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Patho1 > Endocrine > Flashcards

Endocrine Flashcards

1
Q

what hormones does the anterior pituitary gland secrete?

A

ACTH, TSH

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2
Q

what hormones does the posterior pituitary gland secrete?

A

ADH, oxytocin

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3
Q

what are the two components of the adrenal glands?

A

inner medulla and outer cortex

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4
Q

what does the inner medulla of the adrenal gland secrete?

A

epinephrine and norepinephrine

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5
Q

what does the outer adrenal cortex of the adrenal gland secrete?

A

glucocorticoids, mineralocorticoids (aldosterone), androgens [sugar, salt, sex]

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6
Q

what is cushings?

A

a collection of s/s associated with HYPERcortisolism

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7
Q

what are the potential causes of cushings?

A

primary hyperfunction = a disease involving the adrenal cortex (syndrome)
secondary hyperfunction = a disease involving the anterior pituitary gland (disease)
exogenous steroids = most common (syndrome)

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8
Q

if the normal function of cortisol is to increase glucose availability, what is the clinical manifestation in cushings?

A

glucose intolerance, hyperglycemia

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9
Q

if the normal function of cortisol is to maintain the vascular system, what is the clinical manifestation in cushings?

A

hypertension, capillary friability (causing bruising)

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10
Q

if the normal function of cortisol is to breakdown protein, what is the clinical manifestation in cushings?

A

muscle wasting
muscle weakness
thinning of skin
osteoporosis
bone pain

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11
Q

if the normal function of cortisol is to breakdown fat, what is the clinical manifestation in cushings?

A

redistribution of fat to the face, shoulder, and abdomen

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12
Q

if the normal function of cortisol is to suppress the immune and inflammatory responses, what is the clinical manifestation in cushings?

A

impaired wound healing
impaired immune response
risk for infection

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13
Q

if the normal function of cortisol is to excite the CNS, what is the clinical manifestation in cushings?

A

insomnia, mood swings

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14
Q

what is Addison’s disease?

A

disease of the adrenal cortex that causes hyposecretion of all adrenocorticoid hormones

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15
Q

what is the cause of Addison’s disease?

A

can be idiopathic, autoimmune, or something else - not real sure

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16
Q

how much of the adrenal cortex needs to be non-functional before symptoms show up related to Addison’s disease?

A

90%

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17
Q

what hormones are in excess with Addison’s disease?

A

ACTH and melanocyte stimulating hormone (MSH)

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18
Q

what are the early symptoms of Addison’s disease?

A

anorexia
weight loss
weakness
malaise
apathy
electrolyte imbalance
skin hyperpigmentation

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19
Q

what are the effects associated with hypoaldosteronism with Addison’s ?

A

hypotension (not able to retain salt and water)
decreased vascular tone
decreased cardiac output
decreased circulating blood volume
salt craving (low serum Na+)
increased K+
dehydration

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20
Q

what are the effects associated with hypocortisolism with Addison’s?

A

hypoglycemia
weakness and fatigue
unsuppressed ACTH
hyperpigmentation

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21
Q

what are the short term side effects of steroids?

A

increased intraocular pressure
fluid retention
weight gain
hungry
mood swings
increased BP

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22
Q

what are the long term side effects of steroids?

A

cataracts
increased blood sugar (can develop or worsen DM)
increased risk of infection
osteoporosis
decreased adrenal gland function
fatigue, anorexia, nausea, weakness
thin skin
bruising
slow wound healing

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23
Q

what is the drug of choice for Addison’s?

A

hydrocortisone

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24
Q

what are the nursing implications of a patient with Addison’s taking life long steroids?

A

taking the doses at the right time to mimic natural release
never to abruptly stop these
dosing will need to be increased (3x3) during stress
always have an emergency supply
wear a medical alert bracelet

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25
Q

what is a severe cushings adrenal crisis?

A

characterized by massively elevated random serum cortisol or a 24-hour urine cortisol that is 4x the upper limit

26
Q

what does potassium look like with a severe cushing’s adrenal crisis?

