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Drugs Flashcards

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1
Q

Streptomycin

A
  • rapidly bactericidal against aerobic Gram-negative bacteria
  • used for one and one thing only, tuberculosis (used in combination with other drug, rifampin and INH)
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2
Q

Tobramycin

Gentamicin

A

mainly used in cases of severe infection by aerobic Gram-negative infections that are likely resistant to other drugs

-usually used in combination with Beta-lactam antibiotics for synergistic effects and prevent emergence of resistance.

Gentamicin is the preferred simply due to cost.

Gentamicin, Tobramycin are some of the most nephrotoxic aminoglycosides. Nephrotoxic effects are reversible upon discontinuation

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3
Q

Amikacin

A

the preferred drug if gentamicin and tobramycin don’t work.

It is a cyborg of kanamycin (part synthetic) but is less toxic.

again, gram negative aerobic bacteria

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4
Q

Neomycin

Kanamycin

A

both drugs are too toxic for ingestion and are primarily topical use.

They are used on infected surfaces- skin or eyes, or injected into joints, pleural cavities, tissue spaces and abscess cavities.

ointments are often formulated as a neomycin-polymyxin-bacitracin combination - neosporin

Neomycin is one of the most nephrotoxic

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5
Q

Aminoglycoside toxicity

A

All aminoglycosides are nephrotoxic, most likely if taken more than 5 days.

Neomycin, gentamicin, tobramycin
are some of the most toxic

All aminoglycosides are ototoxic: auditory damage (tinnitus, high frequency hearing loss, or vestibular damage, vertigo, ataxia

Again, ototoxic effects most likely to appear if taken more than 5 days or at higher doses in elderly.

Neomycin, kanamycin and amikacin cause the most auditory damage while streptomycin, gentamicin cause the most vestibular damage.

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6
Q

What are the mode of action of Aminoglycosides, Tetracyclines

A

Aminoglycosides; they can be bacteriocidal and act be performing 3 things. They inhibit protein initiation, protein elongation and inhibit proofreading leading to the post antibiotic effect.

Tetracyclines only do one of those things, they bind to the 30S subunit and prevent elongation so they are bacteriostatic. They are however much broader and can cover aerobic, anaerobic GN GP bacteria some protozoa.

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7
Q

Tetracyclines have basically all the same activity, what differs between them?

A

The half life, the longer the half life, the more compliance:

Short (6-8) :
Oxytetracycline
Tetracycline
(oral)

intermediate (12):
Demeclocycline
(oral)

Long (16-18):
*doxycycline (oral or IV)
minocycline (oral)

Superfucking long
*Tigecycline (IV) only 36 hours

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8
Q

Tetracycline uses

A

Rickettsial infections:
________________________
Rocky mountain spotted fever, typhus, Q fever

Sexually Transmitted Infections:
______________________________
Chlamydia, urethritis, epididymitis, cervicitis

Respiratory Tract infections:
_______________________________
community-acquired pneumonia

Skin and Soft-tissue infections:
________________________________
community-acquired staph, severe acne

**Anthrax, malaria, Lymes disease: doxycycline

***community acquired pneumonia, MDR bacteria, MDR S. aureus (MRSA), MDR enterococci (VRE) , MDR acinetobacter, Penicillin-resistant streptococci

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9
Q

Tetracycline toxicities

A

Absorption of orally administered drugs is impaired by food (except for doxycycline
and minocycline) and alkaline pH. • Tetracyclines chelate multivalent cations (Ca2+, Mg2+, Fe2+, and Al3+). • Absorption is therefore also impaired by these cations and by products that contain
them (e.g., dairy products and antacids).

(GI disturbances): fine

(Bony structures and teeth): tetracyclines will bind to the calcium on newly deposited teeth and is of primary concern for young children.

(Photosensitization): systemic administration can produce mild-to severe sensitivity reactions in skin of treated individuals

Liver disturbances:
-contraindicated during pregnancy because of hepatoxic effects

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10
Q

What are the pharmacokinetics of macrolides (50S inhibitors)

A

Aminoglycosides: aerobic gram negative

Macrolides: mostly aerobic gram positive

Include erythromycin, clairthromycin, telithromycin, azithromycin

they inhibit the translocation step of elongation.

Antibacterial properties of all are again similar like tetracycline, they have difference in half lifes.
(**only thing is that telithromycin is active against many macrolide resistant bacteria)

Erithromycin - short, 1.5 hours
Clarithromycin: 6 hours
Telithromcyin 10 hours
Azithromycin (Z pack) -3 days

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11
Q

What are the uses of macrolides?

