Renal Flashcards
(121 cards)
1
Q
About how much of total body weight is water
A
~60%
varies with gender, age, body fat%
↑Muscle=↑Water
2
Q
ECF is fluid outside of cells (______ & ______) = _____ volume of TBW
A
ECF is fluid outside of cells (ISF & Plasma) = < 1/2 volume of TBW
ECF is more immediately altered by kidneys
3
Q
Osmolar Homeostasis is mainly mediated by which sensors located where
A
osmolarity sensors in the anterior hypothalamus
4
Q
osmolar homestasis stimulates
A
stimulates thirst
pituitary release of vasopressin (ADH)
cardiac atria release ANP decreasing Na+/Water excretion
5
Q
what mediates volume homeostasis
A
juxtaglomerular apparatus sense changes in volume
↓Vol @ JGA triggers Renin-Angiotensinogen-Aldosterone system (RAAS)→Na+/H20 reabsorption
6
Q
normal Na+ level?
Na+ level okay for surgery?
A
135-145 mEq/L
≤125 or ≥ 155 mEq/L for elective surgery
7
Q
signs of hypovolemia
A
Na+/H2O loss
-decreasd skin turgor, flat neck veins, dry mucous membranes, orthostatic hypotension, tachycardia, oliguria
renal or extrarenal losses
8
Q
euvolemia causes of hyponatremia
A
Urine Na < 20: salt restricted diet
Urine Na > 20: glucocorticoid deficiency, hypothyroidism, high sympathetic drive, drugs, SIADH
9
Q
signs of hypervolemia
A
peripheral edema, rales, ascites
10
Q
example of renal losses leading to hypovolemia/hyponatremia
A
diuretics
mineralocorticoid deficiency
salt-losing nephritis
renal tubular acidosis
ketonuria
osmotic diuretic
Urine Na+ > 20
11
Q
example of extrarenal losses leading to hypovolemia/hyponatremia
A
vomiting
diarrhea
3rd space losses
burns
pancreatitis
muscle trauma
Urine Na+ < 20
12
Q
hypervolemia causing hyponatremia
A
Urine Na> 20: renal losses
-ARF, CKD
Urine Na< 20: avid sodium reabsorption
-nephrotic syndrome, cardiac failure, cirrihosis
13
Q
most severe consequences of hyponatremia
A
seizure, coma, death
14
Q
treatment of hyponatremia
A
treat underlying cause - look at volume status
*electroylte drinks
* normal saline
* diuretics
* hypertonic saline/3% NaCl
15
Q
hypertonic saline/ 3% NaCl
A
80 ml/hr over 15 hours
Na+ correction should not exceed 1.5 mEq/L/hr
16
Q
what can happen if Na+ correction of >6 mEq/L in 24 hours occurs
A
osmotic demyelination syndrome (can lead to permenent neuro demage)
17
Q
common causes of hypernatremia (6)
A
excessive evaporation
poor oral intake (very old, very young, AMS)
overcorrection of hyponatremia
Diabetes Insipidus
GI losses
excessive sodium bicarb (treating acidosis)
17
Q
hyponatremic seizures treatment
A
hyponatremic seizures= medical emergency
3-5mL/kg of 3% over 20 minutes until seizure resolves
18
Q
renal water loss leading to hypernatremia hypovolemia
A
osmotic diuretic
loop diuretic
postrenal obstruction
intrinsic renal disease
profound glycosuria
19
Q
euvolemia causes of hypernatremia
A
renal water loss:
Diabetes Inspidus: central, nephro, gestational
extrarenal water loss:
insensible losses- respiratory tract and skin
20
Q
hypervolemia causing hypernatremia (8)
A
sodium gains
hyperaldosternosism
Cushings
Hypertonic Dialysis
IV Sodium Bicarb
Hyperalimentation
Hypertonic saline enemas
Salt water drownings
Urine Na > 20
21
Q
extrarenal water loss leading to hypernatremia hypovolemia
A
diarrhea
GI fistulas
burns
sweating
22
Q
s/s of hypernatremia
A
orthostasis
restlessness
lethargy
tremor/muscle twitching/spasticity
seizures
death
23
Q
treatment for hypernatremia
A
root cause, assess volume status (VS, UOP< turgor, CVP)
hypovolemic: normal saline
euvolemic: water replacement (PO or D5W)
Hypervolemic: diuretics
24
Want Na+ reduction rate ≤____ mmol/L/hr and ≤ ____ mmol/L per day to avoid _____ _____, ____, and ______ damage.
