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Renal > Lecture 4 - Renal Pathology, Diuretics, and Anesthesia > Flashcards

Lecture 4 - Renal Pathology, Diuretics, and Anesthesia Flashcards

1
Q

What produces Atrial Natriuretic Peptide (ANP)?

A

-Atrial myocytes

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2
Q

What is the function Atrial Natriuretic Peptide (ANP)?

A
  • Relax smooth muscle

- Promote NaCL and water excretion by kidney

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3
Q

What is the stimulation for ANP?

A

-Atrial stretch

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4
Q

T/F: ANP will stimulate the release of renin.

A

FALSE (ANP will inhibit the release…)

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5
Q

T/F: ANP will will inhibit Anti Diuretic Hormone release from the posterior pituitary.

A

TRUE

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6
Q

What is the action of Atrial Natriuretic Peptide (ANP)?

A
  • Increased GFR via vasodilation of the afferent arteriole and constriction of the efferent arteriole
  • Acts directly on the collecting duct to decrease NaCl reabsorption
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7
Q

T/F: Atrial Natriuretic peptide stimulates aldosterone secretion.

A

FALSE ( Atrial Natriuretic Peptide inhibits aldosterone secretion.)

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8
Q

Nesiritide (Natrecor) is produced by the _________ myocardium.

A

ventricle

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9
Q

T/F: Nesiritide (Natrecor) is also called the brain natriurectic peptide.

A

TRUE

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10
Q

Nesiritide (Natrecor) has been shown to be linked with increase _______ and ______ dysfunction.

A
  • mortality

- renal

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11
Q

What is Nesiritide (Natrecor) used for:

A

-Treat CHF patient by causing vasodilation, diuresis, and natriuresis

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12
Q

Nesiritide (Natrecor) has also been used as a lab marker of ______ ________ (>500 pg/ml is very positive).

A

-Heart Failure

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13
Q

MOST diuretics act by decreasing the rate of _______ reabsorbtion from the ________ which causes ________ output to increase (Natriuresis) Which then results in diuresis (water output).

A
  • Sodium
  • Tubules
  • Sodium
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14
Q

T/F: Although many diuretics work within minutes this effect decreases over the next few days with chronic use.

A

TRUE

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15
Q

What effects eventually override the effects of diuretics?

A

DECREASE

  • ECF
  • MAP
  • GFR

INCREASE

  • Renin
  • Angiotension II
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16
Q

What are the different types of diuretics?

A
  • Osmotic
  • LOOP
  • Thiazide
  • Carbonic anhydrease inhibitors
  • Aldosterone antagonists
  • Na+ Channel blockers
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17
Q

What are some osmotic diuretics?

A
  • Urea

- Mannitol

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18
Q

T/F: Glucose can act like a osmotic diuretic in the diabetic that has glucose in their urine?

A

TRUE

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19
Q

What are some examples of LOOP diuretics?

A
  • Furosemide (Lasix)
  • Bumetanide (Bumex)
  • Ethacrynic acid
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20
Q

How do LOOP diuretics work?

A

-Inhibits the Na-2CL-K co-transporter in the TAL of Henle’s loop

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21
Q

T/F: LOOP diuretics disrupts the counter-current multiplier system and the interstitium cannot become hyperosmolar.

A

TRUE

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22
Q

What are some drugs that are thiazide diuretics?

A

-Hydrochlorothiazide (HCTZ)

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23
Q

How do Thiazide diuretics work?

A

-Inhibit sodium chloride reabsorbtion in the EARLY DISTAL TUBULE.

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24
Q

What are some drugs that are carbonic anhydrase inhibitors:

A
  • Acetazolamide (Diamox)
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25
Q

What is the disadvantage of using carbonic anhydrase inhibitors (Diuretics)?

A
  • Causes acidosis through bicarbonate loss in the urine.
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26
Q

How does carbonic anhydrase inhibitors work? -

A

Reduce reabsorbtion of Na+ by decreasing bicarbonate reabsorbtion in the PROXIMAL TUBULE.

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27
Q

What are dome drugs the are Aldosterone antagonist (Diuretics)?

