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
