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Apex > Endocrine > Flashcards

Endocrine Flashcards

1
Q

What two hormones does the posterior pituitary release?

A

Oxytocin
ADH

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2
Q

What six hormones does the anterior pituitary release?

A

FLAG PiT

F: follicle-stimulating hormone
L: Luteinizing hormone
A: Adrenocorticotropin
G: growth hormone

P: prolactin
“Ignore I”
T: thyroid-stimulating hormone

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3
Q

What are the primary hypothalamic hormones?

A

“Let’s Come Together and release”

“Promote Growth (in and out) “

Luteinizing hormone-releasing hormone
Corticotropin-releasing hormone
Thyrotropin-releasing hormone
Prolactin hormone releasing/inhibiting hormone
Growth hormone releasing/inhibiting hormone

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4
Q

Luteinizing hormone -releasing hormone targets what in the anterior pituitary?

A

Follicle stimulating hormone (FSH)
Luteinizing hormone

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5
Q

Corticotropin-releasing hormone stimulates what in the anterior pituitary?

A

Andrenocorticotropic hormone (ACTH)

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6
Q

What does the thyrotropin-releasing hormone stimulate in the anterior pit?

A

Thyroid stimulating hormone (TSH)

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7
Q

What does prolactin-releasing factor and prolactin-inhibiting factor stimulate in the anterior pituitary?

A

Prolactin (either increase or decrease)

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8
Q

What does the growth hormone releasing/inhibiting hormone stimulate in the anterior pituitary?

A

Growth hormone (increase or decrease)

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9
Q

What does hypersecretion of follicle stimulating hormone cause?

A

Early puberty

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10
Q

What does hyposecretion of follicle stimulating hormone create?

A

Infertility

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11
Q

What does hypersecretion of Luteinizing hormone do?

A

Early puberty

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12
Q

What does HYPOsecretion of Luteinizing hormone produce?

A

Infertility

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13
Q

What does hypersecretion of adrenocorticotropic hormone produce?

A

Cushing’s disease

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14
Q

What does hyposecretion of adrenocorticotropic hormone produce?

A

Addison’s

Secondary adrenal insufficiency

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15
Q

What does hypersecretion of thyroid stimulating hormone produce?

A

Hyperthyroidism

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16
Q

What does hyposecretion of thyroid stimulating hormone produce?

A

Hypothyroid or cretinism

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17
Q

What does hypersecretion of prolactin hormone produce?

A

Infertility

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18
Q

What does hyposecretion of prolactin hormone produce?

A

Menstrual dysfunction

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19
Q

What does hypersecretion of growth hormone produce?

A

Acromegaly
Gigantism

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20
Q

What does hyposecretion of growth hormone produce?

A

Dwarfism

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21
Q

What two hormones are NOT affected by a negative feedback?

A

Oxytocin
Prolactin (neural control)

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22
Q

What is syndrome of inappropriate ADH secretion?

A

Too much ADH

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23
Q

What is diabetes Insipidus?

A

Too little ADH

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24
Q

What are some traits of SIADH?

A

HYPOnatremia (< 135)
Euvolemia/hypervolemic
PLASMA ~ osmolarity < 275
URINE ~ hyperosmolar (low volume)

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25
Q

What is the tx for SIADH?

A

Fluid restriction
Demeclocycline
Give NaCl if symptomatic

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26
Q

What are some traits with Diabetes Insipidus?

A

Polyuria
PLASMA: euvolemic/hypovolemic
PLASMA: hypertonic > 290
PLASMA Na: > 145

URINE: osmolarity low
Normal Na

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27
Q

What is the treatment for DI?

A

DDAVP or vasopressin

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28
Q

What does over-secretion of growth hormone AFTER adolescence cause?

A

ACromegaly

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29
Q

What does over secretion of the growth hormone BEFORE puberty cause?

A

Gigantism

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30
Q

What are some anesthetic consideration for acromegaly?

