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PHASE 3B > Intro Lectures > Flashcards

Intro Lectures Flashcards

1
Q

What are the 6 domains of Health Quality? Consider what?

A

STEEEP: safe, timely, effective, efficient, equitable and patient-centred
LEAN models

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2
Q

What is geroscience? What is senescence? What is autophagy?

A

A research paradigm based in addressing the biology of ageing and biology of age-related diseases together
The condition or process of deterioration with age
Your body’s process of reusing old and damaged cell parts

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3
Q

What makes a safe prescription?

A

Date, identification of the patient, name of the drug, formulation, dose, frequency of administration, route of administration, amount to be supplied, prescribers signature, must be legible

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4
Q

What are never events?

A

Serious and avoidable medical errors for which there should be preventative measures in place to stop their occurrence

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5
Q

Legal responsibility for prescribing lies with who?

A

The doctor who signs the prescription

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6
Q

How should prescriptions be written? Prescription for controlled drugs have additional what? Wherever appropriate the prescriber should state what? Consideration also to what?

A

Written legibly in ink or otherwise so as to be indelible, should be dated, should state the name and address of the patient, the address of the prescriber, an indication of the type of of prescriber, signed in ink by the prescriber, age and DOB of the patient, age for <12 y/o
Additional legal requirements
Current weight of the child to enable the dose to be checked, dose per unit mass e.g. mg/ kg or dose per m2 body-SA

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7
Q

What should be noted on a prescription?

A

Strength/ quantity to be contained in capsules, lozenges, tablets etc- liquid preps in particular
Avoid unnecessary decimal points- <1g in mg, <1mg in micrograms
Micrograms/ nanograms/ units should not be abbreviated
The term millilitre is used
Dose and dose frequency should be used- minimum dose interval for preparations to be taken ‘as required’
doses other than multiples of 5 mL are prescribed for oral liquid preparations the dose-volume will be provided by means of an oral syringe, (except for preparations intended to be measured with a pipette). Suitable quantities:
Elixirs, Linctuses, and Paediatric Mixtures (5-mL dose), 50, 100, or 150 mL
Adult Mixtures (10 mL dose), 200 or 300 mL
Ear Drops, Eye drops, and Nasal Drops, 10 mL (or the manufacturer’s pack)
Eye Lotions, Gargles, and Mouthwashes, 200 mL
The names of drugs and preparations should be written clearly and not abbreviated
The quantity to be supplied may be stated by indicating the number of days of treatment required in the box provided on NHS forms
it is recognised that some Latin abbreviations are used.

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8
Q

Prescriptions for Schedule 2 and 3 controlled medicines must include specific details about the medicine such as what?

A

It’s name and what form it’s in, strength and dose, total quantity or number of doses, shown in both words and figures
https://www.gov.uk/government/publications/controlled-drugs-list–2

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9
Q

How to perform a medication review?

A

Assess each medicine individually, identify the indication for the medication, if the medicine requires any monitoring ensure this is up to date
Assess for any CIs and interactions for each medicine
Review the suitability of the medication in the context of the patient’s current medical presentation- can be considered by weighing up the risks and benefits of each medication

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10
Q

What is the STOPP START Toolkit? What risk score predicts bleeding risk in patients on anticoagulation for AF?

A

Screening Tool of Older People’s potentially inappropriate prescriptions
Screening tool to alert doctors to right treatments
ORBIT bleeding risk score- similar to HASBLED

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11
Q

2 points for what on ORBIT bleeding risk score?

A

Reduced Hb<13 mg/dL in men and <12 mg/dL in women, haematocrit<40% in men and <36% in women or hx of anaemia
Bleeding history

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12
Q

1 point for what in ORBIT bleeding risk score? Low, medium and high risk groups?

A

Older 75 y/o, insufficient kidney function eGFR<60mg/dL/1.73m2
Tx with an antiplatelet agent
0-2/ 3/ 4-7

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13
Q

Go-to model for clinical reasoning? Context of a consultation that has an impact on our clinical reasoning?

A

Dual process model
Location of the consultation, background noise, clinical presentation, affect of both parties, additional people in the consultation, skill of the clinician, knowledge of the patient, expectations of both parties

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14
Q

What is inductive reasoning? What is deductive reasoning?

A

The premise provides some evidence for the validity of the conclusion but not all- we induce the conclusion
Based on the assumption of two factually correct statements allowing a valid conclusion- more analytical

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15
Q

What is abductive reasoning?

A

The realistic norm of most clinical encounters- plausability is determined based on the evidence presented with the most plausible explanation sought(continuum between inductive and deductive reasoning)- fall onto this based upon the context in which we are functioning

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16
Q

What is probabalistic reasoning? What is categorical reasoning?

A

The probability of some conditions is much higher than others
If something fits a clear category then a specific approach is applicable- fits well with EBM

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17
Q

What is bounded rationality in relation to clinical reasoning? What are heuristics? What is cognitive biases?

A

The process by which we are happy that we have a good enough answer- linked to heuristics and biases
Rules of thumb or mental short cuts- can be linked to pattern recognition/ non-analytical reasoning
A systematic pattern of deviation from norm or rationality in judgement

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18
Q

What is the framing effect? What is anchoring bias? What is confirmation bias? What is search satisficing?

A

Who/ how story previous info “triage cueing”
Early salient feature- we rely on the first piece of information
Searching for info supporting hypothesis- ignoring info refuting
Where a clinician call off a search once they’ve identified a cause for a patient’s complaint

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19
Q

What is availability bias? What is representativeness?

