pharm logbook interview Flashcards

Question

effects of thiazide

Answer 1

* Reduced reabsorption of sodium, chloride and water * Vasodilation (through an unknown mechanism)

Answer 2

oral, once/twice daily

Answer 3

* Glucose intolerance * DM * Gout * Pregnancy

Answer 4

* Postural hypotension * Dizziness * Hypokalaemia * Hyperuricaemia  gout * Hyperglycaemia  diabetes

Answer 5

* Electrolyte imbalances (sodium, potassium, calcium, magnesium) * Acute gout flare in pt with family or personal history of gout * BP monitoring * Blood glucose levels in pt with impaired glucose metabolism

Answer 6

- phenylalkylamaines - verapamil - benzothiazepines - diltiazem dihydroppyridines - amlodipine

Answer 7

Blocks L-type calcium channel in cardiac and smooth muscle, which causes smooth muscle relaxation since Ca2+ is needed for contraction - Vascular-selective: reduce systemic vascular resistance - Cardio-selective: reduce CO

Answer 8

* Cardiac-selective CCBs will decrease HR, AV conduction, contractility, and thus CO  causes an overall reduction in BP * Vascular selective CCBs will decrease vascular smooth muscle contraction, vascular tone (vasodilation), which cause a decrease in vascular resistance and an overall reduction in BP

Answer 9

oral, q8-12h IV

Answer 10

oral, once daily IV

Answer 11

oral once daily

Answer 12

- HTN - angina - arrhythmias (a-fib)

Answer 13

- HTN - angina - arrhythmias (a-fib)

Answer 14

- HTN - angina

Answer 15

* Bradycardia * AV block * Constipation

Answer 16

* Bradycardia * AV block * Constipation * Reflex tachycardia * Peripheral oedema * Headache * Flushing * Hypotension * Dizziness

Answer 17

* Reflex tachycardia * Peripheral oedema * Headache * Flushing * Hypotension * Dizziness

Answer 18

Vascular selective: * Tachyarrhythmias * Heart failure * Hypersensitivity Cardio-selective: * Heart failure * Bradycardia * AV block

Answer 19

* Routine BP measurement * Adverse effects such as peripheral oedema, dizziness and flushing * ECG * HR

Answer 20

atenolol metoprolol

Answer 21

* Block beta1 receptors in cardiac muscle – which then inhibits noradrenaline * Inhibits SNS action on cardiac muscle: - decreased HR - decreased AV conduction - decreased contractility - decreased automacity (spontaneous AP generation) - less O2 consumption by myocardium - Negative inotropic and chronotropic (contractility and rate) - decreased CO and arterial P

Answer 22

* Activation of beta 1 receptors normally increases intracellular Ca2+ (via increased cAMP and PKA) – so inhibition of this will cause decreased intracellular Ca2+ * Opposing action of SNS - decreased HR, AV conduction, contractility * decreased CO, thus decreased arterial BP

Answer 23

very little portion metabolised by liver

Answer 24

oral once daily

Answer 25

oral once/twice daily

Answer 26

- HTN - HF - tachyarrhythmia (a-fib) - angina - post-AMI

Answer 27

* Asthma, COPD * Bradycardia * Peripheral vascular disease * DM * AV block

Answer 28

* Bradycardia * Fatigue * Cold extremities * Bronchoconstriction * Nightmares * Hypoglycaemia

Answer 29

* Blood glucose monitoring * Routine BP measurement

Answer 30

prazosin terazosin

Answer 31

* Blocks alpha1 receptors in vascular smooth muscle -> at postsynaptic receptors on peripheral blood vessels, NA binds to alpha1 receptors --> increased phosphalipase C --> increased IP3 and DAG --> increased intracellular Ca2+ and vasoconstriction --> blockade of alpha1 receptor causes vasodilation --> reduce systemic vascular resistance

Answer 32

Vasodilation -> decreased TPR and BP

Answer 33

mainly biliary

Answer 34

mainly biliary, some renal

Answer 35

oral, 2-3 times daily

Answer 36

oral, once daily or q12h

Answer 37

* Postural hypotension * Dizziness * Headache * Oedema * Nasal congestion – due to peripheral vasoconstriction

