AIP Flashcards

1
Q

What do leads are present for anterior, lateral, inferior and posterior MI?

A
  • V1, V2, V3 - LAD, anterior MI
  • 1, aVL, V5, V6 - circumflex, lateral MI
  • 2, 3, aVF, RCA, inferior MI
  • V1, V2, V3 ST depression, RCA, posterior MI (also bradycardia)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What investigations needed for ACS?

A

o Observations including ECG
o Bloods
 FBC, U+Es, LFTs and clotting, CRP
 Troponins T and I (3x normal limit, rising), CK, AST, LDH
o Imaging
 CXR to exclude differentials

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is the management of STEMI?

A

Morphine (for pain), cyclizine for nausea, oxygen if <94%, GTN 2mg unless hypo, aspirin 300mg oral and prasugrel (P2Y12 antag), unfractionated heparin before PCI(within 2 hrs)- transfer to CCU.
If fails or triple vessel - do CABG, graft from long saphenous vein or internal mammary artery
thrombolysis - 12 hour - alteplase - repeat ecg after 90min. <50% better = PCI needed still

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Post MI complication? (DARTH VADER)

A

Death, Dressler’s, Arrhythmia, Aneurysm, Rupture, Recurrence, Tamponade, HF/CCF, Valve disease, Embolism

Fever, pleuritic pain relieved by leaning forwards, raised ESR
 Dressler’s syndrome tends to occur around 2-6 weeks following a MI
 Treated with NSAIDs
o Bradycardia
 AVN block can occur following inferior MI as the RCA supplies the AVN leading to bradycardia
Persistent ST elevation
 Aneurysm after MI
o Tamponade
 Beck’s triad of raised JVP, low BP, muffled heart sounds
o Acute fall in BP
 Cardiogenic shock following acute LVF - (inotropes and vasodilators eg. Noradrenaline)
o Systolic murmur and pulmonary oedema
 Acute mitral regurgitation due to ischaemia of papillary muscle causing fluid backlog
 POOR SOD (Pour away/stop fluids, sit up, oxygen, loop diuretic IV Furosemide)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Secondary prevention of MI (ABCDE)

A

o Conservative
 Exercise, Mediterranean diet, less alcohol, smoking cessation, cardiac rehabilitation, HTN/DM management, avoid sex for 4 weeks, avoid driving for 4 weeks if not treated with PCI (1 week if treated with PCI)
o Medical ABCDE
 Ace inhibitor Ramipril 10mg OD
 BB (Atenolol)
 Cholesterol (Atorvastatin 80mg OD)
 Dual AP therapy (Aspirin 75mg OD for life + another antiplatelet (clopidogrel, ticagrelor, prasugrel) 12 months)
 ECHO +/- Eplerenone Aldosterone antagonist eg. Eplerenone/Spironolactone if LV dysfunction (EF < 50% on echo_

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

NSTEMI and UA mangement

A

 Conservative
* Scans (stress ECG, myocardial perfusion scan)
* GRACE score to determine risk of death or MI within 6 months)
* If low risk <3% then conservative
* Diet, exercise, cardiac rehabilitation, HTN/DM management
 Medical
* Medium or high risk GRACE score >3%
o Aspirin plus Fondaparinux if PCI not planned immediately
o Then angiogram and PCI or CABG within 3 days/72 hours
 When to do an angiogram?
* Hypotensive – immediate
* GRACE score >3% - angiogram within 3 days
* GRACE score <3% - angiogram after 3 days

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Causes of Interstitial Lung Disease

A

Idiopathic Pulmonary Fibrosis

Iatrogenic
 Nitrofurantoin, methotrexate, amiodarone

Inflammatory
 Sarcoidosis -> Erythema nodosum, uveitis, hypercalcaemia

Infective
- TB

Toxins
- Coal, silicosis, asbestosis
- Farmers’, bird owner

Autoimmune
 SLE, RA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are the signs and symptoms of Interstitial Lung Disease?

