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136 Cards in this Set
- Front
- Back
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Stuff that blood transports (6) |
O2, glucose, nutrients, hormones, electrolytes, cell waste |
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Ways that blood promotes homestasis (4) |
1. distributes core body heat 2. maintains BP and fluid levels 3. constantly circulates complement system and clotting factors 4. Carbonic acid buffer system maintained to RBCs to maintain pH |
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What is in plasma and what color is it? |
Clear fluid containing clotting factors and Ig's -Called FFP -Given to people with liver disease who need clotting factors and Ig's but don't need more RBCs |
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What is in Plasma protein (3)? |
1. Alubumin (for osmotic pressure) 2. Globulins and antibodies 3. Fibrinogen |
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What is in Serum (2)? |
Electrolytes and glucose |
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What is another name for a RBC? |
Erythrocyte |
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What is polycythemia? |
Increased amounts of RBCs |
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What is Hematocrit and what is a normal level? What do high and low levels indicate? |
Proportion of blood volume that is composed of RBCs (36-50%, women normally lower)
High: dehydration (high viscosity) Low: blood loss, anemia, blood dilution (low viscosity) |
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Correlation between hemoglobin and hematocrit |
There is approx 3x the amount of Hct as there is Hgb ex) Hgb = 8, then Hct = 24
-Tx needed if Hgb under 9 |
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What is the function of Hemoglobin? |
Its the molecule in RBCs that carries Oxygen |
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Erythropoientin |
Hormone released from kidneys to stimulate bone marrow to increase RBC production |
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What are the 5 steps of Hemolysis? |
1. Phagocytized in spleen or liver where they are broken into heme and globin unit 2. Fe+ is recycled 3. Heme becomes unconjugated bilirubin 4. Unconjugated bilirubin goes to liver to become more soluable (aka conjugated bilirubin) 5. Conjugated bilirubin is then excreted in the bile and released in stool |
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What is Hemolytic Anemia cased by (2) and what can it lead to (3)? |
-Caused by the rapid destruction of RBCs or Liver dz (when there is decreased ability to conjugate bilirubin)
-Unconjugated bilirubin in blood = jaudice, pruritis, icteric sclera
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What does Hgb consist of, what are the globin inits called that circulate in the arterial and venous systems? |
4 globin subunits that each have an iron atom that allow oxygen to attach -Oxyhemoglobin: oxygen rich RBCs -Deoxyhemoglobin: oxygen reduced RBCs that carry carbon dioxide |
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Acidosis |
Favors O2 release + CO2 binding to heme group in venous system |
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Alkalosis |
Favors CO2 release and binding to heme group in arterial system |
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What is Valine? |
The amino acid that replaces glutamic on the Hgb beta chain. -this small change causes Sickle cell anemia |
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WBC's (aka leukobytes) constitute what % of total blood volume and what are the 5 types? |
-1% -Granulocytes: Neutrophils, basophils, eosinophils -Agranulocytes: Lymphocytes (t&b cells), monocytes |
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Leukopoiesis |
production of WBCs stimulated by colony stimulated factors released by macrophages and T-cells |
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Tell me 5 things about Neutrophils |
-Granulocyte -Most abundant leukocyte -First responder to tissue damage -immature ones called "bands" or "scabs" -Increase (aka left shift) indicates a bacterial infection (aka Neutrophilia)
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Tell me 4 things about Basophils |
-Granulocyte -becomes a "mast cell" after migrating into tissue to phagocotize -releases histamine and heparin -involved in vasodilation |
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Tell me 4 things about Eosinophils |
-Granulocyte -increased amounts response to Type 1 allergic reaction -release histamine -activates IgE for allergic reaction |
