Pathophysiology Exam 3 with more Questions and Answers Graded A

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Diabetes Mellitus (DM) - ANSWER Systemic metabolic disorder in which there is chronic hyperglycemia (high blood sugar over years) Insulin does what to blood sugar? - ANSWER Lowers Eating carbohy ... drates does what to blood sugar? - ANSWER Raises Diabetes Mellitus is due to: - ANSWER -a decrease in production and secretion of insulin (type 1) -a decrease in the cells ability to utilize the insulin (type 2) Insulin deficiency results in impaired use of: - ANSWER CHO, fats, proteins Chronic hyperglycemia causes ___________ ______________ in the vasculature of many organs - ANSWER Structural abnormalities ____ to _____ million Americans have DM. - ANSWER 12 to 15 million There is high incidence of DM in: Low incidence in: - ANSWER -Blacks, Hispanics, American Indians -Japanese Insulin is produced by pancreas ______ cells of the islets of Langerhans - ANSWER beta Insulin acts like a _____, opening up cells so they can take in sugar and use it as an energy source - ANSWER key Insulin attaches and stimulates ____________. Glucose then enters cell by ____________ _______________. - ANSWER GLUT 4; facilitated diffusion Type I (Insulin dependent diabetes mellitus) - Juvenile onset - Etiology/Pathophysiology - ANSWER -10% of diabetes -onset usually before age 30 -etiology is probably multifactorial -theory that beta cells are destroyed by an inappropriate autoimmune response -inherited susceptibility (hereditary cause) -viruses possibly trigger immune response/cause inflammation -LITTLE OR NO PRODUCTION OF INSULIN Type II (non-insulin dependent diabetes mellitus) - adult onset - Etiology/Pathophysiology - ANSWER -85-90% of diabetes -onset usually after age 30 (but this trend is changing) -etiology is multifactorial -resistance to insulin or a decrease in number of receptors is present -obese at onset Type I (IDDM, Juvenile onset) - Clinical Manifestations - ANSWER *Related to osmotic action of glucose in blood -Polyuria: (increased urine output), high blood sugar pulls fluid into vasculature -Polydipsia: (thirst in the hypothalamus), high osmolarity stimulates *Related to cellular starvation -Polyphagia: (increased hunger) -Weight loss - fats and proteins broken down (lipolysis, proteinolysis) and used for energy (gluconeogenesis) -weakness/fatigue - poor use of food products Gluconeogenesis - ANSWER -formation of new glucose for new energy -the liver makes glycogen from fats/proteins (that were just broken down by lypolysis, proteinolysis) Type II (NIDDM, Adult onset) - Clinical Manifestations - ANSWER -Polyuria -Polydipsia -Polyphagia -Weakness/fatigue -may be asymptomatic Diagnosis of DM - ANSWER -high fasting blood sugar -presence of islet cell antibodies -Hgb A1C test for glycosolated hemoglobin: average amount of glucose hemoglobin has bound to over time -glucose tolerance test Criteria for Good Control - ANSWER -maintain optimal weight and in good health -glycosylated hgb <7% -fasting blood sugar under 140mg/dl -postprandial blood sugar no higher than 180mg/dl Diabetic Ketoacidosis (Diabetic Coma) - ANSWER Extreme hyperglycemia of 300 to 800mg/dl with ketonuria Diabetic Ketoacidosis Etiology: - ANSWER -not enough insulin -illnesses -psychologic stress Diabetic Ketoacidosis Pathophysiology: - ANSWER -marked decrease in insulin (causes decreased glucose transport into cells) -the body senses this lack of cellular fuel/glucose (but still high in the bloodstream) (causes glycogenolysis and gluconeogenesis - makes BS higher so makes things worse) -the high BS leads to osmotic diuresis (causes dehydration, polyuria, polydipsia) -increased lipolysis (breaking down lipids) leads to ketone production and accumulation, then ketonuria (ketones in urine) and acidosis, then ketone acids excreted by lungs (breathe hard, deep, fast) -acidosis (hyperkalemia) -increased proteinolysis and lypolysis (increase in gluconeogenesis) Diabetic Ketoacidosis clinical manifestations: - ANSWER -hyperglycemia -ketonuria -polyuria, polydipsia, polyphagia -nausea, vomiting, abdominal pain -Kussmaul's respirations (fast, hard, deep) -fluid loss (can lead to hypotension, tachycardia, shock, cardiac arrhythmias) Diabetic Ketoacidosis treatment: - ANSWER -give insulin -correct fluid and electrolyte imbalance -correct the cause Hypoglycemia (insulin reaction) - ANSWER Blood sugar levels less than 60mg/dl (very low BS) -often called insulin reaction/shock Hypoglycemia etiologies: - ANSWER -overdose of insulin -inadequate food intake -increased