N-120 Exam 2
Reglan
(Antiemetic) Treatment of postsurgical and diabetic stasis. Management of gastroesophageal reflux. Therapuetic effects- Decreases N/V decreases symptoms of gastric stasis. Peripherally releases acetycholine resulting in increased gastric emptying.
Vistaril
(Antihistamine) Prevents N/V. Drug is also known as Hydroxyzine.
Phenergan
(Antihistamine) Prevents N/V. Drug is also known as Promethazine. Has an anticholinergic effect to control N/V.
Zofran
(Seratonin Antagonist) Prevents N/V. Drug is also known as Ondansetron. It is an antagonist to specific serotonin (5-HT) receptors (that act centrally and peripherally to prevent N/V.
11. What is the relationship between an incompetent lower esophageal sphincter (LES) and GERD?
- Short A: This sphincter when incompetent allows gastric juices and contents to escape from the stomach to escape into the esophagus causing irritation and inflammation. The esophagus has a mucus lining and is not designed to withstand the acidic nature of gastric juices. This acidity can lead to esophageal erosion and possible bleeding and/or infections. certain foods can cause this like caffeine, chocolate (say it ain't so!), drugs like anticholinergics, etc. (The list is longer like onions, garlic, alcohol... pretty much all the stuff we like to eat or that make recipes taste better.) Off topic but bulimia exacerbates LES and these patients often has acid reflux. So if you get a young woman with heart burn, look at the back of her hand (for teeth marks) and assess for chronic GERD.
Who is at risk of developing Type 2 diabetes?
-80-90% of people w/ type 2 DM are overweight, calorie and fat reduction is goal -most prevalent type of DM, 90% of patients w/ DM -most powerful risk factor = obesity, specifically abdominal and visceral -individuals w/ metabolic syndrome (characterized by insulin resistance, elevated insulin levels, high levels of triglycerides, decreased levels of HDLs, increased levels of LDLs, and HTN) are at increased risk for development of type 2. -risk factors for metabolic syndrome incl.: central obesity, sedentary lifestyle, urbanization/westernization, certain ethnicities (native American, Hispanics, African Americans) -ADA recommends routine screening for all obese adults > 45 yo
Is oxygen an appropriate intervention for Kussmaul breathing? Why or why not? -
-Kussmaul breathing: rapid, deep breathing associated w/dyspnea, body's attempt to reverse metabolic acidosis (from DKA) through exhalation of excess carbon dioxide. -Yes, O2 therapy is an appropriate intervention for DKA as an attempt to compensate for the metabolic acidosis. Ensure a patent airway and administer O2 via nasal cannula or non-rebreather mask
What is metformin?
-a biguanide glucose-lowering agent -used alone or w/ sulfonyluras (which increase insulin production in pancreas), other OAs, or insulin to treat type 2 DM -primary action is to reduce glucose production by liver -enhances insulin sensitivity at tissue level and improves glucose transport into cells -does NOT promote weight gain (unlike insulin and sulfonylureas); beneficial effects on plasma lipids; used to prevent DM w/ those w/ prediabetes, esp those who are obese and have genetic predisposition -combo therapies w/ other drugs in tablet form available -it is the generic name
What is hypoglycemic protocol?
-causes of hypoglycemia are often related to mismatch in timeing of food intake and peak action of insulin or oral hypoglycemic agents that increase indogenous insulin secreation -balance b/t blood glucose and insulin can be disrupted by the admin of too much insulin or meds, the ingestion of too little food, delaying time of eating, performing unusual amts of exercise -if blood glucose is below 70 mg/dl, pt should immediatedly begin tx for hypoglycemia Treatment If alert enough to swallow: -15 to 20 g of a simple carbohydrate -4 to 6 oz fruit juice -Regular soft drink -Avoid foods with fat -Decrease absorption of sugar -Do not overtreat -Recheck blood sugar 15 minutes after treatment -Repeat until blood sugar >70 mg/dl -Patient should eat regularly scheduled meal/snack to prevent rebound hypoglycemia -Check blood sugar again 45 minutes after treatment If no improvement after 2 or 3 doses of simple carbohydrate OR Patient not alert enough to swallow: -Administer 1 mg of glucagon IM or subcutaneously -Side effect: Rebound hypoglycemia -Have patient ingest a complex carbohydrate after recovery -In acute care settings -20 to 50 ml of 50% dextrose IV push -after correction is made, determine cause of hypoglycemia...remember, hypoglycemia can be verrrrry bad. (side note: in case you haven't seen this already, any time you have a diabetic patient in the hospital and you look at their MAR, in addition to the insulin therapy indicated, you will also so therapies for hypoglycemic therapies for hypoglycemic protocol - in the event that this should occur. In my experience thus far, I've seen multiple interventions indicated which all depend on the severity and status of the patient...)
