Pathophys final- cell, acid/base, inflam, immun, infect, hem
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| homeostasis | state of balance, maintained by brain and self regulating mechanisms
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| why study? | understanding diseases
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| Nosocomial | originating in the hospital
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| Sequelae | things caused by disease (scars)
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| Complications | adverse rxn
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| Risk Factors | predisposed to disease/illness
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| Prevalence | # of people that have the disease
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| Incidence | new cases that are diagnosed in amt of time
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| Acute Dz | rapid onset, acute infection, short course
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| Epidemiology | incidence, distribution, possible control of diseases & other health related factors
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| Syndrome | symptoms that occur together; condition w/ associated symptoms
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| Latent Period | period between infection w/ virus and onset of symptoms
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| Exacerbation | made worse
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| Remission | temporary recovery
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| Chronic Dz | long lasting, recurrent
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| Carrier Status | dz is there, but quiet
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| 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
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| Membrane Transport types | active- need energy- low to high gradient;
passive- no energy needed
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| Cell Membrane | Control movement of substances btw of compartments; gatekeeper
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| atrophy vs hypertrophy | Atrophy- cell size decrease,
hypertrophy- cell size increase
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| hyperplasia | # of cells increase
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| metaplasia | mature cells replaced by another cell type
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| autosomal | not sex linked
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| Recessive | has to come from both parents
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| Dominant | dominant trait/gene, can come just from 1 parent
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| X-linked | sex linked
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| DNA | double helix with nucleotide bases
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| strand of DNA in nuclei of cells | chromosome
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| gene | DNA sequence w/ heredity traits
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| Fluid & pH | Normal body fluid composition pH- 7.4, isovolemic, isotonic, more negative inside cell
Fluid movement btw spaces
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| Sodium | Major extracellular ion- Na+
Magnet with water
Effects of changes (hyponatremia mainly) Hyponatremia- coma, confusion, lethargy
Hypernatremia- agitation, restless, LOC, convulsions, DEATH
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| 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+
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| Diffusion | Hydrostatic and osmotic pressure/gradients- movement of ions across space
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| acids/bases | acid- lower pH
base- higher pH
Metabolic acids= byproducts of cellular metabolism
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| Carbonic acid-bicarbonate buffer | kidneys- regulate HCO3
lungs- regulate CO2
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| Acidosis | Metabolic, Respiratory; Control mechanisms- kidneys excrete excess H+ ions in urine, raise bicarb
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| Alkalosis | Metabolic, Respiratory; Control Mechanisms- kidneys excrete more bicarb in urine, lungs decrease RR- retain CO2
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| innate resistance | natural barriers, skin membrane
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| 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
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| inflammatory response | protective host response, dilute toxins, remove bacteria, initiate healing/repair, block infection- cant spread
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| inflammation | Purpose- bodily protection for injury and infection
Causes- “All of the above”
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| 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
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| Histamine | increase blood flow, endothelial cell contrax, increased leukocyte adherence to endothelium, hyperemia, edema
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| Chemotaxis | causes directional movement of cells toward inflammation
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| 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
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| cellular response | mast cells- rapid; slower/secondary cell response- eosinophils, basophils, monocytes/macrophages, lymphocytes, fibroblasts, polymorphonuclear neutrophil
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| Neutrophils | (granular, first major phagocyte)- bacterial response, WBC granulocytic; 6-12 hrs after injury- short lived
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| Opsonization | coat bacteria w/ antibody/complement, susceptible to PMN; facilitates phagocytosis; easier for body cells to recognize & engulf enemy materials
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| Phagocytosis | primary function of PMN; extend pseudopods toward bacteria/ debris, engulf, release hydrolytic enzymes & O2 radicals to digest
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| Eosinophils | anaphylaxis and allergy
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| Monocytes/Macrophages | largest normal blood cell; WBC; appear 24 hrs after injury- replace neutrophils; prolong cell response; process antigen; secrete monokines; promote wound healing
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| Basophils | release histamine, leukotrienes, prostaglandins
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| inflammation manifestations | local- heat, redness, edema;
systemic effects- fever, leukocytosis, plasma protein synthesis
BIG 3: erythema, calor, swelling)
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| stem cell | “totipotential”
Myeloid >>> erythrocytes, monocytes, PLTs, granulocytes
Lymphoid >>> lymphocytes, NK cell
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| Monocyte/Macrophage | antigen ingestion/processing/presentation; APC when presenting antigen circulating in blood/lymph; made more available to lymphocytes; Antigen Presenting Cell
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| T cell- Lymphocyte | immunity;
CD3- antigen- specific receptor on surface
CD4 >>> T-helper cell, IL2= CD4 receptor w/ CD3
CD8- T cytotoxic w/ CD3
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| B cell- Lymphocyte | humoral (antibody)- produce/ release antibodies that enter blood and react w/ specific antigen; released from bone marrow as mature
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| 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
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| 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
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| 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
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| Antigen/Antibody complex | CD4/ APC
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| Plasma cells | mature B cell; can produce all other types of antibody proteins specific to that antigen (IgG, IgE, IgA, IgD)
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| Natural active | encountered vaccine, produced immunoglobins to fight it off again
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| Natural passive | body already has them- usually from mom
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| Artificial passive | you’re given antibodies (IVIG)
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| Artificial active | immunization
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| Secondary immune response | natural or artificial (vaccines); prepared to respond/attack
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| Immunogens | antigens that will induce an immune response resulting in the production of antibodies or functional T cells.
