General Flashcards
What is a massive PE
PE with obstructive shock or SBP <90mmHg
What is a submassive PE
Acute PE without systemic hypotension >90 BUT either RV dysfunction or myocardial necrosis
Initital investigations for ?P.E
A-E ECG CXR if acutely unwell WELLS score ABG - D-dimer CT pulmonary angiogram
Gold standard PE investigation
CTPA
Main ECG finding for PE?
Sinus tachy
Why can’t you prescribe verapamil and bisoprolol together?
complete heart block
Main finding on ECG for complete heart block
prolonged PR interval (>200ms, >6 squares)
Main feature of Mobitz type 1 heart block on ECG
Increasing PR interval then missed QRS complex
Main feature of complete heart block on ECG?
P and QRS are both regular but completely separate rhythms
Differentials for stroke
Migraine
Hypoglycaemia
Seizure
Old stroke symptoms exacerbated by concurrent illness (e.g. sepsis)
Ischaemic stroke management
Alteplase (thrombolysis) <4.5 hours
/Thrombectomy
Aspirin 300mg for 2 weeks then Clopidogrel
BP control
Haemorrhagic stroke management
Neurosurgery referral BP control (usually <140)
?Stroke investigations
Blood glucose
CT within 24 hours
Stroke assessment score
Rosier score
LOC -1 Seizure activity -1 Asymmetrical facial weakness +1 Assymmetrical arm weakness +1 Asymmetrical leg weakness +1 Speech disturbances +1 Visual field deficit +1
Stroke is likely if score is >0
A-E assessment: Breathing
Examine: Observe for signs of resp distress Resp rate Quality of breathing Chest deformity O2 sats and FiO2 Tracheal position Brief resp exam: chest expansion, auscultation, percussion
Investigations
ABG
CXR
Action
O2
Nebulisers
Investigation of ?PE
PERC calculation –> If >0 then..
Wells score –> if <4 (unlikely): D-dimer. If >4 (likely) –> CTPA + CXR + ECG.
If CTPA positive –> Anticoagulate
In what scenario is CTPA for ?PE contraindicated? What should you do instead?
Pregnancy
Renal impairment
Contrast allergy
Radiation risk (breast cancer)
Ventilation-perfusion scan
Treatment for massive PE
Thrombolyse (alteplase)
Treatment for unprovoked submassive / non-massive PE?
Anticoagulate –> DOAC (apixaban/rivaroxaban)
Investigate if unprovoked --> FBC, U&E, LFTs, Clotting, Calcium, PSA Breast/prostate/testicular/rectal examination Systems review (CT if cancer suspicion)
Sx of aortic dissection
Sudden ripping or tearing chest pain (migrates over time, maximal at time of onset)
Hypertension
Differences in BP between arms
Collapse
Tx of aortic dissection
Analgesia
IV access
BP and HR control (beta-blocker)
Surgical intervention
Tx for pericarditis
Bed rest
NSAIDs (+ PPI cover)
Oral prednisolone if severe
Treatment for large/ unstable pneumothorax
Aspiration (2nd/3rd intercostal space, mid-clavicular line).
If aspiration fails:
Chest drain in triangle of safety (5th ICS, midaxillary line, anterior axillary line)
What is the triangle of safety?
Mid-axillary line
Anterior axillary line
5th ICS
3 criteria for exacerbation of COPD
Increased SOB
Increased sputum production
Increased purulence of sputum
Most common causes of COPD exacerbation
Haemophilus influenzae
Strep pneumoniae
RSV
Treatment pathway for COPD exacerbation
1) Nebs –> salbutamol 2.5mg QDS, ipratropium 0.5mg QDS
2) Steroids –> prednisolone 30mg OD / hydrocortisone 100mg QDS
3) Abx - amoxicillin, doxycycline, clarithroymcin
4) Oxygen therapy (venturi, NIV, mechanical)
Tests which must be done before starting NIV
ABG - to ensure T2RF
CXR - to rule out pneumothorax
CURB-65 score and interpretation
Confusion Urea >7 Resp rates >30 BP <90 systolic or <60 diastolic 65 - age >65
1 –> home tx
2 –> hosp admission
>3 –> ICU
How to measure calf swelling for ?DVT
Measure 10cm below tibial tuberosity
Difference of >3cm = significant.
