Pcl QI. What is this black discolouration? = 1 Q2. Define this pathological process. 1 Q3. What are the causes? 1 au What are the different types of this pathological process? 1 Fig. 16.1 PC 2 QU. Whatis this intensely eosinophilic cell in the epidermis? 1 2, Give two examples of physiological itions of this process? , cat P che) heal’ (Aenbayfiows) — dose Problem Ae fe y/ ae LY om Cards at vr A Wy A oA mth MOG? C fain wg’ Q3. Give two examples of pathologica 1 conditions of this process. 1 Q4. What is the most characteristic morpho- logical feature? 1 Pc3 52-year-old poor man suffering from fever and cough for 2 months with cervical lymphadenopathy, Cervical lymph node shows following, histological features: Ql. What is the diagnosis of the disease? 1 Q2. What particular cells have bee’ focused by arrows? 1 Q3, Which cytokines play an important role in pathogenesis? 2 239 rere NE lsED Pathology Practicals 7 Fig. 16.3, Pc4 47-year-old female who had varicose veins in left leg and was on prolonged rest after hystéfectomy. She suddenly developed swelling of left leg, pain and red or discoloured skin of left leg. Ql. What is the diagnosis? 1 Q2. Name the triad and component which predisposes to the pathophysiology. 1 Name some hereditary (primary) factors which can cause it. 1 What are the microscopic features of this pathologic lesion? 1 Qs. lor Fig. 16.4 T— PC5 A patient had clinical diagnosis of splenic artery occlusion following thromboem. bolism. Cut section of the spleen shows following morphological features: QI. What is the diagnosis? 1 Q2. Why this pathologic lesions are white? { QB. In which organs red-coloured lesions of same pathologic process are seen? Q4. What are the properties of this patho- logic lesion? 1 Fig. 16.5 PC6 A baby was born with severe mental retardation (IQ 30) with flat facial profile, oblique palpebral fissures, epicanthic folds and congenital heart defects, Ql. What is this genetic disorder? 1 Q2. What are the chromosomal changes? 1 Q3. What is the most common cause? 1 Q4. What are the future complications? 1 4S vk “~ Fig. 16.6pc7 A person was given penicillin injecti treatment without a test dose, Within steve minutes (10 minutes) he develops mucosal secretion (nasal, conjunctival), smooth muscle contraction and oedema, Ql. What is the diagnosis? Q2. Which cell is res; reaction? Q3. Which chemical mediators ponsible for this? 1 Q4. Which antibody is most important to cause this reaction? 1 ‘Ponsible for this 1 are res- PC 8- An adult person presents with fever, severe weight loss, generalized lymphadenopathy and opportunistic infections. History reveals that he had unprotected sex in brothels. QL. What is the diagnosis? 1 @. How does CD4+ T cell count help to diagnose the disease? 1 Q3. What neoplasms may develop in these patients? 1 QL. What are the most sensitive and specific tests? 1 co A patient had died of multiple myeloma and chronic inflammatory diseases. During autopsy, liver was found to be enlarged. Cut section of liver was firm and had a waxy appearance. Painting the cut surface with Fig. 16.7 [Problem Garda iodine imparts a yellow colour which transformed to blue violet after application of sulphuric acid (H,SO,). Ql. What is the diagnosis? 1 Q2. "What other organs may be involved? 1 disease and their colours. Q4. What are the biopsy sites for aod scopic examinations? aére,fynus, LS CODName two special stains to diagnose ee 1 PC 10. A patient had a small firm tumour (1.5 x 1.3 cm) on arm for several years. It was surgically resected. Grossly, the tumour is well circumscribed and white-glistening. Microscopically it is found to benerve sheath origin. QL. From: history and gross, is it a benign raour or malignant tumour? 