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| Antigen | becomes immunogen if- Foreignness to the host; Adequate size; Adequate chemical complexity; Present in sufficient quantity (not too much OR too little)
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| 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
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| Endogenous | antigen fragmented and presented on surface of damaged cell; combined w/ Class 1 MHC; recognizable to T cytotoxic (CD8) lymphocytes
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| Antigen specificity | host cells can recognize an antigen
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| anaphylaxis vs cytotoxic | Anaphalaxis- immediate rxn, can cause death
Cytotoxic- usually cause by adverse drug rxn
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| 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
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| Tolerance vs autoimmunity | Tolerance- most individuals accept own antigens- otherwise body would attack antigen
Autoimmunity- immune system reacts to self- usually attacks
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| ABO blood type antibodies | A- anti-B
B- anti-A
AB- universal recipient- no antibodies
O- universal donor- anti-A, anti-B
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| Apoptosis | programmed cell death (suicide); removed neg selected autoimmune lymphocytes, clear activated lymphocytes after antigen clearance, remove damaged lymphocytes
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| Immunodeficiency | failure of immune system to protect the body adequately from infection due to absence or insufficiency of some component process or substance
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| Bacteria | prokaryotes; aerobic/anaerobic; cocci/bacilli; gram pos/neg/acid fast; virulence factors- capsules, fimbriae-pilli, enzymes, exotoxins, endotoxins
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| Parasites | different from fungi, bacteria, and viruses; big problem worldwide
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| fungi | mold/yeast
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| Viruses | Replication depends on host cell, DNA or RNA
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| 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)
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| Gram staining, culturing | potentially infected specimens; Sensitivity testing to various antimicrobial agents determines which are most effective in inhibiting growth of that particular pathogen
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| CA, Benign | uncontrolled invasive cell growth
grow slowly, capsule, non-invasive, differentiated, low mitotic index, doesn’t metastasize
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| malignant tumors | grow rapidly, no capsule, invasive, poorly differentiated, high mitotic index, can metastasize
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| Dysplasia | “pre-cancer” abnormal change in size, shape, organization of mature cells
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| TNM | staging for solid tumors- Tumor size Nodes Metastasis;
Tumor cell markers not diagnosis but progression/risk
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| Carcinoma in situ | preinvasive growth of epithelial tissue of glandular/ squamous cell origin
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| Proto-oncogene | produce growth factors, proteins that accelerate cell proliferation
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| Tumor Suppressor Gene | mutations (p53, inheritance)- produce tumor suppressor factors, proteins that regulate (slow down) cell proliferation
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| Oncogenes | c-ras, inheritance; abnormal cells, mutated proto-oncogenes
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| multi- hit principle | CA is a dz of aging typically- experience more genetic hits over time & these mutation add up
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| Lymphatic | picked up by lymph channels, #1 route
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| 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
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| direct/continuous extension | tissue spaces/lymph/vessels/cerebrospinal
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| risk factors for CA | genetic, viral, bacterial, immune, environmental
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| Chemo- tx CA | kills cells with high rate of proliferation- bone marrow, hair, skin, GI epithelial cells;
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| biotherapy- tx CA | no damage to healthy tissue, restore/augment host immune response
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| radiation- tx CA | damage cells during different phases of cell division;
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| Formed Elements- blood comp | cellular components; 45-50% of blood; erythrocytes, leukocytes, PLTs
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| Plasma- blood comp | fluid portion of blood; 50-55% of blood; water 90% of plasma; plasma proteins- albumin, globulins, clotting factors
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| Other materials- blood comp | electrolytes, complement, enzymes, nutrients
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| 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)
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| WBC | Granulocytes- neutrophils/Bands, Eosinophils, Basophils; Agranulocytes- Lymphocytes, Monocytes; leukopoiesis (development of WBCs), colony stimulating factors- drive WBC production- leukocyte specific
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| Lymphatic System | Primary- bone marrow/ thymus
Secondary- spleen, Lymph nodes, Tonsils, Peyer’s patch (in GI)
