Critical Care Qs

Question 1

Post - Op Colectomy

Tachycardic and Unwell

i) Differentials
ii) Investigation of choice for PE

Answer 1

i) Differentials

Anastamotic leak, VTE, ARDS, Infection

Late- Wound Infection, Post-operative collection,

ii) CTPA - look for filling defect in the pulmonary arteries

Question 2

Trauma Patient - LOC + Vomiting + Concomitant ankle fracture

GCS subsequently Drops

i) Points of contact
ii) Possible CT Head findings
iii) Early CT Head Criteria

Answer 2

i) Contact - Anaesthetist/ITU, Neurosurgeons, Radiology, Senior Support
ii) CT Head findings - EDH, SDH, Contusion, DAI
iii) Canadian CT Head Rules - CT required for minor head injury if :

GCS < 15 After 2 Hours

>2 Episodes Vomiting

Depressed Skull Fracture Concern

Base of SKull Fracture Concerns

Age >65

Medium Risk - Retrorade amnesia, Dangerous Mechanism

Question 3

Raised ICP

i) What is the monroe kelly doctrine?
ii) Normal ICP/MAP/CPP
iii) How to measure ICP?
iv) Causes of raised ICP
v) Signs
vi) management
vii) Regulation of cerebral blood flow?

Answer 3

i) Monroe Kelly Doctrine centres around that there are three constituents in the brain - parenchyma, CSF and Blood. As the brain is contained inside a closed vault (skull) if any one of the constituents increases the others become displaced/the ICP rises.

ii) ICP - <25 (5-15) mmHg CPP - >65mmHg MAP - 90mmHg

iii) MAP - ICP = CPP

Need ICP monitoring + MAP monitoring to accurately gauge the CPP

Invasive MEasurement via - IVD, EVD (parenchymal, subarcachnoid, epidural)

Non invasive measurement via - Doppler, CT, Introcular pressure

iv) Causes - SOL, Bleed, Blockage in CSF drainage or decreased resorption/increased production/ cerebral oedema, obstructed venous outflow
v) signs - CN palsies, Cushings Triad (bradycardia, low RR + hypertension), pappilodoema
vi) management - Head up, normocapnea, IV mannitol, sedation, oxygenation, targeted BP management
vii) Cerebral Blood Flow:

Autoregulation between 50-150mmHg Systolic Pressure by myogenic stretch reflex in vessels

Low CO2 leads to vasoconstriction

High CO2 leads to vasodilation

Question 4

Burns:

i) How to manage airway and breathing?
ii) Calculating percentage area of burns
iii) Calculating fluid requirement?
iv) type of fluid?
v) RFs for Smoke Inhalation Injury

Answer 4

Burns should be managed in a specialist burns unit and some patients will need ITU management (multi organ failure)

i) - High index of suspicion for inhalation injuries - These patients need early intubation as intubation becomes more difficult with time

Escharotomy if required for circumferential thoracic burns

ARDS is associated with burns

Suspect Carbon Monoxide poisoning

Ix -Serial ABGs, CXR, Capnography, Laryngoscopy

ii) Wallace Rule of 9s

Head + Neck - 9

Arm - 9 each

Chest/Upper back - 9 each

Abdomen / Lower back - 9 each

Leg -18 each

(Lund and Browder Chart is more accurate)

iii)Fluid requirement ( if >15% affected)

Parkland’s Formula - 4 x body weight x percentage burn.

1/2 in 8 hours 1/2 in 16 hours

(There is also a mount vernon formula)

iv) Fluid type

Crystalloid - prefered Hartmann’s to prevent hyperchloraemic acidosis

v) HO Fire in enclosed space, Soot around nostrils, Carbon sputum, singed nasal hairs, hoarse, Upper airway sounds, Drooling, COHb - >10

Question 5

i) Which nutrition sources in critical patients?

ii) What percentage of enteral feeding target in sick patients?

iii) Early parenteral feeding?

iv) Feedin in malnutritioned criticlaly ill patients

Answer 5

i) Carbohydrates are favourable. Protein is indeterminate - currently thought that critically ill patients have higher protein requirements. Fats thought to not be metabolised well in sick state.

ii) <30%. Agressive nutritional treatment was shown in trials to be associated with increased mortality

iii) Early parenteral feeding is associated with increased HAIs

iv) Traditionally patients who have moderate starvation have been treated with enteral/parenteral feeding as appropriate however mortality/hospital stay date have not validated these observations

Question 6

Criteria for malnutrition

Answer 6

i) Bmi <18.5
2) Weight loss of 2.3kg/ 5% in 1 month
3) Weight loss of 4.5kg/10% in 6 months

Question 7

Contraindications to enteral feeding?

Answer 7

i) Severe haemodynamic instability
2) Bowel Obstruction
3) Ileus (severe/protracted)
4) Major UGI bleeding
5) Prolonged vomiting/diarrhoea
6) GI Ischaemia
7) High output fistula

Question 8

Contraindicatiosn to parenteral nutrition?

Answer 8

i) Hyperosmolarity
ii) Severe hyperglycaemia
iii) Volume overload
iv) Poor IV access

Question 9

Feeding Calculations

i) in normal weight/ underweight

iii) obese patients

Answer 9

i) Initially 8-10 kcal/kg —> 18-25 kcal/kg in the first week and this can be increased in subsequent weeks
ii) Penn State University Prediction

Dosing Weight = IBW + 0.4(ABW-IBW)

Then with the dosing weight use the same kcal/kg parameters

Question 10

i) Types of delivery

ii) Basic components of feed)

iii) Normal or concentrated feed in CCI patients?

iv) Complications of PEG/PEJ

v) Complications of Nasoenteric tubes

vi) Contraindications to nasoenteric tubes

Answer 10

i) Pyloric:

NG Tube or PEG Tube

Post-pyloric (Gastric dysmotility, Gastric outflow obstruction, duodenal obstruction, oesophageal injury):

ND/NJ tube or PEJ Tube

ii) Feed Components

Isotonic,

1kcal/ml (can be more concentrated)

Protein - 40g/L (can be nonhydrolyzed protein)

Long chain fatty acids

Vitamins, nutrients + minerals

Simple and complex carbs

iii)

CCI patients usually given concentrated feeds yet lack of supportive evidence

iv) General - Tube dysfunction, Wound Infection, Nec Fasc, bleeding, leakage, ulceration, gastric outlet obstruction, removal, peritonitis,

Early - Pneumoeritoneum, ileus, visceral perforation,

Late - Deterioration of site, buried bumper syndrome (tight tube), fistulation, seeding along PEG tract,

v) Placement - pulmonary, Kinking/coiling

Nasal ulceration/necrosis

Visceral perforation

Increased risk of reflux due to sphincter dysfunction

vi ) Oesophageal stricture, oesophageal varices, base of skull fractures + bleeding risk

Question 11

i) Complications Enteral

ii) Complications Parenteral

Answer 11

i) Complications

Aspiration,

Diarrhoea (can be helped with fiber feeds),

Metabolic - refeeding syndrome, hyperglycaemia, nutrient deficienceis

Hypovolaemia

Constipation

High residual volumes
Nausea/Vomiting

ii) Line Related - Damage to structures, Thrombosis related to feed viscosity

Feed Related - Electrolyte, TGs, Glucose (High/Low), Thrombosis

Expensive , Gut atrophy, increased acute phase response

Question 12

ARDS

1) Causes
2) Features
3) Pathology
4) Management

Answer 12

Causes: Trauma, Sepsis, Pancreatitis, Cardiac operations, Pneumonia, Burns, TRALI, Drugs

Features:

Dyspnoea

Hypoxaemia despite high FiO2 (Early alkalosis on ABG then acidosis w/ tiredness)

CXR - Diffuse bilateral alveolar infiltrates

Decreased Lung Compliance

Absence of pulmonary oedema (Pul. Wedge. Pressure <20, absence of clinical signs of fluid overload)

Pathology:

Early - Exudative phase (oedema, inflammation, hyaline membrane formation)

Late - Development of fibroplasts, Collagen Deposition

Resolution - Fibrosis

Management:

Supportive: Sedation ( reduce oxygen requirement), Analgaesia, PPI, VTE Prophylaxis, Steroids (severe ARDS)

Oxygenaton:

FiO2 - generally high requirement but goal is PaO2 of 55-80, Prone positioning, ECMO,

Generally require invasive ventilation, Low tidal volume ventilation (mitigates alveolar injuries)

Question 13

i) Constituents

ii) Pulse deficit?

Answer 13

i) Cardiac Output = HR x SV (SV = End Diastolic Volume - End Systolic Volume)
ii) Pulse Deficit - Difference between palpated pulses and heart beats. Some pulse pressures may not be significant enough to generate a radial pulse esp. as seen in arrhythmias.

Question 14

1) Intitial Stabilisation
2) Type 2 RF
3) Initial Management
4) Initial Imaging

Answer 14

1) NEXUS Clearance (low risk) - if none of the following present then CT C Spine can be avoided:

i) Focal Neurology, ii) spinal tenderness, iii) altered consciousness iv) distracting injury v) intoxication

If high risk mechanism (or significant intracranial trauma/pevlic trauma/neurological sx) - Immobilisation with C Spine Collar and blocks. Some centres use a spinal board.

2) T2RF - i) Think Cord Injury/spinal shock (apraxia) ii) phrenic nerve injury iii) Think Head injury iv) Obstruction to airway

C3 and above - Immediate resp. paralysis

Below - delayed phrenic nerve palsy

3) Initial Management:

After in line stabilisation.

Hypoxaemia - Supplemental oxygenation with some mechanical ventilation. May need early intubation (and later on trachy placement)

Hypotension - Due to other injury/ spinal shock - Legs up, IV therapy + ?Pressor Support

Bradycardia - Consider Atropine

Urinary Retention - may need catheter insertion

medical - PPIs, Steroids,

4) A-P X Ray + Lateral (Need to be able to see up to T1).

Swimmer’s View - helpful to view C7/T1. Aim is to anteriroly displace the humeral hads

Question 15

1) Types of shock
2) BP components
3) Shock Categories

Answer 15

1) Types: Distributive (Septic, SIRS, Inflammatory) , Hypovolaemic, Neurogenic, Cardiogenic, Obstructive (pulmonary)

2) BP Components - CO x Systemic Vascular Res.
3) Categories

I (<750ml/15% loss) - no features

II (750ml-1.5L/ 15-30% loss) - Signs, HR >100, RR>20, UO 20-30ml

III (1.5l-2L/30-40% loss) - Signs, HR>120, RR> 30, UO 10-20ml

IV (>2L/>40% Loss) - Signs, HR >140, RR>40, UO <10

Question 16

What to say in the case of a septic patient?