A

Distorted face (diff mask)
Large tongue, teeth ~ diff intubation
Subglottic narrowing ~ smaller ETT
Turbinate enlargement ~ avoid nasal

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31
Q

What is the most common cause of SIADH?

A

Traumatic brain injury

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32
Q

What is the most common cause of diabetes Insipidus?

A

Pituitary surgery

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33
Q

What are 4 differing traits of T3 when compared to T4?

A

Higher potency
Shorter half life
Less protein bound
Smaller concentration in the blood

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34
Q

What are four traits about T4?

A

Higher concentration in blood
More protein binding
Less potency
Longer half-life

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35
Q

What does T4 and T3 stimulate in the negative feedback loop?

A

The ANTERIOR PIT! Not the hypothalamus

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36
Q

how does an increased thyroid hormone affect the body?

A

Increased Thyroid hormone > ^ BMR > ^ O2 consumption > ^ CO2 production

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37
Q

How does HYPER thyroid affect the heart?

A

Increased inotropy
Increased contractility
Increased lusitropy (rate of relaxation)
Decreased SVR

*** this also increased the number and sensitivity to beta receptors

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38
Q

How does hyperthyroidism affect the resp system?

A

Increased BMR > ^ O2 consumption ^ Ve (Increased RR)

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39
Q

How does hyperthyroidism affect the MAC?

A

Does not affect MAC

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40
Q

How does hyperthyroidism affect the GI system?

A

Hypermotility

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41
Q

How does hyperthyroidism affect the musculoskeletal?

A

Tremors

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42
Q

What is the diagnosis for hyperthyroidism?

A

Low TSH and high T3 and T4

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43
Q

What is the diagnosis for HYPOthyroidism?

A

High TSH, low T3 and T4

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44
Q

what is the most common cause of HYPERthyroidism?

A

Graves’s disease

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45
Q

What is the most common cause of HYPOthroidism?

A

Hashimoto’s thyroiditis

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46
Q

What is a complication of severe hypothyroidism?

A

Myxedema coma

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47
Q

Emergency surgery of a patient with hyperthyroid warrants administration of what?

A

Beta-blockers, glucocorticoids, potassium iodine and PTU should be started at this time

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48
Q

If a patient has a goiter, how should you anticipate the airway?

A

Awake intubation

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49
Q

When does hypocalcemia following Thyroid surgery usually occur?

A

24-48 hours after surgery

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50
Q

What is thyroid storm?

A

Medical emergency ~typically happens 6-18 hrs after surgery

Fever > 38.5
Tachycardia/afib
HTN
CHF
Shock
N&V

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51
Q

How do you manage thyroid storm?

A

Remember the 4 Bs

Block synthesis ~ PTU
Block Release ~ radioactive iodine
Block Conversion of T4 to T3 ~ PTU/propranolol
Block beta receptors ~ esmolol

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52
Q

What is the medical management for hypothyroidism?

A

Levothyroxine (synthetic T4)

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53
Q

Is an inhalation induction fast or slower with hypothyroidism?

A

FASTER

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54
Q

How does hypothyroidism affect MAC?

A

It doesn’t

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55
Q

What do osteoblasts do?

A

Bones cells that PROMOTE BONE DEPOSITION ~ they add Ca to the bone > reducing serum ionized Ca

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56
Q

What do osteoclasts do?!

A

Promote bone RESORPTION ~ remove Ca from bone to increase free ionized Ca

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57
Q

What is PTH MOA?

A

Site of release: parathyroid
Effect: ^ ionized Ca
^ Ca resorption from bone
Activates Calcitriol (increases Ca absorption in the gut)
^ Ava reabsorption from kidneys

58
Q

What is Calcitonin MOA?

A

Site of release: thyroid gland
Effect: decreases ionized Ca
Increased Ca deposition (into bone)
Increases phosphate

59
Q

What is the most common cause of hypercalcemia?

A

Primary hyperparathyroidism

60
Q

What is the most common cause of secondary hyperparathyroidism?

