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MARYVILLE PATHO 611 EXAM 1: WUNDERLICH
Terms in this set (71)
Describe the characteristics of apoptosis.
A programmed cell death that is regulated or programmed.
Necrosis: characterized by rapid loss of the plasma membrane structure, organelle swelling, mitochondrial dysfunction. Hypoxia is the #1 major cause of cellular injury leading to necrosis especially to the kidneys and heart. (Myocardial infarction)
Page 52: What's new: Current research supports that after muscle heart injury that stem cells exist in the heart and differentiate into various cardiac cell lineages and is profoundly changing the understanding of myocardial biology!!
Cellular adaptation: Atrophy
Physiologic: thymus gland atrophy (childhood)
Cellular adaptation: Hypertrophy
Increase in size of cell
Another cellular adaptation that can actually be beneficial is hypertrophy of myocardial cells such as an endurance training-this is referred to as physiologic hypertrophy. Versus pathologic hypertrophy that occurs secondary to HTN.
Cellular adaptation: Hyperplasia
Increase in number of cells
Compensatory: removal of 70% off liver-can regenerate in about 2 weeks.
Pathologic: endometrial hyperplasia
Cellular adaptation: Metaplasia
Replacement of cells
Normal columnar ciliated epithelial cells of the bronchial lining have been replaced by stratified squamous epithelial cells. Can be reversed if irritant is stopped.
Cellular metabolism: During ischemia, what effect does the loss of the adenosine triphosphate (ATP) level have on cells?
ATP = energy BUT needs oxygen - aerobic metabolism
A reduction in ATP levels causes the plasma membrane's sodium-phosphate (Na+, K+) pump and sodium-calcium exchange to fail, which leads to an intracellular accumulation of sodium and calcium and diffusion of potassium out of the cell. (The Na+, K+ pump is discussed in chapter one). Sodium and water then can enter the cell freely, and cellular swelling results.
Anaerobic metabolism (glycolysis)
Results when oxygen reserves are depleted.
Free radicals play a major role in the initiation and progression of which diseases?
A free radical is an electrically uncharged atom or group of atoms having an unpaired electron. Having one unpaired electron makes the molecule unstable; thus to stabilize, it gives up an electron to another molecule or steals one. Therefore, it is capable of injurious chemical bond formation with proteins, lipids, carbohydrates—key molecules in membranes and nucleic acids.
Cardiovascular, HTN, IHD. Emerging data indicate that reactive oxygen species play major roles in the initiation and progression of cardiovascular alterations associated with hyperlipidemia, diabetes mellitus, hypertension, ischemic heart disease, and chronic heart failure.
Cellular injury: What is a consequence of leakage of lysosomes during chemical injury?
Lysosomes: Enzymatic digestion of cellular organelles, including the nucleus and nucleolus, ensues, halting synthesis of DNA and ribonucleic acid (RNA).
Ethanol: Liver enzymes metabolize ethanol to acetaldehyde which causes hepatic cellular dysfunction. Peroxisomes helps detoxify ethanol - if not functioning properly the ethanol is turned to Fat in the liver
Deoxyribonucleic acid (DNA)
The cell component most vulnerable to the target of radiation.
Aging and the cell/tissues:
Every physiologic process can be shown to function less efficiently.
Muscular atrophy (Sarcopenia)
o "Stiffness" or "rigidity" of systems:
Peripheral vascular resistance increases.
Decreased production of HCL and delayed emptying of stomach.
Decreased immune response
F & E: Total body potassium concentration also decreases because of decreased cellular mass.
An increased sodium/potassium ratio suggests that the decreased cellular mass is accompanied by an increased extracellular compartment.
Indications of dehydration
Marked water deficit is manifested by S & S of dehydration: headache, thirst, dry skin and mucous membranes, elevated temperature, weight loss, and decreased or concentrated urine. Skin turgor may be normal or decreased. Symptoms/signs of hypovolemia, including tachycardia, weak pulses, dizziness and postural hypotension, may be present.
Thirst: Osmoreceptors are activated by an increase in osmotic pressure of the plasma
Vulnerable populations to FVD:
--Infants: 75-80% TBW
--Obese: fat is water repelling
--Older: thirst sensation is diminished
At the arterial end of capillaries, fluid moves from the intravascular space into the interstitial space because the [fill in the blank]:
...capillary hydrostatic pressure (influenced by the Cardiac system) is higher than the capillary oncotic pressure.
Heavily influenced by plasma proteins.
