Learn — Systemic pathology: diseases of the organs

3 notes · 3 questions on the topic

Respiratory pathology — tuberculosis, pneumonia, COPD and bronchogenic carcinoma

Respiratory pathology is the morphology and mechanism of the diseases of the airways, lung and pleura that fill Indian wards — tuberculosis above all, the pneumonias, the chronic obstructive diseases, asthma, the occupational lung diseases and bronchogenic carcinoma — read on the sputum smear, the chest film and the biopsy. The paper asks the Ghon complex, the stages of lobar pneumonia, the difference between chronic bronchitis and emphysema, and the types of lung cancer, and the nurse meets them as the cough that must be sent for acid-fast bacilli, the sputum that changes colour and the haemoptysis that does not stop.

Tuberculosis is a caseating granulomatous inflammation caused by Mycobacterium tuberculosis spread by droplet nuclei: primary infection produces the Ghon focus (a subpleural lesion in the mid-zone) with its draining hilar lymph nodes, together the Ghon complex, which usually heals with calcification and leaves latent bacilli; secondary or reactivation tuberculosis sits in the apices, cavitates, sheds bacilli into the sputum and spreads to the pleura, larynx, gut, spine (Pott's disease), meninges and, as miliary tuberculosis, everywhere by the blood.
The diagnosis rests on sputum (an upfront nucleic acid amplification test — the cartridge-based CBNAAT or the chip-based Truenat — which also reports rifampicin resistance, with the acid-fast Ziehl-Neelsen smear kept for follow-up and where a molecular test is not available), the chest film, the tuberculin test (induration of 10 mm or more at 48 to 72 hours is positive, 5 mm in HIV) which shows infection rather than disease, and histology showing epithelioid granulomas with Langhans giant cells and caseation; the complications are haemoptysis, pleural effusion, pneumothorax, bronchiectasis, empyema and aspergilloma in an old cavity.
Lobar pneumonia, classically pneumococcal, consolidates a whole lobe through four stages — congestion (day 1 to 2), red hepatisation (day 2 to 4, the lung liver-like with red cells and fibrin), grey hepatisation (day 4 to 8, fibrin and neutrophils) and resolution (after day 8) — whereas bronchopneumonia is patchy, bilateral and basal, follows the bronchioles and afflicts infants, the elderly and the bedridden; interstitial or atypical pneumonia (Mycoplasma, viruses, Pneumocystis in HIV) inflames the septa with few sputum findings, and aspiration pneumonia (anaerobes, the right lower lobe) follows a depressed cough reflex.
Chronic obstructive pulmonary disease: chronic bronchitis is defined clinically — a productive cough for at least three months in each of two consecutive years — with hypertrophy of the mucous glands (a Reid index above 0.4), and the patient is the blue bloater with hypoxia and cor pulmonale; emphysema is defined anatomically — permanent enlargement and destruction of the air spaces beyond the terminal bronchiole without fibrosis — centriacinar in smokers (upper lobes) and panacinar in alpha-1 antitrypsin deficiency (lower lobes), and the patient is the pink puffer; smoking causes both, and the loss of elastic recoil traps air.
Asthma is reversible airway obstruction from bronchial hyper-reactivity — smooth muscle spasm, mucosal oedema and thick mucus plugs — with eosinophils, Charcot-Leyden crystals and Curschmann spirals in the sputum; bronchiectasis is permanent dilation of bronchi from destruction of their walls by chronic infection (cystic fibrosis, tuberculosis, childhood pneumonia, obstruction) with copious foul sputum; acute respiratory distress syndrome is diffuse alveolar damage with hyaline membranes after sepsis, aspiration, trauma or pancreatitis.
Bronchogenic carcinoma, the commonest cancer death in men worldwide and overwhelmingly a disease of smokers: squamous cell carcinoma is central and cavitating and may secrete parathyroid-hormone-related peptide (hypercalcaemia); adenocarcinoma is peripheral, the commonest type overall and the type in non-smokers and women; small cell carcinoma is central, neuroendocrine, the most aggressive and the one that produces ectopic ACTH and antidiuretic hormone; large cell carcinoma is the rest; a tumour at the apex (Pancoast) invades the brachial plexus and sympathetic chain (Horner's syndrome), and a mediastinal mass compresses the superior vena cava.
The pneumoconioses are dust diseases of work: silicosis (quartz, mining and stone-cutting — nodular fibrosis, egg-shell calcification of hilar nodes, a high risk of tuberculosis), coal-workers' pneumoconiosis, asbestosis (fibrosis, pleural plaques, bronchogenic carcinoma and mesothelioma decades later), byssinosis (cotton dust — Monday-morning chest tightness), bagassosis (mouldy sugarcane) and farmer's lung (mouldy hay — a hypersensitivity pneumonitis); pleural effusion is a transudate in heart failure and an exudate in tuberculosis, pneumonia and malignancy, told apart by protein, lactate dehydrogenase and cells.

