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Mar: Sem 2 - Health Assessment > Renal (Bri/Jia) > Flashcards

Renal (Bri/Jia) Flashcards

1
Q

_____TBW is water (varies w/ gender, age, body fat %)

slide 3

A

60%

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2
Q

What is ECF? What is it composed of? How much of it is TBW?

A
  • ECF is the fluid outside of cells
  • ISF +Plasma
  • < 1/2 volume of TBW
  • ECF is more immediately altered by kidneys

Slide 3

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3
Q

What are 2 types of homeostasis?

A

osmolar homeostasis
volume homeostasis

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4
Q

What is osmolar homeostasis mediated by? What does it cause?

A
  • Mediated by osmolality-sensors in anterior hypothalamus
  • Stimulate thirst
  • Cause Pituitary Release of Vasopressin (ADH)
  • Cardiac atria releases ANP→act on kidney to excrete Na+/H20.

3

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5
Q

What is volume homeostasis mediated by? what does it cause?

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

3

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6
Q

Increased mucles =

A

increased water

3

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7
Q

What does ADH do?

A

Helps body ↑H20/Na+ retention

3

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8
Q

how do you calculate TBW?

A
  • 60% body weight.

3

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9
Q

What are the categories/cause of hyponatremia?

A
  • Hypovolemia
  • Euvolemia
  • Hypervolemia

4

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10
Q

Hypovolemia leads to?

A
  • decreased skin turgor
  • flat neck vein
  • dry mucous membrane
  • orthostatic hypotension
  • tachycarda
  • oliguria.
    TOD-FOD (say it like hypovolemia: ta-da!!!)

4

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11
Q

Hypervolemia leads to?

A
  • peripheral edema
  • rales
  • ascites
    Hypervolemia…that’s PAR for the course

4

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12
Q

When hypovolemic, if Una ____ it due to renal losses. If Una is ____, its due to extrarenal loses.

A
  • Una >20 [renal loss]
  • Una <20 [extrarenal loss]

4

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13
Q

Renal loss due to hypovolemia if Una is > 20 is because of?

A
  • diuretic excess
  • mineracorticoid deficiency
  • salt losing nephritis
  • renal tubular acidosis
  • metabolic alkaloss
  • ketonuria
  • osmotic diuretic
    Ren Might Die So Keaton Met Ozzie
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14
Q

Renal loss due to hypovolemia if Una is < 20 is because of?

A
  • Vomiting
  • diarrhea
  • 3rd space losses
  • burns
  • pancreatituss
  • muscle traume

My 3rd pan burned vomit and diarrhea

4

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15
Q

Hypovolemic hyponatremia is caused by?

A
  • Na/H20 Loss like with diuretics, GI loss, Burns and trauma

Slide 4 comment

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16
Q

Howto treat euvolemia if Una is <20?

A

Salt restricted diet

4 + comment

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17
Q

What are the causes of euvolemia if Una is >20?

A
  • glucocorticoid deficiency
  • hypothyroid
  • high sympathetic drive
  • drugs
  • SIADH

4

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18
Q

When hypervolemic, if Una ____ it due to renal losses. If Una is ____, its due to extrarenal loses.

A
  • Una >20 [renal loses]
  • Una < 20 [Avid sodium reabsorption]

4

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19
Q

What are the causes of hypervolemia if Una is >20?

A
  • acute renal failure
  • chronic renal failure

4 comment

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20
Q

What are the causes of hypervolemia if Una is <20?

A
  • nephrotic syndrome
  • cardiac failure
  • cirrhosis

4

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21
Q

____ hospitalized pts are hyponatremic. Why?

A
  • 15%
  • over fluid-resuscitation
  • ↑endogenous vasopressin

4

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22
Q

Normal Na levels?
What levels do you stop surgery?

A
  • 135-145mEq/L
  • look at trends, more concerned with acute changes; ≤125 or ≥ 155, want correction prior to elective case

4

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23
Q

S/Sx of hyponatremia: 130-135 (8)

A
  • Asymtomatic
  • headache
  • nausea
  • vomitting
  • fatigue
  • confusion
  • mucle cramp
  • depressed reflexes

slide 5

Starts with HA.

