Med 1 Flashcards
What is an aneurysm
•Permanent + irreversible dilation of blood vessel. Abdominal or thoracic. Dilation of all 3 layers of arterial wall. Usually asymptomatic.
SYmptoms and signs of a TAA
• Pain (severe sharp back/intrascapular), aortic regurg, systemic symptoms (eg fever if infective cause), thrombo-embolic presentation (DIC), symptoms of compression of local structures )hoarseness, cough, stridor, back pain). If dissection then the severe pain may migrate, inequal upperlimb pulses. If ruptured acute pain, collapse, shock or sudden death.
Physiology of TAA
•Probably inflammation, proteolysis, reduced survival of smooth muscle cells in aortic wall and when reached a diameter, it looses all distensibility so rise in BP can exceed arterial wall strength and may trigger dissection or rupture.
What are causes and RFs of a TAA
- Causes = genetic, CT tissue disorders (Marfan’s, Ehler’s Danlos), infections (HI), aortitis, trauma
- RFs = hypertension, increasing age, smoking, aortic valves, atherosclerosis, COPD, CKD, previous AA repair, Turner syndrome . Marfans – structural weakness in wall of aorta
IX and management for TAA
- Ix = Non acute is bloods, ECG, lung function, US, CT/MRI, coronary angiography. Acute is bloods, ECG, CT with contrast, MRI
- Surveillance, repair, replace
- Complications – dissection, rupture, AV regurg
- Surgery:Immediate(ruptured, acute symptoms), symptomatic 9regardless size), asymptomatic (>5.5cm ascending or ?6cm descending or risk of expansion big
WHat are the types/causes of chest pain
- Ischaemic cardic pain = stable angina, ACS, hypertorphic cardiomyopathy, aortic stenosis…
- Non-ischaemic cardiac = arrhythmias, aortic dissection/aneurysm, mitral valve disease
- Respiratory = pneumothorax, PE, Pneumonia, oleurisy, lung cancer.
- MSK = costochondritis , trauma, rib pain
- Breast disease / Skin – herpes zoster infection . Others – sickle cell crisis, diabetea mononeuritis
- GI = GORD, Oesophageal rupture/spasm, peptic ulcer disease, pancreatiis
- Psychological = anxiety, depression, panic disorder
Investigatiobs for chest pain
ECG, CXR, ABG, Bloods, repeat ECG/enzymes, ECHO/ETT.MPS.CTCA/Angiography/MRI, exam
What is the patho of a wheeze
•whistling sound as air passes through a narrowed airway and stops oxygen getting into bloodstream effectively so causes SOB and some chest tightness.
What causes a wheeze
- Asthma – bronchospasm. Cough, wheeze, breathless, chest tightness
- COPD – Chronic bronchitis (inflamm airways), and emphysema (damage to alveoli) mainly form smokinh
- Bronchiectasis – abnormal widening of one or more airways, extra mucus made, prone to infection, cough with sputum and possible blood.
- Bronchiolitis – infection of bronchioles, by RSV
- Inhaled objects (block bronchi), other infections, lung cancer, lung disorders
What is the pathophysiology of breathlessness
•= Body needs more oxygen so try breathe faster to increase flow of air into lungs which then goes into bloodstream and pumped round the body by the heart.
WHta are the respiratory and non respiratory causes of breathlessness
- Respiratory: Airways (COPD, bronchiectasis), Tissue (interstitial lung disease), Perfusion (V/Q mismatch), PE, PA hypertension and other.
- Non-respiratory: Hypoxia related (anaemia, HF, MI), compensatory (acidosis, anxiety)
What are the Types of Hypoxia
•Types Hypoxia: Hypoxic (not enough O2 getting in blood eg, high altitude), Anaemic(insufficient Hb), stagnant (o2 in blood ineffectively circulated, histotoxic (cells cant use sufficient O2)
What is hyperventilation
•= rate or tidal volume breathing eliminates more CO2 than body can produce. Caused by psychological stress, anxiety, head injury, resp disease, cv disease, acidosis. Might also get heart palpitations, numbness, dizziness.
What is cyanosis and the two types
•= blue discolouration skin/mucous membranes form low o2. Central (resp, CV, CNS) or peripheral (reduced CO, hypothermia)
Oxygen Therapy - basic options and target sats
- Oxygen therapy: Mostly should be 94-98% but those at risk of hypercapnic respiratory failure (Eg COPD) needed 88-92% as chronic CO2 retainer so less sensitive response to CO2 and need hypoxic drive.
- Nasal cannula up to 4L, Venturi mask (controlled), simple mask (highly variable 1-15L O2), non re-breathe mask (high percentage O2) 10L/15L
What is COPD?
•COPD =
- Airflow limitation + destruction of lung parenchyma. Increased mucus secreting goblet cells in bronchial mucosa and bronchi can become overly inflamed with pus in lumen.
- Decreased mucociliary clearance so increased risk resp infections and need abs and routine vaccinations.
- Microscopic – inflammation, scarring thickening of walls airways, loss elastic recoil, V/Q mismatch
RFs of COPD
•RF = Smoking (over distention of lungs as loss surfactant), Alpha-1-antitrypsin deficiency (inhibits proteolytic enzymes which can destroy alveolar wall CT)
Symptoms and Signs of COPD
- Symptoms = Productive cough with white or clear sputum, wheeze, breathlessness usuallya ftermany years of smokers cough. Colds settle on chest, can have hypertension, osteoporosis, depression, weight loss, reduced muscle mass.
- Signs = May be none or quiet wheezes through chest and in severe then tachypneic with prolonged expiration and accessory muscles, hyperinflated lungs. HF/oedema are terminal events and respiratory failure.
- Pulm Hypertension – cor pulmonale in advanced copd (sign of fluid overload secondary to lung fisease) and RV hypertrophy.
- FEV1<70
Invetsigations for COPD
•Ix = lung function tests (FEV1:FVC reduced), CXR (flattened diaphragms), high res CT, Hb level, packed cell vol (can be elevated), blood gas, sputum exam, ECG normal, ECHO, a1 antitrypsin level
Management of COPD
•Mx = Reg ass lung function -> smoking cessation -> pneumococcal and annual influenza vacc -> SABA bronchodilator for acute relief, LABA -> add in muscarinic bronchodilator -> consider theophylline or Combo ICS + LABA -> Pulm rehab -> eval+ treatment of hypoxaemia -> lung reduction surgery/ transplany.
Pathology of Ischaemia heart disease
- Atheroma: endothelial dysfunction -> monocyte adhesion/emigration, smooth muscle cell migration to intima, smooth muscle cell migration to intima and proliferation, ECM elaboration, lipid accumulation, inflammation, plaque growth.
- Patho: Coronary arteries become blocked with atheroma.
Symptoms of Ischaemic heart disease
•Symptoms = Chest pain (Angina/HA, central crushing), breathless, tired, dizzy palpitations
RFs of Ischaemic heart disease
- Diabetes – High blood glucose can damage blood vessels and the nerves that control your heart and blood vessels and over time this can lead to heart disease
- Obesity – Fatty material builds up in arteries and this can lead to heart attack.
- High LDL + triglycerides and low HDL linked to heart disease
- HBP (make arteries less elastic, decrease flow blood + o2 to heart and hear disease.
- smoking FH heart disease, inactivity
Invetsigations for Ischaemic heart disease
•Specialist IX= CT with contrast. Coronary angiogram if blockage then angioplasty
Complications of Ischaemic heart disease
•Complication -> ACS ( Unstable angina, NSTEMI, STEMI)
Stable Angina - what is it and how does it occur?
•Stable angina= (fixed atherosclerotic plaque)-> unstable plaque with platelet aggregation (unstable angina) -> plaque ruptures (thrombus which is NSTEMI and STEMI)
What are the signs + symptoms stable angina
•S/S = breathless, chest pain, nausea, ehart murmurs, sweaty, fever, acute confusion, syncope…
Invetsigations for stable angina and the scorign system
- Ix = bedside (obs, ECG, BM), bloods (routine + cardiac enzymes, amylase), image (CXR), Special (ECHO, Angiography)
- TIMI scoring = risk cardiac events in next 30 days. Age>65, known CAD, aspirin in last 7/7,s evere angina (>2hrs in 24hrs), ST deviation>1mm, elevated torponins, >CAD RFS
Acute coornary syndrome - what makes up this and the general management
- Unstable angina, NSTEMI, STEMI
- MX = MONAC: •Morphine (5-10mg slow IV injection), Oxygen, Nitrate (GTN spray), Apsirin (300mg chewed), Clopidogrel (or fondaparinx etc and antiemetic).
What is heart failure
- HF = Complex syndrome that can result form any structural or functional cardiac disorder that impairs the ability of the heart to function as a pump to support physiological circulation. Decreased CO, increased venous congestion so increased afterload/preload and increased cardiac work.
- CO = MAP/TPR
Causes and RFs of HF
- Causes: Mainly ischaemic heart disease, cardiomyopathy (dilated- many caused like infection, infiltrative) + hypertension. Also get valvular heart disease (endoc, degenerate, congenital). RHF (RV infarct, pulmonary hypertension, PE, COPD),
- RFs = Age >65 (weaker, stiffer heart), FH, genetics, lifestyle, medical conditions, race, sex (men at younger)
Symptoms/Signs of HF
- Symptoms – Exertional dyspnea, orthopnea, paroxysmal nocturnal dyspnoea, fatigue. Oedema (cant pump blood effectively so backs up causing oedema).
- Signs – Tachycardia, elevated JVP, cardiomegaly, 3/4h heart sounds, bi-basal crackles, pleural effusion, peripheral ankle oedema, ascites, tender hepatomegaly
- NY Heart Association classification = I (no limitation), II (marked L- fine rest, nroml activity produce fatigue), III (marked L – gentle PA produced marked symptoms), IV (HF symptoms at rest then exacerbated).
- HR-REF (Symptoms, signs, reduced LV ejection), HR-PEF (S/S, normal/mildy reduced LV ejection fraction, no LV dilation, relevant structure disease + diastole dysfunction)
Invetsigations for heart failure
•Ix = Bloods, CXR, ECG, ECHO, nuclear cardio, cardiac MRI, cardiac cath, cardiac biopsy, CP exercise test, 24h ECG.
NP ProBNP in HF and referrall criteria
•NTProBNP = >2000 urgent specialist ass within 2w, >4000, further assessment CXR,12LECG, ECHO
Heart fialure effect on sodium
•Patients with heart failure may exhibit hyponatremia due to a decrease in water excretion, which may be related to the enhanced release of both angiotensin and vasopressin and can be exaggerated by diuretic therapy. Along with potassium and calcium, magnesium influences cardiovascular function.
Cardiomyopathy - the Types
- Dilated cardiomyopathy = LV enlarged, cant effectively pump blood out of heart, mostly middle aged men from CAD/MI and genetic defects
- Hypertrophic cardiomyopathy = Abnormal thickening of heart muscle so harder for heart to work. Mostly affects LV. More severe if childhood, often FH.
