NU 545 Study Guide Unit 1/FINAL COPY unit 1_FB Complete test, Exams of Nursing

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Study Guide Unit 1 NU 545

1. What is metabolic absorption? (pg. 3) ◆ the process by which all cells take in an use nutrients and other substances from their surroundings ◆ example: cells of kidney tubules and the intestinal epithelial cells reabsorb fluids and synthesize proteins. Thus the kidney and intestines function to absorb fluids. ◆ Cells become specialized through the process of differentiation, or maturation in order to eventually perform one of the 8 chief cellular functions (including movement, conductivity, metabolic absorption, secretion, excretion, respiration, reproduction, and communication). 2. During cell injury what is released that is capable of cellular autodigestion? (pg. 7, 8, 64) ◆ Lysosomes - are membrane-enclosed organelles filled with enzymes that digest macromolecules and defunct intracellular organelles and particles from outside the cell by endocytosis; function as the intracellular digestive system ◆ Lysosomal enzymes are capable of digesting most cellular constituents completely to their basic components (ie amino acids, nucleotides and carbs) ◆ lysosomal enzymes aid in cellular self-digestion - Lysosomal storage diseases: Pompe disease, Tay-Sachs disease, and gout. - Lysosomes are crucial for normal digestion of cellular nutrients, intercellular debris, and potentially harmful extracellular substances that must be removed from the body. - As cells complete their life span and die, lysosomes digest the resultant cellular debris in a process called autodigestion. - In living cells, cellular debris is encapsulated within a vesicle that reacts with a lysosome to complete its degradation in a process called autophagy, which promotes homeostasis through continuous biosynthesis and cell turnover. 3. Where is the genetic info contained in the cell? (pg. 3) ◆ nucleus contains the nucleolus – a small dense structure composed largely of RNA, most of the cellular DNA, and the DNA-binding protein (histones) that regulate its activity - primary functions of nucleus = cell division & control of genetic info, as well as the replication and repair of DNA and the transcription of the info stored in DNA

4. Cell membranes contain which major chemical components? (p. 12-15)

strands of chromatin (the substance that gives the nucleus its granular appearance) begin to coil, causing them to shorten and thicken. The M phase of the cell cycle, mitosis and cytokinesis, begins with prophase , the first appearance of chromosomes. As the phase proceeds, each chromosome is seen as two identical halves called chromatids , which lie together and are attached at some point by a spindle attachment site called a centromere. (The two chromatids of each chromosome, which are genetically identical, are sometimes called sister chromatids .) The nuclear membrane, which surrounds the nucleus, disappears. Spindle fibers are microtubules formed in the cytoplasm. Spindle fibers radiate from two centrioles located at opposite poles of the cell. The role of the spindle fibers is to pull the chromosomes to opposite sides of the cell. During metaphase , the next phase of mitosis and cytokinesis, the spindle fibers begin to pull the centromeres of the chromosomes. The centromeres become aligned in the middle of the spindle, which is called the equatorial plate (or metaphase plate ) of the cell. In this stage chromosomes are easiest to observe microscopically because they are highly condensed and arranged in a relatively organized fashion in the two- dimensional equatorial plate. Anaphase begins when the centromeres split and the sister chromatids are pulled apart. The spindle fibers shorten, causing the sister chromatids to be pulled, centromere first, toward opposite sides of the cell. When the sister chromatids are separated, each is considered to be a chromosome. Thus the cell has 92 chromosomes during this stage. By the end of anaphase, 46 chromosomes are lying at each side of the cell. Barring mitotic errors, each of the 2 groups of 46 chromosomes is identical to the original 46 chromosomes present at the start of the cell cycle. During telophase , the final stage, a new nuclear membrane is formed around each group of 46 chromosomes, the spindle fibers disappear, and the chromosomes begin to uncoil. Cytokinesis causes the cytoplasm to divide into roughly equal parts during this phase. At the end of telophase, two identical diploid cells, called daughter cells, have been formed from the original cell.

