Med 1

Question 1

Thoracic Aortic Aneurysm

Answer 1

• TAA = premant + irreversible dilation (all 3 layers) of TA, usually asymptomatic
• S/S = severe sharp back/intracapsular pain, aortic regurg, systemic symptoms, TE presentation (DIC), symptoms of compression of nearby structures (hoarse voice)
• Physiology = inflammation, proteolysis, reduced smooth muscle cell survival then loose distensibility so rise in bP can exceed arterial wall strength and trigger dissection/rupture.
• Causes = Genetic, CT disorder (marfans/turners_, infections, aortitis, trauma
• RFs = HBP, older, smoking, athersclerosis, previos AA,
• Ix = Bloods, ECG, lung function, US, CT/MRI, coronary angiography.
• Surveillance, repair, replace
• Surgery = Immediate, symptomatic, asymtpomatic but >5.5Asc/>6cm Ascending or growing more than 1cm a year.

Question 2

Wheeze

Answer 2

• Wheeze = whistling sound as air passes through narrowed airway and stops O2 gettign into bloodstream effectively so causes SOB and some chets tightness
• Causes:
  
  • Asthma - bronchospasm. Cough, wheee, breathless, chets 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

Question 2

Breathlessness (Dyspnea)

Answer 2

• Patho = Body need smor eoxygen so we try to breathe faster to increase dlow of air into the lungs whcih then goes into bloodstream and pumped around the body by the heart.
• Causes: Respiratory (airways-COPD, Tissue-interstitial lung disease, Perfusion-V/Q mismatch, PE, PAhypertension) and non respiratory (hypoxia related, compensatory-acidosis, anxiety)
• Types of 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)
• Cyanosis = blue discolouration skin/mucous membranes from low O2. Central (resp,CV, CNS) or peripheral (reduced CO, hypothermia)
• Hyperventilation = more CO2 eliminated than produced, lots causes (acidosis, anxiety…). Might also get dizzy, palpitations
• O2 therapy = 94-98% or 88-92% for co2 retainers. Nasal cannula (up to4l), venturic mask (controlled), smple mask(1-15l), non re breathe (10/15l)

Question 3

COPD

Answer 3

• COPD = airflow limitation + destruction of lung parenchyma. Increased mcuus secreting goblet cells in bronchial mucosa and bronchi can become obverly inflamed with pus in lumen. Decreased mucociliary clearance so increased risk of resp infections and needs Abs and routine vaccinations. Inflammation, scarring, thickening of wall airways, loss elastic recoil, V/Q mismatch
• RF = smoking, alpha 1 antitrypsin def.
• Symptoms = productive cough (white/clear psutum), wheeze, breathless after many years smokers cough.
• Signs (possible) = quiet wheezes through chest and in severe thentachypneic with prolonged expiration and accessory muscles, hyperinflated lungs. HF/oedema are temrinal events. In advanced then pulmonary hypertension
• FEV1<70
• Ix = lung function tests (FEV1:FVC reduced), CXR, high res CT, Hb, packed cell vol, blood gas, sputum exam, ECG normal, ECHO,a1 antitrypsin level
• Mx = Keep assessing function, stop smoking, pneumococcal + influenza vacc, SABA for acute, LABA, muscarinic bronchodilator, consider theophylline or combo ICS + LABA, pulm rehab, treatment hypoxaemia, lung reductions urgery/transplant.
  *

Question 4

Ischaemic heart Disease/ CHD: (most common type HF)

Answer 4

• Patho = coronary arterues become blocked with atheroma.
• Symptoms = Chest pain, breathless (angina), tired, dizzy, palpitations
• RF = Diabetes, obesity, high LDL, HBP, smoking, FH, inactivity
• Reduce risk = meditarranean diet
• Specialist Ix = CT with contrast, coronary angiography then angioplasty if blcokage.
• Ix = Bedisde (obs, ECG, BM), bloods (routine + cardiac enzymes, amylase), image (CXR), possible ECHO.
• TIMI scoring = risk cardiac event in next 30days. Age >65, known CAD, Aspirin in last 7/7, severe angina (>2hrs in 24hrs), ST deviation ?1mm, elevated tropnonins, >CAD RFs.
• Complications = ACS (unstable angina, NSTEMI, STEMI)
• Stable angina (fixed atherosclerotic plaque)-> unstable plaque with platelet aggregation (unstable angina) -> plaque ruptures (thrombs which is NSTEM/STEMI).

Question 5

Chest Pain

Answer 5

• Types: ischaemic cardiac pain, non-sichaemic cardiac, respiratory, MSK, Breast disease, GI, psychological
• 1st steps = Assess, stabilise, oxygen, iV cannula, analgesia, Re-assure
• History taking
• Mx = initial, symptomatic (GTN/nitrates, nicorandil, CCBs, sympathectomy, sympathetic ganglion blocks) , disease modifying/prognostic, based on anatomy. Prognostic meds like antiplatelets.

