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Week 7-9

Sarah Purcell Med 1 Metabolism Englisch 114 Karten

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Karten in diesem Stapel (114)

  1. 1Bolus Insulinsshort acting and rapid acting. Given to cover carbohydrates or to quickly lower a high BG
  2. 2Short acting insulins- Clear, form hexamers that need to dissociate into monomers once injected → slow absorption
    - Can be used for meals, give 30 to 45 min prior
    - Rarely used in children with diabetes
    - Agent of choice - IV insulin infusions
  3. 3Rapid Acting Insulins- Clear, do not associate easily
    - Ideal for 0-15 min before or right after meals
    - Ideal bolus insulins
    - Correct a high glucose or cover carbohydrate in a meal/snack
  4. 4Basal Insulins:Background insulin Fasted state
  5. 5- Intermediate actingo Addition of Protamine makes it longer acting
    o Cloudy, combined with protamine → delays its absorption after injected
    o Useful as a basal insulin and can cover lunch or rise in glucose occurring overnight
    o When given at night, peak can lead to hypoglycemia
    o Peak 5-8 hours after they are giving and can last up to 18 hours
  6. 6- Long acting insulinso True basal insulins, lower incidence of nocturnal hypoglycemia compared with N or NPH
  7. 7Metformin = BiguanideUnless contraindicated is the major 1st line agent in the management of T2DM
    - Most important effect is reduction of hepatic glucose production (gluconeogenesis)
    Can cause lactic acidosis
    NO hypoglycemia
     Stop metformin prior to IV contrast (EG. CT scans) or before anesthetic
  8. 8Acarbose (Alpha Glucosidase Inhibitor)Reduces the digestion of complex carbohydrates and reduces their absorption from gut
    NO hypoglycemia
    - Side effects: flatulence and diarrhea = Lead to high rate of discontinuation
  9. 9Incretin based therapy- DPP-4 Inhibitors
    - GLP-1 receptor agonists = big weight loss
    - NO hypoglycemia
  10. 10Incretinsbody makes GIP and GLP-1 in the gut after a meal which is broken down by DPP-4. Incretins increase insulin secretion and sensitivity and act on the brain to reduce appetite and improve feeling of fullness, decrease glucose production in liver and increase glucose uptake in the muscle.
  11. 11SGLT2 Inhibitors- Sodium glucose co-transporter 2 inhibitors
    - SGLT2 in proximal renal tubules mediate reabsorption of ~ 90% of filtered glucose load
    - Lowers blood glucose by increasing urinary losses of glucose
    NO hypoglycemia
    - Associated with weight loss
  12. 12Insulin Secretagogues- Act on potassium channels to increase calcium influx which then triggers insulin to move to membrane to be secreted
    - Sulfonylureas
    - Metiglinide
    YES hypoglycemia
  13. 13- Sulfonylureaso Metabolized by the liver and excreted by liver and kidney
    o Duration of action: shortest is 6-12 hours and longest is 24 hours
  14. 14- Metiglinideo Metabolized and excreted by liver
    o Duration of action: up to 6 hours shorter duration than sulfonylureas
    o Effective in early insulin release that occurs after a meal → targets post meal rise in BG
    o Taken 1-30 min before meals
  15. 15Thiazoledinediones (TZDs)- Increase insulin sensitivity by acting on muscle, adipose tissue and liver to increase glucose utilization and reduced glucose production = Mechanism not well understood
    - Bind to and activate one or more PPARs (peroxisome proliferatoractivated receptors) in adipocytes
  16. 16Insulin Regimens- Once daily basal insulin – commonly start with this
    - Basal Plus = Once daily basal insulin AND Once daily rapid acting insulin at breakfast or largest meal
    - Basal-Bolus = 3 or more injections per day (intensive insulin therapy)
    - Once or twice daily premixed insulin = Intermediate and rapid or short acting insulin combination. EG 70/30 Humulin (30% Regular and 70% N)
  17. 17Basal Insulin regimen specificAdd evening (usually before bed) basal or intermediate acting insulin
    o Check BG at least once a day fasting
    o Suggested starting dose 10 units (either Lantus or N/NPH)
    o Increase by 1 unit per day until fasting glucose < 4-7 without nighttime hypoglycemia
    o Lower by 1-2 units per day if fasting BG consistently below 5.5
  18. 18Bolus Insulin regimen specifics- Bolus Insulin
    o Check BG 2 hours post meal or prior to next meal •Increase dose by 1 unit daily to target
  19. 19What percent of calcium is bound40%
  20. 20what percent of calcium is ionized50%
    this is free to use
    VERY tightly regulated
  21. 21Calcium correction equation for albuminIncrease sCa2+ by 0.2 mmol/L for each decrease of 10 g/L (below 40 g/L) in serum albumin.
