Archive for Presentations

ICU Reflection & EMERG Day 1

Antibiotics that DO NOT need to be renally adjusted:

  • penicillin VK
  • cloxacillin
  • ceftriaxone
  • moxifloxacin
  • azithromycin
  • erythromycin
  • clindamycin
  • metronidazole
  • doxycycline
  • linezolid

ICU Presentation Reflection- Antibiotic dosing in obesity

  • PREPARATION, organization and MESSAGE
  • antibiotics that are hydrophilic do not require dosage adjustment in obesity ( generally, assume that Vd and Cl is the same to that of a patient with normal BMI)

Emerg Rotation day 1

  • CoQ10 can interact with antihypertensives (add-ative) and warfarin ( decrease effect)
  • PERL: pupil equal and reactive to light
  • if a patient is receiving warfarin therapy, they do not require DVT prophylaxis with heparin

STROKE 101

  • Dx: Ct is definitive
  • Primary:
    • alteplase?
    • antiplatelets
    • BP
    • LOC?
    • glucose ( BG less than 10)
    • seizure ( do not need empiric tx)
    • Na
    • DVT prophylaxis ( delay if alteplase given…wait 24 hours)
  • Secondary:
    • HTN
    • statin
    • afib: ECG, 24 hour horter for proximal afib
    • CEA ( Carotid endarterectomy-A procedure by which a surgeon gently removes atherosclerotic plaque that has accumulated inside the internal carotid artery) for carotiid artery stenosis <– U/S ( cause?)
    • diabetes  (Hba1c, FPG, STT, 2HR post prandial glucose, random glucose)

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ID- Week 3

Presentation this Wednesday on need for double coverage in patients with pseudomonal pneumonia. The presentation was well attended and there was some discussion on the increasing resistance of 3rd gen ceph for pseudomonas aeruginosa.
  • For patients with c diff and toxic megacolon, TOC is po vanco
  • staph epi with hardware: vanco
  • sildenafil  & nitroglycerin=  Nitroglycerin works by increasing nitric oxide, and it helps with angina by opening up the arteries that supply the heart with oxygen. If you take nitroglycerin and Viagra together, the increased nitric oxide plus the blocking of PDE5 can lead to problems. Consistent with its known effects on the nitric oxide/cGMP pathway, sildenafil was shown to potentiate the hypotensive effects of nitrates. Deaths have been reported in men who were using sildenafil while taking nitrate or nitrite therapy for angina. Nitrates amplify the vasodilatory effects of sildenafil or other phosphodiesterase inhibitors (e.g., vardenafil) if coadministered and result in severe hypotension
  • perforation = rupture
  • enterococcus coverage endocarditis with prosthetic valve= gent + vanco x 6 wk
  • yeast= branching fungi= aspergillus
  • enterococcus found in GI (gut) and GU (bladder)
  • echo doesn’t exclude endocarditis
  • meningitis: ceftriaxone q12h in guidelines, but q24 h in study
  • UTI diagnosed by (1) urinalysis (2) urine culture (3) clinical signs and symptoms
  • pre- renal: Prerenal causes of AKI are those that decrease effective blood flow to the kidney. These include low blood volumelow blood pressure, and heart failure. Changes to the blood vessels supplying the kidney can also lead to prerenal AKI. These include renal artery stenosis, which is a narrowing of the renal artery that supplies the kidney, and renal vein thrombosis, which is the formation of a blood clot in the renal vein that drains blood from the kidney.

ex) Ramipril, an angiotensin-converting enzyme (ACE) inhibitor, is metabolized to a more potent ramiprilat (active drug). Both prevent the conversion of angiotensin I to angiotensin II, a vasoconstrictor agent, which decreases vasopressor activity and aldosterone secretion

ex) Furosemide is an anthranilic acid derivative and a potent diuretic that works by blocking the absorption of sodium and chloride in the kidney tubules (proximal and distal tubules, also in the loop of Henle), causing a profound increase in urine output .

