community/GP Flashcards
what are the three characteristics of asthma ?
- airflow limitation - usually reversible spontaneously or with treatment
- airway hyper-responsiveness
- bronchial inflammation with T lymphocytes, mast cells, eosinophils with associated plasma exudation, oedema, small muscle hypertrophy, mucus plugging and epithelial damage
what are the two main types of asthma?
allergic/eosinophilic asthma (allergens e.g. fungal allergens and pets etc) and atopy
Non-allergic/non-eosinophilic - exercise, cold air and stress, smoking and non smoking associated, obesity associated.
what is atopy?
individuals who readily develop IgE against common environmental antigens such as house-dust mites, grass pollen and fungal spores leading to elevated IgE serum levels is linked to airway hyper-responsiveness and the prevalence of asthma
what environmental factors can influence asthma?
early childhood exposure to allergens and maternal smoking has a major influence on IgE production
growing up in a clean environment may predispose towards an IgE response to allergens where as growing up in a dirtier environment may allow the immune system to avoid developing allergic reaction
what are the risk factors for asthma?
personal history of atopy family history of asthma or atopy obesity inner-city environment premature birth socio-economic deprivation
what are precipitating factors for asthma?
occupational sensitizers such as wood dust, bleaches and dyes, isocyanates and latex can cause occupational asthma
- cold air and exercise
- atmospheric pollution and irritant dusts
- diet - more fruit and veg is protective
- drugs such as NSAIDs particularly aspirin which can trigger attacks, also beta-blockers have a direct parasympathetic innervation that results in bronchoconstriction which results in airflow limitation and potential attack - do not give beta blockers to someone who has asthma
- allergen induced asthma
what is the clinical presentation on asthma?
intermittent dyspnoea wheeze cough sputum symptoms worse at night episodic shortness of breath
during an asthma attack what would you see?
reduced chest expansion
prolonged expiratory polyphonic time
bilateral expiratory polyphonic wheeze
tachypnoea
what are the symptoms of uncontrolled asthma?
PEFR less than 50%
respiratory rate less than 25
pulse less than 110
normal speech
what are the symptoms of a severe asthma attack?
inability to complete sentences
pulse greater than 110 bpm
resp rate greater than 25/min
what are the symptoms of a life threatening asthma attack?
silent chest confusion and exhaustion cyanosis bradycardia PEFR less than 33%
how do you manage an acute asthma attack?
O SHIT ME
O - ocygen therapy to maintain sats at 94-98%
S - salbutamol - back to back nebulisers 5mg per hour
H - hydrocortisone or prednisolone
I - ipratropium nebulised - if there is poor response or if life threatening
T - theophylline - Aminophylline if unresponsive
M - magnesium sulphate
E- escalate care
ABG and repeat within 2 hours if severe attack or if the patient is detonating
CXR - if fails to respond to treatment
check PEFR within 15-30 mins/regularly
oximetry to ensure Sao2 is greater than 93%
what are some DD for asthma?
pulmonary oedema, COPD, large airway obstruction cause by foreign body/tumour, pneumothorax, bronchiectasis
what are the questions you would ask to try and help diagnose uncontrolled asthma?
RCP3 questions - recent nocturnal waking usual asthma? - usual asthma symptoms in the day? - is it interfering with you ADLs?
what are the methods you can use to see if asthma is controlled?
RCP3 questions
asthma control test (25=well controlled, 20-24 = on target, less than 20 = off target)
lung function tests
exercise tests
trial of corticosteroids
exhaled nitric oxide - means of eosinophilic inflammation and an index of corticosteroid response - used to assess the efficacy of corticosteroids
blood and sputum tests
skin prick tests to help identify allergic trigger factors
how can you distinguish between asthma and COPD?
COPD is a later disease and more dominantly smokers
more of a relentless progressive shortness of breath with wheeze as part of the symptom complex
less day-day variation
winter symptoms and sputum production in COPD overlap can occur
how is asthma treated?
first of all control extrinsic factors when specific allergen triggers are identified
- mild SABA - 2 puffs when required
- SABA + ICS (low dose)
- SABA + LABA or tiotropium + ICS (low or medium dose)
- SABA + LABA or tiotropium + ICS (medium)
- SABA + LABA or tiotropium + ICS (high dose) plus immunomodulator (omalizumab)
- oral corticosteroid + ICS (high dose) + LABA or tiotropium + immunomodulator + SABA
what are some examples of SABA?
salbutamol
Terbutaline
what are some examples of LABA?
salmeterol
formoterol
what is ipratropium and tiotropium?
muscarinic antagonists
what are some examples of inhaled corticosteroids that can be used?
beclomethasone, prednisolone, budesonide
what is COPD?
a disease state characterised by airflow limitation
NOT fully reversible
usually progressive and associated with abnormal inflammatory response of the lungs to noxious particles or gases
what is COPD associated with the envelopment of?
chronic bronchitis - cough with sputum for 3 months for 2 or more years
Emphysema - histologically its enlarged airspaces distal to terminal brocnhioles with destruction of alveolar walls
what are the causes of COPD?
