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Anesthesia Practice T3 > Endocrine Diseases > Flashcards

Endocrine Diseases Flashcards

1
Q

what does the anterior pituitary gland produce? (6)

A
  • adrenocorticotrophic hormone (ACTH)
  • thyroid stimulating hormone (TSH)
  • growth hormone (GH)
  • follicle-stimulating hormone (FSH)
  • lutenizing hormone (LH)
  • prolactin
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2
Q

what does the posterior pituitary gland secrete?

A
  • anti-diuretic hormone (ADH)

- oxytocin

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3
Q

how is secretion from the anterior pituitary regulated?

A

the hypothalamus

*transported via capillary portal system

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4
Q

what is the difference in how hormones are produced and secreted by the anterior and posterior pituitary?

A
  • anterior PRODUCES hormones and releases them into circulation under hypothalamus control
  • posterior SECRETES hormones produced in the hypothalmus after neural stimulation
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5
Q

where does prolactin act?

A

prolactin acts on the milk producing cells in the breast, causing lactation

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6
Q

where does ACTH act?

A

the adrenal cortex, releasing adrenalin

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7
Q

where does GH act?

A

the body’s cells, causing growth

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8
Q

what does TSH do?

A

acts on the thyroid, causing thyroxin secretion, stimulating growth and metabolism

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9
Q

where does FSH and LH act?

A

the testes and ovaries, causing
- androgen and sperm production
or
- egg production

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10
Q

where does oxytocin act?

A

the uterus, causing labour contractions

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11
Q

where does ADH act?

A

the kidneys, regulating water levels

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12
Q

what is the difference between T4 and T3?

A

T3 is more potent and less protein bound,

but glands release more T4 (10:1)

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13
Q

whats T4 called?

A

thyroxine

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14
Q

whats T3 called?

A

tri-iodothyronine

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15
Q

what is hyperthyroidism?

A

overproduction of T3 and/or T4

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16
Q

what can cause hyperthyroidism?

A
  • grave’s disease
  • TSH-secreting pituitary tumors
  • iatrogenic (caused by medicine)
  • thyoiditis
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17
Q

what are symptoms of hyperthyroidism?

A
  • weight loss
  • fatigue
  • arrhythmias
  • anxiety
  • exopthalmos (eyeballs popping out)
  • widened pulse P
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18
Q

what do T3 and T4 act on?

A

adenylate cyclase

- affects speed of rxns, O2 use, and energy output (heat production)

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19
Q

whats the most common cause of hyperthyroidism?

A

graves disease

*in women 20-40 yo

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20
Q

how do you treat hyperthyroidism?

A
  • antithyroids or beta antagonist

- surgical total, subtotal or lobar thyroidectomy

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21
Q

what intra-op considerations would you have for a PT with hyperthyroidism?

A
  • esmolol
  • no SNS stimulants
  • PTs usually hypovolemic
  • NO change of MAC
  • exaggerated hypotensive response upon induction
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22
Q

what are some post op concerns for hyperthyroidism?

A
  • RLN injury (horseness)
  • hematoma/tracheomalacia
  • hypocalcemia
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23
Q

what does radioiodine do? Specific to the thyroid?

A

destroys thyroid cell function

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24
Q

what pre-op info is relevant for elective thyroidectomy?

A
  • RHR
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25
Q

what is the most serious post-op threat for thyroid PTs?

A
  • thyrotoxic crisis (thyroid storm)

* usually 6-18hrs post-op

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26
Q

what are symptoms of thyrotoxic crisis?

A
  • abrupt axiety
  • fever
  • tachycardia
  • cardiovascular instability
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27
Q

treatment of thyrotoxic crisis?

A
  • IV cooled crystalloids
  • continuous esmolol infusion
  • dexamethasone (2mg q6)
    or cortisol (100-200 mg q8)
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28
Q

what can inhibit conversion of T4 to T3?

