All of the drugs Flashcards

Question

Spiro: drug class

Answer 1

K+ sparing diuretic Aldosterone antagonist

Answer 2

Competitive inhibition of aldosterone by binding to R Interfere with Na+ reabsorption → ↑ max excretion of Na+ to 2% Preserve K+ excretion

Answer 3

Slow onset Peak 2-3days

Answer 4

Extensively/rapidly metabolized - Metabolites active but less potent

Answer 5

CHF Hepatic cirrhosis (inhibit ascites)

Answer 6

Steroid-like effect Facial dermititis Antiandrogenic effects (Hu): gynecomastia, hisurtism, impotence

Answer 7

Caution with K+ supplementation and NSAIDs

Answer 8

Thiazide diuretic

Answer 9

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

Answer 10

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

Answer 11

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

Answer 12

Low ceiling diuretic: max response reached at low dose

Answer 13

CHF/edema → chronic use of diuretics Antihyper-tensive Ca2+ excretion (Ca2+ oxalate urolithes)

Answer 14

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

Answer 15

Steroids: salt retention → ↓ effect Indomethacin/ NSAIDs → interfere w PG → ↓ effect Antiarrhythmics: class IA or III → prolong QT Nephrotoxic ATB Probenecid (gout tx) → block effect

Answer 16

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

Answer 17

- ↓ 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

Answer 18

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

Answer 19

ACEi > AngI - 200 000x greater

Answer 20

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

Answer 21

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

Answer 22

Bioav. 60% - Well absorbed by GI tract

Answer 23

Metabolized in liver → become pharmacologically active Secreted by kidneys

Answer 24

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

Answer 25

Pregnancy RA stenosis HyperK+ Renal dz Angioedema Hypotension

Answer 26

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

Answer 27

Same to enalapril

Answer 28

Non sulfhydryl ACEi

Answer 29

Metabolism: liver → hydrolysed into benazeprilat to become active Excretion: bile and urine - Less dependent on kidneys

Answer 30

Same enalapril

Answer 31

Vasodilator

Answer 32

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

Answer 33

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

Answer 34

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

Answer 35

Rapid onset (almost immediate) Duration: min

Answer 36

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

Answer 37

Acute CHF Hypertension

Answer 38

Hypotension Cyanide toxicity Venous hyperO2 Lactic acidosis Dyspnea

Answer 39

*protect from light Expensive!

Answer 40

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

Answer 41

Vasodilator

Answer 42

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

Answer 43

Blood volume redistribution: central → peripheral ↓intraventricular pressure → ↓ edema ↓SVR → ↑ SV, ↓LAP, ↓edema

Answer 44

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

Answer 45

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

Answer 46

CHF PH Angina pectoris (Hu) Laminitis (Eq) → ↑ blood flow to feet

Answer 47

Hypotension MetHb Tolerance

Answer 48

inotrope +

Answer 49

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

Answer 50

Biosynthetic precursor of NE → stimulates NE release

Answer 51

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

Answer 52

½ life = 1-2min - Rapid clearance

Answer 53

Plateau [CRI] achieved in 8min

Answer 54

*Inotropic effects w/o tachycardia

Answer 55

Acute CHF Cardiogenic shock Acute renal failure

Answer 56

Arrhythmias

Answer 57

Vasodilator

Answer 58

↑ [prostacyclin] → direct arteriolar SMcells

Answer 59

↑ 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

Answer 60

Metabolism: hepatic 1st pass → acetylation

Answer 61

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

Answer 62

- Reflex ↑∑ tone → ↑ contractility and HR → ↑CO → stable BP - Addition of β-blocker blocks reflex Not seen with CHF: ↓ response to ∑ tone

Answer 63

Systemic hypertension Cases refractory to ACEi Regurgitation/ shunt refractory to tx

Answer 64

Renal failure: affect hepatic metabolism →↑ [plasma] Hypotension Anorexia Vomiting Diarrhea Systemic lupus erythematosus Fever Peripheral neuropathy