Question 6

Acute coronary syndrome

Answer 6

•Unstable = Unprovoked/prolonged episode of chest pain.At rest. Without definitive ECG or lab evidence. Platelet adhesion. Typically precipitated by stress/exertion (3+m), lasts <20mins, relieved by GTN or resting.

• Normal troponin, ECG normal, Possible ST depression
• LMWH (fondaparinux), Ticagrelor, B-Blocker (Bisoprolol), statin (atorvastatin, ACEi(Ramipril), Nitrates (V infusion if severe pain with hypertension), consider coronary angiography within 72hr, senior RITA trial?

•NSTEMI = Chest pain suggestive of AMI. Platelet aggregation.

• Raised troponin, ST depression, possible T wave inversion, can be normal.
• GRACE scoring: Predicts 6/12 mortality in NSTEMI patients

•STEMI = Sustained chest pain, suggestive of AMI. Complete occlusion.

• Raised troponin, ST elevation (>1mm LL, >2mm chest leads), Hyperacute T waves, new LBBB, T inversion, Q waves more than 25% down or R pathological Q wave.
• Mx =PCI

•MX = MONAC: Morphine (5-10mg slow IV injection), Oxygen, Nitrate (GTN spray), Apsirin(300mg chewed), Clopidogrel (or fondaparinx etc and antiemetic).

Question 7

Cardiomyopathy

Answer 7

•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, often genetic

•Presentation = Breathless, swelling, bloated abdo, cough when lying down, fatigue, heartbeats feel rapid/pounding/fluttering, chest discomfort or pressure, dizziness…

•RF = FH, long term HBP, Conditions affecting heart, long term lcohol abuse, obesity, drugs, cemo drugs, diseases like diabetes/amyloidosis/Ct disorder etc.

•Diagnosis = CXR, ECG, ECHO, treadmill stress test, cardiac catheterisation, cardiac MRI, Cardiac CT, bloods, genetic testing or screening

•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.

Question 8

Heart Failure

Answer 8

• HF = from structural/function cardiac disorder -> heart cant function to support physiological ciruclation needs. Decreased CO, Ibcreased venous congestion so increased afterload/preload and increased cardiac work. CO= MAP/TPR.
• Causes - Mianly ischaemic heart disease, cardiomyopathy, hypertension.
• RFs = Age >65, FH, genetics, lfiestyle, med conditions, race, sex (men younger)
• Symptoms= exertional dyspnea, orthopnea, paroxysmal nocturl dyspnea, fatigue.
• Signs = tachyc, elevated JVP, cardiomegaly, 3/4 heart sound,s 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 / HR-PEF
• Ix = Bloods, CXR, ECG, ECHO, nuclear cardio, cardiac MRI, cardiac cath, cardiac biopsy, CP exercise test, 24h ECG.
• NTProBNP = >2000 urgent specialist ass within 2w, >4000, further assessment CXR,12LECG, ECHO

Question 9

Valcular heart disease

Answer 9

• Valvular heart disease = Damaged/diseased, leaky and cause regurgitation with not enough blood being pushed forward through heart.
• Causes = rheumatic hert disease, endocarditis, congenital heart disease, heart disease, marfans syndrome (structural weakness in walla orta), autoimmune, high dose radiation exposure, ageing.
• Symptoms = SOB, Chets pain, fatigue, dizzy, daint, fever, rapid weight gain, irregular heartbeat.
• Dx = listen to heart (Murmurs) and ECHO
• Tx = if not severe then medicines to treat symptoms. if mroe serious then surgery like replacement in open/non open heart surgery

Question 10

Gastroenteritis

Answer 10

• GE = non sepcific term, combo of nausea, vomiting, diarrhea and abdo pain
• Causes = Viral, bacteria, parasitic
• RFs = poor perosnal hygience, lack sanitation, compromised immune system, achlorhydia, poor cooked food (notifiable), travelling
• Presentation = incubation for viruses usually day, for bacterial dysentery (notifiable) few hours-4days, parasites 7-10days. Usually rotsvirus/norovirus in UK. Blood diarrhea then E.COLI 0157 usually.
• Assess - dehdyration, BP, pulse, temp, abdo exam etc
• Ix = stool culture, bloods if unwell.
• Tx = Advice on preventing dehydration, not usually drug treatments, hygiene, dont work until after 48hours last episode.

Question 11

Pneumococcal/ TB vaccines

Answer 11

•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 – 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.

