Intro Lecture weeks

Question 1

What is chemsex?

Answer 1

Sex between men under the influence of drugs taken immediately before and/ or during a sex session to sustain, enhance, disinhibit or facilitate the experience and performance e.g. crystal methamphetamine, mephedrone and GHB/ GBL

Question 2

Incubation of monkeypox? Lasts how long? How does the monkeypox rash develop?

Answer 2

Macular, papular, vesicular, pustular, crusted, desquamation
Firm or rubbery, well-circumscribed, deep-seated, and often develop umbilication, maybe painful then itchy
Single genital lesion, sores on mouth or anal mucosa

Question 3

Other symptoms of monkeypox?

Answer 3

Fever, backache, lymphadenopathy, myalgia
Resp= sore throat, nasal congestion, cough
Anal/ rectal pain, bleeding
Penile swelling
Erectile dysfunction
Rash can be on palms and soles

Question 4

Primary or secondary prevention (post-exposure) of monkeypox? Tx?

Answer 4

Smallpox vaccine
Tecovirimat

Question 5

When to do a CT/GC DNA NAAT? What about syphilis and HIV? Refer for what with ulcers/ discharge/ pain?

Answer 5

2 weeks, 4 weeks post LSI- men= urine, women= self-taken vulvovaginal swab for CT/GC
HIV= using 4th generation test but need final test at 12 weeks if high risk, Hep B(and C for some) at 12 weeks
Specialist assessment, HSV positivity doesn’t exclude co-infection, requires STS and repeat

Question 6

Ix for STIs in MSM and transgender?

Answer 6

CT/GC DNA NAAT and 2 weeks after LSI: urine, pharynx, rectum

Serology baseline plus: syphilis 4-6 weeks post LSI, HIV 4-6 weeks using 4th generation test but need final test at 12 weeks if high risk, Hepatitis B and C at 12 weeks, Hep C PCR if recent high risk exposure (includes some chemsex)

LGV (infection caused by chlamydia bacteria) testing if rectal positive CT

Question 7

What is PEP(SE)? What things to consider?

Answer 7

A type of medication that can be taken up to 72 hours after exposure to HIV to stop you becoming infected-

Type of sexual activity, HIV status of contact, contact characteristics- sexual orientation, IVDU, country of origin, viral load of contact, country where SI occurred, sexual assault/ trauma, discuss with local STI/ ID specialist

Question 8

Drugs used for PEP(SE)? Repeat HIV testing how many months after treatment end? What does PrEP involve?Need what, but don’t do what? Consider what?

Answer 8

Truvada (tenofovir/ emtracitabine) + raltegravir- triple drug therapy for 28 days

3 months + can do at 4-6 weeks

Truvada 2-24 hours before sex

Baseline HIV test- wait for results

Wishes of the patient

Question 9

Symptoms of HIV 2-6 weeks after exposure?

Answer 9

Glandular fever/ flu symptoms- fever, sore throat, rash, lymphadenopathy, muscle + joint pain, mouth ulcers/ candida, pneumonia, viral meningitis/ other neurological symptoms, any age

Question 10

Presentations of primary syphilis? Secondary syphilis?

Answer 10

Single painless genital ulcer 9-90 days, maybe multiple and painful esp if co-infected

Secondary= 6-12 weeks, generalised rash- PAINLESS, palms and soles of feet, wart-like lesions of genitals, snail-track ulcers of mouth, hair loss, flu, lymph nodes enlarged, bone/ joint pain, liver + kidney problems, viral meningitis, iritis
Rash goes away, but long-term effects

Question 11

Presentations of other STIs?

Answer 11

Herpes: blisters, ulcer(s,) usually painful, dysuria, systemic illness, tropical(chancroid/ donovanosis,) pustule, painful/ painless ulcer(s,) lymphadenopathy, LGV in MSM= proctocolitis

Question 12

4 pillars of inflammation? Causes of acute swollen joint?

Answer 12

Rubor(redness,) dolor(pain,) calor(heat,) tumor(swelling)
Infection, crystal arthritis, inflammation, trauma

Question 13

Presentation of infected joint?

Answer 13

Very painful/ hot, difficulty moving the joint/ weightbearing, fever(sometimes,) WCC(neutrophils,) high CRP/ ESR, may be systematically unwell, are there RFs(elderly, diabetes, source of bacteraemia/ direct entry–> open skin,) immunosuppression(remember steroids)

Question 14

What things make a crystal arthritis more likely?

Answer 14

Gout= very hot, swollen, painful- excruciating, pseudogout can be less severe, previous episodes/ known episodes, RFs= dehydration, diuretics, renal impairment

Question 15

Joints affected in gout vs pseudogout?

Answer 15

1st MTPJ, midfoot, ankles, knees, olecranon, bursitis, less commonly upper limb
Wrists, 2/3 MCPJs, knees other large joints, cervical spine

Question 16

Causes, microscopy, X-rays and tophi in gout vs pseudogout?

Answer 16

Uric acid vs calcium pyrophosphate
- birefringent rods vs + birefringent rhomboids, punched out erosions vs linear calcification “chondrocalcinosis”
Tophi vs vs no tophi

Question 17

What to do for an acute hot joint?

Answer 17

Blood tests: CRP, ESR, WCC, blood cultures, uric acid, renal function, clotting screen
X-rays- infections, take 2 weeks to show osteomyelitis, pseudogout- chondrocalcinosis, gout- old gouty erosions, trauma
Joint aspirate

Question 18

Tx of infection in acute swollen joint? Crystal arthritis? Inflammation? Trauma?

Answer 18

Blood culture/ synovial fluid- antibiotics guided b this/ microbiology discussion, analgesia, off-load the joint, ortho- wash out in theatre
Gout= continue pre-existing allopurinol/ febuxostat, add NSAIDs/ colchicine(low dose) or steroids, pseudogout= NSAIDs/ colchicine or steroids, both= contact rheum SpR on call for intra-articular steroid
Inflammation- NSAIDs/ simple analgesia/ IM steroids/ PO steroids, reactive= screen/ tx underlying trigger if still present
Ortho, bleeding disorders= refer haem

Question 19

Acronym for red flag sx of back pain?

Answer 19

TUNAFISH: trauma/ thoracic pain, unexplained weight loss, neurologic sx/ nocturnal pain, age>50, fever/ TB/ recent UTI, IVDU, steroids/ other immunosuppression (incl HIV,) hx of cancer
Also in diabetes and the very young

Question 20

Red flag back pain causes? Sx of inflammatory back pain?

Answer 20

Infection, malignancy incl multiple myeloma, fractures- trauma/ osteoporosis/ pathological, inflammation
Early morning stiffness, eases with movement, thoracic and anterior chest wall, buttock pain, typically age<45, duration> 3 months, wakes during second half of night, relief with NSAIDs

Question 21

What to do for back pain?

Answer 21

Bloods= CRP, ESR, WCC, blood cultures, urine dip, MSU
X-rays- if suspect infection/ trauma, inflammatory= no utility unless Sx>8-10 years, urgent further imaging: MRI in most cases, CT if suspected bony injury/ trauma, involve spinal surgeons/ neurosurgeons/ ID

Question 22

S+S of GCA?

Answer 22

Temporal headache/ tenderness, jaw/ tongue claudication, PMR symptoms(proximal limb girdle,) visual changes, amaurosis fugax, sudden loss of vision, diplopia, cranial nerve palsy (VIth and others)
Tortuous swollen temporal artery, skin changes, loss of TA pulse, vascular bruits- carotid, subclavian, check BP in both arms

Question 23

What to do for large vessel vasculitis- GCA?

Answer 23

Bloods- ESR+ CRP, FBC(high WCC & platelets)
Exclude other causes of raised ESR/ CRP- infection, malignancy, normal for the patient
Exclude other headache causes- cervicogenic, migraine, tension headache, cluster headache

Question 24

Who to refer to for visual symptoms in GCA? No visual symptoms? Out of hours/ unable to contact the above?

Answer 24

Ophthalmology SpR on call
Rheumatology SpR on call
Treat, pred 40-60mg PO once daily, ophthalmology may use IV methylprednisolone if severe visual symptoms, PPI, calcium/ vit D, consider bisphosphonate, DEXA, blood glucose monitoring

Question 25

Examples of ANCA small vessel vasculitis? Cryoglobulin associated? IgA vasculitis? Non-specific?

Answer 25

GPA granulomatous polyangiitis, MPA microscopic polyangiitis, eGPA eosinophilic polyangiitis
Hep C, haem malignancy
HSP, URTI often strep throat infection
Infection, drugs, malignancy

Question 26

What to do investigate small vessel vasculitis?

Answer 26

Bloods: FBC, U&E, LFT, ESR, CRP, Igs & SPE, ANCA, consider cryoglobulins
Urine dip- blood & protein?, microscopy: casts? red cells?, uPCR: protein leak
CXR
Infection screen incl. strep throat
Stop any potentially triggering drugs e.g. newly started antibiotics

Question 27

Complications of treatment for rheumatic disease?

Answer 27

Sepsis, steroids, drug side-effects
Sepsis: high index of suspicion, patients on immunosuppressive treatment may not mount fever or high WCC, stop DMARDs and biologic therapy, take appropriate cultures, contact rheum team

Question 28

What can steroids cause?

Answer 28

Hyperglycaemia, increased risk of sepsis, adrenal sepsis- remember steroid sick day rules, osteoporotic fractures

Question 29

When to suspect adrenal crisis in patients on steroids?

Answer 29

N&V, dizziness, general malaise, extreme fatigue, fever or shivering, confusion, low BP, +/- low Na
(Usually in context of intercurrent illness or sudden cessation/ drop in medication)

Question 30

Tx for adrenal crisis? If admitted to hospital unwell?

Answer 30

100mg hydrocortisone by IV or IM injection at the start of surgery followed by continuous IV infusion of 200mg over 24 hours/ 50mg IV or IM every 6 hours
Double dose when eating and drinking and reduce to usual dose over the next 1-2 weeks as you recover
100mg hydrocortisone by IV or IM injection followed by continuous IV infusion of 200mg hydrocortisone over 24 hours/ 50 mg of hydrocortisone IV or IM every 6 hours

Question 31

SEs of DMARDs and biologics?

Answer 31

Bone marrow suppression due to intercurrent renal impairment, methotrexate & trimethoprim, allopurinol and azathioprine
Hepatotoxicity, pneumonitis acute reaction to MTX, sepsis

Question 32

The big 5 CV risk factors?

Answer 32

Smoking, HTN, diabetes mellitus, hypercholesterolaemia, family hx
Also CKD, PAD, inflammatory conditions (RA etc,) ethnicity

Question 33

Ix for cardiology?

Answer 33

Vital signs, ECG, bloods- FBC, LFT, clotting screen, troponin +/- D dimer, cholesterol, glucose/ HBA1c, CXR, ABG if hypoxic/ PE suspected

Question 34

Criteria for PPCI in STEMI? Superior to what?

Answer 34

ST elevation>2mm in 2 contiguous chest leads/ >1mm in 2 contiguous limb leads, chest pain or other evidence of ischaemia
New/ presumed new LBBB in right clinical context
Thrombolysis

Question 35

Management of STEMI?

Answer 35

Morphine- only if needed and give with metoclopramide, oxygen to maintain SATs, nitrates, aspirin 300mg stat, meet criteria–> PPCI

Question 36

When to measure troponin? Score used to decide whether to discharge or admit someone with chest pain?

Answer 36

ASAP, then again in 3 hours- significant rise or fall suggests MI
HEART score

Question 37

Other ED management of non-STE ACS?

Answer 37

Cardiac monitoring, management of complications such as arrhythmias, acute heart failure, load with P2Y12 inhibitor- ticagrelor 180mg or prasugrel 60mg, clopidogrel use in ACS 2nd line, anticoagulation e.g. fondaparinux 2.5mg SC, do not give beta blocker, ACEi etc. at this stage without specialist supervision, IV GTN infusion if ongoing pain

Question 38

In-patient management of non-STE ACS?

Answer 38

Cardiac monitoring>24 hours, medical vs invasive management PCI vs CABG, commence on secondary prevention, length of stay about 72 hours, monitor for complications, physio, optimisation of RFs

Question 39

What to write on the TTO for an MI?

Answer 39

Big 5, aspirin 75mg OD, potent P2Y12 inhibitor- ticagrelor 90mg BD or prasugrel 5-10mg OD for >1 year
Cardioselective beta blocker e.g. bisoprolol 2.5mg OD (caution if asthmatic, bradycardic, conduction disease)
ACE-i e.g. ramipril 2.5mg OD, caution if hypotensive, severe CKD
High intensity statin e.g. atorvastatin 80mg OD
PRN GTN
Consider if poor LV function, MRA- eplerenone or spironolactone 12.5-25mg OD
Consider if pericarditic pain- colchicine 500mcg BD
Consider if clinical HF- Loop diuretic e.g. Furosemide 40mg OD, SGLT2 inhibitor e.g. Dapagliflozin or Empagliflozin
Consider if non-revascularised significant coronary artery disease- anti-anginals- beta blocker, nitrates, amlodipine etc.

Question 40

Follow-up to write on TTO for MI?

Answer 40

Clinical 1 month- consider device therapy if significant LVSD
TTE if not had an inpatient, cardiac rehab programme, smoking cessation, GP- uptitrate secondary prevention e.g. ramipril and bisoprolol towards 10mg OD
Don’t drive 1 week if PCI, 4 weeks if no PCI, gradual return to usual activity levels, typically 6 weeks off work, stop smoking

Question 41

Ix for stable angina?

