RN License: ACHIEVED

I relate to all these faces on many levels

ANTIBIOTICS CHEAT SHEET :)

Also, REMEMBER!!!!

* Sulfonamides compete for albumin with:

Bilirrubin: given in 2°,3°T, high risk or indirect hyperBb and kernicterus in premies

Warfarin: increases toxicity: bleeding

* Beta-lactamase (penicinillase) Suceptible:

Natural Penicillins (G, V, F, K)

Aminopenicillins (Amoxicillin, Ampicillin)

Antipseudomonal Penicillins (Ticarcillin, Piperacillin)

* Beta-lactamase (penicinillase) Resistant:

Oxacillin, Nafcillin, Dicloxacillin

3°G, 4°G Cephalosporins

Carbapenems 

Monobactams

Beta-lactamase inhibitors

* Penicillins enhanced with:

Clavulanic acid & Sulbactam (both are suicide inhibitors, they inhibit beta-lactamase)

Aminoglycosides (against enterococcus and psedomonas)

* Aminoglycosides enhanced with Aztreonam

* Penicillins: renal clearance EXCEPT Oxacillin & Nafcillin (bile)

* Cephalosporines: renal clearance EXCEPT Cefoperazone & Cefrtriaxone (bile)

* Both inhibited by Probenecid during tubular secretion.

* 2°G Cephalosporines: none cross BBB except Cefuroxime

* 3°G Cephalosporines: all cross BBB except Cefoperazone bc is highly highly lipid soluble, so is protein bound in plasma, therefore it doesn’t cross BBB.

* Cephalosporines are "LAME“ bc they  do not cover this organisms 

L  isteria monocytogenes

A  typicals (Mycoplasma, Chlamydia)

M RSA (except Ceftaroline, 5°G)

E  nterococci

* Disulfiram-like effect: Cefotetan & Cefoperazone (mnemonic)

* Cefoperanzone: all the exceptions!!!

All 3°G cephalosporins cross the BBB except Cefoperazone.

All cephalosporins are renal cleared, except Cefoperazone.

Disulfiram-like effect

* Against Pseudomonas:

3°G Cef taz idime (taz taz taz taz)

4°G Cefepime, Cefpirome (not available in the USA)

Antipseudomonal penicillins

Aminoglycosides (synergy with beta-lactams)

Aztreonam (pseudomonal sepsis)

* Covers MRSA: Ceftaroline (rhymes w/ Caroline, Caroline the 5°G Ceph), Vancomycin, Daptomycin, Linezolid, Tigecycline.

* Covers VRSA: Linezolid, Dalfopristin/Quinupristin

* Aminoglycosides: decrease release of ACh in synapse and act as a Neuromuscular blocker, this is why it enhances effects of muscle relaxants.

* DEMECLOCYCLINE: tetracycline that’s not used as an AB, it is used as tx of SIADH to cause Nephrogenic Diabetes Insipidus (inhibits the V2 receptor in collecting ducts)

* Phototoxicity: Q ue S T  ion?

Q uinolones

Sulfonamides

T etracyclines

* p450 inhibitors: Cloramphenicol, Macrolides (except Azithromycin), Sulfonamides

* Macrolides SE: Motilin stimulation, QT prolongation, reversible deafness, eosinophilia, cholestatic hepatitis

* Bactericidal: beta-lactams (penicillins, cephalosporins, monobactams, carbapenems), aminoglycosides, fluorquinolones, metronidazole.

* Baceriostatic: tetracyclins, streptogramins, chloramphenicol, lincosamides, oxazolidonones, macrolides, sulfonamides, DHFR inhibitors.

* Pseudomembranous colitis: Ampicillin, Amoxicillin, Clindamycin, Lincomycin.

I’ve made some corrections and added ABs that didn’t include before!!! Here’s the link if you want to download the corrected chart:  [Antibiotics doc]

Also, I’m gonna add a couple of things that didn’t mention before:

* MRSA: Ceftaroline, Telavancin, Dalbavancin, Oritavancin, Vancomycin, Linezolid, Tidezolid, Daptomycin, Tigecyclin.

* Skin MRSA: TMP/SMX, Clindamycin, Doxycycline, Linezolid

* FQ: Gemi, Levo, Ciprofloxacin cover Pseudomona but do NOT cover anaerobes. Moxifloxacin covers anaerobes but do NOT cover Pseudomona.

* Ertapenem DOES NOT cover Pseudomona

* mAcrolides DO NOT cover stAph.

* ciPRofloxacin DOES NOT cover stReP

* Cefoxitin, Cefotetan: the only 2°G cephalosporins that cover anaerobes. Also deplete prothombin, so there’s increase risk of bleeding. 

* VRE: Tigecycline, Linezolid, Quinupristin/Dalfopristin, Daptomycin

* ESBL: (BLEE en español)  carbapenems, beta lactam+beta lactamase inhibitors

The Changing Colors Of Bruises And What They Mean

The color of bruises comes from the presence of blood within your skin, which goes through specific stages of breakdown and cleanup as the area heals. Unsightly though they may be, the changing colors of bruises represent different stages in the healing process.

You develop a bruise when some type of trauma causes bleeding near the surface of your body without breaking the skin. With minor injuries — like bumping your arm or pinching your finger — the bleeding is usually confined to your skin and the bruise becomes apparent within minutes to hours.

With more forceful trauma — like twisting your ankle or getting hit with a baseball — bleeding typically occurs in the deeper tissues and the blood gradually seeps into your skin over a period of hours to days. This is why you may not see a bruise for a day or two after you’ve had a fall or other injury.

The size of a bruise depends on what caused your injury and the amount of force involved. The more forceful the injury, the greater the amount of bleeding and the larger your bruise will be. The closer to your skin surface the bruise is, the more intense the colors you will see.

Fresh to Early Bruise Colors

Fresh bruises develop within minutes to a few days, depending on how deep below your skin surface the bleeding is. You’ll typically see a new bruise progress from red to blue to purple within the first couple of days after an injury.

Red bruises: when you first get a bruise — especially one near the surface of your skin — it usually appears red. The color comes from fresh blood leaking into your tissues. Fresh blood is bright red because it contains both iron and oxygen.

Blue bruises: within a few hours, blood that has leaked from your injured blood vessels loses the oxygen it was carrying. As this occurs, the blood becomes darker and your bruise begins to look more bluish or purple. Note that if you have a deep bruise, the red stage may have already passed by the time you are first able to see the bruise. So the first color you see may be a bluish purple color.

Purple bruises: typically, over one to three days (depending in the severity of your injury), a bruise becomes more intensely purple and may even appear black. This occurs as red blood cells break down and iron is released into the injured area.

Healing Bruise Colors

When red blood cells break down, they release an iron-containing protein called hemoglobin. As your bruise begins to heal, your body converts the hemoglobin into other colored chemicals. The presence of these chemicals causes your bruise to change color as it heals.

Green bruises: you’ll know your bruise is beginning to go away when you notice it turning green. You’re likely to first notice the transition from purple to green at the edges or center of a bruise. The green color is due to the presence of a hemoglobin breakdown product called biliverdin.

Yellow bruises: at long last, your green bruise will eventually turn yellow as it enters the final stage of healing. The yellow color is from the final breakdown product of hemoglobin in your skin, a chemical called bilirubin. The yellow fades as your body clears away the last of the debris from the bleed, leaving you with bruise-free skin.

As you’ve probably noticed with bruises you’ve had in the past, most are multicolored. This is because the amount of blood in different areas of the bruise varies, and the stages of healing overlap.