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Tell me 5 things about Lymphocytes |
-Agranulocyte -B-cells: humoral immunity -T-cells: cell mediated immunity -Activated by macrophages and other T-cells -increased (right shift) indicates viral or fungal infection (aka lymphocytosis) |
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Tell me 2 things about Monocytes |
-Agranulocyte -migrate into tissue and become marcophages to phagocytize and antigen presenting |
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Differential |
-Indicates the proportion of the specific types of WBCs in the blood -Normal: 50-70% neutrophils and 30-40% lymphocytes |
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Thrombocytes (5 key points) |
-also known as Platlets -essential for clotting -Non-nucleated fragments of megakaryoblast in bone marrow (aka NOT A CELL!!) -attach to each other, rough surfaces and foreign materal -repair small breaks in vessels |
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Hemostasis (other name, electrolyte require and process) |
-coagulation cascade -Ca+ 1. Tissue damage causes vasoconstriction and vasospasms thus inhibiting blood flow 2. Thrombocytes adhere to tissue to create platelet plug and attract coagulation factors 3. Inactive prothrombin, fibrinogen, thrombocytes and RBCs form clot |
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Intrinsic pathway |
coagulation cascade activated by endothelial injury in blood vessels -check aPTT due to heparin |
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Extrinsic pathway |
coagulation cascade activated by tissue and platelet injury -check PT/INR due to coumadin |
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Hemophilia Classic A indicates the deficiency of which Factor? |
VIII |
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Prothrombin is activated by which Vitamin and what does it change into? |
-Vitamin K turns into thrombin (sticky tar'ish stuff) |
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Fibrinogen turns into... |
Fibrin |
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Where are prothrombin and fibrinogen made? |
made in the liver, so if patient has liver problem they can have bleeding problems |
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PT/INR |
-Prothrombin time is the amount of time it takes prothrombin to turn into thrombin -should be 1.0 -Want to check this on someone taking Coumadin (vit K antidote) |
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aPTT |
-Partially activated thromboplastin time -Want to check this on someone taking Hepatrin |
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Thrombolytic drugs are also known as |
clot busters |
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Universal donors have which type of blood? |
O negative |
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Universal Recipients have which type of blood? |
AB+ |
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What is PRBC and who usually gets it? |
-Packed Red blood cells -common for anemia |
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What blood product do patients usually get for thrombocytopenia or bleeding disorders? |
Packed platelets |
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Which blood product can be given without concern for Type II cytotoxic reaction? |
Colloid Expander (contain albumin) |
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What type of blood products are Procrit and Eprex, what does it do and how is it given? |
-Epotin alfa: stimulate bone marrow to increase RBC production -given SubQ |
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What is pancytopenia and what is an example? |
-systemic bone marrow suppression (reduction in RBCs, WBCs and platelets) Ex) Aplastic anemia's |
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Bone marrow transplants are given to those with... |
Severe immunodeficiencies or pancytopenia |
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Lymphatic system consists of: |
1. Vessels 2. Nodes (immune systems surveillance system) 3. tonsils 4. Thalamus 5. Spleen (left upper quad) 6. Bone marrow |
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Lymphatic fluid |
similar to plasma but higher % of lymphocytes |
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3 Functions of the Lymph system: |
1. Return 1-2% of interstital fluid back to blood after going thru nodes or spleen 2. Capture unwanted material 3. Monitors for foreign material and initiates immune response as needed |
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The 3 blood Dyscrasias: |
1. Anemias 3. Blood clotting disorders 4. Myelodysplasia syndromes