- Restrictive cardiomyopathy = Heart muscle becomes stiff and less flexible so cant expand and fill with blood between heartbeat. Least common, often in older and can be idiopathic or from amyloidosis.
- Arrhythmogenic RV dysplasia = rare, RV muscle replaced by scar tissue so hert rhythm problems, often genetic mutations.
Presentation of cardiomyopathy
•Breathless, swelling legs/ankles/feet, bloating abdo from fluid, cough when lying down, difficulty lying flat to sleep, fatigue, heartbeats feel rapid/pounding/fluttering, chest discomfort or pressure, dizziness/lightheadedness/fainting
RFs of cardiomyopathy
•RF = FH, long term HBP, Conditions affecting heart, long term lcohol abuse, obesity, drugs, cemo drugs, diseases like diabetes/amyloidosis/Ct disorder etc.
Complicatiosn of cardiac myopathy
•Complications = HF, blood clots, heart valve problems, cardiac arrest, sudden death
Dx of cardiomyopathy
•Diagnosis = CXR, ECG, ECHO, treadmill stress test, cardiac catheterisation, cardiac MRI, Cardiac CT, bloods, genetic testing or screening
Treatment of cardiomyopathy
•Tx = Manage S/S, prevent worsening, meds to improve heart pumping/blood flow, lower BP, remove extra fluid, prevent blood clots. Therapies (septal ablation, radiofrequency alation). Surgery (Implantable cardioverter defib, ventricular assist device, pacemakers. Septal myectomy heart transplant.
How do to BLS
Valvular Heart Disease - wat is it and what causes it?
•Valvular heart disease = any heart valve damage or diseased. They become leaky and cause regurgitation and not enough blood can be pushed forward through the heart.
•Causes:
- Rheumatic Heart disease – after infection form bacteria that causes strep throat is not treated with Ab. Can causing scarring of heart
- Endocarditis – infection of endocardium caused by severe infeciton in bloods
- Congenital heart disease 0 malformations e, missing a leaflet
- Heart disease- HF, Atherscleroisis, TAA, HBP, MI
- Marfans syndrome, autoimmune (like lupus), high dose radiation exposure, ageing.
Symptoms of valvular heart disease
•Symptoms = SOB, chest pain, fatigue, dizziness or fainting, fever, rapid weight gain, irregular heartbeat.
Dx od valvular heart disease
•Dx – listen to heart (Murmurs), and ECHO.
Treatment of valvular heartd disease
•If not severe then medicines to treat symptoms. If more serious then surgery such as replacement in open heart surgery or not open heart.
Why does CT disease lead to valvular heart disease
•CT disease – Marfan syndrome leads you to be at an increased risk of heart valve disease due to structural weakness in the wall of aorta. Also more at risk of aortic aneurysm and aortic dissection.
How can muscular dystorphies lead to repsiratory failure
•Muscular dystrophies can lead to respiratory failure due to inability of respiratory system to provide proper oxygenation and CO2 elimination.
What is pharmacogenetics
•Pharmacogenetics = Study of how genes affect a personsresponse to drugs. Combines pharmacology and genomics to develop effective, safe medications and doses that will be tailored to persons genetic makeup
What is gastroenteritis and what can be a cause/RF
- Gastroenteritis – non specific term used to describe condition where combination of nausea, vomiting, diarrhea and abdominal pain.
- Causes- Viral, bacterial, parasitic pathogens
- RFs – Poor personal hygiene and lack of sanitation, compromised immune system, achlorhydia, poor cooked food, travelling.
Presentaiton of gastroenteritis
•– incubation for viruses usually day, for bacterial dysentery few hours to 4days and parasites can be 7-10days. In this country usually rotavirus but norovirus is known as winter vomiting bug. Blood diarrhea espect bacterial, esp E.Coli 0157.
How to asses and investigate gastroenteritis
- Ass – temp, BP, pulse, RR, abdo exam to exclude other, assess for dehydration. Can range form mild (lightheaded, anorexia) to severe (weaknes,s confusion, shock)
- Ix – stool culture (unwell, blood, mucus, suspected food poisoning, recent Abs/PP, hospital admission, been abroad, recurrent diarrhea not improving, uncertain about diagnosis). Bloods for unwell etc
Treatment gastroenteritis
•Tx – advice on preventing dehydration, leaflets, NOT drug treatment with antidiarrheal/antiemetics (not usually recommended nor Abs). Hygiene advice, don’t attend work until 48horus after lats episode.
CV compensatory mechanisms in anaemia
- CV compensatory mechanisms = Tachycardia, increase CO, hyperdynamic state due to reduced blood viscosity and vasodilation to enable tissue perfusion.
- Anaemia leads to tiredness and breathlessness
Pneumococcal vaccine
•Pneumococcal vaccine – protects against pneumococcal infections caused by bacterium streptococcus pneumonia which can lead to pneumonia, blood poisoning (sepsis) and meningitis. For those higher risk so babies, 65+, long term health conditions. Inactivated
TB Vaccine
•TB vaccine – BCG vaccine – For babies up to 1year where TB rates high, close relatives in a country with high rate or close contact of someone infectious. Also 16 and under for similar reasons. For adults its 16-35 when high risk from work. Small scar. Weakened strain Tb bacteria.
How is HIV transmitted
•Transmission = sexual, perinatal, blood transfusion, sharing needles, occupational
SYmptoms of HIV
- Most infectious shortly after infection and many unaware till later stages
- First few weeks after infection – influenza like illnesss (fever, headache, rash, sore throat),seroconversion illness
- As infection progressively weakens immune system – swollen lymph nodes, weight loss, fever, diarrhea, cough
- Without treatment – risk severe illness like TB, cyptococcal meningitis, severe bacterial infections, lymphomas and Kapoi’s sarcoma.
COmplications and presentations of hIV
- Karposi’s sarcoma – HHV-8, purple/brown lesions/patches on legs, mouth, genitalia
- Oral Hairy leucoplakia – EBV, white patches on tongue can’t be scraped.
- Esophageal candidiasis – white plaques on mucosa, scraped off, pain eating/drinking.
- Cryptosporidium – Protozoan infection through ingestion contaminated water.food. Abdo cramo, diarrhea, weight loss
- Toxoplasmosis – protozoan parasite, commonest cause brain lesion in HIV Fever, seizures
- Shingles – herpes zoster infection. Painful vesicle lesions.
- Pneumocystitis jiroveci pneumonia – dyspnea, fever, malaise alveolar infiltrates on CXR
- Progressive multifocal leukonencephalopathy – from kc virus, muscle control loss, paralysis, blind, speech problems…
- Mycobacterium TB - cough, tired, weight loss, fever, haemoptysis, night sweat. Acid fast bacilli
- CMV – herpes virus. Viral infection that can cause pneumonia, colitis, encephalitis, retinitis
- Ryptococcus neoformans – commonest cause meningitis in hIv people.
Primary immunodeficiency syndromes
- Primary immunodeficiency syndromes: Mostly inherited single gene disorder that present in infancy/early childhood. B cell/ t cell defects. B cell immunodeficiencies (adaptive) – loss antibody production, severe recurrent bacterial infection risk
- T cell IDs (adaptive) – killing activity disrupted and problems with B cell function
- SCID – complete lack T cells and variable number B cells so little to no immune function.
- Phagocyte disorders (innate) – bacterial and fungal are serious
- Complement defects (innate) – can lead to SLE, RA.
Secondayr immunodeficiency
- Secondary Immunodeficiency – many possible causes. Environmental factors (HIV/AIDS or malnutrition) , in hematological malignancies.
- Malnutrition – t cell numbers + function decrease in proportion to levels protein ef so susceptible to diarrhea an dRTIs
- Drug regiments – immunosuppression
- Chronic infections – AIDS from HIV infection
Presentaiton o immunodeficiency and what to ceck in history
- Presentation: frequent infections (opportunistic, severe/persistent bacterial, common gI symptoms. Neuro problems, autoimmune problems
- History – check FH, RFs, history adverse reactions, previous antibiotic prescriptions.
What is a lympoproliferative disorder
•Lymphoproliferative disorders = uncontrolled production lymphocytes that cause monoclonal lymphocytosis, lymphadenopathy and bone marrow infiltration. Often in immunocompromised.
how is malaria transmitted and the incubation period
- Transmission – bite infected by female mosquito. Lifestyle has blood and liver stages.
- Incubation period 7-30days
Early symptoms of malaria and the complciations
- Early symptoms – fever, chills, sweats, headaches, muscle pains, nausea, vomiting.
- Severe malaria/complciations – primary by plasmodium falciparum. Confusion, coma, neurological focal signs, severe anaemia, resp failure. RFs are <5, pregnancy, low endemic area travelers.
5 species of mosquito
•5 species = Plasmodium falciparum (highest mortality rate) plasmodium ovale (latent liver stage), Plasmodium vivax (latent liver stage), Plasmodium malariae not latent stage, but can persist for 30days), plasmodium knowlesi (only species with animal reservoir).
Diganosis malaria
– demonstration parasites on blood film or detection of antigens using immunochromatographic tests.
Treatment malaria and prevention
- = depends on severity, species, likelihood resistance.
- Severe – IV artesunate
- Non-severe – options include ACT, quinine, chloroquine, doxycycline. P vivax and P ovale – need to treat latent liver stage to prevent relapse (primaquine)
- Prevention – Anti-malaria prophylaxis, insecticide treated bed nets, long clothes + insecticides, residual indoor spraying, larvicidal agents, intermittent preventative therapy. New is vaccination
What is sinus rhythm
Signal originates SA node -> depolarize R/L atrium -> reaches AV node + pass to ventricles -> travels from HIS bundle to L/R bundle branches into purkinje fibres.
What does each part represent on this ECG
What is First degree AV block?
= impulses take longer to pass through AV node. Prolonged PR interval >200ms. One P wave for every QRS
What is second degree AV block
- AV node intermittently fails to conduct impulses. Not every P wave produces a QRS. Two types:
- Mobitz I (Wenkebach) = AV node does not recover fully following conduction of impulse. PR interval prolongs gradually. Eventually QRS dropped as AV node unable to conduct
- Mobitz II = AV node unable to conduct impulses at regular interval, normally 2:1, also can be 3:1, 4:1 Etc.
What is third degree AV block
•Third Degree AV Block = Complete heart block, the AV node is unable to conduct impulses from the atria. No relationship between P waves and QRS complexes.
Why might the ST segment be elevated and why might it be depresseed
- ST elevation – Acute MI, coronary vasospasm, pericarditis, benign early repolarization, LBBB, LV hypertrophy…
- ST depression – MI/NSTEMI, reciprocal change in STEMI (posterior MI), digoxin effect, hypokalaemia, SVT, RBBB, RV hypertrophy.
4 main phases in cardiac cycle
Cardiac cycle:
- Ventricular filling – Ventricular diastole, atrial systole
- Isovolumetric contraction – ventricular systole
- Ventricular ejection – ventricular systole
- Isovolumetric relaxation
What is atrial fibrillation
• Irregularly irregular QRS rhythm (can have fast or slow ventricular response), no clear P waves. Need amiodarone, cardioversion, anticoag. Chaotic rhythm in atrium, microcirucits so bombardments of AV node hence irregular rhythm. Not constant as around AV node is refractor period (cells recovering) and atria cant contract in coordinated manner hence no PV wave.