Question 12

HIV - immunodeficiency

(HIV1/ HIV-2-W.africa)

Answer 12

• Transmission - sexual, perinatal, blood transfusion, shring needles, occipational
• Symptoms:
  
  • Most infectious shortly after infeciton, usually unaware
  • Firts few weeks after infection - influenza like symptoms
  • As infection progressively weakens immune system - swollen lymph nodes, weight loss, fever, diarrhea, cough
  • Withotu treatment - risk severe illness like tB, cyptococcal meningitis, severe abcterial ifnections, lymphomas, Kapois sarcoma
• Complications/Presentations:
  
  • Karpois sarcoma (HSV, purple/brown lesions)
  • Oral hairy leucoplakia (EBV)
  • CEsopahgeal candidiasis
  • Cryptosporidum (protozoan inf, abdo cramp, diarrhea, weight loss, contam food/drink)
  • Toxoplasmosis - protozoan paasite -> brain lesion
  • SHingles - HSV
  • Pneumocystitis jiroveci pneumonia - dyspnea, fever, malaise, alvoelar infiltrates on CXR
  • Progressive multifocal leukoencephalopathy - from kc virus
  • TB
  • CMV - herpes virus
  • Ryptococcus neoformans - commonest cause mneingitis if have HIV.

Question 13

Immundoeficiency

Answer 13

• Immunodeficiecy disrorders = full/partial impairment of immune system
• Primary immunodeficiency syndromes: Mostly inherited single gene disorder that present in infancy/early childhood.
  
  • 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.
• 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
• Presentation: frequent infections (opportunistic, severe/persistent bacterial, common gI symptoms. Neuro problems, autoimmune problems
• History – check FH, RFs, history adverse reactions, previous antibiotic prescriptions.

Question 14

Lymphoproliferative disorders

Answer 14

•Lymphoproliferative disorders = uncontrolled production lymphocytes that cause monoclonal lymphocytosis, lymphadenopathy and bone marrow infiltration. Often in immunocompromised.

Question 15

Malaria

Answer 15

• Transmission – bite infected by female mosquito. Lifestyle has blood and liver stages.
• Incubation period 7-30days
• 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 = 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).
• Dx – demonstration parasites on blood film or detection of antigens using immunochromatographic tests.
• 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

Question 16

Normal ECG parameters and basics

Answer 16

• LL - Ride Your Green Bike = Right arm (red), Left arm (Yellow), Left leg (green), Right leg (Black)
• HR = 300/number big swuares between R-R or number QRS complexes rhythm strip x6.
• SInus rhythm = p waves before very QRS
• brad <60, tachy >100

Question 17

AV Block

Answer 17

• 1st degree AV block = impulses take longer to pass through AV node. Porlonged PR interval >200ms. 1 P wave for every QRS
• 2nd degree AV block = not every P wave rporduces QRS.
  
  • Mobitz Type I (Wenkebach)- AV node doesnt recover fully followign conduction of impulse. PR intervl prolongs gradually. EVentually QRS dropped as AV node unable to conduct.
  • Mobitz Type II = av node unable to conduct impulses at regular interval, normally 2:1, also can be 3:1, 4:1
• 3rd degree AV Block = Complete heart block, AV node unable to conduct impulses from atria. No relationship between p waves and QRS complexes.

Can have av block with atrial tachycardia (120-200bpm)

Question 18

Describe the relevance of ST segment on ECG

Answer 18

• ST elevation - Acute MI, coronary vasospasm, pericarditis, benign early rpeolarisation, LBBB, LV hypertrophy
• ST depression - MI/NSTEMI, reciprocal change in STEMI (posterior mI), digoxin effect, hypokalaemia, SVT, RBBB, RV hypertrophy.

Question 19

Atrial Fibrillation

Answer 19

• AF = irregularly, irregular QRS rhythm, no clear P waves. microcirutis in atrium so bombard AV node. Atrial rate 300-600bpm
• Ix = ECG, history, CV exa, pulse, BP, fbc, coag, enal function _ electrolytes, thyroud, liver function, CXR, ECHO.
• Types - first diagnosied, paroxysmal (<7days), persistent (>7days), long standing (>12m), permanent (accepted by patient and physician.)
• Causes - CV (hyeprtension, CAD), resp (PE, COPD), metabolic (thyroid), sepsis
• Stroke risk so NOACs, vit k antagonist INR 2-3 or lMWH. Do CHA2DS2-VASc/ HAS-BLED
• Symptoms = most -> least common = •palpitations, breathless on exertion, light-headed, breathless on rest, chest tightness, syncope. Check if hemodynamically stable
• Mx = Thromboembolic Risk assessment. Rate vs rhythm control. B, blockers, CCB, digoxin. Cardioversion (if <48hrs otherwise give anticoag first). Amiodarone.

