Pathology: ALL Flashcards

Question

Explain the components and, indications and benefits of the cardiac rehabilitation program. | what is it, components and benefits.

Answer 1

* Support, exercise & education to help strengthen patient’s hearts after a cardiac event such as ACS * Timing: early referral, early attendance Components: * Thorough assessment of MH, smoking, medications, exercise capacity and QOL * Health behaviour change, lifestyle risk factor management (physical activity, diet, smoking cessation) * Intermittent reassessment and adjustment of plans * Follow up (transfer of care) Benefits * Reduced CVD mortality * Reduced hospital admissions * Improvement in quality of life * Improved cardiovascular risk profile

Answer 2

When pain comes on 1. glyceryl trinitrate spray 400 micrograms sublingually, repeat every 5 minutes if pain persists, up to a total of 3 doses if tolerated TO decrease risk 2. education of patients 3. Antiplatelet: aspirin and P2Y12 inhibitor: PCSK9 enzyme that normally reduces the number of available LDL receptors on cells, mainly hepatocytes. Inhibitors of this enzyme thereby ↑ the number of receptors, resulting in more LDL cholesterol being removed from circulation. Statins: Inhibit HMG CoA reductase - the rate limiting enzyme in cholesterol synthesis in liver, thereby ↓ the amount of cholesterol produced by the liver - liver cells respond to ↓ cholesterol by activating the transcription factor (SREBP) to ↑ LDL receptor expression on cells. Thus, ↑ cholesterol is extracted from blood and taken up into cells for storage or excretion. Beta blockers: bind to B1 and 2 receptors (B1 are heart ones) and stop nor-adrenalin and adrenalin from increasing cardiac function. Angiotensin converting enzyme inhibitors: inhibits angiotensin 1 converting to A2 therefore, vasodalation of blood vessels Calcium channel blockers: preventing calcium from entering myocytes. Calcium causes the heart and arteries to squeeze (contract) more strongly. By blocking calcium, calcium channel blockers allow blood vessels to relax and open.

Answer 3

STATIN: Inhibit HMG CoA reductase, ↓ the amount of cholesterol produced by the liver - liver cells respond to ↓ cholesterol by activating the transcription factor (SREBP) to ↑ LDL receptor expression on cells. Thus, ↑ cholesterol is extracted from blood and taken upfor excretion. * first line * cannot take while breastfeeding or preg * SE: myalgia, GI upset EZETIMIBE:Inhibits absorption of cholesterol from the duodenum by blocking transport protein NPC1L1 in the brush border of enterocytes → ↓cholesterol concentration. * cannot take while breatfeading * GI upset, pain, headache. FIBRATES: stimulate cellular fatty acid uptake, conversion to acyl-CoA derivatives, and catabolism by the beta-oxidation pathways, which, combined with a reduction in fatty acid and triglyceride synthesis, results in a decrease in VLDL production. * avoid use with statins * rhabdomyolysis, GI symtoms PCSK9 inhibitors: PCSK9 is an enzyme that normally reduces the number of available LDL receptors on cells, mainly hepatocytes. Inhibitors of this enzyme thereby ↑ the number of receptors, resulting in more LDL cholesterol being removed from circulation. * do not use in pregnancy * flu like symtoms, sores and ithcing.

Answer 4

Demographics: M>F, Risk factors: FHx or PMH CKD, hypertension, diabetes, dyslipidaemia, stroke, early onset coronary heart disease and low birth weight * Modifiable lifestyle factors include: smoking, diet, weight control, obesity, exercise, recreational drug use, alcohol intake Clinical features: * Often asymptomatic * Blood pressure ≥ 140/90 mmHg * Retinopathy * Other: headache, visual changes, dyspnoea, chest pain Investigations: * Cardiac exam * Urine dip stick * Blood tests: fasting metabolic panel with estimated GFR, lipid panel * 12-lead ECG * Blood pressure treatment targets: Generally, for patients who require BP-lowering therapy the aim is to reduce BP to below 140/90 mmHg. * Lifestyle Advice * Pharmacological Treatments: * ACE inhibitors, (ARB), calcium channel blockers, Thiazide and thiazide-like diuretics (Beta Blocker not recommended) Complications: Stroke, CAD, Kidney disease, Heart Failure, AF, retinopathy, PVD, Aortic dissection, death

Answer 5

The Framingham Heart Study (launched 1948) was originally designed to identify common risk factors contributing to cardiovascular disease (CVD). The study now spans over 3 generations, studying the family patterns of CVD, and includes diverse populations. Risk Factors Identified in Framingham Study: high blood pressure, high cholesterol (HDL vs LDL + total triglycerides), unhealthy eating patterns (fat, sugar, alcohol etc.), age (particularly >50yrs), smoking, physical inactivity and unhealthy weight. Sex and race changes the impact of risk factors and CVD development. Australian CV risk calculator Differences: * Australian calculator measures 5-year risk while Framingham measures 10-year * Australian calculator doesn’t include information on the presence of hypertension, and whether there is Tx for hypertension being provided * Australian calculator incorporates ECG LVH while Framingham does not

Answer 6

Screening is defined as “the examination of asymptomatic people in order to classify them as likely or unlikely to have a disease”. Criteria used for screening * Condition should be an important health problem Coronary heart disease leading cause of death * Recognisable latent or early symptomatic stage CVD is progressive and has a variety of early symptoms * Natural history of the condition should be adequately understood pathophysiology of most of CVD are well understood * Accepted treatment for patients with recognised disease there are several methods of treatments for CVD including medications, surgery and rehabilitation * Suitable test or examination that has a high level of accuracy sensitivity of 80% and specificity of 69% * Test should be acceptable to the population this test is simple, fast and non-invasive * Agreed policy on whom to treat as patients * Facilities for diagnosis and treatment should be available can be done online or by a healthcare professional * Cost of screening (including diagnosis and treatment of patients diagnosed) should be economically balanced in relation to possible expenditure on medical care as a whole no cost * Screening should be a continuing process and not a ‘once and for all’ project screening is recommended every 2 years

Answer 7

Who to Assess * >45 every 2 years for people at medium to high risk * Blood tests for people of low risk * >74 documented as 74 years. This may underestimate the five year risk, but it will give an estimate of the minimum risk. * Patients with a family history of premature CVD (in a first-degree relative – men aged <55 years, women aged <65 years) or obesity may be at greater risk. Similarly, patients with depression and atrial fibrillation (AF) may also be at increased risk. * Indigenous Australians greater than 35 Management Low absolute risk: <10% cardiovascular disease (CVD) risk * Provide lifestyle advice and education * Offer pharmacotherapy for hypertension * Review blood pressure of 140-159 mmHg after two months of lifestyle advice Moderate risk: 10-15% absolute CVD risk * Provide intensive lifestyle advice * Consider pharmacotherapy if systolic blood pressure is 140-159 mmHg or diastolic blood pressure is 90-99 mmHg * If systolic blood pressure is 130–139 mmHg or diastolic blood pressure is 85–89 mmHg, review BP in six months * Offer pharmacotherapy for HTN and lipid therapy simultaneously with lifestyle intervention if BP persistently over 160/100 mmHg or if family history of premature CVD or patient is of South Asian, Middle Eastern, Maori, Aboriginal, Torres Strait Islander or Pacific Islander descent High risk: >15% absolute CVD risk * Provide intensive lifestyle advice * Commence pharmacotherapy (simultaneously with lipid therapy unless contraindicated)

Answer 8

clinical presentation * history of precipitating aetiology * autoimmune/inflammatory - SLE, RA, ARF * bacterial/viral infection - TB, COVID, coxsackie, etc. * cancer - malignancy * uraemia, post MI/Dressler’s syndrome, trauma * fever * chest pain * sharp, retrosternal, radiates to neck/shoulder * worse on inspiration, coughing, swallowing, lying supine * relieves leaning forward * pericardial friction rub * pericardial effusion with cardiac tamponade * triad of hypotension, raised JVP, muffled heart sounds * tachycardia, pulsus paradoxus investigations * ECG * widespread ST elevation (with concavity) & PR depression * reciprocal ST depression & PR elevation in aVR * electrical alternans if effusion * ECHO * can show pericardial effusion * CXR * increased cardiac silhouette if effusion * FBC * leukocytosis, elevated CRP & troponin management * treat underlying cause (e.g. dialysis for uraemia) * anti-inflammatories * high dose NSAID * colchicine (continued for 3 months) * pericardiocentesis or pericardial drain if pericardial effusion * follow-up as outpatient

Answer 9

AORTIC DISSECTION Demographics * 60-80 yr olds: 8.6 per 100 000 people * Over 80 yrs: 32 per 100 000 * 75% occur in patients aged between 40-70 yrs * 3 times more common in males than females Risk Factors * Male sex * >65 years old * Hypertension * Smoking * Aneurysm * Congenital disorders: marfan syndrome, * Inflammatory disease: aortitis, giant cell arteritis, Takayasu arteritis, Systemic lupus erythematous * Aortic wall stress: previous cardiovascular surgeries, wall thinning, structural abnormalities Clinical Features Abrupt onset of severe chest, back or abdomen pain (ripping or tearing). Precordial or interscapular pain. * Less than half patients will also present with: * Pulse deficit * Murmur of aortic regurgitation * Hypotension * Syncope * Symptoms of malperfusion (stroke, MI, intestinal infarction, renal insufficiency, paraparesis or paraplegia) Investigation Findings 12-lead ECG – presence of nonspecific ST-segment or T-wave changes. Chest X-ray – widened mediastinum or abnormal aortic contour (50% patients) (Sensitivity and specificity of X-ray and ECG are too low for rule-out or rule-in of aortic dissection). Troponin – elevated if dissection causes myocardial ischemia FBC – leucocytosis, creatinine elevated with renal artery involvement CT, echocardiogram and MRI (highly accurate in diagnosis)

Answer 10

AORTIC ANEURYSM Demographics * More common over 50 yrs old * Affects 4-7% men and 1-2% women over the age of 65 Risk Factors * Smoking (accounts for about 75% of all abdominal aortic aneurysms) * Male sex * Advancing age * Family history * Hypertension * Hypercholesterolaemia * Atherosclerosis * Congenital disorders: marfan syndrome, Loeys-Dietz syndrome, Vascular Ehlers- Clinical Features Can develop and grow before causing any symptoms. * Pulsatile mass * Pain and tenderness on palpation * May present with abdominal, back or flank pain * Bruit on auscultation Ruptured aneurysm: shooting abdominal or back pain with a pulsatile abdominal mass + severe hypotension. Investigation Findings * Ultrasound * CT – size, shape, potential for rupture

Answer 11

Starling Forces * Capillary Hydrostatic Pressure: * Plasma Colloidal Pressure: o Osmotic pressure caused by blood proteins draws fluid in * Interstitial Fluid (Hydrostatic) Pressure: o Hydrostatic pressure in tissues, may draw or oppose flow from capillary o Varies with capillary bed: positive in glomerulus, negative in loose tissues like the skin * Interstitial Fluid Colloidal Pressure: o Proteins in tissues causes osmosis out of capillary Pitting vs non-pitting Pitting oedema: * Indentation in the affected areas * Excess fluid mainly composed of water Non-pitting oedema : * Associated with conditions affecting the thyroid or lymphatic system * Build up of proteins, salts & water

Answer 12

↑ Capillary Hydrostatic Pressure → ↑ Venous Pressure: DVT, congestive HF (R), liver cirrhosis. ↓ Plasma Colloidal Pressure: IBD, malnutrition, nephrotic syndrome Pulmonary Oedema CARDIOGENIC · Decrease in left ventricular systolic function & increase in systemic vascular resistance will lead to increased capillary hydrostatic pressure · Causes exudation of fluid from vessels into lung interstitium & alveoli NON-CARDIOGENIC * Increased capillary permeability results in exudation of protein rich fluid into the alveoli * Common causes include sepsis and pneumonia (usually infective causes) Signs & Symptoms * Reduced pulmonary compliance * Dyspnoea, cough * Orthopnoea * Paroxysmal Nocturnal Dyspnoea (PND) * Cyanosis due to inefficient gas exchange * Crackles on auscultation

Answer 13

Mitral stenosis: At the beginning of diastole, the mitral valve opens but is narrowed so there is decreased filling into LV: Opening snap at beginning of S2 followed by a mid-diastolic rumble (EXPIRATION) Mitral regurgitation: Mitral valve leaks when LV contracts & blood flows backward into LA: Pansystolic murmur high pitched, soft S1 (EXPIRATION) Aortic stenosis: Blood is unable to flow freely from LV to aorta during systole. Initial ejection click then crescendo-decrescendo pattern as pressure of blood flow ↑ then ↓ Systolic ejection murmur(EXPIRATION) Aortic regurgitation: Valve does not close completely, leaking blood into LV: Early diastolic decrescendo murmur (EXPIRATION) Tricuspid regurgitation: Valve does not close completely, leaking blood backward into RA: Pansystolic murmur high pitched (INSPIRATION)

