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Pathophys Final pt 1
Pathophys final- cell, acid/base, inflam, immun, infect, hem
| Question | Answer |
|---|---|
| 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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