Endocrine PATHO

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Author:
cmatthews
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209673
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Endocrine PATHO
Updated:
2013-03-26 17:06:32
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BC CRNA PATHO EXAM
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Endocrine Patho Exam 2 Spring 2013
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  1. Hormones may travel by circulation in what two ways?
    As free unbound molecules or attached to transport carriers
  2. What kind of hormones usually circulate unbound in the blood?
    • Peptide hormones
    • Protein hormones
  3. Do hormones that are unbound in the blood have long or short half lives?
    SHORT
  4. What kind of hormones travel through the blood with a carrier?
    • Steroid hormones
    • Thyroid hormones
  5. Where are the carrier proteins (that help hormones travel in the blood) made?
    In the liver
  6. What does a paracrine hormone act on?
    to a nearby cell (not itself!)
  7. What does an autocrine hormone act on?
    ITSELF!
  8. Can unbound (Water soluble) hormones cross the cell membrane?
    NO, they need cell surface receptors. They exert effects through intracellular second messengers (like cAMP)
  9. TRUE or FALSE
    Bound hormones (lipid soluble) easily pass through the cell membrane and act on the nuclear or cytoplasm receptors (INSIDE the cell)
    TRUE
  10. TRUE or FALSE
    Each hormone must have it's own second messenger
    FALSE. Multiple hormones can use the same second messenger.
  11. ↑ Protein binding will _____ half life
    increase
  12. Describe UP regulation
    LOW hormone level concentration = ↑ in # of receptors per cell 

    AKA the cells get MORE sensitive
  13. Describe DOWN regulation
    HIGH hormone circulation = ↓ in # of receptors per cell


    AKA the cells get LESS sensitive (less effect of the hormone)
  14. What are the three ways hormones have effect on cells?
    • Enter blood stream and effect cells in rest of body (distal to release site)
    • Paracrine 
    • Autocrine
  15. Receptor modulation involves UP regulation and DOWN regulation. Does this have to do w/hormone concentration?
    YES!
  16. Hormone regulation is accomplished via complex interactions with nervous system, circulatory system and immune system. Name three ways of regulation.
    • Receptor modulation
    • Negative feedback
    • Neural regulation
  17. Describe Negative feedback
    • target organ hormone inhibits secretion of releasing hormone and tropic hormone.
  18. Give an example of positive feedback
    • Giving birth (contractions get stronger)
    • Breastfeeding
  19. What two hormones does the posterior pituitary secrete?
    • Oxytocin
    • ADH
  20. What hormones doe the Anterior Pituitary secrete?
    • GH
    • TSH
    • ACTH
    • FSH/LH
    • Prolactin
    • MSH
  21. What are the hormones that the Hypothalmus secretes to the Anterior Pituitary?
    • Think R!
    • GHRH
    • TRH
    • CRH
    • GnRH
    • Somatostain
    • Dopmaine
  22. Oxytocin is secreted by the posterior pituitary. What is does it do?
    • chemically similar to ADH
    • It's primary target organ in in mammary tissue and also stimulates uterine contractions. May have role in sperm motility in men.
  23. ADH (also called vasopressin) is secreted from the posterior pituitary and does what?
    Controls the serum osmolality by increasing H2O re-absorption in the DISTAL tubules and collecting ducts of the nephron.

