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Anesthesia 101 > Basic ENDO/Metabolic > Flashcards

Basic ENDO/Metabolic Flashcards

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1
Q

Glucagon is secreted by pancreatic alpha cells in response to hypoglycemia and INHIBITS (Gluconeogenesis/Glycolysis) to IMPROVE blood glucose concentration

A

Glycolysis

*glucagon STIMULATES glycogenolysis and gluconeogenesis

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2
Q

Glucagon raises blood sugar indirectly how? (3)

A
  1. Stimulates lipolysis
    - produces glycerol and FFA
  2. Inhibits Glycolysis
    - stops consumption of glucose
  3. Inhibits glycogen synthesis
    - available glucose can be released into bloodstream instead of being stored in liver
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3
Q

How does glucagon affect the heart?

A

inotropic and chronotropic effects

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4
Q

How to differentiate Malignant hyperthermia from Thyroid storm?

A
  1. Muscle rigidity
  2. Rate of EtCO2 ( MH&raquo_space; TS)
  3. Temperature (MH&raquo_space; TS)
  4. MH (hyperkalemia), TS (hypokalemia)
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5
Q

Treatment for MH vs Thyroid storm?

A

MH: Dantrolene

Thyroid storm: Sodium iodide and PTU

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6
Q

AVP (aka ADH) regulates diuresis and antidiuresis. The most potent trigger for its release is ____

A

systemic arterial hypotension (mediated by aortic and carotid baroreceptors)
-> AVP vasoconstricts by stim V1a receptors

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7
Q

AVP (aka ADH) acts on receptors in the collecting ducts to induce water and Na reabsorption that causes what changes to urine and plasma osmolality?

A

Increases urine osmolality

Decreases plasma osmolality

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8
Q

Why are clinically hypothyroid pts susceptible to hypotensive effects of anesthesia?

A
  1. Decreased CO
  2. Blunted autonomic reflexes
  3. Decreased Intravascular volume
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9
Q

Primary vs secondary hypothyroidism

  • TSH, T4
  • primary dysfunction?
A

Primary

  • High TSH, low T4
  • primary dysfunction: lack of T4 feedback on pituitary (ie: hashimotos, iodine deficiency)

Secondary

  • Low TSH, Low T4
  • primary dysfunction: pituitary gland (ie: adenoma, hemorrhage, radiation)
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10
Q

What is a bad idea for management of pts with thyrotoxicosis (hypermetabolic state d/t Thyroid hormone?

A

RAI

- destroys thyroid gland - can worsen thyrotoxicosis bc thyroid hormone is released into the blood

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11
Q

What can you pretreat hyperthyroid pts with prior to RAI to prevent thyrotoxicosis (aka thyrostatic medications)?

A

Methimazole or propanolol

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12
Q

What is the treatment for Hashimotos (thyroid gland is attacked by immune system)?

A

L-thyroxine (levothyroxine)

*pts are hypothyroid

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13
Q

What is the treatment for Graves disease (thyroid gland is hyperfunctioning)?

A

Methimazole, or PTU, or Iodide

*Pts are hyperthyroid

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14
Q

Why are pts hyperglycemic after surgery/stress?

A

Body release hormones (cortisol, catecholamines, glucagon) that are counter-regulatory to insulin -> insulin resistance –> increase production and release of glucose

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15
Q

Diabetic autonomic neuropathy results in resting tachycardia that does NOT compensate well for changing hemodynamics, which can cause ______

A

orthostatic hypotension

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16
Q

Why is starting a BB prior to a-blocker dangerous in pts with pheochromocytoma?

A

Hypertensive emergency
- unopposed alpha vasoconstriction

Ideally: initiate a-adrenergic receptor antagonist (phenoxybenzamine, phentolamine, doxazosin, terazosin, or prazosin) 10-14 days prior to and including morning of surgery.
- can add BB only if indicated (persistent tachycardia, hypertension, dysrhythmias)

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17
Q

In DKA pts, what is recommended once plasma glucose is approximately down to 200 mg/dL?

A

Switch from 0.45% NaCl to D5 in 0.45% NaCl

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18
Q

________ is the combination of euvolemia, hypotonic plasma (low serum osm), hypertonic urine (urine osm > 100mOsm), and high urine sodium (>20 mEq/L).