How to measure calf swelling for ?DVT
Measure 10cm below tibial tuberosity
Difference of >3cm = significant.
Complications of DVT
CV event
ASD –> stroke
Post-thrombotic syndrome –> chronic venous hypertension which causes limb pain, swelling, dermatitis, ulcers.
Difference between periorbital and orbital cellulitis?
Periorbital is ANTERIOR to orbital septum, and does not affect vision or cause pain on eye movement.
Treatment for cellulitis
Flucloxacillin for 5-7 days (7 if facial)
If not systemically unwell / not significantly unwell = oral
If significant systemic upset / sepsis = IV
Explain DKA
High blood glucose and low cell glucose causes ketogenesis - liver converts fatty acids into ketones (which can be used as fuel in the brain). When ketones can no longer be buffered by bicarbonate, they cause METABOLIC ACIDOSIS.
Hyperglycaemia also causes diuresis which causes DEHYDRATION and total body hypokalaemia, but serum HYPERKALAEMIA as insulin normally drives K+ into cells.
Symptoms of DKA
Nause and vomiting Fatigue Abdo pain Polyuria and polydipsia Weight loss Acetone smell to breath Kussmaul breathing Hypovolaemic shock
Triad of diagnosis for DKA?
+ other important investigations
THINK : D(diabetes), K(ketosis), A(acidosis)
Blood glucose >11mmol/L (or known diabetic!)
Ketones >3mmol/L (or ++ on dipstick)
Acidosis –> pH <7.3 with bicarb <15mmol/L
ECG
Treatment for DKA
FIG PICK
FLUIDS: (If shocked - fluid boluses until SBP >90) 1L over 1 hour 1L over 2 hours 1L over 2 hours 1L over 4 hours 1L over 4 hours 1L over 6 hours 1L every 8 hours onwards
INSULIN - Fixed rate infusion of 0.1unit/kg/hour
GLUCOSE - start IV dextrose when <14mmol/L
POTASSIUM - add 40mmol/L if potassium <5.5mmol/L
INFECTION - treat triggers
CHART FLUIDS
KETONES - monitor hourly
Complications of DKA
Dehydration
Hypokalaemia
Cerebral oedema
Investigations if hypoglycaemia and diabetic status unknown
LFTs, U&Es, TFTs, glucose, HbA1c, insulin and C-peptide (measured to investigate insulinoma - endogenous source of insulin)
Treatment for hypoglycaemia
Conscious: 10-20g glucose (tablet, gel, coke, fruit juice)
Unconscious: IV 50% dextrose 25ml STAT (or IM glucagon 1mg/kg)
SEPSIS management
Blood cultures Urine ouput Fluids Antibiotics Lactate Oxygen
What is HHS? Diagnostic triad.
Very high blood glucose in T2DM which causes severe intracellular dehydration. Severe hyperglycaemia, serum hyperosmolarity, without significant ketosis
Hypovolaemia Marked hyperglycaemia (>30mmol/L) Without hyperketonaemia (<3mmol/L)
Treatment for HHS
Fluid replacement –> 3-6L by 12 hours, remaining in next 12 hours (100-220ml/kg)
Monitor response –> osmolarity, Na+, glucose hourly
Insulin –> only if significant ketonaemia = 0.05units/kg/hr
Potassium replacement
VTE prophylaxis
How to assess capacity
- Does the patient have a potential impairment of mind or brain?
IF YES - Can they: understand, retain, weigh up, communicate decision
Define shock
What does it cause?
Clinical syndrome caused by inadequate tissue perfusion and oxygenation, leading to abnormal metabolic function
Intracellular calcium overload –> reduced myocardial contractility
Anerobic metabolism –> lactic acidosis –> further exacerbation of myocardial issues
4 types of hypoxia
Hypoxic
Anaemic (due to ↓ Hb)
Stagnant (↓ citruclation)
Histotoxic (Impaired metabolism)
Define preload and after load
Preload = initial stretching of cardiac myocytes prior to contraction
Afterload = force/load against which the heart has to contract to eject the blood
How much does one unit of blood increase Hb?
