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336 Cards in this Set
- Front
- Back
- 3rd side (hint)
Do all arteries carry only oxygenated blood? |
Nope |
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What is autonomic neuropathy associated with? |
Silent (painless) myocardial ischemia |
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T\F a widened pulse pressure is found in shock and congestive heart failure |
False |
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Does skeletal muscle or cardiac muscle have a higher oxygen demand? |
Cardiac muscle is higher |
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What does cessation of blood flow to the myocardium produce? |
Immediate ischemia |
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Does unstable atherosclerotic plaques compared to stable plaques have |
Blah |
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Risk factors for atherosclerotic heart disease |
Obesity Male Inflammation Sedentary lifestyle High LDL Low HDL |
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Does cocaine promote thrombosis by activating platelets? |
Yes |
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Is cocaine a vasodilator? |
No it's a vasoconstrictor |
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Does cocaine decrease heart rate? |
No it increases it |
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Neutral pH |
7.0 |
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In humans normal arterial blood pH |
7.4 (7.35-7.45) Slightly alkalotic, slight base excess, slight HCO3- excess |
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Acid = |
H+ which = protons |
Charge |
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Increase H+ does what to pH |
Decreases pH so it's more acidic/ less base |
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Decrease H+ does what to pH |
Higher pH so less acid and more base |
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pH equations |
pH=-log[H+] Or pH= [HCO3] / [paCO2] |
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Metabolic and respiratory parts that make up pH |
Metabolic = HCO3 levels Resp = paCO2 levels |
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How does the body deal w acid? |
By using HCO3 buffers protons, takes away acid but leaves conjugate base - that has negative charge (aka an anion) |
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Kidney and HCO3 |
It is made by kidney but takes few days to make significant level, kidney also saves/re absorbs HCO3 to elevate levels |
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H2O and CO2- what happens to them in the body |
Water/co2 are exhaled by lungs, some h2o is used by body, h2co3 (carbonic acid) an intermediate metabolite is present in very small concentrations, H+ is buffered (removed by proteins) |
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H2o + co2 <-> ______ <-> ______ |
H2co3 H+ + hco3 |
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Normal arterial paco2 |
35-45 |
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Arterial bicarbonate normal levels |
Hco3: 24-31 Kidney related |
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Normal levels of pH, Paco2 and hco3 in arterial blood |
PH: 7.35-7.45 Paco2: 35-45 Bicarbonate: 24-31 |
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Respiratory alkalosis blood levels |
PH= greater than 7.45 PCo2 = less than 35 |
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Etiology of resp alkalosis |
Hyperventilation, anxiety, stress Drugs. Aspirin/caffeine intoxication High fever |
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Metabolic acidosis blood levels |
PH less than 7.35 Hco3 less than 22 |
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Metabolic acidosis etiology |
Diarrhea, renal tubular acidosis, lactic acidosis, ketoacidosis, shock, cardiac arrest, toxins ethanol, methanol, ethylene glycol |
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Respiratory acidosis blood leveks |
Ph less than 7.35 Paco2 greater than 45 |
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Respiratory acidosis etiology |
Narcotic overdose, severe CNS injury Airway obstruction Severe asthma pneumonia copd |
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Metabolic alkalosis |
Ph higher than 7.35 Hco3 greater than 31 |
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Metabolic alkalosis etiology |
Vomiting Gastric drainage Loop diuretics Too much antacid |
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If bicarbonate level goes down you can become... |
Acidodic |
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Major buffer for H+ in the body |
Hemoglobin / proteins in general |
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Arterial vs Venous blood |
arterial: higher O2 levels, standard for blood gases Venous: lower O2, higher co2, more acidodic |
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2 types of immunity |
Innate (natural/native) Adaptive (acquired, specific) |
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List innate immunity traits |
Physical/molecular/cellular defenseman place before infection Low levels, always ready Always present Antigen nonspecific Respond immediate No immunologic memory Attacks nonself Doesn't distinguish between different microbes |
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What does innate immunity recognize |
General classes of molecules shared by related groups of microbes that are essential to their survival Does not recognize specific antigens |
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Examples of innate immunity |
Epithelial barrier (skin, cilia, mucus, stomach acid, saliva, tears) Macrophages, neutrophils, eosinophils, nk cells, dendritic cells Plasma proteins Lysosomes |
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Immune system that doesn't distinguish between different mucrobes |
Innate |
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Physical/molecular/cellular defenseman place before infection Low levels, always ready Always present Antigen nonspecific Respond immediate No immunologic memory Attacks nonself Doesn't distinguish between different microbes |
Innate immunity |
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Epithelial barrier (skin, cilia, mucus, stomach acid, saliva, tears) Macrophages, neutrophils, eosinophils, nk cells, dendritic cells Plasma proteins Lysosomes |
Innate immunity |
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Natural killer cells are part of__ immunuty |
Innate |
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Less rapid but more effective immunity |
Adaptive |
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Initially naive but then develops memory, 1st must recognize foreign agen then process then produce amplified response |
