Pass the PSA revision Flashcards

Question

What are appropriate prescriptions for: No pain Mild pain Severe pain?

Answer 1

With No pain: no need for regular prescription, can prescribe paracetamol 1 g PRN, 6 hourly oral (Max 4g) Mild pain: regularly prescribe paracetamol 1g 6 hourly, and as required codeine 30 mg up to 6 hourly oral Severe pain: cocodamol 30/500 (meaning 30 mg codeine and 500 mg paracetamol) 6 hourly oral. Prescribe as required morphine sulphate 10 mg up to 6 hourly oral. NSAIDS may be introduced either regularly or as required as long as they are not contraindicated. E.g. ibuprofen 400 mg 8 hourly.

Answer 2

check the total amount the patient has prescribed. If on two formulations e.g. paracetamol or co-codamol they could overdose over the maximal dose of 4g/ day. Underyling rule when correcting this is to ensure no more than 4g of paracetamol is given, whether this is stopping the paracetamol or the cocodamol is driven by the patients pain.

Answer 3

Metoclopramide and domperidone are both dopamine antagonists. Metoclopramide crosses the BBB therefore exacerbating parkinsonian symptoms by acting on central dopamine receptors. Domperidone does not cross the BBB so is safer to use in parkinson's disease. (remember cyclizine is an antihistamine antiemetic).

Answer 4

Cough - due to increased levels of bradykinin, the cough can present up to a year after starting ACEi. Hyperkalaemia - Due to the blockade of ACE, no Angii therefore no aldosterone release. Aldosterone normally leads to Na+ uptake and K+ loss --\> therefore less K+ lost -- \>increased serum K+ levels. This is in contrast to Loop, thiazide and aldosterone antagonists which lead to hypokalaemia.

Answer 5

Ibuprofen inhibits prostaglandin synthesis needed for gastric mucosal protection from acid. Therefore risk of inflammation and ulceration

Answer 6

Oral steroids inhibit gastric epithelial renewal therefore predisposing to ulceration

Answer 7

NSAIDS --\> ibuprofen inhibits prostaglandin synthesis, reducing renal artery diameter (needed to vasodilate the afferent arterioles), therefore reduces kidney perfusion and function. ACE i's --\> reduces angiotensin ii production, which is needed to constrict the efferent arteriole, required to increase the filtration pressure at the glomerulus when renal blood flow is reduced.

Answer 8

Opiates! E.g. cocodamol, codeine should not be prescribed to patients presenting with constipation.

Answer 9

Ibuprofen & other NSAIDS can cause bronchoconstriction in asthmatics therefore avoided unless strictly necessary & under close supervision i.e not at home.

Answer 10

Methotrexate or being on another antifolate medication. This is because trimethoprim is a folate antagonist too, using both together increases the risk of bone marrow toxicity. This can lead to pancytopenia and neutropenic sepsis.

Answer 11

Methotrexate suppresses the immune system, therefore this medication should be witheld in the septic patient as we need to determine whether this is neutropenic sepsis. Whilst septic, withold methotrexate.

Answer 12

Verapamil is a CCB that should not be used with beta blockers due to the risk of bradycardia and at worst asytole! They also cause hypotension.

Answer 13

**_Microcytic anaemia: TAILS_** Thalassaemia, anaemia of chronic disease, iron deficiency anaemia, lead poisoning, sideroblastic anaemia **_Normocytic anaemia: RAAAHH_** Renal disease, Anaemia of chronic disease, aplastic anaemia, acute blood loss, haemolytic anaemia, hypothyroidism **_Macrocytic anaemia:_** Megaloblastic anaemia (B12 B9 deficiencies) **Normoblastic macrocytic anaemia:** HARD Liver Hypothyroidism, alcohol, reticulocytosis (haemolytic anaemia or blood loss), drugs (azathioprine), liver disease.

Answer 14

High neutrophils: bacterial infection, tissue damage (infarct, inflammation, malignancy), steroids High lymphocytes: viral infection, lymphoma, chronic lymphocytic leukaemia Low neutrophils: viral infection, chemotherapy/ radiotherapy (note this leads to neutropenic sepsis), clozapine(antipsychotic), carbimazole (antithyroid)

Answer 15

Increase in platelets as a reaction to : bleeding, tissue damage (infection/ inflammation/ malignancy), post splenectomy or due to primary problem - i.e myeloproliferative disorder.

Answer 16

Reduced production: * infection (viral) * drugs - penicillamine e.g. in rheumatoid arthritis treatment. * myelodysplasia, myelofibrosis, myeloma Increased destruction: * heparin * hypersplenism * DIC * Idiopathic thrombocytopenic purpura * haemolytic uraemic syndrome * thrombotic throbocytopenic purpura

Answer 17

Hypovolaemic hyponatraemia: * Fluid loss --\> vomiting, diarrhoea * addison's (lack of aldosterone) * diuretics (any type) Euvolaemic hyponatraemia: * SIADH (causes remembered by mnemonic SIADH, small cell lung Ca, infection, abcess, drugs (carbmazepine and antipsychotics), head injury * Primary polydipsia * hypothyroidism Hypervolaemic hyponatraemia: * Renal F * Heart F * Liver F (due to low albumin) * nutritional deficiency - low albumin * thyroid failure

Answer 18

Dehydration Drips - too much IV saline Drugs - e.g. effervescent tablets or IV preparations with high sodium diabetes insipidus

Answer 19

normal range sodium 135- 145 mmol/L

Answer 20

Hyperkalaemia: DREAD * Drugs - ACEi and aldosterone antagonists * Renal failure * Endocrine - Addison's disease * Artefact (due to clotted sample) * DKA (insulin drives K+ into cells, lack of insulin leads to K+ EC) Hypokalaemia: DIRE * Drugs - loop and thiazide diuretics, insulin, salbutamol * Inadequate intake/ intestinal loss (diarrhoea, vomiting) * Renal tubular acidosis * Endocrine - Cushing's syndrome and Conn's syndrome

Answer 21

Prerenal: * 70% AKI, urea \>\> creatinine e.g. urea 19 (3-7.5 mml) and creatinin 110 (35-125umol/L). * Shock --\> haemorrhagic, septic shock * Dehydration * renal artery stenosis (often precipitated by ACEi or NSAID Renal: * 10% of AKI, creatinine \>\> urea * INTRINSIC * ischaemia (due to prerenal AKI causing acute tubular necrosis) * nephrotoxic antibiotics - gentamycin, vancomycin, tetracyclines * Tablets - ACEi, NSAID * Radiological contrast * injury - rhabdomyolysis * negatively birefringent crystals (Gout) * syndromes - glomerulonephritis * inflammation (vasculitis) * Cholesterol emboli Post renal: * 20% of AKI * creatinine rise \>\> urea ruse. Bladder or hydronephrosis may be palpable * In lumen --\> stone * in wall --\> tumour renal cell carcinoma, transitional cell carcinoma * external pressure --\> BPH, prostate cancer, lymphadenopathy, aneurysm

Answer 22

1) for hepatocyte injury or cholestasis: bilirubin, ALT and less commonly AST 2) Synthetic function : albumin, vitamin K dependent clotting factors (2,7,9,10) measured via PT/INR.

Answer 23

Prehepatic --\> solely raised bilirubin, from the increased breakdown of RBCs leading to increased levels of bilirubin that overwhelms the capacity of the liver to degrade it. (e.g. haemolysis from sickle cell/ thalassemia, Gilbert's syndrome, crigler najjar syndrome). Intrahepatic --\> raised bilirubin & raised ALT/AST (greater than ALP rise). E.g. due to fatty liver, hepatitis, cirrhosis, malignancy (primary or secondary), wilsons disease, haemochromatosis, heart failure with hepatic congestion. Posthepatic --\> bilirubin raised and raised ALP. E.g. due to gallstones, drugs causing cholestasis, cholangiocarcinoma, primary biliary cirrhosis, sclerosing cholangitis, extrinsic pressure e.g. pancreatic cancer or gastric cancer

Answer 24

Alcoholic liver disease fatty liver disease viral - hepatitis B/C (Hep A-E and EBV) Drugs - paracetamol overdose, statins, rifampicin autoimmune - primary biliary cirrhosis, primary sclerosing cholangitis, autoimmune hepatitis

Answer 25

COCP antibiotics --\> flucloxacillin, coamoxiclav, erythromycin, nitrofurantoin steroids sulphonylureas - (gliclazide) Chlorpromazine, prochlorperazine (1st gen antipsychotic D2 antagonists, antiemetics)

Answer 26

No, raised alkaline phosphatase can indicate bone damage and there are a number of causes of raised ALP Liver disease e.g. cholestasis, hepatitis, fatty liver and neoplasia Bone disease --\> pagets, osteomalacia, bone metastases Hyperparathyroidism Renal failure (can't absorb Calcium for bone mineralisation, leads to bone damage) Physiological --\> fracturs, pregnancy, growing children Mnemonic ALKPHOS - Any fracture, liver disease (Post hepatic), Kancer, pregnancy& paget's disease, hyperparathyroidism, osteomalacia, surgery

Answer 27

Primary hypothyroidism --\> low T4 from damaged thyroid causing compensatory raise in TSH . E.g. Hashimoto's thyroiditis or drug induced hypothyroidism Secondary hypothyroidism --\> low TSH from damaged pituitary gland, leading to low T4. Primary hyperthyroidism (high T4 from thyroid, causing a low TSH). E.g. Graves disease, toxic nodular goitre, drug induced hyperthyroidism Secondary hyperthyroidism (high TSH from pituitary causing high T4) e.g. pituitary tumour

