CAM 2013: Exam One

  1. Addison's Disease:  S/S & Labs
    partial/complete destruction of adrenal gland (primary adrenal insufficinecy)

    • Can be precipitated by (Keto, Phen, Pheno, Rif)
    •      Ketoconazole
    •      Phenytoin
    •      Phenobarbital
    •      Rifampin

    • S/S
    •      increased ACTH causes increased pigmentation
    •      weight loss, fatigue/weakness, hair loss, depression, ab pain

    • Labs
    •      hypnatremic
    •      hyperkalemia
    •      elevated BUN & sCr
    •      metabolic acidosis
    •      increased ACTH; decreased aldosterone
  2. Addison's Disease:  Tx
    • Glucocorticoid therapy:  cortison/hydrocortisone
    •      SE:  wt gain, edema, HTN, hypokalemia, insomnia, DM, electrolyte imbalance, GI upset
    •      Monitor sxs q 6-8 wks
    •      ADE w/ prolonged use:  iatrogenic Cushing's (weight gain, moon face, buffalo hump), increased infection risk, edema, electrolyte imbalance

    • Mineralcorticoid therapy:  fludrocortisone
    •      SE:  same as glucorticoids + excitability
    •      Monitor sxs, electrolytes, BP

    • Supplement:  DHEA
    •      positive effects on wellbeing & mood
    •      reserved for patients in which G and M are not working; limited efficacy
    •      Monitor:  lipids, breast & prostate cancers
  3. Secondary Adrenal Insufficiency
    cause:  exogenous steroid use/hypothalamic-pituitary tumor

    Presentation:  normal to low ACTH causing hypopigmentation; ALD secretion preserved

    Tx:  G/M therapy
  4. Acute Adrenal Insufficiency (Adrenal Crisis):  presentation, labs, causes
    Presentation:  weakness, dizziness, weight loss, ab pain, myalgia, tachycardia

    Labs:  hyperkalemia, hypoglycemia, hyponatremia, hypotension leading to shock

    Causes (CISTS):  chronic exogenous CS use, infection, stress, trauma, surgery
  5. Acute Adrenal Insuffiency (Adrenal Crisis):  Tx
    • hydrocortisone via rapid infusion, then PO taper
    • fluid replacement
    • supportive therapy
  6. Hypoaldosteronism:  presentation/labs
    usually part of a larger insufficency such as Addison's

    Presentation/Labs:  hyponatremia, hyperkalemia, hypercholremic metabolic acidosis
  7. Hypoaldosteronism:  Tx
  8. Virilism
    excessive secretion of androgens from adrenal gland via an androgen secreting tumor

    Sxs:  hirsutism, voice deepening, acne, increase muscle mass, menstrual abnormality, lose female figure, hair recession
  9. Virilism tx
    Glucocorticoids to suppress HPA-axis
  10. Hirsutism
    Etiology can be genetic, med related, adrenal/ovary overproduction

    Tx:  cosmetic approaches, eflonithine HCl cream, glucocorticoid suppression therapy
  11. Monitoring/Couseling/Adminstration for Glucocorticoid Therapy
    Monitor:  glucose, electrolytes, growth and development

    Counseling:  don't stop abruptly; increase dose during stress; take second dose 6-8 hours after first dose which is taken in the AM

    • HPA-axis suppression problem:  use shortest duration, taper slowly, QOD therapy
    • Osteoporosis:  consider Ca2+ or BPh; NOT QOD therapy
    • Weight gain:  monitor and use shortest possible duration
  12. Primary Hyperaldosteronism:  Clinical Presentation
    adrenal cortex abnormality

    • 65% of cases is bilateral adrenal hyperplasia (BAH)
    • 30% are aldosterone-producing adenoma (APA, Conn's Syndrome

    Clinical presentation:  hypernatremia (HTN), hypokalemia (muscle weakness/fatigue/arrythmias), low plasma renin, increased ALD, polydipsia, polyuria, metabolic alkalosis
  13. Primary Hyperaldosteronism:  BAH tx
    First line = meds

    • Spironolactone
    •      MOA:  ALD receptor antagonist
    •      salicyclates increase elimination of active metabolite
    •      SE:  gynecomastia, menstrual irregularites, GI discomfort, impotence



    Surgery is last line
  14. Primary Hyperaldosteronism:  APA tx
    First line = surgery:  laparoscopic resection of adenoma