Question 20

Atrial Flutter

Answer 20

•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

Question 21

Broad complex tachycardia:

Answer 21

• BCT = 3+ successive beats >120bpm. AV dissocition. QRS>120, Ventriculsr rate>120. Potentially life threatening, can degenerate into VF. Causes are LQT, electrolyte disturbances, cardiomyopathy, acute MI, IHD. Durgs, cardioverison, pacing
• Ventricular tachycardia = broad complex tachy originating in ventricles. May impair CO with conseuent hypotension, collapse + acute cardiac failure due to extrmee HR and lack coordinated atrial contraction.
• Ventricular fibrillation = shocable. ventricles suddenly attemp to contract at rates up to 500bpm. This rapdi + irregular electrical activity renders the ventricles unabel to contract in synchronised manner, so immediate loss CO. Heart no longer effective pump + reduced to quiverign mess.

Question 23

Atrial and Ventricular Ectopics

Answer 23

•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.

•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.

Question 24

Broad QRS complexes - Bundle branch block

Answer 24

• 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.

Question 25

Ischaemia and Infarction on ECG (STEMI/NSTEMI)

Answer 25

•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.

•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)

•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.

Question 26

Meningitis

Answer 26

• Meningitis = inflammation of the tissues around the brain
• Pathogens = Most common is Neisseria meningitidis (meningococcus). other bacterial (strep penumoniae, Hib, E.coli) and there are many viral causes and rare fungal/TB.
• Symptoms: Generally ynwell, cold hands/feet, pale colour around lips which leads to a ras (red/purple blotchy dots, non blanching). In babies may also may be excessive crying, hight temp etc and in adults high temp, shivering, stif neck, headache, fast breathing, photophobia, drowsiness
• Dx : bloods, lumbar puncture, CT/MRI
• Tx: In viral most make full recovery but in bacterial you need antibiotics injects, fluid, o2 etc as complciations are hearing loss, learning problems, epilepsy, oint/kidney/bone problems.
• Prevention: meningitis vaccine + immunisations
• Contacts - household and kissing <7days, short course Abs and vaccine offered

Question 27

Common sites bacterial infections

Answer 27

• UTI/Cystitis = pain, increased freqm blood c,oudy/smelly, possible abdo pain. Drink lots, Abs if doesnt go
• SKin infections = swelling, redness, heat then pain + pus or weeping from wound.
  
  • Impetigo = epidermis, mosty children
  • Cellulitis = dermis + subcut tissue in ulcers + surgical wounds
  • MRSA suerbig on small score on skin + can spread
• Respiratory infections = coughs/colds, pneumonia (cough, thick mucus, rapidHR, fever, brethless…)
• STIS - abdo pain, bleeding between periods, fever, sores, painful intercourse, painful urination, pus liek discharge, swelling or tenderness of vulva, anal itching etc.

Question 28

Common leg infections/ changes

Answer 28

• Cellulitis = skin + superficial soft tissue infection, usually staph aureus or other strep. Red, hot, tenfer, defined edges, unilateral usually. Swabs, cultures, bloods, imaging, mark borders and Abs/surgical debrdiement if severe
• Necrotising fascitis = severe soft tissue infection caused by G A strep. Release of toxins by S/Pyogenes. Hot, red, swollen, necrotic tissue areas, not demarcated well. Skin swabs, broad then narrow spectrum Abs, IV fluid, surg debridement and possible amputation
• Chronic venous changes = lipodermatosclerosis: from chronic inflammation and fibrosis of dermis and subcut tissue of lower legs. Painful inflamm above ankles with oedema and hemosiderin deposition. Uusally bilateral
• DVT = red, hot , sweollen, unilateral LL. Calf tenderness (trhombophlebitis) and possible two grad epyrexia. Need doppler US imaging, D dimer, WELLs score.
• Osteomyelitis

Question 29

Myeloproliferative disorders - pyrexia unknown origin

Answer 29

• Myeloprliferative neoplasms - group rare disorders of bone marrow that cause increase in number of blodo cells. Most are 60+ y/o.

Question 30

What is pericarditis and the symptoms?

Answer 30

• Pericardial disease (pericarditis) = inflammation of any of the layers of the pericardium (thin tissue sac surroudnign the heart)
• Pericarditis = causes sharp chest pain when irritated layers of pericardium rub against each other. Uusally mild and goes away without treatment.

Question 31

Pleural disease

Answer 31

• Pleural space = lubricate pleura to allow sliding as lungs inflate/deflate.
• Pleural fluid:
  
  • 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 = pleural plaques. Indicator for asbestos exposure.
• Mesothelioma = maligannt tumour of serosal surfaces (mostly pleura), usually from asbestos expsoure.

