New User Special Price Expires in

Let's log you in.

Sign in with Facebook


Don't have a StudySoup account? Create one here!


Create a StudySoup account

Be part of our community, it's free to join!

Sign up with Facebook


Create your account
By creating an account you agree to StudySoup's terms and conditions and privacy policy

Already have a StudySoup account? Login here

Introduction to Pathology

by: Miss Zena Toy

Introduction to Pathology PATH 300

Marketplace > West Virginia University > Pathology > PATH 300 > Introduction to Pathology
Miss Zena Toy
GPA 3.76

Beverly Kirby

Almost Ready


These notes were just uploaded, and will be ready to view shortly.

Purchase these notes here, or revisit this page.

Either way, we'll remind you when they're ready :)

Preview These Notes for FREE

Get a free preview of these Notes, just enter your email below.

Unlock Preview
Unlock Preview

Preview these materials now for free

Why put in your email? Get access to more of this material and other relevant free materials for your school

View Preview

About this Document

Beverly Kirby
Class Notes
25 ?




Popular in Course

Popular in Pathology

This 17 page Class Notes was uploaded by Miss Zena Toy on Saturday September 12, 2015. The Class Notes belongs to PATH 300 at West Virginia University taught by Beverly Kirby in Fall. Since its upload, it has received 19 views. For similar materials see /class/202675/path-300-west-virginia-university in Pathology at West Virginia University.


Reviews for Introduction to Pathology


Report this Material


What is Karma?


Karma is the currency of StudySoup.

You can buy or earn more Karma at anytime and redeem it for class notes, study guides, flashcards, and more!

