pathology 1 st practical exam part 1
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PATHOLOGY 1 ST PRACTICAL EXAM part 1. THANK YOU FAISAL FOR MOST OF THE PICTURES. Please do read your manuals. Don’t solely rely on this reviewer. There are other questions in the manual that I did not include in the slides. Cellular injury, adaptation, and death. CELLULAR SWELLING, kidney. - PowerPoint PPT PresentationTRANSCRIPT
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PATHOLOGY 1ST PRACTICAL EXAM part 1
THANK YOU FAISAL FOR MOST OF THE PICTURES.
Please do read your manuals. Don’t solely rely on this reviewer. There are other questions in the manual that I did not include in the slides.
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CELLULAR INJURY, ADAPTATION, AND DEATH
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CELLULAR SWELLING, kidney
Organ: Kidney – convoluted tubules
Size of lumen: decreasedCytoplasm: enlarged, increased pinkish colorReversible cell injury, but may become irreversible if stress is not removed
Pathogenesis: Swelling Is due to failure of membrane pumps because of lack of cellular ATP allowing the cell to accumulate fluid
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FATTY CHANGE, liverHISTO:Organ: Liver – hepatic cordsCytoplasm: lipid vacuoles replacing the normal cords of hepatocytesNucleus: displaced peripherallyPathogenesis: impaired metabolism of fatty acids that leads to accumulation of triglyceridesConditions that give rise to fatty liver:1.Alcoholism2.Obesity3.Diabetes Mellitus
GROSS:Yellow and glossy appearancePale liver
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BROWN ATROPHY, heartPigment: LIPOFUSCINCell: Cytoplasm of Myocardial CellColor: brown or golden yellow granular appearance
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ANTHRACOSIS, hilar lymph nodePigment: CARBON/coal dustCell: Parenchymal cellsColor: black
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MALARIA, liverPigment: HEMOZOINCell: Kupffer cells
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CHRONIC PASSIVE CONGESTION (CPC), lungPigment: HEMOSIDERINCell: alveolar/laden macrophageColor: yellow, golden brown
“heart failure cells (macrophages) in the alveoli are indicative of left sided heart failure”
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BILE NEPHROSIS, kidneyPigment: BILIRUBINCell: Tubular LumenColor: Reddish or golden brown
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SQUAMOUS METAPLASIA, lungsOrgan: Bronchi, lungs
Lining Epithelium: pseudostratified ciliated columnar epithelium was replaced by stratified squamous epithelium
Adaptive change: METAPLASIA
Seen in: chronic smokers and vitamin A deficiency
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FAT NECROSIS, pancreas“acute pancreatitis” – pancreatic enzymes leak out of the acinar cells and liquefy the membranes of fat cells in the peripancreatic adipose tissue
Presence of numerous chalky white spots; necrosis of surrounding peripancreatic adipose tissue
Fat cells: pinkish-shadowy outline
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TUBERCULOSIS, lungsCASEOUS NECROSIS
White cheese-like appearance(granular amorphous debris)
MICROSCOPIC: formation of granulomas
NOTES:Other types of necrosis:1.Coagulative – common in kidney2.Liquefactive – brain3.Gangrenous – DM4.Fibrinous – connective tissue
GROSS:-Decrease in size of organ-White lesions on cut surface
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INFLAMMATION AND REPAIR
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ACUTE APPENDICITISCells: PMN,
Edema present in mucosa, muscularis, and propria
(+) congestion of vessels and thrombosis
Type of necrosis: Suppurative Inflammation
Pathogenesis: initiated by progressive increase in intraluminal pressure that compromises venous outflow
APPEARANCEGROSS: dilated lumen; thickened wall; serosal surface has fibrinopurulent exudateHISTO: thickened edematous cell wall with neutrophilic infiltrates and vascular congestion with focal hemorrhages; eroded mucosa; presence of segmenters densely occupying the appendiceal wall
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BRONCHOPNEUMONIA, lungsGROSS: with patches of consolidation, multiple abscess in the lungs
HISTO: bronchi, alveoli filled with NEUTROPHILS; congested septal capillaries
Tissue damage or necrosis
Acute inflammation
Marked neutrophilic response with tissue destruction
Abscess formation
OUTCOMES:1.Complete resolution2.Healing by CT replacement3.Progression to chronic inflammation
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TUBERCULOSIS, lungsGRANULOMATOUS-Epitheloid cells, Langhans giant cells
Role of lymph nodes:-Filters and drains extravascular fluids that have seeded out of the capillaries
Conditions that cause chronic granulomatous inflammation:1.Leprosy2.Syphilis3.Cat-scratch disease4.Sarcoidosis5.Chron’s Disease
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BENIGN ULCER, stomachExcavation of surface produced by the shedding of inflamed necrotic tissue; breach on the mucosal layer and penetrates into muscularis mucosa, submucosa, or deeper
EARLY PHASE – intense PMN infiltration and vascular dilation in margins
CHRONIC PHASE – fibroblastic proliferation, lymphocytes, macrophages, plasma cells
It is caused by an imbalance between damaging factors (gastric acid and peptic enzymes) and protective factors (gastric mucus secretion, local secretion of alkali)
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GRANULATION TISSUESeen in the vagina
Presence of highly lymphocytic infiltrates with numerous angiogenesis
Plasma cells are also present and fibroblastic formation is seen
*Granuloma – no angiogenesis and focal accumulations of activated macrophages *Granulation tissue – angiogenesis, mononuclear cells (lymphocytes, plasma cells), some fibroblasts
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END OF PART 1SHOUTOUTS:
hi to elmer, choy, kent, trixie, arlyn, and mark. i love you guys.Reinald, when is our next ice cream test? –ratatouille
To my thesis mates: HANS AND GIL. Good job to us! Kahit tatlo lang tayo. ICS 9, may our 15th member rest in peace.
Med Group 8. HI GUYS! I think dr. rosario will be leaving for 2 weeks. According to choy.Madame, sino na ang pipiliin mo? Si P, si M, si E, or si R? hihi. <3
Santi, my ever sipag patho lab buddy, thank you sa notes! Perfect dapat to ha!To justin, hi. I miss you. I love you. Hahaha. Adik lang!
Irene, get well soon. Good luck with the 2nd long exams. Kaya mo yan!
2013 a, good luck. 100% passing rate kahit dito lang sa patho exam. God bless everyone!
Love lots, RENEE GULA. 2013 A.
Hello to the Mann Hann Boys, CO6, ICS groupmates, and to the conyo people of sec A (Sam, Fifi, Ana, Xtian B.)Faisal, Salam-alaikum sibal! Koos arnab!
GOOD LUCK AND GOD BLESS 2013A!-Santi. 2013A