Answer 16

1 - A-E Approach

2 - Meets SIRS criteria

3 - Management:

Early Goal-Directed Therapy with Circulatory Optomisation

• Which setting can she be managed in?
• Urine output, Cardiac Output, CVP Monitoring

Early Goal-Directed Therapy with Circulatory Optomisation is:

• when lactate >4 –> 20 ml/kg crystalloid minimum as an initial resuccitation measure
• Where the initial resuscitation measure does not work –> Vasopressors to aim for MAP >65 mmHG / CVP >8mmHg/ Central Venous Oxygen Sats >70%

Question 17

i) Bloods for patient with abdominal pain + SIRS

ii) Imaging for same clinical scenario

Answer 17

i) FBC, U+E, CRP, LFT (+GGT, ALT, AST), Clotting, Blood Cultures

Pancreatitis: LDH, Albumin, Lab GLucose, Amylase, Lipase, ABG

Group + Save

ii) Erect Chest XR

USS Abdo

CT (if no cause found)

Question 18

Scoring Systems for Pancreatitis:

Answer 18

i) Modified Glasgow Criteria (>3 = Severe and should be escalted to intensive care team):

Pao2 <8

• *Age** >55
• *Neutrophils** >15
• *Calcium** <2.0
• *Renal** Urea >16
• *Enyzmes** LDH>600/ AST>100
• *Albumin** <32

Sugar >10

Ranson Criteria

Balthazar CT Scoring

APACHE II

Note CRP >140 confers poor prognosis

Question 19

i) Potential Complications of Panreatitis

ii) What is a pancreatic pseudocyst

iii) Complications of chronic pancreatitis

Answer 19

i) Early

Local - Necrotising Pancreatitis, Superimposed Infection, Paralytic Ileus, Haemorrhage Pancreatitis

Systemic - SIRS, ARDS, Hypocalcaemia, Pleural effusion (Left), Hypovolaemic Shock

Late

Local - Pseudocyst, SMV/SV/SMA/SA thrombosis/heamorrhage, Intrabdominal Collection

ii) Pancreatic Pseudocyst - encapsulated fluid collection encased within a fibrous capsule

1/2 -Resolve spontaneously 1/2 - Require drainage (IR/Endoscopic/ Open)

iii) Malnutrition (Lipase,Proteinase Deficiency)

Osteoporosis

Chronic pain

Diabetes

Structural - Collections, Fistulation, Biliary Obstruction(strictures), Abscess

Question 20

Pancreas Function

Answer 20

Endocrine:

B Cells - Insulin

Alpha Cells - Glucagon

D Cells - Somatostatin

PP Cells - Panceratic Polypeptide

Exocrine: (activated by CCK)

Proteins- Trypsinogen - activated by enterokinase –> Trypsin

Lipase - Fats

Amylase - Carbs

Alkaline - Neutralises stomach acid

Question 21

Acid Base

i) What is the Henderson-Hesselbach Equation?

ii) What is chloride shift?

iii) Normal Anion Gap? Causes of normal/High anion gap acidosis

iv) Causes of metabolic alkalosis

v) Causes of Respiratory Acidosis?

vi) Causes of respiratory alkalosis?

Answer 21

i) CO2 + H20 <–> HCO3- + H+
ii) Chloride Shift:

Process by which RBCs can exchange Chloride Ions for Bicarbonate Ions.

Pulmonary Blood: More H+ than CO2. So RBCs produce H2O+ CO2 leading to less HCO3- in RBCs. Therefore Chloride ions move out of RBCs and HCO3- moves in

Systemic Blood: More CO2 than H+. So RBCs produce HCO3- + H+. THis leads to HCO3- moving out of RBCs and Chloride ions moving in.

iii) Anion Gap: 10-14

Normal - RTA, Tubular Damage, Loss of HCO3- (intestinal), Hyperparathyroidism, Hypoaldosteronism (RTA IV)

High - Lactate, Methanol, Hyperkalaemia, Salicylates

iv) Metabolic Alkalosis - H+ Loss (Vomiting/ Renal), Hypochloraemia, Diuretics, Antacids

v) Airway Obstruction - Asthma/COPD,

Altered gas diffusion - pneumonia, ARDS, oedema

Central Causes - Head Inj, Myaesthenic, Drugs, flail segment, polio

vi) Respiratory Alkalosis - Hyperventilation, Saliclylate, Pulmonary Embolus

Question 22

i) DDx for a cool/painful leg

ii) Causes of embolus

iii) Where do emboli tend to get stuck?

iv) Investigations for ALI?

Answer 22

i) Acute on Chronic, Acute embolic, Vascular injury, Venous Thrombosis, Neurological

ii) Embolus:

AF/Cardiac Thrombus, Proximal Aneursym, Atherosclerotic Plaques

iii) Emboli tend to get stuck at bifurcations

iv) If evidence for emboli is clear argument for immediate embolectomy without imaging.

If the event may be thrombotic useful to have Angiography CT beforehand to plan procedure

Investivation choice also depends on clinical severity - If muscular paralysis the limb is non salvageable. If Paraesthesia - urgent revascularisation is necessary. If approaching 6 hour mark consider urgent intervention

Question 23

Acute Assessment of Sick Patient (CCRISP)

Answer 23

A - Assess airway. If concerns of compromise assess further - with look listen and feel approach:

• Attempt Suction
• Airway Adjuncts
• Oxygen

B - SaO2/ABG

Chest Exam - tracheal deviation, Good air entry, any added sounds, good expansion

C - IV Access + Bloods, ECG, Cardiac Monitoring (Incl BP)

Fluid Assessment - JVP, CRT (central+peripheral), Heart Rate, Ausculate chest, Look for oedema

D - Pupils, Glucose, Neurological status (GCS/ AVPU)

E - Expose and full examination

Question 24

Acute Limb Ischaemia Classification

Answer 24

I + IIa - May have time for imaging

IIb + III - Probably not time for imaging

Question 25

**What consitutes SIRS:**

Answer 25

**2 or more of:** Temp \>38 / \<36 RR \>20 / PaCO2 \<4.3 Pulse \>90 WCC \> 11 / \<4

Question 26

# Define: **i) Acute Renal Failure** **ii) Timeframe to develop acute renal failure** **iii) Causes of renal failure** **iv) Causes of ATN (main 2)** **v) Investigations for Acute Renal Failure (immediate)** **vi) Basic Management (+ if there is concomitant pulmonary oedema)** **vii) Oliguria**

Answer 26

i) An acute accumulation of toxic metabolites due to impaired renal excretion ii) Over the course of 48 hours iii) **Pre Renal -** Hypovolaemia, Shock States, Renal Artery Stenosis **Renal -** ATN, Glomerulonephritis, Interstitial nephritis, Hepatic Renal Syndrome **Post Renal -** Urinary Tract obstruction (ureters, bladder, Urethral), Abdominal Compartment Syndrome iv) **ATN -** Ischamic Hit (renal hypoperfusion), Nephrotoxins (Aminoglycosides, Tetracyclines, Paracetamol, Myoglobin, Myeloma, Heavy Metals) v) **Urine Dip, MC&S, LFTs (**HRS), **ABG** (Lactate), **CRP, Bone Profile (?High Ca++)** Not first line - US KUB/CT KUB, ACR/PCR, Renal Screen (myeloma, autoimmune) vi) Treat precipitant! Then - Stop nephrotoxins, Input/Output Monitoring (Cathter/CVP pressure monitoring .UO 0.5 ml/kg/hour in Adult, 1 ml/kg/hour in Child) , IV Fluid Provision (20-30 ml kg day is maintenace so if under filled will need more than this) **Pul. Oed.** - Sit patient up - oxygenate. CXR. ABG. No fluids. IV Furosemide (If SBP \<100 then can try GTN infusion) . Strict input/output monitoring **vii) Oliguria** - \<400 ml urine output per day

Question 27

**Hypoxic Patient:** i) Initial Investigations ii) Define ARDS iii) Causes of ARDS iv ) Management of ARDS v) Mortality

Answer 27

**i)** CXR, ABG, ECG, Fluid Balance Chart Bloods - FBC, CRP, ?Troponin, Us + Es ?Pul. Oedema CTPA - if high Well's Score **ii)** **ARDS -** Acute respiratory failure and non cardiogenic pulmonary oedema with reduced lung compliance + hypoxia . Often refractory to oxygen therapy. **All of these are required -** **a)** Normal/ Low Pulmonary Capillary Wedge Pressure (\<18 mmHg) **b)** Diffuse bilateral pulmonary infiltrates **c)** PaO2/FiO2 Ratio - \<26.6 kPA iii) **Causes -** **Pulmonary** - Pneumonia, PE, Aspiration, Fat embolus, Smoke ihalation, Trauma **Cardiac** - Cardiothoracic Surgery **Systemic** - Sepsis, Pancreatitis, Trauma, Massive Transfusion, DIC iv) **Management:** Oxygenation Ventilation - Prone, Prolonged inspiration (reverse I:E ratio), High PEEP (risk of alveolar trauma) Drugs - (no evidence) Prostacyclin, Steroid, NO v) **Mortality -** 50-60% **With sepsis - 90%**

Question 28

**Present This**

Answer 28

PID, Date, Time, PA/AP, **Diffuse Bilateral Pulmonary Infiltrates:** Suggestive of **ARDS, Pulmonary Oedema, Pneumonitis, TRALI (If transfused recently)** **Technical Adequacy Points:** Rotation - Equal distance between clavicles and spinous processes Insipiration - 5 Anterior Ribs Penetration - Vetebral bodies behind the heart should just be visible Exposure - Costophrenic Angles + Apices included?

Question 29

**AIrway:** **i) Indications for surgical airway** **ii) Location of cricothyroidotomy** **iii) Location of tracheostomy**

Answer 29

**i) Indications for surgical airway -** Failed intubation + Laryngeal Trauma **ii)** **Cricothyroidotomy -** Through cricothyroid membrane/ligmanet **iii) Tracheostomy -** Through the 2nd - 5th Tracheal Rings

Question 30

**Which layers do you traverse when creating a tracheostomy?**

Answer 30

Skin Subcutaenous Fat Fascia + Platysma Investing layer of deep cervical fascia Pretracheal Fascia Infrahyoid Strap Muscles (retracted) Thyroid Isthmus Trachea

Question 31

**i) Consequences of poor pain management** **ii) Gross description of pain pathway** **iii) Indications for PCA (another card somewhere too) - Dosing**

Answer 31

i) Poor Patient Experience Poor Mobility --\> Incr. DVT risk and delayed recovery Poor cough --\> Incr. risk of HAP Incr. Sympathetic tone --\> Incr. myocardial oxygen demand, delays gastric emptyinh ii) **Noiciceptors** **--\> A Delta Fibers (**Fast and sharp pain**)** **--\> C Fibers (**Slow and diffuse pain**)** Both synapse in **ipsilateral substantia gelatinosa** --\> decussate and travel more ventrally up the spinal cord to synapse in the thalamus. ---\> Through corona radiata to cerebral hemispheres **iii)** Severely painful conditions + major surgery: Purely bolus w/ time lockout period **or** Basal Bolus administration **Dosing -** 0.5mg-1.5mg Diamorphine with 3-5minute lock out period

Question 32

**Risk factors for chronic post surgical pain**

Answer 32

Pre operative pain Chemotherapy Long Surgery Severe post operative pain

Question 33

**Blood Transfusions:** **i) Shelf life of blood products** **ii) Infections screened for in blood** **iii) Complications of transfusion** **iv) What is a massive transfusion + Complications** **v) Ratio of blood products in massive transfusion?**

Answer 33

**i) Blood -** 35 Days (2-6 degrees) **Platelets -** 5 Days (20 degrees) **Cryoprecipitate/FFP -** 1 year (-30 degrees) **ii) Infections screened -** HIV, Hep B +C, Sphyllis, HTLV CMV - in FFP **iii) Immediate** - Febrile Transfusion reactions, Haemolytic Transfusion Reactions, Anaphylaxis, Coagulopathy **Delayed** - Delayed Haemolytic Transfusion Reaction, TRALI, Overload, Hyperkalaemia, Hypocalcaemia, Infection, GvHD, Post-transfusion purpura **iv)** When 50% circulatory volume is given within 4 hours/ 100% circulatory volume in 24 hours. Complications are : - Electrolyte disturbance(High K+, Low Ca++), ARDS/TRALI, Fluid overload, Coagulopathy, Hypothermia, Metabolic Alkalosis **v) 2:1:1** RBC:Platelets:FFP Inter-trust variation.

