalemic patients are often
Acidotic
As H+ inside the cells, potassium
Leave the cell –> patient becomes Hyperkalemic
Treatment of hyperkalemic
Albuterol insulin, Calcium gluconate B-agonist
Acid-base balance where is almost all bicarb reclaimed ________ Is bicarb lost in neutralization regenerated? New bicarb= ___________in ________
◦ Almost all bicarbonate (HCO3-) reclaimed in proximal tubule ◦ Bicarb lost via neutralization of acid = regenerated New bicarb = product of breakdown of carbonic acid (H2CO3) in distal nephron
Infants normally slightly _____have less ____compared to adults They have limited _______
Infants normally slightly acidotic (pH=7.37) have less bicarb (22 mEq/L) compared to adults ◦ Limited in ability to respond to acid load, esp. premies
Acute Kidney Injury = _____onset ◦ Multifactorial; classified as
(AKI, formerly acute renal failure) = abrupt prerenal, intrarenal, postrenal
2 issues in AKI you must know
- deterioration in ability of kidneys to clear nitrogenous wastes (urea and creatinine) + - ↓ability to excrete solutes and maintain normal water balance
◦ Clinical presentations of renal insufficiency:
edema, HTN, HyperK+, uremia
Children more likely to have renal disease from______such as (SS)
systemic diseases (e.g., sickle cell disease, systemic lupus erythematosus)
Harmful to kidney among other INTRARENAL
Contrast dye Acute Glomerulonephritis NSAIDS Antibiotics (Aminoglycosides, AMPHOTERICIN B)
POST-RENAL
Obstruction (stone, tumor, BPH)
Pre-renal is (LCS) Exacerbated by : NSAIDS, ACEI, ARBs.
the most common Loss of ECF , cardiac failure, sepsis DIMINISHED RENAL PERFUSION Major hemorrhage, V/D, severe burns, CHF
Intra-renal causes
20-30% Infants: Birth ASPHYXIA, SEPSIS, cardiac surgery Older: TUHS (Trauma, Uremia (hemolytic), sepsis
Post renal Obstruction can be intrarenar
1.INTRARENAL Tumor lysis myoglobinuria Hemoglobinuria Meds: acyclovir, antiviral 2. URETER: Stones, compression pressure from lymph/tumor Post renal
Exact pathophysiology of AKI________
what factors increases renal vasoconstriction?
Unknown Profound renal vasoconstriction –>
GFR Increase renal vasoconstriction RAAS , SNS and endothelial dysfunction (Increase endothelin, decrease NO)
Therapy for Vasodilation
Prostaglandin, Dopamine, ACEI, CCB Endothelin antagonists, however does not significantly reverse AKI
Opposing forces to pressure tissue
Protein want to hold on fluid Decrease GFR Less pressure pushing forward, same pressure pushing backwards, DECREASE GRF–> decrease in Renal output
AKI can result also from
renal tubule cell injury
Nephrotoxin or ischemic insult
Obstructs within minutes Decrease GFR via obstruction of lumen of tubule.
With reperfusion injury after ischemia metabolic BYPRODUCT call in
Neutrophils.
Reperfusion injury increases intracellular adhesion molecule 1 (ICAM-1) on endothelial cells promoting the adhesion of circulating neutrophils and their eventual infiltration into the parenchyma.
Blood flow down–>
ischemia –> Low GFR –> Dialysis
PRE renal AKI Look at the _______ .
if ratio____Prerenal
if ratio______ renal
Prerenal = FEna _____%children ___% infants
Intrarenal = FEna > __%
What does FEna Stands for
Look at BUN: CR ration >20 Prerenal <20 Renal
FENA prerenal Children < 1% 2.5% infants
Fena INTRARENAL > 1%
Differentiate between pre-renal
look at FENA Renal US
Interventions : Hypovolemic
Fluid resuscitation of at least 20ml/kg over 30-60min
RULE OF THUMB: give 500 or less
Diuretics should only be used
After circulation volume is adequate restored
Dialysis for patients- indications
When is dialysis indicated?
Hyperkalemia Fluid overload refractory to diuretics
Severe metabolic acidosis
S/S of uremia (pericarditis, encephalopathy)
BUN approaches 100mg/dL
CKD
Decrease in RF about 30-50% of normal Measure with GFR, CrCl etc.
Renal function under
30%
Different stages of CKD
5 stages, and percentage of normal kidney function
1- 90% or more % of normal kidney function
2- 60-89%
3- 30-59%
Stage 1-3 There are no specific symptoms, but kidney function can slowly decline
4 15-29% (kidney function is very low, and treatment for kidney failure may be needed soon.
