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1
Q

What is the function of apolipoprotein E and what expresses it?

A

Mediates remnant upake.

Chylomicron
Chylomicron remnant
VLDL
IDL
HDL

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2
Q

What is the function of apolipoprotein A-1 and what expresses it?

A

Activates LCAT
(LCAT catalyzes esterification of cholesterol, making nascent HDL –> Mature HDL)

HDL
Chylomicrons

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3
Q

What is the function of apolipoprotein C-II and what expresses it?

A

Lipoprotein lipase cofactor
Required for LPL function on the surface of vascular endothelial cells

Chylomicron
VLDL
HDL

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4
Q

What is the function of apolipoprotein B-48 and what expresses it?

A

Mediates chylomicron secretion

Chylomicron
Chylomicron remnant

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5
Q

What is the function of apolipoprotein B-100 and what expresses it?

A

Binds LDL receptro and mediates VLDL uptake in liver

VLDL
IDL
LDL

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6
Q

Penicillin G, V
MOA
Clinical Use
Toxicity
Resistance

A

MOA: Bind PBP (transpeptidases
Block transpeptidase cross-linking of peptidoglycan
Activagte autolytic enzymes

Clinical Use: Gram+
(S. pneumo, S. pyogenes, actinomyces)
Also, N. meningitidis, T. pall

Toxicity:
Hypersensitivity reactions, hemolytic anemia

Resistance: Penicillinase cleaves b-lactam ring

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7
Q

Ampicillin, Amoxicillin

MOA
Clinical Use
Toxicity
Resistance

A

MOA: Bind PBP’s and block transpetidase cross-linking of peptidoglycan
Also, combine with clavulanic acid to protect against b-lactamase (augmentin)
Amoxicillin = oral
Ampicillin = IV

Clinical Use: HELPSS
H. influenzae, E. coli, Listeria, Proteus, Salmonella, Shigella, Enterococci

Toxicity: Hypersensitivity, rash, pseudomembranous colitis

Resistance: Penicillinase

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8
Q

Oxacillin, Nacillin, dicloxacillin
MOA
Clinical Use
Toxicity
Resistance

A

Penicillinase resistant penicillins
MOA: Bind to PBP, block transpeptidase cross-linking of peptidoglycan
Resistant to penicillinase because of bulky R group blocking b-lactam ring

Clinical Use: S. aureus
Use naf for staph

Toxicity: hypersensitivity, interstitial nephritis

Resistance: Modification of PBP’s

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9
Q

Ticarcillin, Piperacillin

MOA
Clinical Use
Toxicity
Resistance

A

Antispeudomonals

MOA: Binds to PBP’s, inhibits transpeptidases cross-linking of peptidoglycan

Clinical Use: Pseudomonas and gram- rods

Toxicity: Hypersensitivity

Resistance: Penicillinase, use with clavulanic acid, sulbactam, or tazobactam

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10
Q

1st Generation Cephalosporins

MOA
Clinical Use
Toxicity
Resistance

A

Cefazolin, cephalexin

MOA: b-lactam drugs that inhibit cell wall synthesis, but are less susceptible to penicillinases
Bactericidal

Clinical Use: PECK
Proteus, E. coli, Klebsiella

Toxicity: Hypersensitivity, Vit. K deficiency, low cross-reactivity with penicillins
Increases nephrotoxicity of aminoglycosides

Resistance: modification of PBPs

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11
Q

2nd Generation Cephalosporins

MOA
Clinical Use
Toxicity
Resistance

A

Cefoxitin cefaclor, cefuroxime

MOA: b-lactam drugs that inhibit cell wall synthesis but are less susceptible to penicillinases
Bactericidal

Clinical Use: HEN PECKS
H. influenzae, Enterobacter, Neisseria, Proteus, E. coli, Klebsiella

Toxicity: Hyeprsensitivity, Vit. K Deficiency, Low cross-reactivity with PCN’s, Increases nephrotoxicity of aminoglycosides

Resistance: Modification of PBP’s and b-lactamases

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12
Q

3rd Generation Cephalosporins

MOA
Clinical Use
Toxicity
Resistance

A

Ceftriaxone, Cefotaxime, Ceftaxidime

MOA: b-lactam drugs that inhibit cell wall synthesis but are less susceptible to penicillinases. Bactericidal

Clinical Use:
Serious Gram - infections
Ceftriaxone for CSF penetration

Toxicity: Hypersensitivity, Vit. K Def., low cross-reactivity with PCN’s increases nephrotoxicity of aminoglycosides