Atrial fibrillation
Atrial flutter
Invetsigations of AFib
•After ECG then History + CV exam, pulse + BP (manual), FBC, coag profile, renal function + electrolytes (potassium, calcium, magnesium), thyroid and liver function, CXR, ECHO
Types of AFib and causes
- Types/Definitions: First diagnosed, paroxysmal (<7days), persistent (>7days), long standing (>12m), permanent (accepted by patient and physician.)
- Causes – Surgical sieve. CV (hypertension, valvular hear disease, CAD), Resp (infection, PE, COPD), metabolic (thyroid, autonomic), other (sepsis).
Causes of AFib
•Surgical sieve. CV (hypertension, valvular hear disease, CAD), Resp (infection, PE, COPD), metabolic (thyroid, autonomic), other (sepsis).
How to decrease stroke risk with AFib and what do we use to estimate the risk
NOACs (for stroke risk), Vitamin K antagonist (Warfarin) aim INR 2-3, LMWH.
SYmptoms of AFib
•most-> least common) – palpitations, breathless on exertion, light-headed, breathless on rest, chest tightness, syncope. Check if hemodynamically stable
Management Atrial Fibrillation
•Mx: Thromboembolic Risk assessment. Rate vs rhythm control. B, blockers, CCB, digoxin. Cardioversion (if <48hrs otherwise give anticoag first). Amiodarone.
Describe Atrial flutter and what causes it
- Saw tooth pattern irregularly regular. Short circuit in the heart causes atria to pump rapidly. Managed the same as atrial flutter.
- Re-entrant circuit in the LA or RA. Atrial rate about 300bpm. Ventricular rate can be regular or irregular.
- Causes - Surgical sieve. CV (hypertension, valvular hear disease, CAD), Resp (infection, PE, COPD), metabolic (thyroid, autonomic), other (sepsis).
- Risk of clot formation like atrial fibrillation
WHat is broad complex tachycardia and what are the causes
Broad complex Tachycardia – 3 or more successive beats at >120bpm. AV dissociation. QRS >120ms, ventricular rate >120bpm. Can be monomorphic or polymorphic. Concordance of the chest leads. Can be sustained >30secs. Potentially life threatening and can quickly degenerate into VF. Causes include LQT, Electrolyte disturbances, cardiomyopathy, acute MI, IHD. Include VT and VF below. Need drugs, cardioversion and pacing.
Ventricular Tachycardia and the consequences
•Broad complex tachycardia originating in the ventricles. May impair cardiac output with consequent hypotension, collapse and acute cardiac failure. This is due to extreme heart rates and lack of coordinated atrial contraction. Decreased CO may result in decreased myocardial.
Describe Ventricular fibrillation
•Most important shockable cardiac arrets rhythm. Ventricles suddenly attempt to contract at rates up to 500bpm. This rapid and irregular electrical activity renders the ventricles unable to contract in a synchronized manner, resulting in immediate loss of cardiac output. The heart is no longer an effective pump and is reduced to a quivering mess.
Descrieb Atrial tachycardia
•– depolarization of atrial form ectopic focus. Rate between 120-200bpm. Can have AV block.
What are atrial ectopics
• (Atrial Extrasystoles), Supraventricular extrasystoles (SVE), atrial premature beats (APB). A pwave earlier than expected usually with a QRS following. Can sometimes flal in refractory period, resulting in no QRS.
What are ventricular ectopics
•An early broad QRS without preceding P wave (P wave can follow QRS if VA conduction occurs). Can be unifocal or multifocal. Can be single or more frequent (Couplets/triplets/salvo, bigeminy, trigeminy). Also known as ventricular extrasystole, premature ventricular beats.
What can a broad QRS complex idnicate and hwo to distinguish between the differentials
- Left bundle branch block: Broad QRS>120 dominant QS/Rs in . Broad dominant RsR in V7. V1 neg has to be LBBB
- Right bundle branch block: Broad QRS>120 dominant R wave in V1 and Slurred S wav in V6. V1 positive has to be RBBB
- Cant really analyze T waves and ST segment with BBB as this masksproblems
- With axis deviation look at axes on ECG written which should be -30 to +90.
What is a STEMI and what does it look like on an ECG
•ST Elevation MI (STEMI): Due to area of cardiac muscle having reduced flow of blood leading to necrosis. After the MI Q waves and T wave inversion can normally be seen in the region. Patient symptoms and troponin levels.
On an ECG and leads etc what areas do they correspond to
Describe NSTEMI and the appearance on an ECG
•NonST Elevation MI (NSTEMI): Necrosis of cardiac muscle in the absence of ST elevation with elevation of cardiac markers. Blood test for Troponin levels. ST depression/ T wave inversion on ECG. Patient symptoms (SOB, tightnes,s pain, dizzy, sweating, lightheaded, grey, clammy etc)
What is ischaemia and how does it typically show on an ECG
•Ischaemia: Reduced flow in coronary arteries. Eg, stable to unstable angina. Can be treated with GTN spray to help dilate the artery and increase blood flow. Shows typically as ST depression/T wave inversion on ECG.
WHat is meningitis and the msot common pathogens
- Meningitis = inflammation of the tissues around the brain.
- Most common = Neisseria meningitidis (meningococcus). Less common are Strep penumoniae, Hib, E.Coli
- Viral meningitis – more common and complication of various viral illness and less severe than bacterial.
- Rare causes – fungal/TB.
What are the symptoms of meningitis
•Symptoms = Often develops quickly.
- Common early warning symptoms – generally unwell, leg pains, cold hands/feet, pale colouraround lips.
- Rash. In meningococcal. Red/urple, small blotchy dots. Do not fade under pressure. Also sign sepsis.
- Other symptoms (babies) – excessive crying, fats breathing, high temp, wont take feedsmirritable, drowsiness, bulging fonanelle.
- Older children/adults – High temp, shivering, stiff neck, headache, fast breathing, aches/pains, pale or blotchy or blue skin, photophobia, drowsiness or confusion, repeated vomiting
What is the diagnosis for meningitis
•Dx = Bloods, lumbar puncture, CT/MRI,
Treatment for meningitis, the prveention and process for contacts
•Tx =
- Bacterial – antibiotic injections. Fluids, O2, possible steroid injections, ICU. Complications are hearign loss, learning problems, epilepsy, kidney problems, joint or bone problems
- Viral – antibiotics when cause not known but when know viral then stop Ab and let body clear it. Most make full recovery.
•Prevention – meningitis vaccine and immunization (Hib, GB/C meningococcus, pneumococcus, mumps.
•Contacts – increased risk (household or intimate kissing within 7days). Short course Abs to prevent possible infections and also offer GC meningococcus.
Describe the symptoms of UTI/Cystitis
•Pain during urination, increased need to urinate and blood in urine. Urine may also be cloudy and/or smeloy with possible pain in tummy and more tired. Drink water and if don’t go away Abs.
What are the common symptoms of skin infections, and some common examples
•Skin infections: Swelling, redness, heat then pain and pus or weeping from the wound.
- Impetigo – affects epidermis, mostly in children (honey crusted lesions around mouth)
- Cellulitis – dermis + subcutaneous tissue in uclers or surgical wounds.
- MRSA superbug on small score on skin and can spread.
Common repsiratory infections and symptomd
•Respiratory infections: Coughs/colds, pneumonia (cough, thick mucus, rapid HR, fever, breathless, sweat, shiver, chets pain).
What are common symtpoms of STIs
: Chalmydia, Gonorrhea, mycoplasma genitalium, syphilis, bacterial vaginosis and pelvic inflammatory disease.
Abdo pain, bleeding between periods, fever sores, painful intercourse, painful urination, pus like discharge, swelling or tenderness of vulva, anal itching, painful bowel movements
What are the 4 main causes of infection
- Bacteria – 1 of 3 domains of taxonomy. Single celled organisms with phospholipid bilayer membranes. Only tiny subset infect humans.
- Fungi - on of the 5 kingdoms of eukaryotes. Usually divided to moulds vs yeasts.
- Viruses – Non-cellular, replicate inside living cells of cellular organism.
- Parasites – loose term covering various non-closely related, multicellular organisms.
Describe cellulitis, IX and Tx.
•Skin and superficial soft tissue infection, usually staph aureus or other strep. Red, hot, tender, swollen area tissue, Edges infective areas well demarcated. Usually unilateral. Need to ix with swabs, cultures, bloods, imaging (US/MRI). Mark borders, Give Abs if severe (flucloxacillin usually) and possible surgical debridement if spreading.
Describe necrotising fasciits, the symptoms, IX and Tx
•Severe soft tissue infection caused by G A strep. Release of toxins by S/pyogenes exacerbates extent of tissue damage by infection. Hot, red, swollen area of skin with necrotic tissue and severe pain (extends further than rash)with poorly demarcated edges and purple/black tissue areas. Skin swabs which are sent for MC&S. Need broad spectrum IV Abs, analgesia, IV fluid and surgical debridement and possible amputation
Chronic venous changes - signs and symptoms
•Chronic Venous Changes: Lipodermatosclerosis: from chronic inflammation and fibrosis of dermis and subcutaneous tissue of lower legs. Characterized by painful inflamm above ankles. Oedema + hemosiderin deposition (brown discoloration). Almost always bilateral.
Symptoms of DVT and IX
•DVT – Red, hot swollen unilateral LL. Calf tenderness (thrombophlebitis) and possible two grade pyrexia. Need doppler US imaging, D dimer, WELLS score.
What are myeloproliferative neoplasms
•Myeloproliferative neoplasms – group rare disorders of bone marrow that cause increase in number of blood cells. Most people ar eover 60years old.
What is percarditis and the symptoms
- Pericardial disease (pericarditis) = inflammation of any of the layers of the pericardium (thin tissue sac surrounding the heart).
- Pericarditis causes sharp chest pain when irritated layers of pericardium rub against each other. Usually mild and goes away without treatment
What is the pleural space and whata re the two types of pleural fluid
•Pleural space = lubricate visceral and parietal pleura to allow sliding as lungs inflate and deflate. To help create vacuum as we breathe in order to suck air in.
•Pleural fluid production 15ml/day, absorption 15ml/day, drainage by lymphatic pump and max drainage 300ml ish a day/ Can increase flow rate if increased production.
•Transudate: Low fluid protein (fluid protein/serum protein <0.5, protein less than 25). Low LDH – (fluid LDH/Serum LDH<0.6)
•Exudate: High fluid protein (fluid protein/serum protein >0.,5, protein greater than 35). High LDH (fluid LDH/serum LDH>0.6)
Benign pleural disease- what is this
•Benign Pleural Disease: Pleural plaques. Indicator for asbestos exposure. Not eligible for compensation unless associated asbestos or development of mesothelioma.