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24
Q

S/Sx of hyponatremia: 120 - 130 (8)

A
  • malaise
  • unsteadiness
  • headache
  • nausea
  • vomitting
  • fatigue
  • confusion
  • muscle cramps

slide 5

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25
Q

S/Sx of hyponatremia:<120 (7)

A
  • Headache
  • Restless
  • lethargy
  • seizure
  • Brainstemp herniation
  • respiratory arrest
  • death

slide 5

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26
Q

the most severe consequences of hyponatremia

A

Seizures, coma, death.

slide 5

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27
Q

What is the treatment for mild hyponatremia?

A
  • Treat underlying cause (look at volume status)
  • Electrolyte drinks
  • Normal saline
  • Diuretics
    Mildhyponatremia TENDs to be treated by…

slide 6

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28
Q

What is the treamtent for extreme hyponatremia [<120?]

A
  • Hypertonic Saline/3% NaCl

sllide 6

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29
Q

Hypertonic saline is adminsitered for hyponatremia. What is the dose and consideration?

A
  • 80ml/hr over 15h
  • Na+ correction should not exceed 1.5 mEq/L/hr

slide 6

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30
Q

What happens if you correct hyponatremia fast? What is considered fast?

A

Rapid correction (>6 mEq/L in 24 h) can cause Osmotic Demyelination Syndrome (often permanent neuro damage)

slide 6

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31
Q

With low sodium levels, what is a medical emergency?
How do you treat it?

A
  • Hyponatremic seizures=medical emergency (neurological damage)
  • 3-5ml/kg of 3% over 20 min, until seizures resolve

slide 6

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32
Q

Common causes of Hypernatremia

A
  • Excessive evaporation
  • Poor oral intake (very young, very old, altered mental status)
  • Overcorrection of hyponatremia
  • Diabetes insipidus
  • GI losses
  • Excessive sodium bicarb (treating acidosis)
    PODGEE

slide 7

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33
Q

What are the s/sx of hypernatremia?

A
  • Orthostasis
  • Restlessness
  • Lethargy
  • Tremor/Muscle twitching/spasticity
  • Seizures
  • Death

slide 9

hypernatremia sx mirror hyponatremia sx

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34
Q

What is the treatment for hypernatremia?

A
  • Route cause, Assess volume status (VS, UOP, Turgor, CVP)
  • Hypovolemic: normal saline
  • Euvolemic: water replacement (po or D5W)
  • Hypervolemic: diuretics
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35
Q

What should be the sodium reduction rate for hypernatremia and why?

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

slide 9

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36
Q

Normal K+ levels?
% in the ECF?

A
  • 3.5-5 mmol/L
  • < 1.5% in ECF

slide 10

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37
Q

______ reflects transmembrane K+ regulation more than total body K+

A

Serum K+

slide 10

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38
Q

_____ causes the distal nephron to secrete K+ (and reabsorb Na+)

A

Aldosterone

slide 10

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39
Q

____ is inversly related to K.

A

Aldosterone

slide 10

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40
Q

In renal failure, what happens to K excretion>

A

K+ excretion declines.
Excretions shifts towards GI system

slide 10

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41
Q

What are the 3 major categories for the cause of hypokalemia?

A
  1. Renal loss
  2. GI loss
  3. Transcellular loss

slide 11

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42
Q

Causes of hypokalemia due to renal loss include?

A
  • Diuretics
  • hyperaldosteronism
  • Mineralcorticoids
  • high-dose glucocorticoids
  • abx (penicillin, nafcillin, ampicillin)
  • Drugs associated with magnesium depletion
  • Surgical Trauma
  • Hyperglycemia

slide 11

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43
Q

Causes of hypokalemia due to GI loss include?

A
  • N/V/D
  • Malabsorption
  • Zollinger-Ellison Syndrome
  • Jejunoileal bypass
  • Chemo
  • Nasogastric suction

slide 11

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44
Q

Causes of hypokalemia due to transceullar shift include?

