PATHO STUDY GUIDE: FINAL EXAM!

PATHO STUDY GUIDE: FINAL EXAM! Stress increases functional demand  adaptations: hypertrophy, hyperplasia, atrophy, metaplasia, dysplasia)  Stress is reversible – when it’s relieved cell returns to normal  Irreversible stress – too much damage  necrosis Reversible Stress Types 1. Atrophy: decreased size of cell due to decreased functional demand  Overall decrease tissue mass  Muscle can atrophy if not used because of injury, neuromuscular dysfunction (i.e. spinal cord)  Bones, glands, vagina can also atrophy  Prednisone/steroids can atrophy adrenals and testes 2. Hypertrophy: increased size due to increased demand  Beneficial for skeletal muscle  Not good for heart tissue – leaves less space for blood to flow & restricts C.O. 3. Hyperplasia: enlarged tissue mass due to fxn demand or stress that leads to an increased # of cells  Hyperplasia of epithelial tissue = calluses  Gums overriding teeth due to drug use = gingival hyperplasia 4. Metaplasia: extreme stress but still reversible, mature cell type becomes replaced by different mature cell type due to stress increase, new cell is normal but not what you’d usually find @ that location  Change in PSCCE of smoker  squamous epithelium (if they quit PSCCE can return)  Unresolved GERD changes epithelia of esophagus 5. Dysplasia: so much stress that cells become abnormal shape, structure, and size  Uniformity is lost, nuclei look different  “Precancerous” easy to become neoplasia or anaplasia i. ex: papsmear screening for cervical cancer Irreversible Stress Types 1. Anaplasia: totally undifferentiated cells that are cancerous  Nucleus and cell structures are variable 2. Neoplasm: new grow, tumor forms Causes of injury/death  Ischemia/hypoxia: lack of blood, lack of O2  cell can’t make energy o Ischemia is worse than hypoxia alone because no blood = no nutrients at all  Free radicals: damage membrane or cells  Nutrition: too high or too low (macro and micro nutrients) o With poor intake, poor absorption, poor circulation (nutrients can’t get in)  Infectious/immunologic: bacteria and viruses, body’s immune response can create more damage  Chemical: toxins, poisons, alcohol, drugs  Physical & mechanical: extreme temp, change in pATM, trauma, electrical, ionizing radiation Reversible cell injuries  Hydropic swelling: 1st manifestation of reversible cell injury due to accumulation of h2o caused by malfunction of Na/K pump o Sodium builds up in cell and h2o follows o Large pale cytoplasm b/c of increased h2o o ER + mitochondria  swollen and dilated o Increased size & weight of organ o “-MEGALY” organ enlarges suffix  Intracellular accumulation: lipid accumulation/deposition o Normal body substances build up o Not metabolizing well  build up (ex: Taysachs) o Exogenous products can also build up (coal dust in lungs)Irreversible cell injuries  Free radical: charged atom that has unpaired electron (neg charge) when cell is exposed to lots of energy (UV, radiation) o Can damage membrane, protein, transport pumps, DNA (cancer), lipid oxidation o Prevented by peroxisomes that rid free radicals, antioxidants (vit C, A, E, coQ, carotenes, uric acid in blood, melatonin o *MEMBRANE DAMAGE = IRREVERSIBLE  Necrosis: tissue destruction o Ruptures due to membrane damage  products spill out  inflammatory process starts  further injury o Coagulative necrosis: most common type  Starts w/ ischemia  loss of energy  Na/K pump can’t work  Na rises in cell so h2o rushes in  swelling, cell tries to make ATP  acid h2o build up  rupture and spill  organ becomes gray firm mass o Liquefactive necrosis: cells release contents and are destroyed  Lysosomal enzymes eat dead cell AND healthy cell  Dissolved dead tissue becomes liquid abscesses/cyst o Fat necrosis: death of adipose tissue as result of trauma  Pancreatitis – chalky white appearance related to chronic alcoholism o Caseous necrosis: seen with lung damage secondary to TB  Chunky cheese appearance o Consequences of necrosis…  Loss of fxn – dead tissue doesn’t work  Inflammation & fever – spilled contents  Foci of infection – vulnerable to bacteria  Release of intracellular proteins (can be used as serum markers)  Gangrene: tissue death in large area caused by ischemia o Dry gangrene – large scale coagulative necrosis  Slow spreading  Seen in someone w/ poor circulation to lower extremities (diabetes, peripheral artery disease)  Dry, black, wrinkles  Clear demarcation from healthy to dead  Tissue won’t return, must remove o Wet gangrene – large scale liquefactive necrosis, large abscess formation  Fast spreading  Usually seen w/ internal organs but can be seen outside  No demarcation o Gas gangrene – could’ve been dry or wet but now infected with anaerobic clostridium bacteria  makes gas bubbles in damaged tissue Apoptosis: made too many cells, worn out, developed improperly, genetically damaged  Programed cell suicide thru cascade signaling process  No inflammatory response!  Killed neat, clean  Room for new, healthy cells Cancer  Cell-based diseases w/ systematic manifestations  Risk increases w/ age  Prevalence 14 mil, causes 1 in 4 deaths o Men – prostate o Women – breathe o No disparity in lung, colorectal, urinary, lymphoma, etc.  More + better treatment  increased longevity (“5 year survival rate”) o Pancreatic – poor prognosiso Prostate – 99% survival  Definition: altered cell differentiation and growth o Neoplasia = new growth o Dysplasia = disorganized & somewhat differentiated (pre-cancer)  Growth is uncoordinated and autonomous (no regulatory controls)  IN SITU (confined to initial area) or INVASIVE (goes to other tissues)  Neurons and cardiac muscle can’t divide/reproduce so they don’t usually become cancerous  Skin, liver, blood, bone can reproduce mutated cells very quickly – cont. to grow and divide  Undifferentiated stem cells – can be triggered thru abnormal process to start making progenitor cells (usually helpful) but with mutations, they become cancer cells  Tumor = cancer cells forming mass (malignant or benign) Suffixes:  “oma” benign  “carcinoma” malignant tumor of epithelial  “sarcoma” malignant tumor of connective Benign Malignant -slow growing -well differentiated -resemble cells of origin -encapsulated (no shedding/metastasis) -can eventually shrink -stays local -seen in fatty tissue, cherry hemangioma -only life threatening w/ brain pressure -fast growing -undifferentiated -cannot recognize origin -no capsule (spread by breaking off and moving through lymph and blood to seed and start 2*/metastatic tumor elsewhere) -capable of angiogenesis (own blood supply, steals nutrients from tissue in need causing necrosis) -can release enzymes & toxins to destroy healthy tissue -paraneoplastic syndrome: excrete hormones to mimic body’s hormones Anaplasia – irreversible adaptation, loss of differentiation  Undifferentiated cancer cells – change size, shape (pleomorphism), nucleus, DNA Cancer causing factors  Body ignores own growth signals (insensitive to antigrowth signal)  Cells aren’t being destroyed (avoiding apoptosis when necessary)  Sustained angiogenesis  Limitless replicative potential  No contact inhibition (bump into other cells but don’t realize that there’s no space to continue growth)  Abnormal membranes w/ altered surface antigens that affects how body responds  No adherence (break loose  distant sites) Cancer spread  Local – malignant tumor invades