    Last line is meds
  15. Secondary Hyperaldosteronism
    Causes:  extra-adrenal factor, RAAS, excessive potassium, OC use, pregnancy

    Tx Goal:  correct extra-adrenal issue, but use spironolactone unitl etiology found
  16. Cushing's Syndrome:  Presentation
    most common cause is exogenous adminstration of cortisol

    • endogenous overproduction
    •      90% ACTH-dependent hypercortisolism via ACTH- secreting pituitary tumor (Cushing's) or ectopic ACTH secretion

    Presentation:  wt gain, central obestiy, moon face, buffalo hump, brusing, stretch marks, hirsutism, osteoporosis, muscle weakness, HTN, hypokalemia, edema, DM, depression, decreased WBC
  17. Cushing's Syndrome:  Dx
    Establish presence of hypercortisolism by 24-hour urinary free cortisol secretion and dexamethasone overnight test  (Normal cortisol:  10-100 mcg)

    • Establish cause and location of problem
    •      low ACTH --> ACTH-independent adrenal tumor
    •      normal/high ACTH --> ACTH dependent
  18. Psudeo-Cushing's Syndrome sxs
    • obestiy
    • alcoholism
    • depression
    • acute illness
  19. Cushing's Syndrome 1st line Tx
    selective removal of pituitary corticotrope tumor

    • Other options:
    •      Bilateral adrenalectomy - take out adrenal gland
    •      Adrenal adenoma resection - take out portion of adrenal gland that's not working
  20. Cushing's Syndrome tx for Refractory/Post-surgery patients
    • Metyrapone
    • Aminoglutethimide
    • Ketoconazole
    • Etomidate 
    • Mifepristone
    • Mitotane 
    • Cyproheptadine
    • Pasiretoide
  21. Metyrapone
    • MOA:  inhibits cortisol production     
    • SE:  hypotension, hair growth, voice deepening
  22. Aminoglutethimide
    • MOA:  suppresses adrenal cortex     
    • Should NOT use alone --> use metryapone to allow for lower doses     
    • SE:  severe sedation
  23. Ketoconazole
    • inhibits adrenal & gonadal steroidogenesis  
    • potent inhibitor of 17, 20 desmolase and 17α-hydroxylase     
    • at high doses, inhibitor of CE --> pregnenolone (aminoglutethimide) and DHEA --> androsternedione (3β-dehydrogenase)    
    • SE:  low cortisol & hepatoxicity
  24. Etomidate
    • MOA unknown; parenteral use only     
    • SE:  myoclonus (muscle twitching)
  25. Mifepristone
    • MOA:  competitve antagonist of cortisol effects on GLU metabolism and increases circulating cortisol concentration     
    • SE:  edema, HTN, fatigue, HA, hypokalemia, N/V
  26. Mitotane
    • MOA:  decreases production of cortisol & alters steroid metabolism
    • CNS side effects
  27. Cyproheptadine
    • MOA:  decreases ACTH secretion     
    • SE:  sedation, increased appetite
  28. Pasireotide
    GHIH (somatostatin) analog that inhibits ACTH secretion and decreases cortisol

    SE (HAD No CHF):  HA, ab pain, diarrhea, nausea, cholethiasis, hyperglycemia, fatigue
  29. Pheochromocytoma:  Presentation & Causes
    • Classic Triad:  HA, sweating, palpitations
    • persistent HTN
    • Sxs:  anxiety, chest pain, polyuria, polydypsia, heat intolerance

    Genetic Causes:  autosomal dominant multiple endocrine neoplasia (MEN) syndrome, Von Hippel-Lindaw (VHL) disease, family history

    Med Causes:  glucagon, histamine, contrast dyes, metoclopramide, TCAs BB, opiates
  30. Pheochromocytoma:  Biochemical Markers
    • chromogranin A
    • neuropeptide Y
    • biogenic amines - Epi, Norepi, dopamine
  31. Pheochromocytoma:  Tx
    TOC:  complete tumor removal

    Preoperative tx:  phenoxybenzamine - alpha blocker to maintain BP of 160/90; may add another BB for tachycardia (propanolol, which shouldn't be used alone)

    Postop tx:  maintain BP

    Malignant Pheochromocytoma:  tumor mass reduction +/- alpha blockers +/- chemo +/- radiation

    Monitor:  BP, catecholamines q 6-12 mos, sxs of excess catecholamines
Card Set
CAM 2013: Exam One
Adrenals, Asthma, COPD