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What is going on with Anemias, what are normal RBC levels and what are the symptoms if low? |
-reduction in O2 carrying capacity of blood = cellular hypoxia -women: 12-14 -men: 14-16 -CNS irritability, decreased energy, metabolism, reproduction, Erythropoiesis, tachycardia, peripheral vasoconstriction, decreased GI regeneration |
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Erythropoiesis |
-cellular hypoxia compensation mechanism leading to renal excretion of erythropoietin -this then stimulates the bone marrow to increase RBC production and leads to the release of immature RBCs (aka increased reticulocyte count) |
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Tachycardia and peripheral vasoconstirction lead to: |
SOB, exercise intolerance, cool skin |
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decreased GI regeneration causes: |
1. Stomatitis 2. chapped lips 3. dysphagia 4. brittle hair/nails |
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CBC includes which 5 things? |
1. WBC count 2. Hgb, 3. Hct 4. Platelet 5. measure of corpuscular RBC morphology |
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-Chromic refers to the: |
-hemoglobin (aka iron) content in blood -Hypochromic: low Hgb -Normachromic: normal Hgb
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-Cytic refers to the: |
-size of cell -Microcytic - small cell suggesting low Hgb -Macrocytic - large cell suggesting an RBC production error |
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what is MCV and what does it tell us? |
- mean corpuscular volume tells us our RBCs oxygen carrying capasity |
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What is MCHC? |
-mean corpuscular hemoglobin content |
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RDW |
-reticulocyte distribution width -Increased RDW = anisocytosis
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The 4 Types of Anemia |
1. Iron deficiency 2. Pernicious 3. aplastic 4. hemolytic (sickle cell, Thalassemia, polycythemia) |
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Iron Defiency anemia (Patho, CBC, Causes, S/sx) |
Patho: lack of Fe+ impedes production of RBCs CBC: hypochromic, microcytic, decreased Hgb, MCV, MCHC (RDW unaffected) Causes: diet lacking green veg/red meat, chronic blood loss, bad duodenal absorption of Fe+, liver dz S/Sx: regular anemia s/sx, stomatitis, amenrrhea, delayed healing |
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Pernicious Anemia aka megaloblastic anemia (patho, CBC, causes, s/sx) |
Patho: malabsorption of B-12 that is needed for RBC production in bone marrow CBC: macrocytic reticuloctes, increased RDW Causes: diet (rare), destroyed parietal cells due to autoimmune reaction or chronic gastritis (alcoholics), gastroectomy due to surgery S/sx: macroglossia, acholorhydria. ataxia, tingling, burning due to peripheral demylination
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Pernicious anemia diagnosis and tx |
Diagnosis tests: achlorhydria (decreased production of HCL confirms diagnosis), large megaloblastic cells, decreased b-12 Tx: B-12 injection, oral for prophylaxis only, cannot treat with oral supplement |
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Aplastic Anemia aka pantocytopenia (patho, CBC, cuases, S/sx, Tx) |
Patho: impairment of bone marrow leading to lack of stem cells to make RBCs, WBCs, platelets CBC: neutorphilia, MCV, Hgb/Hct/Plt all low Causes: idiopathic (most common), myelotoxins, SLE (autoimmune dz), Fanconi's (hereditary dz) S/sx: regular anemia s/sx, leukopenia, opportunitic infections, thrombocytopenia Tx: tx underlying causes, bone marrow trans |
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Hemolytic Anemias (3 types, patho, causes) |
Include Sickle cell, thalassemia, polycythemia Patho: excessive hemolysis Causes: genetic, neoplastic, cytotoxic immune reaction, toxins, malaria |
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Sickle cell anemia (causes, fact, s/sx, diagnosis, tx) |
Causes: HgS gene inherited from parents as homoxygous recessive. needs to be from both parents for abnormal Hgb (african/middle eastern) Fact:inherit from one parent (heterozygous) its protective against malaria S/sx: regular anemia s/sx, hyperbilirubinemia, splenomegaly, vascular occlusions causing sickle cell crisis, growth/development delays, CHF Diagnosis: hemoglobin eletophoresis, DNA test for HgS Tx: hydrea, avoid high altitudes/infections/stress, prophylactic meds, 20 year life expectancy |
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Thalassemia (causes, s/sx, CBC, tx) |