A

Hallmark of SIADH
- Hypotonic plasma d/t increased free water retention from ADH

INAPPropriate ADH
- Increased NA in the PP

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19
Q

ADH is released from the _______ in response to _____

A

Posterior pituitary

Hyperosmolar state or hypovolemia

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20
Q

ADH can be inappropriately be released by ______

A
  1. Stress
  2. Major trauma
  3. Severe pain
  4. Use of opioids
  5. Sepsis
  6. Nausea
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21
Q

Primary hyperaldosteronism (Conn syndrome) is most commonly caused by _____

A

unilateral adrenal adenoma

- mineralocorticoid excess (aldosterone)

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22
Q

________ increases the reabsorption of Na and secretion of K in the distal tubule for volume expansion. What happens to Na and K if a pt has hyperaldosteronism?

A

Aldosterone

  • Hypernatremia
  • Hypokalemia
  • (Metabolic alkalosis)
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23
Q

Stress dosing steroids.

- Low risk for pts taking < ____

A

< 5 mg prednisone

*conflicting data on superiority

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24
Q

Steroid Trivia

  • Mineralocorticoids regulate
  • Glucocorticoids regulate
  • Corticosteroids regulate
A
  • Mineralocorticoids regulate: sodium and water levels (aldosterone)
  • Glucocorticoids regulate: metabolism and inflammation (cortisol)
  • Corticosteroids regulate: both gluco/mineralocorticoid effects
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25
Q

Adrenal cortex three diff layers and what they secrete

A
  1. Outer: zona glomerulosa
    - Mineralocorticoids (aldosterone)
  2. Middle: zona fasiculata
    - Glucocorticoids (cortisol)
  3. Inner: zona reticularis
    - Gonadocorticoids
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26
Q

Adrenal medulla is made of ______ and secretes ____

A

chromaffin cells

catecholamines (adrenaline, noradrenaline)

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27
Q

Best way to intraoperatively manage diabetic pt’s insulin pumps

A

Continue at programmed rate in uncomplicated surgery

If complicated surgery/expecting large hemodynamic shifts, electrolyte imbalances, and acid-base balance, turn OFF basal rate, and start continuous insulin infusion

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28
Q

_____ is the most common cause of hyponatremia in pts with CNS disturbances

A

SIADH

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29
Q

What condition looks exactly like SIADH, but is treated differently?

  • Hyponatremic (<280)
  • High ur Na (>40)
  • High ur Osm (>100)
A

Cerebral salt wasting

*Cerebral salt wasting is either euvolemic or hypovolemic

In SIADH: treatment is fluid restriction, PO NaCl, Lasix

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30
Q

What type of acid base disturbances do loop and thiazide diuretics cause?

A

Hypochloremic metabolic alkalosis

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31
Q

What type of electrolyte is needed in the treatment of alkalosis?

A

Potassium

  • since alkalosis causes hypokalemia
  • K+ is driven into cells and exchanged for intracellular H+ in attempt to buffer alkalosis
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32
Q

Most pts with primary hyperparathyroidism are asymptomatic, but what is the most common presenting symptom if any?

A

nephrolithiasis

- secondary to elevated calcium levels

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33
Q

Aldosterone (mineralocorticoid) and cortisol (glucocorticoid) promote renal potassium (uptake/secretion)

A

secretion

- hypokalemia

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34
Q

Insulin and thyroid hormones promote cellular potassium (uptake/secretion)

A

uptake

- hyperkalemia

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35
Q

What happens to Na and K with glucocorticoid administration?

A

Stimulate Na reabsorption and K excretion

- Hypernatremia and hypokalemia

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36
Q

How to change the non-depolarizing neuromuscular blocker in pts with hyperparathyroidism?

A

Increase the dose

- Hypercalcemia antagonizes effects of non-depolarizing NMB

37
Q

How can hyperparathyroidism lead to respiratory insufficiency?

A

Hypercalemia is assoc w/ muscle weakness

38
Q

Most common cause of stridor 24-96 hours post thyroidectomy?

A

hypocalcemia

*recurrent laryngeal n damage is more likely to cause early stridor and difficulty with phonation

39
Q

Why does damage to the superior laryngeal n cause change in pitch of pts voice?

A

SLN innervates cricothyroid muscle

40
Q

The normal pulse rate variability that occurs with inhalation and exhalation is 10/min. Baroreceptors sense changes to preload with inspiration -> increase pulse rate, and expiration -> decrease rate.
Loss of this variability is a sign of _____

A

early autonomic neuropathy.

41
Q

(T3/T4) exerts direct effects on the myocardium and may result in thyrotoxic cardiomyopathy

A

T3

42
Q

In primary hyperthyroidism, what levels are increased and decreased (TSH, T3, T4, THBR)

A

TSH: decreased

T3 and T4: increased

Thyroid hormone binding ratio (amt of free T4 circulating): increased

*The hormones themselves are affected

43
Q

Most common initial presentation of pts with primary hyperaldosteronism?

