CPTP Flashcards
1
Q
In liver disease patients, WHICH 5 drugs which have high extraction rates (high first pass metabolism) should be given a reduced dose if taken orally as that first pass metabolism does not take place
Equally name the pro-drugs that is not themselves active, they need to be metabolized into the active drug and so in liver disease less drug is turned into the active form - requires increased dose
A
Aspirin Levodopa Morphine Salbutamol Propranolol
PPI
2
Q
List common medicines that are especially likely to cause harm to patients with impaired liver function
A
Antibiotics Paracetamol Statins Methotrexate Phenytoin Aspirin Alcohol Oral contraceptives Isoniazid
3
Q
Drugs which can precipitate hepatic encephalopathy
diabetic drug which is not affected by liver too much so ok to use in liver disease
A
Sedatives, opioids, diuretics, drugs that cause constipation
Sulphonylureas - Gliclazide
4
Q
Peptic ulcer disease
Causes
Sx
Perforation management
A
H.Pylori, Zollinger-Ellison syndrome, steroids, NSAIDs, bisphosphonates, alcohol, smoking, diet or obesity
Gastric ulcers are worse on eating (worse on eating with back pain indicates pancreatitis) and thus patients lose weight. Duodenal ulcers are better on eating and thus patients can gain weight. Patients can be anaemic due to blood loss.
Malaena, haematemesis or shock indicates an upper GI bleed or perforation = Adrenaline + endoscopy with clip/burn of arteries.
5
Q
Upper GI conditions, definition and Ix Dyspepsia Peptic ulcer Gastritis GORD Achalasia
A
Dyspepsia or indigestion often has no known cause, with normal hb, negative urea breath test and psychosocial factors
Peptic ulcer refers to visible ulceration on endoscopy due to increased acid production, often H.pylori
Gastritis is inflammation of the stomach, endoscopy is gold standard, hb will be normal
GORD is due to failure of the LOS which allows acid to wash up the oesophagus and risks Barret’s Oesophagus. Hiatus hernia often present,
improves symptoms, OGD can show Barrett’s, ambulatory pH monitoring is gold standard
Achalasia is due to inability of LOS to relax, oesophageal manometry is gold standard
6
Q
With regards to upper GI what alarm Sx would prompt endoscopy before PPI?
VBAD
A
VBAD Vomiting Bleeding/anaemia Abdominal mass/weight loss Dysphagia
7
Q
If heartburn is not due to NSAIDs or GORD then what Ix next?
A
H.pylori test – carbon 13 urea breath test – as H.pylori produces urease which breaks down urea, creating hydrogen, which is detected in the breath
OR stool antigen test
OR if during an endoscopy then urea rapid urease test from endoscopy biopsy
If H.pylori positive then start eradication (PAC/PAM 1 week)
If H.pylori negative then start empirical PPI or H2 receptor antagonist treatment
Then if still Sx endoscopy
8
Q
PPI
Mechanism
Contraindications
Examples
A
PPIs cause irreversible inhibition of H/K ATPase responsible for H+ secretion from parietal cells
Potent acid reduction thus increased risk of c.diff and pseudomembranous colitis – thus maybe stop PPIs during antibiotics
Can interact with clopidogrel and impair its effect
Acute interstitial nephritis
Omeprazole, lansoprazole
9
Q
H2R antagonists
Mechanism
Contraindications
Examples
A
H2 receptor antagonists competitively block the action of histamine on the parietal cell by antagonising the H2 receptor thus less acid secreted
Cimetidine should be avoided in patients on warfarin, phenytoin as it inhibits the p450 enzyme thus warfarin will be stronger etc
Ranitidine, cimetidine
10
Q
H.pylori eradication regime
A
PAC/PAM PPI, amoxicillin + clarithromycin PPI, amoxicillin + metronidazole 1 WEEK! Continue PPI for 2months!
11
Q
Drugs causing upper GI Sx NSAIDs Steroids CCR antagonists Theophyllines Bisphosphonates Nitrates
A
NSAIDs = gastritis and peptic ulcers Steroids = gastritis and peptic ulcers CCR antagonists = gastritis Theophyllines = gastritis Bisphosphonates = Oesophageal erosion and ulceration Nitrates = reflux
12
Q
Bulk forming laxative
Mechanism
Contraindications
Examples
A
When taken with water, it increases the volume of non-absorbable material (fibre) in the gut, which increases colon distension and stimulates peristaltic movement
Intestinal obstruction/atony, dysphagia, not for opiate induced
Ispaghula husk
13
Q
Osmotic laxative Mechanism Contraindications Examples Other use
A
Sit inside the lumen of the gut, attract water via osmosis, increase the water content of the stool (this adds to the bloated feeling), this distends colon and stimulates peristaltic movement
Not for obstruction
Lactulose, movicol, macrogel
Also for hepatic encephalopathy (higher dose)
14
Q
Stimulant laxative Mechanism Indication Contraindications Side effects Examples
A
Increase GI peristalsis + Increase water and electrolyte secretion by the mucosa
Good to empty bowel before procedures + for opiate induced
Obstruction (peristalsis against an obstruction) = bad
Danthron is carconogenic
Damage to nerve plexuses – atonic bowel
Senna
15
Q
Faecal softners Mechanism Indication Side effects Examples
A
Promote defecation by softening the stool (Docusate sodium)
Promote defecation by lubricating the stool (Liquid paraffin)
Allows water to enter stool more readily. Requires another laxative to really work!
Faecal impaction
Haemorrhoids
Anal fissures
Long term Liquid paraffin use can impair absorption of fat soluble vitamins
Docusate sodium, Liquid paraffin
16
Q
What can be used when rapid bowel evacuation is required?
A
Magnesium salts
17
Q
NICE guidelines for under 55s and over55s concerning dyspepsia Sx
A
<55y = ‘Test and Treat’
Test for H.pylori (Urea breath test or stool antigen)
Treat with 4 weeks full dose PPI (low dose when proven non-ulcer)
> 55y with unexplained/persistent Sx = URGENT endoscopy referral
Don’t prescribe PPI pre-endoscopy as need to be off acid suppression for >2weeks prior to endoscopy
18
Q
Therapeutic pathway for h.pylori +ve and -ve PEPTIC ULCERS with caveat for -ve gastric ulcer
A
H.pylori +ve:
PAC/PAM (Triple therapy)
PPI, amoxicillin + clarithromycin
PPI, amoxicillin + metronidazole
1 WEEK!
Then PPI for 2 MONTHS! Then retest for H.pylori + follow up endoscopy IF gastric ulcer
Stop NSAIDs until ulcer healed and then reassess need
H.pylori -ve:
PPI for 2 MONTHS
+ endoscopy after 2 months if gastric ulcer
19
Q
Therapeutic pathway for NON-ULCER dyspepsia
So theyve got Sx and had an endoscopy but no ulcer
A
‘Test and treat’
- ‘Test’ for H.pylori
- ‘Treat’ with 4 weeks low dose PPI (high dose if didn’t know there was no ulcer)
20
Q
Post upper GI bleed care (after the adrenaline / clipping at endoscopy)
IV PPI shown to reduce risk of rebleeding!