What is mesothelioma and the bigegst RF
•Mesothelioma = Malignant tumour of serosal surfaces (mostly pleura) usually resulting from asbestos exposure. Median survival 9-12m from diagnosis. Identification of asbestos exposure is essential for claiming compensations.
Pleural effusion - what is the pathology and causes
•Patho = When rate of production of pleural fluid exceeds the rate of reabsorption of fluid leading to accumulation of fluid in pleural space (contains 1-20ml fluid).
•Causes:
- Transudates – fluid leaks into pleural space from elsewhere. Too much fluid in body (HF, renal failure, liver cirrhosis), fluid leaking from elsewhere (hypoalbuninaemia, ascites/peritoneal dialysis) or hypothyroidism, Meigs syndrome, PE
- Exudates – Too much fluid produced/ failure of reabsorption due to damage to pleural surface. Pleural malignancy (primary or secondary), pneumonia, TB, empyema, pulmonary infarction, ct disease, pancreatitis.
History of symptoms and signs for pleural effusion and what you would see on a general exam
- History – progressive breathlessness (days to weeks), may have pleuritic chest paina nd often cough (dry or white phlegm). Also symptoms underlying cause (weight loss, haemoptysis, fever, ankle oedema).
- Sign – reduced chest wall movement, Reduced TVF, dull percussion not, reduced air entry. Reduced vocal resonance
- General Exam – breathless, hypoxia, evidence underlying causes (cancer, CHF, Signs liver disease)
Invetsigations in pleural effusion
•Ix – History + exam, bloods (normal and LDH, Abs, amylase..), CXR, pleural US, consider CT chest.
Management in pleural effusion
- Thoracentesis pleural aspiration = US guided, pass needle into pleural fluid and aspirate a sample.
- Ix – Biochem (LDH+ protein), MC&S, cytology, pH (low pH- less than 7.35-45 indicates parapneumonic one so needs draining as may have pain/trappe dlung) and possibly Colour, viscosity, smell, glucose-RA ,cytology, extra (amylase, triglycerides), Acid fast bacilli+TBculture, ADA
Lights criteria for if pleural fluid is exudate
•Lights criterial for if fluid is exudate: Pleural fluid protein/serum protein >0.5, LDH/Serum LDH>0.6, Pleural fluid LDH>2/3 upper limit of lab normal value for serum LDH
WHat to do with a unilateral pleural effusion
•BTS algoritm. Suggest transudcate, treat cause and if not resolved then chets physicicana dnpleurla aspiration and if no answers then CT thorax. Then consider LA thoracoscopy or surgical VAT3 or radiologically guided pelural biopsy. Still not fund then HF, PE etc checl and wait.
What is a pneumothorax and the 2 types?
•Pneumothorax = Air enters pleural space from outside the chest or form the lung itself via mediastinal tissue planes or direct pleural perforation. Intrapleural pressure increases and lung volume decreases.
•Primary spontaneous – no underlying disease, usually form rupture of pleural blebs that lie within or immediately under visceral pleura. Second-hand smoke, air poll, genetic predisposition, underlying CT disorder etc.
•Tx = if >2cm + breathless, needle aspirate and unsuccessful then chest drain + admission, Otherwise small then consider discharge review. Hospital stay 4-8days.
•Secondary spontaneous penumothorax – discernible lung disease
•Tx = If >2cm + breathless then chest drain, if 1-2cm then aspirate and smaller then high flow O2 unless O2 sensitive and observe. Minimally symptomatic need no treatment, usually admit for obs and/or drain
HPC of pneumothroa and PMH RFs
- HPC – pleuritic chest pain- suddent onset, breathlessness, “pop” sensation, sometimes trigger like heavy lifting.
- PMH= previous PTX, COPD, Alpha-1-antitrypsin def, underlying lung disease
Signs on examination in pneumothorax
- General – breathless, inhalers/o2 conc, nicrotine replacement patches etc, drains, Obs/vitals.
- Respiratory = trachea, reduced chest wall movement/expansion, acc muscle use, intercostal/subcostal recession, hyper-resonant note, absent breath sounds.
- CV (displaced apex beat, murmurs (Marfans). Tall stature, high arched palate, thumb sign etc
recurrent pneumothroax - what to do
Surgical candidates – pleurodesis, bleb/bulla losure, lung vol reduction. Non surgical candidates (chemical pleurodesis) – tetracycline derivatives, Talc, others. .
What general invetsigations might you do for URTi and general symptom
- General: Throat swab x2, 1 direct exam, 1 culture, nasopharyngeal aspirate, Bloods, Microscopy, culture
- URTI/LRTI: Strep pneumoniae+VE COCCI, H.Influenzae –VE BACILLI, Staph Aureus +VE COCCI, catalase, coag positive, Gram-VE also E.Coli, Klebsiella, pseudomonas
- Cough, sore throat, running nose, nasal congestion, headache, low grade fever, facial pressure.
Descrieb tonsilitis symptoms and common cause
•red, swollen, white tonsillar exudate (bacterial or EBV), surrounding LN enlargement, halitosis, cough, runny nose. Commonly G A strep or viruses.
Describe peritonsillar abscss and the IX and MX
•complication acute tonsilitis, pus collects in peritonsillar space. Mostly G A beta-haemolyticstreptococci. Odynophagia with poss referred ear pain. Uvula deviation, hot potato voice. Throat swab, monospot, EBV Abs, bloods. Liverpool peritonsillar abscess score. Analgesia/IV fluids, Abs, corticosteroids. Surgery for aspiration, incision and drainage.
What is pharyngitis and the common causes
•Pharyngitis – ‘sore throat’. Many causes. Rhinitis or common cold – mostly viruses.
Sinusitis - what it is, symptoms, IX.
– infection of paranasal sinuses. RFs like septal deviation. Acute is mostly viruses like RSV or bacterial like strep pneumonia, H.Influenza. Chronic is oblihae anaerobes, staph aureus. Symptoms/Dx–Acute <4w, subacute 4-12, chronic >12. (sudden onset >/2 symptoms): nasal blockage/obstruction/congestion, +/- facial pain/pressure, +/- anosmia/hyposmia, +/- cough. Anterior rhinoscopy (swelling, erythema, pus, polyps.) 10days bacterial. Elevated CRP/ESR, deterioration, severe local pain, purulent discharge is bacterial.
Laryngitis - symptoms, causes, IX
•Can lead to oedema of true vocal cords. Often hoarseness over period <7days usually preceded by viral URTi and self limiting. Also aphonia dysphagia, dyspnea, increased saliva…Check airway. Viral/bacterial/fungal. Non infectious is inhaled fumes etc. Diagnosis (laryngoscopy -oedema + erythema true vocal cords, secretions in glottis), chronic TB laryngitis (lesions), reflux (no exudative change), oropharyngeal cultures, nasal swab.
Laryngotracheobronchitis
•– Croup - <3yrs, inspiratory stridor, hoarseness, fever, cough, coryza. Parainfluenza mostly,. Needs corticosteorids, epinephrine, mechanical ventilation sometimes. Steeple sign.
Epiglottitis - symptoms causes, MX
•Oedema + inflamma. 2-6yrs. Dyspnoea, dysphagia, drooling, dys[honia, inspiratory stridor, fever. Hib in unvaccinated. Notify ENT don’t look in mouth, nebulized adrenaline, IV Abs, fluids and secure airway.
LRTi - Bronchitis vs Bronchiolitis
- Bronchitis (inflamm of bronchus)– extension of URTi or bacterial agents directly like Bordetella. Fever, productive cough, dyspnea, wheeze in those with asthma. CXR, sputum culture, pulmonary lung function, CT scan. Chronic >3m in year for 2+years. Bacterial or viral or non-infectious like irritant exposure.
- Bronchiolitis – Inflammation bronchioles – presents as acute viral infection less than 2 years. Acute onset wheeze, dyspnea, cough, rhinorrhoea, respiratory distress. Mostly RSV
What are the main types of pneumonia
- Pneumonia – inflammatory condition of lung parenchyma (alveoli) so alveolar filling with fluid (consolidation). Most common is strep pneumonia.
- CAP: Acute infection in those not in hospital or long-term care for >14 days before onset symptoms. Spread by resp droplets.
- RFs – extremities age, comorbidities, resp conditions, lifestyle, iatrogenic
- Types – pneumococcal typically acute onset + high fever but atypical (mycoplasma pneumoniae, chlamydophilia pneumoniae and legionella penumophilia) tend to be slower onset, more extrapulmonary symptoms and don’t respond to penicillin’s (macrolides+ doxycycline)
- HAP – 48 or more after admission. New onset cough, purulent sputum, Xray with consolidation. HCAP- non-hospitalized but recent +substantial healthcare exposure. Empirical therapy (-VE=piperacillin-tazobactam or meropenem and +VE=vancomycin). Then definitive. Noocomial infection ishealthcare acquired.
- VAP – 48+ hours after endotracheal intubation
- Aspiration pneumonia – chemical pneumonitis as food inhalation promotes infective environment. Mostly in right lung.
- In immunocompromised – opportunistic pathogens like pneumocytis pneumonia. Try do indirect immuno-fluorescence on induced sputum or bronchoalveolar lavage fluid.
Signs and invetsigatuons of pneumonia
•Dx = Fever, brethless cough (+sputum_, pleuritic chest pain, SOB. Reduced chest expansion, dull percussion, increased vocal resonance, coarse crackles, temp, low O2 and new unexplained xray shadows.
•Ix = Bedside (Obs, NEWS, sputum, ECG, Urine antigens (atypical suspicious), Bloods + cultures if pyrexial, CXR (consolidation) and sometimes bronchoscopy/bronchiolar lavage or pleural fluid aspiration.
CURB 65 score and implications
•CRUB 65 = Confusion, Urea>7, RR>30, BP<90/<60, >65y/0. = 0-1 (Oral Ab home), 2(oral Ab inpatient), 3(admit, IV Abs, urgen senior review), 4-5 (IV Abs, ITU)
Complications of pneumonia
•Complications = Effusion, empyema (infective infusion, need USS guide chest drain) lung abscess, pericarditis
The differentce between infection, SIRS, sepsis and septic shock
- Infection = invasion of the body by pathogenic microorganisms causing tissue damage and disease
- SIRS = systemic inflammatory response syndrome in response to infective or non infective insult. Dysregulated inflammation where physiological mechanisms of repair go into over drive.
- SEPSIS = life threatening organ dysfunction caused by dysregulated host response to infection. Presence of SIRS with evidence of infection. Ongoing vasodilation, capillary leak, inflammatory response leads t o hypoperfusion (low GCS, lactic acidosis). Think sepsis when 3= in one parameter NEWS and known infection.