Causes: genetic defect where one or more genes of globin (protein portion of Hgb) are variant/ missing = premature destruction of RBCs S/sx: reg anemia s/sx, hyperbilirubinemia, hyperactive bone marrow, growth retardation CBC: microcytic, hypochromic RBCs, increased erythropoietin/reticulocytes, high iron levels Tx: transfusion, iron chelation, splenectomy, survive into 30s
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More about Thalassemia |
-Thalassemia minor when only one globin unit -Thalassemia major (cooley's dz) when 2+ globin units -Named after which globin affected (alpha or beta -Alpha: seen more in Indian, Chinese, South Asian -Beta: Mediterranean |
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Polycythemia (patho, causes, CBC, S/sx, Tx) |
Patho: increased bone marrow stimulation Causes: neoplastic/idiopathic (primary/vera type), lung dz, high altitudes, increased excretion of erythorpoietin due to renal tumor (secondary) CBC:high RBC/granulocytes/platelets, low erythropoietin, hyperuricemia S/sx: high viscosity blood, increase throbocytes, cyanosis, hepatomegaly, plenomegaly, full/bounding pulse, visual probs Tx: phlebotomy, marrow suppression, meds, radiation |
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The 2 Blood Clotting disorders |
1. Hemophilia A (classic hemophilia) 2. Disseminated intravascular coagulation |
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The 3 Myelodysplasia syndroms |
1. Leukemias 2. Lymphomas 3. Multiple Myeloma |
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Hemophilia A (patho, S/sx, Diagnosis, Tx) |
Patho: genetic deficiency of clotting factor VIII (x-linked recessive trait manifested in men but carried by women) S/sx: bleeding, hemarthrosis, hematrua, hematochezia Diagnosis: prolonged PTT and aPTT Tx: blood or factor VIII transfusions
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Hemarthrosis |
hemorrhage in joint |
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Hematuria |
blood in urine |
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Hematochezia |
blood in stool |
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Disseminated intravascular coagulation |
Patho: excessive fibrinogen and throboplastin Causes: obstetric, infection, major trauma, burns S/sx: bleeding, clots, petechia, bruising, strokes, MI, vasodilation, septic shock Diagnosis: low fibrinogen, high aPTT times. very poor prognosis |
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Leukemias (patho, etiology, s/sx, diagnosis, Tx) |
Patho: very high leukocyte levels (20-40 thousand) causing lymphadenopathy Etiology: type determined by type of cell affected S/sx: infections, hemorrhage, anemia, bone pain, wt loss, enlarged lymph nodes, hepatosplenomegaly, CNS depression Diagnosis: leukocytosis, low RBC/platelets, bone marrow biopsy confirms Tx: chemo, nurtrition, bone marrow transplant
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Hodgkins Lymphoma (patho, s/sx, tx, prognosis) |
Patho: malignant T-cell proliferation in lymph nodes happens in orderly fashion S/sx: painless/non-tender nodes, splenomegaly, weight loss, night sweats, pruritus, Tx: radiation, chemo, surgery Prognosis: pretty good |
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Non-Hodkins lymphoma (patho, tx) |
patho: malignant T-cell proliferation in lymph nodes typically in intestinal/abd area (no order) Tx: radiation, chemo, surgery |
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Multiple Myeloma |
Patho: involves B-cells in older adults where malignant cells replace bone marrow S/sx: decreased immune function due to decreased B and T cell production, pain, kidney stones, clots, renal failure from hypocalcemia Tx: chemo, palliative tx, 3 year survival |
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The 4 steps of the electrical impulse in the heart |
1. SA node: pacemaker controlled by ANS and stimulated directly or by catecholomines 2. AV node: slows impulse a little to allow blood to full empty from RA to RV (location of 1,2, 3 degree heart blocks) 3. Bundle of His: splits signal an sends it to ventricles (location of BBB, IVCD) 4. Perkinje Fibers: ventricular contraction highway (apex to aorta) |
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What is happening for the P-wave and which node is involved? |
-atrial depolarization (aka contraction) -SA node |
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What is happening for the PR interval and which node is involved? |
-time between atrial and ventricular contraction - AV node |
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What is happening for QRS and what is involved? |
-Rt and Lt ventricular contraction -Bundle of His and the purkinje fibers |