tissue it’s in  Direct extension – grown past basement membrane of tissue into surrounding  Seeding – cells break off from malignant tumor thru lymph/blood to go thru body  lands & seeds  replicates  Metastasis – seeds grow & replicate into 2* tumor How malignant tumors affect other parts of the body  Compress blood vessels  downstream ischemia  necrosis  inflammatory response  Enzymes secreted break down cells and proteins  Hormones secreted mimic our own hormones (affect h2o, Na, Ca balance)  Abnormal cells initiate inflammatory process and immune response  decrease organ integrity & function  Angiogenesis – stimulates growth of BV to tumor taking away nutrients from good tissueGenes: control proliferation and differentiation  Neoplastic cells ignore genetic control  Increased proliferation = autonomy  Decreased differentiation = anaplasia  Mutator genes: more mutations, faster  Protooncogenes: (good) required for normal prolif, but when mutated they become an oncogene (bad)  Genes for apoptosis: damaged cells stick around  Tumor suppressor genes: prevent growth of cancerous cells  Genes for DNA repair: radiation, chemicals, etc. damage DNA but need to repair, instead cells w/ bad DNA replicate Mutations in somatic cells (ex: epithelial) won’t replicate Mutations in germ/stem cells will be passed onto future generations Carcinogens: environmental, cause mutations that form malignant tumors  Radiation – UV, nuclear disasters  Hormones – beef, milk, etc.  Chemicals – cole mines, smokers Diseases that cause cancer (r/t chronic inflammation)  GERD – esophagus inflammation  Chronic pancreatitis (alcoholism) Viruses insert own genetic structure into our DNA  cells can replicate  shed viral particles & infect other cells Chronic inflammation  cytokine release  inflammatory response  Free radicals are produced which damage DNA  Decrease response to DNA damage = cancer Immune system: immunosuppressed (HIV, meds that decrease immune response) are at higher risk of cancer Warning signs of cancer  Bleeding/discharge  Change in bowel/bladder habits  Change in warts/moles  Sores that don’t heal  Unexplained weight loss  Anemia & fatigue  Cough/hoarseness w/o reason  Solid, painless lumps Clinical manifestations of tumors LOCAL  Pain: usually seen in late stages, well advanced tumors, severity depends on what tumor is pushing on  Tissue integrity: compressed BV  ulceration & necrosis, if BV erode then there will be bleeding/hemorrhage  Obstruction: BV, lung tumors block airway, GI tract impedes flow of feces, superior vena cava syndrome (blood coming back to heart)* needs immediate treatment SYSTEMIC  Weight loss/cachexia: ano, tired, pain, stress  Release of cytokines  inflammation  Anemia due to blood loss @ tumor site, nutrition deficit (tumor taking it from body), decreased Hgb synthesis  Fatigue: inflammation, cachexia, anemia, psychological factors  Effusions: fluid build up in body cavities due to inflammation caused by tumor  Infection due to decreased resistance, anemia, undernourished, fatigued, or on radiation/chemoDiagnostic tests: 2* level of prevention  Routine screening to ID early  Self exams (breast, testicular, skin)  Blood tests – levels during treatment (WBC for immune fxn and RBC for anemia), blood measure of tumor markers (ex: PSA prostate specific antigen)  X-ray (radiographic), ultrasound, MRI, CT – none are diagnostic because you can’t tell WHAT lump is, may be cyst  Biopsy *most dependable – only way to confirm cancer, test the sample, histologic and cytologic exam to find stage and tumor type TNM classification system: T = size of primary tumor (TX can’t tell, Tis in situ, T0 none, rest are 1-4) N = # of lymph nodes it is in (NX can’t tell, N0 none) M = is it distant yet? (MX can’t tell, M0 no spread, M1 spread) Treatment:  Curative = not advanced prognosis, hopefully remission (when cancer becomes undetectable)  Control = keep it from growing or metastasizing  Palliative = keep person comfortable  Chemo: antineoplastic drugs, attacks dividing cells, same bad effects as radiation, can damage kidney and esp. liver  Radiation: destroys dividing cells and good cells, effect depends on cancer type, can decrease tumor cell # and size  Surgery: good if tumor is small, if it’s large it can affect function based on amount of tissue removed  Debulking: can decrease size by chemo or radiation  Immunotherapy and hormones can be used as well 1 st line of defense = mechanical barriers (non-specific) 2 nd line of defense = inflammation & phagocytosis 3 rd line of defense = immune response (Ab & lymphocytes act following exposure to specific antigens) Purposes: neutralize/destroy invaders, limit spread to other tissues, prepare for repair Causes: physical damage, infection, trauma, chemicals, temp extremes First… chemokines or bacteria entering skin cause WBC to migrate (chemotaxis, margination, diapedesis, and selections which help WBC adhere to extravascular tissue) into tissue (neutrophils which arrive 1 st and macrophages) BRADYKININ released from injured cells Pain receptors are activated Sensation of pain causes MAST CELLS and BASOPHILS to degranulate HISTAMINE is released Bradykinin & Histamine cause CAPILLARY PERMEABILITY VASODILATION, increasing blood flow Plasma proteins can move into ISF and brings fluid with it Increased fluid dilutes toxins Fibrinogen forms mesh to localize invader (Leukotrienes and prostaglandins are released later) Cytokines = communicators  Send message to lymphocytes and macrophages, immune system, & hypothalamus for fever Leukos are attracted by chemotaxis as cells release contents  Neutrophils and macrophages collect along capillary wall and migrate out into interstitial area via diapedesis  Neutrophils that have engulfed pathogens die, enzymes are released and surrounding tissues are destroyed (prolonged inflammation) Complement system: group of circulating proteins that are normally inactive precursors  Can be activated by classic mechanism (antigen antibody complex form) or alternative mechanism  Includes mast cell degranulation (histamine), opsonization (negative coating for recognition), chemotaxis (movement of WBC to injured tissue), anaphylatoxins (bronchospasms), cell lysis, increased vascular permeability (vasodilation), recruitment & activation of neutrophils Cardinal signs of inflammation: redness (inc blood flow), swelling (vasodilation brings in fluids and proteins), pain (increased nerve pressure and bradykinin), loss of fxn (lack of nutrients or too much swelling), heat (inc blood flow) Systemic effects of inflammation: fever (pyrogens), malaise, fatigue, headache, anorexia Inflammatory exudates  Function: transport leukos and Abs, dilute toxins, transport nutrients for tissue repair  Types: o Serous – mostly water, some proteins and WBC o Sanguineous – bloody o Serosanguinous – mostly serous w/ RBCs o Fibrinous – thick, sticky, high cell & fibrin content o Purulent – pus, yellow/green, leukocytes, debris, microorganisms Changes in blood with inflammation  Leukocytosis - o Increased WBC, especially neutrophils o Increased CRP (only shows up in inflammation, not normally there) o Increased plasma proteins o Increased cell enzymes (released from necrotic tissue) WBC differential  Total #: 4,500-11,000 cells/mL  Neutrophils: 50-62% - phagocytes and first responders  Lymphocytes: 25-40% - B & T cells  Monocytes: 3-7% - immature macrophage  Eosinophils: 0-3% - allergic responses, parasites  Basophils: 0-1% - heparin, histamine, mediators of inflammation  Bands: 3-6% - immature neutrophils When there is leukocytosis and in INCREASE IN BANDS  SHIFT LEFT Acute inflammation Chronic inflammation -2 weeks -discrete events -minimal scarring -can come after acute if cause isn’t eradicated, or can dvlp gradually -due to chronic irritation (ex: smoking) -LESS swelling & exudate -more lymphocytes, macrophages, fibroblasts -more scar tissue, granuloma can develop Complications of inflammation:  Infection (microorgs can easily penetrate tissues w/ edema)  Deep ulcers (cell necrosis and lack of regeneration)  Skeletal muscle spasm (protects against pain)  Local complication of obstruction & decreased cell fxnTreatment = RICE therapy Pharm treatments:  Acetylsalicylic acid (aspirin) - decreases PG synthesis, reduce inflammation  Acetaminophen (Tylenol) - reduces fever and pain  NSAIDs (ibuprofen/advil, naproxen/aleve) - reduces inflammation, reduces pain, reduces fever reduces PG synthesis **everything!  