A

-Spironolactone (Aldactone)

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28
Q

How does Aldosterone antagonists diuretics work?

A
  • Decreases reabsorbtion of Na+ and decreases K+ secretion by competing for aldosterone binding sites in the distal tubules
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29
Q

T/F: Spironolactone (Aldactone) will NOT spare potassium.

A

FALSE

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30
Q

What are some drugs that are Na+ channel blockers diuretics?

A
  • Amiloride

- triamterene

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31
Q

Where does Na+ channel blocker diuretic work?

A

-Collecting tubules

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32
Q

T/F: Na+ channel blockers will spare potassium within the body.

A

TRUE

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33
Q

Acute renal failure that is pre-renal means:

A
  • Kidney not getting enough blood flow and therefore becomes ischemic (EXAMPLES: Heart Failure, hypovolemia, ETC..)
34
Q

Acute renal failure the is Intra-renal means:

A

-Damage to the kidney itself. (Example: Toxins, infections, autoimmune disease, direct renal injury,)

35
Q

Acute reanl failure that is Post-renal means:

A

-Obstruction to the collecting system. (Example: Stones, urethral valves, tied off ureter, kinked foley)

36
Q

When does Chronic renal failure occur?

A
  • When the number of functioning nephrons drop below 70% of normal.
37
Q

What would be mechanisms of injury for chronic renal failure to the renal vasculature.

A
  • Atherosclerosis of largee vessels
  • Fibromuscular dysplasia
  • Nephrosclerosis
38
Q

What would be the mechanisms of injury for chronic renal failure with glomerulonephritis?

A
  • Deposition of antigenantibody complexes in glomerular membranes
  • Can be post strptococcal infetion
  • Lupus can also cause this
39
Q

What would cause nephrotic syndrome in CRF:

A

-Large amounts of protein are lost in the urine due to destruction of or loss of negative charge on the capillary basement membrane in the glomerulus

40
Q

What are the effects of renal failure on the body:

A

-Edema from water and salt retention
-Acidosis
-Increase in urea, creatine, uric acid, potassium, phosphates, phenols
-Decrease of Erythropoetin
-Increase in CO to compensate for decrease oxygen carrying capacities
-prone to fluid overload and pulmonary edema
-Minute ventilation is increased
-abnormal glucose tolerance
-Platelet and WBC dysfunction occurs
Hypersecretion of gastic acid increases the risk of ulcers-Autonoic neuropathy can slow gastric empying
-Peripheral neuropathy is common

41
Q

What is osteomalacia?

A

-When the kidney cannot assist in the production of 1,25 hydroxycholecalvciferol which promotes the absorption of calcium in the intestine.

42
Q

What causes hypertension in renal failure?

A

-Lesions in the kidney prevent sodium and water excretion which causes HTN

43
Q

What are the determining factors of the rate of movement of solute across the dialysis membrane?

A
  • Concentration gradient of the solute
  • permeability
  • surface area of the membrane
  • length of time the blood and fluid remain in contact with the membrane
44
Q

Usually there is about ____ cc of blood in the dialysis machine at any time.

A

500

45
Q

Place in order from greatest to least the most common causes of ESRD.

  • DM
  • HTN
  • Glomerulonephritis
  • Polycystic kidney disease
  • Other/Unknown
A
  1. DM
  2. HTN
  3. Other/unknown
  4. Glomerulonephritis
  5. Polycystic Kidney disease
46
Q

List the indication for dialysis.

A
  • FLuid overload
  • Hyperkalemia
  • Severe acidosis
  • Metabolic encephalopathy
  • Pericarditis
  • Coagulopathy
  • Refractory GI symptoms
  • Drug toxicity
47
Q

Increased BUN can be from decreased ___ or increased _______ breakdown (also seen in ______ or ___________ of blood in the GI tract).

A
  • GFR
  • Protein
  • sepsis
  • degradation
48
Q

__ to __ % of urea is passively reabsorbed in the nephron, hypovolemia will increase this.

A
  • 40

- 50

49
Q

Normal BUN is __ to __ mg/dL.

A

10

20

50
Q

Normal creatinine is __ to __ mg/dL in men and __ to __ in women.

