Human and Animal Disease
Human and Animal Disease MIP 315A
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This 114 page Class Notes was uploaded by Winona McClure on Tuesday September 22, 2015. The Class Notes belongs to MIP 315A at Colorado State University taught by Gerald Callahan in Fall. Since its upload, it has received 46 views. For similar materials see /class/210244/mip-315a-colorado-state-university in Microbiology at Colorado State University.
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Date Created: 09/22/15
3 May Hypertension Normal Systolic lt120 Diastolic lt80 Stage 1 S 140 159 D 90 99 Stage 2 S 2 160 D 2 100 Types amp Causes Primary Essential 90 No identifiable cause Associated with obesity Secondary Caused by another conditionmedication Sudden onset Higher BP than primary Risk Overweight Age Family history High salt diet stress Hypertension is main risk for cardiovascular disease Oftentimes shows no symptoms Lifestyle changes Weight reduction DASH diet Decrease in sodium Exercise Medications Diaretics usually prescribed first Ebola RNA virus Filoviridae Zoonotic 5 Types Zaire Ivory Coast Suda Bundibugyo Reston Reston is not known to affect humans Contact w body fluids use of contaminated medical supplies possibly aerosol Abrupt onset Incubation 2 21 days Symptoms Fever rash muscle aches ampc at first Internalexternal bleeding low effective circulating blood interstitial edema DIC amp cerebral edema 9 death 50 90 infected die Lifelong disease No immune memory No treatments Isolation pain medications Crohn s Disease Inflammatory disease of GI Skip lesions ileum amp colon Diarrhea pain vomiting anorexia bloody stools 3 possible causes autoimmune genetic environmental Autoimmune chronic inflammation ulcers TNFot overproduction proinflammatory cytokines Caucasian amp JewishFamily Risk decrease pasteurized milk fruit Risk increase meat Diet amp stress trigger flareups Against normal gut flora CD4 most damaging reagent Therapy TNF blocker humira Natalizumab works against another inflammatory factor Antimicrobial Corticosteroids Surgery Helminthic worms Q Fever Zoonotic Bacteria coxiellaburnetii Similar to flu Airborne Associated w aborted fetuses of domestic livestock 60 asymptomatic Treated w strong antibiotics Infected birthing fluids mix w soil churned up as dust and sent around in wind 27 April Feline Leukemia Virus Retrovirus Shed in salivanasal secretionsurinefecesmilk Cattocat bite grooming sharing litterfood Symptoms Weight loss Poor coat condition Enlarged lymph nodes Fever Pale gums Skinbladderupper respiratory infection Diarrhea Seizuresbehavioral changes Virus enters through nosemouth Travels to lymph Causes viremia presence of virus in blood Therapy Prevent stress amp exposure Vaccinations Treated as symptoms develop Fatal familial insomnia Autosomal dominant gene mutation Avg 50 years old onset Caused by deterioration of thalamus Responsible for sleep regulation sensory amp motor function Early symptoms Sleeplessness Sweating Pinprick pupils 4 Stages of Onset Stage 1 4 months Sleeplessnesspanic attacksphobia development Stage 2 5 months Worseninghallucinations Stage 3 3 months Total insomniaweight lossdiminished mental processes Stage 4 6 months Dementialoss of reactions Progression into coma 9 death Treatment Symptom management Prion malformation blockers possible Chaga s Disease Caused by Trypanosomacruzi Vector reduviid bug Bug feces or blood enter body Symptoms Acute weeks months Swellingfeverrashnausea diarrhea Intermediate No signssymptoms Chronic 10 20 years after infection Irregular heartbeatsudden cardiac arrest Heart failure Enlarged colonesophagus Treatment Manage symptomskill parasite 20 January Objectives Understand the nature and function of the normal flora Know the general characteristics of bacteria Understand how intercellular bacteria cause disease Understand how endotoxins cause shock Understand how exotoxins cause disease DNA surveys of the belly button inner elbows and elsewhere reveal diverse microbial communities Belly button has many more bacteria than between the toes Largest concentration of bacteria is in the gut especially the large intestine Bacteria and individuality Identical twins may share appearances mannerisms even clothes but the microbes living in their guts are anything but the same Communities of bacteria in adult identical twins differ dramatically Classification Spherical Cocci Rodlike Bacili or Spiral Spirochetes in shape Gramnegative grampositive Bacteria have cell walls 9 referred to as flora Have chromosomes ribosomes enzymes capable of reproducing Bacterial Pathogenesis Attachment to and invasion of cells followed by cellular destruction or alteration of cellular physiology n Bacteria grow in body fluids eg blood I 39 39 or 39 and urine quot Production of toxins Endotoxins only come from gram negative bacteria Endotoxins lipopolysaccharide LPS Septic Endotoxic shock Results from getting gram negative bacteria into the blood Bacteria die 9 release LPS Attaches to macrophages Release TNF and Ll TNF is a stimulator of inflammation Cause blood vessels to dilate and get leaky vasodilation Blood pressure drops Person goes into shock Multiple organ failure 9 death Exotoxins are proteins produced by living bacteria or that bind to specific receptors on host cells and interfere with normal host cell function Toxicgenic9 Produce toxins E Coli 0157H7 Produces a toxin that binds to kidney cells 9 interferes with kidney function 9 death November 2009 beef recall Ground beef Produces Shiga toxin Gets inside kidney cells nterferes with normal assembly of ribosomes Can t create proteins Kidney failure Leads to death in 35 of cases TeNT Tetanus nervous toxin Inhibits neuron Muscle cannot relax llLockja w Botulinum Toxin Paralytic Possibly the most acute toxic substance known Botox Staphylococcus aureus Toxic shock Produces exofoliative toxin amp TSSTl toxic shock syndrome toxin one TSSTl activates T cells T cells release gamma interferon Binds with macrophages Produces TNF 9 shock 9 death Salmonella Often leading cause of death in children worldwide Fecal oral 2008 US Outbreak Jalape o chiles Peanut butter Pepperoni chiles eggs Domestic animals 9 human food 9 human 9 sewage 9 domestic animals Ingested 9 small intestine 9 penetrates cells 9 multiplies in lymphoid tissue 9 cells cannot absorb water 9 diarrhea 9 death if hydration is not available 27 January Objectives from last lecture Understand the nature of prion and viruses Understand how prions and viruses cause disease Know the pathogenesis of influenza A Antigenic Shift 9 RNA is swapped from one virus to another H5N1 Birds hemorrhaging fever Humans die from pneumonia Spongiform Encephalopathy Similar to disease recognized in sheep for years Transmissible Can take brain from infected inject in healthy and symptoms show after a period of time TSEs as a group Kuru In the humans of Papua New Guinea Prion Protein Holes in the brain Large black veins on the brain Other TSEs Chronic Wasting Disease CWD Sheep elk moose Creudztfeld Jacob Disease CJD Humans PRPC form found in everyone PRPSC form found in diseased animals Have the same amino acid sequence Arranged differently a helix vs 6 pleated sheet PRPSC transforms PRPC into PRPSC Amyloid protein coat Kuru caused by ritualistic cannibalism Peyer s patches 9 part of lymphoid tissue in gut Lymphoid tissue is wired to the brain directly through neurons Mad Cow Disease When killing a cow they hit it on the head trying to eliminate pain Before it dies bits of the brain are circling around the body Some cuts of meat may contain lymphatic tissue Prions Ignored by immune system Not affected by cooking Objectives Understand the nature of fungi Understand the pathogenesis of mycotoxicoses Understand the pathogenesis of mycoses Know the difference between protozoa and helminthes Understand the pathogenesis of malaria Understand the pathogenesis of filarial worm infections Myco refers from fungus Eukaryotic with cell walls Mycose fungus is actually inside the body Single cell yeast Multiple cell mold Mycotoxicoses To be infected by a bacterial toxin you normally have to be have the bacteria inside you The fungus is never present inside the infected animal One sort releases aflotoxins The toxins remain after the fungi is dead Resistant to cooking Not destroyed by heating Pathogenesis Aflotoxins produce acute necrosis cirrhosis and carcinoma of the liver in a number of animal species no animal species is resistant to the acute toxic effect of aflotoxins Mycotoxicose exa m ple Ergot 29 March Endocrines are secreted into blood Exocrines are secreted into glands 9 surface Pancreas produces insulin Also secretes enzymes necessary for digestion Dumped into small intestine through duct Pancreatitis Abdominal pain greatest in upper leftmiddle Nauseavomiting Sweating Anxiety Fever Mild jaundice Objectives Lecture 20 and 21 Know the glands of the endocrine systems Know the types of hormones produced Understand the etiology and pathogenesis of hypo and hyper thryoidism Understand the etiology and pathogenesis of Addison s and Cushing s disease Understand the etiology and pathogenesis of diabetes types and II Mammalian Stress