A

propylthiouracil (250-500 mg q6 PO)

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29
Q

what muscle relaxant should we avoid with hyperthyroid PTs?

A

pancuronium

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30
Q

what condition does thyrotoxic crisis mimic?

A

malignant hyperthermia

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31
Q

what is a primary cause for hypothyoidism?

A

dysfunction/destruction of thyroid tissue

  • Hashimoto’s Thyroiditis
  • high TSH but low T3/T4
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32
Q

what is a secondary cause for hypothyroidism?

A

hypothalmic/pituitary axis disfunction

  • normal or low TSH and low T3/T4
  • iatrogenic
  • myxedema coma
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33
Q

what are sympoms of hypothyroidism?

A
  • lethargy
  • weight gain
  • cold intolerance
  • hypoactive reflexes
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34
Q

how can you treat hypothyroidism?

A

PO T4

*synthroid

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35
Q

what is an extreme case of hypothyroidism more common in elderly women with a long history of hypothyroidism?

A

myxedema coma

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36
Q

What should be done with hypothyroid PTs preop?

A
  • minimize premed
  • gastric emptying
  • TAKE YOUR SYNTHROID
  • warm
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37
Q

what are some intraop concerns for hypothyroid PTs?

A
  • hypotension and increased sensitivity to agents
  • blunted baroreceptors
  • maybe avoid GA if possible
  • use KETAMINE if you must do GA
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38
Q

why might hypothyroid PTs have impaired pulmonary function?

A

TH aids in surfactant production

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39
Q

how does PTH affect serum calcium and phosphate?

A
  • increases calcium (bone resorption, dec. excretion)

- decreases phosphate (renal excretion)

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40
Q

what can cause primary hyperparathyroidism?

A
  • adenoma
  • carcinoma
  • hyperplasia of PTH glands
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41
Q

what can cause secondary hyperparathyroidism?

A

PTH increase due to hypocalcemia

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42
Q

what are symptoms of hyperparathyroidism?

A
  • hypercalcemia

* renal stones, HTN, constipation, fatigue

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43
Q

what medical treatment can be done for hyperparathyroidism?

A
  • saline

- loop diuretics

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44
Q

what causes hypoparathyroidism?

A

decreased PTH by iatrogenic causes

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45
Q

what symptoms result from hypoparathyroidism?

A

result from hypocalcemia

  • acute paresthesia, NM irritability
  • chronic EKG changes, lethargy, cataracts
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46
Q

what should we avoid in hypoparathyroid PTs?

A

don’t hyperventilate

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47
Q

what is a positive chvostek’s sign?

A

facial muscle twitching with tapping the mandible

*for nerve hypersensibility

48
Q

what is a positive trousseau’s sign?

A

occluding brachial artery for 3 minutes, causes spasm of forearm due to hypocalcemia

  • for nerve hypersensibility
  • more sensitive than chvosteks sign
49
Q

what is DiGeorge syndrome?

A

congenital hypoplasia of the thymus and parathyroid

50
Q

what does the thymus do?

A

immune organ that develops lymphocytes into T-cells for adaptive immune function

51
Q

what may you see in your airway exam for PTs with DiGeorge syndrome?

A

micrognathia

52
Q

what concerns do you have for Digeorge syndrome peri-op?

A
  • NMB unpredictable
  • hypervent could exacerbate hypocalcemia
  • micrognathia
53
Q

What does the adrena medulla secrete?

A

catecholamines (epi, norepi, dopamine)

54
Q

what does the adrenal cortex secrete?

A
  • glucocorticoids (cortisol)

- minerocorticoids (aldosterone, Na, K)

55
Q

what stimulates the adrenal cortex to release cortisol?

A

corticotropin

56
Q

glucocorticoids have a role in what metabolic pathway?

A

gluconeogenesis (inhibiting peripheral glucose use, causing hyperglycemia)

57
Q

what is the net effect of aldosterone? (3)

A
  • increased extracellular fluid volume
  • decreased plasma K+
  • metabolic alkalosis
58
Q

how are androgens significant for anesthetic management?

