endo Flashcards
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decreased libido
kallman syndrome
defective hypothalmic gonadotropin realsing hormone and is associated with anosmia or hyposmia due to olfactory bulb agenesis or hypoplasia
prevents progression through puberty
postpartum women with hyperprolactinemia and prominent pituitary mass
lymphocytic hypophysiitis
empty sella
empty or partially empty sella
can hve normal pitutary function implying tht surrounding rim of pitutary tissue is functional
silent infarction csf filling
pitutary apoplexy
spontaneously postpartum ( sheehan) diabetes hypertension sicklecell anaemia shock
tt
high dose glucocorticoids if no evident visual loss
if loss of vision consiousness cn palsy them surgical decompression
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normal or high growth hormone level
low insulin groeth levels
sequence of hormone liloss in adult gh deficiency
GH 》FSH/LH》TSH》ACTH
igf level provide useful index of therapeutic respinses but not sufficient for diagnosis
because its level can be normal in gh deficiency
contraindications of gh replacement
active neolalsm
intracranial hypertension
uncontrolled diabetes
retinopathy
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male testosterone gnrh therapy for infertilty
females estrogen progestron
features of sellar mass
table 4031Impacted StructureClinical ImpactPituitaryHypogonadismHypothyroidismGrowth failure and adult hyposomatotropismHypoadrenalismOptic chiasmLoss of red perceptionBitemporal hemianopiaSuperior or bitemporal field defectScotomaBlindnessHypothalamusTemperature dysregulationAppetite and thirst disordersObesityDiabetes insipidusSleep disordersBehavioral dysfunctionAutonomic dysfunctionCavernous sinusOphthalmoplegia with or without ptosis or diplopiaFacial numbnessFrontal lobePersonality disorderAnosmiaBrainHeadacheHydrocephalusPsychosisDementiaLaughing seizures
stalk section phenomenon
pituitary stalk compression
disrupting pitituary of hypothalmic hormone and dopamine
decreasing all hormones except prolactin
physiologic pituary enlargement in?
adoloscent and pregnancy
prolactin suppresion by dopamine agonist doesnot neccesarily indicate tht underlying lesion is prolactinoma why?
because hyperprolactinemia caused by mass effect of nonlactotrope lesion is also corrected by treatment with dopamine agonist
mainstay of tratment with micro macro prolactinemia
oral dopamine agonist
dopamine agonist used pitutary prolactinoma
cabergoline
bromocriptine
men tend to present with larger tumors why
because features of male gonadotropin deficiency r les likely evident
causes of acromegaly
•Excess Growth Hormone Secretion
Pituitary Densely or sparsely granulated GH cell adenoma Mixed GH cell and PRL cell adenoma
Mammosomatotrope cell adenoma
Plurihormonal adenoma
GH cell carcinoma or metastases
Multiple endocrine neoplasia 1 (GH cell adenoma)
McCune-Albright syndrome
Ectopic sphenoid or parapharyngeal sinus pituitary adenoma •Extrapituitary tumor
Pancreatic islet cell tumor
Lymphoma Although these tumors usually express positive GHRH immunoreactivity, clinical features of acromegaly are evident in only a minority of patients with carcinoid disease.
Excessive GHRH
also may be elaborated by hypothalamic tumors, usually choristomas or neuromas. Presentation and Diagnosis Protean manifestations of GH and IGF-I hypersecretion are indolent and often are not clinically diagnosed for 10 years or more. Acral bony overgrowth results in frontal bossing, increased hand and foot size, mandibular enlargement with prognathism, and widened space between the lower incisor teeth. In children and adolescents, initiation of GH hypersecretion before epiphyseal long bone closure is associated with development of pituitary gigantism (Fig. 403-4). Soft tissue swelling results in increased heel pad thickness, increased shoe or glove size, ring tightening, characteristic coarse facial features, and a large fleshy nose. Other commonly encountered clinical features include hyperhidrosis, a deep and hollow-sounding voice, oily skin, arthropathy, kyphosis, carpal tunnel syndrome, proximal muscle weakness and fatigue, acanthosis nigricans, and skin tags. Generalized visceromegaly occurs, including cardiomegaly, macroglossia, and thyroid gland enlargement. The most significant clinical impact of GH excess occurs with respect to the cardiovascular system. Coronary heart disease, cardiomyopathy with arrhythmias, left ventricular hypertrophy, decreased diastolic function, and hypertension ultimately occur in most patients if untreated. Upper airway obstruction with sleep apnea occurs in more than 60% of patients and is associated with both soft tissue laryngeal airway obstruction and central sleep dysfunction. Diabetes mellitus develops in 25% of patients with acromegaly, and most patients are intolerant of a glucose load (as GH counteracts the action of insulin). Acromegaly is associated with an increased risk of colon polyps and mortality from colonic malignancy; polyps are diagnosed in up to one-third of patients. Overall mortality is increased about threefold and is due primarily to cardiovascular and cerebrovascular disorders and respiratory disease. Unless GH levels are controlled, survival is reduced by an average of 10 years compared with an age-matched control population. Laboratory Investigation Age-matched serum IGF-I levels are elevated in acromegaly. Consequently, an IGF-I level provides a useful laboratory screening measure when clinical features raise the possibility of acromegaly. Due to the pulsatility of GH secretion, measurement of a single random GH level is not useful for the diagnosis or exclusion of acromegaly and does not correlate with disease severity. The diagnosis of acromegaly is confirmed by demonstrating the failure of GH suppression to <0.4 μg/L within
Excess Growth Hormone–Releasing Hormone Secretion Central Hypothalamic hamartoma, choristoma, ganglioneuroma
Peripheral Bronchial carcinoid, pancreatic islet cell tumor, small cell lung cancer, adrenal adenoma, medullary thyroid carcinoma, pheochromocytoma
features of acromegaly
•Acral bony overgrowth results in frontal bossing, increased hand and foot size, mandibular enlargement with prognathism, and widened space between the lower incisor teeth. In children and adolescents, initiation of GH hypersecretion before epiphyseal long bone closure is associated with development of pituitary gigantism
•Soft tissue swelling results in
increased heel pad thickness,
increased shoe or glove size,
ring tightening,
characteristic coarse facial features, and a large .