6. What allows potassium to diffuse in and out of cells? (pg. 32,36) ◆ The sodium (Na+)–potassium (K+) pump (or sodium-potassium-dependent ATPase pump, or sodium-potassium antiport system ) continuously regulates the cell's volume by controlling leaks through pores or protein channels, as well as maintains the ionic concentration gradient necessary for cellular excitation and membrane conductivity. ◆ This pump system moves Na+ out of the cell and K+ into the cell using energy directly from ATP via a transporter protein called adenosine triphosphatase (ATPase). The resting plasma membrane is more permeable to K+ than to Na+, K+ can diffuse easily from its area of higher concentration in the ICF to its area of lower concentration in the ECF. - For every ATP molecule hydrolyzed, three Na+ move out of and two K+ move into cell. - Channel protein: a protein transporter creates a water-filled pore or channel across the bilayer through which specific ions can diffuse. The channels are sometimes called ion channels , and because they are permeable mainly to K+, they are also called K+ leak channels.

7. How is the cell protected from injury? (p. 12, 49-51)

- Neurohormonal signaling- hormones released into the blood by neurosecretory neurons that release blood-borne chemical messengers (angiotensin II) - Neurotransmitters - chemicals that allow neurons to communicate directly with the cells they innervate at the chemical synapses. ⟶ diffuses across the synaptic cleft and acts on the postsynaptic target cell ◆ important differences is the speed and selectivity which signals are delivered to target 11. How is glucose transported from the blood to the cell? (pg. 29-31) ◆ Glucose can be transported two ways depending on the need of the cell - Passive (facilitated diffusion) mediated mechanism using a uniport protein transporter down a concentration gradient with no energy expenditure. ⟶ Demonstrates saturation kinetics- transport system is saturated when all the glucose-specific receptors on the membranes are occupied at max capacity - Active transport of sugars and amino acids across the plasma membrane in the small intestine and kidneys involves the simultaneous movement of Na+ or Na+-dependant transport; ATP indirectly involved in glucose transport b/c Na+ gradient is ATP dependant 12. Understand the transportation of potassium and sodium across plasma membranes. (p.31) ◆ Active transport of Na and K involves in antiport system where Na moves out while K moves in ◆ Cell membrane use the direct energy of ATP to move these cations via the transporter protein enzyme ATPase ◆ 1 hydrolyzed ATP= 3 Molecules of Na move out of the cell and 2 K move into the cell electrical potential (inside o cell more negative than outside) ◆ Electrical potential where inside of the cell is more negative than outside of the cell - Na is greater in ECF and K greater in ICF. resting plasma membrane is more permeable to K than to Na which makes it easier for K to travel to its lower area of concentration in the ECF resulting in more anions inside the cell (electrical impulses) ◆ The 3 Na+ ions bind to the carrier while at the same time ATP binds to the same carrier. ATP is hydrolyzed, the carrier then changes shape and release the Na+. The carrier then attracts and binds two K+ ions, and then returns to its original shape and release the K+ and ATP remnant.

13. Understand membrane transport. (p, 27-35, 43) ◆ Depends on membrane transport proteins that span lipid bilayer and provided private thoroughfares of select molecules. The two main classes of membrane transport proteins are transporters and channels. ◆ Electrolytes as Solutes are electrically charged ions. Exhibit polarity by orienting themselves toward the positive or negative pole. Cations (positive charge) and Anions (negative charge) migrate toward pole of their opposite charge. Anions and cations are located in the ECF and the ICF, concentration of particular ions varies and depends on the area they are in. - PASSIVE TRANSPORT - water and small electrically uncharged molecules move easily through pores in plasma membrane’s lipid bilayer. Occurs naturally through semipermeable barrier. Molecules will flow easily from area of HIGH concentration to area of LOW concentration. Does not require energy. Driven by the following: ⟶ Diffusion – passive movement of a solute from area of greater concentration to area of lesser concentration (concentration gradient) - The rate is influenced by differences of electrical potential across the membrane (C++ on lipid bilayer) and the substances size (more hydrophobic or small molecule is the faster it will diffuse) ⟶ Filtration (hydrostatic pressure) – mechanical force of water pushing against the membrane ⟶ Osmosis – water moves down the gradient from area of lesser concentration to area of lower concentration - ACTIVE TRANSPORT - requires life, biologic activity, and expenditure of cell’s metabolic energy “UPHILL” (**SEE QUESTION 16 FOR FURTHER INFO) Movement of solute against a concentration gradient occurs by special types of transporters called pumps ⟶ Sodium-Potassium Active Transport System (question 12) ⟶ ATP-dependent Ca++ active transport system – seen in the sarcoplasmic reticulum of the heart and skeletal muscle. Regulates Ca++ in cell’s cytoplasm regulates muscle contraction and relaxation cycles of those muscles ⟶ Na+ - dependent transport – the simultaneous (symport) movement of Na+; ATP dependent - Transport of sugars and amino acids across the plasma membrane in the epithelial cells of the small intestines and kidneys - Transport by vesicle formation ⟶ ENDOCYTOSIS - cellular internalizing process where a section of plasma membrane enfolds substances from outside the cell, invaginates and separates from plasma membrane forming an endocytic vesicle that moves into the inside of the cell - Clathrin-mediated endocytosis - Caveolae-mediated endocytosis

