NSG5003 Advanced Pathophysiology Final Study Guide (Latest): South University

NSG5003 Advanced Pathophysiology Final Study Guide (Latest): South University Week 1 Cell & Tissue Function/Dysfunction Atrophy: decrease in size of cells. Hypertrophy: increase in cell size. Hyperplasia: increase in number of cells. Metaplasia: mature cell type is replaced by a different mature cell type. Dysplasia: cells vary in size & shape within a tissue. Anaplasia: undifferentiated cells with variable nuclear & cell structure. Neoplasm: tumor. Cell Damage Ischemia: oxygen deficit due to respiratory or circulatory problems. Hypoxia: reduced oxygen in tissue. Oxygen Deficit: decreased energy production, loss of Na pump ↑ intracellular Na. Temperature: inactivation of some enzymes, damages organelles, protein coagulation, disruption of cell membrane. Micro-organisms Abnormal Metabolites: caused by genetic disorders or altered metabolism. Nutritional Deficits Cell Death Apoptosis:programmed cell death controlled by genetics. Necrosis:lysis of a cell, cell components leak into blood. Liquification:dead cells liquefy due to release of enzymes. Coagulation:cell proteins are altered or denatured causing coagulation. Caseous:form of coagulation necrosis, thick, yellowish, cheesy. Fat: fatty tissue is broken down into fatty acids. Tissue Damage from Chemicals Exogenous: from environment. Endogenous: from inside the body, Tissue Damage from Physical Agents Hypothermia: vasoconstriction, ↑ blood viscosity, hypovolemic shock ↓ blood pressure. Hyperthermia: causes general vasodilatation, decrease in circulating blood volume. Radiation: primarily affects actively dividing cells Biological Agents Insects/Animals: direct injection of toxin, transmission of infectious agent, allergic reaction to insect proteins. Food Poisoning Normal Defenses of the Body 1st Line Defense Physical Barriers: unbroken skin, mucous membranes, nasal hair, clots. Fluids: may contain enzymes or chemicals:saliva, tears, gastric, sweat. 2nd Line Defense-non-specific Phagocytosis:neutrophils & macrophages engulf cells, debris, foreign mat. Inflammation: automatic response to cell injury. 3rd Line Defense-specific defense produced by Antibodies Cell Mediated Immunity Cellular Defenses Mast Cells: located in tissue & release histamine & bradykinin. Macrophages: monocytes that enter tissue & act as phagocytes. Interferons: small proteins made by lymphocytes to prevent virus replication. White Blood Cells Granulocytes Neutrophils: work by phagocytosis. Basophils: release histamine leading to inflammation. Eosinophils:combat the effects of histamine. Agranulocytes Monocytes:can enter tissue to become macrophages which function as phagocyte. Lymphocytes: B & T Acute Inflammation Vascular Response: vasodilatation & increased capillary permeability. Cellular Response: migration of inflammatory cells through chemotaxis to injury site to destroy ineffective organism, remove damaged cells,releasedinflammation mediators. Exudate Serous: watery, mostly fluids, some proteins and WBC’s. Fibrinous: thick, sticky, high fibrin content. Purulent: thick, yellow-green, contains leukocytes, cell debris & microorganisms. Abscess: Pocket of purulent exudates or pus in a solid tissue. Local Effects of Inflammation-Cardinal Signs of Inflammation Redness & Warmth: due to increased blood flow to area. Swelling: shift of protein & fluid into interstitial space. Pain: pressure on free nerve endings, chemical mediators irritate nerves. Loss of Function: edema may restrict movement. Systemic Effects of Inflammation Mild Fever: due to resetting of hypothalamic thermoregulatory setpoint, release of endogenouspyrogens. Malaise Fatigue Headache Anorexia Treatment of Inflammation: drugs may decrease capillary permeability, reduce number of leukocytes & mast cells. Types of Healing Resolution: minimal tissue damage, cells can repair themselves. Regeneration: damaged tissue is replaced by identical tissue. Replacement: functional tissue replaced by scar or fibrous tissue. 1st Intention: wound is clean, edges are close together with minimal gap. 2nd Intention: large break in tissue, longer healing process with more scar tissue. Scar Formation: fibroblasts proliferate, abnormal amount of collagen. Hypertrophic: overgrowth of fibrous tissue, keloid. Ulceration: blood supply around scar is impaired resulting in tissue breakdown. Wound Staging 1. Partial thickness ulcer-red or pink ie.Sunburn. 2. Partial thickness ulcer-blister, scrape,abrasion. 3. Full thickness ulcer- throughdermis. 4. Full thickness ulcer that includes muscle orbone. Drainage Transudate: clear & watery. Serosanginous: clear w/ tinge of red/brown. Contains serum/blood thin & watery. Exudate: creamy yellowish. Contains proteins & WBC’s Thick. Purulent: yellowish. Contains leukocytes and necrotic debris, thick. Infected Pus: hues of yellow, green or blue. Contains pathogens, thick. Venous Insufficiency ClinicalPresentation IncompetentValves medial legarea InefficientCalfPump edema DistendedCapillaryBed wet wound DecreasedFibrolysis scaring, red base FibrinLeakage hemosiderin deposits(purple/brown on leg) Trauma Ulcer Documentation of Pulses Normal: 2 Diminished: 1 Absent: 0 Arterial Insufficiency: decreased arterial bloodsupply. Acute(thrombosis) vs Chronic(arteriosclerosis) Characteristics Dry Gangrene: nonviable dry tissue. Wet Gangrene: tissue necrosis bacterial infection. Drainage w/ odor. Black Gangrene: gangrenous borders, mummified skin. Pain w/ walking=Claudication Skin is atrophic(no hair) slow nail growth & Diminished Pulse Ankle Pressure Index: SBP LE/SBP UE 1 no arterial occlusivedisease .9-1 min sx in LE .5-.9 claudication pain(leg pain w/walking) .3-.5 ischemic restpain .3 ischemic w/ tissuenecrosis Assessment of arterial flow, skin color w/ elevation/dependency 1. LE Elevation to 60º for 1 minute. Normal=no color change. 2. Lower the LE & record time for color toreturn.30seconds means arterial insufficiency. Will look hyperemic(brightred). Week 2 Immune Response-Third Body Defense Humeral Immunity: antibodies are produced to protect body & stored in blood. Cell Mediated Immunity:lymphocytes are programmed to attack non-self cells. Antigens:immunogens, proteins, polysaccharides, glycoproteins on cell surface. Cells Macrophages:present throughout the body, derived from monocytes, initiate immune response, engulf foreign materialprocess & display foreign antigens & present them to lymphocytes, secrete monokines & interleukins . Lymphocytes:primary cell in immune response, T: has 3 subgroups made in bone marrow & differentiate in thymus, cell mediated immunity, can target certain cells. 1.Cytotoxic T:cells destroy cells bind to antigen & release enzymes 2.Helper T: facilitate immune response by activating & regulating 3.Memory T: remember antigens. B:Made in bone marrow, located in spleen & lymphoid tissue, produce antibodies. Natural Killer:kill tumor or virus infected cells w/o prior exposure Antibodies IgG:most common, can activate compliment, cross placenta, primary & secondary immune response. IgM:can activate compliment, natural antibodies ie. Involved in blood type IgA:not in blood, is in tears, saliva & colostrums. IgE IgD Compliment System:antigen-antibody complex, activated during immune rxn w/ IgG or IgM. Causes cell damage when activated, causes macrophagestorelease enzymes. Immune Response Primary: 1st exposure to antigen, 1-2 weeks needed for effective antibodies Secondary:repeat exposure to same antigen, effective response in 1-3 days Immunity: Innate-always present. Or acquired. Hypersensitivity Reactions Type 1 Hypersensitivity:allergic rxn, exposed to allergen causes development of IgE’s,activate mast cells and causes inflammation. Ie. Hay fever, allergies, asthma Type 2 Hypersensitivity:cytotoxic hypersensitivity. Antigen oncellmembrane reacts w/ circulating IgG’s, activates compliment, cells w/ antigen destroyed. Ie incompatible blood type exposure. Type 3: Immune complex hypersensitivity-antigen & antibody combine forming