Renal Flashcards
(174 cards)
1
Q
_____TBW is water (varies w/ gender, age, body fat %)
slide 3
A
60%
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
3
Q
What are 2 types of homeostasis?
A
osmolar homeostasis
volume homeostasis
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
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
6
Q
Increased mucles =
A
increased water
3
7
Q
What does ADH do?
A
Helps body ↑H20/Na+ retention
3
8
Q
how do you calculate TBW?
A
- 60% body weight.
3
9
Q
What are the categories/cause of hyponatremia?
A
- Hypovolemia
- Euvolemia
- Hypervolemia
4
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
11
Q
Hypervolemia leads to?
A
- peripheral edema
- rales
- ascites
Hypervolemia…that’s PAR for the course
4
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
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
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
15
Q
Hypovolemic hyponatremia is caused by?
A
- Na/H20 Loss like with diuretics, GI loss, Burns and trauma
Slide 4 comment
16
Q
Howto treat euvolemia if Una is <20?
A
Salt restricted diet
4 + comment
17
Q
What are the causes of euvolemia if Una is >20?
A
- glucocorticoid deficiency
- hypothyroid
- high sympathetic drive
- drugs
- SIADH
4
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
19
Q
What are the causes of hypervolemia if Una is >20?
A
- acute renal failure
- chronic renal failure
4 comment
20
Q
What are the causes of hypervolemia if Una is <20?
A
- nephrotic syndrome
- cardiac failure
- cirrhosis
4
21
Q
____ hospitalized pts are hyponatremic. Why?
A
- 15%
- over fluid-resuscitation
- ↑endogenous vasopressin
4
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
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.
24
Q
S/Sx of hyponatremia: 120 - 130 (8)
A
- malaise
- unsteadiness
- headache
- nausea
- vomitting
- fatigue
- confusion
- muscle cramps
slide 5
25
S/Sx of hyponatremia:<120 (7)
* Headache
* Restless
* lethargy
* seizure
* Brainstemp herniation
* respiratory arrest
* death
| slide 5
26
the most severe consequences of hyponatremia
Seizures, coma, death.
| slide 5
27
What is the treatment for mild hyponatremia?
* Treat underlying cause (look at volume status)
* Electrolyte drinks
* Normal saline
* Diuretics
Mildhyponatremia TENDs to be treated by...
| slide 6
28
What is the treamtent for extreme hyponatremia [<120?]
* Hypertonic Saline/3% NaCl
| sllide 6
29
Hypertonic saline is adminsitered for hyponatremia. What is the dose and consideration?
* 80ml/hr over 15h
* Na+ correction should not exceed 1.5 mEq/L/hr
| slide 6
30
What happens if you correct hyponatremia fast? What is considered fast?
Rapid correction (>6 mEq/L in 24 h) can cause Osmotic Demyelination Syndrome (often permanent neuro damage)
| slide 6
31
With low sodium levels, what is a medical emergency?
How do you treat it?
* Hyponatremic seizures=medical emergency (neurological damage )
* 3-5ml/kg of 3% over 20 min, until seizures resolve
| slide 6
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Common causes of *Hyper*natremia
* 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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What are the s/sx of hypernatremia?
* Orthostasis
* Restlessness
* Lethargy
* Tremor/Muscle twitching/spasticity
* Seizures
* Death
| slide 9
## Footnote
hypernatremia sx mirror hyponatremia sx
34
What is the treatment for hypernatremia?
* Route cause, Assess volume status (VS, UOP, Turgor, CVP)
* Hypovolemic: normal saline
* Euvolemic: water replacement (po or D5W)
* Hypervolemic: diuretics
35
What should be the sodium reduction rate for hypernatremia and why?
* 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
36
Normal K+ levels?
% in the ECF?
* 3.5-5 mmol/L
* < 1.5% in ECF
| slide 10
37
______ reflects transmembrane K+ regulation more than total body K+
Serum K+
| slide 10
38
_____ causes the distal nephron to secrete K+ (and reabsorb Na+)
Aldosterone
| slide 10
39
____ is inversly related to K.
Aldosterone
| slide 10
40
In renal failure, what happens to K excretion>
K+ excretion declines.