Answer 14

Demographics: ATSI, younger, rual Aetiology: autoimmune reaction to the bacteria group A streptococcus (S. Pyogenes) Risk factors: Overcrowding, Poor living, reduced immunity, reduced health literacy Pathophysiology 1. Molecular mimicry GAS M protein shares proteinswith cardiac myosin, tropomyosin, and laminin--> T, B cells & antibodies target streptococcal M protein and cardiac myosin. CD4 causing realease of TNF a, IL2 and IFg Clinical features: Fever, Migratory polyarthritis most commonly in the knees, ankles, elbows, and wrists, congestive heart failure, including chest pain, shortness of breath, fast heartbeat, Fatigue, Chorea, Erythema marginatum, Subcutaneous nodules DIAGNOSTICALLY must have symptoms - and initial gas infection. Investigation findings: Positive ASO and anti-DNAase-B titre AND Raised CRP ≥30 mg/L and ESR ≥30 mm/hr Management: Following confirmation of ARF diagnosis, IM benzathine penicillin G injections must be given every 3-4 weeks for a minimum of 10 years as secondary prophylaxis

Answer 15

Demographics: around 20 ys, more likely female Aetiology: Repeated bouts of ARF due to GAS result in the development of RHD Risk factors: GAS infection, Overcrowding, Low SES, Poor hygiene Pathophysiology: Damage to heart tissue occurring in ARF leads to the formation of lesions in the cardiac tissue --> Aschoff bodies Aschoff bodies in the endocardium, inflammation occurs in the L sided valves, and results in fibrinoid necrosis within cusps and/or tendinous cords. This inflammation leads to progressive fibrosis consisting of leaflet thickening, commissural fusion and shortening and thickening and fusion of the tendinous cords resulting in valvular dysfunction. Clinical Features: Chest pain, Fatigue, Breathlessness, Swelling of the legs. * Others: Arrhythmia, stroke, endocarditis, and complications during pregnancy. Ix findings: Characteristic features on ECHO are valve dependent: Mitral valve features o Prolapse of anterior leaflet o Thickened leaflet tips o Restricted posterior leaflet o Chordal thickening o Leaflet calcification o Diastolic doming of anterior leaflet (dog leg appearance) Management: 1. Secondary prophylaxis 2. Valve specific * MR → mitral valve repair is the operation of choice OR mitral valve replacement with biological or mechanical prosthesis o Avoid mechanical prosthesis if concerns about warfarin adherence or future pregnancy * MS → diuretics are indicated for patients with symptomatic pulmonary venous congestion or pulmonary edema o Surgically: Percutaneous balloon mitral valvuloplasty (PBMV) or mitral valve repair or replacement * AR, AS, TR, TS→ valve replacement/ repair Fertility considerations * RHD is exacerbated by pregnancy due to the increased CO demand therefore use IUDs or implants * planning pregnancy or are pregnant require coordinated health care to avoid multiple appointments and incurring of high travel costs and increased time away from their community * Anticoagulants required post surgery pose serious risks in pregnancy to mum and baby including haemorrhage and teratogenicity Dental considerations - All those with ARF and RHD need regular dental review to reduce their risk of infective endocarditis Complications: HF, Arrhythmia, PuL HTN Prognosis: Severe carditis at first presentation is correlated with poorest prognosis

Answer 16

Primordial: improvements in living conditions that aim to decrease poverty and overcrowding. 1. Bathing and washing clothes 2. Safe disposal of waste water 3. Improving nutrition 4. reduce environmental impacts - pests, dust, temperature, hazards causing trauma Primary: prevents the autoimmune response to the group A streptococcal infection from occurring. If primary prophylaxis is given during the early stage of the infection, antibiotics will interrupt the autoimmune response, and therefore ARF does not occur. Antibiotics given for infection. Secondary: reduce the spread of new group A streptococcal strains. These strains may induce acute, chronic or repeated ARF attacks. Through the use of penicillin, group A streptococcus can be eradicated, preventing initial ARF attacks, as well as recurrences of ARF. Tertiary :prevention of morbidity and mortality, which ultimately works by preventing the complications associated with RHD. This is achieved through the medical management of heart failure, operative management of valve lesions and treatment for the consequences of RHD, including stroke, infective endocarditis and arrhythmia. Quaternary: Medical surveillance to ensure the patient is not over medicalised.

Answer 17

* Stenosis = failure of complete valve opening obstructs forward flow of blood from one heart chamber into another o due to cusp abnormality e.g. calcification or scarring MS - dyspnea, orthopnea, PND, ascietes, increased JVP AS - dyspnea, angina, excertional TS - increased JVP, arrhythmias PS - cynosis and raised JVP * Regurgitation = failure of complete valve closure allows back flow of blood from one heart chamber into the previous o due to diseased cusps or supporting structures e.g. chordae tendineae or papillary muscles MR - pulmonary oedema, enlarged heart AR - wide pulse pressure, hyperkinietic heart beat, displaced heart TR- hepatomegarly, increased JVP, ascites PR- right ventricular dialation.

Answer 18

RIGHT HEART FAILURE BODY o Decreased appetite, anorexia, nausea o Peripheral oedema o Weight gain o Hepatomegaly o Ascites o Splenomegaly o Jugular vein distention SYSTOLIC DYSFUNCTION * Ventricles are still being filled but contraction force is reduced, reducing SV and CO DIASTOLIC DYSFUNCTION * Heart failure of inadequate filling due to the inability of the cardiac muscle to relax DEMOGRAPHICS: caused by L Aetiology: HTN, CAD, TM, Arrhythmias, alcohol, drugs, Pathophysiology: RV failure  increased RV preload (from accumulation) increased RA pressure,  systemic venous congestion As the blood builds up in systemic circulation, peripheral oedema occurs (blood cant drain into IVC) – pitting oedema causing weight gain Investigation finding CXR : 1) pulmonary vessel (venous) dilatation, moderate and marked, 2) pulmonary oedema, patchy and diffuse, 3) Kerley's (septal) lines, and 4) pleural effusion.

Answer 19

LEFT HEART FAILURE * LUNGS o Dyspnoea on exertion o Orthopnoea o Cough o Paroxysmal nocturnal dyspnoea o Cyanosis o Restlessness o Fatigue o Basilar crackles o Elevated pulmonary capillary wedge pressure o Tachycardia SYSTOLIC DYSFUNCTION * Ventricles are still being filled but contraction force is reduced, reducing SV and CO DIASTOLIC DYSFUNCTION * Heart failure of inadequate filling due to the inability of the cardiac muscle to relax DEMOGRAPHICS: more common than right Aetiology: HTN, CAD, TM, Arrhythmias, alcohol, drugs, Blood pushed into the aorta is reduced increased blood in the ventricle LV pressure rises preventing the LA from emptying, raising LA pressure backlog of fluid into lungs Causes pulmonary congestion (increased pulmonary venous pressure) and the increased pulmonary hydrostatic pressure This backlog increases RV afterload  RV hypertrophy and eventual RV failure as well Investigation finding CXR : 1) pulmonary vessel (venous) dilatation, moderate and marked, 2) pulmonary oedema, patchy and diffuse, 3) Kerley's (septal) lines, and 4) pleural effusion.

Answer 20

ACUTE * Furosemide IV/IM * GTN sublingual/oral * Dobutamine 2.5-15 microg/kg/min IV * Treat underlying arrhythmia/infection * <94% O2 = non-invasive ventilation via high-flow O2 mask * CPAP if unresponsive * Intubate if unresponsive * IDC to monitor urine output LONG-TERM * All patients: ACE-I/ARB + beta-blocker * If symptomatic despite max. dose, substitute ACE-I/ARB with ARNI * Loop diuretics to decrease symptoms General Education: * Fluid management advice * Na/K/dietary intake (e.g. via dietician) * Physical activity support + obesity advice * Control other modifiable CVD risk factors * Management of night-time symptoms via pillows/recliner * Heart transplantation * Ventricular-assist devices (till transplant/permanent)

Answer 21

* Acute infective endocarditis o Sudden onset o Rapidly progressive with high fevers, rigors and sepsis * Subacute infective endocarditis o Slower, insidious onset Demographics: M>F, over 60y Aetiology: 60% Strep. Viridans, 20% Staph aureus Pathophysiology 1. Preparation of the cardiac valve for bacterial adherence 2. Adhesion of circulating bacteria to the prepared valvular surface 3. Survival of the adherent bacteria on the surface with propagation of the infected vegetation risk factors: IVDU, weakenned immune system, prostetic valve. birth defects clinical features: ACUTE * Sudden high fever * Tachycardia * Fatigue * Rapid and extensive heart valve damage causing symptoms of heart failure SUBACUTE * Fatigue * Mild fever * Moderately tachycardia * Weight loss * Sweating * Anaemia investigation findings: * Blood cultures – primary investigation and yield the causative micro-organism * Echocardiography – show heart valve vegetations and damage to the heart

Answer 22

Pathophysiology: supraventricular arrhythmia There is pre-excitation of the atria due to bursts of electrical activity from other foci or from aberrant pathways Atrial fibrillation is sustained by re-entry rhythms. -->Due to the abnormal conduction, the atria contract rapidly but ineffectively, and uncoordinatedly. This leads to stasis of blood within the atra and risk of formation of thromboembolism and stroke causes P - Pulmonary causes I - ischemia/infarction/CAD R - Rheumatic heart disease/mitral valve regurgitation A - Alcohol, anaemia T - Thyrotoxicosis/toxins E - Electrolytes/Endocarditis S - Sepsis investigation findings ECG * Irregularly ireegular RR intervals * Tachycardia is common * P waves are not discernable (fibrillatory waves) * Typically narrow QRS complex FBC: check for anaemia Electrolytes: check for imbalance Serum glucose TSH and T4 levels: screen for hyperthyroidism Renal Function: eGFR and albumin management: 1. Reduction of thromboembolism and stroke risk -Use NOACs, antiplatelets 2. Symptoms relief (rate/rhythm control) Rate control: atenolol or metoprolol 25mg Rhythm control - Electrical cardioversion to restore sinus rhythm 3. Treatment of associated co-morbidities CHA2DS2-VASc Score helps to determine the 1 year risk of a thromboembolic event * Congestive heart failure or LV dysfunction * Hypertension * Age 75 years or older * Diabetes mellitus * Previous stroke, transient ischemic attack or thromboembolism * Vascular disease (peripheral arterial disease, complex aortic plaque or prior MI) * Age 65-74 years * Sex (female) complications: Ischemic stroke, Heart failure , Cardiac arrest

Answer 23

L-R - Atrial Septal Defect (ASD) Small → asymptomatic until adult, CHF, pulmonary HTN (late, rare). RV hypertrophy - Ventricular Septal Defect (VSD) Most are small → asymptomatic, RV hypertrophy, pulmonary HTN and CHF - Patent Ductus Arteriosus (PDA) IE common, Small → asymptomatic, Large → pulmonary HTN → shunt reversal, Eisenmenger syndrome with cyanosis and CHF R-L (cynotic) Tetralogy of Fallot (FT): Clubbing, polycythaemia and paradoxical embolism, Enlarged boot shaped heart on CXR. Mild (pulmonary stenosis) → like VSD, no cyanosis Obstruction Coarctation of Aorta (COA) Infantile/pre-ductal (with PDA) → cyanosis of lower half of body → severe, die early, Calf pain from claudication

Answer 24

Demonstrating Understanding Personal Communication · Rapport: · Language: · Listening · Time · Non-verbal communication · Personal Space · Touch · Silence · Eye contact · “Yes”

Answer 25

Venous ulcer: Varicose veins and Venous stasis Location: Gaiter region Lateral and medial malleoli Pathogenesis: Venous stasis fluid accumulation in tissue + chronic low grade ischaemia → loss of skin integrity → ulceration Features: Wet + shallow + irregular, Itchy & often painful Arterial ulcer: Atherosclerosis, Buerger’s disease Location: Toes, M/L malleolus Pathogenesis: Occlusion of arterial lumen → ischaemia → tissue damage/death → ulceration Features: Dry + dark, Painful, Absent limb pulses, No bleeding, Trophic changes of the skin Neuropathic ulcer: Location: Pressure points Foot pads, ankles, Pathology: Loss of sensation → repeated trauma → hard callus formation and necrosis of tissue → ulcer formation Features: Deep + clean + punched out, Surrounding callus, Painless, Bleeds on probing Malignant / benign tumour Ulcer: Pathology: Sun exposure epithelial cell → mutation → epithelial cell proliferation and neoplasm → ulceration SCC: ulcerated, nodular mass, hyperkeratotic, commonly seen on the face but limbs are also affected. BCC: an elevated nodule with a central, ulcerated crater surrounded by telangiectatic vessels. Melanoma: A mole like growth with ABCDE (asymmetrical, border irregular, colour multiple, diameter >6mm, evolution), ulceration is rare Infective Ulcer: Infection with pathogenic organism → Direct virulence effect of the organism / immune response of the host damage --> tissue ulceration - Random, Often multiple ulcers, Pus + bleeding, Associated dermatitis

Answer 26

ARTERIES: · abdominal aorta o > common iliac arteries § > internal iliac artery § > external iliac artery · becomes FEMORAL artery o palpate midway between ASIS & pubic symphysis o becomes POPLITEAL artery § palpate midline of popliteal fossa (posterior knee) § > anterior tibial artery · becomes DORSALIS PEDIS artery o palpate lateral to EHL tendon § > POSTERIOR TIBIAL artery · palpate posterior & inferior to medial malleolus

Answer 27

VEINS: · varicosities: superficial veins of upper & lower leg > branches of long saphenous vein & short saphenous vein · DVTs: o thigh > Superficial femoral veins, popliteal veins o calf > Posterior tibial veins, peroneal veins