A

can be normal or severely hypokalemic

27
Q

what is a severe cushing’s syndrome adrenal crisis usually associated with?

A

the onset of sepsis, HF, or opportunistic infections

28
Q

how do you treat someone who is in a severe cushing’s adrenal crisis?

A

manage F&E and metabolic disturbances and try to rapidly resolve the problem (what ever is causing it)

29
Q

what is an Addisonian crisis?

A

sudden insufficiency of serum corticoids, this will lead to the body crashing and can be fatal

30
Q

what is pheochromocytoma?

A

a rare tumor of the adrenal inner medulla that produces excess epinephrine and norepinephrine

31
Q

who is most at risk of a pheochromocytoma?

A

young - middle age adults

32
Q

what are the clinical manifestations of pheochromocytoma?

A

hypertension - headache, diaphoresis, tachycardia

33
Q

what is the biggest concern with pheochromocytoma?

A

a stroke

34
Q

what is the preferred and secondary treatment of pheochromocytoma?

A

preferred - surgery
secondary (if inoperable or need to reduce HTN before) alpha-adrenergic blockers

35
Q

what is the function of ADH?

A

fluid retention via the kidney

36
Q

what is SIADH?

A

syndrome of inappropriate antidiuretic hormone - this is an abnormally excessive amount of ADH

37
Q

how is SIADH characterized?

A

fluid retention, serum hypoosmolality, hyponatremia, concentrated urine

38
Q

what are the potential causes of SIADH?

A

malignant tumor such as small cell lung cancer - this causes a wild release of ADH
CNS disorders like a head trauma, stroke, or tumor
drug therapies like morphine, SSRI, and some chemos
hypothyroidism (d/t a massive decrease in CO)
infection

39
Q

serum osmolality in SIADH is:

A

low

40
Q

urine osmolality and specific gravity in SIADH is:

A

high

41
Q

serum Na+ in SIADH is:

A

low

42
Q

urine output in SIADH is:

A

low

43
Q

does a patient lose or gain weight with SIADH?

A

gain

44
Q

what are the clinical manifestations of a patient with SIADH?

A

hyponatremia - dyspnea, fatigue, lethargy, confusion, muscle twitching, convulsions, anorexia, vomiting, cramps, impaired taste, dulled sense
FVE

45
Q

for a patient with SIADH, what Na+ level causes irreversible neurological damage?

A

100-115

46
Q

what happens with water intoxication?

A

serum Na+ levels become lower than intracellular Na+, the cells rapidly pull fluid in causing severe swelling - this is a problem specifically when the brain cells do this

47
Q

what can water intoxication lead to?

A

confusion, lethargy, coma, death

48
Q

what is used to treat chronic SIADH?

A

demeclocycline

49
Q

what is diabetes insipidus?

A

a deficiency in ADH or a decreased renal response to it

50
Q

what is DI characterized by

A

excessive loss of water by urine

51
Q

what are the potential causes of neurogenic DI?

A

hypothalamus / posterior pituitary damage
some brain injury (stroke, TBI, brain surgery, cerebral infection)

52
Q

onset and duration of neurogenic DI?

A

sudden onset, usually permanent

53
Q

what are the potential causes of nephrogenic DI?

A

loss of kidney function (usually drug related, could be lithium)
CKD

54
Q

onset and duration of nephrogenic DI?

A

slow onset, progressive

55
Q

serum osmolality in DI is:

A

high

56
Q

urine osmolality and specific gravity in DI is:

A

low

57
Q

serum Na+ in DI is:

A

high

58
Q

urine output in DI is:

A

high

59
Q

what are the clinical manifestations of DI?

A

polyuria
polydipsia
dehydration
electrolyte imbalance
hypovolemia shock - if severe enough

60
Q

what are the treatment options for neurogenic DI?

A

need a synthetic ADH replacement

61
Q

what are the treatment options for nephrogenic DI?

A

need a thiazide diuretic (somehow this works to decrease polyuria and allows urine to concentrate)

62
Q
A

Patho1 (22 decks)

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