- cigarette smoking is the major cause of COPD
- chronic exposures to: pollutants at work, outdoor air pollution, inhalation of smoke from biomass fuels used in heating and cooking in poorly ventilated areas
- alpha-1 antitrypsin deficiency causes early onset COPD
what is alpha-1 antitrypsin deficiency?
causes early onset COPD (due to proteolytic lung damage)
a rare cause of cirrhosis (due to an accumulation of the abnormal protein in the liver mutations in the alpha-1 antitrypsin gene on chromosome 14 lead to reduced hepatic production of alpha 1 antitrypsin which normally inhibits proteolytic enzyme - neutrophil elastase
what is chronic bronchitis?
airway narrowing - hypertrophy and hyperplasia of mucus secreting glands of the bronchial tree, bronchial wall inflammation and mucosal oedema
inflammation is followed by scarring and thickening of the walls which narrows the small airways
chronic bronchitis = blue bloaters
what is emphysema?
dilatation and destruction of the lung tissue distal to the terminal bronchioles
results in loss of elastic recoil, which normally keeps the airways open during expiration
leads to expiratory airflow limitation and air trapping
patients with emphysema are referred to as the pink puffers
what do patients with COPD get V?Q (ventilation/perfusion) mismatch?
mismatch is partly due to damage and mucus
plugging of smaller airways from the chronic inflammation and partly due
to rapid closure of smaller airways in expiration owing to the loss of
elastic support
what does V/Q mismatch cause?
- this mismatch leads to a fall in PaO2 and increased
work or respiration - CO2 excretion is less affected and many patients will have normal PaCO2 due to increasing alveolar ventilation in an attempt to correct their hypoxia (pink puffers)
- other patients fail to maintain their resp efforst and their PaCO2 levels increase - in the long term this can cause these patients to become insensitive to CO2 and come depend of hypoxaemia to drive ventilation - such patients appear less breathless and because of renal hypoxia they start to retain fluid and increase erythrocyte production which can lead to polycythaemia - typical appearance of a blue bloater
what is the presentation of COPD ?
Characteristic symptoms are productive cough with white or clear
sputum, wheeze and breathlessness, usually following many years of a
smokers cough
cold seem to settle on the chest and frequent infective exacerbations occur with purulent sputum
symptoms can be worsened by cold or damp weather and atmospheric pollution
what are some systemic effects of COPD?
hypertension osteoporosis depression weight loss reduced muscle mass with general weakness
what would you see on examination of someone with COPD?
breathless at rest with prolonged expiration, chest expansion is poor and the lungs are hyper inflated
pursed lips
DD fir COPD?
asthma CHF bronchiectasis allergic fibrosing alveolitis pneumoconiosis asbestos
how is COPD diagnosed?
- based on history of breathlessness and sputum production in a chronic smoker
lung function tests show progressive airflow limitation with increasing severity and breathlessness - post bronchodilator FEV1/FEV of <70% on spirometry
CXR - may be normal or may show evidence of hyperinflated lungs
High res CT
ABG
BMI
how is COPD staged?
breathlessness
• FEV less than 80% predicted value
• FEV1/FVC less than 0.7 - airway obstruction
• Stages:
- Stage 1 - FEV1 less than 80% of predicted value
- Stage 2 - FEV1 50-79%
- Stage 3 - FEV1 30-49%
- Stage 4 - FEV1 less than 30% of predicted value
• Multiple peak flow measurements may be necessary to exclude
asthma
how is COPD treated?
smoking cessation is the most useful - even in advanced disease it may slow down the rate of deterioration
encourage exercise
influenza and pneumococcal vaccination, pulmonary rehab
PRN SABA - salbutamol or short acting antimuscarinic - ipratropium
if severe combine LABA or combo of B2 agonist and corticosteroid e.g. Symbicort (budesonide plus formoterol)
anti mucolytic agents can help by reducing sputum viscosity
diuretic can be used to treat oedema
good diet
reduce weight and obesity
what is normal blood pressure?
less than 140/90 mmHg
what are the stages of hypertension?
stage 1 - more than or equal t0 140/90 clinic BP, or ambulatory BP (ABPM)/home blood pressure monitoring (HBPM) greater than or equal to 135/85
stage 2: more than or equal to 160/100 clinic BP, or ABPM or HBPM great or equal to 150/95
Severe hypertension: systolic BP greater than or equal to 180mmHg and/or diastolic BP greater than ore equal to 110mmHg
what are some endocrine causes of hypertension?