1 Q2. What morphological features (micro- scopical) differentiate a benign and malignant tumour? 2 Q3. Mention two differences between carcinoma and sarcoma. 1 Fig. 16.8 PC 1 A 58-year-old male patient developed— Pathology Practicals PC 13_ a. Q. What is this clinical condition? What is the normal value of bilirubin in adults? 3. Mention some causes of unconjugated hyperbilirubinaemia. 1 . Mention some causes of conjugated hyperbilirubinaemia 1 Fig. 16.9 PC 12. A 52-year-old patient had tuberculosis and chest X-ray show following features, Qi. Q2. Qs. Qt. What is the provisional diagnosis based on chest X-ray? 1 What will be glucose and protein value in this fluid compared to plasma? 1 What will be LDH content and fluid LDH/serum LDH ratio? 1 What is anasarca? 1 Fig. 16.10 A5- year-old girl is suffering from fever anaemia, bone pain and generalise, lymphadenopathy. Peripheral blood smea, and flow cytometry reveal the following features. Ql. What is the diagnosis? 1 Q2. What will be the bone marrow picture? 1 Q3. Which marker/markers are positive in Qs. CD34 FITC the flow cytometry? w 1 Which special stain can be use Foy theses! abnormal cells? a yh 10° cp19 Pcs. 8 10' Fig. 16.114 and B- ——_—_ re ” Problem Cards pc 14 Qi A middle-aged man suffering from fatigue, Q2 fever and gum bleeding. His bone marrow sméar shows the following Q3- features: Ql. What is the diagnosis? 1 Q2. What is that constituent in the cyto- plasm of cells indicated by arrow? 9 Q3. Why there is gum bleeding? a 4 What markers are positive in flow cytometry (immunophenotyping)? 10° 10° 10° CD34 B c Fig. 16.12A to C PC 15 _ A 56-year-old female from moderate anaemia, bility and dragging sensation in men. TLC is 108,0007mm’. Peripheral blood smear has following features: patient is suffering weakness, fatiga- the abdo- 1 sensation in the 1 What is the diagnosi Why there is dragging abdomen? Which particular chromosome © detected in this case? What will be the NAP (neutrophil alkaline phosphatase) score? 1 ‘an be 1 Fig. 16.13 PC 16 A 60-year-old male patient is suffering from anaemia and symmetrically enlarged, dis- crete and non-tender lymph nodes. Peri- pheral blood smear shows the following features: . What is the diagnosis? 1 | Why 10-15% of these patients develop haemolytic anaemia? . What aggressive tumour may develop in these patients? 1 . What immunomarkers will be posi- ive? ee O13 CO, O23 Fig. 16.14Pathology Practicals ng adult presented with painless phadenopathy (potato size cervical lymph node). He also had constitutional symptoms like fever, night sweats and weight loss. Microscopy of lymph node and THC staining have following features: QI. What is the diagnosis? 1 2. Which variant of the disease is shown in the upper right picture? 1 23. Which markers are positive for the neoplastic cells (lower left)? 1 pe Which variant of the disease is shown in the lower right picture? Fig. 16.15A to D PC 18 Anelderly woman suffering from bone pain, pathologic fractures and renal failure. Bone marrow aspirates have following micro- scopic features: Ql. What is the diagnosis? 1 2. What will be found in serum electro- phoresis? 1 Q3. What may be found in X-ray of skull? 1 Q4. What will be urinary findings? 1 Fig. 16.16year-old female presented with pinpoint haemorrhages (petechiae) in the dependent areas 8nd ecchyniOsts. Spleen is of normal size, But microscoy Seng aire py of spleen has Q1. What is the diagnosis? Q2. What will be the peripheral bood picture? . What will be bone marrow picture? i Q4. Is there any antibody for the patho- genesis? 1 Problem Cards Q3. What biochemical investigations will help to reach the diagnosis? 