- Septic shock = Sepsis with persisting hypotension despite fluid correction + inoptropes (requiring vasopressors to maintain MAP>65) and serum lactate >2mmol/l. BP<90 (clinical shock)
Management of sepsis
- GIVE high flow O2 (>95% maintain unless COPD)
- TAKE Blood cultures – and others if needed
- GIVE Broad spectrum Abs – protocol
- GIVE IV fluid challenge – SBP<100, 500ml Hartmann’s STAT(15m) if SBP>100, 250ml Hartmann’s over 1hour and review
- TAKE serum lactate and Hb – If lactate >2mmol/L give 500 Hartmanns stat unless give and repeat lactate every 2hours till normal
- TAKE urine output
SIRS - what is it defined as
2 or more…
Temperature >38.3 or <36c
- HR >90
- RR> 20
- WCC >12 or <4 x 10^9 cells/L
- Altered mental state
Capillary glucose >7.7mmol/L (non diabetics
Red flags which raises suspiscion of sepsis
- GCS
- SBP 90 (or drop of >40 from normal)
- HR>/130
- RR>/25
- Needs O2 to keep Sp02 >/92% (88% in COPD)
- Non-blanching rash/mottled/ashen/cyanotic
- Recent chemo
- Not passed urine in 18hours (<0.5ml/kg/hr if catheterized)
qSOFA
qSOFA: For diagnosing seps- induced organ failure. 2+ factors suggest likely poor outcome.
- RR > 22
- SBP >100
- GCS >15 (altered mental status)
Core features and explanations in inflammation
- Inflammation = part of complex biological response of body tissues to harmful stimuli such as pathogens, damaged cells.
- S/S = heat (calor), pain (dolor), rednesss (rubor), swelling (tumor), loss of function (function laesa)
- Vasodialtion, increased blood flow (redness)+ temp), extravasation fluid (oedema + swelling), stimulation aff nerves (pain), more inflammatory cells to site (neutorphils, NK cells, monocytes)
What is innate immunity
- Layer defence – enzymes, skin…
- TLRs (PRPR) on mast cells/macrophage recognize PAMP/DAMPs
- Dilation capillaries, margination white cells, recruit neutrophils
- Phagocytosis from neutrophils. Mracrophages to eat bacteria.
- Completements – plasma proteins activated by pathogen bound antibody to cascade reactions fp ropsonisation, pore formation, intracellular pathogen
- NK cells – apoptosis
Adaptive immunity
Adaptive immune = time to activate, specific, memory, T lymphocytes, B lymphocytes. B cells to plasma cells then Abs formed.
- T lymphocytes. Cell mediated immunity
- B lymphocytes. Antibody mediated immunity (humoral)
- T lymphocytes: Macrophages are the APC. Present HLA/MHCI (-> CD8+ T lymphocytes-> cell lysis, extensive damage), HLA/MHCII (CD4+ (Helper) T lymphocytes which control macrophages, cytotoxic T cells(CD8+), eosinophils, B lymphocytes then become memory cells.).
- B lymphocytes: Helper t cells help B lymphocytes become plasma cells (produce antibodies- coats antigens to help I phagocytosis, agglutinate + neutralize toxin, activate compliment system).
What are the different types of shock and their effect on CO,HR,CVP,PCWP,SVR,O2 sats
- Caridiogenic = due to heart problems
- Hypovalaemic = caused by too little blood volume
- Anaphylactic = allergic reaction
- Septic shock = infection
- Neurogenic = damage to nervous system
What is a PE and the presentign signs and symtpoms
•Pulmonary embolism = blockage in blood vessel in the lungs which can be formed by thrombosis, fat (bone fracture, ortho surgery), amniotic fluid or air (following cannulation)
•Presenting symptoms + signs = (not specific with PE can lead to sudden collapse/death).
•Symptoms = dyspnoea, pleuritic chest pain retrosternal chest pain, cough, haemoptysis, chest symptoms for those with DVT signs, for severe dizziness/syncope, calf swelling.
•Signs = Tachypnoea, tachycardia, hypoxia (may cause anxiety, restlesness, agitated, impaired consciousness), pyrexia, elevated JVP, gallop rhythm, pleural rub, systemic hypotension, cardiogenic shock.
•Small PE may have no symptoms or breathless, chets pain, cough up blood, fever, fats HR
Examinationa and investiagtions for a PE
- Exam – Obs, general, resp (normal- unexplained hypoxia, reduced air entry), CV (features RHF) – raised JVP etc, other signs DVT.
- Ix – ECG, Normal CXR, D-Dimer (elevated), CTPA (gold standard), V/Q scan . Tests for underlying causes like CT TAP, autoantibody screen etc. Prognostication with troponin, ECHO.
Wells score for PE
What do you see on an ECG for PE
•On ECG PE = Sinus tachy/ SQ Q3 T3
What is the Mx for PE and complications
- Mx = Anticoagulation (usually rivaroxaban or apixaban or LMWH), Thrombolysis , oxygen, embolectomy, fitlers
- Complications = collapse, strain on heart, recurrent PE, S/E from treatment
Risk factors for PE
What are coagulation disorders and the major causes that lead to too much clotting
•Coagulation disorders = disruptions in the bodys ability to control blood clotting. Can result in haemorrhage or thrombosis.
- Major causes that lead to too much clotting;
- Factor V Leiden – genetic disorder, this fsctor overreacts
- Antithrombin III (ATIII) deficiency - Helps regulate bleeding and clotting, genetic disorder of low levels
- Protein C or Protein S deficiency – they help reg bleeding and clotting so low levels
- Prothrombin (PT) gene mutation – factor II mutation. Genetic disorder, too much clotting factor made
- Antiphospholipid antibody syndrome – autoimmune with increase in certain blood proteins that may increase risk of clotting.
- Symptoms – DVT, PE, heart attack or stroke at young age, recurrent pregnancy loss or stillbirth.
DVT clinical signs, differentials. and RFs
- Clinical = limb pain/tenderness, swelling of calf, pitting oedema, colour + temp changes (warm, red as blood diverted to outer veins).
- DDx = trauma, superficial thrombophlebitis, post thrombotic syndrome, peripheral oedema, hf, cirrhosis…
IX, MX, complciations for DVT
•NICE recommendations = General medical, physical, 2 level wells. Leg vein US and if negative then D dimer. Repeat US for those with positive D dimer 6-8days later. Can give parenteral anticoag if US not within 4hours.
- Tx = Anticoag (usually DOACs or LMWH or warfarin), compressions stockings, walking regularly but raising leg when resting, also possible thrombolytic therapy, embolectomy or filter in large vein.
- Complications – post thrombotic syndrome, pain, discomfort, swellignin calf.
What are the otucomes after tB infection?
- TB – cause mycobacterium tuberculosis complex.
- Outcomes after infection = 1) Clearance by immune system, 2? Latent infection, 3) reactivation.
- Latent = infected, no symptoms, cant spread, immune system stop bacteria growing. Active = immune system cant stop bacterial growing so symptoms etc.
Key RFs for TB
•Key RFs = Poverty + overcrowding, undernutrition, alcohol misuse, HIV, Silicosis, CKD, DM, smoking, immunosuppression.
SYmptoms fo TB
•= Fever, night sweats, weight loss, malaise. Pulmonary 85% (productive cough, haemoptysis), extra-pulmonary (back pain, lymphadenopathy, meningitis, GU), military TB (disseminated haematogenous spread of TB)
Diagnosis of tB and treatment
- Dx = Active TB – sputum smear x2, sputum culture (gold standard but slow), sputum PCR (quick + easy, detects resistance to rifampicin)
- Tx = Standard treatment of drug sensitive TB (Isoniazid + rifampicin 6m AND Pyraziniamide + ethambutol first 2m). MDR TB (resistant to isoniazid + rifampicin), XDR TB – additional resistance to injectable second line drug and fluoroquinolone.)
What is a UTI, the symptoms and common bacterial causes
- UTI = bacteria proliferation in sterile urinary tract. Causes irritation of urothelium.
- Symptoms – dysuria, frequency, urgency, haematuria.
- Common bacterial causes – E.Coli, proteus, staph saprophyticus
RFs for UTI
•Pregnancy (renal pelvis dilation as more urinary stagnation), menopause (thins urothelium- vulnerable to damage + infection), chronic health conditions (DM- excess glucose), sexual activity (bacteria migrates sites), tract blockage (renal stones), catheter (introduce foreign body and colonise around).
Red flags in UTI
= haematuria, flank pain, rigors. Check sexual intercourse and PMH that increases risk.
Managamenet UTI
- Mx – conservative (fluids/hydration), medical (Abs) – 1st line…
- Unwell elderly – Iv co-amoxiclav (possible add gentamicin)
- Symptomatic lower UTI + catheter ass – PO nitrofurantoin or trimethoprim (possible add gentamicin)
- UTI pregnancy – PO nitrofurantoin
- Pyelonephritis or lower UTI complicated by sepsis – IV co-amoxiclav
Complications of a UTI
•Complications = Urinary tracts tones, sepsis, pyelonephritic (flank pain, fever, rigors, haematuria)
Lung cancer symptoms and signs and what to check
•Symptoms (non specific)= Cough (change in quality/ 2-3w+), weight loss, fatigue, SOB (may be from spread), Haemoptysis, chest pain (non specific ache), hoarse voice and other features of intrathoracic invasion eg, SVC obstruction, elevated diaphragm.
•Signs = cachexia/weight loss, finger clubbing, pleural effusion, lymphadenopathy, stridor, tracheal deviation, SVC obstruction
- Things to check – PC, PMH, drugHx, SHx, Fhx, systems review
- Q cancer risk calculator
RFs of lung cancer
•RFs = smoking, asbestos exposure, underlying interstitial lung disease, COPD.
WHO functional status with lung cancer
•WHO Functional status = 0 (fully active), 1 (no heavy physical work), 2 (ambulatory + self care, not work activities), 3 (limited self care, confined to bed/chair for 50%hours), 4 (disabled, no self care).
TNM staging (lung cancer)
Diagnosis of lung cancer and the signs of metastasis
- Dx: CXR -> chest clinic -> CT scan -> assess fitness then Bronchoscopy/EBUS/CTguidedFNA/ pleural tap/ mediastinoscopy for tissue diagnosis. Then PET scan if curative treatment feasible.
- Metastasis signs: Spinal mets (pain), neuro (diff walking, sensory loss, bowel/bladder), spinal cord compression, SVC obstruction, extra thoracic spread (lymphadenopathy, horner’s, brain, bone, liver) and paraneoplastic syndromes (eg, hypercalcaemia, SIADH).
What is NSCLC, the types, RFs, and therapy
NSCLC 75-80% cases:
- Epithelial lung cancer
- Types: Squamous (men- tends to be smokers with elevated Ca+), adenocarcinoma (women, usually non-smokers), bronchiolar alveolar cells.
- Early stage disease is curable (surgery) and radioT/Chemo can help symptoms
- New Tx is immunotherapy + biological agents
- Stage 1-2b (some 3a) – radical tx –surgery, radical RT, sterotactin radiotherapy
- S3a-3b – chemo +/- radiotherapy and consider chemo-RT with radican intent if good fitness
- 4 – palliative chemo/radio
- Some mutations have direct drugs for tx like EGFR mutation (Erlotinib,tarceva or Gefinitib,Iressa, Alk- alikinase (crizotinib), PDL1 (pembroluzimab).
