Basal Cell Carcinoma

Background and Epidemiology

  • The most common malignancy in caucasian individuals (rare in patients with darker skin), with an incidence of up to 0.2% of the population (100-200/100,000)
  • Lifetime risk is estimated at 30%

Risk Factors/Aetiology

  • UVR exposure
    • The exact importance of duration/magnitude is unknown, so it is important to ask about any over-exposure
    • Sub-burn and overexposure as a child seems much more significant than that as an adult
  • Skin type I
  • Red/blonde hair and blue/green eyes; freckling in childhood
  • Family history
  • Previous skin cancer
  • Age
  • Immunosuppression
  • PUVA treatment
  • Rarely, genetic syndromes can predispose to BCC (i.e. basal cell naevus syndrome associated with Gorllin’s syndrome)


  • Arise from the pluripotent cells of the basal cell layer of the epidermis
  • One of the important signalling pathways thought to be dysregulated in the development of BCC is the Hedgehog-patch pathway
    • Hedgehog gene encodes an extracellular protein that binds to a cell membrane receptor complex (Patch and SMO) to start a cascade of cellular events responsible for cell proliferations
      • mutations of Patch, hedgehog and SMO, as well as other tumour suppressor genes, can all increase the risk of BCC development

Presentation and types of BCC

  • Typically occur on sun-exposed areas e.g. head and neck (80%)
  • Early lesions are small, may be translucent or pearly and have raised border with telangiectasia and an ulcerated centre (rodent ulcer)
  • Nodular
    • Solitary, shiny, red/pearly nodule with large telangiectasic vessels
      • may be cystic
      • may be ulcerated with rolled edges
    • Commonly on the face
    • Typical history is of spontaneous bleeding and healing
  • Superficial
    • Tends to occur in younger patients and at multiple sites, most commonly the upper trunk/shoulders
    • Pink/red, scaly, irregular plaques, well-demarcated and often larger than 20mm at presentation
    • Slowly grow over months/years
    • Can bleed/ulcerate
  • Morphoeic (or sclerosing/infiltrative)
    • Usually found on the face
    • Generally more aggressive
      • May infilltrate peripheral nerves and more likely to recur after surgery
    • Thickened, yellowish/skin-colour, waxy/scar like, poor demarcated plaques


  • The principle investigation is biopsy for histology.  Because BCCs are usually small and localised, surgical excision of the lesion is usually performed for both diagnostic and therapeutic purposes.
    • Surgical excision is treatment for the majority (certainly nodular BCC) of tumours
      • 4mm margin is recommended
  • Other options include
    • Mohs surgery
      • Mainly used for large (>2cm) tumours at high risk sites e.g. alar crease of the nose, near the vermillion border of the lips, on the ear etc
      • Also used for BCC recurrences
      • BCC without clear margins
    • Curettage and cautery
      • May be used for low risk BCC (small, well-defined, non-critical sites)
    • Radiotherapy
    • Topical treatments may be preferred for superficial BCC e.g.
      • imiquimod
      • topical fluorouracil 5% (body/trunk/limbs- not face)
      • cryotherapy
    • Rarely light therapy (PDT) can be used (patients are made photosensitive)

Prognosis, Prevention and follow-up

  • 5-year cure rate of about 90%
    • A minority of patients may relapse
    • (Almost no patients will ever die of BCC)
  • Make sure to advise about UV protection
  • Also ask to return early if symptoms/features recur


Gentamicin, Tobramycin, Neomycin

Structure and efficacy

  • Composed of an essential 6-membered ring with amino-group substitutions
  • Excellent activity against aerobic gram-negative organisms including enterobacteriaceae (e.g. E coli, Klebsiella, Proteus), also Pseudomona aeruginosa
  • Can be used in combination with beta-lactams and glycopeptides for synergy against Staphylococci and Streptococci (gram-positive)
  • Not effective against anaerobic organisms


