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360 Cards in this Set
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- Back
- 3rd side (hint)
What is the difference between substance dependence and substance abuse?
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Dependence: not only do you have a diminished control over your use, but you have a physiological dependence on the substance
Abuse: behavioral; failure to maintain social roles, participate in hazardous behaviors. |
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What is the mechanism of action of Anabuse?
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Blocks aldehyde dehydrogenase causing an immediate rxn: flushing, nausea, dizziness, tachy
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What must be done prior to administering the loading dose of Anabuse?
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Patient must breath zero on breathilizer
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What is naltrexone used for and what is the mechanism of action of Naltrexone?
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Alcohol addiction.
Pure opioid antagonist; blocks the mu opioid receptors; blocks the euphoria from alcohol |
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What is acamprosate used for and what is its mechanism of action?
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Alcohol addiciton
Structurally similar to GABA->enhances GABA transmission --> interferes with glutamate transmission -->decreases anxiety from protracted withdrawal |
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What is the main contraindication to acamprosate?
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severe renal impairment (Cr clearance <=30mL/min)
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What are the three medications available for nicotine dependence?
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Buproprion (Zyban)
Nicotine replacement (gums/patch) Varenicline (Chantix) |
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What are the contraindications to buproprion?
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lowers sz threshold, eating disorders
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What is the approximate dosing of nicotine replacement medications?
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1 mg per cigarette (20 mg for a ppd smoker)
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What are the three medications used for opioid dependence?
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Methadone
Buprenorphine Naltrexone |
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What is the MOA of methadone?
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mu opioid agonist; competes with heroin for the receptor so you can't get the same high from heroin. Long acting
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What are the con's of using benzos?
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dependency
anterograde amnesia interacts with other CNS depressants (e.g., alcohol) Rebound Psychomotor impairment |
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What is the tx for circadian rhythm d/o?
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Light and melatonin
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What is the tx for conditioned insomnia?
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stimulus control and sleep restriction
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What is the first line tx for generalized anxiety d/o?
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SSRI, SNRI
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What are the main drugs used for alcohol w/d?
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Clorazepate
Chlordiazepoxide Lorazepam |
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What is the surgical stress response?
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afferent neural message from spinal cord to brain --> efferent back to trauma site and adrenals --> activation of the hypothalamic-pituitary-adrenal axis --> adrenals release catecholamines, cortisol and stress hormones --> tachy, HTN, hypercoag, immunosuppression
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What is the term used to describe the peripheral and central sensitization to acute pain that eventually leads to chronic pain?
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Neuroplasticity
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What is allodynia?
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perception of pain when no pain should be present
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Is acute pain primarily somatic or visceral?
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Somatic (muscles, bones, tissues)
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How will neuropathic pain be described by your patient?
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burning, tingling, shooting, electric-like, lightening-like
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How do opioids work to control acute pain?
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diffuses across the dura mater into the CSF --> binds with receptors in the dorsal horn of the spinal cord --> modifies transmission of pain impulses to the brain
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What is the main advantage of the IV-PCA?
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there are fewer fluctuations between side fx of too much opioid and the acute pain
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Which analgesia provides the best postop analgesia?
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Epidural
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What is the most significant side effect of opioid analgesics?
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Respiratory depression
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Are NSAIDs helpful in managing acute pain?
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Yes. Unless contraindicated, NSAIDs have been shown to reduce opioid requirements by 20-40%
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What is the MOA of NSAIDs?
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inhibition of COX enzyme --> supression of prostaglandin synthesis
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What is the only injectable NSAID?
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Ketorolac (Toradol)
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What is the rule of thumb for dosing opioid in opioid-dependent patients?
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pt will need 2-3x the pre-op dose for adequate post-op control in first 24-48 hrs (may need up to 10x)
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What is the treatment protocol (drugs, doses, and timeline) for seizures?
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Pt Found: Airway/position/oxygen/IV/suction; 3-5 minutes: Lorezapam (2-4mgIV q 5 min); 10-15 Min: Phenytoin (20mg/kg @ 50mg/min); 30-45 Min: Paralyze/Intubate c/ Pentobarbital (12mg/kg) or Phenobarbital (20mg/kg)
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What is the last resort for intractable agitation unresponsive to Benzos or Antipsychotic Meds?
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Intubation/Paralysis to prevent potentially fatal acidosis/hypoxia/hyperthermia
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What are the four types of allergic reactions?
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Local(skin); Local(airway); Systemic; Anaphylactic shock
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What are the three drug categories used in allergic reactions?
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Anithistamines (i.e. Diphenhydramine 25-50mg PO/IV); Steriods (i.e. Methylprednisolone 120mg IV); Pressors (i.e. epinephrine 0.3mg im 1:1000)
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What are the three main causes of respiratory distress?
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Airway Problem (i.e. Allergic, infection, trauma); Lung Problem (i.e. Asthma, COPD, CHF); Systemic Problem (DKA, Toxicity, Anxiety)
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What three drugs are the current standard for advanced testis cancer chemotherapy?
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BEP: Bleomycin, Etoposide (recently took place of Vinblastine), cisPlatin
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What are the major toxicities associated with BEP therapy?
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Hematologic (marrow suppression), Nausea, Nephrotoxicity, Lung toxicity, Neuropathy
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What are the three essential elements necessary to make therapeutic decisions in testis cancer?
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Histology, Stage, Organ Function
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What factor limits the maximum chemotherapy dose in testis cancer, and how can this be overcome?
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Bone marrow toxicity of BEP chemo; adjuvant Tx c/ Autologous stem cell rescue can allow for higher chemo doses - used for relapse after standard-dose chemo
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What 4 classes of drugs are used in the prophylaxis of migraine headaches?
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Anti-epileptic drugs (Depakote, Topamax and Zonisamide), Beta blockers (propranolol due to good lipid solubility), Calcium re-entry blockers, and Tricyclic antidepressants.
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For what 2 reasons would a female of child-bearing age not want to take Depakote?
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Due to weight gain and the risk of neuro tube defects.
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Describe the use, MOA, and limiting factor of the drug Mehysergide.
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Methysergide is a serotonin antagonist and can be used for short-term interruption of a difficult migraine cycle. Its use is limited by retroperitoneal fibrosis. (common board question)
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What are limiting factors in the use of TCADs for headache?
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Excess sedation, weight gain, dry mouth, and refusal to take a "psych" med.
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What is Ergotism?
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Excess use of ergots can lead to Ergotism which is a progressive arterial occlusive syndrome of the extremities. (another common/archaic board question)
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What drugs are 1st line therapy for migraine sufferers? What patients would want to avoid these medications?
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Ergots (typically given in preparation with caffeine) and triptans (more expensive). These meds are restricted to patients without CV disease due to inducing vasospasm.
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What is our natural defense mechanism against headache?
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Sleep! This is why sedatives and analgesics with sedative properties can sometimes be helpful in migraines and headaches.
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What is the most life threatening headache and what is it? What are some causes?