immune complexes that cause inflammation & tissue destruction. Type 4:Cell Mediated or delayed response by T-lymphocytes. No antibodies present. Ie. Tb test, contact dermatitis. Immune System Malfunction Hypersensitivity: full system immune response to non-noxious stimulus. Asthma: central windpipe or airway disorder. Interventions/Treatment:avoid triggers, medicate. Peak flow 50-80% of person’s best signal moderate attack, 50% below best PF = major attack. Autoimmune Multiple Sclerosis: autoimmune demyelinization of nerves in brain &CNS Classification Clinically Isolated Syndrome-only suffer 1attack. MS-multiple attacks at least 1 month apart & damage toat least 2 separate CNS areas & r/o all other possiblecauses. Tests & Measures: MRI, visual evoked potentials, CSF analysis. Interventions: modify disease course, treat attacks, manage sx. Myasthenia Gravis: antibodies destroy Ach receptors at NM junction. Guillen Barre Syndrome: demyelination of peripheralnerves. Fibromyalgia: generalized musculoskeletal pain 3 months, multiple tender points affecting all 4 quadrants, 11/18 points, 4Kg forcepainful Rheumatiod Arthritis:autoimmune destruction of joints affects multiple joints in symmetrical pattern, inflammation can affect organs. Scleroderma:affects microvessels causing hypoxia in all tissue. Skin & organs commonly affected. Sjogren’s Syndrome: autoimmune disease » loss of fluid for tears/saliva Hashimoto’s Disease: autoimmune thyroid disease, causes hypothyroidism Graves Disease: hyperthyroidism, Type 1 Diabetes: autoimmune destruction of pancreas cells » no insulin. Inflammatory Bowel Disease: group of disorders with inflammation of intestines Crohn’s: ulcers throughout intestines, except rectum. Ulcerative Colitis: ulcers in lower intestines, may begin in rectum. Immunosufficiency HIV Meningitis: photophobia is red flag. Toxoplasmosis: parasitic infection. Contaminated cat feces in 1st trimester. Histoplasmosis: fungal infection diagnoses based on organ involved Micro-organisms Bacteria-unicellular organisms, no nucleus, divide by binary fission. Cocci-staph, strep, diplococci-pneumococcus Bacilli-tetanus, botulinum. Spirochetes-syphillis, cholerae. Gram Positive: doesn’t retain crystal violet, has outer membrane layer. Gram Negative: retains crystal violet, no outer layer, thick peptidoglycan layer Toxins Exotoxins: produced by gram bacteria. Endotoxins: gram- bacteria. Released when bacteria die causing shock. Virus Active Viral Infection: virus attacks host cell injects genetic material, uses host cell to produce viral proteins & nucleic acids. New viruses made in cytoplasm & released by lysis or budding from host cell. Latent Viral Infection: virus enters cell similar to activeinfection, replicates slowly or delays replication, viral proteins are insertedintocell membrane of host cell causing immune response. Ie. Herpesvirus. Fungi: eukaryotic organisms, primarily affect skin or mucous membranes. Protozoa: eukaryotic organisms, usually parasites. Ie. Malaria, dysentary Prions: protein like agent that can change shape of proteins in host cell. Mad Cow. Modes of Transmission Direct Contact IndirectContact Droplet Aerosol Vector Nosocomial Infections: infections that occur in healthcare setting. Development/Stages of Infection Incubation Period: time of organism entering body to appearance of clinical signs Prodromal Period: infection is developing, nonspecific symptoms. Acute Infection: fully developed infectious disease with peak clinical signs. Chronic Infection: microorganism continues to replicate in body, sx milder. Subclinical Infection: Microbe can reproduce in body but no signs present. Septicemia: bacteria reproducing & circulating in bloodstream. Complimentary Medicine Red Flags: refer toDr. Chest pain/discomfort, unusual SOB w/ acute pain in chest, arm, throat or jaw, unexplained dizziness, persistent hoarseness or cough, difficulty swallowing, persistent abdominal pain/discomfort, coughing up blood, unexplained weight gain/loss, persistent unexplained fatigue, changes in a mole,changein bowel/bladder habits, blood in stool, unexplained vaginal bleeding, lumpinbreast or discharge or change in size or shape, changes in testicles, severeHA, blurred vision, sores that don’t heal, persistent unexplainedlumps/swelling,persistent back pain even w/ rest, unexplained leg swelling/pain. ScreeningLab Fingernails Absent Lunula: anemia, malnutrition. Pyramidal Luluna: trauma or excessive manicures. Red Luluna: cardiovascular disease, collagen disease of vessels, blood CA Mee’s Lines: metal toxicity, chemotherapy exposure. Longitudinal Lines: Addison’s disease, breast CA, melanoma, trauma. Splinter Hemorrhages bacterial endocarditis, lupus, renal failure, psoriasis Terry’s Nails:half& half appearance:edema & anemia »renal/liver disease. Cancerous Moles-asymmetry, border, color, diameter Week 3 General Cancer Info General Genetics Info Cancer rundown BladderCancer : -Early stages bleeding in urine but little nopain -Hematuria 1st sign with changes in urination BreastCancer: -New lump is most commonsymptom -Manual palpation better catch than mammogram Cervixcancer: -often asymptomatic -vaginal discharge, abnormal bleeding, pain during intercourse Colorectalcancer: -change in bowel habits mostcommon -Diarrhea, constipation, more narrow stools, blood in stool -Bright blood-lower GI, Dark/black blood-Upper GI Lungcancer: -persistent cough with or w/o chestpain -Feeling of an infection that just won’t go away Prostatecancer: -weak interrupted urine flow, frequent urination esp. @night Renalcancer: -low back pain, especially if pain not assoc. w/injury SkinCancer: -Any new growth on skin should beexamined -Spot or bump that changes size, irregular borders -Sore that will not heal Change in bowel/other habits A sore that does not heal Unusual bleeding or discharge Thickening or lump in breast Indigestion or difficulty swallowing, unexplained weight loss Obvious change in wart or mole Nagging cough/hoarseness Fluid/Electrolyte imbalance Water -60% adult body wt, 70% infants, higher % in females Fluid compartments -Intracellular 2/3 waterinbody -ECF1/3 *Interstitial 3/4, Intravascular 1/4, Cerebro Spinal Fluid 1% Control Fluid Balance-Thirst mechanism -Antidiuretic Hormone (ADH): fluid output -Aldosterone: Reabsorption of water and sodium -Atrial Natriuretic Peptide (ANP): lowers BP by controlling blood volume EDEMA: fluid excess in interstitial compartment DEHYDRATION: Signs-decreased skin turgor, sunken eyes, low BP, rapid weak pulse, high temp ELECTROLYTES Intracellular electrolytes: potassium, phosphate, magnesium Blood electrolytes: sodium, calcium, less extent bicarbonate EXCESS/DEFICIENT ELECTROLYTE CAUSES of EFFECTS of HypoNatremia Excessive sweating, vomiting, diarrhea, insufficient aldosteerone, kidney failure, excessive water- intake Impaired nerve conduction, fatigue, mm cramps, Abdom issues, decreased Osmotic pressure in ECF- THUS fluid into cells HyperNatremia Insufficient ADH, loss of thirst mechanism, watery diarrhea, rapid respiration, Fluid shift out of cells, weakness, dry tongue mucous membranes, increased BP HypoKalemia Diarrhea, diuresis, excessive aldosterone, low dietary intake, Insulin forces K into cell Cardiac Dysrythmias, interference with neuromm junc, decreased dig. Tract motility HyperKalemia Renal failure, deficit aldosterone, leakage of K from ICF into ECF, prolonged acidosis (H replaces) Cardiac dysrythmias, mm weakness common progressing to paralysis, respiratory arrest HypoCalcemia Hypothyroidism, malabsorption syndrome, deficient serum albumin, increased serum pH Increased permeability/ -- excitability of nerve membranes,spont stim of skeletal mm, Tetany, weak Heart contractions HyperCalcemia Uncontrolled release from bones - demineralization from immobil. -increased intake Depressed neuromm activity -interference with ADH function -increased strength cardiac contractions HypoMagnesmia Malabsorption of assoc with alcoholism, use of diuretics Neuromuscular hyperirritability - heart