1. Fever (>38C/100.4F) or Hypothermia (<36C/96.8F)

2. Tachypnea (RR>20-24 breaths/min)

3. Tachycardia (HR>90bpm)

4. Leukocytosis (>12-14cells/mm3 or microL), Leukopenia (<4000), or >10% immature bands

1. Systemic Inflammation

2. Procoagulant State

3. Reduced Fibrinolysis

1. Pulmonary

2. Intraabdominal

3. Urinary Tract

1. Age: infants, >65

2. Weak immune system

3. Hospitalized

4. Urinary cath, artificial joints, breathing tubes, surgical incisions, wounds, burns

5. Long term AB use

1. Nitric Oxide

2. B-endorphin

3. Bradykinin

4. PAF

5. Prostacyclin

Type 1: Pro-inflammatory

Type 2: Anti-inflammatory

1. Progressive high-output cardiac failure - cannot sustain high CO 

2. Circulatory failure - severe vasodilation and hypotension refractory to resuscitation 

2 organs ~50%

3 organs ~ 70%

5 organs ~100%

1. Respiratory (~18% of pt)

2. Circulatory

3. Renal (~15%)

1. refractory hypoxia

2. decreased lung compliance

3. noncardiogenic pulmonary edema

4. pulmonary hypertension

hyperdynamic state

- high cardiac output

- abnormally low systemic vascular resistance

1. adequate renal perfusion

2. trial of loop diuretics

1. respiratory alkalosis

2. leukocytosis

3. mild liver function abnormalities

leaky capilaries and altered protein binding = increased Vd

drugs (esp. AB) will have lower serum concentrations

Levofloxacin (Levaquin)

Moxifloxacin (Avelox)

Gemifloxacin (Factive)

Imipenem - G(+)

Meropenem - G(-)

Seizures rates are probably similar.

1. amphotericin B based preparations

2. azole antifungals

3. echinocandin antifungals

4. combo of fluconazole with amphotericin B

Of the amphotericin-B products available, what is the brand name for:

1. Convential amphotericin B (C-AMB)

2. Colloidal dispersion (ABCD)

3. Liposomal (L-AMB)

4. Lipid Complex (ABLC)

1. Fungizone 

2. Amphotec, Amphocil 

3. Ambisome 

4. Abelcet

What happens when CAMB is given with the addition of electrolytes?

CAMB - Fungizone

ABCD also has more chills and hypoxia than CAMB and premedication can be used to reduce febrile reactions

What are the ADE related to LAMB?

How should Ambisome be administered?

Nephrotoxicity, hypokalemia, infusion-related reactions

In D5W with initial doses infused over 2 hours (doses up to 10mg/kg)

Amphotericin B + dimyristoylphosphatidylcholine + dimyristoylphosphatidylglycerol = ?

Which is more nephrotoxic, LAMB or ABLC?

ABLC - Abelcet

ABLC

binds to sterol moiety (primarily ergosterol) in membranes -->

polyenes appear and form pores/channels -->

increased membrane permeability -->

leakage of small molecules

Which amphotericin-B formulation acheives the highest blood levels?

Which formulation has the worst infusion-related reactions?

What is used for pretreatment?

Rankings for nephrotoxicity?

LAMB - Ambisome

ABCD (Abelect) > CAMB (Fungizone) >

ABLC (Amphotec, Amphocil) >LAMB (Ambisome)

APAP (po) or IV hydrocortisone hemisuccinate (0.7mg/kg)

ABLC<LAMB<ABCD (lipid formulations are less nephrotoxic)

1. Supplemental K -1/3 of pts on prolonged therapy should get it

2. Saline loading - administer 1 L of IV NS on the day CAMB is given

What are the 2 broad classes of azole antifungals? Which agents are in each class? Differences between the two classes?

What is their shared MOA?