Answer 28

DRSABCDE ## Footnote Details - patient name, dob, sex, type of film PA or AP, erect or supine, correct L/R marker, inspiration or expiration? Date and time of Xray. RIPE : Rotation - medial of clavicle equidistant from spinous processes Inspiration - 5-6 anterior ribs or 8-10 posterior ribs above the diaphragm. Projection - AP or PA? Majority of CXR's are PA (xray goes from back to front). Cardiothoracic ratio can only be done on PA, AP overestimates the size of the heart. Exposure- vertebrae should be visible behind the heart Soft tissues and bones - ribs/ sternum & clavicles (fractures), breast shadows, calcifications in great vessels or carotids. Airways - trachea central, paratracheal or mediastinal masses, carina, hilum (look for asymmetry) Breathing - assess lungs, divide each lung into three zones and assess each for lung markings, inspect the pleura (not normally visible, if visible can indicate mesothelioma), fluid or blood in pleural space, pneumothorax (absent lung markings) Cardiac - cardiothoracic ratio less than 0.5 on PA. Cardiomegaly if \> 50% thoracic width on PA (valvular heart disease, cardiomyopathy, pulmonary hypertension, pericardial effusion). Heart borders, right atrium makes up most of right heart border, left ventricule makes up most of left heart border. Borders can become less visible with consolidation of overlying lung tissue. Diaphragm - Right hemidiaphragm higher than left due to liver, stomach underlies left hemidiaphragm - gastric bubble. On erect CXR, air under diaphragm indicates pneumoperitoneum and bowel perforation. Costophrenic angles --\> Should be clearly visible with acute angle, costophrenic blunitng or loss of this angle indicates fluid or consolidation. Or due to hyperinflation of lung leading to diaphragmatic flattening Everything else --\> mediastinal contours (containing heart, great vessels, lymphoid tissue). Aortic knuckle (L lateral edge of aorta), aortopulmonary window space between arch of aorta and pulmonary arteries (can be lost due to mediastinal lymphadenopathy ). Bones & soft tissues, tubes (NG tube), lines, artificial heart valves, pacemakers Make sure to look at review areas - lung apices, retrocardiac regions, behind the diaphragm, peripheral region of lungs, hilar regions

Answer 29

Pushing of trachea --\> large pleural effusion, tension pneumothorax pulling of trachea --\> consolidation with associated lobar collapse Apparent tracheal deviation: rotation of patient can give appearance of apparent tracheal

Answer 30

PA projection --\> standard CXR with patient standing up with Xray passing from posterior anterior. Image is viewed as if looking from the front face to face. AP projection --\> sometimes not possible to acquire PA, if the patient is too unwell to stand. CXR is still viewed face to face. Heart is an anterior structure therefore is magnified by the AP view as there is a shorter distance between the Xray source & patient. Therefore do not consider cardiothoracic ratio on AP view. Scapular edges - PA images often have scapula edges retracted with only small proportion over each lung. In AP images scapulae are often not retracted and remain projected over each lung.

Answer 31

ABCDE Alevolar oedema (in a batwing distribution) Kerley B lines - interstitial odema Cardiomegaly upper lobe Diversion (diversion of blood to upper lobes) pleural Effusion

Answer 32

1) rate --\> 300 / number of large squares inbetween QRS complexes. Normal 60-100 bpm 2) Rhythm --\> regular or irregular? (if irregular then count the number of complexes in the rhythm strip which is 10 seconds long & multiply by 6 for the rate). For regularity mark out consecutive R-R intervals on a piece of paper and move them along the rhythm strip to check if subsequent intervals are similar. 3) P waves present? If P before every QRS then sinus rhythm. Do P waves look normal? (Sawtooth baseline, flutter waves, Chaotic baseline fibrillation waves, flat line, no atrial activity at all) 4) P-R interval (3-5 small squares, 120-200 ms/ 0.2 seconds). (from start of P wave to beginning of QRS complex) is not constant or over 0.2 seconds this suggests heart block. * Heart blocks: * 1st degree fixed prolonged PR interval * 2nd degree type 1 progressive prolongation followed by dropped QRS * second degree type 2 fixed number of intermittently dropped QRS complexes. * Third degree heart block no association between P and QRS complex. * Shortened PR interval: * atrial impulse using short cut to ventricles, delta wave e.g. wolff parkinson white syndrome 5) QRS complex: * narrow or broad? should be under 0.12 s or under 3 squares * narrow QRS is normal, conduction via bundle of his to purkinje fibres to ventricles. * broad QRS if abnormal depolarisation sequence e.g. ventricular ectopic where impulse spreads slowly. Or bundle branch block, broad QRS as umpulse gets to one ventricle rapidly but has to spread slowly across the myocardium to get to the other ventricle. * Height QRS: small or tall (should be under 5mm), tall complex implies ventricular hypertrophy. * morphology: * delta wave with WPW = slurred upstroke of QRS * Q waves --\> small deflection at start of QRS complex, can indicate previous MI, look for it in a territory. Single Q wave not pathological. 6) J point ( where QRS joints ST segment) & 7) ST segment * J point --\> Can be elevated resulting in "high take off" = benign early repolarisation. Mostly occurs under 50 yrs, J point will be raised with widespread ST elevation in multiple territories making ischaemia less likely. T waves also raised in benign early repolarisation (unlike STEMI in which T wave remains same size and ST segment is raised). Plus ECG will not evolve unlike STEMI. * ST segment elevation --\> Significant when greater than 1mm (1 small sq) in 2 or more contiguous limb leads or \> 2mm in 2 or more chest leads. Indicates STEMI. * ST segment depression --\> \> 0.5 mm in \>= 2 contiguous leads indicates myocardial ischaemia 8) T waves : tall T waves ---\> hyperkalaemia or hyperacute STEMI Inverted T waves ---\> (inversion in V1 and lead 3 is normal). Otherwise indicates ischaemia, bundle branch blocks, PE, LVH in lateral leads, hypertrophic cardiomyopathy if widespread. Biphasic T waves indicate ischaemia and hypokalaemia, flattened indicates ischaemia and electrolyte imbalance 9) u waves: not common, wave after T wave \> 0.5 mm best seen in V2 or V3, seen in electrolyte imbalance, hypothermia and antiarrythmic therapy e.g. digoxin procainamide or amiodarone

Answer 33

1st - QRS comple must be wide in BBB, \> 0.12 s Then look at V1 and V6. **In Left BBB = WiLLiaM** * V1 - QRS deflection is W shaped * V6- QRS deflection is M shaped **In Right BBB = MaRRoW** * V1 - QRS deflection is M shaped * V6- QRS deflection is W shaped

Answer 34

narrow therapeutic index = small difference in blood concentration between therapeutic and toxic effects. Most common: Digoxin theophylline lithium phenytoin abx - gentamycin, vancomycin

Answer 35

Malignancy --\> small cell lung cancer (pancreatic, prostate) Neurological --\> stroke, subarachnoid haemorrhage, subdural haemorrhage, meningitis/ encephalitis/ abscess Infections --\> Tuberculosis, pneumonia Drugs --\> sulfonylureas, SSRIs, TCAs, carbamazepine, vincristine, cyclophosphamide Management --\> correction must be done slowly to avoid precipitating central pontine myelinolysis, fluid restriction, demeclocyline reduces responsiveness of collecting tubulutes to ADH, ADH antagonists (tolvaptan)

Answer 36

Phenoxymethylpenicillin benzylpenicillin flucloxacillin amoxicillin ampillicin coamoxiclav - ***augmentin*** cofluampicil ***(magnapen)*** piperacillin with tazobactam - ***Tazocin*** Ticarcillin with clavulanic acid - ***timentin***

Answer 37

Increase the dose by the smallest increment possible

Answer 38

No change is required as clinical response is more important. No mpoint increasing dose just to get patient into what is considered a therapeutic range - already having an adequate response

Answer 39

You need to decrease the dose. If there is evidence of toxicity then omitting the drug for a few days is appropriate. only excpetion is gentamycin - if there is a high serum level without toxicity then this leads to decreased frequency by 12 hours rather than reduced dose. e.g. every 24 hours to every 36 hours.

Answer 40

Gentamicin is an IV antibiotics used for severe infections Doses calculated according to patients weight and renal function most patients are on a high dose regimen of 5-7 mg/ kg once daily those with renal failure or endocarditis may be on a 1mg/ kg 12 hourly (in renal F) or 8 hourly (in endocarditis) divded daily dosing regimen

Answer 41

Usually gentamicin levels are measured at particular times e.g. 6-14 hours after the last gentamicin infusion was started. then using a normogram (different for either the 5mg/kg dose or 7mg/kg dose), you can determine if the levels are too high. Plot blood concentration on y axis against the time between starting last infusion and taking blood. If resultant point on graph falls in 24 hour area then continue at the same dose. If it falls above the 24 hr area then you need to change the dosing interval: - falls in 36 hours area then change to 36 hr dosing - if it falls in 48 hr area then change to 48 hr dosing - if it rests above 48 hr area then repeat gentamicin level and only re-dose when concentration is below \< 1mg/L You adjust the frequency of the dose instead of the dose itself as you need sufficient dose to provide required peak to hit minimum inhibitory concentration of the organism

Answer 42

usually peak and trough levels are used. One hour " peak" serum concentration should be 5-10 mg/ litre Trough concentration (i.e just before the next dose) should be less than 2mg/ litre. For endocarditis the one hour peak should be between 3-5 mg / litre Trough concentration should be less than 1mg/ litre serum gentamicin conc should be measured after 3 or 4 doses then at least every 3 days after a dose change. If the predose trough concentration is high then the interval between the doses must be increased. If the post dose peak concentration is high the dose must be decreased.

Answer 43

paracetamol is metabolised in the liver into a toxic compound known as NAPQI. This is then conjugated by glutathione an antioxidant. The liver had limited stores of glutathione which are quickly depleted allowing toxic metabolite NAPQI to accumulate and cause acute liver damage. The treatment is with NAC (N acetyl cysteine) which replenishes the stores of glutathione, reducing formation of NAPQI, protecting against liver damage.

Answer 44

Paracetamol normograms are used at least 4 hours after ingestion, if the plasma paracetamol level is below the line then the patient does not require NAC, if the plasma level is above the line then they do. We give NAC regardless in paracetamol OD if time of ingestion is unknown, or a staggered overdose was taken.

