Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
235 Cards in this Set
- Front
- Back
|
Characteristics of Prokaryotes |
-less defined nucleus or no nucleus -single, circular chromosome -lack histones -examples: cyanobacteria, bacteria, and ric kettsiae |
|
|
Characteristics of Eukaryotes |
- complex cellular organization -membrane bound organelles -well-defined nucleus, nucleic acids w/ nuclear membrane -examples: higher animals, plants, fungi, protozoa, algae |
|
|
What are some cellular functions |
-movement -conductivity -metabolic asorption -Secretion -excretion -respiration -reproduction -communication |
|
|
What is contained in a eukaryotic cell nucleus |
-nuclear envelope and nuclear pores -nucleolus -DNA -Histone proteins -Laminins -Cell division |
|
|
What is contained in the eukaryotic nucleolus |
ribosomes: r-RNA & ribosomal proteins |
|
|
Functions of DNA |
-Replication -repair -transcription ( creates RNA) |
|
|
What are histones |
highly alkaline proteins found in eukaryotic cells that package and order DNA into structural units called nucleosomes -chief protein component of chromatin |
|
|
what are laminins |
high molecular weight proteins of the extracellular matrix -play important role in cell differentiation, migration, and adhesion |
|
|
Nuclear DNA controls the production of... |
cellular enzymes, membrane receptors, structural proteins and other proteins that define the cell's type and behavior |
|
|
What composes the nuclear envelope |
outer membrane, lumen, and inner membrane |
|
|
Cytoplasm of Eukaryotic cell |
-cytoplasmic matrix -cytosol -cytoplasmic organelles |
|
|
What are ribosomes composed of? |
rRNA & Proteins -free ribosomes -polyribosomes -attached ribosomes ( rough ER) |
|
|
ER |
-site of protein synthesis -smooth and rough |
|
|
Golgi Complex |
( post office of cell) -flattened, smooth membranes, cis& trans -cisternae -Secretory vesicles, storage vesicles, lysosomes -Proteins from ER( transport vesicles) modified, sorted, and packaged in golgi complex, bud off as vesicles |
|
|
lysosomes |
bud off golgi apparatus in cells -filled with enzymes that digest molecules and parts of the cell -Tay Sachs disease--> person has cytoplasmic bodies storing a fat that lysosomes are unable to digest |
|
|
v-Snares in golgi aparatus |
bind lock and key fashion with help of t-snare docking marker -specificity ensures secretory vesicles fuse only with surface membrane of cell and empty contents onto cell exterior |
|
|
What do lysosomes catalyze |
proteins, lipids, nucleic acids, and carbs -ph=2 to 3 ( acidic) |
|
|
What is the substrate to the enzyme ribonuclease |
RNA |
|
|
What is the substrate to the enzyme deoxyribonuclease |
phosphate esters |
|
|
what is the substrate to the enzyme glycosidases |
complex carbs, glycosides, and polysaccharides |
|
|
what is the substrate to enzyme arylsulatases |
sulfate esters |
|
|
what is the substrate to collagenase |
collagens |
|
|
what is the substrate to enzyme cathespins |
proteins |
|
|
What oxidative enzymes do peroxisomes contain |
peroxidase, and catalase - important in detoxification reactions such as hydrogen peroxide ( catalase) - helps break substances down into harmless products |
|
|
How can peroxisomes modify protein synthesis |
- form by budding off er -when active, bind to DNA and modify synthesis of RNA which modifies protein synthesis |
|
|
Mitochondria |
( power houses of cell) -double lipid bilayer membrane -electron transport chain -have mitochondrial dna |
|
|
What 2 processes do mitochondria participate in |
oxidative phosphorylation, ATP |
|
|
what purpose do cristae serve in mitochondria |
provide increased inner membrane surface area |
|
|
What do molecular chaperones do? |
bind and stabilize unfolded or partly folded proteins -prevent proteins from aggregating and being degraded ex: heat shock proteins |
