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NURS 5315 Advanced Patho Exam 1
Questions & Answers
Steps of the Action Potential - ANSWERSDepolarization Repolarization Hyperpolarization Depolarization - ANSWERSmovement of the intracellular charge towards zero (more positive charge) Voltage gated Na channels open and allow Na to enter the cell -> voltage inside the cell moves towards zero Repolarization - ANSWERSOnce the intracellular charge reaches zero, the negative polarity of the inside of the cell is restored back to its baseline of -70 to -85 mV -Na channels close, K channels open Hyperpolarization - ANSWERSwhen the cell's resting membrane potential is greater than -85mV. Is less excitable, because there is a greater distance between the resting membrane potential and the threshold potential. In order for the action potential to be sucessful - ANSWERSt has to depolarize by 15- mV (threshold potential) to reach -55 to -65 mV. An alteration in action potential may result from - ANSWERSneurologic diseases, muscle disease or electrolyte imbalances. What is the main protein responsible for maintaining the correct balance of extracellular Na and intracellular K, which is needed for cellular excitation and membrane conductivity. - ANSWERSNa+-K+ ATPase Resting membrane potential - ANSWERSwhen the cell is in a nonexcited state and is at -70 to -85 mV.
Refractory Period - ANSWERSis a period of time during most of the action potential which the cell membrane resists stimulation and it cannot depolarize Absolute refractory period - ANSWERSoccurs when the membrane will not respond to ANY stimulus no matter how strong. Relative Refractory Period - ANSWERSoccurs when the membrane is repolarizing and will only respond to a very strong stimulus. Hyperpolarized - ANSWERSwhen the cell's resting membrane potential is greater than - 85mV. Is less excitable, because there is a greater distance between the resting membrane potential and the threshold potential. Hypopolarized - ANSWERSwhen the cell's resting membrane potential is closer to zero, for instance it is -65mV. Is more excitable because the resting membrane potential is closer to the threshold potential, there is less distance between them. Action potential altered by hypokalemia - ANSWERS(serum outside of cell is low) -Hyperpolarized (cell becomes more negative, ex: -100) -Affects the resting membrane potential of cells -The cell is less likely to depolarize and transmit impulses Can cause a decrease in neuromuscular excitability and leads to weakness, smooth muscle atony, paresthesias, and cardiac dysrhythmias Action potential altered by hyperkalemia - ANSWERSHypopolarized -Also has an effect on the resting membrane potential -If the ECF potassium increases without any change in the ICF potassium levels, the resting membrane potential of the cell becomes more positive. -The cells are more excitable and conduct impulses more easily and more quickly because the resting membrane potential is closer to the threshold potential. Therefore, the person will have peak T waves on EKG. -As potassium rises, the resting membrane potential will continue to become more positive and it will eventually become equal to the threshold potential. As this happens the EKG will show a widening QRS complex. If the resting membrane potential equals the threshold potential, an action potential will not be generated and cardiac standstill will occur. Paralysis and paresthesias may also occur. Action potential altered by hypocalcemia - ANSWERS-Causes an increase in the cell permeability to Na causing a progressive depolarization -Causes the RMP and the TP to be closer to one another & making it easier to initiate an action potential - the cells are more excitable. -Results in tetany, hyperreflexia, circumoral paresthesias, seizures, dysrhythmias