Question 34

**Alternatives to blood in Jehova's Witness**

Answer 34

**Fluids** **Pharmacology** - Fe+, EPO, TXA, Factor VIIa **Blood -** Autologous, Cell Saver **Intraoperative -** Haemostasis, Monitoring and optomisation of homeostasis

Question 35

* *Brainstem Death: i) Reversible Causes of coma?** **ii) Who assesses for brainstem death?** **iii) Examination?** **iv)** **Absolute/Relative CIs to organ donation**

Answer 35

**i) Toxins - Lots of drugs** **Hypothermia,** **Shock, Endocrine -** thyroid, addison's, glucose, **Electrolyte-** Na+, uraemia, ammonia **ii)** 2 independent doctors at different times - 1 consultant and both \>5 years experience . Neither should be involved with patients who have patients potentially receiving the organs. **iii)** **5 things -** Absent VOR, Fixed Pupils, Absent Corneal response, Absent motor responses to pain, Absent cough/gag reflex **Then** - **Apnoea Test:** Oxygenate to \>95% Decrease ventiltion rate to - ETCO2 \>6.0 and confirm ABG CO2 \>6.0 and pH \<7.4 Then stop ventilation, continue oxygenation with 5L through ET Observe 5 minutes. If ABG shows \>0.5 rise in CO2 then confirmed loss of respiratory drive **iv) Absolute - vCJD + HIV** **Relative -** Liver failure, TB, Metastatic cancer and high age

Question 36

**Types of ventilation**

Answer 36

**Supplementary** - NC, Venturi, non re breathe, adjuncts **Non** invasive - BiPAP, CPAP, Optiflow **Invasive** - ET, Trachy

Question 37

**Burns Classification**

Answer 37

Question 38

**i) Criteria for admission to specialist burns unit** **ii)** **Particulars of Hydrofluoric Acid Burns**

Answer 38

**i) Area -** \>10%(Adult)/ \>5%(child) Total SA **Location -** Face, Flexural Surfaces, hands, feet and circumferential burns **Type -** Steam, Electricity, Chemicals **Patient Specific -** \<5/\>60 years old, Severe Comorbidities **ii) Hydrofluoric acid burns can be devestating:** **Electrolytes (**Hypocalcaemia, Hyperkalaemia, Hypomagnesaemia) **Necrosis including of the bone**

Question 39

**Central Line:** **i) Indications** **ii) Complications** **iii) Insertion Guidelines** **iv) IJV Surface Marking** **v) Describe procedure - IJV + SCV** **vI) Removal**

Answer 39

i) **Indications** include - TPN, Drugs (amiodraone/K+), CVP monitoring, Transvenous Pacing, Haemodialysis, Failed IV access ii) **Complications** include - Arterial Puncture, Pneumothorax, Air Embolus, Thrombosis, infection, Cardiac Arrhthmias, Atrial Perforation, Thoracic Duct Damage **iii) A)** US GUidance **B) X Ray** to check **- SVC Cannulated** and **no pneumothorax** **iv)** Apex of both SCMs (Lateral to Carotid) **v) IJV -** Head Down. Turn head other way. US Guidance. Palpate carotid and go lateral. **Seldinger Technique.** Introduce needle at 30 degree angle pointing at the nipple. Keep aspirating and when you get blood advance catheter **SCV -** Same technique except needle insertion at midpoint inferior to clavicle pointing towards suprasternal notch. **vi)** Removed either flat/ head down - prevents air embolus Check clotting plateleets before hand Send tip for MC&S if concerns about infection

Question 40

**Which layers do you pass through to insert a subclavian line?**

Answer 40

Skin Subcut Fat + Fascia Pec Major Subclavius Muscle Subclavian Vein

Question 41

**i) What is Frank-Starling's Law?** **ii) What would it imply if the curve of cardiac output x venous return shift to the right?**

Answer 41

i) With increased Pre-Load ( Left Ventricular- End Diastolic Volume ) there is increased Stroke Volume: Due to the effect of stretch on the ventricular wall leading to increased contractility. ii) Indicates reduced contractility of the myocardium so reflects redued ability to cope with increased venous return and preload. **inversely** in exercise/fit hearts and reduced systemic resistance (afterload) left shift can be observed where contractility is increased

Question 42

**i) Describe a CVP Trace** **ii) Causes of increased/decreased CVP**

Answer 42

**i) Ascents - ACV** **Descents - XY** **a - atrial contraction** **c- tricuspid closure (**during isometric contraction of ventricles**)** **x - atrial relaxation** **v - venous return to the atria** **y - tricuspic valve opening** **ii)** **Decreased -** Hypovolaemia, Vasodilation **Increased -** Fluid Overload, Cardiac - Failure, Tamponade, Cor Pulmonale,

Question 43

**Outline ATLS appraoch**

Answer 43

Know resources available to you. Ask for monitoring to be attached including cardiac monitoring. **C -** Hard Collar, Sandbags and tape until such time as the C Spine could be cleared using a tool such as the NEXUS criteria / Imaging **A -** Airway assessment - talking? upper airway sounds? no breath on face? Suction/Adjuncts/Tube/Surgical Airway **B -** SaO2/ABG/RR Examine - Expansion, Percussion + Auscultation Emphysema/ Trachea position Observe for any open chest/penetrating chest injuries/ asymmetrical chest movements Attach Oxygen if indicated and start with highflow **C -** 2 Large bore Cannulae - take bloods BP/Cardiac Monitoring/ECG. Central + Peripheral Pulse/ CRT / Skin mottling **Look** for blood - Chest/ Abdo/ Long bones/ Pelvis/Floor Warmed Crystalloid **D -** PEARL/ GCS / Peripheral neurological examination **E -** Environment assessment Expose the patient and perform a log roll carefully Urinary Catheter / NG Tube / Trauma Series (Chest, Pelvis, + C- Spine) / Low Res CT

Question 44

**Describe**

Answer 44

AP Radiograph of ? taken at ? Communited mid-shaft tib / fib fracture with some varus displacement of distal fragments noted. Knee and Ankle appear to be intact however I would like: Lateral Tib/ Fib and dedicated knee/hip/ankle films to be certain. Risk of neurovascular compromise due to vascular/nervous/compartment syndrome is high so i would assess for these. Another risk would be rhabdomyolysis is this was a crush injury Also be certain to not miss other injuries as this is likely to be a distracting injury

Question 45

**i) Causes of rhabdomyolysis** **ii) Lab Testing** **iii) Complications** **iv) Management** **v) Myoglobin vs Haemoglobin in terms of oxygen dissociation**

Answer 45

**i)** Crush Injury Fracture Burns Hypothermia/Hyperthermia Acute Limb Ischaemia Connective Tissue Disorders/Haemophilias **ii)** CK, Renal Function, Electrolytes, (High K+, High PO4-, Low Ca+), Blood Gas (pH, lactate), LDH, Urinary Casts (brown) **iii)** AKI / Acute Renal Failure (ATN) + DIC **iv) Management:** Fluid Balance Monitoring (likely needs to be intensive) May need haemodialysis to remove the toxins Some extensive dialysers (high-flux) Can remove myoglobin (muscle oxygen binding protein) themselves **v) Myoglobin** has a steeper dissociation curve as it only has 1 binding site for oxygen cf haemoglobin. Therefore at lower partial O2 pressures oxygen won't dissociate allowing muscles to utilise oxygen in low/no oxygen environment.s

Question 46

**WRT Compartment Syndrome:** **i) Weak pulses/paraesthesia mean?** **ii) What is compartment syndrome?** **iii) Causes of compartment syndrome** **iv) How to measure compartment pressure?** **v) Management**

Answer 46

i) Bad- Late signs. Require urgent treatment at this point. Pain out of proportion with clinical picture is the earlier sign of compartment syndrome. ii) **Compartment syndrome** - is where the intracompartmental pressure exceeds capillary pressure thus reducing vascularisation of muscles/ nerves iii) **Causes -** Fractures, Crush, Burns, Dressings, Extravasation injury, Postischaemic, iv) **Compartment pressure measurement probe/ Arterial Line** **v)** Keep limb at level of heart. Release any pressure (Plaster) Two incision four compartment debridement (either side of the tibia)

Question 47

**i) What test of coagulation is most effected in liver damage / obstructive jaundice?** **ii) Why does ALP rise in obstruction?** **iii) Where is GGT found?** **iv) WHat does bile do?** **v) What is bilirubin precursor and how is unconjugated bilirubin transported to the liver?** **vi) Is bilirubin reabsorbed?** **vii) Correcting hepatic coagulopathy**

Answer 47

**i) Prothrombin Time (Measure of Extrinsic Pathway - I, II, V, VII, X):** This is because the liver is the site of production of the vitamin k dependent clotting factors (II, VII, IX, X), which tend to have short half lives. In obstruction vitamin k absorption is impaired. **ii)** **ALP** rises in obstruction as it is concentrated in the epithelial cells of biliary canuli. Disruption to this epithelium will therefore release ALP. **iii) GGT-** Small Bile Ducts + Hepatocytes **iv)** **Bile** - Emulsifies fats --\> Fatty Acids --\> Allows absorption of Vit ADEK Bile is reabsorbed in distal ileum **v) Haem -\> Biliverdin -\> Bilirubin (Unconjugated -\> Transported to liver on albumin --\> Conjugated Bilirubin ( Glucoronyl Transferase )** **vi)** Bilirubin is converted to stercobilinogen -\> stercobilin by oxidation in the bowel. Some stercobilinogen is reabsorebd --\> becomes urobilinogen in the liver -\> urobilin (answer is no) **vii)** Vitamin K \< FFP \< PTCC

Question 48

**i) Define: DIC** **ii) Why is the D Dimer raised in DIC?** **iii) List causes of DIC**

Answer 48

**i) A pathological consumptive coagulopathy** whereby there is simultaneous activation of coagulation factors leading to fibrin deposition and fibrinolysis. This leads to platelet and coagulation factor consumption. Combined risks of microvascular thrombosis + severe bleeding risk **ii) D Dimer is raised** as it is a breakdown product of fibrin. Due to enhanced fibrinolysis activity there is increased fibrin breakdown and increased D Dimer levels. **iii) Infectious -** Any systemic infection **Malignancy -** APML (M5) **Pregnancy-** Abruption, Ecclampsia **Haematological -** MAHA **Transfusion Reaction** **Trauma -** Burns, Polytrauma **Hepatic Failure**

Question 49

**Hypothermia:** **i) Definition** **ii) Consequences** **iii) Intraoperative causes**

Answer 49

**i) \<36 degrees** **Mild - 35-32** **Moderate - 32-28** **Severe - 28-20** **ii) Consequences:** Decreased Oxygen Dissociation from Hb - myocardial ischaemia, cerebral ichaemia, limb ischaemia, bowel ischaemia Hypocalcaemia Met. Acidosis Arrhythmias Coagulopathy - Enzyme Function impiarment + Platelet Dysfunction Enzyme Dysfunction Renal Failure Pancreatitis **iii)** **Intraoperative Causes:** Preop hypothermia, Major Surgery, Long Surgery, Using GA + LA, Blood Loss/Transfusion

Question 50

**EPidural:** **i) Which Space/which layers do you go through?** **ii) What could thoracic epidural do to respiration?** **iii) What could a thoracic epidural do to the cardiovascular system?** **iv) Consequences of high thoracic block**

Answer 50

**i)** Between dura and ligamentum flavum ultimately. Goes through - Skin, Subcut Fat, Fascia, Suprasinous Lig., Interspinous Lig., Ligamentum Flavum. **ii)** It could paralyse the intercostal muscles at and below the level it is insreted at thus impairing chest wall expansion **iii)** Distributive shock - cause vasodilation Bradycardia - due to the drug cocktail used T1-T5 level could impair the sympathetic stimulation to the heart thus preventing an appropriate rise in HR Above C4- Respiratory Depression/ Arrest **iv)** Hand paralysis, Respiratory Compromise (intercostal nerves), Cardiovascular compromise (cardiac sympathetics), Urinary Retention Other complications: Haemorrhage (Be careful when using antiplatelets/anticoagulants)

Question 51

**Petechial rash over fat, neck and axillae** **i) Features** **ii) Causes** **iii) Pathophysiology** **iv) Mode of death** **v) Test Results** **vi) Mx**