|
|
Accessory proteins |
stimulate the hydrolysis of ATP and conformational change in Hsp70 -results in closed form -facilitates proper folding -facilitates exchange of ATP for bound ADP---> converts Hsp70 back to open form and releases properly folded substrate |
|
|
Chaperonins |
-form small folding chambers that allow unfolded proteins to fold properly |
|
|
GroEl ( chaperonin mediated protein folding) |
in absence of ATP or presence of ADP, GroEL exists in tight conformational state that binds partly folded or misfolded proteins |
|
|
What does binding of ATP do to GroEL |
shifts it to more open relaxed state that releases folded protein. During process, one end of open GroEL is blocked by co-chaperonin GroES |
|
|
Proteasomes |
protein destroying organelle -breaks down regulatory, abdnomal and misfolded proteins one at a time -tagged with ubiquitins ( protein gets unfolded, breaks in pieces and is released) |
|
|
Parkinson disease and proteasomes |
proteasomes fail to destroy improperly folded proteins and forms plaques and tangles that destroy neurons |
|
|
How are proteins targeted for proteasomal degradation |
by polyubiquitination |
|
|
cytoskeleton |
-"bones and muscle of cell -maintains cell shape and internal organization -permits movement of external projections -microtubules -microfilaments |
|
|
3 key structures of cytoskeleton |
1) microtubules( centrioles, aster formation, inside core of cilia, flagella) 2) Microfilaments ( actin or thin filaments) 3) Intermediate filaments |
|
|
Intermediate Filament 1)cytokeratins 2)desmin 3)glial fibrilary acidic protein(GFAP) 4)neurofilament protein 5)nuclear lamin 6)vimentin |
Localization 1) epithelial cells 2)smooth & striated muscle 3)astrocytic glial cells 4) neurones 5)nucleus of all cells 6)many mesodermal tissues |
|
|
Motor proteins |
myosin, kinesin, and dynein -move along microfilaments or microtubules -pull larger structures such as vesicles, fibers, or particles -used for intracellular transport or movement into cell's entire framework |
|
|
centrosomes |
acts as microtubule organizing center for cell's cytoskeleton |
|
|
Formula for microtubule arrangement for cilia and flagella |
9 outter/peripheral microtubules + 2 Central microtubules. - outer microtubules are doublet, central microtubules are single |
|
|
Formula for microtubule arrangements for centriole and basal body |
9 outter/ peripherap microtubules ( triplets) - 0 central microtubules |
|
|
Microvilli |
microfilaments as core but no microtubules -found mainly with intestinal cells |
|
|
what is the function of the plasma membrane |
controls composition of a space or compartment it encloses |
|
|
What is the plasma membrane composed of? |
-Caveolae -lipids -carbs ( glycoproteins) |
|
|
What are the two classes of lipids |
-ampiphathic lipids * hydrophillic and hydrophobic phospholipids, glycolipids, and cholesterol |
|
|
What 2 proteins are present in plasma membrane |
1) integral ( transmembrane) and 2) peripheral |
|
|
What are functions of the plasma membrane proteins? |
receptors, transport, enzymes, surface markers, cell adhesion molecules(CAMs), catalysts |
|
|
Where do you find gap junctions? |
cardiac tissues |
|
|
What are 3 types of cell junctions? |
Desmosomes, tight junctions, gap junctions |
|
|
Gap Junctions |
highly permeable -permeability controlled by gating |
|
|
What is gating in gap junctions |
premeability dependent upon concentration of cytoplasmic calcium ions: - high Ca++ = decreased permeability * gating allows uninjured cells to seal off from injured neighbors * Ca++ is released from injured cells |
|
|
Forms of Cellular Communication |
1) direct link up 2) gap junctions ( contact signaling) 3)chemical signaling 4) neurotransmitters: chemical synapses |
|
|
Hormonal chemical signaling |
Endocrine cells- hormones- bloodstream- target cells/ organs |