  • intrinsic: Those causes that lead to damage to the kidney itself are dubbed intrinsic. Intrinsic AKI can be due to damage to the glomerulirenal tubules, or interstitium. Common causes of each are glomerulonephritisacute tubular necrosis (ATN), and acute interstitial nephritis (AIN), respectively.
  • postrenal: Postrenal AKI is a consequence of urinary tract obstruction. This may be related to benign prostatic hyperplasiakidney stones, or an obstructed urinary catheter.
  • mucomucosa: erode into bone, in sinus, TOC: surgery, then amph B x months
  • azole: always check interactions
  • azole: static
  • echinocandin: static
  • amph: cidal
  • static: rely on immunsystem
  • invasive endocarditis: echinocandin
  • cidal for : (1) endocarditis (2) meningitis (3) neutropenic or immunosuppressed patients
  • combo antifungal use in the future
  • echinocandin work on cell wall
  • ketoconazole is oldest azole with the narrowest coverage, poor CNS penetration
  • fluconazole: good absorption, penetrate CNS
  • itraconazole: not well absorbed, good for aspergiosis, but not as good as voriconazole; liquid is better absorbed
  • posaconazole: same as vori, but better coverage
  • albican cultures are differentiated by: (1) pseudopod (2) germ tube
  • candiasis is a yeast; aspergillosis is a mold
  • azole is not as good for candida krusei or glabrata

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Surgery- Day 5

We continued to review our patients today. I am now following up with 5 patients.

Patient 4:  DRP- Patient is currently receiving daily glucose testing for insulin s/s; however, her BG has been consistently normal for +4 days and does not have a history of diabetes. Patient is experiencing x 8-9 bouts of diarrhea daily, c. difficile? Awaiting culture. Monitor for magnesium and potassium levels + dehydration .

Patient 5: Upon discussion with the patient, the patient brought up that she has been on an antidepressant for 4 weeks. She has been receiving this as a sample from her doctor, so it did not show up on PharmaNet. Pt does not have the medication with her/ no friend or family to retreive med from home. Pt does not know the dose of the medication ( thinks it’s cipralex?). I phoned her family doctor to gather more info and found that she has been receiving escitalopram (cipralex) 10 mg qam x 3 weeks. Her last follow up with the doctor was 3 days ago and her mood has been improving. VGH does not carry escitalopram on formulary. Suggest giving patient an equivalent dose of citalopram 20 mg instead ( 1/2 the potency of escitalopram).

Patient 6: impaired renal clearance with history of acute renal failure 1 week ago? current creatinine clearance: 40 mL/min. Renal adjust vanco and fluconazole. pre-vanco level : 17.2 mg/L ( target : 15-20mg/L)

FMI:

  • CPAP- A continuous positive airway pressure (CPAP) machine was initially used mainly by patients for the treatment of sleep apnea at home, but now is in widespread use across intensive care units as a form of ventilation. Obstructive sleep apnea occurs when the upper airway becomes narrow as the muscles relax naturally during sleep. This reduces oxygen in the blood and causes arousal from sleep. The CPAP machine stops this phenomenon by delivering a stream of compressed air via a hose to a nasal pillow, nose mask or full-face mask, splinting the airway (keeping it open under air pressure) so that unobstructed breathing becomes possible, reducing and/or preventing apneas and hypopneas.
  • What is considered a major surgery that requires q8h for heparin dosing in DVT prevention? laparotomy, surgery requiring general anesthesia, surgery that is greater than 30-40 minutes
  • serum creatinine 5mg/dL= 44mmol/L
  • erythromycin : prokinetic effect for ileus paralysis
  • resis oxacillin: resis methacillin: MRSA
  • bactrum: SMX/TMP
  • pip, carbapenem and pen high can lead to seizures
  • fluconazole: liver toxicity
  • diltazem and verapamil (CCB): primarily afib
  • swallowing assessment is done by the speech language pathologist (SLP)

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Distribution- Day 7

Hayley and I went over our workflow recommendations to Jeremy today. We also had some discussion about whether the paperless system has decreased frequency of errors.

Eric and I did our presentation for lytes during the academic half day today.

The presentation went well. I think that the latter section about the cases was more helpful for everyone. The cases provided a good overview about all the material that we had previously covered during the ppt. Eric was a very good presenter. He went at a very good pace and asked many thought provoking questions that led to constructive discussions. This is some thing I should work on.