  • Interferes with bacterial protein synthesis by binding to the 30S ribosomal subunit.
    • Note that, in order for aminoglycosides to reach this target, it requires an oxygen-dependent transport system
      • this is inhibited by divalent cations e.g. Ca2+ and Mg2+; low pH; anaerobic conditions and hyperosmolarity
    • However, once achieved, these are rapidly bactericidal (efficacy increases with concentration).  They also continue to kill bacteria after levels have dropped
      • Once daily dosing is adequate (see prescribing below)


  • Poor GI absorption- IV route needed
  • Distributed well into the urine, kidney (nephrotoxic), inner ear (ototoxic), bone, synovial and peritoneal fluids.  Generally poor CSF levels.
  • Majority excreted by the kidneys


See Gentamicin prescribing protocol for NHS tayside

(Also the Hartford Gentamicin Calculator)

Side effects

  • Nephrotoxicity- requires eGFR and U&Es monitoring (usually reversible)
  • Ototoxicity- usually irreversible (early symptoms include tinnitus, vertigo)
  • Neuromuscular blockade- gentamicin is contraindicated in patients with e.g. myaesthenia gravis
    • reversed by calcium gluconate


Mechanism of action

  • Inhibits bacterial RNA-dependent protein synthesis by binding to the 50S subunit of the 70S ribosome, which causes dissociation of t-RNA from the ribosome and prevents protein synthesis
  • Protein synthesis can resume once the antibiotic is removed i.e. bacteriostatic
    • The bacteria are then killed by WBCs
  • Effective against
    • gram-positive aerobic organisms e.g. Strep pneumoniae;
    • some gram-negative aerobic organisms e.g. Legionella, Neisseria gonorrhoea, Moraxella and Bordetella (Enterobacteriaceae are resistant)
    • useful against other intracellular pathogens e.g. mycoplasma, Chlamydia


  • Absorption via the gut is poor due to destruction by gastric acid and poor water solubility.  (Better absorbed in a fasting state)
  • Excreted mainly by the liver, biliary system and into the gut (little renal excretion)
  • Clarithromycin has a fairly short half life (requires bi-daily dosing) but azithromycin has an extended half-life which means a single dose can often be effective

Adverse effects

  • GI upset is common
  • Prolongation of the QT interval is a potentially serious side effect in patients with either an already prolonged QT interval or WPWS


Vancomycin and Teicoplanin

Mechanism of Action and Range

  • All glycopeptides act on the bacterial cell wall (bacteriocidal)
    • Inhibits cell wall peptidoglycan synthesis by forming complexes with D-alanine residues on peptidoglycan precursors
  • Because they are unable to penetrate the outer liposaccharide layer of gram-negative organisms, their use is restricted to gram-positive organisms
    • Useful against gram-positive cocci which are resistant to penicillins
    • However, their use should be restricted as more strains are becoming resistant


  • Both require IV/IM administration except in C diff infection where vancomycin can be given orally
  • Little distribution to the CSF
  • ~55% bound to plasma proteins
  • Eliminated mainly by kidneys (>80%), the majority within 24 hours
    • Note, however, that glycopeptides generally take a while to work (>24 hours), therefore multiple doses must be given.
    • Due to risk of nephrotoxicity, patients must have vancomycin levels and U&Es/eGFR monitored regularly (trough concentrations.  Note that the loading dose is also based on patient weight (see prescribing below)
      • Aim for levels >10mg/l
  • Synergistic effect with aminoglycosides


For NHS Tayside Vancomycin prescribing protocol, see Vancomycin Protocol June 11

NB There are also teicoplanin dosing protocols (see formulary)

Typically used for serious infections e.g. endocarditis.

