GP Flashcards
define domestic abuse
any incidence or pattern of incidents of controlling, coercive, threatening behaviour, violence or abuse between those aged 16+ who are, or have been, intimate partners or family members, regardless of gender or sexuality.
can encompass, but not limited to:
psychological, physical, sexual, financial, emotional.
list the different types of domestic abuse
psychological physical sexual financial emotional
- not limited to these, can be more than one type
give some ways domestic abuse impacts on health
- traumatic injuries following an assault e.g. fractures, miscarriage
- somatic problems or chronic illness consequent on living with abuse e.g. headaches, GI problems, chronic pain
- psychological or psychosocial problems secondary to abuse e.g. PTSD, attempted suicide, substance misuse, depression etc
in triaging a woman in A&E with injuries, what are some flags that could suggest domestic violence?
'reported as unwitnessed by anyone else' repeat attendance delay in seeking help multiple minor injuries not requiring treatment presenting 7pm-7am
what must you always consider if you identify a woman as being a victim of domestic abuse?
are there any children in the household - child safeguarding is utmost priority!!
what is the role of doctors in responding to domestic/sexual abuse?
- display helpline posters and contact cards, helps create an environment where people feel able to talk
- focus on patient’s safety (and safety of children)
- acknowledge and be clear that behaviour is not ok
- give information and refer on where appropriate
- be part of their process of recognising and escaping abuse
- be open to working with other agencies
what are the components of Maslow’s hierarchy of needs, from base to top?
physiological - breathing, food, water, sex, sleep etc
safety - security of body, of employment, of resources, of the family, of health, of property
love/belonging - friendship, family, sexual intimacy
esteem - self-esteem, confidence, achievement, respect of others
self-actualization - morality, creativity, spontaneity, problem solving, lack of prejudice, acceptance of facts
what is the main stated cause of homelessness?
“relationship breakdown”
caused by - mental illness, domestic abuse, disputes with parents, bereavement
list some health problems faced by homeless adults
- IDs incl TB and hepatitis
- poor condition of feet and teeth
- respiratory problems
- injuries following violence/rape
- sexual health, smears, contraception
- serious mental illnesses
- poor nutrition
- addictions/substance misuse
what are some of the barriers to healthcare faced by homeless people?
- difficulties with access - opening times, getting appointments, perceived discrimination
- lack of integration between primary care services and other agencies (housing, social sector, criminal justice system, third sector)
- other things on their mind - focussed on pure survival, not getting a smear
- don’t know where to find help
what are some barriers to healthcare faced by Gypsies and Travellers?
- reluctance of GPs to register these groups, and to visit sites
- poor reading and writing skills (many are illiterate)
- communication difficulties
- too few permanent and transient sites
- mistrust of professionals
- lack of choice
define refugee
an adult/child that ‘owing to a well founded fear of being persecuted for reasons of race, religion, nationality, social group/political opinion is outside the country of his nationality, and is unable, or owing to such fear, unwilling to avail himself of the protection of that country’
define asylum seeker
someone who has submitted an application to be recognised as a refugee and is waiting for their claim to be decided by the home office
define internally misplaced person
someone who’s had to leave their home for similar reasons to refugees/asylum seekers, but has not crossed international borders.
what is indefinite leave to remain?
when a person is granted full refugee status and given permanent residence in the UK.
they have all the rights of a UK citizen.
eligible for family reunion - one spouse and any child of that marriage under age of 18
what are asylum seekers entitled to?
money (£35 per week)
housing - no choice dispersal
NHS care
if under 18, have a social services key worker and able to attend school
NOT allowed to - work or claim any other benefits.
FAILED asylum seekers - not entitled to money/housing/NHS care
what are some barriers to accessing healthcare faced by asylum seekers?
- lack of knowledge of where to get help
- lack of understanding of how NHS works
- language/culture/communication
- hyper-mobility
- not homogenous group
- health not a priority
what physical health problems might an asylum seeker/refugee face?
- common illnesses
- illness specific to country of origin
- injuries from war/travelling
- no prev health surveillance/screening/imms
- malnutrition
- torture, sexual abuse
- infestations
- communicable disease / blood borne diseases
- untreated chronic disease / congenital problems
what mental health problems might an asylum seeker/refugee face?
PTSD depression sleep disturbance psychosis self harm
also, any mental health conditions anybody else could get!
what are some flags that might make you consider loneliness in a patient?
- body language, appearance, talkative, clinging
- denial, boredom
- living alone
- male 50+
- bereavement, recent transition
- mobility
- sensory impairment
- close family nearby?
- quality not quantity of social contact
define social exclusion
dynamic process of being shut out, fully or partially, from any of the social, economic, political or cultural systems which determine the social integration of a person in society
what are the 5 domains of social exclusion?
material resources civic activities basic services neighbourhood social relationships
give some causes of social exclusion
poor health, sensory impairment, poverty, housing issues, fear of crime, transport issues, discrimination, poor coordination, fragility of networks
define disability
relates to anyone who has a physical, sensory or mental impairment which seriously affects their daily activities
what is age related macular degeneration?
central part of retina that’s used for detailed work is called the macular - macular disease is the collective term for conditions causing damage
no cure but can sometimes be slowed or halted in some cases with medical treatment, drug therapy or laser treatment.
most common eye condition in the UK.
what is retinitis pigmentosa?
inherited diseases of retina - leads to gradual reduction in vision, initially night and peripheral vision then difficulties in reading and colour vision
what is glaucoma?
condition affecting optic nerve.
once affected, can’t be reverse.
often the nerve is damaged before vision loss is noticed
what is diabetic retinopathy?
blood supply to retina is impaired.
if caught early can be treated by laser - stops progression but doesn’t restore loss.
what are cataracts?
very common - lens changes with ageing, becoming less transparent - turns misty or cloudy.
how do you calculate a unit of alcohol?
% ABV * ml / 1000
give some social/psychological risk factors for problem drinking
- drinking within the family
- childhood problem behaviour relating to impulse control
- early use of alcohol, nicotine and drugs
- poor coping responses to life events
- depression as a cause (not a result!) of problem drinking
what are the most common causes of death related to alcohol?
- accidents and violence
- malignancies
- cerebrovascular disease
- coronary heart disease
what is foetal alcohol syndrome?
occurs if persistent drinking throughout pregnancy
small underweight babies, slack muscle tone
mental retardation, behavioural and speech problems. characteristic facial appearance.
cardiac, renal and ocular abnormalities.
list some screening tools for alcohol problems
AUDIT
CAGE
also - PAT, FAST, abbreviated AUDIT
DON’T use blood tests
what is the role of brief structured advice in managing potential alcohol abuse in the GP setting?
well-researched technique - use 5-15 mins to cover potential harm caused, reasons for changing incl health and well-being benefits, cover obstacles to change, strategies to combat and goals.
briefly explain the NYHA staging of heart failure
Stage I - No limitation on ordinary physical activity
Stage II - Normal at rest. Ordinary physical activity causes breathlessness.
Stage III - Normal at rest. Less-than-ordinary activity causes breathlessness.
Stage IV - Symptoms at rest.
what is ‘heart failure’?
when output of the heart is inadequate to meet the needs of the body - end stage of all cardiac diseases
give some high output causes of chronic heart failure (and explain what that means!)
high output heart failure occurs when heart is working at normal/increased rate, but needs of the body are increased.
causes - hyperthyroidism, anaemia, Paget’s disease, AV malformation
what are some low output causes of heart failure?
low output = due to reduced heart function, due to either increased preload, pump failure or chronically excessive afterload.
causes - mitral regurg, fluid overload, ischaemic heart disease, cardiomyopathy, MI, AF, aortic stenosis, restrictive cardiomyopathy, constrictive pericarditis, tamponade, chronic HTN
drug causes - beta blockers (if making them really bradycardic), verapamil, diltiazem
what investigations would you order in suspected heart failure?
BNP (serum B type natriuretic peptides) and NTproBNP (N-terminal-pro-BNP) - if raised, refer to cardiology for review.
ECG (if ECG and BNP normal, NICE says it’s probs not heart failure)
might do an echo - can identify cause.
also - CXR, lung function tests if trying to exclude respiratory cause, bloods (FBC, U&E, creatinine, eGFR, TFTs, BM/HbA1c) - these are to test for exacerbating factors and things you can treat!
what are the Farmingham criteria for congestive cardiac failure?
diagnosis of CCF needs 2 major or 1 major + 2 minor criteria:
MAJOR - paroxysmal nocturnal dyspnoea, neck vein distension, crepitations, acute pulmonary oedema, S3 gallop, hepatojugular reflux, cardiomegaly, increased central venous pressure, weight loss >4.5kg in 5 days in response to treatment
MINOR - bilateral ankle oedema, nocturnal cough, dyspnoea on ordinary exertion, tachycardia >120, pleural effusion, hepatomegaly, reduced vital capacity
describe the non-drug aspects of managing a patient with chronic heart failure in GP land
6 monthly review - check functional capacity, fluid status, screen for depression, medication review etc
educate - about disease and prognosis
lifestyle measures - stop smoking, low salt diet, weight loss, healthy diet, regular exercise. discuss needs for benefits, disabled badge etc.
give annual flu and pneumococcal vaccines.
describe the use of diuretics in management of a patient with chronic heart failure
diuretics - used to relieve congestion/fluid retention - use a loop diuretic (e.g. furosemide 20-40mg or bumetanide 1-2mg). add thiazide if problems with oedema/HTN continue.
monitor for hypokalaemia - treat with amiloride or K+ supplements if needed.
list some classes of drug used in management of heart failure, and name the drugs commonly used
diuretics - usually loop (furosemide), might add thiazide
ACE inhibitors - ramipril, start low and titrate up
beta-blockers - bisoprolol - ‘start low, go slow’
might substitute an ARB in if the ACEi gives a cough (e.g. candesartan)
how does management of heart failure differ if the patient has a preserve ejection fraction?
this is less common - basically can’t do anything beyond give diuretics and treat co-morbidities
when might you consider referring a heart failure patient to cardiology?
- making initial diagnosis (should have a routine referral)
- unable to manage at home
- severe
- not controlled by first line medication
- angina, AF, other symptomatic arrhythmia
- heart failure due to valve disease
- comorbidity that might impact heart failure e.g. COPD, renal failure, anaemia, thyroid disease, PVD, urinary frequency, gout
- woman with heart failure planning pregnancy
give some examples of drugs that might be used by a cardiologist in the management of heart failure
aldosterone antagonists e.g. spironolactone
hydralazine + nitrate in combo
ARB - in combo with ACEi and beta blocker
digoxin - anti-arrhythmic and positive inotrope
amiodarone - used for arrhytmias
what is the prognosis of chronic heart failure?
progressive deterioration to death, high BNP is poor prognostic factor
50% dead at 5 years - this is improving though
what symptoms are seen if a patient has left ventricular heart failure?
dyspnoea, poor exercise tolerance, fatigue, orthopnoea, PND, nocturnal cough, wheeze, nocturia, cold peripheries, weight loss
what symptoms are seen if a patient has right ventricular heart failure? what causes right ventricular heart failure?
peripheral oedema, ascites, nausea, anorexia, facial engorgement.
causes - left ventricular failure, pulmonary stenosis, lung disease
what signs would you expect to see on a CXR of a patient with chronic heart failure?
ABCDE! Alveolar oedema Kerley B lines Cardiomegaly Dilated upper lobe vessels pleaural Effusion
how does furosemide work? side effects?
laymans terms = works on kidneys to help you get rid of excess fluid, which can make symptoms better
acts on ascending limb of loop of Henle to inhibit the Na/K/2Cl co transporter
SEs - hypokalaemia, renal impairment.
monitor U&Es!
how do ACE inhibitors work in heart failure? side effects?
angiotensin-converting enzyme inhibitors - ramipril, lisinopril.
first line for chronic heart failure - improves symptoms and prognosis
laymans - reduces the strain on your heart by lowering your blood pressure, makes it easier for heart to work.
block action of ACE, preventing conversion of angiotensin I to angiotensin II - reduces peripheral vascular resistance, so lowers BP (and afterload!)