amounts of exercise Hypoglycemia clinical manifestations: - ANSWER -neurologic reaction when the hypothalamus senses decreased glucose levels (brain can't store glucose, so it is affected immediately) -increased HR, RR -diaphoresis, pallor, tremors, cool skin -cellular malnutrition (mostly brain) -headache, dizziniess, irritability, confusion, fatigue -vision changes, hunger, seizures, coma Hypoglycemia treatment: - ANSWER -give glucose -correct fluid and electrolyte imbalances -correct the cause Chronic Diabetic complications: - ANSWER -macrovascular degenerative disease -microvascular disease (degenerative changes) -neuropathy -infection Acute Diabetic complications: - ANSWER -Diabetic Ketoacidosis (Diabetic Coma) -hypoglycemia (insulin reaction) Macrovascular degenerative disease (changes) - ANSWER Probably related to: -lypolysis (leads to) -hyperlipidemia (leads to) -atherosclerosis (leads to) -CAD/PVD/CVA Microvascular disease (degenerative changes) - ANSWER Affects the capillary 1. Glycosolation of proteins/collagen leads to formation and deposits of advanced glycosolation end products in vessel walls 2. Protein kinase C (enzyme) is activated (inappropriately) by high BS SOO... Both 1&2 lead to vascular cell proliferation and thickens the basement membrane -vascular cell proliferation thickens basement membrane of capillaries - leads to decreased perfusion, hypoxia, ischemia Microvascular disease major places affected: - ANSWER -kidneys (nephropathy, renal failure) -retina (Diabetic retinopathy) 1/4 new cases of blindness are related -also affects extremities Neuropathy Etiology: - ANSWER Related to Microvascular disease: -vascular ischemia leads to nerve endings being destroyed in ischemic areas Neuropathy clinical manifestations: - ANSWER Peripheral: -pain and tingling in extremities (paresthesia) -decreased sensation Autonomic nervous system: -gastroparesis (slow GI) -neurogenic bladder -sexual dysfunction -CV - no, HR variability Infection - ANSWER Poor wound healing -glucose is a good media for growth, so bloodstream with lots of glucose is a good location for bacteria to grow -decreased sensation decreases possible prevention -hypoxia/ischemia causes poor wound healing Gene - ANSWER -fundamental unit of information storage -blueprints of protein synthesis Deoxyribonucleic acid (DNA) - ANSWER -where genetic information is stored -genes are composed of DNA sections DNA backbone is composed of? - ANSWER Alternating sugar and phosphoric acid DNA center portions are? - ANSWER Nitrogenous base pairs that carry genetic information Purines center portions: - ANSWER Adenine, Guanine Pyrimadines center portions: - ANSWER Thymine, Cytosine Adenine always pairs with: - ANSWER Thymine Guanine always pairs with: - ANSWER Cytosine DNA is located inside the _____________, therefore, each _____________ can have thousands of genes. - ANSWER Chromosomes, chromosome Somatic cells: - ANSWER -non sex cells -46 chromosomes Gametes: - ANSWER -sex cells (sperm, ova cells) -23 chromosomes - one member of each chromosome pair ____________ connects the base pairs at the middle. - ANSWER Hydrogen Genetic mutations - ANSWER An error in duplication of DNA (can be accidental or inherited) Most common type of genetic mutations? - ANSWER Single gene disorders Base pair substitution: - ANSWER A different pair is substituted for the normal pair in the DNA Frameshift mutation - ANSWER Either insertion or deletion of one or more base pairs in the DNA Genotype - ANSWER Describes the genetic constitution of an individual (hereditary information) Phenotype - ANSWER The measurable expression of genes in a person (what we see, what is observed) Chromosomes are found in pairs in ____________ cells with matching genes - ANSWER Somatic Alleles - ANSWER Alternative forms of a gene at a given place on the pair of chromosomes that controls a specific trait; they are inherited genetic coding for that particular trait; two alleles per gene, one from each parent Homozygous - ANSWER Two identical alleles for the trait Heterozygous - ANSWER Two different alleles for the trait Dominant traits - ANSWER Only one allele is needed to express the trait; dominant alleles mask recessive alleles (if present) Recessive traits - ANSWER Two identical alleles for the trait must be present to be expressed (exception is male offspring in x-linked recessive inheritance) -a recessive trait(allele) can be hidden ("unaffected carrier") if heterozygous The formal laws of inheritance - ANSWER -autosomal dominant -autosomal recessive -x-linked dominant -x-linked recessive Autosomal