    If someone has 1.8 serum calcium but a 30g/L albumin the adjusted number is 2.0mmol/L
  22. 22Normal Serum calcium levels2.2-2.6 mmol/L
  23. 23Normal ionized levels of calcium1.2 mmol/L
  24. 24Normal minimum albumin level40g/L
  25. 25Actions of PTHif calcium is low, PTH will be elevated
    If calcium is high, PTH will be suppressed
  26. 26Vitamin D regulation and conversionActivated in the liver to 25(OH)D3 and then it is regulated to active vitamin D in the kidney to 1,25(OH)2D3 by using 1a hydroxylase enzyme which is regulated by Parathyroid hormone
  27. 27Calcitonin action on calcium1. Bone - inhibits osteoclasts, therefore decreases resorption of Ca2+ + PO4
    2. Kidney - decrease tubular resorption of Ca2+ → increases urinary Ca2+ excretion
  28. 284 reasons for hypercalcemic disorderso Increase in Osteoclastic bone resorption
    o 2. Excess GI Ca2+ absorption
    o 3. Impaired renal excretion of Ca2+
    o 4. Impaired bone mineralization – not getting rid of depositions in bone
  29. 29With malignancy, patients have ______ levels of PTH since the hypercalcemia ______ endogenous normally responsive and functioning parathyroid glandsLOW
    SUPRESSES
  30. 30Agents the increase urine Ca losssaline
    Lasix
    calcitonin
    dialysis
  31. 31Epidemiology of osteoporosis- 1 in 3 women and 1 in 5 men will have an osteoporotic fracture in their lifetime
    - Over 1.4 million affected during lifetime in Canada
    - Female > male ▪ Hip fracture rates in Canada are among the highest in the world (in the top quarter)
    - One in 3 sustain another osteoporotic fracture in the first year after a hip fracture
    - Over one quarter of hip fractures in Canada occur in men (total number of hip fractures ~ 30,000 a year)
    - In the first year after a vertebral or hip fracture there is at least a doubling in the risk of death and 1 in 4 will require long term care
  32. 32Bone Density Status and T-score- Normal is +2.5 to -1.0
    - Osteopenia is ≤-1.0 and ≥-2.5
    - Osteoporosis is < -2.5
    - Severe osteoporosis <-2.5 + fragility fracture
  33. 33o CAROC (Canadian Association of Radiologists/Osteoporosis Canada) Semi-quantitative estimation of 10-year absolute risk of a major osteoporotic fracture* in postmenopausal women and men over age 50
     3 fracture risk categories: Low: < 10%, Moderate 10-20%, High: > 20%
     Base risk category is obtained from age, sex, and done density T-score of the femoral neck
     Fragility fracture after age 40 bumps up a category
     Prolonged corticosteroid use pumps up a category
  34. 34o FRAX (Fracture Risk Assessment Tool) Model designed to predict the 10 year probability of hip fracture and major osteoporotic fracture
     Parameters include: prior fracture, parental hip fracture, rheumatoid arthritis, glucocorticoid use, current smoking and high alcohol intake
  35. 35BISPHOSPHONATESinhibits osteoclast form resorption
     bind to hydroxyapatite crystals in bone
     Adverse effects: Osteonecrosis of the jaw which is associated with invasive dental procedures, atypical femur fractures which are associated with long term use and can be bilateral fractions from minimal or no trauma
  36. 36RANKL inhibitors (Denosumab)interferes with osteoclast signaling pathway
     High affinity for human RANKL, blocks binding of RANK-L to RANK
     Results in inhibition of osteoclast differentiation, proliferation, and function
     In a 3 year study, has been shown to reduce vertebral fractures by 68%, nonvertebral fractures by 20%, and hip fractures by 40% compared to placebo
     Given as 60 mg sc every 6 months
  37. 37Parathyroid hormone (Periparatidestimulates bone formation
     Treatment of OP in postmenopausal women at high risk for fracture
     Men with primary or hypogonadal osteoporosis at high risk for fracture
     Main issue is cost! (~$800 a month)
  38. 38List of Pituitary masses- Non-functioning adenoma 38.7%
    - Prolactinoma 34.3%
    - Rathke’s cleft cyst 6.5%
    - GH secreting adenoma 6.5%
    - Craniopharyngioma 4.5%
    - ACTH secreting adenoma 3.8% (Cushing’s)
    - Other 5.8%
  39. 39What percentage of acromegaly cases also have prolactin secreting tumors30%
  40. 40what is the prolactinoma treatmentdopamine agonist
     (Cabergoline, bromocriptine, quinagolide)
  41. 41Diabetes Insipidus- Don’t have enough ACTH so you aren’t regulating your water absorption the way you should
    - Symptoms: polyuria, extreme thirst (polydipsia), excessive water intake (up to 20 liters per day), dry skin, and constipation.
