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*year 5 > 4) infection, MSK > Flashcards

4) infection, MSK Flashcards

1
Q

What is often given to patients during surgery to reduce the risk of post-op infections?

where to find further guidance on this?

A

normally give single dose of one or more ANTIBIOTICS just before or during surgery

which Abx are used depend on the type of surgery an local guidelines

check trust guidelines!!

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2
Q

Locations to look for infection on a post-op patient? 7

A
  • peritonism (ie intra-abdo)
  • wound infection
  • cannula site infection
  • chest infection
  • UTI
  • meningism
  • endocarditis
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3
Q

PYREXIA in post-op patients:

  • possible benign causes? 3
  • investigations to consider? (5 bloods, 2 other, 3 imaging)
  • what non-infection complication should you also check for? 1
A

MILD pyrexia in first 48hrs post-op may be from:

  • atelectasis (needs prompt physio, not Abx)
  • tissue damange / necrosis
  • blood transfusion

HOWEVER have a low threshold for infection screen!!

  • FBC
  • U+E
    (- LFT)
  • CRP
  • blood cultures
  • urine dip
    (-MSU)
  • CXR

(- USS)
(- CT scan)

ALWAYS check for DVT!!!
- can cause a temp!

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4
Q

C. DIFF:

  • what type of colitis does it cause?
  • which CLASSES of antibiotics are highest risk? 3
  • other risk factors? 6
A

pseudomembranous colitis (PMC)

CAUSATIVE ABX

  • cephalosporins
  • macrolides (esp clari)
  • fluroquinolones (anything with ‘floxacin’ - eg ciprofloxacin)

“remember that often start with C for C diff”

  • long hospital stay
  • ITU stay
  • NG tube
  • elderly
  • co-morbidities
  • immnocompromised
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5
Q

SYMPTOMS of C. DIFF

  • how long post-Abx do these tend to occur?
  • main symptoms? 3
A

symptoms typically appear 5-10 DAYS post-Abx therapy

1) WATERY DIARRHOEA
- resolves 1-2 weeks post-Abx
- Varies from asymptomatic carrier (1-3% all adults)→ self limiting → severe + debilitating
- Can be BLOOD stained

2) COLICKY ABDO CRAMPS
3) FEVER w/ Rigors

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6
Q

INVESTIGATIONS for C. DIFF:

  • bedside test to get? 1 (how many times?)
  • important bloods to get? 4
A

1) STOOL SAMPLE (get 3!)

nb this is a stool cyto toxins test - some C Diff produce toxins, others don’t - can also do culture and other fancy tests! - ask micro!

  • FBC (↑↑WCC – 80%, often v.high),
  • ↑↑CRP
  • ↓Albumin (inf/sepsis/protein losing enteropathy)
  • U+Es – essential to determine electrolyte loss

nb consider colonoscopy w biopsy if really severe!! (or think may be a DDx)

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7
Q

C. DIFF:

  • approach if pt critically unwell?
  • antibiotic options? 2 (incl route)
  • additional supportive / nursing management that should also always do? 4
A

A-E approach

1st) ORAL METRONIDAZOLE
2nd) ORAL VANCOMYCIN

nb only indication for oral vancomycin!

nb use both if severe!

nb if asymptomatic may not need abx!

1) STOP causative abx!
2) put pt in side room
3) give fluids (PO + IV) to replace losses
4) inform public health england!!

nb Adjuvant pro-biotics, IV immunoglobulin or rifampacin used in refractory or recurrent C.diff (also Faecal transplant - Colectomy if Toxic megacolon)

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8
Q

DDx for C Diff? 4 (ie watery diarrhoea)

A
  • side effect of Abx (esp macrolides)
  • IBD
  • food poisoning
  • typhoid etc (always askl Travel Hx)
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9
Q

Which Abx is given to treat MRSA? 1

A

Vancomycin

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10
Q

HIV

- four main stages of infection? (just name them - do descriptions on later flashcards)

A

stage 1 = SEROCONVERSION

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11
Q

HIV:

  • how long take to become established in body post-exposure?
  • time scale of seroconversion?
  • 3 main presentations of seroconversion?
A

48-72 hours to become established in body post-exposure

SERO CONVERSION
- transient illness 2-6 weeks after exposure

1) FLU-LIKE symptoms
- headache, fever, malaise, myalgia, pharyngitis

2) EXACERBATION of CHRONIC inflamm conditions
- eg eczema, mouth ulcers, lymphadenopathy

3) MACULOPAPULAR RASH on TRUNK

nb can rarely get meningoencephalitis too

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12
Q

HIV:

  • typical presentation of clinical latency?
  • what may some patients have? 1
A

after initially seroconversion illness, pts are normally ASYMPTOMATIC for a period

30% will have persistent generalised LYMPHADENOPATHY (PGL)
- nb this is nodes >1cm for >3 months

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13
Q

HIV: AIRDS related complex (ARC)

  • what is it considered as?
  • possible systemic symptoms? 4
  • common opportunistic infections/conditions? 10
A

AIDS related complex (ARC) = ↓CD4 + ↑HIV viral load

Regarded as a prodrome to AIDS

SYSTEMIC

  • fever
  • night sweats
  • DIARRHOEA
  • weight loss

OPPORTUNISTIC INFECTIONS

  • TB (most common)
  • candida (norm oesophagus)
  • EBV
  • shingles
  • atypical pneumonia (incl; pneumocystis)
  • cryptococcal meningitis
  • toxoplasmosis
  • kaposi’s sarcoma
  • invasive cervical cancer
  • lymphoma
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14
Q

Stage 4 of HIV infection

  • aka?
  • prognosis if no HAART?
A

aka AIDs (although this name is going out of favour dt stigma! - say serious HIV infection etc)

2 years prognosis if no HAART

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15
Q

What 3 conditions are associated with HIV and should consider testing for HIV if someone presents with them? 3

A
  • Syphilis
  • EBV
  • TB
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16
Q

Who should have a HIV test? 8

A
  • Anyone who requests it
  • All registering in GP where prevalence exceeds 2/1000
  • Sexual intercourse w/ person from high risk country (Africa, middle east, Caribbean)
  • Sexual partner w/ HIV +ve person
  • Homosexual men or MSM
  • IVDU
  • Anyone with STI
  • Anyone with suspicion of HIV as differential
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17
Q

HIV testing:

  • 2 types of point of care tests? 2
  • window period for antigen test?
  • window period for antibody test?
A

POCT

  • self-sampling (blood or saliva)
  • rapid test kit (30 mins)

HIV antigen
- use 2-4 weeks after exposure

HIV antibody
- can use if >4weeks post-exposure

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18
Q

If someone is HIV positive, other things to consider testsing for? 7

A

TB

Hep B+C

Tocoplasma

CMV

Syphilis

other STIs

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19
Q

Management of HIV:

  • mainstay of treatment? 1
  • what should be monitored? 1
  • how to prevent opportunistic infections? 2
A

Highly active anti-retroviral therapy (HAART)

monitor viral load, CD4 count AND FBC every 3 months
- nb do other routine blood tests every 6 months

prevent:

  • vaccines (pneumococcal, fluy, hepatitis, tetanus)
  • prophylactic antivirals and/or antibiotics (if CD4 count is below certain level)
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20
Q

HIV positive mothers:

  • how to reduce risk of transmission to baby?
  • vaginal birth or c-section?
  • breast or bottle feeding?
A

Suppress mums viral load with HAART

Measure viral load @ 36wk

Can have normal vaginal delivery if VL suppressed (<50 copies/ml @ 36 wks)

May require C-Section

Neonate PEP for 4 wks

Avoidance of breast feeding

nb if do all this risk drops from 45% to <1%

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21
Q

When can give PEP to avoid sero-conversion?