SEs - hypotension (esp first dose), dry cough (due to excess bradykinin), hyperkalaemia, renal impairment
be aware of first-dose hypotension, especially if starting on loop diuretic at the same time!
how do ACE inhibitors work in hypertension? side effects?
angiotensin-converting enzyme inhibitors - ramipril, lisinopril.
first line if <55yrs and not afro-carribbean
laymans - improves blood pressure by encouraging veins and arteries around your body to relax a bit, reduces strain on your heart.
block action of ACE, preventing conversion of angiotensin I to angiotensin II - reduces peripheral vascular resistance, so lowers BP.
SEs - hypotension (esp first dose), dry cough (due to excess bradykinin), hyperkalaemia, renal impairment
be aware of first-dose hypotension, especially if starting on loop diuretic at the same time!
how do beta blockers work in heart failure? side effects?
e.g. bisoprolol, atenolol
first line option - improves prognosis
via beta1-adrenoreceptors (in heart, beta2 ones are in vessels and airways) these drugs reduce force of contraction and speed of conduction in heart - ‘protects’ heart from effects of chronic sympathetic stimulation.
start low, go slow - might initially impair cardiac function, so don’t just whack the dose straight up - titrate up every 2+ weeks.
SEs - fatigue, cold extremities, headache, GI upset, erectile dysfunction.
CONTRA-INDICATED IN ASTHMA
how does spironolactone work in heart failure? what kind of drug is it? side effects?
used if at least moderate severity, or heart failure arising within 1 month of an MI, generally as addition to beta blocker and ACEi/ARB.
it’s an aldosterone antagonist.
inhibits action of aldosterone by competitively binding to the aldosterone receptor - increases sodium and water excretion, and potassium retention (risk of hyperkalaemia when combined with ACEi).
SEs - hyperkalaemia, gynaecomastia, erectile dysfunction
define polypharmacy. when does it become “inappropriate polypharmacy”?
5+ medications.
inappropriate as soon as 1 drug prescribed that shouldn’t be there:
- no evidence based indication, expired indication, dose too high
- medicines that aren’t working
- combination of, or any one, drug(s) causing adverse reaction
patient doesn’t want/isn’t able to take as intended
list some potential consequences of polypharmacy
increasing costs of healthcare increasing adverse drug events drug interactions medicines non-adhesive cognitive impairment, functional impairment, falls, urinary incontinence, nutrition
what community support is available for patients with heart failure?
cardiac rehab (psuchological support, education, structured exercise programme, RF modification)
regular reviews - heart failure nurses
support groups
list some causes of hypertension
unknown/'essential' (95%) renal disease endocrine - Cushing's, Conns, phaeochromocytoma, acromegaly, hyperparathyroidism Pregnancy Coarctation of the aorta
what is the treatment threshold for hypertension?
> 160/100 if otherwise healthy.
If >140/90 might treat if other risk factors/co-morbidities.
how is hypertension staged/classified?
stage 1 = clinic BP >140/90 and subsequent daytime average ABPM/HBPM >135/85
stage 2 = clinic BP >160/100, average ABPM/HBPM >150/95
severe = clinica systolic >180 or diastolic >110
what is the difference between ABPM and HBPM?
ABPM = ambulatory BP monitoring - continuous BP monitoring usually for 24 hours. HBPM = home BP monitoring - BP taken at home, not a continuous machine.
when would you initiate antihypertensive treatment, if patient has stage 1 hypertension?
if <80y age and 1+ of:
- target organ damage
- established CVD
- diabetes
- renal disease
- 10y CVD risk 20+% (Q risk)
when would you initiate antihypertensive treatment, if patient has stage 2 hypertension?
all stage 2 hypertension needs drug treatment!
sneaky trick qu
what are some non-drug measures that can be taken in managing hypternsion?
education - to make sure pts understand why it’s important they take drugs etc
lifestyle - smoking cessation, regular exercise, reduce alcohol intake, reduce dietary salt, increase fruit and veg intake, reduce caffeine, encourage relaxation/stree management
when would you prescribe a statin in a hypertensive patient?
if existing CVD - give statin regardless of baseline cholesterole/LDL levels
OR - for primary prevention in patients >40y with HTN and 10y CVD risk 20+%
describe the flowchart of antihypertensive drugs
first line = ACEi (or ARB) if <55yrs.
if >55 or african/caribbean = CCB (e.g. amlodipine)
Step 2 = ACEi + CCB
Step 3 = ACEi + CCB + thiazide-like diuretic
Step 4 = add spironolactone or higher dose thiazide-like diuretic. consider alpha/beta blocker.
what are the treatment targets used in hypertension management?
non-diabetic, no CKD = <140/80 diabetic, T2DM = <140/90 T1DM = <135/85 if any renal, foot, eye or cardiovascular complications in a diabetic patient - need tighter control, aim for <130/80 CKD = <130/80
what would be included in an annual hypertension review appointment?
- check BP (obvs) and look for signs of end-organ failure (incl urine dip for proteinuria)
- discuss symptoms and medication
- assess and treat other modifiable RFs
- reinforce lifestyle advice
what features in a hypertension patient would prompt you to consider referring to secondary care?
- accelerated hypertension
- renal impairment
- suspected secondary hypertension
- patients <40yr
- BP difficult to treat (got to step 4)
- pregnancy
what is the first line treatment for a white patient <55yrs old requiring antihypertensives?
ACE inhibitor - ramipril or lisinopril
how do ACE inhibitors work as antihypertensives? important side effects?
reduce risk of stroke, MI and death from CVD.
block action of ACE to prevent conversion of angiotensin I to angiotensin II. angiotensin II would normally be causing vasoconstriction, so blocking it means peripheral vascular resistance drops.
SEs - dry cough!! due to increased levels of bradykinin, which is usually inactivated by ACE. also first dose hypotension, hyperkalaemia, renal failure.
what is the first line treatment for a Afro-Carribbean patient, or a patient >55yrs old requiring antihypertensives?
calcium channel blockers e.g. amlodipine, nifedipine
how do CCBs work as antihypertensives? important side effects?
reduce calcium entry into vascular and cardiac cells - causing relaxation and vasodilation in arterial smooth muscle - lowers BP
amlodipine/nifedipine (dihydropyridines) are selective-ish for vessels, while diltiazem/verapamil (non-dihydropyradines) are more cardio-selective.
SEs (of dihydropyridines) = ankle swelling, flushing, headache and palpitations.
what is the second line / step 2 of antihypertensives?
ACEi / ARB + CCB
what is the third line / step 3 of antihypertensives?
ACEi + CCB + thiazide-like diuretic
what is the fourth line / step 4 of antihypertensives?
add spironolactone or higher dose thiazide-like diuretic. consider alpha/beta blocker.
probs refer to cardiology - this is resistant hypertension
how do thiazides/thiazide-like diuretics work as antihypertensives? important side effects?
e.g. bendroflumethiazide (no longer NICE recommended though), indapamide
inhibit Na/Cl co-transporter in distal convoluted tubule of nephron - prevents reabsorption of sodium and so more water excreted.
tell patient - offering you a ‘water tablet’ for your high BP, will also help with leg swelling if they have it - ask about difficulty getting to toilet on time!
SEs - erectile dysfunction, hyponatraemia, hypokalaemia
give an example of an alpha-blocker. what common chronic condition are they used fourth line?
doxazosin, tamsulosin, alfuzosin
used in resistant hypertension
(also first line option for BPH)
act on alpha1 adrenoceptors, which are mostly found in smooth muscle and urinary tract. so block those to induce relaxation, can drop BP.
SE - hypotension! esp. postural. dizziness and syncope.
what tip can you give patients when playing with their BP meds to avoid them having a fall?
if risk of first dose hypotension - take at bed time!
what drugs should a patient be offered as part of secondary prevention post-MI?
all patients should be offered the following drugs:
dual antiplatelet therapy (aspirin plus a second antiplatelet agent, typically clopidogrel)
ACE inhibitor
beta-blocker
statin
what lifestyle advice might be given for secondary prevention post-MI?
diet: advise a Mediterranean style diet, don’t recommend omega-3 supplements or eating oily fish
exercise: advise 20-30 mins a day until patients are ‘slightly breathless’ (cardiac rehab programmes helpful)
sexual activity may resume 4 weeks after an uncomplicated MI. Reassure patients that sex does not increase their likelihood of a further MI.
advise weight loss, reduce alcohol.
if a patient is diabetic, how does that change first line hypertension management, and why?
first line always an ACE inhibitor in diabetes, as they’re renoprotective
what non-drug, non-lifestyle advice treatment should be given to all post-MI patients as part of secondary prevention?
cardiac rehabilitation!
including an exercise programme of some kind
what are ‘red’ features on the traffic light system for assessing a febrile child?
- pale/mottled/ashen/blue skin, lips or tongue
- no response to social cues
- appearing ill to a healthcare professional
- doesn’t wake/stay awake if roused
- weak, high pitched or continuous cry
- grunting
- RR >60
- moderate/severe chest indrawing
- reduced skin turgor
- bulging fontanelle
what are the ‘amber’ features on the traffic light system for assessing a febrile child?
- pale skin/lips/tongue reported by carer
- not responding normally to social cues
- no smile
- wakes only with prolonged stimulation
- reduced activity
- nasal flaring
- dry mucous membranes
- poor feeding in infants
- reduced urine output
- rigors
what are the ‘green’ features on traffic light system for assessing a febrile child?
green if they have all of the below, and no amber/red signs:
- normal colour of skin/lips/tongue
- responds normally to social cues
- content/smiles
- stays awake/wakens quickly
- strong, normal cry/not crying
- normal skin and eyes
- moist mucous membranes
what are the steps involved in assessing a febrile child?
1) check your ABCDEs
2) assess against red/amber/green criteria
3) measure and record - HR (tachycardia = at least amber), RR, CRT (3+ is amber sign), temp (if < 3 months, 38+ C = red risk, if 3-9 months and 39+ C = at least amber)
4) assess for dehydration (prolonged CRT, abnormal skin turgor, abnormal resp pattern, weak pulse, cool extremities)
explain Gillick competence
a competent child is one who can understand the nature, purpose and possible competence of a proposed procedure + the consequences of not undergoing the procedure.
competent child (<16) can consent to treatment, but if they refuse they can be overruled by parents/court.
if not competent - only someone with parental responsibility can authorise/refuse
UNLESS it’s an emergency - can provide any medical treatment, limited to what is necessary for saving life
what 4 criteria need to be met for a patient to be deemed capacitous? what needs to be done before we can declare a patient incapacitated?
Patient needs to be able to:
1) understand the information
2) retain the information
3) weight it up
4) communicate decision back
You have a duty to take all reasonable steps to attempt to make them capacitous e.g. Braille/sign language, giving lots of time to explain and weigh it up etc.
if a patient is deemed incapacitated, what should you as the GP do before giving at treatment?