What is glucophage?
-this is a brand name of metformin -as per above, used for type 2 DM
What information does hemoglobin A1C give the health professional? What is normal?
-useful in determining glycemic levels over time -not diagnostic but monitors success of tx and make changes to tx modalities -shows the amt of glucose attached to hgb molecule over RBC lifespan - 90-120 days -ideal goal is <6.5% -NI AIC reduces risk of retinopathy, nephropathy, neuropathy -anemias (or other blood disorders) may alter the lab results due to screwy glucose attachment to hgb, so just be aware
How are HHS & DKA similar? Different?
DKA vs. HHS Similarities: -Both DKA and HHS occur because of hyperglycemia -Treatment is similar and includes immediate IV administration of either 0.9% or ).45% NaCl at a rate that is dependent on cardiac status and the degree of fluid volume deficit. Differences - DKA occurs mostly with type 1 DM; HHS occurs mostly with people >60yo w/ Type 2 DM - DKA occurs with people whose circulating supply of insulin is insufficient; HHS there is enough circulating insulin so that ketoacidosis does not occur. - With DKA the person experiences polyuria; with HHS there is a reduction in renal perfusion which leads to oliguria and then possibly no urine formation -There are ketone bodies in the urine (ketonuria) with DKA because glucose cannot be properly used for energy (due to insufficient circulating supply of insulin) so the body breaks down fat stores as a secondary source of fuel; HHS does not have ketones in the urine because there is enough circulating insulin - HHS requires greater fluid replacement treatment -Hypoglycemia is not as significant in HHS as it is in DKA, although fluid losses may result in milder potassium deficits that require replacement. When treating HHS, why is insulin withheld until fluid resuscitation is underway? What effect does this have on potassium blood level? You withhold insulin until fluid resuscitation is underway to aid in reducing the hyperglycemia. Hypokalemia is not as significant in HHS as it is in DKA, but you may have a mild potassium deficit that requires IV fluid replacement.
2. List three potential problems associated with prolonged nausea and vomiting.
Dehydration- water plus essential electrolytes (K+, NA+, CL-, H+) are lost -severe electrolyte imbalanceloss of extracellular fluid, decreased plasma volume, and even circulatory failure Metabolic Alkalosis- results from loss of gastric HCL Threat of pulmonary aspiration - A concern with patient who is elderly, unconscious or other conditions that impair gag-reflex. -patient who cannot manage self care should be placed in semi-fowler or side lying position to prevent aspiration.
What is DKA?
Diabetic Ketoacidosis (DKA) Also referred to as diabetic acidosis and diabetic coma is caused by profound deficiency of insulin Characterized by: hyperglycemia, ketosis, acidosis, dehydration Most likely to occur in people with Type 1 diabetes, but may also be seen in type 2 with severe illness or stress when the pancreas can't meet the extra demand for insulin. Decrease insulin & excess glucagon lead to increase release of glucose by liver from glucagon through glucogenesis. Increase glucose level spills into urine (taking water and solution Na & K) Leads to dehydration Precipitating factors: Illness and infection, Inadequate insulin dosage, Poor self management, Neglect, Undiagnosed Type I Signs and symptoms: Dehydration. Lethargy and weakness, Abdominal pain - N/V, Kussmaul respirations - sweet fruity odor. An abnormal slow deep respiration; A respiratory compensation for metabolic acidosis. Blood gases will show a low partial pressure of CO2 in conjunction with low bicarbonate because of a forced increased respiration, blowing of CO2. When acidosis is less severe, the breath is rapid and deep gasping. Common lab values: Blood glucose > 300mg/dl, Arterial blood pH below 7.3, Serum bicarbonate level < 15 mEq/L, Ketones in blood and urine
13. List four foods that can aggravate symptoms of GERD.
Diet does not cause GERD but food can aggravate symptoms. Foods that cause reflux should be avoided. Foods that decrease LES (lower esophageal sphincter) pressure, such as chocolate, peppermint, coffee, and tea should be avoided because they are predisposed to reflux. Milk products also should be avoided at bedtime to decrease gastric acid secretion.