A
  • Signs and symptoms
    o Gradual onset sob, non-productive cough, haematemesis, wheeze, chest pain, fever and myalgia
    o Occupational history - smoking, farming, dust, birds, asbestos, coal
    Examination
    o Finger clubbing, cyanosis, wheeze, fine end-inspiratory crackles, tachycardia, RHF
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are the investigations needed for Interstitial Lung Disease?

A

Observations
 Temp, BP, HR, RR, sats
o Blood tests
 FBC, U+E, LFT, CRP, ESR
 Antibodies RF, anti-CCP, ANA, dsDNA

Bedside
 ABG, peak flow, spirometry, ECG
 Restrictive pattern with FEV1/FVC > 0.7 and reduced total lung capacity

o Imaging
CXR, HRCT (honeycombing, nodular opacities, BHL, ground-glass changes), lung biopsy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Management of Interstitial Lung Disease?

A

o Conservative
 Smoking cessation
 Avoid triggers - dust, allergens, coal, asbestos, bird droppings
 Seasonal influenza vaccinations
 Physio
 LTOT
o Medical
 Corticosteroids (if symptomatic) - not for EAA
 Pirfenidone (antifibrosis) - especially for IPF
o Surgical
 Lung transplantation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are the causes of PE?

A

Cause
o Thrombosis from DVT
o Fat embolism (surgery), amniotic fluid (pregnancy), tumour (cancer), air (trauma)
Pathophysiology
o Causes reduced blood flow to lungs resulting in VQ mismatch
o A massive PE will increase right ventricle afterload and cause right ventricular failure leading to haemodynamic compromise

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

PE presentation

A

Symptoms
 Pleuritic pain and haemoptysis
 Isolated SOB/dyspnoea/cough
 Circulatory collapse and LOC (a massive PE)/light headedness
Signs
 DVT (cause)
 Hypotension, raised JVP, parasternal heave (RV failure)
 Tachypnoea (most common sign), Tachycardia
 Decreased O2 (VQ mismatch)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

PE Investigations

A

NOTE: IF PE SUSPECTED, START DOAC IMMEDIATELY
Observations
Bloods: FBC, U&Es, LFTs, clotting, CRP, d-dimer, troponin
Bedside: ECG (Sinus tachycardia, S1Q3T3)
Wells PE is used to determine the investigations used
o D dimer IF WELLS SCORE IS <4
 If negative, then stop DOAC
 If positive, then CTPA or VQ
 If PE suspected, start DOAC
 If Wells PE <4, do d dimer
 D dimer negative then stop DOAC
If Wells PE >4 or D dimer positive, then do CTPA (gold standard)
If CTPA contraindicated (renal impairment or contrast allergy) then do VQ scan instead
 If CTPA or VQ is negative, stop DOAC
 If CTPA or VQ is positive, continue DOAC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

WELLs Score for PE

A

Wells PE is used to determine the investigations used
 Suspected DVT: 3
 PE most likely diagnosis: 3
 Tachycardia: 1.5
 3 days immobilisation in past 30 days: 1.5
 Hx of thrombosis DVT/PE: 1.5
 Haemoptysis/coughing blood: 1
 Malignancy/cancer: 1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

PE management

A

Immediate
 A to E and stabilisation
 Senior input as the patient is unwell
Conservative
 If PESI score is low, can be managed as outpatient
Medical
 Start DOAC immediately if PE suspected (Rivaroxaban, Apixaban)
* If provoked: 3 months DOAC
* If unprovoked: 6 months DOAC
 IF ANTIPHOSPHOLIPID SYNDROME OR SEVERE RENAL IMPAIRMENT (<15/min): LMWH plus VKA (Warfarin) instead
 IF MASSIVE PE WITH HYPOTENSION: thrombolysis with 50mg Alteplase bolus is first line
Surgical
 IF REPEATED PEs: can try an IVC filter to stop clots getting into pulmonary circulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

PE in pregnancy management

A

PE in pregnancy
 D-dimer cannot be used as it will be raised
 If leg symptoms, do leg USS first
 If PE suspected, do CXR
 If CXR normal, do leg USS
 If normal, do VQ scan (preferable to CTPA)
 Consult obstetrician

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What are the causes of COPD excarcebations

A

 Most common cause is H.Influenza (annual influenza vaccine) and S.pneumoniae (one-off pneumococcal vaccine), or Moraxella
 Rhinovirus is the most common viral cause

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Investigations for COPD exacerbations?