Low plasma albumin
______ causes edema as a result of a reduction in plasma oncotic pressure.
They decrease blood pressure and increase sodium and water retention. Natriuretic peptides are hormones that include atrial natriuretic peptide (ANP) produced by the myocardial atria, brain natriuretic peptide (BNP) produced by the myocardial ventricles, and urodilatin within the kidney. Natriuretic peptides decrease blood pressure and increase sodium and water excretion. (ANTAGONIST OF THE RAAS)
RAAS - Renin angiotensin-aldosterone system
When circulating blood volume or blood pressure is reduced, renin, an enzyme secreted by the juxtaglomerular cells of the kidney, is released in response to sympathetic nerve stimulation and decreased perfusion of the renal vasculature.
Increase in plasma osmolarity
ADH: Secretion of antidiuretic hormone (ADH) and the perception of thirst are stimulated by an increase in __________
What does Na+ do?
Regulator of fluids; maintenance of neuromuscular irritability for conduction of nerve impulses (134-145)
Clinical manifestations of severe hypernatremia
confusion, convulsions, cerebral hemorrhage, and comma
Water is drawn from the intracellular space to the extravascular space in an effort to restore fluid balance.
BRAIN: The high sodium in the blood vessels pulls water out of brain cells into the blood vessels, causing brain cells to shrink. Cerebral hemorrhage from stretching/contraction of veins.
Manifestations and causes of hyponatremia (less than 135)
Pure sodium deficits: diuretics, vomiting, diarrhea.
Dilutional hyponatremias: hypotonic IV solutions (post-op)
Diseases: Kidney failure, Heart failure; liver failure (ascites)
S & S: headache, lethargy, confusion; seizures, coma
Role of potassium (K+)
Major determinant of the resting membrane potential necessary for transmission of nerve impulses.
The ratio of K + in the ICF to K + in the ECF is the major determinant of the resting membrane potential, which is necessary for the transmission and conduction of nerve impulses, maintenance of normal cardiac rhythms, and skeletal and smooth muscle contraction.
Causes of hyperkalemia
Renal failure and Addison's disease (decreased production of aldosterone thus body holds onto K+). Hyperkalemia should be investigated when there is a history of renal disease, massive trauma, insulin deficiency, Addison disease, use of potassium salt substitutes, or metabolic acidosis.
If extracellular potassium concentration increases without a significant change in intracellular potassium, the resting membrane potential becomes more positive (i.e., changes from -90 to -80 mV) and the cell membrane is hypopolarized (the inside of the cell becomes less negative or partially depolarized (increase excitability - demonstrated with Tall-peaked T waves). Page 118
Why do hyperkaliemia and acidosis often occur together?
In states of acidosis, hydrogen ions shift into the cells in exchange for ICF potassium.
How is insulin used to treat hyperkalemia?
Insulin transports potassium from the blood to the cell along with glucose. Insulin contributes to the regulation of plasma potassium levels by stimulating the Na + , K + -ATPase pump, thereby promoting the movement of potassium into liver and muscle cells simultaneously with glucose transport after eating. The intracellular movement of potassium prevents an acute hyperkalemia related to food intake.
Insulin also can be used to treat hyperkalemia.
What are causes and manifestation of hypokalemia?
Hyperaldosteronism causes which fluid and electrolyte imbalances: Hypokalemia, hypernatremia, and fluid volume excess
Manifestations: Cardiac: flattened-T waves; AV block; bradycardia; paralytic ileus
Inadequate intestinal absorption, massive blood administration, decreases in PTH and vitamin D levels; nutritional deficiencies -malnutrition; alkalosis, elevated calcitonin level; pancreatitis; hypoalbuminemia
Increased neuromuscular excitability; tingling, muscle spasms (particularly in hands, feet, and facial muscles), intestinal cramping, hyperactive bowel sounds; osteoporosis and fractures; severe cases show convulsions and tetany; prolonged QT interval, cardiac arrest
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
Normal calcium level
Many nonspecific; fatigue, weakness, lethargy, anorexia, nausea, constipation; impaired renal function, kidney stones; dysrhythmias, bradycardia, cardiac arrest; bone pain, osteoporosis, fractures
Hypophosphatemia (<2.0) causes
Intestinal malabsorption related to vitamin D deficiency, use of magnesium- and aluminum-
containing antacids, long-term alcohol abuse, and malabsorption syndromes; respiratory alkalosis; increased renal excretion of phosphate associated with hyperparathyroidism
Hypophosphatemia manifestations (<2.0)
Conditions related to reduced capacity for oxygen transport by red blood cells and disturbed energy metabolism; leukocyte and platelet dysfunction; deranged nerve and muscle function; in severe cases, irritability, confusion, numbness, coma, convulsions; possibly respiratory failure (because of muscle weakness), cardiomyopathies, bone resorption (leading to rickets or osteomalacia)
Normal phosphorus level
Hyperphosphatemia causes (>4.7)
Acute or chronic renal failure with significant loss of glomerular filtration; treatment of metastatic tumors with chemotherapy that releases large amounts of phosphate into serum; long-term use of laxatives or enemas containing phosphates; hypoparathyroidism
Symptoms primarily related to low serum calcium levels (caused by high phosphate levels) similar to symptoms of hypocalcemia; when prolonged, calcification of soft tissues in lungs, kidneys, joints
Hypomagnesemia causes (<1.5)
Malnutrition, malabsorption syndromes, alcoholism, urinary losses (renal tubular dysfunction, loop diuretics)
Hypomagnesemia manifestations (<1.5)
Behavioral changes, irritability, increased reflexes, muscle cramps, ataxia, nystagmus, tetany, convulsions, tachycardia, hypotension
Normal magnesium level
Hypermagnesemia causes (>3.0)
Usually renal insufficiency or failure; also excessive intake of magnesium-containing antacids, adrenal insufficiency
Hypermagnesemia manifestations (>3.0)
Lethargy, drowsiness; loss of deep tendon reflexes; nausea and vomiting; muscle weakness; hypotension; bradycardia; respiratory distress; heart block, cardiac arrest
Which three substances influence the calcium and phosphate balance?