A
- Monitor for signs of rebleeding (Rockall score)
- 80mg omeprazole bolus IV STAT
- 8mg/hour omeprazole for 72hours IV
- High dose oral PPI for 2 months
- Avoid NSAIDs
- Repeat endoscopy after 8weeks for gastric ulcer
21
Q
Treatment for c.diff (ABx use, PPI use, old, profuse, fever, CRP, WCC, toxic megacolon)
A
Metronidazole + Vancomycin
22
Q
Loperamide indications and contraindications
A
Indications: Mild infective diarrhoea IBS Chronic IBD High output stomas
Contraindications: Severe UC or c.diff > Toxic megacolon Severe infective diarrhoea Dysentery (bloody stool) Liver disease (risk of accumulation)
(Doesnt cross BBB so no euphoria)
23
Q
Management for uncomplicated faecal loading constipation
A
First line treatment is dietary modification and attempt to mobilise and change lifestyle factors, only then consider drugs
Use drugs for short durations only
Oral/IV rehydration + laxative
24
Q
Type2Diabetes drugs
BIGSS
A
Biguanides - Metformin Incretins - DPP-IV inhibitors (Gliptins) + GLP-1 mimetics Glitazones - Pioglitazone Sulphonylureas - Gliclazide SGLT2 inhibitors
25
```
Metformin
Mechanism
Indications
Side effects
Weight
Hypoglycemia?
```
Inhibits hepatic gluconeogenesis + increases peripheral uptake of glucose
Good for metabolic syndrome + lipids
Nausea + diarrhoea, lactic acidosis due to accumulation of metformin metabolites, made worse if CKD
Weight loss
No hypos
26
Sulphonylureas (gliclazide)
Mechanism
Weight
Hypoglycemia?
Mimic action of glucose and bind to SU receptor in pancreatic B cells, which closes K+ channels > depolarization > calcium influx > insulin secretion from Beta cells
-SU Secretes insulin-
Weight gain + hypos!
27
```
Glitazones (pioglitazone)
Mechanism
Side effects
Weight
Hypoglycemia
```
Bind to Peroxisome proliferator activated receptors (PPARs) to increase insulin sensitivity/performance thus:
1. Increased lipogenesis = use of glucose
2. Decreased lipolysis = release of glucose
Heart failure/ fluid retention
Weight gain + hypos (small risk)
28
SGLT2 inhibitors (sodium glucose reabsorption channel)
Mechanism
Side effects
Weight
Prevent renal glucose (and sodium) reabsorption from the SGLT2 channel in the proximal tubule – lose sugar in the urine, less in the bloodstream > weight loss
UTIs + oral thrush
Weight loss
29
What are Incretins?
Incretins are hormones released by intestinal endocrine cells in response to food/glucose, resulting in insulin release from beta cells in a glucose dependent manner, and reduced hepatic gluconeogenesis via less glucagon secretion from alpha cells. However only last 1-2hours. We can either give GLP-1 (incretin) mimetics or DPP-IV inhibitors as that usually inactivates incretins.
30
```
DPP-IV inhibitors (Gliptins)
Mechanism
Indication
Side effects
Weight
Hypoglycemia
```
Inhibits DPP-IV which prolongs the half-life of GLP-1 to release insulin
Can be used in advanced renal failure
Pancreatitis
Weight loss
No hypos - only stimulate pancreas when blood glucose is rising
31
```
GLP-1 mimetics (Liraglutide, Exenatide)
Mechanism
Indication
Side effects
Weight
Hypoglycemia
```
DPP-IV resistant (usually breaks incretin down) but this drug is not affected = enhances incretin effects
Causes early satiety and thus good for weight loss
Sc injection + pancreatitis
Weight loss
No hypos
32
Type2 DM NICE guidelines
1. Lifestyle only
2. If HbA1c rises to 48 then add metformin
3. Increase metformin dose to achieve sub 48 HbA1c
4. If HbA1c rises to 58 then begin dual therapy by adding one of: sulfonylurea, DPP-4 inhibitor/gliptin, pioglitazone or SGLT-2 inhibitor
5. If HbA1c is still above 58 then begin triple therapy OR consider insulin (NPH isophane) therapy (Keep on metformin)
6. If triple therapy not effective, not tolerated or contraindicated and BMI >35 then add GLP-1 mimetic to metformin and sulfonylurea
33
Primary prevention statin
Secondary prevention statin
Primary prevention:
10 year CVD risk >10% OR T1DM OR eGFR <60 CKD = Atorvastatin 20mg
Secondary prevention:
Known IHD, CVD, PAD = Atorvastatin 80mg
34
Explain DKA and HHS
Relative (HHS) or absolute (DKA) insulin deficiency stimulates hepatic glucose production, which results in hyperglycaemia, osmotic diuresis and dehydration. In severe insulin deficiency, the liver will augment ketone body production, culminating in hyperketonaemia and, eventually, acidosis.
35
Diagnostic criteria for DKA
11,3,15
and other non diabetic causes
In the name: DIABETIC11 KETONE3 ACIDOSIS15
Capillary blood glucose >11mmol/L
Capillary ketones >3mmol/L OR Urine ketones ++ or more
Venous pH <7.3 and/or bicarbonate <15mmol
Other causes: Atkins diet, liver failure, starvation
36
Anion gap
(Na +K) - (HCO3 + Cl): N= 16+/- 4
(Na) - (HCO3 + Cl): N= 12+/- 4
Assess metabolic acidosis to see if its due to:
High = DKA or renal failure or lactic acidosis
Normal: Drop in HCO3-, covered by Chlorine
Low = Hypoalbuminemia
37
DKA guidelines
1. Fluid (Kcl if <5.5)
2. Insulin
3. Glucose
4. SC insulin (discontinue insulin infusion 30mins later)
1. ABC then check hospital protocol
2. Commence FLUID repletion 0.9% NaCl – large bore cannula via infusion pump – then KCl/potassium replacement (if K<5.5)
3. Commence fixed rate IV insulin infusion – rapid acting 6u/hour (0.1u/kg) or weight dependent (Alongside their normal insulin regime)
4. Further Ix – GCS, get usual DM Dr, blood glucose + all bloods, ECG, cultures, CXR, MSU, anion gap
5. Establish monitoring regime – hourly BM, hourly ketones, hourly/2hourly venous bicarbonate and K+, 4 hourly U&Es + cardiac monitoring, pulse oximeter
6. If patient alert, parameters normalising- commence 10% glucose alongside 0.9% saline infusion (avoid hypo)
7. Once patient eating & drinking normally- switch to fast-acting SC insulin with a meal and discontinue insulin infusion 30 minutes later, stop IV fluids
38
Once patient is recovering from DKA and has had first SC insulin how long do you continue running the insulin infusion for?
