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

KLE-Endocrine modules 10-19 Flashcards

(143 cards)

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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
3 treatments for Cushing's disease
1. transsphenoidal resection of pituitary gland 2. pituitary radiation 3. adrenalectomy
26
What are 3 intraoperative anesthetic considerations for Cushing's disease
1. Strict aseptic technique 2. Careful positioning to reduce skin and bone injury 3. Consider s/sx for hyperaldosteronism (dec K+, alkalosis)
27
What are 2 postop consideration for pt w/ Cushing's disease
1. postop steroids | 2. DI post pituitary resection
28
Pathophysiology of primary adrenal insufficiency (Addison's)
1. Adrenal glands don't secrete enough hormone | 2. ACTH increases to try and stimulate failing adrenal gland
29
What are 3 causes of Addison's disease
1. autoimmune destruction of both adrenals 2. HIV 3. TB
30
What are 5 causes of secondary adrenal insufficiency
1. exogenous steroid administration 2. HPA dz d/t tumor 3. infection 4. surgery 5. radiation
31
What is the pathophysiology of secondary adrenal insufficiency
decreased CRH or ACTH release
32
Causes of acute adrenal crisis
chronic AI in the presence of stress
33
What are 8 clinical features of adrenal insufficiency
1. muscle weakness/fatigue 2. HoTN 3. Hypoglycemia 4. Hyponatremia 5. Hyperkalemia 6. Metabolic acidosis 7. N/V 8. Hyperpigmentation
34
Electrolytes altered by adrenal insufficiency
1. hyponatremia | 2. hyperkalemia
35
Acid base imbalance of adrenal insufficiency
metabolic acidosis
36
What are 4 clinical features of adrenal crisis
1. hemodynamic instability 2. fever 3. hypoglycemia 4. impaired mental status
37
Treatment for adrenal insufficiency
steroid replacement w/ 15-30 mg cortisol daily (prednisone)
38
What are treatments for acute adrenal crisis
1. steroid replacement therapy (hydrocortisone) 2. ECF volume expansion w/ D5NS 3. Hemodynamic support
39
How does exogenous steroid administration affect the HPA
It suppresses ACTH release from the anterior pituitary gland Pts will not be able to increase cortisol in response to perioperative stress
40
When is the risk for HPA suppression greatest for pts on chronic steroids
Taking prednisone >20 mg/day for >3 weeks
41
When is there a possibility of HPA suppression for pts taking chronic steroids
When taking prednisone 5-20 mg/day for >3 weeks
42
Should a pt taking prednisone <5 mg/day or less than 3 weeks receive a stress dose of steroids
It is not needed
43
Stress dose for steroids for pts having moderate surgeries (colon rsxn, total joint, total abd hyst)
50 - 75 mg IV
44
Stress dose for steroids for pts having major surgery (CV, thoracic, liver, whipple)
100-150 mg IV
45
How can etomidate cause adrenocortical suppression
By inhibiting 11-beta-hydroxylase | It is dose-dependent
46
What are the two hormone types secreted by the pancrease
``` Exocrine = secretion into duodenum Endocrine = secreted into systemic circulation ```
47
What type of tissue in the pancreas secretes exocrine vs endocrine hormones
Acini tissue = exocrine | islets of Langerhans = endocrine hormones
48
``` What hormones do the following pancreatic cells secrete Alpha Beta Delta PP ```
``` Alpha = glucagon Beta = insulin Delta = somatostatin PP = pancreatic polypeptide ```
49
What type of hormone is insulin
Anabolic hormone that promotes energy storage
50
6 ways insulin facilitates energy storage
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
51
Why does insulin decrease serum K+
by stimulating the Na/K-ATPase pump move K+ inside the cell
52
What is the primary stimulator of insulin release
Glucose
53
What hormones can stimulate insulin release
Anything that increases blood glucose: 1. glucagon 2. catecholamines 3. cortisol 4. growth hormone
54
What drug can increase insulin release
beta agonists
55
How does ANS affect insulin release
It can stimulate release by -PNS stimulation after meal- SNS stimulation
56
What are 2 drugs that can reduce insulin release
1. volatile anesthetics | 2. beta antagonists
57
How does insulin increase glucose uptake
It binds receptors. The beta subunits activate tyrosine kinase which activates insulin-receptor substrate The cascade turns on GLUT4 transporter, allowing glucose uptake
58
Structure of insulin
2 alpha and 2 beta subunits joined by disulfide bonds
59
Which organs do not require insulin for glucose uptake
liver | brain
60
How is glucose uptake unique in the liver and brain
insulin is not required for glucose uptake
61
At what glucose level does cerebral function decline
50 mg/dl or less
62
What type of hormone is glucagon
Catabolic to promote energy release from adipose and liver
63
What is the relationship of insulin and glucagon
they are physiologic antagonists
64
What is the half-life of insulin vs glucagon
``` insulin = 5 minutes glucagon = 3-6 minutes ```
