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Transcript
Endocrinology
Edward Buckingham, M.D.
Faculty Advisor: Francis Quinn, M.D., FACS
The University of Texas Medical Branch
Department of Otolaryngology
Grand Rounds Presentation
December 15, 1999
Pituitary - Embryology and
Anatomy
• posterior pituitary- neurohypophysis
– outpouching floor 3rd ventricle
– nervous connection to hypothalamus
– octapeptides-oxytocin, vasopressin (ADH)
• anterior pituitary-adenohypophysis
–
–
–
–
Rathke’s pouch
no direct nerve supply
chemical hypophyseal-portal system
ACTH, TSH, GH, PRL, FSH, LH
Pituitary - Embryology and Anatomy
Pituitary - Sella tercica, sphenoid bone
Pituitary - Relation to sphenoid sinus
Pituitary - Soft tissue boundaries
Pituitary - Vasculature
Pituitary - Embryology and Anatomy
Pituitary - Embryology and Anatomy
Pituitary - antidiuretic hormone (ADH)
(vasopressin)
• CNS osmoreceptors supraoptic,
periventricular nuclei hypothalamus
– plasma osmolality changes
• baroreceptors, aortic arch, carotid sinus, left
atrium
– CN IX, X
• renal action
– ADH increases H2O permiability of DCT and
CD
Pituitary - ACTH
•
•
•
•
•
proopiomelanocortin precursor
melanotropins, lipotropins and B-endorphin
circadian rhythm peaks am,
stimulus, CRF- stress, hypoglycemia,
CRF-feed back from glucocorticoids in
circulation
• action- adrenal cortex secrete
glucocorticoids, lesser aldosterone
Pituitary - TSH
• glycoprotein hormone, thrytopic cells, level
constant
• stimulus, TRH
• feedback free T3
• c-AMP mediated
• action-early increased formation of colloid,
uptake of iodine, formation of TH
• action-late increased volume and number of
cells
Pituitary - GH
• via somatomedins
promotes longitudinal
growth
• anabolic protein
metabolism, lipolytic,
stimulates insulin
release, decreases
peripheral tissue
utilization of glucose
Pituitary - Prolactin
• acts on prepared mammary tissue to initiate
and maintain lactation
Pituitary - FSH, LH
• Kallmann’s syndromemaldevelopement
olfactory lobes, related
hypothalamic lesions,
hyposmia, anosmia,
isolated Gn-RH
deficiency
Pituitary - Diabetes Insipidus
• partial or complete
absence of vasopressin
• tumor, inflammation,
granuloma, trauma,
vascular
Pituitary - Diabetes Insipidus
• clinical features
– polyuria- 3-15 L/day 4-5 L common, SG <
1.005, urine osmolality <200 mOsm/kg, plasma
osmolality > 287 mOsm/kg
– polydipsia- compensatory mechanism,
hypothalamic thirst center destruction
disastrous
– associated features- visual field loss, optic
atrophy, papilledema, other pituitary hormone
abnormalities
Pituitary - Diabetes Insipidus
• treatment
– acute- liberal fluid
replacement, shortacting aqueous
vasopressin
– chronic- dDAVP
intranasally BID
Pituitary - SIADH
• continued secretion of
antidiuretic hormone
despite hypotonicity
• secreted by pituitary
or ectopic source
Pituitary - SIADH
• clinical features
– fatigue, muscle
weakness, dizziness,
behavioral changes,
drowsiness, Na < 120
stupor, convulsions,
coma
– urine osmolality not
maximally dilute
despite hypotonicity
Pituitary - SIADH
• diagnostic criteria
– hyptonicity of plasma
– hyponatremia
– less than max dilute
urine
– naturesis
– exclusion of other
causes
• treatment
– water restriction 600800 ml/day
– demeclocycline 9001200 mg/day- blocks
vasopressin at DCT
– hypertonic saline if
sodium < 115 mEq/L
Pituitary - Tumor classes
•
•
•
•
Class 1 - microadenomas < 10mm diameter
Class 2 - macroadenomas >10 mm diameter
Class 3 - part of sellar floor involved
Class 4 - all of the floor destroyed
Parathyroid- Embryology and
Anatomy
• third and fourth
branchial pouches
– third migrates with
