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19 Cards in this Set
- Front
- Back
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Discuss the role of hydrogen ion concentration in cellular function and dysfunction |
Acid: a molecule that can release a hydrogen ion (H+) Ex. HCl --> H+ plus Cl- Base: an ion or molecule that can accept or combine with a H+ Ex. HCO3 plus H+ --> h2CO3 the more hydrogen present the lower the pH (more acidic) pH measures hydrogen ions |
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Describe how the plasma buffering systems help prevent significant fluctuations in pH |
Chemical buffering systems in the ICF and ECF regulate pH on a moment to moment basis. a buffer system consist of a weak back and the acid that its paired with or a weak acid and its base. there are three major buffering systems in our body: - Bicarbonate system ECF - Phosphate ICF -Hemoglobin -Proteins mostly ICF (largest buffer system in body and most are ICF but albumin and plasma globulins are intravascular. proteins are amphoteric (can be an acid or a base) - Transcellular H+/K+ Exchange system (both move freely between ICF and ECF) these systems are available immediately to combine with excess acid or base to prevent large changes in pH from occurring during the time it takes for the respiratory and renal mechanisms to take effect. |
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Explain how the lungs and kidneys regulate acid-base balance |
-Lungs control CO2 (more ventilation = lower PCO2) (lower ventilation = higher PCO2) the change in blood PCO2 and pH triggers changes in respiratory rate. the response is rapid and reaches maximal effectiveness in 12-24 hours -The kidneys take longer to act than other mechanisms but can return Ph to normal or almost normal and can function for days. renal mechanisms include H+ elimination, resorption of filtered bicarb and production of new bicarb, tubular buffer systems (phosphate and ammonia), potassium hydrogen exchange, and chloride bicarb exchange. |
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Differentiate between respiratory and metabolic acid-base disorders by causes and mechanisms of compensation |
- Respiratory acidosis --decrease in ventilation causes increase in H2CO3 --Causes of hypoventilation are respiratory depression(paralysis) and disorders of the lung (asthma and pneumonia) --clinical mans are headache, restlessness, disorientation, tremors, convulsions and eventually coma if not treated --renal compensation is the increase HCO3 reabsorption and increase in H+excretions -Respiratory alkalosis --Hyperventilation and reduction in CO2 --causes = hypoxemia, hyper metabolic state (sepsis) --clinical mans = dizzy, confusion, extremity tingling, convulsions and eventually coma if not treated --renal compensation is increase in H+absorption and increase HCO3 extretion -Metabolic acidosis --increase in H+ or loss in HCO3 --causes = hypoxia, over production of lactic acid, ketosis, ASA poisoning, diarrhea, renal failure --clinical mans = early(headache and lethargy) and GI symptoms --respiratory compensation = kussmaul respirations (rapid deep breathing) -Metabolic alkalosis --Excess HCO3 or Loss acid --causes = excessive antacid use, hyperaldosteronism, low K+, vomiting --clinical mans = confusion, weakness, hyperactive reflexes --respiratory compensation = slow deep breathing |
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Explain the components of atrial blood gases and use them to interpret clients acid - base status |
what to evaluate in a patient: -what is pH (acidotic, alkalotic?) -what is the PCO2 (bicarb) -What is the HCO3 (in lungs) -does the CO2 or the HCO3 match the pH alterations and the clinical picture and finally what is the clinical picture? is the body attempting to compensate and if so how well is the body compensation? |
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Discuss the two functional fluid compartments of the body |
ICF = 40% of body weight ECF = 20% of body weight in the ECF is the intravascular space (within blood vessels), interstitial space (between cells but not in vascular system), and transcellular (separated by an epithelial layer and its 1%) |
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Describe the causation, patho, and clinical mans of edema |
Edema = palpable swelling produced by an excessive accumulation of fluid in the interstitial spaces. it may be localized or generalized -dependent edema is due to gravity dependence -pitting edema can pit when pressed down -it takes 2.5-3L of excess interstitial volume to produce edema Physiologic mechanisms of edema -increased capillary filtration pressure (increased vascular volume, venous obstruction, and increased arterial pressure) -decreased capillary colloidal osmotic pressure (increased loss of plasma proteins, decreased plasma protein production) -Increased capillary permeability (Inflammation, allergic reactions, malignancies, tissue injury) -obstruction of lymphatic flow (lymphedema, malignancy and surgical removal of lymph nodes) |
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Discuss the regulatory processes for sodium and water balance in the body, including the role of ADH, RAAS, and ANH |
Water has gain and loses in the body. NA is a cation mostly in ECF. Na has gains and loses as well (gain through GI losses through kidney) -water and sodium balance (mechanisms of regulation) --thirst (controlled thirst center in hypothalamus, responds to changes in the extracellular osmolality, cellular dehydration, or decreased blood volume) --sympathetic nervous system outflow (responds to changes in circulatory volume and blood pressure by adjusting the GFR. changes in the GFR result in adjustment of sodium filtration. the SNS also regulated tubular reabsorption of sodium and release of renin) --ADH (produced in the brain and stored in the posterior pituitary gland. controlled by hypothalamus. increases permeability of renal collectin tubules so more water can be reabsorbed. ADH is secreted when plasma osmolality increases or when circulating blood volume decreased/bp drops --ANP (horomone excreted by cells in the lining of the atria. secretion is in responce to increased blood volume/BP raises. ANP inhibits sodium reabsorption in the distal and collecting tubules in the kidney which leads to increased sodium excretions) --RAAS 0 renin = protein enzyme released by kidney in response to changes in ABP, GFR, and Na in tubular fluid. it concerts to renin substrate to angiotensin I 0 Angiotensin I = concerted to angiotestin II by ACE 0 Angiotensin II = acts directly on renal tubules to increase Na reabsorption and this also regulates aldosterone 0 Aldosterone = secreted by adrenal cortex, secretion stim by decrease sodium level in ECF or increase level in urine. increases sodium reabsorption and increases potassium elimination in the collecting tubules in kidneys. |