arrythmia HyperMagnesmia Renal failure Depressed neuromm funct GENETIC DISORDERS CAUSE(S) CHARACTERISTICS Angelman syndrome X-linked, lose “bit” of chromosome Flat head. PROTUDING TONGUES odd bouts of Laughter, Balance disorders Cri du Chat Missing part chromosome 5, mutation at Hi “CAT-like” cry, webbed toes & fingers, DOWNward slant to wide set eyes, skin tags ant. ears Downs syndrome Trisomy 21 Flat face, Upward slanted eyes, single DEEP crease palm of hand, HYPOtonia (low muscle tone), Fragile X syndrome Fragile x retardation protein Large head w/ prominent forehead, boys develop long face, tactile defensiveness Neurofibromatosis Autosomal dominant, Esp. effects nervous syst and skin, birthmarks called café-au-lait, freckles in armpits and groin, purplish RUBBERY lesions on skin GENETIC DISORDERS CAUSE(S) CHARACTERISTICS Prader Willi syndrome Chromosome XV Extreme hunger/overeating, obsessed w FOOD, temper tantrums, violent outbursts, @ 1 Y.O. become ravenously hungry Smith-Magenis Syndrome Deletion @ XVII Broad nasal bridge, PROTRUDING jaw, ear anomalies, SPEECH & middle ear problems, SLEEP disturbances Sudden Mood changes Klinefelter’s Syndrome Men w/ extra X chromosome Teenagers less developed, prepubescent testosterone helps, testosterone levels to diagnose, infertility Turner Syndrome Females w/ only 1 X chromosome WEBBED neck!! Underdeveloped BREASTS High BP, Type II diabetes Triple X syndrome Extra X chromosome Girls TALL, often not diagnosed, no long term problems Williams syndrome Random mutation chrom. 4 50% retardation, PUFFINESS around eyes, long neck, sloping shoulders, Poor DEPTH perception Cystic Fibrosis Single point mutation CFTR Life limiting (30s), frequent coughing w/ thick sputum, salty- skin, frequent lung infections, Muscular Dystrophy Dystrophin-over 30 different genetic diseases -Duschenne most common (missing dystrophin), affects skeletal & cardiac Muscle -Fascioscapulohumeral-faulty dystrophin -Myotonic; congenital, juvenile, adult, late onset-over 50 ACID-BASE Imbalance-Normal 7.4, ranges from 7.35 to 7.45 o Enzymes act in narrow pHrange • 20:1 base to acidratio  Respiratory system- alters carbonic acid levels Acidosis- CO2up  Kidneys- modifies excretion rates of acids, Most effective control system Acidosis: excess Hydrogenions Alkalosis: deficit in Hydrogen ions AcidosisHCO3-down Alkalosis HCO3-down **compensation occurs to balance relative ratio (20:1), NOT total concentration Week 4 Cardiovascular Disorders -general treatment -Low Na , fat -Decrease weight -exercise – Increase HDL, decrease LDL (high and low density lipoproteins) -smoking cessation -Vasodilators, (e.g. nitroglycerin for coronarya.’s) -Beta-blockers – prevent CNS stimulation ofheart -Ca2 channel blockers – decrease contractility of heart - anti-hypertensives – ACE inhibitors (angiotensin converting enzyme – work via renal system), diuretics, cholesterol decreasing drugs, anticoagulates to prevent clots Arteriosclerosis – hardening, narrowing of arteries – fibrous tissue formation (tunica adventicia grows)  constriction -caused by hypertension Atherosclerosis – plaque buildup in arteries, “atheromas” -coronary occlusion angina, MI -clot to brain TIA or stroke -clot in periphery  can lead to aneurysm Cholesterol -HDL – mostly protein, little fat – carries lipids to liver for excretion -LDL – mostly fat, little protein – carries lipids to cells of body -largely responsible for atheroma formation Risk factors for cardiovasc problems – age, heredity, obesity, sedentary lifestyle, smoking, glycemic control, serum lipids Angina Pectoris – O2 low in heart muscle  severe, crushing chest pain, “angere”= “to choke” Myocardial infarction – cell death from O2 deprivation  replaced with fibrous tissue -majority occur in left ventricle Congestive Heart Failure -Forward effect – Not enough blood going out, pump FAILURE -Backward effect – CONGESTION of blood behind failing ventricle -One side fails first, ultimately leads to failure of other side -Decreased CO (cardiac output) one side compensation mechanisms – vasoconstriction, water & sodium retention, increased blood volume increased work for the heart -Eventually muscles of affected side weaken congestion behind affected side  unaffected side pumps against increased resistance  Previously unaffected side weakens Right side failure – systemic congestion Left side failure – pulmonary congestion -pericarditis  effusion  fibrous adhesions -myocarditis  arrhythmias -endocarditis  infection of heart valves can lead to fibrosis Dx tests for heart diseases -auscultation – listen to valves -exercise stress test -imaging -doppler blood flow -blood test – can detect enzymes release from infracted myocytes -EKG EKG – usually 12 leads – at least 3 The basics – -P wave – depolarization of atria -QRS complex – depolarization of ventricles -T wave – Repolarization of ventricles EKG Abnormalities -PAC –premature atrial contrx – slight flutter, benign -PVC – premature ventricular contrx – many times benign, can lead to ventricular fib (life threat) -atrial flutter – atria contract quickly, but in rhythm – P waves not always followed by QRS -atrial fibrillation – atria quiver ineffectually (can live without coordinated atrial contraction) -ventricular tachycardia -ventricular fibrillation – will die without swift intervention Heart block – problem with SA node communication with AV node -1st degree AV block – long PR interval – slow communication -2nd – Missing QRS after P wave -3rd – 2 consecutive missing QRS after P waves Auscultation -Sound 1 = tricuspid and mitral valves -Sound 2 = semilunar valves Nervous control of heart -medulla of brain stem – control center of heart -baroreceptors in aorta and internal carotid (peripheral a’s - stretch recepts for BP monitoring) -Autonomic system – increase and decrease HR Vasculature Arterylayers -tunica intima –endothelial cells -endothelial cells respond to hormones, signal smooth muscle to contract, relax -tunica media – muscle cells -tunica externa (adventicia) – connective tissue Venous return – thinner walls, valves prevent backflow Hypertension -95% idiopathic -can cause endothelial cells to shear off -epinephrine in blood stream = inhibitory for endothelial cells, excitatory for smooth muscle underneath  vasoconstriction and incr. BP -fat deposits in hole in intima atheroma -blood can begin running between tunica intima and media dissecting aneurysm Angiotensin Renin complex -angiotensinogen renin -Angiotensin I ACE (angiotensin converting enzyme) -Angiotensin II **ACTION = angiotensin II  receptor  vasoconstriction, incr. BP Aneurysms -fusiform – bulge in all directions -saccular – sac forms on one side – pooling of blood causing clotting thrombus formed -dissecting – most dangerous – blood runs between tunica intima and media – dissecting aortic aneurysm =ticking time bomb Circulatory shock – severe hypotension -causes = hypovolemic, cardiogenic, septic, distributive (vasogenic, neurogenic, anaphylactic) -compensations – SNS incr. HR, force of heart contraction; kidneys release renin, aldosterone, ADH Diff Dx Kawasaki’s Disease -antibod’s produced against endothelial cells and smooth mm -Presentation – red tongue, rash @ distal extremity, skin sloughing, edema -recovery usually spontaneous Raynaud’s Disease -insufficient blood supplied to distal phalanges – Womenmen -prolonged ischemia can  gangrene. Venous insufficiency -valves fail due to age, injury, sendentary life, obesity -chronic pooling of blood in LE -brown, blue, purple skin in feet and toes – waste accumulation! -minor trauma  large wound! Hard to treat Lymphomas – cancer of T-cells and B-cells -Hodgkins – Tcell; Non-Hodgkins- B-cell -large lymph nodes and spleen -good prognosis if tx’d before metastasis Respiratory Disorders – Week 5 How to Breathe – the basics -respiratory muscles contract & thoracic cage expands, creating negative pressure in lungs -air goes in -elastic fibers around alveoli passively contract -air goes out -Sympathetic activation  smooth mm relaxation, bronchodilation -alveoli = squamous epithelium – maximizes gas exchange -covered with surfactant – reduce surface tension of fluid, prevent collapse -macrophages! -intrapleural pressure a shade under atmospheric pressure -feeling when you hold breath due to chemoreceptors for CO2. Hypercapnia – Increased CO2 in blood – compensate with hyperventilation Hypocapnia – decr. CO2 – compensate with hypoventilation Hyper/hypoxemia – O2 sats -As more O2 binds to hemoglobin, affinity for O2 rises – aids in acquisition and release of O2. Pneumonia -viral, bacterial, or fungal; 1 lobe or both lungs Tuberculosis -spread by oral droplet, can survive in dry sputum -TB takes root in primary infection stage, symptoms present in reinfection stage -can go dormant for long periods, bacilli walled off in localized area of lung - resurfaces when immune compromised -tissues of lung die in active infection -dx with skin test, chest x-ray, sputum culture -Long multidrug treatment, 6 mos- 1 yr. -grown more resistant to drugs in recent years. Obstructive Pulmonary Disorders – impaired ability to push air out of lungs -Cystic Fibrosis -Single gene mutation -increased mucus in the lungs, increased risk of infections -Lung Cancer -90% smoking related, 3rd most common cancer -can be result of metastasis -Lung Tumor -inflammation and bleeding in lungs cough blood -pleural effusion, pneumothorax -can secrete hormones –“paraneoplastic syndrome” -Asthma -Type 1 hypersensitivity – IgE formed in response to allergen -inflammation of mucosa  bronchoconstriction, obstructive mucus -can cause atelectasis –collapse of lung because of airway blockage (-pneumothorax involves a collapsed lung caused by mechanical damage or a rupture of a small airsac or “bleb” on outside of lung) -presents with hypoxia, respiratory alkalosis (initially due to hyperventilation), cyanosis, cough, tightness in chest, thick mucus, tachycardia -treat with inhalers and glucocorticoids COPDs –progressive degeneration -Emphysema –“pink puffers” – red face, overinflation -destruction of alveolar walls permanent inflation -smoking eliminates anti-trypsin that inhibits enzyme that destroys elastin elastin of alveoli destroyedloss of septae between alveolar sacs decreased surface area for gas exchange -presents with “barrel chest” – ribs fixed in inspiration position -Chronic Bronchitis – “blue bloater” -inflammatory obstruction repeat infections, progressive, irreversible damage of bronchioles -hypertrophy, hyperplasia of mucus glands, fibrosis -Present with constant cough, SOB, cyanosis -treat by Stopping Smoking, O2 supplementation, available vaccinations for at risk infections Emphysema Chronic Bronchitis Alveoli affected Bronchioles affected Septae walls destroyed Increased secretions Some cough Lots of coughing Little sputum Lots of sputum No cyanosis Cyanosis Some infections Frequent infections -Bronchiectasis -permanent dilation of medium-to-large-sized bronchi -caused by recurrent inflammation Restrictive Pulmonary Disorders – impaired lung expansion -often abnormal chest wall or lung inself -Pneumoconiosis -exposure to irritants – coal workers -inflammationfibrosis, “stiff lung” - insidious onset -Vascular Disorders -Fluid collects in alveoli and interstitial fluid -lung expansion decr, O2 in blood decr, -leads to pulmonary hypertension and edema -Pulmonary embolism -blood clot from veins pumped to lungs – deadly -Atelectasis -collapse of lung caused by: obstructed airway, compression (tumor), increased surface tension preventing expansion -small areas asymptomatic, large areas –dyspnea and chest pain -Pleural effusion – “hydrothorax” -fluid in pleural cavity protiens and WBCs follow, respond to inflammation -Incr pressue in pleural cavity, layers separate, prevent expansion -presents with incr RR and HR, cyclic chest pain -Pneumothorax -air in chest cavity, lung collapse -open – air enters through hole in chest cavity; -closed – air in chest cavity from rupture on inside -tension – air allowed to enter cavity, no natural way to remove it -Adult Respiratory Distress Syndrome -rapid, shallow resp, incr HR, confusion -caused by shock, sepsis, burns, multiorgan failure Diff Dx - Sputum -yellow-green = infection -rusty-dark = pneumonia -purulent and foul odor = bronchiectasis -Breathing -labored breathing – obstruction -wheezing, whistling – obstruction of small airways -stridor – high crowing noise – obstruction of small airways BLOOD DISORDERS - Week 6 Week 6- Blood Disorders Hemocrit - proportion of cells(RBC) -indicates viscosity & inc or dec inhydration Hemoglobin: Tetramer-4 hemes which carry 1 oxygeneach Hemostasis: Hemophilia A: 90% of cases, deficit of clotting FACTOR III, an X-linked recessive trait Hemophilia B: Xmas disease, deficit FACTOR IV Hemophilia C: factor XI, milder form Blood therapies: o Whole blood: for severeanemia o Artificial EPO (stimulates RBCproduction) o Bone marrow Transplants: some cancers, immune deficiencies, blood celldisease ANEMIAS-can lead to ANGINA or CHF  Hemoglobin deficit= reduction in oxygentransport  Generalsigns • Fatigue, pale face, dyspnea,tachycardia  Causes • Nutrientdeficiency • Impaired bonemarrow • Blood loss or excessive destruction ofRBCs Iron deficiency: impairs hemoglobin, very common, usually underlying CAUSE Pernicious Anemia o Large, immature, nucleatederythrocytes(RBCs) o SYMPTOMS-Tongue large, RED, sore,shiny o • AplasticAnemia o Temporary or permanent impairment or failure of bonemarrow o Bone marrow cells replaced byFAT o Cause must be ID’d for prompt treatment & marrow recover or is LIFEthreatening • Hemolytic anemia o CAUSE: excessive destruction of RBCs via manycauses • Sickle Cell Anemia- abnormalhemoglobin o Genetic condition; autosomal rec., heterozygous Rcarrier  More common n AFRICANancestry o Sickle cell crisis occurs when LOW O2levels  When deoxygenated HbS is unstable and crystallizes=sickleshape • Thalassemia o Most common blood disorder inworld o Abnormal hemoglobin due to missinggenes ANEMIAS CONT. • Polycythemia o Primary polycythemia-Increased rate of RBCproduction  Secondary polycythemia-Increased RBC production due to prolongedHypoxia o Concerns for both: Category Sytemic disease Musculoskeletal  Sluggish bloodflow  Increased BP & hypertrophiedheart • Indications of Blood clottingDisorders o Persistent bleeding in gums & nose bleeds, bleeding into joint, coughing up/vomitingblood, blood in feces, vomiting, lowBP • Causes of clottingdisorders o Defective plateletfunction o Long term use ofwarfarin • Hemophilia A(classic) o Most common inherited clottingdisorder o Varyingseverity o Spontaneous bleeding intojoints • Disseminated IntravsascularCoagulation o Excessive clotting & excessive bleeding incirculation o Clotting factors reduced to dangerouslevel o Widespread uncontrollablebleeding o HIGH fatalityrate THE LEUKEMIAS Acute High proportion of IMMATURE, nonfunctional cells in marrow andcirculation Onset is abrupt SIGNS: Frequent uncontrolled infections ,BONE PAIN, Weight loss, fatigue, drowsiness, vomiting Chronic Higher proportion of MATURE cells Insidious onset Mild signs & better prognosis Diagnostics for all leukemias Peripheral blood smears Bone marrow biopsy confirmation Treatment- Chemo, Biologic therapy using INTERFERONS, Can stimulate immune system Histology: Differential diagnosis of Systemic Pain versus Musculoskeletal Course/duration Cyclic, progressive symptoms Constant or may come & go Sudden(gradual when related to overuse) Relieving Factors Usually NONE : if relieved by rest or position, there is typically cyclic progression of increasingfrequency, intensity, or durationuntil rest/position doesn’twork Decrease with Rest Aggravating Factors None specific Increase with useaffected region Quality DEEP, ACHING, throbbing DIFFUSE or waves/spasm SHARP Intensity Severe if cancer spread to nerves surrounding a visceral organ Depends on if acute, subacute, or chronic Location From Upper back, middle to low back regions. May also be in front of trunk frequently in abdomen over affected organ Located