thymus
– aberrant in 15% to
20%
– ICA to AP window ant
or post to arch
– usually 4 glands may
be 6 or more
Parathyroid- Ectopic glands
Parathyroid- Blood supply
• inferior/superior
parathyroid arteries
– branches of inferior
thyroid artery
– occas. superior from
sup. thyroid artery
Parathyroid- Calcium metabolism
• actions of PTH
–
–
–
–
–
increases serum calcium level
increases urine phosphate
increases bone osteoclast and osteoblast activity
increases bicarbonate excretion by kidney
increase GI calcium and phosphate absorption
through Vit D
– increases conversion of 25-OH Vit D to 1,25
di-OHVit D
Parathyroid- Calcium metabolism
• calcitonin
– parafollicular cells response to increased Ca
– inhibit bone resorption, increase phos excretion
by kidney
• vitamin D
–
–
–
–
absorbed through skin or GI tract
liver 25 OH
kidney 1,25 OH most active form
increases calcium and phosphate absorption and
retention
Parathyroid - Hypercalcemia
Parathyroid - Assoc. conditions
Parathyroid- Hypercalcemia
•
Parathyroid - laboratory evaluation
Parathyroid - definitions
• primary hyperparathyroidism
– single adenoma 85%, 12% hyperplastic glands,
3% multiple adenomas
• secondary hyperparathyroidism
– hyperplastic glands
– malfunction of another organ system
– usually renal failure
Parathyroid - definitions
• tertiary hyperparathyroidism
– similar to secondary
– PTH production now autonomous
– renal transplant
Parathyroid hyperparathyroidism
• Laboratory values
– low serum phosphorus (<2.5 mg/dL)
– hyperchloremia (>107 mEq/L)
– alkaline phosphatase elevated in 10%
• indicates osteitis fibrosis cystica
– subperiosteal bone resorption
Hyperparathyroidism - surgery
• asymptomatic
hyperparathyroidism
– Kaplan
• compared metabolic
benefits
• 6 pt asymptomatic with
7 symptomatic before
and after surgery
• concluded
asymptomatic received
same benefits
Hyperparathyroidism - surgery
• Other pros
–
–
–
–
postmenapausal women
Cogan psychologic function and EEG improved
avoid hypercalcemia if sick or dehydrated
cost effective
• surgery indicated
– hypertension, mildly reduced creatinine
clearance, increased urine calcium, decreased
bone density, clinical symptoms
Thyroid - Embryology and
Anatomy
• embryology
– pharyngeal floor,
foramen cecum
– decent with
parathyroids
– lateral to TE groove
– assoc. with RLN
Thyroid - Embryology and Anatomy
• vasculature
– arterial
• sup. thryroid artery
ECA
• inf. thyroid artery TCT
– venous
• superior and middleIJV
• inferior BCV
– lymphatics
• pretracheal,
paratracheal
Thyroid - Physiology
• hormonogenesis
–
–
–
–
–
–
–
trapping - iodine oxidized
organification - tyrosyl incorporation
MIT, DIT, T3, T4
secretion
95.5% bound. 0.5% free biologically active
TBG primarily, prealbumin, albumin
T4 > T3 liver and kidney
Thyroid - Physiology
• hormonogenesis
– inhibited by
• renal, hepatic disease
• acute or chronic illness
• drugs- propylthiouracil, glucocorticoids,
propranolol, iopanoic acid
– reverse T3
• regulation
– feedback of free T3 on TRH and TSH
• action
– metabolic rate, thermogenesis
Thyroid - TFT’s
• T4 radioimmunoassay
– measures bound and unbound hormone
• T3RU
–
–
–
–
–
determines TBG capacity
radiolabeled T3 given
bound to TBG open sites
resin given 25-35% normally binds to resin
increased TBG decreased T3RU
Thyroid - TFT’s
• FTI
– product of T3RU and T4
– good initial determination of hyper or hypo
thyroidism
• T3 radioimmunoassay
– reflects peripheral metabolism not thyroid
function
– T3 thyrotoxicosis
Thyroid - TFT’s
• TSH
– hypothyroidism
– replacement therapy
– euthyroid goiters
Thyroid imaging
• thyroid scans
