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Pharm II (Elise) > Exam 1 Pharm II > Flashcards

Exam 1 Pharm II Flashcards

1
Q

4 Types of drugs that act on the blood

A

(1) Antianemic
(2) Colony Stimulating Factors (CSF)
(3) Drugs affecting hemostasis - pro and anti
(4) Drugs to Treat thromboembolism in cats

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2
Q

4 Classifications of Anemia that require Antianemic Drugs

A

1. Microcytic (hypochrome) anemia = Fe and Cu

2. Macrocytic (megaloblastic) anemia - cobalt

  1. Normocytic anemiadue to CRF or bone marrow suppression - EPO, iron, anabolic steroids

4. Immune- mediated hemolytic anemia (IMHA) - supportive, blood transfusion, Immunosuppresives, IV gamma globulin

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3
Q

Iron preparations

A

Classification: Anti-anemic

MOA: component of heme

Use: Microcytic (hypochromic) anemia in DOGs and PIGLETs

Problems: heavy metal issues (toxic, irritation, estringent), carbohydrates added to parental preparations causes histamine release, SQ & IM administration causes yellow discoloration

ADME: Oral (stable use- less irritating) or Parental (emergency use) divalent is better than trivalent requires carrier protein (epotherotin) to move through body no excretion method- be careful with dose

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4
Q

Copper Preparation

Copper Sulfate & Copper Glycinate

A
  • Classification: Anti-anemic
  • MOA:
    • (1) involved in Fe absorption and metabolism
    • (2) component of cytochrome oxidase
  • Use: Microcytic (hypochromic) anemia in DOGs and PIGLETs
  • Problems: heavy metal issues
  • ADME:
    • –Copper Sulfate= Oral
    • – Copper Glycinate = SC or IM
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5
Q

Cobalt

A

Classification: Antianemic

Use: Macrocytic (megaloblastic) anemia in RUMINANTs

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6
Q

Erythropoeitin, EPO (Epogen)

A
  • Classification: Antianemic
  • MOA:
    • (1) replacement of reduced EPO due to decreased renal production
    • (2) bone marrow stimulation of RBC precursor
  • Use: Anemia due to CRF or bone marrow suppression
  • Problems: vasoconstriction, allergic reaction
  • ADME: inject 2x a week, made by recombination DNA technology ( Dog and human available?)
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7
Q

How do you treat immune-mediated hemolytic anemia?

A

(1) Supportive Therapy = fluids, acid-base balance, organ perfusion

(2) Blood transfusion

(3) Immunosuppresives -

  • — GLucocorticoids (prednisone, presnisolone)
  • — Cytotocic drugs (cyclophosphamide, azathioprine)
  • –Danazol
  • —Cytosporin A

(4) Intravenous gamma globulin

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8
Q

What are the problems associated with heavy metals (such as Iron and Cooper)?

A

Heavy Metals are:

  • –very potent & toxic
  • – large doses cause GI irritation (ulcers, nausea, diarrhea)
  • –estringent–> precipitate proteins –> constipation
  • – animals lack removal mechanisms

can provide chelating agents as antidotes (bind to metal to form water soluble and easily excreted complex that is less toxic)

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9
Q

Colony Stimulating Factor

Filgrastin (G-CSF) vs Sargramostim (GM-CSF)

A
  • Classification: drugs acting on the blood
  • MOA: stimulate maturation, differentiation and proliferation of proginator cells
    • (a) G-CSF stimulates neutrophils
    • (b) GM- CSF stimulates myeloid precursor to increase neutrophils, eosinophils, basophils, erythocytes and macrophages
  • Use: prevent and treat neutropenia induced by anti-cancer chemotherapy
  • Problems: Bone pain & Sargramostim causes fever and cardiopulmonary toxicity
  • ADME: injectable
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10
Q

Filgrastin (G-CSF)

A
  • G-CSF stimulates neutrophils
  • Use: prevent and treat neutropenia induced by anti-cancer chemotherapy
  • Problems: Bone pain
  • ADME: injectable
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11
Q

Sargramostim (GM-CSF)

A
  • Sargramostim (GM- CSF) stimulates myeloid precursor to increase neutrophils, eosinophils, basophils, erythocytes and macrophages
  • Use: prevent and treat neutropenia induced by anti-cancer chemotherapy
  • Problems: Bone pain & Sargramostim causes fever and cardiopulmonary toxicity
  • ADME: injectable
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12
Q

What are the 2 Groups of Hemostatic Drugs

A

Local (Styptics) and Systemic

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13
Q

Local Hemostatics (Styptics)

A

For topical use only (thrombus is used systemically)

  • (1) Vasoconstrictors - epinephrine
  • (2) Astringents - tannic acid & ferric chloride – precipitated proteins form crust/seal over injured vessel
  • (3) Surgical- oxidized cellulose, gelatin sponge, collagen
  • (4) Physiological - Thromboplastin, thrombin, fibrinogen, fibrin foam
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14
Q

what drug is a Vasocontrictive local hemostatic?

A

Epinephrine

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15
Q

What two drugs are Astringent Local Hemostatics? How do they work?

A

tannic acid (in coffee and tea) & ferric chloride

– precipitated proteins form crust/seal over injured vessel

(ferric= local/topical, ferous= systemic)

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16
Q

What drug is a Surgical Local Hemostatics?

A

oxidized cellulose gelatin sponge collagen

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17
Q

Physiological Local Hemostatics

A

Thromboplastin

thrombin

fibrinogen

fibrin foam

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18
Q

What is Benzocaine? What product is it in

A

local anesthetic in Clot-it- PLUS Ester

(most amides have “i” before -caine)

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19
Q

What are the 5 systemic hemostatics?

A
    1. Clotting factors- can be used in ANY type of hemorrage - in blood transfusions & fresh frozen plasma (FFP)
    1. Vitamin K for warfarins
    1. Protamine sulfate – for heprin bleeding
    1. Aminocaproic acid – for thrombolytic agent bleeding
    1. Desmopressin (DDAVP) – for vWF disease ( and ADH/Vasopressin analog)
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20
Q

Vitamin K- classification, MOA, Use, ADME?

A

Classification: Systemic Hemostatics

  • (a) *Vitamin K1 (phytonadione) from plants *
  • (b) Vitamine K2 (menaquinone) formed by bacteria in the GI tract - not available as drug
  • (c) Vitamin K3 (menadione) synthetic - DO NOT USE IN HORSES

MOA: active/reduced K1 is a co-factor for carboxylase enzyme that is required to activate precursors of factors 2, 7, 9 & 10 (PIVKA) in the liver

Use:

  • (1) antidote to warfarins (both 1st and 2nd genration)
  • (2) treatment of spoiled sweet clover poisening in cattle (releases glycosides that act similar to warfarin)
  • (3) Treatment of rare vitamin K deficiency in ulcerative colitis and liver cirrhosis (abundant in diet and thus must have alteration in K ADME)
  • (4) treat epistasis in dogs Problems: K3 causes renal failure in horses, slow onset, IV–> hypersensitivity

ADME: slow onset (24 hours) due to mechanism acting on precursors

  • –oral (K-Caps)
  • – Prenterally - IV, SC, IM –
  • fat soluble and widely distributed
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21
Q

Protamine sulfate- classification, MOA, Use, ADME?

A

Protamine sulfate

  • Classification: Systemic hemostatic
  • MOA: highly basic drug that binds with acidic heparin to form a inactive salt (=Chemical antagonism)
  • Use: antidote for heparin Problems: overdose has anticoagulant effect
  • ADME: give slow IV
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22
Q

Aminocaproic acid- classification, MOA, 3 uses?

A

Classification: Systemic hemostatic

MOA: inhibits conversion of plasminogen to plasmin

Use:

  • (1) antagonism of thrombolytic agent
  • (2) treatment of hyperfibrinolysis hemorrhage
  • (3) treatment of degenerative myelopathy in German shepards by antiprotease activity
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23
Q

Desmopressin (DDAVP) - classification, MOA, Use

A

Classification: Systemic hemostatic

MOA: increases VWF levels for two hours in dogs by causing release from endothelial cells and macrophages.