    - Causes of Central DI – deficiency of ADH. It is made in the hypothalamus not the pituitary, therefore the causes are more general/systemic.
  42. 42Results of water deprivation testo If urine osmolality concentrates to normal, diabetes insipidus is ruled out (likely psychogenic polydipsia)
    o After DDAVP administration
     If urine osmolality increases by >50% → Central DI
     If no change in urine osmolality → Nephrogenic DI
  43. 43Normal Timing of Puberty - Females8-13 years • Thelarche (breast development) < 8 years = precocious >13 years = delayed
  44. 44Normal Timing of Puberty - Males9-14 years • Testicular enlargement (Gonadarche) < 9 years = precocious >14 years = delayed
  45. 45Female Tanner Staging: Breast- Tanner 1: none
    - Tanner 2: breast bud, beneath areola
    - Tanner 3: breast tissue extending beyond areola
    - Tanner 4: secondary mound
    - Tanner 5: full maturity
  46. 46Testicular volume Tanner Stages- Tanner 1: < 4mL
    - Tanner 2: 4-6 mL (4 mL) = 2.5 cm length
    - Tanner 3: 8-10 mL
    - Tanner 4: 12-15 mL
    - Tanner 5: 15-25 mL
  47. 47Pubic Hair Tanner Staging- Tanner 1: none
    - Tanner 2: Straight, coarse hairs on labia or at base of penis
    - Tanner 3: curled hairs extending to mons pubis
    - Tanner 4: triangular pattern
    - Tanner 5: extending to medial thigh
  48. 48- Hypogonadotropic hypogonadism(low LH/FSH) = problem with hypothalamus or pituitary
  49. 49- Hypergonadotropic hypogonadismhigh LH/FSH) = problem with gonads themselves
  50. 50Amenorrhea - Primary:No menarche 3-5 years after onset of secondary sexual characteristics or no menarche beyond 16 years
  51. 51Differential Diagnosis for 16 year old girl with no period yet- ***Pregnancy*** - ALWAYS on the differential
    - Hypothalamic anovulation/Pituitary insufficiency
    - Hyperprolactinemia
    - Hypothyroidism, Cushing’s
    - Androgen excess
    - Ovarian Failure – congenital/acquired
    - Outflow tract abnormalities (absent/small uterus, imperforate hymen)
  52. 52Distinguishing Central vs Peripheral Causes of Puberty- LH = Helps if detectable - indicates central. However, often not elevated in early stages
    - GnRH Stimulation test
    o If LH rises above 8 then this means the pituitary is responding to GnRh and they are in central puberty
    o If after 40 mins and LH and FSH are still low it is not responding to GnRH so there is a peripheral problem
  53. 53- How to STOP the precocious periodo GnRH agonist (Depot Leuprolide) – gives constant level which instant pulsatile and that can actually stop puberty
    o Injection every 3-4 weeks
    o Given until a more normal timing of puberty – 11 or 12 years
  54. 54Oxidation and organification of iodideo iodide is oxidized by thyroid peroxidase (TPO) in the presence of H2O2
    o TPO also mediates the iodination of tyrosyl residues in thyroglobulin to form monoiodotyrosine (MIT) and diiodotyrosine (DIT)
  55. 55- ‘Thyrotoxicosis’clinical syndrome that results when tissues are exposed to high levels of circulating thyroid hormone
  56. 56- Graves’ diseaseo Most common form of hyperthyroidism
    o Females affected 5:1, peak incidence 20-40y, frequently familial predisposition
    o Due to overproduction of an antibody that binds and stimulates the TSH receptor (TSHr Ab) = autoimmune disorder, thus may be associated with other autoimmune disorders
  57. 57Cretisnmrefers to infants with severe neonatal hypothyroidism and is characterized by:
    o puffiness of the face and hands
    o thick protruding tongue
    o protruding abdomen
    o poor muscle tone