Answer 28

Demographics: Older age. female. Aetiology: Virchow’s triad * Stasis of blood, Endothelial injury and Hypercoagulability state Risk factors - recent plaster, immobilisation of lower extremities, increasing age, family hx, cancer, surgery, flights, trauma, smoking, pregnancy, obesity, HF Pathophysiology Excess thrombosis leading to obstruction and stasis (acute) 1. Risk factors of Virchow’s triad 2. Thrombosis in deep vein of leg 3. Leads to clinical presentation Clinical features * Unilateral pain and swelling in the affected area – usually calf or thigh * Red or discoloured skin * A firmness or thickening of the vein (cord) If progressed to PE – dyspnoea, tachycardia, pleuritic chest pain, cough, haemoptysis or syncope Investigation findings * Bloods – FBC, INR, aPTT * D-dimer – if negative can rule out DVT, positive does not confirm * Duplex ultrasonography – detect blockages or blood clots in deep veins Management Primary approach is anticoagulation * Direct oral anticoagulants * Low-molecular-weight heparin Complications * PE – clot breaks free and travels to lung * Post-thrombotic syndrome – development of long-term symptoms in the calf. Damage to the veins results in venous hypertension. * Increased risks of recurrent thrombosis

Answer 29

DEMOGRAPHICS Mostly occurs in people >60yrs + those with risk factors identified in PERC/Well’s criteria AETIOLOGY - Clots RISK FACTORS Condition of stasis: e.g. surgery, long flights etc.) Acute and chronic medical illness (particularly MI, HF, COPD, atherosclerosis) Well’s score > 4 warrants imaging If the answer to all of PERC is no, PE can be excluded PATHOPHYSIOLOGY Virchow’s Triad: hypercoagulable state, venous stasis, vessel injury → blood clot develops → clot dislodges + migrates to inferior vena cava, RA, RV + gets lodges in pulmonary artery → PE Dec. perfusion to lung parenchyma distal to clot (leading to ischaemia of lung tissue) Blood pumped from RV to pulmonary arteries cannot pass clot → inc. pulmonary + RV pressure → inc. RV strain → inc. RV workload + dec. RCA perfusion → symptoms of MI/RHF Inc. dead space ventilation + V/Q mismatching → chemoreceptors detect inc. CO2 + dec. O2 → signal to the brain to inc. breathing rate CLINICAL FEATURES Sharp, pleuritic chest pain + dyspnoea: ischemia of lung tissue distal to clot (chest pain can also be from inc. RV + pulmonary pressure) Tachypnoea: dec. arterial O2 Tachycardia: inc. RV + pulmonary pressure Hypotensive: inc. RV workload + dec. RCA perfusion Pleural rub “velcro sound”/”walking on snow” on inspiration + expiration May also be calf swelling + tenderness on examination INVESTIGATION FINDINGS Positive D-Dimer: body attempts to break down clot (fibrinogen breakdown products in blood) CXR: Hampton’s hump (rare but specific sign of PE), may also get Westermark’s sign (oligaemia) or pleural effusion - ischemia of lung tissue distal to clot CT-PA: filling defect - blood pumped from RV cannot pass clot | GOLD STANDARD ECG: S1Q3T3 pattern - inc. RV + pulmonary pressure

Answer 30

Warfarin MOA: Warfarin competes with vitamin K and inhibits epoxide reductase thus inhibiting the synthesis of vitamin K- dependent clotting factors, thereby leading to reduced clotting Indications: Prevention and treatment of emboli. Contraindications: Alcoholism, pregnancy, active bleeds, Route and frequency: Taken orally, usually at night - and must be taken at the same time each day Side effects: Severe bleeding, rash, bruising, nausea and vomiting, Reversibility - Vitamin K1 NOACs: non-vitamin-K-antagonist Oral anticoagulants MOA: Direct thrombin inhibitors - dabigatran * Reversibly inhibit both free and fibrin-bound thrombin. Prevents conversion of fibrinogen to fibrin Factor Xa inhibitors - rivaroxaban and apixaban * Selective for factor Xa rather than thrombin Thus blocks thrombin production, conversion of fibrinogen to fibrin Indications: Moderate to high risk unstable angina, STEMI undergoing early invasive management including PCI Contraindications: Renal impairment (CrCl <30 ml/min), Bleeding risks: Active bleeding, bleeding disorders etc, Pregnancy Route: All NOACs are taken orally Side effects Typically well tolerated - SE mainly bleeding ranging from minor Reversibility Only for dabigatran → Idarucizumab 5g IV, by bolus or infusion Heparin MOA Unfractionated Heparin * Potentiates the activity of antithrombin III which inhibits factor 2 (thrombin) and factors 9 and 10 Low Molecular Weight * Has a greater effect on factor Xa than on thrombin (only inhibits factor Xa, not II) * Advantages over regular heparin include: longer half life, less bleeding risk, less monitoring, and can be administered by the patient subcutaneously Indications:Prevention and treatment of thrombotic events such as deep vein thrombosis (DVT) and pulmonary embolism (PE) as well as atrial fibrillation (AF). Contraindications Absolute: Heparin-induced thrombocytopenia Hx, Known hypersensitivity, Active bleeding Relative: Bleeding disorders e.g. Hemophilia, Conditions w/ catastrophic bleeding e.g. haemorrhagic stroke, CrCl <30 ml/min Route and frequency of administration UFH * Typically taken IV * Route of administration and dosage of LMWH varies according to indication * Typically parentally once or BD Side effects: Bleeding from puncture sites, Wounds, Anaemia Reversibility Stop UFH or LMWH immediately - Protamine

Answer 31

Peripheral Artery Disease (Ischemia) Aetiology * Insufficient tissue perfusion due to atherosclerosis in the aorta and peripheral arteries (Atherosclerotic plaques reduce the arterial lumen → arterial insufficiency distal to the occlusion.) * Often coexists with coronary artery disease (CAD), stroke Risk Factors (same as Atherosclerosis) * Smoking * Diabetes mellitus * Arterial HTN * Dyslipidaemia * FHx: cardiovascular events in the first-degree relatives below the age of 55 (male)/65 (female) * High homocysteine levels (homocystinuria) * Obesity * High fibrinogen levels * Hyperphosphatasemia * Stress * Increased alcohol consumption

Answer 32

Intermittent claudication (10-35% of patients) * Pain, cramps, or paresthesia (burning, prickling, tingling) distal to arterial occlusion * Worsens upon exertion * Completely relieved by rest * Reproducible Critical Limb Ischemia/Chronic Limb Threatening Ischemia with Rest Pain * Severe pain or numbness in the legs and feet while not moving. Worsens when in a reclined position and improves when feet hang off the bed or standing * Shiny, smooth, dry skin in the legs or feet, * Absent or diminished pulse in the legs o Rest pain lasting > 2 weeks, Nonhealing ulcers , Tissue loss (gangrene) Acute Ischemia: Medical emergency, Sudden onset severe ischemia associated with sensory loss, motor loss and intense pain

Answer 33

Management of PAD Conservative: Smoking cessatio, exercise therapy, Foot care Medical Therapy o Antiplatelet therapy reduced morbidity and mortality  Aspirin: irreversible COX inhibition → decreased thromboxane A2 synthesis → decreased plt aggregation o Cholesterol/Lipid-lowering agents (usually statins)  Statin therapy (ezetimibe, PCSK9 inhibitors) lowers lipids. Lowering LDL-C in particular to the lowest possible target greatly improves cardiovascular outcomes. o Antihypertensive treatment  ACE-I, ARBs, CCBs, o Hyperglycaemia control Revascularisation * Minimally invasive interventional radiology: percutaneous transluminal angioplasty (PTA) with or without stenting * Surgical procedures o Operative vascular reconstruction (bypass surgery): used when a long portion of an artery is completely blocked, causing the patient to experience severe symptoms o Stenting or stent grafts- for occlusive or aneurysmal disease Amputation * Last resort o in the event of gangrene

Answer 34

Demographic: Women with a BMI greater than 30 are three times as likely to develop varicose veins. Aetiology caused by weak vein walls and dysfunctional valves. Risk factors: Age. women, pregnancy, standing. Pathology: Tortuous veins : Stasis and increased pressure of blood causes veins to change shape Enlarged, visible veins : Defective deep vein valves leads to backflow, which leads to increased pressure in superficial veins, causing enlargement Only superficial veins affected: Deep veins rely on surrounding musculature to assist with venous return, superficial veins have no assistance from muscle if valves are defective Stasis dermatitis : Blood is not able to flow out of superficial veins due to deep vein valve defectiveness, causing stasis and venous hypertension. There is subsequent leakage of blood into tissues and cutaneous inflammation. Skin will be erythematous, dry and itchy. Venous ulcers (gaiter region): Often follows stasis dermatitis. A wound of the skin has inhibited healing- due to venous insufficiency from varicose vein stasis (lack of oxygen and nutrients) and weakened skin (due to swelling). This inhibited healing leads to ulceration.

Answer 35

Demographics: - BCC can develop in younger people however common in people over 40 - SCC most commonly occurs in people over 50 Risk factors - UV radiation - causes damage to DNA - Immunosuppression- especially SCC Melanomas  Family history and genetic susceptibility * Suggested that one or more first degree relatives with melanoma are at a greater risk of being diagnosed with melanoma * People with fair skin (lack of melanin) are more susceptible to cancer * There is an association with the number of benign nevi or moles on the person’s body and melanoma diagnosis- large number of benign nevi and moles, the greater the likelihood of melanoma diagnosis

Answer 36

Henoch Schonlein Purpura (IgA Vasculitis) DEMOGRAPHICS: Children 2-8 yrs. urti PATHOGENESIS: IgA immune complexes within small blood vessels (arterioles & capillaries) necrotising inflammation CLINICAL FEATURES: Immune mediated haematuria, Proteinuria, Palpable, purpura, Abdominal pain (colicky) INVESTIGATIONS: Biopsy of affected organ = IgA deposition COMPLICATIONS: Renal disease; nephritis, chronic kidney disease, Arthritis – large joints Wegener’s Polyangitis DEMOGRAPHICS: Middle-aged adults PATHOGENESIS: Infectious exposure ANCA BV necrosis neutrophil activation endothelial cell injury & inflammation thrombosis CLINICAL FEATURES: Ear/nose/throat = sinusitis, nasal disease, subglottic stenosis (specific – loss of nasal septum), otitis media, hearing loss, ear pain, oral lesions INVESTIGATIONS: Positive (ANCA), BIOPSY COMPLICATIONS: Glomerulonephritis chronic kidney failure, Orbital mass Polyarteritis Nodosa (PAN) DEMOGRAPHICS: Middle-aged or older adults PATHOGENESIS: Necrotising, Immune complex mediated systemic inflammation of arteries CLINICAL FEATURES: Systemic features – fever, anorexia, weight loss, myalgia, arthralgia Skin – cutaneous or subcutaneous nodules, palpable purpura, livedo reticularis, skin infarction INVESTIGATIONS: Biopsy of affected tissue Angiography COMPLICATIONS: Acute renal failure, Polyneuropathy Buerger’s Disease DEMOGRAPHICS: MALES, JEWISH, smoking PATHOGENESIS: Inflammation of arteries hypersensitivity reaction thrombosis segmental, transmural inflammation + lumen thrombosis gangrene CLINICAL FEATURES: General systemic signs, Pain, Raynaud’s phenomenon COMPLICATIONS: Gangrenous toes amputation Kawasaki Disease DEMOGRAPHICS: children; seen before 5 yrs old PATHOGENESIS: Delayed hypersensitivity reaction in genetically susceptible individuals – triggered by viral infection CLINICAL FEATURES: Fever, bilateral nonexudative conjunctivitis, cervical lymphadenopathy, polymorphous rash, oral cavity changes (erythema, cracked lips, strawberry tongue) INVESTIGATIONS: Coronary artery lesions seen on echocardiogram COMPLICATIONS: Acquired cardiac disease in children Giant Cell Arteritis DEMOGRAPHICS: Older age group: >50 yrs old PATHOGENESIS: Immune dysfunction to unknown antigen; T cell inflammation and formation of granuloma giant cells = damages blood vessels and causes thrombosis CLINICAL FEATURES: increasing headache Diplopia, Tender temporal arteries INVESTIGATIONS: Thickened palpable, nodular tender temporal artery COMPLICATIONS: vision loss

Answer 37

Dyspnoea is the subjective sensation of breathlessness that is excessive for any given level of physical activity. Pathophysiology is complex – involves activation of several pathways that lead to increased work of breathing, stimulation of receptors of upper or lower airway, lung parenchyma or chest wall and excessive stimulation of the respiratory centre by central and peripheral chemoreceptors. Pulmonary Embolism: Pleuritic chest pain or Previous PE, Immobilization Pneumothorax: Trauma/ Malignancy/ Tall and thin :Marfans Syndrome, Tracheal deviation, Absent or reduced breath Asthma: atopy, Cough at night/ morning, accessory muscles , Bilateral Consolidation Pneumonia: Cough painful & dry at first, Fever and rigor, Increased vocal fremitus, Reduced breath sounds , Bronchial breath sounds crackles Pleural effusion: Transudate- cardiac failure, Exudate- Pneumonia, Pulmonary infarction, Displaced trachea and apex beat, Stony Dullness over fluid Interstitial Lung disease: Drug & occupational Hx, Travel Hx , Reduced Expansion, Cough Clubbing Crackles (3 Cs)