A
  • Akalosis
  • Beta-agonist
  • Insulin
  • Tocolytic drugs
  • alkalosis
  • Hypercalcemia
  • Hypomagnesemia

slide 11

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45
Q

Common cause of hypokalemia

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

slide 11

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46
Q

List the s/sx of hypokalemia

A
  • Generally cardiac and neuromuscular
  • Muscle weakness/Cramps
  • Ileus
  • Dysrhythmias, U wave

s;ode 12

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47
Q

Tx for hypokalemia?

A
  • Underlying cause
  • 10-20meq/L/hr IV [Potassium PO > IV ]

slide 12

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48
Q

____ meq of IV K+ increases serum K by ____

A
  • 10 meq
  • 0.1 mmol/L

slide 12

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49
Q

To prevent hypokalemia what needs to be avoided?

A

Avoid excessive insulin, β-agonists, bicarb, hyperventilation, diuretics

slide 12

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50
Q

List the causes of hyperkalemia (8).

A
  • Renal failure
  • Hypoaldosteronism
  • Drugs that inhibit RAAS
  • Drugs that inhibit K+ excretion
  • Depolarizing NMB (Succs)
  • Acidosis (Respiratory/Metabolic)
  • Cell death (trauma, tourniquet)
  • Massive blood transfusion

slide 13

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51
Q

What are the s/sx of hyperkalemia

A
  • Chronic may be minimally symptomatic (malaise, GI upset)
  • Skeletal muscle paralysis,↓fine motor
  • Cardiac dysrhythmias

slide 13

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52
Q

What EKG changes can be seen with hyperkalemia?

A
  • peaked T wave
  • P wave disappearance
  • prolonged QRS complex
  • sine waves
  • asystole

slide 13

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53
Q

_____ causes K+ secretion & excretion

A

Aldosterone

slide 13

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54
Q

How much does Succinylcholine increases serum K+ by ?

A

0.5-1 mEq/L

slide 13

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55
Q

Hyperkalemia treament includes (7)? And what do avoid (3)

A
  • Dialyze within 24h prior to surgery
  • Calcium- 1st initial treatment (quickly stabilize cell membrane)
  • Hyperventilation
  • Insulin +/- glucose
  • Bicarb
  • Loop Diuretics
  • Kayexalate (hrs to days)
  • Avoid Succs, hypoventilation, LR & K+ containing IV fluids

slide 14

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56
Q

How much does hyperventilation decrease K levels?

A

↑pH by 0.1 →↓K+ by 0.4-1.5 mmol/L

slide 14

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57
Q

What dose is insulin and glucose adminsterd at for hyperkalemia?
How long does it take to work?

A
  • 10u IV: 25g D50
  • works in 10-20 min

slide 14

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58
Q

How much % of calcium is stored in the ECF vs bone?

How much plasma calcium is protein bound?

A
  • ECF: 1%
  • Bone: 99%
  • 60% and its mainly to albumin. this is inactive.

slide 15

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59
Q

What types of calcium is physiologically active? Normal values?

A
  • Only ionized plasma Ca++ is physiologically active (Not PB Ca++)
  • Normal iCa++: 1.2-1.38 mmol/L

slide 15

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60
Q

What is calcium level effected by?

A
  • albumin levels and pH
  • ↑pH/Alkalosis→↑Ca++ binding to albumin (therefore ↓iCa++)

slide 15

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61
Q

What are the hormones that regulate Ca++ and how?

A
  • Parathyroid hormone: ↑’s GI absorption, renal reabsorption and pulls from bone
  • Vitamin D: augments intestinal Ca++ absorption
  • Calcitonin: promotesbone reabsorption (decreases plasma Ca++)

slide 15

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62
Q

Causes of Hypocalcemia include?

A
  • ↓Parathyroid hormone (PTH) secretion
  • Magnesium deficiency [required for PTH production]
  • Low Vit D or disorder of Vit D metabolism [aids in absorption]
  • Renal failure (kidneys not responding to PTH)
  • Massive blood transfusion (citrate preservative binds Ca++)

Maggie D. Rents Paragliders and Bikes

slide 16

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63
Q

PH acts where to increase calcium absorption?

A

bones, kidneys, GI system

slide 16

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64
Q

After __ units of PRBCs, __ is checked to see if it needs to be replaced.

A
  • 4+
  • iCa++

Slide 16

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65
Q

Causes of hypercalcemia include?