A

Easily recalled experience dominates evidences
When we’re trying to assess how likely a certain event is, we often make our decision by assessing how similar it is to an existing mental prototype

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20
Q

Causes of raised ALP?

A

HPB disease, bone disease: Paget’s disease, osteomalacia + rickets, renal osteodystrophy, bone mets, primary bone tumour e.g. sarcoma, recent fracture, growing child- especially at puberty, pregnancy, vitamin D deficiency, drugs: penicillin derivatives, erythromycin, aminoglycosides, carbamazepine, phenoarbital, phenytoin, cetirizine, captopril, dilitiazem, felodipine, penicilliamine, sulfa drugs, OCP, steroids, MOIs, chlorpromazine

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21
Q

What is osteolytic bone mets characterised by? Osteoblastic? Mixed?

A

Destruction of normal bone present in MM, RCC, melanoma, non-small cell lung cancer, non-Hodgkin’s lymphoma, thyroid cancer or Langerhans- cell histiocytosis
Deposition of new bone, present in prostate cancer, carcinoid, small cell lung cancer, Hodgkin lymphoma or medulloblastoma
Both lesions types/ individual metastasis has both osteolytic and osteoblastic components- in BC, gastrointestinal cancers and squamous

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22
Q

Complications of untreated coeliac disease?

A

Malabsorption and malnutrition, iron, B12 and folate deficiencies, osteoporosis, lactose intolerance, mild increase in lymphoma + small bowel cancer risk, neurological disorders- ataxia, brain fog, migraines, peripheral neuropathy

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23
Q

Function of the spleen? Causes of splenomegaly?

A

Filters out old and damaged RBC, produces lymphocytes, stores RBC and platelets
Viral infections- EBV, bacterial infections- syphilis, endocarditis, parasitic- malaria, liver disease, haemolytic anaemia, metabolic- Gauchers disease(build up of fatty substances,) Niemann- Pick disease(inability to metabolise fat in cells)

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24
Q

When is prognosis worse in infective endocarditis? Increased mortality? Most common cause of death?

A

When the organism isn’t identifiable/ there’s a resistant organism
Fungal infections and prosthetic valve endocarditis
Intractable heart failure

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25
Q

Causes of AF? What can amiodarone cause? Suspect what if new/ progressive SOB?

A

Stretch: HTN, PE, cardiomegaly
Rub: pericarditis, tamponade, tumour
Toxins: alcohol, drugs, infection
Thyrotoxicity and hepatotoxicity
Pneumonitis

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26
Q

What does the liver do?

A

Protein, clotting factors, bile and glucagon
Detoxification: alcohol, drugs, ammonia, bilirubin
Storage: energy, vitamins and minerals
Part of the immune system

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27
Q

Components of acute liver failure?

A

A complex multisystem illness occurs after an insult to the liver: jaundice, coagulopathy INR>1.5, hepatic encephalopathy, absence of chronic liver, within 12 weeks

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28
Q

When does hyperacute acute liver failure occur? Acute? Sub acute? Causes?

A

Within 7 days (best prognosis)- paracetamol, drugs, viral hepatitis
8-28 days- viral hepatitis, ischaemic hepatitis
29 days- 12 weeks- seronegative and autoimmune hepatitis

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29
Q

Most common cause of ALF in the UK and in developing countries? Types of viral hepatitis? Rarely what viruses?

A

Paracetamol, viral hepatitis, mushrooms- amanita phalloides
Paracetamol, viral hepatitis, mushrooms- amanita phalloides
A, E and B
Herpes simplex virus, CMV, EBV and parvoviruses

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30
Q

Rare causes of ALF?

A

Ischaemic hepatitis, AI hepatitis, acute fatty liver of pregnancy, Wilson’s disease, Budd Chiari syndrome, mushrooms- amanita phalloides, post hepatectomy

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31
Q

Factors leading to poor prognosis without liver transplant for ALF?

A

Female 20-40 y/o
Recent jaundice and coagulopathy with previously normal LFT, liver biopsy, trial of steroids, liver transplant

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32
Q

Ix for hepatitis A? Hep B+D? Hep E? Paracetamol? Idiosyncratic drug reactions? Autoimmune? Pregnancy fatty liver? HELLP syndrome? Toxaemia? Wilson’s disease? Budd-Chiari syndrome? Malignancy? Ischaemic hepatitis?

A

IgM anti-HAV
HBsAg- may be negative, IgM anti-core, HBV DNA
Anti-HEV
Drug concs in blood
Eosinophil count
Autoantibodies, IgGs
US, uric acid, histology
Platelet count
Serum transaminases
Urinary copper, ceruloplasmin, slit-lamp examination
US or venography
Imaging and histology
Transaminases

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33
Q

Factors increasing paracetamol hepatotoxicity?

A

Staggered overdose, excessive alcohol consumption, malnutrition, HIV, cancer, CLD, liver enzyme inducers drug- antiepileptics, rifampicin, spironolactone

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34
Q

POD treatment?

A

IV NAC, IV crystalloids, IV broad spec ABx and antifungal if patient has encephalopathy, call liver transplant centre

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35
Q

Complications of ALF?

A

Grades 1-4 of encephalopathy, high levels of ammonia may–> cerebral oedema
CR= hypotension, acute respiratory distress syndrome and pneumonia
Renal failure- multifactorial
Sepsis- immune-suppressed, bacterial and fungal infection in 80% and 30%
Malnutrition- hypermetabolic state

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36
Q

Who is the critically ill patient? How to assess them?

