Pharmacology Block 8 (1-4)

Front 1

What drug class is enalapil?

Back 1

It is an Angiotensin Converting Enzyme Inhibitor (ACEI)

Front 2

Where and what is enalapril conveted to?

Back 2

It is converted to enalaprilat within the liver.

Front 3

What are the contraindications and adverse reactions associated with enalapril?

Back 3

hypersensitivity to ACE inhibitors; GI distress (anorexia, vomiting, diarrhea); potentially: weakness, hypotension, renal dysfunction and hyperkalemia

Front 4

What are the primary indications or uses of enalapril?

Back 4

ACE inhibitors are used primarily as a vasodilator in the treatment of heart faiulre or hypertension; may also be of benefit in the treatment of chronic renal failure or protein losing nephropathies

Front 5

What is the MOA of enalapril?

Back 5

it is converted in the liver to the active compound enalaprilat; which prevents the formation of angiotensin II ( a potent vasoconstrictor) by competing with angiotensin I for the enzyme angiotensin-converting enzyme (ACE). ACE has a much higher affinity for enalaprilat than for angiotensin I; because angiotensin II concentrations are decreased aldosterone secretion is also reduced and plasma renin activity is increased.

Front 6

What drug class is colchicine a part of?

Back 6

It is a unique antiinflammatory agent.

Front 7

What are the most likely adverse effects of colchicine?

Back 7

GI distress (early sign of toxicity) but several serious effects are possible, including bone marrow suppression

Front 8

What is the MOA of colchicine?

Back 8

The MOA is not completely understood but it probably is related to the drug's ability to reduce inflammatory response to the disposition of monosodium urate crystals. It inhibits cell division during metaphase by interfering with sol-gel formation and mitotic spindle. Also blocks the synthesis and secretion of serum amyloid A (SAA; an acute phase reactant protein) by hepatocytes thereby preventing the formation of amyloid-enhancing factor and preventing amyloid disposition

Front 9

What are the uses/indcations of colchicine?

Back 9

treatment of amyloidosis, however once the amyloid A is deposited into the kidney it can not effectively remove it but may be able to prolong the life of the patient by providing anti-inflammatory effects in the kidney and preventing some accumulation of amyloid. Also used in hepatic fibrosis. (increases the breakdown of collagen)

Front 10

What is the absorption, metabolism,excretion and half-life of colchicine?

Back 10

absorbed in the GI, metabolized in the liver (first pass effect), "recycling activity in the GI" half-life 20 minutes, leukocyte half-life 60 hours, and excreted in the urine

Front 11

What is the use/indications of pentobarbital agents?

Back 11

For the humane euthanasia of animals, but not animals for food

Front 12

What is the MOA of pentobarbital?

Back 12

Pentobarbital causes death by severly depressing the medullary respiratory and vasomotor centers when administered at high doses

Front 13

What are the contraindications/percautions of pentobarbital?

Back 13

must not be used in animals for food purposes, extreme care in handling filled syringes and proper disposal of used injection equipment must be undertaken. AVOID any contact with open wounds or accidental infection.
Prior to use a tranquilizing agent may be necessary when the animal is in pain or agitated.

Front 14

What are the adverse effects/warnings of pentobarbitol?

Back 14

minor muscle twitching may occur after injection. Death may be delayed or not accomplished if injection given perivascularly.

Front 15

What is the use/indication of Nitrofurantoin?

Back 15

It is an antibacterial used for susceptible UTI's

Front 16

What are the contraindications of Nitrofurantoin?

Back 16

renal impairement; hypersensitivity to it

Front 17

What are the adverse effects of Nitrofurantoin?

Back 17

gastrointestinal distrubances and hepatopathy of most concern; may cause infertility in males or peripheral neuropathy

Front 18

What is the MOA of Nitrofurantoin?

Back 18

It is a bacteriostatic antimicrobial but may be bactericidal depending on the concentration of the drug and the susceptibility of the organism. The exact MOA has not been fully elucidated but the drug apparently inhibits various bacterial enzyme systemc, including acetyl coenzyme A.

Front 19

What is the activity (against what organisms) of nitrofurantoin?

Back 19

It is affective against several gram-negative and some gram-postitive organisms, including many strains of E.coli, Klebsiella, Enterobacter, Enterococci, Staphylococcus aureus and epidermidis, Enterobacter, Citrobacter, Salmonella, Shigella and corynebacterium. Little or no activity against most strains of Proteus, Serratia or Acinetobacter and has no activity agsint Pseudomonas spp.

Front 20

What are the pharmacokinetics of nitrofurantoin?

Back 20

eliminated into urine unchanged via both glomerular filtration and tubular secretion. Some of the drug is metabolized primarily in the liver. Half-life is about 20 minutes for humans. Absorbed from the GI tract and absorption is enhanced in the presence of food.

Front 21

What is xylazine?

Back 21

It is an alpha2-adrenergic agonist structurally related to clonidine. It is classified as a sedative/analgesic with muscle relaxant properties.

Front 22

What are the effects of xylazine?

Back 22

causes sedation and CNS depression, skeletal muscle relaxation through central mediated pathways, emesis is often seen in cats, occasionally in dogs, depresses thermoregulatory mechanisms and either hypothermia or hyperthermia is a possiblity depending on ambient air temperatures, initial increase in totoal peripheral resistance with increased blood pressure followed by a longer period of lowered blood pressure, enhances the arrhythmogenic effects of epinephrine, high doses respiratory depression, increases blood glucose.

