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Advanced Anesthesia > Endocrine/Renal > Flashcards

Endocrine/Renal Flashcards

1
Q

Where is EPO produced?

A

Peritubular cells in the kidneys with a small amount (10%) also in perisinusoidal cells of the liver.

Stimulated by hypoxia and suppressed by polycythemia –> accelerates release of erythroid precursors and reticulocytes from bone marrow

Uses include treatment of anemia, bone marrow suppression, Jehovah’s witnesses but takes several weeks to improve Hb levels

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2
Q

The most sensitive indicator of failing thyroid function?

A

Increased TSH

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3
Q

Difference between subclinical hypothyroidism and hypothyroidism?

A

FT4 is normal in subclinical hypothyroidism and low in hypothyroidsim. (TSH elevated in both).

Subclinical hypothyroidism is thought to have little or no perioperative significance. It is common in people aged 65 years or older. It is often transient and presents with minimal or nonspecific symptoms such as fatigue, depression and hyperlipidemia.

Hypothyroidism affects respiratory control mechanisms, fluid homeostasis, electrolytes particularly sodium, temperature regulation, muscle relaxation (with a higher incidence of myasthenia gravis), and increased MI risk.

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4
Q

Almost all hormones increase during a stress response EXCEPT?

A

T3/T4 and GRH are DECREASED

TSH and insulin can go up or down in response

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5
Q

Posterior pituatary hormones?

A

Vasopressin (ADH) and oxytocin - these hormones typically not altered with pituitary tumors because ANTERIOR pituitary typically involved

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6
Q

Normal serum osmolality?

A

290 mOsm/kg

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7
Q

Normal urine sodium?

A

20 mEq/L

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8
Q

Normal urine osmolality?

A

100 mOsm/kg

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9
Q

Treatment for diabetes insidious?

A

vasopressin

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10
Q

How to differentiate between SIADH versus cerebral salt wasting syndrome?

A

volume status:
SIADH is euvolemic to hypervolemic
CSW is hypOvolumic

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11
Q

treatment for SIADH?

A 
fluid restriction to < 800mL/day
Salt/solute intake
vasopressin ANTagonists such as conivaptan, demeclocycline or lithium
Hypertonic saline (reserved for severe cases)
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12
Q

Mnemonic for Conn’s syndrome versus Addison’s

A

Conn’s
imagine a cone of SALTed caramel: INCR sodium, decr potassium

Addison
imagine a cone of vanilla: DECR sodium but INCR calcium from the dairy, and incr potassium

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13
Q

Treatment for diabetes insipidus?

A

Induce an SIADH picture: give desmopressin, vasopressin or even carbamazepine (which sensitizes collecting duct to ADH)

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14
Q

Plasma osmolality formula

A

Posm = 2 * Na + [Glu/18] + BUN/2.8

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15
Q

FeNa, FeUrea and Urine Na in prerenal azotemia?

A

FeNa < 1%
FeUrea <35%
Urine Na <20

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16
Q

FeNa, FeUrea and Urine Na in ATN?

A

FeNa > 1%
FeUrea >35%
Urine Na >40

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17
Q

Most common changes seen in ESRD?

A

anemia from decreased EPO
hypOcalcemia
hypERkalemia

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18
Q

How does magnesium change in setting of ESRD?

A

increases

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19
Q

How does cholesterol change in setting of ESRD?

A

hyperlipidemia

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20
Q

How does BP change in setting of ESRD?

A

hypertension

21
Q

How does phosphate change in setting of ESRD?

A

hyperphosphatemia

22
Q

How does parathyroid hormone change in setting of ESRD?

A

Secondary hyperparathyroidism

23
Q

Cause of platelet dysfunction in ESRD?

A

Uremia

24
Q

Why is extreme caution needed when treating DI with desmopressin in setting of cerebral edema?

A

because DDAVP limits excretion of dilute urine –> rapid normalization of serum sodium may result in an acute and critical increase in intracranial pressure.

25
Q

Formula for FeNa?

A

[Pcr * Una / Pna * Ucr] x 100

26
Q

What is Conn’s syndrome? What electrolyte abnormalities exist?