    o Caused by iodine deficiency during pregnancy
  58. 58Chronic autoimmune thyroiditis (Hashimoto’s) Most common cause of hypothyroidism
     An autoimmune disorder where lymphocytes become sensitized to thyroid antigens = autoantibodies are produced = massive lymphocytic infiltration of the thyroid with destruction of normal architecture
  59. 59Hashimotos treatment• Treat hypothyroidism with levothyroxine (Synthroid)
    • T3 therapy generally not recommended due to rapid absorption, short half-life and transitory effects (can cause palpitations)
    • Measure serum TSH every 4-6 weeks and adjust levothyroxine dose until TSH normal
  60. 60Congenital Hypothyroidism- The term “cretin” – referred to individuals with untreated congenital hypothyroidism
    - Clinical features are NOT present at birth
  61. 61Neonatal Thyroid Screening Interpretationo TSH shows a big surge within 30 min of birth which comes down to near normal within 24 to 36 hours of life – Test done at 24-48 hours – may still be high at early discharge
    o TSH result (in Maritime screening program) – >20 IU/L triggers physician notification and immediate investigation of the baby
  62. 62Positive Screen for Congenital Hypothyroidismo Treat as an urgent/emergent problem
     Confirm with serum TSH, Free T4
     If available, obtain Tc99 thyroid scan to assess for presence, size and location of thyroid
     Priority - start l-thyroxine therapy
  63. 63Incidence of Congenital Hypothyroidism in Canada1:3000 to 4000
  64. 64Rickets- Failure of normal bone mineralization, particularly at the metaphysis and epiphyseal plate (growth plate)
    - When body is calcium deficient it leads to elevation in parathyroid hormone which….
    o Activates osteoclasts releasing Ca and PO4 from bone
    o Increases Ca re-absorption and PO4 excretion in kidneys
    o Increases conversion of Vitamin D to active form
  65. 65Normal/minimum growth velocitieso Early → late infancy 23-28 cm/y → 13 cm/y
    o 1-2 years: 10 cm/y
    o 2-3 years: 7 cm/y
    o 3-4 years: 6 cm/y
    o 5y-onset of puberty: 5 cm/y
  66. 66- Peak height velocity o GirlsEarly puberty growth spurt (Tanner 2-3). Girls grow on average < 2 inches after menarche
  67. 67Peak height velocityt boyso Boys – Mid to Late puberty growths spurt (Tanner 3-4)
  68. 68Below ____ or above ____ percentile needs attention3rd
    97th
  69. 69Mid-parental Height = Target Height equationMother’s Ht + Fathers Ht ± 13 cm* (5 in)/ 2
  70. 70BMI equationBMI equation
  71. 71Kg to lb In to cm1 kg = 2.2 lb
    1 inch = 2.5 cm
    12 inches (foot) = 0.3m = 30cm
    6 feet tall (72 inch) = 182cm
  72. 72ApoBApoBs are proteins found in lipoprotein particles that are artery-clogging.
    The apoB-containing lipoprotein particles that are the most damaging to our arteries include not only LDL cholesterol but also remnants of chylomicrons and VLDL (very low density lipoproteins). All three – LDL, VLDL, and chylomicrons – promote atherosclerosis.
  73. 73A ____ mmol/L reduction in LDL was associated with ____% reduction in major coronary events and a ____% reduction in major vascular events1mmol
    23%
    21%
  74. 74Conditions for which pharmacotherapy with statins is indication- Clinical atherosclerosis = if they have a heart attack don’t even need to test their blood start treating, they have the disease
    - Abdominal aortic aneurysm
    - Diabetes mellitus
    - Chronic kidney disease
    - LDL-C >5.0 mmol/L
  75. 75Statins- Interfere with HMG-CoA reductase which is the critical enzyme in the biosynthesis of cholesterol.