Answer 38

* For adverse effects like dizziness, oedema * Routine BP measurement

Answer 39

- CCBs - beta blockers

Answer 40

alpha 1 antagonists

Answer 41

alpha 2 agonists (except use of methyldopa in pregnancy)

Answer 42

clonidine methyldopa

Answer 43

* Mimics autoinhibitory response in CNS -> less SNS outflow > less NA effects > less vasoconstriction > less SNS effects on heart > less CO > less BP * Constant reduction of SNS outflow -> up-rego of SNS receptors -> increased sensitivity to sympathomimetics (avoid sudden drug cessation and drug interactions like alpha1 agonists – can cause sudden and dangerous increase in BP)

Answer 44

* Inhibit further NA release through negative-feedback (autoinhibitory) control by NA at pre-synaptic 2 receptors * 2 receptor agonists activate 2 receotors in CNS and inhibit NA release, and thus SNS outflow

Answer 45

mainly renal

Answer 46

oral q6-12h

Answer 47

* Bradycardia * AV block * Peripheral vascular disease * Depression * Diabetes

Answer 48

* Drowsiness * Fatigue * Bradycardia * Dizziness -> all due to SNS activity

Answer 49

* For adverse effects like dizziness, bradycardia * Routine BP measurement

Answer 50

atorvastatin simvastatin

Answer 51

* Competitively inhibit HMG-CoA reductase (normally HMG-CoA converts into mevalonic acid through HMG-CoA reductase, which mevalonic acid turns into cholesterol) * Inhibition of HMG-CoA reductase -> decreased hepatic cholesterol synthesis -> increased demand for cholesterol -> increased expression of LDL receptors -> increased LDL clearance from plasma (due to decreased hepatic cholesterol and increased demand) -> decrease plasma LDL cholesterol

Answer 52

* Decrease plasma LDL cholesterol * Other actions: - Decreased plasma TG - Increased plasma HDL - Improved endothelial function (reduces % of atherosclerotic plaque forming) - Reduced vascular inflammation (reduces % of atherosclerotic plaque forming) - Reduced platelet aggregability (which can limit pathogenesis of atherosclerotic plaque) - Increased neovascularisation of ischaemic tissue - Stabilisation of atherosclerotic plaque - Antithrombotic actions - Enhanced fibrinolysis

Answer 53

mainly biliary

Answer 54

oral once daily

Answer 55

oral once daily (at night - due to shorter half life so take at night when cholesterol metabolism is highest)

Answer 56

* Drugs that inhibit CYP450 enzymes * Acute liver disease

Answer 57

* Hypercholesterolaemia * High risk of coronary heart disease (e.g., patients post-acute MI), with or without hypercholesterolaemia

Answer 58

* Myalgia * Mild GI disturbances – nausea, stomach pain * Elevated aminotransferase actions * Rhabdomyolysis (rare)

Answer 59

* Liver function? * Blood lipid levels * Protein kinase levels

Answer 60

* Decreases absorption of exogenous cholesterol by blocking transport protein (NPC1L1) in small intestine absorptive enterocytes > increase demand for cholesterol > increase LDL receptor expression > increase plasma LDL clearance > reduced plasma concentration of LDL

Answer 61

* Reduce plasma LDL cholesterol

Answer 62

enterohepatic circulation

Answer 63

oral once daily

Answer 64

* Hypercholesterolaemia (when statins are not tolerated/ added to statins)

Answer 65

* Hypersensitivity * Acute liver disease

Answer 66

* Headache * Abdominal pain * Diarrhoea

Answer 67

* Blood lipid levels

Answer 68

cholestyramine

Answer 69

Bind bile acids in intestinal lumen, which prevents their reabsorption through enterohepatic circulation, which then increases bile acid excretion in faeces > decreased absorption of exogenous cholesterol and increased metabolism of endogenous cholesterol into bile acids > increased demand for cholesterol (since exogenous absorption of cholesterol decreased) > increase LDL receptor expression > increase plasma LDL clearance > decrease plasma concentration of LDL-cholesterol

Answer 70

* Decrease plasma LDL levels

Answer 71

oral q12-24h

Answer 72

Combination treatment for hyperlipidaemia when statin alone is inadequate

Answer 73

- hypertriglyceridemia - Pt with complete biliary obstruction

Answer 74

* GI disturbances – constipation, abdominal pain, flatulence, dyspepsia, nausea, vomiting, diarrhoea, anorexia * Can increase TG levels * Decrease fat soluble vitamins levels (vit A D E K) – due to interference with absorption of dietary lipids

Answer 75

* Blood lipid levels, esp. TG?