Answer 38

community-acquired: sick contacts, smoking, Strep pneumoniae (gram +ve diploccoci) Young, healthy, 1-3 days high fever. Pleuritic chest pain, Rusty sputum, purulent cough, fever, cyanosis, enlarged tonsils, cervical lymphadenopathy, confusion, ↑HR, ↑RR, ↓BP, ↓ expansion, ON XRAY:Unilateral consolidation of lobe. hospital-acquired:seen in unhealthy, hospital stay >2 days, Gram negative: Klebsiella, haemophillus influenzae, 1-3 days high fever. Pleuritic chest pain, fever, cyanosis, ↑HR, ↑RR, ↓BP, ↓ expansion, dull percussion, increased fremitus (consolidation), CXR: bronchial (patchy consolidation, usually bilateral lower lobes atypical: Young people, Mycoplasma pneumoniae, HPC: slow onset, sever dyspnoea, wheeze, dry cough, flu-like symptoms, CXR: interstitial consolidation, appears worse than symptoms suggest. aspiration: People with dysphagia, Parkinson’s, Accidental ingestion of mixed oral flora, bronchospasms, crackles on auscultation, cough with foul-smelling sputum, CXR: superior segment of right lower lobe (most common site of aspiration) – infiltrates on X-ray

Answer 39

assess severity via severity scores: CURB-65 · 1 point each for: acute confusion, urea >7, resp rate >30, BP <90/<60, age >65 · 0-1 = treat in community, 2 = inpatient, 3-5 = inpatient & consider ICU · can use abbreviated version CRB-65 if access to bloods unavailable § if any red flags present – tachypnoea >22, tachycardia, hypotension SBP <90, hypoxia <92%, lactate >2, multi-lobar, acute confusion § also consider social circumstances e.g. support at home, comorbidities, etc. o to identity requirement of ICU or higher risk of MORTALITY: § SMART-COP · 2 points each for: SBP <90, oxygen low (PaO2 <70 or O2 sat ≤93% or PaO2/FiO2 <333 if age ≤50 ; , arterial pH <7.35 · 1 point each for: multi-lobar, albumin <35, resp rate >25 if age ≤50 or >30 if age >50, tachycardia >125, acute confusion · low if 0-2, moderate if 3-4, high if 5-6, very high if 7+ empirical antibiotics o based on severity § low: · usually managed in community with oral therapy · monotherapy with amoxicillin OR doxycycline or clarithromycin (if clinical suspicion of atypical pathogens or penicillin allergy) · combination therapy with amoxicillin + doxycycline (if unable to review or no improvement with monotherapy within 48 hours) § moderate: · combination therapy with oral amoxicillin OR IV benzylpenicillin + oral doxycycline OR clarithromycin § high: · combination therapy with IV ceftriaxone or cefotaxime + IV azithromycin · additional therapy based on pathogen e.g. staph aureus · switch once stable to oral amoxicillin + doxycycline or clarithromycin

Answer 40

Assessing pneumonia: shortage of healthcare staff, particularly those trained in the management of severe pneumonia Stoic attitude resulting in fewer presentations to health clinics for pneumonia. CXR machines may not be available in some rural settings. This is an essential component in the diagnosis of pneumonia There is a delay in diagnosis because certain/most investigations are not available, and thus must be outsourced Management of pneumonia * Patients who need intensive care support must be transported to a centre with appropriate equipment. o Some rural and remote areas do not have equipment necessary to treat severe pneumonia – such equipment include ventilators, oxygen machines, specialist medications. o Lack of specialist access. o Delay in arriving to a specialist centre/hospital that can manage pneumonia, leading to progression of symptoms.

Answer 41

COPD = chronic pulmonary disease that presents with progressive shortness of breath caused by airway inflammation. It is subdivided into chronic bronchitis and emphysema. Demographic: M, >60, Smoker, occupation. Aetiology:Tobacco use, Air pollution, Recurrent pulmonary infections and TB, Premature birth, Alpha-1-antitypsin deficiency Pathophysiology C Bronchitis:Bronchial Inflammation IL, TNF, IFNγ, Excess mucous & narrowing (fibrosis) of bronchi Emphyema: 1. Neutrophil Protease - macrophage MMP. -Alveolar wall & elastic fiber loss. -Loss of recoil, air trap, No inflam/fibrosis. Clinical features CB: Cough & Wheezing. Bronchial inflam. & recurrent infections Emph: Dyspnea, Barrel chest, Alveoli & elastic fiber loss. Management:COPD X COnfirm diagnosis, optimise function, prevent deteriation, develop support and stop exaccerbations.

Answer 42

First-line management (all cause): * Salbutamol 100 micrograms, up to 10 separate actuations by inhalation via pMDI with spacer, repeated as necessary * OR terbualine 500 micrograms, 1 or 2 actuations inhalation * OR ipratropium 21 micrograms, up to 6 separate actuations by inhalation via pMDI with spacer * Systemic corticosteroids shorten duration of hospital admission and hastens return to previous lung function and stable symptom control. o Should be used routinely for severe exacerbations of COPD o 5-day course is adequate of Prednisone 30-50mg orally, once daily. * Oxygen therapy if patient is hypoxaemic aiming for saturations of 88-92% o Caution due to risk of hypercapnic respiratory failure during an exacerbation Antibiotic regime: * Do not use antibiotic therapy unless the patient has clinical features suggestive of bacterial infection * Shared decision making to determine whether antibiotic therapy is useful * If indicated – use oral antibiotic therapy for all patients, including hospitalised. o Amoxicillin 500mg orally, 8-hourly for 5 days OR o Amoxicillin 1g orally, 12-hourly for 5 days o Doxycycline 100mg orally, daily for 5 days.

Answer 43

Infleunza Annual vaccinations is the most important measure to prevent influenza and its complications and is recommended for all individuals aged 6 months and over. * Recommended to get in April * Best protection occurs within the first 3-4 months following vaccination. Not immediately effective Free flu vaccinations from about May-June for certain population groups: 6m-5y, >65, preg, ATSI, Pneumococcal * Bacteria Strep pneumoniae - can cause: meningitis, pneumonia and bacteremia etc. * Vaccine recommended for: infant/ kids, >70, ATSI >50, conditions, * Vaccines available in Aus: 13vPCV, 15vPCV and 23vPPV * All children are recommended to receive 13vPCV in a 3-dose schedule at 2, 4 and 12 months of age. Can be received as early as 6 weeks, then next dose would be 4 months. * Some Infants and children including Aborigional and Torrest Strait Islander children or those with a risk condition(s) for pneumococcal disease need extra doses. * A single dose of 13vPCV or 15vPCV is recommended for all non-Indigenous adults at 70 years of age.

Answer 44

Contraindications Absolute: * Anaphylaxis Precautions: * Egg allergy, Latex allergy, Guillain-Barre syndromimmune-oncology therapy Effectiveness/ Benefits * About 70-90% strain-specific effectiveness in healthy adults for 1-3 years * In healthy adults is associated with reduced absenteeism and reduced demand on healthcare resources * Effectiveness does not wane however yearly antigenic drift in the circulating strains of influenza virus results in yearly vaccinations * In elderly people, the protection conferred against influenza is about 30-60%, but efficacy of preventing hosptalisation and pneumonia is around 50-60%. Complications * Injection site reactions - induration, swelling, redness pain * Systemic reactions few hours after administration and lasts for 1-2 days: fever, malaise, myalgia * Immediate adverse reaction: hives, angioedema, anaphylaxis * Fever and febrile convulsions in children under 5 years (associated with vaccines not currently available in Aus) * Guillain-Barre syndrome

Answer 45

DEMOGRAPH: rural, ATSI, SDOH, W, kids. AEITOLOGY: Obstructive lung disease associated with an impaired host defence or result of an infectious insult. PATHOPHY: Initial infection → inflammation → impaired mucocilliary clearance → airway mucus hypersecretion + obstruction → microbial colonization/infection → bronchial dilation + airway destruction RISK FACTORS: post-infection, primary/secondary immune deficiency, asthma CLINICAL FEATURES Chronic cough, sputum +/- recurrent chest infections (exacerbations), haemoptysis, chest pain, SOB, lethargy + exercise initiation, chronic sinus inflammation + GORD INVESTIGATION FINDINGS Pathology: FBC, immunoglobulin deficiencies, CRP Sputum MCS: mostly bacteria Functional assessment: spirometry + DLCO + 6min walk test Imaging: CXR, CT Additional: sweat test, genetic testing

Answer 46

DEMOG: overseas-born residents AEITOLOGY Caused by Mycobacterium tuberculosis - spread when a person with active TB in lungs coughs/sneezes PATHO: Aerosolization → phagocytosis → phagolysozome blockage + replication → T-helper response (TH1) → granuloma formation → clinical manifestations → active disease + transmission A) Aerosolization occurs when a person with active tuberculosis forcefully expires through actions such as coughing. B) Inhaled droplets small enough to reach the alveolar sacs, where they will encounter macrophages, dendritic cells + monocytes. The macrophages will phagocytose the bacteria and attempt to destroy the invader. Dendritic cells migrate to lymph nodes to activate T-helper cells. C) M. tuberculosis prevents the phagolysosome fusion (combination of phagosome and lysozyme that contains acidic products + degradation enzymes), avoids destruction, begins replicating, and releases DNA, RNA, proteases, and lipids. Additionally, the macrophages will release cytokines + VEGF. VEGF triggers angiogenesis and inc. vascularisation to the lesion. The cytokines will initiate the innate response and recruit NK cells, dendritic cells, neutrophils + macrophages. D) The T-helper cell response will involve the migration of TH1, Tregs + B cells. These cells will combine to form the granuloma. E) The granuloma is a prison to wall off the bacteria from spreading systemically. F) Later, or present, immunocompromisation prevents the granuloma from containing the bacteria. The bacteria will spread and multiply in multiple clinical manifestations. G) During this phase, the bacteria can be aerosolized by the new infected host and begin the cycle anew. RISK FACTORS: Close contacts , Medical conditions that worsen, IVDU, homeless, HIV infection, young and old CLINICAL FEATURES: Sickness/weakness, sudden weight loss, fever, night sweats, (chronic) cough, chest pain (sometimes pleuritic), appetite loss and haemoptysis INVESTIGATION FINDINGS TST/Mantoux: skin raised if infected with TB IGRA: blood interferon-gamma release assay test immune response to TB Culture: most sensitive - acid-fast staining bacteria Sputum: generally 3 samples - preferably in the morning CXR: air space consolidation, cavitation + fibrous contraction, particularly in upper lobes

Answer 47

Aetiology * Viral o Influenza A and B o Parainfluenza o Adenovirus o RSV o Rhinovirus o Coronavirus * Bacterial * Environmental (allergens, smoking) Clinical Features * Cough o Coughing bouts with/without sputum production * Coryzal symptoms o Runny nose and sore throat o Headache o Malaise o Myalgia o Chest pain o Mild dyspnoea o Fever * Auscultation findings o Rhonchi (coarse loud sounds due to large airway constriction) o Wheezing o Fine crackles (rare)

Answer 48

Acute Respiratory Failure Causes * Acute respiratory distress syndrome, COPD or Asthma (obstruction), Opioid overdose or alcohol abuse, Stroke Clinical Features * Dyspnoea, Extreme fatigue, Peripheral cyanosis * With high carbon dioxide levels people experience o Tachypnoea, Confusion, Blurred vision , Headaches Atelectasis Causes: * Airway obstruction -> nonventilated alveoli -> reabsorption of gas -> lung collapse * Compression atelectasis: external space occupying lesion (e.g. pleural effusion) -> compresses lung -> forcefully pushes air out of the alveoli * Adhesive atelctasis: surfactant deficiency or dysfunction -> increase in surface tension of alveoli -> instability and collapse * Contraction atelectasis: parenchymal scarring leads to contraction of the lung * Relaxation atelctasis: loss of contact between parietal an visceral tissue (pneumothorax) * Replacement atelectasis: all alveoli in an entire lobe are replaced by tumour -> loss of volume -> lung collapse * Post operative atelectasis Clinical Features * Can be asymptomatic if small number of alveoli are affected, Acute dyspnoea, Chest pain, Tachypnoea, Tachycardia, Cyanosis, Dullness to percussion, Diminished breath sounds, Decrease tactile/vocal fremitus over affected lung, Possible tracheal deviation

Answer 49

Microscopy Light microscope: the most commonly used method of examining individual cells (cytology) as well as normal (histology) and pathological tissue (histopathology) for diagnostic and teaching purposes * Visualisation of structures using stains (e.g., H&E stain) Electron microscope: method primarily used for research purposes and in the diagnosis of certain kidney, muscle, and CNS diseases, with a higher resolution than light microscopy * Visualisation of the structures through compounds of heavy metals (e.g., osmium tetroxide) Culture: Bacterial culture is a method that allows the multiplication of bacterial cells in or on a culture medium under controlled laboratory conditions. The exact conditions required for optimal replication will depend on the target bacterial species. NAAT- Nucleic Acid Amplification Test A test that detects a particular pathogen in a specimen of blood, tissue, or bodily fluid by amplifying the RNA or DNA of the pathogen. Examples include polymerase chain reaction and ligase chain reaction. Serology A laboratory study of the serum. Most commonly refers to the detection of specific antibodies and/or antigens in the blood (e.g., ANA, Lyme IgM).

Answer 50

acute tonsillitis/pharyngitis caused by GAS without antibiotic treatment → development of antibodies against streptococcal M protein → cross-reaction of antibodies with nerve and myocardial proteins (most commonly myosins) due to molecular mimicry → type II hypersensitivity reaction → acute inflammatory sequela IMAGE SHOWN: A collagenous nodule (green overlay) is seen within the myocardial tissue. The nodule contains a loose lymphoplasmacytic infiltrate and large eosinophilic cells with an ovoid nucleus (Anitschkow cells, arrowheads). Anitschkow cells are thought to be histiocytes. These nodules, referred to as “Aschoff bodies,” are thought to represent myocardial granulomas, which are typically found in rheumatic heart disease. Pathogenesis: Inflam.  plasma leak into pericardium  coagulation  fibrin. Gross: White ‘fibrin’ covering the surface of heart (Bread & Butter) Micro: Inflamed pericardium, Fibrin deposits on the surface. Clinical: Friction rub, weak heart sounds, fibrillations, murmur.

