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32 Cards in this Set
- Front
- Back
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AUTOCRINE SIGNALING
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SECRETORY CELL TARGETS ITS OWN RECEPTORS
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PARACRINE SIGNALING
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SECRETORY CELL TARGETS RECEPTORS ON ADJACENT CELLS
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ENDOCRINE SIGNALING
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HORMONE IS SECRETED INTO BLOOD BY ENDOCRINE GLAND AND EFFECTS DISTANT CELLS
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SIGNAL TRANSDUCTION MECHANISMS
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CYCLIC NUCLEOTIDES: cAMP AND cGMP
PROTEIN KINASES: EGF RECEPTORS, ras, AND MAPK MEDIATED BY REVERSIBLE PHOSPHORALATION RXNS KINASES - PHOSPHORALATE PHOSPHOPROTEIN PHASPHATASES - REMOVE PHOSPHATES 5% OF GENES ENCODE FOR EITHER KINASES OR PHOSPHATASES |
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SIGNAL TRANSDUCTON PATHWAYS
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PI3 KINASE PATHWAY
MAP KINASE PATHWAY IP3 PATHWAY cAMP PATHWAY JAK/STAT PATHWAY ALL LEAD TO TRANSCRIPTION FACTOR ACTIVATION ALL SIMULTANEOUS, ALL NORMAL |
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PATHWAY FOR EPIDURMAL GROWTH FACTOR
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EGF RECEPTOR EXISTS AS TWO SEPARATE INACTIVE MONOMERS
EGF BINDS THE RECEPTORS WHICH FORM AN ACTIVE DIMER AUTOPHOSPHORALATION LEADS TO THE PHOSPHORALATION OF TARGET PROTEINS TARGET PROTEINS ARE ACTIVATED |
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TYPES AND EXAMPLES OF STRESSFUL STIMULI
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GENETIC - GENETIC DEFECT IN CLOTTING FACTOR
NUTRITIONAL - VITAMIN K DEFICIENCY IMMUNE - ANTIBODY TO PART OF OWN BODY ENDOCRINE - ADDISONS PHYSICAL AGENTS - SUN CHEMICAL AGENTS - DRUG TOXICITY INFECTIVE - VIRAL ETC - MOST COMMON ANOXIA OR HYPOXIA |
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DEGREE OF STRESS DEPENDS ON ...
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NATURE OF STRESSFUL STIMULI
DURATION OF EXPOSURE DOSE LOCATION OF EXPOSURE |
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REVERSIBLE CELL INJURY
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INJURY IS USUALLY MILD OR SHORT-LIVED
INJURY CESSATION-->CELL REVERTS BACK TO NORMAL CHARACTERIZED BY CELLULAR SWELLING --> LEADS TO DECREASED ATP-->DECREASED NA+,K+-ATPASE ACTIVITY-->INCREASED MEMBRANE PERMEABILITY--> WATER INFLUX SWOLLEN MITOCHONDRIA-->ATP PRODUCTION BY ANAEROBIC GLYCOLYSIS--> INCREACED LACTIC ACID PRODUCTION, DECREASE IN pH-->DECREAED CELLULAR METABOLISM |
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ATP STARVATION LEADS TO
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CELL SWELLING
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CONSEQUENSES OF CELLULAR SWELLING
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INTERIOR AND EXTERIOR FUNCTIONS DECREASE
JUNCTIONS ARE CONPROMISED CELL DOESN'T COMMUNICATE WELL WITH NEIGHBORING CELLS |
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IRREVERSABLE CELL INJURY
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INJURY IS USUALLY OVERWHELMING OR LONG-LIVED
INJURY CESSATION-->CELL IRREVERSABLY DAMAGED CHARACTERIZED BY LOSS OF CELL INTEGRITY, CELL MEMBRANE RUPTURE, AND DISTINCTIVE NUCLEAR CHANGES DAMAGED MITOCHONDRIA--> VASTLY DECREASED ATP PRODUCTION-->LOSS OF CELL FUNCTION-->LOSS OF PLASMA MEMBRANE FUNCTION-->RUPTURE OF CELL MEMBRANE-->RELEASE OF CYTOPLASMIC ENZYMES--> LDH IN SERUM/BLOOD |
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NUCLEAR CHANGES/DAMAGES
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1. PYNKNOSIS - CONDENSATION OF CHROMATIN
2. KARYORRHEXIS - FRAGMENTATION INTO SMALLER PEICES 3. KARYOLYSIS - DISSOLUTION OF NUCLEAR STRUCTURE, LYSIS OF CHROMATIN BY ENZYMES |
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EXAMPLES OF REVERSIBLE INJURY
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HYPOXIA
OXYGEN RADICALS |
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ACCIDENTAL RELEASE OF CA+ IN RESPONSE TO STRESSFUL STIMULI
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CAUSES VAST EXCESS IN CYTOSOLIC CA++
HARMFUL ENZYMES ARE ACTIVATED OR RELEASED PHOSPHOLIPASE - DEGRADES MEMBRANES ATPASE - REMOVES ATP ENDONUCLEASE - DEGRADES DNA |
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CELLULAR DEFENSES
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GLUTATHIONE - TRIPEPTIDE OF GLY-CYS-GLU
ANTIOXIDANT ENZYME p53 - PROTEIN DETERMINES CELLULAR DEATH OR REPAIR THE PROTEOSOME HEAT SHOCK PROTEINS |