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Subarachnoid hemorrhage - when blood contacts the dural surface causing severe pain. Causes include a ruptured aneurysm, bleeding AVM, and trauma. (Worst headache of my life)
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What could you use to treat atypical face pain?
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Indomethacin
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What can be used to treat trigeminal neuralgia?
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Antiepileptics (phenytoin,carbamazepine, etc).
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What are 4 classes of drugs that are harmful in heart failure?
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NSAID's (b/c they affect renal blood flow), Ca channel blockers (b/c they are negative inotropes), Diabetes drugs (b/c they cause fluid retention), and anti-arrhythmic drugs (b/c these will often act pro-arrhythmic in HF pts.)
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What 3 classes of drugs treat the symptoms of heart failure? What 3 classes actually improve survival?
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Reduce sx = diuretics, digoxin, ACE-I's/ARB's, Reduce mortality = ACE-I's, B-blockers, Spironolactone
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Why give diuretics for a pt with heart failure (how do they work)? What side effects could occur?
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Diuretics improve symptoms such as dyspnea and leg edema because they up salt/water excretion thus decreasing IV fluid. Side effects include hypokalemia, hyponatremia, hypotension, renal failure, and the activation of the renin/angio/aldo system.
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How does spironolactone work (for heart failure) and what are two side effects?
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Spironolactone is an aldosterone receptor blocker preventing sodium and water retention. Side effects are hyperkalemia and gynecomastia. (this med actually helps survival when added to an ACE-I)
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Why use ACE-I's in heart failure (what is their MOA)? And what are the side effects you would expect?
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ACE-I's cause vasodilation by blocking angiotensin II from being formed, thus lowering afterload, decreasing SNS activity, lessening remodeling (by decreasing aldosterone), and increasing bradykinin and thus NO (vasodiltor and antiplatelet). Side effects are hypotension, renal failure, hyperkalemia, and cough/angio-edema (BK mediated).
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What do Beta blockers help with in heart failure and what are their side effects?
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As long as they are started slowly/titrated slowly and carefully they help decrease tachycardia and help with the adverse effects caused by high catecholamine levels on the heart. Side effects include increased HF sx, bradycardia, hypotension, fatigue, and decreased libido. (They do not cause depression)
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Between SSRI's and TCA's, which has a lesser side effect profile?
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SSRI's have less side effects than TCA's. (This will affect patient adherence!)
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What are some side effects of TCA's? (Esp trazadone?)
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Trazadone = Priapism in males. Other side effects include sedation, orthostatic hypotension, anticholinergic effects, cardiac arrhythmias, and weight gain.
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What are some side effects of SSRI's (acute and delayed onset)?
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Acutely = insomnia, somnolence, diarrhea, nausea (will likely diminish with time). Delayed onset = sexual dysfunction, weight gain, cognitive blunting.
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What class of drug is Bupropion and what are two advantages and two disadvantages of this med?
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NDRI - Norepi-Dopamine Reuptake Inhibitor. Advantages are less sex dysfxn, less wt gain. Disadvantages are it's not effective for anxiety disorders, and it is contraindicated in pt's with sz d/o's and eating d/o's.
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Name some 1st line antidepressants and some 2nd first line drugs.
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1st line = sertraline (best overall), Fluoxetine (qday dosing), Citalopram. 2nd first line = Escitalopram (good drug but very expensive), Bupropion if wt gain and sex dysfxn are main concerns.
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When would you want to switch vs. augment antidepressant meds?
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Switch meds if side effects are an issue. If not, augmenting is going to probably give max benefits.
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What is the best test for thyroid function?
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TSH
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What is the starting dose for thyroid replacement?
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1.6mcg/kg (100mcg)
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What is the TSH treatment goal for thyroid replacement?
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0.5 - 2.5 mU/L
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What is the next step for a pt with symptoms of hyperthyroidism and a low TSH?
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Thyroid uptake
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For a pt with low TSH and low thyroid uptake, what is the likely dx?
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thyroiditis
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What should a thyroid scan look like in pt with low TSH?
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suppressed, not normal (i.e. remember to interpret results in context of TSH)
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What changes might you make to a pregnant pt's thyroid replacement? Why?
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increase by about 50%, reduced Free T4 due to increased TBG
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Is the TSH normal if checked early in pregnancy?
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low
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What are the two main defects that can be affected in diabetes management?
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loss of beta cell function and increased insulin resistance
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How would you initiate Metformin treatment in a diabetic patient?
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start slow (500mg at bedtime), titrate to 1000 BID, warn about bloating and loose stools
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What are the pharmacologic options for augmenting insulin secretion?
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Sulfonylureas, meflintides, sitagliptin, exenatide
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How would you initiate basal insulin dose in diabetic patient?
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Start with evening dose around 10U, adjust each week based on fasting glucose (up 4 if >140, up 2 if 120-140)
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What the hell is the correction factor?
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1500/Total Daily Insuilin - tells you FPG reduction per Insulin Unit
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What are the choices for 1)rapid-acting insulin? 2)Short Acting? 3)Intermediate? 4)Long Acting?
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1) Lispro, Aspart, Gluilisine 2) Regular 3) NPH, lente 4) Glargine
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Why might someone take NPH and regular insulin in the morning?
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Regular for breakfast, NPH for lunch (single injection instead of 2)
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How do the thiazolidinediones work?
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increasing glucose uptake in fat and muscle cells
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What are the two "hits" that lead to diabetes?
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insulin resistance and decreased insulin production by beta cells
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What are the principles of DKA treatment?
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IVF, insulin (0.1U/kg bolus, 0.1U/kg/hr pump), replace K+, add Glu when blood glucose is normal but AG persists
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What are the 4 classes of antiarrhythmic drugs?
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Class I - Na channel blockers, Class II - Beta blockers, Class III - mostly K channel blockers (act to prolong repolarization), Class IV - Ca Channel Blockers
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Describe "use dependence" and which class of antiarrhythmic meds has this? Which has "reverse" use dependence?
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This is when during faster heart rates, less time exists for the drug to dissociate from the receptor, resulting in an enhanced drug action. Class I agents show this (IC>IA>IB). Class III show the reverse of this.
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What are some notable side effects of Class IA drugs?
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Vagolytic effects, anticholinergic effects, GI symptoms, hypotension, and immune-mediated reactions.
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What are the notable side effects of Class IB drugs?
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Neurologic toxicity!!! Also GI, and Dermatitis.
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What are the notable side effects of Class IC antiarrhythmics?
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"Class IC Flutter" (slow Afib with wide complex), and extracardiac effects such as metallic taste in the mouth.
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What is the side effect/arrhythmia you worry about with Class III drugs?
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Torsda de Pointes
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What are some of the many effects of amiodarone toxicity?
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Hypo and hyperthyroid, liver function abnormalities, optic neuropathy, sinus bradycardia, photosensitivity, skin discoloration, pulm fibrosis, tremor, constipation, loss of appetite, etc.
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When a person is on Sotalol or Dofetelide, what organ system do you want to monitor? (Hepatic or renal?)
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Renal!
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What four drugs does amiodarone enhance the effect of?