Glucocorticoids – synthetic hormones that decrease capillary permeability, reduce leukocytes and mast cells, block immune response o Side effects…  Atrophy of lymph tissue  reduced WBC  increased infection risk and decreased immune response  Bone demineralization, muscle wasting, thin skin/mucosa  Reduce secretion of natural hormones  atrophy adrenal glands (aldosterone like effects retain H2o and Na)  Delayed growth in kids  Reduced hematopoiesis (formation of blood cells in marrow) NOW ONTO … 3 types –  Resolution – occurs w/ minimal tissue damage, cells can fix and return to normal quickly (ex: sunburn)  Regeneration – damaged cells can do mitosis and be replaced w/ functional cells  Replacement – cells can’t do mitosis, functional tissue replaced by scar tissue, can’t function Healing by 1* intention: wound edges can be approximated, all areas heal simultaneously, like a surgical incision w/ sutures Healing by 2* intention: takes longer, more scar tissue, doesn’t heal all at same time but from bottom up, like a pressure ulcer Phases of healing 1. Inflammation – occurs w/ clotting, removal of foreigners by neutros, macros, and monos 2. Proliferative – key cell is fibroblast (produces GF), you see moist pink granulation tissue 3. Remodeling – development of fibrous scar, collagen synthesis Promoters of healing: youth, nutrition, vitamins, Hgb, effective circulation, no infection/cleanliness Inhibitors of healing: hemorrhage, hypovolemia, altered nutrition (O2 & nutrients), infection, impaired collagen synthesis, impaired epithelialization Scar: loss of function & specialized structures (follicles, nerves, receptors), not elastic (contractures & obstructions), adhesions (things that aren’t supposed to fuse together) Complications of scars –  Hypertrophic – scar tissue w/ excessive collagen deposits  Keloid – overgrowth of fibrous tissue  Ulcerations – blood supply impaired around scar  more breakdown  Dehiscence – wound reopens Communicable: spread person to person Non-communicable: opportunistic infection in someone immune-compromised Pathogenicity: ability to cause disease Virulence: degree of pathogenicity, depends on…  How invasive? Motility (flagella) or enzymes  Toxins released by bacteria  Adherence – pili and fimbrae make it hard to get rid of Avoid host defenses – body can’t recognize Epidemiology –  Sporadic: single individual  Endemic: continuous transmission w/in population  Epidemic: higher than normal, spread to new area (increased incidence)  Pandemic: world wide across continents Chain of infection Means of transmission:  Can be direct contact – w/o any intermediary or indirect with an intermediary like an inanimate object (fomites) or dirty hands  Universal precautions – hand hygiene, etc.  Contact – gloves and gown, with patients like MRSA, used in addition to standard  Droplet – respiratory/salivary secretions, expelled from infected individuals, must wear mask  Aerosol – small particles suspended in air, can travel far like TB or chicken pox, must wear N95 mask  Vector borne: insect/animals as intermediate host, like mosquitos with malaria or a dog with rabies Nosocomial infections: acquired in health care settings, should be prevented but effect 10-15% of pts Infection control: standard/universal precautions should be used with everyone (esp when in contact with body fluids) Process of infection:  Pathogen enters host  incubation period  immune system kicks in  inflammatory process starts  Prodromal period (subclinical): disease is there w/ a few symptoms but it’s vague and systemic (fever, weak, nauseous)  Acute illness phase: local (inflammation, heat, pus, loss of fxn, etc) & worse systemic effects  W/ adequate immune response we can defeat and enter convalescent phase (recovery w/ general malaise) o Might never happen w/ chronic infections, instead we treat outbreaks or need life long treatments  Septicemia: immune-compromised, infection gets in blood stream causing circulatory shock, maybe death o Shock can be controlled to get you back to convalescence Clinical manifestations  Specific: can be seen whatever part of body it’s infecting (i.e. bad food  GI symptoms with nausea, respiratory infection  pneumonia)  Non-specific: symptoms can be seen w/ many different diseases  Obvious: predictable patterns like chicken pox  Covert: can’t tell so have to perform lab tests to detect, asymptomatic Local  Viral – serous, clear exudates Bacterial – green/yellow purulent exudate Systemic  Fever, headache, fatigue, nausea, malaise Blood tests:  WBC count – o Leukocytosis – increase WBC, indicates bacterial infection  Neutrophilia also indicates bacterial infection o Leukopenia – decrease WBC, indicates viral infection  Specific increase in T lymphocytes indicates virus  Serum antibody levels – used in HIV testing, sees if you’ve made Ab to HIV causing pathogen  Cultures – used from exudate to test for presence of microorganisms  Sensitivity – done w/ culture @ same time, sees what rx it’ll respond to Treatment:  Antimicrobial drugs (antibacterial, fungal, viral) o Over perscription causes resistance o Virus doesn’t have many rx (they exist for HIV and hepatitis)  Symptom reduction – fluids, rest, analgesics, antipyretics o Don’t give children aspirin  Reye’s syndrome  permanent neuro and liver damage  Surgical – access to infected site (i.e. draining abscess), clean site (wound debridement rids necrotic/infected tissue), remove if it’s really bad (appendectomy) Influenza: viral infection of epithelial cells of airway (upper respiratory)  Causes cell rupture, death, necrosis  Contain cilia to cough/sneeze what we trap – if we destroy cells we destroy process of trapping debris and pathogens  Can lead to bacterial infection (increased susceptibility)  Types A (more severe, seen in general population), type B (mild, in children), type C (don’t know)  Droplet transmission – only travel 3-4 ft  Secretions should be serous/clear  Local manifestation – cough, throat, congestion  Systemic manifestation – fever, lost appetite, malaise  Diagnosis based on clinical judgment, rapid viral assays can be used w/ special types like bird or swine flu  Treat by addressing symptoms (rest, water, nutrition, pain/fever control) o Antivirals not used w/ general flu o Primary prevention is vaccine Cells of innate immunity:  Neutrophil – phagocytosis  NK cell – nonspecific cellular antigen destruction  Dendritic cell – antigen presentation  Monocyte/macrophage – phagocytosis Cells of adaptive immunity:  B lymphocytes o Memory cells – rapid antibody response to antigen recognition o Plasma cells – secrete IGs/antibodies  T lymphocytes o Killer T CD8 – specific cellular antigen destruction o Helper T CD4 – activation of killer T cell 3 rd line of defense is adaptive immunity  Specific Defends against antigen invasions HLA – how body recognizes self cells (labels them so immune system doesn’t attack)  Non-self can be antigens, microorgs, deformed self cells  Located on MHC o MHC 1: on all nucleated cells  Prevents immune system attack on good cells  If self cells become cancer or invaded by virus body will recognize MHC1 cells and CD8 cells will kick in to destroy  Alloimmunities (transplants) try to match up MHC/HLA to prevent rejection o MHC 2: on all immune cells, they engulf pathogen and present it through MHC 2 receptor  Immune cell engulfs pathogen and puts fragments on surface  CD4 sees fragments and triggers immune response  Can pull other T’s and B’s to help destroy 2 types of immunity Cell Mediated Humoral -uses specific T lymphos that originate from thymus -defends against viruses in particular -CD 8 cells are cytotoxic -CD 4 cells are helper  TH1 call other T’s to area to help destroy, TH2 signal B lymphos -also make memory cells -B lymphocytes that orginate from bone marrow -can develop into plasma cells which become different antibodies -also make memory cells Antibodies:  IgG “the intern” o Most common 75-80% o Secreted by B cells o Smallest – crosses placenta for passive immunity to baby o Responsible for action at 2nd exposure (otherwise, after 1st exposure follows after IgM)  IgM “the boss” o Too big to cross capillary wall  stays in vasculature, circulates blood o First responder upon exposure to antigen for 1st time o Works best to activate complement system o Triggers response to transfusions  IgA “security” o Works in innate immunity w/ 1st line of defense – secretions of GI, mucous, saliva o Can pass from mother to child via colostrum  IgD “CEO” o Only makes 1% of cells o Function unknown but possibly tells B cells to differentiate and multiply into plasma/memory cells o May work closely with IgM o Found in tissue & stomach lining  IgE “janitors” o Important to fight parasites, allergic reactions *type 1 hypersensitivity o Bound to surfaces of masts and basophils  degranulation  histamine Functions of antibodies  Precipitation & agglutination – binds w/ antigen to form antigen/Ab complex, makes entire antigen larger so it can precipitate out of serum and be easily recognized by macrophages  Neutralization – anti-toxins can neutralize toxins (ex: snake bite)  Opsonization – coating of antigen for easy recognition  Complement activation –inflammatory response keeps infection local & prevents spreadDiagnostic tests  Elisa – detects HIV antibodies and other disease  Titers – level of IG circulating in serum, ready to fight specific antigens  Indirect Coombs Test – Rh blood compatibility, no transfusion issues, mother to child issues (Rh NEG mom with Rh POS baby)  MHC typing – match tissue based on MHC/HLA before transplant Types of immunity  Natural active immunity: natural exposure to antigen (getting chicken pox)  Artificial active immunity: antigen introduced to body on purpose (chicken pox vaccine in weak/dead form)  Passive natural immunity: mother to child (IgG & IgA) *temporary  Passive artificial immunity: injection of Ab for short term protection, your body doesn’t build up it’s own (ex: snake bite and anti-venom) *temporary … Autoimmune disease: can’t distinguish self from non-self  Develop Ab to self  Cause is unclear but can lose immune tolerance after tissue damage, aging, genetic Normally… With autoimmune disease… -invaders come and Ab forms -Ab removes invading antigens -Ab remains for future protection -Immune system makes Ab to self -auto-antibodies attack self antigens -inflammation and tissue damage occur Alloimmunity: immune response to cells from same species  Type 4 hypersensitivity – occurs with any transfusion or transplant  Rejection causes inflammation, necrosis organ needs to be replaces after few years but less likely when HLA match, donor is living, person takes immunosuppressant  Host vs. graft disease: you reject the graft you get (ex: you reject donated kidney)  Graft vs. host disease: graft tissue has T cells that reject you (ex: bone marrow transplant) Hypersensitivities (allergies) – B cells for type 1, 2, 3 & T cells for type 4  Type 1: “allergic reaction” o Exposure causes B cells to make IgE  binds to mast cells  mast cells become sensitized  secrete histamine  inflammation, vasodilation, capillary permeability o RAPID response (15-30 min) o Skin rash, eczema, hay fever, vomiting, anaphylaxis, wheezing, tachycardia o Causes: food allergy, seasonal, pet, dermatitis, drug reaction o Can tell by skin tests o Pharm: antihistamines, corticosteroids, B adrenergics, IgE, epi o Can be inherited  atopic hypersensitivity o 1 st phase – mast cell degranulation, chem mediators o 2 nd phase – leukotrienes, prostaglandins  Type 2: “cytotoxic” *tissue specific o Antigen is present on cell membrane o IgG mediated – causes phagocytosis and release of cytolytic enzymes o Usually RAPID can be slow o Caused by skin graft rejection, transfusion rxn, hemolytic disease of new born o Also caused by autoimmune diseases: Graves (hyperthyroid) or mysethenia gravis (neuromuscular disorder where Ab attack receptors on nerves)  Type 3: immune COMPLEX reaction *NOT tissue specific o Antigen-antibody combine to make complex o Complex deposits in BV wall o Activates complement system – massive inflammationo Ex: Lupus (SLE), glomerulonephritis (caused by strep infection), rheumatoid arthritis, serum sickness, farmers lung  Type 4: delayed response o Mediated by sensitized T cells that react to antigen, release chemicals that cause inflammatory response and destruction of antigen o Ex: contact dermatitis (cosmetics, dye, latex, plants), Hashimotos (hyperthyroid), celiac, Guillain barre, type 1 diabetes, transplant rejection, cutaneous basophil hypersensitivity (skin graft rejection) o TB Moutaux test – checks prior exposure, positive reaction shows past exposure doesn’t mean active infection (X-ray or sputum culture tells you if it’s active) Causes of immunodeficiency  Young and elderly have decreased immune response  Alcohol, drug abuse in developed countries  Malnutrition in developing countries o Lack protein = impaired cell mediated immunity, complement system, phagocytosis, IgA production, cytokines Body systems involved: kidney, lung, heart, GI Body fluid found in: arteries, veins, lymph, joints, cerebral ventricles, intestinal lumen WATER is 40-60% of total body weight (70% in infant)  Populations w/ LESS water: women, elderly, obese ICF = most of total body fluid *2/3  O2, electrolytes (K**, Mg, HPO), glucose ECF =* 1/3, most of which is interstitial  Carries nutrients and waste from cells  Contains electrolytes – Na**, Cl, bicarb, Ca  Higher amount in newborn ~50% Types of ECF:  Intravascular – in vessels (includes electrolytes and proteins)  Interstitial – btwn cells, makes up ¾ ECF (has NO protein, electrolytes Na, Cl, bicarb)  Transcellular – special cavities (synovial, cerebral, pleural, pericardial, GI) makes up least of ECF Fluid balance managed by intake (drink, food, IV, cell metab), absorption (GI, lungs), distribution (vasculature movement due to pressure and concentration gradients), excretion (urine, feces, insensible loss) Cell membrane:  Pores allow h2o & h2o soluble molecules to pass  Lipid membrane allows lipid soluble to go directly thru  Large proteins can’t pass thru Transport:  Active: low  high (ions, glucose, aminos) uses ATP  Passive: high  low (rates depend on cell membrane permeability) no ATP o Diffusion: hi  lo based on temp, size, concentration o Facilitated diffusion: special transport proteins (ex: glucose) o Filtration: fluid & solute move from high hydrostatic pressure (HP)  low HP, depends on weight of fluid causing actual physical force  *HP is PUSH FORCE o Osmosis: water from low solute concentration (low osm pressure)  high solute concentration (high osm pressure)  Osmolality = concentration in 1 kg  Osmolarity = concentration in 1 L  OSMOTIC PRESSURE is PULL FORCEHow is fluid regulated internally? THIRST, ADH/VASOPRESSIN, ALDOSTERONE, DIURETICS Water balance  Hypothalamus: osmoreceptors located here  Pituitary: posterior releases ADH to regulate water only retention by kidneys  water and electrolytes In the kidneys…ADH & ALDOSTERONE 1. ADH/vasopressin: ONLY responsible for water reabsorption  From hypothalamus, stored in posterior pituitary Fluid deficit (hypovolemia) or increase osmolality/solute concentration is sensed by receptors Thirst & ADH release are triggered ADH acts on distal collecting tubules in kidneys, makes them more permeable H2o is reabsorbed and not excreted in urine *in reverse situation with fluid excess (hypervolemia) or decreased solute concentration, osmoreceptors sense this so ADH is suppressed and water is secreted 2. RAAS: Decreased renal perfusion/decreased sodium Release of renin (signals to kidney) Renin converts Angiotensin 1  Angiotensin 2 (w/ help of ACE enzyme) Adrenal cortex causes release of aldosterone Aldosterone causes kidney tubules to increase reabsorption of Na & H2o, excretion of K Increases BP and increases volume body fluid In the heart…ANP & BNP  ANP – vasodilator  BNP (from ventricle in response to stretching/fluid overload) – decreases vascular resistance & venous pressure  ANTAGONISTS of RAAS! (decrease BP and blood volume) Balance is related to extracellular saline imbalances, body fluid imbalances or both Closely related to SODIUM in ECF (normal, low, elevated) Alterations:  Hypovolemia – hemorrhage, dehydration  Hypervolemia – increased fluid volume, edema HYPOVOLEMIA – ECF deficit that is isotonic, depletion of WATER and SODIUM  Causes: decreased intake (nauseous, no appetite, coma, NPO), increased loss (trauma/loss of blood, burn victims, polyuria/diabetes, diuretics, diarrhea, vomiting, NG suction tubes, 3rd spacing fluid shifts, shock, diaphoresis)  Diuretics cause FLUID and ELECTROLYTE loss o Treats HTN or heart failure o Loop diuretic (Lasix) – inhibits SODIUM and CHLORIDE reabsorption from loop of Henley  Inhibits Ca & Mg reabsorptiono Thiazide (HCTZ): inhibits SODIUM and CHLORIDE reabsorption from distal convoluted tubules in kidneys  Increases Ca reabsorption o Potassium Sparing (aldoctone): competitive antagonist of aldosterone which holds onto Na and excretes K  Stimulation of Na/K exchange in kidney’s tubules doesn’t occur so patients lose but KEEP POTASSIUM and DO NOT REABSORB SODIUM  Manifestations: dry mouth, thirst, decrease turgor, light headed/dizzy (poor brain perfusion due to low BP), oliguria (dec output), weight loss (1L=1kg)  Treatment: replace with normal saline/lactated ringers, monitor INO, daily weight, safety, skin integrity risk  Dehydration: insufficient body fluid because of inadequate intake or major loss of fluids or both o Loss affects ECF first o Mild deficit loss of 2% body weight, moderate 5%, severe 8% or more o Manifestations: dry membranes, poor turgor, low BP, weak pulse, fatigue, inc HCT (proportion of RBC/water), dec mental fxn o Compensation: inc thirst, inc heart rate, constrict BV (pale an cool), dec urine, inc ADH and aldosterone o Diagnosis:  Physical exam – dry membrane, dec turgor, low BP, high BUN and creatinine to show kidney malfunction, high urine specific gravity because urine has a lot of solutes and not a lot of water  BUN – liver makes urea as product of protein digestion, kidney is responsible for getting rid of it  Creatinine – byproduct of muscle breakdown, supposed to be excreted by kidneys o Treatment: oral IV fluids, correct electrolyte imbalance o Types of dehydration (due to amount of sodium intra and extra vascular):  Isotonic dehydration – serum electrolytes are NORMAL  Caused by fasting (food and water), diarrhea, vom, burns, hemorrhage  Dry membranes, decreased urine output, hypovolemia  Treated w/ normal saline & lactated ringers  Hypertonic dehydration – INCREASE serum electrolytes (esp. Na)  Caused by long fever, dec fluid intake, diabetes insipidus, DM  Thirst, lethargy, agitation, seizure, coma  Treat w/ hypotonic solution – ½ normal saline, D5W  Diabetes insipidus – decrease in ADH (which is responsible for reabsorption of water)  Caused by brain tumor, head injury, infection, kidney damage, meds (lithium)  Ducts and tubules don’t reabsorb well  Decreased water absorption, increased urine output, increased serum osmolality  Symptoms of dehydration and hypernatremia  Hypotonic dehydration – DECREASE serum electrolytes  Caused by Addison’s disease (aldosterone deficiency), overuse diuretic, marathon/exercise w/o replenishing  Symptoms of hyponatremia (nausea, vom, seizures, coma)  Treat with hypertonic solutions 3% saline HYPERVOLEMIA – ECF excess w/o change in osmolality, WATER and SODIUM excess  Causes: renal failure (can’t excrete enough urine), CHF (heart can’t pump blood normally), hormone imbalance (Cushing’s, steroid therapy), liver failure  Manifestations: edema, weight gain, circulatory overload (bounding pulse, jugular venous distention, elevated BP)  Treat: diuretics (CHF), dialysis (renal failure), fluid restriction  Monitor INO, weigh daily, check resp status (risk of dyspnea – short breath), monitor for skin breakdown (edema)  Overhydration: o Hyperosmotic – oral/IV hypertonic OD  fluid shifts in vasculature  inc plasma volume, dec ICF, HTN crisis (inc BP) o Hypotonic – caused by syndrome of inappropriate ADH (SIADH) or ingestion of too much water o Isosmotic – oral/IV OD o SIADH – overproduction of ADH  Caused by CNS disorder, cancer, meds (thiazides, opioids)  Leads to dilution hyponatremia, dec serum osmolality, increase urine osmolality, dec urine volume (retain more h2o but salt can be excreted)  Shows symptoms of fluid overload & hyponatremiaEdema – main causes  Increased capillary HP – prevents blood from going from ISF  venous end of capillary, forces extra fluids out of capillary into tissues o Caused by kidney fail that inc blood volume, pregnancy, congestive heart failure, admin of too many fluids  Loss of plasma proteins (albumin) – dec osmotic pressure of plasma o When there are less plasma pros in capillary, more fluids are allowed to leave and can’t return to venous end o Seen in kidney/liver disease  Blockage of lymph circulation – usually cause local edema because fluids and proteins can’t return to circulation o Caused by tumor, infection, removal of lymph from surgery  