Renal Diseases (Exam III-Mordekai) Flashcards

1
Q

Which vertebrae are the kidney’s typically situated between?

A

T12 - L4

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2
Q

Which kidney is slightly more inferior/caudal? Why?

A

Right kidney is more inferior to accommodate the liver.

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3
Q

What stimulates erythropoietin release from the kidneys?

A

Inadequate O₂ to the kidneys

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4
Q

How much of CO do the kidneys receive?

A

20 - 22% ( 1-1.25L/min)

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5
Q

What is Azotemia?
What causes it?

A
  • Abnormally high levels of nitrogen containing compounds in the blood such as urea and creatinine.
  • Azotemia is causes by dysfunctional kidneys.
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6
Q

Where are your osmolality sensors located?
What occurs when you have hyperosmolality?

A
  • Anterior Hypothalamus
  • Hypothalamus signals pituitary gland to stimulate thirst and secrete ADH.
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7
Q

What degree of hyponatremia would give you pause for surgery?

A

Less than 125 mg/dL

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8
Q

6 listed here, theres alot more though

What are some conditions (discussed in lecture) that can cause hyponatremia?

A
  • Prolonged diuretic use
  • SIADH
  • Acute or chronic renal failure
  • Vomiting/diarrhea
  • Insufficient aldosterone
  • Excessive H₂O intake
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9
Q

5 treatments. Na+ correction should not exceed?

How would hyponatremia be treated?

A

This is highly dependent on underlying pathology.

  • Treatment of underlying disease
  • NS
  • Hypertonic Saline- 80ml/15 hours
  • Lasix
  • Mannitol

Na+ correction should not exceed 1.5meq/L/Hr

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10
Q

What pathology could occur with rapid over-correction of hyponatremia?

A

Osmotic Demyelination Syndrome (“Locked-in Syndrome”)

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11
Q

At what degree of hypernatremia would you typically cancel surgery?

A

155 mg/dL or greater

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12
Q

7 listed

What are common causes of hypernatremia?

A
  • Insufficient replacement of water loss
  • Excessive sweating
  • DI
  • Gi losses
  • Overcorrection of hyponatremia
  • Poor oral intake
  • too much bicarb
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13
Q

What is the complication from rapid correction of hypernatremia?

A

There is little evidence of morbidity from rapid hypernatremia correction. 0.5 mmol/L/hr to an absolute change of 10 mmol/L/day would be best to avoid cerebral edema, seizures, and other neurological sequelae.

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14
Q

Severe hyponatremia/hypernatremia both result in what?

A

Seizures, coma, and death

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15
Q

What are normal levels of serum potassium?

A

3.5 - 5 mg/dL

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16
Q

Excessive intake of what food is known to cause hypokalemia?

A

Licorice

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17
Q

When does hypokalemia need to be treated with K⁺ repletion?

A

Serum K⁺ < 3 mg/dL

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18
Q

What types of symptoms are generally seen with hypokalemia?

A

Cardiac & neuromuscular

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19
Q

What EKG sign is seen with hypokalemia?

A

“U”-waves

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20
Q

What other lab(s) needs to be check when replenishing K⁺ ?

A

Serum Phosphorus and Mg⁺⁺

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21
Q

A patient presents with a gun shot wound to the thorax necessitating exploratory thoracostomy. The patient’s serum K⁺ level is 5.7 mg/dL, what do you do?

A
  • Emergent surgery so proceed and treat the hyperkalemia

If the surgery was not emergent you would treat the K⁺ til it was below 5 mg/dL.

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22
Q

What are hyperkalemia’s effects on on EKG?
What about on the cardiac cellular membrane?

A
  • Peaked “T” Waves
  • ↑ Vᵣₘ and ↓ APD (action potential duration)
  • HYPERkalemia HYPOpolarizes the cell membrane
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23
Q

CH BIG K

What is the treatment for hyperkalemia?

Avoid what?

A

“CH BIG K”

  • Calcium gluconate (1° treatment)
  • Hyperventilation
  • Bicarbonate
  • Insulin
  • Glucose
  • Kayexelate

Avoid succs, LR & K containing fluids

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24
Q

Best measure of what?

What is a normal GFR?

A
  • 125 - 140 mL/min
  • Best measure of renal function overtime
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25
Q

Correlates w/? Influenced by?

What is normal serum creatinine?

Double serum creatinine causes what change to GFR?

A
  • 0.6 - 1.2 mg/dL
  • Correlates w/ muscle mass
  • Can be influenced by high protein diet, supplements, muscle breakdown –> having a baseline is critical
  • Double serum creatinine can decrease GFR by 50% acutely
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26
Q

What is better for acute monitoring of renal function, GFR or creatinine?

