Emergency medicine

Question 1

Target time for treatment 95% A+E pts?

Answer 1

4 hours

Question 2

Factors increasing A+E strain?

Answer 2

warm, dry and sunny weather; local music festivals; national sports teams winning (mainly assault); major natural disasters; Mondays and Fridays/Saturdays (drinking)

Question 3

How to deal with inappropriate A+E attendance and who?

Answer 3

triage by nurse; GPs working alongside ED Drs; patients prefer ED sometimes and can put strain on it rather than go to primary care where problem can be solved without a trip to the ED; may get some patients that turn up loads and are ‘crying wolf’

Question 4

Major burn definition?

Answer 4

15% burn surface area (BSA) or 10% in child

Question 5

When referred to burns specialist unit?

Answer 5

major then require resus and burns specialist treatment; also referred = inhaled, face, hands, feet, genitalia

Question 6

First aid treatment for burns?

Answer 6

remove burnt clothing; irrigate for 10 mins (cool sterile saline); chemical burns = continuous irrigation; keep clean, cover with cling film, warm pt to stop shock

Question 7

Assessing airways in burns?

Answer 7

assess from ICU; high flow O2; accurate hx vital (suspicion if injury in enclosed space); intubate if hypoxaemia/hypercapnia

Question 8

S+Ss inhalational burns?

Answer 8

injury to face/neck, singed nasal hair, carbonaceous sputum, voice change, dyspnoea, soot area; systemic oedema can happen after fluid resus

Question 9

Treatment for inhalational burns?

Answer 9

give continuous 100% O2 until carboxyhaemoglobin levels known, if raised continue until 10% for 6 hours; if high COHb levels then can be high cyanide from burning foam and suspect if also tissue poisoning; anaesthetist assessment needed, usually intubation with nasogastric before swelling needed (uncut endotracheal tube with >7.5mm diameter so bronchoscope passed)

Question 10

C spine/chest injuries result in what?

Answer 10

can result in pneumothorax or flail chest (explosion)

Question 11

Fluid resus in burns victims what and regime?

Answer 11

– extreme inflammatory response means lots of Hartmann’s needed to stop shock, using Parkland’s formula (vol in mils = 4 x body weight in kg x BSA % of burn); give 50% of this in first 8 hours then other half in next 16; may need other specific fluids; avoid colloid in first 24hrs due to colloid permeability; blood and clotting where needed and avoid IV in burnt skin; all products should be warmed and arterial and venous monitoring; minimum 0.5ml urine output for formula to work

Question 12

How to measure BSA?

Answer 12

estimated by rule of nines (SEE BOOK FOR WALLACE RULE OF NINES) or palm of pt to estimate 1% BSA; Lund and Browder chart more accurate but longer to do; need to modify for burns in children

Question 13

What S+Ss can be misleading and shouldn’t be taken into acc when assessing burn depth?

Answer 13

erythema, mild redness, blisters, oedema

Question 14

What is a superficial burn?

Answer 14

red, painful with blistering but hair follicles intact

Question 15

Deep dermal burn?

Answer 15

red, painful, peeling sheets rather than blistering, a few hair follicles intact

Question 16

Full thickness burn?

Answer 16

pale and charred grey/black, no erythema, no hairs intact, skin is insensate, leathery and causes constriction if circumferential

Question 17

Burn management?

Answer 17

• Analgesia should be given as painful; elevate to minimise risk of compartment syndrome and peripheral pulses monitored

Question 18

Prognostic factors for burns?

Answer 18

BSA, pre-morbid conditions, inhalational injury and age

Question 19

Most likely to drown?

Answer 19

usually in <5yrs and in adults can be associated with alcohol

Question 20

Difference between distress and drowning?

Answer 20

• Distress = pending danger as shouting for help but still afloat but struggling
• Drowning = person already started to suffocate and usually silent

Question 21

Initial management of drowning pt?

Answer 21

no CPR in water, immobilise C-spine, keep pt prone when out of water as water helps maintain venous return so don’t want venous collapse, hypoxaemia causes cardiac arrest so 100% oxygen and intubation with high PEEP (water dilutes surfactant so atelectasis more common)

Question 22

Management of drowning pt after admission?

Answer 22

observe pt after drowning; can get pulmonary oedema; monitor = haemoptysis, basal crackles, CXR changes, hypoxia; asymptomatic after 4hrs discharge; 2wk CXR after to see if infected with anything

Question 23

Other things to bear in mind with drowning pts?

Answer 23

hypothermia can mask clinical death so keep resussing until back at hospital aggressively (no pulse, breathing, muscle rigidity); hyperkalaemia = poor prognosis, ECG and end-tidal CO2 for diagnosing cardiac arrest

Question 24

Causes of electric shock injuries?

Answer 24

utility working, poorly earthed appliances, appliances near water

Question 25

Consequences from electric shocks?

Answer 25

physiological changes, thermal tissue destruction, secondary damage from muscle spasm and falls

Question 26

Poor prognostic factors and explanations for electric shocks?

Answer 26

type of current (AC more dangerous than DC as can cause muscle spasm so victim won’t let go of source, AC cause VF and DC causes systole); energy delivered (applied voltage x current; can cause extreme heating meaning internal/external burns, coagulation necrosis); current pathway (where it goes through body, head and chest is worse); resistance encountered (fluid and electrolyte tissues conduct well; bone is most resistant and skin thickness can limit amount of current into body, hearts and nerves do badly so check these as they conduct electricity the best); contact duration (briefer = better)

Question 27

Treatment of electric shocks?

Answer 27

turn source off; paradoxical triage (treat apparent dead first; resus long and aggressively); more fluids needed if burnt than normal burns as can go deeper; check of rhabdomyolysis; treat arrhythmias; usually can cause compartment syndrome in legs

Question 28

3 types of lightning strike injuries?

Answer 28

direct = strikes and enters ground through pt; side flash = lightning hits object first then jumps sideways; ground strike = strikes nearby and travels through ground to pt

Question 29

Consequences of lightning strikes?

Answer 29

pt usually unaware what happened and confused with tympanic rupture; safe to touch pt; full trauma assessment; visual acuity assessed (can cause electrical cataracts)

Question 30

Immediate S+Ss of lightning strikes?

Answer 30

asystole due to secondary hypoxic arrest; generalised muscle aches and neuro usually resolve in 24hrs

Question 31

Associations with altitude problems?

Answer 31

• Usually from skiing, trekking or working; ascend faster than bodies can acclimatise

Question 32

Patho of acclimatisation?

Answer 32

in ascent pO2 drops from barometric pressure drop, this means chemoreceptors respond to the hypobaric hypoxia by increasing resp rate and depth; kidneys prevent resp alkalosis by excreting bicarb and reabsorbing hydrogen ions; long-term increase in EPO increases RBCs and takes weeks

Question 33

Rules for ascension to reduce risk of altitude sickness?

Answer 33

above 3000m = each night’s sleep should only be 300m higher with a rest of 2-3 days or 1000m ascended; >5500m will be physical and mental deterioration

Question 34

Diagnosis and S+Ss acute mountain sickness (ACS)?

Answer 34

headache plus one of GI upset, fatigue/weakness, dizziness, difficulty sleeping couple of hours after ascent; common at >2500m, high cerebral blood flow, mild cerebral oedema, oxidative stress from oxygen free radicals

Question 35

Moderate and severe management of ACS?

Answer 35

managed by rest, hydration, analgesia, antiemetics for mild; severe = acetazolamide (250mg/8h po) and/or dexamethasone (4mg/6h po) but can’t descend on dexamethasone

Question 36

RFs for ACS?

Answer 36

rate of ascent, absolute altitude, blunted ventilatory response to hypoxia, level of exertion, home above >900m, previous AMS, concurrent URTI, neck irradiation/surgery

Question 37

Patho and definition of high-altitude cerebral oedema?

Answer 37

potentially fatal encephalopathy, change in mental state and/or ataxia usually preceded by AMS; patho = vasogenic cerebral oedema from disruption of BBB with/out cytotoxic oedema; needs more descent than HAPE

Question 38

Treatment high-altitude cerebral oedema?

Answer 38

acetazolamide, dexamethasone, consider O2, portable hyperbaric chamber, descent

Question 39

S+Ss and patho high-altitude pulmonary oedema?

Answer 39

– more common than HACE; usually 2-4 days after ascending to >3000m; S+Ss = cough, dyspnoea at rest, haemoptysis, lethargy, tachycardia, tachypnoea, cyanosis, crackles; patho = patchy pulmonary vasoconstriction so stress failure of pulmonary caps and pulmonary oedema

Question 40

RFs high-altitude pulmonary oedema?

Answer 40

strong hypoxic vasoconstrictor response, concurrent resp infection, congenital absence of pulmonary artery

Question 41

Treatment high-altitude pulmonary oedema?

Answer 41

descent, portable hyperbaric chamber, O2, nifedipine, acetazolamide and dexamethasone, sildenafil PO, inhaled salmeterol

Question 42

What is acetazolamide and what is it for?

Answer 42

carbonic anhydrase inhibitor causing more bicarb excretion from kidneys and aids acclimatisation; can use as prophylaxis 250mg/12h for those with previous AMS or rapid ascent; doesn’t hide AMS symptoms; helps sleeping; may have an allergy and give test dose prior to travel

Question 43

Precautions to take if working at high altitudes?

Answer 43

climb high, sleep low; avoid undue exertion; avoid alcohol/sedating antihistamines/sedating hypnotics; feel unwell is from altitude unless proved otherwise; don’t ascend with AMS S+Ss; never leave AMS pt alone; descend if HAPE or HACE

Question 44

Important points for wound management (6 points)?

Answer 44

o Irrigation with 0.9% saline asap o Infiltrate with lidocaine (works by blocking voltage-gated Na+ channels to stop depolarisation) 3mg/kg or 7mg/kg adrenaline, lidocaine is vasodilator so clears itself systemically and adrenaline vasconstricts to help reduce bleeding is useful and lidocaine is needed over 3mg/kg – SEE PAGE 773 FOR SPECIFIC DOSE CALCULATION o Can add some local anaesthesia 1% for suturing and put into devitalised tissue o Remove debris, foreign objects and material and necrosis; trim ragged edges; avoid excessive resection of facial tissue as reconstruction tricky; abrasions scrubbed/debrided thoroughly immediately o Avoid skin tension/wound inversion and use absorbable subcut sutures to bring skin together; use interrupted monofilament on the skin, 6’0 on the face and 5’0 or thicker elsewhere; brush suture knots away after 1 week o Remove sutures: face = 5 days, upper limb/body = 7-10, lower limb = 14

Question 45

Alternatives to sutures?

Answer 45

steri-strips = good for non-hairy strips and don’t get wet or rub, can be used with buried dermal absorbable sutures; glues (dermabond) = after haemostasis put on top of accurately apposed and dry skin edges, avoid thick layers as exothermic reaction can hurt, 30secs to dry then another layer, don’t get inside wound, don’t soak or scrub it

Question 46

When to use abx in wound management?

Answer 46

animal bite, hand wound

Question 47

Problems with pretibial lacerations?

Answer 47

poor blood supply and vulnerable to flap wounds (flap retracts back so can’t appose)

Question 48

Treatment for pretibial lacerations?

Answer 48

iron out all flap, evacuate haematoma so no tension, skin closure with adhesive strips not sutures as can be loosened, wound glue, dress and give supportive bandage and elevation; review = infection, necrosis, wound tension

Question 49

Wound healing limitations?

Answer 49

less easy with higher age, malnutrition, DM, steroids, smoking, peripheral vascular disease, irradiation

Question 50

What is chloramphenicol for?

Answer 50

cosmetic on face when scarring due to infection

Question 51

What is keloid and hypertrophic scarring?

Answer 51

keloid scarring = exaggerated as excess type 3 collagen production beyond wound and progressively; hypertrophic scarring = exaggerated scarring in the wound usually across a joint; both keloid and hypertrophic commoner in darker skin

Question 52

Problem and treatment for a hammered finger?

Answer 52

subungual haematoma, relieve blood pressure by trephine hole in the nail with a 19G needle, no force needed

Question 53

Problems with a swallowed fish bone and treat?