- RF = Tobacco + smoking, asbestos radon, air pollution.
SCLC - RF, Tx
SCLC: 20-25% cases:
- Develops in tissues of the lungs
- RF = smoking (rare in non)
- Freq metastatic at diagnosis, usually more aggressive
- Not amenable to surgery
- Often very chemosensitive +/- RT
- Surgery only if only very early stage (1)
Mesothelioma - RF, Tx
Mesothelioma:
- 80-90% form asbestos
- Huge latency period for presenting with it 40-50ys later
- Tx – radiotherapy (pain control), surgery (small proportion people), chemo, palliative/supportive
What is an aortic dissection and in whom is it most common
- Aortic dissection = tear occurs in inner layer of body’s main artery. Blood rushes through the tear, causing inner and middle layers of the aorta to split (dissect). If the blood goes through the outside aortic wall, its often fatal.
- Usually in men 60s and 70s but uncommon.
Symtpoms aortic dissection
•Symptoms = May be similar to MI. Sudden, severe chest pain or upper back pain, sudden severe stomach pain, loss consciousness, SOB, symptoms similar to stroke, weak pulse in one arm compared with other, leg pain, difficulty walking.
TA/TB of aortic dissection
- TA = tear in aorta where exits heart or upper aorta which may extend into abdomen. Surgery (graft to reconstruct aorta or replace) and medications to prevent it worsening.
- TB = Tear in lower aorta only 9descending) which may also extend into abdomen. Meds , surgery (sometimes stents)/.
RF of aortic dissection
•Rf = hypertension, atherosclerosis, aortic aneurysm, aortic valve defect, aortic coarctation. Also Turner syndrome (HBP, heart problems), Marfans(CT disorder), Other ct (ehlers danlos, loeys-dietz syndrome (wistedarteries esp in neck). Male, older, cocaine, pregnancy, high intensity weight lifting.
COmplications and Dx of aortic dissection
- Complications – death form itnenrla bleeding organ damage,storke.
- Dx = Transesophagela ECHO, CT, MRA
WHat is cyanosis and how would you invetsiagte it
- Cyanosis = Abnormal blue discolouration of the skin and mucous membranes.
- Ix = ABG, FBC, ECG, XR, Sputum+ blood cultures, V/Q scan, echo, Hb
Central Cyanosis VS Peripheral cyanosis
•Central cyanosis: diseases of heart/lungs or abnormal Hb, seen in tongues/lips as shunting DeO2 venous blood to systemic circulation. Also may have dyspnea, tachypnea, secondary polycthaemic and peripheral cyanosis.
- Neonates – transient after delivery, TOF/stenosis/TAPV/PA, resp distress syndrome, birth asphyxia, penumothroax, pulm oedema, pleural effusion, meconium aspiration
- Adults – lung disease (PE, Pulm oedema…) r->L cardiac shunt, abnormal Hb
- Peripheral: Peripheral vasoconstriction and bluish or purple discolouration of affected area, usually cold. Decreased local circulation and increased extraction of oxygen in the peripheral tissues. In conditions with peripheral vasoconstriction + stasis blood in extremeities eg, CHF, circulatory shock, reduced co, Raynauds.
Lymphadenopathy - what is this, the causes and Dx
- Lymphadenopathy = swollen lymph nodes. Tenderness, pain in LNs, swelling and other symptoms depend on cause
- Causes – common infections (strep throat, ear infections, HIV), uncommon (TB, STIs..), immune system duiorders (lupus, RA), Cancers (lymphoma, leukaemia, other mets)
- Dx/IX – MH, physical exam, bloods (CRP), imaging (XR,CT, US), lymph node biopsy
What is infective endocarditis and the symptoms/clinical findings
- Infective endocarditis = infections of endocardial surface of heart, deposition of platelets and fibrin -> colonization by bacteria -> development vegetation. Native or prosthetic valves.
- Symptoms = fevers, rigors, malaise, dyspnea, anorexia, weight loss.
- Clinical findings = Roth spots, Janeaways lesions (palms hands), splinter haemorrhages, Osler’s nodes (fingertips)
RFs/ causes of infective endocarditis
•RFs = congenital heart disease, rheumatic heart disease, IVDU, mitral vale prolapse, IV devices
Causes = •80% from strep or staphs. IVDU (S.aureus), Prosthetic valve (coagulase negative staphylococci), GI/GU source (enterococci), rare (HACEK, fungi), culture negative causes (Coxiella burnetiid, chalmydia sp. , bartonella, brucella.)
Diagnosis of Endocarditis
- Dx = 3 sets blood cultures and ECHO. Need 2 major criteria/one major + 3minor/ 5minor:
- Major – pos blood culture (from 2 separate cultures), evidence endocardial involve (ECHO or new valvular regurg)
- Minor – predisposition, fever, vascular phenomena, immunological phenomena, microbiological phenomena, ECHO findings (doesn’t meet above criteria).
Treatment endocaritis
•Tx = Depends on causative organisms, native/prosthetic valve and patient factors (eg, renal function. Usually 4-6weeks IV Abs and may require therapeutic drug monitoring and surgery. Eg, amoxicillin, gentamicin, vancomycin.
Bronchiectasis - what is this and what causes it and Rfs
•Bronchiectasis = Abnormal and permanently dilated airways characterized by viscous circles of neutrophilic inflamm, recurrent infection + damage to airway. Further impairs mucociliary clearance + persistent inflamm leads to impairment of immunity.
•Causes = Congenital, mechanical bronchial obstruction, post infective bronchial damage, granuloma, diffuse disease lung parenchyma, immune def, mucociliary clearance defects
•RFs = CF, chronic + inflamm lung disease, chronic/severe lung infections, defects in immune system
Clinical features of bronchiectasis and the invetsigations
- Clinical = Cough (usually persistent), sputum production, breathlessness, hemoptysis (infection), pleuritic chest pain, coarse crackles, clubbing.
- Ix = High Res CT, CXR, sputum exam, immune assessment, sweat test + CF genetic ass, nasal nitric oxide, total IgE(aspergillus testing).
Managaement bronchiectasis
Mx = airway clearance techniques, anti-inflammatories (long term azizthromycin + ICS), treat infection
What is cystic fibrosis, the most comon mutation and patho
- Mutations in cystic fibrosis transmembrane and conductance regulator, CFTR gene on chromosome 7. This encodes for epithelial chloride channel regulated by cyclic AMP.
- Most common mutation is delta-F508.
- These genes can lead to: No functional CFTR, abnormal intracellular processing of proteins, abnormal reg of channel, abnormal conduction of chloride through channel or reduction in functional CFTR reaching cell membrane
- Patho: Dehydration of airway surface fluid resulting in mucociliarydysfunction.
Presentation of Cystic fibrosis
- Presentation: Most picked up on newborn heel prick (immuno reactive trypsin test) or before from USS (confirmed with chorionic villus sampling + amniocentesis). Supported by sweat/gene test (sweat chloride >60). May be suspect when meconium ileus and children failing to thrive, fatty stools or recurrent chest infections. In adulthood rare but resp symptoms, diabetes, infertility.
- Clinical: Resp disease (productive cough, recurrent chest infections which an lead to cor pulmonale, bronchiectasis, haemoptysis, pneumothorax), pancreatic disease (fatty stools and malabsorption), GI disease (meconium ileus, constipation), malignancies (GI)
Management Cystic fibrosis
•Mx = Encouraging clearance of secretions and treating/preventing infections. Airway clearance techniques combined with mucoactiveagents (rhDNase-reduce viscosity, hypertonic sodium chloride-neb+hydrate secretions, mannitol dry powder for inhalation last resort). Pulmonary infections need managing (staph aureus flucloxacillin prop up to 3yrs and pseudomonas auruginosa then eradication therapy and extended course. Lung transplant for progressive respiratory failure mostly both lungs so not infected secretions left.
The cough reflex
- Cough reflex = Defence mechanism which clears airways of irritants by forcefully expelling air from respiratory tract.
- Acute cough <3w (URTi, LRTi, asthma, irritants) Subacute 3-8w (whooping cough infections like TB) and Chronic >8w (postnasal drip, acid reflux, asthma, lung disease, cigarette smoke). Also lung cancer foreign body CF, bronchiectasis etc
- Sensory afferent pathway: Irritation cough receptors (to afferent nerves), rapid/slow adapting stretch rceptors and C fibres -> Central pathway: sensory info to nucleus tractus solitarius of medulla. Vagusnerve synapses with motor neurons to deliver to effector muscles and cough reflex ->
- Motor efferent pathway: Diaphragm contracts + flattens, laryngeal muscles contract to close vocal cords, external intercostals contract and rectus abdominis contracts to depress rib cage and decrease space in thoracic cavity.
- Phases of Cough reflex: inspiratory phase (receptor cause vocal cord open and more air in, chest expands), compression phases: epiglottis and vocal cords close, trap air, increase intrathoracic pressure) then Expiratory phase: internal intercostals and contract and depress thoracic cavity. Vocal cords relax, epiglottis opens and air expelled.
- Causes = ACE inhibtors dry cough due to bradykinin accumulation. This causes chemical irritation of C fibres of resp tract through release of proinflammatory peptides and histamine so hyperstimualiton of cough reflex.
WHta is hyperventilaton and the causes
•Hyperventilation = excessive ventilation of the lungs, beyond what is required for normal ABGs. Lowers pCO2 and prodcues respiratory alkalosis. Secondary hypocalcaemia also occurs.
•Causes:
- Mostly from increasing RR and depth in exercise.
- Metabolic acidosis – compensatory hyperventilation (DKA/Acute kidney injury)
- Problems respiratory exchange – V/Q imbalance (PE)
- Hypoxia – altitude
- Fever, toxins, drugs (aspirin overdose)
- Iatrogenic – over ventilating those with head injruies
- Anxiety
- Dysfunctional breathing with asthma
Acute and chronic symptoms of hyperventilation.
- Symptoms -Paroxysmal complaint, SOB, pain/discomfort, parasthesiae in arms. Also dizzy, perioral tingling, weakness, tinnituds, palpitations, wheezing.
- Chronic - may be persistently low arterial pCO2 iwht high renal excretion of bicarb so pH normal. Occaisonal deep, sighing breaths.
Invetsigations and treatment for hyperventilation
- Ix = ABG, ECG, Pulmonary function tests, toxicology (eeg if syndrome)
- Tx = = rebreathing to paper bag, relaxation, treat cause, breath exercises, pharmacological.
•
Interstitial lung disease (diffuse parenchymal lung disease) - what is this and the physiology
- Group of conditions characterized by carrying degrees of inflammation and fibrosis, initially affecting interstitium of the lung, which typically presents with exertional dyspnoea, with or without cough. Often irreverisbel and gets worse with time. Chest paid
- Physiology = Loss of lung volume, increase ratio FEV1:FV2, decrease CO diffusion capacity. Causes stiffness in lungs from scarring (fibrosis) so difficult to breathe and don’t get as much oxygen into bloodstream.
Causes/RFs of Interstitial lung disease
- Causes: Occupation/environment (silica dust, asbestos), medications, medical conditions like RA, mixed CT disease.