A

within 72 hours of exposure

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22
Q

INFLUENZA:

- when is a person with flu infective from and to?

A

infective from 1 day before symptoms to 7 days after symptoms end

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23
Q

INFLUENZA:

- main symptoms? 7

A

Fever

Headache

Malaise

↓Mood

Myalgia

Nausea and Vomiting

Conjunctivitis, eye pain – conjunctivitis ± photophobia

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24
Q

INFLUENZA:

- which four broad groups most at risk of complications? 4

A

Chronic resp disease – COPD, bronchiectasis, CF, interstitial lung fibrosis, asthma

Chronic heart disease – congenital, HF, IHD

CKD or CLD or DM

Immunosuppression

BASICALLY any serious chronic disease or immunosuppression!

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25
Q

INFLUENZA:

  • two main tests? (which norm done)
  • when done?
  • serious DDx which it can be mistaken for? 1
A

PCR – 36hrs

Nasopharyngeal swab culture – takes 1 wk

test if unwell in hospital or unclear over diagnosis

can mimic MENINGITIS with fever, phtophobia, generally unwell etc (also Covid….)

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26
Q

INFLUENZA:

  • symptomatic medication to advise for everyone? 1
  • who can consider giving antivirals to? when to give them?
A

PARACETAMOL for all!

(also fluids and bed rest)

Antivirals – Oseltamivir – if ALL of the following apply

1) Person is an at risk group
2) National surveillance scheme indicates flu is circularting
3) Person can start Rx within 48hrs of Sx onset

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27
Q

MUMPS:

  • type of virus?
  • prevention? (when?)
A

highly infectious RNA Paramyxovirus illness spreads via droplet infection

MMR vaccine

  • 1 year
  • 3 years 4 months
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28
Q

MUMPS

  • symptoms of prodrome? 3
  • main feature? 1 (+ 4 associated symptoms)
  • how diagnose? 1
A

PRODROME

  • Fever
  • malaise
  • myalgia

PAROTITIS
– swelling of parotid glands begins U/L → B/L

  • Painful swelling
  • causes ear ache or pain whilst eating
  • Dry mouth (salivary glands become blocked)

Clinical diagnosis is often adequate ☺

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29
Q

MUMPS:

- possible complications? 4

A

ORCHITIS in males → infertility: 50% of post-pubertal males (nb uncommon in pre-pubertal boys)

  • Chills, sweats, headache, backache, swinging fever
  • Severe local testicular pain + tenderness (U/L common)
  • Swollen scrotum – testes may be impalpable

Hearing loss – U/L and transient

Acute Pancreatitis (4%) or Myocarditis –

Meningitis (15%) – usually mild and self-limiting

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30
Q

MUMPS:

- management? (1 if in hospital, 2 if anywhere)

A

isolation (if in hospital)

  • fluids + nutrition
  • paracetamol

(can give antivirals if severe!)

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31
Q

RUBELLA

  • prodrome? 1
  • describe rash?
  • associated symptoms? 2
  • feature common in older pts? 1
A

Prodrome = Low grade fever

MACULAR RASH
– pink discrete on face → coalesce whole body (fades after 3-5d)

Forcheimer spots – red spots on palate of mouth

Lymphadenopathy – post-auricular, sub-occipital, cervical

Arthralgia – in older patients (common)

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32
Q

RUBELLA:

  • how diagnose?
  • gold-standard test? 1
  • management? 3 (2 for pt, 1 Q re contacts)
A

Diagnosis is unreliable as Sx are fleeting and mimicked by other viruses

Serology ± PCR testing of saliva = gold standard, detect IgM +ve

  • fluids + nutrition
  • paracetamol
  • ask about contact w pregnant women!
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33
Q

RUBELLA:

  • main complication? 1
  • other complication? 1
A

FOETAL DAMAGE – teratogenic during 1st 8-10 wks

  • encephalopathy (6 d post rash)
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34
Q

If someone presenting with diarrhoea, what 3 questions should you always ask them (about risk factors) to narrow down cause?

A
  • any foreign travel?
  • any new foods?
  • any recent Abx? (or other meds changes)
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35
Q

INFECTIVE GASTROENTERITIS:

  • seasons most common in? 2
  • risk factors? 4
A

winter + spring

  • poor hand hygiene
  • undercooked food
  • travelling
  • immunocmpromised

(also recent Abx for C diff)

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36
Q

INFECTIVE GASTROENTERITIS:

  • most common cause in adults? 1
  • most common cause in children? 1
  • other viral cause?
  • bacterial causes? 4
A

Norovirus (adults)

Rotavirus (child)

Adenovirus (10-15%)

BACTERIAL CAUSES (rare)

  • campylobacter
  • E.coli
  • salmonella
  • cholera
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37
Q

INFECTIVE GASTROENTERITIS:

  • two main symptoms?
  • duration of each of these?
  • what other features to ask about? 3
A 
WATERY DIARRHOEA  (lasts 5-7 d, resolves in 2 wks)
- ↑Frequency + Loose consistency

VOMITING
(lasts 1-2 d, resolves in 1 wk)
- Causes dehydration

stomach cramps

fever

blood or mucus in stools

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38
Q

Infective gastroentertis: what examining for on physical exam?

A

signs of DEHYDRATION

Sunken eyes, ↓skin turgor, ↓exhaustion, ↓Urine output (not weeing),↑HR (weak), ↓BP, ↑CRT

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39
Q

What is dysentry?

A

Dysentery is ANY infection of the intestines that causes diarrhoea containing BLOOD or MUCUS

can also get fever, vomiting and stomach cramps

nb norm bacterial cause!

