Drugs For Cptp4

Front 1

Metformin

Back 1

inhibits hepatic gluconeogenesiso Weight neutral or can induce weight loss, low cost and long track recordo GI adverse effects (nausea, loose stool, flatulence), lactic acidosis (renal impairment, heart failure, liver disease), unsafe if GFR<30

Front 2

Sulphonylureas

Back 2

Sulphonylureas increase insulin secretion but can cause hypoglycaemia and weight gain

Front 3

Thiazolidenediones

Back 3

Eg. pioglitazone enhance lipogenesis, decrease lipolysis and decrease plasma FFAs (PPAR-γ agonists), but may cause fluid retention and weight gain and increase peripheral fracture rate. They may have an association with bladder cancer and are now rarely used, mostly in NAFLD

Front 4

DPP-IV inhibitors

Back 4

Eg Sitagliptin Inhibits the DPP-IV enzyme which breaks down GLP-I (Incretin). Therefore DPP-IV inhibitors prolong the incretin activity

Well-tolerated, don’t cause hypoglycaemia, some licensed for use at low GFR. High cost, long term effects uncertain

Front 5

GLP-I mimetics

Back 5

Eg. exenatide, agonists of the GLP-1 receptor

Are resistant to DPP-IV, so enhance incretin effects. No hypoglycaemia, weight loss. SC injection, nausea and vomiting, long term effects unknown, high cost

Front 6

SGLT2 inhibitors

Back 6

Sodium/ glucose cotransporter 2 inhibitor

Prevent renal glucose reabsorption in the PCT, causing weight losso can cause UTIs, is high cost with uncertain long term effects

Front 7

NPH

Back 7

Intermediate acting insulin eg. Isophane insulin

Front 8

Human insulin

Back 8

made using recombinent DNA

Front 9

Insulin analogs

Back 9

Based on human inslulin but slight tweeks have been made to make it more effective. Therefore more of an insulin receptor ligand. These are useful as they reduce nocturnal hypos and allow for lower fasting glucose

Front 10

Constant infusion rapid acting analogue

Back 10

Allow more predictable absorption and smaller SC volume. Basal rate with meal-time boluses reduces hypoglycaemia but active self-management with high incidence of DKA if not used properly and high cost

Front 11

Statins

Back 11

By inhibiting HMG-CoA reductase, statins block the pathway for synthesizing cholesterol in the liver. This is significant because most circulating cholesterol comes from internal manufacture rather than the diet. When the liver can no longer produce cholesterol, levels of cholesterol in the blood will fall

Serious side effects are rare; myositis or myopathy, hepatitis, with increased risk in renal impairment, hypothyroidism and drug interactions

Front 12

Criteria for diagnosis of DKA

Back 12

ketonaemia >3mmol/l or significant ketonuria (>2+ on dipstick)

BM>11 or known DM

bicarbonate <15mmol/l or venous pH<7.3

Front 13

What is the management of DKA?

Back 13

-500ml 0.9% saline rapidly in DKA; can give up to a litre

-Begin potassium replacement early in DKA in adults, with frequent monitoring for the development of hypokalaemia.

-Insulin should be administered via short-acting insulin IV infusion at 0.1unit/kg/hour using infusion pump it should be mixed with saline

-Commence glucose alongside insulin when patient more alert with lower ketones

Front 14

What regular investigations should be undertaken for a patient in DKA?

Back 14

Hourly BM, hourly ketones, venous bicarbonate and potassium 2 hourly, 4 hour plasma electrolytes

Front 15

Define the resolution of DKA

Back 15

Resolution is defined as blood ketones <0.3mmol/l and venous pH>7.3

Front 16

Once DKA resolution has been confirmed how is management stopped?

Back 16

fast-acting insulin SC with meal and discontinue insulin infusion 30 minutes later

Front 17

How should a hypo be managed?

Back 17

If IV access in unconscious patient, give 75-80ml 20% dextrose or 150-160ml 10%.  If no IV access, give Glucagon 1mg IM, recheck in 10 minutes, and repeat if below 4  Give long-acting oral carbohydrate after immediate recovery

Front 18

Define Pharmacogenetics

Back 18

The study of the genetic basis for variability in drug response

Front 19

Pharmacogenomics

Back 19

The use of genetic information to guide the choice of drug and dose on an individual basis; for personalised therapy

Front 20

Describe the effects of a Polymorphism in the TPMT gene

Back 20

Polymorphisms in the TPMT gene result in decreased TPMT enzyme activity, reducing breakdown of the thiopurine drugs used to treat acute lymphoblastic leukaemia and increasing risk of severe bone marrow toxicity

Front 21

Give some examples of idiosyncratic (bizarre) drug reactions which now seem to be associated with genomics

Back 21

SJS due to carbamazepine, hepatitis with flucloxacillin, aplastic anaemia with chloramphenicol and rhabdomyolysis with simvastatin

Front 22

What is the basic diagnostic criteria for PD?

