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Patho Midterm 1

pathophysiology the study of the underlying changes in body physiology that results from or is caused by disease or injury.
etiology cause of disease
idiopathic disease of unknown cause
iatrogenic disease as a result of medical/surgical treatment
nosocomial disease that results from being in a hospital environment
diagnosis naming or identification of a disease
clinical manifestations evidence of disease
sign objective alterations that can be observed or measured by another person
symptom subjective experience by the patient
prognosis expected outcome of a disease
acute disease sudden appearance of signs or symptoms of disease(short time period)
chronic disease slow development, long time period of signs or symptoms of disease
remissions periods when symptoms disappear or diminsh significantly
exacerbations periods when symptoms are much worse/severe
complication onset of another disease in a person who is already coping with a pre-existing disease
sequelae unwanted outcomes of having disease or result of trauma
prodrome/prodromal period time(usually at illness start) when patient has vague symptoms before onset of specific disease signs and symptoms
insidious slow, vague, nonspecific feelings of change in the body
latent period time during which no symptoms are apparent, but disease is present
syndrome group of symptoms and/or signs that occur together that may be caused by interrelated problems or a specific disease
disorder abnormality of function
risk factors/predisposing factors increase probability that disease will occur (but are not causes)
precipitating factor a condition or event that causes a pathologic event or disorder
purpose of DNA synthesis of proteins- genetic code
mutation any alteration of genetic material
pyrimidines cytosine and thymine
purines adenine and guanine
transcription RNA is synthesized from the DNA template, results in formation of mRNA, RNA Polymerase binds to promoter and txn continues until termination sequence
translation process by which RNA directs the synthesis of a polypeptide
Chromosomes condensed DNA and protein(chromatin) into dark staining organelles. Contain genes
genes basic units of inheritance
somatic cells all cells besides gametes. Contain 46 chromosomes(23 pairs). Diploid Cells
Gametes sperm and egg cells. Contain 23 chromosomes. Haploid Cells. Contain one member of each chromosome pair
autosomes the first 22 of the 23 pairs of chromosomes in males and females. Homologous
Homologous Chromosomes identical chromosomes
sex chromosomes remaining pair of chromosomes(23rd pair). In females it is XX and in males it is XY
karyotype ordered display of chromosomes
Euploid Cells have a multiple of the normal number of chromosomes
Polyploid Cell when a euploid cell has more than the diploid number
Triploidy a zygote having 3 copies of each chromosome (69 total) - polyploid
tetraploidy a zygote having 4 copies of each chromosome (92 total)- polyploid
aneuploidy a somatic cell that does not contain a multiple of 23 chromosomes
Trisomy a cell containing 3 copies of one chromosome
monosomy presence of only one copy of any chromosome (lethal)
nondisjunction Failure of homologous chromosomes or sister chromatids to seperate normally during meiosis or mitosis. Usually the cause of aneuploidy
partial trisomy only an extra portion of a chromosome is present in each cell
chromosomal mosaics trisomies occurring only in some cells of the body
Down Syndrome Trisomy 21. Mentally retarded, low nasal bridge, epicanthal folds, protruding tongue, poor muscle tone
Trisomy X female that has 3 X chromosomes. "Metafemales". Variable symptoms: sterility, menstrual irregularity, mental retardation
Turner Syndrome females with only one X chromosome. Absence of ovaries, sterile, short stature, webbed neck. edema, underdeveloped breasts, wide nipples, usually inherited from mother
Klinefelter Syndrome At least 2 X's and one Y. Can be XXY or XXXY. Male appearance, female like breasts, small testes, sparse body hair, long limbs
Cri du Chat Syndrome rare genetic disorder. Deletion of short arm of chromosome 5. Low birth weight, mental retardation, microcephaly
deletions broken chromosomes and lost DNA
fragile sites areas on chromosomes that develop distinctive breaks or gaps when cells are cultured
fragile X syndrome fragile site on long arm of the X chromosome. Associated with mental retardation. Higher incidence in males b/c they dont have another X to compensate. Females can be carriers. Caused by CGG repeats
genetics mechanisms by which an individuals set of paired chromosomes produces traits
locus position of a gene along a chromosome
allele a different form of a particular gene at a given locus
homozygous loci on a pair of chromosomes have identical genes/alleles
heterozygous loci on a pair of chromosomes have different genes/alleles
genotype the genetic makeup of an organism. "What the have"
phenotype the observable, detectable, or outward appearance of the genetics of an organism. "What they demonstrate"
dominant allele Allele with observable effects in a heterozygote. Capital Letter
recessive allele Allele with hidden effects in a heterozygote. Lowercase Letter.