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40
Q

INFECTIVE GASTROENETERITIS:

  • causes of bloody diarrhoea? 3
  • cause of ‘rice water stools’? 1
A

CAUSES OF BLOODY DIARRHOEA

  • shigella
  • campylobacter
  • E.Coli 0157

‘rice water stools’ = CHOLERA

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41
Q

INFECTIVE GASTROENTERITIS:

  • when to send a stool culture? 6
  • when to admit a patient? 2
A

SEND STOOL CULTURE IF:

  • blood OR mucus in stools
  • been abroad
  • immunocompromised
  • septicaemia
  • diarrhoea not improved in 7 days
  • uncertain over Dx

admit pt if:

  • patient is septic
  • patient is severly dehydrated
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42
Q

INFECTIVE GASTROENTERITIS:

  • mainstay of management? 1
  • when to consider Abx?
  • when can go back to work?
A

oral rehydration solution = mainstay
- and lots of fluids

(IV fluids if not taking things orally)

consider Abx if severe AND suspect bacterial infection (eg blood/mucus)

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43
Q

Possible complication of E Coli gastroenteritis? 1

what is this? (3 main features)

management? 4

A

HAEMOLYTIC URAEMIC SYNDROME (HUS)
- most common cause of AKI in children

E Coli 0157 produces toxins

  • >
  • abdo pain
  • bloody diarrhoea
  • fever
  • lethargy
  • seizures

1) anaemia
2) thrombocytopenia
3) renal insufficiency

MANAGEMENT

  • mainly supportive
  • NO antibiotics
  • dialysis
  • plasmaphoresis / IVIG
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44
Q

Possible complication of bacterial gastroenteritis? 1

A

Post-dysentric reactive arthritis

– due to salmonella, shigella or campylobacter (HLAB27 related)

→ Urethritis, Arthritis, Conjunctivitis

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45
Q

MALARIA

  • causative organism?
  • vector? 1 (be specific)
A

parasitic disease caused by species of the genus PLASMODIUM, travels in 1st vector (ANOPHELES mosquitos)

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46
Q

MALARIA:

  • risk factors? 6
  • protective factors? 2
A
  • African countries
  • lower socioeconomic groups
  • pregnancy
  • elderly
  • travellers
  • foreign aid workers

Protective factors:

  • G6PD lack
  • Sickle-cell trait
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47
Q

MALARIA:

  • most severe type? 1 (incl incubation period + frequency of fevers)
  • other types? 3
A

Plasmodium FALCIPARUM = most severe disease

  • incubation 7-14 d
  • travellers present within 8 wks
  • DAILY Sx are common
  • plasmodium vivax
  • plasmodium ovale
  • plasmodium malariae

nb in these less severe strains tend to get fever paroxysms every 3 or 4 days!

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48
Q

MALARIA:

- main feature? describe how this presents? (incl associated symptoms)

A

FEVER PAROXYSMS
= cyclical fevers (reflect synchronous release of flocks merozoites from mature schizonts)

Phase 1 (≤ 1hr) 
- Shivering / rigors

Phase 2 (2-6hr)

  • Fever (HIGH temp > 41)
  • flushed
  • dry skin
  • nausea + vomiting
  • headache
  • myalgia
Phase 3 (3hr) 
– Cold Sweats as temp falls (to norm or below)

then tend to sleep and be asymptomatic for 1-3 days until have another cycle!

nb Sx may occur from 6 d of infection → many months later

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49
Q

MALARIA:

- possible signs on examination? 2

A

Spleno/hepatomegaly ± abdominal tenderness

Jaundice

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50
Q

MALARIA:

  • stain used on blood film to see? (what see if falciparum)
  • what to do if can’t see on blood film but high clinical suspision?
A

Serial Thick + Thin Blood Films – stained w/ GIEMSA STAIN (gold standard)

SCHIZONTS = falciparum

If –ve, at least 2 further films should be obtained over 48 hrs to exclude malaria

nb also do other blood tests: FBC, U+Es, LFTs (can be deranged), glucose, VBG, clotting

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51
Q

Main DDx of malaria? what test to do to exclude this? 1

A

sepsis!!!!

look for source of infection AND do blood cultures

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52
Q

Management of MALARIA

  • 1st line drug if non-falciparum?
  • how to manage if drug-resistant or uncomplicated falciparum?
A

NON-falciparum
= oral CHLOROQUININE

if drug-resistant (common) or uncomplicated falciprum
= oral QUININE and some other drugs… (don’t bother learning names!)

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53
Q

Malaria prophylaxis if travelling to high-risk areas? 1

A

doxycycline

54
Q

COMPLICATED FALCIPARUM INFECTION:

  • additional features? 9
  • 5 grim signs? 5
  • where manage and with what?
A

nb these are features in addition to the norm: headache, malaise/myalgia, anorexia, fever paroxysm etc

  • dyspnoea
  • bleeding (DIC)
  • fits
  • hypovolemia
  • hypoglycaemia
  • AKI
  • nephrotic syndrome
  • ARDS
  • jaundice
    ^don’t worry if don’t remember all of these!

FIVE GRIM SIGNS:

1) ↓GCS or coma
2) Convulsions
3) Co-existing chronic illness
4) Acidosis – esp. bad if HCO3- < 15
5) Renal failure (from acute tubular necrosis)

NB High mortality if pregnant or elderly

IV Rx required in ICU (mortality 15-20% if treated, 100% if untreated)
- IV Artesunate or
IV Quinine

55
Q

FEBRILE TRAVELLER: which tropical infection is being described:

  • fever
  • relative bradycardia
  • dry cough
  • abdo pains
  • constipation (then diarrhoea)
  • lymphadenopathy
  • headache
  • splenomegaly
    +/- rose spots on torso (40%)
  • causative organism? 1
  • investigations to diagnose? 4
  • management? 2
  • main complication? 1
A

= TYPHOID

Bacteria = salomonella typhi

  • blood cultures (1st 10days)
  • bone marrow culture (gold standard)
  • urine culture
  • stool culture
    ^positive for longer than blood
  • fluid replacement
  • antibiotics

GI perf = main complication

nb can also get cholecytitis, myocarditis, meningitis, abscess etc

56
Q

FEBRILE TRAVELLER: which tropical infection is being described:

found in central + west africa and south america

  • fever
  • headache
  • myalgia
  • rash (flushing or petechial)
  • thrombocytopenia
  • leucopenia

if severe, can get:

  • jaundice, hepatosplenomegaly and anuria
  • haemorrhagic signs (petechiae, GI, gum or nose bleeds)
  • shock
  • causative organism? 1
  • incubation period?
  • investigations to diagnose? 1
  • management? 1
A

DENGUE FEVER

virus spread by AEDES mosquitos

max 14 days incubation
- so if symptoms start >14 days after leaving endemic area then dengue can be ruled out!

serology to diagnose

supportive management - lots of IV fluids!

57
Q

FEBRILE TRAVELLER: which tropical infection is being described:

  • swinging fever
  • RUQ pain
  • sweats
  • jaundice
  • causative organism?
  • what condition is it associated with? 1
  • investigation to diagnose? 1
  • management?
A

AMOEBIC LIVER ABSCESS

type of amoebia (nb called entamoeba histolytica)

50% will also have a Hx of amoebic dysentry (loose stools w blood + mucus)
- but 50% won’t so don’t rely on this!

Liver USS with biopsy (can also do ct biopsy)
- get ‘anchovy sauce’ pus on aspiration

antibiotics! - drainage if large!

58
Q

Causative organism of ‘traveller’s diarrhoea’?