Answer 65

Can ↑ furo delivery to nephron → ↑ GFR

Answer 66

Anti arrhythmic class 1A

Answer 67

Na+ channel blocker - ↓ upstroke velocity of phase 0

Answer 68

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

Answer 69

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

Answer 70

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

Answer 71

- Dosing difficult since short ½ life - Sustained release tablets: allow q8h o ↓ peak serum

Answer 72

Ventricular tachy-arrhythmias Preexcitation SVT

Answer 73

Hypotension and peripheral vasodilation ↓ inotropy → SLOW IV administration Pro arrhythmic effect Auto immune response → production of anti nuclear antibodies

Answer 74

Anti arrhythmic class 1B

Answer 75

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

Answer 76

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

Answer 77

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

Answer 78

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

Answer 79

40-100min Variable clearance rate

Answer 80

Rapid onset Short duration Effective

Answer 81

withdraw +/- diazepam

Answer 82

Ventricular arrhythmias Local anesthesia

Answer 83

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

Answer 84

Cimetidine Propanolol Halotane →↓ liver clearance (↓ dose) Hepatic enzyme inducers → ↑ clearance (↑ dose)

Answer 85

Anti arrhythmic class 1B

Answer 86

Na+ channel blocker - ↓ upstroke velocity of phase 0

Answer 87

Interrupt re-entry circuits: - Slow conduction - ↓ membrane responsiveness Suppress abnormal automaticity ↓ DADs formation induced by digitalis ↑ fibrillation threshold in ventricles

Answer 88

Analog of lidocaine

Answer 89

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

Answer 90

urine 80%, feces

Answer 91

similar to lidocaine

Answer 92

- Vomiting - Disorientation - Ataxia

Answer 93

seizures/ neuro signs

Answer 94

Anti arrhythmic class 1C

Answer 95

Na+ channel blocker - ↓ upstroke velocity of phase 0

Answer 96

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

Answer 97

Excretion: hepatic + renal - Unchanged

Answer 98

Paroxysmal SVT Sustained VT Catecholamine polymorphic Vtach → block open RyR channels

Answer 99

Pro arrhythmic effects - Structural heart dz: non uniform slowing of conduction - More common w ventricular ectopy ↓LV fct CNS side effects RBBB, LAFB, SSS

Answer 100

Amiodarone (kinetic) ↑ - inotrope: βB quinidine, disopyramide ↓AV cond: quinidine, procainamide

Answer 101

Anti arrhythmic class II

Answer 102

β blocker: selective β1 antagonist

Answer 103

Water soluble - ↓liver clearance

Answer 104

½ life = 5-6h dog, 3.5h cat

Answer 105

Excretion: urine - Unchanged

Answer 106

Acute withdrawal may exacerbate original issue

Answer 107

Afib → ↓HR SV and ventricular arrhythmias SAS: ↓ sudden death HOCM: ↓SAM

Answer 108

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

Answer 109

Anti arrhythmic class II

Answer 110

β blocker: non selective β1 and β2 antagonist

Answer 111

- ↓ catecholamine dependent automatic rhythms: normal + abnormal - Slow conduction in normal ventricular myocardium AV node: - ↑ refractory period - Slow conduction velocity ↓ myocardial contractility → ↓ O2 consumption

Answer 112

Lipophilic molecule

Answer 113

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

Answer 114

- 1.5h (1st dose) - 2h (2nd dose)

Answer 115

Dose dependent change in myocardial contractility and SVR

Answer 116

Afib → ↓HR SV and ventricular arrhythmias

Answer 117

Similar to atenolol

Answer 118

Anti arrhythmic class III mixed

Answer 119

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

Answer 120

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+

Answer 121

Highly lipophilic - Rely on liver - Accumulates 300x [plasma] in adipose tissue [Myocardial] = 15x plasma

Answer 122

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

Answer 123

Metabolism: liver → Desethylamiodarone: block fast Na+ channels

Answer 124

slow onset

Answer 125

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

Answer 126

Clearance: rapid except adipose tissue

Answer 127

SVT →Afib/ flutter Ventricular arrhythmias OK with structural heart dz

Answer 128

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

Answer 129

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

Answer 130

Anti arrhythmic class III/mixed

Answer 131

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

Answer 132

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

Answer 133

L isomer - 50% > β blocker activity

Answer 134

Absorption: rapid Bioav. 85-90%

Answer 135

SVT Ventricular arrhythmias

Answer 136

Similar to propranolol/ atenolol Use with caution: - ↓ cardiac contractility - Slow HR