Adaptive immunity |
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Antigen specific immunity |
Adaptive |
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Immunity that attacks specific microbes at specific antigens |
Adaptive |
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2 types adaptive immunity |
Humoral (antibody proteins in blood) Cell mediated (phagocytic cells) |
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Humoral immunity |
B cell Antibody proteins in blood |
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Cell mediated immunity |
T cells Phagocytic cells |
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Immunity that recognizes general class of lipopysaccharide molecules in gram- bacterial walls |
Innate |
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Immunity recognizes antibody specific to endotoxins o antigen of e.coli in cell wall |
Adaptive |
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T cells come fron |
Thymus |
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B cells come from |
Liver, then thymus, then bone marrow, then blood |
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Immunity you need to be exposed a second time for response |
Adaptive |
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More specific immunity |
Adaptive |
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First identified as antigens that evoke rejection of transplanted organs |
Mhc ( majorhistocompatabity complex) |
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Aka HLA (human leukocyte antigen) in humans |
Mhc |
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Mhc |
Major histocompatibility complex Important in organ transplant The better the match of similar antigens between recipient and donor, the less rejection of organ by recipient |
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Where are different lymphocytes generated and where do they mature |
Generated from stem cells in bone marrow or fetal liver B cells mature in bone marrow T cells mature in thymus then go to lymph nodes to wait to be activated by antigen presenting cells |
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T lymphocyte functuon |
Functions in cell mediated immunity - virus -rejection of tissue grafts -delayed hypersensitivity reactions (ex. Tb skin test) -intracellular microbes (ex. Legionella pneumonophila) -graft vs host - contact sensitivity |
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CD4+ |
Type of t lymphocyte Master regulator for the immune system Important in aids |
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Types of t lymphocytes |
Memory cells Cd4+ Cd8 (become cytotoxic T cells) Regulatory T cells (suppress immune response) |
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Cytokines |
Small cell signaling proteins Act through cell surface receptors After releasing cells itself, immediate adjacent cells, distant cells Specific kinds released by different types of cells |
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Cytokines difference from hormones |
-Higher initial concentration - much greater increase 1000 fold trauma and infection -made by different types of cells - erythropoietin is a cytokine hormone |
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Erythropoietin |
Cytokine hormone made by fibroblasts in kidney and CNS neurons and astroglia for memory Tells precursor to Rbcs to start making rbcs |
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Are cytokines hirmones |
No |
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Def of hormones |
Secreted by discrete glands (ie B cells in pancreas) and affect distant cells and tissues |
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Effect of low concentration of cytokines |
Local effects |
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Effects of high concentrations of cytokines |
Systemic effects |
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1918 flu pandemic |
Relatively more deaths in young people Healthy immune system liability (produce stronger immune response, greater cytokine response, caused cytokine storm) |
Cytokines |
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Cytokine storm |
Cause of 1918 flu pandemic deaths Fever, erythema, swelling, cachexia, fatigue, lack of cytokine regulation, loss of feedback loop Implicated in sirs (systemic inflammatory respond syndrome) So many cytokines killed virus but good cells too |
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What does cytokine storm cause |
Inflammation, organ failure, infection |
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Plasma cells |
Typically not in peripheral blood- found in lymph nodes Part of B cell humoral adaptive immunity Short lived, needs continuous colony stimulator factor Produces antibody against antigen |
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Typically not in peripheral blood- found in lymph nodes Part of B cell humoral adaptive immunity Short lived, needs continuous colony stimulator factor Produces antibody against antigen |
Plasma cells |
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Immuniglobulins secreted by plasma cells |
Igg Igm Iga Ige |
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IGG |
Immunoglobulin secreted by plasma cells 75% of all antibodies in normal individual Crosses placenta, protects fetus |
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Igm |
Immunoglobulin secreted by plasma cells 1st antibody to respond to antigen Does not cross placenta |
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IGA |
Immunoglobulin secreted by plasma cells Mucosal production Tears, gut, milk, saliva |
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IGE |
Immunoglobulin secreted by plasma cells Lowest concentration of any immunoglobulin Parasites, allergy, hypersensitivity (anaphylaxis) |
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Immunoglobulin of highest concentration |
IGG |
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First antibody to respond to antigen |
IGM |
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Immunoglobulin in mucosal |
(Tears, saliva, milk, gut) IGA |
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Lowest concentrated immunoglobulin |
IGE |
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Immunoglobulin associated with parasites and allergy |
IGE |
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Immunoglobulin that c tosses placenta |
IGG |
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Immunoglobulin levels at birth |
Newborn has high IGM and no IGG, if elevated IGG it is from mom so the baby had an infection in utero |
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At birth origin of IGG is... |
