pathology final practical
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Pathology Lab 3rd Dec’09
Last practical of 1st SemesterSlides for finals
Ravi A Patel
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Leprosy of Skin
Acute Appendicitis
Meningitis (In given slide meningitis is around Cerebellum)
Lung Abscess
Viral Hepatitis
Intestinal amoebiasis
Schistosoma Ova (Schistosoma japonicum)
Wilm’s Tumor
Lobar Pneumonia(bacterial)
Viral Pneumonia
M++
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EpidermisDermis
Causative organism- Mycobacterium leprae
Organs affected- Skin and Peripheral nerves--------------------------------------------------------------------------------------------- **** Granulomatous formation – In upper dermis layer ****Foam cells harbouring the organism ****Fibrosis
Observation :---
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LPO
Granulomas
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LPO
Granuloma
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HPO
Foam cells– Modified macrophagesso called because of foamy cytoplasm
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HPO
Dark Stained are lymphocytes
Fibrosis
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Mucosa
SubmucosaTunica muscularis
Tunica Serosa
Primary casue - 80% Obstruction of lumen producing increased pressure with compression of blood vessels and ischemia.
Secondary cause- bacterial infection and pus formation (suppurative exudates)
Observation ***** PMNs – mainly neutrophil infiltration in muscularis
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LPO
Lumen
Mucosal layer
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LPO
Tunica muscularis
Wtih infiltrationOf neutrophils
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LPO
Blood vessel with clot within
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LPO
Lymph nodules
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HPO
PMNs ---- Mostly Neutrophils inTunica muscularis layer
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Section taken from cerebellum
Molecular layer of cerebellarcortex
Granular layerOf cerebellar cortex Medullary
Layer of cerebellum
Meningeal layer* Site of Meningitis
Causative organism:- Pnemococcus
Observation **** Subarachnoid space filled with suppurative exudates(pus) **** Presence of Neutrophils confirmed in exudates in HPO
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LPO
bloodVessels congestedBy the exudatesSurrounding them
Suppurativeexudates
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LPO
Congested blood vessel
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LPO
Suppurative exudates
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LPO
bloodVessels congestedBy the exudatesSurrounding them
Suppurativeexudates
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HPO
Blood vessel surrounded byThe exudates
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HPO
Predominant NeutrophilsIn exudate
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HPOPredominant NeutrophilsIn exudate
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HPO Predominant NeutrophilsIn exudate
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• Liquefactive type of necrosis• When this necrotic tissue is absorbed from the
organ a cystic space is produced
• Observation ** Total digestion of lung tissue ** Granular debris
** Lymphocyte in filtration
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LPO
There is total destruction of lung tissue As observed in these slides the debris of Dead tissue
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HPO
Granular debris
Neutrophil infiltrates
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HPO
Neutrophil infiltrates
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• Morphologic changes in acute and chronic phase of viral hepatitis are the same.
• Slide is in acute phase
• Observation ***Lobular dissray ***Cell necrosis in portal area
***Mononuclear infiltrate in portal areas and sinusoids
Viral Hepatitis
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LPOWe might mistake it as lung Abscess if given in low poweras this one
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Central vein
illustration of lobular rays in normal liverWhere in the sinusoids(draining to central vein) seems to form rays aroundThe central vein
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LPO Lobular dissray- hard to distinguish sinusoids
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HPO
HepatocytesSeems to have Undergone cytolysis
Swollen hepatocyte In Viral hepatitis Some cells get swollenAnd some undergo cytolysis
MonnuclearCells infiltrate insinusoids
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HPO
Infiltrates inThe sinusoids
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HPO
Mononuclear cell infiltrated in the portal area
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PV
HA
BD
Lymphatic vessel
Id space : Hepatic sinusoid
Normal Liver
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Portal Area
HPO
There is cell necrosis in portal area---
Portal area in normal liver
Portal area in liver with Viral hepatitis showingViral hepatitis
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• Causative organism- Entamoeba histolytica• Infective stage of organism- Cyst• Pathologic state of Organism- Trophozoite• Observation *** Cyst
*** Trophozoites *** Mononuclear infiltrates
Intestinal Amoebiasis
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LPO
Area where in the mucosa is Ulcerated because of the Proteolytic invasion by trophozoites
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HPO
Trophozoites harbouringRBC
Mononuclear infiltrates
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HPO
Trophozoites
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HPO
Cysts– because it doesnothave RBC within the cytolasm
One pointed is a trophozoite
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HPOIdentify Trophozoites and cysts in this slide
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HPO
Mononuclear Infiltrates
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Schistosoma ova
• Organism- Blood fluke (Schistosoma japonicum)
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LPO
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HPO
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HPO
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HPO
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HPO
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HPO
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• Wilm’s tumour is a common primary tumour of childhood.
• Observation *** Area of tumour *** Immature tubules and glomerulus
*** Sphindle shaped cells *** Dark stained cells
Wilm’s Tumour
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LPO
Sphindle shaped cells
There are attempts to form tubules and Glomerulus but they are immature
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HPO
Blastemal component
Immature glomerulusand tubules surroundingthem
Sphindle shaped cells
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HPO
Immature glomerulusand tubules in high power
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HPO
Sphindle shaped cells In high power
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HPOObservation slide
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HPO
Blastemal component
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Lobar Pneumonia
Pneumonia- Inflammation of the lung parenchyma when it affects a part of a lobe it is designated ad lobar
Bacterial in origin
Observation *** Lung alveoli filled with fibrino-purulent exudates *** Congested alveolar walls
*** In HPO there is fibroblasts growing into exudates
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LPO
Lung Alveoli
Lung alveoli filled with purulentexudates
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LPO
Lung alveoli filled with Purulent exudates
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HPO
Congested alveolar wall
There is fibrosis in the alveoli Along with purulent exudate (at the pointer)
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HPO
Purulent exudate in High power shows presence of neutrophils
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HPO
Fibrosis in high power along with neutrophils
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HPO Scanty Neutrophils and at the pointeris the congested alveolar wall
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Hallmark :- Inflammation in the interstitium and septa but the alveolar spaces are very clear meaning there is no exudate in the space as compared to the bacterial pneumonia.
Viral Pneumonia
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LPO Observe clear alveolar spaces withoutExudates, but the alveolar walls are edematous
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LPO Patchy Inflammation of the Interstitium and Septa
Mononuclear infiltrates in alveolar wall
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LPO
Mononuclear infiltrates inThe alveolar walls
Edematous walls
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HPO
Compare the alveolar walls with the normal onesTo appreciate the edema in the viral Pneumonia
Mononuclear infiltrates in alveolar wall
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HPO Observation Slide
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Differentiating Viral and Bacterial Pneumonia
LPO
Exudates in Alveolar spaces No exudates in the alveolar space, butPatchy inflammtion and edema in The alveolar walls
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Thanking to the entire Universe