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Health Assessment > Renal > Flashcards

Renal Flashcards

1
Q

About how much of total body weight is water

A

~60%
varies with gender, age, body fat%

↑Muscle=↑Water

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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

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3
Q

Osmolar Homeostasis is mainly mediated by which sensors located where

A

osmolarity sensors in the anterior hypothalamus

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4
Q

osmolar homestasis stimulates

A

stimulates thirst
pituitary release of vasopressin (ADH)
cardiac atria release ANP decreasing Na+/Water excretion

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5
Q

what mediates volume homeostasis

A

juxtaglomerular apparatus sense changes in volume
↓Vol @ JGA triggers Renin-Angiotensinogen-Aldosterone system (RAAS)→Na+/H20 reabsorption

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6
Q

normal Na+ level?
Na+ level okay for surgery?

A

135-145 mEq/L
≤125 or ≥ 155 mEq/L for elective surgery

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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

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8
Q

euvolemia causes of hyponatremia

A

Urine Na < 20: salt restricted diet
Urine Na > 20: glucocorticoid deficiency, hypothyroidism, high sympathetic drive, drugs, SIADH

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9
Q

signs of hypervolemia

A

peripheral edema, rales, ascites

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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

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11
Q

example of extrarenal losses leading to hypovolemia/hyponatremia

A

vomiting
diarrhea
3rd space losses
burns
pancreatitis
muscle trauma

Urine Na+ < 20

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12
Q

hypervolemia causing hyponatremia

A

Urine Na> 20: renal losses
-ARF, CKD

Urine Na< 20: avid sodium reabsorption
-nephrotic syndrome, cardiac failure, cirrihosis

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13
Q

most severe consequences of hyponatremia

A

seizure, coma, death

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14
Q

treatment of hyponatremia

A

treat underlying cause - look at volume status
*electroylte drinks
* normal saline
* diuretics
* hypertonic saline/3% NaCl

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15
Q

hypertonic saline/ 3% NaCl

A

80 ml/hr over 15 hours
Na+ correction should not exceed 1.5 mEq/L/hr

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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)

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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)

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17
Q

hyponatremic seizures treatment

A

hyponatremic seizures= medical emergency
3-5mL/kg of 3% over 20 minutes until seizure resolves

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18
Q

renal water loss leading to hypernatremia hypovolemia

A

osmotic diuretic
loop diuretic
postrenal obstruction
intrinsic renal disease
profound glycosuria

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19
Q

euvolemia causes of hypernatremia

A

renal water loss:
Diabetes Inspidus: central, nephro, gestational

extrarenal water loss:
insensible losses- respiratory tract and skin

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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

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21
Q

extrarenal water loss leading to hypernatremia hypovolemia

A

diarrhea
GI fistulas
burns
sweating

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22
Q

s/s of hypernatremia

A

orthostasis
restlessness
lethargy
tremor/muscle twitching/spasticity
seizures
death

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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

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24
Q

Want Na+ reduction rate ≤____ mmol/L/hr and ≤ ____ mmol/L per day to avoid _____ _____, ____, and ______ damage.

A

Want Na+ reduction rate ≤0.5 mmol/L/hr and ≤ 10 mmol/L per day to avoid cerebral edema, seizures, and neurologic damage.

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25
Q

potassium

A

3.5-5 mmol/L
major ICF cation
<1.5% in ECF

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26
Q

what does serum K+ reflect

A

transmembrane K+ regulation more than total body K+

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27
Q

aldosterones effect on potassium

A

aldosterone causes the distal nephron to secrete K+ and reabsorb Na+

aldosterone inversely effects K+

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28
Q

renal failure and potassium

A

in renal failure, K+ excretion declines
excretions shifts toward the GI system
which is a slower process leading to buildup

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29
Q

hypokalemia common causes (7)

A

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

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30
Q

additional causes of hypoK+

A
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31
Q

symptoms of hypoK+

A

cardiac and neuromuscular
* muscle cramps/weakness
* ileus
* dysrhytmias, U-wave

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32
Q

treatment of hypoK+

A

underlying cause
Potassium PO> IV (CVC) which may require days

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33
Q

IV K+ dose

A

10-20 mEq/L/hr IV
each 10 mEq IV K+ increases serum K+ by ~ 0.1 mmol/L

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34
Q

avoid what during hypoK+

A

excessive insulin
beta agonists
bicarb
hyperventilation
diuretics

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35
Q

hyperK+ causes (7)

A

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)

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36
Q

symptoms of HyperK+

A

chronic may be minimally symptomatic (malaise, GI upset)
skeletal muscle paralysis, decreased fine motor
cardiac dysrhtymias

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37
Q

EKG progression with HyperK+

A

Peaked T wave
P wave disappearance
prolonged QRS complex
sine waves
asystole

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38
Q

hyperK+ treatment

A

Calcium 1st inital treatment to stabilize the cell membrane

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39
Q

when should the pt be dialyzed before surgery

A

within 24 hrs
dialysis also initially causes hypovolemia, the day prior allows them to re-equillibrate

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40
Q

Fastest to slowest hyperK+ treatment

A

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)