A

e. coli

59
Q

Spinal cord compression:

  • most common portion of spine affected?
  • oncological causes? 2 (mechanism not specific Cancers)
  • MSK causes? 3
  • inflammatory causes? 1
A

Typically THORACIC spine (66%) (also cervical and lumbar (33%))

ONCOLOGICAL CAUSES

  • Extradural metastasis (common)
  • Extension of tumour from vertebral body (ie bone mets)

MSK CAUSES

  • crush fracture (think osteoporosis)
  • trauma
  • prolapsed intervertebral disc (commonly L4-L5 or L5-S1)

INFLAMM CAUSES
- rheumatoid arthritis (high cervical spine)

nb in RA: weakness of ligaments holding odontoid peg → rupture causes atlas to slip forward → compress high cervical spine

60
Q

name of condition that results from injury / dissection of half of the spinal cord?

what symptoms do you get?

A

BROWN-SEQUAD SYNDROME

rare neurological condition that results from an injury or damage to one side of the spinal cord

results in weakness or paralysis on one side of the body (hemiparaplegia) and a loss of sensation on the opposite side (hemianesthesia).

61
Q

SPINAL CORD COMPRESSION

  • most common early symptom? (describe this, exacerbating, relieveing etc)
  • other groups of symptoms? 3
A

BACK PAIN (90%)

  • Localised, band-like or radicular (radiates to extremities along course of spinal nerve root)
  • Nocturnal (lying flat)
  • UL or BL
  • Aggravated by straining, coughing, lying flat (nocturnal)

MOTOR (LEG) WEAKNESS / PAIN

  • norm symetrical
  • subtle or rapid onset

SENSORY DISTURBANCE

  • paraesthesia/numb, below level
  • Saddle anaesthesia (buttocks, perineum, inner thigh)

BOWEL / BLADDER DYSFUNCTION
- urinary retention (often insidious), constipation or incontinence

nb not all patients present with back pain!! - have a high index of suspision!!

62
Q

SPINAL CORD COMPRESSION

  • what examinations to do? 4
  • where else to palpate? 2
A

EXAMINATIONS

  • cranial nerve exam
  • UL neuro exam
  • LL neuro exam
  • DRE examination (anal tone + saddle anaesthesia)

PALPATE

  • spine (tenderness)
  • abdo (urinary retention)

nb Reflexes: ↑below compression, absent at level, normal above

nb clonus may be present

63
Q

SPINAL CORD COMPRESSION

  • investigation to diagnose? how quickly needed?
  • immediate management? 2
  • what else to prescribe? 2
A

URGENT MRI spine
- within 24hrs

1) IMMOBILISE spine (lie flat)
2) DEXAMETHASONE (16mg)

  • PPI cover (Omeprazole)
  • PLUS analgesia for the back pain
64
Q

SPINAL CORD COMPRESSION

  • definitive management options? 2
  • prognosis?
  • additional management? (1 if hospitalised, 1 if in urinary retention)
A

dependent on cause:

  • radiotherapy
  • neurosurgical decompression

If all motor function is lost for 48hrs, recovery is unlikely
- nb TKCC score predicts prognosis

  • LMWH if hospitalise
  • Catheterise if urinary retention
65
Q

OSTEOPOROSIS

  • primary causes / risk factors? 4
  • secondary causes? 9 (incl acronym)
A

= increased age
= female > male

= FHx
= prolonged

SHATTERED

S = Steroids
H = Hyperthyroidism / hyperparathyroidism
A = Alcohol + smoking
T = Thin (BMI<20)
T = low Testosterone 
E = Early menopause
R = Renal or liver failure
E = Erosive/inflam bone disease
D = Diet low in Calcium
66
Q

OSTEOPOROSIS

  • most common presentation?
  • complication that pts normally present with? 1
  • common locations of these? 5
A

mainly ASYMPTOMATIC

present with FRAGILITY FRACTURES

  • vertebrae (crush fractures)
  • proximal femur (NOF)
  • distal radius
  • humerus (neck)
  • pubic rami
67
Q

OSTEOPOROSIS

  • investigation if suspect fracture?
  • gold standard investigation? (what result is abnormal?)
  • bloods to do? 4
A

X-ray (if suspect fracture)

DEXA scan (gold standard ∆) – measures bone density via T-scores

T > -1.0 (normal);
T -1 to -2.5 (osteopenia);
T < -2.5 (osteoporosis)

  • TFTs
  • Vit D + Ca
  • Phosphate
  • ALP levels
    (Ca, Ph and ALP are on bone profile)

nb FRAX score used to risk assess severity based on DEXA result and other risk factors

68
Q

OSTEOPOROSIS

- lifestyle advice? 4

A

Quit smoking

↓Alcohol

increase Weight bearing exercise → ↑Bone density

ddo Balance exercises (Tai Chi) → ↓Falls risk

69
Q

OSTEOPOROSIS

  • class of drugs used to manage? 1 (most common example of this? 1)
  • other drugs to give if deficiency? 2
A

Bisphosphonates for pts. With T score < -2.5

Alendronate is 1st line

Vit D and Calcium if deficiency

70
Q

OSTEOPOROSIS PREVENTION:

  • what to offer post-menopausal women? 1
  • what to offer hypogonadal men? 1
  • what to offer all at risk? 2
A

HRT – can prevent osteoporosis in post-menopausal women

Testosterone – hypogonadal men

Ca2+ supplements and Vit. D to all post-menopausal women

71
Q

BISPHOSPHONATES:

  • how to take medication? (freq and when to take in day)
  • side effects? 4
  • adverse effects? 4
A

eg alendronate (1st line)

take Once weekly, standing 30 mins, before breakfast;

SIDE EFFECTS:

  • fever
  • myalgia
  • arthralgia (acute)
  • GORD

ADVERSE EFFECTS

  • oesophagitis (stop)
  • osteonecrosis jaw
  • stress fractures
  • ↓Ca2+

nb can’t use if eGFR <35

72
Q

POLYMYALGIA RHEUMATICA:

  • which condition associated with?
  • two main risk factors? 2
A 
temporal arteritis (aka giant cell arteritis)
- about 50% have both
  • female
  • aged over 55

nb pathology is unclear - not a true vasculitis

73
Q

POLYMYALGIA RHEUMATICA:

  • what body part mostly affected? how affected? speed of onset?
  • additional systemic features? 4
  • what other body parts may be affected? 2
  • what is NOT a symptom? 1
A

SHOULDER and PELVIC girdle

  • aching + tenderness bilaterally
  • MORNING stiffness
  • mild poly arthritis / arthralgia

^ 2 weeks - 1 month

  • fatigue
  • fever
  • weight loss
  • loss of appetite
  • tendosynovitis (pain, tender, swelling or lump of tendon)
  • carpal tunnel (10%)

weakness is NOT a feature
- if find objective weakness, consider alternative diagnosis!

