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Adv. Health Assessment (Spring 2024) > Spring 2024 (Exam III) Renal Assessment > Flashcards

Spring 2024 (Exam III) Renal Assessment Flashcards

1
Q

The kidneys sit retroperitoneal between _______ and _______.

Which kidney is slightly more caudal (lower) to accommodate the liver?

A

T12 and L4

Right

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2
Q

What is the functional unit of the kidney and what are its components?

A
  • Nephron
    -Glomerulus
    -Tubular system
  • Bowman capsule
  • Proximal Tubule (PCT)
  • Loop of Henle
  • Distal Tubule (DCT)
  • Collecting duct
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3
Q

The kidneys receive ________% (range) of CO
The _____ _____ receives the majority of RBF (85-90%)

A
  • 20% (1 L)
  • Outer Layer
    *LOH particularly vulnerable for developing necrosis in response to HoTN ((↓kidney perfusion)
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4
Q

Besides the kidneys, what organ is retroperitoneal?

A

Spleen

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5
Q

Primary functions of the kidneys (6 functions).

A
  1. Maintain extracellular volume and composition (RAAS and ANP)
  2. Blood Pressure Regulation (Intermed/Long)
  3. Excretion of Toxins and Metabolites
  4. Maintain Acid-Base Balance (excretion of HCO- and H+
  5. Hormone Production (Renin, Erythropoietin, Calcitrol, PGs)
  6. Blood glucose homeostasis (Gluconeogenesis and glucose reabsorption)
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6
Q

Calcium requires ________ for adequate absorption and utilization.

A

Calcitriol (Active Vitamin D)

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7
Q

How does Vitamin D get activated?

A

Through the kidneys

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8
Q

What hormone will stimulate the release of Ca++ from the bones and which hormone promotes storage of Ca++?

A

PTH; Calcitonin

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9
Q

____-% of body weight in non-obese patients is composed of water.

A

about 60%

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10
Q

What are the two main fluid compartments?

A

ECF and ICF

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11
Q

Per this lecture ECF is _______ the volume of ICF.

A

< 1/2 volume of TBW

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12
Q

____ ____ is mainly mediated by osmolality-sensors in anterior hypothalamus

A

Osmolar homeostasis

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13
Q

_____ _____ is mediated by juxtaglomerular apparatus

A

Volume homeostasis

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14
Q

What are the ways osmolality sensors in the anterior hypothalamus regulate fluid?

A
  • Stimulate thirst
  • Release Vasopressin (ADH)
  • Cardiac atria releases ANP→ act on kidney to ↓Na+/H20 reabsorption
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15
Q

What are ways JGA regulates fluid?

A
  • ↓Vol @ JGA triggers Renin-Angiotensinogen-Aldosterone system (RAAS)→Na+/H20 reabsorption
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16
Q

What is a normal sodium level?

A

135-145 mEq/L

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17
Q

There are no absolute cut offs for sodium level for surgery, but these numbers will be a good reference.

Na level below _________ mEq/L and above _______ mEq/L are a no go for surgery.

A

Below 125 mEq/L
Above 155 mEq/L

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18
Q

What are some causes of hyponatremia?

A
  • Prolonged sweating
  • Vomiting/diarrhea
  • Insufficient aldosterone secretion
  • Excessive intake of water
  • Burns
  • Trauma
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19
Q

What percent of people in the hospital have hyponatremia and why?

A
  • 15%
  • over fluid-resuscitation
  • ↑endog vasopressin
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20
Q

There are two patient populations where we are most concerned about sodium levels.

A

Neuro patients
Kids

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21
Q

The most severe consequence of hyponatremia are these three things:

A
  • Seizures
  • Coma
  • Death
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22
Q

What are treatments for hyponatremia?

A

Treat underlying causes
* Normal Saline
* Hypertonic 3% Saline
* Lasix
* Mannitol

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23
Q

What is the correction rate when supplementing Na with 3% saline?

A
  • Na+ correction should not exceed 1.5 meq/L/hr
  • Dose: 80 mL/hr over 15h
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24
Q

Rapid correction of Na faster than 6 mEq/L in 24 hours can cause __________ syndrome.

What could this result in?

A

osmotic demyelination

Seizures, coma, death

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25
Q

What is the dose and rate of 3% hypertonic saline for patients that are hyponatremic and seizing?