1. Imidazoles - 

(clotrimazole, miconazole, ketoconazole, econazole, butoconazole, oxiconazole, sertaconazole, sulconazole)

2. Triazoles -

(terconazole, itraconazole, fluconazole, voriconazole, posaconazole, isavuconazole) - systemic drugs, metabolized more slowly and less effects on sterol synthesis.

MOA: inhibition of 14-alpha-sterol demethylase (microsomal CYP)

- impairs the biosynthesis of ergosterol (for cytoplasmic membrane)

- results in accumulation of 14-alpha-methylsterols (causes disruption of packing of acyl chains of phospholipids = impaired function of membrane enzymes and inhibited growth)

Fluconazole:

1. Class

2. CYP inhibitor

3. Route of Elimination

4. T½

5. CSF availability?

6. PPB?

7. ADE?

8. Pregnancy category? Breast milk?

9. Formulations

Diflucan(R):

1. Triazole

2. CYP3A4, 2C9

3. >90% renal excretion (adjust interval based on creatinine clearance)

4. 25-30h

5. yes, 50-90% of plasma levels

6. ~10%

7. reversible alopecia may occur, rare hepatic failure or SJS

8. Preg C, + breast milk

9. T(50,100,150,200), Susp(10,40mg/mL), IVwNaClorDextrose(200mg/100mL;400mg/200mL), 

Voriconazole:

1. Class

2. Metabolism/Inhibition

3. T½

4. IV formulation component that is excreted entirely by the kidneys and accumulates if CrCl<50mL/min

5. Preg Class?

6. ADEs

7. Formulations

B: Vfend

1. Triazole "conazole"

2. CYP2C19 (Asians=poor 2C19), 2C9, 3A4

3. 6h

4. SBECD - sulfobutyl ether B-cyclodextrin

5. Preg Class D

6. hepatotox, QTc prolongation, visual, anaphylactoid, rash

7. T(50,200mg), Susp(40mg/mL), IV(200mg)

Echinocandins:

1.  MOA

2. Susceptible fungi

3. Resistant mutation

1. inhibit glucan synthesis complex in plasma membrane that catalyzes the sythesis of glucan = reduced integrity of cell wall = osmotic instability and death

2. Candida and Aspergillus

3. Fks1p, a subunit of glucan synthase

1. Caspofungin (Cancidas) 70mg

2. Micafungin (Mycamine) 75mg

3. Anidulafungin (Eraxis) 200mg

Which echinocandin:

1. has the shortest t½ and smallest Vd?

2. is water insoluble and diluted in ethanol for IV infusion?

3. is a mild CYP3A4 inhibitor?

4. has the longest t½ and largest Vd?

1. Cancidas (Caspofungin)

2. Anidulafungin (Eraxis)

3. Micafungin (Mycamine)

4. Anidulafungin (Eraxis)

1. increases intravascular volume

2. enhances cardiac output 

3. delays development of refractory hypoxia

What is mean arterial pressure (MAP)?

Equation?

average arterial pressure during a single cardiac cycle

MAP = (CO*systemic vascular resistance)+ central venous pressure

Where do crystalloids increase volume?

Which fluids are crystalloids?

Extracellularly: 25% intravascular and 75% extravascular

NS (0.9% sodium chloride/154mEq/L-NaCl), lactated ringer solution (130mEq/L of Na), & hypertonic saline(513mEq/L-NaCl)

Which are colloids?

What are some advantages of colloids over crystalloids?

How do colloids distribute in the body?

1. 5% albumin, 6% hetastarch (synthetic)

2. more rapid restoration of intravascular volume (> expansion per quantity infused), preferred when serum albumin <2.0g/dL

3. intravascularly, albumin can shift fluids from intracellular and interstitial spaces

What are 2 inotropic agents used to improve CO?

When do you use vasopressors?

What are some complications of inotropes and vasopressors?