Answer 45

Warfarin - vitamin K antagonist, inhibits the enzyme VKORC1 required to make vitamin K dependent clotting factors 10 9 7 2. INR = ratio of a patient prothombin time compared to the general population. Normal INR is 1. Target INR on warfarin is 2.5 Target INR on warfarin with metal heart valves or recurrent VTE is 3.5

Answer 46

Major bleed and warfarin: stop warfarin give 5-10 mg IV vitamin K Give prothrombin complex (e.g. beriplex) (replace the clotting factors immediately)

Answer 47

INR \> 8 with no bleeding: stop warfarin, give oral vitamin K 1-5mg using IV prep orally. Repeat dose of vitamin K if INR still too high after 24 hours. restart warfarin when INR below 5. INR \> 8 minor bleed: stop warfarin, give IV vitamin K 1-3 mg, repeat dose of vitamin k if INR still too high after 24 hours. restart warfarin when INR below 5. INR 5-8: with minor bleed --\> stop warfarin, give IV vitamin K 1-3 mg , restart when INR below 5. INR 5-8 no bleeding --\> withold 1 or 2 doses of warfarin, reduce subsequent maitenance dose.

Answer 48

Digoxin - confusion, naisea, visual halos and arrythmias Lithium - early tremor, intermediate tiredness, later features - coma, seizures, renal failure, diabetes insipidus Phenytoin - gum hypertrophy, ataxia, nystagmus, peripheral neuropathy and teratogenicity Gentamicin - ototoxicity and nephrotoxicity Vancomycin - ototoxicity and nephrotoxicity

Answer 49

ACEi - teratogenic (especially in the first trimester) therefore unsuitable in pregnancy - an alternative to blood pressure control i.e labetalol should be initiated prior to conception. ACEi increase the risk of hyperkaaemia Cough is common in with ACEi Caution should be taken with ACEi when a patient has diarrhoea or vomiting, there is because of increased risk of AKI when a patient is elderly or unwell. ACEi can cause renal failure Monitoring - important to monitor renal function (K+) after starting ACEi, this is done 1-2 weeks after starting treatment.

Answer 50

Tamoxifen - SERM, acts as an oestrogen receptor antagonist in breast tissue and partial agonist in other tissues. Tamoxifen increases the risk of endometrial cancer, VTE. tamoxifen increases the efficacy of warfarin and high INR readings (increased risk of bleed) timing that tamoxifen is taken will not influence SE's Common SE's - hot flushes (those similar to menopause), menstrual disturbance (vaginal bleeding, amenorrhoea), VTE, endometrial cancer. Leg cramps, vulvovaginal disorder and alopecia.

Answer 51

Metformin: MOA --\> Biguanide, increases insulin sensitivity and inhibits hepatic gluconeogenesis First line in T2DM in patients that are overweight. Contraindications: Note those underweight or have CKD with creatinine \> 150 umol/L or eGFR \< 30 ml/min should not have metformin Can cause lactic acidosis if taken when there is tissue hypoxia, therefore avoid in recent MI/Sepsis/ AKI or dehydration. Metformin should be avoided on day of and 48 hours after a procedure with iodine containing contrast - e.g. angiography Common SE's: GI upset - nausea, anorexia, diarrhoea (intolerable in 20%). Lactic acidosis with liver disease or renal Failure. Starting metformin - titrate slowly to reduce incidence of SE's. If patients develop unacceptable SEs then modified release metformin should be considered.

Answer 52

Sulphonylureas - e.g. gliclazide, glimepridie, glipizide, tolbutamide. MOA -stimulate pancreatic beta cells to secrete insulin Key SE - hypoglycaemia, weight gain, hyponatraemia. Hypoglycaemia more common with long acting sulfonylurea e.g. glibenclamide. Sulfonylureas should be taken in the morning with breakfast, if taken at bedtime it increases the risk of nocturnal hypoglycaemia. Patients should not miss meals as this increases the risk of hypoglycaemia. Where more than 160 mg is requred then total daily dose should be divided but still given with meals.

Answer 53

MOA - inhibition of dihydrofolate reductase and DN synthesis for lymphocyte proliferation, indicated in rheumatoid arthritis, psoriasis, ALL. SE -nausea, hair loss, infection, mucositis, pneumonitis and pulmonary fibrosis, liver fibrosis Pregnancy - women should avoid pregnancy for at least 6 months after treatment has stopped, men need to use effective contraception for at least 6 months after treatment. Interactions - folate antagonists e.g. trimethoprim, cotrimoxazole should NEVER be used with methotrexate (increased risk of SE and bone marrow suppression). interactions - high dose aspirin, increases risk of methotrexate toxicity secondary to reduced renal excrection Folic acid should be used alongside methotrexate to limit its toxicity to bone marrow. Folic acid 5 mg once weekly should be coprescribed, taken more than 24 hours after methotrexate dose. Methotrexate for non oncological reasons is only ever taken once weekly. Starting dose is 7.5mg weekly, only one strength should be prescribed usually 2.5 mg. Regular monitoring of WBCs is required due to risk of neutropenia. FBC, U&E and LFT needs to be regularly monitored, both before starting treatment and repeated weekly until therapy stabilised. Then monitored every 2-3 months.

Answer 54

Warfarin MOA - inhibits vitamin K epoxide reductase, inhibiting the formation of vitamin K dependent clotting factors 10/9/7/2. Indicated in DVT & prophylaxis of stroke from underlying AF. Largely superseded by DOACs as they require less monitoring. SE --\> haemorrhage, teratogenic (especially 1st trimester, 3rd trimester risk of bleeding during labour) (can be used in breastfeeding), skin necrosis/ blue toe syndrome. Alopecia, N & V. Monitoring --\> monitored using INR ratio of prothrombin time for the patient over national average prothrombin time. Monitored daily or on alternate days in early treatmnet then at longer intervals, then up to efvery 12 weeks. interactions: NSAIDs (inhibit platelet function, also displace warfarin from albumin). Diuretics - think this increases bleeding risk General factors that potentiate warfarin - cranberry juice, NSAIDS, liver disease, inbibitors of P450 system

Answer 55

Abx --\> ciprofloxacin, clarithromycin, erythromycin, isoniazid (TB) omeprazole amiodarone allopurinol imidazoles - ketoconazole fluconazole SSRIs Sodium valproate acute alcohol intake

Answer 56

AEDs - phenytoin, carbmazepine, barbiturates rifampicin st johns wort chronic alcohol intake (clotting increases) smking

Answer 57

Long term steroids increases risk of diabetes mellitus and blood sugar should be monitored regularly. Patients are also at increased risk of hypertension therefore BP should be monitored regularly. Steroids increase the risk of osteoporosis, if a patient is predicited to be on steroids for longer than 3 months e.g. polymyalgia rheumatica then prophylactic tx with a bisphosphonate is an option. small increased risk of gastric irritation and ulceration therefore PPI should be considered. Other SE's: * Endocrine --\> impaired glucose regulation, increased appetite & weight gain, hirsutism, hyperlipidaemia * cushings syndrome - moon face buffalo hump, striae * MSK - osteoporosis, proximal muscle weakness, AVN femoral head * immunosuppression * psychiatric - mania, depression, psychosis * GI - ulceration and acute pancreatitis * opthalmic- glaucoma and cataracts * growth suppresion in children * mineralocorticoid SE --\> fluid retention & HTN Those on long term steroids should never stop medication abruptly due to risk of addisonian crisis. BNF suggests gradual withdrawal of systemic steroids if patients have had more than 40 mg prednisilone daily for more than 1 week, recieved more than 3 weeks treatment or recently received repeated courses.

Answer 58

SSRIs - sertaline, citalopram, fluoxetine, paroxetine Inhibit reuptake of serotonin in the synaptic cleft Uses - depression and GAD SE: - SIADH - hyponatraemia (drowsiness, confusion, convulsions) - Sickness- nausea, gastritis, appetite loss, vomiting, weight change - Shakes (tremor) - Sleep disturbance - insomnia - Sexual disturbance - loss of libido, anorgasmia - suicidal ideation (worsening in initial 6 weeks) - slippery blood - increased risk of GI bleeding - sun sensitivity - citalopram makes you UV sensitive, precautions should be taken in sunlight Others - concentration impaired, confusion, headache, memory loss, palpitations and QT interval prologation Patients should be reviewed every 1-2 weeks at the start of antidepressant treatment treatment should be continued for at least 4 weeks before considering switch antidepressant tx should be continued for a further 6 months following remission in depression and 12 months in GAD (risk of relapse is high)

Answer 59

N & V Agitation, confusion, drowsiness, hallucinations tremor, nystagmus dilated pupils hyperthermia tachycardia & hypertension convulsions & muscle rigidty rhabdomyolysis

Answer 60

Alendronate, pamidronate, risedronate MOA - drives osteoclast apoptosis, interrupts formation of the ruffled border inhibiting bone resorption Indicated in osteoporosis or hypercalcaemia. Once weekly preparation SEs: * Oesophageal reaction - oesophagitis, ulcers * osteonecrosis of jaw * increased risk atypical stress fractures in proximal femoral shaft * acute phase response - fever myalgia arthralgia Patients should take bisphosphonates swallowed with a full glass of water sitting or standing up, on empty stomach at least 30 minutes before breakfast or other medication. (eg. with adcal D3 which is a calcium salt that reduces absorption).