generalized visceromegaly occurs, including cardiomegaly, macroglossia, and thyroid gland enlargemen
Other commonly encountered clinical features include hyperhidrosis, a deep and hollow-sounding voice, oily skin, arthropathy, kyphosis, carpal tunnel syndrome, proximal muscle weakness and fatigue, acanthosis nigricans, and skin tags. Get.
additional treatment of growth hormone secreating adenoma
surgical correction
medical treatment of growth hormone secreating adenoma
somatostatin analges octrotide lanreotide
therapeutic effects somatostatin receptors whuch r presnt of gh secreating tumors
Adverse effects are
git mainly
short-lived and mostly relate to druginduced suppression of gastrointestinal motility and secretion. Transient nausea, abdominal discomfort, fat malabsorption, diarrhea, and flatulence
. Octreotide suppresses postprandial gallbladder contractility and delays gallbladder emptying; develop long-term echogenic sludge or asymptomatic cholesterol gallstones. Other side effects include mild glucose intolerance due to transient insulin suppression, asymptomatic bradycardia, hypothyroxinemia, and local injection site discom
•gh receptor antagonst
pegvisomant
• dopamine agonist
suppress growth hormone secretion cabergoline
clinical features of cushing syndrome
Obesity or weight gain (>115% ideal body weight) Thin skin Moon facies Hypertension Purple skin striae Hirsutism Menstrual disorders (usually amenorrhea) Plethora A bnormal glucose tolerance Impotence P roximal muscle weakness Truncal obesity Acne B bruising Mental changes Osteoporosis Edema of lower extremities Hyperpigmentation Hypokalemic alkalosis Diabetes mellitus
use of petrosal sinus venous sampling
differntiate between pitutary adenoma and acth secreating tumors
treatment of choice cushing ds
selective transpenoidal resection
drugs used in cushing syndrome
somatostatin analogue
pasirotide
hyoerglycemia diabetes due to suppressed secretion of pancreatic secretion of insulin and increatins
glucocorticoids receptors antagonists
mifepristone
steroidogenic inhibitors
ketoconazole inhibit cytp450
metrapone inhibits 11b hydroxylasenelson syndrome
Adrenalectomy in the setting of residual corticotrope adenoma tissue predisposes to the development of Nelson’s syndrome, a disorder characterized by rapid pituitary tumor enlargement and increased pigmentation secondary to high ACTH levels. Prophylactic radiation therapy may be indicated to prevent the development of Nelson’s syndrome after adrenalectomy.
most common type of pituitary adenoma
non functional
MOA of AVP
Antidiuresis is mediated via binding to G proteincoupled V2 receptors on the serosal surface of the cell, activation of adenyl cyclase, and insertion into the luminal surface of water channels composed of a protein known as aquaporin 2
constriction of smmoth muscles in blood vessels and git
drug essential in sheehan syndrome
glucocorticoids
All are associated with pituitary apoplexy except-
1) Hyperthyroidism
2) Diabetes mellitus
3) Sickle cell anemia
4) Hypertension
hyperthyroidism
most common cause of GHRH mediated acromegaly
chest or abdominal carcinoid
Nelson’s syndrome is most likely seen after -
1) Hypophysectomy
2) Adrenalectomy
3) Thyroidectomy
4) Orchidectomy
adrenalectomy
Tolvaptan is approved for use in-
1) High Na
2) High K
3) High Ca
4) Low Na
low na
Treatment of lithium induced diabetes insipidus -
1) Vasopressin
2) Mineralocorticoid antagonist
3) Amiloride
4) Loop diuretic
amiloride
causes of diabetes insipidus
pituitary di
gestational DI
secondary DI due to ongibition of avp by excess fliud intake
also known as primary polydypsia
3 subcategories
dipsogenic di
psychogenic di
ioatrogenic di
nephrogenic di
most common cause of preventable mental retardation
iodine deficiency
most common cause of preventable mental retardation
iodine deficiency
cause of cretinism
congenital hypothroidism
thyroid hormone synthesis begin at 11 wks of gestation if there is no thyroid gland / hormone mother thyroid will compensate till birth so chance sof cretinism will be more in first few yrs of life
if mother is also hypothyroid during pregnancy child will be born with cretinism
TSH is realsed in pulsatile manner but single measurement is effective why
long half life of TSH
wolff chaikoff effect
excess iodine transiently inhibits thyroid iodide organification
CAUSE OF INCREASE and DECREASE IN TBG
increase in pregnancy ocp inflammatory liver ds tamoxifen serm
decrease in
androgens
nephorotic syn
seum TBG levels are increased in all type of thyrotoxcossis except
thyrotoxic factitia caused by self admininstration of thyroid hormone
function of tpo
oxidation of iodine
coupling of monoidottrosines and diiodotyrosines
antibodies found in hypothyroidism
antiTPO
antithyroglobulin
anti TSH
they r useful markers of autoimmunity
