Block 3 questions

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  1. List factors that put pt at risk for candida
    Broad spectrum antibiotics, neutropenia, immunosuppression, prolonged antibiotic use, implantable prosthetic device, prolonged ICU stay > 7-14 days, High APACHEE II score, central venous catheter, TPN, > 2 days mechanical
  2. When would you use an echinocandin over azol
    Severe infection or recent azol exposure
  3. 2 pros and 2 cons of using echinocandin vs fluconazole in candidiasis
    • Pro: broader spectrum cover C. galbrata and C. krusei, no adjustment for renal, fewer D/D interactions
    • Con: only IV, Cost, no clear evidence of superiority, resistance in the future
  4. Duration of therapy for Candida infection
    Treat for 2 weeks past documented clearance from blood stream
  5. What are risk factors for infection with C. glabrata
    Elderly, cancer, DM
  6. What are sepsis, severe sepsis, and shock
    • Sepsis: 2 SIRS + infection
    • Severe sepsis: sepsis + organ dysfunction
    • septic shock: severe sepsis + hypotension
  7. Name 2 pros and 2 cons of using Echinocandin vs fluconazole in candidiasis
    • Pro: broader spectrum cover C. galbrata and C. krusei, no adjustment for renal, fewer D/D interactions
    • Con: only IV, Cost, no clear evidence of superiority, resistance in the future
  8. What are the SIRS criteria?
    RR > 20, HR > 90, WBC < 4000, >12000, 10% bands, Tem < 36 or > 38
  9. How much do you want to lower BG and why
    Lower by 10 % 1st hr then 50-75 mg/dl/hr to prevent cerebral edema and electrolyte abnormalities
  10. Ketones in DKA and how to measure them
    Acetone, acetoacetate, beta hydroxybutyrate Measure in blood and urine, dos a nitroprusside reaction which estimates the acetoacetate and acetone levels. Measure the serum B-hydroxybutyrate if possible
  11. When can you transition to SQ insulin
    When ketones have cleared, anion gap normalized and pt able to eat
  12. When do you stop the infusion after you have given SQ insulin
    1-2 hrs
  13. What electrolytes are important to monitor in DKA
    Mg+, Phos, Na+, K+
  14. Difference btwn HHS and DKA
    • HHS: mostly in type 2 DM, slower onset, normal pH, Glucose > 600
    • DKA: fast onset, mostly in type 1 DM, low pH acidosis, glucose > 250
  15. What is the pathophysiology of DKA
    1. Insulin deficiency 2. ↑ counter regulatory hormones (cortisol, glucagon, catecholamines)lead to insulin resistance
  16. What are the components of a diabetic foot exam
    Dermatologic, Musculoskeletal, Neurological assessment, vascular assessment
  17. What does LOPS stand for
    Loss of protective sensation
  18. What is the triad of causes that interact and ultimately result in ulceration
    Neuropathy, deformity, and trauma
  19. Risk factors for DFI
    • Poor glycemic control,
    • peripheral neuropathy
    • duration of DM > 10 yrs
    • high plantar pressure
  20. 3 differences btwn AACE and ADA guidelines
    • ADA: A1C < 7, pre-prandial 70-130, post prandial < 180
    • AACE: A1C < 6.5, pre-prandial < 110, post prandial < 140
  21. Sitagliptin and Byetta give one pro and one con of each
    • Sitagliptin-
    • Pro: weight neutral, oral, well tolerated 1% ↓ A1V
    • Con: expensive, may ↑ digoxin levelsb.
    • Byetta-
    • Pro: weight loss, A1C ↓ by 0.5-1%
    • Con: injection bid, expensive, GI SE
  22. What is insulin and what is its major role in the body
    Anabolic/anti-catabolic hormone Plays major role in protein, CHO, and fat metabolism
  23. What peptide can be used as and endogenous marker of insulin production
    Peptide C, cleaved when insulin is made
  24. What does the DOSE trial tell us about bolus vs. continuous infusion of furosemide in ADHF
    There is no difference in outcomes, start with bolus easier to use, continuous if resistant
  25. 2 pros and 2 cons of using nitroglycerin in ADH
    • Pro: improves PCWP, slight ↓ in MAP
    • Con: tolerance so have to continually titrate, pro-arrhythmic
  26. How much K + do you give a pt in a central line vs. peripheral
    Central 20 mEq, Peripheral 10 mEq
  27. How much Mg+ do you give a pt in a central line vs. peripheral
    Central 2 gram/hr, peripheral 1 gram/hr
  28. What is the mechanism by which a thiazide added to a loop produces more diuresis
    Loop work on the ascending loop of Henle, leading to more Na+ reaching the distal convoluted tubule which atrophies and therefore takes up more Na+, Thiazides block this
  29. What are the causes of hyperglycemia in the hospital setting
    Acute metabolic and hormonal changes due to injury and stress, counter regulatory hormones (glucagon, cortisol) lead to alteration in CHO metabolism, insulin resistance, gluconeogenesis, lipolysis
  30. What is the risk of hyperglycemia in the hospital
    ↑ Mortality, prolonged length of hospital stay, poor long term outcomes, high health costs
  31. When would you leave a patient on their home regimen
    Clinically stable, and have normal nutritional intake, normal BK and stable renal and cardiac function
  32. which echinocandind do you not need to dose adjust for hepatic impairment
  33. Name two pros and two cons to S/S insulin
    Pro: convenient, easy to implement, doesn’t depend on physician for dosing Con: reactive not proactive, hyper or hypoglycemia, can lead to DKA
  34. 2 pros and 2 cons of Milrinone in ADHF
    • Pro: can use with BB and it is ver effective at increasing cardiac output and cardiac index
    • Con: has long half-life so SE will last longer, and can cause arrhythmias so must monitor EKG
  35. Name a inotropic agent and what you need to monitor while using them
    Dobutamine, Milrinone, Dopamine