Answer 76

evolucumab

Answer 77

* Monoclonal Ab – they have monovalent affinity – they bind to the same epitope * PCSK9: crucial role in cholesterol homeostasis – binds to LDL receptors and promotes lysosomal degradation > which then decreases hepatic LDL uptake, and increases plasma LDL * Evolocumab specifically bind to PCSK9 > increase LDL receptor (and inhibition of lysosomal degradation of LDL rcts > increases hepatic LDL uptake) > decreased plasma LDL concentration

Answer 78

* Decrease plasma LDL concentration by 55-75%

Answer 79

mainly through saturable binding to PCSK9

Answer 80

subcutaneous injection every 2 weeks or once monthly

Answer 81

Combination therapy with statin in familial hypercholesterolaemia, or primary hypercholesterolaemia after inadequate response or intolerance of statins

Answer 82

hypersensitivity

Answer 83

- injection site reactions - infections - angioedema

Answer 84

- for angioedema - for infections - blood lipid levels

Answer 85

fenofibrate gemfibrozil

Answer 86

* Agonists at PPARa w nuclear receptors which is usually located in cytoplasm of cell * Increase transcription of genes for lipoprotein lipase * Enhanced lipoprotein lipase results in increased TG uptake by VLDL and chylomicrons > increased removal of plasma TG

Answer 87

* Decrease TG by 40-80% * Decrease LDL by 5-15% * Increase HDL by 10-30%

Answer 88

hepatic CYP450

Answer 89

enterohepatic circulation

Answer 90

mainly renal

Answer 91

oral once daily

Answer 92

* Severe hypertriglyceridemia * Combination therapy with statin for mixed hyperlipidaemia with predominant hypertriglyceridemia * Second-line option when statins are not tolerated or are contraindicated

Answer 93

Severe renal and hepatic impairment – primary biliary cirrhosis, gallstones, gall bladder disease, photosensitivity due to fibrates

Answer 94

* GI disturbances * LDL levels can increase in pure hypertriglyceridemia (rather than mixed hyperlipidaemia) * Rhabdomyolysis (rare, but high risk if used in combination with statins) * Headache * Dry mouth * Myalgia

Answer 95

- protein kinase levels - blood lipid levels

Answer 96

* Exact MoA unknown, but is thought to decrease release of free fatty acids from adipose tissue > decreases hepatic synthesis of TG > decreased hepatic VLDL secretion > decreased plasma TG and LDL

Answer 97

* Reduced TG by 25-40% * Reduced LDL by 15-30% * Increases HDL by 20-35%

Answer 98

oral, once daily

Answer 99

* Use is limited by its poor tolerability * May be used for hypertriglyceridaemia * Combination therapy for mixed hyperlipidaemia if tolerated

Answer 100

* Recent MI * Gout * Hyperuricaemia * Hepatic or renal impairment * DM

Answer 101

* Vasodilation effects – flushing, hypertension, headache * Nausea * Vomiting * Diarrhoea

Answer 102

* Blood lipid levels * For adverse effects like hypotension and nausea

Answer 103

- GTN: IV/ sublingual/ transdermal - isosorbide mononitrate (tablet)

Answer 104

In endothelial cells, nitrates react with tissue sulfhydryl groups to release NO – NO diffuses into smooth muscle cell and activates guanylate cyclase > increased cGMP > increased protein kinase G – PKG induces smooth muscle relaxation by decreasing intracellular calcium and K, and increasing MLC phosphatase activity

