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
Causes of hyperkalemia?
- Hypoaldosteronism - Succinylcholine - Acidosis - Cell death (trauma/tourniquet) - MTP
26
S/S of hyperkalemia?
- If chronic, may not have symptoms - Skeletal muscle paralysis - ↓ fine motor movement - Dysrhythmias
27
EKG progression with hyperkalemia?
- Peaked T wave - P wave abscence - Prolonged QRS - Sine waves - Asystole
28
How much does succinylcholine increase serum K+?
0.5-1 mEq/L
29
Hyperkalemia treatments?
- Dialyze w/i 24 hrs of surgery - Calcium **1st treatment** - Hyperventilation - 10 units IV insulin - Bicarb - Loop diuretics - Kayexalate
30
Hyperventilation's affect on pH?
each ↑ pH by 0.1 = ↓K+ by 0.4-1.5 mmol/L
31
Where is 99% of the body's calcium stored?
Bone
32
What is physiologically active calcium and it's normal value?
Ionized calcium - 1.2-1.38 mmol/L
33
What affects ionized calcium levels?
* Albumin and pH - ↑pH/Alkalosis = ↑Ca++ binding to albumin (therefore ↓iCa++)
34
What hormones affect calcium levels?
- PTH: ↑’s GI absorption, renal reabsorption, and regulates bone/bloodstream levels - Vitamin D: augments intestinal Ca++ absorption - Calcitonin: promotes storage of Ca++ in bone
35
Causes of hypocalcemia?
- ↓PTH secretion - Mg deficiency (required for PTH production) - Low Vitamin D - Renal failure (not responding to PTH) - MTP (citrate in blood products)
36
Complication of thyroid/PT surgery?
Laryngospasm d/t hypocalcemia
37
Causes of hypercalcemia?
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
S/S of hypercalcemia?
- Confusion - Lethargy - Decreased DTR - N/V/abd pain - Short QTi ## Footnote Chronically can cause kidney stones
39
S/S of hypocalcemia?
- Parasthesia - Irritability - Hypotension - Seizures - **Prolonged QTi**
40
Causes and symptoms of hypomagnesia?
Causes: Decreased intake or absorption, renal wasting Symptoms: Muscle weakness or excitation, seizures, VTach/Torsades
41
Treatments for hypomagnesia?
Dependent of severity of symptoms Slow replacement if not urgent Torsades/seizures → 2 g Mg sulfate
42
Causes for hypermagnesemia?
Very rare - d/t over treatment, eclampsia, pheochromocytoma
43
S/S of hypermagenesia at different serum levels?
4-5 mEq/L: Lethargy, N/V, Flushing >6 mEq/L: HoTN, ↓DTR >10 mEq/L: Paralysis, apnea, heart blocks, cardiac arrest
44
Treatment of hypermagnesemia?
- Diuresis - IV calcium - Dialysis
45
Location of kidneys (specifically)?
- Retroperitoneal between T12-L4 - Right kidney lower than left to accomodate for the liver
46
The kidneys recieve how much of the CO? Where does most of it go? Which part of the kidney is most vulnerable to ischemia?
- 20% of the CO - Cortex gets 85-90% - Medulla most sensitive to changes in BP
47
Role of calcitriol and prostaglandins?
Calcitriol: Maintains serum Ca++ PG's: inflammatory mediators, cause vasodilation, maintain RBF
48
What is the best measure of renal function overtime? Normal value?
GFR 125-140mL/hr - heavily influenced by hydration status
49
What is the best lab value for measuring GFR and acute changes? Normal value?
Creatinine clearance 110-140 mL/min ## Footnote Creatinine is freely filtered and not reabsorped
50
Normal serum creatinine? When is it useful?
0.6-1.3 mg/dL (correlates with muscle mass) Good for acute monitoring, need to know baseline
51
How is serum creatinine related to GFR?
- Inversely related - Acutely, an double in serum creatinine and mean GFR has dropped by half
52
Normal BUN? Causes of low and high BUN?
Normal: 10-20 mg/dL Low BUN: malnourishment or volume diluted High BUN: ↑protein diet, dehydrated, GI bleed, trauma, muscle wasting
53
What lab value is a good indicator of hydration status? Normal value?
BUN:Cr ratio 10:1 BUN is reabsorped and Cr is not
54
Normal urine protein levels? What do high levels indicate?
