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115 Cards in this Set
- Front
- Back
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Diabetes Mellitus
Diabetic Neuropathy Definition |
Progressive deterioration of nerves that result in loss of nerve function.
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Diabetes Mellitus
Diabetic Neuropathy Types |
Focal = affects a single nerve or nerve group
Diffuse = involve widespread nerve function loss |
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Diabetes Mellitus
Diabetic Neuropathy Focal neuropathy |
Caused by [1]acute ischemic event: blood supply to nerve is disrupted, Sx begin suddenly, affect only one side of body and are self-limiting; or [2]physical entrapment: compression of nerve in body compartment or btwn tissues, Sx begin gradually, can occur anywhere (e.g., carpal tunnel syndrome)
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Diabetes Mellitus
Diabetic Neuropathy Diffuse neuropathy |
• Most common diab neuropath
• Slow onset • Affect both sides of body • Involve motor & sensory nerves • Progress slowly • Permanent • Include ANS dysfunction • Late complications: foot ulcers |
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Diabetes Mellitus
Diabetic Neuropathy Causes |
Hyperglycemia leads to neuropathy thru blood vessel changes that cause nerve hypoxia;
Nerve cells swell and become scarred; Damaged nerve cells send incorrect signals or no signals |
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Diabetes Mellitus
Diabetic Neuropathy Focal damage S/S |
• Burning, tingling, sharp pain, crawling sensation in feet, legs, hands, arms
• Numbness or weakness in feet, legs, hands, arms • Restless legs at night • Hypersensitivity |
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Diabetic Neuropathy
ANS neuropathy causes the following: |
CV: orthostatic hypotension, syncope
GI: gastroparesis, dysphagia, heartburn, N & V, bowel elimination problems GU: incomplete emptying of bladder |
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Diabetes Mellitus
Pathophysiology Vicious Cycle: 1 |
Cells are not absorbing glucose the way they should, i.e.,
insulin resistance of cells, e.g., the door gets stuck shut (door lock is cell receptor site, insulin is key) |
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Diabetes Mellitus
Pathophysiology Vicious Cycle: 2 |
Pancreas is not making enough or adequate insulin to metabolize glucose
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Diabetes Mellitus
Pathophysiology Vicious Cycle: 3 |
Liver makes too much sugar
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Diabetes Mellitus
Sick Day Management |
Stress causes glucagon & epinephrine to be released, which increases blood glucose levels
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Diabetes Mellitus
Sick Day Management |
Illness, injury, surgery & esp. infection stimulate the stress response,
which in turn increases blood glucose levels |
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Diabetes Mellitus
Sick Day Management |
Teach clients to check their blood sugar more often during periods of illness, injury, surgery, or infection
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Diabetes Mellitus
Sick Day Management |
Do not hold medication without consulting the health care provider, i.e., check with doctor before holding insulin prior to surgery
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Diabetes Mellitus
Sick Day Management |
Teach clients to finish all of their antibiotics
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Diabetes Mellitus
Sick Day Management |
Teach clients to check their urine for ketones during periods of infection or illness
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Diabetes Mellitus
Critical Nursing Care |
DM treatment –
Whole Pancrease Transplant: Pancreas transplant is attached to bladder. If urine amylase decreases 25%, indication that pancreas transplant is not working well; treat rejection. High blood glucose levels are a later marker of rejection and usu. indicate irreversible graft failure |
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Diabetes Mellitus
Critical Nursing Care |
Maintain a blood glucose level of 120 – 200 mg/dL during the periop period to decrease complications and increase wound healing
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Diabetes Mellitus
Polyuria |
Frequent and excessive urination resulting from an osmotic diuresis caused by excess glucose in the urine. As a result of diuresis, sodium, chloride, and potassium are excreted in the urine and water loss is severe.