A

 Observations
* Temp, BP, HR, RR, sats
 Routine bloods
* FBC, U+Es, LFTs and clotting, CRP
 Bedside
* ABG, peak flow, ECG
 Sepsis six and infection screen
* UOP, lactate, blood cultures, sputum culture
 Imaging
* CXR
o If consolidation then pneumonia, otherwise infective exacerbation of COPD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is the management of COPD Excacerbation

A

 Immediate
* A to E assessment and stabilisation
* Senior input as this is an unwell patient
* 15L non-rebreathe mask if life threatening, otherwise Venturi titrated to 88 - 92% O2
* REPEAT ABG to assess for hypercapnic respiratory acidosis (need NIV)
 Medical
* OSHIT AE (NV)
* Nebulised SABA salbutamol (2.5mg) +/- SAMA Ipratropium (0.5mg)
* Prednisolone 30mg for 5 days (40mg in Asthma exacerbation)
* IV theophylline with senior input
* Oral antibiotics ONLY IF purulent YELLOW or GREEN sputum or signs of pneumonia
o Amoxicillin (not if penicillin allergy) or clarithromycin (not if long QT syndrome) or doxycycline
* Non-invasive ventilation
o If respiratory acidosis <7.35, then NIV needed in an ITU setting (better outcomes than ET)
o Bilevel positive airway pressure with IPAP and EPAP
o Next step up could be intubation and ventilation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What are the different types of bowel ischaemia?

A

o Acute mesenteric ischaemia
o Chronic mesenteric ischaemia
o Ischaemic colitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What are the causes of mesenteric ischaemia?

A

 Mostly arterial embolus due to AF, as well as MI, IE
 Venous due to hypercoagulation, tumours, infection
 Also, non-occlusive due to hypovolaemia and blood vessel constriction (COCAINE –> acute mesenteric ischaemia)
Blocks the small bowel

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Investigations for mesenteric ischaemia

A

 Observations
 Bloods – FBC, U+Es, LFT, CRP, lactate (ischaemic)
 Bedside – urinalysis, ECG/echo
 Imaging
* CXR and AXR (may show thumb printing due to oedema and inflammation)
* CT Angiography is gold standard

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Management of mesenteric ischaemia?

A

 Immediate
* A to E
* Senior input
* Morphine, Oxygen, anti-emetic, NBM
 Medical
* Antibiotics
* Possibly thrombolytics or heparin
 Surgery
* Embolectomy or angioplasty if bowel if viable
* Emergency laparotomy with resection usually required due to necrosis or sepsis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Chronic Mesenteric Ischaemia causes investigation and management

A

o Atherosclerosis of gut blood vessels
o Post-prandial (after food) colicky, transient pain
o Intestinal angina, (also have TIA, angina etc)
o Examination
 Upper abdominal bruit (atherosclerosis)
o Investigation
 Bloods, ECG, CVD RFx, ANGIOGRAPHY is gold standard
o Management
 Surgery
* Angiography and stenting (stent)
* Bypass graft

25
Q

Ischaemic Colitis (large bowel ischaemia usually in spenic region - watershet between inferior and SMA supply

Presentation, investigation, managment

A

o Can lead to inflammation (thumb-printing), ulceration (bleeding in colonoscopy), and haemorrhage (loose stool with blood)
o Presentation
 Acute abdominal pain in LIF, transient, less severe than acute mesenteric ischaemia, N/V/D, loose stools with BLOOD
o Investigations
 CXR and AXR
 CT
 Colonoscopy: blue swollen mucosa with bleeding
 Barium enema: thumb-printing (mucosal oedema and inflammation)
o Management
 Usually conservative (acute mesenteric ischaemia needs urgent surgery usually)
* IV fluids and rest
 Surgery
* If perforation, necrosis, strictures

26
Q

What is epilepsy?