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What is happening during the T-wave? |
-Ventricular repolarization -irritable time for heart so if stimulated heart is at risk for arrhythmias |
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Systole |
-ventricular contraction/close of AV valves -time between 'lubb-dupp' -only 1/3 of cycle |
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Diastole |
-ventricular relaxation/coronary prefusion -pause after 'dupp' -2/3 of cycle |
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What is Cardiac Output and what are its 2 determinants? |
Amount of blood pumped through heart in 1 min 1. Stroke Volume: mL of blood pumped by ventricle with each contraction -factors: pre/afterload 2. Heart rate: approx 5000mL/min - # of ventricular beats per min -factors: epinephrine, fever, fluid status, exercise |
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What is cardiac reserve? |
Ability for heart to increase CO when Oxygen demand increases |
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Preload and afterload |
-Ventricular stretch that facilitates myocardial contraction (want to increase) -Pressure ventricle must overcome to push blood forard (want to decrease) |
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Systemic autoregulators that will cause vasodilation (4) |
1. Acidotic tissue 2. hypoxic tissue 3. fever 4. histamine |
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Systemic autoregulators that will cause vasoconstriction (3) |
1. catecholamines 2. angiotensin 3. hypothermia |
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What is blood pressure? Systolic and Diastolic? |
-hydraulic pressure that the blood exerts against the walls of the arteries (BP = CO x PVR) S: pressure exerted during left ventricular contraction D: pressure exerted during ventricular relaxation |
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Variables that effect BP (6) |
1. Blood volume 2. viscosity 3. venous return 4. elasticity of arteries 5. rate of contractions 6. force of contractions |
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What is PVR and what might affect it? |
-Force opposing blood flow through the arteries -friction inside vessel wall, vasocontrict/dilation, blood viscosity, hormones, SNS/catecholamines |
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SNS influences on heart |
Beta 1 adrenergic receptors: stimulated by adrenal catecholamines to increase HR, force of contraction, therefor incrased CO Alpha 1 adrenergic receptors: stimulated by adrenal catecholamines cause skin/viscera/arteriole constriction to increase venous return and PVR |
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The 4 types of Cardiac disorders |
1. Heart Disorders 2. Arterial Vascular Disorders 3. Venous vascular disorders 4. Shock |
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The 7 types of Heart disorders |
1. CAD (arterio vs atherosclerosis) 2. Angina 3. MI 4. CHF (left and right) 5. Valvular defects 6. Cardiac infections/inflammations 7. Tamponade |
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The 5 types of arterial vascular disorders |
1. HTN 2. PAD 3. Thrombophlebitis obliterans 4. Raynauds 5. Aortic aneurysm |
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The 2 types of Venous vascular disorders |
1. Varicose veins 2. Thrombophlebitis |
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CAD aka Heart disease (2 types, risk factors, tx) |
Arteriosclerosis: normal degeneration of arteries Atherosclerosis: formation of atheroma (lipid filled plaques) causing narrowing of arteries Risk factors: SMOKING, age, gender, genetics, bad nutrition, DM, sedentary lifesyle Tx: stop smoking, lower cholesterol, meds, decrease Na+ angioplasty, CABG |
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Angina (Patho, causes, s/sx, types) |
Patho: heart attempting to compensate for ishcemia but usually atherosclerosis present so vessels unable to dilate normally thus causing oxygen deprivation Causes: the sclerosis's, Prinz-metal, anemias, tachy, resp dz, HTN S/sx: CP triggered by emotional/physical stress Types: Stable, Variant, Unstable |
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Major cause, patho and the 3 Etiologies of MI |
Cause: atherosclerosis ischemia Patho: ischemia -> inflammation -> necrosis -> scarring -> decreased CO -> CHF 1. Thrombus build up forms anetheroma causing arteries to be blocked (stable angina early warning sign) 2. Vasospasm 3. Embolus (broken off thrombus) |
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Pain in MI (type, description, DM, women) |
