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APEX-KLE > KLE-Endocrine modules 10-19 > Flashcards

KLE-Endocrine modules 10-19 Flashcards

1
Q

What are the 2 most potent synthetic steroids

A

Dexamethasone

Betamethasone

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2
Q

What are the 2 least potent synthetic steroids

A

Prednisone

Prednisolone

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3
Q

Which synthetic steroids have glucocorticoid effects but no mineralocorticoid effect

A

Dexamethasone
Triamcinolone
Betamethasone

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4
Q

How does methylprednisolone and dexamethasone glucocorticoid potency compare

A

dexamethasone is 5 times more potent

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5
Q

Which synthetic steroid is the best choice for adrenocortical insufficiency and why

A

Prednisone

It is an analog of cortisol

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6
Q

Which endocrine disease would be treated with prednisone

A

Addison’s disease

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7
Q

What are the 3 most relevant endogenous steroids

A

Cortisol
Cortisone
Aldosterone

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8
Q

Which steroid is best for addison’s disease

A

Prednisone

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9
Q

What is Conn’s disease

A

Excess of aldosterone

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10
Q

What is primary hyperaldosteronism

A

Inc aldosterone release from adrenal gland

normal renin activity

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11
Q

What is secondary hyperaldosteronism

A

Inc aldosterone stimulus from extra-adrenal source

Increased renin activity

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12
Q

What are causes of primary hyperaldosteronism

A
  1. Aldosteronoma
  2. pheochromocytoma
  3. primary hyperthyroidism
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13
Q

What are causes of secondary hyperaldosteronism

A

Renovascular HTN

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14
Q

What are 3 clinical features of hyperaldosteronism

A
  1. HTN (Na+/H2O retention)
  2. Hypokalemia (K+ wasting)
  3. Metabolic acidosis (H+ wasting)
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15
Q

What are 4 treatments of hyperaldosteronism

A
  1. removal of aldosterone secreting tumor
  2. Aldosterone antagonist (spironolactone, eplerenone)
  3. K+ supplementation
  4. Na+ restriction
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16
Q

What are 2 aldosterone antagonists

A
  1. spironolactone

2. eplerenone

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17
Q

What are anesthetic considerations for the hyperaldosterone pt w/ hypokalemia

A
  1. muscle weakness/cramping
  2. inc sensitivity to ND-NMB
  3. U wave on EKG
  4. avoid hyperventilation (activates H/K pump and dec serum K)
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18
Q

What are CV anesthetic considerations for the hyperaldosterone pt

A

HTN = caution w/ fluid overload

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19
Q

What herbal supplement can cause a syndrome that resembles hyperaldosteronism

A

licorice

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20
Q

What is Cushing’s syndrome

A

Result of cortisol excess either from overproduction or exogenous administration

Excess ACTH

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21
Q

What are 3 causes of Cushing’s syndrome

A
  1. Pituitary adenoma
  2. Adrenal tumor
  3. Acute ectopic ACTH syndrome
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22
Q

What are 6 glucocorticoid effects of Cushing’s syndrome

A
  1. hyperglycemia
  2. weight gain (central obesity)
  3. increased risk of infection
  4. osteoporosis
  5. muscle weakness
  6. mood disorder
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23
Q

What are 3 mineralocorticoid effects of Cushing’s syndrome

A
  1. HTN
  2. Hypokalemia
  3. Metabolic alkalosis
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24
Q

What are 5 androgenic effects of Cushing’s syndrome (gender specific)

A

Women

  1. hirsutism
  2. hair thinning
  3. acne
  4. amenorrhea

Men

  1. gynecomastia
  2. impotence
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25
Q

3 treatments for Cushing’s disease

A
  1. transsphenoidal resection of pituitary gland
  2. pituitary radiation
  3. adrenalectomy
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26
Q

What are 3 intraoperative anesthetic considerations for Cushing’s disease

A
  1. Strict aseptic technique
  2. Careful positioning to reduce skin and bone injury
  3. Consider s/sx for hyperaldosteronism (dec K+, alkalosis)
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27
Q

What are 2 postop consideration for pt w/ Cushing’s disease

A
  1. postop steroids

2. DI post pituitary resection

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28
Q

Pathophysiology of primary adrenal insufficiency (Addison’s)

A
  1. Adrenal glands don’t secrete enough hormone

2. ACTH increases to try and stimulate failing adrenal gland

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29
Q

What are 3 causes of Addison’s disease

A
  1. autoimmune destruction of both adrenals
  2. HIV
  3. TB
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30
Q

