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__Y6 Finals Revision > __One2one > Flashcards

__One2one Flashcards

1
Q

Bruising on face in a Cardio exam?

A

Evidence of anti-coagulation
Think AF or valve replacement

Potentially also evidence of a fall with LOC (if face hit)

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2
Q

Cardio exam

Midline sternotomy scar

Differentials? (X3)

A
  • Valve replacement (look for Warfarin, listen HS)
  • CABG (look for saphenous graft scar, tar staining, xanthelasma)
  • Congenital cardiac disease repair (if young, more rare)
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3
Q

Graft options in CABG (x3)

A

Great saphaenous vein
Left internal mammary artery (aka internal thoracic)
Radial artery

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4
Q

No scar
No Warfarin
Normal pulse
Ejection systolic murmur

Differentials? (x3)

A 
Aortic stenosis (slow rising pulse, narrow pulse pressure)
Aortic sclerosis

+- CCF (look at JVP, lungs, oedema)

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5
Q

Cardio exam

No scar, no Warfarin, normal pulse

Most likely differentials? (x2)

A 
Valvular disease (see pulse, BP, HS)
CCF (look for JVP, lungs, oedema)
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6
Q

What is a slow rising pulse?

A

Seen in Aortic stenosis
No quick upstroke
Peak pressure is prolonged over a period of time

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7
Q

Define pulse pressure

What is considered a narrow pulse pressure?

Where is this seen?

A

Difference between systolic and diastolic BP

Narrow if difference is <25% of the systolic

Seen in aortic stenosis
Stenosis means pressures are very similar before and after due to restriction of flow

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8
Q

Cause of narrow pulse pressure? (x4)

Cause of wide pulse pressure? (x4)

A

Narrow - aortic stenosis, HF, shock, tamponade

Wide - pp increases with exercise, wider in athletes
If prolonged - stiffness of great vessels, aortic regurg, AVM

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9
Q

Systolic murmur differentials (x3)

A

Aortic stenosis/sclerosis - Loudest in upper chest, radiates around chest wall

Mitral regurgitation - (Only) heard at apex

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10
Q

Aortic stenosis vs sclerosis

A

Stenosis - radiates to carotids, slow-rising, narrow PP, heaving apex beat (sign of severity)

Sclerosis - murmur only

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11
Q

Things to remember when presenting a murmur?

A

TIPQRS

Type - sys/dias
Intensity (usually 3/6)
Position
Quality
Radiation
Systemic features
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12
Q

Main symptoms of aortic stenosis (x3)

Main causes (x2)

A

SAD

Syncope
Angina
Dyspnoea - with LV failure

Causes: calcific degeneration, bicuspid valve (presents 10 yrs earlier)

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13
Q

Signs of severity in Aortic stenosis

x5

A

Haemodynamic involvement - Narrow pulse pressure

Delayed closure of A2 (due to prolonged time for SV to leave heart)

Heaving apex beat (LVH, cardiac remodelling)

Features of CCF
Symptomatic

(i.e. NOT the intensity of the murmur)

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14
Q

Indications for surgery in aortic stenosis (x4)

A

Symptomatic
CCF
Mean transvalvular pressure gradient >44mmHg
Concomitant CABG

Overall relies on clinical judgement of pt suitability

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15
Q

Grading of murmurs

A 
1 - just audible to expert
2 - just audible to non-expert
3 - clearly audible
4 - clearly audible with thrill
5 - audible with stethoscope only lightly applied
6 - audible without stethoscope
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16
Q

Cardio exam

Sternotomy scar and evidence of Warfarin use

Top differentials?

A

Metallic valve
(possibly tissue valve)

Also possibly AF or CCF

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17
Q

Metallic vs tissue valves

A

Metallic valve - clicks, evidence of Warfarin
Lasts 20 years
Flow murmur okay but regurg indicates failure

Tissue valve - no click, lasts 10 years (although improving)
Small amount of regurg is okay

Metallic valves have higher INR targets (cannot use DOAC, must be warfarin) with life ling Warfarin - vs aspirin after 3 months for tissue

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18
Q

Major surgery with a metallic valve

How to manage anticoagulation?

