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12. Pharmacology > All of the drugs > Flashcards

All of the drugs Flashcards

1
Q

Furosemide: drug class

A

Diuretic
Loop diuretic

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2
Q

Furosemide: MOA

A
  • Inhibit Na+/K+/2Cl- (ascending loop of Henle)
  • ↓Na, K, Cl reabsorption → retained in tubule → presented to distal nephron → retain H2O (dilute urine)
  • ↑ max fractional excretion of Na+ to 15-25% filtered load
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3
Q

Furosemide: other effects

A
  • ↑intrarenal PGE2 synthesis → ↑ renal blood flow
  • Initial ↓ renal vascular resistance w/o changing GFR
  • Anti inflammatory
  • ↑ thoracic duct lymph flow (high dose)
  • Bonchodilation in Hu, Eq, Guinea pigs
  • ↑ renin secretion
  • Initial direct effect on macula densa
  • 6h 2nd effect to ↓ volume and activation of ∑ system
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4
Q

Furosemide: 1/2 life

A

1.5-3h

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5
Q

Furosemide: bioavailability

A

variable
- Incomplete 40-50%
- Eq: almost no PO

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6
Q

Furosemide: IV, IM, PO onset, peak, duration

A

IV: onset 5min, peak 20-30min, duration 2h

IM: onset 10-15min, peak 30min, duration 4-8h

PO: onset 30-60min, peak 1-2h, duration 6-8h

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7
Q

Furosemide: pharmacoK

A

Protein bound: 86-91%

[Kidney to plasma] = 5:1

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8
Q

Furosemide: excretion

A

45% bile, 55% urine

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9
Q

Furosemide: indications

A

CHF
Edema
Congestion

Hyper Ca2+
HyperK+

Oliguric renal dz

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10
Q

Furosemide CI

A

Renal failure
- ↓ renal clearance to 15%
- 1/3 of diuretic effect
- 2x serum ½ life
- Constant rate of diuresis

HypoNa, hypoK, hypoCl, hypoMg
Metabolic acidosis
Hypovolemia

HF w/o fluid retention

Nonketotic hyperglycemic state
Ergogenic blood lipid changes
Ototoxicity
Nursing

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11
Q

Furosemide: drug interactions

A

Aminoglycoside
Amphotericine B → nephro/ ototoxicity

NSAIDs → can ↓ effect

Not mix with acidifying solution

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12
Q

Furosemide: MOA ototoxicity

A

Electrolyte disturbance in endolymphatic system

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13
Q

Furosemide: storage

A

Protect from light

Room Temp

Poorly soluble in water: can be used in dextrose 5% (D5W), saline 0.9%, LRS → stability 8h

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14
Q

Torsemide: drug class

A

Loop diuretic: high ceiling

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15
Q

Torsemide: MOA

A

Inhibit Na+/K+/2Cl- (ascending loop of Henle)

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16
Q

Torsemide: other effects

A

K+ sparing

Anti aldosterone/ mineralocorticoid effect
- Inhibit aldosterone R: bind cytoplasmic fraction of kidney

Antifibrotic effect
- Mineralocorticoid R blockade in 
- ↓ lysyl oxidase & collagen cross linking → correlates w myocardial fibrosis and ventricular stiffness

Vasodilatory

Coronary protective

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17
Q

Torsemide: moelcule

A

Lipophilic anilinopyrimidine sulfonylurea derivative

Unique chemical structure → not related to furo

10x more potent vs furosemide

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18
Q

Torsemide 1/2 life dogs

A

120min

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19
Q

Torsemide bioav dogs

A

80-100%

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20
Q

Torsemide IV, PO peak, onset, duration dogs

A

IV: [peak] 2-5min, peak effect 20-25min, duration 90min
- Low urinary excretion rate

PO: onset 20min, peak 2h, duration 12h

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21
Q

Torsemide PO peak, onset, duration cats

A

PO: onset 20min, peak 4h, duration 12h

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22
Q

Torsemide 1/2 life eq

A

9h

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23
Q

Torsemide PO peak eq

A

3h

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24
Q

Torsemide: studies in Hu and rats

A

differences in myocardial fibrosis in torsemide patients (vs furo + spiro)