Back 22

characterised by bradykinesia with at least one of rigidity, resting tremor and postural instability

Front 23

How are abnormal proteins involved in PD

Back 23

abnormal protein aggregations of α-synuclein often collected into intracellular inclusions (Lewy bodies)

Front 24

Co-careldopa

Back 24

The combination of the two medications carbidopa and levodopa. Levodopa is a precursor of dopamine with a 60 minute half-life, given with dopa-decarboxylase inhibitor, which degrades dopamine peripherally)

Front 25

Levadopa

Back 25

-L-DOPA crosses the protective blood–brain barrier, whereas dopamine itself cannot. Thus, L-DOPA is used to increase dopamine concentrations.

-SE's: postural hypotension, insomnia, vivid dreams, nightmares, confusion, visual hallucinations, delusions, nausea, vomiting --Abnormal involuntary movements (dyskinesia) and end-of-dose deterioration in the long term -Consider fractionating dose or giving adjuvant treatment

Front 26

Carbidopa

Back 26

Dopa-decarboxylase inhibitor. A drug given to people with Parkinson's disease in order to inhibit peripheral metabolism of levodopa. This property is significant in that it allows a greater proportion of peripheral levodopa to cross the blood–brain barrier for central nervous system effect.

Front 27

Dopamine agonists

Back 27

Eg ropinirole. Act directly on the post-synaptic dopamine receptors in the striatum; with oral, transdermal, or SC administration. Similar side effects with impulse control disorders; gambling, hypersexuality, compulsive buying, binge eating

Front 28

Describe the management pathway for patients with PD

Back 28

Front 29

MOA-B inhibitors

Back 29

selegiline irreversibly inhibit monoamine oxidase B, reducing breakdown of dopamine so more remains in the synaptic cleft

Possibly neuroprotective so used first line in younger patients

Nausea, vomiting, confusiono Potential interaction with SSRIs, may cause serotonin syndrome

Front 30

COMT inhibitors

Back 30

(entacapone) inhibit catechol-O-methyltransferase so more levodopa is available to cross BBB for prolonged effect

diarrhoea, discolouration of body fluids, may increase dyskinesia

Front 31

Amantadine

Back 31

An antiglutaminargic and NMDA receptor antagonist, which increases dopamine release, used as an adjuvant treatment in late PD to treat dyskinesia o confusion, hallucinations, psychosis, ankle oedema

Front 32

Anticholinergics in PD

Back 32

only used in young patients with a prominent tremor, reducing effects of relative central Ach excess that occurs due to dopaminergic deficiencyo May cause cognitive impairment in elderly, dry mouth, constipation, dizziness, blurred vision, urinary retention, glaucoma

Front 33

What are the general principles for management of epilepsy

Back 33

-Generally, valproate used for generalised; carbamazepine (+ lamotrigine) for partial

-Lamotrigine or levetiracetam in women of child-bearing age for generalised

Front 34

What is the management of absent seizures?

Back 34

Treated with ethosuximide or lamotrigine if not tolerated.

Front 35

Describe the adverse drug effects associated with anti-convulsants

Back 35

-Anti-epileptic drugs can cause acute allergic reactions with a skin rash, or toxic effect reactions with unsteadiness, blurred vision, tremor and confusion

-hair loss, overgrown gums, memory loss, mood change, anaemia, osteomalacia

-Valproate associated with Parkinsonism, weight gain, teratogenicity (spina bifida)

Front 36

Describe the problems that epileptic women face when using long term contraception

Back 36

Lamotragnine, Phenytoin and Carbomazapine are CYP450 inducers, therefore they speed up the breakdown of OCP, so be careful. Does for the COCP should be at least 50 micrograms a day. Implant, POP, patches should be avoided

Front 37

Describe the management of status epileptics

Back 37

 Secure airway, give oxygen, take collateral history, gain IV access, check glucose + thiamine IV lorazepam 0.07mg/kg or 4mg or diazepam 10-20mg, up to 40mg; repeat after 5 minutes Phenytoin 15-18mg/kg after 20-30 mins; 0.5-1g if already on

Front 38

What are the risk factors for SUDEP?