Maternal |
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If elevated IGG at birth... |
Baby got infection from mom in utero |
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Primary immune response |
Macrophages phagocytize antigen, present to t helper cell that processes it, TH then activate B cells that produce antibodies Takes 2-3 weeks |
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How long does primary immune response process take |
2-3 weeks |
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What kind of response to vaccines produce |
Primary immune response |
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Secondary immune response |
B memory cells respond to antigen immediately Plasma antibody levels rise w/in days |
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Boost shot produces what type of immune response |
Secondary |
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IGG in response to antigen exposure (describe graph) |
Primary antibody response levels go up then start to decline but in response to 2nd exposure go way up even higher |
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IGM in response to multiple exposures to antigen (graph) |
Levels go up in each response but quickly got back to zero after each response so each response is the same level as before |
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What is Passive immunity |
ATB pass directly into body from external source instead of body making them |
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Artificial examples of passive immunity |
Diphtheria antitoxin Antivenom IV immunoglobulin Rabies vaccine |
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Examples natural passive immunity |
IGG through the placenta IGA through breast milk |
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Natural active immunity |
Exposed to antigen, develop disease and acquire immunity |
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Artificial active immunity |
Vaccine exposed to antigen but no symptoms or very mild |
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Vaccination |
Substance that produces immunity |
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Immunization |
Process by which person becomes protected from disease By vaccines or being exposed to the disease |
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Vaccination vs immunization |
Vaccination: substance that produces immunity Imm: process by which person becomes protected from the disease |
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Active immunity produces _____ so if re exposed, b and T cell response if _____ |
Immunologic memory Rapidly mobilized |
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Types of vaccines |
Inactivated or dead Part of microbe Attenuated live or viable |
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Inactivated or dead vaccines typically.. |
Need a booster |
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Live or viable vaccines |
Less need for boosters Can be excreted and inoculate others Cannot be used in immunoconpromised (ex. Polio persists in intestines) Do better job at stimulating cell mediated immunity |
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Do most vaccines do a good job of stimulating cell mediated immunity |
No they do a poor job But live attenuated do it better |
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Do vaccines stimulate innate immunity |
None do currently |
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Immunoconpromised people and vaccines |
May not develop immunologic response to vaccine antigen Can develop vaccine associated disease from live attenuated virus |
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Can host develop disease from vaccine? |
Very rarely and typically milder Immunosuppressed can from live vaccines |
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Very rare things vaccines can cause |
The illness itself Act as super antigen and overstimulate immune system Cause allergic reaction to egg protein because it is produced in embryonic chicken eggs |
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Vaccine autism myth |
Thine risk (ethyl Hg) does not cause autism, it is almost never used anymore but autism is increasing |
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Adjuvant |
Added to vaccine to stimulate immune response to target antigen |
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Hapten |
Small molecule that can elicit immune response when attached to lrg protein carrier cannot elicit response by itself |
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Hapten is associated with... |
Type IV cell mediated immunity |
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Immunosnescense |
Deterioration of immune system w/ age Decreased response to infection Decreased immunologic memory especially to vaccination |
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What decreases in immunosenescence |
Hematopoietic stem cells |
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Why do hematopoietic stem cells decrease in immunosenescence |
With increasing age, oxidative damage to DNA and telomere shortening cause this |
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Disorders caused by the immune response are called |
Hypersensitivity reactions |
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What are Hypersensitivity reactions |
Excessive or inappropriate activation of immune response Damage to body by immune response rather than by antigen |
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Types of hypersensitivity reactions |
Type I - IV |
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Type I hypersensitivity reaction mediated by |
IGE mediated
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Type I hypersensitivity reaction aka |
Immediate hypersensitivity Antigens are called allergens Pollen, dust, animal dander, food, chemical, drug Can be localized or systemic, mild to life threatening |
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Anaphylaxis |
Type I hypersensitivity Acute, potentially fatal Multi organ involvement Release mediators from mast cells, basophils, eosinophils |
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Where are mediators released from in anaphylaxis |
Release mediators from mast cells, basophils, eosinophils |
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What does anaphylaxis require |
Previous sensitization and reexposure |
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Steps of anaphylaxis |
1: previous exposure 2: reexposure 3: IGE release 4: mediator release (mast cells, basophils, eosinophils) 5: symptoms |
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Non IGE hypersensitivity reaction |