Dopamine + Dobutamine

SBP<90mmHg or MAP <60-65mmHg after adequate LV preload and inotropic therapy

tachycardia, myocardial ischemia, myocardial infarction

1. Which cardiovascular agent used in septic shock has dopaminergic activity?

2. Which agent has no activity at B2 receptors?

3. Which agent has the most activity at both alpha and beta receptors?

4. Which agent has the least activity at the alpha receptors?

1. Dopamine

2. Phenylephrine

3. Epinephrine

4. Dobutamine

Which receptors does epinephrine affect at low doses? high doses?

What are the benefits of epinephrine?

ADE?

Administration/Formulation?

1. Low doses - B2 stimulation (skeletal muscle dilation)

2. High doses - Alpha stimulation (constriction of blood vessels in kidney, skin, mucosa)

↑ contractility (inotropic) + ↑ HR (chronotropic)= ↑ CO (also ↑ SV and LV work/beat)

increased lactate level, impaired bloodflow to splanchnic system

IV infusion, SQ, IM inj, nebulized, inhaled

1. What are the brand names for injectable epinephrine devices?

2. Injectable solution? Nasal solution?

3. What is the name of the OTC aerosol solution?

1. Adrenaclick & Twinject (0.15mg/0.15mL, 0.3/0.3)

EpiPen (0.3/0.3) and EpiPenJR (0.15/0.3)

2. Adrenalin 1mg/mL and 0.1%

3. Primatene Mist (0.22mg/act)

1. increased relative duration of diastole at higher HR

2. Increased strenght of contraction and myocardial oxygen consumption from direct effects of epi on cardiac myocytes → metabolic dialator effect

How does epinephrine affect the tone of the stomach?

What are the metabolic effects of epinephrine?

If tone is relaxed it causes contraction.

If tone is high it causes relaxation.

1. Elevated glucose and lactate concentration in blood.

-Insulin secretion is inh by an int with a2 and enhanced by act of B2

-Glucagon secretion is enhanced by action at B receptors on pancreatic alpha-cells 

-Epi stimulates glycogenolysis (through B receptors)

2. Elevated FFA concentration

- stimulation of B receptors in adipocytes activates TG lipase and increases metabolism

1. increases Hct and plasma protein conc. by reducing circulating plasma volume (loss of protein-free fluid to extracellular space)

2. increases circulating PMN leukocytes

3. Accelerates blood coagulation and promotes fibrinolysis

4. decreased glandular secretions

5. mydriasis

6. stimulates K uptake into cells (decreased renal K excretion)

Which epinephrine dosage is used as/for:

1. SQ, IM, or IV

2. hypersensitivity reactions to drugs/allergens

3. IV inj for acute hypersensitivity uncontrolled by other formulations

4. respiratory distress from bronchospasm

5. Stokes-Adams syndrome

1. 1mg/mL (1:1,000)

2. 1mg/mL (1:1,000)

3. 0.1mg/mL (1:10,000)

4. 1mg/mL (1:1,000)

5. 0.1mg/mL (1:10,000)

When comparing NE, Epi, and Isoproterenol, which agent:

1. Reduces pulse rate?

2. Increases blood pressure?

3. Increases peripheral resistance?

4. Has the most moderate effects on pulse rate, BP, peripheral resist?

1. NE

2. NE

3. NE

4. Epinephrine

Norepinephrine has more or less B-adrenergic activity than epinephrine?

What "tropic" effect(s) are seen with NE?

ADE?

LESS

Positive inotropic

Positive chronotropic effects are overcome by baroreflex compensation

Like epinephrine, extravasation can occur - use long plastic cannula

Warmth

NTG application

Phentolamine (a-receptor antagonist)

What is the brand name for NE?

What is NE's BBW?

What is a sign of NE overdose?

Dilution?

Levophed (1mg/mL)

Antidote for extravasation ischemia - phentolamine ASAP

HA

In D5W or NaCl with D5W (not just saline because oxidation=loss of potency)

pure a-adrenergic agonist

vasoconstriction → increased SBP, DBP, and MAP

no B-effects so reflex bradycardia

↑ afterload + myocardial O2 consumption → ↑ coronary blood flow

Which stimulating agent is the least likely to produce tachycardia?