A
  • Pertusis
  • Chlamydial infections
  • **Streptococcal pharyngitis the best!
  • for those allergic to penicillin, useful alternative for Staph infections of skin or soft tissue

So mostly respiratory tract infections (community acquired pneumonia (telithromycin), chronic bronchitis

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12
Q

What is toxicity of macrolides?

A

GI effects: anorexia, nausea, vomiting and diarrhea
(just eat food)

Liver toxicity: can produce acute cholestatic hepatitis, likely a hypersensitive reaction

Telithromycin can only be used for community acquired pneumonia because of toxicity.

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13
Q

Clindamycin

A

A lincosamide - it is only for gram positive bacteria and bacteriostatic. Used for treatment of skin and soft tissue infections. It was once ideal for staph but now MRSA will not be effected.

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14
Q

Quinupristin/Dalfopristin

A

These are streptogramins that are taken in combination through IV.

Used for treatment of infections caused by vancomycin resistent enterococcus faecium. Also used for complicated skin infections caused by methicillin sensitive S:aureus

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15
Q

Linezolid: super important

A

One of the newest drug, wonderdrug for Multi Drug resistant bacteria including MRSA VRE and penicillin resistant streptococci.

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16
Q

What are the two functional classes of DNA synthesis inhibitors and their members/

A

Antifolate drugs: which inhibit bacterial biosynthesis of DNA (can’t make purines)

  1. Sulfonamides (PABA analogs)
  2. Trimethoprim
  3. Both

DNA gyrase/topo 4 inhibitors: block bacterial DNA synthesis by blocking bacterial topoisomerase II (DNA gyrase) and Topoisomerase 4

  1. fluoroquinolones.
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17
Q

What is the mechanism of action of

Sulfonamides, trimethoprim

A

Sulfonamides are PABA analogs which act as competitive inhibitors of dihydropteroate synthase which converts PABA to dihydrofolic acid.

bacterial DHFR is inhibited by Trimethoprim which converts Dihydrofolic acid to THF.

Combination is often bacteriocidal, alone they are bacteriostatic

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18
Q

Sulfisoxazole

Sulfamethoxazole

A

Rarely used, these are sulfonamides used only for treating UTIs

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19
Q

Sulfasalazine (**)

A

Worth knowing because it is widely used in ulcerative colitis, enteritis and other IBDs. It is the front line for it.

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20
Q

Adverse effects of TMP-SMX

A

Sulfonamides:
They are all partially cross-allergenic so they promote allergies. (short course of treatment< 5 days)

  • fever, skin, rashes, dermatitis, photosensitivity, urticaria, nausea, vomiting, diarrhea
  • may precipitate in urine** causing crystalluria (super painful), hematuria or even obstruction

Longer course of treatment > 5 days
-megaloblastic anemia and leukopenia

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21
Q

What are uses of TMP-SMX (Bactrim)

A
  • UTIs
  • Pneumocystis jiroveci pneumonia - number one opportunistic killer of AIDS
  • Acute exacerbations of chronic bronchitis

**-systemic salmonella infections

  • prostatitis
  • shigellosis
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22
Q

Fluoroquinolones: pharmacodynamics and uses and toxicities

A 
Ciprofloxacin
Lomefloxacin
Levofloxacin
Ofloxacin 
-(gram negative activity-gyrase)

Gemifloxacin, moxifloxacin
(gram positive-topo IV)

-bacterial diarrhea caused by Shigella, E. coli and Campylobacter

**Ciprofloxacin is the drug of choice for anthrax

Levofloxacin, gemifloxacin, moxifloxacin (aka the “respiratory FQs”) used increasingly for treatment of upper and lower respiratory tract infections

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23
Q

Sulfasalazine:

A

Used for IBD (ulcerative colitis, enteritis .