Response Threat 9 hypothalamus 9 CRA 9 pituitary 9 ACTH 9 adrenals 9 cortisol 9 immune system suppression Hormones Protein and peptide hormones Insulin Amine and amino acids hormones Thyroid hormones Steroid hormones Testosterone estrogen Made from cholesterol All are produced at one point and act distantly Autocrine cell secretes something it itself uses Paracrine other cells use All hormones affect through specific receptors Cell will do something different Most changes occur because of change in genetics Switching genes onoff Hypothalamus Coordination of autonomous nervous system Regulation of body temperature Maintenance of water balance Control of anterior pituitary Through hormones GHRH TRH CRH Growth hormone GH Stimulates fat cells to break down triglyceride suppress ability to take up and accumulate circulating lipid Stimulate liver production of IGF1 insulin growth factor1 9 stimulates growth Stimulates production of adrenal glucocorticoids Mainly cortisol Follicle Stimulating Hormones Females acts on follicle to stimulate it to release estrogen Leutinizing hormone Secrete estrogen Testosterone Adrenal hormones Adrenal Cortex outer portion Mincaralocorticoids Aldosterone Adrenal androgens DHEA dehydroepiandrosterone Glucorticoids Cortisol Medulla inner portion Epinephrine Everything produced by cortex starts as cholesterol Medulla Adrenaline Triggered by neurons Thyroid T4 amp T3 T3 is active Regulate metabolism Only a tiny amount is unbound and active Most bound to something else Lots of effects throughout the body Participates in direct activation of genes Growth hormone Too muchtoo little gigantismdwarfism Children Deficiency Interferes wnormal bone and muscle growth Excess Gigantism Adults Excess Overgrowth of cartilaginous parts of skeleton enlarged heart other organs liver intolerance Thyroid dysfunction Graves disease Autoimmune Antibodies against own TSH thyroid stimulating hormone receptors Thyroid thinks antibody is TSH Produces T4 amp T3 a lot of it Ketoacidosis Thyroid storm One of most common symptoms bulging eyes Goiter enlarged thyroid bulge in neck Thyroid grows to try to produce more Removedestroy thyroid Hypothyroidism Congenital most common Cretinism mental retardation impaired growth Acquired Often iatrogenic Fatigue weight gain cold intolerance myxedema Myxedema accumulation of fluid between fascia and outer layer causes swelling Adrenals Actions of Cortisol Glucoseproteinfat metabolism Emotional stability Antiinflammatory Immune suppression StressInduced Hypercortisolism Chronic fatigue syndrome Immune suppression Chronically abused sexually children Pelvic pain Headache G symptoms Musculoskeletal pain Mood disorders High medical care use as adults Addison s Disease Hypocortisolism Most common cause US autoimmune Underdeveloped tuberculosis Symptoms Chronic fatiguemuscle weakness Loss of appetite Blood pressure drop Blotchy dark tanning Cushing s disease Hypercotisolism Cause usually pituitary tumor excess ACTH Buffalo hump deposition of fat around neck Affects testosterone production Cure aim to reduce mass ofadrenal gland remove pituitary tumor 22 February Objectives Lectures 9 and 10 Know the leading types of cancers and the leading causes of death from cancer in the US Understand the difference between benign and malignant tumors Understand the role of environmental factors in carcinogenesis Understand the nature and function of oncogenes and tumorsuppressor genes Understand the pathogenesis of breast cancer Most frequent cancer Men prostate Females breast Most killing cancer Lungin M amp F Tumor excessive cell division Malignant tumors can metastasize spread from point of origin Benign usually have a capsule Malignant Grows Reaches a blood or lymphatic vessel Dead cells in the center of the growth Often more fatal than benign 9 metastases are difficult to findtreat singular of metastases 9metasis which is the same as the name of the process Classification of Malignant Tumors Carcinomas Epithelial Origin Sa rcomas Connective Tissue Origin Gliomas Nervous Tissue Origin Lymphomas Solid Tumors of Lymphoid Tissue Leukemias Bone Marrow Tumors Benign tumors are named with place of origin oma usually Malignant transformation the process of a normal cell becoming a tumor cell Generally few mitochondria ER no Golgi and a new antigen on the membrane Basically though it divides too rapidly Angiogenesis Happens at primary amp metastatic sites Cause blood vessels to grow getting more blood for the tumor Carcinogens Environmental factors that can cause cancer They are carcinogenetic can cause cancer Carcinogenesis the process oh terminology Sunlight UV radiation radiation cigarettes aflotoxins produced by fungus 9 ingested 9 liver turns it to a carcinogen viruses HTLVl for example some processed meats contain nitrites and nitrates which the liver converts damn you coal tar ampc Apoptosis Programmed cell death Cancer is due to an imbalance of cell growth and death Genes Involved in Malignant Transformation Oncogenes promote cell division Tumor suppressor genes regulate cell division DNA repair genes Genes that regulate apoptosis P53 Activated amp binds to DNA if it is damaged Slows replication Repair can take place Mutated Does not work DNA is not repaired Mutant cells Neoplasm tumor Activation of growthpromoting oncogenes Inactivation of tumor suppressor genes Alteration in genes that regulate apoptosis Cause imbalance of growthdeath Cachexia Loss of appetiteweightmuscle tone Risk ofa woman developing breast cancer in her lifetime is 1 in 7 Risk is highest in the developed world Environmental factors Lifestyle factors 24 March Celiac disease Malabsorption Most common autoimmune disease Probably also most common inflammatory bowel disease Immune attack on villi in small intestine Small bowel biopsy shows absence of villi Improvement on glutenfree diet Some genetic predisposition Villi lost 9 surface area drops 9 much less can be absorbed Most common symptom diarrhea Often misdiagnosed as Crohn s or ulcerative colitis Gastrointestinal symptoms Abdominal pain distention bloating Decreased appetite Constipation Diarrhea Nonintestinal symptoms Anemia Bone and joint pain Bone disease Breathlessness Wide range of other symptoms Glutens increase inflammation exacerbates disease f gluten is not in system villi will be present Gliadin piece of gluten Gluten presented to immune system Production of antibody and inflammatory cells Cholera Bacteria interferes with cyclic AMP Water is not absorbed in gut Diarrhea Oralfecal transmission Multiplies in gut produces toxins ATP metabolism is screwed up 9 cell pumps dependent on ATP fail 9 water does not get absorbed Objectives Lecture 19 Understand the physiology of the liver Know the symptoms of liver disease and their causes Understand the pathogenesis of cirrhosis Know the causes of cholecystitis and cholelithiasis Know the causes and consequences of pancreatitis Liver gallbladder and pancreas produce things which empty into small intestine Liver disease Symptoms portal hypertension ascites jaundice Liver functions Detoxification Protein production most of those that are in the blood Bile Portal hypertension Veins go from gut and stomach directly to liver Everything gets detoxified Leads to inferior vena cava Liver problems blood does not flow easily Varicose veins in the gut have a tendency to bleed Ascites Caused by builtup blood pressure portal hypertension Fluid forced out of portal system Accumulates in peritoneal cavity Painful Can be drained but will come back unless something is done to fix liver function Bile Bilirubin comes from hemoglobin Heme is broken into biliverdin broken into bilirubin By macrophages Bilirubin normally binds to albumin travels to liver combined into bile With liver disease albumin is not as available to pick up bilirubin Excess bilirubin in blood 9 jaundice Yellowing of skin and eyes Cirrhosis Characterized by fibrosis and the conversion of normal liver architecture into abnormal nodules Among top 10 causes of death in developed world Caused by alcohol chronic infections autoimmune diseases Deposition of fats 9 accumulation of inflammatory cells 9 areas where liver cells die and are replaced by scar tissue fibrosis reversible turning point 9 extensive fibrosis loss of liver function Alcohol ethanol goes to liver 9 converted to acidaldehyde hard on cells causes them to die inflammation 9acetic acid 9 Krebs cycle Symptoms Varicose veins Swelling Jaundice Hepatitis Different routes of transmission depending on type A Oralfecal route Least severe type Jaundice B Most commonly sexual transmission Most commonly malemale Usually acute 9 immune response 9 virus disappears Sometimes chronic 9 liver inflammation C No vaccine Most commonly parenteral Shared needles between drug users Usually acute Chronic has no apparent immune response whereas B has failed immune response C is worst Most likely to establish chronic infection Gallbladder Stores bile Bile water cholesterol fats bile salts proteins bilirubin Gallstones Salt concentrations in bile are high Can harden into stones Can put pressure on gallbladder Block bile duct Backup into liver Block pancreatic duct 15 February Exam is through lecture 