dominant - ANSWER Abnormal allele is dominant (the one causing disease) -ex: Huntington's disease Autosomal dominant characteristics - ANSWER -males=females -no skipping of generations -affected heterozygous individuals have a 50% chance to transmit the trait to each offspring Autosomal recessive - ANSWER Abnormal allele is recessive, so needs 2 to be expressed (tt) -having 1 makes you an "unaffected carrier" of the trait (Tt) -ex: cystic fibrosis Autosomal recessive characteristics: - ANSWER -males=females -usually skips a generation -both parents of an affected child are carriers, usually X-linked inheritance - ANSWER Not everyone gets two x chromosomes -females: two x (one from mom, one from dad) -males: one x (always from mother) If only one allele present (one x chromosome), then that is what is expressed (regardless of dominant or recessive) Of the 23 pairs of chromosomes that make up the karyotype of an individual, 22 are __________, one pair is _____ _____________. - ANSWER Autosomes; sex chromosomes X-linked male offspring - ANSWER Mom donates her x (2 t's); dad does not contribute (use 0) X-linked female offspring - ANSWER Mom donates her x (2 t's); dad donates his x (1 t) X-linked dominant characteristics - ANSWER -males=females -on males, traits (the one allele present) are expressed as phenotype -usually, affected dad's have unaffected sons, but affected daughters -heterozygous moms have a 50% chance of transmitting the trait to each daughter or son X-linked dominant example - ANSWER Polydactyly X-linked recessive examples - ANSWER Color blindness, muscular dystrophy, hemophilia A, hemophilia B X-linked recessive characteristics - ANSWER -males>females -affected dads cannot transmit to sons, but transmit to ALL daughters -sons of mom carriers have a 50% chance of being affected -daughters of mom carriers have a 50% chance of being carriers Chromosome disorders - ANSWER -may be either numeric or structural -may affect either autosomes or sex chromosomes Numerical abberations (disorders) - ANSWER Loss or gain of chromosome sets Nondisjunction - ANSWER The failure of one or more pairs of chromosomes to separate and segregate during meiotic division; so both chromosomes end up in one daughter cell and none in the other Trisomy 21 - ANSWER Down syndrome -3 chromosomes in a daughter cell; nondisjunction on chromosome 21 Trisomy 21 risk - ANSWER -1 in 700 live births -increased with maternal age -20-30% of paternal origin Sex chromosome aberrations: - ANSWER -Turner's syndrome -Klinefelter syndrome Turner's syndrome - ANSWER 45 chromosomes, XO- one x chromosome, (female phenotype) but are infertile, hypogonadism present -1 in 2500 female births Klinefelter's syndrome - ANSWER 47 chromosomes, XXY (male phenotype) female body traits, infertility -1 in 1000 male births Multifactorial inheritance - ANSWER More than one genetic factor is involved (polygenic); also many times environmental factors are involved -ex: intelligence, cleft lip/palate, obesity Molecular tests: - ANSWER Study small genes/ short lengths of DNA Chromosomal tests: - ANSWER Analyze whole chromosomes/ long lengths of DNA Biochemical tests: - ANSWER Study proteins activity or amount Teratogens - ANSWER An agent that acts on the fetus causing genetic abnormalities -infections, diseases (DB, CMV, Rubella) -alcohol -smoking -radiation There are never any "unaffected carriers" with? - ANSWER Autosomal dominant Girls are more likely than boys to be affected with the disorder in? - ANSWER X-linked recessive Arteries - ANSWER -elastic (constrict and dilate) -maintain BP and perfusion (deliver O2 and nutrients) Veins - ANSWER -can stretch, but not as elastic -adequate "venous return" requires valves and muscles Factors affecting blood flow: - ANSWER -pressure -resistance -viscosity Clots forming in the heart (with afib) travel to? - ANSWER Brain Clots forming in veins (calves) travel to? - ANSWER Lungs Which is more common? Venous or arterial thrombosis? - ANSWER Venous thrombosis (r/t less flow than in artery) Thrombus - ANSWER A clot Thrombosis - ANSWER A thrombus occludes a vessel Embolus - ANSWER A foreign object that circulates Arterial thromboembolism - ANSWER Acute blockage of artery Arterial thromboembolism Etiology: - ANSWER -atherosclerotic disease -stimulation of coagulation system (irritation, trauma, inflammation, stasis (immobility, afib)) Arterial thromboembolism clinical manifestations - ANSWER R/t ischemia (not enough O2) -pain (cramping, squeezing; during or after exercise; relieved by rest) -diminished pulses -pallor, cyanosis -cool