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70 Cards in this Set

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Morphology
The appearance of organs, tissues, and/or cells on a gross, microscopic, and ultrastructural level.
Etiology
The agent or agents that initiate a chain of events, ultimately causing disease. Intrinsic (genetics) or extrinsic (acquired).
Pathogenesis
Mechanisms (chain of events) connecting the etiology (cause of disease) and the disease itself.
4 types of cellular adaptation
Hyperplasia
Hypertrophy
Atrophy
Metaplasia
Hyperplasia
More cells than there should be. Often associated with hypertrophy but not same thing. Since involved cell division, only cells which undergo cell division can undergo hyperplasia (ergo not permanent cells).
Different cell types according to replication
Labile - Always in cell cycle making new cells.
Stable - Not constantly dividing but can make new cells.
Permanent - Incapable of cell division, uve got all ur gonna get.
Types of physiological hyperplasia and examples
Hormonal - Breast epithelium during puberty/pregnancy
Compensatory - Regrowing liver.
Pathologic Hyperplasia and example.
Usually due to excess hormonal stim or GF influence. Often associated with increased risk of neoplasia.
Ex. endometrial hyperplasia caused by imbalance of estrogen/progesterone.
Hypertrophy
Increase in cell size not due to swelling. Associated with increased risk of neoplasia
Causes of phisiological hypertrophy and examples
Hormonal stimulation - Estrogen effect on uterine smooth muscle in pregnancy.
Increased functional demand - skel muscle.
Pathologic Hypertrophy example
Myocardial hypertrophy - Changes in signal transduction lead to changes which are adaptive at first but become pathologic.
Atrophy
Decrease in cell size due to loss of cellular components other than water. Often associated with apoptosis.
Physiologic atrophy examples
Embryonic structures (notocord, thyroglossal duct)
Post partum myometrium
Endometrium in menopause
Causes of pathologic atrophy
1) Workload reduction
2) Loss of innervation
3) Loss of blood supply
4) Inadequate nutrition
5) Aging
6) Pressure (like a tumor pushing up against other cells).
Atrophy Mechanisms
Decrease in protein synthesis with an increase in protein degradation (via lysosomes and proteases)
Metaplasia
Reversible change where one cell type becomes another. It is named after the new cell type. Cells dont acutally morph; stem cells just start producing a new cell type due to change in signals (cytokines, GF, ECM components ect).
What type of metaplasia is:
1) Smoking
2) Barretts esophagus
3) Duct obstruction
4) Vitamin A deficiency
Smoking = Squamous metaplasia
Barrett = Columnar metaplasia
Duct obstruction = squamous metaplasia
Vit A deficiency = squamous metaplasia.
Connective tissue metaplasia examples
Myositis ossificans - soft tissue undergoes metaplasia into bone.
Necrosis
Cell death often due to hypoxia leading to:
1) Cell Swelling
2) Protein denaturation
3) Organelle breakdown
4) Random breakdown of nucleic acids
Apoptosis
Programmed cell death leading to:
1) Cell shrikage
2) Formation of apoptotic bodies
3) Ordered breakdown of nucleic acids
Necrosis vs Apoptosis (Cell size, Nucleus, Plasma membraine, Cellular contents, Adjacent inflamation, physiologic or pathologic)
Necrosis = Swelling . Apoptosis = Shrinkage
Necrosis = Karyolysis/pyknosis/karyorrhexis . Apoptosis = Fragmentation into nucleosome sized fragments (pyknosis or karyorrhexis)
Necrosis = plasma membrane disrupted . Apoptosis = intact but altered structure
Necrosis = enzymatic digestion, may leak out of cell . Apoptosis = intact, may be released in apoptotic bodies.
Necrosis = adjacent inflammation frequent . Apoptosis = Not
Necrosis = always pathologic . Apoptosis physiologic or pathologic
5 intracellular systems most vulnerable to to injury
1) Aerobic respiration
2) Cell membrane integrity
3) Protein synth
4) Cytoskeleton
5) Genetic integrity
Depletion of ATP consequences
1) No Na+ pump > influx of Na+ and water (and efflux of K+) > cell swells (as do ER).
2) Increase in anarobic glycolysis > decrease in glycogen and increase in lactic acid > decrease in pH > clumping of chromatin
3) Detachment of ribosomes > decrease in protein synth and lipid deposition.
4) Calcium pumps fail > increase in intracellular calcium > activation of damaging enzymes
5) Proteins undergo misfolding leading to unfolded protein response.
What can cause irreversible mitochondrial damage and what does it lead to?