Answer 51

**Fat Embolus Syndrome** **i) Described by Bergmenn in 1873 as a triad:** **Petechial Rash- a)**Due to thrombocytopenia (purpura) and **b)** cutaneous vessel embolsiation **Respiratory Compromise - a)** VQ Mismatch **b)** Capillary Permeability (due to inflammation) -\> oedema **c)** Pneumonia **Cerebral Features** - **a)** Microembolisation leading to hypoxia **b)** Lipase degradation of cerebrum (Renal, Retina, Tachycardia, Pyrexia) **ii) Causes:** **Traumatic -** Long Bone Fractures/ Orthopaedic Procedures (reaming/ KR)/ Massive soft tissue injury **Atraumatic -** Pancreatitis, Omental Fat Necrosis, BM transplant, Liposuction, Cardiopulmonary bypass, Sickle Cell, **iii) Patho:** **Mechanical -** Local ischaemia and tissue injury due to fat globule impaction in pulmonary and systemic vasculature **Biochemical -** Catecholamines + Steroids --\> activeate lipases --\> break down fat to FFA which cause capillary permeability + lead to pul. damage **Coagulation -** Thromboplastin from marrow --\> activate coagulation/complement cascade --\> intravascular coagulation **iv)** Mode of death is usually **right heart failure.** This is rare and only apparent with **fulminant fat embolus syndrome (most severe of three clinical presentations)** **v)** ABG - Increased pulmonary shunt fraction ECG - Tachycardic/ RHS FBC - Low Hb, Low Plt, CLotting - looks like DIC Impaired renal function Low Albumin Low Ca++ Urine and Sputum contain lipids CXR - Pulmonary Infiltrates (fluffy snow storm appearance) MRI- Multiple acute infarcts **vi)** **Prophylactic** - Early Steroid Therapy, Ex-Fix device, Over-reaming femur in TKR, Decreased shaft width reamers, Early Fixation **Intensive Care Setting** **Oxygenation**/**Ventilation** - Early on CPAP **Albumin** - Binds FFAs **Fluid Balance Monitoring (Invasive)** **Correcting of electrolyte abnormalities** **DVT prophylaxis**

Question 52

**i) Define : Fistula** **ii) Define: Sinus** **iii) Define: Abscess**

Answer 52

**i)** A fistula is an abnormal connection between two endothelial/epithelial surfaces lined by granulation tissue **ii)** A sinus is a blind ending tract lined by granulation tissue **iii)** A localised collection of pus surrounded by granulation tissue

Question 53

**Fistulae:** **i) Causes of Enterocutaneous Fistula** **ii) Classifying Fistulae** **iii) Complications of high output fistulae** **iv) Enterocutaneous Fistula Management**

Answer 53

**i)** **Abdominal** **Surgery** (3/4) **Spontaneous** (1/4): - Inflammatory Conditions - Malignancy - Irradiation - Ischaemia **ii) a)** Congenital/ Acquired **b)** Type - Enterovesicular, enterocolic, enterocutaneous, **c)** aetiological **d) Output:** **Low- \<200ml** **Moderate - 200-500 ml** **High - \>500 ml** **iii) Complications:** - Dehydration (Kidney Injury) - Electrolyte Imbalances (HypoK+, HypoNa+, Acidosis) - Malnutrition - Infection - Abscess, cellulitis - Intestinal Failure **iv)** Initial Resuscitation with A-E MDT approach - Surgeon, Dietitian, Stoma Nurse **SNAP** **S** epsis control **N** utrintional Support (Initially TPN) **A** natomical assessment / **A**dequate fluid/electrolyte management **P** lan treatment / rotection of skin **60% Spontaneously resolve if -** not infected/ adequate nutrition/ no distal obstruction **Surgery can be considered if** : Conservative management fails Ongoing infectious concerns **Surgery aims to:** Excise Tract Resect affected segment of bowel Exteriorisation/anastamosis

Question 54

**i) What prevents spontaneous healing of fistulae?** **ii) Imaging modalities for fistulae**

Answer 54

**i) 60% Spontaneously Heal:** Otherwise causes are: Distal Obstruction Inflammatory Conditions / Sepsis Malignancy Foreign Body Radiation High Output Malnutrition **ii)** CT is Usually First Line but the **best modality is a fistulogram (contrast being given through fistula outlet)** **Anorectal fistulae -** Endoanal ultrasound / MRI are other modalities considered

Question 55

**i) Normal Calorific Requirements** **ii) Calorific Requirements in extensive trauma patients** **iii) Caveats in critically ill patients?** **iv) Complications of TPN**

Answer 55

**i)** 25-30 Kcal/kg/day **ii)** 45-55 kcal/kg/kday **iii)** In critically sick patients: There is disparity in the practice that is performed. Some data suggests early agressive nutritional support is associated with increased mortality and early parenteral support is assocaited with increased HAI. Generally a stepwise increase in calorific provision starting at less than \<20 kcal/kg/day gradually increasing this. **iv)** TPN Complications: Related to Central Line Insertion Electrolyte abnormalaties - HypoK+, Mg++, PO4- Glucose high/low TGs - High Ess. Fat. Acid - Low

Question 56

**Portal System:** **i) normal pressure** **ii) Sites of anastamosis with systemic system?** **iii) What are oesophageal varices?** **iv) Emergency Endoscopic Treatment Options for Varices? If Refractory to these?**

Answer 56

**i) \<10 mmHg** **ii) 6 -** Lower oesophageous, Upper Rectum, Retroperiotoneum, Bare Area of the liver, Patent Ductus Venosus, Umbilicus **iii)** Resultant from portal hypertension leading to venous engorgement of the oesophageal venous plexus (2/3 develop acute bleeding) **iv) a) Band** **Ligation** **b) Sclerotherapy** **--\>** **c) Sengstaken**-**Blakemore** **Tube** (Baloon position need to be checked - Oesophagus & Cardia of stomach by X Ray before inflated) - **can be complicated by** oesophageal necrosis, perforation and aspiration pneumonia **Further d) TIPS** (shunt between HV + PV) **e) Surgical Shunt f) Liver Transplant** **g) Both Terlipressin** (V1\>V2 receptor agonist) + Octreotide ( Somatostatin analogue) Both cause splanchnic/portal vasoconstriction reducing blood flow flow to the varices + **Prophylactic Antibiotics for all patients** **h) Propranolol for prophylaxis**

Question 57

**i) What specifics do you look for when assessing head injury?** **ii) Preventing secondary brain injury**

Answer 57

**i) Base of Skull/ Cribiform Plate injury -** CSF Rhinorrhorea/Otorrhoea, Raccoon Eyes, Battle Sign **PEARL -** Anisocoria/Absent VOR (if C Spine clear)/ Gaze Palsy **GCS** **Neurological Exam - CN/ UL/ LL. Hoffman's/ Babinski** **ii)** 1. Rapid Sequence Induction 2. Ventilate to PO2 \>13 / PCO2 \<5.3 (decreases Cerebral Perfusion Pressure 3. Head up position on bed 4. Osmotic Diuresis (Mannitol/ Hypertonic Saline 5. invasive monitoring - central line/art line/ ICP monitoring 6. Extras - Dex, Antibiotics, Fluids, Vasopressors

Question 58

**Hydrocephalus**: ## Footnote **i) Definition** **ii) Causes** **iii) Describe production and circulation of CSF**

Answer 58

**i) Presence of increased CSF within the ventricular system of the brain** **ii) Categorised into:** **Communicating (Non- obstructive)** **i) reduced absorption -** Venous Sinus Thrombosis, haemorrhage **ii) inreased production** - Choroid Plexus Carcinoma **Non- Communicating (Obstructive) -** Arnold-Chiari Malformation, Colloid Cyst, haemorrhage, abscess, tumour, head injury/oedema **iii)** Produced in **Ventricular Choroid Plexus:** Lateral ventricles --\> Third Ventricle (via foramen of monroe) --\> Fourth Ventricle (via aqueduct of sylvius) --\> Subarachnoid space (Foramen of Luschka/lateral arpetures either side of pons and Foramen of Magendie/median aperture between medulla/cerebellum) **Absorbed by Arachnoid Villi located in the subarachnoid space**

Question 59

**Types of hypersensitivity reaction**

Answer 59

**+ ?Type V -** Formulation of stimulatory antibodies

Question 60

**i) What are the sequalae of T1HS reaction?** **ii) What causes airway compromise?** **iii) Size Guedel + NP airway** **iv) What can interfere with pulse ox readings?**

Answer 60

**Antigen** - **IgE**(On **Mast** **Cell**) Linking --\> **Degranulation** of **mast** **cell** releasing **inflammatory** **cytokines**: Histamine, Leukotrienes, Prostoglandins --\> **Vasodilation, Smooth Muscle Spasm, Vascular Permeability, Increased secretions** **--\>** **Symptoms -\>** Tingling, Itching, Flushing, Urticaria, Mucosal Oedema, Upper Airway Compromise, Decreased SVR, Hypotension + CV compromise **ii) Airway compromise caused by -** Bronchospasm + oedema **iii) Guedel -** Incisors --\> Angle of Mandible **NP -** External Nares --\> Tragus **iv)** Nail Polish, Peripherally shut down, Carbon Monoxide (overestimate), Bilirubin (Underestimate)

Question 61

**i) Constiutents of NS vs hartmann's?** **ii)** **Complications associated with Colloids?** **iii) What is a colloid?** **iv) Colloids vs Crystalloids in sick patients?** **v) Distribution of crystalloid? Dextrose?**

Answer 61

**i) Normal Saline:** 154 mmol/L Na+ 154 mmol/L Cl- **Hartmann's:** 131 mmol/L Na+ 5 mmol/L K+ 111 mmol/L Cl- 2 mmol/L Ca++ 29 mmol/L HCO3- (in the form of lactate) **ii)** Interfere with platelets and vWF, Anaphylaxis, VTE **iii) Colloid -** contain large insoluble molecules **Crystalloid -** contain water-soluble molecules **iv) SAFE Study - Saline vs Albumin (4%)** found no survival benefit between the two. **v) Crystalloid** distribution is confined to the **ECF compartment:** 25% - Intravscular 75% - Extravascular **Dextrose -** 5% Dextrose quickly becomes water --\> 1/3 - **Extracellular** (1/4 intravascular 3/4 interstitial) 2/3 - I**ntracellular** As the overall intravascular contribution of dextrose would be minimal it is not useful in resus situations

Question 62

**Levels of care**

Answer 62

0 - Ward Care 1 - Ward Care with CCOT input 2 - HDU. One Failing System/ Major Surgery 3 - ITU. \>1 Failing System / Advanced monitoring.