2 PC 21 A 62-year-old female is suffering from anaemia. Bone marrow has following features: Ql. What is the diagnosis? 1 Q2. Whatare the features seen in Peripheral blood? Q3. Describe the particular cell in the bone marrow. 1 Fig. 16.17 PC 20 A pregnant lady is suffering from weakness, extreme fatigue and skin pallor. Peripheral blood smear shows the following features: Ql. What is your diagnosis? 1 Q2. What will be bone marrow findings? 1 Fig. 16.18 Fig. 16.19 PC 22 A7-year-old child is suffering from anaemia, priapism and bone pain. Peripheral blood smear has the following features: Ql. What is the diagnosis? 1 Q2. What is the molecular defect? 1 ove 0 3 Burts ge On ©.0°e9 o Se @*o8o % 250" ao 26° 6° 83 o 00, ©0920 o8, 3 Qo oO” © S02 8 ° one “* oo wy 0 5583 > n Fig. 16.20Pathology Practicals Q3. Which organs are affected by vaso- occlusive or pain crises? 1 sa What particular blood test is helpful? 1 PC 23 A patient presented with anaemia, spleno- megaly and jaundice. Peripheral blood smear has following features: QU. What is the diagnosis? Q2. What is the molecular defect? 1 S What is the cause of aplastic crises in these patients? poets cn 1 Q4. Which particular laboratory test (simple and cost-effective) will help to diag- nose? 1 10 wy @ oS eo Fig. 16.21 24 Xenuta is suffering from growth retardation, severe anaemia, hepatosplenomegaly and prominent cheek bones. Mother is also known to suffer from the disease. Haemo- globin electrophoresis shows the following features: a. Upper panel—normal control b. Middle panel—affected mother c. Lower panel—affected child Ql. What is the disease in child? ik Q2. What is the disease in affected mother? Q3. What will be peripheral blood pic- es? il Wily there is crew-cut appearance on ay? quay Movers i are Beery te Fig. 16.22 During marriage negotiation both the bride and groom underwent blood testing for HPLC. The groom has the following HPLC features: ™ tA 1.12 xm ae games 1.36 oses5 3.38 166 1.74 10866 6 IF nee 66 wma mie , — 30% 20% 10%: @ o [hit ° 1 2 3 4 Snag Fig. 16.23; Pe LL Cll ( —— 1. What is your diagnosis? Q2. What will be genotypi person? a i 1 (QI) What are the radiological features and Notypic defect in this « your diagnosis? — 1 i an’ 1 2. hat i: Q3. Wither bey anaemic? | tate yanceel rg shores? inding in Hb electro. Q3 Which special stain is commonly used to 1 diagnose the case? Why causative organisms give positive colour with this rey stain? paid 2 A 56-year-old male is suffering fi roductive cough and chest pane 18000/mm' with neutrophilia. Chest X-ra shows following features; z Ql. What is your diagnosis? 1 Q2. What is the finding fn air bi (chest X-ray)? : eee Q3. What is the commonest organism in nosocomial form of this disease? "1 Q4. What will be’histologic findings in lung vaatw ' biopsy? - wat ee Fig. 16.25 PC 28 An elderly patient had barrel-shaped chest and presents with dyspnoea, prolonged expiration, and sits forward. Spirometry reveals the following features: 7 Normal spirogram IRV Fig. 16.24 Volume (Iters) lower socioeconomic background presents with fever, dyspnoea, cough and hacmo- ptysis for 3 months. Chest X-ray has the _ following features: Fig, 16.264 PC 27 A 45-year-old female, a sum dweller withPathology Practicals Fig. 16.268 1. What is your diagnosis? (Q Why these patients are called pink — puffers? Q3. Which hypothesis explains the patho- genesis? 1 (QA. What are the causes of death? 1 PC 29 A patient presented with chest tightness, dyspnoea and wheezing. Peripheral blood shows eosinophilia. Sputum reveals Curs- chmann spirals and Charcot-Leyden crystals. QI. What is your diagnosis? 