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TPN Clinical – Day 5

Last day of TPN Clinical on Friday. I did my presentation to Corry and Ken on my last day. The presentation went well. I should try to condense some of the material in the future because the presentation may have been too comprehensive for a 25 minute presentation. Nevertheless, I think that it went well. I feel that I benefited alot from putting the presentation together. It was a good overview of all the knowledge that I’ve learned from this week. This will come in useful with any future patients I have who are also on TPN.

FMI:

  • not many medications are incorporated into the TPN bag. Some that can be incorporated include regular insulin, heparin or ranitidine

Mouth is sore today. Took all 4 wisdom teeth out at once…..oww. I plan on sleeping through the weekend.

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Medicine- Day 19

Last day at LGH today for the medicine rotation. I am sad to see it end. The staff at the LGH have all been extremely friendly and supportively towards my learning. I will miss them alot.

Yesterday, I received news from Beth that one of my patients had passed away after been transferred to SPH. He had a history of alcoholic cirrhosis and was awaiting a liver transplant. Unfortunately, his kidney made a turn for the worse on Wednesday and he passed away later that evening. I feel very sad for the patient and his wife.

Didatic on alcohol withdrawal:

  • DMS IV: dependence: ( 3 of following): tolerance, withdrawal, use more or longer than intended….
  • Abuse: example being social problems–> essentially, it is anything that affects functionality
  • mild withdrawal: sx in 0-48 hr, peak 24-48 hr, resolve: 48-72 hr
  • 40% pt die if not treated: mostly from CV reasons or metabolic disturbances or infections
  • DT: delirium tremens: delirium, horors, fears, disorientation, tremors, hallunciations, diarrhea anxiety
  • CAGE: cut down, annoyed, guilty, eye opener
  • agitation is the most common side effect
  • CIWA: clinical institute withdrawal assessment for alcohol
  • disadvantage of CIWA: need to communicate ( sedated patient or language barrier)
  • advantage of CIWA: prn
  • evidence for CIWA: decrease treatment duration, decrease BDZ dose, decrease sx
  • reason for thiamine: (1) thiamine deficiency (2) wernicke’s encephalopathy: ataxia, confusion, memory problems, eye paralysis
  • thiamine is found in grains and eggs, some patients are put on multivit ( help with other nutritional deficiency- ex. B12)
  • CIWA protocol : option A: diazepam, option B: lorazepam
  • lorazepam is more easily broken down compared to diazepam in renal/hepatic impairment
  • lorazepam has less risk of respiratory depression on diazepam
  • MOA of alcohol withdrawaL: alcohol bind gaba, gaba is an inhibitor, increase stimulation from SNS –> seizure, gaba is up regulator b/c of alcohol ; therefore, more gaba receptors; bdz bind gaba receptor
  • watch for decrease opioid or pt will be over sedated
  • overadherence of CIWA: agitated for other reasons
  • CIWA protocol : duration of 5 days usually

Case presentation today

The presenation went well today. The pharmacists asked lots of thought provoking question about the case, which led me to think of other alternatives and also to question my own recommendation. The case was a discussion about the use of clopidogrel and ASA combination for a post MI patient. I discussed a few trials, including the MATCH, CHARISMA and CAPRIE trial. I think that I will spend more time looking into the recent landmark trials discussion the interaction between clopidogrel and PPI. These studies will play a significant role in the interpretation of the case. It would also be more helpful if I can remember specific population inclusion criterias and the absolute event rates for the trials included. One of the pharmacist also explained to me that the CAPRIE trial was not an ITT trial. When he recalculated the numbers, the data was not ss. The absolute risk is likely very miniscule, or less than 1%.

Procedure Log:

I was able to order a pre and post level for a new gent dosing for a patient. The patient has renal impairment and we were not sure how the medication was going to be cleared. In addition, the patient is also a very big, tall man, so conventional dosing may not be appropriate.
Secondly, I was able to interpret a digoxin level for the same patient. The level came back as 2.1 and it was taken 19 hours post dose, which is within the ideal 12 to 25 hour range. The target for our elderly patient is less than 1 to 1.5 because he is experiencing sx of weakness and anorexia when he was first admitted. Digoxin experiences linear pharmacokinetics. His current dose is 250mcg daily. Our patient weights 170 lbs, IBW: 86.8. It was suggested that the patient’s dose be decreased to 185.7 mcg daily to achieve a trough digoxin dose of approx 1.5. We would then monitor the patient for sx improvement and heart rate control. Bisoprolol was also added to the patients’s current therapy for better rate control.

