Exam 4: Endocrine Flashcards

1
Q

Type of disturbance typically seen with tumors/cancer:

A

Hyperfunction; sometimes mass effect

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2
Q

Types of target cell failure:

A
↓ in # of receptors
Impaired receptor function
Presence of antibodies against receptors
Antibodies acting as agonists
Unusual expression of receptors
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3
Q

Hormones secreted by the hypothalamus:

A
GnRH (→ FSH/LH)
TRH (→ TSH)
CRH (→ ACTH)
PIF (→ prolactin)
GHRH (→ GH)
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4
Q

Hormones secreted by the anterior pituitary:

A

FLAT PEG

FSH
LH
ACTH
TSH

Prolactin
Growth hormone

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5
Q

Posterior pituitary syndromes:

A
DI
SIADH
Oxytocin deficiency
Hypopituitarism
Null cell adenoma
Ischemic necrosis/Sheehan syndrome
Ablation
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6
Q

Pituitary adenomas:

A
Prolactinomas
GH adenoma
ACTH adenoma
Gonadotroph adenoma
TSH cell adenoma
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7
Q

Hypothalamus site of hormone synthesis:

A

Supraoptic and paraventricular nuclei

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8
Q

Requirement for hormones to be transported in blood:

A

Bound to proteins

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9
Q

Clinical manifestations of SIADH:

A

Water retention
Hyponatremia
Hypoosmolarity

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10
Q

Cause of neurogenic vs. nephrogenic DI:

A

Neurogenic: insufficient ADH produced
Nephrogenic: inadequate response to ADH

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11
Q

S/s of DI:

A

Polyuria
Polydipsia
Unconcentrated urine

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12
Q

Sheehan syndrome is:

A

Ischemic necrosis of pituitary due to heavy blood loss during delivery

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13
Q

Panhypopituitarism usually from:

A

Cell destroying/null cell tumors

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14
Q

Non-neoplastic causes of panhypopituitarism:

A

Head trauma, infection, etc

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15
Q

Most common cause of hyperpituitarism:

A

Slow-growing benign pituitary adenoma

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16
Q

S/s of pituitary adenoma:

A

Headache/fatigue
Visual changes
Hyposecretion of neighboring ant.pit. hormones

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17
Q

Cause of acromegaly:

A

↑ GH during adulthood

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18
Q

Cause of gigantism:

A

↑ GH during childhood/adolescence

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19
Q

S/s of acromegaly:

A

Overgrowth in nose, face, scalp, forehead

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20
Q

Anesthesia implications of acromegaly:

A

Can be difficult to intubate/manage airway

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21
Q

S/s of gigantism:

A

Proportional growth beyond typical sizes

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22
Q

Cause of dwarfism:

A

↓ GH in childhood

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23
Q

S/s of dwarfism:

A

Proportionally stunted growth; 1/3rd are able to go through puberty/reproduce

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24
Q

Three major effects of panhypopituitarism:

A

Hypothyroidism
Depressed cortisol production
Suppressed sex hormone production

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25
Q

Three major effects of panhypopituitarism:

A

Hypothyroidism
Depressed cortisol production
Suppressed sex hormone production

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26
Q

Causes of hyperthyroidism:

A

Graves disease
Hyperfunctioning adenoma
TSH cell adenoma
Iatrogenic

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27
Q

Causes of hypothyroidism:

A

Hashimoto’s
Iodine deficiency
Ablation
Idiopathic

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28
Q

Carcinomas of the thyroid:

A

Papillary
Anaplastic
Medullary
Follicular

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29
Q

Part of anterior pituitary that secretes TSH:

A

Pars distalis

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30
Q

Short feedback loop goes between thyroid and:

A

Anterior pituitary gland/pars distalis

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31
Q

Long feedback loop goes between thyroid and:

A

Hypothalamuc

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32
Q

Conditions that cause ↑ TSH and ↑ T3/T4:

A

Pituitary adenoma secreting TSH

Ectopic TSH production (small cell carcinoma in lung)

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33
Q

Conditions that cause ↑ TSH, ↓ T3/T4:

A

Hashimoto’s thyroiditis

Iodine deficiency

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34
Q

Conditions that cause ↓ TSH, ↑ T3/T4:

A

Graves’ disease
Toxic goiter
Thyroxine-secreting thyroid cancer

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35
Q

Conditions that cause ↓ TSH, ↓ T3/T4:

A

Panhypopituitarism
Null cell adenoma
Sheehan’s syndrome

36
Q

Pathogenesis of Grave’s disease:

A

Antibodies called TSIs (thyroid stimulating globulins) act like TSH and cause constant T3/T4 production via ↑ cAMP

37
Q

Half-time of TSH and TSIs:

A

TSH: 1 hr
TSIs: 12 hrs

38
Q

S/s of hyperthyroidism:

A
Anxiety
Irritability
Insomnia
Rapid/irregular heartbeat
Tremors
Diaphoresis
Heat-sensitivity
Weight loss
Brittle hair
Goiter
Light menstrual periods
Diarrhea
Exophthalmos
39
Q

Tx for hyperthyroidism:

A

β blockers
Anti-thyroid meds
Radioactive iodine
Surgery

40
Q

Pathogenesis of Hashimoto’s thyroiditis:

A

Autoimmune destruction of receptors and gland, causing inflammation

41
Q

S/s of hypothyroidism:

A
Cold sensitivity
Constipation
Pale, dry skin
Puffy face
Goiter/hoarse voice
Elevated cholesterol
Weight gain
Muscle aches/tenderness/stiffness
Heavy menstrual periods
Depression
42
Q

Tx of hypothyroidism:

A

Levothyroxine

Iodine if deficient

43
Q

Role of immune system in Hashimoto’s:

A

Thyroid-specific helper T cells (CD4) stimulate cytotoxic T cells (CD8) and B cells (humoral)

CD8 cells responsible for parenchymal destruction

B cells secrete antibodies against TSH receptors et al.

44
Q

Role of antithyroglobulin and antithyroid peroxidase antibodies in Hashimoto’s:

A

Not pathogenic, but useful serologic markers of disease

45
Q

Pathogenesis of myxedema:

A

↑ chondroitin and hyaluronic acid cause interstitial fluid ↑ and edema

46
Q

Pathogenesis of cretinism:

A

Hypothyroidism (extreme) in fetal life, infancy, or childhood

47
Q

S/s of cretinism:

A

Skeletal growth stunted more than soft tissue; obesity, large tongue, etc

Dwarfism
Unique facial features
Absent/scant secondary hair
Poorly developed breasts
Potbelly
Umbilical hernia
48
Q

Role of PTH glands:

A

Regulator of serum Ca++
Antagonizes calcitonin
Excretes PO4-

49
Q

Role of PTH glands:

A

Regulator of serum Ca++
Antagonizes calcitonin
Excretes PO4-

50
Q

S/s of hyperparathyroidism:

A
Hypercalcemia
Hypercalcuria
Kidney stones
PUD
Pancreatitis
N/V/anorexia
Osteoporosis
Confusion/poor memory
Muscle weakness/fatigue
51
Q

Tx of hyperparathyroidism:

A

Surgery

52
Q

Anesthetic considerations for hyperparathyroidism surgery:

A

Positioning - weak bones, muscles

Avoid benzos and muscle relaxants

53
Q

S/s of hypoparathyroidism:

A

Hypocalcemia

Tetany, esp. in smaller muscles

54
Q

Hypocalcemic tetany in the hand is called:

A

Carpopedal spasm

55
Q

Tx for hypoparathyroidism:

A

PTH

Vitamin D

56
Q

Mineralocorticoid hormones produced in:

A

Zona glomerulosa of adrenal cortex

57
Q

Activity of mineralocorticoid hormones:

A

↑ activity of epithelial Na+ pump

Na+ retention, K+/H+ loss

58
Q

Most potent naturally occuring mineralocorticoid hormone:

A

Aldosterone

59
Q

Glucocorticoid hormones produced in:

A

Zona fasciculata of adrenal cortex

60
Q

Glucocorticoid hormone release stimulated by:

A

ACTH

61
Q

Activity of glucocorticoid hormones:

A

Hyperglycemia
Anti-inflammatory
Growth suppression
Sleep/awareness

62
Q

Most potent naturally occuring glucocorticoid hormone:

A

Cortisol

63
Q

Adrenal estrogens and androgens produced in:

A

Zona reticularis of adrenal cortex

64
Q

Adrenal estrogens and androgens produced in:

A

Zona reticularis of adrenal cortex

65
Q

Production of strong androgens like testosterone:

A

Weak androgens (DHEA, androstenedione) produced in adrenal cortex and converted to stronger androgens in periphery

66
Q

Catecholamines produced in:

A

Chromaffin cells/pheochromocytes in adrenal medulla

67
Q

Endogenous causes of hypercortisolism/Cushing’s:

A

Pituitary tumor
Adrenal tumor
Ectopic secreting tumor
Iatrogenic

68
Q

Causes of hyperaldosteronism/Conn’s:

A

Overrelease of aldosterone

Overrelease of renin

69
Q

Most common cause of Cushing’s:

A

Excess ACTH

70
Q

S/s of Cushing’s:

A
Hyperglycemia
Hypertension
Fat redistribution to trunk/face
Fatigue
Muscle weakness
Moon face
Stretch marks
Thin skin, easy bruising
Slow healing
Depression, anxiety, anger
Acne
Thicker hair
Absent menstrual periods
ED
71
Q

Tx for Cushing’s:

A

↓ steroid use if iatrogenic
Surgery
Radiation
Medical/drugs

72
Q

Cause of Conn’s disease:

A

Tumors in zona glomerulosa

73
Q

S/s of Conn’s:

A
Hypokalemia
Metabolic alkalosis
↑ ECF/blood volume
↑ Na+/H2O retention
HTN
74
Q

S/s of adrenogenital syndrome:

A

Virilization

75
Q

Tx of adrenogenital syndrome:

A

Cortisol

76
Q

S/s of Addison’s:

A
Muscle weakness/fatigue
Weight loss
Anorexia
Hyperpigmentation
Hypotension/syncope
Hypoglycemia
Hyponatremia/salt craving
N/V/D
Irritability
Depression
77
Q

Tx of Addison’s:

A

HRT

Salt tabs

78
Q

S/s of pheochromocytoma:

A
Tachycardia
Arrhythmias
Sweating
Chest pain
Upper abdominal pain
Headaches
Tremors
Anxiety/fright
Pale skin
Hypertension
79
Q

Tx of pheochromocytoma:

A

α blockers

β blockers

80
Q

Tx of pheochromocytoma:

A

α blockers

β blockers

81
Q

Reticular activating system response to acute stress:

A

Activates so we won’t sleep

82
Q

Amygdala response to acute stress:

A

Behavioral changes

83
Q

Arcuate nucleus response to acute stress:

A

Release of NE from the locus coeruleus
Release of neuropeptide Y (NPY)
Drives BP/HR up

84
Q

Hypothalamus response to acute stress:

A

Secretes CRH to stimulate ACTH release from ant pit

85
Q

Cortisol role in acute stress:

A

Negative feedback to pituitary and hypothalamus to bring levels back down to normal when appropriate

86
Q

Effect of chronic stress on stress pathway:

A

Dampens the negative feedback of cortisol so that you have perpetually ↑ levels of CRH, ACTH, cortisol

87
Q

Effect of chronic stress on anesthesia:

A

Labile BPs d/t catecholamine depletion

Hyperglycemia