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Patho 2
| Question | Answer |
|---|---|
| Stem cells | Pluripotent cells in bone marrow that differentiate into B and T-cells |
| Hematopoiesis | production of blood cells and platelets in bone marrow |
| Endothelial cells | line blood vessels and release inflammatory mediators that regulate migration of WBCs (from circulation to injured tissue) |
| Mast cells | in tissues, release histamine by degranulating when activated |
| Monocytes | leave circulation and migrate to tissue |
| Macrophages | used to be monocytes, ingest bacteria/viruses and undergo apoptosis |
| Esinophils | involved in allergic reactions and inflammation; acts like neutrophils against parasites |
| Basophils | act like mast cells (release histamine into blood) |
| afebrile | no fever |
| febrile | fever (core temperature above normal range) |
| Defervescence | breaking/absence of fever |
| immunogenicity | ability for immunogen to generate specific immune response |
| self-tolerance | ability for immune system not to react to self antigens |
| immunogen | substance that can cause immune response (AKA antigen) |
| Immunoglobulin | class of proteins in serum and cells that are antibodies |
| gluconeogenesis | body using other sources (amino acids and fats) to create glucose |
| glucagon | raises glucose in the bloodstream by stimulating breakdown of glycogen in liver (glycogenolysis) and activates lipase to breakdown fat |
| glycogen | stored glucose |
| glycogenesis: | making glycogen |
| glycogenolysis | breaking of stored glycogen to make glucose |
| lipolysis | breakdown of fat |
| insulin | transports glucose into cells, inhibits lipolysis, stimulate glycogenesisoverall lowers blood sugar |
| alpha cells | secretes glucagon, increases BS |
| beta cells | secrete insulin, lowering BS |
| petechiae | pinpoint, round spots due to bleeding |
| hemoptysis | coughing up blood |
| epistaxis | nosebleed |
| occult blood | blood in stool |
| ecchymosis | hematoma |
| pancytopenia | deficiency of WBCs, RBCs, and platelets |
| Non-specific Defenses | Includes first and second lines of defensesFirst: physical, chemical, and flora barriersSecond: phagocytes, inflammation, fever, plasma protein systems (complement, kinin, clotting) |
| specific (immune) system | third line of defense: antibody and cell-mediated response |
| Third line of defense | lymphocytes interact with antigen, specific activation and effectiveness |
| Leukocyte production is from… | colony stimulating factors |
| Megakaryocyte production is from… | thrombopoietin (from liver) |
| erythrocyte production is made from… | erythropoietin (from kidneys) |
| WBC Differential | Never Let a Man Enter the Back |
| Diseases that have too many WBCs (6) | leukocytosis, neutrophilia, eosinophilia, lymphocytosis, leucocythemia, leukemia |
| leukocytosis | overall high WBC count (>11,000/mcL) |
| Neutrophilia | increase in neutrophils; commonly points to infection |
| Eosinophilia | increase in eosinophils, commonly points to parasitic worm or allergies |
| lymphocytosis | increased number of lymphocytes |
| leucocythemia | extremely high WBC count, commonly points to malignancy like leukemia or lymphoma |
| leukemia | low count of circulating blood cells because ONE type is overpopulated; causes proliferation of WBCs |
| Diseases of not enough WBCs (2) | leukopenia and neutropenia |
| leukopenia | overall decrease of all WBCs (<4,000 mcL) |
| Neutropenia | decrease of neutrophils (<1500 mcL) |
| Precautions to neutropenia | handwashing, infection risk, monitor CBC, temp Q4 >100.5 |
| histamine | inflammatory mediator, releases mast cells and basophils quicklycauses vasodilation and increased capillary permeability at injury site |
| cytokines | inflammatory mediators, released by WBCs that regulate inflammatory reaction and can cause local or systemic effects |
| interleukins (IL) | attracts WBCs to area and enhance inflammatory response |
| tumor necrosis factor (TNF) | cytokines release inflammatory cells to enhance inflammation and initiate fever |
| interferons (IFN) | interfere with a virus using a cell, stimulate fever |