Areas of improvement for the future:

1. Pay attention to the small details when doing a work up… they can make a big difference! 
2. Try to go the next level with your formal topics… memorization or better understanding will help you apply the knowledge to your patients.

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Academic Half Day- Project Presentation

Code Black= bomb

Code Red= fire from bomb

Code Yellow= missing patient who set off the bomb

We had our project presentation at SPH. I got many good feedback that I plan on implementing for my project. Some of these suggestions include:

  • classifying adverse events into either severe or minor events
  • defining shock
  • define DKA and HHS diagosis

Other things that I’ve learned at the AHD:

  • cohort study –> look at % of pt receiving drug and go forward to see outcomes
  • case study–> look at outcome and go back to see % of pt receiving drug

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Medicine- Day 11

Today, I lead a journal club discussion on the use of dabigatran vs warfarin in afib patients at risk of experiencing a stroke. My journal CONSORT assessment is available at my e-portfolio for viewing. There was a good discussion that happened after the paper presented. Some interesting questions were brought up that lead to interesting ideas.

Below is the CONSORT assessment on the trial assessed:
Dabigatran versus Warfarin in Patients with Atrial Fibrillation

Didactics on DVT/PE:

  • DVT- virchow’s triad : (1) abnormalities of blood flow ( afib, obestity, bed rest, tumor), (2) abnormalities of clotting ( estrogen, preg, malignancy, thrombocytosis- platelet only, myloproliferative disorder – increased WBC and others) (3) abnormaliities of surfaces in contact with blood ( vasuclar injury, trauma)
  • for temporary DVT risk that can be resolved: bridging warfarin therapy can last 3 to 6 months
  • heparin tx for DVT: (1) 1 mg/kg BID enoxaparin or 1.5 mg /kg daily enoxaparin  (2) 175 units/kg daily for tinazparin (3) dalteparin : mostly for prophlaxis and surgery
  • (1) enoxaparin: more cardiac (2) tinzaparin : least renaly affected (3) dalteparin: mostly prophylaxis & surgery
  • LMWH: antiXa: antiIIa (2:1- 4:1); no aPTT monitoring, sc only; longer action–> pk stable- less binding; reversible
  • UFH: iv or sc ; irreversible; half life: 30 min to 2 1/2 hour ( short)
  • aPTT monitoring : q6 h, then daily when PTT stable
  • LMWH monitoring: anti-Xa
  • UFH switch to LMWH–> wait 12 hour ( based on half life)
  • no IM heparin–> cause hemotoma ( bruising)
  • heparin: ( large dose) affect Xa & IIa directly; ( small dose) affect Xa, indirectly inhibit IIa
  • DVT Prevention: (1) enoxaparin 30 mg BID or 40 mg daily (2) dalteparin 2500-5000 daily for surgery (3) 15 units/ g tinzaparin
  • venography: use contrast dye–> anaphylactic rx sometimes
  • HIT type 1: happens in 1st several days; moniroting –> don’t D/C  heparin
  • HIT type 2: happens between day 5 to 14–> d/c heparin ; don’t switch to LMWH
  • PE: Dx by VQ scan–> breath in –> check where blood perfuses to –> X ray to see if blood stops somewhere–? ventolation perfusion
  • PE: tx in hospital, not for outpatient therapy
  • vit K: take orally, given quickly–> anaphylactic rxn ( SOB, flushing)
  • INR more than 5, no bleed: skip dose
  • INR 5-9 , no bleed:  vit K 0.5- 2.5 mg orally
  • INR more than 9, no bleed: vit K 5-10 mg orally
  • DIC (Disseminated Intravascular Coagulopathy)–> clot & bleed at the same time; trigger: infection/malignancy; increase INR; increase aPTT; decrease pH; Clot in microvascular area ( brain, kidney, etc); don’t tx with anticoagulant; tx cause, fluid replacement, sx management; controversy on the use of heparin and fibrinolytic for management

FMI:

  • topiramate = aka the stupid drug
  • potassium: KCl elixir and Slow K ( 8mmol KCl) are available at the hospital
  • K-Dur  ( 20 mmol KCl) is not available at the hospital

CSHP Clinical Symposium

It has been a few years since my last CSHP clinical symposium. From what I remember from my last encounter, the material flew right over my head. It was very different this time. I felt that I understood the material and was eager to implement it in real practice.