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25
Q

Spiro: drug class

A

K+ sparing diuretic

Aldosterone
antagonist

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26
Q

Spiro MOA

A

Competitive inhibition of aldosterone by binding to R

Interfere with Na+ reabsorption → ↑ max excretion of Na+ to 2%

Preserve K+ excretion

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27
Q

Spiro PO onset/peak

A

Slow onset
Peak 2-3days

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28
Q

Spiro: metabolism

A

Extensively/rapidly metabolized
- Metabolites active but less potent

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29
Q

Spiro: indications

A

CHF

Hepatic cirrhosis (inhibit ascites)

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30
Q

Spiro: CI

A

Steroid-like effect

Facial dermititis

Antiandrogenic effects (Hu): gynecomastia, hisurtism, impotence

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31
Q

Spiro: drug interaction

A

Caution with K+ supplementation and NSAIDs

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32
Q

Hydrochlorothiazide: drug class

A

Thiazide diuretic

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33
Q

Hydrochlorothiazide: MOA

A

Inhibit Na+ reabsorption in distal tubule
- ↓ diuretic effect compared to loop diuretic → most H2O already reabsorbed in distal tubule

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34
Q

Hydrochlorothiazide: other effects

A

Can lead to hypoK+

Can ↑ effect of other diuretic and anti-hypertensive agents

Will block region where hypertrophy occurs during long term use of loop diuretics

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35
Q

Hydrochlorothiazide: PO onset/peak/duration

A

PO:
- Onset 1-2
- Peak 4h
- Duration 12-24h

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36
Q

Hydrochlorothiazide: features

A

Low ceiling diuretic: max response reached at low dose

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37
Q

Hydrochlorothiazide: indications

A

CHF/edema
→ chronic use of diuretics

Antihyper-tensive

Ca2+ excretion (Ca2+ oxalate urolithes)

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38
Q

Hydrochlorothiazide: CI

A

Renal failure/azotemia: marked ↓ effect

HypoK+, hypoNa+
HyperCa2+

Ventricular arrhythmias: ↓K+, Mg2+
Proarrhythmic drugs

Pregnancy:
- ↓ circulating volume
- Cross placental barrier

Sulfonamide type IM side effects: hepatic jaundice, pancreatitis, blood dyscrasia, angiitis, pneumonitis, interstitial nephritis, photosensitive dermatitis

Diabetogenic effects: ↑ risk of new diabetes

Urate excretion and gout: ↓ urate excretion + ↑ blood uric acid

Atherogenic changes in blood lipids: ↑ LDL cholesterol and triglycerides

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39
Q

Hydrochlorothiazide: drug interactions

A

Steroids: salt retention → ↓ effect

Indomethacin/ NSAIDs → interfere w PG → ↓ effect

Antiarrhythmics: class IA or III → prolong QT

Nephrotoxic ATB

Probenecid (gout tx) → block effect

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40
Q

Enalapril: drug class

A

ACEi

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41
Q

Enalapril: MOA

A

Block conversion of AngI → Ang II by binding AngI site on ACE

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42
Q

Effects of decr Ang II

A
  • ↓ vasopressor effect
  • ↓ H20/Na+ retention
    o ↓ aldosterone release from adrenal gland
    o ↓vasopressin (ADH) release from posterior pituitary
  • ↓ central/peripheral ∑ tone
  • ↓ GFR preservation when ↓ blood flow
  • ↓ myocardial hypertrophy/remodel
    o ↓AngII
    o ↑ [bradykinin]
  • ↓ myocardial collagen synthesis and ↑ degradation → prevent fibrosis from AngII/aldosterone
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43
Q

Enalapril: other effects

A

Mild vasodilator (arterial + venous)
- ↓SVR by 25-30% (↓afterload) → ↑SV and CO
- ↓venous tone: ↑ peripheral circulation, ↓PCWP, LV, LAP

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44
Q

Enalapril: affinity

A

ACEi > AngI
- 200 000x greater

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45
Q

Enalapril: 1/2 life

A

½ life = 7-8h initially, 11-19h additive

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46
Q

Enalapril: PO peak/duration

A

Peak 2-4h
Duration 12-24h
[Steady state] in 4days

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47
Q

Enalapril: bioav

A

Bioav. 60%
- Well absorbed by GI tract

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48
Q

Enalapril: metabolism

A

Metabolized in liver → become pharmacologically active

Secreted by kidneys

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49
Q

Enalapril: indications

A

Hypertension

CHF

Asympto patients w LV dysfct → can ↓ development of CHF (Hu)