Question 63

**i) Indications for tracheostomy** **ii) Types of trachy** **iii) Types trachy tubing** **iv) Complications of Trachy** **v) What constitutes trachy care**

Answer 63

**i) Congenital** **Conditions** - Laryngeotracheomalacia, Treacher-Collins Syndrome, Laryngeal Stenosis **Acquired Conditions -** Head and neck tumours **Emergency Airway -** Ludwig's Angina, Epiglottitis, Largyngeal Oedema, Upper Airway Trauma **Long term ventilation** **ii) Elective Surgical Trachy -** Horizontal incision midway between cricoid cartialge and sternal notch **Emergency Surgical Trachy -** Vertical incision [Tracheal access via a) vertical incisions between 2nd - 4th rings b) Bjork flap c) window cut] **Percutaneous -** Seldinger technique **Mini-Trachy -** 4mm tube through cricothyroid lig. under LA **iii)** Material - metal vs plastic Tube- Fenustrated vs unfenestrated Cuff - Cuffed vs un-cuffed **iv) Early -** Bleeding (Thyr. Isthmus+ AJV), Tracheal inj/, oesophageal inj., RLN Injury, Pneumothorax/mediastinum **Tube related -** Displacement, Extubation, blockage **Intermediate -** Infection (chest, trachea, wound), Trache-inominate/oesophageal fistula, Tracheal ulceration **Late -** Tracheal Stenosis **v)** **Trachy Care -** Humidified oxygen, Regular suction and cleaning of inner tube, Emergency trachy kit availability

Question 64

**Causes of hyponatraemia**

Answer 64

**Hypervolaemic - Ur Na+ \<20 -** CCF, Cirrhosis, Nephrotic Syndrome **Ur NA+ \>20 -** Renal Failure **Euvolaemia -** **Ur Na+ \>40 -** SIADH (Low serum osmolality, Increased urine osmolality, raised urinary sodium), Hypothyroidism, Low glucocorticoids **Ur Na+ \<40 -** Dietary, Psychogenic Polydypsia **Hypovolaemic -** **Ur Na+ \<20 -** Burns/Skin loss, GI loss **Ur Na+ \>20 -** Adrenocorticol deficiency, Renal Failure, Diuretics, Cerebral Salt Wasting **Pseudohyponatraemia:** **Normal serum osmolality -** Lipids / Proteins High (myelomatous states) **High serum osmolality -** High glucose, Mannitol, alcohols Drip arm

Question 65

**i) Causes of SIADH:** **ii) Rx**

Answer 65

**i) Drugs -** Psychiatric, Opiates, NSAIDs AEDs, Cytoxic **Pulmonary -** Malignancy, Pneumonia, PE **Cranial -** Tumour, Meningitis, Trauma **Many Malignancies.** **ii) Rx -** Water Restrict. Demecloycline - DDAVP Receptor Antagonist Vaptan - V2 Receptor Antagonist

Question 67

Answer 67

**J Osborn Waves - Seen in hypothermia (\<32 degrees)** Upward deflection between QRS and ST Segment

Question 68

**Clostridium Tetani:** **i) Describe** **ii) When are you fully vaccinatd?** **iii) Exotoxin vs endotoxin?**

Answer 68

**i)** Gram Positive Spore Forming Anearobic bacteria that produces toxin (tetanospasmin) **ii)** Full Vaccination is conferred - when you have had all five boosters within a ten year period iii) **Exotoxin** - Secreted immunogenic protein from poth Gram + and Gram -. Specific Host Response **Endotoxin -** LPS from the cell wall present on gram -. Widespread systemis stress resposne

Question 69

**WRT MODS:** **i) What is it?** **ii) Which organs can fail?**

Answer 69

**i)** Multi-Organ Dysfunction Syndrome ## Footnote **ii) Renal Failure, Intestinal Failure, Cardiovascular Compromise, Liver Failure, Bone Marrow Failure, Respiratory Failure**

Question 70

**i) Adrenergic Receptors - What acts on them?** **ii) When would you consider vasopressors/inotropes?** **iii) What's best for fluid refractory hypotension?** **iv) Target for patients in septic shock?** **v) What is MAP? Calculate it?** **vi) What does CVP Monitoring measure?**

Answer 70

**i) B1** - Cardiac Muscle --\> **Inotropic** and **Chronotropic** effect. **Dobutamine** (increases cardiac output) **B2** - Vascular walls --\> **Vasodilation. Dobutamine (**Reduces Afterload) **A1 -** Vascular walls/ Heart. --\> **Vasoconstriction. Noradrenaline** --\> Increased Blood Pressure (SVR) **Dopamine 1/2** - Diuresis **Dopamine Administration -** has effect on a broad range of adrenergic receptors which differ at different doses. **ii)** **Hypotension** unresponsive to fluid **Tachycardia, Distributive Shock (**peripheral vasodilation/ low SVR**),** **Low CO** **iii) Dopamine** + **Noradrenaline** **iv) MAP** \>65 mmHg Other things to monitor (End-Organ perfusion, BP, HR) **v) MAP =** (COxSVR) +CVP **MAP calculation =** Diastolic BP + 1/3(SBP-DBP) **vi)** Cardiac Filling Pressure which is related to **End Diastolic Ventricular Pressure.** This is used as a surrogate for preload **Preload cannot be actually measured as it is the stretching of cardiac myocytes before contraction**

Question 71

**i) Distribution of water** **ii) How much water in the 70 kg man?**

Answer 71

**i)** **2/3 Intracellular Water** **1/3 Extracellular Water (3/4 - Interstitial 1/4 - Intravascular)** **ii)** 42L in the 70 kg man (60% of body weight)

Question 72

# Define: **i) Respiration** **ii) Breathing** **iii) Respiratory Failure** **iv) Minute ventilation** **v) Indications for intubation and Ventilation** **vi) Confirmation of ET Tube position?** **vii) Components of ventilation**

Answer 72

**i)** Transfer of oxygen from air to tissue/ CO2 from tissue to air **ii)** The passing of air in and out of the lungs **iii)** Inadequate gas exchange (low O2 / high CO2 in arteries) Type 1 - PaO2 \<6.5 Type 2 - PaCO2 \> 6 PaO2 \<8 **iv)** Minute Ventilation - **RR** x **Tidal** **Volume** **v)** Low GCS State, Upper Airway Injury/Obstruction, ARDS/TRALI, Chest Injury, Neuromuscular Disease, Prophylaxis - Smoke inhalation, angiodoema **vi)** Chest: Symmetrical chest movements/ Ausculation of air in both lungs **not** in stomach **Gold Standard -** Waveform Capnography **imaging -** CXR **vii)** Ventilation involves: a) Ventilator (Insp. + exp. circuits) - Can be spontaneously controlled - Volume Controlled - Pressure Controlled b) Patient c) Connection between a and b

Question 73

**i) Calculation of Minute Ventilation** **ii) Complications of mechanical ventilation** **iii) When to consider ventilation wean**

Answer 73

**i) Minute Ventilation = Tidal Volume x RR** **Tidal Volume =** 5-10ml/kg **RR-=** 15 **For a 70 kg man** 700 x 15 = 10.5 L **ii)** Ventilator Associated Lung Injury - Barotrauma (pneumothorax/mediastinum/emphysema) VAP, Diaphragamtic Atrophy, CV (Decreased preload/ Stroke Volume), Laryngeotracheal damage **iii)** Can be weaned when with **trials of spontaneous ventilation:** **Fio2\< 50 %** **Low PEEP (**\<8cm H2O)

Question 74

**i) Risk Factors for development of acute AF after surgery** **ii) Mx of Acute new onset AF**

Answer 74

**i) Preoperative:** Age, CV Disease, Comborbidities (thyroid/ Lung disease/ diabetes/ alcoholism) **Postoperative:** Hypovolaemia, Electrolyte abnormalities, Infection, Hypoxia, Acute Myocardial Event, Pulmonary Embolus **ii)** Ascertain an precedent. If hypovolaemic/septic - Fluid Resuscitation may be enough If no adverse features - Pharmacological management with digoxin/amiodarone (guided by medical/cardiology teams) If adverse features - involve arrest/peri-arrest team and emergency DC Cardioversion/ Pharmacological cardioversion may be required

Question 75

**i) Open AAA repair complications**

Answer 75

**i) Graft** **Related** - Haemorrhage, Infection, Spinal Ischaemia/ Renal Failure/ Ischaemic Bowel, Distal embolus, Graft Thrombosis **Operation** **Related** - Acute Renal Failure, Ischaemic bowel (branch occlusion), Abdominal compartment syndrome, Ileus

Question 76

**Causes of ischaemia**

Answer 76

Arterial Occlusion Venous Congestion Hypoxia - Pulmonary/ Anaemia/ Carbon monoxide poisoning Impaired tissue oxygenation due to impaired oxygen dissociation

Question 77

**i) What does clopidogrel do?** **ii) What does aspirin do?** **iii) When does more care need to be given to stopping antiplatelet agents?**

Answer 77

**i) Clopidogrel** irreversibly **inhibits platelet** **ADP** **receptor** preventing platelet **aggregation** **- this lasts for 8 days** as the average platelet lifespan is eight days **ii) Non** **specific** **COX-1 + COX-2 Inhibitor preventing prostaglandin + thrombaxane generation** **-** Thromboxane is a promotor of platelet aggregation and activation **iii)** When the indication is for **stent insertion (cardiac/vascular)**

Question 78

**Methods for reduction of intraoperative blood loss**

Answer 78

Meticulous Haemostasis Cell Savers Tourniquets Optomising coagulation Physiological Hypotension

Question 79

**NSAIDs sytemic effects**

Answer 79

**GI (**Reduced prostalgandin production which contribute to the production of protective mucous**) -** Dyspepsia, Gastritis, Peptic Ulceration **Renal -** Interstitial Nephritis, Reduces afferent vasodilation **Cardiovascular -** Salt/Water Retention -\> Heart Failure **Coagulopathy -** Reduce platelet aggregation (due to reduced thromboxane production) **Bronchospasm-** Due to increased leukotriene production

Question 80

**i) Metabolic Respone to Injury** **ii) What is the respiratory Quotient?**

Answer 80

**i) Ebb Phase -** Reduced metabolic rate/ cardiac output/ core temperature **Flow Phase -** Catabolic Phase then Anabolic Phase **ii) Respiratory Quotient = CO2 Excreted / O2 Consumed** Used to suss out which foods are being metabolised

Question 81

**Why is NJ preferred in pancreatitis to NG?**

Answer 81

**NJ preferred-** as it bypassed the DJ flexure. Fatty Acids in the duodenum cause the release of **CCK --\>** Stimulates pancreatic enzyme secretion and worsen the inflammatory process

Question 82

**i) Features of opiate overdose** **ii) Managing overdose**

Answer 82

**i)** Confusion, Itchiness, Visual/Tactile Hallucinations Hypotension, Pinpoint Pupils Apnoea, Respiratory Failure **ii)** A-E approach Nalaxone following trust policy (0.4-2mg IV which can be repeated evert few minutes up to 10mg) Contact critical care team regarding Nalaxone infusion

Question 83

**Causes of pancreatitis**

Answer 83

**I**diopathic **G**allstones **E**thanol **T**rauma **S**teroid * *M**umps * *A**utoimmune **S**corpion bite **H**ypercalcaemia/hyperlipidaemia **E**RCP **D**rugs (Azathiaproine, Sulfasalazine, Trimethoprin, Tetracycline)

Question 84

**Define: Shock**

Answer 84

Inadequate tissue perfusion for metabolic requirement

Question 85

**Classification of Shock**

Answer 85

Question 86

**TURP Syndrome** **i) Features** **ii) Rx**

Answer 86

i) **Hyponatraemia** - restlessness, blurred vision, confusion **Hypovolaemia -** overload/cardiac failure **High Ammonia -** Confusion This is due to the glycine rich instillation fluid used which when asborbed causes a: dilutional hyponatraemia raised ammonia **ii)** If intraoperative - stop and stop instillation of fluid C- A-E Assessment: Consider intubation if necessary Take bloods and an ABG to look at the electrolytes Enlist anaesthetist/ITU support in maanaging the electrolytes as the patient is also overloaded - ?hypertonic saline - ?fluid restrict - ?diuresis Treat complications such as arrhythmias/ seizures

Question 87

**Diuretics MOA** **i) Loop** **ii) Thiazide** **iii) Aldosterone Antagonist** **iv) Amiloride** **v) Osmotic Diuretic**

Answer 87

**i) Loop -** Furosemide, Bumetanide Inhibit Na/K/Cl- Transporter in the thick asending loop of henle. Prevents sodium resorption/concentration gradient formation. Prevents concentration of urine. **ii) Thiazine -** Bendroflumethiazide Inhibits Na/Cl- transporter in DCT. **iii) AR Antag. -** Spironolactone, eplenorone Prevents the insertion of eNAC channels in the collecting tubules which prevents Na+ resorption and K+ excretion **iv)Amiloride -** K+ Sparing diuretic **v) Osmotic Diuretic -** Mannitol. Large molecule that is filtered but not reabsorbed. Causes water to be retained in the tubules.