| prostaglandins | released from WBCs and other cell membranes |
| leukotrienes | made by leukocytes and cause vasodilation and stimulate nerves endings to cause pain |
| Enzyme pathway COX 1 | produces prostaglandins that protect GI and enhance kidney perfusionstimulate platelet aggregation and vasodilation during inflammation |
| Enzyme pathway COX 2 | produces prostaglandins that promote inflammation and sensitize pain receptors so pain is felt |
| lipoxygenase | used during enzyme pathways to produce leukotrienes to cause bronchospasms in bronchial edema |
| complement system: opsonization | codes invaders (pathogens) and targets them for elimination through phagocytes |
| complement system: anaphylatoxin | complement peptides that induces degranulation of mast cells |
| complement system: chemotaxis | chemical signal that calls for more neutrophils to come to site |
| kinin system | forms bradykinin (stimulates nerves to cause pain) |
| clotting system | series of reactions to stop blood loss |
| pyrogens | specialized cytokines that travel through blood to hypothalamus to cause fever |
| mast cells | releases histamine via degranulation |
| two types of mast cell receptors: | H1 and H2 |
| H1 histamine receptors | on mast cells and produce acute inflammation and hypersensitivity reactions, dilates blood vessels, increase permeability, redness, edema, and hives |
| H2 histamine receptors | on mast cells and secretes hydrochloric acid |
| acute inflammation signs | erythema, warmth, edema, pain |
| acute inflammation signs that affect vascular permeability | erythema, warmth, edema |
| acute inflammation signs that affect chemotaxis | margination and clotting |
| pain in acute inflammation | edema causes pressure to stimulate nerve endings to stimulate pain along with bradykinin and prostaglandins guards injury site and healing can begin |
| serous/transudate exudates | watery, plasma seeping out of vessels due to increased capillary permeability |
| hemorrhagic exudate | blood cells are injured and RBCs seep into tissue |
| purulent/pus exudate | contains degraded phagocytes, proteins, and debris |
| systemic indicators of inflammation | leukocytosis, C-reactive protein (CRP), erythrocyte sedimentation rate, and fever |
| C-reactive protein | used in systemic inflammation; made in liver in response to cytokines (released by macrophages) and opsonizes/activates other complement proteins |
| erythrocyte sedimentation rate | measures how quickly RBCs settle at the bottom of a sample tubefaster than normal = inflammationused to determine illness that causes inflammation |
| AV shunts affect on thermoregulation | open shunts = heat dissipates into environmentclose shunts = heat is retained also causes vasodilation (dissipates)/constriction (conserves) |
| AV shunts | passage of blood from arteries to veins without going through capillaries |
| sweat glands affect on thermoregulation | regulates heat loss via evaporation |
| pilimotor reflex affect on thermoregulation | contracts hair muscles to conserve heat |
| hypothalamus affect on thermoregulation | releases pyrogens (stimulate fever) |
| benefits of fever | stimulates body’s defenses and may inactivate certain bacteria |
| stages of fever | prodromal → chill → flush/defervescence |
| prodromal | vague symptoms most contagious |
| chill | feeling cold, heat conservation initiated/vasoconstriction, till shivering generates heat/fever |
| flush/defervescence | skin is warm and red to dissipate heat |
| populations vulnerable to fever | infants/children (infants can't shiver); elderly (poor circulation, may not have febrile response); immunocompromised (no normal reaction to pathogens) neurogenic (hypothalamus is affected in traumatic brain injury and baseline can be affected) |
| labile cells in tissue repair | skin, GI, bone marrowcontinually going through cell cycle and reproducing, healing has predictable phases |
| stable cells in tissue repair | bone cellsusually in resting state, but can divide when stimulated |
| permanent cells in tissue repair | cardiac and neuronswhen they die, they are lost forever |