- take all factors affecting the decision into consideration
- involve the patient with decision making as far as possible
- take the patient’s previously known wishes into consideration
- consult everyone else involved in patient’s care/welfare (but remember, up to you to make best interests decision, not giving relative power to decide)
how would you manage an unwell child falling into the ‘red’ category?
refer for immediate/same day review by a paediatrician
how would you manage an unwell child falling into the ‘amber’ category?
treat cause if found
if no cause located, decide based on concerns of you and family:
- advise parent’s to ring up if any deterioration/failure to improve
- arrange to review within a few hours
- refer for paediatric review
SAFETY NET - advise on warning symptoms (amber/red) and how to access further healthcare e.g. walk in/OOOH
what are some common causes of pyrexia in a child <5yrs?
infection most common cause - consider UTI if no localizing symptoms/signs.
non-infective causes - malignancy (leukaemia, lymphoma), immunological (Still’s, Kawasaki’s disease), drugs, liver or renal disease
what symptoms/signs in a febrile <5yo would make you consider meningococcal disease?
non-blanching rash - particularly with 1+ of:
- ill-looking child
- lesions >2mm in diameter (purpura)
- CRT 3+
- neck stiffness
what symptoms/signs in a febrile <5yo would make you consider a pneumonia?
tachypnoea (>60 if 0-5m, >50 if 6-12m, >40 if >12m) crackles in chest nasal flaring chest indrawing cyanosis O2 sats <95%
what symptoms/signs in a febrile <5yo child would make you consider bacterial meningitis?
neck stiffness
bulging fontanelle
decreased level of consciousness
convulsive status epilepticus.
what symptoms/signs in a febrile <5yo child would make you consider herpes simplex encephalitis?
focal neurological signs
focal seizures
decreased level of consciousness
what symptoms/signs in a febrile <5yo child would make you consider UTI?
vomiting poor feeding lethargy irritability abdominal pain or tenderness urinary frequency or dysuria
what symptoms/signs in a febrile <5yo child would make you consider septic arthritis/osteomyelitis?
swelling of a limb or joint
not using an extremity
non-weight bearing
what symptoms/signs in a febrile <5yo child would make you consider Kawasaki disease?
bilateral conjunctival injection
change in mucous membranes in the upper respiratory tract (for example, injected pharynx, dry cracked lips or strawberry tongue)
change in the extremities (for example, oedema, erythema or desquamation)
polymorphous rash
cervical lymphadenopathy
what home care advice would you give a parent/carer who you’re sending home with a febrile child (no red/amber features)?
- to look out for red/amber signs, how to access healthcare if deteriorate e.g. OOOH
- temperature management - DON’T use tepid sponging/underdressing/over-wrapping - can use alternating paracetamol and ibuprofen if child distressed
- regular fluids (breastmilk if breast fed) - any fluid fine, watch for signs of dehydration - if present, encourage fluids, seek advice if worried (111, walk i centre)
- how to identify non-blanching rash
- check child during night
- keep off school - notify them of febrile illness
you’ve just seen a febrile 2 year old in your GP surgery - you assessed him against the traffic light criteria and he’s currently green. there’s no identifiable cause, but you aren’t particularly concerned at present, you give safety-netting and explain how to call OOOH or find the walk in if they need more help later this evening.
Mum asks - “when should I seek further advice?” (or something that sounds more like what a Mum would actually say)
- if child has a fit
- develops non-blanching rash
- if parent/carer feels child is getting worse
- if parent/carer becomes more worried
- fever lasts >5 days
- carer is distressed or worried they can’t look after their child
what signs of dehydration would you advise a parent caring for a febrile <5 yo looks out for?
sunken fontanelle (if young enough) dry mouth sunken eyes absence of tears poor overall appearance
how would you explain the importance of vaccination to a mother concerned about their safety and considering not allowing her child to be vaccinated? include an explanation of herd immunity
- immunisations have caused massive improvements in health since they were introduced
- their quick, safe and effective
- child’s body will then be able to fight off diseases better - there’s a greater risk of them being exposed to harm if they aren’t vaccinated (due to risk of catching, a being very ill from, the illness)
herd immunity = when a large portion of population have been vaccinated, everyone benefits from herd immmunity - important that all healthy children are vaccinated, as there’s a proportion who can’t due to immune problems - herd immunity helps to protect them. it also prevents large outbreaks, and can lead to virus eradication.
what common side effects of childhood immunisations would you inform the parents about?
- redness or swelling around the injection site
- might be irritable/unwell/slight fever for a couple of days (esp common with MenB - advised to give 3 doses paracetamol after to prevent/treat fever)
- after MMR - can get a rash about a week later, may also get fever/swollen glands
what % of population need to be vaccinated to achieve herd immunity?
WHO targets >95%, PHE targets >94% (we don’t normally meet that in England!)
higher unemployment and lower household income significantly associated with low uptake.
list the notifiable diseases
- acute encephalitis
- acute infectious hepatitis
- acute meningitis
- acute poliomyelitis
- anthrax
- botulism
- brucellosis
- cholera
- diphtheria
- enteric fever (typhoid/parathyroid)
- food poisoning
- haemolytic uraemic syndrome
- infectious bloody diarrhoea
- invasive group A strep disease and scarlet fever
- Leggionnarie’s
- leprosy
- malaria
- measles
- meningococcal septicaemia
- mumps
- plague
- rabies
- rubella
- SARS
- smallpox
- tetanus
- TB
- typhus
- viral haemorrhagic fever
- whooping cough
- yellow fever
who do you notify of a notifiable disease?
public health england / local health protection team
what immunisations are given at 8 weeks old?
diphtheria, tetanus, pertussis, polio, Hib, hep B - (DTaP/IPV/Hib/HepB)
pneumococcal conjugate vaccine (PCV)
MenB
Rotavirus
what immunisations are given at 12 weeks old?
diphtheria, tetanus, pertussis, polio, Hib, hepB
rotavirus
what immunisations are given at 16 weeks old?
Diphtheria, tetanus, pertussis, polio, Hib and HepB
pneumococcal (PCV)
MenB
what immunisations are given at one year old?
Hib and MenC
pneumococcal (PCV)
MMR
MenB
which children are eligible to receive the live attenuated flu vaccine?
children aged 2 and 3 on August 31st of that year children in reception class and school years 1, 2, 3, 4 and 5 piloting all primary school-aged children in some parts of country children aged 2 to 17 with long-term health conditions
delivered via nasal spray
what immunisations are given ‘pre-school’ (3y 4m old or soon after)?
diphtheria, tetanus, pertussis and polio
MMR (confirm first dose given)
what immunisations are given to girls age 12-13?
HPV types 6, 11, 16, 18 - protects against genital warts and cervical cancer.
two doses given 6-24 months apart.
what immunisations are given at 14 years old (school year 9)?
tetanus, diphtheria and polio (confirm MMR status)
MenACWY
how is the rotavirus vaccine delivered?
orally - drops
do you adjust the immunisation schedule for prematurity i.e. if gestational age 30 weeks when delivered, would you give first imms at 18 weeks (+10 weeks)?
NO - prematurity means the babies are at greater risk of infection, so important to give them as normal from 2 months after birth.
when is the DTap/IPV/Hib/HepB vaccine given? what does it protect against?
8 weeks
12 weeks
16 weeks
protects against diphtheria, tetanus, pertussis, polio, Hib, hepB
further DTap/IPV at 3y 4m.
also tetanus/diphtheria and polio given at 14yrs
when is the PCV (pneumococcal) vaccine given?
8 weeks
16 weeks
1 year old
When is the MenB vaccine given?
8 weeks
16 weeks
1 year
when is the rotavirus vaccine given?
8 weeks
12 weeks
when is a MenC vaccine given?
combined with Hib at one year.
as part of MenACWY for 14 year olds.
when is the MMR vaccine given?
one year
3y 4m
when is Hib vaccinated against?
8/12/16 weeks as part of DTap/IPV/Hib/HepB
one year as part of Hib/MenC
what are the most common conditions presenting with abnormal vaginal discharge in GP land?
bacterial vaginosis
candidiasis
also - normal changes!
consider STIs and other non-infective causes
describe normal vaginal discharge
white/clear, non-offensive, varies with menstrual cycle
give some symptoms that might indicate abnormal vaginal discharge
- heavier than usual
- thicker than usual
- pus-like discharge
- white and clumpy discharge
- greyish/greenish/yellowish/blood-tinged
- foul-smelling discharge
- discharge accompanied by bloodiness, itching, burning, rash, soreness
describe the vaginal discharge typically seen in BV
thin, profuse, fishy-smelling - no itch or soreness
describe the vaginal discharge typically seen in candidiasis
thick, curd-like/cottage cheese, white, non-offensive - associated with vulval itch and soreness
can cause mild dyspareunia and dysuria
describe the vaginal discharge typically seen in chlamydia
asymptomatic in 80%
but - can see copious purulent discharge
describe the vaginal discharge typically seen in trichomonas infection
can cause offensive yellow discharge, often profuse and frothy
associated w/ vulval itch, soreness, dysuria, abdo pain, superficial dyspareunia
describe the vaginal discharge typically seen in gonorrhoea
often asymptomatic
may present with purulent vaginal discharge
give some basic info on the rules re. chaperones in GP
patients need to be offered a chaperone for all intimate examinations.
should ideally be another medical professional - NOT a relative/friend (impartial observer).
record that chaperone present and who it was.
explain the ‘UPSSI’ acronym for remembering what to do re <16yo requesting contraception - Fraser criteria
U - understands advice and risks involved
P - parents - can you persuade/encourage them to speak to parents
S - suffer - without the contraception, their physical/mental health is likely to suffer
S - sex - still gonna have sex either way!
I - interests - it’s in the best interests of the patient to have the contraception without parental consent
if under 25 - offer chlamydia screening
what types of contraception are ideal for use in teenagers/under 16s?
CONDOMS - high failure rate but advise essential for preventing STIs!!!! remember, <25yrs = chlamydia screening
LARC - suggest use in combination with condom (for STI cover) - implant/IUCD/IUS - injection if needed, but raises osteoporosis risk (defs don’t use for >2 yrs)
COCP/POP - suitable method, but compliance issues - relatively high failure rate. POP only really used if LARCs not wanted and COCP CI’ed due to menstrual irregularity.
what investigations should be ordered before a GP puts a referral in to memory clinic?
bloods - FBC, U&Es, LFTs, renal function, TFTs, glucose, B12, folate, syphilis serology
ECG
BP
urine dip
will probs also get a CT head, can be organised by GP or memory clinic
what are the different types of dementia?
alzheimer’s
vascular
dementia with Lewy bodies
Frontotemporal dementia
mixed
Parkinson’s
briefly explain the pathophysiology of Alzheimers
progressive degeneration of cerebral cortex - cortical atrophy
neurones affected develop amyloid plaques, neurofibrillary tangles, and produce less ACh
“irreversible global, progressive impairment of brain function leading to reduce intellectual ability”
give some risk factors for Alzheimer’s
increasing age (obviously) Caucasian family hx female apoplipoprotein E4 variant (genetic) head injury the usual vascular RFs
describe the presentation/disease progression of Alzheimer’s disease
insidious!
initially - memory lapses, forgetting names, word-finding-difficulty, forgetting appts
then - language difficulties, apraxia, problems with planning and decision making, confusion
later - wandering, disorientation, apathy, psychiatric symptoms, behaviour problems, altered eating habits, incontinence
what are the pharmaceutical options for management of alzheimers disease?
acetylcholinesterase inhibitors - donepezil, galatamine, rivastigmine
these slow progression, but don’t stop it. only work for some people. can have GI side effects.
memantine - NMDA antagonist
what are some non-pharmaceutical management options for alzheimer’s disease?
memory aids - notes, lists, diaries etc
CBT
aromatherpay etc
also - think about advanced planning. memory clinic referral.
what is vascular dementia? what are the main subtypes?
- cognitive impairment caused by ischaemia or haemorrhage, secondary to cerebrovascular disease.
main subtypes = stroke-related, subcortical, mixed dementia (e.g. vascular dementia and alzheimers)
risk factors for vascular dementia?