Answer 53

examine throat and tonsils, bone usually only grazed mucosa; if stuck remove with forceps; refer to ENT if fail

Question 54

Problems with fish-hooked barbed finger and treatment?

Answer 54

infiltrate with plain lidocaine and push barb through finger unless important structures; cut barb off once through and remove hook

Question 55

How to do a plaster cast for undisplaced forearm fxs?

Answer 55

remove anything stopping circ (rings); protect yourself and pt with apron; measure length for backslab (knuckles to below elbow); cut piece of plaster-impregnated bandage 5x longer and fold 5x; cut off corner for thumb hole and one on other side for the elbow; roll stockinette over forearm above elbow; wind roll of wool around this to protect from plaster; immerse hard plaster in water and apply to arm dorsum; reflect stockinette above and below over the hard plaster to protect at the edges; put bandage right around everything; takes 4mins to set; arm in sling for 1 day then encourage shoulder, elbow and finger movement

Question 56

Cautions for plaster casts?

Answer 56

return to ED if fingers swell/blue/can’t move them; don’t get plaster wet; do not lift heavy objects with hand

Question 57

How to remove a tight ring?

Answer 57

trauma and pregnancy; no.4 silk suture through ring distal to proximal, wind the suture at the distal end around the finger, then unwind from the proximal end distally; lubrication + compression + traction; can use a ring cutter

Question 58

Caught penis in zip management?

Answer 58

lots of lubrication with mineral oil; cut bridge of zip with strong wire cutters so zip falls apart; can use Savile Row technique (lidocaine and gently unzip)

Question 59

Mammal bites management in not risky?

Answer 59

clean well with soap and water/debride; avoid suturing unless deffo needed; give abx like co-amoxiclav

Question 60

High risk for mammal bites?

Answer 60

>50yrs, immunosuppressed, wound to hand/face/foot, delayed presentation, crush, reaches underlying structures

Question 61

Treatment for monkey bites?

Answer 61

use valaciclovir to stop cercopithecine herpesvirus 1 leading to encephalitis

Question 62

Dog bites treatment?

Answer 62

can give crush wounds so image, can transfer Pasteurella multocida streps and fusibacteria; check rabies and tetanus

Question 63

S+Ss snake bites?

Answer 63

only adder in UK usually in summer in long grass; S+Ss = nausea, ptosis, reduced GCS, weakness, coagulopathy, muscle pain

Question 64

Treatment for a snake bite?

Answer 64

immobilise limb and hospital (don’t do wound sucking, incisions, bandages and tourniquets), identify species asap; ABC = resp paralysis, hypotension, cardiac arrest, seizures

Question 65

Investigations for snake bites?

Answer 65

check clotting time, renal function, CK, D-dimer, FBC, urine for myoglobinuria, venom detection kits

Question 66

Specific treatments for snake bites?

Answer 66

UK use European viper venom antiserum, adrenaline to hand, if outside of UK antiserum in Liverpool/London, only admit if systemic symptoms under 2 hours for adders (advise rest, abx for secondary infection and antihistamine for swelling as can damage 4-5days after)

Question 67

Specific treatments for lesser weaver fish stings?

Answer 67

5-20 min in water as hot as tolerated/>45degrees

Question 68

S+Ss scorpion stings and treatment?

Answer 68

S+Ss = high/low bp, renal failure, LVF; treat = lidocaine, antidotes, prazosin/levocarnitine may help

Question 69

What foreign objects swallowed that need romving?

Answer 69

; if ingested mainly children/drug smugglers and do X-ray, if below level of diaphragm then discharged and observed, button batteries can cause oesophageal necrosis and need urgent removal

Question 70

S+Ss chronic oesophageal compaction?

Answer 70

poor feeding, FTT, stridor, PUO, repetitive aspiration pneumonia

Question 71

Treatment for chronic oesophageal compaction?

Answer 71

most pass it, may need Foley catheter and bougienage if obstruction and endoscopy for impacted oesophagus

Question 72

Treatment for bee stings?

Answer 72

scrape out with knife/credit card quickly; sting lasts longer if left in; pheromones released attracting more bees so run away; fatal >200 stings; treat = ice, calamine, antihistamines if severe itch, treat anaphylaxis

Question 73

Definition of major trauma?

Answer 73

multiple, serious injuries that could cause serious disability/death; high global mortality cause; mostly in 17-45yrs male from sport

Question 74

3 peaks of death from trauma?

Answer 74

trimodal distribution: first peak from major neurovasc disruption and not easy treat; second peak = head, thorax, limb, abdo haemorrhage; 3rd peak = sepsis and organ failure days later; mainly death in 1st two stages

Question 75

Definition of hypotensive?

Answer 75

low if <90; low if >40 lower than normal, MAP <65

Question 76

What does CABCDE stand for?

Answer 76

Control catastrophic haemorrhage, airway with C-spine protection, Breathing with ventilation, Circulation with haemorrhage control, Disability (Neuro status), Exposure/Environment (any limb injuries, pt warm, some bedside test, analgesia); THIS IS PRIMARY SURVEY IN TRAUMA

Question 77

What to do if NEWS2 >7?

Answer 77

escalate to senior and immediate review, sepsis 6, hourly fluid monitoring, contact critical care, consultants

Question 78

What to do if catastrophic injury?

Answer 78

clear any clots obscuring bleeding source; direct pressure; more direct pressure; indirect pressure; torniquet (2/3 inches above, not first line, less severe); haemostatic agents (ceelox)

Question 79

How long to secure airway in catastrophic injury?

Answer 79

try and secure in 45 mins; rapid sequence induction = for even more severe and should happen quicker (for absolute indications for intubation)

Question 80

Relative indications for intubation?

Answer 80

haemorrhagic shock when metabolic acidosis happening, agitated pt, multiple painful injuries, transfer to another hosp

Question 81

Absolute indications for intubation?

Answer 81

Can't maintain airway in any consciousness; can't keep oxygenation with less invasive manoeuvres; can't maintain normocapnia; deteriorating consciousness; significant facial injuries; seizures

Question 82

Airway and c-spine management and main indications?

Answer 82

immobilise C-spine, provide O2, assess airway, go to RSI if indicated; 3 main indications for immobilisation = mechanism or injury, head/neck/facial injury and low GCS

Question 83

Pathophysiology of clinical shock?

Answer 83

inadequate perfusion, cellular hypoxia, energy deficit, lactate build up (anaerobic resp), metabolic acidosis (vasoconstriction), cell membrane dysfunction, intracellular lysozyme release, cap endothelial damage, cell death

Question 84

Causes of clinical shock?

Answer 84

distributive (neurogenic and endocrine [addison’s crisis]), endocrine, septic, cardiogenic (ischaemic, arrhythmia), spinal, obstructive (tension ptx, PE, tamponade), hypovolaemic, anaphylactic, haemorrhagic

Question 85

Treatment pathway for clinical shock?

Answer 85

DR ABC; hypovolaemic (fluids lots and some vasopressor), septic/anaphylactic (fluid, vasopressor and sometimes inotrope), cardiogenic (maybe fluid but lots of inotrope)

Question 86

Basic life support for choking and not breathing?

Answer 86

• DRS ABC; CPR (100bpm, 5cm depth); for choking encourage coughing then 5 back blows then 5 abdo thrusts then alternate then CPR

Question 87

ABCDE in advanced life support in trauma?

Answer 87

ABCDE; A = airway, jaw thrust to protect C-spine (sometimes chin lift), 100% O2; B = breathing and auscultate lungs and heart, percuss chest; C = circ and haemorrhage control (2 points of venous access, replace blood if over 1.5L, younger and symptomatic tends to be severe, cardiogenic/neurogenic shock, use hypotensive resuscitation); D = disability (GCS/AVPU, pupillary reflexes, lateralising injury, spinal cord, BM, head injury); E = exposure (rewarm body if hypothermia; secondary survey after all this)

Question 88

What is ATMIST stand for and when is it applied?

Answer 88

age, time, mechanism, injuries, signs, treatments (how to handover in trauma)

Question 89

What is SBAR stand for and when is it applied?

Answer 89

in normal handover; situation, background, assessment, recommendation

Question 90

Reasons to send to a major trauma centre?

Answer 90

o Assessing vital signs and level of consciousness – GCS <14, sustained systolic <90, RR <10 or >29 or abnormal paeds value o Assess anatomy of injury – chest injury with altered physiology, traumatic amputation, penetrating trauma (neck, chest, abdo, back, groin), suspected open/depressed skull fx, suspected pelvic fx, spinal trauma from abnormal neuro, trauma with facial/circumferential burns, time critical (>20% burns) o Evaluate mechanism of injury – traumatic death in same passenger compartment, falls >20ft, person trapped under vehicle, bullseye window o Others – trauma with: >55yrs, >20wks preggaz, bleeding disorder, morbidly obese

Question 91

Main adjuncts to primary survey?

Answer 91

• CT scan within 30 mins rather than XRs and reported within 60; peripheral XRs in secondary survey also urinary catheters for outflow, NGT insertion if no facial injuries, ABG in cold pts for O2

Question 92

What is a FAST and pros and cons of its use in major trauma?

Answer 92

focussed assessment sonography in trauma; don’t use if delays CT, low negative predictive value (good for ruling in not ruling out), good for triaging in major incident scenario

Question 93

Portable CXR for in major trauma?

Answer 93

portable easily acquired; evaluate flail chest, massive pneumothorax, haemothorax, ET tube placement and widened mediastinum; lung contusion can look like atelectasis as blood fills lung from ruptured vessels; straight fluid line in lung is haemothorax and pneumothorax as air pushing against blood; flail chest just looks like a bit of rib cage floating

Question 94

Airway management?

Answer 94

weigh C-spine injury against hypoxia etc; look at rib fxs; reasons to intubate = GCS <9, sustained seizures, facial/airway trauma, high aspiration risk, flail segments, resp failure

Question 95

How to logroll a pt?

Answer 95

moving from bed to bed; keep spine secure and warn pt and person at head in charge; can disrupt: internal clots, induce spinal and pelvic movement, heighten distress; can move supine in a scoop too; try not to move if don’t have to

Question 96

XR of spine features looking for?

Answer 96

look at bones, cartilage, soft tissues and alignment; soft tissue should be less than 1/3 width of vertebrae above C4 but then after less than its width on XR; can view C-spine through mouth as well (PEG view)

Question 97

What is a jefferson's fx?

Answer 97

C1/atlas fx; from load on top of head; usually a burst/4 part fx in posterior and anterior arches

Question 98

What is a hangman fx?

Answer 98

C2; high force hyperextension; involved pedicles of C2 and anterior displacement of body and pedicle C2

Question 99

Teardrop fx?

Answer 99

fx of anterior and inferior aspect of vertebra from traction of anterior longitudinal ligament connecting them both; from severe hyperextension; soft tissue swelling as well

Question 100

Flexion teardrop fx?

Answer 100

opposite mechanism to above; bit lower; anterior cord compression

Question 101

Burst fx?

Answer 101

squash vertically into vertebra and bursts out from vertical load

Question 102

What is a normal facet alignment?

Answer 102

C-spine injury without radiological abnormality (SCIWORA); dislocation can return back spontaneously or remain in dislocated position; do an MRI if suspect this

Question 103

When to do intraosseus access and how?

Answer 103

no peripheral venous access; so go for this to deliver drugs if having difficulty finding a vein (trauma, DKA, severe burns); pushed into bone matrix to infuse through bone marrow into systemic circ; take sample of glucose, venous blood gas, electrolytes, haemoglobin first here before giving drugs

Question 104

CIs for intraosseus access?

Answer 104

failed attempt, infections, trauma at site, surgery near site; can lead to compartment syndrome and fxs but this is rare; remove asap to prevent osteomyelitis

Question 105

Initial fluid management for damage control resuscitation?

Answer 105

o Early haemostasis with surgery, splintage or angiography o Treat the lethal triad o Reduce crystalloid/colloid use if can (dilutes blood and doesn’t contain blood coagulants so can increase trauma based coagulopathy) o Early RBC, plasma, platelets use 1:1:1 o Hypotensive resus o May need damage control surgery

Question 106

Hypovolaemic shock S+Ss?