Answer 105

- Therapeutic effects are dose-related - At low doses: * Venorelaxation, with little effect on arterial resistance vessels > venorelaxation > peroopheral pooling > decreased venous return > decreased preload and VEDP > increased coronary perfusion (perfusion window) > decrease cardiac workload anad O2 demand - At higher doses: * Dilation of arteries: > coronary arterial vasodilation > increased cardiac perfusion > systemic arterial vasodilation > decreased afterload > decreased cardiac workload and O2 demand - Nitrates also diverts blood from normal to ischaemic areas of myocardium – due to the dilatation of collateral vessels that bypass narrowed coronary artery

Answer 106

mainly renal

Answer 107

not subject to first pass metabolism in liver - hepatic via conjugation

Answer 108

* IV: for acute treatment * Sublingual: every 5 minutes up to 3 times * Transdermal: once daily for no more than 12 hours

Answer 109

Oral, twice daily (immediate release); once daily (extended release)

Answer 110

* Angina > prophylactic (transdermal) and acute (sublingual tablets and sprays)

Answer 111

angina > prophylactic

Answer 112

* Hypotension * Inferior and posterior MI/ RV infarct * Fixed cardiac output – aortic stenosis, tamponade * Significant tachycardia or bradycardia * Hypersensitivity

Answer 113

Vasodilatory effects: * Headache * Postural hypotension * Reflex tachycardia * Flushing * Fainting * Palpitations * Peripheral oedema

Answer 114

- for adverse effects like peripheral oedema

Answer 115

* Do not administer with PDE5 inhibitors (sildenafil, vardenafil, tadalafil) – increase nitrate effects – systemic vasodilation and severe hypotension * Hypersensitivity to nitrates

Answer 116

* Irreversibly and non-selectively inhibits cyclo-oxygenase enzyme (COX) – thus inhibits the production of prostanoids > inhibits production of prostacyclin and thromboxane A2 - COX-1: present in most cells as a constitutive enzyme, regardless of needs – produced prostanoids that function as homeostatic regulators (e.g., gastric protection, renal blood flow, platelet function) - COX-2: not normally present, inducible – induced during inflammation and tissue repair and has physiological roles to play in reproduction and renal function * Irreversible inhibition of COX reduces both TXA2 synthesis in platelets and PGI2 synthesis in endothelium – vascular endothelial cells can continue to synthesise new COX-1 because these cells are nucleated, but platelets are not so they cannot continue to synthesise COX-1, so once it is irreversibly inhibited by aspirin, they cannot continue to produce TXA2

Answer 117

* Inhibition of TXA2 synthesis and inhibition of platelet aggregation and activation ** after administration of aspirin TXA2 synthesis does not recover until more platelets are produced (turnover, which is 7-10day)

Answer 118

mainly renal

Answer 119

oral, 75-300mg daily

Answer 120

* ACS * Thrombosis prevention * Post-AMI * History of symptomatic atherosclerosis

Answer 121

* Hypersensitivity - especially people with pre-existing allergies like asthma * Bleeding GI ulcers

Answer 122

* Bleeding * GI disturbances – discomfort, dyspepsia, ulceration – due to direct irritation and COX-1 inhibition * Allergic reactions – urticaria, bronchoconstriction

Answer 123

monitor for adverse effects like allergic reactions and bleeding

Answer 124

clopidogrel

Answer 125

Irreversibly inhibits P2Y12 platelet (which usually acts as a chemoreceptor for ADP) – this prevents ADP-mediated activation of GP iib/iiia complex and thus inhibit platelet aggregation

Answer 126

anti-platelet effects via inhibition of platelet aggregation

Answer 127

hepatic CYP450

Answer 128

mainly renal

Answer 129

oral once daily - loading dose for pt >75y

Answer 130

-ACS -thrombosis prevention

Answer 131

* Hypersensitivity * Active pathologic bleeding – peptic ulcer, intracranial haemorrhage

Answer 132

* Bleeding * GI disturbances (upset stomach/ pain, diarrhoea, constipation)

Answer 133

for adverse effects

Answer 134

* Inhibits the phosphodiesterase enzymes (PDE3) that break down cAMP > increased cAMP > activation of PKA > phosphorylation of IP3 receptors > decreased Ca2+ release from ER > decreased release of granules * Block of adenosine uptake into RBC (adenosine then binds to A2 receptors, which increases platelet cAMP)