  • ALLHAT: 1/3 black patients; 7 years old trial
  • BB: usually not 1st line in HTN management, no mortality benefit
  • ACCOMPLISH- 11,000 pt at high risk for HTN; CCB outperformed thiazides ( more peripheral edema in CCB; more hypotension in thiazide group; no difference in adverse events); 18% pt had less than 60ml/min GFR~ impaired diuretic efficacy; HCT inferior in bp effect in 24 hr post therapy; chlorthalidone ( half life : 12 hours) –> longer half life than HCTZ; chlorthalidone is twice as potent as HCTZ and they are non-interchangeable
  • risk factors for thiazide induced hyponatremia: lean women, elderly
  • controlled hypokalemia doesn’t correlate with controlled hyponatremia
  • low salt diet may be more effective than initiating therapy? sustained difference?
  • Aliskiren- direct renin inhibitor
  • Olmesartan–> most potent ARB
  • Predialysis solution may interfere with home glucose monitoring–> give false high reading
  • intermetant IP–> concentration dependent antibiotic curve
  • continuous IP–> time dependent antbiotics
  • COPD: nicotine replacement has best cessation rate for COPD smokers
  • inhaled anticholingerics doesn’t increase all cause morality ( meta-analysis: JAMA 2008)

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Day 14- Home IV Program

The morning picked up quickly.

A patient had been accidentally discharged before the CADD pump was connected and the home IV counseling was done. The nurse had overlooked the note saying that the patient should be discharged after these tasks were done. Not only so, the nurse also gave to the patient a prescription for a few weeks of pip/taz IV bags that was clipped inside the chart and asked the patient to fill it at a local pharmacy. It is worthy to note that the prescription had a note on it that said, “Not needed- Home IV program will …have meds sent to the clinic.” This created alot of inconvenience and confusion for the patient and his family. Fortunately, we were able to contact the patient’s son, who was able to bring the patient back to the hospital. The down side was that the patient missed his 12 o’clock dose of antibiotic and this dose was given an hour later than scheduled. An incident report was filed regarding this matter. This incident could have easily been avoided if the nurse had checked the notes or if she had contacted the CML, resident or pharmacist for confirmation of discharge.

This afternoon, I did a presentation for the nurses on “Antibiotics- Spectrum of Activity, a review”. I wish I had done better. One of my goals from my midpoint evaluation was to become more confident and concise in my speech. I wish I had done better. Nevertheless, the nurses told me that they found it very helpful. They also brought up some interesting scenarios from real practice during the discussion portion of the presentation. It was interesting to hear things from their point of view and I felt comfort in that they may have benefited from the presentation.

There was a new patient assessment near the end of the day. This assessment brought up an unique assessment factor that had never came up so far during my rotation, the patient’s social history. Because this had never played a big factors in my previous assessment, it became a challenge in learning to weight the importance of recreational drug use and compliance to home iv therapy.

Useful link: http://www.vhpharmsci.com/

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Day 10 – Didactics

Things I learned from my PICOS presentation ( the “S” in PICOS stands for studies):

1. Be more confident and try not to apologize so much.

2. Have a clear game plan ( preferrable written) of things to say ( a powerpoint presentation does not count as a game plan)

3.  TABLES are always good when presenting results

It was sad to see everyone part, but we look forward to seeing all the residents again in our next case presentation. If ever any of the out of town residents are in Vancouver for a rotation, we have set up plans to have dinner together.It is interesting to hear what the other residents do for their health authority.

For example, the Fraserhealth residents has a seminar series every week. They also have a separate kinetics and evidence based rotation as part of their schedule. However, their rotations are not planned with the idea of having the more advanced clinical based rotation later on in the year, which can be difficult for a resident who has his/her basic pharmaceutical rotation at the end of the year.

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