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Define Hypotonic, isotonic, and hypertonic alterations in water balance and give example of each |
Isotonic = solutions have the same osmolality as body fluid. for fluid loss or fluid excess and cells stay the same hypertonic = solutions have a higher effective osmolality than body fluid. for hypernatremia and water deficit. vells shring hypotonic = solutions have lower osmolality than body fluid. for hyponatremia and cells bloat. |
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Identify the basic causes and clinical mans of hyper/hyponatremia |
-Hyperna = it is caused by sodium retention and a over secretion of aldosterone or ACTH, infusion of sodium, decrease intake of water, or loss of water. it results in intracellular dehydration and hyperchloride often accompanies. --manifestations- caused primarily by ECF loss and cellular dehydration, thirst, fever, decreased urine, tachy, decreased BP, dry skin, decreased reflexes etc -hyponatremia- two types translocational and dilutional. translocational is caused by osmotic shift of water from ICF to ECF and dilutes Na in ECF. --manifestations are muscle cramps, weakness, fatigue, n/v diarrhea, apathy lethargy, etc |
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Clinical manifestations of water deficit |
-dry mucous membranes, decreased skin turgor, weight loss, tachy, thirst, dizzy, weak, shock, fever, no urine, increase BUN, increased specific gravity |
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Discuss the distribution, function, and regulation of potassium in the body |
K is in the intracellular cation (ICF = 140-150 and ECF 3.5-5) and kidneys are the main source of loss -renal regulation is aldosterone and the K/H+ exchange -trancellular shift between ICF and ECF compartments (K/Na pump is within membranes of all body cells, it moves K into cells when plasma levels are high and out when levels are low |
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identify the basic causes and clinical mans of hypo/hyperkalemia |
-hypokalemia - causes include inadequate intake, renal loss, gi loss, and transcellular shift. --manifestations include all body differences (renal polyuria, Gi anorexia, neuromuscular weakness, lab less than 3.5, postural hypotension, cns depression, and metabolic alkalosis hyperkalemia - causes include inadequate elimination from kidneys, release from intracellular compartment, and excessive intake --manifestations are labs high, N/V, paresthesias, ecg changes, and metabolic acidosis |
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describe physiologic basis of the GAS response |
The "syndrome of being sick" is from the HPA and its a state manifested by symptoms that arise when a body responds to situations in specific ways 1. alarm stage - stressors trigger the HPA axis and activates the SNS. arousal of body defenses occurs 2. resistance/adaption stage - begins with the actions of the adrenal horomones, mobilization contributes to fight or flight 3. Exhaustion stage (allostatic overload) - occurs only if stress continues and adaption unsuccessful. leads to disorders. it is also called the generalized stress response. CRH productions, ADH release, SNS activation and RAAS activated. |
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Explain interactions among the components of the nervous system, endocrine, and immune system in mediating a stress response |
Immune system- stress directly related to proinflammatory cytokines, link between stress, immune function and disease. immune system affected by nueroendocrine factors and stress response decreases T cell cytotoxicity and B cell funtions Nervous system - SNS > adrenal gland > catecholamines > Epi and Norepi > target cells in heart lungs muscles blood vessels and liver Endocrine system - hypothalamus CFR>ACTH>adrenal gland>gluco and mineral corticosteroids>target cells kidneys, liver (increased Na and glucose and decrease K) |
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List the effects of cortisol and catecholamines on stress |
cortisol mobilizes substances needed for cellular metabolism and stim of glucogenesis -cortisol promotes hormones (mineral and glucocortisol) which increases blood glucose levels, increases glucagon and increase sodium and cholesterol leve overall its an increase of oxytocin and endophins, raas and a decrease of TSH -catecholamines - epi is the chief effect of CVS and its increased cardiac output and blood in dilating vessels to heart, brain and skeletal, also plasma glucose goes up and sweat, blood,pupil -catecholamines - norepi effect complement those of epinephrine. constricts blood vessels of viscera and skin which shifts the blood flow. also mental alertness RAS |
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identify cations and anions for cell transport |
ion = particle with a charge --cation (K icf, Mg icf, Na ecf, Ca ecf) --anion (Ph icf, Su icf, Ch ecf, Bicarb ecf) electrolyte is a substanse that dissociates in solution to form ion nonelectrolyte does not dissociates (glucose, uria) |
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compare active and passive transport |
-Active =from low to high using atp (Na/K pump) -Passive = high to low and no energy (osmosis, filtration, diffusion) -osmosis --osmolarity = concentration in 1KG of water inside the body --osmolality = concentration of 1L of water outside the body -tonicity = iso, hyper, hypotonic and cell size change -filtration = hydrostatic pressure (BP) -passive mediated transport = intergral or transmembrane proteins and channel proteins |
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discuss diffusion and osmosis and the clinical manifestations |
-Diffusion - molecules from high to low as water moves across the membrane it generates osmotic pressure. the magnitude of osmotic pressure represents whats called hydrostatic pressure, which opposes movement or water across the membrane. solvent and solute equalize concentrations -osmosis - movement of water from low to high. only solvent particles move and solute does not. both equalize the two solutions |