Answer 135

Decrease platelet aggregation via decreased activation of platelets

Answer 136

oral twice daily w aspirin

Answer 137

Thrombosis prevention/ ischaemic stroke, TIA prevention

Answer 138

* Hypersensitivity * Thrombocytopenia

Answer 139

Vasodilatory effects: * Headache * Flushing * Dizziness

Answer 140

for adverse effects

Answer 141

* Block GPIIb/IIIa receptors > prevents fibrinogen from binding to the GP IIb//IIIa receotors > prevents linkage of adjacent platelets * Block all pathways to platelet aggregation since GP IIa/IIIb receptors constitute at a point at which the pathways converge

Answer 142

* Decrease platelet aggregation due to inhibition of fibrinogen crosslinking

Answer 143

negligible

Answer 144

mainly renal

Answer 145

IV – loading dose with 5 minutes, then post loading dose for up to 18h

Answer 146

thrombosis high risk unstable angina

Answer 147

* Hypersensitivity * Thrombocytopenia * Active internal bleeding or history of bleeding diathesis * Major surgical procedure or severe physical trauma within previous month

Answer 148

* Dizziness * Allergic reaction * Nausea * Headache * Bleeding

Answer 149

adverse effects

Answer 150

* Convert plasminogen to plasmin, which catalyses fibrin breakdown > plasminogen deposition on fibrin strand within thrombus – exogenous plasminogen activators then diffuse into thrombus and cleave plasminogen to release plasmin – plasmin breaks down the thrombus

Answer 151

* Dissolves clots through plasmin-mediated fibrinolysis

Answer 152

mainly renal

Answer 153

IV – initial bolus over 1 minute (10% of total dose), then remainder over 60 minutes

Answer 154

* STEMI * Ischaemic stroke

Answer 155

* Active internal bleeding * Stroke or serious trauma within 3 months * Severe uncontrolled hypertension * Bleeding diathesis

Answer 156

* Bleeding * Angioedema * Anaphylaxis * Unusual bleeding * Headache * Dizziness

Answer 157

* For adverse effects like angioedema, bleeding, anaphylaxis

Answer 158

ARNI - sacubitril with valsartan

Answer 159

* Valsartan: decreased vasoconstriction > decreased aldo secretion > decreased sodium and water retention > decreased potassium secretion > decreased blood volume and pressure > decreased venous pooling and oedema * Sacubitril: Inhibits the degradation of natriuretic peptides, which causes more vasodilation, natriuresis and diuresis

Answer 160

* Help maintain sodium and fluid balance, and protect CVS from effects of fluid overload (sacubitril acts to raise NP levels and results in vasodilation, natriuresis, and diuresis

Answer 161

Sacubitril: mainly renal Valsartan: faeces

Answer 162

oral twice daily

Answer 163

heart failure with reduced ejection fraction

Answer 164

* Elderly * Renal and hepatic impairment * Hyperkalaemia * Angioedema * Hypotension

Answer 165

* Hypotension * Hyperkalaemia * Dizziness * Angioedema

Answer 166

* Monitor hypotension, hyperkalaemia, renal impairment, angioedema

Answer 167

spironolactone

Answer 168

* Antagonises aldosterone * Inhibits aldosterone-induced increase in sodium channels in luminal membrane, and Na/K ATPase pumps in basolateral membrane of collecting tubules * increased loss of sodium and water, and decreased excretion of potassium in urine

Answer 169

decreased aldosterone effects helps with pathophysiology of heart failure and improve outcomes

Answer 170

hepatic and renal

Answer 171

Oral, once daily initial dose, if not tolerated, then once every other day

Answer 172

* Hypersensitivity * Conditions associated with hyperkalaemia

Answer 173

* Hyperkalaemia * Gynaecomastia * Menstrual disorders * Testicular atrophy

Answer 174

monitor adverse effects like hyperkalaemia - K levels

Answer 175

dapagliflozin empagliflozin

Answer 176

* Inhibit sodium-glucose co-transporter 2 (SGLT2), which reduce glucose reabsorption in the kidney, and increase its secretion in urine * Inhibiting SGLT2 produces glycosuria and osmotic diuresis, reducing fluid load

