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Pharmacology Flashcards

1
Q

What is the primary site for most oral drug absorptions?

A

Small intestine

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2
Q

What is the first pass effect?

A

A phenomenon of drug metabolism at a specific location in the body which leads to a reduction in the concentration of the active drug, specifically when given PO, before it reaches the site of action or systemic circulation

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3
Q

What method of drug administration skips first pass metabolism?

A

TM and rectal allow for absorption through GIT segments that are not drained by the portal circulation

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4
Q

Why is respiratory drug administration highly effective?

A

The alveoli are thin with excellent surface area and lined heavily with capillaries, allowing a drug to rapidly and directly enter systemic circulation

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5
Q

What 4 factors is drug distribution dependent on?

A
  1. Physicochemical properties of the drug
  2. Concentration gradient established between blood and site of infection
  3. Ratio of blood flow to site of action
  4. Affinity of the drug for tissue constituents
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6
Q

Where are lipid soluble drugs distributed to?

A

All body water, therefore found in both the ICF and ECF

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7
Q

What are water soluble drugs distributed to?

A
  • Only in the ECF
  • Important to remember that the volume of ECF is altered in disease
  • In hypovolemia, the ECF shrinks as the depleted water volume shifts to the ICF = increased concentration of drug confined in ECF = potential toxicity
  • In edema, ECF volume increases = lowers concentration of drug = subtherapeutic level
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8
Q

What effect do liver shunts have on drug distribution?

A

Shunts prevent the distribution of drugs to the liver for essential metabolism which can result in toxicity if the drug if the drug is active and remains in circulation, or in failure of therapy if drug relies on biotransformation in liver

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9
Q

What is the MDR1 gene?

A
  • P-glycoprotein 1 or ATP binding cassette subfamily B member 1 (ABCB1)
  • A protein (drug transporter) highly distributed within GIT, kidney, liver, and BBB that can remove foreign substances, including drugs, out of cells
  • It can transport substances from brain tissue back into capillary lumen, limiting brain exposure to drugs
  • Certain breeds lack full expression of the MDR gene and are susceptible to toxic brain exposure/increased sensitivity to drugs
  • Herding dogs, aus shepherds, collies
  • Avermectins, chemo, loperamide
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10
Q

How does hypoalbuminemia affect drug efficacy?

A
  • Drugs can exist bound to plasma proteins = inactive to the body, or unbound to plasma proteins = active and available to cross cell membranes
  • Drugs must be in the unbound state for metabolism and elimination
  • The fraction of unbound/active drug may shift and produce a greater effect
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11
Q

What is the cytopchrome P450 (CYP) dependent system?

A
  • The primary microsomal enzyme system responsible for the oxidative metabolism of endogenous compounds
  • It catalyzes a diverse range of oxidative reactions
  • It is essential for the metabolism of many medications
  • CYPs are expressed in liver (primary), intestine, brain, kidneys
  • This system can convert drugs to inactive metabolism, active prodrugs, or create toxic metabolites
  • Any time 2 drugs rely on CYP metabolism there is the potential for drug interaction
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12
Q

What is glucuronidation?

A
  • A metabolic pathway that involves the conjugation of glucose with other compounds to form glucuronides, which are then excreted in urine and bile
  • An elimination and detoxification mechanism for a host of lipophilic compounds
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13
Q

Why do cats have a decreased ability to effectively perform phase II metabolism?

A
  • Cats can’t synthesize glucuronic acid to the extent needed to metabolize some drugs, leading to toxicity
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14
Q

What is an enzyme inducer?

A
  • A drug that can activate or enhance P450, resulting in increased drug mnetabolism
  • Pheno, St. John’s Wort
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15
Q

How are most drugs eliminated from the body?

A

Via the urine through the kidney by glomerular filtration

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16
Q

What form must drugs be in to be eliminated?

A

Drugs must be water soluble, smaller in molecular weight, polar, ionized, and unbound to plasma proteins to be eliminated

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17
Q

Why are kidneys susceptible to drug induced toxicity?

A

Due to their high blood flow, tendency to concentrate drugs in glomerular infiltrates and passively reabsorb them

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18
Q

What is enterohepatic recycling?

