Cases Flashcards
Ob-Gyn patient, s/p episiotomy – during suturing, very little bleeding, and no complaints of pain. Pt becomes disoriented, mumbling, barely responsive. Warm, flushed diaphoretic, P 140 reg, BP 70/40. H/o - 23yo female, first deliver, no PMH, no meds. Had had an amniocentesis 7d earlier, PROM (30h earlier).
- How would you treat this patient?
- What was the issue?
- Pathophysiology?
- Drugs?
How would you treat this patient? – Stabilize. Start IV, fluids (NS). Trendelenberg position.
What was the issue? – Chorioamnionitis (RF’s - amnio, PROM).
Pathophysiology? – GI/GU/urethral [GNR, anaerobes – Bacteroides, Prevotella, Enterobacteracea, C. trachomatis, Group A,B strep]; skin [Staph, Strep]
Drugs? – Doxycycline (for Chlamydia)+ Pip/Tazo OR Clinda + Gentamicin (or ceftriaxone)
65yo male requires hand surgery, but has extensive CAD and severe HTN. Decided to provide regional IV anaesthesia with lidocaine (what is this?)
Regional IV anaesthesia
1 ) Nerve block
2) Venous then arterial tourniquet [45min] + numbing of nerves – Lidocaine +/- epinephrine
65yo male requires hand surgery, but has extensive CAD and severe HTN. What is the problem with giving him IV epinephrine.
Arrhythmia –> sinus tach –> V tach, V fib
Hypertensive crisis
26yo female in clinic - acute onset of dysruia, freq, urgency, slight hematuria (no fever, chills, abd pain, back pain, flank pain). PE: T 37.5, P 80, BP nml, R 12, very mild suprapubic tenderness, no CVA tenderness. U/A dipstick pos for WBCs, blood. What do you do?
- Dx?
- Pathophysiology?
- Drugs?
Dx - UTI (cystitis)
Pathophysiology - (1) E. coli; (2) Enterobacter, Serratia, Staph saprophyticus, Enterococcus
Drugs - Nitrofurantoin, TMP/SMX, Ciprofloxacin, Cephalexin
–> Phnazopyridine for symptomatic relief of dysuria
In treating an uncomplicated UTI, what are the usual drugs, and which would be problematic with the following?
1) known hives to penicillin
2) known G6PD deficiency
3) She lived in an area with >25% E. coli resistant to co-trimoxazole
5) She had known liver disease
6) She was known to be pregnant
7) She was treated for a UTI one week earlier
Nml drugs = Nitrofurantoin, TMP/SMX, Ciprofloxacin, Cephalexin
1) known hives to penicillin - Cephalexin
2) known G6PD deficiency - TMP/SMX
3) lived in an area with >25% E. coli resistance - TMP/SMX (–> Nitrofurantoin)
4) She had known renal disease
5) She had known liver disease - Ciprofloxacin
6) She was known to be pregnant - Nitrofurantoin in the in T3 or during labor; TMP/SMX 2 wks before EDC (d/t potential increase in kernicterus)
7) She was treated for a UTI one week earlier
A 60-year old man was admitted to evaluate double vision and weakness. His hypertension had been well controlled for 15 years on HCTZ. Six months ago he was placed on penicillamine for refractory rheumatoid arthritis. In retrospect, he feels he has not felt “right” since starting that drug. He mentioned that the double vision was not present on waking, but progressed throughout the day. His PE demonstrated weakness of several extra-ocular muscles. When he received edrophonium 2 mg IV there was prompt resolution of his ocular problems for several minutes. How would you proceed?
- Penicillamine: rare side effect of MG
(improved with edorphonium = acetylcholinase inhibitor - short-acting)
Penicillamine mimics acetylcholine antibody –> attacking the Nm receptors on the NMJ end-plates
A 68-year old man received two weeks of intravenous mezlocillin and gentamicin in the hospital to treat a severe pseudomonal external otitis media. He was discharged home to receive the same drugs for another four weeks (iv home administration by his wife through a PICC line). Five days after he went home, at about 9 PM, his wife presented to a local ER with a severe allergic reaction. She had acutely developed diffuse skin itching with classic urticarial lesions, then wheezing and shortness of breath. She received diphenhydramine and prednisone )no Epi???) in the ER, and her symptoms resolved over the next few hours. What happened to the patient’s wife?
Immediate allergic rxn in penicillin-sensitive wife of pt receiving parenteral mezlocillin ==> high seminal level in wife.
Timing == it was 5 days after (first time they had had vaginal sex), she had been mixing the drug previously without problems.
Type I rxn == should have gotten diphenhydramine + prednisone + Epi (if really having breathing problems).
Possible that could have dripped on hand – but have to assume that can be absorbed transcutaneously
A patient with known chronic stable angina is admitted to the CCU with new onset unstable angina and pancreatitis. His usual outpatient medications include nitroglycerin 0.4 mg SL when necessary for chest pain, hydrochlorothiazide 25 mg by mouth once daily for hypertension, and prompt release metoprolol 25 mg by mouth thrice daily to control hypertension and chronic angina. In the CCU, you wish to continue (or possibly increase) his metoprolol to prevent withdrawal (or “rebound”) worsening of his angina, but the surgical consultant insists that he remain “NPO” with an NG tube to put the pancreas at rest.