Ex - removal of part of the liver and the cells regenerating, uterine and mammary gland enlargement occur during pregnancy to meet the demands of the increased work load, callus on foot Ex: (Hormonal) Breast and uterine enlargement during pregnancy. Pathological Example of Hyperplasia - ANSWERS-Is an abnormal proliferation of normal cells usually caused by increased hormonal stimulation Ex - endometrial hyperplasia (imbalnce in estrogen & progesterone with increase in estrogen - risk for cancer), Benign prostatic hyperplasia (BPH), thyroid enlargement - thyroid goiters Pathological Example of Hypertrophy - ANSWERSleft ventricular hypertrophy cardiomegaly Physiological Example of Hypertrophy - ANSWERSSkeletal muscle, when a kidney is removed and the other kidney steps in to function as both and increases in size Physiological Example of Atrophy - ANSWERSShrinking of the thymus gland during childhood, uterus decreasing in size after childbirth Disuse - skeletal muscle atrophy that occurs from a person being immobilized or bed ridden for a period of time (arm in a cast, Pathological Example of Atrophy - ANSWERSDecrease in workload, pressure, use, blood supply, nutrition, hormonal stimulation, or nervous stimulation Cellular Injury - ANSWERS-Occurs when the cell is no longer able to maintain homeostasis with the result being disease. May or may not be reversible. This is dependent on the type of cell, level of differentiation, ability to adapt and the type, severity and duration of the injury. Causes of cellular injury - ANSWERShypoxia, free radicals, chemicals, radiation, direct mechanical trauma, genetics, nutrition, infections, immunologic reactions and inflammation. Mechanisms of Cellular Injury - ANSWERS-ATP Depletion -Oxygen and Oxygen derived free radicals -Intracellular Calcium and loss of calcium steady state Cellular Injury (partially ischemia) triggers an increase in - ANSWERSIintracellular calcium -The more damage which is done, the higher the calcium concentration becomes. The elevated calcium level causes damage to the cell membrane. It also causes damage to the intracellular contents by activating enzymes which cause the damage directly.
ATP Depletion - ANSWERSresults from the loss of mitochondrial production of ATP. This contributes to cellular swelling, decreased protein synthesis, and impairs cellular membrane transport systems. All of these changes impair cellular membrane integrity. Oxygen and Oxygen derived free radicals - ANSWERSdecrease oxygen delivery to cells results in the production of activated oxygen species (free radicals, H2O2, NO) which destroy the cell membranes and structures. Most common cause of cellular injury - ANSWERSHypoxic Injury Clinical Manifestations of Hypoxic Injury - ANSWERSReduced ischemia, loss of hemoglobin, diseases, etc. Heart attack, etc Pathophysiology of Hypoxic Injury - ANSWERSIschemia - ↓ mitochondrial oxygenation, ↓ATP, Na-K & Na-Ca pumps fail -> ↑ intracellular Na & Ca -> K to diffuse out of cell -> acute cellular swelling (from ↑ Na in cell), anaerobic glycolysis, ↑Lactate, necrosis Reperfusion Injury - ANSWERSReoxygenation, Tissue transplantation, ischemic syndromes of heart, liver, GI, kidneys, and cerebrum. Clinical Manifestations of Reperfusion Injury - ANSWERSNeutrophils especially affected, causing neutrophil adhesion to endothelium Serious complication in transplantation and ischemic diseases Patho of Reperfusion Injury - ANSWERS-Triggers the production of highly reactive oxygen intermediates (hydroxyl radical & hydrogen peroxide -> cell membrane damage & mitochondrial Ca overload). -WBC function is impaired as result of injury. * Xanthine dehydrogenase -> converts to xanthine oxidate -> creates massive amounts of free radicals, superoxide & hydrogen peroxide -> etc... apoptosis Free Radical - ANSWERSAny molecular species capable of independent existence that contains a single unpaired electron in an outer orbit Highly reactive Clinical Manifestations of Free Radical - ANSWERS-Redox reactions in normal metabolic processes (respiration) -Absorption of extreme energy sources (UV light, radiation) -Enzymatic metabolism of exogenous chemicals, drugs, and pesticides -Process of transition metals (iron, copper) (fenton reaction) -Nitric oxide (NO) acting as an important chemical mediator, colorless gas Reactive Oxygen Species (ROS) - ANSWERS-Chemically reactive molecules from molecular oxygen formed as natural oxidant species in cells during mitochondrial respiration & energy generation. -This form of injury is called oxidative stress