Pain: sudden substernal CP that may radiate into jaw, arm, shoulder Described as: crushing, heavy, dull Diabetics: may just feel like indigestion Women: typically have atypical symptoms thus harder to catch early |
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MI diagnosis |
EKG ST elevation helps to diagnosis occluded arteries (stemi vs. nstemi) STEMI: ST elevation - EKG abnormal, patient goes strait to cath lab NSTEMI: Non-ST elevation, EKG normal but elevated enzymes indicate damage (CK-MG, Toponin-1), Na+/K abnormal, leukocytosis, low grade fever |
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MI Mortality and complications |
Mortality: 30-40% in first year after Complications: Arrhythmias (major cause of death for few hours after MI), heart block, ventricular irritability, CHF, ventricular aneurysm, thromboembolism Tx: MONA, meds, surgery, pacemaker |
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What does MONA stand for and what is it given for? |
Morphine, Oxygen, Nitrages, Asprin -MI |
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Normal sinus rhythm, low, high? |
NSR: 60-100 BPM Sinus Bradycardia: <60 BPM (could be athlete, due to Vagal stimulation) Sinus tachycardia: >100 BPM (due to exercise, SNS stimulation, hypovolemia, fever) |
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Tell me about Sinus node abnormalities? |
-The P-wave is affected causing atrial conduction delays |
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Premature atrial contractions (type, patho) |
Type: arryhthmia/dysrhythmia Patho: early impulse generates beat causing to be slightly off but no serious issue -often lack P-wave |
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Atrial Flutter (type, other name, patho, risk) |
Type: arrhythmias/dysrhythmias Other name: saw tooth Patho: more than one P-wave for every QRS complex (2:1 or 3:1 ratio) Risk: tachycardia
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Atrial Fibrilation (type, patho, risk) |
Type: arrhythmia/dyshythmia Patho: abnormal/irregular P-wave and HR RIsk: clots |
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AV blocks (Type, patho, 3 degress) |
Type: arryhthmia/dyshythmia Patho: PR internal delay causing delay at the AV node or bundle of his First degree: fixed, prolonged PR interval second degree: PR elongates with each beat, then resets and starts to elongate again Third: no communication between P and QRS (also knows as a COMPLETE HEART block) |
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Bundle Branch Block (type, patho) |
Type: arrhythmia/dysrhythmia patho: bundle branch conduction interference - no change in CO but QRS widens because ventricles don't contract together |
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V-Tach (type, patho, nurse, risk) |
Type: arrhythmia/dysrhythmia Patho: no atrial coordination with ventricular rate of 100-150 (no SV = no CO) Nurse: SHOCKABLE only if patient is pulseless risk: if cardiac ischemia occurs this will lead to Vfib |
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V-Fib (type, patho, nurse) |
type: arrhythmia/dysrhythmia Patho: quivering of ventricles with no coordination Nurse: ALWAYS pulseless so always SHOCKABLE |
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Premature ventricular contractions (type, risk) |
Type: arrhythmia/dysrhythmia Risk: typically don't affect CO but frequent can cause ischemia or Vfib |
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Asystole aka Cardiac arrest (type, patho, nurse, causes) |
Type: arrhythmia/dysrhythmia Patho: no contraction Nurse: total flatline so not shockable Causes: drugs, acidosis, vagal stimulation |
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CHF (patho, etiology, compensation, s/sx) |
patho: heart unable to pump enough blood to supply the bodies demands etiology: usually a secondary condition to CAD, HTN, MMI, heart defects Compensation: heart wants to maintain CO but this ends up being even more damaging (aka a positive feedback loop) S/sx: decrased bf to organs, exercise/cold intolerance, cool extremites, daytime oliguria |
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The vicious cycle of CHF (5 steps) |
1. decreased CO 2. increased SNS and RAAS (Epi/nori and Na+/H20 retention) 3. Increased PVR and Fluid retention (vasoconstrict/BP) 4. Increased LV Afterload and LV overstretch (starlings law) 5. thus decreasing CO agian |
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Left CHF (patho, etiology, S/sx) |
Patho: traffic jam from increased pressure downstream from ventricle Etiology: high pressure/afterload against left ventricle, HTN, MI, faulty aortic valve S/sx: Pulmonary edema from congestion, paroxysmal nocturnal dyspnea, rales/crackles |