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Diabetes Mellitus
Hyperglycemia S/S |
• Polyuria = increased urine
• Polydipsia = increased thirst • Polyphagia = increased hunger • Fatigue = tired • Drowsiness = sleepier than usual • Dry, itchy, skin • Blurred vision • Weight loss • Decreased healing • Hot & Dry = Sugar High |
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Diabetes Mellitus
Hypoglycemia S/S |
Cold and Clammy = Need Some Candy
Adrenergic: Tachycardia – heart pounding Irritability - nervous/anxious Restless – shaking/tremulous Depression Cholinergic: Excessive hunger Diaphoresis - sweating Tingling Neuroglycopenic: Confusion – difficulty thinking Emotional lability – behavior changes Seizures – loss of consciousness Brain Damage > Death |
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Diabetes Mellitus
Type 1 |
• Autoimmune
• Beta cells are destroyed • Absolute insulin deficiency |
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Diabetes Mellitus
Type 2 |
• Progressive
• Pancreas makes less insulin over time • Reduced ability of cells to respond to insulin (resistance) • Poor control of liver glucose metabolism • Decreased Beta cell function progressing to Beta cell failure |
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Diabetes Mellitus
Cardiovascular Disease |
Clients with DM2 have as much risk of CVD events as client who already have a Hx of CVD. CVD causes most diabetic deaths.
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Diabetes Mellitus
PRIORITY |
MAINTAIN BLOOD GLUCOSE LEVEL WITHIN NORMAL LIMITS!!
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Diabetes Mellitus
Acute Complications |
Hypoglycemia:
-too much insulin -too little glucose Hyperglycemia: -DKA diabetic ketoacidosis -HHNK hyperglycemic-hyperosmolar-nonketotic syndrome |
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Diabetes Mellitus
Chronic Complications |
Microvascular:
• Diabetic neuropathy • Diabetic nephropathy • Retinopathy • Erectile dysfunction Macrovascular: • Cardiovascular disease (CVD) • Cerebrovascular disease • Peripherovascular disease (PVD) |
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Diabetes Mellitus
Risk Factors |
• Obesity
• Sedentary Life Style • Family History • Hypertension • Triglycerides > 250 mg/dL • Low HDL < 35 mg/dL |
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Diabetes Mellitus
Ketones |
Ketones are a waste product of fat metabolism. Their presence in urine may indicate impending ketoacidosis. The ADA recommends testing urine for ketones during acute illness or stress, when blood glucose levels are consistently > 300 mg/dL, during pregnancy, or when any symptoms of ketoacidosis are present. Ketone testing is recommended for diabetic clients following a weight loss program.
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Diabetes Mellitus
Diet - Fiber |
Eat 20 - 35 g/day of FIBER:
raw fruit, beans, cereals, unpeeled vegies, legumes, whole grain breads FIBER decreases insulin in blood & decreases blood lipid levels 50 g/day of FIBER decreases blood glucose levels by 10% |
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Diabetes Mellitus
Diet - Goals |
1. Control blood sugar & lipids without compromising overall health
2. Provide appropriate calories 3. Prevent, delay, minimize DM complications 4. Improve overall health |
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Diabetes Mellitus
Diet - Servings/Day |
Meat: 2-3 [protein]
Milk: 2-3 [protein] Veg: 5-7 [low index carbs] Fruit: 2-3 [low index carbs] Starch: 4-5 [high index carbs] |
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Diabetes Mellitus
Diet - Protein |
20-30% total daily calories
7-8 oz/day Adults with kidney damage = 0.8g/kg/day |
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Diabetes Mellitus
Diet - CHO [carbs] |
50-60% total daily calories
15g=1/2-1cup=1serving Any food that is not protein or fat is carb Eat complex [unrefined] carbs with fiber |
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Diabetes Mellitus
Diet - Fat |
15-20% total daily calories
Avoid saturated & transfats, use polyunsaturated Limit cholesterol < 300 mg/dL/day Per day: 3 tsp/6 oz meat/1 egg |
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Diabetes Mellitus
Diet - Vitamin C |
Eat one good source of vitamin C per day -- 2 if smoker