Extracellular changes associated with aging - ANSWERSbinding of collagen, ↑ free radical damage, structural changes of fascia, tendons, ligaments, bones, joints, & development of arteriosclerosis. The extracellular matrix is affected by decreased synthesis and increased degradation of collagen. These changes result in dehydration and wrinkling of the skin. What are the labs that are elevated as we age and are markers of increased risk for morbidity and mortality - ANSWERSInterleukin 6, Interleukin 1, tumor necrosis factor - alpha and C-reactive protein Frailty - ANSWERSis a condition of vulnerability and debility which occurs after one has experienced a health stressor and has not recovered from it completely ETOH in blood metabolizes to - ANSWERSAcetaldehyde in cytoplasm of cell -> Pyruvate to be changed to LA, Oxaloacetate -> malate, this prevents gluconeogenesis -
fasting hypoglycemia. Also Glyceraldehyde-3-phosphate -> glycerol 3- phosphate combines with fatty acides to form triglycerides -> hepatosteatosis. Also ↓ citric acid cycle production of NADH -> utilization of Acetyl-CoA for ketogenesis -> ketoacidosis & lipogenesis -> hepatosteatosis Hepatic Changes in ETOH - ANSWERS(inflammation, deposition of fat, enlargement of liver, interruption of microtubular transport of proteins & their secretions, ↑ intracellular water, ↓ fatty acid oxidation in mitochondria, ↑ membrane rigidity, development of liver necrosis. Ketogenesis - ANSWERSis the formation of ketone bodies and occurs mostly in the mitochondria of the hepatocytes. Occurs as a result of the unavailability of glucose. Role of the Hepatocytes in Ketogenesis - ANSWERSThe major parenchymal cells in the liver: metabolism, detoxification, and protein synthesis Role of the mitochondria in ketogenesis - ANSWERSMembrane-bound cell organelles (mitochondrion, singular) that generate most of the chemical energy needed to power the cell's biochemical reactions. Chemical energy produced by the mitochondria is stored in a small molecule called adenosine triphosphate (ATP) Triggers for ketogenesis - ANSWERSstarvation, lack of glucose Effect on oxaloacetate in ketogenesis - ANSWERS-Is used in gluconeogenesis. During starvation & uncontrolled diabetes, these levels are insufficient bc it is completely used by gluconeogenesis- The depletion of ______________ increases the amount of acetyl-CoA -> acetyl-CoA is processed by hepatocytes -> undergoes transformation to 3 ketone bodies: acetoacetate, acetone, β-hydroxybutyrate = basis for ketoacidosis
Tumor Markers - ANSWERSare substances produced by the cancer cells that are found on tumor plasma membranes or in the blood, spinal fluid, or urine. An elevated tumor marker may suggest a specific diagnosis, but it is not used alone as a definitive diagnosis test. Alpha Fetoprotein (AFP) tumor marker can be found in - ANSWERSliver or germ cell cancers Carcinoembryonic Antigen (CEA) tumor marker can be found in - ANSWERSGI, Pancreatic, Lung, and Breast cancers Beta Human Chorionic Gonadotropin (Beta HCG) tumor marker can be found in - ANSWERSgerm cell cancers or choriocarcinoma Prostate Specific Antigen (PSA) tumor marker can be found in - ANSWERSprostate cancer Benign Tumors - ANSWERSa nonmalignant new growths, slow growing, do not spread locally or to distant sites and are well encapsulated. Malignant Tumors - ANSWERSrapidly growing and poorly differentiated, do not look like the tissue or origin, rapid cell growth, and can metastasize to local tissues or distant sites. Not encapsulated, anaplasia, pleomorphic (various shapes/sizes). Are named after the cell of origin but in addition to the "oma" they have the root words "carcino" or "sarco". Adeno refers to - ANSWERSthe glandular epithelial tissue (deeper epithelial tissue or glands) Carcino- - ANSWERSCancer arising in the epithelial tissue Sarco- - ANSWERSCancers arising from mesenchymal tissue (connective tissue, muscle, bone) Oma- - ANSWERSTumor or Mass Ex: lipoma Carcinoma in Situ - ANSWERSVery early and preinvasive carcinoma of the glandular or squamous epithelial tissue, it has not broken through the basement membrane -blastoma - ANSWERSMalignant tumors of nervous tissues are based on the nerve cell type Site of Metastasis for Lung Cancer - ANSWERSMultiple organs including brain, adrenal glands