Excretions shifts towards GI system
| slide 10
41
What are the 3 major categories for the cause of hypokalemia?
1. Renal loss
2. GI loss
3. Transcellular loss
| slide 11
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Causes of hypokalemia due to renal loss include?
* **Diuretics**
* **hyperaldosteronism**
* Mineralcorticoids
* high-dose glucocorticoids
* abx (penicillin, nafcillin, ampicillin)
* Drugs associated with magnesium depletion
* Surgical Trauma
* Hyperglycemia
## Footnote
slide 11
43
Causes of hypokalemia due to GI loss include?
* **N/V/D**
* **Malabsorption**
* Zollinger-Ellison Syndrome
* Jejunoileal bypass
* Chemo
* Nasogastric suction
## Footnote
slide 11
44
Causes of hypokalemia due to transceullar shift include?
* **Akalosis**
* **Beta-agonist**
* **Insulin**
* Tocolytic drugs
* alkalosis
* Hypercalcemia
* Hypomagnesemia
## Footnote
slide 11
45
Common cause of hypokalemia
* 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
46
List the s/sx of hypokalemia
* Generally cardiac and neuromuscular
* Muscle weakness/Cramps
* Ileus
* Dysrhythmias, U wave
| s;ode 12
47
Tx for hypokalemia?
* Underlying cause
* 10-20meq/L/hr IV [Potassium PO > IV ]
| slide 12
48
____ meq of IV K+ increases serum K by ____
* 10 meq
* 0.1 mmol/L
| slide 12
49
To prevent hypokalemia what needs to be avoided?
Avoid excessive insulin, β-agonists, bicarb, hyperventilation, diuretics
| slide 12
50
List the causes of hyperkalemia (8).
* 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
51
What are the s/sx of hyperkalemia
* Chronic may be minimally symptomatic (malaise, GI upset)
* Skeletal muscle paralysis,↓fine motor
* Cardiac dysrhythmias
| slide 13
52
What EKG changes can be seen with hyperkalemia?
* peaked T wave
* P wave disappearance
* prolonged QRS complex
* sine waves
* asystole
## Footnote
slide 13
53
_____ causes K+ secretion & excretion
Aldosterone
| slide 13
54
How much does Succinylcholine increases serum K+ by ?
0.5-1 mEq/L
| slide 13
55
Hyperkalemia treament includes (7)? And what do avoid (3)
* 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
56
How much does hyperventilation decrease K levels?
↑pH by 0.1 →↓K+ by 0.4-1.5 mmol/L
| slide 14
57
What dose is insulin and glucose adminsterd at for hyperkalemia?
How long does it take to work?
* 10u IV: 25g D50
* works in 10-20 min
| slide 14
58
How much % of calcium is stored in the ECF vs bone?
How much plasma calcium is protein bound?
* ECF: 1%
* Bone: 99%
* 60% and its mainly to albumin. this is inactive.
| slide 15
59
What types of calcium is physiologically active? Normal values?
* Only ionized plasma Ca++ is physiologically active (Not PB Ca++)
* Normal iCa++: 1.2-1.38 mmol/L
| slide 15
60
What is calcium level effected by?
* albumin levels and pH
* ↑pH/Alkalosis→↑Ca++ binding to albumin (therefore ↓iCa++)
| slide 15
61
What are the hormones that regulate Ca++ and how?
* Parathyroid hormone: ↑’s GI absorption, renal reabsorption and pulls from bone
* Vitamin D: augments intestinal Ca++ absorption
* Calcitonin: promotes bone reabsorption (decreases plasma Ca++)
| slide 15
62
Causes of Hypocalcemia include?
* ↓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
63
PH acts where to increase calcium absorption?
bones, kidneys, GI system
| slide 16
64
After __ units of PRBCs, __ is checked to see if it needs to be replaced.
* 4+
* iCa++
| Slide 16
65
Causes of hypercalcemia include?
* Hyper-parathyroid or cancer [majority]
* Vit D intoxication
* Milk-alkali syndrome (excessive GI Ca++ absorption)
* Granulomatous diseases (sarcoidosis)
Scar Hypes VitD Milk
| slide 17
66
Hyperparathyroid serum Ca++?