Question 32

Pleural Effusion

Answer 32

• Pathology = Rate production of pelural fluid > rate absorption so acucmulation pleural fluid in pleural space.
• Causes = Fluid leaks in from elsewhere (HF, renal failure, ascites…) or too much fluid produced (pleurla malignancy, pneumonia)
• Symptoms = progressive breathlessness, may have pleuritic chets pain and often cough and symptoms depending on underlying cause
• Sign = reduced chets wall movement, reduced TVF, dull percusiion, reduced air entry, reduced vocal resonance.
• Ix = Hist, exam, bloods (+LDH), CXR, pleural US, CT chest
• Mx = thoracentesis pleural aspiration = US guided/
• Lights criteria determines if exudate fluid.

Question 33

Pneumothorax

Answer 33

• Pneumothroax = air enters pleural space, intrapleural pressure increases and lung vol decreases.
• Primary spontaneous PT = no undelryign disease, usually rupture of pleural blebs under visceral pleura. Also 2nd hand smoke, air poll, genetic predisposoition, underlying cT disorder. >2cm + breathless = aspirate, then if unsuccessful chest drain + admission 4-8days. Small then discharge + review.
• Secondary spontaneous PT = Discernable lung disease. >2cm+breathless then chets drain, if 1-2cm aspirate, if smaller high flow O2 (unless o2 sensitive) and observe. Minimally symptomatic dont need treatment.
• S+S = Pleuritic chest pain, sudden onset, breathleless, “pop” sensation, sometimes trigger like heavy lifting. Reduced chets wlal movement, acc muscle use, absent breath sounds, CV signs/
• RFs = previous pTX, a-1 antitrypsin def, underlying lung disease
• Recurrent PTX = surgical candidates - pleurodesis, bleb/bulla closure, lung vol reduction. Non surgical then chemical pleurdesis (tetracycline derivates, Talc,…)

Question 34

Describe some comon upper respiratory tract infections

Answer 34

• Tonsillitis = Red, swollen, white tonsillar exudate (Bacterial/EBV), LN enalrgement, halitosis, cough, runny nose. Commonly G A strep/ viruses
• Peritonsillar abscess (quinsy) = complciation acute tonsilitis, pus in peritonsillar space. Mostly G A beta aemolytic streptococci. uvula dev, hot potato vob,. Throat swab, monospot, ECB Abs, bloods. Analgesia/IV fluids, Abs, Surgery for incision and drainage.
• Paryngitis = sore throat. Rhinitis or common cold - mostly viruses
• Sinusitis = infection paransal sinuses. Acute (<4w)is mostly RSV or strep pneumonia, H.influenza. Chronic (12w) is oblhae anaerobes, staph aureus. Suddent onset >/2 = nasal blockage/obstruction/congestion, facial pain/pressure,- anosmia/hyposmia, cough. Ant rhinoscopy (swelling, erythema, pus, polyps_. <10d viral, >10days bacterial with elevated CRP/ESR, deterioration, sever elocal pain, purulent dischare.
• Laryngitis = can lead to oedema of true vocal cords, often hoarse voice <7days, dyspnea, dyspahgia. V/bac/fungal/non infectious. Dx on laryngoscopy.
• Laryngotracheobronchitis - croup <3yrs, sinpiratory strdor, hoarsenes,s fveer, cough, coryza.
• Epiglottis - oedema, inflamm 2-6yrs, dyspnea, dyspahgia, drooling, dysphonia,fever. Hib in unvacc. Notify EnT, dont look in mouth, neb adrealine, IV Abs, fluids, secure airway

Question 35

Bronchitis vs Bronchiolitis (LRTi)

Answer 35

• 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+ year. Bacterial or viral or non infectius like irritant exposure.
• Bronchiolitis - inflammation bronchioles - presents as acute viral inection less than 2 uears. Acute onset wheeze, dyspnea, cough, rhinorrhoea, resp distress. Mostly RSV.

Question 36

The types of Pneumonia

Answer 36

• Pneumonia - inflammatory condition of the lung parenchyma (alveoli) so alveolar filling with fluid (consolidation). Most comonly strep pneumonia.
• CAP = Community aquired. Acute infection not in hops or long term care for >14days before onset symptoms.
  
  • RFs are extremities in age, comorbidities, resp conditions, lifestyle, iatrogenic.
  • Types - pneumococcal typucally acute onset + high fever but atypical (mycoplasma pneumoniae, chlamydophilia pneumoniae and legionella pneumophilia) tend to be slower obset, more extrapulmonary symptoms and dont respond to penicillins (macrolifes + doxycycline)
• HAP = 48h+ after admission. New onset ocugh, purulent sputum Xray with consolidation. Empirical therapy (-VE piperacillin=tazobactam or merpenem and +VE vancomycin) then definitie.
• HCAP - non hospitalise dbut recent and substantial healthcar exposure.
• VAP- 48+hours after endotracheal intubation.
• Aspiration pneumonia = chemicla pneumonitis as food inhalation promotes infective environment. Mostly right lung.
• If immunocompromised - opportunisti pathogens liek pneumocytitis pneumonia. try to do immuno-fluoresence on induced sputum or bronchoalveolar lavage fluid.