A

Patient with impaired organ failure which can progress to organ failure and the need for critical care treatment
ABCDE- do not move on quickly from one thing to the next: look, listen, feel

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37
Q

Causes of gurgling, snoring, stridor, wheeze, silent airway noises?

A

Secretions, tongue obstructing pharynx, perilaryngeal obstruction, airways collapse, complete obstruction

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38
Q

Tx for airway obstruction? Caution with what? What if gurgling noises continue?

A

Headtilt and chintilt, jawthrust
Gurgling and secretions= gentle suction
C-spine injury
Guedel airway

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39
Q

Other options for airway management?

A

Recovery position, nasal airway, intubation, gentle suction

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40
Q

Things to consider for breathing in A-E approach for look? Listen? Feel?

A

RR, dyspnoea, SATs, cyanosis, symmetry of chest expansion
Air entry, added sounds
Trachea, percussion, symmetry of chest expansion, generally before listening

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41
Q

Breathing treatments? If respiration absent or inadequate?

A

High flow O2 with reservoir mask + 15 l/ min O2, bag and mask ventilation

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42
Q

Things to look for in circulation part of A-E approach? Listen? Feel?

A

Perfusion- CRT, SATs, peripheral cyanosis, bleeding, other organ perfusion, brain: reduced LOC, kidneys urine output, trauma/ surgical patient= blood or fluid loss
Heart sounds
Peripheral= radial and central= femoral and carotid, rate, volume, rhythm, BP

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43
Q

When is someone hypotensive?

A

If SBP<90mmHg systolic, >40mmHg lower than normal, MAP<65mmHg(DBP+ pulse pressure/3)

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44
Q

How to tx circulatory problems? Circulation tx aims? After fluid challenge check for what volume overload signs? Max volume to give? If still hypotensive?

A

Fluid challenges- large bore IV access, take bloods- FBC, U&E, coag, cultures, glucose
Fluid replacement, haemorrhage control, restoration of tissue perfusion
Increases resp distress, bulging neck veins, crackles in the chest
2000mls- may need critical care for invasive monitoring and vasoactive drugs

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45
Q

3 components to measure for disability in A-E approach? Exposure? Scoring system designed to identify early patients at risk of deterioration? If NEW 2>7, obs how often?

A

Level of consciousness, pupils, glucose
Focussed clinical examination
NEWS 2- RR, O2, pulse and BP, level of consciousness, temperature
Every 30 minutes- escalate to nurse in charge, immediate medical/ HOOH review within 15 minutes, escalation to senior clinician if no attendance within 30 minutes, hourly fluid monitoring, complete sepsis screening tool, critical care outreach team
No improvement after 2 hours= contact patient’s consultant to review management plan

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46
Q

What is sepsis defined as? Patients with suspected infection who are likely to have a prolonged ICU stay or to die in the hospital can be promptly identified at the bedside with what? What is septic shock?

A

Life-threatening organ dysfunction caused by a dysregulated host response to infection- acute change in total SOFA score 2 points consequent to that infection
qSOFA i.e. alteration in mental status, systolic BP 100mmHg or RR 22/ min
Subset of sepsis in which underlying circulatory and cellular/ metabolic abnormalities are profound enough to increase mortality- persisting hypotension requiring vasopressors to maintain MAP 65mmHg and having serum lactate>2mmol/L despite adequate volume resus

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47
Q

Inflammatory cytokines involved in sepsis? Recommendations for sepsis?

A

TNF, IL-1, IL-6, IL-8
ABx within 1 hour- MRSA, infusion> bolus, don’t rely on qSOFA alone, use lactate to guide fluid resus, 30ml/kg crystalloid within 3 hours- not saline
HFNO>NIV
6ml/kg Vt
30cmH20 peak pressure
PEEP good
Prone >12hrs
Bolus NMBD > infusions

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48
Q

Cardiovascular aims in sepsis?

A

CO Monitoring ?POCUS ?LiDCO
Aim MAP >65mmHg
Noradrenaline +/- Vasopressin +/- Adrenaline
Dobutamine for CF
Add steroids if you’re not winning
Start vasopressors peripherally of delay to central access
Arterial line

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49
Q

Any patient with a SHEWS>3 should be screened for what? Anyone with red flags for sepsis should get what done?

A

Sepsis
BUFALO 6- blood cultures, urine output, IV fluid challenges, broad spec Abx, serum lactate, high flow oxygen

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50
Q

What is osmolality? Osmolarity? Tonicity?

A

Osmoles per kg of solvent- usually water
Osmoles per litre
Ability of a solution to cause water movement

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51
Q

Examples of crystalloid fluids? Colloids- artificial, organic?

A

Any salty water- 0.9% saline, Hartmann’s, or not: 5% dextrose, 10% dextrose
Gelofusine, Hetastarch
Blood, albumin solutions

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52
Q

Requirements of sodium and potassium in a 70kg adult? Approach to fluid prescribing?

A

70-140mmols, 70mmols
Calculate deficit, ongoing requirements, monitor results of therapy
New fluid charts

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53
Q

Causes of coma? (CNS, CVR, Resp, metabolic, pharmacological)?