A
  1. hypokalemia metabolic alkalosis
    - urinary loss of K+ and H+ in exchange for absorbing Na+
  2. Increased BP
  3. Reduced renin
44
Q

MEN I tumors

A

Pituitary tumor
Parathyroid tumors
Pancreatic tumors

45
Q

MEN IIa tumors

A

Parathyroid tumors
Thyroid tumor (medullary)
Pheochromocytoma

46
Q

MEN IIb tumors

A

Ganglioneuromas
Parathyroid tumors
Thyroid tumor (medullary)
Pheochromocytoma

47
Q

Glucagon release is triggered by (hyper/hypoglycemia) and its release is stimulated by ______

A

Hypoglycemia
- indicated in cases of insulin overdose

Epinephrine (catecholamines)

48
Q

________ are the most effective drugs to block release of thyroid hormone from the thyroid gland

A

Iodides, but should only be used after a thyrostatic agent is given (ie: PTU or methimazole) d/t the “escape phenomenon” where new thyroid hormones are actually synthesized and worsen the hyperthyroidism

49
Q

________ consists of episodic flushing, diarrhea, wheezing and R sided heart disease

A

carcinoid syndrome

50
Q

Pancuronium (stimulates/blunts) the sympathetic nervous system

A

stimulates

- use with caution in pts with hyperthyroidism

51
Q

When can you stop BB in hyperthyroid pts getting thyroidectomy

A

several weeks

- half life of T4 is 7-8 days

52
Q

Primary adrenal insufficiency (addison disease) is characterized by: (5)

A
  1. Hyponatremia
  2. Hyperkalemia
  3. Metabolic acidosis
  4. Hyperpigmentation
  5. Hypocortisolism
53
Q

Primary adrenal insufficiency develops adrenal gland dysfunction/exacerbation. What is treatment?

A

100mg IV hydrocortisone q6h for 24hrs

*adrenal gland is unable to produce sufficient mineralocorticoid, glucocorticoid, and androgens

54
Q

Primary vs secondary disorders

A

Primary: something affects the production or quantity or quality of the hormone itself

Secondary: Something disrupts the hormone axis that is usually able to respond to fluctuating hormone level

55
Q

Destruction of ___% of the adrenal glands must occur before clinical signs of adrenal insufficiency appear

A

> 90%

56
Q

Type 1 diabetes occurs d/t injury to ____ in the pancreaas

A

Beta cells, responsible for insulin production

57
Q

Statins are _____ inhibitors. Which

A

HMG-CoA reductase inhibitors

- increase HDL:LDL

58
Q

How does metformin help control blood sugars in pts with diabetes?

A

Decreases hepatic gluconeogenesis and increases insulin sensitivity

59
Q

Malignant hyperthermia is closely associated to which 3 diseases?

A
  1. Central core disease
  2. Multi-minicore disease
  3. King-Denborough syndrome
60
Q

Lipolysis will increase or decrease with:

  • alpha 2 stimulation
  • beta 2 and 3 stimulation
A
  • alpha 2 stimulation: inhibit

- beta 2 and 3 stimulation: stimulate

61
Q

Benefits of carbohydrate rich drinks given 2h before surgery ?

A

increases insulin sensitivity (decrease insulin resistance)

Stress of sx = hyperglycemia
Fasting state = low insulin

62
Q

What catecholamine predominates in this type of pheochromocytoma?

  • Paroxysmal
  • Sustained
A

Paroxysmal: EPi

Sustained: Norepi

63
Q

How does a pt’s insulin regimen get affected perioperatively if they are on:

  • Rapid/short acting:
  • Intermediate:
  • Long acting:
A

Rapid/short acting:
- continue

Intermediate:

  • take 75% nl dose night before sx
  • take 50% nl dose day of sx

Long acting:
- take 50% nl dose morning of sx

64
Q

Concern about pts on chronic glucocorticoid therapy?

A

Can suppress the hypothalamic-pituitary adrenal axis ->

insufficient response by adrenal glands to the stress of major sx

65
Q

Categories of risk of adrenal insufficiency: (what dose of steroids are they on)
Low
Intermediate
High

A

Low:

  • Any dose GC < 3 weeks
  • Prednisone <5mg/d or 10mg q other day

Intermediate:

  • Prednisone 5-20mg/d > 3 weeks
  • Chronic inhaled or topical GC

High:

  • Cushing syndrome 2/2 to GC
  • Prednisone >20mg/d > 3 weeks

*High risk pts should be considered for periop stress dose steroids

66
Q

During a stress response (ie. surgery), which hormones decrease?