A
  • Medical Emergency
  • 3-5 mL/kg of 3% saline
  • Give dose of over 20 minutes until seizures resolve
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26
Q

Hyponatremic seizures are a medical emergency and can cause __________ brain damage.

A

Irreversible

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27
Q

What are the causes of hypernatremia?

A
  • Excessive evaporation
  • Poor oral intake(very young, old)
  • Overcorrection of hyponatremia
  • Diabetes Insipidus
  • GI losses
  • Excessive sodium bicarb to tx acidosis
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28
Q

Symptoms of hypernatremia

A
  • Orthostasis
  • Restlessness
  • Lethargy
  • Tremor/ Muscle Twitching/ spasticity
  • Seizures
  • Death
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29
Q

How do we treat hypernatremia?

A
  • Hypovolemic: 0.9% NaCl
  • Euvolemic: water replacement (PO or D5W)
  • Hypervolemic: diuretics
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30
Q

What is the recommended Na+ reduction rate and what are the side effects if reduced too quickly?

A
  • ≤0.5 mmol/L/hr and ≤ 10 mmol/L per day
  • Cerebral edema, seizures, and neurologic damage
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31
Q

Be cautious when using sodium bicarb to treat acidosis, what is a good alternative to use if you want to avoid raising sodium?

A

Tromethamine injection (THAM) is indicated for the prevention and correction of metabolic acidosis.

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32
Q

Treatments for hypernatremia?

A

First, assess volume status (tachycardic, hypotensive, u/o, skin turgor, CVP, SV variation)

Then treat the cause.

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33
Q

Treatments for the following.

Hypernatremic Hypovolemia:
Hypernatremic Hypervolemia:
Hypernatremic Euvolemic:

A

Hypernatremic Hypovolemia: normal saline
Hypernatremic Hypervolemia: diuretic
Hypernatremic Euvolemic: water replacement (PO or D5W)

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34
Q

What is normal potassium level?

A

3.5 to 5 mEq/L

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35
Q

Patients will not go to surgery if potassium is less than ______ or greater than _______ mEq/L.

A

K+ less than 3 mEq/L
K+ greater than 5 mEq/L

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36
Q

What are the causes of hypokalemia?

A

Excessive release of aldosterone
Diuretics drugs (Lasix, hydrochlorothiazide)
Kidney disease
Excessive intake of licorice (kids eating too much licorice.)
DKA (frequent urination)

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37
Q

Effects of hypokalemia

A

Generally, cardiac and neuromuscular (K+ of 2mEq/L)
Dysrhythmias (K+ of 2mEq/L)
Muscle weakness
Cramps (Eat a banana)
Paralysis
Illeus (lose parastalsis)

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38
Q

What changes in EKG will you see with hypokalemia?

A

U-waves

You will see this on the exams and boards.

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39
Q

Treatments for hypokalemia

A
  • Treat the underlying cause
  • PO > IV Potassium
    May require days to correct
    Avoid excessive insulin, β-agonists, bicarb, hyperventilation, diuretics
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40
Q

10 mEq of potassium will increase serum K+ by ________ mEq/L.

A

0.1 mEq/L

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41
Q

Why may PO potassium be faster in increasing serum potassium levels?

A

A larger dose can be given PO compared to 10-20 mEq/hr with IV.

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42
Q

When replacing potassium levels, what other electrolytes do you need to keep an eye on?

A

Phosphorus (normal levels 2.5 - 4.5 mg/dL)

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43
Q

Who are at the most risk of dysrhythmias when getting potassium replacement?

A

CHF patients
Digoxin patients

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44
Q

What are the causes of hyperkalemia?

A

Renal failure
Hypoaldosteroinism
Drugs that inhibit RAAS
Drugs that inhibit K-secretion
Use of depolarizing NMBD (Succs)
Acidosis (Resp./ Metabolic)
Cell Death (trauma, tourniquet)
Massive Blood Transfusion

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45
Q

With hyperventilation, a pH increase of 0.1 will cause a ____ in potassium.

A

0.4 to 1.5 mEq/L decrease in potassium

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46
Q

Succynlcholine will increase serum K by ______

A

about 0.5-1.0 mEq/ L

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47
Q

What are the effects of hyperkalemia?

A
  • Potentially asymptomatic
  • GI upset
  • Malaise
  • Skeletal muscle paralysis, ↓fine motor
  • Severe cardiac dysrhythmias (cardiac arrest)
  • Lowers resting membrane potential
  • Decreases action potential duration
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48
Q

What are EKG presentations of hyperkalemia?

