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NURS 323 - Pathophysiology/Pharmocology

Terms in this set (34)

A 12-year-old boy develops pancreatic atrophy with loss of his beta cells. Which of the following conditions does this boy most likely have?
A. Impaired glucose intolerance (IGT)
B. Impaired fasting intolerance (IFG)
C. Diabetes type 1
D. Diabetes type 2
c.Type 1 diabetes mellitus is demonstrated by pancreatic atrophy and specific loss of beta cells. Diabetes type 2 occurs in ethnic minorities, females, and those with obesity or metabolic syndromes. IGT occurs when 2-hour postload glucose level is greater than or equal to 140 mg/dl but less than 200 mg/dl. IFG is defined as a fasting glucose greater than or equal to 110 mg/dl but less than 126 mg/dl.
Which of the following is NOT a typical symptom of new-onset diabetes?
A. Polydipsia
B. Anuria
C. Polyphagia
D. Weight loss
b.The classic symptoms of diabetes include polyuria, polydipsia, polyphagia, and unexplained weight loss. Anuria is the absence of urine production or a urinary output of less than 100 mL per day.
Which of the following contributes to insulin resistance?
A. A thin body habitus
B. Illness
C. Active lifestyle
D. Young age
b.Resistance of the receptors to insulin is heightened by obesity, inactivity, illnesses, medications, and age.
Which of the following is a TRUE statement regarding diabetic ketoacidosis (DKA)?
A. Increase in insulin
B. Decrease in catecholamines
C. Peak in the older adult
D. Accelerated gluconeogenesis and ketogenesis
d.DKA develops when there is an absolute or relative deficiency of insulin or increase in insulin counterregulatory hormones. This includes an increase in catecholamines, cortisol, glucagon, and growth hormone. Emotional factors and stress, especially in children, can contribute to the development of DKA. Profound insulin deficiency results in decreased glucose uptake, increased fat mobilization with release of fatty acids, and accelerated gluconeogenesis and ketogenesis. Also glucose production increases, peripheral glucose usage decreases, and fat mobilization increases.
A person develops severe dehydration and hyperglycemia. There is an absence of ketosis. Which of the following conditions does this person have?
A. Hyperosmolar hyperglycemic nonketotic syndrome (HHNKS)
B. DKA
C. Hypoglycemia
D. Somogyi effect
a.HHNKS is different from DKA in the degree of insulin deficiency and fluid deficiency. It is also characterized by a lack of ketosis. Somogyi effect occurs when hypoglycemia stimulates glucose counterregulation of hormones. This causes a rebound hyperglycemia.
Which of the following BEST describes the Somogyi effect?
A. Hyperglycemia followed by hypoglycemia
B. Hypoglycemia followed by rebound hyperglycemia
C. Early morning rise in blood glucose with no hypoglycemia
D. Early morning hypoglycemia without rebound hyperglycemia
b.The Somogyi effect is a unique combination of hypoglycemia followed by rebound hyperglycemia.
Insulin
- Binds to insulin receptors on the cells membrane
- Allows glucose to move from the blood into the cells to be used as energy
Ketones
- Byproduct of fat metabolism for energy
- Leads to metabolic acidosis
Type 1 DM
- Little or no insulin is produced by the pancreas
- Formerly known as juvenile onset or insulin dependent diabetes mellitus (IDDM)
- Most often occurs in people under 30 y/o
Type 1 DM etiology and pathophysiology
- Result of pancreatic islet cell destruction and a total deficit of circulating insulin
- T-cells attack and destroy pancreatic beta cells
- Auto-antibodies cause a reduction of 80% to 90% of normal beta cell function before manifestations occur
- Causes: genetic predisposition and exposure to a virus, unknown non-immune factors
Type 1 DM clinical manifestations
- Weight loss
- Classic triad signs of hyperglycemia (polyuria, polydipsia, polyphagia)
- Weakness and fatigue
- Ketoacidosis
Classic triad of s/sx of hyperglycemia
3 P's = Polyuria, polydipsia, polyphagia
Type 1 DM treatment
Requires insulin injections for LIFE
No oral hypoglycemic agents
Type 2 DM
- Formerly known as non-insulin dependent diabetes mellitus (NIDDM) or "adult onset"
- Encompasses over 90% of persons with diabetes
- 80% to 90% of patients are overweight at time of diagnosis
- Pancreas continues to produce some endogenous insulin, insulin is produced in insufficient quantity AND/OR insulin is poorly used by the tissues (insulin resistance)
Type 2 DM risk factors
- Obesity, especially abd. and visceral adiposity
- Sedentary (sitting around) lifestyle
- Family history
- Impaired glucose tolerance
- Ethnic ancestry
- HTN, high cholesterol, previous gestational diabetes
Insulin Resistance (Type 2 DM) etiology and pathophysiology
- Body does not respond to endogenous insulin (insulin from originating from within the body)
