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Stage 4 > CPTP > Flashcards

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

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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
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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

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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.

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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

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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
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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

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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

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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

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10
Q

H.pylori eradication regime

A 
PAC/PAM
PPI, amoxicillin + clarithromycin
PPI, amoxicillin + metronidazole
1 WEEK!
Continue PPI for 2months!
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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
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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

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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)

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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

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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

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16
Q

What can be used when rapid bowel evacuation is required?

A

Magnesium salts

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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

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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

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19
Q

Therapeutic pathway for NON-ULCER dyspepsia

So theyve got Sx and had an endoscopy but no ulcer

A

‘Test and treat’

  1. ‘Test’ for H.pylori
  2. ‘Treat’ with 4 weeks low dose PPI (high dose if didn’t know there was no ulcer)
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20
Q

Post upper GI bleed care (after the adrenaline / clipping at endoscopy)

IV PPI shown to reduce risk of rebleeding!

A
  1. Monitor for signs of rebleeding (Rockall score)
  2. 80mg omeprazole bolus IV STAT
  3. 8mg/hour omeprazole for 72hours IV
  4. High dose oral PPI for 2 months
  5. Avoid NSAIDs
  6. Repeat endoscopy after 8weeks for gastric ulcer
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21
Q

Treatment for c.diff (ABx use, PPI use, old, profuse, fever, CRP, WCC, toxic megacolon)

A

Metronidazole + Vancomycin

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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)

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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

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24
Q

Type2Diabetes drugs

BIGSS

A 
Biguanides - Metformin
Incretins - DPP-IV inhibitors (Gliptins) + GLP-1 mimetics
Glitazones - Pioglitazone
Sulphonylureas - Gliclazide
SGLT2 inhibitors
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25
Q 
Metformin
Mechanism
Indications
Side effects
Weight
Hypoglycemia?
A

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

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26
Q

Sulphonylureas (gliclazide)
Mechanism
Weight
Hypoglycemia?

A

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!

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27
Q 
Glitazones (pioglitazone)
Mechanism
Side effects
Weight
Hypoglycemia
A

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)

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28
Q

SGLT2 inhibitors (sodium glucose reabsorption channel)
Mechanism
Side effects
Weight

A

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

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29
Q

What are Incretins?

A

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.

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30
Q 
DPP-IV inhibitors (Gliptins)
Mechanism
Indication
Side effects
Weight
Hypoglycemia
A

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

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31
Q 
GLP-1 mimetics (Liraglutide, Exenatide)
Mechanism
Indication
Side effects
Weight
Hypoglycemia
A

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

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32
Q

Type2 DM NICE guidelines

A
  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
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33
Q

Primary prevention statin

Secondary prevention statin

A

Primary prevention:
10 year CVD risk >10% OR T1DM OR eGFR <60 CKD = Atorvastatin 20mg

Secondary prevention:
Known IHD, CVD, PAD = Atorvastatin 80mg

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34
Q

Explain DKA and HHS

A

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.

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35
Q

Diagnostic criteria for DKA
11,3,15

and other non diabetic causes

A

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

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36
Q

Anion gap

A

(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

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37
Q

DKA guidelines

  1. Fluid (Kcl if <5.5)
  2. Insulin
  3. Glucose
  4. SC insulin (discontinue insulin infusion 30mins later)
A
  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
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38
Q

Once patient is recovering from DKA and has had first SC insulin how long do you continue running the insulin infusion for?

A

30 minutes

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39
Q

DKA fluid repletion based on BP

A

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

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40
Q

Hypoglycemia
Definition
Sx
Mx

A

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
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41
Q

Diabetes and pregnancy
Folic acid
During labour
Post-partum

A

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%

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42
Q

Type2 DM guidelines

A
  1. Lifestyle
  2. Metformin at 48
  3. Metformin + 1 at 58
  4. Metformin + 2 OR insulin if still above 58 with double therapy
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43
Q

Diabetes surgical management

A

Type1: Stop insulin + GKI infusion

Type2: Stop sulfonylurea (risk of hypo) on morning / metformin 48hours before

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44
Q

Statins
Indication
Adverse effects
Contraindications

A

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

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45
Q

Dopamine mechanism pathway

A
  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
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46
Q

Levodopa
Indication
Adverse effect

A

Gold standard + first line
Give with dopamine decarboxylase inhibitor

Long term patients WILL get involuntary abnormal movements – dyskinesias – manage with smaller doses more frequently

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47
Q

Levodopa + dopamine agonist side effects

A

GI
Dementia
Postural hypotension
Sleep disorders

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48
Q

Dopamine agonists
Indication
Adverse effects

A

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!