Write specific orders in the chart for giving this man his metoprolol.
Cannot stop metoprolol abruptly = rebound
Can convert metoprolol PO –> IV
2.5:1
F = 1/2.5 == 40%
Metoprolol = 75mg/d PO ==> 30mg/d IV
You admit a 70-year old alcoholic man to the hospital to treat a large carbuncle, and he begins to demonstrate signs and symptoms of alcohol withdrawal. To prevent the development of delirium tremens, you begin treatment with diazepam 5 mg by mouth four times daily. After three days, the patient seems quieter and less agitated, and you decide to continue the drug. He is discharged on the fourth hospital day, with strict instructions to continue his diazepam and oral antibiotic as ordered. The patient was apparently very scared during this admission, and promises that he will take his drugs faithfully; his daughter states that he will be staying with her for the next two weeks, and promises to make sure that he takes his medicines as ordered.
One week later (10 days after starting the diazepam), his daughter brings the patient back to your clinic, saying that he keeps falling asleep and can barely stay awake to eat or dress himself. She says that she can’t care for him in this state, and you will have to either admit him, or place him in a nursing home. Also, she is worried because she has never seen him like this before, except when he has been drinking heavily. She is sure this is not the case, because she has no alcohol of any kind in the house. How do you explain this patient’s course based upon pharmacokinetic principles?
Diazepam is very lipid-soluble ( can stop a seizure in 2-4min)
==> if lipid-soluble ==> metabolized by the liver
Pt could also have alcoholic fatty liver / cirrhosis
t 1/2 of elimination in healthy liver (diazepam) = 24h
Steady-state concentration @ 3.5d
t 1/2 of elimination in cirrhotic liver (diazepam) = 72h
Steady-state concentration @ 10-12d
He was discharged at 3-4days at 5mg of diazepam ==> reaching steady state at 10-12d later –> he should have been kept longer, or given a lower amt.
t(1/2) = 0.7 * Vd/Cl
b/c the pt is likely cirrhotic == increased t (1/2) –> decreased clearance of the drug.
When epinephrine is added to a 1% lidocaine solution to be used as a local anesthetic, the main therapeutic goal is to:
A. Help prevent vasovagal syncope with the local injection
B. Reduce the initial pain from the local injection/infiltration
C. Prolong the duration of action of the local anesthetic with local infiltration
D. Buffer the pH of the solution to prolong the shelf life of the local anesthetic
E. Help maintain the patient’s blood pressure during the procedure
C. constricts the blood flow, decreasing the uptake of the drug – increasing its duration of action.
bupiviaine is better for reducing bleeding (specifically)
You are treating a woman for a case of cystitis, and the gram stain of her urine reveals lots of PMN’s and plump gram negative rods. She tells you that she has been healthy prior to this acute problem, but she does know from a prior drug experiences that with her Mediterranean background, she is deficient in the enzyme glucose-6-phosphate dehydrogenase. Which one of the following possible oral antibiotics that you are considering prescribing would be most strongly contraindicated for use in this patient?
A. Ampicillin B. Cefuroxmine C. Doxycycline D. Nitrofurantoin E. Ciprofloxacin
D. nitrofurantoinn == on the DANGER list of drugs NOT to give people with G6PD deficiency.
quinolones are on the “likely do not give”
A fourth-year medical student is planning to go into a general surgery residency, and then pursue further training in plastic surgery. Why is it important for that student to learn about the advantages and disadvantages of the newer or atypical antipsychotic drugs (such as quetiapine) as compared to the older drugs of this class like haloperidol or chlorpromazine?
A. One of the intern’s post-op patients may develop an acute dystonic reaction after receiving Compazine™ (prochlorperazine), given for post-op nausea and vomiting
B. One of the intern’s plastic surgery patients may develop post-op ICU psychosis, and may require treatment with an optimal neuroleptic drug in the ICU
C. Step 3 (at the end of internship) will test the intern’s knowledge in this area
D. The intern may become concerned about potential anesthesia/drug interactions with one of these newer drugs
E. All answers are correct
F. One of the intern’s plastic surgery patients may be on one of these newer drugs preoperatively
E. the 2nd generation / atypical antipsychotics are more likely to cause extrapyramidal sxs.
In this course, when we discuss a particular medication, we will always refer to that drug with its generic name, and often with its brand name as well. It’s useful for you to learn both names for a drug primarily because:
A. On board examinations, all drugs will be referred to by their generic names
B. In most states, you can order a drug by either its generic name or its brand name
C. Some smaller pharmacies will stock only one version of a drug, sometimes generic, sometimes branded
D. In most states, if you prescribe a drug by its generic name, the pharmacist will dispense the generic version of the drug
E. You will usually want to prescribe the drug by its generic name, but patients and doctors often remember the brand name better
E. Best answer - “you will usually want to prescribe the drug in generic form”
In his 2015 paper in The Lancet, Dr. Simon Maxwell discussed the importance of every medical school in Great Britain making sure that its graduates received adequate training the the knowledge and skills necessary for their graduates to become safe and effective prescribers when they became new interns. They also developed a national on-line exam that could be taken (and is now required to be taken) by all senior medical students in the UK, prior to graduation, and passing the exam prior to beginning their internships. This national effort involving all UK medical schools, and all UK teaching hospitals, was motivated in part by the earlier discovery that some percentage of prescriptions (or drug orders) written by newly graduated doctors in UK teaching hospitals contained errors ranging from minor to life-threatening. How large was this problem, according to his paper?
