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"My FLAT PiG"
List all the hormones secreted by the anterior pituitary
MSH - melanotropin FSH - stimulates sex organs LH - stimulates sex organs ACTH - adrenal growth and steroidogenesis Prolactin - stimulates lactation GH - stimulates somatic growth via IGF-1 and is counter-regulatory to insulin B FLAT
Which hormones in the Anterior pituitary are produced by the basophils?
Basophils produce FSH, LH, ACTH, TSH These hormones have a common alpha subunit. The beta subunit determines speciﬁcity.
Which hormones in the Anterior pituitary are produced by the acidophils?
GPA GH, Prolactin are produced by Acidophils
Impotence Amenorrhea (Prolactin inhibits GnRH) Gynecomastia (male breasts), Galactorrhea (abnormal milk production) Headache Bitemporal hemianopsia (loss of peripheral vision) General hypopituitary symptoms (if "mass effect" is present)
List 6 signs and symptoms of a prolactinoma
List a common clinical correlation that can mimic a prolactinoma
Dopamine antagonists (ex: antipsychotics) cause galactorrhea, amenorrhea, impotence, etc due to loss of dopamine inhibition on prolactin
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First line: Bromocriptine or cabergoline (dopamine agonists)
What is the treatment for a prolactinoma?
Second line: Transsphenoidal surgical resection for large tumors NOTE: Bromocriptine can also be used in the treatment of Parkinson's disease.
Bitemporal hemianopsia (loss of peripheral vision) You must do a visual ﬁeld test (during the PE) on a patient with signs or symptoms of a prolactinoma! Other sx: amenorrhea, gynecomastia, galactorrhea, etc. What classic sign/symptom is this patient most likely experiencing? Both are caused by pituitary adenoma that secretes growth hormone GH secretion in childhood prior to skeletal epiphyseal closure = Gigantism Lengthening of long bones GH secretion in adulthood after epiphyseal closure = Acromegaly Thickening of bones Coarsening of skin/facial features Thickening hands and feet Prognathism (an overbite or underbite) Large tongue with deep furrows Deep voice Peripheral neuropathies due to nerve compression 1) Surgery or radiation 2) Octreotide: somatostatin analogue that inhibits GH release from the anterior pituitary
Compare and contrast Acromegaly and Gigantism
List 6 clinical signs and sx of Acromegaly
List three treatments for a pituitary adenoma that secretes growth hormone
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3) Pegvisomant: GH receptor antagonist blocking the production of IGF-1
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TSH GnRH ---(+)--> FSH LH <---(-)--.Prolactin The anterior pituitary is derived from which embryological tissue? Oral ectoderm (Rathkeʼs pouch) The posterior pituitary is derived from what embryological tissue? Neuroectoderm Vasopressin..StudyBlue Flashcard Printing of Endocrinology http://www. MSH Dopamine --(-)--> Prolactin GHRH ---(+)--> GH Somatostatin ---(-)--> GH. has 2 functions: List the two major function of vasopressin and it's other names. especially after a glucose tolerance test (should be less than 1ng/nL after ingesting 75g of glucose) MRI 5 of 47 2/1/12 8:57 PM . 1) Moderate vasoconstriction 2) Antidiuretic effect. aka AVP (arginine-vasopressin) or ADH (antidiuretic hormone). increases passive water reabsorption in renal collecting ducts When ADH is present you make Dark urine How do you diagnose a GH sectreing toumor? Increased serum IGF-1. Prolactin CRH ---(+)--> ACTH.com/servlet/printFlashcardDeck?deckId=. List the hormones involved in the hypothalamic pituitary axis and their relationships (inhibition/stimulation) TRH --(+)--> TSH..studyblue.
Exercise 3.StudyBlue Flashcard Printing of Endocrinology http://www.Trauma to pituitary . List three normal reasons for an increase in GH 1..Pituitary tumor What are the types and causes of diabetes insipidus? 2) Nephrogenic diabetes insipidus: Kidney is not responding to ADH . the patient my recover ADH production in a 3-5 days.. Hypoglycemia Ingesting glucose should cause a decrease in IGF-1. What is the treatment for Central diabetes insipidus? 6 of 47 2/1/12 8:57 PM .studyblue. Stress 2. urine osmolarity is very low (<150mOsm/L). intranasal desmopressin (ADH analog) for replacement Note: if the DI was caused by trauma. be careful not to over-hydrate!! Lack of ADH >7 days indicates permanent DI.com/servlet/printFlashcardDeck?deckId=.Hereditary Response to desmopressin distinguishes the two Adequate hydration. if it doesn't. together with an inability to concentrate urine Serum osmolarity is high (>290 mOsm/L).Lithium . and urine speciﬁc gravity is low (<1. you dx GH secreting tumor List two physiologic controls that cause and increase in AVP secretion 1) An increase in serum osmolality is sensed by osmoreceptors in hypothalamus which release AVP into the systemic circulation 2) Baroreceptors sense a decrease in blood volume (5-10%) and afferent inputs to the hypothalamus for more ADH What are the signs and symptoms of diabetes insipidus? Intense thirst and polyuria (over 3L/24hrs).006) 1) Central diabetes insipidus: pituitary is not secreting ADH .
no edema. Medications such as chlorpropamide can also cause inappropriate ADH secretion Euvolemic hyponatremia . but cognitive Name three treatments for SIADH Discuss central pontine myelinolysis and its cause 7 of 47 2/1/12 8:57 PM .studyblue. a lung tumor... or a lung infection. bringing in free water and dumping Na) Abnormal mental status List 5 signs and symptoms of SIADH? Convulsions Fatigue Headache Irritability Normal blood pressure. 3) Hypertonic (5%) saline if severe CNS changes.StudyBlue Flashcard Printing of Endocrinology http://www. etc Urine osmolarity will usually be be higher than serum osmolarity 1) Free water restriction if asymptomatic 2) Demeclocycline: inhibits the actions of ADH in the kidney.. or amiloride * Thiazides increase renal Na excretion → ECF volume contraction → ↓ GFR → ↑ proximal tubular reabsorption of water and Na ∴ less water and Na are lost as urine What is the Syndrome of Inappropriate Antidiuretic Hormone and what are the causes? SIAHD occurs when too much ADH is produced by the posterior pituitary (tumor). hydrochlorothiazide*. indomethacin.com/servlet/printFlashcardDeck?deckId=.(Body responds by decreasing Aldo/Na reabsorption. What is the treatment for nephrogenic diabetes insipidus? Adequate hydration.. such as seizures CAUTION: Rapid correction of hyponatremia can lead to central pontine myelinolysis Rapid correction of hyponatremia can lead to central pontine myelinolysis Damage of myelin sheath of pons → patient becomes "locked in": muscles paralyzed with exception of eye blinking.
com/servlet/printFlashcardDeck?deckId=.studyblue...StudyBlue Flashcard Printing of Endocrinology http://www. function is intact 8 of 47 2/1/12 8:57 PM .