- hx of stroke/TIA
- AF
- hypertension
- DM
- hyperlipidaemia
- smoking
- obesity
- CHD
- FHx stroke/CVD
how does vascular dementia present and progress?
progression may be sudden or gradual but is classically stepwise
imaging shows cerebrovascular disease
features indicating possible vascular cause:
- focal neurology
- difficulty w/ attention and concentration
- seizures
- depression ± anxiety
- early present of disturbance in gait/falls
- bladder symptoms
brief explanation of treatment and prognosis of vascular dementia
- no pharmacological options - AChE inhibitors and NMDA antagonists should NOT be used for anything other than Alzheimer’s dementia.
occasionally donepezil used
prognosis - bad - life expectancy 3-5yrs
what is dementia with Lewy bodies?
‘eosinophillic intracytoplasmic neuronal inclusion bodies’ (Lewy bodies) in the brainstem and neocortex
how does Lewy body dementia present?
- dementia symptoms - memory loss, decline in problem solving etc
- characteristic fluctuation in levels of awareness and attention
- signs of mild Parkinsonism
- visual hallucinations
- sleep disorders
- fainting spells - “drop attacks”
brief explanation of treatment and prognosis of Lewy body dementia
- avoid anti-Parkinsonian treatment
- cholinesterase inhibitors e.g. rivastigmine at >6mg/day can treat cognitive decline according to NICE when I did GP - disputed in Cochrane review - maybe check this??
prognosis = 5-8y survival from onset
what is frontotemporal dementia?
atrophy of fontal and temporal lobes - compared to diffuse atrophy in Alzheimer’s
what are the 3 main syndromes that frontotemporal dementia presents with?
1) behavioural variant - loss of inhibition, inappropriate social behaviour, loss of empathy etc - most common
2) semantic dementia - loss of vocab with fluency of speech maintained, word finding difficulty, loss of facial recognition, memory comparatively well-preserved
3) progressive non-fluent aphasia - slow, hesitant speech, loss of literacy, difficulty with complex sentences
what support services are in place for people with dementia?
care and support plan / support plan for carers - gets put in place after health and social needs assessment
Admiral nurses - dementia experts
Alzheimer’s society/other charity sector things - memory cafes, befriending, singing for the brain etc
Community care - home care / personal assistants, day hospitals/services
Memory clinic - does CT head, extensive questionnaire’s/assessments, treatment, take detailed collateral history
what is an IMCA?
independent mental capacity advocate
service that provides advocacy for people deemed lacking in capacity - they know lows about the Mental Capacity Act, human rights, ethics/law stuff etc, spend time with patient trying to understand their wishes.
used when making decisions about:
- long-term care move;
• serious medical treatment;
• adult protection procedures; or
• a care review.
appointed when someone has no nominated friend/family to help make these decisions, or anyone with power of Attorney (personal and welfare) or a personal welfare Deputy
what does it mean to make a ‘best interests decision’?
- everything that’s done on behalf of someone who lacks capacity must be in that persons best interests
- the person is able to put wishes in a written statement, and these must be taken into account (even if lacks capacity)
- carers/family have right to be consulted
what are the five key principles of the mental capacity act?
1) every adult has the right to make decisions and must be assumed to have capacity until proved otherwise
2) every adult must be given all possible help and support to make and communicate decisions before being consider to have lost capacity
3) making an unwise decision doesn’t mean they lack capacity
4) anything done or decision made on behalf of them must be in their best interests
5) it must also be the least restrictive of their basic rights and freedoms
what does “lasting power of attorney” mean?
legal document an individual might have drawn up to appoint someone else to make decisions for them - can be written any time whilst the person has capacity - no legal standing till registered with Office of the Public Guardian.
two types - property and affairs vs personal welfare.
personal welfare is the healthcare one, only works when registered and the individual lacks capacity. Attorney can only make decisions about life-sustaining treatment if the LPA specifies that.
give some basics of how advanced decisions work
- these are statements about wishes regarding medical treatment in case individual become incapable later - legally binding, don’t have to be written except for refusal of life-sustaining treatment
- if refusing life-sustaining treatment, must be: written, specific (e.g. CRP), signed by individual and a witness
- respect any refusal of treatment as long as clearly applicable to given circumstances!
- cannot include decisions about what patient would like, only refusals - can’t include directions to prematurely end life
- if a Dr is unwilling to carry through an advance directive, should pass over care to another doctor who is
- BMA recommends don’t withhold ‘basic care’ (e.g. symptom control) even in face of directive specifying no treatment
- if no formal advance decision - take patients wishes into consideration where known
what is Deprivation of Liberties Safeguarding (DoLS)?
used in care homes and hospitals, written document, aims to make sure people can be given the care they need in the least restrictive regimes possible.
‘deprivation of liberty’ is where someone is under continuous supervision and control, is not free to leave, and they lack capacity to consent to these arrangements.
DoLS helps prevent arbitrary DoL, allows patients the right to challenge unlawful detention
list a load of differentials for memory loss - acronym Memory VANISHED
Medications Vascular */+ Alzheimer's + Alcohol */+ Arrhythmias Normal pressure hydrocephalus ICP (raised) Insomnia */+ Subdural haematoma HIV Hypothyroid + Hypoglycaemia * Hypertension Head trauma * Emotional (severe depression) + Dementia + Delirium * Drug abuse */+ Deficiency (B12) *
- = acute, + = chronic
others - Parkinson’s, Syphilis, Stress, Wilson’s disease, CJD, renal failure
give some examples of deprivations of liberty that might be placed on an individual with dementia
deciding on the person’s routine, stopping them from walking about at night, or preventing them from leaving.
anything that restricts someone/makes decisions for them
define deprivation of liberty
‘The person is under continuous supervision and control and is not free to leave, and the person lacks capacity to consent to these arrangements.’
what are the three key elements of the DoLS?
- to provide the person with a representative – a person who is given certain rights and who should look out for and monitor the person receiving care
- to give the person (or their representative) the right to challenge a deprivation of liberty through the Court of Protection
- to provide a mechanism for a deprivation of liberty to be reviewed and monitored regularly
who orders a DoLS assessment? who performs?
care home/hospital requests assessment/authorisation from local authority if think person is/will be deprived of liberties
Two people do assessment - best interests assessor, mental health assessor - appointed by local authority, need experience/trained
best interests assessor = qualified social worker, nurse, occupational therapist or chartered psychologist - must not know patient.
mental health assessor = doctor capable of determining if has ‘mental illness’ and impact of DoL on that
what 6 things are checked for in a DoLS assessment?
Age – Is the person aged 18 years or over?
Mental health – Does the person have a ‘mental disorder’?
Mental capacity – Does the person lack ‘capacity’ (the ability) to make their own decisions about treatment or care in the place that is applying for the authorisation?
Best interests – Is a deprivation of liberty taking place? If so, is it:
– in the person’s best interests?
– needed to keep the person safe from harm?
– a reasonable response to the likelihood of the person suffering harm (including whether there are any less restrictive options and if they are more appropriate)?
Eligibility – Is the person already liable to detention under the Mental Health Act 1983, or would they meet the requirements for detention under this Act?
No refusals – Does the authorisation contradict or conflict with any advance decision the person has made refusing treatment, or with any decisions made by, for example, a court-appointed deputy or someone with Lasting power of attorney?
Has to meet all 6 to be approved
how long can a DoLS last?
A DoLS authorisation should last for as little time as possible, and only up to a maximum of 12 months. Each individual DoLS authorisation will state the date it lasts until. However, during this time both the care provider and local authority should:
make regular checks to see if the authorisation is still needed
remove the authorisation when it is no longer needed
provide the person’s representative with information about their care and treatment.
define food poisoning. what actions should be taken if there’s an outbreak?
‘any disease of an infectious or toxic nature caused by, or thought to be caused by, the consumption of food/water’
includes illness caused by toxic chemicals if transported in food.
actions:
- identify affected cohort
- identify source
- ?close restaurant
- people sampling, food sampling, questionnaires (to detect cause)
list some differentials for low mood
depression
schizophrenia
other psych conditions - anxiety, eating disorders
dementia
SAD
bereavement
organic cause - hypothyroid/hyperthyroid, endocrine (Addison’s, Cushing syndrome, prolactinomas)
some medications - methyldopa, propanolol, benzodiazepines, progesterone contraceptives
give some risk factors for depression
- female sex
- pregnancy and postnatal period
- past history of depression (alters how you treat)
- physical illnesses
- other mental health problems e.g. dementia
- bereavement
- divorce, illness, redundancy, financial worries
- family history
- isolation
- learning disabilities
- asylum seekers/refugees
- African and Asian communities
- elderly people
give some risk factors for suicide
- previous suicide attempt/self harm
- male
- age (40-44yrs = highest group)
- concurrent mental disorders or prev psych treatment
- unemployment
- homelessness
- alcohol and drug abuse
- physically disabling or painful illness
- low SE status, loss of a job
- isolation
- significant life events
- institutionalised e.g. prisons, army
what screening questions do NICE recommend asking patients to detect symptoms of depression?
During the last month, have you often been bothered by:
feeling down, depressed or hopeless?
having little interest or pleasure in doing things?
what options do NICE recommend for initial management of a patient presenting with persistent subthreshold depressive symptoms or mild-moderate depression?
sleep hygiene advice
active monitoring (if you think they’ll recover without other intervention, arrange to see in 2 weeks and re-assess)
low-intensity psychosocial interventions e.g. online/guided self-help CBT, group exercise programme
group-based CBT (if decline self-help style CBT)
typically - DON’T use antidepressants, but consider if past history of depression or no response to the above
what options do NICE recommend for management or a patient with persistent subthreshold depressive symptoms or mild-moderate depression and no response to initial treatment options? same options used for presenting with moderate-severe depression.
anti-depressant (usually SSRI)
high-intensity psychological intervention e.g. CBT, IPT
if moderate/severe depression - provide combination of the above
if a patient presents with depression to GP, what are the first things you should do?
- assess severity, comprehensive assessment
- consider degree of functional impairment, duration of episode
- assess past history
- always ask directly about suicidal ideation!
when would you consider starting antidepressant treatment if a patient has mild-moderate depression?
NOT used typically, only use if:
past history of moderate/severe depression
symptoms persist after other interventions
outline the key points to know about antidepressant treatment from the NICE guidelines
start with SSRI normally - citalopram, sertraline (not in older people), fluoxetine, paroxetine
warn patients of SEs and importance of continuation, discuss gradual development of full antidepressant effect and the need to continue beyond remission
monitoring - see at 2 weeks, then every 2-4 weeks for first 3 months, then longer intervals.
initial lack of response at 3-4 - check compliance, increase dose if no SEs, switch drug - different SSRI, or try TCA/MAOI/venfalaxine - may be less well tolerated.
REFER if need to start combining/augmenting
if a patient’s mood improves and you feel they’re in remission from depression, when do you stop anti-depressant treatment?
encourage them to keep taking it for at least 6 months - this reduces risk of relapse.
taper doses down before stopping - including taking lowest dose every other day etc.
what screening tools are available for assessing depression?
PHQ-9 is the classic - should also do GAD-7 (anxiety version) at the same time.
edinburgh PND questionnaire - done by health visitors for all postnatal women.
HADS = hospital anxiety and depression scale, can be used in primary care setting.
Also alcohol ones to be aware of - CAGE, AUDIT, SADQ
when should antidepressants be started?
Consider for:
Patients with moderate/ severe depression ± psychological therapy
Dysthymia (subthreshold depressive symptoms lasting > 2y)
Mild depression if other treatment strategies have failed
what should you tell the patient before starting antidepressants?
- The reasons for prescribing
- Timescale of action— unlikely to have any effect for 2wk; effects build up to maximum effect at 4– 6wk, and
- Likely side effects including possible exacerbation of anxiety in the first 2wk of treatment
what are some common side effects of SSRIs?