over injury sight. If severe may also refer proximal and distal to injury sight Associated signs & symptoms Jaundice, skin rash, weight loss, fatigue, low-grade fever, muscular weakness, frequent infections Usually none- trigger pts may be accompanied by nausea/sweat Week 7 Digestive Disorders Digestive System Overview 5 layers of gut wall (inner to outer): mucosa, submucosa, circular muscle layer, longitudinal muscle layer, serosa *Peristalsis (involuntary contractions) occurs in circular and longitudinal smooth muscle layers Stomach Gastrin cells (G cells): initiated by food entering stomach, stimulates chief and parietal cells Intrinsic factor (parietal cells): needed for absorption of vitamin B12 HCL (parietal cells): activates pepsinogen, creates optimal pH ~2, denatures proteins Pepsinogen (chief cells): pepsin not activated until pH of 6 Liver “Metabolic factory of the body” 1) Storage of nutrients 2) Maintains blood glucose 3) Blood reservoir 4) Produces bile, plasmaproteins, blood clotting factors, cholesterol/lipoproteins 5) Metabolic processes (detoxification,conversions) Glucose - Glycogen = Glycogenesis (when glycogen supply low) Protein, Fat - Glycogen = Glyconeogenesis Glycogen - Glucose = Glycogenolysis (maintains blood glucose levels) Pancreas Exocrine (secreting digestive enzymes and electrolytes) and endocrine organ Trypsin, chymotrypsin, carboxypeptidase-break proteins Ribonuclease-break nucleic acids Pancreatic amylase-break starch Lipase-break lipids GI tract Ileum=major site of nutrient absorption, villi (folds of mucosa) Large intestine=fluid and electrolyte reabsorption, movement slow to allow absorption of water, vitamin K synthesis (essential for blood clotting) Neural and hormonal control PNS (vagus mainly): increased motility and secretions, SNS: inhibits GI activity Gastrin: increases gastric motility and promotes stomach entering, Secretin: decreases gastric secretions, Cholecystokinin: inhibits gastric emptying Upper GI Tract Disorders (includes differential diagnosis) Disorder Description Causes Dysphagia Difficulty swallowing 1) Neurologicaldeficit 2) Musculardisorder 3) Mechanicalobstruction -congenital atresia -stenosis -esophageal diverticulum -tumors Esophageal Cancer Squamous cells in distal esophagus, poor prognosis Chronic irritation -chronic esophagitis -hiatal hernia Hiatal hernia Part of stomach protrudes into thoracic cavity Gastroesophag eal Reflux Disease Gastric substances reflux into distal esophagus,often seen with hiatal hernia Decreased competence of lower esophageal sphinctor Gastritis Stomach mucosa inflamed (either acute or chronic) *Helicobacter pylori infection typically present w/ chronic Acute: Infection, allergies to food, spicy food, excessive alcohol, ulgerogenic drugs Chronic: Most idiopathic Gastroenteritis Inflammation of stomach AND intestine Usually an infection Peptic Ulcers (gastric and duodenal) Erosion in mucosa Common in proximal duodenum and antrum of stomach (ulcers in general rarely found in large intestine) 1) H. pylori infection 1) Increasedacid-pepsin secretions 2) Inadequate bloodsupply 3) Excessiveglucocorticoid secretion 4) Ulcerogenicsubtances Stress Ulcers Rapid onset, may form within hours of precipitating event Severe trauma: Burns (curling’s ulcers), head injury (cushing’s ulcers) Systemic: hemorrage, sepsis (ischemic ulcers) Gastric Cancer Primarily in mucous glands and in antrum or pyloric area, poor prognosis Gone down bc we have preservatives w/ food Pyloric Stenosis Narrowing and obstruction of pyloric sphinctor May be developmental anomaly or acquired later in life Liver and Pancreas Disorders (includes differential diagnosis) Gallbladder Disorders Description Cholelithiasis Formation of gallstones* Cholecystitis Inflammation of gallbladder and cystic duct Cholangitis Inflammation related to infection of bile ducts Choledocholithiasis Obstruction of biliary tract by gallstones (due to larger stones) *Risk factors for developing gallstones: Women (2x more likely), high cholesterol, obesity, multi parity (several children), use of oral contraceptives or estrogen supplements, hemolytic anemia, alcoholic cirrhosis Disorder Description Causes Jaundice Yellowish color of skin (not disease itself but sign of other disorders) Prehapatic: unconjugated bilirubinelevated Intrahepatic: unconjugated and conjugated bilirubin elevated Posthepatic: conjugated bilirubin elevated Prehepatic: excessive destruction of RBCs Intrahepatic: disease or damage to hepatocytes Posthepatic: obstruction of bile flow into gallbladder or duodenum Hepatitis Inflammation of liver Mild: impaired hepatocyte function Severe: necrosis and obstruction of blood/bile flow along w/ impaired hepatocyte function 1) Idiopathic (fattyliver) 2) Infection (viral ornon-viral)* Cirrhosis Progressive destruction of liver Stage 1=fatty liver (asymptomatic &reversible) Stage 2= alcoholic hepatitis (irreversible) Stage 3=end stage cirrhosis (liver failure when 80-90% of liver destroyed) 1) alcohol (mostcommon) 2) biliary: obstruction of bileflow 3) post-necrotic: linked w/ chronic hepatitis or long-term toxicexposure 4) metabolic Liver Cancer Initial signs mild, diagnosis occurs with advanced stages Hepatocellular carcinoma (most common primary tumor of liver) Secondary/metastatic cancer (arises from areas served by hepatic vein) Acute Pancreat itis Chronic or acute(medical emergency for acute) Spreads to tissue surrounding the pancreas Very painful (different than pancreatic cancer) Chronic in 15% of cases Results from auto digestion of the tissue (Premature activation of pancreatic proenzymes) Precipitating factors=alcohol (most common), biliary tract obstruction, gallstones, mumps Pancreat ic cancer Adenocarcinoma-most common form Asymptomatic until advanced (metastasizes quickly) Mortality=95% Risk factors=smoking, pancreatitis, and dietary factors *Viral Hepatitis Hepatitis A: Infectious hepatitis, RNA virus, transmitted by fecal-oral route in areas of inadequate sanitation, no carrier or chronic stage, vaccine available Hepatitis B: Serum hepatitis, DNA virus, incubation period of 2 months, primarily transmitted by infectious blood (may also be sexual transmission or from mother to fetus), carriers asymptomatic but contagious, vaccine available, chronic hepatitis B (ascites) =engorgement of blood vessels, can’t filter toxins anymore Hepatitis C: RNA virus, most common type transmitted by blood transfusion, has carrier state, increases risk of hepatocellular carcinoma Hepatitis D: Delta virus, incomplete RNA virus (needs hepatitis B to produce active infection), transmitted by blood Hepatitis E: RNA virus, transmitted by oral-fecal route, no chronic or carrier state Lower GI tract disorders (includes differential diagnosis) Disorder Description Causes Celiac disease Malabsorption syndrome: prevents further digestion of gliadin (breakdown product of gluten) Atrophy of villi Primarily a childhood disorder Autoimmune disease (1% of US population) -defect in intestinal enzyme Crohn’s disease (included in chronic Inflammatory Bowel Disease) Progressive inflammation and fibrosis cause obstructed areas Normally affects small intestines (but may affect any part of GI tract) Inflammation occurs in “skip lesions” Genetic factor (often occurs during adolescence) Ulcerative Colitis (included in chronic IBD) Blood and mucous in stool Inflammation starts in rectum and progresses to colon Genetic factor (often occurs during 2nd or 3rd decade) Appendicitis Obstruction of appendiceal lumen, wall inflamed as fluid builds in appendix Occurs in 10% of population Symptoms=LRQ rebound tenderness, periumbilical pain Fecalith, gallstone, or foreign object cause obstruction Diverticular Disease Diverticulum=outpouching of mucosa through muscular layer of colon Diverticulosis=asymptomatic Diverticulitis=inflammation of diverticula (very painful) Symptoms=cramping, tenderness nausea, fever, elevated WBC, do NOT see blood in stool May be genetic link Colorectal Cancer Early diagnosis essential