Exam 3

  1. What causes pathophysiology of the endocrine system
    • hyperfunction: glands produce too much of a hormone
    • hypofunction: glands produce too little of a hormone
    • tumors: neoplasia- either functioning or nonfunctioning
  2. How can hypofunction of a gland happen
    • synthesis or release is affected: deficiency
    • there is abnormal target tissue: resistance
    • there is an abnormal target response: resistance
  3. functioning vs nonfunctining tumors
    • functioning: the tumor is producing a particular hormone
    • nonfunctioning: the tumor is not producing a hormone
  4. types of endocrine syndromes and examples
    • autoimmune: Hashimotos, type 1 diabetes
    • Post-surgical: removal or thyroid gland causing hypothyroidism/hypoparathyroidism
    • Neoplasia: tumor production of hormone 
    • Inflammation: destruction of endocrine glands from inflammatory cells
    • Receptor defect/resistance: type II diabetes mellitus. cells have insulin resistance
  5. hyperpituitarism
    a result of a functioning tumor in the cells of the pituitary gland in the skull
  6. symptoms of hyperpituitarism
    • visual field defects
    • increased ICP due to incereased pituitary size
    • Sxs related to overproduction of certain hormones
  7. why do pituitary adenomas cause visual defects
    the pituitary gland is in the sella turcica- this is where the optic chiasma also is so the increased size of the pituiary pushes on it and causes visual problems
  8. what hormones can be affected by a functional pituitary adenoma
    • growth hormone
    • prolactin
    • ACTH (adrenocorticotrophic hormone)
  9. difference in symptoms between a functioning pituitary tumor and a nonfunctioning one
    • functioning tumors are often caught earlier because there are early signs- the overproduction of hormones
    • nonfunctional tumors have late sx because no hormone secreted. 
    • sx only show up in a nonfunctional when its size is pushing on and affecting something else.
  10. when do most pituitary tumors happen
    • between your 40s and 60s. 
    • these tumors account for 10% of cranial tumors
  11. mass effect
    • this is the effect from growth in tumor size
    • in pituitary mass effect causes visual field changes and increased cranial pressure, headache, nausea and vomiting.
  12. Apoplexy Triad
    • headache
    • vomiting
    • visual impairment
    • and altered consciousness with hemodynamic instability
    • can happen in patients who have a pituitary tumor which leads to bleeding in the pit gland and ends up as pit hypofunction
  13. Hypopituitarism
    • due to death of the cells in the gland from...
    • ischemic injury
    • radiation
    • inflammation process that has affected the pituitary gland and therefore its hormone production
  14. symptoms of hypopituitarism
    • depend on which hormone is decreased
    • can happen due to a variation, inflammation, infection or some kind of compression of the gland like a tumor
  15. hormones affected by pituitary failure and what they cause
    • lutenizing hormone and follicule stimulating hormone
    • in men: testosterone levels drop leading to decreased sexual drive and impotence
    • in women: infertility
  16. pituitary stalk effect
    • infundibulum (the tube like strucutre that connects the posterior pituitary to the hypothalamus) can get inflamed or compressed by something like a tumor, giving us the stalk effect. 