    Monitor: BP
  36. When is it appropriate/ or not appropriate to use Nesiritide
    Only in the absence of symptomatic hypotension, in addition to diuretic therapy for rapid improvement of congestive symptoms or if persistent ADHF despite aggressive treatment w/ diuretics and standard oral therapy
  37. When would you use migraine prophylaxis
    > 2 HA a month, pt expresses desire to not experience HA and wants therapy
  38. Name 3 diffrences btwn migraine and tension HA
    • migraine can be accompained by N/V and photophobia
    • Migraine typically last 24 + hrs, tension HA are shorter duration
    • Tension HA are bilateral, migraines are unilateral (but can go bilateral)
  39. What are the diffrences btwn Sumatriptan, Eletriptan and Frovatriptan
    • Sumatriptan: fast onset, short duration of action
    • Eletriptan: fast onset, long duration of action
    • Frovatriptan: slower onset, longer duration
  40. What two triptans come in ODT
    Rizatriptan and Zolmitriptan
  41. What are the 4 potent vasodilators released in migraine HA
    NO, CGRP, Neurokinin A, Substance P
  42. What is the risk of using triptan w/i 24 hrs of using a ergotamine
    they both cause vasoconstriction so it will produce extreme basoconstriction, which leads to hypertensive crisis, MI
  43. Why would you not use and SSRI and a triptan together
    Risk of serotonin syndrome
  44. What is the mechanism of action for triptans
    agonist of the 5HT receptor leading to vasoconstriction
  45. list 3 AED medications that are renally eliminated
    Levtiracetam, Gabapentin, Pregabalin, Lacosamide, Zonisamide
  46. List 3 AED that are enzyme inducers
    Phenytoin, Phenobarbital, Primidone, Carbamazepine,

    at high doses: Oxcarbazepine, Topiramate, Gelbamate
  47. Describe the diffrence btwn saccades and nystagmus
    Saccades: break up of smooth pursuit- choppy eye movement when following finger (marker that pt is taking med)

    Nystagmus: eye darts back and forth (or up and down) very rapidly when following finger (indication of toxcity)
  48. What 2 AED have FDA indication for migrain prophylaxis
    Topiramate, Valproic acid
  49. What are the hematology class effects of all AED
    decrease WBC, PLT and RBC
  50. What is an auto inducer and name one AED example
    • auto inducer is a drug that induces the metabolism of itself
    • Carbamazepine
  51. What two seizure medications should not be give in hyponatremia
    • Carbamazepine
    • Oxcarbazepine
  52. What do you need to screen pt for before starting Levetiracetam
    History of psychosis, can unmask
  53. What is a mojor adveres effect of Ezogabine
    Need to do bladder scan, pt can't feel bladder/if it is empty
  54. What are the two newest AED
    • Clobazam
    • Ezogabine
  55. 2 pro and 2 cons of using bivalirudin in HIT
    • Pro: no hepatic/renal adjustment, short half-life
    • Con: not FDA approved, fewer studies compared to other agents
  56. 2 pros and 2 cons of Argatroban in HIT
    Pro: FDA approved, no renal adjustment, reversible

