Phar 342 - Material For Midterm 1 (Kumar Part 2/3)

Front 1

Which Aminoglycoside was the first one used for clinical purposes?

Back 1

Streptomycin

Front 2

What are the most common Aminoglycosdies?

Back 2

Tobramycin, Amikacin, Gentamicin. Gentamycin is the most used, and Amikacin is used when the organims is resitant to Gentamycin.

Front 3

Do Aminoglycosides work well against Anaerobes?

Back 3

No

Front 4

What are the theraputic uses of Aminoglycosides?

Back 4

1)Severe infection of abdomens/urinary tract/bacteremia and endocarditis

2) CNS infections [meningitis, ventriculties]

3) Bone and Joint infections

4) Plague

5)Pneumonia

6) Tuberculosis

7) Skin and Soft Tissue infection s

Front 5

How are Aminoglycosides are administered?

Back 5

Usually given by IV and Intrathecal routes

Front 6

"Aminoglycosides are rarely seen in CSF and Brain unless given by IV and Intrathecal" True or False?

Back 6

True

Front 7

What is the MOA of Aminoglycosdies ?

Back 7

It works by blocking Protein synthesis, through the irreversible binding to the 30S bacteria ribosome, interefering with initation between mRNA and 30S subunit.

Front 8

"Are aminoglycosides given with penicillin"?

Back 8

No

Front 9

What are the pharmacokinetics of Aminoglycosides?

Back 9

Not absrobed well orally, but given via IM or IV. Found in all the tissues except the CNS (unless given with IV/Intrathecal) . No metabolism of Aminoglycosides occurs in the hos, but is rapidly excreted by glomerular filteration

Front 10

What are the charactersisitcs of Aminoglycosides?

Back 10

highly polar cation, and this is why its poorly absorbed from GI tract

Front 11

"Elimination of Aminoglycosides takes 30-60hrs for anephric patients" True or False?

Back 11

TRUE

Front 12

What are the toxcities of Aminoglycosides?

Back 12

1) Nephrotoxcity

2) Ototoxcity

3)Neuromuscular Blockade

Front 13

"Aminoglycoside intracellular concentration is low in ALL cells of the body"True or False?

Back 13

False, proximal renal tubules stores relatively higha amount of Aminoglycosides

Front 14

"Nephrotoxcitiy is a reversible side effect of Aminoglycosides" True or False?

Back 14

TRUE

Front 15

"Ototoxcity is a reversible side effect of Aminoglycosides" True or False?

Back 15

FALSE

Front 16

How do you treat a Nerumoscular Blockade caused by Aminoglycosides?

Back 16

Treat with Calclium Gluconate or Neostigmine

Front 17

"All Aminoglycosides have the same toxcity profile" True or False?

Back 17

TRUE

Front 18

What are the common side effects of Aminoglycosides?

Back 18

Headache, Dizzines, Vertigo, Skin Rash, Fever and Parasthesia

Front 19

What are the drug interactions of Aminoglycosides?

Back 19

1) Increased effects of anticoagulants

2) Cephalothin may increase renal toxcity 3)Diuretics increase renal toxcity and ototoxcity

Front 20

What are the causes of mechanims of resistance of Aminoglycosides?

Back 20

1) Drug does not reach to the target

2) Drug is not active due to acetylation /phosphrylation

3)Target is altered via mutation

Front 21

Which Aminoglycoside is the preffered one for the treatment of Pseudomonas aeruginosa or when th organism is unknown?

Back 21

Tobramycin

Front 22

What are the characteristics of Chloramphenicol?

Back 22

Bacteriostatic against a wide range of bacteria but is bacteriacdial against Hemophilus, Neisseria and Pneumoccus

Front 23

"Chloramphenicol is a derivative of _________"

Back 23

Dichloroacetic Acid

Front 24

What are the uses of Chloramphenicol?

Back 24

1) CNS infections when the patient is allergic to penicillins

2) Typhoid fever in patients unable to to tolerate ampicillin/amoxcillin or cotrimaxozole

3) Rickettsial infections when tetracyclines are not tolerated

4) Topically in skin and ophtalmic preparetions

Front 25

"Chloramphenicol is not effective against Chlamydial infections" True or False?