Question 88

**Classic time for anastamotic leak**

Answer 88

Day 4/5

Question 89

**Causes of post-operative pyrexia**

Answer 89

**Blood -** Transfusion **Physiological -** SIRS (0-1 Days) **Infection -** Pulmonary atelectasis (1-2) days, UTI, Cellulitis, SUperficial thrombophelbitis, Wound Infection **Drug Reaction -** Suxamethonium **Anastamotic leak (**4-5 days**)** **Thrombosis -** PE, Pneumonia

Question 90

**i) Risk of aortic stenosis in surgery?** **ii) Coronary Perfusion Pressure Equation** **iii) Voltage criteria for LVH** **iv) Warfarin MOA**

Answer 90

**i)** Due to the outflow obstruction there isn't a capacity to modulate cardiac output! Anaesthetic agents/ spinal anaesthetics can reduce the afterload/SBP. Myocardium is compromised due to lack of coronary perfusion **ii) Coronary Perfusion Pressure =** Systemic Diastolic Pressure - LV End Diastolic Pressure **iii) Either** **S** in **V1** or **R** in **V5/V6** \>35 mm / 7 small squares **iv )Warfarin -** Inhibits Vitamin K Epoxide Reductase

Question 91

**i) What are the desired effects of sedatives?** **ii) Contraindications to sedation?** **iii) General risks to sedation?** **iv) Monitoring requirement for sedation?**

Answer 91

**i)** Reduced state of consciousness, analgaesia, anxiolytic **Light -** Patient can maintain their airway and respond to stimuli easily **Deep -** Patient airway is not always patent and needs sizable stimuli to rouse **GA -** Patient airway is not patent and they are not responsive **ii)** **CIs to sedation -** patient choice, long procedures, lack of monitoring, not starved appropriately (food \>6 hours, water \>2 hours), **unstable patients.** **iii)** **Risks -** Respiratory Depression, Airway Compromise, Confusion, Hypotension, Impaired gastric emptying/ regurgitation **iv)** **Monitoring -** General Obs, Three lead ECG, ETCO2, If conscious then monitoring of symptoms

Question 92

**Features of different sedation agents:** **i) Midazolam** **ii) Ketamine** **iii) Propofol** **iv) Nitrous Oxide** **v) Morphine** **vi) Etomidate**

Answer 92

**i) Midazolam. 1-2mg.** Good for amnesia/anxiolytic. not for pain. Minimal cardiorespiratory compromise **ii) Ketamine.** Good for amnesia/Pain. Marked dissocative psychiatric effects / nausea/ vomiting. **iii) Propofol.** Rapid Onset. CVS/Resp Depression. Good antiemetic properties **iv)** **Nitrous Oxide.** Inhaled. SACD in chronic use. **v) Morphine.** Good for pain. Caution in renal patients. Causes vomiting/constipation/ nausea/ CV+ resp compromise. **vi) Etomidate.** Induction agent. Adrenocortical suppression. Less CV/Resp effect.

Question 93

**Signs of Lidocaine Toxicity** **Max dose w/ w/o adrenaline**

Answer 93

**Max Dose:** With adrenaline - 7 mg/kg . Without adrenaline 3mg/kg **Signs of toxicity:** Perioral Paraesthesia Hypotension Convulsions Dizziness Cardiac Arrhythmias Collapse

Question 94

**Nutritional Requirements:** Sodium Potassium Calories Protein/Fat/Glucose

Answer 94

Sodium - 1-2 mmol/kg/day Potassium - 1mmol/kg/day Calories - 25-30 kcal/kg/day Protein/Fat/Glucose - 20:30:50

Question 95

Adrenaline vs Noradrenaline

Answer 95

Adrenaline Alpha and Beta Noradrenaline predominantly alpha Alpha - peripheral vasoconstriction Beta - cardiac chronotropic and inotropic

Question 96

What is dopexamine

Answer 96

Splanchnic vasodilator

Question 97

**Anion Gap** **Calc** **Causes**

Answer 97

Calculation (Na+K+)-(Cl+HCO3) Normal **10-18** **Low Anion Gap** hypoalbuminaemia, increased cations (MG++, Ca++, IgG), **Normal Anion Gap** - **Hyperchloraemic** Bicarb Loss, Renal Tubular Acidosis (moreso in type II), Drugs (Acetozolamide), Chloride Injection, Addison's Disease (Type IV RTA) **High Anion Gap** Lactate, Ketoacidosis, Urate, Exogenous Acids

Question 98

**JVP** Absent a waves Large a waves cannon waves prominent v waves slow y descent steep y descent JVP rises during inspiration Fixed Raised JVP

Answer 98

Absent A Waves - AF Large A Waves - Right ventricular hypertrophy, triscupid stenosis Cannon Waves - Complete Heart Block Prominent v waves - Tricuspid Regurgitation Slow y descent - Tricuspid stenosis, Right Atrial Myxoma Steep y descent - Right ventricular failure, Constrictive pericarditis, Tricuspid regurgitation JVP rises during inspiration - Kussmaul's sign of constrictive pericarditis Fixed Raised JVP - Superior Vena Cava Obstruction

Question 99

**Four mechanisms of vomiting**

Answer 99

**Gag** - Touch Receptors in throat (CN IX), Pharyngeal Cosntrictors (CNX + CNIX for stylopharyngeus) **Labyrnthine** disorders - Motion Sickness **Stomach and duodenal distension -** stretch receptors **Central (brain) -** chemically induced (drugs etc.)

Question 100

**When to admit for acute lower GI bleeding**

Answer 100

Age \>60 Significant Co-Morbidity Unstable Profuse bleeding Aspirin/NSAID use

Question 101

By what mechanism does ECF Volume depletion cause Metabolic Alkalosis

Answer 101

Losing significant bodily fluid through vomiting or diuretics results in a loss of Na+ + Cl- This leads to RAAS activation --\> aldosterone causes increased ENaC channels so more Sodium crosses from lumen into cells. Luminal K+ channels upregulated so potassium is lost to the lumen. Na+K+ATPase at interstitial side of cells is upregulated ---\> K+ is moved into the cell whereas Na+ is moved into interstitium. These three transporter changes lead to an increase loss of K+ to the collecting duct lumen and a preservation of Na+ Loss of K+ Leads to K+/H+ Buffering. K+ moves from cells into ECF in exchange for H+ -----:\> **Alkalosis**

Question 102

Managing local anaesthetic toxicity Max Doses

Answer 102

Intralipid: Bolus- 1.5 ml/kg over 1 minute Infusion - 0.25 ml/kg/minute If prilocaine is used then administere methylene blue 1st dose - neat/ 2nd dose w/adrenaline **Lignocaine -** 3 mg/kg. 7 mg/kg Bupivicaine - 2 mg/kg 2 mg/kg Prilocaine - 6 mg/kg 9 mg/kg **Prilocaine**

Question 103

**Best test for vWD**

Answer 103

Bleeding Time (factor VIII may also be low) vWD can be Autosomal Dominant: Type I - Quantitative deficiency of vWF Type 2 - Qualitative impariment of synthesis of vWF Autosomal Recessive Type 3 - Absolute deficiency in vWF

Question 104

Which Coag factors to the following influence: Heparin Warfarin Liver Disease Disseminated Intravascular Coagulation

Answer 104

**Heparin -** 2,9, 10, 11 **Warfin -** 2, 7, 9 , 10 **Liver disease -** 1, 2 , 5 , 7, ,9, 10, 11 **DIC -** 1, 2, 5, 8, 11

Question 105

**Which hormones are reduced in stress response?**

Answer 105

Insulin Oestrogen Testosterone

Question 106

**principles for operating in acute cholecystitis**

Answer 106

\<48 hours surgery is a good idea \>5 days - surgery is best left deferred to 3 months to allow inflammation to settle

Question 107

**Fistulae** **When is it safe to conersvatively manage?** **Drug therapy for high output fistula** **Contraindication to probing perianal fistulae** **How to delinieate fistula tract?**

Answer 107

**Conservative management -** In the absence of IBD or distal obstruction **Octreotide** si used to reduce pancreatic secretions in the context of high output fistulae **Perianal fistulae** should not be probed in teh context of **acute inlammation** Fistula anatomy can be delineated using CT and barium studies

Question 108

Why use bupivicaine post-operatively over lidocaine?

Answer 108

It has a much longer duration of action than lignocaine and therefore can provide longlasting wound-site analgaesia

Question 109

**What would be the LA of choice in regional block?**

Answer 109

Prilocaine - this is much less cardiotoxic

Question 110

**Sulphur Granules and Gram Positive Organisms -** Histology

Answer 110

Actinomycosis - Forms multiple sinuses The sulphur granules (round or oval basophilic masses)

Question 111

**Within what time should an open fracture be internally fixated?**

Answer 111

72 hours

Question 112

Scaphoid abdomen

Answer 112

Abdomen sucked inwards: Think diaphragmatic hernia in newborn

Question 113

**Wound healing - Predominant Cell Types** **Inflammation** **Regeneration** **Remodelling (Contraction)**

Answer 113

**Inflammation** Neutrophils. Early phase (first week) **Regeneration** Fibroblasts. (8 weeks) Microvascularisation **Remodelling (Contraction)** Differentiated fibroblasts. Microvessels regress so the scar looks pale.

Question 114

**Ileostomy effluent**

Answer 114

Na - 126 mmol/ L K+ - 22 mmol/L

Question 115

**What is in cryoprecipitate**

Answer 115

VIII Fibrinogen XIII vWF

Question 116

**Ventilation** **What are the three cerebral areas responsible for ventilation and what do they respond to?** **Any non-cerebral areas involved?**

Answer 116

**Medulla** **Oblongata** This responds to increased interstitial H+ to increase ventilation (to blow off CO2). The **Apneustic** Centre in pons instigates inspiration whereas the **Pneumotaxic** Centre, also in the pons, inhibits inspiration. **Peripheral chemoreceptors** are in the carotids and arch of aorta --\> these respond to arterial pO2, pCO2 and H+

Question 117

**Below which blood pressure does renal autoregulation of flow fail?**

Answer 117

\<80 systolic blood pressure

Question 118

Management of traumatic pneumothorax and why?

Answer 118

Chest drain - Usually in context of traumatic pneumothorax there is damage to lung parenchyma = High chance of tension pneumo development

Question 119

Which drug prevents conversion of plasminogen to plasmin?

Answer 119

Tranexamic Acid

Question 120

Which clotting factors are particularly heat sensitive?