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50
Q

Enalapril: CI

A

Pregnancy

RA stenosis

HyperK+

Renal dz

Angioedema

Hypotension

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51
Q

Enalapril: side effects

A

Damage to kidneys confined to proximal tubules
- Juxtamedullary region of cortex
- Necrosis of tubular cells

Regeneration possible

2 studies
- Lower incidence of azotemia in enalapril group
- Enalapril had no effect on [creatinine]

Effects on kidney thought to be mainly from ACEi 2nd hypotension → ↓ renal blood flow and GFR

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52
Q

Benazepril: drug class

A

ACEi

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53
Q

Benazepril: MOA

A

Same to enalapril

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54
Q

Benazepril: molecule

A

Non sulfhydryl ACEi

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55
Q

Benazepril: peak

A

1-3h

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56
Q

Benazepril: 1/2 life

A

22h

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57
Q

Benazepril: metabolism

A

Metabolism: liver → hydrolysed into benazeprilat to become active

Excretion: bile and urine
- Less dependent on kidneys

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58
Q

Benazepril: indications

A

Same enalapril

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59
Q

Nitroprusside: drug class

A

Vasodilator

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60
Q

Nitroprusside: MOA

A

NO formation → stimulate guanylate cyclase → ↑cGMP → vascular SM relaxation

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61
Q

Nitroprusside: Other effects

A

Arteriole: ↓SVR → ↑SV and CO

Venous: ↓PVR, ↑peripheral flow, ↓ cardiac volume, ↓ venous P

May ↑ LV compliance

↓LVP diastolic and end diastolic

↓LAP, LAD and LV diameter

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62
Q

Nitroprusside: molecule

A

NO compound w/o ester bound
- Release NO when non enzymatically metabolized

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63
Q

Nitroprusside: onset/duration IV

A

Rapid onset (almost immediate)
Duration: min

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64
Q

Nitroprusside: absorption

A

well GI

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65
Q

Nitroprusside: metabolism

A

Metabolism: hepatic → rapidly by nitrate reductase to <10%
- Rarely used PO

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66
Q

Nitroprusside: indications

A

Acute CHF

Hypertension

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67
Q

Nitroprusside: CI

A

Hypotension

Cyanide toxicity

Venous hyperO2
Lactic acidosis
Dyspnea

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68
Q

Nitroprusside: storage

A

*protect from light

Expensive!

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69
Q

Nitroprusside: other effects

A

*Tolerance does not develop
- Reflex ↑∑ drive can occur

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70
Q

Nitroglycerine: drug class

A

Vasodilator

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71
Q

Nitroglycerine: MOA

A

NO formation → stimulate guanylate cyclase → ↑cGMP → vascular SM cell relaxation

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72
Q

Nitroglycerine: other effects

A

Blood volume redistribution: central → peripheral

↓intraventricular pressure → ↓ edema

↓SVR → ↑ SV, ↓LAP, ↓edema

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73
Q

Nitroglycerine: molecule

A

Ester of NO
- Parent compound: 10-14x more potent

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74
Q

Nitroglycerine: 1/2 life

A

1-4min

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75
Q

Nitroglycerine: absorption

A

well GI

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76
Q

Nitroglycerine: metabolism

A

Metabolism: hepatic → rapidly by nitrate reductase to <10%
Rarely used PO

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77
Q

Nitroglycerine: indications

A

CHF

PH

Angina pectoris (Hu)

Laminitis (Eq) → ↑ blood flow to feet

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78
Q

Nitroglycerine: CI

A

Hypotension

MetHb

Tolerance

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79
Q

Dobutamine: drug class

A

inotrope +

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80
Q

Dobutamine: MOA

A

β1 = β2 > α1 agonist
Bind D-1R in kidneys → vasodilation

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81
Q

Dobutamine: molecule

A

Biosynthetic precursor of NE → stimulates NE release

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82
Q

Dobutamine: effect depends on

A

Low doses: inotropic effect + ↓ SVR
High doses: ↑SVR as action on lower affinity αR

