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Pathophys Final pt 1

Pathophys final- cell, acid/base, inflam, immun, infect, hem

homeostasis state of balance, maintained by brain and self regulating mechanisms
why study? understanding diseases
Nosocomial originating in the hospital
Sequelae things caused by disease (scars)
Complications adverse rxn
Risk Factors predisposed to disease/illness
Prevalence # of people that have the disease
Incidence new cases that are diagnosed in amt of time
Acute Dz rapid onset, acute infection, short course
Epidemiology incidence, distribution, possible control of diseases & other health related factors
Syndrome symptoms that occur together; condition w/ associated symptoms
Latent Period period between infection w/ virus and onset of symptoms
Exacerbation made worse
Remission temporary recovery
Chronic Dz long lasting, recurrent
Carrier Status dz is there, but quiet
sign vs sx Sign- indication of a disease, not always apparent to pt Symptom- physical or mental feature that indicates a condition of disease- apparent to patient
Membrane Transport types active- need energy- low to high gradient; passive- no energy needed
Cell Membrane Control movement of substances btw of compartments; gatekeeper
atrophy vs hypertrophy Atrophy- cell size decrease, hypertrophy- cell size increase
hyperplasia # of cells increase
metaplasia mature cells replaced by another cell type
autosomal not sex linked
Recessive has to come from both parents
Dominant dominant trait/gene, can come just from 1 parent
X-linked sex linked
DNA double helix with nucleotide bases
strand of DNA in nuclei of cells chromosome
gene DNA sequence w/ heredity traits
Fluid & pH Normal body fluid composition pH- 7.4, isovolemic, isotonic, more negative inside cell Fluid movement btw spaces
Sodium Major extracellular ion- Na+ Magnet with water Effects of changes (hyponatremia mainly) Hyponatremia- coma, confusion, lethargy Hypernatremia- agitation, restless, LOC, convulsions, DEATH
Potassium Major intracellular ion- K+ Effects of changes (hypokalemia, hyperkalemia)- hypokalemia- Cardiac/respiratory arrest, arrhythmias, dizzy; hyperkalemia- same, but more dangerous risk Link with acidosis- increase in H+
Diffusion Hydrostatic and osmotic pressure/gradients- movement of ions across space
acids/bases acid- lower pH base- higher pH Metabolic acids= byproducts of cellular metabolism
Carbonic acid-bicarbonate buffer kidneys- regulate HCO3 lungs- regulate CO2
Acidosis Metabolic, Respiratory; Control mechanisms- kidneys excrete excess H+ ions in urine, raise bicarb
Alkalosis Metabolic, Respiratory; Control Mechanisms- kidneys excrete more bicarb in urine, lungs decrease RR- retain CO2
innate resistance natural barriers, skin membrane
adaptive immunity allows immune system to remember pathogen for next time it is encountered- stronger response each time (body’s immune system prepares itself for future
inflammatory response protective host response, dilute toxins, remove bacteria, initiate healing/repair, block infection- cant spread
inflammation Purpose- bodily protection for injury and infection Causes- “All of the above”
Mast Cell Activation- initiates acute vascular response to injury Degranulation (some agents preformed and others formed as response)- substances and synthesizes more in response to injury/infection- prolong inflammation
Histamine increase blood flow, endothelial cell contrax, increased leukocyte adherence to endothelium, hyperemia, edema
Chemotaxis causes directional movement of cells toward inflammation
vascular response acute arteriolar vasoconstriction (few seconds); fluid exudation (depends on amt of cells/proteins in fluid); dilation of vessels, bring in cells, promote edema- RED/WARM/ SWELLING
cellular response mast cells- rapid; slower/secondary cell response- eosinophils, basophils, monocytes/macrophages, lymphocytes, fibroblasts, polymorphonuclear neutrophil
Neutrophils (granular, first major phagocyte)- bacterial response, WBC granulocytic; 6-12 hrs after injury- short lived
Opsonization coat bacteria w/ antibody/complement, susceptible to PMN; facilitates phagocytosis; easier for body cells to recognize & engulf enemy materials
Phagocytosis primary function of PMN; extend pseudopods toward bacteria/ debris, engulf, release hydrolytic enzymes & O2 radicals to digest
Eosinophils anaphylaxis and allergy
Monocytes/Macrophages largest normal blood cell; WBC; appear 24 hrs after injury- replace neutrophils; prolong cell response; process antigen; secrete monokines; promote wound healing