1 Q2. If the attack remains for a prolonged time (days or week) instead of a few minutes to hour; what is that condition known as? 1 Which constituent of eosinophils causes epithelial damage? 1 ~={Q4) What is Charcot-Leyden crystals? 1 hs Pc 30 A 75-year-old man ;-resented with weight loss, cough, chest pain and dyspnoea. Contrast-enhanced CT scan of lung shows a 5.5 cm, round, completely enhanced mass in left lobe of lung (arrow). 11. What is your provisional diagnosis? 1 2.How would you confirm the diagnosis? 1 Q3. What are the histologic types? 2 Fig. 16.27 31 ~Arrélderly woman is suffering from hyper. tension for years. Now she develops oedema over ankle (pedal) and pretibial. USG reveals hepatosplenomegaly and ascites. Echo- cardiography reveals left ventricular hyper. trophy (LVH). Ql. What is your diagnosis? 1 Q2. If there were pulmonary congestion and edema along with LVH and hype, tension, then what was your diagnosis What particular cells may be found in this case? 1 Q3. What particular colour change may be observed in liver? 1 32 A 56-year-old man (smoker and diabetic) suddenly developed acute chest pain and presented with rapid, weak pulse, profound sweating (diaphoresis) and dyspnoea Ql. What is your diagnosis? Q2. Whatare the most sensitive and specific biomarkers? 1 What gross features and light micto- scopic features will be seen in the affected organ(s) after 1-3 days? ? PC 33 A child has mitral valve prolapse a4 bicuspid aortic valve. He develops feverQ3. What are the clinical features of this condition? 1 Q4. What further examination would you find out the cause? 1 Answers to Problem Cards Mor 6 petiely, This is dry ganghGé'a W6St necrosis. . Necrosis is a localised area of death in living tissue and is accompanied by inflammatory reaction. This cell death is irreversible, Causes are hypoxia, ischaemia and toxins (poisoning). Coagulative necrosis, liquefactive necro- sis, caseous necrosis, fat necrosis, fibri- noid necrosis and gangrenous necrosis pe 2 S (dry and wet gangrene). Pc2 1. Apoptotic body. 2. Programmed cell death during embryo- genesis and endo down during menstruation. Councilman bodies in viral hepatitis and graft-versus-host disease (GVHD). Chronfatin condensation. tt 3. 4. PC3 1. Tuberculosis 2. Langhans giant cells 3. i, IL-1 and IL-2: Stimulate proliferation of more T cells ii, IFN-yactivates macrophages. iii, TNF-o. promotes fibroblast proli- feration and activates endothelium, iv. Growth factors (TGF-B, PDGF) stimulate fibroblast growth. —__-—-——_- Pc4 J. Deep vein thrombosis D Virthow’s triad: Endothelial injury, alteration in t od flow and blood hypercoagulability ee Problem Cards 3, © Mutation of factor Y (most common) * Antithrombin III deficiency * Protein C or potein S deficiency 4, Fibrin, moge"enmeshed red celJs and few platelets (therefore called red or stasis thrombi). Also, lines of Zahn, which cof 1 cu ipon OG, t pale platelet ibrin deposit vot ty dashecon | fotos se .¢present pale platelet and fibrin deposits PAL fests alternating with red cell layers (hence apparent laminations). une te-B : pn ia Beige OT Trt 1, Splenic infarction (white infarct) wo 2. Solid organs (like spleen.kidney or heart) have increased tissue density and it limits the seepage of blood from adjoining capillary beds into the necrotic area. Organs with loose tissues like lung and small intestine (arterial occlusion). Organs with dual blood supply like ovary and testis (venous occlusion). _ Red infarcts: Ill-defined haemorrhagic margins which change in colour to brown. ‘ite infarcts: (Well defined margins and progressively pallor with time. » - Pcé 1. Down syndrome 2. # In 95% of cases, there is trisomy 21 - (extra copy of chromosome of 21; so total chromosome 47). © In 4% of cases, robertsonian