| phases of tissue repair | inflammatory → proliferative → remodeling |
| inflammatory phase of tissue repair | first few days after injuryhemostasis stops bleeding and inflammatory cells migrate to site to contain injury/being healing |
| proliferative phase of tissue repair | can last several weeksfibroblasts migrate and deposit extracellular matrixangiogenesis is stimulated to create new blood vessels (via new growth factors) granulation tissue appears |
| remodeling of tissue repair | 3+ weeks to monthscollagen synthesis and lysis helps prevent re-injury |
| primary intention cutaneous wound healing | wounds closed surgically or with staples |
| secondary intention cutaneous wound healing | remains open and heals with epithelization of marginscommon for pressure injuries |
| tertiary intention cutaneous wound healing | combination of primary and secondaryuse skin grafts to close bed once cleaned |
| cellulitis | DIAGNOSTIC TOOLcaused by bacteria, bites, surgical woundssymptoms include inflammationsystemic: increase in WBC, fever, C-reactive protein, ESR |
| dehiscence | edges of primary intention spread apart |
| evisceration | organs pop out from dehiscenceput sterile saline on organsavoided by splinting (pillow over abdomen when coughing) |
| keloids | abnormal scar tissue (from genetics) |
| contractures | scar tissue shrinks and is inflexibleseen in burn pts |
| strictures | same as contractures, except on interior opening/tube of body |
| adhesions | internal scarring post-op |
| factors that impair healing | blood flow (hypoxic injury = less blood flow), ischemia (less likely to heal), and nutritional status (need proteins, vitamins, etc) |
| chronic inflammation | long term effects: cardiovascular disease, neurological disease, cancer, lupus, etc-can also lead to DNA damage → neoplasia and dysplasia -caused by cancerous processes |
| Adaptive Humoral Immunity | B-lymphocytes which produce antibodies or immunoglobulins |
| Adaptive Cell-mediated immunity | t-lymphocytes which use subsets of t-cells |
| central lymphoid organs | bone marrow (b-cells or lymphocytes production) or thymus (t-cells become immunocompetent) |
| peripheral lymphoid organs | lymph nodes (remove foreign material before bloodstream/space to stimulate immune cell proliferation), spleen (filters antigens from blood), etc (contains b/t-cells, macrophages, and dendritic cells) |
| What cells help initiate immune response or recognize foreign matter? | Antigen-presenting cells (APCs) or self-tolerance |
| Antigen-presenting cells: epitope | phagocytes present the epitope on its cell surface |
| antigen-presenting cells: macrophage and dendritic cells | Main APCs in humans; alert adaptive immune cells when foreigners are present |
| self tolerance: MHC | major histocompatibility compleximmune cells that distinguish self from nonself |
| self tolerance: HLA | human leukocyte antigenHLA tissue typing required for successful body tissue transplants |
| Universal donor | type O (has both antibodies) |
| universal recipient | AB (no antibodies) |
| IgM | “me first”1st immunoglobulin to appear as response to immunogen1st produced by newborns (distinguished maternal infections from newborn infections) |
| IgA | “any orifice”secretory immunoglobulin found in saliva, tears, and colostrumFound in GI/pulmonary tractprimary protective shield in mucus tissue |
| IgD | Primarily in cell membranes of B-lymphocytes serves as antigen receptor for initiating differentiation of B cells |
| IgG | “greatest amount”most abundant immunoglobulin in circulationpresent in most body fluidsactivates complement system to heighten inflammatory reactionONLY one to CROSS placenta |
| IgG vs IgM in antibody mediated timeline | 1st exposure: IgM is higher than IgG2nd exposure” IgG is higher and antibody concentration is longer while IgM is lower |
| passive immunity | transferred from one to anotherNatural: placenta/breastmilk from mom to babyArtificial: monoclonal antibodies (short-term protection to specific exposure but NO MEMORY) |
| active immunity | stimulated to produce antibodiesnatural: infectionartificial: vaccine |