carrier an individual who has a disease gene but is phenotypically normal
pedigrees summarizes family relationships and shows which members of a family are affected by a genetic disease
proband first person in the family diagnosed or seen in a clinic
autosomal dominant disorder abnormal allele is dominant, normal allele is recessive, and the genes exist on a pair of autosomes
recurrence risk the probability that parents of a child with a genetic disease will have yet another child with the same disease. Same for each subsequent child
penetrance the percentage of individuals with a specific genotype who also express the expected phenotype
expressivity variation in a phenotype associated with a particular genotype
autosomal recessive disorder abnormal allele is recesssive and a person must be homozygous for the abnormal trait to express the disease
Sex Linked(X-linked) disorders usually expressed in males because females have other X to mask abnormal gene. Recessive. Males have only one X chromosome so they are hemizygous for genes on the X chromosome. If they inherit a recessive gene, on Xm he will be affected
polygenic variation in traits caused by the effects of multiple genes
multifactorial trait variation in traits caused by genetic and environmental or lifestyle factors
quantitative traits traits that are measured on a continuous numeric scale
5 types of adaptations atrophy, hypertrophy, hyperplasia, metaplasia, dysplasia
atrophy decrease or shrinkage in cellular size(can lead to entire organ shrinkage). Most common in skeletal muscle, heart, secondary sex organs, brain.
physiologic atrophy occurs with early development (ex. thymus glad during childhood)
pathologic atrophy occurs as a result of decreases in workload, pressure, use, blood supply, nutrition, hormones, and nervous stimulation
hypertrophy increase in size of cells (and affected organ); most common in heart and kidneys. Due to protein accumulation
triggers for hypertrophy 1) Mechanical- stretch 2) Trophic- growth factors, hormones, vasoactive agents
physiologic hypertrophy occurs in response to heavy work; diminishes with lighter workload. Occurs when kidney adapts to removal of part of damaged kidney and during pregnancy with mammary glands and uterus
pathologic hypertrophy example is in the heart due to hypertension
hyperplasia increase in number of cells resulting form an increased rate of cellular division
Compensatory Hyperplasia (Physiologic) enables certain organs to regenerate . example is regeneration of liver cells.
Hormonal Hyperplasia(Physiologic) occurs chiefly in estrogen dependent organs such as uterus and breast. Hyperplasia(along with hypertrophy) allows these to enlarge.
Pathologic Hyperplasia abnormal proliferation of normal cells, usually in response to excessive hormonal stimulation or growth factors on target cells
dysplasia abnormal changes in the size, shape, and organization of mature cells; not a true adaptive process, often occurs in epithelial tissue of the cervix and respiratory tract
metaplasia reversible replacement of one mature cell type by another, sometimes less differentiated cell type.
cellular injury occurs if the cell is unable to maintain homeostasis. Can be reversible/recovery or irreversible/death.
4 common biochemical themes of cell injury ATP depletion, oxygen and oxygen-derived free radicals, calcium alterations, defects in membrane permeability
ATP depletion loss of mitochondrial ATP and decreased ATP synthesis; results in cellular swelling, decreased protein synthesis, decreased membrane transport, lipogenesis, loss of integrity of plasma membrane
Oxygen and Oxygen derived free radicals lack of oxygen leads to injury, free radicals(O2-,H2O2, OH.) cause destruction of cell membrane/structure
Calcium Alterations normally intracellular Ca concentrations are low; ischemia and chemicals cause an increase in cytosolic Ca++ concentrations. Causes intracellular damage
Defects in membrane permeability early loss of selective membrane permeability is found in all forms of cell injury
3 common forms of cell injury Hypoxia, free radicals/reactive oxygen species injury, chemical injury
hypoxia lack of sufficient oxygen; single most common cause of cell injury
ischemia reduced blood supply, not enough oxygen
anoxia total lack of oxygen
Cellular Responses to Hypoxic Injury decrease in ATP production, increased anaerobic metabolism, decreased glycogen, failure of sodium potassium pump and sodium calcium exchange, cellular swelling vacuolation, damage to membrane
Free Radicals/Reactive Oxygen Species Injury (oxidative stress) occurs when excess ROS overwhelms endogenous antioxidant systems. Cause damage by lipid peroxidation, membrane damage, increased permeability, attacking proteins, fragmenting DNA, and damaging mitochondria
free radical electrically uncharged atom or group of atoms that has an unpaired electron. To stabilize, they give up or steal an electron. When the attacked molecule loses its electron, it becomes a free radical. Hard to control
antioxidants SOD, glutathione peroxidase, catalase, vitamin E. ROS overwhelm them
chemical injury biochemical interaction between toxic substance and the cell's plasma membrane(leads to increased permeability); CCl4, lead, CO, ethanol, mercury, drugs
lead a heavy metal in the environment, hazardous mostly for children and pregnant mothers; affects nervous system, hematopoietic system, and kidneys.