7 Type III Hypersensitivities Immune Complex Diseases Antibodies amp antigens can link into a big complex and becomes no longer soluble Fall out of solution Large amount of preexisting antibody large amount of antigen Complex activates complement Inflammation Neutrophils come Blood vessels dilate Leakiness Blood pressure crashes Multiple organ failure Death First339 quot quot areall39 quot type Mediated by antibody Can lead to anaphylaxis inflammation caused by an immune event Anaphylactic shock can result Type IV Delayedtype Take a few days to develop Eg poison ivy Poison ivy Catechol on leaves contact skin Modify proteins APCs take cells break down present CD8 cells activated find cells presenting altered protein and destroy them Didn t really pose a threat but the immune system thinks it did Rheumatoid arthritis Includes at least type II amp hypersensitivities Hard to categorize some hypersensitivities since several symptoms can be present at once Systemic inflammatory disease affecting 2 million people in the United States Autoimmune etiology Age of onset 20 45 yea rs Results in average of 5 to 10 years decrease in life expectancy Treatment is expensive Person makes antibodies against their own antibodies Immune complexes form Deposited in joints Type II since it s antibodies against own antibodies Type I because of immune complexes Most commonly affects joints in fingers ankles amp knees Bone degrades Pannus forms overgrowth of synovial membrane Treatment involves immune suppression Exam 33 questions Multiple choice and true false Objectives Lecture 1 Understand the nature of the science of pathology Know the leading causes of death in the US Know the leading causes of death in the underdeveloped world Know the reasons for the differences Understand symbiosis and its various forms Objectives Lecture 2 Understand the nature and function of the normal flora Know the general characteristics of bacteria Understand how intracellular bacteria cause disease Understand how endotoxins cause shock gram negative death Understand how exotoxins cause disease either living Understand the pathogenesis of salmonella Understand why antibacterial antibiotics work Objectives Lecture 3 Understand the nature of prions and viruses Understand how prions and viruses cause disease Know the pathogenesis of influenza A PRPCvs PRPSC C 9 good sc 9 bad Prion causes good to change to bad Virus is nucleic acid in protein coat Have to be inside a cell to reproduce Bind to host cell Objectives Lecture 4 Understand the nature of fungi Understand the pathogenesis of mycotoxicoses Understand the pathogenesis of mycoses Know the difference between protozoa and heminthes Understand the pathogenesis of malaria Understand the pathogenesis of filarial worm infections Malaria Transported by mosquito Blood 9 liver 9 blood cells till they burst Cycles No immunity Objectives Lecture 5 Know the soluble and cellular elements of the inflammatory response Know the process and consequences of inflammation Understand the differences between acute and chronic inflammation Histamine and TNF are stimulators of inflammation Objectives Lecture 6 Know the organs and the cells of the immune system thymus bone marrow lymph nodes Understand the adaptive immune response Understand how T cell and B cells protect against infection Immune responses take place in lymph nodes Macrophages and dendritic cells are antigenpresenting cells T cells deal with intracellular B cells deal with antigen in the fluid free 3 March Exam covers Lectures 8 17 33 questions Multiple choice TF 80 of heart attacks are caused by atherosclerosis Buildup of plaque inside arteries Contains cholesterol ampc Arteries narrow Blood clots Blood vessels become more fragile Causes turbulent blood flow Features Fibrous cap over top Crystals of cholesterol Process Damage to vascular endothelium Monocytes amp lowdensity lipoproteins move into the space between the layers of the vessel walls Macrophages from monocytes eat LDL Smooth muscle cells that are part of artery wall proliferate Cells that eat LDL 9 foam cells Inflammation Pathogenesis Endothelial injury Infiltration of lipoproteins LDL Adhesion of monocytes Monocytes migrate in to vessel wall become macrophages Macrophages take up lipids foam cells Triggers more inflammation Vessel wall fills with cellular debris and cholesterol Smooth muscle proliferation and fibrosis Especially bad in coronary arteries At risk for heart attack Can possibly occlude an artery up to 50 before there are symptoms Angina 9 pain Pain can radiate to various areas not just chest Angina pectoris Caused by ischemia reduced blood flow Usually reversible Gets worse with exercisestress The longer a blood vessel is blocked the more tissue will die Myocardial infarction 20 40 minutes causes permanent damage due to prolonged ischemia Results in scarring Most people die from ventricular fibrillation Most due to clot formed on arterial plaque occlusion Scarring inhibits contraction Symptoms Chest discomfort Discomfort in other areas of upper body Shortness of breath Can vary What to do Angioplasty usually balloon angioplasty Insert catheter from femoral artery 9 aorta 9 blocked vessel Expand balloon Forces artery open Balloon is surrounded by stent metal cage left to hold artery open Coronary artery bypass If it can t be pushed open Take vein or artery piece and sew it in place so blood uses that and bypasses blockage Triple bypass three arteries have to be bypassed Objectives Lecture 15 Understand the causes of heart failure Know the different manifestations of left and rightside failure and be able to explain the underlying mechanisms Know the several forms of shock Be able to explain the pathogenesis of each form of shock Congestive heart failure Pathological decrease in cardiac output Blood tends to pool in places Primarysecondary Primary cardiac Causes Myocardial infarction Hypertension Cardiomyopathies Degenerative conditions of the heart Infectious agents Rightside Body 9 lungs Blood pools in periphery Peripheral edema Swelling in handsfeet Accumulation of fluid in peritoneal cavity Leading cause of rightside failure is leftside failure Other cause chronic lung diseases congenital heart disease primary pulmonary hypertension PPH heart valve disease Leftside Lungs 9 body Blood pools in lungs Pulmonary edema Frothy cough fluid in lungs Causes heart attack chronic blockage of heart arteries ampc Common consequence of heart attack Circulatory shock Critical decrease in tissue perfusion caused by a loss or redistribution of blood Can be a result of a heart attack Cardiogenic shock Decreased contractility Pulmonary congestion Shock Hypovolemic Sudden drop in blood volume Distributed Sudden change in capacity of circulatory system Cause vasodilation Shock is a sudden change in blood flow Consequence multiple organ failure Hypovolemic Damage to multiple organs Loss of consciousness Anaphylactic shock Caused by immune response Form of distributive shock Symptoms respiratory system closes down vasodilation Septic shock Caused by infection by gramnegative bacteria Distributive Inflammation Vasodilation Blood pressure falls Multiple organ failure Objectives Lecture 16 Know the basic anatomy and physiology of the respiratory system Understand the pathogenesis and symptoms of acute pneumonia Excess C02 causes a drop in blood pH Trachea 9 bronchi 9 bronchioles 9 alveoli Walls get thinner as the layers go down Acute Upper Respiratory Tract Infections Colds and flus Selflimiting Viral Pneumonia Lower respiratory tract Inflammation of the lungs Typical inflammation inside alveoli Atypical inflammation between alveoli Most common cause bacterial infection Symptoms of typical Comes on quickly Cough Chest pain Sputum coughed up Pathogenesis Inhalation of bacteria aerosol Upper resp tract infection 9 inhale organisms from there to lower Inhale gastric contents stomach contents Typical alveolar Bronchial inflammation of bronchioles fluid builds up in alveoli Evenly distributed Lobar confined to one lobe Atypical quotWalking pneumonia slower onset Lower body temperature Dry cough Inflammation outside alveoli Less life threatening 12 April Lecture 25 and 26 Objectives 139 39 Ithe role of and Know the epidemiology pathogenesis risk and treatments for osteoporosis Understand the etiology and pathogenesis of osteomalacia rickets Understand the pathogenesis of osteoarthritis Understand the etiology and pathogenesis of gout Osteoporosis Epidemiology 28 mil cases in the US Bone Remodeling Activation Preosteoclasts mature into active osteoclasts Resorption Osteoclasts digest mineral matrix old bone Reversal End of resorption Vitamin D3 and parathyroid hormone play a big role in preosteoblasts activation of osteoclasts Effects of Parathyroid Hormone Ultimately activates osteoclasts but only in the presence of osteoblasts Osteoporosis weak bones due to breaking down faster than rebuilding Spine column gets compressed Breaks in bones can t support weight Primarily in elderly especially women Risk factors Overproduction of parathyroid hormone Inactivitybed rest Aging Insufficient vitamin BS or calcium Hormonal imbalance Genetic predisposition WhiteAsian women Greater risk 