Pass the PSA revision

Question 1

What are the basic principles of prescribing?

Answer 1

All prescriptions should be:

1) legible
2) unambigous (no range of doses)
3) an approved name e.g. salbutamol not ventolin
4) written in capitals
5) no abbreviations
6) signed - name and bleep
7) if a drug is PRN - provide two instructions both the indication and the maximum frequency (e.g. twice daily, max dose in 24 hours)
8) if antibiotics then give indication & stop/review date
9) duration of treatment if not long term

Question 2

What system is the most important in metabolism of drugs within the body?

What is an inducer vs inhibitor and how will this affect drug metabolism?

Answer 2

Most drugs are metabolised to inactive metabolites by the Cytochrome P450 enzyme system in the liver.

An enzyme inducer increases cytochrome P450 enzyme activity increasing metabolism of other drugs therefore leading to a reduced effect - therefore require increased doses of these drugs.

An enzyme inhibitor will decrease cytochrome P450 activity and therefore there will be increased levels of other drugs - therefore required reduced doses of these drugs.

Question 3

Examples of enzyme inhibitors

Answer 3

Drug inhibitor –> decreases enzyme activity therefore increases drug concentration.

A DOSE VICE (squeezing the liver so enzymes cant work).
Allopurinol
Disulfiram
Omeprazole
Sulphonamides
Erythromycin
Valproate
Isoniazid
Ciprofloxacin
Ethanol (acute intoxication)

Question 4

Examples of enzyme inducers

Answer 4

Enzyme inducer –> increases enzyme metabolic activity therefore reduced drug concentration.

BS CRAP (when you crap you get rid of drugs…)
Barbiturates
Sulphonylureas
Carbamazepine
Rifampicin
Alcohol (chronic excess)
Phenytoin

Question 5

Prescribing for surgery - Which drugs are never stopped intraoperatively?

Answer 5

CCB & BB must be continued during the operation

Question 6

Prescribing for surgery - drugs to increase during surgery?

Answer 6

Patients on long term corticosteroids (e.g. prednisilone) commonly have adrenal atrophy therefore unable to amount an adequte physiological stress response post operatively.
This results in profound hypotension if steroids are discontinued.
As with sick day rules - where patients on long term steroids double their daily dose when ill to counter increased steroid requirement, at induction of anaesthesia patients should be given IV steroids.

Question 7

Prescribing for surgery - drugs to stop during surgery?

Answer 7

I LACK OP
Insulin
Lithium
Anticoagulants/ antiplatelets
COCP/HRT
K sparing diuretics
Oral hypoglycaemics
Perindopril & other ACEi

Question 8

What is a mnemonic for safe prescribing?

Answer 8

PReSCRIBER
Patient details
Reactions –> drug allergies and what happens?
Sign the front of the chart
Contraindications
Route
IV fluids required?
Blood clot prophylaxis
Antiemetics
Relief- pain relief

Question 9

What key parts are needed for patient details?

Answer 9

Need three pieces of patient identifying information e.g. Name/ DOB/Hospital number.
(or hospital sticker)

If the patients details do not match, do not prescribe.

Question 10

What do we need to check with reactions?

Answer 10

If new chart - need to complete allergy box including any drug reactions mentioned by the patient.
If amending the chart then check allergies before prescribing.

Question 11

What common antibiotics contain penicillin?

Answer 11

Coamoxiclav - contains amoxicillin (a penicillin)
Tazocin - piperacillin with tazobactam (should always prescribe as piperacillin with tazobactam not Tazocin, as this masks the fact the drug contains penicillin.

Question 12

What are the key drug classes to know contraindications for?

Answer 12

Drugs that increase bleeding –> antiplatelets, heparin, warfarin

Steroids

NSAIDS

Antihypertensives

Question 13

General contraindications for antiplatelets/ heparin/ warfarin

Answer 13

Do not give these drugs to patients that are bleeding, suspected of bleeding or at risk of bleeding (e.g. prolonged prothrombin time with liver disease).

Prophylactic heparin is contraindicated in acute ischaemic stroke due to risk of bleeding into the stroke.

Question 14

What antibiotic may affect warfarin and how?