A
  • A tendency towards unprovoked seizures (2 or more within a year)
  • Seizures are synchronised neuronal discharge leading to disturbance of consciousness, behaviour, emotion, motor function, or sensation
27
Q

What are the causes of seizures?

A

o The majority of cases are idiopathic
o Vascular (stroke, hypertensive encephalopathy, pre-eclampsia), infection (encephalopathy/meningitis), trauma (head injury or cranial surgery), toxins (hepatic, alcohol, TCAs), autoimmune (vasculitis), metabolic (hypoglycaemia, hypocalcaemia, hyponatraemia), neoplasm, neurodegenerative, CNS (tuberous sclerosis, hamartomas)

28
Q

Epilepsy differentials

A

o LOC
 Vasovagal syncope: short post-ictal period but CAN be associated with twitching/jerking
 Cardiac syncope
o Seizures
 Febrile convulsions
* Recurrent tonic-clonic seizures in children <5 due to viral infection
 Alcohol withdrawal seizures
 Psychogenic non-epileptic seizures/Non-epileptic attack disorder (NEAD)
* Female, mental/psychiatric health, pelvic thrusting, crying, gradual onset
* No tongue biting or raised serum prolactin
* Important to refer to psychiatry

29
Q

Classifiction of epilepsyy

A

 Generalised
* Motor:
o Stiffening (tonic - contraction and cyanosis)
o Loss of tone (atonic drop attacks)
o Jerking (clonic, myoclonic)
o Tonic-clonic/Grand mal (stiffening/contraction and extension, back arching, then jerking)
* Non-motor:
o Absence/Petit mal (child unresponsive staring for 10 seconds with eyelid fluttering and no loss of tone)
 Focal
* Motor:
o Twitching, jerking
o Automatisms (brief unconscious behaviours): lip licking, rubbing hands
o Spreading from one area to another: Jacksonian march
* Non-motor:
o Auras: thinking, sensation, emotion, experience (Déjà vu, Jamais vu)
 If it lasts more than 5 minutes: status epilepticus
 Other seizure syndromes in children: West’s syndrome, Lennox-Gastaut, benign Rolandic, juvenile myoclonic

30
Q

Seizure history

A

o Onset: trigger, prodrome, onset
o Character: duration, awareness, motor symptoms (rigid jerking/myoclonic, stiffness/tonic, tonic-clonic, floppy body/drop attack (atonic), absence, automatisms (lip licking, rubbing hands), changing (Jacksonian march))
o Associated symptoms: Aura, light headedness, dizziness palpitations, LOC, seizures, cyanosis, incontinence, trismus/lateral tongue biting, frothing at the mouth, >2 minutes post-ictal phase confusion, fatigue, headache, myalgia, speech difficulty, Injuries (shoulder dislocation), Brief period of ipsilateral paralysis/weakness: Todd’s post-ictal paresis (key stroke ddx)

31
Q

Ix for Epilepsy

A

o Observations
o Bloods
 Routine, glucose
o Bedside
 Urinalysis, ECG, 24-hr ECG, lying and standing BP, tilt table
o Imaging
 CT
 MRI
 LP
 EEG

32
Q

Immediate and conservative Mx of Epilepsy (including DVLA informing)

A

o Immediate
 A to E
 Senior input
o Conservative
 Ketogenic diet (high fat, low carb)
 Must inform DVLA and Cannot drive for 12 months after a seizure

33
Q

Generalised(same as myoclonic and tonic seizure) and focal seizure medication

A

Generalised seizures
* Sodium valproate is 1st line (NOT for women of child-bearing age)
* Lamotrigine is 2nd line (for females)
myoclonic female - levetiracetam

Focal seizures
first line: lamotrigine or levetiracetam
second line: carbamazepine, oxcarbazepine or zonisamide

 Starting treatment
* Only started after a confirmed diagnosis - after a second seizure
* Start with monotherapy and gradually titrate up to maximum
* Consistent supplier
* Baseline FBCs, U+Es, and LFTs before starting

