1.

Myocardial Hypertrophy

A. Lesion: increase in the amount of cytoplasm and size of nuclei of cardiac cells (?) B. Mechanism: increased metabolic demand, increased protein synthesis, increased synthesis of filaments C. Causes: increased functional demand/increased cardiac workload (most common stimulus), increased pressure load, increased valve load D. Growth Factors: TGF - B, IGF - 1, FGF E. Vasoactive agents: alpha - adrenergic agonists, endothelin - 1, angiotensin II

2 main biochemical pathways 1. Phosphoinositide 3 - kinase/Akt pathway 2. Signaling downstream of G - protein coupled receptors

cardiac hypertrophy - associated with reinduction of ANF gene expression

2. Benign Prostatic Hyperplasia

A. Lesion: stromal and glandular hyperplasia B. Mechanism: impaired cell death - main component of hyperplastic process C. Cause: increase in dihydrotestosterone responsible for androgen - dependent prostatic growth D. Growth Factors: FGF 1 & 2, TGF B, FGF 7 (most important)

Nodularity - hallmark of BPH Nodular hyperplasia - originates in the transition zone

Composition of Nodules: 1. purely stromal fibromuscular nodules 2. fibroepithelial nodules with a glandular predominance

3. Fatty liver

A. Lesion: clear vacuoles (triglycerides) pushing the nucleus of the hepatocytes to the periphery B. Mechanism: excessive entry of FFA into the liver (starvation, DM, corticosteroids), increased FA synthesis (alcohol), decreased FA oxidation (anemia, hypoxia), increased alpha glycerophosphate (alcohol), decreased apoprotein synthesis (carbon tetrachloride, phosphorus, protein malnutrition), impaired lipoprotein secretion from the liver (orotic acid)

Fatty Change - abnormal accumulation of triglycerides within hepatocytes often seen in liver because it is a major organ involved in fat metabolism

SUDAN IV or OIL RED - O - stains orange - red color to the contained lipids

4. Cloudy Swelling

A. Lesion: cellular swelling, blebs, condensed mitochondria - proximal tubule B. Mechanism: impaired sodium - potassium pump - Hypotonicity C. Causes: Hypoxia, Decreased ATP

pigmented RBC cast - red color hyaline cast - pink to purple color

5. Pulmonary Tuberculosis A. Lesion: Caseous necrosis B. Mechanism: granulomatous response by macrophage in response to Mycobacterium tuberculosis

TB Granuloma - characteristic abnormality in TB Macrophage - predominant cell; primary cells to be infected: endocytosis mediated IFN gamma - critical mediator that enable macrophage to ocntain MTB infection; released by TH1 cells macrophages --> epitheloid histiocytes --> giant cells

Epithelioid histiocytes - characterized the granulomatous response Granuloma collection/aggregates of epitheliod cell Giant cell - fused epitheloid cells; multinucleated Langhan's giant cell - nucleus at the periphery; due to fusion Foreign body giant cell - haphazard arrangement of nucleus Fibroblast - limits the granuloma

6. Myocardial infarction

A. Lesion: Coagulative necrosis - characterized by pyknosis, karryohexis, karyolysis B. Mechanism: sudden loss of blood supply

infarct - localized area of coagulative necrosis; appears as unstained pale zone wavy fibers periphery of infarct; due to forceful systolic tugs of the viable fibers on adjacent noncontractile dead fibers vacuolar degeneration/myocytolysis - margins of infarct; large vacuolar spaces within cells that contain water

left anterior descending coronary artery - most common

Sequence of events: 1. sudden change in atheromatous plaque 2. platelets adhere to exposed subendothelial collagen, become activated, release granule contents and aggregate 3. vasospasm 4. tissue factor activates the coagulation pathway 5. thrombus evolves to occlude the lumen of the vessel

Early biochemical consequence: 1. cessation of aerobic metabolism 2. accumulation of noxious metabolites (lactic acid)

Ultrastructural changes: 1. myofibrillar relaxation 2. glycogen depletion 3. cell & mitochondrial swelling

7. Pseudomembranous colitis

A. Lesion: Pseudomembranes - made up of neutrophils, dead epithelial cells and fibrin B. Mechanism: disruption of the normal colonic flora by antibiotics causing Clostridium difficile overgrowth