Answer 61

Serum creatinine should be monitored --\> this is because two classic SE of vancomycin are ***ototoxicty and nephrotoxicity (can go on to cause renal failure) .*** Renal function must therefore be taken into account when choosing dosing regimen for vancomycin as renal dysfunction will mean reduced renal clearance and increased risk of toxicity. Other key SE's: Neutropenia - more uncommon, and occurs at least a week after starting treatment. Monitor WBC in patients on long term vancomycin. Thrombocytopenia is a rare SE Severe cutaneous adverse reactions , hypersensitivity, tinnitus, vertigo, vasculitis, pseudomembranous enterocolitis, red man syndrome with IV administration/ 1st dose (flushing of face and neck, hypotension & pruritus). Vancomycin - glycopeptide antibiotics used in treatment of gram positive infections, particularly MRSA, clostridium difficile

Answer 62

Serum ALT. Answer: statins are associated with myopathy but in those with risk factors for it. E.g. in the elderly, women, low BMI, personal or family hx of muscular disorder, prev hx of muscular toxicity, high alcohol intake, renal impairment, hypothyroid/ diabetes. When prescribing a statin creatinine kinase level should be checked at baseline in these patients, but if clinical situation reveals no RFs for myopathy then creatinine kinase levels are not the most suitable monitoring options. (only check CK baseline in pts with risk factors for myopathy). Liver impairment - statins are metabolised in the liver, use with caution in liver disease as reduced metabolism can lead to increased levels and therefore myopathy. NICE guidelines recommend checking LFTs at baseline, 3 months and 12 months. If there is any active liver disease and transaminases ALT/AST are raised more than three times normal range then statins are contraindicated/ should be stopped if already being taken.

Answer 63

Phenytoin - VG Na+ channel blocker, increasing refractory period. Used in treatment of tonic clonic and focal seizures, status epilepticus, acute symptomatic seizures with head trauma or neurosurgery. Monitoring - phenytoin levels do not need to be monitored routinely but trough levels immediately before the dose should be checked if ? adjustment of dose or suspected toxicity. post dose phenytoin levels are not routinely required, T1/2 of is 24 hrs therefore after 2 weeks of treatment it is unlikely to have diurnal variation in plasma level. normal range is quoted in the BNF, consider level in context of the patient. If there are no seizures and trough levels within range no adjustment required. If there are side effects despite normal "trough" level then dose should be decreased if seizure control is adequate or alternative sought.

Answer 64

Lithium MOA - neuronal calcium channel blockade, mood stabiliser. used in treatment of bipolar disorder or refractory cases of depression. Very narrow therapeutic range 0.4 - 0.8 mmol/L. It has a long plasma half life and is renally excreted. Toxic effects are likely to manifest at serum concentrations above 1.5 mmol/L. SE: * N&V, diarrhoea * tremor * nephrotoxicity - polyuria secondary to nephrogenic diabetes insipidus * hypothyroidism and thyroid enlargement * ECG - t wave flattening / inversion * hyperparathyroidism and hypercalcaemia Monitoring: * Recommended sampling for lithium is 12 hours post dose * routine lithium monitoring should be done weekly after initiation and after each dose change until concentrations are stable, then every 3 months thereafter. * thyroid and renal function should be checked every 6 months * FBC not routinely required for patients on lithium Sodium depletion can increase the risk of toxicity --\> advise patients to avoid making changes in their diet that can lead to increased or decreased sodium intake

Answer 65

Monitoring methotrexate: - FBC, U&E, LFT need to be regularly monitored , taken before starting, and weekly until stabilised. Afterwards monitored every 2- months. Methotrexate has been known to cause fatal blood dyscrasias therefore FBC monitoring at regular intervals is required, and once therapy has been stabiised FBC can be monitored every 2-3 months. BNF - CXR not required at baseline but british society for rheumatology recommend one or is needed if pulmonary toxicity suspeted. Treatment with methotrexate should not be started if LFTs are abnormal due to risk of liver cirrhosis. If there is a significant drop in WBC then methotrexate should be stopped immediately. Patients should be advised to report all symptoms of infection, especially a sore throat. Note - regular renal monitoring not as important as methotrexate not cleared renally

Answer 66

Olanzapine is one of the atypical 2nd generation AP's. More selective block of D2 receptors in the mesolimbic pathway associated with less extrapyramidal effects. More associated with metabolic effects. Now first line schizophrenia. Adverse effects --\> weight gain, dyslipidaemia, hyperglycaemia and obesity, diabetes, hyperprolactinaemia (breast enlargement, galactorrhoea), increased risk of stroke & VTE in elderly. Monitoring of olanzapine: * blood lipids & weight at baseline, then at 3 months. For olanzapine these are needed every 3 months for the first year then yearly. * Fasting blood glucose should be measured at baseline, after 1 month, then 4-6 months. * Advisable to monitor prolactin concenration at start, 6 months then yearly.

Answer 67

COCP MOA - suppressed ovulation, reduces LH and FSH Uses - contraception, PCOS, dysmenorrhoea and menorrhagia. SE - acne, fluid retention & weight gain, metrorrhagia, depression, Alopecia, hypertension, increased risk DVT (strokes and heart attack too) There is a small increase in risk of breast cancer and small increase in risk of cervical cancer with use \> 5 yrs. Monitoring: blood pressure is monitored due to HTN increasing the risk of arterial disease.

Answer 68

MOA - ovulation is inhibited by the oestrogen and progesterone components of the COCP (reduce LH and FSH needed to stimulate ovulation). Benefits - more effective contraception than barrier methods, does not interrupt intercourse, menstrual bleeding usually lighter & less painful, reduced risk of ovarian and endometrial cancer, reduced acne severity, normal fertility returns immediately after stopping COC. Disadvantages: * Does not protect against STI, less effective than IUD. * Increased risk of HTN, MI, stroke, VTE, breast CA, cervical CA. SE mood change, breast pain, menstrual irregularities. Drug interactions: St johns wort - enzyme inducer will reduce efficacy of COCP. Antibiotics - rifampicin, antivirals, AEDs Advise : - If COC is started in first 5 days of the cycle then there is no need for additional contraception if started at another point in the cycle then alternative contraception should be used for 7 days - importance of taking pill same time everyday - do not have to have a bleed every 21 days, can tailor their regimen but this is off licence Missed pills: If missed only 1 pill or started 24 hours late - still protected against pregnancy. Take last pill now, even if that means taking 2 in a day, then carry on taking the rest as normal, taking 7 day pill free break as normal. If missed 2 pills \> 48 hours late then not protected. Take last pill that was missed, even if that means 2 in a day, leave earlier missed pills, then take rest of pack as normal, use condoms for next 7 days. If UPSI has occured in the last 48 hours they might need emergency contraception. Vomiting: If vomited within 3 hours of COC then advise to take another ASAP. If vomiting / diarrhoea occurs more than 24 hours then advice to follow instructions for missed pills, counting each day of vomiting / diarrhoea as a missed pill. Avoid sexual intercourse and use barrier contraception during illness & 7 days afterwards. If illness occurs in last 7 pills then omit pill free interval/ inactive tablets and start next cycle immediately.

Answer 69

Amiodarone - class 3 antiarrythmic used in tx of atrial/ nodal and ventricular tachycardias. Blocks K+ channels inhibits repolarision therefore prolongs AP. Monitoring: * A baseline CXR should be carried out owing to risk of pulmonary toxicity with amiodarone. * TFT, LFT, U&E & CXR prior to treatment * TFT and LFT every 6 months Adverse effects: - Thyroid dysfunction - hypo and hyper - corneal deposits - pulmonary fibrosis / pneumonitis - liver fibrosis/ hepatitis - peripheral neuropathy / myopathy - photosensitvity & slate grey appearance - thrombophlebitis at injection sites - proarrythmic effects as lengthens QT interval

Answer 70

Carbimazole --\> inhibits thyroid peroxidase from coupling and iodinating tyrosine on thyroglobulin therefore reducing thyroid hormone production. Indication --\> thyrotoxicosis, given in high doses for 6 weeks until patient becomes euthyroid before being reduced. Adverse effects --\> agranulocytosis (bone marrow suppresion), therefore all patients asked to report symptoms of infection e.g. sore throat. WBC should be performed in this case, and stop carbimazole promptly if any evidence of neutropenia Pregnancy - congenital malformations in 1st trimester, need effetive carbimazole. Only used in pregnancy after thorough risk assessment and at lowest effective dose.

Answer 71

ACE i are known to cause hyperkalaemia, hyponatraemia, and in some cases AKI. U&Es should be checked at baseline and after every dose change rise in creatinine and K+ may be expected after starting ACE i, acceptable changes are increase in serum creatinine up to 30% from basseline and increase in K+ up to 5.5 mmol/L.

Answer 72

Therapeutic drug monitoring: Plasma digoxin assay only measured if toxicity, non compliance or inadequate effect are suspected. Blood taken 6 hours after dose. ***U&Es and renal function (creatinine and urea) --\> monitoring required as digoxin is primarily renally excreted, patients with renal dyfunction at increased risk of toxicity.*** Serum K+ relevant as ***hypokalaemia increases the risk of digoxin toxicity.*** ***Digoxin normally binds ATPase pump at same site as K+ , if low K+ binds more easily therefore increased effects.***

Answer 73

Digoxin toxicity may occur even if concentration is within therapeutic range. Toxicity increased progressively from 1.5 to 3 mcg/l Features: * unwell, lethargy, N& V, anorexia, confusion, yellow green vision * arrythmia - AV block & bradycardia * gynaecomastia Causes of digoxin toxicity - hypokalaemia - renal F - myocardial sicahemia - hypothermia, hypothyroidism, hypomagnesaemia - hypernatraemia, hypercalcaemia, acidosis - increased age - other drugs - amiodarone, verapamil, diltaizem, spironolactone, thiazides and loop D (last 2 cause hypoK).

Answer 74

Sodium valproate - 1st line for generalised seizures, inhibits GABA. Monitoring sodium valproate : plasma valproate concentrations are not used as not index of efficacy. Monitor LFTs before therapy and during first 6 months - due to risk of hepatotoxicty. Adverse effects: * teratogenic * hepatotoxicity * pancreatitis - amylase only needed if ? Pancreatitis * Thrombocytopenia - FBC and clotting checked before surgery to ensure no risk of bleeding * ataxia, tremor * alopecia * increased appetite/ weight gain *

Answer 75

Common drug reactions and dangerous drug reactions Common drug reactions e.g myalgia with statins vs dangerous drug reaction e.g. rhabdomyolysis with statins Type A drug reactions - common, predicatable and dose related Type B reactions - idiosyncratic reactions, unexpected reaction related to host/gene/environmental factors.