Beta-lactam Antibiotics


  • Contain a ‘beta-lactam’ ring structure
    • Note that a drawback of these antibiotics is that some bacteria can secrete beta-lactamases which breaks down this ring and thus inhibits the agent’s action

Mechanism of action/Pharmacokinetics

  • Bactericidal- inhibits enzymes involved in cell wall synthesis (preventing cross-linking of peptidoglycan in the cell wall)
  • Mostly metabolised/excreted via the kidneys (ceftriaxone has a biliary excretion component also)
  • Penicillins can distribute well to the urine, synovial fluid, pleural fluid, CSF.  They are useful for skin/soft tissue infections (Strep pyogenes), meningitis (N meningitidis or S pneumoniae)
  • Cephalosporins also have a fairly good distribution to the CSF and are used in a number of infections in the hospital setting.
  • Generally safe (see below for allergy)


  • Penicillins
    • Natural penicillins e.g. benzylpenicillin and phenoxymethylpenicillin provides good cover against Gram-possitive organisms and anaerobic organisms: staphylococci, streptococci, neisseriae, spirochaetes and certain other organisms e.g. oral anaerobic organisms (e.g. in dental disease)
      • However, resistance (beta-lactamases) is largely found in staphylococci and gonnococci
      • Other staphylococci and pneumococci can be resistant to penicillin via other mechanisms
    • Aminopenicillins e.g. amoxicillin and ampicillin have the added ability to cover some Gram-negative organisms (enterobacteria)
      • Resistance is quite common so they are not routinely used first line for the treatment of gram-negative infections
        • Mostly due to beta-lactamase production.  This can be overcome by the addition of a beta-lactamase inhibitor e.g. clavulanic acid (e.g. co-amoxiclav) or sulbactam
    • Carboxypenicillins (e.g. ticarcillin) and ureidopenicillins (e.g. piperacillin) are very effective against Gram-negative organisms, particularly Pseudomonas spp. which is resistant to other types of antibiotics
      • Can also be enhanced by beta-lactamase inhibitors (e.g. tazocin: piperacillin + tazobactam)
  • Cephalosporins
    • Structure
      • Beta-lactam ring is fuse with a dihydrothiazide ring (cf thiazolidine ring of penicillins)
    • Efficacy/Clasification
      • Generally good broad-spectrum agents.
      • No effect against Enterococcus spp
      • First-generation cephalosporins (e.g. cephalexin)
        • Rarely used in hospital setting, (occasionally in the community)
        • Effective against Gram-Positive aerobic cocci e.g. Strep pyogenes (group A strep), Group B strep and streptococcus viridans
      • 2nd generation (e.g. cefuroxime)
        • less active against gram-positive but more active against gram-negative organims.  Cephamycins are also active against anaerobic Gram-negative bacilli
      • 3rd generation (e.g. cefotaxime, ceftriaxone)
        • generally broad-spectrum, covering a spread of both gram-positive (e.g. S aureus, Group A and B strep, Strep pneumoniae) and gram-negative organisms (e.g. H influenzae, Moraxella, Neisseria and Enterobacteriaceae)
        • generally used in hospital-acquired/severe gram-negative organism infection e.g. bacterial meningitis
  • Others 
    • Carbapenems e.g. Imipenem
      • Often an antibiotic of last resort and is truly broad-spectrum

NOTE: Beta-lactam antibiotics tend to work synergistically with aminoglycoside

Adverse effects

  • Penicillin allergy affects 0.7-10% of patients
    • Note it is important to ask about the features of the ‘allergy’ (distinguish from an intolerance)
    • DO NOT prescribe penicillins to a penicillin allergic patient. Avoid cephalosporins also where possible
  • Cephalosporins are associated with C difficile infection and so they are rarely used without a laboratory (and C&S) diagnosis

Aortic Aneurysm

In general, an aneurysm is a localised or diffuse dilatation which is at least 50% greater than the normal size of an artery.

An abdominal aortic aneurysm is a permanent dilation of the abdominal aorta >3cm in diameter.

true aneurysm is one where the 2 or more layers of the vessel wall forms the wall of the aneurysm (i.e. vessel wall is intact).

false aneurysm is one where a collection of blood is held close to the vessel by a wall of connective tissue (i.e. contained leak from a vessel).

fusiform aneurysm is one where the aneurysm is tapered at both ends.  A sac-like aneurysm is more rounded.