A

Seizure, infection, SOL, CVA
Low CO state
Hypoxia, hypercapnia, CO poisoning
Uraemia, hepatic encephalopathy, hypoglycaemia, hypo/ hypernatraemia, hypothyroidism, hypothermia
Opiates, benzos, tricyclics & alcohol

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54
Q

How to assess level of consciousness? What does AVPU stand for?

A

AVPU, GCS, glucose
Alert, voice, pain, unresponsive

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55
Q

What does a secondary survey involve?

A

Head-to-toe evaluation of the trauma patient and involves taking a thorough history and performing a comprehensive examination

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56
Q

What RFs should warrant a CT head scan within 1 hour of them identified after sustaining a head injury?

A

GCS<13 on initial assessment
GCS<15 at 2 hours after injury on assessment in the ED
Suspected open or depressed skull fracture, any sign of basal skull fracture, post-traumatic seizure, focal neurological deficit, more than one episode of vomiting since the head injury

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57
Q

Risks of EDH?

A

Airway at risk
Secondary brain injury- hypo/ hyperperfusion, autoregulation loss/ CO2 reactivity loss, vasospasm, oedema/ inflammation, metabolic dysfunction, excitotoxicity, oxidative stress, necrosis/ apoptosis

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58
Q

Indications for intubation?

A

Failure to maintain and protect airway- GCS 8 and below, seizures, hypoxia, hypercarbia, agitation, pain (polytrauma pts,) anticipatory

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59
Q

What does the Monroe-Kellie doctrine describe? What 3 components exist in equilibrium within the cranium? If the volume of one increases, what must happen? An increase of any one of these components will also cause what? Normal ICP value? Above what value may intervention be required?

A

The relationship between the contents of the cranium and intracranial pressure
Blood volume, brain parenchyma volume, CSF fluid
The volume of another must be decrease
An increase in pressure
5-15mmHg, 20mmHg

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60
Q

What are the main compensatory mechanisms that can be used to maintain a normal ICP? What happens when the equilibrium is disrupted? What’s it called when the brain parenchyma shifts position?

A

Increased drainage of CSF fluid/ blood from the intracranial cavity
ICP will begin to rise
Herniation

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61
Q

Most serious types of herniation? As a pathology increases in size, the patient enters a decompensated state which is what? What is this termed as?

A

Uncal- displacement of the medial part of the temporal lobe (uncus) below the tentorium cerebelli
Tonsillar- when the cerebellar tonsils are forced downwards through the foramen magnum, causing compression on the brainstem
Whereby small increases in intracranial volume result in a large increase in intracranial pressure which can lead to herniation
Volume- pressure relationship

62
Q

Uncal herniation putting pressure on CN III leads to what? What is Cushing’s reflex?

A

Mydriasis
ICP obliterates CBF (blood volume that flows per unit mass per unit time in brain tissue,) increasing sympathetic tone HR and BP- both rise, baroreceptors detect high BP, parasympathetic stimulation, reflex bradycardia

63
Q

What is CPP and how is it measured? How to optimise cerebral perfusion in terms of BP and ICP?

A

CPP= MAP- ICP (net pressure gradient that drives oxygen delivery to cerebral tissue)
Get BP up, get ICP down

64
Q

Blood, brain and box methods of treating raised ICP/ Cushing’s reflex?

A

Blood: head up 30 degrees, hypercarbia and hypoxia increase CBV, avoid hypoxia, aim for normocarbia (4.5-5kPa)
Brain: mannitol or hypertonic saline, CMRO2(temp/ seizures/ shivering,) NMBD, glucose
Box: decompress- skull put back craniotomy, skull not put back= craniectomy

65
Q

Definition of shock? Causes of shock- fluid, pump and pipes?

A

Circulator failure, tissue hypo-perfusion, energy deficit, accumulation of metabolites
Fluid- hypovolaemic= dehydration(acute/ chronic,) haemorrhagic= bleeding(trauma, GI bleed, AAA)
Obstructive= tension PTX, PE, tamponade/ cardiogenic= ischaemic, arrhythmias, other
Distributive= neurogenic/ endocrine, septic, anaphylactic

66
Q

What can hypothyroidism be considered as? Does what in critically ill patients? Thyrotoxicosis may induce what?

A

Reduces CO, can lead to hypotension and respiratory insufficiency
Reversible cardiomyopathy

67
Q

How can acute adrenal insufficiency result in distributive shock?

A

From discontinuing corticosteroid tx without tapering the dosage, surgery and intercurrent disease in patients on CS therapy without adjusting the dosage to accomodate for increased requirements may result in this condition

68
Q

Where can relative adrenal insufficiency in critically ill patients lead to distributive shock?

A

Where present hormone levels are insufficient to meet the higher demands

69
Q

General therapies for hypovolaemic, septic/ anaphylactic and cardiogenic shock?

A

Hypovolaemic= +++fluid, + vasopressor, - inotrope
Septic/ anaphylactic= ++ fluid, ++ vasopressor, +/- inotrope
+/- fluid, - vasopressor, ++ inotrope

70
Q

What do inotropes do? What do vasopressors do? Review what algorithm?

A

Drugs that tell your heart muscles to beat or contract with more power or less power
Causes the constriction of blood vessels
Adult tachycardia algorithm (with pulse)

71
Q

E.g. of a selective NSAID? Both what and what action? Things to check before paracetamol prescription? NSAIDs?

A

Celecoxib
Central and peripheral action

Liver impairment- reduce dose/ consider avoiding if severe, severe cachexia- <50kg= max 500mg QDS

Renal and platelet count, CI= GI bleeding or ulcer hx, asthma
Concurrent medications: warfarin, digoxin, steroids

72
Q

E.g. of weak opioids? All have a what on analgesia?