  • vWF is important for adherance of platelets to an injured vessel, platelet aggregation, & stabalizing factor 8

Use:

  • (1) control bleeding in dogs with vWF disease
  • (2) surgery in dogs with vWF disease
  • (3) in blood donor dogs with vWF disease ProblemsL short duration (2 hours)
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24
Q

3 types of Antithrombotic drugs

A
  1. Anticoagulants (heparin and warfarin)
  2. Thrombolytics
  3. Antiplatelet drugs
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25
Q

Heparin

classification, MOA, use, PK problems?

A

Classification: Anticoagulant antithrombotic

MOA: activates anti-thrombin III resulting in :

  • (1) inhibition of thrombin
  • (2) inhibition of activated coagulation factors 9, 10, 11 & 12 in the liver

Pharmacokinetics:

  • Give IV (not absorbed orally, SC is slow, and should not be used IM)
  • Fast onset and short duration
  • give as IV infusion or IV intermittent
  • Rapid metabolism in liver
  • Does NOT cross the placenta or enter milk

Use: anticoagulant of choice in pregnant animals

  • (1) treat acute thromboembolism
  • (2) anticoagulant in-vitro

Problems: narrow safety margins, **bleeding**, cause allergies.

  • Low molecular weight heparins (LMWHs) are less antigenic and less likely to cause allergies BUT are more $$$$
  • Treat toxicities with protamine sulfate, blood transfusion or fresh frozen plasma (FFP)
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26
Q

Warfarin

A

Classification: Anticoagulants

MOA: inhibits vitamin K epoxide reductase –> depletion of redued vitamin K –> less carboxylation–> inhibition of prothrombin (expires first) and coagulation factors 7, 9 & 10

PK:

  • ORAL, Slow onset (2 days) - because have to deplete existing coagulation factors.
  • Slow absorption (2 hours).
  • Widely distributed. Crosses placenta & milk.
  • Long duration 2-5 days (due to high plasma protein binding- 99% of albumin).
  • Metabolized by the liver microsomal enzymes (altered by enzyme induction/inhibition).

Use: long term prevention in thromboembolic diseases (too slow for acute thromboembolism), Rodenticide

Problems: narrow safety margin, bleeding, teratogen (bone defects), Drug interactions (weakly bound to plasma proteins, easily displaced), crosses placenta.

Antidote: Vitamin K (slow onset) and blood/plasma transfusion (acute replacement of clotting factors)

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27
Q

Drugs that increase warfarin effect

A
  • –Phenylbutazonee, salicylates
  • –Heparin
  • –Chloramphenicol
  • –Sulfonamides and broad-spectrum antibiotics (displacement & inhibit intestinal flora production of vitamin K)
  • –anabolic steroids- increase binding affinity to receptors
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28
Q

Drugs that decrease warfarin effect

A

enzyme inducers (phenobarbitol)

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29
Q

What are STREPTOKINASE, UROKINASE, TPA, & ANISTREPLASE all an example of?

What is their MOA? Use? Problems? Antidote?

A

Classification: Thrombolytic agents

MOA: activates conversion of plasminogen to plasmin (breaks down clots/fibrinolysis)

–tPA is clot-specific at low therapeutic doses by binding to plasminogen bound to fibrin

Use: Acute thromboembolic disorders, tPA is used in opthalmology

Problems: narrow safety margin (monitor for 48 hours), bleeding, allergy

Antidote: Aminocaproic acids (prevents conversion)

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30
Q

Which drugs are Anti-platelet drugs?

A

Asprin

Dipyridamole

Abciximab

Lepirudin

Clopidogrel

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31
Q

Asprin

A

Classification: Anti-platelet Drug

MOA:

  • Low does –| Cox inhibit synthesis of thromboxane A2 (TXA2) by irreversibly (For whole lifespan of the platelet) inhibiting cyclooxygenase. Also –| PGI2 (antiaggregant).
  • TXA2 is the main proaggregant
  • Action behinds to cyclooxygenase irreversibly, called “Acetylation”
  • Non-selective COX inhibitor –> side effects by blocking protective PGE

Problems: ulceration & bleeding.

Clinical Uses

  • Low doses of aspirin are used in prevention of thrombotic disorder
  • Low doses > large doses
    • Large doses inhibit the proaggregant activity (TXA2) and also the antiaggregant activity (PGI2), which will decrease the effect.
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32
Q

Dipyridamole

A

Classification: Antiplatelet

MOA: Inhibits enzyme that breaks down cAMP (Phosphodiesterase) and causes an increase in cAMP ( Which –I aggregation)

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33
Q

Abciximab

A

Classification: Antiplatelet (human)

MOA:block receptor that links platelets together by fibrinogen (GPIIb/IIIa receptor)

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34
Q

Lepirudin

A

Classification: antiplatelet

MOA: Binds to thrombin

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35
Q

Clopidogrel

A

Classification: anti-platelet

MOA: inhibit binding of pro-aggretive ADP

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36
Q

What is the definition of a Diuretic?

A

Diuretics are drugs that increase the rate of urine floe or increase urine volume

They also increase the rate of Na excretion, usually as NaCl in water

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37
Q

What are Diuretics Classified as?

A

Caridovascular

Physiological

Osmotic diuretics

Loop/high ceiling diuretics

Thiazide diuretics

Potassium-sparing diuretics

Carbonic anhydrade inhibitors (used to treat glucoma)

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38
Q

What are examples of Cardiovascular Diuretics? How do they work?

A

Cardiovascular Diuretics: Digitalis (digoxin), Phosphodiesterase inhibitors (Aminophylline, inamrinone, Milrionone)

MOA: Positive ionotrophs that increase the GFR.

Use: treatment of edema associated with congested heart failure.

Not diuretic if also cause vasoconstriction as well as increase heart contractivity.

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39
Q

What are physiological diuretics? how do they work?

A

(1) WATER!

MOA: inhibit ADH production (which acts on DCT and collecting duct)

Use: compensate chronic interstitial nephritis in dogs

(2) Sodium Chloride

Use: urolithiasis in sheep, calves and cats.

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40
Q

What are 4 examples of Osmotic diuretics? MOA? PK? Use?

A

Osmotic Diuretics: Mannitol* (action depends on route of administration), urea, glycerin, Isosorbide.

MOA: osmotically draw water into tubules.

  • Acts on loop of Henles and PCT
  • Has very insignificant interferance on Na, K, Ca, Mg, Cl, Bicarb and phosphate
  • Increases renal blood flow (use in oliguric renal failure
  • Stays in the blood or interstitium (contraindicated in generalized edema)

Use:

  • Local edema in cerebral edema & acute glaucoma.
  • Treat acute renal failure
  • Mobilization of edema fluid
  • Drug overdose/ toxicity ( because weak diuretic, does not alter electrolyes and increases renal perfusion)

PK:

  • Mannitol = IV (oral is a laxative), not metabolized, eliminated rapidly
  • Urea= IV
  • Glycerin and isosorbide= ORAL
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41
Q

List the effectiveness of diuretics from most to least? What are the relative precentages?

A

Most effective= 25% = Loop diuretics

5%= Thiazide diuretics (act on early DCT)

2%= Potassium Sparing (act on late DCT and CD)

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42
Q

What are examples of Loop or High ceiling diuretics?

A

Furosemide

Bumetanide

Ethacrynic acid

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43
Q

What is the MOA of Loop or High Ceiling Diuretics?

A

Furosemide, Bumetanide, Ethacrynic acid

MOA:

  • Inhibit Na-K-Cl symporter on the luminal membrane of the aLOH (Most effective, block 25% of Na reabsortion)
  • Results in inhibition of paracellular reabsorption of Na, Ca, and Mg
  • Negative luminal transmembrane potential in the DCT and collecting duct facilitates K excretion (principal calls) and H secretion (a cells) –> hypokalemia and systemic acidosis
  • Stimulates RAAS –> hypokalemia and systemic acidosis
  • Increases total renal blood flow (may involve PG)
  • Increases systemic venous capacitance (vasodilating) via PG
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44
Q

What are therapeutic uses of Loop diuretics?

A

Loop diuretics= Furosemide, Bumetanide, Ethacrynice acid

Uses:

  • Generalized and localized edema
  • Treat hyperkalemia (if combined with isotonic saline)
  • Used in acute renal failure patients
  • Treat increased IOP and udder edema
  • Treat exercise-induced pulmonary hemmorage in horses = Furosemide only
  • Drug overdose (be careful of hypovolemia)
  • Treat life-threatening hypernatremia (combined with hypertonic saline)
  • Treat edema of nephrotic syndrome
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45
Q

What are the adverse effects of Loop Diuretics?