|
|
neurohormonal chemical signaling |
neuro- secretory neurons |
|
|
Paracrine chemical signaling |
local chemical mediators act on near or by cells - destroyed or imobilized quickly |
|
|
Autocrine chemical signaling |
auto stimulation( act back on the cells of origin) - part of normal growth regulatory mechanisms secreting cells targets itself |
|
|
What are neuro transmitters |
chemical synapses |
|
|
ct occurs by Merocrine secretion |
secretion of cell product occurs by exocytosis from the cell apex into lumen |
|
|
Apocrine secretion |
pinching off of cell cytoplasm containing cell product..... aka exocrine secretion |
|
|
holocrine secretion |
shredding of the whole cell containing the cell product |
|
|
endocrine secretion |
endocytosis from the cell base into the blood stream |
|
|
3 forms of signal transduction |
-extracellular messengers * convey instructions to cell's exterior * transfer, amplify, distribute, and modulate - channel regulation - second messengers 1) cAMP 2) Ca++ |
|
|
what does cAMP do? |
triggers cellular response by activating protein kinase A adenly cyclase-->converts ATP to cAMP-->activates protein kinase A-->phosphorylates intracellular protein-->protein changes shape-->cell response accomplished |
|
|
Ca++ as 2nd messenger process |
Binding of extracellular messenger-->activates G protein--->phospholipase C activated-->Pip2 converted to DAG + IP3--->IP3 mobilizes Ca++ from organelles--->Ca++ as second messenger activates calmodulin---> calmodulin induces change in shape and function of protein---> altered protein produces desired cell response |
|
|
anabolism |
dehydration= synthetic reaction - uses energy |
|
|
catabolism |
degradation= hydrolysis reaction - energy releasing |
|
|
example of dehydration |
synthesis of a molecule, H2O is released |
|
|
hydrolysis reaction example |
2 monomers separate / degrade and releases water |
|
|
What are GTP and UTP |
nucleotides -high energy compouns that can transfer energy |
|
|
Glycolysis |
occurs in the cytoplasm -anaerobic: 2 net ATP produced from one glucose molecule |
|
|
Citric acid cycle |
aka Krebs cycle -occurs in mitochondrial matrix |
|
|
Where does the electron transport chain occur |
In cristae of inner mitochondrial membrane - generates most of ATPs aerobically -oxygen is acceptor of electron at end of chain |
|
|
passive transport |
needs no energy * diffusion- concentrated gradient * filtration= hydrostatic pressure |
|
|
Transport Processes: Channels |
specific, facilitate movement of materials only with electrocemical gradients - ion channels control flow of electrical current through membrane |
|
|
Transport Processes: Pumps |
move ions against electrochemical gradient ( low to high conc) -use ATP |
|
|
Caveole (microdomains) |
Functions: regulation and transport of cholesterol, localization of estrogen receptors, uptake of vit B, Folic acid |
|
|
What phase of cell division does DNA duplication occur |
S phase |
|
|
when is cyclin D highest |
should plateau and not go down during any phase |
|
|
When is cyclin E highest |
Between G and S phase |
|
|
When is cyclin A highest |
Between G and M phase, but highest point is during G2 phase |
|
|
When is cyclin B highest |
between G2 and M phase |
|
|
Where are simple squamous Epithelium cells found |
kidney glomeruli, air sacs of lungs, lining of heart, blood vessels, and lymphatic vessels, lining of ventral body cavity |
|
|
simple cuboidal |
fxn: secretion and absorption Location: kidney tubules, ducts, and secretory portions of small glands, ovary surface |
|
|
Simple columnar epithelium |
fxn: absorption, secretion of mucus, enzymes. ciliated ones propel mucus location: nonciliated types line the digestive tract, gallbladder, and excretory ducts -cilliated: line small bronchi, uterine tubes, and some regions of the uterus |
|