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Warfarin, Cyclosporine, Dig, Statins
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How is the new med Dronederone improved from Amiodarone?
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You remove the iodine moieties from amiodarone to get dronederone and this stops the toxicities you will see with amiodarone.
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Describe the mechanism by which tPA, streptokinase, and urokinase work for thrombolysis. (ie. direct vs. indirect)
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tPA - indirectly activates plasminogen to plasmin, streptokinase - directly lyses because it is plasmin-like, urokinase - indirectly activates plasminogen to plasmin
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Why do you not want to treat thromboemboli with Warfarin acutely?
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Warfarin takes 5-7 days to reduce the pool of "activatable" factors, it does not affect the factors already activated.
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How are LMWH and Fondaparinux cleared and what might you monitor while pts take these?
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They are renally cleared and you want to monitor Creatinine, do not use if CrCL<30
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If a pt has a history of HIT, what might you want to use? If a pt has active HIT, what would you use? What type of heparin is most likely to cause HIT?
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h/o HIT - use fondaparinux, active HIT - use argatroban, lepirudin, bivalirudin. Unfractionated Heparin is most likely to cause HIT.
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What should you remember about the timing of converting from IV heparin to LMWH?
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The drip should be turned off at the SAME TIME the sq injection is given!
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What is the MOA of Warfarin? ***likely test questsion***
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Warfarin inhibits the carboxylation of vitamin K dependent factors so the factors are still produced but can't promote thrombus, it will not interact with already activated factors!
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What is the MOA of Aspirin?
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it is an irreversible inhibitor of COX thus inhibiting prostacyclin synthesis, decreasing TXA 2 thus reducing platelet aggregation and vasoconstriction
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What antiplatelet therapy is recommended for the prevention of thromboembolic events in pts with A fib?
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Aspirin, if pt fails, then use Warfarin
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(Pharmacokinetics 2/1)
What is the equation to calculate the loading dose |
Loading dose = Cp * Vd
(Cp = plasma drug concentration, Vd = volume of distribution) |
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What is the equation to calculate the maintenance dose (using clearance)
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Dose/time = Cpss * (clearance)
(Cpss = steady state plasma drug concentration) |
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What is the equation to calculate the maintanance dose (using half-life for 1st order drugs)
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Dose = 1/2 * (loading dose every half life)
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What is the equation for drug clearance
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clearance = Ke * Vd
(Ke is 1st order rate constant) |
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What is the equation for Ke (the 1st order rate constant)
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Ke = 0.693 / half-life
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what are two mechanisms in which liver disease changes drug pharmacokinetics
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1) altered metabolism from impaired clearance
2) altered volume of distribution from poor protein production |
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what are two mechanisms in which kidney disease changes drug pharmacokinetics
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1) altered metabolism from impaired clearance
2) altered volume of distribution from microalbuminemia or acid/base changes |
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what is first-pass metabolism?
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metabolism of drug before systemic effects due to the fact that all orally absorbed drug must enter the liver via the portal vein before reaching the systemic circulation
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how can cirrhosis effect first-pass metabolism
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reduces first-pass metabolism - due to shunting of portal blood around remaining functional hepatocytes
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what is bioavailability?
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overall fraction of orally administered drug that reaches the circulation
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(Treatment of drug overdoses 2/1)
what is the treatment of cyanide toxicity |
thiosulfate
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how does thiocyanate work to treat cyanide toxicity
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converts cyanide to thiocyanate which can be excreted
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major symptoms of carbon monoxide poisoning
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headache, hypoxemia (normal pulse Ox, low O2 sat on arterial blood draw)
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treatment of insulin toxicity
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50-100 ml 50% glucose IV
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5 ways to prevent poison absorption
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1) wash the skin
2) emesis - 1 oz Ipecac + H20 3) lavage - 36F tube + H20 4) charcoal - 10x weight of estimated drug 5) cathartic - MgSO4 or Mg citrate |
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Dx of narcotic overdose
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1) pinpoint pupils
2) shallow or absent respirations 3) needle tracks (or heroin needle sticking out of arm) |
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Rx of narcotic overdose
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Naloxone (Narcan) 2mg IV; repeat upt o 10 x if suspicion is strong every 2-3 hrs.
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Dx of ethylene glycol and methanol intoxication
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1) history
2) intoxication 3) metabolic acidosis 4) ethylene glycol - oxylate crystals in urine 5) methanol - blurred vision 6) blood levels |
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Rx of ethylene glycol or methanol intoxication
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1) ethanol bolus - 0.6 g/kg
2) hemodialysis and ethanol infusion |
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Rx of acetaminophen toxicity
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N-acetylcysteine (Mucomyst)
loading dose - 140 mg/kg, 70 mg/kg q 8 hrs x 3 days |
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Dx of anticholinergic toxicity
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1) Dry as a bone
2) Hot as a hare 3) Mad as a hatter 4) tachycardia |
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Rx of anticholinergic toxicity
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physostigmine 2mg IV
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Effect organophosphates have on nervous system
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cholinesterase inhibitors -> increased parasympathetic effect
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Dx of organophosphate toxicity
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1) history (exposure to insecticides)
2) lacrimation 3) salivation 4) defection 5) bradycardia |
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Rx of organophosphate toxicity
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Atropine 1mg. Keep doubling until desire effect (up to 100mg)
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Tx of salicylate and phenobarbital toxicities
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alkaline diuresis or dialysis
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management of digoxin overdose
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1) correct low sodium K, if present
2) try phenytoin 5-10mg/kg IV 3) use transvenous pacemaker for complete heart block 4) avoid cardioversion; may lead to V fib |
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symptoms of thenothiazine overdose (thorazine and haldol)
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1) oculogyric crisis
2) pseudo parkinsonism 3) toricolus |
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Rx of phenothiazine overdose
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diphenhydramine 50mg IV q 6 hr for 1-3 days
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Rx of iron toxicity
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gastric lavage with 2gm/liter deferoxamine
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drug overdoses that require supportive care
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1) most barbiturates, benzodiazepines
2) tricyclic antidepressants 3) ethanol 4) hydrocarbons 5) theophylline (maybe dialysis) 6) amphetamines 7) hallucinogens |
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treatment of lidocaine overdose
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ECMO - extracorporeal pump
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What are the most common place for fractures in osteoporosis?
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Vertebral
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What are the TWO main diagnostic criteria for osteoporosis?
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Low T-score (<2.5) OR fragility fracture
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What are the TWO main categories of osteoporosis meds (and how do they work)?
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Anti-resorptive agents: inhibit osteoclast activity (i.e. PTH analogs) and Anabolic agents: stimulate formation/osteoblast activity (i.e. everything else - SERMS/estrogen, calcitonin, bisphosphonates)
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What mechanisms account for statins’ role in both long AND short-term benefit in cardiac-event reduction?
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Long-term: regression of atherosclerotic lesions; Short-term: Stablize lesions, reduce inflammatory stimuli, increase vasodilation
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What THREE platelet-driven mechanisms account for atherosclerotic plaque formation (and what drug classes attack each one)?