Which agent has a BBW instructing physicians to become familiar with the complete monograph before prescribing it as an IV, IM, or SQ injection?

Phenylephrine

Phenylephrine(Neo-Synephrine)-1%;10mg/mL;1+5mL vials, 1mL amp

How does dopamine affect

1. MAP?

2. CO?

3. SV?

4. HR?

5. CI?

What is the MOA of dopamine?

Which component of BP does dopamine affect primarily?

Drug interactions?

stimulates D1 receptors → activation of adenylyl cyclase→ raises intracellular cAMP→vasodilation (increases GFR, renal blood flow, and Na excretion)

SBP, may have no effect on DBP or slight increase

MAOIs, TCAs

What is dopamine's BBW for?

Onset of action? Half-life? Duration?

Metabolism?

Elimination?

Antidote for peripheral ischemia - extravasation; use phentolamine (0.1-0.2mg/kg up to 10mg per dose)

5min, 2min, 10min

MAO and COMT; ~25% hydroxylated to NE in specialized neurosecretory vesicles (adrenergic nerve terminals)

80% excreted in urine within 24h

Which isomer of dobutamine is:

1.a1 agonist?

2. a1 antagonist?

3. a more potent B-ag by about 10x?

1. negative(-): pressor responses

2. positive(+): can block the effects of the negative isomer

3. positive(+): both are full beta agonists

Relative to dopamine, dobutamine has increased OR decreased: 

1. CO

2. myocardial oxygen demand

3. pulmonary shunting

1. increased

2. decreased 

3. decreased

What are the major metabolites of dobutamine?

What is the t½?

conjugates of dobutamine and 3-O-methyldobutamine

2min

What are the initial resuscitation goals:

1. CVP

2. MAP

3. UO

4. CV or mixed venous O2-sat

1. 8-12mmHg

2. > 65mmHg

3. > 0.5mL/kg/h

4. > 70%

What are the goals for adjunctive therapy with:

1. Oxygen

2. Insulin (if hyperglycemia requires)

1. >90% O2 sat

2. glucose <150mg/dL 

Is it appropriate to have adjunctive therapy with:

1. corticosteroids? (hydrocortisone, fludrocortisone)

2. DVT prophylaxis (UFH, LMWH)

3. Stress ulcer prophylaxis (PPI, H2RA)

1. controversial - maybe IV hydrocortisone 200-300mg/day for 7 days in 3-4 divided doses for pt with septic shock

2. yes

3. yes

What are the brand names for the following sedatives that can be used in pt with sepsis in the ICU?

1. Propofol

2. Midazolam

3. Lorazepam

4. Dexmedetonidine

1. Diprivan

2. Versed

3. Ativan

4. Precedex

Which goes with which?!

(propofol, midazolam, lorazepam, dexmedetonidine):

1. Maximum dose of 20mg

2. Risk of propylene glycol toxicity

3. Maximum dose of 0.7mcg/kg/hr

4. An onset of 1-2 mins + duration <20 min

5. Monitor for TG

6. Approval for use <24h

7. Not good for renal dysfunction

8. Not for IV push bolus

9. Increased delerium

10. No respiratory depression

11. Onset in 5-10min with duration of 1½-2h

12. Infusion syndrome

1. Propofol (Diprivan)

2. Lorazepam (Ativan)

3. Dexmedetonidine (Precedex)

4. Propofol

5. Propofol

6. Dexmedetonidine

7. Midazolam (Versed)

8. Propofol, Dexmedetonidine

9. Midazolam, Lorazepam

10. Dexmedetonidine

11. Midazolam 

12. Propofol

What is the MOA of Drotrecogin Alpha?

Brand name?

Dosage formulations?

Infusion duration?

Administration information?