Answer 14

Erythromycin is an enzyme inhibitor that will prolong warfarin’s half life. Therefore prothrombin time and INR will increase despite a stable dose.
Consider other drugs when a patient is over coagulated.

Question 15

Steroids: what are the common side effects?

Answer 15

Remember with the mnemonic STEROIDS

Stomach ulcers
Thin skin
Edema
R&L HF
Osteoporosis
Infections
Diabetes - tendency towards hyperglycaemia and rarer can precipitate diabetes
cushing’s Syndrome

From BNF - weight gain, psychotic disorder/ cognitive impairment, GI discomfort & nausea, impaired healing, hirsutism, menstrual irregularities

Question 16

What are some of the contraindications for steroids?

Answer 16

Congestive heart failure
diabetes mellitus (including Fhx)
Glaucoma
Infections - TB, herpes simplex
peptic ulcer
osteoporosis
recent intestinal anastomoses
recent MI
affective disorders- e.g. psychosis
diverticulitis and UC
thromboembolic disorders

Question 17

NSAIDS - cautions and contraindications?

Answer 17

Remember with mnemonic NSAID
No urine - renal failure
systolic dysfunction - heart failure
Asthma
indigestion
dyscrasia (clotting abnormality)

Question 18

ACEi’s

MOA
Common SE
Caution and contraindications?

Answer 18

ACEi - inhibit ACE from converting Angiotensin 1 into angiotensin 2

Common SE:
Dry cough - due to increased bradykinin levels
angiooedema
hyperkalaemia
first dose hypotension

Cautions & contraindications:
Avoid in pregnancy and breastfeeding
renovascular disease - renal artery stenosis
aortic stenosis
hereditary idiopathic angioedema

Question 19

Beta blockers

Uses

Side effects

Contraindications

Answer 19

Uses:
HTN
Angina (reduce cardiac work)
MI - secondary prevention
Arrhythmias - BB + digoxin in AF/ SVT / thyrotoxicosis
Heart failure - Bisoprolol and carvedilol
thyrotoxicosis - propanolol

Side effects:
Bronchospasm
Fatigue
cold peripheries
sleep disturbances & nightmares

Contraindications:
2nd or 3rd degree heart block
unstable / worsening heart failure
Asthma
COPD (with significant reversible airways obstruction)
Not contrainidicated in diabetes but can mask hypoglycaemia by masking symptoms e.g. tachycardia.

Question 20

Calcium channel blockers:
Common examples & uses

Common side effects of calcium channel blockers?

Specific SE’s for each CCB class?

Answer 20

Dihydropyridine CCB’s –> Nifedipine and amlodipine –> more influence on vessels than myocardium & no antiarrhythmic activity. Used in angina and hypertension.
Verapamil hydrochloride –> angina, hypertension & arryhthmias.
Diltiazem hydrochloride –> angina, long acting for hypertension

Note CCB’s (with exception of amlodipine) should be avoided in heart failure as can further depress cardiac function & lead to HF.

peripheral oedema
flushing

Specific SE:
verapamil –> constipation common SE, can precipitate HF, hypotension at high doses, do not use with BB.
Dihydropyridines –> SE with vasodilation –> flushing, headache, ankle swelling.
Diltiazem –> less negative inotropy than verapamil, but risk of bradycardia, used with caution with BB.

Question 21

Name the loop diuretics

MOA

Indication

Common SE

Contraindications

Answer 21

Furosemide, bumetanide

MOA- inhibit NKCC2 in the TAL of the LOH reducing absorption of NaCl.

Indications - Hypertension (resistant hypertension with renal failure), heart failure (acute (IV) and chronic (orally)

Common SE’s:

• hypotension
• hypokalaemia, hyponatraemia, hypomagnesaemia, hypochloraemia, hypocalcaemia
• metabolic alkalosis
• ototoxicity (high doses or rapid IV can cause tinnitus and deafness)
• renal impairment
• can exacerbate diabetes (less common than thiazides), can exacerbate gout

Contraindications: careful in patients on digoxin too (hypokalaemia), careful in BPH can lead to urinary retention, can cause AKI.

