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Patho II > Endocrine Pt. 1 > Flashcards

Endocrine Pt. 1 Flashcards

1
Q

cAMP mechanisms

A 
ACTH
LH, FSH,
TSH
ADH (V2 receptor)
HCG
B1 & B2 receptor
a2 receptor
Calcitonin
PTH
Glucagon
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2
Q

IP3 mechanisms

A 
GnRH
TRH
GHRH
ADH (V1 receptor)
Oxytocin
a1 receptor
Angiotensin II
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3
Q

Steroid Hormone mechanisms

A 
Glucocorticoids
Estrogen
Testosterone
Progesterone
Aldosterone
Vit. D
Thyroid hormone
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4
Q

Activation of tyrosine kinase

A

Insulin

IGF-1

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5
Q

cGMP

A

Nitric oxide

atrial natriuretic peptide (ANP)

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6
Q

In embryogenesis, _______ is a depression in the roof of the developing mouth in front of the buccopharyngeal membrane that gives rise to the anterior pituitary

A

Rathke’s pouch

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7
Q

What 2 hypothalamic nuclei syntheisze posterior pituitary hormones for release into the circulaiton?

A

Supraoptic and paraventricular nuclei

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8
Q

Where is the pituitary gland located?

A

Sella turcica of the sphenoid bone

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9
Q

Which lobe of the pituitary gland is linked to the hypothalamus by the hypothalamic-hypophysial portal system?

A

Anterior

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10
Q

MCC of hypopituitarism

A

Pituitary tumors

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11
Q

Anterior pituitary infarct during childbirth d/t post partum hemorrhage

A

Sheehan’s syndrome

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12
Q

Clinical features a/w hypopituitarism

A
  1. Growth failure/ ⬇️ muscle mass in adults (⬇️ GH)
  2. Adrenal insufficiency (⬇️ ACTH)
  3. Failure to lactate (⬇️ Prolactin)
  4. Hypothyroidism (⬇️ TSH)
  5. Impotence & testicular atrophy in male; amenorrhea & sexual organ atrphy in female (⬇️ FSH/LH)
  6. Decrease skin & hair pigmentation (⬇️ MSH)
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13
Q

Dx & Tx for hypopituitarism

A

Low level of target hormones & MRI;

Hormone replacement

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14
Q

Hormones of the anterior pituitary

A

GH, Prolactin, TSH, LH, FSH, ACTH

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15
Q

ACTH, MSH, B-lipoprotein & B-endorphin are derived form what single precursor?

A

pro-opiomelanocortin (POMC)

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16
Q

Hormones of posterior pituitary

A

ADH & oxytocin

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17
Q

GH secretion is increased by?

A

Sleep, stress, puberty, starvation, exercise, & hypoglycemia

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18
Q

GH secretion is decreased by?

A

Somatostatin, obesity, hyperglycemia, & pregnancy

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19
Q

Actions of GH

A

⬇️ glucose uptake into the cells (diabetogenic)
⬆️ lipolysis
⬆️ protein synthesis, lean body mass, & organ size
⬆️ protein synthesis in chondrocytes and linear growth (puberty growth spurt)

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20
Q

Failure to grow, short stature, mild obesity, & delayed puberty.

A

GH deficiency

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21
Q

Caused by pituitary adenoma.
Causes enlargement of hand & feet, facial features, & internal organs.
Anti-insulin effect —> HYPERGLYCEMIA

A

GH excess

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22
Q

How do you tx GH excess?

A

Somatostatin analogs (Octreotide)

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23
Q

Hypersecretion of GH before puberty causes what?

A

Gigantism

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24
Q

Hypersecretion of GH after puberty causes what?

A

Acromegaly

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25
Q

Why is tunnel visions (bitemporal hemianopia) a/w pituitary adenoma/acromegaly?