Increased capillary permeability o Can result from inflammation or infection o Histamine and bradykinin are released from cells after tissue injury  increase cap permeability  inc fluid to ISF o Plasma proteins leak into ISF which increases pressure  Pitting = if fluid moves aside and indent remains  Functional impairment: restricted joint movement, pain due to pressure on nerves (headache with cerebral edema, stretching of organs with capsule i.e. kidney and liver), impaired arterial circulation (ischemia  tissue breakdown), susceptible to skin breakdown Third spacing: fluid shifts from blood  body cavity and can’t reenter vasculature  Ex: liver failure  ascites (inc abdominal fluid) can’t e used in circulation  Ex: burns with high osmotic ISF  Causes fluid deficit in vasculature and fluid excess in ISF  Weight can’t be used to determine fluid shift Electrolytes balanced by intake (meds, IV transfusion, saline, supplements, food), absorption (concentration, binding proteins, pH of intestine, meds), distribution (hormones, insulin for glucose and K, PTH for calcium, meds, epinephrine), excretion (urine, sweat, feces, meds specifically Kaexalate for high K pts, abnormal loss from drain) Imbalance:  Common causes: 2* to vomiting, diarrhea, treatment (perioperative NPO, GI prep, blood loss)  Manifestations: dehydration, arrhythmia, death  At risk: o Infants - immature kidneys, rapid respiration, more body SA to lose fluid o Elderly - low total body water, dec thirst, kidney changes (dec renal flow, GFR, creatinine clearance), can’t concentrate urine or conserve water, decreased rennin + aldosterone production, inc ADH & ANP, loss of skin thickness (moisture loss) Tonicity: basis of IV fluid, determines direction of diffusion  Isotonic = same osmolality as ICF (normal saline)  Hypotonic = lower osmolality than ICF (1/2 normal saline)  Hypertonic = greater osmolality than ICF (3% saline) Electrolyte Lab Values Na 135-145 mEq/L K 3.5-4.5 mEq/L Ca 9-11 mg/dL Mg 1.5-2.5 mEq/L PO 2.5-4.5 mg/dL Cl 96-100 mEq/L SODIUM 135-145  Primary extracellular cation 90%  Diffuses between vasculature and ISF  Transport across membrane controlled by Na/K pump (active)o Makes Na levels HIGH OUTSIDE cell and LOW INSIDE cell  Exist in body as salt, NaCl, sodium bicarb  Lost via sweat, urine, feces  Controlled by KIDNEYS via ALDOSTERONE  Important for acid base balance, osmotic forces, conducting nerve impulses, muscle contraction o Change in sodium  CNS issues HYPONATREMIA: 135  Causes: o Results from direct loss (vom, diarrhea, diuretics) o Results from excess h2o (too much hypotonic IV fluid, SIADH, dilution of sodium)  Manifestations: o Neuro – lethargy, confusion, seizure coma o If due to Na loss  hypovolemia symptoms (light head, thirsty, 0 urine) o If due to h2o dilatational hyponatremia – s/s fluid overload  Treatment: salt tabs, hypertonic solution (3.5% saline), restrict h2o HYPERNATREMIA: 145  Causes: o Results from ingestion w/o proportionate h2o intake o Results from loss of h2o that’s faster than loss of Na o Deficient ADH (diabetes insipidus) o Cushing’s disease  Manifestations: o Neuro – same as hyponatremia o Due to Na gain – think fluid overload o Due to fluid loss – hypovolemia s/s  Treatment: restrict Na, give hypotonic solutions POTASSIUM  Major ICF cation  Ingested in foods (bananas, citrus fruits, tomatoes)  Excreted in urine via ALDOSTERONE, also INSULIN moves K into cells  Fxn is nerve conduction and muscle contraction (*cardiac)  Regulates ICF volume  Regulates cell metabolism  High/low levels have serious heart effects, changed EKG  Influenced by acid base levels in body o Acidosis: H+ ions come in cell and take place of K+ ions so they have to move out of cell  K+ moves into blood  hyperkalemia o Alkalosis: moves K+ into cell HYPOKALEMIA: 3.5  Causes: o Low K diet, alcoholism, malnutrition o Abnormal loss – vom and diarrhea o Mg deficiency causes renal K wasting o Metabolic alkalosis o Treatment of DKA w/ insulin (causes K to go into cell, decreasing K in ECF)  Manifestations: sort of a “slow down” incl bradycardia, skeletal muscle weak, weak resp muscles, dec GI motility, impaired arteriolar blood flow, polyuria  Treat: IV/oral KCl supplements, K sparing diuretics (aldoctone), inc diet K HYPERKALEMIA: 5  Causes: o Increased intake (IV, diet, supps, oral) o Metabolic acidosis (low in cell but high in ECF) o Renal failure, decreased excretion o Hyperglycemia, Insulin deficiency, can’t be brought into cells o Transfusion ptso Drugs: digoxin – blocks Na/K ATPase (normally makes Na leave and K come in but K can’t come in when pump is blocked)  Also ACE inhibitors, K sparing diuretics o Aldosterone deficit due to Addison’s (adrenal glands can’t make hormones)  Manifestations: tingling, cramps, diarrhea, neuromuscular irritability o Severe: muscle weakness, loss of tone, flaccid paralysis, arrhythmia, cardiac arrest  Treat: D50 dextrose w/ insulin, IV calcium, kaexalate (makes K excreted in stool), diuretics CALCIUM  Important ECF cation  Fxn: bone, teeth, blood clot, hormones, cell receptor  Ingested in dairy food  Stored in bone as hydroxyapatite o Balance controlled w/ PTH, calcitonin, vitamin D, phosphate  Low blood Ca  PTH secretion  increased Ca absorption in stomach and reabsorption from bone  Vit D – made in skin w/ UV rays and must be ACTIVATED by kidneys, then it will promote Ca to move from bone + intestine  blood  Ca & phosphate have inverse relationship HYPOCALCEMIA 9  Causes: o Retention of phosphate o Vit D isn’t activated o Alkalosis can reduce free # Ca o Hypomagnesaemia o Hypoparathyroidism o Acute pancreatitis o Sepsis o Severe burns  Manifestations: o Muscle cramps, hyperactive reflexes, hyperactive bowel sounds, parasthesia, delayed heart conduction o Chvostek (cheek) – tremor of nose, lips o Trousseau – tetany of hands w/ BP constriction o Skeletal muscle spams result from inc nerve irritability, they have enough Ca for contractions in own reserves o Cardiac muscle relies on available Ca in ECF passing thru channel, directly r/t Ca deficit in ECF  Treatment: IV/oral Ca HYPERCALCEMIA 11  Causes: o Cancer warning sign (bone cancer, tumor on PTH) o Hyperparathyroidism o Diets, supps, vit D overdose o Prolonged immobilization  body reabsorbs Ca from bone o Diuretics (thiazide HCTZ)  Manifestations: o Weak muscles, slow reflex, tingling, intestinal cramps, hypoactive bowel, constipation, cardiac arrest, lethargy, decreased neuromuscular excitability  Treat: hydration to reduce Ca stones, calcitonin, biphosphates (meds that treat bone loss), loop diuretics, isotonic saline infusion MAGNESIUM: 1.5-2.5  Intracellular cation  Most body Mg (50%) stored in bone  Linked to K and Ca levels  Used in enzyme rxns, protein & DNA synthesis  Imbalance is rare HYPOMAGNESEMIA 1.5  Causes:o Malabsoprtion, malnutrition, alcoholics o Loop diuretics o DKA o Hyperthyroidism o Hyperaldosteronism o Hypercalcemia (Mg competes w/ Ca in kidney)  Manifestations: sort of a “speed up”… o Neuromuscular hyperirritability (reflexes, tetany, convulsions, tachycardia, HTN, arrhythmias w/ increased HR), insomnia, personality chg HYPERMAGNESEMIA 2.5  Causes: o Renal failure o Excessive antacids (Maalox & milk of magnesia)  Manifestations: sort of a “slow down”… o Decrease neuromuscular fxn, dec reflexes, lethargy, muscle weakness, respiratory depression  Treat: stop intake, start dialysis PHOSPHATE 2.5-4.5  