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Cell reg + Genetics
pathophysiology week 1
| Question | Answer |
|---|---|
| Why is it important that our body stay in aerobic cellular respiration most if not all of the time? | This form of cellular respiration not only makes significant more ATP than its anaerobic counterpart, but if we go into anaerobic metabolism it can form lactic acid which can build up and lead to acidosis, sepsis, etc. |
| What is the difference between cellular edema and cellular dehydration? | In cellular edema extracellular fluid enters the intracellular space, vs in cellular dehydration fluid moves the opposite direction. |
| What does the sodium potassium pump do? Do you have to use some energy for it to work? | This pump moves 3 Na ions out of the cell and 2 K ions into the cell (simultaneously). It does require ATP, meaning this is a form of active transport. |
| What is an example of a drug class that can alter the Na/K pump? | cardiac glycosides |
| Is mitochondrial DNA derived maternally or paternally? | maternally |
| What is one major source of damage to mitochondrial DNA? | free radicals |
| Describe the general steps of aerobic respiration and its yield. | glucose becomes pyruvate in glycolysis, and pyruvate undergoes the krebs cycle. Net yield 34 ATP. |
| Describe the general steps of anaerobic respiration and yield. | glucose becomes pyruvate in glycolysis, and pyruvate becomes lactic acid through other processes. Net yield 2 ATP. |
| What is the difference between allostatic load and overload? | Allostatic load refers to a new normal homeostasis with chronic allostasis. Allostatic overload refers to the "crash and burn" when your body can no longer maintain balance. |
| What are the main extracellular and intracellular electrolytes? | Extracellular: Na Intracellular: K |
| Hypertrophy stimulates __________ | angiogenesis |
| Hyperplasia | increased number of cells, usually from a specific stimulus and will stop when the stimulus ceases. |
| Metaplasia | one cell type replaces another, usually a protective measure but is reversible. |
| Dysplasia | deranged cell growth, not cancer, within a specific tissue. |
| Anaplasia | progression to no differentiation, potentially cancer |
| Neoplasia | disorganized/uncontrolled new growth, considered cancerous, can be benign or malignant. |
| Describe four primary characteristics of a benign neoplasia. | well differentiated, with defined borders and progressive/slow growth that doesn't metastasize. |
| Describe four primary characteristics of a malignant neoplasia. | undifferentiated/atypical structure, typically rapid growth that grows by invasion/metastasizes and accesses the blood and lymph. |
| What does VEGF do? | stimulates synthesis of collateral branches when increased blood flow is needed. |
| Nitric oxide and endothelin are _______. | Opponents. NO triggers vasodilation whereas endothelin triggers vasoconstriction. |
| What is the difference between atherosclerosis and arteriosclerosis? | athero is the buildup of plaque that can lead to occlusions; arterio is the narrowing/hardening of the arterial wall and thus loss of elasticity. |
| Give one pathological example of decreased and increased apoptosis. | decreased: prostate cancer increased: spinal muscular atrophy (infantile ALS) |
| What is ischemia? What can it lead to? | Ischemia is lack of oxygenated blood to the tissue, which can lead to ischemic necrosis otherwise known as an infarction. |
| What is necrosis? | death to the tissue from injury, irreversible lysosomal activation and autolysis. |
| What is gangrene and what bacteria does it come from? | Gangrene is prolonged ischemia, infarction, and eventually necrosis. It comes from clostridium perfringens. |
| What is the telltale sign of gangrene and what causes this? | Gangrene emits a very identifiable gas as it destroys tissue, which comes from the bacteria causing the problem. |
| What is the difference in cause between wet and dry gangrene? | wet gangrene is from bacterial infection, dry is from lack of blood supply. |
| What are the signs/symptoms of wet gangrene? | area swells, with odor and oozing |
| What are the signs/symptoms of dry gangrene? | tissue shrinks, turns black (ex frostbite) |
| Do exons or introns actually encode proteins? | exons are the portions of DNA that actually encode proteins. |
| Does one of your alleles come from both of your parents? | No, an allele only comes from one parent but will have a counterpart from your other parent that codes for the same trait. |
| What are the designations for the short and long arms of the chromosome? | short=p; long=q |
| What is the function of the X chromosome in sex linked inheritance? | X is bigger than Y, so it carries more genes and also sometimes has alleles without a corresponding one on the Y. In this case, those with XY genes will always express the X allele regardless of dominance without another allele to silence it. |
| What is penetrance? | ratio of ppl w/ phenotype vs genotype. higher ratio indicated nearly all ppl with the gene express the phenotype. |
| What is a single nucleotide polymorphism? | change in one nucleotide in the sequence |
| What are proto oncogenes? | normal genes that control proliferation, mutation leads to active oncogene. |
| What do oncogenes do? | enable uncontrolled proliferation and synthesis of oncoproteins. |
| What do oncoproteins do? | regulate the cell cycle, direct cell to uncontrollably proliferate |
| What do tumor suppressor genes do? | inhibit uncontrolled proliferation. |
| What is aneuploidy? | different number of chromosomes than 46 |
| Where is the gene for familial hypercholesterolemia? | short arm of chromosome 19 |
| What are the different genotypic forms of FH, and which is more severe? | There are heterozygous and homozygous forms, but the homozygous forms are more severe. |
| What is the pathophysiology of FH? | lack of LDL receptors leads to increased LDL which can lead to widespread atherosclerosis. |
| What is the specific gene/location/mutation in marfan's syndrome? Is it dominant? | Fibrillin 1 mutation on chromosome 15. It is autosomal dominant, but can be from a sporadic mutation. |
| What structures does marfan's syndrome impact? | The myofibrils which are structural components of many cells. |
| What are some implications of marfan's syndrome? | young death around 30-40, CV disease especially aortic dissection and dilation |
| What is the karyotype of Turner syndrome? | 45 XO |
| Symptoms of Turner syndrome | lack of breast development and amenorrhea |
| Complications/implications of Turner syndrome | possible spontaneous abortion, varying severity |
| Gene locus and general genotype of fragile x syndrome | Xq27.3, repeating CGG sequences |
| Fragile x syndrome symptoms | cognitive impairment, FMR, autistic behaviors |
| Down syndrome genotype and risk factors | trisomy 21, maternal age has a strong link |
| Down syndrome symptoms | flat facial profile, epicanthic folds, often a low IQ. |
Created by:
earwe
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