What are 5 causes of secondary adrenal insufficiency

A
  1. exogenous steroid administration
  2. HPA dz d/t tumor
  3. infection
  4. surgery
  5. radiation
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31
Q

What is the pathophysiology of secondary adrenal insufficiency

A

decreased CRH or ACTH release

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32
Q

Causes of acute adrenal crisis

A

chronic AI in the presence of stress

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33
Q

What are 8 clinical features of adrenal insufficiency

A
  1. muscle weakness/fatigue
  2. HoTN
  3. Hypoglycemia
  4. Hyponatremia
  5. Hyperkalemia
  6. Metabolic acidosis
  7. N/V
  8. Hyperpigmentation
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34
Q

Electrolytes altered by adrenal insufficiency

A
  1. hyponatremia

2. hyperkalemia

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35
Q

Acid base imbalance of adrenal insufficiency

A

metabolic acidosis

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36
Q

What are 4 clinical features of adrenal crisis

A
  1. hemodynamic instability
  2. fever
  3. hypoglycemia
  4. impaired mental status
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37
Q

Treatment for adrenal insufficiency

A

steroid replacement w/ 15-30 mg cortisol daily (prednisone)

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38
Q

What are treatments for acute adrenal crisis

A
  1. steroid replacement therapy (hydrocortisone)
  2. ECF volume expansion w/ D5NS
  3. Hemodynamic support
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39
Q

How does exogenous steroid administration affect the HPA

A

It suppresses ACTH release from the anterior pituitary gland

Pts will not be able to increase cortisol in response to perioperative stress

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40
Q

When is the risk for HPA suppression greatest for pts on chronic steroids

A

Taking prednisone >20 mg/day for >3 weeks

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41
Q

When is there a possibility of HPA suppression for pts taking chronic steroids

A

When taking prednisone 5-20 mg/day for >3 weeks

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42
Q

Should a pt taking prednisone <5 mg/day or less than 3 weeks receive a stress dose of steroids

A

It is not needed

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43
Q

Stress dose for steroids for pts having moderate surgeries (colon rsxn, total joint, total abd hyst)

A

50 - 75 mg IV

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44
Q

Stress dose for steroids for pts having major surgery (CV, thoracic, liver, whipple)

A

100-150 mg IV

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45
Q

How can etomidate cause adrenocortical suppression

A

By inhibiting 11-beta-hydroxylase

It is dose-dependent

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46
Q

What are the two hormone types secreted by the pancrease

A 
Exocrine = secretion into duodenum 
Endocrine = secreted into systemic circulation
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47
Q

What type of tissue in the pancreas secretes exocrine vs endocrine hormones

A

Acini tissue = exocrine

islets of Langerhans = endocrine hormones

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48
Q 
What hormones do the following pancreatic cells secrete
Alpha
Beta
Delta
PP
A 
Alpha = glucagon
Beta = insulin
Delta = somatostatin
PP = pancreatic polypeptide
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49
Q

What type of hormone is insulin

A

Anabolic hormone that promotes energy storage

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50
Q

6 ways insulin facilitates energy storage

A
  1. increases glucose permeability of skeletal muscle, liver, and fat
  2. converts CHO to glycogen in liver and muscle
  3. Converts excess CHO into fat
  4. Promotes cellular uptake of AA, K+, Mg++, and phos
  5. encourages protein synthesis
  6. stimulates Na/H-ATPase pump
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51
Q

Why does insulin decrease serum K+

A

by stimulating the Na/K-ATPase pump move K+ inside the cell

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52
Q

What is the primary stimulator of insulin release

A

Glucose

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53
Q

What hormones can stimulate insulin release

A

Anything that increases blood glucose:

  1. glucagon
  2. catecholamines
  3. cortisol
  4. growth hormone
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54
Q

What drug can increase insulin release

A

beta agonists

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55
Q

How does ANS affect insulin release

A

It can stimulate release by
-PNS stimulation after meal-
SNS stimulation

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56
Q

What are 2 drugs that can reduce insulin release

A
  1. volatile anesthetics

2. beta antagonists

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57
Q

How does insulin increase glucose uptake

A

It binds receptors. The beta subunits activate tyrosine kinase which activates insulin-receptor substrate

