NP3: Module 3

SCD: s/s, Tx

-SCD: RBC is a sickle shape, cells clump together, causing clots, poor perfusion of O2 and tissue perfusion, increased risk of infection, Death (due to poor blood perfusion). -S/S: Severe pain—dehydration increases pain. Clumping causes vaso-occlusive event. -Heart: HF as a result of anemia -Skin: pallor -ABD: spleen and liver damage. Spleen/liver full of blood, for clumping blood/sickled cells—have ischemia from blockages, hypoxia from low O2 blood to these organs. Further exacerbating issues. -Musculo-skeletal changes: edema occurs because of BV occlusion of arms and legs. Stasis and fluid pooling in lower extremities (legs and arms) -Respiratory: can cause pulmonary HTN, recurrent pneumonia, acute chest syndrome (heart attack feeling, most common cause of death). -Tx Priorities: Pain due to poor tissue perfusion and joint destruction with low oxygen levels. Potential for infection, sepsis, multiple organ dysfunction syndrome (MODS), and death. --Hydration: PO or IV route helps reduce the duration of pain episodes. Urge the patient to drink water or juices. Patient is often dehydrated and blood is hypertonic, hypotonic fluids are usually infused at 250 mL/hr for 4 hours. Once the patient's blood osmolarity is reduced to the normal range of 270 to 300 mOsm, the IV rate is reduced to 125 mL/hr if more hydration is needed. No caffeine is allowed, increased dehydration. --Pain: Tx starts with at least 48hrs of IV analgesics. Morphine and hydromorphone are given IV on a routine schedule or by infusion pump using PCA. When relief obtained IV dose can be tapered, and the drug given orally. Moderate pain may be managed with oral doses of opioids or NSAIDs. Non-opioids are better. --Barometric Pressure Tx: disease acts up when pressure changes, exacerbated in dehydrated states. --Penicillin: for risk of penumonia. --Oxygen Tx --Blood transfusions: PRBCs; admin HgbA to dilute the HgbS. In 120 days, HgbS will outnumber the HgbA. Watch for iron overload. --Hematopoietic stem cell transplantation (HSCT) may correct abnormal Hgb permanently during childhood.

Bone marrow aspiration and biopsy: Pre-Op, Intra-Op, Post-Op, RN considerations, Priorities

Bone marrow aspiration and biopsy, similar invasive procedures, help evaluate hematologic status when other tests show abnormal findings that indicate a possible problem in blood production or maturation. Results provide info about BM function, including the production of all BCs and platelets. In a BM aspiration, cells and fluids are suctioned from the BM. In a BM biopsy, solid tissue & cells are obtained by coring out an area of bone marrow w/ a large-bore needle. -Pre-OP: HCP prescription & signed informed consent form. May be performed at the patient's bedside, in an examination room, or in a laboratory. After learning which specific tests will be performed, check w/ the hematology lab to determine how to handle the specimen. Some tests require that heparin or other solutions be added to the specimen. -RN: help reduce anxiety/fears by providing accurate info & emotional support. Some patients like to have their hand held during the procedure. Explain the procedure and reassure the patient that you will stay during the entire procedure. Tell the patient that the local anesthetic injection will feel like a stinging or burning sensation. Tell him or her to expect a heavy sensation of pressure and pushing while the needle is being inserted. Sometimes a crunching sound can be heard or scraping sensation felt as the needle punctures the bone. Explain that a brief sensation of painful pulling will be experienced as the marrow is being aspirated by mild suction in the syringe. If a biopsy is performed, the patient may feel more discomfort as the needle is rotated into the bone. Help the patient onto an examining table and expose the site (usually the iliac crest). If this site is not available or if more BM is needed, the sternum may be used. For iliac crest, place the patient in prone or side-lying. Depending on the tests to be performed on the specimen, a lab tech may be present to ensure its proper handling. -Op: usually 5-15min. A local anesthetic agent is injected into the skin around the site. The patient may also receive a mild tranquilizer or a rapid-acting sedative, such as midazolam, lorazepam, or etomidate. Some patients do well with guided imagery or autohypnosis. Aspiration or biopsy procedures are invasive, & sterile technique must be observed. The skin over the site is cleaned. For an aspiration, the needle is inserted with a twisting motion, and the BM is aspirated by pulling back on the plunger of the syringe. When sufficient marrow has been aspirated to ensure accurate analysis, the needle is withdrawn rapidly while the tissues are supported. For a biopsy, a small skin incision is made & needle is inserted. Pressure and several twisting motions are needed to ensure coring and loosening of an adequate amount of marrow tissue. Apply external pressure to the site until hemostasis is ensured. A pressure dressing or sandbags may be applied to reduce bleeding at the site. -Post-Op: nursing priority after a BM aspiration/biopsy is prevention of excessive bleeding. Cover the site with a dressing after bleeding is controlled, and closely observe it for 24hrs for s/s of bleeding & infection. A mild analgesic (aspirin-free) may be given for discomfort, and ice packs can be placed over the site to limit bruising. If the patient goes home the same day as the procedure, instruct him or her to inspect the site every 2hrs for the 1st 24hrs to assess for active bleeding or bruising (indicated internal bleeding). Advise the patient to avoid any activity that might result in trauma to the site for 48hrs. -Info obtained from BM aspiration/biopsy reflects: degree & quality of BM activity present. The counts made on a BM specimen can indicate whether different cell types are present in the expected quantities & proportions. In addition, BM aspiration/biopsy can confirm the spread of cancer cells from other tumor sites.

Managing DKA & HHS

Tx of DKA and HHS are the same: --DKA in Type 1 DM; HHS more likely in Type 2: -Glucose: Monitor for DKA/document to evaluate Tx: first assess the airway, LOC, hydration status, electrolytes, and blood glucose level. Check the patient's BP, pulse, and RR every 15min until stable. Record UO, temp., and MS every hour. When a CVAD is present, assess central venous pressure every 30min or as prescribed. After treatment starts and these values are stable, monitor and record VS every 4 hours. Use blood glucose values to assess therapy and determine when to switch from saline to dextrose-containing solutions. Insulin therapy is used to lower serum glucose by about 50 to 75 mg/dL/hr. Unless the episode of DKA is mild, regular insulin by continuous IV is the usual management. An initial IV bolus dose is given, followed by an IV continuous infusion. Continuous insulin infusion is used because insulin half-life is short and subcutaneous insulin has a delayed onset of action. Subcu insulin is started when the patient can take PO fluids and ketosis has stopped. DKA is considered resolved when blood glucose is less than 200 mg/mL along with a serum HCO3 level >18 mEq/L, venous pH is >7.30, and anion gap is <12 mEq/L. Assess therapy effectiveness by monitoring BS levels and electrolyte levels. -F&E: Assess for acute wt loss, thirst, decreased skin turgor, dry mucous membranes, and oliguria with a high SG. Assess for weak and rapid pulse, flat neck veins, increased temp, decreased central venous pressure, muscle weakness, postural hypotension, and cool, clammy, and pale skin to determine if the patient is at risk for dehydration. Fluid Tx & return glucose to baseline level with IV insulin—done slowly over 36-72hrs. Return of baseline cognitive function is evidence that the tx is working. Priority for fluid Tx is to maintain perfusion to vital organs: Typically initial infusion rates are 15-20 mL/kg/hr during the 1st hour. 2nd priority is to replace total body fluids more slowly, hypotonic fluids are infused at 4-14 mL/kg/hr after the initial fluid bolus. When blood glucose levels reach 250 mg/dL, give 5% dextrose in 0.45% saline. This solution helps prevent hypoglycemia and cerebral edema, which can occur when serum osmolarity declines too rapidly. 1st 24hrs of Tx: patient needs enough fluids to replace the actual vL lost, as well as any ongoing losses, and the total may be as much as 6-10 L. Assess cardiac, kidney, and MS to avoid FVO. Watch for symptoms of HF &pulmonary edema. Assess the status of fluid replacement by monitoring BP, I&O, and changes in daily wt. -Electrolytes: Hyperglycemia causes hyperkalemia—when using insulin and other drugs to tx hyperkalemia, its possible to lower the K so much that it causes hypokalemia. Be aware of this, monitor K levels, and tx very slowly. Prevent hypokalemia: K replacement is initiated after serum levels fall below normal. Assess for signs of hypokalemia: fatigue, malaise, confusion, muscle weakness, shallow respirations, ABD distention or paralytic ileus, hypotension, and weak pulse. An ECG shows conduction changes related to alterations in potassium. Hypokalemia is a common cause of death in the treatment of DKA. Action Alert: Before giving IV K-containing solutions, ensure that UO >30 mL/hr.

Accessory Organs of Blood Formation

Accessory Organs of Blood Formation: -Spleen and liver are important accessory organs for blood production. Help regulate the growth of BCs & form factors that ensure proper blood clotting. Problems with either the spleen or the liver result in impaired hematologic function, which usually decreases adequate perfusion or clotting to some degree. -Spleen: contains white, red, and marginal pulp—tissues help balance BC production with BC destruction and assist with immunity. --White pulp- filled with WBCs and is a major site of antibody production. As whole blood filters through the white pulp, bacteria and old RBCs are removed. --Red pulp is the storage site for RBCs and platelets. --Marginal pulp contains the ends of many blood vessels (the "glue"). -Spleen destroys old/imperfect RBCs, breaks down the Hgb released from these destroyed cells for recycling, stores platelets, and filters antigens. -Splenectomy- causes reduced immune functions and an increased risk for infection and sepsis. -Liver: produces prothrombin & other blood clotting factors. Proper liver function is important in forming vitamin K in the GI tract. --Vitamin K- needed to produce clotting factors VII, IX, and X and prothrombin. --Large amounts of whole blood and BCs can be stored in the liver. --Liver also stores extra iron within the protein ferritin.

Cushing's Disease & Syndrome

Adrenal Gland Hyperfunction: Hypersecretion by adrenal cortex results in: Cushing's syndrome or disease, Hypercortisolism, Excessive androgen production. -Cushing's Disease: pituitary adenoma→excessive ACTH→Increased cortisol --S/S: weight gain, muscle loss, hyperglycemia, and sodium retention. -Dietary modifications: include reduction of total calories and CHO to prevent or reduce the degree of hyperglycemia. -Cushing's Syndrome: adrenal adenoma→excessive cortisol→decreased ACTH. Rt to use of steroids or ACTH for other dz. -Assessment: Fatigue, Muscle weakness, Stress intolerance, Poor wound healing, Heavy trunk, thin extremities. Moon face, Buffalo Hump, Osteoporosis. Fragile, think skin - striae, Virilzation, female-amenorrhea & Hirsutism, personality changes, gynecomastia, fat on back of shoulders & face, GI upset from increased acid, Na+H2O retention-edema, CNS irritability, hyperglycemia. -Analysis: Risk of infection, F&E imbalance. -Dx: cushing's dz Dx by cortisol in urine/saliva. ACTH levels Dx if its an adrenal or pituitary problem, or if from chronic steroid use (Prednisone-moon face, wt gain-not permanent). -Implementation: Monitor fluid I&O. Weigh daily, check for edema. Monitor for signs of infection. Balance restored through radiation, surgery, or drugs. --Post-operative: Hypovisectomy (pituitary is cause) or adrenalectomy (adrenal are the cause). Monitor for signs of adrenal hypofunction: Lack of cortisol→ hypoglycemia. Lack of aldosterone→ orthostatic hypotension. Can cause an addisonian crisis. Adrenalectomy--Give Solu-cortef/Hydrocortisone succinate in post-op.

Anti-Clotting Forces

Anti-Clotting Forces: Blood clotting is rapid, it keeps forming fibrin clots whenever the cascade is set into motion until all blood throughout the entire body has coagulated and perfusion stops. This would lead to death. To counteract this, anticlotting forces are also started to limit clot formation only to damaged areas so normal perfusion is maintained everywhere else. Clotting is balanced by anti-clotting, so the clot only occurs where it is needed & perfusion is maintained. -Anticlotting- ensures that activated clotting factors are present only in limited amounts and also cause fibrinolysis to prevent over enlargement of the fibrin clot. -Fibrinolysis- process that dissolves fibrin clot edges with special enzymes. Starts by activating plasminogen to plasmin. Plasmin, an active enzyme, then digests fibrin, fibrinogen, and prothrombin, controlling the size of the fibrin clot. -Additional anticlotting substances are also activated (protein C, protein S, and antithrombin III). --Protein C and S: increase the breakdown of clotting factors V and VIII. --Antithrombin III inactivates thrombin and clotting factors IX and X. --Actions prevent clots from becoming too large or forming in an area where clotting is not needed. Deficiency of any anticlotting factor increases the risk for VTE (ex. pulmonary embolism), MI, and strokes.

Care of Patient in sickle cell crisis

Care of Patient in sickle cell crisis: -Administer oxygen. -Administer prescribed pain medication. -Hydrate the patient with normal saline IV and with beverages of choice (without caffeine) orally. -Remove any constrictive clothing. -Encourage the patient to keep extremities extended to promote venous return. -Do not raise the knee position of the bed. -Elevate the HOB no more than 30 degrees. -Keep room temperature at or above 72°F (22.2°C). -Avoid taking BP with a standard or automatic external arm cuff. -Check circulation in extremities every hour: -Pulse oximetry of fingers and toes -Peripheral pulses -Capillary refill

Risk factors, age of onset, manifestations and pathologic mechanisms of Type 2 DM

DM Type 2: -Type 2 Diabetes (T2DM): Ranges from insulin resistance with relative insulin deficiency to secretory deficit with insulin resistance -Former Names: Adult-onset diabetes, Ketosis-resistant diabetes, Non-insulin-dependent diabetes mellitus (NIDDM) -Age at onset: May occur at any age in adults -S/S: Frequently none; thirst, fatigue, blurred vision, vascular or neural complications -Etiology: Not known, genetic predisposition -Pathology: Insulin resistance, Dysfunctional pancreatic beta cell -Antigen Patterns: none -Antibodies: none -Endogenous insulin and C-peptide: Low, normal, or high -Inheritance: Autosomal dominant, multifactorial -Nutritional status: 60% to 80% obese -Insulin: Required for 20% to 30% -Medical Tx: Mandatory -Ketoacidosis: rare -Type 2, Dx more often in people >30yrs old, most of these patients are overwt (70-90%). Has a gradual onset and a strong genetic component. It increases risk of elevated BP and cholesterol—increasing the incidence of CVD & stroke. 75% of type 2 cases are Dx when testing for other diseases. It's the result of insulin resistance, impaired insulin secretion, or both. Also have inappropriate hepatic gluconeogenesis. -Risk factors (causes): overwt (esp. if BMI >27), family Hx of DM—esp. in Hispanics, African Americans, & Native Americans/Alaskan Natives. Veterans w/ exposure to toxic chemicals (agent orange, Digoxin). -Metabolic Synd.- high risk for developing T2DM, ABD obesity, hyperglycemia, HTN, hyperlipidemia. Any of these S/S alone increase risk for CVD, but together can be devastating. ABD obesity: waist circumference of 40in+ (100cm) for men; 35in+ (88cm) for women. Hyperglycemia: fasting blood glucose level of 100 mg/dL+ or on drugs for elevated blood glucose levels. HTN: systolic BP of 130+ or diastolic BP of 85 mg Hg or more or on drugs for HTN. Hyperlipidemia: triglyceride level of 150 mg/dL+ or on drugs for elevated triglycerides; HDL cholesterol <40 mg/dL for men; <50 mg/dL for women.

Diet for DM

Diet for DM: CHO intake avoids nutrient deficient sources and focuses on sources from vegetables, fruits, whole grains, legumes, and dairy products. -Adults with diabetes should eat 25g of fiber daily Teach patient with DM or prediabetes to avoid sugar sweetened beverages and sucrose to prevent weight gain and adverse effects on metabolism. Dietary fat and cholesterol intake for adults with DM focuses on the quality of fat rather than on the quantity of fat -MEDITERRANEAN DIET: rich in monosaturated fatty acids--Avocados, Nuts and seeds, Olives, Dark chocolate, Omega 3 fatty acids, EPA and DHA from fish or fish oil supplements are recommended -LIMIT TRANS FAT -Limit Alcohol consumption: Teach patients that 2 alcoholic beverages for men and 1 for women can be ingested with, and in addition to , the usual meal plan. -CHO counting: Because fat and protein have little effect on after-meal blood glucose levels. It focuses on the nutrient that has the greatest impact on these levels.