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83
Q

Dobutamine: 1/2 life

A

½ life = 1-2min
- Rapid clearance

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84
Q

Dobutamine: pharmacoK

A

Plateau [CRI] achieved in 8min

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85
Q

Dobutamine: w/ tachycardia

A

*Inotropic effects w/o tachycardia

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86
Q

Dobutamine: indications

A

Acute CHF

Cardiogenic shock

Acute renal failure

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87
Q

Dobutamine: CI

A

Arrhythmias

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88
Q

Hydralazine: drug class

A

Vasodilator

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89
Q

Hydralazine: MOA

A

↑ [prostacyclin] → direct arteriolar SMcells

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90
Q

Hydralazine: other effects

A

↑ Ao compliance

↓ SVR by 40% and in vascular beds:
- Renal
- Coronary
- Cerebral
- Mesenteric
> skeletal

No effect on systemic venous tone

↑ contractility: reflex from NE release → histamine release

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91
Q

Hydralazine: metabolism

A

Metabolism: hepatic 1st pass → acetylation

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92
Q

Hydralazine: onset/peak/stability

A

Onset: 30min-1h
Peak 3h
Stability 8-10h

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93
Q

Hydralazine: When used for systemic hypertension w/o heart dz

A
  • Reflex ↑∑ tone → ↑ contractility and HR → ↑CO → stable BP
  • Addition of β-blocker blocks reflex

Not seen with CHF: ↓ response to ∑ tone

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94
Q

Hydralazine: indications

A

Systemic hypertension

Cases refractory to ACEi

Regurgitation/ shunt refractory to tx

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95
Q

Hydralazine: CI

A

Renal failure: affect hepatic metabolism →↑ [plasma]

Hypotension

Anorexia
Vomiting
Diarrhea

Systemic lupus erythematosus
Fever
Peripheral neuropathy

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96
Q

Hydralazine: drug interactions

A

Can ↑ furo delivery to nephron → ↑ GFR

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97
Q

Procainamide: drug class

A

Anti arrhythmic class 1A

98
Q

Procainamide: MOA

A

Na+ channel blocker
- ↓ upstroke velocity of phase 0

99
Q

Procainamide: other effects

A

May slow conduction or induce bidirectional block in re-entrant circuit

100
Q

Procainamide: action depend on

A

extracell [K+]: if ↑ → ↓ resting membrane potential → ↑ effect
- ↓ tissue excitability
- ↑ duration of repolarization and effective refractory period

101
Q

Procainamide: 1/2 life

A

3h

102
Q

Procainamide: metabolism

A

Metabolism: liver
- Hu: metabolized into n-acetyl procainamide → class III anti arrhythmic properties
- May need higher dose in dogs vs Hu

103
Q

Procainamide: PO pharmacoK

A
  • Dosing difficult since short ½ life
  • Sustained release tablets: allow q8h
    o ↓ peak serum
104
Q

Procainamide: indications

A

Ventricular tachy-arrhythmias

Preexcitation

SVT

105
Q

Procainamide: CI

A

Hypotension and peripheral vasodilation
↓ inotropy
→ SLOW IV administration

Pro arrhythmic effect

Auto immune response → production of anti nuclear antibodies

106
Q

Lidocaine: drug class

A

Anti arrhythmic class 1B

107
Q

Lidocaine: MOA

A

Inhibit impulse/nerve conduction via Na+ channel block
- ↓ phase 0 depolarization
- W/o affecting conduction
- Little effect on atrial conduction and refractoriness

108
Q

Lidocaine: other effects

A

Abolishes automatic/re-entrant ventricular tachyarrhythmias
- ↑ or ↓ conduction velocity w/I circuit
- Prolong refractory period

109
Q

Lidocaine: incr effects

A

Better effect on damaged cells
- ↑ effect with ↑ extracell [K+]
- Hyperpolarization of partially depolarized cell → improve conduction in damaged myocardium regions

110
Q

Lidocaine: metabolism

A

Metabolism: into monoethyl-glycinexylidide (MEGX)
- Primary liver
- Critical factors:
- Liver flow (↓CHF, βB)
- Liver microsomal activity