Diet Breast milk is relatively vitamin D DEFICIENT! It is important to supplement this vitamin. vaginal distention and uterus contraction Used clinically for: acute postpartum hemorrhage and to induce labor After labor: in the presence of oxytocin.StudyBlue Flashcard Printing of Endocrinology http://www.25 OH2 vitamin D (via 1α-hydroxylase in kidney) Macrophages can also convert vitamin D to it's active 1.Sunlight/Skin and MILK!! Vitamin D2 (ergocalciferol) . What are the functions of oxytocin? During labor: stimulates cervical.studyblue..25 OH2 form (cause of hypercalcemia in sacroidosis) Increase in both [Ca2+] and [phosphate] List the four effects of Vitamin D on Ca2+ and Phosphate Increase intestinal Ca2+ absorption via (calbindin-D-28K) Increase intestinal phosphate absorption Increase renal Ca2+ and phosphate reabsorption 9 of 47 2/1/12 8:57 PM ..com/servlet/printFlashcardDeck?deckId=. nipple stimulation will "let down" breast milk What are 3 adverse effects of oxytocin? 1) Hyponatremia 2) Seizures 3) Subarachnoid hemorrhage Name the types of vitamin D and their sources Vitamin D3 (cholecalciferol) . especially in darker skinned newborns Explain how vitamin D is activated Vitamin D3 (skin) and Vitamin D2 (diet) → 25OH vitamin D (in liver) ----> 1.
Increase bone resorption of Ca2+ and phosphate 10 of 47 2/1/12 8:57 PM .studyblue...com/servlet/printFlashcardDeck?deckId=.StudyBlue Flashcard Printing of Endocrinology http://www.
which stimulate osteoclasts to break down bone and release calcium.com/servlet/printFlashcardDeck?deckId=. Intermediate phase 3. Excessive ↑ in osteoclastic activity → shaggy lytic bone lesions. paramyxoviruses such as measles or respiratory syncytial virus).25-OH2 vitamin D inhibits its own production by inhibiting 1α-hydroxylase. ↓serum phosphate. Hypervascular/Osteolytic phase 2.studyblue. List the three phases of Paget's Disease 1.. ↓ serum calcium. ↑ PTH levels --. 11 of 47 2/1/12 8:57 PM . Mosaic bone is replaced areas of highly cellular lamellar bone with irregular "cement lines" List the three stages of bone activity in the hypervascular/ostolytic phase of Paget's disease..All INCREASE activity (more D) 1. thick and highly vascular 3. Name 4 factors that regulate 1α-hydroxylase and their effect on this enzyme. Describe the mechanism of Paget's Disease and a possible underlying cause Massive bone turnover due to ↑ osteoclastic and ↑ osteoblastic activity → abnormal bone architecture May be caused by a slow virus infection (eg. 2.StudyBlue Flashcard Printing of Endocrinology http://www. Quiescent phase 1. Massive osteoblastic response (↑↑ alkaline phosphatase) → ↑ production of woven "mosaic bone" that is weak (radiolucent). Note: High phosphate from CKD inhibits 1α-hydroxylase How does PTH effect bones? (describe the biochemistry) Binding of PTH to its receptor on osteoblasts → osteoblasts secrete M-CSF and RANK-L.
StudyBlue Flashcard Printing of Endocrinology http://www. but osteoblastic activity predominates Descrive the activity and physical features of bone during the Quiescent phase of Paget's disease osteoblastic activity eventually declines Sclerotic bone: .. phosphate. pathologic fractures Pagetoid bone is highly vascular with extensive arteriovenous shunting that may signiﬁcantly ↑ blood ﬂow → ↑ cardiac output → compensatory left ventricular hypertrophy and. parathyroid hormone . Describe the bones activity in the intermediate stage of paget's disease Osteoclastic activity is still present. Small risk of developing into osteogenic sarcoma What are the 2 potential complications of Paget's disease What are the characteristic lab ﬁndings of Paget's disease Serum levels: ..enlarged/widened bones .absent Haversian systems . ↑ hat size.marrow spaces replaced by vascular ﬁbrous tissue Enlarged/widened bones that are weak: List the signs and symptoms of Paget's disease. Skull → headaches.studyblue. hearing loss (if ear canal involvement) Weight bearing bones → bone pain especially at night. in severe cases.normal calcium.↑ alkaline phosphatase 12 of 47 2/1/12 8:57 PM .com/servlet/printFlashcardDeck?deckId=. high-output heart failure. List at least 4 key symptoms.
GI malabsorption of fat-soluble vitamins 2. etidronate) are ﬁrst-line agents What is the mechanism for Primary Osteoporosis Type I (Postmenopausal) Estrogen deﬁciency → increased activity of RANKL/RANK and therefore osteoclasts 1. Renal osteodystrophy: chronic renal failure → ↓ 1-α-hydroxylase activity → 3.2 Deletion Syndrome (aka DiGeorge Syndrome or velocardiofacial syndrome) CATCH-22: microdeletion of central portion of chromosome 22 Cardiac defects Abnormal facial features Thymic aplasia .. ↑ ↑ Osteoclast activity (bone resorption) 2.studyblue. Vitamin D deﬁcient diets (most common) 1. Aluminum-containing phosphatebinding antacids (mechanism?) 4. Phenytoin (seizure drug) 5.StudyBlue Flashcard Printing of Endocrinology http://www.leads to T cell malfunction Cleft palate Hypocalcemia: due to hypoparathyroidism 22 1. alendronate. pamidronate. Obesity (D is trapped by fat!) Calcepenic rickets (most common) Serum levels: ↓ Calcium ↓ Phosphate ↑ Parathyroid hormone (PTH) ↑ Alkaline Phosphatase List 5 common causes of vitamin D deﬁciency What are the two types of ricketts? What are the common lab ﬁndings for both? 13 of 47 2/1/12 8:57 PM .. ↑ Osteoblast activity (bone formation compensates but unable to keep up with osteoclast activity) Name 5 classic characteristics of 22q11. What is the treatment for Paget's disease? Bisphosphonates (eg.com/servlet/printFlashcardDeck?deckId=.
