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1
Q

define primary endocrine disease

examples?

A

disease is within gland

neoplasms, autoimmune, vascular injury, infection, trauma, infiltrative process, molecular

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2
Q

secondary disease

A

caause of disease is outside gland (too high or too low trophic factor?? includes hormones?? which affects the gland

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3
Q

in glands, what should you think when you see heterogenous cells?
homogenous?
chronic inflammatory?

A

hetero?? hyperplasia
homo?? neoplasm (adenoma and carcinoma)
chronic inflammatory?? autoimmune

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4
Q

how much of the gland tissue must be gone for hypofunction to occur?

A

80?90%

atrophy of secretory cells or destruction/necrosis

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5
Q

what is most common endocrine neoplasia? benign or malignant? how do you diagnose?

A

adenoma more common
histopath of benign and malignant are often similar, so you diagnose based on presence of mets and/or local vascular/neural invasion

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6
Q

how do autoimmune endocrine diseases work?

A

can either interact with endocrine cell receptors to stimulate or block
or can cause tissue destruction (cell/humoral mediated immune injury with lymphocytes, macrophages, plasma cells)

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7
Q

what is the anterior pituitary called?

posterior pituitary?

A

anterior=adenohypophysis=pars distalis (80%)
portal vessels connect hypothalamus and adenohypophysis

posterior=neurohypophysis=pars nervosa?? extension of hypothalamic neuronal axons

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8
Q

adenohypophysis

describe the embryology

A

arises from oral cavity invagination called rathkes/hypophyseal pouch
extends dorsally
loses connection with oral cavity

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9
Q

neurohypophysis

describe the embryology

A

arises as ventral extension of hypothalamus

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10
Q

what is the anterior lobe of pituitary composed of?

A

clusters of secretory cells in richly vascular stroma

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11
Q

which secreetory products are acidophilic?

basophilic?

A

aciophils: somatotrophs (GH)
lactotrophs (prolactin)

basophils:
thyrotrophs (TSH)
corticotrophs (ACTH)
gonadotrophs (FSH and LH)

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12
Q

what is posterior lobe of pituitary composed of?

A

nervous tissue

composed of axons (whose neuronal bodies are in the hypothalamus) and modified glial cells (piuticytes)

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13
Q

where do pituitary adenomas and carcinomas arise from?

how do characterize macroaednoma vs microadenoma?

A

anterior pituitary cell

macro: >1cm??> mass effect
micro: no mass effect

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14
Q

where do craniopharyngiomas arise from?
who gets them?
gross?
microscopy?

A

bimodal: children/adolescents then >65 yrs

arise from remnant cells of rathkes pouch in neighborhood of pituitary, not from pituitary iteslf
can also be in suprasellar location
gross: cystic and solid regions
micro: nests/cords of stratified squamous cells edged with columnar cells, keratin, cholesterol rich cysts, fibrosis, calcification

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15
Q

sheehans syndrome

A

postpartum necrosis of anterior pituitary
anterior pituitary enlarges during pregnancy, majority of blood supply is venous

hemorrhage during/after surgery leads to hypotension then ischemia and necrosis of anterior pituitary

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16
Q

what is pituitary apoplexy?

A

sudden expanding hemorrhage (usually in adenoma) that leads to destruction of adjacent pituitary cells
leads to hypopituitarism

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17
Q

panhypopituitarism

A

involves both anterior and posterior pituitary

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18
Q

empty sella sydnrome

A

destruction of all or part of pituitary

can be from surgery, radiation, congenital defect (when there is no diaphragm so CSF goes into sella)

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19
Q

what happens when there is posterior pituitary destruction?

A

low ADH??> central diabetes insipidus

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20
Q

what is the most common pituitary tumor?

A

prolactinoma

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21
Q

what are natural causes of hyperprolactemia?

A

sleep, physical exertion, food, stress, ovluation, coitus, prenancy, suckling, lactation

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22
Q

pathologic causes of hyperprolactinemia

A

prolactinoma
acromegaly, sellar masses, infiltrative, pituitary stalk disease, primary hypothyroidism

seizures, polycystic ovary disease, chest wall trauma, surgery, herpes, renal insufficiency, cirrhosis

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23
Q

pharmacologic causes of hyperprolactinemia

A

antihypertensives (verapamil, methydopa, reserpine)
GI meds (chlorpromazine, metocolpramide, domperidone)
antipsychs (atypicals, haloperidol, reserpine, phenothiazines)
antidepressants
cocaine, opiates, protease inhibitors

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24
Q

how do women with hyperprolactinaemia present?

men?