    - Excellent for lowering LDL
    - Neutral for HDL and triglycerides
  76. 76Presence of _____ ____ requires the discontinuation of the statinmuscle toxicity
  77. 77Niacin/ Nicotonic Acid- Best agent to raise HDL-C = brings it up by 30%
    - Decreases both VLDL (get down 30%) and LDL (get down 15%) levels
    - causes flushing
    - causes hepatotoxicity
    - decreases hepatic production of VLDL and of ApoB
    - not well understood
  78. 78Ezetimibe- acts at the brush border of the small intestine and inhibits the absorption of cholesterol
    o reduction in hepatic cholesterol stores and increase in clearance of cholesterol from the blood
    o decrease in delivery of intestinal cholesterol to the liver
  79. 79Bile acid sequestrants- Binds bile acids, thus increasing the excretion of cholesterol in stool
    - Lowers LDL-C by 15-20%
  80. 80Fibrates- Excellent for lowering TG’s and good at raising HDL
    - Mechanism: increase peripheral lipolysis and decrease hepatic TG production
  81. 81Steps to Minimize the Risk of Muscle Toxicity with Fibrate–Statin Combination Therapy- Use statin alone for non-HDL-C goals
    - Use fish oils or niacin rather than fibrates
    - Keep the doses of the statin and fibrate low
    - Dose the fibrate in the AM and the statin in the PM
    - Avoid (or cautiously use) combo in renal impairment
    - Assure no interactions
    - Teach the patient to recognize muscle symptoms
    - Discontinue therapy if muscle symptoms are present and CK is >10 times the upper limit of normal
  82. 82PCSK9 inhibitionEvolocumab
    PCSK9 in blood will mark LDL receptor and kill the receptor.
    Having functional LDL receptors = good
    BLOCK the PCKS9 = receptors are good longer
  83. 83Target LDL-C <___mmol or >_____% reduction2.2mmol
    50%
  84. 84Cortisol is ____% bound to corticosteroid binding globulin (CBG or transcortin) and ____% to albumin75%
    15%
  85. 85Testosterone and estradiol are _____% bound to sex hormone binding globulin (SHBG) and ____% to albumin60%
    38%
  86. 86CBG levels are _____ by in high estrogen states (e.g. OCP use), hypothyroidism, and geneticsincreased
  87. 87CBG levels are ______ in protein deficiency states (cirrhosis, nephrotic syndrome), critical illness, hyperthyroidism, and familial CBG deficiencydecreased
  88. 88Cushing’s Diseasedue to excessive ACTH secretion from a pituitary tumor
  89. 89ACTH independent causes of cushings- exogenous glucocorticoids *most common**
    - adrenal neoplasm (adenoma, carcinoma)
    - nodular adrenal hyperplasia
  90. 90ACTH dependent causes of cushings- pituitary adenoma (Cushing’s disease) = 2nd commonest
    - nonpituitary neoplasm = ectopic ACTH = 3rd commonest
    o small cell lung CA
    o carcinoid tumors
    o pancreatic tumors
  91. 91Who should be investigated for Cushing’s syndrome?- Patients with multiple and progressive features suggestive of hypercortisolism
    - Patients with unusual features for age
    - Patients with adrenal incidentaloma
    - Children with decreasing height percentile and increasing weight 30
  92. 9224 hour Urine Free Cortisol (UFC)= quantitative test
    Demonstrates cortisol excess
    wide discrepancy of reported sensitivity and specificity
    o Can be influenced by variations in renal function
  93. 93- 1 mg Overnight Dexamethasone Suppression Test (DST)= qualitative test
     normal patient will suppress to < 50 nmol/L
    o Sensitivity better than UFC (> 95%) but specificity is limited (~80%)
  94. 94Two-Day Low-Dose DST0.5 mg dexamethasone EVERY 6h over 48 hours
    9am, 3pm, 9pm and 3am = shitty times
    sensitivity is high (~100%) and specificity is much improved (88-96%)
  95. 95Loss of more than _____% of adrenal cortex results in the clinical manifestations of adrenocortical insufficiency90%
    occurs with 1/100,000 people
  96. 96Addison's diseasePrimary Adrenal Insufficiency
    - Most common cause is autoimmune adrenalitis