Answer 51

Photograph of a dissected heart specimen opened to show the endocardial aspect of left atrium and ventricle The mitral valve is thickened (indicated by arrow) and shows numerous yellow vegetations on the atrial (superior) aspect of the valve (examples indicated by arrowheads). This gross appearance is typical of infective endocarditis of the mitral valve. Pathogenesis [1] Damaged valvular endothelium → exposure of the subendothelial layer → adherence of platelets and fibrin → sterile vegetation (microthrombus) Localized infection or contamination → bacteremia → bacterial colonization of vegetation → formation of fibrin clots encasing the vegetation → valve destruction with loss of function (valve regurgitation) [11] Valve involvement [10] Frequency of valve involvement: mitral valve > aortic valve > tricuspid valve > pulmonary valve The tricuspid valve is the most commonly affected valve in persons who inject drugs (associated with Pseudomonas, S. aureus, and Candida). Clinical consequences [1][11] Bacterial vegetation → bacterial thromboemboli → vessel occlusion → infarctions Emboli can lead to metastatic infections of other organs. Formation of immune complexes and antibodies against tissue antigens → glomerulonephritis, Osler nodes

Answer 52

* Can occur on normal (ABE), abnormal (SBE) & Artificial valves. * Abnormal valve, Immunosupp., IV drug abuse, Diabetes – Risk factors. * 60% Strep. Viridans, 20% Staph aureus, Enterococci, HACEK gp. * Fever, anemia, New murmur, glomerulonephritis, septic embolisms* . SBE: Subacute bacterial endocarditis * Common (60%) , any age, * Common on abnormal valve * Usually in Immunocompetent. * Lower virulence (Strep viridans) * Onset slow weeks-months. * Prognosis is good – recover with antibiotic – low mortality. ABE: Acute bacterial endocarditis Less common 20% elderly. Common on normal valve. Immuno supp. / IV drug abuse. High virulence (Staph aureus) Onset sudden: fever & murmurs. Prognosis is poor even with therapy – High mortality

Answer 53

A defect in the ventricular septum leads to a left-to-right shunt, the volume of which is dependent on the size of the defect. Blood flows from the left ventricle to the right ventricle (white arrow) along the pressure gradient (1). This leads to increased RV and LV preload (due to increased end-diastolic volume), ventricular hypertrophy and dilation (double-headed white arrows), and pulmonary hypertension resulting from excessive pulmonary blood flow (2). In end-stage disease, the pressure gradient is reversed because of Eisenmenger syndrome (shunt reversal), leading to the flow of mixed blood to the systemic circulation (white arrow) and subsequent cyanosis (3). Blue: structures that contain deoxygenated blood; Red: structures that contain oxygenated blood; Purple: structures that contain mixed blood

Answer 54

Cardiac hemodynamics in atrial septal defect An atrial septal defect causes blood to flow from the left to the right atrium (left-to-right shunt; white arrow), resulting in volume overload of the right atrium and ventricle (1). As a result, there is dilation and compensatory hypertrophy (double-headed white arrows) of the right atrium and ventricle (2). In the late stages, Eisenmenger syndrome with shunt reversal (right-to-left shunt; white arrow) and cyanosis can occur (3). Blue: structures that contain deoxygenated blood; Red: structures that contain oxygenated blood; Purple: structures that contain mixed blood

Answer 55

Cardiac hemodynamics in patent ductus arteriosus In patent ductus arteriosus, there is a left-to-right shunt, with blood flowing from the aorta to the pulmonary arteries during both systole and diastole (1). This shunt leads to volume overload (recirculation) of the blood within the pulmonary vessels, the left atrium, and left ventricle (2). Eventually, because of the increased blood flow to the pulmonary circulation, pulmonary hypertension may develop as well as Eisenmenger syndrome, which involves a shunt reversal. The left-to-right-shunt without cyanosis becomes a right-to-left shunt with cyanosis (3). Blue: structures that contain deoxygenated blood; Red: structures that contain oxygenated blood; Pink: structures that contain mixed blood

Answer 56

Coarctation of the aorta (1) Stenosis distal to the left subclavian artery results in hypertension (↑ BP) in the upper extremities and the head, and hypotension (↓ BP) in the lower extremities and abdomen. (2) If coarctation involves the origin of the left subclavian artery, BP in the right arm and head will be higher than in the left arm, lower extremities, and abdomen. Genetic defects and/or intrauterine ischemia → medial thickening and intimal hyperplasia → formation of a ridge encircling the aortic lumen → narrowing of the aorta → ↑ flow proximal to the narrowing and ↓ flow distal to the narrowing acyanotic Brachial-femoral delay: weak femoral pulses ↑ Blood pressure (BP) in upper extremities and ↓ BP in lower extremities

Answer 57

Tetralogy of Fallot Tetralogy of Fallot is the simultaneous occurrence of: (a) Pulmonary stenosis (b) Right ventricular hypertrophy (c) Ventricular septal defect (VSD) (d) An overriding aorta (above the VSD) The hemodynamic effects depend on the extent of right ventricular outflow tract obstruction. With mild obstruction (1), a left-to-right shunt is more pronounced and there is mild cyanosis. With severe obstruction (2), a right-to-left shunt is more pronounced, which results in severe cyanosis. Pulmonary circulation may be supplied via a patent ductus arteriosus Untreated children tend to squat: squatting → ↑ SVR → ↓ right-to-left shunt → ↑ blood flow to pulmonary circulation → ↓ hypoxemia → relief of symptoms Cardiac examination findings Harsh systolic ejection murmur at the left upper sternal border Single S2 Possible RV heave and systolic thrill

Answer 58

Hypertrophic cardiomyopathy Pathophysiology: Concentric hypertrophy of the left ventricle (including the interventricular septum) → ↓ ventricular relaxation → ↓ diastolic filling and systolic output → ↓ myocardial and peripheral perfusion Obstructive type (HOCM): left ventricular outflow tract (LVOT) obstruction and mitral regurgitation due to systolic anterior movement (SAM) of the mitral valve [1] Clinical features: Frequently asymptomatic Signs of left heart failure (dyspnea, syncope, dizziness) Arrhythmias S4 gallop Possible holosystolic murmur from mitral regurgitation Sudden death LV cavity size: Decreased EF: Normal Wall thickness: increased

Answer 59

Dialated cardiomyopathy Pathophysiology: Eccentric hypertrophy of the left ventricle → ↓ ventricular contractility → ↓ LVEF CLinical features: Signs of left heart failure and right heart failure S3 gallop Systolic murmur LV cavity size: increased EF: Decreased Wall thickness: Decreased MOST COMMON

Answer 60

Restrictive Cardiomyoapthy Pathology: Proliferation of connective tissue → ↓ Elasticity of cardiac tissue Atrial enlargement and severe diastolic dysfunction Clinical features: Signs of left heart failure and right heart failure LV cavity size: decreased EF: Normal Wall Thickness: Increased

Answer 61

Myocarditis Viral: Coxsackie, CMV, EBV, HIV Bacterial : Diphtheria, leptospirosis etc. Parasitic : Trypanosoma, Toxoplasmosis, Trichinosis.  Clinical: chest pain, fever, arrhythmias, HF / sudden death.  Microscopy: Lymphocytic Inflammation.fibrosis (late).

Answer 62

Left-sided heart failure (HFrEF and/or HFpEF) Increased left ventricular afterload: increased mean aortic pressure (e.g., arterial hypertension), outflow obstruction (e.g., aortic stenosis) Increased left ventricular preload: left ventricular volume overload (e.g., backflow into the left ventricle caused by aortic insufficiency) Symptoms of pulmonary congestion Dyspnea , orthopnea (a sensation of shortness of breath that occurs upon lying down and is relieved by sitting up) Pulmonary edema Paroxysmal nocturnal dyspnea Nocturnal bouts of coughing and acute shortness of breath Caused by reabsorption of peripheral edema at night → increased venous return Cardiac asthma Increased pressure in the bronchial arteries → airway compression and bronchospasm Symptoms mimic asthma, with shortness of breath, wheezing, and coughing. [8] Physical examination findings [9] Bilateral basilar rales may be audible on auscultation. Laterally displaced apical heart beat (precordial palpation beyond the midclavicular line) Coolness and pallor of lower extremities

Answer 63

Right-sided heart failure Increased right ventricular afterload: increase in pulmonary artery pressure (e.g., pulmonary hypertension) Increased right ventricular preload: right ventricular volume overload (e.g., tricuspid valve regurgitation, left-to-right shunt) Symptoms of fluid retention and increased CVP Peripheral pitting edema: as a result of fluid transudation due to increased venous pressure Hepatic venous congestion symptoms Abdominal pain Jaundice Other symptoms of organ congestion (e.g., nausea, loss of appetite in congestive gastropathy) Physical examination findings Jugular venous distention: visible swelling of the jugular veins due to an increase in CVP and venous congestion Kussmaul sign Hepatosplenomegaly: may result in cardiac cirrhosis and ascites Hepatojugular reflux: jugular venous congestion induced by exerting manual pressure over the patient's liver → ↑ right heart volume overload → inability of the right heart to pump additional blood → visible jugular venous distention that persists for several seconds

Answer 64

* ANCA Positive Vasculitis: (AntiNeutrophil Cytoplasmic Ab) o Microscopic polyangiitis – MPO (P-ANCA) perinuclear. o Granulomatosis with polyangiitis (Wegener’s) – PR3 (CANCA) cytopl. o Eosinophilic granulomatosis with polyangiitis - C-ANCA * ANCA negative Vasculitis: o Adults: Giant cell arteritis, Behcet’s, Takayasu (Aorta) o Children: Kawasaki (coronary) IgA vasculitis (Buerger’s).

Answer 65

Venous ulcers: wet, oozing, dermatitis. * Cause: Varicose veins 90% (1in5 men, 1in3 women). * Location: Gaiter region. * Pathogenesis: Venous stasis  Ischemic Injury  ulcer. * Features: * large, multiple, irregular, shallow. * Wet oedematous, oozing. * Moist granulating base – bleeds on touch. * Surrounding eczematous stasis dermatitis. * Hemosiderin deposition  dark skin. * Mild pain, relieved by elevation. * Compression bandage - relieve congestion.

Answer 66

Arterial Ulcers: dry, dark, painful * Cause: Atherosclerosis (Peirpheral Vascular Disease) * Pathogenesis: Ischemia. * Location: tips of toes, distal shin, foot, * Features: * Feet: Cold, pale, absent or weak pulses. * Skin: Shiny, loss of hair – atrophy. * Ulcer: Dry, Irregular clear border, black necrotic. * Does not bleed on touch. * Painful Nocturnal, elevation worsens. * Note: no compression bandage…!

Answer 67

Neuropathic ulcer: Clean, Caving, Callus, painless * Cause: Neuropathy, Diabetes* * Location: Distal leg, pressure points*. * Pathogenesis: neuronal loss  loss of * sensation injury  ulcer (painless) * Features: * Painless. Punched-out, deep caving. * Surrounding callus (hyperkeratosis) * Probing leads to brisk bleeding (intact artery) * May also have Impaired sensation and diminished * positional sense or 2-point discrimination * (neuropathy).

Answer 68

Malignant ulcers: tumour, irregular. * Cause: BCC, SCC, Melanoma & others * Location: Sun exposed*, Old scars (Marjolin’s ulcer) * Features: * Refer to individual tumors (MB3-SSS) * Irregular tumor / raised edges. * Painless, Lymphadenopathy, metastases, cancer cachexia.

Answer 69

Pressure Ulcers (decubitus ulcers or bedsores) Deep, excavating, Over a bony prominence, heel & sacrum. Elderly, immobile, poor nutrition, vascular disease, diabetes etc. Pathogenesis: Sustained pressure induced, ischemic skin and soft tissue injury & inflammation furthering tissue damage. Early sign of red/blue skin discoloration to ulcers within hours* Sustained compression induced ischemia leading to cellular damage 5 clinical stages: 1. Non-blanching erythema of intact skin. 2. Partial thickness skin loss, exposed dermis. 3. Full thickness skin loss, subcutaneous fat visible. 4. Exposed deep tendons, fascia or bone 5. Un-stageable: Obscured by slough or eschar.

Answer 70

* Rare, Acute, febrile, usually selflimited illness of children <5y. * Arteritis of mainly large to medium-sized vessels, Coronary  MI*. * Delayed type hypersensitivity in Genetically susceptible triggered by Viral infection. * Cross reacting vascular endothelial antigen. * Transmural coronary arteritis: * Self limited healing - 80% * Aneurysm / Intimal thickening & Obstruction MI (20%). Erythema, blisters & rashes of Hand, Foot & Mouth with cervical lymphadenopathy. Strawberry toungue. Boys 2:1 Rx: Immunoglobulins + Aspirin

Answer 71

* Antibodies to platelet phospholipids. * Lupus Anticoagulant Antibody syndrome (old name). * Secondary AAS: In autoimmune disorders or drugs. 30% of SLE Pts develop AAS. & Following Infections in children. * Primary AAS when not associated with other disorders. * These auto antibodies activate coagulation in vivo but block phospholipid reagent in the laboratory to prolong PTT. * Clinical: Recurrent venous thrombosis (DVT), repeated miscarriages. Cardiac valve vegetations, and thrombocytopenia. Rarely  TTP. * Lab Diagnosis: Prolonged PTT and remains prolonged even after adding 50% normal plasma, unlike factor deficiency.