|
pseudostratified columnar epithelium |
fxn: secretion, particularly of mucus; propulsion of mucus by ciliary action location: non ciliated type in sperm ducts and ducts of large glands -ciliated ones line trachea and most of upper respiratory tract |
|
|
stratified squamous epithelium |
fxn: protects underlying tissues in areas subjected to abrasion location: nonkeratinized type is in moist linings of esophagus, mouth, and vagina - keratinized: epidermis of skin ( dry membrane) |
|
|
transitional epithelium |
fxn: stretches readily and permits distension of urinary organ by contained urine location: lines the ureters, urinary bladder, and part of the urethra |
|
|
Where is the sight for blood formation |
inside marrow of bones |
|
|
appositional growth |
increase in diameter |
|
|
endochondral growth |
increase in length |
|
|
apocrine glands |
mammary glands generally found in animals but not in humans |
|
|
merocrine glands |
Pancreas, most salivary glands, mammary glands |
|
|
holocrine glands |
sebaceous glands ( oil glands) |
|
|
Ribosomal structure of prokaryotes |
70s ( 65% RNA + 35% proteins): 30s and 50s |
|
|
Ribosomal structure of Eukaryotes |
80s (50% RNA + 50% proteins) |
|
|
Why weren't mitochondria and chloroplast destroyed by antibiotics |
because they have a double membrane -70s |
|
|
How are antibiotics created? |
structural differences are exploited which selectively harm prokaryotic ribosomes but not eukaryotic ribosomes |
|
|
Digestion |
break down of glucose 1 mol glucose- aerobically breakdown= 686 kcal chemical energy released |
|
|
Name 2 types of enzymes present in peroxisomes |
1) catalase 2) oxidase |
|
|
Why do cells adapt to their environment? |
to escape and protect themselves from injury |
|
|
physiologic adaptation |
occurs with early development |
|
|
pathologic adaptation |
result of pathology from: *decreased workload *pressure *use *blood supply *nutrition *hormoal stimulation *nervous stimulation |
|
|
atrophy |
decrease or shrinkage in size * most common in skeletal and heart muscles * secondary sex organs *brain |
|
|
2 classifications of atrophy |
1) physiologic: occurs during development ex thymus gland incolution 2) pathologic: occurs due to decrease in workload, pressure, use, blood supply, nutrition, hormonal stimulation, nervous stimulation |
|
|
what is an example of atrophy |
skeletal muscle disuse |
|
|
Characteristics of an atrophic cell |
-less ER, less mitochondria, myofilaments, etc -increase in autophagic vacuoles, increase in lipofuscin( yellow-brown pigment) primarily in liver, myocardial cells -decreased O2 and amino acid uptake - decreased protein synthesis -increased protein catabolism---> incolces proteosomes ( Ub- proteosome pathway) |
|
|
What does deregulation of the Ub-proteosome pathway lead to? |
abnormal cell growth and is associated with cancer and other diseases |
|
|
Hypertrophy |
increase in size of cells ex: cells of heart, kidneys, muscles, uterus, mammary glands -increase in protein and not fluids in cytoplasm |
|
|
what specifically causes hypertrophy |
hormone stimulation or increased functional demand |
|
|
what are triggers of hypertrophy |
1. mechanical signals (stretch) 2. trophic signals( growth factors, hormones, vasoactive agents) |
|
|
Hyperplasia |
increase in number of cells & increase in rate of cell division |
|
|
What can cause hyperplasia |
prolonged injury or severe injury |
|
|
Physiologic hyperplasia ( compensatory) |
adaptive mechanism/ regeneration ex...part of liver removed leads to hyperplasia ex epidermis, intestinal epithelia, bone marrow cells, callus (skin) |
|
|
What types of cells do not regenerate |
nerve cells, skeletal muscles, myocardial cells, lens of eye |
|
|
hormonal hyperplasia |
estrogen dependent organs...uterus & breast |
|
|
patholigic hyperplasia |