Activated protein C; inhibits coagulation by proteolytic inactivation of factors Va (5a) and VIIIa (8a)

Xigris - indicated for sepsis

5 & 20mg IV solution

96h

administer via IV infusion pump or syringe pump, use a dedicated IV line or lumen of a multilumen CVC, can only be admin through same line as NS, RL, dextrose, and NaCl inj

1. HSR to drotrecogin alfa or any component

2. active internal bleeding

3. hemorrhagic stroke within 3 mo

4. intracranial or intraspinal surgery or severe head trauma within 2 mo

5. trauma with increased bleeding risk

6. epidural catheter

7. intracranial neoplasm or mass lesion or evidence of cerebral herniation

1. concurrent heparin use
2. plt <30,000*10^6/L
3. INR >3
4. GI bleed within 6 weeks
5. thrombolytic therapy within 3 days
6. oral anticoags or GP2b/3a inh within 7 days
7. ASA >650mg/day or other platelet inh within 7 days
8. ischemic stroke within 3 mo
9. intracranial arteriovenous malformation or aneurysm
10. known bleeding diathesis
11. chronic severe hepatic disease
12. any other conditions where bleeding would be hazardous or particularly difficult to manage

Which antibiotic drug class inhibits protein synthesis by binding to 50S ribosomal subunit to block aminoacyl translocation reaction and formation of an initiation complex?

Static or Cidal?

Spectrum?

Preg Class?

Misc:

Macrolides (Erythromycin, Azithromycin, Clarithromycin, Dirithromycin)

Static

G+/- cocci, G+ bacilli

staph/strep/mycobacterium, good atypical, no g(-)bacilli

B (Clarith = C)

QT prolongation; renal dosing for clarithromycin

Which antibiotic drug class inhibits acetylation of transpeptidases in bacterial cell walls by binding to PBPs?

Static or Cidal?

Penicillins 

natural: Pen G Na, PenVK, Pen G Benz, Pen G Pro

amino: amoxicillin, ampicillin

penicillinase-resistant: methicillin, nafcillin, oxacillin, cloxacillin, dicloxacillin

extended spectrum: piperacillin, ticarcillin

Cidal

What is the spectrum of PCNs?

Preg Cat?

MISC:

G(+), little G(-)

not good for staph, blactam-G+, Staph only

extended spectrum for pseudomonal activity, some anaerobes

B

time-dependent, extended-spectrum after pH function

Which antibiotics inhibit peptidoglycan synthesis by binding to PBPs?

Static/Cidal?

Spectrum?

Pregnancy Cat?

Renal Dosing?

Misc:

Penems:

Primaxin (imipenem/cilastatin)

Invanz (ertapenem)

Merrem (meropenem)

Doribax (doripenem)

Static/Cidal

broad spec G(+/-), not for MRSA or enterococcus, no pseudomonas with ertapenem, good anaerobes

B (C for Primaxin)

Yes

concentration independent, high risk of seizures

Which antibiotics bind to the 30S and 50S ribosomal subunits to interfere with protein cell wall synthesis?

Static/Cidal?

Spectrum?

PregCat?

Renal dosing?

MISC:

Aminoglycosides

(gentamicin, tobramycin, amikacin, streptomycin, netilmicin)

Cidal

some G+, some staph, good G-, good pseudomonas

D

Yes

Concentration-dependent nephrotox and ototox, post antibiotic effect 

Which antibiotics inhibit DNA gyrase and Top IV relaxing supercoiled DNA and promoting strand breakage?

Static/Cidal?

Spectrum?

PregCat?

Renal Dosing?

Misc:

Fluoroquinolones(ciprofloxacin, levofloxacin, moxifloxacin, ofloxacin, norloxacin, gemifloxacin)

Cidal

BS, pseudomonas, some atypical, Moxi covers anaerobes, not for MRSA, g+ coverage improves with newer agents

C

Yes

QT prolongation, tendonopathy

Which antibiotics inhibit mucopeptide cell wall synthesis?

Static/Cidal?