Front 23

What are the pharmacokinetics of xylazine?

Back 23

absorption: rapid following IM injection
HORSES:
Onset of action: 1-2 minutes with a max effect 3-10 minutes after injection
duration: dose dependent but may last for approx. 1.5 hours
half-life: approx. 50 minutes
DOGS AND CATS:
Onset: IM or SC 10-15 minutes, and 3-5 min. IV
duration: analgesic properties 15-30 min, sedative actions 1-2 hours
serum half-life: 30 minutes

Front 24

What class of drugs does amikacin belong to?

Back 24

aminoglycoside

Front 25

What is the action of amikacin?

Back 25

it is a bactericidal agent

Front 26

What is the MOA of amikacin?

Back 26

like other aminoglycosides it acts on susceptible bacteria presumably by irreversibly binding to the 30S ribosomal subunit thereby inhibiting protein synthesis

Front 27

How is amikacin eliminated?

Back 27

kidneys

Front 28

What are the main toxicity features of amikacin?

Back 28

nephrotoxic, ototoxic (vestibular and deafness), NM blockade

Front 29

What is the spectrum of activity for amikacin?

Back 29

may aerobic gram-negative, and some aerobic gram-postitive bacteria (E. col, Klebsiella, Proteus, Pseudomonas, Salmonella, Enterbacter, Serratia, and Shigella, Mycoplasma, and Staph)
**inactive against fungi, vruses and most anaerobes

Front 30

What are the active ingrediants of Clavamox?

Back 30

amoxicllin and clavulanic acid

Front 31

What is the drug class of clavamox (amoxi and clavulanic acid)?

Back 31

potentiated penicillin

Front 32

What is the action of clavamox?

Back 32

it is a bactericidal agent

Front 33

What is the site of action of clavamox?

Back 33

amoxicillin works on the cell wall and clavulanate is a penicillnase inhibitor

Front 34

What is the distribution of amikacin?

Back 34

extracellular

Front 35

What are the local factors that decrease efficacy?

Back 35

purulent debris

Front 36

What is the distribution of amikacin?

Back 36

extracellular

Front 37

What are the local factors that decrease efficacy of clavamox?

Back 37

purulent debris for amoxi

Front 38

What is the spectrum of action of clavamox?

Back 38

staph, strep, coliforms, obligate anaerobes

Front 39

What is the drug class of ampicillin?

Back 39

beta-lactam (broad-spectrum penicillin)

Front 40

What is the action of ampicillin?

Back 40

bactericidial

Front 41

What is the site of action for ampicillin?

Back 41

cell wall

Front 42

What is the primary site for elimination of ampicillin, and clavamox?

Back 42

renal

Front 43

What is the distribution of ampicillin?

Back 43

extracellular

Front 44

What are the local factors that decrease efficacy of ampicillin?

Back 44

purulent debris

Front 45

What is the spectrum of action of ampicillin?

Back 45

strep, +/- colforms, obligate anaerobes (not B. fragilis), possibly sensitivie to staph but really an inferior agent (other agents used instead)

Front 46

what is the special spectra of ampicillin, penicillin G, and amoxicillin?

Back 46

corynebacteria some spirochetes

Front 47

What is the drug class of trimethoprim/sulfa (TMP/SMZ)?

Back 47

potentiated sulfonamide

Front 48

What is the site of action of TMP/SMZ?

Back 48

it is bactericidal; however Trimethoprin: bacteriostatic
Sulfadiazine: bacteriostatic

Front 49

What is the site of action of TMP/SMZ?

Back 49

Trimethoprin: enzyme dihydrofolc acd reductase
sulfadiazine: competes with PABA

Front 50

What is the site of elimination for TMP/SMZ?

Back 50

renal

Front 51

What is the potential toxicities that can occur with TMP/SMZ?

Back 51

Trimethoprine: bone marrow suppression (high dose and/or long term use)
Sulfadiazine: crystalluria, hepatotoxicity (rare), hypothyroidism (long-term use), immune mediated KCS and polyarthropathy
*no risk of crystalluria for the combo because sulfa dose is much lower in the pot. sulfa

Front 52

What is the drug class of Trimethoprim?

Back 52

benzylpyrimidine

Front 53

What is the drug class of sulfadiazine?

Back 53

sulfonamide

Front 54

What is the distribution of trimethoprim and sulfadiazine?

Back 54

trimethoprim: intraceullular and across bbb and blood-aqueous barrier
sulfadiazine: intracellular to milk, prostate, phagocytes, intraceullar and across bbb and blood-aqueous barrier (most sulfa are extracellular but this one has low protein binding)

Front 55

What are the local factors that decrease efficacy of sulfadiazine?

Back 55

purulent debris

Front 56

What is the spectrum of action with TMP/SMZ?

Back 56

staph, strep, coliforms, and could be sensitive to obligate anaerobes
Trimethoprim: (NEVER USED AS A SINGLE AGENT)
Sulfadiazine: possibly susceptible to staph, strep, coliforms and resistant to obligate anaerobes

Front 57

What is the action of penicillin G?

Back 57

bacteriocidal

Front 58

What is the site of penicillin G?

Back 58

cell wall

Front 59

What is the potential toxicity of K-PEN?

Back 59

potential cardiac arrhythmias if given too fast IV