The cascade turns on GLUT4 transporter, allowing glucose uptake

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58
Q

Structure of insulin

A

2 alpha and 2 beta subunits joined by disulfide bonds

59
Q

Which organs do not require insulin for glucose uptake

A

liver

brain

60
Q

How is glucose uptake unique in the liver and brain

A

insulin is not required for glucose uptake

61
Q

At what glucose level does cerebral function decline

A

50 mg/dl or less

62
Q

What type of hormone is glucagon

A

Catabolic to promote energy release from adipose and liver

63
Q

What is the relationship of insulin and glucagon

A

they are physiologic antagonists

64
Q

What is the half-life of insulin vs glucagon

A 
insulin = 5 minutes
glucagon = 3-6 minutes
65
Q

Where are insulin and glucagon eliminated

A

Kidney’s and liver

66
Q

What are 5 setting that stimulate glucagon release

A
  1. hypoglycemia
  2. stress
  3. trauma
  4. sepsis
  5. beta agonists
67
Q

what are 2 settings glucagon secretion is reduced

A
  1. insulin

2. somatostatin

68
Q

What are cardiac effects of glucagon

A
  1. increase myocardial contractility
  2. increase HR
  3. increase AV conduction by increasing intracellular cAMP
69
Q

In what 4 situations can glucagon assist with CV function

A
  1. beta blocker OD
  2. CHF
  3. low CO after CPB or MI
  4. improve MAP during anaphylaxis
70
Q

Why is glucagon given during ERCP

A

to relax the biliary sphincter

71
Q

Side effects of glucagon

A

N/V

72
Q

What is another name for somatostatin

A

growth-hormone inhibiting hormone

73
Q

What does somatostatin regulate

A

hormone output from islet cells

74
Q

Somatostatin:
release=
primary function=
secondary function=

A

release= pancreatic delta cells
primary function= inhibits insulin and glucagon
secondary function= inhibits splanchnic BF, gastric motility, gall bladder contraction

75
Q

What is the function of pancreatic polypeptide

A

to inhibit pancreatic exocrine secretion, gallbladder contraction, gastric acid secretion and gastric motility

76
Q 
What pancreatic cells release the following hormones
pancreatic peptide
glucagon
somatostatin
insulin
A

pancreatic peptide = PP
glucagon = alpha
somatostatin = delta
insulin = beta

77
Q

Diagnostic criteria for DM

A
  1. Fasting plasma gluc >126
  2. Random gluc >200 + symptoms
  3. Two-hour plasma glucose >200 w/ oral glucose tolerance test
  4. Hgb A1C >6.5%
78
Q

Classic triad of DM symptoms

A
  1. polyuria
  2. dehydration
  3. polydipsia
79
Q

What are 5 features associated with metabolic syndrome

A
  1. fasting plasma glucose 100-110
  2. abd obesity
  3. serum trig >150
  4. serum HDL <40 men, <50 women
  5. BP >130/85
80
Q

5 Clinical features of DKA

A 
Gap acidosis
Hyperglycemia
ketoacidosis
hyperosmolarity
dehydration
81
Q

Why is ketosis not present with hyperglycemic hyperosmolar states

A

There is enough insulin produced to prevent ketosis

82
Q

6 Clinical features of hyperglycemic hyperosmolar states

A
  1. Ketosis not present
  2. Hyperglycemia extremes >660
  3. Extreme osmo elevation >330
  4. glycosuria
  5. non-anion gap acidosis
  6. hypovolemia
83
Q

Describe the insulin vs glucagon concentrations in DM1 vs DM2

A

DM 1:
insulin = very low, absent
Glucagon = high

DM2:
insulin = normal to high
glucagon = high, resistant to suppression

84
Q

What are 3 DM long-term effects in microvasculature

A
  1. neuropathy
  2. retinopathy
  3. nephropathy
85
Q

What are 3 DM long-term effects in macrovasculature

A
  1. CAD
  2. PVD
  3. Cerebrovascular dz
86
Q

What are 4 long-term physiologic effects of DM (not CV)

A
  1. Stiff joint syndrome
  2. Poor wound healing and infection
  3. Cataracts
  4. Glaucoma
87
Q

What are anesthetic concerns for diabetic ANS dysfunction

A
  1. Reduced vagal tone = tachycardia
  2. Risk of dysrhythmia
  3. Orthostatic HoTN
  4. impaired respiratory compensation to hypoxia and hypercarbia
  5. delayed gastric emptying
  6. impaired thermoregulation
  7. RA avoided in neuropathy
88
Q