A

Stop Warfain 1 week before
Use LMWH as bridging until day before
Then switch to unfrationated heparin the day before (as reversible)

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19
Q

Cardio exam

Sternotomy scar
Normal pulse
No Warfarin
No click

Differentials? (x2)

A

Tissue valve

CABG (look for graft sites, tar staining, xanthelasma)

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20
Q

Indications for CABG (x4)

A

Failure of medical management
Left main stem disease
2 or more vessel disease
Concomitant valvular replacement

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21
Q

Types of saphenous graft scars

A

Longitudinal (old) scar down medial aspect of leg

Newer shorter endoscopic scars

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22
Q

Medication post CABG

A 
Dual antiplatelets (aspirin and clopidogral/ticagralor)
For 12 months then aspirin alone

ACE-inhibitor (or ARB)
Beta-blocker (eg. bisoprolol)

If HF assoc CABG then add Spironalactone

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23
Q

Causes of mitral regurg (x4)

A

Chronic - myxomatous degeneration (CTD), functional (with LV dilatation and distortion of papillary muscles)

Acute - infective endocarditis, papillary muscle rupture (2ndary to inf/post MI)

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24
Q

Signs of severity in mitral regurg (x3)

A

Symptoms - eg. CCF
LVF
Displaced or thrusting apex beat

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25
Q

Raised JVP in cardio exam

A

Right sided HF

Congestive cardiac failure (indicates increased R heart pressure)

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26
Q

Signs of R HF vs L HF

A

Right ventricular failure:

  • Acute: raised JVP, hepatomegaly (deranged LFTs)
  • Chronic: pedal/sacral oedema, ascites

Left ventricular failure:
- Acute/chronic: pulmonary oedema, poor peripheral perfusion, tachyopnoea, tachycardia

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27
Q

Causes of R HF and L HF
(acute and chronic)
(x9)

A

Right ventricular failure:

  • Acute: MI, PE, infective endocarditis
  • Chronic: LVF, cor pulmonale

Left ventricular failure:

  • Acute: MI, infective endocarditis
  • Chronic: cardiomyopathy (ischaemia or hypertensive), valvular heart disease
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28
Q

Management of CCF

A

Conservative:
Lifestyle (smoking), Education, Monitoring (disease and complications), Nutrition
Long term O2 for cor pulmonale

Medical:
ACE-i, BB, tx underlying cause (HTN, AF)
Aggressive management of RFs

Surgical:
LVAD or transplant

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29
Q

Stages of clubbing

A

Staging of clubbing (FACE)

  • Fluctuancy of nail bed increased
  • Angle Loss
  • Curvature increased
  • Expansion (drumsticking)
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30
Q

Causes of clubbing

A

Resp - pulmonary fibrosis, malignancy, suppurative lung diseases (bronchiectasis, abscess, empyema, CF)

Cardio - infective endocarditis, atrial myoxma, congenital cyanotic HD

Abdo - coeliac/malabsorption, IBD (crohn’s/UC), malignancy, cirrhosis

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31
Q

Spider naevi

What number are abnormal?
Definining features?
What conditions are they seen in?

A

> 3 is abnormal

Found in distribution of SVC
Fill from CENTER when blanched

Seen in chronic liver disease
also pregnancy, HRT (due to increased oestrogen)

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32
Q

Signs of chronic liver disease?

General, face, hands, abdo

A

General - cachexia, jaundice, excoriations, bruising

Hands - Dupuytren’s, palmer erythema, digital clubbing

Face - icteric sclerae

Abdo - spider naevi, caput medisae, gynaecomastia, ascities, splenomegaly

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33
Q

Chronic liver disease signs plus obesity, diabetes

A

Think NAFLD (increasingly common cause of CLD)

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34
Q

Chronic liver disease signs and xanthelasma

A

Think of cholestatic disorders (PSC, PBC)

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35
Q

Traube’s space and relevance to abdo exam

A

Below left hemidiaphragm above spleen
Should be resonant on percussion due to stomach
Dull to percussion if splenomegaly as spleen moves into this space

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36
Q

Causes of chronic liver disease

How would you investigate specifically for these?

