Exam 3 - Renal Assessment Flashcards

1
Q

How is osmolar homeostasis maintained?

A
  • Mediated by osmolality sensors in anterior hypothalamus
  • Stimulates thirts via release of ADH from pituatary gland
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2
Q

How is volume homeostasis maintained?

A
  • Mediated by the JGA
  • ↓ in volume activates the RAAS → Na+/H2O reabsorption
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3
Q

What can cause someone to have a TBW > 60%?

A

Increased muscle mass

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4
Q

What degree of hypo-/hypernatremia would give you pause for surgery?

A
  • < 125 mg/dL or > 155 mg/dL
  • More concerned about acute changes in Na+; monitor trends
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5
Q

Some causes of hypovolemic hyponatremia?

A

d/t Na+ and H20 losses:
- Diuretics
- GI losses
- Burns
- Vomiting
- 3rd spacing

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6
Q

Some causes of euvolemic hyponatremia?

A
  • Salt restriction
  • Hypothyroidism
  • Drugs
  • SIADH
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7
Q

Some causes of hypervolemic hyponatremia?

A
  • Renal failure
  • Heart failure
  • Cirrhosis
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8
Q

Why are 15% of hospitalized patients hyponatremic?

A
  • Over resuscitated
  • ↑ endogenous vasopressin
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9
Q

What are the most severe consequences of hyponatremia?

A

Seizures, coma, death

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10
Q

How would hyponatremia be treated?

A
  • Treatment of underlying disease (look at volume status)
  • Electrolyte drinks
  • NS
  • Hypertonic Saline: 80mL/hr over 15 hrs
  • Diuretics
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11
Q

How quickly should you correct low Na+?
How often should you check serum levels?

A
  • Do not exceed > 1.5 mEq/L/hr
  • q4h
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12
Q

What might happen if you correct the sodium > 6 mEq/L in 24 hr?

A

Osmotic Demyelination Syndrome - leads to permanent neuro damage

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13
Q

What is the treatment for hyponatremic seizures?

A

3-5mL/kg of 3% NS over 20 min until seziures resolve

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14
Q

What are some causes of hypovolemic hypernatremia?

A
  • Diuretics
  • Post renal obstruction
  • GI losses
  • Sweating
  • Burns
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15
Q

What are some causes of euvolemic hypernatremia?

A
  • DI
  • Insensible losses
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16
Q

What are some causes of hypervolemic hypernatremia?

A

Sodium Gains
- Hyperaldosteronism
- Cushing’s
- Sodium bicarbonate

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17
Q

S/S of hypernatremia?

A
  • Restlessness
  • Lethargy
  • Tremor
  • Seizures
  • Death
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18
Q

Treatment of hypernatremia?

A

Hypovolemic: NS
Euvolemic: Water replacent (PO or D5W)
Hypervolemic: Diuretics

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19
Q

At what rate should you aim to correct hypernatremia?

A

< 0.5 mmol/L/hr and < 10 mmol/L/day

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20
Q

Aldosterone’s relationship to K+?

A
  • Inversely affects K+ levels
  • Causes distal nephron to secrete K+ and reabsorp Na+
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21
Q

Common causes of hypokalemia?
Not so common..?

A
  • Renal losses: diuretics, hyperaldosteronism
  • GI losses
  • Intracellular shifting: alkalosis, beta agonists, insulin
  • DKA (osmotic diuresis)
  • HCTZ
  • Excessive licorice - board question
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22
Q

S/S of hypokalemia?

A
  • Muscle weakness/cramps
  • Ileus
  • Dysrhythmias (u wave)
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23
Q

Treatments for hypokalemia?

A
  • Treat underlying cause
  • PO K+ preferred over IV
  • Avoid excessive insulin, bicarb, β agonists, hyperventilation, and diuretics
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24
Q

How much does IV K+ increase serum K+?

A

Every 10 mEq IV increases serum K+ by ~0.1 mmol/L

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25
Q

Causes of hyperkalemia?