-Stop cell division in damaged cells & prevent mutations Known as anti-oncogenes - ANSWERSTumor Suppressor Genes *2 of these genes in each cell must be turned off by the cancer to halt their effects P53 Tumor Suppressor Gene - ANSWERS-monitors cellular stress and activating caretaker genes, maintain integrity of the genome. -Produces proteins that repair damaged or mutated DNA. Controls initiation of cellular senescence (stop cell division), apoptosis, and suppresses cell division until DNA is repaired BRCA gown increases the risk of - ANSWERSovarian, breast, and prostate cancer BRCA gene in men increases risk of - ANSWERSprostate, melanoma, colon, pancreatic, breast cancer Paraneoplastic Syndromes - ANSWERS-Are a constellation of symptoms which are ignited by cancer but are not caused by direct local effects of tumor mass -Typically triggered by the release of substances from a tumor These patients have an increase in apoptosis and impaired ability to regenerate cells - ANSWERSCachexia Is a catabolic process and results in a wasting syndrome - ANSWERSCachexia S/S of Cachexia - ANSWERS-Loss of appetite, cardiac atrophy and dysfunction, gut barrier dysfunction, the release of proinflammatory mediators, release of acute thermogenesis, weight loss and muscle wasting Na is important in maintaining - ANSWERS-Neuromuscular Nerve Impulse Conduction -Acid Base Balance -Cellular Chemical Processes -Cell Membrane Transport Systems Sodium is regulated by - ANSWERSADH, RAAS, Kidneys This type of syndrome is most commonly found in the GI tract or lungs - ANSWERSparaneoplastic syndromes What is responsible for shifting potassium intracellularly - ANSWERSInsulin What shifts potassium extracellularly - ANSWERS-Insulin Deficiency -Aldosterone Deficiency -Acidosis -Strenuous Exercise
Alpha adrenergic antagonists will cause K to shift - ANSWERSinto the cell Beta 2 antagonist (Beta Blockers) causes K to shift - ANSWERSextracellularly Intracellular - ANSWERSAll fluids contained inside the cells by their plasma membrane. Consists of cytosol and fluid in cell nucleus. Interstitial fluid - ANSWERSExtracellular space Tissue space that surrounds cells in body Contains 20% of body water Intravascular - ANSWERSBlood. Mixture of blood cells, colloids and solutes (glucose and ions). It's the fluid inside blood cells and blood plasma. Contains 20% of body water What happens to the BP when fluid moves out of the intravascular compartment - ANSWERSBP drops Intravascular Volume is regulated by - ANSWERShydrostatic pressure and reabsorption by kidneys When excessive fluid accumulates in this space, edema, develops and fluid shifts into brain cells causing high cranial pressure - this is called - ANSWERSinterstitial space Allows for movement of ions, proteins and nutrients across cell barrier. When fluid shifts out of cells, cellular processes slow down or cease from - ANSWERSdehydration Osmolality - ANSWERSThe measure of solute concentration in a solution (Concentration of plasma). Plasma Osmolality value is - ANSWERS280-295 mOsm/kg Osmosis - ANSWERS-Movement of water between compartments from areas of low concentration of solutes to areas of high concentration of solutes (areas of high water to low water). Passive Force -> does not require energy Osmotic Pressure - ANSWERSAmount of pressure or force that is exerted by solute molecules of a compartment. ↑ osmolality = ↑ this This pulling force will pull water into a compartment. This pulling force must be overcome by hydrostatic pressure to oppose osmosis. Hydrostatic Pressure - ANSWERSForce within a fluid compartment - the mechanical force of fluid against the walls of a compartment (blood pressure)