Back 38

uncontrolled epilepsy, young age, generalised seizures, learning disability, seizures in sleep, unwitnessed seizures, and poor compliance.

Front 39

What is the management of Delirium Tremens

Back 39

Give chlordiazepoxide PO (benxodiazapine used in alchohol withdrawl) as needed based on symptom score, and IV thiamine for three days

Front 40

Describe the ADR's of Carbamazopine

Back 40

-can cause drowsiness at first but it wears off

-hypersensitivity, mouth ulcers,

lymphadenopathy, fever, neutropenia

-toxicity causes double vision, unsteadiness (cerebellar signs); reduce dose, supportive

-γ-GT can be raised as it is an enzyme inducer; contraindicated with Warfarin, can induce its own metabolism

-hyponatraemia as it causes SIADH; only discontinue if symptomatic

Front 41

Describe the common symptoms of drug induced parkinsonisism?

Back 41

bilateral (disease unilateral initially) subacute onset, early presence of postural tremor, with progression concurrent with medication intake.

Front 42

What drugs are likely to lead to drug induced parkinsonism?

Back 42

With any dopamine antagonists, such as anti-emetics (metoclopramide, prochlorperazine) as well as haloperidol, risperidone, valproate, lithium, calcium channel blockers and SSRIs such as fluoxetine

Front 43

List the main hepatotoxic drugs

Back 43

Paracetamol, isoniazid, statins methotrexate, phenytoin, aspirin, alcohol, antibiotics, and oral contraceptives

Front 44

Describe hepatic drug clearance

Back 44

-The volume of blood perfusing the liver that is cleared of the drug per unit of time, dictated by blood flow through the liver (Q) and:

-Fraction of the drug that is free of unbound plasma proteins and capable of interacting with hepatic enzymes (f)

-intrinsic clearance (Cl), the ability of the liver to metabolise the drug in absence of flow limitations and protein binding

Front 45

What is the hepatic extraction ratio?

Back 45

The percentage of the drug removed from the perfusing blood during passage through the organ is the extraction ratio; the ratio of hepatic clearance to hepatic blood flow

Front 46

What does a 'large first pass effect mean'?

Back 46

Drugs with high hepatic Extraction ratio have a large first pass effect and low oral bioavailability. Therefore loads of the drug is cleared in the liver before reaching the target tissues. Therefore it would be better to not give this drug orally

Front 47

What is oral bioavalibility?

Back 47

Normal dose- extraction ratio

Front 48

What should you do differently when prescribing drugs for patients with hepatic impairment?

Back 48

-use drugs eliminated by routes other than the liver

-avoid hepatotoxic drugs, sedatives, diuretics,

-avoid drugs which cause constipation as these precipitate encephalopathy

-avoid drugs that interfere with haemostasis e.g. aspirin, warfarin

-avoid drugs that cause sodium retention e.g. NSAIDs, steroids or sodium-containing drugs such as antacids, which exacerbate fluid overload and ascites

Front 49

What lifestyle interventions can help with the management of dyspepsia?

Back 49

stop smoking, reduce alcohol, lose weight, increase exercise, reduce fatty or spicy foods, eat small regular meals, raise head of bed

Front 50

What drugs should be removed to help eliviate the symptoms of dyspepsia?

Back 50

-Calcium antagonists and theophyllines cause gastritis

-nitrates cause reflux

-bisphosphonates cause oesophageal erosion and ulceration

Front 51

How can you differentiate between gastric and duodenal ulcers?

Back 51

Gastric ulcer pain is worse with meals, whereas duodenal ulcer pain is relieved by eating

Front 52

What does the Blatchford score measure?

Back 52

severity of upper GI bleed

Front 53

What investigations can be used to identify the presence of H.Pylori?

Back 53

H. pylori tests include faecal antigen test, Carbon 13 urea breath test, serum H. pylori antibody test, rapid urease test of endoscopic biopsy sample (not really used as unpleasant)

Front 54

How do PPI's work and what ADR's are associated with their use?

Back 54

PPI diffuses out of blood and is activated by acid in canaliculus and binds proton pump on parietal cells;can cause electrolyte disturbance (lowmagnesium), microscopic colitis, acute interstitial nephritis, C. difficile (especiallywith antibiotics)s

Front 55

Antacids?