GI upset is the most common
appetite and weight disturbance (loss or gain)
hypersensitivity reactions e.g. rash
initial increase in anxiety and suicidal ideation
can lower seizure threshold
prolong QT interval
can increase risk of bleeding
what is serotonin syndrome?
SSRIs given at high doses or in overdose can cause this - triad of autonomic hyperactivity, altered mental state and neuromuscular excitation
what side effects might a patient experience when withdrawing from SSRIs?
GI upset neurological symptoms flu-like symptoms sleep disturbance avoid sudden withdrawal!!
list some differential diagnoses for acute cough
URTI (would have coryzal symptoms, normal chest) acute bronchitis common cold LRTI - viral or bacterial pneumonia asthma acute exacerbation of COPD inhaled foreign body pertussis PE pneumothorax/tension pneumothorax lung cancer GORD ACE inhibitors
list some differential diagnoses for sub-acute cough
foreign body aspiration lung cancer pulmonary TB post-infectious cough bronchitis pneumonia asthma pertussis
list some differential diagnoses for chronic cough
foreign body lung cancer pulmonary TB smoking-related cough ACE inhibitor induced cough asthma GORD eosinophilic bronchitis COPD pertussis heart failure bronchiectasis interstitial lung disease
give some risk factors for TB
- born in high prevalence areas
- close contacts
- prev (especially incomplete) treatment for TB
- comorbidities e.g. HIV, diabetes, CKD
- drugs - steroids, chemo
- social risk factors - homeless, institutionalised, overcrowding
- alcohol/drug misuse
- low body weight
- old/young
- malnourished
outline some measures to prevent spread of TB
- if diagnosed in GP clinic - leave via back door, consider home visits/telephone consultations to avoid spread in waiting room, or have TB clinics (this is all if GP practice is high risk area)
- BCG vaccine for at risk groups
- main thing is just identifying and treating adequately
- within households - adequate ventilation, educate on cough etiquette, hand washing, avoid public transport/crowded places, sleep separately
what investigations would you order if you suspected a patient had TB?
CXR
Sputum samples for culture (state on the form that you are looking for acid-fast bacilli)
Tuberculin test + ve (may be − ve if immunocompromised) If diagnosis is confirmed, refer for treatment and contact tracing.
how is TB treated?
RIPE!
2 months on Rifampicin, Isoniazid, Pyrazinamide, Ethambutol
then further 4 months of just isoniazid and rifampicin
what are the main side effects of the drugs used to treat TB?
Rifampicin - raised LFTs, low platelets, ORANGE WEE, inactivation of Pill, flu symptoms
Isoniazid - can get neuropathy - switch to pyridoxine if so
Pyrazinamide - hepatitis, arthralgia (don’t give if they have gout)
Ethambutol - optic neuritis (first symp. is loss of colour vision)
briefly explain ABG interpretation
not really GP but needed to do it at some point
PaO2 - want this >10 if healthy and room air. if on O2, should be well above 10. <10 = hypoxaemic, <8 =severely hypoxaemic.
Type 1 resp failure = hypoxaemic but normal CO2
Type 2 resp failure = hypoxaemic but high CO2
pH <7.35 = acidotic, >7.45 = alkalotic
if pH change is respiratory driven - abnormal CO2
if metabolically driven - abnormal HCO3
HCO3 should be 22-26
Base excess > +2 indicates metabolic alkalosis or compensated respiratory acidosis
< -2 indicates metabolic acidosis or compensated respiratory alkalosis
give some causes of respiratory acidosis
(pH low, CO2 high)
Respiratory depression (e.g. opiates)
Guillain-Barre – paralysis leads to an inability to adequately ventilate
Asthma
Chronic obstructive pulmonary disease (COPD)
Iatrogenic (incorrect mechanical ventilation settings)
give some causes of respiratory alkalosis
(pH high, CO2 low)
Anxiety – often referred to as a panic attack
Pain – causing an increased respiratory rate
Hypoxia – resulting in increased alveolar ventilation in an attempt to compensate
Pulmonary embolism
Pneumothorax
Iatrogenic (excessive mechanical ventilation)
give some causes of angina
usually - coronary artery disease
Rarer - HOCM, valve disease, hypoperfusion during arrhythmia, arteritis, anaemia, or thyrotoxicosis.
how does angina present?
episodic central-crushing or band-like chest pain that may radiate to jaw/neck and/or one or both arms
precipitated by exertion, cold, emotion, and/or heavy meals - stops with rest or GTN spray
associated with palpitations, sweating, nausea, and/ or breathlessness during attacks
has risk factors - smoking, FHx, hx of other vascular disease, peripheral vascular disease
what investigations would you order for a patient presenting for the first time with angina?
Bloods - FBC, fasting lipid profile, fasting blood glucose. Consider checking ESR (to exclude arteritis) and TFTs if clinical suspicion of thyrotoxicosis
ECG - for arrhythmias, presence of heart block, previous MI, myocardial hypertrophy, and/or ischaemia
ECG doesn’t rule out coronary artery disease, but identifies those at bigger risk of future MI etc
how would you manage a patient with stable angina?
general advice - avoid heavy manual labour, might need to inform DVLA, stop smoking/modify other RFs where poss
cardiac rehab
PRN drugs - GTN spray (1-2 puffs in response to pain or before exertion)
regular meds - beta blockers or CCB first line, then long acting nitrates (e.g. ivabradine, nicorandil)
secondary prevention - aspirin, statins, ACEi - give to all with angina
when might you admit/refer a patient with angina?
Admit: unstable angina/rapidly progressive symptoms
Urgent referral: aortic stenosis with angina, angina following MI, abnormal ECG at diagnosis
Routine referral: angina not controlled by medication with two drugs, if diagnosis is in doubt, strong family history, other factors, e.g. occupation affected
what is unstable angina? how should you manage it?
angina pain occurring at rest, in the night, or which is rapidly worsening in frequency/severity etc
do urgent referrral to cardiology
what surgical options are there in the management of angina?
PCI/CABG - consider if not responding after trialling 2 drugs
what is Prinzmetal angina?
occurs with coronary artery spasm, rather than on exertion
ECG will show ST elevation - cardiology referral to exclude MI and atherosclerotic angina.
GTN spray will offer immediate release always, CCBs used to prevent attacks.
what are the classic ECG features seen in AF?
rapid irregularly irregular narrow QRS complex tachycardia with absence of P-waves.
risk of embolic stroke.
give some causes of AF
No cause (isolated AF) (12%) Coronary heart disease hypertension (especially if LVH) Cardiomyopathy Valvular heart disease (especially mitral valve disease)
give some factors that can precipitate acute AF
acute infection high alcohol intake surgery MI electrocution PE hyperthyroidism
how does AF present?
typically detected as part of testing for other reasons, being asymptomatic
can cause - palpitations, chest pain, syncope, stroke/TIA, fatigue, dyspnoea
how would you investigate a patient with AF?
Routine investigations - resting ECG, CXR, Bloods - TFTs, FBC, U&E
further investigations - ambulatory ECG or cardiac memo (measures ECG trace when triggered by patient e.g. to see if symptoms are due to arrhythmia) if paroxysmal AF.
echo if < 50y or murmur/ heart failure detected
consider exercise tolerance test if exercise-related
what are the aims/principles of managing AF?
to relieve symptoms (e.g. palpitations, fatigue), maintain cardiac function and prevention thromboembolism and stroke risk
if infrequent paroxysmal AF can consider no drugs/’pill-in-pocket’ approach but if chronic or frequent paroxysms need to think about continuous treatment/anticoagulation
what would an ECG trace show in a patient with atrial flutter?
regular, sawtooth baseline at rate of 300bpm, with a narrow QRS complex tachycardia superimposed at a rate of 150bpm or 100bpm.
managed similar to AF
what is the ‘pill-in-the-pocket’ approach to managing AF?
self-medication with PRN beta blocker (e.g .atenolol 50-100mg)
describe the medical management of AF (controlling the actual AF rather than anticoagulation management)
either rate or rhythm control
rhythm control = electrical/chemical cardioversion to sinus rhythm - used if - associated heart failure, new onset AF, atrial flutter suitable for ablation, AF secondary to a treated/corrected precipitant, rate control not successful
rate control - with beta blocked (e.g. atenolol, bisoprolol) or rate-limiting calcium channel locker (e.g. diltiazem). can also use digoxin (but getting into specialist areas here)
how do beta blockers work to manage AF? any side effects to warn patient of?
drug that slows how fast your heart goes - prolongs refractory period of the AV node.
SEs - fatigue, cold extremities, headache, GI upset, sleep disturbance, erectile dysfunction
CI in asthma!!!!!!!! can cause bronchospasm as they block the beta 2 adenoreceptors in the airways
how do CCBs work to manage AF? any side effects to warn patient of?
diltiazem and verapamil are the ones used for this (cardioselective)
they suppress cardiac conduction across the AV node, slowing ventricular rate.
SEs - ankle swelling, flushing, headache, palpitations, constipation (verapamil), bradycardia, heart block.
DON’T prescribe with beta blockers - can cause heart failure/block
what is the CHA2DS2-VASC score? what are the components?
score used to assess risk of stroke in AF patients to decide whether oral anticoagulants are needed.
Get points for the following:
Congestive heart failure Hypertension Age: ≥ 75 (2 pts) or 65-74 (1pt) Diabetes mellitus Stroke/TIA/thrombo-embolism (2 pts) Vascular disease Sex - Female
score of 1 = consider anticoagulating if male
score 2+ for female to consider anticoagulating
target INR = 2-3
what is the HASBLED score?
used to weigh benefits of anticoagulating against risk of bleeding.
one point for each of:
Hypertension - uncontrolled, > 160 mmHg systolic
Abnormal liver function
Abnormal renal function
Stroke
Bleeding
Labile INRs
Elderly (Age >65)
Drugs/alcohol
score 3+ means consider carefully whether need to anticoagulate
what drugs are used for anticoagulation of a patient with AF to prevent stroke?
lots of people on warfarin for this (target INR 2-3) - NICE now says to use NOACs only: apixaban, dabigatran etexilate, rivaroxaban or a vitamin K antagonist.
when would you offer rate vs rhythm control to someone with AF?
Offer rate control as first-line to people with AF, except in people:
whose AF has a reversible cause
who have heart failure thought to be primarily caused by AF
with new-onset AF
with atrial flutter whose condition is considered suitable for an ablation strategy to restore sinus rhythm
for whom a rhythm control strategy would be more suitable based on clinical judgement.
what does NICE say about how to assess if people are eligible for medications etc as part of primary prevention of heart disease? what should they receive?
Use the QRISK2 scoring system.
decide between statins and lifestyle adjustments only - depends on overall risk, willingness to change etc.
offer atorvastatin 20mg OD to anyone with 10yr CVD risk >10% as determined by Q Risk
if dealing with secondary prevention (e.g. after MI) - always give statin - usually 80mg atorvastatin
you are assessing a patient to decide whether to offer statins as part of a primary prevention strategy for CVD - his 10yr risk is 11% - what lifestyle advice should you give before starting the statin?
stick to alcohol recommendations
reduce intake of (saturated) fatty foods - eat more mono-unsaturated fats e.g. olive oil
reduce sugar intake, get 5 a day, 2 portions fish per week, 4-5 portions unsalted nuts/seeds/legumes per week
150 mins of moderate intensity aerobic exercise per week, + 2 days of muscle strengthening exercises
STOP smoking
maintain normal BMI
how do statins work? any side effects to warn patients about?
reduce serum cholesterol levels - given to everyone with a 10 yr CVD risk of >10% (some places say 20% but think it’s been lowered to 10)
inhibit 3-hydroxy-3-methyl-glutaryl coenzyme A (HMG CoA reductase) - enzyme that makes cholesterol. this decreases cholesterol production in liver, and increases clearance of LDL-cholesterol from blood. also reduce triglycerides and slightly increase HDL levels - slows atherosclerotic process and poss even reverses
SEs - headache and GI upset most common. but can affect muscles - aches, myopathy or rhabdomyolysis
give some causes of obesity
Physical inactivity
Smoking cessation— mean weight ↑ 3– 4kg
Cultural factors
Low education
Polygenic genetic predisposition - around 1 in 3 obese people - more prone to obesity again after successful dieting
Childbirth— especially if not breastfeeding
Drugs— steroids, antipsychotics (e.g. olanzapine), contraceptives (especially depo-injections), sulfonylureas, insulin
Endocrine causes (rare) - hypothyroidism, Cushing’s syndrome, PCOS
Ongoing binge eating disorder
what are the management options for obesity?