◆ requires life, biologic activity, and metabolic energy. Occurs only living membranes that have to drive the flow UPHILL by pairing it to an energy source (such as ATP). Movement of a solute against its concentration gradient occurs by transporter PUMPS. These pumps must harness an energy source to power the transport (ATP hydrolysis). ◆ Na-K pump continuously regulates the cell’s volume by controlling leaks through pores or protein channels and maintains ionic concentration gradients ◆ Vesicle formation

- Endocytosis- taking in - Exocytosis- taking out ◆ Also called ACTIVE MEDIATED TRANSPORT = movement of a substance across a membrane via a carrier that requires expenditure of energy for activation. Only occurs across living membranes. - Most active transporters use ATP as their primary energy source. - Larger molecules or molecular complexes (ligand-receptor complexes) are moved into the cell by active transport 17. What are cytokines? (pg. 38) ◆ Cytokines also called growth factors, are peptides that transmit signals within and between cells. Major role in the regulation of tissue growth and development. Growth factors stimulate an increase in cell mass or cell growth by promoting the synthesis of proteins and other macromolecules and inhibiting their degradation. Chapter 7 18. When normal columnar ciliated epithelial cells of the bronchial lining are replaced by stratified squamous epithelial cells, the process is called? (pg. 49) ◆ Metaplasia- is the reversible replacement of one mature cell type by another less mature cell type. - New cells mature along a different pathway from the existing type of cells due to signal generated by cytokines and growth factors in the cell’s environment. ◆ In this example, the newly formed squamous epithelial cells do secrete mucus or have cilia, causing a loss of a vital protective mechanisms. usually seen with smokers and effects can be reversed if smoking is stopped and cells are allowed to heal. 19. What is the relation between ischemia and ATP? (pg. 51-51) ◆ Ischemia is most commonly caued by hypoxia (arteriosclerosis) or (thrombosis) decreased mitochondrial oxygenation (mitochondrial phosphorylation) mitochondrial damage in the form of membrane permeability changes and loss of membrane potential which ultimately decrease ATP production ◆ decreased ATP can lead to further mitochondrial damage if oxygenation is not restored. May cause pro-apoptotic proteins between inner and outer membranes to be activated which may activate cell’s suicide pathway (apoptosis)

◆ further ischemia leads to further decrease in ATP and can cause:

- failure of Na-K and Na/Ca pump cellular swelling, and diffusion of K out of cell as well as a release of Ca intercellularly ultimately causing cell death 20. When does sodium enter the cell and cause swelling? (p.51) ◆ During ischemia/hypoxia sodium the Na-K pump fails thus resulting in an intercellular accumulation of Na (swelling) and a diffusion of K out of the cell. ◆ Results when there is a depletion in the level of ATP to fuel the movement of Na+ from the ICF to the ECF. This is seen in hypoxia, when there is a decrease in mitochondrial oxygenation needed for ATP production.

◆ Cellular swelling is reversible with restoration of oxygen to the injured cell. If oxygenation is not restored there is vacuolation within the cytoplasm, swelling of lysosomes, and marked swelling of the mitochondria resulting from mitochondria membrane damage.

21. What are free radicals in relation to cell damage? Progression of diseases? (pg. 54) ◆ cell injury produced by free radicals (especially ROS) is a important mechanism of cell damage in many conditions including chemical and radiation injury, ischemia-reperfusion injury, rapid burst, cellular aging. ◆ Free radicals are capable of inuring chemical bond formation with DNA, RNA, proteins, lipids, carbs – ofter occurs due to excess reactive oxygen species (ROS) through oxidative stress - oxidative stress which is important mechanism of cell damage in many conditions including cell injury, cancer, certain degenerative diseases, and aging. - 3 important effects: ⟶ Peroxidation of lipids: destruction of fatty acids ⟶ Alterations of proteins causing fragmentation of polypeptide chains ⟶ Alterations of DNA, including breakage of single strands 22. Know all about lead poisoning. How does it cause damage within the cell? (pg. 64-67) ◆ LEAD is a heavy toxic metal found in home <1978, environment and workplace. ◆ primary hazard in children (they absorb lead more easily) - damage to brain and nervous system, slowed growth and development, learning/behavior problems, hearing/speech problems lower IQ, ADHD, poor in school ◆ The organ systems affected include nervous, hematopoietic, reproductive, gastrointestinal, cardiovascular, renal and musculoskeletal. Exposure through ingestion, inhalation, and skin (rare). ◆ PATHO: - alteration of cellular ion status: disrupt divalent cations, alter ion transport, and disrupt protein function from displaced metal enzyme cofactors

