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76 Cards in this Set
- Front
- Back
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What causes SER hypertrophy?
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CYP-metabolized drugs
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What are the characteristics of hypertrophied cardiomyocytes?
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enlarged, boxy, hyperchromatic nuclei
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What is a keloid?
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excess COLLAGEN from fibroblasts
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What is a hypertrophic scar?
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Excess MYOfibroblasts
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What causes warts?
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HPV virus in squamous cells promotes growth via cell cycle inhibitors - viral E6, E7
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How does marasmus get the protein out of the muscles?
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autophagy of cytoplasmic organelles to yield energy or recycle damaged structure
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How does Cachexia get the protein out of the muscles?
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degradation via ubiquitin-proteosome path
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What are the 3 pathways of cell death?
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necrosis
apoptosis autophagy |
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What is autophagy regulated by?
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autophagy genes, Atgs
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What is the earliest change seen in reversibly injured cells?
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hydropic change/swelling
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When is injury irreversible?
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when mitochondrial dysfunction is irreversible
when membranes are lost when nuclear dissolution occurs |
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What are the 2 sources of lysosomal enzymes that degrade cells during necrosis?
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Autolysis - enzymes intrinsic to injured cell
Lyosomal enzymes from immigrant leukocytes of the inflammatory response |
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What is oxidative stress?
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imbalance between free radical generation and free radical scavenging systems
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What is the key characteristic of shock?
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Systemic Hypoperfusion
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Why does acidemia occur in cases of shock?
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increased serum lactic acid/lactic acidosis (defines shock after giving pressor drugs to increase BP)
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What is the initial presentation of a patient in septic shock?
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warm, dry skin, febrile
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What are the inflammatory mediators from leukocytes?
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TNF
IL-1 HMGB1 |
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What complement products are important in septic shock?
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C3a, C5a, C3b
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What are the inflammatory cytokines important in septic shock?
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IL-10 and also Lymphocyte apoptosis
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What happens to the kidneys during shock?
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acute tubular necrosis
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What happens to the lungs during shock?
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diffuse alveolar damage
morphology of ARDS/shock lung |
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What happens to the liver during shock?
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steatosis (fatty change)
ischemic necrosis |
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What happens to the GI during shock?
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Hemorrhagic necrosis
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What happens to the hear during shock?
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necrosis and hemorrhages
steatosis may occur |
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What happens to the CNS during shock?
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ischemic necrosis pattern
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What happens to the disseminated intravascular coagulation during shock?
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Widespread clots with consumption of procoagulants and platelets- leads clinically to bleeding
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What cells cannot recover from shock?
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cardiomyocytes
neurons |
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How is apoptosis executed?
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Execution caspases cleave cytoskeletal protein
Activate DNAses DNA breaks into oligonucleosomes |
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What does apoptosis leave on an agarose gel electrophoresis plate?
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DNA "ladders"
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What does apoptotic bodies look like on an H&E stain?
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single cells
Round, intensely eosinophilic with dense pyknotic nucleus or nuclear fragments |
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Which T cells are selected for apoptosis by the Thymus early in life?
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Those cells that/which/with:
inappropriate affinity to antigen respond to self antigens |
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Which genes play a role in the process of apoptosis in the Thymus?
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Fas/FasL
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What are some anatomic structures that undergo apoptosis in fetal development?
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aortic arches
digital webs mesonephros excess neurons in developing brain |
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What are the pro-apoptotic members of the BCL-2 family?
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Bax,
Bak |
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What are the anti-apoptotic members of the BCL-2 family?
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Bcl-2
Bcl-x Mcl-1 |
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What does the gene Bcl-2 do?
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keeps mitochondrial membrane channels closed
(Cells with Bcl-2 overexpression CANNOT die) |
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what activates Bax, Bak to open channels and release cytochrome C among other mitochondrial proteins?
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BH3-only proteins (Bim, Bad, Bid)
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What kinds of things to cytotoxic t-lymphocytes mediate apoptosis?
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immune response to viral infection
immunity to cancer, esp viral induced some types of transplant rejection some type IV hypersensitivity rxns |
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What is the mechanism of CTL mediated apoptosis?
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Perforin forms a transmembrane pore --> granzyme B enters cytoplasm; activates caspase 9 and others
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Where do accumulations occur?