Date Created: 09/12/15
Pathology is the study of disease and the structural amp functional changes in cells tissues and organs that underlie disease Etiology cause Pathogenesis is the sequence of events in the response of cells or tissues to the etiologic agent Morphologic changes are structural alterations in cells or tissues Functional derangements and clinical significance determine clinical features course and prognosis Nucleus is the overseer of all cytoplasmic events Cytoplasm contains the nucleocytoplasmic ratio NC ratio which is the differentiated v undifferentiated cells Mitochondria generate energy Ribosomes are small granules of RNA and are involved in protein synthesis They are attached to the RER Free ribosomes are polysomes and are structural proteins that maintain cell function Endoplasmic reticulum is the meshwork of membranes RER is the site of protein synthesis SER has complex functions catabolism drugs hormones nutriets synthesis of steroids Golgi apparatus is where proteins synthesized in ER pass through They are biochemically modified and packaged into secretory glandslysosomes Lysosomes are membranebound digestive organelles Hyaloplasm is the main structure in cytoplasm with no structure and is uid with organelles Mostly water Cytoskeleton maintains cell shape It contains filaments such as intermediate filaments which are cell type specific proteins Plasma membrane is the outer surface of the cell and the living structure requires energy Autocrine stimulation is self and has surface receptors for own secretory product T lymphocytes and IL2 Paracrine stimulation have mediators released from one cell and taken up by another neuroendocrine cells and chief cells GastringtHCl Endocrine stimulation has higher integration anatomically distinct organs and hormones are released into blood circulation erythropoietin helps bone marrow produce RBC Homeostasis is a state ofbalance between opposing pressures operating in and around a celltissue Steady equilibrium Interdependent Reversible cell injury is within range ofhomeostasis Stopping of injury results in a return to steady state Cellular swelling is where water enters hyaloplasm with mitochondrial swelling With Na K pump to have cellular swelling there will be excess Na and Cl and water into the cell Pathogenesis of cellular swelling has altered membrane permeability In reversible cell injury is the nucleus is not injured and energy is restored toxin neutralized cell will return to normal Pyknosisis condensation of chromatin Karyorrhexis is fragmentation of the nucleus Karyolysis is dissolution of nuclear structure with lysis of chromatin Cell injury causes hypoxia anoxia toxic injury microbial pathogens immunein ammatory mediators and geneticmetabolic disturbances Atrophy is the decrease in size of cell tissue organ or organism Hypertrophy is the increase in size of tissues or organs due to enlargement of single cells Occurs in heart increased workload and striated muscle exercise Hyperplasia is the increase in size of tissues or organs cause by increased number of cells These are usually combined benign prostatic and endometrial Hypertrophy Hyperplasia urinary bladder with obstruction and pregnant uterus Metaplasia changes one cell type into another smoker s bronchial mucosa columnar to stratified squamous and can be reversible Dysplasia is a disorderly arrangement of cells nuclear atypia Apoptosis cell death is dropping out and endogenously programmed Necrosis is exogenously programmed and irreversible Autolysis is in a dead organism Coagulative necrosis is most common and retains firmness This involves solid internal organs Liquefactive necrosis is the dissolution of tissue and occurs in brain Caseous necrosis is coagulative found with TB and is cheesy white Fat necrosis is liquefactive with lipolytic enzymes In ammation is a complex process Changes in blood circulation vessel wall permeability WBC response and release of soluble mediators Circulatory response is relaxation of precapillary sphincter in arterioles and oods the capillary network Plasma derived in ammation must be activated Cell derived in ammation may be stored synthesized Histamine has gaps that increase permeability Fluid and cells into interstitial space Bradykinin has effects similar to histamine but is slower Incites pain Complement system contains cascade proteins 19 Forms MAC Lipoxygenaseforms leukotrienes and slow reacting substances of anaphylaxis Cyclooxygenase forms prostaglandinsvasodilation PMNs are primary mediators of in ammation Segmented Phagocytosis Platelets make blood clot with proliferation of connective tissue cells Eosinophilsreact with basophils in allergic reactions and are the in ammatory response to parasites Basophils are IgE reaction Monocytes contain phagocytes Antigen presentation to lymphocytes and become tissue macrophages In ammation events has leakage of uid into tissue emigration of leukocytes and phagocytosis Serous is mildest clear uid and early stages of in ammation Fibrinous is severe strep bacterial pneumonia and pericarditis Purulent caused by pus forming bacteria High in lytic enzymes Abcessis localized collection ofpus Sinusabcess to skin Fistula is between cavities or cavity to skin Empyema is accumulation of pus in formed cavity Ulcerative is body surfaces or mucosa of hollow organs Pseudomembranous is ulcerative fibrinous pus CDIF Chronic is prolonged extensive loss of function PID Granulomatous is not preceded by acute Fever is where IL1 and TNF act on hypothalamus Labile cells are continually dividing skin hair nails Stable cells can be stimulated to divide parenchymal liver kidneys Permanent cells are nondividing with no proliferative brain heart Wound healing has PMNs scavenging the site Macrophages produce cytokines growth factors and