Systems - Endocrine

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Systems - Endocrine
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2014-11-30 13:01:13
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Systems - Endocrine
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  1. Describe the normal axis of thyroid hormone production
    • 1) hypothalamus makes TRH stimulates anterior pituitary to make TSH
    • 2) TSH increases the production of T3 and T4
    • 3) Rising levels of T3 and T4 inhibits TRH release by the hypothalamus and TSH levels by the anterior pituitary
  2. Describe the 5 avenues of investigation we have available to us in investigating the thyroid
    • 1) PE (HR, sweating, fine tremor, hair loss)
    • 2) Palpation of thyroid 
    • 3) Labs (fT3, fT4, TSH, thyroid autoantibodies)
    • 4) U/S
    • 5) Iodine uptake scan
  3. How does thyroid hormone increase BMR? (2)
    • 1) increases synthesis of Na-K-ATPase pumps
    • 2) Increases SNS by increasing expression of Beta1 receptors
  4. 6 Causes of hyperthyroidism Investigations to confirm each.
    • 1) Autoimmune: Graves (most common; TSH receptor antibodies), Hashimoto's (transient; anti Tb and Tg antibodies)
    • 2) autonomy of the thyroid (not TSH dependent; uptake scan, absence of abs)
    • 3) Exogenous hyperthyroid (too many pills; Hx)
    • 4) Thyroid cancer (rare; uptake, U/S)
    • 5) Pituitary dysfunction (high TSH)
    • 6) Amiodarone therapy
  5. Describe Hashimoto's Thyroiditis (4)
    • 1) initial hyperthyroid (release of stored T4) and then hypo (tissue is destroyed)
    • 2) Look for high antithyroglobilin (Tg-abs) and anti-thyroperoxidase (TPO-abs) (these are the destructive antibodies causing the damage)
    • 3) infiltration of lymphocytes
    • 4) Heurthel cells
  6. Describe the pathophysiology of Graves' disease
    IgG (TSI) stimulates the TSH receptors which causes the overproduction of thyroid hormone in the thyroid. In addition it increases GAG production in fibroblasts behind the eyes and on the shins causing the proptosis and tibial myxedema, respectively.
  7. Describe the labs that you see in Graves' disease and what inflammatory disorder gives similar results
    • Decreased TSH, increased fT3 and fT4
    • TSH-receptor abs are increased
    • anti-TPO and anti-Tg abs are increased. 
    • Diffuse increased RAIU (radioactive iodine uptake)

    With the exception of the TSH-receptor abs and the these results are the same as what you would see in early Hashimoto's thyroiditis
  8. When do you see "hot" nodules on RAIU and when do you see diffuse increased iodine uptake?
    • -Hot: autonomous adenomas
    • -diffuse increase: disseminated autonomy and Graves
  9. What are the 5 P's of pheochromocytoma. What is the 6 P?
    • Pressure - HTN (90%)
    • Pain - headache (80%)
    • Perspiration (70%)
    • Palpitations (65%)
    • Pallor (40%)

    The 6th P is paroxysmal. These events are severe and transient (some insult causing release)
  10. Describe the 4 main types of thyroiditis
    • 1) Hashimoto's: chronic lymphocytic infiltration
    • 2) de Quervain's (subacute thyroiditis): tender, granulomatous infiltration
    • 3) Post partum: subacute
    • 4) Riedel: hard a wood, nontender
  11. What are the three levels of thyroid problems?
    • Primary: thyroid
    • Secondary: pituitary
    • Tertiary: hypothalamus
  12. 5 causes of secondary hypothyroidism?
    • -empty sella
    • -pituitary adenoma
    • -post hypophyseal surg
    • -post traumatic brain injury
    • -apoplexy (Sheehan-syndrome)
  13. Describe the dual pathophysiology of iodine deficiency goiter. What are the labs you see for this?
    • 1) increased TSH levels cause cell hypertrophy
    • 2) decreased Iodine in thyrocytes causes cell hyperplasia