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cytoplasm (including ER)
Within lysosomes Nucleus |
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What is antrhacosis?
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Black carbon accumulation universally seen in lungs of urban dwellers and increased in lungs of tobacco smokers and coal miners
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What are the causes of hepatic steatosis?
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Obesity, DM
Alcohol abuse toxins and drugs (CCL4, etc) Protein malnutrition; rapid weight loss Shock/anoxia |
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What is the pathogenesis (generally) of steatosis?
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lipid peroxidation = no apoprotein production
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Which enzymes are elevated in hepatic steatosis?
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AST and ALT serum enzymes are elevated
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Grossly, what does hepatic steatosis look like?
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enlarged, greasy, yellow, and soft liver
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Microscopically, what does hepatic steatosis look like?
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smalle, liposomes expand to vacuoles in cytoplasm, cells may rupture leading to globules
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What causes lipid in cardiac muscle?
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prolonged, moderate hypoxia as in profound anemia
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What does the term "hyaline change" refer to?
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nonspecific descriptive histological term widely used to describe accumulation of protein
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What does hyaline change look like?
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homogenous, glassy, pink material on H&E stain
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What diseases are associated with glycogen accumulation?
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DM: develops glycogen in
- renal tubular epithelial cells - liver cells, beta cells, islets of langerhans - myocardial cells Glycogen storage diseases/glucogenoses-genetic enzyme defect |
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What does glycogen accumulation look like?
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Clear vacuoles by H&E, PAS positive!!!!
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What is lipofuscin?
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insoluble residual bodies; derived of lipid peroxidation of subcellular membranes
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What is the morphology of lipofuscin?
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yellow brown, perinuclear, granular pigmentation of cytoplasm
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Where does lipofuscion occur?
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heart, liver of aging patients; often associated with atrophy = brown atrophy
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What is Mallory Hyaline?
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ubuitinated damaged intermediate filamentskeratins;
associated with alcohol toxicity |
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What is hemosiderin?
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iron-overload
- hemoglobin-derived aggregates of ferritin micelles |
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What does hemosiderin look like in H&E?
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golden-yellow granular intracellular iron pigment
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What stain is used to demonstrate pigment of hemosiderin/iron?
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prussian blue stain
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What does localized hemosiderin accumulation follow?
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hemorrhage (bruises....accumulates in macrophages)
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What are some causes of hemosiderin?
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Hereditary hemochromotosis
certain disorders of RBCs, esp hemolytic anemias repeated transfusion of RBCs |
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Where does hemosiderin accumulate? (which organs)
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liver
bone marrow spleen lymph nodes joints glandular tissue myocardium |
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What is hemosiderosis?
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deposit of iron in parenchymal cells
usually with no organ dysfxn |
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What is hemochromatosis?
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massive accumulation of iron
produces organ damage, including cirrhosis of the liver |
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What does localized hemosiderin accumulation follow?
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hemorrhage (bruises....accumulates in macrophages)
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What are some causes of hemosiderin?
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Hereditary hemochromotosis
certain disorders of RBCs, esp hemolytic anemias repeated transfusion of RBCs |
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Where does hemosiderin accumulate? (which organs)
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liver
bone marrow spleen lymph nodes joints glandular tissue myocardium |
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What is hemosiderosis?
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deposit of iron in parenchymal cells
usually with no organ dysfxn |
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What is hemochromatosis?
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massive accumulation of iron
produces organ damage, including cirrhosis of the liver |
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What is jaundice/icterus?
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excess accumulation of bilirubin
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What is kernicterus?
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accumulation of unconjugated bilirubin in brain of young infants
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What is exudate?
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fluid, proteins, blood cells move into tissue
extracellular fluid with high protein content, cell debris and high specific gravity >3 grams Due to small BV changes = inflammation increased LDH |
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What is transudate?
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low protein content, little cell debris, low specific gravity
ultrafiltrate of plasma due to hydrostatic or osmotic imbalance across vessle wall no increased vessel permeability |
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What endothelial-leukocyte adhesion molecules are found on the endothelial cell?
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selectins
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What endothelial-leukocyte adhesion molecules are found on the luekocyte?
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integrins
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What is pressure overload also called?
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concentric hypertrophy
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What is volume overload also called?
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eccentric hypertrophy
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