Study your flashcards anywhere!

Download the official Cram app for free >

  • Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off

How to study your flashcards.

Right/Left arrow keys: Navigate between flashcards.right arrow keyleft arrow key

Up/Down arrow keys: Flip the card between the front and back.down keyup key

H key: Show hint (3rd side).h key

A key: Read text to speech.a key


Play button


Play button




Click to flip

88 Cards in this Set

  • Front
  • Back
  • 3rd side (hint)
What are Sulfonamides analogs of?

What is this term referred to as?

Sulfonamides are COMPETITIVE inhibitors of what enzyme and synthesis of what product?
Dihyrdopteroate synthase

Definition: A substance inhibiting cell growth by competing with, or substituting for, a natural substrate in an enzymatic process
What is the Efficacy of Sulfonamides based on? (3)
1. how tight they bind
2. how well it is recognized by the enzyme
3. Relative concentrations of PABA
Sulfonamides: Static or Cidal?
How are Sulfonamides administered?

Topical (burns)
Describe the distribution of Sulfonamides
Good distribution including CNS
What chemical modification (metabolism) yields inactive Sulfonamide?
How are Sulfonamides excreted?
90% in urine by glomerular filtration
Where in the body do Sulfonamides concentrate?
Urine = 10-20X the blood concentration in the urine
Sulfonamide used topically for burns
Silver Sulfadiazine
Sulfonamide used as Ophthalmic preparations (eye drops)
Sodium Sulfacetamide
What infection are Sulfonamides particularly used for?

*b/c they concentrate in the urine
Sulfonamide used for Ulcerative Colitis
-Explain the mechanism
-not absorbed by the gut but split by gut bacteria to release Aminosalicylate = anti-inflammatory
What drug are Sulfonamides commonly combined with?
Major adverse effect of Sulfonamides
Allergic reactions
What other drugs may Sulfonamides cross-react with?
1. Carbonic anyhydrase inhibitors
2. Diuretics = Thiazide, Furosemide
3. Sulfonylurea hypoglycemics
Sulfonamides are the DOC for this infectious agent
Syndrome that can occur as an adverse effect of Sulfonamides
Stevens-Johnson Syndrome
-erythema multiform that involves the skin and mucus membranes
-hypersensitivity reaction
List the 4 Adverse effects of Sulfonamides
1. Allergic reaction (SJS)
2. Crystalluria / Hematuria
3. Hematopoietic effects = depression in blood cell counts
4. Hemolytic anemias in G6PDH deficiency
List 3 ways in which microbes may become resistant to Sulfonamides
1. overproducing PABA
2. loss of permeability
3. new form of Dihydropteroate synthetase which discriminates between PABA and sulfonamide
Drug that inhibits Bacterial Dihydrofolate Reductase?
Drug that inhibits Protozoan Dihydrofolate Reductase?

Name a specific microbe

Toxoplasma gondii
Drug that inhibits Mammalian Dihydrofolate Reductase
Describe the distribution of Trimethoprim
Wide distribution including CNS
What enzyme does Trimethoprim inhibit?
Dihydrofolate Reductase
What is Trimethoprim usually combined with?
What is the name of Trimethoprim-Sulfamethoxazole
Co-trimoxazole (TMP-SMX) = synergistic
What are 2 clinical uses of TMP-SMX?
1. Pneumocystis pneumonia

2. complicated UTI
TMP-SMX: Static or Cidal?
Name 3 adverse effects of Trimethoprim
1. Megaloblastic anemia = causing cells to be Folate deficient
2. Leukopenia
3. Granulocytopenia

**you're inhibiting THF synthesis so you kill cells
with high proliferation rates
**TMP = Treats Marrow Poorly
With what drug may the toxicity of Trimethoprim be alleviated?
Folinic Acid
What patients receiving Co-trimoxazole have a much higher incidence of adverse effects such as:
-fever, rashes, leukopenia, diarrhea
AIDS patients with Pneumocystis
What is the mechanism of action of Quinolones?
Inhibits DNA gyrase (Topoisomerase II) = inhibit DNA replication
Are Quinolones STATIC or CIDAL

What is the spectrum of Fluoroquinolones?

Gram + & -
What was the protype Quinolone? Why was its use stopped? What was done to correct the drug?
Nalidixic Acid

It was rapidly absorbed, metabolized, and EXCRETED = poor pharmacokinetics

Added Fluorine to diminish metabolism
What ending do alot of Fluoroquinolones have?

(Ciprofloxacin, Levofloxacin)
What can decrease the renal excretion of Fluoroquinolones?
List the adverse effects of Fluoroquinolones (-floxacins) (6)
1. NVD syndrome
2. headaches, dizziness, insomnia
3. **Abnormal liver fxn tests**
4. **block Theophylline and Caffeine clearance**
5. **effects on collagen metabolism and cartilage development**
6. **Tendonitis and tendon rupture in adults**
What 2 things does Fluoroquinolones (-floxacins) block the clearance of?
1. Theophylline

2. Caffeine
What group of people is Fluoroquinolone contraindicated in and why?
Pregnant women and children b/c animal studies show damage to CARTILAGE
How does resistance to Fluoroquinolones arise?