Answer 72

DVT CASE: 42y woman. Swollen, painful leg. H/O long flight / surgery / drugs (OCP), familial. Etiopathogenesis: Stasis of blood in deep veins of leg. Virchow’s triad: Blood: Hypercoag, FV leiden, Lupus, etc. Flow: immobility, long flight, preg., Obesity BV injury: Thrombophlebitis. Gross: swelling / inflam. Thrombosed vein. Microscopy: Thrombosis. Complications: Pulmonary embolism.(paradoxical embolism ?). MB2-HRM-Hemostasis

Answer 73

Varicose Veins CASE: 62y traffic police man. Heavy legs, prominent veins, non healing ulcers in gaiter region. Etiopathogenesis: Defective valves (Acquired or congenital)  backflow of blood  varicosity. Gross: dilated tortuous superficial veins. Microscopy: nil significant. Complications: Venous stasis, non healing ulceration, dermatitis.

Answer 74

Giant Cell Arteritis, Etiopathogenesis: late age >50y, immune dysfunction to an unknown antigen. (like sarcoidosis). Large arteries, temporal & Aorta. Responds to steroids or Anti-TNF therapy. Gross: Thickened palpable, nodular tender temporal artery. Micro: Focal Chronic inflam, granuloma giant cells. Complications: visual loss  optic nerve ischemia. Takayasu Arteritis: similar, young age, <50y, Aortic arch mainly. AKA: pulseless disease.

Answer 75

Wegener’s granulomatosis Etiopathogenesis: Lung & ANCA +ve* Triad: Necrotizing granulomas: URI, nose, Lungs etc.Necrotizing polyangiitis: Small BV, URI, lungs etc, Glomerulonephritis Crescentic:,P3ANCA in 95%,Immunosuppressive / Anti TNF. Gross: URI, nose, lungs, skin.. Microscopy: segmental transmural, acutenecrotizing inflame. of small & medium arteries. Complications: debilitating, recurrent, fatal*, Behcet’s disease, Churg-Strauss Syndrome: allergic vasculitis..

Answer 76

Polyarteritis Nodosa Etiopathogenesis: unknown / Post viral immune complex. HBV (30%). Renal, heart, liver & GIT. (not pulmonary*, No ANCA*) Gross: arterial ulcers. Kidney hematoma. Microscopy: segmental transmural, acute necrotizing inflam. of small & medium arteries. Complications: Acute Renal Failure. Responds to immunosuppression.: children < 4y. Post viral, Coronary vasculitis, MI, self limited, aneurysms. Kawasaki Disease

Answer 77

AS-Aorta Etiopathogenesis: Life style, HPTN, DM, Obesity. US Plaque embolism  Stroke. Gross: multiple atheromatous plaques of all stages, some with marginal ulceration. Microscopy: Atheroma, unstable. Complications: CHF / SCD, PVD, plaque / thromboembolism, Aneurysm, renal artery block. PVD, GI Ischemia,

Answer 78

Old healed MI + Gross: Lateral wall infarction – now healed with thin scar replacing myocardium. Area of scar is protruding out – ventricular aneurysm. Complications: if alive, this patient would have had hypercoagulability due to scar, mural thrombosis and thromboembolism  stroke. (anti plt. Drugs - to prevent). If large area of scar – pt. would have had congestive cardiac failure. (low output)

Answer 79

Floppy Mitral Valve: Mitral Valve Prolapse (MVP) Gross: ballooning and prolapse of mitral valve into atrium. Microscopy: degeneration, myxoid or mucoid material. Reduced normal fibrous tissue. Etiopathogenesis: reduced fibrous tissue and increased mucoid material in the valve. Some cases of Marfans syndrome have MVP.. Differential: Ischemia, MI. Complications: Bacterial endocarditis, thromboembolism, stroke, CCF.

Answer 80

Calcific Aortic Stenosis Gross: calcified mounds within cusps (Valsalva sinus). Microscopy: calcification, bone & bone marrow in valvular fibrosa. Varying inflammation. Etiopathogenesis: Age associated senile change. Aorta common. Wear & tear, damage  Dystrophic calcification. Over normal / bicuspid valve.* Deposits prevent opening of valve  stenosis. Differential: Rheumatic AS. Complications: Bacterial endocarditis, CCF.

Answer 81

Infective Endocarditis Gross: Large irregular destructive vegetation's. Destruction of chordae tendinae, yellow / pus. Microscopy: Necrosis, bacterial clumps,inflammation Etiopathogenesis: Acute: normal valve, highly virulent bacteria (Staph aureus). Subacute: abnormal valve/Immunosuppression. Low virulence (Strep viridans), Differential: Non Bacterial (NBTE) plts, no inflame., along the line of closure (in DVT, PE etc..) RHD: young, linear, along free border, Immune. SLE: Libman-Sacks – plt. Complications: septicemia, emboli, septic infarcts, mycotic aneurysm, Glomerulonephritis, Janeway lesion

Answer 82

MS-RHD Gross: excised mitral valve. Fusion of thickened opaque leaflets, fused chordae tendinae, narrow fish mouth mitral opening. Microscopy: at this time there would be just fibrous scarring (collagen bundles) early stagewould have Aschoff bodies (perivascular T cell mediated granuloma around fibrinoid necrosis with macrophages/Anitschkow, giant cells & T lymphocytes) in machH/O recurrent URTI as child. Fever, arthritis and heart problems several years ago. Undergoes mitral valve replacement. Etiopathogenesis: Genetic, Environmental, Autoimmune. GABH streptococcal M Protein. Cardiac Ag.

Answer 83

ARF Vegetations Gross: mitral valve linear, small vegetation's & inflammation along the occlusal borders. (Area of damage & exposure of Ag.) Microscopy: inflammation, T lymphocytes, Aschoff bodies, platelet rich thrombus overlying area of ulceration. Normal valve Vegetations Etiopathogenesis: Genetic, Environmental, Autoimmune. GABH streptococcal M Protein. Cardiac Ag. Differential: Bacterial Endocarditis (large irregular, destructive both sides). Non Bacterial – only platelets, no inflammation, along the line of closure. Complications: Bacterial endocarditis, thromboembolism, stroke, CCF.

Answer 84

AAA: Rupture * Abdominal Aortic Aneurysm * (A) External view, gross large aortic aneurysm that ruptured (arrow). * (B) Opened view, rupture tract indicated by a probe.The wall of the aneurysm is exceedingly thin, and the lumen is filled by a large quantity of layered thrombus. * Note atherosclerotic obstruction of Iliac arteries.

Answer 85

AS-Aorta Gross: multiple atheromatous plaques of all stages, some with marginal ulceration. Microscopy: Atheroma, unstable. Etiopathogenesis: Life style, HPTN, DM, Obesity. US Plaque embolism  Stroke. Complications: CHF / SCD, PVD, plaque / thromboembolism, Aneurysm, renal artery block. PVD, GI Ischemia,

Answer 86

Healed MI (LAD) Gross: Horizontal section of ventricles. Anterior wall replaced by white scar. Multiple small scars in posterior wall. anterior wall dilatation - aneurysm. Microscopy: Collagen bundles (fibrosis) inbetween normal myocardium. No inflam. Etiopathogenesis: Coronary block, atherosclerosis (others rare). Life style, HPTN, DM, Obesity. Chronic, multiple Healed / Scar (collagen / fibrosis). Complications: CHF, Aneurysm thromboembolism, stroke, Arrhythmia..

Answer 87

Gross: Horizontal section of ventricles. Dark brown mid zone (Infarction & Acute inflam) in the posterior wall of LV & posterior 1/3 of septum. Dilated RV, Mural thrombus in LV. Microscopy: Hemorrhage / dead myocardium (no nucleus). LDH & glycogen loss*. (Special stain). Etiopathogenesis: Coronary atheroembolism (others rare). Risk Fac: Life style, HPTN, DM, Obesity. US Plaque  inflam. Complications: HF/SCD, Mural thrombus, embolism, Arrhythmia, progressive block.

Answer 88

Clinical classification: Community Acquired Pneumonia (CAP) * Acquired in community * In healthy individuals * Or in hospital <2days * Bacterial or viral * Inhalation, haematogenous * Lobar pneumonia pattern * Most common bacteria: o Strep pneumoniae, H.influenzae, Mycoplasma, Legionella, Staph aureus Hospital Acquired Pneumonia (HAP) * Acquired in hospital >2days or 7-10days after discharge from hospital * Dangerous because usually multidrug resistant pathogens such as MRSA * Pseudomonas, Kleibsella etc (usually Gram negative rods) * Bronchopneumonia pattern

Answer 89

* First bacterial entry occurs early in life in developing countries. Primary TB. activation of macrophages. * 1-2cm caseating granuloma in lung(Ghon focus) with involvement of lymph node (Ghon Complex). * Stimulation of cell mediated immunity leads to healing with fibrosis & calcification in majority and in few it may spread (progressive pr.) * Second entry of bacteria in a immunocompromised adult leads to secondary TB. Typical cavitary pulm. TB & many other organ TB*

Answer 90

COPD + Pneum * Gross: Lung section, distended, Upper zone black spots. Lower solid grey white. * Microscopy: Lower Zone: alveoli show different stages of acute inflammation (Bronchopneumonia) Upper zone: carbon pigment in centrilobular area with loss of alveolar wall (Centrilobular emphysema). * Etiopathogenesis: Smoking  loss of cilia, occumulation of sputum  secondary infection  Broncho pneumonia. * Complications: COPD, emphysema, bronchiectasis, Endstage LD, Carcinoma.

Answer 91

Lobar Pneumonia * Gross: Lung section, grey white solid upper lob. Normal lower lobe* * Microscopy: upper lobe: alveoli are full of WBC neutrophils & macrophages. (one stage only) lower lobe: relatively normal. * Etiopathogenesis: Community acquired pneumonia in healthy adult. infection by pneumococci (Strep pneumoniae). Gram +ve diplococci. Intact architecture, no destruction of alveoli. Spread through pores * Complications: rare now. Septicemia, fatal, pleural adhesions.

Answer 92

COPD Emphysema * Gross: Lung section, distended, black spots all over, more in upper zone. * Microscopy: Loss of alveolar wall (bullae) carbon pigment in centrilobular area (emphysema) * Etiopathogenesis: Smoking  neutrophil elastase breakdown & loss of alveolar wall – emphysema more in upper zone (CO2). * Complications: End stage Lung dis, Ca. * COPD / Chronic Bronchitis / Emphysema...?

Answer 93

* Gross: Focal, dilated irregular bronchi filled with pus. (visible till pleural margin) * Microscopy: Destruction of bronchial epithelium replaced by acute/chronic inflammation, necrosis, (pus). * Etiopathogenesis: Smoking  loss of cilia / sputum accumulation / obstruction (tumour / foreign body) infection wall destruction Bronchiectasis. (normal commensal over growth) * Complications: Septicemia

Answer 94

Tuberculosis* Etiopathogenesis: mycobacterium tuberculosis, infection. (HIV, DM, steroid therapy, travel, nutrition, country). Gross: Lung, apical cavity (opening to bronchus), pleural adhesion / fibrosis. Microscopy: Caseating granuloma. Epitheloid macrophages, giant cells, lymphocytes, central caseation. Complications: Milliary, extrapulm spread, lung fibrosis, amyloidosis. (immunosupp*)

Answer 95

Miliary TB Etiopathogenesis: when bacteria spread through lymphatics / veins to RV  Lungs only (pulmonary) or into arteries to whole body (systemic). Gross: Lung section, multiple grey white small foci / nodules). Microscopy: Caseating granuloma. Epitheloid macrophages, giant cells, lymphocytes, central caseation. Complications: systemic can be fatal.

Answer 96

Relatively normal lung tissue (green overlay) can be seen next to pathologic lung tissue (white overlay) with alveolar infiltrates of mainly neutrophils as well as exudation of erythrocytes. A cross-section of an airway (white outline) also shows purulent infiltrates (examples indicated by black arrows) consisting predominantly of neutrophils.

Answer 97

Neutrophilic pleuritis is seen at the bottom left of the sample (red overlay). There is also neutrophil invasion with fibrinopurulent exudate seen in the alveoli (green overlay in black circles). These are typical findings in lobar pneumonia.

