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Health Assessment > Renal Assessment Ex 3 > Flashcards

Renal Assessment Ex 3 Flashcards

Dr Morderca

1
Q

How is osmolar homeostasis maintained?
What are 3 functions?

A

-Osmolar homeostasis mainly mediated by osmolality-sensors in anterior hypothalamus
-Cause pituitary release of ADH
-stimulate thirst
-Cardiac atria releases ANP→act on kidney to ↑Na+/H20 reabsorption

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2
Q

How does the juxtaglomerular apparatus mediate volume homeostasis?

A

It senses changes in volume and triggers RAAS to reabsorb Na and water

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3
Q

Interstitial fluid makes up __ of ECF
Plasma makes up ___ of ECF

A

3/4

1/4

ecf is more immediatly altered by kidneys

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4
Q

Which Na+ level do you correct prior to elective surgery?

A

less than 125 and >155!!

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5
Q

What are some causes of hypovolemic hyponatremia?

What are some causes of euvolemic hyponatremia?

A

hypovolemic: diuretics, gi loss, burns, trauma

euvolemic: Salt resitriction, endocrine related like hypothyroidism & SIADH (holding on to H2O and Na)

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6
Q

What are some causes of hypervolemic hyponatremia?

A

ARF, CKD, heart failure

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7
Q

Why are 15% of hospitalized patients hyponetremic?

A

-The are over fluid resiscuitated
-They have high levels of endogenous vasopression (inc H20 reabsorption)

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8
Q

S/S of Na 130-135

A

asymptomatic, H/A, N/V, fatigue, confusion, muscle cramps, depressed reflexes

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9
Q

Whare are s/s of Na 120-130?

A

120-130: HA, NV, fatigue, confusion, muscle cramps, malaise, unsteadiness

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10
Q

What is the treatment of hyponatremia?

Correction should not exceed what?

How fast do you infuse 3% NS?

A

treat underlying cause (volume status), REPLACE (electrolye drinks, NS), diuretics, hypertonic Saline

***should not exceed correction of 1.5 meq/lL/hr *

3% NS @ 80 mL/hr for 15 hr & check Na level q4h

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11
Q

What can happen if you correct Na+ too fast?

What is the treatment for hyponatremic seizures?

A

rapid correction (>6 meq/L in 24 hr) can cause** osmotic demyelination syndrome **and result in permanent neuro damage

3-5 mL/kg 3% NS over 20 min! until seizures resolve.

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12
Q

What are common causes of hypernatremia?

A

Hypovolemic-Renal or GI loss
Euvolemic- DI, insensible loss (skin, respiratory)
Hypervolemic- ↑Na+ intake( IV), hyperaldosteronism, Cushings

-overcorrection of hyponatremia, excessive sodium bicarb when treating acidosis

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13
Q

What are s/s of hypernatremia?

What is the treatment?

A

-orthostasis, restleness, lethargy, tremor, muscle twitching, seizures, death

-Assess volume status (US, UOP, turgor, cvp)
hypovolemic: NS
euvolemic: water replacement; or D5W
hypervolemic: diuretic

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14
Q

Goal for treatment for hypernatremia ?

A
  • want reduction rate of <0.5 mmol/L/hr and <10 mmol/L/day to avoid cerebral edema seizures, neuro damage
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15
Q

Serum K+ reflects more ____ K+ regulation than total body K+.

Aldosterone causes the distal nephron to ____ K+ and ____ Na+

A
  • Serum K+ reflects transmembrane K+ regulation more than total body K+

secrete k+ and reabsorb Na

<1.5% of K in ECF

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16
Q

What are common causes of hypokalemia?

A
  • Low PO Intake
  • Renal loss- Diuretics, Hyperaldosteronism
  • GI loss – N/V/D, malabsorption
  • Intracellular shift- Alkalosis, beta agonists, Insulin
  • DKA (osmotic diuresis)
  • HCTZ (in BP meds)
  • Excessive licorice

3 categories- renal loss, GI loss, trancellular shift

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17
Q

What are symptoms of hypokalemia?

What is the treatment?