10g/L
What 3 blood products are needed in haemorrhagic shock? In what ratio?
Packed red cells
FFP
Platelets
1:1:1
Explain how ionotropes and vasopressors are used in the management of shock
Inotropes = increase contractility of heart by increasing calcium availability and thus increasing stroke volume
Vasopressors = increase systemic vascular resistance, which increases BP and increases tissue perfusion
Management of hypovolaemic shock
Oxygen IV access Fluids (500ml 0.9% NaCL, then bloods) Activate MHP (if fluids insufficient, or Hb <70g/L) Vasopressors and ionotropes
Management of anaphylactic shock
ABCDE IM adrenaline IV fluid challenge Antihistamines Steroids
What is cariogenic shock? Causes?
Treatment?
Low cardiac output state due to failure of heart to pump
Causes: MI, dysrhythmia, myocarditis, cardiac rupture
MONAT
Morphine, oxygen, GTN, aspirin, tricagelor
Rapid PCI
Ionotropic support
What is distributive shock?
Vasodilation +/- endothelial leakage.
Caused by sepsis, anaphylaxis, neurogenic shock (damage to spinal cord)
What do the different NEWS scores mean?
0 = Low risk. Continue monitoring every 12 hours.
1-4 = Low risk. Nurse assessment and escalate if necessary. Review 4-6 hourly.
5-6 or >3 in one area = High risk. Urgent ward based response, nurse to urgently inform medical team. Review 1 hourly
Score >7 = emergency response. Critical care and airway management team needed. Continuous monitoring.
What are the 3 steps of the WHO pain ladder?
1) Non-opioid –> paracetamol, aspirin, NSAID
2) Weak opioids –> Codeine, co-codamol
3) Strong opiod –> morphine, fentanyl, oxycodone
Nephrotic syndrome triad and Tx
- Oedema
- Hypoalbuminaemia
- Proteinuria (High urinary PCR)
Tx = Long term steroids (prednisolone) + reduced salt diet
What is Cushing’s syndrome?
Causes and symptoms.
Prolonged cortisol elevation.
Sx: Moon face, central obesity, proximal muscle wasting, striae, buffalo hump (think man on AMU!), T2DM
Causes: exogenous steroids (iatrogenic or mediation abuse), adrenal adenoma, paraneoplastic, Cushing’s disease (pituitary adenoma releasing excessive ACTH)
What is the correct sequence of actions in basic life support?
Safety (approach with care), Stimulate, Shout for help, Airway opening manoeuvres, Look listen feel, Rescue breaths
Commonest cause of airway obstruction in an anaesthetised patient is:
Tongue
How do you assess breathing during BLS?
Look listen and feel
During CPR what it the best indicator of effective breaths in an un-intubated patient?
Visualising the chest rise and fall
What type of shock is commonly seen in anaphylaxis?
Distributive shock
Two types of definitive airway
ET tube
Tracheostomy
Two types of definitive airway
ET tube
Tracheostomy
What does the size of ET tube indicate?
internal diameter in mm
What colour and size cannula should be inserted in cardiac arrest?
16G (grey)
15G (orange)
What is the best indicator of correct placement of ET tube?
CO2 in expired gas
Scoring systems for upper GI bleed
Glasgow-Blatchford score - predictor of risk of GI bleed
Rockall score - predictor of re-bleed and morbidity after endoscopy
GI bleed causes
Mallory-weiss tear Gastro/duodenal ulcer Oesophageal varices Cancers Oesophagitis
Acute upper GI bleed management
ABATED
A-E assessment Bloods - Hb, platelets, clotting, urea, LFTs, cross match Access - IV access Transfusion: blood, platelets, FFP Endoscopy - urgent within 24h Drugs - stop anticoagulants and NSAIDs
+ Test for H.Pylori –> Rapid urease test usually carried out during endoscopy / breath test can be done.