Cancer serum Ca++?
* Hyperparathyroid serum Ca++ <11
* Cancer serum Ca++ >13
| slide 17
67
With parathyroidectomy, what is the biggest complication?
* Hypocalcemia-induced laryngospasm (life threatening complication)
* caution when extubating parathyroidectomy
| slide 18
68
Hypercalcemia s/sx
* Confusion, lethargy
* Hypotonia/↓DTR
* Abd pain
* N/V
* Short QT-I
| Slide 18
69
What does a chronic ↑Ca++ causes ?
Hypercalciuria & nephrolithiasis
| slide 18
70
Hypocalcemia s/sx
* Paresthesias
* Irritability
* HoTN
* Seizures
* Myocardial depression
* Prolonged QT-I
71
What can cause Hypo-magnesemia
* Low dietary intake or absorption
* Renal wasting
| slide 19
72
What are the s/sx of hypo-magnesium
* Muscle weakness or excitation
* seizures
* Ventricular dysrhythmia (Polymorphic V-tack/Torsades De Pointes)
| slide 19
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What is the tx for hypo-magnesium
* depends on severity of sx
* Slower infusions for less severe
* Torsade's/seizures→ 2g Mag Sulfate
| Slide 19
74
What are the causes of hypermagnesemia?
* Very rare
* Generally due to over treatment: Pre-eclampsia/Eclampsia and Pheochromocytoma
| slide 20
75
Symptoms at magnesium levels of 4-5 mEq/L
Lethargy, N/V, Flushing
76
Symptoms at magnesium levels >6 mEq/L
HoTN, ↓Deep tendon reflexes
77
Symptoms at magnesium levels >10 mEq/L
Paralysis, apnea, heart blocks, cardiac arrest
78
What is the treatment for hypermagnesemia?
Diuresis, IV Calcium (stabilize cell mbrn), Dialysis
*Check mag levels at regular intervals if on a gtt*
79
Location of the kidney
* Located retroperitoneal btw T12-L4
* Right slightly caudal to left to accommodate liver
| slide 21
80
____ is the primary “Structural/Functional Unit
nephron
| slide 22
81
how many nephrons does each kidney have?
* 1 million/kidney
| * 2 million total.
## Footnote
slide 22
82
What is the nephron composed of?
1. Glomerulus
2. Tubular system
* Bowman capsule
* Proximal Tubule (PCT)
* Loop of Henle
* Distal Tubule (DCT)
* Collecting duct
## Footnote
slide 22
83
How is the CO distributed within in the kidney?
* The Kidneys receive 20% COP = 1-1.25 L/M
* Cortex (outer layer) which receives majority RBF (85-90%)
| slide 23
84
What portion of the kidney is particularly vulnerable for developing necrosis in response to HoTN
Loop of henle within the medulla (inner layer)
| slide 23
85
List the primary functions of the kidney (6)
* 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
How is BP and volume regulated by the kindeys?
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
How is PH balanced by the kindeys?
by reabsorption & excretion of HCO- & H+
| slide 24
88
List the hormones that the kidney produces .
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
# LABS
GFR value?
What does it tell us?
* GFR: 125-140 mL/min
* Best measure renal function over time
* Heavily influenced hydration status
| slide 25
90
Creatinine Clearance normal range
* 110-140 mL/min
* 24 hr urine test
* Creatinine freely filtered, not reabsorbed
* Most reliable measure of GFR
| slide 25
91
Serum Creatinine normal range
* 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
SC _____ related to GFR
* inversely
* In acute case, double SC can mean drop in GFR by 50%
| slide 25
93
Blood Urea Nitrogen normal range
* 10-20 mg/dL
* Urea is reabsorbed into blood
* BUN affected by diet, intravascular volume
| slide 26
94
What does a low vs high bun indicate?
* Low BUN could mean malnourished, or volume diluted
* High could mean ↑protein diet, dehydrated, GI bleed, trauma, muscle wasting
| slide 26
95
BUN:Creatinine ratio normal ratio
* Norm 10:1
* BUN (reabsorbed) to Creatinine (not reabsorbed)
* Good measure of hydration status
| slide 26
96
Proteinuria
normal?
abnormal?