A

Peaked T-waves (can progress into sine waves if hyperkalemia is severe)
* P wave disappearance
* Prolonged QRS
* Asystole

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49
Q

Treatment of hyperkalemia

A
  • Dialyze within 24h prior to surgery (can also cause hypovolemia)
  • Calcium- 1st initial treatment (quickly stabilize cell membrane)
  • Hyperventilation (↑pH by 0.1 →↓K+ by 0.4-1.5 mmol/L)
  • Insulin +/- glucose (10u IV: 25g D50) * works in 10-20 min
  • Bicarb
  • Loop Diuretics
  • Kayexalate (hrs to days)
  • *Avoid Succs, hypoventilation, LR & K+ containing IV fluids
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50
Q

What do CRNAs do that can cause hyperkalemia in a patient?

A

Massive Transfusion Protocol and Blood Products

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51
Q

How much Ca++ is in the ECF?

A

Only 1% body’s Ca++ is in ECF; 99% stored in bone

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52
Q

What is the normal range of iCa?

A

Normal iCa++: 1.2-1.38 mmol/L

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53
Q

How does alkalosis affect Ca++?

A
  • ↑pH/Alkalosis→↑Ca++ binding to albumin;** therefore ↓iCa++**
54
Q

What are the causes of hypocalcemia?

A
  • ↓Parathyroid hormone (PTH) secretion
  • Complication of thyroid/PT surgery
  • Magnesium deficiency
  • Low Vit D or disorder of Vit D metabolism
  • Renal failure (kidneys not responding to PTH)
  • Massive blood transfusion (citrate preservative binds Ca++)
55
Q

What is required for PTH production?
________ can lead to laryngospasms

A
  • Magnesium
  • Parathyroidectomy
56
Q

The majority of patients with hypercalcemia have ____ or cancer

A

Hyper-parathyroid

57
Q

Less common causes of hypercalcemia

A
  • Vitamin D intoxication
  • Milk-alkali syndrome (excessive GI Ca++ absorption)
  • Granulomatous diseases (sarcoidosis)
58
Q

Signs and symptoms of hypercalcemia

A
  • Confusion, Lethargy
  • Hypotonia/ ↓DTR
  • Abd pain
  • N/V
  • Short QT-I
  • Chronic ↑Ca++→ Hypercalciuria & nephrolithiasis
59
Q

What are the causes of hypomagnesemia?

A
  • Low dietary intake or absorption
  • Renal Wasting
60
Q

What are the signs and symptoms of hypomagnesemia?

A
  • Muscle weakness
  • Seizures
  • Ventricular Dysrhythmias (Polymorphic Vtach/ Torsades)
61
Q

What is the treament for hypomagnesemia?

A
  • depends on severity of sx
  • Slower infusions for less severe
  • Torsade’s/seizures→ 2g Mag Sulfate
62
Q

What are the causes and S/S of Hypermagnesemia?

A
  • Very uncommon
    Generally due to over treatment
  • Pre-eclampsia/Eclampsia
  • Pheochromocytoma
    Symptoms
  • 4-5 mEq/L: Lethargy, N/V, Flushing
  • > 6 mEq/L: HoTN, ↓DTR
  • > 10 mEq/L: Paralysis, apnea, heart blocks, cardiac arrest
63
Q

What is the treatment for Hypermagnesemia?

A
  • Diuresis
  • IV Calcium (stabalize cell membrane)
  • Dialysis
64
Q

What are lab tests for renal function?

A

GFR (best measurement) 125-140 ml/min
best measure for renal function overtime
Heavily influenced by hydration status
**Creatinine Clearance ** 110-140 mL/ min
Freely filtered, not reabsorbed
Most reliable measure of GFR
Serum Creatinine 0.6-1.2mg/dL- correlates with muscle mass
Good for acute monitoring; inversely related to GFR
Double SC= 50% decrease in GFR

65
Q

What is creatinine?

A

A substance produced by skeletal muscle and is a byproduct of creatine breakdown.

66
Q

Creatinine production is constant and directly __________ to muscle mass.

A

proportional

A emaciated individual will probably have a lower creatinine level compared to a bodybuilder. But if you see that a cachectic person has a high creatinine level, it might be a sign that the kidneys are not working well.

67
Q

Creatinine undergoes renal _________ but not _________, making it a useful indicator of GFR.