Question 22

Name the thiazide diuretics

MOA

Indications

SE’s

Contraindications

Answer 22

Bendroflumethiazide, Indapamide, chlorthalidone, hydrochlorothiazide

MOA - inhibit Na/Cl symporter in the DCT.

Indications - hypertension (chlortalidone and indapamide are preferred), lower doses administered in the morning (to prevent night time urination), chronic heart failure.

SE’s:

• hypotension (postural), hypovolaemia (dehydration & dry mouth & dizziness))
• hypokalaemia (K+ lost as a result of more Na+ reaching collecting ducts)
• hyponatraemia, hypercalcaemia
• precipitates gout (hyperuricaemia)
• precipitates diabetes (hyperglycaemia)
• impotence
• skin reactions

Uncommon –> photosensitivity rash, pancreatitis , agranulocytosis or thrombocytopenia

Question 23

Antiemetics:

Which antiemetics are commonly prescribed?

What route is used?

What are the standard doses? Does this change with the route given?

Answer 23

Cyclizine and metoclopramide

If a patient is vomiting then antiemetics should be given by non oral routes - IV/ IM/ SC

Doses of common antiemetics are the same regardless of the route taken e.g. cyclizine 50 mg 8 hourly, metoclopramide 10 mg 8 hourly.

Cyclizine is a better first line antiemetic however should be avoided in patients with heart failure as it can lead to fluid retention

Metoclopramide is better if the patient has heart failure but caution in parkinsons disease and young women. Metoclopramide is a dopamine anatagonist therefore exacerbates parkinsons and can lead to acute dystonia (unwanted movements) in younger patients.

Question 24

A patient at risk of bleeding should not be prescribed what?

A patient with peripheral arterial disease should not be prescribed what?

Answer 24

Do not prescribe heparin, antiplatelet, anticoagulants to patients with risk of bleeding

Do not prescribe compression stockings to patients with peripheral arterial disease (check peripheral pulses), can precipitate acute limb ischaemia.

Question 25

What are appropriate prescriptions for:

No pain

Mild pain

Severe pain?

Answer 25

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.

Question 26

What is a common trap with paracetamol?

Answer 26

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.

Question 27

Out of the dopamine antagonists which is more likely exacerbate parkinsonian symptoms?

Metoclopramide

domperidone

Answer 27

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).

Question 28

What are two commonly examined SE’s of ACEis?

Why do these SE’s occur?

Answer 28

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.

Question 29

What is the mechanism behind ibuprofen leading to gastric ulceration?

Answer 29

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

Question 30

What is the mechanism behind steroids leading to gastric ulceration?

Answer 30

Oral steroids inhibit gastric epithelial renewal therefore predisposing to ulceration

Question 31

What are two common classes of drugs that can precipitate renal failure?

How do they do this?

Answer 31

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.

Question 32

What drugs might commonly need to be stopped in a patient presenting with constipation?

Answer 32

Opiates!

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

Question 33

Why might you be cautious to use ibuprofen in a patient with asthma?

Answer 33

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

Question 34

What is a direct contraindication to trimethoprim as an antibiotic?

Answer 34

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.

Question 35

Why is caution needed in continuing methotrexate in a patient that is unwell?

Answer 35

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.

Question 36

Why should CCB and BB not be prescribed together?

Answer 36

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.

Question 37

Data interpretation:

Common causes of anaemia:

Microcytic

Normocytic

Macrocytic

Answer 37

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.

Question 38

Data interpretation:

Causes of High white blood cells:

Neutrophils

Lymphocytes

Causes of low neutrophils

Answer 38

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)

Question 39

Data interpretation:

Causes of thrombocytosis (high platelets)

Answer 39

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

Question 40

Data interpretation:

Causes of thrombocytopenia (low platelets)

Answer 40

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

Question 41

Data interpretation:

Causes of hyponatraemia:

Hypovolaemic

Euvolaemic

Hypervolaemic

Answer 41

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

Question 42

Data interpretation: Causes of hypernatraemia:

Answer 42

Dehydration

Drips - too much IV saline

Drugs - e.g. effervescent tablets or IV preparations with high sodium

diabetes insipidus

Question 43

data interpretation:

normal range of sodium?

