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114 Cards in this Set
- Front
- Back
- 3rd side (hint)
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Which one of the following reasons would indicate caution when prescribing nebulised ipratropium? Glaucoma Bradycardia peptic ulceration liver cirrhosis |
Glaucoma |
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Which drug does not directly cause bronchodilation? Salbutamol thephylline ipratropium prednisolone |
Prednisolone |
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How do inhaled or systemic corticosteroids improve bronchial function? |
By moderating airway inflammation |
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Which one of the following is not a side effect of theophylline? hypokalaemia tachycardia paradoxical bronchospasm convulsions |
Paradoxical bronchospasm |
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What class of drug does cause paradoxical bronchospasm? |
selective beta2 agonist drugs antimuscurinic bronchodilators |
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Inhaled corticosteroid therapy can cause? Candidiasis gum hyperplasia dyslipidaemia dental discolouration |
Candidiasis |
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Why does candidiasis arise when taking inhaled corticosteroids? |
local compromised immunity from oral contact with corticosteroid drugs |
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Which of the following medications does not interact with theophylline? St Johns wart Carbamazepine propranolol warfarin |
warfarin |
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One benefit of using a spacer device for inhaled salbutamol therapy? |
Administration of salbutamol increases |
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Why should a steroid card be issued with high dose steroids? |
Increased risk of adrenal suppresison |
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If a patient has liver impairment, which one of the following would require a dose change? Salbutamol ipratropium theophylline budesonide |
Theophylline |
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If a patient taking theophylline stops smoking, what effect will this hasve on the plasma theophylline concentration? |
It will increase and there is a risk of toxicity |
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Montelukast is a leukotrience receptor antagonist which blocks effects of cysteinyl leukotriences in the airway. What best describes the actions of leukotriences such as LTC4 and LTD4 in the airway? |
Contraction of airway smooth muscle, recruitment of inflammatory mediators and mucus secretion. |
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Montelukast blocks cysteinyl leukotrienes in the bronchus from doing what? |
Spasmogenic affect on bronchial smooth muscle and suppress inflammatory effects on mucus production |
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30% of COPD exacerbations are of no obvious cause, true or false? |
True |
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What type of infection is Pseudomonas aeruginosa? What do you treat it with? |
Gram-neg infection, most common hospital aquired infection (nosocomial). |
Ciprofloxacillin |
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What class of drug is ciprofloxacillin? |
Quinolones |
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LIst Beta-2 agonist inhalers |
Salmeterol Terbutaline Formoterol |
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List leukotrienes inhibiting inhalers |
Monkelukast |
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List corticosteroid inhalers |
Budesonide Fluticasone Beclomethasone |
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List anti-muscarinic inhalers |
Ipratropium ipratropium |
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What are the three main aims of treating asthma and COPD? |
Bronchodilatation reduce inflammation increase mucus clearance |
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What happens when you stimulate beta adrenergic receptors? |
Bronchodilation |
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What happens when you stimulate muscarinic receptors? |
Bronchoconstriction |
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What are the side effects of beta-2 agonists? |
Fine tremor nervous tension tachycardia low potassium |
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What is the MOA of antimuscarinic agents? |
Direct antagonism of muscrinic receptors on bronchial smooth muscle causing bronchodilation. |
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Main side effects of anticholinergic agents? |
Dry mouth impaired memory blurred vision dry eyes glaucoma urinary retnetion dyspepsia constipation |
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Pharmacodynamic effects of xanthines? |
Relaxation of smooth muscle in the lungs, reduces bronchospasm, reduces inflammatiory effects, respiratory stimulant |
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Why should theophylline be used with caution? |
Narrow theraputic window and interaction with other medications |
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List systemic side effects associated with corticosteoids |
OA Adrenal suppression skin thinning hyperglycaemia peptic ulcers susceptibility to infections |
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List local effects associated with corticosteroids? |
Dysphonia candidiasis pharyngitis reflex cough sensation of thirst pharyngitis |
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Pharmacodynamic effects of corticosteroids in the lungs? |
Reduce bronchial inflammation reduce oedema reduce mucus secretion |
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How can side effects associated with inhaled corticosteroids be minimised? |
titrate to effective dose use spacer add LABA rather than increase corticosteroid dose |
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What is the rationale for using a leukotreine antagonist? |
LTA's prevent the action of cysteinyl leukotrienes which are potent inflammatory mediators can be used alone with ICS also used for symptomatic relief of seasonal allergic rhinitis in pathients with asthma |
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Common/very common side effects of leukotriene antagonists? |
Abdominal pain headache thirst hyperkinesia in paeds |
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Describe the paharmacdynamic action of Beta-2 agonists |
