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patho ch 2
| Question | Answer |
|---|---|
| peripheral proteins | membrane protein for signaling/scaffolding only on 1 side of cell membrane |
| transmembrane proteins | spans membrane bilayer communication and transport |
| integral proteins | membrane proteins that often act as channels bound to the tail |
| Smooth Endoplasmic Reticulum | lipid and steroid synthesis (fats for membrane/hormones) calcium storage |
| Endoplasmic reticulum in cell signaling | ion storage and control center for cell signaling |
| Golgi Apparatus | Packaging in the cell for excretion or exocytosis |
| Lysosome | Autophagy and debris cleaning via acid hydrolysis |
| Peroxisomes | oxidases neutralize reactive oxygen species |
| What organelle plays key function in apoptosis signalling | mitochondria |
| Mitochondria | aerobic respiration and oxidative phosphorylation = ATP + CO2 + H2O + Heat |
| Microtubules | tubulin |
| Microfilament | actin |
| thick filaments | Myosin |
| What are the 4 things that form cytoskeleton | microtubules, microfilaments, intermediate filaments and thick filaments |
| What are the 6 core cellular functions | transport ingestion secretion respiration communication reproduction |
| Types of Channels | Leak channel and Gated Channels |
| What are the types of gated channels | Voltage gated, ligand gated, mechanically gated |
| Mechanically gated channel | activation via mechanical force, ie pressure |
| Voltage gated | activation via voltage/action potential |
| Ligand gated | activated via ligands (cell signaling molecules) |
| Example of Primary Active Transport | Na/K--ATPase, Na+ out, K+ in |
| Primary Active transport | Direct transport involving ATP use |
| Secondary Active Transportation | Transport via energy from primary gradient to secondary gradient cotransport (symport)/countertransport (antiport) |
| Cotransport | secondary active transportation moving 2 molecules in the same direction symport |
| Countertrasnport | secondary active transport moving 2 molecules in opposite direction |
| Pinocytosis | small fluid filled vesicles which are ATP dependent |
| Phagocytosis | engulfment of large particles by phagocytes |
| Endocytosis process | endocytosis by phagocyte, merging phagocyte and lysosome, formation of secondary lysosome (degradation), exocytosis by |
| Glycolysis | anaerobic respiration (cytosol) with 2 ATP/glucose yield with pyruvate byproduct |
| Citric Acid Cycle | breakdown of sugars/fats/proteins via electron carriers |
| Oxidative Phosphorylation | aerobic respiration yielding 30-38 ATP/glucose |
| Lactic acidosis | low O2 state leads to anaerobic metabolism, lactic acid byproduct |
| Paracrine | Local/rapid signaling |
| Endocrine | Hormonal/systemic signaling, slower and longer lasting |
| How is cell production regulated | via growth signals and checkpoint control during tissue renewal or repair |
| what regulates the cell membrane/transport | phospholipid bilayer, integral/transmembrane/peripheral proteins, diffusion, osmosis, facilitated diffusion, active transport, Na+/K+-ATPase, symport/antiport |
| what are the 4 types of vesicle traffic | endocytosis, exocytosis, pinocytosis, phagocytosis |
| what can occur when normal cells encounter stress? | atrophy, hypertrophy, hyperplasia, metaplasia, dysplasia occurs as a result of prolonged stress |
| what are the 2 types of cellular mechanism of death | apoptosis and necrosis |
| possible causes of injury | mechanical, chemical, thermal |
| what is cerebral atrophy and some causes | injury and reduced stimuli to brain, progressive reduction in size of neurons |
| how can cerebral atrophy manifest clinically | it can be focal or global |
| how is cerebral atrophy diagnosed | identification of loss of brain function (memory loss, difficulty speaking, movement/balance issues) onset/duration/severity neurologic examinations imaging in form of PET/CT/MRI/SPECT scans |
| What is a SPECT scan | nuclear imaging study, Single Photo Emission Computerized Tomography |
| how is cerebral atrophy treated | prevention methods interruption of injury process slowing disease progression down |
| What is Cardiac Hypertrophy and causes | AKA HOCM increased cardiac muscle mass (enlarged heart) possible etiology from excessive cardiac workload, increased functional demand, inherited genetic trait |
| Primary vs secondary cardiac hypertrophy | primary hypertrophy is inherited secondary is due to other underlying conditions leading to increased workload and increased myocardial cell size (left ventricle more likely to occur) |
| HOCM | hypertrophic obstructive cardiomyopathy usually 2/2 hypertension |
| clinical manifestations of cardiac hypertrophy | (with severity from mild to severe) SOB, chest pain, syncope, impaired cardiac function |
| diagnostic criteria of cardiac hypertrophy | genetic testing, HTN, reduced MET, ventricular arrhythmia, heart murmur EKG/ECHO to check cardiac function |
| treatment for cardiac hypertrophy | medication to relax ventricular fn or reduce heart workload (ie. b-blocker/CCB) surgical (risky, alcohol septal ablation alternative) activity restrictions |
Created by:
sleepingbear
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