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79 Cards in this Set
- Front
- Back
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Hypothalamus hormones
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1.) thyrotropin releasing hormone (TRH)
2.) Gonadotropin releasing hormone (GnRH) 3.) Corticotropin releasing hormone (CRH) 4.) Growth hormone releasing hormone (GHRH) 5.) Somatostatin 6.) Dopamine |
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thyrotropin releasing hormone (TRH)
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Release of:
thyroid stimulating hormone (TSH) and prolactin (PRL) |
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Gonadotropin releasing hormone (GnRH)
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Release of:
luteinizing hormone (LH) and follicle-stimulating hormone (FSH) |
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Corticotropin releasing hormone (CRH)
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Release of adrenocorticotropin (ACTH)
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Growth hormone releasing hormone (GHRH)
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Release of growth hormone (GH)
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Somatostatin
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Inhibits thyroid stimulating hormone (TSH) and growth hormone (GH) release
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Dopamine
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Inhibits prolactin (PRL) release
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Kallman's syndrome
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- hypogonadotropic hypogonadism due to GnRH deficiency
- hypothalamus problem, not releasing enough GnRH |
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Hormone Tests
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1.) Glucose load
2.) Clonidine supression 3.) Cosyntropin stimulation 4.) Dexamethazone supression |
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What are the Anterior pituitary hormones, how are they secreted?
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- pulsatile secretion
* amplitude & frequency - LH: Luteinizing hormone and FSH: Follicle-stimulating hormone - TSH: Thyroid stimulating hormone - ACTH: Adrenocorticotropin - GH: Growth hormone - PRL: Prolactin |
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Adrenocorticotropin (ACTH) Circadian (diurnal) rhythm
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- nadir 11PM – 3 AM
- peak upon awakening 6-9 AM |
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Thyroid stimulating hormone (TSH) Circadian (diurnal) rhythm
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- nocturnal levels are 2x the daytime levels
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What organ does LH and FSH work on?
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gonads
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What organ does TSH work on?
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thyroid
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What organ does ACTH work on?
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adrenal
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What organ does GH work on?
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multiple organs
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What organ does PRL work on?
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breast
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Tropic hormones
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- actions are specific for another endocrine gland
- LH, FSH, TSH, ACTH |
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Direct effector hormones
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- act directly on peripheral tissues
- GH and PRL |
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What is Growth Hormone also known as, what hormone does it oppose,
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- GH aka somatotropin
- an amphibolic hormone (in catabolism and anabolism) - hypothalamus releases GHRH and somatostatin (SS) to the anterior pituitary that releases GH - a single random measurement may not be diagnostic - lvl modulated by many factors - opposes the action of insulin * promotes hepatic gluconeogenesis * promotes lipolysis |
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Highest level or growth hormone
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- dirunal variation
- sleep onset (at other times extremely low or undetectable) |
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Somatomedins
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- Mediators of the action of GH
- referred to as Insulin Like Growth Factors (IGF) - IGF-1 produced in liver amplifies the effect of GH |
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What is the cause of Acromegaly?
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- excess GH
- most common cause:pituitary tumor or may be accompanied by overt diabetes |
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Diagnosis of acromegaly
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- Measure GH @ 0, 60, 120 min following an oral glucose load
* GH level will not be suppressed (normal glucose load response: GH will decrease to undetectable levels) |
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GH Deficiency
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- genetic causes
* no hormone production * failure of hormone secretion * defective GH or IGF receptors - GH deficiency in children may be accompanied by hypoglycemia |
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Hypopituitarism
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- secondary failure
- associated with low or normal target gland hormone levels |
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Primary failure
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- refers to dysfunction of target gland
- if hypofunctioning target gland, pituitary gland will be producing excessive quantities of the tropic hormone |
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Posterior pituitary hormones
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1.) antidiuretic hormone (ADH)
2.) oxytocin |
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Antidiuretic hormone (ADH), what does it regulate?
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- vasopressin
- regulation of water retention * Hypothalamic osmoreceptors * Vascular baroreceptors |
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Hypothalamic osmoreceptors
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- osmotic threshold for ADH = 284 mOsm/kg (<284:ADH release is supressed)
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Vascular baroreceptors
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- initiate ADH release
* in response to - fall in blood volume and decrease in blood pressure * stimulus for ADH release is exponential * can override osmotic supression of ADH release |
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Diabetes Insipidus
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- decreased ADH levels
- accompanied by elevated serum osmolality |
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Oxytocin
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lactation by posterior pituitary hormone
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Adrenal function
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- adrenal medulla
- adrenal cortex |
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What does Adrenal medulla secrete?
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- secretes catecholamines: epinephrine and norepinephrine
- actions similar to sympathetic nerves |
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Adrenal cortex
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1.) aldosterone
2.) cortisol, corticosterone 3.) dehydroepiandrosterone (DHEA) |
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aldosterone
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- salt
- mineral balance (Na,K) |
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cortisol, corticosterone
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- sugar
- glucose metabolism - stress response - immune system regulation |
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Dehydroepiandrosterone (DHEA) &DHEAS
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- sex
- adrenal sex hormone precursor - Androgens – important at puberty & in adult female * less potent than testosterone |
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G-zone of adrenal cortex
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- salt
- blood pressure: serum potassium - aldosterone |
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F-zone of adrenal cortex
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- sugar
- blood pressure: glucose - cortisol |
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R-zone of adrenal cortex
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- sex
- virilization - testosterone |
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Pregnenolone
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- parent cpd
- from cholesterol |
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Catecholamines
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- Vasoactive amines
- first responders to stress |
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plasma catecholamines
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- hydrophobic
- short half life - low levels which fluctuate |
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24 hour urine catecholamines
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- free norepinephrine
- epinephrine - catecholeamine metabolites * metanephrines & vanilly mandelic acid (VMA) |
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Clonidine supression test
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- drug suppress release of catecholamines by adrenal gland
- use to r/o phaeochromocytoma * phaeochromocytoma - no suppression of adrenal gland, catecholamines stay high - total plasma catecholamines < 500 pg/ml |
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Salt: Renin-Angiotensin system, what is hypoperfusion?