A

Chronic kidney disease

(Remember renal osteodystrophy)

61
Q

What is the most common cause of primary hypoparathyroidism?

A

Iatrogenic gland removal during thyroidectomy

62
Q

What does the zona glomerulosa contain?

A

Mineralcorticoids (aldosterone)

“Minerals glow ~ merulosa”

63
Q

What does the zona fasciculata contain?

A

Glucocorticoids

“Glucose/steroids make you fast ~ciculata”

64
Q

What does the zona reticularis contain?

A

Androgens

“Reticular = testicular

65
Q

What is the mnemonic for the adrenal cortex?

A

Glomerulosa ~ SALT
Fasciculata ~ SUGAR
Reticularis ~ SEX

66
Q

What two catecholamines does the adrenal medulla create?

A

Epi (80%)
Norepinephrine (20%)

67
Q

What 3 things is Aldosterone release increased by?

A

RAAS
Hyperkalemia
Hyponatremia

68
Q

What is the primary glucocorticoid?

A

Cortisol

69
Q

How does cortisol improve hemodynamics?

A

Increases the number and sensitivity of beta receptors on the myocardium ~ also required for the vasculature to respond to catecholamines

70
Q

What medication is an analog of cortisol making it a perfect med to treat adrenocortical insufficiency (ADDISONS?

A

Prednisone
Equivalent dose is 5 mg

71
Q

Which three synthetic steroids have ZERO mineralocorticoid effects?

A

Dexamethasone, betamethasone, and triamcinolone

72
Q

What are the 3 most relevant endogenous steroids?

A

Cortisol
Cortisone
Aldosterone

73
Q

What is cushing’s disease?

A

Excessive cortisol

74
Q

What is addison’s disease?

A

Insuffiencient cortisol

75
Q

What is Conn’s syndrome?

A

Excess aldosterone

76
Q

What are the clinical features of Conn’s syndrome?

A

Increased aldosterone

Hypokalemia
HTN
Metabolic Alkalosis

77
Q

Ingestion of what can mimic hyperaldosteronism?

A

Licorice!

78
Q

What is an ACTH-dependent cause of Cushing disease?

A

Increase in ACTH stimulate cortisol release ~ pituitary adenoma

79
Q

What is an ACTH-independent cause of Cushing’s disease?

A

Tumor releases cortisol regardless of ACTH

Adrenal cortex is messed up!

80
Q

What are some glucocorticoid effects in Cushing’s disease?

A

HYPERglycemia
Weight gain (moon face, hump, central obesity)
Risk of infection
Osteoporosis musc weakness

81
Q

What are some of the mineralocorticoid effects in Cushing’s disease?

A

Hypokalemia
HTN
Metabolic alkalosis

82
Q

What are some of the androgens effects in Cushing’s disease?

A

Women become masculinized (hirsutism)
Men become feminized (impotence)

83
Q

What is the treatment for Cushing’s disease?

A

Depends on type

Transsphenoidal resection if the pituitary gland (pituitary problem)

Adrenalectomy (if adrenal tumor)

84
Q

What is Addison’s disease?

A

Primary Adrenal insufficiency (destruction of all cortical zones)

Autoimmune destruction of both adrenal glands > glands don’t secrete enough steroid hormones

Decreased production in all the zones! GFR!!

85
Q

What is Acute adrenal crisis?

A

Medical emergency

Chronic adrenal insufficiency faced with a stressful moment.

Hemodynamic instability
Fever
Hypoglycemia
Impaired mental state

86
Q

What are some features of Addison’s/AI?

A

Hypotension
Hypoglycemia
Hyperkalemia
Muscle weakness/fatigue
Metabolic acidosis
**hyperpigmentation

87
Q

How do you treat acute adrenal crisis?