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24
Q

Sulfisoxazole and sulfamethoxazole

A

are used almost exclusively for UTIs

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25
Penicillin G
blocks the activity of transpeptidase by being a D-ala-D-ala mimic. Broad spectrum useful for Gram negative cocci, Gram positive, and anaerobes. Beta-lactamase sensitive
26
Cloxacilin
blocks the activity of transpeptidase by being a D-ala-D-ala mimic. It is used almost only for Gram positive and is not useful for enterococci, Gram negative rods, cocci and anaerobes. Beta lactamase resistant
27
Amoxicillin
blocks the activity of transpeptidase by being a D-ala-D-ala mimic. It is broad spectrum and covers Gram positive and Gram negative. Beta lactamase sensitive.
28
Penicilin characteristics other than mode of action
Remarkably nontoxic. They do all however have cross reactivity and 2nd generation cephalosporins can substitiute
29
Clavulonic acid
It is a beta-lactamase inhibitor. It will bind to beta-lactamase and irreversibly disable it. It preferentially works on plasmid encoded beta lactamase over chromosomally encoded beta lactamase. Avibactam is a more broad spectrum.
30
Cefazolin
First generation Cephalosporin. It is broad spectrum but works preferentially on Gram positive. Used only for surgical prophylaxis, does not penetrate the CNS and has allergic cross reactivity with penicillin
31
Cefamandole
2nd generation, beginning of no cross reactivity with penicillin. Still broad spectrum but extends the coverage of Gram negative
32
Ceftazidime
3rd generation, increases coverage of Gram negative at the expense of Gram postive and it crosses the blood brain barrier, some of them do.
33
Cefepime
4th generation, (4th generation and up all cover Gram positive and negative. It is more resistant to beta lactamases, penetrates CNS
34
Ceftaroline
The newest Cephalosporine. It attacks Gram negative and Gram positive. It is useful for MRSA, most effective for skin infections.
35
Aztreonam
It is a monobactam. It is exclusively used for Gram negative rods. Relatively resistant to Betalactamases. No activity to GP or anaerobes. No cross reactivity or toxicities
36
Imipenem
Its a carbapenem. Its broad spectrum useful for Gram negative rods, Gram positive bacteria and anaerobes, commonly used for mixed infections. Imipenem is resistant to beta lactamases but not metallo beta lactamases. FYI (cilastatin increases half life of imipenem because imipenem is a inactivated by dehydropeptidases in the kidneys)
37
Vancomycin
A lipopeptide that targets gram positive bacteria. It binds directly to D-ala-D-ala, compromising the cell wall. It is bacteriocidal for growing cells. VRE use D-ala-D-lactic acid Dosing is for 7-10 days
38
Dalbavancin and Oritavancin
Dalbavancin, gram positive and the dosage is less. Just two IV doses separated by 7 days Oritavancin: gram positive, one dose. Both are effective for MR gram positive skin infections.
39
Daptomycin:
Forms pores in the cell walls of gram positive bacteria. Potassium efflux but the cell does not rupture. it is useful for MRSA
40
Polymyxin
It compromises the cell wall after binding to outermembrane of gram negative bacteria. Thick membrane perforations rather than pores. It binds to the LPS molecule that is specific for gram negative.
41
Fosfomycin:
It inhibits enzyme murA which converts NAG-UDP to NAM-UDP. Can't form peptidoglycans. It is therefore effective against Gram positive and Gram negative. Pretty safe to use.
42
Bacitracin:
Prevents lipid phosphatase that dephosphorylates the lipid carrier of peptidoglycan subunits. Only used topically because it is so nephrotoxic. It is specific for gram positive bacteria
43
D-cyclosporine
An analog of D-ala. Inhibits D-ala racemase and D-ala ligase. It is a second line drugs with serious side effects (CNS toxicity) Used primarily to treat Tb
44
Isoniazid (when used alone, 9 months)
Inhibits mycolic acid, a component of the mycobacterium cell wall. Mechanism: it inhibits Fas II. The active form, INH-NAD binds to Fab1 preventing the final step of FasII cycle. Isoniazid needs to converted to active form by KatG) Activity of Isoniazid also depends on if you are a fast acetylators or rapid acetylators. (the faster you acetylate, the faster you get rid of it so you need to prescribe more) Toxicity: - Hepatitis - Peripheral neuropathy because structurally similar to pyrodoxine. Mechanisms of resistance: 1. mutation in KatG 2. The binding region of Fab1 is altred. 3. Increasing expression of target enzyme (Fab1) 4. Increasing level of normal metabolite (NADH) which outcompetes.
45
Rifampicin
