General Practice Flashcards
Define ischaemic heart disease (IHD)
Cardiac myocyte damage (and eventual death) due to insufficient supply of oxygen-rich blood
In ascending order of severity: stable angina> unstable angina > NSTEMI > STEMI
Main cause of IHD
- Atherosclerosis leading to the formation of atherosclerotic plaques that narrow the lumen of the coronary arteries
Risk factors for atherosclerosis and IHD
Non-Modifiable Risk Factors
- Older age
- Family history
- Male
Modifiable Risk Factors
- Smoking
- Alcohol consumption
- Poor diet
- Low exercise
- Obesity
- Poor sleep
- Stress
- Diabetes
- Hypertension
Define stable angina
A condition where a narrowing of the coronary arteries reduces blood flow to the myocardium.
During increased oxygen demand e.g., exercise, insufficient supply to meet demand > ischaemia > angina symptoms
Symptoms of stable angina
- Constricting chest pain with/without radiation to jaw or arms, brought on by exposure to cold/exercise
- Lasts 1-5 minutes
- Pain relieved by rest/GTN (glyceryl trinitrate) spray
Investigations for stable angina
Bedside:
- Physical examination (e.g., heart sounds, signs of heart failure, blood pressure and BMI)
- ECG (a normal ECG does not exclude stable angina)
- FBC (anaemia)
- U&Es (required before starting an ACE inhibitor and other medications)
- LFTs (required before starting statins)
- Lipid profile
- Thyroid function tests (hypothyroidism or hyperthyroidism)
- HbA1C and fasting glucose (diabetes)
- Cardiac stress test - assesses heart function during exertion e.g. walking on treadmill, and assess using ECG, echo, or MRI
- Gold standard: CT Coronary Angiography
Management plan for stable angina
- R – Refer to cardiology (urgently if unstable)
- A – Advise them about the diagnosis, lifestyle changes, management and when to call an ambulance
- M – Medical treatment
- P – Procedural or surgical interventions
Immediate symptom relief for stable angina
- GTN spray, repeat after 5 minutes if no relief
- Call ambulance if no relief after repeat dose
Long-term symptom relief for stable angina
Use one or a combination if uncontrolled on one:
Beta blocker (e.g. bisoprolol) and/or Calcium channel blocker (e.g. amlodipine)
Primary prevention of stable angina
- Lifestyle changes
- Low-dose aspirin (75mg once daily)
Secondary prevention of stable angina
4As
- Aspirin (i.e. 75mg once daily)
- Atorvastatin 80mg once daily
- ACE inhibitor
- Already on a beta-blocker for symptomatic relief.
Define acute coronary syndrome
Acute Coronary Syndrome is usually the result of a thrombus from an atherosclerotic plaque blocking a coronary artery.
Three types:
- Unstable angina
- ST Elevation Myocardial Infarction (STEMI)
- Non-ST Elevation Myocardial Infarction (NSTEMI)
Symptoms of ACS
- Chest pain
Central, ‘heavy’, crushing pain
Radiation to the left arm or neck - Certain patients, such as diabetics, may not have chest pain (‘silent MI’)
- Shortness of breath
- Sweating
- Nausea and vomiting
- Palpitations
- Anxiety: often described as a ‘sense of impending doom’
ECG + troponin results in unstable angina
ECG normal + troponin levels not raised
NSTEMI: ECG and troponin results
- ECG - ST depression or T wave inversion or pathological Q waves
- Troponin level raised (released during heart muscle damage)
STEMI: ECG and troponin results
- ECG - ST elevation or new left bundle branch block
- Troponin level raised (released during heart muscle damage)
Atypical presentations of ACS
Usually diabetics
Silent MI:
- no pain
- low-grade fever
- pale, cool, clammy skin
- hyper/hypotension
Additional investigations for ACS
- Baseline bloods, including FBC, U&E, LFT, lipids and glucose
- Chest x-ray
- Echocardiogram once stable
Initial management for ACS
CPAIN
C – Call an ambulance
P – Perform an ECG
A – Aspirin 300mg
I – Intravenous morphine for pain if required (with an antiemetic, e.g., metoclopramide)
N – Nitrate (GTN)
Definitive management of STEMI
- Primary PCI: symptom onset < 12hrs and available within 2hrs
- Thrombolysis: symptoms onset > 12 hours and PCI unavailable within 2hrs
- PCI: Percutaneous coronary intervention is first-line method of revascularization
- Insertion of a catheter via the radial or femoral artery to open up the blocked vessels using an inflated balloon (angioplasty), and a stent may also be inserted
2) Anticoagulation and further antiplatelet therapy:
- Aspirin + clopidogrel
- Unfractionated heparin and a glycoprotein IIb/IIIa inhibitor
STEMI: what treatment would be provided if the patient is unsuitable for PCI?
Thrombolysis e.g. alteplase or tenecteplase
- Offered if symptom onset is greater than 12h OR PCI not available within 120 mins
- IV administration of a thrombolytic or ‘clot-busting’ agent
Definitive management of NSTEMI
BATMAN-O
B – Base the decision about angiography and PCI on the GRACE score
A – Aspirin 300mg stat dose
T – Ticagrelor 180mg stat dose (clopidogrel if high bleeding risk, or prasugrel if having angiography)
M – Morphine titrated to control pain
A – Antithrombin therapy with fondaparinux (unless high bleeding risk or immediate angiography)
N – Nitrate (GTN)
O2 if sats <95% without COPD
Angiography (type of Xray to visualise blood vessels) in NSTEMI
Unstable patients are considered for immediate angiography as in STEMI
GRACE score = 6m probability of death after NSTEMI
If medium to high risk = angiography with PCI within 72hours
Ongoing management for ACS
- Echocardiogram
- Cardiac rehabilitation
- Secondary prevention
Secondary prevention for ACS
6As
- Aspirin 75mg once daily
- Another antiplatelet: e.g. clopidogrel or ticagrelor for up to 12 months
- Atorvastatin 80mg once daily
- ACE inhibitors (e.g. ramipril)
- Atenolol (or other beta blocker)
- Aldosterone antagonist for those with clinical heart failure
Lifestyle changes for ACS as secondary prevention
- Stop smoking
- Reduce alcohol consumption
- Mediterranean diet
- Cardiac rehabilitation (a specific exercise regime for patients post MI)
- Optimise treatment of other medical conditions (e.g. diabetes and hypertension)
Possible complications of MI
Heart Failure (DREAD)
- D – Death
- R – Rupture of the heart septum or papillary muscles
- E – “Edema” (Heart Failure)
- A – Arrhythmia and Aneurysm
- D – Dressler’s Syndrome (pericarditis secondary to injury)
Define chronic heart failure
Refers to the clinical features of impaired heart function, specifically the function of LV to pump blood out of the heart and around the body.
This impaired LV leads to a chronic backlog of blood waiting to flow into the left side of the heart.
The left atrium, pulmonary veins and lungs experience increased volume and pressure, and start to leak fluid, resulting in pulmonary oedema
Ejection fractions in chronic heart failure
Ejection fraction is the % of blood in the LV squeezed out with each ventricular contraction
EF > 50% = normal
HFrEF = EF < 50%
HFpEF = EF > 50% - issues with LV filling during diastoles
Causes of chronic HF
- Ischaemic heart disease
- Valvular heart disease (commonly aortic stenosis)
- Hypertension
- Arrhythmias (commonly atrial fibrillation)
- Cardiomyopathy
Presentation of chronic heart feature
- Breathlessness, worsened by exertion
- Cough, which may produce frothy white/pink sputum
- Orthopnoea, which is breathlessness when lying flat, relieved by sitting or standing (ask how many pillows they use)
- Paroxysmal nocturnal dyspnoea (PND) sudden night waking with severe SOB, cough and wheeze)
- Peripheral oedema
- Fatigue
Signs of HF on exam
- Tachycardia
- Tachypnoea
- Hypertension
- Murmurs on auscultation indicating valvular heart disease
- 3rd heart sound on auscultation
- Bilateral basal crackles (sounding “wet”) on auscultation of the lungs, indicating pulmonary oedema
- Raised jugular venous pressure (JVP),
Diagnosis of heart failure
- Clinical assessment (history and examination)
- N-terminal pro-B-type natriuretic peptide (NT‑proBNP) blood test
- ECG
- Echocardiogram
Others:
- Blood
- CXR
New York Heart Association Classification for Heart Failure
- Class I: No limitation on activity
- Class II: Comfortable at rest but symptomatic with ordinary activities
- Class III: Comfortable at rest but symptomatic with any activity
- Class IV: Symptomatic at rest
Management of HF
RAMPS
- R – Refer to cardiology
- A – Advise them about the condition
- M – Medical treatment
- P – Procedural or surgical interventions
- S – Specialist heart failure MDT input, such as the heart failure specialist nurses, for advice and support
Urgency of referral dpedns on NT-proBNP results:
400 - 2000ng/L = specialist and echo < 6 weeks
> 2000ng/L = specialist and echo < 2 weeks
Additional management of HF
- Flu, covid and pneumococcal vaccines
- Stop smoking
- Optimise treatment of co-morbidities
- Written care plan
- Cardiac rehabilitation (a personalised exercise programme)
First line medical management of chronic HF
ABAL
A – ACE inhibitor (e.g., ramipril) titrated as high as tolerated
B – Beta blocker (e.g., bisoprolol) titrated as high as tolerated
A – Aldosterone antagonist when symptoms are not controlled with A and B (e.g., spironolactone or eplerenone)
L – Loop diuretics (e.g., furosemide or bumetanide)
Define atrial fibrillation
A type of supraventricular tachycardia (SVT), characterised by a chaotic irregular atrial arrhythmia.
Common causes of AF
SMITH
S – Sepsis
M – Mitral valve pathology (stenosis or regurgitation)
I – Ischaemic heart disease
T – Thyrotoxicosis
H – Hypertension
Alcohol and caffeine = lifestyle causes
Pathophysiology of AF
Normally, the SA node produces electrical activity that coordinates the contraction of the atria and heart.
In AF, atrial contractions are uncoordinated and irregular because the uncoordinated electrical discharges produced in the atria override the regular impulses produced in the SA node.
Symptoms of AF
Often asymptomatic and diagnosed after a stroke (5x risk of stroke with AF)
- Palpitations
- Shortness of breath
- Dizziness or syncope (loss of consciousness)
- Symptoms of associated conditions (e.g., stroke, sepsis or thyrotoxicosis)
Key examination finding in AF
- Irregularly irregular pulse
Investigations for AF
ECG
- Irregularly irregular ventricular rhythm
- Absent P waves
- Narrow QRS complex (<120ms) tachycardia
What is paroxysmal AF
Episodes of AF that reoccur and spontaneously resolve back to sinus rhythm.
Lasts between 30s to 48 hours
If normal ECG but suspected paroxysmal AF:
- 24-hour ambulatory ECG (Holter monitor)
- Cardiac event recorder lasting 1-2 weeks
Management of AF
- Rate or rhythm control
- Anticoagulation
Complex but remember from zero to finals
Most patients = beta blocker for rate control, often bisoprolol, and a DOAC for anticoagulation.
If you remember one thing about the treatment of atrial fibrillation, remember this combination.
Define hypertension
Hypertension is defined as a blood pressure reading of ≥140/90 mmHg (ambulatory blood pressure monitoring ≥135/85 mmHg).
Secondary causes of hypertension
ROPED
R – Renal disease
O – Obesity
P – Pregnancy-induced hypertension or pre-eclampsia
E – Endocrine
D – Drugs (e.g., alcohol, steroids, NSAIDs, oestrogen and liquorice)
Complications arising from hypertension
- Ischaemic heart disease (angina and acute coronary syndrome)
- Cerebrovascular accident (stroke or intracranial haemorrhage)
- Vascular disease (peripheral arterial disease, aortic dissection and aortic aneurysms)
- Hypertensive retinopathy
- Hypertensive nephropathy
- Vascular dementia
- Left ventricular hypertrophy
- Heart failure
3 stages of hypertension
1) Stage 1 Hypertension
Clinic Reading: >140/90
Ambulatory / Home Readings >135/85
2) Stage 2 Hypertension
Clinic Reading: >160/100
Ambulatory / Home Readings >150/95
3) Stage 3 Hypertension
Clinic Reading: >180/120
Ambulatory / Home Readings: >180/120
Diagnosis for hypertension
Clinic BP: 140/90 mmHg - 180/120 mmHg = 24-hour ambulatory blood pressure or home readings to confirm the diagnosis.
White-coat syndrome involves more than 20/10mmHg difference in clinic and home/ambulatory reading
How often should patients have their blood pressure checked?
NICE guidelines: every 5 years if no end organ damage, consider more often if clinical readings are near 140/90
Investigations for hypertension for patients with new HTN diagnosis (to assess for end organ damage)
- Urine albumin:creatinine ratio (proteinuria) and dipstick for microscopic haematuria to assess for kidney damage
- Bloods for HbA1c, renal function and lipids
- Fundoscopy for hypertensive retinopathy
- ECG for LVH
- Calculate QRISK (risk of stroke or MI in next 10 years) if above 10% = statin
Lifestyle advice for patients with hypertension
Healthy diet, stopping smoking, reducing alcohol, caffeine and salt intake and taking regular exercise.
Medications for hypertension
A – ACE inhibitor (e.g. ramipril 1.25mg up to 10mg once daily)
B – Beta blocker (e.g. bisoprolol 5mg up to 20mg once daily)
C – Calcium channel blocker (e.g. amlodipine 5mg up to 10mg once daily)
D – Thiazide-like diuretic (e.g. indapamide 2.5mg once daily)
ARB – Angiotensin II receptor blocker (e.g. candesartan 8mg to up 32mg once daily)
ARB is used if ACEi is not tolerated or the patient is of Afro-Caribbean or African descent.
Steps in medical management of hypertension
There are slightly different guidelines for younger patients and those aged over 55 or black:
Step 1: Aged less than 55 and non-black use A.
Aged over 55 or black of African or African-Caribbean descent - use C.
Step 2: A + C. Alternatively A + D or C + D.
If black then use an ARB instead of A.