mediators Myfibroblasts contract and secrete Angioblasts are blood vessel precursors Dehiscence is separation deficient scar formation Contractures are immobilization from excess scar formation Keloids are from defective remodeling Type III collagen Cell mediated immunity is mediated by T lymphocytes Humoral immunity is production of antibodies and mediated by B lymphocytes T lymphocytes mature in thymus CD4 are helper cells and CD8 are suppressor cells CD4CD8 is 21 B lymphocytes mature in bone marrow Humoral immunity differentiated by plasma cells which produce immunoglobulins Immunoglobulins are antibodies Fc fragment Fab fragment Antigen binding site IgMis largest and first to appear IgGis smallest but most abundant Small amount with initial immunization Reexposure boosts production IgA is mucoal secretions IgE mediates allergic reaction and anaphylactic shock Antibody production is contact between antigen and immune system cells Antigen presentation must have antigen present to B lymphocyte Most are presented by antigenpresenting cells macrophages amp are Tcell dependent Primary immune response has IgM as first but weak and IgG as temporary Secondary immune response has anamnestic reaction IgG production and is much stronger Complement activation is where antigen binds to Fab portion of antibody Fc region is binding site for complement and attaches cells to Fc receptors Type I hypersensitivity is hay fever rhinitis or anaphylactic shock Type II hypersensitivity is where antibodies react with antigens Hemolytic anemia and Goodpasture s syndrome Type III hypersensitivity is mediated by formation of immune complexes Lupus Type IV hypersensitivity is contact dermatitis most common poison ivy Transplant rejection Autograftis where patient is donor and recipient Isograftis genetically identical individuals twins Homograft is same species not genetically identical Xenograft is animals of different species Graftv Host is cell mediated Type IV Recipient is immunocompromised A blood has anti B antibodies Receive A or O B blood has anti A antibodies Receive B or O 0 blood has anti A and anti B antibodies Receive 0 AB blood has neither anti A or anti B Receive all dD is only Rh group that is clinically significant D or Dd is Rh positive dd is Rh negative Hemolytic disease of newborn is where ABO incompatibility is less important because IgM doesn t cross placenta Anti D is IgG which crosses placenta Negative mother exposed to positive cells produces anti D Subsequent pregnancy is where mother s antibody attacks baby cells Autoimmune disease is breakdown of autotolerance Lupus has antibodies to nuclear components DNA RNA nuclear proteins and antinuclear antibodies ANA Primary immunodeficiency disease severe combined immunodeficiency lacks T and B cells and can be fatal without isolation AIDS caused by HIV Selective affinity for CD4 helper cells Neoplasiais uncontrolled growth of cells whose proliferation can t be adequately controlled by normal regulatory mechanisms in normal tissue Normal cells stop proliferating and assume specialized function They have differentiation tumor cells do not Autonomous is independent of growth factors and stimuli Excessive don t respond to normal regulators unregulated Disorganized don t follow the rules of formation lack of contact inhibition Filing of cells Benign tumors limited growth good outcome sharp borders easy to remove cells resemble tissues arisen from differentiation regular shape and size low NC ratio normal number of chromosomes some complex function Malignant tumors uncontrollable growth no sharp borders harder to remove anaplasia undifferentiated vary in size and shape little cytoplasm high NC ratio abnormal number of chromosomes aneuploidy no specialized function rapid growth Metastasis spread cancer cells from primary location to another site Cells from one site to another Only tumor cells metastasize and not all malignant cells can metastasize Oma is benign tumors ofmesenchymal cells Adenoma is benign tumors of epithelial cells renal cell adenoma salivary gland adenoma intestinal adenoma which is a polyp Sarcoma malignant tumors ofmesenchymal cells fibrosarcoma liposarcoma Carcinoma Malignant tumors of epithelial cells squamous cell carcinoma Adenocarcinoma malignant glands or ducts neoplasia Lymphomas malignant tumors of lymphoid cells Gliomas malignant tumors of glial cells Seminomas malignant tumors of testicular seminiferous epithelium Blastoma malignant tumor from embryonic cells Teratoma derived from germ cells benign or malignant hair teeth etc Tumor staging is the clinical assessment of extent of spread More predictive value than grading Tumor grading is based on histologic examination of tumor Malignant cells have simpler metabolism Better adaptation and survival In vitro survives more easily and may be immortal In vivo is autonomous excessive and disorganized mentioned above Promotion is cells stimulated to proliferate Progression even if you take away carcinogen you still develop malignancy Conversion is new cell type Clonal expansion is rapid growth with identical daughter cells Selection is where best adapted clone outgrows others DNA viruses integrate directly into genome of infected cell RNA viruses reverse transcriptase makes DNA to incorporate into cellular genome with message in viral RNA RNA tumor virus HTLVl DNA tumor virus is linked to cancer but no proof Papillomavirus Epstein barr and hep B are strongly implicated Mutated normal genes are protooncogenes which normally encode proteins Dysregulation results in neoplasia Tumor suppressor genes are regulatory genetic mechanisms that protect normal cells against acquired oncogenes Wilms tumor is renal malignant tumor of infants and children Chromosomal fragility syndromes are Bloom s and Fanconi s Inherited tendencies