effects of lead Alters calcium, interferes neurotransmitters, inhibits enzymes involved in hemoglobin synthesis, causes anemia, convulsions, delirium, paralysis, nausea, weight loss, etc
carbon monoxide odorless, colorless, undetectable gas produced by incomplete combustion of fuels. Produces hypoxic injury- affinity for hemoglobin is higher than oxygen so oxygen cant bind
ethanol causes nutritional disorders and liver injury
4 Unintentional and Intentional Injuries blunt force injuries, sharp force injuries, gunshot wounds, asphyxial injuries
blunt force injuries application of mechanical energy to the body resulting in the tearing, shearing, or crushing of tissues
contusion bruise; bleeding into skin or underlying tissues as a result of a blow that squeezes or crushes the soft tissues and ruptures blood vessels without breaking the skin. Color changes (red/purple->blue/black-> yellow/green/brow) reflect healing process
hematoma collection of blood in soft tissue or an enclosed space
subdural hematoma collection of blood between inner surface of dura mater and brain resulting in shearing of small veins that bridge the subdural space
epidural hematoma collection of blood between inner surface of the skull and the dura. Caused by a torn artery
abrasion scrape; results from removal of the superficial layers of skin that was caused by friction between skin and injuring object
laceration tear or rip resulting when the tensile strength of the skin or tissue is exceeded. Jagged or irregular
avulsion wide area of tissue pulled away, creating a large skin flap
sharp force injuries cutting and piercing injuries
incised wound cut that is longer than it is deep. sharp, distinct edges without abrasion
stab wounds a penetrating sharp force injury that is deeper than it is long; depths of wound are clean and distinct, no underlying or associated crush injury; a lot of internal bleeding
puncture wounds caused by instruments or objects with sharp points but without sharp edges
chopping wounds combo of sharp and blunt force; axes, hatchets, etc
gunshot wounds can be penetrating(bullet retained in body) or perforating(bullet exits)
contact range entrance wounds occur when gun is held so the muzzle rests on or presses into the skin surface
blowback occur in hard contact wounds of the head; gas and explosive energy sent into wound causes severe tearing and disruption of tissues, giving the wound a large, gaping and jagged appearance
muzzle imprint patterned abrasion that mirrors the features of the weapon
intermediate range entrance wound surrounded by gunpowder tattooing or stippling
indeterminate range entrance wound occurs when the only thing striking the body is the bullet
exit wounds shape can be round or slit like to completely irregular
ashpyxial injuries caused by failure of cells to receive or use oxygen
suffocation oxygen failing to reach the blood; results from lack of oxygen in environment or blockage of airways. Includes choking asphyxiation- obstruction of internal airways
strangulation caused by compression and closure of the blood vessels and air passages resulting from external pressure on the neck; results in stop of blood flow to brain; hanging, ligature, manual strangulation
chemical asphyxiants cyanide and hydrogen sulfide
drowning alteration of oxygen delivery to tissues resulting from breathing of fluid/water.
dry lung drowning in as many as 15% of drownings, little or no water enters lungs because of vagal nerve mediated laryngospasms
Infectious injury when a microorganism has disease producing potential(can invade and destroy cells, produce toxins and produce hypersensitivity reactions)
Immunologic and Inflammatory Injury cellular membranes are injured by direct contact with cellular and chemical components of the immune and inflammatory responses
complement responsible for many of membrane alterations that occur during immunologic injury (causes leakage of K+ out of cell and rapid influx of water)
cellular accumulations(infiltrations) occur in normal and injured cells;WATER, lipids, carbs, glycogen, proteins, etc
cellular swelling most common degenerative change;caused by shift of extracellular water into cells.(Hypoxia-> decreased ATP->Na and water move into cell and K diffuses out-> increased osmotic pressure->more water moves into cell->vacuolation->ONCOSIS/VACUOLAR DEGENERATION
hemosiderin yellow brown pigment derived from hemoglobin. How iron is stored in tissue cells when iron levels are high.
