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NURS 611 EXAM 1 STUDY GUIDE/KEYPOINTS EXAM|
150+FREQUENTLY TESTED QUESTIONS AND VERIFIED
ANSWERS |A+ GRADE (MARYVILLE UNIVERSITY)
Key Points Exam 1: Know Cell components and what they do:
- Nucleus- contains and stores DNA
- Ribosomes- Make proteins, vital for cell growth and survival
- Mitochondria- powerhouse of the cell, make ATP
- Golgi apparatus- Package newly synthesized proteins and lipids from the ER to send within the cytoplasm and to the plasma membrane
- Lysosome- Break contents down using enzymes, release contents to be recycled
- Peroxisome- (peroxide) break things down using oxygen, byproduct is H2O (hydrogen peroxide) too much can lead to free radicals
- What are Free Radicals or Reactive Oxygen Species? How do they cause damage? o Unstable atoms that can cause damage (aging, illness) ▪ Atom with outer shell not full—will bond with another atom to completeits electron shell o Difficult to control and can initiate chain reactions o Can cause alteration of proteins or DNA, lipid peroxidation **Cell membrane
- What is the Plasma Membrane made up of?** o Polar head (hydrophilic head) with nonpolar (hydrophobic tail) o Fluid mosaic model: fluidity of the lipid bilayer, the flexible, self-sealing properties, and selective impermeability of the plasma membrane. o Water moves freely by diffusion through the lipid bilayer through aquaporins - Why do we need a Cell membrane? o Keep ICF and ECF separate, hold cells together so they can function as a unit - How is Osmolality different between ICF and ECF? o Due to water permeability, osmolality should be equal. - What do proteins do for the cell? How much of the Cell membrane is made up ofprotein? o Carry out 55% of all physiologic processes o Recognition and binding units (receptors) for substances moving in and out of thecell o Pores or transport channels o Enzymes that drive active pumps o Cell surface markers, such as glycoproteins o Cell adhesion molecules - What is a protein?
o Large, complex molecules that are required for the structure, function, andregulation of the body’s tissues and organs. o Made from amino acids (chains), each amino acid coded from 3 nucleotides→ major structural unit of the cell o Functions: antibody, enzyme, messenger, structural, transport/ storage (enzymaticand hormonal functions) 3 types of Cell junctions:
- Describe what Tight junctions are and why we need them? o Help cells move together and don’t allow things in - Describe what Gap junctions are and why we need them? o Junctions are channels that allow for conductivity- like the heart and nerve cells o Provide the most intimate means of intercellular communication (don’t have toenter the extracellular fluid) o Protein channels - Describe what Desmosomes are and why we need them? o Hold cells together by forming either continuous bands of belts of epithelialsheets or button like points of contact **Energy
- What is Oxidative phosphorylation?** o Occurs in the mitochondria and is the mechanism in which energy is producedfrom carbohydrates, proteins and fats and this energy is transferred to ATP - What is the Inside of cell main Cation? o Potassium - What is the outside of cell main Cation? o Sodium - Is the inside of the cell positively or negatively charged? o Negatively charged - Is the outside of the cell positively or negatively charged? o Positively charged **Transport:
- Diffusion** o A passive movement of a solute from an area of higher solute concentration to anarea of lower solute concentration - Facilitated diffusion o KEY and LOCK….. This is a carrier mediated process that will allow particlesthat are too big or charged to get through the membrane. AGAIN there is no energy to do this process, but you have a limited capacity. o Back up—glucose and ETOH