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41
Q

what to avoid during hyperK+ treatment

A

succinycholine
hypoventilation
LR and K+ containing fluids

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41
Q

presence of calcium in the body

A

1% in ECF
99% stored in bone

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41
Q

ionized Ca++ vs non ionized Ca++

A

only ionized Ca++ is physiologically active
nonionized Ca++ is protein bound to albumin (60%)

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42
Q

ionized ca++ level and influences

A

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++

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43
Q

hormones that regulate Ca++

A

PTH stimulates release of Ca++ from bone into plasma
Calcitonin promotes calcium storage
vitamin D augments intestinal Ca++ absorption

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44
Q

causes of hypocalcemia

A

↓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

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45
Q

hypercalcemia major causes

A

hyper-parathyroid or cancer
hyper-parathyroid serum Ca++<11
Cancer serum Ca++>13

Normal Ca++ 9-11

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46
Q

hypercalcemia less common causes

A

vitamin D intoxication
milk-alkali syndrome (excessive GI Ca++ absorption)
granulomatous disease (sarcoidosis)

47
Q

s/s of hypocalcemia

A

parasthesias
irritability
hypotension
seziures
myocardial depression
prolonged QT-interval
post parathryoidectomy - hypocalcemia-induced laryngospasm

extra caution when extubating parathyroidectomy always have laryngospasm plan

48
Q

s/s of hypercalcemia

A

confusion, lethargy
hypotonia, decreased DTR
ABD pain
N/V
Short QT-I
Chronic hypercalcemia - hypercalcuria & nephroliathiasis

49
Q

hypomagnesemia
causes, symptoms, treatment

A

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
Q

hypermagnesemia

A

very uncommon
generally due to over-treatment
- pre-eclampsia
- pheochromocytoma

51
Q

hyperMg++ symptoms

A

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
Q

hyperMg++ treatment

A

diuresis, IV calcium, dialysis

53
Q

where are the kidneys located

A

located retroperitnoeal between T12-L4
right slightly caudal (lower) to the left to accomodate liver

54
Q

nephron

A

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
Q

what percent of the Cardiac output do the kidneys receive

A

20%
1-1.25L/min

56
Q

which layer of the kidneys recieves 85-90% of renal blood flow

A

cortex = outer layer

medulla = inner layer is vulnerable to developnig necrosis in response to hypotension (decreased renal perfusion)

57
Q

primary functions of the kidneys

A

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
Q

renal function labs

A

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
Q

GFR best measures renal function over ______. heavily influcence by ______ ________

A

GFR best measures renal function over time. heavily influcence by hydration status

GFR is better for trending

normal GFR 125-140 mL/min

60
Q

which renal function test is the most reliable measure of GFR

A

creatine clearance

61
Q

serum creatinine can be influenced by what and used when?

A

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
Q

blood urea nitrogen

A

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
Q

what is the BUN: creatinine ratio used for

A

hydration status
BUN (reabsorbed): Creatinine (not reabsorbed)

64
Q

proteinuria

A

> 750 mg/day could suggest glomerular injury or UTI
*frothy bubbly urine (albumin)

Normal < 150 mg/dL

65
Q

what does specific gravity test

A

the neprhons ability to concentrate urine
compares 1mL of urine to 1mL distilled water

Normal 1.001-1.035

66
Q

assessing volume status

A

H&P
orthostatic pressure changes
decreased base excess
increased lactate
*drop in UOP is late sign

67
Q

normal UOP

A

30 mL/hr; 0.5-1 mL/kg/hr

68
Q

oliguria

A

<500 mL in 24hr

69
Q

volume monitors

A

US to assess IVC collapse
CVP, RAP
LAP, PCWP (powerful stimuli for renal vasoconstriction)
PAP
SVV

70
Q

Ultrasound assessment of IVC and hydration

A

> 50% collapse indicates fluid deficit
* consider passive leg raise to determine fluid resposiveness

71
Q

SVV measurement

A

Compares inspiratory vs expiratory pressure
Assumes ventilated patient
Assumes sinus rhythm

72
Q

AKI

A

failure to excrete nitrogenous waste products or maintain fluid/electrolyte homeostasis
*caused by hypotension, hypovolemia, and nephrotoxins (IV contrast)

73
Q

azotemia

A

buildup of nitrogenous products (urea and creatinine)

hallmark of AKI

74
Q

AKI with multisystem organ failure requiring dialysis carries what mortality rate

A

> 50% mortality rate

75
Q

what percent of hospitalized and ICU patients have AKI

A

20% hospitalized pts
50% ICU patients

76
Q

risk factors of AKI (9)

A

Pre-existing renal disease
Advanced age
CHF
PVD
Diabetes
Sepsis (hypotension)
Jaundice
Major operative procedures
IV Contrast

77
Q

AKI diagnositc criteria

A

↑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
Q

pre-renal AKI causes (9)

A

hemorrhage
GI fluid loss
trauma
surgery
burns
cardiogenic shock
sepsis
aortic clamping
thromboembolism

Pre-renal= ↓ renal perfusion

79
Q

intrarenal AKI causes (7)