30 minutes
39
DKA fluid repletion based on BP
SBP <90: 500ml 0.9% NaCl over 10-15mins – repeat until >90
SBP >90: 1000ml 0.9% NaCl over 60mins
Continue fluid replacement with addition of KCl if <5.5
40
Hypoglycemia
Definition
Sx
Mx
Treat any capillary BM <4mmol/L as a hypo
Lack of glucose causes autonomic (sweats + palpitations), neuroglycopenic (confusion) and general malaise
1. Food 2. Glucogel 3. Glucagon
Conscious and able to swallow:
1. 15-20g quick acting carbohydrate, repeat with BM reading every 10-15mins until >4.
2. If no improvement, consider 1mg glucagon IM.
3. Once recovered give long acting carbohydrate – biscuit or toast + insulin injection if due
Conscious but confused, but able to swallow:
1. As above but with glucogel every 10-15mins
2. Use IM glucagon if glucogel not effective
Unconscious +/- seizures +/- aggressive:
1. ABCDE
2. Glucagon 1mg IM OR 80ml 20% glucose IV over 10-15mins (faster than IM)
3. Recheck BM after 10mins
4. If BM <4 repeat glucose bolus
5. If BM >4 give long acting oral carbohydrate
41
Diabetes and pregnancy
Folic acid
During labour
Post-partum
5mg/day Folic Acid pre-conception until 13weeks post conception
During labour give GKI (Glucose, potassium, insulin) infusion OR separate Dextrose and Insulin infusion (allows alteration to insulin dose) to maintain glucose at 4-7, monitor every 30mins-1hour
Diabetes worsens during pregnancy as insulin resistance increases via placental hormones, as such more insulin is required during pregnancy. Post-partum there is increased insulin release by body and so decrease insulin infusion by 50%
42
Type2 DM guidelines
1. Lifestyle
2. Metformin at 48
3. Metformin + 1 at 58
4. Metformin + 2 OR insulin if still above 58 with double therapy
43
Diabetes surgical management
Type1: Stop insulin + GKI infusion
Type2: Stop sulfonylurea (risk of hypo) on morning / metformin 48hours before
44
Statins
Indication
Adverse effects
Contraindications
10 year CVD risk of 10% OR GFR <60 = 20mg atorvastatin
OR 80mg if known severe CVD
Myositis - high CK, hepatitis - jaundice, LFTs
Macrolide antibiotics + antifungals + grafefruit + amiodarone = AKI due to rhabdomyolysis
Don't use in hypothyroid or renal impairement
45
Dopamine mechanism pathway
1. Pre-syn neurone: Tyrosine > L-Dopa > DA (Via DA decarboxylase)
2. Degraded by COMT in synapse
3. Then re-taken up into pre-syn neurone- degrade by MAO-B
46
Levodopa
Indication
Adverse effect
Gold standard + first line
Give with dopamine decarboxylase inhibitor
Long term patients WILL get involuntary abnormal movements – dyskinesias – manage with smaller doses more frequently
47
Levodopa + dopamine agonist side effects
GI
Dementia
Postural hypotension
Sleep disorders
48
Dopamine agonists
Indication
Adverse effects
Treat motor features in early disease and cause less dyskinesia than levodopa so useful in young
Cognitive impairment thus dont use in elderly
IMPULSE CONTROL DISORDER!
ORTHOSTATIC HYPOTENSION!
49
```
Mono-Amine Oxidase B inhibitors
Mechanism
Indication
Adverse effects
Example
```
Inhibits MAOB thus less breakdown of dopamine and so more left in the synaptic cleft
Weak clinical effect thus used in mild/adjuvant
First line? in young as may be neuroprotective
Serotonin syndrome if combined with an SSRI
Rasagiline
50
First line Ix in Parkinsons
Dopaminergic agent trial
51
Catechol-O-methyl transferase COMT inhibitors
Mechanism
Indication
Adverse effects
Inhibits L-dopa from being peripherally broken down by COMT into 3-0 methyl dopa, increasing the amount available for conversion to dopamine in the brain and reducing fluctuations in plasma levels.
Usually given alongside carbidopa/levodopa
Discolourisation of bodily fluids
52
Amantadine (antiviral)
Indication
Adverse effects
Used later in disease to control dyskinesia complications
Can cause dementia so avoid in elderly
Also can cause Livedo reticularis
53
Anticholinergics
Indication
Adverse effects
Best in young to combat prominent tremor
not in elderly as can cause cognitive impairment
AcH SEs: Dry, glaucoma, blurred vision
54
Parkinsons disease treatment pathway
Young
Old
Complications
Young:
MAO-B inhibitor + Dopamine agonist >>> L-dopa + COMTi
Old:
L-dopa >>> MAO-B inhibitor + COMTi
Complications:
Dyskinesia >>> Reduce l-dopa + amantadine
Severe tremor etc >>> SC apomorphine + deep brain stimulation
Given the higher risk of dyskinesias in young patients with carbidopa/levodopa, and the higher risk of orthostasis and hallucinations in older patients with dopamine agonists, dopamine agonists are often the initial treatment of choice in younger patients (<70 years), while carbidopa/levodopa may be the initial treatment in older patients (>70 years).
55
Drug induced parkinsonism
| Sx
Sudden onset, bilateral (unusual) OR increase in symptoms of known PD patient
Dopamine antagonists: Neuroleptics – Clozapine, Haloperidol, Olanzapine
Metoclopramide, CCBs
Amiodarone, sodium valproate
56
Epilepsy classification
Generalised = Seizure involves both brain hemispheres and consciousness is affected - Absence, Tonic Clonic, Myoclonic (sudden muscle jerks), Clonic, Tonic, Atonic (drop attack)
Partial = Seizure activity starts in one area of the brain
Simple: Retains some awareness as to whats going on
Complex - Altered awareness and behaviour
Can progress to generalised seizure aka tonic clonic
57
```
Epilepsy Mx
Generalised tonic clonic
Absence
Myoclonus
Partial
```
TREAT ONLY AFTER 2 SEIZURES - only 50% have 2nd seizure
Generalised tonic clonic:
Sodium valproate
(?lamotrigine or levetiracetam in women)
Absence:
Ethosuximide (absences only) or Sodium valproate
(Lamotrigine if above unsuitable or not tolerated)
Myoclonus:
Sodium valproate
Partial:
Lamotrigine or carbamazepine
In myoclonus/absence- avoid carbamaz, phenytoin, pregabalin, etc
58
```
Anti-epileptic drugs side effects
Sodium valproate
Lamotrigine
Carbamazepine
Phenytoin
Diazepam
```
Sodium valproate: Weight gain, parkinsonism, teratogenicity, displaces phenytoin from albumin = phenytoin toxicity
Carbamazepine and Lamotrigine: Tiredness, double vision, unsteadiness, hyponatremia, neutropenia, RASH!