A

Loop diuretics= Furosemide, Bumetanide, Ethacrynice acid

Uses:

  • Ototoxicity- due to electrolyte inbalance in the inner ear fluid
  • Hypokalemia**
  • HypoMg
  • Hypovolemia
  • Hypotension & arrhythmia
  • Hyperglycemia (only issue in diabetes)
  • Hyperuricemia (in human gout patients)
  • Hypersensitivity in patients with sulfonamide allergy
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46
Q

How do you give furosemide? What are its pharmacokinetics?

A

IV or Oral

Rapid onset, short duration

partly metabolized by conjugation

actively secreted in urine by organic acid transportes

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47
Q

Spironolactone

A

Spironolactone

Classification: Potassium-Sparing Diuretic

MOA: Competitively block aldosterone binding to aldosterone/mineralcorticoid receptors in the late DCT and collecting duct

  • Results in exretion of NaCl and retention of K & H
  • Diuretic effect depends on the endogneous levels of aldosterone
  • Mild diuretic because only 2% of Na reabsorption occurs in the late DCT to collecting duct

Use:

  1. mild diuretic (use with other diuretics in heart failure)
  2. Treatment of primary and secondary hyperaldosteronism

Problems

  • Hyperkalemia
  • Systemic acidosis
  • Reproductive issues (acts on androgen and progesterone receptors)

PK:

  • Oral
  • prodrug
  • highly plasma protein bound
  • slow onset (2-3 days) and long duration
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48
Q

Triamterene & Amiloride

A

Triamterene & Amiloride

Classification: potassium-sparing diuretic

MOA: Block Na channels on the luminal membran eof the principal cells of the late DCT and collecting duct.

  • Excretion of Na, diuresis and retention of H & K

Use:

  • Treatment of hypokalemia and hypomagnesemia
  • very week diuretic, occasionally used in edematous disorders and hypertensio

Problems: Hyperkalemia & Systemic acidosis

PK: Oral

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49
Q

Acetazolamide

Methazolamide

Dorzolamide, Brinzolamide

A

Acetazolamide, Methazolamide, Dorzolamide, Brinzolamide

Classification: Carbonic anhydrase inhibitors (CAI’s)

MOA: reversible inhibition of carbonic anhydrase (which inhibits the exchange of H for Na in the PCT (primary site) and Collecting duct (secondary site)

  • Lower intraocular pressure (IOP) by inhibiting CA in the eye –> decrease formation of aqueous humor

Use:

  • Treatment of chronic glaucoma (topical dorzolamide is best)
  • Acetazolamid for udder edema

Problems

  • Systemic acidosis (vomit, diarrhea, hyperventilation, PU/PD, prutitus of paws)
  • Hypokalemia
  • Hyperglycemis

PK:

  • Acetazolamide = oral
    • onset is 30 minutes, duration 4-6 hours in small animals
    • eliminated by kidney - actively excreted in urine bt organic acid secretory mechanism
  • Dorzolamide= opthamlic topical
    • less systemic acidosis
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50
Q

ADH (vasopressin)

A

Stims reabsorption of water in the DCT and collecting duct

Results in decrease ECF osmolarity and increase water in the ECF

Natural= pitressin = used IM/IV for 1 hour to differentiate central from peripheral diabetes insipidus (DI)

Synthetic= Desmopressin (DDAVP)= more potent, longer duration= drug of choice to treat central DI in cats and dogs

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51
Q

What are your drugs of choice for diabetes insipidus?

A

Central = Desmopressin

Nephrogenic = Thiazide Diuretics

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52
Q

What is oliguric renal failure and how can you treat it (3 drugs)?

A

Acute renal failure

Treat with Mannitol, furosemide and dopamine

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53
Q

What drug will you use to treat an incomplete AV block?

A

ATROPINE

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54
Q

What drug do you use to treat a complete AV block?

A

Epinephrine!

Low dose acting on B2, high dose acting on a2

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55
Q

List the Beta-1 agonist in order of potency

A

Most potent=Isoproterenol

epinephrine

norepinephrine

Least potent= dopamine

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56
Q

Norepinephrine

A

Acts on alpha-1 and beta-1 (with no counteracting beta-2)

Not commonly used due to too much vasoconstriction that is more likely to cause a reflex bradycardia than epinephrine

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57
Q

What are non-drug therapies you can use for congested heart failure

A

Restrict Salt

Restrict Exercise

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58
Q

What drugs can you use to treat CHF?

A

Positive Inotrophic drugs

Vasodilators

Inodilators

Diuretics

B-Blockers

PImobendan is the drug of choice for CHF

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59
Q

What is the MOA of Digitalis glycosides?

A

Block Na/K ATPase –> increase Na available for exchange for Ca –> Increase intracellular Ca –> positive inotrophic

Increases the mechanical efficency of heart & slows heart down by allowing the parasympathetic system to predominate (?)- things he said

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60
Q

What is significant of Digitalis glycosides undergoing enterohepatic recycline?

A

Prolongs duration of action

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61
Q

What are Inodilators?

A

Inodilatos are both vasodilators and increase cardiac output

Include:

Phosphodiesterase inhibitors (Amrinone & Milrinone) - use in emergency

Pimobendan - used in CHF in dogs-increases sensitivity to Ca & causes mixed vasodilation

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62
Q

What is so great about using Spironolactone in CHF?

A

blocks aldosterone (which is elevated in CHF)

K-sparring diuretics-thus will correct the decrease K

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63
Q

Which are better to use in CHF?

a. Non-selective B Blockers (Carvedilol)
b. Selective B-Blockers (Metoprolol & atenolol)

A

Selective B Blockers (Metoprolol & atenolol)

You maintain your B2 function –> more vasodilation, bronchodilation, less hypoglycemia

B1 is used in CHF because it prevents the RAAS which decreases angiotensive II and aldosterone

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64
Q

Carvedilol

A

Carvedilol

Classification: B- Blocker

Use: Treat CHF due to dilated cardiomyopathy to blunt the harmful effects of the SNS on the heart

MOA:

(1) nonselective B blocker and a1 blocker (prevents RAAS & vasodilator)
(2) antioxidant
(3) inhibits endothelin release

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65
Q

How does nebulization of ethanol (20%) help severe cases of CHF?

A

Prevents foaming

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66
Q

What is the drug of choice for atrial fibrillation in equines?

A

Quinidine

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67
Q

What is the MOA of Class I antiarrythmic drugs?

A

Class I= block volatge sensitive Na channels

IA: prolongs AP = Quinidine & Procainamide

IB: shortern AP= Lidocaine, Phenytoin, Mexiletin

IC: no effect on AP= flecainide

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68
Q

What is the drug of choice for ventricular arrythmias in DOGs?

A

Lidocaine-IV Only

Lidocaine can also be used to treat digitalis induced arrhythmias (with Phenytoin)

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69
Q

What drugs can you use to treat digitalis induced arrythmias?

A

Lidocaine

Phenytoin = DOGs only

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70
Q

What is great about mexiletin?

A

It is similar to lidocaine, but can be given ORALLY

Lidocaine has a very high first pass effect and thus can only be given IV

Both are Class IB Antiarrythmic drugs

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71
Q

What is the drug of choice for supraventricular and ventricular arrythmias in CATS?

A

Propranolol ( B blocker- Class II antiarrythmic)

Also effective if induced by hyperthyroidism

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72
Q

Why are B-blockers effective to treat cats with hyperthyroidism?

A

They block B1

B1 is upregulated in hyperthyroidism –> tachyarrythmias and tachycardia

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73
Q

What are Class III (K-channel blockers) anti-arrythmias useful for?

A

Refractory ventricular arrythmias

Includes Bretylium, Amiodarone and Sotalol

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74
Q

What are Class IV antiarrythmic drugs?

A

Class IV= Ca channel blockers

Only Verapamil and Diltiazem are anti-arrythmic

Work ONLY for supraventricular tachyarrythmias (Ca channels are not within the ventricle)

Also used for Myocardial hypertrophy

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75
Q

What is the drug of choice for dogs with supraventricular tachyarrythmias (atrial tachycardia, atrial flutter, atrial fibrillation)?

A

Digoxin

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76
Q

What is the drug group of choice for cats with supraventricular and/or ventricular tachyarrythmias?

A

B- Blockers (Propranolol)

May or may not be due to hyperthyroidism

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77
Q

What is the drug of choice for cardiac asystole (aka cardiac resuscitation)?