Anaphylactoid Mast cell and basophils activation rather than IGE Can occur rarely in humans Need prior sensitization unless complement activation on first exposure |
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Ex. Anapgylactoid hypersensitivity reaction |
Radiocontrast dyes |
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What cells are covered with IGE and what happens when an antigen specific to IGE binds to it |
Basophils, mast cells, eosinophils Inflammatory agents are released like histamine |
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Routes of anaphylaxis |
Oral Parenteral Topical Inhalational |
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What does histamine do |
Increases capillary permeability to allow WBCs and proteins to disperse to infected areas Stimulates parietal cells to produce stomach acid |
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Morphine and histamine |
Certain drugs like morphine displace histamine in granules release |
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List what histamine causes |
Bronchoconstriction Vasodilation Separation of endothelial cells which inc capillary permeability Arrythmogenic and myocardial depressant |
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Leukotrienes |
More potent but slower than histamines in anaphylaxis |
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What is atopy |
Exaggerated tendency to mount IGE response to a wide variety of environmental allergens Inc circulating ige |
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% affected by atopy in western world |
40 |
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What is atopy frequently associated with |
Eosinophilia |
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Examples of atopy |
Hay fever, eczema, asthma |
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Local (atopic) reactions in type 1 hypersent reaction |
Strong genetic component but contact w allergen must occurred before reaction develops Hay fever rhinitis Food allergies Atopic dermatitis Hives |
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Type II hypersensitivity reaction |
Antibody mediated, cytotoxic IGE and IGM bind to antigens on own cell surface |
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2 types of antigens |
Intrinsic- part of own cell wall Extrinsic- foreign antigen absorbed on to cells |
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Antibody mediated hypersensitivity reaction aka |
Type II cell mediated |
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Steps of type II hypersensitivity reaction |
1- drugs bind to Rbc membrane recognized as different 2-IGM or IGG bind to antigen 3- activate complement pathway 4- acute inflammation 5-cell membrane attacked 6- cell lysis |
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Example of type II cell mediated hypersensitivity |
Penicillin induced hemolysis (not anaphylaxis) |
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Type III immune complex mediated hypersensitivity reaction |
Formation of insoluble antigen-antibody complexes form in circulation Localized or systemic |
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Steps of type III hypersensitivity reaction |
1- deposited on endothelial blood vessels or tissues 2- activate complement 3- attract neutrophils 4- release inflammatory response 5- necrosis |
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Ex of type III immune complex mediated hypersensitivity reaction |
Glomerulinephritis |
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Serum sickness |
Immune complexes deposited in heart, joints, kidney, and skin |
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Causative agents of serum sickness |
Antiserum Horse antitoxin to diphtheria Anti venom snake bites Human blood products Penicillin NSAID Monoclonal bodies |
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Type IV hypersensitivity reaction. Aka |
Cell mediated |
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Type IV cell mediated hypersensitivity reaction T cells attack what |
Antigen, not antibody-antigen |
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What does type IV hypersensitivity reaction primarily respond to |
Mycobacterium species Virus Fungi Protozoa |
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Type IV delayed type hypersensitivity |
tB skin test ex. Mantoux Allergic reactions ex. Poison ivy Hypersensitivity pneumonitis |
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Def self tolerance |
Ability of immune system to differentiate self vs nonself |
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What happens in autoimmune disease |
Self tolerance breaks down and immune system destroys body tissue Can be types I, II, III, or IV |
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Why can't autoimmune disease be type I |
No disease mimics type I |
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Factors associated with autoimmune disease |
Genetic: familial clustering Environment: molecular mimicry |
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Environmental factor of autoimmune disease molecular mimicry |
Microbe shares epitope with host, and cell walls hve human antigens in streptococci |
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Examples of Environmental factor of autoimmune disease molecular mimicry |
Heart: rheumatic fever Kidney: glomerulonephritis |
Heart Kidney |
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Superantigens |
Coca using hyperactivation and release of large amounts of cytokines |
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Types of grafts |
Xeno:different species Allo: same species ISO: identical twins |
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Host vs graft |
Immunocompetent host recognizes foreign antigens on grafted tissues or cells and mounts an immune response which results in rejection |
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Graft vs host |
Immunocompromised host grafted with foreign immunocompetent lymphoid cells with immunoreactive T cells in the graft recognize the host tissue as foreign and mount immune reaponse |
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Hygiene hypothesis |
Lack or early childhood exposure to antigens such as infections, symbiotic flora, parasites, increased susceptibility to allergic disease later in life Lack of exposure leads to defective immune tolerance When exposed later in life exaggerated response |
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Groups with higher allergic disorders because of hygiene hypothesis |
Small families Not go to daycare Live in clean, like city vs farm Used antibiotic in 1st year Inc in affluence |