are polygenic in uenced by exogenous factors Colon cancer and breast cancer BRCA1 and BRCA2 are in 5 of all breast cancers Tumor antigens are recognized as foreign Incidence is number of new cases over time in specific population Prevalence is numb er of all cases within a time in a population Mortality is number of deaths in a specific time and population Asbestos causes lung cancer and mesothelioma Dietary fat may cause colon cancer Cachexia is wasting weakness and weight loss anorexia and is a symptom of cancer Hypercoagulability is also a symptom of cancer Congenital present at birth but may not show up Malformations 75 have unknown causes usually genetic Deformations caused by extra fetal factors usually mechanical Teratogens agents that induce fetal malformation drugs etc FAS common in USA TORCH toxoplasma other varicella Epstein barr rubella cytomegalovirus herpes Deletions piece of gene missing Translocations piece of gene adjoins to another Monosomy loss of one chromosome Trisomy additional chromosome Trisomy 21 Down s most common chromosomal abnormality Turner s Syndrome 45 X monosomy X Klinefelter s Syndrome XXY 47 trisomy sex Autosomal dominant disorders Marfan syndrome and familial hyp ercholesterolemia Autosomal recessive disorders cystic fibrosis lysosomal storage diseases phenylketonuria Cystic fibrosis Most common autosomal recessive disease in US Affects chloride transport channel Lysosomal storage diseases accumulation of metabolites that can t be processed due to inborn enzyme deficiency Phenylketonuria Deficiency of enzyme that metabolizes phenylalanine into tyrosine X linked recessive evident in males by asymptomatic female Common disorders are hemophilia lack ofVIII or IX and muscular dystrophy Fragile X Syndrome 80 of males have mental deficiency Multifactorial inheritance several genes interacting with each other also environment and lifestyle Diabetes mellitus and anencephaly Neural tube defects incomplete fusionimportance of folic acid Acute leukemia most common malignancy in children Nephroblastoma most common extracranial solid cancer Premature before 37th week and less than 2500 grams Neonatal respiratory distress syndrome immature lungs deficient in surfactant lecithin needed for alveoli Capillaries site of most uid exchange Fluid movement controlled by hydrostatic pressure oncotic pressure albumin and lymphatics Imbalance results in edema Arterial end hydrostatic gt oncotic Venous end oncotic gt hydrostatic Edema excess uid in interstitial spaces body cavities Abdominal ascites or hydroperitoneum Pleural hydrothorax Pericardialhydropericardium Generalized edemaanasarca Effusion excessive uid can be transudate water or exudate pus In ammatory edema mediatorsincreased vessel permeability Hydrostatic edema increased vascular and arterial blood pressure Hypertension venous stagnation and congestive heart failure Oncotic edema reduced colloid osmotic pressure ofplasma Hypoalbuminemia Obstruction of lymphatics is less common Parasites elephantiasis Hypervolemic edema retention of sodium and water Active hyperemia blood into capillaries mediated by neural signals Blushing or exercise Acute in ammation Passive hyperemia increased venous backpressure Hematoma blood filled swelling blood boil Hemoptysis coughing up blood Hematemesis vomiting up blood Hematocheziaanorectal bleeding bright red Melena black discolored blood in stool Hematuria blood in urine Menorrhagia abnormal menstrual bleeding Metorrhagiauterovaginal bleeding non menstrual menopause Shock collapse of circulation Hypoperfusion of tissues with blood Cardiogenic shock pump failure of heart Infarct myocarditis valvular Hypovolemic loss ofvolume Bleeding diarrhea vomiting burns Hypotonic loss oftone pooling ofblood in vessels Anaphylaxis sepsis Compensated shock tachycardia quot heart rate vasoconstriction reduced urine production Decompensated shock hypotension oliguria acidosis Primary hemostasis formation of platelet plug Secondary hemostasis formation of fibrin clot Fibrinolysis clot breakdown Pathologic thrombi endothelial cell injury hemodynamic changes hypercoagulability of the blood Inherited abnormalities Factor V Leiden Disseminated intravascular coagulation coag system excessively stimulated Microthrombi formed in vascular system Excessive bleeding Venous thrombi most common and found in dilated veins varicose veins Embolism Occlusion of blood vessel by embolus Interrupt ofblood supply Venous thromboemboli cause of pulmonary embolism Arterial thromboemboliorginate in left atrium ventricle aorta Cause of cerebral embolism and organ ischemia If embolus becomes trapped it becomes embolism Infarction sudden ischemic necrosis resulting from insufficient blood supply White Pale infarcts arterial occlusion in solid organ Red infarcts venous obstruction Thrombolytic drugs streptokinase Anticoagulant drugs Anti platelet Plavix aspirin heparin Oral anticoagulants Coumadin MONITOR INR Systole left ventricular contraction Arterial pressure rises Blood forced into aorta and large arteries Diastole Left ventricle relaxes Pressure maintained by elastic squeeze Blood pressure modulated by kidneys blood vessel constriction preserve water for blood volume Reninangiotensin aldosterone system Total cholesterol LDL HDL VLDL cholesterol LDL bad cholesterol Promotes atherosclerosis HDL good cholesterol Protective against atherosclerosis VLDL amplifies atherosclerosis risk of high LDL or low HDL Triglycerides Total cholesterol 200 mgdl LDL cholesterollt 100 mgdl HDL cholesterolgt 60 mgdl not associated with risk Arteriosclerosis disease of small blood vessels Pts with htn and diabetes Atherosclerosis atheroma is basic lesion Soft fatty cholesterol followed by fibrous hard scar tissue with calcium Pathogenesis endothelial injury lipid accumulation in