A

Infective - hep B, hep C
Toxic - alcohol
Metabolic - NAFLD, (Wilsons, haemochomatosis A1AT)
Autoimmune - AI hep, PSC, PBC

Hp B/C serology
Hx of alcohol
Bloods - ferritin, A1AT, caeruloplasmin
Immunoglobulins, autoabs

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37
Q

Signs of decompensation in chronic liver disease

A

ABC

Ascites
Bilirubin - worsening jaundice
Coagulopathy

Encephalopathy - asterixes

Hypoglycaemia (late stage sign)

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38
Q

Complications of cirrhosis

A

Portal HTN - variceal haemorrhage, SBP (ascites), thrombocytopaenia (splenomegaly)

Hepatocellular failure - encephalopathy, HCC, hypoalbuminaemia, coagulopathy

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39
Q

Causes of splenomegaly

4 main categories

A

Haem - CML, myelofibrosis ,spherocytosis

Infective - malaria, EBV

Congestion - portal HTN, RHF, thrombosis/blockage (Budd Chiari)

Infiltration - amyloidosis

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40
Q

Differentials for splenomegaly AND hepatomegaly

x4

A

CML, infective (malaria, EBV), infiltration eg. amyloidosis, sarcoidosis

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41
Q

Indications for splenectomy (x4)

A

Traumatic rupture
Spherocytosis
Idiopathic thrombocytopaenia (less common now better meds)
Sometimes in lymphoma to reduce sx of hypersplenism

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42
Q

Signs to look for in renal transplant (x6)

A 
Scar and abdo mass
Signs of renal failure
AV fistula (old or active)
Insulin injection sites (aetiology)
Cushingoid
Skin malignancy (immunosupp)
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43
Q

RRT scar (Rutherford Morrison) and nephrectomy scars?

A

Old kidneys usually left in in RRT

There would need to be an indication for their removal eg. polycystic kidney disease, renal cell carcinoma, haemorrhage (cyst)

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44
Q

Indications for renal transplant (x3)

A

Diabetic nephropathy
Polycystic kidney disease
Glomerulonephritis

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45
Q

Complications of renal transplant (x43

A

Short term - bleeding, infection, thrombosis, acute rejection (+ renal failure)

Long term - immunosuppresant side effects (skin malignancy, gum hypertrophy, increased infection risk, high BP)

Cushing syndrome

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46
Q

Signs of renal failure to look for in exam (x4)

A

Scars - old AV fistula, neck line, peritoneal dialysis catheters

Cachexia
Pulmonary and peripheral oedema
Pallor

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47
Q

Stoma differentials (x4)

A

IBD - if YOUNG, pallor, ileostomy
Diverticulitis - elderly, colonostomy
Malignancy
Urostomy

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48
Q

Signs of IBD on examination (x6)

A

Young pt
Pallor, slim
Oral ulcers
Pyoderma gangrenosum (or erythema nodosum)
Clubbing
Medications at the bedside (sulfasalazine, azathioprines, steroids)

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49
Q

Signs of complications of IBD to look for on examination (x5)

A 
Scars from Hickmann lines (for parental nutrition)
Cushingoid
Gum hypertrophy and HTN (ciclosporin)
Jaundice (PSC)
Hepato-splenomegaly - amyloidosis
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50
Q

Extra-intestinal manifestations of IBD?

A

Eyes - episcleritis, posterior uveitis, scleritis

Skin - pyoderma gangernaosum, erythema nordosum

Other - clubbing, oligoarthritis, anaemia

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51
Q

Complications of IBD (x6)

A

Crohn’s - strictures, obstruction, fistulae

UC - toxic megacolon, colonic carcinoma, PSC

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52
Q

Indication for stoma in IBD (x5)

A 
Failure of medical management (severe disease activity)
Obstruction (from strictures)
Fistulae
Toxic megacolon 
Malignancy
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53
Q

Complications of PKD (x4)

A 
HTN
UTI
Cyst haemorrhage
Haematuria
End stage renal failure
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54
Q

Associations with PKD

A

Hepatic cysts
Berry aneurysms
Mitral valve prolapse

55
Q

Differentials for bilateral renal masses (x6)

A 
Polycystic kidney disease
Bilateral renal cysts/RCC
Bilateral hydronephrosis
Hepatomegaly and splenomegaly
Amyloidosis
Tuberous sclerosis
56
Q

Definition of COPD

A

Chronic bronchitis - cough with sputum for most days fro 3 months of 2 years (clinical diagnosis)

Emphysema - permanent dilation with destruction of alveolar walls distal to terminal bronchioles (histological diagnosis)

FEV1/FVC <0.7 and FEV1 <80% predicted

57
Q

COPD vs alpha1-AT deficiency histologically?