A
  • Hypoaldosteronism
  • Succinylcholine
  • Acidosis
  • Cell death (trauma/tourniquet)
  • MTP
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26
Q

S/S of hyperkalemia?

A
  • If chronic, may not have symptoms
  • Skeletal muscle paralysis
  • ↓ fine motor movement
  • Dysrhythmias
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27
Q

EKG progression with hyperkalemia?

A
  • Peaked T wave
  • P wave abscence
  • Prolonged QRS
  • Sine waves
  • Asystole
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28
Q

How much does succinylcholine increase serum K+?

A

0.5-1 mEq/L

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29
Q

Hyperkalemia treatments?

A
  • Dialyze w/i 24 hrs of surgery
  • Calcium 1st treatment
  • Hyperventilation
  • 10 units IV insulin
  • Bicarb
  • Loop diuretics
  • Kayexalate
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30
Q

Hyperventilation’s affect on pH?

A

each ↑ pH by 0.1 = ↓K+ by 0.4-1.5 mmol/L

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31
Q

Where is 99% of the body’s calcium stored?

A

Bone

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32
Q

What is physiologically active calcium and it’s normal value?

A

Ionized calcium - 1.2-1.38 mmol/L

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33
Q

What affects ionized calcium levels?

A
  • Albumin and pH
  • ↑pH/Alkalosis = ↑Ca++ binding to albumin (therefore ↓iCa++)
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34
Q

What hormones affect calcium levels?

A
  • PTH: ↑’s GI absorption, renal reabsorption, and regulates bone/bloodstream levels
  • Vitamin D: augments intestinal Ca++ absorption
  • Calcitonin: promotes storage of Ca++ in bone
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35
Q

Causes of hypocalcemia?

A
  • ↓PTH secretion
  • Mg deficiency (required for PTH production)
  • Low Vitamin D
  • Renal failure (not responding to PTH)
  • MTP (citrate in blood products)
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36
Q

Complication of thyroid/PT surgery?

A

Laryngospasm d/t hypocalcemia

37
Q

Causes of hypercalcemia?

A

Most common: Hyperparathyroid (serum Ca++ < 11) and cancer (serum Ca++ >13)
Less common: Vitamin D intoxication, milk-alkali syndrome (excessive GI absorption), and sarcoidosis

38
Q

S/S of hypercalcemia?

A
  • Confusion
  • Lethargy
  • Decreased DTR
  • N/V/abd pain
  • Short QTi

Chronically can cause kidney stones

39
Q

S/S of hypocalcemia?

A
  • Parasthesia
  • Irritability
  • Hypotension
  • Seizures
  • Prolonged QTi
40
Q

Causes and symptoms of hypomagnesia?

A

Causes: Decreased intake or absorption, renal wasting
Symptoms: Muscle weakness or excitation, seizures, VTach/Torsades

41
Q

Treatments for hypomagnesia?

A

Dependent of severity of symptoms
Slow replacement if not urgent
Torsades/seizures → 2 g Mg sulfate

42
Q

Causes for hypermagnesemia?

A

Very rare - d/t over treatment, eclampsia, pheochromocytoma

43
Q

S/S of hypermagenesia at different serum levels?

A

4-5 mEq/L: Lethargy, N/V, Flushing
>6 mEq/L: HoTN, ↓DTR
>10 mEq/L: Paralysis, apnea, heart blocks, cardiac arrest

44
Q

Treatment of hypermagnesemia?

A
  • Diuresis
  • IV calcium
  • Dialysis
45
Q

Location of kidneys (specifically)?

A
  • Retroperitoneal between T12-L4
  • Right kidney lower than left to accomodate for the liver
46
Q

The kidneys recieve how much of the CO?
Where does most of it go?
Which part of the kidney is most vulnerable to ischemia?

A
  • 20% of the CO
  • Cortex gets 85-90%
  • Medulla most sensitive to changes in BP
47
Q

Role of calcitriol and prostaglandins?