Symptoms=alternating diarrhea and constipation, bleeding,weight loss, anemia, fatigue, red blood in stool, pain doesn’t often occur Most diagnosed cancer next to skin cancer Most from adenomatous polyps (polyp does not always mean cancer!) Risk factors: familial multiple polyps, long-term ulcerative colitis, diet low in fiber (why susceptibility has increased) Intestinal Obstruction Lack of movement of intestinal contents (most common in small intestine) Mechanical obstruc. -tumors, adhesions, etc Functional obstruc. -impairment of peristalsis -Ex: spinal cord injury Peritonitis Inflammation of peritoneal membranes Symptoms: sudden severe and generalized abdominal pain, abdominal distention, dehydration, low blood pressure,tachycardia, vomiting 1) Chemical peritonitis:caused by foreign chemical in peritoneal (bile, chyme,etc) 2) Bacterial peritonitis: direct trauma affecting intestines, ruptured appendix 1) Abdominal surgery (infection maydevelop) 2) Pelvic inflammatory disease in women Irritable Bowel Syndrome 1) Change in bowel motility thatis associated withpain 2) Must be there 12 weeks out ofthe year 3) Do NOT see blood instool Week 8- Urinary Disorders Urinary System Overview Kidney Nephron=functional unit of the kidney (1 million), consists of renal corpuscle (filtration unit) and renal tubule ADH-prevents water loss (increases reabsorption of water in distal convoluted tubules and collect. duct) Aldosterone-prevents water loss (increases sodium reabsorption in distal convoluted tubules) ANP-allows water loss in response to high blood pressure Glomerular rate: 1)afferent arteriole dilation=increased filtrate 2) efferent arteriole constriction=increased filtrate 3) afferent arteriole constriction=decreased filtrate Renin(kidney) ACE(lung) ↓ ↓ Angiotensinogen → Angiotensin I → AngiotensinII (plasma) vasoconstrictor (Renin secreted in response to reduced afferent arteriole blood flow) Urinalysis Cloudy-presence of large amounts of protein, blood, bacteria, and pus Blood: if large amount=increased glomerular permeability or hemorrhage, if small amount=infection, inflammation or tumors in urinary tract Dark color-hematuria, excessive bilirubin, highly concentrated urine Unusual smell or odor-infection, diet, or medication Elevated BUN and creatine=failure to excrete nitrogen waste Metabolic acidosis (low pH, low bicarbonate)=failure of tubules to control acid/base balance Urinary System Disorders (includes differential diagnosis) systemic sign of high fever *can lead to renal failure* Glomerulonephritis Decreased GFR rate (decreased urine output, elevated blood pressure and edema) Metabolic acidosis Bloody, foamy urine and pain Acute poststreptococcal glomerulonephritis caused by presence of anti-streptococcal antibodies Nephrotic Syndrome Increased permeability in glomerular capillaries Hypoalbuminemia,increased aldosetrone, severe edema Bladder cancer Often develops as multiple tumors Early signs:hematuria and dysuria Predisposing factors: working w/ chemicals (analine dyes, rubber, aluminum), smoking, recurrent infections, heavy analgesics intake Vascular Disorders Thickening/hardening of walls and small arteries Reduces blood to kidney-stimulation of renin (increases blood pressure) Some normal w/ aging Adult Polycystic kidney disease Manifests around 40 Multiple cysts in both kidneys-leads to chronic renal failure Autosomal dominant gene on chromosome 16 Polycystic disease in children Manifested at birth, child dies in first month or is stillborn Autosomal recessive mutation Acute Renal Failure Rapid onset Metabolic acidosis and hyperkalemia Ogliuria, increased serum urea 1) Acute bilateral kidney diseases 1) Prolonged/severe circulatory shock orheart failure 2) Nephrotoxins 3) Mechanicalobstruction 4) Burns Chronic Renal Failure Gradual, irreversible destruction of kidneys (10%=end stage) Asymptomatic w/ up to 40% left Symptoms later on=polyuria with dilute urine, anemia, fatigue Axotemia=renal insufficiency25% 1) Chronic kidneydisease 2) Polycysticdisease 3) Systemicdisorders 4) Low-level nephrotoxin exposure over longtime Kidney Stones Calcium (sharp),magneisum, uric acid, cystine 1-5mm can be passed Wilms Tumor Usually unilateral and gives purely kidney symptoms Most common tumor in children, defects in tumor- suppressor on chromosome 11 Diabetic Neuropathy Leading cause of chronic renal failure 1/3 ppl on dialysis have Type 1 diabetes, 2/3 have Type 2 Reflux Neuropathy Flow of urine from bladder to upper tract Can lead to end stage renal disease Primary (congenital) Secondary (obstruction) Associated with hypertension Incontinence 1)Stress: most common Ex:sneeze Associated w/ aging, most 2) Urge:spasm 3) Overflow: can’t fully emptybladder 4)Functional: bladder normal, something else keeps them from going to bathroom Ex: spinalcord injury common in women Dialysis-provides filtration and reabsorption (hemodialysis=blood moves from shunt into machine, 3x per week for 4 hours)(Peritonal dialysis= peritoneal membrane serves as semipermiable membrane, usually done at home during night) Acute Neurologic Disorders- Week 9 Neurons and Conduction of Impulses • Neurons: highly specialized, non-mitotic cells which conduct impulses through the CNS andPNS • Myelin sheath: insulates, speeds up conduction, formed by Schwann cells, Nodes ofRanvier • Glial cells: astroglia, oligodendroglia, microglia, ependymalcells • Regeneration of Neurons: neuronal cell body damaged = death of neuron; CNS = neuronsdo NOT regenerate; PNS = neurons may be ableto • Conduction of impulses: depolarization (sodium influx) generation of action potential repolarization (outward movement of potassium) sodium – potassium pump moves ionsinto their normal position; myelinated fibers: salutatory conduction = rapidconduction • Chemical neurotransmitters: stimulated released into synaptic cleft; inactivated byenzymes or reuptake; postsynaptic neuron dendrites or cells body depolarizes depending on neurotransmitters • Neurotransmitters: o Acetylcholine: (excitatory and inhibitory) located: neuromuscular junction, autonomic nervous system (SNS and PNS), peripheral nervous system,CNS o Catecholamines: (excitatory) present in the brain, norepinephrine: neuromuscular junction and SNS, epinephrine: SNS,dopamine o Seratonin: (excitatory) located in the CNS (brain) and GI; regulates behavior, attention, digestive processes; implicated in moodchanges o Glutamate:(excitatory) o Y-Aminobutyric acid (GABA): (inhibitory) located inbrain • Autonomic NervousSystem: o Involuntary, motor and sensory innervation: cardiac muscle, smooth muscle, glands, sympathetic/parasympathetic, neural pathway: preganglionic fibers (in brain orspinal cord) postganglionic fibers (outsideCNS) • Sympathetic NervousSystem: o “Fight or flight”; stress response, increase general level of activity: cardio, respiratory, neurologic, Neurotransmitters: preganglionic fibers release acetylcholine (cholinergic); postganglionic fibers release norepinephrine (adrenergic) • Parasympathetic NervousSystem: o Dominates digestive system, aids recovery after sympathetic activity, vagus N: innervates heart and GI, neurotransmitter: acetylcholine; receptors (cholinergic): nicotinic andmuscarinic Acute Neurologic Disorders Problem/Disorder Description Treatment Increased Intracranial Pressure Expansion of fluids/tissue  Increase in pressureIschemia and infarction Herniation Displacement of brain tissue caused by large mass (clot/tumor) Brain Tumors Lesions that cause increased ICP If accessible then removal Vascular Disorders Hemorrahagic (increased ICP) or ischemic Transient Ischemic Attacks Temporary reduction of blood flow in the brain Small mini-strokes occurring continually Connected to dementia Cerebrovascular Accidents Infarction of the brain due to lack of blood Clot busting agents, surgery, glucocorticoids, team approach Cerebral Aneurysms Localized dilation in the wall of an artery Surgery before rupture, antihypertensive drugs Meningitis Bacterial infection of the meninges of the CNS Antimicrobial