Calcium and phosphate balance is regulated by three hormones: parathyroid hormone (PTH), vitamin D, and calcitonin.
Respiratory acidosis - full compensation
pH = 7.36
pCO 2 = 75.1
HCO 3 = 40.6
Metabolic alkalosis - partial compensation
pH = 7.59
pCO 2 = 49
HCO 3 = 48.2
Respiratory acidosis - no compensation
pH = 7.31
pCO 2 = 58.5
HCO 3 = 24
Metabolic acidosis - full compensation
pH = 7.36
pCO 2 = 30
HCO 3 = 15
Respiratory alkalosis - no compensation
pH = 7.49
pCO 2 = 34
HCO 3 = 26
Metabolic acidosis - partial compensation
pH = 7.30
pCO 2 = 33.9
HCO 3 = 18.2
Respiratory acidosis causes
Chronic respiratory disease (e.g., COPD)
Barbiturate or sedative overdose
Chest wall abnormality
Respiratory muscle weakness
Respiratory acidosis pathophys
↑ CO 2 retention from hypoventilation
Compensatory response is ↑ HCO 3 − retention by kidney
Respiratory acidosis lab findings
↓ Plasma pH
↑ PaCO 2
HCO 3 − normal (uncompensated)
↑ HCO 3 − (compensated)
PaCO 2 54 mm Hg
HCO 3 − 25 mEq/L
Respiratory Alkalosis causes
Hyperventilation (e.g., hypoxia, anxiety, fear, pain, exercise, fever)
Stimulated respiratory center (e.g., septicemia, stroke, meningitis, encephalitis, brain injury, salicylate poisoning)
Respiratory alkalosis pathophys
↑ CO 2 excretion from hyperventilation
Compensatory response is ↑ HCO 3 − excretion by kidney
Respiratory alkalosis lab findings
↑ Plasma pH
↓ PaCO 2
HCO 3 − normal
↓ HCO 3 − (compensated)
PaCO 2 27 mm Hg
HCO 3 − 24 mEq/L
metabolic acidosis causes
INCREASED NON-CARBO NIC ACIDS (ELEVATED ANION GAP): BICARBONATE LOSS (NORMAL ANION GAP)
Increased H +load: Diarrhea
Ketoacidosis (diabetes mellitus): Ureterosigmoidoscopy and Renal failure
Lactic acidosis (shock): Proximal renal tubule acidosis
Ingestions (ethylene glycol, salicylates)
Metabolic acidosis pathophys
Gain of fixed acid, inability to excrete acid or loss of base
Compensatory response is ↑ CO 2 excretion by lungs (Kussmaul respirations)
Metabolic acidosis lab values
↓ Plasma pH
PaCO 2 normal (uncompensated)
↓ PaCO 2 (compensated)
↓ HCO 3 −
PaCO 2 38 mm Hg
HCO 3 − 18 mEq/L
Metabolic alkalosis causes
Excess NaHCO 3 intake
Metabolic alkalosis pathophys
Loss of strong acid or gain of
Compensatory response is ↑
CO 2 retention by lungs
Metabolic alkalosis lab values
↑ Plasma pH
PaCO 2 normal (uncompensated)
↑ PaCO 2 (compensated)
↑ HCO 3 −
PaCO 2 40 mm Hg
HCO 3 − 34 mEq/L
Chromosomal aberrations and Associate diseases:
PAGE: 146: Aneuploid cells are defined as those that do not contain a multiple of 23 chromosomes. An aneuploid cell containing three copies of one chromosome is said to be trisomic (a condition termed trisomy).