Mechanisms to maintain acid-base balance - ANSWERS-Physiologic (chemical) buffer systems (plasma carbonate, phosphate, hemoglobin, and protein) - 1st line of defense -Respiratory acid-base control - 2nd line of defense -Renal acid-base control - 3rd line of defense Chemical Buffer System - ANSWERSBicarbonate Phosphate Plasma Proteins Hemoglobin Metabolic Acids - ANSWERSCarbonic Acid Lactic Acid Sulfuric Acid Phosphoric Acid Ketone Bodies Carbonic Acid - ANSWERSH2CO Is a byproduct of aerobic metabolism Lactic Acid - ANSWERSByproduct of anaerobic metabolism of glucose Sulfuric Acid - ANSWERSResults from oxidation of sulfur containing aminoacids Phosphoric Acid - ANSWERSResults from metabolism of phosphoproteins and ribonucleotides which are used as an energy source Ketone Bodies - ANSWERSAcids that result from breakdown of fats pH - ANSWERS-Is the measure of the body alkalinity and acidity. -The value is inversely proportional to the concentration of hydrogen ions in the blood. Total Body Weight decreases as we age due to - ANSWERS-Increase in body fat -Decrease in muscle mass -Decrease in ability to regulate sodium and water balance -Decrease in renal function -Elderly are very susceptible to dehydration d/t increased insensible water loss PCO2 - ANSWERS-Measures the partial pressure of arterial CO2 in the blood (dissolved in the blood) and reflects ventilation. -The higher this level is, the faster the respirations are and vice versa. HCO3 - ANSWERS-Is a direct measurement of the amount of bicarbonate in the blood. -It reflects the metabolic component of acid base balances, specifically the kidney.
PaO2 - ANSWERSIs a measure of the partial pressure of arterial O2, which is the amount of oxygen content that is dissolved in the arterial blood. Base Excess/Deficit - ANSWERS-Is a value which is calculated from the pH, PCO2, and the hematocrit. -It represents the amount of anions available for buffering. A negative base excess represents - ANSWERSmetabolic acidosis A positive base excess represents - ANSWERSmetabolic alkalosis or compensation for respiratory acidosis A-a Gradient - ANSWERS-Measures the differences between the alveolar (A) to arterial (a) O2. -It is a calculated value which indicates the difference between alveolar and arterial O content. An elevated A-a gradient can happen in such diseases such as - ANSWERSpulmonary edema, pulmonary fibrosis, and ARDS. Roles of the kidney in maintenance of acid base balance - ANSWERSReabsorption of Bicarbonate Renal Excretion of Hydrogen Excretion of Hydrogen as Ammonium What inhibits HCO3 reabsorption - ANSWERSAcetazolamide (carbonic anhydrase inhibitor): blocks the action of carbonic anhydrase Order of RAAS - ANSWERS-release of renin -renin -> angiotensin -angiotensin -> angiotensin 1 -ACCE converts angiotensin1-> angiotensin II -> causes art VC -> release of aldosterone -> stimulates renal Na reabsorption and K excretion Works opposite of RAAS to decrease blood volume - ANSWERSANP and BNP Natriuretic Hormones -promote urinary excretion of Na and water may be used interchangeably with osmolality - ANSWERStonicity What causes an increase in hydrostatic pressure - ANSWERSvenous obstruction or retention of Na & water what causes a decrease in oncotic pressure and osmotic pressure - ANSWERSdecreased plasma protein production