Answer 43

normal range sodium 135- 145 mmol/L

Question 44

Data interpretation: Causes of hyperkalaemia and hypokalaemia

Answer 44

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

Question 45

AKI : Picture of the U&E’s in each of the categories and causes of each category

Prerenal

Renal

Post renal

Answer 45

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

Question 46

What markers are important to look at in the context of liver damage?

Answer 46

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.

Question 47

What pattern of derangement on LFTs would be see in:

Prehepatic jaundice

intrahepatic jaundice

Post hepatic jaundice

Answer 47

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

Question 48

What are the common causes of hepatitis and cirrhosis?

Answer 48

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

Question 49

What drugs cause cholestasis?

Answer 49

COCP

antibiotics –> flucloxacillin, coamoxiclav, erythromycin, nitrofurantoin

steroids

sulphonylureas - (gliclazide)

Chlorpromazine, prochlorperazine (1st gen antipsychotic D2 antagonists, antiemetics)

Question 50

Does a raised alkaline phosphatase always mean posthepatic damage?

What are the common causes of raised alkaline phosphatase?

Mnemonic for remembering causes of raised ALP?

Answer 50

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

Question 51

What would the thyroid function tests look like for:

1) primary hypothyroidism
2) secondary hypothyroidism
3) primary hyperthyroidism
4) secondary hyperthyroidism

Answer 51

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

Question 52

How should you go about interpreting a chest xray?

Answer 52

DRSABCDE

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

Question 53

Causes of tracheal deviation?

Answer 53

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

Question 54

PA VS AP on CXR

Answer 54

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.

Question 55

What are the signs of heart failure on a CXR?

Answer 55

ABCDE

Alevolar oedema (in a batwing distribution)

Kerley B lines - interstitial odema

Cardiomegaly

upper lobe Diversion (diversion of blood to upper lobes)

pleural Effusion

Question 56

Best technique for interpreting ECG?

Answer 56

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

Question 57

Bundle branch blocks: how do you work this out on ECG?

Answer 57

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

Question 58

What does a narrow therapeutic mean?

What are drugs known to have a narrow therapeutic index?

Answer 58

narrow therapeutic index = small difference in blood concentration between therapeutic and toxic effects.

Most common:

Digoxin

theophylline

lithium

phenytoin

abx - gentamycin, vancomycin

Question 59

Data interpretation:

SIADH causes

Answer 59

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)

Question 60

What are the penicillin antibiotics?

Answer 60

Phenoxymethylpenicillin

benzylpenicillin

flucloxacillin

amoxicillin

ampillicin

coamoxiclav - augmentin

cofluampicil (magnapen)

piperacillin with tazobactam - Tazocin

Ticarcillin with clavulanic acid - timentin

Question 61

How do we respond to inadequate response to drug and low serum level?

Answer 61

Increase the dose by the smallest increment possible

Question 62

How do we respond to an adequate response to a drug and normal or low serum drug level?

Answer 62

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

Question 63

How do we respond to adequate response to drug but high serum levels?

Answer 63

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.

Question 64

Gentamicin - what type of antibiotic is it?

What is it used for?

what are common doses used? under what circumstances?

Answer 64

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

Question 66

How do we monitor gentamicin levels with the once daily regimen?

Answer 66

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

Question 67

How do monitor gentamicin on the daily divided dosing?

Answer 67

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.

Question 68

How is paracetamol metabolised in the body & how does this relate to toxicity?

How do we treat paracetamol OD?

Answer 68

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.

Question 69

How do you use a paracetamol normogram?

when do we just give NAC regardless in paracetamol OD?

Answer 69

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.

Question 70

Warfarin

MOA

INR meaning

INR target on warfarin normally?

INR target on warfarin with metal heart valves or recurrent VTE?

Answer 70

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

Question 71

How do we manage major bleed and warfarin dosing?

Answer 71

Major bleed and warfarin:

stop warfarin

give 5-10 mg IV vitamin K

Give prothrombin complex (e.g. beriplex) (replace the clotting factors immediately)

Question 72

Management of high INR on warfarin:

If INR > 8?

INR > + minor bleed?

INR 5- 8 minor bleeding?

INR 5-8 no bleeding?

Answer 72

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.