Cushing’s syndrome
Conn’s syndrome
Phaemochromocytoma
why does Cushing’s disease cause hypertension?
Hypersecretion of corticosteroids (which enhance adrenalines
resulting in a vasoconstrictive effect) is associated with
systemic hypertension
why does Conn’s syndrome cause hypertension ?
Adrenal tumour that secretes ALDOSTERONE (resulting in Na+
retention and thus water retention thereby increasing blood
volume and pressure) can cause hypertension
what drugs are associated with hypertension?
corticosteroid cyclosporine erythropoietin some types of the contraceptive pill alcohol amphetamines ecstasy cocaine
what are some risk factors for hypertension ?
age race - more common in blacks fam history overweigh and obese little exercise smoking too much salt alcohol diabetes stress
what are the vascular changes in hypertension?
hypertension accelerates atherosclerosis
it also causes thickening if the media of muscular arteries
it is the smaller arteries and arterioles that are especially affected in hypertension
the resulting endothelial cell dysfunction is associated with impaired nitric oxide-mediated vasodilatation and enhance secretion of vasoconstrictors including endothelin’s and prostaglandins
what are the complications of HTN?
vascular damage
heart: major risk of IHD
nervous system: intracerebral haemorrhage
Kidneys: renal disease, kidney size is often reduced
what tests would you perform to diagnose complications of HTN?
look for end-organ damage (LV hypertrophy, retinopathy, proteinuria) - it indicates the severity and duration of hypertension and associated with poor prognosis
Urinalysis - protein, albumin: creatine ratio and haematuria
Bloods - serum creatinine, eGFR, glucose
fundoscopy/ophthalmoscopy - look for retinal haemorrhage or papilloedema
ECG
ECHO
24hr ambulatory BP monitoring
what lifestyle modifications would be made for hypertension?
change diet regular physical exercise reduce alcohol intake reduce salt intake lose weight stop smoking
what is step one and step two management for <55 years (not of black African or afro-Caribbean) with hypertension?
step 1: angiotensin converting enzyme inhibitor (Ramipril or Enalapril) or angiotensin 2 receptor blocker (Candesartan or Losartan)
Step 2 : CCB (amlodipine) or thiazide diuretic (if CCB not tolerated)(Bendroflumethiazide)
what is step one and two for patients over 55 or if they are black African or afro-Caribbean origin with hypertension?
step 1: CCB (nifedipine or amlodipine)
Step 2: ACE inhibitor (Ramipril) or angiotensin 2 receptor blocker (candesartan) or thiazide diuretic (Bendroflumethiazide)
what is the third and fourth and fifth step of hypertension management?
ACE inhibitor or ARB + CCB + thiazide like diuretic
if this doesn’t work they are considered to have resistant hypertension
STEP 4: add a 4th drug - spironolactone
step 5: consider a Beta-blocker - bisoprolol
what is type 1 diabetes?
disease of insulin deficiency usually caused by autoimmune destruction of beta-cells of the pancreas
what is the cause of T1DM?
autoimmune
idiopathic
genetic susceptibility
RF for T1DM?
- Family history - HLA-DR3-DQ2 or HLA-DR4-DQ8 in > 90%
- Associated with other autoimmune disease:
• Autoimmune thyroid
• Coeliac disease
• Addison’s disease (excess cortisol)
• Pernicious anaemia
what is T1DM characterised by?
polyuria
polydipsia
lethargy
weight loss
ketosis
what is T2DM?
combination of insulin resistance and less severe insulin deficiency
RF for T2DM?
fam history
increasing age
obesity and poor exercise - can trigger DMT2 in genetically susceptible individuals
ethnicity - middle eastern, south east Asian and western pacific
what is the normal presentation of T1DM?
usually young people - often present with a 2-6 week history and report the classic triad of symptoms:
- polyuria and nocturia
- polydipsia
- weight loss
what is the tests for diagnosing DM?