DIET AND EXERCISE - target weight loss of 1-2lbs per week, equivalent to calorie deficit of 600kcal/day (decrease consumption and increase expenditure)
drugs - orlistat, decreases fat consumption, trial if >3m consistent weight loss effort has failed
surgery - adjustable gastric band most common. use if BMI >40 and all non-surgical options have failed. Complications: band slippage/ damage; gastric erosion, pouch dilatation; infection; malabsorption.
describe the medical options to aid smoking cessation
NRT e.g. patches, gum, sprays - swap out for cigarettes, use for 8 weeks then stop completely
bupropion - an atypical antidepressant shown to aid smoking cessation. don’t give if seizure prone.
varenicline - alpha-4 beta-2 (α4β2) nicotinic acetylcholine receptor partial agonist - both blocks and stimulates the receptor - both reduces nicotine cravings, and reduces pleasure effect of smoking.
what is osteoporosis?
reduced bone mass and deterioration of bone architecture - usually described as low bone density. means bones are more fragile and prone to fracture.
fracture risk assessed using FRAX (can calculate with or without BMD) or QFracture (based on UK pop, doesn’t use BMD)
give some causes of osteoporosis
Endocrine - hypogonadism (e.g. premature menopause, anorexia, androgen blockade, taking aromatase inhibitors), hyperthyroidism, hyperparathyroidism, hyperprolactinaemia, Cushing’s disease, type 1 DM
GI - coeliac disease or other causes of malabsorption, inflammatory bowel disease, chronic liver disease, chronic pancreatitis
Rheumatological - RA, other inflammatory arthropathies
Other - immobility, multiple myeloma, haemoglobinopathy, systemic mastocytosis, CF, COPD, CKD, homocystinuria
STEROIDS
define ‘fragility fracture’. what types are common?
Fracture sustained falling from ≤ standing height— includes vertebral collapse (may not be as a result of a fall).
commonly - hip, wrist (Colle’s #), osteoporotic vertebral collapse (get pain, reduced height, kyphosis)
give some risk factors for osteoporosis
Female sex.
Low body mass (<19 kg/m2) and anorexia nervosa.
Parental history of hip fracture.
Past history of fragility fracture (especially hip, wrist and spine fracture).
Corticosteroid therapy (current treatment at any dose orally for three months or more).
Cushing’s syndrome.
Alcohol intake of three or more units per day.
Smoking.
Falls and conditions increasing the risk of falls, such as:
Visual impairment.
Lack of neuromuscular co-ordination or strength.
Cognitive impairment.
Sedative medication and alcohol.
what is a T score?
scoring system for osteoporosis that compares bone mineral density (BMD) of patient to the young adult mean.
osteoporosis then defined as anything below -2.5 SDs away from that mean.
osteopenia = between -1 and -2.5 (reduced density but not osteoporosis yet)
what are DEXA scans and when should they be used in investigation of osteoporosis?
dual energy X ray absorpimetry - only use after assessing fracture risk with FRAX or Qfracture.
often wouldn’t bother if >75yo as likely will treat anyway, so doesn’t change the management much.
in a patient taking moderate/high dose steroids, when should you add bone protection?
add it from the start if think they'll be on it for >3 months - don't wait till 3 months have passed! use alendronate (bisphosphonate) - common side effect of GI upset, switch to risedronate
what treatment options are there for osteoporosis?
advise adequate calcium/vit D intake - consider supplementation.
regular weight bearing exercise, stop smoking, reduce alcohol consumption.
bisphosphonates = alendronic acid/alendronate 70mg once weekly - take on empty stomach, 30 mins before any other food/meds, sitting upright for 30 mins after, drink loads of water. common GI upset - switch to risedronate if so.
other meds - strontium (not recommended any more)
raloxifene (works on oestrogen) - used if bisphosphonates CI’d
denosumab - monoclonal ab, used further down line of treatment
what is osteoarthritis? how does it present?
‘wear and tear’ arthritis - now thought to be metabolically active.
usually localised to knee or hip or base of thumb initially - pain on movement, crepitus, worse at end of day, background pain at rest, gelling (stiffness after rest), joint instability
what are the classic X ray features of osteoarthritis?
LOSS Loss of joint space Osteophytes Subarticular sclerosis Subchondral cysts
give some risk factors for development of osteoarthritis
↑ age (uncommon < 45y) F > M black and Asian populations genetic predisposition obesity abnormal mechanical loading of joint, e.g. instability poor muscle function post-meniscectomy certain occupations, e.g. farming
describe the initial management of osteoarthritis
reduce load on joint - physio, walking aids
exercise improves local muscle strength and reduces pain and disability
avoid pharmacological treatment where poss - local heat, TENS etc
then 1g paracetamol QDS first line ± topical NSAIDs (if knee or hand)
second line - codeine, NSAIDs (+ omeprazole), topical capsaicin
describe further management of osteoarthritis (beyond lifestyle changes + drugs)
intra-articular steroids - short-term can really relieve
intra-articular hyaluronic acid - not NICE recommended cos expensive
if severe - joint replacement (hips or knees)
what is rheumatoid arthritis? how does it present?
chronic systemic inflammatory disease - symmetrical, deforming peripheral polyarthritis
typical presentation = symmetrical swollen, painful and stiff small joints of hands and feet, worse in morning.
what hand signs are seen in rheumatoid arthritis?
ulnar deviation of fingers
dorsal wrist subluxation
Boutonniere and swan-neck deformities of fingers
Z deformity of thumbs
what investigations would you do for rheumatoid arthritis?
rheumatoid factor (positive in 70%) anticyclic citrullinated peptide antibodies (ACPA/anti-CCP) - very specific for RA inflammation means - raised platelets, ESR and CRP XR - may be normal, show periarticular osteoporosis or soft tissue swelling - late on shows loss of joint space, erosions and joint destruction
when should you refer a patient with suspected rheumatoid arthritis?
all patients with persistent synovitis should be reviewed.
refer urgently if:
- the small joints of the hands or feet are affected
- more than one joint is affected
- there has been a delay of 3 months or longer between onset of symptoms and seeking medical advice.
new NICE guidelines say they should be seen by rheumatology within 3 weeks
what non-pharmacological management options are there for RA?
use the MDT!!
physio
OT
hand exercise programmes
podiatry
psychological therapies - consider IAPT referral, ensure regularly screening for depression
encourage mediterranean diet - but no link between any particular foods and RA generally
complementary therapy - welcome to try, but shouldn’t replace conventional treatments
when should you consider referring a patient for surgical management of RA?
if any of the following do not respond to optimal non-surgical management:
persistent pain due to joint damage or other identifiable soft tissue cause
worsening joint function
progressive deformity
persistent localised synovitis.
ALSO -
if they have any of the following complications for a specialist surgical opinion before damage or deformity becomes irreversible:
imminent or actual tendon rupture
nerve compression (for example, carpal tunnel syndrome)
stress fracture.
describe the initial drug management of RA
treat-to-target - patients should have regular disease monitoring/reviews e.g. monthly rheumatology appts until they’re in remission/meet disease control target (generally should be remission!)
first line - monotherapy with conventional DMARD - methotrexate, sulfasalazine, hydroxychloroquine - ideally start < 3 months after symptom onset.
titrate dose up to have effect - if that doesn’t work, try the above in combination (step-up strategy)
describe the further drug management of RA (after conventional DMARDs have failed)
biologics - sarilumab, dalimumab, etanercept, infliximab, certolizumab pegol, golimumab, tocilizumab and abatacept - all used in combination with methotrexate
rituximab used if the above don’t work/are intolerated
tocilizumab also used later on in treatment steps.
how should RA ‘flares’ be managed?
oral NSAIDs + PPI
short term course of steroids - oral, or intra-articular injections if disease quite localised
list some extra-articular complications of RA
respiratory: pulmonary fibrosis, pleural effusion, pulmonary nodules, bronchiolitis obliterans, methotrexate pneumonitis, pleurisy
ocular: keratoconjunctivitis sicca (most common), episcleritis, scleritis, corneal ulceration, keratitis, steroid-induced cataracts, chloroquine retinopathy
osteoporosis
ischaemic heart disease: RA carries a similar risk to type 2 diabetes mellitus
increased risk of infections
depression
list symptoms/signs of acute asthma attack (not life-threatening)
PEFR 33– 50% predicted or best (if recorded)
Sats ≥ 92%
Unable to talk in sentences
Intercostal recession
Tachypnoea (respiratory rate ≥ 25 breaths/ min)
Tachycardia (heart rate ≥ 110bpm)
list signs of a life-threatening asthma attack
PEFR < 33% predicted or best (if known) Sats < 92% Arrhythmia Hypotension Cyanosis Exhaustion Poor respiratory effort Silent chest (inaudible wheeze) Altered consciousness
how should you manage a patient presenting with an acute severe asthma attack, in the GP surgery?
give oxygen
salbutamol nebs (or via spacer if no nebuliser available)
steroids - po pred or iv hydrocortisone
if no response - ADMIT
if any life-threatening signs/symps - ADMIT
what is asthma? what are the 3 characteristic features?
paroxysmal, reversible airways obstruction
3 characteristic features:
- Airflow limitation— usually reversible spontaneously or with treatment
- Airway hyper-responsiveness to a wide range of stimuli
- Inflammation of the bronchi
what clinical features increase likelihood that a patient has asthma?
> 1 of: Wheeze Breathlessness Chest tightness Cough
Particularly if: Symptoms are worse - at night/ early morning, with exercise, allergen and/ or cold air exposure, after aspirin/ beta-blockers PMH of atopy FH asthma and/or atopy Widespread wheeze Unexplained low FEV1 or PEFR Unexplained eosinophilia
what clinical features make it less likely that a patient has asthma?
Prominent dizziness, light-headedness, peripheral tingling
Chronic productive cough without wheeze/breathlessness
Normal examination of chest when symptomatic
Voice disturbance
Symptoms with colds only
Smoking history (> 20 pack y)
Cardiac disease
Normal PEFR/ spirometry when symptomatic
what tests should be done to diagnose asthma?
spirometry preferred - FEV1/FVC ratio <70% = airway obstruction - but this can be normal if asymptomatic at the time of assessment!
peak flow diaries more useful in monitoring controlled asthma, but are sometimes used
fractional exhaled nitric oxide testing can be used if “intermediate” probability - more nitric oxide meant to indicate more inflammation in lungs
might use reversibility testing - if airflow obstruction at time, test FEV1 before and after give salbumatol inhaler. if no airflow obstruction, test before and after trial of treatment with beclometasone
describe the step-wise management of asthma in adults
1) SABA - reliever inhaler, salbutamol (blue)
step up if using blue inhaler 3 times a week
2) add low dose ICS
3) add leukotriene receptor agonist, review in 4-8 weeks
4) add LABA, continue LTRA if helpful
5) SABA ± LTRA, plus switch ICS/LABA for a maintenance and reliever therapy (MART), that includes a low-dose ICS
5) increase ICS to moderate dose - either as MART, or switch to LABA + ICS maintenance with SABA reliever
6) SABA +/- LTRA + one of the following options:
- increase ICS to high-dose (only as part of a fixed-dose regime, not as a MART)
- a trial of an additional drug (for example, a long-acting muscarinic receptor antagonist or theophylline)
- seeking advice from a healthcare professional with expertise in asthma
what is COPD? what causes it?
slowly progressive disorder characterized by airflow obstruction with little or no reversibility
SMOKING
Genetic— bronchial hyperresponsiveness; alpha1-antitrypsin deficiency
Race— Chinese and Afro-Caribbeans have reduced susceptibility
Diet— poor diet and low birthweight
what features of a history would make you consider COPD?