(Withhold PPI until after endoscopy)
Management of H.pylori infection
Triple therapy for 7 days –> PPI + 2 antibiotics (e.g. amoxicillin + clairthromycin)
How do you know if NG tube is placed correctly?
Aspirate = test pH. CXR = Dissects carina and sits under left hemidiaphragm
Management of tricyclic antidepressant overdose
Check TOXBASE
IV bicarbonate to correct acidosis
IV lipid emulsion to bind free drug
Supportive
(no specific antidote)
DO NOT give antiarrthymics
Trauma to the face often causes which type of bleed?
Extra dural haematoma
Guidelines for CT post-head injury
WITHIN 1 HOUR:
GCS <13 on initial assessment, or <15 two hours post injury
Suspected open/depressed skull fracture
Signs of basal skull fracture (CSF leak, battle sign, racoon eyes, haemotympanum, subconjunctival haemorrhage)
Post-traumatic seizure
Focal neurological deficit
>1 episode of vomiting
WITHIN 8 HOURS: >65 yo Bleeding/clotting disorder Dangerous injury mechanism >30 mins retrograde amnesia Warfarin patient
CT SPINE within 1 hour IF:
Need for CT head in 1 hour
Suspicion of C-spine injury
Neck pain/tenderness
Management of head injury
CT following CT head rules
Maintain CPP (control BP (fluids, pain relief), control ICP (IV mannitol))
Neurosurgery referal
- Haematoma –> depressive craniotomy / drainage
- Depressed skull fracture –> surgical correction
What are the Canadian C Spine rules?
If ANY of the following, must have C-Spine immobilisation:
- Age >65
- Dangerous mechanism
- Numbness/tingling in extremities
- Not ambulatory at any time at scene
- Neck pain
- Pain on midline C-spine palpation
- Cannot rotate neck 45 degrees left/right
Need CT spine within 1 hour (X-ray if neck pain/tenderness)
Diagnosis and management of HHS
DIAGNOSIS
= Hypovolaemia, hyperglycaemia (>30), and raised serum osmolarity (>320mosmol/kg) in T2DM, without acidosis or ketonaemia
MANAGEMENT
- Fluid replacement 0.9%NaCl (first 50% in 12 hours, second 50% in 12 hours)
- Monitor: osmolarity, potassium, glucose, sodium
- Target glucose 10-15mmol/L
Treatment guidelines for hyperkalaemia
TREAT IF :
- K+ >6 + ECG changes
- K+ >6.5
Treatment:
- Stop K+ sparing drugs (ACE-i, ARBs, Spironolactone)
- 10% calcium gluconate 30mls over 10 minutes (cardio protective)
- IV insulin + 50% dextrose
Mechanism of action of Amiodarone
Class II anti-arrhythmic
Blocks potassium currents causing repolarisation of the heart muscle à increases duration of action potentials and refractory period
This reduces cardiac muscle cell excitability and restores normal sinus rhythm.
Mechanism of action of adrenaline
Increases myocardial force of contraction (positive inotrope) and heart rate (positive chronotrope)
Mechanism of action of adenosine (CCB) & contraindications
Slows cardiac conduction through AVN à resets rhythm back to normal
Causes brief period of asystole, very quickly metabolised
Contraindications: asthma, COPD, heart failure, HTN
Mechanism of action of atropine
Anti-muscarinic –> inhibits parasympathetic nervous system which increases HR
SE: pupil dilatation, urinary retention, dry eyes, constipation
AAA classification and management
Normal - <3cm
Small = 3-4.4cm
Medium = 4.5-54.cm
Large = >5.5cm
Small = yearly screen (CT angiogram)
Medium = 3 monthly screen
Large or growing >1cm a year = Elective repair & graft (end-vascular aneurysm repair: EVAR)
What is the screening programme for AAA
Men routine USS screen at age 65
Women considered if age >70 with CVD/COPD
What is ascending cholangitis and what is Charcot’s triad ?
Blockage in common bile duct preventing the flow of bile, which causes infection and leads to biliary sepsis.
Mirrizzi syndrome = blockage of common bile duct by a stone.