-Acute pain transfusion reaction (APTR) -Transfusion-associated circulatory overload (TACO) -Transfusion-associated graft-versus-host disease (TA-GVHD) -Bacterial transfusion reactions

-Acute pain transfusion reaction (APTR): rare event w/ unknown cause, can occur during or shortly after transfusion of any blood product. S/S: severe chest pain, back pain, joint pain, HTN, anxiety, & redness of the head & neck. Rx does not appear to be life threatening, & most patients respond well with drugs for pain and rigors. S/S are general, but Dx can be supported with a positive direct antibody test (DAT), indicating some degree of hemolysis has occurred but is not widespread. APTR management focuses on patient support & drugs to control or reduce s/s. -Transfusion-associated circulatory overload (TACO): can occur when a blood product is infused too quickly, esp. in an older adult. It is a pulmonary rx that may be difficult at first to differentiate from TRALI. Most common w/ whole-blood transfusions or when the patient receives multiple PRBC transfusions. S/S: HTN, Bounding pulse, Distended jugular veins, Dyspnea, Restlessness, Confusion. Manage/prevent by monitoring I&O, infusing blood products more slowly, and giving diuretics. -Transfusion-associated graft-versus-host disease (TA-GVHD): rare but life-threatening problem that occurs more often in an immunosuppressed patient. Its cause in immunosuppressed patients is similar to that of GVHD that occurs with allogeneic stem cell transplantation, discussed in the interventions section of Leukemia and Preleukemia, in which donor T-cell lymphocytes attack host tissues. S/S: usually occur w/in 1-2wk & include thrombocytopenia, anorexia, n/v, chronic hepatitis, wt loss, & recurrent infection . TA-GVHD has an 80-90% mortality rate but can be prevented by using irradiated blood products. Irradiation destroys most T-cells and their cytokine products. -Bacterial transfusion reactions: occur from infusion of contaminated blood products, esp. those contaminated with a gram-negative organism. S/S: tachycardia, hypotension, fever, chills, and shock. The onset of a bacterial transfusion reaction is rapid.

-Vitamin B12 anemia: assessment, Dx, Tx -Folic Acid Anemia: assessment, Tx

-Vitamin B12 anemia: caused by diets lacking protein, small bowel resection, chronic diarrhea, diverticula, tapeworm, intestinal bacteria. Megaloblastic or macrocytic anemia, pernicious anemia - deficiency of intrinsic factor - autoimmune. RBCs large/oval & fragile, w/ reduced life span. -S/S: pallor and jaundice, glossitis (Smooth/beefy red tongue & ulcers at corner of mouth), fatigue, weight loss, paresthesias, poor balance. -Dx: shilling test, measure B12 uptake after RA B12 dose. CBC: Hgb, Hct, RBCs. -Interventions: -Increase B12: animal proteins, fish, eggs, nuts, dairy, dried beans, citrus fruit, leafy green. Vitamin supplements may be prescribed. Pernicious anemia: B12 injections weekly. -Folic Acid Anemia: decrease in RBCs due to poor nutrition- lack of green leafy vegs, liver, yeast, citrus fruits, beans, nuts. Malabsorption: Crohn's. Drugs: anticonvulsants, contraceptives. Women higher risk, pregnant higher risk. -S/S: similar to B12 but no paresthesia ( w/o NS dysfunction) -Interventions: diet high in B12 & Folic Acid -Identify pt at risk and prevent: older adults, ETOH dependency, malnourished, and those with increased folic acid requirements (preggys women need more). Folic acid and B12 nutrition + replacement therapy.

Hyperglycemia S/S, patho, manifestations

Hyperglycemia- w/o insulin, glucose builds up in the blood, which disturbs F&E balance , leading to the classic symptoms of diabetes: polyuria, polydipsia, and polyphagia. Releasing free fatty acids (FFAs), to get energy from fat stores--Ketone bodies ("ketones"), Dehydration leads to hemoconcentration, hypovolemia, poor tissue perfusion, and hypoxia, especially to the brain. Anion-gap metabolic acidosis- excess acids caused by absence of insulin increase H+ and CO2 levels in the blood. -Kussmaul respiration- acid triggers brain to increase the RR and depth to exhale CO2/acid. Acetone is exhaled, giving the breath a "rotting citrus fruit" odor. When the lungs fail to offset the acid, the pH drops. ABG: show metabolic acidosis, w/ compensatory respiratory alkalosis. Dx DKA: kushmaul respirations indicate DKA, 2 labs are drawn to confirm it. ABGs show anion gap, CBC shows lactic acid levels. Both are needed to confirm the Dx of DKA. -Hypokalemia- Insulin lack first causes potassium depletion. With the increased fluid loss from hyperglycemia, excessive potassium is excreted in the urine, leading to low serum potassium levels. -Hyperkalemia- may occur in acidosis because of the shift of potassium from inside the cells to the blood in exchange for hydrogen ions. -Serum potassium levels in DM, may be low, high, or normal, depending on hydration, the severity of acidosis, and the patient's response to treatment. Patients with BS 250+ & ketonuria should avoid exercise. -Chronic Hyperglycemia: leads to many health problems—micro/macrovascular issues, nerve damage from reduced BF (irreversible & unresponsive to meds), increased wound healing time from low blood O2 to outer layers of skin, increased cholesterol leads to CVD (angina, MI, stroke), Diabetic nephropathy causes CKD and failure, retinopathy from reduced BF to retina. Main S/S hyperglycemia: 3 P's for 1& 2 1: N/V, headache, anxiety or aggression, blurred vision (S/S similar to hypoglycemia) Type 2: DKA Kushmaul resp., sweet breath, N/V, ABD pain, wt loss, blurred vision Normal hospital algorithm: tx BS of 150+. Critical hyperglycemia: S/S develop quickly—if left untreated can progress to DKA or HHS. DKA: Catabolic state causes muscle weakness/loss, and ketone production. Dehydration, electrolyte abnormalities, and cardiac dysrhythmias may also be present. Causes by infection, stress, inadequate insulin dose. -HHS: hyperosmolar (increased blood osmolarity) state caused by hyperglycemia. HHS results from a sustained osmotic diuresis leading to extremely high blood glucose levels. Differs from DKA in that ketone levels are absent or low and blood glucose levels are much higher. Blood glucose levels may exceed 600 mg/dL, and blood osmolarity may exceed 320 mOsm/L. Caused by infection, stressors, dehydration. -HHS & DKA: caused by hyperglycemia and dehydration

Managing Hypothyroidism at Home: patient teaching

Hypothyroidism at Home: if fatigue is severe—1 floor living. S/S not improved at D/C, extra clothing or heat may be needed, Drug Tx may need to be done by 1 family member if patient is unable. -Education: most important is about hormone replacement therapy and its SE. Emphasize the need for lifelong drugs, and review the s/s of both hyper/hypothyroidism. Wear a medical alert bracelet. When to seek medical tx for dosage adjustment & the need for periodic blood tests of hormones. Do not take OTC meds w/o talking to HCP -Diet: well-balanced diet with adequate fiber and fluid intake to prevent constipation, use of fiber supplements may interfere with the absorption of thyroid hormone. -Drugs: TH should be taken on an empty stomach, at least 4 hours before or after a meal. -Lifestyle: Remind the patient about the importance of adequate rest. Recovery of S/S may take a long time. Teach the family to orient the patient often and to explain everything clearly, simply, and as often as needed. -Monitor Tx effectiveness: two easiest parameters to check are need for sleep and bowel elimination. Needing more sleep and having constipation indicate the dose needs to be increased.

Interventions for Hyperthyroidism

Interventions for Hyperthyroidism: -Diet Tx: until the thyroid is better controlled, extra kCals and protein may be necessary, along w/ possible Ca supplementation. Hyperglycemia occurs from reduced glucose tolerance. Avoid stimulants and caffeine. -Graves: drug Tx and radioablation. Surgery is reserved for severe disease that is not responsive to other forms of management. -Medical management: used to decrease the effect of TH on cardiac function & reduce TH secretion. -Priorities for RN care: focus on monitoring for complications, reducing stimulation, promoting comfort, and teaching the patient and family about therapeutic drugs and procedures. --Monitoring: measuring the patient's apical pulse, BP, and temp at least every 4hrs. Instruct the patient to report immediately any palpitations, dyspnea, vertigo, or chest pain. Increased temp, indicates worsening of condition and possible thyroid storm. Immediately report a temp increase of even 1°F. If delegated to AP, instruct them to report temp to imediately. If elevated immediately assess the patient's cardiac status. If the patient has a cardiac monitor, check for dysrhythmias. --Reduce stimulation & promote comfort: put patient in a quiet/comfortable room, limit visitors, shut door, give cool clothes, and ice-water available. Helps prevent increasing the symptoms of hyperthyroidism and the risk for cardiac complications. For patients with exophthalmos, prevent eye dryness by encouraging the use of artificial tears. Change the bed linen whenever it becomes damp from diaphoresis. Suggest patient take a cool shower or sponge bath daily. -Drug Tx, RAI, Surgery.

Interventions for Hypoglycemia

Interventions for Hypoglycemia: -Prevention is better than Tx: Monitor glucose levels before giving antidiabetic drugs, before meals, before bedtime, and when the patient is symptomatic. All patients who take insulin, those taking long-acting insulin stimulators (glyburide), and those taking metformin in combination with glyburide are at risk for hypoglycemia. This risk is increased if they are older, have liver or kidney impairment, or are taking drugs that enhance the effects of antidiabetic drugs. In the hospital setting, mealtime insulin must be coordinated with timely monitoring and food delivery to avoid episodes of hypoglycemia. Blood glucose should be checked no more than 1 hour before a meal, and rapid-acting insulin given just before the meal to avoid hypoglycemia. -Hospital: we tx blood glucose < 70. -If patient is awake: drink 15-20g of fast CHO, recheck BS in 15min, if not above 70 give another 15g CHO, recheck BS in 15min, if not above 70 you need to call the MD and repeat steps above. Avoid high-potassium options such as orange juice. Concentrated sweet fluids, such as chocolate, may slow absorption because of the fat content. -Patient is unable to swallow: IV dose of concentrated dextrose or subcutaneous glucagon is indicated. For extremely low BS, cant swallow or unconscious. Its very quick acting and will increase BS (converts glycogen to glucose). May be repeated every 20min, dilute as instructed. RN: after admin, patient often vomits. Position them on their side to prevent aspiration. SE are temporary, after N/V stops give them a small snack. Before D/C patient/family needs to verbalize understanding of DM diet, S/S of hypoglycemia & hyperglycemia. Stress that delaying a meal for more than 30 minutes raises the risk for hypoglycemia when using some insulin regimens. Instruct him or her to keep a CHO source nearby at all times. Teach the patient and family how to inject glucagon. -Home: patient can use glucose tabs or 4oz juice or a tbs honey (anything with fast CHO), follow with a light snack of protein and CHO (ex PeanutButter, meat) Book said: Adding protein to CHO does not improve blood glucose response and does not prevent subsequent hypoglycemia. Eat additional food, such as low-fat milk, after 10 to 15 minutes.

Interventions for Thyroid storm or thyroid crisis

Interventions for Thyroid storm or thyroid crisis: Thyroid storm or thyroid crisis: life-threatening event- thyroid storm after surgery is less common because of drug therapy before thyroid surgery, it can still occur. Even with treatment, thyroid storm may lead to death. -Assess: temp often because an increase of even 1°F (1.8°C) may indicate an impending thyroid crisis. If a temperature increase occurs, respond by reporting it immediately to the HCP. -Tx: focus on maintaining airway patency, promoting adequate ventilation and gas exchange , reducing fever, and stabilizing the hemodynamic status. -Maintain a patent airway and adequate ventilation. -Give oral antithyroid drugs as prescribed: methimazole or propylthiouracil. -Admin sodium iodide solution IV daily as prescribed. -Give propranolol IV as prescribed, slowly over 3 minutes. The patient should be connected to a cardiac monitor, and a central venous pressure catheter should be in place. -Give glucocorticoids as prescribed: hydrocortisone, prednisone, or dexamethasone. -Monitor continually for cardiac dysrhythmias. -Monitor vital signs every 30 minutes. -Provide comfort measures, including a cooling blanket. -Give nonsalicylate antipyretics as prescribed. -Correct dehydration with normal saline infusions. -Apply cooling blanket or ice packs to reduce fever.

Leukemia: types, risks, S/S, Dx, & Tx

Leukemia: Blood cancer, uncontrolled production of immature/malignant WBCs in the bone marrow (usually blast cells). Myelodysplastic syndromes can progress to leukemia. -Acute: rapid onset w/o Tx- result of infection or hemorrhage. ALL (3-7yrs, fair Px), s/s fatigue, weakness, anorexia, fever, petechia, ecchymosis. AML (all ages, poor Px), s/s fatigue, weakness, anorexia, fever, petechia, ecchymosis, lymphadenopathy, splenomegaly, Auer rods in myeloblasts. --Chronic: CML (50yrs, poor Px) s/s fatigue, weakness, anorexia, fever, night sweats, splenomegaly, philidelphia chromosone. CLL (70yrs, fair Px) s/s insidious onset, few s/s, low lg levels, infections. --Overcrowding of nonfunctional cells in BM, leads to reduction of normal cells: low RBCs & platelets. Leads to anemia, splenomegaly, & bleeding. -Risk factors: exact cause unknown, interaction of genetics+environment-- exposure to chemicals, Genetics-down's synd or Blooms synd, antineoplastics, chemo/radiation. Any condition/drug that chronically suppresses the immune system. Recent increases in patient with hypoplastic/aplastic anemia. -Cell Type: classified by type of abnormal cell -Lymphocytic or lymphoblastic: coming from lymphoid pathways. Myelocytic, myelogenous, or myeloblastic: coming from myeloid path. Biphenotypic leukemia is acute, shows both types. -S/S: Anemia from low Hgb, Neurtopenia- risk of infection, Thrombocytopenia-risk of bleeding. Wt loss, fever, frequent infections, SOB, weakness, bone/joint pain & tenderness, fatigue, anorexia, swollen lymph nodes, spleen/liver enlargement, pallor, night sweats, easy bleeding/bruising, purple patches or spots. -Dx: low Hgb/Hct, low platelet, abnormal WBC count (higher= poor prognosis). --BM Exam: shows abnormal cell type. AML: abnormal myloblasts, ALL: lymphoblasts, CML: lymphocytes. Definitive test of aspirated cells. Protein/Ag on surface of Blast cells ID type. --Clotting studies: time & factors abnormal w/ Acute Leukemia, clotting time generally increased. --Chromosomal analysis: ID type of leukemia, & predict prognosis & Tx. -Tx: Induction- goal is rapid/complete remission of disease. 1st Tx given, often standardized, Chemo is the most common, may be used w/ BM transplant. Consolidation- used early in remission to try to cure cancer. Maintenance- in acute cases, used after induction/Consolidation to maintain remission of cancer. Stem cell transplant, std for acute--closely matched donor, Tx done when in temporary remission after induction. -RN: patient on reverse isolation, monitor neutrophils: <1000 mod risk, <500 severe risk. Risk of bleeding: platelets <50,000 moderate; <20,000 severe risk. Fatigue reduces appetite, need to increase Kcal to fight cancer. Stomatitis & Candida can further reduce kcal intake (result of chemo/radiation).

Describe common factors in the care of a child with anemia and develop a plan of care to improve the condition.

PEDS Iron Deficiency Anemia: most common nutritional deficiency in kids age 9-15mo. -Dx: CBC--Low hemoglobin (6-11). Microcytic, hypochromic RBCs. Decreased mean cell volume (MCV). Decreased mean cell hemoglobin (MCH). Reticulocyte normal or slightly elevated. Total Iron-binding capacity (TIBC) elevated. Serum ferritin / iron low. -Assessment--Obtain Hx from parents: Decrease in child's activity level? More tired than usual? Increased desire to be held? Cow milk before age 12 months? Increased milk consumption? No solid foods? Heart races when at rest? Detailed nutritional Hx--What is the usual diet? -Physical s/s: Pallor, Tired appearance, Mild to severe tachycardia, Heart murmur. Babies: extreem pallor (wt porcilan doll), tachycardia, increased RR, lethargic, fatigue, irritable. Iron is stored in fetus in 3rd trimester, premature babies at higher risk. IDA rarely seen in healthy babies before 4-6mo old. -Interventions: -Dietary Changes to increase Iron: <12mo old- Iron fortified formula or breast milk, premature babies may need iron-supplements earlier; >12mo old- limit cow's milk to < 24oz/day (moderate Tx), Increase iron-rich foods: Liver, dried beans, Iron fortified cereal (Cream of Wheat), apricots, prunes, other dried fruits, egg yolks, dark green leafy vegetables. -Drugs: daily PO iron preparation admin 3x/day. -Keep a dietary diary -RN Teaching: Explain need of iron for RBCs, labs, potential outcome if not follow interventions, lack of iron in cow's milk, irons effect in the body. Keep meds out of child's reach. Monitor for black, tarry stools. Increase vitamin C--increases iron absorption. Follow up labs to monitor: reticulocyte count, HgB, Hct. -Administration of Iron: Admin in 1-3 divided doses. Give between meals (1- 2hrs before meals), on an empty stomach. Dosage: 3-6 mg/kg/day or 2-4 mg/kg/day for premature infants. Give with vit-C rich fluids - orange juice, Admin w/ a straw or medicine dropper placed at the back of mouth, away from the teeth to avoid stains. Can cause black, tarry stools, and constipation. Do not admin iron with milk, impeding absorption.