65
Where are insulin and glucagon eliminated
Kidney's and liver
66
What are 5 setting that stimulate glucagon release
1. hypoglycemia 2. stress 3. trauma 4. sepsis 5. beta agonists
67
what are 2 settings glucagon secretion is reduced
1. insulin | 2. somatostatin
68
What are cardiac effects of glucagon
1. increase myocardial contractility 2. increase HR 3. increase AV conduction by increasing intracellular cAMP
69
In what 4 situations can glucagon assist with CV function
1. beta blocker OD 2. CHF 3. low CO after CPB or MI 4. improve MAP during anaphylaxis
70
Why is glucagon given during ERCP
to relax the biliary sphincter
71
Side effects of glucagon
N/V
72
What is another name for somatostatin
growth-hormone inhibiting hormone
73
What does somatostatin regulate
hormone output from islet cells
74
Somatostatin: release= primary function= secondary function=
release= pancreatic delta cells primary function= inhibits insulin and glucagon secondary function= inhibits splanchnic BF, gastric motility, gall bladder contraction
75
What is the function of pancreatic polypeptide
to inhibit pancreatic exocrine secretion, gallbladder contraction, gastric acid secretion and gastric motility
76
``` What pancreatic cells release the following hormones pancreatic peptide glucagon somatostatin insulin ```
pancreatic peptide = PP glucagon = alpha somatostatin = delta insulin = beta
77
Diagnostic criteria for DM
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
Classic triad of DM symptoms
1. polyuria 2. dehydration 3. polydipsia
79
What are 5 features associated with metabolic syndrome
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
5 Clinical features of DKA
``` Gap acidosis Hyperglycemia ketoacidosis hyperosmolarity dehydration ```
81
Why is ketosis not present with hyperglycemic hyperosmolar states
There is enough insulin produced to prevent ketosis
82
6 Clinical features of hyperglycemic hyperosmolar states
1. Ketosis not present 2. Hyperglycemia extremes >660 3. Extreme osmo elevation >330 4. glycosuria 5. non-anion gap acidosis 6. hypovolemia
83
Describe the insulin vs glucagon concentrations in DM1 vs DM2
DM 1: insulin = very low, absent Glucagon = high DM2: insulin = normal to high glucagon = high, resistant to suppression
84
What are 3 DM long-term effects in microvasculature
1. neuropathy 2. retinopathy 3. nephropathy
85
What are 3 DM long-term effects in macrovasculature
1. CAD 2. PVD 3. Cerebrovascular dz
86
What are 4 long-term physiologic effects of DM (not CV)
1. Stiff joint syndrome 2. Poor wound healing and infection 3. Cataracts 4. Glaucoma
87
What are anesthetic concerns for diabetic ANS dysfunction
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
Why do pts with diabetic ANS dysfunction have increased sensitivity to anesthetic drugs
D/t impaired respiratory compensation to hypoxia and hypercarbia
89
How is thermoregulation altered in patients with diabetic ANS dysfunction
It is impaired, increasing risk for hypothermia
90
Why is regional anesthesia a risk in diabetic pts w/ ANS dysfunction
It can worsen neurologic deficits in pts w/ diabetic polyneuropathy
91
How does stiff joint syndrome in the diabetic pt affect airway management
reduced AO joint ROM increasing risk of difficult intubation
92
What are initial symptom distribution of peripheral neuropathy
stocking and glove (lower legs and hands)
93
What are 3 primary treatments for peripheral neuropathy
NSAIDs Antidepressants Anticonvulsants
94
Why should LR be avoided in diabetic pts
the lactate can be converted to glucose and contribute to hyperglycemia
95
What are 3 factors that can mask intraoperative hypoglycemia in the diabetic pt
1. general anesthesia 2. diabetic autonomic neuropathy 3. use of beta-blockers
96
List 4 CV changes in patients with diabetic autonomic neuropathy
1. painless myocardial ischemia 2. reduced vagal tone => tachycardia 3. risk of dysrhythmias 4. orthostatic hotn
97
Metformin: Class MOA
Class= biguanides MOA= inhibits gluconeogenesis and glycogenolysis in the liver. decreases peripheral insulin resistance
98
When should metformin be dc'd before surgery
24 hrs
99
Which 5 oral hypoglycemic classes can lead to hypoglycemia
1. Sulfonylureas 2. megalitinides 3. glucagon-like peptide-1 receptor agonists 4. dipeptidyl-peptidase-4 inhibitors 5. amylin agonists
100
Which 3 oral hypoglycemic classes don't have a risk of hypoglycemia
1. biguanides 2. thiazolidinediones 3. a-glucosidase inhibitors
101
What acid-base imbalance are pts at risk for taking metformin
Lactic acidosis
102
Sulfonylureas MOA
stimulates insulin secretion from pancreatic beta cells
103
Which oral hypoglycemics should be avoided in pts w/ sulfa allergy ex:
sulfonylureas glyburide glipizide glimepiride tolbutamide
104
Which oral hypoglycemics should be dc'd before surgery
Biguanides | Sulfonylureas
105
Megalitinides: MOA examples
