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Clinical Med > endocrine > Flashcards

endocrine Flashcards

1
Q

primary v. secondary endocrine disorders

A

Primary: disorder or abnormality of gland;organ itself is malfunctioning
- target endocrine organ does not produce hormones

Secondary: erroneous message to the gland (defect is further up, and the gland is not stimulated properly)
- hypothalamic or pituitary dysfunction are secondary disorders

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2
Q

what are the anterior pituitary hormones?

A

FSH
LH
ACTH
TSH

Prolactin
Growth hormone

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3
Q

why might a pituitary tumor give a HA?

A

Traction on dura mater

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4
Q

what differentiates maco from microadenomas?

A

microadenomas are 10mm

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5
Q

what important structures can pituitary tumor compress?

A

carotid artery or optic chiasm or CNs

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6
Q

what is SHeehan’s syndrome?

A

postpartum bleed that can cause pituitary insufficiency

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7
Q

Growth hormone is secreted in response to what 2 things?

A

1) Stress (hypoglycemia)

2) GHRH (GH Releasing Hormone)

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8
Q

what is the Growth horm target?

A

targets liver – production of insulin-like growth factor 1 (IGF-1) which acts on peripheral tissues to modulate GH effects

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9
Q

Growth hormone is inhibited in response to what 3 things?

A

1) somatostatin,
2) IGF-1 (negative feedback where when IGF-1 is successfully secreted, GH should be shut off),
3) glucose

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10
Q

what’s the difference between gigantism and acromegaly?

A

Gigantism: Excess hormone before epiphyses closed
-so if GH tumor occurs when still young

Acromegaly: Overgrowth of bone and soft tissues
-so if GH tumor occurs later in life

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11
Q

what 3 metabolic conditions are people with gigantism or acromegaly at risk for?
what else?

A

DM, heart disease, HTN

-myopathy, weakness, excess sweating

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12
Q

what tests can help diagnose acromegaly or gigantism?

A

1) elevated IGF-1 (check in the morning especially)
2) oral glucose load (oral glucose tolerance test) – try to suppress GH
3) since GH levels vary, a random GH level isn’t very helpful

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13
Q

what are some clues that might indicate childhood GH deficiency?

A

short stature (but normal proportions) and fasting hypoglycemia (counterregulation)

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14
Q

why does prolactin release increase with injury to pituitary stalk?

A

PRL release increases with injury to the pituitary stalk because the dopamine doesn’t arrive to the gland

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15
Q

what hormone regulates release of prolactin?

A

PRL production constantly inhibited by dopamine from hypothalamus (block dopamine to the pituitary, release PRL)
**some stimulation from TRH, which explains increased PRL in hypothyroid (where more TRH is being secreting)

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16
Q

what are some accompanying symptoms you might see in hyperprolactinemia?

A

menstrual irregularity or complete lack (amenorrhea), impotence/erectile dysfunction, infertility, galactorrhea (milk draining), osteoporosis

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17
Q

most common pituitary adenoma cause?

A

prolactinoma

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18
Q

micro vs macroprolactinomas: which populations are they common in?

A

microprolactinomas – more commonly seen/detected in pre-menopausal women bc big impact on the menses so more noticable medically

macroprolactinomas (>10mm size) – more common in men or post-menopausal women, take longer to notice

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19
Q

what drug could you use to treat prolactinoma?

A

dopamine agonist

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20
Q

Give an example of 2 gonadotropins

A

leutenizing hormone (LH) and follicle stimulating hormone (FSH)

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21
Q

describe how GnRH secretion works

A

GnRH secretion is pulsatile – if it is steady or constant it turns off LH and

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22
Q

describe primary vs secondary amenorrhea:

A

amenorrhea: lack of menses
primary = no menstruation by 16y = no menses ever
secondary = no menses for ≥3 months after had previously had

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23
Q

Primary vs secondary ovarian failure:

A 
Primary = ovary won’t ovulate
Secondary = otherwise normal ovary is not stimulated in normal cyclic manner
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24
Q

what are some possible endocrine issues that would cause amenorrhea:

A

1) very low body weight – hypothalamic amenorrhea
2) hyperprolactinemia – i.e. from prolactinoma
3) thyroid dysfunction
4) hypopituitarism – low gonadotropin levels – bleed, tumor, infiltration?
5) androgen excess

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25
Q

causes of ED?

A

1) primary hypogonadism – gonads/testis themselves are malfunctioning – low testosterone or elevated LH (bc attempting to stimulate the testes)
2) secondary hypogonadism – could be hypopituitarism (low testosterone or low LH), or hyperprolactinemia
3) meds: most anti-hypertensives, SSRIs (i.e. Prozac), GnRH agonists or antagonists
4) vascular disease: smoking, HTN, hyperlipidemia, diabetes, peripheral vascular disease (PVD)
5) neurological disease: diabetic neuropathy, spinal cord injury
6) psychological stressors

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26
Q

phosphodiesterase-5 inhibitors (PDE-5) are taken for what and can cause what kind of ocular side effects?