Answer 41

FBC + U&E, CT coronary angiogram, MPS, invasive coronary angiogram, ETT, screen for other RFs- hypercholesterolaemia, HTN, DM, rule out valve disease on examination- no ECHO for no murmur/ evidence of HF

Question 42

Tx for stable angina?

Answer 42

Aspirin, statin, antianginal- Beta blocker, CCB, nitrates, nicorandil, ivabradine, ranolazine
Refer to intervention if failed on 2 antianginals

Question 43

PCI for what benefit? Some evidence of improved hard outcomes if for what? More and more what? Requires DAPT for how long?

Answer 43

Symptomatic benefit
Proximal disease
Variations
6 months

Question 44

What is CABG used for?

Answer 44

3 vessel disease, left main stem disease, concurrent valvular disease requiring intervention

Question 45

RV strain assessment in PE? How to anticoagulate if considering anticoagulation?

Answer 45

Troponin, CTPA, echocardiography, if so? thrombolyse, UFH if considering thrombolysis, provoked vs unprovoked, unprovoked- look for underlying cause

Question 46

Overall strategy with AF?

Answer 46

Rate vs rhythm control- may need neither, ALWAYS consider anticoagulation

Question 47

Tx if male scores higher or equal to 2 for CHADVASc? Score of 1? Above or equal to 3 for female? Score of 2? Prefer what to VKA?

Answer 47

OAC, consider OAC
OAC, consider OAC
NOAC

Question 48

Tx for acute AF if HD compromise? What else? If <48 hours- can try what? If >48 hours or unclear what? Can consider cardioversion when?

Answer 48

DC cardioversion
Anticoagulate
Cardioversion- DC vs chemical
Rate control- can consider cardioversion later after 4 weeks anticoagulation or after TOE
Beta blocker or CCB, digoxin if concern about HD status

Question 49

Tx of acute pulmonary oedema?

Answer 49

High flow oxygen, sit forward, decide if shocked or not- BP usually sky high, if cardiogenic- will need immediate cardiology/ critical care input
Vasodilation- opiates e.g. 5mg IV diamorphine stat, GTN either SL/ IV infusion
Diuresis e.g. furosemide 80mg IV stat- vasodilates before diuresis
Consider CPAP
Tx underlying cause- start ACS tx if indicated, R/O STEMI, discuss with cardiology, ASAP if not improving

Question 50

Key drugs in heart failure?

Answer 50

Aspirin and statin if ischaemic
ACE-i or ARB if not tolerated: hydralazine & nitrates if poor renal function, Beta blocker
MRA if significantly reduced LV ejection function- spiro or eplerenone
If refractory- can upgrade ACE to ARNI(sacubitril- valsartan,) can start SGLT2 inhibitor

Question 51

Permanent pacemaker typically set up what? Able to do what?

Answer 51

DDD(R)(dual chamber system)
Mode switch e.g. pAF, unipolar vs bipolar pacing

Question 52

Patients with LBBB/ RV pacing can get what? Not a significant issue if what is normal? But worsens symptoms/ prognosis if what is impaired? Can be reduced in RV paced pts by what?

Answer 52

Dysynchrony
Left ventricle, left ventricle
Septal pacing- does not eliminate

Question 53

Who is cardiac resynchronisation therapy used in? Leads in dual chamber PPM? Biventricular PPM also known as what?

Answer 53

Patients with LVSD + LBBB/ needing a PPM or very wide RBBB
RA + RV leads
CRT-P

Question 54

What groups of patents have significant risk of VT/ VF?

Answer 54

Severe LVSD, previous VT/ VF- not if ass with acute infarct, inherited cardiac conditions- HCM, Brugada

Question 55

An implantable cardioverter defibrillator (ICD) adds what to pacing function? If added to a single lead/ dual chamber PPM is what? What if it’s added to a CRT device?

Answer 55

ICD, CRT-D

Question 56

Purpose of death certification?

Answer 56

Confirm that the death has occurred, give an indication of the probable cause of death, support the bereaved by giving reasons for a person’s death, assist the appropriate investigation of sudden/ unexplained deaths and identify possible criminality prior to disposal of the deceased, provide accurate statistical information via the Office for National Statistics (ONS) in order to better inform public health policy

Question 57

How do you verify death?

Answer 57

Full and extensive attempts at reversal of any contributing cause to the CR arrest have been made where appropriate, one of the following is fulfilled: individual meets the criteria for not attempting CP resus, attempts at CPR have failed, tx aimed at sustaining life has been withdrawn because it has been decided to be of no further benefit to the patient and not in his/ her best interest to continue and/ or is in respected of the patient’s wishes in an advance decision

Question 58

The individual should be observed for a minimum of how long to establish irreversible CR arrest has occurred? In primary care, the absence of mechanical cardiac function is normally confirmed using a combination of what?

Answer 58

5 minutes
Absence of a central pulse on palpation, HSs on auscultation, in hospital can be supplemented by: asystole on continuous ECG display, absence of pulsatile flow using direct intra-arterial pressure monitoring, absence of contractile activity using echocardiography

Question 59

What else should be confirmed after 5 minutes? What is recored too?

Answer 59

Absence of the pupillary responses to light, of the corneal reflexes, and of any motor response to supra-orbital pressure should be confirmed
Time of death, document findings

Question 60

What is completed to verify a death? Who can complete this?

Answer 60

Medical Certificate of the Cause of Death (MCCD) and cremation form if applicable- any doctor when it is impractical for the attending doctor to do so
Must have attended the deceased within 28 days of death or seen after death by a doctor

Question 61

What is the death certification process?

Answer 61

Death is verified, doctor completes MCCD and cremation forms, family provide MCCD to registrar’s office and death certificate and certificate for burial or cremation obtained by family, family provide certificate for burial or cremation to funeral director so that body can be released by mortuary

Question 62

Doctors have a legal obligation to report certain categories of death under what act?

Answer 62

Coroners and Justice Act 2009: reason to suspect the death was unnatural, unexplained, violent or occurs in prison/ detention, occurring during/ following an operation or operations from previous admission which contributed to death, OGD, chest drain, catheter, PEG, external ventricular drain are not operations but reportable if complications arouse, ERCP, stents, PPM insertion, angioplasty require colonial referral
Neglect/ self-neglect

Question 63

What deaths are referred to a coroner?

Answer 63

Trauma, injury or violence
Conditions linked to occupation e.g. asbestosis
Medical act/ omission that contributed to death/ accelerated death e.g. neutropenic sepsis following recent chemo
Poisoning/ exposure to toxic substance- not smoking/ alcohol
Linked to use of medicinal product, controlled drug e.g. haemorrhagic stroke and was taking anticoagulation
Cause of death is unknown
No doctor attended to the patient 28 days before death/ saw the patient after death
The deceased cannot be identified
Condition may have occurred many years earlier however if contributory to death must be reported

Question 64

HMC Referrals of death are sent how? Who will send you an electronic referral to complete? They will send this and medical examiner notes to who? They will then do what?

Answer 64

Electronically
Medical Examiner Team
HMC
Notify the Medical Examiner team the outcome of the referral

Question 65

Outcomes of coronial referrals?

Answer 65

Form A and Death Report- no further investigation and MCCD can be issued, post mortem, inquest, post mortem and inquest

Question 66

2 parts to the MCCD form?

Answer 66

Part 1: sequence of causes, conditions or events directly leading to the death and is split into 3 parts: a, b and c- 1a= caused 1b which is caused by 1c
Causes in part II are other significant conditions contributing to the death but not directly related to the disease or condition causing it

Question 67

How to write cause of death if more than one condition?

Answer 67

On the same line

Question 68

If there are more than 3 conditions for cause of death? If due to a single disease?

Answer 68

Write more than one condition on a line indicating clearly that one is due to the next
Enter on line 1a

Question 69

Do not include what? Conditions in part 2 must have done what?

Answer 69

‘Mode’ of death- doesn’t explain why
Cardiac arrest, coma, kidney failure, respiratory arrest
Contributed to death- not just a list of co-morbidities

Question 70

The Registrars of Births and Deaths will refer to who the cause of death list during what? They’ll do what if an unacceptable cause of death is recorded on the MCCD?

Answer 70

Royal Society of Pathologists death registration
Refer to the coroner

Question 71

Doctors completing the MCCD will also complete what? Currently is not what required due to the coronavirus act? Need to declare whether what is in the body?

Answer 71

Cremation Form Part 4
Cremation Form Part 5
A hazardous implant in the body e.g. pacemaker, radioactive device or ‘fixion’ intramedullary nailing system in body so that it can be removed prior to cremation

Question 72

What are medical examiners? Assisted by who?

Answer 72

Senior medical doctors contracted for a number of sessions a week to undertake medical examiner duties, outside of their usual clinical duties- trained in legal and clinical elements of death certification processes
Medical examiner officers, new statutory role across England and Wales

Question 73

What does the medical examiner service do?

Answer 73

Discuss causes of death and come to an agreement, use the Royal College of Pathologists Cause of Death list to ensure MCCDs are not rejected at the Registrar’s office, facilitate referrals–> Coroner’s office and are informed of outcomes, ME scrutiny sent to coroner’s office for consideration
Refer cases for structured judgement review(SJR) based on 6 national criteria, speak to bereaved about cause of death and answer any Qs, inform clinical governance teams or SJR process if concerns raised about care provided

Question 74

What do bactericidal antibiotics do? Generally do what? What do bacteriostatic antibiotics work?

Answer 74

Kill>99.9% bacteria in 18-24 hours generally by inhibiting cell wall synthesis e.g. Beta lactams, glycopeptides
Agent prevents growth of bacteria- kill>90% in 18-24 hours, inhibit protein synthesis, DNA replication or metabolism e.g. clindamycin, linezolid

Question 75

When are bactericidal antibiotics useful? Bacteriostatic antibiotics used to do what?

Answer 75

Useful if poor penetration e.g. endocarditis, difficult to treat infections or need to eradicate infection quickly e.g. meningitis
Used to reduce toxin production e.g. s. pyogenes- severe cellulitis/ necrotising fasciitis, s.aureus- toxic shock syndrome STSS, gram negative bacteria LPS ‘endotoxin surge’ less likely

Question 76

Is a high/ low MIC better for antibiotics? What is key parameter?

Answer 76

Low- less is needed to inhibit the growth of the organism: peak conc/ MIC ratio- aminoglycosides, quinolones
How high the concentration is above MIC, the time that serum concentrations remain above the MIC during the dosing interval: t>MIC- Beta-lactams, clindamycin, macrolides, oxazolidinones

Question 77

What does time and concentration dependent mean in practice for antibiotics?

Answer 77

Conc dependent- ensure ‘peak’ post dose concentration high enough
Give drug frequently enough, IV penicillin four hourly x6 a day, IV fluclox 6 hourly- or continuous IVI

Question 78

What does antibiotic pharmacokinetics include?

Answer 78

Its release from the dosage form, its absorption from the site of administration into the bloodstream, its distribution to various parts of the body, including the site of action and its rate of elimination from the body via metabolism(LIVER) or excretion (KIDNEY) of unchanged drug

Question 79

Things to consider for safety with antibiotics? 5 C drugs causing c.difficile?

Answer 79

Intolerance, allergy and anaphylaxis, SEs, age, renal + liver function, pregnancy and breast feeding
Ciprofloxacin, clindamycin, cephalosporins, co-amoxiclav, carbapenems

Question 80

Why do bacteria develop resistance?

Answer 80

Intrinsic- naturally resistant
Acquired- spontaneous gene mutation(new nucleotide base pair, change in amino acid sequence, change to enzyme or cell structure, reduced affinity or activity of antibiotic–> point mutations,) horizontal gene transfer- conjugation- most concerning aspects, transduction- viruses that infect bacteria mediate transfer of DNA between bacteria, transformation- bacteria take up free DNA from the environment and incorporate it into their chromosome

Question 81

Examples of intrinsic antibiotic resistance?

Answer 81

All subpopulations of a species will be equally resistant
Aerobic bacteria are unable to reduce metronidazole to its active form
Anaerobic bacteria lack oxidative metabolism required to uptake aminoglycosides
Vancomycin cannot penetrate outer membrane of gram negative bacteria
PBP in enterococci are not effectively bound by the cephalosporins
S.aureus all produce penicillinase so resistant to penicillin

Question 82

MRSA contains what gene? Encodes what protein? Confers resistance to what? Exposure to what promote MRSA?

Answer 82

Resistance gene mecA
Penicillin-binding protein 2a(PBP2a)
All Beta-lactam antibiotics in addition to methicillin(= flucloxacillin)
Fluoroquinolone and cephalosporins

Question 83

What is VRE? Promoted by use of what?

Answer 83

Plasmid mediated acquisition of gene encoding altered amino acid on peptide chain preventing vancomycin binding
Cephalosporin use

Question 84

How do ESBLs provide resistance? TEM-1 in what bacteria? SHV-1 in what? More extensive plasmid mediated CTX-M cephalosporinase in what? Such strains remain sensitive to what?

Answer 84

Mutation at active site - hydrolyse oxyimino side chains of cephalosporins: cefotaxime, ceftriaxone, and ceftazidime and monobactams: aztreonam
E.coli, H.influenzae and N.gonorrhoea
K.pneumoniae
Enterobacteriacae
B-lactamase inhibitors

Question 85

What is co-amoxiclav made of? Tazocin?