MOA= stimulates insulin secretion from pancreatic beta cells Examples = repaglinide, nateglinide
106
Thiazolidinediones: MOA Examples
MOA = decreases peripheral insulin resistance and increases hepatic glucose utilization Examples = rosiglitazone, pioglitazone
107
Which oral hypoglycemics can lead to edema
Thiazolidinediones expand ECF leading to edema
108
Which oral hypoglycemic agents should be avoided in liver failure
1. biguanides | 2. thiazolidinediones
109
Which oral hypoglycemics affect cardiac morbidity and how
sulfonylureas The close Katp channels => inhibition of myocardial precondition => inc cardiac morbidity
110
a-glucosidase inhibitors: MOA examples
MOA = slow digestion and absorption of CHO from GI tract Ex= acarbose, miglitrol
111
Glucagon-like peptide-1 receptor agonists: MOA Ex
MOA= increase insulin release from pancreatic beta cells, decrease glucagon release from alpha cells, prolong gastric emptying Ex = exenatide, liraglutide
112
Dipeptidyl-peptidase-4 inhibitor: MOA Ex
MOA = inc insulin release from pancreatic beta cells, decrease glucagon release from alpha cells Ex= -liptin
113
Amylin agonist: MOA Ex
MOA = inhibits glucagon release from pancreatic alpha cells and reduce gastric emptying Ex = pramlintide
114
Which 2 oral hypoglycemic classes promote peripheral glucose uptake
1. biguanides | 2. thiazolidinediones
115
Which 3 oral hypoglycemic classes promote insulin secretion
1. GLP-1RA (glucagon-like peptide-1 receptor agonists 2. Sulfonylureas 3. Meglitinides
116
Under normal conditions, how much insulin is secreted by the pancreas How it affected by a meal
~1 unit/hr into portal circulation Meal = insulin output increases 5-10 fold
117
What is total insulin output per day
40 units
118
What type of ANS stimulation increases insulin secretion
Beta-2 | PNS
119
What type of ANS stimulation inhibits insulin secretion
Alpha-2
120
Regular insulin: onset peak duration
``` onset = 30 min peak = =2-4 hrs duration = 6-8 hrs ```
121
What are 3 classes of drugs that counter insulin effect
1. epinephrine 2. glucagon 3. adrenocorticotrophic hormone
122
Treatment for hypoglycemia
D50 (50 - 100 mL) | Glucagon (0.5 - 1.0 mg IV/SQ)
123
What are 3 drug classes that can extend or enhance the hypoglycemic effect of insulin
1. MAO-is 2. Salicylates 3. Tetracycline
124
What effect does beta-2 and PNS stimulation have on insulin release
increases release
125
What effect does alpha-2 stimulation have on insulin release
Decreases release
126
What is the goal A1c for insulin therapy
<7%
127
What is carcinoid syndrome
An inappropriate secretion of vasoactive substances from enterochromaffin cells usually from tumors in the GI tract
128
How does hepatic function affect carcinoid hormone
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
What are the most common signs of carcinoid syndrome
Flushing | Diarrhea
130
What are 3 carcinoid hormones
1. histamine 2. kinins and kallikrein 3. serotonin
131
What are 4 effects of carcinoid syndrome histamine release
1. bronchoconstriction 2. vasodilation 3. HoTN 4. flushing
132
What are 5 effects of carcinoid syndrome kinin/kallikrein release
1. bronchoconstriction 2. vasodilation 3. HoTN 4. flushing 5. increases histamine release from mast cells
133
What are 6 effects of carcinoid syndrome serotonin release
1. bronchoconstriction 2. vasoconstriction 3. HTN 4. SVT 5. Diarrhea 6. abd pain
134
2 ways concurrent cardiac disease manifests with carcinoid syndrome
1. pulmonic stenosis | 2. tricuspid regurgitation
135
5 things that should be avoided to minimize RV cardiac problems in patients with carcinoid syndrome
Protect RV by avoiding increased PVR 1. hypoxia 2. hypercarbia 3. acidosis 4. nitrous oxide 5. light anesthesia
136
What are 5 s/sx of carcinoid crisis
1. tachycardia 2. hyper-hypotension 3. intense flushing 4. abd pain 5. diarrhea
137
5 drugs appropriate for anesthetic use in pts with carcinoid syndrome
1. somatostatin (octreotide) 2. antihistamine (H1 and H2) 3. 5-HT3 antagonists 4. steroids 5. phenylephrine for HoTN
138
Why is somatostatin used in carcinoid syndrome
It inhibits the release of vasoactive substances from carcinoid tumors to improve hemodynamic stability
139
Which antihistamines should be used in carcinoid syndrome
H1 and H2 | benadryl and ranitidine
140
4 drugs classes to avoid in pts with carcinoid syndrome
1. histamine releasers 2. Succinylcholine 3. exogenous catecholamines 4. sympathomimetics
141
What histamine releasing drugs should be avoided in carcinoid syndrome
1. morphine 2. meperidine 3. atracurium 4. thiopental 5. Succinylcholine
142
Why should succinylcholine be avoided with carcinoid syndrome
1. histamine release | 2. fasciculations can cause hormone release from tumor
143
How is hypotension addressed with carcinoid syndrome
1. phenylephrine | 2. octreotide

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