Answer 98

Upper respiratory tract infection: 1-3 days onset, Others sick in the house, unvaccinated Vitals: Fever, Tachycardia , EXAM: Clammy, phlegm, TESTS: Nasopharyngeal swab Lower respiratory tract infection: Pneumonia, bronchitis, exacerbation of COPD Days to Week , older patients >65 (COPD, Asthma, Stroke, Immunosuppression), Smoking Vitals: Fever, Tachycardia, increased RR , EXAM: Crackles or wheeze in part of lung, Resonant to percuss. TESTS: * Sputum MCS, – Blood and sputum culture, - CXR, * Respiratory viral panel during respiratory virus season, * COVID-19 testing Melioidosis Days – years onset fever, headache, loss of appetite (anorexia), cough, shortness of breath, chest pain, and general muscle soreness. VITALS: Fever. EXAM: Rigor, confusion, dyspnea, abdominal pain, muscle tenderness, pharyngitis, diarrhea, and jaundice. TESTS: Burkholderia pseudomallei COPD—smoking history Years Smoker, PMH asthma, Occupational hazards. VITALS: Tachycardia, hypertension, RR change, O2 stat low. EXAM: hyperinflation of the chest, reduced chest expansion, hyperresonance to percussion, soft breath sounds and a prolonged expiratory phase. SIGNS: clubbed fingers, barrel chest, cyanosis. TESTS: Spirometry - if infective symptoms do Sputum and once recovered spirometry. Asthma Child onset, Lasts hours Cold, Exercise, worse in winter, Allergies, worse at night. VITALS: increased RR, tachycardia. EXAM: audible Wheeze. TESTS: decreased FEV1, Spirometry shows relief with bronchodilators Gastro-oesophageal reflux— After food occurs when lying down, burning central chest pain. horse cough potentially worse after spicy food and alcohol. Post nasal drip: Morning, everything fine Bronchiectasis Chronic Recurrent infections as a child Cough with copious, foul smelling purulent sputum & Dyspnea.Smoking. VITALS: Decreased SPO2, Fever, Tachycardia, Tachypnoea, Hypotension.. EXAM: One or more lobes, Lower lobes common - crackles, wheezing, and inspiratory squeaks may be heard. General findings may include clubbing, cyanosis, plethora, wasting, and weight loss. Nasal polyps and signs of chronic sinusitis may also be present.. TESTS: HRCT scan Carcinoma of the lung Chronic Smoking Cancer history , Haemoptysis, Weight loss, Anorexia VITALS: Low-grade fever., Decreased SPO2, Tachypnoea, Tachycardia, Hypotension.EXAM: decreased BMI, decreased/absent breath sounds, reduced chest expansion, Horner’s syndrome, wasting of the hands, increase in the tactile fremitusTESTS: Chest x-ray, CT, MRI, PET, Needle biopsy OTHER: HF, Ace inhibitor cough, Occupational, TB, psychological, Fire/ smoke.

Answer 99

DEMOGRAPHICS: M>F (child) F>M adults, inner regional PATHOPHYSIOLOGY: * bronchoconstriction/bronchial hyperresponsiveness, airway inflammation and mucous impaction Ag binding leads to T cell differentiation (Th1 + Th2 components): -->Th2 response: mast cells/ basophils/ eosinophils (IgE release) → mediators of inflammation released (histamine, PGs, LK, enzymes etc.) → bronchial hyperresponsiveness + airway obstruction → asthma symptoms | more important response -->Th1 response: cell mediated immunity + neutrophilic inflammation RISK FACTORS + TRIGGERS: * Risk factors: family hx, allergies, viral respiratory infection, occupational exposures, smoking, air pollution, obesity etc. * Triggers: tobacco smoke, dust mites, outdoor air pollution, pests, pollen, pets, mold, cleaning + disinfection, sinus infection, allergy, physical exercise, breathing cold + dry air/bad weather (esp. cold), foods, fragrances, (respiratory) infection etc.

Answer 100

Asthma diagnostic criteria · No single test to diagnose asthma, thus based off clinical suspicion supported by spirometry · Recurrent episodes of wheeze, dyspnoea, cough & chest tightness o Typically occur nocturnally & early morning o Specific triggers e.g. exercise, aeroallergens o Personal or history of atopy (allergic rhinitis, dermatitis) · Widespread wheeze on chest auscultation, signs of atopy ·Spirometry shows airflow limitation/obstruction which is variable & reversible o Reduced FEV1/FVC ratio <0.7 o Increase in FEV1 or FVC by at least 200mL AND at least 12% 10-15mins post-bronchodilator (SABA)

Answer 101

General principles * Self monitoring via peak flow meter * Influenza and pneumococcal vaccination * Avoid triggers eg. take puffer before exercise * Avoid smoking Pharmacotherapy * Preventer - inhaled corticosteroid +/- LABA * Reliever - inhaled bronchodilator SABA

Answer 102

Personal: Inadequate knowledge of the disease and its complications therefore unlikely to seek help/treatment when needed, have greater Fear of adverse effects from medications and dont understand that medications take time to work. Inability to afford medications leading to non-adherence Age-Related: Difficulty differentiating asthma from COPD in elderly community. Young children cannot comply with medication regime by themselves, Adolescents may have unique difficulties regarding adherence due to shame. Family Genetic component : Many family members may have asthma and will want to follow same routine, and if one grows out of it, might say they will too. Family Caregiver: Inadequate knowledge of the disease, Not recognising environmental or other triggers Societal Stigma regarding asthma, so people may not want to administer medications in front of others; this prevents timely administration of medications Socioeconomic status: cost of medications can prevent adherence, unable to regularly check with GP Environmental There are many different environmental triggers for asthma. A number of these triggers are non-modifiable, and thus it is a serious barrier to appropriate asthma control Health system Poor referral programs for pulmonary function testing, Inadequate education for patients newly diagnosed or suspected cases

Answer 103

Primordial prevention: preventing the development of risk factors for disease. - exposre to allegens ? - Exposure to house dust mite is reported to cause asthma whereas dog or cat allergen exposure might be protective - Smoking ban during pregnancy Primary Prevention: reduce the individuals at risk of developing disease.Prevention of sensitization (IgE) to factors that may subsequently induce disease / atopy (Avoidance of personal exposure to common risk factors) - Smoking Ban - Avoid Pollutants - Respiratory Infections (get vaccinated) -Breast feeding exclusively for the first 6 months of life Secondary Prevention: Early detection of all types of asthma and preventing the development of an allergic disease following sensitisation - Avoid allergens - Increased testing in suspected cases – early detection - Treat atopic eczema / atopic dermatitis topically - Treat upper airway diseases (e.g. allergic rhinitis) to reduce progression of asthma - Correct usage of inhalers - Asthma first aid Tertiary Prevention: Efficient long term management of asthma - Reduced allergen exposure - Efficient drug therapy - Smoking cessation - Pulmonary rehabilitation - Check inhaler technique - Asthma action plan Quaternary Prevention - Prevent complications - Influenza vaccination - Patient education re: precipitants of asthma, allergic symptoms and anaphylaxis - Corticosteroid → Cushing syndrome

Answer 104

Clinical features of severe acute asthma: * Hypoxia (SpO2 of 90 - 94%) * Increased work of breathing indicated by use of accessory muscles (eg. tracheal tug, intercostal or subcostal recession, marked abdominal breathing, chest wall recession in children) * Obvious respiratory distress * Unable to complete sentences in one breath Clinical features of life threatening asthma: * Decreased work of breathing indicated by exhaustion (poor respiratory effort) * Reduced level of consciousness * Collapse * Soft or absent breath sounds * Cyanosis * Hypoxia (SpO2 less than 90%)

Answer 105

Pneumoconiosis: group of restrictive lung diseases caused by the inhalation of certain dusts, which are often associated with mining and agriculture. Coal miners lung --> A more severe form of anthracosis . Complications: Chronic bronchitis that progresses to progressive massive pulmonary fibrosis, ↑ Risk of Caplan syndrome. CXr: Fine nodular opacifications (< 1 cm) in upper lung zone Asbestosis: Airborne asbestos fibers, caused by exposure. Symptoms typically develop 15–20 years after initial exposure.Exertional dyspnea, Dry cough that transforms into productive cough, Digital clubbing Complications: Lung cancer, Diffuse bilateral infiltrates predominantly in the lower lobes, Interstitial fibrosis Calcified pleural plaques (usually indicate benign pleural disease), Pleural effusion (BAPE) Sarcoidosis: Highest in African American and Scandinavian populations. Dry cough, mild rales, bilateral hilar lymphadenopathy, Erythema nodosum, Uveitis, Arthralgias and/or arthritis CXR, Noncaseating granulomas, Giant cells, BLOODS: ↑ CD4:CD8 ratio in bronchoalveolar lavage, ↑ serum ACE levels Idiopathic pulmonary fibrosis (IPF): irreversible pulmonary fibrosis and impaired pulmonary function, M>f older. Requires the absence of other known causes of interstitial lung disease (e.g., medication, environmental exposures, CTD-ILD), Presence of usual interstitial pneumonia , Honeycomb appearance with or without traction bronchiectasis Gradual onset of non-productive cough- Progressive dyspnoea- Dry or “velcrolike” crackles on inspiration- Weight loss

Answer 106

A collection of air within the pleural space between the lung (visceral pleura) and the chest wall (parietal pleura) that can lead to partial or complete pulmonary collapse. Spontaneous pneumothorax: - Primary spontaneous pneumothorax occurs in patients without clinically apparent underlying lung disease o family history, male sex, young age, slim, tall stature, smoking - Secondary spontaneous pneumothorax occurs as a complication of underlying lung disease o COPD, CF, marfans, malignancy, infections (TB, pneumocystis pneumonia) Traumatic pneumothorax: - A type of pneumothorax caused by a trauma (e.g. penetrating injury) Tension pneumothorax: - A life- threatening variant of pneumothorax characterised by progressively increasing pressure within the chest and cardiorespiratory compromise Clinical features: P-THORAX - Pleuritic pain that is sudden, severe, stabbing. - Tracheal deviation (opposite side) - Hyperresonance to percussion if pneumothorax is large - Onset sudden, subcutaneous emphysema - Reduced /absent BS + Dyspnoea + distended neck veins - Absent vocal fremitus - X-ray – collapse of lung First-line management - Small (<2cm from chest wall) with no SOB: o discharge – resolves spontaneously - Shocked o remove free air with needle decompression (blunt cannula/intercostal catheter) - Not shocked o needle aspiration/intercostal catheter into triangle of safety o oxygen via non-rebreather o analgesia = NSAIDS, consider intercostal nerve block o advise smoking cessation

Answer 107

Pathophysiology: Occurs when an allergen binds to and cross-links membrane-bound IgE on mast cells in a susceptible individual, causing release of histamine, tryptase and other vasoactive mediators from mast cells. These mediators have a variety of effects, including vasodilation, increased capillary permeability leading to hypotension, and bronchoconstriction. (Type 1 Hypersensitivity reaction) Clinical features Mild to moderate: * Swelling of lips, face, eyes * Hives or welts * Tinglinging mouth * Abdominal pain, vomiting Anaphylaxis (severe) * Difficulty/noise breathing * Swelling of tongue * Swelling/tightness in throat * Difficulty talking and/or hoarse voice * Wheeze or persistent cough * Persistent dizziness or collapse * Pale and floppy (young children) Symptoms usually begin 5-30 mins from time of exposure but can occur up to 2 hours later. Initinal management * Primary Survey with evaluation of (and immediate management of concerns with) airway, breathing, circulation and disability. * Administer Adrenaline IM immediately into the thigh if anaphylaxis is suspected 1. Adrenaline - Intramuscular and nebulised (repeat every 5 mins if necessary) 2. Oxygen 3. Fluids 4. Steroids 5. Histamine blockers Additional * Remove allergen * Salbutamol (for bronchospasms) * 4-hour observation

Answer 108

Direct effects of climate change include injuries and deaths from: - Increased heat stress - Floods - Fires - Droughts - Increased frequency of intense storms Indirect effects: - Adverse changes in air pollution causing increasing rates of respiratory illness - Increase in incidence of food and water borne diseases (storms -> contamination; droughts -> concentrate pathogens in water supplies which are a danger to rural Australians and livestock) - Spread of disease vectors (In Aus, concerns about dengue moving from Northern QLD south) - Lost work capacity and reduced labour productivity - Food insecurity and undernutrition (ocean acidification, damaged crops and pastures) - Displacement - Declining mental health (especially acute in rural areas where climate change places additional stress on livelihoods) Vulnerable groups in Australia: - Rural Australians - Low incomes individuals and families - People with chronic diseases - Children and elderly - Physical and outdoor workers - Tourists - Indigenous Australians (heavy reliance on climate-sensitive primary industries, strong connections to the natural environment and constraints to adaption)

Answer 109

Bronchitis:Small amounts of blood with sputum Vital Signs: fever and tachypnoea, ENT: normal-to-pharyngeal erythema , Lungs: localized lymphadenopathy, and rhinorrhoea to coarse rhonchi and wheezes that change in location and intensity after a deep and productive cough. Bronchial carcinoma Frank blood, history of smoking, hoarseness Appearance of the Patient: Well-appearing, Lethargic, Confused, cachexia. , Vital Signs: Low-grade fever, Decreased (SpO2), Tachypnoea, Tachycardia, Skin: Pallor. , Neck: Lymphadenopathy, Lungs, Hoarseness, Rapid rate of breathing, Pleural friction rub, Crackling or bubbling noises, Decreased/absent breath sounds, Hypo resonance, Dull percussion, Tactile fremitus, Reduced chest expansion , Clubbing of fingers, Weakness. Bronchiectasis Large amounts of sputum with blood General appearance: Lethargy, Weight loss, Wasting, Syncope with activity, Vital Signs: Vital signs are generally within normal limit, but could be Decreased SPO2, Fever, Tachycardia, Tachypnoea, Hypotension, :Course crackles, Wheeze, Inspiratory squeaks, Right ventricular hypertrophy (RVH),Skin: Cyanosis, ENT: Nasal polyps, Breath odor, Increased jugular venous pressure, Prominent neck and facial veins, Extremities: Digital clubbing, Pedal edema Pneumonia, PE