Resistance: Modification of PBP’s

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13
Q

4th Generation Cephalosporins

MOA
Clinical Use
Toxicity
Resistance

A

Cefepime

MOA: b-lactam drugs taht inhibit cell wall synthesis but are less susceptible to penicilinases
Bactericidal

Clinical Use: Pseudomonase and gram + organisms

Toxicity: Hypersensitivity, Vit. K def., low cross-reactiity with PCN’s, increased nephrotoxicity of aminoglycosides

Resistance: Modification of PBP’s

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14
Q

5th Generation Cephalosporins

MOA
Clinical Use
Toxicity
Resistance

A

Ceftaroline

MOA: b-lactam drugs taht inhibit cell wall synthesis but are less susceptible to penicilinases
Bactericidal

Clinical Use: Broad Gram+/- coverage, including MRSA
No pseudomonal coverage

Toxicity: Hypersensitivity, Vit. K def., low cross-reactiity with PCN’s, increased nephrotoxicity of aminoglycosides

Resistance: Modification of PBP’s

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15
Q

Aztreonam

MOA
Clinical Use
Toxicity
Resistance

A

MOA: Monobactam, resistant to b-lactamases
Prevents peptidoglycan from cross-linking by binding to PBP 3

Clinical Use: Gram - Rods only
For PCN allergic patients or those with renal insufficiency who cannot tolerate aminoglycosides

Toxicity: Occassional GI upset

Resistance: modification of PBP

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16
Q

Carbapenems

MOA
Clinical Use
Toxicity
Resistance

A

Imipenem, meropenem, ertapenem, doripenem

MOA: broad-spectrum, b-lactamase-resistant
Binds to PBP to inhibit cell wall synthesis

Clinical Use:
Imipenem is administered with cilastatin to reduce deactivation of drug in renal tubules
Gram+ cocci, Gram- rods, and anaerobes

Toxicity: GI distress, skin rash, CNS toxicity/seizures at high plasma levels (Meropenem has less CNS toxicity)

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17
Q

Vancomycin

MOA
Clinical Use
Toxicity
Resistance

Study These Flashcards
A

MOA: inhibits cell wall peptidoglycan formation by binding D-ala D-ala portion of cell wall precursors
Bactericidal

Clinical Use: MRSA, enterococci, C. diff
Gram+ ONLY

Toxicity: NOT many issues
Nephrotoxicity
Ototoxicity
Thrombophlebitis
Red Man Syndrome (pretreat with antihistamines and slow infusion rate)

Resistance: Amino acid modification of D-ala D-ala to D-ala D-lac

18
Q

What antibiotics target protein bacterial ribosomes/protein synthesis and how?

Study These Flashcards
A

Buy AT 30, CCEL at 50

  • *30**s ribosome:
  • *A**minoglycosides (cidal)
  • *T**etracyclines (static)
  • *50**s ribosome:
  • *C**loramphenicol (static)
  • *C**lindamycin (static)
  • *E**rythromycin (macrolides = static)
  • *L**inezolid (variable)
19
Q

Aminoglycosides

MOA
Clinical Use
Toxicity
Resistance

Study These Flashcards
A

Mean GNATS caNNOT kill anaerobes
Gentamycin, Neomycin, Amikacin, Tobramycin, Streptomycin

MOA: Inhibit formation of initiation complex and cause misreading of mRNA. Also, blocks translocation
Requires O2 for uptake

Clinical Use: Gram- Rods
Synergistic with b-lactams
Neomycin for bowel surgery

Toxicity:

  • *N**ephrotoxicity (esp. w/Cephalosporins)
  • *N**euromuscular blockade
  • *O**totoxicity (esp. w/loop diuretics)
  • *T**eratogen

Resistance: Anearobes
Bacterial transferase enzymes inactivate the drug by acetylation, phosphorylation or adenylation

20
Q

Tetracyclines

MOA
Clinical Use
Toxicity
Resistance

Study These Flashcards
A

Tetracycline, Doxycycline, Minocycline

MOA: Bind to 30s and prevent attachment of aminoacyl-tRNA.
Do not take with Ca, Mg, or Fe containing foods; they inhibit resorption

Clinical Use: Borrelia burgdorferi (Lyme dz), M. pneumoniae, Rickettsia (RMSF), Chlamydia, and acne

Toxicity: GI distress, discolorationo f teeth, inhibition of bone growth (chelates to Ca), photosensitivity. Contraindicated in pregnancy

Resistance: Decreased uptake or increased efflux by plasmid-encoded transport pumps