A

Codeine, dihydrocodeine, tramadol, nefopam sometimes included
A ceiling effect

73
Q

Generic strong opioids? Specialist palliative care only?

A

Morphine, oxycodone, buprepnorphine, fentanyl, diamorphine
Hydromorphone, alfentanil, methadone

74
Q

What to consider before starting a strong opioid?

A

Co-morbidities, patient concerns, renal function, age and frailty, are they driving, will they take them as prescribed, have you prescribed medications for any side effects?

75
Q

Common opioid SEs? Less frequent? Rare SEs? What improves after the first week or so? What remains and needs what?

A

Constipation, nausea, sedation, dry mouth
Psychomimetic effects, confusion, myoclonus
Allergy, respiratory depression, pruritus
Nausea and drowsiness- constipation, a stimulant laxative

76
Q

What is background and breakthrough pain? Tips when prescribing strong opioids?

A

Pain at rest, ongoing pain
Transient exacerbation- can be predictable such as movement or unpredictable
Always start low, titrate dose according to pain and PRN usage
PRN doses= generally 1/10th- 1/6th of the 24 hour dose

77
Q

Duration of action for modified release of morphine and oxycodone? Immediate release for breakthrough pain? E.g. of modified release morphine? Immediate release? For oxycodone?

A

12 hours, 4 hours
MST- tablet, zomorph capsule
Oromorph (liquid,) sevredol(tablet)
Oxycontin, oxynorm (liquid or capsule)

78
Q

How potent is oxycodone compared to morphine? Why is morphine most commonly used? Active metabolites?

A

Twice as potent- 30mg MST BD = 15mg oxycontin BD Cheaper and more readily available, although oxycodone less side effects(switch when unable to tolerate morphine)
M3G, M6G

79
Q

Codeine and tramadol are how potent compared to oral morphine?

A

1/10th
Codeine phosphate= 60mg QDS, 240mg/ 24 hours, divide by 10, equal to 24mg morphine
Start 10mg BD morphine modified release morphine

Tramadol= 100mg QDS, 400mg/ 24 hours, divide by 10, equal to 40mg morphine, start 20mg BD morphine modified release

80
Q

PRN doses of morphine are usually what fraction of the 24 hour dose? Prescribe what along with oromorph?

A

1/10th- 1/6th of the 24 hour dose
Stimulant laxative, PRN antiemetic

81
Q

When are fentanyl and buprenorphine patches indicated? Takes how long to reach analgesic concentrations when first increased? Don’t use in what? Apply how and avoid what?

A

For intolerable side effects, oral route difficulties: compliance or dysphagia, renal impairment
1-3 days- acute/ unstable pain
To hairless, dry and non-inflamed skin
Heat pads- increases rate of absorption

82
Q

Options for palliative care analgesia in renal impairment?

A

Stay on current opioid- reduce dose and frequency
Switch opioid to a more renal-friendly option- oxycodone, fentanyl, buprenorphine, methadone, alfentanil

83
Q

Antidepressants and antiepileptics useful in neuropathic pain? Antispasmodics for muscle spasms? Steroids for compression symptoms? Benzos for spasms and neuropathic pain? Local anaesthetics for local areas of pain? Bisphosphonates for bone pain?

A

Amitriptyline and duloxetine, pregabalin and gabapentin
Baclofen, tizinidine
Dexamethasone
Clonazepam, diazepam
Topical lidocaine plasters
Zolendronic acid

84
Q

Injectable opioids are how strong as oral ones? If stable on a fentanyl patch, but needing to start a syringe driver, don’t do what? Don’t write what in one prescription for opioids? Always write what things and always check what before prescribing?

A

Twice as strong
Remove the patch
PO/SC in one prescription, a minimum interval and an appropriate max in 24 hours
Allergy status

85
Q

Don’t prescribe in what? Always prescribe in what and always prescribe what? Use what if advised by palliative care or a more senior doctor? When re-writing a continuing CSCI chart, the start date is what?

A

Millilitres, milligrams, the formulation i.e. MR or IR
Syringe pump form- add onto your EPR
The date that particular CSCI dosage commenced- not the current date, signature/ name are yours, not original prescriber’s

86
Q

Mnemonic for thoracic/ chest injury?

A

ATOM FC: airway obstruction/ disruption, tension pneumothorax, open pneumothoax, massive haemothorax, flail chest (2 or more ribs become detached from the rest of the ribcage, cardiac tamponade

87
Q

What points towards a tension pneumothorax? What is a massive haemothorax classed as?

A

Consistent history, air hunger/ agitation, hypoxia, hypotension
>1500ml blood, reduced air sounds, hyporesonant, obtain IV access prior to decompression, >1500ml blood or >200ml/hr= consideration urgent thoracotomy

88
Q

What is an open pneumothorax?

A

Wound–> chest wall communicating with pleural cavity, more than 2/3 aperture of trachea, air moves down pressure gradient into pleural space, wound seals on expiration

89
Q

What is a flail chest? Signs of cardiac tamponade? How to treat?

A

Fracture of 2 or more ribs in 2 or more places, moves paradoxically during respiration, ventilatory failure
Beck’s triad- hypotension, diminished heart sounds, distended neck veins
Thoracotomy

90
Q

Secondary survey injuries can that the ability to deteriorate and cause morbidity? Features of a bleeding patient?

