Flashcards
Endocrine System
Cards in this deck (85)
- 1Most common cause for hyperpituitarismPituitary adenoma
- 2causes of hyperpituitarismpituitary adenoma, hyperplasia, carcinoma, extra pituitary tumors, certain hypothalamic lesions
- 3manifestations of hypopituitarismGH secretion impairment; hypogonadism; hypothyroidism (due to TSH deficiency); Adrenocorticotropic hormone deficiency (most serious)
- 4treatment of hypopituitarismtreat identified underlying cause; replacement therapy of hormone deficiency
- 5Insulin in relation to growth and deficienciesEssential role in growth, and carbohydrate and fat metabolism
(e.g. children with DM and normal GH levels fail to grow normally) - 6Thyroid hormone related growth and deficienciesDeficiency leads to bone growth and epiphyseal closure delay
- 7Androgens related to growth and deficienciesexert anabolic growth effects through their actions on protein synthesis
- 8glucocorticoids related to growth and deficienciesExcess leads to inhibition in growth
- 9Growth hormone disorders: what stimulates growth hormone?hypoglycemia, fasting, starvation, increased blood levels of amino acids, and stress conditions
- 10GH disorders: what inhibits GH?increased glucose levels, free fatty acid release, cortisol, and obesity
- 11Examples of GH disordersGH deficiency, short stature in children, tall stature, and GH excess in adults
- 12Causes of short stature (attained height below third percentile)Chromosomal abnormalities, malnutrition, chronic kidney disease, DM, malabsorption syndrome, and excessive glucocorticoid administration
Emotional disturbances - functional endocrine disorders (causing psychosocial dwarfism) - 13Diagnosis of short statureHeight measurements, tests to exclude non-endocrine and hormonal causes, imaging
- 14Constitutional delay in growth and pubertychildren of moderately short stature, thin build, delayed skeletal and sexual maturation, and absence of other causes of decreased growth
- 15Psychosocial dwarfismfunctional hypopituitarism seen in some emotionally deprived children
- 16Etiology of GH deficiency in childrenIdiopathic GH deficiency; pituitary tumors or genesis of pituitary; congenital GH deficiency; acquired GH deficiency
- 17effects of GH deficiency in childrennormal intelligence, short stature, obesity with immature facial features, delay in skeletal maturation, and puberty delayed
- 18treatment of GH deficiency in childrenGH replacement therapy and IGF-1 replacement therapy
- 19Treatment of tall statureSex hormones
- 20GigantismGH excess in children - GH excess occurring before puberty and before fusion of epiphyses of long bones
- 21AcromegalyGH excess in adults: occurs after the epiphyses of the long bones have fused
- 22signs of acromegalyexaggerated growth of the ends of extremities (fingers, hands and toes); metabolic effects
- 23treatment of GH excesspituitary tumor removal, radiation therapy and other pharmacological agents
- 24How does precocious puberty occur?qEarly activation of the hypothalamic-pituitary-gonadal axis; or idiopathic, gonadal, adrenal, or hypothalamic disorders, and tumors of the CNS
- 25Diagnosis of precocious pubertyBased on physical findings and radiologic findings of advance bone age
- 26Diagnosis of precocious puberty in girlsearly thelarche, adrenarche, and menarche,
- 27diagnosis of precocious puberty in boysearly genital enlargement
- 28bones in precocious pubertyRadiologic findings of advance bone age; tall as children but short as adults because of early closure of epiphyses
- 29Treatment of precocious pubertyMRI or CT, surgery, medication, or no treatment, and patient support
- 30Shape of the thyroidShield shaped structure - lateral lobes and a connecting isthmus
- 31Hormones of thyroidT3 (10%) and T4 (90%) go to circulation - T3 in active form?