Answer 106

tachypnoea, pallor, hypotension, anxiety, tachycardia, bradycardia, arrest

Question 107

Causes of hypovolaemic shock?

Answer 107

blood on the (external haemorrhage) and 4 more (chest, abdo, pelvis and long bones = humerus, radius, femur, fibula, tibia, metacarpals)

Question 108

Total blood volumes in adult, child and neonates?

Answer 108

70mls/kg in adults; 80 mls/kg in kids and 90 mls/kg in neonates

Question 109

Osmolality definition?

Answer 109

osmoles per kg of solvent

Question 110

Osmolarity definition?

Answer 110

osmoles per litre of solution

Question 111

Tonicity definition?

Answer 111

ability of a solution to cause water movement

Question 112

What electrolyte moves out of cells during burns and crush injuries?

Answer 112

K+

Question 113

What is a crystalloid?

Answer 113

dissolved in water (Hartmann’s), more of this needed to give to pt than colloid

Question 114

What is a colloid?

Answer 114

suspension and not mixed (gelloplasma etc); most fluid resus now with colloid

Question 115

How to do a maintenance fluid calculation?

Answer 115

o For 0 - 10 kg = weight (kg) x 100 mL/kg/day; For 10-20 kg = 1000 mL + [weight (kg) x 50 ml/kg/day]; For > 20 kg = 1500 mL + [weight (kg) x 20 ml/kg/day] o Replace deficit over 12/24 hours; 4mls/kg then 2 mls/kg then replace with 1mls/kg o Need to do a U+Es everyday minimum if doing fluid resus

Question 116

Treatment for internal haemorrhage?

Answer 116

– IV tranexamic acid (1g over 10min then 1g over 4h) in 3hrs of injury; avoid crystalloid (can contribute to hypothermia, haemodilution of clotting factors and Hb so worsens coagulopathy); can have permissive hypotension as higher bp hydrostatic forces can disrupt clotting; aim for bp: 70-80mmhg in penetrating trauma, 90mmhg in blunt and cerebration in awake pt; resus after haemostasis achieved

Question 117

Best fluids to use?

Answer 117

see RBC, FFP and platelet ratio above (1:1:1); but the best is warm fresh whole blood but only really used by military due to difficulty storing; also fibrinogen for early clotting

Question 118

What is trauma induced coagulopathy and how to assess and treat?

Answer 118

treat if clinical suspicion from the lethal triad; lab tests hard to determine; younger can compensate and mask the blood loss and hypoxia (cryptic shock); can assess lactate, base excess, central venous oxygenation for blood loss; starting to do point of care coagulation testing; give Orh-ve blood until blood type determined and beriplex if warfarin

Question 119

When to fluid resus?

Answer 119

systolic below 90, HR >130mmHg, reduced consciousness, obvious massive ongoing blood loss

Question 120

Causes of shock?

Answer 120

from hypovolaemia; haemothorax with chest drain, abdo = surgery, splint long bones and pelvis for haemorrhage control, other causes of shock = neurogenic (spinal), cardiac tamponade, drug effects and tension pneumothorax

Question 121

What is FAST?

Answer 121

free fluid in pericardium/peritoneum (blood for trauma); 90% sensitivity and 200mLs+ detected; not for liver/spleen tears and hollow viscous injuries; extended FAST (eFAST) for haemo and pneumothoraces better than CXR, for hypotensive pt and no obvious bleeding; can be performed immediately after primary survey during secondary and non-invasive (don’t need diagnostic peritoneal lavage)

Question 122

What is the lethal triad?

Answer 122

• Three parameters interacting in major trauma – cascade of inflammatory mediators with neuroendocrine compensatory mechanisms can lead to death from organ failure; hypothermia, coagulopathy and acidosis interaction can all be caused by and cause each other that makes pt condition worse

Question 123

Definition of hypothermia?

Answer 123

<35degrees but <36 in trauma

Question 124

RFs for hypothermia?

Answer 124

elderly, intoxicated, burnt and exposed

Question 125

Patho for hypothermia?

Answer 125

dampens CVS compensation against hypovolaemic shock and worsens tissue hypoxia

Question 126

Acidosis patho?

Answer 126

tissue hypoperfusion and lactic acid production with resp acidosis from hypoventilation (flail chest, COPD, opiates); temp and pH influence clotting and platelets so small changes = life-threatening coagulopathies which is exacerbated by haemorrhage

Question 127

Coagulopathy patho?

Answer 127

¼ of severely injured and 4x mortality increase; can be from haemorrhage and haemodilution due to fluid resus, in minutes from tissue hypoperfusion, pre-existing medical conditions and anti-coagulating drugs

Question 128

Lethal triad, what to do on scene?

Answer 128

early hypothermia and haemorrhage control (apply pressure to bleeds and pelvic binder for internal; use blankets [bear hugger] and warmed fluids)

Question 129

Mnemonic for secondary survey?

Answer 129

Has My Critical Care Assessed Patient’s Priorities Or Next Management Decision? (Head/skull, Maxillofacial, C-spine, Chest, Abdo, Pelvis, Perineum, Orifices, Neuro, MSK, Diagnostic care)

Question 130

Overview of RTA assessment?

Answer 130

• Some clinical signs may not appear til later due to compensation and catecholamines; assessing injuries before removing from scene is v helpful; need a good handover from first on scene to hospital; pictures useful

Question 131

4 components leading to injury?

Answer 131

vehicle impacting with object; occupants hit in vehicle; organs jerked to a halt (rupture liver, aortic arch over 40mph); impact from unrestrained objects/people

Question 132

4 points of occupant injury?

Answer 132

impact of vehicle with object; pelvic and femoral fxs from handlebars and fuel tank; impact of landing; organs jerked to halt

Question 133

Questions to ask and general signs from RTA leading to injuries?

Answer 133

airbag deployed; state of car; other passengers; major injury visible; seatbelt worn and what type; relate vehicle damage to passenger injuries • Bullseye on windscreen – facial fxs and internal head injuries • Impact onto steering wheel – severe chest injuries/abdo compression (diaphragmatic rupture); seatbelt worn = clavicle, sternal, internal organ damage • Intruding dashboard – compress femur and dislocate hip posteriorly; patellar injury • Intruding engine compartment – tibia/fibular injuries/trapped feet • Lateral impact – worse than frontal impacts; complications = aortic dissections, lateral chest/abdo/pelvic compression injuries • Rear impact – lower back and whiplash • Fall from height – onto heels = calcaneum fx, pilon ankle fx, tibial plateau fx, hip injury, spinal compression, base of skull fx

Question 134

What is see saw movement of chest in resp mean?

Answer 134

obstruction as abdo sucked into chest during inspiration

Question 135

Most serious feature of chest injury?

Answer 135

hypoxia (give 15L O2 in rebreather bag)

Question 136

ATOM FC stands for what in primary survey?

Answer 136

Airway obstruction, tension pneumothorax, open pneumothorax, massive pneumothorax, flail chest, cardiac tamponade

Question 137

Airway obstruction S+Ss and treatment?

Answer 137

trauma to neck/face/larynx (also posterior dislocations of clavicular head); S+Ss = noisy breathing, stridor, altered voice; suction available for vomit and stop aspiration; after recovery position and jaw thrust doesn’t work use guedel airway (don’t insert if resisting – nasal airway, intubate, gentle suction)

Question 138

Tension pneumothorax S+Ss and treatment?

Answer 138

from penetrating injury making one way valve to thoracic cavity; can collapse lung and less venous return with other lung compression; S+Ss = diminished breath sounds, hyperresonance, distended neck veins, deviated trachea, hypoxia, tachycardia, hypotension (less venous return from increased intrathoracic pressure); treat = large-bore cannula into 2nd intercostal space in midclavicular line to decompress, chest tube if not work

Question 139

Open pneumothorax S+Ss and treatment?

Answer 139

sucking chest wound (wound seals on expiration and more air in when inspire – turns to tension); immediate occlusion with sterile dressing taped on 3 sides so flutter-valve; complete seal with chest drain

Question 140

Massive haemothorax S+Ss and treatment?

Answer 140

>1500mL blood in hemithorax; causes = wounds to intercostal vessels, great vessels, heart; S+Ss = hyporesonant; treat = large-bore chest drain (32G) with IV fluid/blood and maybe auto-transfusion of blood; may need thoracotomy; can cause haemopneumothorax

Question 141

Flail chest S+Ss and treatment?

Answer 141

section of fractured ribs with no bony continuity with rest of chest wall; can cause = serious hypoxia from bad chest wall movement and pulmonary contusions; S+Ss = looks abnormal on respiration; treat = high flow O2, may need to intubate/ventilate depending on resp distress; can get pulmonary contusions in blunt trauma too

Question 142

Cardiac tamponade S+Ss and treatment?

Answer 142

clinical diagnosis with Beck’s triad (rising JVP, falling BP and muffled HS) but easier with potable US; treat = pericardial aspiration before thoracotomy if needed; pericardial aspiration = 18G needle left to xiphisternum, aim at left shoulder with needle down, elevate legs for venous return; this is only temporary (can fail if clotted blood) and definitive treatment is pericardiotomy; afterwards = need cardiothoracic input, frequent ECHOs, invasive monitoring in ITU

Question 143

Injuries of chest identified in secondary survey?

Answer 143

simple pneumothorax, simple haemothorax, tracheobronchial tree/aortic dissection, blunt cardiac injury, oesophageal rupture

Question 144

Problems with simple pneumothorax?

Answer 144

can develop to tension

Question 145

Management simple haemothorax and problems?

Answer 145

<1500ml, if lung/blood vessel lacerations no surgery needed, large-calibre chest tube if big enough to be visualised on CXR, if left can clot leading to lung entrapment and infection

Question 146

Problems and management tracheobronchial tree/aortic disruption?

Answer 146

usually death at scene and urgent treatment, CXR and clinical diagnosis, if left can cause resp distress/bowel strangulation

Question 147

Problems with blunt cardiac injury?

Answer 147

most die on-scene, ECG and US monitoring (serious arrhythmias), if troponin rise can be cardiac contusion

Question 148

Problems with oesophageal rupture?

Answer 148

= if v unwell compared to injury, with left pleural effusions and/or pneumomediastinum

Question 149

Definition and causes of ventilation perfusion mismatch?

Answer 149

when blood volume circulating the lungs doesn’t get a high perfusion of O2 even when 100% O2 (low O2); usually due to shunts in lung and alveoli not ventilated (causes: alveolar collapse (atelectasis)/bronchoconstriction – pneumonia, post-op, lying down; oedema)

Question 150

Definitions of the different stages of CKD?

Answer 150

stage 1 = 1.5x, <0.5ml/kg/hr for >6 hours; stage 2 = 2x creatinine, <0.5ml/kg/hr for >12 hours; stage 3 = 3x creatinine, <0.3/kg/hr for 24 hours or anuria >12 hours or RRT

Question 151

Patho of electrolytes in renal failure?

Answer 151

when renal failure K+ and H+ stay in capillaries and Na+ stays in tubules as pumps for these stop working (hyperkalaemia and acidaemia)

Question 152

STOP causes of renal impairment?

Answer 152

sepsis/shock, toxins, obstruction, pressure optimisation

Question 153

Pre-renal causes of renal failure?

Answer 153

S and P (S = hypovolaemic, septic [cap walls become leaky and less fluid, less O2 to proximal convoluted tubules so die and get acute tubular necrosis], cardiogenic [less blood pumped round]; P = )

Question 154

Renal causes of renal failure?

Answer 154

T (acute interstitial nephritis = renal lesion meaning decline in kidney function and means inflammatory infiltrate in kidney interstitium [from NSAIDs]; T = tubular toxicity, contrast from scans, gentamicin esp with furosemide)

Question 155

Post-renal causes of renal failure?

Answer 155

O (can be stones and calculi or cancer) | o For all forms acute kidney injury - CVVH machine or haemodialysis

Question 156

Types and definitions of resp failure?

Answer 156

pO2 <8kpa; type 1 = low O2, low/normal CO2; type 2 = low O2, high CO2 (stop being able to hyperventilate to get rid of O2), respiratory acidosis

Question 157

Types of O2 flow for different resp failure types?