– radioactive isotopes of iodine
– one month to clear contrast agents
– indications
•
•
•
•
hot and cold nodules
metastatic thyroid cancer
ectopic tissue
Hashimoto’s
Thyroid imaging
• ultrasonography
– solid vs. cystic
– FNA
– suppression
Thyroid - Hyperthyoidism
Thyroid - Hypofunction
Adrenal Gland
• cortex
– zona glomerulosa
• mineralocorticoids- aldosterone
– zona fasciculata
• glucocorticoids- cortisol
– zona reticularis
• androgens- estrogen, progesterone, testosterone
• medulla
– norepinephrine, epinephrine
Adrenal Gland - Physiology
• zona glomerulosa
– renin JG cell
• respond to Na, and volume
–
–
–
–
–
–
angiotensinogen > angiotensin I
angiotnsin I > angiotensin II by ACE
angiotensin II potent pressor > aldosterone
hyperkalemia promotes independently
hypokalemia inhibits
ACTH
Adrenal Gland - Physiology
• zona fasciculata
– ACTH as discussed
– cortisol actions
• zona reticularis
– ACTH controls
– no feedback
– adrenarche
Hyperadrenocorticism
• cushing’s sydndrome
• 3rd - 6th decade, 4 to1 females
• causes
–
–
–
–
pharmocologic
pituitary adenoma 75-90%
adrenal adenoma, carcinoma
ectopic ACTH
• treatment based on cause
Adrenocortical insufficiency
• primary causes, ie. Addison’s disease
– autoimmune disease, tumors, infection,
hemorrhage, metabolic failure,
• secondary causes
– hypopituitarism, suppression exogenous
steroids
Adrenocortical insufficiency
• symptoms, signs
– fatigability, weakness, anorexia, nausea, weight
loss, hyperpigmentation, hypotension, women
loss of axillary and pubic hair
– can lead to severe volume depletion and shock
• treatment
– glucocorticoid replacement, mineralocorticoid
replacement
Overproduction of aldosterone
• primary causes, ie. Conn’s syndrome
– adenoma, nodular hyperplasia zona
glomerulosa
• secondary
– cirrhosis, ascites, nephrotic syndrome, diuretic
use
• symptoms, signs
– headache, hypokalemia causing muscle
weakness, nocturnal polyuria, hand cramping
Overproduction of aldosterone
• treatment
– surgical for adenoma
– medical for hyperplasia with sprionolactone
Pancreas
• alpha cells- glucagon
• beta cells- insulin
– stimulus
• glucose, amino acids, glucagon, GI hormones, vagal
nerve
– inhibition
• B-adrenergic blockers, sympathomimetics,
somatostatin
Diabetes
Surgical care
• 120-250 mg/dL
• 1-2 hr checks
• 3 g/kg/day prevent catabolism and lipolysis
– 5% dextrose at 100 ml/hr
Ketoacidosis
–
–
–
–
–
–
–
ketone bodies metabolic acidosis-lipolysis
IV insulin 12-20 u bolus
.05 to 0.1 u/kg/hr
IVF - 0.9 NS
glucose approx. 200 add dextrose
potassium electrolytes as needed
monitor anion gap for endpoint
Hyperosmotic nonketotic coma
–
–
–
–
similar to above
disagreement isotonic/hypotonic saline
severe dehydration
watch electrolytes closely
Case Presentation
• 45 year old with craniopharyngeoma now
24 hrs post-op from a transphenoidal
approach to tumor excision
• Nurse notifies you patient urinated 3L over
the last 8 hrs and 5L over the last 16 hrs
Case Presentation
• PE
– The patient is slightly somnolent, but arousable,
oriented to person and place, but not to time or
situation, this is new over last 4-5 hrs
– No polydipsia
– Neuro-exam is otherwise normal
• Labs
– CBC, Chem 7, plasma osmolality pending,
urinalysis SG - 1.003, urine osmolality 185
mOsm/kg.
Case Presentation
• CT Head
– post-operative changes, otherwise normal
• Labs
– WBC 10.5, HGB 14.5, HCT 45.2, Plt 567K,
– Na-162, K-5.4, Cl-110, CO2-18, BUN-45, Cr.76, Glucose 120
– Osmolality - 300 mOsm/kg
Case Presentation
• Diagnosis
– Diabetes insipidus with injury to hypothalamic
thirst center
• Therapy
– Fluid boluses with isotonic saline
– aquous vasopressin