ux of smooth muscle cells and macrophages in ammation proliferation of smooth muscle collegen deposition Coronary artery atheroma angina is chest pain from ischemia and myocardial infarct is from coronary occlusion Brain infarction stroke Peripheral vascular insufficiency Atherosclerosis or aorta or major branch Intermittent claudication leg pain or cramps w exercise Renovascular insufficiency one cause of htn Bowel infarction Essential hypertension 90 no known cause Secondary hypertension specific cause identified kidney disease etc Malignant hypertension 16 011 0 progressive fatal w 0 treatment Vasculitis in ammation of blood vessels Autoimmune Angiitis small vessels involved Arteritis large arteries affected Necrotizing vasculitis small vessels are usually necrotizing Acute in ammation leads to death ofvessel Polyarteritisnodosa autoimmune Temporal arteritis most common LOCAL vasculitis Giant cell arteritis Blindness Thromboangiitisobliterans small vessels of handsfeet Most common in young cigarette smokers Raynaud phenomenon exaggeration of normal vasoconstriction amp vasodilation reactivity to cold or emotional stress Varicosities tortuous dilated veins Superficial are most common From hydrostatic pressure and leads to edema Epicardium membrane that covers surface of heart Endocardium membrane that lines heart continuation of vascular membrane Myocardium heart muscle SA node heart s natural pacemaker in the right atrium Dysrhythmia mechanically inefficient interrupt normal filling and emptying of chambers Normal cardiac rhythm 70 beats per min Bradycardia less than 60 beats per min Tachycardia more than 100 beats per min normal response to stress or work Congestive heart failure heart unable to eject volume ofblood as delivered and becomes engorged with blood Uncompensated heart failure too stretched fibers wweaker contractions Failed cardiac output Forward failure low ventricular output Backward failure venous congestion Left heart failure damaged heart muscle excess strain of high blood pressure aortic or mitral valve disease cardiomyopathy Symptoms uid retention dyspnea rapid heartbeat rales Right heart failure most common cause is left heart failure Pure right heart failure corpulmonale results from pulmonary hypertension Ischemic heart disease coronary artery disease caused by atherosclerosis Four syndromes angina pectoris myocardial infarct cardiac death chronic ischemic heart disease wcongestive heart failure Angina pectorisStable is relieved by rest medication exertion emotion cold Unstableis platelets aggregating on atherosclerotic plaque old angina angina at rest prolonged or nocturnal angina Unremitting doesn t uctuate and can t be relieved caused by myocardial infarct Myocardial infarction Myocardial necrosis caused by ischemia Complete occlusion of a coronary artery sudden Chronic Myocardial Ischemia ischemic cardiomyopathy Ventricular muscular deterioration Hypertensive heart disease strain leads to ventricular hypertrophy High metabolic requirements More susceptible to infarct and arrhythmia Decreased movement and stroke volume Valvular heart disease stenosis is obstructed ow and insufficiency is regurgitationback ow valves don t close properly Both mechanically inefficient and can occur together Rheumatic heart disease in amed valve cusps Susceptible to bacterial infection erosion Acute autoimmune disease group A strep pharyngitis molecular mimicry Acute rheumatic fever or chronic rheumatic valvulitis Infective endocarditis bacterial infection or valve Most common infective lesion of the heart Myocarditis viral or autoimmune Congenital heart disease develops in first 10 weeks of gestation Pericarditis usually viral Hemopericardium undiluted blood but just bloody effusion Allergic rhinitis hay fever irritated by allergic reactions Mucosal edema redness mucous secretion Prominent EOSINOPHILS Acute Upper Res Infections infections rhinitis common cold Caused by viruses Clear nasal dischargefever Acute Pharyngitis Sore throat viral Acute strep pharyngitis rheumatic fever and glomerulonephritis Vocal cord nodules reactive nodules vocal cord polyps Atelectasis incomplete expansion of lungs neonatal or collapse of previously in ated lungs COPD emphysema andor chronic bronchitis Emphysema abnormal permanent enlargement of airspaces distal to the terminal bronchiole accompanied by destruction of their walls wo obvious fibrosis Chronic bronchitis chronic cough that produces sputum for 3 consecutive months 2 years in a row Hypersecretion of mucous in large airways Bronchiectasis Permanent dilation ofbronchi and bronchioles caused by destruction of the muscle and elastic tissue Associated wchronic necrotizing infections Asthma chromic in ammatory disorder Hyperreactive airways Episodic reversible bronchostriction Increased responsiveness of tracheobronchial tree to stimuli Restrictive lung diseasePneumoconioses inhalation of mineral dusts Hypersensitivity pneumonitis immunologically medicated interstitial lung disorder T cell occurs after prolonged exposure to dust and occupational antigens Pneumonia lower respiratory infection infection of lungs Lung abscesssuppurative process characterized by necrosis Pneumothorax air within pleural space Pleual effusion excess uid within pleural space Pleuritis in ammation of the pleura Mesothelioma Pleural malignancy associated wasbestos exposure Gingivitis in ammation of the soft tissue surrounding the teeth Superficial Periodontitis In ammation of supporting structures Deeper in ammation Stomatitis in ammation of the mouth Glossitis In ammation of the tongue Precancerous lesions Leukoplakia white plaque patch that can t be scraped Sialadenitis in ammation of the salivary gland Dysphagia difficulty swallowing Heartburn re ux of gastric juices Hematemesis Vomiting of blood Stomach