A

Epinephrine

(aso used for COMPLETE AV block)

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78
Q

Drug of choice for treating dogs with CHF?

A

Pimobendan

Classification: Inodialtor

MOA: sensitizes heart to Ca by enhancing interaction b/w Ca and troponin C

should NOT be used in conditions where an increase of cardiac output is not possible

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79
Q

Vasoconstrictors

A

Used in vasodilatory shock, as nasal decongestion, and in severe hypotensive shock

Nonselective a-­‐agonists
? Epinephrine
? Norepinephrine

? Selective a1-­‐agonist
? Phenylephrine

? Direct and indirect sympathomimetics
? Ephedrine, pseudoephedrine, phenylpropanolamine(PPA)

Given orally. Tolerance is an issue.

High dose Dopamine

Vasopressin

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80
Q

Sympatholytic Vasodilators

A

? Nonselective a-­‐blockers

? Phentolamine & ? Phenoxybenzamine
? Selective a1-­‐blocker
? Prazosin
? Presynaptic a2-­‐agonist
? Clonidine
? Nonselective B-­‐blockers
? Propanolol
? Selective B1-­‐blockers
? Atenolol
? B and a1-­‐blocker

Carvedilol

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81
Q

ACE Inhibitors

A

Captopril, Enalapril, Benazepril, Lisinopril

MOA: by inhibiting ACE they reduce actions of angiotensin II and aldoserone

Use:

  • CHF
  • Hypertension (= Drug of choice for systemic hypertension in dogs)
  • Progressive renal failure - improve renal perfusion from internal mechanisms

Problems:

  • Hypotension
  • May lower GFR
  • Ideopathic glomerular disease
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82
Q

Losartan

A

Angiotensin II antagonist

MOA: Competitive antagonist of angiotensin II receptors

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83
Q

Direct- Accting Vasodilators (2)

A

Hydralazine- arterial vasodilator
? MOA: Increases local concentrations of PGI2/block Ca influx

? Nitrates- low dose on veins, high dose on arteries
(Sodium nitroprusside, Nitroglycerin, Isosorbide dinitrate)
? MOA: Formation of the reactive radical nitric oxide? Only used in emergencies because of their potent vasodilatory effect

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84
Q

Calcium Channel Blockers

A

Verapamil, Diltiazem, Amlodipine, Nifedipine

? MOA: Inhibit influx of extracellular calcium across myocardial and smooth muscle cell membranes.
? Effects: ?

  • Negative intotrope, ?
  • Negative chronotrope, ?
  • Increased O2 delivery to myocardial tissue, ?
  • Decreased afterload (due to vasodilatory effect)

Use:

  • Class IV Antiarrhythmic
  • Antihypertensive- Amlodipine is drug of choice in cats (unless due to hyperthyroidism)
  • Myocardial hypertrophy - Diltiazem is drug of choice in cats
  • Antianginal
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85
Q

What is the first line antihypertensive drug in cats?

A

Amlodipine (Ca channel blocker)

UNLESS caused by hyperthyroidism (then use B-Blockers)

(Dogs = Ace inhibitors)

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86
Q

What are the drugs of choice for myocardial hypertrophy?

A

Diltiazem

(Benzodiazapine- Ca Channel Blockers)

-and-

B Blockers

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87
Q

How do you treat normal and emergency hypertension?

A

Normal cases:
? Diuretics
? Beta
blockers
? Vasodilators
? Caclium Channel Blockers

? Emergency:
? Hydralazine or sodium nitroprusside IV?Propanolol or acepromazine IV

Phemtolamine IV? Oral calcium channel blockers, prazosin or ACE inhibitors

? Pheochromocytoma-­‐induced
? Phenoxybenzamine

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88
Q

What is the drug of choice for pheochromocytoma induced hypertension?

A

Phenoxybenzamine

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89
Q

Drug of choice for CHF?

A

Pimobenden

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90
Q

Which of the following is NOT a use for Ca Channel Blockers?

A. Posi;ve Inotrope
B. Treatment of CHF
C. Antiarrhythmic
D. Antihypertensive
E. Treatment of myocardial hypertrophy

A

B. Treatment of CHF

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91
Q

Which of the following drugs could be used to treat a subventricular tachyarrythmia?

A. Digoxin
B. Captopril
C. Lidocaine
D. Diltiazem
E. Epinephrine

A

C. Lidocaine

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92
Q

Which if the following drug would be the first choice antihypertensive drug in hyperthyroid cat?

A. Furosemide
B. Captopril
C. Amlodipine
D. Propanolol
E. Diltiazem

A

D. Propanolol

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93
Q

Who produces T4?

A

100% the thyroid gland

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94
Q

Who produces T3?

A

20% thyroid gland

80% liver kidney and muscle tissue by deiodinating T4 into T3

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95
Q

T4 and T3 are _____ plamsa bound

A

99% plasma bound

Only 1% ‘free’

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96
Q

What is the thyroids function?

A

ALOT (dont have to memorize all of them)

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97
Q

How do you treat Hypothyroidism?

A

Replace the hormone!

Levothyroxine (T4) > T3

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98
Q

What are the difference between Liothyronine and Levothyroxine?

A
99
Q

Why do you use L4 over L3to treat hypothyroidism?

A

L4 allows intracellular autoregulation, providing only L3 to cells as they have a need for it

T4 has a longer half-life, which makes its easier to dose (SID to BID)

The higher potency of L3 puts the animal at greater risk of thyrotoxicosis

100
Q

Levothyroxine Sodiume (Soloxine)

A

Levothyroxine Sodiume (Soloxine)

  • Oral tablet (scored)
    • 0.02 mg/kg PO BID, 0.5 mg/ m^2
    • should try not to give >0.8 mg BID
  • Should monitor peak plasma concentration 4-12 hours post dose (very high variation of half-life)
    • check thyroid levels after 4-8 weeks
  • Problems (chronic > acute) = thyrotoxicosis usually due to chronic overdose
  • Not all formulations are equal (but not always a big deal)
  • In dogs over 50 lbs, use the body surface area to calculate the dose (0.5 mg/m^2)
  • Injectable ONLY for Myzedema Coma -rare- also warm patient, provide respiratory and fluid support
101
Q

What drug should you use for a Myxedema Coma?

A

Injectable Levothyroxine sodium

(this is the only condition you use the injectable form of this drug)

Also warm patient and provide fluid/electrolyte and respiratory support

102
Q

What are the clinical signs of Thyrotoxicosis?

A

Thyrotoxicosis – vomiting/diarrhea, tachycardia, tachypnea, weight loss, hyperactivity, hypertension

Should recheck dose/weight (maybe try calculating by surface are in large dog) and decrease the dose.

Thyrotoxicosis is usually due to chronic overdose

103
Q

What AED will NOT interfere with thryoid testing?

A

Levetiracetam or Potassium Bromide (KBr)

One that do: Phenobarbital, Zonisamide

104
Q

Which drugs interfere with thyroid testing?

A
105
Q

What care common causes of hyperthyroidism in cats?

A

***Functional adenomatous hyperplasia ****

Less commonly thyroid adenomas

Uncommonly thyroid carcinomas

106
Q

What are common causes of hyperthyroidism in dogs?

A

Iatrogenic or functional neoplasia

107
Q

What are the three best treatment options for hyperthyroidism?

A
  1. Radioactive iodine (I-131)
  2. Antithyroid drugs (Thioureylenes, Iodides, Iodinated contrast agents)
  3. Diet (Hill’s y/d)

Surgical thyoidectomy and intrathyroid injection of ethanol are not commonly used. Risky and other options are better.

108
Q

Radioactive Iodine Therapy

A

Drug to Treat Hyperthyroidism (also thyroid carcinoma)

MOA: selectively destroys thyoid tissue

Pros: single injection, permanent cure, no anesthesia, safe, usually dont have to supplement thyroid hormone after.