  • The majority (~75-95%) of aortic aneurysms are abdominal and below the level of the renal arteries (~30% also involve the iliac arteries)
    • Of those that are thoracic, the majority are either in the ascending or descending sections (rarely found in the arch)
    • Occasionally, you can also get thoracoabdominal aneurysms.  These can be classed using the Crawford classification
  • The prevalence of AAAs is between 1.3-12.7%.  AAA frequency increases with age (25/100,000 in 50 year old men vs 78/100,000 in >70 year old men)- around 1 in 20 men >65 increasing to almost 1 in 10 >75
    • Male : Female ratio 6:1


  • Family history/genetics are becoming increasingly apparent as a causal factor
  • Smoking
  • Male
  • Age
  • Hypertension
  • COPD
  • Heart disease/atherosclerotic disease
  • Hyperlipidaemia
  • Rarely, other causes e.g. trauma, infection (e.g. TB, HIV); inflammatory diseases (Behcet’s, Takayasu’s); connective tissue diseases (Marfan’s; Ehlers-Danlos type IV)
  • Diabetes seems to be protective
  • Can be associated with aneurysms elsewhere e.g. popliteal aneurysms


  • In patients >50, the normal aortic diameter is 1.5cm in women and 1.7cm in men.
  • Aneurysms are thought to arise due to failure of major structural proteins of the aorta (elastin and collagen)
    • This can be genetic
    • Inflammatory processes are also thought to contribute
      • Proteases and metalloproteinases may be important, as are interleukins and various cytokines
  • Atherosclerosis (degenerative disease) is a common finding in patients with AAA.  However, not all patients with severe atherosclerotic disease will develop AAA.  The association is not thought to be causative, but there may be a common underlying process in predisposed individuals.  Some patients exhibit an inflammatory mechanism whereby vessel wall inflammation causes adhesions to adjacent structures e.g. duodenum, small bowel etc.
    • Other causes include
      • Mycotic/infective
      • Traumatic (more commonly cause false aneurysms)
      • Connective tissue disorders e.g. Marfan’s syndrome; Ehler Danlos; Tuberous sclerosis


  • Size is the best indicator of likelihood of rupture.  Note that rate of growth is also a powerful indicator.
    • <5cm have a <4% chance per annum
    • 5-6cm have a 7% chance
    • >6cm have a >20% chance (i.e. exponential increase with size)
    • a growth of >10% per year significantly increases risk


  • Incidental- The majority of patients with an unruptured AAA will be asymptomatic and the diagnosis will be incidental either from
    • Physical examination
      • Expansile mass (i.e. expands – not just pulsatile as with normal pulses and in false aneurysms)
    • Imaging (commonly abdominal USS, but x-ray/CT/MRI also possible)
  • Patients may present with central abdominal pain, back pain, loin pain or pain in the iliac fossa/groin (rarer)
    • NB this is more common in inflammatory type aneurysms
  • Rarely, AAAs can allow thrombi to form.  These can then embolise to the lower limb causing acute ischaemia
  • Occasionally patients may have features of compression/obstruction e.g. vomiting (duodenal obstruction); oedema/DVT (IVC obstruction)
  • Rupture
    • A ruptured TAA can cause sudden onset, severe chest pain (may be similar to MI).  This can radiate to the back.  This may also deteriorate rapidly.
    • A ruptured AAA causes a ‘classical triad’ (few patients have all 3) of
      • Back/flank pain
      • Hypotension
      • Pulsatile abdominal mass
    • The patient may also feel nauseous (+/- vomit); light-headed (+/- syncope); pale/sweaty/cold; may also have bruising in flanks
    • The pulse may be weak, rapid and ‘thready’.
    • Mild cases may present with features similar to renal colic