A

Simple pneumothorax, aortic injuries, diaphragmatic injuries, fractured ribs, lung contusion, cardiac contusion
Sweaty/ diaphoretic, anxious/ confused, pallor/ peripherally cool, tachycardia, tachypnoea, >CRT, narrow pulse pressure, hypotension, bradycardia, arrest

91
Q

Where can patients bleed to death from? What can abdominal bleeding be from? Signs?

A

External haemorrhage, chest, abdomen, pelvis, long bones
Blunt force trauma/ penetrating trauma, signs can be subtle- not always peritonitic, liver/ spleen/ retroperitoneal injuries, perforation hollow viscus, CT in all but the most unstable patient

92
Q

Things regarding pelvic fractures?

A

Massive haemorrhage possible, closing potential space stops bleeding, use of binder mandatory in haemodynamically unstable blunt trauma patients

93
Q

What is a long bone? Clinically important?

A

Anything longer than it is wide- humerus, radius, femur, fibula, tibia, metacarpals
Femur, humerus and tibia

94
Q

What to avoid what with bleeding patients in major trauma? What is trauma-induced coagulopathy? Aims of resus in major trauma?

A

More shocked= less able you are to clot
High MAPs
Replace volume, address coagulopathy, prevent from becoming hypothermic(administer packed red cells)

95
Q

What does TXA prevent? Usually administered when? Indications for fluid administration in trauma?

A

Fibrinolysis- in pre-hospital setting
Systolic BP<90, HR>130mmHg, reduced conscious level, obvious massive ongoing blood loss

96
Q

Methods for stopping bleeding in major trauma?

A

Pelvic binder, splint long bone fractures, permissive hypotension, TXA 10min then 1g infusion, emergent damage control surgery, interventional radiology, limit crystalloid(not sepsis, crystalloid)

97
Q

Assessment of neurology in a primary survey?

A

AVPU, pupillary size and response, motor score of GCS most predictive outcome, sensory level if able

98
Q

Primary and secondary head injuries? Aim for?

A

Primary= the incident, secondary= hypoxic injury/ hypoperfusion, can do little about former and can cause later
CPP= MAP - ICP, trade off, systolic >100 ideal, aim for normal everything else

99
Q

Cushing’s triad- ICP rise? Head injury tx in major trauma?

A

HTN, bradycardia, irregular bradycardia
Prevent secondary brain injury, secure airway GCS<8 or need control ventilation, maintain normal - ICP/ glucose/ oxygen/ CO2

100
Q

E assessment in major trauma?

A

Look for obvious limb threatening injuries, ensure patient is being kept warm, consider few bedside tests, don’t forget pain

101
Q

Respiratory differences in elderly patients? CV differences?

A

Respiratory muscle weakness, kyphosis thoracic spine, chest wall rigidity, impaired central response to hypoxia, reduced alveolar GE SA
Total body water lower, total peripheral resistance higher–> CO affected, myocardium replaced by fat and collagen, AN + baroreceptor dysfunction, atrial pacemaker atrophy

102
Q

What is SV a product by?

A

Preload- total body water, afterload- total peripheral resistance and contractility- cardiac power index

103
Q

Normal BP? Check what before immobilising C-spine in elderly? Rib fractures in elderly mortality?

A

Depends on the patient
If spine anatomically normal or not
>3 fractures, each additional= 10% mortality

104
Q

Abdominal injuries in elderly patients? Most common diagnosis after fall? % incorrectly diagnosed with UTI? Better diagnostic criteria in elderly?

A

Protective cage= weaker, abdominal examination= unreliable
UTIs
40%- tests inaccurate, sterile bacteriuria
New urinary sx/ fever with change in urinary character or haematuria or loin tenderness

105
Q

What is FAST? Other radiology methods?

A

Focussed Assessment Sonography in Trauma, CT= modality of choice in major trauma, MRI= not routinely used in acute setting, role later on

106
Q

What is FAST Scan used for? Issues?

A

USS LUQ and RUQ- LUQ= looking for blood between kidney and liver, RUQ= between spleen and kidney, suprapubically between bladder and bowel and subxiphisternally- free fluid in pericardium and abdomen
Not <250ml blood seen, doesn’t rule out if normal

107
Q

Plain film views? CXR pros?

A

AP chest, pelvis and C-spine series
CT recommended for C-spine imaging
Pneumothorax, aortic injury, flail chest, endotracheal tube in right place- CT chest likely needed too

108
Q

Straight white- dark interface is what in radiology? What is flail chest? Used for what and almost always associated with what?

A

Fluid level
2/ more contiguous ribs fractured in 2 or more places, marker for chest trauma severity
Pulmonary contusion/ laceration, pneumothoax, haemothorax

109
Q

Widened mediastinum often due to what? Suspicion based on what? How to Ix?

A

Aortic injury- if transection often dead
Mechanism of injury, CT angio
If AP at 5th rib- should be no more than 8cm, if PA, think about widened mediastinum if>6cm

110
Q

If pelvic fracture look for what? Uncontrolled bleeding into what? Other comps?

A

Other fracture- think POLO mint, carry significant morbidity
Pelvic rim and retroperitoneally
Bladder, urethral rupture, rarely= perforation

111
Q

AP compression–> pelvic fracture type? What does a vertical shear fracture result in? Ipsilateral fracture called? Contralateral?