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Activation (ASA), Adhesion (Thienopyridines), Aggregation (2B/3A receptors)
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Why does protamine completely reverse Heparin but not Enoxaparin (LMWH)?
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Both indirectly inhibit thrombin (activity reversed by protamine), but LMWH is 40% Factor Xa blocker, which remains unaffected
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Of the following drugs, which is NOT a vasopressor? Phenylephrine, Dopamine, Norepinephrine, Epinephrine, Dobutamine
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Dobutmine is an INOTROPE b/c only has B1 activity (the rest have alpha/beta 1 and 2)
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What are the main pros/cons of drug-eluting stents compare to bare-metal?
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Pro - less renarrowing, Con - increased thromboses due to decreased endothelialization (necessates longer period of anti-coagulation)
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Why is it so important to reduce the overall use of antibiotics?
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Resistance is increasing, emergance of new drugs is decreasing, so we must conserve the utility of current Abx
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What is the best strategy for avoiding Abx-associated C.diff infections?
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Always switch to the narrowest Abx possible as soon as culture/sensitivity data available
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List THREE strategies for decreasing antibiotic resistance
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Remove invasive devices ASAP, always document abx therapy status (i.e. day 3/7) on notes, use the shortest abs Tx duration within allowable limits
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What is the Port Pneumonia Severity Index (PSI)?
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Risk stratification for CAP: 5 classes based on 19 variables, including Age, Comorbidity (i.e CHF< cancer, CRD), Physical Exam (i.e high BP/HR/RR), Lab Values (i.e. low HCT/Na, high Gluc)
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List THREE typical and THREE atypical bugs causing CAP
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Typical: s. pneumo, H. influenzae, S. aureus; Atypical: M. pneumoniae, Legionella, C. pneumo
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What is the preferred treatment for outpatient vs. inpatient CAP?
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OP: flouoroquinolone; IP: Macrolide + Beta-lactam (2nd line for each is the 1st for the other)
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Which race had the most TB on navy ships in the 70s - Whites, negroes, or orientals?
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The correct answer is ASIANS, you racist old white man!
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Who should get treated for TB?
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High risk pts (empirically), pts w/abnl CxR, pts w/Pos sputum smear/culture (NOTE: pos. TST not enough alone!)
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How should TB drug-induced hepatitis be treated?
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Stop TB drugs, assess for other causes, check LFTs, bridge with other Abx if necessary (FQ, EMB, aminogly), re-challenge w/TB drugs individually once LFTs resolve
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What is the current multi-drug TB treatment standards?
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6-9 months of IRZE or IRZ+streptomycin; short course (1-2 drugs for 3-4 months under study, but not yet proven)
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In patients with infections on corticosteroids, explain how one could have a neutrophilia but NOT be fighting the infection?
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While neutrophils are released from the bone marrow in increased fashion with steroids, there is decreased margination of neutrophils. It is the marginated neutrophils that go to site of inflammation.
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How do corticosteroids produce anti-inflammatory effects?
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1. vasoconstriction
2. antipyresis 3. inhibition of accumulation and activation of inflammatory cells 4. inhibit synthesis of prostaglandins and many cytokines. |
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How do you measure HPA activity?
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1. Fasting cortisol >15mcg/dL is good
2. Peak cortisol from cosyntropin stim test 3. CRF stimulation of anterior pituitary 4. corticoid metabolite urinary excretion Test don't correlate |
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At what point after the administration of corticosteroids does the suppression of the HPA axis occur?
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10-14 days after beginning steroids
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|
What are stress doses of steroids, how are they administered?
|
An increase in steroid administration above normal human production in pts with long term disease or extensive surgery to prevent system collapse from the chronic suppression of the HPA axis. 100-2--mg/day IV hydrocortisone
|
|
|
Are steroids helpful or harmful in severe infections?
|
Depends: steroids bad for viral illnesses (measles, varicella, hepatitis); make them worse.
Helpful in bacterial infections, thyphoid, PCP and EBV, septic shock (low doses). Often used as adjunct. |
|
|
What are the consequences of short-term and long-term (>10 days) use steroids?
|
short-term: not many
Long-term: increase in opportunistic infections |
|
|
How do you dose corticosteroids for antiinflammatory purposes?
|
Induction: 1mg/kg/day pred in divided doses (IV not better than po); as disease improves, taper to 0.5mg/kg/day and eventually to 0. Maintenance usually not necessary.
|
|
|
Why do you taper the dose of corticosteroids when discontinuing for antiinflammatory purposes?
|
to prevent the rebound of the illness.
|
|
|
How do you dose steroids in a crisis situation (translpant rejection, asthma/COPD exacerbation)?
|
1-4g of methyl pred IV/day
|
|
|
What are the acute side effects of systemic steroids?
|
1. salt/water retention
2. edema 3. increased BP 4. K loss 5. mood changes in either direction 6. insomnia Also exacerbates preexisting HTN, glucose intolerance, PUD, acne vulgaris depending on dose |
|
|
Side effects of high-dose sustained therapy of corticosteroids?
|
1. cushing's syndrome
2. HPA axis suppression 3. weight gain 4. mood disturbance 5. impaired wound healing 6. increase risk of infxn 7. hypercalciuria 8. increased protein catabolism |
|
|
Side effects with large cumulative doses of corticosteroids (high dose for years)?
|
1. osteoporosis
2. cataracts 3. skin atrophy 4. growth retardation 5. atherosclerosis |
e.g transplant pts
|
|
What are the rescue medications for asthma?
|
short-acting b-agonists
anticholinergics systemic corticosteroids |
|
|
What are the medications for daily LT control of asthma?
|
steroids
leukotriene modifiers mast cell stabilizers Anti-IgE mab Beta agonists for bronchodilation |
|
|
Which asthma medication can enhance the efficacy of the glucocorticoid receptor, making steroid use more effective?
|
b-agonists
|
|
|
Do inhaled corticosteroids stunt the growth in children?
|
there is a decrease in growth rate, but they compensate and catch up.
|
|
|
Why are b-agonists not appropriate for monotherapy for asthma?
|
there are no inherent anti-inflammatory actions; effective with ICS treatment 2/2 heightening the activity of the GC receptor in the nucleus
|
|
|
What is the treatment for asthmatics not controlled with ICS?
|
add a b-agonist. Do not increase the dose of the corticosteroid
|
|
|
What is the MOA of leukotriene modifiers?
|
5-LO inhibitors or leukotriene receptor antagonists; interrupt the arachadonic acid cascade
|
|
|
What is the first line of treatment for mild, persistent asthmatics starting therapy?
|
ICS
|
|
|
What is the first drug targeting severe, poorly controlled allergic asthma?
|
anti-IgE; binds to IgE molecules and clears them from the body
|
|
|
What are the barriers to asthma control?
|
1. Technique
2. Adherence 3. Misdiagnosis 4. location of inflammation 5. lack of eos inflammation 6. genetics |
|
|
What is inoculation and when would you want to inoculate?
|
Inoculation: purposeful infection
done to assure person has disease when less dangerous; bioterrorism; to attenuate disease in an individual. |
|
|
What is vaccination?