Answer 85

Amoxicillin + clavulanate
Pipericillin + tazobactam

Question 86

AmpC Beta-lactamase provides resistance to what? Encoded on the chromosome in bacteria such as what? Also what resistant? What expression type? Can be treated with what but may require?

Answer 86

Broad spec penicillin, cephalosporin and monobactam resistance
Citrobacter spp., serratia marcescens, enterobacter spp.
Beta-lactamase inhibitor resistant
Inducible- only turned on by antibiotic(may be carried on plasmids on E.coli where not inducible)
Quinolones or trimethoprim, carbapenem tx/ agents such as fosfomycin

Question 87

Examples of carbapenemases? Option for CBEs?

Answer 87

Metallo-B-lactamases, OXA, KPC
Colistin- a polymyxin(bind to LPS and phospholipids in outer cell membrane)

Question 88

What does start smart mean in relation to antibiotic stewardship?

Answer 88

Do not start antimicrobial therapy unless there is clear evidence of infection, take a thorough drug allergy history, initiate prompt effective antibiotic tx within one hour of diagnosis in patients with severe sepsis or life-threatening infections- avoid inappropriate use of broad-spec ABx, comply with local antimicrobial prescribing guidance, document clinical guidance, drug name, dose and route on drug chart, include review/ stop date or duration, obtain cultures prior to commencing therapy where possible, single dose ABx for surgical prophylaxis where ABx shown to be effective, exact indication on drug chart for clinical prophylaxis

Question 89

‘Focus’ in relation in antibiotic stewardship?

Answer 89

Reviewing clinical diagnosis and continuing need for ABx at 48-72 hours and documenting clear plan of action- ‘antimicrobial prescribing decision,’ 5 options are:
1) Stop antibiotics if no evidence of infection
2) Switch from IV–> oral
3) Change ABx ideally to narrower spectrum/ broader if needed
4) Continue and document next review date or stop date
5) Outpatient parenteral antibiotic therapy (OPAT)- document all in clinical notes and on drug chart where possible

Question 90

Red flag makers for sepsis? Lab markers?

Answer 90

Systolic BP<90mmHg, BP>40mmHg drop norm, HR>130 BPM, RR>25 BPM, O2 SATS<90%, urine output<0.5ml/kg/hr, lactate>2 mmol/L, acute confusional state or reduction in GCS
Creatinine>120micromol/L, platelets<100 x10^9/L, APTT>60 seconds, INR>1.5

Question 91

SEPSIS 6? Antibiotic? No signs of red flag sepsis? When should they be reviewed along with sputum and blood culture results?

Answer 91

Administer oxygen, IV fluids, IV ABx, urine output, take blood cultures, measure lactate
Piperacillin/ tazobactam (IV) 4.6g QDS + clarithromycin (IV) 500mg BD
Empirical antibiotic treatment guidelines
At 48 hours

Question 92

How does amoxicillin work? Gram +ve organisms it targets? Gram -ve? Different penicillins have different what?

Answer 92

Bind to penicillin binding proteins, inhibit cell wall formation
Strep spp., listeria
N.meningitidis, E.coli + clostridium perfringens, E.faecalis
PBP affinities

Question 93

Clarithromycin is a what that binds to what? What gram +ve and -ve organisms and non-culturable? Other macrolides? What group is clindamycin in?

Answer 93

Strep spp., s.aureus
Bordetella pertussis, campylobacter spp.
Legionella spp, chlamydia spp, mycoplasma pneumoniae
Erythromycin and azithromycin
Lincosamides- struggles to enter through the gram -ve cell membrane hence lack of activity

Question 94

Gram +ve and gram -ve organisms targeted by co-amoxiclav?

Answer 94

S.aureus
Klebsiella spp., proteus spp.
Anaerobes

Question 95

What is cefuroxime? What happens as generation rises? What is ceftazidime?

Answer 95

2nd generation cephalosporin
Gram -ve cover broadens as generation rises, gram +ve falls a bit
3rd generation cephalosporin

Question 96

What is aztreonam? What is teicoplanin?

Answer 96

A monobactam- gram -ve bacteria only, safe in almost all pen allergies
Glycopeptide, along with vancomycin- prevents cell wall formation, broad coverage vs gram +ve, minimal to no gram -ve, NEPHROTOXIC (teic= easy to dose, takes longer to reach steady state, less suitable for acute sepsis)

Question 97

Qs to ask when a patient is failing on their antibiotics?

Answer 97

Is there a resistant organism, is there an organism we aren’t covering, is this failure of source control i.e. walled off abscess/ area where the ABx aren’t getting to, should we re-image- is there an empyema/ abscess that wasn’t fully treated (always check recent cultures for comparison, explain how plan may change)

Question 98

What does tazocin target?

Answer 98

As co-amox, plus pseudomonas aeruginosa and more anaerobes

Question 99

What is doxycycline? Gram +ve organisms? Gram -ve organisms? Non-culturable?

Answer 99

Tetracycline, bacteriostatic binds reversibly to ribosome, inhibits mitochondrial protein synthesis in parasites
Strep spp., s.aureus
H.influenzae, rickettsia spp., coxiella burnettii
Legionella spp, chlamydia spp, mycoplasma pneumoniae
Poor urine penetration, minimal gram -ve cover really

Question 100

What is gentamicin? Gram +ve and gram -ve organisms targeted?

Answer 100

Aminoglycoside punches holes in the cell wall, changes shape of ribosome
S.aureus (inc MRSA)
Enterobacteraciae- E.coli, Klebsiella, enterobacter, salmonella, pseudomonas

Question 101

Piv-mecillinam?

Answer 101

Extended spec oral only beta lactam
Gram -ve only

Question 102

What is ciprofloxacin? Gram +ve and -ve organisms? Non-culturable?

Answer 102

Fluoroquinolone, inhibits topoisomerase and DNA gyrase- stops DNA from coiling
Strep spp., s.aureus
Enterobacteraciae, salmonella, pseudomonas, campylobacter, neisseria
Legionella spp, chlamydia spp, mycoplasma pneumoniae
TB

Question 103

SEs from ciprofloxacin?

Answer 103

Tendon rupture, lowering of seizure threshold, prolongation of QT interval, aortic dissection

Question 104

What is trimethoprim? Gram +ve and -ve organisms? Adding sulfamethoxazole forms what?

Answer 104

Diaminopyridamine, interferes with folic acid synthesis, prevents DNA synthesis, inhibits dihydrofolate reductase, used for UTIs and prostatitis
S.aureus
Enterobacteraciae- E.coli, Klebsiella, enterobacter, salmonella
Co-trimoxazole

Question 105

What is nitrofurantoin? Gram +ve and -ve organisms?

Answer 105

Only drug in its class available in the UK- predominantly renally excreted, minimal in serum
Staph saprophyticus, enterococcus spp., enterobacteraciae- E.coli, Klebsiella

Question 106

What is fidaxomicin?

Answer 106

First member of a class of narrow spectrum macrocyclic antibiotic drugs called tiacumicins
Targets c.diff, minimal GI flora disruption

Question 107

What makes flucloxacillin stable vs Beta lactamases produced by MRSA? Plus what else?

Answer 107

Its structure
Beta haemolytic steps (A C G)

Question 108

Inflammation x time is what? What is reversible and irreversible?

Answer 108

Tissue damage
Inflammation= reversible
Damage= irreversible

Question 109

Acute tx for gout? Those associated with lowest CV risk?

Answer 109

NSAID unless renal failure(only if eGFR>40,) peptic ulcer disease, some pts with asthma
Colchicine 500micrograms 2-3 times daily
Corticosteroids intra-articular, oral- low dose (5-10mg short course)
Other analgesics don’t work
Ibuprofen and naproxen

Question 110

Indication for long-term tx of gout?

Answer 110

1) Recurrent attacks
2) Evidence of tophi or chronic gouty arthritis
3) Associated renal disease
4) Normal serum uric acid cannot be achieved by lifestyle modifications
Meds: allopurinol, febuxostat= more potent xanthine oxidase inhibitor, benzbromarone/ probencid - if allergic/ intolerant

Question 111

Process for purine synthesis in gout?

Answer 111

RNA/ DNA–> adenine/ guanine–> inosine–> hypoxanthine(xanthine oxidase)–> xanthine(xanthine oxidase)–> uric acid

Question 112

Aim of chronic gout management? Dose etc?

Answer 112

Reduce uric acid below 300 micromol/L, start at 100mg allopurinol and increase every 2-4 weeks until target met, engage patient in this- more likely to comply and make lifestyle modification

Question 113

Dose of febuxostat as alternative to allopurinol? What cover for first 2 months? Leflunomide dose? Washout with what if significant toxicity? Monitor what? Sulfasalazine?

Answer 113

80mg daily, can increase to 120mg
Colchicine
10-20mg- cholestyramine
BP as it causes HTN
2-3g daily (2 divided doses), occasionally severe rash and neutropenia, monitoring not needed after 1 year

Question 114

How long does methotrexate take to work in RA? What acts as bridge? What if disease doesn’t respond? What given once weekly on different day to reduce risk of SEs?

Answer 114

6- 8 weeks, taken weekly
Steroid
Biologic medications
Folic acid, avoid 3-6 months pre pregnancy, alcohol restriction

Question 115

How do corticosteroids work at a cellular level?

Answer 115

Reduce number and activity and leucocytes, proliferation of blood vessels, activity of mononuclear cells, activity of cytokine secreting cells, production of cytokines, histamine release

Question 116

Adverse effects of steroids?

Answer 116

Cushing’s disease
Sleep disturbance/ activation, mood disturbance, psychosis
Cushingoid appearance, abdominal striae, acne, hirsutism, oedema, neuropathy, pseudomotor cerebri, HTN, osteoporosis, asceptic necrosis of bone, myopathy, diabetes mellitus, adrenal cortex suppression, lymphocytopenia, immunosuppression, false negative skin, cataracts, narrow-angle glaucoma, growth retardation

Question 117

How to avoid unwanted effects of corticosteroids?

Answer 117

Use short courses/ low doses if possible
Use steroid sparing drugs
Withdraw chronic steroids slowly
Give dose once daily and in morning, give prophylactics if possible, give product locally, remember CIs, educate patient

Question 118

Goal of DMARD tx? Drugs used- often in combination? Mode of action? Response rates best when?

Answer 118

Reduce disease activity, rate of joint damage, improve quality of life
Methotrexate, sulfasalazine, leflunomide, hydroxychloroquine
Non specific inhibition of the inflammatory cytokine cascade- “the immune messengers”
If introduced within 3 months of initial symptoms, onset of action is slow

Question 119

Possible SEs of DMARDs? Blood tests?

Answer 119

Bone marrow suppression- low WCC, Hb, platelets, abnormal liver enzymes, GI effects- nausea, diarrhoea, oral ulceration and hair loss, teratogenic except sulfasalazine, azathioprine
FBC, U&Es and LFT monthly for 3 months, then every 3 months

Question 120

Methotrexate and sulfasalazine not working? Onset of action of anti-TNF inhibitors?

Answer 120

Anti-TNF meds: infliximab(MAB,) etanercept(receptor fusion proteins,) adalimumab (MAB,) certolizumab, golimumab
Rituximab= anti CD20- anti-B cell(every 6-18 months)
Abatacept= anti-T cell, binds to CD80/ 86, better with MTX
Tocilizumab= anti-IL 6, best as monotherapy
Baricitinib/ tofacitinib- JAK inhibitors(not biologics)- oral, interrupt intracellular signalling that happens after cytokines bind their receptors
1-3 weeks

Question 121

Adverse effects of TNF inhibitors?

Answer 121

Increased risk of bacterial, viral and/ or fungal infections
More severe and may present later
Injection site reactions
Generation of antibodies to drugs–> reduced efficacy over time
Emergence of skin cancers over long-term use

Question 122

JAK inhibitor SEs?

Answer 122

Short half life 2-3 days, high infection risk, particularly shingles, increased risk of DVT/ PE and possibly malignancy, overall risk similar to biologics

Question 123

Epidemiology of GCA? Comps of GCA?

Answer 123

Peak incidence= 70-80 y/o, most common in white Northern European populations particularly Scandinavian, F:M= 3:1
Strokes 1%, blindness<20%

Question 124

Clinical features of GCA?

Answer 124

New localised headache (abrupt, temporal,) visual sx- blurring, amaurosis fugax, diplopia, photophobia, visual loss, scalp tenderness, jaw and tongue claudication, polymyalgia, constitutional sx(fever, malaise), limb claudication

Question 125

Physical signs of GCA? What could cause normal CRP/ESR GCA?

Answer 125

Scalp tenderness, temporal artery tenderness thickening- visible distension, reduced/ absent pulsation
Previous corticosteroid use/ immunosuppressants

Question 126

How to calculate upper limit of normal ESR in women? In men? What things influence?

Answer 126

Age+10/2
Age/2
BMI, insulin resistance, metabolic syndrome

Question 127

Score used to calculate probability of GCA? What should be used as a checklist to aid diagnostic accuracy and assess probability?

Answer 127

Southend probability score
GCAPS

Question 128

What tests should all patients with suspected GCA have?

Answer 128

USS, temporal artery biopsy, or both
PET-CT and axillary US for extra-cranial disease

Question 129

Initial management in GCA?

Answer 129

No delay in corticosteroid tx
40-60mg oral pred(up to 60mg in those with hx of ischaemic sx: visual loss, limb, tongue or jaw claudication)
IV methylpred
No evidence aspirin beneficial- follow CVD guidelines for secondary prevention
PPI in high risk patients- OLDER AGE

Question 130

Sx of major relapse of GCA? Minor relapse?