Phenytoin: Gum hyperplasia, osteomalacia, coarsening of skin, SLE
59
Which receptor do Sodium val and benzos work on? And which do all other anti-epileptic drugs work on?
GABA agonist
Na channel blocker
60
Epilepsy drugs that induce CYP450 and thus reduce levels of COCP
Drug which is inhibited by COCP
If COCP used with epilepsy what dose?
Carbamazepine + Phenytoin + Ethosuximide
Lamotrigine
50ug (any breakthrough bleed = ineffective)
Use depo or mirena coil
61
Status epilepticus
Definition
Mx
> 30 mins single seizure or multiple seizures without full recovery in between
1. ABC + >5mins give IV lorazepam or rectal diazepam if no IV
2. Repeat benzo at 20mins + alert anaesthetist
3. Give phenytoin infusion
4. Still fitting then intubate + induce coma
62
Indications for epilepsy surgery
Epilepsy refractory to medical treatment
Localised onset (if resective surgery)
Likely benefits outweigh risks
Disabling
63
Since lamotrigine + sodium valproate can cause fetal abnormalities which drug should be used in epilepsy during pregnancy?
Eclampsia Dx
Breastfeeding is fine
Carbamazepine is 1st line + 5mg/day folic acid + vit K
ANY fit during pregnancy and upto 24hrs after delivery = eclampsia until proven otherwise = MgSO4
64
First things to do when finding fitting patient
collateral Hx + capillary blood glucose
65
Phenytoin monitoring
Ideal range
Toxicity Sx
10-20
In pregnancy, the elderly, and certain disease states where protein binding may be reduced, careful interpretation of total plasma-phenytoin concentration is necessary; it may be more appropriate to measure free plasma-phenytoin concentration.
In patients with renal failure associated with hypoalbuminemia, free phenytoin levels may be more accurate than total phenytoin levels.
Symptoms of phenytoin toxicity include nystagmus, diplopia, slurred speech, ataxia, confusion, and hyperglycaemia.
Phenytoin may cause coarsening of the facial appearance, acne, hirsutism, and gingival hyperplasia and so may be particularly undesirable in adolescent patients.
66
Acute alcohol withdrawal
Mx
complications
1. ABC
2. Chlodiazepoxide (lorazepam if hepatic failure)
3. IV thiamine + Mg + PO4 (PROTECT AGAINST SEIZURES)
Long term thiamine/B12 def = Wernickes encephalopathy
Sx: Ataxia + confusion + Opthalmoplegia (eyes) = ACE!
If goes untreated = Korsakovs syndrome = hallucinations and confabulations
67
Carbamazepine:
continue if on warfarin?
continue if raised GGT and low sodium?
Maybe better to use lamotrigine BUT regular INR monitoring can allow for both carbamazepine + warfarin together.
Raised GGT results from enzyme induction - monitor but if stable continue
Hyponatremia is due to SIADH (too much water absorbed from collecting ducts) - if asymptomatic then continue!
If nystagmus/ataxia occurs then reduce dose
68
Features which indicate drug induced parkinsonism?
Antipsychotics + anti-emetics + sodium valproate + lithium + CCBs + SSRIs
Subacute bilateral onset
Progression of symptoms concurrent with medication intake
Early presence of postural tremor
L-dopa MAY be useful for symptomatic relief
69
Would you perform a DAT scan following drug induced parkinsonism?
May help determine whether the patient already had a pre-existing dopamine deficit that was exposed by the Stemetil, or whether full recovery is unlikely
Expensive approx £800
70
ased on the relationship with levodopa dosing, dyskinesia most commonly occurs at the time of peak L-DOPA plasma concentrations and is thus referred to as peak-dose dyskinesia.
how do we prevent this?
How do we treat this?
Prevention:
Delaying use of L-dopa –”sparing” strategy
```
Treatment:
Reduce dose of L-dopa
Amantadine
Duodenal infusion of L-dopa
Apomorphine infusion
```
71
Pros and cons of Deep brain stimulation for PD
Deep brain stimulation of subthalamic nucleus:
Improves motor fluctuations
Improves PD features and may permit drug dose reduction
Does not improve axial problems
May worsen speech
72
Beta2 agonists
Mechanism
Indication for short and long acting
Adverse effects
Act on beta2adrenergic receptor to cause smooth muscle relaxation
SABA: Salbutamol - quick Sx relief
LABA: Salmeterol - slow onset
Fine tremor, tachycardia, palpitations, hypokalemia
73
Muscarinic antagonists
Mechanism
Indication
Adverse effects
Antagonise effects on acetylcholine at M3 receptors to cause smooth muscle relaxation
Useful in patients who are unable to tolerate adrenergic agonists (patients with ischaemic heart disease or tachycardia)
Generally reserved as adjunct in the management of acute severe asthma
Short-acting muscarinic antagonists (SAMA) e.g ipratropium bromide
Long-acting muscarinic antagonists (LAMA) e.g tiotropium bromide
Dry mouth
74
Theophylline / phosphodiesterase inhibitor
Mechanism
Adverse effects
Loading dose
Inhibits phosphodiesterase to cause an increase in cAMP in smooth muscle cells
Nausea, diarrhoea, tachycardia, arrhythmias, irritability, Ha, toxicity- narrow TI = seizures (not great drug!)
Metabolised by CYP450
Do not give loading dose during acute emergency attacks of asthma IF already taking theophylline regularly
75
Leukotriene receptor antagonist/ Montelukast
Mechanism
Indication
Adverse effects
Leukotriene antagonists inhibit the cysteinyl L1 receptor
Not used in acute situations. Better for prophylaxis
Good for nasal polyps/allergic asthma
Because the leukotriene pathway is just one of several process responsible for the inflammatory response in asthma, they are less effective than inhaled corticosteroids, but have very few side effects
76
Corticosteroids
Mechanism
Indication
Adverse effects
Bind to glucocorticoid receptors in airway and reduce lung inflammation and mucus production - o ↑FEV1, ↑am PEF, ↓AHR (measure of inflam)- night sx resolve before day sx
ALL patients with asthma should take ICS to control inflammation!
Can increase incidence of LRTI in elderly
Oral candida (rinse mouth out after use), hoarseness, cushings, bruising.