Why do pts with diabetic ANS dysfunction have increased sensitivity to anesthetic drugs

A

D/t impaired respiratory compensation to hypoxia and hypercarbia

89
Q

How is thermoregulation altered in patients with diabetic ANS dysfunction

A

It is impaired, increasing risk for hypothermia

90
Q

Why is regional anesthesia a risk in diabetic pts w/ ANS dysfunction

A

It can worsen neurologic deficits in pts w/ diabetic polyneuropathy

91
Q

How does stiff joint syndrome in the diabetic pt affect airway management

A

reduced AO joint ROM increasing risk of difficult intubation

92
Q

What are initial symptom distribution of peripheral neuropathy

A

stocking and glove (lower legs and hands)

93
Q

What are 3 primary treatments for peripheral neuropathy

A

NSAIDs
Antidepressants
Anticonvulsants

94
Q

Why should LR be avoided in diabetic pts

A

the lactate can be converted to glucose and contribute to hyperglycemia

95
Q

What are 3 factors that can mask intraoperative hypoglycemia in the diabetic pt

A
  1. general anesthesia
  2. diabetic autonomic neuropathy
  3. use of beta-blockers
96
Q

List 4 CV changes in patients with diabetic autonomic neuropathy

A
  1. painless myocardial ischemia
  2. reduced vagal tone => tachycardia
  3. risk of dysrhythmias
  4. orthostatic hotn
97
Q

Metformin:
Class
MOA

A

Class= biguanides
MOA= inhibits gluconeogenesis and glycogenolysis in the liver.
decreases peripheral insulin resistance

98
Q

When should metformin be dc’d before surgery

A

24 hrs

99
Q

Which 5 oral hypoglycemic classes can lead to hypoglycemia

A
  1. Sulfonylureas
  2. megalitinides
  3. glucagon-like peptide-1 receptor agonists
  4. dipeptidyl-peptidase-4 inhibitors
  5. amylin agonists
100
Q

Which 3 oral hypoglycemic classes don’t have a risk of hypoglycemia

A
  1. biguanides
  2. thiazolidinediones
  3. a-glucosidase inhibitors
101
Q

What acid-base imbalance are pts at risk for taking metformin

A

Lactic acidosis

102
Q

Sulfonylureas MOA

A

stimulates insulin secretion from pancreatic beta cells

103
Q

Which oral hypoglycemics should be avoided in pts w/ sulfa allergy
ex:

A

sulfonylureas

glyburide
glipizide
glimepiride
tolbutamide

104
Q

Which oral hypoglycemics should be dc’d before surgery

A

Biguanides

Sulfonylureas

105
Q

Megalitinides:
MOA
examples

A

MOA= stimulates insulin secretion from pancreatic beta cells

Examples = repaglinide, nateglinide

106
Q

Thiazolidinediones:
MOA
Examples

A

MOA = decreases peripheral insulin resistance and increases hepatic glucose utilization

Examples = rosiglitazone, pioglitazone

107
Q

Which oral hypoglycemics can lead to edema

A

Thiazolidinediones expand ECF leading to edema

108
Q

Which oral hypoglycemic agents should be avoided in liver failure

A
  1. biguanides

2. thiazolidinediones

109
Q

Which oral hypoglycemics affect cardiac morbidity and how

A

sulfonylureas

The close Katp channels => inhibition of myocardial precondition => inc cardiac morbidity

110
Q

a-glucosidase inhibitors:
MOA
examples

A

MOA = slow digestion and absorption of CHO from GI tract

Ex= acarbose, miglitrol

111
Q

Glucagon-like peptide-1 receptor agonists:
MOA
Ex

A

MOA= increase insulin release from pancreatic beta cells, decrease glucagon release from alpha cells, prolong gastric emptying

Ex = exenatide, liraglutide

112
Q

Dipeptidyl-peptidase-4 inhibitor:
MOA
Ex

A

MOA = inc insulin release from pancreatic beta cells, decrease glucagon release from alpha cells

Ex= -liptin

113
Q

Amylin agonist:
MOA
Ex

A

MOA = inhibits glucagon release from pancreatic alpha cells and reduce gastric emptying

Ex = pramlintide

114
Q

Which 2 oral hypoglycemic classes promote peripheral glucose uptake

A
  1. biguanides

2. thiazolidinediones

115
Q

Which 3 oral hypoglycemic classes promote insulin secretion

A
  1. GLP-1RA (glucagon-like peptide-1 receptor agonists
  2. Sulfonylureas
  3. Meglitinides
116
Q