Question 73

Common signs of drug toxicity with :

Digoxin

Lithium

Phenytoin

Gentamicin

Vancomycin

Answer 73

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

Question 74

Communicating information:

Key points for ACE inhibitors

Answer 74

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.

Question 75

Communicating information:

Tamoxifen

MOA

Risks

Timing and side effects?

SE

Answer 75

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.

Question 76

Communicating information:

Metformin

MOA

1st line for what?

Contraindications?

Common SE?

Starting metformin?

Answer 76

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.

Question 77

Communicating information:

Sulfonylureas

MOA?

SE’s

Special information on timings of taking, how to take, splitting doses

Answer 77

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.

Question 78

Communicating information: Methotrexate

MOA

SE

Pregnancy

Interactions

Key information - frequency of dosing

Monitoring

Answer 78

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.

Question 79

Communicating information:

Warfarin

MOA

Indication

SE

Monitoring

Interactions

Answer 79

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

Question 80

Inhibitors of P450 system (that increase bleeding risk with warfarin)

Answer 80

Abx –> ciprofloxacin, clarithromycin, erythromycin, isoniazid (TB)

omeprazole

amiodarone

allopurinol

imidazoles - ketoconazole fluconazole

SSRIs

Sodium valproate

acute alcohol intake

Question 81

Inducers of P450 system - makes warfarin less therapeutic

Answer 81

AEDs - phenytoin, carbmazepine, barbiturates

rifampicin

st johns wort

chronic alcohol intake (clotting increases)

smking

Question 82

Communicating information: Steroids

Key SE’s and monitoring of those?

Other SEs

Stopping treatment

Answer 82

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.

Question 83

Communicating information: SSRIs

MOA & names

SEs

Treatment duration / switching antidepressant

Answer 83

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)

Question 84

Serotonin syndrome : symptoms

Answer 84

N & V

Agitation, confusion, drowsiness, hallucinations

tremor, nystagmus

dilated pupils

hyperthermia

tachycardia & hypertension

convulsions & muscle rigidty

rhabdomyolysis

Question 85

Communicating information:

Bisphosphonates

Answer 85

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).

Question 86

Drug monitoring:

Vancomycin

Which parameter should be monitored?

serum creatinine, serum ALT, CRP , neutrophil count or platelet count?

Other SE’s?

Answer 86

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

Question 87

Drug monitoring:

Statins

Which should be monitored?

serum ALT, BP, creatinine kinase, serum albumin or weight?

Answer 87

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.

Question 88

Drug monitoring: Phenytoin

Key points

Answer 88

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.

Question 89

Drug monitoring: Lithium

MOA

Indication

Therapeutic range

SE

Monitoring

what can increase the risk of toxicity?

Answer 89

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

Question 90

Drug monitoring: Methotrexate

Key points to remember:

When to monitor and what/ how often

How does this differ when stabilised?

An important risk with treatment that should be monitored? What should patients be told to look out for?

When should treatment not be started?

How is it excreted?

Answer 90

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

Question 91

Drug monitoring :

Olanzapine

Type of antipsychotic

SE’s associated

monitoring required

Answer 91

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.

Question 92

Drug monitoring: COCP

MOA

Uses

SE ‘s to counsel patients on

Increase in risk of what?

Monitoring required

Answer 92

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.

Question 93

COCP : advise for patients:

MOA

Benefits / disadvantages

Drug interactions

Missed pill rules

Vomiting and diarrhoea

Answer 93

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.

Question 94

Drug monitoring:

Amiodarone

MOA

SE

Monitoring

Answer 94

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

Question 95

Drug monitoring:

Carbimazole

MOA

Indication

SE/ Drug monitoring

Answer 95

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.

Question 96

Drug monitoring: ACE i

Answer 96

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.

Question 97

Drug monitoring: Digoxin

Answer 97

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.

Question 98

Digoxin toxicity

when does it occur

Features

causes

Answer 98

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).

Question 99

Drug monitoring : sodium valproate

Answer 99

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
  *

Question 100

Adverse drug reactions:

what are the two important types of reaction to know about?

How do they differ?

Answer 100

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.

Question 101

ADR’s

The most important SEs for:

Gentamicin

&

Vancomycin?