A

Compresses optic chiasm

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26
Q

Major hormone responsible for lactogenesis & breast development

A

Prolactin

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27
Q

Prolactin secretion is tonically inhibited by ____ secreted by the hypothalamus and is increased by _____ using negative feedback control

A

Dopamine (PIF); TRH

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28
Q

Prolacitn inhibits ovulation in women by decreasing synthesis and release of _______. How does this affect men?

A

Gonadotropin-releasing hormone (GnRH) (no FSH/LH); impotence & loss of libido

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29
Q

Prolactin excess leads to? Tx?

A

Glactorrhea & amenorrhea;

Bromocriptine (dopamine agonist to reduce prolactin secretion)

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30
Q

Factors ⬆️ prolactin secretion

A 
Estrogen (pregnancy)
Breast feeding
Sleep
Stress
TRH
Dopamine antagonists (antipysch)
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31
Q

Factors ⬇️ prolactin secretion

A

Dopamine
Bromocriptine
Somatostatin

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32
Q

Where are ADH (vasopressin) & oxytocin synthesized?

A

In hypothalamic supraoptic & paraventricular nuclei

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33
Q

_____ serum osmolarity increases ADH, while _____ serum osmolarity decreases ADH

A

Increased; Decreased

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34
Q

ADH regulates serum osmolarity by ___ H2O reabsorption (aquaporin 2, AQP2) from late distal tubules and collecting ducts via what receptor and mechanism?

A

⬆️; V2 receptor and cAMP

35
Q

Through what mechanism is ADH a potent vasoconstrictor?

A

V1 receptor and IP3/Ca mechanism

36
Q

______ is d/t an ADH deficiency. 50% idopathic, the other d/t trauma during neurosurgery

A

Central Diabetes Insipidus

37
Q

ADH secretion is normal but renal tubules do not respond to ADH. A/w CKD. Sicklers, & drugs (lithium)

A

Nephrogenic diabetes insipidus

38
Q

What is the Desmopressin challenge test?

A

⬆️ urine osmolarity after test dose = Central DI;

No change in urine osmolarity = Nephrogenic DI

39
Q

Tx for Central DI

A

Desmopressin

Chlorpropamide (oral hypoglycemic drug) ⬆️ ADH secretion

40
Q

Tx for Nephrogenic DI

A

Thiazide diuretics (depletes body of Na which leads to ⬆️ reabsorption of Na and Water in PT —> less pee)

41
Q

Overproduction of ADH.
CF: acute hyponatremia (reabsorb too much H2O),
Urine osmolarity > serum osmolarity, signs of brain swelling (lethargy, weakness, seizures, coma, death)

A

SIADH

42
Q

Tx for SIADH

A

Remove underlying cause, fluid restriction, demeclocycline (antagonizes ADH on renal tubules), lithium (use for its side effects), 3% NaCl, loop diuretics, non-peptide vasopressin antagonists

43
Q

Causes ejection of milk from breats “let down reflex”.

Contraction of myoepithelial cells in the breast and contraciton of uterus

A

Oxytocin

44
Q

Increase oxytocin secretion

A

Suckling, dilation of cervix, orgasm

45
Q

Oxidation of iodide (I-) to iodine (I2) is catalyzed by ____ enzyme. This enzyme is inhibited by ______?

A

Peroxidase (PO); propylthiouracil (PTU)

46
Q

Coupling of monoiodotyrosine (MIT) and diodotyrosine (DIT) result in production of?

A

T4 (thryoxine 93%) and T3 (more potent)

47
Q

In circulation, most of the T4 and T3 is bound to?

A

Thyroxine-binding globulin (TBG) or thyroglobulin

48
Q

In _____ TBG levels decrease leading to decrease in total T3 and T4 level, but normal levels of free T3 and T4

A

Hepatic failure

49
Q

In ____ TBG levels increase leading to an increase in total T3 and T4 level, but normall levels of free T3 and T4. Also a normal TSH level

A

Pregnancy

50
Q

What controls TRH and TSH

A

Hypothalamic-pituitary

51
Q

IgG type. Release form reticuloendothelial system.