Consider in any patient > 35y with a risk factor for COPD (generally smoking) and ≥ 1 of:
SOBOE - use an objective measure, e.g. MRC dyspnoea scale to grade breathlessness
Chronic cough
Wheeze
Regular sputum production
Frequent winter ‘bronchitis’
list some possible signs of COPD
might be none! or any of: Hyperinflated chest ± poor chest expansion on inspiration ↓ cricosternal distance Hyperresonant chest with ↓ cardiac dullness on percussion Wheeze or quiet breath sounds Paradoxical movement of lower ribs Use of accessory muscles Tachypnoea Pursing of lips on expiration (purse lip breathing) Peripheral oedema Cyanosis ↑ JVP Cachexia
what results on spirometry indicate airflow obstruction?
FEV1/FVC <70%, FEV1 <80% (some places say 70%) predicted
what investigations should be ordered if a patient presents with symptoms that sound like COPD?
spirometry
CXR to exclude other pathologies
FBC
calculate BMI
if early onset/family linked - consider testing for alpha1 antitrypsin deficiency
what does NICE recommend regarding management of stable COPD?
general - smoking cessation, pneumococcal vaccine, annual flu jab
SABA or SAMA (ipatropium) is first line - if remain symptomatic then treat according to FEV1
FEV1 > 50% predicted - add LABA (salmeterol) or LAMA (tiotropium)
next:
if on LABA, switch to LABA + ICS combi
if on LAMA, keep that and add LABA + ICS combi
then maybe try theophylline
mucolytics can be ‘considered’
how does an acute exacerbation of COPD present?
One or more of:
↑ dyspnoea— marked dyspnoea, tachypnoea (> 25 breaths/min), use of accessory muscles at rest and purse lip breathing are signs of severe exacerbation
↓ exercise tolerance— marked ↓ in activities of daily living is a sign of severe exacerbation
↑ fatigue
↑ fluid retention— new-onset oedema is a sign of severe exacerbation
↑ wheeze
Chest tightness
↑ cough
↑ sputum purulence
↑ sputum volume
Upper airways symptoms, e.g. colds, sore throats
New-onset cyanosis— severe exacerbation
Acute confusion— severe exacerbation
what causes acute exacerbations of COPD?
infections or pollutants
organisms:
Haemophilus influenzae (most common cause)
Streptococcus pneumoniae
Moraxella catarrhalis
what does NICE say about managing acute exacerbations of COPD?
increase frequency of bronchodilator use and consider giving via a nebuliser
give prednisolone 30 mg daily for 7-14 days (useful qu if assessing severity of COPD - how many times were you on steroids last winter?)
it is common practice for all patients with an exacerbation of COPD to receive antibiotics. NICE only recommend giving oral antibiotics ‘if sputum is purulent or there are clinical signs of pneumonia’
if giving abx - Use broad-spectrum antibiotic, e.g. clarithromycin 500mg bd or doxycycline 100mg od/ bd
when should a COPD patient be put on LTOT?
Assess patients for suitability if any of the following:
very severe airflow obstruction (FEV1 < 30% predicted). Assessment should be ‘considered’ for patients with severe airflow obstruction (FEV1 30-49% predicted)
cyanosis
polycythaemia
peripheral oedema
raised jugular venous pressure
oxygen saturations less than or equal to 92% on room air
Assessment is done by measuring ABGs on 2 occasions at least 3 weeks apart in patients with stable COPD on optimal management.
Offer LTOT to patients with a pO2 of < 7.3 kPa or to those with a pO2 of 7.3 - 8 kPa and one of the following: secondary polycythaemia nocturnal hypoxaemia peripheral oedema pulmonary hypertension
LTOT involves 15h a day of supplementary O2 via oxygen concentrator.
what are some risk factors for GORD?
Smoking Alcohol Coffee Fatty food Big meals Obesity Hiatus hernia Tight clothes Pregnancy Systemic sclerosis Drugs (NSAIDs, TCAs, SSRIs, iron supplements, anticholinergics, nitrates, alendronic acid) Surgery for achalasia
what causes GORD?
retrograde flow of gastric contents through incompetent gastro-oesophageal junction - gives heart burn type symptoms.
conditions causing GORD:
Oesophagitis (defined by mucosal breaks) ± oesophageal ulcer
Benign oesophageal stricture
Intestinal metaplasia: Barrett’s oesophagus
Oesophageal haemorrhage
Anaemia
how does GORD present?
Heartburn: most common symptom. Burning retrosternal or epigastric pain which worsens on bending, stooping or lying, and with hot drinks. Relieved by antacids.
Other symptoms:
Waterbrash— mouth fills with saliva
Reflux of acid into the mouth (bad/funny taste) - especially on lying flat
Nausea and vomiting
Nocturnal cough/ wheeze due to aspiration of refluxed stomach contents
when would you consider ordering an endoscopy for a patient with likely GORD?
symptoms for >4 weeks persistent vomiting GI bleeding/iron-deficient anaemia palpable mass age >55 dysphagia symptoms despite treatment weight loss
what types of investigations might be ordered for a GORD patient?
endoscopy
barium swallow - identifies hiatus hernia
oesophageal pH monitoring / manometry - useful if endoscopy normal
outline management options for GORD
lifestyle - raise bed head, weight loss, smoking cessation, avoid spicy food/alcohol/citrus/hot drinks/choc, small regular meals
drugs - antacids or alginates, PPI if oesophagitis or unresponsive to initial treatment.
surgery - aims to increase resting LOS pressure, consider in severe GORD - Nissen fundoplication
what kind of inhalers are seretide/symbicort? side effects?
compound inhalers - contain ICS and LABA
Seretide = fluticasone and salmeterol
Symbicort = budesonide and formoterol
SEs - ICS’s cause oral thrush (rinse mouth out), hoarse voice.
LABAs can cause tremor, tachycardia, arrhythmias, muscle cramps.
advise patient - must use every morning to work, might take a few days to feel benefit. rinse mouth and gargle immediately after - prevents oral thrush/hoarse voice.
what are alginates? what are they used for? side effects to warn patient?
used in GORD/dyspepsia - act to increase viscosity of stomach contents, reducing reflux of stomach acid into oesophagus - forms floating ‘raft’ on top of acid as well.
usually used with antacids as Gaviscon/Peptac.
antacids work by buffering stomach acids.
SEs - rare, but diarrhoea or contraception. can reduce absorption of other drugs.
what are bisphosphonates? how do they work? important SEs?
e.g. alendronate
used first line for pts at risk of osteoporotic fragility fractures
they reduce bone turnover, by inhibiting action of osteoclasts (cells responsible for bone resorption)
patients take it once a week, before any food/drink, with lots of water, sitting upright for 30 mins after.
SEs - oesophagitis, hypophosphataemia. avoid in severe kidney failure, CI if hypocalcaemia or upper GI disorders.
how do beta2-agonists work? how are they classified? important SEs?
SABA (salbutamol, terbutaline) or LABA (salmeterol, formoterol)
beta2 receptors are found in smooth muscle of bronchi, GI tract, uterus and blood vessels - stimulation by SABA/LABA causes smooth muscle relaxation, improving airflow, reducing breathlessness.
SEs - tachycardia, palpitations, anxiety, tremor. LABAs can cause muscle cramps.
how do antimuscarinic bronchodilators work? how are they classified? important SEs?
SAMA (ipratropium) vs LAMA (tiotropium)
bind to muscarinic receptor, competitively inhibiting acetylcholine - reduce smooth muscle tone and secretions by blocking action of muscarinic receptor.
SEs - none really, might get a dry mouth.
how do inhaled corticosteroids work? SEs?
e.g. beclometasone, budesonide, fluticasone
used in asthma and COPD
‘dampen down’ inflammation in lung - hardly any absorbed into the body.
basically pass into cytoplasma, activate receptors then modify transcription of loads of genes - results in downregulation of pro-inflammatory interleukins, cytokines etc, and upregulation of anti-inflammatory ones - reduces mucosal inflammation, widens airways, reduces mucus secretion.
both improves symptoms and reduces exacerbations.
SEs - very local - oral thrush and hoarse voice.
what are proton pump inhibitors? important SEs?
e.g. omeprazole, lansoprazole
reduce gastric acid secretion - irreversibly inhibit H+/K+-ATPase in gastric parietal cells (proton pump) which normally secretes H+ - can suppress gastric acid production almost completely cos they act on this last step.
SEs - GI disturbance, headache
what are H2-receptor antagonists? important side effects?
e.g. ranitidine
used in GORD/peptic ulcer disease
reduce gastric acid secretion - not completely though, so PPIs better really - ranitidine only blocks one pathway from stimulating proton pump
SEs - usually well tolerated, might get diarrhoea, headache, dizziness
what would histology of a biopsy taken at endoscopy from someone with coeliac disease show?
villous atrophy, raised intra-epithelial lymphocytes, and crypt hyperplasia
what is coeliac disease? how does it present?
gluten sensitivity resulting in inflammation of bowel and malabsorption - T cell mediated autoimmune disease of small bowel.
associated with HLA-DQ2 and HLA-DQ8, and other autoimmune diseases
usually presents with kinda vague history of diarrhoea and weight loss/anaemia. also steattorrhoea, abdo pain, bloating, N&V, aphthous ulcers, angular stomatitis, fatigue, weight loss, osteomalacia
how is coeliac disease investigated?
tissue transglutaminase
anti-endomyseal antibodies
alpha-gliadin
(pt must have eaten 1+ meal with gluten per day for >6 weeks for tests to work)
also do - FBC, ESR/ CRP, B12, folate, ferritin, LFTs, Ca2 +, TFTs, and stool sample for M, C& S (if diarrhoea)
how is coeliac disease managed?
gluten free diet - can prescribe gluten free breads, biscuits etc. refer to dietician.
give pneumococcal vaccine - at risk due to secondary hyposplenism
what are some complications of coeliac disease?
anaemia, secondary lactose-intolerance, GI T cell lymphoma (rare), general raised risk of malignancy (gastric, oesophageal, bladder, breast, brain), myopathies, hyposplenism, osteoporosis
what is IBD?
ulcerative colitis and crohns:
chronic, relapsing-remitting diseases characterized by acute, non-infectious inflammation of the gut.
UC - inflammation limited to mucosa. varies from disease limited to the rectum (proctitis) to affecting the whole colon (pancolitis).