A

muscle weakness/ cramps, ileus, U waves

-PO, or 10-20 meq/L/hr
-each 10 meq rises K by 0.1 mmol/L

Avoid excessive insulin, B agonists, hyperventilation and diuretics

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18
Q

What are causes of hyperkalemia? (8)

A
  • Hypoaldosteronism
  • Renal failure
  • Drugs that inhibit RAAS- Aldosterone inhibitors
  • Drugs that inhibit K+ excretion
  • Depolarizing NMB (Succs)
  • Acidosis
  • Cell death (trauma, tourniquet)~ cell rupture
  • Massive blood transfusion

Succ increases serum K+ by 0.5-1 mEq/L

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19
Q

Symptoms of hyperkalemia?

A
  • Skeletal muscle paralysis,↓fine motor
    Cardiac dysrhythmias:
  • peaked T wave ; first sign
  • P wave disappearance
  • prolonged QRS complex
  • sine waves
  • asystole

Chronic intially minimal symptomatic (malaise, GI upset)

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20
Q

What is treatment for hyperkalemia?

A

-Dialyze~ 24 hr before surgery
-Ca+ (First)
-Hyperventilation- inc pH by 0.1 and lowers K by 0.4-1.5 mmOl/L
-10 u insulin and 25g D50 (works in 10-20 min)
-bicarb, loop diurettics, Kayexalate

avoid succ, hypoventilation, LR

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21
Q

Only 1% of Ca+ is in ___; 99% is stored in ___

60% of plasma Ca+ is ___ bound.

Ionized Ca+ level is affected by ___ levels and ___

A

ECF; stored in bone

protein bound

albumin levels and pH- high pH= low iCa+

Only ionized Ca+ is active

normal Ca= 1.2-1.38

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22
Q

What hormones regulate Ca+? (3)

A
  • Parathyroid hormone: ↑’s GI , renal, and bone absorption
  • Vitamin D: augments intestinal absorption
  • Calcitonin: inhibits bone resorption
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23
Q

What are some causes for hypocalcemia? (6)

A

-Low PTH secretion (thyroid complication)
-parathyroidectomy* common complication is laryngospasm*
-Mg deficiency (Mg required for PTH production)
-Low Vit D
-Renal failure
-massive blood tranfusion

citrate preservative binds to Ca+, check iCa+ after 4 pRBC

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24
Q

Majority of pt’s w/ hypercalcemia have _____ or _____

A

hyper-parathyroid or cancer

Hyperparathyroid serum Ca++ <11
Cancer serum Ca++ >13

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25
Q

Less common causes of hypercalcemia

A

Vit D intoxication
Milk-alkali syndrome (excessive GI Ca++ absorption)
Granulomatous diseases (sarcoidosis)

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26
Q

S/S of hypercalcemia

A

confusion, lethargy, hypotonia, drop in DTR, abd pain, D/V, short QT.

Chronic: high Ca+–>hypercalcicurla and nephrolithiasis

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27
Q

s/s of hypocalcemia

A

paresthesias, irritability, HTN, seizures, myocardial depression, prolonged QT
Post-Parathyroidectomy-hypocalcemia-induced laryngospasm (life threatening complication)

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28
Q

What are s/s of hypomagnesia

Treatment?

A

Muscle weakness or excitation
seizures
Ventricular dysrhythmia (Polymorphic V-tack/Torsades De Pointes)

Slower infusions for less severe
Torsade’s/seizures→ 2g Mag Sulfate

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29
Q

What are the symptoms for Mag of 4-5 meq/L?
>6 MEQ?
>10?
What are treatments for hypermagnesium?

A
  • 4-5 mEq/L: Lethargy, N/V, Flushing
  • > 6 mEq/L: hypotension, ↓DTR
  • > 10 mEq/L: Paralysis, apnea, heart blocks, cardiac arrest
    -Treatment: diuresis, IV calcium, dialysis

common causes: preclampsia, or pheochromocytoma

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30
Q

What part of the kidney recieves 85-90% of RBF?

What part is vulnerable for developing necrosis in response to hypotension?

A

cortex

loop of henle

31
Q

What is AKI?
What are the causes?