Basophils release histamine, leukotrienes, prostaglandins
inflammation manifestations local- heat, redness, edema; systemic effects- fever, leukocytosis, plasma protein synthesis BIG 3: erythema, calor, swelling)
stem cell “totipotential” Myeloid >>> erythrocytes, monocytes, PLTs, granulocytes Lymphoid >>> lymphocytes, NK cell
Monocyte/Macrophage antigen ingestion/processing/presentation; APC when presenting antigen circulating in blood/lymph; made more available to lymphocytes; Antigen Presenting Cell
T cell- Lymphocyte immunity; CD3- antigen- specific receptor on surface CD4 >>> T-helper cell, IL2= CD4 receptor w/ CD3 CD8- T cytotoxic w/ CD3
B cell- Lymphocyte humoral (antibody)- produce/ release antibodies that enter blood and react w/ specific antigen; released from bone marrow as mature
NK cells tumor surveillance- similar to T cytotoxic cell (CD8)- kills tumor cells; uses own NK receptor to bind, doesn’t require MHC molecule or activation of CD4 cells
B cell immunoglobulin types IgM- ~10%; made first, largest immunoglobin, initial immune action; c mu IgG- ~75%; largest quantity, later immune response, fetal blood via placenta; c gamma
B cells immunoglobulin types IgA- ~15 %; body fluids/mucus/secretions; mucus membranes, colostrum; c alpha IgE- <1&; binds mast cells for allergic rxn; role in parasitic infection; c epsilon
Antigen/Antibody complex CD4/ APC
Plasma cells mature B cell; can produce all other types of antibody proteins specific to that antigen (IgG, IgE, IgA, IgD)
Natural active encountered vaccine, produced immunoglobins to fight it off again
Natural passive body already has them- usually from mom
Artificial passive you’re given antibodies (IVIG)
Artificial active immunization
Secondary immune response natural or artificial (vaccines); prepared to respond/attack
Immunogens antigens that will induce an immune response resulting in the production of antibodies or functional T cells.
Antigen becomes immunogen if- Foreignness to the host; Adequate size; Adequate chemical complexity; Present in sufficient quantity (not too much OR too little)
Exogenous antigen fragmented in macrophage/B cell, presented on macrophage (now called APC) increase recognition to T helper- CD4; antigen remains whole, floats in blood/lymph or presented whole on surface of APC, recognizable to B lymphocytes
Endogenous antigen fragmented and presented on surface of damaged cell; combined w/ Class 1 MHC; recognizable to T cytotoxic (CD8) lymphocytes
Antigen specificity host cells can recognize an antigen
anaphylaxis vs cytotoxic Anaphalaxis- immediate rxn, can cause death Cytotoxic- usually cause by adverse drug rxn
immune complex vs cell mediated Immune complex- 3-10 hrs; antigen-antibody rxn; lupus, serum sickness Cell mediated- takes 48 hrs-28 days to show rxn; contact dermatitis, transplant rejection
Tolerance vs autoimmunity Tolerance- most individuals accept own antigens- otherwise body would attack antigen Autoimmunity- immune system reacts to self- usually attacks
ABO blood type antibodies A- anti-B B- anti-A AB- universal recipient- no antibodies O- universal donor- anti-A, anti-B
Apoptosis programmed cell death (suicide); removed neg selected autoimmune lymphocytes, clear activated lymphocytes after antigen clearance, remove damaged lymphocytes
Immunodeficiency failure of immune system to protect the body adequately from infection due to absence or insufficiency of some component process or substance
Bacteria prokaryotes; aerobic/anaerobic; cocci/bacilli; gram pos/neg/acid fast; virulence factors- capsules, fimbriae-pilli, enzymes, exotoxins, endotoxins
Parasites different from fungi, bacteria, and viruses; big problem worldwide
fungi mold/yeast
Viruses Replication depends on host cell, DNA or RNA
Manifestations of infection direct (fever, redness, edema, pain, exudation, increased mucus, bleeding, dysfunction); systemic (cough, diarrhea, emesis, stiffness, increased WBC); Toxic (shock, cachexia, rigors); immune (anaphylaxis, rashes, organ dysfunction)
Gram staining, culturing potentially infected specimens; Sensitivity testing to various antimicrobial agents determines which are most effective in inhibiting growth of that particular pathogen
CA, Benign uncontrolled invasive cell growth grow slowly, capsule, non-invasive, differentiated, low mitotic index, doesn’t metastasize
malignant tumors grow rapidly, no capsule, invasive, poorly differentiated, high mitotic index, can metastasize