Cons: isolation for 1-4 weeks, permanent (issue if kidney disease), expensive. If animal dies, it remains radioactive for months/years

PK: single injections, eliminated in urine

109
Q

Methimazole

A

Treats Hyperthyroidism (drug of choice) - Felimazole/ Tapazole

MOA: inhibits synthesis of thyroid hormone by inhibiting organification and coupling. Lowers T4, but T3 is normal due to autoregulation mechanism in the tissue

PK: good oral availability, can be compounded to transdermal paste (does NOT prevent adverse effects)

Cons:

  • monitor T4 levels adter 2-4 weeks (in cats, time of day does not matter)
  • common (10-15%) side effects (vomiting, anorezia, depression, hematology changes)
  • rare idiosyncratic reactions (facial excoriations, hepatopathy, bleeding, agranulocytosis, bleeding, thrombocytopenia)
110
Q

Carbimazole (Vidalta)

A

Treats Hyperthyroidism

MOA: converted in body into Methimazole (=inhibits synthesis of thyroid hormones)

Long acting formula - UK/Aus only

111
Q

Propylthiouracil (PTU)

A

Treat Hyperthyroidism

Inhibits conversion of T4 to T3 in tissue

112
Q

What drugs should you use for hyperthyroidism if mehtimazole, radioactive iodine, and diet are NOT options?

A

Iodines & Iodinated radiographic contrast agents

Not first-line drugs due to transient effects and efficacy.

Iodides: Lugol’s solution, Potassium/Na iodide

  • Inhibit thyroid hormone organification & Inhibit preformed hormone secretion. May inhibit binding of iodine

Iodinated radiographic contrast agents: Ipodate (Oragrafin®), Iopanoic Acid

  • Inhibit the conversion of T4 to T3 in peripheral tissues
  • Monitor T3 levels (T4 may not change)
113
Q

Hill’s Y/D Diet

A

Treats Hyperthyroidism

MOA: Restricts dietary iodine –> reduces T4/T3

Pros: does not cause hypothyroidism

Cons: has be fed exclusively (indoors, no treats etc.). Still have to monitor T4 levels

In multi-cat house hold, you should supplement non-hyperthyroids cats 1 tablespoon of normal food.

114
Q

What are the kidneys, guy, and bones roles in calcium metabolism?

A

 Bone – storage pool for calcium, can be mobilized
 Kidney – resorption or excretion of calcium. Converts vitamin D2 to calcitriol (=PTH minion)
 GIT – absorption (or not) of dietary calcium

115
Q

What are 3 top causes of hypocalcemia? What are less significant causes?

A 
Parturient paresis (“milk fever”) in cattle and sheep
Parturient eclampsia in lactating bitches
Primary hypoparathyroidism (canines)

ALSO: Contamination of EDTA will cause decrease Ca levels, as well as increased K.

Other causes: With hypomagnesemia or mastitis (cattle), Pancreatitis (cats), Sepsis (horses), Acute/chronic renal disease (variable), Iatrogenic

116
Q

What are clinical signs of hypocalcemia?

A

May be medical emergency!

 Hyperesthesia, muscle tremors, muscle fasciculations or tetany
 Progression to flaccid paralysis (cattle)
 Seizures
 Hyperthermia, bradycardia
 Pawing/rubbing at face (dogs/cats)

117
Q

What are you two overal treatment goals for hypocalcemia?

A

(1) Correct calcium deficit - short term, for transient issues (increase need), provide oral or parenteral Ca supplementation
(2) Correct underlying problem - long term, provide oral vitamin D therapy

118
Q

Which parenteral calcium can you ONLY give IV?

A

Ca Chloride

119
Q

Which Parenteral Ca can you possibly give IM?

A

Ca (Boro) Gluconate

Should be diluted forms only, it can be caustic to tissues

120
Q

What are two concerns you should have when giving patenteral calcium to rapidly correct hypocalcemia?

A
  1. Monitoring for arrythmias/cardiac arrest (if give too rapidly)
  2. Can precipitate with bicarbonate, acetate, or lactate
121
Q

Oral calcium requires the _______ to be able to absorb the calcium.

A

gut

122
Q

What is a benefit of using oral Ca Gluconate/Lactate?

A

tablets have a small quantity of element (90-130 mg/g) and thus ideal for smaller patients

123
Q

What is good and bad about oral Ca Carbonate?

A

good= 400 mg/g - better for larger animals

Bad= may cause alkalosis

124
Q

What is an issue with Ca Chloride?

A

It is acidic, thus more likely to cause GI irritation

125
Q

Ca Acetate can be used to…

A

bind dietary phosphorus/phosphate binder

(but Aluminum is more common)

126
Q

Ca propriote is used in which species as a food supplement?

A

Cattle (250 mg/g)

127
Q

What is the most recomended form of Oral calcium to use?

A

Ca Carbonate

128
Q

How does long term use of Vitamin D help with hypocalcemia?

A

Increase intestinal absorption of calcium/phosphorus
Increase renal tubular re-absoption of calcium/phos
Increase mineral bone resorption

129
Q

Which form of Vitamin D supplement is most commonly used?

  1. Ergocalciferol (Vitamin D2)
  2. Dihydrotachysterol (DHT, synthetic Vit D2 analog)
  3. Calcitriol (1,25-dihydroxycholecalciferol)
A

Calcitriol

130
Q

What is the drug of choice for prmiary hypoparathyroidism?

A

Calcitriol

(also used to manage chronic renal failure)

131
Q

Compare the followings potency and time to clinical response:

Ergocalciferol (Vitamin D2)
Dihydrotachysterol (DHT, synthetic Vit D2 analog)
Calcitriol (1,25-dihydroxycholecalciferol)

A

Ergocalciferol- need large dose, is slow, and needs liver& renal activation

DHT- potent, faster than ergocalciferol, NO PTH activation

Calcitriol: most potent, fastest, no renal or liver activation

132
Q

What are your top differentials for hypercalcemia?

A
133
Q

What is the most common,and often only, clinical sign of hypercalcemia?

A

PU/PD

134
Q

What is most important when treating hypercalcemia?

A

Treat underlying disease!!! and maybe short term measures to correct hypercalcemia

If unknown, or untreatable, or Ca is still too high you can then provide longer term measures to manage Ca.

135
Q

What are short term and long term treatment options of hypercalcemia?

A

Short Term ( supplement K, provide fluids)

  1. Saline diuresis- Na competes for Ca tubular reabsorption
  2. Furosemide- prevents Ca reabsorption
  3. Sodium bicarbonate- decreasesactive Ca, short term
  4. Calcitonin - reduces osteoclast activity

Long term

  1. Glucocorticoids - reduces absorption and excretion, antineoplastic (may interfere with Dx)
  2. Bisphosphonates - Inhibits osteoclast activity, $$$, side effects
  3. Plicamycin (mithramycin)- inhibits RNA synthesis in osteoclasts, toxicity concerns
136
Q

What should you use to treat cholecalciferol toxicity?

A

Calcitonin

137
Q

What stimulates insulin secretion?

A
  • Rise in blood glucose concentration
  • GI hormones
  • Amino acids and fatty acids in the GIT
  • Vagal stimulation (M receptors)
  • Catecholamines (β2 receptors)
138
Q

What decreases insulin secretion?

A

Decrease in blood glucose concentration
Somatostatin
Catecholamines (α2 or I3 receptors)

139
Q

What are the 4 effects of insulin in the boday?

A
  • Storage and building- Stimulates glycogenesis, lipogenesis & protein synthesis
  • Inhibits glycogenolysis, gluconeogenesis, lipolysis
  • Stimulates uptake of potassium into cells
  • Anabolic (especially in the fetus)
140
Q

What is an artifactual cause of hypoglycemia?

A

Leaving blood out too longs before spinning down

RBC continue to metabolize glucose while in tube.

141
Q

What are the Therapeutic considerations of hypoglycemia if NOT involving insulin?

A

Give dextrose (if severe) and Treat the underlying disease

142
Q

What are the Therapeutic consideration of treating hypoglycemia if involving insuling? How will it differ from iatrogenic vs endogenous insulin?

A

Iatrogenic: Stop insulin/hypoglycemic agent and implement supportive care until metabolized.
Endogenous: Treat the hypoglycemia, treat the underlying disease (if possible).

143
Q

True or False

Glucagon is commonly used in treatment of hypoglycemia

A

FALSE- it is not commonly used

It has to be given IV and the liver must have glycogen stores in order for it to work

144
Q

True or False

Dextrose is the 1st line drug to use until you figure out the underlying cause of hypoclycemis

A

True

___

It can be given for acute casees at 50% dextrose solution or for mainteneance (IV) at 2.5-5% dextrose

Consideration: hyperosmolality/irritation, rising glucose stimulates insulin secretion

145
Q

Why should you nod use 50% dextrose for maintenance?

