DM

characterized by inappropriate hyperglycemia caused by a relative or absolute deficiency of insulin or by cellular resistance to action of insulin

  1. type1: result of pancreatic islet cell destruction and a total deficit of circulating insulin

  2. type2: results from insulin resistance with a defect in compensatory insulin secretion

  3. gestational diabetes: condition in which blood sugar levels become high during pregnancy affecting pregnant women who has never been diagnosed with diabetes


DM: hormones produced by several different cells of the endocrine pancreas along with hormones produced by small intestine are responsible for glucose homeostasis in the body.

-TYPE1: characterized by hyperglycemia, a breakdown of body fats and proteins and development of ketosis. Result of destruction of beta cells of islets of langerhans in insulin is no longer produced.

-TYPE2: condition of fasting hyperglycemia that occurs as a result of progressive insulin resistance. Level of insulin produced varies and is impaired by insulin resistance in peripheral tissues. Liver produces more glucose than normal thus dietary carbs are not metabolized well and eventually the pancreas secretes less than adequate amounts of insulin. Insulin production is usually sufficient to prevent breakdown of fats with resultant ketosis thus T2DM is a nonketotic form of DM. However, the function of insulin available is not sufficient to lower blood glucose levels through the uptake of glucose by muscle and fat cells.


pathophysiology of T2DM:

  • body either produces inadequate amounts of insulin to meet demands of body or insulin resistance has developed

  • insulin resistance: when cells of body such as muscle, liver and fat cells fail to respond to insulin even when levels are high

  • in fat cells, triglycerides are broken down to produce free fatty acids for energy, muscle cells are deprived of an energy source and liver cells fail to build up glycogen stores

  • leading to an overall rise in level of glucose in blood. Glycogen stores become reduced thus less glucose available for release when needed

  • obesity and lack of physical activity are major causes of insulin resistance


RISKS:

  1. history of DM in parents or siblings

  2. obesity

  3. physically inactive

  4. race/ ethnicity


manifestations: (in case)

  • polyuria— hyperglycemia causes serum hyperosmolality, drawing water from intracellular spaces into vascular circulation. The increased blood volume increases renal blood flow, and hyperglycemia acts as an osmotic diuretic. This increases urine output and causes loss of electrolytes.

  • polydipsia— the decrease in interstitial and later intracellular volume and the increase urinary output causes dehydration. the mouth becomes dry and thirst sensors are activated causing a person to drink more fluids.

  • blurred vision— result from osmotic effect that cause swelling of lenses


diagnostic test:

  1. HbA1c: measures amount of glucose attached to haemoglobin, shows average amount of glucose attached to haemoglobin over past three months

  2. OGTT: performed in morning at least 3 days of unrestricted diet and usual physical activity, fast pt 8-14h overnight and collect 3ml fasting blood specimen. Administer 75g glucose in water orally over course of 5mins and pt shld engage in minimal physical activity. No eating after glucose is administered. Collect a second blood specimen 2h after test load

  3. urine analysis

  4. fasting lipids


acute complications:

  1. hyperglycemia— somogyi effect and dawn phenomenon: cause people with DM to have high blood sugar in morning

  • somogyi effect: involves a surge of hormones but due to a low blood sugar episode overnight.

  • dawn phenomenon: doesnt happen because of low sugar but happens when hormones in body naturally makes blood sugar higher (more common)

  1. hypoglycemia: results in primarily mismatch between insulin intake, physical activities and lack of carb availability

CLINICALS:

  • slurred speech

  • blurred vision

  • nausea

  • sweating

  • decreasing level of consciousness

  • shakiness

  • irritability

  • rapid pulse

  • pale, cool skin

MANAGEMENTS:

  • 15g of rapid-acting sugar

  • if manifestations cont, 15/15 rule: wait 15, eat another 15g of carbs if sugar level still low

  • if conscious and alert, give 10-15g of an oral carbs

  • if altered levels of consciousness, paternal glucose administered by intravenous push (D50)

  1. DKA*

  1. HHS— very high blood sugar leads to severe dehydration and highly concentrated blood. Involves lack of insulin but still can produce enough insulin to prevent the production of ketones. Thus, theres an underlying condition such as an infection thats also contributing to high blood sugar.

chronic complications:

  1. cardiovascular disease— effect of hyperglycemia from impaired glucose tolerance and insulin resistance sets off an inflammatory process in the vascular endothelial lining

  2. peripheral vascular disease

  3. diabetic retinopathy/ nephropathy— microvascular damage and hemorrhages lead to scarring of retina leading to cause of blindness, risk of developing cataracts as a result of increased glucose levels within the lens itself/ microvascular disease of kidneys characterized by presence of albumin in urine, hypertension, and progressive renal insufficiency, microvascular damage results in thickening of the basement membrane of glomeruli impairing renal function. Glomerulosclerosis thickens the basement membrane and simultaneously makes it functionally leaky, allowing large molecules such as protein to be lost in urine.