stimulation of beta 2 receptors on airway causing relaxtion of bronchial smooth muscle and dilatation |
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Side effects of beta-2 agonists |
Tremor tachycardia hypokalaemia |
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MOA of antimuscarinic agents? |
Direct antagonism of muscarinic receptors on smooth muscle cells of airway causing bronchodilation. |
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Why should theophylline be used with caution? |
Narrow theraputic window and interactions with other medicines. |
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MOA of corticosteroids |
Anti-imflammatory properties by inhibiting inflammatory mediator synthesis. |
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Issues with high dose corticosteroids? |
Adrenal suppression muscle wasting hypergylcaemia OA susceptibility to infections |
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What other drug helps reduce inflammation of the airways? |
Leukotriene receptor antagonists, Beta-2 agonists, Xanthines (weak) |
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What is likely to happen if an enzyme INDUCING drug is administered with another drug that is metabolised via the same pathway? |
1. increased metabolism causes decrease in active drug. 2. or if it's a pro-drug more will be metabolised into an active drug. |
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What is likely to happen when an enzyme INHIBITING drug is adminsitered with another drug that is metabolised via the same pathway? |
1. Reduced metabolism causes an increase in active drug. 2. or will convert less pro-drug into active drug. |
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What is likely to happen to the level of a highly protein bound drug if the patient has reduced levels of albumin in the blood? |
Less protein available for binding to drug, hence more drug will be in the 'free' form leading to potential toxicity. |
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List key pharmacodynamic effects of corticosteroids... |
Reduce inflammation reduce bone mineral density increased salt and water retnetion - HTN Skin thinning, depigmentation reduced immune response increased blood glucose |
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Acute withdrawl of corticosteroids can cause acute adrenocortical insufficiency, what are those symptoms... |
Fever, myalgia (pain in a muscle), arthralgia (pain in a joint), weight loss. |
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Non-selective NSAID's |
IbuproFEN's PiroxiCAM |
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Selective COX-2 NSAID's |
XIB's only. |
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Why include paracetamol in the WHO pain ladder? |
1. Additive effect when given with other analgesics. 2. Safest 3. Useful alternative to NSAID's |
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In which patients are opioids contraindicated in? |
HI, comotose patients, raised intracranial pressure, respiratory depression, paralytic ileus. |
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MOA of opioids? |
Bind to opioid receptors causingthem to be stimulated, this blocks the transmission of pain signals, inducing an analgesic effect. |
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MOA tramadol? |
Selective agonist mu nociceptors spinal cord and brain AND inhibits reuptake of serotonin and norepinephrine. |
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MOA of Amitriptylline? |
Elevates serotinin.noreadrenaline or both and blocks Na+ channels. |
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Which opioid is most potent, Fentanyl codeine DF118 morphine |
Fentanyl |
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Opiates cause nausea because? |
They STIMULATE the chemoreceptor trigger zone |
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Which of the following is NOT due to the increased smooth muscle tone effected by opiates? Biliary spasm urinary retention pruritus increased bronchial airway resistance |
Pruritus |
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Which statement best describes the mechanism of action of opioid drugs? They are agonists for serotonin receptors in the brain and spinal cord? They are antagonists for noreadrenaline receptors in the brain and spinal cord? They are agonists for neuronal endorphin receptors They are antagonists for neuronal endorphin receptors? |
They are agonists for neuronal endorphin receptors |
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Which of the following is a partial opioid agonist? Morphine alfentanyl tramadol buprenorphine |
Buprenorphine |
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What distingushes tramadol from other opioids? |
It increases noradrenaline and serotonin levels in the brain. |
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Which of the following enhances the effects of morphine? Warfarin cimetidine SSRI's levothyroxine |
Cimetidine |
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Pharmacodynamics of codeine? |
Analgesic effect- mild- moderate pain Antitussive- for non-rpoductive cough Anti-motility effect- for symptomatic relief of acute diarrhoea |
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Codeine ADR's |
1. Resp depression- Opioid receptors in control ctrs 2. N+V- stimulation of CTZ |
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Codeine toxicity signs and why? |
Reduced GCS, pin-point pupils CYP2D6 |
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Pharmacodynamics naloxone? |
Selective opioid antagonist to reverse respiratory depression, high affinity for the mu-receptors and blocks these. |
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Half-life of naloxone? |
20mins |
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MOA of tramadol? |
selective agonist mu nociceptors spinal cord and brain, Inhibits re-uptate of serotonin and norepinephrine. |
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Why use tramadol? |
Half-life 4-6 hrs less constipating lower addiction potential less resp depression |
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Where is tramadol metabolised? |
Liver |
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Rationale for using Methadone? |
Slow metabolism - high lipid solubility, longer lasting then morphine. OD administration Withdrawl symptoms less demanding |
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MOA of Buprenorphine? |
Partial u-agonist, and K-antagonist Long acting Moderate/severe pain and opioid addiction S/L, transdermal patches Only partly reversed by naloxone |