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Primary immunodeficiency disorders |
Congenital: most recessive (autosomal or xlinked) |
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Secondary immunodeficiency disorders |
Loss immunoglobulins through GI tract T cell deficiency after viral disease Drugs and toxins Aging |
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Importance of early detection of immunodeficiency disorders |
Prevention of exposure Available treatment Avoid live virus vaccines when indicated |
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IGA deficiency |
Most common (1/700 Caucasians) GI/eye/nasopharyngeal infections because that's where IGA is secreted Treatment with IVIg can cause anaphylaxis |
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Most common immunodeficiency |
IGA deficiency |
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Combined T and B cell defects |
Lymphoid progenitor cells defective so bothT and B cell lineages are affected Infants suffer recurrent infections, especially opportunistic Spectrum from mild to fatal |
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SCID |
Severe combined immunodeficiency disorder -absent t and B cell immunity and absence of circulating T and B cells -infants course resembles aids |
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Treatment of scid |
Bone marrow transplant |
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Infants with SCID symptoms |
Like aids - failure to thrive - diarrhea - opportunistic infections |
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HIV |
Human immunodeficiency syndrome is a single strand of RNA retrovirus that incorporates into host cell dna 12 genes |
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What does hiv attack |
Cd4 t lymphocytes which coordinates with response to infection Until cd4 count very low patient is asymptomatic |
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In hiv, what does infection risk correlate with |
Cd4 count |
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Are antibodies to hiv protective |
No but it is helpful in diagnosis |
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Hiv causes |
Immunosuppression Infection Malignancy Waisting CNS degeneration |
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___ is the virus ____ is the disease |
Virus- hiv Disease- aids |
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How hiv is transmitted |
Blood (transfusion, needles) Semen Vaginal secretions Breast milk |
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First stage of hiv |
Acute infection 2-4 weeks after expose influenza like synptoms Very high viral load but may be seronegative (test negative) |
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Second stage of hiv |
Clinical latency 3-20 years (avg 8 years) Generalized lymphadenopathy, weight loss, fever |
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3rd stage of hiv |
AIDS ( acquired immunodeficiency syndrome) Typically initial symptom is respiratory |
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HIV in infants |
Failure to thrive CNS abnormalities, higher incidence of encephalopathy than older patients Developmental delay Maternal antibodies can persist for up to 18 months |
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How is hiv transmitted to infants |
Vertical -in utero -birth canal Breast feeding |
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Signs of congenital hiv |
Most appear clinically normal Neurodevelipmental disorders Early encephalopathy with microencephaly Failure to thrive and growth retardation |
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Why some congenital hiv will show synptoms |
Comirbidities such as ETOH or drug exposure or other congenital infections especially CMV are present |
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How to reduce mother to child hiv transmission |
Cdc through key interventions reduced it from 35% to 5% - testing - antiretroviral medication to mother and exposed infant - safe feeding practices |
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Hiv drug resistance |
Hiv mutations common because virus replicates rapidly and doesn't contain proteins to correct mistake in replication Reduce risk by using 2 antiretrovirals |
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Ebola barrier protection |
Fluid impermeable gown, gloves, mask Goggles or face shields If copious secretions double glove and leg and shoe covering If aerosol generating N95 mask and negative pressure room |
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Cardiac output= Equation |
Heart rate x stroke volume |
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3 major determinants of stroke volume |
Preload Contractility afterload |
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Statins |
Lower cholesterol in liver |
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70% of cholesterol is made where |
In the liver |
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Co= |
Hr (heart rate per min) x sv (stroke volume ml) |
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Flow = |
Pressure / resistance |
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Radius of blood vessel= |
Blood pressure - 1/r^4 Factor in resistance |
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Total blood volume is about... |
5.5L |
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Def stroke volume |
Blood pumped/ beat by each ventricle |
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Cardiac output def |
Volume of blood pumped/ min by each ventricle |
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Thrombus |
Blood clot, stationary |
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Emboli |
Blood clot, migrates |
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Blood in pulmonary artery is.. |
Unoxygenated |
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Normal co for adult women and men |
Men- 5.5 Women- 4.9 |
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Normal HR |
75 |
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Normal stroke volume |
70ml |
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What happens if co goes down a little, a lot, or to zero |
A little: congestive heart failure A lot: shock Zero: cardiac arrest |
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Fick equation |
Calculates blood flow to an organ |
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Preload is blood.. |
Pumped into the heart to be pumped out |
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Preload when standing |
Blood pools in lrg veins in legs |
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Preload when laying down |