A

Calcitriol: Maintains serum Ca++
PG’s: inflammatory mediators, cause vasodilation, maintain RBF

48
Q

What is the best measure of renal function overtime?
Normal value?

A

GFR
125-140mL/hr - heavily influenced by hydration status

49
Q

What is the best lab value for measuring GFR and acute changes?
Normal value?

A

Creatinine clearance
110-140 mL/min

Creatinine is freely filtered and not reabsorped

50
Q

Normal serum creatinine?
When is it useful?

A

0.6-1.3 mg/dL (correlates with muscle mass)
Good for acute monitoring, need to know baseline

51
Q

How is serum creatinine related to GFR?

A
  • Inversely related
  • Acutely, an double in serum creatinine and mean GFR has dropped by half
52
Q

Normal BUN?
Causes of low and high BUN?

A

Normal: 10-20 mg/dL
Low BUN: malnourishment or volume diluted
High BUN: ↑protein diet, dehydrated, GI bleed, trauma, muscle wasting

53
Q

What lab value is a good indicator of hydration status?
Normal value?

A

BUN:Cr ratio
10:1
BUN is reabsorped and Cr is not

54
Q

Normal urine protein levels?
What do high levels indicate?

A

< 150 mg/dL
>750mg/day could suggest glomerular injury or UTI

55
Q

What lab measures the nephrons ability to concentrate urine?
Normal values?

A

Specific gravity
1.001-1.035

56
Q

What is a late sign of volume loss?

A

Decreased UOP

57
Q

What defines oliguria?

A

< 500 mL/day

58
Q

What can we monitor to assess for volume status?

A
  • US for IVC collapsibility (>50% collapse = fluid deficit)
  • CVP
  • LAP/PAWP
  • SVV (compares inspiratory and expirartory pressure; pt must be ventilated and in SR)
59
Q

What is a hallmark finding of AKI?

A

Azotemia - buildup of nitrogenous products (urea, creatinine)

60
Q

Some risk factors for AKI?

A
  • Pre-existing renal dx
  • Elderly
  • CHF
  • DM
  • Sepsis (hypotension)
  • IV contrast
  • Major operations
61
Q

4 diagnostic criteria for AKI?

A
  • Serum Cr ↑ by 0.3 mg/dL in 48 hrs
  • Serum Cr ↑ by 50% in 7 days
  • ↓ in CrCl by 50%
  • Abrupt oliguria (not always)
62
Q

Physical S/S of AKI?

A
  • Malaise
  • Hypotensive
  • Hypo/hypervolemic
  • Asymptomatic
63
Q

Causes of prerenal AKI?

A
  • Hemorrhage
  • Traume
  • Surgery
  • Sepsis

Anything that decreases renal perfusion

64
Q

Causes of intrarenal AKI?

A
  • Vasculitis
  • ATN
  • Contrast dye

Anything that caues injury to the nephron

65
Q

Causes of postrenal AKI?

A
  • Kidney stone (nephrolithiasis)
  • BPH

Anything that blocks urine outflow (easiest to treat and most common)

66
Q

Lab values that indicate preranal AKI?
Treatment?

A

BUN:Cr > 20:1
Tx: Restore RBF → Fluids, diuretics, maintain MAP (pressors)

67
Q

Lab values indicative of intrarenal AKI?

A
  • ↓ GFR (late sign)
  • ↓urea reabsorption and ↓Cr filtration leads to BUN:Cr < 15:1
68
Q

Neuro complications of AKI?

A
  • Uremic encephalopathy
  • Neuropathies
  • Myopathies
  • Seizures
  • Strokes
69
Q

CV complications of AKI in order of incidence?

A
  • Hypertension
  • LVH
  • CHF
  • Pulm. edema
  • Arrythmias
70
Q

Hematologic complications of AKI?