< 150 mg/dL >750mg/day could suggest glomerular injury or UTI
55
What lab measures the nephrons ability to concentrate urine? Normal values?
Specific gravity 1.001-1.035
56
What is a late sign of volume loss?
Decreased UOP
57
What defines oliguria?
< 500 mL/day
58
What can we monitor to assess for volume status?
- 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
What is a hallmark finding of AKI?
Azotemia - buildup of nitrogenous products (urea, creatinine)
60
Some risk factors for AKI?
- **Pre-existing renal dx** - Elderly - CHF - DM - Sepsis (hypotension) - IV contrast - Major operations
61
4 diagnostic criteria for AKI?
- 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
Physical S/S of AKI?
- Malaise - Hypotensive - Hypo/hypervolemic - Asymptomatic
63
Causes of prerenal AKI?
- Hemorrhage - Traume - Surgery - Sepsis ## Footnote Anything that decreases renal perfusion
64
Causes of intrarenal AKI?
- Vasculitis - ATN - Contrast dye ## Footnote Anything that caues injury to the nephron
65
Causes of postrenal AKI?
- Kidney stone (nephrolithiasis) - BPH ## Footnote Anything that blocks urine outflow (easiest to treat and most common)
66
Lab values that indicate preranal AKI? Treatment?
BUN:Cr > 20:1 Tx: Restore RBF → Fluids, diuretics, maintain MAP (pressors)
67
Lab values indicative of intrarenal AKI?
- ↓ GFR (late sign) - ↓urea reabsorption and ↓Cr filtration leads to BUN:Cr < 15:1
68
Neuro complications of AKI?
- Uremic encephalopathy - Neuropathies - Myopathies - Seizures - Strokes
69
CV complications of AKI in order of incidence?
- Hypertension - LVH - CHF - Pulm. edema - Arrythmias
70
Hematologic complications of AKI?
- Anemia (↓ EPO) - PLT dysfunction - vWF disruption from uremia - prophylactic DDAVP
71
Metabolic complications of AKI?
- Hyperkalemia - Water/Na+ imbalance - Hypoalbuminemia (renal loss) - Met. acidosis - Malnutritin - Hyperparathyroidism (in OD to try to stimulate kidneys to reabsorb Ca++)
72
Volume status managemet for patients with AKI?
- 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
Why would we give sodium bicarbonate prophylactically to AKI pts?
- ↓ free radical formation - Prevents ATN from causing renal failure
74
Leading cause of CKD? When are seeing them in the OR?
- DM and hypertension - Surgery for dialysis access - Diabetic amputations/debridements - Non-healing wounds
75
How does GFR change with aging?
Decreases by 10 mL/min/decade beginning at 20 yo
76
Describe the stages of CKD?
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
CV effects of CKD? Treatments?
* 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
Why are ACEi and ARB beneficial in CKD? Anesthesia concerns?
* ↓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
Hematologic treatments and risks for CKD?
- Exogenous EPO (goal is hgb of 10) - Transfusion of blood products (can lead to sluggish circulation, acidosis, and hyperkalemia)
80
Indications for dialysis?
AEIOU Acidosis Electrolyte imbalance Intoxication Overload Uremia
81
Best type of dialysis? Leading cause of death for patients of dialysis?
- HD more efficient - Infection (impaired immune system and healing)
82
Why might we be concerned for bleeding in patients with CKD? Treatments for surgery?
Uremia inhibits vWF = bleeding Assess coag function Transfuse if needed DDAVP - tachyphylaxis, choose wisely if multiple operations
83
Best NMB for CKD patients?
Nimbex - is not dependent on renal elimination
84
Why should you avoid giving lipid insoluble drugs to CKD patients?
Prolongs the medications duration of action d/t unchanged renal elimination - need renal dosing
85
Some drugs we give that are renally excreted?
- Phenobarbital - Pancuronium/vecuronium - Neostigmine - Glycopyrrolate - Atropine - Hydralazine - PCN - Vancomycins
86
What 2 drugs should we avoid in CKD patients d/t their active metabolites?
Morphine - M-3 glucuronide/M-6 glucuronide (can cause profound resp depression) Meperidine - Normeperidine has half life of 15-30 hrs → neurotoxicity
87
What K+ is acceptable for elective surgeries?
< 5.5 mEq/L
88
Why should we aim to blunt the SNS outflow in CKD patients in surgery?
Catecholamines activate ⍺1 receptors and constrict the afferent arteriole ↓RBF