A more broad spectrum drugs (works for Gram positive, negative, anaerobes) Targets mycobacteria RNA polymerase. It binds to the large subunit (b) of RNAP. It does not let the RNA polymerase leave the promoter (blocks elongation) This is bactericidal for fast growing extracellular mycobacteria but also effective against slow growing intracellular mycobacteria: It is useful for leprosy. It also penetrates the CSF actively and useful if meninges is enflamed. Adverse effects: It affects CYP3A which leads to increased metabolism of other drugs, possibly increasing their toxicity. If administered less than twice weekly, can lead to flu like symptoms. Causes discoloration of urine which is harmless
46
What are rifabutin | Rifapentine
They are better versions of rifampin. 1. Greater potency 2. Longer half life: 3. Less active in inducing CYP3A so its better to be used with other medications 4. Increased membrane permeability so it gets into the macrophage better.
47
For patients with HIV and Tb, what kind of treatment regiment is proposed and how does it vary?
If someone is on Antiretroviral therapy, just do the standard 6 months. If someone with HIV is not on ART, then extend by 3 months. Be careful with 3 times weekly regimen during continuation phase but never give only 2 times weekly. There is adverse effects with Rifampin so Rifabutin is preferred
48
Pyrazinamide
only used for Tb. It is a prodrug that is turned into active metabolite by PcnA enzyme, aka PZase, into POA (pyrazinoic acid). This binds to Rsp-A which prevents the recruitment of tmRNA to a stalled ribosome. *it is a persistent killer of dormant Tb Resistance via PcnA is rather fast. It does reduce the time of therapy from 9 months to 6 months. No toxicities
49
EMB - ethambutol
It blocks EmbA and EmbB arabinosyl transferases. It blocks incorporation of Arabinose into the cell wall making it more vulnerable for damage. *used for actively dividing extracellular tuberculosis. Toxicities: Optic neuritis Can cause red green color blindness.
50
What class of bacteria are aminoglycosides used against -
Gram negative or Yersinia pestis: Think Francis the rabbit.
51
Tetracyclines are bacteriostatic for which bacteria, useful for which infections, and what adverse effects.
Tetracyclines are broad spectrum useful for gram postive, negative aerobes and anaerobes. 1. Rickettsial infections 2. STIs 3. Community acquired pneumonia 4. MDR bacteria (tigecycline) 5. Anthrax 6. Lyme disease Adverse: 1. GI disturbances 2. Teeth deposition. 3. Photosensitivity 4. Hepatotoxicity during pregnancy.
52
What are macrolides bacteriostatic for, what are they used for and what are the adverse effects?
Bacteriostatic for mainly aerobic Gram positive and some gram negative 1. Community acquired pneumonia (like tetracyclines) All that telithromycin is used for 2. Skin and soft tissue infections (penicilin substitute) Acute otitis media Strep throat (real good) Cornebacterium Diptheria Pertussis. Adverse effects: Hepatotoxicity GI disturbances
53
What classes of drugs bind to the 50S ribosomal subunit and interfere with protein synthesis by blocking the ribosomal translocation step?
1. Macrolides 2. Clindamycin (a lincosamide) 3. Quinupristin + Dalfopristin 4. Linezolid
54
What is bactrim -TMP-SMX used for and its adverse effects?
1. Uncomplicated UTIS 2. Shigella 3. Salmonella 4. Pneumocystis jiroveci - common disease in HIV 5. Prostatitis 6. Bronchitis Treatment less than 5 days leads to allergic reactions (photosensitivity, uriticaria, hives, rashed) Treatment more than 5 days can lead to megaloblastic anemia and leukopenia
55
What are the bacteria that are targeted by fluoroquinolones, its uses and adverse effects
Gram negative - Topo II, DNA gyrase Gram positive - Topo IV DNA gyrase 1. UTIs 2. Anthrax - ciprofloxacin 3. Diarrhea- shigella, salmonella, EHEC 4. Respiratory infections: (levofloxacin, moxifloxacin, gemifloxacin) 5. Intra-abdominal infections 6. joint infections
56
Probenecid
Coprescribed with penicillins (beta lactam antibiotics) which will competitively inhibit renal excretion
57
Cilastatin
An inhibitor of renal dehydropeptidases to increase concentrations and extend half life
58
What would you prescribe to someone with a possible MRSA?
Vancomycin and Ceftaroline
59
What would you someone with a known penicillin allergy
Cephalosporines or aztreonam. Aztreonam is a monobactam with no cross reactivity of penicillin
60
An asian dude has a sore throat with a fever which turns into pneumonia with a severe prolonged hacking cough. Cryoagglutinins are present, what is the agent?
Mycoplasma pneumoniae
61
A sexually active female develops PID, what is the likely agent
Chlamydia trachomatis. N. gonorrhea is much less common especially in the general population. It is more common in the economically disadvantaged city teens.
62
A person had multiple flea bites resulting in daily fevers, headaches, chills and malaise. He has a maculopapular rash on his trunk, arms and thighs. What is the likely cause of the condition.
Rickettsia typhi i. The vector is the rat flea, and the reservoirs are the rat and the rat flea. Unlike other rickettsial infections, R. typhi is frequently acquired in cities in the developing world with inadequate rodent control

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