A

Open book- pubic symphysis and SIJ, may be ass w/ sacroilial joint disruption–> can bleed heavily
Vertical unilateral fractures of the pubic rami, and vertical fracture of the sacral foramina on the same side
Malgaigne, bucket handle

112
Q

Lateral compression causes what pelvic fracture?

A

Sacral fracture with diastasis of the pubic symphysis
Oblique fractures of the pubic rami bilaterally, impacted fractures of the sacral foramina ipsilateral to the force, with infolding of the hemipelvis

113
Q

3 standard views for C-spine X-rays? Look for what?

A

Lateral, anterior-posterior(AP,) and odontoid peg- open mouth for C2, low threshold for CT
Any obvious fractures and alignment

114
Q

C1 Jefferson fracture usually from what mechanism?

A

Axial load- top of head, space between odontoid peg of C2 and lateral masses of C1 is widened on both sides, lateral masses of C1= both laterally displaced and no longer align with lateral masses of C2

115
Q

Hangman cervical fracture?

A

High force hyperextension injury- may involve odontoid peg, vertebral body or posterior elements, pedicles of C2 and often results in anterior displacement of the body and peg of C2

116
Q

Flexion teardrop cervical fracture?

A

Sudden pull of anterior longitudinal ligament on anterior, inferior aspect of vertebral body following extreme hyperextension of the neck

117
Q

Burst cervical fracture?

A

Axial loading most often secondary to RTAs and falls
Usually–> comminuted vertical fracture through the vertebral body, anterior wedging
Convexity to posterior vertebral surface
Fragments may be retropulsed into the spinal canal injuring the cord

118
Q

Interpreting a CT head?

A

Brain tissue= grey, CSF= dark grey, gas= black, bone and acute blood= bright white

119
Q

Hyperacute blood(1st hour or so) looks like what? Acute? Chronic?

A

Relatively isodense to the adjacent cortex with a swirled appearance due to mixture of clot, serum and ongoing unclotted blood
High attenuation to brain parenchyma= 6-24 hours
Clot starts to degrade and density drops= 3-21 days

120
Q

Sub-arachnoid blood includes what? Can cause what?

A

Ventricles, sulci and basal cisterns
Hydrocephalus, midline shift and raised ICP pressure, not always traumatic

121
Q

Subdural haematoma caused by what? 95% what? Crosses what?

A

Traumatic tear or bridging veins
Supratentorial
Crescentric shape along brain surface
Suture lines

122
Q

EDH ass w/ what?

A

Acute head injury and skull fracture
Normally torn meningeal artery
Biconvex in shape, can cause mass effect and herniation- EMERGENCY

123
Q

Want to assess what with body CT? Common visceral injuries?

A

Viscera, vessels, spaces and bones, chest, abdo, pelvis= CAP
Spleen, liver, kidney

124
Q

Polytrauma indications for CT? Imaging technique most often used?

A

HD instability, mechanism of injury- more than one system/ body part, RTC with fatalities, findings on plain film/ FAST scan= inconclusive/ suggestive of injury, obvious severe injury
Head-to-thigh contrast enhanced multi-detector computed tomography (MDCT)

125
Q

Role of intervational radiologists?

A

Image-guided endovascular techniques to stop haemorrhage- minimally invasive, can keep spleen, stabilise before theatre/ avoid altogether
Coiling/ embolisation, stenting

126
Q

Most common mechanism causing hypoxia? 3 ways disease affect alveoli?

A

V/Q mismatch
Fills with fluid, terminal bronchiole constricts, collapse
Collapse= pneumonia, post-op, lying down
Oedema- LVF
Asthma/ COPD

127
Q

Respiratory failure paO2 value? Normal paCO2 (4-6kPa) in asthma means what? T1RF vs T2RF?

A

<8kPa
Life threatening asthma
1= low pO2, low/ normal CO2, 2= high CO2

128
Q

Expiratory pressure does what to oedematous alveoli? EPAP/ CPAP improves what? IPAP? what is BiPAP?

A

Reduces the work of the left ventricle- pushes fluid back into the pulmonary vasculature
V/Q mismatch, high CO2
BiPAP

129
Q

What is NIV? CPAP is for what? BiPAP? Used for what? Not?

A

Covers CPAP/ EPAP and BiPAP(EPAP + IPAP)
T1RF, T2RF
Post-op, COPD, pneumonia, oedema, COVID
Asthma, PTX, airway loss

130
Q

EPAP improves what?

A

Oxygenation

131
Q

What happens to K+ and H+ in the kidneys during shock? Common drug causing acute interstitial nephritis? What causes tubular toxicity?

A

Less efficiently into Bowman’s capsule–> acidosis and hyperkalaemia
NSAIDs
Contrast, gentamicin(stop toxic drugs)

132
Q

What happens in the kidney (Na+,K+ and H+)? Tubular toxicity?

A

Retains Na+, rid of H+ and K+
Retain K+, H+, rid of Na+–> hyperkalaemia, acidosis and hyponatraemia

133
Q

Kidney obstruction causes causing AKI? 2 modes of renal replacement? What are indications for renal replacement therapy (RRT)?

A

Stones and cancer
Haemofiltration and haemodialysis
Symptomatic uraemia + confused, poisoning- lithium, ethylene glycol, hyperkalaemia, acidosis

134
Q

pO2 in ABG tells you what? pCO2(regardless of pH)? High means that? Low? Base excess <-2 in ABG means what? >+2?

A

Resp failure or not
Type 1 or 2
Acidosis, alkalosis
Metabolic acidosis
Metabolic alkalosis

135
Q

Normal bicarb? What does pH tell you? Most of the time dealing with what?