9 shorter period of time exposed to estrogen Increased fractures result Reducing chance of fractureslow osteoporosis Balance training Strength training Weight bearing exercise Bone can be regained through hormone replacement therapy Add estrogen Increased risk of cervical cancer Add estrogen and progestin Decreased risk of cervical but increased risk of breast Medicine slows process of bone absorption Osteomalacia Inadequate mineralization of bone Calcium or phosphate deficiency False fracture so much mineral in removed Xray does not show any bone there Bones are soft and spongy Greater risk for fracture Osteoarthritis 1 in 13 people in USA Debilitating disease Most common type of arthritis Damage to cartilage Development of bone spurs Bits of bone in joint Joint lining becomes inflamed Causes of secondary OA Being overweight Age Joint injury Stresses on joints Functions of Cartilage Lubricates joint Reduces friction Spreads load 9 easier weight distribution Bone cysts form Open spaces Joint space narrows Symptoms pain stiffness Moving joint helps pain Knees more common in women Hips more common in men Gout Dramatically swollen joints Urate crystals inflammatory cells Risk gt2030 years of age Genetic predisposition Heavy alcohol consumption Obesity Urate crystals 9 inflammation Objectives Lecture 27 Know the basic elements of the skin Understand sunburn and skin cancer Understand the basic mechanisms of infectious diseases of the skin Know the etiology and pathogenesis of acne Know the pathogenesis of eczema All layers ofepidermis begin as basal cells Above keratinocytes All products of basal cells Dendritic cells defense Melanocytes source of melanin Skin color Lesion abnormal tissue in the body Rash inflammatory spots reddening at surface of skin Pruritus itching 3 February The Acute Inflammatory Response Occurs over minutes to days A defensive response of vascularized living tissue to cellular injury caused by endogenous or exogenous agents Signs of inflammation rubor calor tumor dolor Inflammatory stimuli Infections complement and macrophage activation Trauma Tissue necrosis cell death Foreign bodies splinters dirt Immune reactions Vasodilation and become leaky One reason skin turns red is that blood vessels get larger closer to the surface Swelling from increased fluid from veins Warmth from increased blood flow Mast cells Full of granules Granules released when cell is perturbed Degranulation Affected by pathogenesis allergens stem cell factor ampc First degranulation Then synthesizes new proteins Produces histamine TNF ot leukotrines All cause increased vascular permeability smooth muscle contraction Mediators of inflammation Histamines Vasodilation Increased vascular permeability Bowel parastalsis can lead to diarrhea Effect in stomach Raises production of hydrochloric acid Smooth muscle contraction Mast cell produces new things These maintain inflammatory response NonSteroidol Antiinflammatory Drugs NSAIDs n aspirin aleve ampc but not Tylenol Alleviate pain Phosphoglandin production blocked Decrease mucus production in the stomach Leukotrines and phosphoglandins created by mast cell 9 maintain inflammation pain Transudate moves out of blood vessels first Proteins liquid ampc Then exudate 9 cells Receptors on macrophage bind to bacteria Pulled into phagosome Fuses with lysosome Oxidative burst Toxic environment inside macrophage 9 bacterial death Bacteria destroyed Release of Ll and TNF Inflammation increased Macrophage gathers and kills bacteria increases inflammation 9 results in more macrophages in the area Actions of neutrophils Adhesion to microorganisms Phagocytosis Intracellular killing of microorganisms Oxygen dependent mechanisms Oxygen independent mechanisms lysozyme lactoferrin which chelates iron required for bacterial growth cationic proteins and the low pH inside phagocytic vacuoles Release of lysosomal products Pus is mostly bunches of dead neutrophils Resolution and Healing Neutrophils and macrophages clean produce growth factors Repair blood vessels New vessel growth Acute inflammation Abscesses and granulomas can form Most dead cells in an abscess 9 neutrophils Giant cells are present in granulomas most dead cells 9 macrophages Vaccine first encounter with pathogen 7 10 days 9 no response lag phase Response for a few weeks IgM antibody is present These make up the primary response Boost at end of that response same sort amp a new sort 3 day lag phase and then a high response IgG for same sort Primary response to new Immunologic memory Response is different the next time they encounter Large antibody response Adaptive immunity Dendritic cell Just underneath skin Eats pathogen MHC molecules class 1 amp 2 Bind with bits of pathogen Stick on outside of cell Immune system then recognizes something s wrong T helper cells cytolytic T cells Bone marrow 9 thymus 9 these cells Once through the thymus they have acquired Tcell receptor Thymus picks out cells that are danger to host amp eliminates T helper cell Recognizes pathogen on cell surface Produces series of cytokines Cytokines drive the rest of the immune response These knocked out in AIDS B cell can bind to antibody Receptive to cytokines Divides Can become plasma cells Release particular type of antibody IgM sotype switch Plasma cell that releases lgG These will be predominant cells second time invader is present Memory B cell Specific for antibodies 31 March Dia betes There are 208 million children and adults in the United States or 7 of the population who have diabetes Estimated 146 million have been diagnosed 62 million nearly 13 are unaware they have the disease Pancreas produces insulin 9 blood Energy metabolism Decreased glycolysis Glycogen synthesis increase in muscle amp liver Type Juvenile onset or insulindependent Not always in juveniles Major lesion insulinproducing islet cells destroyed by autoimmune response Positive family history Exposure to certain viral infections or other environmental toxins may serve to trigger abnormal antibody Autoantibodies produced against insulin islet cells product of islet cells Symptoms Increased thirst Increased urination Weight loss in spite of increased appetite Fatigue Nausea Vomiting Type II adult onset or insulinresistant Normal production of insulin but it doesn t do anything Glucose cannot enter cells stays in blood Risk Obesity metabolic syndrome Metabolic syndrome Obesity high blood pressure high blood lipids lack of exercise Metabolic syndrome also includes type II diabetes Pancreas thinks there s not enough insulin Makes more Fails Prevalence Type II 16 mil Americans incl undiagnosed 72 mil diagnosed Rate of people infected is increasing dramatically Type II Symptoms Same as Blurred vision Slowhealing infections No single cause Being over 40 Overweight Family Gestational diabetes during pregnancy AfricanAmericansHispanics at greater risk Cannot use glucose Use glycogen and fats instead Blood pH lowers due to fat digestion 9 diabetic coma Hypoglycemia symptoms Confusion Difficulty speaking Dizziness Hunger Feeling weak Effects of high blood glucose on vessels Blindness Atherosclerosis Numbness of feet and hands Due to nerve damage Sensory motor autonomic nerves can be affected Lecture 2223 Objectives Know the basic elements of the nervous system Understand the nature and classification of hematomas Understand the nature and classification of strokes Understand the epidemiology and pathogenesis of multiple sclerosis and Parkinson s disease Know the pathogenesis of encephalitis and meningitis Neuron Cell body with nucleus Axon main fiber signal transmission Dendrites smaller signal reception Synapses gaps between neurons Neurotransmitters released into synapse to continue signal Myelin sheath fat rolled around the axon White matter wrapped in myelin Gray matter unwrapped Myelinated transmits faster Oligodendrocytes produce myelin Astrocytes are involved in memorysupport Microglial cells immune defense Membranes meninges Outermost dura Next arachnoid Inner pial Traumatic head injury Hematoma Results in bruise in brain hemorrhage Epiduralsubdural most common Blood leaking into brain inflammation Pressure builds until it equals arterial pressure the blood to brain stops schemia Brain Stroke Brain cells die 9 coma 9 death Subdural arteries burst Epidural veins burst More sudden onset of symptoms Headaches vomiting Subdural Loss of consciousness Chronic unexplained headache personality change or hemiparesisplegia 12 body weight 15 resting cardiac output 20 total oxygen consumption Very susceptible to ischemia reduced blood flow Same factors amp process as heart attack schemic Clot Portion begins to die Cerebral infarct Hemorrhagic stroke Blood vessel bursts Pressure rises Unconsciousnessampc Thrombolytic clot forms inside brain itself Embolytic forms somewhere else moves into brain Sooner it s found more likely it can be stopped lschemic is most common Symptoms Risk Numbness weakness Motor amp cognitive function Difficulty raising both arms Speech difficulty Gender males at higher risk High blood cholesterol Obesity Smoking AfricanAmerican 8 February Lecture 6 Objectives Know the organs and the cells of the immune system Understand the adaptive immune