A
  • Creatinine for acute monitoring
  • GFR for chronic/trending
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27
Q

What populations would have lower creatinine levels?
Who would have higher?

A
  • ↓ in women and elderly
  • ↑ in body builders
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28
Q

What is the normal BUN:Creatinine ratio?

A

10:1

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29
Q

What is normal urine specific gravity?

A

1.001 - 1.035

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30
Q

Affected by? High vs low?

What is normal BUN?

A
  • 10- 20 mg/dL
  • Affected by diet and intravascular volume
  • low= malnourished or fluid overload
  • high= dry, high protein diet
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31
Q

Large amounts of what macromolecule would be suggestive of glomerular injury?

A

protein

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32
Q

What is the primary metabolite of protein metabolism in the liver?

A

Urea

Amino acids → ammonia → urea

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33
Q

Which of these two compounds is subject to filtration at the glomerulus?
- Creatinine
- Urea

A

Trick question. Both are subject to filtration

34
Q

Which of these two compounds is subject to reabsorption in the nephron?
- Creatinine
- Urea

A

Urea is reabsorbed unlike creatinine ( and therefore can’t be used to measure GFR)

35
Q

What would a BUN:Creatinine ratio of greater than 20:1 indicate?

A

Pre-renal Azotemia

36
Q

What is normal urine output in adults?

A

1 mL/kg/hr

37
Q

Your pre-operative patient has had less than 500 mLs of urine output in the past 24 hours. How would you classify this patient?

38
Q

What’s the greatest risk factor for AKI?

A

Pre-existing renal disease

39
Q

Four

What lab values would be indicative of acute kidney injury?

A
  • Serum creatinine increase by > 0.3 mg/dL w/in 48hrs
  • Serum creatinine increase by 50% w/in 7 days
  • 50% decrease in creatinine clearance
  • Oliguria (although not always seen)
40
Q

And treatment? If untreated?

What is the most common cause of pre-renal AKI?

A

Renal Hypoperfusion

shock, burns, trauma, blood loss, aortic clamping, etc.

Tx by restoring renal blood flow
If untreated –> renal azotemia

41
Q

Other lab values we would see?

What is a typical BUN:Creatinine ratio in intra-renal AKI?

A
  • < 15:1
  • Decreased urea reabsorption in proximal tubule–> decreased BUN
  • Low creatinine clearance, high serum creatinine
  • Low GFR –> late sx
42
Q

Why are urea levels (in the urine) higher in intra-renal AKI?

A

Whole nephron is failing so urea is not being reabsorbed in the PCT.

43
Q

What is the cause of intra-renal AKI?

A

Renal parenchymal (inner kidney) damage

ATN, glomerulonephritis, CKD, etc.

44
Q

What is the cause of post-renal azotemia?

A

Urinary tract blockage

45
Q

What BUN:Creatinine ratio is typically seen in post-renal AKI?

A
  • Initial: > 15:1
  • Chronic = ↓ BUN:Cr
46
Q

What is the most common neurological complication of AKI?

A

Uremic Encephalopathy

47
Q

4

What are the most common cardiac complications of AKI?

A
  1. Volume Overload → Heart Failure / Pulmonary Edema
  2. Electrolyte Imbalances → Arrhythmias
  3. Uremia → Pericarditis
  4. Hypertension –> Can worsen LV hypertrophy
48
Q

Two major complications

What are the most common hematologic complications of AKI?

A
  • Anemia
    - Due to decreased EPO & hemodilution
    -
  • The relationship between vWF and platelets is disrupted by uremia –> Uremic toxins interfere with platelet glycoprotein receptors that are needed for vWF-mediated adhesion and aggregation.
49
Q

5

What are the most common metabolic complications of AKI?

A
  • Hyperkalemia
  • H₂O & Na⁺ retention
  • ↓ albumin
  • Metabolic acidosis
  • Hyperparathyroidsm (this is actually more commonly seen in CKD)
50
Q

Benefit of Prophylactic Na+ bicarb in CKD patients?

A
  • Decreases formation of free radicals
  • Chronic acidosis can lead to tubulointerstitial injury and fibrosis, accelerating CKD progression.
51
Q

What are the leading causes of ESRD?

52
Q

On average, GFR decreases by _____ per decade starting from age 20.

53
Q

It is usually helpful to assume that everyone with CKD also has this condition.

54
Q

What drugs are often used to combat chronic kidney disease?

A

ACEi’s and ARBs

55
Q

How do ACEi’s and ARBs help treat CKD?

A
  • Decrease systemic & glomerular HTN
  • Decrease proteinuria
  • Decrease glomerular sclerosis
56
Q

What antihypertensive drugs need to be held on the day of surgery to decrease the risk of intraoperative hypotension?

A

ACEi’s & ARBs

57
Q

Which populations are at a higher risk for silent MI?