Question 37

Pneumonia in general

Answer 37

• Pneumonia = inflammatory condition of lung parenchyma (alveoli) so alvolar fillign with fluid (consoldiation). Most commonly strep pneumonia.
• Dx = Fever, breathless, cough (+sputum), pleuritic chest pain, SOB, reduced cehst expansion, dull percussion, increased vocal resonance, coarse crackles, temp, low O2 and new unexplained xray shadowns.
• 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.
• 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 = Effusion, empyema (infective infusion, need USS guide chest drain) lung abscess, pericarditis
  *

Question 38

Infection -> SIRS

Answer 38

•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

SIRS Defined as having 2 or more of:

• 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

Question 39

Sepsis and septic shock

Answer 39

• Sepsis = Life thretening organ dysfunciton 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)
• Ix = Bedside (obs, news, ecg, sputum), Bloods (blood cultures, lactate)
• Mx = GIVE: High flow O2, braod spectrum Abs + IV fluid challenge. TAKE: Blood ucltures, serum lactate + Hb, urine output.
• Red flags = GCS130, RR>25, needs o2 for SpO2>92%, non blanching rash, recent chemo, not passed urine in 18hrs.
• qSOFA for diagnosises sepsis induced organ failure. 2+ factors poor outcome usually RR>22, SBP>100, GCS>15

Question 40

Pulmonary Embolism

Answer 40

• PE = bloclage in blood vessel in the lungs whcih can be formed by thrombosis, fat, amniotic fluid or air.
• S/S (not specific but can lead to sudden collapse/death) =
  
  • Symp = dyspnea, pleuritic chets pain (retrosternal), cough, haemoptysis, chest symp for those with DVTm in severe then dizzy/syncope, calf swelling. Small may have nothing.
  • Signs = tachypnea, tachycardia, hypoxia, pyrexia, elevated JVP, gallop rhythm, pleural rub, systemic hypotension, crdiogenic shoc
• Ix = ECG, normal CXR, Ddimer elevated, CTPA (godl standard), V/Q scan, tests for undelryign causes
• Wells score =3 level is 0-1low, 206 intermediate, >7high) (2level unlikely 0-4, >5 likely/ For simplified wells 0-1 unlikely, >2 likely)>
• On ECG PE = Sinus tachy/ SQ Q3 T3
• Mx = Anticoagulation (usually rivaroxaban or apixaban or LMWH), Thrombolysis , oxygen, embolectomy, fitlers
• Complications = collapse, strain on heart, recurrent PE, S/E from treatment
• Venous thrombosis = stasus (poor mobility, obesity), vessel wall damage (trauma), hypercoaguability (malignancy, prgenancy)

Question 41

Coagulation disorders - Thromboembolism

Answer 41

•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.

•Too much bleeding – hemophilia, von willebrand disease (VWF low), Disseminated iV coagulation, vit K def, platelet dysfunction.

Question 42

DVT

Answer 42

• 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…
• 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.
• Veneous thrombosis triad - hypercoagulability stasis, vessel wall damage

Question 43

TB

Answer 43

• Cause = mycobacterium Tuberculosis complex
• Outcomes after infection:
  
  • Clearance by immune system
  • latent infection = no symp, cant spread, immune system stop bacteria growing
  • Reactivation - immune system cant stop bacteria growing so symptoms. (More risk if HIV)
• Key RFs = poverty + overcrowding, undernutrition, alcohol misuse, hIV, silicosis, CKD, DM, smoking, immunosuppression
• SYmp = fever, night sweats, weight loss, malaise. Pulmonary (porductive cough, haemoptysis), extra-pulm (back pain, lymphadenopathy, meningitis, GU), Miliary TB (disemminated haematogenous spread of TB)
• Dx = Active TB - sputum smear x2, sputum culture (gold standard but slow), sputum PCR (quick + easy + detects resistance to rifampicin)
• Tx =
  
  • Standrad of drug sensitive TB = pyraziniamide + ethambutol first 2m and isoniazis + rifampicin for 6m.
  • MDR - reisstant to isoniazid + rifampicin
  • XDR TB - add resistance to injectable second line drug and fluoroquinolone