Answer 130

Headache + features of ischaemia e.g. tongue, jaw, limb claudication, scalp necrosis, visual sx, restart from beginning as if newly presented, 60mg oral pred daily, inform rheum urgently to expedite review
Return of headache without features of ischaemia, urgent CRP/ ESR required, back to last effective dose of steroids until next clinical review, inform rheum to expedite review

Question 131

How is tocilizumab taken for GCA? Can be used in patients with what? Available for how long? Requires what for eligibility?

Answer 131

SC injection once weekly
In patients with refractory disease/ in relapsing disease
12 months
Tissue or imaging diagnosis for eligibility

Question 132

Suspect GCA in who?

Answer 132

Patients over 50 with severe new onset headache AND elevated CRP especially if specific GCA characteristics in the hx

Question 133

DDx of fever in a returning traveller?

Answer 133

Malaria, typhoid, dengue fever, TB, Ebola, Marburg fever, Rocky mountain fever, Lassa fever, Schistomiasis, Chikungunya, Scrub typhus, Rift valley fever, yellow fever, West nile virus, TB, Hantavirus, paratyphoid fever, monkeypox, leptospirosis, influenza, meningitis, tick borne encephalitis

Question 134

5 species of plasmodium parasite? The deadliest species of plasmodium causing malaria in humans? Common symptoms of malaria? Severe disease? More in what type of people? Incubation period?

Answer 134

Plasmodium falciparum, malariae, vivax, ovale, knowlesi
Falciparum
Diarrhoea, headache, fever, chills and shivers, cough, body ache, sweat, N&V
Cerebral malaria, renal failure, liver failure, severe anaemia, respiratory distress
Pregnant women, children, elderly, immunocompromised- e.g. splenectomy, HIV/ AIDs
<1 month, can be up to 1 year

Question 135

Cause of typhoid fever?

Answer 135

Gram negative bacilli- salmonella typhi

Question 136

Symptoms of Ebola? Examples of viral haemorrhagic fever?

Answer 136

Headache, red eyes, hiccups, sore throat, difficulty breathing, difficulty swallowing, chest pain, stomach pain and vomiting, rash and bleeding, aches, diarrhoea, aches and weakness, fever, lack of appetite, internal bleeding
Lassa fever, Ebola, Marburg disease, Crimean-Congo haemorrhagic fever

Question 137

Signs of severe malaria? Check what things? How Ix? What should be used for blood samples?

Answer 137

Impaired consciousness, confusion, hypotension, respiratory distress, jaundice
BP, pulse, oxygen SATs, RR, temperature, for hepatomegaly/ splenomegaly and pallor
Microscopy of thick and thin blood films(GOLD standard) or antigen detection test- most need secondary care referral
EDTA

Question 138

What should be done if the first blood films for malaria are negative? Thick films can be negative in who?

Answer 138

Further blood testing must be arranged 12-24 hours later and again after a further 24 hours to rule out infection
Pregnant women

Question 139

DDx for malaria? Ix?

Answer 139

Viral haemorrhagic fevers, enteric fevers like typhoid and paratyphoid, arboviruses such as Dengue, West Nile virus, and Japanese encephalitis, ricksettial disease like like scrub typhus + relapsing fever, rabies
FBC, U&E, LFTs, clotting, CRP, blood cultures before ABx, malaria RDT + haem sample for thick + thin blood film, blood-borne virus testing- HIV, Hep B, Hep C and syphilis serology, ABG- pH, CXR, urine dip for haematuria

Question 140

Empirical tx for malaria?

Answer 140

Ceftriaxone, doxycycline, IV artesunate- phone ID SpR

Question 141

How can medication errors be classified? Most common type seen amongst F1 doctors? How else can they be classified?

Answer 141

Mistakes- knowledge or rule based errors
Lapse- memory based errors e.g. forgetting the patient is allergic to penicillin
Slip- action based error i.e. picking up digoxin instead of diltiazem
Slips+ knowledge-based mistakes
As to where in the prescribing cycle they occur- prescribing, dispensing and administration errors

Question 142

Types of medication incident?

Answer 142

Omission, wrong drug, wrong dose, wrong frequency, wrong duration, wrong route, wrong patient, inappropriate prescribing

Question 143

How might the wrong dose be administered?

Answer 143

Decision to prescribe, when creating, from prescriber–> pharmacy, pharmacy process, pharmacy–> ward, administration of drug

Question 144

How might the wrong patient occur when prescribing?

Answer 144

Transitions in care- moving ward, changing team, communication e.g. phone messages handover, complex and high risk systems such as emergency medicine

Question 145

E.g. of high risk prescribing moments?

Answer 145

Rewriting a drug chart, amending a previous prescription, being distracted whilst prescribing, writing up drugs with more than 1 drug card/ set of notes in front of you, unfamiliar drugs, prescribing parenteral drugs, time pressured, high risk drugs, calculating drug doses, look-alike drugs

Question 146

Who should have a PSA test? What can elevate PSA levels?

Answer 146

Abnormal feeling prostate on DRE, symptoms of locally advanced or metastatic disease, >50 years on request if appropriately counselled, >45 if FH/ Black ethnicity on request if appropriately counselled, men w/ LUTS, can be prognostic for progression of LUTs, haematuria, erectile dysfunction

UTIs- avoid within 4- 6 weeks proven UTI, retention

Question 147

E.g. Ix for prostate cancer?
E.g. of prostate cancer treatments? What is androgen deprivation therapy used for?

Answer 147

Transrectal (TRUSS)/ transperineal biopsy
Transurethral resection of the prostate (TURP)
EBRT(external beam radiation therapy)/ ADT(androgen deprivation therapy,) brachytherapy(internal radiation,) focal therapies, active surveillance, WW- unwilling/ co-morbidities–> ADT
Locally advanced and metastatic disease

Question 148

Typical settings of an ECG? 5 big squares is how long on X-axis? 2 big squares on Y-axis?

Answer 148

25mm/sec, voltage= 10mm/mV
1 second
1 mV

Question 149

How to calculate HR on ECG?

Answer 149

300/ number of large squares between R waves or QRS complexes in 10 seconds x 6

Question 150

Classification of tachycardia?

Answer 150

Narrow complex tachycardia- sinus tachycardia, SVT, AF with fast ventricular response
Broad complex tachycardia- ventricular tachycardia, sinus tachycardia/ SVT/ AF with aberrant conduction (bundle branch block)

Question 151

Rhythms on ECG?

Answer 151

Regular- P waves present= normal sinus rhythm, absent= ectopic pacemaker rhythms, atrial flutter
Regularly irregular–> sinus arrhythmia/ 2nd heart block/ regular ectopics (bigeminy etc.)
Irregularly irregular= AF, irregular ectopics

Question 152

How does atrial flutter appear on an ECG?

Answer 152

Organised atrial activity- 300/min, ventricular capture at ratio to atrial rate - usually 2:1 so 150 bpm, usually regular, can be irregular if ratio varies

Question 153

If QRS is positive in both lead I and II, what is this? What is lead I is positive and lead II is negative?

Answer 153

Normal axis
Left axis deviation- Leaving each other

Question 154

What if lead I is negative and lead II is positive?

Answer 154

Right axis deviation- Reaching towards each other

Question 155

What is a normal P wave axis? What is P mitrale? P pulmonale?

Answer 155

Positive in all leads except avR, abnormal suggests non-sinus origin
Notch in the P wave
Tall peaked P waves

Question 156

Normal PR interval? Is it long and constant? Is it long and not constant?

Answer 156

120-200ms
1st degree heart block
2nd degree heart block/ 3rd degree heart heart block (complete)

Question 157

Mobitz type I 2nd degree heart block also known as what? What is it? What about Mobitz type II?

Answer 157

Wenckebach phenomenon- PR interval gets longer and longer, then missed beat, then PR interval resets, P-P interval remains constant

2:1 block, every other P wave fails to conduct, atrial rate twice the ventricular rate, PR interval remains constant, P-P interval remains constant

Question 158

How dangerous is Mobitz Type I and type II 2nd degree heart block?

Answer 158

Not typically dangerous- can be a normal variant e.g. at night in young people, but if pathological can progress to higher grade block
Almost always pathological, next stage is complete heart block and risk of ventricular standstill so warrants urgent pacemaker insertion

Question 159

What is complete (3rd degree heart block)?

Answer 159

No relationship between P waves and QRS, QRS typically broad, risk of ventricular standstill, broader the escape rhythm, the more dangerous, mandates urgent pacemaker insertion unless congenital

Question 160

What is a Delta wave? What does a short PR interval with a delta wave and broad QRS indicate? Short PR interval and no delta wave + symptoms?

Answer 160

A slurred upstroke in the QRS complex
Wolff-Parkinson-White Syndrome + symptoms
Lown-Ganong-Levine syndrome

Question 161

Normal length of QRS complex? Most common cause of prolonged QRS complex? Other causes of prolonged QRS?

Answer 161

<120ms
Bundle branch block- WILLIAM- LBBB/ MARROW- RBBB
Ventricular origin of QRS e.g. ventricular ectopic, ventricular tachycardia, complete heart block, pre-excitation(delta wave)

Question 162

What is a Q wave? What is a pathological Q wave?

Answer 162

Any negative deflection before an R wave- can be more prominent in lead III, but disappear on inspiration as a normal variant
Deeper and broader- may represent full thickness infarction in that territory

Question 163

Diagnostic criteria for LVH on an ECG?

Answer 163

S in V1 + R in V5 or V6>35 mm

Question 164

What leads look at the lateral view of the heart? Which artery? Inferior view? Artery? Septal view? Artery? Anterior view? Artery?

Answer 164

Leads I, aVL, aVF, V5 + V6= CIRCUMFLEX
Leads II, III and aVF= RCA
V1, V2
V3, V4= LAD

Question 165

What does the QT interval measure? Best measured in what leads? Normal values in men and women?

Answer 165

Measure of time to ventricular repolarisation
Leads II, V5 or V6
Prolongation (or shortening) confers increased risk of arrhythmia and sudden death
Men= 350-440ms, women= 350-460ms

Question 166

Causes of abnormal QT?

Answer 166

Congenital- genetic(long/ short QT syndrome)
Acquired- ischaemia, electrolyte disturbance
DRUGS e.g. macrolide antibiotics, anti-epileptics, antidepressants, 1st generation antihistamines

Question 167

How does QT vary with faster and slower rates? What do reference ranges apply to? How to calculate QTc? Also known as what?

Answer 167

Shortens at faster rate, lengthens at slower rate
60bpm therefore correct for rate
QT duration/ square root of RR interval
Bazett formula

Question 168

What does the T wave measure? T waves should always be upright in what leads and inverted in what lead? What is T wave inversion + appropriate sx/ blood tests suspicious for?

Answer 168

Ventricular repolarisation
I, II, V3-V6
aVR, can be upright or inverted in other leads and still be considered normal
Infarction

Question 169

Tall ‘tented’ T- waves is what?

Answer 169

Hyperkalaemia, ‘hyperacute T waves’ in MI

Question 170

Tx for mild hyperkalaemia? Moderate? Severe?

Answer 170

Non-K+ sparing diuretics e.g. furosemide 40-80mg IV/ KAYEXALATE 15-30G to 100ml of 20% Sorbitol orally/ by retention enema

Glucose + insulin- 50ml D50 + 10U regular insulin over 15-30 minutes/ sodium bicarbonate 50 mEg oIV over 5 minutes/ albuterol 10-20mg
nebulised over 15 minutes

All of above, also calcium chloride (10%) 500-1000mg IV over 2-5 minutes to reduce the effects of K+- lowers the risk of VF

Question 171

What is prevalence? What is incidence?

Answer 171

The proportion of a population who are positive for a disease at any point in time
The number of new cases presenting in a population over a period of time

Question 172

How do you calculate cumulative incidence? What is pre-test probability? Post-test probability?

Answer 172

Diseased/ population at risk
The probability before a diagnostic test is performed that someone has the disease
Probability of the patient having the disease after obtaining test results

Question 173

What is specificity? Sensitivity?

Answer 173

The proportion of people without the disease, who have negative test result- problem= false negatives
The proportion of people with the disease, who have a positive test result- problem= false positives

Question 174

4 reasons for doing tests?

Answer 174

Rule in a diagnosis, rule out a diagnosis, check for complications, assess severity
Plan treatment, monitor progress, confirm recovery, monitor health

Question 175

What is a valid test? Reliable test? What is an accurate test?

Answer 175

One that test what we need to test
One that gives the same result irrespective of the operator
One that is sensitive and/ or specific enough to answer the clinical question

Question 176

What is negative predictive value?

Answer 176

Of all the people with a negative test, what proportion don’t have the disease

Question 177

What is adolescence?

Answer 177

The period following the onset of puberty during which a young person develops from a child into an adult

Question 178

Developmental tasks during adolescence?

Answer 178

Move from dependence–> independence
Physical= puberty, sleep, appetite
Social= peers, romantic relationships, independence from parents, peer pressure/ social media
Emotional= intensity, identity development, depression/ anxiety/ eating disorders/ aggression/ anti-social behaviour
Neurocognitive

Question 179

What is the HEEADSSS psychosocial screening tool?