Want Na+ reduction rate **≤0.5 mmol/L/hr and ≤ 10 mmol/L** per day to avoid **cerebral edema, seizures, and neurologic damage.**
25
potassium
3.5-5 mmol/L
major ICF cation
<1.5% in ECF
26
what does serum K+ reflect
transmembrane K+ regulation more than total body K+
27
aldosterones effect on potassium
aldosterone causes the distal nephron to secrete K+ and reabsorb Na+
| aldosterone inversely effects K+
28
renal failure and potassium
in renal failure, K+ excretion declines
excretions shifts toward the GI system
which is a slower process leading to buildup
29
hypokalemia common causes (7)
low PO intake
**renal loss** - diuretics, hyperaldosteronism
**GI loss**- N/V/D, malabsorption
**intracellular shift** - alkalosis, B-agonists, insulin
DKA (osmotic diuresis)
HCTZ
excessive licorice
30
additional causes of hypoK+
31
symptoms of hypoK+
cardiac and neuromuscular
* muscle cramps/weakness
* ileus
* dysrhytmias, U-wave
32
treatment of hypoK+
underlying cause
Potassium PO> IV (CVC) which may require days
33
IV K+ dose
10-20 mEq/L/hr IV
each 10 mEq IV K+ increases serum K+ by ~ 0.1 mmol/L
34
avoid what during hypoK+
excessive insulin
beta agonists
bicarb
hyperventilation
diuretics
35
hyperK+ causes (7)
renal failure
hypoaldosteronism
drugs that inhibit RAAS
drugs that inhibit K+ excretion
depolarizing NMB (succ increases K+ by .5-1 mEq/L)
acidosis (metabolic/respiratory)
cell death (trauma, tourniquet)
massive blood transfusion (storage and death of cells)
36
symptoms of HyperK+
chronic may be minimally symptomatic (malaise, GI upset)
skeletal muscle paralysis, decreased fine motor
cardiac dysrhtymias
37
EKG progression with HyperK+
Peaked T wave
P wave disappearance
prolonged QRS complex
sine waves
asystole
38
hyperK+ treatment
Calcium 1st inital treatment to stabilize the cell membrane
39
when should the pt be dialyzed before surgery
within 24 hrs
dialysis also initially causes hypovolemia, the day prior allows them to re-equillibrate
40
Fastest to slowest hyperK+ treatment
**hyperventilation**
*increasing the pH by 0.1 decreases K+ by 0.4-1.5 mmol/L
**insulin +/- glucose**
*10 units iV: 25g D50
*works in 10-20 min
**bicarb**
*drives K+ back into the cell
**loop diuretics**
**kayexalate** (hrs to days)
41
what to avoid during hyperK+ treatment
succinycholine
hypoventilation
LR and K+ containing fluids
41
presence of calcium in the body
1% in ECF
99% stored in bone
41
ionized Ca++ vs non ionized Ca++
only ionized Ca++ is physiologically active
nonionized Ca++ is protein bound to albumin (60%)
42
ionized ca++ level and influences
Normal iCa++ = 1.2-1.38 mmol/L
iCa++ is affected by albumin levels and pH
* alkalosis (increased pH) increases Ca++ binding to albumin decreasing iCa++
43
hormones that regulate Ca++
PTH stimulates release of Ca++ from bone into plasma
Calcitonin promotes calcium storage
vitamin D augments intestinal Ca++ absorption
44
causes of hypocalcemia
↓Parathyroid hormone (PTH) secretion
**complication of thyroid/PT surgery - drop in Ca++ that leads to laryngospasm**
Magnesium deficiency
Magnesium required for PTH production
Low Vit D or disorder of Vit D metabolism
Renal failure (kidneys not responding to PTH)
Massive blood transfusion (citrate preservative binds Ca++ rendering it inactive)
**Check iCa++ after 4+ units of PRBCs may need to give Ca++**
| Normal Ca++ 9-11
45
hypercalcemia major causes
hyper-parathyroid or cancer
hyper-parathyroid serum Ca++<11
Cancer serum Ca++>13
| Normal Ca++ 9-11
46
hypercalcemia less common causes
vitamin D intoxication
milk-alkali syndrome (excessive GI Ca++ absorption)
granulomatous disease (sarcoidosis)
47
s/s of hypocalcemia
parasthesias
irritability
hypotension
seziures
myocardial depression
prolonged QT-interval
post parathryoidectomy - hypocalcemia-induced laryngospasm
## Footnote
extra caution when extubating parathyroidectomy always have laryngospasm plan
48
s/s of hypercalcemia
confusion, lethargy
hypotonia, decreased DTR
ABD pain
N/V
Short QT-I
Chronic hypercalcemia - hypercalcuria & nephroliathiasis
49
hypomagnesemia
causes, symptoms, treatment
**causes**: low dietary intake or absorption; renal wasting
**symptoms**: muscle weakeness or excitation, seizures, ventricular dysrhythmia (torsades)
**treatment**: dependent on severity of symptoms, slower infusions for less severe
**Torsades/seizures: 2g Mag Sulfate**
50
