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Bio 203 Res/ur/fluid
Respiratory, urinary, fluids, electrolytes
| Question | Answer |
|---|---|
| COPD diseases - 2 (obstructing gas exchange) | * chronic bronchitis --> chronic edema/mucous of airway *emphysema --> cig smoke destroy alveoli walls -->dec sa for gas exchange --> ducts so fragile, they collapse and air gets stuck |
| Restrictive diseases (respiratory) | asthma --> trachea cartilagenous rings, smooth muscle, and mucous mem. Usually in sensitive airways (env, allergic) type response. |
| asthma bwo of allergic/sensitivity response | is inflamm response too-->edema-->reflexive contraction of sm musc (attempt to keep irritant out) |
| asthma tx edema with corticosteroid for inflamm (interferes with inflamm response). How do we tx sm reflexive contranction | epinepherine which binds B2 receptors in sm muscle (B2 agonist)to relax sm muscle |
| ABGs drawn on arterial blood because | venous blood has too much fluctuation dependent upon metabolic needs (cell type, if at rest or active like sk musc cells) |
| How to interpret ABG labs using C02 + H20 --> H2C03 --> H+ + HC03- | *if pC02 is elevated --> pH is decreased acidic *if pC02 is decreased --> pH is increased alka |
| if pulm disease COPD --> pC02 elevated --> | pH low, acidosis bwo hypoventilation (respiratory acidosis) |
| if hyperventilation occurs --> blowing off C02--> | then pC02 decreases,pH increases alkalosis usually bwo panic attack, increased ventilator rate (respiratory alkalosis) |
| have receptors that detect both C02 and O2 | *central chemo receptors in medulla oblongota (resp rate controller)Pons controls depth of respiration. *peripheral receptors in carotid bodies, aorta |
| chemo receptors are sensing (bwo vagus, glossopharyngeal innervation) | pC02, p02, pH |
| In acidosis conditions, less 02 sat | in alkalosis conditions, more 02 sat |
| ANP & BNP cause podocyte pedicles to move away from glomerulus to allow increased filtration | acting like diuretic opposing ADH & Aldosterone |
| everything gets filtered through glomerulus must be at the proper GFR by using | *ANP, BNP *size of afferent arteriole (const/dil) * |
| renin-->AT I --> AT II (vasopressin) | --> aldosterone (dopamine also a pressor drug) |
| everybody filters glucose through glomerulus and reabsorb it in | PCT |
| If sodium is actively transported from filtrate to blood)(in reabsorption then these guys follow | Cl-, K+, Ca, Mg, urea . . .hyperosmol, therefore water now follows. Glucose transport also linked to Na crossing. When glucose levels too high >200, then all transporters are full and it spills (can't be reabsorbed) into urine |
| Hallmark signs of diabetes mellitus | *polyuria (if glucose in filtrate, osmolarity high, draws in water - called osmotic diuretic effect of glucose in filtrate. *polydispia *polyphasia |
| Loop of Henle- thick ascending imperm to water, with vasa recta, and transporter for Na which brings Cl and K --> | water will follow Na, Cl and K |
| loop diuretics (furosemide) | blocks transporter of Na, cl, K which is excreted, so give K (not sure if I got this right) |
| K sparing diuretic - aldactone, spirnolactone | block Na transporter, so now K can't follow and it stays in blood |
| Lab tests (venous blood) mark for kidney issue evidenced by waste products | *BUN (hydration status indicator) *creatinine (kidney function indicator) if they start to rise, then there is renal dysfunction * |
| urea is temporarily reabsorbed as a solute in counter current exchange mechanism to attract water to blood | then urea is excreted |
| can lose 75% nephron system for renal disfunction and 90% loss is | renal failure |
| in dialysis, take blood out of pt and place in artifical, external tubule, which is semipermeable and contains dialysate, which is hypotonic --> | --> filtrate wastes can leave hypertonic blood for filtration in the dialysis tube |
| UA tests for microalbumin, which is a big protein which is not to be filtered | if it appears in UA, then indicator of glomerular issue |
| angiotensin II also stimulates | hypothalamus thirst center, in addition to RAA pathway |
| hypotonic hydration, overhydration, water intoxication, hyponatremia | all synonyms . . .they got super dehydrated and then chugged a whole bunch of water which rushes from blood-->ECF-->cells. *a lot of plain water moves super fast, now too much water at once, dec Na+ (diluted) *cells swell--> *convulsions, coma, death |
| hypotonic hydration s/s due to | we messed with the Na/K balance by over-dilution by the hypotonic intake of xs water |
Created by:
lorrelaws
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