response Understand how T cells and B cells protect against infection Characteristics of the Acquired Immune Response Hallmarks Specificity and Memory Primary and Secondary Immune Responses Humoral vs Cellular Immunity Humoral Serum extracellular pathogen Cellular Lymphocytes intracellular pathogen Primary lymphoid organs thymus amp bone marrow Secondary lymphoid organs sites of immune response lymph nodes ampc Cells of the immune system B cells T cells macrophages amp dendritic cells T cells capable of initiating immune response when find invaders MHC molecules pick up antigen break it up display it Once the T cell recognizes it lots of processes begin Antigen shows up processed 9 T cells arrive find antigen 9 B cells arrive 9 B cells proliferate and specialize Every virus that infects a cell has to use a specific molecule to bind to another specific molecule on a cell Antibodies cover the virus so it can t bind Same thing is true with bacterial toxins Virus toxin neutralization Opsonization Coating of antibodies Gives traction so the invader can be eaten Antibodies are too big to get inside cells Cellular immune response Deals with intracellular 9 infected cells are killed by T cells After B cell reacts with T cell invader B cell 9 plasma Releases antibodies in blood Basically T cells deal with virus B cells deal with bacteria Lecture 7 Objectives Understand primary immune deficiencies Understand acquired immune deficiencies Understand etiology epidemiology and pathogenesis of HIV AIDS Immunodeficiencies Primary of congenital immune deficiency syndromes Defect in any of the components of normal immune response or normal inflammatory response Secondary or Acquired Immune Deficiencies Nutritional Iatrogenic drug induced Traumatic eg burns amp head injuries Stressinduced Microbial Most frequent cause of AIDS transmission in US is male male HIV is a retrovirus Uses RNA Absorption 9Uncoating Creates DNA from its RNA using reverse transcriptase 9 DNA inserted into host genome Reverse transcriptase creates lots of mutations which leads to the person being infected by multiple strains AIDS symptoms AIDS is the description of the disease HIV is the virus Oral thrush Lymphoma Kaposi sarcoma Things we normally deal with become problems 7 April Control of bone remodeling Parathyroid hormone Controls serum CaH by mobilization from bone hormone binds to osteoblasts and activates osteoclasts Calcintonin Lowers serum CaH stores to bone Vitamin D Increases intestinal absorption of CaH and activates osteoclasts Tendons points at which muscle attaches to bone Ligaments connect bone to bone Sprains and Strains A sprain is a stretch andor tear of a ligament a band of fibrous tissue that connects two or more bones at a joint A strain is an injury to either a muscle or a tendon fibrous cords of tissue that connect muscle to bone Depending on the severity of the injury a strain may be a simple overstretch of the muscle or tendon or it can result from a partial or complete tear ACL can be torn by hyperextension or sudden pressure to the bottom half of the leg 25 January Salmonella Intracellular bacteria nterferes with host cell function Feces 9 oral route Attaches to wall of small intestine Replicates in lymphoid follicles Leads to diarrhea Messes up cyclic aMP 24 48 hours to occur 9 fast Selflimiting will go away by itself Treatment fluids let it solve itself Vomiting diarrhea ampc for 2 3 days 9 most likely food poisoning not flu Antibiotics interfere with the bacteria creating a cell wall So you poison the bacteria without poisoning the host Antivirals are much less effective 9 you have to kill host cells Prion protein Virus DNA RNA protein Viruses 1 Adsorption virus sticks to viral receptor on host cell No one virus infects all cells Different viral receptors 2 Penetration virus enters the cells 3 Uncoating protein coat stripped DNA RNA is free 4 Replication uses host cell mechanisms to copy 5 Assembly uses host cell ribosomes to make proteins to make more viruses 6 Release Type 1 Replicate until there are so many viruses the host cell bursts Type 2 Budding Virus pushes out of host taking membrane with it Enveloped virus When an enveloped virus attaches to the host the envelope fuses with the host s cell membrane Host reacts9 inflammation Enveloped viruses do not last long outside of host cells The envelope is essential to its function and it denatures quickly Non enveloped viruses are very sturdy Influenza A RNA virus Enveloped Neuramidase and hemogglutin are in the envelope These are the molecules referred to in something like HlNl Molecules that attach to host cell Route of transmission Aerosol coughing sneezing Aerosol transmission 9 Infection 9 Immune System hopefully 9 Recovery Host sheds virus for 10 days with proper immune response If immune system can t beat the virus 9 pneumonia inflammation of the lungs HSNl Outbreak 1999 12 year old boy in Hong Kong Flulike symptoms Dead in 4 days Next 2 weeks 12 people with same symptoms 6 died Traditionally a fowl influenza First time it appeared that there was direct transfer from animals to humans Resulted in chicken slaughter 2001 returned Southeast Asia particularly Deaths of millions of birds 2030 people As of today 220 infected 150 deaths 60 kill rate Cannot move from human to human 24 February Women are at higher risk of breast cancer the longer they are exposed to estrogen Menstruating earlier in life Menopause later in life Hormone replacement therapy Also obesity lack of physical activity alcohol use diet high in saturated fats Genetic Factors About 5 to 10 of breast cancers occur in women with an inherited susceptibility to cancer The majority of these are women with hereditary breast and ovarian cancer syndrome which is explained by deleterious mutations in the BRCA1 and BRCA2 genes In approximately 25 of women with breast cancer there s a genetic alteration in the HERZ gene that produces an increased amount of the growth factor receptor protein on the tumor cell surface The TP53 gene p53 is found altered in breast carcinomas in approximately 20 40 of all cases Most breast cancers are ductal carcinomas Usually die due to metastases BRCAl amp 2 DNA repair Form a complex interact w p53 Objectives Lecture 11 Understand the process of hematopoiesis and its cellular products Understand the pathogenesis of irondeficiency anemia Know the symptoms and pathogenesis of mononucleosis Understand the differences between Hodgkin s and nonHodgkin s lymphomas Inside bone marrow is a hematopoietic stem cell In adults spinehipribs are marrow bones In children all are Pluripotent stem cell Lymphoid stem cell Lymphocytes Bamp T Myeloid stem cell Monocytes become macrophages when they leave the blood Granulocytes or Polymorphonuclear leukocytes or PMN s Eosinophil Neutrophil Basophil Megakaryocyte 9 platelets Erythrocytes RBC White Blood Cells Neutrophils 60 70 Eosinophils 1 3 Basophils 03 05 Lymphocytes 20 30 MonocytesMacrophages 3 8 Function of Eosinophils Cationic granule proteins and their release by degranulation Reactive oxygen species such as superoxide peroxide andhypobromite Growth factors Cytokines Functions of Basophils Contain anticoagulant heparin prevents blood from clotting too quickly Contain vasodilator histamine promotes blood flow to tissues Lots found at sites of ectoparasite infections Anemia too few RBC Iron deficiency anemia Most common nutritional deficiency in the developing world Abnormal palenesslack of skin color rritability Lack of energyfatigue Tachycardia high heart rate Pica 9 desire to eat peculiar substances Enlarged spleen Causes of ID Dietary insufficiency Malabsorption Increased demands pregnancyinfancy Chronic blood loss most common Ulcers Hemorrhoids Hookworms Colon cancer osis9 excess of Etiology of IM mononucleosis More than 90 secondary to EBV infection Risk Being a collegeHS student Kissing Blood transfusion 95 people worldwide infected Some immune suppression 9 strep throat Swollen lymph nodes esp under jaw on neck Soft swollen spleen risk of rupture Pathogenesis Transmitted in saliva nfects epithelia of mouth 9 lyses cells Spreads to bloodlymphoid tissues nfects liver spleen B cells Immune response Some infected B cells persist for life 19 April Exam This Thursday Lectures 18 29 Turner s Syndrome 45 X0 Female Nondeveloped ovaries Tend to be short webbed neck coarctation of aorta narrowing Klinefelter s Syndrome 37 XXY Male Sometimes partial development of breasts Sterile Taller longer arms Can have more X chromosomes XXXY XXXXY likelihood of mental problems increases with additional X s XXY normally has no mental problems Autosomal genetic disorders Dominant Heterozygous express Recessive Homozygous recessive only express Testosterone amp 5otdihydrotestosterone Necessary to develop a male 5otReductase Deficiency Absence of 5alpha reductase type 2 limits 5otdihydrotestosterone XY fetus does not undergo virilization External genitalia female or nearly At puberty genitalia become masculine or nearly 5otreductase type 1 becomes present at puberty Single point mutation causes deficiency LeschNyhan disease Purine salvage pathway doesn t function uric acid created Point mutation in Xchromosome Selfmutilation