hemosiderin accumulation accumulates in areas of bruising and hemorrhage and in lungs and spleen after congestion from heart failure. Skin appears red-blue and then lysis of escaped rbcs occurs, causing hemoglobin to be transformed to hemosiderin
calcium accumulation causes cellular calcification- influx of extracellular calcium in injured mitochondria. Also can be caused by excretion of acid which leads to OH- ions which leads to precipitation of calcium hydroxide and hydroxyapatite
dystrophic calcification occurs in dying and dead tissue
metastatic calcification consists of mineral deposits that occur in undamaged normal tissues as a result of hypercalcemia
necrosis cellular death leading to cellular dissolution; the sum of cellular changes after local cell death and the process of cellular self digestion
autolysis process of cellular self digestion known as autodigestion
karyolyisis nuclear dissolution and chromatin lysis
pyknosis nucleus shrinks and becomes a small dense mass of genetic material
karyorrhexis fragmentation of the nucleus into smaller particles or "nuclear dust"
4 major types of necrosis + 2 other types coagulative, liquefactive, caseous, fatty, gangrenous,gas gangrene
coagulative necrosis occurs in kidneys, heart, and adrenal glands; commonly results from hypoxia caused by ischemia or chemical injury,; caused by PROTEIN DENATURATION
liquefactive necrosis commonly results from ischemic injury to neurons and glial cells in the brain. Brain cells are rich in digestive hydrolytic enzymes and lipids. The cells are digested by their own hydrolases. Tissue becomes soft, liquefies, walled off from healthy tissue.
caseous necrosis usually results from tuberculosis pulmonary infection. Combination of coagulative and liquefactive necroses. Tissues resemble clumped cheese
fat necrosis cellular dissolution caused by lipases that occur in the breast, pancreas, and abdominal organs. Necrotic tissue appears opaque and chalk white
lipase break down triglycerides, releasing free fatty acids, which combine with calcium, magnesium and sodium ions, creating soaps(saponification)
gangrenous necrosis death of tissue from sever hypoxic injury (b/c of arteriosclerosis, blockage of arteries) usually in lower leg
dry gangrene usually the result of coagulative necrosis. skin becomes dry and shrinks, color changes to dark brown or black
wet gangrene develops when neutrophils invade site, causing liquefactive necrosis. Ususally occurs in internal organs. Site becomes cold, swollen, black, foul odor,
gas gangrene special type of gangrene caused by infection of injured tissue by Clostridium sp. Death caused by shock
Clostridium anaerobic bacteria that produce hydrolytic enzymes and toxins that destroy connective tissue and cellular membranes and cause bubbles of gas to form in muscle soft tissue.
apoptosis "dropping off"; programmed cellular death. Affects scattered, single cells
physiologic apoptosis important in development of body tissue
pathologic apoptosis result of intracellular events or adverse exogenous stimuli (example: viral hepatitis induces apoptosis). Includes increase in apoptosis or the absence of apoptosis(leads to proliferation/accumulation of cells)
characteristics of cellular aging atrophy, decreased function, loss of cells, .
tissue and systemic aging progressive stiffness and rigidity, sarcopenia(loss of skeletal muscle mass and strength)
frailty mobility, balance, muscle strength, motor activity, cognition, nutrition, endurance, falls, fractures, bone density
somatic death death of an entire person. followed by postmortem changes
algor mortis postmortem reduction of body temperature
livor mortis pooling of blood in most dependent/lowest tissues which develop a purple discoloration
rigor mortis without ATP, detachment of myosin from actin is compromised and the muscles remain in a contracted position
postmortem autolysis release of enzymes and lytic dissolution
total body water the sum of fluids within all body compartments
intracellular fluid all the fluid within cells (2/3 of TBW and 40% of body weight)
extracellular fluid all the fluid outside the cells; interstitial fluid and intravascular fluid (1/3 of TBW and 20% of body weight)
interstitial fluid between cells an outside blood vessels(15% of body weight)
intravascular fluid blood plasma(5% of body weight)
effect on aging to TBW elderly have less TBW because of increase adipose tissue/decrease muscle mass, renal decline results in less retention of water and diminished thirst perception leads to dehydration
antidiuretic hormone secreted by the posterior pituitary gland in response to increased osmolality, decreased blood volume, or decreased blood pressure. Increases water retention by the kidney
osmoreceptors stimulated by hyperosmolality. Stimulate thirst and signals posterior pituitary to release ADH
baroreceptors nerve endings that are sensitive to changes in volume and pressure. When there is a decrease in blood volume and blood pressure, they stimulate ADH
Sodium accounts for 90% of the ECF cations. Regulates extracellular osmotic forces and regulates water balance
Chloride the major anion in the ECF and provides electroneutrality in relation to sodium. Passive transport following active transport of sodium. Maintains acidity of gastric secretions
aldosterone a mineralocorticoid secreted form the adrenal cortex that increases the reabsorption of sodium and the secretion of potassium.
