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Nursing Adult Health Exam 1
Terms in this set (74)
How soon the insulin starts to lower blood glucose after it is administered.
The time after administration, that the insulin is working the hardest to lower blood glucose.
Duration of action
How long the insulin lasts-the length of time from administration, that it keeps lowering the blood glucose.
Rapid Acting Insulin
Rapid effect, most like endogenous insulin in response to a meal. Shorter duration than regular insulin. Covers immediately after the injection, patient to eat within 5-15 min.
Onset: 10-15 minutes
Peak: 1 hour
Duration 2-4 hours
Short acting Insulin Regular
Humulin - R
Is clear. Given 20-30 minutes before a meal. Covers the increase in glucose after meals. May be given alone or with a longer acting insulin. Can't be mixed with Glargine and Glulisine.
Humulin - Time
Onset: 30-60 minutes
Peak: 2-3 hours
Duration: 4-6 hours
Intermediate Acting Insulin
White and cloudy. Onset: 2-4 hours
Peak: 4-12 hours
Duration: 16-20 hours
Very long acting Insulin
Glargine and Detimir
Glargine and Detimir
Peakless, absorbed very slowly over 24 hours. This insulin can't be mixed. Given once a day at the same time, to provide a relative constant level of insulin.
A group of metabolic diseases characterized by increased levels of glucose in the blood resulting from defects in insulin secretion, insulin action or both.
Type 1 Diabetes
Loss of beta cell function and absolute insulin deficiency. Not making any insulin.
Type 2 diabetes
Results from insulin resistance accompanied by relative lack of insulin (beta cell dysfunction). Tissues do not respond to insulin. Do not always need insulin med.
Occurs in Type 1 Diabetes. Liver breaks down free fatty acids in the absence of insulin which cause increased production of ketone bodies. Leads to diabetic ketoacidosis. Causes nausea, vomiting, abdominal pain, and can progress to cerebral edema, coma, and death.
Type 1 Manifestations
Sudden symptoms onset. 3 Ps - Polyuria, polydipsia, polyphagia. May have sudden weight loss and ketoacidosis.
Type 2 Manifestations
Slow onset, may have 3 Ps. Fatigue, weakness, vision changes, tingling or numbness in extremities, dry skin, slow wound healing, and recurring infections.
Criteria for Diabetes
Fasting blood glucose - ≥ 126 mg/dl (No caloric intake for 8 hours)
Random Blood Glucose - ≥ to 200
HgbA1C - ≥ to 6.5%
Monitoring Blood Glucose levels
BG monitoring - cornerstone of diabetes management. Before meals, snacks, and bedtime. Before and after exercising. Learn how to respond to results.
Occurs when the BG falls to <70 mg/dl. Severe if BG < 40 mg/dl. Can be caused by too much insulin, hypoglycemic medicine, too little food, or excessive physical activity.
Sympathetic nervous system is stimulated. Adrenergic response - surge of epinephrine and norepinephrine. Sweating, tremor, tachycardia, palpitations, nervousness, and hunger.
Drop in glucose level deprives brain cells of needed fuel. Signs of impaired CNS function: Poor concentration, headache, lightheadedness, confusion, memory lapse, slurred speech, impaired coordination, double vision, and drowsiness.
CNS is so impaired that the patient needs the assistance of another person for treatment. Symptoms - disoriented behavior, seizures, difficulty arousing from sleep, and loss of consciousness.
2. Cardiac monitor
3. Potassium Replacement
4. Insulin Drip
Hyperglycemic Hyperosmolar Syndrome (HHS)
Metabolic disorder usually of type 2 diabetes. Result of insulin deficiency caused by an illness that raises the demand for insulin. Type 2 patient who is able to produce enough insulin to prevent DKA but not enough to prevent hyperglycemia.
Hypotension, profound dehydration, tachycardia and variable neurologic signs.