How does illness effect blood glucose?
From the textbook • Acute illness, injury and surgery are situations that may evoke a counter-regulatory hormone response resulting in hyperglycemia. Even minor illness, such as a cold or flu can cause this. • When pts with DM are ill, they should continue their regular meal plan while increasing intake of non-caloric fluids, such as broth, water, diet gelatin and other decaffeinated beverages. • Blood glucose should be checked at least every four hours. • The health care provider should be notified promptly if the pt is unable to keep any fluids or food down.
Identify the clinical manifestations of acute and chronic complications of diabetes mellitus.(neuropathy, retinopathy and nephropathy)
From the textbook Acute complications: o Hypoglycemia Can result from too much insulin or an excessive dose of an oral agent. Important that health care provider is able to distinguish btw hyper and hypoglycemia, because hypo worsens rapidly and constitutes and serious threat if not treated immediately. Blood glucose level of below 70/mg/dL requires treatment for hypo. Treat by giving pt 15 - 20 g of simple carb, such as 4-6 oz of fruit juice. Treatment with sweet foods that also contain fat should be avoided. o Diabetic ketoacidosis (DKA) - also referred to as diabetic acidosis or diabetic coma. Is cause by a profound deficiency of insulin and is characterized by hyperglycemia, ketosis, acidosis, and dehydration. Most likely to occur in Type 1. When the circulating supply of insulin is insufficient, glucose cannot be properly used for energy so that the body breaks down fat stores as a secondary souce of fuel. Ketones are acidic by-products of fat metabolims that can cause serious problems when they become excessive in the blood stream - altering pH balance and causing metabolic acidosis to develop. Ketonuria is a process that begins when ketone bodies are excreted in the urine. During this process, electrolytes b/c depleted as cations are eliminated along w/the anionic ketones in an attempt to maintain electrical neutrality. Renal failure may eventually occur from hypovolemic shock. This causes the retention of ketones and glucose, and the acidosis progresses. Untreated, the pt b/c comatose as a result of dehydration, electrolyte imbalance and acidosis. If untreated, death is inevitable. o Hyperosmolar hyperglycemic syndrome (HHS) A life-threatening syndrome that can occur in the DM pt who is able to produce enough insulin to prevent DKA, but not enough to prevent severe hyperglycemia, osmotic diuresis and extracelluar fluid depletion. HHS is less common than DKA. Most often occurs in pts over the age of 60 with Type 2. Pt with HHS produces fewer symptoms (than DKA) in the earlier stages, blood glucose levels can climb quite high before the problem is recognized. High blood glucose levels produce more severe neurologic manifestations, such as somnolence, coma, seizures, hemiparesis, and aphasia. Often related to impaired thirst sensation and/or a functional inability to replace fluids. There is usally a history of inadequate fluid intake, increased mental depression and polyuria. Lab values in HHS include blood glucose of greater than 400 mg/dL. Ketones are absent or minimal in both blood and urine. HHS is a medical emergency and has a high mortality rate. Chronic complications: • Those of organ disease from damage to blood vessels (angiopathy) secondary to chronic hyperglycemia. Angiopathy is one of the leading causes of DM-realated deaths, with about 65% of those due to cardiovascular disease and stroke. These chronic blood vessel dysfunctioons are divided into two categories: macrovascular complications and microvascular complications. • Macrovascular complications - disease of the large and medium blood vessels that occur w/greater frequency with an earlier onset in people with DM. These include: cerebrovascular, cardiovascular, and peripheral vascular disease. • Microvascular complications - result from thickening of the vessel membranes in the capillaries and arterioles in response to conditions of chronic hyperglycemia. They most noticeably affect the eyes (retinopathy), the kidneys (nephropathy), and the skin (dermophathy). • Infection - people with DM are more susceptible to infections than other pts because of a defect in the mobilization of inflammatory cells and an impairment of phagocytosis by neutrophils and monocytes. Pts may not feel their infections, which can delay detection/treatment.
Describe the nursing management of a patient with newly diagnosed diabetes mellitus.