A
  • Hyper-parathyroid or cancer [majority]
  • Vit D intoxication
  • Milk-alkali syndrome (excessive GI Ca++ absorption)
  • Granulomatous diseases (sarcoidosis)

Scar Hypes VitD Milk

slide 17

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66
Q

Hyperparathyroid serum Ca++?
Cancer serum Ca++?

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

slide 17

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67
Q

With parathyroidectomy, what is the biggest complication?

A
  • Hypocalcemia-induced laryngospasm (life threatening complication)
  • caution when extubating parathyroidectomy

slide 18

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68
Q

Hypercalcemia s/sx

A
  • Confusion, lethargy
  • Hypotonia/↓DTR
  • Abd pain
  • N/V
  • Short QT-I

Slide 18

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69
Q

What does a chronic ↑Ca++ causes ?

A

Hypercalciuria & nephrolithiasis

slide 18

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70
Q

Hypocalcemia s/sx

A
  • Paresthesias
  • Irritability
  • HoTN
  • Seizures
  • Myocardial depression
  • Prolonged QT-I
71
Q

What can cause Hypo-magnesemia

A
  • Low dietary intake or absorption
  • Renal wasting

slide 19

72
Q

What are the s/sx of hypo-magnesium

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

slide 19

73
Q

What is the tx for hypo-magnesium

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

Slide 19

74
Q

What are the causes of hypermagnesemia?

A
  • Very rare
  • Generally due to over treatment: Pre-eclampsia/Eclampsia and Pheochromocytoma

slide 20

75
Q

Symptoms at magnesium levels of 4-5 mEq/L

A

Lethargy, N/V, Flushing

76
Q

Symptoms at magnesium levels >6 mEq/L

A

HoTN, ↓Deep tendon reflexes

77
Q

Symptoms at magnesium levels >10 mEq/L

A

Paralysis, apnea, heart blocks, cardiac arrest

78
Q

What is the treatment for hypermagnesemia?

A

Diuresis, IV Calcium (stabilize cell mbrn), Dialysis
Check mag levels at regular intervals if on a gtt

79
Q

Location of the kidney

A
  • Located retroperitoneal btw T12-L4
  • Right slightly caudal to left to accommodate liver

slide 21

80
Q

____ is the primary “Structural/Functional Unit

A

nephron

slide 22

81
Q

how many nephrons does each kidney have?

A
  • 1 million/kidney

* 2 million total.

slide 22

82
Q

What is the nephron composed of?

A
  1. Glomerulus
  2. Tubular system
    * Bowman capsule
    * Proximal Tubule (PCT)
    * Loop of Henle
    * Distal Tubule (DCT)
    * Collecting duct

slide 22

83
Q

How is the CO distributed within in the kidney?

A
  • The Kidneys receive 20% COP = 1-1.25 L/M
  • Cortex (outer layer) which receives majority RBF (85-90%)

slide 23

84
Q

What portion of the kidney is particularly vulnerable for developing necrosis in response to HoTN

A

Loop of henle within the medulla (inner layer)

slide 23

85
Q

List the primary functions of the kidney (6)

A
  • Regulate EC volume, osmolarity, composition
  • Regulate BP (intermediately & LT) *RAAS, ANP
  • Excrete toxins/metabolites
  • Maintain acid/base balance
  • Produce hormones
  • Blood glucose homeostasis

Reginold Brian Olson the V Manspalins At Her Toxic Grass

slide 24

86
Q

How is BP and volume regulated by the kindeys?

A

1- Renin Angiotensin Aldosterone system (RAAS)→↑Na+/H20 reabsorption
2- Atrial Natriuretic Peptide (secreted from cardiac atria, binds to receptor in kidney) →↑Na+/H20 reabsorption

slide 24

87
Q

How is PH balanced by the kindeys?

A

by reabsorption & excretion of HCO- & H+

slide 24

88
Q

List the hormones that the kidney produces .

A
  1. Renin
  2. Erythropoietin: involved in RBCs production.
  3. Calcitriol: maintains serum Ca++
  4. Prostaglandins: key inflammatory modulators, vasodilatory effects, maintain renal blood flow

slide 24

89
Q

LABS

GFR value?
What does it tell us?