acid alters blood quotcoffee grounds Esophagus stomach duodenum Hematochezia unaltered red blood mixed with stool Lower colon or rectum Melena digested blood Black tarry stools Any intestinal site including esophagus Achalasia failure to relax Spasm of esophageal sphincter Result is dysphagia and regurgitation Hiatal hernia where esophagus passes through the diaphragm Diverticula outpouching of the alimentary canal MalloryWeiss Syndrome longitudinal tears in the GE junction as a result or severe retching or vomiting Laceration Esophageal varices varix dilated tortuous vein result of portal hypertension Most common cause of portal hypertension is cirrhosis of liver Esophagitis in ammation of esophagus GERD gastroesophageal re ux Gastroesophageal re ux consequences of GERD bleeding ulceration stricture and Barrett s Esophagus intestinal metaplasia gt dysplasia Risk factor for cancer Pyloric stenosis congenital anomaly Infants males wsevere projectile vomiting Gastritis in ammation of gastric mucosa Chronic gastritis is precursor for carcinoma Gastritis 1 cause of H pylori Peptic ulcer disease due to H pylori Atresia complete obstruction Stenosis just narrowing Obstruction causes in congenital anomalies 1 Herniation slipping out through weakened area 2 Adhesions sticking together 3 Intussusception telescoping 4 Volvulus twisting Angiodysplasia tortuous dilitations of small blood vessels in mucosa and submucosa of right colon and cecum that are prone to bleeding Vascular dis Hemorrhoids dilated anal veins varix Diarrhea high volume frequent watery unformed stool Dysentery low volume bloody painful Irritable bowel disease abdominal pain bloating varied in bowel movements or consistency No path findings Mostly women Temporary relief with bowel movement Enterocolitis in ammation of bowel associated with diarrhea Pseudomembranous colitis broad spectrum antibiotic C dif Celiac sprue malabsorption syndrome Gluten sensitive eteropathy gluten is in wheat oats barley rye Autoimmune Try to have gluten free diet Crohn s disease transmural in ammation lumen strictured Granulomas skip lesions fistulas fissures creeping fat Ulcerative colitis limited to colon Affects mucosa and submucosa Extends continuously proximally from rectum Bloody mucoid diarrhea that persists for days weeks or months Ileus occurs leading to toxic megacolon Precancerous treatment is total colectomy Diverticulitis In amed diverticulum Colon is the site for more neoplasms than any other organ in the body Digestive Exocrine Pancreas secretes 23 liters of alkaline pancreatic juice per day water bicarbonate mucus digestive agents Protease enzymes inactive form zymogen digest proteins in active form Lipase enzymes digest fats Amylase enzymes digest carbs Hormonal Endocrine Pancreas Islets of Langerhan secrete hormones into blood Alpha cells secrete glucagon Beta cells secrete insulin Delta cells secrete somatostatin Insulin acts on cell membranes to allow glucose to enter cell to be burned for energy Decreases blood glucose by allowing it to leave blood amp into cells Glucagon releases energy from body stores Somastostatin inhibits secretion of insulin and glucagon Acute pancreatitis is acute in ammation of pancreas Usually a sterile chemical in ammation Chromic pancreatitis repeated episodes of acute results in fibrosis Acute may be well documented or not In general treatment for pancreatitis is supportive Acute hemorrhagic pancreatitis medical emergency Lab tests are critical Blood amylase rises and falls quickly Blood lipase rises slower remains high longer Chronic alcoholism is responsible for 23 of chronic pancreatitis Carcinoma of pancreas adenocarcinoma common Mature to older men and women Smokers have twice the risk ofnonsmokers Very grave prognosis Diabetes mellitus hormonal pancreas disease Disorder ofinsulin action and secretion resulting in high blood glucose hyperglycemia Fasting BGL 126 mgdL or more BGL 200 mgdL on any occasion Hemoglobin A1C 65 or more Type 1 Diabetes deficiency of insulin resulting from autoimmune destruction ofislets Usually appears in otherwise healthy person under 20 Type 2 Diabetes 90 of cases Resistance to action of insulin by peripheral tissues Common in older obese adults Glycosuria polyuria most common symptom of diabetes too much urine Polydipsia excessive thirst electrolyte imbalance Polyphagia excessive hunger Acidosis may progress to diabetic coma Long term complications of Diabetes Vascular disease Accelerated atherosclerosis in large vessels Also microvascular disease Kidney disease Eye disease Brain amp peripheral nerva damage Hepatocytes liver cells They are facultative mitotic which means they can regenerate themselves Liver functions detoxification lipid and carb metabolism and storage regulates triglyceride and cholesterol protein synthesis functions regulation of albumin transport proteins and clot factors blood filter aging or damaged RBCs exocrine secretion bile Iaundice yellow color of skin and sclera resulting from retention of bile bilirubin gives skin yellow color Cholestasis impaired bile ow Cirrhosis diffuse and chronic fibrosis Caused by alcohol abuse Portal hypertension quot resistance to portal blood ow Hepatitis A fecaloral transmission Vaccine Hepatitis B Parenteral transmission Vaccine Hepatitis C Parenteral transmission Hepatitis D Parenteral transmission Hepatitis E Fecaloral transmission Alcoholic Liver Disease Phase 1 Hepatic Steatosis fatty liver Phase 2 Alcoholic Hepatitis Stage 3 Cirrhosis Hereditary Hemochromatosis HH excessive accumulation of iron through intestinal absorption Wilson Disease accumulation of toxic levels of copper Metastatic tumors of the liver more common than primary liver tumors Gallbladder regulates bile release Gallstones cholelithiasis Cholecystitis in ammation of the