A

Around 22-26
Is the acidosis/ alkalosis compensated or decompensated
Acidoses

136
Q

What does T2RF cause? What is mixed?

A

Respiratory acidosis
Resp + metabolic acidosis

137
Q

What colour is air on CXRs? White bits are what? Blacker/ darker grey bits are what?

A

Black
Opaque/ opacities
Lucent/ lucencies

138
Q

Describing stuff CXR?

A

Is opacity well-defined/ ill-defined, ill-defined= think consolidation, well-defined= is it a mass, or if it’s at the lung bases- an EFFUSION

139
Q

What does atelectasis mean?

A

Alveoli have collapsed and stuck together

140
Q

Pleural effusion on CXR? Dense white triangle, some mediastinal shift? ABCDE meaning?

A

Meniscus, solid white
Lobar collapse- possibly cancer
Airway, breathing, borders, cardiac- <50%, diaphragm, everything else

141
Q

Things to consider with lines/ tubes on CXR? Link to help with this?

A

Right place? Safe to use? Complications of insertion or removal?
http: tinyurl.com/ycqradhn, also Radiology Masterclass CXR galleries

142
Q

What is rapid tranquilisation? First think what?

A

Use of medication by parenteral route if de-escalation & oral medication not possible/ urgent sedation necessary for safety because of disturbed/ dangerous behaviour
DDx- OD, HI, brain disorder, substances, hypoxia
De-escalation techniques- voice, posture, kindness, low stimulus environment, empathy, physical health checks if possible including ECG, CI- resp/ CVDs, support of team and trained staff for restraint, discussion with senior staff if possible

143
Q

Medication for tranquilisation? Post-tranquilisation?

A

Revisit oral options- lorazepam 1-2mg/ haloperidol 5-10mg + promethazine 25-50mg(helps with EP SEs of haloperidol,) IM= lorazepam 1-2mg/ haloperidol 2.5-5mg + promethazine 25-50mg
Documentation, physical health checks- SE= dystonia, resp depression, urinary retention, debrief with team

144
Q

When neuroleptic malignant syndrome occur? Sx? Tx?

A

1-2/52 of start of changed dose
All neuroleptics and other dopaminergic meds
Fever, altered mental state, muscular hypoactivity & severe(lead pipe rigidity,) increased CK, WCC & LFTs, low Fe, AN dysfunction, ileus

145
Q

When does serotonergic syndrome occur?

A

Within 24 hours- all SSRIs, other 5HT-1 & 2 meds, tramadol
Fever, altered mental state, NM hyperactivity, hyperreflexia, clonus
Often none, can be high CK & WCC, AN hyperactivity, shivering hyperactive bowel, dilated pupils
Stop SSRI & supportive care

146
Q

Common SEs of lithium? Rare SEs? Lithium toxicity sx? Ix? Tx? Prevention?

A

Nausea, diarrhoea, dry mouth, metallic taste, thirsty, mild tremor
Renal dysfunction, hypo/ hyperthyroidism, foetal abnormality if used in 1st trimester pregnancy
Narrow TI, levels 0.4-1.0mEq/L: polyuria, incontinence, nausea, drowsy, confusion, blackouts, faints, blurred vision, shaking/ muscle twitches, spasms in face, tongue and neck
U&E, TFT, lithium levels
Supportive, haemodialysis
Regular bloods, avoid dehydration, don’t reduce Na suddenly, care with diuretics, SSRIs, epilepsy meds, ABx, NSAIDs

147
Q

Acute dystonic reaction related to what? Sx? Tx?

A

Antipsychotic use, arms held in dystonic posture, neck spasm to side, mouth open, dysarthria(tongue dystonia,) upward eye gaze(oculogyric crisis,) pain and distress
Procyclidine 5-10mg IM

148
Q

Other SEs of antipsychotics?

A

Akathisia(mins-days)= motor restlessness + agitation- switch to 2nd generation/ reduce dose
Drug induced Parkinsonism(days- months)= brady/ akinesia, rigidity- switch to 2nd gen or procyclidine
Tardive dyskinesia(years)- jaw, tongue, face, choreiform/ tics, no rx
Metabolic: weight gain, diabetes mellitus, hyperlipidaemia, HTN, arrhythmias, QT prolongation, stroke and venous thrombosis, liver impairment
GI: hypersalivation, constipation, hyperprolactinaemia, gynaecomastia
Sexual dysfunction/ glaucoma- muscarinic
Neutropenia- esp clozapine(ask about bowels)

149
Q

Definition of death? Reflexes checked for when verifying death? Wait how long after CPR to verify death? Next step?

A

Irreversible loss of capacity for consciousness, irreversible loss of capacity to breathe
Painful and pupillary stimulus
10 minutes
5 minute examination period- central pulse and listen to heart

150
Q

Once observed for 5 minutes for death, next step?

A

Neurological: painful stimulus in CN distribution/ jaw thrust, pupillary reflex, corneal reflex(not usually done)
Verify time of death- wait after CPR done(write up paperwork)

151
Q

Neurological criteria of verifying death?

A

Heart is still beating- done in ICU, brain injury, strokes, rule out high spinal injury, CN abnormalities, hypothermia, 2 doctors: 5 years GMC registration + 1 consultant
Test each CN, apnoea test
Second test by 2nd doctor- time of death= 1st set of deaths

PHASE 3B (11 decks)

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