77
IgE monoclonal Ab e.g omalizumab
Monoclonal Ab binds to IgE
Treatment of severe persistent confirmed IgE-mediated asthma needing continuous or frequent (≥4 courses/yr) oral corticosteroids
Only used by specialists respiratory physicians
78
Asthma diagnostic algorithm
1. Hx indicates asthma (night time, wheeze, chest tightness)
2. Reversibility of airflow obstruction - improvement in FEV1 by 12% and 200 mL
OR
2. PEFR varies by at least 20% for 3 days in a week over several weeks or PEFR increases by at least 20% in response to asthma treatment
3. Challenge tests - try to induce asthma
4. Test for eosinophilic inflammation or IgE atopy
Only symptoms when cold > less chance of being asthma
79
Stepwise chronic asthma management
1. SABA
if using 3 or more times a week
2. ICS
3. LABA
If no response to LABA then STOP LABA then increase ICS dose
If some response from LABA then continue LABA but increase ICS
4. Theophylline, montelukast, muscarinic etc + increase ICS + Refer to specialist
5. Oral steroids
80
Drugs which may exacerbate asthma
B-blockers:
Cause bronchospasm > give prostaglandin analogues - Bimatoprost, Travoprost
NSAIDs:
Cause bronchospasm in sensitive > give clopidogrel
81
Stepwise acute asthma EMERGENCY management
O SHIT Mg
1. Oxygen - maintain 94-98%
2. Salbutamol nebuliser
3. IV hydrocortisone / Prednisolone (follow with oral for 5days)
4. Ipratropium nebuliser
5. Try nebulisers again
6. Magnesium salts
Do ABGs and CXR
82
```
COPD vs Asthma
Demographic
Sx
Variation
Reversibility
```
COPD occurs after 35 and is due to smoking/pollution
chronic dyspnoea and slowly progressing symptoms with sputum production = COPD
Asthma features diurnal variation AND PEFR improves by 15% post bronchodilator whereas COPD is not reversible
83
NICE guidelines for COPD FEV1/FVC = <70%
>50% predicted = ?
<50% or exacerbation Hx predicted = ?
Pneumococcal and influenza vaccination
Smoking cessation
Pulmonary rehabilitation
1. Everyone gets SABA as required
2. FEV1 >50% use LABA or LAMA
3. FEV1 <50% use LABA + ICS + LAMA
84
COPD exacerbation management
1. Oxygen - 88-92%
2. Nebulised SABA
3. 7-14day steroids
4. Antibiotics if purulent sputum or signs of consolidation > culture
5. Non-invasive ventilation NIV if hypercapnic failure
85
```
Pros and cons of:
Nebuliser
Nasal prongs
MC mask
Venturi mask
```
Nebuliser: High dose and easy for patient and carer BUT huge dose may cause systemic effects and expensive
Nasal prongs: Difficult to tell how much O2 patient is getting
MC mask: Standard
Venturi: Delivers precise O2 - best for COPD
86
Admit to hospital if WHICH features persist after initial therapy?
Acute severe asthma criteria
PEF 33-50% best/predicted
RR >25
HR >110
Inability to complete senteces in one breath
87
Admit if PEF is below WHAT %
50
88
Acute asthma severe and life threatening distinguished
Life threatening is <33% whereas severe is just 50%.
Severe is RR and HR whilst life threatening is silent chest, altered consciousness etc
89
What drug do you not give in asthma attacks
Lorazepam
90
Asthma attack penumonia
Pathogens
Theophylline CYP450 by Clarithromycin and ciprofloxacin complication
Strep pneumoniae
H. influenzae
M. catarrhalis
Atypicals e.g Mycoplasma
Note patient on theophylline
Clarithromycin and ciprofloxacin inhibit theophylline metabolism and increase theophylline concentrations
91
Discharge policy following asthma attack
PEF >75% + <25% variability - own PEF meter
Treatment with oral and inhlaed steroids
92
Name COPD drug used to decrease secretions/mucus
Mucolytic - Carbocisteine!
93
pH 7.31, pO2 6.8, pC02 7.4, Bicarbonate 34
| What does the ABG show?
Acute on chronic respiratory acidosis
Normally with respiratory acidosis the bicarbonate is LOW. The bicarbonate goes HIGH here to try and compensate for the acidosis, thus chronic, usually here the pH corrects to normal
94
Type 1 respiratory failure / VQ mismatch
Type 2 respiratory failure / Ventilatory failure
Type 1: o2 is low, pco2 is normal/low
Type 2: o2 is low, co2 is high - MUST BE GIVEN CONTROLLED OXYGEN WITH VENTURI MASK AND AIM FOR 88-92% - also monitor ABGs
95
If patient is in respiratory acidosis or tiring or type2 respiratory failure then instead of messing around with venturi mask use...
NIV
96
Long term oxygen therapy for COPD
Right sided ventricular strain + cor pulmonale
PaO2 <7.3
PaO2 7.3-8.0 and cor pulmonale
97
NICE definitions
Stage 1 HTN
Stage 2 HTN
Severe HTN
Stage 1: 140/90 + ABPM 135/85
Stage 2: 160/100 + ABPM 150/95
Severe: 180 / 110
98
Diagnosis of HTN
If the clinic BP is >140/90
Offer ABPM to confirm
99
Ix to check organ damage due to HTN
Kidneys: Urine dip (protein/blood), U&E, creatinine, GFR
Blood: glucose, cholesterol
Fundoscopy: hypertensive retinopathy
ECG
100
BP target for
Under 80
Over 80
Diabetes patients
Under 80: <140, ABPM <135
Over 80: <150, ABPM <145
Diabetes: <130
101
HTN NICE stepwise management
refer to specialist if under 40 and stage 1 to look for secondary causes
If only stage 1 HTN then only offer drugs if end organ damage or QRISK >20% and under 80
1: Under 55 = ACEi (or ARB if cough)
Over 55 or Afro-Caribbean = CCB
(A before C, younger first)
2. ACEi/ARB + CCB
3. + Thiazide
4. + Further diuretic or a/b blocker
102
```
ACEi
Mechanism
Indication
Contraindications
Adverse effects
Examples
```
Inhibit ACE > Reduced activity of RAS
Indication: young + HF. Post MI
Contraindication: Pregnancy + renal artery stenosis
Adverse effects: Hyperkalemia + angioedema + cough (not in ARB)
RENAL FAILURE! + in ARBs
Avoid with NSAIDs = renal damage (ACEi dilate efferent, NSAIDs constrict afferent)
Lisinopril + Ramipril
103
Calcium channel blockers
Mechanism
Indication
Contraindication
Examples
Block calcium = less excitation = less contraction = vasodilation + less force of contraction
Afrocarribean, elderly, ANGINA
Not to be used in HF > heart block
Amlodipine, Nifedipine
104
```
Diuretics
Mechanism
Types
Indications
Adverse effects
```
Decrease BP = decrease preload unlike CCBs which decrease afterload.