1) Increased intracellular calcium
2) Oxidative stress
3) Breakdown of phospholipids

Leads to expression of a mitochondrial permeability transition (MPT) causing leakage of protons and cytochrome C screwing up oxphos.
What happens when calcium levels become elevated in a cell?
Enzymes become activated:
-Phospholipases damage membranes
-Endonucleases damage DNA
-Proteases damage proteins
-ATPases decrease ATP stores resulting in more calcium influx enhancing the effect.
What are free radicals and what are their effects
Highly reactive, autocatalytic molecules with an unpaired electron. Cause:
1) Lipid peroxidation - leads to membrane damage
2) Oxidative protein dmg - causes degredation of critical enzymes
3) DNA damage - causes single stranded breaks possibly related to aging and cancer.
How can one inactivate a radical
1) Antioxidants (vit A, E, ascorbic acid, glutathione)
2) Binding reactive molecule (like a transition metal) to a transport protein to prevent redox reactions
3) Chemical modification via enzymes (catalase, superoxide dismutase, glutathione peroxidase).
Causes of free radical formation
1) Normal redox Rxs
2) Redox Rxs involving transition metals
3) NO can act as a free radical
4) Absorbtion of radiant energy
5) Enzyme mod. of endogenous chemicals
3 main causes of membrane permeability defects
Decreased ATP, activation of phospholipases, cytoskeleton damage via proteases.
2 major types of reversible cell injury the characteristics of reversible cell injury
Can be either swelling or fatty change.
Tissue has pallor, increased turgor, and increased weight.
Characteristics of of irreversible cell injury
Extensive plasma membrane damage, lysosomal swelling, mitochondrial vacuolization.
Pkynosis, Karyolysis, Karyorrhexis
Types of nuclei of necrotic cells:
Karyolysis - Blue nucleus fades to pink losing basophilia.
Pyknosis - Shrinkage and increase basophilia (blueness) of nucleus (also seen in apoptosis).
Karyorrhexis - Fragmentation of a pyknosis nucleus (also seen in apoptosis).
Coagulative necrosis
Most common kind in general and during ischemia.
Firm Texture
LM: -loss of cytologic detail
-retains basic cell outline
-retains tissue architecture.
Liquefactive necrosis
Typical necrosis of CNS and certain infections.
Viscous mass due to complete digestion of cells
LM: -loss of cytologic detail
-loss of basic cell outline
-loss of tissue architecture
Caseous necrosis
Typical of tuberculosis.
Cheese like.
LM: -loss of cytologic detail
-retention of basic cell outline
-loss of tissue architecture.
Gangrenous necrosis
Coagulative necrosis of a big chunk of tissue due to aschemia:
Dry gangrenous necrosis - coagulative necrosis of tissue that has lost its blood supply.
Wet gangrenous necrosis - Same as previous but has also been secondarily infected, converting it into liquefactive necrosis.
Fat Necrosis
Coagulative necrosis of fat cells that have developed calcium deposits.
Fibrinoid necrosis
Typical of vascular immune Rxs with complexes deposited in walls of arteries making them look like fibrin.
Reverseible hypoxic injury
Leads to decreased aerobic respiration causing reduced ATP and the following results:
1) Influx of Na and water
2) Stimulation of glycolysis decreasing pH, causing nuclear chromatin clumping
3) Detachment of ribosomes from rough RER decreasing protein synth
4) Dispersion of cytoskeleton causing reduction of microvilli and bleb formation
5) Membrane injury leading to myelin figures
6) Swelling of mitochondria and RER
Irreversible hypoxic injury
2 main features:
1) Permanent mitochondrial dysfunction and inability to turn oxphos back on.
2) Loss of cell membrane integrity disallowing separation of internal mileu and external environment.
Reperfusion Injury
In a setting of ischemia, is increased injury after bloodflow is restored. Caused by new free radicals, cytokines, and inflammatory cells entering the wounded region causing additional damage.
Chemical injury mechs
2 general mechanisms:
1) Direct action to a critical molecular component or organelle
-Mercury poisoning
-cyanide
-chemo drugs
2) Metabolism of drug to a toxic metabolite
-Acetaminophen OD
-carbon tetrachloride poisoning
Physiologic Apoptosis examples
1) Embryogenisis
2) Hormone dependent involution in adults (ex. ovaries post menopause, breasts post breastfeeding)
3) Cell deletion in a proliferating cell pop (crypt cells in intestine)
4) Neutrophil death in inflammation
5) Deletion of self reactive T cells
6) Death induced by cytotoxic T cells
Pathologic Apoptosis examples
1) Cell death from DNA damaging stimuli
2) Cell death in certain viral diseases
3) Cell death in organs with duct obstruction
4) Cell death in neoplasms
5) Cell death in other processes that may also induce necrosis (the process).