hypermagnesemia
very uncommon
generally due to over-treatment
- pre-eclampsia
- pheochromocytoma
51
hyperMg++ symptoms
4-5 mEq/L: lethargy, N/V, flushing
>6 mEq/L: hypotension, decreased DTR
>10 mEq/L: paralysis, apnea, heart blocks, cardiac arrest
| Check mag level at regular intervals if on gtt
52
hyperMg++ treatment
diuresis, IV calcium, dialysis
53
where are the kidneys located
located retroperitnoeal between T12-L4
right slightly caudal (lower) to the left to accomodate liver
54
nephron
strucutral/functional unit
1M per kidney
Consists of:
Glomerulus
Tubular system
Bowman capsule
Proximal Tubule (PCT)
Loop of Henle
Distal Tubule (DCT)
Collecting duct
55
what percent of the Cardiac output do the kidneys receive
20%
1-1.25L/min
56
which layer of the kidneys recieves 85-90% of renal blood flow
**cortex = outer layer**
## Footnote
medulla = inner layer is vulnerable to developnig necrosis in response to hypotension (decreased renal perfusion)
57
primary functions of the kidneys
Regulate EC volume, osmolarity, composition
Regulate BP (intermediately & Long-Term) *RAAS, ANP
Excrete toxins/metabolites
Maintain acid/base balance
Produce hormones (Renin, Erythropoietin, Calcitriol, Prostaglandins)
Blood glucose homeostasis
58
renal function labs
GFR (125-140 mL/min)
creatinine clearance (110-140 mL/min)
serum creatinine (0.6-1.3 mg/dL)
BUN (10-20 mg/dL)
BUN: creatinine ration (10:1)
Proteinuria (<150 mg/dL)
Specific gravity (1.001-1.035)
| Lab values can be effected by factors outside of renal function
59
GFR best measures renal function over ______. heavily influcence by ______ ________
GFR best measures renal function over **time**. heavily influcence by **hydration status**
| GFR is better for trending
## Footnote
normal GFR 125-140 mL/min
60
which renal function test is the most reliable measure of GFR
creatine clearance
61
serum creatinine can be influenced by what and used when?
influeneced by a high protein diet, supplements, muscle breakdown
good for acute monitoring, Serum creatinine is inversely related to GFR.
in acute case, doubled serum creatinine means a drop in GFR by 50%
| Normal 0.6-1.3 mg/dL
62
blood urea nitrogen
urea is reabsorbed into the blood
affected by diet and intravsacular volume
lower BUN could mean malnourished or volume diluted
higher BUN could mean increased protein diet, dehydration, GI bleeding, trauma, muscle wasting
| Normal 10-20 mg/dL
63
what is the BUN: creatinine ratio used for
hydration status
BUN (reabsorbed): Creatinine (not reabsorbed)
64
proteinuria
>750 mg/day could suggest glomerular injury or UTI
*frothy bubbly urine (albumin)
| Normal < 150 mg/dL
65
what does specific gravity test
the neprhons ability to concentrate urine
compares 1mL of urine to 1mL distilled water
| Normal 1.001-1.035
66
assessing volume status
H&P
orthostatic pressure changes
decreased base excess
increased lactate
*drop in UOP is late sign
67
normal UOP
30 mL/hr; 0.5-1 mL/kg/hr
68
oliguria
<500 mL in 24hr
69
volume monitors
US to assess IVC collapse
CVP, RAP
LAP, PCWP (powerful stimuli for renal vasoconstriction)
PAP
SVV
70
Ultrasound assessment of IVC and hydration
>50% collapse indicates fluid deficit
* consider passive leg raise to determine fluid resposiveness
71
SVV measurement
Compares inspiratory vs expiratory pressure
Assumes ventilated patient
Assumes sinus rhythm
72
AKI
failure to excrete nitrogenous waste products or maintain fluid/electrolyte homeostasis
*caused by hypotension, hypovolemia, and nephrotoxins (IV contrast)
73
azotemia
buildup of nitrogenous products (urea and creatinine)
| hallmark of AKI
74
AKI with multisystem organ failure requiring dialysis carries what mortality rate
>50% mortality rate
75
what percent of hospitalized and ICU patients have AKI
20% hospitalized pts
50% ICU patients
76
risk factors of AKI (9)
Pre-existing renal disease
Advanced age
CHF
PVD
Diabetes
Sepsis (hypotension)
Jaundice
Major operative procedures
IV Contrast
77
AKI diagnositc criteria
↑SCr by 0.3 mg/dL within 48 h
↑SCr by 50% within 7 days
↓Creatinine clearance by 50%
Abrupt oliguria *although not always seen in AKI
Physical sx:
Asymptomatic
Malaise
HypoTensioN
Hypovolemic or hypervolemic
78
pre-renal AKI causes (9)
hemorrhage