Thiazide - Bendroflumethiazide - Inhibits NaClCa channel = Less NaCl more Ca
Loop - furosemide - ~Fast acting, short duration - inhibits reabsorption of NaKCl = hypokalemia
ONLY DIURETIC SAFE I PREGNANCY
K+sparing - Amiloride (blocks ENaC), spironolactone - competitive aldosterone antagonist = hyperkalemia
Can cause gynaecomastia
good for patients with HF as treats both
Contraindicated in GOUT, RENAL FAILURE and ?? DM, hyperlipidemia, sexually active males
105
```
Beta blockers
Mechanism
Indication
Contraindication
Examples
```
blocks beta drenergic receptors = vasodilation, slower HR and weaker beat, reduced renin secretion
Angina, post MI, tachycardia, HF, AF
Don't use asthma, COPD, heart block
Atenolol, propanolol
106
Alpha blockers
Doxazosin
good for men - helps prostate
Contraindicated in women due to urinary incontinence
107
HTN and pregnancy
High risk eclampsia/HTN prophylaxis
BP target
Only HTN drugs used in pregnancy
75mg aspirin 12w-birth
Aim for <150/100
Methyldopa + nifedipine + labetalol
All others CI!
108
Heart Failure
| Ix
Audible third heart sound (‘gallop rhythm’)
ECG and BNP - if both normal HF unlikely
If ECG abnormal ie ST depression (old infarct) or BNP then do ECHO
ECHO confirms presence of LV dysfunction ie ejection fraction <55%
```
CXR: ABCDE
Alveolar oedema (bat wings)
Kerley B lines
Cardiomegaly
Upper lobe Diversion
Effusion
```
109
Acute heart failure management
1. Sit up and give high flow oxygen - IV access
2. furosemide 80mg IV as bolus injection
After stabilisation: ACEi + b blocker
110
Chronic heart failure management
Contraindicated drugs
Lifestyle
1st: ACEi (ARB if intolerant)
B blocker
2nd: Spironolactone
Sx control: Furosemide
Digoxin
CCBs are contraindicated in systolic HF!
111
```
Step 2 (alongside paracetamol)
NSAIDs
Mechanism
Indications
Dose
contraindications
```
Good for MSK / inflammatory pain
Work by inhibiting COX2 pathway
1st: Ibuprofen - 400mg tds > 800mg tds
2nd: Naproxen - 250-500mg bd
```
Contraindications: INCREASED IN ELDERLY
HF exacerbation > MI
Peptic ulcer
IBD?
Asthmatic with sensitivity
Liver or renal disease
Coagulation disorders
Inhibits bone healing
```
112
```
Step 2
Codeine + Tramadol
Mechanism
Indication
Adverse effects
```
```
Codeine:
First line!
Metabolised to morphine, extent varies by person
Require laxatives
Causes nausea
30-60mg QDS
```
Tramadol:
Synthetic opioid with multiple active metabolites.
Most commonly using following bowel surgery + chronic pain
Less constipation but more nausea
Avoid in elderly as can cause delirium + renal/hepatic failure
50-100mg QDS
113
```
Step 3
Morphine
Mechanism
Adverse effects
Overdose treatment
```
Morphine:
Acts on u-opioid receptor in CNS
Resp depression, sedation, pruritus, constipation - dont forget to exclude other causes!
Toxicity:
Features - myoclonic jerks, pin-point pupils, hallucinations, confusion, reduced RR
Action - reduce opiate dose by 30-50%.
consider Naloxone if RR <8 sats <90%
114
Pain ladder
```
Step 1: Non-opioid
1. Paracetamol
2. NSAIDs
Step 2: Weak opioids
1. Codeine
2. Tramadol
3. Dihydrocodeine
Step 3: Strong opioids
1. Morphine
2. diamorphine
3. Oxycodone
4. hydromorphone
5. Fentanyl
```
115
Adjuvant medications which can reduce opiate requirement in:
1. Muscle spasm
2. Bone pain
3. Bowel colic
4. Neuropathic pain
5. Raised ICP
1. Muscle relaxant - diazepam
2. Bisphosphonates
3. Antispasmodics
4. Antidepressants/Anticonvulsants
5. Corticosteroids
116
End of life prescriptions
1. Pain and breathlessness
2. Nausea and vomiting
3. Agitation
4. Excess secretions
1. Morphine
2. Cyclizine
3. Midazolam
4. Hyoscine Hydrobromide
117
1. Analgesia for #NOF
2. for post op pain
3. neuropathic pain
1. IV morphine (will be nil by mouth, maybe give anti-emetic and watch resp depression)
2. Co-codamol 30/500 2 tablets 6hrly and oramorph when required.
3. amitriptyline, gabapentin, pregabalin
118
Opiate drug calculations
General
Rules
Add regular dose to PRN dose to get a total 24 hour dose. This should then be given as the new regular dose.
The PRN dose should be between 1/6th and 1/10th of the total regular dose
Only increase dose by max 50%
119
```
Penicillin Beta lactams
Mechanism
Resistance
Adverse effects
Examples and indications
```
All have a beta lactam ring which helps inhibit cell wall formation by inhibiting cross linking peptidoglycan.
Beta lactamase (enzyme) producing bacteria stop the beta lactam ring from working. To overcome this resistance, β-lactam antibiotics are often given with β-lactamase inhibitors such as clavulanic acid.
ALLERGY + ANAPHYLAXIS (penicillin allergy)
Co-amoxiclav can cause cholestasis/LFTs. amoxicillin given to patients with EBV = rash
Flucloxacillin = s.aureus
120
Cephalosporins beta lactams
Generation
Route + indication
1st: Cephalexin > UTIs oral
2nd: Cefuroxime - IV
3rd: Cefotaxime/Ceftriaxone - IV crosses BBB for meningitis
121
Metronidazole
Mechanism
Indication
Adverse effects
Kills anaerobes by targeting the cytoplasm. Forms oxygen free radicals after activation inside the bacteria which interact with nucleic acid.
Good for protozoa and abscesses
Disulfiram reaction with alcohol
122
```
Macrolide
Examples
Mechanism
Contraindications
Adverse effects
```
Erythromycin, Clarithromycin, Azithromycin
Inhibit protein synthesis at ribosomal 50S
CYP450 inhibitor thus can increase dose of warfarin + phenytoin
Can cause prolonged QT interval - torsades de pointes thus ECG first
clindamycin is similar but technically not a macrolide and causes c.diff!
123
Tetracycline
Examples
Mechanism
Contraindications
Doxycycline
BacterioSTATIC - Inhibit protein synthesis, at ribosomal 30S
DO NOT give to CHILDREN as stains TEETH
124
Aminoglycosides
Examples
Mechanism
Adverse effects
Gentamicin
Inhibits protein synthesis at ribosomal 30S and 50S
Can precipitate Myasthenia Gravis
Ototoxicity
Nephrotoxic
125
Quinolones
Examples
Mechanism
Adverse effects
Ciprofloxacin
Chromosome target -
Inhibits DNA gyrase
Reduces seizure threshold
Tendon rupture
126
Trimethoprim
Mechanism
Adverse effects
Chromosome target - Inhibits DNA synthesis by inhibiting FOLATE
risk of neural tube defects in first trimester!