74
Q

POLYMYALGIA RHEUMATICA:

  • key bloods for diagnosis? 2
  • which blood should be normal? 1 (what does it rule out? 1)
A

raised CRP and ESR

CK should be normal (would be raised if myositis / myopathies)

75
Q

POLYALGIA RHEUMATICA:

  • management? 1
  • how quickly expect to see improvement?
  • how long need to be on medication for?
  • what medications should you co-prescribe to reduce risk of side effects of treatment? 2
  • what to monitor for?
A

ORAL PREDNISOLONE (15mg/day - don’t need to know dose but just fyi)

Dramatic response in 1wk, consider alternate Dx if not!

need pred for at least 2 years (slowly wean down dose)

nb also tell pt that whenever they get ill to tell the dr that they’re on steroids (these may need to be upped if acutely unwell)

CO-PRESCRIBE

  • gastro-protection (PPI)
  • bone protection (bisphosphonates)

monitor for steroid side effects and treatment efficacy (see 1 week after every dose change and bloods every 3 months)

76
Q

GOUT

  • what is it? (incl be specific about what is in joints)
  • which joint most commonly affected?
  • what other joints can be affected? 6
A

deposition of MONOSODIUM URATE crystals in and near joints forming tophi → ACUTE monoarthropathy and severe joint inflammation

Commonly occur at MTP joint of BIG TOE

Also occur at Ankle, foot, hand, wrist, knee, elbow

77
Q

RISK FACTORS for GOUT

  • gender?
  • lifestyle factors? 3
  • comorbidities? 4
  • preceeding events? 3
  • class of medication? 1
A

M > F (4:1)

  • high purine diet
  • alcohol
  • high BMI
  • CKD
  • CV disease
  • HTN
  • DM
  • startvation
  • surgery
  • infeciton
  • diuretics (esp furosemide)
78
Q

symptoms of GOUT

  • main symptom? speed of onset of this?
  • severity? how described?
  • systemic symptoms? 2
  • findings on examination of joint? 3
A

SEVERE pain (crescendo over 6-12 hrs, resolution 5-15 d – “Attack sign”)

Localised to specific area – typically 1st MTP

“Blanket pain” – minor contact causes sev pain

  • fever
  • malaise

JOINT is:

  • swollen
  • erythematous
  • very tender
79
Q

atypical gout attacks? (ie where apart from joints can it affect)? 3

A

Tenosynovitis

bursitis

cellulitis

80
Q

GOUT

  • 1st line investigation? what find?
  • bloods to consider doing? 5
  • findings on joint x-ray? (1 early, 1 late, 1 very late)
A

Aspirate synovial fluid of joint (1st line ∆)
Crystallography =
NEGATIVE BIREFRINGENT URATE CRYSTALS

  • CRP (raised)
  • ESR (raised)
  • serum urate (raised)

consider FBC + U+E

JOINT X-RAY

  • early = soft tissue swelling
  • late = punched out erosions
  • very late = reduced joint space
81
Q

GOUT

  • main severe DDx to rule out? 1
  • other main DDx? 1
A

ALWAYS rule out SEPTIC ARTHRITIS!!

pseudo gout is other main DDx

(nb if multiple joints affected then think more RA or reactive arthritis)

82
Q

GOUT

  • 1st line management during attack?
  • what to consider co-prescribing?
  • normal length of an attack?
  • alternative medication if 1st line contraindicated? 1
A

NSAIDs (eg diclofenac or naproxen!)

  • consider PPI

attack = 7-10 days
(continue treatment until 48hrs after attack resolved!)

if NSAIDs contraindicated use COLCHICINE (nb or steroids if can use neither)

83
Q

GOUT:

  • lifestyle advice to prevent recurrence? 3
  • medication to prevent future attacks? when to start this?
A
  • less purine-heavy diet
  • less alcohol
  • loose weight

ALLOPURINOL
- start TWO WEEKS after acute attack resolved

nb if someone has an attack while on allopurinol, don’t stop this!! - just don’t START allopurinol during acute attack

nb caution use in renal disease!

84
Q

PSEUDO GOUT:

  • what is it? (incl specifically what find on joint aspiration?)
  • main risk factor? 1
  • other risk factors? 3
A

(Acute CPP crystal arthritis) – calcium pyrophosphate deposition (RHOMBOID) (CPPD) → acute monoarthropathy of larger joints in ELDERLY

Weakly POSITIVE birefringent crystals (RHOMBOID)

= OLD AGE

  • increased PTH
  • low phosphate
  • haemopchromatosis

nb often provoked by illness, surgery, trauma

85
Q

PSEUDO GOUT:

  • supportive management? 2
  • medical management options? 3
A

attacks are self-limiting

  • Cool packs
  • Rest
  • Intra-articular steroid
  • NSAIDS ± Colchicine
86
Q

VASCULITIS:

  • what is it?
  • two main groups of types?
  • what % idiopathic?
  • what % infective?
  • what % inflam disease?
  • what % drug-induced?
A

umbrella term for conditions that cause inflammation of blood vessel walls (huge range of subtypes)

infective and non-infective

Idiopathic (45-55%), Infection (15-20%), Inflammatory disease (15-20%), Drug induced (10-15%)

87
Q

Which groups of drugs can cause vasculitis? 5

A
  • sulphonamides
  • ß-lactams
  • NSAIDS
  • OCP
  • thiazide diuretics
88
Q

Which of these vasculitises are:

  • large vessel 2
  • medium vessel 2
  • small vessel (which ANCA +ve and which -ve - 2 of each)
  • variable 1
  • bechetts
  • churrg strauss
  • giant cell arteritis
  • good pasteur’s
  • henoch-schönlein purpura (HSP)
  • kawasaki
  • microscopic polyangitis
  • polyarteritis nodosa
  • takayasu’s
A

LARGE VESSEL

  • giant cell arteritis
  • Takayasu’s (basically GCA but < 55years)

MEDIUM VESSEL

  • Kawasaki
  • polyarteritis nodosa (often causes renal aneurysms)

SMALL VESSEL (immune complex)

ANCA +ve

  • Churrg strauss
  • microscopic polyangitis

ANCA –ve

  • henoch-schönlein purpura
  • Goodpasteur’s

VARIABLE
– Bechet’s

89
Q

which of these groups of symptoms of VASCULITIS’ are characteristic:

1) small vessel
2) medium vessel
3) large vessel

A)

  • End-organ ischaemia – TIA, CVE, HTN
  • Aneurysms
  • Dissection ± haemorrhage or rupture

B)

  • Nodules, Ulcers, Digital infarcts
  • HTN (dt damage to renal vessels)
  • Livedo reticularis (mottled, purplish, lace-like discolouration of skin), - Papulo-necrotic lesions

C)

  • Palpable purpura (1-3mm) – may become confluent to form plaques ± ulcer
  • Papules, urticaria, vesicles, splinter haemorrhages
A

SMALL VESSEL =
- Palpable purpura (1-3mm) – may become confluent to form plaques ± ulcer
- Papules, urticaria, vesicles, splinter haemorrhages
= “purpura and splinter haemorrhages are small - think small vessel”

B) MEDIUM VESSEL =
- Nodules, Ulcers, Digital infarcts
- HTN (dt damage to renal vessels)
- Livedo reticularis (mottled, purplish, lace-like discolouration of skin), - Papulo-necrotic lesions
= “think kawasaki -> coronary artery aneurysms (aneurysms norm a/w HTN)”

A) LARGE VESSEL =
- End-organ ischaemia – TIA, CVE, HTN 
- Aneurysms 
- Dissection ± haemorrhage or rupture 
= "think TIA with giant cell!"

nb vasculitises can affect all organs of the body!!! - there is a long list of possible symptoms depending on organ system affected…

90
Q

specific bloods to consider if suspect a vasculitis? 4

(ie in addition to routine)

gold standard test for diagnosis?