Parathyroid Gland

Parathyroid Gland: consist of 4 small glands located close to or within the back surface of the thyroid gland. These cells secrete PTH-- regulates Ca & P metabolism by acting on bones, the kidneys, & GI tract. -PTH: increases bone resorption (bone release of Ca into the blood from bone storage sites), thus increasing serum calcium. -PTH acts on the kidneys and increases their activation of vit D—increases absorption of Ca & P from the intestines. In the kidney tubules, it increases the absorption of Ca back into the blood. -Serum Ca high- PTH secretion goes down -Serum Ca low- PTH secretion goes up -PTH and Calcitonin work together to maintain normal serum and ECF concentrations of Ca. --Note the location of the parathyroid gland and the laryngeal nerve, inflammation post-op can compress the nerve.

Subcutaneous Insulin Administration: w/ vial & syringe, w/ pen device

Subcutaneous Insulin Administration -With Vial and Syringe: -Wash your hands. Inspect the bottle for the type of insulin and exp. Gently roll the bottle of intermed-acting insulin in the palms of your hands to mix. Clean the rubber stopper with an alcohol swab. -Remove the needle cover and pull back the plunger to draw air into the syringe. The amount of air should be equal to the dose. Push the needle through the rubber stopper and inject the air into the insulin bottle. Turn the bottle upside down and draw the insulin dose into the syringe. Remove air bubbles in the syringe by tapping on the syringe or injecting air back into the bottle. Redraw the correct amount. Make certain the tip of the plunger is on the line for your dose of insulin. Magnifiers are available to assist in measuring accurate doses of insulin. Remove the needle from the bottle. Recap the needle if the insulin is not to be given immediately. -Select a site within your injection area that has not been used in the past month. Clean your skin with an alcohol swab. Lightly grasp an area of skin and insert the needle at a 90-degree angle. Push the plunger all the way down. This will push the insulin into your body. Release the pinched skin. Pull the needle straight out quickly. Do not rub the place where you gave the shot. Dispose of the syringe and needle without recapping in a puncture-proof container. -With a Pen Device: -Wash your hands. Check the drug label to be sure it is what was prescribed. Remove the cap. Look at the insulin to be sure it is evenly mixed if it contains NPH and that there is no clumping of particles. Wipe the tip of the pen where the needle will attach with an alcohol swab. Remove the protective pull tab from the needle and screw it onto the pen until snug. Remove both the plastic outer cap and inner needle cap. Look at the dose window and turn the dosage knob to the appropriate dose. -Holding the pen with the needle pointing upward, press the button until at least a drop of insulin appears. This is the "cold shot," "air shot," or "safety shot." Repeat this step if needed until a drop appears. Dial the number of units needed. -Hold the pen perpendicular to and against the intended injection site with your thumb on the dosing knob. Press the dosing knob slowly all the way to dispense the dose. Hold the pen in place for 6-10sec, then withdraw from the skin. -Replace the outer needle cap; unscrew until the needle is removed, and dispose of the needle in a hard plastic or metal container. Replace the cap on the insulin pen.

Surgery for Hyperthyroidism

Surgery for Hyperthyroidism: Removal all/part of thyroid, when other Tx not working, & if goiter is compressing esophagus/trachea. -Pre-Op: Tx w/ thionamide first to have near-normal thyroid function (euthyroid) before thyroid surgery. Iodine prep also used to decrease thyroid size & vascularity, reducing the risk for hemorrhage & storm. HTN, dysrhythmias, and tachycardia must be controlled before surgery. May need to follow a high-protein, high-carbohydrate diet for days-weeks before surgery. -Teach: deep-breathing exercises. Importance of supporting the neck when coughing/moving by placing both hands behind the neck to reduce strain on the incision. Explain the surgery and the care after surgery to the patient. Remind him or her that a drain and a dressing may be in place after surgery. -Op: Thyroidectomies- usually MIS. The parathyroid glands & laryngeal nerves are avoided to reduce the risk for complications & injury. Subtotal thyroidectomy- remaining thyroid tissues are sutured to the trachea. Total thyroidectomy- entire thyroid gland is removed, but the parathyroid glands are left with an intact blood supply to prevent causing hypoparathyroidism. -Post-Op: RN Priorities-maintain airway & adequate ventilation because of proximity to parathyroid, frequently assess for hypocalcemia, assess for drainage (Quantity/Quality), stridor indicates obstruction. -Monitoring for complications is the most important nursing action after thyroid surgery (hemorrhage 1st 24hrs post). Monitor VS every 15 minutes until stable, then every 30 minutes. Assess for discomfort & give drugs for pain control PRN. Use pillows to support the head and neck. Place the patient, while he or she is awake, in a semi-Fowler position. Avoid positions that cause neck extension. Help the patient deep-breathe every 30 minutes to 1 hour. Suction oral and tracheal secretions when necessary. -Remain alert to the potential for complications and identify s/s early. Hemorrhage may be seen as bleeding at the incision site or as respiratory distress caused by tracheal compression. Mod amount of serosanguineous drainage is normal. Respiratory distress and reduced gas exchange can result from swelling, tetany, or damage to the laryngeal nerve, resulting in spasms. Laryngeal stridor is heard in acute respiratory obstruction. Keep emergency tracheostomy equipment in the patient's room. Check that oxygen and suctioning equipment are nearby and in working order. HypoCa & tetany may occur if the parathyroid glands compromised, causing low PTH- assess for S/S of hypocalcemia. Ca gluconate or Ca chloride for IV use should be available in an emergency situation. Laryngeal nerve damage- problem results in hoarseness and a weak voice. Assess the patient's voice at 2-hour intervals and document any changes. Reassure the patient that hoarseness is usually temporary.

Tx for Hyperpituitarism

Tx for Hyperpituitarism: -Acromegaly: provide emotional support for alt. body image. Check for s/s of DI: polyuria/polydipsia. Prep for surgery. -Radiation: can be used to reduce tumor size, but can damage eyes/optic nerve. -Drugs: dopamine agonists bromocriptine & cabergoline (inhibit PRL & GH) decrease tumor size. Somatostatin analogs, especially octreotide and lanreotide, & GH receptor blocker, pegvisomant. -Hypophysectomy: most common OP, remove tumor & pituirary. If successful, relieve headache, sexual dysfunction, & reduce H-levels. -Pre-Op: teach what to expect; nasal packing 2-3days post-op, so breath through mouth; drip pad will be under nose. DO NOT: brush teeth, cough, sneeze, blow nose, or bend forward. -Op: depends on tumor size/location. Transsphenoidal, or MIS endoscopic transnasal w/ smaller instruments is used under general anesthesia instead of a more invasive procedure. Nasal packing inserted after transsphenoidal incision closed, mustache dressing applied (not needed for MIS). If tumor isn't reached by either of these 2 Ops, then craniotomy may be indicated. -Post-Op: Monitor VS hourly for the 1st 24hrs, then every 4hrs. Monitor fluid balance, esp. if UO>Intake. Encourage DB exercise. Instruct not to cough, blow the nose, or sneeze. Use dental floss & oral PO rinses, no toothbrush till surgeon approves (2wks). Avoid bending at the waist (prevent increased ICP). Monitor nasal drip pad, type/amount of drainage (glucose +). Teach methods to avoid constipation/straining. Teach admin of the H's. Keep HOB elevated. Decreased smell will last 3-4mo. -Report: increased swallowing or post-nasal drip (CSF leak), persistent/severe headache, return of hyperpit. s/s. -Observe: for indications of increased ICP, DI, CSF leak, infection. Infection (meningitis)-headache, fever, neck rigidity--Tx with ABs, antipyretics, analgesics. Halo s/s- light yellow color at the edge of the clear drainage on the dressing, indicates CSF, usually resolves w/ bedrest, rarely need Op. DI-polyuria, polydipsia, tachycardia. Tx w/ desmopressin (DDVAP). -Entire pit removed: replacement of thyroid H's & glucocorticoids is lifelong. (cortisol, thyroid, gonadal, vassopressin).

Aplastic Anemia: assessment, Tx

-Aplastic Anemia: impaired cellular regulation of the BM, fail to produce RBC cells; or Pancytopenia: low RBCs, WBCs, & platelets. Caused by injury to pleuipotent ST cell--Long exposure to toxic agents, radiation, infection, Fanconi (hereditary), drugs that impair the hematologic system. -S/S: pallor, weakness, fatigue, tachycardia, bleeding, weak immunity (if low WBC). Severe anemia, CBC macrocytic anemia, leukopenia and thrombocytopenia. Biopsy shows replacement of the red BM that forms RBC with fat. -Interventions: risk of infection & hemorrhage -Isolation precautions if low WBCs -Blood transfusion - just when life threatening thrombocytopenia, due risk of immune reactions to platelets -ST Cells transplant: most successful Tx -Drug discontinuation -Immunosuppressive therapy: if autoimmune ds present; Steroids-Prednisone, antithymocyte globulin (ATG), and cyclosporine for remission. Moderate aplastic anemia: daclizumab to improve blood counts and transfusion requirements. Splenectomy may be needed. HSCT when pt is able to undergo and have a suitable donor

Leukemia (Class Notes)

-Assess leukemia: reduction of platelets causing excessive bleeding. S/S—bruising, minor trauma, nose or rectal bleed, blood in gums & urine. Low WBC increase risk of infection. -Present: w/ anemia, fatigue. -Changes w/ body systems: · Cardiac: low BP, high pulse. · Respiratory: reduced gas exchange from infection and anemia · Skin: anemia causes poor tissue perfusion, so skin looks pale, cool to touch. · GI: anorexia, wt loss, nausea · Headaches, Risk of seizure or coma, Papilla edema, Joint/bone tenderness, Large lymph nodes, on armpit & neck. -Dx: low Hgb/Hct, low platelet, abnormal WBC count (higher= poor prognosis). -Aggressive Tx: results in suppression of bone marrow—this reduces immunity & increases risk of infections. Takes 2-3 weeks to recover from bone marrow procedure, need to "live in a bubble". -RN: protect from infection, monitor WBC & CBC daily or multiple times day. WBC increase/elevate- at risk of infection & their immune system has weakened.

Transfusion complications vs reactions, & interventions

-Complications and acute transfusion rx can occur with any type of RBC component therapy, rx are more common when components >30 days old & when multiple transfusions are admin. -Transfusion rx: febrile, hemolytic, allergic, or bacterial reactions; circulatory overload; or transfusion-associated graft-versus-host disease. -Prevent complications: remain alert during transfusions to detect early rx & initiate appropriate management. Instructing pt to immediately report any change in physical or emotional status, such as new-onset joint, back, chest, or abdominal pain; chills; nausea; feeling unwell; or feeling uneasy, may help identify a possible transfusion reaction. -Interventions for reactions: occurring during transfusion (hemolytic reactions, allergic reactions, and bacterial reactions) begin with stopping the transfusion and removing the blood tubing. (For hemolytic and suspected bacterial reactions, return the component bag, labels, and all tubing to the blood bank or laboratory.) Initiate the RRT. If the patient has no other IV access, keep the access and flush w/ NS. Do not flush the contents of the blood transfusion tubing, which would allow more of the reaction-causing blood to enter the patient. Usually O2 is applied, & diphenhydramine is given by IV push. If shock is present, fluid resuscitation and hemodynamic monitoring are needed. BP support w/ vasopressors may be needed. Other drug tx is supportive, ex. antipyretics for fever, antibiotics for possible bacterial contamination, & meperidine for rigors.

-Dawn phenomenon vs Somogyi phenomenon

-Dawn phenomenon results from a nighttime release of adrenal hormones that causes blood glucose elevations at about 5 to 6 a.m. It is managed by providing more insulin for the overnight period (e.g., giving the evening dose of intermediate-acting insulin at 10 p.m. instead of with the evening meal). -Somogyi phenomenon is morning hyperglycemia from the counterregulatory response to nighttime hypoglycemia. It is managed by ensuring adequate dietary intake at bedtime and evaluating the insulin dose and exercise programs to prevent conditions that lead to hypoglycemia. --Both problems are diagnosed by blood glucose monitoring during the night. Help identify these problems and teach the patient and family about management.

Drugs for Leukemia

-Drugs for Chronic Leukemia: -CML: Imatinib mesylate is a common first-line drug therapy for CML that is Philadelphia chromosome positive; interferon alfa also used which slows the growth of leukemic cells. -CLL: standard chemotherapy, monoclonal antibody therapy (e.g., rituximab, ofatumumab, alemtuzumab, obinutuzumab), or targeted therapy such as ibrutinib (a Bruton tyrosine kinase [BTK] inhibitor), idelalisib (a highly selective inhibitor of the delta isoform of PI3K, which plays a critical role in B-cell function through BCR signaling), or venetoclax (a selective BCL2 inhibitor), can cause remissions but does not cure the disease. Monoclonal antibody therapy is often combined with standard chemotherapy drugs or used as a single agent. -Allogeneic hematopoietic stem cell transplantation in patients with CLL is an option for cure or increased survival at time of relapse, but has considerable risk for mortality and is not an appropriate alternative for all patients. -Drugs for MSD: Antitumor immunomodulating agents have improved blood counts in patients who have less severe MDS, especially those whose abnormal cells have a specific chromosome aberration. For higher-grade MDS, azacitidine and decitabine have been approved, although positive responses usually require 3 to 6 months of therapy and not every patient responds. -Drugs for infection: Drugs used depend on the sensitivity of the organism causing the infection, as well as on infection severity. Drugs for infection include antibacterial, antiviral, and antifungal agents.

-Febrile transfusion reactions -Hemolytic transfusion reactions -Allergic transfusion reactions (anaphylactic transfusion reactions) -Transfusion-related acute lung injury (TRALI)

-Febrile transfusion reactions : most often in pt w/ anti-WBC antibodies, which can develop after multiple transfusions, WBC transfusions, and platelet transfusions. S/S: chills, tachycardia, fever, hypotension, and tachypnea. Giving leukocyte-reduced blood or single-donor HLA-matched platelets reduces the risk for this type of reaction. WBC filters may be used to trap WBCs and prevent their infusion into the patient. -Hemolytic transfusion reactions: caused by blood type or Rh incompatibility. When blood containing Ag different from the patient's own Ag is infused, Ag-antibody complexes are formed in his or her blood. Complexes destroy the transfused cells and start inflammatory responses in the BV walls and organs. Onset immediate, or after mult units transfused. Rx may be mild, w/ fever/chills, or life threatening, with DIC & circulatory collapse. Other S/S: Apprehension, Headache, Chest pain, Low back pain, Tachycardia, Tachypnea, Hypotension, Hemoglobinuria, & sense of impending doom. -Allergic transfusion reactions (anaphylactic transfusion reactions): most often in pt w/ other allergies. S/S: may have urticaria, itching, bronchospasm, or anaphylaxis. Onset usually occurs during or up to 24 hours after the transfusion. Patients with an allergy history can be given leukocyte-reduced or washed RBCs, in which the WBCs, plasma, and immunoglobulin A have been removed, reducing the risk for an allergic reaction. -Transfusion-related acute lung injury (TRALI): life-threatening event, occurs most often when donor blood contains antibodies against the recipient's neutrophil antigens, HLA, or both. S/S: rapid onset of dyspnea & hypoxia w/in 6hrs of the transfusion. Early recognition is key to survival. Most patients require intubation and mechanical ventilation for respiratory support.

-G6PD: assessment, Tx -Immuno-hemolytic anemia: assessment, Tx

-G6PD (Glucose 6 Phosphate dehydrogenases): genetic deficiency enzyme G6PD - how RBC produce ATP. Genetic, severe in males (x-linked recessive-mild in carrier females), African americans, middle east and asia. Triggered by agents, drugs, or severe infection -Interventions: Prevention is best! -Men, high risk group should be tested; genetic counceling for families. -Hydration is important to prevent AKI, flushes out cellular debris. -Enzyme RT -Autoimmune hemolytic anemia: own antibodies attacking and destroying own RBCs - followed by accelerated production of abnormal RBCs (erythropoiesis). S/S: Weakness, fatigue, malaise, pallor, jaundice. --Warm antibody: IgG excess, activated at 37C, triggered by drugs, chemicals, or autoimmune problems --Cold antibody anemia: IgM, activated at 30C, Raynaud-like response, arteries in the hands and feet constrict to cold temperatures or stress -Interventions: Tx depends on severity. Steroid therapy, Immunotherapy with rituximab, Splenectomomy (if no Tx working), Chemo, plasma exchange (aphaeresis).