A

Conn’s syndrome is primary hyperaldosteronism from excess secretion of a functional tumor of the adrenal cortex (zona glomerulosa).

Distal renal tubules absorb Na+ ions in exchange for urinary LOSS of K+ and H+ ions –> volume expansion because H2O follows Na+ ions –> decreased renin production

(hypokalemia and metabolic alkalosis)

27
Q

Preop management of Conn’s syndrome? Intraop treatment?

A

Spironolactone because it is an aldosterone antagonist, potassium repletion, and antihypertensives. May take several weeks to achieve some level of homeostasis.

Intraoperatively, avoid hyperventilation because will further reduce K+ and cortisol supplementation if BOTH adrenal glands are being removed. Otherwise cortisol can worsen hypokalemia and sodium retention because of mild mineralocorticoid activity.

28
Q

What happens to urine in ATN?

A

kidney loses the ability to concentrate urine and reabsorb salt so
urine osmolality < 350
specific gravity < 1.0035
urine Na > 40

If situation is pre-renal, kidney can still concentrate urine and reabsorb Na so
urine osmolality > 500
specific gravity > 1.01
urine Na < 20

29
Q

Highest risk for post cardiopulmonary bypass acute kidney injury?

A

elevated preop Cr
complex cardiac procedures
emergency surgery
preop intraaortic balloon pump

30
Q

hyperparathyroidism causes what type of acid-base abnormality and electrolyte disorder?

A

high PTH inhibits RENAL bicarb absorption and inhibits Na/Cl cotransporter leading to hyPERchloremia.

hyperchloremic (non-gap) metabolic acidosis (think same as excessive normal saline administration)

31
Q

primary pharmacologic treatment of acromegaly?

A

ocreotide because it suppresses growth hormone production

32
Q

Risk of recurarization with neostigmine in renal failure?

A

unlikely because neostigmine is MORE prolonged than rocuronium in renal failure

33
Q

Factors that distinguish HHS from DKA?

A

glucose very high > 600 whereas DKA is >250

pH typically > 7.3 whereas DKA is usually more acidotic

minimal to no ketones

34
Q

Treatment for hyperthyroidism or thyrotoxicosis?

A

Methimazole or propylthiouracil which blocks conversion of T4 to T3

Radioactive iodine is another option

adjuvant therapy includes propranolol, atenolol or calcium channel blockers

35
Q

Earliest sign of diabetic autonomic neuropathy?

A

increased resting tachycardia with loss of HR variability

36
Q

Later signs of diabetic autonomic neuropathy?

A

HR fails to respond to exercise
gastroparesis
impaired ventilatory reflexes to hypoxia and hypercapnia
hypOglycemia unawareness

37
Q

first line treatment for carcinoid syndrome?

A

ocreotide

38
Q

potassium in setting of high aldosterone or high cortisol?

A

hypokalemia due to potassium LOSS

39
Q

potassium in setting of high insulin or high thyroid hormone?

A

hypERkalemia due to potassium uptake

40
Q

acid-base and chloride in hyperparathyroidism?

A

NON anion gap hyPERchloremic metabolic acidosis

Similar to NSS administration

41
Q

acid-base and chloride in pyloric stenosis?

A

hypOchloremic metabolic ALKalosis

42
Q

Avoid these drugs in carcinoid syndrome?

A

histamine releasing agents: “MAST”

mivacurium/morphine
atracurium
SUX
tubocurarine/thiopental

43
Q

Diuretic site of action: carbonic anhydrase inhibitors

A

PCT

44
Q

Diuretic site of action: osmotic diuretics like mannitol

A

PCT, thin descending LOH, and collecting ducts

45
Q

Diuretic site of action: loop diuretics

A

THICK ASCENDING loop of henle

46
Q

Diuretic site of action: potassium sparing

A

collecting ducts and tubules

47
Q

metabolic alkalosis with which diuretics?

A

loops and thiazides

48
Q

metabolic acidosis with which diuretics?

A

acetazolamide and potassium-sparing

Advanced Anesthesia (11 decks)

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