A

THEYRE NOT

59
Q

what important disease process is associated with the adrenal medulla?

A

PheoChromoCytoma (PCC)

60
Q

what causes cushing’s syndrome?

A

excess cortisol by ACTH -secreting adenoma

61
Q

what are symptoms of cushing’s?

A
  • obesity
  • HTN
  • muscle wasting
  • glucose intolerance
  • osteoporosis
62
Q

what are some preop considerations for cushing’s syndrome PTs?

A
  • BP, electrolytes, hypervolemic and hypokalemic

- blood sugar

63
Q

intraop considerations for cushings

A

osteoperosis and obesity

64
Q

post op considerations for cushings

A
  • poor would healing

- infection

65
Q

what is conn syndrome?

A

hyperaldosteronism, usually caused by a tumor

66
Q

what are symptoms of conn syndrome?

A
  • metab. alkalosis
  • hypokalemia
  • headache, cramps
67
Q

what can be done to treat conn syndrome?

A
  • spironolactone

- surgery

68
Q

what can be done perioperatively for PTs with Conn syndrome?

A
  • treat hypokalemia

- treat any HTN

69
Q

what is spironolactone?

A

an aldosterone antagonists

- a K+ sparing diuretic

70
Q

what is a primary adrenocorticoid deficiency?

A

addison’s disease (autoimmune)

71
Q

what is a secondary adrenocorticoid deficiency?

A

cortisol deficiency with normal aldosterone, caused by chronic steroid use

72
Q

what are some symptoms of adrenocorticoid deficiency?

A
  • hypotension
  • hyponatremia
  • hypovolemia
  • hyperkalemia
  • fatigue
  • hyperpigmentation
73
Q

how do you treat adrenocorticoid deficiency?

A

replace minero/glucocorticoids

*hydrocortisone 100 mg q6 hrs

74
Q

what should you be aware of peri-op for PTs with adrenocorticoid deficiency?

A

addisonian crisis

  • keep stress free
  • avoid etomodate
75
Q

what causes hypoaldosteronism?

A
  • congenital deficiency of aldosterone synthase
  • hyporeninemia
  • adrenalectomy procedure
76
Q

how do you treat hypoaldosteronism?

A

fludrocortisone (a minerocorticoid)

77
Q

what is pheochromocytoma?

A

PCC is a catecholamine secreting tumor of the medulla, secreting NE and Epi 85:15

78
Q

what are some signs of PCC?

A
  • sudden malignant HTN
  • cardiac dysrhthmias
  • headache
  • perspiration
79
Q

how much NE does the average PCC tumor contain?

A

100-800 mg NE

80
Q

how do you treat PCC?

A

cut out the tumor, manage BP with alpha-antagonists and B blockers

81
Q

what can result peri-op with PCC PTs?

A
  • HTN before removal
  • Hypotension after
  • HTN crisis can cause blindness
  • CVA
  • have an A-line
82
Q

what causes acromegaly?

A

excess GH, usually from a tumor on pituitary gland

83
Q

what will a PTs airway with acromegaly look like?

A

excess soft tissue & catilage, making DL difficult

*increased subglottic stenosis incidence

84
Q

what is diabetes insipidus?

A

deficiency or resistance to vasopressin

85
Q

what are symptoms of diabetes insipidus?

A

extreme thirst, excess urination

86
Q

how do you treat neurogenic diabetes insipidus?

A
  • synthetic vasopressin (desmopressin)

* due to lack of vasopressin secretion

87
Q

how do you treat nephrogenic diabetes insipidus?

A
  • keep Na+ levels low w/ diuretics

* vasopressin levels should be normal, just decreased response

88
Q

what should we monitor peri-op with diabetes insipidus?