Stopping medication
* If seizure-free for 2 years, consider SLOW withdrawal over 2-3 months
* Relapse risk is highest in first year

34
Q

Tx for Absence seizures (Petit mal)

A

first line: ethosuximide
second line:
male: sodium valproate
female: lamotrigine or levetiracetam
carbamazepine may exacerbate absence seizures

35
Q

Surgical treatment for epilepsy

A

 Vagal nerve stimulation
 DBS
 Surgical focal resection

36
Q

GBS signs and symptoms

A

o Acute ascending neuropathy due to campylobacter infection in the past week leading to cross-reaction of antibodies leading to demyelination
- Signs and symptoms
o Ascending neuropathy from the lower limbs
o Sensory: reduced sensation
o Motor: weakness and reduced reflexes (LMN)

37
Q

GBS Ix

A

o Observations
 Temp, BP, HR, RR, sats
o Bloods
 FBC, U+Es, LFTs, CRP, lactate, glucose
o Bedside
 Diagnosis: Nerve conduction studies are diagnostic
 Cause: Infection screen (blood, sputum, stool, urine, LP cultures), urinalysis
 Impact:
* LP will show raised protein
* Spirometry is important - reduced FEV1/FVC is an indication for ITU admission
 Cauda equina: DRE
 Claudication: ABPI
 Peripheral neuropathy: B12, folate, glucose

38
Q

Mx of GBS

A

Immediate
 A to E assessment and stabilisation
 Senior input
 Monitor spirometry for the need for ventilatory support
Medical
 Plasma exchange or IVIG to remove the autoantibodies
 DVT prophylaxis

39
Q

Stroke Differentials

A

o Todd’s paresis (post epilepsy weakness)
o VITAMIN CDEF
o TIA, amaurosis fugax, cerebellar
o Carotid/vertebral artery dissection

40
Q

Bamford classification of strokes

A
41
Q

Stroke recognition scoring tools

A

 General public: FAST criteria
 Medical professionals: ROSIER score (FAST + LV) - Recognition Of Stroke In ER
o Severity of a stroke
* NIH Stroke Severity Scale (NIHSS)
* 11 items: Face, arms, legs, aphasia, dysarthria, visual fields, gaze palsy, inattention, consciousness, ataxia

42
Q

Stroke Examination findings

A

o CN exam (visual inattention, visual field defect), upper limb, lower limb (UMN lesion - acutely diminished tone, and absent reflexes, weakness –> becomes hypertonic, hyperreflexia, spastic paralysis, Babinski positive), speech (receptive or expressive aphasia, dysarthria), cerebellar (DANISH)
o General examination (AF, carotid bruit - carotid dissection is an important cause)
o Special test: Hoover’s test to differentiate organic/psychogenic cause (if organic, when asked to raise normal leg, the supposed weak leg will flex at the hip)

43
Q

Cerebellar Signs (DANISH)

A

dysdiadochokinesis
ataxia
nystagmus
intention tremor
scanning dysarthria(stuttered speech)
heel-shin test positivity

44
Q

Ix for strokes

A

o Observations
o Bloods
* FBC, U&Es, LFTs, ESR/CRP
* CK, glucose, lipids
* NOTE: IF ‘young’ <55 year old with no obvious cause: thrombophilia and autoimmune screening is indicated (syphilis serology, antibodies, clotting)
o Bedside
* ECG, urinalysis, BP lying standing
o Imaging
* CT head
* Urgent NON CONTRAST CT head if within 4.5 hours (candidate for thrombolysis - to exclude haemorrhagic), taking anticoagulants (DOACs, warfarin), GCS <13, getting worse, meningism (headache, neck stiffness, photophobia, N/V, Kernig (pain on extending knee when hip flexed), Brudzinski (knees bend when head is raised lying down)), or severe headache (SAH)
* Indicated in ALL suspected stroke within 24 hours
* Diffusion weighted MRI is gold standard (done at QE)
* Carotid doppler (stenosis, dissection)