extremities -tissue death Venous thrombosis - ANSWER Thrombus formation in a vein -thrombus range from partial to complete occlusion -emboli may develop, loosen, and circulate Venous thrombosis Etiology: - ANSWER -inflammation/infection -trauma -stasis (immobility, afib) -hypercoagulability -incompetent valves -poor muscle contraction -aging Severity of venous thrombosis is related to 2 things: - ANSWER 1. Degree of obstruction 2. Degree that collateral circulation can compensate When collateral circulation compensates (venous thrombosis): - ANSWER There is near-normal venous return When collateral circulation cannot compensate (venous thrombosis): - ANSWER -increased venous pressure in distal veins (then) -distention of veins (then) -congestion/pressure changes (then) -edema/damaged venules Thrombophlebitis - ANSWER Venous thrombosis with inflammation Symptoms of thrombophlebitis can occur ______ after thrombus, and usually persist _______ weeks. - ANSWER Hours; 1-3 weeks Thrombophlebitis pathophysiology: - ANSWER Inflammatory cells accumulate and cause congestion of capillaries/venules Thrombophlebitis clinical manifestations - ANSWER R/t swelling, congestion, inflammation -pain (localized tenderness) -redness/warmth -edema Chronic venous insufficiency and venous stasis - ANSWER Inadequate return over time which leads to stasis -over time will cause problems on venous AND arterial side Mechanisms that fail with chronic venous insufficiency and venous stasis - ANSWER -muscles (calf) -elastic veins -valves Chronic venous insufficiency and venous stasis pathophysiology - ANSWER -mechanisms fail (then) -venous hypertension (then) -upsets capillary fluid exchange (increased capillary hydrostatic) (then) -congestion and edema (leads to) -stasis Chronic venous insufficiency and venous stasis clinical manifestations - ANSWER -pain (dull ache, worse with legs in a dependent position or standing still, relieved with walking or leg elevation) -brawny edema -dermatitis, hyperpigmentation -poor circulation -stasis ulcers Arterial atherosclerosis occlusive disease (chronic) - ANSWER -arteriosclerosis -atherosclerosis Arteriosclerosis - ANSWER Stiffening r/t hypertension and aging (Arterial atherosclerotic occlusive disease -chronic) Atherosclerosis - ANSWER Development of calcium deposits and then plaque in arteries (Arterial atherosclerotic occlusive disease - chronic) Arterial atherosclerotic occlusive disease common sites: - ANSWER -coronary arteries -abdominal aorta -iliac/femoral arteries -carotid arteries Arterial atherosclerotic occlusive disease clinical manifestations - ANSWER Related to ischemia (occlusion leads to decreased blood flow leads to decreased perfusion) -pain (cramping, squeezing; during or after exercise; relieved by rest) -diminished pulses -pallor, cyanosis -cool extremities -tissue death -prolonged capillary refill/loss of hair -slowed nail growth/muscle weakness Three factors in the maintenance of arterial blood pressure: - ANSWER -blood volume -peripheral (systemic) vascular resistance -cardiac output (HR and stroke volume in L/min) Neural control of BP is mostly the _____________ system. - ANSWER Sympathetic (Parasympathetic controls HR) Cardiovascular control center is in the adrenal _________. - ANSWER Medulla Adrenal medulla releases SNS impulses which are: - ANSWER Norepinephrine and epinephrine SNS impulses excite ________ receptors to cause vasoconstriction. - ANSWER Alpha SNS impulses excite ________ receptors (in the heart) to cause increased HR and increased force of cardiac contraction. - ANSWER Beta1 Types of receptors responding to changes in BP - ANSWER -baroreceptors -arterial pressoreceptors -atrial receptors (volume receptors) -arterial chemoreceptors Arterial pressoreceptors - ANSWER -in aorta and carotid -sense changes in "pressure" in the major arteries -send impulses to the CV control center to decrease or increase SNS INHIBITION (will increase inhibition to decrease activity) Atrial receptors (volume receptors) - ANSWER -in vena cava and right atria -venous side (right) -sense tension (volume) in large veins How body brings low BP back up: - ANSWER -Low BP (leads to) -decrease in blood flow through major arteries and decrease in venous return (sensed by baroreceptors) (leads to) -decrease in SNS inhibition by CV control center -increased SNS response (increased HR, increased force of contraction, vasoconstriction) (leads to) -increased BP BP control by renin-angiotensin-aldosterone system - ANSWER Angiotensin II has 3 functions: 1. Stimulates adrenal cortex, which increases aldosterone