Answer 177

Reduces fluid load through glycosuria and osmotic diuresis

Answer 178

minimally metabolised - primarily metabolised via glucuronidation

Answer 179

oral daily

Answer 180

heart failure with preserved ejection fraction

Answer 181

hypersensitivity pt on dialysis

Answer 182

* Urinary and genital tract infection * Thirst

Answer 183

monitor adverse effects

Answer 184

furosemide

Answer 185

* Inhibit Na/K/2Cl symporter in luminal membrane of thick ascending limb of loop of Henle * Increases loss of Na, K, Cl, and water in urine * Decreases venous return and venous pooling

Answer 186

* Reduces fluid load through glycosuria and osmotic diuresis * Decreases venous return and venous pooling due to reduced sodium chloride reabsorption > aims to reduce signs and symptoms of congestion, and improve exercise tolerance

Answer 187

renal and hepatic - glucuronidation

Answer 188

mainly renal

Answer 189

oral once or twice daily

Answer 190

heart failure with reduced ejection fraction

Answer 191

hypersensitivity anuria

Answer 192

* Hyperuricaemia * Hypokalaemia * Dizziness * Orthostatic hypotension

Answer 193

- for adverse effects - uric acid levels

Answer 194

* after arriving at vascular space, it will diffuse into interstitial space * the sodium does not enter intracellular space due to active sodium extrusion * which then causes immediate expansion of intravascular volume, and equilibration between vascular and interstitial spaces (these two spaces have higher osmolarity than that of intracellular space) * which then ultimately results in water movement from intracellular space in order to equalise osmolarity throughout intracellular, interstitial, and intravascular space.

Answer 195

* Immediate expansioin of intravascular volume – corrects hypovolaemia

Answer 196

- crystalloid: normal saline - colloids: albumin

Answer 197

hypovolaemic shock

Answer 198

* Oedema * Heart disease * Cardiac decompensation * Hyperchloremic metabolic acidosis

Answer 199

injection site infection

Answer 200

* clinical and laboratory findings of patient – electrolyte concentrations, volume status, acid-base disturbances * evaluation for dehydration/ fluid overload

Answer 201

* expansion of intravascular compartment  the fluid does not leave across the blood vessel walls and other compartments are unaffected

Answer 202

* more blood volume – restoration of hypovolaemia

Answer 203

intestinal mucosa

Answer 204

hypersensitivity severe anaemia HF

Answer 205

hypovolaemic shock

Answer 206

* Hypersensitivity * Flushing * Urticaria * Fever * Chills * Nausea * Vomiting * Tachycardia * Hypotension

Answer 207

* Monitor for any adverse effects * Patient’s fluid status

Answer 208

noradrenaline adrenaline vasopressin dopamine

Answer 209

* Preferentially activates alpha-1 receptors in the vasculature, causing vasoconstriction and increased peripheral resistance * Some activation of beta-1 receptor in the heart, but since increased TPR is coupled with compensatory baroreceptor reflexes, there is either no change or HR and CO

Answer 210

* Vasoconstriction and INCREASED TPR helps raise BP and establishes a more adequate circulation

Answer 211

monoamine oxidase in adrenergic neuron

Answer 212

hypovolaemic shock

Answer 213

hypersensitivity

Answer 214

* Headache * Dizziness * Reflex bradycardia * Blurred vision * Chest pain/ discomfort * Nervousness * unusual tiredness or weakness

Answer 215

adverse effects pt fluid status

Answer 216

* at low doses, beta 1 and 2 receptors are activated – beta 1: increased HR and contractility; beta 2: decreased TPR * at higher doses, alpha 1 receptors are activated, which increases peripheral resistance

Answer 217

* Alpha 1 and beta 2 effects helps raise BP and establishes a more adequate circulation

Answer 218

hypovolaemic shock

Answer 219

* Non-anaphylactic shock * Thyrotoxicosis * Diabetes

Answer 220

* Tachyarrhythmia * Ischaemia * Headache * Flushing * Dizziness * Palpitations * Hypertension