  • Abdominal USS is the first line imaging investigation in patients with a stable AAA.
    • CT is usually the gold-standard investigation for evaluation of the aneurysm
  • Other investigations to consider would include an ECG, CXR, bloods


  • Uncomplicated aneurysm
    • <5.5cm are generally monitored
      • 3-4.4cm annually (USS)
      • 4.5-5.4cm 3-monthly (USS)
      • >5.5 (if unsuitable for surgery) 3 monthly (USS)
    • >5.5cm – consider surgery (particularly for patients with high risk of rupture e.g. large diameter, smokers, female, hypertension, family history, rapid expansion, onset of sinister symptoms/signs e.g. pain/tenderness)
      • Endovascular stent-graft repair preferred due to
        • avoids open surgery and aortic clamping
        • reduced mortality within 4 years
  • Ruptured aneurysm
    • Surgical emergency
    • ABCDE until theatre ready
    • 95% overall mortality (50% in theatre)
      • Most patients won’t survive (for those who even reach theatre, surgery mortality is 60-80%, more if there are impacting factors e.g. >80yo; shock non-responsive to resuscitation); cardiac arrest prior to/during surgery)
  • Open repair
    • Indication
      • Elective if >5.5cm or if rapidly expanding or if patient presents with pain; all emergency cases (rupture)
    • Pre-operative assessment
      • BP control
      • Smoking cessation
      • Co-morbidity/mortality assessment
    • Consent
      • 5% mortality (significant)
      • DVT; Chest infection; wound infection
      • Graft infection (~1 in 500)
    • Procedure
      • Supine position
      • Midline incision (usually)
      • Retract bowel and duodenum to right
      • Divide the posterior peritoneum and dissect the AAA
      • Define the proximal and distal neck/extent of AAA
      • Administer IV heparin
      • Apply distal then proximal aortic clamps (warn anaesthetist) before incising sac
      • Oversew arteries e.g. lumbars/IMA if patent

AAA Screening

  • Offered to all males >65 years old
  • Those with small aneurysms are monitored and those with larger ones (>5.5cm) are offered surgery


Hypertension is a blood pressure >140/90mmHg.


  • Around 30% of adults have a BP of >140/90mmHg
  • Prevalence increases with age (30% aged 45-54; about 70% in peopler ages 75+ years)
  • More common in African-Caribbean than in Caucasian people
  • Hypertension is one of the most common conditions seen in patients and one of the most common reason for prescribing medications
    • Accounts for >£1 billion worth of drugs per year


  • In the majority of individuals, a specific cause of hypertension is not found (essential hypertension)
  • There are many factors that are thought to contribute to primary hypertension:
    • renal dysfunction (via RAAS as well as salt/water excretion)
    • peripheral resistance and vessel tone
    • endothelial dysfunction
    • autonomic tone
    • insulin resistance
    • neurohumoral/immunological factors
    • genetic factors
  • Secondary hypertension can be caused by
    • Alcohol
    • Obesity
    • Pregnancy
    • Renal disease
    • Endocrine disease
    • Drugs
      • e.g. OCP, anabolic/cortico-steroids, NSAIDs, sympathomimetic agents

NB It is important to take a full history from a patient with hypertension to rule out any underlying causes for secondary hypertension and to evaluate whether the patient has any target organ damage.  E.g. Full drug hx; do they have any symptoms e.g. headache, sweats/palpitations (could this be a phaeochromocytoma?).  Is there a family history of renal disease? Does the patient appear cushingoid?