45
Q

Mx of stroke

A

o Overall: Imaging, medication, surgery, secondary prevention. CT angiography within 4.5 hours, Aspirin 300mg for 2 week and Clopidogrel 75mg for life, Thrombolysis with alteplase if within 4.5 hours, Thrombectomy within 6 hours (24 if viable penumbra), Carotid endarterectomy if >70% stenosis. Then Anticoagulation if AF after 2 weeks, Atorvastatin if high cholesterol after 2 days,
o Immediate
* A to E assessment and stabilisation
 Maintain oxygen, fluid status, temperature, glucose (IV insulin)
 Senior input
o Conservative
* Physio, OT, SALT, MUST score +/- NGT/PEG
o Medical
* Aspirin 300mg oral or rectal (if dysphagia) ONCE HAEMORRHAGE EXCLUDED
 Different to MI: Continued for 2 weeks DAILY 300mg Aspirin
 Then 75mg Clopidogrel daily indefinitely
 OR Aspirin PLUS MR Dipyridamole if Clopidogrel not tolerated (diarrhoea, constipation)
* Thrombolysis with Alteplase (tPA) ONCE HAEMORRHAGE EXCLUDED
 IF 1) within 4.5 hours from onset and 2) Once haemorrhage excluded on non-contrast CT head and 3) No contraindications - seizure, head injury, uncontrolled HTN, INR >1.7, GCS <8, abnormal blood glucose, rapidly improving signs
* Anticoagulation and statins
 If AF: start ANTICOAGULATION 14 DAYS AFTER THE STROKE
 If cholesterol >3.5mmol/L: start ATORVOSTATIN 48 HOURS AFTER STROKE
o Surgical
* Thrombectomy (PLUS Aspirin and thrombolysis)
 Within 6 hours
 Within 24 hours IF evidence of salvageable brain matter “viable penumbra” (small infarct volume on CT angiogram or MRI)
* Carotid endarterectomy if >70% stenosis (continue antiplatelets due to risk of clot)

46
Q

TIA definition and key differential

A

 NEW DEFINITION: transient neurological dysfunction caused ischaemia without infarction
 Hemiparesis, hemisensory loss, cortical signs (dysphagia), vision (monocular loss, amaurosis fugax, hemianopia), cerebellar signs
 Key differential is hypoglycaemia

47
Q

Management

A

 Conservative
* Not allowed to drive until seen by specialist
* If dysphagia, consider a variable rate insulin
* Specialist neuro rehab ward
 Medical
* Same: 300mg aspirin once bleed excluded
* 75mg Clopidogrel for life
* OR If Clopidogrel not tolerated (diarrhoea), then Aspirin plus MR Dipyridamole
 Referral criteria
* IF repeated “crescendo” TIAs, carotid stenosis, or AF: urgent referral
* IF TIA in the past 7 days: referral within 24 hours
* IF TIA >7 days ago: referral within 1 week
 Surgical
* Same: IF carotid stenosis (doppler US) >70% occlusion : carotid endarterectomy - to remove atherosclerosis

48
Q

Falls Ix and Mx

A

 Observations
 Bloods including glucose, lipids, clotting, CK
 Bedside urinalysis, ECG
 Imaging consider CXR, AP and Lat hip XR
Management
 Immediate
* A to E
* Senior input
* MDT discussion
 Conservative
* Physio, OT, MUST score (NGT or PEG)
* Close follow-up with GP

49
Q

What is counted as a paracetamol overdose?

A

> 4g a day
1 dose <1 hour or staggered over 1 hour needs NAC
Dx is with Nomogram, Tx is with charcoal, NAC, and vitamin K, KCH criteria is used for transplantation

50
Q

How does paracetamol overdose present

A

o The first 24 hours there is some nausea, vomiting, and abdominal pain
o After 24 - 72 hours there is jaundice, RUQ pain, hypoglycaemia, encephalopathy, as well as increased INR
o A key feature is lactic acidosis

51
Q

Paracetamol OD Ix

A

o NOTE: if paracetamol overdose is likely from the history, initiate treatment before results come back
o Observations
o Bloods
 FBC, U+E, LFTs, clotting, glucose, plasma paracetamol
o Bedside
 ABG (lactic acidosis), ECG