    • usualy leads to slight elevation in prolactin levels, much less than in prolactin producing tumors but still enough to cause women to get galactorrea and loose periods
  17. severe hypopituitarism
    • can affect thyroid gland and cause hypothyroidism 
    • or affect adrenal gland and cause low cortisol levels which can be LIFE THREATENING
  18. General symptoms of hypopituitarism
    • they are general so a diagnosis has to be done by looking at hormonal effects
    • weight loss or gain
    • fatigue, decreased energy
    • dizziness
    • headaches
    • pituitary apoplexy
  19. growth hormone produciing tumor
    • gigantism
    • acromegaly
  20. prolactin producing tumor
    • galactorrhea (milk production)
    • amenorrhea
  21. ACTH producing tumor
    • cushings disease
    • nelsons syndrome (post adrenalectomy- if a patient has both adrenal glands removed which is rare)
  22. prolactinoma
    • the most common pituitary adenoma
    • hyperprolactinemia (prolactin is greater than 200ug/L)
    • clinical status determines detection
  23. types of prolactinomas
    • mircoadenomas: smaller nodules in female
    • macroadenomas: larger nodules in males
  24. symptoms of prolactinomas
    • increased prolactin levels leading to 
    • amenorrhea
    • galactorrhea
    • libdo loss
    • infertility
  25. Growth hormone- secreting adenoma symptoms
    • if it happens before epiphseal closure (replacement of the epiphyseal plate with the epiphyseal line which happens after puberty)prepubertal: gigantisism
    • if it occurs after epiphyseal closure (in adults): acromegaly
  26. Gigantism
    • large body stature, increased height, delayed puberty
    • long legs/arms
    • longer bones
    • enlarged hands, feet, tongue, nose, lips
    • enlarged forehead and jaw, spreading of teeth
    • artrhitis- bc of weight their joints dont work
  27. what are people with pituitary gigantism at risk of developing
    • high blood pressure
    • Diabetes mellitus
    • heart disease 
    • thyroid cancer
    • colon polyps
    • arthritis
    • osteoporosis
    • CHF
  28. bob wadlow
    • died at 22 due to infection
    • 8ft 4in
    • had gigantism
  29. acromegaly
    • abnormal growth
    • frontal bossing- protruding forehead
    • prognathism (bulging of lower jaw)
    • enlarged hands/feet/nose/tongue
    • problems with perspiration
    • galactorrhea
    • enlarged colon, hepatomegaly, nephromegaly
    • many other abnormalities due to GH late in life
  30. what are those with acromegaly at risk for
    • carpal tunnel
    • diabetes mellitus
    • hypertension
    • arthritis
    • osteoporosis
    • CHF
    • they also have a complicated histor after having extra doses of growth hormone after puberty
  31. pathway of pituitary dependent cortisol production
    • hypothalamus secreates corticotrophin releasing hormone which stimulates the anterior pituitary to secrete ACTH which stimulates the adrenal coretex to make cortisol
    • when cortisol high this inhibits the hyp from making CRH
  32. ACTH Adomas
    • corticotrophin cell adomas
    • corticotrophin cells in the anterior pituitary are responsible for producing ACTH
    • A lot of ACTH is produced here due to the tumor 
    • ACTH acts on the adrenal cortex and stimulates production of cortisol so you get high cortisol levels which causes Cushings disease (pituitary dependent increase in cortisol)
    • the tumor is unresponsive to the bodys negative feedback to stop cortisol production (normally the hypothalamus would stop making corticotrophin releasing hormone and stop it but even when this happens the tumor still makes ACTH)
    • High ACTH, high cortisol
  33. symptoms of ACTH adenomas
    • weight gain
    • increased BP
    • truncal obesity
    • decreased muscle mass
    • diabetes mellitus
  34. what gender is ACTH cell adenomas more common in
    women
  35. Posterior pituitary hormones
    • antidiuretic hormone (ADH) aka vasopressin
    • oxytocin
  36. ADH
    • antidiuretic hormone/vasopressin
    • increased absorption of water from the kidney resulting in...
    • decreased urinary volume
    • increased sodium conc. in urine
    • increased serum volume
    • decreased serum sodium conc.
    • increased blood pressure due to increased volume

    ADH IS RESPONSIBLE FOR RETENTION OF WATER ONLY, it does not stimulate sodium retention, the sodium effects are a secondary effect to water retention.