A
  • GFR: 125-140 mL/min
  • Best measure renal function over time
  • Heavily influenced hydration status

slide 25

90
Q

Creatinine Clearance normal range

A
  • 110-140 mL/min
  • 24 hr urine test
  • Creatinine freely filtered, not reabsorbed
  • Most reliable measure of GFR

slide 25

91
Q

Serum Creatinine normal range

A
  • 0.6-1.3 mg/dL
  • Correlates with muscle mass
  • Can be influenced by high protein diet, supplements, muscle breakdown
    Good for acute monitoring.

slide 25

92
Q

SC _____ related to GFR

A
  • inversely
  • In acute case, double SC can mean drop in GFR by 50%

slide 25

93
Q

Blood Urea Nitrogen normal range

A
  • 10-20 mg/dL
  • Urea is reabsorbed into blood
  • BUN affected by diet, intravascular volume

slide 26

94
Q

What does a low vs high bun indicate?

A
  • Low BUN could mean malnourished, or volume diluted
  • High could mean ↑protein diet, dehydrated, GI bleed, trauma, muscle wasting

slide 26

95
Q

BUN:Creatinine ratio normal ratio

A
  • Norm 10:1
  • BUN (reabsorbed) to Creatinine (not reabsorbed)
  • Good measure of hydration status

slide 26

96
Q

Proteinuria
normal?
abnormal?

A
  • Proteinuria (<150 mg/dL)
  • > 750mg/day could suggest glomerular injury or UTI

slide 26

97
Q

Specific gravity

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

slide 26

98
Q

Orthosttic pressure changes, a decrease in base excess [BE] and an increase in lactate can indicate?

What is a late sign of volume loss?

A
  • That the patient is probably dry.
  • Low urine output

slide 27

99
Q

Normal UOP?
Oliguria?

A
  • UOP- 30 ml/hr; 0.5-1ml/kg/hr
  • Oliguria: <500mL in 24h

slide 27

100
Q

What are some of the monitors that help assess volume status.

A
  • US to assess IVC; Compressed IVC = dehydration
  • CVP, RAP
  • LAP, PCWP (Powerful stimuli for renal vasoconstriction)
  • PAP
  • SVV

slide 28

101
Q

SVV is a type of a monitor. What does it do to assess volume status?

What criteria needs to be met to use SVV?

A
  • Compares inspiratory vs expiratory pressure
  • It automatically assumes ventilated patient and sinus rhythm

Sldie 28

102
Q

What is acute kidney injury?
Effects what % of hospitalized pts?
What is it complicated by?
Is it reversible?

A
  • Failure to excrete nitrogenous waste products or maintain fluid/electrolyte homeostasis
  • AKI effects 20% hospitalized pts & 50% ICU pts
  • characterized by hypotension/hypovolemia & nephrotoxins
  • Reversable w/timely interventions. Can be placed on CVVHD to get through the temporary insult.

slide 30

103
Q

What is the hallmark of AKI?

A
  • Azotemia: Buildup of nitrogenous products s/a urea & creatinine

slide 30

104
Q

AKI w/_____ requiring dialysis carries > ____% mortality rate

A
  • MSOF = multi system organ failure.
  • 50%

slide 30

105
Q

What are the risk for factors for AKI (9).

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

Slide 31

106
Q

What is the diagnostic criteria for AKI?

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

Slide 32

107
Q

What are the physical sx of AKI?

A
  • Asymptomatic
  • Malaise
  • HoTN
  • Hypovolemic or hypervolemic

Slide 32

108
Q

What are the 3 major classes that cause of AKI?