Answer 157

* EPAP – expiratory positive air pressure; for low O2 problem; same as CPAP (continuous positive air pressure) * IPAP – inspiratory for high CO2 * NIV – non-invasive ventilation * BiPAP – biphasic positive air pressures; includes inspiratory and expiratory for type 2 * Treatment – PEEP (positive end expiratory pressure) for oedema to push fluid back into capillaries

Question 158

What does a high base excess mean?

Answer 158

Metabolic acidosis

Question 159

What does a high pCO2 mean?

Answer 159

Resp acidosis

Question 160

What does normal pH with high/low pCO2 mean?

Answer 160

Compensating

Question 161

Sepsis definition?

Answer 161

life threatening organ dysfunction by dysregulated host response to infection (body response to infection damages itself) o HAT – hypertension, altered mental state, tachypnoea (resp rate above 20)

Question 162

Patho of sepsis?

Answer 162

TLRs activate macrophages releasing inflammatory cytokines; arachidonic pathway activated; coagulation system activated (pro-thrombotic) and anticoagulation down regulated; decrease contractility, vasodilate, RV dilatation, arrhythmias, PAH (TLRs, cytokines and NO)

Question 163

What is septic shock?

Answer 163

sepsis and hypotension unresponsive to fluid and lactate more than 2

Question 164

What's BUFALO?