Cardiovascular pathology — atherosclerosis, ischaemic heart disease and rheumatic heart disease

Cardiovascular pathology is the study of the lesions behind the country's leading cause of death — the atherosclerotic plaque that narrows and ruptures, the infarct that follows when a coronary artery closes, the rheumatic scar that deforms a valve after a streptococcal sore throat, the vegetation of infective endocarditis, and the vessel changes of hypertension. The paper asks the layers of the plaque, the timeline and markers of a myocardial infarct, the Jones criteria and the Aschoff body, and the nurse reads them as the chest pain, the new murmur and the fever that must not wait.

Atherosclerosis begins as the fatty streak of childhood, becomes the fibrous plaque of adult life — a fibrous cap over a core of lipid, foam cells (macrophages full of cholesterol), necrotic debris and calcium in the intima — and ends as the complicated plaque that ulcerates, thromboses, bleeds into itself, calcifies or weakens the wall into an aneurysm; the sites in order are the abdominal aorta, the coronary arteries, the popliteal arteries, the internal carotids and the circle of Willis, and the modifiable risks are smoking, hypertension, dyslipidaemia, diabetes, obesity and inactivity, the fixed ones age, male sex and family history.
Ischaemic heart disease is the plaque's clinical face: stable angina from a fixed narrowing, unstable angina from a ruptured plaque with a non-occlusive thrombus, variant angina from spasm, and myocardial infarction when the thrombus occludes — transmural in a full-thickness infarct with ST elevation, subendocardial in the inner third; the left anterior descending artery is the commonest culprit (the anterior wall and septum), then the right coronary (inferior wall) and the circumflex (lateral wall).
The infarct evolves on a timetable the exam asks: no visible change under 4 hours, coagulative necrosis and wavy fibres by 4 to 12 hours, neutrophils from 12 to 24 hours to 3 days, macrophages clearing dead muscle from day 3 to 7 (the wall is softest and rupture likeliest then), granulation tissue at 1 to 2 weeks and a firm fibrous scar by 6 to 8 weeks; grossly the infarct is pale, then yellow with a red rim, then grey-white.
The markers: myoglobin rises first (1 to 3 hours) but is non-specific; troponin I and T rise at 3 to 6 hours, peak around 24 hours and stay up for 7 to 10 days, and are the most specific and sensitive; creatine kinase-MB rises at 4 to 6 hours, peaks at 24 and returns to normal in 48 to 72 hours, which makes it the marker for reinfarction; lactate dehydrogenase rises late and stays for days; a normal troponin at the door and at 6 hours effectively excludes infarction.
Complications of infarction: arrhythmia (the commonest cause of death in the first hours — ventricular fibrillation), cardiogenic shock when more than 40 per cent of the left ventricle is lost, rupture of the free wall, septum or papillary muscle at day 3 to 7, mural thrombus and embolism, ventricular aneurysm, acute pericarditis at day 2 to 3, Dressler's autoimmune pericarditis at 2 to 10 weeks, heart failure and sudden death; hypertension adds its own lesions — hyaline arteriolosclerosis in benign disease, hyperplastic onion-skinning and fibrinoid necrosis in malignant hypertension, concentric left ventricular hypertrophy, nephrosclerosis and retinopathy.
Rheumatic fever is an immune cross-reaction, two to three weeks after a group A streptococcal pharyngitis, between the bacterium's M protein and the heart, joints, skin and brain (molecular mimicry); the revised Jones criteria need evidence of the streptococcal infection (raised anti-streptolysin O, a throat culture or rapid antigen test) plus two major criteria — carditis, migratory polyarthritis, Sydenham's chorea, erythema marginatum, subcutaneous nodules — or one major and two minor (fever, arthralgia, raised ESR or C-reactive protein, a prolonged PR interval); the Aschoff body with its Anitschkow cells is the pathognomonic lesion, the MacCallum patch its atrial scar, and the mitral valve the one most deformed — the fish-mouth stenosis of chronic rheumatic heart disease, with the aortic valve next.
Infective endocarditis grows vegetations of fibrin, platelets and organisms on valves: subacute disease from Streptococcus viridans after dental work on a rheumatic or congenitally abnormal valve, acute disease from Staphylococcus aureus on a normal valve — the tricuspid in the intravenous drug user; the signs are fever, a new or changing murmur, splinter haemorrhages, Osler's nodes, Janeway lesions, Roth spots, splenomegaly and emboli, the diagnosis rests on repeated blood cultures and echocardiography (the Duke criteria), and the vegetations embolise to brain, kidney and spleen; the aneurysms complete the chapter — atherosclerotic in the abdominal aorta, syphilitic in the thoracic aorta, berry aneurysms in the circle of Willis, and dissection in the hypertensive and the Marfan patient.

Gastrointestinal, hepatic and renal pathology — peptic ulcer, cirrhosis and glomerulonephritis

The gastrointestinal, hepatic and renal chapters carry the lesions the ward sees every day — the peptic ulcer that bleeds or perforates, the gastritis behind pernicious anaemia, typhoid's ulcer in the third week, the two inflammatory bowel diseases, the adenoma that becomes a colonic carcinoma, the hepatitis viruses and the cirrhosis they and alcohol produce, and the two faces of glomerular disease, nephritic and nephrotic. The paper asks the differences in pairs — duodenal versus gastric ulcer, Crohn's versus ulcerative colitis, nephritic versus nephrotic — and the nurse turns them into what to watch for at the bedside.

