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NRSG 2300 (2)
Midterm

PP Exam 2.docx

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Department
Nursing
Course
NRSG 2300
Professor
Stephan Wood
Semester
Fall

Description
Exam 2 Study Guide • Blood o Specialized fluid that carries oxygen, 2, nutrients, hormones, water, proteins and a variety of cells for use by the tissues o Approx. 5.5 L in average human o 60,000 miles of blood vessels o Water ~ 92% ~ 8 % dissolved solutes • Functions of blood o Delivery of substances needed for cellular metabolism o Removal of the waste products of cellular metabolism: urea, CO2 o Defense against antigens and injury o Maintenance of Acid/Base balance • Constituents o Plasma: contains water, electrolytes, proteins, gases, carbohydrates, lipids  Albumin: class of proteins, made in liver • 60% of plasma proteins • globular, spherical protein • ionized • carries negative charge: primary job is to carry things around (hormones, drugs, electrolytes) • secondary job is to create oncotic pressure • low levels o hypoalbuminemia: w/o liver function  no proteins  low pressure  fluid leaks out  Globulin (immunoglobulin made in B cells) • Heterogenous group of proteins: composed of different sizes and shapes • Water soluble • Most produced in liver • Alpha-1: protease inhibitors o Antitripson: elastin in lungs  elastase recycles broken down elastin • Alpha-2: binding to other proteins, will bind free Hb, guide other proteins (?) o Hemoglobin: Contains iron, can bind O & other gases o Ciruloplasmin: defect in levels results in accumulation of copper  Wilson’s disease, autosomal, CYP450  Copper depositied in hypatocytes, interrupts brain w/ Parkinson- like symptoms  Kelator: lots of treatments to get copper out + dietary changes o Fibrin & fibrinogen • beta • Gammaglobulins = immunoglobulins  Fibrinogen: protein involved in clotting • Most abundant cell in blood o Biconcave shape in order to increase surface area for interaction w/ other tissues o Reversible deformity: can shrink or expand o Flip and flopases change  show reached useful age  taken to spleen for recycling and reuse o Nitric oxide: vasodilator, causes more blood flow when given for angina etc. • CBC: complete blood count o Hgb: measure of the amount of circulating hemoglobin. (12 – 16 F, 13.5 – 17.5 M) o Hct: The percent of RBCs in the blood (as a ration compared to the solute) (36 – 46 F, 41- 53 M) • Anemia: classified by cause or by cell shape, low blood cell count o Cytic: refers to cell size  Macrocytic anemia: large • Megaloblastic anemia: inhibition of DNA synthesis, happens in bone marrow, can’t move from G2 growth phase to mitosis  not B12 or folate cause it  Pernicious anemia: low intakes of B12 (in chronic alcoholics or malnourishment) • Kelitis, astomatitis (inflamed mouth areas)  Mircrocytic anemia: small RBC’s, also usually hypochromic (low Hb), iron deficiency • Blood loss most common cause usually from lower GI bleeding o Symptoms: Fatigue, pale, shortness of breath, indentation in nail o Can measure iron level and pheretin level o Anesocytosis: change in cell size o Treatment: IV iron, tablets, blood transfusion • Worms, Diverticulotis develops (pouches in colon) and may leak blood  Normocytic anemia: normal RBC’s but still anemic, normal size/ Hb content, insufficient number • Aplastic: bone marrow isn’t producing enough RBC’s  Polycythemia: bone marrow producing too many RBC’s o Chromic: refers to cell Hgb content  Posthemorrhagic: after bleeding  Asplastc  Chronic inflammation  Sickle cell: one amino acid • Too much iron o Hemochromatosis: hereditary cause (deregulation/ deficiency of Hfe) , autosomal, recessive, or too much iron deposited in tissues (symptoms manifest depending on organ), macrophages engulf • Porphyria o Effects porphyron: Hb (protophorphyron 9) o Big compounds able to absorb bands of light o Can’t break them down, end up with big compounds instead of Hb o Symptoms: neuropathy, ab pain, psychiatric symptoms, photosensitivity o VAMPIRES: pale, crazy, need blood b/c • Thrombocytopenia o Platelets < 150,000 mm 3 o Increased risk for hemorrhage o Pathophysiology o Congenital o Acquired Endocrine System • the system of glands that produce endocrine secretions that help to control bodily metabolic activity • Glands are duct-less: hormones released directly into the blood • Hormones secreted in 3 patterns o Diurinal: every 24 hours, circadian rhythm  EX cortisol: produced by adrenal glands, stress hormone, inc glucodeogenesis, peaks in morning, dec at night o Pulcitial or cyclic: basal levels oscillate in response to food intake o Response to levels of substrate: Negative feedback system, emergent fashion  EX low Ca levels in blood  calcitonin to inc Ca levels • Negative feedback: release of hormone signals release of other hormones, return of initial o EX thyroidism • Positive feedback: signals to secrete more hormones  keeps amplifying o EX oxytocin: childbirth, uterus contracts, stimulates secretion, stimulate stronger contractions, stimulates more hormones, etc • Hormones need to travel o Most peptide hormones water soluble (free, travel around, unbound)  EX epinephrine: responds to stress, causes vasoconstriction o Lipid soluble: less water soluble, bounded  EX thyroid hormones • After secreted  will bind to receptor  signal process to take place • Hormonal dysfunctions o Pituitary gland: pea sized part of brain connected to master hypothalamus, produces many (10ish) hormones  2 parts: anterior and posterior  management of BP  thyroid function (thyroid