therapy, glucocorticoids, vaccines Brain Abscess Localized infection; necrosis of tissue Surgical drainage, antimicrobial therapy Encephalitis Infection of the parenchymal or conn tissue in the brain and spinal cord Antimicrobial therapy, antiviral drugs (depends on the type of encephalitis) Rabies Viral transmitted by bite of rabid animal or transplantation of contaminated tissues Prophylactic immunization Tetanus Infection by puncture wound Immunizations advised Poliomylitis Polio virus; attacks motor neurons of the spinal cord and medulla Immunization available Herpes – Zoster (shingles) Caused by varicella – zoster in adults Vaccine available for ages 60 Post-polio syndrome Occurs 10 – 40 years after initial infection Reye Syndrome Viral infection linked to children treated with aspirin No immediate cure Guillain – Barre syndrome Inflammatory condition of the PNS Recovery usually spontaneous; supportive treatment Chronic Neurologic Disorders Problem/Disorder Description Treatment Hydrocephalus Excess CSF within the skull Non-communicating (flow of CSF through ventricular system is blocked) Communicating: absorption of CSF through subarachnoid villi impaired Spina Bifida Failure of the posterior Diagnostic Tests: alpha – spinous processes to fuse  meninges and spinal cord herniated fetoprotein (AFP) elevated, ultrasound Surgical repair,OT/PT afterwards Cerebral Palsy Motor impairment due to brain damage: intellectual function, behavior, communication / speech, seizures, visual or hearing deficits Causes: genetic mutations, abnormal fetal formation, brain damage, difficult delivery, hypoxia (ischemia) Spastic paralysis: hyperreflexia Dyskinetic: loss of coordination with fine movement Ataxic: loss of balance and coordination Speech, PT/OT, assistive devices, monitor hearing/vision, alternate modes of communication Multiple Sclerosis (MS) Progressive demyelination of neurons in brain, spinal cord, and cranial nerves Cause: unknown S&S: blurred vision, diplopia, scotoma, weakness in legs, progressive weakness and paralysis, paresthesia, dysarthria, loss of coordination, bladder / bowel / sexual dysfunction, chronic fatigue MRI for diagnosis and monitoring Research treatments: interferon beta – 1b, glucocorticoids PT/OT Muscle relaxants Parkinson’s Disease Progressive degeneration in basal nuclei; imbalance between excitation and inhibition Excess stimulation affects movement and posture S&S: resting tremors (“pill rolling”), muscular rigidity, difficulty initiating movement, postural instability, decreased flexibility, fatigue, lack of facial expressions, propulsive gait, bradykinesia Removal of cause if known Dopamine replacement therapy Anticholinergic drugs Speech/language, PT/OT Treatment of respiratory or urinary tract infections Amyotrophic Lateral Sclerosis Muscle wasting, progressive Stem cell therapy under (ALS) degenerative disease affecting motor neurons Cause: unknown Cognition, sensory neurons, neurons of eye are unaffected Loss of upper motor neurons: spastic paralysis and hyperreflexia Loss of lower motor neurons: Flaccid paralysis, decreased muscle tone and reflexes investigation Moderate exercise and rest Electronic communication devices Team approach No specific treatment to slow degeneration Myasthenia Gravis (MG) Autoimmune disorder: auto- antibodies to acetylcholine receptors at NMJ S&S: muscle weakness in face/eyes, weakness in arms/trunk, impaired vision and speech, difficulty chewing and swallowing, head droops, upper respiratory infections Diagnostic tests: EMG, serum antibody test, acetylcholine esterase inhibitor Treatment: antiacetylcholine esterase agents, gludocorticoids, plasmaphoresis, thymectomy Huntington’s Disease Rapid, jerky movements, chronic progressive neurodegenerative chorea, hereditary, autosomal dominant (~40 years of age) Progressive atrophy of brain S&S: mood swings, personality changes, restlessness, choreiform movements in arms and face, intellectual impairments Diagnositc test: DNA analysis Treatment: no therapy to slow progress, only symptomatic therapy Dementia Intellectual deterioration that interferes with occupational or social function S&S: impaired cognitive skills, impaired thinking, judgment, and learning, memory loss, confusion, behavioral and personality changes Causes: vascular disease, infections, toxins, genetic disorders Alzheimer’s Disease Progressive cortical atrophy: neurofibrillary tangles and amyloid plaques 1st stage: short term memory loss, social withdrawal, no sense of humor Cause: unknown S&S: onset insidious, behavioral changes (irritability, hostility, mood swings), gradual loss of memory and lack of concentration, impaired learning, poor judgment, decline in cognitive function, memory and language, change in food intake, inability to recognize family, environment unawareness, incontinence 2nd stage: general confused stage, wandering (sundown syndrome) 3rd stage: terminal stage, incontinent, apathetic, institutionalized No diagnostic tests available Treatment: anti-acetylcholine esterase drugs, OT/PT, psychologists, speech therapists, team approach Creutzfeld – Jacob Disease (Mad Cow Disease) Rapidly progressive Cause: prion ingested or transmitted through contaminated blood S&S: memory loss, behavioral changes, motor dysfunction, progressive disorders, dementia Diagnosis: blood tests Fatal: within 6 months = dead AIDS Dementia Common in later stages of AIDS, virus invades brain tissue Gradual loss of memory and cognitive ability, impaired motor function Complex Regional Pain Syndrome (CRPS) • Pathogenesis: abnormal activity of the SNS, gate control theory, reflexive musclespasm • Stages ofCRPS: o Stage 1 (acute): right after injury, weeks to 3 mo., excess sympathetic activity, persistent burning pain and swelling, hyperesthetic, hyperhidrosis, increased nail/hair growth, pain will be severe o Stage 2: dystrophic stage, 3 – 6 mo., persistent pain and stiffness, trophic skin changes, muscle atrophy, flexion contractures, pain exacerbated by stimulus, limb: edematous, cool, cyanotic, mottled, hair loss, cracked brittle nails, skin cool totouch o Stage 3: atrophic stage, ~6 mo., pain can increase or decrease, progressive atrophy of skin, subcutaneous tissue, muscle, and bone, bone demineralization, skin: cool, thin and shiny o Stage 4: existence of stage 4 is questionable, 2 years, psychosocial level, swelling is gone, atrophy is permanent (muscle, bone, skin), no NOC firingnow • Definite CRPS: pain and tenderness in extremity, S&S of vasomotor instability, swelling, dystrophic skinchanges • Probable CRPS: pain and tenderness OR swelling, dystrophic skin changes oftenpresent • Possible CRPS: vasomotor instability AND/OR swelling, NO pain but tenderness, dystrophic skin changes occasional • Doubtful CRPS: unexplained pain and tenderness in anextremity PAIN • How we interpret pain: NOC perception interpretation emotions social • Pain: the perception of nociception that is not directlymeasurable • Pain behavior: the observed consequence of a painful experience (distress response); Pain behaviors: verbal, vocal, facial expressions, physical actions, function, socialactions • Benign pain: not associated with terminal illness vs. Malignant: associated with terminaldisease Acute Pain Chronic Pain Recent onset (3 mo.) 3 mo. Close link with pain generator Loose link with pain generator Not a learned response even though there will be pain behavior Learned behavior, positive reinforcement for pain behavior Objective findings coincide with generator No lab or clinical findings to support pain Unlikely to have errors in stimulus discrimination Pt. may confuse pain with other forms of distressful stimuli Brief in nature lengthy Differential Diagnosis of Chronic Pain Test Description Wadell’s Signs Distracted SLR, rotation of back, superficial tenderness, regional pain, migrating trigger points, sham axial loading of spine, regional weakness Mankopf’s Test Pain should raise pulse rate of person by 5% O’ Donoghue’s Maneuver AROM PROM = sign McBride’s Test