52
Q

Mx of Paracetano,

A

o Immediate
 A to E and stabilisation + ABG to assess acidosis
 Senior input
 Plot plasma paracetamol on Nomogram
o Conservative
 Refer to psych liaison team
o Medical
 Consult TOXBASE for latest guidelines
 IF WITHIN 1 HOUR: activated charcoal
 Antidote is NAC N-acetylcysteine AKA Parvolex
 Also, a 10mg single dose of vitamin K
- NAC guidelines
o Indications:
 Paracetamol above treatment line on the Nomogram (>150mg/kg at 4 hours (OR if staggered overdose, persistent high LFTs or detectable after 24 hours)
o Infusion over 21 hours
 Bag 1 (150mg/kg in 200ml 5% glucose 1 hr) (repeat blood tests after first bag - stop NAC if fine)
 Bag 2 (50mg/kg in 500ml 4hrs
 Bag 3 (100mg/kg 1000ml 16hrs)
o Commonly causes NON-IgE mediated mast cell release anaphylactoid reaction - urticaria rash and facial flushing (not angioedema)
 Treated by stopping the infusion then restarting at a lower rate. 50mg/kg over 4 hours
 If bronchospasm or O2 saturations fall, give nebulised salbutamol
 IM adrenaline or a peri-arrest call is UNNECESSARY

53
Q

KCH criteria for liver transplantation

A

o Arterial pH <7.3 at 24 hours after ingestion
o OR ALL OF these 3:
 PT >100 seconds (11 - 13.5) or INR >6.5 (0.8 - 1.1)
 Creatinine >300umol/L
 Grade 3/4 encephalopathy (1: irritability, 2: confusion, 3: incoherence, 4: coma) - asterixis is at grade 2

54
Q

What do you need to examine in a pre op anaesthetic examination?

A

Neck movement limitation/jaw opening limitation/dentures

Airway assessment: use Mallampati classification and note BMI
See all soft palate and uvula
See half of uvula
See a small gap at end of soft palate
Can only see hard palate

Back examination (if having spinal/epidural): look for skeletal malformations

55
Q

Pre op multisystem examination what do you need to check in general, hands, neck, check, abdomen, calves

A

General: GCS, limb movements

Hands: cyanosis, warm peripheries, cap refill, peripheral pulses

Neck: JVP, carotid bruits

Chest: heaves/thrills, chest expansion, percussion resonance, lung and heart sounds

Abdomen: tenderness, masses/organomegaly, bowel sounds

Calves: swelling/tenderness, oedema

56
Q

Pre op investigations

A

Tests that may be required for patients having surgery include:

Blood tests: FBC, U&Es, LFTs, clotting, group and save

ECG

Other tests may be considered in advance
Pregnancy test (if chance of pregnancy)
Echocardiogram (if murmur/heart failure/cardiac symptoms)
Spirometry (if significant lung disease)
Pacemaker check(if have pacemaker)
TFTs (if on known thyroid disease)

57
Q

When do you need to stop warfarin, DOAC, LMWH, unfractionated heparin, aspirin/clipidogrel/pasugrel, insulin, oral hypoglycaemic, diuretic, steroid, COCP

A

Warfarin 5 days
DOAC - 24 hr (48 for major surg)
LMWH - 24 hr
Heparin - 4 hr
Aspirin - 7 days
Insulin - avoid morning dose
Oral hypoglycaemic- avoid on day of operation
Diuretics - on the day
Steroid - change to hydrocortisone
COCP - 4 weeks

58
Q

What do you need to correct before surgery?

A

INR - if >1.4, 5-10mg Vit K repeat INR in 6 hrs, if still hgih then prothrombin complex concentrate - discuss with haem,
INR due to liver - 10mg IV vit K, repeat INR in 6 hours
Blood transfusion - <9g/dl,<10g/dl if elderly
Platelet concentrate if platelet <50 x 10^9
correct electrolytes
Correct iron - iron tablet or infusions