Question 44

UTI

Answer 44

• UTI = bacteria prolfieration in sterile urinary tract. Causes irritation of urothelium
• Symp= dysuria, freq, urgency, haematuria
• Common bacterial causes - E.Coli, proteus, staph saprophyticus
• RFs = prgenancy, menopause, chronic health conditions, sexual activity, tarct blockage, catheter
• Ix = bedside (obs, urien cultures, urine dip (leukocytes +/- nitrates), bloods, x in recurrent UTIs
• Red flags = haematuria, flank pain, rigors. Check sexual intercouse and pM that increases risk.
• Mx = conservative (fluids/hydration), medial (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 = Urinary tracts tones, sepsis, pyelonephritic (flank pain, fever, rigors, haematuria)

Question 45

Lung cancer

Answer 45

• Symptoms = cough (change in qual, 2-3wks), weight loss, fatigue, SOB, haemoptysis, chest pain, hoarse coice, other features intrathroacic invasion
• Signs = cachexia/weight loss, finger clubbing, pleural effusion, lymphadenopathy, stridor, tracheal deviation, SVC obstruction
• Q cancer risk calc, WHO functional status
• RFs = smoking, asbestos exposure, underlying interstitial lung disease, COPD
• 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).
• SABR – stereotactic ablative radiotherapy – high focused, high dose, limited damage to surrounding tissues, can be for those with poor lung functiona nd poor cardiac reserve. Also target molecular therapy.
• Screening – trials done but expensive, many downsides.

Question 46

Types of lung Cancer

Answer 46

NSCLC - 75-80%

• EPithelial lung cancer. Lots types eg, Squamous (male smokers), adenocarcinom (women, non smokers), broncheolar alveolar cells
• Early stage disease is curable (surgery) and radioT/chemo to help symp
• New Tx is immunotherapy + biological agents. Some mutations have direct drugs.
• RF = tobacco, smoking, asbestos, radon, air poll

SCLC = 20-25%

• Decelops in tissues of lungs
• RFs = smoking (rare in non)
• Freq mets at diagnosis, usually more aggressive. Not amenable to surgery, often very chemosensitive +/-RT. SUrgeyr only if very early stage.

Mesothelioma - 80-90% form asbestos, huge latency period 40-50yrs after exposure. Radiotherapy (pain control), surgery (small proportion), chemo, palliative/supportive

Question 47

Aortic dissection

Answer 47

• AD = tear in inner layer of aorta, blodo rushes through and causes inner and middle layers to split. Often fatal if blood goes through outside wall. Uuslaly men 60s/70s but uncommon
• Symp = sudden, severe chets pain or upper back pain, sudden severe stomach pain, loss consciousness, SOB, symptoms similar to stroke/MI, weak puls ein one arm vs other, leg pain, difficulty walking.
• TypeA = (ascending) Type b = (descending, lower aorta)
• RFs = HBP, atherosclerosis, AA, aortic valve defec, aortic coarcations, turners, marfans, male, cocaine, pregn, high intensity weight lifting.
• Complications = death from internal bleeding, organ damage, stroke
• Dx = transesopahgeal ECHO, CT, MRI

Question 48

Cyanosis

Answer 48

• Cyanosis = abnromal blue discolouraiton of skin and mucous membranes
• Ix = ABG, FBC, ECG, XR, Sputum, bloods cultures, V/Q scan, ECHO, Hb
• 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.

Question 49

Lymphadenopathy

Answer 49

•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

Question 50

Endocarditis

Answer 50

• Infective endocarditis = infections of endocardial surface of heart, deposition of platelets and fibrin -> colonisation by bacteria -> development vegetation. nativ eor prostehtic valves.
• RFs = CHD, rheumatic heart disease, IVDU, mitral valve prolapse, oV decies.
• Symptoms = fevers, rigors, malaise, dyspne, anorexia, weight loss
• Clinical findigns = roth spots, janeways lesions (palms hands), splinter haemorrhages, oslers nodes (fingertips)
• Causes = 80% from strep or staphs.
• Dx = 3sets blood cultures and ECHO. Need 2 major/one major+3minor/5 minor
  
  • 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).
• 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.

Question 51

Bronchiectasis

Answer 51

• 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
• 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).
• RFs = CF, chronic + inflamm lung disease, chronic/severe lung infections, defects in immune system
• Mx = airway clearance techniques, anti-inflammatories (long term azizthromycin + ICS), treat infection usually 2weeks (high dose ciprofloxacin useful) and treat complications (eg pulm rehab).

Question 52

CF

Answer 52

• CF = mutations in CFTR gene on chromsoome 7 which encodes for epithelal chloride channel regulated by cyclic AMP. Most commonly delta-F508.
• Patho = dehydration of airway surface fluid resulting in mucociliary dysfunction
• Presentation = most picked up on newborn heel prick or before from USS. Supported by sweat/gene test. May suspect when meconium ileus, children failing to trhie, fatty stools or recurrent chest infections. in adults rare but resp symptoms, diabetes, inferility.
• 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)
• Mx = Encouraging clearance of secretions and treating/preventing infections. Airway clearance techniques combined with mucoactiveagents (rhDNase). 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.