abnormal proliferation ex uterus, prostatic gland, urinary bladder |
|
|
Dysplasia |
abnormal changes in size, shape and organization of mature cells ex cervix, respiratory tract, associated with common neoplastic growts |
|
|
how is dysplasia classified |
mild/ moderate/ severe/ or low grade/ high grade - once stimulus is removed, may be reversible |
|
|
metaplasia |
replacement of one mature differentiated cell type with another....often occurs in smokers ( loss of cilia) |
|
|
hypoxic injury |
lack of sufficient oxygen ( most common cause is ischemia) |
|
|
causes of hypoxia |
-decreased O2 in air -loss of Hb or fxn -decreased production of RBC -decreased respiratory and or CV fxn -poisoning of oxidative enzymes |
|
|
Ischemia causes |
narrowing of arteries ( stenosis), arteriosclerosis, blood clots, thrombus, embolus |
|
|
anoxia |
total lack of oxygen |
|
|
Cellular response to decrease in oxygen |
-decrease in ATP -failure of Na+/K pump, Na+/Ca++ pump exchange -cellular swelling -vacuolation |
|
|
allergy |
exaggerated response against environmental anitgens
* least life threatening |
|
|
autoimmunity |
misdirected response against the host's own cells |
|
|
alloimmunity |
directed response against beneficial foreign tissues - ie in transfusions or transplants |
|
|
immune deficiency |
insufficient to protect the host |
|
|
hypersensitivity |
altered immunologic response to an antigen that results in disease or damage to the host |
|
|
ypersensitivity : allergy |
deleterious effects to environmental ( exogenous) antigens -ex medicine, pollen, bee stings, foods, infectious agents |
|
|
hypersensitivity: autoimmunity |
disturbance in immunologic tolerance of self antigens |
|
|
hypersensitivity: alloimmunity |
immune reaction to tissue of another individual |
|
|
What occurs during autoimmunity |
- disturbance in tolerance of self antigens -produce antibodies against own antigens( autoantibodies) -auto reactive T-cells cause damage to tissues, clinical disorders= autoimmune diseases |
|
|
When is alloimmunity commonly seen? |
in reactions against transfusions, transplanted tissue/ organ - fetus during pregnancy |
|
|
Type I hypersensitivity |
-IgE mediated and products of mast cells -peak action: 15-30 mins |
|
|
Type II hypersensitivity |
tissue specific reactions -peak 15-30 mins - hypersensitivity against tissue specific antigens, only found on certain specific cells ex... platelets, erythrocytes is target of an immune response ex: Graft rejection, blood transfusion reaction, Myasthenia gravis |
|
|
type III hypersensitivity |
immune complex mediated |
|
|
type IV hypersensitivity |
cell mediated |
|
|
Anaphylaxis |
most rapid hypersensitivity reaction...occurs w/in munures after exposure to antigen -symptoms: itching, erythema, vomiting, cramps, diarrhea, breathing difficulties, edema of throat, decreased BP, shock, death |
|
|
How does IgE in type I facilitate a response |
IgE binds to Fc receptors on surface of mast cells ( cytotropic antibody)---> individual now considered sensitized - Further exposure of a desensitized person to allergen= degranulation of mast cells |
|
|
Histamine release in Type I |
-Binds H1 receptors---> bronchial constriction, vasodilation( increased blood flow), increased vascular permeability ( edema) -Binds H2 receptors---> increased gastric secretion - can be controlled with antihistamines |
|
|
Clinical manifestations of Type I hypersensitivity |
-itching -Urticaria -Conjunctivitis -Rhinitis -Hypotension -Bronchospasm, edema, thick & heavy mucus -dysrhythmias -GI cramps and malabsorption |
|
|
Atopic |
Individuals genetically predisposed to develop allergies - one parent has allergies: 40% offspring will have allergies -2 parents have allergies: 80% - have more fc receptors for IgE on mast cells |
|
|
symptom |
what a patient describes - headache is a symptom but not a sign...cant measure it |