* Proteinuria (<150 mg/dL)
* >750mg/day could suggest glomerular injury or UTI
| slide 26
97
Specific gravity
* 1.001-1.035
* Comparing 1ml urine to 1ml distilled water
* measures nephron’s ability to concentrate urine
| slide 26
98
Orthosttic pressure changes, a decrease in base excess [BE] and an increase in lactate can indicate?
What is a late sign of volume loss?
* That the patient is probably dry.
* Low urine output
| slide 27
99
Normal UOP?
Oliguria?
* UOP- 30 ml/hr; 0.5-1ml/kg/hr
* Oliguria: <500mL in 24h
| slide 27
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What are some of the monitors that help assess volume status.
* US to assess IVC; Compressed IVC = dehydration
* CVP, RAP
* LAP, PCWP (Powerful stimuli for renal vasoconstriction)
* PAP
* SVV
| slide 28
101
SVV is a type of a monitor. What does it do to assess volume status?
What criteria needs to be met to use SVV?
* Compares inspiratory vs expiratory pressure
* It automatically assumes ventilated patient and sinus rhythm
| Sldie 28
102
What is acute kidney injury?
Effects what % of hospitalized pts?
What is it complicated by?
Is it reversible?
* 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
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What is the hallmark of AKI?
* Azotemia: Buildup of nitrogenous products s/a urea & creatinine
| slide 30
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AKI w/_____ requiring dialysis carries > ____% mortality rate
* MSOF = multi system organ failure.
* 50%
| slide 30
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What are the risk for factors for AKI (9).
* **Pre-existing renal disease**
* Advanced age
* CHF
* PVD
* Diabetes
* Sepsis (hypotension)
* Jaundice
* Major operative procedures
* IV Contrast
| Slide 31
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What is the diagnostic criteria for AKI?
* ↑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
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What are the physical sx of AKI?
* Asymptomatic
* Malaise
* HoTN
* Hypovolemic or hypervolemic
| Slide 32
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What are the 3 major classes that cause of AKI?
1. Prerenal Azotemia: = ↓ renal perfusion
2. Renal azotemia: nephron injury
3. Postrenal azotemia: outflow obstruction *easiest to treat
| Slide 33
109
What can cause prerenal azotemia? (9)
* basically everything on here narrows down to ___
* Hemorrhage
* GI fluid loss
* Trauma
* Surgery
* Burns
* Cardiogenic shock
* Sepsis
* Aortic clamping
* Thromboembolism
**poor perfusion**
| Slide 33
## Footnote
Anesthesia meds + volume & blood loss →↓RBF
110
What can lead to renal azotemia? (7)
* Basically everything on here narrows down to ____
* Acute glomerulonephritis
* Vasculitis
* Interstitial nephritis
* ATN
* Contrast dye
* Nephrotoxic drugs
* Myoglobinuria
**Injury to kidney itself**
| Slide 33
111
What can lead to postrenal azotemia? (4)
* Basically everything on here can be narrowed down to ___
* Nephrolithiasis
* BPH
* Clot retention
* Bladder carcinoma
**Obstruction to outflow**
| Slide 33
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# 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?
1. True
2. ½
3. >20:1
4. Na+ & H20
5. Restore RBF: Fluids, Mannitol, Diuretics, maintain MAP, Presso
| Slide 34
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# Renal Azotemia
1.Renal azotemia is an ____ renal disease, and it potentially __
2. Diagnositic criteria?
1. Intrinsic, reveraible
2.
↓GFR(late sx)
↓urea reabsorption in prox tubule →↓BUN
↓Creatinine filtration→↑blood creatinine
BUN:Cr often < 15:1
| Slide 35
## Footnote
Renal AKI BUN:Cr decreased from pre-renal AKI (>20)
114
Post renal azotemia is a ____ obstruction which causes ____ nephron tubular hydrostatic presssure.
* outflow
* increased
| slide 36
115
what is helpful with identifing post-renal azotemia?
renal ultrasonography
| slide 36
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# w
with post renal azotemia reversibility is inversely related to ____. We treat this how?