A. 10% B. 15% C. 30% D. 20% E. 5%
A. 7-10% of prescriptions written by interns are incorrect
A 32-year-old Caucasian female needs analgesia after oral surgery for a root canal/ tooth implant preparation. She is prescribed PO tramadol 37.5 mg combined with acetaminophen 325 mg two tablets twice a day. She contacts her dentist the following morning saying she is still in significant pain and the dentist increases her dose to two tablets every six hours. A day later she goes to see his PCP still complaining of severe tooth and jaw pain on the side of her dental surgery. Oral examination shows edema and inflammation at the surgical site. Altered activity of which of the following enzymes is MOST LIKELY responsible for the therapeutic failure of the analgesic regimen in this patient?
A. Prostaglandin synthase B. CYP 450 3A4 C. CYP450 2D6 D. Cyclo-oxygenase-1 & 2 E. CYP450 2C9 F. Cyclo-oxygenase 3
C. Acetaminophen and tramadol metabolized by both Cyp450 3A4 and 2D6
Tramadol esp. a substrate for 2D6
74 year old male with congestive heart failure and atrial fibrillation is well controlled on the following drug regimen, furosemide, spironolactone, lisinopril, carvedilol and warfarin. His most recent INR is 2.6 and has been stable on his current warfarin dose of 3 mg/ day. The patient develops a community acquired pneumonia, which has progressed over 5 days despite azithromycin treatment, and requires hospitalization. Concomitant prescription of which of the following as part of combination drug therapy to treat his refractory pneumonia will necessitate an INCREASE in warfarin dose to maintain anti-coagulation?
A. Piperacillin/tazobactam B. Azithromycin C. levofloxacin D. cefoperazone E. rifampin
E. Rifampin is the only one of the group that is a Cyp inducer
A 55-year-old liver transplant patient is on cyclosporine as part of his immunosuppressive therapeutic regimen. His trough cyclosporine concentrations have been stable at 200-250 mcg/L (therapeutic range 150-300 mcg/L). He develops what was treated as a lower respiratory tract infection and received a course of antibiotics. Several days after starting the antibiotic he noted bilateral hand tremor and was taken to the ED having sustained a self-limiting seizure. A random cyclosporine concentration done in the ED was 775 mcg/L. Which of the following drugs was he MOST LIKELY prescribed, that caused this adverse outcome?
A. Minocycline B. Amoxicillin/clavulanate C. Clarithromycin D. Doxycycline E. Cefditoren
C. Clarithromycin is the only of the group that is a Cyp inhibitor
A 52 year old man is admitted to hospital with a one week history of dark urine and pale stools. On examination he is jaundiced without physical signs of chronic liver disease. His total bilirubin is 14.9 mg/dL (direct bilirubin is 13.5 mg/dL) ALT and AST are 45 and 39 iu/L respectively and the Alk phosphatase is 90 iu/L . His prothrombin time is 18 seconds (INR 2.0). Further investigation does not identify an extra hepatic anatomical/viral/toxicological or immunological cause for his elevated bilirubin. His comorbidities, CAD and mild CHF are well controlled on his current drug therapy. Which of the following drugs this patient is taking is the MOST LIKELY cause of his jaundice?
A. Eplerenone B. Atenolol C. Clopidogrel D. Lisinopril E. Rosuvastatin
C. Clopidogrel
+ Rosuvastatin
==> intrahepatic cholestasis
A 25-year-old healthy man who weighs about 70 kg goes into a bar at 6 PM (mostly empty stomach). While he is there he drinks 3 beers, and 4 shots of vodka.
He leaves the bar at 8 PM, and drives to his girlfriend’s house
He drives for about ½ hour, and then arrives at her town
As he is driving down the street, at about 8:30 PM he strikes an elderly man with a cane who is crossing the street. He does not see him, and does not stop.
The next day, he sees blood on his front fender, and a large dent, and vaguely remembers something from the night before. He learns that there was a hit-and-run accident the night before two blocks from his girlfriend’s house.
He turns himself into the police that next morning, and his BAC is zero at that time. The police determine that his car is the one that hit and killed the little old man in the crosswalk.
What was his approximate BAC at the time of the accident? Was he driving “under the influence”?