|
|
sign |
can measure certain things... ex fever |
|
|
Desensitization occurs via what? |
IgG blocking antibodies |
|
|
What occurs in type I hypersensitivity in a 1st exposure? |
1) allergen binds to macrophage cell 2)B lymphocyte activates plasma cell to release IgE antibodies 3) IgE antibodies bind to Fc receptor on sensitized cell * reaction does not occur during first exposure |
|
|
What happens during 2nd exposure during type I |
1)Antigen binds to IgE antibodies on cell 2) Degranulated mast cell is triggered to release histamine 3) allergic reaction initiated 4) histamine causes things like edema |
|
|
What is the mechanism of hypersensitivity for Foods? |
Type I |
|
|
What is the mechanism of hypersensitivity for Drugs? |
Type 1, II, III |
|
|
What is the mechanism of hypersensitivity for Pollen, dust, molds |
Type I |
|
|
What is mechanism of hypersensitivity for Aspergullus Fumigatus? |
Types I, III |
|
|
What is mechanism of hypersensitivity for thermophillic actinomycetes |
Types III, IV |
|
|
What is mechanism of hypersensitivity for Drugs |
types I, II, III |
|
|
What is mechanism of hypersensitivity for bee venom |
Type I |
|
|
Mechanism of hypersensitivity for vaccines |
type III |
|
|
mechanism of hypersensitivity to serum |
types I, III |
|
|
mechanism of hypersensitivity for poison ivy, metals |
type IV |
|
|
Type II : Mechansim (1) |
cell is destroyed by antibodies IgM or IgG ex autoimmune hemolytic anemia, alloimmune reaction to mismatched transfused blood cells |
|
|
Type II: Mechanism (2) |
cell destruction through phagocytosis (Macrophage) -activate complement -deposition of C3b on cell surface -receptor on macrophage bind opsonin or antibody-phagocytosis ( ex platelet specific antigen & Rh antigen) |
|
|
Type II: Mechanism (3) |
soluble antigen( medication, substances/ toxins released by microbes or own cells) -may enter circulation and deposit on tissues -antibodies bind, complement activation, C3a & C5a produced, chemotactic, neutrophils bind to C3b ( attached to cells) |
|
|
Type II: Mechanism (4) |
antibody dependent cell mediated cytotoxicity (ADCC) -involves natural killer cells, antibody attached to target cells (RBCs) -Fc receptor of NK cell bind to antibody -NK cells release toxic substances -destroy target cell |
|
|
Type II : Mechanism (5) |
Does not destroy but does cause target cell malfunction -specific cell surface receptors are antigenic -antibodies are produced/ targeted against these receptors |
|
|
Type II What happens once the antibody binds the receptor? |
It changes the function of cell ex....Graves disease= hyperthyroidism -antibody against Tsh receptor produced, tsh receptors are on thyroid gland cells, auto antibodies binding= prologed activation of thyroid cell= high levels of thyroxines -feedback on pituitary decreases tsh level but antibody production is not affected |
|
|
reperfusion of injury |
- results from oxidative stress -free radicals cause further membrane damage and mitochondrial Ca++ overload |
|
|
How are neutrophils affected by reperfusion injury |
neutrophil adhesion to endothelium |
|
|
What reverses neutrophil adhesion and neutrophil mediated heart injury |
antioxidant treatment |
|
|
early dilation( swelling) of cell's endoplasmic reticulum results in? |
decreased sodium/ potassium pump function |
|
|
A common pathway of irreversible cell injury involves increased intracellular |
Calcium |
|
|
Free radical |
-electrically uncharged -unpaired electron that makes molecule unstable -gives up or steals an electron to become a free radical |
|
|
What damage does a free radical cause |
injurious chemical bonds are formed with proteins, lipids, carbs and nucleic acids |
|
|
When does oxidative stress occur |
when Reactive oxygen species overwelms endogenous antioxidant systems |
|
|
What do free radicals cause |