Dysplasia “pre-cancer” abnormal change in size, shape, organization of mature cells
TNM staging for solid tumors- Tumor size Nodes Metastasis; Tumor cell markers not diagnosis but progression/risk
Carcinoma in situ preinvasive growth of epithelial tissue of glandular/ squamous cell origin
Proto-oncogene produce growth factors, proteins that accelerate cell proliferation
Tumor Suppressor Gene mutations (p53, inheritance)- produce tumor suppressor factors, proteins that regulate (slow down) cell proliferation
Oncogenes c-ras, inheritance; abnormal cells, mutated proto-oncogenes
multi- hit principle CA is a dz of aging typically- experience more genetic hits over time & these mutation add up
Lymphatic picked up by lymph channels, #1 route
Hematogenous (shed in vessels, lodge in target organ, enveloped in fibrin/ plt complex & invade parenchyma or organ, lungs/brain- common sites due to increased blood supply
direct/continuous extension tissue spaces/lymph/vessels/cerebrospinal
risk factors for CA genetic, viral, bacterial, immune, environmental
Chemo- tx CA kills cells with high rate of proliferation- bone marrow, hair, skin, GI epithelial cells;
biotherapy- tx CA no damage to healthy tissue, restore/augment host immune response
radiation- tx CA damage cells during different phases of cell division;
Formed Elements- blood comp cellular components; 45-50% of blood; erythrocytes, leukocytes, PLTs
Plasma- blood comp fluid portion of blood; 50-55% of blood; water 90% of plasma; plasma proteins- albumin, globulins, clotting factors
Other materials- blood comp electrolytes, complement, enzymes, nutrients
RBC erythropoiesis(development of RBCs), function, reticulocytes- (immature RBC~1%), MCV (mean corpuscular Volume, avg size of 1RBC, hypochromic(decrease MCHC)/ hyperchromic(increase in MCHC), bilirubin (byproduct of breakdown of RBC), hemoglobin)
WBC Granulocytes- neutrophils/Bands, Eosinophils, Basophils; Agranulocytes- Lymphocytes, Monocytes; leukopoiesis (development of WBCs), colony stimulating factors- drive WBC production- leukocyte specific
Lymphatic System Primary- bone marrow/ thymus Secondary- spleen, Lymph nodes, Tonsils, Peyer’s patch (in GI)
Anemia- causes Insufficient Production- iron deficiency, vit B12 or folate deficiency, alcoholism, marrow dz, renal dz w/ decreased erythopoietin Increased Destruction- immune hemolytic anemia, hereditary spherocytosis, sickle cell dz, thalassemias (dif structure)
Anemia- manifestations mild (nonspecific fatigue, weakness, pallor, mild dyspneas, dx lab; moderate to severe (gradual onsent)- stron pulses, pallor-skin/mucosa, labs/clinical findings; acute- weakness SOBm orthostatic changes, tachy, decreased urinary output, shock/code
Iron-deficiency anemia Labs (MCV, ferritin), appearance of cells- low MCV, low retic, low ferritin (low stores of iron) Causes- result of blood loss or inadequate iron intake High risk populations- infants & pregnant
Chronic Dz/Renal Dz Anemia Labs, appearance of cells- renal- low erythropoietin- low RBC production; chronic dz- low RBC/HCT, microcytic/normocytic, ferritin may be +/- Erythropoietin- long term tx can lead to iron deficiency
Macrocytic Anemias Causes: Alcoholism, B12/folate deficiency, pernicious anemia- MACRO- megaloblastic, alcohol, cirrhosis (liver dz), reticulocyte related, other (thyroid, meds, etc) Labs- high MCV, low serum B12, Schilling test +, low folate level
Pernicious Anemia (Macrocytic) Cause- lack of intrinsic factor needed for B12 uptake Intrinsic Factor role (antibody to this)- destroyed by hypersensitivity autoimmune rxn
Hemolytic Anemias Destruction of RBCs antibodies bind to RBC; idiopathic, secondary- neoplasia, collagen vascular disorders inherited- Hgb electrophoresis Labs- ↓ RBC/HCT, ↑ retic count, peripheral smear w. polychromasia & schistocytes, serum antibody
Sickle Cell Anemia Cell appearance- stiff, angular Risk populations- African Americans – 8% Manifestations- - pain, spleen dysfunction, delayed growth/development, organ dysfunction/failure
Polycythemia myeloprolifertive dx, ↑ RBC, granulocytes, PLTs Sxs- weakness, weight ↓, diaphoresis, fatigue, HA, visual disturbances, claucation, pruitis, abd pain, HTN, blood shot eyes, ↑ viscosity (stroke, MI, organ damage, thrombosis, hemorrhage) ↑ mortality rate
“-philia” attraction or affinity to something
“-cytosis” kind of active transport mechanism for the movement of large amounts of molecules into and out of cells.