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49
Q 
Mono-Amine Oxidase B inhibitors
Mechanism
Indication
Adverse effects
Example
A

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

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50
Q

First line Ix in Parkinsons

A

Dopaminergic agent trial

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51
Q

Catechol-O-methyl transferase COMT inhibitors
Mechanism
Indication
Adverse effects

A

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

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52
Q

Amantadine (antiviral)
Indication
Adverse effects

A

Used later in disease to control dyskinesia complications

Can cause dementia so avoid in elderly

Also can cause Livedo reticularis

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53
Q

Anticholinergics
Indication
Adverse effects

A

Best in young to combat prominent tremor

not in elderly as can cause cognitive impairment

AcH SEs: Dry, glaucoma, blurred vision

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54
Q

Parkinsons disease treatment pathway
Young
Old

Complications

A

Young:
MAO-B inhibitor + Dopamine agonist&raquo_space;> L-dopa + COMTi

Old:
L-dopa&raquo_space;> MAO-B inhibitor + COMTi

Complications:
Dyskinesia&raquo_space;> Reduce l-dopa + amantadine

Severe tremor etc&raquo_space;> 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).

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55
Q

Drug induced parkinsonism

Sx

A

Sudden onset, bilateral (unusual) OR increase in symptoms of known PD patient

Dopamine antagonists: Neuroleptics – Clozapine, Haloperidol, Olanzapine
Metoclopramide, CCBs
Amiodarone, sodium valproate

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56
Q

Epilepsy classification

A

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

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57
Q 
Epilepsy Mx
Generalised tonic clonic
Absence
Myoclonus
Partial

TREAT ONLY AFTER 2 SEIZURES - only 50% have 2nd seizure

A

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

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58
Q 
Anti-epileptic drugs side effects
Sodium valproate
Lamotrigine
Carbamazepine
Phenytoin
Diazepam
A

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

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59
Q

Which receptor do Sodium val and benzos work on? And which do all other anti-epileptic drugs work on?

A

GABA agonist

Na channel blocker

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60
Q

Epilepsy drugs that induce CYP450 and thus reduce levels of COCP

Drug which is inhibited by COCP

If COCP used with epilepsy what dose?

A

Carbamazepine + Phenytoin + Ethosuximide

Lamotrigine

50ug (any breakthrough bleed = ineffective)
Use depo or mirena coil

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61
Q

Status epilepticus
Definition
Mx

A

> 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
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62
Q

Indications for epilepsy surgery

A

Epilepsy refractory to medical treatment
Localised onset (if resective surgery)
Likely benefits outweigh risks
Disabling

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63
Q

Since lamotrigine + sodium valproate can cause fetal abnormalities which drug should be used in epilepsy during pregnancy?

Eclampsia Dx

A

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

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64
Q

First things to do when finding fitting patient

A

collateral Hx + capillary blood glucose

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65
Q

Phenytoin monitoring
Ideal range
Toxicity Sx

A

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.

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66
Q

Acute alcohol withdrawal
Mx
complications

A
  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

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67
Q

Carbamazepine:
continue if on warfarin?
continue if raised GGT and low sodium?

A

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
Q

Features which indicate drug induced parkinsonism?

Antipsychotics + anti-emetics + sodium valproate + lithium + CCBs + SSRIs

A

Subacute bilateral onset

Progression of symptoms concurrent with medication intake

Early presence of postural tremor

L-dopa MAY be useful for symptomatic relief

69
Q

Would you perform a DAT scan following drug induced parkinsonism?

A

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
Q

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?