From the textbook • Assessment of the pt who is new to insulin must include an eval of his/her ability to manage this therapy safely. This includes the ability to understand the interaction of insulin, diet, and activity and to be able to recognize and treat the symptoms of hypoglycemia appropriately. • Many pts are fearful when they first begin using insulin. Some find it difficult to self inject b/d they are afraid of needles or the pain. Some are afraid they will hurt themselves by giving too much or too little insulin. • Some pts believe that using insulin is a "last-ditch" effort and that he/she has to be in the final stages of the disease process therefore it is important to explore the patient's underlying fears before beginning and teaching. • The potential for microvascular complications and infections requires diligent skin and dental hygiene practices on the part of the pt. Daily brushing/flossing and regularly dental visits must be encouraged. • Emphasis s/b given to foot care. • The pt should be instructed to carry medical ID at all times, indicating he/she is a DM pt. (medical alert bracelet) • Travel requires advanced planning to ensure a full set of diabetic care supplies.
Describe the nursing management of the patient with diabetes mellitus in the ambulatory and home care settings.
From the textbook • Successful management requires ongoing interaction among the pt, family and the health care team. • A diabetes nurse educator should be involved in the care of the pt and family • Many w/DM face challenges for self-care due to poor vision, mobility issues and cardio-vascular disease. In some cases, a nurse will make referrals to others who can help the pat achieve self-care. • Pt's support system should be id'd. If it is the family, they need to be involved in teaching so they can care for the pt when self-care is no longer possible. • Nurses teach proper admin of insulin, assess pt response to insulin therapy, and educate pt regarding side affects and adjustments that may need to be made. • DM can profoundly affect pt's life. Careful assessment of what it means to the pt to have DM should be the starting point of pt teaching. Goals of teaching s/b mutually determined by the pt and the nurse, based on the individual's needs as well as therapeutic requirements.
How does exercise influence blood glucose?
From the textbook • Exercise increases insulin receptor sites in the tissue and can have a direct effect on lowering the blood glucose levels. • Pts who use insulin, sulfonylureas, or meglitinides are at increased risk for hypoglycemia when there is increased physical activity. • Glucose-lowering effects of exercise can last up to 48 hours. • Strenuous activity can be perceived by the body as a stress, causing a release of counter-regulatory hormones that result in a temporary elevation of blood glucose.
Describe the role of nutrition and exercise in the management of diabetes mellitus.
From the textbook (see question 12 for exercise info) • Nutrition therapy is the cornerstone of care for the person with DM - yet it is the most challenging for pts. • DM is a general metabolic disorder that involves three energy nutrients: carbohydrates, fats, and proteins. In a diabetic meal plan: a. carbs and mono-unsaturated fats should provide 45-65% of total energy intake b. Low-carb diets are not recommended for pts with DM c. Carbs include sugars, starches and fiber. Carbs from whole grains, frits, vegetables and low-fat milk s/b included in meal plan. d. Fats should compose no more than 25-30% of the meal plan's total cals, with less than 7% coming from saturated fats. e. Protein should contribute less than 10% of the total energy consumed. f. Alcohol promotes hypertriglyceridemia. It can cause severe hypoglycemia in pts on insulin or on oral hypoglycemic meds. DM pts should only drink alcohol with food, use sugar-free mixes, and drink dry, light-wines. No more than one drink per day for women, and two for men. • The Glycemic Index (GI) is a term used to describe the rise in blood glucose levels after a person has consumed a carb-containing food. A GI of 100 refers to the response of 50 g of glucose or white white bread in a normal person w/out DM. All other food with an equivalent carb value is measured against this standard. For example: GI of an apple is 52, regular milk is 27, baked potato is 93. • According to the ADA, the overall goal of nutritional therapy is to assist people w/diabetes in making healthy nutritional choices eating a varied diet, and maintaining exercise habits that will lead to improved metabolic control. Specific goals include: a. Maintain blood glucose levels to as near normal as safely possible to prevent or reduce the risk for complications of DM. b. Achieve lipid profiles and bp levels that reduce cardiovascular disease risk. c. Modify lifestyle as appropriate for the prevention and treatment of