[citrus, stawberries, papaya, broccoli, cabbage, brussel sprouts] |
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Diabetes Mellitus
Diet - Vitamin A |
Eat one good source of vitamin A every other day
[dark green or yellow fruits or vegies] |
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Diabetes Mellitus
Diet - Alcohol |
1 serving alcohol = 2 fat servings
Raises triglycerides, induces hypoglycemia > drink with or after meal Men = 2 servings, Women = 1 serving |
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Diabetes Mellitus
HHNK = Hyperglycemic-Hyperosmolar Nonketotic Syndrome Manifestations...... |
Blood sugar > 600, high blood osmolality (thick blood) = extreme dehydration
No ketosis, No acidosis Gradual onset, pancreas still functioning Altered neurologic function profound, seizure possible = appear drunk |
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Diabetes Mellitus
HHNK = Hyperglycemic-Hyperosmolar Nonketotic Syndrome Interventions....... |
• Improved LOC is best indicator of adequate treatment
• Fluid therapy = rehydrate • Restore normal blood glucose in 36-72 hrs • Continued therapy often needed • IV regular insulin @ 10 units/hr until blood glucose levels reduced |
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Diabetes Mellitus
DKA [Diabetic Ketoacidosis] |
• Occurs in the absence of insulin
• Breakdown of fat • Results in metabolic acidosis • Osmotic diuresis causes dehydration • Life-threatening |
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Diabetes Mellitus
DKA [Diabetic Ketoacidosis] manifestations...... |
• Sudden onset
• Blood sugar > 250-300 mg/dL • Sx of hyperglycemia • Infection most common cause • Ketosis = Kussmaul’s respirations & fruity breath • Nausea & abdominal pain |
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Diabetes Mellitus
DKA [Diabetic Ketoacidosis] labs...... |
Profound electrolyte loss:
• Potassium elevated with acidosis, then low following dehydration • Metabolic acidosis = pH < 7.35, HCO3 < 22 • Dehydration = elevated BUN & Creatinine • Urine = + ketones |
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Diabetes Mellitus
DKA [Diabetic Ketoacidosis] interventions......fluids...... |
IV Fluids (to decrease blood viscosity):
• 1 L NS in first 30-60 minutes • 1 L NS in second 60 minutes • 6-10 L in first 24 hours • When glucose drops to less than 250 mg/dL then change from NS to D5% 0.45NS |
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Diabetes Mellitus
DKA [Diabetic Ketoacidosis] interventions......insulin...... |
• IV insulin drip to decrease glucose by 75-150 mg/dL/hr (0.1 unit/kg bolus followed by 0.1 unit/kg/hr)
• Low dose insulin prevents hypokalemia |
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Diabetes Mellitus
DKA [Diabetic Ketoacidosis] interventions......electrolytes...... |
• With insulin therapy, potassium shifts rapidly into cells
• Before giving IV potassium to correct this shift, make sure urine output is at least 30 mL/hr • Acidosis is corrected with fluid replacement and insulin therapy, rarely with bicarbonate • Hypokalemia is a significant cause of death in DKA, leads to fatal cardiac dysrhythmias |
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Diabetes Mellitus
Prevention of Exacerbations with Lifestyle Modifications |
• Low carb, low fat, low cholesterol diet
• Exercise 30min every day • Maintain a healthy weight • Stop smoking • Limit alcohol • Get adequate sleep • Get regular check-ups |
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Diabetes Mellitus
Exercise - Benefits DM type 1 |
Regular, moderate-intensity exercise in type 1 DM:
1. helps regulate blood glucose levels 2. lowers insulin requirements 3. improves control by increasing insulin sensitivity and enhancing cell uptake of glucose 4. promotes weight loss 5. decreases risk factors for CVD 6. decreases blood lipid levels and increases HDLs 7. decreases BP 8. improves CV function |
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Diabetes Mellitus
Exercise - Benefits DM type 2 |
Regular vigorous physical activity prevents or delays type 2 DM by reducing body weight, insulin resistance and glucose intolerance.
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Diabetes Mellitus
Exercise - Benefits |
Benefits of exercise last about 24-36 hours.