3rd generation cephalosporins - most common antibiotic associated with p. colitis

toxins cause: 1. ribosylation of small GTPases 2. disruption of the epthelial cytoskeleton 3. tight junction barrier loss 4. cytokine release 5. apoptosis

8. Pyogenic abscess, Liver A. Lesion: Liquefactive necrosis B. Mechanism: deep seeding of pyogenic bacteria into the tissue (Staphylococcus)

Suppurative/Purulent inflammation - neutrophils, liquefactive necrosis and edema fluid Abscess - central region that appears as a mass of necrotic leukocytes and tissue cells; zone of preserved neutrophils around the necrotic focus and outside this region, vascular dilation and parenchymal and fibroblastic proliferation occur

9. Acute Appendicitis

A. Lesion: Liquefactive necrosis - neutrophilic infiltration of the lumen, muscular wall and periappendiceal soft tissues B. Mechanism: Ischemic injury and stasis of luminal contents favroing bacterial proliferation

Active hyperemia - hemodynamic abnormality lymphocytes - black neutrophil - red & black

10. Acute Suppurative Meningitis

Lesion: neutrophilic infiltrates in the leptomeninges Mechanism: inflammation in response to .. causative agent: neonates - E - coli & group B streptococci adolescents and young adults Neisseria meningitidis others - Strep pneuomoniae and Listeria monocytogenes

11. Congestion

Mechanism: impaired venous outflow

Congestion - passive process - cyanosis due to red cell stais and accumulation of deoxygenated hemoglobin

12. Pulmonary Edema

Lesion: engorged alveolar cappilaries, intra alveolar granular pink precipitate, alveolar microhemorrhages & hemosiderin - laden macrophages ?? Mechanism: increased hydrostatic pressure - most common cause, injury to the capillaries of alveolar septa

13. Systemic Lupus Erythematosus

Lesion: thickening of the subendothelium GBM; wire - loop lesion Mechanism: immune complex deposition

immune complexes: DNA, anti - DNA antibodies, histones antigen + antibody

Mesangial lupus glomerulonephritis - mildest Diffuse proliferative glomerulonephritis - most common and most severe

DOC PILONES REVIEW:

FATTY LIVER 1. What stain? -Oil Red O -Sudan 4 2. Eventual consequence of fatty liver? Cirrhosis

MYOCARDIAL HYPERTROPHY 1. Why is there hypertrophy? -Increase cardiac workload

BENIGN PROSTATIC HYPERPLASIA 1. Target cell -Stromal cells 2. What triggers the hypertrophy? -Increase DHT

PULMONARY TUBERCULOSIS 1. Characteristic abnormality in TB? -TB Granuloma 2. Predominant cell? -Macrophage

MYOCARDIAL INFARCTION 1. Why is there infarction? -(due to) Sudden, severe ischemia

PSEUDOMEMBRANOUS COLITIS 1. Clinical significance? -Impaired reabsorption of water 2. What makes up the pseudomembrane? -Fibrin

PYOGENIC ABSCESS 1. What is pyogenic abscess? -Localized collection of pus/abscess

PULMONARY EDEMA 1. Basic mechanism of PE and CHF? -Imbalance of hydrostatic and oncotic pressure (increase h.p, decrease o.p)

CONGESTION 1. Basic mechanism of congestion. Why is there congestion? -Impaired venous outflow

SLE 1. Where is the site of lesion? -GBM (specifically: subendothelial area) 2. Basic mechanism of SLE -type III hypersensitivity

CLOUDY SWELLING 1. Biochemical mechanism? -Impaired NaK pump (Sodium-Potassium Pump) 2. What is the trigger? -absence of ATP 3. Most common cause? -hypoxia

Hypoxia-->No oxygen for oxidative phosphorylation-->impaired cristae production of ATP--> absence of ATP

ACUTE APPENDICITIS 1. What is the inflammatory process/hemodynamic abnormality? Active hyperemia 2. What layer is involved -All layers

ACUTE MENINGITIS 1. How can you say it's acute? -Presence of neutrophils

(by the way, the cristae is a part of the mitochondria that produces the ATP...and wa njud koy recollection ana nga term. hahahaha!)