-lipid peroxidation -alteration of critical proteins -alteration of DNA -alteration of mitochondrial structure and function |
|
|
lipid peroxidation |
-destroys polyunsaturated lipids - membrane damage + increased permeability |
|
|
alteration of critical proteins |
destroy ion pumps, transport proteins, damage enzymes |
|
|
Alteration of DNA |
decreases protein synthesis, prevent cell division , growth, repair, regeneration, etc |
|
|
slteration of mitochondrial structure and function |
liberation of Ca++ into cytosol, reduced ATP formation, etc |
|
|
What is a common pathway of irreversible cell injury |
increased intracellular calcium |
|
|
chemical injury |
-interaction with toxic substance and plasma membrane -formation of free radicals, lipid peroxidation results |
|
|
Signs and symptoms of lead toxicity |
-hyperactive behavior -convulsions -delirium -wrist/ finger/ foot paralysis -mental retardation -anemia -renal lesions -loss of appetite -abdominal cramping |
|
|
Is Carbon Monoxide's affinity for Hb (RBCs) high or low? |
high - 300 times greater than that of Oz |
|
|
Symptoms of CO poisoning |
headache, giddiness, tinnits ( ringing in the ears), nausea, weakness, vomiting |
|
|
Nutritional deficiencies due to alcoholism |
Magnesium, Folate ( anemia, prenfancy= spinal bifida), vit B6 ( neuronal damage), thiamine ( deficiency= glossy tongue), phosphorus |
|
|
Acute alcoholism |
CNS |
|
|
Chronic alcoholism |
affects CNS, Liver and stomach and other organ systems |
|
|
what slows alcohol absorption |
fatty foods and milk |
|
|
major enzyme in alcohol metabolism? |
ADH ( alcohol dehydrogenase |
|
|
Hepatic changes from alcoholism |
-deposition of fat -enlargement of liver ( hepatomegaly) |
|
|
Prenatal alcohol exposure |
Fetal alcohol syndrome - microcephaly ( small head) -thinned upper lip, -small eye openings ( palpebral fissures) -epicanthal folds - receded upper jaw ( retrognathia) |
|
|
Blunt force injuries |
-mechanical energy to the bodhy resulting in tearing , shearing, or crushing of tissues - contusion vs hematoma - abrasion -laceration -fractures |
|
|
Sharp injuries |
incised wounds -stab wounds -puncture -chopping |
|
|
asphyxial injuries |
caused by a failure of cells to receive or use oxygen |
|
|
cellular accumulations ( infiltrations) |
water,
-lipids and carbs -glycogen -proteins |
|
|
Cell injury: water |
cellular swelling, most common degenerative change
|
|
|
cell injury: hypoxia |
- decreased ATP & ATPase -inactive Na+/K+ pump, transport proteins - Na+ accumulates in cell -K diffuses out of cell |
|
|
Lipid accumulation in Tay-Sachs, Niemann-Pick, and Gaucher |
- lipid accumulation after cellular injury 1) increase movement of fatty acid in liver ( starvation increases breakdown of triglycerides in adipose tissue, releasing Fatty acids into liver cells 2)failure of metabolic processes that convert FA to phospholipids 3) increased synthesis of TG and alpha glycerophosphatase= increased TG 4)decreased synthesis of apoproteins 5) failure of lipids to bind APs= less lipoproteins 6) failure to transport LPs out of cell |
|
|
Carb accumulation |
-mucopolysaccharidoses cause clouding of the cornea -joint stiffness -mental retardation |
|
|
albinism |
unable to convert tyrosine to DOPA intermediate in melanin synthesis |
|
|
Vitiligo |
white patches on skin, destruction of existing melanocyted |
|
|
hemoproteins |
essential endogenous pigments HB and cytochromes ( oxidative enzymes) |
|
|
what is the iron transport protein |
transferin |
|
|
What are the two forms iron is stored in the tissue? |
1) ferritin 2)hemosiderin ( when increased levels of iron are present) |
|
|
What is hemosiderin |
yellow brown pigment derived from Hb |
|
|
What does an excess of iron cause |
himosiderin to accumulate in cells in areas of -bruising -hemorrhage -lungs & spleen |
|
|
hemosiderosis |