111
Q

Lidocaine: 1/2 life

A

40-100min
Variable clearance rate

112
Q

Lidocaine: onset/duration/effective

A

Rapid onset
Short duration
Effective

113
Q

Lidocaine: toxicity

A

withdraw +/- diazepam

114
Q

Lidocaine: indications

A

Ventricular arrhythmias

Local anesthesia

115
Q

Lidocaine: CI

A

SSS → slow rate of phase 4 depol. In Purkinje Fibers → slow ventricular escape beat

Toxic on CNS: drowsiness, emesis, nystagmus, muscle tremors, seizures
- Cats > common

Depress ventricular fct → myocardial failure

Can induce AVB if conduction system dz

Hypotension

116
Q

Lidocaine: drug interaction

A

Cimetidine
Propanolol
Halotane
→↓ liver clearance
(↓ dose)

Hepatic enzyme inducers → ↑ clearance
(↑ dose)

117
Q

Mexiletine: drug class

A

Anti arrhythmic class 1B

118
Q

Mexiletine: MOA

A

Na+ channel blocker
- ↓ upstroke velocity of phase 0

119
Q

Mexiletine: Other effects

A

Interrupt re-entry circuits:
- Slow conduction
- ↓ membrane responsiveness

Suppress abnormal automaticity
↓ DADs formation induced by digitalis
↑ fibrillation threshold in ventricles

120
Q

Mexiletine: molecule

A

Analog of lidocaine

121
Q

Mexiletine: metabolism

A

Metabolism: not extensive 1st pass by liver (10%)
- Well absorbed GI

122
Q

Mexiletine: 1/2 life

A

3-4h

123
Q

Mexiletine: excretion

A

urine 80%, feces

124
Q

Mexiletine: indications

A

similar to lidocaine

125
Q

Mexiletine: side effects

A
  • Vomiting
  • Disorientation
  • Ataxia
126
Q

Mexiletine: overdose

A

seizures/ neuro signs

127
Q

Flecainide: drug class

A

Anti arrhythmic class 1C

128
Q

Flecainide: MOA

A

Na+ channel blocker
- ↓ upstroke velocity of phase 0

129
Q

Tips and tricks class 1 anti arrhythmics

A

Class IA: Double Quarter Pound
Class IB: Lettuce, Mayo, Pickles
Class IC: Fries Please!

130
Q

Flecainide: 1/2 life

A

13-19h

131
Q

Flecainide: excretion

A

Excretion: hepatic + renal
- Unchanged

132
Q

Flecainide: indications

A

Paroxysmal
SVT

Sustained VT

Catecholamine polymorphic Vtach
→ block open RyR channels

133
Q

Flecainide: CI

A

Pro arrhythmic effects
- Structural heart dz: non uniform slowing of conduction
- More common w ventricular ectopy

↓LV fct
CNS side effects
RBBB, LAFB, SSS

134
Q

Flecainide: drug interaction

A

Amiodarone (kinetic)

↑ - inotrope: βB quinidine, disopyramide

↓AV cond: quinidine, procainamide

135
Q

Atenolol: drug class

A

Anti arrhythmic class II

136
Q

Atenolol: MOA

A

β blocker: selective β1 antagonist

137
Q

Atenolol: pharmacoK

A

Water soluble
- ↓liver clearance

138
Q

Atenolol: bioav

A

80-90%

139
Q

Atenolol: 1/2 life

A

½ life = 5-6h dog, 3.5h cat

140
Q

Atenolol: excretion

A

Excretion: urine
- Unchanged

141
Q

Atenolol: features

A

Acute withdrawal may exacerbate original issue

142
Q

Atenolol: indications

A

Afib → ↓HR

SV and ventricular arrhythmias

SAS: ↓ sudden death

HOCM: ↓SAM

143
Q

Atenolol: CI

A

Exacerbation of:
- CHF
- SA node dysfct
- AV node dysfct

↓ rate of subsidiary PM

↑ lower airway resistance: not use if lower airway dz

Diabetes: ↓∑ compensation for hypoglycemia → ↓ insulin secretion

HyperK+ → ↓ K+ flux from intra to extra

Hypotension

144
Q

Propanolol: drug class

A

Anti arrhythmic class II

145
Q

Propanolol: MOA

A

β blocker: non selective β1 and β2 antagonist

146
Q

Propanolol: other effects

A
  • ↓ catecholamine dependent automatic rhythms: normal + abnormal
  • Slow conduction in normal ventricular myocardium