A

electrolyte imbalances

  • high Na+
  • low K+
  • low Mg2+
89
Q

___ % of glucose production comes from hepatic glycogenolysis and ___ % comes from hepatic gluconeogensis during the postabsorption phase of digestion.

A

75%, 25%

90
Q

what is a normal hemoglobin A1C?

A
91
Q

what do the Islets of Langerhans do?

A

75% B cells - secrete insulin

20% a-cells - secrete glucagon

92
Q

what does glucagon do?

A

increases glycogen breakdown in the liver (gluconeogensis)

93
Q

what does insulin do?

A

lowers blood glucose by transporting glucose into the cell

94
Q

what does somatostatin do (from Delta cells)?

A

decreases motility of stomach, duadenom, gall bladder to increase absorption time
*inhibits insulin, glucagon, growth hormon, gastrin, motilin

95
Q

how is glucagon and insulin affected by parasympathetic and sympathetic innervation? (T5-T10)

A
  • sympathetic stimulates glucagon release

- parasympathetic stimulates insulin release

96
Q

what hormones can stimulate insulin release?

A

GH and cortisol

97
Q

what effect can lack of insulin have on glucose, fat and protein?

A
  • cells cant use glucose
  • increase fat as energy source, increase lipase and LDL
  • increase muscle wasting
98
Q

what are the type of DM?

A

type I - 5-10% of cases, autoimmune destruction of B cells
type 2 - 90%, insulin resistance
gestational - 2-3% of pregnancies, resolves post partum, dangerous for baby

99
Q

what are symptoms of DM?

A
  • polyurea, polydypsia, polyphagia
  • weight loss from muscle/fat used as energy
  • asthenia (no strength)
  • sweet breath from acetone
  • vision problems until blood sugar controlled
100
Q

long term complications of DM

A
  • HTN
  • vascular disease
  • neuropathy
  • renal failure
101
Q

what is the most common cause of death in older diabetics?

A
  • MI

* 20x greater risk periop

102
Q

what is diabetic ketoacidosis? (DKA)

A

decreased insulin activity leading to more metabolism of fatty acids and an accumlation of organic acids by-products
*occurs when exogenous insulin isn’t given

103
Q

how do you treat DKA?

A

crystalloid and insulin

104
Q

what are clinical signs of DKA?

A 
blood sugar 320+
fatigue
polyuria
mental stupor
ketones in urine
105
Q

what is a hyperosmolar non-ketotic coma?

A

hyperglycemic (600+ BS) diuresis that results in dehydration and hyperosmolality

106
Q

what do you do to treat hyperosmolar non-ketotic coma?

A

hypotonic solution and insulin

107
Q

what causes hypoglycemia?

A

insulin > carb intake

  • BS ~50mg/dL
  • mostly Type I DM
108
Q

how do you treat hypoglycemia?

A

IV administration of 50% glucose (each mL will raise BS about ~2mg/dL

109
Q

regular insulin can be given IV. All other insulin products must be given how?

A

subcutaneously

110
Q

what is metformin for?

A

1st line for obese type II DM PTs. decreases insulin requirements

111
Q

what are the four major classes of oral hypoglycemics?

A
  • secretagogues (sulfonylureas)
  • biguanides (metformin)
  • glitazones
  • a-glucosidase inhibitors (acarbose)
112
Q

when do you treat high glucose intra-op?

A

when BS is >150 mg/dL

*check every hr

113
Q

how do you treat high blood sugar intra-op?

A

give insulin

*(bs-100)/40 = units of insulin to give

114
Q

how much will 1 unit of insulin lower blood sugar?

A

25-30 mg/dL

115
Q

what is carcinoid syndrome

A

tumors of the GI tract causing massive serotonin and histamine release

116
Q

what will you see with carcinoid syndrome?

A

flushing and diarrhea, maybe massive hypotension

117
Q

what can you do to treat carcinoid syndrome?

A
  • a line
  • zofran
  • octreotide, somatostatin

Anesthesia Practice T3 (6 decks)

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