    Con: metabolized by the liver, difficult to transition to warfarin
  57. What is the difference btwn HIT assay and SRA
    • ASSAY: more sensitive ( many ppl will have antiboidies), faster, doesnt tell if diesease is present
    • SRA: more specific, expensive, takes long time, tells that disease is present
  58. 4 T's of HIT
    Thrombosis, thrombocytopenia, time and other causes
  59. What is the role of fondaparinux in HIT
    For pt with history of HIT but not active HIT
  60. If pt has gonorrhea what partners need to be treated
    all partners w/i 60 days
  61. What does of acyclovir would you give for initial treatment of herpes
    Acyclovir 400 mg TID x 7 days
  62. What are contraindications to metformin
    SCr > 1.5 men > 1.4 women
  63. How would you initiate rapid insulin in pt uncontrolled on basal insulin
    start with highest meal of the day and have pt take 4 units or aspart, lispro, apidar and titrate by 2 units q 3 days until BG is w/i goal of < 180 2 hrs post
  64. Sitagliptin vs Exenatide 1 pro and 1 con of each
    • Sitagliptin: pro: available PO and no hypoglycemia
    • Con: expensive, long term safety not established

    • Exenatide: Pro: weith loss and improved satiety
    • Con: renal adjustment and injection
  65. What did the ACCORD trail teach us about BP, Lipids and glucose in DM
    • BP: compared lower BP 120 to 140 w/no diffence in outcomes
    • Lipids: statin+ fibrate vs. statin alone: no diff in outcomes
    • Glucose: A1C < 6 showed a increase in mortality with no CV venefits
  66. Diffrence btwn pioglitazone and rosiglitazone
    rosiglitazone has a BB warning for HF and increase risk of MI
  67. Metfromin and SU MOA and how it relates to hypoglycemia
    • Metromin is an insulin sensitizer and does not cause hypo alone
    • SU stimulate insulin release form the pancreatic beta cell and can cause hypoglycemia
  68. Pt in ED w/ asthma exacerbation and has had several doses of SABA and oxygen with no relief what can you give him and why
    Ipratropium can be added bc it is short acting anticholinergic that will work quickely to decrease the exacerbation. Studies have shown that in combo with SABA in ED it helps to decrease the severity of exacerbation and length of hospital stay
  69. what is the diffrence btwn allergic rhinitis and asthma
    • Asthma: chronic inflammatory condiciton of the lower airways characterized by reversible airflow obstruction, hyper responsiveness and episodic respiratory symptoms
    • Allergic rhinitis: disorder of upper airway, resulting for IgE mediated inflammation of the nose upon contace with allergen
  70. what is the diffrence btwn albuterol and levalbuterol
    Levalbuterol is R isomer of albuterol so it has less SE of tachycardia and tremor compared to albuterol which is a racemic mixture
  71. when to use IV vs. PO steroids in acute exacerbations of asthma
    IV is for life threatening only, PO for mild-moderate and severe
  72. Role of IV Mag sulfate in asthma exacerbation
    used when incomplete response to initial treatment w/i 1-2 hrs, used to avoid the need for intubation
  73. what is the role of omalizumab in asthma
    treatment step 5 and 6 with allergic component
  74. what is an asthma action plan and why is it used
    to help assist the pt in understanding their disease and teach how to self manage it. Focuses on 2 things: daily managment and how to recognize worsening symptoms
  75. 3 counseling pts for oral inhalers
    store at room temp, wash mouth piece w/ soap and water, prime before use, inhaler technique
  76. when would you use spironolactone for resistant HTN
    Refractory HTN, advanced HF or CKD
  77. 50 yr old perimenopausal female give 2 reasone venlafaxine is a good option
    treats the vasomotero symptoms and is non-hormonal so no increased risk of CV event
  78. Name two drug that are used to treat hot flashes
    Venlafaxine, prempro, OC, gabapentin
  79. What does ACHES stand for
    abdominal pain, chest pain, headache, eye pain, sever leg pain
  80. What does PAINS stand for, and when would you use it
    Period late, Abdominal pain, Infection exposure, Not feeling well, String missing (what to look for with the use of IUD)
  81. when and why would you add on progesterone to estrogen hormone therapy in perimenopause
    add when pt still has uterus to decrease the risk of endometrial cancer and endometrial hyperplasia
  82. What is the role of glucosamine in OA
    Guidelines say not to use it but it does prevent cartilage loss
  83. what is the mechanism of orlistat and the SE
    • reversible inhibitor of intestinal lipases, prevents TG absorption
    • SE: fatty stool, decreased absorption of fat soluble vitamins
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Block 3 questions
Block 3 questions
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