Answer 164

``` sepsis 6 (blood cultures, hourly urine output, intravenous fluid challenges, broad spectrum abx, serum lactate, high flow O2) • EARLY TREATMENT IMPORTANT ```

Question 165

Give the GCS scoring system?

Answer 165

eyes (4 – spontaneous, to speech, to pain, none); verbal (5 – orientated, confused, words, sounds, none); motor (6 – obeys commands, localising, normal flexion, abnormal flexion [decorticate], abnormal extension [decerebrate], none)

Question 166

When do blast injuries occur?

Answer 166

– domestic (gas explosion), industrial (mining), military/terrorist bombings; multiple casualties

Question 167

4 phases of blast injuries and explanations for each?

Answer 167

o PRIMARY INJURIES – absence of external features so easily missed; types = compress gas-filled spaces from pressure generated (ears, intestinal perforation, haemorrhage, fatal air embolism in coronary/cerebral arteries), pulmonary barotrauma most common cause of death for those that survive, intra-alveolar haemorrhage can cause ARDS o SECONDARY INJURIES – from missiles and projectiles giving blunt and penetrative trauma; most common injuries o TERTIARY INJURIES – victim thrown by blast and striking surrounding objects o QUARTERNARY – other injuries = burns, asphyxia, crush, toxic substance exposure (radiation, CO, cyanide)

Question 168

Psych support for blast injuries?

Answer 168

stop the aim of the terrorist (fear and panic); long-term = chronic intrusive thoughts, anxiety, PTSD, poor conc

Question 169

First on scene for blast injuries to bear in mind?

Answer 169

• Don’t approach scene until know it’s safe; don’t disturb crime scene unless to help pt

Question 170

Problems with trauma in the elderly?

Answer 170

• Kyphosis, resp difficulties, less preload and more afterload so lower (less body water, peripheral vasculature more rigid, less myocardium) CO, IHD; frailty; polypharmacy

Question 171

Why more likely to have ICP that ruptures brain vessels in the elderly?

Answer 171

• ICP more likely to rupture vessels in brain as more rigid but less CSF; more space due to brain atrophy so can bleed more whilst compensating before it’s too late

Question 172

Complications of elderly trauma?

Answer 172

* Prognosis of survival of head injury declines after 56yrs * High risk of C-spine injury as more rigid and fixed and softer bones and methods to immobilise an be hazardous to elderly * More likely to get secondary pneumonia and larger risk from minor injuries in thoracic injuries * Abdo – protection weaker and examination unreliable

Question 173

I HATE FALLING in elderly for trauma RFs?

Answer 173

inflammation of joints, hypotension, auditory and visual abnormal, tremor, equilibrium problem (balance), foot problem, arrhythmias (heart block/valvular), leg-length discrepancy, lack of conditioning (generalised weakness), illness, nutrition, gait disturbance

Question 174

Influencing factors in gunshot wounds?

Answer 174

* Either high (military rifles) or low (handguns more likely to lacerate/crush) velocity * Influencing factors – weapon used, bullet speed, distance, trajectory, yaw (how tip deviates in flight) and tumble (how travels directly through body)

Question 175

Injury usually from gunshot wounds?

Answer 175

most lethal to head then myocardium; chest usually cause haemopneumothorax

Question 176

Definition of primary and secondary head injuries?

Answer 176

• Primary = at the time; secondary = mins/days after from neurophysical and anatomical (high ICP, cerebral oedema, expanding haematomas, seizures, infection, hypoxic/hypoperfusion)

Question 177

What things to measure first in head injuries?

Answer 177

o AVPU, pupillary size and response, motor score of GCS (most predictive outcome), sensory if able to

Question 178

Leading causes of head injuries?

Answer 178

assaults, falls, RTAs; alcohol gives most complications and can mask it

Question 179

Things to check in head injury?

Answer 179

unequal pupils big red light in unconscious; assess power, tone, reflexes, sensory upper/lower/left/right; check for priapism and anal tone (spinal injury), spinal shock syndrome can also cause transient neuro features; low bp with low pulse = sympathetic disruption in c-spine

Question 180

Types of head injuries?

Answer 180

cranial (skull fx and c-spine); intracranial (diffuse axonal injury, extradural injury, subdural bleed, subarachnoid bleed, intracerebral bleed, cerebral contusion)

Question 181

Head injury imaging criteria?

Answer 181

head injury + low GCS need head CT within 1 hour and report with 1 hour scan; if no Rfs then pts on anti-coagulants need one within 8hrs

Question 182

RFs for urgent CT head?

Answer 182

GCS <13, GCS <15 2hrs post injury, open/depressed/basal skull fx, fit after, focal CNS deficit, >1 ep vomiting; any LOC/amnesia with: >65yrs, dangerous mechanism of injury, coagulopathy, retrograde amnesia >30mins

Question 183

Adding c spine CT with CT head criteria?

Answer 183

GCS <13 initially, intubation, multi-region trauma; any suspicion of spinal trauma + >65yrs/dangerous mechanism/focal CNS deficit/paraesthesia in any limbs

Question 184

Management of head injury?

Answer 184

admit with consultant specialist in head trauma; if not concerning then discharged with head injury advice leaflets

Question 185

Minor head injury considerations in elderly?

Answer 185

symptoms and INR not always reliable; consider INR reversal if high to stop ICH (higher risk with clopidogrel than warfarin); minimise haematoma expansion

Question 186

What is a high ICP definition?

Answer 186

>20mmHg

Question 187

Patho high ICP?

Answer 187

mass can be accommodated up until a point by displacement of vessels and CSF but after a while will cause hypoperfusion

Question 188

Treatment of high ICP?

Answer 188

enhance perfusion by normalising ICP and monitoring mean arterial pressure (MAP), target MAP = 90mmHg and CPP >60mmHg

Question 189

What is Cushing's triad?

Answer 189

for indicating high ICP = bradycardia, irregular resps, widened pulse pressure

Question 190

Medical management of head injuries?

Answer 190

avoid hypotension (bp>90 but better over 100, use isotonic solutions for normovolaemia, don’t overload or use glucose), avoid hypercapnia and hypoxia (O2>11 kpa, CO2 4.5-5 kpa to optimise CPP, hyperventilation reduces CO2 so cerebral vasoconstriction and lower ICP but not for too long as can cause hypoperfusion), opiates (mitigate stress response from intubation and increase ICP), mannitol (0.25-1g/kg of 20% solution causes osmotic diuresis to reduce ICP in acute but careful of systemic hypotension), seizure control (IV lorazepam/buccal midazolam to stop high ICP, can also use prophylaxis), raise head to 30 degrees (improve jugular venous return), avoid of hyperglycaemia and hyperpyrexia, urgent neurosurgical input; secure airway GCS <8; try and get normal ICP/gluc/O2/CO2

Question 191

Borders of abdo?

Answer 191

T4 (nips) to groin and to iliac crests posteriorly, diaphragmatic rupture can mean contents in chest

Question 192

Key questions for abdo injury?

Answer 192

peritoneum breached, intra-peritoneal organs damaged, don’t deny analgesia for fear of masking signs

Question 193

Penetrating trauma in abdo overview?

Answer 193

high-velocity missiles harder to predict than stab wounds; liver most commonly injured; surgery if posterior rectus sheath breached; only no surgery for v superficial

Question 194

Most common injuries and how in blunt trauma in abdo?

Answer 194

deceleration can mean bowel comes from mesentery, liver from vena cava, bladder from its neck, pancreas from retroperitoneum and aorta; spleen most commonly injured (suspect rupture if shock, abdo tenderness/distension, left shoulder tip pain, overlying rib – bit like ectopic pregnancy and may not be as painful as other abdo trauma)

Question 195

How pts unstable in abdo trauma and management?

Answer 195

from bp, shock, GI/GU/PR bleeding, evisceration, peritonitis; immediate laparotomy; FAST scan for haemoperitoneum; portable CXR quickly; hypotensive resus and cross match >6L blood

Question 196

Management stable pts in abdo trauma?

Answer 196

still suspicious as bp doesn’t drop til 30% blood loss; mainstay invest = constant vitals, abdo examine, FAST scans; CVP/CT/US can be misleading; consider diagnostic laparoscopy for seeing damage to peritoneum/diaphragm; observe for minimum 24hrs

Question 197

Management in asymptomatic pts with anterior abdo stab wounds?

Answer 197

many don’t penetrate abdo cavity and more don’t need surgery; wound assess first to see if rectus fascia intact and comprehensive wound exploration to see if can discharge (can use local anaesthesia); further invest if needed = FAST scans and serial examinations; careful for chest exploration for pneumothorax, use contrast CT rather than exploration for posterior tracking wounds

Question 198

Why do emergency laparotomy in abdo trauma?

Answer 198

peritonism, radiological evidence of free air, GI haemorrhage, persistent/resistant haemodynamic instability (won’t respond to treat)

Question 199

Why to do radiology in trauma?

Answer 199

• Unrecognised haemorrhage contributes to lethal triad and deaths in trauma

Question 200

What type of radiology first line in trauma?

Answer 200

use interventional radiology to stop haemorrhaging (transcatheter embolization and stents to realign and plug up bleeds) without the stress of surgery; this can be for abdo but also endovascular techniques for organs (spleen [don’t lose immunity from splenectomy], liver etc)

Question 201

What surgical interventions first line in trauma?

Answer 201

* Move towards trying to do endovascular techniques before surgery if can (didn’t use to be the case in the past) even in those who are haemodynamically unstable * Still no rigid guidelines and should go by what most senior person thinks

Question 202

What is RAPTOR?

Answer 202

resuscitation with angiography, percutaneous techniques and operative repair suite is a new concept where interventional radiology, surgery and resus equipment in one place

Question 203

Common things to think about in pelvic injuries?

Answer 203

• Only when >2 fxs in pelvis is its protection unstable and usually need to worry about internal injuries more; usually break in 2 places

Question 204

How to assess a pelvic injury?

Answer 204

don’t rock the pelvis (can disturb tamponade of retroperitoneal haematoma, exacerbating haemorrhage); gently compress to assess stability; Tile classification is best (CHECK PAGE 794 FOR DIFFERENT TYPES)

Question 205

What is AP compression in pelvic injury?

Answer 205

open book injury (pubic symphysis wider than 5mm); crush injury; v bad news bears

Question 206

What is vertical shear in pelvic injury?

Answer 206

vertical, unilateral fractures of pubic rami; bucket handle; malgaigne (ipsilateral so fxs on same side)

Question 207

What is lateral compression in pelvic injury?

Answer 207

oblique fxs of pubic rami, sacral fx, impaction, diastasis of pubis symphysis; lateral force from crush or something

Question 208

S+Ss in pelvic fx?

Answer 208

leg length discrepancy, abdo distension, loin bruising, perineal/scrotal haematoma, # line on PR/PV exam (if rectal injury then can get sepsis)

Question 209

S+Ss GU injury in pelvic injury?

Answer 209

urethral injury in 15% males; extra-peritoneal bladder rupture can give false +ve FAST scan; blood at tip, frank/microscopic haematuria, PR exam to assess bowel integrity and presence of blood, urology if urethral damage suspicion (blood at tip) and retrograde urethrography performed; may need suprapubic catheterisation

Question 210

Reducing blood loss in pelvic injury?

Answer 210

apply pelvic splints (put over greater trochanters) but don’t compress to less than normal circ; use orthopaedic scoops not logrolls; check foot pulses and urine often; high chance of mortality from shock

Question 211

Associated injuries to pelvic fx?

Answer 211

usually internal injuries, splenic lesions, diaphragm and bladder ruptures, liver lacerations, urethral lesions, intestinal lesions and kidney rupture

Question 212

Radiology for pelvic injury?

Answer 212

FAST scan for intraperitoneal fluid; only XR if don’t need CT; use endovascular embolization for haemorrhage control; fx can be fixed when pt stable

Question 213

Stats for trauma in pregnancy?

Answer 213

affects 1 in 12 pregnancies and leading cause of maternal death

Question 214

Mitigating risks to trauma in pregnancy?

Answer 214

road safety, educate on seatbelt use, educate on falls (more susceptible from weight gain and joint laxity)

Question 215

Consequences of trauma in pregnancy?

Answer 215

blunt trauma usually causes placental abruption and high risk of feto-maternal haemorrhage; penetrative is better maternal but poorer foetal survival; foetal death usually from hypoxia secondary to cardiovascular disruption

Question 216

Management of trauma in pregnancy?

Answer 216

3rd trimester+ put woman in left lateral tilt position to stop aortocaval compression and increases CO by 30%; give Rh-ve mothers IM anti-D within 72hrs abdo trauma; primary survey normal but in secondary also do vaginal/perineal/rectal examination and continuous foetal monitoring; foetal distress in asymptomatic mum = early sign of hypovolaemia; get gestational age quick help predict outcome and treatment; resus of mother is resus to foetus; mother gets priority

Question 217

Indication for C section after trauma in pregnancy?

Answer 217

laparotomy to assess internal organs, uterine rupture, foetal distress with viable foetus, maternal cardiac arrest within 5 mins of CPR (no foetus improves CPR

Question 218

Functions of the liver?

Answer 218

o Protein, clotting factors, bile and glucagon synthesis o Alcohol, drugs, ammonia, bilirubin detox o Energy, vitamins and mineral storage o Part of immune system

Question 219

Consequences of liver failure?

Answer 219

• ALF (acute liver failure) – acute liver injury results in jaundice, coagulopathy (INR >1.5) and hepatic encephalopathy, in 12 weeks; rare with high mortality; occurs after insult to liver

Question 220

Definitions for acute, hyperacute and subacute liver failure?

Answer 220

o Hyperacute – within 7 days ALF (usually paracetamol) o Acute – 8 to 28 days (HBV cause) o Subacute – 29 days to 12 wks

Question 221

Common causes of ALF in the UK?

Answer 221

paracetamol, mushrooms, legal highs, anabolic steroids, herbal medicines; hep A and E with B, abx and MDMA; HELLP in pregnancy

Question 222

Patho for paracetamol?

Answer 222

Metabolised through CYP450 to make N-acetyl-p-benzoquinoneimine (toxic metabolite) detoxed by glutathione (in OD may not be enough glutathione)

Question 223

Factors increasing paracetamol hepatotoxicity?

Answer 223

Staggered OD, excessive alcohol, malnutrition, HIV, cancer, chronic liver disease, liver enzyme inducer drugs (antiepileptics, rifampicin, spironolactone)

Question 224

Treatment paracetamol OD?

Answer 224

n-acteylcysteine, abx, fluids, rest

Question 225

Inhalational and IV anaesthesia examples?

Answer 225

INHALATIONAL (sevoflurane, desflurane [mostly in the obese – not good for greenhouse gases], isolfurane); IV (propofol, thiopentone); IV propofol is the best for inducting