Crohn’s, any part of the gut from mouth to anus can be affected with normal bowel between affected areas (skip lesions).
what is the impact of smoking on UC?
protective factor!
briefly describe the pathology of UC
relapsing and remitting inflammatory disorder - hyperaemic/haemmorrhagic granular colonic mucosa ± pseudopolyps formed by inflammation - might see punctate ulcers extedning into lamina propria, but inflammation not normally transmural
symptoms/signs of UC
symps - episodic or chronic diarrhoea (± blood/mucus), crampy abdo discomfort, urgency/tenesmus (rectal UC) - frequency of bowel movements relates to severity.
signs - might be none, or clubbing, aphthous oral ulcers, erythema nodosum, pyoderma grangrenosum, conjunctivity, episcleritis, iritis, sacroiliitis etc etc
what investigations would you do for a patient with suspected UC?
bloods - FBC, ESR, CRP, U&E, blood culture
stool MC&S to exclude infection
colonoscopy - shows disease extent, allows biopsy
give some complications of UC
perforation
bleeding
toxic megacolon
venous thrombosis - higher risk
how do you manage UC?
induce remission with a 5-aminosalicylic acid (sulfasalazine or mesalazine), steroids (prednisolone) can also help.
maintenance - often stay on 5-ASA
also - suppositories (e.g of pred or mesalazine) helpful in proctitis, foams PR can help procto-sigmoiditis.
immunomodulation (e.g. azathioprine, methotrexate, infliximab) used if steroids not inducing remission
surgery - eventually - resulting in stoma usually.
what is Crohn’s disease/describe pathology
characterized by transmural granulomatous inflammation - affects any part of gut from mouth to anus, can have skip lesions.
symptoms/signs of Crohn’s
symps - diarrhoea with urgency, abdo pain, wt loss, fever/malaise/anorexia, steattorrhoea
signs - aphthous ulcers, abdo tenderness, perianal abscess/fistulae, skin tags, anal strictures.
give some complications of Crohn’s disease
small bowel obstruction toxic megacolon abscess formation fistulae e.g. colovesical malnutrition osteomalacia
how would you investigate a patient with suspected Crohn’s?
blood - FBC, ESR, CRP, U&E, LFT, INR, ferritin, B12, folate
stool - MC&S to exclude infection
colonoscopy and rectal biopsy
management of Crohn’s
mild attack - mesalazine or prednisolone
severe - admit, IV hydrocortisone, consider surgery
there’s loads of weird and wonderful drugs can try in specialist care e.g. azathioprine, methotrexate, TNF alpha inhibitors etc
surgery usually last resort if other management failed - never curative
what is IBS?
chronic (> 6mo) relapsing and remitting condition of unknown cause, with symptoms including ABCs: Abdominal pain or discomfort; Bloating; and Change in bowel habit.
what symptoms would suggest a diganosis IBS?
Abdominal pain or discomfort that is:
Relieved by defecation, or
Associated with altered bowel frequency or stool form
and ≥ 2 of the following:
Altered stool passage (straining, urgency, incomplete evacuation)
Abdominal bloating (F > M), distension, tension, or hardness
Symptoms made worse by eating
Passage of mucus
other common symptoms - lethargy, nausea, backache and bladder problems
how do you manage a patient with IBS?
reassurance, dietary advice e.g. limit/increase fruit and veg intake, trial various diet changes
try bisacodyl/sodium picosulfate for constipation
for diarrhoea can try bulking agent and loperamide
for cramping/colic/bloating - antispasmodis (mebeverine)
psychological therapies
try not to over medicalise
list some causes of CKD
DIABETES hypertension SLE hypercalcaemia Urinary tract obstruction Chronic pyelonephritis Polycystic kidneys (familial) Glomerulonephritis e.g. IgA nephropathy Renovascular disease Interstitial nephritis Amyloid Myeloma PAN
CKD - features of history, symptoms, signs
History features - FH (polycystic kidneys); UTI; drugs (especially analgesics) - often none really
Symptoms - often no symptoms, or - nausea, anorexia, lethargy, itch, nocturia, impotence.
Later symptoms - oedema, dyspnoea, chest pain (from pericarditis), vomiting, confusion, fits, hiccups, neuropathy, coma
Signs - pallor, ‘lemon tinge’ to skin, pulmonary/ peripheral oedema, pericarditis, pleural effusions, metabolic flap, ↑ BP, retinopathy
define CKD
impaired renal function for >3 months with abnormal structure/function - OR - GFR <60 for >3 months ± evidence of kidney damage
explain the classification system for CKD
normally no symptoms till stage 4+:
stage / GFR / notes
stage 1 = >90 = normal or high GFR with evidence of renal damage
stage 2 = 60-89 = slightly low GFR with evidence of renal damage
stage 3A/B = 45-59 / 30-44 = moderately low GFR with or without evidence of renal damage
stage 4 = 15-29 = severely low GFR, ± evidence of renal damage
stage 5 = <15 = established renal failure
evidence of renal damage = proteinuria, haematuria, evidence of abnormal anatomy/systemic disease
who should be screened for CKD?
patients with:
diabetes
hypertension
cardiovascular/cerebrovascular disease
structural renal disease, known stones or BPH
recurrent UTIs or childhood hx of vesicoureteric reflux
multisystem disorders which could involve the kidney eg. SLE
FHx of end-stage renal failure or known hereditary disease e.g polycystic kidneys
what investigations might you order for a patient with newly diagnosed CKD?
Urine - MC& S, microalbuminuria, albumin:creatinine ratio protein:creatinine ratio, RBCs, glucose
Bloods - U& E, creatinine, eGFR, glucose, Ca2 +, PO4 – urate, protein, FBC, ESR, serum electrophoresis
Renal tract USS If progressive or advanced (stage 4/ 5) disease, refractory ↑ BP, haematuria, or palpable bladder/ lower urinary tract signs
consider renal biopsy if rapidly progressive/unclear cause and normal size kidneys
when should you refer a patient with CKD?
- stage 4 or 5
- moderate proteinuria unless due to DM and already appropriately treated
- proteinuria with haematuria
- rapidly falling eGFR
- poorly controlled hypertesion despite 4+ antihypertensives
- known/suspected rare/genetic cause
- suspected renal artery stenosis
how do you manage CKD?
- find and treat reversible causes
- limit progression/complications - tight BP control, treat raised PTH to prevent renal bone disease, reduce CVD risk factors, dietician advice
- symptom control - monitor for anaemia, acidosis, oedema, restless legs
- prepare for renal replacement therapy
give some basic info on renal replacement therapy options
dialysis normally started at GFR of about 8-10
haemodialysis - need AV fistula normally to get good enough access, blood passed over membrane and waste removed, can do ultrafiltration to remove excess fluid as well
haemofiltration - used in critically ill but inappropriate for long term as takes too long
peritoneal dialysis - uses the peritoneum as membrane - catheter inserted into cavity, infusion of fluid, then solutes can move across - can be done at home, quite simple.
dialysis has a massive impact on QoL!!
the ultimate in renal replacement therapy is renal transplant - but major surgery, long term immunosuppression, risk of complications etc
what causes type 1 diabetes?
insulin deficiency due to autoimmune destruction of insulin-secreting pancreatic beta cells.
associated with HLA DR3 ± DR4 - and other autoimmune diseases.
they will be insulin dependent, can present in DKA
what causes type 2 diabetes?
reduced insulin secretion and raised insulin resistance - associated with obesity, sedentary lifestyle, calorie and alcohol excess.
progresses from preliminary phase of impaired glucose tolerance or impaired fasting glucose.
what are the WHO cut offs for diabetes?
symptoms of hyperglycaemia (e.g. polyuria, polydipsia, weight loss, vision blurring, genital thrush, lethargy) AND raised blood glucose once - fasting = 7+, random = 11.1+ mmol/L
OR
2 separate occasions of raised blood glucose using above cut offs OR oral glucose tolerance test 2h value 11.1+ mmol/L
HbA1c noraml at 48+ mmol/L (or 6.5%) - doesn’t exclude DM, don’t bother using in kids, pregnancy or T1DM
describe the non-drug management options for T2DM
LIFESTYLE - education programme, smoking cessation, weight loss, good nutrition
start statin, control BP, foot care
inform DVLA - don’t drive if hypo spells - loss of hypo awareness = loss of license (permanent if HGV driver)
influenza and pneumococcal jabs
what are the drug management options for T2DM?
1) metformin (biguanide) - only effective if some insulin production still, no hypo risk, can aid weight loss
second-line / if metformin CI’ed - DPP4 inhibitors, pioglitazones or sulfonyureas
sulfonyurea - e.g. glicazide - increase insulin secretion, can cause hypos and weight gain
pioglitazone - increases insulin sensitivity, can cause hypos, fractures, fluid retention
DPP4 inhibitors - aka gliptins e.g. sitagliptin
3rd line is basically combinations of the above
then you go to insulin
contra-indications for pioglitazone
heart failure or history of heart failure hepatic impairment diabetic ketoacidosis current, or a history of, bladder cancer uninvestigated macroscopic haematuria.
when would you avoid using metforming for T2DM?
reduce eGFR (<36) also if very elderly, severe heart disease, liver disease, alcohol problems
what different types of insulin therapy are available?
Rapid-acting analogues (e.g. insulin lispro— fastest acting; peak 0– 3h after injection; last 2– 5h; give just prior to meals)
Soluble (clear) human, porcine, or bovine (e.g. Actrapid — short-acting; peak 2– 6h after injection; last 8h; give 15– 30min before meals)
Intermediate- or longer-acting (cloudy) human, porcine, or bovine (e.g. Humulin I)— peak 4– 12h after injection; last up to 30h. Taken alone, od/ bd to provide background insulin, or with short/ rapid-acting insulin
Long-acting insulin analogues (e.g. insulin glargine)— last 24h; provide background insulin; as no peak, associated with ↓ risk of hypoglycaemia
Pre-mixed— combination of short- + long-acting insulin, e.g. 30%: 70%
list some complications of diabetes
- infection/lipohypertrophy and injection sites (advise rotation)
- vascular disease - CVD, stroke - MASSIVE issue
- nephropathy
- diabetic retinopathy
- cataracts
- peripheral neuropathy / foot ulcers
how does diabetes mellitus present?
Acute - ketoacidosis or hyperosmolar non-ketotic coma Subacute - weight ↓, polydipsia, polyuria, lethargy, irritability, infections (candidiasis, skin infection, recurrent infections slow to clear), genital itching, blurred vision, tingling in hands/ feet
With complications - skin changes, neuropathy, nephropathy, arterial or eye disease
Asymptomatic - incidental finding or through risk stratification
list some causes of hyperthyroidism
Graves’ disease
Toxic nodular goitre— older women with past history of goitre
Thyroiditis - inflammation of thyroid - e.g. postpartum
Amiodarone
Exogenous e.g. thyroid replacement post hypothyroidism
Kelp ingestion
how might hyperthyroidism present?
Weight loss Tremor Palpitations Hyperactivity AF Hyperhidrosis Eye changes Infertility Alopecia
what are the management options for hyperthyroidism?
beta blockers - rapid symptom control
carbimazole - anti-thyroid meds - often given as ‘block-replace’ in combo with thyroxine
radioiodine - absorbed into thyroid then destroys it - usually become hypothyroid after so then need replacement
thyroidectomy - risk of damage to recurrent laryngeal nerve (hoarse voice) and hypoparathyroidism, might need thyroxine
symptoms/signs of hypothyroidism
symps - tired, lethargic, low mood, cold disliking, weight gain, constipation, menorrhagia, myalgia, cramps, weakness signs - BRADYCARDIC Bradycardic Reflexes relax slowly Ataxia Dry, thin hair and skin Yawning - drowsy Cold hands ± cold intolerance Ascites ± non-pitting oedema (lids/hands/feet) Round puffy face/double chin/obese Defeated demeanour Immobile ± ileus CCF
what TFT results would you expect in hyper vs hypo thyroidism?
hyper = TSH low (suppressed), T4 and T3 high hypo = TSH high, T3/T4 low
give some causes of hypothyroidism
primary atrophic hypothyroidism
Hashimoto’s thyroiditis
iodine deficiency
post-thyroidectomy or radioiodine treatment
how do you treat hypothyroidism?
replacement with levothyroxine (T4)