A

(1) more likely to overdose
(2) high osmolality –> phebitis

146
Q

If you need to make a 2.5% dextrose solution for a patient. If you have a bottle of 50% dextrose on your shelf, how much do you need to add to a 1L bag of LRS to make a 2.5 % dextrose drip?

A

50 mL

(2.5% /50%) * 1000mL = 50 mL

147
Q

How due use dietary management to treat hypoglycemia?

A

Acute: karo syrup/corn syrup
Chronic: (if not severe) Frequent, small meals of Complex carbs (simple carbs may stimulate insulin secretion) that are Easily digestible and have Moderate fat and protein

–

commonly used in isulinomas in whivh you are unable to treat itand thus just managing it with diet and other therapy

148
Q

True or False

The goal of hypoglycemia therapy is always to maintain a “normal” blood glucose

A

FALSE!!!

Goal of therapy is to eliminate/minimize clinical signs associated with hypoglycemia

_________

This may not mean maintaining a ‘normal’ blood glucose!

“treat the patient, not the glucose numbers

149
Q

Will a dog with a glucose of 50 show clinical signs?

(reference interval is 76-119)

A

Maybe, it is more likely if acute/rapid progression

150
Q

What is your go to drug for treating hypoglycemia?

A

Glucocorticoids

____

Use Diazoxide, Streptozotocin or Somatostatin only if glucocorticoids are not working

151
Q

What is the MOA of glucocorticoids (predmisone, Prednisolone) in treating hypoglycemia?

A

Increasing gluconeogenesis
Decreasing glucose utilization
Stimulating glucagon secretion

side effects are mild at low doses (pu/pd, panting) and progressively severe as the dose is increased (immunosuppresion)

there is hepatic metabolism/activation of prednisone to prednisolone

152
Q

Prednisone is metabolized into active prednisolone in the ________

A

liver

153
Q

What are side effects of Diazoxide?

A

Hypersalivation, anorexia/vomitting/D, tachycardia, blood changes, diabetes, fluid retention (most are in humans)

_____

this drug is usually only used to treat hypoglycemia IF glucocorticoids and diet are no longer working.

Efficacy is iffy

154
Q

What drug activates K channels in islet cells, switches off voltage-gated Ca channels to inhibit insulin release, increases glycogenolysis in the liver, and inhibits tissue/brain uptake of glucose?

A

Diazoxide (proglycem®, hyperstat IV ®)

Used to treat hypoglycemia if diet and glucocorticoids are not working

155
Q

What somatostatin analogue is sometimes used for:

Insulinomas (dogs, ferrets)
Gastrinomas (dogs, cats)
Chlyothorax (dogs, cats)
Acromegaly (dogs)

A

Octreotide

_____

somatostatis efficacy is very iffy and should be used as a last resort.

MOA: inhibits release of insulin, GH, CCK, glucagon

156
Q

What drug selectively destroys beta cells in the pancreas or metastatic sites?

A

Streptozotocin (Zanosar®)

Given IV

very narrow therapeutic index (nephrotoxic, vomiting in ~30%)

Survival may not be significantly improved over other therapies - not worth the risk

157
Q

Which two species are most likely going to get an insulinoma?

A

dogs and ferrets

158
Q

What are your top two differential for hyperglycemia?

A
  1. Physiologic hyperglycemia–Stress, postprandial, diestrus
  2. Diabetes Mellitus

Others:  Hyperadrenocorticism  Pheochromocytoma  Pancreatitis/Exocrine pancreatic neoplasia  Some drugs/toxins (eg. amitraz)  Head trauma

159
Q

True or False

Type I diabetes (IDDM) is a Absolute deficiency of insulin from destruction (autoimmune) of pancreatic β cells

A

True!

160
Q

True or false

Type II (NIDDM) diabetes is a Relative insulin deficiency and insulin resistance seen generallu in dogs

A

FALSE

Type II (NIDDM) diabetes is a Relative insulin deficiency and insulin resistance, NOT generally seen in dogs

Can be seen in cats, horses and humans

161
Q

True/False: Diabetes insipidus is due to an ADH deficiency

A

True

162
Q

What are the 4 frequent signs of diabetes?

A
  1. Catabolism (muscle loss/weight loss)
  2. Accumulation of glucose in the blood (~180-220 mg/dL)
  3. PU/PD- Glucose in urine causes osmotic diuresis
  4. Polyphagia- Lack of glucose entering ‘satiety center’ of the brain leads to polyphagia
163
Q

What are the goals of hyperglycemia therapy? (5)

A

Reduce hyperglycemia
Reverse catabolic effects
Reverse ketosis
Control clinical signs
Maintain patient in a mild hyperglycemic state (150- 200mg/dL)

164
Q

Why not aim for normoglycemia in hyperglycemia therapy?

A

Do not want to enter hypoglycemic state

glucose fluctuates throughout the day and “at home” levels may be lower than “at vet” levels due to stress

If animal has decrease demand, or misses a meal, the medication may send them into a hypoglycemic state

hypoglycemic states signs are crude, thus owners may not notice if animal is hypoglycemic

165
Q

What kind of diet do you want to used for a cat and a dog with diabetes?

A

Canine: High fiber/Complex Carbs (Hill’s R/D or W/D, Purina DCO)
Feline: Low Carb (Hill’s M/D, Purina DM)

166
Q

What diabetes drug decreased postprandial rise/ inhibits glucose uptake from the GI by Inhibiting alpha amylases and brush border oligo/disaccharides?

A
  • *Acarbose (precose®)**

Not used often, NOT effective as solitary treatment

Sometimes used as an adjunct in dogs and cats
Can cause diarrhea, weight loss

167
Q

Which Sulfonylureas is most commonly used to treat diabetes?

A

Glipizide (glucotrol®)

____

Stimulates insulin secretion by blocking potassium channels in the beta cells, increases Ca++ and increases release of insulin

Increases tissue sensitivity to circulating insulin

REQUIRES FUNCTIONAL BETA CELLS TO WORK!!! - CAN ONLY USE IN TYPE 2 DIABETES

168
Q

T/F: Glipizide is a oral drug that can be used for both type 1 or type 2 diabetes?

A

FALSE!!! REQUIRES FUNCTIONAL BETA CELLS TO WORK!!!

CAN ONLY USE IN TYPE 2 DIABETES (NOT effective in dogs)

  • Stimulates insulin secretion by blocking potassium channels in the beta cells, increases Ca++ and increases release of insulin
  • Increases tissue sensitivity to circulating insulin
169
Q

What (mostly human) Biguanide causes Causes inhibition of hepatic glycogenolysis and increases peripheral glucose utilization?

A

Metformin (glucophage®) - limited vet studies

does NOT affect insulin secretion

170
Q

T/F: Insulin injection are only for type 1 diabetes

A

False- they can be used for either type 1 or 2

171
Q

What are the vet approved insulin product? Why are they better to use than human forms, even though the peptide is highly conserved?

A

ProZinc™, Vetsulin/Caninsulin

It is better to use due to the concentration (40 IU/mL) is easier to dose for smaller patients

Human preperations = 100 IU/mL

172
Q

Can you use U40 insulin in U100 syringes?

A

NO

173
Q

Is insulin function maintained if you shake it vigerously to reconstitute it, have it dilutes, or id it is expired?

A

nope, nope, nope

__________

You should:

Roll GENTLY to reconstitute
Avoid using diluted insulin
Pay attention to expiration date- get new bottle if close to expiration date before upping the dose

174
Q

T/F: All insulins are pretty much the same

A

FALSE: there are different durations, potency and variations

175
Q

Which insulin is most commonly used for DKA management?

A

“Short acting insulin” as CRI/intermediat injection in hospital

Regular/crystalline/neutral insulin (Humulin®-R)

Lispro (Humalog), aspart, glulisine

176
Q

What is a good starting insulin type for canines with diabetes?

A

“Intermediate acting” insulin = Isophane (NPH), Lente, Vetsulin

SC only

Protamine (NPH) or zinc (Lente)are added to delay absorption and extend clinical effect

May not provide adequate duration for cats

177
Q

What insulin should be used for a cat with diabetes?

A

“Long acting” insulin= Glargine (Lantus®)

SC only- pH causes microprecipitates =‘flat curve’

178
Q

T/F: Levemir/Insulin detemir has a similar potency compared to other insulins

A

FALSE- exception to the rule

Canine insulin receptors are 4x more sensitive than human receptors to detemir thus dose must be lower in dogs ( 0.1-0.2 IU/kg BID)

179
Q

How do you correct a sick DKA(not eating)?