- RFs = age, exposure to dust etc, GORD, smoking, radiation + chemo
Dx, Tx and complications of interstitial lung disease
- Complications = Pulm hypertension, RHF, resp failure
- Dx = Bloods, CT, ECHO, Pulm function test, lung tissue analysis.
- Tx = corticosteroid meds, medications that slow progression idiopathic pulmonary fibrosis, meds that reduced stomach acid, O2 therapy, pulmrehab, surgery
WHat is pulmonary hypertension and the classifications
- Pulmonary hypertension = increase in mean pulmonary arterial pressure which can be caused by or associated with many conditions. Increase in mean PAP>25 at rest as assessed by right heart catheterization.
- Classifications:
- Idiopathic/familial, cardiac, pulmonary, CTEPH, Misc
- WHO - group 1 (idiopathic), G2 (secondary to left heart disease, valvular heart disease, restrictive cardiomyopathy), G3 (secondary to chronic lung disease + environmental hypoxaemia), G4 (due to chronic thrombotic disease, embolic disease or both) and G5 (metabolic disorders, systemic disorders, haem diseases.
What can pulmonary hypertension lead to symptom wise
- History – Exertional dyspnea, palpitations, syncope
- Exam – Elevated JVP, Loud P2, LPH, Pedal oedema.
What are the DDx, IX for hypertension
- DDx – cor pulmonale, cardiomyopathies, MI, congestive HF, recurrent PE, pulmonary stenosis
- Ix – ECHO, BBP, CTPA, V/Q Scan, RHC (bloods, CXR, ECG, pulm function tests, MRI, lung biopsy )
TX for Pulmonary hypertension
•Tx – as per cause. Cardiosupportive therapy, prostacyclin analogues, endothelin-A receptor antagonsits, phosphodiesterase-5-inhibitors, possible thrombo-arterectomy or transplant.
Asthma - what is it and the patho
•Asthma = Chronic inflammatory airway disease characterized by bronchial hyper-responsiveness and bronchoconstriction. Day t day variability in symptoms manifesting as PEFR variation >20%. Commonly starts in childhood. T1 hypersensitivity (iGe bidnign to mast cells)
•Pathology: Eosinophils play a role and can cause Hypereosinophiliasyndrome. Also trait specific inflammation (Th2 cell CD4 mediated inflammation-allergic eosinophilc pathway) and NK/Macrophage induced inflammation ‘non-allergic eosinophilic pathway).
•Airflow limitation (usually reversible spontaneously or with treatment), airway hyper-responsiveness, bronchial inflammation
Diagnosis of asthma and some types
•Diagnosis = Symptomology – day to day variability in core symptoms. History of triggers (allergic/non allergic). Functional PEF with diurnal variability 20%, dynamic airflow obstruction >15% post BD FEV1. Tests for bronchia hyper-responsiveness or eosinophilic tests (FENO). Also CXR, E0, IgE sputum eosinophilia, RAST.
- Late- onset (adult) =Factors like different illness’s, virus’s, infections can contribute. Smoking doesn’t cause it but can provoke asthma symptoms.
- Atopic asthma – (Allergic) is asthma triggered by allergens like pollen, pets and dust mites.
Chronic Asthma - RFs, presentation, Tx
- RFs – personal history, FH/atopy, inner city, obesity, LBW, viral infections, smoking…
- Presentation: More than one: Wheeze, breathlessness, chest tightness and cough particular if: Symptoms worse at nigh/early morning, present
- in response to exercise, allergen exposure + cold air and present after taking aspirin or beta blockers. History atopy, FH asthma, widespread wheeze on auscultation. Otherwise low FEV1/PEV or peripheral blood eosinophilia.
- DDx – Children’s (bronchiolitis, CF, CHD, GORD), adults (COPD, angina, HF, malignancy)
- Assess and review at least annually: affecting activities, sleep, control questionnaire, lung function, check inhaler technique, review exacerbations and review meds.
- Tx: Beta 2 agonist inhaler -> regular inhaled steroids and if exacerbations use beta 2 agonist -> initial add on therapy (LTRA (before LABA) -> increase inhaled steroid -> referral to respiratory physician -> Omalizumab (allergenic severe persistent IgE)
- New alternative therapies – MART therapies, Omaluzimab (MAB to IgE), Reslizumba/Mepoluzimab/Benralizumab (Mab to IL-5), bronchial thermoplasty.
Acute asthma - what is it and mx
- Reduction in baseline obj measure Pulm function like PEFR and FEV1. Mild (PEFR 75%predicted+), mod (PEFR 50-75%), Severe (can to complete sentence, HR>110, RR>25, PEFR 30-50%), Life threatening (ehasution, confusion, coma, silent chest, central cyanosis, Pao2<8KpA)
- Mx = 1) Salbutamol neb 5mg +/- ipratropium 2) PO prednisolone 40mg5days or IV hydrocortisone and possible antibiotics. May need BIPAP/intubation/ECMO if life threatening and ICU.
What is osteomyelitis and the types
- Osteomyelitis = Infection of bone marrow which may spread to bone cortex and periosteum via harversian canals. Results in inflammatory destruction of the bone and if the periosteum becomes involved, necrosis. Can be acute or chronic
- Hematogenous osteomyelitis – infection from hematological bacteria seeding from remote source. In long bone clasisically acutely febrile and bacteremic patient with markedly painful immobile limb, nay be swelling + extreme tenderness, warm, redness, effusion of neighboring joints. In vertebrae then usually following acute septicaemic episode with selling, erythema, tenderness , chronic back pain. Potts disease is vertebral osteomyelitis form hematogenous spread of TB.
- Direct (contiguous) osteomyelitis – direct contact of infected tissue with bone. Classically with fever, pain, erythema but may be associated history accidental or surgical trauma.
- Chronic = previous joint infeciton, localized bone pain, erythema + swelling, no-healing ulcer, draining sinus tract, decreased ROM of adjacent joints, chronic fatigue, generalized malaise.
Pathogens in osteomyelitis, and RFs
- Pathogens = Staphylococcus aureus is most common. Others are strains of MRSA, H.influenzae, streptococcus spp., E.Coli, proteus spp., Pseudomonas spp., coagulase negative staphylococcus spp., mycobacteria, fungi.
- RF = trauma, prosthetic orthopedic device, diabetes, PAD, chronic joint disease, alcoholism, IV drug abuse, chronic steroid use, immunosuppression, hIV etc.
Ix and MX of osteomyelittis
- Ix = Labs (fbc, blood cultures, bone cultures), Imaging (MRI is choice but plain XR may be helpful in chronic signs etc). Godl standard is boen b
- Mx = Locla bone + soft tissue debridement, stabilization of bone, local Ab therapy (for acute 4-6weeks, chronic is 3-6m), reconstruction of soft tissue, reconstruction of osseous defect zone. analgesia ETC
Describe chicken pox , incubation period, symptoms, treatment and complications
Acute disease, mostly in childhood. Varicella zoster virus. Can reactivate and call shingles. Prodromal symptoms (nausea, myalgia, headache) then small erythematous macules then papules the clear vesicles then pustules. Intubation 1-3weeks, infectious 1-2days before rash and until crusted over. Can lead to bacterial skin irritation etc. Paracetamol, topical calamine lotion and possible acyclovir for immunocompetent within 24hours onset
Bacterial mneingitis - symptoms,. tx
Bacterial Meningitis: Mostly babies and children. Non-specific symptoms like fever, nausea, vomiting, lethargy, irritability. More specific is stiff neck, confusion, drowsiness, non-blanching rash, photophobia, kernigs, brudzinskis sign. Parenteral Abs (IM benzylpenicillin) earliest chance
Erythema multiforme - what is it and how does it appear, tx
Erythema multiforme – cutaneous hypersensitivity reaction, usually by infection (HSV, mycoplasma pneumoniae) and less commonly by drug sensitivity. Can appear as many types like macules or papules but always has targetoid or iris appearance. Usually acral distribution. Usually self limited 2-4weeks, no treatment
Impetigo - what is it, treatment,
Impetigo – Common superficial bacterial infection of skin. Ostly young children and clinical dx but can do swabs etc for persistent. Advice on higience to sotp spreading, stay from school till scabbed or 48hours after Abs, ensure skin conditions optimally treated. Treat localised non bullous infection with topical hydrogen peroxide for 5dts or topical Ab. Moral extensive is oral antibiotics like flucloxacillin.
Non-bullous impetigo (staph aureus, strep pyogenes) – rapidly rupturing esicles releasing exudate forming Golden/brown crust. Usually asymptomatic but might be itchy
Bullous impetigo – staph aureus – fluid filled lesions 2-3days and rupture to leave thin flat yellow/brown curst.
Lymes Disease
Lymes disease: Infection from bacteria group Borrelia burgdorfrie form infected tick. Complications are severe neuro symptoms and lyme arthritis. Erythema migrans rash. I fno focal symptoms then oral antibiotics but focal symptoms like neuro then referral to specialist. Doxycycline for 21says
How can herpes simplex complicate eczema
Herpes simplex may complicate eczema. – grouped vesicles and punched out erosions. Fever, lymphadenopathy and malaise (in eczema herpeticum). Medical emergency in <2 and urgent referral. Immediate hospital admission
Cellulitis - what is it, symptoms, organism, Tx
Cellulitis – Acte bacterial infection of dermis and subcutaneous tissue. Ain, warmth, swelling, erythema and possible blisters + bullae may form. Fever, malaise, nausea and rigors. When microorganisms like strep pyogenes and staphylococcus aureus gain entry to dermis and subcut tissue. Systemic symptoms manage in hospital. Primary care is Abs (usually Flucloxacillin), advise on analgesia, fluids etc. Manage underlying RFs and identify comorbidities
Necrotisiing Fascitis
Necrotising Fasciitis – destructive and rapidly progressive soft tissue infection in deep subcutaneous tissues and fascia, characterised by extensive necrosis and gangrene of skin and underlying structures. Immediate hospital admission, IV Aba, IV fluid
What is septic arthritis and the most common organisms
- Septic arthritis = infection of a joint. Can cause irreversible articular cartilage damage leading to severe OA.
- Most common pathogen = staphylococcus aureus but also gonorrhoea (in sexually active).Bacteria will seed the joint from a bacteremia.
RFs for septic arthritis
•RF = Increasing age, dm, Prior joint damage, joint surgery, hip/knee prosthesis, skin infection in combo with joint prosthesis, immunodeficiency
Symptosm and signs for septic arthritis
- Symptoms = Single, swollen joint with pain on active/passive movement, may get polyarticular arthritis (rare), fever and rigors, if shoulder/sternum then chest wall pain, if sacroiliac then but/hip/ant thigh pain. In children then fever, joint pain, unwilling to move affected joint,.
- Signs = swollen, warm , tended, extremely pain, may be effusion. Occasionally abscess. Invetsiaget psotehtic joint if applicable.