Avoid if patient on another anti-folate drug such as methotrexate
127
Reasons for inadequate response with ABx
```
Wrong diagnosis
Wrong drug – site, spectrum,
Resistant organisms
New infection
Poor penetration eg abscess
Insufficient duration/dose/route
```
128
Man with meningitis Sx, what do?
IM benzylpenicillin before referring to hospital
129
Single most important investigation with meningitis?
Lumbar puncture for CSF examination (after CT scan if confused/ depressed GCS)
130
difference between meningitis and meningococcal disease
Meningitis is a disease caused by inflammation and irritation of meninges
Meningococcal disease is a blood disease which can then go to inflame the meninges causing meningitis but generally just causes THAT RASH = ANY DISEASE CAUSED BY Neisseria meningitides – gram negative
131
Most common meningitis pathogens and then ones in neonates and elderly
Neisseria meningitidis
Strep. pneumoniae
Haemophilus influenzae
Group B strep (neonates)
Listeria monocytogenes (neonates)
E.coli (neonates)
Staph. Aureus (elderly)
132
After LP what ABx should be used to treat meningitis and what additional ABx in elderly AND if suspected bacterial meningitis early use of WHAT is important
1. IV ceftriaxone 2g after LP
2. Amoxicillin
3. Corticosteroids
133
Meningococcal disease prophylaxis for close contacts
Rifampicin 600 mg bd for 2 days OR
Ciprofloxacin 500 mg po stat OR
Ceftriaxone 250 mg im stat (pregnancy)
134
1. Native valve endocarditis pathogen + treatment
| 2. Prosthetic valve pathogen + treatment
```
1. Strep viridans
IV Amoxicillin (or BenzylPenicillin) + IV Gentamicin
```
2. S Aureus
IV Flucloxacillin + IV Gentamicin + PO Rifampicin
135
Infective endocarditis prophylaxis given after invasive procedures IF
And ABx
Valve surgery/disease
Structural heart disease
Previous infective endocarditis
No longer give prophylaxis for dental procedures (needs to v invasive procedures)
Amoxicillin or clindamycin
136
Trough level
Peak level
Trough level: Immediately before administration of the next dose
Peak level: 1 hour after administration
With once daily gentamicin we only need trough level
But twice daily you check both peak and trough
137
What can be done to reduce the risk of hospital-acquired infections?
Hand washing
Antibiotic stewardship
Avoid prolonged broad spectrum antibiotic therapy
Care in prescribing for over 65 years
138
Anti-TB Mx
```
RIPE
Rifampicin (CYP450 inducer + red urine)
Isoniazid (peripheral neuropathy)
Pyrazinamide
Ethambutol (optic neuritis/colourblind)
```
139
Acute AF Mx
1. Treat underlying cause
2. Haemodynamicaly unstable? DC cardioversion + heparin
3. Onset >48hours = only attempt RATE control. Rhythm control is for early intervention only as stroke risk increases with duration
4. Rhythm control: Amiodarone or Flecainide (CI in structural heart disease/IHD)
140
AF classification
1. Acute
2. Paroxysmal
3. Persistent
4. Permanent
1. Suddenly comes on with Sx
2. Spontaneous termination within seven days and most often within 48 hours. Comes and goes.
3. Doesn't go away within 72hours, usually longer than 7 days but you can terminate it
4. Cannot achieve sinus rhythm
141
Most common side effect of IV amiodarone?
List others Photo Bitch
Hypotension
```
Photo BITCH
Photosensitivity
Bradycardia/blue
Interstitial lung disease
Thyroid
Corneal/cutaneous
Hepatic/hypotension (IV)
```
142
Once AF is stable RATE control is preferred over RHYTHM. When is RHYTHM preferred?
AF has a reversible cause
Heart failure
First episode AF
HR below 90
143
Cardioversion rules
Electrical cardioversion as emergency if patient is haemodynamically unstable
Onset <48 hours:
1. Heparin
2. Electrical or pharma - flecainide or amiodarone if structural heart disease
Onset >48 hours:
1. Anticoagulate for 3 weeks prior to cardioversion OR
2. Transoesophageal echo to exclude atrial thrombus > immediate heparin + cardioversion
Consider AMiodarone 6 weeks before and up to a year after cardioversion to maintain sinus rhythm
144
Consider RHYTHM control if Sx, or keen to avoid long term anticoagulation, or young. Describe guidelines for rhythm control in persistent and paroxysmal
Persistent AF
1. Cardiovert if acute AF under 48hours
2. If over 48 hours then either -
a) Echo for thrombus + cardioversion
b) 3 weeks anticoagulation then cardioversion
c) if already on anticoagulation then go ahead and cardioversion
Paroxysmal AF:
1. Pill in the pocket (infrequent episodes)
2. Beta blocker (CI in asthma)
3. Amiodarone
145
If old, unsuitable for cardioversion, CAD and in permanent AF then do RATE control. Guidelines:
1. B blocker or CCB (CI in HF)
2. Digoxin if sedentary lifestyle
3. Any 2 of the above
4. Rhythm control
5. Ablation
146
Stroke prophylaxis in AF
Warfarin
NOAC
Consider CHADVASC and HASBLED
147
CI to cardioversion
Abnormal heart features
Valvular heart disease
Left atrium dilatation / structural heart disease etc
148
```
Warfarin
Mechanism
INR target (PT time)
Adverse effects
Antidote
```
Inhibits Vitamin K clotting factors 2 7 9 10
2-3
Teratogenic! Change to IV heparin
Affected by CYP450!
Vitamin K + prothrombin complex or FFP
149
CYP450 enzyme inducers and inhibitors
```
SICKFACES.COM/GA
Sodium Valproate
Isoniazide
Cimetidine
Ketoconazole
Fluconazole
Alcohol (Acute)
Chloramphenicol
Erythromycin (macrolides)
Statin
Ciprofloxacin
Omeprazole
Metronidazole
Grapefruit juice
Amiodarone
```
```
CRAPGPS induces me to madness
Carbamazepine
Rifampicin
Alcohol (chronic)
Phenytoin
Griseofulvin
Phenobarbiturates
Sulphonylureas / St Johns Wort
```
150
Digoxin
Antiarrhythmia mechanism
Positive inotropic mechanism
Adverse effects
Antiarrhythmic: Increases vagal tone / parasympathetic = reduces rate and conduction velocity in sinus and AV nodes
Negative inotrope: Na/K channel, with Na on inside of cell, next to Na/Ca channel with Ca on inside of cell. If Digoxin blocks Na/K then less Na leaves cell thus more is in cell thus Na/Ca channel has less activity as Na is already present in cell so it doesnt want to swap with calcium, so more calcium remains in the cell = more binds to troponin
Narrow therapeutic window
Less effective at controlling rate during exertion than beta blockers or CCBs, so only consider in sedentary elderly patients only
151
Methods to reduce absorption during poisoning
Only beneficial within 1hour!