3 beers
4 shots of vodka
BEER: 12oz * 3 * 14g ethanol = 42g EtOH
VODKA: 1oz * 4 * 14g ethanol = 46g EtOH
==> 98g EtOH
Vd = 0.6 L/kg == 42L
Cp(max) = 98g/42L == 2.3g/L == 2300mg/L
(if he absorbed all of it without clearing it)
legal limit of alcohol == 800 mg/L
LIVER METABOLISM = 120mg/kg/h
==> 120mg/70/h
== 8.4g/h * 2h
== 16.8g cleared by the time he left the bar
98g EtOH - 16.8g == 81.2g EtOH left in his system
Which of the following drugs is CORRECTLY paired with the urological tract adverse effect it is MOST often associated with?
A. Sulfamethoxazole + Trimethoprim/nephrolithiasis
B. Ketorolac/ureteric strictures
C. Omeprazole/increased tubular reabsorption of sodium
D. Atenolol/reduced renal efferent arteriolar resistance
E. Dobutamine/acute tubular necrosis
A. Sulfa drugs cause obstructive uropathy (post-renal)
not very soluble
An 81 year old man has been noted to have blood pressure recordings of between 185/110 and 175/100 mm Hg for the last three visits to his PCP’s office. His home blood pressure monitoring revealed a BP average of 168/102 mm Hg. He is not overweight, does not smoke cigarettes or imbibe ethanol. His serum creatinine is normal for his age but his eCrCl is 45 mL/min (eGFR 50 ml/min/1.73 m2). His PCP initiates therapy with hydrochlorothiazide 12.5 mg daily. In this patient which of the following effects would this therapy MOST LIKELY cause?
A. Hypomagnesemia B. Hyperphosphaturia C. Hyperoxaluria D. Hypo-osmolar urine E, Hypocalcemia
A. Hypomagnesemia
–> hypercalcemia == leading to stones
In patients with normal renal function, 80 % of the administered dose of a newly FDA approved H2 receptor antagonist (pergeiseldine) is excreted unchanged in the urine. In patients with normal renal function, the standard persgeiseldine dose is 100 mg PO q 12h. Your patient who is 84 years old and has an estimated creatinine clearance (eCrCL) of 25 mL/min (~ 1/4 of normal). What dose of pergeiseldine would you give 12 hourly to achieve the same average serum steady state concentration (Css-av) as a patient with normal renal function?
A. 40 mg B. 10 mg C. 25 mg D. 75 mg E. 60 mg F. 85 mg
A. 40mg
Consider nml clearance = 100mL/min
80% - kidneys ==> 100mL/min
20% - liver
Consider pt’s clearance = 25mL/min (25%)
(1/4) 80% - kidneys ==> 20mL/min
20% - liver==> 20mL/min
== 40mL/min cleared
If given 40mg,
• A 21-year old woman sees you in the clinic, complaining of 4 days of dysuria, frequency, and urgency. Over the last 12 hours she has noted shaking chills, fever, nausea, vomiting, malaise, and right flank pain. She had several urinary tract infections in high school, but none in the last few years. She is taking no other meds. Her last period was one week ago. She says that when she last received ampicillin several years ago, she passed out and required epinephrine because of a breathing problem. On exam, she is a fit young woman lying uncomfortably on the stretcher who appears warm, diaphoretic, and flushed. Her temperature is 103 F orally, BP 95/60 (lying) and 85/50 (sitting), pulse 120, respirations 16. There is marked right costovertebral angle tenderness, mild right flank tenderness, and moderate suprapubic tenderness. Pelvic and rectal exams are unremarkable except for some bladder tenderness. Urinalysis reveals many white cells and bacteria; gram stain of the unspun urine reveals many WBCs and many plump gram negative rods per high-power field. Creatinine is 0.7 mg/dl. Approach this case using the framework that we discussed in class. Discuss the diagnosis, and present your detailed plans for management.
o Dx – pyelonephritis, with concern for distributive sepsis
o Pathology – GNRs = likely E. coli (she is young, prior hx of UTIs)
o Typical methods of treatment = Outpatient (Ciprofloxacin 500mg BID, Levofloxacin 750mg q24h, Ofloxacin 400mg BID x5-7d); Inpatient (Ciprofloxacin 400mg IV q12h; Ampicillin 2gm IV q6h + Gentamicin 5mg/kg q24h OR Ceftriaxone 1-2g IV q24h OR Piperacillin-Tazobactam 3.375g IVq4-6h)
o Tx for this pt - she is an outpatient, but she likely need to be admitted for concerns of sepsis, and she had an anaphylactic/anaphylactoid rxn to ampicillin so no penicillins or cephalosporins if other good regimens exist – Get cultures/sensitivities + empiric Ciprofloxacin 400mg IV q12h x5-7 days.