Step 3: A + C + D
Step 4: A + C + D + additional (see below)
For step 4, if the serum potassium is ≤ 4.5 mmol/l then consider a potassium-sparing diuretic such as spironolactone.
If the serum potassium is > 4.5 mmol/l, consider an alpha blocker (e.g. doxazosin) or a beta blocker (e.g. atenolol).
Specialist mx if the blood pressure remains uncontrolled despite treatment at step 4.
Targets for blood pressure control on hypertension treatment
< 80 years
Systolic Target: < 140
Diastolic Target: < 90
> 80 years
Systolic target: < 150
Diastolic target: < 90
Complications of hypertension
1) IHD
2) Cerebrovascular accident (hypertension is biggest risk factor)
3) Heart failure
4) Chronic kidney disease
Define asthma
Asthma is a chronic inflammatory airway disease characterised by intermittent airway obstruction and hyper-reactivity.
One of the atopic conditions: eczema, hay fever and food allergies
Risk factors for asthma in adults
- History of other atopic conditions
- Family history
- Viral URTI
- Other triggers: cold weather and exercise
- Occupational exposure (10-15%): e.g. spray paint, flour (bakers) - requires specialist referral
Presentation of asthma
- Episodic - periods where symptoms are better or worse
- Diurnal variability
Typical symptoms:
- SOB
- Chest tightness
- Dry cough
- Wheeze
Improve with bronchodilators
What findings would you note in a patient with asthma?
- Normal if patient is well
- Key finding = widespread “polyphonic” expiratory wheeze
TOM TIP: a localised monophonic wheeze is not asthma, differentials include inhaled foreign body, tumour = CXR
Typical triggers for asthma
- Infection
- Nighttime or early morning
- Exercise
- Animals
- Cold, damp or dusty air
- Strong emotions
Non-selective beta-blockers e.g. propranolol and NSAIDs can worsen asthma
Investigations for asthma
- Spirometry - FEV1:FVC ration < 70% = obstructive disease e.g. asthma or COPD
- Bronchodilator reversibility testing - > 12% increase in FEV1 indicates asthma
- Fractional exhaled nitric oxide (FeNO) - measures concentration of NO exhaled, marker of inflammation (> 40ppb = positive)
- Peak flow variability - peak flow diary, variability of > 20% = positive
Diagnosis of asthma
NICE guidelines recommends the following in patients with suspected asthma:
- Fractional exhaled nitric oxide (FeNO)
- Spirometry with bronchodilator reversibility
- If diagnostic uncertainty = peak flow variability by keeping peak flow diary, twice a day, for 2 to 4 weeks
Medications for managing asthma
1) SABA (short-acting beta-agonist); e.g. salbutamol
2) ICS (inhaled corticosteroid); e.g. beclomethasone.
3) LTRA (leukotriene receptor antagonist); e.g. montelukast (reduces inflammation, not a steroid)
4) LABA (long-acting beta-agonist); e.g. salmeterol
5) MART (maintenance and reliever therapy); combined fast-acting LABA and ICS for symptomatic relief and maintenance in a single inhaler.
Management for asthma in adults
Occupational exposure = they should be referred to a specialist.
Occupational asthma = symptoms and reduced PEFR during the working week and improvement when not at work.
Step 1: Newly-diagnosed asthma: SABA (PRN)
Step 2: If symptoms not controlled through SABA: SABA + low-dose ICS
Step 3: SABA + low dose ICS + LTRA
Step 4: SABA + low dose ICS + LABA +/- LTRA dependent on response
Step 5: consider MART regime
- Increase ICS to moderate dose
- High dose ICS
- Specialist management (e.g. oral corticosteroids)
Presentation of acute asthma exacerbation
- Progressively shortness of breath
- Use of accessory muscles
- Raised respiratory rate (tachypnoea)
- Symmetrical expiratory wheeze on auscultation
- The chest can sound “tight” on auscultation, with reduced air entry throughout
ABG in asthma exacerbation
Initially respiratory alkalosis as tachypnoea causes decrease in CO2
Normal pCO2 or low pO2 (hypoxia) = concerning as it means patient is getting tired - life-threatening asthma
Respiratory acidosis due to high pCO2 is very bad sign
Moderate asthma exacerbation features
Peak flow 50 – 75% best or predicted
Severe asthma exacerbation features
- Peak flow 33-50% best or predicted
- Respiratory rate above 25
- Heart rate above 110
- Unable to complete sentences
Life-threatening exacerbation
- Peak flow less than 33%
- Oxygen saturations less than 92%
- PaO2 less than 8 kPa
- Becoming tired
- Confusion or agitation
- No wheeze or silent chest
- Haemodynamic instability (shock)
Treatment of asthma exacerbations
Involve seniors
Mild exacerbations
- SABA (e.g., salbutamol) via a spacer
- 4x dose of their inhaled corticosteroid (for up to 2 weeks)
- Oral steroids (prednisolone) if ICS ineffective
Follow-up within 48 hours
Moderate exacerbations may additionally be treated with:
- Consider hospital admission
- Nebulised beta-2 agonists (e.g., salbutamol)
- Steroids (e.g., oral prednisolone or IV hydrocortisone)
Severe exacerbations may additionally be treated with:
- Hospital admission
- Oxygen to maintain sats 94-98%
- Nebulised ipratropium bromide
- IV magnesium sulphate
- IV salbutamol
- IV aminophylline
Might need:
- Admission to HDU or ICU
Intubation and ventilation
Why does serum potassium need to be monitored with salbutamol treatment?
Salbutamol can cause potassium to be absorbed from blood to cells, resulting in hypokalaemia
Define chronic obstructive pulmonary disease (COPD)
Chronic obstructive pulmonary disease (COPD) is a progressive, irreversible obstructive lung disease characterised by airflow limitation that is not fully reversible. It encompasses both emphysema and chronic bronchitis.
What is emphysema?
Loss of alveolar integrity due to an imbalance between proteases and protease inhibitors (e.g. alpha-1 antitrypsin).
Elastase breaks down elastin, which decreases surface area fir gaseous exchange.
Triggered by chronic inflammation, such as smoking.
What is chronic bronchitis?
Bronchitis involves excessive mucus secretion secondary to ciliary dysfunction and increased goblet number and size → lung parenchymal destruction → impaired gas exchange. Chronic bronchitis is long-term bronchitis.
Presentation of COPD
Typical presentation of COPD is a long-term smoker with persistent symptoms of:
- Shortness of breath
- Cough
- Sputum production
- Wheeze
- Recurrent respiratory infections, particularly in winter
Signs on examination of COPD
- Tachypnoea
- Barrel chest (bulging of the chest)
- Hyperresonance on percussion
- Tar staining of fingers with peripheral cyanosis
Risk factors for COPD
- Age: usually diagnosed > 45
- Tobacco smoking: greatest risk factor
- Occupational exposure: dust, coal, cotton
- Alpha-1 antitrypsin deficiency: younger patients that present with COPD features
MRC dyspnoea scale for assessing breathlessness
- Grade 1: Breathless on strenuous exercise
- Grade 2: Breathless on walking uphill
- Grade 3: Breathlessness that slows walking on the flat
- Grade 4: Breathlessness stops them from walking more than 100 meters on the flat
- Grade 5: Unable to leave the house due to breathlessness
Diagnosis of COPD
Clinical diagnosis and spirometry results
Spirometry:
- FEV1:FVC < 70%
- No response to bronchodilator testing with beta-2 agonists (e.g., salbutamol).
Severity
- Stage 1 (mild): FEV1 > 80% of predicted
- Stage 2 (moderate): FEV1 50-79% of predicted
- Stage 3 (severe): FEV1 30-49% of predicted
- Stage 4 (very severe): FEV1< 30% of predicted
Other investigations for COPD
- BMI
- Chest x-ray to exclude lung cancer
- CT thorax to rule out fibrosis or bronchiectasis
- FBC for polycythaemia (raised haemoglobin due to chronic hypoxia), anaemia and infection
- Sputum culture
- ECG and echocardiogram
- Serum alpha-1 antitrypsin
What is FEV1/FVC?
FEV1: forced expiratory volume; the volume of air exhaled in the first second of forced exhalation
FVC: forced vital capacity; the volume exhaled after maximal expiration following full inspiration
Normal FEV1/FVC = above 0.75-85
Medications used to manage COPD
1) SABA: short-acting beta-adrenoceptor agonist (e.g. salbutamol) - leads to bronchodilation
2) SAMA: short-acting muscarinic antagonist (ipratropium) - inhibits smooth muscle contractions
3) LABA: long-acting beta-adrenoceptor
agonist (e.g. salmeterol) - leads to bronchodilation
4) LAMA: long-acting muscarinic antagonist (e.g. tiotropium) - inhibits smooth muscle contraction
5) ICS: inhaled corticosteroid (e.g. beclomethasone
Long-term management of COPD
- Smoking cessation
- Annual flu and pneumococcal vaccine
Step 1: SABA or SAMA (e.g. ipratropium bromide)
Step 2: if no asthmatic or steroid-responsive features = combination inhalers containing LABA and LAMA
If asthmatic or steroid-responsive features = LABA and ICS combination inhalers
Step 3: LABA, LAMA and ICS combination inhalers
Long-term oxygen for severe COPD with O2 sats < 92%
Symptoms of acute COPD exacerbation
Rapidly worsening symptoms
- Cough
- SOB
- Sputum
- Wheezing
Triggers: viral or bacterial infection
Define bronchiectasis
Permanent dilatation of the bronchi, the large airways that transport air to the lungs. Sputum collects and organisms grow in the wide tubes, resulting in a chronic cough, continuous sputum production and recurrent infections.
Causes of bronchiectasis
Results from damage to the airways
- Idiopathic (no apparent cause)
- Pneumonia
- Whooping cough (pertussis)
- Tuberculosis
- Alpha-1-antitrypsin deficiency
- Connective tissue disorders (e.g., rheumatoid arthritis)
- Cystic fibrosis
- Yellow nail syndrome
What is yellow nail syndrome?
Triad of yellow fingernails, bronchiectasis and lymphoedema
Symptoms of bronchiectasis
- Shortness of breath
- Chronic productive cough
- Recurrent chest infections
- Weight loss
Signs of bronchiectasis
- Oxygen therapy (if needed)
- Weight loss (cachexia)
- Finger clubbing
- Signs of cor pulmonale (e.g., raised JVP and peripheral oedema)
- Scattered crackles throughout the chest that change or clear with coughing
- Scattered wheezes and squeaks
Investigations for bronchiectasis
Sputum culture, most common infective organisms are:
- Haemophilus influenza
- Pseudomonas aeruginosa
CXR findings:
- Tram-track opacities (side-view of the dilated airway)
- Ring shadows (dilated airways seen end-on)
- Gold standard: high-res CT (HRCT) to establish diagnosis
Management of bronchiectasis
- Vaccines (e.g., pneumococcal and influenza)
- Respiratory physiotherapy to help clear sputum
- Pulmonary rehabilitation
- Long-term antibiotics (e.g., azithromycin) for frequent exacerbations
- Inhaled colistin for Pseudomonas aeruginosa colonisation
- Long-acting bronchodilators if SOB
- Long-term oxygen therapy if low sats
Surgery:
- Surgical lung resection
- Lung transplant for end-stage disease
Management for infective exacerbation of bronchiectasis
- Sputum culture (before antibiotics)
- 7–14 days antibiotics
- Ciprofloxacin if Pseudomonas aeruginosa
TOM TIP: key things to remember with bronchiectasis
- Finger clubbing
- Diagnosis by HRCT
- Pseudomonas colonisation
- Extended 7 - 14 days course of antibiotics
Define community-acquired pneumonia (CAP)
Pneumonia is an infection of lung tissue, causing inflammation in the alveolar space
CAP develops in the community
It is a lower respiratory tract infection - the lower the infection, the more likely it is bacterial
Presentation of pneumonia
- Cough
- Sputum production
- Shortness of breath
- Fever
- Feeling generally unwell
- Haemoptysis (coughing up blood)
- Pleuritic chest pain (sharp chest pain, worse on inspiration)
- Delirium (acute confusion)
Key findings on examination for pneumonia
- Bronchial breath sounds (harsh inspiratory and expiratory breath sounds)
due to consolidation around the airways - Focal coarse crackles caused by air passing through sputum in the airways
- Dullness to percussion due to lung tissue filled with sputum or collapsed
Describe CRB-65
CRB-65 is a scoring system used in community to assess the severity + mortality risk of pneumonia
- C – Confusion (new disorientation in person, place or time)
- U – Urea > 7 mmol/L (only in hospital)
- R – Respiratory rate ≥ 30
- B – Blood pressure < 90 systolic or ≤ 60 diastolic.
- 65 – Age ≥ 65
Consider hospital assessment when CRB-65 score is > 0
Infective organisms that cause pneumonia
- Streptococcus pneumoniae (most common)
- Haemophilus influenzae
Investigations for pneumonia
In community, CRB 0 or 1 pneumonia = don’t always need investigations.
Point of care test for CRP levels used to guide diagnosis and abx in primary care
Hospital investigations for pneumonia
- Chest x-ray - seen as a consolidation
- Full blood count (raised white cell count)
- Renal profile
- CRP
Moderate/severe infection
- Sputum cultures
- Blood cultures
- Pneumococcal and Legionella urinary antigen tests
WBCC and CRP levels roughly = severity of infection, used to monitor patient progress to recovery
Management of community-acquired pneumonia
Mild - abx according to local guidelines, usually:
- Amoxicillin
- Doxycycline
- Clarithromycin
Moderate/severe = hospital for IV abx
Complications of pneumonia
- Sepsis
- Acute respiratory distress syndrome
- Pleural effusion
- Empyema
- Lung abscess
- Death
Define type 1 diabetes
An autoimmune disease that causes the destruction of beta cells in the islets of Langerhans in the pancreas, so it is unable to produce adequate insulin. This leads to chronic hyperglycemia due to insulin dysfunction.
