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Pathophys.
| Question | Answer |
|---|---|
| levels of organization | cells, tissues, organs, organ systems, organism |
| an error in cell function/structure results in | disease and symptoms |
| Cell theory principles (4) | 1. chemicals make up cells 2. cells are derived from pre-existing ones 3. cells are the smallest functional/structural unit of the human body 4. each cell maintains homeostasis at the cellular level |
| Homeostasis is acquired through the coordinated actions of _____ | cells |
| composition of the plasma membrane | phospholipid bilayer composed of polar heads, nonpolar tails, phosphate heads are hydrophilic, lipid tails hydrophilic |
| the cytoplasm consists of everything inside the plasma membrane besides _______ | the nucleus |
| types of proteins on the plasma membrane | transmembrane proteins, integral proteins, and peripheral proteins |
| carbs composing the plasma membrane | glycolipids, glycoproteins |
| structures within the cytoplasm with distinct functions | organelles |
| the fluid within the cytoplasm | cytosol |
| What does the ER produce | fats and proteins |
| Types of Er and their functoins | rough ER- synthesizes proteins and produces lysosomal enzymes smooth ER- synthesizes lipids, lipoproteins, and steroid hormones, regulates intracellular calcium |
| function of the golgi apparatus | prepares substances from ER to be secreted out of the cell, produces lysosomes |
| what is a lysosome | small sac that digests cellular waste |
| what is a peroxisome | smaller than a lysosome, neutralizes free radicals and promotes cell survival by neutralizing harmful substances |
| site of aerobic cellular respiration, produces ATP | mitochondrion |
| what surrounds the nucleus | nuclear envelope |
| each cell contains how many pairs of chromosomes | 23 pairs |
| what are the different forms of the chromosome | chromosome: condensed DNA chromatin: DNA + Histone = not yet condensed Chromatid: duplicated chromosome = sister chromatids |
| area inside the nucleus that synthesizes RNA | nucleolus |
| forms the framework of the cell | cytoskeleton |
| main components of the cytoskeleton | microtubules and microfilaments |
| Functions of the Cell | transportation, secretion, ingestion, communication, respiration, and reproduction |
| types of passive transport | simple diffusion, facilitated diffusion, osmosis |
| facilitated diffusion uses what types of channels | ion channels and transport channels |
| what are the passive transport ion channels on the PM | leaky channels and gated channels |
| what do gated channels require what are the three different types | require a stimulus. voltage gated channels, ligand gated channels, and mechanically gated |
| types of active transport | primary active transport: direct use of ATP and secondary active transport: does not directly use ATP |
| what are the types of secondary transport relative to direction | cotransport: substances transported in the same direction and counter transport: substances transported in the opposite direction |
| what method do cells use to ingest substances | endocytosis |
| what are the categories of endocytosis, describe them | pinocytosis: ingestion of small vesicles phagocytosis: ingesting large particles |
| what two organelles aid in the process of secretion, how? | golgi apparatus and the endoplasmic reticulum, golgi apparatus packages material from the ER and fuses to PM to release them |
| process of releases substances from the cell | exocytosis |
| metabolic process that transform fuel molecules into ATP and wastes | respiration |
| ATP produced without oxygen | anaerobic respiration |
| ATP produced with oxygen | aerobic respiration |
| initial step of cellular respiration, what does it do | glycolysis, breaks down glucose into ATP |
| cycle in respiration that breaks down fats, lipids, and proteins into energy | citric acid cycle |
| what produces the proteins needed for cell function | genes (via transcription and translation) |
| what happens if proteolytic enzyme activity is impaired | impaired protein breakdown = impaired cell function and impaired production of needed products |
| what is the main purpose of cell communication | to coordinate cell behavior by sending and receiving signals (ligands) |
| what is signal transduction | the process where a ligand binds a receptor and triggers an internal cellular response |
| what are feedback mechanisms why do cells use them | they regulate gene activation to control proten production and prevent over/under production |
| what are the two types of signal transduction in the cell, function? | paracrine signaling: signal transduction with a local/rapid response endocrine signaling: affects cell behavior within whole organism |
| what are the ligands involved with endocrine signaling called | hormones |
| how do cells react when faced with damage/injury | they either adapt or die |
| potentially damaging conditions to cells | toxins, changes in 02, temp, electrolytes, |
| what are some of the ways cells respond to change | atrophy, hypertrophy, hyperplasia, metaplasia |
| decrease in cell size | atrophy |
| what are 7 of the causes of atrophy | loss of function, ischemia, denervation, loss of endocrine stimulation, malnutrition, aging, chronic disease/infection |
| What process causes normal tissue/organ shrinkage but is NOT considered a cellular adaptation? | involution |
| increase in cell size | hypertropy |
| 2 causes of hypertropy | trophic (growth) signals increase, and demand increase |
| increase in cell number | hyperplasia |
| 3 causes of hyperplasia | hormone signaling, increased workload, oxygen |
| what two cellular adaptations are often seen together | hypertrophy and hyperplasia |
| reversible process of a mature cell being replaced by another cell type not normally found in that tissue | metaplasia |
| describe the process of how metaplasia comes about, what happens when that process stops | stressor causes metaplasia, when stressor removed cells go back to normal, pathological changes can occur if stressor progresses |