A

Some drugs are eliminated in the bile and can be reabsorbed later in the GIT and re-enter the circulatory system

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19
Q

What is the purpose of a CRI?

A

To administer new drug to the body at the same time the drug is being metabolized and eliminated, thus ‘ins and outs’ is balanced

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20
Q

Why should a loading dose be given when starting a CRI?

A

In the absence of a loading dose, a CRI will reach steady state plasma concentrations in 3-5 drug half lives

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21
Q

What is pharmacokinetics?

A
  • The study of absorption, distribution, metabolism, and excretion/eliminating of drugs and their metabolites
  • What the body does to the drug
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22
Q

What is pharmacodynamics?

A
  • The study of the responsiveness of receptors to a drug and the mechanisms by which these effects occur and impact the body
  • What the drug does to the body
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23
Q

What is a ligand?

A
  • Any chemical that binds to receptors: drugs, hormones, neurotransmitters
  • When a ligand and receptor bind, a cellular response occurs which serves a biological purpose
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24
Q

What is chelation?

A

Chelating agents work independently of receptors. They bind directly to heavy metals in the body and promote their excretion

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25
Q

Why can drug distribution be altered in pediatrics and geriatrics?

A
  • Due to increased total body water, decreased fat stores, and hypoproteinemia
  • Pediatrics may have fewer P450 enzymes and decreased ability to perform glucuronidation, making drug metabolism immature
  • The pediatric renal system is not fully developed until ~ 8 weeks, which may decreases drug clearance
  • Pediatrics may have increased BBB permeability, giving some drugs more profound CNS effects
  • Geriatrics are at increased risk for CKD, which reduces GFR and decreases drug clearance
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26
Q

How does apomorphine induce emesis?

A

It stimulates the CRTZ to induce emesis as a nonselective dopamine agonist

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27
Q

Why is apomorphine highly effective in dogs?

A
  • Histamine and dopamine are significant neurotransmitters in the canine CRTZ, making dopaninergic and histaminergic receptor antagonists important antiemetic classes
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28
Q

Why is apomorphine less effective in cats?

A
  • Alpha 2 adrenergic and 5HT3 serotonergic receptors are the significant neurotransmitters in the feline CRTZ
  • Cats have fewer dopamine receptors
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29
Q

Why is xylazine the emetic drug of choice for cats?

A

It is an alpha 2 adrenergic agonist and stimulates the feline CRTZ

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30
Q

How do phenothiazine derivatives exert their effects as antiemetics?

A

They block dopamine receptors in the CRTZ

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31
Q

How does Ondansetron reduce nausea/emesis?

A

It is a serotonin antagonist

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32
Q

How does maropitant work?

A

It is a neurokinin-1 (NK) antagonist that blocks substance P (a neurotransnitter) at the VC

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33
Q

Why should maropitant only be given for 5 days?

A

It utilizes two P450 enzymnes, one of which has low capacity, leading to accumulation

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34
Q

What effect can maropitant have in dogs under 8 weeks old?

A

Bone marrow suppression

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35
Q

How do proton pump inhibitors work?

A

They inhibit Na+/K+-ATPase pump activity, thereby controlling proton deposition into the gastric lumen and hydrochloric acid production

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36
Q

How does omeprazole work?

A

Binds to the secretory surface of parietal cells, inhibiting transport of H+ ions into the stomach

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37
Q

How do H2 histageneric antagonists exert their effects?

A

They are specific antihistamines that reduce the action of histamine at histamine receptors on gastric parietal cells, thereby reducing stomach acid production

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38
Q

All H2 antagonists can cause ____ if given too rapidly IV

A

Bradycardia

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39
Q

Cimetidine is a known P450 enzyme ____?

A
  • Inhibitor
  • Decreased metabolism, prolonged 1/2 life, and increased serum level of many drugs
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40
Q

How can Ranitidine exert a weak prokinetic effect?

A

Due to inhibition of acetylcholinase, thereby stimulating parasympathetic innervations of gastric and intestinal motility

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41
Q

How does sucralfate work?

A
  • It prevents stomach acid from reaching the site of injury and reduces breakdown of mucus
  • It promotes bicarbonate production and may increase production of prostaglandins
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42
Q

What is misoprostol?