  • Note that “white coat” hypertension can be confounding.  This is blood pressure that is unusually high simply due to the anxiety and/or concerns about seeing the doctor.
  • Measuring blood pressure
    • It is important to try and keep the environment constant whilst measuring blood pressure e.g. relaxed, quiet, seated with arm outstretched and supported at heart level (ideally the arm should be bare)
    • If there is a difference of >20mmHg between arms, record measurements from the arm with higher BP
    • If the first reading is >140/90mmHg, take a second after a minute interval.  If this is substantially different, record a third measurement too.  Use the lower of the last two measurements.
    • If all measurements are consistently >140/90mmHg, recheck BP on 2-3 occasions over the next few weeks
      • If clinic BPs are persistently above 140/90mmHg, offer ambulatory blood pressure monitoring or home blood pressure monitoring
  • Classification
    • Mild (Stage I)
      • clinic BP >140/90mmHg and ABPM average is >=135/85mmHg
    • Moderate (Stage II)
      • clinic BP >160/100mmHg and ABPM average is =>150/95mmHg or there is isolated SBP of >=160mmHg
    • Severe (Stage III)
      • clinic BP >180/110mmHg
      • NB if a patient has this high a BP, check the retina for hypertensive retinopathy (papilloedema and/or retinal haemorrhage).  Also take bloods (FBC, U&Es and LFTs), urinalysis and do an ECG for signs of other system failure e.g. acute kidney injury
        • Malignant hypertension is defined as grade III hypertension with signs of secondary organ damage

Other investigations

  • As well as BP, ECG, Bloods and urinalysis
    • Test glucose (diabetes)
    • Test cholesterol for cardiac risk


  • Lifestyle advice
    • Alcohol consumption; caffeine consumption; salt consumption
    • Smoking
    • Stress
    • Don’t take electrolyte supplements
    • Exercise/physical activity
    • Weight loss
    • Diet
  • Assess cardiac risk
    • There are several ways of assessing risk
      • QRISK2 (see here)
      • ASSIGN score (see here– more commonly used in Scotland)
      • In general, a score of >20(% in 10 years) and age >50 years suggests intervention, including low-dose aspirin (75mg), statin treatment
  • Antihypertensive medication
    • Offer if
      • <80yo; mild hypertension and one or more of
        • Target organ damage, established CVD, renal disease, diabetes and/or a 10 year CV risk of 20% or more (using ASSIGN or QRISK2)
      • Moderate Hypertension (all)
    • If <55yo (and not African-Caribbean)
      • start an ACE inhibitor or (if intolerant/contraindicated) an Angiotensin-II-receptor blocker
        • In Moderate to severe renal disease, reduce the dose of ACEIs (cleared by the kidney)
        • Relatively contraindicated in bilateral renal artery stenosis
        • Drug interactions (important ones): DO NOT CO-PRESCRIBE ACEI, NSAID +/-  ARB
      • Alternatively, a beta-blocker can be used in young patients
        • who can’t tolerate ACEIs/ARBs
        • women who might become pregnant or are planning a pregnancy
        • NOTE that whilst beta-blockers are recommended by NICE for the treatment of hypertension, SIGN does not recommend their use first line (only after 3-combination therapy has been tried)
          • this is because ‘beta blockers were the least clinically and cost effective drug at preventing major CV events’
        • Use can be limited by side effects: cool peripheries, fatigue and impotence are common.  Headache/postural hypotension is also possible.
    • If >55yo or Afro-Caribbean
      • Offer a calcium-channel blocker (dihydropyridine type e.g. amlodipine) unless there is evidence of oedema, heart failure (or risk of heart failure), or drug intolerance
        • In this case, offer a thiazide diuretic or a thiazide-like diuretic
    • Note that if BP remains uncontrolled on one drug
      • Offer combination of CCB/TD/TLD and ACEI/ARB*/BB
        • Preferred in African/Caribbean patients
      • If the patient’s BP remains high with 2 drugs at optimal doses
        • consider ACEI/ARB + CCB + TD/TLD
      • If still resistant to treatment (resistant hypertension)
        • sensible to refer to a specialist
        • It is possible to combine all 3 drug types.  Alternatively, low dose spironolactone can be added (or higher dose thiazide diuretic)
          • the former if K < 4.5 and the latter if >4.5
          • patients require close monitoring of their U&Es (particularly K+)
  • Admit a patient if they have
    • Malignant hypertension
    • Hypertensive encephalopathy
    • Suspected phaeochromocytoma and severe hypertension
    • Severe hypertension and high risk of vascular complications

Sepsis & Systemic inflammatory response syndrome (SIRS)

Sepsis and SIRS are common and can be a major cause of morbidity and mortality in the critically ill.