AV node:
- ↑ refractory period
- Slow conduction velocity

↓ myocardial contractility → ↓ O2 consumption

147
Q

Propanolol: pharmacoK

A

Lipophilic molecule

148
Q

Propanolol: metabolism

A

Metabolism: liver
- Extensive 1st pass
- ↑ [blood] with ↓ liver blood flow

149
Q

Propanolol: 1/2 life

A
  • 1.5h (1st dose)
  • 2h (2nd dose)
150
Q

Propanolol: effects depend on

A

Dose dependent change in myocardial contractility and SVR

151
Q

Propanolol: indications

A

Afib → ↓HR

SV and ventricular arrhythmias

152
Q

Propanolol: CI

A

Similar to atenolol

153
Q

Amiodarone: drug class

A

Anti arrhythmic class III mixed

154
Q

Amiodarone: MOA

A

Block outward K+ channel
- ↓ slope of phase 4 → ↓ SA rate
- Prolong AP duration → delay myocardial repol

155
Q

Amiodarone: other effects

A

Prolong refractory period of atrial/ ventricular myocytes + AV node
- W/o changing resting potential

Interrupt re-entry circuit
- Anti fibrillatory effect

Other effects:
- Block α and β R
- Ability to block slow Ca2+
- Ability to block fast Na+

156
Q

Amiodarone: pharmacoK

A

Highly lipophilic
- Rely on liver
- Accumulates 300x [plasma] in adipose tissue

[Myocardial] = 15x plasma

157
Q

Amiodarone: absorption

A

Absorption: slow GI → distribution in adipose tissue
- Fill peripheral tissue depot, then
- [Blood/cardiac]
- Slow onset

158
Q

Amiodarone: metabolism

A

Metabolism: liver
→ Desethylamiodarone: block fast Na+ channels

159
Q

Amiodarone: onset

A

slow onset

160
Q

Amiodarone: 1/2 life

A

Long ½ life = 3.2 days
- Up to 6mo
- Withdrawal: ↓ [plasma] in 3-10days + slow ↓ of tissue store

161
Q

Amiodarone: clearance

A

Clearance: rapid except adipose tissue

162
Q

Amiodarone: indication

A

SVT →Afib/ flutter

Ventricular arrhythmias

OK with structural heart dz

163
Q

Amiodarone: CI

A

GI disturbance

Neurologic problems

Corneal deposits → visual impairment

Dermatologic → pruritus when given IV

Hepatotoxicity: ↑ liver enzyme

Pulmonary fibrosis → inhibit phospholipase A → phospholipidosis

Exacerbation of  dz

Hyper/hypothyroidism → inhibit T4-T3 secretion

Bone marrow toxicity: neutropenia

Hypotension → vasodilation

164
Q

Amiodarone: drug interaction

A

↑ [serum]
- Diltiazem
- Digoxin
- Quinidine
- Procainamide
- Phenytoin
- Warfarin

165
Q

Sotalol: drug class

A

Anti arrhythmic class III/mixed

166
Q

Sotalol: MOA

A

Potent/non selective
- β blocker: β1 and B2
o Similar to propranolol but 1/3 potency

167
Q

Sotalol: other effect

A

Prolong AP duration
↑ effective refractory period of atrial/ ventricular myocardium
↑AV node refractory period

↑ fibrillation threshold

168
Q

Sotalol: pharmacoK

A

L isomer
- 50% > β blocker activity

169
Q

Sotalol: absorption/bioav

A

Absorption: rapid
Bioav. 85-90%

170
Q

Sotalol: clearance

A

renal

171
Q

Sotalol: indications

A

SVT

Ventricular arrhythmias

172
Q

Sotalol: CI

A

Similar to propranolol/ atenolol

Use with caution:
- ↓ cardiac contractility
- Slow HR

173
Q

Diltiazem: drug class

A

Anti arrhythmic class IV

174
Q

Diltiazem: MOA

A

Slow voltage dependent Ca2+ channel blocker → block Ca2+ entry into cell

175
Q

Diltiazem: other effects

A

PREDOMINANT ACTION
AV node: negative dromotrope
- Slow conduction
- Prolong refractory period