CEPHS - CIDAL

1st generation:

Keflex (cephalexin) - PO

Duricef (cefadroxil) - PO

Ancef (cefazolin) - IV

2nd generation:

Ceclor (cefaclor) - PO

Cefzil (cefprozil) - PO

Lorabid (loracarbef) -PO

Ceftin/Kefurox (cefuroxime) - PO/IV/IM

Mefoxin (cefoxitin) - IV

3rd generation:

Suprax (cefixime) - PO

Omnicef (cefdinir) - PO

Vantin (cefpodoxime) -PO

Spectracef (cefditoren) -PO

Fortax (ceftazodime) -IV/IM

Cefobid (cefoperazone) - IV/IM

Claforan (cefotaxime) - IV/IM

Cefizox (ceftizoxime) - IM/IV

Rocephin (ceftriazone) - IV/IM

4th generation:

Maxipime (cefepime) - IV/IM

5th generation:

Teflaro (ceftaroline) - IV

1. mod broad (~amox/amp); best G+ act, stable to B-lactamases and penicillinases but not to cephalosporinases
2. broader G- with less G+; stable to BLase, PCNases, and some CEPHases
3. broad G- with less G+; some pseudomonas, stable to BLases, PCNases, many CEPHases
4. broad G- with significant G+, very active against pseudomonas and enterobacteriaceae, not for anaerobes, stable to BLases, PCNases, and almost all CEPHases
5. selective G-/+; MRSA, S pyogenes, S agalactiae, E coli, K pneumonia, K oxytoca

More on Cephs:

1. pregnancy category

2. renal dosing

3. misc

1. B

2. Yes, except Rocephin (ceftriaxone)

3. concentration independent

Which antibiotics bind to 30S ribosomal subunit to inhibit protein synthesis?

Static/Cidal?

Spectrum?

PregCat?

Renal Dosing?

Misc:

Tetracyclines [Tetracycline, Doxycycline, Minocycline, Demeclocycline, Tygacil (tigecycline)]

Static

BS, good anaerobes, good atypical, good against Rickettsia and Chlamydia, Tige good for MRSA

PregD

NO

works on actively dividing only; avoid dairy/antacids

Which antibiotics bind to D-ala-D-ala precursor in bacterial peptidoglycan and prevent cell wall formation as well as some protein synthesis?

Static/Cidal

Spectrum

PregCat

Renal dosing

misc:

Vancomycin

Cidal

G+, MRSA, C.difficile

Preg: PO-B; IV-C

yes

concentration-independent; trough >10best at 15-20

Which AB have high risk of seizures?

Which should you not take with daily/antacids?

tendonopathy?

1. penems

2. tetra

3. fluoroquinolones

penems

cephs

vanc

Which FQ works on anaerobes?

Which tetracycline has MRSA activity?

Which CEPHs can be give IM?

Which 2nd generation Ceph has anaerobic coverage?

Moxi

Tigecycline

cefuroxime, ceftazodime, cefoperazone, cefotaxime, ceftizoxime, rocephin, cefepime 

cefoxitin (Mefoxin)

Piperacillin

Ticarcillin

Ticarcillin/Tazobactam (Zosyn)

Ampicillin/Sulbactam(Unasyn)

Meropenem (Merrem)

Gentamicin (Garamycin, Septopal, Cidomycin)

Tobramycin (Tobi, Tobradex)

Levofloxacin (Levaquin)

Ciprofloxacin (Cipro)

Cefepime (Maxipime)

Which drug class inhibits synthesis of beta (1-3)-glucan resulting in disruption of the cell wall synthesis = cell death?

static/cidal?

spectrum?

Renal dosing?

PregCat?

echinocandin antifungals 

Cancidas (caspofungin), Mycamine (micafungin), Eraxis (anidulafungin)

Cidal

Candida, Aspergillus, no C neoformans, zygomycosis or mucomycosis

No

Preg C

Common causes of sepsis (pathogen classification)?

Risk factors for septic shock?

What non-specific blood levels are elevated in severe sepsis?