• A 68 year-old Caucasian woman with no significant past medical history, was unwell with a non productive cough, intermittent fevers and muscle and joint aches for over a week. She lost her appetite during this period, and had been taking extra strength acetaminophen (Tylenol) two 650 mg tablets every 6-8 hours most days during this illness, to relieve her symptoms. Over the prior 24-36h she noticed her urine had become dark and her skin rather yellow. Her bilirubin was 4.2 mg/dL, AST and ALT were 1350 and 1140 U/L respectively; Alk. Phos. - 230 u/L; Tot. Protein - 7.2 g/dL and Albumin - 3.2 g/dL; PT - 19 seconds (INR 2.2). Plasma acetaminophen conc. = 13 mg/L (therapeutic range 10-20 mg/L). What is the diagnosis and how would you manage this patient? How could this clinical situation have been prevented?
o Dx: acetaminophen-induced acute liver injury
o Risk factors for drug-induced acute liver injury (DILI): female (likely d/t smaller size); alcohol abuse; malnutrition.
o Prevention:
1) improved nutrition
2) advice on cautious use of acetaminophen use. The recommended limit of acetaminophen is 3000mg per day (she was taking 1300mg every 6-8h, so ranging from 3900-5200mg).
3) Review of other medications – if she was concurrently taking medications for what may have been a flu, she may have taken a Cyp inhibitor, which would have lead to accumulated, toxic levels of acetaminophen (though the serum level was not supratherapeutic).
• A 58 year old man with moderately severe coronary artery disease and is being treated with metoprolol 100 mg bid, diltiazem SR 160 mg bid and sublingual nitrates prn. He takes atorvastatin 40 mg at night for hypercholesterolemia. He comes to your office complaining that he feels tired and depressed since started on the combination anti-anginal therapy, though his angina is well controlled. You decide his symptoms are, in part, drug induced but also in part due to depression. Treatment with nefazodone 100 mg bid (a non-SSRI antidepressant) is begun. Two weeks later the patient says he feels no better, the nefazodone dose is increased to 200 mg bid. When reviewed one week later he complains that for the past week his muscles have been aching especially after some exercise and that his legs feel weak. What assessments/labs should you perform? What is the etiology of this problem? What precipitants should he avoid? What genetic test may show him to be predisposed to this? How would you manage the patient clinically?
o Assessment: The major point from his history was the increase in his nefazodone, which is a Cyp3A4 inhibitor. His current symptoms mimic statin toxicity, as statins are as well metabolized through the liver. It is likely that higher doses of nefazodone led to decreased Cyp3A4 activity, causing accumulated statin levels. o Labs: Assessment of his liver, since nefazodone toxicity can cause acute liver injury – AST, ALT, Alk phos, Tbili, DBili. o Avoid: Any Cyp inhibitors. If he continues to require the nefazodone, he should also avoid drugs that are metabolized by the liver. However, it is more likely that he would be switched to a different antidepressant since he will require the statins for his moderately severe CAD. o Genetic test: Cytochrome p450 3A4 mutation panel and Cytochrome p450 3A5 DNA test – since 5% of those of European origin have a slow-acting, intermediate metabolizer form of Cyp3A4. o Management: 1) Gradual taper of nefazodone over weeks to months as tolerated 2) Start on an alternative anti-depressant. Bupropion is in the similar class of non-SSRI antidepressants. Bupropion is a Cyp450 2D6 inhibitor, but statins are processed through the Cyp450 3A4 pathway, so this is a potentially safer option than SSRIs, which are processed through Cyp450 3A4.
• Write a complete prescription for yourself for a ten-day course of ampicillin for a UTI. This is legal, but what are you “missing” if you go this route??? What are the eight essential parts of this Rx, and why are they important?
o Ampicillin will cover most of the gram-positives, but would miss some of the gram negatives (E.coli, Klebsiella that are the common culprits of UTIs) and beta-lactamase producing bacteria (which would be better covered by a regimen of Amoxicillin-Clavulanate).
o Prescription
1) Date: 01/30/2018
2) Name: Stacey T Chu
3) Rx: Augmentin
4) Formulation: Amoxicillin-Clavulanate 875/125mg tablets
5) Dispense: #14 tablets
6) Label: Take 1 tablet, twice daily, for 7 days for urinary tract infection
7) Renewal: none
8) Prescriber contact info: Stacey T Chu, (818)470-8414
• A 60-yo man (otherwise in good health, creatinine 1.6 mg/dl) developed acute, severe pustular psoriasis. After several weeks of not responding to topical treatments, he was referred to a dermatologist. He decided that the most appropriate treatment given the severity and acuity of the disease would be oral methotrexate (MTX). He explained this to the patient (regimen Monday 8 PM, Tuesday 8 AM and 8 PM), handed him a pamphlet about use of MTX in psoriasis, and gave him a prescription for
o Methotrexate 2.5 mg tablets
o Dispense #60
o Label: Take 2 tablets every 12 hours 3x/week.
o Patient was instructed to have CBCs checked every Monday morning for weeks 1,2,4, and 6, and to return to Derm clinic in week 6. Patient was seen in drop-in clinic 3 days after beginning this regimen for complaints of burning of his skin, and some worsening of his skin lesions. CBC and LFTs were checked because of his history of having been recently started on oral MTX; all were normal. He was discharged on antihistamines. Four days later he was admitted with sepsis and severe pancytopenia. Any thoughts?
o Per UptoDate: methotrexate dosing is 15mg-25mg/week (maximum), with absorption of oral methotrexate reduced at higher doses – such that subcu or IM administration is preferred. This patient was 22.52 = 10mg per day, 30mg per week, which is an incredibly high dose.