  97. 97the 3 H's of addisons diseaseo hypotension = decrease in vascular tone
    o hyponatremia = glucocorticoids necessary for free water excretion
    o hypoglycemia = decrease in cortisol = decrease in glucose
  98. 983 main symptoms of addisonsweakness and fatigue
    weight loss
    hyperpigmentation
  99. 99Secondary Adrenal Insufficiency Similar to Addison’s except:o Features of mineralocorticoid deficiency not seen (hyperkalemia, severe volume depletion)
    o No hyperpigmentation
  100. 100ACTH stimulation test resultsA normal response excludes primary adrenal insufficiency (Addison’s) but not partial secondary insufficiency (ACTH deficiency)
    - An abnormal response confirms the presence of adrenal insufficiency but does not distinguish between primary and secondary insufficiency
  101. 101Insulin-induced hypoglycemiao Tests the full hypothalamic-pituitary-adrenal axis
    o For determining presence of secondary adrenal insufficiency if clinical picture unclear
    Normal response to Plasma ACTH and Insulin tolerance means the person does not have a primary or secondary insufficiency
  102. 102Management of Addison’s - Maintenance hormone therapyo hydrocortisone 10-20 mg daily, usually divided BID or TID (e.g. 10 mg am, 5 mg pm or 10-5-5 mg) it is short acting, trying to mimic diurnal variation
    o fludrocortisone 0.05-0.10 mg daily
  103. 103Adrenal Crisisacute adrenal insufficiency
     hypotension and shock*
     dehydration, volume depletion
     fever
     nausea, vomiting, anorexia, abdominal pain
     weakness, apathy, confusion, decreased LOC, coma
     hypoglycemia
     hyponatremia, hyperkalemia
  104. 104the 5 s's of adrenal crisissalt, sugar, steroids, support, and search for precipitating illness
  105. 105Pheochromocytoma- Tumour in the adrenal medulla (chromaffin cells)
    - Secretes catecholamines = Epinephrine, Norepinephrine, Dopamine
    0.01-0.1% of hypertensive population = 0.5% of those screened for it
  106. 106Signs and symptoms of Pheochromocytomao Paroxysms – on and off symptoms
    o Pain (headache) 90%
    o Pressure (hypertension) 80%
    o Perspiration 71%
    o Palpitations 64%
    o Pallor 42%
  107. 107Screening for pheochromocytoma should include a 24-hour urine for _______________ and __________metanephrines and creatinine
  108. 108Unilateral adenomaConn’s syndrome
    o Excess aldosterone leading to hypertension
    o 10-60%
    o Higher BP and lower potassium
    o Younger age
  109. 109Have to stop certain medications before screening for aldosterone problems Aldosterone/mineralocorticoid receptor antagonists (ex. Spironolactone)
     Potassium-wasting diuretics
     Licorice root
     May need to stop x 2 weeks: Beta blockers, clonidine, NSAIDs, ACEi, ARB, direct renin inhibitors, CCBs
  110. 110Black licorice problem- Has glycyrrhizin acid
    - Inhibits 11BHSD  this enzyme normally changes cortisol to cortisone which CAN’T fit into mineralocorticoid receptors  if the enzyme is inhibited it causes stimulation of mineralocorticoid receptors by cortisol
    - Get an aldosterone like effect  hypernatremia, hypokalemia  hypertension
  111. 111Why does Cushing’s cause hypertension?o Cortisol secreted from the adrenal cortex also has some mineralocorticoid effect
    o Can activate the mineralocorticoid receptor that is normally activated by aldosterone
    o Aldosterone is 3000x stronger so you need a lot to overpower it
    o But if you make SO much cortisol it will take over (same as black licorice affect)
  112. 112Cold nodule is __-___% chance of being malignant16-20%
  113. 113types of thyroid cancer and %well differentiated
    - papillary 85%
    - follicular 10%
    poorly differentiated 2%
    undifferentiated 1% = cure rates are poor
    C cell/parafollicular type 3% = medullary thryoid cancer
  114. 114—

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Med 1 Metabolism Karteikarten am Week 7-9, erstellt von Sarah Purcell am 28/02/2020.
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