A

Correct fluid/electrolyte/acid-base abnormalities

Supplemental K+ (+/- PHOS supplementation)

IV CRU of insulin to start (Can also do intermittent IM injections)

Goal is to reverse the metabolic situation - It is not urgent to get the glucose down to normal

180
Q

How do you treat a hyperosmolar nonketotic diabetic?

A

Start on fluids- do not give insulin initially

Want to Treat like a DKA but the goal is to bring glucose down VERY SLOWLY

181
Q

What type of response is happening in the graph? how do you treat it?

A

Somogyi response
Significant drop in blood glucose (due to too much insulin) triggers a glucagon/epinephrine response –> Blood glucose rises very high (‘Overswing’)

TREATMENT= REDUCE DOSE

this response may give you altered readings that may make you believe you should up the dose when the dose is already way to hig

182
Q

What is produced in the zona glomerulosa, fasiculata and reticularis of the adrenals?

A
183
Q

What are the genomic and non-genomic effects of glucocorticoids?

A

Genomic - binds to cytoplasm receptor to have a slow feedback on ACTH secretion by down regulating ACTH’s genomic expression

Non-genomic - binds to membrane receptors to have a fast (immediate/hours) feedback on ACTH secretion by reducting ACTH release

184
Q

T/F: Glucocorticoids effect almost all body systems in some way but clinical signs will vary depending on if there are too high/low levels of glucocorticoids

A

True

they have to most effects on energy metabolism and water/electrolytes

185
Q

What are clucocorticoids effects of energy metabolism?

A
  • *Generally catabolic**= if excess–> muscle wasting
  • *Antagonistic to insulin**- Increase gluconeogenesis, lipolysis, protein catabolism

(Steroids and diabetes do NOT work well together)

186
Q

What are glucocorticoids effects on water/electrolytes?

A
  • *Alter calcium metabolism**- Decrease GI absorption, increase urinary excretion
  • *Polyuria-** Decrease ADH secretion, increase GFR
  • *Polydipsia**- central and due to polyuria
187
Q

What effects do glucocorticoids have on hematology?

A

Increased PCV and RBC lifespan
Increased platelets
Increased clotting/platelet function
“Stress leukogram”- eosinopenia

(in addisons you will see normal to increase eosinophils)

188
Q

Glucocorticoids can mask a febrile response by inhibiting _________ production in the thermoregulatory center

A

PGE2

189
Q

What causes calcinosis cutis?

A

chronic excess of steroids

190
Q

How do glucocorticoids affect the musculoskeletal system?

A
  • Increase osteoclast activity /decrease osteoblast activity
    • Osteoporosis, decreased bone growth
    • Depletion of cartilage matrix
  • Inhibition of fibroblasts
191
Q

How do glucocorticoids affect the repro system?

A
  • Fetal maturation
  • Teratogenic (cleft palate)
  • Induce abortion/parturition
  • Inhibit spermatogeneiss or ovulation
192
Q

How do glucocorticoids affect the GI and hepatic systems?

A
  1. GI ulcerations
    • Increased gastric acid secretion
    • Decreased gastric mucus secretion
    • Significant risk if concurrent use of NSAIDs!!
  2. Fatty liver
    • Increased fat absorption from GIT
    • Increased fat deposition in the liver
    • Alteration of liver enzymes

Does not directly affect the pancrease

193
Q

What are glucocorticoids most commonly used for?

A

Anti-inflammatory (low dose) and immunosuppression (high dose)

Clinical uses:

 Treat allergies
 Suppress inflammation/fibrosis
 Immunosuppression
 Induction of parturition
 Treatment of neoplasia
 Replacement therapy (Addison’s disease)
 Trauma/shock therapy (?)
 Endocrine function testing (LDDS, HDDS)
 Treat hypercalcemia, bovine ketosis, stimulate appetite,
adjunct to treatment of certain infectious diseases

194
Q

What are some (7+) clinical uses of glucocorticoids?

A
  • Treat allergies
  • Suppress inflammation/fibrosis - ie if want to prevent esophageal stricture or slow liver fibrosis
  • Immunosuppression
  • Induction of parturition
  • Treatment of neoplasia
  • Replacement therapy (Addison’s disease)= pysiologic dose
  • Trauma/shock therapy (?)- very case dependent
  • Endocrine function testing (LDDS, HDDS)
  • Treat hypercalcemia, bovine ketosis, stimulate appetite, adjunct to treatment of certain infectious diseases
195
Q

T/F: glucocorticoids are highly protein bound

A

True

  • *Transcortin ‘corticosteroid-binding protein CBP**’ - high affinity, low capacity
  • *Albumin** – low affinity, high capacity
196
Q

Methylprednisolone, prednisone and cortisone require ________ metabolism to become active

A

hepatic

anything that is given topically/not intended for systemic use, must be in an active form

197
Q

What are contraindication/cautions to glucocorticoids?

A

Diabetes mellitus
Pre-existing catabolic disease
Infections (most of the time)
Corneal ulceration
Young, growing animals
Pregnancy
Wounds (that you want to heal)
Concurrent use of NSAIDs
Caution with underlying liver, cardiac disease, etc.
Numerous drug interactions (NSAIDs, digoxin, etc)

198
Q

What are SHORT term side effects of glucocorticoids?

A

Lab changes - stress leukogram, hepatic enzyme increase, decrease thyroid values

PU/PD/PP

Fetal abnormalities /abortion

199
Q

What are LONG term (>1 week) side effects of glucocorticoids?

A

Increased susceptibility to infection
Skin changes (hyperpigmentation, thinning, alopecia)
Collagen disease (cruciate injury due to weakening of ligaments)
Hypertension, thromboembolic disease
Panting
Addisonian signs (w/ withdrawal – ‘iatrogenic Addison’s due to rapid withdrawal and decrease ACTH production)
Less common: myopathy, calcinosis cutis, osteoporosis

200
Q

What are the three “types” of doses you will use for glucocorticouds?

A
  • *Physiologic** dose ~ 0.1-0.2 mg/kg/day
  • *“Anti-inflammatory**” dose
  • *Immunosuppressive”** dose ~2-4mg/kg day
201
Q

T/F: If dosing glucocorticoids for more than a few days, you need to taper the dose before discontinuing

A

True!
____

Can reduce dose amount or increase dose interval

The longer the time on, the slower the tapering of dose

202
Q

if want to dose a patient with 2mg/kg of prednisone but we only have dexamethasome available, what dose would you use?

[HINT: Dex antiinflammatory potency is 30, while prednisole is 4]

A

0.27 mg/kg

Dex is more potent, dose need to be less

203
Q

Which is longer acting: Prednisone or Dexamethasone?

A

Dexamethasone

204
Q

T/F: Chemical form (compound) of the steroid can facilitate different routes of administration, delay onset and prolong the effect.

A

True

205
Q

T/F: Salt Ester glucocorticoids are highly soluable and thus can be given by IV injection

A

True

Onset is faster with IV, but the duration is similar to normal

206
Q

T/F Insoluable esters glucocorticoids are less soluable and have a shorter duration than salt ester glucocorticoids

A

FALSE

Insoluable esters glucocorticoids are less soluable and have a LONGER duration than salt ester glucocorticoids

———–

due to the low soluability, it is absorbed slower (slow onset), and thus has a longer duration

CANNOT be used IV= opaque

207
Q

What 2 glucocorticoids are often used for topical use?

A

Prednisolone and cortisol

must not require liver activation

Fluorination or esterification with fatty acids or cyclic acetonides to increases lipid solubility

208
Q

Which propellant is preferred?

  1. Chloroflurocarbon (CFC) = particle size 35μm
  2. Hydrofluoroalkane-I34a (HFA) = particle size 1.1μm
A

Hydrofluoroalkane-I34a (HFA) = particle size 1.1μm

209
Q

What type of glucocorticoid is commonly used? what excipient is prefered? and how much is systemically absorbed?

A

Fluticasone diprioprionate with HFA excipient

Systemic absorption: 0% in cats, 30% in humans

210
Q

Which glucocorticoid is highly potent (~15x prednisolone) and has a high topical activity in the GIT but unknown/variable systemic absorption?