25. Where do lipids accumulate? (p. 84) ◆ Mainly in the spleen, liver and CNS. Intracellular accumulation (fatty change) is most commonly in the liver. Accumulation of lipids in liver cells is called fatty liver. As lipids fill the cells, vacuolation pushes the nucleus and organelles aside, and give the liver a yellowish and greasy appearance. - Fatty liver caused by alcohol can lead to a form of liver fibrosis called cirrhosis. - The accumulations of both lipids and carbohydrates are called mucolipidoses. Accumulations of excess carbohydrates are called mucopolysaccharidoses. MLs and MPSs are classified as lysosomal storage diseases as they involve increased storage of carbs or lipids in lysosomes - lipids and other such substances tend to accumulate in these organelles). Examples: Tay-Sachs disease, Fabry disease, Gaucher disease, Niemann-Pick disease, and Pompe disease. 26. What is hemosiderosis? (p. 86) ◆ Condition where excess iron is stores as hemosiderin in the cells of many organs and tissues. Common in people who have received repeated blood transfusions or prolong parenteral iron infusions. Associated with increased absorption of iron, conditions that impair iron storage/transport, and hemolytic anemia as well as excessive alcohol injestion. 27. What causes free calcium in the cytosol? (pg. 87) ◆ Causes of free calcium in cytosol: abnormal permeability of calcium ion channels, direct damage to membranes, and depletion of ATP (as seen w/ hypoxia). ◆ If free calcium cannot be buffed out uncontrolled enzyme activation further damage. Important final pathway in many causes of cell death: - Dystrophic calcification: chronic TB of lungs and lymph nodes, advanced atherosclerosis, injured heart valves, center of tumors - Metastatic calcification: mineral deposits in bones from hypercalcemia (hyperparathyroidism, Addison’s disease) 28. What happens to sodium and water during cell injury? (pg. 84) ◆ Pump that transports Na ions out of the cell is maintained by ATP and ATPase ◆ Metabolic failure d/t hypoxia reduced level of ATP/ATPase permits Na to accumulate in the cell (ICF) and pushes K out increase in osmotic pressure which draws water into the cell ◆ Cisternae of the ER become distended, rupture, and coalesce to form vacuoles to isolate the water from the cytoplasm which results in oncosis or cytoplasm swelling. 29. During cell injury caused by hypoxia, what happens to osmotic pressure? ◆ It increases and allows for water to be drawn into the cell 30. What causes mammary glands to enlarge in pregnancy? (pg. 49) ◆ Hormonal hyperplasia (??)