Perpheral Vascular Disease
Disorders of the arteries or veins that cause a malfunction with the natural flow of the circulatory system outside the brain and heart circulatory system. It is when a (failure) change occurs within the system.
Partial or total occlusions = ischemia and tissue death.
Caused by atherosclerotic plaques (90% of reason for arterial disease). Can lead to altered flow rate, platelet aggregation, low oxygenation levels, and turbulence. Arterial will not have edema.
Incompetent valves, venous hypertension, and Deep vein thrombosis. Can cause fluid back up (edema).
A disease in which plaque builds up inside your arteries. Decreases diameter of vessel, limiting the flow of oxygen enhanced blood.
Arterial embolism or thrombi
Cessation of distal blood flow. 5 P's - severe pain, pallor, pulselessness, paresthesia, hypothermia, and paralysis. Loss of function and purplish, cyanotic coloring. This is an emergency situation.
Abdominal Aortic Aneurysm (AAA)
A confined, blood-filled abnormal dilation of an artery caused by disease or a debilitated vessel wall. Most common AAA is distal to the renal arteries. Only 40% of patients have symptoms.
AAA - Signs and Symptoms
Throbbing sensation in abdomen while supine. Mass visible in abdomen (depending on girth and weight), and systolic bruit. Prior to rupture - sudden, constant severe back or abdominal pain. Diaphoresis/clamminess, loud bruit.
Physical Assessment of PAD
Pain, pallor, rubor with coolness (severe PAD), shiny, taut, dry skin, thick yellowish nails, ulceration dependent (toes, heel) that is dry pale, minimal exudate and usually symmetric ulcers.
Chronic Venous Insufficiency (CVI)
Necrotic and inflamed tissue due to diminished blood flow and dysfunctional valves. Lower extremity ulcerations - 75% of all cases come from insect bites, cellulitis or previous trauma, or acute edema.
Physical Assessment Venous Vascular
Erythema and warmth, edema in dependent position, wet irregular shallow wounds (large), weeping, hemosidorous staining, diminished pulses, thickening and scaling of skin, minimal leg pain (superficial).
Deep Vein Thrombosis Signs and Symptoms
Limp pain with swelling and tenderness in one leg (usually your calf). Heavy ache in the affected area, warm to touch, red skin, particularly at the back of your leg below the knee, prominent vasculature.
Intermittent arterial vasoconstriction, vasospasm with ischemia. Causes coldness and pain of extremities, hyperhidrosis may accompany it, defect in temperature regulation, sudden vasoconstriction produces pallor and vasodilation produces hyperemia. Numbing, tingling and burning.
Avoid stress and anxiety and limit exposure to cold. Teach patient: insulated clothing, warm vehicles, sweaters in air conditioning, avoid nicotine, and caution with trauma.
Unilateral - rapid onset, upper or lower extremity, indistinct area, trauma, Peau'd Orange tissue appearance. Erythema with pain and fever = sepsis. Blistering, joint and muscle aches, high occurrence with CVI and diabetes, independent of VI with infection.
Prevent sepsis, elevation of affected leg, warm moist packs, monitor size and shape of area. Asses wound for changes, review labs and cultures. Monitor for and educate patient on compliance with antibiotic treatment and analgesic and increased pain or swelling.
Systolic BP > 140
Diastolic BP > 90
Determined on the "average of two or more accurate blood pressure measurements taken during two or more contacts with a healthcare provider"
Stage 1 Hypertension
Stage 2 Hypertension
>30% known as essential hypertension. High blood pressure from an unidentified cause. Silent killer.
Identifiable, 5-10% of population. Renal disease, narrowing of renal arteries, hyperaldosteronism, pheochromcytoma, medications, coarctation of aorta, pregnancy, etc.
Extremely high BP that must
Acute and life threatening with target organ damage. Must be lowered IMMEDIATELY. >180 systolic or >120 diastolic. Therapeutic goal = 20-25% BP reduction within first hour. Further reduction to 160/100 within 6 hours.