A

acute gloemerulonephritis
vasculitis
intersitial nephritis
ATN
contrast dye
nephrotoxic drugs
myoglobinuria

Renal = direct nephron injury

80
Q

postrenal AKI causes (4)

A

nephrolithiasis
BPH
clot rention
bladder carcinoma

Post Renal= outflow obstruction *easiest to treat

81
Q

BUN: Creatinine ratio for all the forms of AKI

A

pre-renal BUN:Cr > 20:1
intrarenal BUN:Cr < 15:1
postrenal BUN:Cr varies

82
Q

pre-renal azotemia

A

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
Q

most common cause of acute tubular necrosis is

A

pre-renal AKI if not reversed will transition into renal AKI

84
Q

drug treatmemt for pre-renal azotemia

A

fluids, mannitol, diuretics, maintain MAP, pressors
- volumize to restore renal flow but addding tone may increase RBF

85
Q

renal azotemia

A

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
Q

post renal azotemia

A

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
Q

neuro complications of AKI

A

Related to protein/amino acids buildup in blood
Uremic Encephalopathy (Dialysis improves)
Mobility disorders
Neuropathies
Myopathies
Seizures
Stroke

88
Q

CV complications of AKI

A

Systemic hypertension
Left ventricular hypertrophy
CHF
Pulmonary edema
Uremic cardiomyopathy
Arrhythmias

In order of incidence HTN→ LVH→ CHF→ ischemicheartdisease→ anemicheartfailure→ rhythm disturbances → pericarditis with or without effusion→cardiactamponade, uremic cardiomyopathy

89
Q

hematological complications of AKI

A

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
Q

metabolic complications of AKI

A

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
Q

AKI anesthesia implications

A

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
Q

why vasopressin during AKI

A

Vasopressin-preferentially constricts the Efferent arteriole, better than alpha agonists (constrict afferent arteriole) for maintaining RBF

93
Q

anesthesia implications for AKI

A

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
Q

drugs to avoid with acute kidney injury

A

Avoid drugs w/active metabolites, drugs that ↓RBF, and renal toxins
Morphine/Demerol

95
Q

leading cause of CKD

A

DM, HTN

96
Q

what procedures do pts with CKD come to the OR for

A

dialysis access
DM, toe/foot debridement’s & amputations
Non-healing wounds
Often frequent flyers

97
Q

stages of CKD

A

GFR decreases by 10 per decade starting from age 20

98
Q

CKD CV effects

A

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
Q

why ACE-Is, ARBs for CKD

A

↓systemic BP and glomerular pressure
↓proteinuria by reducing glomerular hyperfiltration
↓glomerulosclerosis

100
Q

ACE-I/ARB anesthesia considerations

A

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
Q

CKD and dyslipidemia

A

Dyslipidemia
Triglycerides often > 500
LDL often > 100

Predisposed to “Silent MI”
Peripheral & autonomic neuropathy, sensation may be blunted.

Which populations are high risk for silent MI? Women and Diabetics

102
Q

CKD and anemia

A

Responsive to exogenous erythropoietin
Target Hbg 10
Platelet dysfunction
Transfusion -Risks vs benefits: excess hgb leads to sluggish circulation

103
Q

inidications to consider dialysis

A

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
Q

HD or PD?

A

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
Q

anesthesia concerns with CKD

A

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
Q

Anesthesia concerns for uremic bleeding

A
  • normal platelet count/PT/PTT. Assess plt function.
  • Cryo, F VIII, vWF
  • Desmopressin
  • Peak 2-4h; lasts 6-8h
  • Tachyphylaxis
  • Give preop
107
Q

best NMB for CKD

A

cisatracurium

not dependent on renal elimination

108
Q

Many anesthetic agents are _____-______ and ________ by renal tubular cells

A

Many anesthetic agents are lipid-soluble and
Reabsorbed by renal tubular cells

109
Q

lipid insoluble drugs

A

eliminated unchanged in the urine, prolonged duration of action
*renal dosing - usually based on GFR
thiazides
Loop diuretics
Digoxin
many ABX

110
Q

induction agents that use renal excretion

A

phenobarbital
thiopental

111
Q

muscle relaxants that use renal excretion

A

pancuronium
vecuronium*

112
Q

cholinesterase inhibitors excreted by kidneys

A

edrophonium
neostigmine*

113
Q

CV drugs that use renal excretion

A

atropine
digoxin
glycropyrrolate
hydralazine
milrinone

114
Q

antimicrobials excreted by the kidneys

A

aminoglycosides
cephalosporins
penicillins
vancomyocin

115
Q

is sugammedex recommended for renal patients

A

sugammedex creates a covalent bond - theorectically not recommened for renal patients

116
Q

how much of morphine is excreted through the urine

A

40%
*failure to clear leads to signficant active metabolites
*dialysis to clear metabolites

117
Q

demerol

A

Analgesic and CNS effects
main adverse effect is neurotoxicity (nervousness, tremors, muscle twitches, seizures)
Multiple doses of meperidine result in the accumulation ofnormeperidinedue to its long elimination half-life (15-30 h) compared with meperidine (2-4 h)

118
Q

preoperative concerns (6) for CKD

A

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

Health Assessment (16 decks)

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