Hyperpituitarism: Assessments, Complaints, Complications, Dx

-Hyperpituitarism: over secretion of H's, caused by tumors or tissue hyperplasia. Tumors (adenomas) most common cause. Can be pre or post-puberty. -1st s/s: headache, visual changes from the tumor pressure increasing ICP. -Complaints: back/joint pain, vision problems, headaches, bone enlargement. -High GH in children: Gigantism--S/S frontal bossing-prominent forehead, heavy brow ridge, prominent jaw, gaps in teeth, thick facial features. Large hands/feet w/ thick fingers/toes. Double vision, bad peripheral vision (ICP). Sleeping problems/apnea. Muscle weakness-risk of falls. Late childhood-early adulthood, height & organ growth, extremely large for age & delays puberty (hypogonadism). -High GH in adults: Acromegaly--similar s/s to gigantism. Gradually changes musculo-skeletal system. Early detection necessary, to minimize overgrowth of soft tissue in hands, face, feet, skin, tongue. Organ damage can also occur. Menstrual changes. -Pituitary tumors often secrete prolactin, inhibits secretion of gonadotrops & sex H's. causes galactorrhea, impotence, low libido in men. Amenorrhea, infertility, galactorrhea in women. -High ACTH: s/s of excess glucocorticoids & mineralocorticoids. -Dx: high serum somatotropin (GH), X-ray, MRI, Physical exam, PO glucose challenge test (level doesn't go down) admin 100g of glucose or 0.5 g/kg of body wt, followed by serial GH level measurements. GH levels not <5 ng/mL (mcg/L) indicate positive/abnormal result. CT of Head-shows enlarged sella turcica. -Complications: may have hyperglycemia bc GH blocks action of insulin. Increased ICP w/ tumor.

-Iron deficiency anemia: assessment, Tx

-Iron deficiency anemia: most common, any pt diagnosed with it should be evaluated for abnormal bleeding, esp. GI. RBCs are small (microcytic). Ferritin <10 (normal 10-300). Usually due to poor diet. Higher in women bc mentrurate. -S/S: Pallor/Cool to the touch, Intolerance to cooler temp, Brittle nails and concave, Rapid HR increased after meals and with activity, Murmurs and gallops, Orthostatic hypotension, Breathless on exertion, Decreased O2sat, Fatigue, Increased need for sleep, Reduced energy -Interventions: -Increase oral intake of iron: red meat, liver, iron fortified cereal, organ meat, egg yolks, kidney beans, leafy greens, raisins. Iron intake 10-15g/day. -Dextran, Ferumoxytol parenterally - iron solutions. Take w/ citrus to increase absorbtion, milk inhibits absorbtion, use straw to prevent teeth staining, brush teeth after admin. Can cause constipation, GI upset. -PEDS: premature babies high risk iron deficiency, in healthy babies IDA rarely seen before 4-6mo. Increase PO intake--infants: breast milk, iron fortified formula (need till 12mo old). Older child: diet same as adults, PO supplement 3x/day. Moderate Tx: limit cows milk to 24oz/day.

S/S of Hyperglycemia vs Hypoglycemia

-Main S/S of hyperglycemia: All patients with diabetes have this. Polyuria- excessive urination, because the body needs to excrete the excess water intake. Polydipsia- excessive thirst, because the body needs more water to dilute the glucose. Polyphagia- excessive hunger, because glucose cant enter the cells, the body thinks its starving. Polyphagia is more common with hypoglycemia than hyper. -Causes: too much food, too little insulin, stress, or certain meds. -Other S/S: skin is warm, dry, vasodilated. Dehydration present. Respiratory- rapid, deep; Kussmaul type; acetone odor (rotten "fruity" odor) to breath. MS- varies from alert to stuporous, obtunded, or frank coma. Acidosis; hypercapnia; ABD cramps, N/V. Dehydration: decreased neck vein filling, orthostatic hypotension, tachycardia, poor skin turgor. BS >250mg/dL. Ketones in urine or blood. -Main S/S of hypoglycemia: skin is cool, clammy, "sweaty". Dehydration absent. Respiratory: No particular or consistent change. MS- Anxious, nervous, irritable, mental confusion, seizures, coma. Weakness, a double vision, blurred vision, hunger, tachycardia, palpitations. BS <70mg/dL. No ketones in urine or blood.

Interventions for Thrombocytopenic purpura

-Platelet transfusions: platelets are <10,000/mm3 or when the patient has an acute life-threatening bleeding episode. Platelets don't go on a pump, bc quicker is better (gravity)! -Maintaining a safe environment: protect the patient from bleeding. Closely monitor the amount of bleeding that is occurring. -Drug therapy: to control ATP & TTP, drugs that suppress immune function. Ex. corticosteroids, azathioprine, eltrombopag, rituximab, and romiplostim are used to inhibit production of antibodies directed against platelets or endothelial cells. --ATP: IV immunoglobulin & IV anti-Rho, help prevent the destruction of antibody-coated platelets. --Aggressive Tx: low doses of chemo. --TTP & HIT: also Tx w/ anticoagulants. --TTP: platelet inhibitors such as aspirin, alprostadil, & plicamycin. Plasma removal and the infusion of FFP (plasma exchange) reduce the clumping caused by elements in the pt blood. This Tx for autoimmune TTP has been responsible for dramatically increasing the survival rate. FFP doesn't go on a pump, but on gravity! --HIT: includes a direct thrombin inhibitor such as argatroban or lepirudin -Surgical management ATP: splenectomy for those patients who do not respond to drugs. (In ATP the spleen is the site of excessive platelet destruction.) --Splenectomy is usually not for TTP & HIT. --Depending on spleen size & risk for bleeding, may be open ABD Op or MIS by laparoscopy. RN post-op care is same as ABD Op. Post-op, increased risk for infection bc the spleen performs many protective immune functions, esp antibody generation. Vaccinations against pneumococcal and meningococcal disorders and Haemophilus influenzae are recommended- 2wks before planned Op or 2wks after. Teaching patients about their increased risk for infection, avoiding crowds and people who are ill, and when to consult with the primary HCP is RN priority.

Hematologic Assessment: Normal Ranges and Significance of Changes

-RBC: Females: 4.2-5.4 × 106/mcL, Males: 4.7-6.1 × 106/mcL. Decreased levels: possible anemia or hemorrhage Increased levels: possible chronic hypoxia or polycythemia vera. -Hemoglobin (Hgb): Females: 12-16 g/dL, Males: 14-18 g/dL. Decreased levels: possible anemia or hemorrhage Increased levels: possible chronic hypoxia or polycythemia vera. -Hematocrit (Hct): Females: 37%-47%, Males: 42%-52%. Decreased levels: possible anemia or hemorrhage Increased levels: possible chronic hypoxia or polycythemia vera. -Mean corpuscular volume (MCV): 80-95 fL. Increased levels: macrocytic cells, possible anemia. Decreased levels: microcytic cells, possible iron deficiency anemia. -Mean corpuscular hemoglobin (MCH): 27-31 pg. Increased levels: macrocytic cells, possible anemia. Decreased levels: microcytic cells, possible iron deficiency anemia. -Mean corpuscular hemoglobin concentration (MCHC): 32-36 g/dL or 32%-36%. Increased levels: spherocytosis or anemia. Decreased levels: iron deficiency anemia or a hemoglobinopathy. -WBC: 5000-10,000/mm3. Increased levels: associated with infection, inflammation, autoimmune disorders, and leukemia. Decreased levels: prolonged infection or bone marrow suppression. -Reticulocyte: 0.5%-2.0% of RBCs. Increased levels: possible chronic blood loss or recovery from anemia. Decreased levels: possible inadequate RBC production. -Total iron-binding capacity (TIBC): 250-460 mcg/dL. Increased levels: iron deficiency. Decreased levels: anemia, hemorrhage, hemolysis. -Iron (Fe): Females: 60-160 mcg/dL, Males: 80-180 mcg/dL. Increased levels: iron excess, liver disorders, hemochromatosis, megaloblastic anemia. Decreased levels: possible iron deficiency anemia, hemorrhage. -Platelet: 150,000-400,000/mm3. Increased levels: polycythemia vera or malignancy. Decreased levels: bone marrow suppression, autoimmune disease, hypersplenism. -Direct and indirect Coombs test: Negative. Positive findings: antibodies to RBCs. -International normalized ratio (INR): 0.8-1.1 times the control value. Increased values: longer clotting times (desirable for therapy with warfarin). Decreased values: hypercoagulation and increased risk for VTE. -Prothrombin time (PT): 11-12.5 sec, 85%-100%. Increased time indicates possible deficiency of clotting factors V and VII. Decreased time may indicate vitamin K excess.

PCV: assessment, Tx

-S/S PCV: initially asymptomatic. Headache, facial skin and mucous membranes have a dark, purple or cyanotic, flushed (plethoric) appearance with distended veins. Intense itching caused by dilated BVs and poor perfusion. Thick blood moves more slowly and causes HTN. BF may be so slow in some areas that stasis occurs. Vascular stasis causes thrombosis/clot within the smaller BVs, occluding them, which interferes with perfusion and leads to tissue hypoxia, anoxia, and, later, infarction and necrosis. Tissues most at risk are the heart, spleen, and kidneys, damage can occur in any organ. Organs enlarging causes ABD tenderness/fullness--leading to nutritional deficits. Death usually from vascular complications. -Tx: Goal is to reduce blood viscosity & vL. -PCV is malignant, lack of Tx will lead to death w/in 2yrs. Manage w/ repeated phlebotomy w/ apheresis (2-5x/week), the patient may live 10-15yrs or longer. --Phlebotomy/Apheresis- withdrawal of whole blood (pints- amount determined by HCP) and removal of some of the patient's blood components (for PCV, RBCs). Plasma is then reinfused back into the patient. Periodic labs drawn to monitor Tx effectiveness. --Hydration: increase to >3L/day & promoting venous return help prevent clot formation. --Lifestyle: wear support stockings, elevate legs when sitting, wear non-binding clothing. Smoking cessation is important. --Drugs: anticoagulants--aspirin Tx, decreases clotting, but increases risk of GI bleeding. Hydroxyurea, PO chemo drug, may be prescribed for severe s/s. Pegylated interferon has also shown some benefit in controlling RBC production. --Avoid leafy greens/veg, anything high in iron, bc they hold onto it more than normal. --Need lifestyle changes w/ apheresis in order to live.

Addison's Disease & Crisis

Addison's Disease: Adrenal hypofunction (usually due to autoimmune disease). Idiopathic atrophy of adrenal cortex. Not enough secretion of glucocorticoids (sugar), & mineralcorticoids (Na). Primary when dz originates w/ adrenals. -Assess: Characteristic pigmentation of skin folds (in primary)--bronze, from over absorption of iron in GI. Changes in distribution of hair. Fatigue, light headed, postural hypotension, weakness, GI upset, hypoglycemia, wt loss, poor coordination, dry skin/muc-memb, sparse axially/pubic hair. -Lack glucocorticoids: Anorexia, weight loss, apathy, Stress intolerance, Hypoglycemia. -Lack mineralocorticoids: Sodium loss→dehydration/hypotension, Hyperkalemia, Metabolic acidosis. -Dx: plasma/urine testing, show decrease of cortisol. Also ACTH stimulation tests. -Tx: Monitor fluid and electrolyte balance, Watch for signs of hypoglycemia. --Diet: high protein, high kCals, w/ extra Na. Na needed to replace what is lost due to lack of aldosterone, to conserve Na. Restrict K intake. --Education: Explain need for lifelong replacement of gluc- and mineralocorticoids, Advice to avoid infections trauma or stress: risk of Addisionian crisis. Take more hormones when under stress. Carry medical identification card. -Addisonian crisis: Lack of glucocorticoids→minor stress or illness may cause fatal crisis. -Assess: Acute hypotension, shock, Renal failure due to hypovolemia, Hypoglycemia, Hyperkalemia, Hyponatremia. Profound fatigue, dehydration, vascular collapse, renals shut down (low Na, high K). -Dx for Crisis: low Na, high K/Ca/BUN, hypoglycemia common, Hct elevated from hemoconcentration, cortisol low (often <10). -Tx Crisis: Don't wait for cortisol results--Tx quickly & usually resolves, Assist with IV administration of NaCl and Hydrocortisone (solucortef, prompt IV bolus), Monitor vitals signs, Monitor urine output every hour.

Assessing DM

Assessing DM: -Ask woman how large their children were at birth: GDM or glucose intolerance during pregnancy. -Assess wt & wt change: obesity risk factor for DM2. DM1 often has wt loss w/ increased appetite in wks before Dx. -Fatigue, polyuria, polydipsia (1 &2) -Ask about recent major/minor infections & assess overall immunity. Ask women about frequent vaginal yeast infections. -Small injuries that become infected easily or take longer to heal. -Changes in vision and sense of touch -Ongoing Assessment: A test result indicating DM should be repeated to rule out laboratory error unless s/s of hyperglycemia or hyperglycemic crisis are also present. Screening for DM usually is done with labs of both A1C levels and FGB. -Glycosylated hemoglobin (A1C): is the average blood glucose over the past 120 days. Meas how much glucose permanently attaches to the Hgb molecule & indicates the effectiveness of blood glucose control measures. Because glucose binds to proteins, including Hgb, through a process called glycosylation, the higher the blood glucose level is over time, the more glycosylated the Hgb becomes. Long-term glycemic control, Predict risk for complications, Results are not altered by the eating habits on the day before the test, Recommended at least twice yearly to evaluate treatment outcomes, For patients whose therapy has changed should be done quarterly. -Fasting plasma glucose (FPG or FGB): along with A1C, is used to diagnose DM in nonpregnant adults. Dx of DM is made w/ 2 separate test results >126 mg/dL. -Random or casual plasma glucose: greater than 200 mg/dL (7.0 mmol/L) is used to diagnose DM in patients with classic hyperglycemia symptoms or hyperglycemic crisis. -Oral glucose tolerance test (OGTT): sensitive test for the diagnosis of DM. It is often used to diagnose gestational diabetes mellitus (GDM) during pregnancy and is not routinely used for general Dx. -Type 1: Markers of destruction include islet cell autoantibodies (ICAs), autoantibodies to insulin, zinc transporter antibodies (ZnT8), and autoantibodies to glutamic acid decarboxylase (GAD65). ICAs are present in 85% to 90% of patients with new-onset type 1 DM. -Fructosamine assays: ST follow-up of Tx or in patients with Hgb abnormalities in which A1C does not accurately reflect glucose levels. When glucose binds to amino groups on serum proteins, esp. albumin, the glycosylated protein product is called fructosamine. This product increases w/ elevated blood glucose levels as Hgb does but can indicate blood glucose control over a shorter period.

Assessing a thyroid storm, causes, Tx

Assessing a thyroid storm: -Thyroid storm or thyroid crisis (thyrotoxic crisis): life-threatening event that occurs in patients with uncontrolled hyperthyroidism, most often with Graves disease. Excessive T-H release, which dramatically increases metabolic rate. Acute exacerbation of hyperthyroidism. Overproduction of epi & hypermetabolism. S/S develop quickly & are fatal if untreated. Causing cardiac, renal, and hepatic failure. -Causes: often triggered by stressors such as trauma, infection, DKA, and pregnancy. Other conditions are vigorous palpation of the goiter, exposure to iodine, and RAI therapy. Post-op after thyroid surgery (less common). -S/S: initially marked tachycardia, vomiting, stupor. Then fever, severe tachycardia, and systolic HTN. May have ABD pain, N/V, and diarrhea. Often patient is anxious w/ tremors. As the crisis progresses, the patient may become restless, confused/delirium, or psychotic and may have seizures, leading to coma. HF and shock can also occur. Hyperthermia w/ temp up to 105.3F. -Tx: even w/ Tx, thyroid storm may lead to death. --RN Critical Rescue: When caring for a patient with hyperthyroidism, even after a thyroidectomy, assess temperature often because an increase of even 1°F, may indicate an impending thyroid crisis. If a temp. increase occurs, report immediately to the HCP.

Blood components

Blood components: -Plasma is the liquid portion of the blood that contains the cells, ECF fluid that's similar to interstitial fluid, but with more proteins. 3 types of proteins: Albumin- maintains the osmotic pressure of the blood, preventing the plasma from leaking into the tissues. Globulins- have many functions, ex. transporting other substances, as antibodies they protect the body against infection. Fibrinogen- activated to form fibrin, which is critical in the blood clotting process. -RBCs: (erythrocytes) are the largest proportion of blood cells. Biconcave, flexible disk with no nucleus, transports oxygen & CO2. When healthy/mature, they live about 120 days. Iron is needed to let the RBC carry O2, each Hgb molecule can carry 4 molecules of O2. Hgb molecules carry CO2 at a different site from O2. Substances needed for RBC/Hgb production: iron, vitamin B12, folic acid, copper, pyridoxine, cobalt, and nickel. Lack of any can cause anemia (reduced numbers of function of RBCs), which results in unmet tissue oxygen needs because of a reduction in the number or function of RBCs. -WBCs, leukocytes: also are formed in the BM. The many types of WBCs all have specialized functions that provide protection through inflammation and immunity. -Platelets/thrombocytes- smallest blood cells, formed in the BM from megakaryocyte precursor cells. Activated platelets stick to injured BV walls and form platelet plugs that can stop the flow of blood at the injured site. They produce substances important to blood clotting and aggregate (clump together) to perform most of their functions. Platelets help keep small BVs intact by initiating repair after damage. Platelet production: controlled by growth factor thrombopoietin. Platelet storage: after they leave the BM, they are stored in the spleen, released slowly per the bodys demands. Normally 80% of platelets are circulating, 20% stored in the spleen.

