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AP II > Endocrine Diseases > Flashcards

Endocrine Diseases Flashcards

1
Q

which hormones are associated with the anterior pituitary?

A

FLATPeG

FSH
LH
ACTH
TSH
Prolactin
GH
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2
Q

which hormones are associated with the posterior pituitary?

A

ADH and Oxytocin

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3
Q

which thyroid hormone is the most active and most potent?

A

T3

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4
Q

pathophysiology of hyperthyroidism

A

hyperfunction of the thyroid gland

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5
Q

causes and symptoms of hyperthyroidism

A

Causes: Graves disease, TSH-secreting pituitary tumors, iatrogenic, thyroiditis
Symptoms: weight loss, fatigue, arrhythmias, anxiety, exopthalmos

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6
Q

anesthetic complications and treatments for hyperthyroidism

A

Treatment: medical (antithyroids, beta antagonists) and surgical (total, subtotal, or lobar thyroidectomy)
Anesthesia: anxiolytics, discontinue drugs to increase sympathetic discharge, can have RL nerve damage

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7
Q

what is a thyrotoxic crisis?

A

Life-threatening exacerbation of hyperthyroidism that may be caused by trauma, infection, surgery, or medical illness
Most often appears in post-op period, esp. if surgery was emergent

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8
Q

what are the symptoms and treatments for thyrotoxic crisis?

A

Symptoms – anxiety, fever, tachycardia, cardiovascular instability
Treatment – immediate: supportive; then decrease circulating hormone levels

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9
Q

what can thyrotoxic crisis mimic?

A

malignant hyperthermia

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10
Q

pathophysiology of hypothyroidism

A

Primary: dysfunction/destruction of thyroid tissue
Secondary:Hypothalamic-pituitary axis dysfunction
Autoimmune – Hashimoto’s thyroiditis
Iatrogenic – thyroidectomy, antithyroid medications

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11
Q

symptoms and treatments for hypothyroidism

A

Symptoms: lethargy, weight gain, cold intolerance, hypoactive reflexes (high TSH, low T3/T4)
Treatment: PO T4 (Synthroid)

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12
Q

anesthesia complications of hypothyroidism

A

hypotension intraop
decreased gastric emptying
slow to wake up
*myxedema coma (precipitated by stress)

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13
Q

pathophysiology of hyperparathyroidism

A

Primary: adenoma, carcioma, hyperplasia of parathyroid glands (which stimulate calcium circulation in blood)
Secondary: Compensatory increase in PTH secretion due to hypocalcemia (by renal disease or GI malabsorption)

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14
Q

symptoms and treatment for hyperparathyroidism

A

Symptoms: usually due to hypercalcemia (renal stones, hypertension, constipation, fatigue)

Treatment: may be medical or surgical

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15
Q

anesthetic considerations for hyperparathyroidism

A 
decreased response to NMB means an increased requirement 
during parathyroidectomy (constant Ca2+ checks)
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16
Q

pathophysiology of hypoparathyroidism

A

decreased PTH (almost always iatrogenic)

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17
Q

symptoms and treatment for hypoparathyroidism

A

Symptoms: (result from hypocalcemia), muscle and abdominal cramps, irritability, chvostek’s sign

Treatment: Ca2+ infusion

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18
Q

what are patients with hypoparathyroidism prone to intraop?

A

hypotension

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19
Q

pathophysiology for DiGeorge Syndrome (congenital thymic hypoplasia)

A

hypoplasia/aplasia of parathyroid and thymus

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20
Q

considerations of DiGeorge syndrome

A

small jaw, prone to infection

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21
Q

what is the function of glucocorticoids?

A

anti-inflammatory, help fight stress, increase glucose

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22
Q

what is the function of minerocorticoids?

A

(aldosterone) Na+ reabsorption, K+ secretion –> water retention

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23
Q

where are glucocorticoids and minerocorticoids produced?

A

adrenal glands

24
Q

pathophysiology of cushing’s syndrome

A

excessive cortisol (abnormal adrenocortical tissue, microadenoma, small-cell lung carcinoma)

25
Q

symptoms and treatment of cushing’s syndrome

A

Symptoms: obesity, hypertension, muscle wasting and weakness, glucose intolerance
Treatment: radiotherapy, transsphenoidal resection (if microadenoma is the cause)

26
Q

anesthetic considerations for cushing’s syndrome?