Dermatologic toxicity: His symptoms of skin burning and worsened skin lesions is likely a result of methotrexate toxicity, which can cause a dermatologic toxicity ranging from a nonspecific morbilliform drug rash to a bullous formation or desquamation. A secondary bacterial infectious over these bullae or desquamated areas may have led to his sepsis
Hematologic toxicity: methotrexate toxicity can lead to myelosuppression and thus his severe pancytopenia.
o While the major problem is with the initial dosage, I wonder if folate repletion may have helped with his problem.
o 90% of methotrexate is cleared by the kidneys. With the patient’s eCrCl = (140-60)/1.6 = 50, he has roughly 50% of the expected clearance. Renal dosing would have required that the dose be given at 50% of normal (for CrCl 10-50 mL/min).
• What are four important factors that the FDA considers in deciding whether a given drug preparation can be safely sold over the counter without a prescription?
1) Adequate labeling so that consumers with low literacy can understand and so that the consumer can self-diagnose, self-treat, and self-manage the condition being treated
2) No health practitioner is needed for the safe and effect use of the product.
3) Drugs have low potential for misuse and abuse
4) Safety margin such that OTC availability benefits > risks.
When you write an order for a drug to be given “prn” or “as needed” in the hospital chart or EMR, you must also supply what further bit of information that is most often forgotten by the prescriber?
A. Interval of dosing B. Dose of drug C. Indication for repeat dosing D. Name of drug E, DEA number
C. Indication for repeat dosing
Need both interval AND indication (indication is most often forgotten)
In 1906 when the first legislation about the FDA was passed in Congress during the “Progressive Era”, the actual bill stated that in order for drugs to be approved by the FDA, they had to be proven to be:
A. Accurately labeled in terms of content and purity of ingredients
B. Safe
C. Effective
D. More effective than previous treatments for the same condition
E. Non-addicting
A.
Pure Food & Drug Act of 1906 - prohibited mislabeling and adulteration of drugs
Nowadays, most new drugs are first approved for prescription use only, and then later, the FDA might make a decision to allow the drug, often at the lower end of the dose range, to be sold over-the-counter and without a prescription. Recently we have seen such a pathway with drugs such as several antihistamines, several H2 blockers, several PPIs, etc. When the FDA makes the decision to allow a relatively new drug to be sold over the counter without a prescription, they usually are paying close attention to all of the following factors EXCEPT which one?
A. Lack of severe toxicity when the drug is taken as directed (e.g. acetaminophen)
B. Evidence that the drug is not habit-forming or addicting, or regulated by the DEA
C.Cost of the drug
D. The ability of the patient to make an accurate self-diagnosis (e.g. GERD)
E. The ability of a typical patient with 8th grade reading ability to understand the necessary safety information printed on the box
C. cost of the drug -yes, they’re usually cheaper, but the FDA is not interested in that
These OTC are for drugs that can reasonably help pt’s self-diagnose
(not like cancer drugs, etc.)
In 2009, three faculty members at DMS (Drs. Lisa Schwartz, Steven Woloshin, and Gil Welch) published a paper advocating that direct-to-consumer ads about prescription drug typically fail to provide fundamental information that consumers need to make informed decisions about how well a particular drug might work for them. They proposed that providing patient a drug facts box—a carefully formatted table quantifying important outcomes with and without the drug (or comparing one drug with a second drug)—could improve patient knowledge and affect patient judgments about prescription medications. The authors concluded that the specially formatted drug facts box, when present in such direct-to-consumer advertisements:
A. All answers are correct
B. Helped consumers appreciate how well each of the drugs actually worked
C. Resulted in better choices by consumers between two drugs for current symptoms
D. Corrected overestimation of drug benefit in the setting of drugs used for prevention
A.
of course all of these are correct dummy
Which one of the following is the most important way that an allergic drug reaction (such as red macular rash from penicillin) differs from the more common type of pharmacologic adverse drug reactions (such as hypokalemia from hydrochlorothiazide)?