A
  • Anemia (↓ EPO)
  • PLT dysfunction
  • vWF disruption from uremia - prophylactic DDAVP
71
Q

Metabolic complications of AKI?

A
  • Hyperkalemia
  • Water/Na+ imbalance
  • Hypoalbuminemia (renal loss)
  • Met. acidosis
  • Malnutritin
  • Hyperparathyroidism (in OD to try to stimulate kidneys to reabsorb Ca++)
72
Q

Volume status managemet for patients with AKI?

A
  • NS preferred (no K+)
  • Correct fluid, electrolyte, and acid/base imbalance pre-op
  • Maintain MAP 20% of baseline
  • Vasopressin > ⍺ agonists - preferentialy constricts the efferent arteriole (better for increasing RBF)
73
Q

Why would we give sodium bicarbonate prophylactically to AKI pts?

A
  • ↓ free radical formation
  • Prevents ATN from causing renal failure
74
Q

Leading cause of CKD?
When are seeing them in the OR?

A
  • DM and hypertension
  • Surgery for dialysis access
  • Diabetic amputations/debridements
  • Non-healing wounds
75
Q

How does GFR change with aging?

A

Decreases by 10 mL/min/decade beginning at 20 yo

76
Q

Describe the stages of CKD?

A

1 - Kidney damage with normal or increased GFR (>90)
2 - Kidney damage with midly decreased GFR (60-89)
3 - Moderately decreased GFR (30-59)
4 - Severely decreased GFR (15-29)
5 - Kidney failure (GFR < 15)

77
Q

CV effects of CKD?
Treatments?

A
  • Systemic HTN (cause and consequence): d/t ↑RAAS (↑Na+/H2O retention)
  • Dyslipidemia (↑triglycerides and LDL) - can lead to slient MI from decreased sensation
  • Tx: 1st = Thiazides, may need ACEi/ARB
78
Q

Why are ACEi and ARB beneficial in CKD?
Anesthesia concerns?

A
  • ↓systemic BP and glomerular pressure
  • ↓proteinuria by reducing glomerular hyperfiltration
  • ↓glomerulosclerosis
  • Hold before surgery to prevent profound hypotension - have pressors on hand if not held
79
Q

Hematologic treatments and risks for CKD?

A
  • Exogenous EPO (goal is hgb of 10)
  • Transfusion of blood products (can lead to sluggish circulation, acidosis, and hyperkalemia)
80
Q

Indications for dialysis?

A

AEIOU
Acidosis
Electrolyte imbalance
Intoxication
Overload
Uremia

81
Q

Best type of dialysis?
Leading cause of death for patients of dialysis?

A
  • HD more efficient
  • Infection (impaired immune system and healing)
82
Q

Why might we be concerned for bleeding in patients with CKD?
Treatments for surgery?

A

Uremia inhibits vWF = bleeding
Assess coag function
Transfuse if needed
DDAVP - tachyphylaxis, choose wisely if multiple operations

83
Q

Best NMB for CKD patients?

A

Nimbex - is not dependent on renal elimination

84
Q

Why should you avoid giving lipid insoluble drugs to CKD patients?

A

Prolongs the medications duration of action d/t unchanged renal elimination - need renal dosing

85
Q

Some drugs we give that are renally excreted?

A
  • Phenobarbital
  • Pancuronium/vecuronium
  • Neostigmine
  • Glycopyrrolate
  • Atropine
  • Hydralazine
  • PCN
  • Vancomycins
86
Q

What 2 drugs should we avoid in CKD patients d/t their active metabolites?

A

Morphine - M-3 glucuronide/M-6 glucuronide (can cause profound resp depression)
Meperidine - Normeperidine has half life of 15-30 hrs → neurotoxicity

87
Q

What K+ is acceptable for elective surgeries?

A

< 5.5 mEq/L

88
Q

Why should we aim to blunt the SNS outflow in CKD patients in surgery?

A

Catecholamines activate ⍺1 receptors and constrict the afferent arteriole ↓RBF