Back 55

Antacids (aluminium hydroxide, magnesium carbonate, magnesium trisiliate) raise the pH of stomach, neutralise stomach acid, and bind to and inactivate pepsin

Avoid in hypophosphatemia; can cause constipation and diarrhoea

Front 56

H2 receptor antagonists

Back 56

(ranitidine) competitively inhibit action of histamine on parietal cell

Front 57

How is H.Pylori eradicated?

Back 57

H. pylori eradicated using triple therapy, usually a PPI, amoxicillin and clarithromycin (or metronidazole) for 7 days; PPI for 2 months, then re-test¬

Front 58

Bulk-forming laxatives

Back 58

(bran, methylcellulose, isphagula husk) increase volume of non-absorbable material in gut, distend colon and stimulate peristaltic movement

-Contraindicated in dysphagia, intestinal obstruction, colonic atony, faecal impaction

-May cause flatulence, abdominal distension and obstruction

-Useful in poor diet but not opioid use

Front 59

Osmotic laxatives

Back 59

Osmotic (lactulose, macrogols) increase water content in bowel via osmosis, distend colon and stimulate peristaltic movement. They are contraindicated in bowel obstruction

-May cause flatulence, cramps and abdominal discomfort

-Caution is older adults and renal impairment

Front 60

Stimulant laxatives

Back 60

Stimulants(senna, danthron, bisacodyl)increase peristalsis and water and electrolyte secretion bythe mucosa; usually used with opioids but contraindicated in obstruction.

-In the shortterm, they may cause cramps and discomfort

-In the longterm, they may damage nerve plexuses, causing deterioration of normal intestinal function

Front 61

Faecal softener

Back 61

-Faecal softeners (liquid paraffin, docusate sodium) promote defecation by softening or lubricating stool, but they should not be administered in children under 3.

-Long term use of liquid paraffin can impair absorption of fat soluble vitamins (A, D)

-No effect alone; must be used with another laxative

Front 62

How should you manage an upper GI bleed?

Back 62

For upper GI bleeds, consider adrenaline injection, clips, argon-plasma coagulation, heat probe, haemospray

Withhold NSAIDs, 80mg omeprazole IV STAT, then 8mg/hour IV for 72 hours

High dose oral therapy for 2 months

Repeat endoscopy 6-8 weeks following treatment for a gastric ulcer

Front 63

What does a rasied faecal calprotectin indicate?

Back 63

Elevated faecal calprotectin indicates the migration of neutrophils to the intestinal mucosa, which occurs during intestinal inflammation, including inflammation caused by inflammatory bowel disease

Front 64

What does a raised faecal elastase indicate?

Back 64

Measurement of stool Elastase 1 allows the diagnosis or exclusion of pancreatic exocrine insufficiency

Front 65

Loperamise

Back 65

-An opiate GI-specific anti-motility agent which reduces GI smooth muscle tone and peristalsis.

-Indicated- Mild infective diarrhoea, IBS, chronic IBD, diarrhoea, and high output stomas.

-Contraindicated in severe infective diarrhoea, dysentery and liver disease (risk of accumulation); also in severe UC or C. diff as increases risk of toxic megacolon.

Front 66

SABA

Back 66

-(salbutamol) have an acute bronchodilator effect;

- SE's- Fine tremor, anxiety, headache, muscle cramps, palpitation, hypokalaemia (tachycardia, arrhythmia), peripheral vasodilation, myocardial ischaemia, sleep or behaviour disturbance

Front 67

LABA

Back 67

(salmeterol) are chemical analogues of salbutamol with a long lipophilic side chain which anchors the drug to the lipid membrane allowing the active portion of the molecule to remain at the receptor site; slow onset, not for relief of acute attack

Front 68

Muscarinic antagonists

Back 68

-(ipratropium bromide, tiotropium) competitively antagonise effects of endogenous Ach at M3 receptors, relaxing bronchial smooth muscle and decreasing mucus secretion.

-Used more in COPD or adjunct in severe asthma

-Used in patients who cannot have SABA or LABA; IHD, tachycardia

Front 69

Theophylline

Back 69

-causes acute bronchodilation as a competitive, non-selective phosphodiesterase inhibitor, causing an increase in cAMP in smooth muscle cells. This activates PKA, inhibiting TNF-α and leukotriene synthesis to reduce inflammation. They may also inhibit the delayed phase, are usually oral with sustained release, and have a narrow therapeutic index and many drug interactions including antibiotics

-Nausea, diarrhoea, tachycardia, headaches, insomnia, irritability, dizziness, arrhythmias in overdose

-clarithromycin and ciprofloxacin inhibit its metabolism

Front 70

Leukotriene antagonists

Back 70

(montelukast) inhibit cysteinyl L1 receptor, and extensively metabolise; the metabolites undergo biliary excretion.