A
  • A synthetic prostaglandin analogue
  • Improves gastric blood flow, decreases gastric acid production, increasing mucus production, and bicarbonate secretion and promoting cell turnover, leading to accelerated healing of gastric ulcers
  • Used to prevent NSAID induced GI injury and ulceration
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43
Q

Why is a furosemide CRI superior to intermittent boluses?

A

Creates more diuresis and Na & Ca excretion with less K loss

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44
Q

Where does Spironolactone exert its effect?

A
  • It competitively binds to its receptor site in the distal tubule and collecting duct
  • Permits Na, Ca, & H2O excretion but limits K excretion
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45
Q

Where do thiazide diuretics exert their effects?

A

They inhibit the Na Cl ion transporter within the distal tubule of kidney, enhancing excretion of H2O, Na, Cl, K, and Mg

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46
Q

How does pimobendan exert its effect?

A
  • Phosphodiesterase III inhibitor that increase the concentration of intracellular Ca, ultimately enhancing the cardiac contractility and cardiac output
  • Does not increase myocardial oxygen consumption
  • An inodilator: combo of positive inotrope and vasodilation
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47
Q

How do ACE inhibitors exert their effect?

A

By blocking the conversion of Angiotensin I to II, which lowers arteriolar resistance, increases venous capacity, increases natriuresis, decreases BP, and decreases ventricular remodeling and ventricular hypertrophy

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48
Q

How do the calcium channel antagonists exert their effects?

A
  • Classified as dihydropiridines or non dihydropiridines; bind to different sites to the Ca channel
  • Non-dih: more myocardial selective, tend to reduce HR (Diltiazem)
  • Dih: more vascular selective, dilates vascular smooth muscle, reduces afterload, lowers BP
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49
Q

How do nitrates exert their effects?

A
  • The treatment of fulminant CHF often depends on rapidly reducing vascular resistance, reducing afterload, and improving cardiac function
  • The nitrate drugs, sodium nitroprusside and nitroglycerin, are metabolized in the body to form nitric compounds
  • Their production and subsequent diffusion into vascular smooth muscle cells mediate relaxation, venodilation and vasodilation, thus reducing afterload
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50
Q

How does nitroprusside exert its effect?

A
  • Immediately produces a decrease in SVR, which can cause a decrease in arterial BP
  • Reduces afterload
  • Used for acute hypertensive crisis or fulminant CHF
  • Can be used in conjunction with inotropes
  • Easily titratable
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51
Q

How does Hydralazine exert its effect?

A
  • It is a direct acting vascular smooth muscle relaxant that works primarily on arteries and arterioles
  • Causes vasodilation, afterload reduction, and lowering of BP
  • Primarily used for hypertensive crisis, but can be used for CHF
  • Harder to titrate than n/p, can result in hypotension and a baroreceptor reflex causing increased HR
52
Q

How do alpha-1 adrenergic antagonists/alpha blockers exert their effects?

A
  • They can be selective and work solely on alpha-1 receptor OR
  • Non selective and also work on the alpha-2 adrenergic receptor
  • They relax vascular smooth muscle, producing vasodilation, afterload reduction, and decreased SVR
  • Phenoxybenzamine, Prazosin, Phentolamine
53
Q

What is dopamine?

A
  • The precursor to norepinephrine
  • A catecholamine and sympathomimetic agent
  • A beta and alpha adrenergic agonist
  • Administer as CRI, do not give loading dose
54
Q

What is epinephrine?

A
  • A catecholamine with A2 & B2 adrenergic agonist properties
  • Low dose: predominant beta-agonist effect: vasodilation, bronchodilation, increased cardiac contractility & CO, increased HR
  • High doses: more alpha 1 adrenergic effects predominate, & pronounced vasoconstriction occurs
55
Q

What is norepinephrine?

A
  • A sympathomimetic & catecholamine with alpha 1 and beta 1 adrenergic agonist effects utilized to improve BP in patients unresponsive to IVFT
56
Q

What is dobutamine?

A
  • A sympathomimetic agent with beta 1 adrenergic agonist effects
  • Increases
57
Q

Why is vasopressin used for cases of refractory hypotension?