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Diabetes Mellitus
Exercise - Guidelines |
1. Check blood glucose before & 30 minutes after exercising
2. For levels > 250, test urine for ketones 3. If ketones are present = do NOT exercise 4. Stay hydrated = 8 oz/15-20 minutes of exercise 5. Risk for hypoglycemia increases when insulin is injected into an area that is exercised within 1 hour of injection 6. Extra carbs may be needed for up to 24 hrs after exercise to prevent hypoglycemia 7. Eat an extra 15-30 g of carbs for every 30-60 minutes of long, vigorous exercise 8. Exercise 30-60 minutes after eating |
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Diabetes Mellitus
Dawn phenomenon |
• Results from a nighttime release of growth hormone that causes blood glucose elevations at about 5-6am
• Treated by providing more insulin for the overnight period (e.g., giving intermediate-acting insulin at 10pm) |
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Diabetes Mellitus
Somagyi's phenomenon |
• Morning hyperglycemia from the effective counterregulatory response to nighttime hypoglycemia
• Treated by ensuring adequate dietary intake at bedtime and evaluating the insulin dose and exercise program to prevent conditions that lead to hypoglycemia |
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Diabetes Mellitus
Insulin Injection Site |
1. Site affects speed of absorption
2. Absorption is fastest in abdomen (preferred site), then deltoid, thigh, buttocks 3. Rotate injection sites to prevent lipoatrophy & lipohypertrophy 4. Rotation within one anatomic site is preferred to prevent day to day changes in absorption |
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Diabetes Mellitus
Insulin Teaching |
1. Use needles only once
2. Wash hands and site with soap & water 3. Give at 90 degree angle, do not aspirate 4. Can be stored at room temp for 1 month 5. Prefilled syringes can be stored upright for 3 weeks 6. Refrigerate to maintain potency, inhibit bacterial growth, avoid heat and sunlight 7. Cold insulin can irritate injection site 8. Do not freeze insulin 9. Roll, don’t shake, intermediate-acting insulin 10. Discard needles in hard plastic container marked “not for recycling” with household trash |
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Diabetes Mellitus - Medications
Meglitinides Action |
Stimulates release of insulin from pancreatic Beta cells; similar to sulfonylureas, but shorter action
nateglinide (Starlix) repaglinide (Prandin) |
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Diabetes Mellitus - Medications
Sulfonylureas Precautions |
1. Do not give with NSAIDs
2. Contraindicated in hepatic disease, sulfa allergies, pregnancy, alcohol (antabuse affect) 3. Betablocker may induce or mask hypoglycemia 4. Underweight older adults with CVD, liver or kidney impairment are more prone to hypoglycemia 5. Many drug interactions 6. Weight gain 7. No longer recommended because of hypoglycemia side effects glimepiride (Amaryl) glipizide (Glucotrol) glyburide(DiBeta,Micronase,Glynase) |
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Diabetes Mellitus - Medications
Biguinide Side Effect |
• Does NOT cause hypoglycemia
• N & V, GI upset, flatulence, diarrhea • Fatigue, unusual muscle pain (myalgia) • Dyspnea • Dizziness, lightheadedness • Irregular heart beats • May cause weight loss & favorable effect on triglycerides, LDL, HDL metformin (Glucophage) |
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Diabetes Mellitus - Medications
Biguinide Action |
1. Decreases liver glucose production by inhibiting glycogenolysis & gluconeogenesis
2. Reduces absorption of glucose from small intestine 3. Increases insulin sensitivity in tissue, which improves glucose uptake in peripheral muscle & adipose cells metformin (Glucophage) |
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Diabetes Mellitus - Medications
Sulfonylureas Action |
1. Stimulates insulin secretion in pancreatic Beta cells
2. Reduces liver glucose production & metabolism 3. Increases cell uptake of glucose 4. Enhances sensitivity of cell receptor sites for interaction with insulin glimepiride (Amaryl) glipizide (Glucotrol) glyburide(DiBeta,Micronase,Glynase) |
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Diabetes Mellitus - Medications
Thiazolidineiones (TZD) Side Effect |
• 15% Mild weight gain (4-6 lbs, mostly fluid)
• Edema, peripheral • Not susceptible to hypoglycemia, unless using other hypoglycemic meds • Headache • Increased BP does not cause hypoglycemia • Improves triglycerides, HDLs • Reduced effectiveness of oral contraceptives • Do not use with CHF Pioglitizone (Actos) Rosiglitizone (Avandia) |
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Diabetes Mellitus - Medications
Incretin Mimetic Action |
1. mimics incretin hormone produced in gut
2. represses glucagon release from alpha cells inhibits gluconeogenesis in liver 3. stimulates body’s natural insulin response to sugar levels after meals gila monster venom (Byetta exenatide) |
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Diabetes Mellitus - Medications
Incretin Mimetic Side Effects |
• Appetite suppression
• Weight loss • N & V, diarrhea gila monster venom (Byetta exenatide) |
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Diabetes Mellitus - Medications
Incretin Mimetic Precautions |
• Not used in DM type 1 or 2 insulin dependent
• By injection only, degraded in intestines • Subcut. Inj. 30 min. ac b.i.d. at least 6 hours apart • Not as effective if given after meals • May be given with other oral diabetic meds gila monster venom (Byetta exenatide) |
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Diabetes Mellitus - Medications
Insulin Nursing Actions |
Know onset, peak, and duration of insulin given so you know when client needs to eat or not eat. Teach clients so they don’t “bottom out” their blood sugar (hypoglycemia).