21
Q

Macrolides

MOA
Clinical Use
Toxicity
Resistance

Study These Flashcards
A

ACE
Azithromycin,Clarithromycin,Erythromycin

MOA: Inhibits protien synthesis by blocking translocation (“macroslides”); bind to the 23s rRNA of 50s ribosome

Clinical Use: Atypical pneumonias, STD (chlamydia), Gram+ cocci (Strep ifnxn if allergic to PCN)

Toxicity: MACRO
Gastrointestinal Motility issues, Arrhythmia/prolonged QT, acute Cholestatic hepatitis, Rash, eOsinophilia. Increases [] of theophyliines, oral anticoags

Resistance: Methylation of 23s rRNA-binding site prevents drug binding

22
Q

Chloramphenicol

MOA
Clinical Use
Toxicity
Resistance

Study These Flashcards
A

MOA: blocks peptidyltransferase at 50s ribosomal subunit

Clinical Use: Meningitis (H. influenzae, N. meningitidis, S. penumo) and Rickettsia rickettsii (RMSF)

Toxicity: Anemia (dose dependent), aplastic anemia (dose independent), gray baby syndrome (premies lack UDP-glucuronyl transferase)

Resistance: Plasmid-encoded acetyltransferase inactivates drug

23
Q

Clindamycin

MOA
Clinical Use
Toxicity
Resistance

Study These Flashcards
A

MOA: Blocks peptide transfer (translocation) at 50s subunit

Clinical Use: Treats anaerobes above the diaphragm Anaerobic infxns (Bacteroides, C. perfringens) in aspiration pneumonia, lung abscesses, and oral infections
Affective against invasive GAS

Toxicity: C. diff colitis, fever, diarrhea
Resistance: active transport out of cells

24
Q

Sulfonamides

MOA
Clinical Use
Toxicity
Resistance

Study These Flashcards
A

Sulfamethoxazole (SMX), sulfisoxazole, sulfadiazine

MOA: Inhibit folate synthesis. PABA antimetabolites inhibit dihydroperoate synthesis

Clinical Use: Gram+, Gram-, Nocardia, Chlamydia, simple UTI

Toxicity: Hypersensitivity, hemolysis of G6PD deficient, Interstitial nephritis, photosensitivity, kernicterus in infants, displace other drugs from albumin (i.e. warfarin)

Resistance: Altered enyzme (bacterial dihydropteroate synthase), decreased uptake, or increase PABA synthesis to overcome drug competitively

