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Module 1 Study Questions should be answered after reviewing objectives, lectures, text and additional resources such as links.

1. What is the major difference between a prokaryotes and eukaryotes cells? A. The eukaryote cells contain membrane-bound organelles (nucleus) Prokaryotes do not. **Note Prokaryotes were on Earth before eukaryotes came into being.** 2. Discuss how a cell is affected when damage occurs to a cell membrane. A. Cell membrane damage will cause a cell to swell and burst to the loss of integrity. This process is called necrosis. Inflammation and injury to neighboring cells may occur if the contents linger. 3. What are four mechanisms that cause cellular injury? A. 1. ATP depletion 2. Oxygen and Oxygen derived free radicals 3. Intracellular calcium and loss of calcium steady state 4. Defects in membrane permeability 4. What is the difference between active and passive transport? A. Active transport is the movement of substances in the direction opposite to their electrochemical gradients for diffusion {low to high concentration}. Cellular energy (ATP) is needed. Sodium potassium pump and Proton pump are examples. B. Passive transport is the movement of substances along the gradient {high to low concentration} No cellular energy is needed. Osmosis and Diffusion are examples. 5. How does damage to the cell affect the Na+- K+ pump? A. When cell membrane permeability is altered the Na+-K+ pump kicks in and attempts to rid the cell of all the extra Na. As you know water follows salt, causing pressure to be applied to the mitochondria. When under duress the mitochondria can not produce the needed ATP required for energy production. Without energy to run the Na+-K+ pump can not run efficiently to keep the swelling down in the cell. If not corrected the cell will swell and burst allowing the intracellular contents out. The Lysosomes released help and hurt at the same time. They will clean up the debris and irritate the surrounding cells, causing injury and the process begins again. 6. What happens to the membrane potentials during an electrical impulse? P.32 A. A membrane potential (resting potential) is -70 to -85 mV (millivolts) K+ has a greater potential in ICF and Na+ has a greater potential in ECF. The concentration difference is maintained by the active transport of Na+ and K+ pump which moves Na+ outward and K+ inward. The resting 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. Because Na+ and K+ are both cations, the net result is an excess of anions inside the ell, resulting in the resting membrane potential. 7. How would you distinguish between the four types of tissues? Tissue Type

Epithelia Connecti ve Muscle


Act as protective linings and coverings. In some locales, absorption and secretion are important functions of these lining and covering cells. As secretory cells, epithelia form most glandular structures of the body. Serve as connective and supportive tissues that bind and hold body structures together. Specialized fluid connective tissue types serve as liquid media important intransport, exchange, and body defense. Tissues with the unique capability to contract or shorten. This enables muscle types to be involved in functions of support and movement. Nerve cells are specialized for conduction. Nervous tissues therefore serve as the complex telecommunications network of the body. These tissues act in a sensory capacity, to receive, disseminate, and store information collected from receptors. In a motor capacity, nervous tissues provide response potential by controlling effectors such as muscles or glands.

A. The epithelial tissue or epithelium in dermatology is a tissue composed of a layer of cells. In humans, it is one of four primary body tissues. Epithelium lines both the outside (skin) and the inside cavities and lumen of bodies. The outermost layer of our skin is composed of dead stratified squamous epithelial cells, as are the mucous membranes lining the inside of mouths and body cavities. Other epithelial cells line the insides of the lungs, the gastrointestinal tract, the reproductive and urinary tracts, and make up the exocrine and endocrine glands. Functions of epithelial cells include secretion, absorption, protection, transcellular transport, sensation detection, and selective permeability. Endothelium (the inner lining of blood vessels) is a specialized form of epithelium.

-Connective tissue: is one of the four types of tissue in traditional classifications (the others being epithelial, muscle, and nervous tissue.) It is largely a category of exclusion rather than one with a precise definition, but all or most tissues in this category are similarly: Involved in structure and support. Derived from mesoderm (there are exceptions). Characterized largely by the traits of non-living tissue. Blood, cartilage, and bone are usually considered connective tissue, but because they differ so substantially from the other tissues in this class, the phrase "connective tissue proper" is commonly used to exclude those three. There is also variation in the classification of embryonic connective tissues; on this page they will be treated as a third and separate category. Also, labrums, facia, tendons, & ligaments are connective tissues.