Peptic ulcer: the duodenal ulcer is four times commoner, sits in the first part of the duodenum, is almost always Helicobacter pylori related, hurts when the stomach is empty and at night and is relieved by food, and is never malignant; the gastric ulcer sits on the lesser curvature, follows NSAIDs and H. pylori, hurts after food, and must be biopsied because a gastric ulcer can be a carcinoma; the complications are bleeding (the commonest — a posterior duodenal ulcer eroding the gastroduodenal artery), perforation (an anterior duodenal ulcer — a rigid, silent abdomen with gas under the diaphragm), pyloric obstruction and penetration into the pancreas; Curling's ulcer follows burns and Cushing's ulcer follows head injury.
Gastritis is acute and erosive after NSAIDs, alcohol, stress and shock, or chronic — type B in the antrum from H. pylori (the road to ulcer, adenocarcinoma and MALT lymphoma) and type A in the body from autoimmune destruction of parietal cells, which removes acid and intrinsic factor and gives pernicious anaemia; gastric carcinoma is intestinal (glandular, on chronic gastritis) or diffuse (signet-ring cells, linitis plastica) and announces itself late as Virchow's node in the left supraclavicular fossa, Sister Mary Joseph's nodule at the umbilicus or the Krukenberg tumour in the ovaries.
The small and large bowel: typhoid ulcers lie along the long axis over the Peyer's patches of the ileum and perforate in the third week, tuberculous ulcers lie across the bowel and stricture; appendicitis begins with obstruction by a faecolith and is diagnosed on the slide by neutrophils in the muscle wall; Crohn's disease is transmural, patchy with skip lesions, cobblestoned, fistulating and granulomatous, favouring the terminal ileum, while ulcerative colitis is mucosal, continuous from the rectum, with crypt abscesses and pseudopolyps and a real risk of carcinoma after ten years; colorectal carcinoma grows from an adenoma through the adenoma-carcinoma sequence (APC, KRAS, p53), presents on the left with obstruction and bleeding and on the right with anaemia, and is followed with carcinoembryonic antigen.
Viral hepatitis: A and E spread by the faecal-oral route, cause acute self-limiting disease and never become chronic, though E kills pregnant women; B, C and D spread by blood, sex and birth, become chronic and lead to cirrhosis and hepatocellular carcinoma; the B markers to read are HBsAg (current infection), anti-HBs (immunity from infection or vaccine), HBeAg (high infectivity), IgM anti-HBc (recent infection) and HBV DNA; on the slide the dying hepatocyte is the acidophilic Councilman body.
Cirrhosis is diffuse fibrosis with regenerative nodules that destroys the liver's architecture — micronodular in alcohol, macronodular after viral hepatitis — reached in alcohol through fatty liver, then alcoholic hepatitis with Mallory bodies and neutrophils, then scar; its consequences are portal hypertension (oesophageal varices, ascites, splenomegaly, caput medusae), hepatic encephalopathy, the hepatorenal syndrome, coagulopathy, hypoalbuminaemia and hepatocellular carcinoma (alpha-fetoprotein); jaundice is pre-hepatic and unconjugated in haemolysis, hepatic in hepatitis, and post-hepatic and conjugated in obstruction, with pale stools, dark urine and itching; gallstones are mostly cholesterol stones in the fat, fertile female of forty, and acute pancreatitis follows gallstones and alcohol with fat necrosis, a raised amylase and lipase, and flank and periumbilical bruising when it bleeds.
Glomerular disease has two syndromes: the nephritic syndrome — haematuria with red-cell casts (smoky or cola-coloured urine), oliguria, hypertension and periorbital oedema, classically post-streptococcal glomerulonephritis in a child one to three weeks after a throat or skin infection, with a low C3 and subepithelial humps on electron microscopy; and the nephrotic syndrome — proteinuria above 3.5 g a day, hypoalbuminaemia, generalised oedema, hyperlipidaemia and lipiduria — from minimal change disease in children (foot-process effacement, steroid-responsive), membranous nephropathy and focal segmental glomerulosclerosis in adults, and diabetic nephropathy with its Kimmelstiel-Wilson nodules.
The rest of the kidney: acute pyelonephritis is an ascending Escherichia coli infection with white-cell casts and flank pain, and chronic pyelonephritis scars the cortex and 'thyroidises' the tubules; acute tubular necrosis follows ischaemia or toxins with muddy-brown granular casts and recovers if the patient is carried through; stones are calcium oxalate most often, struvite staghorns in Proteus infection and radiolucent uric acid stones in gout; adult polycystic kidney disease is autosomal dominant and travels with berry aneurysms; renal cell carcinoma is a clear-cell tumour with the triad of haematuria, flank pain and a mass, and Wilms tumour is the abdominal mass of the child under five.

Free today: the 10-question daily quiz · the NORCET 11 recall paper · what ₹999 unlocks — once, no auto-renewal.