Question 226

Recommendation speed for IV?

Answer 226

give any IV drug over 1 minute so even spread and slower if low CO (reduce side effects like hypotension); give opioid before anaesthesia so less needed to sedate

Question 227

Types of analgesia?

Answer 227

opioids (morphine, codeine, diamorphine, oxycodone, dihydrocodeine), synthetic opioids (pethidine, fentanyl, alfentanil, remifentanil); synthetic partial agonists (buprenorphine); antagonists of opioids (naloxone)

Question 228

Recommendation for dosage of opioids depending on route?

Answer 228

as 50% metabolised first pass by liver so give half the dose parenterally than orally for same dosage (10mg oral = 5mg parenteral); PCA = patient controlled analgesia

Question 229

Patho of morphine metabolism and OD?

Answer 229

metabolised to morphine 6 glucuronide and more potent but cleared quickly in normal renal function but can build up in failure and quickly cause resp depression (not in <30% renal function) can use oxycodone instead

Question 230

Types of muscle relaxants?

Answer 230

neuromuscular blocking agents (block ach at binding site; depolarising [suxamethonium] or non-depolarising [atracurium or rocuronium])

Question 231

Treating opioid induced resp depression?

Answer 231

IV fastest route; titrate drug accordingly and don’t give all at once (1ml in 10ml saline); short half-life of naloxone and be careful of OD in addicts; one ampoule is usually enough for an adult

Question 232

Drug targets?

Answer 232

ion channel (ach receptor at nmj), G protein coupled (opioid receptors), enzyme inhibitors (anticholinesterases, COX inhibitors)

Question 233

Types of local anaesthetics?

Answer 233

lidocaine, xylocaine (lido with adrenaline), spaff, prilocaine (least toxic), bupivacaine (most toxic, use for post-op analgesia); myelinated fibres harder to block and need stronger conc of anaesthesia

Question 234

Max dosage lidocaine 2%?

Answer 234

300mg

Question 235

Max dosage mepivacaine 3% plain?

Answer 235

300mg

Question 236

Max dosage articaine 4%?

Answer 236

500mg

Question 237

Max dosage prilocaine 4% plain?

Answer 237

400mg

Question 238

`Max dosage bupivocaine 0.5%?

Answer 238

90mg

Question 239

Toxicity symptoms opioids?

Answer 239

tingling, CV collapse, tinnitus

Question 240

CIs opioids?

Answer 240

regular paracetamol reduces morphine efficacy by 20%; NSAIDs should be fine

Question 241

Drugs for sedation and antagonist to it?

Answer 241

midazolam (1mg at a time); flumazenil is antagonist to benzos; can cause apnoea if too much midazolam

Question 242

Types of anti-emetics?

Answer 242

5HT3 antagonists (ondansetron), antihistamines (cyclizine), antidopaminergic (metoclopramide)

Question 243

What does a high lactate mean?

Answer 243

lactic acidosis from dehydration, blood problems (leukaemia), liver disease/damage meaning it can’t break down lactic acid

Question 244

Dx of scalp/facial haematoma management?

Answer 244

discharge with advice and safety net with symptoms of possible ICP/brain injury (unless on anticoags)

Question 245

Gold standard for diagnosing PE?

Answer 245

CTPA (CT pulmonary angiography)

Question 246

What is PERLA?

Answer 246

pupils equal and reacting to light and accommodating

Question 247

Troponin results for suspected ACS?

Answer 247

>5 = repeat in 2 hours and if increase by 7 then ACS; >50 = ACS

Question 248

Difference between exudative and transudative pleural effusion?

Answer 248

exudative = malignancy/infection, protein >30, fluid sucked out; transudative = HF, protein <30, fluid pushed out

Question 249

Treatment for ACS?

Answer 249

300mg aspirin, fondaparinux, ticagrelor

Question 250

Investigation targeted at ACS?

Answer 250

Troponin T

Question 251

Investigation targeted at PE?

Answer 251

D-dimer

Question 252

What is ABCD2 for TIA?

Answer 252

A — Age: 60 years of age or more (1 point) B — BP (at presentation) 140/90 mm Hg or greater (1 point) C — Clinical features Unilateral weakness, 2 points Speech disturbance without weakness, 1 point. D — Duration (60 minutes or longer, 2 points, 10–59 minutes, 1 point) D — presence of diabetes: 1 point

Question 253

What happens with high risk from ABCD2?

Answer 253

MRI, carotid US and consult neuro

Question 254

What is CHADSVASC for AF?

Answer 254

congestive HF (1), hypertension (1), age >75 (2), DM (1), stroke/TIA/systemic embolism (2), vascular disease (1), 65-74yrs (1), sex = female (1)

Question 255

What is a moderate to high risk score from CHADSVASC and what should be done?

Answer 255

Above 2 and consider anticoag

Question 256

What is HASBLED?

Answer 256

hypertension, abnormal renal/liver function, stroke, bleeding, labile INRs, >65yrs, drugs/alcohol; higher the score the more carefully should consider if need anticoagulants

Question 257

Aortic stenosis/ejection systolic murmur?

Answer 257

Collapse from vasovagal syncope

Question 258

Pleuritic chest pain causes?

Answer 258

PE, pulmonary oedema, pleural effusion

Question 259

AEIOU tips mnemonic for causes of collapse?

Answer 259

alcohol, epilepsy, infection, OD, uraemia, trauma, insulin, poisoning, stroke

Question 260

T waves tall cause?

Answer 260

Hypokalaemia

Question 261

Consequences of COVID?

Answer 261

Pneumonitis, hypercoagualable state so leads to stroke/PE and can show up on D dimer test

Question 262

What is zero point survey/STEPUP?

Answer 262

self [danger to self], team [leader, roles allocated, briefing], environment [danger, space, light etc], patient [primary survey – ABCDE], update [check pt status], priorities [identify team goals and set mission trajectory]); secure the airway, give O2, assess cardioresp function (O2 sats, HR, bp, BM

Question 263

Drugs for fitting pt if no IV access?

Answer 263

Status epilepticus (seizure longer than 5 mins or more than 1 seizure in 5-minute period) so buccal/rectal midazolam 10mg first line in children/young people/adults; check if on opioids (can give resp depression), so for methadone in IVDU, previous coma from benzos, lung problems (CNS depression, severe resp depression, compromised airway)

Question 264

Drugs for pt if IV access?

Answer 264

IV access then give IV lorazepam 4mg

Question 265

SEs of benzos?

Answer 265

give women and partners (of childbearing age) info of AEDs and benzo effects on neurodevelopment of unborn children (sodium valproate risks if on it), give with combined hormonal contraception/COCP; dependence problems and withdrawal effects (confusion, muscle twitching, seizures, paranoia, depression etc)

Question 266

If benzo therapy not working for fitting pt?

Answer 266

Diazepam 10mg if midazolam and lorazepam unavailable; second dose of benzos if unresponsive; after this then additional maintenance treatment with AEDs (IV phenytoin)

Question 267

Things to check whilst on IV phenytoin?

Answer 267

Rate of infusion changed if hypotension/arrhythmias/renal/hepatic impairment; ECG monitoring and EEG

Question 268

Alternatives to IV phenytoin?

Answer 268

also can use sodium valproate but probs not in women of childbearing age or IV levetiracetam

Question 269

Causes of status epilepticus?

Answer 269

alcohol withdrawal; hypoglycaemia; poorly controlled epilepsy; stroke; renal failure; liver failure; encephalitis; HIV; drug abuse; genetic diseases (fragile X/angelman syndrome); head injuries

Question 270

Invest and treatments of causes of status epilepticus?

Answer 270

chlordiazepoxide, thiamine/pabrinex (alcohol withdrawal); methadone (opioid addiction/withdrawal); FBC, U+Es, LFTs, calcium, glucose, clotting, antiepileptic drug levels, serum drug levels, EEG, ECG, blood gases to assess acidosis; evacuate haematoma in brain (craniotomy); mannitol for high ICP; encephalitis = benzylpenicillin etc

Question 271

Medical complications of status epilepticus?

Answer 271

physical disability, mental disability, coma, death

Question 272

Early alcohol withdrawal signs?

Answer 272

insomnia, autonomic dysfunction, tremor, N+V, agitation, anxiety, seizures (generalised), hallucinations

Question 273

Treating features of alcohol withdrawal?

Answer 273

pabrinex, chlordiazepoxide, benzos

Question 274

Features of delirium tremens?

Answer 274

tremors, hallucinations, seizures, confusion, agitations, hyperactivity, LOC, insomnia, fever, high BP, rapid HR, excessive sweating, dehydration

Question 275

Treating delirium tremens?

Answer 275

continuous sedation through the administration of benzos; IV fluids; antipsychotic meds for agitation and hallucinations

Question 276

Assessing alcohol dependence?

Answer 276

FAST, AUDIT, Glasgow Modified Alcohol Withdrawal Scale (GMAWS)

Question 277

Possible causes of chest pain?

Answer 277

MI – serious, possible; angina – not too serious but needs to be treated, very likely; anxiety attack – not serious, possible; PE – serious, possible; gastritis – possible (can lead to ulcers with blood brought up), possible; MSK – depends how much is affecting the person to it’s seriousness (broken bones, flail chest), possible if after trauma; pneumothorax – more in young men, serious if becomes tension; pericarditis – serious, less common; pleural effusion/pulmonary oedema from pneumonia or infection – serious at a certain point; stab/gunshot wound – v serious to chest, unlikely and usually visually seen; aortic dissection; ischaemic cardiac pain

Question 278

RFs for IHD?

Answer 278

male gender, active smoker, positive family history; others = previous coronary artery disease, advanced age, diabetes, hypertension, hypercholesterolaemia, obesity, sedentary lifestyle, aspirin

Question 279

Causes of chest pain associated with chest wall tenderness?

Answer 279

pulmonary oedema, PE, pleural effusion, bruising to intercostals/rib fxs, angina, MI, ACS, pericarditis; more likely to be MSK injuries if chest wall tenderness

Question 280

Significance of chest pain on exertion?

Answer 280

less likely to be MSK and more likely to be vascular/cardiac/resp cause (ischaemic cardiac cause); more likely to be stable angina than unstable and can be controlled more effectively with medication, not as significant risk to health

Question 281

Bedside test in first few mins of finding coma pt, why and treat?

Answer 281

blood glucose (BMs), hypoglycaemia/hypers, diabetic ketoacidosis can lead to cerebral oedema and then to uncal herniation which is imminent death if untreated; can also mean hypokalaemia, pulmonary oedema and fluid loss causing kidney/organ damage; get IV access and give dextrose if hypoglycaemic (5mls per kg)

Question 282

Further assessment of coma pt after ABCD?

Answer 282

E – exposure (hypothermia); secondary survey for broken bones/c-spine injury; immediate CT; needs a GCS 12 or less, full neuro exam?; GCS is 7; maintaining airway even though in coma (recommended to secure airway manually if GCS <8); FBC (WBCs, hb); U+Es (hyponatraemia in the elderly, hypo/hyperkalaemia [3.5-4.5 is normal], urea [uraemia from renal failure]); LFTs for liver failure; coag screen; VBG (lactate and pH and CO2 and base excess); head CT

Question 283

Normal temp range in pt?

Answer 283

36.5-37.5

Question 284

Give the GCS scorign system?

Answer 284

out of 15; eyes (4 – spontaneous, to speech, to pain, none); verbal (5 – orientated, confused, words, sounds, none); motor (6 – obeys commands, localising, normal flexion, abnormal flexion [decorticate], abnormal extension [decerebrate], none)

Question 285

Where to apply pain stimulus?

Answer 285

under the eye socket, behind the ear and sternal rub, under the floating ribs

Question 286

Possible diagnoses for coma?

Answer 286

head injury (hypotension, hypoxia, extradural haematoma), no head injury (acute CVS event, acute hypoglycaemia/hyperglycaemia), no head injury/no neuro signs (infection like meningitis, cerebral malaria – abx therapy), no head injury/no neuro signs, infection unlikely (poisoned, toxin like CO, tricyclics, narcotics or something arising from end organ failure like DKA, myxoedema coma, resp failure – use ABG, serum anion gap and serum electrolytes), alcohol (acute intoxication), decorticate (injury to midbrain), decerebrate (brainstem lesion)

Question 287

Treatment for opioid OD?

Answer 287

IV naloxone hydrochloride; initially 400micrograms then 800 for up to 2 doses at 1 minute intervals if not responding to preceding dose then to 2mg if still no response; can be given subcut, IM routes (400mg every 2-3mins) only if IV not feasible; also intranasal (1.8mg)

Question 288

Why danger still remains in IVDU treated with naloxone?

Answer 288

if still high serum opioid then naloxone has shorter half-life than most opioids like heroine and could be discharged but may go into resp depression again; also may be angry and withdrawal effects

Question 289

Uncal herniation signs?

Answer 289

uncal herniation (the bruising are battle scars and then yellow liquid is CSF); will be from high ICP from cerebral oedema/haematoma/extradural haemorrhage from middle meningeal artery after lucid interval; depressed brain fx can introduce infection (meningitis) or focal epilepsy when presses on the brain

Question 290

Causes of tachycardia in major trauma?

Answer 290

anxiety, pain, internal bleeding, hypothermia (lethal triad – hypothermia, coagulopathy, acidosis); distributive (neurogenic and endocrine [addison’s crisis]), endocrine, septic, cardiogenic (ischaemic, arrhythmia), spinal, obstructive (tension ptx, PE, tamponade), hypovolaemic, anaphylactic, haemorrhagic

Question 291

Priorities of what to do after assessing major trauma pt?

Answer 291

obtain IV access and start IV normal saline, catheterise, FAST scan, feel for foot pulses and manipulate, carry out secondary survey

Question 292

Normal blood tests to do for major trauma?

Answer 292

FBC, VBG, U+Es, LFTs, clotting, trop T, D dimer, group and save

Question 293

What is permissive hypotensive resuscitation?

Answer 293

use of restrictive fluid therapy (mainly in trauma pt) to increase systemic bp without achieving normotension (get to around 90 systolic which is enough to maintain vital perfusion)

Question 294

What is major haemorrhage protocol?

Answer 294

more than 5L of blood loss in 24 hours/150ml per minute; source of haemorrhage (use SCALPeR – scalp and external, chest, abdo, long bones, pelvis, retroperitoneum); approach to control (help, cause, direct pressure/elevation/adrenaline/tourniquets; invasive measures if needed; correct coagulopathy); pulse palpation to guide bp (carotid = 60-70mmHg, femoral = 70-80mmHg, radial = >80); 4 classes of haemorrhagic shock (4th is worse = >200mL and with bradycardia); hypothermia prevention and treatment; damage control resus (DCR – permissive hypotension, early haemostatic resus and damage control surgery)

Question 295

Indications for WBCT?

Answer 295