Morphology of apoptosis
1) Cell shrinkage
2) Chromatin condensation
3) Formation of surface blebs that pinch off into apoptotic bodies
4) Phagocytosis of apoptotic bodies
5) Maintenance of cell membrane integrity until late part of process
6) Absence of inflammatory response
Biochemistry of apoptsis
1) Protein cleavage by caspases
2) Ordered DNA breakdown
3) Expression of phosphotidyl serine on outer membrane signaling non-inflammatory phagocytosis
Extrinsic Apoptosis Initiation
Initiated via engagement of cell surface death receptors which have a cytoplasmic death domain (ex. fas and fas ligand).
Intrinsic Apoptosis Initiation
Initiated by a withdrawal of survival factors (GHs, hormones), or application of certain injurious stimuli.
Mitochondria expresses more pro-apoptotic genes and less anti-apoptotic genes. This increases mito. membrane permeability causing proteins like cytochrome c to activate caspases in cytoplasm.
Decreased Apoptosis and disease
Malignant neoplasms and autoimmune disorders (lack of t cell pruning)
Increased Apoptosis and disease
Neurodegenerative disorders, ischemic injury, death of virus infected cells.
Steatosis
When TGs and cholesterol accumulate in heart, liver, kidney, muscle due to toxins, protein malnutrition, diabetes mellitus, obesity, or anorexia.
What causes steatosis in liver and heart
Liver:
-Alcohol
-Carbon tetra chloride
-protein malnutrition
-Starvation
Heart:
-Hypoxia
Pathologic accumulation of cholesterol examples
-Athrosclerosis
-Xanthomas
-Foamy macs in necrosis
-Cholesterosis
-Type C Niemann-Pick disease.
2 methods of protein accumulation and examples
1) Exceeding catabolic activity of the cell. (ex Reabsorbtion droplets in proximal tubule, russell bodies in chronic inflamation).
2) Defect in protein folding (trypsin deficiency, amyloidosis).
Unfolded protein response
Initially leads to increased chaperone production and decreased protein translation.
If unfolded proteins continue to accumulate, leads to apoptosis via caspase activation.
Endogenous pigment examples
1) Lipofuscin
2) Melanin
3) Hemosiderin
4) Bilirubin
Lipofuscin
Endogenous pigment. Looks brown, granular. Telltale of free radical injury and lipid peroxidation. Also known as the wear and tear or aging pigment. Seen in liver and heart of elderly as well as malnourished people or people with cancer cachexia.
Melanin
Endogenous pigment. Brown-black pigment.
Hemosiderin
Endogenous pigment. Golden yellow to brown, granular or crystalline. Formed in the breakdown of hemaglobbin and is the major storage form of iron. Lots of it is seen in hemachromatosis and hemosiderosis
Bilirubin
Endogenous pigment. Yellow green. Hemoglobbin derrived, non iron containing, found in bile. Leads to color of jaundice.
Morphology of calcification
Fine white granuals, hard.
Microscopically appears basophilic granuals, sometimes clumped.
Dystrophic Calcification
Occurs in dying tissue despite normal calcium levels/metabolism. Is initiated by the calcium buildup in the mitochondria of dying cells.
Metastatic calcification
Occurs in living tissue and is due to hypercalcemia usually due to problem with calcium metabolism. Can be caused by:
^PTH secretion
-destruction of bone (bone tumors or paget disease)
-Vitamin D disorders
-Renal failure
Hyaline Change
Is a Morphologic Descriptor implying homogenous, glassy, eosinophilic microscopic appearance. Can be intracellular or extracellular. Examples include:
-Reabsorbtion dropletts and Russell bodies.
-old scars
-amyloidosis
-Arterial walls in HTN/DM
3 enzymes which inactivate radicals
1) Catalase
2) Superoxide Dismutase (SOD)
3) Glutathione Peroxidase
What would cause a strawberry appearance in a gall bladder?
Lipid deposition
Russel Body
Expanded eosinophilic ER of a plasma cell caused by Ig synthesis in chronic inflammation. Is a mech of protein accumulation in a cell.
Reabsorbtion Droplet
Caused by increased protein in the epithelial cells of the proximal tubules during excessive protein catabolic activity. Look granular and eosinophilic. Is a mech of protein accumulation in a cell.
Diseases with misfolded protein problems
A1 antitrypsin deficiency
CF
Familial hypercholestermeia
Parkinsons/huntingtons
Amyloidosis
Types of diseases which cause glycogen accumulation
diabetes and storage diseases.