Answer 221

fluid status electrolyte levels ECG BP

Answer 222

* Causes vasoconstriction by acting on V1 (Gq GPCR) receptors * This activation in vascular smooth muscle causes increased phospholipase C and IP3 * V2 receptors in kidneys are also activated to increase water reabsorption

Answer 223

* Helps raise BP and thus establish a more adequate circulation

Answer 224

hepatic and renal

Answer 225

hypovolaemic shock

Answer 226

hypersensitivity

Answer 227

* Sweating * Nausea * Diarrhoea * Angina

Answer 228

adverse effects pt fluid status and electrolytes level

Answer 229

* At low dose: Activate D1 receptors in renal and mesenteric arteries, which increases adenylate cyclase > increased cAMP and PKA > inhibition of MLCK > vascular SM relaxation and vasodilation * At medium dose: Activates D1 and beta 1 receptors – increases CO and maintain renal blood flow * At high dose: Activated alpha-1 and beta-1 receptors

Answer 230

* Helps raise BP and thus establish a more adequate circulation

Answer 231

hepatic, renal, and plasma (monoamine oxidase)

Answer 232

hypovoalemic shock

Answer 233

* Hypersensitivity * Uncorrected tachyarrhythmias * Ventricular fibrillation

Answer 234

* Arrhythmia * Tachycardia * Angina * Palpitation * Bradycardia * Hypotension * Hypertension * Vasoconstriction * Headache * Nausea * Ectopic beats

Answer 235

for adverse effects - ECG, BP pt fluid and electrolyte levels

Answer 236

dobutamine isoprenaline

Answer 237

* beta agonist (positive inotropes) * increases CO via positive chronotropic (HR) and inotropic (contractility) actions * minor effect at alpha-1 receptors, hence little effect on peripheral vascular resistance

Answer 238

* increase CO via positive chronotropic and inotropic actions

Answer 239

hepatic and tissue

Answer 240

hypovolaemic shock

Answer 241

hypersensitivity

Answer 242

* Tachyarrhythmia * Hypertension * Angina * Headache * Nausea * Ectopic beats * Palpitations

Answer 243

ECG, BP fluid levels

Answer 244

* beta agonist (positive inotropes) * increases CO via positive chronotropic (HR) and inotropic (contractility) actions * no effect on alpha-1 receptors, so either maintain or increase systolic BP, and decrease diastolic BP by lowering peripheral resistance (beta 1 and 2 effects)

Answer 245

* increase CO via positive chronotropic and inotropic actions

Answer 246

* Hypersensitivity * Concomitant use with adrenaline * Pre-existing ventricular arrhythmias * Tachyarrhythmia * MI * Angina

Answer 247

* Tachycardia * Ectopic beats * Arrhythmias * Platelet aggregation inhibition * Hypotension * Tachyarrhythmia * Ischemia * V-fib

Answer 248

* Nonselective muscarinic receptor antagonist * Blocks M2 receptors via Gi on myocardial cells causes an increased rate of firing at SA node and increased conduction velocity through AV node

Answer 249

* Increased conduction at AV node * Increased rate at SA node

Answer 250

mainly renal

Answer 251

bradycardia AV block

Answer 252

hypersensitivity

Answer 253

* M3 receptor antagonist effects (relaxation of smooth muscle and decreased glandular secretions): - Constipation - Urinary retention - Blurred vision - Dry mouth - Dry eyes

Answer 254

1. Increases PNS activity (vagal tone) > slow SA node (decreased HR) and AV conduction (negative chronotrope and dromotrope) 2. Blocks Na/K ATPase on cardiac muscle cell membrane > blocks sodium efflux > Na+ accumulates intracellularly > affects Na+ gradient for Na/Ca exchanger > exchanger is indirectly inhibited by the accumulation of sodium > Ca2+ cannot leave via exchanger as there’s no gradient for sodium influx > calcium accumulates intracellularly as well

Answer 255

* Decreased HR via SA node and decreased AV conduction (negative chronotropic and dromotropic effects) * More intracellular sodium and calcium > positive inotropic effects * Proarrhythmic effects

Answer 256

mainly renal

Answer 257

* A-fib (rate control) > slows HR and increase contractility)

Answer 258

* Hypersensitivity * V-fib **increased risk of toxicity: * Renal impairment * Hypokalaemia (decreased competition for K binding site on Na/K ATPase – toxic effects but no increase in digoxin plasma levels)

Answer 259

**narrow therapeutic index – ineffective below the range, and toxic above the range: - anorexia – below - nausea – mid-range - vomiting – above * Other signs of toxicity: - Diarrhoea - Vision disturbances (halo around objects) - Confusion - Agitation - Life-threatening arrhythmias (atrial or ventricular) - AV block

Answer 260

* Digoxin plasma levels * Renal function * K levels * ECG recording?