Conservative Management of Hyperparathyroidism

Conservative Management of Hyperparathyroidism: Non Surgical Tx: Diuretics and fluid Tx to reduce Ca levels—usually furosemide with large vL of saline. --Drug Tx: used if diuretics are unsuccessful—PO phosphates and Ca chelators as a short term Tx. Ca levels must be controlled >14 can lead to coma. Severe s/s of hyperparathyroidism or who have hypercalcemia related to parathyroid cancer involves the use of cinacalcet, a calcimimetic. Drug binds to calcium-sensitive receptors on parathyroid tissue, reducing PTH production/release. The result is decreased Ca levels, stabilization of other minerals, and decreased progression of PTH-induced bone complications. Etelcalcetide- for CKD-associated hyperparathyroidism in patients undergoing dialysis. It is a synthetic calcium-sensing receptor agonist given IV three times weekly at the end of a dialysis session. Both cinacalcet and etelcalcetide require serum calcium monitoring for hypocalcemia on a regular basis for the duration of therapy. PO phosphates are used to inhibit bone resorption and interfere with calcium absorption. IV phosphates are used only when serum calcium levels must be lowered rapidly. Calcitonin decreases the release of skeletal calcium and increases kidney excretion of calcium. It is not effective when used alone because of its short duration of action. Therapeutic effects are enhanced if calcitonin is given with glucocorticoids. --Monitor cardiac function and I&O every 2 hours during hydration therapy. Continuous cardiac monitoring may be necessary. Compare recent ECG tracings with the patient's baseline tracings—changes in the T waves and the QT interval, as well as changes in the rate and rhythm. --Monitor serum calcium levels, and immediately report any sudden drop to the primary health care provider. Sudden drops in Ca levels may cause tingling and numbness in the muscles. -Preventing injury: w/ chronic hyperparathyroidism often has significant bone density loss and is at risk for fragile fractures. Teach AP to handle the patient carefully and to use a lift sheet to reposition the patient rather than pulling him or her.

Conservative Management of Hypoparathyroidism

Conservative Management of Hypoparathyroidism: -Non surgical Tx: Focus is correcting hypocalcemia, vitamin D deficiency, and hypomagnesemia. If low mg is the cause, it may be from alcoholism, malnutrition, malabsorption syndromes. Assess for S/S of hypocalcemia (Chvostek, trouseau). -Drug Tx: Acute and severe hypocalcemia, IV calcium is given as a 10% solution of calcium chloride or calcium gluconate over 10 to 15 minutes. Acute vitamin D deficiency is treated with daily oral calcitriol. Acute hypomagnesemia is corrected with IV magnesium sulfate. LT PO Tx for hypocalcemia involves the intake of calcium, 0.5 to 2 g daily, in divided doses. LT Tx for vitamin D deficiency is replacement with PO ergocalciferol daily. Dosage is adjusted to keep the patient's calcium level in the low-normal range (slightly hypocalcemic), enough to prevent s/s of hypocalcemia. It must also be low enough to prevent increased urine calcium levels, which can lead to stone formation. -Diet Tx: RN management includes teaching about the drug regimen and interventions to reduce anxiety. Teach the patient to eat foods high in calcium but low in phosphorus. Milk, yogurt, and processed cheeses are avoided because of their high phosphorus content. -Teaching: Stress that therapy for hypocalcemia is lifelong. Advise the patient to wear a medical alert bracelet. Tell patient that with adherence to the prescribed drug and diet regimen, the calcium level usually remains high enough to prevent a hypocalcemic crisis.

Dx DMCriteria for the Dx of Diabetes 1 & 2

Criteria for the Dx of Diabetes: -A1C >6.5%. The test should be performed in a lab using a method that is NGSP certified & std. to the DCCT assay. -AND Fasting blood glucose >126 mg/dL. Fasting is defined as no kCal intake for >8hrs. (DM Case Study: Dx of DM made after 2 fasting BS tests >126.) -OR 2-hr blood glucose > 200 mg/dL during oral glucose tolerance testing. The test should be performed using a glucose load containing 75 g anhydrous glucose dissolved in H20. -OR In a patient w/ classic S/S of hyperglycemia or hyperglycemic crisis, a casual or random blood glucose concentration >200 mg/dL. Casual is defined as any time of the day w/o regard to time since last meal. Classic S/S: polyuria, polydipsia, and unexplained weight loss. Note : In the absence of unequivocal hyperglycemia, the first 3 criteria should be confirmed by repeat testing. -A1C% & Mean Glucose levels: -A1C 6%= 126mg/dl -A1C 7%= 154mg/dl -A1C 8%= 183mg/dl -A1C 9%= 212mg/dl -A1C 10%= 240mg/dl -A1C 11%= 269mg/dl -A1C 12%= 298mg/dl Type 1 screening: Markers of pancreas cell destruction include islet cell autoantibodies (ICAs), autoantibodies to insulin, zinc transporter antibodies (ZnT8), and autoantibodies to glutamic acid decarboxylase (GAD65). ICAs are present in 85% to 90% of patients with new-onset type 1 DM. Type 2 screening: Testing to detect pre-diabetes & type 2, is recommended for patients >45yrs & those defined as overwt (BMI >25 kg/m2). Testing is considered for younger pt who are overwt if they have additional risk factors for DM or other health problems associated w/ it. Screening for DM usually is done with lab testing of both A1C levels and fasting plasma glucose levels. -Labs: -Fasting BS: normal 60-110mg/dl -Glycoesated Hgb: normal 4-6% -LDL: normal <130mg/dl -HDL (Good): normal >35mg/dl 45 mg/dL for men; >55 mg/dL for women -Tryglycerides: normal 40-160 mg/dL for men & 35-135 mg/dL for women -Total Cholesterol: normal <200mg/dl

Clinical Indicators of DKA & HHS

DKA: sudden onset. Caused by infection, stressors, inadequate insulin dose. S/s Ketosis: Kussmaul respiration, "rotting fruit" breath, nausea, abdominal pain. Dehydration or electrolyte loss: polyuria, polydipsia, weight loss, dry skin, sunken eyes, soft eyeballs, lethargy, coma. -Serum glucose >300 mg/dL -Osmolarity/osmolality Variable -Serum ketones Positive at 1:2 dilutions -Serum pH <7.35 -Serum HCO3 <15 mEq/L -Serum Na+ Low, normal, or high -BUN >30 mg/dL: elevated bc dehydration. -Creatinine >1.5 mg/dL: elevated bc dehydration. -Urine ketones Positive HHS: gradual onset. Caused by infection, stressors, poor fluid intake. S/S: Altered central nervous system function with neurologic symptoms, Dehydration or electrolyte loss: same as for DKA. -Serum Glucose >600 mg/dL -Osmolarity/osmolality >320 mOsm/L -Serum ketones Negative -Serum pH >7.4 -Serum HCO3 >20 mEq/L -Serum Na+ Normal or low -BUN Elevated -Creatinine Elevated -Urine ketones Negative

Risk factors, age of onset, manifestations and pathologic mechanisms of Type 1 DM

DM Type 1: -Type 1 Diabetes (T1DM): Beta cell destruction leading to absolute insulin deficiency, Autoimmune, Idiopathic -Former Names: Juvenile-onset diabetes, Ketosis-prone diabetes, Insulin-dependent diabetes mellitus (IDDM) -Age of onset: Usually younger than 30yrs -S/S: Abrupt onset, thirst, hunger, increased urine output, weight loss -Etiology: Viral infection, autoimmunity -Pathology: Pancreatic beta cell destruction -Antigen Patterns: HLA-DR, HLA-DQ -Antibodies: Often present at diagnosis -Endogenous insulin and C-peptide: None to very low -Inheritance: complex -Nutritional status: Usually nonobese -Insulin: All dependent on insulin -Medical therapy: mandatory -Ketoacidosis: common -Type 1 is approx. 5% of DM cases, pancreas produces little to no insulin from Beta cell destruction -Causes: unknown, but suspected to be a combination of genetics and environmental triggers. -Autoimmune disfunction causes islet cell antibodies to destroy Beta Cells. -Male with type 1 has 1:17 odds of passing to children -Women with type 1, who has child before age 25yrs, has a 1:25 risk. Women with type 1, who have child after age 25, risk is 1:100. -Triggers: Mumps, coxsackie B, congenital rubella, cows milk, cold temperatures (Dx increases in winter), common cold, children who did not breastfeed & began eating solid food early.

Drug Tx & education for Hyperthyroidism

Drug Tx & education for Hyperthyroidism: --Drugs: antithyroid drugs are the initial Tx, causes some to go into remission for 10yrs. Block TH production by preventing iodide binding in the thyroid gland. Response is delayed because they may have large amounts of stored THs that continue to be released. --Propylthiouracil/Methimazole: Avoid crowds bc risk of infection, monitor for hypothyroidism, Report jaundice & darkening of urine, bc liver toxicity/failure can occur. Drug is not for pregnant bc birth defects. -Lugol solution/Saturated solution of potassium iodide (SSKI): Admin 1hr after thionamide has been given because initially iodine agents can cause an increase in production of THs, giving thionamide 1st prevents the initial increase. Assess for fever, rash, metallic taste, mouth sores, sore throat, or GI distress—indicate idoism, a toxic effect of drug, may need to discontinue med. -Solutions with iodine agents—temporary Tx to reduce size and vascularity of thyroid gland, and prep for removal. Drug can result in hypothyroidism, and the patient is monitored closely for the need to adjust. -Beta-adrenergic blocking drugs such as propranolol may be used as supportive therapy. These drugs relieve diaphoresis, anxiety, tachycardia, and palpitations but do not inhibit TH production.

Exercise for DM

Exercise • Remember that exercise helps control blood glucose levels and blood lipid levels and helps reduce complications of diabetes. • Perform level of exercise recommended to you by your diabetes health care provider. • Wear appropriate footwear designed for exercise. • Examine your feet daily and after exercising. • Stay hydrated and do not exercise in extreme heat or cold. • Do not exercise within 1 hour of insulin injection or near time of peak insulin action. • Prevent hypoglycemia during exercise by: • Do not exercise unless blood glucose level is at least 80 and less than 250 mg/dL. • Have a carbohydrate snack before exercising if 1 hour has passed since the last meal or if the planned exercise is of high intensity. • Carry a simple sugar to eat during exercise if symptoms of hypoglycemia occur. • Carry identification information about diabetes during exercise. • Check your blood glucose levels more often on days you exercise and remember that extra carbohydrate and less insulin may be needed during the 24-hour period following exercise.

Hematologic system

Hematologic system: involves all the components & organs responsible for blood formation, circulation, function, storage, and recycling. -Components of Blood formation: blood cells, lymph, and lymph nodes, along with the bone marrow, spleen, liver, and thymus. Formation and circulation of normal blood are critical to tissue perfusion and gas exchange (oxygenation) because the blood is the oxygen delivery system. -Perfusion: total arterial blood flow through the tissues and blood that is pumped by the heart. Peripheral perfusion- BF through the tissues & extremities. Central perfusion- blood flow through the heart/pump. -Problems with the hematologic system: All organs and tissues require oxygen to function and live, problems in this oxygen delivery system lead to body wide disfunction. To achieve whole body health/perfusion, liquid blood must be able to carry and deliver O2 via circulation—but clotting is also an important factor for this system to function properly. -Clotting: a complex, multistep process by which blood forms a protein-based structure (clot) in an appropriate area of tissue injury to prevent excessive bleeding while maintaining whole-body blood flow (perfusion). -Bone Marrow (BM): functional site of blood formation in adults and produces RBCs/erythrocytes, WBCs/leukocytes, & platelets/thrombocytes. BM also involved in the immune responses. --Blood cell production: in adults is present only in flat bones (sternum, skull, pelvic and shoulder girdles) and the ends of long bones. Aging causes fatty tissue to replace active red BM, and only a small portion of the remaining marrow continues to produce blood in older adults. Step 1: BM makes immature stem cells, unspecialized cells that are capable of becoming any blood cell, depended on body needs. Step 2: committed stem cell (precursor cell) enters one growth pathway and can at that point specialize (differentiate) into only one cell type. These cells actively divide, but need a specific growth factor to specialize. Ex. erythropoietin (kidneys) is a growth factor specific for the RBC.

Hematopoietic stem cell transplantation (HSCT)

Hematopoietic stem cell transplantation (HSCT): is standard treatment for the patient with acute leukemia who has a closely matched donor and who is in temporary remission after induction therapy. -It can also be used for some forms of chronic leukemia, MDS, lymphoma, multiple myeloma, aplastic anemia, sickle cell disease, and many solid tumors. -Stem cells for transplantation can be obtained directly from the donor's bone marrow or, more often, from his or her peripheral blood. -Before HSCT, additional chemotherapy with or without total-body irradiation (TBI) is given to purge (clear) the marrow of leukemic cells. -These treatments are lethal to the bone marrow, and without replacement of stem cells by HSCT, the patient would die of infection or hemorrhage. -After conditioning, new healthy stem cells are given to the patient. The new cells go to the marrow and then begin the process of hematopoiesis, which results in normal, properly functioning blood cells and ideally a permanent cure. -Autologous: self donation -Syngeneic: Patient's HLA identical twin or other identical sibling -Allogeneic: HLA-matched relative, Unrelated HLA-matched donor, Mismatched or partially HLA-matched family member or unrelated donor (donor registries)

Hematostasis & Blood Clotting

Hematostasis & Blood Clotting: -Hemostasis- the multistep process of controlled blood clotting, resulting in localized blood clotting in damaged BVs to prevent excessive blood loss while continuing perfusion of liquid blood and individual cells to all other areas. Balances blood clotting actions with anticlotting actions. -Injury- results in the formation of a platelet plug, other steps result in the formation of a fibrin clot. -3 steps for blood clotting: platelet aggregation w/ platelet plug formation, the blood clotting cascade, and the formation of a complete fibrin clot. -1) Platelet plugs: not clots and last only a few hours. They cannot provide complete hemostasis but only trigger the start of the hemostatic process. Substances that activate clumping: adenosine diphosphate (ADP), calcium, thromboxane A2 (TXA2), and collagen. Platelets self-activate by secreting some of these substances. Platelet aggregation causes plugs, which start the cascade, w/o adequate numbers risk of bleeding. -2) 2 paths for cascade: Extrinsic- outside of BV, usually trauma that damages BVs and exposes the collagen within BV walls. Collagen then activates platelets to form a platelet plug within seconds. This causes a quicker cascade. Other conditions or substances that can activate platelets in the extrinsic pathway include inflammation, bacterial toxins, or the presence of foreign proteins. Intrinsic- w/in the BV, changes in the blood not trauma. Ex. impaired BF (venous stasis) or the presence of excessive amounts of substances that promote blood clotting within the blood itself that can activate platelets and trigger the blood clotting cascade. This is less of a protective response and results from problems that promote abnormal clotting. -3) Fibrin Clot: last phase of blood clotting. Fibrinogen is an inactive protein made in the liver. The activated enzyme thrombin removes the end portions of fibrinogen, converting it to active fibrin molecules that can link together to form fibrin threads. Fibrin threads make a mesh like base to form a blood clot. -After mesh is formed- clotting factor XIII tightens up the mesh, making it dense and more stable. More platelets stick to the threads of the mesh and attract other BCs and proteins to form an actual blood clot. As this clot tightens (retracts), the serum is squeezed out, and clot formation is complete. -Cascade, from the formation of a platelet plug to the formation of a fibrin clot, depends on the presence of specific clotting factors, calcium, and more platelets at every step. -Last 2 critical steps in the cascade: activation of thrombin from prothrombin and the conversion (by thrombin) of fibrinogen into fibrin. Only fibrin molecules can begin the formation of a true clot.

Hemophilia

Hemophilia: Group of bleeding disorders where there is a deficiency of one of the factors necessary for coagulation. --S/S: Bleeding--Mild to Severe, Pain, Swelling, Neuropathy, Parasthesia, Hemarthrosis, Excessive bruising, Prolonged bleeding after minor injuries, Nosebleeds -Hemophilia A: Factor VIII deficiency X-linked recessive, S/S: Intra cranial & GI hemmorage, prolonged nose bleeds, bruise easily, warm/painful/swollen joints w/ less movement. -Hemophilia B: Factor IX deficiency -Von Willebrand's: Deficiency of von Willebrands Factor, vWD carrier protein for coagulation factor VIII--Co-factor for binding of platelets to damaged tissue; Autosomal recessive or dominant. S/S: Epistaxis, bleeding from gums/muc-memb, menorrhagia, Prolonged bleeding from cuts, after surgery/trauma. Dx: Family hx of bleeding disorders, Quantitative immunoelectrophoretic assay. Tx: Replacing missing or dysfunctional factor, DDAVP. -Dx: Prolonged bleeding after circumcision. PT/PTT, bleeding time, fibrinogen level, platelet count, factor VIII, IX assays. -Implementation: When bleeding--elevate and apply pressure for 10-20min. Avoid taking rectal temperatures. Tx hemarthroses early to preserve mobility of joint (elevation, ice packs, may require splinting). -Tx: Replace coagulation factors VIII or IX (heat-treated to inactivate viruses or recombinant), Recombinant antihemophilic factor, DDAVP intranasal spray, Amicar or Cyclokapron, Avoid activity that induce bleeding, Protect joints during activities, Immobilize joints affected by hemarthrosis, Treat bleeding with RICE, Aspirin is contraindicated. -Home Care: Administer factor per home care protocol. Immobilize joint, apply pressure to superficial wounds, apply ice. Call MD if child sustains blunt trauma. Safe environment. No contact sports. Precautions with other sports/activities. Good dental hygiene, good nutrition. -Genetic Counseling: X-linked recessive disease, Transmitted by asymptomatic female carriers - 50% of male offspring will have disease - 50% of female offspring are carriers.