Mostly in bone  Used in metabolism, bone & tooth mineralization, phosphate buffer system  Reciprocate relationship w/ Ca HYPOPHOSPHATEMIA 2.5  Causes: o Malabsoprtion, diarrhea, excessive antacids, alkalosis, hyperparathyroidism  Manifestations: impairs neuro fxn (tremors, slow reflex, parasthesia, confusion) HYPERPHOSPHATEMIA 4.5  Caused by renal failure CHLORIDE: 98-106  Major ECF anion  Follows Na because of electrical charge attraction (high Na = high Cl)  Cl and bicarb are both negative can exchange places as blood circulates thru body  Maintains acid-base balance: bicarbs bind w/ metabolic acids, Cl ions diffuse into serum to take their place and maintain same # negative ions in blood o If Cl levels drop then bicarb can leave RBCs to maintain electrical neutrality o Low serum Cl = high serum bicarb  alkalosis “chloride shift” HYPOCHLOREMIA 98  Causes: o Acid lost from vomiting  alkalosis o Excessive sweating/fever  loss of NaCl  hyponatremia, hypochloremia and dehydration HYPERCHLOREMIA 102  Caused by excessive NaCl intake (IV) or hypernatremia Physiological pH arterial/O2 blood = 7.35-7.45 so blood is slightly basic pH = % of H+ ion Acid sources in body:  Stomach acid  Respiration (cellular – mitochondria makes energy and releases co2) o Co2 in blood is volatile acid  Non-volatile acids: metabolism of dietary proteins, fats, oxidation of glucose, anaerobic metabolism (lactic acid)… these are *fixed acids Co2 in blood = dissolved as gas, combined w/ h2o to make bicarb, or as carbaminohemoglobinRatio bicarbonate:acid should normally be 20:1 – determines pH  Concentration of metabolic acids and bicarb is regulated by kidney  Concentration of Co2 is regulated by respiratory system BUFFER SYSTEMS  Plasma buffer – reacts in seconds, w/in blood, constantly active o Bicarbonate: principle ECF buffer, bicarb can bind with H+ to decrease acid or release H+ to increase acid o Phosphate: can attach/release H+ o Protein: end groups of pros can attach to H+ or bicarbs  Respiratory buffer – reacts in minutes **compensatory o Hyperventilate or hypoventilate (CO2) to balance  Renal buffer – reacts in hours-days **compensatory o Rid thru urine or hold in tubules of nephron o Can help make bicarb ABG sampling  CO2 = 35-45mmHg  O2 = 80-100mmHg  Bicarb = 22-26mEq/L Acidosis = pH 7.35 (systemic inc in H+) Alkalosis = pH 7.45 (systemic dec in H+) ANION GAP is a type of acidosis  Anions = Cl, HCO3, lactate  Cations = Na, K, Ca, MG  CATIONS – ANIONS  quick calc Na – (Cl + HCO3)  If anion gap increases, typically indicates bicarb is being replaced from Na because bicarb is being used up to help balance out acids  A lot less bicarb = bigger anion gap  HIGH GAP = METABOLIC ACIDOSIS Decompensation: balance is so whack that plasma, renal, respiratory buffers can’t keep anything in check so we have to intervene or it can be deadly  Ph 7.4 or 7.5  death 4 categories of acid base imbalance 1. Respiratory acidosis: elevated co2 as result of breathing issues and ventilation depression 2. Respiratory alkalosis: decrease co2 from hyperventilation/blow off too much co2 3. Metabolic acidosis: decrease HCO3 or increase non carbonic acid 4. Metabolic alkalosis: increase HCO3 or decrease non carbonic acid RESPIRATORY ACIDOSIS: retaining too much co2 in body  Caused by hypoventilation o Could be due to neuromuscular – diaphragm doesn’t work o Rx overdose, head injury  respiratory depression o Airway obstruction o COPD, pneumonia, other lung disease  CNS manifestations: dizzy, lethargic, headache, convulse, coma  Compensation: only renal o Respiratory = 0 o Renal: w/ fxn kidneys you can excrete H+ or make/reabsorb bicarb RESPIRATORY ALKALOSIS: lose too much co2  Caused by hyperventilation o Pain, anxiety, injury, tumor to head, overventilating people  CNS manifestations: parasthesia, confused, tachypnea Compensation: only renal o Respiratory = 0 o Renal: w/ fxn kidneys you can retain/reabsorb H+, decrease bicarb reabsorption/production METABOLIC ACIDOSIS: increase production of metabolic acids or loss off too many bicarbs  Caused by lactic acidosis (anaerobic metabolism)  DKA – not getting glucose into cells so aminos are broken down instead  ketones  Excessive diarrhea = loss of bicarb  Kidney failure – can’t reabsorb bicarb  CNS manifestations: headache, hyperpnea, lethargy, confusion  Compensation: BOTH! o Respiratory: hyperventilate to decrease CO2 o Renal: can excrete H+ and increase bicarb reabsorption/production METABOLIC ALKALOSIS: keep too much bicarb or lose too much acid  Caused by suction/vomiting which removes lot of acid form GI tract  OD on antacids, overcorrection of acidosis  CNS manifestations: numb, tingling fingers and toes, muscle cramps, tetany  Compensation: BOTH! o Respiratory: breathe deep and slow to keep CO2 in blood longer  Can’t do that much slowing because we still need O2 in o Renal: can increase H+ excretion, decrease reabsorption/production of bicarb o Ammonia increase in urine can get rid of H+ Mixed acid base disorder: respiratory and metabolic  Example is COPD which causes respiratory acidosis and renal failure which causes metabolic acidosis ABG calculations: 1. pH midline is 7.4 – which way is it leaning? a. anything 7.4 is leaning towards acidosis  acidic b. anything 7.4 is leaning towards alkalosis  basic 2. If CO2 trend matches with pH it is a RESPIRATORY IMBALANCE a. 45 mmHg  acidosis b. 35 mmHg  alkalosis 3. If bicarb trend matches with pH it is a METABOLIC IMBALANCE a. 22 mmHg  acidosis b. 26 mmHg  alkalosis 4. Determine compensation a. Uncompensated: no change in CO2/bicarb values to get pH back to normal i. *2 abnormal values b. Partially compensated: change in CO2/bicarb values but pH is still off i. *3/all abnormal values c. Fully compensated: change in CO2/bicarb values and pH is good again! (7.35-7.45) i. *pH is normal Pathophysiology Study Guide: Exam 2 EYES 3 types of issues: 1. Errors of refraction a. Hyperopia b. Myopia c. Presbyopia d. Astigmatism2. Eye movement impairment a. Strabismus b. Amblyopia c. Diplopia d. Nystagmus 3. Structural impairment a. Glaucoma b. Cataracts c. Macular degeneration Refraction – eyes unable to accommodate/focus  Hyperopia: farsighted, can’t see close up o A:P dimension of eyeball is too short o Image focuses behind retina o Uses convex lenses  Myopia: nearsighted, can’t see far away o A:P dimension is too long o Image focuses in front of retina o Uses concave lenses  Presbyopia: aging o Lens is less flexible o Difficult to read up close Eye movement –  Strabismus: abnormality of eye coordination and alignment that results in loss of binocular vision o R/t paralysis or non-paralytic weaknesses o Eye moves towards strong muscle & away from weak muscle  Amblyopia: diminished vision w/o detectable lesion in eye o One eye sees blurred, brain starts to block out blurry eye until it becomes permanent blindness (if untreated) o Nothing structurally wrong, has to do with signaling of brain  Diplopia: double vision, issues w/ eye muscles, binocular vision isn’t lined up o Caused by drugs, strained eyes o Corrective lenses or surgery to fix/tighten muscles  Nystagmus: involuntary rhythmic oscillation of eye movements o Trying to focus on object but looking way off to L or R o R/t semicircular ducts & vestibular apparatus in ears o Not always r/t disease or disorder Eyelid disorders –  Ptosis: weak levator muscle o Caused by bells palsy, stroke  