- 32What are thyroid hormones bound to?Thyroid hormones bound to protein (thyroxine binding globulins - TBG) are not active
- 33What are free thyroid hormones?Responsible for pituitary feedback
- 34What alters protein binding of thyroid hormones?Medical conditions, medications, and genetic predisposition can alter protein binding of T3 and T4
- 35What regulates thyroid hormones?Regulated by HPT (hypothalamic-pituitary-thyroid) feedback system
- 36What stimulates the thyroid gland?TSH from anterior pituitary
- 37What causes feedback inhibition of HPT system?Increased thyroid hormones
- 38Actions of thyroid hormonesMetabolic rate - Increases - energy production increases
Resp functions - increase O2 consumption, ventilation
Cardiac functions - vasodilation - increase blood volume & cardiac output
GI functions - diarrhea, increase appetite, weight loss
Neuro- increase muscle contract, fine tremors, tachycardia, nervous, anxiety, insomnia - 39Thyroid tests1) Immunoassay: free T4, TSH levels, Primary hypo: low T3, T4 and free T4 levels and high TSH
2) Auto-antibodies
3) Radioiodine uptake test
4) Thyroid scans
5) US, CT, MRI, Biopsy - 40GoiterIncrease in size of thyroid gland; hypothyroid, euthyroid, hyperthyroid; toxic or nontoxic; produces signs of hyperthyroid; diffuse; entire thyroid gland; multi nodular goiters
- 41Congenital hypothyroidismlack thyroid gland or deficient TSH secretion; mental retardation and impaired physical growth
- 42Acquired hypothyroidismslows down metabolic process and causes myxedema; non-pitting edema
- 43Signs and symptoms of hypothyroidismgradual weakness, fatigue; weight gain despite lack of appetite; cold intolerance; dry and rough skin, thick-brittle hair; conductive deafness, constipation, bradycardia, lethargy, impaired memory
- 44Treatment of hypothyroidReplacement therapy (T3 or T4)
- 45Hashimoto thyroiditisAutoimmune disorder (thyroid destroyed); hyperthyroid state can occur midcourse; signs and symptoms of hypothyroidism
- 46Myxedematous comalife threatening end-stage of hypothyroidism; S/S: coma, hypothermia, CV collapse, hypoventilation, severe metabolic disorders (CO2 retention & hypoxemia, fluid-electrolyte imbalance, hypothermia)
- 47Treatment of myxedema Comamanage cardiopulmonary system -- thyroid replacement
- 48What is hyperthyroidism?high levels of circulating thyroid hormone; increased oxygen consumption and metabolism
- 49Signs and Symptoms of hyperthyroidismweigh loss despite large appetite; tachycardia, palpitations, SOB; excessive sweating, muscle cramps, heat intolerance; restlessness, muscle tremors; thin and silky hair; abnormal retraction of the eyelids and infrequent blinking
- 50Treatment of hyperthyroidismReduce levels of thyroid: radioactive iodine, surgical removal, anti-thyroid drugs
- 51Graves DiseaseAutoimmune disorder = abnormal stimulation of thyroid gland (thyroid stimulating antibodies)
- 52Clinical features of Graves DiseaseTriad of Symptoms:
hyperthyroidism
goiter
opthalmopathy
Cytokine activation of fibroblast in orbital tissue causes eye problem - 53Treatment of Graves DiseaseGlucocorticoids with radio iodine
- 54What is Thyroid Storm?Life-threatening form of thyrotoxicosis - due to undiagnosed or ineffective treatment
- 55Cause of thyroid storm?stress (infection), DKA, physical or emotional trauma, manipulation of hyperthyroid (surgery)
- 56Manifestations of Thyroid StormVery high fever; CVS effects - tachycardia, angina, congestive heart failure; CNS effects - agitation, restlessness and delirium
- 57Treatment of Thyroid StormRapid diagnosis is crucial; peripheral cooling; replace fluids, glucose, electrolytes, beta-blockers, anti-thyroid medication
- 58Where are the adrenal glands?bilateral at apex of kidneys
- 59What are the parts of adrenal glandsMedulla (inner portion) produces the catecholamines epinephrine and norepinephrine
Cortex:
Mineralocorticoids - outer layer
Glucocorticoids - middle layer
Adrenal androgens and estrogens - inner layer - 60MineralocorticoidsAdrenal hormone of the cortex
Aldosterone: regulates ion transport; essential role in the regulation of potassium and sodium levels and water balance; controlled by the renin-angiotensis system and potassium levels; promotes the kidneys to hold on to sodium and excrete potassium - 61glucocorticoidsAdrenal hormone of the cortex
Cortisol: the main glucocorticoid produced by the adrenal cortex; controlled by the hypothalamic-pituitary- adrenal system; when body is stressed > hypothalamus releases corticotrophin releasing hormone > on anterior pituitary > ACTH > adrenal gland > cortisol; ACTH controls the release of cortisol; when cortisol levels rise ACTH levels fall (NEGATIVE FEEDBACK) - 62Functions of GlucocorticoidsDirect effect on CHO metabolism; increases blood glucose concentration ; promotes gluconeogenesis by the liver; protein breakdown into amino acids; promotes mobilization of fatty acids from adipose tissue; promotes cell metabolism to use fatty acids for energy; suppresses the immune response; when cortisol (hydrocortisone) is administered it blocks inflammation; inhibits prostaglandin synthesis