A

Steroid replacement therapy (hydrocortisone ~ 100 + 100-200 q 24h)
ECF volume expansion (D5NS)
Hemodynamic support

88
Q

What would be the preoperative hydrocortisone dose for a superficial surgery? This is with a patient in continuous steroid therapy

A

None

89
Q

What would be the preoperative hydrocortisone dose for a minor surgery? This is with a patient in continuous steroid therapy

A

25 mg IV

90
Q

What would be the preoperative hydrocortisone dose for a moderate surgery? This is with a patient in continuous steroid therapy

A

50-75mg

91
Q

What would be the preoperative hydrocortisone dose for a major surgery? This is with a patient in continuous steroid therapy

A

100 mg

92
Q

What cell produces glucagon?

A

Alpha cells

93
Q

What cells produce insulin?

A

Beta cells

94
Q

What cells produce somatostatin?

A

Delta cells

95
Q

What cells produce pancreatic polypeptide?

A

PP cells

96
Q

What are some things that stimulate insulin release?

A

Anything that raises glucose will stimulate insulin release.

PNS stimulation (after eating a meal)
SNS stimulation
Beta agonists
Cortisol
catecholamines

97
Q

What are some things that reduce insulin release?

A

Anything that reduces blood glucose will inhibit insulin.

Volatile anesthetics
Beta antagonists

98
Q

What are some things that stimulate glucagon release?

A

Anything that reduces blood glucose will stimulate glucagon release

Hypoglycemia
Stress
Trauma
Sepsis
Beta agonists

99
Q

What are some things that reduce glucagon release?

A

Anything that increases blood glucose will inhibit glucagon release

Somatostatin/insulin

100
Q

What are some other indications for glucagon?

A

Glucagon increases myocardial contractility by increasing cAMP

Great for beta blocker overdose
CHF
Low CO after CPB
Improving MAP with anaphylaxis

101
Q

What is somatostatin?

A

Growth hormone-inhibiting hormone ~ regulates hormone output from the islet cells.

Released by pancreatic delta cells
Inhibits insulin and glucagon
Inhibits splanchnic blood flow, gastric motility, and gall bladder contraction

102
Q

What does pancreatic polypeptide do?

A

Inhibits pancreatic exocrine secretion, gallbladder contraction, gastric acid secretion, and gastric motility

103
Q

Which two organs don’t need insulin for glucose uptake?

A

Brian and liver

104
Q

What is the criteria for diabetes?

A

Fasting plasma glucose > 120
Random glucose > 200 (with symptoms)
Two-hour plasma glucose > 200 mg/dL during oral glucose test
A1C > 6.5%

105
Q

What is type 1 DM characterized by?

A

Lack of insulin production

106
Q

What is type II DM characterized by?

A

Lack of insulin + insulin resistance

107
Q

What are the characteristics of metabolic syndrome?

A

Fasting glucose of 100-110
Abdominal obesity (> 40 in in men; > 35 in women)
Triglyceride > 150
HDL < 40 in M; < 50 in F
BP > 130/85

108
Q

What is the BBG for a DMI patient in diabetic ketoacidosis?

A

> 250

109
Q

What is the BBG for a DM II patient in hyperglycemia hyperosmolar state?

A

> 600 mg/dL

110
Q

What is the classic triad of symptoms associated with diabetes mellitus?

A

Polydipsia
Polyuria
Dehydration

111
Q

What sign is suggestive of an increased risk of difficult intubation in the DM patient?

A

Prayer sign.

112
Q

What are four CV changes in a diabetic patient with autonomic neuropathy?

A

Orthostatic hypotension
Reduced vagal tone ~ tachycardia
Painless myocardial ischemia
Risk of dysrhythmias

113
Q

What are the 3 main medications used to treat peripheral neuropathy?

A

Anticonvulsants
NSAIDs
Antidepressants

114
Q

What are biguanides?

A

Metformin

Inhibit gluconeogensis and glycogenolysis in the liver and decrease insulin resistance

***THESE DO NOT CAUSE HYPOGLYCEMIA

115
Q

What are the risks of biguanides?