obesity, dyslipidemia, cardiovascular disease, and nephrophathy. d. Improve health through healthy food choices and physical activity. e. Address individual nutritional needs while taking into personal and cultural preferences and respecting the individual's willingness to change. • For Type 1 DM: a. Meal planning s/b based on the individual's usual food intake and balanced w/insulin and exercise programs. b. The insulin regimen s/b developed w/the pt's eating habits and activity pattern in mind. c. Day-to-day consistency in timing and the amount of food eaten is important for those using conventional, fixed insulin regimens. d. Pts using rapid-acting insulin can make adjustments in dosage before the meal based on the current blood glucose level and the carbohydrate content of the meal. e. Intensified insulin therapy, such as multiple daily injections or the use of an insulin pump, allows considerable flexibility in food selection and can be adjusted for deviations in food/exercise habits. • For Type 2 DM: a. Emphasis should be placed on achieving glucose, lipid, and bp goals. b. Because 80-90% of those with Type 2 DM are overweight, calorie and fat reduction is a goal. c. A weight loss of 5-7% of body weight often improves glycemic control, even if the desirable body weight is not achieved. On Exercise, from the textbook • Regular exercise is considered an essential part of diabetes and prediabetes management. • Exercise increases insulin receptor sites in the tissue and can have a direct effect on lowering the blood glucose levels. • Exercise contributes to weight loss, which decreases insulin resistance. • Regular exercise may also help reduce triglyceride and LDL cholesterol levels, increase HDL, reduce BP, and improve circulation. • Any new exercise program started by a diabetic pt s/b started only after medical clearance and should be started slowly. • Pts who use insulin, sulfonylureas, or meglitinides are at increased risk for hypoglycemia when there is increased physical activity. • Glucose-lowering effects of exercise can last up to 48 hours. • Several small carbohydrate snacks can be taken every 30 minutes during exercise to prevent hypoglycemia. Pts using meds that place them at risk for hypoglycemia should always caring a fast-acting source of carb with them, such as glucose tabs or hard candy. • Strenuous activity can be perceived by the body as a stress, causing a release of counter-regulatory hormones that result in a temporary elevation of blood glucose.
15. What is the pathophysiology of gastritis?
Gastritis occurs as the result of a breakdown in the normal gastric mucosal barrier. This mucosal barrier normally protects the stomach tissue from autodigestion by HCL acid and the proteolytic enzyme pepsin. When the barrier is broken, HCL and pepsin can diffuse back into the mucosa. This back diffusion results in tissue edema, disruption of capillary walls with loss of plasma into the gastric lumen, and possible hemorrhage. (See Table 42-16)Pg 1013.
List the manifestations of hyperglycemia
Gradual onset. s/s include: Three Ps: polyuria (frequent urination), polyphagia (excessive thirst) and polydispsia (excessive hunger)
What is HHS?
Hyperosmolar Hyperglycemic Syndrome (HHS) sometimes called Hyperosmolar Hyperglycemic Nonketotic Syndrome (HHNS) -It is a life-threatening syndrome that is less common than Diabetic Ketoacidosis -More common in patients over 60 years old with Type 2 Diabetes When someone with Type 2 diabetes eats a lot of carbohydrates, their insulin resistance increases causing hyperglycemia. Since the concentration of solutes is increased, water and essential ions are going to be released from the kidneys leads to osmotic diuresis which leads to fluid volume deficit. This leads to a depletion in sodium, potassium and phosphorus causing an electrolyte imbalance. Since most of the people that suffer from HHS already have a history of dehydration, this electrolyte imbalance makes them even more susceptible to profound dehydration leading to hyperosmolarity and hypovolemia. Hypovolemia causes a decrease in renal profusion, hypotension and a hyperviscosity of the blood which can all lead to seizure, shock, coma and possibly death. Lab values (for HHS) include: Blood Glucose > 400 mg/dl (22.25 mmol/L), marked increase in serum osmolality. Ketone bodies are absent (or minimal) in both blood and urine. Treatment includes administration of IV fluids to correct dehydration, admin insulin therapy to reduce blood glucose and serum acetone, admin of electrolytes to correct electrolyte imbalance, assessment of renal status, cardiopulmonary status related to hydration and electrolyte levels, and monitoring level of consciousness. Monitor signs of potassium imbalance resulting from osmotic diuresis.
If the patient has manifestations of hypoglycemia and monitoring equipment is not available, what action should the nurse take?