RAA Mechanism(Renin Angiotensin Aldosterone) When blood volume and bp are reduced Renin is secreted by kidney, combines with angiotensinogen to make Angiotensin I. Angiotensin I is converted to Angiotensin II in the lungs by ACE. Angiotensin II stimulates vasoconstriction and stimulates aldosterone
Atrial Natriuretic Factor functions in renal elimination of sodium to control sodium and water balance. Blocks the effects of aldosterone. Also reduces blood pressure.
Hypovolemia fluid volume deficit; fluid loss, reduced fluid intake, fluid shift out of vascular space(3rd spacing). Caused by hemmorhage, polyuria, vomiting, diarrhea, fistulas, fever, nasogastric suctioning, etc
1 L of water lost is equal to ??? lbs 2.2 lbs is equal to ??? L of water lost
detecting dehydration thirst, poor skin turgor, dry mucous membranes, tachycardia, weak pulse, postural hypotension. shock, decreased urinary output, elevated hematocrit and serum sodium, skin tenting,
electrolytes substances whose molecules dissociate into ions when placed in water
simple diffusion movement of molecules from areas of high concentration to areas of low concentration; requires no external energy.
facilitated diffusion movement of molecules from areas of high concentration to low concentration; combine with a carrier molecule. Passive(requires no external energy)
active transport passage of ions or molecules across a cell membrane by an energy consuming pricess ; takes place against an electrochemical gradient(low-->high). Example: sodium potassium pump
osmosis movement of fluid through a semipermeable membrane; from area of low solute concentration to area of higher solute concentration until equilibrium is reached. Requires no external energy. Stops when conc. differences disappear or hydrostatic pressure inc.
osmolality osmotic force of solute per unit weight of solvent (describes fluids inside the body)
osmolarity total milliosmoles of solute per unit of total volume of solution (describes fluids outside of the body)
isotonic/iso-osmolar solutions have same osmotic pressure as blood (same amount of solutes); Normal Saline (0.9%), Lactated Ringers Solution, 5% dextrose in water(D5W).
hypotonic/hypo-osmolar solution lower osmotic pressure than blood/fewer solutes; 1/2 normal saline(.45% NaCl) or 2.5% dextrose in water (D2.5W)--> fluid moves into cell to compensate
hypertonic/hyper-osmolar solution higher osmotic pressure than blood/more solutes; hypertonic saline (>5% NaCl), 5% dextrose in NS(D5NS) or 5% dextrose in lactated Ringers solution (D5LR).-->fluid moves out of cell to compensate
hydrostatic pressure force within a fluid compartment that pushes water out. "pushes"
oncotic pressure (colloidal osmotic pressure) osmotic pressure from colloids in solution. Wants to keep water inside. "pulls"
What pushes water out of capillaries? capillary hydrostatic pressure and interstitial oncotic pressure
What pulls water into capillaries? plasma oncotic pressure and interstitial hydrostatic pressure
filtration movement of water and solutes by forces of pressure
forces favoring filtration capillary hydrostatic pressure and interstitial oncotic pressure
forces favoring reabsorption plasma oncotic pressure and interstitial hydrostatic pressure
edema accumulation of fluid in the interstitial spaces. Caused by an increase in plasma hydrostatic pressure, lowering of plasma oncotic pressure, increased capillary membrane permeability, and lymphatic channel obstruction.
