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
causes of ED?
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
26
phosphodiesterase-5 inhibitors (PDE-5) are taken for what and can cause what kind of ocular side effects?
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)
27
3 situations where you wouldn't give phosphodiesterase-5 inhibitors (PDE-5)
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
28
ADH is made where? what does it control?
posterior pituitary hormone synthesized in the magnocellular neurons that regulates water balance
29
Name 2 target tissues for ADH and what it does there?
1) kidney (resorp free water/anti-getting-rid-of-fluid) – concentrates urine 2) blood vessels (vasoconstriction and increased BP)
30
ADH is triggered by what 2 things?
1) increased serum osmolality – want to hold water (sensitive to 1% changes) 2) volume contraction/decrease – want to hold all the fluid you can
31
what is syndrome of inappropriate ADH (SIADH)?
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
32
Causes of syndrome of inappropriate ADH (SIADH)?
* pulmonary disease (i.e. tuberculosis or pneumonia) * bronchogenic carcinoma – certain lung cancers * central nervous system diseases * drugs: SSRI really only if elderly (Prozac), ecstasy
33
ACTH release of what from what gland?
ACTH stimulates cortisol, aldosterone, androgens from adrenal gland
34
what are some stimuli for ACTH?
Stress, psychological, surgery, serious infection, trauma, physical, Hypoglycemia
35
when does ACTH peak and trough?
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
what are the 3 adrenal cortex zones and what do they secrete?
Zona glomerulosa→Aldosterone Zona fasciculata→ Cortisol Zona reticularis→Androgen (DHEA / S)
37
adrenal medulla secerets:
catecholamines (epi and norepi)
38
T/F: too much ACTH can give DM?
ACTH is counterregulatory hormone – too much cortisol can give diabetes
39
excess cortisol can cause what kind of effects or conditions to occur?
```  hyperglycemia/DM  irregular menses  immune suppression  depression, insomnia, various mood and sleep disorders  weight gain  osteoporosis  cataracts  secondary HTN *Proximal Muscle weakness ```
40
what is a stimulus for aldosterone release?
stimulated by renin-angiotensin | Also ACTH, hyperkalemia, hypovolemia
41
Cushing's disease vs syndrome?
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
what could be an ACTH independent cause of Cushing's syndrome?
``` Adrenal tumor (primary) Exogenous glucocorticoid ```
43
what are some options for screening for Cushing's syndrome?
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
what is Nelson's syndrome? when would you get it? how can you prevent it
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
what stimulates production of aldosterone?
Angiotensin 2
46
angiotensin is produced where? where is renin?
kidneys produce renin | angiotensin is produced in liver
47
Describe the effects of aldosterone on these 3 ions: sodium, potassium, hydrogen
Na ↑ K ↓ H ↓
48
Name a secondary cause of hyperaldosteronism:
renovascular hypertension (i.e. renal artery stenosis) -> renal artery is narrowed so the kidney senses volume depletion
49
you would be suspicious of hyperaldosteronism if you see HTN with what:
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
Chronic vs acute symptoms of adrenal insufficiency?
Chronic: -weakness, fatigue, hypOtension (postural) - hyperpigmentation (PRIMARY only) -Hyponatremia, Hypoglycemia, Hyperkalemia (primary), -Metabolic acidosis Acute=collapse, emergency
51
what is Addison's disease?
Addison’s disease is an autoimmune that usually gives both mineralo- and glucocorticoid deficiency *primary adrenal insufficiency
52
For adrenal insufficiency, elevated plasma ACTH will only be seen in primary causes
elevated plasma ACTH will only be seen in primary causes
53
what is adrenal virilism?
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
How can you diagnose pheocromocytoma?
Elevated catecholamines in plasma or 24 hour urine
55
what is pheochromocytoma and what kind of side effects does it cause?
pheochromocytoma: adrenal tumors that secrete catecholamines - adrenergic hyperactivity (tachycardia, sweating, palpitations) - secondary hypertension - weight loss - may be episodic
56
how do you treat pts with pheochromocytoma before surgery?
α-block (phenoxybenzamine) first, then β-block (propranolol), then calcium channel block (nifedipine)
57
what is MEN and what is the difference between MEN 1 and 2?
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
what is diagnostic/pathognomic for neurofibromatosis (type 1)
``` 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
what are some findings you might see with neurofibromatosis type 2?
``` 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
thyroid gland primarily produces which, T4 or T3?
gland mostly produced T4, but T3 is more biologically active
61
Total T4 influenced by what hormone?
TBG •Low TBG: liver disease, nephrotic kidney disease, nutritional deficiency •High TBG: pregnancy, estrogen therapy
62
free vs total T4
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
Primary vs secondary hypothyroidism: what would free T4 and TSH levels be?
Primary hypothyroidism Free T4 ↓; TSH ↑ Secondary hypothyroidism Free T4 ↓; TSH ↓
64
Primary vs secondary hypERthyroidism: what would free T4 and TSH levels be?
Primary hyperthyroidism Free T4 ↑; TSH ↓ Secondary hyperthyroidism Free T4 ↑; TSH ↑
65
what are some ocular features of hypothyroid?
``` Loss of lateral 1/3 of eyebrows Periorbital edema Ptosis Cataracts Graves-type ophthalmopathy (autoimmune) Keratoconjunctivitis sicca (dry eye syndrome) ```
66
T/F: can also get hypercholesterolemia with hypothyroid?
true
67
how does hyperthyroid affect fertility and bone mass?
causes osteoporosis, infertility
68
what is thyroid storm?
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
what is Apathetic Hyperthyroidism?
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
Thyroid Ophthalmopathy causes?
Graves/hyperthyroid | -Hashimoto's
71
T/F: Most common cause of proptosis in adults is Graves
true *Clinically significant in 20-40% of Grave’s patients Present in up to 50%
72
what are some methods to limit swelling/inflam/edema in Graves?
decrease swelling (inflammation, edema) Glucocorticoids Diuretics Elevate head of bed
73
what would you see on thyroid iodine scan in Grave's
if Graves’ – avid iodine uptake
74
what is subacute painful thyroiditis?
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
what is painless thyroiditis?
- 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
should be most concerned with optic nerve compression when what EOM affected?
medial rectus
77
calcium plays a major role in what functions?
``` Skeletal structure Muscle contraction Neurological function Coagulation Intracellular signaling ```
78
osteoclasts vs blasts
osteoclasts resorb bone matrix to let Ca2+ free | osteoblasts lay down bone matrix and incorporate Ca2+
79
parathyroid hormone (PTH)… if you need more calcium it will:
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
what are 3 functions of vitamin D in body?
Increase calcium absorption (small bowel) Increase calcium resorption (bone) Decrease PTH synthesis
81
where does vitamin D need to be activated?
liver and kidneys
82
PTH stimulates what?
osteoclasts
83
what are some symptoms of hypercalcemia? what do you see in the eye?
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
what are some meds that cause increased risk of bone loss?
``` Heparin Thyroxine (excess) Glucocorticoid Anticonvulsants Cyclosporine (blood thinners, seizures, steroids) ```
85
what are the screening recommendations for osteoporosis?
USPSTF recommends women 65+ are screened routinely | -start screening at age 60 for women who are at increased fracture risk
86
T score vs Z score?
T score: Comparison w/ peak adult bone mass | Z score: Age comparison