Blood evenly distributed in veins Inc central venous pressure-> inc diastolic volume -> inc sv-> inc pulse pressure |
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In the frank starling mechanism as ventricular end diastolic volume increases... |
Stroke volume increases until a certain point it evens out and then too high will plummet |
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When patient was placed laying down with head lower than feet |
Adverse outcome when used in shock Called trendelenburg position |
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Increased preload effect on stroke volume |
It will inc sv to an extent but will eventually overstretched the heart muscles and dec sv such as in fluid overload in congestive heart failure |
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When does the heart get blood |
During diastole |
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Perfusion of the myocardium is during.. |
Diastole |
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Arteriosclerosis |
Gardening and loss of elasticity of medium and larg arteries |
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What kind of disease is atherosclerosis |
Chronic and slowly progressive A symptomatic for decades Symptoms depend on which artery and organs are involved Very abrupt onset of symptoms when narrowing or obstruction of blood flow to organs occurs |
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Steps of atherosclerosis formation |
1- endothelial cell injury 2- migration inflammatory cells 3- lipid accumulation & smooth muscle proliferation 4- plaque formation 5- occlusion and or rupture with thrombosis |
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First step of atherosclerosis formation |
Endothelial cell injury - smoking/pollution/ldl/mechanical stress(hypertension)->>> endothelial injury->> adhesion monocytes and platelets |
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Second step of atherosclerosis formation |
Migration inflammatory cells -endothelial cells express chemotaxic adhesion molecules Monocytes and other inflammatory cells accumulate Monocytes migrate to intima, become macrophages and engulf lipoproteins (especially ldl) |
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Third step of atherosclerosis formation |
Lipid accumulation and smooth muscle proliferation - activated macrophages release ROS that oxidize ldl-> macrophages ingest oxidized ldl and form foam cells-> macrophages induce migration and proliferation of smooth muscle cells and increase extracellular matrix |
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Fourth step of atherosclerosis formation |
Superficial fibrous plaque made of smooth muscle cells and extracellular matrix (especially collagen) secreted by smooth muscle cells ->> necrotic core of fatty debris and lipid filled foam cells -> monocytes continue to infiltrate |
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Fifth step of atherosclerosis formation |
Occlusion, rupture, and thrombosis - rupture, ulceration, or erosion of fibrous cap initiates activation of extrinsic clotting system that forms thrombosis and obstruction Can totally stop blood and kill tissue May reorganize and cause stenosis |
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Determinants of plaque instability |
Inflammation Size of lipid rich core Lack stabilizing smooth muscle cells Stability and thickness of fibrous cap |
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What triggers plaque rupture? |
Sympathetic stimulation often triggered by anger |
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How much occlusion or coronary artery can you have w/out symptoms |
70% |
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Trigger for acute cardiovascular events |
Outbursts of anger (sympathetic activity) causing changes in blood flow |
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Major risk factors for atherosclerosis |
Hypertension Diabetes Smoking Family history Low levels of HDL High levels of ldl |
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HDL vs ldl good and bad |
Good- HDL Bad- ldl |
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Importance of hdl |
Takes days back to liver to be recycled So if low levels foam cells accumulate causing plaque to accumulate and stick out more |
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Treatment of atherosclerosis |
Lifestyle modifications (diet, exercise) Stop smoking Lower bp Drugs (statins, low dose aspirin) Invasive procedures (stents, bypass) |
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What gives blood flow a pulse |
Contraction/ relaxation of left ventricle |
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Nicotine effect on blood flow |
Causes vasoconstriction, so has a dose response curve with strain on the heart and blood vessel damage Also causes inflammation and dysplasia |
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Vasoconstriction effect on peripheral vascular resistance, blood flow, and co |
Periph resist- higher Blood flow- lower Co- less |
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What is blood flow proportional to |
Radius^4 |
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Systolic pressure |
Peak pressure in arteries Higher value in blood pressure notation Occurs near end of cardiac cycle when ventricles contracting |
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Contributing factors to systolic pressure |
Closure of aortic valve Force and rate blood is ejected Elasticity of aorta and large arteries Ventricle contracting |
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Peak pressure in arteries is called |
Systolic pressure |
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In blood pressure notation top number is ___ and bottom number is ____ |
Top is systolic bottom is diastolic |
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Diastolic pressure |
Minimal pressure in arteries Occurs when ventricles are relaxed and filling w blood |
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Contributing factors to diastolic pressure |
Closure of aortic valve Energy (rebound) stored in elastic fibers Resistance to flow through arterioloes and capillaries |
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Pulse pressure what is |
Difference between systolic and diastolic pressure Proportional to sv (but not =) About 40mmhg (120-80) |
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Autonomic nervous system regulation of heart |
Parasympathetic via vagus nerve lowers HR Sympathetic inc. HR (chrinitropic) and inc contractil it's (inotropic) |
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Autonomic nervous system regulation of blood vessels |
Sympathetic vasoconstriction leads to inc peripheral resistance |