|
the administration of less virulent infection or dead organisms with the intent of immunization even though not all people will develop immunity.
|
|
|
Is influenza vaccine active or inactive virus?
|
inactive or live/attenuated (nasal)
|
|
|
What are the problems with attenuated virus?
|
1. disease in the immunocompromised
2. contomination with virulemt strain of other organisms 3. quality control 4. reversion to virulence |
|
|
What are examples of subunit vaccines?
|
toxoid: protein from the organism
polysaccharides: from bacterial capsule conjugate polysaccharides: linking the sugar to a protein (t-dependent) recombinant protein: genetically engineered protein |
|
|
What is the level necessary to achieve herd immunity?
|
90-95% of population need to be immune
|
|
|
Parkinson's Drugs (2/4)
4 cardinal signs of Parkinson's Dz |
1) Resting Tremor
2) Rigidity 3) Bradykinesia 4) Postural Instability |
|
|
6 other signs of Parkinson's Dz
|
1) decreased facial expression
2) small handwriting 3) shuffling gait 4) low speech volume 5) hesitation in initiating movements 6) freezing |
|
|
3 major forms of Parkinson's Dz and relative prognosis
|
1) Tremor Predominant - best prognosis
2) Rigid/Bradykinesia Predominant - intermediate prognosis 3) Postural Instability and Gait Difficulty Form - worst prognosis |
|
|
Parkinson's Dz is associated with loss of neurons in which part of the brain
|
substantia nigra
|
|
|
3 neuroprotective therapies for treatment of Parkinson's Dz
|
1) Vit E
2) Coenzyme CoQ10 3) Aerobic exercise |
|
|
5 classes of drugs used to treat symptomatic Parkinson's Dz
|
1) Dopaminergics (Levodopa)
2) MAO-B inhibitors 3) COMT inhibitors 4) anticholinergics 5) non-motor treatments (antidepressants, anticholinesterases) |
|
|
what symptoms of Parkinson's Dz does MAO type B treat?
|
tremor and freezing
|
|
|
relative contraindication for MAO type B
|
peptic ulcer dz
|
|
|
what symptoms of Parkinsons Dz does anticholinergics treat?
|
tremor
|
|
|
side effects of anticholinergics
|
dry mouth, urinary retention, decreased memory, psychosis
(hot as a hare, blind as a bat, dry as a bone, red as a beet, and mad as a hatter) |
|
|
mechanism of action of amantadine in Parkinson's Dz
|
releases dopamine stores, inhibits dopamine reuptake
|
|
|
3 side effects of amantadine
|
mental status changes, peripheral edema, Livedo reticularis (lacey rash)
|
|
|
example of 1st generation dopamine agonist
|
bromocriptine
|
|
|
3 examples of 2nd generation dopamine agonist
|
1) pramipexole (Mirapex)
2) Ropinirole (Requip) 3) Neupro (Rotigotine) |
|
|
why should you avoid dopamine agonists in the elderly
|
results in cognitive dysfunction and orthostasis
|
|
|
4 common side effects of 2nd generation dopamine agonists
|
1) nausea
2) orthostasis 3) excessive daytime sleepiness 4) compulsive behaviors (gambling, shopping, porn, etc) |
|
|
what two drugs make up Sinemet?
|
carbidopa and levodopa
|
|
|
what enzyme does carbidopa inhibit?
|
dopa-decarboxylase
|
|
|
what benefit does carbidopa have on side-effects of levadopa?
|
decreases nausea (does not cross blood-brain barrier)
|
|
|
4 side effects of sinemet
|
nausea, postural hypotension, mental status changes, dyskinesias
|
|
|
long-term complication of Sinemet at >5yrs?
|
75% at >5 yrs have motor fluctuations between overmedication (dykinesias) and undermedication (rigidity)
|
|
|
why do motor fluctuations occur as a side-effect of long-term Sinemet use?
|
therapeutic window becomes narrower over time, and easier to over/under treat
|
|
|
Most effective treatment at time of motor fluctuations due to long-term Sinemet use?
|
deep brain stimulation
|
|
|
(Hormonal Contraception 2/8)
the spike of which hormone causes ovulation? |
LH
|
|
|
what two hormones are in combined OCPs?
|
estradiol and progestin
|
|
|
what are 3 actions of progestins that result in contraception?
|
1) suppresses LH surge
2) results in atrophic endometrium 3) results in thick cervical mucous |
|
|
what 4 actions of estradiol results in contraception?
|
1) suppress FSH surge (no follicles)
2) edematous endometrium 3) potentiates progesterone receptors 4) decreased ovum transport time |
|
|
4 ways OCP decrease dysmenorrhea
|
1) longer progestin response
2) decreased endometrial thickening 3) decreased prostaglandin relase 4) suppression of endometrial implants |
|
|
how do OCPs decrease acne?
|
estrogens increase sex hormone binding globulins (SHBGs) which decrease androgen levels
|
|
|
OCPs decrease the risk of what 4 diseases in older women?
|
1) ovarian CA
2) endometrial CA 3) benign breast dz 4) osteoporosis |
|
|
what two cancers are shown to not correlate with OCP use
|
1) breast ca
2) cervical ca |
|
|
the estrogen in OCPs cause what two side effects
|
nausea, breast tenderness
|
|
|
what is the cause of break through bleeding when first starting OCPs?
|
decidual changes in endometrium
|
|
|
what is the cause of break-through bleeding during long term use of OCPs?
|
thin and fragile endometrium
|
|
|
treatment of break-through bleeding during long-term use of OCPs
|
7 day course of ethanol estradiol (EE) during bleeding period
|
|
|
what can be the cause of amenorrhea when OCPs are used long-term?
|
thinned endometrium
|
|
|
treatment of amenorrhea when OCPs are used long-term?
|
reassurance or ethanol estradiol during next cycle
|
|
|
7 absolute contraindications of OCPs?
|
1) current or past PE, MI, CVA, or thrombophebitis
2) active liver dysfunction 3) known breast CA 4) undiagnosed vaginal bleeding 5) suspected pregnancy 6) smoker over age 35 7) migraines with aura |
|
|
what should you do if you miss a OCP pill
|
take two the next day
|
|
|
what should you do if you miss 2 OCP pills (within first 2 wks)?
|
take 2 the next day, and use condoms for 7 days
|
|
|
what should you do if you miss 2 OCP pills (during 3rd wk)?
|
will probably start period - use condoms for 7 days and start a new pack. pray.
|
|
|
why dose the vaginal ring have lower serum estrogen levels than OCPs?
|
vaginal ring has no first-pass effect
|
|
|
3 adverse effects of depoprovera
|
1) irregular menses (30% within 1st yr, 10% after 1st yr)
2) depression and weight gain (5%) 3) delay in ovulation of 9 months |
|
|
how long does norplant last?
|
5 yrs
|
|
|
how long dose implanon work?
|
3 yrs
|
|
|
adverse effect of implanon
|
unpredictable bleeding
|
|
|
how long does mirena work? (hormonal IUD)
|
5 yrs
|
|
|
how long does copper IUD work?