Bind to TSH receptor on thyroid & act like TSH by stimulating the thyroid to secrete T3 & T4

A

Thyroid stimulating immunoglobulins

52
Q

Actions of thyroid hormone

A
  1. Thermogenic (⬆️ heat production, BMR, O2 consumption)
  2. Growth, bone formation/maturation
  3. Maturation of CNS (TH deficiency cause mental retardation)
  4. Beta stimulating actions (bblocker for hyperthyroid)
  5. ⬆️ CO
  6. ⬆️ glucose production & oxidation
  7. Catabolic effect on proteins & fats
53
Q

Autoimmune antibodies to TSH receptors (TSI)

A

Grave’s dz (hyperthyroidism)

54
Q

Autoimmunie thyroiditis or myxedema

A

Hashimoto’s (hypothyroidism)

55
Q

S/Sx of hyperthryoidism

A 
THYROIDISM:
Tremor
Heart rate up
Yawning (fatigability) 
Restlessness
Oligomenorrhea & amenorrhea
Intolerance to heat
Diarrhea
Irritability
Sweating
Musle wasting & weight loss
56
Q

S/sx of hypothyroidism

A 
SLUGGISH:
Sleepiness, fatigue
Loss of memory
Unusually dry skin
Goiter
Gradual personality change
Increase in body weight
Sensitivity to cold
Hair loss, sparseness of hair
57
Q

Labs & Tx with hyperthyroidism

A

⬆️ T3 and T4, ⬇️ TSH;

Propylthiouracil (PTU), thyroidectomy, radioactive iodine, B blockers

58
Q

Labs and Tx with hypothyroidism

A

⬇️ T3 and T4, ⬆️ TSH;

Levothyroxine (T4) replacement

59
Q

Preop hyperthyroidism

A

No sx until pt is euthyroid.

PTU, high dose of sodium iodide (⬇️ size of gland and risk of bleeding), bblockers, benzos for sedation

60
Q

Drug of choice intraop for hyperthyroidism? Drugs to avoid?

A

Drug of choice: thiopental (has anti-thyroid activity in high doses)
Avoid: Ketamine, pancuronium, & indirect acting adrenaergic agonists. (Stimulate SNS and ⬆️ BP & HR). Prone to hepatic injury with halothane

61
Q

Most important threat postop with hyperthyroidism? Tx?

A 
Thryoird storm (excessive release of T3 & T4);
Hydration & cooling, BB, PTU, sodium iodide (⬇️ release of TH), cortisol (⬇️ relase, synthesis, & conversion of T4 to T3 (active form))
62
Q

Intraop considerations with hypothyroidism

A

More susceptible to hypotensive effect of anesthetics (⬇️ CO, baroreceptor reflex, IV volume); no change in MAC. May have hypoglycemia, anemia,hyponatremia, difficult intubation d/t large tongue!!, hypothermia

63
Q

Postop considerations with hypothyroidism

A

Delayed recovery d/t hypothermia, resp depression, & slow drug biotransformation. Prolonged mech ventilaiton. Non-opioids (ketorolac) for postop pain

64
Q

Secretion of adrenocortical hormones by different zones

A

Zona Glomerulosa - aldosterone
Zona Fasiculata - Cortisol
Zona Reticularis - Androgen
GFR = salt (Na), sugar (glucocorticoids), and sex (androgen)

65
Q

Actions of glucocorticoids (cortisol)

A

Stimulation of gluconeogensis,
Anti-inflammatory effect (inhibits PG, IL-2, histamine, & serotonin),
Suppression of immune response (IL-2 & T lymophocytes),
Upregulates a1 receptors (⬆️ sensitivy to vasoconstrictor effect)

66
Q

Glucocorticoid secretion is highest at ___ and lowest at _____

A

8am; midnight

67
Q

Controlled by ACTH byt separately regulated by the renin-angiotensin system

A

Mineralocorticoids (aldosterone)

68
Q

Actions of mineralocorticoids (aldosterone)

A

⬆️ renal Na reabsorption “saves Na”
⬆️ renal K secretion “gets rid of K”
⬆️ renal H secretion “gets rid of H”