StudyBlue Flashcard Printing of Endocrinology http://www.. normal PTH.. and Vit D 14 of 47 2/1/12 8:57 PM . Phosphopenic rickets (rare): low Phos. Calcium.com/servlet/printFlashcardDeck?deckId=.studyblue.
e. which is distinctly different from osteoporosis. What is the common mechanism for Rickets and Osteomalacia?` Vitamin D Deﬁciency leads to decreased Ca → increased PTH levels → decreasing phosphate.. not found Osteomalacia) Genus varus Rachitic "rosary chest": bony prominence at costochondral junctions Harrison's sulci: indentations in lower ribs Craniotabes: softening of skull bones Growth retardation Genus varus in Rickets What is the correct term for this condition? What disease causes this? What are the symptoms of osteomalacia? Diffuse bone pain. bowing) List the clinical ﬁndings speciﬁc to Rickets (i.. which is painless.StudyBlue Flashcard Printing of Endocrinology http://www.. unless there is a fracture. and ↓ mineralization of newly formed bone matrix (osteoid) → Rickets (children) & osteomalacia (adults) Qualitative defects in bone formation — versus a quantitative defect like osteoporosis Failure of mineralization leads to changes in the growth plate (increased width and disorientation) and bone (cortical thinning.com/servlet/printFlashcardDeck?deckId=. 15 of 47 2/1/12 8:57 PM .studyblue.
studyblue.com/servlet/printFlashcardDeck?deckId=. What are the two types of parathyroid cells and what are their functions? Chief cells: produce parathyroid hormone (PTH) Oxyphil cells: function is unknown 16 of 47 2/1/12 8:57 PM ..StudyBlue Flashcard Printing of Endocrinology http://www..
1) ↑ bone resorption of calcium and phosphate 2) PTH stimulates 1α-hydroxylase in the kidney → increased 1..com/servlet/printFlashcardDeck?deckId=. while severe decreases in Mg2+ inhibit PTH secretion and produce symptoms of hypoparathyroidism.StudyBlue Flashcard Printing of Endocrinology http://www. What are common causes of magnesium deﬁciency? Common causes of ↓ Mg2+: diarrhea. Mild decreases in Mg2+ stimulate PTH secretion. causes (bone) pin What are the three primary causes for primary hyperparathyroidism? Single benign adenoma: majority of cases Hyperplasia of parathyroid glands: rare incidence MEN (multiple endocrine neoplasia) I and IIA 17 of 47 2/1/12 8:57 PM . ↑ serum Ca2+ and ↓ serum Phos List the 4 actions of Parathyrdoid Hormone and the overall result. bones and groans" What are 5 signs and symptoms of hypercalcemia? 1) Mental status changes 2) Kidney (stones) 3) Muscle weakness 4) Cardiac Arrythmias 5) Constipation (groans) 6) Osteitis ﬁbrosa cystica . aminoglycosides.. diuretics.25-(OH)2 vitamin D production leading to ↑ intestinal absorption of Ca2+ 3) ↑ renal Ca2+ absorption (↑ urinary cAMP) 4) ↓ kidney reabsorption of phosphate ↓ free serum Ca2+ causes ↑ PTH Explain how PTH is regulated by serum Ca2+ and Mg2+ secretion.studyblue.cystic bone ﬁlled with brown ﬁberous tissue. Ca2+-sensing receptors on chief cells mediate these effects. and alcohol abuse "Stones.
. normal. sarcoidosis. therefore decreasing serum Ca This hormone opposes PTH Not normally important in Ca homeostasis 18 of 47 2/1/12 8:57 PM . thiazidediuretics. progresses into autonomous hypersecretion of PTH even after correction of chronic hypocalcemia What are the lab values for primary hyperparathyroidism Calcium: High PTH: High (or inappropriately normal) Serum phosphate: low Urine phosphate: high Urine cAMP: high If the PTH is normal consider Vit Dtoxicity. milk-alkali syndrome is a possible cause for the hypercalcemia Calcium: LOW (this is the cause!) PTH: High Serum phosphate: low.com/servlet/printFlashcardDeck?deckId=. or high depending on kidney function Alk phosphatase: high P will be low hypocalcemia is due to a GI problem. What do they all have in common? Chronic renal failure: decreases Ca absorption and decreased hydroxylation of Vit D GI Malabsorptive disorder Rickets List the primary cause of tertiary primary Long standing hyperparathyroidism. and high if due to CKD Parafollicular cells (C cells) of thyroid produce calcitonin What are 5 pertinent lab ﬁndings for secondary hyperparathyroidism What cells produce calcitonin and what is its function? Calcitonin is released due to increased serum calcium. or high depending on kidney function Urine phosphate: low. usually due to chronic renal failure.StudyBlue Flashcard Printing of Endocrinology http://www. It serves to decrease bone resorption of calcium. normal.studyblue. Occurs when parathyroid glands are chronically stimulated by hypocalcemia to release PTH List the three most common causes of secondary hyperparathyroidism..
neuromuscular irritability.Low serum calcium . What are 4 classic signs and sx of hypocalcemia 1) Tetany 2) Carpal-pedal spasms (Trousseau's sign) 3) Prolonged QT interval 4) Parasthesias (numbness and tingling of extremities) What is the cause of Vitamin D dependent Rickets Type 2 NOT ON BOARDS (1/5/12) .A mutation in the alpha 1 hydroxylase enzyme Type 1 = alpha 1 . carpal-pedal spasms What are the 4 characteristic lab ﬁndings of hypoparathyroidism What are 3 classic signs and sx of hypoparathyroidism? 19 of 47 2/1/12 8:57 PM .Commonly associated with allopecia What is the cause of Vitamin D dependent Rickets Type 1 NOT ON BOARDS (1/5/12) .studyblue..Low PTH Hypocalcemic symptoms: tetany.com/servlet/printFlashcardDeck?deckId=.High serum phosphate .A mutation in the vitamin D receptor (on liver? kidney?) .Low serum Vit D .StudyBlue Flashcard Printing of Endocrinology http://www..
. Renin-Angiotensin.com/servlet/printFlashcardDeck?deckId=.. Potassium ---> Zona Glomerulosa 2) ACTH (from CRH) --> Zona Fasiculata 3) ACTH (from CRH) --> Zona Reticularis List the primary regulatory control for the adrenal medulla Preganglionic sympathetic ﬁbers to the chromafﬁn cells in the medulla 20 of 47 2/1/12 8:57 PM . short stature Pseudohypoparathyroidism is caused by a fault in the G protein receptor signaling pathway in the kidney leading to decreased urinary cAMP levels What are the two PE signs that indicate hypoparathyroidism Chvostek's sign: tapping the facial nerve --> elicit spasm of facial muscles Trousseau's sign: cut off blood ﬂow to distal arm with BP cuff --> carpal spasm List all ﬁve layers of the adrenal gland and the hormones they make (if applicable) 1) Capsule Cortex 2) Zona Glomerulosa --> Mineralocorticoid Aldosterone (salt) 3) Zona Fasiculata --> Glucocorticoid Cotrisol (sugar) and sex hormones 4) Zona Reticularis --> Sex hormones (sex) 5) Medulla --> Catecholamines (Epi & Norepi) List the primary regulatory control for the three layers of the adrenal cortex 1) ACTH. How is this mutation inherited? Autosomal dominant kidney unresponsiveness to PTH Classic sign: Shortened metacarpals 4th and 5th digits. hypocalcemia.StudyBlue Flashcard Printing of Endocrinology http://www. Describe the mutation responsible for Pseudo-hypoparathyroidism and three classic features of this disease.studyblue.