A

ESR
CRP

ANCA (if think churg strauss or microscopic polyangitis)

rheumatoid factor

nb can also do urine screen for Proteinuria, Glucosuria, Haematuria (+/- casts)

Angiography +/- Biopsy (GOLD standard Δ)

nb other tests may be done depending on suspected type and/or organ stystem affected

91
Q

VASCULITIS MANAGEMENT

  • medication often used to control acute symptoms? 1
  • medication used in some small / med vessel vasculitis? 1

what blood test normally used to monitor response to treatment? 1

A

COSRTICOSTEROIDS
- used to control acute symptoms

CYCLOPHOSPHAMIDE

  • used in some small/medium vasculitis
  • or other IMMUNOSUPPRESSION used!

ESR normally used to measure response to treatment

92
Q

what score should you use to assess someone’s risk of a fragility fracture?

what is it used to determine

what main things does it take into account? 3

A

FRAX score

used to determine if start on bisphosphonates or not

  • any previous fragility fracture
  • bone mineral denisty (from dexa scan)
  • other risk factors (eg age, sex, weight, smoking, medications incl steroids, RA, alcohol)
93
Q

ANKYLOSING SPONDYLITIS:

  • describe pathophysiology
  • what gene associated with?
  • gender most affected? and age it presents?
A

chronic, inflammatory disease of SPINE + SACROILIAC JOINTS → forms bony outgrowths due to ENTHESITIS → fusion of spine (BAMBOO)

(Unknown aetiology), 90% are HLA-B27 +ve

MALE present earlier > Female (6:1 at 16yo, 2:1 at 30yo)

94
Q

ANKYLOSING SPONDYLITIS:

  • norm presenting symptom?
  • SOCRATES of this?
A

LOWER BACK PAIN
– Gradual onset
- Radiates from sacroiliac joints → hips/buttocks
- a/w morning STIFFNESS
- Worse mornings/night, improves as day progresses
- Relieved by exercise

95
Q

ANKYLOSING SPONDYLITIS:

- main findings on physical exam? 2

A

is PROGRESSIVE

1) ↓ SPINAL MOVEMENT
- ↓Lateral flexion
- ↓Forward flexion (< 5cm = +ve Schober’s test)

2) DEFORMITY
- May cause kyphosis, neck hyper-extension + spino-cranial ankylosis
- Results in thoracic expansion – question mark deformity (hunched back)

96
Q

ANKYLOSING SPONDYLITIS:

  • extra-articular manifestations? 7 (the 7 A’s - which most common?)
  • what other non-A complication are they at risk of? 1
A

7 Extra-articular manifestations (rule of A’s)

= Anterior UVEITIS or IRITIS (30%) (painful red eye!)

  • Apical fibrosis
  • AV node block
  • Aortic regurgitation

= Achilles tendon rupture,
- Amyloidosis (kidneys + heart)

= CaudA EquinA syndrome

= OSTEOPOROSIS!!! (60% - give bisphosphonates!)

97
Q

ANKYLOSING SPONDYLITIS:

  • how diagnosis made?
  • who to refer to?
  • 1st line imaging? (1 early, 1 middle, 1 late sign)
A

CLINICAL diagnosis (though norm following x-ray!)

refer to RHEUMATOLOGIST if suspect clinically!

X-Ray (1st line preferred) or MRI spine/pelvis –

early = SACROILIITIS
– subchondral erosions, sclerosis

middle = VERTEBRAL SYNDESMOPHYTES (common at T11-L1)
– bony outgrowth due to enthesitis at ligament + vertebra
(these fuse with vertebral body above →) Ankylosis

late = BAMBOO SPINE (calcification of supraspinous and interspinous ligaments w/ ankylosis)

98
Q

ANKYLOSING SPONDYLITIS:

  • possible finding on FBC? 1
  • other blood tests to do? 2
A

FBC (normocytic anaemia)

↑↑ESR/CRP

nb HLA B27 +ve in 90% - doesn’t mean much though!

99
Q

ANKYLOSING SPONDYLITIS:

  • lifestyle advce? 1
  • 1st line management?
  • other medical management options? 4
  • surgical management option? 1
A

1) Exercise
– improves backache and posture

2) NSAIDs (Ibuprofen, Naproxen) ± PPI – 1st line
- relieve Sx in 48hrs, may show slow radiographic progression

nb use slow release NSAID (if night pain + morning stiff remains)

3) Add paracetamol ± codeine
4) IA injections of corticosteroids

5) TNF-a inhibitors (adalimumab, etanercept, golimumab)
– for severe active AS if Sx poorly controlled with NSAIDs
- Must be monitored by rheumatologist

6) Surgery = Hip Replacement (↓pain, ↑mobility)

100
Q

ANKYLOSING SPONDYLITIS:

  • prognosis?
  • what indicates poor prognosis? 4
A

AS is a chronic condition with NO CURE

POOR prognosis if

  • ESR > 30
  • onset < 16yo
  • early hip involvement
  • poor response to NSAIDs
101
Q

REACTIVE ARTHRITIS:

  • what is it?
  • what two groups of conditions can cause this? 2
  • give 3 specific examples for each of these two groups?
  • gender as a risk factor?
A

sterile inflammation of synovial membrane, tendons and fascia → affects lower limb

SEXUALLY-TRANSMITTED INFECTION
= Chlamydia
= Trachomatis
= Gonorrhoea

POST-DYSENTERIC
= Shigella
= Salmonella
= Campylobacter

(nb HLA-B27 mediated 60-80% cases)

remeber that dysentry means diarrhoea with blood and/or mucus!

post-STI form much more common in men (e.g. 10:1)

post-dysenteric form equal sex incidence

102
Q

REACTIVE ARTHRITIS:

  • what are the three main symptoms? 3 (name of triad of symptoms?)
  • how long after the triggering infection do these arise?
  • additional symptoms? (2 systemic, 3 localised to certain body parts)
  • how long do symptoms last?
A

TRIAD of REITER’S SYNDROME
– typically FOUR WEEKS post-initial infection (gastric or STI normally)

1) ARTHRITIS – usually one joint in lower limb (occurs 1-4wks after infection)
2) UVEITIS or CONJUNCTIVITIS (50%)
3) URETHRITIS or CERVICITIS

“Can’t see, pee or climb a tree”

Other symptoms:

  • Malaise + fatigue
  • Fever
  • Circinate BALANITIS – painless penile ulceration (secondary to chlamydia)
  • KERATODERMA BLENORRHAGICA – Brown, raised plaques on soles/palms
  • Mouth ULCERS – painful

symptoms last 4-6 months

103
Q

REACTIVE ARTHRITIS:

  • key blood tests? 2
  • blood test to rule out DDx?
  • possible tests for cause? 3
A

Bloods – ↑ESR, ↑CRP

rheumatoid factor (will be negative!)