- What part does albumin do with keeping fluid in blood vessels? o Main protein the blood that stays in the blood, help pull water back into thecapillary o Responsible for plasma oncotic pressure o Carries a NEG charge - What is happening in edema or third spacing if albumin is low? o Loss of plasma proteins/ albumin fluid leaves the vasculature and enters the third space/ interstitial space dehydration can develop o Decreased synthesis of plasma protein (malnutrition, cirrhosis), increased loss of plasma proteins (nephrotic syndrome), increased plasma Na+ and H2O retention (dilution of plasma proteins ▪ All decrease capillary oncotic pressure - What happens to calcium if albumin is low? o Hypoalbuminemia Since a significant portion of calcium circulates bound toalbumin, low serum albumin levels may result in a low serum total calcium despite normal ionized calcium levels **Electrical Impulses and Membrane potential
- Resting Membrane Potential** o The difference in voltage across the plasma membrane when it is at rest - Action Potential: o The cell membrane acts as a capacitor o Stores electrical charge o Membrane potential is the electrical energy difference between the inside and outside of the cell - Depolarization: o A rapid rise in membrane potential which opens sodium channels in the cellmembrane - causes a large influx of Na+ ions. - Repolarization: o Refers to the change in membrane potential that returns the cell to anegative value just after the depolarization phase of an action potential. This phase occurs after the cell reaches its highest voltagefrom depolarization. - What is the difference between the relative refractory and Absolute refractory period? o Absolute refractory – new action potential cannot be initiated o Relative refractory – new action potential can be initiated but may need morestimulus
Key Points WEEK 2: Altered Cell metabolism and GeneticsAltered Tissue Define and give examples of each Condition Define Example Atrophy - Physiologic: with earlydevelopment
- Pathologic: Decrease in cell size (due to decreases in workload, use, pressure, blood supply, nutrition, hormonal or nervous stimulation Can affect any organ but most common in skeletal muscle, heart, secondary sex organs, and the brain
- Physiologic: thymus gland duringchildhood
- Pathologic: aging causes brain cells toatrophy Hypertrophy increase in the size of cells by increased work demands or hormonal stimulation-- increases thesize of the affected organ; physiologic (increased demand, stimulation of hormone and growth factors) or pathologic (chronic hemodynamic overload) Physiologic hypertrophy: pregnancy(hormone-induced uterine enlargement) Pathologic hypertrophy: hypertension or heart valve dysfunction Hyperplasia increase in the number of cells caused by an increased rate ofcellular division
- Occurs as a response to injury thatresults when the injury has been severe and prolonged
- Growth factors stimulate the remaining cells to synthesize newcell components
- Compensatory hyperplasia enables certain organs to regenerate. (normal) *Removal of the liver leads to hyperplasia of the remain in liver cellsto compensate for the loss
- Hormonal hyperplasia is stimulated by hormones to replace lost tissue orsupport new growth, such as during pregnancy. (normal)
- Pathologic hyperplasia is the abnormal proliferation of normal cells in response to excessive hormonal stimulation of growth factors on targetcells.
o Decreased levels of oxygen and increased levels of oxygen-derived free radicals, increased concentration of intracellular calcium and loss of calcium steady state,defects in membrane permeability Which is worse, Hypoxia or Ischemia? Why?
- Ischemia causes hypoxia o Ischemia: cessation of blood flow to vessels that supply the cell with oxygen andnutrients ▪ Oxygen applied after can result in reperfusion injury o Hypoxia: can induce inflammation and inflamed lesions can become hypoxic What is the difference between necrosis and apoptosis?