symptoms of edema weight gain, swelling, puffiness, limited movement of affected joints, pitting of skin when pressed,
second spacing abnormal accumulation of interstitial fluid (edema)
third spacing fluid accumulation trapped and unavailable for functional use (ascites and edema associated with burns)
ascites accumulation of fluid in the peritoneal space
hypothalamus contains osmoreceptors that sense increases in plasma osmolality. Stimulates thirst and ADH release (ADH is syntehsized here)
Pituitary region releases ADH in response to increased plasma osmolality, decrease in blood volume, stress, nausea, nicotine, morphine
Syndrome of Inappropriate Antidiuretic Hormone Secretion occurs when factors other than hyperosmolality or hypovolemia stimulate secretion of ADH. Causes water to be retained in excess (decrease renal excretion of water)
Renal Regulation (function of kidneys) primary organ for regulating fluid and electrolytes, ADH and aldosterone work on its tubules, impairment causes edema, potassium and phosphorus retention, acidosis
ways of losing water vaporization from lungs and skin, increased body temp/exercise, excessive sweating
hypovolemia fluid volume deficit; fluid loss, reduced fluid intake, fluid shift out of vascular space(3rd spacing). Caused by hemmorhage, polyuria, vomiting, diarrhea, fistulas, fever, nasogastric suctioning
clinical manifestations of hypovolemia restlessness, drowsiness, lethargy, confusion, thirst, dry mouth, decreased skin turgor, dizziness, postural hypotension, weakness, weight loss, increased respiratory rate, seizures, coma, etc
hypervolemia fluid volume excess; caused by excessive isotonic/hypotonic IV fluids, renal/heart failure, polydipsia, SIADH, etc.
clinical manifestations of hypervolemia headache, confusion, lethargy, peripheral edema, distended neck veins, bounding pulse, increased BP and CVP, polyuria, muscle spasms, weight gain, seizures, coma
osmotic pressure pressure needed to oppose the movement of water across the membrane
Hypernatremia excess of serum sodium; caused by a loss of water or a gain in sodium intake. Leads to cellular dehydration.
Causes of hypernatremia deficiency in synthesis/release of ADH, decrease in kidney response to ADH, primary aldosteronism, too rapid infusion of hypertonic saline, sodium bicarb, or isotonic saline, drinking salt water, high salt intake, diarrhea, diabetes insipidus, dehydration
clinical manifestations of hypernatremia intracellular dehydration, convulsions, pulmonary edema, hypotension, tachycardia, etc. Thirst, fever, dry mucous membranes, restlessness
Treating Acute Hypernatremia if it occurs in a period of 48 hours or less, correct it rapidly
Treating chronic hypernatremia corrected more slowly due to risks of brain edema( if extracellular tonicity is decreased to quickly, water will move into brain cells)
Hyponatremia deficit of serum sodium; cause plasma hypo-osmolalty and cellular swelling
Dilutional Hyponatremia occur when proportion of TBW to total body sodium is excessive
Hypo-osmolar Hyponatremia When renal excretion of water is impaired and TBW and sodium are increased, but the retention of water exceeds increase in sodium
Hypertonic Hyponatremia increases in plasma lipids and proteins displace water volume and decrease sodium concentration(hyperglycemia attracts ICF and increase in ECF dilutes concentration of sodium)
clinical manifestatins of hyponatremia decreased osmolality, free water excess, ECF goes into cells and causes hypovolemia, free water excess can also cause hypervolemia/water intoxication; lethargy, confusion, decreased reflexes, seizures, coma
causes of hyponatremia excessive diuresis, excessive sweating, GI loss, adrenocortical insufficiency, excess IV fluids, SIADH
Hyperchloremia excess of chloride, occurs with hypernatremia or deficit in bicarbonate. Manifestations include metabolic acidosis, stupor, deep rapid respirations, weakness, coma
hypochloremia deficit in serum chloride, result of hyponatremia or elevated bicarbonate. Develops as a result of vomiting and loss of HCL. Manifestations include metabolic alkalosis, muscle hypertonicity, depressed respirations, tetany
potassium major intracellular cation. regulates intracellular osmolality, excreted by kidneys, concentration maintained by Na+/K+ pump, regulate intracellular electrical neutrality, essential for action potentials, normal cardiac rhythm, muscle contraction
things that affect potassium levels changes in pH(H+ ions accumulate in ICF during acidosis. K+ shifts out to balance), aldosterone, insulin, epinephrine, alkalosis(all make K+ move into cells)
hyperkalemia elevation of ECF potassium above 5.5 mEq/L.
causes of hyperkalemia increased intake of K+, shift of K+ from the ICF to the ECF, decreased renal secretion, insulin deficiency, or cell trauma
ECG changes with hyperkalemia tall peaked T wave, wide QRS complex, ventricular fibrillation, cardiac arrest
clinical manifestations of hyperkalemia mild: neuromuscular irritability; severe:cell cant repolarize, muscle weakness, loss of muscle tone, flaccid paralysis
hypokalemia decrease in the ECF potassium concentration below 3.5 mEq/L.