69
Q

Primary adrenal insufficiency d/t autoimmune destruciton of the adrenal cortex (adrenal crisis)

A

Addison’s dz

70
Q

S/Sx of Addison’s dz

A

Hypotension (hyponatremic volume contraction),
⬆️ ACTH (low cortisol stimulates ACTH secreation),
Hypoglycemia, wt loss, weakness, N/V, Hyperpigmentation,
Hyperkalemia/hyponatremia & met acidosis

71
Q

Anesthesia considerations for Addison’s Dz

A

Steroid coverage during perioperative period

72
Q

How is secondary adrenal insufficiancy different than primary?

A

Caused by deficiency of ACTH (chronic steroid use casuing atrophy of adrenal cortex);
Does not exhibit hyperpigmentation, volume contraction, hyperkalemia, or met acidosis.
Aldosterone levels are NORMAL

73
Q

Excess of glucocorticoids, (MCC prolonged intake of steroid) vs pituitary adenoma that releases excessive ACTH

A

Cushing’s syndrome vs Cushing’s disease

74
Q

S/sx of cushings

A 
⬆️ cortisol & androgen
⬆️ ACTH if dz, ⬇️ ACTH if prolong steroid use
Hyperglycemia
⬆️protein breakdown/muscle wasting
Central obesity (moon face, buffalo hump)
Poor wound healing
Virilization of women 
Na/H20 retention -> HTN 
Hypokalemia
75
Q

Dexamethasone suppresion test

A

Normal: 1mg Dex inhibits pituitary & adrenal gland by - feeback > suppression of cortisol
Cushing’s: only with 8mg Dex will pituitary shut off (pituitary adenoma producing too much ACTH)
Adrenal gland tumor: Dex does NOT suppress but there is ⬇️ ACTH
Ectopic ACTH (small cell Ca): Dex does not suppress, but there is ⬆️ ACTH

76
Q

Conn’s Syndrome

A

Primary hyperaldosteronism d/t aldosterone-secreting tumors.

HTN, Hypokalemia, Hypernatremia, Met alkalosis, & low plasma renin (- feedback inhibition by high BP & ECF)

77
Q

Caused by CHF. Kidney misperception of low intravascular volume, resulting in an overactive renin-angiotensin system. A/W high plasma renin

A

Secondary hyperaldosteronism

78
Q

Tx for hyperaldosteronism

A

Spironolactone (aldosterone antagonist)

79
Q

D/t an enzymatic deficiency in cortisol syntheis.

A

Congenital Adrenal Hyperplasia (CAH)

80
Q

MC type of CAH.
⬇️ cortisol & aldosterone level (enzyme block);
⬆️ ACTH (by decreased feedback inhibition by cortisol)
⬇️ mineralocorticoids, hypotension, hyperkalemia.
⬆️ 17 a-hydroxyprogesterone (above block) —> ⬆️ adrenal androgens. Ambiguous genitalia in girls + virilization

A

21 b-hydroxylase defeciency

81
Q 
Block that ⬇️ cortisol & androgen.
⬆️ aldosterone
Lack of pubic hair,
Hypoglycemia, hypertension, hypokalemia, met alkalosis
⬆️ ACTH
A

17 a-hydroxylase deficiency

82
Q

Anesthetic considerations with cushing’s syndrome

A

Tend to be volume-overloaded & have hypokalemic met alkalosis.
Supplement K. Osteoporosis = risk of fractures.
⬆️ sensitivity to muscle relaxant.
May need supplemental steroids if syndrome d/t exogenous steroids

83
Q

5 P’s of pheochromocytoma

A
  1. Pressure (paroxysmal HTN)
  2. Pain (headache)
  3. Perspiration
  4. Palpitation
  5. Pallor
84
Q

Why should droperidol be avoided in pheochromocytoma?

A

It inhibits dopamine release & dopamine inhibits release of catecholamines…. No dopamine = lots of catecholamines —> hypertensive crisis

Patho II (11 decks)

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