A

COPD - centriacinar emphysema

A1AT - panacinar emphysema

58
Q

Chronic COPD management

A

Smoking cessation, annual influenza, one-off pneumococcal

  1. SABA or SAMA first line
  2. 2nd line:
    • FEV1 >50% - LABA or LAMA
    • FEV1 <50% - [LABA and ICS] combo or [LAMA]

Note: discontinue SAMA when starting LAMA

  1. If persistent SOB or exacerbations
    • If taking LABA switch to [LABA + ICS] combo
    • Or give triple therapy: LAMA and [LABA + ICS]

Consider theophylline if above therapies ineffective
Consider mucolytics if chronic productive cough

Smoking cessation and long term O2 only factors that improve survival

SABA – salbutamol or terbutaline
LABA – salmeterol or forameterol
LAMA – tiotropium
ICS – fluticasone

59
Q

When do you give long term O2?

A

Non smoker

PaO2 <7.3

PaO2 <8 AND evidence of pulm HTN, polycythamia, paroxysmal nocturnal dyspnoea, pulm effusion

Pallative

60
Q

Resp exam

Clubbing, dry cough, fine crackles

A

Fibrosis

61
Q

Causes of pulmonary fibrosis (apical and basal)

A

Apical - CHARTS

Coal miners lung
Hypersensitivity pneumonitis
Ankylosing spondylutus 
Radiotherapy
TB
Sarcoidosis/silicosis

Basal:

Idiopathic
Connective tissue disease (rheumatoid arthirtis, SLE, systemic sarcoidosis)
Asbestos
Recurrent aspiration

62
Q

4 most common causes of pulmonary fibrosis

A

Idiopathic
Rheumatoid arthitis
Drugs - methotraxate, amiodarine, nitrofuratoin
Hypersensitivity

63
Q

Differentials for chest asymmetry when testing expansion (x4)

A

Pneumothorax (not in PACES)
Kyphoscoliosis
Effusion
Lobectomy (/pneumonectomy)

64
Q

Most likely reasons for lobectomy

chest asymmetry and a scar

A 
Malignancy (look for tar staining)
Old TB (>60 years, old management, absent ribs)
65
Q

Signs of old TB on examination (x6)

A 
Scars, deformity, absent ribs
Apical fibrosis with tracheal traction
Crackles, bronchial breathing
Reduced expansion
Kyphosis (Pott's disease)
Dullness on percusion (if pneumonectomy - with lobectomy, healthy lung tends to expand into space)
66
Q

Current TB treatment and their SEs?

A

RIPE

Rifampacin - hepatitis, orange secretions
Isoniazid - hepatitis, peripheral neuropathy (give with pyridoxine)
Pyrazinamide - hepatitis
Ethambutol - hepatitis

67
Q

Resp exam

Wet cough, SOB

Top two differentials?

A

Bronchiectasis (look for signs of CF)

pneumonia (less likely in PACES)

68
Q

CF observations on exam (x6)

A 
Young and thin
Gastostomy (PEG)
Creon at bedside
Port-a-cath
Transverse abso scar (meconium ileus, obstruction)
PEP devices (+ve expiratory pressure)
69
Q

CF treatment

A

Conservative - postural drainage, active cycle breathing, nutrition

Medical - Creon and fat soluble vitamens, immunisations
DNase, abx (prophylactic and exacerbations)

Surgical - lung transplant

70
Q

Causes of bronchiectasis (3 main categories)

A

Post-infectious - severe pneumonia, recurrent aspiraitons, TB, pertussis, ABPA

Congenital - CF (50%), primary ciliary dyskinesia

Mechanical - foreign body, obstructing tumour

71
Q

Causes of pleural effusion

A

Transudate (protein <25g/L) - cardiac failure, renal failure, liver failure, hypoalbuminaemia

Exudate (protein >35 g/L) - parapneumonic effusion, empyema, malignancy, inflammatory pleuritis (RA, SLE)

72
Q

Pleural effusions - what parameters define transudate and exudate?