|
10 yrs
|
|
|
active hormone in Plan B
|
levonorgestrel
|
|
|
within how many hours after doing it must Plan B be taken?
|
72 hrs
|
|
|
(Hormone Replacement Therapy 2/8)
what changes occur to the endometrium during early menopause? |
chronic proliferation due to anovulation and continued estrogen production
|
|
|
what changes occur to the endometrium during late menopause?
|
atrophic changes once estrogen production decreases
|
|
|
what causes hot flashes in menopausal women?
|
a relative decrease in estrogen levels
|
|
|
4 hormonal treatments of hot flushes?
|
1) combined OCPs
2) oral progestins 3) injectable progesterone 4) transdermal patches |
|
|
2 non-hormonal treatments shown to decrease hot flashes
|
1) clonidine
2) SSRIs |
|
|
current recomendation of HRT for CAD prevention
|
do not start HRT for CAD prevention
|
|
|
5 contraindications to HRT
|
1) undiagnosed vaginal bleeding
2) acute liver disease 3) active thrombosis 4) hx of breast ca 5) recent endometrial ca |
|
|
What are some of the physiologic changes in the elderly affecting drug absorption?
|
1. decrease gastric acid production
- less absorption of weakly acidic drugs -increased absorption of weakly basic drugs (TCAs) 2. decrease gastric emptying and GI motility 3. decrease splanchnic blood flow |
|
|
What are the physiologic changes in the elderly that affect distribution?
|
1. decrease in total body water and lean muscle mass
-decrease VOD of water-soluble drugs 2. increase in adipose tissue -increases VOD of lipid soluble drugs |
|
|
What are the two main treatments for prostate cancer?
|
Radiation oncology and prostatectomy...no real benefit of one over the other.
|
|
|
What are some possible side effects from radiation oncology as treatment for prostate cancer? What about surgery?
|
Rad onc - bowel and bladder urgency, surg - ED or urinary leakage.
|
|
|
What is the main controversy about screening for prostate cancer?
|
Screening probably over-diagnoses PCA, only 3% of men actually die from their PCA, should men over 65-70 yoa actually be screened? ultimately, you need to consider the pt's co-morbid conditions and the decision is the patient's
|
|
|
What drugs are studies saying should augment radiation in the treatment of prostate CA?
|
Hormones, but be careful of side effects like hot flashes, wt gain, decreased muscle strength.
|
|
|
What side effect made DES now prohibited in the treatment of prostate cancer?
|
Blood clots!
|
|
|
What are the 7 drugs we need to memorize that inhibit the CYP450 3A4 metabolism system?
|
macrolides, CCBs, antidepressants, azole antifungals, protease inhibitors, antiarrhythmics, herbal supplements like grape fruit juice.
|
|
|
In someone who is in renal failure, what do you want to remember about using Digoxin?
|
NEVER load a pt with Dig who is in renal failure since it is renally cleared.
|
|
|
What are the 6 drug classes that inhibit the P-gp pathway of metabolism?
|
antiarrhythmics, macrolides, ccb's, azole antifungals, calineurin inhibitors, and protease inhibitors
|
|
|
What are the inducers of the CYP450 3A4 and P-gp pathways?
|
St. Johns wart, rifampin, phenytoin
|
|
|
What are the ABCs of anyphylactic treatment?
|
Adrenaline, Benadryl, Corticosteroid
|
|
|
What should you do prior to the ABCs of anyphylactic treatment?
|
Start an IV line, oxygen
|
|
|
What is the dose of Epinephrine used in anaphylactic treatment?
|
0.3-0.5ml (EPI 1:1000) IM in the thigh
|
|
|
What is the differential diagnosis for anaphylaxis?
|
vasovagal (bradycardia), hereditary angioedema (will not respond to ABC), carcinoid syndrome, arrhythmia/sudden death
|
|
|
How was the lecture on Colorectal Cancer Chemotherapy?
|
Really boring.
|
|
|
Why should people stay in the ER for several hours after you've treated them for anaphylaxis?
|
risk of protracted/Recurrent anaphylaxis
|
|
|
How is uric acid formed?
|
by the ez xanthine oxidase in purine pathway
|
|
|
What are risk factors for developing gout?
|
obesity, alcohol, drugs (CANT LEAP)
|
|
|
What are the CANT LEAP drugs that may raise uric acid levels?
|
Cyclosporine, Alcohol, Nicotinic acid, Thiazides, Loop diuretics, Ethambutol, ASA at lose dose, Pyrazinamide
|
|
|
What are your options for treatment of acute gouty attack?
|
prednisone, NSAIDs, colchicine, analgesics
|
|
|
When should you treat symptomatic hyperuricemia with a daily prophylactic med?
|
tophaceous disease, multiple attacks in first 1-2 yrs, renal stones
|
|
|
Who should get allopurinol vs. probenecid?
|
Allopurinol for overproducers, tophaceous, renal stones, CrCl <50, more than 81mg ASA
|
|
|
What are the potential benefits of Febuxostat over allopurinol?
|
no renal dosing, greater inhibition of xanthine oxidase, achieve a goal of uricemia <6mg
|
|
|
what 2 drugs should you NOT prescribe pts with eye conditions?
|
1) topical anesthetics
2) topical steroids |
|
|
where do eye drops drain that cause local side effects?
|
nasolacrimal duct and nose
|
|
|
what class of drugs are dilating drops? And what color tops do the eye droppers have?
|
parasympathetic antagonists, red top
|
|
|
when should you not dilate a pupil?
|
history of narrow angle attack or glaucoma
|
|
|
what is the first line drug for bacterial conjunctivits
|
polytrim gtt (polymixin, trimethoprim)
|
|
|
what is the history that is associated with bacterial keratitis of the eye?
|
contact lens use or other trauma to epithelium
|
|
|
What are 2 treatments for HSV keratitis of the eye?
|
1) trifluidine gtt
2) acyclovir PO |
|
|
treatment of viral conjunctivitis
|
nothing
|
|
|
what two drugs are most effective as eye allergy drops?
|
1) mast cell stabilizers (cromolyn)
2) antihistamine (levostin) or combination drop |
|
|
why should you avoid vasoconstrictors for eye allergy drops?
|
causes rebound scleral injection
|
|
|
2 mechanisms of action of glaucoma drugs
|
1) increase drainage through trabecular meshwork
2) decrease intraocular fluid production |
|
|
which type of glaucoma is chronic (open/closed angle) and which is associated with acute pain and loss of vision?
|
open angle - chronic,
narrow or closed angle - acute and ocular emergency |
|
|
two types of glaucoma drugs that increase drainage from eye
|
1) pilocarpine
2) latanoprost (Xalastan) |
|
|
3 classes of drugs that decrease aqueous production in the eye
|
1) beta-blockers (timolol, levobunolol)
2) alpha-agonists (iodipine, brimonidine) 3) carbonic anhydrase inhibitors (acetazolamide) |
|
|
what are the dangers of beta-blocker drops for glaucoma?