    ADH responds to multiple stimuli.
  24. SIADH (HIGH ADH) is caused by what?
    • Ectopic secretion in several carcinomas
    • Post-op Crani/pituitary surgery
    • MEDS (antidepressants, anesthetics, barbitiuates, morphine, vincristine, etc)
  25. How do you treat SIADH?
    • Fluid restrict
    • Correct hyponatremia
  26. Is serum Na+ low or high in SIADH?
    • Low (diluted from all the water retention)
    • Get lethargy, Nausea, anorexia, and Coma from HYPOosmolarity
  27. Diabetes INSIPIDUS (DI) is when there is a LOW level of ADH. What are two types of DI?
    • Neurogenic (decreased synthesis of ADH)
    • Nephrogenic (failure of nephron to respond to ADH)
  28. What are some s/s of low ADH (DI)?
    • ↑ thirst
    • ↑ urine volume
    • ↓ specific gravity (1.001-1.005)-very dilute urine!
  29. How do you treat low ADH (DI)
    Replace deficiency (vasopressin or DDAVP)
  30. Give an example of neural regulation of hormones.
    adrenal medulla releases epinephrine in response to SNS stimulation
  31. TRUE or FALSE
    Hyperprolactinemia is the most common anterior pituitary disorder.
    • TRUE!
    • Cause is tumor or meds (specially antipsychotics and tricyclic antidepressants)
    • Treat with drugs that stimulate dopamine receptors in the brain
  32. If there is an excess of Growth Hormone (from anterior pituitary) it will cause ____ in adults and ____ ____ in kids.
    Acromegaly in adults. Proportional giantism in kids. 

    S/S Big hands/feet, metabolic imbalances, increased glucose
  33. A deficiency of Growth hormone (from anterior pituitary) will cause ____ ___ in adults and ____ in kids.
    metabolic syndrome in adults and dwarfism (or short stature) in kids (interferes with bone growth)
  34. Adrenal glands secrete mineralcorticoids like ______ and glucocorticoids like _____.
    Aldosterone (mineral): secreted in response to Angiotensin II. (Causes water retention by conservation of Na in nephron)

    Cortisol (gluco): immunologic and anti-inflammatory effects
  35. Low cortisol could be from a primary cause like _____ disease. Describe it!
    Addison's. (could be from autoimmune or TB) Destruction of all layers of adrenal cortex, so they can't secrete adrenal cortical hormones (see an increase in ACTH because pituitary really wants adrenal gland to secrete these hormones)
  36. A secondary cause of low cortisol could be from _______.
    Hypopituitarism. Could be surgical removal of pituitary or iatrongic (rapid removal of glucocorticoids)
  37. What are some s/s of low cortisol?
    • weakness
    • GI disturbances
    • Hyperpigmentation (bronzed skin)
    • hypoglycemia
    • hypotension
  38. In an acute adrenal crisis (or Addison's crisis) there is an drop in BP. Why?
    Aldosterone is unable to conserve water so you get low blood volume which leads to low BP
  39. Why do you get bronzed skin from adrenal insufficiency?
    Melanin Releasing hormone and ACTH share same progenitor (parent) hormone

    So if there is an increase in the parent hormone because thinks it needs more ACTH to stimulate the cortisol secretion
  40. What is Cushing's disease?
    Chronic increase in the function of the adrenal cortex (or iatrogenic) so there is an INCREASE in cortisol
  41. In Cushing's syndrome you get excessive ACTH from the pituitary. TRUE or FALSE?
    TRUE
  42. What is the difference between primary and secondary causes of Cushing's syndrome?
    • Primary: problem with the adrenal gland
    • Secondary: pituitary adenoma (70%)
  43. There are a lot of s/s of Cushing's, list them! (think high cortisol)
    • Weight gain (truncal obesity, moon face, buffalo hump)
    • Abdominal striae
    • glucose intolerance leading to DM
    • protein wasting
    • osteoporosis
    • hypercalcuria
    • poor wound healing
    • HTN
    • Mood disturbances
    • Impaired inflammation/immune response
    • GI bleeding
  44. Whey is hyperfunction of the adrenal medulla a bigger problem than hypofunction?
    • Adrenal medulla secreted Epi and Norepi. If too much, can cause too much fight or flight response.
    • Other areas in body also secrete these hormones so hypofunction is less of problem.
  45. What is the usual cause of hyperfunction of the adrenal medulla?
    Usually a tumor (pheochromocytoma)
  46. What happens when there is hyperfunction of the adrenal medulla?
    • Chronic secretion of catecholamines. Leads to severe HTN (fight or flight). 
    • Tumors are usual cause and are very vascular and may rupture
  47. TRH is secreted by the ____ gland and T3/T4 are secreted by the ____
    • Pituitary
    • Thyroid
  48. TRUE or FALSE
    T4 is the active form of thryoxine
    FALSE. It's T3 (T4 is converted into T3)
  49. What do the thyroid hormones control?
    The rate of metabolic processes
  50. What is the most common cause of hyperthyroidism?
    GRAVES disease (other causes adenoma, carcinoma, hyperplasia, pituitary adenoma, thyroiditis)
  51. What is GRAVE's disease
    An autoimmune phenomenon that results in a hypermetabolic state (HYPERthyroidism)
  52. What is common symptom of Hyperthyroidism?
    • Opthomopathy (bulging eyes)
    • Other s/s include:
    • diaphoresis, palpitations, chest pain, ↑BP, weight loss, amenorrhea
  53. Hypothyroidism in which the patient would was born without a thyroid gland is called____
    Cretinism. Autosomal Recessive disorder!
  54. TRUE or FALSE
    Hypothyroidisim in the newborn must be detected in newborn screening during first 6 weeks of life
    TRUE. During the first 6 weeks, 1/2 of brain development occurs.
  55. What is the autoimmune cause of hypothyroidism called?
    Hashimoto thyroiditis. (Hypothyroidism also caused by thryoiditis, iodine deficiency, and iatrogenic)
  56. What are some s/s of hypothyroidism?
    ↓metabolism (opposite of hyperthyoidism). Weight gain, cold, tired, etc.
  57. What happens if hypothyroidism is left untreated?
    Myxedema (from alterations in composition of dermis and other tissues)