Hormones of the Anterior & Posterior Pituitary

Hormones of the Anterior & Posterior Pituitary: -Pituitary Gland: 2 parts; anterior lobe (adenohypophysis) and the posterior lobe (neurohypophysis). -Anterior: shares circulation w/ hypothalamus, releases trophic hormones that travel to other endocrine glands (target tissues), other hormones directly produce an effect on target tissues. --TSH (Thyrotropin): goes to thyroid & causes synthesis/release of thyroid hormones. --ACTH (Corticotropin): goes to the adrenal cortex, causes the synthesis/release of cortical steroids, & stimulates adrenocortical growth. --LH (LCSH in men): in the ovaries, causes ovulation & progesterone secretion. Travels to testes & causes testosterone secretion. --FSH (Interstitial/Sertoli stim. H): in ovaries causes estrogen secretion & follicle maturation. In testes, causes spermatogenesis. --PRL: in mammary glands causes production of breast milk. --GH: in bones & soft tissue, causes growth growth through lipolysis, protein anabolism, and insulin antagonism. --MSH: promotes pigmentation in skin. -Posterior: directly connected to hypothalamus by nerve fibers. --ADH (Vasopressin): made by hypothalamus, stored in P-Pit. In the kidneys, promotes H20 reabsorption. --Oxytocin: made by hypothalamus, stored in P-Pit. In mammary glands causes ejection of milk. In uterus causes contractions.

Hyperparathyroidism: causes, S/S, Dx

Hyperparathyroidism: Over secretion of PTH, causing hypercalcemia and hypophosphatemia. Increases bone resorption by decreasing osteoblastic activity, and increasing osteoclastic activity. -Causes: 90%+ of cases are caused by a single parathyroid tumor. Primary: when 1+ parathyroid glands do not respond to the normal feedback of serum calcium levels. Secondary: benign tumor in one parathyroid gland and CKD. Parathyroid tumor or cancer, Congenital hyperplasia, Neck trauma or radiation, Vit D deficiency, CKD w/ hypocalcemia, PTH-secreting carcinomas of the lung, kidney, or GI tract. -S/S: rt excessive PTH or hypercalcemia. Bone fractures, recent wt loss, arthritis, or psychological stress. High PTH causes kidney stones and deposits of Ca in the soft tissue of the kidney. Bone lesions are caused by an increased rate of bone destruction and may result in fractures, bone cysts, and osteoporosis. --High Ca: anorexia, n/v, epigastric pain, constipation, weight loss. Hypercalcemia causes elevated serum gastric levels & leads to PUD. Fatigue & lethargy present, and worsen as Ca increases. Ca >12, psychosis w/ confusion, followed by coma & death if unTx. --In Chronic dz: may have a waxy pallor of the skin, & bone deformities in the extremities & back. Dx Hyperparathyroidism: -Ca Total: 9.0-10.5 mg/dL, increased in primary -P: 3.0-4.5 mg/dL, decreased -Mg: 1.3-2.1 mEq/L, increased -PTH Whole: 10-65 pg/mL, increased -Vit D (Calciferol): 25-80 ng/mL, variable

Hypoparathyroidism: causes, types, S/S, labs/Dx

Hypoparathyroidism: Decreased function of the parathyroid gland (PTH), rare disease. Hypocalcemia results. Problems related to lack of PTH or a decreased effectiveness of PTH on the target tissue. -Causes: Surgical or radiation-induced thyroid ablation, Parathyroidectomy, Congenital dysgenesis, Idiopathic (autoimmune)hypoparathyroidism, Hypomagnesemia. -Types: Iatrogenic-most common form, is caused by the removal of all parathyroid tissue during total thyroidectomy or surgical removal of the parathyroid glands. Idiopathic- can occur spontaneously. The exact cause is unknown, but an autoimmune basis is suspected, and it may occur with other autoimmune disorders. Hypomagnemia- Low Mg levels are seen in patients with malabsorption syndromes, CKD, and malnutrition. Low magnesium levels suppress PTH secretion and may interfere with the effects of PTH on the bones, kidneys, & Ca regulation. -S/S: May range from mild tingling/numbness to muscle tetany. Mild-to-moderate hypocalcemia: tingling and numbness around the mouth or in the hands & feet. Severe hypocalcemia: Severe muscle cramps, spasms of the hands & feet, & seizures (with no loss of consciousness or incontinence). The patient/family may notice mental changes ranging from irritability to psychosis. Check for Chvostek and Trousseau signs; positive responses indicate potential tetany. Excessive or inappropriate muscle contractions that cause finger, hand, and elbow flexion. Bands or pits may encircle the teeth, which indicates a loss of tooth Ca & enamel. Dx Hypoparathyroidism: -Ca Total: 9.0-10.5 mg/dL, decreased -P: 3.0-4.5 mg/dL, increased -Mg: 1.3-2.1 mEq/L, decreased -PTH Whole: 10-65 pg/mL, decreased -Vit D (Calciferol): 25-80 ng/mL, decreased

Hypothyroidism: causes, assessment

Hypothyroidism: reduced/absent thyroid hormone secretion, results in whole-body decreased metabolism from inadequate cellular regulation. Deficits of T3/T4. -Early stages—disorder can be missed; onset is gradual & undramatic. -S/S widespread, reflecting reduced metabolism from low TH. Low metabolism causes hypothalamus & anterior pituitary to make TSH, to try to get the thyroid gland to release T3. TSH binds to the thyroid gland & causes a goiter, but T3/T4 production does not increase. Cellular energy decreased, causing buildup of metabolites in the cell, called glycosaminoglycans (GAGs= sugars+proteins). GAGs buildup increases the mucus and water, forms cellular edema, and changes organ texture. -S/S: Fatigue, Loss of appetite, Cold intolerance, wt gain, Constipation, Bradycardia, Puffy face, Dry and course skin, Thin and brittle nails and hair. -Myxedema: cellular edema from mucus and water buildup (GAGs). Seen in severe hypothyroidism. NON-pitting edema everywhere (esp. around the eyes, in the hands/feet, between shoulder blades). The tongue thickens, edema of the larynx causes the voice to be husky. -Myxedema Coma- aka hypothyroid crisis, a serious complication of untreated/poorly Tx hypothyroidism. Dangerously reduced cardiopulmonary and neuro functioning, but coma in adults is rare. Can cause orgain failure/dysfunction. Slow progression, but stress, infection, cold, or trauma can intensify it. S/S: hypotension, hypothermia, hypoglycemia, enlarged tongue, slow/slurry speech.

Indications for Testing People for Type 2 Diabetes

Indications for Testing People for Type 2 Diabetes: • Testing for diabetes is considered at any age in adults with a BMI greater than 25 kg/m2 (or greater than 23 kg/m2 in Asian Americans) with one or more of these additional risk factors: • Have a first-degree relative with diabetes • Are physically inactive • Are members of a high-risk ethnic population (e.g., African American, Hispanic American, American Indian, or Pacific Islander) • Give birth to a baby weighing more than 9 lb (4.1 kg) or have been diagnosed with GDM • Are hypertensive (>140/90 mm Hg) • Have a high-density lipoprotein (HDL) cholesterol level less than 35 mg/dL (0.90 mmol/L) and/or a triglyceride level greater than 250 mg/dL (2.82 mmol/L) • Have polycystic ovary syndrome • Have A1C greater than 5.7%, or IFG or IGT on previous testing • Have a history of vascular disease • If the tested adult has normal glucose values at this time but other conditions and risk factors remain the same, testing should be repeated at 3-year intervals.

Hyperthyroidism: causes, types, labs

Lab Assessment of Hyperthyroidism (thyrotoxicosis): -Over secretion of T-H's causes hypermetabolism, increased SNS activity. Stimulate hrt, increase HR & SV—causing increased CO, BP, and BF. -Can be permanent or temporary. -Types: many, Graves is most common (AKA toxic diffuse goiter)--Autoimm. dz, antibodies to TSH receptors stimulate thyroid. More often Dx in women age 20-40yrs--autosomal recessive, limited to females. Also Toxic multinodular goiter, usually occurs >50yrs, affects women 4x more. S/S are milder than Graves disease, and no exophthalmos or pretibial myxedema. Nodules may be enlarged thyroid tissues or benign tumors (adenomas). Patients usually have goiter for yrs. Exogenous, ingestion of T-H meds. Hyperthyroidism also co-occurs w/ autoimm/endocrine ds (DM, hyperparathyroidism). Serum T3: normal 70-205ng/dL, increased. Serum T4 total: normal 4-12mcg/dL, increased. Free T4 index: normal 0.8-2.8ng/dL, increased. TSH stimulation test (thyroid stimulation test): normal >10% in RAIU or >1.5 mcg/dL, N/A this test is used only to differentiate primary from secondary hypothyroidism Thyroid-stimulating immunoglobulins (TSI): normal <130% of basal activity, Elevated in Graves disease. Normal in other types of hyperthyroidism. Thyrotropin receptor antibodies (TRAbs): normal titer 0%, 80%-95% indicates Graves. TSH: normal 0.3-5mcU/mL. Low in Graves disease. High in secondary or tertiary hyperthyroidism. -Other Dx: Thyroid scan w/ RAI (meas. size, position, function--not for pregnant), measures RAIU--normal 5-35% in 24hrs; hyper-increased, ID active thyroid nodules. US-IDs size/composition of nodules or masses. ECG- usually shows supraventricular tachycardia, others include a-fib, dysrhythmias, & premature ventricular contractions.

Labs for Hypothyroidism, incidence, causes

Lab Assessment/Dx for Hypothyroidism: -Serum T3: normal 70-205ng/dL, decreased. -Serum T4 total: normal 4-12mcg/dL, decreased. -Free T4 index: normal 0.8-2.8ng/dL, decreased. -TSH stimulation test (thyroid stimulation test): normal >10% in RAIU or >1.5 mcg/dL, No response in primary hypothyroidism; Normal response in secondary hypothyroidism. -Thyroid-stimulating immunoglobulins (TSI): normal <130% of basal activity, no change. -Thyrotropin receptor antibodies (TRAbs): normal titer 0%, no response. -TSH: normal 0.3-5mcU/mL, High in primary disease; Low in secondary or tertiary disease. -Other labs : -CBC w/ differential: to rule out other possible causes of s/s (anemia or infection). -Blood Chemistries: needed to evaluate F&E status. -Triglycerides & cholesterol: Hypothyroidism can cause increase in these levels, leading to coronary atherosclerosis. -Common in: women, downs synd., DM. Occurs more often in women between 30-60yrs. Women are affected 7-10x more often than men. -Causes: primary- thyroidectomy, inflammatory conditions, autoimmune ds (HT). Secondary-inadequate intake of iodine, use of anti-thyroid meds.

Low-molecular-weight heparin

Low-molecular-weight heparin. Subcutaneous LMWHs such as enoxaparin or dalteparin have a consistent action and are preferred for prevention and treatment of DVT. LMWHs bind less to plasma proteins, blood cells, and vessel walls, resulting in a longer half-life and more predictable response. These drugs inhibit thrombin formation because of reduced factor IIa activity and enhanced inhibition of factor Xa and thrombin. -Some patients taking LMWH may be safely managed at home with visits from a home care RN. Candidates for home therapy must have stable DVT or PE, low risk for bleeding, adequate renal function, and normal vital signs. They must be willing to learn self-injection or have a family member, friend, or home care nurse administer the subcutaneous injections. -Some HCP place the patient on a regimen of IV UFH for several days and then follow up with an LMWH. In this case, the UFH is discontinued at least 30min before the 1st LMWH injection. Assess all stools for occult blood. The aPTTs are not checked on an ongoing basis because the doses of LMWH are not routinely adjusted. The anti-Xa factor can be assessed to monitor the effect of the LMWH. Therapeutic range of the anti-Xa factor for LMWH therapy is 0.5 to 1.2 IU/mL --LMWH is used more commonly today because of the complications involved with UFH.

Preventing Sickle Cell Crisis

Preventing Sickle Cell Crisis: -Drink at least 3 to 4 liters of liquids every day. -Avoid alcoholic beverages. -Avoid smoking cigarettes or using tobacco or nicotine in any form. -Contact your HCP at the first sign of illness or infection. -Be sure to get a "flu shot" every year. -Ask your HCP about receiving the pneumonia vaccine. -Avoid hot and cold temperature extremes. -Be sure to wear socks and gloves when going outside on cold days. -Avoid airplanes with unpressurized passenger cabins. Avoid travel to areas at high altitudes (e.g., Denver, Flagstaff, Santa Fe, Lake Louise). -Be sure all your HCP know that you have SCD, especially the anesthesia provider and radiologist. -Consider genetic counseling before becoming sexually active. -Avoid strenuous physical exercise. -When you are not in crisis, perform mild, low-impact exercise three times a week. Increases O2, prevents FVO.

Perform focused physical assessment including laboratory values for patients with suspected or actual Hypo-Pituitary conditions.

Perform focused physical assessment including lab values for patients with suspected or actual Pituitary conditions: -Hypopituitarism: deficiency of 1+ anterior or posterior hormones. Causes metabolic problems & sexual dysfunction. ACTH & TSH are the most life threatening. -Caused by: tumors, malnutrition (ex. AN), trauma (ex infection). -Results: -Low FSH/LH: decreased sex-H--irregular menses, amenorrhea, decreased hair, impotence, & bone density. -Low ACTH: decreased cortisol--weakness, malaise, N/V, hypoglycemia, hyponatremia, pale. -Low TSH: decreased thyroid-H--depression, apathy, wt gain, low cold tolerance, low libido, lethargy, slow cognition, scalp alopecia, hirsutism. -Low ADH: DI--increased UO & thirst, low SG (<1.005), dehydration, increased plasma Osm & elec. (esp. Na). UO doesn't decrease when fluid intake decreases. -Tx: lifelong HRT (Androgen/testosterone, estrogen, GH).

Physical Assessment of Hyperthyroidism

Physical Assessment of Hyperthyroidism: -Onset: will often follow an acute episode of physical/emotional stress. -Causes: Graves -Hallmark: heat intolerance, visual changes—may be earliest detectable problem. -Main S/S: Nervousness, Increased appetite, Heat Intolerance, Weight loss, Fine tremor of hands, Tachycardia, Warm/moist skin, Fine/soft hair. -Graves: exophthalmos- big/protruding eyes, can cause corneal ulcers & vision problems. Pretibial myxedema- dry/waxy swelling of the front of lower legs; resembles benign tumors or keloids. Enlarged thyroid/goiter, nervousness, heat intolerance, wt loss despite increased appetite, diaphoresis, & diarrhea. -Cardiopulmonary: Palpitations, Chest pain, Increased systolic BP/decreased diastolic BP--wide PP, Tachycardia, Dysrhythmias, Rapid/shallow respirations -Metabolic: Increased BMR, Heat intolerance, Low-grade fever, Fatigue -Neuro: Blurred or double vision, Eye fatigue, Increased tears, Injected (red) conjunctiva, Photophobia, Eyelid retraction, eyelid lag, Globe lag, Hyperactive DTR, Tremors, Insomnia -Skin: Diaphoresis. Fine, soft, silky body hair (straight). Smooth, warm, moist skin. Thinning of scalp hair. -GI: Weight loss, Increased appetite, Increased stools/diarrhea -Reproductive: Amenorrhea, Increased libido -Psychosocial: Decreased attention span, Restlessness and irritability, Emotional instability, Manic behavior -Other: Goiter, Wide-eyed or startled appearance (exophthalmos), Enlarged spleen, Muscle weakness and wasting -Eyelid lag- upper eyelid fails to descend when the patient gazes slowly downward. -Globe lag- upper eyelid pulls back faster than the eyeball when the patient gazes upward.