|
same side effects as systemic beta-blockers - arrhythmia, asthma, low blood pressure
|
|
|
side effects of alpha-agonists for eye drops
|
1) dry mouth
2) redness in eye 3) in peds - hypotension, hypothermia, bradycardia |
|
|
side effect of carbonic anhydrase inhibitors for tx of glaucoma
|
acidosis, K deficiency, GI upset
|
|
|
what do you use fluoroscein stain for in eye diagnosis?
|
can see trauma or dendrites from HSV better with fluoroscein stain under blue light
|
|
|
in conjunctivitis what lymph node will be inflammed?
|
pre-auricular node (anterior to ear)
|
|
|
some diagnostic clues for narrow angle glaucoma?
|
pupil is mid-dilated,
cornea is ground glass, occured during twilight |
|
|
oral iron preparations
|
1) ferrous gluconate
2) ferrous sulfate 3) fumarate salts 4) heme iron polypeptide (Proferrin) |
|
|
4 side effects of oral iron pills?
|
nausea, abdominal pain, constipation, black stools
|
|
|
4 uses of IV iron
|
rapid replacement
dalysis patients malabsorption severe GI toxicity from oral iron |
|
|
3 side effects of IV iron
|
anaphylaxis, arthalgias, fever
|
|
|
what two serum proteins are elevated in B12 and folate deficiency?
|
1) homocysteine
2) methylmalonic acid |
|
|
what serum protein is elevated in B12 deficiency (not folate)
|
methylmalonic acid
|
|
|
what labs should you draw if you suspect B12 or folate deficiency? (and cut-off levels)
|
1) serum B12 (low is <350 pg/ml
2) serum folate (low is <3-5 ng/ml) |
|
|
if yellow IV bag is already hanging and you suspect B12 or folate deficiency, what two labs should you draw?
|
1) methymalonic acid
2) homocysteine |
|
|
3 major causes of B12 deficiency?
|
1) pernicious anemia
2) malabsorption (post-gastrectomy) 3) poor intake (vegan or alcaholic) |
|
|
6 causes of hyperhomocysteinemia?
|
1) B12 deficiency
2) folate deficiency 3) cystathionine B-synthase deficiency 1/100,000 4) inborn error of B12 and folate metabolism 1/500.000 5) anti-folate drugs (methotrexate) 6) renal failure |
|
|
4 conditions that require vitamin B6 therapy
|
1) homocystinuria
2) X-linked siderblasic anemia 3) drug toxicity (INH, theophylline) 4) acquired sideroblastic anemia |
|
|
symptom of B6 toxicity
|
sensory neuropathy
|
|
|
4 reasons for vit K replacement
|
1) prevent hemorrhagic dz of newborn (no gut flora)
2) correct over anticoagulation with warfarin 3) correct or prevent deficiency from malabsorption, antibiotics, or NPO 4) augment poor liver synthesis in obstructive jaundice |
|
|
why do you need to give IV vitamin K slowly?
|
prevent anaphylaxis
|
|
|
What is the MOA and histamine antagonists? When are these drugs helpful?
|
Blocks H2 receptors on parietal cells in the stomach. Good for acute treatment of PUD -- 2 to 3 months.
|
|
|
What is the MOA of proton pump inhibitors?
|
Irreversibly blocks the release channel of any acid-releasing cell at the H/K ATPase pump --> make more parietal cells that secrete acid.
**Inappropriate use of these drugs will create the symptoms you are trying to avoid-->create an addiction. -prazoles |
|
|
When should patients take a proton pump inhibitor?
|
before breakfast for full day coverage
single dose covers about 17 hrs/day |
|
|
Omeprazole and esomeprazole decrease the clearance of which drugs?
|
Diazepam, phenytoin, warfrin
|
|
|
What are the differences in efficacy of PPIs for PUD and GERD?
|
PUD = no difference
GERD = marginal benefit using emeprazole |
|
|
What is the one major side effect of PPIs?
|
All PPIs (save pantoprazole) decrease the efficacy of clopidodrel (consider H2)
KNOW THIS |
|
|
What is the role of IV proton pump inhibitors?
|
reduce risk of bleeding of high risk peptic ulcers treated endoscopically
|
|
|
What is a non-system approach to PUD?
|
mucosal protection - sucralfate
|
|
|
What is the MOA of metaclopramide?
|
Prokinetic agent; increase esophageal and gastric emptying
best anti-nausea (zofran is an anti-emetic) |
|
|
What is the main side effect of metaclopramide in people > 60yo?
|
Parkinsonism
tardive dyskinesia irreversible |
|
|
When does H. pylori infection occur?
|
First 5 years of life; not everyone gets PUD/cancer/lymphomA
|
|
|
T/F: H pylori causes GERD.
|
FALSE - NO ASSOCIATION
|
|
|
What is the easiest test for eradication of H pylori?
|
Stool antigen after 2 weeks of being OFF PPI.
|
|
|
What are the four drugs needed to eradicate H pylori?
|
PPI
2 antibiotics (ampicillin, tetracyl, metro, biaxin) Pepto Bismol for 10-14 days |
|
|
What are the three drugs to treat anti-diarrheals?
|
Loperamide (imodium)
Diphenoxylate/atropine (Lomotil) Bismuth subsalicylate (Pepto) |
|
|
When do you give antibiotics for diarrhea?
|
Before stool tests come back:
fever > 101 or dysentery Travelers (not asia): cipro or rifaximin Travelers (Asia): azith Hx of antibiotics: Metro |
|
|
What is the treatment for first episode of genital herpes?
|
1. Nucleoside analog - terminates DNA strand of viral DNA polymerase
Acyclovir - drug of choice Famciclovir Valacyclovir |
|
|
What is the reatment for recurrent genital herpes?
|
Nucleoside analogs with different doses (Famcyclovir 125) and shorter duration (5 days)
|
|
|
What is the treatment for frequently recurring genital herpes?
|
Nucleoside analogs bid or qd
recurrences decrease over time; consider stopping therapy yearly to reasses |
|
|
Which form of HSV is the main cause of encephalitis?
|
HSV-1
|
|
|
What is the treatment for HSV1 encephalitis?
|
Acyclovir - only nucleoside analog available IV
treat before LOC and within 24hr of symptoms onset; nucleoside analogs only prevent disease from moving to adjacent neurons, it can't help neurons already infected |
|
|
What is the treatment for influenza?
|
(old school)M2 inhibitors-blocks the M2 protein which forms a proton channel necessary for replication;amantidine and rimantadine
new school = neuraminidase inhibitors; inhibit the release of new progeny virons from infected cells; oseltamavir and zanamavir; only decrease duration of symptoms |
|
|
Which influenza virus is M2 inhibitors useful?
|
type A
|
|
|
In which patients must you be careful with zanamavir?
|
COPD or asthma
zanamavir is inhaled |
|
|
Treatment for mild-moderate RSV
|
Supportive care (o2, ventilation, bronchodilators)
Ribovirin approved but not shown to be affective; non-toxic |
|
|
How do you define chronic HBV?
|
HBV present and replicating > 6mos.