    can get COMA (hypothermia, progressive respiratory depression, high mortality rate!)
  58. TRUE or FALSE
    Type 1 diabetes could have an enviornmental triggering event (like an infection) prior to diagnosis?
    • TRUE. It results from an interaction between genetic and environmental factors.
    • Immune mediated destruction of beta cells!
  59. What is insulin resistance?
    Impaired ability of tissue to use insulin.
  60. Is Type 2 diabetes an inflammatory disease?
    YES, always a low level of inflammation
  61. What is metabolic syndrome?
    • DIABESITY! Need three of the following!
    • Central obesity
    • HTN
    • HIGH triglycerides
    • LOW HDL cholesteral
    • Insulin resistance
  62. What are s/s of metabolic syndrome?
    • Polyuria (excessive urine)
    • Polydipsia (excessive thirst)
    • Polyphagia (excessive hunger)
  63. What are some common complications of diabetes?
    • Macrovascular (Coronary artery, cerebral vascular,peripheral vascular disease)
    • Foot ulcers 
    • Microvascular (Nephropathy, retinopathy, neuropathy)
  64. DKA happen in Type ___ diabetes. This causes an inhibition of fat breakdown and release →
    converts to ketones.
    1!
  65. What are some causes of DKA?
    infection, stressors, inadequate insulin dose
  66. What are some s/s of DKA?
    • Ketosis (Kussmauls' respirations, fruity breath, nausea, abdominal pain)
    • Dehydration or electrolyte loss
    • polyuria, polydipsia, weight loss
    • dry skin, lethargy, coma
  67. how do you diagnose DKA?
    • Serum glucose >200
    • Serum & urine ketones: +
    • Serum pH <7.3
    • Low bicarb
  68. What population gest Hyperosmolar Hyperglycemic State (HHS)?
    • mostly in elderly type 2 diabetics 
    • (type 2 is better able to prevent ketosis because they have some insulin!)
  69. Besides Diabetes, who else can cause HHS?
    Pancreatitus, or pt receiving TPN
  70. What causes HHS?
    • infection, stressors, poor PO intake
    • (occurs in dehydrated people w/insufficient insulin, almost always has concurrent illness)
  71. What are s/s of HHS?
    • Neurologic: confusion, seizures, hemiparesis
    • Marked dehydration
    • Fluid and electrolyte imbalances
    • Acute Renal Failure may result from renal hypoperfusion
  72. What labwork would you expect for HHS?
    • Serum glucose >600
    • serum/urine ketones = NEGATIVE
    • serum pH >7.4
    • serum bicarb >20
    • Hyperosmolar state (>310)

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