Describe the pathophysiology of type 1 diabetes
Autoantibodies attack beta cells in the Islets of Langerhans leading to Insulin deficiency = chronic hyperglycaemia
As the body cannot use glucose as fuel, cells think the body is starved. So continuous breakdown of glycogen from liver (gluconeogenesis) > glycosuria (glucose in urine)
Risk factors for type 1 diabetes
- Northern European ancestry
- Genetic susceptibility
- Certain viral infections (e.g. coxsackie B virus or enterovirus)
Classic triad of Type 1 diabetes
- Polyuria (excessive urine)
- Polydipsia (excessive thirst)
- Weight loss (mainly through dehydration)
Or Diabetic ketoacidosis
Tests to diagnose type diabetes
- Random plasma glucose >11.1 mmol/L (along with symptoms, this alone is enough for a diagnosis)
- Fasting plasma glucose >7 mmol/L
- HbA1c (glycated haemoglobin) > 6.5% / 48mmol/mol.
What is diabetic ketoacidosis?
In type 1 DM, cells cannot use glucose as fuel and think they are starving. They undergo ketogenesis so that they have usable fuel.
- Over time the patient gets higher and higher glucose and ketones levels.
- Initially, the kidneys produce bicarbonate to counteract the ketone acids in the blood and maintain a normal pH.
- Over time the ketone acids use up the bicarbonate and the blood becomes acidic > metabolic acidosis (pH < 7.3). This is called ketoacidosis.
Key features of DKA?
- Ketoacidosis
- Dehydration
- Potassium imbalance (serum K high or normal but total body K low as none stored in cells)
Presentation of DKA
- Polyuria
- Polydipsia
- Nausea and vomiting
- Acetone smell to their breath
- Dehydration
- Weight loss
- Hypotension (low blood pressure)
- Altered consciousness
Diagnosis of DKA
- Hyperglycaemia (blood glucose > 11 mmol/L)
- Ketosis (e.g., blood ketones above 3 mmol/L)
- Acidosis (e.g., pH below 7.3)
Treatment of DKA
FIG-PICK
Fluid
Insulin
Glucose (monitor and add glucose when < 14mmol/L)
Potassium
Infection (treat underlying)
Chart fluid balance
Ketone (monitor ketones, pH and bicarbonate)
Long-term management of type 1 diabetes
Basal-bolus regime
- Basal (long-acting) insulin - once a day
- Bolus (short-acting) insulin - injected 30mins before carb consumption
Insulin pumps
Small devices that continuously infuse insulin at different rates to control blood sugar levels
Symptoms of a hypo
Some patients might not be aware until they are severely hypoglycaemic
Hunger
Tremor
Sweating
Irritability
Dizziness
Pallor
Reduced consciousness
Coma
Death
Long-term complications of diabetes
Macrovascular:
- Coronary heart disease = significant cause of death in diabetics
- Peripheral ischaemia = poor skin healing and diabetic foot ulcers
- Strokes
- Hypertension
Microvascular complications
- Diabetic neuropathy leads to lack of sensation in feet > occult foot ulcers
- Diabetic retinopathy
- Diabetic nephropathy particularly glomerulosclerosis
Infections:
- UTI
- Skin and soft tissue infection particularly in the feet
Describe type 2 diabetes
A disease characterised by abnormally low insulin secretions and peripheral insulin resistance, which leads to chronic hyperglycemia due to insulin dysfunction
Pathophysiology of type 2 diabetes
Repeated exposure to glucose and insulin causes insulin resistance in the body.
Increasing levels of insulin are required to stimulate cells to take up and use glucose. The pancreas eventually becomes fatigued and damaged from producing so much insulin, and insulin production is reduced.
A high carb diet, insulin resistance and reduced pancreatic function leads to chronic hyperglycaemia
Chronic hyperglycaemia leads to microvascular, macrovascular and infectious complications (see type 1 diabetes)
Risk factors for type 2 diabetes
Non-modifiable
- Older age
- Ethnicity (Black African or
Caribbean and South Asian) - Family history
Modifiable
- Obesity
- Sedentary lifestyle
- High carbohydrate (particularly sugar) diet
Presentation of type 2 diabetes
Consider type 2 diabetes in patients with risk factors
- Tiredness
- Polyuria and polydipsia
- Unintentional weight loss
- Opportunistic infections (e.g., oral thrush)
- Slow wound healing
- Glucose in urine (on a dipstick)
Acanthosis nigricans - thickening and darkening of the skin (giving a “velvety” appearance), often neck, axilla and groin, associated with insulin resistance.
Diagnosis of type 2 diabetes
HbA1c ≥ 48mmol/L, repeated after a month to confirm diagnosis
Management of type 2 diabetes
- A structured education program
- Low-glycaemic-index, high-fibre diet
- Exercise
- Weight loss (if overweight)
- Antidiabetic drugs
- Monitoring and managing complications
Treatment targets for type 2 diabetes
- 48 mmol/mol for new type 2 diabetics
- 53 mmol/mol for patients if on more than 1 med
- The HbA1c is measured every 3 to 6 months until under control and stable.
Medical management for diabetes type 2
1st line: metformin
SGLT-2 inhibitor (e.g. dapagliflozin) if CVD or HF (NICE says consider if QRISK > 10%)
2nd line: add sulfonylurea, pioglitazone, DPP-4 inhibitor or SGLT-2 inhibitor.
3rd line:
- Triple therapy with metformin and two of the second-line drugs
- Insulin therapy (initiated by the specialist diabetic nurses)
If above ineffective and BMI above 35, change one medication to GLP-1 mimetic (e.g., liraglutide).
Main concerning side effect of SGLT-2 inhibitors
DKA
Glycosuria and therefore increased UTIs
What is pre-diabetes
Pre-diabetes is an indication that the patient is heading towards developing T2DM. They do not fully fit the diagnostic criteria for T2DM but should be educated on diabetes and lifestyle changes
Not recommended to start treatment - weight loss and lifestyle changes first
Diagnosis of pre-diabetes
HbA1c of 42 – 47 mmol/mol
What is hyperosmolar hyperglycaemic state?
Rare but potentially fatal complication of type 2 diabetes
Characterised by hyperosmolality (water loss = very concentrated blood), hyperglycaemia) and absence of ketones (different from DKA)
Presents with polyuria, polydipsia, weight loss, dehydration, tachycardia, hypotension and confusion.
Medical emergency, experienced seniors and treatment with IV fluids and monitoring
Describe hyperthyroidism
Hyperthyroidism is a disease characterised by the over-production of thyroid hormones T3 and T4 by the thyroid gland.
Causes of hyperthyroidism
GIST
G – Graves’ disease - most common, autoimmune disease where TSH receptor antibodies stimulate TSH receptors
I – Inflammation (thyroiditis)
S – Solitary toxic thyroid nodule - usually adenomas removed via surgery
T – Toxic multinodular goitre - nodules on thyroid that produce excessive thyroid hormones
Presentation of hyperthyroidism
- Anxiety and irritability
- Sweating and heat intolerance
- Tachycardia
- Weight loss
- Fatigue
- Insomnia
- Frequent loose stools
- Sexual dysfunction
- Brisk reflexes on examination
- Oligomenorrhea
Specific features of Graves’ disease due to the presence of TSH receptor antibodies
- Diffuse goitre (without nodules)
- Graves’ eye disease, including exophthalmos (bulging of the eyes)
- Pretibial myxoedema
- Thyroid acropachy (hand swelling and finger clubbing)
Management of hyperthyroidism
1st line: carbimazole (taken for 12 to 18m). Once levels stable after about 4 - 6 weeks, titrated to maintain normal levels
Significant side effects of carbimazole
- Acute pancreatitis - look out for a patient in your exam taking carbimazole with severe epigastric pain radiating to the back
- Agranulocytosis - dangerously low WCC - key presenting feature is a sore throat, urgent FBC and aggressive infection treatment
Define hypothyroidism
Insufficient thyroid hormones, triiodothyronine (T3) and thyroxine (T4).
Primary hypothyroidism = thyroid produces inadequate hormones. Negative feedback is absent = raised TSH and low T3 and low T4.
Secondary hypothyroidism (central hypothyroidism) is where the pituitary behaves abnormally and produces inadequate TSH. TSH, T3 and T4 will all be low.
TSH levels in primary and secondary hypothyroidism
Primary - TSH levels are high
Secondary - TSH levels are low
Causes of hypothyroidism
- Hashimoto’s thyroiditis, most common cause in developed world
Autoimmune condition causing inflammation of the thyroid gland.
Presence of anti-thyroid peroxidase (anti-TPO) and anti-thyroglobulin (Anti-Tg) antibodies
Iodine deficiency - most common in developing countries
Causes of secondary hypothyroidism
Lack of other pituitary hormones e.g. ACTH (hypopituitarism)
- Tumour (e.g. pituitary adenomas)
- Surgery
- Radiotherapy
- Sheehan’s syndrome (post-partum haemorrhage causes avascular necrosis of the pituitary gland)
- Trauma
Presentation of hypothyroidism
- Weight gain
- Fatigue
- Dry skin
- Coarse hair, hair loss and thinning or loss of the outer third of the eyebrows
- Fluid retention (including oedema, pleural effusions and ascites)
- Heavy or irregular periods
Constipation
Iodine deficiency = goitre
Hashimoto’s thyroiditis - initially goitre then atrophy of the thyroid gland
Treatment for hypothyroidism
Oral levothyroxine (synthetic version of T4 and metabolises to T3 in the body
Dose is titrated based on TSH level - initially every 4 weeks
TSH = high, increase levothyroxine
TSH = low, decease levothyroxine levels
Define Gastro-oesophageal reflux disease (GORD)
Acid from the stomach flows through the lower oesophageal sphincter and into the oesophagus and irritates the lining and causes symptoms
Causes and triggers of GORD
- Greasy and spicy foods
- Coffee and tea
- Alcohol
- NSAIDs
- Stress
- Smoking
- Obesity
- Hiatus hernia
Presentation of GORD
- Dyspepsia (non-specific term to describe indigestion):
- Heartburn
- Acid regurgitation
- Retrosternal or epigastric pain
- Bloating
- Nocturnal cough
- Hoarse voice
What are some red flag symptoms that warrants 2ww referral for endoscopy?
- Critical!!! Dysphagia at any age = immediate two week wait referral
- Aged over 55 (urgent referral)
- Weight loss
- Upper abdominal pain
- Reflux
- Treatment-resistant dyspepsia
- Nausea and vomiting
- Upper abdominal mass on palpation
- Low haemoglobin (anaemia)
- Raised platelet count
What is an oesophago-gastro-duodenoscopy (OGD)?
Insertion of a camera through the mouth down to the oesophagus, stomach and duodenum to assess for:
- Gastritis
- Peptic ulcers
- Upper gastrointestinal bleeding
- Oesophageal varices (in liver cirrhosis)
- Barretts oesophagus
- Oesophageal stricture
- Malignancy of the oesophagus or stomach
Management of GORD
Lifestyle changes: reduce tea, coffee and alcohol, weight loss, avoid smoking, smaller, lighter meals, stay upright after meals
- Review meds (stop NSAIDs)
- Antacids (e.g. Gaviscon)
- PPI (e.g. omeprazole)
- Histamine H2-receptor antagonists (e.g. famotidine)
TOM TIP for GORD
The usual medical strategy when someone presents for the first time is to exclude red flags, address potential triggers, offer a 1 month trial of a proton pump inhibitor and consider H. pylori testing.
What is Helicobacter pylori (H.pylori)
- Gram-negative aerobic bacteria that can live the stomach
- It causes damage to the epithelial lining, resulting in gastritis, ulcers and increased risk of stomach cancer
- Offer test for H.pylori to patients with dyspepsia, need 2 weeks without PPI before testing for accurate result
Investigations for H. pylori
- Stool antigen test
- Urea breath test using radiolabelled carbon 13
- H. pylori antibody test (blood)
- Rapid urease test performed during endoscopy (also known as the CLO test)
Treatment for H. pylori infection
Triple therapy with PPI and two antibiotics e.g. amoxicillin and clarithromycin for 7 days.
What is Barrett’s oesophagus?
When the lower oesophageal epithelium changes from squamous to columnar epithelium (metaplasia - change from one cell type to another)
It is a pre-malignant condition and increases risk of oesophageal adenocarcinoma
Histology of Barrett’s is a common exam question
What are gallstones (cholelithiasis)?
Small stones that form in the gallbladder
Most are made of cholesterol
Define biliary colic
Intermittent right upper quadrant pain caused by gallstones irritating bile ducts
Define cholestasis
Blockage to the flow of bile
Define cholelithiasis
Presence of gallstones
Define cholecystitis
Inflammation of the gallbladder
Define choledocholithiasis
Gallstones in the common bile duct
Define cholangitis
Infection and Inflammation of the bile ducts.
Surgical emergency, high mortality rate due to sepsis and septicaemia
Define cholecystectomy
Cholecystectomy: surgical removal of the gallbladder
Define cholecystostomy
Inserting a drain into the gallbladder
Risk factors for gallstones
4Fs
Fat
Fair
Female
Forty
Presentation of gallstones
- Might be asymptomatic
- Typical symptom: biliary colic - severe epigastric or RUQ pain
- Often after meals especially if high in fat
- 30 mins to 8 hours
- Nausea and vomiting
- Sometimes patients can present with the complications e.g. acute cholecystitis, acute cholangitis, obstructive jaundice , pancreatitis
Why does high fat meals trigger biliary colic
Fat causes cholecystokinin (CCK) secretion from the duodenum.
CCK triggers contraction of the gallbladder = biliary colic
Patients with gallstones and biliary colic told to avoid high fat meals
Possible exam question
LFT results in cholelithiasis
- Raised Alkaline phosphatase (ALP) is non-speific marker = biliary obstruction if alongside RUQ pain and/or jaundice
- Raised ALT and AST = hepatocellular injury
- Cholestasis (due to gallstones) = slight increase in ALT and AST with higher increase in ALP, known as “obstructive picture”
- Raised bilirubin (jaundice) with pale stools and dark urine - biliary obstruction)
Investigations for gallstones
1st line = ultrasound scan, helps identify:
- Gallstones in the gallbladder
- Gallstones in the ducts
- Bile duct dilatation (normally < 6mm diameter)
- Acute cholecystitis
2nd line - magnetic resonance cholangio-pancreatography
Define irritable bowel syndrome (IBS)
- A condition resulting from a disturbance of the gut-brain interaction
- Functional disorder
- More common in women than menn j
Symptoms of IBS
IBS mnemonic
I – Intestinal discomfort (abdominal pain relating to the bowels)
B – Bowel habit abnormalities
S – Stool abnormalities (watery, loose, hard or associated with mucus)
Common symptoms (varies between individuals):
- Abdominal pain
- Diarrhoea
- Constipation
- Fluctuating bowel habit
- Bloating
- Worse after eating
- Improved by opening bowels
- Passing mucus
IBS is a diagnosis of exclusion, what serious underlying pathology do you need to consider?