A

Transudate (protein <25g/L)
Exudate (protein >35 g/L)

Light’s criteria if between 25-35

Effusion albumin/plasma alb >0.5
Effusion LDH/plasma LDH >0.6
Effusion LDH >2/3 x upper limit of normal for plasma LDH

73
Q

Neuro exam

Abnormal gait
Flexed arm, extended leg

A

Hemiplegia - pyramidal weakness

Likely stroke

74
Q

Post-stroke signs on neuro exam (x7)

A 
Pyramidal weakness (flexed arm, extended leg)
Walking aids
Wasting on affected side
Increased tone and clonus
Clasp knife spasticity
7th nerve palsy in UMN distribution
Brisk reflexes, upgoing plantars
75
Q

Additional examinations you would like in a stroke patient (as well as the neuro limbs)

(x5)

A

Gag and swallow assessment (aspiration risk and nutrition, need for PEG or NGT)

Visual fields and neglect (needed for Bamford stroke classification)

Blood pressure (cause: hypertensive haemorrhagic stroke)

AF - as a cause

Carotid bruit if anterior circulation stroke

76
Q

MRC grading of power

A 
0 - none
1 - flicker
2 - moves with gravity neutralised
3 - vs gravity but not resistance 
4 - reduced power vs resistance 
5 - normal
77
Q

Bamford classification of stroke

A

Clinical classification

Total anterior circulation stroke - hemiplegia, homonymous hemianopia, higher cortical dysfunction

Partial anterior circulation stroke - 2 of 3

Lacunar circulation stroke - hemi-motor or hemi-sensory only

Posterior circulation stroke - cerebellar, brainstem

78
Q

Parkinsonism signs

A

Gait - slow, shuffling, slow start/turn, limited arm swing
Face - expressionless, glabellar tap +ve, slow monotonous speech

Pill rolling tremor, bradykinesia, rigidity
Cogwheel rigidity

79
Q

Parkinsonism causes and features of each

A

Idiopathic parkinsons disease

Lewy body dementia - dementia present also
Drug-induced - look at med hx (anti-psychotics)

Parkinson plus syndromes:

  • Multisystem atrophy: low BP (postural hypotension)
  • Progressive supranuclear palsy: palsy of vertical eye movements
  • Corticobasal degeneration: apraxia, myoclonus, acalculia
80
Q

Neuro exam

Broad and unsteady gait

A

Ataxia

Look for further cerebellar signs

81
Q

Cerebellar signs in the arms (x5)

A

Rebound overshoot
Dysdiadochokinesia
Hypotonia, hyporeflexia
Past-pointing and intention tremor

82
Q

Cerebellar sign localisation within the cerebellum?

A

Cerebellar vermis - more trucal ataxia, minimal limb signs

Cerebellar hemisphere lesions - ipsilateral limb signs, less truncal involvement

83
Q

Cerebellar syndrome causes and features (x4)

A

Multiple sclerosis - young, female, spasticity, internuclear opthalmoplegia

Stroke - older, AF, CABG, tar staining

Alcohol - chronic liver disease

Phenytoin - gingival hypertrophy

84
Q

What is internuclear opthalmoplegia?

What is seen?

A

Failure of lateral conjugate gaze

lesion of median longitudinal fasiculus tract which connects the nuclei of CN III IV, VI

On examination:

  • Ipsilateral - failure of ADduction
  • Contralateral - nystagmus when in ABduction

Can be bilateral

85
Q

Main two categories of a facial palsy-causing lesion

A

Cerebral hemispheric lesion - contralateral and preservation of frontalis

Facial nerve (or nucleus) lesion - ipsilateral and frontalis wekaness

86
Q

Facial palsy PLUS corticospinal tract signs, VI palsy

Site of lesion and underlying cause?

A

Pons

Stroke or MR

87
Q

Facial palsy PLUS V, VI, VIII and cerebellar signs

Site of lesion and underlying cause?

A

Cerebello-pontine angle

Acoustic neuroma

88
Q

Facial palsy PLUS VIII palsy

Site of lesion and underlying cause?

A

Inner ear

eg cholesteatoma

89
Q

Facial palsy PLUS parotid scar/swelling

Site of lesion and underlying cause?

A

Parotid tumour

90
Q

Treatment of Bell’s palsy?