what other tests would you perform?
random plasma glucose >11.1mmol/L
fasting plasma glucose >7mmol/L
* if symptomatic - one test is diagnostic, if asymptomatic 2 tests = diagnostic
for borderline cases - oral glucose tolerance test
HbA1c
screen for urine microalbuminuria to assess for kidney disease
FBC, U&Es, liver biochemistry, fasting blood sample for cholesterol and triglycerides
blood pH
what conditions might diabetes be secondary to?
pancreatitis trauma/pancreatectomy neoplasia of pancreas acromegaly Cushing syndrome addisons Drugs: thiazide diuretics, BB, immunosupressives, thyroid hormone
how do you manage diabetes other than medications?
educate patient on disease and risks
maintain lean weight
stop smoking
take care of feet
encourage regular physical activity and reduction in bodyweight in the obese
good glycaemic control with good diet (low in sugar, high in starchy carbs with low glycaemic index, high in fibre, low in fat
how is T1DM managed?
insulin is always indicated in a patient who has been in ketoacidosis and is usually required in lean patients who present under the age of 40
for good control it is vital to educate to self-adjust dose
- SC recombinant human insulin into abdo, thighs or upper arms
- inform DVLA if on insulin
- change injection sites to avoid fatty lumps
- finger prick before meal to inform about long-acting insulin
- finger prick after meal to inform about short acting insulin doses
what are the different types of insulin?
short-acting (soluble) insulins: start working within 30-60 minutes and last for 4-6 hours - given 15-30 mins before meals
Short-acting insulin analogues - human insulin analogies - insulin aspart, insulin lispro, insulin glulisisne)have a fast onset and a short duration than the soluble insulin but overall do not improve diabetic control
long acting insulins - insulin premixed with retarding agents - can be intermediate (12-24 hours) or long acting (>24 hours)
what are the complications of insulin treatment?
hypoglycaemia
injection site lipohyertrophy
insulin resistance
weight gain
what are the first line treatments for type 2 diabetes?
lifestyle and dietary changes dietary factors - low sugar high in starch nutrient load should be spread throughout the day blood pressure control - Ramipril cholesterol control - statins exercise weight loss orlistat in obesity
second line management for T2DM?
used in association with diet and lifestyle changes
initially give oral metformin
if not controlled add a sulfonylurea - oral gliclazide
if still not controlled add insulin or a glitazone
what are the positive factors of metformin?
- Reduces rate of gluconeogenesis in the liver
- Increases cells sensitivity to insulin
- Helps with weight issues
- Reduces CVS risk in diabetes
what are the side effects of and contraindications of metformin?
- S/E; anorexia, diarrhoea, nausea, abdominal pain, NOT
HYPOGLYCAEMIA - Contraindicated in heart failure, liver disease or renal disease,
since can induce lactic acidosis
what are sulfonylureas?
how do they work
what are the side effects?
which is the safest on in the elderly?
- Promotes insulin secretion
- These are ineffective in patients without a functional beta-cell
mass - Avoided in pregnancy
- Effect wears off as beta-cell mass declines
- S/E; hypoglycaemia (must monitor glucose), promote weight
gain (so best avoided in the overweight!!) - Should be used with care in people with liver disease and those
with renal impairment should use sulfonylurea’s primarily
excreted by the liver - The safest drug in the very elderly is ORAL TOLBUTAMIDE
since it has a very short duration of action
what is chronic congestive heart failure?
Develops from any structural or functional cardiac disorder that impairs the ability
of the heart to function as a pump and maintain sufficient cardiac output to meet
the demands of the body
• Occurs when output of the heart is inadequate to meet the needs of the body
what are the two types of CCF?
high out put CCF - heart is working at a normal rate but the needs of the body are increased beyond that which the heart can supple
low out put CCF - reduced heart function
what are some causes for high output CCF?
hyperthyroidism, anaemia, Paget’s disease, AV malformation
what are some causes of low output CCF?
• Increased pre-load e.g. mitral regurgitation and fluid overload
• Pump failure e.g. IHD, Cardiomyopathy
• Reduced expansion of heart and restricted filling e.g. restrictive
cardiomyopathy, constrictive pericarditis, tamponade
• Arrhythmia - AF is most common
• Chronic excessive afterload e.g. HTN or aortic stenosis
what is cardiac failure, systolic failure and diastolic failure?
- Cardiac failure = CO is inadequate for the body’s requirements
- Systolic failure = inability of the ventricle to contract normally
- Diastolic failure = inability of the ventricle to relax and fill normally
how does left ventricle failure present?