  37. oxytocin
    • stimulates contraction of uterus
    • stimulated lactiferous ducts during pregnancy
  38. ADH deficiency
    • also called diabetes insipidous
    • diabetes not related to hyperglycemia
  39. symptoms of ADH deficiency
    • polyuria
    • polydipsia
    • dehydration
    • no hyperglycemia
  40. lab values for ADH deficiency/diabetes insipidus
    • large volumes of dilute urine
    • decreased specificy gravity
    • decreased urinary sodium concentration due to increased water
    • increased serum sodium concentration
    • increased serum osmolarity- because increased sodium concentration and water follows
  41. why could ADH deficiency happen
    • no pituitary gland
    • lesions of posterior pituitary
    • Rathke's cleft cyst (a pouch between ant. and pos. pituitary)
    • infection- ie tuberculosis of the pit
    • tumors- pushes on post pit and leads to cell death.
  42. SIADH and why does it happen
    • Syndrome of inappropriate antidiuretic hormone
    • usually bc of an ADH producing small cell (oat cell) carcinoma of the lung
    • can also happen bc of CNS tumors or trauma
  43. what happens in SIADH
    ADH produced by a tumor leading to increased water reabsorption from the renal tubules which causes increased blood volume, decreased urine ouput, increased urine sodium [], decreased serum sodium [ and decreased sodium osmolarity in serum bc its too dilute
  44. sx of SIADH
    • ADH excess
    • concentrated urine
    • dilute serum
    • hyperosmolarity of urine- bc high sodium there
    • hypoosmolarity of serum- bc low sodium there
  45. Consequences of SIADH in order of progression
    • increased body water but no edema
    • overhydration in general but the danger is in overhydration of the brain cells
    • confusion if sodium drops below 125mM
    • convulsions if sodium drops below 115mM
    • coma/death
  46. what can be done about SIADH
    • Remove the cause (tumor, medication)
    • resolve the trauma- the SIADH should resolve once the trauma heals
    • restrict fluids
    • give ADH antagonist- diuretics
  47. thyroid gland
    • anterior and inferior to the larynx 
    • has a left and right lobe connected by the isthmus
    • contains most of the body's iodine
  48. average amount of iodine each type of person needs per day
    • adults and adolescents: 150ug
    • pregnant women: 220ug
    • Lactating women: 290ug
    • children 1-11 years: 90-120ug
    • infants: 110-130ug
  49. where does most of our iodine intake come from
    • food and salt
    • avg adult needs 100-150 ug/day to make thyroxin (aka T4)
  50. thyroid on the microscopic level
    • spherical follicles lined by cuboidal epithelium- this is what synthesizes the hormone tetraiodothyronine (T4)
    • There is a protein called thyroglobulin in the colloid that stores T4 in the gland
    • there are also 4 groups of cells called the parafollicular C cells (aka clear cells) that secrete calcitonin
  51. regulation of thyroid gland function
    • regulated by the anterior pituitary gland through the secretion of thyroid stimulating hormone (TSH)
    • TSH stimulates the thyrooid gland to produce T4 
    • When T4 level goes up, that negatively affects the hypothalamus and ant. pit. gland and stops the hyp from producsing thyroid releasing hormone and therefore when this stops the ant. pit. is no longer stimulated to produce TSH
    • hypothalamus, ant. pit and thyroid all participate in a connected negative feedback loop
  52. how does thyroid hormone affect metabolism
    you produce T4 that eventually becomes T3 at the level of the tissue and then enters the cell and induces protein synthesis to increase the basal metabolic rate
  53. physiologic effects of thyroid hormones
    • they increase the BMR and therefore the temperature
    • when high thyroid hormone and BMR there is increased heart rate and CO
    • increased gi motility
    • increased bone turnover
    • increased muscle contraction
    • increased RBCs and 2,3DPG
    • Increased gluconeogenesis
    • increased cholesterol
    • increased stimulation of symp NS
    • increased b-adrenergic activity
    • increased catecholemines
  54. what causes a hypermetabolic state