- Necrosis: the sum of all changes after local cell death (inflammation, cellular lysis,autolysis) o Rapid loss of the plasma membrane structure, organelle swelling, mitochondrialdysfunction, lack of typical features of apoptosis o Cell SWELLS; plasma membrane disrupted; frequent adjacent inflammation
- Apoptosis: programmed cell death characterized by the “dropping off” of cellular fragments called apoptotic bodies o CELL SHRINKS; plasma membrane intact o Occurs with severe cell injury, accumulation of misfolded proteins, infections(viral), obstruction in tissue ducts **Necrosis: explain the difference
- Gangrenous necrosis** : death of tissue resulting from severe hypoxic injury - Dry gangrene o The result of coagulative necrosis: hypoxia caused by severe ischemia or hypoxia caused by chemical injury; coagulation is caused by protein denaturation→ causesAlbumin to change from gelatinous, transparent state to a firm, opaque state→ area of infarct o Skin becomes very dry and shrinks, resulting in wrinkles, color change to darkbrown/ black - Wet Gangrene o Develops when neutrophils invade the site, causing liquefactive necrosis o Occurs in internal organs→ site becomes cold, swollen and black, foul odor, pus **Cells and Aging:
- What happens to cells as we age?** o Atrophy, decreased function, loss of cells (apoptosis)--> causes hypertrophy and hyperplasia which can lead to metaplasia, dysplasia, neoplasia
▪ DNA, RNA, cellular proteins, and membranes more susceptible to injury(decreased ability to repair) o Progressive loss of tissues and organs over time o Senescence: a process of permanent proliferative arrest on cells in response tostressors → may be important in age-related disease ▪ Loss of tissue-repair capacity because of cell cycle arrest ▪ Produces proinflammatory and matrix-degrading molecules o Hallmark of aging: accumulation of damaged macromolecules from telomereerosion, DNA damage, epigenetic stress, ROS accumulation, ER stress o Increased levels of cytokines and proinflammatory markers o Increased activation of the coagulation system with age o Adaptive immunity declines with age but innate immunity may result in mildhyperactivity o Extracellular changes: decreased binding of collagen, increased free radicals, structural alterations of fascia, tendons, ligaments, bones, and joints, developmentof peripheral vascular disease (atherosclerosis) ▪ Decreased elastin, degradation of collagen, changes in proteoglycans and plasma proteins→ result in dehydration and wrinkling of the skin
- What is somatic death? o Death of an entire organism/ person, cessation of respiration, circulation, graduallowering of body temperature, pupil dilation, loss of elasticity, increased transparency in the skin, muscle stiffening, skin discoloration (livor mortis) Free Radical Injury– Explain what happens with ROS? Reactive oxygen species (ROS)- can cause irreversible damage to DNA as they oxidizeand modify some cellular components and prevent them from performing their original functions.
- Target cell membrane → oxidative stress can activate intracellular signaling pathways
- Can cause lipid peroxidation or the destruction of unsaturated fatty acids, alterations ofproteins, protein loss, and protein misfolding, and mutations in the DNA Chemical Injury List common types of chemical injuries and what happens in the body?
- Accumulations of water, lipids, carbohydrates, glycogen, proteins, pigments,hemosiderin, bilirubin, calcium, urate o Systemic manifestations: fever, leukocytosis, increased HR, pain, serum elevations of enzymes in the plasma
- Long-term exposure: air pollutants, insecticides, herbicides cause cell injury
- Carbon monoxide, carbon tetrachloride, social drugs significantly alter cellular function and injure cellular structures
o Are agents, such as radiation and chemicals, that increase the frequency ofmutations
- Which part of the cell can be damaged the most by radiation? o DNA from ionization **Explain the process of how we make a Protein?