SCREEN FOR STIs
- Urine MSU (men) +/- discharge culture or vaginal swab (women)

STOOL CULTURE if diarrhoea – screen for shigella, salmonella or campylobacter

104
Q

REACTIVE ARTHRITIS management:

  • acute management to reduce pain?
  • 1st line medical management? 2
  • what considered if symptoms go on for a long time?
A

Splint affected joint acutely

FIRST LINE

  • NSAIDs
  • Local steroid injections

Sulfasalazine or Methotrexate if symptoms are persistent > 6months

nb treating the original infection makes little difference to the arthritis (but should still do!)

105
Q

REACTIVE ARTHRITIS:

  • prognosis?
  • how long do symptomas tend to last for?
  • main possible complication? 1
  • what increases chance of recurrence?
A

prognosis is very good – a self-limiting illness, usually resolves within 3-12 months (average 4-6m)

In isolated patients symptoms may persist → destructive arthtitis

can be chronic or relapsing!

Recurrence is likely if HLA-B27 +ve

106
Q

What is meant by a ‘sero-negative’ arthritis?

- give 5 specific common examples? 5

A

an inflammatory arthritis which is rheumatoid-factor (and other specific factors like ANCA etc) negative

  • psioriatic arthritis
  • arthritis associated w IBD (aka enteropathic arthritis)
  • ankylosing spondylitis
  • reactive arthritis
  • sero-negative rheumatoid arthritis (more controversial)
107
Q

Main 5 examples of sero-POSITIVE arthritis?

A
  • rheumatoid arthritis
  • lupus
  • scleroderma
  • vasculitis
  • sjorgen’s
108
Q

What do seronegative arthritises tend to be positive for? (specific blood test)

which bones/joints do they tend to affect?

A

HLA-B27

often bones in the SPINE and NEARBY JOINTS.

nb That’s why they’re sometimes called seronegative spondyloarthritides, where spondylo means vertebra.

also cause peripheral arthritis that’s generally asymmetric, and axial arthritis like sacroiliitis and spondylitis, affecting the sacroiliac and vertebral joints, respectively

109
Q

Asied from affecting spine + nearby joints, what other groups of features do you tends to find with SERONEGATIVE ARTHRITISES? 3

What tends to be the predominant medical management? 1

A

1) ibnflammatory back pain (30 mins morn stiffness)
2) ENTETHESIS (inflammation at the sites where tendons or ligaments insert into the bone) and DACTYLITIS (aka sausage fingers)

3) EXTRA-ARTICULAR features:
- anterior uveitis
- skin (psoriasis)
- aortic regurg / pericarditis
- genitourinary symp (secondary to nerve compression)
- GI features (IBD)

nb (as mentioned in Q) also cause peripheral arthritis that’s generally asymmetric, and axial arthritis like sacroiliitis and spondylitis, affecting the sacroiliac and vertebral joints, respectively

nb w psoriatic psoriasis the rash and arthralgia often don’t occur at the same time and the arthrtitis can present first!

NSAIDs often work very well!!

110
Q

PAGETS disease of BONE

  • BRIEFLY describe pathophysiology
  • % that are asymptomatic
  • main symptom? 1
  • which bones normally affected? 4
A

basically increased osteoblast and osteoclast activity in the bone -> remodelling and structural weakness

Asymptomatic (70%)

BONE PAIN! (boring, deep)

  • lumbar spine
  • pelvis
  • femur
  • skull

nb can get increased skin temp over areas of active disease

111
Q

PAGETS disease of BONE

  • two types of imaging? 2 (+ findings)
  • main blood test that is abnormal?
A

X-RAY

  • Localised enlargement of bone
  • Asymmetric and patchy cortical thickening w/ sclerosis (radio-opaque), osteolysis (radiolucency), deformity
BONE SCAN (radionucleotide)
- reveals hot spots and extent of disease severity

↑↑ALP (need serial monitoring)

nb Ca2+, Phos, PTH often normal

112
Q

PAGETS disease of the BONE

  • boney-related complications? 5
  • metabolic complication? 1
A
  • pathological FRACTURES
  • OSTEOARTHRITIS (if joint involvement)
  • SPINAL STENOSIS or nerve damage from compression (rare)
  • DEAFNESS / TINNITUS (dt bone overgrowth in bones of ear)
  • OSTEOSARCOMA (need to monitor for!)
  • HYPERCALCAEMIA

nb can also get high output congestive HEART FAILURE (if >40% skeleton involved) dt increased blood flow through vasculature of bones

nb management is with NSAIDs and paracetamol, CA/Vit D replacement if deficient and BISPHOSPHONATES!

113
Q

PAGETS disease of the BONE

- main DDx? 3

A
  • osteoarthritis
  • osteoporosis
  • osteomalacia

nb also bone tumours! (or infective bone if fevers etc

114
Q

OSTEOMALACIA

  • what is it?
  • what deficient in? 3
  • what blood test is high? 1
  • what called if in kids?
A

recduced mineralisation of the bone

deficient in Vit D, calcium AND phosphate!

ALP is raised

RICKETTS (kids)

  • growth retardation
  • hypotonia
  • Genu valgum (knock) or varum (bow) deformity
115
Q

OSTEOMALACIA

- main cause is vit D deficiency - other secondary causes? 5

A
  • renal failure (lack of activated vit D)
  • liver failure
  • malabsorption (eg IBD)
  • drug-induced (anti-convulsants)
  • tumour-induced (type of paraneoplastic sndrome)
116
Q

OSTEOMALACIA

  • two main symptoms? 2
  • complication that can be initial presentation? 1
A

can be asymptomatic!!!

  • BONE PAIN + muscle tenderness
  • PROXIMAL MYOPATHY → waddling gait

Fragility FRACTURES – especially NOFF

117
Q

Which cancers commonly metastasise to the bone? 5

(acronym to remember this)

which are norm sclerotic lesions and which normally lytic?

A

“Lead kettle = Pb KTL”

SCLEROTIC

  • Prostate
  • Breast

LYTIC

  • kidney
  • thyroid
  • lung

nb melanoma’s also (and others)

118
Q

What is the most common primary bone tumour?

three groups of symptoms it presents with? 3

A

MYELOME (see haematology falshcards for more info!)