• Dyspnoea, poor exercise tolerance, fatigue, orthopnoea (shortness
of breath when lying flat), paroxysmal nocturnal dyspnoea (PND),
nocturnal cough, wheeze, nocturia, cold peripheries, weight loss,
muscle wasting
how does right ventricle failure present?
peripheral oedema ascites nausea anorexia facial engorgement pulsation in neck and face epistaxis
what are some general features of heart failure?
raised RR +/- cyanosis
increased pulse rate, JVP
displaced apex beat
right ventricular heave
DD of CCF?
obesity
respiratory disease
drug-induced ankle swelling e.g. Ca2+ blockers or fluid retention e.g. NSAIDs
what criteria/classifications are used for heart failure diagnosed?
Framingham criteria
New Your Heart associated classification of heart failure
what tests would you perform for heart failure?
CXR - will show cardiac enlargement and features of LVF
ECG - may show evidence of underlying causes e.g. arrhythmias, ischaemia or LV hypertrophy
FBC - look for anaemia
TFTs - rule out thyroid pathology
brain natriuretic peptide - elevated in CCF
N terminal fragment realised from pro-BNP - also elevated
ECHO should be performed in ALL patients with suspected CCF
how do you treat CCF?
education, physical activity, stop smoking, lose weight
Diuretics - to relieve congestive symptoms/fluid retention in all types of failure - first of all loop diuretic (furosemide) then add thiazide diuretic (indapamide)
First line treatments for LV systolic function - ACE inhibitor (Ramipril) or ARB if ACE not tolerated (candesartan) and a BB (bisoprolol)
If still symptomatic ass vasodilators e.g. isosorbide mononitrate
what are some notifiable diseases?
Acute encephalitis Acute infectious hepatitis Acute meningitis Acute poliomyelitis Anthrax Botulism Brucellosis Cholera Diphtheria Enteric fever (typhoid or paratyphoid fever) Food poisoning Haemolytic uraemic syndrome (HUS) Infectious bloody diarrhoea Invasive group A streptococcal disease Legionnaires’ disease Leprosy Malaria Measles Meningococcal septicaemia Mumps Plague Rabies Rubella Severe Acute Respiratory Syndrome (SARS) Scarlet fever Smallpox Tetanus Tuberculosis Typhus Viral haemorrhagic fever (VHF) Whooping cough Yellow fever
at 8 weeks what vaccinations should a child be given
- 6 in 1 vaccine (Diptheria, Tetanus, Pertussis, Hep B, Poliomyelitis and Haemophilus Influenza type B
(HiB)) - 1st dose - Meningococcal group B - 1st dose
- Pneumococcal polysaccharide conjugate vaccine (PCV) - 1st dose
- Rotavirus - 1st dose
at 12 weeks what vaccinations should children be given ?
6 in 1 vaccine (Diptheria, Tetanus, Pertussis, Hep B, Poliomyelitis and Haemophilus Influenza type B)
- 2nd dose
Rotavirus - 2nd dose
at 16 weeks what vaccinations should an infant be given?
6 in 1 vaccine (Diptheria, Tetanus, Pertussis, Hep B, Poliomyelitis and Haemophilus Influenza type B)
- 3rd dose
Meningococcal group B - 2nd dose
Pneumococcal polysaccharide conjugate vaccine (PCV) - 2nd dose
at 1 year what vaccinations should children be given?
Measles, mumps & rubella (MMR) - 1st dose
Meningococcal group B - Booster
Pneumococcal polysaccharide conjugate vaccine (PCV) - Booster
Haemophilus Influenzae Type B with Meningococcal group C (Hib/Men C) - Booster
at 2-10 years what vaccine should children be given?
influenza vaccine
at 3-4 years what vaccinations should children be given?
4 in 1 pre-school booster - diphtheria, pertussis, poliomyelitis and tetanus
at 11-14 years what vaccination should children be given?
HPV
at 13-18 what vaccinations should children be given?
3-in-1 teenage booster (tetanus, diptheria, poliomyelitis)
Meningococcal A with C & W & Y
BB - action and s/e
action - makes heart pump slower but with more force = less stressed heart
s/e = light headed, GI upset
Statins - action and S/E
action = Lowers the cholesterol in the blood, helping prevent build up in the arteries, s/e = leg pain and GI upset
clopidogrel - action and S/E
action = blood thinner - antiplatelet s/e = GI upset, bleeding