| T-helper cells (CD4) | “cops patrolling”calls in reinforcement when neededuses cytokine to call B-cells/more T-helper cellssignify macrophages |
| T-cytotoxic cells (CD8) | “killers”release perforinssees infected cells antibodies cannot detect |
| T-memory cells | mediate a faster/more potent response from repeat encounter with an antigen |
| T-suppressor cells | blocks action of other lymphocytes to keep immune system from becoming overactive |
| Type 1 hypersensitivity reactions | immediate, classic allergic reactionIgE and histamine released s/sx: urticaria (itchy rash), bronchoconstriction (serious), anaphylaxis (potentialy fetal - can be delayed up to 12 hrs), anaphylactic shock |
| anaphylactic shock | worse case scenario of type 1 reactionssudden spread of histamine causes widespread vasodilation that leads to sudden drop of BP and then vasoconstriction |
| Type 2 hypersensitivity reactions | Cytotoxic Ag-IG reactions (blood transfusions) IgG or IgM attack target cells and inflict damageexamples: hemolytic transfusion reactions, type 1 diabetes, Rh hemolytic disease in newborns |
| type 3 hypersensitivity reactions | plasma immune complexes deposit everywhere (antigen-antibody complexes/incited inflammation)IgG or IgM examples: lupus, rheumatoid arthritis, glomerulonephritis |
| Type 4 hypersensitivity reactions | Cytotoxic T-cellsexamples: contact dermatitis (PPD, poison ivy), host vs. graft, graft vs host |
| host v. graft | type 4 reaction where hosts immune defends against graft because transplant’s foreign MHCs |
| graft v. host | immunocompetent t-cells attack receipt body cells as foreign and attackcan be prevented with immunosuppressant drugs |
| autoimmune disorders | breakdown of immune cell tolerance or hypersensitivity → systemic/local injury OR molecular mimicry (microbe has similar genetic sequence as self cells) |
| molecular mimicry | microbe has similar genetic sequence as self cells |
| autoimmune factors and examples | geneticMG, ITP, DM, RA, SLE, sarcoidosis, scleroderma |
| Type 1 DM etiology | autoimmune destruction of beta cells (cannot produce insulin) or benign viral infections idiopathic in asian/african americans |
| Type 1 DM risk factors | White > non-white |
| Type 1 DM manifestations | hyperglycemia, glycosuria (glucose in urine), polyuria (inc. urine output), polydipsia (inc. thirst), polyphagia with weight loss (inc hunger), fatigue, recurrent infections, poor wound healing |
| What are the 3 “polys” | polyuria (inc urine), polydipsia (inc. thirst), polyphagia (inc. hunger but losing weight due to cells starving) |
| Type 1 DM treatment | diet (counting carbs)activity (balancing with insulin and food intake)insulin replacement |
| Type 2 DM etiology | insulin resistance (glucose cannot get into cells)liver glucose production (makes glucose from stored glycogen) |
| Type 2 DM risk factors | genetics and age (45+)obesitylifestyle |
| Type 2 manifestations | hyperglycemia, polyuria, polydipsia, polyphagia, fatigue, recurrent infections, neuropathy |
| Similar manifestations of type 1 and 2 DM | hyperglycemia, polyuria, polydipsia, polyphagia, fatigue, recurrent infections |
| Type 2 DM treatment: | lifestyle changes (diet and exercise)OHAs (oral hypoglycemic agents)insulin |
| gestational DM | diabetes in the second or third trimester of pregnancy |
| Labs that Diagnose DM | FBG > 126AgbA1C >/= 6.6%urinalysis (showing glucose and ketones in urine)2 hr Postprandial (Oral glucose tolerance test) BS >/= 200 blood sugar with eating |
| Amylin | Associated with DM; secreted by beta cells and turns off alpha cells to decrease glucagonsuppresses action of glucagon and promotes satiety |
| IgE | “allergieeeeeees”inflammation and allergic reactionsbinds to mast cells/basophils to trigger release of histamine |
| Incretins | involved with DM; secreted by GI cells after we eatsignals pancreas that we ate, so pancreas can release insulin |
| epinephrine and GH (somatotropin) | involved with DMgrowth hormone; stimulates glycogenolysis and lipolysissomatostatin inhibitor |