Short onset and short-lived effects. Sodium nitroprusside, nicardipine hydrochloride, Enalaprilat, and nitroglycerin.
Acute without target organ damage. Extremely high BP that must be lowered within 24-48 hours. >180 systolic and/or >120 diastolic. Therapeutic goal = oral agents. Symptoms = severe headache, nose bleeds, and anxiety.
Consistent pattern of onset, duration and symptomology. Usually precipitated by physical or emotional stress or exertion. Resolved by nitroglyceride.
Often occurs during rest, thought to be caused by coronary artery vasospasm, rare: sometimes associated with Hx of migraines or Raynaud's syndrome.
Unpredictable, longer lasting, occurs at rest. UA is an emergency.
Low hemoglobin or hematocrit and/or symptomatic. Possible symptoms include short of breath especially with exertion, tachycardia, low BP, dizziness, decreased O2Sat.
Packed Red Blood Cells (PRBC)
A concentrated preparation of red blood cells that is obtained from whole blood by removing the plasma and is used in transfusion.
Blood Administration Reaction
Itching, hives, rashes, swelling, shortness of breath, back pain, blood in urine, fever or chills develop.
Blood Administration Procedure
Administer slowly (no faster than 5ml/minute) for first 15 minutes - most common time frame for reactions to occur. At 15 minutes - check breathe sounds and VS. Assess for signs of reaction. If stable, administration rate can be increased.
Blood Administration: Adverse Reaction Procedure
Stop Transfusion, hang normal saline using new tubing to keep vein open, assess patient, while monitoring vital signs have someone notify provider (do not leave patient), implement ordered treatment, notify blood bank. Blood and tubing may need to be brought to blood bank.
Hemolytic Transfusion Reaction
Life threatening due to blood incompatibility. S/S: Fever, chills, low back pain, nausea, chest tightness, dyspnea, anxiety, hypotension, bronchospasm, circulatory collapse, and death.
Febrile nonhemolytic reaction
Caused by antibodies to donor leukocytes that remain in the blood component. Most common type of reaction, most likely in pt. who has had a lot of transfusions. S/S: chills, fever (more than 1+ C or 1.8+ F.
Allergic transfusion reaction
Allergic reaction to plasma proteins. S/S: rash, hives, itching, flushing. Can develop bronchospasm, laryngeal edema, and shock.
S/S: Shortness of breath, orthopnea, tachycardia, and sudden anxiety. Given Lasix IVP.
Usually controls the heart, has the fastest signals. 60-100 for SA node.
Imaginary lines formed between two electrodes. The provide a snapshot of electrical activity in the heart. Each lead provides a different view.
P-Wave before QRS complex
Shows that the SA node is controlling the heart. Without P-wave before QRS, then SA node is not in control and something else is.
Normal 0.12-.20 seconds. Longer = AV blocks.
Width should be < 0.12 seconds. Wider = likely ventricular in origin. Narrower = SA or AV node in origin.
Normal Sinus Rhythm
Rate is less than 60. Some people in the hospital will have heart rate in the 50s due to inactivity and that is normal for them.
Rate is 100-200 BPM
Premature Atrial Contractions
An electrical impulse begins in the atria, but outside the SA node (It's an ectopic beat). The impulse is faster than the SA node, and causes an early beat that leads to early contraction. PACs are common in healthy individuals and usually don't require treatment. However, frequent and/or symptomatic PACs may indicate a worsening condition, and could lead to more serious dysrhythmias.
Atrial Fibrillation - A-Fib
The most common sustained cardiac arrhythmia. Reaching epidemic proportions, affects nearly 15% of those >85. Loss of arterial kick (the last little squeeze of blood into ventricles), increased risk of emboli due to pooled, clotted blood in the atria. Heart gets stretched from hear failure, can cause A-fib. Atria aren't able to squeeze properly.
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