Answer 179

A practical, time-tested strategy that can be used to obtain a Psychosocial Review of Systems (PROS) for adolescent patients who attend ED with self-harm/mental health concerns
Home, education, eating, activities, drugs and alcohol, sexual health, suicide/ spirituality/ sleep, social media/ general safety

Question 180

Risk and protective factors for mental health difficulties?

Answer 180

Negative parenting experiences, stressful life events, physical health problems, learning/ developmental difficulties, parental mental health problems, conflictual family relationships, poverty, low SE status, inequality, discrimination and bullying
Positive parenting experiences, sense of self-esteem + self efficacy, positive social relationships, sense of belonging, social skills, problem solving skills, communication skills

Question 181

What are health risk behaviours?

Answer 181

Any activity undertaken with a frequency or intensity that increases risk of disease or injury- leading cause of morbidity and mortality in young people

Question 182

Types of eczema?

Answer 182

Atopic dermatitis, contact dermatitis- irritant and allergic contact dermatitis, discoid/ nummular eczema, stasis/ gravitational dermatitis, seborrhoeic dermatitis

Question 183

Epidemiology of atopic dermatitis? PPx?

Answer 183

10-30% children, 2-10% adults, early, late and senile onset AD
Genetics: FH of atopy, FLG mutations
Environment- hygiene hypothesis/ infection, allergens, irritants

Question 184

Must have an itchy skin condition/ parental report of scratching or rubbing in a child plus 3 or more of what?

Answer 184

1) Hx of involvement of the skin creases such as elbow folds, behind the knees, fronts of ankles or around the neck- including cheeks in children <10
2) Personal hx of asthma or hayfever/ hx atopic disease in 1st degree relative in children <4 y/o
3) Hx general dry skin in last year
4) Visible flexural eczema or involving cheeks/ forehead and outer limbs in children< 4 y/o
5) Onset under the age of 2- not used if child is under 4

Question 185

Acute and chronic changes in atopic dermatitis?

Answer 185

Erythema, swelling, crusting, erosions, (fissuring, scaling= subacute)
Scaling, lichenification, prurigo like lesions, xerosis(dry skin)

Question 186

Atopic stigmata?

Answer 186

Dennie Morgan folds- under eyelids, keratosis pilaris- goosebump feeling, peri-orbital darkening, xerosis

Question 187

Causes of eczema flares? Scores to assess severity of eczema?

Answer 187

Allergens, irritants, stress, compliance with emollients, topicals, infections
DLQI, PGA, EASI

Question 188

Tx of atopic dermatitis?

Answer 188

Basic skin care- avoid irritants, gloves, emollients- use liberally and very regularly, direction of hairs, ointments, gels, creams, lotions, bath additives, soap substitutes, topicals- steroids cream vs ointment, frequency, duration, flare vs maintenance, topical calcineurin inhibitors, other tx, phototherapy- narrowband UVB, PUVA, systemic therapy- prednisolone courses, methotrexate, ciclosporin, azathioprine, biologics- dupilumab- IL 4 &13, tralokinumab- IL 13, JAK inhibitors-JAK 1 and 2= baricitinib, JAK1 selective- upadacitinib

Question 189

How to use topical steroids for eczema?

Answer 189

Use weakest effective steroid with written and verbal instructions of duration/ step down:
Mild= hydrocortisone
Moderate= 2-25x potency vs hydrocortisone- clobetasone butyrate(Eumovate)
Potent= 100-150x- betamethasone valerate (Betnovate)
Very potent= up to 600x- clobetasol propionate (Dermovate)

Question 190

Local SEs of topical steroids?

Answer 190

Skin thinning- atrophy & striae, easy bruising and skin tearing, telangiectasia, susceptibility to infection, triggering/ worsening other skin conditions, allergy to ingredient

Question 191

Systemic SEs of topical steroids?

Answer 191

Adrenal suppression, Cushing’s syndrome
Weakest effective, sensitive areas- flexures, face, children vs adults
Duration, plan for weaning down, verbal and written advice

Question 192

What is a finger-tip unit?

Answer 192

Amount from a tube with a 5mm diameter nozzle from distal skin- crease to tip of index finger- 0.5g, treats area roughly size of x2 adult palms

Question 193

What causes irritant contact dermatitis? Ix? Tx?

Answer 193

Direct chemical or physical irritation to skin, anyone can be affected, no diagnostic test, standard eczema tx, avoid irritants

Question 194

Type of hypersensitivity reaction of allergic contact dermatitis? Ix? Tx?

Answer 194

Type IV, prior sensitisation needed, only people with an allergy react
Patch testing, standard eczema tx, avoid allergens

Question 195

What is nummular dermatitis also known as?

Answer 195

Discoid eczema

Question 196

Who does stasis dermatitis occur in? Due to? Hx of?

Answer 196

Middle-older aged, venous insufficiency, DVT, cellulitis, varicose veins, venous ulcers

Question 197

What does seborrhoeic dermatitis usually affect? How does infantile seborrhoeic dermatitis affect infants? When does adult usually start?

Answer 197

Sebaceous-gland rich areas on scalp, face and trunk
Babies under the age of 3 months and usually resolves by 6-12 months of age
In late adolescence. Prevalence is greatest in young adults and in older people. It is more common in males than in females
Very common in those with darker skin types

Question 198

Adult associations with seborrhoeic dermatitis? Tx?

Answer 198

Psoriasis, immunosuppression, Parkinson’s, stroke, Down syndrome
Emollients, medicated shampoos, topical antifungals, topical steroids, topical calcineurin inhibitors

Question 199

Where can melanoma grow?

Answer 199

Commonly in the skin, other= mucosal, ocular(uvea,) leptomeninges

Question 200

RFs for melanoma?

Answer 200

Age- 25%= >75 y/o, UV exposure, skin type, >100 melanocytic naevi, >5 atypical naevi, multiple solar lentigines, family hx, personal hx

Question 201

Gene responsible for 2% and 20% familial melanomas? Increased risk of what?

Answer 201

CDKN2A- pancreatic cancer

Question 202

How to assess a lesion? Major features of the lesion(2 points each)? Minor features(1 point each)?

Answer 202

ABCDE- asymmetry, border, colour, diameter, evolution
Change in size, irregular shape or border, irregular colour
Largest diameter 7mm or more, inflammation, oozing or crusting of the lesion, change in sensation including itch

Question 203

Most common subtype of melanoma? Commonest sites?

Answer 203

Superficial spreading- prolonged radial growth phase
Trunk in males, legs in females

Question 204

Who is nodular melanoma more common in? Common sites?

Answer 204

Males- trunk, head and neck
Early vertical growth phase

Question 205

Who is lentigo maligna melanoma more common in? Ass with what? Often occurs on what? Commonest site?

Answer 205

Elderly
Chronic accumulative sun exposure
Sun damaged skin
Face

Question 206

Most common melanoma type in darker skin types? Often presents when and where?

Answer 206

Acral lentiginous melanoma
Late + has worse prognosis- palms, soles or nail apparatus

Question 207

ABCDEF of acral lentiginous melanoma?

Answer 207

Age range 20-90 y/o, peak 5th-7th decades, African-American, Native American, Asian
Nail band, brown-black, breadth>3mm, irregular border
Rapid increase in size/ growth rate of nail band
Thumb>hallux>index finger, single> multiple digits dominant hand
Extension of pigment to involve proximal or lateral nail fold(Hutchinson’s sign) or free edge of nail plate
Family/ personal hx previous melanoma

Question 208

What is the depth of the melanoma from the surface of the skin down through to the deepest part called? How is melanoma staged?

Answer 208

Breslow thickness
TNM staging system

Question 209

Stage 0, 1, 2, 3 and 4 of melanoma?

Answer 209

In situ, thinner tumours confined to skin, thicker tumours confined to skin, LN involvement, distant metastasis

Question 210

Management of melanomas? Secondary care?

Answer 210

GP= 2 WW- NO BIOPSY
Diagnostic excision of the pigmented skin lesions with a 2mm peripheral margin
WLE- margins dependent on staging

Question 211

What in IIC who have not had a sentinel lymph nodes biopsy? Including what for suspected stage IV disease? Consider what for children and young people?

Answer 211

CT scans
Brain, MRI

Question 212

What is found in 40-50% melanomas?

Answer 212

BRAF mutations

Question 213

Tx of stage 3 and 4 melanoma?

Answer 213

Targeted therapy: BRAF inhibitors- Dabrafenib
MEK inhibitors- Trametinib

Question 214

Checkpoint inhibitor examples?

Answer 214

Anti CTLA4 antibody- ipilimumab
Anti PD1 antibody- Nivolumab, Pembrolizumab

Question 215

What are non-melanocytic skin cancers? Actinic and keratosis can turn into what?

Answer 215

Tumours of keratinocytes- BCCs and SCCs
SCC

Question 216

RFs for NMSC?

Answer 216

UV exposure: SCC= chronic cumulative, BCCs- intermittent intense UV exposure, Fitzpatrick’s skin types I-II (fair skin,) increasing age, immune suppression (SCC>BCC,) ionising radiation, chronic wounds(SCC,) cigarette smoking (SCC,) HPV(SCC,) genetic syndromes

Question 217

Genetic syndromes increasing risk of NMSC?

Answer 217

Xeroderma pigmentosum, albinism, epidermodysplasia, dystrophic epidermolysis bullosa, Muir-Torre syndrome, basal cell nevus syndrome, Bazex- Dupre- Christol and Rombo syndrome

Question 218

What is actinic keratosis and it begins where? No what or what?

Answer 218

Partial thickness dysplasia of epidermal keratinocytes
In the basal layer
Invasion through the basement membrane or ability to metastasise

Question 219

How does actinic keratosis present?

Answer 219

Develops over years, at sun exposed sites, no hx of rapid growth/ pain/ bleeding or ulceration, base not raised

Question 220

% actinic keratoses spontaneously resolve over a 1-year period? Tx?

Answer 220

20%
Topical txs= 5-flurouracil, imiquimod, diclofenac
photodynamic therapy
Discrete lesions= cryotherapy, C&C, topical treatments

Question 221

What is Bowen’s disease? Diagnosis along with actinic keratosis?

Answer 221

Full thickness dysplasia of epidermal keratinocytes- no ability to metastasise
Develops over years, sun exposed sites, no hx of rapid growth, pain, bleeding or ulceration, base not raised
Clinical Ix, dermoscopy, biopsy

Question 222

Bowen’s disease tx? What is SCC? Presentation? Tx?

Answer 222

5-flurouracil, cryotherapy, C&C, PDT
Invasion past the basement membrane- potential to metastasise
Rapid growth- week to months, raised base, keratotic or scaly lesions, may ulcerate and/ or bleed, may be painful, sun exposed sites- face, lips, ears, hands, forearms, lower legs
Surgery- standard excision, Mohs surgery, radiotherapy

Question 223

Presentation of BCC? Tx?

Answer 223

Slowly growing plaque or nodule, skin coloured, pink or pigmented, often shiny or pearly, rolled edges, telangiectasia, ulceration + spontaneous bleeding, very rarely metastasise
Surgery- standard, Mohs, radiotherapy

Question 224

Indications for Mohs micrographic surgery?

Answer 224

Tumour site- especially central face, around the eyes, nose, lips and ears
Tumour size- especially>2cm
Histological subtype- especially morphoeic, infiltrative, micronodular and basosquamous subtypes
Poor clinical definitions of tumour margins
Recurrent lesions
Perineural or perivascular involvement

Question 225

Tx of superficial BCCs?

Answer 225

Curretage and cautery, cryotherapy, cryotherapy, topical- imiquimod, 5-flurouracil, photodynamic therapy

Question 226

What is interoception?

Answer 226

The neurological and nonconscious process of sensing, interpreting and regulating the body

Question 227

2 types of reassurance?

Answer 227

Affective: generic, engages emotions, often no further questions, transient, relief
Cognitive: specific, engages thoughts, often involves further questions, sustained assurance

Question 228

4-step approach to dealing with persistent physical sx(REAL)?

Answer 228

Recognition, explanation, action, learning
Recognition: of the patient, symptoms/ syndrome, their concern by using generic reassurance
Explanation: cognitive reassurance, plain language
Action: what to do when things are bad, how reduce risk of future episodes, safety netting
Learning: acute management, ongoing: continuity and trust, learn together what works for you

Question 229

What is acute inflammation? Chronic inflammation results from what?

Answer 229

An immediate response to a trigger: tissue invasion- infection, tissue damage- trauma, tissue response to antigen- allergy(primarily innate immune system)
Persistent triggering: abnormality of immune system- RA, lupus, of metabolism- gout, medicines/ therapies- immunotherapy(innate + adaptive immunity)

Question 230

What is HLH (Hemophagocytic Lymphohistiocytosis)? 3 Fs? Score that estimates the risk of having reactive haemophagocytic syndrome

Answer 230

When histiocytes and lymphocytes become overactive= immune dysregulation with ++ macrophage (haemo) phagocytosis- immune chaos
Fever(cytokine storm,) falling counts (haemophagocyosis,) ferritin highly elevated (high TG, low fibrinogen, abnormal LFTs)

Question 231

‘At risk’ person with some/ all of 3 Fs, HPB dysfunction, CNS signs, coagulopathy, multi-organ failure, check what? H score 169 tx? Day 2-3 further tx with anakinra may be needed if what?

Answer 231

Ferritin, triglycerides, fibrinogen, clotting screen, FBC, LFTs, review imaging to calculate H score
1st line tx for HLH= 1g IV OD for 3 days of methylprednisolone–> daily HLH screen, stage 1 tests
If after dose 2 of corticosteroids- no improvement/ H score worsening, multi-organ failure develops and/ or there are CNS signs/ myocarditis

Question 232

How does COVID-19 enter cells? Root cause of severe disease? Most common complication of COVID-19?