- 63What do adrenal androgens do?Produces dehydroepiandrosterone (DHEA) which promotes pubertal growth of body hair in women; Production declines in women as they age and is referred to as adenopause; replacement of DHEA may help improve overall wellbeing and sexuality
- 64Adrenal SuppressionLong term therapy of glucocorticoids causes atrophy of the adrenal gland due to depression of the HPA system; Abrupt stopping of glucocorticoids can cause acute adrenal insufficiency; the recover phase to normal function can take up to 12 months or more
- 65Adrenal function testingBlood levels of cortisol, aldosterone and ACTH; 24 hour urine collection measuring for the end products of adrenal cortical hormones; 24 hour urinary free cortisol; late night serum or salivary cortisol levels; overnight 1 - mg dexamethasone suppression test; Test dose of ACTH; insulin-induced hypoglycemic test
- 66What is congenital adrenal hyperplasia?Autosomal recessive disorder: lack of synthesis of cortisol leading to abundance of ACTH and over production of androgen hormones
- 67Diagnosis of congenital adrenal hyperplasiaMale infants are usually not diagnosed; female infants have civilization syndrome
- 68Treatment of congenital adrenal hyperplasiaOral or parenteral glucocorticoid replacement; reconstructive surgery (consists of reducing the size of the clitoris; separating the labia; exteriorizing the vagina)
- 69Addison's diseaseCaused by a destruction of the adrenal gland, mainly related to autoimmune (TB can do this. not common in US)
- 70What is primary adrenal insufficiency (cortical)?Mainly related to autoimmune:
1) Addison's disease (all adrenal glands are destroyed)
2) TB
3) Adrenal hemorrhage secondary to anticoagulant therapy, open heart surgery, child birth
4) AIDS
5) Drugs - 71Secondary adrenal insufficiencyresults from disorders of the HPA system
- 72Signs and Symptoms of Addison's diseasesparse axillary and pubic hair in women; hyponatremia/hyperkalemia; decreased cardiac output; loss of extra cellular fluid; orthostatic hypotension; anorexia/weight loss; nausea/vomiting; hyper pigmentation of the skin
- 73Treatment of Addison's DiseaseOral replacement of glucocorticoid and mineralocorticoid agents (hydrocortisone, fludrocortisone, DHEAs in females); Educate about regular meals and exercise; need for medial attention during times of infection, trauma or unusual stress; may need to wear medical bracelet
- 74Secondary adrenal cortical insufficiency causes and treatmentHypopituitarism (remove pituitary gland); hypothalamic effect (tertiary); rapid withdrawal of glucocorticoids; treatment with glucocorticoids can cause adrenal atrophy and loss of cortisol production; long lasting effects; critical in stress or surgery
- 75Causes of Acute adrenal crisisLife threatening illness caused by:
Uncontrolled Addison's disease; salt losing forms of CAH; massive bilateral adrenal hemorrhage; meningococcal septicemia; adrenal trauma; anticoagulant therapy; adrenal vein thrombosis; adrenal metastasis - 76Signs and symptoms of adrenal crisisNausea/vomiting
muscular weakness
hypotension
dehydration
vascular collapse - 77Treatment of adrenal crisisfluid replacement
glucocorticosteroid replacement
oral hydrocortisone
fludrocortisone
broad spectrum antibiotics - 78What is Cushing syndrome?Secondary to Glucocorticoid excess
- 793 main forms of hypercortisolismPituitary form (increased ACTH)
Adrenal form (caused by benign/malignant tumor)
Ectopic Cushing syndrome (non-pituitary ACTH source, e.g. small cell lung carcinoma)
Long term use of glucocorticoids (iatrogenic) - 80Signs and Symptoms of Cushing SyndromeSecondary to exaggerated cortisol actions:
Altered fat metabolism (moon face, buffalo hump)
muscle weakness; skin changes; osteoporosis; DM/hypertension; immunocomporomise; GI bleeding; androgen effects (facial hair); emotional disturbances - 81Diagnosis of Cushing syndrome24 hour excretion of cortisol in the urine; elevated cortisol levels between 11pm and midnight; overnight dexamethasone suppression test; elevated plasma ACTH level (pituitary tumor, ectopic ACTH); low plasma ACTH levels (adrenal tumor); MRI or CT scans to locate adrenal or pituitary tumors
- 82What happens if Cushing syndrome is not treatedserious morbidity and mortality
- 83Goal of treatment of Cushing Syndrometo remove or correct the source of hypercortisolism with least possible pituitary or adrenal damage
- 84Treatment of Cushing's syndromeTranssphenoidal, hemihypophysectomy - removal of pituitary; pituitary radiation; adrenalectomy; cortisol replacement therapy; removal of ectopic ACTH producing tumors; medications that block steroid synthesis for inoperable ectopic tumors or adrenal carcinomas; pneumonia prophylaxis
- 85—
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- Flashcards on Endocrine System, created by Marian Baxter on 22/07/2017.
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- Marian Baxter
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