A
  • It increases SVR as a vasoconstrictor
58
Q

Drugs that target platelet function are for ______ thromboemobolism

A

Arterial

59
Q

Drugs that inhibit coagulation cascade directly are for ____ thrombosis

A

Venous

60
Q

How does aspirin exert its effect?

A
  • It results in the blockade of platelet COX 1, which causes inhibition of thromboxane A2
  • TXA2 plays an important role in the recruitment & activation of platelets to the site of vascular injury
  • Its inhibition results in a decreased rate & degree of platelet aggregation
  • Primary use is in hypercoagulable states or states of increased platelet reactivity (IMHA)
61
Q

How does clopidogrel exert its effect?

A
  • It blocks adenosine diphosphate (ADP) induced platelet aggregation
  • Has potential to interact with other drugs that alter P450 enzymes
62
Q

Heparins

A
  • A naturally occuring substance stored within secretory granules of mast cells
  • Prophylactic agents only
  • Indirect anticoagulants = they work by enhancing the pre-existing properties of antithrombin
  • In situations where antithrombin may be decreased, such as PLE< they may have decreased efficacy
63
Q

What is the reversal for heparin?

A
  • Protamine sulfate
  • Does not fully reverse LMWH
64
Q

How does heparin exert its effect?

A
  • Binds to antithrombin
  • Inactivates thrombin
  • Inhibits factors IIa, IXa, Xa, XIa, XIIa
65
Q

What are direct Factor Xa inhibitors?

A
  • Rivaroxaban, apixaban
  • Does NOT require antithrobim for clinical effect
  • PO only
  • Does not dissolve clots
  • No antidote
66
Q

Can thrombolytics be given for cardiac thrombi?

A

No, contraindicated

67
Q

Why should thrombolytics be given immediately after clot identification?

A

Older clots contain more extensive fibrin, making them more resistant to dissolution

68
Q

What class of drug is diphenhydramine?

A

An inverse agonist of the H1 histageneric receptor

69
Q

What effects do beta 2 adrenergic agonists have?

A
  • They are effective bronchodilators and enhance mucus clearance
  • They relax smooth muscle in respiratory passages and can cause vasodilation in muscle
70
Q

What are methylxanthines?

A
  • Bronchodilators that inhibit phosphodiesterase and block adenosine and reduce inflammation
  • Second choice to beta 2s because of their narrower therapeutic window
71
Q

Why does diphenhydramine cause sedation in people?

A

It can cross the BBB and produce a CNS effect

72
Q

List some other antihistamines

A
  • Meclizine (used for motion sickness)
  • Cyproheptadine (appetite stimulant and serotonin antagonist)
  • Mirtazapine (antiemetic effects, and affects histamine, serotonin, adrenergic, dopamine, muscarinic receptors)
73
Q

What is arachadonic acid?

A

An essential fatty acid and a precursor in the biosynthesis of prostaglandins

73
Q

NSAIDs reduce peripheral ________

A

sensitization along the transduction part of the nociceptive pathway and may also work centrally

74
Q

Do NSAIDs have a direct effect on pain receptors?

A

No. The modulation of inflammation results in analgesia

75
Q

What are the four main classes of NSAIDs?

A
  • Carboxylic acids (aspirin, salicylates)
  • Propionic acids (ibuprofen, ketoprofen, carprofen, naproxen)
  • Enolic acids (phenylbutazone, piroxicam)
  • Acetic acids (etodolac)
76
Q

Why should NSAID administration be avoided with concurrent use of highly protein bound drugs?

A

They will compete for binding sites in plasma proteins, leaving more unbound and pharmacokinetically active drug
- NSAIDs decrease the effects of furosemide, thiazides, ACE inhibitors, and beta blocks

77
Q

What are glucocorticoids?

A
  • Primary: cortisol
  • Vitals for normal homeostatic function and have a large impact on the immune system and metabolic function
  • Act on the immune system to upregulate the expression of anti inflammatory proteins and downregulate the expression of pro inflammatory proteins
  • Stimulate gluconeogenesis, inhibition of glucose uptake, and fat breakdown
78
Q

What are mineralcorticoids?