Answer 232

Spike protein binds surface ACE-2 activated by TMPRSS2 on cell surface, fusion medicated by S2 subunit
Hyperinflammation
VTE- PE, DVT, also myopericarditis, ACS/ acute limb ischaemia, gross derangement in blood sugar control, AKI, acute hepatitis

Question 233

When should be anti-virals be given to be effective against COVID-19? Action of remdesivir? Commonly causes what?

Answer 233

Within the first 5-7 days of symptoms- to prevent deterioration by CMDUs as an outpatient
My job as inpatients
Inhibits lots of RNA viruses pre- COVID-19- IV, OD, pro-drug converted intracellularly to inhibit viral RNA polymerase(reduces disease progression by 80% in mild COVID-19)
Hepatitis- monitor U&Es/ LFTs

Question 234

What is paxlovid? Not safe in who?

Answer 234

Viral protease inhibitor, oral, TD- ritonavir used to boost levels of active drug by inhibiting hepatic metabolism(reduces progression by 80% in mild COVID-19)
Significant liver/ kidney disease, also phenomenon of Paxlovid rebound

Question 235

What is Sotrovimab? Ineffective against what?

Answer 235

MAB against spike protein, IV, once only
New strains of COVID-19

Question 236

Treating late/ severe COVID-19?

Answer 236

Oxygen, fluid status, ABx, consider escalation status
Anticoagulation- therapeutic if on O2 and NOT ICU
Prophylactic if on ICU(usually LMWH)
Immunomodulation
Dexamethasone- 6mg OD for 10 days oral/IV, consider PPI, use pred in pregnancy

Question 237

What is Baricitinib?

Answer 237

Non-selective JAK/ STAT pathway inhibitor often in rheumatic disease downstream of IL-6, oral OD for 10 days- evidence of bacterial infection?, modify for renal function

Question 238

What is Tocilizumab? Need CRP above what level? Reserved for what? IS effect can last how long? Patient should have what?

Answer 238

MABs against interleukin-6- single IV dose
75
Most severe COVID-19
3 months, a pre-immunosuppression screen

Question 239

Treating critical COVID-19?

Answer 239

Organ support: ventilator, renal replacement, inotropes/ vasopressors, mechanical support
Superadded infection: bacterial, fungal other viruses
Advanced care planning/ palliative care

Question 240

Oncology emergencies?

Answer 240

Metastatic spinal cord compression (MSCC), hypercalcaemia, SVC obstruction, epilepsy, venous/ arterial thromboembolism, pleural effusion, bowel obstruction

Question 241

Level 0, 1, 2, 3 and 4 on ECOG/ WHO performance status?

Answer 241

0= fully active, able to carry on all pre-disease performance without restriction
1= can carry out work of a light or sedentary nature
2= can’t do any work activities
3= only limited selfcare, confined to bed or chair>50% waking hours
4= completely disable, totally confined

Question 242

Types of systemic anti-cancer therapy?

Answer 242

Cytotoxic, targeted, endocrine therapies, immunotherapy, bisphosphonates

Question 243

What is neoadjuvant vs adjuvant therapy?

Answer 243

Given before surgery/ radiotherapy to shrink cancer down improve outcome of resection and reduce risk of recurrence
Reduces risk of local recurrence/ distant recurrence by treating micrometastatic disease

Question 244

E.g. of endocrine tx of cancer?

Answer 244

Tamoxifen- SERM
Aromatase inhibitors- post-menopausal only
Prostate= GNRH analogues, can cause tumour flare- give with bicalutamide cover initially
Degarelix- GnRH antagonist

Question 245

Aim of targeted therapies?

Answer 245

Act on different parts of pathway/ cascade which lead to cell proliferation- inhibits pathway at various points to stop stimulus to cancer and cause apoptosis

Question 246

High risk cancer regimens given what?

Answer 246

Prophylactic GCSF- granulocyte colony stimulating factor

Question 247

What is sepsis? RFs?

Answer 247

The body’s response to an infection injuring its own tissues and organs
Aged<1 y/o, >75 y/o, frail w/ multiple comorbidities, pregnant/ pregnant within last 6/52, trauma/ surgery/ invasive procedure within last 6/52, reduced immunity, indwelling lines/ catheters, IVDU, skin infections, cuts, burns, blisters

Question 248

Criteria for considering workup for sepsis/ severe sepsis? Issues with SIRS?

Answer 248

SIRS criteria(NO LONGER USED): HR>90, RR>20, WCC>12/ <4 X 10^9/L, temp>38 or <36 degrees, blood glucose>7.7mmol/L(not diabetic)
Not good at separating those who will do badly from those who will do well, overuse of ABx

Question 249

What did the SOFA score describe? Relies on what? What did qSOFA look at?

Answer 249

Sepsis- related organ dysfunction, infection + increase in SOFA score of 2 or more
Blood results not available in most acute circumstances
Just BP/ GCS/ RR- needed interpretation- not as sensitive as SIRS

Question 250

NEWS2 components?

Answer 250

RR, oxygen SATs, breathing air/ supp O2, BP, HR, AVPU, temp(5 or more)

Question 251

Common infections precipitating sepsis?

Answer 251

Pneumonia, urinary tract, abdomen, skin, soft tissue, bone and joint, endocarditis, device-related infection, meningitis

Question 252

Red flag sx of sepsis? If one or more red flags present?

Answer 252

Objective evidence of new or altered mental state, systolic BP<90 mmHg or drop of >40 from normal, HR>130, RR>25, needs O2 to keep SpO2>92%- 88% in COPD, non-blanching rash/ mottled/ ashen/ cyanotic, recent chemo, not passed urine in 18 hours(<0.5ml/kg/hr if catheterised)
SEPSIS 6+ consultant review: blood cultures (before ABx if possible,) urinary output(catheter,) IV fluids, IV ABx, lactate (VBG,) O2 keep to 94-98% or 88% in COPD- complete within 1 hour of red flag sepsis recognition

Question 253

If lactate>4mmol/l or SBP<90 in sepsis do what? Lactate 2-4mmol/L? <2mmol/L? If no improvement?

Answer 253

IV fluid 500ml over less than 15 minutes
500ml IV fluid <15 minutes
Consider IV fluids, consultant to attend

Question 254

Amber flags for sepsis?

Answer 254

Relatives concerned about mental status, acute deterioration in functional ability, immunosuppressed, trauma/ surgery/ procedure in last 8 weeks, RR 21-24, systolic BP 91-100mmHg, HR 91-130 or new dysrhythmia, temp <36 degrees, clinical signs of wound infection

Question 255

If 2 amber flags for sepsis or SBP 91-100mmHg? If lactate>2 or AKI, treat as what? If only one yellow flag criteria or normal lactate and no AKI? No what when prescribing IV fluids?

Answer 255

Blood cultures, FBC, U&E, LFT, coagulation screen, CRP, lactate + glucose on VBG, review within one hour
Red flag sepsis
Repeat assessment of patient and senior review within 3 hours
Colloids or glucose containing fluids

Question 256

Clinical sx of monkeypox? DDx?

Answer 256

D1-5: fever, headache, back pain, muscle aches, lethargy and lymphadenopathy
Then 1-3 days after fever subsides–> rash: macules, papules, vesicles, pustules, umbilication before crusting over and desquaming over a period of 2-3 weeks(sequential stages)
HSV, VZV, orf, moluscum, erythema multiforme etc

Question 257

Tx of monkeypox? COMPS? If genital lesions?

Answer 257

Mostly isolation, 21 days or until complete resolution of all lesions- scabs fall off and intact skin, Imvanex vaccination (i.e. smallpox) + post/ pre exposure prophylaxis, cidofovir and brimcidofovir, tecovirimat, vacinia immunoglobulin
Pain relief, simple analgesia, topical analgesia
Secondary bacterial infection- cellulitis, perforations etc
Refer to GUM

Question 258

What is a probable case of monkeypox?

Answer 258

Anyone with an unexplained rash or lesion on any part of their body or proctitis and who has epidemiological link to a confirmed probable or highly probable case of monkeypox in the 21 days before sx onset or identifies as a gay, bisexual or GBMSM or has had one or more new sexual partners in the 21 days before sx onset

Question 259

What is essential to check on pre-op assessment of gallstones? Blood tests? Imaging?

Answer 259

Whether on blood-thinning medications
Clotting, FBC, LFTs, U&Es, lipase
ERCP, MRCP, USS

Question 260

Scan for bowel obstruction? How sensitive is lipase for pancreatitis? What isn’t as sensitive?

Answer 260

CT scan
98%, amylase

Question 261

Imaging for possible gallbladder cancer? 3 tubes for SBO?

Answer 261

CT scan, biliary tree= MRI
NG tube, IV fluids, catheter, NBM

Question 262

Blood tests for GI conditions? Stool tests?

Answer 262

LFTs, FBC- Hb, increased platelets may indicate inflammatory process, U&Es, coeliac serology- TTG & NOT endomysial antibodies, IgA, blood cultures- pyrexial, inflammatory markers, X match in acute emergencies
FIT test(faecal immunochemical test)- colon cancer, when suspicion is low, reassured if negative, faecal calprotectin- can be reassured if -ve, +ve–> colonoscopy, h.pylori, stool M, C & S

Question 263

When are further investigations needed for GI conditions?

Answer 263

Dysphagia, blood loss, weight loss, nocturnal sx, age>45 y/o, family hx of IBD/ GI cancer, acutely unwell
Examination: jaundice, abnormal mass, lymphadenopathy
Labs: deranged bloods- unexplained anaemia, LFTs, CRP, positive coeliac serology, raised faecal calprotectin, raised FIT

Question 264

DDx for oesophageal cancer? Ix for oesophageal cancer?

Answer 264

Structural disorder- benign stricture, reflux oesophagitis, motility disorder- aperistalsis, achalasia, oesophageal spasm
Bloods- FBC, LFT, U&Es, urgent upper GI endoscopy, CT CAP, refer to upper GI cancer MDT–> surgery, radiotherapy, chemo, palliative

Question 265

What should you do for someone with an upper GI bleed? How to manage?

Answer 265

A PR exam, FBC, U&Es, LFTs, cross-match
Endoscopy, IV PPI, resus, on-call gastroenterologist for urgent upper GI endoscopy

Question 266

What do you give terlipressin for? CI in who? Alternative? Tx for functional dyspepsia?

Answer 266

Variceal bleeds, IHD + PVD, ocreotide
Healthy diet, PPI, antispasmodics, neuromodulators e.g. low dose amitriptyline, self referral to IAPT

Question 267

If microcytic anaemia and positive coeliac serology, do what? If raised platelets, elevated CRP and positive faecal calprotectin? Tx for acute UC?

Answer 267

Duodenal biopsy
Colonoscopy
Steroids, maintain remission= aminosalicylates, immunomodulators- azathioprine/ methotrexate/ anti-TNF
Colonic surgery, advice smoking cessation

Question 268

Causes of hepatitis? Ix? Tx?

Answer 268

Alcoholic liver, NAFLD, viral causes, paracetamol poisoning, A1ATD
Non-invasive liver screen, US abdomen, unknown aetiology= invasive liver biopsy
Thiamine deficiency= IV Pabrinex–> oral thiamine, sedatives for withdrawals= chlordiazepoxide/ lorazepam

Question 269

What is needed for a diagnosis of DKA?

Answer 269

Ketonaemia>3.0mmol/L or significant ketonuria>2+ on standard urine sticks, blood glucose>11.0mmol/L or known diabetes mellitus, bicarbonate(HCO3)<15.0mmol/L and or venous pH<7.3
Can occur in T2D

Question 270

What happens to potassium during DKA? Give what to correct also? Elderly become prone to what and young people? Also high risk of what?

Answer 270

Deficit- want to maintain between 4.0 and 5.5mM
Fixed rate IV insulin infusion
Pulmonary and cerebral oedema
DVT

Question 271

Measure what instead of arterial bicarbonate and pH? Why give SC long-acting insulin instead of IV in DKA?

Answer 271

Venous

Question 272

Emergency more in T2DM? Ix? What can occur?

Answer 272

Hyperosmolar hyperglycaemic state
Hypovolaemia plus marked hyperglycaemia without significant ketonaemia or acidosis
Mixed DKA/ HHS

Question 273

Ix HHS? Tx? High risk of what? Tx targets?

Answer 273

IV access, FBC, U&E, LFT, clotting, CRP, CXR, urine C+S, BC, lab glucose, VBG, IV 0.9% NaCl, IV insulin only when blood glucose no longer falling with IV saline
Aim for +ve fluid balance of 3-6L by 12 hours
Encourage food and drink ASAP
Assess for cerebral and pulmonary oedema
DVT, foot ulcers
Fall in sodium no more than 10mM in 24 hours, fall in blood glucose no more than 5mM/ hour, measure osmolality frequently

Question 274

Clues of bilateral adrenal haemorrhage(acute adrenal insufficiency)? Tx?

Answer 274

High eosinophils, K+, urea, low Na+
Hydrocortisone 100mg IV stat…

Question 275

Sodium of 103mmol/L- severe hyponatraemia? Tx to reduce swelling on brain? If sodium brought up too quickly?

Answer 275

170ml 2.7% hypertonic saline over 20 minutes, VBG + serum sodium immediately following this
Osmotic demyelination syndrome- can lead to paralysis

Question 276

Sign of severe hypercalcaemia?