StudyBlue Flashcard Printing of Endocrinology http://www. and an increase in sex hormones 1) Hypotension (low aldo) 2) Masculinization/female pseudohermaphroditism (clitoromegaly) 3) Hyperkalemia (low aldo) 4) Volume depletion due to salt wasting --> can lead to hypovolemic shock in newborns 5) Increased serum renin (due to volume depletion) with low serum aldo Describe the classic signs and sx of 21-hydroxylase deﬁciency 21 of 47 2/1/12 8:57 PM ..studyblue.com/servlet/printFlashcardDeck?deckId=.. respectively. in congenital adrenal hyperplasia All congenital adrenal enzyme deﬁciencies are characterized by enlargement of the adrenal glands due to an increase in ACTH stimulation (due to the decreased levels of cortisol) Describe the pathophysiology behind 17 alpha hydroxylase deﬁciency A congenital adrenal hyperplasia that results in the inability of pregnenalone and progesterone to convert to 17-hydroxypregnenalone (percursor to cortisol and sex hormones) Leads to increased aldosterone (back-up) and decreased cortisol and sex hormones 1) Hypertension (too much aldo/Na) 2) Males become pseudohermaphroditic due to low levels of testosterone 3) Females will have normal genital development. respectively. Explain the mechanism behind the hyperplasia. but will not have enough estrogen to develop secondary sex characteristics Describe the classic signs and sx of 17 alpha hydroxylase deﬁciency Describe the pathophysiology behind 21-hydroxylase deﬁciency MOST COMMON congenital adrenal hyperplasia that results in the inability of Progesterone and 17-Hydroxyprednisone to convert into 11-deoxycorticosterone and 11 deoxycortisol. Leads to decreased levels of aldo and cortisol.
Associated with MEN 2A and 2B.com/servlet/printFlashcardDeck?deckId=.. and dopamine) into the blood stream Most common tumor of the adrenal medulla in adults.Dopamine --> HVA . The 5 P's of Pheo List the ﬁve episodic hyperadrenergic symptoms of pheochromocytoma Elevated blood Pressure Pain (headache) Perspiration Palpitations Pallor Symptoms occur in spells (unknown mechanism) What is the treatment for pheochromocytoma? Alpha antagonists: phenoxybenzamine (non-selective and irreversible) Followed by surgery to remove the tumor What are the typical lab ﬁndings of pheochromocytoma? Name 4 (three are UA results) 1) Elevated plasma catecholamines Elevated urinary biproducts of the catecholamines . epi.StudyBlue Flashcard Printing of Endocrinology http://www.Norepi --> VMA . Describe the venous drainage of adrenal gland Left adrenal gland drainage: left adrenal vein --> left renal vein --> inferior vena cava Right adrenal gland drainage: right adrenal vein --> inferior vena cava Describe the pathophysiology of Pheochromocytoma Neuroendocrine tumor of adrenal medulla chromafﬁn cells (arise from neural crest cells) that secretes catecholamine (norepi..studyblue.Epinepherine --> metanepherines 22 of 47 2/1/12 8:57 PM .
studyblue. Causes elevation in catecholamines and urinary HVA Most common extracranial solid cancer in infancy 1) Spinal cord compression 2) Weakness 3) Bone lesions 4) Swollen neck and abdomen ** Hypertension is uncommon!** Describe the pathophysiology of Neuroblastoma What 4 complications/clinical symptoms are associated with neuroblastoma. Most often found in adrenal medulla but can also be found anywhere along sympathetic chain. What are the 2 lab ﬁndings of Neuroblastoma? What is the clinical signiﬁcance of the second? 1) Homovanillic acid (HVA) a breakdown product of dopamine is found in urine 2) Overexpression of N-myc oncogene is associated with rapid tumor progression Waterhouse-Friderichsen syndrome Acute adrenocortical insufﬁciency associated with meningococcal septicemia Massive hemorrhage within adrenal glands leads to hypotension and shock.. 23 of 47 2/1/12 8:57 PM . What its the "rule of tens" for pheochromocytoma 10% malignant 10% bilateral 10% extra-adrenal 10% familial (Men 2A or 2B) 10% calcify 10% kids Neuroendocrine tumor derived from neural crest cells.. with widespread purpura.com/servlet/printFlashcardDeck?deckId=.StudyBlue Flashcard Printing of Endocrinology http://www.
What is the pathophysiology of this diagnosis? 24 of 47 2/1/12 8:57 PM .StudyBlue Flashcard Printing of Endocrinology http://www..studyblue..com/servlet/printFlashcardDeck?deckId=.
Adrenal Atrophy or destruction leading to absence of hormone production in all 3 cortical divisions. cortisol will rise appropriately 25 of 47 2/1/12 8:57 PM . Melanocyte-stimulating hormone MSH shares the same precursor molecule as ACTH 1) Hyperpigmentation 2) Abnormal cosyntropin (synthetic ACTH) stimulation test: subnormal response of plasma cortisol following cosyntropin is deﬁnitive and diagnostic of adrenocortical insufﬁciency 3) Abnormal metyrapone test: ↑ ACTH. trying to make more cortisol. Describe the pathophysiology of Primary Addison's disease and 6 common causes.com/servlet/printFlashcardDeck?deckId=. Decreased production of pituitary ACTH Secondary Adrenocortical Insufﬁciency is not associated by hyperpigmentation (no MSH) If given cosyntropin (synthetic ACTH). fatigue 4) Skin hyperpigmentation* *ACTH is high. diarrhea. Caused by: 1) Autoimmune 2) TB granuloma 3) Infarction of adrenal gland 4) HIV 5) Waterhouse-Friderichsen syndrome 6) DIC (disseminated intravascular coagulation) 1) Hyponatremic volume contraction 2) Hyperkalemia 3) Constipation. but no ↑ in 11-deoxycortisol What are the classic signs and symptoms of Primary Adrenocortical Insufﬁciency (Addison's) List three ways to diagnose Primary Addison's What is the treatment of Addison's disease? 1) Fluid replacement for hypovolemin shock 2) IV dexamethasone 3) Eventual syntheic mineralocorticoid replacement What is the pathophysiology of Secondary Adrenocortical Insufﬁciency and name three things that distinguish it from primary disease..studyblue.StudyBlue Flashcard Printing of Endocrinology http://www..