* duration
* tx: remove obstrution if possible because persistent obstrution damages the tubular epithelium
| slide 36
117
What kind of kidney injury is this?
* BUN/Cr: > 20:1
* FeNA < 1%
* FEurea: < 35%
* Urine[Na]: < 20
* urine sediment: bland, hyaline casts
pre-renal
| slide 37
118
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
intrensic
| slide 37
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What kind of kidney injury is this?
* BUN/Cr: varies
* FeNA: varies
* FEurea: varies
* Urine[Na]: normal
* urine sediment: blood
post-renal
| slide 37
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neurological complications of AKI are related to protein/amino acids buildup in the blood. What can this present as? (6)
* Uremic Encephalopathy (Dialysis improves)
* Mobility disorders
* Neuropathies
* Myopathies
* Seizures
* Stroke
| slide 38
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cardiovascular complications of AKI include (9)
*in order of incidence*
* HTN
* LVH
* CHF
* ischemic heart disease
* anemic heart failure
* rhythm disturbances
* pericarditis with or without effusion [pulmonary edema?]
* cardiac tamponade
* uremic cardiomyopathy
Harry Loves Cheap Ice And Reliable Phone Connections Until Curfew
| slide 39
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anemia is a hematological complication of AKI, why does this happen?
* ↓ EPO production
* ↓ red cell production
* ↓ red cell survival
* Platelet dysfunction (plt function assay or TEG are valuable)
| slide 40
123
vWF is disrupted by uremia, how can you fix it?
* Prophylactic DDAVP
* ↑VWF & Factor VIII to improve coagulation
| slide 40
124
what are metabolic complications of AKI? (6)
* Hyperkalemia
* Water/sodium imbalances
* Hypoalbuminemia (kidneys allowing albumin to escape)
* Metabolic acidosis
* Malnutrition
* Hyperparathyroidism
| slide 41
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why can you see hyperparathyroidism in AKI?
Parathyroid in overdrive to in attempt to stimulate kidney to reabsorb Ca++
| slide 41
126
intraoperative anesthesia considerations for AKI
* 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
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why is vasopressin perferred over alpha agonist in AKI anesthesia?
Vasopressin-preferentially constricts the Efferent arteriole, better than alpha agonists for maintaining RBF
| slide 42
128
what does prophylactic sodium bicarb do in AKI anesthesia?
* Decreases formation of free-radicals
* Prevents ATN from causing renal failure
| slide 42
129
preoperative anesthisia implications for AKI
* 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
## Footnote
May need post-op dialysis if they cant clear drugs on their own
130
chronic kidney disease is ____ and ____. with the leading causes being ____ and ____.
* Progressive, irreversible
* Leading causes: Diabetes, Hypertension
| slide 45
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how does CKD present?
* Often getting surgery for dialysis access
* DM, toe/foot debridement's & amputations
* Non-healing wounds
* Often frequent flyers
| slide 45
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GFR decreases by ____ per decade starting from age 20. it is often found during routing testing (focus on trends)
10
| slide 46
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this stage of CKD is where kidney damage with normal or increased GFR >90 ml/min/1.73m^2
stage 1
| slide 46
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this stage of CKD is where there is kidney damage with mildly decreased GFR of 60-89 ml/min/1.73m^2
stage 2
| slide 46
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this stage of CKD is where there is moderately dereased GFR of 30-59 ml/min/1.73m^2
stage 3
| slide 46
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this stage of CKD is where there is severely decreased GFR of 15-29 ml/min/1.73m^2
stage 4
| slide 46
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this stage of CKD is where there is kidney failure with GFR < 15 ml/min/1.73m^2
stage 5
| slide 46
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how do you calculate GFR?
GFR = 186 x (SCr)-1.154x (age)-0.203x (0.742 if female) x (1.210 if African American)
| slide 46
139
____ is a cause and consequence of CKD. Causes retention of sodium and water and activation of RAAS.
systemic hypertension
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how do you treat systemic hypertension in CKD?
* 1st line: thiazide diuretics
* may need ACE-I or ARBs
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why are ACE's and ARB's often used in CKD?