- What is transcription?** o The DNA strand is untwisted and unzipped. This occurs in Nucleus ▪ Single strand acts as a template→ creates mRNA ▪ mRNA (messenger) uses this DNA strand to make a template that can be carried outside of the nucleus happens within the nucleus ▪ RNA Splicing-- many RNA sequences are removed and the remaining sequences are spliced together to form functionalmRNA that will migrate to the cytoplasm ▪ Excised sequences are called introns and exons are those thatremains to code for proteins ▪ RNA polymerase ▪ Single stranded, ribose sugar molecule and Uracil rather than thymine ▪ Polymerase-. polymer- means long chain and - ASE means enzyme. So apolymerase IS an enzyme that helps to create a long chain. - What is translation? o mRNA and translating it into amino acids that will make a protein. o mRNA takes the “recipe” out of the nucleus o RNA directs the synthesis of a polypeptide via the interaction with transfer RNA(tRNA). o tRNA contains a sequence of nucleotides (anticodon) complementary to the triad of nucleotides on the mRNA strand (codon). - Where does protein synthesis occur? o The ribosome o Ribosome (rRNA) helps mRNA and tRNA make polypeptides. o When a ribosome arrives at a termination signal on the mRNA sequence,translation and polypeptide formation cease. o RNA is synthesized from the DNA template via RNA polymerase formation of mRNA mRNA moves out of the nucleus to cytoplasm capable of gene splicing(into introns and extrons) **CHROMOSOMES:
- How many pairs of chromosomes do we have?** o 23: 22 homologous pairs and one sex linked pair (homologous (XX) or nonhomologous (XY))
- What is a Gamete cell? o Germline cells o Haploid cells (only 1 member of each chromosome pair) o Reproductive cells, sperm and egg cells; contain 23 chromosomes - What is a Somatic cell? o Any other cell than a reproductive cell o Contain 46 chromosomes-- 23 base pairs; 22 of the pairs are autosomes - What is a Karyotype? o An ordered display of chromosomes arranged according to length and centromere location **Genetic Diseases: DEFINE THE FOLLOWING
- Aneuploidy** o A somatic cell that does not contain a multiple of 23; usually the result ofnondisjunction o I.e. Trisomy (three copies of one chromosome), monosomy (one copy of any chromosome-- often fatal) ▪ Duplication of genetic material better than the loss of genetic material - Penetrance o Definition: the percentage of individuals with a specific genotype who alsoexhibit the expected phenotype o Incomplete penetrance ▪ Individual who has the gene for a disease but does not express the disease ▪ Has genotype but may not express phenotype ▪ Example: Retinoblastoma (eye tumor in children) (90%) o Age dependent ▪ Does not express a disease until a certain age is reached ▪ Has the genotype and will express disease but will not express until a certain age ▪ Example: **Huntington disease
- Expressivity** o Is a variation in a phenotype associated with a particular genotype. o Can be caused by modifier genes, environmental factors, and mutations. o Example: von Recklinghausen disease ▪ Is autosomal dominant. ▪ Expressivity varies from brown spots on the skin to malignant tumors,scoliosis, gliomas, and neuromas. ▪ Can be expressed very differently
o Occurs 1 in 800 live births. o Manifestations : Mental challenges; low nasal bridge; epicanthal folds; protruding tongue; flat, low-set ears; and poor muscle tone. Can have congenitalheart defects o Risk increases with maternal age. o Has an increased risk of congenital heart disease, respiratory infections, andleukemia. o By the age of 40 develop symptoms almost identical to Alzheimer disease because the gene to cause this disease is also on the Chromosome 21.
- Turners syndrome o Females have only one X chromosome; Denoted as karyotype 45,X. o Characteristics include: Absence of ovaries (sterile ), Short stature, Webbing of the neck, Widely spaced nipples, High number of aborted fetuses, X chromosomethat is usually inherited from the mother o Occurs 1 in 2500 female births. o **Teenagers receive estrogen.