Under normal conditions, how much insulin is secreted by the pancreas

How it affected by a meal

A

~1 unit/hr into portal circulation

Meal = insulin output increases 5-10 fold

117
Q

What is total insulin output per day

A

40 units

118
Q

What type of ANS stimulation increases insulin secretion

A

Beta-2

PNS

119
Q

What type of ANS stimulation inhibits insulin secretion

A

Alpha-2

120
Q

Regular insulin:
onset
peak
duration

A 
onset = 30 min
peak = =2-4 hrs
duration = 6-8 hrs
121
Q

What are 3 classes of drugs that counter insulin effect

A
  1. epinephrine
  2. glucagon
  3. adrenocorticotrophic hormone
122
Q

Treatment for hypoglycemia

A

D50 (50 - 100 mL)

Glucagon (0.5 - 1.0 mg IV/SQ)

123
Q

What are 3 drug classes that can extend or enhance the hypoglycemic effect of insulin

A
  1. MAO-is
  2. Salicylates
  3. Tetracycline
124
Q

What effect does beta-2 and PNS stimulation have on insulin release

A

increases release

125
Q

What effect does alpha-2 stimulation have on insulin release

A

Decreases release

126
Q

What is the goal A1c for insulin therapy

A

<7%

127
Q

What is carcinoid syndrome

A

An inappropriate secretion of vasoactive substances from enterochromaffin cells
usually from tumors in the GI tract

128
Q

How does hepatic function affect carcinoid hormone

A

Carcinoid hormones are cleared by the liver
When significant liver dysfunction occurs, these hormones are cleared

If production of carcinoid hormone d/t tumor exceeds the liver’s clearance ability, then levels increase

129
Q

What are the most common signs of carcinoid syndrome

A

Flushing

Diarrhea

130
Q

What are 3 carcinoid hormones

A
  1. histamine
  2. kinins and kallikrein
  3. serotonin
131
Q

What are 4 effects of carcinoid syndrome histamine release

A
  1. bronchoconstriction
  2. vasodilation
  3. HoTN
  4. flushing
132
Q

What are 5 effects of carcinoid syndrome kinin/kallikrein release

A
  1. bronchoconstriction
  2. vasodilation
  3. HoTN
  4. flushing
  5. increases histamine release from mast cells
133
Q

What are 6 effects of carcinoid syndrome serotonin release

A
  1. bronchoconstriction
  2. vasoconstriction
  3. HTN
  4. SVT
  5. Diarrhea
  6. abd pain
134
Q

2 ways concurrent cardiac disease manifests with carcinoid syndrome

A
  1. pulmonic stenosis

2. tricuspid regurgitation

135
Q

5 things that should be avoided to minimize RV cardiac problems in patients with carcinoid syndrome

A

Protect RV by avoiding increased PVR

  1. hypoxia
  2. hypercarbia
  3. acidosis
  4. nitrous oxide
  5. light anesthesia
136
Q

What are 5 s/sx of carcinoid crisis

A
  1. tachycardia
  2. hyper-hypotension
  3. intense flushing
  4. abd pain
  5. diarrhea
137
Q

5 drugs appropriate for anesthetic use in pts with carcinoid syndrome

A
  1. somatostatin (octreotide)
  2. antihistamine (H1 and H2)
  3. 5-HT3 antagonists
  4. steroids
  5. phenylephrine for HoTN
138
Q

Why is somatostatin used in carcinoid syndrome

A

It inhibits the release of vasoactive substances from carcinoid tumors to improve hemodynamic stability

139
Q

Which antihistamines should be used in carcinoid syndrome

A

H1 and H2

benadryl and ranitidine

140
Q

4 drugs classes to avoid in pts with carcinoid syndrome

A
  1. histamine releasers
  2. Succinylcholine
  3. exogenous catecholamines
  4. sympathomimetics
141
Q

What histamine releasing drugs should be avoided in carcinoid syndrome

A
  1. morphine
  2. meperidine
  3. atracurium
  4. thiopental
  5. Succinylcholine
142
Q

Why should succinylcholine be avoided with carcinoid syndrome

A
  1. histamine release

2. fasciculations can cause hormone release from tumor

143
Q

How is hypotension addressed with carcinoid syndrome

A
  1. phenylephrine

2. octreotide

APEX-KLE (4 decks)

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