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AP Test 2 > Test 2 - Endocrine > Flashcards

Test 2 - Endocrine Flashcards

(59 cards)

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1
Q

Anterior pituitary

A

FLAT PG

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2
Q

Posterior pituitary

A

Oxytocin, ADH (vasopressin)

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3
Q

Anterior under control of

A

hypothalamus

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4
Q

Posterior under control of

A

neural control

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5
Q

Hyperthryoid symptoms

A

weight loss despite caloric intake, a-fib, svt’s widened P

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6
Q

Hyperthyroid concerns

A

No change in MAC. Post-RLN injury

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7
Q

Hyperthyroid hypocalcemia, why?

A

Parathyroid hormone

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8
Q

Thyroid storm manifestations

A

mostly in post-op period. Mimics MH (heat).

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9
Q

Hypothyroid

A

destruction of thyroid gland.

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10
Q

Hypothyroid lab values

A

High TSH, low T3 T4. Secondary: CNS dysfunction, low TSH and low T3 4 (Hashimotos)

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11
Q

Hypothyroid symptoms

A

lethargy, weight gain, cold intolerance, hypoactive reflees.

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12
Q

Hypothyroid treatment/med

A

synthroid T4

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13
Q

Hypothyroid pre-op meds

A

minimal. Sensitive to resp depression

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14
Q

Hyperparathyroidism

A

overactive PTH ^ calcium. in bloodusually due to adenoma, carcinoma. (calcitonin decreases)

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15
Q

Hyperventilation

A

decreases potassium, decreases calcium

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16
Q

if they take out too much parathyroid

A

“my mouth is tingly” muscle irritability.. all due to hypocalcemia (no PTH)

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17
Q

Test Chvostek’s sign

A

tap near tragus, if twitch, hypocalcemic

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18
Q

trousseau’s sign

A

claw hand. Hypocalcemia

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19
Q

DiGeorge Syndrome

A

thymus hypoplasia, thymus produces T cells. Lack of development. Low calcium.

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20
Q

DiGeorge Syndrome

A

Micrognathia. May make difficult DL.

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21
Q

Glucocorticoids produce

A

cortisol, which is antiinsulin

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22
Q

Glucocorticoids, physio, and glycogen

A

produces glycogen (gluconeogenesis). Causes hyperglycemia. Antiinflammatory effects

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23
Q

Aldosterone is involved in

A

fluid and electrolyte balance. Increase sodium, decrease potassium

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24
Q

Adrenal cortex produces

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A

glucocorticoids (cortisol), minerocorticoids (aldosterone), androgens.

25
Cushings Syndrome
Glucocorticoid excess. Excess cortisol. ACTH-secreting pituitary adenoma causes HYPERSECRETION of CORTISOL. Moon face, stomach obesity. Buffalo Hump
26
Conn Syndrome
Excess aldosterone - hypokalemia (treat slow!!), hypernatremia. Alkalemia due to ^ sodium and bicarb that comes with it. HTN!
27
Primary adrenocorticoid deficiency
addison's diease (remember: a - 1st). Auto immune. A A A arenocorticoid (deficiency), Addisons, Autoimmue
28
Secondsary adrenocorticoid deficiency
chronic steroid use. Cortisol deficiency. Down regulation of cortisol receptors from overuse
29
Treatment of secondary adrenocorticoid deficiency
100mg hydrocortisone q6h
30
Pheochromocytoma
Ach secreting tumor of adrenal medulla. Tumor secretes NE and Epi in ratio of 85:15. The average pheochromocytoma contains 100-800mg of NE.
31
What can trigger pheochr.
manipulation. We need an A line for these cases
32
Acromegally
excess GH, excess soft tissue in airway, overgrowth of cartilage, hoarseness and abnormal movement of paralysis of vocal cords.
33
Acromegaly Periop
DL may be difficult. Increase incidence of subglottic stenosis.
34
Diabetes Insipidus
Deficiency or resistance to Vasopressin (ADH) : released from Posterior Pituitary.
35
Diabeetus Mellitus
caused by abnormal glucose metabolism that results in predictable long term morbidity.
36
Normal glucose physiology
balance between glucose utilization and engogenous production or dietary delivery. Liver is the primary source of endogenous glucose.
37
Islet a and b cells
B - 75%, secrete insulin. A - 20%, secrete glucagon
38
Pancrease innervation
t5-10, symp innerv can cause insulin inhibition, glucagon stimulation. Para sym stims insulin release
39
hormones inhibiting insulin secretion
GH & Cortisol - both inhibit insulin
40
Type I DM
decreased beta cell insulin release.
41
Type II DM
^ resistance of receptors to circulatin insulin
42
Type I physiology
idiopathic, auto immune destruction of beta cells
43
Type II serum insulin levels
Plasma insulin normal or high
44
asthenia
sweet breath -from ketones
45
Long term complications of DM
HTN, vascular disease, neuropathy, renal faiure
46
End-organ pathophysiology of DM
20x greater risk of MI, sinus arythmia, variability with breathing.
47
DKA
diabetic ketoacidosis (DKA)
48
DKA cause
decreased insulin activity -> metabolism of free fatty acids. Accumulation of organic acids by-products
49
DKA bold note info
Occurs primarily in IDDM when EXOGENOUS INSULIN source is INTERRUPTED.
50
Treatment of DKA
Restore fluids, give insulin
51
Hyperosmolar nonketotic coma
Hyperglycemic diuresis results in dehydration & hyperosmolality.
52
Treatment of nonketotic coma
hypotonic saline and insulin
53
Hypoglycemia
can happen when patient takes insulin NPO. Can be masked by anesthesia. Causes "hangry"ness. Diabetic HTN could be caused by blood sugar. Happens when insulin > carb intake
54
Metformin
oral insulin
55
hb1ac
checks glycemic control
56
When to administer insulin
when glucose > 150mg/dL
57
How to administer
blood sugar - 100/40 = units of insulin to give.
58
Insulin administration decreases
serum K
59
Bold note in glucose control slide
Many patients may require exogenous insulin during intraoperative and postoperative periods because the stress of surgery causes increases in catecholamines, glucocorticoids, and inflammatory mediators – each of these contributes to STRESS HYPERGLYCEMIA

AP Test 2 (4 decks)

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