Hypoglycemia should be assumed and treatment should be initiated. -Treated by ingesting 15-20 g of simple (fast acting carbohydrates) -4-6 oz of fruit juices or regular soft drink -8 oz of low fat milk -Commercial products (gels or tablets) with specific amounts of glucose - Avoid foods with fat b/c slows absorption -Avoid over-treatment with large quantities of simple sugars to prevent fluctuation to hyperglycemia -If no significant improvement in patients condition after 2-3 doses of 15 g of simple carbohydrates of if patient can't swallow then 1 mg of glucagon may be administered IM or Sub-Q
List the manifestations of Type 1 diabetes
Manifestations of Type 1 diabetes: - PPP (polyuria, polydipsia, polyphagia); - the osmotic effect of glucose produces the manifestations of polydipsia and polyuria; - polyphagia is a consequence of cellular malnourishment when insulin deficiency prevents utilization of glucose for energy; - weight loss, weakness, and fatigue;
List the manifestations of Type 2 diabetes;
Manifestations of Type 2 Diabetes: - fatigue, recurrent infections, recurrent vaginal yeasts or monilia infections, prolonged wound healing, and visual changes; - clinical manifestations occur so gradually that an individual may blame the symptoms on other cause, such as lack of sleep or increasing age;
1. Differentiate between nausea and vomiting.
Nausea is the feeling of discomfort in the epigastrium with a conscious desire to vomit. (subjective) Vomiting is the forceful ejection of partially digested food and secretions (emesis) from the upper GI tract. (objective) Requires coordination -closure of glottis -deep inspiration with contraction of the diaphragm in inspiratory position -closure of pylorus -relaxation of the stomach and lower esophageal sphincter -contraction of abdominal muscles with increasing intra-abdominal pressure
5. Describe the pathophysiology and clinical manifestations of diabetes mellitus.
Pathophysiology of Type 1: - results from loss of beta cell function and an absolute insulin deficiency; - causes are genetic predisposition or exposure to virus; - predisposition to this type of diabetes is believed to be related to HLAs (human leukocyte antigens), when an individual with certain HLA types is exposed to viral infections, the beta cells of the pancreas are destroyed, either directly or through autoimmune process; Manifestations of Type 1: - PPP (polydipsia, polyuria, polyphagia); Pathophysiology of Type 2: 1. insulin resistance (tissue doesn't respond to the action of insulin); 2. marked decrease in the ability of pancreas to produce insulin; 3. inappropriate glucose production by the liver (instead of properly regulating the release of glucose in response to blood levels, the liver does so in hazard way that doesn't correspond to the body's needs at the time); 4. alteration in the production of hormones and cytokines by the adipose tissue; Manifestations of Type 2: - gradual onset with fatigue, recurrent infections, and visual changes;
7. What is the clinical significance of black tarry stools?
Pretty much same as the above. Bottom line: we need to know the color and consistency so we know where the GI bleed is happening. If we're dealing with stool that's brown and has red, then we're dealing with a hemorrhoid and/or anus fissure issue.
What is a random glucose test? Fasting glucose test? Post-prandial glucose tolerance test? What are considered normal ranges
Random glucose test- tests glucose levels any time of day with out regard to time of last meal. Positive test is plasma glucose measurement >= 200 mg/dl & manifestations of Diabetes (polydipsia, polyuria, polyphagia/unexplained weight loss)- Indicative of DM Fasting Glucose test No caloric intake for at least 8 hours. Glucose levels >=126 indicative of DM Glucose levels between 100 mg/dl & 126 considered impaired fasting glucose Post-prandial Glucose tolerance test Test 2 hours after having a standard glucose load of 75 g. Glucose level greater than 200 mg/dl indicative of DM Glucose level between 140mg/dl & 199 mg/dl indicative of Impaired glucose tolerance
6. What is the clinical significance of melena? -
Refers to black, tarry feces associated with a GI hemorrhage. Black is caused by the oxidation of iron in the Hgb as it passes thru the colon. (From p. 688) Gastric bleeds can be a significant source of blood loss. GI bleeding is often not apparent and therefore may take time before the problem is identified. Loss of 50-75ml of blood from the upper GI tract is req'd for stools to appear black (melena). Common causes, peptic ulcer, gastritis, esophagitis, diverticuli, hemorrhoids and neoplasia. Loss of 1500mL of blood = a 25% loss of blood volume = hypovolemia (not good). Most common sites for GI bleeds are Esophagus, stomach and duodenum. Ulcers account for 50% of UGI bleeding. UGI bleeds - 6-10% mortality. Risk factors: Women, age, NSAIDs. Severity depends on venous, cap or arterial hemorrhage source.
What type of insulin can be given IV?
