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pathophysiology BIO2710

by: Jennifer Notetaker

pathophysiology BIO2710

Marketplace > University of New Mexico > > pathophysiology BIO2710
Jennifer Notetaker

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This 7 page Bundle was uploaded by Jennifer Notetaker on Sunday January 31, 2016. The Bundle belongs to at University of New Mexico taught by in Summer 2015. Since its upload, it has received 26 views.


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Date Created: 01/31/16
Exam I Learning Objectives: Chapter 1 (Introduction to Pathophysiology): 1. Define the different classifications of pathophysiology etiologies o Congenital: Occurs before or at birth; can be inherited or due to teratogen  (environmental) exposure  Examples: Down Syndrome, Cystic Fibrosis, Thalidomide o Inherited: Genetic, passed through DNA; apparent at birth or later in life  Examples: Sickle Cell Anemia, Hemophilia, Huntington’s Disease o Idiopathic: unknown cause/etiology   Examples: Drug toxicities, Stevens Johnson Syndrome, Idiopathic  Thrombocytopenic Purpura o Iatrogenic: Caused by a medical intervention  Examples: Post­surgical complications, IV or Catheterizations o Infectious Diseases: Ebola o Immunological Diseases: Rheumatic Fever o Metabolic Diseases: Diabetes o Nutritional Diseases: Ingestion, Uptake, Distribution, Excretion  Example: Iron deficiency 2. Contrast symptoms and signs as they relate to clinical manifestations of disease o Symptoms (Subjective): Only reported by person with disease  Headache  Joint/muscle pain  Nausea o Signs (Objective): Visible to Healthcare professional  Fever  Decrease range of motion  Vomiting  Lab tests 3. Define the different stages of disease o Incubation:   The time b/w etiological event and first signs and symptoms o Prodromal:   First signs and symptoms appear o Acute:   Significant symptoms over a short period of time (hours to days) o Chronic:   Disease that lasts for months to years  May follow an acute disease (Hepatitis)  May be chronic from the start (Subacute endocarditis) o Subclinical:  Active disease without signs or symptoms  Chronic renal disease will almost destroy both kidneys before symptoms  appear  Infectious diseases provide many examples  Typhoid Mary o Latent (Silent period):  Symptoms disappear but can reactive later  Herpes and Chicken pox (Shingles) o Remission:  Decrease or disappearance of signs and symptoms  May relate to a cure but not always  When cancer goes into remission, we are not always sure the cancer  cells have been eliminated o Exacerbations (Flare­ups):  Sudden increase in severity o Convalescence:  Recovery o Sequelae:  Pathology after disease  Scarring from inflammation  Group A Strep Throat o Rheumatic Fever o Glomerulonephritis o Syndrome:  Signs and Symptoms not yet delineated into a disease 4. Describe the reason why a clinical test result within the normal 95% confidence interval may   not be normal for an individual patient. o It depends on the patient. Their age, gender and health play a role in where they  normally fall, which could be lower or higher than the 95% confidence level. 5. Define what factors can influence what is a normal clinical sign or symptom o Validity: P2 is not valid for CO poisoning; diabetics and poor blood flow o Cultural:  May be especially relevant to symptoms more than signs o Situational:  Blood parameters and moving to increased altitude o Time:  Circadian rhythm or diurnal (daylight)  Body temperature a good example  o Gender:  Bone mass o Age:  Normal changes the older a person gets 6. Compare and contrast "reliability", "sensitivity", and "specificity" of lab tests o Reliability:  Give similar results on multiple tests  Says nothing about sensitivity and specificity (accuracy) o Sensitivity:  Ability to accurately detect true positives  Group A strep test is 80% sensitive  20% false negatives­ missed cases  HIV blood test is 99% sensitive o Specificity:  Ability to accurately detect true negatives  Limits the percentage of false positives Chapter 4 (Cell Injury, Aging and Death): 1. Define hydropic swelling and describe why it occurs related to ATP, pumps, osmosis o Hydropic swelling is the accumulation of water in the cells that can lead to the  swelling of an organ. o In metabolic malfunctions there can be a lack of ATP which is needed for the cell  to pump out sodium. Without ATP to bind to the NA+­K+ pump, sodium will back  up in the cell causing water to follow by osmosis and therefore lead to the  swelling of the cell. 2. Describe the processes by which cell size increases from intracellular accumulations o Faulty Metabolism: Dysfunction in enzyme that breaks down compound o Excessive Storage/Intake 3. Describe the mechanisms of intracellular fat accumulation related to chronic alcohol ingestion and Tay­Sachs disease. o The liver is the major site of fat storage and metabolism. The liver will metabolize alcohol before the fat and long term excessive alcohol intake can lead to the  buildup of excess fat in vacuoles. o Tay­Sachs is caused by lack of enzymes that recycle gangliosides, molecules  composed of a glycosphingolipid. Progressive damage caused by the buildup of  GM2 ganglioside leads to the destruction of neurons in the brain and spinal cord. 4. Describe two mechanisms responsible for glycogen and protein accumulation in renal cells o Diabetes Mellitus  Impaired cellular uptake of glucose  Reabsorbed by the renal tubules but can only absorb so much  Stored as excessive glycogen in renal tubules cells, taking up space and  leading to kidney problems o Leaky Glomerular Capillaries  Proteins normally cannot pass through  Endocytosis of escaped proteins by tubule cells  Excessive accumulation, becomes toxic  5. Describe the two mechanisms by which cells handle damaged or misfolded