5 <15% Ki
Medications that can cause disfuction
ACEI Beta Blockers Spironolactone
First line for HYPERK+ stabilized MYOCARDIUM with
CALCIUM (tell cell to become more + ions) (Calcium chloride 10%) 10-33mg/kg/IV Albuterol requires asthma dose x8
How does Kayexalate works
Help decrease total body K+
Metabolic acidosis : what happend?
proximal renal tubules UNABLE TO INCREASE AMMONIUM FORMATION Unable to generate bicarb
Secondary Hyperparathyroidism
Decrease Vit D activation–> Hypocalcemia –> Parathyroid overcompensates
Calcium and phosphate
Not friend, if one in, the other out.
Phosphate is normally
What happens with Phosphate containing ENEMA?
excreted, but decrease in failing kidneys
cannot deal with large phosphate load
phosphate =containing enema can lead to
hypocalcemia and hyperphosphatemia
Erythropoietin
Synthesized and excreted By PERITUBULAR CELL in renal cortex responding to decrease tissue O2
Inefficient in renal insufficiency
Tx: Erythropoietin therapy
Complications of ERYTHROPOIETIN THERAPY
Hypotension and thrombosis of AV grafts
CV for Kidney issues
know dry weight (when no signs of Overload) and CURRENT WEIGHT TO compare
Volume overload there is
increase CO –>and peripheral vasoconstriction –>Hypertension
Childhood associated KNOW PRUNE BELLY
NO TONE IN ABDOMEN SHRINKLED BELLY PRUNE BELLY PROBLEMS WITH KIDNEYS
urethral obstruction in utero leads to dilatation of the urethra (megaurethra is a common finding), which, combined with bladder distention and ascites, causes distention of the abdomen in utero. This ultimately leads to vesicoureteral reflux and ureteral dilatation in 80% of affected children.
Preop preparation
What kind of anemia is usually present?
Oliguria (do not let lead to overload) Check dehydration
Fluids and electrolytes
Changes in compartment volume affect volume distribution and pharmacokinetics
NormocytiC NORMOCHOROMIC ANEMIA –> Decrease erythopoietin
In the children in preop
They are at risk for aspiration
Increase uremia can lead to seizure.
Biggest peri-operative insults
CPB (hypoperfusion, oxidative stress, activition of inflammatory system)
Risks for AKI increased with kids (CHAR)
CHF
HTN
ASCITES
RENAL INSUFFICIENCY
Most valuable baseline labs to done
Coagulations CBC, BMP BUN/Cr ratiohn
With suspicion of pericardial effusion or cardiomyopathy
GET ECHO
Potassium can be
Antiport Depends on acid base status and trends K+ 5.5-6.0 which is baseline chronically NO TREATMENT REQUIRED
AN acute increase in K of ______requires _______
K+ 5.5 requires intervention
KNOW PRACTICE CALCULATION :Acidosis increase serum K by 0.5 for every
decrease in pH of 0.1
Magnesium needs to be______
why?
corrected PREOPERATIVELY
Can lead to SVT, ventricular arrythmias
Hgb
within 24 hours of procedure
Transfusion not recommended unless: ___Hct
What won’t platelet do?
Will improve with ______, ______ and ________
What can we give?
Hct < 25%
PLATELET WON’T INFUSE But dysfunctional won’t improve w/ platelet tranfusion
WIll improve with dialyisis, PRBC transfusion and Erythropoietin
Desmopression 0.3mcg/kg IV over 15-20 min Improve platelet function for 6-12 hours.
TOo much magnesium
Leads to MUSCLE WEAKNESS POTENTIATES NMB
Platelet count
normal, wont help
Desmopressin for
worried about bleeding give desmopression 0.3mcg/kg/IV over 15-20 min
Dialysis
Helps reduce K and remove excess water and waste produces can results in Fluid electrolytes imbalances and Hypovolemia.
On day of dialysis
Not a good idea to have surgery
Need to know about dialysis?
When should hemodialysis be performed.?
Last dialysis date, output and input,
DRY weight and actual weight.
HD SHOULD BE DONE THE DAY BEFORE SURGERY not the day of surgery
Peritoneal dialysis can you have on day of surgery
Yes just assess pulmonary status.
RENAL FAILURE, Scientifically SPINAL
Not a problem for kidney issues
Adjustments of patients with renal issue?
Chronic HTN can lead to ______
What can you do to prevent that?