Answer 261

* Activates A1 receptors on AV node > inhibits adenylate cyclase > decreased cAMP and PKA > increased outward K current, decreased funny current and Ca influx

Answer 262

decreases AV conduction

Answer 263

Phosphorylation to adenosine monophosphate by adenosine kinase, or via deamination to inosine by adenosine deaminase in cytosol

Answer 264

Via specific nucleoside transporter into RBCs

Answer 265

* Supraventricular tachycardia (SVT)

Answer 266

* Hypersensitivity * Pre-existing second/ third degree AV block * Pt w asthma and COPD

Answer 267

* Flushing * Chest pain * Dyspnoea * Anxiety * Bronchospasm ** short-lived effects – 15seconds

Answer 268

* ECG recordings * Adverse effects

Answer 269

amiodarone sotalol

Answer 270

* Bind and block potassium channels (prevent K efflux) that are responsible for phase 3 repolarisation

Answer 271

* Slows repolarisation and increases effective (absolute) refractory period

Answer 272

* Ventricular/atrial arrhythmia

Answer 273

* Hypersensitivity * Preexisting second/ third degree AV block * Cardiogenic shock

Answer 274

* Hypersensitivity * Preexisting second/ third degree AV block * Cardiogenic shock * Sinus bradycardia

Answer 275

* Hyper/hypothyroidism – dependent on pt pre-existing thyroid hormone levels * Pulmonary fibrosis * Skin abnormalities * GI disturbances * Corneal deposits * Peripheral neuropathy * Liver damage * Ventricular arrhythmia (torsades de pointes)

Answer 276

* Proarrhythmic effects – inc. torsades de pointes (due to increased AP duration) * Bradycardia * Fatigue * Cold extremities * Bronchoconstriction * Nightmares * Hypoglycaemia

Answer 277

* Hyper/hypothyroidism (thyroid function test) * Pulmonary fibrosis (chest XRAY)

Answer 278

* For adverse effects * ECG recordings * Plasma levels

Answer 279

1. class Ia: disopyramide (intermediate disso rate) 2. class Ib: lidocaine (fastest disso rate) 3. class Ic: flecainide (slowest disso rate)

Answer 280

* Bind and block fast sodium channels that are responsible for rapid depolarisation (phase 0) of non-nodal cardiac AP

Answer 281

* Blocking sodium channels reduced velocity of AP transmission within the heart (reduced conduction veloity) – this can suppress tachyarrhythmias that are caused by abnormal conduction ** the slower a cell depolarises, the more slowly adjacent cells will become depolarised, which leads to a slower transmission of AP b/n cells

Answer 282

* Orally, either q6h, q12h – doasge dependent on weight

Answer 283

Slow IV bolus over 2-3 minutes

Answer 284

Orally, twice daily / IV

Answer 285

* Serious ventricular arrhythmia (second line)

Answer 286

serious ventricular arrhythmia

Answer 287

* Atrial or ventricular arrhythmia (second line)

Answer 288

* Hypersensitivity * Preexisting second/ third degree AV block

Answer 289

* Hypersensitivity * Preexisting second/ third degree AV block * RBBB

Answer 290

* Cardiovascular effects: - Arrhythmias (effect greatest for flecainide, least for lidocaine) – proarrhythmic effects - AV block and worsening heart failure (flecainide) * CNS effects: - Drowsiness - Dizziness - Confusion * Anticholinergic effects: (only disopyramide) - Tachycardia - Dry mouth - Constipation

Answer 291

plasma levels pt response - adverse effects ECG recordings - arrhythmias