BONE
- eg back pain, fractures, hypercalcaemia

BLOOD
- anaemia, neutropenia, thrombocytopenia

KIDNEY
- renal failure

119
Q

What are the specific findings of these investigations for MYELOMA:

  • urine?
  • blood?
  • serum electrophoresis?
  • bone marrow biopsy?
  • x-ray? (ie type of lesions)
A

urine = BENCE JONES proteins

blood = ROULEAUX formations

serum electrophoresis = MONOCLONAL BANDS

BM biopsy =
↑PLASMA cells, plasmocytoma

x-ray = LYTIC lesions

120
Q

What is the most common presenting symptom of a primary bone tumour?

A

bone pain

pathological fractures and palpable lumps come later

121
Q

for each of these primary bone tumours:

  • osteosarcoma
  • ewing’s sarcoma
  • chondrosarcoma

state:

  • where they affect?
  • normal age of onset?
  • distinctive sign on x-ray?
A

OSTEOSARCOMA

  • metaphysis of long bone (typically knee)
  • often occurs secondary to PAGETS
  • usually 10-20 years
  • bone destruction + periosteal thickening (sun burst sign)

EWING’S SARCOMA

  • diaphysis of long bones and limb girdle
  • adolescents
  • ‘onion ring’ sign

CHONDROSARCOMA

  • malignant transformation of chondromas in axial skeleton
  • middle-aged people
  • ‘popcorn’ calcification

DON’T WORRY TOO MUCH ABOUT SPECIFIC X-RAY SIGNS, just know to have bne tumours on differential for bone pain, swelling or pathological fractures and broadly know ages!

122
Q

Systemic Lupus Erythematosus (SLE):

  • two other autoimmune conditions associated with? 2
  • four antibody tests to do? which 1 most specific?
A

A/w Sjogrens + Antiphospholipid syndrome

+ve ANA (+ve 95%)

Anti-dsDNA +ve (v.specific but only +ve 60%)

Anti-smith (most specific)

Rheumatoid Factor (+ve in 40%)

123
Q

Systemic Lupus Erythematosus (SLE):

  • typical systemic features? 3
  • typical derm features? 2
  • typical MSK features? 2
  • typical renal feature? 1
  • other parts of the body that can get inflammed? 3
  • what can often make symptoms worse? 1 (especially the derm ones!)
A

LUPUS is relapsing + remitting! (+has variable features in everyone!)

  • malaise
  • fatigue
  • fever
    (can also get lymphadenopathy)
  • malar butterfly rash (spares nasolabial fold)
  • discoid rash (red, raised plaques)
  • mylagia
  • ARTHRALGIA (90%) (non-erosive arthritis)
  • persistent proteinuria, can -> kidney failure
  • serositis
  • pleuritis
  • pericarditis

nb can also cause seizures, pancytopenia and immunological disorders

SUNLIGHT -the rashes are PHOTOSENSITIVE (ie get worse in sunlight)

124
Q

SCLERODERMA

  • aka?
  • pathological mechanism?
  • two main types? (incl speed of onset) (specific blood test for each type?)
A

aka Systemic sclerosis

autoimmune disorder characterised by ↑Fibroblast activity → ↑COLLAGEN DEPOSITION →internal ORGAN FIBROSIS + VASC DAMAGE

Limited cutaneous SSC (LcSSC) – common, slow onset, milder aka. CREST syndrome
- ACA (anti-centromere Ab)

Diffuse cutaneous SSc (DcSSC) – less common, rapid onset, high mortality
- Anti-Scl 70 (anti-topoisomerase)

DON’T WORRY ABOUT WHICH BLOOD TESTS TO GET - just know that you need to get antibody blood tests

125
Q

what are the features of CREST syndrome? 5

which of these normally presents first?

A

CALCINOSIS
- chalky nodules, may break skin

REYNAUD’S (1st in 90%)

ESOPHAGEAL DYSMOTILITY
- causes reflux + heart burn

SCLERODACYTLY
- hardening of skin on hands

TELANGIECTASIA
- aka spider veins (similar but not same as spider naevi!)

nb can also get: renal complications, erectile dysfunction, fatigue, weight loss, myalgia, fibrosis/pulm HTN, pericarditis, LVF

126
Q

ROTATOR CUFF TEAR

  • muscle in rotator that’s typically affected?
  • typical cause? (2 main RFs)
A

acute injury (young) or chronic degeneration (elderly) → rotator cuff damaged in subacromial space → tears tendon (typically SUPRASPINATUS, also subscapularis + Infraspinatus)

RF:

  • Age> 40
  • Overuse (sport/profession)

can be full or partial tear

127
Q

ROTATOR CUFF TEAR:

  • two main presenting symptoms? 2
  • typical finding during examination? 1 (nb this is v specific!)
A
  • shoulder pain
  • shoulder weakness (incl reduced range of movement)

worse with movement and at night!

PARTIAL tear = PAINFUL ARC syndrome!
- movement possible at upper bits dt action of deltoid!)

COMPLETE TEAR = abduction limited to 40-50 degs)

nb can also get clicking and catching of joint as moving it

nb treat with analgesia, ice packs, physio, steroid injections + surgery (if complete tear or not responding to Tx)

FULL range of PASSIVE movement ALWAYS present (what differetiates it from DDx)

128
Q

Main differential diagnosis for rotator cuff tear? 3

A
  • sub-acromial impingement
  • calcific tendonitis
  • frozen shoulder
129
Q

FROZEN SHOULDER

  • technical term? 1
  • common age and gender?
  • conditions associated with? 3
A

aka. Adhesive capsulitis

Most common in middle aged females

a/w DM, thyroid disease, cervical spondylosis

130
Q

FROZEN SHOULDER

- the three STAGES of the condition? how does each present and how long each one last?

A

inital symptoms develop over days!

1) PAINFUL PHASE
- shoulder pain, worse at night
- reduced active AND passive range of movement
- esp EXTERNAL rotation (< 30 degs)

2) FROZEN PHASE
- pain resolves
- shoulder remains stiff (6-12 months)

3) THAWING PHASE
- shoulder slowly regains range of movement (1-3 years)

nb Mx is NSAIDs and physio, give early

131
Q

golfer’s elbow and tennis elbow?
- which is lateral and which medial epicondylitis?

which is more common?

A

Inflammation @ the common extensor tendon arising from the lateral epicondyle or at forearm flexor muscles origin at medial epicondyle of humerus

TENNIS elbow = LATERAL epicondylitis

  • “you play LATERALLY from side to side in tennis”
  • 5x more common than golfers!

GOLFER’S elbow = MEDIAL epicondylitis
- “you want to hit straight down the MIDDLE in golf”

132
Q

MEDIAL + LATERAL EPICONDYLITIS:

  • most common cause?
  • what present with?
A

Hx of repetitive strain, heavy lifting, sports

pain and tenderness over medial or lateral epicondyl (depnding on type)
- ? often in dominant arm?

nb Mx is 6-24 months of avoiding causative activity, physio and nsaids

nb 90% recover within a year

*year 5 (8 decks)

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