Answer 76

For the aminoglycoside gentamicin --\> Ototoxicity and nephrotoxicity. Nephrotoxicity occurs most commonly in those with renal impairment, gentamicin is renally excreted therefore it can accumulate in renal disease. For glycopeptide vancomycin --\> ototoxicty (tinnitus) and nephrotoxicity (due to Neutropenia more common after 1 week or cumulative dose 25g. Other SE vancomycin - agranulocytosis, eosinophilia, hypersensitivity, tubulointerstitial nephritis, severe skin reactions, thrombocytopenia, vertigo

Answer 77

Side effects: * Hypekalaemia * 1st dose hypotension * Cough * Angioedema Caution in renovascular disease --\> results in renal impairment! Interactions: * Lithium --\> increases concentration of lithium * Caution with K+ sparing diuretics (hyperkalaemia) * caution with NSAIDS --\> ACE i and NSAIDS should not be coprescribed. Due to ACEi relaxing efferent vessel (need ATii to constrict efferent vessel) and NSAIDs block prostaglandins (required to dilate the afferent vessel) therefore together dangerous drop in perfusion of the kidney and therefore eGFR. * Caution with Loop diuretics --\> increased risk of hypotension

Answer 78

Side effects: * hypotension * bradycardia * cold peripheries * fatigue * sleep disturbance - nightmares * Erectile dysfunction * bronchoconstriction in asthmatics * worsens acute heart failure (helps chronic heart failure) Contraindications: uncontrolled heart failure, asthma, sick sinus syndrome Interactions: do not prescribe VERAPAMIL with BB --\> precipitates severe bradycardia!

Answer 79

Rate limiting CCB - dilitiazem and verapamil --\> both can cause hypotension, bradycardia, need caution in heart failure. Verapamil can cause constipation, dilitazem ankle swelling. Dihydropyridines - nifedipine & amlodipine --\> flushing, headache, ankle swelling. Affects peripheral vasculature more than myocardium therefore do not worse HF.

Answer 80

MR receptor blockade - spironolactione, eplerenone Block of ENAC - Amiloride & triamterene SE: both used with caution with ACE i --\> hyperkalaemia. Enac blockers used with thiazide or loop diuretics to prevent hypokalaemia.

Answer 81

SE thiazides: Hypotension hyponatraemia, hypokalaemia, hypercalcaemia hyperuricaemia (gout) impaired glucose tolerance impotence Rarer- photosensitivity rash, thrombocytopenia, agranulocytosis, pancreatitis

Answer 82

Hypotension hyponatraemia, hypokalaemia, hypomagnesaemia, hypocalcaemia Hypochloraemic alkalosis ototoxicity renal impairment hyperglycaemia gout

Answer 83

Two main types of heparin: Unfractionated heparin and low molecular weight heparin. Heparins generally act by activating antithrombin 3. UF heparin forms a complex that inhibits thrombin, factor Xa, Ixa, XIa and XIIa. LMWH only increases the action of antithrombin 3 on factor Xa. Common adverse effects: - bleeding - thrombocytopenia - heparin induced. Immune mediated where antibodies develop against platelets, it is associated with a greater than 50% reduction in platelets, thrombosis and skin allergy and prothrombotic state. - osteoporosis and increased risk of fractyres - hyperkalaemia - thought to be due to inhibition of aldosterone secretion. UF - uses --\> useful in situations where there is a high risk of bleding as anticoagulation can be terminated quickly. Useful in renal F LMWH - standard in the management of VTE and prophylaxis, used in treatment of ACS

Answer 84

Key SE: haemorrhage, peptic ulcer and gastritis, tinnitus in large doses (& hearing loss + vertigo) Rarely- asthma attack/ bronchospasm

Answer 85

Common - Haemorrhage Rare - alopecia, N&V Not known freq - Blue toe syndrome, skin necrosis & skin reactions

Answer 86

Enzyme inhibitors - A DOSE VICE Allopurinol Disulfiram Omeprazole Sulphonamides - sulfasalazine Erythromycin Valproate Isoniazid Ciprofloxacin Ethanol (acute intoxication). - Most common enzyme inhibitors: Graprefruit juice, ketoconazole, erythromycin and ciprofloxacin.

Answer 87

CYP450 enzymes are also in the duodenum, acting as a backstop for the stomach, preventing toxin foodstuffs or poisons before further absorption in the gut. Drug companies are aware of this and sometimes modify doses accordingly to combat losses sustained in the duodenum. One problem is everyday foods can interact and inhibit their action. E.g. single glass of grapefruit juice can inhibit duodenal cytochrome system for approx 24 hrs. This means excessive drug doses can pass through the duodenum To induce the cytochrome p450 system it takes days to weeks wherease to inibit it, it takes only hours -days. This means ADRs can come on quickly, especially if the duodenum is inhibited in metabolising a drug with a narrow therapeutic index/ that requires dose control.

Answer 88

SEs: * fatigue, confusion and drowsiness * nausea, vomiting and diarrhoea, anorexia * blurred vision and xanthopsia - disturbed yellow/ green visual perception * Arrythmias - AV block, bradycardia * Gynaecomastia Remember hypokalaemia increases the risk of digoxin toxicity!

Answer 89

Amiodarone SE's: * lung and liver fibrosis / pneumonitis/ hepatitis * thyroid dysfunction - hyper and hypo * corneal deposits * slate grey skin & UV sensitivity * peripheral neuropathy * myopathy * thrombophlebitis at injection sites * prolongation of the QT interval therefore proarrythmic * bradycardia *

Answer 90

Lithium - narrow therapeutic range , long plasma half life primarily excreted via the kidneys. SE's: * early - tremor ( fine tremor vs coarse tremor in toxicity) * intermediate - tiredness, N , V , diarrhoea * late - * thyroid enlargement - hypothyroid & goitre * hyperparathyroidism and hypercalcaemia * renal failure - polyuria & polydipsia secondary to nephrogenic diabetes insipidus * arrythmias - T wave flattening / inversion * seizures ( also reduced seizure threshold in epilepsy) * coma * Leucocytosis

Answer 91

Signs of intoxication require withdrawal of treatment. 1. Increasing GI disturbance - vomiting & diarrheoa 2. visual disturbance 3. CNS disturbance - confusion, drowsiness, lack of coordination, restlessness, stupor, abnormal reflexes, myoclonus 4. muscle weakness 5. fine tremor progressing to coarse tremor 6. polyuria (kidney failure) 7. incontinence 8. hypernatraemia 9. Cardiac arrythmia --\> bradycardia and heart block --\> blood pressure changes, circulatory failure --\> renal failure --\> coma & sudden death

Answer 92

1st generation - Haloperidol & chlorpromazine are the typical APs that act on D2 receptors to block dopaminergic transmission in the mesolimbic pathways More commonly has Extrapyramidal SEs and hyperprolactinaemia. Extrapyramidal SE's * Parkinsonism --\> TRAP (tremor, rigidity, bradykinesia, posturla instability) * Akathisia --\> severe restlessness * Tardive dyskinesia --\> occurs after months - yrs of tx, subtle involuntary movements of tongue, lips and jaw, can cause dystonia, ticks and chorea as progressive. * Acute dystonia --\>emergency! occurs within hrs to days of antipsychtoics (more common if AP naive). Stiffness, contracture and pain in msucles of neck (torticollis - contraction of neck causing head to tilt down), oculogyric crises (prolonged upward deviation of the eyes). Treat with Procyclidine. Hyperprolactaemia: In men --\> impotence, loss of libido, breast development and galactorrhoea In women --\> amenorrhoea, loss of libido, breast pain & galactorrhoea

Answer 93

2nd generation APS: Amisulpride, risperidone, quietapine, clozapine, olanzapine, ariprazole. Reduced EPSE compared to 1st generation APS. Increased metabolic side effects, leads to metabolic syndrome: * raised blood sugar * raised cholesterol * low serum HDL * weight gain * HTN * increased risk of VTE and stroke in elderly patients Olanzapine is the worst for metabolic SEs, risperidone is better and ariprazole the best. Clozapine --\> only introduced if schizophrenia not controlled despite sequential use of two or more APs drugs. Significant risk of agranulocytosis, therefore FBC monitoring required during tx.

Answer 94

***Clozapine only introduced if schizophrenia not controlled despite sequential use of two or more antipsychotic drugs one of which should be a second generation AP, each for at least 6-8 weeks.*** Adverse effects of clozapine: * Agranulocytosis - FBC monitored for every week for 18 weeks, then every 2 weeks then if blood count stable after 1 yr every 4 weeks. * neutropenia * reduced seizure threshold * myocarditis & cardiomyopathy- baseline ECG taken before starting treatment * constipation & intestinal paralysis (can lead to obstruction and perforation) * hypersalivation Interactions: - clozapine dose adjustment necessary if smoking is started or stopped during treatment smoking induces cytochrome P450 breakdown of clozapine, therefore if patient takes up smoking they will require higher dose, if patient stops smoking they will be more at risk of SEs.