stimulating hormone)  temp regulation  endorphins regulation o pituitary adenoma: irregular growth of gland  can be small and benign or large and malignant  grow in size and are larger than normal but don’t release more hormones  some secrete more  symptoms depend on hormone secreted  apoplexy: hemorage of tissue, severe headaches, very rrare o diabetes insepidis: low blood pressure, hold on to water o SIADH: inc water retention, over release of ADH, too much water  Most in response to carcinoma, infection (EX meningitis, insefilitis), or trauma  Carcinoma: malignant cell type, can occur in any tissue  ADH: upregulate insertion of aquaporins  inc water intake, delusional problems  Clinical signs/ symptoms: headache (maybe from cerebral adema), thirst, nausea/ committing, lethargy, cramps, osmolarity/ Na levels low in blood  high in urine  Treatment: underlying causes, restricting water to regulate blanace, Na tablets, diuretics o Polyuria: urinating off large amounts of water, opp of SIADH  Loss of water from kidneys  nephrogenic diabetes insipidis  Nocturia: urinating all night  Polydipsia: needing to drink large volules of water to keep up with polyuria o Thyroid gland: release thyroid hormones and calcitonion, largest endocrine gland  Regulated by pituitary gland  Calcium homeostasis  Secrets T3 (active thyroid hormone), t4, calcitonin o Hyperthyroidism  Thyrotoxitosis: too much hormone, primary or secondary • Excessive secretion b/c o Graves disease: autoimmune disorder, creates overactive thyroid, overstimulates tissue, caused by thyroid auto antibodies that bind to/ stimulate THS receptors  Signs/ symptoms: insomnia, tremor, hair loss, eyes, sweating, heat intolerance, weight loss, atrial fibrillation, anxiety/ irritability, goiter  Thyroiditis: inflammation or infection of throid gland  Inc release of thyroid hormone • Diagnosis: measurement of throid hormones  THS low b/c negative feedback loop  it’s over stimulated  Treatment: iodine, thyominides, ADH medications, meds for symptoms, beta blocker to dec overproduction  Thyroid storm: rare but seriously dangerous manifestation of hyperthyroidism • Can occur w/ undiagnosed hyperthyroidism • w/ stressor at hand: meds, PTSD, exaggeration of everything in hyperthyroidism • sweating, nausea, seizures, induced coma o hypothyroidism  not enough throid hormone  causes: • hashi moto’s: initial inc of thyroid hormone • post-pardem • nuclear fallout: exposure to iodine 131  signs/ symptoms: weight gain, cold intolerance, constipation, adema of vocal chords, • Queen Anne’s sign = thinning of lateral portion of eyebrows • goiter b/c thyroid gland produces in hope that they can keep up but mass isn’t producing any hormone  TSH high b/c negative feedback; thyroid hormone levels low  Treatment: give thyroid hormone as pill  when levels normal, done  abuse for weight loss • Diabetes o Type 1: insulin dependent  Failure of pancreas to produce insulin  Management w/ dietary changes, less carbs, insulin foreva o Type 2: insulin resistance  Not producing enough, also have resistance, not able to stimulate receptor  Management w/ education b/c often seen in obesity  BP, cholesterol, oral meds to stim. More insulin or inc sensitivity to cells o Gestational: during pregnancy, producing less insulin o Elevated levels of sugar  In infection: immune response stimulated  From steroids  Cystic fibrosis: chloride channels create mucous in lungs o Diagnosis: measure blood sugar levels  hemoglobin A1C: measure how much hemoglobin attacked by glucose, sugar residues attach to proteins, some reside on RBC  glucose tolerance: measures ability of body response to solution intake o signs/ symptoms: polyuria, polydipsia o treatment: insulin, fluid if heavily lost • hypoglycemia o blood sugar below 70 or 50  range of 10-12 o signs/ symptoms: inc heart rate, confusion, stroke-like symptoms, seizures o treatment: glucose (oral or IV) October 18, 2013 ENDOCRINE PART II Diabetes Complications -glycolysis of other tissues leads to damage Damage such as; cardiovascular disease, strokes, kidney disease, retinopathy, neuropathy -glycolysis of small units (capillaries, muscle cells, end nerves) -Very infection prone, often have systemic infections -chronic, deep ulcers (extremely long to heal) Insulin Before discovery, diabetes used to be death sentence of slow starvation BANTING and BESS -found out importance of pancreas via dog experimentations -together isolated the inlets of Langerhans as the insulin producers -created insulin through ground up pancreas and won nobel prize for it -Leonard Tjompson 1 person to receive insulin Used to be available only very limitedly -had to live in Toronto and be a patient of Bess’ Patent sold for 50 cents Cortisol- steroid hormone from adrenal glands Diurnal Cycle (higher in morning than at night) Funtions: -increases glycogenesis (liver is stimed to produce more sugar via catabolism of fats) -inhibits immune/inflammation response, decreased bone formation Cushing’s Disease (TOO MUCH) Causes: -pituitary adenoma causes an overabundance of precursor which turns into too much cortisol -Steroid use (as found in chronic asthma and COPD) -Over secretions b/c of tumor on adrenal glands (All causes dirupt diurnal pattern and cortisol no longer only appears as a stress hormone to body because of constant levels) S/Sx: -Glucose intolerance (down regulation of glucose receptors, similar to type 2 diabetes) -Catabolic process (muscle and bone wasting) -truncal distribution of fat (moon face and buf
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