Negative chronotrope: ↓HR

Vasodilation

Minimal effect on cardiac contractility or vascular SM cell

176
Q

Diltiazem: absorption

A

Absorption: rapid GI
- 30min

177
Q

Diltiazem: 1/2 life

A

½ life = 2-4h
- Shorter in Eq

178
Q

Diltiazem: indication

A

SVT

Hypertension: 2nd tx or combination

179
Q

Diltiazem: CI

A

Hypotension

Myocardia depression

Bradycardia

AVB

180
Q

Diltiazem: toxicity

A
  • IV fluids
  • Ca2+ gluconate/chloride
  • Sympathomimetics
181
Q

Digoxin: drug class

A

other/class 5 anti arrhythmics

182
Q

Digoxin: MOA

A

Blocks Na+/K+ exchanger
- Competitive binding of K+ site
- ↓ Na+ efflux in diastole → ↑ intra¢ Na+ → activate Na+/Ca2+ exchanger to pump out Na+ in exchange for Ca2+ → ↑ intra¢ Ca2+

183
Q

Digoxin: other effects

A

↑ myocardial contractility from ↑ [Ca2+] = positive inotrope

Diuretic effect: block Na+/K+ pump on renal tubular  → ↑ Na+ and H2O excretion

Stimulate p∑ system and ↓ ∑ tone → ↑ activity of vagal nerve
- Slow SA node d/c rate = negative chronotrope
- ↓AV node conduction and prolong refractory period

184
Q

Digoxin: follow up

A

Test blood levels 5-7 days after starting digoxin, then each 6 months
- 4-6h post administration

Narrow therapeutic range: 1-2.5ng/ml
- Block 30% oof pumps in heart

185
Q

Digoxin: pharmacoK

A

Digitalis glycoside
- Poorly liposoluble

186
Q

Digoxin: bioav

A

PO 60%

187
Q

Digoxin: metabolism

A

Metabolism: small hepatic (15%)

188
Q

Digoxin: 1/2 life

A

23-29h dog

189
Q

Digoxin: PO/IV

A

PO: well absorbed by GI

IV: slowly over 15min
- Rapid can cause peripheral vasoconstriction → ↑ afterload

190
Q

Digoxin: excretion

A

renal mostly

191
Q

Digoxin: indications

A

SVT

Myocardial failure

192
Q

Digoxin: CI

A
  • Muscular atrophy: similar R to K+ in muscles → ↑ [serum]
  • Dehydration
  • HypoK+ → ↓ competition for binding sites
  • HyperNa+/Ca2+: ↑ inotropic/toxic effects
  • Hypoxia: ↑ sensitivity to toxicity
  • HyperT4: ↑ myocardial effects

Pro arrhythmic: ↑Ca
Tachyarhythmias/VT

Neurologic signs: depression

GI signs: V+, D+ (vagally mediated)

Hypotension

193
Q

Digoxin: toxicity

A

↑ intracell Ca2+

194
Q

Digoxin: drug interaction

A

↑ [serum]
- Aminoglyco.
- Amiodarone
- Anticholinerg.
- Diltiazem
- Esmolol
- Flecainide
- Quinidine

Drugs altering microsomal enzymes

195
Q

Pimobendan: drug class

A

PDE3i

196
Q

Pimobendan: MOA

A

Phosphodiesterase 3 inhibition
- inhibit PDE enzyme → ↓ cAMP breakdown → ↑ cAMP
- ↑ inotropy, chronotropy, dromotropy, vasodilation

Ca2+ sensitizer
- ↑ Troponin C sensitivity to Ca2+ → ↑ contractility

197
Q

Pimobendan: other effects

A

Anti inflammatory
↑ sensitivity to baroR
↑ lusitropy
↓ platelet agreggation

198
Q

Pimobendan: PO absorption

A
  • Absorption: can change with food and stomach pH
  • Onset 1h
  • Persist 8-12h
  • [Steady state] 2 days
199
Q

Pimobendan: bioav

A

70%

200
Q

Pimobendan: 1/2 life

A

30-120min

201
Q

Pimobendan: metabolism

A

liver → more potent metabolite

202
Q

Pimobendan: excretion

A

feces 90%

203
Q

Pimobendan: indications

A

CHF

Preclinical CVD and DCM

+/- HCM

204
Q

Pimobendan: CI

A

GI upset

Proarrhythmic: reported but not proven

SAS

205
Q

Pimobendan: drug interaction

A

Ca2+ channel blockers
Β blockers
→ ↓ inotropic effect

206
Q

Sildenafil: drug class

A

PDE5i

207
Q

Sildenafil: MOA

A

Phosphodiesterase 5 inhibition
- Found in pulmonary vasculature
- Inhibit PDE enzyme → ↓ cGMP breakdown → ↑ cGMP → vasodilation