trans- location — © In 1% of cases, mosaic pattern (both 46, XY and 47 chromosomes) 3. Most common cause is maternal meiotic non-disjunction, Meiotic non-disjunction occurs in chromosome 21 in ovum. These children have 10-20-fold increased risk of developing acute leukaemia (more commonly ALL and specifically acute megakaryoblastic leukaemia, AML-M7). * Reduced fertility in females (males are totally infertile) . aa risk of respiratory infections >“<_ Pathology Practicals PC7 1. Immediate (type 1) hypersensitivity? Anaphylaxis Mast cell mainly. Also, TH, (Thelper cells) play some role. Histamine is responsible for early clinical features because it is preformed mediator. PAF is the major mediator of the late phase reaction. 4. IgE. N w Pcs _ Acquired immunodeficiency syndrome (AIDS) with human immunodeficiency virus (HIV) infection. _ According to the Centers for Disease Control (CDC) and Prevention, US in 1993, irrespective of presence of symptoms, any HIV-infected person having CD4+ T cell count of <200/pl is labelled as AIDS. aa ib 3[Kaposi¢s sarcoma, primary CNS lym- phoma, NHL and Hodgkin lymphoma, HPV-associated carcinoma (cervix, vagina, anus) and bacillary angiomatosis. ELISA (enzyme-linked immunosorbent aSsay) is the most sensitive test, and Western blot is the most specific test. sen a PC 9 1. Amyloidosis 2. Kidney, spleen (sago spleen and larda- ceous spleen), heart and oral cavity (gingiva and tongue) -&3. Congo red: Pink or red colour to amyloid feposits in tissue. Metachromatic stains like|crystal violet or methyl violet: Rose pink. ous 4. Biopsy from renal_tissue, rectum, abdominal fat and gingiva. The rectum is the best site for taking the biopsy. The staining of abdominal fat aspirate is quite specific but has low sensitivity. Pc 10 1. Benign tumour 2. Some microscopical features are in malignant tumour which is lage™* absent in benign tumour: king or Pleomorphism: Both is the nuclei display this el Nuclear atypia: Hyperchromat ifegularnuclear membrane "3%, A typical, bizarre mitoses: Increased Zarre mutoses; in Is ang number * Loss of polarity and |. faeces Poanty lack of differen. i. Carcinoma arises from epithelial ca whereas sarcomas arise from m = chymal cells. = ii. Caretsoma metastasizes b: \ xy lym route, while sarcomas ee genous route. PCT 1. Jaundice 2. Normal value of serum bilirubin {0 3- 1.2 mg/dl, about 80% of whichis uncoriu- gated bilirubin. . Physiological jaundice of newbom, haemolytic anaemia, diffuse hepato- cellular disease (viral hepatitis), Crigsier Najjar syndrome, Gilbert syndrom= » Biliary tract obstruction, primary biiay 4, cirrhosis, Dubin-Johnson syndrome Rotor syndrome. PC 12 1, Left-sided pleural effusion due accu mulation of exudate. | cawil 2, Glucose contentof the effusion. fluid hal be low (<60 mg/ dl) and protein com vill be high (2.5-35 gm/al) aa 3, LDH content will be high compan transudate and ratio Will be >" " Anasarca ropsy is @ serpree eneralised oe > viemna with Wi dem 8 e zl . suet OS ing. Causes: enal oedema, cardiaeo* and nutritional a.| | | pc 13 1. Acute lymphoblastic leukaemi . mi 2, The bone marrow is ine ma a shows 20-95% lymphoblasts of Bor ell origin. Megakar Soent, | SY OCyteS are reduced or 3. CD34 and CD19 are positive 4, PAS +ve arid acid phosphatase (focal) +ve eae PC 14 1, Acute myeloid leukaemia (AML) 2, Auer rods 3. Thrombocytopenia cause spontaneous bleeding in AML patients. Also, pro- coagulants and fibrinolytic factors released by the leukaemic cells exacerbate — the bleeding tendency. 4, CD34 and CD22 in the first panel. TdT and CD19 in the second panel. Pc 15 1. Chronic myeloid leukaemia (CML). 2. It is caused by splenomegaly. Spleno- megaly occurs as a result of extensive extramedullary haematopoiesis. 