A

women: galactorrhea (30?80%), amenorrhea, infertility, breast atrophy
men: impotence/poor libido, visual field abnormalities, headache, extraocular muscle weakness, anterior pituitary malfunction, galactorrhea (<30%)
? men present with larger tumor

both: loss of secondary sexual hair

25
Q

tx of hyperprolactinemia

A

primary: dopamine agonist therapy (cabergoline and bromocriptine)?? reduces tumor size
surgery and radiation have limited use

(to diagnose you want to do pregnancy test, TSH, free T4, creatinine)

26
Q

side effects of DA agonist therapy

A

N/V, orthostatic hypotension

uncommon: nasal congestion, headache, fatigue, constipation, psychosis, sleep disturbance

27
Q

pathophysiologic changes caused by effects of excessive GH

A

GH and IGF?I are located in many organs (bone, fat, muscle, liver)
bone growth leads to acral changes (large hands and feet out of proportion)
thickening of skin
hypertension
neuromuscular/psych disorders
neoplasia
respiratory problems
cardiomyopathy (heart grows in response to GH, can lead to right vent dysfunction)

sweating, carpel tunnel sydrome, glucose intolerance (can lead to type 2 diabetes)

28
Q

how do you diagnose agromegaly?

when do you produce the most GH?

A

cant take a single measurement of growth hormone bc secretion is pulsatile (you make most during stage 4 sleep)

measurement of insulin like growth factor level is reliable marker for diagnosis of acromegaly (represents average daily GH secretion, levels remain stable throughout day

29
Q

what happens to normal people’s GH levels when you administer glucose?

A

they drop

30
Q

what is the impact of acromegaly on survival?

A

lowers it more wtih acro + diabetes

even more with acro + cardiac disease

31
Q

how do you treat acromegaly?

A

transsphenoidal hypophysectomy
advantage: induce immediate decline in GH level, eliminate or reduce tumor mass, low morbidity
but mortality risk is higher and you may need hormone replacement

radiotherapy
controls tumor growth, but has a delayed response, can lead to hypopituitarism (cant aim laser?? will have deficiency of TSH, ACTH, gonads)

32
Q

what is medical therapy that targets GH/IGF pathway?
(3)
advantages/disadvantages of each?

A

somatostatin analogs?? directly inhibit GH secretion
?no hypopituitarism, once monthly IM injection, possible tumor size reduction/growth control, signs/symptoms improve
but some patients have dift subtypes, resistant to therapy

dopamine agonists?? directly inhibit GH secretion

growth hormone receptor (GHR) antagonist (pegvisomant)?? blocks GH receptor and directly inhibits IGF secretion
improves perspiration, fatigue, soft tissue swelling
but does not affect tumor size!

33
Q

what is goal of management in acromegaly?

A

reduce effects of elevated GH by normalizing IGF levels (this is the measurement used for disease monitoring, normalization of IGF is associated with reduced mortality/morbidity)

34
Q

what do nonfunctioning pituitary tumors secrete?

how are these tumors found?

A

alpha subunit of pituitary glycoprotein hormones
but the BETA subunit is what confers specificity
alpha subunit has no biologic activity bc no hormone excess syndrome

tumors are slow growing, may present as incidental finding on imaging or with symptoms of mass effect (HA, visual changes, cranial nerve palsies)

35
Q

in what order do you lose hormone function of anterior pituitary?

A

GH then LH/FSH then TSH then ACTH then prolactin

36
Q

symptoms of TSH deficiency in children and in adults?

A

children: growth retardation
adults: dec energy, constipation, sensitivity to cold, dry skin, weight gain

37
Q

symptoms of ACTH def?

A

weakness, tiredness, dizziness on standing, pallor, hypoglycemia

38
Q

how often will a microadenoma will progress macroadenoma

what are indications for surgery?