Prednisone: DM

Prednisone: Instruct the patient to report illness because the usual daily dosage may not be adequate during periods of illness or severe stress. -Once clinical improvement occurs, the corticosteroids are tapered because of the adverse effects that commonly occur with long-term steroid therapy (e.g., hyperglycemia, osteoporosis, peptic ulcer disease, increased potential for infection, adrenal insufficiency). -If you have diabetes and are taking steroid medication, your blood glucose levels are likely to increase. Steroid medications can raise blood glucose levels by reducing the action of insulin (causing insulin resistance) and making the liver release stored glucose into the bloodstream. -Common side effects that appear within a week of corticosteroid therapy include acne, sodium and fluid retention, hypertension, sensation of "nervousness," difficulty sleeping, and emotional changes such as crying easily. Side effects with long-term therapy include weight gain, fat redistribution (moon face; buffalo hump between the shoulders), increased risk for GI ulcers and bleeding, fragile skin that bruises easily, reduced muscle mass and strength, thinning scalp hair, increased facial and body hair, increased susceptibility to colds and other infections, and stretch marks. -Most important precaution to teach patients taking long-term corticosteroids is to never stop taking the drug abruptly because adrenal crisis can result and may be life threatening.

Preventing Injury from Hyperglycemia

Preventing Injury from Hyperglycemia -Non-surgical: nutrition, glucose monitoring, planned exercises, drugs. -Patient Education: blood glucose monitoring -Teach pt to check glucose when: s/s of hypoglycemia or hyperglycemia. Assess: Hx Hypoglycemic unawareness, Periods of illness, BS Before and after exercise, Gastroparesis. -Adjustment / evaluation of drug therapy: Pregnancy, Techniques for SMBG (Accucheck style), Data are evaluated with A1C. Anemia falsely elevates glucose values. Polycythemia falsely depresses glucose values. --Use teach back to appropriate use to use meters, calibration, and retest if obtained results are unusual. Frequency of testing varies with drug schedule, therapy and targe outcomes. Target goals: individualized. Recommendations: -Type 1 DM: A1C <= 7%, Premeal glucose: 70-130, Postmeal glucose: <180. Infection control Hand wash/Do not share equipment, Regular cleaning of the meter, Wear gloves, Alternate site testing. -ALERT: HISTORY OF HYPOGLYCEMIC UNAWARENESS DO NOT TEST AT ALTERNATIVE SITES -Continuous blood glucose monitoring (CGM): real-time glucose reader in interstitial fluid -Exercise: Improves carbs metabolism and insulin sensitivity. Type 1 DM: cannot maintain blood glucose levels during exercise. Without adequate insulin supply, cells cannot use glucose. Low insulin trigger release of glucagon and epi to increase liver glucose production, increasing blood glucose levels. That results in hyperglycemia and ketone body formation. Exercise can also cause hypoglycemia because of the increased muscle glucose uptake and inhibited glucose release from the liver during exercise +24h. -Benefits of exercise: Glucose regulation and reduced insulin requirements. Increase insulin sensitivity, increase glucose uptake and weight loss, Decrease CVD, Decrease LDL, Increase HDL, Decrease BP and improve cardiac function. Type 2 DM: prevents or delays by reducing body weight, insulin resistance, and glucose intolerance. Resistance exercises at least 2x week. Exercise adjustments are needed when complications are present: Uncontrolled HTN, Severe autonomic neuropathy, Severe peripheral neuropathy or foot lesions, Unstable proliferative retinopathy, Blood glucose control in hospitalized patients, Corticosteroids use, Change in nutrition therapy. -Hyperglycemia: leads to higher infection rates, longer stay, need for intensive care, and greater mortality Hypoglycemia (<40) is also a risk factor for mortality Glucose target: Critically ill patients: 140-180. Non-critically ill: premeal <140, random <180. Continuous IV insulin are the most effective method to achieve targets

Preventing PCV

Preventing PCV: -Drink at least 3 liters of liquids each day. -Avoid tight or constrictive clothing, especially garters and girdles. -Wear gloves when outdoors in temperatures lower than 50°F (10°C). -Keep all HC-related appointments. -Contact your primary HCP at the first sign of infection. -Take anticoagulants as prescribed. -Wear support hose or stockings while you are awake and up. -Elevate your feet whenever you are seated. -Exercise slowly & only on the advice of your P-HCP. -Stop activity at the first sign of chest pain. -Use an electric shaver. -Use a soft-bristle toothbrush to brush your teeth. -Do not floss between your teeth. -If you are a smoker, strongly consider smoking cessation.

Primary Polycythemia: Polycythemia vera (PV)

Primary Polycythemia: overproduction of RBCs, blood is hyperviscous. Common in jewish males age 40-70yrs. Erythroid St cells develop hypersensitivity to erythropoietin. --Polycythemia vera (PV): most common type. Not genetic. One of the chronic myeloproliferative neoplasms (MPNs) in which there is loss of cellular regulation with excessive expansion of specific groups of abnormal myeloid cells with decreased function. Differs from MPN because number of RBCs in the blood is greater than normal. -Can be temporary (from other conditions) or chronic. --Hgb levels are > 18 g/dL in men, & > 16.5 g/dL in women. RBC count of 6 million/mm3, hematocrit of >55%. --PV cancer of the RBCs: with 3 major hallmarks: massive production of RBCs, excessive leukocyte production, and excessive production of platelets. This cellular excess in the peripheral blood is known as hypercellularity. -Causes: 90%+ have a mutation of the JAK2 kinase gene in the affected cells; this mutation causes a loss of cellular regulation over blood cells. -Manifestations: Large # of RBC, abnormal, w/ shorter life spans—causes rapid turnover of RBCs—increases cellular debris (uric acid and K), which cause the s/s of gout and hyperkalemia. This further thickens the blood. --Large # RBC, but O2 carrying capacity is reduced, leading to poor gas exchange & severe hypoxia. Clotting/platelets are impaired leading to bleeding problems.

Interventions for Hypothyroidism

Priority problems: Decreased gas exchange and oxygenation due to decreased energy, obesity, muscle weakness, and fatigue. Hypotension and reduced perfusion due to decreased HR from decreased myocardial metabolism. Potential for the complication of myxedema coma. -Tx: Monitor VS, apply O2 if hypoxemia is present. Auscultate lungs for decreased breath sounds and crackles. If condition is severe, may need ventilator support. Sedation is avoided because it depresses the resp. system, if needed a lower dose will be used. -Monitor BP and HR and rhythm and observe for indications of shock (e.g., hypotension, decreased urine output, changes in mental status). -Chronic Hypothyroidism: may have CVD. Instruct the patient to report episodes of chest pain or chest discomfort immediately. Requires lifelong thyroid hormone replacement. Synthetic hormone preparations are usually prescribed (Thyroxine). Used to improve all S/S including GI & Cardiac. -RN teaching: med is life long, teach S/S of too much med causing hyperthyroidism. Ex. irritability, palpitations, tachycardia, diarrhea, tremors, insomnia. -Levothyroxine(Synthroid): start low, go slow. Too high of a dose will exacerbate hrt problems. Take exactly as ordered and try to always use the same brand. Final dosage is determined by levels of TSH and the patient's physical responses. The dosage and time required for symptom relief vary with each patient. -Provide a safe environment. -Diet: high fiber, low kCal, increase fluid intake, meticulous skin care.

RAI for Hyperthyroidism

RAI for Hyperthyroidism: -RAI: destroys part of the thyroid gland that produces hormones-- not used in pregnant women. Thyroid stores H's, so S/S relief may not occur for 6-8wks. Drug Tx will still be needed for first few weeks after RAI. Degree of thyroid destruction varies, some may have hypothyroidism as result and need lifelong HRT. -RAI Pt education: -Use a toilet that is not used by others for at least 2 weeks after receiving the radioactive iodine. Sit to urinate to avoid splashing urine. Flush the toilet (lid closed) 3x after each use. If urine is spilled on the toilet seat or floor, use paper tissues or towels to clean it up, bag them in sealable plastic bags, and take them to the hospital's radiation therapy department. Men with urinary incontinence should use condom catheters and a drainage bag rather than absorbent gel-filled briefs or pads. Women with urinary incontinence should use facial tissue layers in their clothing to catch the urine rather than absorbent gel-filled briefs or pads. These tissues should then be flushed down the toilet exclusively used by the patient. -Using a laxative on the second and third days after receiving the radioactive drug helps you excrete the contaminated stool faster (this also decreases the exposure of ABD organs). -Wear only machine-washable clothing and wash these items separately from others in your household. After washing, run the washing machine for a full cycle on empty before it is used to wash the clothing of others. -Avoid close contact with pregnant women, infants, and young children for the first week after therapy. Remain at least 3 feet away from these people and limit your exposure to them to no more than 1 hour daily. -Some radioactivity will be in your saliva during the first week after therapy. Precautions to avoid exposing others to this contamination (both household members and trash collectors) include: Not sharing toothbrushes or toothpaste tubes. Using disposable tissues rather than cloth handkerchiefs and either flushing used ones down the toilet or keeping them in a plastic bag and turning them in to the radiation department of the hospital for disposal.

Onset, Peak, Duration of Insulins; Mixing Insulin

Rapid-Acting Insulin Analogs: -Aspart injection- onset 0.25hr, peak 1-3hr, duration 3-5hr. -Glulisine- onset 0.3hr, peak 0.5-1.5hr, duration 3-4hr -lispro- onset 0.25, peak 0.5-1.5, duration 5 -human inhalation powder- onset 0.25, peak 1-1.25, duration 2.5 Short-Acting Insulin: -Regular human- onset 0.5, peak 2-4, duration 5-12 -Humulin R (Concentrated U-500)- onset 1.5, peak 4-12, duration 24 Intermediate Acting Insulin: -Isophane insulin NPH- onset 1-4, peak 4-12, duration 10-24+ Long-Acting Insulin Analogs: -glargine: onset 2-4, peak None, duration 24 -detemir: onset 1, peak 6-8, duration 5.7-24 -degludec: onset 1, peak 9, duration 42 -Mixing insulin: clear before cloudy! Do not mix any other insulin type with insulin glargine, insulin detemir, or any of the premixed insulin formulations such as Humalog Mix 75/25. Recommendations for Mixing Insulins: • Patients whose blood glucose levels are well controlled on a mixed-insulin dose need to maintain their individual routine when preparing and administering their insulin. • Do not mix insulin with any other medications or diluents unless approved by the health care provider. • Never mix insulin glargine (Lantus) or insulin detemir (Levemir) with other types of insulin. • Inject rapid-acting insulins mixed with NPH insulin within 15 minutes before a meal. • Verify insulin doses with another nurse while you are preparing the injection. -Steps: Take syringe with needleless device or filter needle and aspirate volume of air equivalent to first medication dose (vial A-cloudy). b. Inject air into vial A, making sure that needle or needleless device does not touch solution. c. Holding on to plunger, withdraw needle or needleless device and syringe from vial A. Aspirate air equivalent to second medication dose (vial B-clear) into syringe. d. Insert needle or needleless device into vial B, inject volume of air into vial B, and withdraw medication from vial B into syringe. e. Withdraw needle or needleless device and syringe from vial B. Ensure that proper volume has been obtained. f. Determine on syringe scale what the combined volume of medications should measure. g. Insert needle or needleless device into vial A (cloudy), being careful not to push plunger and expel medication within syringe into vial. Invert vial and carefully withdraw the desired amount of medication from vial A into syringe. h. Withdraw needle or needleless device and expel any excess air from syringe. Check fluid level in syringe for proper dose. Medications are now mixed.

SCD: Sickle Cell disease (anemia)

SCD: genetic disorder in which a mutation in the gene for the beta chains of Hgb causes chronic anemia, pain, disability, organ damage, increased risk for infection, and early death as a result of poor blood perfusion. Higher incidence in people of African decent. -SCD: >40% of the total Hgb is composed of 2 normal alpha chains and 2 abnormal beta chains (HbS) that fold poorly. HbS is sensitive to low oxygen content of RBCs, which causes them to fold even more, distorting the cells into sickle shapes. Average life span of an RBC w/ 40%+ of HbS is about 10-20 days—causes hemolytic (blood cell-destroying) anemia in patients with SCD. -The average life expectancy of adult men with SCD is 42 years and for women with SCD is 48 years. -Conditions that cause sickling: hypoxia, dehydration, infection, venous stasis, pregnancy, alcohol consumption, high altitudes, low or high environmental or body temperatures, acidosis, strenuous exercise, emotional stress, nicotine use (esp. cigarettes), and anesthesia. -Dx: family Hx-Genetic counseling, Blood tests, xray. Dx based on the HbS% on electrophoresis. AS usually has less than 40% HbS, and the patient with SCD may have 80% to 100% HbS. This percentage does not change during crises. Another indicator of SCD is the # of RBCs w/ permanent sickling. This value is <1% among people with no Hgb disease, 5%-50% among people with AS, and up to 90% among patients with SCD. -Lab tests can indicate complications: -Hct low (between 20% and 30%) because of RBC shortened life span and destruction. Value decreases more during crises or stress (aplastic crisis). -Reticulocyte count is high, indicating anemia of long duration. -Total bilirubin level may be high because damaged RBCs release iron and bilirubin. -WBC count is usually high. This elevation is related to chronic inflammation caused by tissue hypoxia and ischemia. -X-Ray: skull may show changes as a result of bone surface cell destruction and new growth, giving the skull a "crew cut" appearance on x-ray. Joints may show necrosis and destruction. -US, CT, PET, and MRI may show soft-tissue and organ changes from poor perfusion and chronic inflammation. -ECG: changes indicate cardiac infarcts and tissue damage. Specific ECG changes are related to the area of the heart damaged. -Echocardiograms may show cardiomyopathy and decreased cardiac output (low ejection fraction).

Sick-Day Rules: for DM

Sick-Day Rules • Notify your primary health care provider or diabetes health care provider that you are ill. • Monitor your blood glucose at least every 4 hours. • Test your urine for ketones when your blood glucose level is greater than 240 mg/dL. • Continue to take insulin or other antidiabetic agents, unless instructed otherwise by your primary health care provider. • To prevent dehydration, drink 8 to 12 ounces (240 to 360 mL) of sugar-free liquids every hour that you are awake. If your blood glucose level is below your target range, drink fluids that contain sugar. • Continue to eat meals at regular times. • If unable to tolerate solid food because of nausea, consume more easily tolerated foods or liquids equal to the carbohydrate content of your usual meal. • Call your diabetes health care provider for any of these problems: • Persistent nausea and vomiting • Moderate or high ketones • Blood glucose elevation after two supplemental doses of insulin • High (101.5°F [38.6°C]) temperature or increasing fever; fever for more than 24 hours • Treat diarrhea, nausea, vomiting, fever as directed by your diabetes health care provider. • Get plenty of rest.

Surgical Management of Hyperparathyroidism

Surgical Management of Hyperparathyroidism: -MIS parathyroidectomy- only remove the glands containing tumors. RN Care: same as with thyroidectomy. 70% of parathyroidectomies suffer from a decrease of PTH about 8-24hrs post-op. So monitor Ca levels, most doctors will order Ca level to be checked Q4 until the levels stabilize. Remaining glands, which may have atrophied as a result of PTH overproduction, require several days to several weeks to return to normal function—hypocalcemic crisis can occur. -Hypocalcemic crisis- life threatening, early S/S numbness, tingling of mouth, face, extremities. Check for Trousseau and Chvostek signs, either of which indicates potential tetany -Larengeal Nerve damage- assess frequently by asking the patient questions, ex. What is your name? What is your pain level? And other simple assessment questions, you don't need to tell them youre specifically assessing for nerve damage. Assess the patient for changes in voice patterns and hoarseness. -Hyperparathyroidism caused by hyperplasia (tissue overgrowth)- 3 glands plus half of the fourth gland are usually removed. If all four glands are removed, a small portion of a gland may be implanted in the forearm, where it produces PTH and maintains calcium homeostasis. If all these maneuvers fail, the patient will need lifelong treatment with calcium and vitamin D because the resulting hypoparathyroidism is permanent.

Syndrome of inappropriate antidiuretic hormone (SIADH)

Syndrome of inappropriate antidiuretic hormone (SIADH): or Schwartz-Bartter syndrome is a problem in which antidiuretic hormone (ADH, vasopressin) is secreted even when plasma osm is low-normal, resulting in H20 retention and FVO. A decrease in plasma osm normally inhibits ADH production and secretion. SIADH occurs with many conditions (e.g., cancer therapy, pulmonary infection or impairment) and with specific drugs, including selective serotonin reuptake inhibitors. ADH continues to be released when not needed, leading to water retention and disturbances of fluid and electrolyte balance. Water retention results in dilutional hyponatremia & FVO. The increase in bvL increases the kidney filtration and inhibits the release of renin and aldosterone, which increase urine sodium loss and results in greater hyponatremia. --Early s/s: related to the water-retention causing dilution of serum sodium levels. GI disturbances, such as loss of appetite, n/v, may occur first. Weigh the patient and document any recent weight gain. Use to monitor responses to Tx. Free water (not salt) is retained and dependent edema is not usually present, even though water is retained. -Water retention, hyponatremia, and fluid shifts affect CNS function, especially when the Na < 115 mEq/L. The patient may have lethargy, headaches, hostility, disorientation, and a change in LOC. Lethargy and headaches can progress to decreased responsiveness, seizures, and coma. Assess DTR, which are usually decreased. -VS changes include full and bounding pulse (caused by the increased fluid volume) and hypothermia (caused by CNS disturbance). --Water retention causes urine vL to decrease and urine osm to increase. At the same time, plasma vL increases, and plasma osm decreases. Elevated urine sodium levels and SG reflect increased urine concentration. Serum sodium levels decrease, sometimes to as low as 110 mEq/L, because of fluid retention and Na loss. -Initial Tx: restrict fluid (sometimes very low 500-660mL/day). Drugs-vassopressin antagonists (Samska) to excrete H20 w/o Na loss. When Na near normal-give diuretics. Hypertonic solutions, all PO fluid must contain Na. Poor management leads to HR--monitor for bounding pulse, JVD, crackles, edema, reduced UO. Provide a safe enviro when Na low bc increased confusion & seizure risk.