- Klinefelter’s syndrome** o Sex Linked: Individuals with at least one Y and two X chromosomes. o Characteristics include: Male appearance, Female like breasts (gynecomastia), Small testes, Sparse body hair o 1 in 1000 male births o Some individuals can be XXXY and XXXXY; will have male appearance; abnormalities will increase with each X; can also have an extra Y chromosome. o Disorder increases with the mother’s age. - What is a congenital disease? o Medical condition present at or before birth; birth defects **Key Points Chapter 3: Fluid and Electrolytes:
- Review how Aging affects the Distribution of water in the body?** o Show to function less efficiently o Sarcopenia-muscular atrophy o Total body potassium concentration decreases because of decreased cellular mass-
increased sodium/potassium ratio (d/t increased extracellular compartment) - How does have a normal, lean or obese frame affect TBW? o Varies with age and amount of body fat o Increased fat content= Decreased TBW o Infants particularly susceptible to significant TBW changes because of highmetabolic rate and potential for evaporative fluid loss
- How does water move between ICF and ECF? o Water moves between the plasma and interstitial fluid by osmosis and hydrostaticpressure across the capillary membrane - What drives hydrostatic pressure? o Hydrostatic pressure is influenced by osmotic pressure o At the arterial end of capillaries, fluid moves from the intravascular space into the interstitial space because capillary hydrostatic pressure (influenced by the Cardiacsystem) is higher than the capillary oncotic pressure - What drives oncotic pressure? o Aka colloid osmotic pressure, it is pressure exerted by proteins (ALBUMIN) inthe blood vessel’s plasma that pull water into the circulatory system o Oncotic pressure is heavily influenced by plasma proteins - What are the 4 causes of edema? o Decreased capillary oncotic pressure ▪ Decreased synthesis of plasma proteins, increased loss of plasma proteins,increased plasma sodium and water retention o Increased capillary permeability (burns, inflammation)--> loss of plasma proteinsto the interstitial space o Increased tissue oncotic pressure ▪ Caused by lymph obstruction→ decreased transport of capillary filtered protein o Increased capillary hydrostatic pressure ▪ Venous obstruction, salt and water retention, heart failure → increasesfluid movement into the tissues - How does sodium and chloride and bicarb affect water balance? o Cl- and Na+ intimately related o Water balance: regulated by renal response to ADH from the posterior pituitary--thirst, antidiuretic hormone (initiated by increased plasma osmolality or a decrease in circulating blood volume) o Na+ Balance: regulated by renal effects of aldosterone increases reabsorption ofNa+ by the distal tubule of the kidney ▪ Aldosterone secretion influenced by Renin and Aldosterone ▪ Atrial natriuretic hormone decreased tubular reabsorption and promotesurinary excretion of Na+ - What does aldosterone do? o Is a steroid hormone that stimulates reabsorption of sodium and secretion of potassium and hydrogen ions within the kidney - What are natriuretic peptides? Why does an elevated BNP indicate CHF?
emesis/diarrhea. ADH secretes to replete volume Euvolemic hyponatremia: Na+ loss w/o H2O loss. This is SIADH, hypothyroidism, PNA, glucocorticoid deficiency) Dilutional hypotonic hyponatremia (H2O intoxication): large intake of free water or replacement of fluid loss with D5W (glucose is metabolized, leaving hypotonic effect) (from cerebral edema/cellula rswelling) *mild hyponatremia isusually asymptomatic Albumin, Urine osmolality and Na+ levels, as well as urine specific gravity, Differential dx includes: SIADH Dehydration Adrenal insufficiency Hypothyroidi sm Infection (PNA) Glucocorticoid deficiency Hyperchloremia 95 - 105 Fluid retention, high BP, fatigue, muscle weakness, excessive thirst, dry mucous membranes. Hypochloremia^95 -^105 Typically accompanies Metabolic alkalosis, hyponatremia and elevated bicarb. Common in Cystic Fibrosis. Na+ deficit associated with diuretics or restricted intake is typically associated with hypochloremia. Weakness, fatigue, difficulty breathing. Often associated with vomiting and diarrhea - although these are what lead to the low levels. *Can be asymptomatic *In all cases treatment of theunderlying cause is required ABGs, anion gap Good H&P required, review medications closely. Hyperkalemia 3.5- 5 Insulin causes potassium to move into cells patients with deficient Insulin can develop EKG changes: Peaked T wave, prolonged PR, depressed ST, wide QRS EKG, labs, IV fluids if dehydrated. Treat underlyin g