GI fluid loss
trauma
surgery
burns
cardiogenic shock
sepsis
aortic clamping
thromboembolism
| Pre-renal= ↓ renal perfusion
79
intrarenal AKI causes (7)
acute gloemerulonephritis
vasculitis
intersitial nephritis
ATN
contrast dye
nephrotoxic drugs
myoglobinuria
| Renal = direct nephron injury
80
postrenal AKI causes (4)
nephrolithiasis
BPH
clot rention
bladder carcinoma
| Post Renal= outflow obstruction *easiest to treat
81
BUN: Creatinine ratio for all the forms of AKI
pre-renal BUN:Cr > 20:1
intrarenal BUN:Cr < 15:1
postrenal BUN:Cr varies
82
pre-renal azotemia
most common cause of AKI
1/2 of hospital aquired AKI are due to prerenal
aneshesia meds + volume and blood loss decrease RBF
*reversible
*treatment= restore RBF
| BUN: Cr > 20:1
83
most common cause of acute tubular necrosis is
pre-renal AKI if not reversed will transition into renal AKI
84
drug treatmemt for pre-renal azotemia
fluids, mannitol, diuretics, maintain MAP, pressors
- volumize to restore renal flow but addding tone may increase RBF
85
renal azotemia
intrinsic renal disease
potentially reversible continuum
↓GFR (late symptom)
↓urea reabsorption in proximal tubule →↓BUN
↓Creatinine filtration→↑blood creatinine
BUN: Cr often < 15:1
86
post renal azotemia
outflow obstruction
↑Nephron tubular hydrostatic pressure
Renal ultrasonography useful
Reversibility is inversely related to duration
Tx- Remove obstruction if possible
*Persistent obstruction damages the tubular epithelium*
87
neuro complications of AKI
Related to protein/amino acids buildup in blood
Uremic Encephalopathy (Dialysis improves)
Mobility disorders
Neuropathies
Myopathies
Seizures
Stroke
88
CV complications of AKI
Systemic hypertension
Left ventricular hypertrophy
CHF
Pulmonary edema
Uremic cardiomyopathy
Arrhythmias
## Footnote
In order of incidence HTN→ LVH→ CHF→ ischemic heart disease→ anemic heart failure→ rhythm disturbances → pericarditis with or without effusion→ cardiac tamponade, uremic cardiomyopathy
89
hematological complications of AKI
Anemia
↓ EPO production
↓ red cell production
↓ red cell survival
Platelet dysfunction (plt function assay or TEG are valuable)
vWF disrupted by uremia
* Prophylactic DDAVP
* ↑VWF & Factor VIII to improve coagulation
*** Can develop tachyphylaxis – give with anticipated blood loss**
90
metabolic complications of AKI
Hyperkalemia
Water/sodium imbalances
Hypoalbuminemia (kidneys allowing albumin to escape)
Metabolic acidosis
Malnutrition
Hyperparathyroidism
* Parathyroid in overdrive to in attempt to stimulate the kidney to reabsorb Ca++
* Kidney receptor no longer responsive
91
AKI anesthesia implications
Correct fluid, electrolyte, acid/base status
Volume- NS preferred for renal (no K+)
Careful w/colloids
Albumin > synthetic colloids
MAP maintained (20% of baseline)
Vasopressors? (Vasopressin, Alpha-agonists)
Prophylactic sodium bicarb
* Decreases formation of free-radicals
* Prevents ATN from causing renal failure
92
why vasopressin during AKI
Vasopressin-preferentially constricts the Efferent arteriole, better than alpha agonists (constrict afferent arteriole) for maintaining RBF
93
anesthesia implications for AKI
Low threshold for invasive hemodynamic monitoring
Prefer preoperative dialysis
**They may need post-op dialysis if they cannot clear drugs on their own**
Recent labs, especially K+ within 1 hour of surgery
Want POC equipment available
**Tailored drug dosing**
Avoid drugs w/active metabolites
94
drugs to avoid with acute kidney injury
Avoid drugs w/active metabolites, drugs that ↓RBF, and renal toxins
Morphine/Demerol
95
leading cause of CKD
DM, HTN
96
what procedures do pts with CKD come to the OR for
dialysis access
DM, toe/foot debridement's & amputations
Non-healing wounds
Often frequent flyers
97
stages of CKD
## Footnote
GFR decreases by 10 per decade starting from age 20
98
CKD CV effects
**Systemic hypertension**
Cause and consequence
Retention of sodium and water
Chronic activation of renin-angiotensin-aldosterone system
**1st line-Thiazide Diuretics,
May need ACE-I/ARB**
99
why ACE-Is, ARBs for CKD
↓systemic BP and glomerular pressure
↓proteinuria by reducing glomerular hyperfiltration
↓glomerulosclerosis
100
ACE-I/ARB anesthesia considerations
Want ACE-I/ARBs withheld on the day of surgery to ↓risk of profound hypotension.