  4. mood alterations

  5. increased susceptibility to infection

  6. periodontal diseases


diabetic ketoacidosis (DKA)*:

serious complication of DM that can be life-threatening (most common in T1DM)

  • develops when there is a deficiency of insulin resulting in glucose deficiency at the cellular level. Glucose deficit causes fat stores to break down to provide energy resulting in mobilization of fatty acids with a subsequent ketosis

  • glucose production by liver increases, peripheral glucose decreases, fat mobilization increases, and ketogenesis is stimulates

  • severe hyperglycemia results in osmotic diuresis which leads to dehydration and loss of electrolytes. If untreated, fluid volume deficit leads to poor tissue perfusion and lactic acidosis, further complicating the metabolic acidosis.

  • glucose is the primary fuel for human body and when low on glucose, or dont have enough insulin to help cells absorb glucose, the body uses fat for energy (yay)

  • ketone is an alternative source of energy to sugar and is produced by body breaking down fats known as ketosis, is often produced when body has insufficient insulin. Instead of insulin helping cells to absorb glucose, body starts to break down fats for energy. Ketones are byproducts of breaking down of fatty acids.

  • those without DM rely on insulin, glucagon, and other hormones that help prevent ketone levels in blood from getting too high.

  • those with DM have a risk of ketones building up in their blood. High level of ketones produced that can cause blood to become acidic which can cause danger to organs if not treated on time

SYMPTOMS:

  1. high blood sugar and ketones in urine

  2. excessive thirst

  3. polyuria in large amounts

  4. sudden loss of weight

  5. nausea/ stomach pain

  6. vomit

  7. dehydration (sore throat, dry mouth and tongue, dark circles)

  8. deep, heavy breathing

  9. fruity-swelling breath

  10. drowsiness leading to unconsciousness

MANAGEMENT:

  • requires medical attention (blood glucose greater than 13.9 mmol/L, a decreasing pH, and ketones in urine)

  • if pt is alert and conscious, fluids may be replaced orally. In the first 12h of treatment, adults require 8-10L of fluid ro replace losses from polyuria and vomiting

  • initial fluid replacement may be administered with 0.9% saline solution at a rate of 500-1000mL/h

  • when blood glucose levels reach 13.9mmol/L, dextrose added to IV solutions prevent rapid decreases in glucose. There is a risk of fatal cerebral edema if blood glucose is lowered too quickly or fluids are given too rapidly/excessively


nursing considerations for METFORMIN:

  • monitor for GI side effects. Administer after meal to reduce GI upset

  • monitor liver/ renal function tests as impairment increases risk of lactic acidosis

  • monitor blood glucose and HbA1c levels. Monitor signs and symptoms of hypoglycaemia such as tachycardia, palpitations, confusion, sweating, headache, and fatigue


nursing consideration for GLIPIZIDE:

  • monitor blood glucose and HbA1c levels

  • monitor for signs and symptoms of hypoglycaemia such as tachycardia, palpitations, confusion, headache, fatigue and nervousness

  • administer before meals for better efficacy


nursing considerations for EMPAGLIFLOZIN:

  • monitor for burning sensation when passing urine as may cause urinary tract infection especially in females

  • educate pt to practise good genital hygiene

  • monitor for shortness of breath or fruity breath as may cause DKA which is serious, as long as monitoring for blood glucose levels and HbA1c levels


hyperthyroidism:
nursing interventions for imbalanced nutrition:

  • monitor daily weight and keep a record of results— inability to meet metabolic demands results in loss of body weight. Regular monitoring detects continued weight loss

  • refer to dietician to offer a diet high in protein and carbs, including snacks in between meals— increased nutrients to meet metabolic demands. Small frequent meal will increase food intake

  • monitor nutritional status through lab test results— a negative nitrogen balance indicates a catabolic state in which protein is lost and metabolic demands are not being met

  • monitor intake and output chart strictly— to monitor fluid balance and note nausea, vomiting or diarrhoea

  • instruct pt to report any abdominal pain— to allow immediate care for the problems reported by pt and further worsening the condition


pt education:

  1. teach medication indication, side effects and need for continued medical care

  2. provide postoperative wound care since the pt has subtotal thyroidectomy iodine therapy

  3. teach pt to detect hyperthyroidism symptoms if pt is on radioactive iodine therapy

  4. refer pt to community healthcare agencies