gallbladder Endocrine glands secrete hormones directly into the blood Hormones chemicals that stimulate or suppress cellular activity in a distant target tissue or organ Endocrine system pituitary gland master gland and all that it controls Ultimately controlled by hypothalamus Anterior of pituitary gland most involved by disease Hyperpituitarism gigantism general increase in body size child Acromegaly coarse appearance big handsfeet diabetes hypertension arthritis CHF osteoporosis ACTH adenomaCusing syndrome too much cortisol from adrenal Lutenizing hormone adenoma amp folliclestimulating hormone adenoma usually only mass effect Thyroid stimulating adenoma thyroid hyperactivity ADH deficiency diabetes insipidis Risk of dehydration Posterior pituitary disorder Graves disease primary hyperthyroidism 8090 of cases common autoimmune disease Enlargement of thyroid gland overactive metabolic state overactive autonomic nervous system exophthalmos Hypothyroidism usually primary may also result from failure of pituitary or hypothalamus Infantile or early childhood cretinism In older children or adults myxedema Slow metabolic rate T3 and T4 increased in hyperthyroidism and decreased in hypothyroidism TSH decreased in hyperthyroid bc ofnegative feedback from increased T3 and T4 Increased in hypothyroidism Increase in hyperthyroidism is result of pituitary Goiter enlarged thyroid gland Most common thyroid abnormality Thyroiditis in ammation Hashimoto thyroiditis common cause of goiter or hypothyroidismchronic autoimmune Neoplasms of thyroid gland less than 1 of thyroid masses are malignant Hyperparathyroidism primary parathyroid hyp erplasia or adenoma Secondary chronic renal failure Hypoparathyroidism low blood calcium Diseases of adrenal cortex overproduction of cortisol aldosterone androgenic hormones Underactivity of adrenal cortex acute adrenocortical crisis and chronic adrenocortical insufficiency Diseases of adrenal medulla pheochromocytoma and neuroblastoma Cushing Syndrome Anterior pituitary hyp erplasia or tumor Excessive secretion of ACTH excessive adrenal secretion of corticosteroids with high blood ACTH Overproduction of cortisol Hyperaldosteronism high blood pressure low blood potassium low blood renin renal tubules retain sodium Congential adrenal hyperplasia overproduction of androgenic hormones Deficits of aldosterone and cortisol quotsalt wasting Can be fatal Acute adrenocortical crisis fatal wo quick diagnosis and cortisol replacement Addison disease chronic adrenocortical insufficiency Usually autoimmune fatal wo treatment Diseases of the adrenal medulla pheochromocytoma secrete catecholamines Hypertension including paroxysmal Neuroblastoma young children Kidney function primary function is to form excrete urine Secretory function Erythropoietin growth factor stimulates RBC production in bone marrow Renin hormone that raises blood pressure Renin gt Angiotensinogen gtAngiotenson I gtAngiotensin II gt Aldosterone gt Increased sodium reabsorption and vasoconstriction Aldosterone increases blood pressure Antidiuretic hormone ADH regulates osmotic reabsorption of water Atrial natriuretic hormone ANH decreases blood pressure Urinary tract failure prerenal intrarenal postrenal Oliguria decreased output of urine Anuria no urine is produced Pyuria pus in urine Acute Renal Failure sudden onset Renal excretory function ceases Prerenal shock or heart failure Renal glomerular destruction glomerulonephritis tubular necrosis Postrenal obstruction Nephritic Syndrome Disorder of glomeruli characterized by generalized edema hypertension hematuria mildmoderate proteinuria Acute is post strep infection other bacterialviral infections Nephrotic Syndrome Glomerular disorder characterized by severe loss of protein in urine hyper and hypo proteinuria severe edema increased blood lipidsfats in urine increased blood clottinginfections Acute Glomerulonephritis immunemediated in ammatory glomerulopathy Upper respiratory strep Crescentric Glomerulonephritis severe glomerular injury accompanied by the formation of an exudate in the glomerular space In ammatory cells around the compressed capillary loops in a crescent form Membranous nephropathy membranous thickening of glomerular basement membrane Immune complexes Lipoid nephrosis also known as Minimal Change Disease or Nil Disease Responds to corticosteroid threatment Chronic Proliferative Glomerulonephritis chronic course don t respond to treatment EndStage Glomerulopathy Most immunemediated glomerulopathies can progress to endstage kidney disease By the time chronic renal failure develops there s no evidence ofin ammation All ultimately appear identical Glomerular pathology in Diabetes Mellitus basement membrane thickening increased permeability proteinuria Vascular changes in Diabetes Mellitus changes lead to ischemia and tubular atrophy Urinary stones urinary calculi urolithiasis Calcium stones 75 of all stones Struvite stones Complication of UTI Uric Acid stones usually in pts with hyp eruricemia or gout Cystine stones Inborn errors of amino acid metabolism UTIs hematogenous ascending infection Acute pyelonephritis suppurative infection of the kidneys UTI Cystitis infection of bladder Acute tubular necrosis sudden decrease in arterial pressure results in hypoperfucsion of the kidneys Ischemia destroys tubules Renal dialysis necessary Nephroangiosclerosis atherosclerosis of aorta renal artery or major branches Hypertension stimulates renal arterial and arteriolar contraction Renal ischemia stimulates renin production Renin aggravates hypertension Wilms39 Tumor nephroblastoma most common solid tumor in infantsyoung children Often present at birth clinically apparent 24 Carcinoma of urinary bladder 2X more common than renal cell carcinoma but same number of deaths Less invasive early symptoms