| somatostatin | involved with DMGH inhibitor; secretes delta cells of pancreasslows GI transit time and is naturally higher in children (why DM is harder to manage in kids) |
| glucocorticoid hormones | released by adrenal cortex in stressful situationscortisol goes to all available resourcesinduce hyperglycemia |
| Metabolic syndrome s/sx | HTN, dyslipidemia, hyperinsulinism, centralized “apple shaped” obesity, glucose intolerance, predisposition to T2DM, FBS >126 |
| Metabolic syndrome increases risk of… | CAD (coronary artery disease), heart attack, stroke, and peripheral vascular disease |
| Hypoglycemia | BS <70 |
| Hypoglycemia etiology | medications, skipping meals, exercise |
| Hypoglycemia manifestations | Neurological: confusion and lethargy → seizures, coma, and deathANS: liver release of glucose and symptoms of anxiety, tachycardia, diaphoresis and vasodilation and pale skin |
| Hypoglycemia treatment | if alert and can swallow: fast acting carbs + protein to stabilize BS unresponsive: hypoglycemia protocol, administer D50 or glucagon |
| hypoglycemia vs alcohol | alc. blocks gluconeogenesis = dangerous for diabetics |
| DKA etiology: | insulin deficiency, hyperglycemia, lipolysis (ketone buildup in blood = lower pH → metabolic acidosis) |
| DKA s/sx | polyuria, polydipsia, polyphagialower pH, fruity breath, potassium shift (excess ketones)Kussmaul’s respirations |
| DKA treatment | IV fluids/IV insulin drip |
| Hyperosmolar Hyperglycemic State etiology | severe hyperglycemia without ketones |
| Hyperosmolar Hyperglycemic State manifestations | severe hyperglycemia (>600) with polyuria and polydipsiasevere dehydration, altered LOC |
| Retinopathy | Microvascular complication causing scarring and blindness; important to have routine eye exams |
| Retinopathy risk factors | poor glycemic control |
| nephropathy | microvascular complication; worsened by hypertension, microalbuminuria, elevated levels of BUN and creatinine (poor kidney function) |
| microalbuminuria | small amounts of albumin that escape in the urine due to changes in glomerulus |
| neuropathy | microvascular complication; peripheral, thick blood = hard to reach limbs, hands, and feet and increased risk of falls |
| neuropathy causes | numbness, tingling, burning, loss of balance, sensation |
| autonomic neuropathy | microvascular complication; damage to nerves that control autonomic function and causes bladder control issues, infection, and sexual dysfunction affects heart, bladder, stomach, and other organs |
| microvascular complications | CAD/MI (myocardial infarct), CVA, peripheral vascular disease (with increased risk of gas gangrene) |
| somogyi effect | nocturnal hypoglycemia (from excessive insulin dosage/peak of action during sleep) causing glycogenolysis → BS inc → hyperglycemia in the morning |
| dawn phenomenon | growth hormone peak at night → slow cellular use of glucose → BS inc → hyperglycemia in the morning |
| Hemostasis | Physiological process of stopping bleeding at injury site |
| Primary hemostasis | platelets aggregate to form a platelet plug and adhere to site of injury |
| Secondary hemostasis | Fibrin deposit and coagulation cascade → fibrin forms a mesh that is incorporated into platelet plug and stabilizes clot |
| The combination of primary and secondary hemostasis leads to… | thrombus (durable blood clot) which takes average of 6 min |
| components of hemostasis | Von Williebrand factor, tissue factor, platelets, clotting factors (prothrombin) |
| Von Williebrand factor | Synthesized from endothelial cells and megakaryocytes; binds platelet receptors so they can adhere and aggregate to activated site |
| What are the 3 clotting cascades? | Extrinsic, intrinsic, and common pathway |
| Extrinsic clotting cascade pathway | activated with external and vessel wall injury (vert fast to minimize blood loss) → releases ADP which attracts/activates more plateletsClotting time is measured by PT or INR |
| Intrinsic clotting pathway | stimulated by tissue damage to endothelial lining, like inflammation or asteriosclerosisClotting time is measured by PTT |