A

tend to be volume overloaded and hypokalemic (often obese)

27
Q

pathophysiology of Conn syndrome

A

excessive secretion of aldosterone, usually by a tumor, bilateral carcinoma of adrenals (more common in females)

28
Q

symptoms and treatments for Conn syndrome

A

headache, muscle cramps, metabolic alkalosis, HTN, hypokalemic, fluid overload

treatment: supplemental K+, excision of gland, spironolactone (K+ sparing diuretic)

29
Q

in what dosage is K+ given peripherally and centrally?

A

periph: 10 mEq
Central: 20 mEq

30
Q

pathophysiology for hypoaldosteronism

A

congenital deficiency of aldosterone synthase, hyporeninemia, unilateral adrenalectomy

31
Q

symptoms of hypoaldosteronism

A

Hyperkalemia without renal insufficiency (that may result in heart block) , hyperchloremic metabolic acidosis

32
Q

pathophysiology of adrenocorticoid deficiency

A

Primary (Addison’s Disease) –> have to lose 90% of tissue to see it, usually autoimmune
Secondary (Cortisol deficiency with normal aldosterone)

33
Q

symptoms and treatment for adrenocorticoid deficiency

A

Symptoms: hypotension, hyponatremia, hypovolemia, hyperkalemia, fatigue, weight loss

Treatment: steroid administration “stress dose” 100 mg hydrocortisone q 6h

34
Q

what induction drug should you not give to adrenocorticoid deficient patients?

A

etomidate

35
Q

pathophysiology of pheochromocytoma

A

catecholamine-secreting tumor of the adrenal medulla

36
Q

symptoms and treatment for pheochromocytoma

A

Symptoms: sudden onset of malignant hypertension, cardiac dysrhythmias, headache, perspiration
Treatment: excision of the tumor

37
Q

perioperative considerations for pheochromocytomas

A

hemodynamic instability; will become hypotensive once tumor is removed

38
Q

pathophysiology for acromegaly

A

excessive GH, usually because of tumor

39
Q

symptoms and treatments for acromegaly

A

Symptoms: skeletal, connective, and soft tissue overgrowth; papilledema; headache; hoarseness?; stridor?
Treatment: surgical or medical

40
Q

what is an important consideration for pts with acromegaly?

A

airway management!

41
Q

pathophysiology and causes for diabetes insipidus

A

deficiency or resistance to vasopressin (helps body retain H2O)

Causes: neurogenic (lack of vasopressin secretion) or nephrogenic (decreased response to vasopressin)

42
Q

symptoms of diabetes insipidus

A

extreme thirst, excessive urination (very dilute)

43
Q

what is the number one endocrine disease?

A

diabetes mellitus

44
Q

what is diabetes mellitus?

A

Chronic disease caused by abnormal glucose metabolism that results in predictable long-term morbidity

45
Q

in the islet of langerhans, what is produced by the beta cells and by the alpha cells?

A

beta: insulin
alpha: glucagon

46
Q

what are the effects of insulin secretion?

A 
↑ glucose uptake 
↑ glycogen synthesis
↑ protein synthesis and storage
↑ fat synthesis and storage
↓ gluconeogenesis
47
Q

what are the effects of glucagon secretion?

A

↑ glucose output from liver
↑ glycogenolysis
↑ gluconeogenesis (from amino acids)
↑ adipose cell lipase

48
Q

what is the pathophysiology of DM?

A

Causes: decreased secretion of insulin from beta cells or increased resistance of receptors to circulating insulin
Heredity
Obesity

49
Q

90% of all DM cases are what type?

A 
Type II (elderly and obese)
-insulin resistant
50
Q

what is the “triad” of symptoms for DM?

A

PolyDipsia
PolyPhagia
PolyUrea

51
Q

long term complications of DM

A 
Hypertension
Coronary artery disease
Myocardial infarction
Congestive heart failure
Diastolic dysfunction
Vascular disease
Neuropathy
Renal failure
52
Q

what is DKA?

A

Diabetic Ketoacidosis

53
Q

what causes DKA?

A

decreased insulin activity → metabolism of free fatty acids → accumulation of organic acids by-products

54
Q

what are the clinical signs and treatments for DKA?

A 
Clinical Signs
-Tachypnea		-Fatigue
-Abdominal pain		-Polyuria
-N/V			-Altered mental status 
Treatment: hypovolemia w/ NS; insulin, check electrolytes
55
Q

1 unit of insulin is said to lower blood sugar _______ mg/dL

A

25-30

AP II (32 decks)

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