    both of these lead to goiter. Normal TSH, fT3, and fT4
  14. 6 findings that you see in hypothyroidism that you DO NOT see in depression
    • bradycardia
    • cardiac and lipid abnormalities
    • cold intolerance
    • delayed reflexes
    • goiter
    • hair and skin changes
  15. Signs and Sx of hyperthyroidism
    • THYROIDISM mnemonic
    • Tremor
    • Heart rate up
    • Yawning (fatigued)
    • Restlessness
    • Oligomenorrhea/amenorrhea
    • Intolerance to heat
    • Sweating
    • Muscle wasting/weight loss
  16. What kind of f/u do patients with graves need after ablation?
    lifetime f/u. routine TSH, fT4, fT3, thyroid autoantibodies
  17. What should you think if you see a "hot nodule" on RAIU?
    autonomous adenoma (multinodular goitre)
  18. what are the treatment options in Grave's disease? (5)
    • 1) Thionamines: Methimazole (longer half life, usually preferred, teratogenic); Propylthiouracil (PTU, use in 1st trimester of preg)
    • 2) Symptom tmt with beta blockers
    • 3) Thyroid ablation with radioactive iodine
    • 4) Thyroidectomy
    • 5) Use steroids for extreme exopthalmos
  19. Describe thyroid storm and how we treat
    This is a medical emergency. Bascially stress in a hyperthyroid patient has caused a huge hormone release.

    Treat the same as graves, but with higher doses. give supportive tmt. Treat precipitant. Give dexamethasone to decrease inflammation and stop peripheral conversion of T3->T4.
  20. Special tests to investigate hypothyroid (4)
    • Anti-TPO Abs
    • Anti thyroglobulin Abs
    • Uptake scan
    • U/S
  21. Signs and Sx of Hypothyroidism
    • HIS FIRM CAP mnemonic
    • Hypoventilation
    • Intolerance to cold
    • Slow HR
    • Fatigue
    • Impotence
    • Renal impairment
    • Menorrhagia/amenorrhea
    • Constipation
    • Anemia
    • Paresthesia
  22. Why you start a patient with hypothyroidism on levothyroxine when should you check levels to adjust dose? why?
    Six weeks, because it has a one week half life and it takes this long to reach SS in the body
  23. What changes to medication do you do in a hypothyroid patient that has just become pregnant?
    Increase the levothyroxine dose as pregnant women need more in order to stay euthyroidic.
  24. Describe myxedema coma
    a medical emergency! Hypothyroid complicated by some kid of acute stressor. Treat the same as hypothyroidism with supportive care.
  25. What would you tell a patient who wants to take "natural" thyroid meds? (2)
    • -different T3/T4 ratio in animals
    • -a lot of variability between batches
  26. What is the most specific and sensitive test to assess for thyroid malignancy?
    FNA
  27. How does type I diabetes usually manifest?
    DKA
  28. Describe the actions of insulin
    -Insulin receptors on all tissues.

    -induce uptake of glucose into cells

    -Increase storage of glucose (glycogen, protein, and fat production)

    -Decreases gluconeogenesis by liver

    -Inhibits glucagon
  29. How does DM II cause hyperglycemia?
    • 1) relative insulin deficiency
    • 2) Excess hepatic glucose production
    • 3) Insulin resistance (due to obesity and inactivity)
  30. What percentage of the diabetic population have DM II, DM I?
    • DM II - 90-95%
    • DM I - 5-10%
  31. Why is there no role for screening in DM I?
    We cannot prevent it once it is underway
  32. Who should you screen for DM II (age and 11 high risk groups)
    • >40 or part of a high risk group
    • HR Groups
    • -History: 1st degree rel with DM, HR population (e.g. aboriginal), IGT or IFG (pre-diabetes), Hx of GDM or macrosomia
    • -Clinical: DM complications, HTN, dyslip, fat, PCOS, acanthosis nigricans, chronic use of corticosteroids
  33. What is the most effective intervention in people at high risk for DM II?
    Lifestyle changes. 60% reduced risk with 5% weight loss in people with prediabetes.