3. Philadelphia chromosome (Ph). Ph chro- mosome is formed by reciprocal balanced translocation between part of long arm of chromosome 22 arm with part of long arm ofschromosome 9 {t (9;22) (q34; q11)}. NAP score will be reduced. (Remember, NAP score will be high in myeloid leukaemoid reactions. Also, NAP score in CML returns to normal with successful treatment, in infections and corticosteroid administration.) PC 16 1. Chronic lymphocytic leukaemia (CLL). 2. This happens because of production of autoantibodies'by non-neoplastic B cells. 3. There may be prolymphocytic trans- formation (15-30% of patients) or a transformation to diffuse large B cell lymphoma (DLBCL), so-called Richter syndrome (510% of patients). Problem Cards 4, CD23, CD20_and CD19 (pan B cell markers). “eee PC 17 1. Hodgkin lymphoma or Hodgkin disease 2. Classic form of Hodgkin lymphoma, mixed cellularity type. 3. CD30 positive in 98% of cases CDI5 positive in 80% of cases CD20 positive in small subset 4, Classic form of Hodgkin lymphoma, nodular sclerosis type. PC 18 1. Multiple myeloma (plasma cell dys- crasia). Presence of M band (M protein) due to presence of monoclonal (hence the name M) immupoglobulin. This Ig is usually IgG (55%, followed by IgA (25% of cases). . Sharply punched out bone lesions. Present of Bence-Jones protein (light chains of immunoglobulin). Also, increased urinary protein 6 gm/dl. R ee PC 19 1. Chronic immune thrombocytopenic pur- pura (ITP). 2. Decreased platelet count and presence of abnormally large platelets (mega throm- bocytes). — 3. Bore*marrow reveals a modestly increased number of megakaryocytes. Some of them are immature With large, non-lobulated, single nuclei, — . Autoantibodies directed against platelet membrane glycoprotein Ilb-Illa or Ib-1IX may be found in plasma and bound to platelet surface near about 80% of patients. Usually spleen is of normal size. Typically, there. \s congestion of splenic sinusoids and enlargement of the splenic follicles, often (gsggiated with reactive germinal. centres » |Pathology Practicals PC 20 . Iron deficiency anaemia. we Mild to moderate increase in the erythroid Progenitors (normoblasts). erie 8- jue reveals disappearance of stain- able iron from macrophages (sideroblasts) in the bone marrow, 2 Serum iron and ferritin level are low, whereas total iron binding capacity (TIBC) is high (which is a reflection of elevated transferrin level). This results in a reduction of transferrin saturation to <15%. PC 21 1. Megaloblastic anaemia 2. Red blood cells (RBCs) are macrocytic and oval (macro-ovalocytes), Neutrophils are larger than normal (macropolymor- phonuclear) and some hypersegmented, having 25 lobes (normally 3-4 lobes) neutrophils. 3. The characteristic large cells are megalo- blasts. These cells are large with rdeply basophilic cytoplasm, prominent nucleoli and a distinctive, fine nuclear chromatin pattern. PC 22 1. Sickle cell anaemia. 2. Point mutation in the sixth codon of B-globin chain that leads to the replacement of a glutamine residue with a valine residue. 3. These crises are episodes of hypoxic inju and infarction which cause severe pain. _The affected organs srelpnesslungs, iver, brainjspleen and pers 4. Mixing of blood sample with an oxygen- consuming reagent such as meta- bisulphite induces sickling of red cells. This is known as sickling test. It can be done with 2% metabisulfite or dithionite, PC 23 1. Hereditary spherocytosis 2. There are intrinsic defects in the red coy, due to diverse mutations Which lead to an, insufficiency of membrane skeletal com, ponents. The pathogenic mutations com. monly seen in ankyrin, spectrin, bang