Answer 276

Short QT interval

Question 277

What is euglycaemic ketoacidosis?

Answer 277

Characterised by ketoacidosis and and relatively lower blood glucose (less than 11mmol/L)

Question 278

How should fractures of the distal radius be assessed? If manipulation is indicated, it should be undertaken using what? Open fractures should undergo what? Referred to the Fracture Clinic service and assessed when?

Answer 278

Using posteroanterior and lateral views centred at the wrist
Regional anaesthesia as opposed to local haematoma block
Surgical debridement and stabilisation in accordance with BOAST Open Fractures
Within 72 hours

Question 279

Patients with a stable fracture of the distal radius should be considered for what? When using a plaster cast to treat a distal radius fracture, the wrist should be in what? Consider removing the cast and starting mobilisation how long after the injury?

Answer 279

Early mobilisation from a removable support once pain allows
Neutral flexion with 3 point moulding + not forced palmar flexion
4 weeks

Question 280

In patients 65 y/o or older, non-operative tx can be considered as primary tx for what unless there is what? In <65 y/o, consider what when assessing whether they’d benefit from surgical reconstruction?

Answer 280

Dorsally displaced distal radius fractures unless there is significant deformity or neurological compromise
Ulnar variance, intra-articular step, dorsal tilt and the patient’s needs

Question 281

Volar displaced fractures are unstable and should be considered for what? When surgical fixation is indicated for dorsally displaced distal radius fractures, offer K-wire fixation if what? If not possible consider what?

Answer 281

Open reduction and plate fixation
Displacement of the radial carpal joint can be reduced by closed manipulation
Open reduction and internal fixation

Question 282

If surgical intervention is performed for distal radius fractures, should be performed within how long for extra-articular and intra-articular fractures? When operative tx is indicated for re-displacement following manipulation, surgery should be done within how long?

Answer 282

72 hours, 1 week
72 hours

Question 283

Repeat radiographs of the wrist how long after injury where it’s thought that the fracture pattern is unstable and subsequent displacement will lead to surgical intervention? Radiograph at time of removing immobilisation is not required unless what? Assess for what? Referred to who? Given info for what?

Answer 283

1-2 weeks
There is clinical cause for concern
Falls risk and bone health, fracture liaison services and/ or falls service
Expected functional recovery and rehab, advice about return to normal activities

Question 284

For patients who cannot weight-bear and who may have a hip fracture, they should be offered what if AP pelvis and lateral hip XR are negative?

Answer 284

MRI- not available within 24 hours/ CI- consider CT

Question 285

Pain relief for 16 y/o and over for non-complex fractures? <16 y/os?

Answer 285

Oral paracetamol for mild pain, oral paracetamol and codeine for moderate pain, IV paracetamol with IV morphine for severe pain, IV opioids in frail/ older adults
Oral ibuprofen or oral paracetamol or both for mild-moderate pain, intranasal or IV opioids for moderate-severe pain

Question 286

Type of splint pre-hospital with suspected long bone fractures above the knee? All other? <16 with suspected displaced femoral fractures?

Answer 286

Traction splint/ adjacent leg as a splint
Vacuum splint
Femoral nerve block or fascia iliaca block

Question 287

What rules to determine whether an X-ray is needed in people over 5 y/o with suspected ankle fractures? 1st-line imaging in people with suspected scaphoid fractures? Don’t use what in torus fractures?

Answer 287

Ottawa ankle and foot rules
MRI
A rigid cast

Question 288

Tx of unimalleolar ankle fractures? When to do surgical tx?

Answer 288

Immediate unrestricted weight-bearing as tolerated
Ortho follow-up within 2 weeks if uncertainty about stability
Not improving - return after 6 weeks
On the day or next day

Question 289

In children with dorsally displaced distal radius fractures who have undergone manipulation, consider what?

Answer 289

Below-elbow plaster cast or K-wire fixation if fracture is completely displaced

Question 290

Tx of displaced low energy proximal humerus fractures?

Answer 290

Offer non-surgical for def tx of uncomp injuries, consider surgery for injuries comp by open wound, tenting of skin, vascular injury, fracture dislocation or split of humeral head

Question 291

Definitive tx of femoral shaft fractures in prematurity and birth injuries? 0-6 months? 3-18 months? 1-6 years? 4-12 years? 11 years to skeletal maturity?

Answer 291

Padded splint
Pavlik’s harness or Gallows traction
Gallows traction
Straight leg skin traction with conversion to hip spica cast to enable early discharge
Elastic intramedullary nail
Elastic intramedullary nails supplemented by end-caps, lateral-entry antegrade rigid intramedullary nail, or submuscular plating

Question 292

Consider advising what for people who have had surgery for distal femoral fractures?

Answer 292

Unrestricted weight-bearing

Question 293

RFs for distal radius fractures? Associated injuries?

Answer 293

Osteoporosis, more females, women>50 y/o- DEXA recommended
DRUJ injuries, radial styloid fractures, soft tissue injuries- TFCC, scapholunate ligament/ lunotriquetral ligament

Question 294

Non-operative tx of distal radius fractures? Operative options? Complications?

Answer 294

Closed reduction and splint/ cast immobilisation
CRPP, ORIF, external fixation
Median nerve neuropathy, ulnar nerve neuropathy, EPL rupture, FPL fracture, radiocarpal arthrosis, malunion/ nonunion, ECU/ EDM entrapment, compartment syndrome, RSD/ CRPS

Question 295

Examples of traditional hazards? Modern hazards?

Answer 295

Related to poverty and insufficient development e.g. lack of safe drinking water, sanitation, indoor air pollution, inadequate waste disposal, vector control

Related to development that lacks health and environmental safeguards, & to unsustainable consumption of natural resources e.g. environmental contamination, urban air pollution, climate change

Question 296

What is planetary health? Planetary boundaries?

Answer 296

The health of the world’s population and the planetary resources on which it depends on
Biosphere integrity, climate change, stratospheric ozone depletion, atmospheric aerosol loading, ocean acidification, biogeochemical flows e.g. nitrogen and phosphorous–> aquatic deadzones, freshwater use, land-system change

Question 297

Direct, ecosystem mediated and socially mediated effects of global environmental change?

Answer 297

Heat and extreme events
Emerging infectious diseases, vector borne diseases, water borne diseases, impact on food supply and undernutrition
Poverty, migration and conflict

Question 298

Lost 33% arable land to what in the last 40 years? Especially what fields? Losing soil 10-100x faster than what? World per capita cereal production lags behind what, not including what?

Answer 298

Erosion and pollution
Ploughed fields
Soil formation
Cereal production- biofuels

Question 299

What test also if testing for glandular fever? Resources?

Answer 299

HIV test
ABC of Sexually Transmitted Infections

Question 300

Delirium acronym?

Answer 300

Drugs
Electrolyte disturbance
Low O2 levels
Infection
Reduced sensory input
Intracranial
Urinary retention/ constipation
Metabolic

Question 301

PINCH ME mnemonic for delirium?

Answer 301

Pain, infection, nutritional compromise, constipation, hydration, medication, environmental

Question 302

CHIMPS PHONED delirium mnemonic?

Answer 302

Constipation, hypoxia, infection, metabolic disturbance, pain, sleeplessness, prescriptions, hypothermia/ pyrexia, organ dysfunction,, nutrition, environment, drugs

Question 303

5 Ps delirium?

Answer 303

Pain, pee, pills, poo, pus

Question 304

Scores for assessing delirium risk?

Answer 304

RASS- ITU
4AT score
CAM-ICU(critical care)- fluctuation
AMT 10
MoCA
AVPU>GCS, BMs, ketones

Question 305

Delirium info gathering?

Answer 305

Review meds, bloods, collateral from staff/ family

Question 306

What is included in a confusion screen?

Answer 306

FBC, U&Es, LFTs, INR, TFTs, calcium, B12 & folate/ haematinics, glucose, blood cultures, urinalysis, CXR

Question 307

When should a CT head be done in delirium?

Answer 307

Reduced level of consciousness not explained by another cause, hx recent falls, head injury, anticoagulation therapy

Question 308

Non-pharm tx delirium?

Answer 308

Orientation, ensuring have sensory aids, sleep hygiene, mobilisation, pain control, nutrition and hydration, manage retention and constipation, involve family

Question 309

Pharm tx delirium (avoid)?

Answer 309

Haloperidol (oral/ IV/ IM)
2nd line- lorazepam

Question 310

Things to consider when classifying fractures? Depends on location and characterisation according to what?

Answer 310

Displacement
Angulation
Shortening
Rotation
Direction of fracture line, relationship of bone fragments involved, number of fragments involved- simple or comminuted, exposure to outside air- open/ closed

Question 311

Type of distal radius fractures?

Answer 311

Colles- extrarticular with dorsal angulation
Smith- extrarticular with volar angulation
Barton- intraarticular involving radial rim & dislocation of radio-carpal joint

Question 312

Non-op management of fractures?

Answer 312

Reduction- manipulation, stabilisation- plaster/ splint, manipulation under haematoma block/ biers block, reverse the injury pattern, hold reduction with back slab application, complete plaster cast after 1-2 weeks

Question 313

Scoring system predicting 30-day mortality for patients after hip fracture? 7 predictors?

Answer 313

Nottingham Hip Fracture Risk score
Age, number co-morbidities, admission, Hb concentration, living in an institution, presence malignant disease

Question 314

What is Degarelix? Zoladex(Goserelin)? When does testosterone drop within hours? What if Leuprorelin is used?

Answer 314

GnRH receptor antagonist
LHRH agonist
Following bilateral orchidectomy using Degarelix
Within 3 weeks

Question 315

When to give Dexamethasone?

Answer 315

In the morning–> agitated at night otherwise

Question 316

Anyone over the age of 40 with visible haematuria would have what? How does Finasteride affect PSA levels?

Answer 316

Flexi cystoscopy and CTIVU
Halves it

Question 317

Score for LUTS?

Answer 317

IPSS score- also frequency volume chart, post void residual volume

Question 318

Comps of poor bladder emptying? In UTIs of post menopausal ladies check what? In others?

Answer 318

Ob uropathy–> renal failure, bladder stones
Oestrogen levels
Self start ABx/ post-coital/ prophylaxis

Question 319

Ix for kidney stones?

Answer 319

U&Es, calcium, uric acid, exclude sepsis, CT- triple AAA

Question 320

Variable rate IV insulin infusions (VRIII) always accompanied by what? (temporary and aim to step off ASAP)

Answer 320

An infusion of fluid containing glucose and potassium- 0.45% NaCl with 5% glucose and 20 or 40 mmol KCl- prevent hypokalaemia

Question 321

When to use VRIII?

Answer 321

Patients with known diabetes unable to take oral food and own insulin regime not possible
Vomiting- exc DKA/ HHS
NBM- miss more than one meal, severe illness

Question 322

With VRIII, review CBG how often?

Answer 322

Hourly, review need for VRIII daily, hep/ renal impairment- use insulin sensitive regime
Daily U&Es & fluid status

Question 323

Fluid rate with VRIII?

Answer 323

No concern fluid overload- 125ml/ hour, concern- 83ml/ hour, elderly/ frail- 10% glucose at 42ml/ hour

Question 324

Things to do when VRIII running?

Answer 324

Stop OHAs, short-acting insulins, pre-mixed insulins
Continue long-acting and basal insulins- don’t worry about hypos

Question 325

When to come off VRIII?

Answer 325

ASAP
Normal biochem, eating and drinking
Give next meal-related long-acting insulin, wait an hour and remove VRIII (IV insulin only half-life 5 minutes)
Restart all other diabetic meds- review meds & doses

Question 326

Managing hypoglycaemia?

Answer 326

Conscious & orientated- Lucozade etc
Conscious, confused w/IV access- 200mls 10% glucose over 10 mins
W/O IV access= 1mg IM Glucagon
Unconscious, fitting, unable swallow- same as above

Question 327

Tx hypoglycaemia? Common culprits?

Answer 327

QDS BM monitoring
Make note time of hypo, oral intake, meds prior to hypo
Insulins, sulfonylureas, meglitanides- may need to be omitted or have doses reduced

Question 328

Do not do what in type 1 diabetics?

Answer 328

OMIT INSULIN- continue at a reduced dose and contact diabetes team if in doubt
Relatively safe in T2DM

Question 329

How does metformin work? SEs?

Answer 329

Biguanide activates AMP kinase in the liver reducing gluconeogenesis and increasing insulin sensitivity- ideal for overweight patients
Diarrhoea, vomiting, lactic acidosis- stop prior to IV radiology contrast due to risk of renal failure

Question 330

Medications that help to secrete insulin?

Answer 330

Sulfonylureas- bind to ATP-sensitive K+ channels on Beta cells and close them–> Ca2+ influx

Meglitanides- both can lead to weight gain and hypos (sulf >met)
Stop if hypos

Question 331

How do thiazolidediones work? SEs and when to stop?

Answer 331

Glitazones- inhibit the gene PPAR-gamma nuclear receptor regulates genes for lipid metabolism and insulin action- reduce hepatic glucose production and enhance peripheral glucose uptake
Weight gain, fluid retention, HF, increased risk bladder ca
Acute fluid overload and known/ suspected bladder cancer

Question 332

Incretin effect (oral response> IV glucose) mediated by what two peptides?

Answer 332

GLP and GIP–> insulin secretion

Question 333

What do GLP1 agonists do? SEs and stop when? how do DPP-4 inhibitors work?