    Medications can give some prophylaxis, but are not as good
  34. Define diabetes and pre diabetes
    Diabetes: presence of hyperglycemia

    pre-diabetes: abnormal blood glucose, but not to the levels of diabetes. Includes Impaired fasting glucose (b/n 6.1-6.9), Impaired glucose tolerance (b/n 7.8-11.0), of HbA1c 6.0-6.5
  35. Compare and contrast DM I and DM II (4 points each)
    DMI: young, usually no FHx, usually thin, sudden onset (DKA)

    DM II: usually older adults, commonly a +ve FHx, fatty, gradual onset
  36. How do you diagnose diabetes? (4)
    • Any one of these will diagnose (confirm on a later date usually)
    • 1) fasting glucose >= 7 
    • 2) random gucose > 11.1 + Sx of hyperglycemia (Polydipsia, polyuria, weight loss)
    • 3) 75 g OGTT: fasting >= 7 and 2hr blood > 11.1
    • 4) HbA1c >= 6.5%

    Unless one test is SUPER sky high, confirm the next day with any of the above tests (does not need to be the same one)
  37. How to diagnose DKA with lab tests?
    • 1) ketonemia
    • 2) ketouria
    • 3) increased ion gap metabolic acidosis
  38. What are the targets for an adult diabetic patient? (3)
    • 1) A1C: <= 7 (7.1-8.5 in elderly)
    • 2) FPG or pre prandial: PG 4-7
    • 3) 2 hr post-prandial: 5-10

    Achieve one in 3-6 months
  39. What are the general dietary percentages for carbs, protein, and fats?
    • carbs: 40-60%
    • protein: 15-20% protein
    • fat: <35% fat
  40. How much weight do you need to lose in order to have a huge effect on insulin sens, glycemic control, BP, lipid levels?
    5-10%
  41. What is the first oral agent you should try? What are the contraindications?
    metformin

    CI's: renal failure or CHF
  42. Which diabetic medications cause weight gain? (4) Why do we care about this?
    • -thiazolidinedione
    • -insulin
    • -sulphonylurea (glyburide)
    • -meglitinide

    We want to use the ones that cause weight loss first (usually metformin to start)
  43. Describe the 6 major classes of Diabetes meds
    • 1) insulin secretagogues (sulphonylureas, meglitinides
    • 2) Insulin sensitizers (metformin
    • 3) Impair carb absorption (acarbose)
    • 4) Incretin analogues (GLP, or DPP agonists)
    • 5) pee out glucose (SGLT inhibitors)
    • 6) insulin
  44. Describe the 4 types of insulin
    • 1) rapid acting (10-15 mins onset, 1 hr peak): humalog, novorapid
    • 2) short acting ( 30 min onset, 2-5 hr peak): humulin-R, toronto
    • 3) Intermediate (1-3 hr onset, 5-8 hr peak): humulin-N, NPH
    • 4) long acting (90 min onset, lasts 16-24 hrs): Lantus
  45. Besides glucose levels what else do we manage in DM
    • 1) A1c < 7
    • 2) BMI < 25
    • 3) aggressive BP management (<130/80): protect kidney, brain, heart and BVs
    • 4) Aggressive cholesterol management: Target LDL < 2
  46. first line meds for controlling BP in a diabetic patient?
    ACEi or ARB
  47. What causes DKA?
    absolute insulin deficiency and a trigger (e.g. infection, trauma, etc)

    triggers high counterregulatory hormone production (cortisol, glucagon, etc) which breaks down glycogen, proteins, fats which produces ketones and acids.

    Causes dehydration due to diuresis
  48. Lab findings include for DKA 3 categories
    • 1) hyperglycemia (>14)
    • 2) Ketoacidosis: Increased Ion gap metabolic acidosis; ketonemia; ketonuria
    • 3) Dehydration electrolytes: elevated Cr/urea; usually hyperkalemia due to insulin deficiency
  49. Treatment for DKA (3 things)

    When should you stop tmt?
    • IV fluids (NS; they are dehydrated)
    • potassium (prevent hypokalemia as the insulin drives the K intracellularly; wait until urine is being produced)
    • insulin (to correct hyperglycemia; wait until K levels are 3.3-5.5 before giving; usually in conjunction with IV glucose once stabalized)

    • Stop Insulin when:
    •  -Anion gap normal
    •  -patient is eating/drinking without vomiting
    •  -Kenotemia/ketonuria is resolved
  50. similarities (2) and difference (3) b/n hyperosmolar hyperglycemic state (HHS) and DKA?
    similarities: severe volume depletion; hyperglycemia

    difference: no ketoacidosis (no DKA manifestations, no increased ion gap MA, no ketonuria/ketonemia); K+ is usually normal (both due to this only being a RELATIVE insulin deficiency); patients are usually 2x as dehydrated
  51. What is hypoglycemia?
    PG < 4
  52. What do you see in hypoglycemia? (2 categories)
    adrenergic sx (1st): palpatations, tremors, anxiety, sweating, tachycard

    neuroglycopenic Sx (2nd): dizzyness, dullness, confusion, seizures, coma
  53. Describe the macro and microvascular complications of DM
    1) macro: CAD, PAD, CVD