HbeAg + |
|
|
Treatment for Chronic HBV?
|
nucleoside and nucleotide analogs
immune modulators (interferon) can be used but have bad side fx |
|
|
What is the nxt step in a patient failing with monotherapy for HBV?
|
add on a second agent with different resistance pattern
|
|
|
Treatment for HCV?
|
6-12 months of:
Immune modulators: interferon and Inf-alpha Nucleoside analog (ribavirin) |
|
|
How do you dx acute HIV infection?
|
HIV-RNA level
pts may still be HIV Ab neg during seroconversion |
|
|
Where are the targets in the HIV replication cycle for anti-retrovirals?
|
co-receptor binding
viral fusion to host Tcell reverse transcriptase Integrase (insertion into the genome) Protease - regulates nucleocapsid assembly |
|
|
MOA of NRTI (nucleoside reverse transcriptase inhibitors)?
|
competitive inhibition of the active site of viral reverse transcriptase (RNA -> DNA)
e.g. AZT |
|
|
MOA of NNRTIs (non-nucleoside RTI)?
|
non-competitive (allosteric) inhibition of viral reverse transcriptase -- blocks at a different site from the active site
|
|
|
MOA of protease inhibitors?
|
competitively inhibits the processing of Gag and Gag-Pol precursors preventing viral maturation
|
|
|
MOA of fusion inhibitors?
|
block fusion of viral and cellular membranes by binding the GP41 subunit of HIV surface glycoprotein
peptide --> must be injectible |
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What is the combination of HAART (highly active antiretroviral therapy)?
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2 NRTIs + 1 NNRTI + PI (?)
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When do you start a pt on HAART?
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1. AIDS defining illness, regardless of CD4 count
2. asymptomatic infx with < 350 CD4 |
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Why do we use triple therapy?
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Avoid resistance: the virus replicates a lot and makes a lot of mutation BUT simulataneous mutations causing resistance to all drugs in one viron is unlikely
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Why does resistance to anti-retrovirals limit future treatment options permanently?
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Since HIV can go dormant at any time in a lymph node, mutations get archived and become impossible to clear from the patient
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What are the common toxicities from anti-retrovirals?
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hematological toxicity
mitochondrial dysfunction renal toxicity metabolic abnormalities allergic reactions |
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What is the most successful prevention of mother to child transmission?
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HAART reduces transmission by 95%
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What is the course of post-exposure prophylaxis for HIV?
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1. Begin ASAP preferably within hours, def within 48-72 (tx ineffective >72 hrs)
2. triple drug regimens treat for 28 days 2 NRTIs and 1 PI. |
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What is the total lifetime risk of developing breast cancer?
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1/8 (assuming life expectancy of 85)
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What are the THREE categories of breast cancer in the context of chemo-adjuvants?
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ER+ (use anti-estrogens +/- chemo), Her2+ (use herceptin + chemo); Triple-negative (chemo + possible new genetic targets)
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What are the FOUR types of hormone therapy in breast cancer treatment?
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Tamoxifen (partial est. agonist); Aromatase inhibitors (prevent est. production); Fulvestrant (est. antagonist); Ovarian ablation (reduce est + prog production)
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Name the two main categories of dementia, and give a few examples of each
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Reversible (10/20%): Drugs, toxins, neoplasms, infection; Irreversinble (80-90%): Alzheimer’s, Prakinson’s, AIDS, TBI
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What is the overall prevalence of Alzheimer’s for people over 65? Over 85?
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5-10%; 30-40%
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What is the genetic difference between early and late onset Alzheimer’s?
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Early (<65): likely autosomal dominant, APP (amyloid precursor protein) mutation on chrom 21 (reason for assoc. w/down’s); also presenelin 1/2 on chrom 14/1; LATE(>65): APOE gene on chrom 19 (E4 allele = higher risk, E2 = protective)
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What are the two classes of toxic gas inhalation?
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Highly soluble: quickly absorbed so affects eyes, oro/nasopharynx (i.e. ammonia); Low soluble: not absorbed on entry so affects deep pulmonary structures (i.e. Nitrates)
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What is MOA of mustard gas?
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quickly cyclizes in tissue, alkylates cell components (including DNA), causes DNA damage, cell death (Specifically: Eye - corneal damage/blindness, Lung: dyspnea, pulm. fibrosis, lung cancer, bone marrow: immunosupression)
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How is a clinical diagnosis of nerve agent exposure confirmed? What is the Tx?
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cholinesterase test in lab (nerve agents are anti-cholinergic, like organophosphates but more volatile/potent); Tx = decontaminate (remove clothes, wash) and Atropine, Benzos
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What is the best way to dose pediatric drugs?
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Based on weight
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How is the ped's gastric pH different from an adult (thus affecting absorption)?
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They have a basic pH until age 2.
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How is the pediatric body composition different from an adult (thus affecting drug distribution)?
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Babies have lots of water, low protein/fat vs. adults that have less water and higher protein/fat.
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Which phase of drug metabolism (I or II) is more decreased in neonates? How might this change in childhood?
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Phase I is decreased in neonates, but in childhood it may even exceed adult metabolism.
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What drug is an important inhibitor of CYP450 in peds?
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Azoles
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What drug is an important inducer of CYP450 in peds?
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Barbs
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How is renal elimination of drugs affected in premature infants/neonates?
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Decreased, since kidneys were not regulating the fluid in the womb.
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Can you take an NSAID with food?
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Yes
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How are NSAIDs metabolized?
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Via the liver (mostly by CYP450) (check liver fxn at 1 mo and q 4mo.)
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How are NSAIDs eliminated? (they can damage this same organ system)
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Renally (check renal fxn at 1 mo and q 4mo.)
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What is the MOA of an NSAID?
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inhibitor of COX, thus decreasing PG and TXA2 synthesis.
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What are the beneficial effects of NSAIDs?
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analgesia, antipyresis, anti-infalmmatory, decreased platelet aggregation
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What is the major side effect/toxicity seen with NSAID use?
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GI complaints, including esoph erosions and gastric ulcers, also can see hepatotoxicity.
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Is vioxx still on the market?
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HELL NO!!!! and someone was very upset about that!
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what does ASA toxicity cause?
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tinnitus
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What is the standard rx of Stage 1 lung cancer?
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surgery alone!
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With lung cancer, what is important to distinguish for treatment?
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Histology! There are many meds that will work for either squamous cell OR non small cell, but not both!
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What are some toxicities seen with the EGFR inhibitor Erlotinib (used in lung cancer)? How is this drug better than chemo?
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acne-like rash, diarrhea and nausea, conjunctivitis, interstitial pnuemonitis (rare but fatal)......but UNLIKE chemo it does not suppress the bone marrow!
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What is the role EGFR mutations play in the treatment of non small cell lung cancer?
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They are oncogenes (drivers of the cell tumor) and so detecting these mutations may determine which patients are more likely to benefit from EGFR thymidine kinase inhibitors. Watch out for developing resistance tho!
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