What specific species most often have resistance?
Altered DNA gyrase

Pseudomonas, Staph, Serratia
What are 4 agents that are used for UTI's
1. Penicillins
2. Aminoglycosides
3. Sulfas
4. Fluoroquinolones

FAPS for UTI's
What is Nitrofurantoin's mechanism of action?
unknown but may involve oxidative stress
Is Nitrofurantoin STATIC or CIDAL?
Either - depends on the bug
Describe the pharmacokinetics of Nitrofurantoin
rapidly absorbed, metabolized, and excreted in the urine -> 50% as an active drug
What is Nitrofurantoin clinically used for?
UTI's: Gram + and -
This drug is most effective as a urine pH of < 5.5
What are the adverse effects of Nitrofurantoin?
Anorexia, GI disturbances

Hemolytic anemia if G6PDH deficient
What patients do you never give Nitrofurantoin to and why?
Those with Renal Insufficiency b/c will cause systemic toxicity

**rapidly absorbed, metabolized, and excreted in the urine -> 50% as an active drug
What bugs are resistance to Nitrofurantoin?
ALL Pseudomonas

some Proteus
Describe Mycobacterial infections
Chronic infections with long dormant periods separating intermittent active (symptomatic) periods
What are the barriers in treating Mycobacterial infections?
They are INTRACELLULAR pathogens = drug has to get into patient's cell and then into Mycobacteria
How long is treatment for "uncomplicated" TB?
6-9 months
How long is chemoprophylaxis treatment for TB?
1 year
How long is treatment for Complicated TB (TB meningitis, Miliary TB)?
2 years
What is the general rule for treating TB?
Combination chemotherapy due to rapidly developing resistance
What is Isoniazid's mechanism of action?
inhibits Mycolic Acid synthesis
Isoniazid: STATIC or CIDAL?
CIDAL in GROWING cells only
Anti-TB with these pharmacokinetics:
-CNS levels ~20% of serum level

-Intracellular = Extracellular
What is the key factor in the pharmacokinetics of Isoniazid?
Metabolism: acetylated in the liver
Who are "Fast" acetylators of Isoniazid?
1. 50% of US blacks and whites
2. most Eskimos, Asians, Native Americans
What is the half-life for Fast and Slow Acetylators of Isoniazid?
Fast = < 1.5 hrs

Slow = > 3 hrs
In what patients may you have to alter doses when giving Isoniazid and why?
Hepatic disease patients
- due to Acetylating ability

**lower doses in Liver disease
What is excreted in the urine of Isoniazid?
INH and Acetylated product
What are the clinical uses of Isoniazid?
Prophylaxis = used alone

Combo chemotherapy for TB

**only agent used as solo prophylaxis against TB
What drugs is Isoniazid used with in Combination chemotherapy?
- Rifampin
- Isoniazid
- Pyrazinamide
- Ethambutol
What are the adverse effects of Isoniazid dependent on?
Dose and Duration
What are the adverse effects of Isoniazid? (2) (hint)
1. Hepatotoxicity that increases with age
-more common in alcoholics and pregnant women
*induces CYP 2E1 along with alcohol to bioactivate Acetaminophen -> liver toxicity

2. Neurotoxicity
INH = Injures Neurons & Hepatocytes
How do you counter the neurotoxocity of Isoniazid?
give Pyridoxine (vitamin B6)
How do Mycobacteria become resistant to Isoniazid?
deletion of katG gene = enzyme normally activates INH
Where in the world is Isoniazid resistance higher? (2)

What is Ethambutol's mechanism of action?
inhibits synthesis of mycobacterial cell wall arabinogalactan
What is the mnemonic for Anti-TB drugs
- Isoniazid
- Streptomycin
- Pyrazinamide
- Isoniazid
- Rifampin
- Ethambutol
Anti-TB with these pharmakokinetics:

1. CNS level variable = 4-60% of serum

2. most excreted in urine = accumulates in renal failure
Anti-TB that may cause dose-dependent Optic Neuritis
Rifampin mechanism of action
inhibits bacterial RNA synthesis
Rifampin: STATIC or CIDAL
How is Rifampin excreted?
Bile = can cause liver problems
What are the adverse effects of Rifampin?
1. Inducer of Microsomal enzymes
- alters half-life of Anticoagulants, oral contraceptives
2. Hepatotoxic
3. "Flu-like" syndrome
4. Gives orange color to body fluids
What are the 4 R's of Rifampin?
1. RNA polymerase inhibitor
2. Revs up microsomal P-450
3. Red/orange body fluids
4. Rapid resistance if used alone
What are the clinical uses of Rifampin?
1. Combo therapy for active TB

2. Single agent prophylaxis for INH-intolerant patients or INH-resistant bug
Pyrazinamide: Static or Cidal?
What is this Anti-TB:
unknown but is activated by the Mycobacterium
-strains lacking the activating enzyme are resistance
What are the adverse effects of Pyrazinamide?
1. Hyperuricemia
2. Gouty arthritis
3. Hepatotoxicity
Why was Streptomycin rarely used for TB? Why is it now used more often?
Had bad pharmacokinetics and adverse side effects

Resistance to the other drugs
Why are second-line Anti-TB drugs usually not used?
because the toxicity outweights the therapeutic effects EXCEPT for highly resistant strains
List 5 2nd line Anti-TB drugs (hint)
1. Cycloserine
2. Para-aminosalicylate
3. Ethionamide
4. Capreomycin
5. Dapsone

*Others: Amikacin, -floxacin's
ETHIOpian CYCList wearing CAPRis PAS's Da (p) zone but still takes 2nd place