A

Eye protection
Prednisolone if <72 hours

(acyclovir no longer recommended)

75% make a full recovery

91
Q

Secondary causes of Facial Palsy
(x7)
Unilateral and bilateral?

A

Unilateral - Herpes Zoster (Ramsey-Hunt syndrome), Diabetes mononeuropathy, tumour

Bilateral - Guillian Barre syndrome, Lyme disease, Sarcoidosis, Myesthenia Gravis

92
Q

Differential for mixed UMN and LMN signs

A

Motor neurone disease
Dual pathology (e.g. peripheral nephropathy (DM) and stroke)
Cons medullaris lesion (traumatic cauda equina)
B12 deficiency - causes peripheral neuropathy and subacute combined degeneration of the spine

93
Q

Gen surg

Oedematous and pigmented legs differential?

A

Chronic venous insufficiency

94
Q

Gen surg

Toe amputations

A

Diabetic foot disease

95
Q

Gen surg

Shiny, pale legs differential?

A

Peripheral arterial disease

96
Q

Differentials for Groin Lump (x6)

Lateral to medial

A

Lat to med

Psoas abscess (rare)
Femoral artery aneurysms
Vascular - varicose veins, saphena varix (dilation at top of great saphenous) - bluish tinge, disappears on lying down
Inguinal hernia (above inguinal ligament)
Femoral hernia (below inguinal ligament, more rare)
Lymphadenopathy

97
Q

Inguinal hernia signs on examination (x5)

A

Show antomical landmarks (neck lies above inguinal ligament - ASIS to pubic tubercle)
Reduces when lying down, protrudes with cough
Bowel sounds present (exclude obstruction)
Comment on scrotal extension

Indirect - compression at deep ring (just above midpoint of inguinal ligament) prevents protrusion
Direct - still appears

98
Q

Differences between femoral and inguinal hernias?

A

Anatomy - Inguinal (75% indirect, 25% direct through inguinal canal), femoral (through femoral canal, neck inf and lar to pubic tubercle)

Epidiemiology - inguinal much more common

Management - inguinal elective repair (unless irreducible)
Femoral - urgent surgery, at increased risk of strangulation (narrower canal)

99
Q

Anatomy of direct inguinal hernias?

A

Hesselbach’s triangle

Inf - inguinal ligament
Lat - inferior epigastric artery
Med - rectus abdominus

100
Q

Gen surg

On examination of the lower limb:
Callus and toe amputations

Differential?

A

Diabetic foot

101
Q

Gen surg
On examination of lower limb:

Trophic changes, reduced pulses, necrosis

Differential?

A

Arterial disease

102
Q

Gen Surg

On examination of the lower limbs:

Oedema, normal puses, ulcers

Differential?

A

Venous insufficiency

103
Q

Arterial vs venous skin changes in vascular disease?

x5 each

A 
ARTERIAL insufficiency:
Thin, scaly, dry skin
Hair loss
No oedema
Cold
Distal gangrene (at most peripheral part)
VENOUS insufficiency:
Oedema
Lipodermatosclerosis
Eczema
Varicose veins
White, stellate scars from prev ulcers (atrophie blanche)
104
Q

How to measure ABPI?

Which pulses to use?

When might it be unreliable?

What value suggests periperal vasc disease?
What value suggests critical ischaemia?

A

1) Doppler US over pulse
2) Cuff inflated proximal to artery
3) Inflate until doppler pulse stops, then deflate slowly until it returns
- This is the systolic pressure in that artery

Do brachial artery pulse in BOTH arms
Take highest of left and right arm

Do posterior tibial AND dorsalis pedis artery
Take the higher of the two values

  • ABPI is the pressure in the leg divided by the arm

Unreliable in pt with arterial calcification (due to incompressible arteries), such as in diabetic pts

<0.9 in PVD
<0.3-0.5 in critical ischaemia

105
Q

Buerger’s test?

A

Elevation pallor and venous guttering
Legs go white when raised off the bed

Then sit over side of bed with legs hanging down
Sunset sign - rubor of dependancy, purple/red colour
Reactive hyperaemia - all vessles maximally dilated following elevation

106
Q

Where is the location of disease?

1) Absent pulses bilaterally?
2) Absent in one leg only, below femorals?
3) Absent dorsalis pedis only?
4) Absent posterior tibial only?