usually lips tongue fingers Sexlinked 9 nearly always males Rare Rarely live beyond 40 Growth retardation reduced IQ llOrange sand may appear in diapers due to uric acid crystalluria Uric acid damages the brain causing the behavior 10 February Exam Next Thursday Covers through immune deficiencies Look at objectives Iectures 17 Pathogenesis AIDS Contact to HIV Positive 0 90 1 to 2 months flu like symptoms HIV Positive to AIDS 95 3 to 5 years average 10 years It now takes longer to go from HIV positive to AIDS due to medication AIDS to Death 100 1 6 years It s hard to make vaccines for this since the virus is constantly mutating Treatment Reverse transcriptase inhibitors prevents virus from making DNA from its RNA Protease inhibitors Chemokines cytokines squbIe things made by one cell that react with another ceII block the entry of virus into cell HAART Higth aggressive antiretroviraI therapy Protease inhibitors amp reverse transcriptase inhibitors Expensive Objectives Lecture 8 Understand the pathogenesis of each of the four major types of hypersensitivity reactions Understand the pathogenesis of rheumatoid arthritis Hypersensitivities ImmediateType All Antibody Mediated Type allergies Type II autoimmune disorders Type III immune complex disease DelayedType All mediated by T cells DTH Contact dermatitis Allergies First time exposure No allergic response Picked up Presented to T cells Plasma cell produces IgE antibody Mast cell has a receptor Next exposure Binds to IgE on mast cell Mast cell degranulates Inflammatory response Every Type hypersensitivity involves IgE Nonallegic person will produce lgG instead of IgE Repeated injections are meant to force the system towards lgG instead of IgE Type II hypersensitivities make antibodies against cells Most autoimmune diseases occur more often in females than males humans 8 March Exam is on Lectures 8 17 Lecture 17 Objectives Know the epidemiology of COPD Understand the pathogenesis of chronic bronchitis Understand the pathogenesis of emphysema Chronic Obstructive Pulmonary Disease Catchall phrase to describe lung diseases characterized by chronic airway obstruction Chronic bronchitis Affects bronchioes Inflammation Emphysema Affects alveoli Chronic bronchitis Excessive production of mucus causing cough 90 caused by smoking Other causes air pollution ampc Bronchioles become inflamed Fluid leaks into bronchioes Restriction of airflow Can cause rightside heart failure blood flow is restricted peripheral edema Emphysema Enlargement of the airspace with destruction of alveolar walls Rare in nonsmokers Alveolar walls destroyed 9 surface area for gas exchange decreases Shortness of breath with light exertion Rapid labored breathing severe Pinkish skin and barrelshaped chests due to overinflated lungs since they re trying so hard to breathe deeper Because of chronic irritation inflammation begins Lung begins to digest parts of itself Hypersensitivities I II amp III are all immediate They are run by antibodies which are always present Type IV is delayed T cell mediated IgE nothing happens with first exposure Shows up on mast cells Reaction Type II autoimmune Type III immune complex Fall out of solution stick to vessels trigger inflammation Antigen antibody Type I II amp III can lead to anaphylactic shock Caused by immune response Type IV is delayed because it takes a while to develop enough T cells to respond Rheumatoid arthritis Rheumatoid factor is an immune complex Make antibodies against own antibodies Settle in joints cause inflammation Loss of function Cancer Most frequent W breast M prostate Most frequent killer lung Imbalance between cell division death Begins as single transformed cell requires multiple genetic changes Tumors must be able to get into vessel and be able to grow new vessels to be malignant Result of genetic predispositionsenvironmental factors Two types of affected genes Oncogenes normally affect the rate of cell division Tumor suppressor genes affect DNA repair and rate of cell death Most tumors have change in both types Most breast cancers are ductal cancers The metastases usually cause death Products of hematopoiesis Iron deficiency Nutritional deficiency is most common cause Mononucleosis Usually caused by EBV herpesvirus Through saliva Lifelong Mouth epithelia 9 blood 9 B cells Coagulation occurs by 2 pathways Both result in fibrinogen 9 fibrin Hemophilia deficiency of factor VIII easy bruising Xlinked ITP Type II hypersensitivity Against own platelets More bruising Usually caused by gramnegative bacteria infection DIC Little blood clots Get stuck Multiple organ failure Heart failure Major consequence of MI Inadequate pumping Leftside primary symptom pulmonary edema Rightside peripheral edema Shock Insufficient circulation Hyperbolic vs distributive H Loss of body fluid change in volume D Vasodilation Septic caused by bacterial infection Pneumonia Inflammation of lung Infectious cause Typical inside alveoli atypical interstices of alveoli Differences between chronic bronchitis amp emphysema 5 May 40 questions for final from previous exams Etiology pathogenesis amp risk factors from presentations 52 questions total Acute Radiation Syndrome Occurs hours to weeks after exposure to total body irradiation Hematopoietic syndrome least lethal Gastrointestinal syndrome Cerebrovascular syndrome most lethal Targets DNA Direct damage particle breaks bonds Indirect reactive oxygen species formed in cell Indirect more common Rapidly dividing cells most vulnerable Sources environairlinesairportsnuclear accidents warfaremedicalfood Hematopoietic 2 7 Sv Bone marrow stem cell death Depletion of blood cells Susceptible to infection 9 sepsis Uncontrollable bleeding no platelets Death or recovery within 60 days 50 exposed die Gastrointestinal 8 30 Sv Small intestine fastest cell division Stem cell death in crypts Depletion of epithelium Bacteria 9 sepsis Nausea vomiting diarrhea Death in 10 days Cerebrovascular gt30 Sv Burning sensation within minutes Brain swelling Death in hours Treatments Cytokine therapy Decreases apoptosis Helps neutrophils recover Increases hematopoiesis Stem cell therapyradioprotectants in future Drugagent to block effects of exposure Sickle Cell Abnormal hemoglobin Chronic inflammation Point mutation in chromosome 11 A sub w T Gene responsible HBB Autosomal recessive One recessive allele 9 sickle cell trait RBC sicklingrupture Decreased blood flow Clotting quotCrisisquot 9 pooling of blood Strokes acute chest syndrome organ damage Abd pain bone pain excessive thirst poor sight Malaria resistance Parasite lives in RBC Inhibits Malaria growthdevelopment Treatment Bone marrow transplant Relieving pain Prevent infectionsorgan damagestrokes Blood transfusions Gene therapy Nitric oxide NO 9 vessel dilation prevents clumping Dengue Fever Dengue virus Transm by mosquitos Four strains Also caused by organ donation infected blood vertical transmission mother 9 child Selflimiting Attaches to E glycoprotein taken into cells nfects macrophages Fever 9 causes bleeding Result of immune enhancement Shock 50 mortality Muscle acheshigh feverhypotension low BPreddened eyesswollen lymph nodes Treatment None currently Exposure to 1 strain 9 lifelong immunity to that strain Equine Infectious Anemia EIA Group V retrovirus Only equines Through body secretions Lifelong carrier Mosquitos closely confined horses poor sanitation Symptoms Acutesubacutechronic Can relapse between these Acute Sudden onset Abd swelling Weak pulse High mortality Subacute Most common Longer onset Swelling Fever Rarely 9 death Chronic Advanced anemic Retirement Not always present w symptoms No treatment Usually euthanized Developing vaccine Listeria Food borne bacteria Gram positive Listeria listeriosis Surviving bacteria from stomach causes inflammation of small intestine Carried to lymph nodesspleenliver C3 doesn t affect bacteria macrophages using C3 have no effect Amnioitis pregnancy problems Jaundiceshockpressure in skullmeningitis IV antibiotics ampicillin 1 March Exam next Thursday Lymphomas ampleukemias will not be on the exam Objectives Lecture 12 l39 39 Ithe basic 39 39 of U 39 Know the genetics symptoms and effects of hemophilia Understand the pathogenesis and symptoms of ITP and DIC ITP Making antibody against own platelets Reduced number of platelets Thrombus blood clot Hemostasis Stepwise process to stop bleeding Three major components Vascular wall Platelets Coagulation cascade Vascular spasm Platelet plug Fibrin clot Clot retractiondissolution Role of Endothelial Cells Normally inhibit coagulation by actively inhibiting platelet adherence After injury of inflammation release procoagulant proteins Loss of endothelial integrity exposes underlying procoagulant proteins and collagen both of which cause platelet aggregation Tissue factor is releasedplatelets arrive after damage to blood vessel Activation of platelets changes them 9 they become sticky Fibrinogen 9 fibrin Coagulation Intrinsic pathway contact activation pathway SlowActivated when blood contacts lipoprotein exposed at wound site Extrinsic pathway tissue factor pathway RapidActivated by damaged tissues Tissue factor pathway most important Prothrombin 9 Thrombin As a result fibrinogen 