Question 53

Cough reflex

Answer 53

•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.

Question 54

Hyperventilation

Answer 54

• Hyperventilation = excessive ventilation of the lungs, beyond what is required for normal ABGs. Lowers pCO2 and prodcues respiratory alkalosis. Secondary hypocalcaemia also occurs.
• Causes: Exercise, metabolic acidosis, PE, hypoxia (altitude), fever, toxins, drugs, iatrogenic, anxiety, dysfunctional breathign with asthma
• 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.
• Ix = ABG, ECG, Pulmonary function tests, toxicology (eeg if syndrome)
• Tx = = rebreathing to paper bag, relaxation, treat cause, breath exercises, pharmacological.

Question 55

Interstitial Lung diseases

Answer 55

•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: Occupation/environment (silica dust, asbestos), medications, medical conditions like RA, mixed CT disease.

•RFs = age, exposure to dust etc, GORD, smoking, radiation + chemo

•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

Question 56

Pulmonary Hypertension

Answer 56

• 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.
• History – Exertional dyspnea, palpitations, syncope
• DDx – cor pulmonale, cardiomyopathies, MI, congestive HF, recurrent PE, pulmonary stenosis
• Exam – Elevated JVP, Loud P2, LPH, Pedal oedema.
• Ix – ECHO, BBP, CTPA, V/Q Scan, RHC (bloods, CXR, ECG, pulm function tests, MRI, lung biopsy )
• Tx – as per cause. Cardiosupportive therapy, prostacyclin analogues, endothelin-A receptor antagonsits, phosphodiesterase-5-inhibitors, possible thrombo-arterectomy or transplant.

Question 57

Asthma

Answer 57

• 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 = 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.

Question 58

Chronic vs acute asthma

Answer 58

Chronic:

• 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
• 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
• Acute Asthma:
• 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.

Question 59

Osteomyelitis

Answer 59

• 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 = Staphylococcus aureus is most common.
• RF = trauma, prosthetic orthopedic device, diabetes, PAD, chronic joint disease, alcoholism, IV drug abuse, chronic steroid use, immunosuppression, hIV etc.
• 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

Question 60

Common rashes

Answer 60

• Chicken pox - VSV, erythemaotus macules -> papules -> clear vesicles -> pustules
• Bacteral meningitis
• Erythema multiforme - cutaneous hypersensitivity reaction usualy by infection, targetoid or iris appearance. no tx.
• Impetigo
• Lymes disease - borrlia burdgedofrie
• Herpes smplex may complicate eczema
• Cellulitis = dermis - subcut
• Necrotising fascities

Question 62

Septic Arthritis

Answer 62

• 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.
• RF = Increasing age, dm, Prior joint damage, joint surgery, hip/knee prosthesis, skin infection in combo with joint prosthesis, immunodeficiency
• 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 – 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: 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 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.

Question 63

Mechanisms of antibiotic acquired resistance

Answer 63

• Bacterium destroys the antibiotic
• Bacterium modifies its target:
• Bacterium shuts the door:
• Bacterium pushes it out: efflux pumps
• 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.

Question 64

ABG interpretation

Answer 64

Question 65

ECHO key

Answer 65

•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
• RV = primarily longitudinal muscle fibres LV = primary radial muscle fibres. ECHO assess radial function with EF and Longitduinal with tissue doppler.
• 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: 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
• Red – towards probe, blue away. Akinetic – ventricle not contracting at all.
• E/E’ ration = increased with ventricular stiffness and reduced compliance. >1 indicates elevated LV diastolic pressures.
• Global longitudinal train – bulls eye lot assess 17LV segments to show regional/global problems.
• Normally L->R flow in heart as left ventricle higher pressure.

Question 66

Asthma drugs and their MOA

Answer 66

•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 (beclomethasone, dipropionate): Suppress inflammation mainly by switching off multiple activated inflammatory genes through reversing histone acetylation by recruiting HDAC2

•LABA – beta agonists (salmeterol): Act on Beta 2 receptors, causing smooth muscle relaxation + dilation airways. At least 12hours effect.

•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.

Question 67

Antifungals

Answer 67

• 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)

Question 68

Antivirals

Answer 68

• 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)

Question 69

Antiparasitic drugs

Answer 69

• 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.

Question 70

Antibacterials - common ones

Answer 70

•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 – 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 (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– 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 – 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 – Ciprofloxacin, bidn to topoisomerase IV/ DNA gyrase- DNA complexes. Prevents DNA replication > stops cell growing/dividing. Restricted by S/E, when no other options.