into bloodstream, which increases sodium/H2O reabsorption into blood and restores blood volume and BP 2. Causes direct vasoconstriction which increases BP 3. Stimulates the posterior pituitary which increases ADH causing increased H2O reabsorption and also stimulates thirst to increase H2O intake to restore blood volume and BP Aldosterone - ANSWER Increases sodium and water reabsorption into blood Angiotensin II ___________ activity go raise blood volume and pressure. - ANSWER Increases Angiotensin II ___________ activity to lower blood volume and pressure. - ANSWER Decreases Hypertension - ANSWER Abnormal elevation of BP Hypertension types - ANSWER 1. Essential/primary (90%) - no known cause 2. Secondary (10%) - due to a known cause Risk factors in Etiology of HTN: - ANSWER Same as CAD Hypotheses of primary HTN: - ANSWER -increased blood volume -overstimulation of the sympathetic nervous system -water and sodium retention by the kidneys Example of secondary HTN: - ANSWER Renovascular disease: decreased renal perfusion, renal arteries narrowed (renal stenosis, clot) -decreased blood flow to kidneys leads to activation of receptors and the RAA HTN Pathophysiology - ANSWER -high BP causes vascular cellular proliferation and damages arterial walls -thickening of basement membrane of arteries -permanent narrowing and poor perfusion out of capillaries HTN clinical manifestations - ANSWER R/t increased pressure in arterial system and in fragile capillaries -mild to moderate may be asymptomatic or vague -advanced: -headaches, epistaxis -dizziness, unsteadiness, blurred vision -retinopathy -CAD -renal insufficiency Organs most acutely affected by HTN: - ANSWER Heart, brain, eyes, kidneys Management of HTN: - ANSWER -drug therapy -exercise -diet (low sodium) Orthostatic hypotension - ANSWER Decrease in BP upon standing -poor reflex vasoconstriction causes -symptoms: dizziness, blurred vision, fainting Shock - ANSWER Overall or generalized reduction of adequate blood flow and oxygen delivery to the tissues Hypovolemic shock - ANSWER Results from loss of circulating blood volume Hypovolemic shock etiologies - ANSWER -hemorrhage -dehydration -burns/tissue trauma Hypovolemic shock clinical manifestations - ANSWER R/t decreased perfusion and compensatory mechanisms -hypotension -tachycardia -oliguria (low urine output) because blood is shunted to organs that need it -cool/pale skin because blood is shunted to organs that need it -restlessness, altered LOC Three stages of shock - ANSWER 1. Non-progressive 2. Progressive 3. Irreversible Non-progressive stage of shock - ANSWER -initial/early phase -compensatory mechanisms are activated -adequate perfusion to tissues is maintained Progressive stage of shock - ANSWER -compensatory mechanisms are still activated -they are unable to restore BP and perfusion -start to see effects of hypoperfusion to the tissues Irreversible stage of shock - ANSWER -inadequate compensation -ischemic cell death occurs Pathophysiology of physical inactivity - ANSWER Skeletal muscles down-regulate their capacity to burn fuel -decreased capillary density -increased insulin resistance -decreased glucose transport Regular exercise cardioprotective effects change Regular exercise cardioprotective effects DECREASED with physical activity - ANSWER LDL, VLDL, BP, insulin resistance, CRP, platelet aggregation, myocardial O2 demand Regular exercise cardioprotective effects INCREASED with physical activity - ANSWER HDL, CV function, coronary blood flow Blood cells and the hematopoietic system - ANSWER Hematopoietic system - ANSWER Includes: All the blood cells and their precursors Bone marrow - hematopoiesis occurs in stem cells of red bone marrow under hormonal control of erythropoietin (released from the kidneys) to increase RBC count - proliferation, differentiation and functional ability of the initial hemocytoblast is controlled by cytokines that act as growth factors - hemocytoblast becomes RBC after 8 days Lymphoid tissue - site of blood cell maturation of some cells Other hematopoietic growth factors - ANSWER Thyroid peroxidase - antigenic determinant for b cells and t cells G-CSF - stimulates the production of WBC to reduce the risk of infection after cancer treatment - also makes premature blood cells move from the bone marrow to the blood GM-CSF - stimulates the production of WBC Functions of the blood - ANSWER Delivery system - transports O2, metabolic waste, and hormones Regulates - body heat - pH by binding or releasing H+ from hemoglobin - fluid volume Protection - coagulation (prevents excess blood