com/servlet/printFlashcardDeck?deckId=..studyblue.StudyBlue Flashcard Printing of Endocrinology http://www. hypernaremia is rare! Aldosterone is under tonic control by ACTH. List the 5 functions of Cortisol (BBIIG) 1) Upregulates alpha 1 receptors to maintain Blood pressure 2) Decreased Bone formation (inhibits osteoblasts and GI Ca2+ absorption) 3) Anti-Inﬂammatory 4) Decreases Immune function (inhibition of PLA2 IL-2 via lipocortin) 5) Increases nutrient catabolism (Gluconeogenisis) 1) Paraventricular nuclei of the hypothalamus release CRH 2) CRH stimulates corticotrophs in anterior pituitary to synthesize POMC --> ACTH and MSH 3) ACTH increases steroid hormone synthesis in the adrenal cortex by activating cholesterol desmolase 4) Cortisol inhibits the release of CRH 1) Low dose causes suppression of ACTH: Normal 2) ACTH is still produced after low dose dexamethasone: Cushing's disease (pituitary adenoma) 3) ACTH is still produced after high dose dexamethasone: Ectopic ACTH producing tumor Late distal tubule/collecting duct 1) ↑ renal Na+ reabsorption by principal cells + secretion by principal cells 2) ↑ renal K cells + secretion bu α-intercalated 3) ↑ renal H cells Excess aldo = hypokalemia and metabolic alkolosis are common. but is separately regulated by the reninangiotensin-aldo system and by potassium Hyperkalemia & low BP will cause and increase in aldo secretion Angiotensin II increases the activity of aldosterone synthase in the zona glomerulosa List the 3 steps leading to cortisol production and how it is regulated Explain the three results of a Dexamethasone suppression test and what they indicate List the three actions (and the location of action) of Mineralocoritoids (Aldosterone) List three factors that regulate aldosterone secretion 26 of 47 2/1/12 8:57 PM ..
secondary. hypokalemia (K dumping). may or may not be "brown") due to primary or tertiarty hyperarathyroidism caused by chronic kidney faliure What is the pathophysiology of renal osteodystrophy Chronic renal failure → ↓ activity of 1-α-hydroxylase → ↓ 1...25-(OH)-vitamin D → ↓ absorption of calcium from the gut → hypocalemia → ↑ production of parathyroid hormone (PTH) → ↑ osteoclastic resorption of cortical bone → subperiosteal thinning with cystic degeneration → cystic bone lesions/tumors What are three charateristics of Osteitis Fibrosa Cystica and what is the cause? 1) ↑ osteoclastic resorption of calciﬁed bone 2) Peritrabecular ﬁbrosis 3) Cystic "brown tumors" in bone Caused by prolonged.com/servlet/printFlashcardDeck?deckId=.studyblue.StudyBlue Flashcard Printing of Endocrinology http://www. severe hyperparathyroidism (Primary. What is renal osteodystrophy? Bone lesions (osteoclastic resorption of cortical bone → subperiosteal thinning with cystic degeneration. metabolic alkalosis due to cell exchange of H for K. or tertiary) A single benign adrenal tumor (adenoma) or bilateral hyperplasia of the adrenal glands result in overproduction of aldosterone Elevated aldosterone levels → Mild hypertension (due to Na/H2O retention). NO hypernatremia! Describe the pathophysiology of Primary Hyperaldosteronism (Conn's Disease) What are 2 classic signs of hypokalemia? 1) Muscle weakness 2) Cardiac changes visible on EKG (classically described as U-waves) 27 of 47 2/1/12 8:57 PM .
How is it diagnosed? List the four causes of cushings syndrome and their respective levels of ACTH 1) Iatrogenic steroid use --. a high renin level suggests secondary hyperaldosteronism as in reno-vascular hypertension (due to RAS.lots of ACTH 4) Zona Fasiculata Adenoma -.low ACTH due to feed back inhibition 1) Hypertension (excess alpha 1) 2) Weight gain 3) Proximal muscle weakness 4) Buffalo hump 5) Eccymosis over arms and legs 6) Moon face 7) Osteoporosis 8) Amenorrhea 9) Immune diﬁciency 10) Skin thinning and striae What are the 5 of the 10 classic symptoms of Cushing's syndrom 28 of 47 2/1/12 8:57 PM . and renal artery stenosis cause low renal vascular volume --> stimulates renin-angiotensin system which increases aldosterone production Diagnosis: increased aldosterone levels with high plasma renin. etc) What are 2 treatments for primary hyperaldosteronism? 1) Surgery 2) Spirinolactone to block the aldo being produced by the tumor CHF cirrhosis.low ACTH due to feedback inhibition 2) Cushings disease (pituitary adenoma of ACTH) -.studyblue. nephrotic syndrome. low levels of renin are seen.com/servlet/printFlashcardDeck?deckId=.lots of ACTH 3) Ectopic ACTH tumor -. In primary hyperaldosteronism.. By contrast. chronic renal failure. Too much cortisol! What is the cause and effect of Secondary Hyperaldosteronism. How is primary hyperaldosteronism diagnosed? (what do the labs look like) High aldosterone suppresses the secretion of renin.. CHF. chronic renal failure.StudyBlue Flashcard Printing of Endocrinology http://www.
VIPomas.StudyBlue Flashcard Printing of Endocrinology http://www.. the cell lines that give rise to the parafollicular cells in the thyroid and chromafﬁn cells in the medulla. which causes a defect in neural crest cells.studyblue. insulinomas.. Defects = diabetes insipidis 29 of 47 2/1/12 8:57 PM . etc) Clinically presents as: Kidney stones and stomach ulcers All via autosomal dominant inheritance How are all MEN (multiple endocrine neoplasia) syndromes acquired? MEN 2A and 2B are speciﬁcally associated with the ret gene. What are the three key characteristics of MEN 1? And what is the most common clinical complaints? 1) Parathyroid tumors 2) Pitutary tumors (prolactin or GH) 3) Pancreatic endocrine tumors (Zollingerellison syndrome. through the portal blood supply to the posterior pituitary.com/servlet/printFlashcardDeck?deckId=. What are the three characteristics of MEN 2A? 1) Medullary thyroid carcinomas (secretes calcitonin) 2) Pheochromocytoma 3) Parathyroid tumors What are the three characteristics of MEN 2B? 1) Medullary thyroid carcinomas (secretes calcitonin) 2) Pheochromocytoma 3) Marfanoid habitus/mucosal neuromas What are neurophysins and what are their function? Neurophysins are carrier proteins released from the posterior pituitary that carry ADH from the supraoptic nuclei and oxytocin from the paraventricular nuclei.