Front 71

IgE monoclonal antibodies for asthma

Back 71

(omalizumab) bind to IgE, used in severe persistent IgE-mediated asthma requiring continuous or frequent oral corticosteroids (>4 courses per year)

Front 72

Explain the steps of management for asthma

Back 72

Front 73

How is acute asthma managed?

Back 73

give oxygen, steroids (IV hydrocortisone in severe)

IV magnesium sulphate in severe with peak flow <50% of predicted if not responded to nebulised treatments

Front 74

Describe the management pathway of COPD

Back 74

Front 75

What management options are available for Exacerbation of COPD

Back 75

Consider oxygen, short course oral prednisolone, antibiotics (amoxicillin, doxycycline), nebulised bronchodilators and NIV for exacerbations

Front 76

Define acute severe asthma

Back 76

PEF 33-50% of bestor predicted, RR>25, HR>110, orthere is inability to complete sentences in one breathe

Front 77

Describe life threatening asthma

Back 77

PEF<33%, sats <92%, PaO2 <8kPa, normal PaCO2 (getting tired), silent chest, cyanosis, feeble respiratory effort, arrhythmia or hypotension, exhaustion or altered consciousness

Front 78

Describe the steps of management for HTN

Back 78

Front 79

Describe the mechanism of action of Thiazine duiretics

Back 79

They control hypertension in part by inhibiting reabsorption of sodium (Na+) and chloride (Cl−) ions from the distal convoluted tubules in the kidneys by blocking the thiazide-sensitive Na+-Cl− symporter.

Front 80

Describe the ADRs for thiazine diuretics

Back 80

May cause postural hypotension (made worse by alcohol), hyponatraemia, hypokalaemia, hypercalcaemia, gout, impaired glucose tolerance, impotence, fatigue, pulmonary oedema, and pneumonitis

Rarely cause thrombocytopenia, photosensitive rash, pancreatitis, renal insufficiency

Front 81

Describe the contraindications for thiazine diuretics

Back 81

Avoid in pregnancy as suppresses breast milk production and cause oligohydramnios

Avoid in renal failure, gout and caution in diabetes

Front 82

Describe the mechanism of action of loop diuretics

Back 82

Loop diuretics act on the Na+-K+-2Cl− symporter (cotransporter) in the thick ascending limb of the loop of Henle to inhibit sodium, chloride and potassium reabsorption.

Front 83

What are the ADR's on loop diuretics

Back 83

Can cause postural hypotension, tinnitus, photosensitivity, hypokalaemia, renal impairment, gout, urinary retention or frequency

Front 84

What are the SE's of potassium sparing duiretics

Back 84

o May cause electrolyte abnormalities (hyperkalaemia), nausea, vomiting, headache, rash, reduced libido, gynaecomastia

Front 85

How do Calcium channel blockers work?

Back 85

(amlodipine) are particularly effective against large vessel stiffness, a common cause of elevated systolic BP in the elderly. They act on vascular smooth muscle, reducing contraction of arteries and increasing arterial diameter. They also reduce force of contraction of the heart, and slow down electrical activity, slowing the heart rate. They block a calcium signal on the adrenal cortex, reducing aldosterone production

Front 86

What are the SE's of calcium channel blockers?

Back 86

Can worsen proteinuria if patient has nephropathy

Dizziness, headache, redness in face, ankle oedema, rapid or slow heart rate, constipation

Front 87

What are the contraindications of ACE-i's?

Back 87

-Caution in impaired renal function, aortic valve stenosis, cardiac outflow obstruction, bilateral renal artery stenosis, hyperkalaemia, hypovolaemia or dehydration

-Contraindicated in pregnancy; congenital malformations and renal problems

Front 88

What are the SE's of ACE-i's?

Back 88

May cause hypotension, dry cough, hyperkalaemia, headache, dizziness, fatigue, angioedema, nausea and renal impairment

Front 89

Describe the mechanism of action of Beta blockers

Back 89

competitively antagonise the receptor for endogenous catecholamines epinephrine and norepinephrine at β1 adrenergic receptors, located in the heart and kidneys. They also reduce renin secretion.