Answer 120

Factor V Factor VIII Hence FFP is frozen

Question 121

**Dose of heparin for:** ## Footnote **Vascular Bypasses** **Cardiopulmonary bypasses**

Answer 121

**Vascular Bypasses** 3000 units prior to cross clamping **Cardiopulmonary bypasses** 30,000 units priot to initiating bypass

Question 122

**Actions of PTH**

Answer 122

Bone - Osteoblasts binding --\> inreased RANKL expression --\> Activation of osteoclasts ---\> increase resorption Kidney - Resorption of calcium and mangesium from DCT. Decreased resorption of phosphate GI - PTH increases Vit D activation --\> increased GI calcium absorption

Question 123

**in DIC which components of clotting are depleted fastest**

Answer 123

V, VIII and Platelets

Question 124

**Effects of Adrenaline**

Answer 124

**Alpha -** Peripheral Vasoconstriction Insulin inhibition Glycogenolysis in liver/muscle and glycolysis in muscle **Beta -** 1 - Cardiac chronotrope + inotrope, increased renin secretion 2 - Skeletal muscle vasodilation + coronary artery vasodilation. Bronchodilation Glucagon secretion, ACTH secretion, Lipolysis in adipose tissue

Question 125

**DTPA vs MAG3**

Answer 125

DTPA - good for assessment of GFR MAG3 - good for assessment of renal function in patients with known impairment

Question 126

**Rockall Score** **WHen?** **Components?**

Answer 126

Following Endoscopy for UGI haemorrhage Components: A Age B BP C Co-morbidities D Diagnosis E vidence of bleeding

Question 127

**Kocher Criteria for Septic Arthritis**

Answer 127

**WIFE** WCC \>12 I - inability to weight bear Fever ESR \>40

Question 128

**Drug Treatment for Colonic Pseudoobstruction**

Answer 128

Neostigmine

Question 129

**management for biliary leak post lap chole**

Answer 129

ERCP + Stent

Question 130

**Biliary Decompression as an adjunct to curative pancreatic surgery**

Answer 130

ERCP + Stent Do not surgically bypass them

Question 131

**Management of sudden full dehiscence**

Answer 131

Analgaesia, IV fluid, IV abx Cover wound with saline gauze Return to theatre STAT

Question 132

**BEst way to assess for upper airway compression?**

Answer 132

Flow Volume Loop

Question 133

**Anaerobic Organism complicating difficult operations\>**

Answer 133

Bacteroides Fragilis - Gram Neg, Anaerobe, Rod Shaped Involved in majority of peritoneal infections

Question 134

**What does serotonin do to vessels?**

Answer 134

Intact vessels - Vasodilation Damaged vessels/tissue - vasoconstriction

Question 135

**Four drugs commonly associated with parotid enlargement**

Answer 135

Thiouracil Isoprenaline Phenylbutazone Oestrogen Contraceptic pills

Question 136

**Drug cause of SIADH**

Answer 136

Carbamezapine, SSRIs, Sulfonylureas, TCAs, vincristine, cyclophosphamide

Question 137

**ABx MOA** **Inhibiting Cell Wall FOrmation** **Inhibiting Protein Synthesis** **Inhibiting DNA Synthesis** **Inhibiting RNA Synthesis Cell Membrane**

Answer 137

**Inhibiting Cell Wall FOrmation** Penicillin, Cephalosporin, Glycopeptide **Inhibiting Protein Synthesis** **50S -** Macrolide, Linezolid, Chloramphenicol **30 S -** Aminoglycloside, Tetracycline, **Inhibiting DNA Synthesis** **DNA Gyrase** - Fluroquunilone Metronidazole, Sulphonamide, Trimethoprim **Inhibiting RNA Synthesis** Rifampicin **cell Membrane** Polymxin

Question 138

**Perforated appendicitis - where is fluid most likely to collect**

Answer 138

pelvis

Question 139

**Mediators of acute inflammation**

Answer 139

Serotonin Histamine Prostaglandin Leukotrienes TNF Interleukins

Question 140

Why might the APTT be long in someone with Anti Phospholipid Syndrome?

Answer 140

They might have Lupus Anticoagulant. ALthugh in vivo this is prothrombotic, in vitro it increases APTT

Question 141

**Actions of corticosteroids**

Answer 141

**Metabolic** Decreased uptake/utilisation of glucose Increased gluconeogenesis Increased hyperglycaemia Increased protein catabolism Lipolysis **Regulatory** Negative feedback on hypothalamus CNS - decreased vasodilation/ decreased fluid exudation Decreased osteoblastic/ Increased osteoclastic Decreased inflammation

Question 142

**Treatment of pancreatitic pseudocyst**

Answer 142

Endoscopic or radiological cystgastrostomy

Question 143

Laparotomy approach in children

Answer 143

Transverse Supra Umbilical incision

Question 144

**Trotter's Triad**

Answer 144

Nasopharyngeal Carcinoma Unilateral Conductive Hearing Loss Ipsilateral Facial Pain Ipsilateral Palatal Paralysis

Question 145

How does tranexamic acid work\>

Answer 145

Inhibits plasmin which is responsible for fibrin degradation

Question 146

**Where is the intercostal bundle**

Answer 146

Lies in the **subcostal groove** Vein is most superior (least easily damaged) Artery Nerve (most inferior)

Question 147

**Which surgical device is good for managing splenic bleeding?**

Answer 147

Argon plasma coagulation system

Question 148

**Which clotting constituents are consumed most quickly in DIC**

Answer 148

V, VIII and platelets

Question 149

**Treatments for extravasation injury** Doxirubicin Contrast media, TPN, Vinca Alkaloids Vinca Alkaloids ALone

Answer 149

Doxirubicin - COld Compress Contrast media, TPN, Vinca Alkaloids - Hyaluridonase Vinca Alkaloids ALone - Warm Compress

Question 150

**Potential Blood Loss from:** **i) Humeral #** **ii) Tibia #** **iii) Femur #** **iv) Pelvic #**

Answer 150

**i) Humeral # -** 750ml **ii) Tibia #** - 750ml **iii) Femur # -** 1L **iv) Pelvic # -** 3L

Question 151

**Steroids:** i) What is a steroid? ii) Anatomical layers of adrenals and steroids they produce iii) What causes increase in aldosterone production? What acid/base abnormality can increased aldosterone cause? iv) What causes **GC** production?

Answer 151

**i)** Hormonal compound formed from **4 cycloalkane rings** **ii)** **Glomerulosa -** Mineralocorticoids **Fasciulata -** Glucorticoids **Reticularis -** Sex Hormones **Medulla -** Catecholamines **iii) Aldosterone production** is caused by: **a)** Incr. Renin **b)** Hyperkalaemia **c)** Hyponataraemia It can cause a metabolic alkalosis due to K+ excretion (consequnetly H+ being transported intracellularly in exchange for K+) **iv)** The HPA Axis - **Hypothalamus -** CRH/ **Pituitary -** ACTH / **Adrenal** - Glucocorticoid

Question 152

**i) Main effects of glucocorticoids** **ii) Hormones produced by the Anterior Pituitary?**

Answer 152

**i) Hyperglycaemia -** Increased gluconeogenesis / Antagonising Insulin **Protein -** Stimulates hepatic protein synthesis/ Reduced peripheral protein synthesis **Fat -** Stimulates lipolysis **Kidneys -** Exerts mineralocorticoid effect in increased concentrations **Stress -** Key modulator in the body stress response **Anti- Inflammatory + Immunosuppressive** **Other -** Weight Gain, Osteoporosis, Capillary Fragility, Proximal Myopathy, Peptic Ulcer, Psychiatric **ii) Anterior Pituitary:** ACTH, TSH, LH, FSH, Prolactin, Growth Hormone

Question 153

**Addisonian Crisis:** **i) 4 Major Features** **ii) What is a crisis?** **iii) Mx of a crisis** **iv) Who doesn't need perioperative glucocorticoid coverage?** **v) When to cover for glucocorticoid insufficiency perioperatively?** **vi) How to test adrenal function ?** **vii) how to cover with steroids perioperatively?**

Answer 153

**i) Major:** Shock Abdominal Pain Nausea Vomiting Temperature dysregulation **Other:** Hyperkalaemia, Hyponatraemia, Metabolic Acidosis **ii)** Addisonian crisis is where the **glucorticoid supply** is insufficient to meet the **glucorticoid demand:** Primary - Adrenal Insufficiency Secondary - Exogenous Steroids abruptly stopped/not increased **iii)** ATLS/ CCrisp approach IV Hydrocortisone 100mg QDS IV Fluids Electrolyte management **iv)** No need for steroid change if: **a)**Steroid administration **\<3 weeks** **b) 5mg prednisolone OD** (or equivalent)**/ 10mg prednisolone Alternate Days** (or equivalent) **v)** **Perioperative** **coverage** **should** be for patients**:** **a) Cushing's Syndrome** on exogenous steroids **b)** Known to be **addisonian and receiving steroid treatment** **c)** On **\>20 mg prednisolone OD** (or equivalent) **d)** Stopped high dose steroids in the last 3 months **vi) Adrenal Testing** through **early morning cortisol** and **ACTH stimulation test** **vii)** **Minor Procedures -** usual morning dose **and** 25mg at induction **Moderate Procedures -** usual morning dose **and** 25-50mg hydrocortisone at induction **and** 25 mg hydrocortisone every 8 hours for 24 hours **Major procedures -** usual morning dose **and** 50-100mg hydrocortisone at induction **and** 50 mg every 8 hours for 24 hours **and** then reduce by half a day until reaching maintenance

Question 154

**ASA Grading**

Answer 154

**I** - No Comorbidities **II** - Mild Systemic Disease **III**- Severe Systemic Disease **IV** - Severe Systemic Disease that is a constant threat to life **V** - Moribund person who will die without operation **VI** - Brain Dead who is having organ removal for donor purpose

Question 155

**LEMON classification system for difficult intubation**

Answer 155

**Look for visible risk factors -** facial trauma/ small mandible/ short neck **Evaluate -** 3 - 3 -2 rule. 3 fingers - between incisors 3 fingers - between hyoid bone and chin 2 fingers - between thyroid notch and floor of mouth **Mallampati Score -** tongue to mouth opening size (ease of laryngoscopy) **Obstruction -** Trauma/Swelling **Neck Mobility -** C Spine injury/ Rheumatoid Arthritis

Question 156

**Coroner Referrals**

Answer 156

1. Death \<24 hours after admission 2. Suspicious/ accidental/ violent/ suicide deaths 3. Death after operation/procedure 4. Unknown cause of death

Question 157

**What types of response are there to a fluid challenge?**

Answer 157

**i) Full Responders -** Probably only mildly hypovolaemic **ii)** **Transient Responders -** Likely to be hypovolaemics so need more fluid resusictation with fluids - This can also represent a person who is actively haemorrhaging so this needs to be considered **iii) Non responders -** These patients are either profoundly hypovolaemic or there is another cause than hypovolaemia contributing to their hypotension

Question 158

**i)How to approach a trachy patient in respiratory distress?** **ii) What are the components of a trachy kit?**

Answer 158

**i) Some help** would be handy **a)** Ensure patient is **monitored** **b)** Look for chest wall **movement** ( reassures you that they are having air entry ) **c)** Listen for breath **sounds** in the tracheostomy **tubing** itself **d)** Feel for **air** **coming** from the **tracheostomy** **e)** Find out if the trachy has an **inner** **tube/if it is cuffed** **f)** Try to **suction** the tube --\> If this fails then go to **g) and h)** **g) With inner tube-** Take the **inner** **tube** out and **clean** it/ **change** it **h) Without inner tube -** Towel underneath shoulders and **change** **the** **tube** keeping the **stoma** **open** with forceps **ii) Trachy Kit** 2 x Trachy Tube (one same size + one smaller) Bag and Mask Portable Suction Device + catheter NaCl Ampoule + syringe

Question 159

**Indications for Renal Replacement Therapy**

Answer 159

Anuria/Oliguria (persistent) Refractory Hyperkalaemia Ureamia (+complications) Pulmonary Oedema Drug Overdose Severe Acidosis

Question 160

**Types of transplant rejection**

Answer 160

Question 161

**Types of Immunosuppresant**

Answer 161

**Corticosteroids** **Calcineurin inhibitors -** Tacrolimus, Cyclosporin **Anti-purine -** Azathioprine, Mycophenolate **Cytotoxics -** Cyclophosphamide **Antimetabolite -** Methotrexate **Small molecule inhibitors -** -ibs **Antibodies -** abs

Question 162

**What are the constituents of :** **i) FFP** **ii) Cryoprecipitate** **iii) Prothrombin Complex Concentrate**

Answer 162

**i) FFP -** Albumin, All clotting factors, vWF, Complement, Fibrinogen **ii)** **Cryoprecipitate-** VIII, XIII, vWF, Fibrinogen **iii)** **Prothrombin Complex Concentrate -** II, (VII), IX, X, C, S, Heparin

Question 163

**Vomiting:** **i) Classcial Biochemical Abnormality?** **ii) ECG Changes in hypokalaemia?**

Answer 163

**i) Hypokalaemic, Hypochloraemia Metabolic Alkalosis** Due to: **a)** loss of HCl + K+ from gastric secretions **b)** Hypovolaemic/Hyponatraemic mediated RAAS Activation leading to K+ excretion in the collecting tubules **ii)** Flat/Inverted T Waves, U Waves, Long PR, ST depression