Answer 101

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

Question 102

ADR :

important SE to know for ACEi ?

Important interactions to know for ACE i

Answer 102

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

Question 103

ADR

Important Side effects for beta blockers

Important drug interactions to know for beta blockers

Answer 103

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!

Question 104

Important SEs to know for CCBs

Two types & different SE profile

Answer 104

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.

Question 105

ADR

K+ sparing diuretics

Answer 105

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.

Question 106

ADR:

thiazide

Answer 106

SE thiazides:

Hypotension

hyponatraemia, hypokalaemia, hypercalcaemia

hyperuricaemia (gout)

impaired glucose tolerance

impotence

Rarer- photosensitivity rash, thrombocytopenia, agranulocytosis, pancreatitis

Question 107

ADR:

Loop diuretics SEs

Answer 107

Hypotension

hyponatraemia, hypokalaemia, hypomagnesaemia, hypocalcaemia

Hypochloraemic alkalosis

ototoxicity

renal impairment

hyperglycaemia

gout

Question 108

ADR:

Heparin

what are the two types and how do they differ?

What are the SE common to both?

What are the different uses for both?

Answer 108

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

Question 109

ADR:

Aspirin SEs

Answer 109

Key SE: haemorrhage, peptic ulcer and gastritis, tinnitus in large doses (& hearing loss + vertigo)

Rarely- asthma attack/ bronchospasm

Question 110

Warfarin key side effects

Answer 110

Common - Haemorrhage

Rare - alopecia, N&V

Not known freq - Blue toe syndrome, skin necrosis & skin reactions

Question 111

warfarin: drugs that lead to too much anticoagulation

Answer 111

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.

Question 112

Cytochrome P450 system:

What other region of the body contains this enzyme system?

What can cause a problem?

how long does it take to induce the cytochrome p450 system?

how long does it take to inhibit the cytochrome p450 system?

Answer 112

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.

Question 113

ADRs: Digoxin SEs

Answer 113

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!

Question 114

ADRs:

Amiodarone SEs

Answer 114

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
  *

Question 115

ADR: Lithium key side effects

Answer 115

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

Question 116

ADR : lithium toxicity features

Answer 116

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

Question 117

ADRs : 1st generation antipsychotics

Name them

Common SE’s

Answer 117

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

Question 118

ADR’s : second generation (atypical ) AP’s

Common SE profile

Answer 118

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.

Question 119

ADR’s:

Clozapine SE

Blood monitoring required?

Interactions with the environment?

Answer 119

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.

Question 120

ADR: corticosteroid SEs

Withdrawing from steroids - what is the advice?

Answer 120

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

Question 121

ADR : statins KEY SE

Answer 121

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

Question 122

Drugs with potent interactions with alcohol:

GI bleeding by?

increased anticoagulation by?

sweating / flushing/ nausea and vomiting by?

lactic acidosis by?

hypertensive crisis by?

sedation by?

Answer 122

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

Question 123

ADRs :

metformin SE

Answer 123

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.

Question 124

ADR’s: sulphonylureas

Answer 124

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

Question 125

What medications worsen psoriasis?

Answer 125

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.

Question 126

Drug monitoring : Digoxin & renal impairment

Answer 126

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.

Question 127

Prescribing in patients with asthma & COPD

4 drug classes to be aware of in terms of cautions and contraindications?

Answer 127

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.

Question 128

Which drugs may worsen seizure control in epilepsy?

Answer 128

• 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

Question 129

Prescribing in patients with heart failure

Answer 129

• 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)

Question 130

What drugs should be used with caution in ischaemic heart disease?

Answer 130

NSAIDS

Oestrogens - COCP / HRT

Varenicline (nicotine receptor partial agonist to aid smoking cessation)

Question 131

Prescribing in breastfeeding

Drugs to avoid

Answer 131

Avoid:

Antibiotics - ciprofloxacin, tetracycline, chloramphenicol, sulphonamides

Psychiatric dugs - lithium, BZDs, clozapine

Aspirin - risk of reyes syndrome

carbimazole

methotrexate

sulfonylureas

cytotoxic drugs

amiodarone

Question 132

Prescribing in pregnancy

Common examples to avoid

Answer 132

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

Question 133

which drugs are usually taken at night?