Teaching for DM

Teaching for DM: -Teach women with GDM about lifestyle changes to prevent DM -Veterans: prevention strategies to maintain healthy weight and regular exercise -No interventions prevent type 1 DM, but can reduce its long term complications -A healthy lifestyle: Low calorie diet, Increase physical activity - at least 150 min per week. Reducing HTN, increase heart rate, lower triglyceride levels, increase HDL, reduce LDL. Smoke cessation, Avoid alcohol, Keep blood glucose levels within prescribed target Follow up with HCP to check vision and kidney function Weight management. Foot inspection, report ulcers and open areas to HCP. Test blood glucose before exercise, at intervals, and after. When urine ketones are present pt should not exercise.

Focused Assessment: The Insulin-Dependent Patient With Diabetes During a Home or Clinic Visit

The Insulin-Dependent Patient With Diabetes During a Home or Clinic Visit • Assess overall mental status, wakefulness, ability to participate in a conversation. • Take vital signs and weight: Fever could indicate infection. Are blood pressure and weight within target range? If not, why? • Ask the patient about any change in vision; check current visual acuity. • Inspect oral mucous membranes, gums, and teeth. • Ask about injection areas used; inspect areas being used; assess whether the patient is using areas and rotating sites appropriately. • Inspect skin for intactness, wounds that have not healed, new sores, ulcers, bruises, or burns; assess any previously known wounds for infection, progression of healing. • Ask the patient how often and how he or she performs foot care. • Assess lower extremities and feet for peripheral pulses, lack of or decreased sensation, abnormal sensations, breaks in skin integrity, condition of toes and nails. • Ask about the color and consistency of stools and frequency of bowel movements; assess abdomen for bowel sounds. • Review patient's home health diary: Is blood glucose within targeted range? If not, why? Is glucose monitoring being recorded often enough? Is the patient's food intake adequate and appropriate? If not, why? Is exercise occurring regularly? If not, why? • Assess the patient's ability to perform self-monitoring of blood glucose. • Assess the patient's procedures for obtaining and storing insulin and syringes, cleaning equipment, disposing of syringes and needles. • Assess the patient's insulin preparation and injection technique. • Assess the patient's knowledge of drug therapy and which side effects to look for.

The priority collaborative problems for patients with diabetes DM include, TX

The priority collaborative problems for patients with diabetes DM include: 1. Potential for injury due to hyperglycemia 2. Potential for poor wound healing due to endocrine and vascular effects of diabetes 3. Potential for injury due to diabetic neuropathy 4. Potential for Kidney dz due to reduced perfusion 5. Potential for the complications of hypoglycemia, DKA, HHS, and coma. -Tx: Management involves nutrition Tx, blood glucose monitoring, a planned exercise program, and often, drugs to lower blood glucose levels. A1C levels are maintained at 7.0% or below (or as prescribed). The majority of premeal blood glucose levels are 70-130 mg/dL. Peak after-meal blood glucose levels are <180 mg/dL. -Drug therapy. Drug therapy is indicated when a patient with DM2 does not achieve blood glucose control w/ diet changes, regular exercise, & stress management. Several categories of drugs. Patients with DM1 require insulin Tx for blood glucose control & may use other antidiabetic drugs too. Drugs are started at the lowest effective dose & increased over time until the patient reaches desired blood glucose control or the max dosage. May require the use of more than one category of drug. Insulin therapy is indicated for the patient with DM2 when blood glucose goals cannot be met with the use of 2-3 different antidiabetic agents, including GLP-1 agonists. Antidiabetic drugs are not a substitute for dietary modification and exercise. Teach the patient about continuing dietary changes and regular exercise while taking antidiabetic drugs. --Insulin therapy. Insulin therapy is required for DM1 & often is used for DM2. The safety of insulin therapy in older patients may be affected by reduced vision, mobility and coordination problems, and decreased memory, increasing the risk for dosage errors. Many types of insulin and regimens are available to achieve normal blood glucose levels. Because insulin is a small protein that is quickly inactivated in the GI tract, it is usually injected. Rapid/short/intermediate/long-acting forms can be injected separately, & some can be mixed. Insulin is available in concentrations of 100 units/mL (U-100), 200 units/mL (U-200), 300 units/mL (U-300), and 500 units/mL (U-500). Insulin concentrations above 100 units/mL are reserved for when very large doses of insulin are required.

Thrombocytopenic purpura: ATP, TTP, HIT

Thrombocytopenic purpura is the destructive reduction of circulating platelets after normal platelet production. -Two common types: --Autoimmune thrombocytopenia purpura (ATP): formerly called idiopathic thrombocytopenic purpura. Immune system begins making antibodies against their own platelet membranes (antiplatelet antibody). When these antibodies attach to platelets, WBCs attack & destroy the circulating platelets & those stored in the spleen faster than new platelets are produced. As the number of circulating platelets decreases, clotting is impaired. This disorder is most common among women age 20-50yrs & w/ people who have other autoimmune disorders. --Thrombotic thrombocytopenia purpura (TTP): also thought to be an autoimmune disorder, w/ the reaction occurring in small BV cells (endothelial) & triggering abnormal platelet clumping in these BVs. Results in too few platelets remain in circulation. The patient's blood forms clots & platelet plugs where they are not needed, yet the blood fails to clot when trauma occurs. Tissues become ischemic (from blockages), leading to KF, MI, & stroke. W/o Tx, often fatal w/in 3mo. --Heparin-induced thrombocytopenia (HIT): serious immune-mediated clotting disorder with an unexplained drop in platelet count after heparin tx. The problem is increasing bc of increased use of heparin. HIT is an immune-mediated drug rx that is caused by heparin-dependent platelet-activating antibodies that allow heparin to bind with platelet factor 4 (PF4). (The antibodies are directed against the heparin rather than patient's own cells.) Heparin+PF4 creates an immune complex that activates the platelets, causing the formation of many microclots that use up circulating platelets, leading to thrombocytopenia. HIT can occur in patients receiving any type of heparin, more common w/ unfractionated heparin. The incidence is higher among females, Tx w/ unfractionated heparin for >1wk. -S/S: 1st seen in the skin & mucous membs & result from excessive bleeding in these tissues. Changes include large ecchymoses (bruises) or purpura (a reddish-purple fine petechial rash) on the arms, legs, upper chest, and neck. Mucous membranes bleed easily. If the patient has had significant blood loss, anemia may also be present. --ATP: distinguished from TTP by the presence of antiplatelet antibodies in the blood. --TTP & HIT: also have small microclots can block capillaries in major organs, causing tissue ischemia. This problem increases the risk for kidney damage, MI, & stroke. Other problems associated with --HIT: also have venous thromboembolism & pulmonary embolism. Dx made by the clinical s/s & Hx of heparin therapy w/in last 100 days. --Platelets are low in all 3 types of thrombocytopenia. If bleeding, Hct & Hgb levels may be low.

Thyroid Gland & Hormones, functions

Thyroid Gland & Hormones: -Follicular cells: T3/T4, T3 is activated T4. Controls & increases metabolism (BMR), heat production, & causes an increase in O2 use. In infants it stimulates G&D. TSH from hypothalamus, causes A-P to release TSH, causing thyroid to make/secrete T-H's. TRH secreted during stress/cold temp. Conversion of T4 to T3, increased in cold temp, impaired in stress, starvation, certain drugs/dyes. Intake of iodide necessary for production of T-H's. Absorbed by GI, thyroid draws/concentrates it & combines w/ tyrosine to form T3/T4. -Parafolicular cells: produce TCH (thyrocalcitonin, calcitonin). TCH lowers serum Ca and P, by reducing bone resorption/release of them (opposite of PTH). -Functions of Thyroid Hormones in Adults: -Control metabolic rate of all cells -Promote sufficient pituitary secretion of GH and gonadotropins. -Regulate protein, CHO, and fat metabolism -Exert effects on HR and contractility -Increase RBC production -Affect RR and drive -Increase bone formation/decrease bone resorption of calcium -Act as insulin antagonists

Thyroiditis: types, assessments, & Tx

Thyroiditis: inflammation of the thyroid gland. -3 types: acute, subacute, and chronic (Hashimoto's, most common). -Acute thyroiditis: caused by bacterial invasion of the thyroid gland. S/S: pain, neck tenderness, malaise, fever, and dysphagia. Tx: It usually resolves with AB Tx. Often resolves w/o complications. -Subacute or granulomatous thyroiditis: viral infection of the thyroid gland after a cold or other URT infection. -S/S: fever, chills, dysphagia, and muscle and joint pain. Pain can radiate to the ears & jaw. T-gland feels hard/enlarged. Thyroid function can remain normal, although hyperthyroidism or hypothyroidism may develop. -Chronic thyroiditis (Hashimoto thyroiditis [HT]): common type of hypothyroidism that affects women more often than men. -HT: autoimmune disorder that is usually triggered by a bacterial or viral infection. Thyroid is invaded by antithyroid antibodies and lymphocytes, causing selective thyroid tissue destruction. If large amounts of the gland are destroyed, hypothyroidism results. -S/S of HT: dysphagia and painless enlargement of the gland. -Dx: based on circulating antithyroid antibodies and needle biopsy of the thyroid gland. Serum T3/T4 & TSH levels vary w/ disease stage/type. -Tx: lifelong HRT to prevent hypothyroidism & suppress TSH secretions. Surgery is indicated when the goiter doesn't respond to meds or occludes breathing.

Transfusion Therapy, RN Responsibilities

Transfusion Therapy, RN Responsibilities: -Before Infusion: Assess laboratory values to ensure agency guidelines for blood transfusions are followed. Verify the P-HCP prescription for type of product, dose, and duration of transfusion because the therapy legally requires a prescription. Assess VS, UO, skin color, and Hx of transfusion rx to establish a baseline for identifying possible reactions during and after the procedure. Establish or use a venous access with a 19g needle or catheter to prevent catheter occlusion or damage to red blood cells. Transfuse (after all safety checks) soon after receiving them from the blood bank to suppress bacterial growth and prevent product deterioration. W/ another RN, verify the patient by name and #, check blood compatibility, & note expiration time because human error is the most common cause of incompatibility reactions. -During Infusion: Admin the blood product using the appropriate filtered tubing to remove aggregates and possible contaminants. Unless directed otherwise, infuse blood products only with IV NS solutions because some other IV solutions can cause hemolysis. Stay with the patient for the 1st 15-30min of the infusion because this is the time when hemolytic transfusion reactions occur. Infuse at the prescribed rate for the transfusion type to avoid the possible complication of fluid overload. Monitor VS at least as often as agency policy and the patient's condition indicates to identify early indications of adverse transfusion reactions. -After Infusion: When the transfusion is completed, discontinue the infusion and dispose of the bag & tubing according to agency and blood-bank policies to prevent the spread of bloodborne pathogens. Document all aspects of the transfusion (e.g., type of product, product number, volume infused, duration of infusion, VS, and any adverse reactions) to identify patient responses to the transfusion as part of the permanent record.

Interventions for Myxedema Coma

Tx for myxedema coma: Factors leading to myxedema coma include acute illness, surgery, chemotherapy, discontinuation of thyroid replacement therapy, and use of sedatives or opioids. Problems that often occur with this condition include: greatly decreased LOC & Cognition, resp. failure, hypotension, hyponatremia, hypothermia, hypoglycemia. -RN- prevent shock, coma, death: Assess the patient with hypothyroidism at least every 8 hours for changes that indicate increasing severity, especially changes in MS, and report these promptly to HCP. -Emergency care for Myxedema Coma: -Maintain a patent airway. -Replace fluids with IV normal or hypertonic saline as prescribed. -Give levothyroxine sodium IV as prescribed. -Give glucose IV as prescribed. -Give corticosteroids as prescribed. -Check the patient's temperature hourly. -Monitor blood pressure hourly. -Cover the patient with warm blankets. -Monitor for changes in mental status. -Turn every 2 hours. -Institute Aspiration Precautions.

Types of Insulin

Types of Insulin: -Rapid-, short-,intermediate-, and long acting forms of insulin can be injected separately and can be mixed in the same syringe. They are available in concentrations of U-100, U-200, U-300, and U-500. Insulin above 100 units/mL are reserved for when very large dose of insulin are required -Regardless of insulin regimen, adherence to injection schedules is critical in achieving the glycemic control needed to reduce long-term complications. -Single daily injection: One injection of intermediate or long acting insulin or an injection of intermediate or a combination of short and intermediate acting insulin. -Multiple component insulin: combines short & intermediate-acting insulin injected TWICE DAILY. 2/3 of the daily dose is given before breakfast, and 1/3 before the evening meal. -Insulin absorption: Absorption is fastest in the ABD, except for the 2in radius around the navel. This is the preferred injection site. Rotation w/in 1 anatomic site is preferred to rotation from one area to another to prevent day-to-day variability in absorption. Longer duration of action makes absorption less reliable. Larger doses prolong the absorption. Applying heat, massaging and exercising the injected area, will increase insulin absorption. Scarred areas have slow insulin absorption. -IM injection: faster absorption & is not used for routine insulin use. Most patients lightly grasp the fold of skin and inject at a 90 degree angle. 45 degree angle used for elderly who has thin skin. Overweight patients can use 4mm and 5mm needles to inject insulin at a 90 degree angle WITHOUT pinching the skin fold before injection -Insulin with rapid onset: Give within 10min before mealtime when blood glucose is in the target range If hyperglycemia or hypoglycemia is NOT PRESENT, can be given just before eating or even immediately after eating. -Regular insulin: Given at least 20-30 minutes before eating.

Unfractionated heparin therapy

Unfractionated heparin therapy. Some patients with a confirmed Dx of a blood clot are started on a regimen of IV UFH therapy. The HCP prescribes UFH to prevent further clotting, which often develops in the presence of an existing clot, and to prevent enlargement of the existing clot. Over a long period of time, the body slowly absorbs the existing clot. --Before UFH admin, a baseline PT, APTT, INR, CBC w/ platelets, urinalysis, stool for occult blood, and creatinine level are required. Notify the HCP if the platelet count is <100,000-120,000/mm3, depending on agency protocol. --UFH is initially given in a bolus IV dose followed by continuous infusion via pump --infusion is regulated by electronic pump, protects against accidental free flow. HCP or pharmacist prescribes concentrations of UFH (in 5% dextrose in water) & the number of units or milliliters/hr needed to maintain a therapeutic aPTT. --aPTT is measured at least daily, 6 hours after initiation, and 6 hours after any dose change, and the results are reported to the HCP ASAP to allow adjustment of heparin dosage. Therapeutic levels of aPTT are usually 1.5 to 2.5 times normal control levels. --Notify HCP if the aPTT value >70s or follow hospital protocol. Assess s/s of bleeding, which include hematuria, frank or occult blood in the stool, ecchymosis (bruising), petechiae, an altered level of consciousness, or pain. If bleeding occurs, stop the anticoagulant immediately and call the HCP or RRT! --While most patients who receive UFH are monitored using the aPTT value, the heparin anti-factor Xa (anti-Xa) is sometimes used to monitor and adjust therapy. The therapeutic range of the anti-Xa factor for UFH is 0.3 to 0.7 IU/mL. -UFH can also decrease platelet counts. Mild reductions are common and are resolved with continued heparin therapy. Severe platelet reductions, although rare, result from the development of antiplatelet bodies within 6-14 days after the beginning of Tx. Platelets aggregate into "white clots" that can cause thrombosis, usually in the form of an acute arterial occlusion. The HCP discontinues heparin if severe HIT (platelet count <150,000), or "white clot syndrome," occurs. --Dabigatran is a direct thrombin inhibitor that may be used as an alternative or for pt w/ Hx of HIT. These drugs increase the risk for bleeding. Monitor hemoglobin, hematocrit, aPTT, platelet count, urinalysis, fecal occult blood test, and BP for indications of this complication. An oral anticoagulant such as warfarin (Coumadin) may also be substituted for heparin if necessary. --Ensure that protamine sulfate, the antidote for heparin, is available if needed for excessive bleeding. -Prevent DVT: UFH may be given in low doses subcu for high-risk patients, esp. after orthopedic surgery. --Alternatives to UFH include: LMWH (enoxaparin-for orth-surgery), Novel oral anticoagulants (dabigatran, rivaroxaban, apixaban, edoxaban), Warfarin.