loss) - WBC protect against infection Composition of blood - ANSWER Fluid tissue (type of CT) of the body After using a centrifuge blood is divided into 1. Plasma (55%) 2. Formed elements - buffy coat <1% (includes WBC and platelets) - RBC 45% Color depends on oxygenation but it is always red - the more oxygenated the brighter red pH is 7.35-7.45 /slightly alkaline Warmer than body temp (100 degrees) Plasma composition - ANSWER Water (90% of volume) - dissolved solutes (hormones, ions, gases, etc.)use water as a transport medium Proteins (10% of volume) 1. Albumin (54-60% of plasma proteins) - acts as a transport protein - maintains osmotic pressure - buffers blood 2. Globulins (38% of plasma proteins) - alpha globulins transport bilirubin and steroids - beta globulins transport iron and copper - gamma globulins are antibodies 3. Fibrinogen (7% of plasma proteins) - turns into fibrin during clotting process Erythrocytes (RBC) - ANSWER RBC- 99% of cells - no nucleus; biconcave disk (large surface area) - flexible plasma membrane to allow it to slide through capillaries - no organelles so no O2 consumption, but it does transport O2 that binds to the 4 hemoglobin iron binding sites (97%) - useful for 100-120 days but they often stay in the spleen to be engulfed by macrophages (iron is recycled, heme is degraded in bilirubin and excreted in bile, and goblin protein is metabolized for its amino acids) * Haldene effect: describes how O2 concentrations determine hemoglobins affinity for CO2 * Bohr effect: describe how CO2 and H+ affect hemoglobins affinity for O2 *Hematocrit count is the percent of RBC in the blood - 42% in women - 45% in men) Anemia (hematocrit is 30%) - ANSWER Low O2 carrying capacity 1. Insufficient number of cells - hemmoragic (rapid blood loss) - hemolytic (rupture of RBC from infecton) - aplastic (bone marrow destroyed from leukemia) - kidney disease - dietary deficiency 2. Decreased hemoglobin content - iron deficiency (creates microcytes) from malnutrition, malabsorption, or pregnancy - pernicious: B12 deficiency (intrinsic factor is needed for absorption of vitamin and DNA synthesis) 3. Abnormal hemoglobin - thalassemias (faulty globin chains) - sickle cell anemia - polycythemia (excess RBC) Polycythemia (hematocrit 70%) - ANSWER primary - caused by a tumor in the bone marrow secondary - caused by adaptive mechanism to improve O2 carrying capacity * dehydration, smoking, and high altitudes also elevate hematocrit to 70% Leukocytes (WBC) - ANSWER Move through capillary beds (diapedesis) and move through tissues using amoeboid motion Granulocytes (2/3 of WBC) - all of them are produced in the bone marrow - all of them are phagocytic - have visual granules in cytoplasm - includes neutrophils (40-70%), eosinophils (1-4%), and basophils (0-1%) Agranulocytes - lymphocytes 20-45%(produced in lymphoid tissue from other lymphocytes that were originally produced in the bone marrow) - monocytes 4-8% (produced in bone marrow) Neutrophils - ANSWER first cells to arrive stained red and blue 2X bigger than RBC Granules contain Ab 3-6 nuclei Eosinophils - ANSWER Granules contain digestive enzymes to defend against parasites and allergic reactions 2 nuclei stained red Basophil - ANSWER Stained blue 2 nuclei contain histamine, heparin, and other mediators of inflammation - similar to mast cells - involved in allergic and hypersensitive reactions Lymphocytes - ANSWER Mostly in tissues of spleen or lymph nodes large spherical nucleus T-lymphocytes: directly act against virus infected cells and tumors B-lymphocytes: activates plasma cells to produce Ab Natural killer cells Monocytes - ANSWER largest WBC U shaped nucleus Phagotizes the antigen and then presents it to the T cell Important role in chronic inflammation (cells survive for moths to years in the tissues) WBC disorders - ANSWER Leukopenia: lack of WBC due to anti cancer/ AIDS drugs Leukemia: impaired normal bone marrow function - acute (from lymphoblasts) - chronic (from myelocytes) Infectious mononucleosis: caused by Epstein bar virus; no cure but is rarely fatal Platelets - ANSWER cell fragments derived from megakaryocytes - regulated by thrombopoietin aid in coagulation (forms the platelet plug to control bleeding) lasts 10 days Hemostasis (stop bleeding) - ANSWER 1. vascular spasm- constriction of damaged blood vessels reduces blood loss 2. platelet plugging- aggregation of platelets forms a plug 3. clot formation- reinforces the platelet plug and converts the fibrinogen into fibrin via clotting cascade enabled by thrombin Bleeding disorders - ANSWER Von