* ↓systemic BP and glomerular pressure
* ↓proteinuria by reducing glomerular hyperfiltration
* ↓glomerulosclerosis
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142
why do we want ACEI/ARBs withheld on day of surgery?
* to ↓risk of profound HoTN
* **Vasopressin, NE, EPI may be needed if ACE-I or ARB on board**
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143
____ is when triglycerides are >500 and LDL >100
dyslipidemia
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144
which populations are high risk for silent MI?
women and diabetics
*Peripheral & autonomic neuropathy, sensation may be blunted*
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____ is responsive to exogenous erythropoietin, with a target hgb of ____. Pts with CKD may also have ____ dysfunction.
* anemia
* 10
* platelet
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what is associated with blood transfusions in CKD?
* excess Hgb leads to sluggish circulation
* acidosis
* hyperkalemia
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when should you consider dialysis for a patient? (5)
* Volume overload
* Severe hyperkalemia
* Metabolic acidosis
* Symptomatic uremia
* Failure to clear medications
OverKill Ur Aciditic Failures
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when would you choose PD over HD?
* HD is more effcient than PD
* PD is slower with less dramatic volume shifts, so better for pts with poor cardiac function
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149
____ is the most common S/E of dialysis, and ____ is the leading cause of death.
* hypotension
* infection (impaired immune system/healing)
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anesthesia considerations for CKD include (7)
* 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
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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?
* check TEG
* Cryo, F VIII, vWF (cryo has the most factors that we need)
* desmopressin
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for desmopressin:
* what is the peak
* duration
* why do we use it as a last resort?
* peak: 2-4 h
* duration: 6-8H
* causes tachyphylaxis
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what is the best NMB for CKD?
cisatracurium[nimbex] because not dependent on renal elimination
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154
why do we want to avoid morphone and demerol in ckd pts?
they have active metabolites
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155
many anesthetic agents are ____ soluble and ____ by renal tubular cells.
* lipid
* reabsorbed
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with lipid insoluble drugs elimination is unchanged in ____, so they have a ____ duration of action.
* urine
* prolonged
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which medication groups are based on renal dosing (based on GFR)
* Thiazide diuretics
* Loop diuretics
* Digoxin
* Many antibiotics
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which induction agents rely on renal excretion?
Phenobarbital
Thiopental
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159
which muscle relaxants rely on renal exretion?
Pancuronium
Vecuronium
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160
which cholinesterase inhibitors rely on renal excretion?
Edrophonium
Neostigmine
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161
which CV drugs rely on renal excretion?
Atropine
Digoxin
Glycopyrrolate
Hydralazine
Milrinone
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which antimicrobials rely on renal excretion?
Aminoglycosides
Cephalosporins
Penicillins
Vancomycin
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163
what happens if the kidneys cant excrete a drug?
liver will eventually metabolize, provided its funtioning
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164
failure to clear morphine leads to significant active metabolites.
* how much morphine is cleared through urine?
* what are the metabolites?
* what can this cause?
* 40%
* morphine-3 glucuronide and morphine-6 glucuronide
* Life-threatening respiratory depression
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For Demerol[meperidine]:
* what is its metabolite?
* what is the metabolites e1/2?
* normeperidine
* e1/2: 15-30h compared to demerol E1/2 of 2-4h
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Normeperidine has ____ and ____ effects. Its main adverse effect is ____.
* analgesic and CNS effects
* adverse effect is neurotoxicity (nervousness, tremors, muscle twitches, seizures)
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for pts with CKD what should K+ levels be?
< 5.5 meq/l on elective surgery
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168
Dialysis pts should be dialyzed within ____ preceding elective surgery
24 h
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for pts with CKD should have aspiration prophylaxis, especially in ____.
DM
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anesthesia and surgery decrease what?
RBF and GFR
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what happens d/t blood loss activating baroreceptors?
increased SNS outflow
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what happens d/t catecholamines activating alpha1 receptors?
increased afferent arteriole constriction which decreased RBF
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what happens d/t longer periods of hypotension (cross-clamping, hemorrhage,sepsis)
decreased RBF
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what is our responisbility as anesthesia providers?
to minimize risk
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