31. After ovulation what happens to uterine endometrial cells? (Pg. 49) ◆ Hormonal hyperplasia ◆ Estrogen stimulates endometrium to grow and thicken for reception of the fertilized ovum if pregnancy occurs hormonal hyperplasia (as well as hypertrophy) enable the uterus to enlarge 32. What happens to liver cells when a portion of the liver is removed? 49 ◆ Compensatory hyperplasia- adaptive mechanism that enables certain organs to regenerate ◆ Removal of part of the liver hyperplasia of the remaining hepatocytes 33. Understand necrosis in relation to pulmonary TB and gangrene. (Pg. 88) ◆ Caseous necrosis- TB infection is a combo of liquefactive and coagulative necrosis that results in the disintegration of dead cells but the debris is not digested completely by hydrolases. Tissues appear soft and granular (cottage cheese), and are enclosed by and granulomatous inflammatory wall. ◆ Gangrenous necrosis- death of tissue and results from severe hypoxic injury commonly due to blockage or artheriosclerosis of major arteries (esp. in the lower leg). Hypoxia and subsequent bacterial invasion necrosis. - Dry- coagulative necrosis. Skin dry shrinks resulting in wrinkles and color changes to dark brown or black - Wet- neutrophils invade site causing liquefactive necrosis. Usually in internal organs. Foul odor, pus, and systemic symtoms. - Gas- infection of injured tissue by one of many species of Clostridium which produces hydrolytic enzymes and toxins that destroy connective tissues and cell membranes and cause gas bubbles to form in muscle cells 34. Infants are susceptible to significant total body water loss, why? (pg. 105) ◆ Because of their high metabolic rate and potential for evaporative fluid loss attributable to their greater body surface area in proportion to total body size (TBW is abt 70-80% of body weight b/c they store less fat) - Diarrhea loss of fluids and renal mechanisms may not be mature enough to compensate so dehydration can happen quickly 35. Why are obese people at greater risk for dehydration? (pg. 105) ◆ % of TBW varies with the amount of body fat b/c fat is H20 repelling (hydrophobic), very little is contained in the adipose cells. Obese people have less TBW and are more susceptible to fluid imbalances that lead to dehydration. 36. With low plasma albumin you have edema, why? (pg. 75, 106) ◆ Albumin is the plasma protein primarily responsible for the plasma oncotic pressure because it has the highest concentration ◆ Decreased albumin decreased plasma oncotic pressure causes fluid to move into the interstitial space and results in edema. ◆ 4 common mechanisms of edema: Increased capillary permeability, increased capillary hydrostatic pressure, decreased capillary oncotic pressure, lymphedema (obstruction)

◆ Hyperaldosteronism and hypernatremia – excess aldosterone causes sodium retention and loss of hydrogen and potassium. Increases renal sodium reabsorption with hypervolemia and hypertension. ◆ Hyperaldosteronism and HYPOkalemia -- the excessive secretion of aldosterone leading to K wasting (renal loss of K due to increased renal excretion of K by the distal tubule) ◆ Hyperaldosteronism and metabolic alkalosis - mild volume expansion ensues when excess aldosterone causes sodium retention and potassium wasting retention of bicarbonate along with sodium alkalosis

- Treat by administration of potassium to correct the imbalance (causes hydrogen ions to move back into the ECF and decreases the loss of hydrogen from the distal tubules) 41. What causes the neuron symptoms in hypernatremia/hyponatremia? (111-113) ◆ Hyponatremia brain cell swelling and deficits of intracellular Na+ alter cell’s ability to depolarize and repolarize normally irritability, depression, confusion - Shift of fluid to the intercellular space (cerebral edema) and increased intracranial pressure

◆ Hypernatremia shrinking of brain cells and alterations in membrane potentials weakness, lethargy, muscle twitching, hyperreflexia, confusion, coma, and seizures

42. Why does a pt. have decreased urine output with SIADH? (p. 113-114) ◆ ADH encourages renal water reabsorption (not excretion) ◆ SIADH = excess ADH failure of distal tubules to reabsorb Na+ (hyponatremia) and enhanced water retention - Water retention – ADH increases renal collecting ducts permeability to water and thus increases reabsorption by the kidneys which leads to an expansion of ECF fluid volume (dilutional hyponatremia) and decreased urine output (urine is inappropriately concentrated) 43. During acidosis how does the body compensate for increase in hydrogen ions? (PG 122- 125) ◆ The higher level of H the more acidic the pH is (<7.4) ◆ Hemeglobin is a good intracellular buffer that binds to H and makes it a weak acid. Venous blood is better buffer than arterial blood. ◆ Respiratory- increase ventilation (eliminate CO2 and reduce carbonic acid concentration) ◆ Renal- excreting H in the urine (dibasic phosphate binds or ammonia with H and are secreted in the urine and conserve bicarbonate) ◆ Cellular ion exchange- Potassium leaves the intracellular space in exchange for Hydrogen alkalosis (shifts can have serious consequences) ◆ Metabolic acidosis: compensation mechanism is via CO2 elimination through hyperventilation. The respiratory system compensates, in response to decreased

pH, by hyperventilation, or blowing off of CO2, thereby lowering PaCO2 and decreasing H2CO3 (a volatile acid known as carbonic acid ). ◆ Respiratory acidosis: compensation mechanism is via renal bicarbonate retention and hydrogen elimination (t he kidneys conserve HCO3- ions and eliminate H+ ions in acidic urine).