Willebrands disease - platelet adhesion to initiate clotting cascade is impared Thrombocytopenia - deficiency in the number of platelets Impaired liver function - inability to synthesize procoagulants due to vitamin K deficiency Hemophilia - hereditary bleeding disorder due to deficiency in factor VIII in the clotting ascade sex linked (males get it more often) - exercise can cause bleeding in joints - vitamin K deficiency can cause tendency to bleed CBC - ANSWER provides info about number of blood cells and their structural and functional characteristics - includes RBC (hematocrit and hemoglobin), WBC, and platelets *white cell differential count is the percentages of individual white blood cell types Obtaining a blood specimen - ANSWER Skin puncture- capillary blood Venipuncture- infuse Arterial puncture- never infuse Bone marrow aspiration and biopsy Transfusion - ANSWER blood loss greater than 30% can cause severe shock or death there are whole blood transfusions or packed red cells (plasma was removed and heparin is used as anticoagulant) Blood antigens aka glucoproteins - ANSWER *Located on the surface of the RBC ABO Rh - second baby can develop erythroblastosis fetalis if the mother is Rh- M, N, Duffy, Kell, Lewis, etc ABO antibodies - ANSWER A - has A antigen - has anti B B - has B antigen - has anti A AB - has A and B antigens - no antibodies making it universal recipient O - no antigens (making it universal donor) - A and B antibodies Blood pressures and disorders - ANSWER Blood flow - ANSWER Flow rate is proportional to the pressure gradient but inversely proportional to resistance *Poiseulles law - velocity of flow is proportional to the radius but inversely proportional to the length of vessel and viscosity of blood * Law of conservation of mass - volume of blood flowing in must equal the volume of blood flowing out - smaller radius has increased velocity to maintain volume of flow out but volume decreases when pressure out increases bc its a higher opposing force to overcome Blood pressure - ANSWER Pressure gradient between the beginning and end of a vessel - blood flows from high pressure to low pressure - resistance depends on blood viscosity, vessel length, and vessel radius (most impactful, especially for arterioles) - resistance is proportional to 1/r^4 Korotkoff sounds - ANSWER Heard thru a sphygmomanometer Phase 1- sounds like thud/ tap; lub sound Phase 2- sounds like swishing Phase 3- sounds are crisp and intense Phase 4- blowing sound Phase 5- sounds stop Systolic Diastolic (2/3 of cardiac cycle is spent here) - ANSWER Arterial pressure as the heart contracts Arterial pressure as the heart relaxes *Pulse pressure systolic- diastolic - high indicates decreased compliance or atherosclerosis Hypertension - ANSWER Prehypertensive - systolic 120-139 - diastolic 80-89 Hypertensive - systolic 140+ - diastolic 90+ *diabetics is 130+/ 80+ Primary "essential" hypertiension - occurs without disease - can be systolic and diastolic or selective for one ex: systolic hypertension has systolic as 140+ while diastolic is <90 Secondary hypertension - occurs with disease such as kidney Malignant hypertension - accelerated form of hypertension Systolic hypertension - systolic is 140+ while diastolic is <90 MAP - ANSWER Equation diastolic pressure + 1/3(pulse pressure) Primarily determined by radius size changes in smooth muscle (has to do with compliance as well; change in pressure divided by change in volume) - sympathetic stimulation to the arterioles - local metabolic or chemical control - hormones Pulmonary artery wedge pressure - ANSWER As the heart pressure decreases (systole), the wedge pressure increases Used to measure the pressure in - pulmonary capillary bed - left atrium - left ventricle during diastole * normally it is 8mmHg opposing 25mmHg BP - ANSWER COxTPR *CO= HRxSV SV - ANSWER Preload - determined by how much the heart can stretch while filling (during end diastole) with venous return - increased with hypervolemia, cardiac valve disease and heart failure Aferload - resistance to flow aka the peripheral resistance the heart has to pump against during sytole - increased in hypertension and vasoconstriction *atherosclerosis occurs with decreased compliance due to decreased diameter (ability to stretch) * Frank starling Law - increased end diastole increases contractility resulting in increased stroke volume - increased contractility is caused by sympathetic nerve stimulation from the sympathetic trunk and increases blood flow return to the right atria * parasympathetic (vagus nerve) and sympathetic stimulation