  • Note that whilst SIRS can be caused by infection, there are many non-infective causes e.g.
    • Burns
    • Dehydration
    • MI
    • Cirrhosis
    • Haematological malignancy
    • Drugs/medications
    • Surgical procedures etc etc etc.


  • If there is a suspected infection + SIRS- SEPSIS 6
    1. Oxygen (aim for 94-98% unless COPD or sepsis induced hypotension/severe sepsis)
    2. Fluid resuscitation
    3. Blood (and other) cultures (e.g. urine, swabs etc)
    4. IV antibiotics
    5. Lactate, FBC and Biochem (urgent)
    6. Monitor urine output (catheterise if appropriate)
  • see here for protocol sheet
  • Antibiotics
    • IV Amoxicillin, Metronidazole and Gentamicin is protocol in Tayside for infection of unknown source
    • Review antibiotic man and investigation results and ammend as necessary if there is a known (/clinically suspected) source

Peripheral Arterial Disease


PAD is a narrowing or occlusion of the peripheral arteries, affecting the blood supply to (usually the lower) limbs.

Acute limb ischaemia is an acute decrease in limb perfusion, with rapidly worsening clinical symptoms/signs, which may threaten limb viability.

Chronic limb ischaemia can present as intermittent claudication – when decreased circulation leads to pain in the limb on exertion- or as critical limb ischaemia (severe blood flow impairment such that there is an imminent risk of limb loss.

Background and Epidemiology

  • Incidence increases with age- affecting around 4-12% of people aged 55-70 and 15-20% of people >70 years.

Risk factors

  • Smoking (less than 5% of PAD patients have never smoked)
  • Diabetes mellitus
  • Hypertension
  • Hyperlipidaemia
  • Physical inactivity
  • Poor diet/ obesity

I.e. all risk factors for atherosclerosis


See atherosclerosis


  • 5 P‘s
    • Pulseless
    • Paralysis (complete or incomplete i.e. weakness)
    • Paraesthesia
    • Pain
    • Pallor
  •  History
    • Intermittent limb claudication
      • The most common symptom is muscle pain in the lower limbs on exercise/exertion and relieved by rest
        • Severe cramp-like/aching pain
        • Most commonly felt in the calves but the buttock/thigh can also be affected.  Typically found or is worse in one leg.
        • typically worse walking uphill (cf spinal claudication)
    • Critical limb ischaemia (usually indicates more severe disease)
      • Rest pain, particularly on lying down, which can be described as cramping/burning pain
    • Acute limb ischaemia
      • Acute-onset, severe pain which is not relieved by rest, often accompanied by loss of power and paraesthesias
    • There may be other symptoms e.g. weakness; sensory deficits (usually peripheral- glove/stocking- distribution); arterial ulcers
    • Make sure to ask about other cardiovascular disease e.g. hypertension, ACSs (inc MI); hyperlipidaemia; diabetes
    • Take a full remaining history e.g. FHx, SHx, RxHx, Allx etc etc
  • Examination (see here)

Other investigations

  • Blood tests
    • Cholesterol, Glucose (particularly if suspicious of diabetic association), D-dimers (if uncertain of the possibility of DVT)
  • Doppler ultrasound
    • As well as measuring ABPI, doppler USS is first line for the investigation of PAD and can evaluate the site and severity of disease
  • Angiography (MR is recommended but CT can also be used)
    • For patients with severe disease symptoms and evidence on USS (i.e. considering surgery), angiography should be performed