A

ocular/visual symptoms may occur with bluish discoloration (there is PDE-6 in the retina); rare reports of NAAION (but remember this may not be causal because the age ranges and risks overlap); systemic Sx include low BP (so do not take with certain meds to lower BP)

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27
Q

3 situations where you wouldn’t give phosphodiesterase-5 inhibitors (PDE-5)

A

1) nitrates – causes dilated vessels, so if you add med you could cause a serious drop in the blood pressure
2) LV outflow obstruction (e.g. aortic stenosis)
3) alpha-blockers: orthostatic hypotension can be exacerbated

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28
Q

ADH is made where? what does it control?

A

posterior pituitary hormone synthesized in the magnocellular neurons that regulates water balance

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29
Q

Name 2 target tissues for ADH and what it does there?

A

1) kidney (resorp free water/anti-getting-rid-of-fluid) – concentrates urine
2) blood vessels (vasoconstriction and increased BP)

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30
Q

ADH is triggered by what 2 things?

A

1) increased serum osmolality – want to hold water (sensitive to 1% changes)
2) volume contraction/decrease – want to hold all the fluid you can

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31
Q

what is syndrome of inappropriate ADH (SIADH)?

A

ADH level is inappropriately high for the serum osmolality

  • excessive absorption of free water
  • hyponatremia (low Na+) but euvolemic (volume normal)
  • symptoms are related to brain edema: headache, nausea, confusion, neuro defects, seizures, death if untreated
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32
Q

Causes of syndrome of inappropriate ADH (SIADH)?

A
  • pulmonary disease (i.e. tuberculosis or pneumonia)
  • bronchogenic carcinoma – certain lung cancers
  • central nervous system diseases
  • drugs: SSRI really only if elderly (Prozac), ecstasy
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33
Q

ACTH release of what from what gland?

A

ACTH stimulates cortisol, aldosterone, androgens from adrenal gland

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34
Q

what are some stimuli for ACTH?

A

Stress, psychological, surgery, serious infection, trauma, physical, Hypoglycemia

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35
Q

when does ACTH peak and trough?

A

ACTH peaks early morning, troughs in later afternoon/evening

  • cortisol peaks 6-8am (when you are waking up) and troughs at midnight (bedtime)
  • cycling of hormones helps with normal sleep-wake cycle -> this is why it is important to keep consistent wake up and sleep times
36
Q

what are the 3 adrenal cortex zones and what do they secrete?

A

Zona glomerulosa→Aldosterone
Zona fasciculata→ Cortisol
Zona reticularis→Androgen (DHEA / S)

37
Q

adrenal medulla secerets:

A

catecholamines (epi and norepi)

38
Q

T/F: too much ACTH can give DM?

A

ACTH is counterregulatory hormone – too much cortisol can give diabetes

39
Q

excess cortisol can cause what kind of effects or conditions to occur?

A 
 hyperglycemia/DM
 irregular menses
 immune suppression
 depression, insomnia, various mood and sleep disorders
 weight gain
 osteoporosis
 cataracts
 secondary HTN
*Proximal Muscle weakness
40
Q

what is a stimulus for aldosterone release?

A

stimulated by renin-angiotensin

Also ACTH, hyperkalemia, hypovolemia

41
Q

Cushing’s disease vs syndrome?

A

Cushing’s syndrome is a general term for excessive glucocorticoid

Cushing’s disease = specific subset of Cushing’s syndrome where secondary cause of glucocorticoid excess is pituitary oversecretion of ACTH (i.e. in a pituitary tumor)

42
Q

what could be an ACTH independent cause of Cushing’s syndrome?

A 
Adrenal tumor (primary)
Exogenous glucocorticoid
43
Q

what are some options for screening for Cushing’s syndrome?

A

1) Urinary free cortisol (24 hours)-Test for excess production of cortisol
2) Midnight cortisol (serum or saliva) -Test for lack of diurnal variation (nadir around midnight)
3) Overnight dexamethasone supression test
Dexamethasone - synthetic glucocorticoid not detected by lab assay. Exogenous glucocorticoid should suppress AM ACTH and cortisol
Abnormal: Cortisol elevated
False positive: Medical illness, depression, alcoholism

44
Q

what is Nelson’s syndrome? when would you get it? how can you prevent it

A

Nelson’s syndrome – results after bilateral adrenalectomy

  • ACTH-secreting macroadenoma in pituitary – gives hyperpigmentation and compression of local structures (i.e. optic chiasm – think visual impact)
  • prevention: pituitary irradiation after bilateral adrenalectomy
45
Q

what stimulates production of aldosterone?