proteins o Heat shock (Chaperone):  Bind to denatured proteins  Refolds the proteins, if fails then see next mechanism o Ubiquitin:  Pushes denatured proteins into proteasome complex for degradation 6. Describe the mechanisms by which bilirubin accumulates to toxic levels in neonates o Rh­factor mediated hemolysis o Decreased bacterial metabolism of conjugated bilirubin in intestines  Intestinal flora not develop  Pales feces  Conjugated is unconjugated and goes back into blood o Can be associated with breast feeding (B­glucuronidase)  Unconjugated bilirubin which is reabsorbed  o Can pass the blood brain barrier causing encephalopathy (kernicterus) 7. Identify the 5 classifications of cellular adaptation and factors that cause each adaptation o Atrophy:  Decrease in size and function:  Minimize nutrient and energy consumption  Decrease organelles and structures  Causes:  Disuse­ bedridden, not mobile, casting  Lack of nutrients  Ischemia­ long term causes of shrinkage causes hydropic swelling  Endocrine dysfunction  Age  Chronic injury or disease­ Alzheimer’s o Hypertrophy:  Increase in size and function due to increased physiologic or pathologic  demands (workload):  Cardiac muscle due to hypertension  Left ventricle hypertrophy  Bigger in cell size  Skeletal muscles hypertrophy:  Myosin and actin increase to increase load bearing  Add more thickness than length  Stretching can add increased length o Hyperplasia:  Increase in cell number:  Mitotic increase (cloning)  Estrogen increases endometrial cells of uterus  Chronic irritation causes calluses or corns  Increased RBCs at higher altitude  Increased neutrophils­ infection (bacteria) response o Metaplasia:  Conversion from one cell type to another  Adaptive response to chronic injury  Examples:  Chronic smoking: ciliated columnar switch to stratified squamous  for protection in response to smoke and toxins  Chronic acid reflux: Cells of esophagus change to those of the  intestinal tract (squamous to columnar)  Intestinal goblets cells are first sign (mucous and alkaline) o Dysplasia:  Disorderly growth  Abnormal variations in size, shape, arrangement  Significant potential to become cancerous 8. Contrast the two processes of irreversible cell injury o Irreversible Cell Injury:  o Injury is too severe or prolonged for repair o Two Processes: o Necrosis:  Unintended cell death  Cell swells and ruptures (breakdown of cell membrane)  Contents releases causing inflammation o Apoptosis:  Programmed cell death (suicide)  Cell goes through controlled fragmentation  No spilling of contents or inflammation  Not always part of injury, can just be a remodeling process  9. Identify extrinsic and intrinsic signals of apoptosis o Extrinsic Signals: o From the outside o Lack of survival signals activating cell  Growth factors, cell­to­cell interactions, etc. o Activation of death receptors by Fas ligand (pathogens) o Intrinsic Signals: o From the inside o DNA damage too great to repair o Mitochondrial failure  o Oxidative stress o P53 protein is key signal to start apoptosis o Cancer cells do not have P53­ it is usually disabled and cancer cell  becomes immortal 10. Describe the mechanisms by which ischemia and hypoxia lead to cell injury 11. Contrast direct vs indirect cell injury from infectious diseases 12. Describe the mechanisms of direct and indirect injury to cells 13. Describe mechanism responsible for the development of “The Bends” during deep sea  diving 14. Identify cells that are most sensitive to radiation injury and what mechanisms of injury occur 15. Describe the mechanism of DNA damage from ultraviolet radiation exposure 16. Describe the relationship between telomeres and cellular apoptosis in aging cells Chapter 24 (Fluid and electrolyte homeostatis): 1. Describe the physiological triggers of thirst when we need more fluid 2. Describe the mechanisms that drive distribution of fluid between vascular ­ interstitial and       interstitial ­ intracellular compartments 3. Describes the pathophysiology mechanisms that can result in a volume deficit imbalance 4. Identify the clinical hallmark signs of volume deficit 5. Describes the pathophysiology mechanisms that can result in a volume excess imbalance 6. Identify the clinical hallmark signs of volume excess 7. Describe the pathophysiologic mechanisms responsible for hyponatremia and what occurs at  the cellular level due to osmosis 8. Describe the pathophysiologic mechanisms responsible for hypernatremia and what occurs at the cellular level due to osmosis 9. Describe the 5 pathophysiologic mechanisms responsible for edema 10. Contrast the pathophysiologic mechanisms that impact muscle contractions due to  hypokalemia and hyperkalemia 11. Describe the 5 major pathophysiologic mechanisms responsible for hypocalcemia 12. Describe the mechanism by which hypocalcemia leads to excessive muscle contractions 13. Describe the pathophysiological impact of hypomagnesemia on neuromuscular excitability 14. Explain how hyperphosphatemia leads to hypocalcemia and aches/stiffness in joints Chapter 13 (RBC Disorders): 1. Identify which diseases are associated with decreased RBC production and which are  associated with abnormal RBC structures and excessive destruction of RBCs. 2. Describe the primary and secondary mechanisms of anemia associated with chronic kidney  failure 3. Describe the mechanism by which Vitamin B12 and Folate deficiencies cause anemia 4. Describe the mechanism of involved in development of Pernicious Anemia 5. Describe the pathophysiology mechanisms that cause: a. Alpha­Thalassemia and Beta­Thalassemia b. Sickle cell anemia c. Glucose­6­phosphate Dehyrogenase 6. Describe the mechanism of Rh­factor mediated hemolytic disease in newborns 7. Contrast the causes of the 3 categories of polycythemia


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