High pH, high HCO Causes of Metabolic Alkalosis - ANSWERSGastric stomach contents (vomiting or gastric suctioning), diuretic use (thiazide diuretics), diarrhea (laxative abuse), antacid ingestion, excess aldosterone Clinical Manifestations of Metabolic Alkalosis - ANSWERSHypokalemia, hypocalcemia, cardiac arrhythmias from hypokalemia, hypoventilation, and a elevated PCO2, tetany, paresthesias Contraction Alkalosis - ANSWERSResults in an increased production of aldosterone and consequently increased reabsorption of Na+ and HCO3- in the proximal tubule in response to the hypovolemia and hypokalemia. -occurs with diuretic use In order for metabolic alkalosis to occur - ANSWERSa process that causes a rise in serum bicarbonate and a process which prevents the renal excretion of serum bicarbonate must both occur. Respiratory Acidosis - ANSWERSResults from an excess of arterial carbon dioxide (PaCO2), a decrease in alveolar ventilation in relation to the metabolic production of carbon dioxide. Lungs aren't blowing off enough CO2. Causes of Respiratory Acidosis - ANSWERS-Medullary respiratory center depression from opiates, barbiturates, anesthesia, PCO2 retention, or a head injury -Impaired respiratory musculature from Guillain-Barre' syndrome, polio, amyotrophic lateral sclerosis, multiple sclerosis -Airway obstruction aspiration, obstructive sleep apnea, laryngospasm and asthma -Impaired gas exchange from acute respiratory distress syndrome (ARDS), chronic obstructive pulmonary disease, pneumonia and pulmonary edema Clinical Manifestations of Respiratory Acidosis - ANSWERSHypercalcemia, Hyperkalemia, Vasodilation, tremors, disorientation, restlessness, muscle twitching, and seizures, H/A, blurred vision, hypotension Respiratory Alkalosis - ANSWERSResults from a deficiency of PaCO2. Occurs when there is an increase in alveolar hyperventilation - lungs are blowing off too much CO2. Clinical Manifestations of Respiratory Alkalosis - ANSWERSIrritating to the CNS and PNS - neuro s/s: dizziness, confusion, paresthesia's, seizures, and coma Causes of Respiratory Alkalosis - ANSWERSHypoxemia, pulmonary embolism, congestive heart failure, high altitudes, fever, gm negative sepsis, or severe anemia, psychogenic hyperventilation, hepatic failure, salicylate overdose, drugs such as catecholamines, methylphenidate3, nicotine, progesterone, or mechanical ventilation.
Genotype - ANSWERSis a persons genetic composition Actual genes specific to the individual Phenotype - ANSWERSExpression of the gene is a persons observable characteristics Carrier - ANSWERSis a person who has a diseased gene but is phenotypically normal Will a person carrying a recessive diseased allele have s/s of disease - ANSWERSNo DNA is composed of - ANSWERSnucleotides (adenine, thymine, guanine, cytosine) What is the difference is DNA and RNA - ANSWERSRNA contains uracil instead of thyamine Translation - ANSWERSprocess of protein synthesis Transcription - ANSWERSprocess where RNA is formed from DNA and requires the RNA enzyme polymerase Autosomal Chromosomes - ANSWERSall chromosomes which do not have any relation to gender Clastogens - ANSWERSharmful agents which damage chromosomes Ex: radiation Polyploidy - ANSWERSState of having 1/more extra sets of chromosome pairs. E.g. 3 sets of chromosomes, incompatible with life, fetuses are often miscarried. Aneuploidy - ANSWERSAlteration in chromosomal number Results in a Single missing or one extra chromosome. Caused by nondisjunction, failure of chromosomes to divide properly. Uneven number of chromosomes, most are spontaneously aborted. Two main types: monosomy & trisomy Monosomy - ANSWERSstate of having one chromosome in a pair missing Ex: Turner Syndrome Trisomy - ANSWERSstate of having more than two chromosomes to a pair Ex: Down Syndrome (3 chromosomes) Autosomal Aneuploidy - ANSWERSDisorders linked to the first 22 same pair of chromosomes. Ex: Down syndrome - 3 chromosomes on 21st pair
Sex linked chromosome - ANSWERSthe 23rd chromosome that determines sex Autosomal Chromosomes - ANSWERSthe first 22 chromosomes Recessive Allele - ANSWERSCystic fibrosis, 1/25 Caucasians are carriers. Dominant Allele - ANSWERSHuntinton's disease Sex Limited Trait - ANSWERSone that can occur in only one of the sexes, often because of anatomic differences. Uterine & testicular defects. Sex influenced trait - ANSWERSoccurs much more often in one sex than the other. Male pattern baldness, breast cancer. Difference in the transmission of autosomal and sex linked genetic diseases - ANSWERSsex linked - recessive traits males are more affected autosomal - both sexes have equal chances of being affected