A
  1. Prerenal Azotemia: = ↓ renal perfusion
  2. Renal azotemia: nephron injury
  3. Postrenal azotemia: outflow obstruction *easiest to treat

Slide 33

109
Q

What can cause prerenal azotemia? (9)
* basically everything on here narrows down to ___

A
  • Hemorrhage
  • GI fluid loss
  • Trauma
  • Surgery
  • Burns
  • Cardiogenic shock
  • Sepsis
  • Aortic clamping
  • Thromboembolism

poor perfusion

Slide 33

Anesthesia meds + volume & blood loss →↓RBF

110
Q

What can lead to renal azotemia? (7)
* Basically everything on here narrows down to ____

A
  • Acute glomerulonephritis
  • Vasculitis
  • Interstitial nephritis
  • ATN
  • Contrast dye
  • Nephrotoxic drugs
  • Myoglobinuria

Injury to kidney itself

Slide 33

111
Q

What can lead to postrenal azotemia? (4)
* Basically everything on here can be narrowed down to ___

A
  • Nephrolithiasis
  • BPH
  • Clot retention
  • Bladder carcinoma

Obstruction to outflow

Slide 33

112
Q

Pre-renal azotemia

  1. T/F: Pre-renal is the most common form of AKI.
  2. _____ of hospital-acquired AKI cases are Pre-renal
  3. Pre-renal BUN:Cr is
  4. pre-renal is still reabsorbing ___ & ____.
  5. Tx for pre-renal?
A
  1. True
  2. ½
  3. > 20:1
  4. Na+ & H20
  5. Restore RBF: Fluids, Mannitol, Diuretics, maintain MAP, Presso

Slide 34

113
Q

Renal Azotemia

1.Renal azotemia is an ____ renal disease, and it potentially __
2. Diagnositic criteria?

A
  1. Intrinsic, reveraible
  2. ↓GFR(late sx)
    ↓urea reabsorption in prox tubule →↓BUN
    ↓Creatinine filtration→↑blood creatinine
    BUN:Cr often < 15:1

Slide 35

Renal AKI BUN:Cr decreased from pre-renal AKI (>20)

114
Q

Post renal azotemia is a ____ obstruction which causes ____ nephron tubular hydrostatic presssure.

A
  • outflow
  • increased

slide 36

115
Q

what is helpful with identifing post-renal azotemia?

A

renal ultrasonography

slide 36

116
Q

w

with post renal azotemia reversibility is inversely related to ____. We treat this how?

A
  • duration
  • tx: remove obstrution if possible because persistent obstrution damages the tubular epithelium

slide 36

117
Q

What kind of kidney injury is this?
* BUN/Cr: > 20:1
* FeNA < 1%
* FEurea: < 35%
* Urine[Na]: < 20
* urine sediment: bland, hyaline casts

A

pre-renal

slide 37

118
Q

What kind of kidney injury is this?
* BUN/Cr: < 20:1
* FeNA: >2% [ATN, > 1%[AIN], < 1% [GN]
* FEurea: < 50%
* Urine[Na]: > 20
* urine sediment:
*ATN: muddy brown casts
* AIN: WBC casts + neg ucx
* GN: RBC casts
* abx/chol. emboli = urine E.O’s
* NSAID = lymphocytes

A

intrensic

slide 37

119
Q

What kind of kidney injury is this?
* BUN/Cr: varies
* FeNA: varies
* FEurea: varies
* Urine[Na]: normal
* urine sediment: blood

A

post-renal

slide 37

120
Q

neurological complications of AKI are related to protein/amino acids buildup in the blood. What can this present as? (6)

A
  • Uremic Encephalopathy (Dialysis improves)
  • Mobility disorders
  • Neuropathies
  • Myopathies
  • Seizures
  • Stroke

slide 38

121
Q

cardiovascular complications of AKI include (9)

A

in order of incidence
* HTN
* LVH
* CHF
* ischemicheartdisease
* anemicheartfailure
* rhythm disturbances
* pericarditis with or without effusion [pulmonary edema?]
* cardiactamponade
* uremic cardiomyopathy

Harry Loves Cheap Ice And Reliable Phone Connections Until Curfew

slide 39

122
Q

anemia is a hematological complication of AKI, why does this happen?

A
  • ↓ EPO production
  • ↓ red cell production
  • ↓ red cell survival
  • Platelet dysfunction (plt function assay or TEG are valuable)

slide 40

123
Q

vWF is disrupted by uremia, how can you fix it?

A
  • Prophylactic DDAVP
  • ↑VWF & Factor VIII to improve coagulation

slide 40

124
Q

what are metabolic complications of AKI? (6)

A
  • Hyperkalemia
  • Water/sodium imbalances
  • Hypoalbuminemia (kidneys allowing albumin to escape)
  • Metabolic acidosis
  • Malnutrition
  • Hyperparathyroidism

slide 41

125
Q

why can you see hyperparathyroidism in AKI?