Muscular tissue: provides for all body movement. Contracting muscles cause body parts to move. The three types of muscle tissue are skeletal, smooth, and cardiac. Skeletal Muscle Tissue Skeletal (voluntary) muscle fiber is striated, or striped, and is under the control of the individual's will (fig. 1-9). For this reason, it is often called voluntary muscle tissue. Skeletal muscle tissues are usually attached to bones. When muscle fibers are stimulated by an action of a nerve fiber, the fibers contract and relax. This interaction between muscle and nervous fibers produces movement Smooth Muscle Tissue These muscle fibers are smooth, or nonstriated, and are not under the control of the individual's will . For this reason, this type of muscle tissue is called

involuntary. Smooth muscle tissue is found in the walls of hollow organs, such as the stomach, intestines, blood vessels, and urinary bladder. Smooth muscle tissues are responsible for the movement of food through the digestive system, constricting blood vessels, and emptying the bladder. General All living cells have the ability to react to stimuli. Nervous tissue is specialized to react to stimuli and to conduct impulses to various organs in the body, which bring about a response to the stimulus. Nerve tissue (as in the brain, spinal cord and peripheral nerves that branch throughout the body) are all made up of specialized nerve cells called neurons. Neurons are easily stimulated and transmit impulses very rapidly. A nerve is made up of many nerve cell fibers (neurons) bound together by connective tissue. A sheath of dense connective tissue, the epineurium surrounds the nerve. This sheath penetrates the nerve to form the perineurium which surrounds bundles of nerve fibers. Blood vessels of various sizes can be seen in the epineurium. The endoneurium, which consists of a thin layer of loose connective tissue, surrounds the individual nerve fibers. Although the system forms a unit it can be divided into the following parts: the central nervous system (CNS) which consists of the brain and spinal cord, the nervous system consists of the nerves outside the CNS which connect the brain and spinal cord to the organs and muscles of the body and the automatic or involuntary nervous system consists of nerve centers and fibers inside as well as outside the central nervous system. There are three main types of neurons, which are classified according their function: Those that conduct impulses from the sensory organs to the central nervous system (brain and spinal cord) are called sensory (or afferent) neurons; those that conduct impulses from the central nervous system to the effector organs (such as muscles and glands) are called motor (or efferent) neurons. Interneurons (also known as connector neurons or association neurons) are those that connect sensory neurons to motor neurons. 8. What are the major differences between the normal and abnormal ways of cellular adaptation? Cellular Adaptations to Stress Hypertrophy: increased cell and organ size, often in response to increased workload; induced by mechanical stress and by growth factors; occurs in tissues incapable of cell division Hyperplasia: increased cell numbers in response to hormones and other growth factors; occurs in tissues whose cells are able to divide Atrophy: decreased cell and organ size, as a result of decreased nutrient supply or disuse; associated with decreased synthesis and increased proteolytic breakdown of cellular organelles

Metaplasia: change in phenotype of differentiated cells, often a response to chronic irritation that makes cells better able to withstand the stress; usually induced by altered differentiation pathway of tissue stem cells; may result in reduced functions or increased propensity for malignant transformation. A. Physiologic adaptations usually represent responses of cells to normal stimulation by hormones or endogenous chemical mediators (e.g., the hormone-induced enlargement of the breast and uterus during pregnancy). Pathologic adaptations are responses to stress that allow cells to modulate their structure and function and thus escape injury. Such adaptations can take several distinct forms. Hypertrophy is an increase in the size of cells resulting in increase in the size of the organ. In contrast, hyperplasia (discussed next) is characterized by an increase in cell number. Stated another way, in pure hypertrophy there are no new cells, just bigger cells, enlarged by an increased amount of structural proteins and organelles. Hyperplasia is an adaptive response in cells capable of replication, whereas hypertrophy occurs when cells are incapable of dividing. Hypertrophy can be physiologic or pathologic and is caused either by increased functional demand or by specific hormonal stimulation. Hypertrophy and hyperplasia can also occur together, and obviously both result in an enlarged ( hypertrophic) organ. Thus, the massive physiologic enlargement of the uterus during pregnancy occurs as a consequence of estrogenstimulated smooth muscle hypertrophy and smooth muscle hyperplasia (Fig. 13). In contrast, the striated muscle cells in both the skeletal muscle and the heart can undergo only hypertrophy in response to increased demand because in the adult they have limited capacity to divide. Therefore, the avid weightlifter can develop a rippled physique only by hypertrophy of individual skeletal muscle cells induced by an increased workload. Examples of pathologic cellular hypertrophy include the cardiac enlargement that occurs with hypertension or aortic valve disease (see Fig. 12). The mechanisms driving cardiac hypertrophy involve at least two types of signals: mechanical triggers, such as stretch, and trophic triggers, such as activation of adrenergic receptors. These stimuli turn on signal transduction pathways that lead to the induction of a number of genes, which in turn stimulate synthesis of numerous