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Diabetes Mellitus - Medications
Insulin Short Acting |
Regular: Humulin R, Novolin R, Velosulin BR
Onset: ½ hour Peak: 2-4 hours (Humulin R) 2 ½ -5 (Novolin R) 1-3 (Velosulin BR) Duration: 6-8 hours |
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Cardiac
MI Labs Serum cardiac markers |
Serum cardiac markers =
proteins released from necrotic heat muscle |
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Cardiac
MI Labs CK or CPK |
CK = creatine kinase or
CPK = creatine phosophokinase • 4-6 hours after AMI • 12-24 hours = peaks • 48-72 hours = decreases Correlates to the size of the MI |
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Cardiac
MI Labs CK-MB |
CK-MB = subset of CK (creatine kinase) that correlates specifically to the cardiac muscle
Most sensitive indicator of MI > 5% = positive indicator of AMI |
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Cardiac
MI Labs Troponins |
Troponins = proteins released during AMI that are sensitive indicators of myocardial
damage. Remain in blood 10-14 days after an MI. 1. Troponin T-cardiac specific troponinT cTnT 2. Troponin I-cardiac specific troponin I cTnI |
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Cardiac
MI Labs Myoglobin |
Myoglobin – First cardiac marker detectable in the blood after an MI, released within a few hours of Sx, but lacks specificity to cardiac muscle and is rapidly excreted
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Cardiac
MI Labs CBC |
CBC = may show elevated WBC
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Cardiac
MI Labs ESR |
ESR = elevates due to inflammation
(Erythrocyte Sedimentation Rate) |
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Cardiac
PA Pressure Ranges |
Pulmonary Artery Pressure:
15 - 28 mm Hg = systolic 5 - 16 mm Hg = diastolic [constantly visible on the monitor] The tip of the catheter senses pressures transmitted from LA, which reflect LVEDP (left vent. end-diastolic pressure). |
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Cardiac
A Fib |
Atrial Fibrillation:
Decreases Cardiac Output by 30% Rhythm: A = none, V = irreg Rate: A = none, V = varies P Waves? Not discernable PR interval: None QRS interval: < 0.1 [Irreg vent. rhythm with wavy baseline] |
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Cardiac
Cardiac Output |
HR x SV = CO
Conditions that alter CO: • Hypovolemia • Cardiac damage • Neurogenic injury • A-fib • Anything affecting HR or SV |
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Cardiac
S1 |
• Bicuspid & Tricuspid valves closing
• Systole = contraction • PMI = left midclavicular fifth ICS |
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Cardiac
S2 |
• Pulmonary & Aortic valves closing
• Diastole = relaxation • Second ICS just R or L of sternum |
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Cardiac
Elevated ST segment |
Indication of infarction
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Cardiac
Depressed ST segment |
Indication of ischemia
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Cardiac
MVP |
Mitral Valve Prolapse:
1. The valvular leaflets enlarge and prolapse into the L atrium during systole 2. Usually benign, but may progress to pronounced mitral regurgitation 3. Most with MVP are asymptomatic 4. Some report chest pain, palpitations, exercise intolerance 5. Dizziness, syncope, palpitations with A or V dysrhythmias 6. Normal HR & BP 7. Mid systolic click and late systolic murmur audible at apex 8. Intensity of murmur NOT related to severity of prolapse 9. Familial connection – affects 5-10% - common in women 20-54 yrs |
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Hematology
Parkland Calculation |
4 mL LR per kg per % TBSA = Total Volume
1. Half of total volume over first 8 hours 2. Remainder over next 16 hours 3. Time starts at time of burn (not arrival at hospital) 4. Give even drip on pump (avoid bolus) |
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Hematology
Erythrocytes Defined |
• Mature Red Blood Cells
• The largest proportion of blood cells • Lifespan of 120 days |
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Hematology
Erythrocytes Normal Range |
• 4,200,000 to 6,100,000 /mm3
• Number varies according to gender, age, general health |
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Hematology
Erythrocytes Stem cells |
• Immature, undifferentiated RBCs