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- Hypoperfusion: inadequate blood flow
- renin - Angiotensin converting enzyme (ACE) - Angiotensin II |
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What secretes Renin and what does renin do?
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- secretion by juxtaglomerular cells
- angiotensinogen -> angiotensin I |
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Angiotensin converting enzyme (ACE)
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angiotensin I -> angiotensin II
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Angiotensin II
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- vasoconstriction
- aldosterone release * increases BP via Na reabsorption and water retention * stimulates H+ K+ excretion :unchecked this can lead to - metabolic alkalosis (losing acid) - HTN (high blood pressure) - hypokalemia (losing K+) |
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Primary Hyperaldosteronism
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- 18-hydroxycorticosterone
* > 100 ng/dl: aldosterone producing adenoma * < 100 ng/dl: idiopathic - Low renin - Hypokalemia - HTN - Metabolic alkalosis |
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Secondary Hyperaldosteronism
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- not the gland
- Elevated renin |
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Diagnostic criteria for primary hyperaldosteronism
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- HTN with no edema
- Renin does not increase with volume depletion - Aldosterone fails to decrease with saline or angiotensin inhibition |
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Hypoaldosteronism
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- adrenal gland destruction
- enzyme deficiencies in aldosterone synthesis |
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Cortisol "sugar"
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- Primary corticosteroid produced and secreted
- Regulator of carbohydrate metabolism, electrolyte balance, and water distribution - Immunosupressant and anti-inflammatory actions - Plasma levels: max. @ 8-9 am, minimum ~ midnight |
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Elevated cortisol
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- pregnancy, high-dose estrogen therapy, adrenal tumors, pituitary or ectopic ACTH producing tumors
- Cushing’s syndrome: may be primary or secondary |
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Cortisol under-production
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Addison’s disease (adrenal insufficiency): may be primary or secondary
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Laboratory diagnosis: Low Cortisol States
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- Low cortisol
- Cosyntropin stimulation test * promotes cortisol & aldosterone production |
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None to minimal cortisol stimulation
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- primary adrenal insufficiency
- high ACTH (baseline) - gland problem |
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Normal cortisol stimulation
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- secondary adrenal insufficiency
- low ACTH (baseline) - gland is working |
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ACTH
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- adrenal corticotropin hormone
- released from the anterior pituitary - stimulates cortisol secretion |
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Laboratory diagnosis: Cushing’s Syndrome
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- Cortisol excess: 24 hr. urine free cortisol
* most sensitive (95-100%) and specific (98%) screen - No diurnal variation * draw cortisol between 11PM & 12 AM >7.5 mg/dl - Resistance to dexamethasone supression |
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Primary cortisol elevation
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- adrenal makes too much cortisol
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Secondary cortisol elevation
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- pituitary makes too much ACTH
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Male sex: adrenal androgens
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- < 10% DHEA is gonadal in males
- Elevated DHEA suggests adrenal hyperandrogenism - Elevated testosterone suggests either adrenal or gonadal source |
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Femal sex: adrenal androgens
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No gonadal DHEA
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Ovary Gonadal Function
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1.) estradiol (E2)
2.) progesterone |
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estradiol (E2)
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- derived from androgens
- responsible for follicular phase changes in uterus * secondary sex chatacteristics * deficiency: incomplete endometrial development |
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progesterone
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- produced only after ovulation: luteal phase of monthly cycle
* endometrial readiness for implantation of embryo * progesterone lacking in women who do not ovulate - deficiency: 1) women who do not ovulate 2) failure of implantation of embryo androgens - excess: hirsutism, masculinization |
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Testes Gonadal Function
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- Testosterone: the major androgen
- clinical utility: sexual development in male children * sexual dysfunction in male adults - circadian rhythm: highest 8 AM, lowest 8PM - primarily protein bound * 50% to albumin, ~45% to SHBP - Free active form ~ 2.3% * a more accurate indication of hormone status |
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FSH (follicle stimulating hormone)
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- pituitary
- facilitates development and maintenance of gonadal tissues which synthesize and secrete steroid hormones, which then control FSH levels by negative feedback - stimulates growth of the ovarian follicle - increased due to lack of negative feedback * Menopause: ovarian function and steroid secretion cease * primary ovarian/testicular failure * when ovaries/testes fail to mature during puberty |
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LH (luteinizing hormone)
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- promotes ovulation (along with FSH to a lesser degree)
- ovarian steroids are the primary negative feedback control for LH secretion - Elevated: lack of negative feedback * menopause, ovarian failure * during puberty when ovaries/testes fail to mature |
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Prolactin
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- stress hormone
- reproductive hormone * stimulates lactation * release inhibited by dopamine * release of TRH stimulates secretion |
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Hyperprolactinemia
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- most common hypothalamic-endocrine disorder
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Prolactinoma
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most common functional pituitary tumor
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Elevations of Prolactin
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- anovulation, amennhorrhea
- impotence: “hypogonadotropic hypogonadism” - dopaminergic medications: phenothiazines, TCA’s |
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hypogonadotropic hypogonadism
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- dec FSH, dec LH
- pituitary or hypothalamic problem - Males: dec testosterone - Females: dec E2 and progesterone |
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hypergonadotropic hypogonadism
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- inc of FSH and inc LH
- testes and ovary primary gland problem - Males: decrease testosterone - Females: decrease E2 and progesterone |