A

Angiotensin 2

46
Q

angiotensin is produced where? where is renin?

A

kidneys produce renin

angiotensin is produced in liver

47
Q

Describe the effects of aldosterone on these 3 ions: sodium, potassium, hydrogen

A

Na ↑
K ↓
H ↓

48
Q

Name a secondary cause of hyperaldosteronism:

A

renovascular hypertension (i.e. renal artery stenosis) -> renal artery is narrowed so the kidney senses volume depletion

49
Q

you would be suspicious of hyperaldosteronism if you see HTN with what:

A

Hypertension with hypokalemia
(or refractive hypertension – very difficult to control even with multiple meds – much more suspicious of secondary cause if HTN is refractory)

50
Q

Chronic vs acute symptoms of adrenal insufficiency?

A

Chronic:
-weakness, fatigue, hypOtension (postural)
- hyperpigmentation (PRIMARY only)
-Hyponatremia, Hypoglycemia, Hyperkalemia (primary), -Metabolic acidosis
Acute=collapse, emergency

51
Q

what is Addison’s disease?

A

Addison’s disease is an autoimmune that usually gives both mineralo- and glucocorticoid deficiency
*primary adrenal insufficiency

52
Q

For adrenal insufficiency, elevated plasma ACTH will only be seen in primary causes

A

elevated plasma ACTH will only be seen in primary causes

53
Q

what is adrenal virilism?

A

adrenal virilism: overproduction of weak androgens by the adrenal glands
-women undergo a degree of masculinization:
hirsuitism (increased hair), menstrual irregularity, acne, virilization (other male sex characteristics such as voice changes and increased muscle)

-pre-pubertal boys: exaggerated hair growth, premature development of gonads but with small testes resulting
accelerated linear growth but epiphyseal closure is premature -> grow earlier but also stop early – think of it as puberty sort of happening earlier

54
Q

How can you diagnose pheocromocytoma?

A

Elevated catecholamines in plasma or 24 hour urine

55
Q

what is pheochromocytoma and what kind of side effects does it cause?

A

pheochromocytoma: adrenal tumors that secrete catecholamines
- adrenergic hyperactivity (tachycardia, sweating, palpitations)
- secondary hypertension
- weight loss
- may be episodic

56
Q

how do you treat pts with pheochromocytoma before surgery?

A

α-block (phenoxybenzamine) first, then β-block (propranolol), then calcium channel block (nifedipine)

57
Q

what is MEN and what is the difference between MEN 1 and 2?

A

Multiple Endocrine Neoplasia Syndromes

MEN I – not typically assoc. with pheochromocytoma = the “P’s”
-Hyperparathyroidism –
hypercalcemia, osteoporosis, kidney stones
-Pituitary tumors – usually prolactinomas
-Pancreatc islet cell tumors – insulinomas usually (hypoglycemia results) or gastrinomas (give gastic ulcers)

MEN II

  • hyperparathyroidism;
  • medullary carcinoma of thyroid of parafollicular C cells - when this tumor is seen, always think MEN II
  • pheochromocytomas
  • **in MEN type II variant get thickened corneal nerves
58
Q

what is diagnostic/pathognomic for neurofibromatosis (type 1)

A 
o	Café au lait macules 6+ (big freckles)
o	Neurobibromas
****Bilateral Optic nerve glioma- pathognomonic 
o	Lisch nodules
o	Freckles in axillary or inguinal areas
o	Sphenoid bone dysplasia
o	Family Hx
o	Congenital glaucoma
o	Epilepsy
o	Renal artery stenosis
59
Q

what are some findings you might see with neurofibromatosis type 2?

A 
CN VIII tumors (bilateral schwannomas)
Meningiomas (multiple, may involve optic nerve sheeth)
**Juvenile posterior subcapsular lens opacity 
Family history of NF2 or CN VIII tumor
Other
**Gliomas (optic disk)
**Epiretinal membranes
Café au Lait spots
Peripheral neurofibromas
60
Q

thyroid gland primarily produces which, T4 or T3?

A

gland mostly produced T4, but T3 is more biologically active

61
Q

Total T4 influenced by what hormone?

A

TBG
•Low TBG: liver disease, nephrotic kidney disease, nutritional deficiency
•High TBG: pregnancy, estrogen therapy

62
Q

free vs total T4

A

Free T4 measures active thyroid hormone directly
Free T4 corrects for changes in TBG

T4 highly protein-bound (Thyroid Binding Globulin TBG)
Total T4 influenced by TBG

63
Q

Primary vs secondary hypothyroidism: what would free T4 and TSH levels be?

A

Primary hypothyroidism
Free T4 ↓; TSH ↑

Secondary hypothyroidism
Free T4 ↓; TSH ↓

64
Q

Primary vs secondary hypERthyroidism: what would free T4 and TSH levels be?