A
  • AKI: Failure to excrete nitrogenous waste products or maintain fluid/electrolyte homeostasis
    Caused by hypotension, hypovolemia, nephrotoxins

AKI affects 20% hospitalized pt and 50% ICU pt

32
Q

What are AKI diagnostic criteria? (4)

A

-inc Cr by 0.3 mg/dL in 48 hr
-inc Cr by 50% in 7 days
-decrease creatinine clearence by 50%
-obrupt oliguria

normal CR: 0.6-1.3 mg/dL; Creatinine clearence: 110-140 mL/min

33
Q

What is azotemia?

A

Azotemia: hallmark of AKI; buildup of nitrogenous products like urea and creatnine

AKI w/ MODS has 50% mortality rate :(

34
Q

What are causes of prerenal azotemia?
What is the treatment?

A

hemorrhage, GI fluid loss, trauma, surgery, burns, cardiogenic shock, aortic clamping, thromboembolism (low renal perfusion)—-usually a volume issue and reverseable; can turn into renal azotemia

-Tx: Restore RBF: fluids, mannitol, diuretics, maintain MAP, pressors if needed.

BUN:CR >20:1;

35
Q

What are causes of renal azotemia? (7)

nephron injury/ intrinsic

A

-acute glomerulonephritis, vasculitis, interstitial nephritis, ATN, contrast, nephrotoxic drugs, myoglobinuria

most difficult to reverse

36
Q

Common labs in renal azotemia

A

-high serum Cr (d/t low filtration)
-low urea reabsorption –>low BUN
-BUN:CR <15:1
low GFR usually a late symptom

37
Q

What are causes of postrenal azotemia? (4)
Tx?

A

nephrolithiasis, BPH, clot retention, bladder CA. due to obstruction!! causes high nephron tubular hydrostatic pressure
Tx: Remove the obstruction!

easiest to treat!

38
Q

What are neurological complications of AKI? 7

A

R/t protein/ amino acids buildup,
uremic encephalopathy,
mobility disorders, neuropathies, myopathies, seizures, stroke

39
Q

CV complications of AKI?

A

HTN, LV hypertrophy, pulmonary edema, CHF, uremic cardiomyopathy, arrythmias

  • In order of incidence HTN→ LVH→ CHF→ischemic heart disease→ anemic heart failure→ rhythm disturbances→pericarditis & effusion→ cardiac tamponade, uremic cardiomyopathy
40
Q

What are hematological compliations of AKI?

A

anemia (d/t low epo production, low RBC production and low RBC survival), platelet dysfunction, and vWF disrupted by uremia

ddabp to improve vWF and Factor VIII and improve coagulation

41
Q

What are metabolic complications of AKI?

A

hyperkalemia, water and Na imbalances, hypoalbuminemia (kidneys allowing it to escape)
metabolic acidosis, malnutrition, hyperparathyroidism (parathyroid in overdrive to stimulate kidney to reabsorb Ca+)

42
Q

What to consider when giving anesthesia to AKI patients?

A
  • Correct fluid, electrolyte, acid/base status
    = Volume; NS preferred for renal (no K+)
  • Careful w/colloids
  • MAP maintained (20% of baseline)
  • Vasopressors? (Vasopressin, Alpha-agonists)
  • Prophylactic sodium bicarb

vasopressin constricts efferent arteriole and this inc RBF

43
Q

Why give sodium bicarb to AKI patients

A

Sodium bicarb decreases formation of free-radicals
Prevents ATN from causing renal failure

44
Q

CKD stages~ irreversible and progressive

What is the GFR in each stage of CKD?

Stage 1:

Stage 2:

A

1: normal or increased GFR >90

2: mildly decreased GFR, 60-89

GFR decreases by 10 per decade starting from age 20 :(

45
Q

What is the GFR in each stage of CKD?

Stage 3

Stage 4

Stage 5

A

3: moderately dec GFR 30-59

4: severely decreased GFR 15-29 (HD)

5: kidney failure! GFR <15

46
Q

Why are ACE and ARBs used in CKD?

Do you continue them day of surgery

A

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

hold day of surgery cause they cause risk of profound hypotension!

