PATHOLOGY 1 ST PRACTICAL EXAM part 1

1. 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.

2. Cellular injury, adaptation, and death

3. CELLULAR SWELLING, kidney Organ: Kidney – convoluted tubules Size of lumen: decreased Cytoplasm: enlarged, increased pinkish color Reversible 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

4. FATTY CHANGE, liver HISTO: Organ: Liver – hepatic cords Cytoplasm: lipid vacuoles replacing the normal cords of hepatocytes Nucleus: displaced peripherally Pathogenesis: impaired metabolism of fatty acids that leads to accumulation of triglycerides Conditions that give rise to fatty liver: Alcoholism Obesity Diabetes Mellitus GROSS: Yellow and glossy appearance Pale liver DSCN6513

5. BROWN ATROPHY, heart Pigment: LIPOFUSCIN Cell: Cytoplasm of Myocardial Cell Color: brown or golden yellow granular appearance DSCN6516

6. ANTHRACOSIS, hilar lymph node Pigment: CARBON/coal dust Cell: Parenchymal cells Color: black DSCN6519

7. MALARIA, liver Pigment: HEMOZOIN Cell: Kupffer cells

8. CHRONIC PASSIVE CONGESTION (CPC), lung Pigment: HEMOSIDERIN Cell: alveolar/laden macrophage Color: yellow, golden brown “heart failure cells (macrophages) in the alveoli are indicative of left sided heart failure” DSCN6531

9. BILE NEPHROSIS, kidney Pigment: BILIRUBIN Cell: Tubular Lumen Color: Reddish or golden brown DSCN6533

10. SQUAMOUS METAPLASIA, lungs Organ: 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

11. 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 DSCN6542

12. TUBERCULOSIS, lungs CASEOUS NECROSIS White cheese-like appearance (granular amorphous debris) MICROSCOPIC: formation of granulomas NOTES: Other types of necrosis: Coagulative – common in kidney Liquefactive – brain Gangrenous – DM Fibrinous – connective tissue GROSS: Decrease in size of organ White lesions on cut surface DSCN6545

13. Inflammation and repair

14. ACUTE APPENDICITIS Cells: 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 APPEARANCE GROSS: dilated lumen; thickened wall; serosal surface has fibrinopurulent exudate HISTO: thickened edematous cell wall with neutrophilic infiltrates and vascular congestion with focal hemorrhages; eroded mucosa; presence of segmenters densely occupying the appendiceal wall

15. BRONCHOPNEUMONIA, lungs GROSS: 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: Complete resolution Healing by CT replacement Progression to chronic inflammation

16. TUBERCULOSIS, lungs GRANULOMATOUS 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: Leprosy Syphilis Cat-scratch disease Sarcoidosis Chron’s Disease

17. BENIGN ULCER, stomach Excavation 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)

18. GRANULATION TISSUE Seen 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

19. END OF PART 1 SHOUTOUTS: 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