A

Prevention:
Delaying use of L-dopa –”sparing” strategy

Treatment:
Reduce dose of L-dopa
Amantadine
Duodenal infusion of L-dopa
Apomorphine infusion
71
Q

Pros and cons of Deep brain stimulation for PD

A

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
Q

Beta2 agonists
Mechanism
Indication for short and long acting
Adverse effects

A

Act on beta2adrenergic receptor to cause smooth muscle relaxation
SABA: Salbutamol - quick Sx relief
LABA: Salmeterol - slow onset
Fine tremor, tachycardia, palpitations, hypokalemia

73
Q

Muscarinic antagonists
Mechanism
Indication
Adverse effects

A

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
Q

Theophylline / phosphodiesterase inhibitor
Mechanism

Adverse effects

Loading dose

A

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
Q

Leukotriene receptor antagonist/ Montelukast
Mechanism
Indication
Adverse effects

A

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
Q

Corticosteroids
Mechanism
Indication
Adverse effects

A

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
Q

IgE monoclonal Ab e.g omalizumab

A

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
Q

Asthma diagnostic algorithm

A
  1. Hx indicates asthma (night time, wheeze, chest tightness)
  2. Reversibility of airflow obstruction - improvement in FEV1 by 12% and 200 mL
    OR
  3. 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
  4. Challenge tests - try to induce asthma
  5. Test for eosinophilic inflammation or IgE atopy

Only symptoms when cold > less chance of being asthma

79
Q

Stepwise chronic asthma management

A
  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
Q

Drugs which may exacerbate asthma

A

B-blockers:
Cause bronchospasm > give prostaglandin analogues - Bimatoprost, Travoprost

NSAIDs:
Cause bronchospasm in sensitive > give clopidogrel

81
Q

Stepwise acute asthma EMERGENCY management

A

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
Q 
COPD vs Asthma
Demographic
Sx
Variation
Reversibility
A

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
Q

NICE guidelines for COPD FEV1/FVC = <70%
>50% predicted = ?
<50% or exacerbation Hx predicted = ?

A

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
Q

COPD exacerbation management

A
  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
Q 
Pros and cons of:
Nebuliser
Nasal prongs
MC mask
Venturi mask
A

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
Q

Admit to hospital if WHICH features persist after initial therapy?

Acute severe asthma criteria

A

PEF 33-50% best/predicted

RR >25

HR >110

Inability to complete senteces in one breath

87
Q

Admit if PEF is below WHAT %

A

50

88
Q

Acute asthma severe and life threatening distinguished

A

Life threatening is <33% whereas severe is just 50%.

Severe is RR and HR whilst life threatening is silent chest, altered consciousness etc

89
Q

What drug do you not give in asthma attacks

A

Lorazepam

90
Q

Asthma attack penumonia
Pathogens
Theophylline CYP450 by Clarithromycin and ciprofloxacin complication

A

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
Q

Discharge policy following asthma attack

A

PEF >75% + <25% variability - own PEF meter

Treatment with oral and inhlaed steroids

92
Q

Name COPD drug used to decrease secretions/mucus

A

Mucolytic - Carbocisteine!

93
Q

pH 7.31, pO2 6.8, pC02 7.4, Bicarbonate 34

What does the ABG show?

A

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
Q

Type 1 respiratory failure / VQ mismatch

Type 2 respiratory failure / Ventilatory failure

A

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
Q

If patient is in respiratory acidosis or tiring or type2 respiratory failure then instead of messing around with venturi mask use…

A

NIV

96
Q

Long term oxygen therapy for COPD

A

Right sided ventricular strain + cor pulmonale
PaO2 <7.3
PaO2 7.3-8.0 and cor pulmonale

97
Q

NICE definitions
Stage 1 HTN
Stage 2 HTN
Severe HTN

A

Stage 1: 140/90 + ABPM 135/85

Stage 2: 160/100 + ABPM 150/95

Severe: 180 / 110

98
Q

Diagnosis of HTN

A

If the clinic BP is >140/90

Offer ABPM to confirm

99
Q

Ix to check organ damage due to HTN

A

Kidneys: Urine dip (protein/blood), U&E, creatinine, GFR

Blood: glucose, cholesterol

Fundoscopy: hypertensive retinopathy

ECG

100
Q

BP target for

Under 80

Over 80

Diabetes patients

A

Under 80: <140, ABPM <135

Over 80: <150, ABPM <145

Diabetes: <130

101
Q

HTN NICE stepwise management

refer to specialist if under 40 and stage 1 to look for secondary causes

A

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)

  1. ACEi/ARB + CCB
    • Thiazide
    • Further diuretic or a/b blocker
102
Q 
ACEi
Mechanism
Indication
Contraindications
Adverse effects
Examples
A

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
Q

Calcium channel blockers
Mechanism
Indication
Contraindication

Examples

A

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
Q 
Diuretics
Mechanism
Types
Indications
Adverse effects
A

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
Q 
Beta blockers
Mechanism
Indication
Contraindication
Examples
A

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
Q

Alpha blockers

A

Doxazosin

good for men - helps prostate

Contraindicated in women due to urinary incontinence

107
Q

HTN and pregnancy
High risk eclampsia/HTN prophylaxis
BP target
Only HTN drugs used in pregnancy

A

75mg aspirin 12w-birth

Aim for <150/100

Methyldopa + nifedipine + labetalol

All others CI!