Front 90

What are the SE's of B-blockers

Back 90

Nausea, diarrhoea, bronchospasm, cold extremities, exacerbation of Raynaud’s, bradycardia, hypotension, fatigue, dizziness, insomnia, intermittent claudication

Front 91

What are the contraindications for B-blockers?

Back 91

Caution in diabetics, contraindicated in COPD, asthma, heart block

Front 92

How do NSAID's work?

Back 92

NSAIDs block cyclooxygenase and hence prostaglandin synthesis

COX1 has routine physiological functions; COX2 is induced by pain and inflammation

Increased cardiovascular risk with COX2 selective but COX1 associated with GI risk

Caution prescribing in elderly, renal impairment, liver disease, heart failure

Front 93

How does codeine work?

Back 93

Metabolised to morphine by CYP2D6

Front 94

Describe the how codeine metabolism varies person to person

Back 94

Metabolising capacity varies from poor to extensive in population

10% Caucasians poor metabolisers, so have inadequate relief

Rapid metabolisers have higher risk of side effects

Cirrhosis may prevent metabolism, rendering pain relief ineffective

Front 95

What is tramadol?

Back 95

-synthetic opioid with multiple active metabolites

-not completely reversed by naloxone

-inhibits serotonin reuptake → mood boost, but may cause serotonin syndrome in combination with SSRI/SNRI

-anticholinergic side effects such as urinary retention

-contraindicated in severe renal or hepatic failure, raised ICP

Front 96

Give some examples of some common adjunct analgesics

Back 96

Corticosteroids, anti-depressants, anticonvulsants, muscle relaxants, bisphosphonates, antispasmodics

Front 97

What are the indications for using corticosteroids as adjunct analgesia?

Back 97

Raised ICP, nerve compression, liver capsule pain, soft tissue infiltration

Front 98

What are the indications for using antidepressents/ anticonvulsants as adjunct analgesia?

Back 98

Neuropathic pain

Front 99

What are the indications for using muscle relaxants/ bisphosphinates as adjunct analgesia?

Back 99

Muscle spasm/ cramp or bone pain

Front 100

What are the indications for using antispasmodics as adjunct analgesia?

Back 100

Bowel colic, bladder spasm

Front 101

Give some examples of weak opioids

Back 101

codeine, tramadol, dihydrocodeine, co-codamol, co-dydramol

Front 102

Give some examples of strong opioids

Back 102

morphine, diamorphine, hydromorphone, oxycodone, fentanyl

Front 103

Mophine

Back 103

used in acute severe and chronic pain, acts on µ-opioid receptors in CNS

euphoria, bronchospasm, urinary retention, pruritis, hypotension

Consider breakthrough pain (1/6 to 1/10 of total regular dose in 24 hours)

Front 104

Describe how to calculate the doses of strong opiods

Back 104

20-30mg in opioid naïve, 40-60mg for patients switched from regular weak opioid.

Immediate release 4 hourly or modified release 12 hourly with rescue doses

Breakthrough repeated every 2-4 hours as required

Oral to IV/SC is 2:1; morphine to oxycodone is 1.5:1; PO morphine to diamorphine is 3:1

Shouldn’t increase regular dose of morphine by over 50% over 24 hours

Front 105

What are the symptoms of opioid toxicitiy?

Back 105

myoclonic jerks, pinpoint pupils, hallucinations, confusion, reduced RR

Front 106

How should you manage opiod overdose?

Back 106

consider naloxone if difficult to rouse, RR<8 and/or saturations <90%

slow titration as not to reverse pain relief

reduce opiate dose by 30-50%, check renal function, consider alternative

Front 107

How can opioid side effects be managed?

Back 107

-fentanyl or tramadol may be less constipating

-adjunct treatments such as ketamine or lidocaine patches so can reduce dose

-excluding other causes; bowel obstruction, hypercalcaemia in bowel cancer

Front 108

What are the main symptoms that we should manage in end of life care?

Back 108

pain, excess secretions, agitation, nausea, and breathlessness

Front 109

What is commonly prescribed for N&V in end of life care?

Back 109

Cyclizine or haloperidol

Front 110

What is commonly prescribed for agitation in end of life care?

Back 110

Midazolam

Front 111

What is commonly prescribed for resp secretions in end of life care?

Back 111

hyoscine hydrobromide or

hyoscine butylbromide

Front 112

Define allodynia

Back 112

a painful response to a non-painful stimuli

Front 113

Define Dysaesthesia

Back 113

abnormal unpleasant sensation to touch

Front 114

What are the main drugs available for neuropathic pain?