high motor speed vehicle collision, non-trivial motorbike collision, death at scene, fall from height >2m, other concerning mechanism of injury, abnormal FAST/trauma chest/pelvis XR, abnormal vitals; non-contrast, CT brain, face, c-spine, thorax and upper abdo in angiographic/delayed phase, abdo or pelvis in portal venous phase, multiplanar reconstructions of thoracic and lumber spine; interventional radiologist in trauma (help uncover lots of incidental findings and clinical assessment may underestimate injury severity by 30%; they do all the imaging by CT, can use angiography to stop the bleeding on site rather than from outside by pressure, laparoscopy so less recovery time)

Question 296

4 stages of splenic injury?

Answer 296

splenic rupture/internal haemorrhage; splenic injury (1 = capsular, 2 = capsular and bleeding on outside, 3 or 4 = shattered); give prophylactic abx and vaccines as lower immunity

Question 297

Consequences of sertraline OD?

Answer 297

long QT, QRS and torsades de pointes (can all lead to ventricular tachycardia or ventricular fibrillation); hyperthermia

Question 298

Serotonin syndrome S+Ss?

Answer 298

CNS (agitation and coma), autonomic instability, neuromuscular excitability, GI upset, tremor, diaphoresis, dilated pupils, rhadomyolysis leading to renal failure

Question 299

Treatment of torsades de pointes with long QT from sertraline OD

Answer 299

magnesium sulfate

Question 300

Treatment for serotonin syndrome?

Answer 300

activated charcoal, obs, ECG, ABG, electrolyte count, oral/IV lorazepam/diazepam and if too severe then cyproheptadine or chlorpromazine

Question 301

Invest for convulsions?

Answer 301

O2, BMs, U+Es, Ca, Mg, Po4, ABG

Question 302

Drugs for muscle relaxing?

Answer 302

1. suxamethonium (caution for hyperkalaemia, rhabdomyolysis, VT, MI), RSI, rocuronium, atracurium [all paralytic agents]

Question 303

How to calculate rate on ECG?

Answer 303

standard = 1 small square = 0.04secs (40ms); speed = 25mm/sec; so rate or bpm = 300/no. of large squares between r waves or 1500/small squares between R waves (if fast rhythm); tachy >100 and brady <60; multiply number of R waves by 6 in a strip to get rate too

Question 304

How to read pattern of QRS complexes?

Answer 304

regular or irregular (regularly irregular [atrial flutter or ecptopic] or irregularly irregular [AF]); sinus = p wave before each and junctional = missing a p wave

Question 305

How to work out axis deviation?

Answer 305

normal = QRS (-30 and 90+); left deviation (-30); right (more than +90); extreme deviation (-90 and 180); how to estimate (lead I and aVF – determine if QRS complex is positive/equiphasic/negative and compare

Question 306

QRS morphology?

Answer 306

narrow complex (sinus, atrial, junctional origin), wide complex (ventricular origin, supraventricular with abberant conduction, bundle branch block, hyperkalaemia, pre-excitation like WPW, ventricular pacing, hypothermia); should be 70-100ms (3 small squares); broad usually coz of ectopics (from anxiety, alcohol, energy drinks)

Question 307

P wave morphology meaning?

Answer 307

absent (sinus arrest, AF), present (morphology and PR interval may mean sinus, atrial, junctional or even retrograde from ventricles); <0.12s (3 small squares); biphasic in V1; right atrial enlargement = increase in height of wave, left atrial enlargement = widening and deepening of negative bit of P wave, both = combination of the 2; if broad notched waves in lead II then mitral stenosis; if tall-peaked waves in lead II = pulmonary hypertension

Question 308

What is a q wave?

Answer 308

pathological = >40ms wide, 2mm deep, 25% depth of QRS, seen V1-3; mean current or prior MI; absent in V5-6 usually from LBBB

Question 309

Meaning of prolonged QT?

Answer 309

hypokalaemia, hypomagnesaema, hypocalcaemia, hypothermia, myocardial ischaemia, raised ICP, long QT syndrome, meds/drugs; >440

Question 310

Cause of short QT?

Answer 310

<350; hypercalcaemia, short QT syndrome, digoxin

Question 311

What is a j point and what does it mean?

Answer 311

where QRS meets ST segment; J wave = hypothermia; elevated or depressed = ST segment abnormality

Question 312

ST segment elevation meaning and what leads mean what type of MI?

Answer 312

acute MI, coronary vasospasm, pericarditis, LBBB, left ventricular hypertrophy, ventricular aneurysm, raised ICP; acute STEMI (MI); large = tombstoning; different infarction areas (treat with aspirin, fondaparinux and ticagrelor – if not treated can go into VF and cardiogenic shock and die; PCI is first-line treatment):  II, III, AVF = inferior – can lead to heart block  V1, 2, 3 = anterior  V3 and 4 = septal  V4, 5, 6 = lateral and lead I and AVL

Question 313

What is an NSTEMI?

Answer 313

ST depression and post ischaemia

Question 314

What is an R wave?

Answer 314

dominant in V1 (normal in young; right ventricular hypertrophy, RBBB, posterior MI, WPW, hypertrophic cardiomyopathy, dystrophy),

Question 315

Association between P waves and QRS complexes?

Answer 315

AV association (difficult to distinguish from isorhythmic dissociation), AV dissociation (complete = atrial and ventricular activity is always independent; incomplete = intermittent capture); Mobitz I/II/complete block; best place to look for P wave is lead II

Question 316

What cardiac abnormalities respond to vagal manoeuvres?

Answer 316

sinus tachy, ectopic atrial tachydysrhythmia (gradual slowing during vagal manoeuvre but resumes on cessation), AVNRT/AVRT (abrupt termination or no response), AF and atrial flutter (gradual response during manoeuvre), VT (no response)

Question 317

T wave morphology?

Answer 317

look for inversion, concordance/discordance with QRS, T wave flattening; AVR and V1 already inverted so not abnormal

Question 318

U wave morphology and meaning?

Answer 318

are they present or not (hypokalaemia); delayed repolarisation of Purkinje fibres; prominent U waves = bradycardia, severe hypokalaemia, digoxin

Question 319

PR wave elongation?

Answer 319

delayed conduction; 1st degree heart block

Question 320

Delta wave meaning?

Answer 320

characteristic of WPW (short PR, broad QRS and delta wave); slurred upstroke to the QRS complex

Question 321

Osborn wave meaning?

Answer 321

seen in hypothermia; raised ST segment with tiny wave before hand

Question 322

Epsilon wave meaning?

Answer 322

in arrhythmogenic right ventricular dysplasia; tiny little wave after QRS complex

Question 323

Describe SVT on ECG?

Answer 323

narrow complex QRS, regular, no Ps (junctional); vagal manoeuvres to treat can do carotid massage but not in the elderly as can cause a stroke, need to induce bradycardia; adenosine after trying these (short half-life, works on the AV node), if doesn’t work use a beta blocker or CCB

Question 324

Describe RBBB and LBBB on ECG?

Answer 324

o M in V1-3 = RBBB | o LBBB - when all QRS are broad

Question 325

Two types of VT and treatment?

Answer 325

pulse (can feel pulse – accommodating) and pulseless (can’t feel pulse and deteriorating to cardiac arrest); amiodarone is best for tachycardias (broad and non-broad QRS)

Question 326

Types of electric cardioversion?

Answer 326

synchronised shocks (delivered at R wave – stops VF) or asynchronised shock (can be delivered at any time – unconscious and about to die, cardiac arrest)

Question 327

What is a polymorphic ventricular tachycardia?

Answer 327

tachy but QRS peaks are different heights; aka torsades de pointes from mg deficiency and ischaemia

Question 328

What is complete heart block?

Answer 328

atria beating completely independent to ventricles and no conduction between them

Question 329

Treatment for bradycardia?

Answer 329

check if symptomatic by checking bp; can give up to atropine 3 x 1mg doses to treat symptomatic (<40); if this doesn’t work do external pacing; then JVP line to heart and use transvenous pacing; those are all short term measures and if long term then need pacemaker

Question 330

Another name for Mobitz type 2 heartblock?

Answer 330

Wenckebach

Question 331

Differentials for anaphylaxis?

Answer 331

asthma, septic shock (hypotension with petechial/purpuric rash), vasovagal episode, panic attack/hyperventilation syndrome, breath holding in a child, systemic mast cell disorders, idiopathic urticaria/angioedema, obstruction by foreign object, seizure

Question 332

Typical rash associated with allergy?

Answer 332

urticaria (hives – red, itchy, raised areas of skin anywhere on body; maculopapular rash), can be associated with angioedema on deeper layers of skin

Question 333

Specific points to note in anaphylaxis hx?

Answer 333

have they eaten/been exposed to this food/allergen before (more likely to be allergy – type 1 hypersensitivity leading to mast cell activation with histamine and other mediators causing bronchial smooth muscle increase, decreased vascular tone and increase cap permeability); what allergen (food, abx, insect stings) were they exposed to just before having the reaction; has this happened before; do they have other allergies (epi-pen); do they have asthma; what order did symptoms come on; do they suffer from panic attacks; any neuro problems during attack (confusion, agitation, LOC); IV drugs tends to kill sooner (2-3 mins), bee stings in 30ish mins

Question 334

Systems affected in anaphylaxis and sx?

Answer 334

airway (lip and tongue swelling, angioedema, nasal congestion, sneezing, tightness of throat, hoarse, stridor), breathing (tachypnoea, bronchospasm, wheeze, increased mucous, exhaustion, confusion, cyanosis, resp arrest), circ (hypotension, tachycardia, arrhythmia, myocardial ischaemia, cardiac arrest), neuro (confusion, agitation, LOC), skin and mucosa (urticaria, erythema, pruritus), GI (stomach cramps, nausea, vomiting, diarrhoea), feeling of impending doom

Question 335

Mechanism of anaphylaxis and anaphylactoid reactions?

Answer 335

Allergic anaphylaxis is an example of immediate type 1 hypersensitivity. The response is caused by the binding of an antigen to an antigen-specific antibody leading to mediating mast cell activation. Histamine and other mediators, including leukotrienes, tumour necrosis factor and various cytokines, are released from mast cells and basophils following exposure to this antigen. This causes bronchial smooth muscle tone to increase (causing wheeze and shortness of breath), decreased vascular tone and increased capillary permeability (leading to hypotension and an urticarial rash). The response is usually uniphasic, although a biphasic response occurs in approximately 20% of individuals; anaphylaxis = immediate systemic reaction from IgE mediated immune response from mast cells and peripheral blood basophils, anaphylactoid = immediate systemic reactions that mimic anaphylaxis but not IgE-mediated immune responses, no previous exposure (direct nonimmune-mediated release of mediators from mast cells and/or basophils or from direct complement activation)

Question 336

Initial treatments for allergic reaction?

Answer 336

ABCDE; call for help, lie pt flat, raise pt’s legs if breathing unimpaired (recovery position or in comfortable one as well), recognition seriously unwell, remove the trigger, adrenaline therapy if indicated, hydrocortisone and antihistamines

Question 337

Indication for adrenaline in allergy?

Answer 337

best when given early in anaphylaxis; give IM (500 micrograms) unless experienced with IV adrenaline; given when life threatening (stridor, wheeze, resp distress, clinical signs of shock) and give 5 mins later if no improvement

Question 338

Adrenaline dose and route for anaphylaxis?

Answer 338

500micrograms IM, 0.5mL

Question 339

Other treatments than adrenaline for anaphylaxis?

Answer 339

IV fluid challenge (crystalloid 20mL/kg) for circ, chlorphenamine (10mg IM/slow IV), hydrocortisone (200mg IM or slow IV); O2; salbutamol for bronchospasm

Question 340

Who should be delivering adrenaline for anaphylaxis?

Answer 340

alpha receptor agonist (reverses peripheral dilation, reduces oedema; beta-receptor activity dilates bronchial airways, increase myocardial contraction and suppresses leukotriene ad histamine release; beta-2 receptors on mast cells and if given early they inhibit its activation); more likely to have harmful SEs if IV than IM; for specialist use only (specialist anaesthetist, emergency physicians, intensivists) must monitor pt at same time (continuous ECG, O2 sats, frequent non-invasive blood pressure), no recommended dose; can give intracerebral haemorrhage as raises BP if not given properly

Question 341

Factors to consider before discharging after anaphylaxis?

Answer 341

keep and observe for at least 6 hours; biphasic reaction could occur afterwards, allergen may still be in system; review by sr clinician, clear safety netting instructions, anti-histamines and oral steroid up to 3 days after considered, consider for adrenaline auto-injector, plan for follow up

Question 342

Follow up arrangements for anaphylaxis?

Answer 342

all pts referred to allergy clinic to identify cause and prep them for future; may need to wear a medic alert bracelet; if can identify cause then give epi-pen and allow them to use, get them to talk to pharmacist and tell them how to use

Question 343

Test to help with anaphylaxis diagnosis?

Answer 343

3 things = acute onset of illness with sudden progression, skin/mucosal changes, life threatening ABC problems; test = mast cell tryptase (major component of mast cell secretory granules, mast cell degradation means high conc of this from anaphylaxis, better for follow-up treatment not initial) and take one immediately, 1 take 2 hours after onset (at least after 30 mins but before 6-8 hours) and the last after 16 hours

Question 344

How to treat anaphylactoid reaction?

Answer 344

anaphylactoid reaction; IV volume infusion, adrenaline and anti-histamines sometimes but start with ABCD

Question 345

Commonest types of anaphylaxis?

Answer 345

foods (nuts, fish, milk, shellfish, eggs and some fruits), medicines (abx, NSAIDs, general anaesthesia), contrast agents for imaging, latex, insect stings, idiopathic

Question 346

What info needed for poisoning?

Answer 346

how much taken, what was taken, have they done this before, when taken, did they throw up, how did they take it, taken with anything else, what was the intention (accidental or on purpose - suicide), events leading up to, S+Ss, problems with liver/metabolism, was it staggered or single OD, pregnancy

Question 347

Sxs for paracetamol OD?

Answer 347

up to 24 hours (no symptoms); 24-72 = raised ALT, AST, RUQ, elevated LFTs, hepatosplenomegaly, oliguria, renal function abnormalities; 72-96 = jaundice, confusion (hepatic encephalopathy), hepatic enzymes raised, hyperammonaemia, bleeding diathesis hypoglycaemia, lactic acidosis, renal failure, death; 4 days to 2 weeks = recovery 4 days and complete at 7

Question 348

Principal site of paracetamol toxicity?

Answer 348

metabolised in liver producing toxic NAPQI which is inactivated by conjugation with glutathione but once this depleted it can cause hepatic necrosis; can also cause renal failure as this is how it is excreted

Question 349

Time to toxicity from paracetamol?

Answer 349

peak conc 1-2 hours post ingestion (30 mins for liquid); toxicity starts after 8 hours

Question 350

At risk pts to liver damage?

Answer 350

recent OD/staggered OD (more than 2 hours – measure LFTs, INRs [above 1.3 is not normal] instead and start treatment immediately), previous liver damage (hepatitis/alcoholic etc), younger (under 12 yrs), genetic variation, HIV positive, malnutrition