108
Q

Heart Failure

Ix

A

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
Q

Acute heart failure management

A
  1. Sit up and give high flow oxygen - IV access
  2. furosemide 80mg IV as bolus injection

After stabilisation: ACEi + b blocker

110
Q

Chronic heart failure management

Contraindicated drugs

A

Lifestyle
1st: ACEi (ARB if intolerant)
B blocker

2nd: Spironolactone

Sx control: Furosemide
Digoxin

CCBs are contraindicated in systolic HF!

111
Q 
Step 2 (alongside paracetamol)
NSAIDs
Mechanism
Indications
Dose
contraindications
A

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
Q 
Step 2
Codeine + Tramadol
Mechanism
Indication
Adverse effects
A 
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
Q 
Step 3
Morphine
Mechanism
Adverse effects
Overdose treatment
A

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
Q

Pain ladder

A 
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
Q

Adjuvant medications which can reduce opiate requirement in:

  1. Muscle spasm
  2. Bone pain
  3. Bowel colic
  4. Neuropathic pain
  5. Raised ICP
A
  1. Muscle relaxant - diazepam
  2. Bisphosphonates
  3. Antispasmodics
  4. Antidepressants/Anticonvulsants
  5. Corticosteroids
116
Q

End of life prescriptions

  1. Pain and breathlessness
  2. Nausea and vomiting
  3. Agitation
  4. Excess secretions
A
  1. Morphine
  2. Cyclizine
  3. Midazolam
  4. Hyoscine Hydrobromide
117
Q
  1. Analgesia for #NOF
  2. for post op pain
  3. neuropathic pain
A
  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
Q

Opiate drug calculations
General
Rules

A

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
Q 
Penicillin Beta lactams
Mechanism
Resistance
Adverse effects
Examples and indications
A

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
Q

Cephalosporins beta lactams
Generation
Route + indication

A

1st: Cephalexin > UTIs oral
2nd: Cefuroxime - IV
3rd: Cefotaxime/Ceftriaxone - IV crosses BBB for meningitis

121
Q

Metronidazole
Mechanism
Indication
Adverse effects

A

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
Q 
Macrolide
Examples
Mechanism
Contraindications
Adverse effects
A

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
Q

Tetracycline
Examples
Mechanism
Contraindications

A

Doxycycline

BacterioSTATIC - Inhibit protein synthesis, at ribosomal 30S

DO NOT give to CHILDREN as stains TEETH

124
Q

Aminoglycosides
Examples
Mechanism
Adverse effects

A

Gentamicin

Inhibits protein synthesis at ribosomal 30S and 50S

Can precipitate Myasthenia Gravis

Ototoxicity

Nephrotoxic

125
Q

Quinolones
Examples
Mechanism
Adverse effects

A

Ciprofloxacin

Chromosome target -
Inhibits DNA gyrase

Reduces seizure threshold

Tendon rupture

126
Q

Trimethoprim
Mechanism
Adverse effects

A

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
Q

Reasons for inadequate response with ABx

A 
Wrong diagnosis
Wrong drug – site, spectrum, 
Resistant organisms
New infection
Poor penetration eg abscess
Insufficient duration/dose/route
128
Q

Man with meningitis Sx, what do?

A

IM benzylpenicillin before referring to hospital

129
Q

Single most important investigation with meningitis?

A

Lumbar puncture for CSF examination (after CT scan if confused/ depressed GCS)

130
Q

difference between meningitis and meningococcal disease

A

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
Q

Most common meningitis pathogens and then ones in neonates and elderly

A

Neisseria meningitidis
Strep. pneumoniae
Haemophilus influenzae

Group B strep (neonates)
Listeria monocytogenes (neonates)
E.coli (neonates)

Staph. Aureus (elderly)

132
Q

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

A
  1. IV ceftriaxone 2g after LP
  2. Amoxicillin
  3. Corticosteroids
133
Q

Meningococcal disease prophylaxis for close contacts

A

Rifampicin 600 mg bd for 2 days OR
Ciprofloxacin 500 mg po stat OR
Ceftriaxone 250 mg im stat (pregnancy)

134
Q
  1. Native valve endocarditis pathogen + treatment

2. Prosthetic valve pathogen + treatment

A 
1. Strep viridans
IV Amoxicillin (or BenzylPenicillin) + IV Gentamicin
  1. S Aureus
    IV Flucloxacillin + IV Gentamicin + PO Rifampicin
135
Q

Infective endocarditis prophylaxis given after invasive procedures IF

And ABx

A

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
Q

Trough level

Peak level

A

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
Q

What can be done to reduce the risk of hospital-acquired infections?