Back 114

-Gabapentin first line in acute pain, acts on calcium channels, and may cause dizziness and ataxia early on but these usually go away with continued use

-Pregabalin is similar but with a quicker onset than gabapentin

-Amitriptyline has central and peripheral action on histamine, muscarinic and serotonergic receptors, but must wait two weeks for full effects

Front 115

Flucloxacillin

Back 115

beta Lactam. Is only active against gram positive bacteria, used in skin infections due to good penetration of soft tissues and action against Staph. aureus

Front 116

Amoxicillin

Back 116

Beta Lactam

gram positive activity also has some gram negative activity, and can cross the blood-brain barrier if the meninges are inflamed

Front 117

Co-amoxiclav

Back 117

Bea lactam. has good gram positive, gram negative, and anaerobic activity and good soft tissue penetration, used in intra-abdominal and skin infections

Front 118

Tazocin

Back 118

Beta lactam

Has even better gram negative cover than others and may cause less C. diff

Front 119

Cephalexin

Back 119

1st generation cephlasporin

has mixed activity with good skin and urine penetration but poor penetration of the chest and abdomen

Front 120

Cefuroxime

Back 120

2nd generation cephlasporin

can only be used IV, with broader cover but no anaerobic activity

Front 121

Cefotaxime

Back 121

3rd generation cephlasporin

only IV and penetrates the blood-brain barrier if the meninges are inflamed; ceftriaxone is another 3rd generation cephalosporin

Front 122

What are the main differences between 1st/2nd/3rd generation cephlasporins

Back 122

Higher generations have better gram negative cover, however this is at the expense of a loss in gram positive cover

Front 123

How do macrolides work?

Back 123

Inhibit protein synthesis by inhibiting binding at 50S ribosomal subunit

Front 124

How microbes are covered by macrolide treatment?

Back 124

Good penetration to most tissues gram positive, anaerobic and some gram negative cover

Front 125

How do tetracyslines work?

Back 125

Bacteriostatic, inhibit protein synthesis by preventing tRNA binding at 30S ribosomal subunit

Front 126

What SE's and contraindications are associated with tetracyline use?

Back 126

Contraindicated in children, pregnancy and breast feeding as deposited in teeth and bones causing discolouration and hyperplasia

GI disturbance, hepatotoxicity, photosensitivity

Front 127

How are aminoglycosides given?

Back 127

IV or topical, renal excretion, with concentration-dependent killing; more bacteria killed at higher peak concentrations; so one daily dose, calculated by body weight

Front 128

What SE's are associated with aminoglycosides?

Back 128

Nephrotoxic, ototoxic (augmented by furosemide), precipitates myasthenia gravis

Front 129

Metronidazole

Back 129

useful for anaerobes and protozoa, forming oxygen free radicals after activation inside the bacteria which interact with nucleic acid

-IV, oral, and rectal (IBD), penetrate BBB and abscesses

-hepatic metabolism and renal excretion

-disulfiram reaction with alcohol; ‘worst hangover ever’ very soon after drinking

Front 130

Trimethoprim

Back 130

-acts on folate metabolism (dihydrofolate reductase), inhibiting DNA synthesis

-Combined with sulphamethoxazole (co-trimoxazole)

-Good gram positive and gram negative activity, frequently used in UTI

-Caution renal failure, pregnancy (neural tube defects), can suppress bone marrow (avoid with methotrexate)

Front 131

Nitrofurantoin

Back 131

bactericidal by an unknownmechanism, with renal excretion; active concentration only in urine

Front 132

What are the common causes of cellulitis

Back 132

Staph Aureus

The second most common cause is β-haemolytic Strep

Front 133

What is the common cause of infective endocarditis in the prosthetic valve? What Abx would you use?

Back 133

In prosthetic valve, Staph. aureus is most common

flucloxacillin (vancomycin, gentamicin if penicillin allergic) and rifampicin

Front 134

What is the common cause of infective endocarditis in the native valve? What Abx would you use?

Back 134

In native valve, caused by Strep. viridans and other α-haemolytic Strep

Benzylpenicillin and gentamicin

Front 135

What antibiotics are used in MRSA?

Back 135

Use vancomycin and gentamicin for MRSA

Front 136

What are the main management options in sedentary patients with AF?

Back 136

-beta blocker – atenolol, bisoprolol

-don’t use amiodarone for rate control in persistent AF

-CCBs (non-dihydropyridine – diltiazem, verapamil) for L-type calcium channel inhibition; cause negative inotropy and chronotropy.