| common clotting pathway | factor 10 is activated → prothrombin → thrombin/ fibrinogen → fibrinRequires bone marrow to produce platelets and liver to produce prothrombin, fibrinogen, and etc |
| Clotting disorders | inc number or activity of platelets and inc coagulation activity |
| bleeding disorders | dec. number/activity/quality of platelets and defective coagulation activity |
| Types of lab tests for platelet counts | thrombocytosis and thrombocytopenia |
| thrombocytosis | too many platelets → risk of stroke and MI |
| thrombocytopenia | too little platelets → risk of hemorrhage |
| types of lab tests on coagulation tests | prothrombin time, international normalizes ration, activated partial thromboplastin time, D-dimer |
| Prothrombin time (PT) | measures extrinsic pathway |
| International normalized ration | PT of pt/ PT control used to normalize pt results (1-1.4) |
| activated partial prothrombin time (PTT) | measures intrinsic pathway (about 30 sec) |
| D-dimer | measures how much fibrolysis is occurring |
| Types of thrombocytopenia disorders | immune thrombocytopenia purpura (ITP), thrombotic thrombocytopenia purpura (TTP), and drug induce thrombocytopenia |
| Immune Thrombocytopenia | common autoimmune disorder; IgG antibodies develop against platelets → dec platelet count risk for hemorrhage |
| s/sx of Immune thrombytopenia purpura | bleeding (petechiae, purpura, bleeding from gums, epistaxis)spleen enlargement |
| immune thrombocytopenia purpura treatment | platelet transfusion, asteroids, infusion of IVIg |
| thrombotic thrombocytopenia purpura | faulty enzyme that’s inherited/autoimmune related and needed to break vWF or vWF accumulates and platelet aggregate in endothelium → clumping = overall decline of platelet number |
| thrombotic thrombocytopenia purpura treatment | platelet apheresis (remove faulty plasma and replace with FFP) and steroid therapy |
| drug induced thrombocytopenia | Usually caused by Heparin, antimalarial drugs, and sulfonamides; IgG antibodies coat heparin complexes → clumping/thrombus = dec platelet count |
| drug induced thrombocytopenia treatment | stop medication and use low molecular weight heparin |
| Inherited coagulation disorders | hemophilia (A and B), vWF disease, and factor V Leiden Mutation |
| Hemophilia A (classic) | missing factor VIII; X linked recessive disorder carried by females and passed to males |
| Hemophilia B (Christmas Disease) | missing factor IXX linked recessive disorder carried by females and passed to malesbleeding in soft tissue and treatment is to replace missing factor |
| Von Williebrand Disease | missing/defective vWF → inc bleeding riskmilder than classic hemophilia and treatment is synthetic antidiuretic hormone (enhances clotting factors) |
| Factor V Leiden Mutation | causes unwanted thrombus formation/hypercoagulation |
| Acquired Coagulation Disorders | Vit K def, liver disease/failure, and disseminated intravascular coagulation |
| vit K deficiency | fat soluble vitamin needed to synthesize prothrombin and other clotting factors continually synthesized by intestinal bacteria |
| liver disease/failure for acquired coagulation | leads to coagulation problems = inc risk of uncontrolled bleeding |
| disseminated intravascular coagulation | rare condition; causes abnormal clotting throughout body which use up clotting factors → massive bleeding, intravascular clots, and ischemia; pathologic consumption of platelet/clotting factors; massive trauma; replace clotting factors and platelets |
| Thromboembolic disorders | Deep vein thrombosis, virchow’s triad, venous stasis |
| Deep vein thrombosis | term for DVT and pulmonary embolism (PE)thrombus develops in deep leg vein with inflammation → thrombus travels to lung to become PE symptom of PE: extremely out of breath |
| Virchow’s traid | trio of risk factors for DVTendothelial injury, venous stasis, hypercoagulability |
| venous stasis | occurs because of poor venous return (ass. with sedentary behavior, immobility, and valve dysfunction in legs)venous blood pools in lower extremities and stagnant blood form clots |