A
  • Primary: aldosterone
  • Plays a critical role in body’s management of BP & BV
  • Influences electrolytes and water balance in body
79
Q

Which two corticosteroids are specifically used for physiologic replacement only as treatment of hypoadrenocorticism?

A
  • Fludrocortisone: mineralocorticoid activity
  • Desoxycorticosterone: potent mineralocorticoid with questionable glucocorticoid activity
80
Q

What is the minimum inhibitory concentration (MIC)?

A

The least amount of drug that can prevent growth on an agar plate after incubation

81
Q

What is vertical transfer?

A
  • Accomplished by reproduction: a copy of genetic info is given to offspring
82
Q

What is horizontal transfer?

A
  • Achieved by plasmids (small portions of genetic code) that can be take up by other organisms and encoded in their DNA
  • This can achieve resistance in entire colonies
83
Q

Responsible stewardship: are abx indicated when a patient only displays leukocytosis?

A

No

84
Q

Responsible stewardship: are abx indicated when a patient has a fever with toxic neutrophil changes?

A

No - this indicates infection, but they still may not be needed (patient may overcome on their own)

85
Q

Responsible stewardship: are abx indicated when a patient has a fever with neutropenia?

A

Yes

86
Q

What are beta-lactam antimicrobials?

A
  • Broad spectrum drugs that contain a beta-lactam ring in their molecular struction
  • Bactericidal
  • Only effective on cells that are in their growth phase
  • They inhibit the formation of polymers that form the bacterial cell wall
  • Gram positive more susceptible
  • Penicillins, cephalosporins
87
Q

What are aminoglycoside antimicrobials?

A
  • Bactericidals against most gram neg aerobics
  • Gebtamicin, amikacin, neomycin, tobramycin
  • Poorly absorbed from GIT, given parenterally
  • High adverse effect profile & narrow therapeutic window
  • Nephrotoxic & ototoxic (accumulate there)
  • Renal function, UAs should be closely monitored (cast formation, glucosuria)
88
Q

What are fluoroquinolone antimicrobials?

A
  • Bactericidal
  • Widest spectrum is against gram neg
  • Effective against intracellular bacteria
  • Able to reach hard to reach places: CNS, prostate
  • Cartilage deformities have been reported in young, growing animals
  • Cause acute retinal detachment in cats
  • Can chelate with positively charged ions (aluminum and copper; can occur with Mg and Ca)
89
Q

What are macrolide antimicrobials?

A
  • Erythromycin, azithromycin
  • Bacteriostatic
  • Mainly effective against gram pos
  • Effective against intracellular
  • Considered an alternative for patients that can’t have beta-lactams
  • Highly effective as prokinetics at subantimicrobial doses
  • Potent inhibitors of P450 enzyme system & therefore can potentiate effects of other drugs
90
Q

What are lincosamide antimicrobials?

A
  • Clindamycin
  • Effective against gram pos
  • Effective at penetrating bone, soft tissue, potentially CNS
  • Recc as partial abx therapy for necrotizing STI
  • Can see anaphylaxis and hepatopathy
91
Q

What are the tetracyclines?

A
  • Bacteriostatic
  • Broad spectrum: effective against gram pos & neg aerobes
  • Effective against intracellular bacteria & atypical organisms —> mycoplasmas, rickettsiae, protozoa, tick born infections Lyme, ehrlichiosis, RMSF
  • Have an antiinflammatory effect and may help treat hyperalgesia
  • High incidence of GI upset, always give with food
  • Esophageal stricutre has been noted in cats
  • Caution in young animals as it can cause discoloration of teeth and can delay bone growth
92
Q

What are the chloramphenicol antimicrobials?

A
  • Bacteriostatic
  • Broad spectrum
  • Has potential to cause serious side effects in humans, including aplastic anemia & bone marrow suppression - wear gloves
93
Q

What are the nitroimidazole antimicrobials?

A
  • Metronidazole
  • Bactericidal & antiprotozoal, also has anti inflammatory effects within the GIT (effective against anaerobes)
  • Known CNS toxicant
94
Q

What are the sulfonamide antimicrobials?