- Bowel cancer
- Inflammatory bowel disease
- Coeliac disease
- Ovarian cancer (often presents with vague symptoms, particularly bloating in women over 50 years)
- Pancreatic cancer
Investigations for IBS
Investigations can be used to assess for underlying differentials (normal in IBS):
- Full blood count for anaemia
Inflammatory markers (e.g., ESR and CRP) - Coeliac serology (e.g., anti-TTG antibodies)
- Faecal calprotectin for IBD
- CA125 for ovarian cancer
- NICE recommends ruling out differentials before diagnosis and patient should have at least 6 months of abdo pain or discomfort with at least one:
- Pain or discomfort relieved by opening the bowels
- Bowel habit abnormalities (more or less frequent)
- Stool abnormalities (e.g., watery, loose or hard)
For a diagnosis, patients also require at least two of:
- Straining, an urgent need to open bowels or incomplete emptying
- Bloating
- Worse after eating
- Passing mucus
What can trigger or worsen IBS
- Anxiety
- Depression
- Stress
- Sleep disturbance
- Illness
- Medications
- Certain foods
- Caffeine
- Alcohol
Lifestyle advice for managing IBS
- Drinking enough fluids
- Regular small meals
- Adjusting fibre intake according to symptoms (more fibre if predominantly constipated, less with diarrhoea/bloating)
- Limit caffeine, alcohol and fatty foods
- Low FODMAP diet, guided by a dietician
- Reduce stress where possible
- Regular exercise
Medical management for IBS
- Loperamide for diarrhoea
- Bulk-forming laxatives (e.g., ispaghula husk) for constipation (lactulose can cause bloating and is avoided)
Antispasmodics for cramps (e.g., hyoscine butylbromide (buscopan) or peppermint oil)
Define bowel cancer
Usually refers to colorectal cancer, small bowel and anal cancers are less common.
Risk factors for colorectal cancer
- Family history of bowel cancer
- Familial adenomatous polyposis (FAP)
- Hereditary nonpolyposis colorectal cancer (HNPCC)
(Lynch syndrome) - Inflammatory bowel disease (Crohn’s or ulcerative colitis)
- Increased age
- Diet (high in red and processed meat and low in fibre)
- Obesity and sedentary lifestyle
- Smoking
- Alcohol
What is familial adenomatous polyposis?
Autosomal dominant condition that involves dysfunction of the tumour suppressor genes called adenomatous polyposis coli (APC)
Results in many polyps (adenomas) in the large intestines - potential to become cancerous.
Patients have their entire large intestine removed prophylactically to prevent bowel cancer
What is hereditary nonpolyposis colorectal cancer (HNPCC) or Lynch syndrome?
Autosomal dominant conditions that results from mutations in DNA mismatch repair (MMR) genes - increases risk of colorectal cancer
Red flag symptoms that make you think bowel cancer
- Change in bowel habit (usually to more loose and frequent stools)
- Unexplained weight loss
- Rectal bleeding
- Unexplained abdominal pain
- Iron deficiency anaemia
(microcytic anaemia with low ferritin) - Abdominal or rectal mass on examination
- Unexplained anaemia
Criteria for 2 week wait for bowel cancer
- Over 40 years with abdominal pain and unexplained weight loss
- Over 50 years with unexplained rectal bleeding
- Over 60 years with a change in bowel habit or iron deficiency anaemia
Screening for bowel cancer
- Faecal immunochemical tests (FIT) - looks for amount of human haemoglobin in stool
Used for patients that do not fit the two-week-wait criteria
- Over 50 with weight loss only
- Under 60s with change in bowel habit
Patients 60 to 74 do home FIT test every two years
Investigations for bowel cancer
Gold standard: colonoscopy, endoscope to visualise entire large bowel, and lesions biopsied for histology
Staging CT - full CT thorax, abdomen and pelvis
TNM classification for bowel cancer
T for Tumour:
TX – unable to assess size
T1 – submucosa involvement
T2 – involvement of muscularis propria (muscle layer)
T3 – involvement of the subserosa and serosa (outer layer), but not through the serosa
T4 – spread through the serosa (4a) reaching other tissues or organs (4b)
N for Nodes:
NX – unable to assess nodes
N0 – no nodal spread
N1 – spread to 1-3 nodes
N2 – spread to more than 3 nodes
M for Metastasis:
M0 – no metastasis
M1 – metastasis
Management of bowel cancer
- MDT involvement
- Treatment depends on clinical conditions, general health, stage, histology, patient wishes
- Surgical resection: laparoscopic preferred
- Chemotherapy
- Radiotherapy
- Palliative care
Define constipation
- Difficulty in emptying the bowels, usually with hardened stools.
- Primary: dysfunctions of regulation of colonic and anorectal neuromuscular function or brain-gut neuroenteric function. Causes slower transit of stool through the bowel
- Secondary: results from certain medications (opiates, antipsychotics), metabolic disturbances (hypercalcaemia, hypothyroidism)
Risk factors for constipation
- Female
- Age > 65
- Black ethnicity
- Lower SES
- Medications: opiates
- Sedentary lifestyle
- Reduced dietary fibre
Clinical features of constipation
- Difficult defecation
- Infrequent stools: <3 per week
- Hard stools
- Excessive straining
Signs:
- Abdominal mass (stool palpable)
- Anorectal lesions: haemorrhoids, fissures
- PR exams: hard stools
- Delirium (common in elderly)
Investigations for constipation
- Abdominal examination: masses, distention, palpable colon
- PR examination: masses, stool, fissures, haemorrhoids , prolapse, rectocele
Management of constipation
Constipation (< 3 month)
1st line:
- Investigate, exclude or treat secondary cause
- Lifestyle advice: increase daily fibre intake, increase exercise, increase fluid intake
- Bulk forming laxative: fybogel (ispaghula husk), methylcellulose
- 2nd line for hard stool, difficult to pass: Osmotic laxative: macrogol, lactulose
- Soft stool, inadequate emptying - stimulant laxatives: senna, bisacodyl
Chronic constipation
If above ineffective for at least 6 months then:
- 1st line: Oral macrogol +/- stimulant laxative
Define diverticulum
A pouch or pocket in the bowel wall, usually ranging in size from 0.5 – 1cm.
Define diverticulosis
Presence of diverticula, without inflammation or infection.
Diverticular disease = symptomatic diverticulosis
Define diverticulitis
Inflammation and infection of diverticula.
What is the pathophysiology of diverticular disease?
Circular muscle layer in the wall of the large intestine have gaps where blood vessels penetrate
Increased pressure over time allow mucosa to herniate through the circular muscle layer and form pouches (diverticula)
The colon (except rectum) has longitudinal muscles forming ribbons called teniae coli
The areas that are not covered by teniae coli are vulnerable to the development of diverticula.
Rectum - outer longitudinal muscle surrounds it completely > extra support protecting it from diverticula
What is diverticulosis?
- “Wear and tear” of the bowel
- Most commonly affect sigmoid colon
- Common with increased age, low fibre diets, obesity, use of NSAIDs
- Incidental finding on colonoscopy or CT scans
Management of diverticulosis
Asymptomatic = no treatment
But if left abdo pain, constipation or rectal bleeding then:
- Increased fibre
- Bulk-forming laxatives (e.g. ispaghula)
- Avoid stimulant laxatives (e.g. senna)
Presentation of acute diverticulitis
- Pain and tenderness in the left iliac fossa / lower left abdomen
- Fever
- Diarrhoea
- Nausea and vomiting
- Rectal bleeding
- Palpable abdominal mass (if an abscess has formed)
- Raised inflammatory markers (e.g., CRP) and white blood cells
Management of uncomplicated diverticulitis in primary care
- Oral co-amoxiclav (at least 5 days)
- Analgesia (avoiding NSAIDs and opiates, if possible)
- Only taking clear liquids (avoiding solid food) until symptoms improve, usually 2-3 days
- Follow-up within 2 days to review symptoms
- Severe - hospital admission
Complications of acute diverticulitis
- Perforation
- Peritonitis
- Ileus/obstruction
Presentation of cholecystitis
- Inflammation of the gallbladder, key complication of gallstones
- Main presenting symptom: RUQ pain that might radiate to the right shoulder.
Other symptoms:
- Fever
- Nausea
- Vomiting
- Tachycardia and tachypnoea
- Right upper quadrant tenderness
- Murphy’s sign (positive in acute cholecystitis)
- Raised inflammatory markers and white blood cells
Investigations for acute cholecystitis
1st line: abdominal ultrasound scan:
- Thickened gallbladder wall
- Stones or sludge in gallbladder
- Fluid around gallbladder
Magnetic resonance cholangiopancreatography (MRCP) - visualise the biliary tree
Management of acute cholecystitis
- Emergency admission to hospitals
- Nil by mouth
- IV fluids
- Antibiotics
- NG tube if vomiting
- ERCP can be used to remove stones in the common bile duct
Surgery:
- Cholecystectomy
Define appendicitis
- Inflammation of the appendix
- Peak incidence between 10 to 20 years old
Pathophysiology of appendicitis
- Obstruction of appendix > build-up of mucus and resident bacteria > inflammation and infection.
- Increasing pressure leading to engorgement and congestion of the appendix
- Inflammation spreads to the parietal peritoneum (tissue covering the abdominal cavity) > classic LRQ pain
Gangrene + rupture > bacteria and faecal matter leak out > peritonitis
Signs and symptoms of appendicitis
- Key symptom: abdominal that starts centrally then moves down to the right iliac fossa (RIF)
- Tenderness at McBurney’s point
Other features:
- Anorexia
- Nausea and vomiting
- Low-grade fever
- Rovsing’s sign (palpation of the left iliac fossa causes pain in the RIF)
- Guarding on abdominal palpation
- Rebound tenderness in the RIF + percussion tenderness = peritonitis
Diagnosis of appendicitis
- Clinical presentation and raised inflammatory markers
- CT scan to confirm diagnosis and exclude other pathology
- USS in female patients to exclude ovarian and gynae pathology
Key differential diagnoses of appendicitis
- Ectopic pregnancy - consider in female of childbearing age. Pregnancy test to exclude pregnancy
- Ovarian cyst - pelvic and iliac fossa pain, particularly if rupture or torsion
Management of appendicitis
- Emergency admission to hospital for appendicectomy , usually laparoscopic surgery
Define pyelonephritis
Inflammation of the kidneys resulting from bacterial infection.
It affects the renal pelvis (connects kidney and ureter) and parenchyma (tissue).
Causes of pyelonephritis
E.coli is the most common cause - gram-negative, anaerobic, rod-shaped bacteria
Presentation and diagnosis of pyelonephritis
Usually clinical diagnosis with history and examination
Similar presentation to lower UTI (dysuria, suprapubic discomfort and increased frequency) and triad of symptoms:
- Fever
- Loin or back pain (bilateral or unilateral)
- Nausea / vomiting
Investigations for pyelonephritis
- Urine dipsticks - infection (nitrites, leukocytes and blood
- Midstream urine (MSU) for microscopy, culture and sensitivity
- Blood tests - raised WCC and CRP
Management of pyelonephritis
- Referral to hospital if there are features of sepsis or not safe to manage in the community
- 1st line antibiotics for 7 to 10 days in the community:
- Cefalexin
- Co-amoxiclav (if culture results are available)
- Trimethoprim (if culture results are available)
- Ciprofloxacin (keep tendon damage and lower seizure threshold in mind)
What is chronic pyelonephritis?
- Presents with recurrent episodes of infection in the kidneys
- Recurrent infection leads to scarring of the renal parenchyma > CKD and then end-stage renal failure
Define kidney stones
Also known as renal calculi, urolithiasis and nephrolithiasis
They are hard stones that form in the renal pelvis, where the urine collects before going down the ureters
Asymptomatic until they obstruct the ureters - commonly at the vesico-ureteric junction
Most common type of kidney stone
Calcium-based stones (~80%): calcium oxalate (more common) and calcium phosphate
Hypercalcaemia and low urine output = key risk factors
Presentation of kidney stones
- Can be asymptotic
- Main presenting complaint = renal colic which is severe unilateral loin to groin pain (worse than childbirth)
- Colicky (fluctuating in severity) as the stone moves and settles
- Nausea and vomiting from the pain
Look out for symptoms of sepsis
Investigations for kidney stones
- Urine dipstick = haematuria (normal does not exclude stones)
- Blood tests to assess for infection, hypercalcaemia as a cause and kidney function
- Non-contrast CT KUB within 24 hrs = first line investigation
Presentation of hypercalcaemia
Remember: renal stones, painful bones, abdominal groans and psychiatric moans
Three causes of hypercalcaemia to remember
- Calcium supplementation
- Hyperparathyroidism
- Cancer (e.g. myeloma, breast or lung cancer)
Management of kidney stones
- NSAIDs particularly intramuscular or PR diclofenac
- Antiemetics (e.g. metoclopramide)
- Antibiotics if infection
- Watchful waiting if <5mm as usually passes by themselves
- Tamsulosin (alpha-blocker) to help passing stones
- Surgery if > 10mm or does not pass spontaneously
Conservative management for recurrent kidney stones
More likely to recurrent if previous episode
- Increase fluid intake (2.5 - 3L)
- Add fresh lemon juice to water as citric acid binds to urinary calcium
- Salt < 6g daily
- Maintain normal calcium intake (low dietary calcium = increased renal stone risk)
Medical management to reduce risk of recurrent kidney stones
- Potassium citrate
- Thiazide diuretics (e.g. indapamide)
Define psoriasis
A chronic inflammatory skin condition characterised by clearly defined red and scaly plaques.