come from the medulla Resistance - ANSWER Arterial side provides most resistance bc of low capacity (30%) - small changes in volume result in large changes in pressure Venous side has high capacity (70%) - increased contraction (systole) increases blood flow return to the right atria thus increasing preload and thus cardiac output Short term control of blood pressure - ANSWER Baroreceptors sense change in BP Long term control of blood pressure - ANSWER renal compensatory mechanisms - high BP causes release of atrial natriuretic peptide to increase sodium and water loss - low BP causes release of ADH Disorders of blood flow in systemic circulation - ANSWER Endothelail cells - ANSWER -controls the transfer of molecules - controls clotting - regulates blood flow and vascular resistance - metabolism of hormones - regulates immune and inflammatory reactions - influences the growth of other cell types *these functions are altered when there are -products that cause inflammation (cytokines, bacteria, virsus) - hemodynamic stresses - lipids (fats) - hypoxia Lipoproteins - ANSWER Chylomicrons very low density lipoproteins - carries large amounts of triglycerides intermediate density lipoproteins low desity lipoproteins - main carrier of cholesterol high density lipoproteins (good kind) - 50% of protein *genetic abnormality can cause elevated levels without any dietary influence Hypercholesteremia - ANSWER Serum cholesterol levels -240+ Primary - occurs independant of other health problems/ lifestyle Secondary - occurs with other health problems and behaviors Atherosclerosis - ANSWER Deposition of fatty plaque in the arteries Manifestations - fatty streaks (flat, yellow discoloration that progressively enlarges - fibrous atheromatous plaque (formation of scar tissue) - complicated lesions (contain hemorrhage, ulceration and scar tissue) Risk factors for atherosclerosis - ANSWER hypercholesterolemia smoking hypertension CHD family history 45+y/o men or 55+ y/o women HDL cholesterol level <40 CRP (C reactive (inflammation) protein) levels greater than 3 (10 may indicate a passing infection so you should retest in 6 weeks) Major complications of atherosclerosis - ANSWER MI - narrowing of vessels resulting in ischemia stroke peripheral vascular disease clinical manifestations of atherosclerosis - vessel obstruction due to plaque accumulation which can rupture resulting in clot formation that further blocks the artery and may become mobile (emboli) Aneurysms Types - berry (spherical vessel dilation) * found most often in the circle of Willis in the brain - saccular and fusiform (football shape) * often found in the thoracic or abdominal aorta; characterized by gradual enlargement of the aorta -dissecting (worst kind) * acute life-threatening condition that involves hemorrhage into the vessel wall with longitudinal tearing of the vessel wall to form a blood filled channel Signs of acute arterial occlusion - ANSWER pain paresthesia (tingling, pricking or burning sensation) motor weakenss distal to the site of occlusion loss of peripheral pulse cool skin cyanosis or pallor distal to the obstruction site Vesculitides used interchangable with angiitis and arteritis - ANSWER Inflammation of blood vessels Classes Group 1 - systemic necrotizing Group 2 - hypersensitivity Group 3 - giant cell arteritis Group 4 - miscellaneous Arterial disease of the extremities - ANSWER atherosclerotic occlusive disease - sudden occlusion of arterial flow to affected tissues of organ thromboangiitis obliterans - inflammatory arterial disorder that causes thrombus formation raynaud disease and phenomenon - intense arterial vasospasm in the fingers and toes Seven Ps of arterial embolism - ANSWER 1. Pistol shot (acute onset) 2. pallor 3. polar (cold) 4. pulselessness 5. pain 6. paresthesia 7. paralysis Venous circulation - ANSWER Veins have unidirectional valves - veins are also thin walled Disorders - vericose veins (primary is superficial while secondary is deep) - thrombophlebitis (clot that blocks a vein; DVT) Virchows triad (associated with thrombosis) - ANSWER 1. Stasis of blood (abnormal blood flow) ´Bed rest ´Immobility ´Spinal cord injury ´Acute myocardial infarction ´Congestive heart failure ´Shock ´Venous obstruction 2. Increased coagulability 3. Vessel wall injury (endothelial injury) Venous insufficiency - ANSWER Caused by DVT - causes deformity of valve laflets Valvular incompetence - loss of unidirectional flow Combination of both conditions - stasis dermatitis - venous ulcers [Show More]

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