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Inc after load does what to the heart |
Puts a strain on the heart |
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2 systems that regulate bp |
Nervous- autonomic nervous systems (symp and parasympathetic) Humoral (renin-angiotensin-aldosterone, and ADH) |
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Angiotensinogen |
Made by liver and is just circulating in the blood until kidney secreted renin |
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How does the kidney secrete renin |
The juxtaglomerular apparatus senses decreased renal perfusion so it secreted renin |
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Renin |
Secreted by kidney Converts angiotensinogen to angiotensin I |
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What triggers renin-angiotensin-aldosterone |
Dec BP, extracellular fluid volume, and extracellular Na |
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ACE |
From endothelial cells (esp in lungs) converts angiotensin I to angiotensin II Reduce vasoconstriction and dilate arteries so it's used to treat hypertension |
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Angiotensin II |
Active form Strong vasoconstrictor |
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Aldosterone |
Released by adrenal cortex Deans orbs Na in the kidney |
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Systolic and diastolic #s in hypertension |
Syst- greater than 140 Diast- greater than 90 |
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Systolic greater than 140 |
Hypertension LV hypertrophy Inc myocardial O2 |
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Normal diastolic and systolic pressure |
Systolic less than 120 Diastolic less than 80 |
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Per hypertension diastolic and systolic pressure |
Systolic- 120-139 Diastolic- 80-89 |
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Hypertension diastolic and systolic pressure |
Systolic- greater than 140 Diastolic- greater than 90 |
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Studies have shown a reduction of just __mmHg can reduce stroke |
5 mmHg |
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Types of hypertension |
Primary= essential, most common, due to weight gain and sedentary lifestyle Secondary= due to other diseases, only 10% |
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Primary hypertension |
Chronic elevation without other diseases present, no identifiable cause 90% Inc metabolic demands, co inc Ren-ang-ald elevated |
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Secondary hypertension types |
Renovascular Hyperaldosteronism Oral contraceptive pills Amphetamines/cocaine/alcohol Decongestants Hyperthyroidism Sleep apnea |
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Most common secondary hypertension |
Renovascular |
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Renovascular hypertension |
Renal artery stenosis from fibromusculad dysplasia or atherosclerosis dec. blood flow which stimulates renin secretion |
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What causes primary hypertension |
No specific disease but it is associated w excessive Edith gain and sedentary lifestyle |
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What causes secondary hypertension |
Specific lesions |
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Treatment of hypertension |
Lifestyle changes (diet/dec Na, exercise, weight loss, stress reduction) Medications (ace inhibitors, beta blockers, calciumu channel inhibitors, diuretics) |
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Medications that treat hypertension |
ace inhibitors, beta blockers, calcium channel inhibitors, diuretics
ABCD |
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Blood pressure in elderly |
Age related inc in systolic bp Loss elasticity of arteries (dec baroreceptor response, inc peripheral resistance) |
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What happens to blood vessels in elderly |
Aorta and lrg arteries elastin replaced by collagen, increases wall stiffness, inability for vessels to distend and adjust to systolic bp, can't store energy needed to maintain diastolic bp |
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Thrombus vs embolism |
Thrombus in vein with inflammation can occlude or break and cause embolism |
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Risk factors for venous thrombosis |
Immobilization, bed rest, dehydration, surgery and inflammation injury to vessel wall, vein injury or compression, malignancy, inc blood coagulability aquired or inherited coag inhibitor factors |
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Pulse pressure relationship with stroke volume |
Proportional but not equal, so if pulse pressure is 55 sv isn't 55 but it does inc |
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Effect of exercise on pulse pressure |
Increases it |
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Normal pulse pressure |
30-40 |
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High and wide pulse pressure characteristics |
Inc sv Anemia Fever Thyrotoxicosis Av fistula |
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Low and narrow pulse pressure |
Hypovolemia Shock chf |
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Heart failure def |
Not pump well enough to get O2 to peripheral cells |
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MI def |
Myocardial infarction, aka heart attack, myocardial cells die, can be cause of heart failure, a systole, and death |
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Coronary artery disease def |
Impaired blood flow, often to heart due to obstruction of coronary arteries Often caused by atherosclerosis so used synonymously w/ atherosclerotic heart disease but there are other etiologies |
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Dyslipidemia |
Risk factor for Coronary artery disease LDL inc and HDL is lowered |
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Diarrhea effect on sv |
Dec blood flow so less preload to sv dec |
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Vascular volume relationship with sv/bp |
If it goes up so does sv/bp |
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Heart is an ____ organ |
Aerobic |
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Interruption of blood flow to the myocardium causes.. |
Immediate ischemia |
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Heart and oxygen |
Has 70% O2 extraction(very high) so blood flow interruption can cause rapid ischemia and if not reversed necrosis |
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How does cardiac monocyte get O2? |
During diastole, has to go through diffusion and vessels in longer areas |