A

Hand washing

Antibiotic stewardship

Avoid prolonged broad spectrum antibiotic therapy

Care in prescribing for over 65 years

138
Q

Anti-TB Mx

A 
RIPE
Rifampicin (CYP450 inducer + red urine)
Isoniazid (peripheral neuropathy)
Pyrazinamide
Ethambutol (optic neuritis/colourblind)
139
Q

Acute AF Mx

A
  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
Q

AF classification

  1. Acute
  2. Paroxysmal
  3. Persistent
  4. Permanent
A
  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
Q

Most common side effect of IV amiodarone?

List others Photo Bitch

A

Hypotension

Photo BITCH
Photosensitivity
Bradycardia/blue
Interstitial lung disease
Thyroid
Corneal/cutaneous
Hepatic/hypotension (IV)
142
Q

Once AF is stable RATE control is preferred over RHYTHM. When is RHYTHM preferred?

A

AF has a reversible cause

Heart failure

First episode AF

HR below 90

143
Q

Cardioversion rules

A

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
Q

Consider RHYTHM control if Sx, or keen to avoid long term anticoagulation, or young. Describe guidelines for rhythm control in persistent and paroxysmal

A

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
Q

If old, unsuitable for cardioversion, CAD and in permanent AF then do RATE control. Guidelines:

A
  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
Q

Stroke prophylaxis in AF

A

Warfarin
NOAC

Consider CHADVASC and HASBLED

147
Q

CI to cardioversion

A

Abnormal heart features

Valvular heart disease

Left atrium dilatation / structural heart disease etc

148
Q 
Warfarin
Mechanism
INR target (PT time)
Adverse effects
Antidote
A

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
Q

CYP450 enzyme inducers and inhibitors

A 
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
Q

Digoxin
Antiarrhythmia mechanism
Positive inotropic mechanism
Adverse effects

A

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
Q

Methods to reduce absorption during poisoning

A

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
Q

Methods to increase elimination during poisoning

A

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
Q 
Paracetamol poisoning
Mechanism
Antidote mechanism
Presentation
Workup
A

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
Q

Acetylcysteine adverse effect

A

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
Q

Aspirin (salicylate) poisoning
Mechanism
Presentation
Workup

A
  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
Q

Opiate poisoning
Antidote mechanism
Presentation
Workup

A

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
Q

TCA poisoning
Presentation
Workup

A

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
Q

If seizures occur during any overdose what is protocol?

A

Diazepam or Lorazepam.

Reverse using benzodiazepine antagonist flumazenil (caution as pro-convulsive)

159
Q

Iron poisoning
Presentation
Workup

A

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
Q

Organophosphate poisoning
Mechanism
Presentation
Workup

A

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
Q 
Example of each ADR type
A. Augmented
B. Bizarre
C. Chronic effects
D. Delayed effects
E. End/withdrawal of drug
A

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
Q

Common ADR

  1. NSAIDs
  2. Diuretics
  3. Warfarin
  4. ACE/A2Ri
  5. beta blockers
  6. Opiates
  7. Digoxin
  8. Prednisolone
  9. Clopidogrel
  10. PPI
A
  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
Q

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
A
  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
Q

Drugs that cause gynaecomastia/galactorrhoea

A

Both:
Estrogens
Reserpine
Methyldopa

Gynaecomastia:
Spironolactone
Digoxin

Galactorrhoea:
Antipsychotics
Tricylics
Metoclopramide

165
Q

CYP450 enzyme inducers and inhibitors

A 
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
Q

Spyro digs boobs

psycho on a tricycle squirts milk

A

spironolactone and digoxin cause gynaecomastia

antipsychotics and TCAs cause galacatorrhea

and ofc estrogen and methyldopa do both

Stage 4 (12 decks)

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