25
Trimethroprim (TMP) MOA Clinical Use Toxicity Resistance
MOA: Inhibits bacterial dihydrofolate reductase Clinical Use: TMP-SMX = UTI, shigella, salmonella, pneumocystis jirovecii tx and prophy, toxoplasmosis prophy Toxicity: **TMP: T**reats **M**arrow **P**oorly Megaloblastic anemia, leukopenia, granulocytopenia
26
Fluoroquinolones MOA Clinical Use Toxicity Resistance
**Ciprofloxacin, norfloxacin, levofloxacin, ofloxacin, sparfloxacin, moxifloxacin, gemifloxacin, enoxacin, nalidixic acid** MOA: Inhibit DNA gyrase (topoisomerase II) and topoisomerase IV. Must not be taken with antacids Clinical Use: Gram- rods of urinary and GI tracts (including pseudomonas), Neisseria, some Gram+ Toxicity: Fluoroquino**lones** hurt attachments to your **bones** GI, upset, superinfections, skin rashes, headache, dizziness. **Tendonitis**, **tendon rupture**, leg cramps, myalgias. Prolonged QT Resistance: Chromosome encoded mutation in DNA gyrase, plasmid-mediated resistance, efflux pumps
27
Metronidazole MOA Clinical Use Toxicity Resistance
MOA: Forms free-radical toxic metabolites in the bacterial cell to damage DNA Bactercidal, antiprotozoal Clinical Use: **GET GAP** **on the metro!** * *G**iardia, **E**ntamoeba, **T**richomonas, **G**ardnerella vaginalis, **A**naerobes, H. **P**ylori * *Treats anaerobic infxn below the diaphragm** Toxicity: Disulfiram-like rxn with alcohol, headache, metallic taste
28
Treatment for M. tuberculosis
Prophy: Isoniazid Treatment: **RIPE** **R**ifampin, **I**soniazid, **P**yrazinamide, **E**thambutol (+Vit B6)
29
Treatment for M. avium-intracellulare
Prophy: Azithromycin, rifabutin Treatment: Azithromycin or Clarithromycin + Ethambutol Can add rifabutin or ciprofloxacin
30
Treatment for M. leprae
Tuberculoid form: Dapsone and Rifampin Lepromatous form: Clofazimine
31
Isoniazid MOA Clinical Use Toxicity Resistance
MOA: Decreased synthesis of mycolic acids Bacterial catalase-peroxidase needed to convert INH to active metabolite Clinical Use: M. tuberculosis Toxicity: **INH I**njures **N**eurons and **H**epatocytes Neurotoxicity, hepatotoxicity. Use with Pyridoxine (Vit. B6) to prevent neurotoxicity, lupus
32
Rifamycins MOA Clinical Use Toxicity Resistance
**Rifampin, rifabutin** **4 R's: R**NA polymerase inhibitor **R**amps up microsomal cytochrome (P450) **R**ed/orange body fluids **R**apid resistance if used alone **R**if**amp**in **ramp**s up CYP450, **but** rifa**but**in does not MOA: Inhibits DNA-dependent RNA polymerase Clinical Use: M. tuberculosis. Delays resistance to dapsone when used for leprosy. Meningococcal prophylaxis and chemoprophylaxis when in contact with those with H. flu type B Toxicity: Hepatotoxicity and drug interxns orange body fluids
33
Pyraxinamide MOA Clinical Use Toxicity Resistance
MOA: Mechanism uncertain. Acidiy intracellular environment via conversion to pyrazinoic acid? Effective in phagolysosomes Clinical Use: M. tuberculosis Toxicity: Hyperuricemia, hepatotoxicity
34
Ethambutol MOA Clinical Use Toxicity Resistance
MOA: Decrease carbohydrate polymerization of mycobacterium cell wall by blocking arabinosyltransferase Clinical Use: M. tuberculosis Toxicity: optic neuropathy (red-green color blindness) **Eye**thambutol
35
Amphotericin B MOA Clinical Use Toxicity Resistance
MOA: Bidns ergosterol; forms membrane poors that allow leakage of electrolytes "Ampho**ter**icin '**tears**' holes in the fungal membrane" Clinical Use: Systemic mycoses Cryptococcus, Blastomyces, Coccidioides, Histoplasma, Candida, Mucor Administer intrathecally for fungal meningitis Toxicity: Fever/chills ("Shake and Bake"), hypotension Nephrotoxicity, arrhythmias, anemia, IV phlebitis. Hydration decreases nephrotoxicity. Supplement K and Mg because of altered renal tubule permeability
36
Nystatin MOA Clinical Use Toxicity Resistance
MOA: Binds ergosterol; forms membrane pores that allow leakage of electrolytes Clinical Use: Oral candida ("swish and swallow"), diaper rash or vaginal candida Toxicity: Topical only - too toxic for systemic use
37
Azoles MOA Clinical Use Toxicity Resistance
**Fluconazole, ketoconazole, clotrimazole, miconazole, itraconazole, voriconazole** MOA: Inhibit fungal sterol synthesis by inhibiting lanosterol --\> ergosterol Clinical Use: Local and less serious systemic mycoses Fluconazole for chronic suppression of cryptococcal meningitis in AIDS pts and candida of all types Itraconazole for blastomyces, coccidioides, Histoplasma Clotrimazole and miconazole for topical fungal infections ``` Toxicity: Testosterone synthesis inhibition (gynecomastia, esp. ketoconazle) Liver dysfunction (inhibits CYP450) ```
38
Flucytosine MOA Clinical Use Toxicity Resistance
MOA: Inhibits DNA and RNA biosynthesis by conversion to 5-fluorouracil by cytosine deaminase Clinical Use: Systemic fungal infections (Cryptococcal meningitis) in combo with amphotericin B Toxicity: Bone marrow suppression
39
Echinocandins MOA Clinical Use Toxicity Resistance
**Caspofungin, micafungin, anidalafungin** MOA: Inhibits cell wall syntehssis by inhibiting syntehsis of b-glucan Clinical Use: Invasive aspergillosis, candida Toxicity: GI upset, flushing (histamine release)
40
Terbinafine MOA Clinical Use Toxicity Resistance
MOA: inhibits fungal enzyme squalene epoxidase Clinical Use: Dermatophytoses (esp. onychomycosis) Toxicity: GI upset, headaches, hepatotoxicity, taste disturbance
41
Griseofulvin MOA Clinical Use Toxicity Resistance
MOA: Interferes with microtubule fxn; disrupts mitosis. Deposits in keratin-containing tissues (i.e. nails) Clinical Use: Oral Tx of superficial infections; inhibits growth of dermatophytes (tinea, ringworm) Toxicity: Teratogenic, carcinogenic, confusion, headaches, Induces CYP450 and wafarin metabolism
42

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