    2) micro: retinopathy, neuropathy, nephropathy, gastroparesis, erectile dysfunction
  54. What is the vascular protection checklist?
  55. How do you calculate an anion gap? What is a normal gap?
    anion gap = [Na] - ([HCO2-]+[Cl-])

    Normal is 12+-2
  56. What is 1st line tmt for dyslipidemia in a diabetic patient?
    Statins
  57. briefly draw how the hormones are produced in the adrenal cortex
  58. What would you expect to see in someone with 21-hydroxylase def CAH
    • -no cortisol, no aldo, lots of sex steroids
    • -no cortisol: hypotension, excess ACTH makes both glands big, N/V
    • -no aldo: salt waste (hypovol) with hyperkalemia
    • -excess sex steroids: clitoromegaly and precocious puberty
  59. Describe where each of the following is produced in the adrenal cortex: cortisol, aldo, sex steroids
    • it gets better as you get deeper (GFR):
    • -outermost (granulosa): aldo
    • -middle (fasciculata): cortisol
    • -deepest (reticularis): sex steroids
  60. Describe why you see the Sx in Cushings Syndrome (6 things, descriptions for first four)
    • -muscle atrophy: increased m. breakdown for gluconeogenesis
    • -weird fat deposition: increased insulin causes fat storage
    • -abdominal striae: cortisol decreases collagen prod, causing BV rupture
    • -HTN: cortisol increases alpha1 receptors
    • -Osteoporosis (decreased bone prod, increased resorption)
    • -Immunosuppression
  61. What 2 screening tests do we use to test cortisol levels in SK?
    • 1) 24 hour urine free cortisol and Cr: should not be 3x normal upper limite
    • 2) Low dose dex suppression test: 1 mg dex at 11pm should suppress cortisol at 8am (< 50). Dex is not detected in assay. If it is still high then cortisol levels are TRULY elevated and this is not just regular variability
  62. How do you manage cushings Synd?
    • 1) What is causing this excess production
    •  -Adrenal source (ACTH < 5)
    •  -ACTH-dependent (ACTH >15)
    • 2) If ACTH-dependent use high dose dex test and imaging to figure out pituitary or ectopic source (high dose dex will slap the pituitary and decrease ACTH levels, no response in tumor)
    • 3) Manage Sx: Blood sugars, BP, infections, bone health
  63. What is Conn's syndrome?
    hyperaldosteronism due to an adrenal adenoma
  64. What are the effects of aldosterone?
    • sodium reabsorption (water follows)
    • potassium excretion
    • H+ excretion
  65. What are the main clinical presentations in primary hyperaldosteronism (conn's)? (2) Renin/aldo relationship?
    • -Severe HTN on 3 agents or hypokalemia (Use the BP Cuff in Conn's)
    • -electrolyte changes: hypernatremia, met alk, ALMOST ALWAYS HYPOKALEMIA
    • -There will be high aldo and low renin
  66. What stimulates renin release? (1)
    • 1) low sodium
    • 2) dehydration
    • 3) decreased renal blood flow
    • 4) low aldo
  67. Most specific test for primary hyperaldosteronism? Why not straight to MRI?
    • 1) salt loading test: sodium bolus decreases aldo in a normal person but does not change anything with someone with primary hyperaldosteronism. Confirm with MRI.
    • 2) Too many people have adrenal incidentalomas (10%) which will give falkse +ves
  68. How do you treat Conn's? (2)
    • Definitive tmt is surgery
    • Medically manage with spirinolactone (aldo antagonist)
  69. Three things you can test in screening for androgen excess
    • -androsenedone
    • -DHEAS
    • -testosterone
  70. How do you confirm adrenal adenoma is the cause of hirsutism. Why is it important to diagnose early?
    MRI of adrenals after biochemical suspicion

    important to diagnose early because hair that has converted to dark terminal hair will not revert back after tumor is excised.
  71. What are the rule of 10 for pheo? (7)
    • 10% are extramedullary
    • 10% in kids
    • 10% bilateral
    • 10% malignant
    • 10% incidentally discovered
    • 10% re-occur after removal
    • 10% familial (more like 20%)
  72. Describe three associations with pheo
    • -MEN 2A and 2B
    • -von hippel-landau
    • -NF 1
  73. How do you screen for pheo?
    24 hour urine looking for metanephrines and chatechols. (+ve if >2x upper limit)