A

Women and diabetics

58
Q

Which patient population is likely to be dyslipidemic?

What lab values reflect dyslipidemia?

A
  • Triglycerides > 500
  • LDL > 100
59
Q

What are the indications for dialysis?

A
  • Volume overload
  • ↑K⁺
  • Severe metabolic acidosis
  • Symptomatic uremia
  • Drug overdose
60
Q

What is the most common adverse event associated with dialysis?

A

Hypotension

61
Q

What is the leading cause of death in dialysis patients?

62
Q

When would peritoneal dialysis be preferred to hemodialysis?

A

PD is preferred for patients who can’t tolerate large fluid shifts (CHF or unstable angina)

63
Q

What two things reduce the risk of pre-renal azotemia?

A
  • Maintain MAP > 65mmHg
  • Appropriate hydration
64
Q

Excessive use of 0.9% NaCl leads to what condition?

A

Hyperchloremic metabolic acidosis

65
Q

Which of the following fluids are associated with increased risk of renal injury?
- Crystalloids
- Colloids
- Starches

66
Q

Treating oliguric AKI patients with diuretics helps improve their condition via diuresing toxic metabolic byproducts of the AKI. T/F?

A

False. Diuretics in a oliguric AKI can further the renal injury.

67
Q

This drug maintains GFR and urine output better than norepinephrine and neosynephrine via preferential constriction of the efferent arteriole.

A

Vasopressin

68
Q

How is idiopathic hypercalciuria treated?

A

Thiazide diuretics

69
Q

Why might you want to do regional or GA with paraplegic patients undergoing bladder surgeries?

A

To avoid autonomic dysreflexia.

70
Q

Stored where? % bound to albumin? How does pH affect? Normal iCal?

Calcium

A
  • 99% stored in bone, 1% in ECF
  • 60% is bound to albumin and inactive
  • Only iCal is considered physiologically active
    -Normal: 1.2-1.38mmol/L
  • Alkalosis –> ↑ Ca++ binding to albumin –>↓ Decreased iCal
  • Acidosis –> ↓ Ca++ binding to albumin–> ↑ Increased iCal
71
Q

3

Hormones that regulate Ca++

A
  • PTH: Increase GI absorption, renal reabsorption, and regulates bone & plasma levels
  • Vitamin D: Increases GI absorption of Ca++
  • Calcitonin: Promotes storage of Ca++ in bone
72
Q

Causes of Hypo/Hyper Ca++

A

HypoCa++
* Low PTH secretion; thyroid problem or complication of parathyroid surgery –> can lead to laryngospasm
* Low Mg++, Low Vit. D
* Renail failure
* MTP

HyperCa++
* Hyperparathyroid: Ca++ <11
* Cancer: Ca++ >13

73
Q

Life-threatening symptom of hypoCa++

A

Post-parathyroidectomy-hypocalcemia induced laryngospasm

74
Q

HyperMg++

A
  • Very uncommon; due to overtreatment of pre-eclampsia/eclampsia or pheochromocytoma

tx w/ diuresis, IV Ca++, dialysis

75
Q

Medullary Cortex vs Inner Medulla

A

Medullary Cortex:
* Outer layer
* Receives 85-90% of RBF

Inner Layer:
* Most vunerable for developing necrosis in response to HoTN

76
Q

Normal, filtered and not what? most reliable measure of?

Creatinine Clearance

A
  • 110-140ml/min
  • Creatinine freely filtered and not reabsorbed
  • Most reliable measure of GFR
77
Q

IVC Collapsibility Indicates…

A

> 50% collapsibility indicates fluid deficit

78
Q

Hallmark of AKI?

A
  • Azotemia; buildup of nitrogenous products such as urea and creatinine
79
Q

2 medical conditions and predisposed to what?

CKD Cardiovascular Effects

A
  • Systeminc HTN
  • Dyslipidemia
  • Predisposed to MI
80
Q

Many anesthetics are what? Need to avoid what kind of metabolites?

Anesthesia & CKD

A
  • Many anesthetics are lipid soluble and reabsorbed by renal tubular cells
  • Give agents not dependent on renal elimination
  • Avoid active metabolites
    -Morphine
    -Demerol
81
Q

Two conditions

CKD Hematologic Effects

A
  • Anemia (Target Hgb 10)
  • Platelet dysfunction
    *
82
Q

K+? Dialysis needs to happen when?

Preoperative Concerns For Renal Disease

Prophylaxis of what? Blood loss stimulates what?

A
  • K+ <5.5 for elective sx
  • Dialysis pts need to be dialyzed w/in 24 hours prior to surgery
  • Aspiration prophylaxis
  • Blood loss stimulates SNS, resulting in decreased renal blood flow