Entropion/ectropion: fixed w/ surgeries or tapes o Entropion – lid turns in, irritates sclera o Ectropion – lid turns out, dry eye  Hordeolum/Chalazion o Hordeolum: infection of sebaceous gland, external or internal o Chalazion: chronic inflammation of meibomian gland, looks like stye that is constant and may need surgery Eye infections –  Conjunctivitis: infection of conjunctiva o Viral – pink eye, watery discharge, redness, spread between eyes o Bacterial – gonorrhea, chlamydia, purulent with eye crusted shut  Eyes treated @ birth because can be passed from mother o Allergic – itchy, red, drainage, not an infection/contagious  Keratitis – cornea infection o Pain = severe o Photophobia o Caused by herpes (saliva, transferred by fingers) o Can cause erosion and ulceration  scar tissue  vision problems Glaucoma – increase intraocular pressure  damage of optic nerve (optic disc cups and can damage nerves)  Causes: decreased aqueous production decreased outflow of eye fluid Congenital vs. acquired  1* w/o preexisting eye problems or 2* resulting from another inflammatory process, tumors, or hemorrhage  2 types: o Acute angle closure – more painful  Rapid increase in IOP  Emergency  Can cause blindness/blurred vision  Stress and pressure dilate pupil  Head ache and nausea  See rainbows around light @ night  Treat w/ eye drops and likely surgery o Primary open angle  Chronic, slowly progressive  Trabecular network clogged  can’t drain  increased pressure  Blind spots starting @ periphery and spreading central  Eye drops and surgery to treat Cataracts – opacity/cloudiness of lens  Vision is blurry, darker over time, should refrain from night driving  Different situations between 2 eyes and between people  Comes with aging, may be congenital  Other causes: DM, smoking, eye trauma, excessive sun exposure  No medical treatment, only surgery to remove & replace lens Macular Degeneration – affects fovea in back of eye (central part of retina)  blindness  Where vision signals come & get sent to brain via optic nerve  2 types are dry and wet o Dry – slow onset, occurs due to fatty lipid deposits called “drusen”, deposits affect blood flow, causes scar tissue and damage o Wet – rapid and severe, leaky microvasculature (mini hemorrhage), blood gets into eye causing damage, can remove optic disk  Improved by laser procedure or eye injections  Will lead to blindness, can only keep from worsening  No cure  Can’t see faces or colors, can’t read  Spreads inward  out Emergencies  Retinal detachment: no pain, vision change o Bright flashes in periphery, blurry, floaters, shadow blindness o Caused by trauma  Acute angle glaucoma: pressure builds up quickly, blurred vision, blindness, halos  Herpes zoster keratitis: shingles in eye, increases pressure, pain, red, teary, photophobia, blurry  Central retinal artery occlusion: ischemic eye, nonfunctional, painless sudden vision loss EARS Issues with hearing and balance:  Conductive hearing loss  Vertigo  central processing disorder  Sensory neural hearing loss External and middle ear: capture, transmit, and amplify sounds Inner ear: receptor organs stimulated by sound waves and head position/movement Eustachian tube: ventilates and equalizes middle ear when there are pressure changes, protect middle ear from unwanted sound waves and unwanted secretions Disorders of the EXTERNAL EAR:  Obstruction – from cerumen (elderly and young children), mass (bug)  Inflammation – “otitis externa”, swimmers ear – water sits against tympanic membrane which is optimal environment for bacterial growth Drainage – “otorrhea”, comes out of external auditory canal, r/t infection and inflammation Disorders of MIDDLE EAR:  Barotrauma – damage to tympanic membrane due to pressure change  Inflammation – “otitis media” o OTITIS MEDIA –  AOM (acute): from an infection  Has effusion (fluid) – ideal for pathogen growth  Fluid traps because of blocked Eustachian tube  Assoc w/ upper respiratory infection, pathogens are able to enter middle ear  S/S: enlarged lymph, fever, runny nose, acute pain, perforated tympanic membrane, hearing loss  OME (w/ effusion): no infection  S/S: Acute pain, perforated tympanic membrane, hearing loss  Treat – differentiate btwn OME and AOM  Observation, antibiotics if serious  Mastoiditis – infection of mastoid bone, spread from inner ear infection  painful, headache  Otosclerosis – new spongy bone forms btwn stapes and oval window, leads to progressive deafness o 3 bones can’t transmit sound to inner ear because stapes is stuck and can’t vibrate o leads to tinnitus, vertigo, conductive hearing loss (trouble transmitting sound from external to internal ear) and sensory neural hearing loss (affects innervation of ear) Disorders of INNER EAR:  Inflammation – “otitis interna”  Can lead to mastoiditis  Neural dysfunction: o Sensory neural hearing loss (can’t transmit sounds to brain b/c auditory nerve is affected) o Tinnitis (not real ringing, caused from inner ear issue, r/t drug use) o Equilibrium – vestibular apparatus w/ fluid and hair follicles  how these move tells brain our position  Vertigo: illusion that motion is occurring – objective (room spins), subjective (you spin)  Meniere disease: unbalanced feeling w/ rotary vertigo (severe spinning can’t move), r/t trauma, infection (syphilis), endocrine disorder  Benign paroxysmal positional vertigo – dizziness when you move your head to quickly  Motion sickness: repeated vestibular stimulation PAIN: discomfort resulting from stimulation of pain receptors in body when tissue damage occurs; it is a body defense mechanism Threshold: amount of stimulation needed to activate nerve endings for individual to feel pain, so then the nerve fibers are able to send signals to spinal cord and brain  Threshold should be constant/should not change over time Tolerance: ability to withstand pain and perception of its intensity  Tolerance varies a lot depending on past pain experiences and overall health Causes of pain: inflammation, infection, ischemia/tissue necrosis, stretching of tissue, chemicals, burns, muscle spasms  Skeletal muscle – pain caused by ischemia or hemorrhage  Liver, kidney, brain – pain receptors in outer capsule are stretched  Tendons, ligaments, joints – stretching or inflammation  Stomach, intestines – inflamed mucosa, ischemia, distension, muscle spasm STRUCTURES & PAIN PATHWAY… Nociceptors: nerve endings that serve as pain receptors, found almost everywhere in body  Stimulated by thermal (temperature), chemical (can be made in body, like histamine), & physical (pressure) means Afferent fibers: carries impulse towards CNS  Myelinated A fibers – A for acute o Very fast transmission of impulses o Trigger acute pain from thermal & physical stimuli  Unmyelinated C fibers – C for chronic o Slow transmission of impulseso Chronic pain (diffuse, dull) o Receive thermal, physical, chemical stimuli from muscle, tendon, heart, GI, skin o Pain impulse travels to dorsal root ganglia  dorsal horn  spinal cord Dermatome: area of skin that is linked to 1 spinal nerve  Brain maps these areas in somatosensory cortex (area of parietal lobe in brain) so pain can be interpreted  Used to determine areas of injuries during medical tests  Ex: herpes zoster occurs along dermatome Reflex response: occurs at spinal cord synapse when there is sudden pain  Spinal cord sends motor/efferent response back to muscle that is damaged 