208
Q

Sildenafil: absorption

A

GI 90%

209
Q

Sildenafil: metabolism

A

extensive 1st pass (CYP450 → 3A4)
- N-demethylation: 40% potent

210
Q

Sildenafil: bioav

A

PO 54%

211
Q

Sildenafil: 1/2 life

A

3-5h

212
Q

Sildenafil: peak PO

A

1-2h

213
Q

Sildenafil: elimination

A

fecal 70%, urine 15%

214
Q

Sildenafil: indications

A

PH

R to L shunting

215
Q

Sildenafil: CI

A

Hypersensitivity possible

L sided heart dz: can ↑ venous return to L heart → CHF

Hypotension

216
Q

Sildenafil: drug interaction

A

Ketoconazole
Erythromycin
Cimetidine
→ ↑ [drug]

217
Q

Theophylline: drug class

A

Bronchodilator
Sympathomimetic

218
Q

Theophylline: MOA

A

Non-selective phosphodiesterase inhibitor

Adenosine antagonist

219
Q

Theophylline: absorption/bioav

A

well PO
>90%

220
Q

Theophylline: 1/2 life

A

1-6h dogs,
14-18h cats,
12-15h Eq

221
Q

Theophylline: indications

A

Inflammatory airway dz

SSS/SA node dysfct
AVB

222
Q

Theophylline: side effects

A
  • GI: V+, D+
  • Tachycardia
  • Excitement/ agitation
  • Tremors
  • Seizures
223
Q

Theophylline: overdose

A

Overdose: hypoK+

224
Q

Theophylline: drug interaction

A

Cimetidine
Erythromycin
Propanolol
→ ↑ [] by ↓ metabolism

Phenobarbital
Rifampin
→ opposite

225
Q

Lomotil: drug class

A

Opiate agonist

226
Q

Lomotil: MOA

A

Bind to mu-opiate R in intestines
- Stimulate SM segmentation in intestines
- ↓ peristaltis
- ↑ fluid/electrolyte absorption

227
Q

Lomotil: indications

A

Opioid effect used to ↓ inflammation and coughing

Coughing (dogs)

Diarrhea

228
Q

Lomotil: absorption

A

Absorption: PO
- Hu: rapid, peak after 2h

229
Q

Lomotil: metabolism

A

liver

230
Q

Lomotil: elimination

A

60% bile and feces

231
Q

Lomotil: 1/2 life

A

12-14h

232
Q

Lomotil: CI

A

D+ from toxins, parvovirus

Hypersensitivity

Atropinization: hyperT, tachycardia, urinary retention, dry MM

Caution:
- Addison
- ↑ cranial P
- HypoT4
- Liver dz
- Kidney failure

233
Q

Lomotil: drug interaction

A

↑ ½ life of hepatic metabolized drugs

234
Q

Hyoscyamine: drug class

A

anticholinergic

235
Q

Hyoscyamine: MOA

A

Competitive antagonist of Ach effect on muscarinic R
- Parasympatholytic → ↑HR

236
Q

Hyoscyamine: other effects

A

antiemetic

237
Q

Hyoscyamine: absorption PO/IV, peak, duration, onset

A

Absorption: not affected by food
- Peak PO 30-60min, IV 15-30min
- Onset PO 20-30min, IV 2min
Duration 4h

238
Q

Hyoscyamine: 1/2 life

A

3.5h

239
Q

Hyoscyamine: elimination

A

Urine mostly unchanges

240
Q

Hyoscyamine: indications

A

Bradycardia
AVB
SSS

Vomiting: associated w
- Motion sickness
- GI dz, ↓ motility/ secretions

241
Q

Hyoscyamine: CI

A

Glaucoma

Intestinal ileus

Gastroparesis

Tachycardia

242
Q

Hyoscyamine: drug interaction

A

Other anti muscarinics

12. Pharmacology (10 decks)

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