A

Parathyroid in overdrive to in attempt to stimulate kidney to reabsorb Ca++

slide 41

126
Q

intraoperative anesthesia considerations for AKI

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

slide 42

127
Q

why is vasopressin perferred over alpha agonist in AKI anesthesia?

A

Vasopressin-preferentially constricts the Efferent arteriole, better than alpha agonists for maintaining RBF

slide 42

128
Q

what does prophylactic sodium bicarb do in AKI anesthesia?

A
  • Decreases formation of free-radicals
  • Prevents ATN from causing renal failure

slide 42

129
Q

preoperative anesthisia implications for AKI

A
  • Low threshold for invasive hemodynamic monitoring
  • Prefer preoperative dialysis
  • Recent labs, esp K+
  • Want POC equipment available
  • Tailored drug dosing
  • Avoid drugs w/active metabolites, drugs that ↓RBF, and renal toxins

slide 43

May need post-op dialysis if they cant clear drugs on their own

130
Q

chronic kidney disease is ____ and ____. with the leading causes being ____ and ____.

A
  • Progressive, irreversible
  • Leading causes: Diabetes, Hypertension

slide 45

131
Q

how does CKD present?

A
  • Often getting surgery for dialysis access
  • DM, toe/foot debridement’s & amputations
  • Non-healing wounds
  • Often frequent flyers

slide 45

132
Q

GFR decreases by ____ per decade starting from age 20. it is often found during routing testing (focus on trends)

A

10

slide 46

133
Q

this stage of CKD is where kidney damage with normal or increased GFR >90 ml/min/1.73m^2

A

stage 1

slide 46

134
Q

this stage of CKD is where there is kidney damage with mildly decreased GFR of 60-89 ml/min/1.73m^2

A

stage 2

slide 46

135
Q

this stage of CKD is where there is moderately dereased GFR of 30-59 ml/min/1.73m^2

A

stage 3

slide 46

136
Q

this stage of CKD is where there is severely decreased GFR of 15-29 ml/min/1.73m^2

A

stage 4

slide 46

137
Q

this stage of CKD is where there is kidney failure with GFR < 15 ml/min/1.73m^2

A

stage 5

slide 46

138
Q

how do you calculate GFR?

A

GFR = 186 x (SCr)-1.154x (age)-0.203x (0.742 if female) x (1.210 if African American)

slide 46

139
Q

____ is a cause and consequence of CKD. Causes retention of sodium and water and activation of RAAS.

A

systemic hypertension

slide 47

140
Q

how do you treat systemic hypertension in CKD?

A
  • 1st line: thiazide diuretics
  • may need ACE-I or ARBs

slide 47

141
Q

why are ACE’s and ARB’s often used in CKD?

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

slide 48

142
Q

why do we want ACEI/ARBs withheld on day of surgery?

A
  • to ↓risk of profound HoTN
  • Vasopressin, NE, EPI may be needed if ACE-I or ARB on board

slide 48

143
Q

____ is when triglycerides are >500 and LDL >100

A

dyslipidemia

slide 49

144
Q

which populations are high risk for silent MI?

A

women and diabetics
Peripheral & autonomic neuropathy, sensation may be blunted

slide 49

145
Q

____ is responsive to exogenous erythropoietin, with a target hgb of ____. Pts with CKD may also have ____ dysfunction.

A
  • anemia
  • 10
  • platelet

slide 50

146
Q

what is associated with blood transfusions in CKD?

A
  • excess Hgb leads to sluggish circulation
  • acidosis
  • hyperkalemia

slide 50

147
Q

when should you consider dialysis for a patient? (5)

A
  • Volume overload
  • Severe hyperkalemia
  • Metabolic acidosis
  • Symptomatic uremia
  • Failure to clear medications

OverKill Ur Aciditic Failures

slide 51

148
Q

when would you choose PD over HD?