causes of hypokalemia reduced intake of potassium, increased intracellular entry of potassium, increased loss of potassium, alcoholism, alkalosis, DIURETICS/ PROLONGED VOMITING/DIARRHEA, aldosterone, laxative abuse, etc.--> K+ shifts from ECF to ICF
ECG changes with hypokalemia flattened T wave, prolonged PR interval, large U wave
clinical manifestations of hypokalemia decrease in neuromuscular excitability, skeletal muscle weakness, smooth muscle atony, and cardiac dysrhythmias
calcium essential cation, widely distributed, 99% is found in bone as hydroxyapatite, necessary for bone, clotting, hormone secretions, neuromuscular function, muscle contraction, maintenance of membrane permeability
parathyroid hormone released by low serum Ca2+ (raises Calcium levels in blood--> stimulates bone to release Ca). Also helps excrete phosphate.
calcitonin stimulated by high serum Ca2+(lower calcium levels in blood--> stimulates take up of Ca by bones)
vitamin D reabsorbs Ca2+ from GI tract
hypercalcemia excess of serum calcium. Increases the block of Na+ into cell
causes of hypercalcemia hyperparathyroidism, cancer, vitamin D overdose, hypophosphatemia, thyrotoxicosis, acromegaly, renal failure
clinical manifestations of hypercalcemia decreased neuromuscular excitability, muscle weakness, cardiac arrest, constipation, kidney stones, anorexia, nausea, vomiting, decrease in heart rate, confusion
hypocalcemia deficit of serum calcium. Decreases block of Na+ into cell
causes of hypocalcemia hypoparathyroidism, hyperphosphatemia, vitamin D deficiency, hypoalbuminemia
manifestations of hypocalcemia numbness, muscle crams, increased neuromuscular excitability, weakness, hypotension, Chvostek and Trousseaus signs, tetany, seizures, emotional instability, etc
chvostek's sign contraction of facial muscles in response to light tap over the facial nerve in front of ear
trousseau's sign carpal spasm induced by inflating a blood pressure cuff above systolic pressure for a few minutes
Calcium's relationship to Phosphate inverse relationship; if concentration of one increases, the other decreases
phosphate major intracellular anion, essential to muscle function, RBCs, and nervous system; most is located in bone. Needed for ATP.
pH the inverse logarithm of the H+ concentration; ranges from 0-14. H+ high means low pH(acidic) and H+ low means high pH(basic)
3 organs involved in regulation of acid base balance bones, lungs, kidneys
pH of blood 7.35-7.45
functions of acids byproducts of energy metabolism(carbonic acid, lactic acid), digestion(HCl), food for brain(ketoacids)
volatile acid carbonic acid (H2CO3); can be eliminated as CO2
nonvolatile acid lactic acid, sulfuric, phosphoric acids; eliminated through kidneys
An increase in CO2 will cause: increase in CO2, increase in H+, increase in bicarbonate
buffer absorb excessive hydrogen (H+) or hydroxyl (OH-) and prevent significnant change in pH.
important buffering systems carbonic acid- bicarbonate system and hemoglobin
carbonic acid bicarbonate buffer system CO2+H2O<-->H2CO3<-->H+ + HCO3- . The greater the partial pressure of carbon dioxide, the more carbonic acid is formed.
respiratory acidosis increased pCO2, increased carbonic acid, increased H+(low pH), increased bicarbonate. Result of ventilation depression
respiratory alkalosis decreased pCO2, decreased carbonic acid, decreased H+(high pH), decreased bicarbonate. Result of hyperventilation
metabolic acidosis increased levels of ketoacids, lactic acid. Decreased bicarbonate levels, increased H+(low pH)--> heavier breathing causes decreased pCO2
metabolic alkalosis decreased H+ levels, increased bicarbonate levels--> lighter breathing causes increased pCO2
compensations renal and respiratory adjustments to changes in pH . (Production of acidic or alkaline urine, or change in ventilation)
protein buffering proteins have negative charges, so they can serve as buffers for H+
renal buffering secretion of H+ in the urine and reabsorption of HCO3-
cellular ion exchange exchange of K+ for H+ in acidosis and alkalosis
anion gap the difference between the plasma concentration of major cation (Na+) and sum of measured anions (Cl- and HCO3-). Represents concentration of unmeasured anions. Na- (Cl+HCO3-). Normal is 8-12. Increased in lactic acidosis, ketoacidosis
Abnormal anion gap (indications) abnormal anion gap is a result of an increased level of an abnormal unmeasured anion. Examples: diabetic ketoacidosis, lactic acidosis
Respiratory System as regulator of acid base balance eliminates CO2, medulla controls breathing. Increased respirations lead to decreased CO2(hyperventilations).