A

T3/T4
Growth RELEASING hormone

*almost every other hormone increases or stays same

67
Q

Insulin effects on:

Adipocytes

A

Increase glucose uptake
Increase Fatty acid storage/synthesis

*insulin has primarily anabolic effects and inhibits catabolic processes

68
Q

Insulin effects on:

myocytes

A

Increase glucose uptake
Increase amino acid uptake
Increase glycogen storage
Increase protein synthesis

*insulin has primarily anabolic effects and inhibits catabolic processes

69
Q

Insulin effects on:

Hepatocytes

A

Increase macronutrient uptake
Increase Fatty acid storage/synthesis
Increase glycogen synthesis

*insulin has primarily anabolic effects and inhibits catabolic processes

70
Q

During surgical stress, the body enters a state of insulin resistance d/t what?

A

release of stress hormones (catecholamines, cortisol, glucagon)

71
Q

insulin has primarily ______effects and inhibits ______ processes

A

anabolic

catabolic

72
Q

Glucagon STIMULATES _______ and _______

A

glycogenolysis
- break down glycogen to glucose

gluconeogenesis
- glucose synth by liver

*both improve blood glucose [ ]

73
Q

How does glucagon affect gastric motility and biliary sphincter and lower esophageal sphincter tone?

A

DECREASE

74
Q

Lab derangements with corticosteroid use

A
  1. Leukocytosis
  2. Polycythemia
  3. Hyperglycemia
  4. Mild hypernatremia
  5. Hypokalemia
  6. Hypercalciurea
75
Q

Insulin is secreted by ____, and is metabolized by _____

A

B-islet cells of pancreas

Kidneys and liver

76
Q

How does hyperparathyroidism affect neuromuscular blockers?

A

Hypercalcemia Antagonizes nondepolarizing NMBs

- need to increase dose of Roc

77
Q

Which cell is MOST dependent on insulin for the majority of the cells’ glucose uptake?

A

Cardiac myocyte

(Remember insulin's effects on myocytes: 
Increase glucose uptake
Increase amino acid uptake
Increase glycogen storage
Increase protein synthesis)
78
Q

Which cells are dependent on insulin for the majority of glucose uptake?

A
  1. Hepatocytes
  2. Immune cells
  3. Erythrocytes
  4. Brain neurons
  5. Cardiac

*Cardiac cells are MOST dependent on insulin for the majority of the cells’ glucose uptake?

79
Q

Which foods are associated with a latex allergy?

A
  1. Avocados
  2. Bananas
  3. Chestnuts
  4. Kiwi
  5. Papayas
  6. Potatoes
  7. Tomatoes
80
Q

The majority of latex allergies are d/t what type of reaction?

A

Irritant contact dermatitis

*NOT d/t immune mediated hypersensitivity reactions

81
Q

If you suspect a pt is having a latex allergy, what lab should be drawn?

A

serum mast cell tryptase level w/in 15-60min and again after 24 hr
- Increased if +

82
Q

Primary vs secondary disorders

A

Primary: something affects the production or quantity or quality of the hormone itself

Secondary: Something disrupts the hormone axis that is usually able to respond to fluctuating hormone level

83
Q

(Hyperthyroidism / Hypothyroidism) is more commonly associated with pleural effusions

A

Hypothyroidism

84
Q

Hyperthyroidism is associated with hematologic effects?

A

Anemia

Thrombocytopenia

85
Q

Insulin and glucagon utilizes the ____ pathway within the _____

A

cAMP signaling

hepatocyte

86
Q

Which cells in the body specifically use the Inositol triphosphate-3 (IP-3) second messenger pathway?

A

Cardiac myocytes
- increase cytoplasmic calcium ions -> activates ryanodine receptor on sarcoplasmic reticulum -> calcium induced calcium release form SR

87
Q

How does cortisol directly influence potassium homeostasis?

A
  • Enhances sodium and potassium exchange

- Enhances renal potassium secretion

88
Q

Etomidate inhibits the synthesis of cortisol transiently and should be avoided in pts with ______

A

adrenal insufficiency

  • ie: addison disease aka primary adrenal insufficiency
  • adrenal glands unable to produce sufficient quantities of glucocorticoid
89
Q

What happens in secondary adrenal insufficiency?

A

failure in adequate production of CRH or ACTH secondary to hypothalamic/pituitary disease or suppression

*Unlike Addison disease, there is only glucocorticoid deficiency with secondary disease

Anesthesia 101 (38 decks)

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