    Drugs and stress (OSA included) can cause false +ves
  74. 3 ways to confirm a +ve 24 hour urine pheo test?
    • 1) MRI
    • 2) CT
    • 3) MIBG scan (attaches to these specific tumor cells)
  75. What is the best tmt for pheo? What do we always give first? Why? second line tmt?
    Surgical excision

    always give phenoxybenzamine (irreversible alpha blocker) so that when you disturb the gland and release all the catacholamines the patient doesn't die on you

    If they cant tolerate surgery, give them beta blockers
  76. Based on size, how to differentiate adrenal adenoma from adrenal carcinoma? Best Dx test, what must you do first?
    Cancer is large (>4.5) adenoma is small (<4.5 cm)

    Diagnose by biopsy, BUT MUST RULE OUT PHEO BEFORE JAMMING A NEEDLE IN THERE!!!
  77. Describe, by order of prevalence the types of adrenal adenoma
    • non-functioning (most common)
    • Cushings
    • Pheo
    • primary aldo
  78. Describe addison's disease. Describe the skin manifestations
    AI destruction cortical glucocorticoid and mineralocorticoid layers. People get hyperpigmentation and vitiligo (if they have concurrent hash. thyroiditis)
  79. How do you diagnose addison's?
    • Pull 8am cortisol levels ( best screening)
    • if low then do a cosyntropin (ACTH analog) stimulation test. +ve test if no corresponding rise in cortisol (best diagnostic)
  80. when do you see emergency or urgent HTN
    180/120
  81. Why is it unlikely that a patient with pheo has MEN? (2)
    • 80%+ of pheo's are non-familial
    • MEN is autosomal dominant, so she would need a parent with the disease
  82. How do you manage acute adrenal emergency? When should you initiate tmt? What shoiuld you switch to for long term?
    • -1-3 L of NS over 24 hours
    • -glucocorticoids (e.g. dex) IV

    DO NOT WAIT FOR TESTS TO COME BACK!

    use mineralocorticoid replacement (fludrocortisone) for replacement
  83. Describe the 5 major anterior pituitary hormones and the positive and negative feedback hormones for each
    • ACTH: CRH (+ve), cortisol (-ve)
    • GH: GRHR, somatostatin
    • LH/FSH: pulsatile GnRH, constant GnRH, estrogen 
    • TSH: TRH, T4, T3
    • Prolactin: progesterone, under constant dopamine inhibition
  84. Most common pituitary mass effect? Other visual effect?
    bitemporal hemianopsia usually. can get a homonymous hemianopsia if post-optic chiasm compression
  85. Describe what you would do if you found a pituitary adenoma incidentally based on size (2,3 for each)
    • If macroadenoma (>1cm):
    • -evaluate for hyper/hypofunctioning
    • -if <2cm and no Sx-> close followup

    • If microadenoma (<1cm):
    • -evaluate for hyper/hypofunctioning
    • -followup if non-functioning
    • -reassure patient (95% do not enlarge over 4-6 years of observation)
  86. describe pituitary apoplexy
    • -acute infarct/hemorrhage of pituitary tumor
    • -sudden/severe headache
    • -ophthalmoplegia
    • -an emergency!!! need transphenoidal decompression
  87. What do you see in GH deficiency? How would you investigate?
    • Presentation:
    • -Children: (justin fontaine), reduced muscle mass, chubby/cherubic facial features
    • -adults: baldness, fatigue, reduced muscle/bone mass