Answer 110

50-70 years, smoking, * Australia and the most common cause of cancer death. Males > females, Occupational exposure to asbestos Pathophysiology General pathophysiology Can be divided into 6 steps: 1. Smoking (and other carcinogens)/ cell injury causes DNA damage 2. Hyperplasia of cells in resp airways 3. Metaplasia → pseudostratified columnar epithelium change to stratified squamous epithelium 4. Dysplasia whereby there is abnormal cells in a tissue/organ (3p in smokers/ EGFR in non-smokers mutations) 5. Carcinoma in situ 6. Infiltration and metastasis (p53 mutation which allows cells to rapidly divide). The usual role of p53 is to control cell division and death. 2 main types of lung cancer: 1. SCLC * Forms central tumours which metastasize rapidly, but often responds well to chemo 2. NSCLC (80-90%) * Forms both central and peripheral tumours, less metastatic, but less responsive to chemo * Includes adenocarcinoma, squamous cell carcinoma Risk factors: smoking, second hand, occupational, COPD Clinical features including red flags * Cough +/- productive sputum Shoulder tip pain Weakness or wasting of small muscles in hand *** Chest pain (may be pleuritic) ** Hoarse voice *** Haemoptysis * SOB/dyspnoea ** *** Unexplained weight loss or dec. appetite** Headaches *** Persistent tiredness/lack of energy** * Clubbing Horner’s syndrome (miosis, ptosis, anhidrosis) Investigation findings * CXR: mass seen as area of white consolidation * CT scan: size, shape, position of lung tumours + can help find enlarged lymph nodes | can also help find mets in other areas of the body (e.g. brain, liver etc.) | CT-guided needle biopsy * PET scan: fluorescence in areas of malignancy

Answer 111

T (tumour) Indicates the size of the tumour and how far the tumour has grown into the lungs. 1-4 N (nodes) Shows if the tumour has spread to nearby lymph nodes; ranges from N0 (no spread) to N3 (cancer in lymph nodes on the opposite side of the chest, above the collarbone or at the top of the lung) M (metastasis) Shows if the tumour has spread to other parts of the body. 0-1 Staging SCLC - sometimes staged using a 2-stage system Limited stage Cancer is only on one side of the chest and in one part of the lung; nearby lymph nodes may also be affected. Extensive stage Cancer has spread widely through the lung, to the other lung, to lymph nodes on the other side of the chest or to other areas of the body. Survival progressively decreased with increasing time from diagnosis for both early and advanced stage cancers. * Stage 1 cancers at 1 year -91%; 3 years -76% and 5 years 68%. * Stage 2 cancers at 1 year -70%; 3 years -42% and 5 years 32%. * Stage 3 cancers at 1 year -58%; 3 years -25% and 5 years 17%. * Stage 4 cancers at 1 year -19%; 3 years -5% and 5 years 3%.

Answer 112

Lung Metastases -Lymph to thoracic duct to SVC vs straight into pulmonary circulation. Sites of Metastasis - Common sites of lymphatic spread: o Supraclavicular lymph nodes o Mediastinal lymph nodes o Subcarinal lymph nodes o Hilar lymph nodes - Lower lobe tumours usually drain to subcarinal lymph nodes - Upper lobe tumours usually drain to upper mediastinal & supraclavicular lymph nodes - Spread to the pleura either directly or via lymphatic drainage especially by peripheral tumours - Haematogenous route lung cancers often spread to → brain, bone, liver, adrenal glands, kidney

Answer 113

Palliative medicine is a comprehensive, interdisciplinary approach to medical care that aims to relieve suffering and provide optimal quality of life in patients with serious or life-threatening illnesses. Key elements of palliative care * Symptom relief, particularly sufficient analgesia * Care is patient centred * Integrated system of teamwork among all members of the multidisciplinary team * Connecting patients and their families with other psychological or physical support systems Lung cancer * Systemic treatment (chemotherapy, immunotherapy, targeted radiation therapy) and surgery may be used to slow the spread of cancer and prevent complications of further metastases * Removal of fluid from the lungs via medication or manual extraction -> prevents ‘drowning’ feeling * Opioid management of pain * Extra oxygen devices that can be used at home or in hospital * Emotional support and counselling from social workers and psychologists to both patient and family * Nutritional supplements to prevent further weight loss and malnutrition * Medications to reduce nausea (ondansetron for chemotherapy induced nausea/vomiting) * Bronchodilators and supplemental oxygen to relieve dyspnoea and cough associated with metastases

Answer 114

PulmonologistKey role in the prompt diagnosis, staging, and treatment of patients with lung cancer; early intervention improves survival. Pulmonologists lead and participate in multidisciplinary efforts to diagnose and treat patients with lung cancer Oncology Team Oncologist: 3 main areas: - Surgical oncology: Cancer surgery - Radiation oncology: Radiation therapy - Medical oncology: Chemotherapy/hormone therapy/immunotherapy/targeted therapy Oncology Nurse - Identify & assess supportive care needs - Monitor patient’s condition - Administer medication & develop care plans - Patient education Allied Health Professionals Social worker: Coping with a cancer diagnosis and the emotional reactions to illness. Providing counselling to individuals and families in grief, loss and interpersonal concerns. Accessing information about your diagnosis and treatment Physiotherapist: Involve exercise education, improve exercise tolerance, reduce exacerbations and hospitalization, assist in sputum clearance Occupational therapist: Assist people living with lung cancer prioritize their goals while managing the side effects of treatment Psychological/Family Support - These can be provided by counsellors, psychologist, mental health social workers & therapists - Psychological issues patient with cancer face: Depression, anxiety, fatigue, pain, QOL

Answer 115

Paraneoplastic syndromes : are rare disorders triggered by antibodies against a neoplasm which cross react with normal tissue or by the production of a physiologically active substance by the neoplasm. Commonly present with lung, breast, ovarian and lymphatic cancers.

Answer 116

aetiology * accumulation of serous fluid within pleural cavity * two types: o transudate : fluid leakage from pulmonary capillaries due to:increased hydrostatic pressure in HF & renal failure OR decreased osmotic pressure in hepatic failure & nephrotic syndrome o exudate : fluid leakage from pulmonary capillaries due to increased pulmonary capillary permeability. occurs in infection, inflammation, malignancy, trauma OR pneumonia, TB, acute pancreatitis, subphrenic abscess, RA & SLE OR impaired lymphatic drainage due to lymphatic obstruction by e.g. tumour clinical presentation * history of underlying cause - HF, recent pneumonia, malignancy, etc. * pleuritic chest pain, dyspnoea, cough * unilaterally ipsilaterally reduced chest expansion, breath sounds, vocal resonance & tactile fremitis * stoney dull to percussion * tracheal deviation & displaced apex beat away from effusion investigations * CXR (meniscus sign, loss of costophrenic angle, hazy bases, fuzzy hilum, tracheal deviation) * CT, US * thoracentesis o assess colour/texture - clear watery if transudative, cloudy if exudative o biochemical (protein, LDH, glucose, cholesterol, etc.), microbiological & cytological analysis  Light’s criteria - exudative if fluid protein &/or LDH higher than serum

Answer 117

Asthma : Gross & Microscopy * Gross: o Inflamed thick bronchi + mucous plugs. o Excess mucous & mucous plugs (sputum) * Microscopy: o Mucous gland & smooth muscle Hyperplasia o Eosinophilic inflammation. o Curschmann (epithelial) spirals & Charcot Leyden Crystals (Eos. Protein) in sputum.

Answer 118

Microscopy: Eosinophilic inflammation, hypertrophy & hyperplasia of mucous glands. Mucous in the lumen, Curschman spirals & Charcot Leyden crystals (eosinophil granules

Answer 119

Asthma presentation : Eosinophilic inflammation, hypertrophy & hyperplasia of mucous glands. Mucous in the lumen, Curschman spirals & Charcot Leyden crystals (eosinophil granules)

Answer 120

Slinicosis: consentric layers of fiorous tissue as nodule with black carbon pigment inbetween. there are also fibrotic nodules with carbon pigment

Answer 121

Silicosis: CXRay: extensive upper lobe fibrocystic change. Micronodular opacities in the mid zones, superior displacement of the hila (fibrosis), small left pneumothorax.

Answer 122

Pneumonia,

Answer 123

Life-threatening (PEFR <33%): 33, 92 CHASE 33: PEFR <33% predicted 92: Sats <92% Cyanosis Hypotension Arrhythmia Silent chest Exhaustion Severe (PEFR <50%): cannot complete sentences, respiratory rate > 25, heart rate >110 Moderate (PEFR <75%) Mild (PEFR >75%) Mneumonic O-SHIT-MI for the management of Severe/Life-threatening asthma: Oxygen, Salbutamol, Hydrocortisone (Prednisolone), Ippatropium bromide, Theophylline, Magnesium sulphate, Intubation and ventilation

Answer 124

ARDS/ ALI (DAD) : Epithelial & endothelial injury, inflammation Neutrophils. Exudation  Hyaline membrane ( surfactant): Diffuse Alv.Damage (DAD). * Severe hypoxia, atelectasis, wet heavy lungs filled with exudate. ARDS (child) Pathogenesis: Immature lung,  surfactant Atelectasis inflammation & exudation. Gross: Purple congested, wet, airless lungs. Microscopy: collapsed, inflammed alveoli, Hyaline membrane of plasma proteins with necrotic cells.

Answer 125

Clinical features: * Local: o Obstruction, Effusion o Pneumonia*. o Bronchiectasis o Atelectasis, Haemoptysis o SVC syndrome o Pancoast Sy: Ptosis o Horner’s syndrome. * Systemic: o Cachexia o Clubbing, PHOA* o Paraneoplastic sy.  ACTH: Cushing’s  ADH: SIADH (decreased Na)  Hypercalcemia.  Polyneuropathy

Answer 126

 Diagnosis? SCLC+SIADH (ADH like protein by Ca cells)  Why confused? Excess ADH like protein (AVP – Argenine Vasopressin) Anti-diuretic  causes excess reabsorption of water from urine resulting in hyperosmolar urine & hyponatremia causing neurologic dysfunction – confusion, delirium, muscle weakness, tremors/ataxia.  severe cases cause cerebral edema & coma.

Answer 127

 Diag? Ad. Ca + Horner Sy (Sympathetic trunk damage.) Pancoast Tumor:  extreme apex part of lung, left/right, in the superior sulcus (a shallow furrow on the surface of the lung). Invade chest wall > than lungs!. pleura, rib, muscle etc.  Shoulder pain radiating to medial scapula, arm. Compress spinal cord – paraplegia, horner sy – sympathetic stellate ganglion compression.  High grade NSCLC (50% Sq, 30% Ad.Ca, rare SCLC.)

Answer 128

Left recurrent laryngeal nerve paralysis

Answer 129

SCC Etiopathogenesis: smoking (3P deletion), carcinogenesis. Gross: grey white, well demarcated, round tumour growing out of bronchus in the hilum. Note hilar lymphnode with metastases. (cavitation common) Microscopy: pleomorphic hyperchromatic squamous cells with dyskeratosis (keratin pearls). Infiltration, inflammation & necrosis. Clinical: spread late, less hormones (PTH like)

Answer 130

Adenocarcinoma Etiopathogenesis: Scar cancer, non smoker. KRAS / EGFR mutations common. Gross: Large grey white, well demarcated expansile tumour in upper lobe. Separate from major bronchi*. (Peripheral) Microscopy: pleomorphic hyperchromatic cells forming irregular glands. Infiltration, inflammation, necrosis. Clinical: Commonest. Non smoker, female, previous injury / scar lungs.

Answer 131

Small Cell Ca Etiopathogenesis: smoking (3p deletion), carcinogenesis. Rb, P53 mutations. Lack of KRAS / EGFR mutations (NSCC). Gross: grey white tumour in the hilum, growing along bronchi. Not well demarcated. Hilar lymph node with black pigment. Microscopy: small, dark cells. Scanty cytoplasm, necrosis common. Clinical: Poor prognosis, early spread, paraneoplastic sy. (responds to treat). Neuroendocrinehormones.. ACTH

Answer 132

Metastases Etiopathogenesis: hematogenous spread (veins) predominantly by carcinomas. In this case melanoma. BN10: Arterial spread of bronchogenic carcinoma lung. (local spread) Gross: Multiple rounded tumours (coin shadows) with patchy black pigmentation. Microscopy: Melanoma (pleomorphic cells with melanin pigmentation) could be any type of cancer…. Clinical: lungs common site of spread – tumors invade veins  right heart  lungs more easily (thinner than artery).

Answer 133

Carcinoid Tumour: * Neuroectodermal tumours (NETs)* * Young ~40y, No relation to smoking. * Bronchus, nodular submucosal <4cm. * Tumor of neuroendocrine cells, secrete serotonin (5-HT) & other hormones. * Carcinoid syndrome in 40% patients - abdominal cramps & intermittent diarrhoea, facial dry flushing, palpitations, SOB / wheezing. * Benign (typical) to malignant (atypical). Majority behave benign. * Clusters of uniform cells with plenty of BV (endocrine pattern). * Diagnosis: increased 5-HIAA in urine / blood.

Answer 134

* Rounded or nodular, grey white, peripheral. * Presents as coin shadow – DD for cancer / metastasis. * True Neoplasm: Mutation, (not a hamartoma - Misnomer) * Benign Capsulated tumor. * Consists of normal appearing lung tissue - cartilage, smooth muscle, BV, Bronchial epithelium. Embryonic disorganization (Not true neoplasms): 1. Hamartoma: Normal tissue in Normal place. 2. Choristoma: Normal tissue in Abnormal place. (ectopic).

Pathology: ALL Flashcards

These are using CLIs and Pathology information