Front 137

What drugs are available for pharmacological cardioversion?

Back 137

Pharmacological cardioversion is with a class III agent (amiodarone, need an IV loading dose) or a class Ic agent (flecanide, propafenone)

Front 138

Class Ic anti-arrhythmics

Back 138

more effective at sinus rhythm restoration than amiodarone if given early (within 12 hours of onset); by 24 hours, there is no difference. They also increase risk of fatal ventricular arrhythmia in those with structural heart disease. Flecainide most appropriate in younger patient

Front 139

Amiodarone

Back 139

less likely to cause heart failure and hypertension through suppressing myocardial contractility; given in those with structural heart disease

Front 140

Other than for cardioversion itself when is amioderone indicated?

Back 140

6 weeks before and up to a year after cardioversion

Front 141

What are the main CYP450 enzyme inducers?

Back 141

Alcohol, rifampicin, St John’s Wort, carbamazepine, and phenytoin are warfarin enzyme inducers

Front 142

What are the main CYP450 enzyme inhibitors?

Back 142

Amiodarone, simvastatin, macrolides, ciprofloxacin, tramadol and grapefruit juic

Front 143

What drugs can be specifically tested for in poisoning?

Back 143

salicylate, carboxyHb (CO), lithium, paraquat, iron, methanol

Front 144

What dose of activated charcoal should be used?

Back 144

give 10x dose of poison, up to 50g

Front 145

What risks are associated with the use of activated charcoal?

Back 145

Can risk aspiration pneumonia, reduced absorption of therapeutic agents, bowel obstruction

Front 146

What drugs are not affected by activated charcoal?

Back 146

Ineffective for lithium, iron, boron salts, cyanide, glycol, methanol, hydrocarbons, insecticides and strong acids or alkalis

Front 147

When is Haemodialysis or haemoperfusion used in poisoning?

Back 147

may be useful when the poison has a small volume of distribution, low inherent clearance rate, and

is small enough to cross dialysis machine for haemodialysis

is bound to activated charcoal for haemoperfusion

Front 148

What are poor prognostic indicators in paracetamol overdose

Back 148

PT or INR rising after day 3, PT>180s, bilirubin>70, metabolic acidosis, encephalopathy, raised lactate and creatinine>300

Front 149

What is the main side effect associated with N-acetyl cysteine treatment?

Back 149

Anaphylactoid reaction with urticarial rash, wheeze, hypotension

Not immune-mediated, drug reaction due to dose-related histamine release.

reduce infusion rate and give antihistamines, steroids not indicated

Front 150

What are the symptoms of aspirin overdose

Back 150

Dizziness, sweating, tinnitus, vomiting, vasodilation, hyperventilation, agitation, delirium, coma, hypoglycaemia, hypokalaemia

Front 151

How is asprin overdose managed?

Back 151

Use activated charcoal, consider MDAC, and prevent CNS penetration by giving sodium bicarbonate to retain drug in its ionised form in the bloodstream.

Enhance elimination by giving bicarbonate; alkalinise the pH of the urine.

Haemodialysis highly effective at removing salicylate and also corrects metabolic abnormalities. Consider is pH<7.3, salicylate over 700mg/l, or if the patient is in renal failure.

Front 152

What are the signs and symptoms of TCA overdose?

Back 152

Anticholinergic effects including hot dry skin, dilated pupils, tachycardia, urinary retention, agitation, delirium, fits, coma, hypertonia, hyperreflexia. Sodium channel blocking affects cause cardiac arrhythmias (VT), conduction block, prolonged QRS and QT intervals. α-adreno-receptor antagonism causes hypotension

Front 153

What is the management for TCA overdose?

Back 153

ECG is essential- assess QRS duration

Charcoal often not used

If acidotic give sodium bicarbonate

Front 154

What are the symptoms of Iron overdose?

Back 154

Early (<6hours) – nausea, vomiting, abdominal pain, bloody diarrhoea, massive GI fluid loss

Delayed (2-72 hours) - black offensive stools, drowsiness, coma, fits, circulatory collapse, haematemesis, metabolic acidosis, hypotension, positive anion gap

Late (2-4 days) - acute liver necrosis and renal failure; very late (2-5 weeks) - gastric strictures

Front 155

What is the treatment for iron poisoning?

Back 155

Desferrioxaminechelates iron and reduces toxicity; chelate is water-solubleand excreted in urine with red discolouration