Question 351

Blood tests for paracetamol OD?

Answer 351

FBC, U+Es (ca, mg, po4), LFTs, clotting screen, VBG, serum paracetamol conc (at 4 hours), glucose

Question 352

Paracetamol OD serum blood levels taken?

Answer 352

how long it takes for levels to rise to amount metabolised and see if liver can handle it (more than 250 mg/kg = problem time), doesn’t come up on a nomogram before this; more than 20 tablets is a problem; takes this long for toxic metabolite to show; wait up until 8 hours for paracetamol levels and then treat

Question 353

How to decide if treat with N-actylcysteine for paracetamol OD?

Answer 353

if have timed plasma paracetamol level above or on the line with 100 mg/L at 4 hours and 15 mg/L at 15 hours after ingestion (nomogram – only really for single acute paracetamol ingestions of immediate); if any doubt about time of ingestion should be given without delay; if modified release/IV/massive/multiple drug OD should be discussed with toxicology; don’t need NAC; limits formation and accumulation of NAPQI; can also give oral methionine

Question 354

When wold you start NAC infusion for paracetamol OD?

Answer 354

first infusion (150 mg/kg over 1 hour), 2nd 50 mg/kg over next 4 hours, 3rd 100 mg/kg over 16 hours; give within 8 hours of ingestion for best efficacy (almost 100%); if allergic reaction, stop, give anti-histamines and half the dose given

Question 355

Questions for OD?

Answer 355

staggered dose, what was his intention, suicidal ideation/self-harm, does he have regrets about his actions now, mood during episode, does he remember episode, has he done this before, any previous psychiatric illnesses/admissions, any PMH, was it planned

Question 356

Scoring system for risk of repeated OD/suicide?

Answer 356

sad person’s score (male sex = 1, 15-25 or 59+ = 1, depression = 2, previous suicide/psych care = 1, excessive ethanol/drug use = 1, rational thinking loss = 2, single/widowed/divorced = 1, organised/serious attempt = 2, no social support = 1, stated future intent = 2; 0-5 = safe to discharge, 6-8 = psych consultation, >8 = hosp admission

Question 357

When to use activated charcoal in OD?

Answer 357

immediate release 50g activated charcoal within 2 hours and up to 4 hours if >30g paracetamol taken (taken 25g so not necessary); helps absorb the paracetamol before taken up into the body to be metabolised so serum paracetamol conc is lower; reduces absorption 50-90 percent

Question 358

Well's DVT score?

Answer 358

1 point for each: active cancer, bedridden recently >3cm days/surgery, calf swelling >3cm compared to other leg, collateral (non-varicose) superficial veins present, entire swollen leg, localised tenderness along deep venous system, pitting oedema on leg, paralysis/paresis or recent plaster immobilisation, previously documented DVT, alternative diagnosis to DVT more likely = -2, 2+ = likely and should have tinzaparin with doppler and bloods to check (including D dimer)

Question 359

What is ascending cholangitis and S+Ss?

Answer 359

murphy’s sign, inspiratory pain, epigastric pain to back, jaundice, pale stools, dark urine, sick, low bp, fever; can develop from cholecystitis (inflammation of the bile ducts) or from gallstone; infection of the bile duct system

Question 360

Treatment ascending cholangitis?

Answer 360

need abx (co-amoxiclav or cephalosporin + metronidazole if penicillin allergy with gentamicin); if untreated can lead to biliary sepsis; definitive treatment = ERCP

Question 361

What is S1Q3T3 and what does it indicate in ECG?

Answer 361

s wave in lead 1, Q wave in lead 3 and inverted T wave in lead 3 = PE

Question 362

What is the Glasgow Blatchford score for and what does it consist of?

Answer 362

Upper GI bleeds; score of 1 or more = hospital referral; Hb, urea, systolic bp, sex, tachycardiac, melena, recent syncope, hepatic disease hx, cardiac failure hx

Question 363

Differentials for chest pain?

Answer 363

MI – serious, possible; angina – not too serious but needs to be treated (unstable more likely), very likely; anxiety attack – not serious, possible; PE – serious, possible; gastritis – possible (can lead to ulcers with blood brought up), possible; MSK – depends how much is affecting the person to it’s seriousness (broken bones, flail chest), possible if after trauma; pneumothorax – more in young men, serious if becomes tension; pericarditis – serious, less common; pleural effusion/pulmonary oedema from pneumonia or infection – serious at a certain point; stab/gunshot wound – v serious to chest, unlikely and usually visually seen; aortic dissection; ischaemic cardiac pain; pneumothorax

Question 364

RFs for IHD?

Answer 364

male gender, active smoker, positive family history, ethnicity, cholesterol, diabetes, age; others = previous coronary artery disease, advanced age, diabetes, hypertension, hypercholesterolaemia, obesity, sedentary lifestyle, aspirin

Question 365

Causes of chest pain associated with chest wall tenderness?

Answer 365

pulmonary oedema, PE, pleural effusion, bruising to intercostals/rib fxs, angina, MI, ACS, pericarditis; more likely to be MSK injuries if chest wall tenderness

Question 366

Significance of chest pain with exertion?

Answer 366

less likely to be MSK and more likely to be vascular/cardiac/resp cause (ischaemic cardiac cause); more likely to be stable angina than unstable and can be controlled more effectively with medication, not as significant risk to health

Question 367

What is Wellen's syndrome?

Answer 367

prodrome for left main stem infarct

Question 368

HEART for assessing ACS?

Answer 368

hx moderate suspicious = 1, highly suspicious = 2; ECG = non-specific repolarisation disturbance = 1, significant ST deviation = 2; age 45-64 = 1, >65 = 2; 1-2 RF = 1, >3 RF = 2; initial trop 1-3x normal limit = 1, >3 = 2; low score = 0-3, moderate = 4-6

Question 369

Tests for chest pain?

Answer 369

FBC, U+Es, VBG, CK, trop T, LFTs, clotting screen, CK-MB, hs-tropinins; trop measured at presentation and 3 + 12 hours after onset of symptoms to see if MI, use sex specific thresholds; CXR

Question 370

Cardiac enzymes different types?

Answer 370

use trop T (best sensitivity); hs troponin = more sensitive at identifying ACS than troponin (troponin is type of protein found in heart muscle and not usually in blood), CKMB = measures amount of isoenzyme CK in blood (CKMB is one form of CK – more for cardiac), injured heart muscle cells release CKMB so CKMB more specific to cardiac damage than muscle/organ damage in body when normal CK released

Question 371

When cardiac enzymes raised?

Answer 371

maybe if more than 3-12 hours, if less than this then maybe enzymes not released enough to be detected; could be an NSTEMI and therefore not detected on ECG

Question 372

Drugs given for chest pain with cardiac?

Answer 372

GTN spray and morphine; oxygen = not found to improve clinical outcome for ACS but may relieve pain (look at sats), deffo put on O2 for MI

Question 373

How to tell if posterior MI?

Answer 373

inversion of T waves in V2, 3, 4

Question 374

Indications for primary PCI?

Answer 374

if have acute LBBB, acute MI

Question 375

What is PCI?

Answer 375

cardiac catheterisation (insertion of catheter tube and injection of contrast dye with iodine into coronary arteries), use PCI to open up coronary arteries that narrowed/blocked by plaque, will still be awake and fed through arteries via arm/leg to heart; may not be able to do it if no longer in pain as too much necrosis of cardiac tissue

Question 376

Instead of PCI?

Answer 376

fibrinolysis; use streptokinase/alteplase; ideally within an hour but should be less than 12 hours/6 hours; acute PE, acute stroke and DVT

Question 377

Fibrinolytic drug and CIs?

Answer 377

streptokinase, alteplase, tenecteplase; Cis = acute pancreatitis, aortic dissection, bacterial endocarditis, coagulation defects, history of cerebrovascular disease, pericarditis, recent haemorrhage, recent surgery, currently haemorrhaging

Question 378

Main 3 drugs for ACS?

Answer 378

aspirin, fondaparinux and ticagrelor

Question 379

PINCHES ME mnemonic for delirium causes?

Answer 379

delirium: pain, infection, nutrition, constipation, hydration, endocrine/electrolyte, stroke, medication/alcohol, environmental

Question 380

AEIOU TIPS for causes of collapse?

Answer 380

alcohol, epilepsy, infection, OD, uraemia, trauma, insulin, poisoning, stroke

Question 381

What is deconditioning?

Answer 381

decline in physical function of the body as a result of physical inactivity and disuse. The most important feature of deconditioning is a decline in muscle strength and bulk. It is usually reversible. It is often seen in the elderly and the infirm due to bed rest and inactivity

Question 382

What is frailty?

Answer 382

An inevitable consequence of ageing; A state due to multiple long term conditions; A condition in which the person becomes fragile; A state associated with low energy, slow walking speed, poor strength; A condition for which nothing can be done

Question 383

How to assess pts for frailty?

Answer 383

Walking speed reduced, grip strength low, immune deficits, reduced; ability of withstand an “insult”; Useful in clinical trials, difficult to implement on large scale; Walking speed; timed up and go test (TUGT) used

Question 384

What is the ceiling of treatment?

Answer 384

considered to be the predetermined highest level of intervention deemed appropriate by a medical team, aligning with patient and family wishes, values and beliefs

Question 385

What is a ReSPECT form?

Answer 385

gives personalised recommendations for person’s care and treatment in a future emergency when unable to make or express choice; made through talking to pt, family, healthcare; it is a non-legally binding form that can reviewed and adapted; recommended summary plan for emergency care and treatment; not just DNACPR as can include other care to refuse like ITU etc or intubation

Question 386

Examination findings for differentials for PE?

Answer 386

1. PE (Well’s scoring over 2, previous DVT sx), MI (pain radiating to jaw or arms and associated with nausea and sweating), MSK (pain felt on palpation), ACS (relieved by rest and GTN), COVID pneumonitis (COVID sx), pulmonary oedema/effusion (stony dull percussion), pneumothorax (hyper resonant percussion)

Question 387

RFs for PE?

Answer 387

recent surgery (major, pelvic, hip/knee replacement, post op intensive care), obs (later pregnancy, C section, puerperium), lower limb (fx, varicose veins), malignancy (abdo/pelvic, advanced/mets), reduced mobility (hospitalised, institutional care), previous VTE, cardio (congenital HD, CCF, HT, superficial VT, indwelling central vein catheter), oestrogens (HRT, oral contraceptive), misc (COPD, neuro disability, occult malignancy, thrombotic disorders, long distance sedentary travel, obesity)

Question 388

Clinical findings for PE?

Answer 388

dyspnoea, tachypnoea (RR>20), pleuritic chest pain, apprehension, tachycardia (>100), cough, haemoptysis, leg pain, clinically evident DVT (swelling and calf tenderness – Wells score)

Question 389

Investigations for PE?

Answer 389

FBC (any problems with blood/infection, polycythaemia [hb], platelets [check if safe to anti-coagulate, not above 10]), U+Es (electrolyte deficiency cause etc, creatinine clearance for anticoagulation and renal clearance for CTPA), ABG (lactate for infection and hypoxia for hyperventilation and increased arterial-alveolar gradient to support PE), LFTs (any problems with liver causing pain), clotting screen (see if it is any different), trop Ts (see if cardiac cause from MI or sometimes PE), ECG (usually sinus tachycardia or normal; can show cardiac or sometimes indicate PE S1Q3T3), D-dimer (can indicate if embolus present but high in most things, rule out not a rule in), CXR (rule out infection/pneumothorax etc, sometimes find wedge infarct for PE), CTPA (gold standard for PE), could do a V/Q scan (isotype lung scan but less specific for PE)

Question 390

What is pretest probability?

Answer 390

chance that pt has disease before test result known (from the sx relating to the Wells scoring)

Question 391

What is Well's PE score?

Answer 391

clinically suspected DVT (3 points), PE at least as likely or more than alternative diagnosis (3), pulse rate >100 (1.5), immobilisation >3 days (1.5), surgery last 4 weeks (1.5), previous VTE (1.5), haemoptysis (1), malignancy (1); pts scoring 4 or less = low risk and above are high risk of PE

Question 392

What is a d-dimer?

Answer 392

sensitive but not specific investigation (poor positive predictive value); raised in VTE, infection, trauma, cancer and inflammation; used only for PE unlikely pts; is when clot starts breaking down and D-dimer is release (breakdown product of blood clot, enzymatic reaction breakdown of fibrin)

Question 393

Sensitivity vs specificity?

Answer 393

sensitive = low false negative rate, specific = low false positive

Question 394

Alternative to CTPA for pregnancy for PE?

Answer 394

due to contrast and risk to baby; use V/Q SPECT (ventilation perfusion single photon emission computed tomography)

Question 395

Risks from anticoags?

Answer 395

warfarin (heavy bleeding – haematuria, melaena, severe bruising, epistaxis, bleeding gums, vomiting blood, haemoptysis, menorrhagia, stroke, internal bleeding) may interact with other drugs (antivirals, vit K is antagonist), calciphylaxis (painful rash), pomegranate juice increases response to drug, reduce alcohol; alopecia, N+V; warfarin is teratogenic and not for first trimester of pregnancy; INR monitoring daily/alternate days at first then up to every 12 weeks; INR uses PT time test results (may also do platelet count, PT time, activated partial thromboplastin time, fibrin D-dimer, fibrinogen, thrombin time); INR number is a ratio varying according to age, medicines, health problems (bigger number = longer time for blood to clot), should be around 2.5-3.5; check using HASBLED

Question 396

Treatment for PE?

Answer 396

use a DOAC if PE and dose of tinzaparin 10-18000 units (LMWH), test them, anticoagulation clinic and see if need to continue LMWH; if massive PE then can do thrombolysis with alteplase and v risky (not usually thrombectomy as 50% mortality)

Question 397

Range for INR aimed for in PE?

Answer 397

2.5-3.5 (or 2-3); at least 3 months for confirmed DVT/PE need anticoagulant; should be DOAC (apixaban or rivaroxaban) but if not then LMWH for 5 days then DOAC or LMWH with vit K antagonist for at least 5 days or until INR is 2.0 for 2 consecutive readings

Question 398

What is thrombophilia and examples?

Answer 398

imbalance in naturally occurring blood-clotting proteins/clotting factors so more at risk of forming clots; genetic = factor V leiden and prothrombin thrombophilia most common (others = congenital dysfibrinogenemia, hereditary antithrombin deficiency, heterozygous protein C deficiency, heterozygous protein S deficiency); acquired = antiphospholipid syndrome (70% female and more likely if have SLE), prolonged bed rest, cancer, trauma, acquired dysfibrinogenemia