The most well-known example of aneuploidy in an autosome is trisomy of the twenty-first Chromosome: Down syndrome was formerly called mongolism, but this inappropriate term is no longer used. Individuals with this disease typically have intelligence quotients (IQs) between 25 and 70. The facial appearance is distinctive, with a low nasal bridge, protruding tongue, and flat, low-set ears.
Some genetic principles: Penetrance versus Expressivity
PAGE: 154: The penetrance of a trait is the percentage of individuals with a specific genotype who also exhibit the expected phenotype. Incomplete penetrance means that individuals who have a disease-causing allele may not exhibit the disease phenotype at all, even though the allele and the associated disease may be transmitted to the next generation.
a well-known autosomal dominant condition and its main features are progressive dementia and increasingly uncontrollable movements of the limbs. One of the key features is that symptoms/signs are not usually seen until age 40 or later, thus known as age-
dependent penetrance. Most genetic diseases exhibit variable expressivity.
the extent of variation in phenotype associated with a particular genotype. If the expressivity of a disease is variable, the penetrance may be complete but the severity of the
disease can vary greatly. A well-known example of variable expressivity in an autosomal dominant disease is type 1 neurofibromatosis, or von Recklinghausen disease. The expression of this gene can vary from a few harmless café-au- lait spots ("coffee with milk," describing the light brown color) on the skin to malignant tumors, scoliosis, seizures, gliomas, hypertension, learning disabilities, and neuromas.
Cystic fibrosis is caused by what type of gene?
PAGE 154: The most common lethal autosomal recessive disease in white children, cystic fibrosis. Because an individual must be homozygous for a recessive allele to express the disease, the carriers are phenotypically normal. Because most recessive alleles are maintained in normal carriers, they are able to survive in the population from one generation to the next.
Which genes are responsible for an autosomal dominant form of breast cancer
PAGE 174: An autosomal dominant form of breast cancer accounts for approximately 5% of breast cancer cases in the United States. Genes responsible for this form of breast cancer have been mapped to chromosomes 17 (BRCA1) and 13 (BRCA2). Women who inherit a mutation in BRCA1 or BRCA2 experience a 50% to 80% lifetime risk of developing breast cancer. Breast cancer aggregates strongly in families. If a woman has one affected first- degree relative, her risk of developing breast cancer doubles.
How common is a given disease in a population?
PAGE 164: Well-established measures are used to answer this question.
1. The incidence rate is the number of new cases of a disease reported during a specific period (typically 1 year) divided by the number of individuals in the population.
2. Relative risk is a common measure of the effect of a specific risk factor. It is expressed as a ratio of the incidence rate of the disease among individuals exposed to a risk factor divided by the incidence of the disease among individuals not exposed to a risk factor.
Page 165: EXAMPLE: The incidence of death from lung cancer was 1.66 (per 1000 person-years) in heavy smokers (more than 25 cigarettes daily), but it was only 0.07 in the nonsmokers. The ratio of these two incidence rates is 1.66/0.07, which yields a relative risk of 23.7 deaths. Thus, it is concluded that the risk of dying from lung cancer increased by about 24-fold in heavy smokers compared with nonsmokers
A major characteristic of type 1 diabetes mellitus is:
PAGE 174: Type 1 diabetes, which is characterized by T-cell infiltration of the pancreas and destruction of the insulin-producing beta cells. In addition to T-cell infiltration of the pancreas, autoantibodies are formed against pancreatic cells; the latter can be observed long before clinical symptoms occur. These findings, indicate that this is an autoimmune disease.
Genetic processes demystified.
Pg 183 & 189
Epigenetics bridges DNA information and function by modifying gene expression without any alteration in DNA sequence.
Epigenetic modification can cause individuals with the same DNA (IDENTICAL TWINS) to have different disease profiles - For example the occurrence of asthma in only one of a pair of identical twins.
As twins age, they demonstrate increasing differences in methylation patterns of their DNA sequences, causing increasing numbers of phenotypic differences.
Environmental factors, such as diet and exposure to certain chemicals, may cause epigenetic modification.
Unlike DNA sequence mutations, which cannot be directly altered, epigenetic
modifications can be reversed. EXAMPLE: 5-azacytidin
When Messenger RNA (mRNA) is over-expressed it results in metastasis of an already existing cancer. EXPLAIN:
PAGE: 186 Hypermethylation is seen in miRNA genes that bind to the ends of mRNAs, degrading them and preventing their translation.
When miRNA genes are methylated, their mRNA targets are over-expressed, and this over-expression has been associated with metastasis
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