excess iron is stored as hemosiderin |
|
|
hemochromatosis |
- genetic disorder -iron overload -liver and pancreas involved |
|
|
bilirubin |
yellow to green pigment of bile derived from porphyrin structure of Hb - causes jaundice |
|
|
hyperbilirunemia |
occurs from 1) destruction of RBCs/ hemolytic jaundice 2) affects metabolism and excretion of bilirubin in liver 3) causes obstruction of common bile duct 4) caused by Chlorpromazine and Phenothiazine derivatives |
|
|
dystrophic calcification |
-occurs in dying and dead cells, chronic TB , lymph nodes, athersclerosis, heart valve injury, centers of tumors- deprived of oxygen supply , dies and becomes calcified |
|
|
metastatic calcification |
mineral deposits in undamaged normal tissues as a result of hypercalcemia |
|
|
urate ( uric acid) |
major end product of purine catabolism in ansence of urate oxidase |
|
|
hyperuricemia |
deposition of sodium urate crystals in tissues -painful, can cause: * gout ( acute arthritis, chronic gouty arthritis, tophi, nephritis) |
|
|
Where is calcium bound to in normal cells |
buffering proteins: calbindin or paralbumin - contained in ER, mitochondria |
|
|
Where does Ca++ increase if abnormal permeability occurs |
Calcium increases in the cytosol |
|
|
karyolysis |
nuclear dissolution and chromatin lysis |
|
|
pyknosis |
clumping of the nucleus, shrinks, becomes small |
|
|
karyorrhexis |
fragmentation ( dust) of the nucleus |
|
|
coagulative necrosis |
- primarily found in kidneys, heart and adrenal glands - results from hypoxia caused by severe ischemia or hypoxia from chemical injury -protein denaturation |
|
|
how does protein denaturation affect albumin |
causes it to change frolm a gelatinous transparent to a firm opaque state |
|
|
liquefactive necrosis |
- results from ischemic injury to neurons and glial cells of the brain - hydrolytic enzymes and lipids of brain cells are digested by their own hydrolases, tissue becomes soft, liquefies and is walled off from healthy tissue |
|
|
Caseous necrosism |
- results from TB infection ( myobacterium tb infection in lungs) -Dead cells disintegrate but debris is not completely digested by hydrolases |
|
|
how do lipases work |
breakdown triglycerides, releasing free fatty acids |
|
|
gangrenous necrosis |
- caused by arteriosclerosis or blockage og major arteries |
|
|
Dry gangrene |
usually result of coagulative necrosis - dry skin, wrinkles, turns black/ brown |
|
|
wet gangrenet |
develops when neutrophils invade the site causing liquefactive necrosis - occurs in internal organs -site becomes cold, swollen and black |
|
|
gas gangrene |
-caused by Clostridium -anaerobic - cause bubbles of foul smelling gas -found in muscles, RBCs result in death by shock |
|
|
What is the best marker of apoptosis |
Karyohexis ( fragmentation of nucleus to dust) |
|
|
Differences between apoptosis vs necrosis |
necrosis occurs with group of cells due to an exogenous injury. Involves nuclear clumping, swollen mitochondria and ER and rupturing of cell membrane leaving cell into fragments Apoptosis occurs from a suicide gene activation of a single cell. involves nuclear changes, cytoplasmic fragmentation, and apoptotic bodies that are taken up by macrophages |
|
|
Somatic death |
death of an entire person |
|
|
algor mortis |
post mortem reduction of body temperature |
|
|
livor mortis |
settling of blood in the most dependent, lowest, tissues -develops purple discoloration |
|
|
What happens within 6 hours after death |
depletion of ATP and carb breakdown cause acidic compounds to accumulate - inteferes with ATP detachment of myosin and actin---> causes muscle stiffness |
|
|
what is rigor mortis |
muscle stiffening due to inteference of ATP detachment -usually affects the entire body within 12 to 14 hours -36 to 62 hours, rigor mortis dimiishes, body becomes flaccid |