  • Cardiovascular risk
    • Smoking cessation
    • Treat hyperlipidaemia (statin)
    • Manage glycaemic control
    • Treat hypertension (as per guidelines)
    • Give low-dose aspirin (75mg daily) to patients with symptoms
  • Management of symptoms (intermittent claudication)
    • Exercise programmes (increasing duration to maximum severity; increasing the amount of exercise possible) is recommended
    • Angioplasty/stenting is only recommended for patients who have modified risk factors and have had no improvement with exercise (and who have surgically treatable disease identified on angioplasty)
  • Management of acute/critical limb ischaemia
    • Clinical emergency and requires urgent surgical management to avoid limb death
    • Endovascular revascularisation; percutaneous catheter-directed thrombolysis; surgical embolectomy are all options
    • If the limb is not salvageable, amputation may be required (occurs in 5-20%)


Chest pain/discomfort caused by an insufficient blood supply to the heart muscle.

Stable angina is angina which occurs during periods of increased oxygen demand on the heart e.g. exercise.  Symptoms are relieved by rest.

Unstable angina is an acute ischaemia of the heart muscle without any clinical features of infarction.  It, nonetheless, requires immediate attention (see ACSs).


  • Incidence increases with age and it generally has a male preponderance (8% of men 55-64 and 14% 65-74 have, or have had, angina; 3% and 8%, respectively, for women)
  • Most common cause is coronary artery disease
    • Modifiable risk factors include smoking, diet, sedentary lifestyle (commonly associated with poor socio-economic background)
    • Semi-modifiable risk factors include hypertension, diabetes, hyperlipidaemia, obesity


  • Chest pain
    • Often described as central, crushing/heavy, deep pain
    • Usually brought on by exertion.  May also be brought on by the cold, or after a large meal, or with intense stress/emotion.
    • Can be mild, moderate or severe in intensity/severity.
    • May radiate up to the jaw or down the left arm
    • May cause difficulty breathing
    • May be relieved slightly by leaning forward.  Almost always relieved by rest after seconds/minutes
    • Relieved by GTN*
      • If the patient is not on GTN spray and there is a suspicion over anginal pain, give GTN.  If the pain disappears, this is likely to be angina
  • If chest pain is not relieved by rest/GTN, this is unlikely to be stable angina.
  • Make sure to ask about previous cardiac disease (in particular MI).


  • ECG
    • Can be normal at rest or may show signs of an old MI
      • e.g. pathological Q waves (QS>20ms in V2-3 or Q wave >30ms and >0.1mV deep)
    • If symptoms are present
      • reversible ST-elevation/-depression, with or without T wave inversion.
  • Exercise tolerance is often used in patients with suspected angina (note that if the patient describes a clear history, this investigation may not be necessary)
    • ST-downsloping is the classical diagnostic feature
  • If a patient is not suitable for ETT (e.g. heart failure) but have pre-existing ECG abnormalities, an MRI myocardial perfusion scintigraphy can be performed
  • Rarely, angiography is used for the diagnosis of angina.  However, if the patient presents acutely and ACS is suspected, angiography may be performed acutely with the view for thrombolysis.


  • Where possible, give lifestyle advice e.g. smoking cessation, weight loss
  • For the acute attack- prescribe sublingual glyceryl trinitrate (GTN) spray
    • Advise the patient to stop what they are doing and take the nitrate
    • Give another dose after 5 minutes if the pain remains.
    • If the pain persists after a further 5 minutes, call 999
  • For prevention, prescribe
    • A beta-blocker e.g. bisoprolol
    • If the patient is not able to use a beta-blocker (e.g. severe asthma), consider a rate-limiting calcium channel blocker e.g. verapamil
      • Combination (BB and CCB) may be better, depending on the reason for discontinuation/failure of monotherapy
      • Occasionally, if neither is suitable, long-acting nitrates or nicorandil can also be options
  • For underlying heart disease
    • Low dose aspirin (75mg) and statin treatment must be considered
    • If the patient also has diabetes, ACE inhibitor treatments should also be considered
  • Revascularisation therapy (e.g. PCI, CABG) can be considered in patients who are either high risk and/or not responding well to pharmacological treatment