Gram-negative bacilli OR Gram-positive cocci

DM, cirrhosis, leukopenia (esp associated with cancer or cytotoxic drugs), invasive devices (trach tubes, caths, drainage tubes), prior tx with AB or corticosteroids

Procalcitonin and C-reactive protein

Lactic acidemia (metabolic acidosis) may cause compensatory hyperventilation (respiratory alkalosis)

What are some signifiant drug-drug interactions with aminoglycoside ABs?

DDI with Ampicillin?

increased nephrotoxicity (w/ enflurane, cisplatin, possibly vanc)

increased ototoxicity (w/ loop diuretics)

increased paralysis (w/ NM blocking agents)

Increased frequency of rash with allopurinol

Meningococcemia

P. aeruginosa

Aeromonas

Staphylococcus aureus

Streptococcus pneumoniae

Coag-negative staphylococci

All of the following are proinflammatory except:

A. TNF-a

B. IL-6

C. IL-8

D. Activated protein C

What is the preferred treatment option for a 56-year-old male with community-acquired pneumonia who was recently prescribed azithromycin for sinusitis:

A. ertapenem

B. moxifloxacin

C. amoxicillin

D. doxycycline

E. clarithromycin

Complication(s) associated with sesis:

A. persistent hypotension

B. disseminated intravascular coagulation

C. ARDS

D. acute renal failure

E. all of the above

Which of the following agents used against MRSA is incorrectly matched with its clinically significant adverse reaction?

A. Vancomycin - nephrotoxicity

B. Linezolid - neutropenia

C. Quinupristin/dalfopristin-myalgia

D. Daptomycin-hyperbilirubinemia

Polymicrobial infections such as secondary peritonitis can be treated with the following agents except:

A. ceftazidime and gentamicin

B. piperacillin/tazobactam

C. ampicillin plus gentamicin plus metronidazole

D. meropenem

E. ciprofloxacin plus metronidazole

The preferred agent for a 37 yo male with advanced AIDS and candidemia is:

A. fluconazole

B. amphotericin B deoxycholate

C. itraconazole

D. amphotericin B lipid complex

E. ketoconazole

Dopamine affects the following receptors except:

A. a1

B. a2

C. b1

D. b2

The following treatment regimen is preferred in case of nosocomial pneumonia with a suspicion of PA?

A. levofloxacin

B. ceftazidime + azithromycin

C. piperacillin + gentamicin

D. ceftriaxone + levofloxacin

E. vancomycin + ertapenem

Regarding hemodynamic support, which of the following agents is the best initial therapeutic intervention?

A. 5% albumin

B. LR

C. NS

D. NE

E. DA

Invasive candidiasis can be treated with all of the following EXCEPT:

A. fluconazole

B. voriconazole

C. caspofungin

D. amphotericin B deoxycholate

E. itraconazole

Which of the following agents is effective against Candida glabrata?

A. fluconazole

B. voriconazole

C. itraconazole

D. ketoconazole

Of the cephalosporins

1. which agents cover anaerobes?

2. which agents cover Pseudomonas aeruginosa?

1. Cefoxitin (Mefoxin)

2. Ceftazidime (Fortaz)

     Cefepime (Maxipime)

What are the cell membrane agents?

MOA?

Polymixin (Poly-Rx)

Colistin (Coly-Mycin M)

damages the cell membrane and permits leakage of intracellular constituents

1. Quinolones - inh DNA gyrase (topoisomerase 2) relax supercoiled DNA and break

2. Nitroimidazoles - disrupts the helical DNA structure and damages the strands resulting in inh of protein synth

3. Rifamycins - bind to the beta subunit of DNA-dependent-RNA-polymerase to block RNA transcription

SMZ inh dihydrofolic acid formation from PABA

TMP inh dihydrofolic acid reduction to THF

static + static = cidal

Tetracyclines

Glycylcyclines (Tigecycline)

Aminoglycosides

Macrolide

Lincosamide

Chloramphenicol

Streptogrammin (Synercid)

Oxazolidinone (Linezolid)