9 fibrin Fibrin clot forms sticky strands of fibrin Clot retraction Shrinking Pulls platelets more closely together Helps to join the edges of the injured vessel Clot dissolution Allows for reestablishment of blood flow Initiates healing Plasminogen activators formed in vascular endothelium liver and kidneys converts plasminogen to plasmin Disrupts fibrin strands Plasmin chops up clot ITP Acute Occurs most frequently in children Often follows a viral infection Almost always selflimiting Sudden onset of bruising Chronic Occurs most frequently in adults No obvious association with infection Females 2x males Peak age 20 50 ITP Symptoms Bleeding into skin or oral mucosa Bruising Nose bleeds Abnormal menstruation Splenomegaly Hemophilia A Result of deficiency of clotting factor VIII Most common form Usually referred to as quotHemophiliaquot Xlinked recessive Varies from mild to severe Bruising Spontaneous bleeding More commonly males Disseminated Intravascular Coagulation DIC Causes Infections Malignancy Major traumatic injury Other underlying disease states eg connective tissue disorder Various complications associated with pregnancy Incompatible red blood cell transfusions Some snake bites Typically gram negative bacteria infection Little blood clots microthrombi Plateletfibrin activation They get used up Bleedinghemorrhage Tissue damage from clots sticking Early Symptoms Bleeding Thrombosis formation Sudden bruising Organ symptoms Organ failure due to clots Objectives Lectures 13 and 14 Know the basic anatomy and function of the heart arteries and veins Understand the pathogenesis of atherosclerosis Understand the underlying mechanisms of heart attacks I39 39 Ithe and for heart attacks Contraction SA sinoatrial node sends out signal Atria contract Ventricles contract P atria contraction QRS ventricles T relaxation of ventricles Blood flow SuperiorInferior vena cava 9 right atrium 9 right ventricle 9 lungs 9 left atrium 9 left ventricle 9 aorta 9 body Pericardium surrounds heart pericardial space then visceral pericardium epicardium attached directly to heart Blood pressure High when ventricles contract Low resting Arteries big muscular elastic Veins smaller have valves And the lymphatic system 18 January Geraldcalahancolostateedu Sample exam questions and answers on ramct In class review session before each exam 3 exams 33 questions Multiple choice true and false 100 points Final Comprehensive 50 questions from previous exams and new material also derived from presentations Do better on the final than another exam drop lowest score and count final twice Objectives Understand the nature of the science of pathology Know the leading causes of death in the US Know the leading causes of death in the underdeveloped world Know the reasons for the differences Understand symbiosis and its various forms Disease as a Way of Life 88 of Americans over 65 years of age have at least one chronic health problem Conclusion Health as we define it is the unusual state attained by very few ifany human beings It is not our health that determines who we are as human beings it is our illness Infectious Verses Noninfectious Diseases Infectious extrinsic disease involves a transmissible agent that is the ultimate cause of the disease Intrinsic sometimes called chronic diseases do not obviously involve a transmissible agent The terms contagious and infectious are not synonymous Morbidity makes us sick Mortality kills us US deaths 2002 Heart Disease 696947 Cancer 557947 Stroke 162672 Leading Cause of Death Worldwide Heart disease Infectious and parasitic disease Underdeveloped world 55 die from an infectious disease Developed vs Developing Outside of the developed world the greatest threat to human life is infectious disease Why are infectious diseases less in developed areas Vaccines Water treatment sanitation Antibodies Public health Nutrition Why doesn t the rest of the world have these Money Worldwide death causes HIV AIDS Respiratory infection Heart disease Conclusions Infectious diseases leading killer worldwide Symbiosis Two organisms residing in the same space Commensalism One benefits no harm Mutalism Both benefit Parasitism One benefits other harmed Transmissible Agents of Disease Prions Viruses Bacteria Fungi Parasites Protozoa ns Helminths Virulent can cause disease in any apparently healthy animal Opportunistic can only cause disease in any animal that is compromised Defense Mechanisms Innate nflammationampc Adaptive Antibodiesampc Pathogenic Adaptations Both the pathogens and mammalian defense are constantly evolving systems Like a waltz one step forward one step back 1029 bacteria in the world 10M bacteria person 1013 cells person 90 of a person is bacteria 5 April Infectious Diseases Encephalitis Myelitis Cerebral abscess Meningitis There is normally a bloodbrain barrier For an infectious agent to get into the brain Penetrating injury or Damage endothelium more common Breaks bloodbrain barrier Herpes virus usual cause of encephalitis Moves through neurons Inflammation in the brain Also caused by others arbovirus infection ampc Inflammation causes swelling raises pressure decreases blood flow Drowsiness Confusion Sudden fever Headache Cell death in brain Meningitis membranes infected Viral less lifethreatening than bacterial Transmission can be through direct contact with saliva ampc Healthy people may also transmit Fairly rapid onset Neck stiffness fever sensitivity to light Meningococcal sepsis usually is the killing agent Endotoxin Petechial or purpuric rash Hypotension Acute adrenal hemorrhage Multiple organ failure 9 shock Symptoms of MS multiple sclerosis Weakness or fatigue Numbness or tingling Blurred visionvisual loss Poor coordination of muscle movements Spastic muscles Challenges with memorythinking skills Myelin sheath loss Fewer neurons more astrocytes Autoimmune Usually flares up dies down Gets a little worse with each flare Treated with immunosuppressants to slow the immune system oligodendrocytes are being destroyed 9 slow the process Women are more likely to become diagnosed Genetic predisposition Usually diagnosed between ages of 20 and 50 Northern European descent more likely Probably an infectious agent involved Alzheimer s Dementia Mild forgetfulness Begins to interfere with daily activities Loss of motor function speech Unreactive to exterior stimuli Can become aggressive wander sundowners usually wander in evening As much as 30 brain mass can have disappeared by death Amyloid plaques between neurons Destruction of axons Not inflammatory Neurofibrillary tangles Pieces of proteins Genetic factors Parkinson s disease Hunched shoulders shuffle Tremor Worsens over time Occurs in substantianigra of brain Affects muscle movements Controlled movement needs dopamine Lecture 24 Objectives Know the elements and structure of bone Know the designation and pathology of sprains Understand the consequence of ligament and tendon damage Understand the healing process for bone feature Cartilage has no nervesblood vesselslymphatics Cannot be repaired Types Hyaline articular Inside joints inside bones There are also fibro amp elastic Made of collagen and chondrocytes Makes movements smooth Bones function Mechanical Mineral storage Hematopoiesis Bone matrix Collagen fiber give tensilesupportive strength Proteoglycansglycoproteins Bone minerals rigidity Calcium amp phosphate Outer compact cortical Inner spongy cancellous Osteoblastsosteoclastsosteocytes Involved in bone creation Blasts build bone Clasts remove bone Cytes bone matrix creation Formation Begins with cartilage Periosteum forms Center ossifies Rest ossifies form the inside out Remodeling by resorptionreformation Preosteoclasts are activated Digest old bone New bone made Control Parathyroid hormonecaIcitoninvitamin D 22 March Objectives Lecture 18 Know the basic physiology and anatomy of the G system Understand the pathophysiology of peptic ulcers Understand the pathology of celiac disease Understand the pathogenesis of Crohn s disease and ulcerative colitis Understand the pathogenesis of cholera Functions of G System Ingestion Propulsion Secretion Digestion Absorption Excretion Esophagus Moves food from mouth to stomach Doesn t have as many layers as the stomach Doesn t have mucus producing cells Stomach Secretes HCI pepsin and water Stores food while it is being worked with pH usually between 2 and 3 Small intestine Absorption proteins peptides amino acids fats triglycerides nucleic acids Not so much water Goes to liver and gets detoxified through portal system circulation Lots of villi in interior increase of surface area Large intestine Absorbs water some minerals Clinical Manifestations of Gastrointestinal Dysfunction Dysphagia difficulty swallowing Anorexia loss of appetite Vomiting Constipation Diarrhea Abdominal pain Bleeding Inflammed esophagus normally caused by acid reflux Esophagus does not have mucus layer f acid eats through esophagus contents may empty into thoracic cavity May cause esophageal tumors Medications and Gastritis Aspirin and other nonsteroidal antiinflammatory drugs cause gastritis Inhibits prostogladin Prostogladin causes pain and regulates mucus production in stomach Stomach inflames Other causes