Chronially HTN, they tend to TANK their BP , Chronically Hypovolemia, Preload with NS
For lupus and steroids medicaitons
You have to continue those medications
Versed and FENTANYL is lipid soluble
Liver will metabolize OK to give
NOT OK TO GIVE WITH KIDNEY ISSUES
What is the most IMPORTANT strategies for Renal protection
MORPHINE
OPTIMIZATION of hemodynamics and Intravascular volume while avoiding NEPHROTOXIC drugs (abt, contrast, nsaids)
Kidney patients need extra NPO time
NO
If the patient will get contrast
Give some bicarb and NS
Fenoldopam
Dopamine 1 receptor agonist INCREASE GFR WITHOUT HTN
DIURETICS does what to kidney disease
WORSE due to hypovolemia
VASCULAR ACCESS For kidney
what should be avoided and why?
What is a POOR output metric for renal perfusion in children?
ImPORTANT: you always need to have a way to administer this vasocative med?
Arterial access should be avoided
Might affect future shunt sites
URINE OUTPUT
CALCIUM
Average life span
5 years for each shunt site
CORE METRIC
URINE OUTPUT
YOU NEED TO HAVE ACCESS BECAUSE
YOU MAY HAVE TO ADMINISTER LIFE SAVING CALCIUM.
Renal Osteodystropy
High risk Be careful with positioning
Children with Renal failure and hx of HTN risk for both
Balance fluid resuscitation because?
HYPOTENSION and HYPERTENSION
Decrease albumin –> decrease oncotic pressure –>PULMONARY EDEMA
NS vs LR
NS resulted in HyperKalemic and metabolic acidosis, LR did not
Anesthetic agesnt: Requiring RENAL EXCRETION
what should you consider?
meds requiring RENAL EXCRETION (Hydrophillic, highly ionized)
most affected (PCN, Cephalosporine,s, aminoglycosides, digoxin)
INCREASING DOSING INTERVAL
Meds partly dependent on renal elimination
Vec Roc Atropine Glycopyr neostigmine
When high Vd, you generally need
higher bolus and low maintenance
VD
Dose (mg) / plasma concentration (mcg/ml)
Propofol is said d to have
some renal protection
Desflurane and Isoflurance
NOT ASSOCIATED WITH IMPAIRED RENAL FUNCTION
SevoFLURANE should be ran per law with at least
2L of fresh air
Low flow techniques: Best VA
DESFLURANE is the best
NDNMB
◦ May have autonomic neuropathy → ↓gastric emptying → aspiration ◦ RSI? Roc takes longer to work c/renal patients (30 sec more)
NDNMB ________and ________preferred
Atracurium and cisatracurium
Succinylcholine does not
Increase is about _____mEq/L unless peripheral neuropathy is present
increase K+ in renal patients more compared to normal
◦ 0.5-0.8 mEq/L unless peripheral neuropathy present ◦ ↑ Plasma K+ levels in chronic renal failure → no K+ bump after succ administration d/t intra/extracellular equilibrium
↑ Plasma K+ levels in chronic renal failure →
no K+ bump after succ administration d/t intra/extracellular equilibrium
If NMB last longer then expected what should you rule out first ?
Which medication can help
Increased magnesium
Ca2+
Neogstimine might be delayed
NMB sugammadex entirely _______
contraindicated in ____
renally excreted
Severe Renal failure
Intraoperative management
Opioid of choice
What should be done to doses of other meds with Remi?
Which 2 medications has metabolites that build up?
metabolism via nonspecific blood/tissue esterases
Doses of other opiods used should be decrese by 30-50%
MORPHINE and MEPERIDINE
Which 2 medications metabolites DO NOT ACCUMULATE
Fentanyl
Sufentanyl
Prolonged antagonism by
Naloxone expected with renal failure
Actions of dexmedetomidine
Suppresses vasopression secretion
diuretic efffect –> Increases GFR/UOP/RBF
NO active metabolic
Intraop Emergence considerations
Delayed emergence
Vomiting
aspiration
HTN
Resp depression
Pulm edema
Modest hypercapia –> Acidosis + hyperkalemia
IntraOP management PACU
HTN treated with potent vasodilators: Hydralazine diazoxide, nitroprusside
Nicardipine (0.5-5mcg/kg/min; max 20mg/hr)
What is the first line therapy for acute HTN? Dose?
What should you suspect if there is confusion ?
Labetalol 0.1-0.4mg/kg/hr q10min
UREMIC ENCEPHALOPATHY