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Key drug interactions with Opioids... |
Coumarins anti-depressants anti-epileptics anti-fungals antivirals cimetidine Morphine potentiates the effects of tranquillisers, muscle relaxants, and anti-hypertensives. |
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ADR's of Opioids |
Constipation opioid toxicity Sudden stopping and cause withdrawal, abdominal cramps. Hyperalgesia |
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What fatty acid substrate is metabolised by COX and LOX to produce protaglandins and leukotrienes? |
Arachidonic acid |
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Are Leukotrienes D4 powerful bronchodilators? |
YES |
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Prostaglandins regulate renal blood flow, renin release, and gut flow. Do they regulate CYP450 enzymes? |
NO |
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Are NSAID's weak or strong acids? |
Weak acids |
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One advantage of selective COX-2 inhibition is? |
Less COX-1 inhibition |
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The following are contraindicated with NSAID's - a history of hypersensitivity to aspirin -severe HF -dehydration Is aggressive inflammatory joint disease? |
NO |
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At what week in pregnancy should NSAID's be stopped? |
avoided after 30weeks |
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True or False The GI benefits of taking a COX_2 inhibitor are negated by the addition of aspirin at anti-plt doses |
True |
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Small daily doses of aspirin can impair renal function? true or false? |
False |
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Non-selective NSAIDs inhibit COX-1 and 2 with equal potency? True or false? |
False |
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COX-2 inhibitors are poor antu-pyretic agents? True or false? |
False |
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Constriction of the fetal ductus arterious is associated with NSAID's and which trimester of pregnancy? |
Third trimester |
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How many isoforms of COX are known to be relevant to drug therapy? |
3 |
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Paracetamol acts on what COX? |
COX- 3 |
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Why might paracetamol be a problem with ETOH abusers? |
Enzyme induction could mean more hepatotoxic metabolite production |
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Are nociceptors only present in the skin? |
NO |
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True or false? Pain is the product of higher brain processing, whereas nociception can occur in the absense of pain? |
TRUE |
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True or false? Nocicpetors are only present in the skin? |
FALSE |
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True or false? Inflammatory mediators (bradykinin, prostaglandins, cytokines) can directly stimulate nociceptors? |
True |
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True or false? Nociceptors detect noxious stimuli, convert them into electrical signals? |
True |
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What fibres are responsible for conducting rapid, sharp pain? |
A fibres! |
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Is caffiene regarded as an adjuvant analgesic? |
Yes |
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Does caffeine has a direct anti-nociceptive effect? |
Yes |
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Is caffeine known to have psychoactive properties? |
Yes |
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Is lidocaine primary an analgesic? |
No |
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What analgesic is recmmended by WHO at every stage of the WHO ladder? |
Paracetamol |
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Some patients are more liekly to be susceptible to paracetmaol toxicity. Whic of the following is LEAST likely to be a risk factor? 1. liver impairment 2. Occasional alcohol 3. Cystic fibrosis 4. long term carbamazepine |
Occassional alcohol |
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True or false? Neuropathic pain can arise from a stimulus that does not normally cause pain? |
True |
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Which of the following is least likely to be useful for the objective assessment of pain? 1. A visual analogue 2. smiley faces scale 3. body posturing 4. breif pain inventory |
Body posturing |
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The three opioid receptors are? |
Mu, kappa, delta |
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Why use caffeine for pain? |
Enhances analgesic affect in acute pain. |
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MOA of opioids |
Mimic endogenous opioid peptides (endorphins etc), when they bind to opioid receptors it blocks the tranmission of pain signals. |
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Opioids are an? |
Agonist |
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The 3 fibres that transmit pain/touch are? |
A-beta fibre - light touch/non-noxious stimuli A-delta fibre - rapid, sharp, reflex pain C-fibres - Prolonged pain, chemical, mechanical, thermal pain (unmylenated c-fibres, spinothalamic tract). |
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The 3 types of pain are? |
Somatic - Nociceptors, skin, muscle, superficial, deep somatic pain. Visceral - internal organs, poorly localised, assocaited with autonomic changes. Neuropathic - damage to nerves, trauma, surgery, DM, HIV. |
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Two nociceptive pain example... |
Mechanical pain, arthritis. |
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Two neuropathic pain examples... |
Trigeminal neuralagia distal polyneuropathy (DM, HIV). |
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Then theres acute and chronic pain. |
I have nothing to say on this. |
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Autonomic response to pain... |
HTN, tachy, sweatiness, vasoconstriction. |
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Pain assessments |
Smiley face Breif Pain Inventory The Visual Analoge Scale Body Posture |
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Naloxone MOA |
Competitive opioid recepetor antagonist. |
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