. Congenital hypothyroidism is most commonly caused by thyroid dysgenesis due to thyroid aplasia/hypoplasia/ectopy What is/are the most common cause and symptoms of congenital hypothyroidism? Hoarse cry Macroglossia Enlarged fontanelles Pot belly with umbilical hernia Big puffy eyes and faces Jaundice Poor feeding and hypotonia 2/1/12 8:57 PM 30 of 47 .Mental retardation can be minimized when thyroid hormone is administered in neonatal period.studyblue. Explain the process of insulin production. which gets cleaved to insulin & C-peptide (essential for proper folding) and stored in secretion granules List the three types of hypothyroidism and their corresponding TSH values 1) Primary hypothyroidism (caused by thyroid hypofunction): ↑ TSH 2) secondary hypothyroidism (caused by pituitary hypofunction): ↓ TSH 3) tertiary hypothyroidism (caused by hypothalamic hypofunction): ↓ TSH 1) Hashimoto thyroiditis (chronic autoimmune thyroiditis) 2) Post ablation: surgical or I-131 radiation (people treated for Graves) 3) Iodine deﬁciency 4) Drugs: lithium.. amioderone.StudyBlue Flashcard Printing of Endocrinology http://www.com/servlet/printFlashcardDeck?deckId=. make sure to name the cells responsible Synthesized and secreted by pancreatic β cells Synthesized as proinsulin. and sulfonamides 5) Subacute lymphocytic (painless) thyroiditis: 1/3rd of patients become hypothyroid within 10 years Disease due to severe fetal hypothyroidism What are 5 common causes of primry hypothyroidism? What is cretinism? How can it be avoided? mental retardation pot-bellied stomach protruding umbilicus and tongues .
. 31 of 47 2/1/12 8:57 PM .com/servlet/printFlashcardDeck?deckId=..StudyBlue Flashcard Printing of Endocrinology http://www.studyblue.
What are 7 common signs and symptoms of hypothroidism? 1) Cold intolerance 2) Weight gain 3) Fatuige/depression 4) Dry ﬂakey skin 5) Myxedema (facia. anxiety. hypotension Treatment: respiratory support.com/servlet/printFlashcardDeck?deckId=. hypoventilation with CO2 retention. periorbital) 6) Bradycardia 7) Carpal tunnel 8) Slow deep tendon reﬂexes 9) Constipation Emergent hypothyroid condition What are the symptoms of myxedema coma and how do you treat it? S/Sx: hypothermic stupor/coma.g.. ﬂushed skin 4) Tremor. in the rare case that a patient has secondary hyperthyroidism due to a TSH-secreting pituitary adenoma → inject TRH and look for ↑ in TSH What is the pathophysiology behind the clinical manifestations of hyperthyroidism 1) Hypermetabolic state (e. cortis What are the three types of hyperthryoidism and what are their corresponding TSH trends? 1) Primary hyperthyroidism: ↓ TSH 2) Secondary hyperthyroidism: ↑ TSH . palpitations 5) Opthalmopathy 6) Increased bone turnover --> osteoporosis 7) Diarrhea 8) Brisk tendon reﬂexes 32 of 47 2/1/12 8:57 PM .. heat intolerance 2) Weight loss 3) Warm.studyblue. intravenous levothyroxine.StudyBlue Flashcard Printing of Endocrinology http://www.. ↑ Na+/K+ ATPase activity): due to ↑ T4 and T3 2) Sympathetic nervous system overactivity: ↑ T4 and T3 → ↑ synthesis of β adrenergic receptors → ↑ β adrenergic tone List 7 common symptoms of hyperthyroidism 1) Sweating.
lab tests that are important to hyperthyroidism 1) ↑ bone turnover → ↑ serum calcium (hypercalcemia) 2) ↑ glycogenolysis → ↑ serum glucose (hyperglycemia) 3) ↑ LDL receptor synthesis → ↓ serum cholesterol (hypocholesterolemia) List the triad of clinical ﬁndings in Graves Disease? 1) Hyperthyroidism: nontender hyperfunctional enlargement of the thyroid 2) Inﬁltrative ophthalmopathy: due to accumulation of glycosaminoglycans and adipose in retro-orbital tissue 3) Inﬁltrative dermopathy: scaly thickening and induration of the skin overlying the shins with nonpitting edema (pretibial myxedema) What is the would the radioactive iodine study look like in a patient with a Toxic Adenoma of the thyroid? Uneven 123I uptake with occasional autonomous "hot" nodules demonstrating ↑ 123I uptake ↓ 123I uptake .↑ SNS → overstimulation of levator palpebrae superioris → wide-eyed staring gaze and lid lag ...painful cervical lymphadenopathy Course: Hyperthyroid. followed by normalization Cause: Viral or bacterial infection List the triad of clinical ﬁndings Acute Thyroiditis and how a radioactive iodine study would appear. Explain the pathophysiology behind the opthalmopathy in non-graves thyroiditis .StudyBlue Flashcard Printing of Endocrinology http://www. What is the common cause & course of this disease? 33 of 47 2/1/12 8:57 PM .painful thyroid .becuase T4 is in the blood stream.Note: true thyroid ophthalmopathy with exophthalmos (proptosis) is only seen in Graves disease.com/servlet/printFlashcardDeck?deckId=. the exopthalmos has it's own pathophysiology List 3. not in the thyroid . non-thyroid-related. followed by hypothyroid.fever .studyblue.
thyroglobulin and anti-thyroid peroxidase antibodies are often present .decreased T4 in thyroid due to feedback inhibition What is the pathophysiology behind inﬂitrative opthalmopathy? TSI autoantibodies cross-react with orbital preadipocyte ﬁbroblasts (which have TSH receptors..tachycardia out of proportion to fever .coma Most common cause of hypothyroid.studyblue. but not tendon) --> exopthalmos. Describe the radioactive iodine uptake pattern in Iatrogenic hyperthyroidism (accidental or for diet reasons) ↓ 123I uptake .tachyarrhythmias — common cause of death in patients with thyroid storm .StudyBlue Flashcard Printing of Endocrinology http://www.shock due to heart failure and/or vomitinginduced volume depletion .. not easily treated Type II Hypersensitivity TSI (thyroid-stimulating immunoglobulin) auto-ab = IgG that binds and activates TSH receptor relatively speciﬁc for Graves Anti.high fever (hyperpyrexia) ..com/servlet/printFlashcardDeck?deckId=.. fat and T cells in the retro-orbital space (esp muscle. wtf) causing them to synthesize glycosaminoglycans Accumulation of GAGs. Auto-abs → attack thyroid 1) Anti-thyroid autoantibodies (anti-Tg and anti-TPO) 2) CD8+ T-cell mediated cell death 3) Cytokines activate TH1 → IFN-γ recruits and activates macrophages → follicle damage What is the pathophisiology behind Graves disease? What are 5 features of Thyroid Storm What is the pathohysiology behind Hashimoto Thyroiditis 34 of 47 2/1/12 8:57 PM .Normally due to aggravated Graves .