| Hemoglobin and iron recycling (RBC destruction) | GLOBIN → degraded into amino acids → turned into new proteinsHEME → porphyrin + FePorphyrin → Biliverdin → bilirubinCan be unconjugated/indirect (too many RBCs are destroyed) or conjugated/direct (bile duct is blocked) |
| Iron in RBC destruction | transferrin → carry iron in circulationferritin → stores iron |
| CBC | plasma (1/2 of CBC sample, platelets, WBC, RBCs |
| what does inc hematocrit in CBC mean? | pt is dehydrated (less plasma) |
| what does dec. hematocrit in CBC mean? | pt has fluid overload (more plasma = more hematocrit) |
| Mean Corpuscular Volume | measures average size of erythrocytes |
| macrocytic | large RBC (take up more room = higher hematocrit) |
| microcytic | small cells (take up less room = lower hematocrit) |
| Mean corpuscular hemoglobin concentration (MCHC) | average amount of hemoglobin in CBC mean cells hemoglobin is more accurate (correlates hemoglobin content to size of RBC) |
| hemoglobin content via MCHC | hypochromic: low Hgbnormochromic: normal Hgb |
| reticulocyte count | indicates how well bone marrow is responding to low H/H |
| Primary Polycythemia (polycythemia vera) | excess of ALL blood cellsmore common in men; causes non-cancerous proliferation of stem cellincreases blood viscosity = inc risk for thromboembolism |
| primary polycythemia treatment | phlebotomy (removes 300-500 mL of blood to maintain hematocrit to under 45%) |
| secondary polycythemia | overproduction of RBCssomething is causing this, usually hypoxia common in COPD, high altitudes, severe heart or lung diseases |
| secondary polycythemia treatment | focuses on treating hypoxia |
| anemia | s/sx: fatigue, vertigo, dizziness, pale skin and mucous membranescompensation: tachycardia and tachypnea |
| hemochromatosis | genetic disorders that causes free excess iron to become toxics/sx: fatigue and darkening of skin treatment: phlebotomy |
| iron deficiency | from chronic slow blood loss and vegetarians s/sx: microcytic/hypochromic, low H/H, low ferritin, low MHC, red sore tongue, spoon shaped nails, petechiae, and brittle hairtreatment: iron replacement |
| vit B-12 def | from autoimmune destruction of parietal cells s/sx: megaloblastic anemia (macro/normochromic), low H/H, inc MCV, low B-12treatment: B-12 replacement |
| Folic acid def | malabsorption disorder in GI, alcoholism, extreme dieters, elderlys/sx: megablastic anemia (macro/normochromic), tongue being sore, asymptomatictreatment: folate replacement |
| aplastic anemia | exposure to radiation/toxins, viral infection, or chemotherapys/sx: pancytopenia → fatigue, pallor, shortness of breath, petechiae, ecchymosis, bleeding, infection and compromised immunitytreatment: transfusion of RBCs and ATG (anti t-cell globins) |
| hemorrhage/hemolytic anemia | chronic is usually GI related s/sx: low H/H and increased reticulocyte counttreatment: blood transfusion and find source of chronic loss |
| sickle cell trait | recessive genes from one parentmilder symptoms because of less hemoglobin S affect RBCs |
| sickle cell disease | from both parents and 80% of RBCs are prone to sickling |
| thalassemia | genetic disorders caused by mutations of hemoglobin alpha/beta globin chains = less hemoglobin than normalseverity depends on type and amount of hemoglobin affectedleads to deformities and weakening of bones; common in mediterranean, asian, and AA |
| hemolytic transfusion reactions | wrong blood type antigen-antibody mismatch leads to lysis of RBC (newborn could be RH incompatibility) |
| Sickle cell crisis | RBCs sickle and cause log jam that clunks cells together = impeded blood flow; s/sx: pain on other side of log jam; tx: hydration with IV fluid, oxygen, and pain management; pt education: prevention cold, physical exertion, infection, illness, hypoxia |
| phrenic nerve | innervates automatic respirations, deep breaths, and holding one’s breath |
| intercostal muscles | rib cage |
| accessory muscles | located in neck and chest, enable deep inhalation |
| stimulus of pulmonary function | central chemoreceptors (medulla) monitors CO2 and pH (CO2 is the primary stim for breathing)peripheral chemoreceptors monitor oxygen levels |