A
  • TMS
  • Broad spectrum
  • Metabolized in liver via acetylation & glucuronidation; cats can’t metabolize
  • Induce Vit K deficiency & consequently coagulopathies, autoimmune anemias, hepatic necrosis, skin lesions
  • Becoming less desirable to use
95
Q

Antifungals - azoles

A
  • Inhibit fungal P450 enzyme required for development of fungal cell walls
  • Ketoconazole can elevate LE & alter metabolism of other drugs
  • Potential for neuro tox in cats
  • Fluconazole drug of choice bc high volune of distribution, minimally protein bound, readily crosses BBB and eye barrier
96
Q

Antifungals - polyenes

A
  • Amphotericin B
  • Chosen for systemic life threatening mycoses
  • Nephrotoxic: binds to cholesterol in renal tubules, causing renal vasoconstriction, renal tub ular acidosis, & AKI
97
Q

Which type of insulin do dogs receive?

A

Porcine

98
Q

Which type of insulin do cats receive?

A

Bovine

99
Q

How does insulin exert its effect?

A
  • Decreases BG by inhibiting glycogen synthesis from absorbed carbs, reduces hepatic production of glucose via gluconeogenesis & glycogenolysis, activates glucose transporters into skeletal muscle cells & adipocytes, and increaes the creation of lipids and decreases their metabolism for energy use
100
Q

What is the only insulin that can go IV?

A
  • Regular/crystalline
101
Q

How many peaks does intermediate insulin cause in dogs?1

A

2

102
Q

How many peaks does intermediate insulin cause in cats?

A

1

103
Q

How does intermediate insulin achieve its length of duration?

A

Contains protamine, a protein that slows insulin absorption

104
Q

How does long acting insulin achieve its length of duration?

A

Forms microprecipitates at the injection site that lasts for 24 hours

105
Q

What are the most widely used immunosuppressive meds used in vet med?

A

Corticoteroids

106
Q

List some commonly used immunosuppressive drugs used in vet med

A
  • Azathioprine
  • Cyclosporin
  • Mycophenolate
  • Leflunomide
107
Q

Azathioprine should not be given to which animal?

A

Cats - not well tolerate

108
Q

What severe side effect can be seen with administration of Human Intravenous Immunoglobulin Therapy?

A

Type 1 Immunoglobulin E-mediated hypersensitivity reaction, manfesting in anaphylaxis

109
Q

What medication is a mild appetite stimulant and serotonin antagonist?

A

Cyproheptadine

110
Q

What medication is a weak appetite stimulant, antiemetic, and has effect on serotonin, adrenergic, dopamine, and muscarinic receptors?

A

Mirtazapine

111
Q

What occurs after tissue injury? (NSAIDS)

A

Arachidonic acid is released from cell membranes

112
Q

What two pathways are established after the arachidonic acid cascade begins?

A

LOX and COX

113
Q

LOX metabolizes arachidonic acid into____?

A

Various leukotrienes

114
Q

COX metabolizes arachidonic acid into____?

A

Prostaglandins, prostacyclin, and thromboxanes

115
Q

What is the recommended length of time to continue antimicrobial therapy before considering failure?

A

72 hours

116
Q

What are two clinical signs that should NOT be used as a reason to begin antimicrobials?

A

Fever, leukocytosis

117
Q

Antimicrobials are unlikely to be beneficial in____?

A
  • Acute lower urinary tract signs in otherwise healthy male cat
  • URTI most commonly caused by viral infections
  • Acute diarrheas (usually not caused by pathogenic bacteria)
  • Acute hemorrhagic diarrheas (have a low incidence of resulting in bacteremia)
118
Q

Antimicrobials work in what 5 ways?

A
  1. Attack cell wall
  2. Attack cell membrane
  3. Ribosomes
  4. Enzymes
  5. Nucleic acids
119
Q

Fluoroquinolones can chelate with____?

A

Positively charged ions: aluminum, copper, magnesium, calcium

120
Q

What two family classes of antimicrobials should not be given together as they have a similar method of action?

A

Macrolides and lincosamides

121
Q

Liver enzyme increase is common after administration of which antimicrobial?

A

Tetracyclines

122
Q

What class of medications binds to cholesterol in renal tubules?

A

Polyenes - amphtericin B

123
Q

What drug can cause gingival hyperplasia?

A

Cyclosporine

124
Q
A

VTS (17 decks)

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