- Results in hyperglycemia (polydipsia, polyuria, polyphagia)
Type 2 DM clinical manifestations
- Onset usually gradual
- People can go for years with undetected hyperglycemia
- Classic hyperglycemic s/sx
- May be nonspecific, triad of hyperglycemia, fatigue, recurrent infections, recurrent vaginal yeast infections, prolonged wound healing, visual changes, paresthesias
Gestational diabetes
- Develops during pregnancy, detected at 24-28 weeks of gestation following an oral glucose tolerance test (OGTT)
- Higher risk for cesarean delivery, prenatal death, and neonatal complications
- Increased risk for developing Type 2 Diabetes after delivery
Diagnostic Studies (Diabetes)
1.) Fasting plasma glucose level (>126 mg/dL, with at least an 8 hour fast, with repeat on another day)
2.) Random plasma glucose measurement (>200 mg/dL plus clinical manifestations of diabetes, taken anytime during day)
3.) Two hour oral glucose tolerance test (OGTT, level >200mg/dL using a glucose load of 75g)
4.) A1C
5.) Urine Testing
6.) Blood glucose levels
Glycosylated Hemoglobin
- Hemoglobin A1C
- Determines glycemic levels over time: adherence to treatment regime (3 months)
- Measures the amount of glucose attached to a hemoglobin molecule for over their lifespan
- Normal 4.5-6%
- >=6.5% indicated DM
Why do we use Urine Testing (Diagnostic studies)
- Used to monitor hyperglycemia and ketoacidosis in type 1 DM
- Measures ketones in urine
Goals of Diabetes Management
Reduce symptoms, promote well being, prevent acute complications, delay onset and progression of long-term complications
Acute Hygiene (Diabetes)
- Must be diligent with dental and skin hygiene, brush and floss daily, inform dentist of DM diagnosis, visit dentist q 2 years, bathe regularly
- Special care for feet (must see podiatrist to clip toenails)
- Treat cuts, scrapes, or burns promptly and monitor carefully (poor wound healing)
Acute complications of Diabetes
1.) DKA
2.) HHNKS
3.) Hypoglycemia
DKA
- Diabetic Ketoacidosis occurs mainly in Type 1 DM
- Lack of insulin combined with counterregulatory hormone actions
- Caused by increased carbohydrate metabolism
- Result: fat stores are used to provide energy
DKA Signs and Symptoms
Polyuria, polydipsia, polyphagia, weight loss, vomiting, abdominal pain, ketone breath odor, dehydration, weakness, acidosis, Kussmaul respirations, altered mental state, shock, coma
DKA Nursing Interventions
- Assess: airway, LOC, hydration status, electrolytes, blood glucose level, temperature, urine output, mental status q1h, VS q 15 mins until stable, hourly blood glucose
- Treat underlying cause
- Monitor fluid status during aggressive replacement (1-2 L 0.9% NS over first 30 mins - 1 hour, 0.45% saline infused slower)
- If BS = 250mg/dL add dextrose!!
- Regular insulin IV (0.1 unit/kg bolus, 01 unit/kg/hr continuous drip)
- Replace serum K
- Infuse bicarb if severe acidosis occurs
HHNKS
- Hyperglycemic-Hyperosmolar Non Ketone Syndrome
- Type 2 DM, impaired thirst sensation and/or functional inability to replace fluids
- Blood glucose levels >600 mg/dL
- Severe hyperglycemia
-Hyperosmolality
- Dehydration
HHS Signs and Symptoms
Inadequate fluid intake, increasing mental depression, polydypsia, polyuria, somnolence, seizures, aphasia, motor and sensory impairment, coma
HHS Nursing Interventions
- Assess: airway, LOC, hydration status, electrolytes, blood glucose level, temperature, urine output, mental status q1h, VS q 15 mins until stable, hourly blood glucose
- Treat underlying cause
- Monitor fluid status during aggressive replacement (1-2 L 0.9% NS over first 30 mins - 1 hour, 0.45% saline infused slower)
- If BS = 250mg/dL add dextrose!!
- Regular insulin IV (0.1 unit/kg bolus, 01 unit/kg/hr continuous drip)
- Replace serum K IV
Hypoglycemia
- Blood glucose less than 60 mg/dL
- Cause is often mismatch between timing of food intake and peak action of insulin or oral hypoglycemia agents
- Too much insulin/medication, too little food, delayed time of eating, unusual amounts of exercises
- At risk: elderly and people taking beta adrenergic blockers (masks s/sx of hypoglycemia)
Hypoglycemia Signs and Symptoms
- Confusion, irritability, diaphoresis, tremors, weakness, visual disturbances, can mimic alcohol intoxication
- If left untreated: loss of consciousness, seizures, and death can occur
Hypoglycemia Collaborative Care
- Stat blood glucose
- Tx: 15-20g simple carb 4-6 oz fruit juice or regular soft drink, or 8 oz. low-fat milk OR commercial products: gels/tablets
- Repeat in 15 minutes if no improvement, ER if no improvement after 2-3 snacks
- Unconscious/altered LOC: 1 mg glucagon SQ or IM or IV of 50 mL 50% dextrose
Chronic complications of Diabetes
1.) Angiopathy
2.) CAD
3.) HTN
4.) CVA
5.) Diabetic retinopathy
6.) Nephropathy
7.) Complications of feet and lower extremities
8.) Infection
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