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| 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)
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| 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
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| 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
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| 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
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| 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
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| Pernicious Anemia (Macrocytic) | Cause- lack of intrinsic factor needed for B12 uptake
Intrinsic Factor role (antibody to this)- destroyed by hypersensitivity autoimmune rxn
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| 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
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| Sickle Cell Anemia | Cell appearance- stiff, angular
Risk populations- African Americans – 8%
Manifestations- - pain, spleen dysfunction, delayed growth/development, organ dysfunction/failure
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| 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
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| “-philia” | attraction or affinity to something
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| “-cytosis” | kind of active transport mechanism for the movement of large amounts of molecules into and out of cells.
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| “-penia” | deficiency
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| Neutrophlia | "Left shift" -high # of neutrophils in peripheral circulation
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| Neutropenia | low # of neutrophils in peripheral circulation
Risks- limited immune system
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| AML | proliferation of more immature myeloid cell-line cells, more common in adults
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| CLL | neoplastc proliferation of more mature lymphoid cells (usually B cells)
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| ALL | proliferation of immature lymphoid cell-line cells- most common in children
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| CML | neoplastic proliferation of more mature myeloid cells (granulocytes or monocytes)
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| Acute | anemia, bleeding, fever, infections, skin changes, leukemic infiltrates, weight loss, lymphadenopathy, hepatosplenomegaly; malaise, ongoing/frequent infection, diaphoresis, anorexia, bone pain
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| Chronic | Very high WBC count, splenomegaly; LUQ abd pain, fatigue, fever, night sweats, anorexia, early satiety, blurred vision, DOE; pallor, bruising, Jaundice, lymphadenopathy
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| Lymphocytic | WBC
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| Myelogenous | non-lymphocytic WBCs- granulocytes, monocytes, platelets
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| Lymphomas | proliferation of lymphocytes and precursors in lymphoid tissues; 5th most common cause of CA, 3rd common for children
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| Hodgkins | next lymph node is predictable
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| non-hodgkins | can’t predict next lymph node; jump around body, burkitts- rapid growth in jaw, abdomen, eye orbit
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| 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
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| 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
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| hemostasis | arrest of bleeding
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| The intrinsic pathway | activated when Factor XII in the bloodstream encounters negatively charged elements from the damaged subendothelial tissue.
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| The extrinsic pathway | activated when thromboplastin (which is a substance released by damaged endothelial cells) reacts with clotting factors, especially VII.
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| von Willebrand factor | promotes PLT adhesion
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| 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
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| manifestations of bleeding disorders | “rashes” (petechiae), bruising, mucosal membrane bleeding, gum bleeding with tooth brushing, epistaxis, hematomas, bleeding into joints, sustained bleeding, menorrhagia, hematuria
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| Thrombocytopenia | Low # of circulating PLT, increased bleeding
Idiopathic- follows viral illness
PLT dysfunction (PLT disorder suspected but PLT count WNL)
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| Hemophilia | (factor deficiency)- inherited [X linked recessive], factor deficiency) A= factor 8 deficiency; B= factor 9 deficiency
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| von Willebrand Syndrome | decrease/ abnormality in vW factor; decreased adhesion/ aggregation of PLT & shortened half life of factor 8
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| Liver dysfunction (why is clotting affected?) | synthesizes most factors for clotting system, responsible for clearance of activated clotting & fibrinolytic factors
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| Vit K Deficiency | (needed for production of multiple clotting factors)- 2,7, 9, 10, protein C/S
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| DIC | uncontrolled imbalance with increased clotting then increased bleeding)- failure to maintain hemostatic balance- multifactorial process
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