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ANTIOXIDANT ENZYMES
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SUPEROXIDE DISMUTASE (SOD)
CATALASE GLUTATHIONE PEROXIDASE GLUTATHIONE REDUCTASE |
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GLUTATHIONE
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FUNCTIONS TO KEEP SH IN THE REDUCED STATE
ALSO FUNCTIONS TO ELIMINATE FREE RADICALS |
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p53
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GUARDIAN OF DNA
RECOGNIZES DAMAGED DNA ATTACHES TO DNA STOPS DNA REPLICATION UNTIL DAMAGE IS REPAIRED IF THE DAMAGE IS NOT REPAIRED p53 WILL TRIGGER CELL DEATH |
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THE PROTEOSOME
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PROTECTS THE CELL FROM DAMAGED PROTEINS
UNBIQUITIN ATTACHES TO DAMAGED PROTEIN UNBIQUINATED PROTEIN IS DESTROYED AND BROKEN DOWN INTO AMINO ACIDS BY PROTEASES |
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CELLULAR ACCUMULATIONS
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FATTY CHANGE - FAT ACCUMULATIONS IN DAMAGED LIVER CELLS
LIPOFISION - INCOMPLETELY OXIDIZED MASS OF MEMBRANE REMNANTS MELANIN - INADEQUATE FUNCTIONING OF THE ADRENAL CORTEX CAUSES INCREASE IN ACTH CAUSING DARKENING OF THE SKIN |
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PERMANENT CELLS
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NEURONS, SERTOLI CELLS, FAT CELLS, LENSE CELLS
DNA DOES NOT REPLICATE POST NEONATAL SOME PERM CELLS SUCH AS:STRIATED MUSCLE, MYOCARDIUM, GLOMERULAR PODOCYTES RETAIN THE ABILITY TO MULTIPLY (MUSCLE), OR TO BECOMES POLYPLOID (MYOCARDIUM), OR TO MULTIPLY INVITRO (PODOCYTES) |
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STABLE CELLS
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HEPATOCYTES, FIBROBLASTS, ENDOTHELIUM, SMOOTH MUSCLE, ETC
NORMAL MITOTIC RATE IS VERY LOW BUT REGENERATIVE BURST CAN OCCUR IN RESPONSE TO DAMAGE |
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LABILE CELLS
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BONE MARROW AND MOST EPITHELIA
CONTINUE TO REPLICATE THROUGHOUT LIFE |
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IF A CELL CAN DIVIDE, WHAT CHANGES CAN OCCUR?
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CELL NUMBER:
INVOLUTION - DECREASE IN CELL NUMBER HYPERPLASIA - INCREASE IN CELL NUMBER DIFFERENTIATION: METAPLASIA - CHANGE TO ANOTHER CELL TYPSE DYSPLASIA - DERANGED ARCHITECTURE NEOPLASIA - UNREGULATED GROWTH |
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IF A CELL CANNOT DIVIDE, WHAT CHANGES CAN OCCUR?
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ATROPHY - DECREASE IN SIZE
HYPERTROPHY - INCREASE IN SIZE |
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ATROPHY
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DECREASE IN PROTEIN SYNTHESIS
LOSS OF ORGANELLES DURING DEVELOPEMENT AND AGING THYMUS IN ADOLESENCE UTERUS IN MENOPAUSE DURING CHRONIC INFLAMMATION PATHOLOGICAL FROM LACK OF USE - MUSCLES IN A BROKEN LEG FOR EXAMPLE |
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REGENERATION OF THE LIVER
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OCCURS BY HYPERPLASIA
DEPENDANT ON AGE AND SPECIES UNDER HORMONAL CONTROL HGF - HEPATOCYTE GROWTH FACTOR |
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RESPONSE OF TISSUES TO IRREVERSABLE DAMAGE
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CELLULAR DEATH
INCREASED CELLULAR PERMEABILITY LEADS TO ENZYME LEAKAGE APOPTOSIS OR NECROSIS FOLLOWS WHEN CELLS DIE THEY RELEASE SOLUBLE PROTEINS INTO THE BLOOD STREAM |
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NECROSIS
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FOCAL DEATH IN RESPONSE TO INJURY
1. TRAUMA 2. SWELLING 3. DESTRUCTION OF CELLULAR COMPONENTS 4. CELL EXPLODES 5. WHOLE SECTIONS OF TISSUE ARE EFFECTED |
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APOPTOSIS
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CELL SUICIDE OR PROGRAMMED CELL DEATH
REGULATED BY THE CELL DRUG TARGETABLE AFFECTS A SINGLE CELL NO INFLAMMATION HAPPENS DURING DEVELOPEMENT - INFANTS HAVE 50% MORE NEURONS THAN NEEDED CONNECTED NEURONS EMIT SURVIVAL SIGNAL NO CONNECTION = APOPTOSIS CANCER = TOO LITTLE APOPTOSIS DEGENERATIVE DISEASES = TOO MUCH APOPTOSIS |
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DIFFERENCE IN TISSUE EFFECTS BETWEEN APOPTOSIS AND NECROSIS
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APOPTOSIS INVOLVES NO INFLAMMATION, PHAGOCYTOSIS BY ADJACENT CELLS, AND RAPID INVOLUTION WITHOUT COLLAPSE OF OVERALL TISSUE STRUCTURE
NECROSIS NEVER PHYSIOLOGICAL INVOLVES ACUTE INFLAMMATION AND SCARING LATER |