Answer 333

Increase incretin effect
Pancreatitis, AKI
Inactivate GLP-1
Nausea, pancreatitis

Question 334

How do SGLT-2 inhibitors work? SE and when to stop?

Answer 334

Blocking Na-dependent glucose transport protein in proximal renal tubules whose function= resorb glucose- mild diuretic
Increased genital candidiasis & UTI risk, held on admission due to risk of ETA

Question 335

Criteria for GLP-1 therapy if triple therapy not effective or CI?

Answer 335

W/ metformin and sulfonylurea if:
BMI>35 and other obesity related problems HTN, CKD
BMI<35 and insulin would have serious occupational implications or not tolerated
Insulin if HbA1C>58 after 3m dual oral therapy- intermediate i.e. Humulin I

Question 336

Who needs insulin? How is total daily dose calculated?

Answer 336

T1 diabetics, anyone presenting in DKA, OHAs= proving insufficient to control blood glucose
1) Total number units over 24h on VRIII
2) 0.5 units/ kg- intentionally underestimate to avoid hypos
3) Starting small dose= 6-8 units for long-acting/ mixed or 4-6 units for short-acting with meals

Question 337

Who is long-acting insulins good for? Mixed BD? Basal-bolus?

Answer 337

Those who can produce insulin still- T2DM- need extra boost
2x injections with breakfast and dinner- T2DM with hyperglycaemia after meals
4-5 injections for T1DM, long-short acting 50/50W

Question 338

When are pre-mixed insulins taken?

Answer 338

With meals and never at bedtime

Question 339

Symptom mechanisms to aid explanation for medicallyunexplained symptoms?

Answer 339

Central sensitisation, dissociation, brain-body signalling

Question 340

2 types of reassurance?

Answer 340

Affective- generic, engages emotions, often no further Qs, transient, relief
Cognitive- specific, engages thoughts, further Qs, sustained, assurance

Question 341

4- step approach to dealing with persistent physical sx?

Answer 341

Recognition- actively listening & acknowledging sx and concerns, Explanation- cognitive reassurance & plain language
Action- self management, medication & safety netting
Learning- acute tx, ongoing management (REAL)

Question 342

Approach to CXRs?

Answer 342

Ramble, quality- RIPE, lines/ devices, ABCDE, summarise
Airway, breathing spaces, cardiac/ circulation, diaphragm, evil areas- apices, bones/ tissue, cardiac- behind, devices, everything

Question 343

What is LUL in contact with? Lingula? LLL?

Answer 343

Aortic knuckle
Left heart border
Left hemidiaphragm

Question 343

RIPE for quality of CXR?

Answer 343

Rotation- clavicles or anterior ribs
Inspiration- 5-7 anterior ribs in mid-clavicular line, 2 domed hemi-diaphragms
Picture- apices to costophrenic angles, side to side
Exposure- spinous processes, pedicles, bone vs soft tissue

Question 344

What do air bronchograms tell us on a CXR? What does the right lower lobe come into contact with? Right middle lobe? RUL?

Answer 344

Alveoli filled with blood, pus or other material
Right hemi-diaphragm
Right heart border
Right paratracheal stripe

Question 345

What can consolidation be on a CXR?

Answer 345

Pneumonia, pulmonary oedema, pulmonary haemorrhage(look same)
Cancer- persists on repeat CXR 6-8 weeks

Question 346

Opacity, meniscus, uniform density without air bronchograms?

Answer 346

Pleural effusion

Question 347

What are transudates? Exudates? pH for empyema?

Answer 347

Fluid in wrong place
Inflammation
pH<7.2

Question 348

Continuous pleural effusion causes?

Answer 348

Loculated- between fissures/ pleura
Empyema

Question 349

What should an NG tube do on CXR?

Answer 349

Bisect the carina, pass below the diaphragm- tip seen below left hemidiaphragm

Question 350

Common drugs causing exanthematous rashes? Onset?

Answer 350

Antibiotics, sulfonamides, allopurinol, anti-epileptics and NSAIDs
4-14 days

Question 351

Common drugs causing and onset of urticarial drug eruptions? Tx?

Answer 351

Penicillins, NSAIDs or sulfamethoxazole in combination with trimethoprim
Minutes- hours
Oral- 2nd-generation antihistamine- cetirizine, loratadine

Question 352

Features of anaphylactic drug eruptions? Onset? Tx?

Answer 352

Pruritus, urticaria, angioedema
Minutes- hours
Adrenaline may not be needed in skin manifestations alone- antihistamines may be all that is required

Question 353

Onset of AGEP (acute generalised exanthematous pustulosis)? Most common cause?

Answer 353

<4 days
Beta-lactam antibiotics- penicillins and cephalosporins
Also other ABx, oral antifungals, CCBs, hydroxychloroquine, carbamazepine, paracetamol

Question 354

Onset of DRESS (drug hypersensitivity syndrome)? Onset of SJS? TEN?

Answer 354

15-40 days
7-21 days
Up to a month

Question 355

Other patterns of drug eruptions?

Answer 355

Psoriasiform, eczematous, lichenoid, lupus, fixed drug eruption, vasculitic, bullous, phototoxic, skin necrosis, acneiform, hyperpigmentation, nail changes

Question 356

Characteristics of drug eruptions?

Answer 356

Type of lesions- urticaria, papule, pustule, distribution and # of lesions, mucous membrane involvement- eyes/ mouth/ genitals, associated signs- fever, pruritus, lymph nodes, visceral involvement

Question 357

Red flags of skin eruptions?

Answer 357

Mucosal involvement, blistering/ skin peeling off, pain, lymphadenopathy, systemic upset- fever, abnormal LFTs, U&Es

Question 358

Chronological factors for skin eruptions?

Answer 358

Documentation of all drugs and dates administered- OTC and complementary
Date of eruption
Drug time-line
Response to removal suspected agent
Response to re-challenge

Question 359

Tx mild drug eruptions?

Answer 359

Withdrawal, emollients, topical corticosteroids in short-term, urticaria= antihistamines, specialist review if more serious suspected

Question 360

TEN or SJS more severe? Caused by? Erythema multiforme caused by what? 100x more common in ass w/ what?

Answer 360

TEN> SJS in severity
Drugs
Infections
HIV

Question 361

Most common causes of SJS/ TEN?

Answer 361

Allopurinol, carbamazepine, lamotrigine, nevirapine, NSAIDs, phenobarbital, phenytoin, sulfamethoxazole, sulfasalazine

Question 362

Sx of SJS/ TEN? Mucosal involvement? Systemic sx? Detachment % BSA?

Answer 362

Prodrome resp sx, fever, PAIN
Dusky red lesions, atypical targets, erythematous plaques
Yes for both
Usually in SJS, always in TEN
SJS= <10%, TEN>30%

Question 363

Severity of illness score for TEN?

Answer 363

SCORTEN

Question 364

Tx of TEN/ SJS?

Answer 364

Withdraw meds
Support–> ICU/ burns unit
Correct fluid and electrolytes
Caloric replacement
Topical ABx
Ophthalmology consult
Urology if urethral
Oral antacids
Resp syndrome–> pulmonary toilet
Periodic cultures mouth, eyes, skin sputum
Physical therapy
Biological dressings- paraffin

Question 365

Sx of DRESS? Tx?

Answer 365

High fever, morbilliform eruption, lymphadenopathy, atypical lymphocytes, eosinophilia, internal organ involvement
Withdrawal of drug, systemic steroids severe
Dressings
Topical corticosteroids
Emollients
Oral antihistamines
Address fluid status, electrolytes, temp, nutrition
Tx secondary infection

Question 366

Sx of AGEP? Tx?

Answer 366

High fever, small sterile pustules within larger areas oedematous erythema, oedema
Leucocytosis with elevated neutrophils
Pustular psoriasis can look similar
Withdrawal drug, topical corticosteroids, emollients, antihistamines

Question 367

Causes of erythroderma(widespread reddening of skin)? Hx?

Answer 367

Dermatitis, psoriasis, drug eruptions
Hx of inflammatory skin disease, personal & family hx of atopy, detailed drug hx, withdrawal of corticosteroids

Question 368

Examination of erythroderma?

Answer 368

Pre-existing psoriatic plaques
Nail changes
Severe pruritus
Lichenification
Original distribution
Lymphadenopathy
Islands of sparing

Question 369

Ix for erythroderma?

Answer 369

FBC U&Es, LFTs, CRP, total IgE, blood film, consider skin biopsy, consider LN Ix- histology, flow cytometry and T-cell receptor gene analysis

Question 370

Tx erythroderma?

Answer 370

Stop meds
Monitor and tx BP, HR, fluid and electrolytes, temp
Wet wraps/ dressings and emollients
Tx underlying dermatosis- may need systemic tx, topical corticosteroids

Question 371

Causes of drug induced SLE and SCLE?

Answer 371

Procainamide, hydralazine
CCBs, ACE-i, antifungals, PPIs, antiepileptics, biologics

Question 372

Causes of acneiform eruptions?

Answer 372

ABx, steroids, hormones, halogens, immunosuppressants, lithium, anticonvulsants, EGFRIs, vitamins B1, B6 and B12

Question 373

Urgent referral to Derm when?

Answer 373

Systemically unwell, mucosal involvement, blistering, suspected TEN/ SJS, DRESS/ AGEP

Question 374

Discuss with Derm?

Answer 374

Lymphadenopathy, pyrexia, eosinophilia, abnormal LFTs

Question 375

Tx MP rash? Urticarial rash?

Answer 375

Absence systemic sx- stop drug, emollients and topical corticosteroids, discuss with Derm if not improving after 48 hours tx

Stop drug, non-sedating antihistamine, monitor and discuss with Derm if not improving after 48 hours tx

Question 376

What is SSSS?

Answer 376

Detachment of epidermis due to exotoxin release from specific strains of s.aureus
Children<5 y/o
Initial infection ears, eyes, throat, localised wounds
Localised S.aureus infection, exfoliative toxins A and B bind to desmoglein-1
MUCOSA UNAFFECTED

Question 377

Comps of SSSS?

Answer 377

Scarring, loss of bodily fluids–> dehydration and electrolyte imbalance, hypothermia, sepsis, cellulitis, pneumonia, renal failure

Question 378

Tx SSSS?

Answer 378

ABCDE approach
Swabs
BCs
Skin biopsy
IV fluids
IV ABx
Pain relief
Skin care- 50/50, non-adherent dressings

Question 379

Most common AI sub-epidermal blistering disorder? Target protein? Ix? Tx?

Answer 379

Bullous pemphigoid
Elderly
Tense intact blisters
Attack on basement membrane of epidermis by IgG +/- IgE IgGs and activated lymphocytes
BP180 or BP230
Skin biopsy + direct immunoflurescence
Steroids

Question 380

What is pemphigus vulgaris?

Answer 380

AI blistering skin disease and mucous membranes
Most common age= 30-60, Jews and Indians
Paraneoplastic and drug induced subtypes

Question 381

What is pemphigus vulgaris? Tx?

Answer 381

IgG autoantibodies to desmoglein 3 +/- 1 found on desmosomes
Superficial intraepidermal blisters
Mucosal involvement
Ix= skin biopsy and direct immunoflurescence
Steroids

Question 382

What does diclofenac increase risk of?

Answer 382

MIs and CVA

Question 383

More potent xanthine oxidase inhibitor? Aim for uric acid tx?

Answer 383

Febuxostat- if intolerant, can’t achieve control 80mg–> 120mg
Colchicine first 2 months
<300micromol/ L
100mg and increase every 2-4 weeks, lifestyle modifications

Question 384

DMARDs take how long to work? Bridge between? Next step? Routes?

Answer 384

8w, steroids, biologics
oral, IM, intra-articular, IV

Question 385

How do corticosteroids work?

Answer 385

Reduce # and activity leucocytes, proliferate blood vessels, activate mononuclear cells, production cytokines, histamine release

Question 386

SEs steroids?

Answer 386

Sleep and mood disturbance, psychosis, skin- Cushing’s, neuropathy, HTN, osteoporosis, myopathy, diabetes, suppress steroid production, increase in infections, cataracts, growth retardation

Question 387

Avoiding SEs of CSs?

Answer 387

Modify of dose, steroid sparing drugs, withdraw slowly, dose OD and in morning, prophylactics if possible, product locally, CIs, education

Question 388

How do DMARDs work?

Answer 388

Inhibit cytokine cascade

Question 389

SEs of DMARDs?

Answer 389

Bone marrow suppression, abnormal liver enzymes, nausea, diarrhoea, hair loss, mouth ulcers, teratogenic
FBC, U&Es and LFT monthly then every 3m

Question 390

Leflunomide SEs? SEs sulfasalazine?

Answer 390

Monitor BP for HTN and GI SEs
Severe rash and neutropenia

Question 391

Anti-TNF meds end in -MAB are what? Ept? Tociluzimab?

Answer 391

-MAB= monoclonal antibodies
Decoy TNF receptor
IL-6 inhibitor- closely related to CRP for iron, thrombosis
Works best on own rather than other meds
Can increase lipid profile

Question 392

E.g. of JAK inhibitors?

Answer 392

Baricitinib/ tofacitinib

Question 393

What is rituximab?

Answer 393

Anti-B cell antibody for RA, SLE, myositis, ANCA+ vasculitis
Every 6-18 months
Reduce antibody response to vaccines

Question 394

Abatacept?

Answer 394

Anti T-cell tx