cellular proteins, including growth factors and structural proteins. The result is the synthesis of more proteins and myofilaments per cell, which achieves improved performance and thus a balance between the demand and the cells functional capacity. There may also be a switch of contractile proteins from adult to fetal or neonatal forms. For example, during muscle hypertrophy, the -myosin heavy chain is replaced by the form of the myosin heavy chain, which has a slower, more energetically economical contraction. Whatever the exact mechanisms of hypertrophy, a limit is reached beyond which the enlargement of muscle mass can no longer compensate for the increased burden. When this happens in the heart, several degenerative changes occur in the myocardial fibers, of which the most important are fragmentation and loss of myofibrillar contractile elements. The variables that limit continued hypertrophy and cause the regressive changes are incompletely understood. There may be finite limits of the vasculature to adequately supply the enlarged fibers, of the mitochondria to supply adenosine triphosphate (ATP), or of the biosynthetic machinery to provide the contractile proteins or other cytoskeletal elements. The net result of these changes is ventricular dilation and ultimately cardiac failure, a sequence of events that illustrates how an adaptation to stress can progress to functionally significant cell injury if the stress is not relieved. Hyperplasia As discussed above, hyperplasia takes place if the cell population is capable of replication; it may occur with hypertrophy and often in response to the same stimuli. Hyperplasia can be physiologic or pathologic. The two types of physiologic hyperplasia are (1) hormonal hyperplasia, exemplified by the proliferation of the glandular epithelium of the female breast at puberty and during pregnancy; and (2) compensatory hyperplasia, that is, hyperplasia that occurs when a portion of the tissue is removed or diseased. For example, when a liver is partially resected, mitotic activity in the remaining cells begins as early as 12 hours later, eventually restoring the liver to its normal weight. The stimuli for hyperplasia in this setting are polypeptide growth factors produced by remnant hepatocytes as well as nonparenchymal cells in the liver. After restoration of the liver mass, cell proliferation is turned off by various growth inhibitors

(Chapter 3). Most forms of pathologic hyperplasia are caused by excessive hormonal or growth factor stimulation. For example, after a normal menstrual period there is a burst of uterine epithelial proliferation that is normally tightly regulated by stimulation through pituitary hormones and ovarian estrogen and by inhibition through progesterone. However, if the balance between estrogen and progesterone is disturbed, endometrial hyperplasia ensues, a common cause of abnormal menstrual bleeding. Hyperplasia is also an important response of connective tissue cells in wound healing, in which proliferating fibroblasts and blood vessels aid in repair (Chapter 3). In this process, growth factors are produced by white blood cells (leukocytes) responding to the injury and by cells in the extracellular matrix. Stimulation by growth factors is also involved in the hyperplasia that is associated with certain viral infections; for example, papillomaviruses cause skin warts and mucosal lesions composed of masses of hyperplastic epithelium. Here the growth factors may be produced by the virus or by infected cells. It is important to note that in all these situations, the hyperplastic process remains controlled; if hormonal or growth factor stimulation abates, the hyperplasia disappears. It is this sensitivity to normal regulatory control mechanisms that distinguishes benign pathologic hyperplasias from cancer, in which the growth control mechanisms become dysregulated or ineffective (Chapter 6). Nevertheless, pathologic hyperplasia constitutes a fertile soil in which cancerous proliferation may eventually arise. Thus, patients with hyperplasia of the endometrium are at increased risk of developing endometrial cancer, and certain papillomavirus infections predispose to cervical cancers (Chapter 19). Atrophy Shrinkage in the size of the cell by the loss of cell substance is known as atrophy. When a sufficient number of cells is involved, the entire tissue or organ diminishes in size, becoming atrophic (Fig. 14). It should be emphasized that although atrophic cells may have diminished function, they are not dead. Causes of atrophy include a decreased workload (e.g., immobilization of a limb to permit healing of a fracture), loss of innervation, diminished blood supply, inadequate nutrition, loss of endocrine stimulation, and aging (senile atrophy). Although some of these stimuli are physiologic