Answer 133

Statins

Amitryptiline

Question 134

Prescribing in patients with renal failure:

Drugs to avoid?

Drugs that accumulate in CKD?

Answer 134

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

Question 135

What are some of the important types of insulins to know?

Answer 135

• 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

Question 136

Management section:

Stable angina

Answer 136

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)

Question 137

Management:

Nitrate tolerance - what is it?

how do we manage it

Answer 137

• 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

Question 138

Management : STEMI

Common management of ACS

Management specific to STEMI

Answer 138

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

Question 139

Management: NSTEMI / unstable angina

Answer 139

• 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.

Question 140

Hyperglycaemia mangament in ACS?

Answer 140

Keep blood glucose levels below 11 mmol/L

Consider dose adjusted insulin infusion with regular monitoring of insulin levels

Question 141

Management:

Secondary prevention in ACS

Answer 141

• 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

Question 142

Management: HTN

Stages of HTN

How do we manage HTN (draw the flow chart)

What are the BP targets by age?

Answer 142

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

Question 143

CCB for HTN - which is first line?

Answer 143

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

Question 144

Management: Preventing contrast induced nephropathy

Answer 144

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.

Question 145

Management: Hypothyroidism

Drug used?

starting dose for elderly vs younger patients?

Target range TSH

Pregnancy and hypothyroidism?

SE of medication

Interactions

Answer 145

• 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

Question 146

Paracetamol overdose: Management

Answer 146

• 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

Question 147

Management: Emergency contraception:

What are the two methods?

What are the two drugs?

Key information for each drug - MOA, timeframe it can be taken in, SE, can hormonal contraception be started after?

Answer 147

• 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

Question 148

Management T2DM

Answer 148

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

Question 149

Management: Respiratory Infections:

Commonly prescribed for:

Epiglottitis

Bronchietasis

Exacerbations COPD

CAP

Pneumonia by atypical pathogens

HAP

Answer 149

• 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

Question 150

Management: Antibiotics for UTI

Duration of antibiotics for: simple infection (non pregnant women), men, pregnant women, catheter associated UTI. Immunosuppresses/ abnormal anatomy or kidney function.

Lower UTI - non pregnant women

Lower UTI - men

Lower UTI - pregnant women

Prostatitis

Pyelonephritis

Answer 150

• 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

Question 151

Management: Antibacterial for skin infections

Impetigo

Answer 151

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

Question 152

Management: antibacterial for skin infections

Cellulitis

Cellulitis near eyes and nose

Erysipelas

Animal or human bite

mastitis during breastfeeding

Answer 152

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

Question 153

Management: ENT infections

Throat infection

Sinusitis

Otitis media

Otitis externa

Periodontal abscess

Gingivitis

Answer 153

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)

Question 154

Management: Genital tract infections

Bacterial vaginosis

Candidiasis

Chlamydia

Gonorrhoea

Syphilis early & late (cover for contacts)

PID

Answer 154

• 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)

Question 155

Management: GI infections

C diff

Campylobacter

Diverticulitis

Salmonella

Shigella

Typhoid

Answer 155

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

Question 156

ADR’s:

Drugs causing urinary retention

Answer 156

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

Question 157

ADR:

Drugs causing confusion

Answer 157

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

Question 158

Management:

Constipation:

Name the 4 classes of laxatives and the drugs within those classes

Extra - prokinetic laxative

Answer 158

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.

Question 159

Management: Constipation:

Contraindiations to prescribing laxatives?

Answer 159

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

Question 160

Management: constipation < 3 months

Answer 160

• 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)

Question 161

Management: constipation > 3 months

Answer 161

• 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.

Question 162

Constipation:

Drug causes

Answer 162

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

Question 163

Organic causes of constipation

Answer 163

• 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

Question 164

Management: Faecal impaction

Answer 164

• 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

Question 165

Management of stress incontinence in women

Lifestyle advice

1st line management

Medical options

Surgical options

If surgical fails/ is declined?

Answer 165

• 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

Question 166

Urge incontinence management:

1st line option

2nd line medical managment

3rd line medical management

Surgical/ invasive management

Answer 166

• 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