Pharmacology Flashcards
What are some critical concepts to understand when treating infectious endocarditis?
Need long treatment duration Use mainly high dose IV antibiotics Need bactericidal activity Combinations of antibiotics for synergy Use preventative antibiotics for high risk patients
Whats the treatment regimen for an endocarditis caused by enterococcus??
Pen + Gentamicin
OR
Amp + Gentamicin
Synergy = -Cillin + Aminoglycoside.
Describe the pharmacodynamics and Pharmacokinetics of aminoglyosides.
IV or IM admin small volume (can be toxic in high concentrations) Weight based dosing "dosing weight" between ideal and actual. Real function is important consideration (Nephrotoxic in 50% of patients)
Limiting adverse effects:
Pulse dose every few days
De-escalation when possible
serum and renal monitoring
Describes some important characteristics of aminoglycosides
It’s a concentration dependent killer. Peak/MIC
It has a post antibiotic effect; where bacterial growth is inhibited for a time after drug levels drop below the MIC (space out dosing).
Resistance encountered- enzymatic drug inactivation
Used with other drugs b/c (No aerobic activity, and No G+ activity)
Used for aerobic G- : i.e. E.coli, Kleb. P, Pseudomonas
Describe the mechanism of action of aminoglycosides
The aminoglycosides are irreversible inhibitors of protein synthesis and are considered bactericidal.
They diffuse through porin channels to cross the outer membrane in G- bacteria.
It then crosses the cell membrane through an oxygen dependent process and is helped by the penicillins in this process=synergistic effect.
What are the beta-lactam drug families?
How do they work?
When is an allergic reaction of a beta-lactam drug not a condraindication for therapy with another type of beta-lactam drug.
Penicillins, Cephalosporins, Monobactams, and Carbapenems
They prevent the cross linking of peptidoglycan in the bacterial cell-wall by binding to the PBP or transpeptidase.
If the allergy is mild or delayed with a penicillin for example, you can still use another beta lactam drug, such as a cephalosporin, as a drug therapy.
What feature of carbapenems enables them to fight G- bacteria without a aminoglycoside?
They are less sensitive to Beta lactamases produced by bacteria.
Which Carbapenem has no Pseudomonas aeriginosa activity?
Which is combined with cilastatin?
What are some side effects you should be concerned about?
Ertapenem
Imipenem-protect it against renal enzymes that degrade it
Seizures, and allergic reactions with other beta lactams drugs, and C.diff (b/c its a broad spectrum antibiotic)
At the end of gym class you leave the building a step on a nail which penetrates you shoe, through your sweaty sock and causes you to fall down in pain. A swab from the area a few days later is taken from pus coming out of the infected wound and is found to have a green pigment and ferments lactose. Which drug therapy would be mostly reliable in treating this infection?
A) Oxacillin B) Vancomycin C) Ertapenem D) Meropenem E) Aztreonam
Meropenem
Although Ertapenem is also a carbapenem it doesn’t have activity against Pseudomonas Arg.
Aztreonam can have activity against this bacteria but its less reliable 78% and you would have to consult your hospitals antibiogram
The others are not even close because they treat gram +
Your patient has a MSSA infection and you decide to treat it with Tobramycin, because you know it has activity against this type of infection. What else should you consider doing?
A) Treat with Aztreonam
B) Include penicillin
C) use dexamethazone for inflammation
D) Increase the length of time for treatment to increase effectiveness.
B. Tobramycin is an aminoglycoside and works only against aerobic G- bacteria. Another antibiotic must be used with it to fill in its gaps in coverage and work synergistically with it; penicillin could do this.
Aztreonam has the same problem with coverage though its a monobactam
Increasing concentration would be important for an aminoglycoside (be careful of renal toxicity)
List 3 extra-cardiac adverse effects from amiodarone
Pneumonitis leading to pulmonary fibrosis
Decreased AV or SA node function
Decreased Contractility of the heart leading to hypotension
Discuss the impact of the CAST study results on drug treatment of cardiac arrhythmias
Proarrhythmic events can occur in as many as 5-10% of patients receiving antiarrhythmic agents
Catheter ablation and implatable devices to treat arrhythmias has larely relegated drug therapy to a secondary role: 1) Decrease frequency of recurrences in patients with infrequent episodes of benign tachycardias 2) Those with incomplete success with ablation 3) Patients with ICD (intra cardiac devices) to decrease frequency of shocks due to ventricular arrhythmia.
What are four common ways to reduce ectopic pacemaking activity using pharmaceuticals?
1) Na+ block
2) Sympathetic block
3) Increase effective refractory period
4) Ca2+ block
Crash cart antiarrhythmic Drugs. Your patient has SVT which drugs should you use in which order to treat them? Briefly describe each drugs effect and pertinent details?
1 Adenosine: vasodilation, decrease chronotropic and dromotropic effects (SA & AV node) 10 sec half life.
2 Verapamil: L-type Ca2+ channel blocker: decreases inotropic, chronotropic and dromotropic effects as well as vasodilation (which is common to all Ca2+ channel blockers)
3 Diltiazem: Similar to verapamil-Use with Atrial fibrillation
Bradycardia crash cart drugs
Atropine- Anticholinergic: Increases HR & AV nodal conduction
Dopamine & Epinephrine- Sympathetics are basically anticholinergics