(e.g., the loss of hormone stimulation in menopause) and others pathologic (e.g., denervation), the fundamental cellular changes are identical. They represent a retreat by the cell to a smaller size at which survival is still possible; a new equilibrium is achieved between cell size and diminished blood supply, nutrition, or trophic stimulation. Atrophy results from decreased protein synthesis and increased protein degradation in cells. Protein synthesis decreases because of reduced metabolic activity. The degradation of cellular proteins occurs mainly by the ubiquitin-proteasome pathway. Nutrient deficiency and disuse may activate ubiquitin ligases, which attach multiple copies of the small peptide ubiquitin to cellular proteins and target these proteins for degradation in proteasomes. This pathway is also thought to be responsible for the accelerated proteolysis seen in a variety of catabolic conditions, including cancer cachexia. In many situations, atrophy is also accompanied by increased autophagy, with resulting increases in the number of autophagic vacuoles. Autophagy (selfeating) is the process in which the starved cell eats its own components in an attempt to find nutrients and survive. We will describe this process later. Metaplasia Metaplasia is a reversible change in which one adult cell type (epithelial or mesenchymal) is replaced by another adult cell type. In this type of cellular adaptation, cells sensitive to a particular stress are replaced by other cell types better able to withstand the adverse environment. Metaplasia is thought to arise by genetic reprogramming of stem cells rather than transdifferentiation of already differentiated cells. Epithelial metaplasia is exemplified by the squamous change that occurs in the respiratory epithelium in habitual cigarette smokers (Fig. 15). The normal ciliated columnar epithelial cells of the trachea and bronchi are focally or widely replaced by stratified squamous epithelial cells. Vitamin A deficiency may also induce squamous metaplasia in the respiratory epithelium. The rugged stratified squamous epithelium may be able to survive under circumstances that the more fragile specialized epithelium would not tolerate. Although the metaplastic squamous epithelium has survival advantages, important protective mechanisms are lost, such as mucus secretion and ciliary clearance of particulate matter. Epithelial metaplasia is therefore a double-edged sword; moreover, the influences that induce metaplastic transformation, if

persistent, may predispose to malignant transformation of the epithelium. In fact, in a common form of lung cancer, squamous metaplasia of the respiratory epithelium often coexists with cancers composed of malignant squamous cells. It is thought that cigarette smoking initially causes squamous metaplasia, and cancers arise later in some of these altered foci. Metaplasia need not always occur in the direction of columnar to squamous epithelium; in chronic gastric reflux, the normal stratified squamous epithelium of the lower esophagus may undergo metaplastic transformation to gastric or intestinal-type columnar epithelium. Metaplasia may also occur in mesenchymalcells but less clearly as an adaptive response. For example, bone is occasionally formed in soft tissues, particularly in foci of injury. 9. Discuss the mechanisms responsible for cell injury leading to necrotic cell death.

Morphologic Alterations in Injured Cells Reversible cell injury: cell swelling, fatty change, plasma membrane blebbing and loss of microvilli, mitochondrial swelling, dilation of the ER, eosinophilia (due to decreased cytoplasmic RNA) Necrosis: increased eosinophilia; nuclear shrinkage, fragmentation, and dissolution; breakdown of plasma membrane and organellar membranes; myelin figures; leakage and enzymatic digestion of cellular contents Apoptosis: nuclear chromatin condensation; formation of apoptotic bodies (fragments of nuclei and cytoplasm) Mechanisms of Cell Injury

ATP depletion: failure of energy-dependent functions reversible injury necrosis Mitochondrial damage: ATP depletion failure of energy-dependent cellular functions ultimately, necrosis; under some conditions, leakage of proteins that cause apoptosis Influx of calcium: activation of enzymes that damage cellular components and may also trigger apoptosis Accumulation of reactive oxygen species: covalent modification of cellular proteins, lipids, nucleic acids Increased permeability of cellular membranes: may affect plasma membrane, lysosomal membranes, mitochondrial membranes; typically culminates in necrosis Accumulation of damaged DNA and misfolded proteins: triggers apoptosis 10. What is the difference between apoptosis and necrosis? A. Apoptosis is an inner-programmed cell death for a cell that become a threat to the organism or the cell is no longer needed. This process involves a specific proteolytic cascade that causes the cell to shrink and condense, to disassemble its cytoskeleton, and to alter its cell surface so that a phagocytic cell may attach and digest the unwanted cell. P. 40 Inflammation does not occur with Programmed cell death. B. Necrosis- cell death due to unexpected and accidental cell damage. A number of toxic chemicals or physical events can cause necrosis: toxins, radiation, heat, trauma, lack of oxygen due to the blockage of blood flow..etc.. Necrosis can lead to : Vasoconstriction halts blood loss Damaged cells release cellular breakdown products that act as inflammatory signals that cause capillaries to dilate and local blood flow to increase. An increase in tissue temperature and tissue reddening, accompanied by the release of histamines, which cause pain by stimulating pain sensing neurons There is an increase in capillary permeability, which enables wbc, leukocytes and macrophages, to leave the circulatory system and move into the damaged region. Fluid moves from the blood to the tissue, leading to the swelling (water mostly will cause the edema) WBC congregate, engulf and digest cellular debris, bacteria and other foreign materials. The immune system will kill and digest organisms from the damaged site, wbc dying will form pus. The tissue will regrow and the wound will heal. Discuss how age affects the distribution of body fluids. A. Cellular Aging