DDx and IX of septi arthritis
- DDx – Osteomyelitis, crystal arthropathies (Gout), inflammatory artrhopathies (RA) fares, haemarthroso (bleedinginto joint space eg on warfarin). Reactive arthritis.
- Ix = Obs (fever), joint aspiration (before Ab if possible), FBC/CRP/urate level, coag, blood cultures, Xrays (soft tissue swelling etc in late disease). Might check for lymes, immunology.
Tx of septic arthritis
•Tx: long term IV Abs (4-6wks). Infected native joints require surgical irrigation and debridement (washout) to aid in source control. May require several washouts before clearance of infection. Infected prosthetic joint, washout is still required but revision surgery is typically needed also.
Gonococcal ifnection - septic arthritis
•Gonococcal infection: Usually presents with fever, arthralgia, multiple skin lesions, tenosynovitis of hand joints, knees, wrists, ankles and elbows. May also present as monoarticular arthritis with other features negative. Do cultures for gonococcal infection (rectal, cervical, urethral, pharyngeal swabs). Ceftriaxone 2weeks.
What is an antibiotic and how used
- Antibiotic = Chemical with selective toxicity which severely damaged micro-organisms but is much less harmful to human cells and metabolism. This differential toxicity is due to differences in cell structures and processes between bacterial cells and human cells.
- Use – Treatment infection, prevention of infection, empirical therapy, targeted therapy
Empirical use for antibitoics
•Empirical use = Directed against anticipated and likely cause of infectious disease. Think about provision diagnosis, site infection, severity, possible pathogens to predict. Dose, route, duration, review, intolerance, interactions, S/E, AB penetration ability, previous microbiology results to consider. Think about nature of allergy like is it mild and fine to use (B lactam fine if GI disturbance, non-urticarial rash then can try cephalosporins, carbapenems, monobactemswith caution and anaphylaxis none)
Antibiotic stewardship
•Antibiotic stewardship = Optimising antibiotic therapy to improve patient outcomes in cost effective manner with least impact of resistance.
A/E of antitiotivs and mOA for reisstance
- A/E antibiotics – allergy, S/E, interactions, bacterial flora (diarrhea, candidiasis, MDR).
- Resistance + allergy = Alternative Abs may be less effective, more S/E, more expensive, larger doses, more likelu IV than oral.
- MOA- more Abs used, more “selective pressure” favoring resistance strains. Abs don’t cause resistance, they create favorable environment for growth of resistant variation in existence. Don’t start them unless clinical evidence.
Start SMART then FOCUS approach to antibiotics
Start SMART then FOCUS:
SMART:
ØAb within 1hr of life threating infection
ØApp cultures before starting AM if can
ØCheck-document allergies
ØPrescribe according to trust guidelines and document everything
ØFor surgical prop give single dose up to 60mins before inciison
ØCheck alert codes (MRSA/C difficle) and consult infection specialist or pharmacist when needed.
FOCUS:
ØReview diagnosis and need for Ab by 24hrs and clear plan action.
ØSTOP if no ev infection, witch IV to oral, change, if continue review again 72hrs, outpatient parenteral Ab therapy.
ØSTOP unless can justify continuing.
Mechanisms of acquired reisstance with antibioitc
- Bacterium destroys the antibiotic - beta-lactamase, aminoglycoside modifying enzymes
- Bacterium modifies its target: penicillin-binding proteins in PRP, peptidoglycan structure in VRE, ribosomal proteins in macrolide and tetracycline resistance
- Bacterium shuts the door: reduced permeability eg ertapenem resistance in Klebsiella
- Bacterium pushes it out: efflux pumps
- Other than beta-lactamase inhibitors, we have no drug based response to antimicrobial resistance other than to use something else.
- This leads to infections being: harder to treat, more expensive, less convenient ages, infections can be more severe as delayed optimisation of treatment and more common is failure prophylaxis, viscous circles.
Response to AMR
- Global – agreements about antibiotic use in agriculture, environmental standards re antibiotic pollution, development of new drugs
- National – surveillance, patient education, prescribing restrictions
- Local – infection control, antimicrobial stewardship
Common treatment for CDIFF
•C.Difficle – clean healthcare environment (chlorine better than detergent), dontgive to people (wash hands etc) and isolate cases, antimicrobial stewardship
Common treatment for simple UTI
•Simple UTI – Symptomatically, take sample, wait and give targeted treatment. Treat empirically – want to cover E/coli + other ‘coliforms’, want something well absorbed PO, and something well tolerated and preferably cheap (nitrofurantoin, trimethoprim, refer to previous cultures)
Bronchitis common treatment
•Bronchitis - manage symptomatically, take a sample, wait and give targeted treatment. Treat empirically: want to cover Haemophilus influenza, Streptococcus pneumonia and Moraxella catarrhalis, something well absorbed, tolerated + cheap (doxyclycline, amoxicillin, clarithromycin)
Common treatment for skn infection
•Skin infection: manage symptomatically. Take a sample, wait and give targeted treatment. Treat empirically: want to cover Staph aureus, streptococci, well absorbed PO, tolerated + cheap: Flucloxacillin, doxycycline, clarithromycin
Endocarditis - common treatment
•Endocarditis: manage symptomatically, take a sample, wait and give targeted treatment. Treat empirically:want to cover alpha-haemolytic streptococci, in some scenarios want to cover staphylococci and enterococci. Need something bacteriocidal and available IV: high dose amoxicillin plus gentamicin or vancomycin plus gentamicin
Bacterial Meningitis (adult)
• Bacterial Meningitis (adult):manage symptomatically. take a sample, wait and give targeted treatment. Treat empirically: want to cover Neisseria meningitidis, Streptococcus pneumoniae +/- Listeria monocytogenes. Need something IV, which crosses BBB and bacteriodical. Typically cefotaxime +/- amoxicillin
ABGs and acid/BASE disturbances
Under 55 caucasion, HBP - what medication
Firts lien ACE inhibitor
3 stages of hypertension
Ideal HBA1C
48
Why is ECHO good and for in HF
- Positives - cardiac real time moving images, multiple modalities and views. Used to assess cardiac structure, valve function/opening/closing, vessels associated with heart and pericardium. No radiation, safe. (user dependent)
- In HF – use for ventricle function, valves, atrial dimensions, pulmonary hypertension
Difference in musle fibres in RV/LV
•RV = primarily longitudinal muscle fibres LV = primary radial muscle fibres. ECHO assess radial function with EF and Longitduinal with tissue doppler.
What is global dilation good for in ECHO
•Global dilation with no muscles working properly then most likely viral as causes more regional area problems. Ischaemia. Muscle should contract in equally to make smaller darker area. LAD supplies greatest LV muscle mass.
Ejection fraction and how to do
- Ejection Fraction: Measure of pump efficiency, radial function only. Normal >55%, borderline low 50-55%, impaired 36-49% and sveerley impaired is <35%. New HF drugs if <40 and implantable defib <35%. Might need to give contrast enhancement. Poor itner operator reliability. Calculated on EHCO with simpsons biplate 0 draw around, machine calculate and adds up
- EF = EDV-ESV / EDV
Views in ECHO
SABA beta agonists
• (salbutamol): Act on beta 2 receptors, causing smooth muscle relaxation + dilation of airways. Rapid onset action (15mins) lasting up to 4hours.
Inhaled corticosteroids
•Inhaled corticosteroids (beclomethasone, dipropionate): Suppress inflammation mainly by switching off multiple activated inflammatory genes through reversing histone acetylation by recruiting HDAC2
LABA
•LABA – beta agonists (salmeterol): Act on Beta 2 receptors, causing smooth muscle relaxation + dilation airways. At least 12hours effect.
LRTA
•Leukotriene receptor antagonists (Montelukast): Prevent leukotrienes synthesis or block binding at receptor level. Leukotrienes are inflammatory chemicals the body releases after coming in contact with allergen or allergy trigger and cause tightening of airway muscles and excess mucus and fluid.
Antifungals examples
- Fungi are eukaryotes – no peptidoglycan cell wall, ribosomes less distinct from our own and more dififuclt to find drug targets
- Imidazoles – clotrimazole, miconazole, ketoconazole
- Triazoles – fluconazole, itraconazole, voriconazole, Posaconazole, isavuconazole
- Echinocandins – caspofungin, micafungin, anidulafungin
- Amphotericin B
- (flucytosine)
Antiviral examples
- Viruses replicate inside host cells – difficult to target them selectively
- Emphasis on – supportive management (common cold, glandular fever, parvovirus) and prevention (vaccination, lifestyle)
- Aciclovir for HSV/VSV
- AZT for HIV (Now susperseeded)
- Oseltamivir for influenza
- Remdesivir for COVID-19 (if it works)
Antiparasitic drug examples
Antiparasitic Drugs:
Parasites are a disparate group of multicellular eukaryoties
Only couple widely used in UK – Mebendazole for threadworms, permethrin or malathion for head lice and scabies.
Beta lactams
•Beta Lactams – penicillin’s, cephalosporines (cefalexin), monobacteams (aztreonam), carbapenems (meropenem). Beta lactam ring binds irreversibly to enzymes that manufacture bacterial peptidoglycan cell wall so cant make peptidoglycan and cell dies. For streptococcus pyogenes, pyogenic streptococcus or staphylococcus aureus. Typical flucloxacillin.
Glycopeptides
•Glycopeptides – vancomycin, teicoplanin… Molecule sbinds to growing peptidoglycan cross links. Only against gram posiutive and not orally. More for MRSA. PO vancomycin for C/Difficile.
Macrolides
•Macrolides – macrolides (erythromycin), azalides (azizthromycin), lincosamides (clindamycin). Bind t bacterial ribosomes + prevent protein synthesis which stops cell growing/dividing. Alternatives to penicillins usually. Likely for streptococcus penumonias, haemophilus influenza but could be legionella etc. Typically co-amoxiclav and clarithromycin
Aminoglycosides
•Aminoglycosides– Gentamicin, neomycin, by IV or topical. Bind to bacterial ribosomes and prevent protein synthesis so stops cells growing/dividing. Mainly in combo for additive or synergistic effect (or singular for UTI).
Tetracyclines
•Tetracyclines – doxycycline, bind to bacterial ribosomes, prevent protein syntesis and stops cells growing/dividing. Mainly PO for respiratory infections, oK for skin/soft tissue and useful long term for acne, pregnancy, breast feeding.
Quinolones
Quinolones – Ciprofloxacin, bidn to topoisomerase IV/ DNA gyrase- DNA complexes. Prevents DNA replication > stops cell growing/dividing. Restricted by S/E, when no other options
Trimethoprim role
– largely restricted to PO treatment of simple UTI. Co-trimoxazole has niche roles
Nitrfurantoin and Fosfomycin use
- Nitrofurantoin – only for PO treatment of simple UTI
- Fosfomycin – single dose PO treatment of UTI
cOLISTIN/COLOMYCIN USE
– last resort treatment for resistant gram negatives
Lenxoid use
•might see it used for MRSA infections or when patients allergic to other things
Rifampicin use
•Rifampicin – really used as part of multi-drug TB regimes. Sometimes in combo for complex staphylococcal infection.