A
  • 0.8
  • 1.3
  • 0.6
  • 1.0
51
Q

What is the byproduct of muscle metabolism?

A

Creatinine

52
Q

Creatinine concentration is ________ related to body muscle mass and is _________ related to GFR.

A
  • Directly

- Inversely

53
Q

GFR decreases by _% for every ________ past the age of __.

A
  • 5
  • decade
  • 20
54
Q

T/F: Low renal tubular flow rates enhance urea reabsorbtion but do not affect creatinine handling.

A

TRUE

55
Q

A BUN creatinine clearance of 10:1 are seen in:

A
  • Volume depletion
  • decreased tubular flow
  • obstructive uropathy
56
Q

A specific gravity > ______ after an overnight fast is indicative of adequate urinary concentrating ability.

A

1.018

57
Q

A low specific gravity in the face of plasma hyperosmolality is consistent with:

A

Diabetes insipidus

58
Q

Patient with renal disease are more susceptible to barbiturate and Benzodiazepines due to:

A

Decreased protein binding causing more free drug available

59
Q

What does propofol, ketamine and etomidate do to the uremic patient?

A

-There is no significant difference

60
Q

T/F: Atropine and Robinol can be used safely though metabolites may accumulate with repeated dosing.

A

TRUE

61
Q

T/F: Metoclopramide is countraindicated with the patient in renal failure.

A

FALSE (Is excreted unchanged by the kidney and can accumulate in renal railure but is generally safe for a single does.)

62
Q

What is the concern with enflurane and sevoflurane in the renal failure patient?

A

Fluoride accumulation

63
Q

T/F: Succinylcholine is safe in patients with K < 5 mEq/L, but will transiently increase K+ by almost 0.5 mEq/L.

A

True

64
Q

What is the drug of choice for the renal failure patient?

A

Cis-atracurium (due to the Hoffman elimination

65
Q

What agents are to be avoided in the renal failure patient.

A
  • Pancuronium
  • Pipecuronium
  • Alcuronium,
  • Doxacurium
    (This is due to renal excretion)
66
Q

__________ (NDMR) and __________ (NDMR) are primarily eliminated by the liver but there is some mild prolongation in renal failure.

A
  • Vecuronium

- rocuronium

67
Q

What is the concern with reversal agents for NDMR?

A

-They are excreted by the kidney but their half life are prolonged about as much as some of the muscle relaxants. So overall there does not tend to be a problem with the agent.

68
Q

Important pre-op information for the renal failure patient is:

A
  • when was last dialysis
  • Recent K
  • EKG
  • Transfusion of RBC if Hgb < 6-7
  • What is their dialysis access site
69
Q

__________ is a key factor in the causation of periop renal failure.

A

Hypovolemia

70
Q

What is the mortality rate of post op renal failure?

A

~50%

71
Q

T/F: Dopamine has positive outcomes for the acute renal failure.

A

FALSE (Renal dose dopamine has no good data supporting it at present)

72
Q

T/F: It is easier to treat the complications of fluid overload than it is to trat acute renal failure.

A

TRUE

73
Q

What are risk factors for perioperative renal failure.

A
  • Sepsis
  • Hypovolemia
  • Obstructive jaundice
  • Aminoglycoside antibiotics
  • NSAIDS
  • ACE inhibitors
  • Recent dye injections
74
Q

T/F: Calcium oxalate stones are the most common kidney stone.

A

TRUE

75
Q

A struvite stone is:

A

-associated with infection with urea splitting bacteria whcih form ammonia

76
Q

A Uric acid stones:

A

-seen in gout and cell lysis scenarios

77
Q

A Calcium phosphate stones:

A

-Associate with hyperparathyroidism and reanl tubular aciosis

78
Q

A cysteine stone:

A

-an autosomal recessive

79
Q

Most kidney < _ mm pass spontaneously.

A

4

80
Q

T/F: Alpha blockers like terazocin may help decrease tone of ureter and promote passage

A

TRUE

81
Q

If stone has not passed in __ days or if there is renal compromise surgery is indicated.

A

30

Renal (5 decks)

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