A

Primary hyperthyroidism
Free T4 ↑; TSH ↓

Secondary hyperthyroidism
Free T4 ↑; TSH ↑

65
Q

what are some ocular features of hypothyroid?

A 
Loss of lateral 1/3 of eyebrows
Periorbital edema
Ptosis
Cataracts
Graves-type ophthalmopathy (autoimmune)
Keratoconjunctivitis sicca (dry eye syndrome)
66
Q

T/F: can also get hypercholesterolemia with hypothyroid?

A

true

67
Q

how does hyperthyroid affect fertility and bone mass?

A

causes osteoporosis, infertility

68
Q

what is thyroid storm?

A

Thyroid storm / thyrotoxic crisis: acute onset of severe hyperthyroid Sx
-life-threatening (often these pts present to the ER)
-precipitated by infection, trauma, or surgery
-findings: high fever, sweating, tachycardia, restlessness, delirium, psychosis, tremor, coma (if not Dx and treated properly)
(basically – extremes of a lot of hyperthyroid symptoms)

69
Q

what is Apathetic Hyperthyroidism?

A

usually elderly patients with few obvious hyperthyroid symptoms, that present (commonly) for cardio care, esp. new a-fib
•depressed mental function, cardio comps: a-fib, other tachyarrythmias, heart failure

70
Q

Thyroid Ophthalmopathy causes?

A

Graves/hyperthyroid

-Hashimoto’s

71
Q

T/F: Most common cause of proptosis in adults is Graves

A

true
*Clinically significant in 20-40% of Grave’s patients
Present in up to 50%

72
Q

what are some methods to limit swelling/inflam/edema in Graves?

A

decrease swelling (inflammation, edema)
Glucocorticoids
Diuretics
Elevate head of bed

73
Q

what would you see on thyroid iodine scan in Grave’s

A

if Graves’ – avid iodine uptake

74
Q

what is subacute painful thyroiditis?

A

often follows a viral illness: pain in neck that might radiate to the ears and is worse with swallowing (often the patient swears they have an ear infection but the ears appear fine)
-tender thyroid
-basically happens because inflammation causes the preformed thyroid hormones to be released
2 phases:
1) Transient hyperthyroidism with ↑ T4 (very early - normal TSH)
2) Followed by hypothyroid phase (TSH will increase)

75
Q

what is painless thyroiditis?

A
  • may be sporadic or post-partum
  • transient hyperthyroidism (lymphocytic infiltration causes release of preformed thyroid hormone) followed by a hypothyroid phase (TSH lags…)
  • recovery normal function in 1-3 months, typically (this is different than Hashimoto’s hypothyroid which has no recovery)
76
Q

should be most concerned with optic nerve compression when what EOM affected?

A

medial rectus

77
Q

calcium plays a major role in what functions?

A 
Skeletal structure
Muscle contraction
Neurological function
Coagulation
Intracellular signaling
78
Q

osteoclasts vs blasts

A

osteoclasts resorb bone matrix to let Ca2+ free

osteoblasts lay down bone matrix and incorporate Ca2+

79
Q

parathyroid hormone (PTH)… if you need more calcium it will:

A

1) stimulates renal tubular calcium resorption
2) increase calcium resorption from the bones
3) increase renal hydroxylation of vitamin D
- activated vit D (activated by the kidney) allows/increases calcium absorption in gut

80
Q

what are 3 functions of vitamin D in body?

A

Increase calcium absorption (small bowel)
Increase calcium resorption (bone)
Decrease PTH synthesis

81
Q

where does vitamin D need to be activated?

A

liver and kidneys

82
Q

PTH stimulates what?

A

osteoclasts

83
Q

what are some symptoms of hypercalcemia? what do you see in the eye?

A

symptoms: “stones, bones, moans, groans”
• renal stones and nephrocalcinosis – calcium deposits in kidneys
• increased risk of fracture
o osteitis fibrosa cystica (OFC) – high bone turn over
o increased PTH in osteoporosis
• depression, lethargy, if severe seizures -> neuropsych Sx
• abdominal pain, constipation, pancreatitis, gallstones
• also band keratopathy -> subepithelial corneal calcium phosphate deposits – usually asymptomatic and do not require Tx

84
Q

what are some meds that cause increased risk of bone loss?

A 
Heparin
Thyroxine (excess)
Glucocorticoid
Anticonvulsants
Cyclosporine
(blood thinners, seizures, steroids)
85
Q

what are the screening recommendations for osteoporosis?

A

USPSTF recommends women 65+ are screened routinely

-start screening at age 60 for women who are at increased fracture risk

86
Q

T score vs Z score?

A

T score: Comparison w/ peak adult bone mass

Z score: Age comparison

Clinical Med (10 decks)

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