A

1) Aorto-iliac
2) Femoral-popliteal on affected side
3) Anterior tibial (dor pedis is a continuation of this)
4) Posterior tibial

107
Q

Features of critical limb ischaemia?

x6

A
  • Rest pain (often worse at night)
  • Absent foot pulses, reduced cap refill
  • Dependant rubor (red/purple colour)
  • Early pallor on elevation (Buerger’s angle <20 degrees)
  • Skin changes, ulcers, gangrene

ABPI <0.5

108
Q

Management of peripheral arterial disease

A

Smoking cessation, exercise

Medical - ACE-i, clopidogrel, statins, diabetes
Need to agressively manage RISK FACTORS (risk of MI, stroke)

Step up to - angioplasty, stenting, bypass grafting

Last resort - amputation (needs to be quite proximal to ischaemia to enable healing)

109
Q

Top neck lump differentials and defining features on examination (x4)

A

Goitre - midline, firm, thyroid status, moves on swallowing, NOT tongue protrusion

Thyroglossal cyst - in the midline, higher up, moves with tongue

Lymph node - reactive or malignant, will be ant/post cervical chain (not midline), malignant is harder, fixed, larger
Always FLAWS a solitary lymph node

Brachial cyst - fluctuant, in the anterior triangle

110
Q

Thyroid differentials

1) smooth and hyperthyroid
2) nodular and hyperthyroid
3) nodular and euthyroid
4) single nodule and euthyroid
5) smooth and hypothyroid

A

1) Graves
2) Toxic multinodular goitre
3) Non-toxic multinodular goitre
4) Malignancy, adenoma, cyst
5) Hashimoto’s, iodine def

111
Q

Complications of a goitre (x6)

A

Due to underlying cause: eg. malignancy, Graves (arrythmias, bone loss, eye damage if can’t close completely)

Local causes:

  • Thoracic outlet obstruction
  • Dysphagia
  • Upper airway obstruction
  • Recurrent laryngeal nerve compression (hoarseness
112
Q

Treatment of Grave’s disease

And key side effects?

A

Propranolol (symptomatic)
Propylthiouracil or carbimazole for 18-24 months
(Thyroid peroxidase inhibitors)

  • Agranulocytosis with carbimazole
  • Both teratogenic

Radio-iodine as tx of choice to cure
May worsen eye disease, contraindicated in preg
May show late hypothyroidism

Alternative is bilateral subtotal thyroidectomy

113
Q

Vasucular exam

Toe amputations (alongside other healthy toes)
Neuropathic ulcers
Callus

A

Diabetic foot

Callus due to lack of sympathetic innervation, lack of sweating so dry skin

Single toes due to localised osteomyelitis

Check insuline injection sites, fingers for BG monitoring

114
Q

Arterial vs venous vs neuropathic ulcers?

A

Arterial - deep, pale, necrotic
Tend to be distal, +++pain

Venous - shallow, red, scaly, weepy
Tend to be lower leg, achy
May see oedema, haemosiderin

Neuropathic - deep, pink/red, surrounding callus
Tend to be on plantar aspect, pressure points
May see foot deformity, decreased sensation

115
Q

Diabetic foot management (x7)

A

Annual review - med and podiatry
Avoid high risk behaviours (e.g. walking barefoot)
Orthotics with pressure relief
Callus debridement (avoid build up of pressure beneath callus and ulcer progression)
Good glycaemic control
IV abx if infected
MRI if abscess/osteomyelitis (+- drain or amputation)

116
Q

Most common area for venous ulcer?

A

Gaiter area
(superior to medial malleolus lateral and medial)
due to anatomical venous drainage, less efficient perforating veins

117
Q

Signs of chronic venous insufficiency on examination (x7)

A 
Oedema
Lipodermatosclerosis
Eczema
Venous ulcers
Varicose veins
Warfarin (prev DVT)
Abdo mass with compression
118
Q

Two main types of varicose veins?