A

Budesonide (Entocort®)

211
Q

Mineralocorticoids are primarily under the control of ____________

A

Angiotensin II

212
Q

What are the two mineralocorticoids you need to know for this class?

A
  1. Fludrocortisone -more potent Na retention, some anti-inflammatory, PO BID
  2. Desoxycorticosterone (DOCP)- longer acting (q25 days), less potent

Clinical use = Addisons Disease (hypoadrenocorticism)

213
Q

What are Fludrocortisone and Desoxycorticosterone (DOCP) used to treat?

A

Typical Addisons Disease (hypoadrenocorticism)

They are mineralcorticoids

214
Q

What are the fast and late responses of mineralocorticoid administration?

A 
_Fast response (minutes_)= Stimulate Na/K/ATPase & Activate Na/H exchanger
_Late response (hours/days)_- De novo synthesis of Na/K/ATPase by upregulating the nuclear receptor
215
Q

What effects do mineralocorticoids have on the transport of electrolytes in the kidney?

A

Na+ (and water) retention
K+/H excretion
Increase ECF and GFR

216
Q

T/F: Most ‘glucocorticoids’ have sufficient mineralocorticoid
activity to treat deficiency

A

FALSE

Most ‘glucocorticoids’ have insufficient mineralocorticoid activity to treat deficiency

217
Q

In addison, do you need to replace the glucocorticoid, the
mineralocorticoid or both or neither?

A

It depends on the type.

  • Iatrogenic hypoadrenocorticism:
    • You suppressed the adrenals with exogenous steroids, gradually wean off the steroid and they’ll be fine.
  • ‘Typical’ Addison’s:
    • Deficient in both mineralocorticoid and glucocorticoid
    • Florinef or DOCP + prednisone (physiologic doses)
  • ‘Atypical’ Addison’s:
    • Deficient in glucocorticoid ONLY
    • Prednisone (physiologic doses) & monitor for development of mineralocorticoid deficiency
218
Q

How do you treat Iatrogenic hypoadrenocorticism

A

Put back on steroid and then gradually wean off the steroid so that ACTH production can be amped back up

219
Q

How do you treat Typical Addisons?

A

Florinef or DOCP + prednisone (physiologic doses)

——————

Deficient in both mineralocorticoid and glucocorticoid

220
Q

How do you treat atypical addisons?

A

Prednisone (physiologic doses)

Deficient in glucocorticoid ONLY

221
Q

Which drug to treat for hyperadrenocorticism/cushings is cytotoxic to the adrenal glands (Zona fasciculata/reticularis)?

A

Mitotane (Lysodren®, o,p-DDD)

It has a narrow therapeutic index - monitor with ACTH stim testing

Have to give induction dose followed by maintenance dosing

Overtreatment can cause primary addisons

Can treat pituitary or adrenal

222
Q

In europe, vets will overdose Mitotane to make a cushings patient an addisons patient by destroying the adrenal gland. What are the pros and cons of this methos

A

Pros- Addisons is easier to treat than cushings due to a more predictable course of therapy

Cons- if poor compliance, a untreated addisons patient will die, while a cushings patient will have a much milder outcome.

223
Q

What is the most common drug used to treat hyperadrenocorticism in small animals?

A

Trilostane (Vetoryl®)

224
Q

Which drug to treat hyperadrenocorticism (primarily pituitary) is a competitive inhibitory of an enzyme of steroid synthesis (3β-hydroxysteroid dehydrogenase) that requires daily oral dosing?

A

Trilostane (Vetoryl®)

Can treat pituitary or adrenal

Start on low dose, then increase

Excessive dose –> oversuppresion

Monitor with ACTH testing

225
Q

What drug to treat hyperthyroidism is an antifungal that inhibits cortisol synthesis and CYP450 enzymes that requires daily oral dosing and has a high risk of hepatotoxicity and a low efficacy?

A

Ketoconazole

226
Q

Which drug for treating pituitary hyperadrenocorticism is a MAO-B inhibitor that increases dopamine –> decrease ACTH –> decrease cortisol? This drug has few side effects and patients will “feel better: despite a specific response in HAC

A

Selegiline (L-deprenyl, Anipryl®)

227
Q

Which drug to treat pituitary hyperadrenocorticism (pars intermedia dysfuction) in horses acts as a dopamine agonist –> decrease ACTH –> decrease cortisol?

A

Pergolide (Permax®)

NOT in USA

Clinical response seen after ~ 3 weeks of therapy
Anorexia (may be dose dependent)

  • *Cabergoline (Dostinex®)** also dopamine agonist – has been looked at in canines
228
Q

What sydrome do the below drugs all treat?

A

Hyperadrenocorticism

229
Q

What are the two inputs/centers in the brain that contribute to appetite?

A

“Feeding center” and Satiety center

230
Q

When treating anorexia/hyporexia, what is your main goal?

A

ID and treat the underlying cause

231
Q

Which appetite stimulant acts on GABA –> inhibits the satiety center –> increase appetite that is more effective in cats?

What is its main two form? and what are some side effects?

A

Benzodiazepines!

sedation is most commonside effect

Diazepam (IV) and Midazolam (IM) are the two forms

232
Q

T/F: Diazepam is given orally to increase appetite in cats

A

FALSE!- Give IV

Do NOT give orally in cats –> idiosyncratic hepatotoxicity!

IM absorption is slow, incomplete and painful

233
Q

Although the mechanism is not well understod, which very short acting (~15 min) appetite stimulant acts on GABA and inhibits 5-HT at sub-hypnotic doses?

A

Propofol (Propoflo®)

____

CAUTION in cats: Heinz body anemia possible if treating repeatedly >5 days

234
Q

Which serotonin (5-HT) antagonist are you more likely to use in a cat? a dog?

A
  • Cat= Cyproheptadine (Periactin®) -
    • oral, 2-3 days for response, sedation, smaller tablets
  • Dog= Mirtazapine (Remeron®)
    • ​ increase NE, large tablets (7.5 mg)
235
Q

How does prednisone stimulate appetite?

A

Via negative feedback on CRH

236
Q

T/F B-vitamins are most effective at stimulating an appetite if there is a B-vit deficiency

A

True

237
Q

What are the two centers in the brain that control vomiting?

A
  • Emetic Center-
    • inputs from glossopharyngeal, vagal & sympathetic afferents
  • CRTZ-
    • sample blood from outside the BBB
    • Receptors: Serotonin (5-HT), Neurokinin (NK1), Adrenergic (alpha-2), Dopamine (D2), Histamine (H1), Metabolic (toxins)
    • Cats: More: α-2 and 5-HT Fewer: D2 and H1
238
Q

How does 3% hydrogen peroxide induce emesis? What species is it contraindicated in?

A

direct irritation of oropharynx/GI lining

Dont use in cats –> hemorrhagic gastritis

__________

Use only if no other options (ie at home)

239
Q

Which emetic stimulates dopamine receptors? which species is it most effective in?

A

Apomorphine (Apokyn®)

More effective in Dogs (cat ~10%)

_____________

Can give ALL routes- even conjunctival sac!

Reverse respiratory depression with naloxone

240
Q

What is the reversal of Apomorphine? What does it do?

A

Naloxone

Reverses respiratory depression but WONT reverse the emetic effect

_________

If give in the conjunctive, you can flush out the drug when you no longer need the emesis

241
Q

Which emetic is a a-2 agonist? which species is it more effective in?

A

Xylazine or Dexmedetomidine (Rompun®, Dexdomitor®)

More effective in CATS= (cats have more α-2
receptors and fewer D2 receptors)

242
Q

What drug is used to treat old dog vestibular disease?

A

Meclizine (Antivert®)

Antihistamine (H1 receptor antagonist) that reduced vestibular input to the CRTZ

Oral, last 8-12 hours, few side effects

243
Q

Which anti-emetic is a (1) dopamine antagonist, (2) 5-HT antafonist @ high dose and has (3)peripheral effects on GI motility?

What can it be used for? How should it be administered?

A

Metoclopramide (Reglan®)

potent anti-emetic, antagonizes apo-morphine induced emesis

CRI is best, but can give oral TID

244
Q

What types of drugs are Ondansetron (Zofran®) & Dolasetron (Anzemet®)?

A

POTENT Anti-emetics - Serotonin antagonist (5-HT)

_____

Initially used for chemotherapy related nausea
More potent than metoclopramide, but more $$$
Usually given by injection but oral formula available

Pharm II (Elise) (3 decks)

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