Regular (Humulin R, Novolin R) (short-acting)... Aspart (Novolog) (rapid-acting) can be given via IV infusion
3. Differentiate between regurgitation and projectile vomiting.
Regurgitation-a process in which partially digested food is slowly brought up from the stomach. Retching and vomiting seldom precedes it. (although not part of this question-"vomiting" lies between regurgitation and projectile vomiting) Projectile Vomiting- a very forceful expulsion of stomach contents without nausea and is characteristic of CNS tumors
4. What is the clinical significance of "coffee ground" emesis?
Related to gastric bleeding, blood changes to dark brown as a result of interaction with HCL. Commonly causes of upper GI ulcers include- H. pylori, NSAIDs, Stress-Related Mucosal Disease(SRMD) -occurs commonly in patients who sustained severe trauma, burns or had major surgery. -if anyone had a surgical patient in clinicals-this is why they were taking antacids.
12. What is the cause of respiratory complications of GERD?
Respiratory complications of GERD include cough, bronchospasm, laryngospasm, and cricopharyngeal spasm. These complications are due to the irritation of the upper airway by gastric secretions. There is also the potential for asthma, chronic bronchitis, and pneumonia as a result of aspiration of gastric contents into the respiratory system.
14. What are the two types of hiatal hernia?
Sliding hernia: The junction of the stomach and esophagus is above the hiatus of the diaphragm, and a part of the stomach slides through the hiatal opening in the diaphragm. The stomach "slides" into the thoracic cavity when the patient is supine and usually goes back into the abdominal cavity when the patient is standing upright. This is the most common type of hiatal hernia. Paraesophageal or rolling: The esophagastric junction remains in the normal position, but the fundus and the greater curvature of the stomach roll up through the diaphragm, forming a pocket alongside the esophagus.
List the manifestations of hypoglycemia
Sudden onset. s/s include: Weakness, diaphoretic, sweat, pallor, tremors, nervousness, feeling hungry, diplopia (seeing two images at the same time), confusion, aphasia, vertigo, and convulsions Remember that hypoglycemia is more dangerous than hyperglycemia.
10. Regarding gastroesophageal reflux disease (GERD), is it a disease or a syndrome?
Syndrome!!!! GERD is any clinically significant symptomatic condition or histopathologic alteration secondary to reflux of gastric contents into the lower esophagus. GERD is the most common upper GI problem seen in adults. Approx. 14-10% of the US experience GERD at lease once a week!!! There is no single cause. (Side note: For patho this was one of my topics for a paper. Of note, acupuncture and Chinese herbs have proven effective when other Western medicines proved to be ineffective. That came from a study.)
16. What is the rationale for the increasing incidence of peptic ulcer disease in patients over 60 years of age?
The incidence of PUD and gastric ulcers in patients over 60 is on the rise due the the increased use of NSAIDS. For some patients the first manifestation may be frank gastric bleeding (hematemesis melena) or a decrease in hematocrit. The morbidity and mortality rates associated with PUD in the elderly patient are higher than those younger adults because of health problems (ex: cardiovascular, pulmonary) and a decreased ability to with stand hypovolemia. The patient is usually treated with antisecretory agents-PPI's or H2R blockers.
Describe the effect of hyperglycemia on the osmotic pressure of the blood and the symptoms that result
Tissue that don't require insulin for glucose transport (kidney, RBCs, blood vessels, eye lens, nerves) use an alternative metabolic pathway for glucose metabolism known as the polyol pathway. With hyperglycemia, glucose is shunted to this pathway and is converted to sorbitol which is then slowly converted to fructose. The resulting accumulation of sorbitol increases intracellular osmotic pressure and attracts water, leading to cell injury such as: - in the lens of the eye, leads to swelling with visual changes and cataracts; - in nerves, damages Schwann cells, and disrupts nerve conduction; - RBCs become swollen and stiff and interfere with perfusion;
9. List two factors that are linked to development of oral cancer.
Tobacco use (cigar, cigarette, pipe, snuff) excessive alcohol intake, and chronic irritation such as from a jagged tooth or poor dental care. Smothers have a 7-10x great risk of developing oral cancer vs non smokers. Overexposure to UV radiation (sun) is also a factor with lip cancer. HPV too. More common after 40yo. Ave age onset = 60 yo. More common with men. Most occur on the lower lip in men.