- Acute compensation for respiratory acidosis is not effective because the renal buffer mechanism takes time to function (*it may take days, less effective than lungs). 44. What is the significance of deep, rapid breathing in metabolic acidosis? ◆ Hyperventilation (KUSSMALS RESPIRATIONS) eliminates C02 and reduces carbonic acid concentration. Body’s method of compensation during acid-base imbalances - Metabolic acidosis body blows of CO2 in order to lower it’s blood levels and decrease acid levels 45. What causes hyperkalemia? (p. 117) ◆ K >5 = hyperkalemia ◆ Excessive intake, a shift of potassium from the ICF ECF or decreased renal excretion. ◆ ICF ECF shifts of K occur with a change in cell membrane permeability (cell hypoxia, acidosis, or insulin deficiency). - Burns, crush injuries, and extensive surgeries can cause cell trauma and loss of ICF K to ECF ◆ Hypoxia diminish efficiency of cell membrane active transport escape of K to the ECF. In states of acidosis hydrogen ions shift into the cells in exchange for ICF K. (acidosis and hyperkalemia often occur together) ◆ Insulin promotes cellular entry of K, deficiency (diabetic ketoacidosis) ◆ Digitalis OD inhibits Na-K ATPase pump ◆ Renal failure oliguria decreased excretion of K ◆ Hypoaldosteronism (Addison’s Disease) decreased production of aldosterone decreased excretion of K in the urine ◆ Drugs that decrease renal excretion can lead to hyperkalemia if they are not paired with a diuretic 46. What causes hypermagnesemia? (122, 120) ◆ Renal insufficiency or failure ◆ Excessive intake of mg-contain antacids ◆ Adrenal insufficiency- ◆ s/s: lethargy, drowsiness, depression of skeletal muscle contraction and nerve function, loss of DTRs, N/V, muscle weakness, hypotension, bradycardia, respiratory distress, heart block, cardiac arrest. ◆ TX- dialysis or avoiding mg-antacids 47. What influences calcium and phosphate balances? (119-120) ◆ Constant concentration- if one increases or decreases the other does as well

- In the instance of inadequate sources of dairy products or green, leafy vegetables. Excessive amounts of dietary phosphorus also bind with Ca2+, so neither mineral is absorbed when such an excess occurs.

◆ Blood transfusions

- The citrate solution to store blood binds with calcium, making it unavailable to tissues. ◆ Pancreatitis - Due to release of lipases into soft tissue spaces, so the free fatty acids that are formed bind to calcium = decreased concentration of ionized calcium. ◆ Neoplastic bone metastases - Inhibit bone resorption = increased calcium bone deposits = decreased serum calcium. ◆ ↓ PTH and vitamin D - Lack of sunlight = decreased intestinal absorption of calcium due to lack of vitamin D. ◆ **Malabsorption of fat

• Which includes malabsorption of fat-soluble vitamin D, and subsequent deficiency in Ca2+.** ◆ Removal of parathyroid glands - Such as occurs during total thyroidectomy, with the resulting loss of PTH. ◆ Metabolic or respiratory alkalosis - Change in pH enhances protein-binding of ionized Ca2+. ◆ Hypoalbuminemia - Lowers total serum calcium by decreasing the amount of bound Ca2+^ in the plasma. ◆ ↑PTH = ↑ renal activation of vitamin D = ↑ intestinal absorption of calcium, ↑ renal reabsorption of calcium and excretion of phosphate, ↑ bone resorption of calcium 50. When someone vomits extensively, what causes the metabolic alkalosis? (p. 127) ◆ Acid is loss due to the depeletion of ECF sodium, chloride and potassium. Renal compensation not effective because the volume depletion and loss of electrolytes stimulate a paradoxical response by kidneys. - Kidneys increase bicarb reabsorption to maintain an anionic balance b/c ECF chloride is decreased and the resulting excretion of hydrogen and reabsorption of bicarb prevent correction of alkalosis. ◆ Vomiting - Loss of H+ metabolic alkalosis H+ moves from ICF to ECF and K+ moves from ECF to ICF = hypokalemia - Loss of Cl- increase bicarbonate renal reabsorption alkalosis - Loss of fluid increase aldosterone, increased renal Na+ reabsorption, loss of H+ alkalosis - Loss of K+ increased movement of H+ from ECF to ICF increase plasma Bicarbonate levels alkalosis 51. What causes edema during inflammation? What is the purpose of inflammation? (194-195) ◆ Inflammation Vasodilation causes increased vascular permeability and results in leakage of plasma from the vessels in the surround tissue which leads to swelling (EDEMA) at the site of injury