    increased levels of T3 and T4
  55. what can increase levels of T3 and T4 to cause a hypermetabolic state
    • diffuse hyperplasia (graves disease)
    • taking too much exogenous thyroid hormone
    • multinodular goiter
    • adenoma of the thyroid
    • post partum (not common)

    thyrotoxicosis is usually graves disease, but these other things can cause it too
  56. effects of hyperactivity of the symp ns in hyperthyroidism
    • nervousness
    • tremor
    • tachycardia
    • palpitations
    • hyperreflexia
    • hypermotility of GI tract
    • malabsorption
    • diarrhea
    • weight loss
    • gaze
    • warm flush skin
  57. graves disease
    • an autoimmune disorder where you produce antibodies agaist TSH receptor which increases T3 and T4 activity and eventually affects the eyes
    • most common cause of primary hyperthyroidism
    • primarily occurs in women 30s-40s
    • familial: HLA-DR3
    • increased T3 and T4, Decreased TSH
  58. Exophthalamos and Pretibial edema
    • infiltrative opthalmopathy (eye bulging) and infiltrative dermatopathy
    • these happen in graves disease
  59. Hypothyroidism
    • low T3 and T4
    • structural or functional interference with inadequate thyroid levels
  60. hypothyroidism at different ages
    • infancy/childhood hypothyroidism: cretinism- growth is retarded (body and brain function)
    • Adult hypothyroidism: Myxedema
  61. causes of primary hypothyroidism
    • goiter (can be caused by iodine deficiency)
    • iodine deficiency
    • hashimotos thyroiditis
    • thyroid ablation
    • infection of thyroid gland that leads to its destruction
    • inflitration of thyroid gland by something like iodine leading to its destruction
    • idiopathic primary
  62. causes of secondary hypothyroidism
    • pituitary disease
    • hypothalamic disease

    bc both pit and hyp regulate thyroid gland
  63. area causes of hypothyroidism
    • central: hypothalamic/piutitary 
    • thyroidal: thyroid problem itself
    • extrathyroidal: somehow there have been mutations taht lead to resistance to thyroid hormone by cells
  64. Infancy characteristics of hypothyroidism
    • dwarfism
    • enlarged tongue
    • protuberent abdomen
    • delayed epiphyseial union and dentation
    • irreversable mental retardation if not corrected early
  65. adult characteristics of hypothyroidism
    • myxedema
    • weight gain
    • muscle cramps
    • fatigue
    • slowed mentation
    • slowed speech
    • cold intolerance
    • constipation
    • cardiomegaly
    • pericardial effusion
  66. myxedema
    accumulation of mucopolysaccharide in and under skin and visceral sites resulting in non-pitting edema
  67. causes of myxedema
    • chronic thyroiditis
    • radioactive I2 ablation
    • suregical removal of thyroid
    • I2 deficiency
    • drugs (ie lithium)
  68. goiter
    • impaired (decreased) thyroid hormone- T3 or T4
    • enlargement of the thyroid due to TSH stimulation
    • the most common thyroid disease worldwide
  69. how does goiter happen
    iodine or t3 or t4 deficiency which leads to increased TSH to stimulate its production and when this continues to stimulate the thyroid becomes larger (hypertrophy and hyperplasia)
  70. endemic vs sporatic goiter
    • endemic: iodine deficiency in mountainous regions. used to get in US but now Iodine in salt. still a big problem in developing world
    • sporadic: usually unknown or from eating too many cruciferous vegetables
  71. autoimmune thyroid diseases
    • graves: causes hyperthyroidism from anti TSH antibodies
    • hashimotos: anti TSH RECEPTOR antibodies are made- the receptor on the thyroid gland is occupied by the antibodies so the TSH cant bind and the gland cant become stimulated so no t3/t4
  72. main sx of hypo and hyperthyroid
    • hypo: high TSH, low t3/t4. fatigue, weight gain, cold intolerance, dry skin, depression, bradycardia
    • hyper: low TSH, high T3/T4. fatigue, weight loss, heat intolerance, hyperhidrosis (excessive sweating), nervousness, palpitations
  73. Blood
    flows through a closed system in the blood vessels
Author
iloveyoux143
ID
349187
Card Set
Exam 3
Description
Exam of 11/1/19
Updated