1) Preceded by ﬂu-like illness with sore throat and fever. tender thyroid. jaw pain.studyblue. and a markedly elevated ESR 2) Tender thyroid 3) Early phase can manifest as hyperthyroidism. List 4 signs/sx..com/servlet/printFlashcardDeck?deckId=. Hypothyroidism may occur. store and secrete thyroid hormone Colloid: central space in follicle where thyroid hormone is stored as a component of thyroglobulin Parafollicular cells: synthesize and secrete hormone calcitonin Name the cancer that forms in parafolicular cells and its important association Medullary thyroid cancer.B-cell non-Hodgkin lymphomas.. as damaged gland spills T4 4) Resolves in 8ish weeks Describe the pathophysiology of Reidel thyroiditis and the clinical consequences Fibrous tissue replaces thyroid parenchyma. especially extranodal marginal zone lymphomas of MALT (mucosa-associated lymphoid tissue) type Describe the clinical course of subacute thyroiditis. List the three functional parts of the thyroid gland and their functions Thyroid follicular cells: synthesize. associated with MEN 2A and 2B 35 of 47 2/1/12 8:57 PM .StudyBlue Flashcard Printing of Endocrinology http://www. ↑ risk of developing other autoimmune diseases What are some complications of Hashimotos Thyroiditis? ↑ risk of primary thyroid lymphoma: . with ﬁbrosis extending beyond the thyroid capsule into surrounding tissue.
that is NOT taking up iodine becuase cancers do not normally produce thyroid hormone. without peripheral beneﬁt. What would the radioactive uptake scan look like in a patient with thyroiditis? Thyroiditis: ↓ 123I uptake 1) β-blocker to control symptoms of ↑ SNS tone AND decrease peripheral conversion of T4 to T3 (mech unknown) 2) Propylthiouracil: inhibition of the organiﬁcation and coupling steps of T4 & T3 synthesis.StudyBlue Flashcard Printing of Endocrinology http://www. also inhibits peripheral conversion of T4 to T3 3) Methimazole: same as PTU. How would an radioactive iodine study appear in a patient with Graves? Diffusely ↑ 123I uptake in the whole thyroid gland What would the radioactive uptake scan look like in a patient with thyroid cancer A COLD focal nodule... 1) High-dose iodine → blocks release of T4 and T3 into the circulation via Wolffe-Chaikoff cycle 2) High-dose radioactive iodine: 131I (versus the 123I used in imaging studies) → becomes concentrated in the thyroid gland → ablation of thyroid function Name the three most common pharmacologic treatments for hyperthyroidism Compare and contrast the two different treatments involving iodine for hyperthyroidism 36 of 47 2/1/12 8:57 PM .studyblue. Category X.com/servlet/printFlashcardDeck?deckId=.
inhibit thyroid hormone synthesis by blocking the organiﬁcation step. releasing T3 and T4 into the circulation.. follicular cells endocytoses thyroglobulin and lysosomal enzymes digest thyroglobulin.studyblue. Residual MIT and DIT are deiodinated by thyroid deiodinase. Remember high levels of I can come from a CT or angiogram! 37 of 47 2/1/12 8:57 PM .StudyBlue Flashcard Printing of Endocrinology http://www.. (organiﬁcation) Couples MIT and DIT to form T3 and T4 (still attached to thyroglobulin) Iodinated thyroidglobulin is stored in the follicular lumen. Upon stimulation by TSH. I moves to lumen via pendrin channel 2) Thyroid peroxidase: Describe the biochemical pathway that leads to the formation of T4/T3 Oxidizes I. The I2 that is generated is recycled to synthesize more thyroid hormone Describe how T4 & T3 are released into the blood stream? What inhibits the Na-I transporter in the thyroid follicular cell? The Na-I transporter is inhibited by thiocyanate and perchlorate anions Name two medications that inhibit thyroid peroxidase Thyroid peroxidase is inhibited by propylthiouracil (PTU) and methimazole!!! Name the phenomenon in the thyroid that occurs due to Iodine overload? Wolff-Chaikoff effect : High levels of I. 1) Iodine enters the follicular cell via Na-I symporter.to I0 Conjugates the I0 to tyrosine residues on thyroglobulin to form MIT & DIT.com/servlet/printFlashcardDeck?deckId=.
com/servlet/printFlashcardDeck?deckId=. 38 of 47 2/1/12 8:57 PM .studyblue..StudyBlue Flashcard Printing of Endocrinology http://www..
T3 is signiﬁcantly more potent than T4..com/servlet/printFlashcardDeck?deckId=. What HLA type is associated with Hashimotos thyroiditis? HLA-DR5 Explain the pathogensis of Riedel's thyroiditis and two common physical exam ﬁndings 1) Thyroid is replaced by ﬁberous tissue leading to hypothyroidism 2) ﬁxed. Rarely malignant Name the two types of cancer associated with Follicular cells along with their associations and prognoses 1) Papillary carcinoma: associated with childhood radiation exposure.StudyBlue Flashcard Printing of Endocrinology http://www. good prognosis 39 of 47 2/1/12 8:57 PM . excellent prognosis. most common 2) Follicular carcinoma: not associated with radiation. less common. rock-like. painless goiter Describe the pathophysiology behind a Toxic Multinodular Goiter Focal patches of hyperfunctioning follicular cells that work independently of TSH due to a mutation in the TSH receptor Appear as hot nodules (increased uptake) on iodine study.. How and where is T4 converted to T3 T4 is deiodinated in peripherial tissue to T3 by the enzyme 5'-deiodinase.studyblue.
Conditions where TBG is increased or decreased can affect total T3 or T4 levels.com/servlet/printFlashcardDeck?deckId=.studyblue. (Pregnancy increases TGB... What is the prognosis for a patient with Anaplastic Thyroid Cancer. TBG bound T3 or T4 is inactive. Describe the pathophysiology of Carcinoid Syndrome What 4 are the common sx of Carcinoid syndrome? Carcinoid 1) Cutaneous ﬂushing 2) Asthmatic wheezing 3) Right-sided valvular disease 4) Diarrhea 40 of 47 2/1/12 8:57 PM . What is it bound to? Only free T3 or T4 is active.critical in neonatal period Bone growth .↑ Na/K-ATPase activity → More O2 TBG (thyroxine-binding globulin) binds most T3 or T4 in peripheral blood What are the four major effects of thyroid hormone? Explain the difference between free thyroid hormone and bound thyroid hormone.StudyBlue Flashcard Printing of Endocrinology http://www.increases the number of Beta 1 receptors on heart muscle BMR ↑ . but thyroid compensates) Rare syndrome caused by neuroendocrine carcinoid tumors that secrete high levels of 5-HT serotonin. The seritonin will be undetectable in the blood stream due to ﬁrst pass effect by the liver.via synergism with GH and IGF-1 Beta-adrenergic effects . Who gets this cancer? VERY poor prognosis Older patients Brain maturation .
Increased LH and FSH .studyblue.com/servlet/printFlashcardDeck?deckId=. the primary symptoms. How do you diagnose Carcinoid syndrome? Increased urinary secretion of 5 HIAA (5 hydroxyindoleacetic acid) a degradation product of serotonin How do you treat Carcinoid syndrome? Octreotide – somatostatin analogue that neutralizes serotonin Surgical resection and chemotherapy with 5-FU (ﬂuorouracil) and doxorubicin Gastrin secreting tumor of the pancreas or duodenem What is the pathophysiology. clinical consequence and important association of Zollinger-Ellison Syndrome? Causes recurrent ulcers Associated with MEN-1 Describe the hormonal abnormalities in Klinefelters syndrome and their cause Hyaliniaztion and ﬁbrosis of the seminiferous tubules leads to lack of testosterone synthesis . and the cause..Testosterone is low --> infertility and absence of secondary sex characteristics Deﬁne agranulocytosis. How would you proceed with a patient if you suspect this condition? Def: absolute PMN count less than 500/mL Sx: Fever & sore throat Cause: propylthiouracil and methimazole (in patient with a history of hyperthyroidism) Tx: d/c medication and order CBC with diff 41 of 47 2/1/12 8:57 PM .StudyBlue Flashcard Printing of Endocrinology http://www..