There are several types
Clinical features of psoriasis
- Symmetrically distributed, red, scaly plaques with well-defined edges
- Plaques often violet/purple in darker skin, the pinkness of early patches might be difficult to see
- Silvery white plaques
- Most common sites: scalp. elbows and knees
- Auspitz sign - pinpoint bleeding upon removal of scaly layer in plaque psoriasis
- Koebner phenomenon: new plaques at sites of skin injury
- Residual pigmentation or hypopigmentation after lesions resolve
Types of psoriasis
For pictures + info:
https://dermnetnz.org/topics/psoriasis
What is Guttate psoriasis?
Post-streptococcal (often after strep throat infection) acute guttate psoriasis
Widespread small plaques
Often resolves after several months
https://dermnetnz.org/topics/psoriasis
Features of small plaque psoriasis
- Often late age of onset (>50)
- Plaques <3 cm
Features of chronic plaque psoriasis
- Persistent and treatment-resistant
- Plaques >3 cm
- Most often affects elbows, knees, and lower back
- Ranges from mild to very extensive
Features of unstable plaque psoriasis
- Rapid extension of existing or new plaques
- Koebner phenomenon: new plaques at sites of skin injury
- Induced by infection, stress, drugs, or drug withdrawal
Features of flexural psoriasis (inverse psoriasis)
- Affects body folds and genitals
- Smooth, well-defined patches
- Colonised by candida yeasts
Where does scalp psoriasis typically affect?
Scalp - first or only site
Features of palmoplantar psoriasis
- Affecting the palms and/or soles
- Keratoderma (thickening of epidermis)
- Painful fissuring
Features of nail psoriasis
Pitting, onycholysis (separation of nail from nailbed) , yellowing, and ridging
Associated with inflammatory arthritis
Factors that worsen or trigger psoriasis
- Streptococcal tonsillitis (‘Strep throat’) and other infections
- Injuries such as cuts
- Sun exposure in ~10% of psoriasis patients (sun exposure is more often beneficial)
- Dry skin
- Obesity, smoking, or excessive alcohol
- Medications such as lithium, beta-blockers, NSAIDs
- Stopping oral steroids or strong topical corticosteroids
- Stress
Diagnosis of psoriasis
- Diagnosis usually based on clinical appearance of lesions , history and examination
- Tools such as psoriasis area and severity index are used (measures erythema, induration (thickness) and desquamation (scaling))
Management of psoriasis
Depends on severity
- Topical steroids
- Topical vitamin D analogues (calcipotriol)
- Topical dithranol
- Topical calcineurin inhibitors (tacrolimus) are usually only used in adults
- Phototherapy with narrow band ultraviolet B light for extensive guttate psoriasis
- Psychological support, as it can be difficult to treat
What disease is psoriasis associated with?
Psoriatic arthritis in 10% to 20% patients
Define intertrigo
A rash in the flexures e.g. behind ears, under arms, groin, between buttocks, fingers, toe spaces
Risk factors for intertrigo
- Obesity
- Genetic tendency to skin disease
- Hyperhidrosis
- Age
- Diabetes
- Smoking
- Alcohol
Types of intertrigo
- Infection or inflammatory but often overlap
- Infections usually unilateral and asymmetrical
- Atopic dermatitis (inflammatory) usually bilateral and symmetrical, and affect flexures of neck, elbow or knees
Infections that cause intertrigo
- Thrush: Candida albicans
- Tinea (ringworm fugus): Tinea cruris (groin) and athletes foot (between toes)
- Impetigo: staphylococcus aureus, streptococcus pyogenes
- Boils: S. aureus
Inflammatory skin conditions that cause intertrigo
- Seborrheic dermatitis
- Atopic dermatitis (eczema)
- Contact irritant dermatitis e.g. napkin dermatitis in infants in the nappy area
- Contact allergic dermatitis
Investigations for intertrigo
- Swab for microscopy, culture and sensitivity
- Scraping for fungal microscopy and culture
Treatment for intertrigo
- Depends on underlying cause (covered under individual diseases)
Conservative measures:
- Bathing and completely drying after physical exertion
- Reduce sweating with antiperspirant
Define athlete’s foot
Fungal infection of the foot (tinea pedis)
Often results in peeling skin and fissures between the toes (toe clefts)
Causes of athlete’s foot
Proliferation of dermatophyte fungi of the genera Trichophyton rubrum, Trichophyton interdigitale, and Epidermophyton floccosum.
Risk factors for athlete’s foot
- More common in those who participate in sports because:
- They may wear occlusive footwear
- They sweat heavily
- They may fail to dry their feet carefully after showering
- They are exposed to fungal spores in communal areas.
Clinical features of athlete’s foot
- Moist, peeling skin between the toes
- White, yellow, or greenish discolouration
- Sometimes, thickened skin
- Painful fissures
- Unpleasant smell.
Usually mild, severe inflammation indicates bacterial infection
Diagnosis of athlete’s foot
Usually clinical
Differentials of athlete’s foot
- Yeast infection
- Bacterial infection (e.g. staphylococci)
Treatment of athlete’s foot
- Dry carefully between the toes
- Use a dusting powder e.g. talc to keep the affected area dry
- Wear shoes that are loose
around the toes or go bare foot - Topical antifungal agent e.g. Terbinafine
What chronic conditions can cause itchy skin?
- Liver disease
- Renal disease
- Cancer
Define urticaria
Urticaria is characterised by weals (hives) or angioedema or both
Several different types
For pictures: https://dermnetnz.org/topics/acute-urticaria
What is acute urticaria?
It is urticaria with or without angioedema that is present for < 6 weeks and often gone within hours to days
1 in 5 children
More common in patients with atopy.
Pathophysiology of urticaria
Weals result from the release of chemical mediators from tissue mast cells and circulating basophils, they include histamine and cytokines. Bradykinin release causes angioedema.
Causes of acute uritcaria
- Acute viral infection e.g. URTI
- Food allergy (IgE mediated)
- Drug-induced (e.g. penicillin)
- Bee/wasp sting
Clinical features of acute urticaria
For pictures: https://dermnetnz.org/topics/acute-urticaria
Urticarial weals - few mm or cm diameter, white or red with or without red flare
Angioedema is usually more localised, commonly affects the face, and can involve the tongue, uvula, soft palate and larynx (danger!!!)
Diagnosis of acute urticaria
- A patient with a short history of weals that last less than 24 hours with or without angioedema
- Ask about medication and family hx
- Physical examination to identify underlying cause
- Skin prick or radioallergosorbent tests (RAST) might be requested in suspected drug, latex or food
Treatment for acute urticaria
- Adults and children: oral second-gen antihistamine e.g. cetirizine, loratadine or fexofenadine
- Avoid triggers
- IM adrenaline for life-threatening anaphylaxis or throat-swelling
Urticaria severity assessment (UAS7 scoring system)
Score of 0 - 3
Measures number of weals over 24 hours and itch
Score: 0, weals: none, itch: none
Score 1: weals: 20, itch: mild
Score 2: weals: 20 - 50, itch: intense
Score 3: weals: > 50, itch: intense
What is chronic urticaria
Daily or episodic occurrence of weals, angioedema, or both for at least 6 weeks
Persists for 1 - 5 years or longer
What is chronic spontaneous urticaria
Urticaria with no specific cause or trigger
Clinical features:
- White/red weals with red flare, lasting few minutes or hours
- Rings, map-like or giant patches
- Angioedema commonly affecting the face, hands, feet and genitalia
Systemic symptoms: headache, fatigue, joint pain/swelling
Diagnosis of chronic urticaria
- Careful history and examination
Treatment for chronic urticaria
- Identify and eliminate any underlying causes
- Avoid triggers
- Pharmacological treatment e.g. antihistamines, if ineffective after 2 to 4 weeks, then refer to dermatologist, immunologist or medical allergy specialist
Treatment overlaps with chronic inducible urticaria
Define chronic inducible urticaria
Chronic urticaria that has an identifiable cause and classified according to the stimulus that provokes weals to develop e.g. scratching the skin (dermographism), exercise and emotional upset (cholinergic urticaria)
Define exanthem
Medical term for a widespread rash that is usually accompanied by systemic symptoms such as fever, malaise and headache.
Usually caused by a infection, and is either a reaction to toxin produced or damage to skin by the infective organism or immune response
What causes exanthem
Exanthems during children are very common and usually due to specific viral infections e.g.:
- Chickenpox (varicella)
- Measles (morbillivirus)
- Rubella (rubella virus)
- Non-specific viral
Bacterial exanthem:
- Staphylococcal toxin: toxic shock syndrome
- Streptococcal toxin infection: scarlet fever
Signs and symptoms of exanthems
- Non-specific exanthems appear as spots or blotches with or without itch
- Usually more extensive on trunk than extremities
- Most cases, patients might have the following symptoms prior to rash: fever, malaise, headache, loss of appetite, muscular aches and pains
Diagnosis of exanthems
Diagnosis by distinct patterns and prodromal (pre-rash) symptoms which allow for clinical diagnosis
If required, consider viral swab for culture and PCR, blood test for serology or PCR
Treatment for exanthem
Symptomatic:
- Paracetamol to reduce fever
- Moisturising emollients to reduce itch
Exanthem associated with Kawasaki disease
Prodrome of persistent high fever (> 39) for at least 5 days
Widespread erythematous maculopapular rash and desquamation (peeling) on palms and soles
- Strawberry tongue (red tongue with large papillae
- Cracked lips
- Cervical lymphadenopathy
- Conjunctivitis
Exanthem associated with herpes varicella/zoster (chickenpox)
Mild systemic symptoms and few or many pruritic papules, vesicles, pustules and crusted lesions that might scar
Mainly on face and trunk
Pictures: https://dermnetnz.org/cme/viral-infections/specific-viral-exanthems
Exanthem associated with measles
Prodrome of fever, malaise, anorexia, then conjunctivitis, cough and coryza
Then Kolpik spots (oral papules) appear 2 - 3 days into prodrome period
24 to 48 hours later, rash starts on cheeks and spreads to trunk and limbs within a day or two
- Widespread “morbiliform” erythema (5 - 10mm macules), fades in a few days, might scar
Rubella exanthem
Prodrome can be asymptomatic or with slight fever, sore throat, rhinitis and malaise
- Pale pink erythematous rash that starts on the face and spreads to neck, trunk and extremities, lasts up to 5 days
What is herpes simplex
Common viral infection that presents with localised blistering, very common.
Aka cold sores, recurrences triggered by febrile illness e.g. flu
Causes of herpes simplex (cold sores)
Type 1 HSV - oral and facial
type 2 HSV - genital and rectal
After primary episodes of infection, HSV remains dormant in spinal dorsal root nerves that supply the skin. Multiple= clinical lesion, rest and repeat.
How is herpes simplex spread?
Type 1 HSV - usually infants and children in underdeveloped countries and overcrowded places
Type 2 HSV - after puberty and usually sexually transmitted
Clinical features of herpes simplex
Primary type 1 HSV - gingivostomatitis (blisters on gums) and fever, usually resolves by 2 weeks
Primary type 2 HSV - genital herpes - painful vesicles, ulcers, redness and swelling for 2 - 3 weeks.
Diagnosis of herpes simplex
Usually clinical diagnosis but if in doubt then confirm by culture or PCR via viral swab taken from fresh vesicles.
Treatment for herpes simplex
Mild, uncomplicated = no treatment
Severe = aciclovir
Define herpes zoster (shingles)
Herpes zoster is a localised, blistering and painful rash caused by a reactivation of varicella-zoster virus (VZV)
Who gets herpes zoster?
Anyone who has had varicella ( chickenpox)
Common in elderly patients and those with weak immunity e.g. active cancer
Pathophysiology of herpes zoster
After primary infection, varicella (VZV) remains dormant in dorsal root ganglia in the spine for years before reactivation
It migrates down sensory nerves to the skin and causes herpes zoster
Triggers for herpes zoster (shingles)
- Pressure on affected nerve roots
- Radiotherapy at the level of affected nerve root
- Spinal surgery
- Infection
- Injury
Clinical features of herpes zoster
- Early sign - localised pain without visible skin changes, fever, headache
- Then 2 - 3 days later, blisters in dermatomal distribution - blisters confined to cutaneous distribution of one or two adjacent nerve roots
- Unilateral, sharp cut-off at anterior or posterior midline
Treatment of herpes zoster
- Prevention = VZV vaccine for > 60
- Contraindicated in immunosuppressed patients
- Usually supportive management with rest, pain relief, petroleum jelly on blisters
- Abx if secondary infection
- Aciclovir if severe
- Recovery 2- 3 weeks for children and younger adults and 3 - 4 weeks if older
Define impetigo
Common, superficial, highly contagious bacterial skin infection
Pustules (lesions with pus) and honey-coloured crusted lesions
Most common infective organism that causes impetigo
Non-bullous - Staphylococcus aureus and less commonly streptococcus pyogenes
Bullous - always staphylococcus aureus
Risk factors for impetigo
- Young children
- Direct contact with infected person
- Skin conditions e.g. eczema
- Skin injury
- Poor hygiene
- Crowded environments
Clinical features of non-bullous impetigo
- Face or extremities are common sites
- Starts as single erythematous macule (flat <5mm) then becomes pustule or vesicle (small blister < 0.5cm)
- Dries into honey-coloured lesion
Clinical features of bullous impetigo
- S.aureus produces epidermolytic toxin that presents as bullae (blisters > 1cm) that rupture and ooze yellow fluid
- Usually face, trunk, extremities, buttocks and perianal regions
Associated with systemic symptoms of malaise, fever, and lymphadenopathy.