Heliobacterplori H pylori and other infections Pernicious anemia A form of anemia that occurs when the stomach lacks a naturally occurring substance Symptoms of gastritis Pain usually upper left quadrant Diaphragmatic hiatus where esophagus passes through diaphragm Hernias something moves into a space where it s not normally found Section of stomach moves up through hiatus into pleural cavity Pain amp difficulty swallowing Can be surgically repaired Achalasia stenosis scarring of gastroesophageal junction Hard to swallow Treated with balloon Peptic ulcers Occur in stomach or duodenum Also quotgastricquot or quotduodenalquot Part has been destroyed sore opens Imbalance between acid and mucus Also usually H Pylori present Stomach digests itself If it hits a blood vessel 9 bleeding ulcer Inflammatory bowel diseases Major defensive response in gut Two major types Crohn s disease and ulcerative colitis Seems to be genetic predisposition American Jews of European descent are more susceptible Largely a disease of the developed world Crohn s disease Cause unknown Aggravated by diet and stress Usually late teens early twenties An abnormal reaction to infection can play a role Infection could result in immune or inflammatory attack on gut flora Most commonly affects end of small intestine beginning of large intestine Infection with worms can reverse symptoms Can affect any part of GI system Skip lesions areas of infection are not continuous Ulcerative colitis Inflammation in colon large intestine Continuous lesion does not skip Lining of gut becomes more exposed to digestive enzymes Some symptoms anemia due to bleeding fatigue weight loss diarrhea Cause unknown Seems to run in families Intestinal obstructions Herniation of part into another area Adhesions between intestinal loops Intussusception sliding of one part into another telescoping Volvulus twist Pain nausea vomiting occur 1 February Fungal diseases happen after the fungus is dead in mycotoxicoses they are ingested If they are actually still alive mycoses Ergot Releases ergot alkaloids Hallucinogenic Pathogenesis Ergotism Ergot alkaloids have a wide range 9 circulation neurotransmission motor problems vasoconstriction quotSt Anthony s firequot Vasoconstriction can cause limb extremity death Symptoms Convulsive Diarrhea paresthesias itching seizures headaches nausea and vomitingHallucinations and mental effects including mania or psychosisCaused by clavinet alkaloids Gangrenous Result of vasoconstriction induced by the ergotamineergocristine alkaloids of the fungus It affects the more poorly vascularized distal structures such as the fingers and toes Mycoses Superficial Subcutaneous Systemic Opportunistic Example Tinea TineaCorporis skin Tinea Pedis athlete s foot TineaTonsoris Ringworm is a type of TineaCorporis Subcutaneous mycoses are more difficult to treat than superficial Can be longterm Rarely fatal Coccidiomycosis Aka valley fever Fungus lives in SW US soils Wind blows 9 airborne Systemic all begin with inhalation Attaches to lungs 9 circulation 9 bones brain Motor amp cognitive abilities Opportunistic Ex Oral Thrush Found in newborns AIDS Parasites eukaryotic cells Plasmodium falciparum Malaria 13 of the world s population affected Several organisms can cause it this one causes the worst Malaria Transmitted by mosquito human to human Warm moist places DDT spraying wiped out mosquitoes carrying malaria in US Spraying stopped because effects of it got up to raptors ampc softening eggs Malaria gets into the mosquito s salivary glands mosquito injects saliva Liver 9 blood and back Periods of chill and fever lasting several hours and occurring every few days Caused by cycles of rupture of red blood cells Respite can last from several days to several months If not treated the spleen and the liver become enlarged anemia and jaundice develop Most drugs used in treatment are active against the parasite forms in the blood Eg artemisin derivatives It is curable but you can t become resistant because you ve had it Slows blood cell reproduction making it easier to kill Dicroceliumdenriticium Suicidal behavior to complete life cycle Ants cows Rats cats Helminths Nematodes round Trematodes flat Cestodes tape Wucheriabancrofti Causes lymphoid filariasis Mosquito borne Mostly humanhuman transmission Microfilaremia worm is present in the blood In some cases it doesn t show in blood lymphangitis lymphedema flow of lymph through lymph nodes stops 9 elephantiasis Lymph systems brings in all the fluid that leaks from blood vessels Worms block lymph nodes 9 they can t function Canine heartworm Mosquito Dog to dog Inside blood Grows into worm Heart gets plugged up with worms Infectious disease symptoms gen Chills lymphadenopathy leukocytosis fever Countermeasures Vaccines Antibiotics Objectives Know the soluble and cellular elements of the inflammatory response Know the process and consequences of inflammation Understand the difference between acute and chronic inflammation Innate vs Adaptive acquired Adaptive means defensives have to be created Innate a defensive already exist 14 April Exam covers GI system through genetic disease Ultraviolet Light UVC 100280 nm radiation is filtered out by ozone in the stratosphere Only a small amount reaches the earth s surface UVB 280320 nm radiation poses a threat to life on earth even though some of it is filtered out by ozone in the stratosphere The cumulative exposure of UVB radiation may cause sunburn cataracts suppressed immune systems premature aging including wrinkles and skin discolorations as well as skin cancer UVA 321300 nm requires 103 times more than UVB to produce sunburn Most common skin cancer is basal cell carcinomas Rarely metastasize Slowgrowing Squamous cell carcinomas More dangerous Greater risk 9 longer cumulative sun exposure Melanoma Most dangerous Highly metastatic Sometimes arise from preexisting moles but usually a new spot Infectious diseases of skin Fungal superficial mycoses Bacterial staphylococci and streptococci Viral herpes Microsporum causes tinea Fungi growing on skin Athlete s foot Ringworm Impetigo More common in children Bacterial infection on surface of skin Treatable by antibiotic cream Staphylococci or streptococci Fascia living cells surrounding muscle Can become infected Toxins are produced that destroy tissue CO2 causes skin to bubble up Skineating bacteria Herpes Lifelong Genital symptoms Swollen glands in the groin Discharge from vagina or penis Those two are more common Painful or difficult urination Feverheadachemuscle ache Acne Sebaceous glands produce sebum Bacteria is normally carried out In acne there is sebum overproduction Hair follicle is plugged up Bacteria multiply inside Hormones can affect production of sebum Eczema Red scaly inflamed spots of skin Itchy Underlying mechanism Type I Hypersensitivity Type of allergy contact w certain things make it worse Faster shedding of skin Eczema flare risks Illness Physicalmental stress Urticaria Hives Also a Type I Hypersensitivity Smooth raised bumps Lecture 28 and 29 Objectives Understand the mechanisms and importance of gene transcription and translation Understand the forms and consequences of mutations Understand the etiology and pathogenesis of Turner s and Kleinfelter s syndromes Understand the etiology and symptoms of Down s syndromes Understand the etiologies and pathogenesis of LeschNyhan disease and 5alpha reductase deficiency Genetic imprinting Some genes are suppressed father vs mother Mutations changed in DNA that result in changes in genes Point mutation change of a single letter Nondisjunction chromosomes do not separate correctly Wrong number of chromosomes in cell Main cause of birth defects genetic mutations Also infant death Trisomy 21 Down syndrome Slanted eyes Diminished intellect Heart problems Simian crease crease in hand goes straight across Caused by nondisjunction Turner sKlinefelter s Turner s 9 X0 Klinefelter s XXY Turner s female genitalia infertile eggs decrease more rapidly ovaries regressed narrowing of aorta Can be a mosaic 28 April Giardia Diarrheal Giardia lamblia Infection by swallowing Giardia cysts Contaminated foodwater One of the most common causes of waterborne disease in US Fecaloral or persontoperson Attach to intestinal epithelium Symptoms same as most diarrheal illness Antiprotozoal medications antidiarrheal pills Vaccine reduces the number of cysts shed 9 prevents of organisms affected Purify water Glaucoma Build up ofaqueous humor fluid in eye 9 increased pressure in eye Overproduction or decreased outflow Causes damage to optic nerve 4 Types Open angle chronic Angle closure acute Congenital Secondary OP cause unknown AC caused by emergency C birth caused by abnormal development of fluid outflow channels S caused by medications other diseases Rabies Vision loss Surgeries to decrease pressure Neurotropic lyssavirus Transferrable between animals amp humans Infected saliva via bitesscratches Swellinginflammation of brainspinal cord Vaccine Louis Pasteur RNA retrovirus Brain 9 salivary glands Abnormal behavior foaming mouth hallucinations Furious type episodes hyperactive periods of calm Dumb type lethargic
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