. What would the LH. testo is very low and there is no feedback inhibition to the pituitary.. FSH.. What is a lingual thyroid. The mechanism behind this effect is unknown Thyroid hormone also increases the number of beta receptors on cell membranes. 1) Long limbs 2) Arachnodactyly (abnormally long and slender limbs) 3) Hyperlaxity . MEN 2B.com/servlet/printFlashcardDeck?deckId=. What complications can occur with treatment of this problem? Due to failure of migration. Sometimes this may be the only thyroid tissue in the body and removal of the mass can lead to life threatening hypothyroidism. Testosterone. the thyroid ca form at any part along the thyroglossal duct's usual path. Homocystinuria 42 of 47 2/1/12 8:57 PM . and sperm count levels be in a patient with Klinefelters syndrome? What effect does a beta blocker have on thyroid hormone? Mutations in what gene are responisble for the majority of familial medullary thyroid cancers A mutation that activates the proto-oncogene "RET". including the tongue = lingual thyroid.. LH and FSH are high.studyblue. LH: elevated FSH: elevated Testosterone: very low Sperm count: low Due to the ﬁbrosis of the seminiferous tubules & damage to the Leydig cells. This is the underlying mechanism behind medullary thyroid cancers in MEN 2A and 2B List three features of Marfanoid Habitus and three clinical diseases associated with this body type.Marfan syndrome. Beta bockers prevent the conversion of T4 to T3 in peripheral tissues..StudyBlue Flashcard Printing of Endocrinology http://www. Beta blocker will mitigate this and decrease sympathetic tone.
studyblue. leading to transient release of LH and FSH.com/servlet/printFlashcardDeck?deckId=. because ADH can still be secreted from the pituitary stalk. and therefore testosterone However. While ADH is released from the posterior pituitary (hypophysis). Damage to the nuclei or the pituitary stalk results in central DI. Marfanoid habitus 1) long limbs 2) Arachnodactyly 3) Hyperlaxity (double jointedness) Describe this man's appearance ADH is sythesized in the supraoptic nuclei of the hypothalamus.. LH and FSH production is suppressed Describe the mechanism and clinical application of the drug Leuprolide Leuprolide is a long-long acting GnRH analogue that causes eventual suppression of the GnRH/LH-FSH axis and therefore a decrease in testosterone and DHT. Preceded by a "ﬂair up" of testo and DHT..StudyBlue Flashcard Printing of Endocrinology http://www. Used to treat prostate cancer 43 of 47 2/1/12 8:57 PM . if GnRH levels are constantly elevated. Where is ADH synthesized? What does 5-alpha reductase do and where does it function? 5-alpha reductase converts testosterone to DHT in target tissues Describe the effect of GnRH on hormone production from the gametes Normally GnRH release from the hypothalamus is pulsitile. damage to this area only causes transient DI.
com/servlet/printFlashcardDeck?deckId=..studyblue..StudyBlue Flashcard Printing of Endocrinology http://www. 44 of 47 2/1/12 8:57 PM .
hyperpigmentation Tx: urgent administration of glucocorticoids is always warrented when adrenal crisis is suspected. Hypoglycemia. weight loss. Testosterone and LH will be uneffected. but not hypernatremia Hypotension. which causes diurese and compensatory Na loss.StudyBlue Flashcard Printing of Endocrinology http://www. This triggers Atrial natruetic peptide. What happens to the hormone axis involving the testes? No inhibin is produced. and tachycardia Presenting with one or more of the following: voimiting. which allows the FSH to be produced unchecked (inhibin low and FSH high).. Explains why hypernatremia is rare in patients with hyperaldosteronism Explain the concept of aldosterone escape Increaed Na/Cl uptake by excess aldo leads to hypervolemia. What is the clinical presentation of adrenal crisis? What is the treatment? Describe the hormonal axis involving leydig cells Hypothalamus secretes GnRH --> Pituitary secretes LH --> LH stimulates leydig cells to produce testosterone --> Testosterone inhibits the pituitary release of LH and the hypothalamic release of GnRH Describe the hormonal axis involving sertoli cells Hypothalamus produces GnRH --> pituitary secretes FSH --> FSH stimulates sertoli cells to produce inhibin --> inhibin inhibits the pituitary from releasing FSH.com/servlet/printFlashcardDeck?deckId=..studyblue. --> mild hypertension due to volume expansion. abdominal pain. 45 of 47 2/1/12 8:57 PM . You do not need lab conﬁrmation. but has no effect on the GnRH production of the hypothalamus (LH and testo can keep going) Sertoli cells are damaged.
photosensitivity. Rare pancreatic tumor that presents with necrolytic migratory erythema List the 3 key characteristics of a Glucagonoma Patients are usually diagnosed as "diabetic" due to hyperglycemia Other sx: stomatitis (gum inﬂammation). and abdominal pain. cheilosis (corners of mouth). but this problem begins in the hypothalamus.com/servlet/printFlashcardDeck?deckId=..studyblue. so the earlier they are introduced the shorter the stature.. abnormalities of bones and teeth Name four clinical syndromes (all discussed this this section) that can be treated with somatostatin 1) Acromegally 2) Carcinoid syndrome 3) Gastrinoma 4) Glucagonoma What is the effect of testosterone and estrogen on bone growth Sex hormones promote both growth and epiphysial plate closure. What is the function of demeclocycline? What is it used for? Side effects? ADH antagonist used to treat SIADH Side effects: nephrogenic DI. 46 of 47 2/1/12 8:57 PM . This leads to low estrogen production from the ovaries. Explain the cause of amenorrhea in an anorexic patient Patients with anorexia nervosa often experience amenorrhea due to loss of pulsatile secretion of GnRH from the hypothalamus. causes bone growth without epiphyseal closure leading to gigantism.StudyBlue Flashcard Printing of Endocrinology http://www. This is in contrast to GLP-1 (somatostatin-C).
List three scenarios where desmopressin (DDAVP) is the standard treatment 1) Central Diabetes Insipidus 2) Mild Von Willibrand's disease (also useful in hemophelia A) 3) Enuresis (bed wetting) 47 of 47 2/1/12 8:57 PM .com/servlet/printFlashcardDeck?deckId=.studyblue..StudyBlue Flashcard Printing of Endocrinology http://www..
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