Diagnosis of impetigo
- Clinical diagnosis based on appearance of lesions, history and examination
- Swabs of weeping bullae can confirm diagnosis, bacteria and antibiotic sensitivities
Treatment of impetigo
Localised non-bullous impetigo -
- Wash affected areas with soap and water
- Hygiene measures (wash hands, cover affected areas)
- Stay off school or work until all blisters are healed
- Antiseptic cream (hydrogen peroxide 1% cream)
Widespread non-bullous impetigo
- Topical fusidic acid
- Antibiotics usually flucloxacillin
Bullous impetigo:
- Conservative measures as above and oral antibiotics usually flucloxacillin
Define cellulitis
An acute bacterial infection of the dermis and subcutaneous tissue
Risk factors for cellulitis
- Previous cellulitis
- Fissuring of toes or heels (e.g. athlete’s foot)
- Trauma e.g. surgical wounds
- Diabetes
- Chronic kidney and liver disease
Most common infective organisms that cause cellulitis
Streptococcus pyogenes and Staphylococcus aureus
Clinical features of cellulitis
- Most often affects the limbs
- Unilateral
- Malaise, fever, chills and rigor due to bacteraemia
- Localised painful, red swollen skin
Other signs:
- Dimpled skin (peau d’orange)
- Warmth
- Blistering
- Ulceration
- Abscess formation
- Purpura (discolouration of skin due to small vessel haemorrhage
Investigations for cellulitis
- Primarily based on clinical features and physical examination
If systemically unwell:
- FBC: leukocytosis, raised CRP
- Blood culture to identify causative organism
- U + E
- LFTs
Classification of cellulitis
Eron classification system
- Class I - no signs of systemic toxicity + no uncontrolled comorbidities
- Class II - systemically unwell or well with comorbidity
- Class III - significant systemic upset e.g. acute confusion, tachycardia and tachypnoea
- Class IV - sepsis or severe life-threatening infection e.g. necrotising fasciitis
Differentials for cellulitis
- Unilateral redness or swelling:
- Acute gout
- DVT
- Chronic allergic dermatitis
Management of cellulitis
- Refer to hospital if sepsis or infection e.g. necrotising fasciitis
- Consider hospital referral if severely unwell, frail or immunocompromised
- Oral abx treatment usually flucloxacillin
- Analgesia e.g. paracetamol
- Identify risk factors and manage for cellulitis e.g. diabetes mellitus and weight management
Define acne vulgaris
Acne vulgaris is a chronic inflammatory skin conditions affecting the face, back and chest.
Characterised by the blockage and inflammation of pilosebaceous unit (hair follicle)
Presents with non-inflammatory, inflammatory lesions (or a mixture
Clinical features of acne vulgaris
- Non-inflammatory lesions (comedones) must be present for a diagnosis
- Papules and pustules (< 5mm)
- Nodules or cysts (> 5mm)
Conservative management of acne vulgaris
Advice:
- Avoid over-cleaning the skin
- Use non-alkaline synthetic detergent cleansing product
- Avoid oil-based comedogenic products
- Treatment might irritate the skin at the start
Medical management for mild to moderate acne
1st line: 12 week course of any 2 of the following in combination:
- Topical benzoyl
- Topical antibiotics (clindamycin)
- Topical retinoids (tretinoin adapalene)
Medical management for moderate to severe acne
- 1st line: 12 week course of same medicines as above but different doses (NICE CKS)
- Sometimes the combo topical creams are combined with oral tetracycline and doxycycline
- COCP alternative to systemic abx for women
What is rosacea?
A chronic inflammatory skin condition predominantly affecting the central face (cheeks, chin, nose and central forehead) and starts usually between 30 to 60
Clinical features of rosacea
Diagnosis if one diagnostic or two major clinical features
- Diagnostic features — phymatous changes (skin thickening), persistent erythema.
Major features — flushing/transient erythema, papules and pustules, telangiectasia, eye symptoms (ocular rosacea).
Minor features — skin burning and/or stinging sensation, skin dryness, oedema.
Triggers and risk factors for rosacea
- Increasing age.
- Photosensitive skin types.
- UV exposure.
- Smoking, alcohol.
- Spicy foods and hot drinks.
- Heat or cold temperature.
- Emotional stress and exercise.
Clinical features of ocular rosacea (affects 50% patients with rosacea
- Dryness/discomfort
- Foreign-body sensation
- Photophobia
- Tearing
- Itching
- Photophobia
Differentials for rosacea
- Acute vulgaris
- Seborrheic dermatitis
- Contact dermatitis
- SLE
Management of rosacea
Advice: rosacea is chronic condition and relapse may occur
Signpost to support and info: British skin foundation, patient leaflets
- Avoid triggers and identify triggers with diary
- Sunscreen
- Gentle soap-free OTC cleanser
Medical management of rosacea
Persistent erythema - topical brimonidine 0.5% gel PRN once a day as temporary symptom relief
Define head lice (Pediculus humanus capitis)
Parasitic insects that infest the hairs of the human head and feed on blood from the scalp.
Head lice infestation is called pediculosis capitis
Diagnosis of head lice
Detection combing (fine-tooth 0.2-0.3mm)
Diagnosis of active head lice infestation only made if live head louse is found.
Treatment of head lice
Depends on preference of the person and their parents/carers
Affected members of the household should be treated the same day
- A physical insecticide, such as dimeticone 4% lotion (Hedrin®).
- A traditional insecticide, such as malathion 0.5% aqueous liquid (Derbac-M®).
- Wet combing with a fine-toothed head louse comb (such as the Bug Buster® comb).
- Advise children being treated for head lice can go school
- Not possible to prevent head lice infestion, primary school children should be checked regularly
Define scabies
Scabies is an transmissible, intensely itchy skin infestation caused by the human parasite Saroptes scabiei
Classical (typical) scabies is infestation with low numbers of mites (5 - 15 per host)
Crusted (Norwegian) scabies is a hyperinfestation with thousands or millions of mites
Risk factors for scabies
- Close contact with an infested person.
- High levels of poverty and social deprivation.
- Crowded living conditions and institutionalization.
- Winter months, probably due to increased crowding and prolonged survival of mites
Clinical features of scabies
- Classical itchy rash - occurs 4 - 6 weeks following initial infection
- Lesions are symmetrical, mainly affecting the hands, wrists, axillae, thighs, buttocks, waist, soles of the feet, genitalia
- Itch worse at night
Rashes are erythematous papules, excoriated with haemorrhagic crusts on top
Thin, linear line brown/grey in colour (pathogonomic sign)as the mites burrow
Differentials of scabies
- Dermatitis, pubic lice and insect bites
Treatment of scabies
- Seek specialist advice e.g. paediatric dermatologist if patient < 2months
- Admission to hospital if crusted scabies suspected
- Classical scabies: topical permethrin 5% cream
- Patient info and education
- Advise that close contacts must be treated with topical permethrin 5% cream
- Bedding, clothing and towels decontaminated with hot wash cycle and drying
- Itching may persist for up to 4 weeks after treatment
Define osteoarthritis
“Wear and tear” in the joints
Occurs in the synovial joints and results from genetic factors, overuse and injury
Due to imbalance between cartilage damage and chondrocyte response.
Risk factors for osteoarthritis
- Obesity
- Age
- Occupation
- Trauma
- Female
- FHx
Osteoarthritis: commonly affected joints
- Hips
- Knees
- Distal interphalangeal (DIP) joints in the hands
- Carpometacarpal (CMC) joint at the base of the thumb
- Lumbar spine
- Cervical spine (cervical spondylosis)
Osteoarthritis: key X-ray changes
LOSS
- Loss of joint space
- Osteophytes (bone spurs)
- Subarticular sclerosis (increased density of the along the joint line)
- Subchondral cysts (fluid-filled holes in the bone)
Presentation of osteoarthritis
- Pain and stiffness in affected joints
- Better first thing in the morning
- Worse with activity and end of the day
Patients might present with referred pain - e.g. OA of the hip might present as LBP or knee pain
Leads to deformity, instability and reduced joint function
General signs of osteoarthritis
- Bulky, bony enlargement of the joint
- Restricted range of movement
- Crepitus on movement
- Effusions around the joint
Hand signs in osteoarthritis
- Heberden’s nodes (in the DIP joints)
- Bouchard’s nodes (in the PIP joints)
- Squaring at the base of the thumb (CMC joint)
- Weak grip
- Reduced range of motion
Diagnosis of OA
NICE guidelines
Diagnosis can be made without any investigations if:
- Over 45
- Typical pain associated with activity
- No morning stiffness or lasting <30 mins
Conservative management for OA
Patient education and lifestyle changes:
- Therapeutic exercise - improve strength and reduce pain
- Weight loss
- Occupational therapy (e.g. walking aids and adaptations at home
Pharmacological treatment for OA
- Topical NSAIDs first-line for knee osteoarthritis
- Oral NSAIDs where required and suitable (with PPI for gastroprotection)
Why should NSAIDs be used with caution in OA?
Very effective for MSK pain, but best used intermittently, adverse effects:
- GI side effects, such as gastritis and peptic ulcers (leading to upper GI bleeding)
- Renal: AKI
- Cardiovascular side effects, such as hypertension, heart failure, myocardial infarction and stroke
- Exacerbating asthma
Particular caution needed in older patients and those on anticoagulants e.g. aspirin or DOACs
TOM TIP: how does NSAIDs cause hypertension?
NSAIDs block prostaglandins (prostaglandins cause vasodilation).
Define gout
A type of crystal arthropathy associated with chronically high blood uric acid levels
Urate crystals deposited in the joint cause it be inflamed.
Clinical features of gout
Usually a single acute, hot, swollen and painful joint
Typically affected joints are
- Metatarsophalangeal joint (MTP) i.e. base of big toe
- Carpometacarpal joint (CMC joint) i.e. base of thumb
Critical differential is septic arthritis
Diagnosis of gout
Clinical diagnosis supported by raised serum urate levels on a blood test
Analysis of aspirated joint fluid show monosodium urate crystals which are needle-shaped, negatively birefringent (yellow) under polarised light.
This is in contrast to pseudogout where the calcium pyrophosphate crystals are rhomboid-shaped and positively birefringent
Key X-ray findings in gout
- Maintained joint space (no loss of joint space)
- Lytic lesions in the bone
- Punched out erosions
- Erosions can have sclerotic borders with overhanding edges
Conservative management of gout
- Weight loss
- Hydration
- Reduce alcohol and purine-based food consumption (meat, seafood)
Medical management of gout
Acute flares:
- 1st line is NSAIDs co-prescribed with PPI
- 2nd line is colchicine for patients that are unsuitable for NSAIDs e.g. renal impairment or heart disease
Prophylactic management of gout
Xanthine oxidase inhibitors e.g. Allopurinol or febuxostat to reduce uric acid levels
Prophylaxis started weeks after acute attack resolution
Initially NSAIDs or colchicine may be given to prevent a gout attack
Once allopurinol or febuxostat is started, continue during acute attack
COMMON EXAM QUESTION
Define “non-specific” or “mechanical” lower back pain
Lower back pain refers to pain in the lumbosacral area
Non-specific or mechanical back pain is lower back pain not attributable to an underlying cause
Accounts for 90 to 95% of low back pain cases in primary care
Risk factors for mechanical low back pain
- Obesity
- Physical inactivity
- Heavy lifting
- Stress
- Depression
Red flag causes of back pain
- Spinal fracture (e.g., major trauma)
- Cauda equina (e.g., saddle anaesthesia, urinary retention, incontinence or bilateral sciatica)
- Spinal stenosis (e.g., intermittent neurogenic claudication)
- Ankylosing spondylitis (e.g., age under 40, gradual onset, morning stiffness or night-time pain)
- Spinal infection (e.g., fever or a history of IV drug use)
Causes of mechanical back pain
- Muscle or ligament sprain
- Herniated disc
- Degenerative changes
Causes of neck pain
- Muscle or ligament strain (e.g., poor posture or repetitive activities)
- Whiplash (typically after a road traffic accident)
- Cervical spondylosis (degenerative changes to the vertebrae)
Define sciatica
The sciatic nerve is formed of spinal nerves L4 - S3
It supplies sensation to the lateral lower leg and foot, and motor function to posterior thigh, lower leg and foot
Sciatica is unilateral pain from the buttocks to the back of the thigh to below the knee or feet, “electric” or “shooting” pain
Symptoms of sciatica
- “Electric” or “shooting” pain unilaterally from buttocks to the back of the thigh to below the knee or feet
- Paraesthesia
- Numbness
- Motor weakness
Causes of sciatica
Lumbosacral nerve root compression by:
- Herniated disc
- Spondylolisthesis (anterior displacement of a vertebra out of line with the one below)
- Spinal stenosis
What is bilateral sciatica a red flag for?
Cauda equina syndrome
History-taking in back pain
Any pain = SOCRATES
Key symptoms in the history:
- Major trauma (spinal fracture)
- Stiffness in the morning or with rest (ankylosing spondylitis)
- Age under 40 (ankylosing spondylitis)
- Gradual onset of progressive pain (ankylosing spondylitis or cancer)
- Night pain (ankylosing spondylitis or cancer)
- Age over 50 (cancer)
- Weight loss (cancer)
- History of cancer with potential metastasis (cauda equina or spinal metastases)
- Fever (spinal infection)
- IV drug use (spinal infection)
Key findings on examination for back pain that points to a more serious underlying pathology
- Localised tenderness to the spine (spinal fracture or cancer)
- Bilateral motor or sensory signs (cauda equina)
- Bladder distention might indicate urinary retention (cauda equina)
- Reduced anal tone on PR (Cauda equina)
Special test to support diagnosis of sciatica
Sciatic stretch test
What are the main cancers that metastasise to the bone and therefore can cause back pain if spinal metastases are present?
PoRTaBLe
Po - prostate
R - renal
Ta - thyroid
B - Breast
Le - Lung
Investigations for back pain
- Non-specific back pain - usually clinical diagnosis
- X-ray or CT for spinal fractures
- Emergency MRI if suspected cauda equina (within hours of presentation)
Suspected ankylosing spondylitis:
- Inflammatory markers (CRP and ESR)
- Spinal X-ray - “bamboo” spine in later stages
- Spinal MRI - bone marrow oedema
What is the StarT back tool
Stratify risk of a patient developing back pain
9 questions that assess a patient’s function and psychological response to the back pain
- Total score out of 9
- Subscore on 4 psychological questions (out of 4)
Low risk: total score ≤ 3 and subscore ≤ 3
Medium risk: total score > 3 and subscore ≤ 3
High risk: total score > 3 and subscore > 3
Manging acute lower back pain
- Exclude serious underlying pathology, if so, arrange appropriate specialist review
Management of non-specific back pain based on StarT Back tool
Low risk:
- Self-management
- Education
- Reassurance
- Analgesia (1st line is NSAIDs, and codeine as alternative, benzo for muscle spasms)
- Staying active and continuing to mobilise as tolerated
Additional management options for patients at medium to high risk of developing chronic back pain
- Physiotherapy
- Group exercise
- Cognitive behavioural therapy
Safety netting for red-flag symptoms
Management of sciatica
Similar to acute back pain
NICE states NOT to use meds such as gabapentin, pregabalin, diazepam or oral corticosteroids for sciatica.