Renal System as a regulator of acid base balance eliminates H+ and reabsorbs HCO3-. Also reabsorbs/secretes electrolytes. Kidneys decrease/increase urine pH
Respiratory Acid base Imbalances affect carbonic acid concentration (CO2)
metabolic acid base imbalances affect bicarbonate
Respiratory Acidosis Causes hypoventilation(slow breathing gives a carbonic acid/CO2 excess), respiratory failure(raises CO2)
Respiratory Acidosis Compensation kidneys conserve HCO3- and secrete H+ into urine(metabolic alkalosis)
Respiratory Alkalosis Causes hyperventilation(causes deficit in carbonic acid/CO2), hypoxemia from acute pulmonary disorders
Respiratory Alkalosis Compensation rarely occurs due to aggressive treatment of causes of hypoxemia.
Metabolic Acidosis Causes bicarbonate deficit caused by ketoacidosis, lactic acid accumulation, severe diarrhea, kidney disease
Metabolic Acidosis Compensation increased CO2 excretion by lungs (respiratory alkalosis)
Metabolic Alkalosis Causes bicarbonate excess caused by prolonged vomiting and gain of HCO3-
Metabolic Alkalosis Compensation decreased respiratory rate to increase CO2, renal excretion of HCO3-(respiratory acidosis)
main sign of dehydration weight loss (1 L=1 kg=2.2 lbs)
Diagnostic criteria for dehydration a BUN/creatine ratio of >25:1,OR orthostasis, OR a pulse of >100 beats/minute, OR a pulse change of 10-20 beats/minabove baseline with a change in position
orthostasis drop in systolic BP >20 mmHg upon a change of position
Hypertonic Dehydration primarily fluid deficit; more water than salt is being lost
Hypotonic Dehydration primarily sodium deficit; more salt than water is being lost
isotonic Dehydration combined water and sodium deficit; both salt and water are lost proportionately
formula for fluid replacement therapy in hypernatremia calculate free water deficit: .6 x body weight(kg) x [(plasma Na/140) -1] OR Change in serum sodium= (infusate sodium-serum sodium)/(TBW+1)
electrolytes lab tests usually provides info about serum Na, K, Cl, HCO3-
BUN and Cr lab tests indication of renal perfusion; elevated BUN reflects intravascular depletion; Cr indicates acute renal failure
CBC lab test info on hemoconcentration secondary to dehydration; WBCs and differential indicators of infection; platelets can elevate as acute phase reactants
UA lab test specific gravity of urine related to hydration state; in renal disease, can help classify condition; urine ions aid in determining if Na is being retained or not
total protein lab test indirect measures of live function, dietary protein intake, and renal loss.
arterial blood gas test aids in classification of acidosis and alkalosis. Give info on bicarbonate levels
Interpretation of ABGs (5 steps) 1) evaluate pH (tells you if its alkalosis or acidosis). 2) Analyze pCO2. 3) Analyze HCO3-. 4) Determine if CO2 or HCO3- matches the pH alteration (respiratory vs. metabolic). 5) Decide if the body is trying to compensate (is pH normal or not?)
ROME Respiratory Opposite= up pH down CO2(alkalosis) and down pH up CO2(acidosis). Metabolic equal= up pH up CO2 (alkalosis) and down pH down CO2(acidosis)
partial compensation after HOURS of acid bas imbalance, the lungs or kidneys will try to bring pH back to normal. ALL parameters will be outside of normal range
full compensation after days or months of untreated acid base imbalance, the pH will be back to normal range, but all other parameters will be abnormal
acidemia more acidic than normal (pH is acidic compared to normal pH of 7.4 but pH still doesnt tell us if it is a respiratory or a metabolic problem)
bicarbonate levels as an indicator for acid base imbalance bicarbonate levels measure metabolic acidosis when a patient has no respiratory abnormality
alkalemia more basic than normal (when the pH rises above 7.45)
Created by: alexadianna