    • Investigate:
    • -NOT random GH (pulsatile hormone)
    • -IGF-1 (would be low)
    • -Stimulated GH (Insulin Tolerance Test (hypoglycemia))
  88. What tests should you order to investigate for central hypothyroidism?
    TSH (normal to low), free T4 (markedly low)

    if this was primary hypothyroid TSH would be markedly elevated
  89. Describe how hypogonadotrophic hypogonadism presents. One genetic cause
    • Peds: absent puberty (>16 w/o menarche), boys >15
    • Adults: decreased libido, ED, amenorrhea, infertility

    Genetic cause of this is Kallmann syndrome (XXY
  90. How do you test for central adrenal insufficiency (2)
    • AM cortisol (screening test)
    • Hypoglycemia (insulin tolerance test) gold standard
  91. How does central adrenal insufficiency differ from primary (addison's)
    • No hyperkalemia (RAAS is still intact)
    • No hyperpigmentation (no increase in POM-c)
  92. How does diabetes insipitus present? How do we confirm? distinguish central from nephrogenic
    • -Polyuria and polydipsia
    • -hypernat and hyperosm (serum) only if water restricted
    • -inappropriately dilute urine

    We water restrict them and test urine OSM. If even in the presence of increase serum osmolality their urine is still dilute Uosm<300) it is diagnostic.

    Give desmopressin (ADH) to distinguish (no response if nephrogenic, because of shitty kidney receptors)
  93. Describe the triphasic nature of damage-induced diabetes insipitus
    • 1) 1-5 days of DI due to stunned pituitary
    • 2) day 6-11 see heavy release of ADH from degenerating pituitary (SIADH)
    • 3) third phase sees either resolution or permanent DI (almost all resolve (10% stay))
  94. In general, how to we treat a hypofunctioning pituitary?
    we replace the end organ hormones as needed
  95. What is the clinical presentation of prolactinemia? (3)
    • -features of hypogonadism (prolactin inhibits GnRH release)
    • -galactorrhea
    • -may be asymptomatic in post-menopausal women
  96. How do you treat a prolactinoma? (2)
    Dopamine agonists: Cabergoline, bromocriptine, pergolide (work in 90% of patients)

    Trasphenoidal surgery if highly symptomatic and refractory to medical tmt
  97. What do you see in GH excess
    • Children: gigantism
    • Adult (acromegaly): jaw growth, rings and shoes dont fit, coarse facial features, diabetes (GH impairs glucose uptake into cells), hyperhidrosis (lots of sweating), Body Odor
  98. When you suspect someone of GH excess, what should you test?
    • 1) IGF-1 (would be high)
    • 2) OGTT with GH tested (GH would not be successfully suppressed)
  99. How do you treat acromegaly?
    definitive tmt is surgery

    if not resectable: give a somatostatin analog (Octreotide or lanreotide); or a dopamine agonist or a GH-receptor antagonist (not widely avail)
  100. Three most specific features of cushing's syndrome?
    • The fat ones
    • -moon facies
    • -supraclavicular fat
    • -dorsocervical fat (buffalo hump)
  101. Relative prevalence of the following causes of secondary amenorrhea:
    Uterus, pituitary, hypothlamus, other, ovary
    • Ovary: 40%
    • Hypothalamus: 35%
    • Pituitary: 19%
    • Uterus: 5%
    • Other: 1%
  102. If someone is on dopamine for prolactinoma and needs to go in for urgent surgery what must you think of? (3 points)
    • -Prolactinoma can cause hypopit, which may cause low cortisol meaning hypotension and hypoglycemia
    • -dopamine agonists can cause hypo or hypotension depending on the type or dose
    • -NEED TO CAREFULLY MONITOR BLOOD PRESSURE INTRAOPERATIVELY!!!
  103. What if a woman with a prolactinoma wants to get pregnant? (3 points)
    • -try to avoid dopamine agonists
    • -follow tumor size, if it starts enlarging (increased risk of sheehans) use bromocriptine in 1st trimester
    • -Don't use if breast feeding because they decrease production
  104. Effects of GH on Heart and joints
    • heart: basically you get hypertrophy
    • Joints: excess cartilage production, alters joint geometry, eventually causing osteoarthritis
  105. Most sensitive and specific tests for acromegaly?
    • sensitive: IGF-1
    • Specific: OGTT with reading of GH levels after
  106. If someone needs an urgent surgery a month after transphenoidal surgery do they need to be given "stress steroids"? Why?
    Yes, because of their presumed pituitary insufficiency they will likely not be able to make the cortisol they normally would to help during surgery.
  107. TMT of Cushings disease (most common to least) (5)
    • -excise adenoma from pituitary
    • -radiation
    • -drugs (e.g. ketoconazole, mitotaine) which decrease cortisol production by inhibiting adrenal enzymes
    • -Remove adrenals then supplement cortisol
    • -lifestyle: exercise, eat well
  108. Describe the tests you would do for hyper and hypofunctional adenoma's of the pituitary producing the following hormones:
    GH, ACTH, TSH, LH/FSH, PRL, ADH, oxytocin
  109. 4 things that parents can do to help prevent their kids from developing TYPE I DM
    • -ensure adequate Vit D intake
    • -follow current infant feeding guidelines: breastfeed for 6 months
    • -avoid exposure to cow's milk proteins in high risk children (use casein formula instead)
    • -avoid exposure to gluten before 6 months of age
  110. Describe glycemic index and glycemic load
    GI: measure of blood glucose response to 50 g of carbohydrate from a paticular food