**Vasopressin, NE, and EPI may be needed if ACE-I or ARB is on board.**
101
CKD and dyslipidemia
Dyslipidemia
Triglycerides often > 500
LDL often > 100
Predisposed to “Silent MI”
**Peripheral & autonomic neuropathy, sensation may be blunted.**
## Footnote
Which populations are high risk for silent MI? Women and Diabetics
102
CKD and anemia
Responsive to exogenous erythropoietin
**Target Hbg 10**
Platelet dysfunction
Transfusion -Risks vs benefits: *excess hgb leads to sluggish circulation*
103
inidications to consider dialysis
Volume overload
Severe hyperkalemia
Metabolic acidosis
Symptomatic uremia (neuro changes)
Failure to clear medications (active metabolites)
-----------------------------------------
*AEIOU*
Acidosis
Electrolyte imbalance (K+)
Intoxication (active metabolites)
Overload - fluid
Uremia
104
HD or PD?
HD is more efficient than PD*
PD is slower, less dramatic volume shifts, may be more suitable to those that can't tolerate fluid swings/vol shifts (i.e., pts w/poor cardiac function)
Hypotension is the most common SE
Infection leading Cause of death in dialysis pts (impaired immune system/healing)
105
anesthesia concerns with CKD
Assess the stability of ESRD
Body weight pre/post dialysis *within 24 h of surgery
Dose drugs on weight and GFR
Well-controlled BP, Meds continued?
Glucose management, A1C?
Aspiration precautions (DM, obesity)
Pressors
106
Anesthesia concerns for uremic bleeding
* normal platelet count/PT/PTT. Assess plt function.
* Cryo, F VIII, vWF
* Desmopressin
* Peak 2-4h; lasts 6-8h
* Tachyphylaxis
* Give preop
107
best NMB for CKD
cisatracurium
| not dependent on renal elimination
108
Many anesthetic agents are _____-______ and ________ by renal tubular cells
Many anesthetic agents are **lipid-soluble** and
**Reabsorbed** by renal tubular cells
109
lipid insoluble drugs
eliminated unchanged in the urine, prolonged duration of action
*renal dosing - usually based on GFR
**thiazides
Loop diuretics
Digoxin
many ABX**
110
induction agents that use renal excretion
phenobarbital
thiopental
111
muscle relaxants that use renal excretion
pancuronium
vecuronium*
112
cholinesterase inhibitors excreted by kidneys
edrophonium
neostigmine*
113
CV drugs that use renal excretion
atropine
digoxin
glycropyrrolate
hydralazine
milrinone
114
antimicrobials excreted by the kidneys
aminoglycosides
cephalosporins
penicillins
vancomyocin
115
is sugammedex recommended for renal patients
sugammedex creates a covalent bond - theorectically not recommened for renal patients
116
how much of morphine is excreted through the urine
40%
*failure to clear leads to signficant active metabolites
*dialysis to clear metabolites
117
demerol
Analgesic and CNS effects
main adverse effect is neurotoxicity (nervousness, tremors, muscle twitches, seizures)
Multiple doses of meperidine result in the **accumulation of normeperidine due to its long elimination half-life (15-30 h) compared with meperidine (2-4 h)**
118
preoperative concerns (6) for CKD
K+ < 5.5 mEq/L on elective surgery
Dialysis pts should be dialyzed within 24 hours preceding elective surgery
Aspiration prophylaxis, especially in DM
Anesthesia & Surgery decrease RBF & GFR
Blood loss activates baroreceptors→↑SNS outflow
* Catecholamines activate α1-Rs→↑afferent arteriole constriction→↓RBF
Longer periods of hypotension (cross-clamping, hemorrhage, sepsis) →↓RBF