Buy Material

Are you sure you want to buy this material for

25 Karma

Buy Material

BOOM! Enjoy Your Free Notes!

We've added these Notes to your profile, click here to view them now.


You're already Subscribed!

Looks like you've already subscribed to StudySoup, you won't need to purchase another subscription to get this material. To access this material simply click 'View Full Document'

Why people love StudySoup

Bentley McCaw University of Florida

"I was shooting for a perfect 4.0 GPA this semester. Having StudySoup as a study aid was critical to helping me achieve my goal...and I nailed it!"

Jennifer McGill UCSF Med School

"Selling my MCAT study guides and notes has been a great source of side revenue while I'm in school. Some months I'm making over $500! Plus, it makes me happy knowing that I'm helping future med students with their MCAT."

Steve Martinelli UC Los Angeles

"There's no way I would have passed my Organic Chemistry class this semester without the notes and study guides I got from StudySoup."

Parker Thompson 500 Startups

"It's a great way for students to improve their educational experience and it seemed like a product that everybody wants, so all the people participating are winning."

Become an Elite Notetaker and start selling your notes online!

Refund Policy


All subscriptions to StudySoup are paid in full at the time of subscribing. To change your credit card information or to cancel your subscription, go to "Edit Settings". All credit card information will be available there. If you should decide to cancel your subscription, it will continue to be valid until the next payment period, as all payments for the current period were made in advance. For special circumstances, please email


StudySoup has more than 1 million course-specific study resources to help students study smarter. If you’re having trouble finding what you’re looking for, our customer support team can help you find what you need! Feel free to contact them here:

Recurring Subscriptions: If you have canceled your recurring subscription on the day of renewal and have not downloaded any documents, you may request a refund by submitting an email to

Satisfaction Guarantee: If you’re not satisfied with your subscription, you can contact us for further help. Contact must be made within 3 business days of your subscription purchase and your refund request will be subject for review.

Please Note: Refunds can never be provided more than 30 days after the initial purchase date regardless of your activity on the site.