Module 1 Quizco PDF

**[Protein synthesis is transcription and translation and transportation]** - [Transcription]: DNA sequence in a gene is copied into mRNA- DNA-\> RNA code-\> mRNA product - [MRNA= molecule that carries copies of instructions ] - [Translation]: mRNA attaches to ribosomes on r...

**[Protein synthesis is transcription and translation and transportation]** - [Transcription]: DNA sequence in a gene is copied into mRNA- DNA-\> RNA code-\> mRNA product - [MRNA= molecule that carries copies of instructions ] - [Translation]: mRNA attaches to ribosomes on rough ER and transfers RNA, bringing amino acids to ribosomes to build protein. Once that is built, mRNA detaches, and protein is released. - [Transportation]: The finished protein is secreted into a transport molecule, travels to the Golgi apparatus, and is modified as needed. The GA releases the protein into a secretory vesicle, carried to the cell\'s surface for release. **[Waste removal- lysosomes and peroxisomes]** - Both perform clean-up functions in the cells. - [Peroxisomes]: functions to detoxify molecules. It contains the enzyme catalase and oxidases and contains free radicals, especially hydrogen peroxide. - [Lysosomes]: functions to clean up more significant components, including senescent organelles, bacteria, and auto-digested cells after death. They contain digestive enzymes and a low pH. **[Cellular transport: passive mediated and active transport]** - [Passive mediated transport]: no energy is required. Diffused with a gradient - [Simple diffusion]: diffusion across a membrane without a protein channel - [Facilitated diffusion]: diffusion across the membrane that uses a protein channel - [Active transport:] extra energy required diffusion against a gradient - NA-K ATPase Pump: protein channel where cells have a low concentration of sodium and a high concentration of potassium, and outside the cell, there should be a high concentration of sodium and a low concentration of potassium - Pinocytosis( endocytosis for fluids) and phagocytosis - [Adaption/injury] - **[Reversible adaptions]** - [Atrophy]: The same number of cells shrink but stay alive - [Hypertrophy]: same number of cells, but they get bigger - [Hyperplasia]: increase in the number of cells but keep the same shape and size - [Metaplasia:] chance in the morphology of the cell- one type of normal tissue converts into a different kind of normal tissue - **[Dysplasia]**: non-reversible adaption - A physiological change that is constantly pushing it into disease state - **[Cellular injury cause]** - Cellular injury causes include ischemia (lack of blood flow), hypoxia (lack of oxygen), chemical agents, physical agents, infections, psychosocial stressors, genetic defects, nutritional defects, and aging. - **[Biochemical response to cellular injury]** - [Free radicals] are chemically unstable and ready to react with other molecules; they naturally occur. - Too little free radicals= immune system not working well enough - Too many free radicals= immune system sent into overdrive - **[Apoptosis/necrosis ]** - [Necrosis]: type of cell death where the cells swell up and burst. Messy and disorderly and unexpected, but it is linked to pathological disease or threat cell contents spew to healthy cells- it doesn't require energy. - [Apoptosis]: type of cell death where the cells shrivel up normally expected tidy cellular death that requires energy - [Neoplasia] - **[General hallmarks of cancer ]** - Self-sufficient pathways: cells use the RAAS pathway to signal cell growth. This can cause mutations in the oncogenes or tumor suppression gene to cause excessive cellular proliferation. - **[Benign vs. malignant]** - [Benign]: polys and terms ending in -oma - Cells and architecture are similar to normal tissue, but they grow slowly. They push on but do not invade the surrounding tissue, and they do not metastasize - [Malignant]: grow slowly or fast and invade surrounding tissue. They metastasize quickly. The cells lack differentiation of normal - **[Cancer spread initiation phase and promotion phase]** - [Initiation phase]: carcinogen exposure, the electrophilic intermediates bind to DNA and can cause a permeate DNA lesion - [Promotion phase]: cell proliferation with altered DNA and can become a malignant neoplasm or a prenoclasic clone - [Fluid regulation] - **[Common disruptions (hypo/hyper) of electrolytes and how they present clinically ]** - [Sodium imbalances]: hypernatremia and hyponatremia - [Hypernatremia]= high sodium in the blood - [']**fried salts"** - Flushed skin - Restlessness - Increased bp/fluid retention - Edema - Decreased urine output - Skin dry - Agitation - Low fever - Thirst - seizure - [Hyponatremia]=low sodium in the blood - ["]**salt loss"** - Stupor - Anorexia - Lethargic - Tachycardic - Limp muscles - Orthostatic hypotension - Seizures/coma - Stomach cramp - [Potassium imbalances]: hypokalemia and hyperkalemia - [Hypokalemia]=low potassium in the blood - "**Ned h**as **m**any **s**trange **s**ymptoms" - Nausea - Ekg change/arrhythmias - Decreased reflex/fatigue - Hypotension - Muscle weakness/paralysis - Shallow breathing - Slow gi tract - [Hyperkalemia]= potassium is too high in the blood - **"murder"** - Muscle weakness - Urine abnormalities - Respiratory distress - Decreased cardiac contractibility- decrease in bp and hr - Reflex decrease - [Calcium imbalances]: hypocalcemia and hypercalcemia - [Hypocalcemia=] too low calcium in blood - **"cahbs go numb"** - Cramps - Anxiety/irritability - Heart failure - Bronchospasm/stridor - Go numb- tingle, paralysis - [Hypercalcemia]= too much calcium in the blood - **"back me"** - Bone pain - Arrhythmias - Cardiac arrest - Kidney stones - Muscle weakness - Excessive urine output - **[Starlings' forces]** - Interstitial hydrostatic pressure - Interstitial oncotic pressure - [Capillary oncotic pressure]- pulling and causing a reabsorption of fluid from interstitial space back into the capillaries - [Capillary hydrostatic pressure:] pressure of our blood against the capillary walls- pushing fluid out of our vasculature and into the interstitial space - **[Edema formation]** - Hyperfunctioning RAAS and subsequent hypertension can cause increased capillary hydrostatic pressure as RAAS activation increases blood volume by retaining water and sodium as well as causing vasoconstriction. - This change in starling forces will increase fluid filtration out of capillary space and into the interstitial tissue. - This filtrate will be reabsorbed due to the complementary starling force of capillary oncotic pressure, but if filtration exceeds reabsorption, edema will form. - **[RAAS: Renal Angiotensin aldosterone system]** - Regulates blood pressure and blood volume - The kidney senses a [drop in blood pressure via decreased perfusion] and [releases renin], - This [hormone converts angiotensinogen], which the liver constantly releases, [to angiotensin I]. In [the lungs], it is [converted to angiotensin II by ACE (angiotensin-converting enzyme).] - [Angiotensin II] will cause [constriction of blood vessels], which [increases blood pressure], as well as cause the [adrenal glands to produce aldosterone,] a hormone that [causes fluid and sodium retention] in the blood, which [increases blood volume.] - **[ADH]- the hormone of the pituitary gland that produces more concentrated urine to cause the loss of fluid from urine- helps regulate bv and bp** - Allows the circulating volume to be better maintained until more fluids can be consumed - Inadequate ADH= diabetes insipidus - Causes renal water retention - [When plasma volume decreases], it is detected by the volume receptors, which send a message to the hypothalamus, which relays the message to the pars nervosa of the posterior pituitary, which releases adh, causes water retention, and then increases the plasma volume. - [When plasma osmolarity increases], it is detected by the brain receptors who send a message to the hypothalamus that signals the body to increase thirst and fluid intake and also says to pars nervosa, which secretes adh causes renal water retention, decreasing plasma osmolarity