NOT to use opioids for chronic sciatica
Use the following neuropathic meds if symptoms are persisting or worsening:
- Amitriptyline
- Duloxetine
Referral to specialist if no improvement
Define polymyalgia rheumatica (PMR)
Polymyalgia rheumatica is an inflammatory condition that causes pain and stiffness in the shoulders, pelvic girdle and neck
Strongly associated with giant cell arteritis and they often occur together
Presentation of polymyalgia rheumatica
- More common in older white patients
- Rapid symptom onset over days to weeks
- Symptoms should be present for at least 2 weeks before diagnosis is considered
- Core symptoms are pain and stiffness of:
- Shoulders, might radiate to upper arm and elbow
- Pelvic girdle (hip), might radiate to thigh
- Neck
What characteristics of the pain and stiffness in the patient’s history indicate polymyalgia rheumatica?
- Worse in the morning
- Worse after rest or inactivity
- Interfere with sleep
- Take at least 45 minutes to ease in the morning
- Somewhat improve with activity
Associated symptoms:
- Systemic symptoms (e.g., weight loss, fatigue and low-grade fever)
- Muscle tenderness
- Carpel tunnel syndrome
- Peripheral oedema
Differentials of polymyalgia rheumatica
The symptoms are not specific to PMR and there are a long list of differentials
- Osteoarthritis
- Rheumatoid arthritis
- Systemic lupus erythematosus
- Myositis (e.g., polymyositis)
- Fibromyalgia
- Lymphoma or leukaemia
Myeloma
Diagnosis of polymyalgia rheumatica
Based on clinical presentation, response to steroids and excluding differentials
NICE recommends investigations before starting steroids
- Full blood count
- Renal profile (U&E)
- Liver function tests
- Calcium (abnormal in hyperparathyroidism, cancer)
- Thyroid-stimulating hormone
- Creatine kinase for myositis
- Rheumatoid factor for rheumatoid arthritis
- Urine dipstick
Additional investigations to consider:
SLE: Anti-nuclear antibodies (ANA)
RA: anti-cyclic citrullinated peptide (anti-CCP)
Myeloma: Urine Bence Jones protein
Treatment of polymyalgia rheumatica
15mg prednisolone daily initially
Follow up after one week
Should be dramatic improvement after a week (70%)
Steroids for 1 - 2 years, gradually reducing:
- 15mg until the symptoms are fully controlled, then
- 12.5mg for 3 weeks, then
- 10mg for 4-6 weeks, then
- Reducing by 1mg every 4-8 weeks
Additional management for patients on long-term steroids
Don’t STOP mnemonic
Don’t - steroid dependence occurs after 3 weeks of treatment, and abruptly stopping risks adrenal crisis
S – Sick day rules (steroid doses may need to be increased if the patient becomes unwell)
T – Treatment card – patients should carry a steroid treatment card to alert others that they are steroid-dependent
O – Osteoporosis prevention (e.g., bisphosphonates and calcium and vitamin D)
P – Proton pump inhibitors for gastro-protection (e.g., omeprazole)
General symptoms of anaemia
- Tiredness
- Shortness of breath
- Headaches
- Dizziness
- Palpitations
- Worsening of other conditions, such as angina, heart failure or peripheral arterial disease
Generic signs of anaemia
- Pale skin
- Conjunctival pallor
- Tachycardia
- Raised respiratory rate
What is anaemia of chronic disease?
- Anaemia of chronic disease often occurs with chronic kidney disease due to reduced production of erythropoietin by the kidneys, the hormone responsible for stimulating red blood cell production.
- Treatment is with erythropoietin.
Presentation of chronic lymphocytic leukaemia
Non-specific
- Fatigue
- Fever
- Pallor due to anaemia
- Petechiae or bruising due to thrombocytopenia
- Abnormal bleeding
- Lymphadenopathy
- Hepatosplenomegaly
Investigations for the underlying causes of anaemia
- Full blood count for haemoglobin and mean cell volume
- Reticulocyte count (indicates red blood cell production)
- Blood film for abnormal cells and inclusions
- Renal profile for chronic kidney disease
- Liver function tests for liver disease and bilirubin (raised in haemolysis)
- Ferritin (iron)
- B12 and folate
- Intrinsic factor antibodies for pernicious anaemia
- Thyroid function tests for hypothyroidism
- Coeliac disease serology (e.g., anti-tissue transglutaminase antibodies)
- Myeloma screening (e.g., serum protein electrophoresis)
- Haemoglobin electrophoresis for thalassaemia and sickle cell disease
- Direct Coombs test for autoimmune haemolytic anaemia
Define vitamin B12 deficiency
A lack of B12 that leads to macrocytic anaemia (mean cell volume (MCV > 95fL), the key causes of low B12 are:
- Pernicious anaemia (autoimmune disorder that impairs the adsorption of B12)
- Insufficient dietary B12
- Medications that reduce B12 absorption (e.g. PPI and metformin)
Define chronic lymphocytic leukaemia
Slowly progressing cancer of the lymphoid cell line
There is neoplastic proliferation of mature B lymphocytes and underproduction of the other cell types
Pathophysiology of pernicious anaemia
The parietal cells of the stomach produce intrinsic factor, which is needed for B12 absorption in the distal ileum.
In pernicious anaemia, autoantibodies target either parietal cells or intrinsic factor = lack of intrinsic factor and lack of B12 absorption
Symptoms of vitamin B12 deficiency
- Peripheral neuropathy, with numbness or paraesthesia (pins and needles)
- Loss of vibration sense
- Loss of proprioception
- Visual changes
- Mood and cognitive changes
Diagnosis of pernicious anaemia
- Intrinsic factor antibodies (the first-line investigation)
- Gastric parietal cell antibodies (less helpful)
Management of vitamin B12 deficiency
1st line: IM hydroxocobalamin
Maintenance:
- Pernicious anaemia - 2 - 3 monthly injections for life
- Dietary - oral cyanocobalamin or twice a year injections
What is the management plan if the patient has B12 and folate deficiency
- Important to treat B12 deficiency first!
- Giving patients folic acid if they have a vitamin B12 deficiency > subacute combined degeneration of the cord with demyelination of spinal cord and severe neurological problems
Risk factors for CLL
- Age: more common in 60+
- Family History
- Male sex x2 risk
Diagnosis of CLL
- FBC within 48 hours for patients with suspected leukaemia
- 1st line: FBC
- Blood film: increased number of mature lymphocytes and smudge cells
- Immunophenotype
Immunoglobulins: hypogammaglobulinemia
Genetic analysis: identify chromosomal deletions to guide treatment
- Bone marrow biopsy
General management of CLL
Urgent referral to oncology and haematology - MDT involvement
- Chemo and targeted therapies e.g. tyrosine kinase inhibitors (e.g. ibrutinib)
Management of CLL
- Referral to oncology and haematology specialist - MDT involvement
- Chemotherapy and targeted therapies e.g. tyrosine kinase inhibitors (e.g. ibrutinib)
Define myelodysplastic syndrome
A form of cancer caused by a mutation in the myeloid cells in the bone marrow resulting in inadequate production of blood cells (ineffective haematopoiesis)
It has the potential to transform into acute myeloid leukaemia
What low levels of blood components does myelodysplastic syndrome cause?
It causes low levels of blood components that originate from the myeloid cell line:
- Anaemia (low haemoglobin)
- Neutropenia (low neutrophil count)
- Thrombocytopenia (low platelets)
Known as pancytopenia
Risk factors for myelodysplastic syndrome
- Older age
- Previous chemotherapy or radiotherapy
Diagnosis of myelodysplastic syndrome
FBC abnormal (pancytopenia - low RBC, low WBC, low platelets), blasts on blood film
Management of myelodysplastic syndrome
Depending on the symptoms, risk of progression and overall prognosis:
- Watchful waiting
- Supportive treatment (e.g., blood or platelet transfusions)
- Erythropoietin (stimulates red blood cell production)
- Granulocyte colony-stimulating factor (stimulates neutrophil production)
- Chemotherapy and targeted therapies (e.g., lenalidomide)
- Allogenic (donor) stem cell transplantation (risky but potentially curative)
Men’s health: what are the lower urinary tract symptoms (LUTS)?
- Storage symptoms: occurs
when bladder should be storing urine - need to pee
FUNI
Frequency, Urgency, Nocturia, (urgency) Incontinence
- Voiding symptoms - occurs when the bladder outlet obstructed
SHID
- Voiding: (poor) Stream, Hesitancy, Incomplete emptying, Dribbling
Others: straining, terminal dribbling, intermittency (stop then start
Define benign prostatic hyperplasia (BPH)
Benign prostatic hyperplasia is a very common condition affecting men in older age (usually over 50 years).
Cause = hyperplasia of the stromal and epithelial cells of the prostate.
Assessment for men presenting with LUTS
- Digital rectal examination (prostate exam) to assess the size, shape and characteristics of the prostate
- Abdominal examination to assess for a palpable bladder
- Urinary frequency volume chart, recording 3 days of fluid intake and output
- Urine dipstick - infection, haematuria (e.g., due to bladder cancer)
- Prostate-specific antigen (PSA) for prostate cancer, depending on the patient preference
Findings on prostate examination
- Benign prostate feels smooth, symmetrical and slightly soft, with a maintained central sulcus
- A cancerous prostate may feel firm/hard, asymmetrical, craggy or irregular, with loss of the central sulcus
What is the management plan for BPH for patients with non-bothersome symptoms?
1st line: lifestyle advice and modification if the patient has mild (non-bothersome) symptoms: treat constipation, reduce caffeine and fluid intake, medication review, bladder retraining.
Medical management of BPH
- Alpha-blockers (e.g., tamsulosin) relax smooth muscle, with rapid improvement in symptoms
- 5-alpha reductase inhibitors (e.g., finasteride) gradually reduce the size of the prostate
Why is the PSA (prostate-specific antigen) test not reliable?
PSA is usually used to screen for prostate cancer. However, many things can also raise PSA levels, such as benign prostate hyperplasia, prostatitis or UTI.
Therefore, it is not a specific test for prostate cancer as it can be raised even if the patient does not have prostate cancer.
Define lower UTI
AN infection that involves the bladder, causing cystitis (inflammation of the bladder).
It can potentially spread up to the kidneys and cause pyelonephritis
Causes of urinary tract infections
Primary source of bacteria from faeces, and bacteria can easily move from anus to urethral opening
E.coli is the most common causative organism
Presentation of lower UTI
- Dysuria (pain, stinging or burning when passing urine)
- Suprapubic pain or discomfort
- Frequency
- Urgency
- Incontinence
- Haematuria
- Cloudy or foul smelling urine
- Confusion is commonly the only symptom in older and frail patients
What symptoms/signs would indicate pyelonephritis and not just lower UTI?
Fever
Loin/back pain
Nausea/vomiting
Renal angle tenderness on examination
Can potentially lead to sepsis and kidney scarring
What would the urine dipstick results be in an UTI?
- Nitrite present: bacteria present as gram-negative bacteria (e.g. E.coli) break down nitrates to nitrites
- Leukocytes - normal to have a small amount in urine, but raised indicates infection
- RBC= can detect microscopic haematuria
UTI if presences of nitrites or leukocytes + red blood cells
If not, UTI diagnosed only if nitrites are present
Why is a midstream urine sample useful in microscopy?
A MSU sample is sent for microscopy, culture and sensitivity to determine the infective organism and antibiotics
Not all patients with uncomplicated UTI will need a MSU, more important in:
- Pregnant patients
- Patients with recurrent - UTIs
- Atypical symptoms
- If abx ineffective
Antibiotics choice and duration in UTI
- Trimethoprim (Avoid in first trimester)
- Nitrofurantoin (avoided in patients with an eGFR <45 and third trimester)
3 days for simple UTI in women
- 5 to 10 days in immunosuppressed women, abnormal anatomy or impaired kidney function
- 7 days of abx for men, pregnant women
Management of UTI in pregnancy
- 7 days of antibiotics
- MSU for microscopy, culture and sensitivity
Antibiotics:
- Nitrofurantoin (avoid in the third trimester as risk of neonatal haemolysis)
- Trimethoprim (avoid in first trimester as folate antagonist)
- Amoxicillin (only after sensitivities are known)
- Cefalexin
Define prostate cancer
Most common cancer in men.
95% are adenocarcinomas
Key risk factors for prostate cancers
- Increasing age
- Family history
- Black African or Caribbean origin
- Tall stature
- Anabolic steroids
Clinical features of prostate cancer
- Might be asymptotic
- LUTS (similar to BPH) e.g. hesitancy, frequency, weak flow, terminal dribbling and nocturia
- Haematuria
- Erectile dysfunction
- Weight loss, bone pain, cauda equina syndrome indicate advanced or metastatic disease
PSA test is unreliable, what are some common causes of raised PSA?
- Prostate cancer
- Benign prostatic hyperplasia
- Prostatitis
- Urinary tract infections
- Vigorous exercise (notably cycling)
- Recent ejaculation or prostate stimulation
It can lead to early detection of prostate cancer however, high rate of false positive (75%) and false negatives (15%)
What problems might a false positive PSA or false negative PSA result cause?
Counselling a patient about whether to have a PSA test is a common OSCE scenario. Tests whether you understand the implications of false positives and negatives and whether you can explain this to a patient to allow them to make an informed decision.
False positives might lead to further investigations. invasive prostate biopsies and lead to unnecessary diagnosis and treatment of prostate that would never have caused problems .
False negatives might lead to false reassurances
How would be benign prostate vs cancerous prostate feel on examination?
Benign prostate = smooth, symmetrical and slightly soft, with maintained central sulcus (the dip in the middle between the right and left lobe)
Cancerous prostate = firm or hard, asymmetrical, craggy or irregular with loss of central sulcus. There might be hard nodule.
The above might indicate prostate cancer warrants a 2WW urgent cancer referral to urology.