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Steps of Left CHF (5) |
1. left ventricle weakens and cannot empty 2. decreased CO to system 3. decreased renal BF stimulates RAAS 4. backup of blood into pulmonary vein 5. high pressure in pulmonary capillaries leading to pulmonary congestion and edema |
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Right CHF |
Patho: in combo with Left CHF etiology: high pressure/afterload against right ventricle, lung dz, faulty pulmonic valve Sx: systemic edema from congestion
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Steps of Right CHF (6) |
1. right ventricle weakens and cannot empty 2. decreased CO to system 3. decreased renal BF stimulates RAAS 4. backup of blood into systemic circulation (vena cavea) 5. increased venous pressure results in systemic edema 6. venous pressure causes JVD and cerebral edema |
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Stenosis |
patho: valve damage causing turbulent blood flow while open (make grunting/squirt sound)
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Incompetent valave |
Patho: valves don't close properly allowing for backflow when valve supposed to be closed |
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Rheumatic Fever (patho and S/sx) |
Patho: group A hemolytic strep infection after acute strep, bronchitis, tonsillitis resulting in systemic inflammatory condition where Ag-Ab complexes being made and deposited into tissue (especially endocardium) resulting in an autoimmune thing where complement causes valve damage s/sx: leukocytosis, nodules on small joints, basal nuclei in brain, ticks |
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Rheumatic heart dz (patho, s/sx, nurse) |
patho: chronic phase of rheumatic fever due to valaves not being able to heal S/sx: heart murmer and valve defects Nurse: prophaylactic antibiotics prior to dental work and/or valve required |
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Endocarditis (patho and 2 types) |
patho: blood-borne pathogen on endocardium causing damage Etiology: surgery, abnormal valves, bad immune Subacute: invasion by low grade organism (intermittent onset of symptoms) Acute: invasion by high grade organism (sudden onset of symptoms |
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Pericarditis (patho and 2 types) |
patho: inflammation of pericardium Acute: from surger, Rheumatic fever, SLE, cancer, viral infection resulting in rough and sticky pericardial sac causing effision and friction rubs Chronic: from chemo, TB, liver/kidney dz causing fibrinous pericardium that limits movement of heart |
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Arterial diseases (5) |
1. HTN 2. PVD/PAD 3. Thromboangitis obliterans (buergers dz) 4. raynaud's 5. aortic anerursm |
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HTN (patho, facts, s/sx, 3 types) |
Patho: artery diameter decreases which increases LV afterload and thus heart strain Fact: 1/3 of adult population (more in men before 55, then more women) S/sx: insidious 1. Essential - most common (idiopathic) 2. Secondary - from renal/endocrine dz, pheocromocytoma 3. Malignant - uncontrollable and rapid progression |
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PVD/PAD (patho, etiology, s/sx) |
Patho: partial/total arterial occlusion impair muscle and sensory function or infarction of distal extremity Etiology: smoking, DM, HTM S/sx: neuropathy, necrosis, skin ulvers, gangrene of extremities, hard toe nails, decreased hair on extremity |
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THromboangitis obliterans aka Buerger's dz (patho, etiology, s/sx, tx) |
patho: imflammation in med/small arteries of arms and legs leading to vascular occlusion of extremity Etiology: before 35, men, Jewish, Japanese, Indian descent, SMOKING S/sx: pain, ulcer on limb, gangrene Tx: amputation |
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Aortic Anerurysm (patho, etiology, s/sx) |
patho: bulge in arterial wall causing embolus that eventually ruptures resulting in massive internal bleeding etiology: HTN, CAD, syphilis, TB, trauma S/sx: asymptomatic, often discovered on accident in CXR |
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Varicose veins (patho, etiology, s/sx, tx) |
patho: blood pools causing stretching and contorted veins etiology: in legs from crossing legs, restrictive closing on waste, genetic, standing a lot S/sx: edema with shiny skin and visible veins tx: ted hoes, elevation, avoid restritive clothes |
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Shock |
patho: severe hypotension when patient unable to maintain a BP and therefor tissue perfusion many times resulting in multisystem organ failure |