Results from combination of accumulating cellular damage (e.g., by free radicals), reduced capacity to divide (replicative senescence), and reduced ability to repair damaged DNA Accumulation of DNA damage: defective DNA repair mechanisms; DNA repair may be activated by calorie restriction (known to prolong aging in model organisms) Replicative senescence: reduced capacity of cells to divide because of decreasing amounts of telomerase and progressive shortening of chromosomal ends (telomeres) Other factors: progressive accumulation of metabolic damage; possible roles of growth factors that promote aging in simple model organisms


How the difference in hypertonic and hypotonic alterations. A. Summary:

n general, changes in bicarbonate produce compensatory changes in carbon dioxide and vice versa. Compensation causes parallel changes in pCO2 and bicarbonate. 13. Primary metabolic acidosis: The primary abnormality is a decrease in HCO3. The compensatory response includes extarcellular buffering by bicarbonate, intracellular and bone buffering (phosphate, proteins, bone carbonate), respiratory compensation and renal hydrogen excretion. Metabolic acidosis stimulates central and peripheral chemoreceptors, thus stimulating alveolar ventilation (and producing a secondary respiratory alkalosis or reduced pCO2), e.g. dogs with lactate acidosis from hypovolemia often hyperventilate (called Kussmaul's respiration). The maximum expected respiratory compenastion for a metabolic acidosis (the most common acid-base disturbance in small animals) can be calculated using the following formula: Decrease in pCO2 = 1.5 [HCO3) + 8 14. Primary respiratory acidosis: The primary abnormality is an increase in pC02. The compensatory response is intracellular buffering of hydrogen (such as by hemoglobin) and renal retention of bicarbonate (a secondary metabolic alkalosis), which takes several days to occur. 15. Primary metabolic alkalosis: The primary abnormality is an increased HCO3. This is initially buffered by hydrogen from extracellular (mostly) and intracellular buffers (such as plasma proteins and lactate). Chemoreceptors in the respiratory center sense the alkalosis and trigger hypoventilation, resulting in increased pC02 or a compensatory respiratory acidosis. Naturally, the extent of respiratory compensation will be limited by the development of hypoxia with continued alveolar hypoventilation. In addition to respiratory compensation, the kidneys excrete the excess bicarbonate (due to increased filtered bicarbonate and by active HCO3 secretion by a subpopulation of intercalated cells in the collecting tubules). However, this takes several days to occur. 16. Primary respiratory alkalosis: The primary abnormality is a decreased pC02. The compensatory