Answer 95

Corticosteroids have glucocorticoid activity (cortisol - body homeostasis, stress and immune responses) and mineralocorticoid activity ( aldosterone - water and electrolyte balance). Fludrocortisone has high mineralocorticoid activity, followed by hydrocortisone. (has both mineralocorticoid and glucocorticoid activity) In order of increasing glucocorticoid activity and decreasing mineralocorticoid activity: * Hydrocortisone * prednisilone * dexamethasone * betmethasone SEs: * Endocrine --\> hyperglycaemia, hyperlipidaemia, increased appetite and weight gain * cushings syndrome --\> buffalo hump, striae, moon face * MSK --\> proximal muscle weakness, osteoporosis, avascular necrosis of femoral head * GI --\> peptic ulceration acute pancreatitis * psychiatric --\> insomnia, mania, depression, psychosis * opthalmic --\> glaucoma and cataracts * dermatological --\> acne, hirsutism * immunosuppresion Mineralocorticoid effects (Fludricortisone) Fluid retention and hypertension **_Withdrawing from steroids:_** * Gradual withdrawal of steroids if patients have received more than 40 mg prednisilone daily for more than 1 week, received more than 3 weeks treatment or recently had repeated courses

Answer 96

* myopathy * abdominal pain * raised ALT/AST * rhabdomyolysis (can be just asymptomatic rise in creatinine kinase)

Answer 97

GI bleeding and alcohol caused by --\> NSAIDS, aspirin Increased anticoagulation with warfarin and acute alcohol intake. Chronic alcholism is prothrombotic. Sweating/ flushing/ N & V by --\> metronidazole and alcohol lactic acidosis --\> metformin and alcohol hypertensive crisis --\> MAOI and alcohol Sedation by ---\> barbiturates, opiods and bzd's and alcohol

Answer 98

metformin --\> biguanide, used mainly in the treatment of T2DM. Increases insulin sensitvity and inhibits liver gluconeogenesis. By inhibiting hepatic gluconeogenesis, lactate is usually taken up in this process, and it can build leading to lactic acidosis. This is more likely if there has been a recent period of hypoxia (sepsis, MI, AKI, dehydration). Adverse effects: * GI --\> nausea, anorexia, diarrhoea (intolerable in 20%) * lactic acidosis --\> with liver disease or renal failure Caution: CKD --\> stopped if creatinine \> 150 umol/l or eGFR \< 30 ml/ min caution with contrast due to increased risk renal imapirment alcohol abuse also increases lactic acidosis.

Answer 99

Sulphonylureas - gliclazide, glimepiride, glibenclamide Stimulating pancreatic insulin secretion (by modification of calcium channels in beta cells, leads to exocytosis of insulin more easily). Therefore by directly stimulating pancreatic insulin secretion it can lead to ***hypoglycaemia & weight gain.*** * Other SE: * Abdominal pain * Nausea & vomiting * diarrhoea

Answer 100

Beta blockers, ***lithium***, antimalarials (chlroquine and hydroxychloroquine), NSAIDs, ACEi, infliximab Other factors that worse psoriasis are: Trauma, alcohol, withdrawal of systemic steroids. Streptococcal infection can trigger guttate psoriasis.

Answer 101

Digoxin is prescribed to slow the ventricular rate in AF therefore monitoring of ventricular rate at rest is key in determining if the dose is effective. ECG not required to check this. With history of CKD you need to check digoxin levels, this is done at least 6 hours after the last dose. This is often done just before the next dose with morning bloods.

Answer 102

Caution with Beta blockers, NSAIDS and adenosine * BB --\> cause bronchospasm and therefore are best avoided. Not absolutely contraindicated, if no alternatives are available may be started under a specialist. Some beta blockers are more cardioselective * NSAIDS --\> 10-20% of patients experience bronchospasm or worsening of asthma control with NSAIDS. Risk increased in those with nasal polyps or middle aged. If no alternative analgesic available & no hx of hypersensitivity then trial of NSAIDS may be given to asthmatics if informing them of the risks * Adenosine --\> asthma & COPD are contraindications to adenosine. Verapamil may be used as an alternative. * Opiod / benzodiazepines --\> caution in COPD as can cause respiratory depression.

Answer 103

* alcohol, cocaine and amphetamines (amphetamines - CNS stimulator drugs used in ADHD and narcolepsy, illegally examples are speed and meth) * Ciprofloxacin and levofloxacin (fluroquinolones) --\> fluoroquinolones can lower seizure threshold and induce seizures * methylxanthines - theophylline and aminophylline --\> can induce seizure * buproprion (antidepressant)--\> (dual inhibitor of NA/DA uptake) lowers seizure threshold * methylphenidate --\> used in ADHD as CNS stimulant (blocks NA/DA reuptake) * NSAID mefenamic acid --\> seizures

Answer 104

* Following medications exacerbate heart failure: * Thiazolidinediones - e.g. pioglitazone ---\> causes fluid retention * Verapamil --\> negative inotropic effect * NSAIDS/ glucocorticoids --\> used with caution as cause fluid retention (low dose aspirin exception as benefit outweighs risk) * Class 1 antiarrythmics --\> flecainide (negative inotropic and proarrythmic effect)

Answer 105

NSAIDS Oestrogens - COCP / HRT Varenicline (nicotine receptor partial agonist to aid smoking cessation)

Answer 106

Avoid: Antibiotics - ciprofloxacin, tetracycline, chloramphenicol, sulphonamides Psychiatric dugs - lithium, BZDs, clozapine Aspirin - risk of reyes syndrome carbimazole methotrexate sulfonylureas cytotoxic drugs amiodarone

Answer 107

* Antibiotics: * tetracyclines * aminoglycosides - gentamycin, tobramycin * sulphonamides * trimethoprim * ACEi / ARB * AEDs - sodium valproate, carbamazepine, phenytoin * Statins * warfarin * sulfonylureas * retinoids * cytotoxic agents

Answer 108

Statins Amitryptiline

Answer 109

Avoid in renal failure: * NSAIDS * Lithium * metformin * antibiotics - tetracycline, nitrofurantoin Drugs that accumulate in CKD: * Abx - penicillin, cephalosporin, vancomycin, gentamicin, * digoxin * atenolol * furosemide * methotrexate * sulphonylureas * opiods

Answer 110

* Rapid acting - Insulin LISPRO * act within 5 mins, peak within 1 hr, last 3-5 hours * used a bolus dose pre meals in basal - bolus regimen * Short acting - Insulin ASPART (Novorapid) * act within 30 mins, peaks in 3 hours, lasts 6-8 hours * used a bolus in basal bolus regime * Intermediate acting - Isophane insulin * acts within 2 hours, peaks 5-8 hours, lasts 12- 18 hours * often used premixed with long acting as basal insulin * Long acting : Insulin GLARGINE (Lantus) or Insulin DETEMIR (Levemir) * act within 1-2 hours, flat profile no peak, last up to 24 hours

Answer 111

Management of stable angina: * acute attacks of stable angina --\> **sublingual GTN** * all patients should receive a **statin and aspirin** as prevention * long term prevention --\> **BB first line** (atenolol, bisprolol, metoprolol, propanolol). * Long term prevention --\> **rate limiting CCB** (verapamil or diltiazem) is 2nd line. Used if BB are contraindicated (asthma, decompensated heart failure) or prinzmetal's angina (e.g coronary artery vasospasm rather than atherosclerosis, pain on rest relieved by GTN spray). * Of there is poor response to initial treatment then medicaiton should be increased to maximum tolerated dose * If patient still symptomatic on monotherapy (BB fails to control symptoms) then combination of BB and CCB should be used. (NOTE NOT verapamil plus BB this is contraindicated due to bradycardia and heart block). * If using the combination of CCB and BB then a long acting dihydropyridine should be used e.g. modified release nifedipine. * If dual therapy is contraindicated then NICE recommends long acting nitrate, ivabradine, nicorandil or ranolazine. * long acting nitrate e.g. **isosorbide mononitrate,** can be given as modified release forms once daily * **ivabradine** (funny current blocker, reduce pacemaker activity in SA node) * **nicorandil** - vasodilatory drug that works by increasing cGMP and activating K channels to cause hyperpolarisation (smooth muscle relaxation). * **ranolizine** - inhibits sodium and potassium currents (unsure of MOA)

Answer 112

* Nitrate tolerance - reduced efficacy of nitrates in reduction of angina pain * NICE advises those that take standard release Isosorbide mononitrate should use asymmetric dosing interval to maintain daily nitrate free time 10-14 hours to minimise development of nitrate tolerance * Not seen in modified release forms

Answer 113

Common management of ACS: MONAC/MONAT - Aspirin 300 mg - oxygen if sats \< 94% - morphine if patients in severe pain not relieved by GTN - Nitrates - GTN spray or tablets given sublingually first. This is rapidly absorbed. Failure to respond mau indicate current episode of pain is more likely to indicate MI than angina. If chest pain does not subside with GTN spray then IV infusion can be used. Never used without trying sublingual route first as SL is quicker and infusion requires monitoring for bradycardia. STEMI mx: ***300 mg aspirin + P2Y12 platelet inhibitor (ticagrelor, clopidogrel, prasugrel). Choice of second antiplatelet agent depends on planned intervention either PCI, fibrinolysis or medical management. Prasugrel preferred for PCI, unless bleeding risk.*** * ***PCI available?*** * Patient presenting within 12 hrs from onset of pain and PCI delivered within next 2 hours * if patient presents \> 12 hrs but still ongoing evidence of ischaemia PCI considered * further antiplatelet prior to PCI - DAPT. * if patient not anticoagulated use prasugrel * if taking anticoagulant use clopidogrel * During PCI - * with radial access (preferred) --\> unfractionated heparin with bailout Glycoprotein iib/iiia inhibitors * with femoral access --\> bivalirudin (thrombin inhibitor) with bailout glycoprotein iib/iia inhibitor * PCI unavailable (cannot deliver in GDH or transfer within 2 hours), **fibrinolysis** * offered if onset of sx in last 12 hours and PCI unavailable. * Fibrinolytic therapy --\> activated plasminogen, forming plasmin which cleaves fibrin cross links causing thrombus breakdown * examples: ***streptokinase, urokinase, alteplase, tenecteplase, reteplase*** * must be started within 12 after which it will not be effective, need specialist adivce if over * If undergoing fibrinolysis antithrombin agent should be given at the same time (e.g. as in PCI when heparin plus bailout GPiib/iiia inhibitors are used). * check for contraindications (i.e factors that increase risk of bleeding): * recent stroke / prior intracranial haemorrhage/ Cerebrovascular abnormality e.g. aneurysm or AVM, intracranial tumour, trauma, bleeding, major surgery recently, pregnancy, current anticoagulant use. * check ECG 60-90 mins after to check if ischaemia has resolved. If there is persistent ischaemia PCI needs to be considered. * DAPT after fibrinolysis: * Ticagrelor plus aspirin if not high bleeding risk * clopidogrel with aspirin or just aspirin if high bleeding risk

Answer 114

* Give aspirin 300 mg * Fondaparinux (antithrombin iii activator, binds to an inhibits factor xa) given to patients not undergoing immediate angiography * if immediate angiography is planned (unstable patient) or they have renal failure then UF heparin used instead **_Risk assessment:_** GRACE score calculated which takes into account their age/BP/cardiac and renal function, cardiac arrest at presentation, ECG findings or troponin levels Under 3% low risk Greater than 3% intermediate - high risk **_Angiography & PCI: Offered to patients:_** - immediately if clinically unstable (hypotensive) - within 72 hours if GRACE score \> 3% - or those than initially considered low risk but there is subsequent ischaemia, or younger patients that may benefit from early angiography **_Angiography and PCI:_** - offer UF heparin during procedure regardless of fondaparinux prior - offer prasugrel or ticagrelor as part of DAPT with aspirin if no indication for ongoing oral anticoagulation. I/e not on anticoagulant already use prasugrel or ticagrelor. - if separate indication for ongoing anticoagulation use clopidogrel i.e if already on anticoagulation use clopidogrel. - If stenting indicated use drug eluting stent **_PCI not indicated:_** **_-_**consider for those low risk on GRACE score \<3% offer DAPT - aspirin plus Ticagrelor (unless high bleeding risk), in which case use Clopidogrel or just aspirin alone.