A

Creatinine undergoes renal filtration but not reabsorption, making it a useful indicator of GFR.

68
Q

What are normal BUN ranges?

A

10-20 mg/dL

BUN can be misleading. Diet and changes in intravascular volume can increase or decrease BUN.

69
Q

What is BUN: Creatinine ratio?What does it indicate?

A

10:1
good measure of hydration status

70
Q

What is the normal value for proteinuria and what would a high value indicate?

A
  • <150 mg/ dL
  • > 750 mg/ dL could = glomerular injury or UTI
71
Q

What is urine specific gravity?

A
  • 1.001-1.035
  • Comparing 1ml urine to 1ml distilled water
  • measures nephron’s ability to concentrate urine
72
Q

What causes BUN of <8 mg/dL?

A

Overhydration, too much hydration, dilution.
Decrease Urea production (malnutrition, liver dz)

EtOH patients will forget to eat and get calories just from the booze.

73
Q

What causes a BUN of 20-40 mg/dL?

A

Dehydration

Increase Protein Input (high protein, GIB, Hematoma breakdown)

Catabolism (Trauma, Sepsis)

Decrease GFR

74
Q

A medical condition characterized by abnormally high levels of nitrogen-containing compounds (such as urea, creatinine, and various body waste compounds) in the blood. It is largely related to insufficient or dysfunctional filtering of blood by the kidneys.

A

Azotemia

75
Q

Oliguria definition.

A

Oliguria is decreased u/o 500 mL in 24 hours

76
Q

What number indicates good urine output from an anesthesia standpoint?

A

30 mL/hr (no standardization for weight and no clinical picture)

0.5-1 mL/kg/hr is more accurate

77
Q

What should we assess/ consider when determining volume status?

A

Look at the big picture
* H/P
* Orthostatic BPs
* ↓BE
* ↑Lactate
* Drop in UOP ** late sign**

78
Q

What is an early indicator of volume change (arm just got cut off)?

A

-Base Excess or Base Deficits will indicate volume loss (Indicator of acid/base balance in the blood).
-Increase in Lactate

79
Q

What are ways we can monitor volume?

A
  • US to assess IVC
  • CVP, RAP
  • LAP, PCWP
  • PAP
  • Stroke Volume Variation (SVV)
80
Q

_______ is a powerful stimulus for renal vasoconstriction.

A

Left atrial pressure (wedge pressure)

Increase LAP, increase vasoconstriction. Afferent arteriole will increase to decrease hydrostatic pressure.

81
Q

What does stroke volume variation in assess?

A
  • Compares inspiratory v expiratory pressure
    Assumes pt is vented and in NSR
82
Q

An IVC greater than _______% collapse indicates a fluid deficit.

A

50%

To assess, place an ultrasound on IVC and perform a passive leg raise, if the quick change in volume dilates IVC, the patient may be in a fluid volume deficit.

83
Q

What is acute renal failure?

A
  • Deterioration of renal function over hours to days.
  • Failure to excrete nitrogenous waste products or maintain fluid/ electrolyte homeostasis
    *generally caused by hypotension, hypovolemia, and nephrotoxins (ie. IV contrast)
84
Q

If someone with AKI progress to dialysis and MSOF, mortality is now greater than ________.

A

50% (due to sepsis, CV dysfunction, pulmonary compilations)
*Reversible with timely interventions. CVVHD to get through the temporary insult

85
Q

What are the risk factors for AKI?

A
  • Pre-existing renal disease
  • Advanced age
  • Congestive HF
  • PVD
  • DM
  • Sepsis (hypotension)
  • Jaundice
  • Major Operative Procedures (Cross-Clamped)
  • IV Contrast
86
Q

Diagnosing AKI lab and physical symptoms

A

Labs
↑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
Asymptomatic
Malaise
HoTN
Hypovolemic or hypervolemic=

87
Q

What are the types of AKI?

A

Pre-renal Azotemia
Renal Azotemia
Post-renal Azotemia

88
Q

What are the causes of prerenal azotemia (ARF)?

A

Hemorrhage
GI fluid loss
Trauma
Surgery
Burns
Cardiogenic shock
Sepsis
Aortic clamping
Thromboembolism
Anesthesia meds+ volume/ blood loss → ↓RBF

All these will decrease renal perfusion

89
Q

What are the causes of Renal Azotemia (ARF)?