| abnormal growth/development of cells, caused by abnormal differentiation of cells, mutations occur | dysplasia |
| two ways cells die | apoptosis and necrosis |
| programmed cell death that is essential for development, immune system, removing damaged cells, and preventing cancer | apoptosis |
| webbed fingers causes by lack of apoptosis in development of embryonic hands | syndactyly |
| uncontrolled cell death that causes cell welling, inflammation, and membrane puncture | necrosis |
| common cell injuries (TIPS) | toxins, infection, physical injury, serum deficit |
| endogenous toxins | within the body |
| exogenous toxins | external environment |
| a pathological decrease in size of cells in the cerebrum is called | cerebral atrophy |
| cerebral atrophy is a _____ of a disease, but not a disease itself | sign |
| why is cerebral atrophy permanent | our neurons have very little ability to regenerate once they're gone, function is lost |
| why does cerebral atrophy happen? 7 | lack of stimulation, deficit injury (improper nutrition), direct injury (physical or toxins/infection), loss of connections, reduced blood flow, neurotoxic injury, disease specific |
| clinical manifestations of cerebral atrophy | Focal atrophy: one region affected, symptoms dependent on that region, Global atrophy: whole brain affected, widespread cognitive decline |
| Diagnosis for cerebral atrophy | is a sign of an underlying neurologic disease. 1. History: family, symptoms, onset, duration 2. physical/neurologic exam: identifies specific deficits, narrows down brain area affected 3. imaging: measures location and severity of tissue loss |
| types of imaging used for diagnosis of cerebral atrophy | MRI & CT: structural imaging PET & SPECT: functional imaging |
| treatment of cerebral atrophy | the goal is to prevent/slow atrophy. Specific to patient depending on the underlying cause: 1. supportive care 2. rehabilitation therapies 3. medications: improve neural signal transmission 4. individualized plan |
| condition of increase in size of myocardial cells of the heart | cardiac hypertrophy |
| do myocardial cells divide and replace themselves | no |
| physiologic cardiac hypertrophy | the normal growth of the heart cells |
| pathologic cardiac hypertrophy, and its types | abnormal thickening of the heart cells. Primary and Secondary |
| primary cardiac hypertrophy is a | disease |
| what causes the disease of primary cardiac hypertrophy | genetics, can cause sudden cardiac arrest |
| secondary cardiac hypertrophy is a | sign |
| secondary cardiac hypertrophy can occur in | The left or right Ventricles: Left ventricular hypertrophy and right ventricular hypertrophy |
| the underlying conditions of left ventricular hypertrophy can be | aortic stenosis or chronic hypertension |
| left ventricular hypertension is caused by | increased pressure in the systemic circulation |
| stages of LVH | compensated stage: LV walls thicken, chamber size shrinks heart still maintains output decompensated stage: LV dilates, wall thins, pump failure occurs, leads to cardiac decomp |
| ventricular remodeling patterns | concentric hypertrophy: thick walls, small chamber pressure ocerload (decomp stage) eccentric hypertrophy: thin walls, dilated chamber, volume overload (decomp stage) |
| concentric and eccentric hypertrophy are part of the stages of LVH but can be _____ on their own | signs |
| right ventricular hypertrophy is caused by | increased pressure in pulmonary circulation |
| clinical manifestations of Cardiac Hypertrophy | symptoms vary- some people don't have symptoms, symptoms include: SOB, chest PA, fatigue, syncope |
| how does cardiac hypertrophy cause arrhythmias | the large cells disrupt the normal electrical pathways in the heart causing irregular beats |
| diagnosis of primary hypertrophy | diagnosed early with genetic testing |
| diagnosis of secondary hypertrophy | must identify and treat the underlying cause |
| screening tools for cardiac hypertrophy | EKG, electrocardiogram, stress test, echocardiogram |
| physical exam findings that could indicate cardiac hypertrophy | heart murmur during contraction, LV outflow obstruction, may also see atrial arrhythmias, bradycardia, systolic ejection murmur, abnormal vascular response |
| treatment of primary Hypertrophy | treat early once signs appear |
| treatment of secondary hypertrophy | treate the cause before permanent damage |
| Treatments of cardiac hypertrophy | medications to reduce LV muscle mass, surgery to reduce muscle mass/repair valves, lifestyle changes |
| condition caused by excess growth hormone after the growth plates (epiphyses) closed | acromegaly |
| what are the two hormones the hypothalamus secretes that can act on the growth hormone secretion of the pituitary gland | 1. somatostatin: inhibits pituitary GH and growth hormone releasing factor: stimulates GH |
| describe the physiology of acromegaly | the hypothalamus secretes somatostatin and GHRH, when the GH is increased the liver 1GF-1 picks up on it and stimulates the hypothalamus to secrete more somatostatin and decrease GHRH to tell the pituitary gland to stop releasing GH |
| what is usually the cause of acromegaly- Growth hormone oversecretion | a pituitary tumor aka adenoma |
| what growth is affected by acromegaly | bone, cartilage, soft tissues, organs, |
| excessive growth caused by overproduction of the growth hormone after epiphyseal growth plate closure | gigantism |
| who does gigantism effect | infants and children |
| clinical manifestations of acromegaly | 1. soft tissue and skeletal changes 2. neuromuscular symptoms 3. cancer risk 4. respiratory symptoms 5. voice changes 6. reproductive: impotence, menstrual irregularities 7. organ enlargement 8. metabolic effects 9.cardiac effects |
| clinical manifestations of acromegaly from pituitary adenoma | brain tissue pressure: impaired vision and headaches, pituitary gland= altered production of other hormones |
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