Answer 115

Keep blood glucose levels below 11 mmol/L Consider dose adjusted insulin infusion with regular monitoring of insulin levels

Answer 116

* 6 A's * Aspirin - 75mg daily * Antiplatelet - Ticagrelor, or clopidogrel for up to 12 months * Atorvastatin - 8- mg once daily * ACE i - ramipril titrated as tolerated to 10 mg once daily * atenolol or other Beta blocker titrated as high as tolerated * Aldosterone antagonist - for those with clinical heart failure Lifestyle measures: - stop smoking - reduce alcohol consumption - mediterranean diet - cardiac rehabilitation - exercise programme regime - optimise treatment of diabetes and HTN

Answer 117

**_Stages of HTN:_** Stage 1 HTN --\> Clinic SBP \> 140/ 90 or ABPM SBP/DBP \> 135/85 Stage 2 HTN --\> Clinic SBP/DBP \> 160/100 or ABPM SBP/DBP \> 150/95 Severe HTN --\> SBP \> 180 mmHg or DBP \> 110 mmHg **_BP targets by age:_** * Under 80 yrs --\> clinic BP 140/90 or ABPM 135/85 mmHg * Over 80 yrs --\> clinic BP 150/90 or ABPM 145/85 mmHg

Answer 118

Amlodipine is the most common drug for HTN, starting at 5mg Note other CCB e.g. nifedipine m/r or felodipine m//r can be used. Standard release nifedipine is not recommended for HTN

Answer 119

Contrast media nephrotoxicity = 25% increase in creatinine occuring within 3 days of IV administration of contrast, occurs 2-5 days after. Occurs in PCI/ coronary angiography and CT with contrast. Risk factors: * known renal impairment * age \> 70 yrs * dehydration * cardiac failure * nephrotoxic drugs e.g. NSAIDS Prevention: * Use IV 0.9% sodium chloride infusion for 12 hours pre and post procedure * patients at high risk should have metformin withheld for minimum 48 hours and until renal function shown to be normal due to risk of lactic acidosis.

Answer 120

* Key points: * initial starting dose of levothyroxine should be lower in elderly patients and those with ischaemic heart disease * Patients with cardiac disease, severe hypothyroidism or \> 50 yrs initial starting dose 25 micrograms OD with dose titrated * Other patients started on 50-100 micrograms OD * following a change in levothyroxine dose TFTs should be check 8-12 weeks * therapeutic goal is normalisation of TSH to 0.5-2.5 mU/L * women with established hypothyroidism who become prengnacy should have dose increased by at least 25-50 micrograms levothyroxine due to increased demands of pregnancy * Side effects of levothyroxine therapy: * hyperthyroidism * reduced bone mineral density * worsening angina * AF * Interactions: * iron and calcium carbonate --\> absorption of levothyroxine is reduced give at least 4 hours apart

Answer 121

* If within 1 hour and dose \> 150mg/ kg then use activated charcoal * If delayed presentation \> 8 hours, staggered overdose (over \> 1hr) or unsure of the timing of ingestion start NAC. * Take urgent paracetamol levels (4 hours post ingestion) and urgent bloods (FBC/U&E/LFT/INR/vbg * Assess the nomogram: * if above 100mg/kg at 4hours or above 15mg/kg at 15 hours ingestion then need NAC * If above treatment line start NAC

Answer 122

* Emergency contraception can be provided either by the copper IUD or by the "morning after pill". * ***Copper IUD*** can be inserted up to 5 days after UPSI, or up to 5 days after earliest estimated date of ovulation. Antibacterial cover may be considered if there is a significant risk of STI associated with pelvic infection. It may be left to provide long term contraception. * Hormonal methods: * ***Levonogestrel & Ulipristal acetate*** * Levonogestrel * MOA - inhibits ovulation and inhibits implantation * should be taken ASAP as efficacy decreases overtime, must be taekn within 72 hours of UPSI * single dose 1.5mg levonogestrel required, but dose should be doubled for BMI\> 26 or weight over 70kg * disturbance of current menstrual cycle may occur * vomiting in 1% * if vomiting occurs within 3 hours, another dose is needed * can use more than once in each cycle if needed * hormonal contraception can be started immediately after using levonorgestrel * Ulipristal acetate: * progestreone receptor modulator known as ellaone. Inhibits ovulation * 30 mg dose to be taken ASAP, no later than 5 days after UPSI * Ulipristal may reduce the effectiveness of hormonal contraception, contraception needs to be restarted 5 days after having ulipristal. * Barrier methods or abstain for 5 days * can be repeated within the same menstrual cycle

Answer 123

HbAIc targets: * should be checked every 3-6 months until stable then 6 monthly * lifestyle --\> \< 48 mmol * Lifestyle + metformin --\> \< 48 mmol * lifestyle + drugs causing hypoglycaemia (e.g. sulfonylurea) --\> 53 mmol/mol * Patient already on treatment (on one drug but HbA1c has risen to 58 mmol --\> \<53 mmol Two pathways --\> tolerate metformin, doesnt tolerate metformin (e.g. BMI \< 18 or CKD) : Tolerates metformin: * metformin is 1st line, should be offered if HbA1c rises to 48 mmol on lifestyle * If HbA1c rises to 58 mmol then add second drug: * sulfonylurea (gliclazide) * sitagliptin (DPP4 inhibitor) * pioglitazone (thiazolidinedione) * SGLT2 inhibitor (dapagliflozin, canagliflozin) * If despite this HbA1c rises to or remains above 58 mmol then go to triple therapy, or insulin therapy should be considered. * Criteria for exenatide: * If triple therapy contraindicated or not tolerated, consider triple therapy with GLP1 mimetic exenatide. * metformin + sulphonylurea + exenatide * IF BMI \> 35/ obese * If BMI \< 35 but insulin therapy would have significant occupational implications Cannot tolerate metformin: * If HbA1c rises to 48 mmol on lifestyle consider: * sulfonylurea * gliptin * pioglitazone * If it then rises to 58 mmol then consider using two of the above agents * If despite this the HbA1c remains above 58 mmol consider insulin therapy Starting insulin: * metformin should be continued * NICE recommend starting with isophane intermediate acting insulin taken at bedtime or twice a day according to need. Control HTN: 1st line for T2DM is ACEi or ARB. ARB preferred in black african /african carribean. BP targets the same, under 80yrs then clinic BP \< 140/90 or ABPM \< 135/85 older than 80 yrs then clinic BP \< 150/90 or ABPM \< 145/85

Answer 124

* Epiglottitis (H influenza) --\> ceftriaxone or cefotaxime * Bronchiectasis --\> 1st line amoxicillin, clarithromycin or doxycycline 7-14 days, 2nd coamoxiclav, levofloxacin * COPD exacerbation --\> 1st line amoxicillin, clarithromycin, doxycycline 5 days, 2nd line --\> coamoxiclav, levlofloxacin, cotrimoxazole * CAP Pneumonia --\> * 1st line low severity --\> amoxicillin * If pen allergic/ atypical pathogens suspected--\> doxycycline, clarithromycin, erythromycin (pregnancy) * 1st line moderate severity --\> amoxicillin * if atypical pathogens suspected --\> amoxicillin with clarithromycin/ erythromycin (pregnancy) * If pen allergic --\> doxycycline * 1st line high severity * Co amoxiclav WITH clarithromycin or Erythromycin (pregnancy) * If pen allergic --\> levofloxacin (consult microbiology if fluoroquinolone not app). * HAP pneumonia --\> * Within first 5 days of admission (therefore lower chance of resistance) --\> coamoxiclav (if penicillin allergic use doxyxycline, cefalexin) * \> 5 days of admission (higher resistance) --\> IV piperacillin with tazobactam, ceftriaxone, ceftazidime * If MRSA confirmed or suspected add vancomycin

Answer 125

* Duration of antibiotics: * non pregnant woman - 3 days * pregnant women (even if asymptomatic bacteruria) --\> 7 days * Men --\> 7 days * Catheter associated --\> 7 days * Abnormal anatomy or kidney function --\> 10 days * UTI non pregnant women - * 1st line Nitrofurantoin or Trimethoprim * 2nd line (no improvement in 48 hour) --\> Amoxicillin * UTI Men: Nitrofurantoin or trimethoprim * UTI Pregnant women --\> * 1st line --\> nitrofurantoin (note avoided in 3rd trimester, associated with haemolytic anaemia of newborn). * 2nd line --\> amoxicillin or cefalexin * Asymptomatic bacteruria --\> amoxicillin, cefalexin, nitrofurantoin * Prostatitis: * 1st line --\> ciprofloxacin, ofloxacin * 2nd line (unable to take fluoroquinolones) --\> trimethoprim * IV 1st line if severely unwell --\> ceftriaxone, cefuroxime * Pyelonephritis: * Non pregnant women and men * Oral 1st line ***cefalexin, ciprofloxacin*** * IV 1st line - ceftriaxone, cefuroxime, ciprofloxacin * if sensitivity known - ***coamoxiclav or trimethoprim*** * Pregnant women: * oral cefalexin * IV cefuroxime