hyperkalemia *can be caused by decreased renal excretion Symptoms: dysrhythmias, tingling lips/fingers, muscle weakness cause. *buffered solutions (Sodium bicarb), Calcium gluconat e Hypokalemia 3.5-^5 EKG changes: slight prolonged PR, slight peakedP, ST depression, prominent U wave Symptoms: weakness/fatigue ,muscle cramps, dysrhythmias Differential Includes: DKA, reduced K+ intake, aldosterone excretion (from increased Na+ levels) Hypercalcemia (PTH, Vit D, Calcitonin)
Hyperparathyroidism ; bone metastases with calcium resorption from breast, prostate, renal, and cervical cancer; sarcoidosis; excess vitamin D; many tumors that produce PTH; calcium-containing antacids Many nonspecific; fatigue, weakness, lethargy, anorexia, nausea, constipation; impaired renal function, kidney stones; dysrhythmias, bradycardia, cardiac arrest; bone pain, osteoporosis, fractures Hypocalcemi a(PTH, Vit D, Calcitonin) 8.5- 10 Inadequate intestinalabsorption, massive blood administration, decreases in PTH and vitamin D levels; nutritional deficiencies – malnutrition; alkalosis, elevated calcitonin level; Increased neuromuscular excitability; tingling, musclespasms (particularly in hands, feet, and facial muscles), intestinal cramping,
possibly respiratory failure (because of muscle weakness), cardiomyopathies , bone resorption (leading to rickets or osteomalacia) Hypermagnesemia 1.4-2.1 Usually renal insufficiency or failure ; also excessive intake of magnesium- containing antacids, adrenal insufficiency Lethargy, drowsiness; loss of deep tendon reflexes; nausea and vomiting; muscle weakness; hypotension; bradycardia; respiratory distress; heart block, cardiac arrest Hypomagnesaemia 1.4-2.1 Malnutrition, malabsorption syndromes, alcoholism, urinary losses (renal tubulardysfunction, loop diuretics) Behavioral changes, irritability, increased reflexes, muscle cramps, ataxia, nystagmus, tetany, convulsions, tachycardia, hypotension ACID BASE:
- Review normal PH and the buffering system which tries to bring body back into balancePH- 7.35-7.45 perfect is 7. HC03 (Bicarb)- 22 - 26 - used as a buffering system to bring body into balance Know common causes of and pathophysiology of the following:
- Metabolic acidosis: increased non-carbonic acids or loss of bicarb from extracellular fluid o Base is lost from the extracellular fluid and cannot be regenerated by the kidney o Causes: overproduction of acid, ketoacidosis, lactic acidosis, decreased acid excretion, advanced renal failure, diarrhea o S/S: headache and lethargy, anorexia, nausea, vomiting, diarrhea→ lead toconfusion and coma→ Kussmaul respirations
- Metabolic alkalosis: bicarbonate concentration increased, caused by excessive loss of metabolic acids o Vomiting, GI suctioning, excessive bicarb intake, hyperaldosteronism, diuretictherapy o Compensated by rate and depth of ventilation is decreased causing retention ofCO
- Respiratory acidosis : decreased alveolar ventilation, increased CO2 retention o Causes: depression of the respiratory center, paralysis of respiratory muscles,disorders of the chest wall, COPD, pulmonary edema o S/S: headache, restlessness, blurred vision, lethargy, muscle twitching, tremors,convulsions, coma
- Respiratory alkalosis: alveolar hyperventilation, excessive reduction in CO - How do you determine if compensation is occurring? What does compensationmean? o Both Carbon dioxide and bicarb levels are not within normal range but pH is in normal range. Either the lungs or the kidneys are able to compensate to help theother system function normally - Understand how the renal and respiratory systems compensate for imbalances. o The kidney regulates HCO3- by ▪ 1. Reabsorption of virtually all of the filtered HCO3- by the proximaltubule ▪ Can reabsorb bicarbonate or regenerate new bicarbonate from CO2and water ▪ Not as rapid as the lungs ▪ 2. Renal excretion of hydrogen ion ▪ Producing more acidic or more alkaline urine (hours to days) o The lungs regulate CO2 by ▪ Exhaling CO2 and leaving water ▪ Increasing or decreasing ventilation (minutes to hours **Explain the neuronal discharge?
- What do afferent, efferent and interneurons do?**