A
  • HD is more effcient than PD
  • PD is slower with less dramatic volume shifts, so better for pts with poor cardiac function

slide 51

149
Q

____ is the most common S/E of dialysis, and ____ is the leading cause of death.

A
  • hypotension
  • infection (impaired immune system/healing)

slide 51

150
Q

anesthesia considerations for CKD include (7)

A
  • Assess stability of ESRD
  • Body weight pre/post dialysis (within 24 h of surgery)
  • Well-controlled BP, Meds continued?
  • Glucose management, A1C?
  • Aspiration precautions (DM, obesity)
  • Pressors
  • Uremic bleeding

slide 52

151
Q

with uremic bleeding want to check to see if PLT/PT/PTT are normal and assess plt function.
* how dow we assess plt function?
* what can be given to fix this?

A
  • check TEG
  • Cryo, F VIII, vWF (cryo has the most factors that we need)
  • desmopressin

slide 52

152
Q

for desmopressin:
* what is the peak
* duration
* why do we use it as a last resort?

A
  • peak: 2-4 h
  • duration: 6-8H
  • causes tachyphylaxis

slide 52

153
Q

what is the best NMB for CKD?

A

cisatracurium[nimbex] because not dependent on renal elimination

slide 53

154
Q

why do we want to avoid morphone and demerol in ckd pts?

A

they have active metabolites

slide 53

155
Q

many anesthetic agents are ____ soluble and ____ by renal tubular cells.

A
  • lipid
  • reabsorbed

slide 53

156
Q

with lipid insoluble drugs elimination is unchanged in ____, so they have a ____ duration of action.

A
  • urine
  • prolonged

slide 54

157
Q

which medication groups are based on renal dosing (based on GFR)

A
  • Thiazide diuretics
  • Loop diuretics
  • Digoxin
  • Many antibiotics

slide 54

158
Q

which induction agents rely on renal excretion?

A

Phenobarbital
Thiopental

slide 55

159
Q

which muscle relaxants rely on renal exretion?

A

Pancuronium
Vecuronium

slide 55

160
Q

which cholinesterase inhibitors rely on renal excretion?

A

Edrophonium
Neostigmine

slide 55

161
Q

which CV drugs rely on renal excretion?

A

Atropine
Digoxin
Glycopyrrolate
Hydralazine
Milrinone

slide 55

162
Q

which antimicrobials rely on renal excretion?

A

Aminoglycosides
Cephalosporins
Penicillins
Vancomycin

slide 55

163
Q

what happens if the kidneys cant excrete a drug?

A

liver will eventually metabolize, provided its funtioning

slide 55

164
Q

failure to clear morphine leads to significant active metabolites.
* how much morphine is cleared through urine?
* what are the metabolites?
* what can this cause?

A
  • 40%
  • morphine-3 glucuronide and morphine-6 glucuronide
  • Life-threatening respiratory depression

slide 56

165
Q

For Demerol[meperidine]:
* what is its metabolite?
* what is the metabolites e1/2?

A
  • normeperidine
  • e1/2: 15-30h compared to demerol E1/2 of 2-4h

slide 57

166
Q

Normeperidine has ____ and ____ effects. Its main adverse effect is ____.

A
  • analgesic and CNS effects
  • adverse effect is neurotoxicity (nervousness, tremors, muscle twitches, seizures)

slide 57

167
Q

for pts with CKD what should K+ levels be?

A

< 5.5 meq/l on elective surgery

slide 58

168
Q

Dialysis pts should be dialyzed within ____ preceding elective surgery

A

24 h

slide 58

169
Q

for pts with CKD should have aspiration prophylaxis, especially in ____.

A

DM

slide 58

170
Q

anesthesia and surgery decrease what?

A

RBF and GFR

slide 58

171
Q

what happens d/t blood loss activating baroreceptors?

A

increased SNS outflow

slide 58

172
Q

what happens d/t catecholamines activating alpha1 receptors?

A

increased afferent arteriole constriction which decreased RBF

slide 58

173
Q

what happens d/t longer periods of hypotension (cross-clamping, hemorrhage,sepsis)

A

decreased RBF

slide 58

174
Q

what is our responisbility as anesthesia providers?

A

to minimize risk

slide 58

Mar: Sem 2 - Health Assessment (32 decks)

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