A. Allergic drug reactions are usually more severe than pharmacologic drug reactions
B. Drug allergies are more common than pharmacologic adverse drug reactions
C. Allergic drug reactions are usually easier to predict in advance by using skin testing
D. Allergic drugs reactions are not related to the usual pharmacodynamic properties of the drug
E. Allergic drug reactions are usually easier to treat than are pharmacologic drug reactions
D. allergic rxn are not expected from the pharmacodynamic properties
A 54-year-old woman previously in good health presents to the ER with the sudden onset 30 minutes earlier of severe pain in her left flank, which radiates down to her left groin. This pain comes in waves every few minutes. At its worst, she says it is 10 out of 10, subsiding back down to 2/10, but not going away completely. She has not noticed any other symptoms. Her vital signs and abdominal exam are normal except for a tachycardia of 110/min. Her basic lab studies are normal, except for her urinalysis, which is positive for a pink color and is dipstick 2+ positive for blood. She is given ketorolac intravenously for her pain , and that seems to have helped a bit. 30 minutes later she undergoes a CT of the abdomen with IV contrast (Renografin™, or sodium meglumine diatrizoate) in an effort to identify the location of her stone. A few seconds after receiving the iv bolus of contrast (Renografin™), she says she feels warm and flushed all over her body. A few seconds after that, she begins to break out in hives all over her thorax and arms. She then begins to wheeze, and her blood pressure falls from 130/80 on admission to 90/54. She says that she feels woozy and lightheaded, and that her lips feel puffy to her, but she is still alert and oriented. She has most likely experienced:
A. An anaphylactoid reaction to ketorolac
B. An anaphylactoid reaction to Renografin™
C. A Type III reaction to ketorolac
D. An anaphylactic reaction to ketorolac
E. An anaphylactic reaction to Renografin™
B. An anaphylactoid reaction to Renografin™
Anaphylactoid are clinically indistinguishable from anaphylaxis –> but usually are d/t:
- contrast
- morphine
- aspirin (induced bronchospasm)
A 54-year-old woman previously in good health presents to the ER with the sudden onset 30 minutes earlier of severe pain in her left flank, which radiates down to her left groin. This pain comes in waves every few minutes. At its worst, she says it is 10 out of 10, subsiding back down to 2/10, but not going away completely. She has not noticed any other symptoms. Her vital signs and abdominal exam are normal except for a tachycardia of 110/min. Her basic lab studies are normal, except for her urinalysis, which is positive for a pink color and is dipstick 2+ positive for blood. She is given ketorolac intravenously for her pain , and that seems to have helped a bit. 30 minutes later she undergoes a CT of the abdomen with IV contrast (Renografin™, or sodium meglumine diatrizoate) in an effort to identify the location of her stone. A few seconds after receiving the iv bolus of contrast (Renografin™), she says she feels warm and flushed all over her body. A few seconds after that, she begins to break out in hives all over her thorax and arms. She then begins to wheeze, and her blood pressure falls from 130/80 on admission to 90/54. She says that she feels woozy and lightheaded, and that her lips feel puffy to her, but she is still alert and oriented. , which one of the following treatments is most important to deliver to her immediately at this point in her case?
A. Diphenhydramine 50 mg PO stat
B. Cimetidine 150 mg IV stat
C. Normal saline 100 ml IV stat
D. Epinephrine 0.4 mg IM stat
E. Methylprednisolone hemisuccinate 125 mg IV stat
D. Epinephrine 0.4 mg IM stat
Esp. if she is hypotensive
should also give diphenhydramine for the hives and swelling –> but not AS important as her BP crashing
Two pseudo-allergic reactions to ACE inhibitors are cough and angioedema. Cough, which occurs in 15-30% of patients on ACE inhibitors, seems to be mediated by bradykinin, and such patients are often switched to angiotension-receptor blockers, usually with good results. However, 0.2-1.0% of patients taking ACE inhibitors develop angioedema, again thought to be related to the toxic effects of excessive bradykinin. Such patients may benefit from being switched from their ACE inhibitor to an ARB drug, but there is concern about the recurrence of angioedema after such patients are switched to an ARB. If you were faced with such a patient (one who had developed angioedema while taking an ACE inhibitor), what would be your advice to the patient?
A. Such patients should virtually never be switched to an ARB because the risk of developing angioedema is simply too high B. Before switching such a patient to an ARB, the patient should first be switched to a different ACE inhibitor, since angioedema may not be a class effect. C. Such patients may be switched to an ARB, but only if the need for such a drug is great, and appears to outweigh the possible risk of angioedema D. Clinical studies have shown that when such patients are switched from an ACEI to an ARB, the risk of having another episode of angioedema is around 25-50%. E. If such a patient is switched from an ACE inhibitor to an ARB, then the patient should also carry an Epi-PEN in case angioedema recurs. F. If such a patient is switched to an ARB, and if angioedema recurs while on the ARB, then the angioedema that develops on the ARB is usually more severe than the first episode while taking the ACE inhibitor.
C. Such patients may be switched to an ARB, but only if the need for such a drug is great, and appears to outweigh the possible risk of angioedema
usually good to be cautious
At most, cross-reactivity at 10%
This IS a class effect - do not give her another ACE-I!