A

10?15%

do surgery if: enlarging lesion, headaches, hypopituitarism
gonadotrophin and GH deficiencies usually occur first

39
Q

causes of hypopituitarism:
how can you tell if its familial hypothalamic?

what other processes can mess up hypothal?

A

midline CNS/facial defects
cleft lip/palate, single upper central incisor

tumors (craniopharyngiomas, CNS tumors, mets)
non tumor: infiltrative disease (sarcoid, TB, lymphoma), trauma
functional: psychosocial, anorexia nervosa

40
Q

what are causes of pituitary damage?

A

genetic?? mutations in pituitary transcription factors
tumors: adenomas, craniopharyngiomas, mets
non tumors: apoplexy of adenoma, sheehans, trauma

41
Q

whats important about recognizing hypopituitarism?

A

symptoms develop slowly

ALL are treatable!

42
Q 
clinical features of hypopituitarism in children?
FH (2)
birth history (2)
neonates (3)
children (3)

adults?

A

FH: parental heights, history of short stature
BH: trauma/hypoxia
neonates: hypoglycemia, midline defects, micropenis
children: dec growth velocity, delayed/absent puberty, TSH/ACTH deficiency

adults: mass effect symptoms, history of destructive process, FSH/LH def

43
Q

clinical features of ACTH def?

A

fatigue, anorexia, weight loss, postural hypotension

44
Q

TSH deficiency features

A

fatigue, cold intolerance, constipation, dry skin, hair loss

45
Q

FSH/LH deficiency

A

women: oligo or amenorrhea, vaginal dryness, hot flashes
men: loss of libido, erectile dysfunction, diminished strength

46
Q

GH deficiency features

A

increased adiposity, reduced strength and muscle mass

47
Q

symptoms of women with panhypopituitarism

A

slightly overweight
fine wrinkling of skin
decreased pigmentation
decreased/absent pubic and axillary hair

48
Q

how do you diagnose FSH/LH def?

A

estradiol and testosterone are low, FSH/LH low/normal

stimulation not necessary and you have blunted/delayed response to GnRH

49
Q

TSH deficiency

A

T4/T3 low
TSH low or normal
stimulation not necessary, blunted/delayed response to TRH

50
Q

ACTH

A

morning cortisol low, ACTH low/normal

insulin induced hypoglycemia, metyrapone test, ACTH stimulation test

51
Q

tx of FSH/LH
TSH
ACTH

A

FSH/LH: estrogen/progestin
M: testosterone

TSH: levothyroxine (daily pill)

ACTH: hydorcotisone or prednisone, dexamethaxasone (pills)

52
Q

how does sheehans syndrome present?

A

failure to lactate, loss of menses

can manifest immediately or years/decades after

53
Q

how does pituitary aplopexy manifest?

A

sudden hemorrhage into pituitary gland or adenoma
sudden excrutiating headache, diplopia from pressure on CN 3/4/6, hypotension

tx: fluids +glucocorticoids + CV support

54
Q

GHD

what causes it in children? adults?

A

children?? GHD is isolated or idiopathic

in adults?? usually due to pituitary tumor and coexists with other pituitary deficiencies (isolated GH deficiency is controversial)

55
Q

features of GH deficiency in kids

A

growth failure after a period of normal growth

subcutaneous fat, esp around trunk, immature face, delayed dentition, delayed puberty

left hand/wrist x ray estimates bone maturation

56
Q

features of GH deficiency in adults

A

usually 4th?5th decade
symptoms are nonspecific
(dec exercise performance, dec sense of wellbeing, energy, depressed mood)
dec muscle mass, bone density, inc central adiposity, inc LDL chol, low HDL
impaired cardiac fx

57
Q

how do you diagnose GH def?

A

measure IGF
then administer stimulus
insulin?induced hypoglycemai or CNS neuroactive agents such as clonidine, glucagon, arginine

should cause IGF to increase

58
Q

how do you treat GH deficiency?

A

recombinant human growth hormone (hGH)
3X/week subcutaneous injections

improve linear growth, restore body composition, improve strength QOL

risks: Na/H20 retention (athralgias, myalgias, edema, carpal tunnel syndrome)
glucose intoleranse, intracranial HTN,

Endocrine (8 decks)

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