Answer 126

Impetigo: * localised non bullous impetigo (vesicles or pustules that rupture quickly forming golden brown crust) usually offer topical treatment. If systemically unwell offer oral. * Bullous impetigo (fluid filled vesicles & blisters that rupture leaving yellow brown crust), offer oral treatment * Treatment: * localised non bullous impetigo --\> topical hydrogen peroxide 1% cream (unless around eyes) * 1st line if hydrogen peroxide unsuitable: * topical fusidic acid * Oral first line : * Flucloxacillin or erythromycin

Answer 127

Cellulitis & erysipelas = infections of subcutaneous tissue, usually from break in the skin, both characterised by inflammation and oedema. Lesions are more superficial in erysipelas and have well defined raised margin. * Cellulitis --\> Flucloxacillin (clarithryomycin, erythromycin (pregnancy) or doxycycline if penicillin allergic) * Cellulitis near eyes or nose --\> Coamoxiclav (clarithromycin + metronidazole if pen allergic) * Severe infection --\> oral Coamoxiclav/ clindamycin, IV ceftriaxone or cefuroxime * If MRSA --\> add IV vancomycin **_Leg ulcer:_** Same as cellulitis: 1st line flucloxacillin, if pen allergic (clarithromycin, erythromycin, doxycycline) 2nd line - coamoxiclav **_Human or animal bite:_** Coamoxiclav 1st line Doxycyline with metronidazole if pen allergic **_Mastitis during breast feeding:_** Flucloxacillin 10-14 days If pen allerfic Erythromycin 10-14 days

Answer 128

Throat infections - phenoxymethylpenicllin 5-10 days or erythromycin/ clarithromycin if penicillin allergic sinusitis - phenoxymethypenicillin ototis media - 1st line amoxicillin (erythromycin or clarithromycin if penicllin allergic). 2nd line - coamoxiclav otitis externa - flucloxacillin (erythromycin/ clarithromycin if penicillin allergic) Periodontal/ periapical abscess - phenoxymethylpenicillin or amoxicillin. If penicllin allergic use clarithromycin. 5 days treatment. (gum infections) gingitivitis - acute necrotising ulcerative - metronidazole (alternative amoxicillin)

Answer 129

* Bacterial vaginosis: * oral or topical **metronidazole** 5-7 days, alternative topical clindamycin * Thrush/ candidiasis * **clotrimazole** cream or pessary * oral antifungal - **fluconazole** * Chlamydia: * **Doxycycline** or azithromycin 7 days (alternative erythromycin 14 days) * Doxycycline is contraindicated in pregnancy and breastfeeding alternatives are: * **azithromycin** * **erythromycin** * amoxicillin * Gonorrhoea: * Sensitivities not known --\> **single IM ceftriaxone 1g** * Sensitivities known --\> **single dose oral ciprofloxacin 500mg** * Early Syphillis (within 2 yrs) : * **IM benzathine benzylpenicillin** single dose * alternative ***doxycycline*** or erythromycin (14 days) * Late syphillis (\> 2 yrs) : * **benzathine benzylpenicillin** - once weekly for 2 weeks * ***doxycycline*** - 28 days * for contacts of syphillis patients - doxycycline 14 days * PID: * ***Doxycycline*** (cover chlamydia and mycoplasma genitalium) + ***metronidazole*** (cover anaerobes e.g. gardenerella vaginalis) (14 days) + ***single dose of IM ceftriaxone*** (Cover gonorrhoea)

Answer 130

C difficile: * Oral vancomycin 1st line * Oral fidaxoicin 2nd line * For further episodes of C diff infection: * within 12 weeks --\> Fidaxomicin * \> 12 weeks --\> vancomycin or fidaxomycin * Life threatening C diff infection --\> oral vancomycin with IV metronidazole Campylobacter: * Often self limiting treated if immunocompromised / severe infection: * clarithromycin (azithromycin or erythromycin) * ciprofloxacin alternatively Diverticulitis: * 1st line --\> coamoxiclav * 2nd line cefalexin with metronidazole or trimethoprim with metronidazole or ciprofloxacin with metronidazole Salmonella: * Ciprofloxacin Shigella: * Ciprofloxacin or azithromycin Typhoid: Cefotaxime or ceftriaxone

Answer 131

* Anticholinergics: * antipsychotics * antidepressants * ipratroprium/tiotroprium * oxybutinin (detrusor relaxants) * General anaesthetic * Alpha adreno R agonists (phenylephrine, clonidine) * BZD * NSAID * CCB * Antihistamines * alcohol

Answer 132

* Opiods * D2 antagonists - metoclopramide * Anticholinergics (antipsychotics/ antidepressants/ tiotroprium/ oxybutinin) * anticonvulsants * less commonly: * H2 antagonist * Digoxin * BB * Steroids * NSAID * Antibiotics

Answer 133

4 classes of laxatives: BOFS * Bulk forming laxatives --\> methylcellulose, isphagula husk, stercolia * Osmotic laxatives --\> macrogol, lactulose, phosphate and sodium citrate enema * Faecal softeners ---\> docusate, arachis oil * Stimulant laxatives --\> bisacodyl, senna, sodium picosulfate * Prokinetic laxative --\> Prucalopride = 5HT4 R agonist. Stimulates intestinal motiloty and considered in chronic constipation where 2x laxatives at highest dose for 6 months have not worked.

Answer 134

* Bowel obstruction/ perforation/ paralytic ileus/ toxic megacolon * faecal impaction * UC/Crohns * Severe dehydration and bisacodyl * galactosemia and lactulose * Peanut hypersensitivity and arachis oil

Answer 135

* Lifestyle measures first --\> increase dietary fibre, increase fluid intake, exercise, stop any constipating drugs * 1st line = bulk forming laxative = methylcellulose * If this doesnt work --\> osmotic laxative --\> macrogol first, lactulose second. * If they are still symptomatic / feelings of incomplete empyting try stimulant laxative --\> senna or bisacodyl If opiod induced constipation do not give bulk laxative. Osmotic first plus a stimulant (macrogol + senna)

Answer 136

* Lifestyle as before, stop constipating drugs, exclude secondary causes. * 1st line bulk laxative methylcellulose * 2nd --\> osmotic --\> macrogol first then lactulose * 3rd --\> stimulant --\> senna and bisacodyl If two laxatives have been tried at maximal dose for \> 6 months and they are still symptomatic and being considered for enema, then try prokinetic agent: Prucalopride - serotinin receptor agonist that stimulates intestinal motility for 4 weeks.

Answer 137

* Aluminium/ Iron/ Calcium containing meds * Opiates * NSAIDS * Antimuscarinics - procyclidine, oxybutinin * antidepressants - TCA * Antipsychotics * AEDS * Antihistamines * Antispasmodics - dicycloverine hyoscine * CCB - verapamil * Diuretic - furosemide

Answer 138

* Endocrine --\> Diabetes (autonomic neuropathy), hypercalcaemia & hyperparathyroidism, hypothyroidism * Electrolytes --\> hypermagnesaemia, hypokalaemia, uraemia * Neurological --\> stroke/ TIA/ Autonomic dysfunction/ MS/ Parkinsons/ Hirschprungs / spinal cord lesion * GI --\> bowel cancer, anal fissure/stricture/ haemorrhoids, colonic stricture e.g. diverticulitis, IBD (crohns/ UC). * Rectal prolapse/ rectocele * 3rd degree tear postnatal * IBS * slow transit constipation

Answer 139

* 1st line try oral osmotic laxative --\> macrogol at a high dose * if after a few days stools remain hard or have become soft but not cleared add a stimulant (bisacodyl or senna ) * If still remaining impacted consider enema with bisacodyl suppository, glycerol or glycerol plus bisacodyl. * Mini enema - docusate or sodium citrate * If response still inadequate --\> arachis oil enema or sodium phosphate enema

Answer 140

* Lifestyle options: * avoid caffiene / alcohol/ acidic drinks * drink 2L fluid a day (not excessive not too little) * weight loss (Reduce abdominal pressure) * quit smoking (reduces cough) * reduce offending medications eg. diuretics and ACEi if possible * 1st line --\> supervised pelvic floor exercises for 3 months (refer to womens physio) * If conservative management fails refer to a urogynaecologist or urologist for surgical management: * tension free tape TVT --\> mesh support around the urethra, joined back onto pubic symphysis and abdominal wall * Sling procedure --\> similar to above but uses patients own fascia * colposuspension --\> pulls vaginal wall forward to support the urethra * intramural urethral injections to bulk around the urethra reducing diameter and adding support * If surgery is declined/ inappropriate offer 2nd line: Duloxetine * NSRI (Na/5HT reuptake inhibitor) --\> increases NA/5HT in the pudendal nerve increasing sphincter muscle tone

Answer 141

* Lifestyle measures --\> reduce alc/ caffiene/ acidic drinks/ smoking/ drink 2l / day, weight loss * 1st line --\> bladder retraining for 6 weeks (gradually increasing the time between voiding). * 2nd line --\> if the above fails add anticholinergic medication: * oxybutinin * tolterodine * Darifenacin * Note avoid oxybutinin in older and more frail women as anticholinergic effects can exacerbate dementia and cognitive decline. Avoid in myasthenia gravis. * Other SE's --\> blurred vision, dry eyes, dry mouth, urinary retention, constipation, postural hypotension, worsening cognition. * Warn takes 4 weeks to work. * 3rd line --\> if anticholinergic contraindicated or not tolerated: Mirabegron: * B3 adrenoreceptor agonist stimulates SNS (destrusor relaxation). * contraindicated in uncontrolled HTN as risk of hypertensive crisis/ Stroke). * If above fails invasive methods: * botulinum toxin A injection * percutaneous sacral nerve stimulation * augmentation cystoplasty * Urostomy/ urinary diversion