“-penia” deficiency
Neutrophlia "Left shift" -high # of neutrophils in peripheral circulation
Neutropenia low # of neutrophils in peripheral circulation Risks- limited immune system
AML proliferation of more immature myeloid cell-line cells, more common in adults
CLL neoplastc proliferation of more mature lymphoid cells (usually B cells)
ALL proliferation of immature lymphoid cell-line cells- most common in children
CML neoplastic proliferation of more mature myeloid cells (granulocytes or monocytes)
Acute anemia, bleeding, fever, infections, skin changes, leukemic infiltrates, weight loss, lymphadenopathy, hepatosplenomegaly; malaise, ongoing/frequent infection, diaphoresis, anorexia, bone pain
Chronic Very high WBC count, splenomegaly; LUQ abd pain, fatigue, fever, night sweats, anorexia, early satiety, blurred vision, DOE; pallor, bruising, Jaundice, lymphadenopathy
Lymphocytic WBC
Myelogenous non-lymphocytic WBCs- granulocytes, monocytes, platelets
Lymphomas proliferation of lymphocytes and precursors in lymphoid tissues; 5th most common cause of CA, 3rd common for children
Hodgkins next lymph node is predictable
non-hodgkins can’t predict next lymph node; jump around body, burkitts- rapid growth in jaw, abdomen, eye orbit
Multiple Myeloma neoplasm of plasma cells, autonomous production of 1 immunoglobulin Manifestations- proteninuria, lytic bone lesions/ hypercalcemia, anemia, sepsis & infections due to suppression of active B cell
PLT activity and clotting factor activity (after injury) PLT change shape (spiny spheres) reveal receptors & degranulate w/ release of histamine & serotonin→ inflammatory process→ forms into fibrin clot
hemostasis arrest of bleeding
The intrinsic pathway activated when Factor XII in the bloodstream encounters negatively charged elements from the damaged subendothelial tissue.
The extrinsic pathway activated when thromboplastin (which is a substance released by damaged endothelial cells) reacts with clotting factors, especially VII.
von Willebrand factor promotes PLT adhesion
pathways Procession to the common pathway and activation of Factor X, leads to clot formation eventually. Fibrolytic pathway initiated concurrently- dissolve clots to remove them
manifestations of bleeding disorders “rashes” (petechiae), bruising, mucosal membrane bleeding, gum bleeding with tooth brushing, epistaxis, hematomas, bleeding into joints, sustained bleeding, menorrhagia, hematuria
Thrombocytopenia Low # of circulating PLT, increased bleeding Idiopathic- follows viral illness PLT dysfunction (PLT disorder suspected but PLT count WNL)
Hemophilia (factor deficiency)- inherited [X linked recessive], factor deficiency) A= factor 8 deficiency; B= factor 9 deficiency
von Willebrand Syndrome decrease/ abnormality in vW factor; decreased adhesion/ aggregation of PLT & shortened half life of factor 8
Liver dysfunction (why is clotting affected?) synthesizes most factors for clotting system, responsible for clearance of activated clotting & fibrinolytic factors
Vit K Deficiency (needed for production of multiple clotting factors)- 2,7, 9, 10, protein C/S
DIC uncontrolled imbalance with increased clotting then increased bleeding)- failure to maintain hemostatic balance- multifactorial process
Created by: sccrgrl159



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