Answer 137

Anti arrhythmic class IV

Answer 138

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

Answer 139

PREDOMINANT ACTION AV node: negative dromotrope - Slow conduction - Prolong refractory period Negative chronotrope: ↓HR Vasodilation Minimal effect on cardiac contractility or vascular SM cell

Answer 140

Absorption: rapid GI - 30min

Answer 141

½ life = 2-4h - Shorter in Eq

Answer 142

SVT Hypertension: 2nd tx or combination

Answer 143

Hypotension Myocardia depression Bradycardia AVB

Answer 144

- IV fluids - Ca2+ gluconate/chloride - Sympathomimetics

Answer 145

other/class 5 anti arrhythmics

Answer 146

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+

Answer 147

↑ 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

Answer 148

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

Answer 149

Digitalis glycoside - Poorly liposoluble

Answer 150

Metabolism: small hepatic (15%)

Answer 151

23-29h dog

Answer 152

PO: well absorbed by GI IV: slowly over 15min - Rapid can cause peripheral vasoconstriction → ↑ afterload

Answer 153

renal mostly

Answer 154

SVT Myocardial failure

Answer 155

- 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

Answer 156

↑ intracell Ca2+

Answer 157

↑ [serum] - Aminoglyco. - Amiodarone - Anticholinerg. - Diltiazem - Esmolol - Flecainide - Quinidine Drugs altering microsomal enzymes

Answer 158

Phosphodiesterase 3 inhibition - inhibit PDE enzyme → ↓ cAMP breakdown → ↑ cAMP - ↑ inotropy, chronotropy, dromotropy, vasodilation Ca2+ sensitizer - ↑ Troponin C sensitivity to Ca2+ → ↑ contractility

Answer 159

Anti inflammatory ↑ sensitivity to baroR ↑ lusitropy ↓ platelet agreggation

Answer 160

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

Answer 161

liver → more potent metabolite

Answer 162

CHF Preclinical CVD and DCM +/- HCM

Answer 163

GI upset Proarrhythmic: reported but not proven SAS

Answer 164

Ca2+ channel blockers Β blockers → ↓ inotropic effect

Answer 165

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

Answer 166

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

Answer 167

fecal 70%, urine 15%

Answer 168

PH R to L shunting

Answer 169

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

Answer 170

Ketoconazole Erythromycin Cimetidine → ↑ [drug]

Answer 171

Bronchodilator Sympathomimetic

Answer 172

Non-selective phosphodiesterase inhibitor Adenosine antagonist

Answer 173

well PO >90%

Answer 174

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

Answer 175

Inflammatory airway dz SSS/SA node dysfct AVB

Answer 176

- GI: V+, D+ - Tachycardia - Excitement/ agitation - Tremors - Seizures

Answer 177

Overdose: hypoK+

Answer 178

Cimetidine Erythromycin Propanolol → ↑ [] by ↓ metabolism Phenobarbital Rifampin → opposite

Answer 179

Opiate agonist

Answer 180

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

Answer 181

Opioid effect used to ↓ inflammation and coughing Coughing (dogs) Diarrhea

Answer 182

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

Answer 183

60% bile and feces

Answer 184

D+ from toxins, parvovirus Hypersensitivity Atropinization: hyperT, tachycardia, urinary retention, dry MM Caution: - Addison - ↑ cranial P - HypoT4 - Liver dz - Kidney failure

Answer 185

↑ ½ life of hepatic metabolized drugs

Answer 186

anticholinergic

Answer 187

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

Answer 188

antiemetic

Answer 189

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

Answer 190

Urine mostly unchanges

Answer 191

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

Answer 192

Glaucoma Intestinal ileus Gastroparesis Tachycardia

Answer 193

Other anti muscarinics