Investigations for prostate cancer
- 1st line for suspected localised prostate cancer: multiparametric MRI, reported on a Likert scale (1- very low suspicion to 5 - definite cancer)
- Next step = prostate biopsy (if Likert 3 or above) or clinical suspicion
- Isotope bone scan to look for bony metastasis
What is the Gleason grading system?
Grading system for prostate cancer based on histology of prostate biopsies
Made up of two numbers added up: the grade of the most prevalent pattern and grade of the second most prevalent pattern
6: low risk
7: intermediate risk
8 or above: high risk
TNM staging for prostate cancer
T - Tumour, N (lymph node) and M (metastasis)
T for Tumour:
TX – unable to assess size
T1 – too small to be felt on examination or seen on scans
T2 – contained within the prostate
T3 – extends out of the prostate
T4 – spread to nearby organs
N for Nodes:
NX – unable to assess nodes
N0 – no nodal spread
N1 – spread to lymph nodes
M for Metastasis:
M0 – no metastasis
M1 – metastasis
Management of prostate cancer
- Surveillance or watchful waiting in early prostate cancer
- External beam radiotherapy directed at the prostate
- Brachytherapy (implanting radioactive metal “seeds” into the prostate)
- Hormone therapy e.g. androgen deprivation (surgery to lower testosterone levels) or blockade (drugs to block testosterone)
- Surgery e.g. bilateral orchidectomy
Define testicular cancer
Testicular cancer arises from the germ cells in the testes. Germ cells are cells that produce gametes (sperm in males).
Two types:
- Seminomas
- Non0seminomas (mostly teratomas)
Risk factors for testicular cancer
- Undescended testes
- Male infertility
- Family history
- Increased height
Presentation of testicular cancer
Typical presentation:
Painless lump that is:
- Non-tender (or even reduced sensation)
- Arising from testicle
- Hard
- Irregular
- Not fluctuant
- No transillumination
Investigations for testicular cancer
- 1st line: scrotal ultrasound
Tumour markers:
- Alpha-fetoprotein – may be raised in teratomas (not in pure seminomas)
- Beta-hCG – may be raised in both teratomas and seminomas
- Lactate dehydrogenase (LDH) is a very non-specific tumour marker
- Staging CT scans
Staging system for testicular cancer
Royal Marsden staging system:
- Stage 1 – isolated to the testicle
- Stage 2 – spread to the retroperitoneal lymph nodes
- Stage 3 – spread to the lymph nodes above the diaphragm
- Stage 4 – metastasised to other organs
Common areas that testicular cancer metastasise to
- Lymphatics
- Lungs
- Liver
- Brain
Management of testicular cancer
- MDT to decide best course of action for the patient
Depending on the grade and stage of testicular cancer:
- Surgery to remove the affected testicle (radical orchidectomy) – a prosthesis can be inserted
- Chemotherapy
- Radiotherapy
- Sperm banking to save sperm for future use, as treatment may cause infertility
Long-term side effects of testicular cancer
Significant as most patients are young and expect to live for a long time after treatment:
- Infertility
- Hypogonadism (testosterone replacement may be required)
- Peripheral neuropathy
- Hearing loss
- Lasting kidney, liver or heart damage
- Increased risk of cancer in the future
Prognosis of testicular cancer
- Early testicular cancer - 90% cure rate
- Metastatic disease can be curable
- Patients will need follow-up to monitor for reoccurrence - tumour markers, imaging CT scans and CXR
Define hydrocele
A hydrocele is a collection of serous fluid between the layers of the membrane (tunica vaginalis) that surrounds the testis or along the spermatic cord.
The tunica vaginalis is a sealed pouch of membrane that surrounds the testes.
Examination findings with a hydrocele
- Patients will present with a testicular lump
- The testicle is palpable within the hydrocele
- Soft, fluctuant and may be large
- Irreducible and has no bowel sounds (distinguishing it from a hernia)
- Transilluminated by shining torch through the skin, into the fluid (the testicle floats within the fluid)
Causes of hydroceles
- Idiopathic
- Testicular cancer
- Testicular torsion
- Epididymo-orchitis
- Trauma
Management of hydroceles
- Ultrasound to confirm diagnosis
- Exclude serious pathology (e.g. cancer)
- Idiopathic or smaller hydrocele = conservative
- Symptomatic/large - surgery, aspiration or sclerotherapy (injection technique to scar and resolve the hydrocele)
Define varicocele
A varicocele occurs when the veins in the pampiniform plexus become swollen - common (15% men)
It can impair fertility, likely due to impaired temperature control in the affected testicle.
It can also lead to testicular atrophy
What is the pampiniform plexus?
A network of veins in the spermatic cord and drains the testes into the testicular vein.
Regulates temperature of blood entering the testes as the testicles need to be at an optimum temperature for producing sperm.
Why do most varicoceles occur in the left testicle (90%)?
- Varicoceles are due to increased resistance in the testicular vein.
- Right testicular vein drains directly into the IVC and the left testicular vein drains into the left renal vein, so increased resistance.
- Left-sided varicocele may indicate obstruction of the left testicular vein due to renal cell carcinoma
Presentation of varicoceles
- Throbbing/dull pain or discomfort, worse on standing
- A dragging sensation
- Sub-fertility or infertility
Examination findings of varicoceles
- A scrotal mass that feels like a “bag of worms”
- More prominent on standing
- Disappears when lying down
- Asymmetry in testicular size if the varicocele has affected the growth of the testicle
Investigations for varicoceles
- USS with Doppler imaging to confirm diagnosis
- Semen analysis if concerns about fertility
- Hormonal tests (e.g. FSH and testosterone) if concerns about function
Management for varicoceles
- Uncomplicated = conservative management
- Surgery or endovascular embolisation indicated for pain, testicular atrophy or infertility
Define epididymal cysts
Cysts that occur at the top of the tests (epididymis)
Fluid-filled or sperm-filled (spermatocele)
Very common - 30% of adult men
Examination findings of epididymal cysts
- Usually asymptotic
- Examination findings:
- Soft, round lump
- Typically at top of testicle
- Separate from testicle, associated with the epididymis
- Large cysts - transilluminate (separate from testicle)
Management of epididymal cysts
Usually harmless, not associated with infertility or cancer
Occasionally might cause pain or discomfort and removal might be considered.
Define otitis externa
Diffuse inflammation of the skin and subdermis of the external ear canal. Might involve the pinna or tympanic membrane.
Acute: inflammation < 6 weeks
Chronic: inflammation > 6 weeks
Infective organisms that cause otitis externa
Acute - usually bacterial staphylococcus aureus and pseudomonas aeruginosa
Chronic - fungal cause e.g. Aspergillus or candida albicans
What conditions might otitis externa be associated with?
Acute otitis externa: underlying skin conditions e.g. contact dermatitis, otitis media, trauma to ear canal
Chronic otitis externa: diabetes mellitus, immunocompromise, prolonged antibiotic or corticosteroid use
Clinical features of otitis externa
- Ear pain
- Discharge
- Itchiness
- Conductive hearing loss
Examination findings in otitis externa
- Erythema and swelling in the ear canal that might extend to the tympanic membrane
- Tenderness of the ear canal
- Pus or discharge in the ear canal
- Lymphadenopathy (swollen lymph nodes) in the neck or around the ear
Diagnosis of otitis externa
Clinical diagnosis with examination of the ear canal using an otoscope
Ear swab for causative organism but not usually required
Management of otitis externa
Mild = acetic acid 2% (OTC EarCalm) - both antibacterial and antifungal
Moderate = topical antibiotics and steroids:
- Neomycin, dexamethasone and acetic acid (e.g., Otomize spray - most common, so REMEBER THIS)
- Aminoglycosides (e.g. gentamicin or neomycin) = potentially ototoxic if pas the tympanic membrane, so rule out perforated eardrum before prescribing
- Fungal = clotrimazole ear drops
Management of severe otitis externa and systemic symptoms
Oral abx e.g. flucloxacillin
Or discussion with ENT for admission and IV abx
What is malignant otitis externa?
Severe potentially life-threatening form of otitis externa.
The infection spreads to the bones surrounding the ear canal and skull.
Progresses to osteomyelitis of the temporal bone of the skull
Risk factors for malignant otitis externa
- Diabetes
- Immunosuppressant medications (e.g., chemotherapy)
- HIV
Clinical features of malignant otitis externa
Severe, unremitting pain, purulent ear discharge, fever, hearing loss, granulation tissue in the ear canal, possible facial nerve palsy.
Granulation tissue at the junction between the bone and cartilage in the ear canal (about halfway along) is a key finding.
Management of malignant otitis externa
- Emergency!
- Admit to hospital under ENT team
- IV antibiotics
- CT/MRI to assess extent of infection
Key complications of otitis externa
- Facial nerve damage and palsy
- Meningitis
- Intracranial thrombosis
- Death
Define tonsillitis
Inflammation of the tonsils
Most common is viral infection
If bacterial - most common cause is group A streptococcus (S. pyogenes)
Presentation of acute tonsillitis
- Sore throat
- Fever (> 38)
- Pain on swallowing
Examination of the throat = red, inflamed and enlarged tonsils with/without exudates - small, white patches of pus on the tonsils
Centor criteria for tonsillitis
Estimates the probability that tonsillitis is due to bacterial infection and benefit from antibiotics
score ≥ 3 = 40 - 60% possibility of bacterial tonsillitis and abx offered:
1 point for each:
- Fever over 38ºC
- Tonsillar exudates
- Absence of cough
- Tender anterior cervical lymph nodes (lymphadenopathy)
FeverPAIN score for tonsillitis
Alternative to Centor score
Score 2 - 3 = 34 - 40% probability
Score 4 - 5 = 62 - 65% probability of bacterial tonsillitis
- Fever during previous 24 hours
- P – Purulence (pus on tonsils)
- A – Attended within 3 days of the onset of symptoms
- I – Inflamed tonsils (severely inflamed)
- N – No cough or coryza
Management of tonsillitis
- Consider admission if patient is immunocompromised, systemically unwell, dehydrated, has stridor, respiratory distress or peritonsillar abscess (quinsy) or cellulitis.
- Calculate Centor or feverPAIN score
- If viral: educate patients and give safety net advice
- Management with simple analgesia with paracetamol and ibuprofen
- NICE recommends that patients return if pain does not settle after 3 days or fever rises above 38.3 - consider antibiotics or alternative diagnosis
- Antibiotics if the Centor score is ≥ 3, or the FeverPAIN score is ≥ 4.
- Also, consider antibiotics if young infants, immunocompromised patients or significant co-morbidity
- Delayed prescription - antibiotics for collection only if symptoms worsen or do not improve in next 2 - 3 days
Antibiotics choice in tonsilitis
1st line: penicillin V (phenoxymethylpenicillin) for 10 days
Clarithromycin if penicillin allergy
Complications of tonsillitis
- Peritonsillar abscess (quinsy)
- Otitis media
- Scarlet fever
- Rheumatic fever
- Post-streptococcal glomerulonephritis
- Post-streptococcal reactive arthritis
Define conjunctivitis
Inflammation of the conjuctiva - a thin layer of tissue that covers the inside of the eyelids and sclera
It can be caused by viruses, bacteria or allergy
Unilateral or bilateral
Presentation of conjunctivitis
- Red, bloodshot eye
- Itchy or gritty sensation
- Discharge
Please note that conjunctivitis does not cause pain, photophobia or reduced visual acuity
Presentation of bacterial conjuctivitis
- Purulent discharge
- Usually worse in the morning when eyes are stuck together
- Highly contagious
Presentation of viral conjunctivitis
- Common and presents with a clear discharge
- Associated with other symptoms of viral infection e.g. dry cough, sore throat and blocked nose, tender pre-auricular lymph nodes (in front of the ears)
- Contagious
Causes of acute red eye
Causes of an acute painful red eye include:
- Acute angle-closure glaucoma
-Anterior uveitis - Scleritis
- Corneal abrasions or ulceration
- Keratitis (corneal infection)
- Foreign body
- Traumatic or chemical injury
Causes of an acute painless red eye include:
- Conjunctivitis
- Episcleritis
- Subconjunctival haemorrhage
Pain or reduced visual acuity warrant an emergency same-day referral to ophthalmology
Management of conjunctivitis
- Resolves in 1 -2 weeks (viral and bacterial)
- Hygiene measures to reduce spread (e.g. avoid towel sharing and close contact and regular hand washing)
- Clean eye with cool boiled water and cotton wool to clear discharge
- Neonates < 1m need urgent ophthalmology assessment as it might be caused by gonococcal infection and can cause permanent vision loss
What is allergic conjunctivitis?
- Conjunctivitis that occurs due to contact with allergens
- Causes swelling of conjunctival sac and eyelid with itching and watery discharge
- Antihistamines to relieve symptoms
- Topical mast-cell stabiliser can be used in patients with chronic seasonal symptoms
Causes/ risk factors of vitamin D deficiency
- Seasonal e.g. UK only has enough sunlight in spring and summer months (lol not even then)
- Dietary deficiency
- Skin colour - darker skin requires more sunlight exposure
- Clothing cover - e.g. religious/cultural reasons
- Malabsorption diseases e.g. coeliac
- End-stage renal failure
Diagnosis of vitamin D deficiency
Check vitamin D levels by measuring serum 25-hydroxyvitamin D (25[OH]D) only if symptomatic:
- MSK symptoms: e.g. suspected osteomalacia, suspected osteoporosis
- Less than 25 nmol/L – vitamin D deficiency
- 25 to 50 nmol/L – vitamin D insufficiency
Treatment for vitamin D deficiency
Colecalciferol (vitamin D₃)
Example loading regime:
- 50,000 IU once weekly for 6 weeks
- Or 4000 IU daily for 10 weeks
A maintenance dose of 800-2000 IU per day is continued following the loading regime (or as the initial treatment in patients that do not require rapid treatment.)
Treatment for vitamin D deficiency
Colecalciferol (vitamin D₃)
Example loading regime:
- 50,000 IU once weekly for 6 weeks
- Or 4000 IU daily for 10 weeks
A maintenance dose of 800-2000 IU per day is continued following the loading regime (or as the initial treatment in patients that do not require rapid treatment.)