CHARCOT’S TRIAD:
Constant epigastric and RUQ pain
Jaundice
Fever
(+ steatorrhoea, signs of infection)
Management of ascending cholangitis
ABCDE for sepsis - BUFALO
Biliary drainage
ERCP –> dislodge obstruction
Investigations and management of bowel obstruction?
Abdo Xray, Contrast CT, bloods (U&Es, VBG/ABG - metabolic acidosis)
DRIP AND SUCK APPROACH
Nil by mouth, IV fluids, NG tube to aspirate stomach contents (prevent aspiration)
Surgical management
Renal colic investigations and management
Urine dip, bloods, AXR, non-contrast CT KUB
IM diclofenac
Anti-emetics + antibtioics
Stone <5mm = watch and wait
Stone >10mm = surgical intervention
Explain the mechanism of paracetamol overdose? At what level is overdose defined, and at what level is toxic?
Paracetamol is metabolised 95% to glucuronide sulphates, and 5% to NAPQI (n-acetyl-p-benzoquinone) which is further metabolised by glutathione.
In OD, pathway gets saturated so NAPQI builds up and is toxic –> liver cell necrosis
OD = >4g in 25h Toxic = >150mg/kg (21 tablets for average 70kg person)
Which drugs are P450 enzyme inducers and what does this mean?
o BS CRAP GPs o Barbituates o St John's Wart o Carbamazepine o Rifampicin o Alcohol (chronic) o Phenytoin o Griseofulvin (fungal treatment) o Phenobarbitone o Sulphonylureas
Symptoms of liver failure
<24 hours –> (asymptomatic) or Sweating, N&V, abdo discomfort
24-72 hours –> RUQ pain, N&V
3-5 days –> jaundice, confusions, coagulopathy, anuria, hypoglycaemia, seizures
Management of paracetamol OD at different time frames
<1 hour = activated charcoal
0 -4 hours = nothing
4 -8 hours = paracetamol level +/- NAC if needed
8 - 15 hours = NAC then paracetamol level (and stop if necessary)
15+ hours / staggered overdose = NAC
NAC is infused over 1 hour. Takes 12 hours for full protocol.
SE of NAC treatment
Rash, itching, nausea (Anaphylactoid like reaction - because it is a precursor of histamine)
Which patients are at increased risk of OD on paracetamol?
Those taking P450 enzyme inducers Malnourished patients (anorexia, alcohol addiction)
Criteria for liver-transplantation post-paracetamol OD
- Arterial pH <7.3 after 24h
- Prothrombin time >100 seconds
- Creatinine >300umol/L
- Grade III/IV encephalopathy
Scoring system for pneumonia and what do results mean
CURB - 65 Confusion Urea >7 Resps >30 BP S <90 / D< 60 >65yo
Guides treatment
1 –> home (oral amoxicillin 5 days)
2 –> Hospital admission (amoxicillin/clarithromycin azithromycin 7-10 days)
>3 –> Consider ICU (amoxicillin + clarithromycin/azithromycin 7-10 days)
DKA treatment improvements and targets?
Glucose reduce >3 /hour until <14mmol/L
Ketones reduce >0.5 /hour until <0.6mmol/L
Bicard increase >3 /hour until >15 (and pH >7.3)
Initial treatment for bowel obstruction
Drip and suck - NG tube + IV fluids
Amiodarone MOA
Class II anti-arrhythmic
Blocks potassium currents causing repolarisation of the heart muscle –> increases duration of action potentials and refractory period
This reduces cardiac muscle cell excitability and restores normal sinus rhythm.
Atropine MOA
Anti-muscarinic –> inhibits parasympathetic nervous system which increases HR
SE: pupil dilatation, urinary retention, dry eyes, constipation
Adenosine MOA
Calcium channel blocker
Slows cardiac conduction through AVN –> resets rhythm back to normal
Causes brief period of asystole, very quickly metabolised
Contraindications: asthma, COPD, heart failure, HTN
Where would a needle decompression for tension pneumothorax be inserted
2nd intraclavicular space, ICS
Where would a chest drain be inserted?
Triangle of safety - between
5th ICS
Midaxillary line
Anterior axillary line