Back 25

TRUE

Front 26

What is the MOA of Chloramphenicol?

Back 26

Inhibits protein syntheisis in bacteria, by binding reversibly to the 50S ribsomoal subunit and so prevents binding of amino acid containing end of tRNA to Acceptor site on 50S ribosomal subunit and cant form peptide bonds

Front 27

What is the pharmacokinetics of Chloramphenicol?

Back 27

Absorbed rapidly from the GI tract. Widely distributed in body fluids AND CSF AND Brain in normal oral doses. Is also present in bile, milk and placental fluid. It is eliminated by metabolization by the liver and inactivated by glucuronic acid. Excreted in the urine

Front 28

What are the precautions of Chlormphenicol use?

Back 28

Might cause fatal blood dyscrasis, because of this it is now reserved for the treatment of life threatiening infection in patients who cannot take safer alternatives because of resistance or allergies

Front 29

What are the toxcities of Chloramphenicol?

Back 29

GI: Nausea and Vomitting. Hematologic: Aplastic Anemia (the failure to make new RBC)[therefore need to monitor blood cell count every 2-3 days. Aleergic Skin Reactions.

Front 30

Which antibiotic can cause 'Grey Baby Syndrome'?

Back 30

Chloramphenicol

Front 31

What is 'Grey Baby Syndrome'?

Back 31

Toxcity of Chloramphenicol in newborns due to accumulation because of an asbsence of necessary liver enzymes in babies resulting in hypotension (low BP), cyanosis and often death

Front 32

What are the drug interactions of Chloramphenicol?

Back 32

Interferes with the actions of penicillin and cephalosporins. Increases the effects of hypoglycemis, barbiturates, phenytoin and anticoagulatnts by decreased metabolism.

Front 33

How does resistance to Chloramphenicol develop?

Back 33

1)Usually resistance is caused by plasmid encoded acetyltransferase that inactivates the drug.

2)Can also be caused by decreased permeability and from ribosomla mutations.

Front 34

"Acetylated derivatives of chloramphenicol can bind to bacterial ribosomes" True or False?

Back 34

False, They cannot bind to bacterial ribsosomes

Front 35

What are the most common Tetracyclines?

Back 35

Tetracycline, Doxycycline and Minocycline

Front 36

What are the characteristics of Tetracyclines?

Back 36

Bacteriostatic , broad spectrum and works agains anaerobes.

Front 37

"Tetracyclines are obtained from cultures of Streptomyces" True or False?

Back 37

TRUE

Front 38

What is the MOA of Tetracyclines?

Back 38

Tetracyclines inhbit proetin synthesis by binding to the 30S subunit of ribosomal RNA and blocking tRNA binding to the A site

Front 39

Whata are the pharmacokinetics of Tetracyclines?

Back 39

Variable oral absorption, given topical, IM or IV. Distributes to all cells.

Elimination varies

1) Teracycline (glomerular filteration)

2) Minocycline (metabolized)

3) Doxycycline (excreted in the feces)

Front 40

What is the order of absorptions of the Tetracyclines?

Back 40

1)Doxycycline/Minocycline (95-100%)

2) Tetracycline (60-80%)

Front 41

What are the therapeutic uses of Tetracyclines?

Back 41

1) STIs by Chlamydia

2) Community Acquired Pneumonia

3) Ricketttsia infections (Rocky Mountain Spotted fever, Qfever)

4) Lyme disease

5) Anthrax

6)Topical ophthalmic preperations

7) Acne/Skin Infections also in the eye

8) When penicillin is contraindicated

9) Doxycycline for Travellers Diarrhea

10) Minocycline has anti-inflammatory effects (Amylotrophic Lateral Sclerosos ALS, Rhematoid Arthritis)

Front 42

What are the side effects of Tetracycylines?

Back 42

1) Discoloration of permanent teeth and tooth enamel in fetuses and children

2) May retard fetal skeletal development if taken during pregnancy

Front 43

Why does food, antacids and iron salts reduce the absorption of Tetracyclines?

Back 43

Because it binds to Ca2+, Mg2+, Al3+ ions to form insoluble complexes.

Front 44

Toxcity of Tetracyclines?