Question 164

**Describe** **Management** **What delays wound healing/fracture healing**

Answer 164

**Weber C Ankle Fracture ( Weber classification by the distal fibular fragment. A - Below syndesmosis. B - through sydnesmosis. C - above syndesmosis)** **Management -** would consult **BOAST Guidelines** SHould not have had X ray as tehre would have been obvious deformity. Needs urgent reduction. - Make sure neurovascularly intact - Reduction by lifting toes with hand under calcaneum and longitudinal traction. - Check x ray and re-cehck neurovascularly intact after reduction - Below knee plastering - Will need ORIF (either within 24 hours or after 6 days - this is due to swelling) **Complicated by :** **Co Morbidities -** Age, Vascular Disease, Diabetes, neuropathies **Smoking** **MEdications -** NSAIDs, Steroids

Question 165

**What does intact bulbocavernosus reflex intact in the context of acute paralysis?**

Answer 165

This reflex involves pulling clitoris/ or glans penis and assessing reflex anal sphincter contraction. **(S2- S4). Can also be tested by tgging a catheter** **Intact -** Spinal Severance **Not Intact-** Spinal Shock

Question 166

**Assessment in ?spinal injury** **Define cauda equina syndrome** **Red Flag syptoms for back pain**

Answer 166

**History** - Pain- Characteristics (neuropathic, ?bilateral) Urinary function - ?feel full bladder, ?pass urine, ?control stream ?does she void normally at all Bowel Fucntion **Examination** LL / UL exam Reflexes Perianal paraesthesia - sharp testing Anal tone testing Bulbocavernosus reflex testing **Cauda Equina Syndrome:** - Back pain, Neuropathic pain, lower limb weakness, perianal paraesthesia, visceral dysfunction **Red Flag Symptoms** **TUNA FISH** Trauma, Unexplained weight loss, Neurological Symptoms, Age \>50 Fever, IVDU, Steroid Use, History of cancer

Question 167

**All Dermatomes and Myotomes**

Answer 167

Question 168

**i) Management of intertrochanteric NOF** **ii) Classification systems from extracapsular NOF**

Answer 168

**i) Reduction -** In traction stirrup (protected with wool) - Longitudinal traction with patella facing the ceiling and then check x ray before fixing **ii) Intertrochanteric Fracture -** Evan's Classification (1-5). 1 is undisplaced and 5 is displaced + severely communited **Subtrochanteric Fracture -** Russel Taylor Classification System

Question 169

**i) Intracapsular NOF Management** **ii) Intracapsular NOF Classification**

Answer 169

**i)** Non displaced - Can try cannulated screw/DHS Displaced and patient is **independently mobile, cognitively intact** + **fit for surgery -** THR **otherwise** hemiarthroplasty **ii)** Intracapsular NOF: **Pauwel's -** Angle of fracture **Garden's** - based on valgus dispalcement

Question 170

**i) What is acute tubular necrosis + causes**

Answer 170

i) Renal failure due to insult to tubular epithelial cells due to either: **Ischaemia** **Nephrotoxins -** Myoglobin, Antibiotics (Aminoglycosides), Toxins (heavy metals)

Question 171

**Some complications of cholecystitis**

Answer 171

**Chronic Cholecystitis** **Gallbladder mucoceoele** **Gallbladder empyema** **Gallstone Ileus** **Gallbladder perforation**

Question 172

**Risks on consent form for laparoscopy +/- appendicectomy**

Answer 172

Bleeding, Infection, Damage to structures, Pain post-procedure, Anaesthetic Risk, Requirement to open abdomen to resect more bowel / form a stoma

Question 173

**Management of anterior shoulder dislocation**

Answer 173

Analgaesia Neurovascular status X Ray Reduction with analgaesia: Hippocratic - axilla countertraction Stimson - prone with arm hanging over bed and gentle traction for 15-20 minutes Post reduction chest x ray and neurovascular check Polysling for 4 weeks after to allow soft tissue healing

Question 174

**Supracondylar fractures** **i) Common nerve palsies** **ii) How would you assess nerve function of someone in backslab?** **iii) What would you consent the patient for if closed reduction and percutaneous pinning being planned?** **iv) Classification for supracondylar fractures?**

Answer 174

**i) Extension -** Median nerve AIN branch \> Radial Nerve **Flexion -** Ulnar nerve **ii)** **Median Nerve -** Test FDP and FPL (Ok Sign) - Index finger sensation **Ulnar Nerve -** Intrinsic hand muscles abduction and adduction of middle / index fingers - Little finger sensation **Radial Nerve-** Extension of MCPJ - 1st Dorsal web space **iii)** Scar, Infection of metalwork, Vascular Injury, Nerve injury, Conversion to open procedure, COmpartment syndrome, Deformity, Mal-union, Non-union **iv) Gartland I -** Non displaced II - Angulated with intact posterior cortex III - completely displaced

Question 175

**Haematemesis** **i) Causes** **ii) Is initial Hb reading accurate?** **iii) Management**

Answer 175

**i)** Oesophageal - Ulcer, Varices, Mallory Weiss Tear, Malignancy, Fistula Stomach - Ulcer, malignancy, angiodysplasia, varices, Duodenum - ulcer, malignancy, angiodysplasia, varices **ii)** No it can be falsely raised as it takes time for the interstitial fluid to redistribute its volume to the plasma. **iii)** A-E approach cCRISP Replace circulatory volume Stop anticoagulants Give blood ( activate massive transfusion protocol i needed) IV PPI Antibiotics/ Terlipressin if suspect varices Urgent endoscopy

Question 176

**Risk factors for anastamotic leak**

Answer 176

Patient - SMoking, vascular disease, diabetes, steroid use, nutrition Pathology - IBD, Autoimmune, Collagen disordes Technical - site of anasatmosis, quality of anastamosis, blood supply to the two ends, infection

Question 177

**i) Mx of severe Crohn's Flare** **ii) Cx fo crohn's disease**

Answer 177

i) Truelovv and Witt's Criteria Admit. IV Steroids, Fluids, antibiotics ( metro/ cipro ), Infliximab if not improving **ii)** Cx: Abscess, fistula, SBO, toxic megacolon, malignancy, PSC, Surgery related - Gallstones, Short bowel syndrome, malabsorption, further fistulae Extra intestinal manifestations- eye disease, joint disease

Question 178

**Differences between Crohn's and UC**

Answer 178

Question 179

**Arrhythmias** **i) Causes of AF** **ii) When to anticoagulate in AF** **iii) Tachycardias** **iv) Bradycardias**

Answer 179

i) **P -** neumonia, COPD, PE **I**- diopathic, ischaemic heart disease **R**- heumatoid arthritis, respiratory disease **A**-trial enlargement **T**-hyroid disease, caffeine, other stimulants **E-** ethanol **S-** epsis/ sleep apnoea Volume depletion **ii) CHADS VASC - CCF, Hypertension, AGE \>70, Diabetes, Stroke** **iii) AFlut, VT, SVTs** **iv) Heart block, Sinus arrhythmia, Sinus Bradycardia, Drugs, Hyperkalaemia**

Question 180

**i) You see Acute STEMI on ECG** **ii) Complications of acute MI** **iii) Investigations**

Answer 180

i) Assess the patient. **MONA BASH** Morphine, Oxygen (if hypoxic), Nitrates, Aspirin Beta blocker (within 12 hours, ACE - i (within 24 hours), Statin, Heparin (For NSTEMI) **Discuss with interventional cardiologist - ?reperfusion** **?thrombolysis** **ii) Complications -** **Acute -** Rhythm disorders (Heart block, AF), Conduction disorders (BBB) Heart Failure Papillary muscle rupture/infarction Rupture of IV Septum Mural THrombus THromboembolism Pericarditis **Chronic -** Dressler's Syndrome (pericarditis), Rhythm disorder, rate disorder, heart failure **iii)** **immediately -** Serial troponin (I or T) (0 hour -12 hour)

Question 181

**Causes of post operative confusion**

Answer 181

**Infective -** Wound, chest, urine, abdominal **Metabolic -** Oxygen, Hb, Sodium, Calcium, sugar, hepatic, renal **Drug causes -** Benzos, alcohol withdrawal, anticholinergics, anticonvulsants, steroids, opioids **Vascular causes -** Stroke, intracerebral bleed

Question 182

**Six life threatening injuries that might be found during primary survery**

Answer 182

**ATOMFC** Airway Obstruction, Tension Pneumo Open pneumothorax Massive haemothorax Flail Chest Cardiac Tamponade (low BP, engorged neck veins, muffled heart sounds)

Question 183

**Immediate CT Head for..**

Answer 183

**GCS \<12** **GCS \<15 after 1 hour** **Suspicions of base of skull/depressed skull** **2 or more vomiting** **Retrograde amnesia** **persistent headache** **Focal neurology** **Age Elderly and Young** **Bleeding diathesis**

Question 184

**i) Young intracapsular NOF management** **ii) Nerve at risk during posterior approach, lateral approach**

Answer 184

i) Goal is to restore function and preserve the hip unlike with an elderly NOF where you just want them on their feet again. Need to achieve satisfactory reduction and ideally cannulated screw/DHS Long term management will involve NWB for 6 weeks (unlike elderly who you weight bear immediately to avoid secondary complications such as VTE/infection) **ii)** Posterior - sciatic Lateral- Sup. Gluteal nerve

Question 185

**i) Outline Gustillo And Anderson Classification System** **ii) Open fracture management**

Answer 185

**i) I -** Less 1 cm **II -** \> 1 cm **III a -** \> 1cm + Periosteal Stripping **III b -** \>1cm + Periosteal Stripping + Inadequate soft tissue coverage **III c** - \>1cm + periosteal Stripping + inadequate soft tissue coverage + Vascular injury **ii)** NV Status/ wary of compartment syndrome IV antibiotics Reduction and splinting Saline gauze Debridement +/- Soft tissue coverage Soft tissue coverage/ amputation within 72 hours

Question 186

**i) Pelvic fracture mx** **ii) X ray views for acetabular fractures**

Answer 186

**i)** In line with BOAST guidelines ATLS approach Pelvic Binder - Across GTs. If **unstable** - Fast Scan, Angiography, Pre-peritoneal packing, laparotamy If stable - CT Scan **Urological** injury (Difficult catheterisation, blood at the meatus) - CT Urethrography/cystography. Urology input **Open** injury - ?Colostomy ?bladder drainage **ii) Judet views- 45 degree obturator and iliac oblique views**

Question 187

**Important progonstic indicators in trauma patietns**

Answer 187

**Lethal Triad -** Acidosis, Hypothermia, Coagulopathy

Question 188

**Causes of confusion**

Answer 188

**Differentiate between longstanding and acute** **Generally Acute:** Infectious - UTI, Chest, Skin, Abdominal Metabolic - Sodium, Glucose, Ammonia Failures - Hepatic, Renal Endocrine - Thyroid Vitamin - B12, Folate, Thiamine Hypoxia, Anaemia Neurological - Trauma, Bleeding, Stroke Drugs - (Any) but Opiates, Benzos, Steroids

Question 189

**i) 3 Methods of CO2 Carriage in the blood?** **ii) Where does CO2 Buffering occur?**

Answer 189

**i)** Carboxyhaemoglobin, CO2 Dissolved in plasma, Buffered with water as Carbonic Acid **ii) CO2** Bufferring occurs in the red blood cells

Question 190

**Where do opiate receptors act?**

Answer 190

**Mu receptors centrally** - Analgaesc, Respiratory Depression, constipation **Kappa -** Centrally/ Spinal. Also Analgaesia, respiratory depression **Delta Receptors -** Analgaesia