Gastric lavage/aspiration:
Use in massive overdose where poisons are not absorbed by activated charcoal
Activated charcoal:
Binding of the poison to prevent stomach and intestinal absorption
Complications - Aspiration pneumonitis, reduced absorption of therapeutic agents in paracetamol poisoning such as methionine, don’t use with impaired gag reflex or absent bowel sounds (ileus)
Does not work with iron.
152
Methods to increase elimination during poisoning
Multiple dose activated charcoal:
Give 50g followed by 25g every 2 hours + laxative to prevent constipation
Reduces elimination half-life by ‘GI dialysis’ and by interfering with enterohepatic circulation
Haemodialysis and haemoperfusion:
Useful when poison is in the blood and would normally take ages to be removed
153
```
Paracetamol poisoning
Mechanism
Antidote mechanism
Presentation
Workup
```
Oxidation via CYP450 into NAPQI which is then detoxified by glutathione. Eventually glutathione runs out and hepatocellular injury ensues
Acetylcysteine - Replenishes glutathione stores
Nausea + abdo pain > liver failure (metabolic acidosis = poor prognosis)
1. Check paracetamol level at 4 hours (full effect) - above 100 at 4 hours = treat
2. Give large dose 50g activated charcoal within 1 hour, or NAC within 8hours – 8 hours to make a decision regarding risk/benefit of NAC
154
Acetylcysteine adverse effect
Causes an anaphylacTOID reaction 20% = urticarial, wheeze, hypotension.
Not a true allergic reaction but rather caused by dose-related histamine release
1. Temporarily STOP NAC
2. Administer IV antihistamines - Chlorphenamine
3. NOT steroids, then restart once symptoms have settled.
155
Aspirin (salicylate) poisoning
Mechanism
Presentation
Workup
1. Hyperventilation due to aspirin acting on respiratory centre = respiratory alkalosis
2. HCO3- excreted in compensation
3. Progressive metabolic acidosis due to salicylic ACID
Deafness, tinnitus, hyperventilation
1. Plasma salicylate conc
2. 50g activated charcoal within 1 hour, followed by further 25g every hours + laxatives
3. HCO3- to prevent CNS penetration and to enhance elimination via urine
4. Consider haemodialysis
5. KCl for hypokalemia
6. Glucose for hypoglycemia
156
Opiate poisoning
Antidote mechanism
Presentation
Workup
Naloxone - competitive opiate antagonist
Needs to be topped up, and can unmask pain and cause withdrawals
CNS/resp depression
Pinpoint pupils
Hypotension/tachycardia
If RR<10/min or GCS <10/15 = Naloxone
1. 400ug
2. 800ug
3. 800ug
4. 2mg
5. REview
157
TCA poisoning
Presentation
Workup
Anticholinergic: Dry mouth, dilated pupils, hyperreflexia
Sodium channel blocker: Cardiac arrhythmias + prolonged QRS and QT
1. 50g activated charcoal if within 1 hour
2. Enhance elimination via multiple dose activated charcoal 25g every 2 hours
3. HCO3- to correct acidosis and wide QRS
4. DC cardioversion
158
If seizures occur during any overdose what is protocol?
Diazepam or Lorazepam.
Reverse using benzodiazepine antagonist flumazenil (caution as pro-convulsive)
159
Iron poisoning
Presentation
Workup
Black stools > liver/renal failure > gastric strictures, acidosis, bleeding
1. Gastric lavage if large as activated charcoal is ineffective!
2. Check iron level on admission, after 4 hours and then repeat after 2 hours
3. If severe then DESFERRIOXAMINE to chelate iron
4. Correct acidosis with HCO3-
160
Organophosphate poisoning
Mechanism
Presentation
Workup
Inhibition of acetylcholinesterase (AChE), leading to the build up of acetylcholine (ACh) in the body
Muscle weakness, cramps, fasciculation, increased secretions
Anti-cholinergic drug = Pralidoxime + Atropine
161
```
Example of each ADR type
A. Augmented
B. Bizarre
C. Chronic effects
D. Delayed effects
E. End/withdrawal of drug
```
A. Predictable aka insulin > hypo, warfarin >bleeding nitrates > headache
B. Unpredictable aka anaphylaxis, chloramphenicol > agranulocytosis
C. Prolonged use aka steroids > osteoporosis/cushings
D. After discontinuation aka unopposed estrogen > endometrial cancer, immunosuppression > lymphoma
E. Withdrawal of drug aka addisons from steroid withdrawal
162
Common ADR
1. NSAIDs
2. Diuretics
3. Warfarin
4. ACE/A2Ri
5. beta blockers
6. Opiates
7. Digoxin
8. Prednisolone
9. Clopidogrel
10. PPI
1. GI ulcer, renal, wheeze
2. Renal, hypotension, gout
3. Bleeding
4. Renal, hypotension
5. Bradycardia, heart block, wheeze
6. Constipation, urinary retention
7. Liver toxicity
8. Gi ulcer, hyperglycemia, osteoporotic
9. GI bleeding
10. c.diff, gastric ca
163
Essential drug interactions
1. Warfarin + erythromycin/metronidazole
2. Warfarin + aspirin/NSAID/clopidogrel
3. Carbamazepine + erythromycin/clarithromycin/fluconazole
4. Lithium +NSAID/diuretic
5. OCP + Antibiotics
6. OCP + rifampicin/carbamazepine
7. SSRIs + St Johns wort/triptans/MAOI
8. Sildenafil + Isosorbide mononitrate
1. Increases bleeding
2. Increases bleeding
3. Increases carbamazepine
4. Doubles lithium dose
5. ABx lowers OCP effectiveness
6. Requires higher estrogen dose
7. Serotonin syndrome - hypertensive crisis
8. Marked hypotension
164
Drugs that cause gynaecomastia/galactorrhoea
Both:
Estrogens
Reserpine
Methyldopa
Gynaecomastia:
Spironolactone
Digoxin
Galactorrhoea:
Antipsychotics
Tricylics
Metoclopramide
165
CYP450 enzyme inducers and inhibitors
```
SICKFACES.COM/GA
Sodium Valproate
Isoniazide
Cimetidine
Ketoconazole
Fluconazole
Alcohol (Acute)
Chloramphenicol
Erythromycin (macrolides)
Statin
Ciprofloxacin
Omeprazole
Metronidazole
Grapefruit juice
Amiodarone
```
```
CRAPGPS induces me to madness
Carbamazepine
Rifampicin
Alcohol (chronic)
Phenytoin
Griseofulvin
Phenobarbiturates
Sulphonylureas / St Johns Wort
```
166
Spyro digs boobs
psycho on a tricycle squirts milk
spironolactone and digoxin cause gynaecomastia
antipsychotics and TCAs cause galacatorrhea
and ofc estrogen and methyldopa do both