Stand on one leg and raise other leg to chest = should decrease LBP Hoover’s Test Supine, hold pt.’s heels off table and have them raise one leg, feel downward pressure if they try to lift the leg • Symptom magnifier: magnifying their symptoms vs. Malingerer: knowingly manipulating the system for their own gain, purposely deceiving the health careproviders • Look at pt’s workhistory SEIZURES • Review types of seizuretable • Seizure: abnormal discharge of a group of cortical or subcorticalneurons • Epilepsy: syndrome characterized by experience of recurrentseizures • Aura: subjective sensation or motor phenomenon that precedes a seizure(pre-ictal/prodomal) • Ictal period: period of abnormal EEG activity; seizure S&S areevident • Post-ictal period: period following acute seizure, time of confusion, EEG activity =normal • Status epilepticus: series of rapidly repeated epileptic convulsions without any period of consciousness betweenthem Seizures Epilepsy Inappropriate electrical activity Recurrent seizures or neurological syndrome associated with seizures Transient neurological signs (seizure) Seizures occurring with little or no provocation Altered consciousness, involuntary movements, and disturbed perception often occur Individual or multiple seizure types; characteristics may change with age Defined by neurological S&S and EEG patterns Spectrum of seizure types, EEG, clinical settings • Etiology: genetic (inherited metabolic abnormalities, lowered threshold to electrical activity of the brain), structural (disturbed cerebral flow, disorders of blood composition), environmental (anoxia, toxins, drug withdrawal), head trauma, idiopathiccauses • Triggering mechanisms: visually induced, movement induced, hyperventilation, trauma, emotions, hydration/electrolyte imbalance, fever, alcohol or drug withdrawal, premenstrual period, lack of sleep,illness • Diagnosis: medical history, diagnostic tests (lab studies, x-rays, lumbar puncture, CT, MRI, EEG), clinicalobservation • Treatment: drugs, surgery, diet, microcomputers,education • Differentiate from: disorders of cerebral blood flow or blood constitution, structural,psychiatric conditions, and migraineheadaches Week 10 Endocrine System Differential Diagnosis Gigantism Acromagly- thicker skull and jaw (occurs after joint plates fuse) Hyperthyroidism Common cause=Grave’s disease Common symptoms=exopthalmos, goiter, heat intolerance, and anxiety Hypothyroidism Very familial, 4X more likely in women Common symptoms=weight gain, cold intolerance, fatigue Myxedema- lots of fluid (would not pit), can look like fibromyalgia bc of muscle aches and trigger point tenderness, sparse hair, brittle nails, may have buffalo hump Thyroid storm-dumps T3 and T4 into system - causes tachycardia, fever, and agitation Thyroid cancer Very treatable, most are benign (only 5% malignant and they normally dont metastasize) Palpation will be painless, unilateral, and in one spot Parathyroid glands Maintain calcium levels between bone and blood Parathyroid cancer=can’t easily be distinguished from thyroid cancer Renal glands Release epinephrine and aldosterone Trousseau’s sign- positive sign would be tremors and twitching bc of nerve or muscle irritability (Non specific sign) Chvostek’s sign-elicit this by having the patient relax face and then the therapist taps the facial nerve, watch for twitch of mouth or side of face Addison’s Diseases (hypoadrenal)- autoimmune, skin changes color to a slight grey Cushing’s Syndrome (hyperadrenal)- too much glucocorticoids in system, can cause muscle wasting, bone demineralization, and ligaments to be lax, might see buffalo hump on back (does NOT feel like fluid) Diabetes (fasting plasma glucose 126mg/dL) Action of insulin-when insulin gets to cell, it makes glucose transporters close to membrane (Below 100 mg/dL is normal for FPG) Type 1=autoimmune (insulin producing B cell destruction), typically under age 20 Risk factors: sibling has Type 1, parents have type 1 Type 2=obesity (insulin resistance...receptor not binding to insulin as well, pancreas intact), hyperglycemia develops slowly, may have genetic predisposition, 85-90% of all diabetes Risk factors: overweight, over 45 yrs old, inactive, women who had a baby over 9ilbs, low HDL Gestational=associated with type 2, glucose intolerance w/ pregnancy, increased risk of diabetes later on, if continues 6 weeks after pregnancy...no longer GDM Acute Hyperglycemia Early signs: blood sugar 180mg/dL, blurred vision, thirsty, ketones,dry skin, increased urination, tired Late signs: blood sugar 240mg/dL, nausea/vomiting, deep/rapid breathing, large ketones in urine, fruity breath, some diabetes pts don’t sense changes bc of neuropathy Acute Hypoglycemia Caused by: over treatment w/ insulin, missed meal, exercising when insulin peaking, stress Early signs: tachycardia, hunger, headache, dizziness, sweating, shaking, pale skin, tingling around mouth, Late signs: slurred speech, confusion, sudden moodiness, clumsy or jerky movements, seizures, pass out Treatment: Act quickly! Test blood sugar after attempting to raise it with 15 grams of fast acting sugar...if 70 repeat, if 70 eat meal/snack (always assume they will drop 50 mg/dL while exercising) Obesity **Nursing/Allied health professions have greater risk of injury due to rising obesity trends** Underweight = 18.5 Normal weight = 18.5-24.9 Overweight = 25-29.9 Obesity = BMI of 30 or greater Subcutaneous vs. Intra-abdominal fat Subcutaneous fat needed for thermalcontrol Abdominal obesity=most important factor in determining pre-diabetic state (1 out of 5 US adults have metabolic syndrome), want to avoid fat around organs (especially liver) Hormone regulation Fat=largest/most active endocrine organ, releases 50 hormones, Adiponectin=hormone that signals brain we are full (as fat cell gets bigger, releases less of this) More macrophages recruited with obesity, causing chronic inflammation Lifestyle=big factor (obesity trends with US Pima Indians vs Mexican Pima Indians) Epigenetics= We can change which genes we turn on and off by our activitity Mental Health Disorders of Children Autism Spectrum Disorder • Autistic disorder, pervasive developmental disorder, and Asperger’s disorder: differ in whenthe symptoms start, how fast they appear, and severity • Cause is unknown; genetic and environmental factors; structural brain abnormalities: larger total brain mass, smaller frontal cortex, abnormalcerebellum • S&S: lack of social skills, avoid eye contact and physical contact, echolalia, don’t listen, aggressive or passive (may switch), inflict self injury, resistant to change, diff in expressing needs,tantrums • Early indications: no babbling or pointing, no single words, no response to name, loss of language or social skills, poor eye contact, excessive lining of objects, no socialresponsiveness • Later indicators: impaired ability to make friends or initiate conversation, impaired play, echolalia, preoccupation with objects, inflexible adherence to routines andrituals • Screening tests: Childhood Autism Rating Scale (CARS), Checklist for Autism in Toddlers (CHAT), Autism screening questionnaire, screening test for autism in 2 yearolds • Treatment: intensive behaviortherapy Attention Deficit Hyperactivity Disorder (ADHD) • Inability to focus on one thing in all aspects of life impairing function; diagnosis (must have all 3): inattention, hyperactivity, andimpulsivity Tourettes Syndrome • Characterized by tics; tics: involuntary, rapid, repetitive, and stereotyped movements of individual musclegroups • Transient tic disorder: do not persist for more than 1 year vs. chronic tic disorder: duration over many years (unchanging character) vs. chronic multiple tics: several chronic motor tics vs. Tourettes: multiform frequently changing motor and phonic tics, unknowncause Bipolar Disease • Combination of euphoria and depression; in kids: continuous, rapid-cycling, irritable, and mixed symptom state that may co-occur with disruptive behaviordisorders School Refusal/Avoidance • Re