Back 44

1) GI problems

2) Photoxcitiy

3) Hepatotoxcity [pregnant woman are at greater risk]

4) Renal Toxcitiy

5) Teeth and Bone depression and dscoluration if given during development

6) Toxcicity

7) Thrombophlebitis

8) Vestibular

Front 45

"Can we use tetracyclines in young children or pregnant mothers"?

Back 45

NO!!!

Front 46

What are the drug interactions of Tetracyclines?

Back 46

1)Antacids, and iron salts may decrease absorption

2)Tetracycylines block actions of bacteriacidal antibiotics

3) Enhances anticoagulant effects by decreasing prothrombus synthesis

4) Reduces oral contraceptive effect

5)Diuretics increase BUN levels

6) Food decreases absorptions [except Doxycycline]

Front 47

Which tetracycline is unaffected by Antacids or Ions? Why?

Back 47

Doxycyline is missing the Ca2+ and Fe 2+ binding site and so is unaffected by Antacids, Ions or foods.

Front 48

"Tetracyclines can cause Painful Yeast Infections" True or False?

Back 48

TRUE

Front 49

"Tetracyclines can cause Inflammation of small intestine"True or False?

Back 49

TRUE

Front 50

"Tetracyclines can cause Maculpapular rash" True or False?

Back 50

TRUE

Front 51

What are the common names of Macrolides?

Back 51

Erythromycin, Clarithromycin, Azithromycin, Spiramycin

Front 52

What are the chracterisitcs of Macrolides?

Back 52

Bacteriostatic. Narrow Spectrum, Gram Positive bacteria (Mycoplasma, Legionella).

Front 53

How common is resistance in Macrolides?

Back 53

Is very Common

Front 54

What is the MOA of Macrolides?

Back 54

Inhibits translocation, by binding to 50S ribosome, thereby inhibiting translocation of peptides by tRNA.

Front 55

What are the pharmacokinetics of Macrolides?

Back 55

Oral absorption is adequate and it can be given parenterally (IV)

Front 56

"Erythromycin is well known for inhibition of CYP450 enzymes in liver thus increases the half life of other drugs"

Back 56

TRUE

Front 57

What are the uses of Macrolides?

Back 57

1) For infections which would normally be treated with penicillins but the patient is allergic to penicillins

2)Drug of Choice for pulmonary infections especially secondary to mycoplasma or legionella

Front 58

Which Macrolides are preferred for the elderly for H.influenza?

Back 58

Azithromycin, Clarithromycin

Front 59

What is the toxcity of Macroldes?

Back 59

GI: Nausea/vomitting/abdominal cramps. Hepatotoxcity: Cholestatic jaundice. Thrombophlebitis: from IV adminstration.

Front 60

What is cholestatic jaundice?

Back 60

Bile cannot flow from liver to duodenum for excretions

Front 61

What are the drug interactions of Macrolides?

Back 61

1)Anticoagulants

2)Carbamazepine

3)Digoxin

4)Theophylline

5)Triazolom

6)Benzodiazepines

Front 62

What is the MOA of Clindamycin ?

Back 62

Clindamycin blocks protein synthesis.

Front 63

What are the characterisitcs of Clindamycin?

Back 63

Narrow Theraputic index, Gram (+ve) and Anaerobes.

Front 64

What is the toxcity of Clindamycin?

Back 64

More toxic than Macrolides

Front 65

What are the pharmacokinetics of Clindamycin?

Back 65

Oral absorption is very good, paraentrally (IM and IV). Distributes to all tissues well except for CNS. Crosses placenta and is excreted in breast milk. Elimated mainly by the liver.

Front 66

What are the therapeutic uses of Clindamycin?

Back 66

1) For infections where the patient is allergic to penicllins

2)Lung abscess if penicillin is allergic

3) Topically for Acne

4) Cerebral toxoplasmosis in AIDs patients

Front 67

What is "Cerebral Toxoplasmosis"?

Back 67

Parasitic infections deposted in the brain

Front 68

What is the toxcity of Clindamcyin?

Back 68

1)GI: Nausea, Vomitting, Diarrhea, Psuedomembrane Colitis

2)Allergic Reactions

3) Thrombophlebitis (from IV)