A

Lactic acidosis
May cause vitamin B12 deficiency

Discontinue > 24 hours before surgery

116
Q

What are Sulfonylureas?

A

End with “ide” ~ taking a “ride” on the Surf”

Stimulate insulin secretion from beta cells

117
Q

What are the risk of sulfonylureas?

A

***RISK OF HYPOGLYCEMIA

avoid if sulfa allergy
^ cardiac morbidity in high-risk patients (inhibits myocardial conditioning)

***discontinue 24-48 hours before surgery

118
Q

What are megalitinides?

A

End in “glinide” ~ “GLIDING in a MEGA LIT room”

Stimulate insulin secretion from beta cells

119
Q

What are some risks with megalitinides?

A

HYPOGLYCEMIA

120
Q

What are Thiazolidinediones?

A

“Get in the ZONE, the THIAZONE”

**rosiglitazone

Decreased peripheral insulin resistance and increased hepatic glucose utilitization

121
Q

What are the risks of thiazolidinediones?

A

***NO HYPOGLYCEMIA
contraindicated in liver failure
Expands ECF~ risk of edema

122
Q

Which oral hypoglycemia agents cause hypoglycemia?

A

Sulfonylurea
Megalitinides
Glucagon-like peptide-1receptor agonists
Dipeptidyl-peptides-4 inhibitors
Amylin Agonists (with insulin)

123
Q

What is the only insulin that can be given IV?

A

Rapid acting ~ Regular insulin

124
Q

How much total insulin output is there in a day?

A

40 U/day

125
Q

Stimulation of what increases insulin secretion?

A

PNS stimulation
Beta-2

126
Q

Stimulation of what decreases insulin secretion?

A

Alpha-2 stimulation

127
Q

What is very rapid-acting insulin? What is it’s onset, peak, and Duraiton?

A

(Lispro, insulin aspart, glulisine)

O: 5-10
P: 45-75 mins
D: 3 hours

128
Q

What is rapid-acting insulin? What is it’s onset, peak, and Duraiton?

A

Regular

O: 30 mins
P: 3 hours
D: 6-7 hrs

129
Q

What is intermediate-acting insulin? What is it’s onset, peak, and Duraiton?

A

NPH

O: 2 hours
P: 6ish hours
D: 20ish hours

130
Q

What is long acting insulin? What is it’s onset, peak, and Duraiton?

A

Detemir
Glargine

O: 2 hours
P: 7ish
D: 24

131
Q

What is ultra-long acting insulin? What is it’s onset, peak, and Duraiton?

A

Degludec

O: 2 hours
P: ~
D: 40 hours

132
Q

What are the goals of insulin therapy?

A

A1C < 7%
Before a meal ~ BBG 70-130
After a meal ~BBG < 180

133
Q

What are the S&S of hypoglycemia?

A

SNS response

(Tachycardia, increased BP, diaphoresis)

BUT Brian requires glucose too ~ seizures, coma, brain damage, death

134
Q

What drugs should you avoid in carcinoid syndrome?

A

Avoid drugs that precipitate hormone release ~
drugs that:
> release histamine (morphine)
> stimulate the SNS (ketamine)
> augment hormone increase (norepinephrine)

135
Q

What is the primary treatment for carcinoid syndrome?

A

Octreotide

136
Q

What are the most common signs of carcinoid syndrome?

A

Flushing and diarrhea

137
Q

What are the 3 main hormones involved in carcinoid syndrome?

A

Histamine
Kinins and Kallikrein
Serotonin

138
Q

What drugs should you give during carcinoid crisis?

A

Somatostatin (octreotide)
Antihistamines
5-HT3 antagonists
Steroids
Phenylephrine or vasopressin for hypotension

139
Q

What drugs should you avoid in carcinoid syndrome?

A

Histamine-releasing drugs (morphine, meperidine, Atracurium, and sux)

Exogenous catecholamines

Sympathomimetic agents

140
Q

Which drugs antagonize the hypoglycemia effect of insulin?

A

Epinephrine
Glucagon

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