1. Compare the characteristics of type 1 and type 2 diabetes.
Type 1 DM - result of long-standing process in which the body's own T-cell attack and destroy pancreatic b-cells; absolute insulin deficiency; - causes are genetic predisposition (most often African or Asian decent) or exposure to virus; - antibodies present for months to years before symptoms occur; - more common in young persons but can occur at any age; - accounts for 5-10% of all types of diabetes; - islet cell antibodies often present at onset; - nutritional status thin, catabolic state; - symptoms are thirst, polyuria, polyphagia, fatigue, weight loss; - ketosis prone at onset or during insulin deficiency; Type 2 DM - the pancreas usually continues to produce endogenous insulin, but it is insufficient for the needs of body and/or is poorly utilized by the tissue; in contrast, there is a virtual absence of endogenous insulin in Type 1; - developing of type 2 associated with obesity (abdominal and visceral adiposity); - increased rate in African Americans, Asian Americans, Hispanic Americans, and Native Americans; - usually occurs at age 35 yr or older but can occur at any age; - accounts for 90% of all type of diabetes; - ketosis resistant during infection or stress; - symptoms are fatigue, recurrent infections;
What is glucagon? What is a potential adverse effect?
Typically produced by the Alpha cells in the pancreas, Glucagon stimulates a strong hepatic response to convert glycogen to glucose and therefore makes glucose rapidly available. Due to the fast acting nature and the depletion of glycogen stores rebound hypoglycemia is a potential adverse effect of glucagons. Having a patients ingest complex carbohydrates after recovering may prevent this from happening. -Patients with minimum glycogen stores will not respond to glucagons Pts with alcohol related hepatic disease, starvation or adrenal insufficiency
8. After an acute bleeding episode, what patient teaching is indicated in order to help prevent future bleeding episodes?
Ulcer disease, drug or alcohol abuse and liver and respiratory diseases can all result to future UGI bleeding incidents. The patient and family must be made aware of the consequences of noncompliance with diet and drug therapy. Only prescribed drugs are to be taken. NO aspirin or SNAIDs are to be ingested. Smoking and alcohol consumption (my favorite toxic twin combo!) should be eliminated as they are sources of of irritation and interfere with tissue replacement. There is also a need for long term follow-up care. Also tell the pt and the family what to do if an acute hemorrhage occurs in the future. The book doesn't say this but I'm assuming that you'd explain/describe Melena. Call the health care provider. Other indicators for nurses, pts and caretakers are: reduced LOC, VS not WNR (lo BP, rapid weak pulse), appearance of neck veins, skin pallor and slow cap refill. Look for abdomen distention and guarding. Pt could be in shock from blood loss (weak pulse, increased thirst, cold clammy skin.) Monitor BP signs every 15-30 minutes. Also note that 80-85% of massive hemorrhages stop spontaneously. However the cause must be identified and treatment initiated. Ulcers account for 50% of UGI bleeding. Drugs, prescribed and OTC are also major culprits. Aspirins and NSAIDs being major culprits.
Know the peak, onset and duration of the following types of insulin (refer to handout):
a. Lispro b. Regular c. NPH d. Lantus e. Novolin® 70/30
2. Answer the following "why" questions:
a. Why is the person with type 1 diabetes usually thin? Person with type 1 diabetes is thin because insulin deficiency prevents utilization of glucose for energy and body has to turn to other sources of energy such as fat or protein. b. Why is insulin required for people with type 1 diabetes but not necessarily for those with type 2 diabetes? The individual with type 1 diabetes requires a supply of insulin from outside source ( pancreas cannot produce any), such as injection in order to sustain life; otherwise; without insulin the patient will develop diabetic ketoacidosis; while patients with type 2, pancreas can produce some endogenous insulin (self-made). c. Why does hypersecretion of insulin occur in type 2 diabetes? When the insulin isn't used properly, the entry of glucose into the cell is impeded, resulting in hyperglycemia. In the early stages of insulin resistance, the pancreas responds to the high blood glucose by producing greater amounts of insulin, which creates a temporary state of hyperinsulinemia that coexists with the hyperglycemia. d. Why are symptoms more acute in type 1 diabetes? - before any manifestations occur, 80-90% of progressive autoimmune destruction of pancreatic beta cells has already happened; once this happens and pancreas can no longer produce insulin the onset is rapid and more acute; ketoacidosis is usually the first indicator;
5. In what position should the nurse place the patient to prevent aspiration if the unconscious patient who is vomiting?
• 30 degrees. 45-90 degrees is a recipe for pressure ulcers. • She also suggests checking what you think 30 degrees looks like. • One study showed that only 20% of nurses properly gauged 30 degrees.
How does stress effect blood glucose?
• Both emotional and physical stress can increase blood glucose levels and result in hyperglycemia. • Sometimes extra insulin is required to maintain glycemic goals and avoid hyperglycemia.