A

Acute glomerulonephritis
Vasculitis
Interstitial nephritis
ATN
Contrast dye
Nephrotoxic drugs
Myoglobinuria

Real kidney injury. Think infections and inflammation.

90
Q

What are the causes of postrenal azotemia (ARF)?

A

Nephrolithiasis (kidney stones, most common cause)
BPH
Clot retention
Bladder carcinoma
UTI- cellular debris
Trauma to the urinary tract

Think mechanical obstruction post-kidney
Easiest to treat

91
Q

Pre-renal azotemia makes up _________ of hospitalized acquired cases.

If pre-renal azotemia is not treated in time, it will progress to _____.

A
  • Half
  • ATN (Pre-renal → Renal)
92
Q

Treatment of pre-renal azotemia.

A

Restore RBF
* Fluids, Mannitol, Diuretics, maintain MAP, Pressors

93
Q

What will be the BUN: Cr ratio of renal azotemia?

What happens to GFR?

What happens to Urea?

What happens to Creatinine?

A

Less than 15

GFR will decrease, and nothing will get filtered

Urea does not get reabsorbed; low urea in the blood, high urea in the urine.

Creatinine filtration decreases, leading to higher Cr in the blood.

94
Q

Neurological complications from AKI

A
  • Uremic Encephalopathy (improves with HD)
  • Mobility Disorders
  • Neuropathies
  • Myopathies
  • Seizures
  • Stroke
    *Related to protein/ amino acid builid up in blood
95
Q

List the order of incidence of cardiovascular compilations from AKI:

A

Order of incidence:
1. Systemic HTN
2. LVH
3. CHF
4. Ischemic heart disease
5. Anemic Heart Failure
6. Rhythm Disturbances
7. Pericarditis W/ WO effusion
8. Cardiac Tamponade/ Uremic Cardiomyopathy

96
Q

Hematological complications of AKI

A

Anemia
* ↓ EPO production
* ↓ red cell production
* ↓ red cell survival
Platelet dysfunction
vWF disrupted by uremia
* Prophylactic DDAVP
* ↑VWF & Factor VIII to improve coagulation

97
Q

Metabolic complications of AKI.

A

Hyperkalemia
Water and Sodium retention
Hypoalbuminemia - responds slower to medication
Metabolic Acidosis

98
Q

Anesthesia concerns of AKI.

A
  • Correct fluid, electrolytes, acid/base status
  • Volume- NS preffer for renal (no K+)
  • Careful with colloids
  • MAP W/I 20% of baseline
  • Vasopresseors (Alpha-agonists, Vasopressin)
  • Prophylactic sodium bicarb
    • decreases the formation of free radicals and prevents ATN from causing renal failure
99
Q

____ preferentially constricts the efferent arteriole better than ____ ____ for maintaining RBF.

A

Vasopressin; alpha agonists

100
Q

What are anesthesia implications for a patient with an AKI

A
  • Low threshold for invasive hemodynamic monitoring
  • Prefer preopertaive HD
  • Recent labs (esp. K+)
  • Have POC equipment available
  • Tailored drug dosing
  • Avoid drugs w/ active metabolites and renal toxins or drugs that ↓RBF
101
Q

Unlike AKI, CKD is ______ and __________.

What is the leading cause of CKD?

A

Progressive and Irreversible

DM and HTN

102
Q

Describe stages of ESRD and GFR for each stage.

A
103
Q

On average, GFR decreases by ______ per decade starting from age 20.

A

10

104
Q

CV effects of CKD

A
  • Systemic HTN (cause and consequence)
    • Retention of sodium and water
    • Activation of RAAS
  • Dyslipidemia
    - Triglycerides > 500
    - LDL > 100
  • Prediposed to “Silent MI”
    - Peripheral and autonomic neuropathy, sensation may be blunted
105
Q

Which populations are a high risk for silent MI?

A

Women and Diabetics

106
Q

What is the first line treatment for CKD induced systemic HTN?

A
  • Thiazide Diuretics

*ACE-I/ ARBS may be needed as well

107
Q

What are the hematological complications of CKD?

A

Anemia
- responsive to exogenous erythropoietin
- Target HBG 10
Platelet Dysfunction
Transfusion Risk v Benefits
- excess HGB leads to sluggish circulation
Acidosis and hyperkalemia are also associated with blood transfusions

108
Q

What are the five indications of dialysis?