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What do you need for forward flow through the arteries |
Systole |
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Determines coronary artery profusion pressure |
Aortic pressure |
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Myocardial blood flow occurs during ___ and is regulated by ___ |
diastole Metabolic demands of myocardium |
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2 vasocontrictors |
Endothelin Angiotensin II |
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2 vasodilators |
Nitric oxide (NO) Lactate CO2 |
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Made by endothelium |
Nitric oxide and AcE |
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Causes of endothelial dysfunction |
Inflammation such as infection or atherosclerosis |
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Def endothelial dysfunction |
Coronary vessels w atherosclerosis lose ability to release vasodilators substances especially NO |
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Normally if demand inc... Is reduced which inc -- |
Coronary resistance dec Flow inc |
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If blood supply doesn't meet demand in body |
Ischemia will occur such as in an MI |
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What does lactate, co2, and prostacyclin have in common? |
They are vasodilators that will inc blood flow |
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What does nitric oxide do? |
Vasodilators that will inc blood flow |
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What do inc hr and systolic pressure decrease |
Dec diastole and thus myocardial blood flow |
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Determined mvo2 |
Ventricular wall stress Contractil it's Heart rate (higher the hr lower the myocardial blood flow) |
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Afterliad |
Pressure the left ventricle needs to overcome during systole |
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Angina |
Paroxysmal chest pain/ pressure sensation Transient myocardial ischemia Fixed or stable plaque (69-70% occlusion) |
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Most common cause of coronary artery disease |
Atherosclerosis |
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Legit happens in an MI |
Unstable or rupture w platelet adhesion of plaque |
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Stable angina |
Fixed or stable plaque Precipitated by walkin, stress, cold, meal Relieved by nitroglycerin |
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Unstable angine |
Occurs at rest Severe pain Not respond to nitroglycerin |
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Nitroglycerin |
Converted to NO by mitochondrial aldehyde dehydrogenase Causes myocardial blood vessel dilation |
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Nitroglycerin dose for decreased preload |
Lower dose |
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Nitroglycerin dose for a lower after load |
Higher dose |
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Silent myocardial ischemia symptoms and causes |
Painless Autonomic neuropathy ex diabetes Elderly Previous mi |
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Symptoms of heart disease |
Chest pain / pressure/tightness Shortness of breath Dizziness/ fainting Fatigue Pain in neck/ back/ jaw/ both arms |
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Do men and women have same symptoms |
In women more diffuse, have chest pain less often than men |
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Cocaine effect on heart |
Inc hr Coronary artery vasoconstriction Promotes thrombosis by activating platelets Accelerates atherosclerosis |
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3 problems acute blockag of a blood vessel causes |
Goes from aerobic to anaerobic Loss of contractile function Loss normal membrane potential causing arrhythmias |
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Serum biomarkers |
A necrotic monocyte releases into the blood enzymes specific to it Cells become necrotic from ischemia and release intracellular contents Higher levels of Troponin (I and t specific for cardiac) Create kinase |
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ST elevation |
Full thickness injury and necrosis to myocardium can cause this |
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EKG indicators of MI |
ST elevation Wide Q wave T wave inversion May not show up early Many don't have at segment elevation |
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STEMI |
ST segment elevated myocardial infarction |
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NSTEMI |
Partial thickness necrosis, ST segment is not elevated Has partial occlusion |
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What is the st segment |
Between qrs and t wave Ventricular re polarization Initial period of ventricular diastole |
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STEMI has ___ occlusion |
Full// complete |
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7 treatments of mi |
O2 Asa aspirin therapy Pain control (narcotics) Re perfusion (catheter) Beta blockers After load reduction (ace inhibitor) Anticiagulation |
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Consequences of MI |
Cardiac arrest Chf Cardiogenic shock Sudden death (arrhythmia, ventricular fibrillation) Mechanical (aneurysm, papillary muscle necrosis) |
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Major cause of death in sudden cardiac arrest |
Arrhythmia most often ischemic in nature |
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What happens after an MI |
Necrosis becomes scar Macrophages remove necrotic tissue Highly vascularized granulation tissue |
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Characteristics of scar tissue |
Less vascular Non contractile Not conduct action potentials, abnormal rhythm |
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Rheumatic fever |
Group a beta hemolytic streptococcus pyrogenes Typically post pharyngitis but also after skin infection |
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Rheumatic fever body involvement list |
Joints ( poly arthritis) Skin Brain (Sydenham's chorea) Heart |
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Rheumatic fever effect on heart |
Acute phase can have ps carditis inflammation -pericardium 5-10% Myocardium rare Long term heart valves esp mitral and aortic affected |
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What type of reaction is rheumatic fever |
Type II hypersensitivity antibody mediated |
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