Band band 4.2. -——~ . Aplastic crises are usually triggered acute parvovirus jnfection. This virus infects and kills red cell pragemitors (nor. moblasts), causing red cell prodtiction tg cease. . Osmotic fragility test which is increased in hereditary spherocytosis. |herocytes on peripheral blood a not pathognomonic of hereditary sphere. cytosis (HS) as it may be found in autoimmune: haemolytic anaemia, ABO haemolytic disease (out not with RH haemolytic disease) 2 newborn, G6PD deficiency and aad PC 24 1. B-Thalassemia major 2. B-Thalassemia minor (trait) 3. Anisopoikilocytosis, target cell, micro- cytes, basophilic stippling, and fx3g- mented red cells. 4. The marrow is|hypercellular and active The expanding marrow erodes existing cortical bone and induces new bone formation, giving rise to a “crew-cut” appearance, = » - PC 25 1, B-Thalassemia minor (thalassemia trait) 2. The person will be heterozygous B- thalassemia (B°/B, or B*/B). One B globin chain will be normal, other is defective: 3, Anaemia will be either absent or if present mild.& | 257] Problem Cards 4. It will reveal increase in HbA. 5.4% of the total haemnoglit tcoraos +039). Adult haemoglobin or HbA will cee © of total haemoglobin Thormal PC 26 . Lung (pulmonary) infection, broncho- pneumonia 2. Focal opacities due to consolidation in 3. Staphylococcus aureus 4, There willbe suppurative, neutrophil-rich exudate which fills the bronchi, bron- chioles-and adjacent alveolar spaces. PC 27 1. Bilateral “Aufty or wooly’ opacities predo- minantly in the upper TEN fibrotic infiltration. Diagnosis is tuberculosis (Koch). 2. Fn ee by the active pulrftonary lesion, particulary bronchial artery is the source of haemoptySis. 3. Ziehl-Neelsen or ZN stain (acid-fast stain) is used to detect the organism, i.e. tubercle bacilli. The acid fastness of tubercle bacilli is due to mycolic acids, cross-linked fatty acids and oth the cell wall of the bacilli. The bacilli take up stain by heated carbolfuchsin and resist decolourisation by weak acids and alcohol unlike other organisms, which cannot resist decolouri- sation. So, tubercle bacilli are acid fast as well as alcohol (ethanol) fast. ae False positive AFB (acid-fast bacil) staining in 2N stain may be seen due to Nocardia, Legio- nella, Cryptosporidium, Isospora, Rhodo- i us and some protozoa, ea ee ce sn ctacaealal PC 28 1. Emphysaema of lung, a type of COPD (chronic obstructive pulmonary disease) 2. These patients ov, fe and remain well oxygenated as well as tachypnoea Protease-antiprotease imbalance hypo- thesis. There is destructive effect of high protease coupled with low antiprotease lead to tissue damage 4, Death is due to: i. Respiratory acidosis and coma ii. Right-sided heart failure, and iii, Massive collapse of the lungs secondary to pneumothorax. idei ’ PC 29 1. Bronchial asthma 2. Status asthmaticus 3. Major basic protein of eosinophils. 4, These are collections of crystalloids, made up an eosinophil lysophospholipase binding protein called galectin. PC 30 1. Lung cancer (carcinoma). 2. Initially FNAC may be done to determine the malignant nature of the neoplasm. But final diagnosis should be made after lung biopsy and histopathologic examination. 3, There are five main histologic types: i, Adenocarcinoma ii, Squamous cell carcinoma or epider- moid carcinoma . Small cell carcinoma iv. Large cell carcinoma v, Combined*eartinoma, e.g. adeno- squamous caiinoma (combination of adenocarcinoma and squamous cell carcinoma). PC 31 1. Congestive heart failure (CHF) due to right-sided heart failure. 2. Congestive heart failure (CHE) due to left sided-heart failure. In the Tung, Some RBCs extravasate into pulmonary oedema fluid within the