A
  1. Volume overload
  2. Severe Hyperkalemia
  3. Metabolic Acidosis
  4. Symptomatic Uremia
  5. Medication Overdose d/t a failure to clear
109
Q

Considerations of dialysis:

HD is more ______ than PD.

PD is more gradual and favored for patients that can’t tolerate __________ associated with HD (CHF/unstable angina).

__________ is the most common adverse event.

_________ is the leading cause of death in dialysis patients.

A

HD is more efficient than PD.

PD is more gradual and favored for patients that can’t tolerate fluid shifts associated with HD (poor cardiac function).

Hypotension is the most common adverse event.

Infection is the leading cause of death in dialysis patients (impaired immune system/ healing).

110
Q

The risk of pre-renal azotemia is reduced by maintaining a MAP greater than _______ mmHg and providing appropriate hydration.

A

> 65 mmHg

111
Q

Vasopressin preferentially constricts the __________ arteriole. Maintains GFR and UOP better than NE or Neo.

A

efferent

112
Q

Anesthesia concerns of CKD.

A

Assess the stability of ESRD.
Get the accurate weight of the patient within 24 hrs of surgery
Well-controlled BP
Glucose management (A1c).
Aspiration Precaution (increase risk)
Pressors
Uremic bleeding (dysfunctional platelets)

113
Q

What are treatments of uremic bleeding?

Max effect time:
Duration:

A

DDAVP - max effect 2-4 hours, last 6-8 hours, give this in pre-op

Cryo (Factor VIII, vWF)

114
Q

What are some lipid insoluble drugs?

A
  • Thiazide/ Loop diuretics
  • Digoxin
  • Many abx
115
Q

What neuromuscular blockers are not dependent on the kidneys?

A

Atracurium
Cisatracurium

Hoffman elimination- plasma esterases affected by pH and temperature.

116
Q

When taking care of renal patients, what medications do we worry about having active metabolite?

A

Opioids (morphine, meperidine)

Morphine is cleared through the urine, active morphine metabolite will lead to respiratory depression.

117
Q

Lipid insoluble drugs will have a _________ duration of action in renal patients.

A

prolonged duration
*Eliminated unchanged in urine and dosing should be dependant on GFR

118
Q

What induction medications are excreted by the kidneys?

A

Phenobarbital
Thiopental

119
Q

What muscle relaxants (paralytics) are excreted by the kidneys?

A

Pancuronium
Vecuronium

If kidneys do not excrete them, the liver will.

120
Q

What cholinesterase inhibitors are excreted by the kidneys?

A

Edrophonium
Neostigmine

121
Q

What CV drugs are excreted by the kidneys?

A

Atropine
Digoxin
Glycopyrrolate
Hydralazine
Milrinone

122
Q

What antimicrobials are excreted by the kidneys?

A

Vancomycin
Aminoglycosides
Cephalosporins
PCN

123
Q

Patients maintained on dialysis should undergo dialysis _______ hours preceding elective surgery.

A

24 hours

124
Q

What is the concern when giving Sugammadex?

A
  • It covalently binds to NMB but if it is not excreted, it could dissociate and both drugs could be bioavailable in the patient
125
Q

____ of morphine in cleared through the urine
Main concern for Morphine with CKD patients?

A
  • 40%
  • circulating active metabolites –> life-threatening respiratory depression
126
Q

What is the main adverse effect for Meperidine (Demerol)?

A

Active metabolite Normeperidine –> Neurotoxicity
-nervousness, tremors, muscle twitches, seizures

127
Q

Normal serum creatinine concentration for males.

Normal serum creatinine concentration for females

A

Males: 0.8-1.3 mg/dL

Females: 0.6 - 1.0 mg/dL

128
Q

Normal creatinine clearance (range): _________

A

110-140 mL/min

129
Q

These drugs undergo hepatic metabolism and conjugation prior to elimination in the urine (Select all that apply).

A. Pavulon
B. Benzos
C. Opioids
D. Anectine

A

A, B, and C

Anectine (Sch) is metabolized by plasma cholinesterase

130
Q

What is the ideal anesthetic agent for renal patients?

A

Forane (Isoflurane)

131
Q

Which kidney is lower?

A

The right kidney is slightly lower than the left kidney.

132
Q

What is the normal range for BUN and serum creatinine?

A

10-20 mg/ dL and 0.6-1.3 mg/ dL

Adv. Health Assessment (Spring 2024) (25 decks)

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