A

Distriibution of short saphenous vein
Posterior aspect of calf up to knee

OR

Distribution of great saphenous vein
Medial aspect of the leg
From hallux to pubic tubercle

119
Q

Trendelenburg’s test

A
  1. Lie pt down, empty blood out of veins
  2. Compress sapheno-femoral junction
  3. Stand pt up

If no refill whilst compressing (negative) - shows deep veins are competent

Then refill when compression removed (positive) - shows superficial veins are incompetent

The test is reported in two parts, the initial standing up of the patient (positive or negative based on rapid filling) and the second phase once the tourniquet is removed (positive or negative based upon rapid filling)

Superficial veins of the leg normally empty into deep veins, however retrograde filling occurs when valves are incompetent, leading to varicose veins

120
Q

Management of venous insufficiency

x5

A 
Compression bandaging
Emollient (/steroid) for eczema/lipodermatosclerosis
Analgesia if pain
Elevate legs when possible
Lose weight, keep active, avoid injury
121
Q

Management of varicose veins

A

Lose weight, moderate exercise, elevate legs where possible

US prior to intervention (position of SFL is variable)

Refer to vascular for:

  • Injection sclerothrerapy
  • Surgical stripping or ligation
122
Q

Carpal tunnel examination

A

Look for vertical scar on wrists/palm of hand over flexor retinaculae

Test abductor pollicis brevis (palm flat, move thumb to ceiling)
Loss of sensation over index finger
Thenar wasting
Phalen’s test (dorsum of hands together, 30-60s)
Tinel’s test (tap over nerve)

123
Q

Associations of carpal tunned syndrome

A

(Any cause of swelling in carpal tunnel)

Trauma
Pregnancy 
Rheumatoid arthritis
Hypothyroidism
Diabetes
Acromegaly
Exaggerated by occupational repetitive strain injury
124
Q

Top hand differentials in PACES and distinguishing features (x4)

A

Rheumatoid - MCP swelling (tender with gentle squeeze), deformity (z-thumb, Swan-neck, boutonierre’s, ulnar deviation)

Osteoarthritis - bony nodules (Bouchard PIP, Heberdens DIP)

Systemic disease - sclerodactyl, calcinosis, nail changes, Reynauds, dupuytrens

Carpal tunnel - scar, thenar wasting

125
Q

Extra-articular manifestations of rheumatoid arthritis

x11

A

Pulm - pleural effusions, pulm fiborosis, bronchiectasis
Eyes - scleritis
Neuro - carpal tunnel, atlanto-axial subluxation
Haem - anaemia, Felty’s syndrome
Cardiac - pericarditis
Renal - neptrotic synd, amyloidosis

126
Q

RA management

A

Conservative - adaptations, physio

NSAIDs - symptoms
DMARDS - methotrexate, steroids, hydroxychloroquinine
Anti-TNFs - infliximab, gadalinumab (if tried >2 DMARDS)

127
Q

Knee osteoarthritis management

A 
Weight loss, exercise
Physio to prevent fixed flexion deformity and preserve function
OT
Analgesia (NSAIDs and PPI cover)
Intra-articular steroids
Joint replacement
128
Q

Osteoarthritis xray changes

A

Loss of Joint Space
Osteophytes
Subchondral cysts
Subchondral sclerosis

129
Q

Nail pitting in the hands?

Joint examination

A

Psoriasis

Think psoriatic arthritis

130
Q

Psoriasis signs (x3)

A

Extensor plaques with scales - erythematous base, dry scaly flakes on top

Also on scalp and behind ears
Note: auspitz sign (bleeding when scales removed)

Nails - Pitting, Oncholysis, Subungal Hyperkeratosis (POSH)

May see it present as Koebner phenomenom, Guttate psoriasis

131
Q

Psoriatic arthropathy types (x5)

A

LASSA

Large joint mono/oligo-arthitis
Arthitis mutilans
Sacroilitis
Seronegative (similar to RA)
Asymmetrical polyarthritis (including DIP, similar to OA)
132
Q

Management of psoriasis (x6)

A

Avoid precipitants - smoking, BB, stress, alcohol
Calcipotriol (vit D analogue)
Betamethasone (steroids)
Tar or dithranol (antiproliferative agents)
Psoralen and UVA (PUVA)

Methotraxate and anti-TNFs for arthritis

133
Q

How do you confirm anaphylaxis on blood tests?

A

Tryptase
Do at time 0, 1 hour, 12-24 hours

Peak at 30 mins-1 hour post anaphylactic rxn
Fall back to baseline within a few hours

Tryptase contained in mast cells so spike in levels seen with mast cell degranulation

__Y6 Finals Revision (14 decks)

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