| what is less sensitive in COPD pts? | chemoreceptors; primary regulator is oxygen not CO2 |
| Ventilation | process of inhalation of oxygen and exhalation of CO2 |
| hyperventilation | rapid respiration rate to cause CO2 to drop |
| hypoventilation | shallow respirations to cause CO2 to rise |
| perfusion causes | hypercapnia and hypoxia |
| hypercapnia | increase in respiratory rate in order to eliminate CO2 |
| hypoxia in perfusion | low levels of oxygen cause inc respiratory rate to let more oxygen in |
| use of CXR, CT, MRI | visualization of chest and lung structure |
| V-0 scan | measure mismatches in perfusion and ventilationdiagnoses clots |
| PFTs | measures lung volume and gas exchange |
| bronchoscopy | lighted scope to visualize respiratory structures and obtain biopsies |
| what tool do you use in respiratory arrest | ambu bag/ BVM |
| dyspnea | s/sx: nostril flaring, use of accessory muscles, retraction of intercostal spaces |
| Dyspnea on Exertion (DOE) | pulmonary and cardiac pt after ambulating a short distance |
| orthopnea | dyspnea while laying flat |
| nocturnal dyspnea | shortness of breath at night |
| acute cough and sputum | last few weeks; associated with infection |
| chronic cough and sputum | lasts more than few weeks; related to smoking, asthma, or gastric reflex |
| non productive cough and sputum | dry, hacking cough that does not simulate mucus secretion; related to environmental irritants or allergies |
| productive cough and sputum | congestion of mucus secretions; requires removal called expectoration |
| sputum quality | purulent (cloudy)hemoptysis (bloody) |
| other pulmonary s/sx | breathing patterns (Cheyenne strokes and Kussmauls), cyanosis, and pleurisy (pain with breathing) |
| atelectasis | collapse of alveoli/inability of alveoli to stay fully inflated which impairs gas exchangerisk factors: impaired expansion following surgery, pleurisy, narcotics, and prolonged immobilitys/sx: dyspnea, coughprevention: TCDB, incentive spirometer, ambulate |
| TCDB | turn, cough, and deep breathe |
| upper airway inflammation | rhinitis, pharyngitis, sinusitisresponse to pathogen/allergens s/sx: congestion, redness, sneezing, sore throat |
| lower airway inflammation | acute/chronic bronchitis (COPD) |
| asthma - obstructive pulmonary disorder | inflammation, increased mucus, bronchoconstrictions/sx: dyspnea and wheezing, thick secretions (mucus plug) |
| COPD - chronic bronchitis and obstructive pulmonary disorder | irritation → irritationmucus, bronchospasm, air has difficulty getting in because of edema s/sx: productive cough, dyspnea with intermittent wheezing, recurrent respiratory infections, Cor pulmonale, “blue bloaters” |
| cor pulmonale | right sided heart failure |
| COPD - emphysema | loss of alveoli elasticity, hyperinflation, spends a lot of energy breathing, insensitive to high CO2 → hypoxic drives/sx: DOE, barrel chest, pursed lips, red complexion, clubbing, blebs, “pink puffers” |
| pneumothorax - restrictive pulmonary disorder | collapsed lung (air in pleural space), spontaneous blebs, can be traumatic/open or tension/closed s/sx: dyspnea and asymmetrical chest rise treatment: establishing negative pressure using chest tube |
| traumatic/open pneumothorax | hole in both visceral and parietal pleura |
| tension/closed pneumothorax | medical emergency, trapped inspired air causes compression and collapse |
| pleural effusion - restrictive pulmonary disorder | fluid in pleural space; plasma is straw-colored, exudate, or bloodys/sx: pleurisy and dyspnea |
| pulmonary edema - pulmonary vascular disorder | excess fluid in LUNG = inc. hydrostatic pressure in pulmonary capillariess/sx: dyspnea, crackles, pink frothy sputum |
| pulmonary hypertension - pulmonary vascular disorder | elevated arteriole BP in pulmonary bed caused by genetics (primary) or disease (secondary) s/sx: cor pulmonale → pulmonary edema |
| Pulmonary embolus - pulmonary vascular disorder | ventilation and NO perfusions/sx: sudden tachypnea, tachycardia, anxiety diagnostic tests: positive d-dimer |
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AV25
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