response to a respiratory alkalosis is initially a release of hydrogen from extra- and (mostly) intracellular buffers. This is followed by reduced hydrogen excretion (mostly as ammonium phosphate) by the kidneys. This results in decreased plasma bicarbonate which is balanced by an increase in chloride (to maintain electroneutrality), thus producing a secondary hyperchloremic metabolic acidosis. The pH can revert to normal from compensation in chronic respiratory alkalosis. Remember these rules for compensation: 1. Compensation does not produce a normal pH (except in a chronic respiratory alkalosis, in which compensatory metabolic acidosis can correct the pH). 2. Overcompensation does not occur. 3. Sufficient time must elapse for compensation to reach steady-state, approximately 24 hours. Characteristic findings in the different primary acid-based disorders with appropriate compensatory changes are illustrated in the table below. Conditions pH H+ Primary Compensation Low High Low HCO3 decrease pCO2 (hyperventilation) Metabolic acidosis High Low High HCO3 increase pCO2 (hypoventilation) Metabolic alkalosis Low High High pCO2 kidneys retain HCO3 Respiratory acidosis High Low Low pCO2 kidneys excrete HCO3 Respiratory alkalosis The following formulas can be used to determine if compensation is occurring in an acid-base disturbance: Conditions Compensation Metabolic acidosis pCO2 decreases by 0.7-0.9 mmHg for each 1 mEq/L decrease in HCO3 Metabolic alkalosis pCO2 increases by 0.7 mmHg for each 1 mEq/L increase in HCO3 Acute: HCO3 increases by 1-1.5 mEq/L for each 10 mmHg increase in pCO2 Respiratory acidosis Chronic:HCO3 increases by 3-4 mEq/L for each 10 mmHg increase in pCO2 Acute: HCO3 decreases by 2-2.5 mEq/L for each 10 mmHg decrease in pCO2 Respiratory Chronic:HCO3 decreases by 5.5 mEq/L for each 10 mmHg decrease in pCO2 alkalosis Alternatively, the following formulas can be used (in these formulae, N = midpoint of the reference range; obs = measured value): For a primary metabolic disturbance, the expected respiratory compensation is: pCO2(expected) = pCO2(N) + [(HCO3(obs) - HCO3(N)) x 0.7] +/- X; where X = 2 for metabolic alkalosis, and X = 3 for metabolic acidosis For a primary respiratory disturbance, the expected metabolic compensation is: HCO3(expected) = HCO3(N) + [(pCO2(obs) - pCO2(N)) x X]; where X = 0.15 for acute respiratory acidosis, X = 0.35 for chronic respiratory acidosis, X = 0.25 for acute respiratory alkalosis, and X = 0.55 for chronic respiratory alkalosis 1.Hypotonic solutions have less solutes and more solvent while hypertonic solutions have more solutes and less solvent. 2.Hypotonic solutions cause the cell to swell because it promotes shifting of water into it while hypertonic solutions cause the cell to shrink because it pulls the water out of the cell. 3.Hypotonic solutions can be used

for dehydration and hypernatremia while hypertonic solutions can be used for cases of hemorrhage. 4.Examples of intravenous hypotonic solutions are 0.45 Na Cl and 0.25 Na Cl while examples of intravenous hypertonic solutions are D5LR and D5 .45 Na Cl.

17. 18.

What are the classic symptoms / clinical manifestations of hyper and hypo alterations related to potassium, calcium, phosphate and magnesium imbalances. A. Discuss the primary and compensatory changes with metabolic acidosis /alkalosis and respiratory acidosis / alkalosis. A.

The three questions I have come up with: In our 75 year old, female patient who is dehydrated from severe vomiting and diarrhea x 3 weeks, which of the following will likely be higher than normal in her blood: 19. 20. 21. 22. 23. Aldosterone only ADH only-ADH would be high because the body is trying to absorb more water K+ only both ADH and aldosterone both ADH and K+

If our 75 year old patient had a depletion of Na (lab value 123) Bun elevation of >100 and is hypotensive which of the following would you administer? 4. 5. 6. NS 0.9% with 20 mEq/L of K+ at 100cc/hr x 2 bags 0.45% NS with D5 at 50cc/hr NS 0.9% at 50-75cc/hr-Depending on how hypotensive you could run the rate a little faster or give a bolus first then have continous IV fluids. Not completely sure about the K since you didn't give a value, but if their K level is low then it would be good! LR at 100cc/hr


What is the proper rate to run IV replacement for severe Hypokalemia at for our 75 year old patient? 1. 2. 5-10 mEq/hr not to exceed 20 mEq/hr 10-20 mEq/hr not to exceed 25 mEq/hr *I would say this answer just from experience in med surg. Sometimes our MD's would order like 3 or 4 K runs over 3 or 4 hours (so each bag mixed with NS would run for 1 hour each piggybacked with regular IV fluids. But obviously if it's burning their veins you definately need to decrease the rate!) 50-75 mEq/hr not to exceed 100 mEq/hr Elderly can not receive IV K+ due to poor vein structure

3. 4.

Ans: IV replacement for severe hypokalemia 1mEq/10 ml of solution. The maximum rate of infusion is 5-10mEq/hr, never to exceed 20 mEq/hr Potassium is a severe tissue irritant infiltration can cause necrosis and skin sloughing. Stop IV infusion if infiltration occurs 0.45% NaCl Half-strength saline is hypotonic. Lactated Ringer's solution is isotonic. Normal saline (0.9% NaCl) is isotonic. A solution that is 5% NaCl is hypertonic.