    • GL = [GIx(g carbs per serving)]/100
    •   -basically normalizes to carb density
  111. What foods tend to lower GI
    • -slower stomach emptying (acids, protein, fat, soluble fibre)
    • -amylose starch (legumes)
    • -less geletanization of starch (cook pasta al dente)
    • -physical barriers (whole grains)
  112. How does bisphenol-A (BPA) cause diabetes?
    • -mimic estradiol
    • -induces hyperinsulinemia and insulin resistance
  113. 4 big diseases that are preventable with diet and lifestyle
    • -colon cancer
    • -stroke
    • -coronary heart disease
    • -diabetes
  114. 8 lifestyle prevention strategies to prevent Type II DM?
    • 1) maintain normal body weight
    • 2) low GI/GL foods
    • 3) high fibre diet
    • 4) adequate vit C, D, magnesium
    • 5) nuts, fatty fish
    • 6) regular exercise
    • 7) reduce exposure to environmental toxins (e.g. BPA)
    • 8) reduce chronic stress
  115. 5 factors that influence BMR
    • -Gender: males>females
    • -genetics
    • -BMR decreases with age
    • -higher % body fat means lower BMR
    • -starvation decreases BMR
  116. Why is yoyo dieting so bad?
    -as you lose weight you also lose lean tissue, when you regain the weight less lean tissue is regained
  117. What happens if you have leptin resistance?
    You never feel full and you keep eating
  118. General advice for people who want to lose weight (7)
    • -regular balanced meals and always eat breakfast
    • - regular exercise
    • - enough sleep (7-8 hours)
    • -Reduce calories from liquids (other than milk)
    • -increase fibre
    • -take vit D (expecially in winter)
    • -eat more slowly, chew more
  119. What is the purpose of PTH? how? (3)
    PTH increases blood calcium level

    • -resorption of bones
    • -reabsorption from renal tubules (and excretion of PO4)
    • -absorption from GIT
  120. S&S of hypercalcemia
    • CNS: lethargy, stupor, fatigue
    • CV: short QT interval, HTN, bradycardia
    • Renal: polyuria, stones
    • GI: N&V
  121. Most common cause of hypercalcemia?
    primary hyperparathyroidism (usually a single adenoma)
  122. How do you treat hypercalcemia? (4)
    • -HYDRATION!!
    • -furosemide
    • -bisphosphonates
    • -calcitonin acutely
  123. S&S of hypocalcemia
    • enhanced neuromuscular irritability
    • -+ve Chovostek's and trousseau's signs
  124. What is rickets?
    insufficient Vit D in children causes elastic bones that can bend.

    Osteomalacia is the adult version of this and is seen in renal failure
  125. How do you take a fall history?
    • SPLATT
    • S- symptoms
    • P - previous falls
    • L- location of the fall
    • A - activity at the time of fall
    • T - Time of fall
    • T - Trauma
  126. When should you order a DEXA scan for a patient?
    all men and women over 65
  127. Calcium and Vit D intake req's in older women
    • Ca: 1200 mg/day
    • Vit D: 1000-2000 IU/day
  128. What are the three types of tumors you see in MEN1?
    • Pituitary
    • Pancreatic
    • Primary hyperparathyroidism

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