47
Q

What 5 complications indicate need for dialysis

A
  • Volume overload during surgery (maybe surgery took longer than expected)
  • Severe hyperkalemia
  • Metabolic acidosis
  • Symptomatic uremia
  • Failure to clear medications
48
Q

K should be what range on elective surgery?

HD should be dialyzed within ___ of elective procedure

A

K <5.5 MEQ/L

within 24 hr

49
Q

Active metabolite of demerol is _____
What is the half life?
What are the 4 signs of neurotoxicity?

A

Normeperidine.
half life is 15-30 hours, as compared to demerol which is 2-4 hr

nervousness, tremors, muscle twitches, seizures

50
Q

How much of morphine is cleared in urine? What is the active metabolite?

A

40% cleared through urine.
morphine-6 glucuronide which can cause life threatening resp depression
Failure to clear leads to active metabolites

51
Q

normal range for GFR? and why it matters

A

125 - 140 mL/min

best measure of renal fxn over time

52
Q

normal range for creat clearance?
why it matters?

A

110 - 140 mL/min
most reliable measure of GFR

24 hr urine test

53
Q

serum creat normal range?
why does it matter?

A

0.6 - 1.3 mg/dL

inversely r/t GFR, acute doubling of serum creat can mean a drop in GFR by 50%

54
Q

normal range for BUN?
why it matters?

A

10-20 mg/dL
urea is reabsorbed to concentrate our urine and hold more volume

low BUN = volume diluted or malnourished

high BUN = high protein diet, dehydrated, GI bleed, muscle wasting

55
Q

normal BUN:creat ratio?
why it matters?

A

10:1

good measure of hydration status

56
Q

whats the normal value of protein in our urine?

why is this impt?

what does proteinuria look like?

A

< 150 mg/dL

> 750 mg/day could mean glomerular injury or UTI

frothy urine!!

57
Q

normal range of urine specific gravity?

why it matters?

A

1.001 - 1.035

measures nephron’s ability to conc urine

58
Q

what does a drop in urine output suggest?

A

a LATE SIGN of volume loss

59
Q

normal UOP range?

A

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

60
Q

how can we measure volume status using US?

A

assess IVC
>50% collapse indicates fluid deficit

other ways: CVP, RAP, LAP, PCWP, PAP, SVV

61
Q

what’s an easy way to determine fluid responsiveness?

A

passive leg raise

62
Q

Which non-depolarizing muscle relaxer is not dependent on renal elimination that would be best for renal pts? based on her ppt

A

cisatracurium (nimbex), but rmbr its slow-ish onset

63
Q

how much does GFR decrease per decade starting from age 20?

A

decreases by 10 :(

64
Q

What’s the 1st line treatment for patients w/ CKD?

A

thiazide diuretics

65
Q

What drugs do we need to HOLD on day of surgery (that a CKD pt is likely on)?

A

ACE-I and ARBs

to reduce the risk of profound hypotension!

66
Q

Whats our target Hgb for a CKD patient?

A

10
- may need to transfuse and/or give some exogenous EPO if pt anemic

67
Q

What are some risks with transfusing an anemic CKD patient?

A
  • excessive Hgb leads to sluggish circulation
  • acidosis and hyperkalemia also assoc w/ blood transfusions
68
Q

what type of dialysis is more efficient?

A

HD > PD

69
Q

what type of dialysis may be more suitable for a renal pt with poor cardiac function?

A

PD - slower, so less dramatic volume shifts

70
Q

What do we need to give the renal pt if we’re expecting them to bleed a lot during surgery?

A

desmopressin (DDAVP) to help them produce more vWF and improve coagulation

tachyphylaxis risk tho

peaks 2-4h and lasts 6-8h

71
Q

What NMBD is best for aspiration precaution patients especially in DM?

A

high dose roc, no succ

72
Q

What are s/s of Na <120

A

<120: H/a, restleness, lethargy, seizures, brain stem herniation, respiratory arrest, death, coma

73
Q

How are lipid insoluble drugs eliminated?
What are some examples she mentioned

A

Unchanged thru urine, use renal dosing. They will have a prolonged duration

o Thiazide diuretics
o Loop diuretics
o Digoxin
o Many antibiotics

Health Assessment (30 decks)

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