A patient is undergoing anesthesia induction in preparation for a 3-hour abdominal surgical procedure, a complex resection of part of the colon involved with colorectal cancer, with exploration and removal of regional lymph nodes. The patient is premedicated with midazolam and fentanyl, but general anesthesia is induced with intravenous thiopental given as a slow IV push. Once the patient becomes totally unresponsive, the anesthesiologist quickly acts to paralyze the patient, secure the airway by endotracheal intubation, and initiate ongoing general anesthesia with sevoflurane. The anesthesiologist knows that he must complete these tasks within a few minutes because the general anesthetic effects of this bolus of thiopental will end after about 10 minutes because:
A. t ½ alpha is about 3-4 minutes
B. t ½ beta is about 1 hour
C. the drug redistributes quickly from blood into bone
D. the liver clears the drug very quickly
E. the kidneys eliminate the drug very quickly
A. For “this bolus of thiopental to end after 10min” – the t 1/2 of redistribution must be about 3-4 min (for steady state to be reached in about 10min)
Thiopental redistribution from its site of action (the highly perfused brain) into other tissues (e.g. the poorly perfused adipose tissue) NOT BONE
Sometimes when we look up information about a loading dose of a drug, the information that we find is confusing. For example, when we look up a loading dose of gentamicin, the reference books say something like LD = 2 mg/kg, which doesn’t look like the numbers we discussed in class. That number would be correct if it was based on:
A. Our target Cp is 8 mg/L, and Vd=0.25 L/kg
B. Our target Cp is 4 mg/L, and Vd = 0.6 L/kg
C. Our target Cp is 1 mg/L, and Vd = 1.5 L/kg
D. Our target Cp is 10 mg/L, and Vd = 4 L/kg
E. Our target Cp is 20 mg/L, and Vd = 0.5 L/kg
LD = Cw desired * Volume
A. LD = 8mg/L * 0.25L/kg == 2 mg/kg
Sometimes patients present to the ER with an intentional drug overdose, but often they present with an unintentional drug overdose. According to literature describing deaths from unintentional drug overdoses from 2000 to 2007, these have almost quadrupled. The drug during this period mostly responsible for this sharp increase in the death rate per 100,000 population over this time period was:
A. Heroin B. Benzodiazepines C. Opioid analgesics D. Cocaine E. Barbiturates
C. Opioid analgesics
> cocaine
> heroin
In the last 10 years or so (2007-2017), there has been a further sharp increase in deaths due to unintentional drug overdoses. In this more recent time period, the drug found (by medical examiners’ postmortem drug testing) to be primarily responsible for this sharp increase in drug overdose deaths has been:
A. Oxycodone B. Hydromorphone C. Heroin D. Fentanyl E. OxyContin™
D. Fentanyl
cutting bags of heroin with fentanyl
When balancing the potential benefits and risks of administering a slurry of activated charcoal to a patient with a recent (< 2 hours ago) intentional drug overdose, the largest potential risk in this situation would be is:
A. Precipitation of torsades de pointes by the charcoal
B. The drug ingested does not adsorb to the activated charcoal
C. Anaphylaxis from the activated charcoal
D. Aspiration of the charcoal slurry
E. Severe diarrhea from the cathartic agent given with the charcoal (e.g. sorbitol)
D. Aspiration of the charcoal slurry
esp. if have seizure and vomit –> then aspirate
A 17 yo high school student runs away from home with his girlfriend. After a few days, she decides to return to North Carolina, and he becomes very depressed. He decides to ingest a bottle of mercuric chloride, which he had stolen from his high school chemistry lab back in NC before he drove to NH. You call your poison information center, and find that this chemical is very likely to cause severe acute renal failure, and sloughing of the lining of the GI tract, as well as other toxic effects related to absorption of the inorganic form of Hg++. Which of the following antidotes would be indicated in this particular overdose case?
A. Flumazenil iv B. Desferoxamine iv C. Naloxone iv D. Desferoxamine po E. Calcium disodium EDTA iv F. Dimercaptosuccinic acid (DMSA) po
F. Dimercaptosuccinic acid (DMSA) po
Flumazenil - Benzos
Desferoamine - Iron
Naloxone - Opioids
Over the last two years, in both NH and VT, we have seen a sharp increase in deaths related to use of heroin. This recent increase has been termed a crisis in both states, and has led to legislation to permit broader distribution of naloxone to doctors, users, and first responders likely to witness such events.
The main factor which has led to heroin use to be associated with so many more ER visits and deaths in the last two years or so appears to be:
A. As bags of heroin have become much less expensive, users are buying and then injecting larger and larger doses of heroin
B. Increasing but unknown amounts of fentanyl have been added to heroin powder to make it appear to be more potent to users
C. The heroin is cut by levamisole, which itself is acutely toxic
D. Drug dealers are distributing heroin in a more pure and therefore potent form
E. As drug cartels in Mexico have changed recently, heroin for intravenous use has become more contaminated with endotoxin, which is highly toxic
B. Increasing but unknown amounts of fentanyl have been added to heroin powder to make it appear to be more potent to users
You are Medical Director for the development of a novel compound with new mechanism of action in treating diabetic ulcers. You are working with your development team to design the first in human study of this compound. Which of the following clinical trial characteristics is MOST important in the trial design?
A. The study provides categorical data on the therapeutic efficacy of the vaccine
B. A phase 0 study must be performed prior to the dose escalation study
C. The study cohorts do not treat normal healthy volunteers
D. The study cohorts receive sequentially escalating doses of the vaccine
E. The study does not have subjects treated with placebo
D. The study cohorts receive sequentially escalating doses of the vaccine
Phase I (first in human)
- no need for therapeutic efficacy
- phase 0 is optiona
- normal healthy volunteers
- escalating doses
- placebo controlled