• RBCs start as stem cells, enter myeloid pathway, and progress in stages to mature RBCs (i.e., erythrocytes) |
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Hematology
Erythrocytes Destruction |
1. As RBCs age, their membranes become more fragile
2. Old cells are trapped and destroyed in tissues, spleen and liver 3. Parts of RBCs (e.g., iron) are recycled into new RBCs |
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Hematology
Erythrocytes Hemoglobin |
• RBCs produce hemoglobin (Hgb)
• Each RBC contains thousands of Hgb molecules • The heme part of each hemoglobin molecule needs a molecule of iron |
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Hematology
Erythrocytes Iron |
• Critical component of hemoglobin
• Only when the heme molecule is complete with iron can it transport up to four molecules of oxygen |
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Hematology
Erythrocytes Erythropoiesis |
• Selective maturation of stem cells into mature erythrocytes
• Carefully controls the number of RBCs a person has circulating • Ensures enough RBCs for good oxygenation but not too many to thicken blood and slow its flow • The trigger for control of erythropoiesis is tissue oxygenation *dialysis causes low H & H *high altitude causes elevated H & H |
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Hematology
Erythrocytes Erythropoietin |
• RBC growth factor produced in kidneys that stimulates bone marrow RBC production
• Produced at a rate to match destruction to maintain a constant normal level of circulating RBCs • Synthetic forms (Procrit, Epogen, EPO) have the same effect on bone marrow as naturally occurring erythropoietin |
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Hematology
Platelets Defined |
• Fragments of a giant precursor cell in the bone marrow = megakaryocyte
• Smallest of the blood cells • Lifespan of 1 to 2 weeks |
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Hematology
Platelets Function |
• Stick to injured blood vessel walls
• Form platelet plugs that can stop flow of blood from injured site • Produce substances important to coagulation |
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Hematology
Platelets Thrombopoietin |
Growth factor that controls production of platelets in bone marrow
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Hematology
Platelets Storage |
• After they leave bone marrow, stored in spleen and released slowly to meet the body’s needs
• 20% stored in spleen • 80% circulate |
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Hematology
Spleen Functions |
1. Destroys old or imperfect RBCs
2. Breaks down hemoglobin from these old cells 3. Stores platelets 4. Filters antigens 5. Cannot palpate a healthy spleen |
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Hematology
Spleen Splenectomy |
Surgical removal of the spleen
After splenectomy: 1. client has reduced immune functions forever 2. not as efficient at ridding body of disease-causing organisms 3. at greater risk for infection and sepsis |
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Hematology
Liver Functions |
1. Main production site for prothrombin and most of the clotting factors
2. Stores large quantities of whole blood and blood cells 3. Converts bilirubin to bile 4. Stores extra iron within the protein ferritin 5. Produces small amounts of erythropoietin |
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Hematology
Blood Clotting Hemostasis |
Hemostasis is a complex process that balances the production of clotting and dissolving factors.
Localized blood clotting occurs in damaged blood vessels while blood continues to circulate to all other areas. |
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Hematology
Blood Clotting Process |
Three sequential processes result in blood clotting:
1. Platelet aggregation with formation of a platelet plug 2. The blood clotting cascade 3. The formation of a complete fibrin clot |
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Hematology
Blood Clotting Platelet aggregation |
1. Platelets normally circulate as individual cell-like structures
2. They are not attracted to each other and do not clump together until activated 3. Activation causes platelet membranes to become sticky, allowing clumping to occur 4. These clumps form large, semisolid plugs within the lumens and walls of blood vessels and disrupt blood flow 5. Platelet plugs are not clots and cannot provide complete hemostasis 6. Platelet plugs start the cascade reaction that leads to fibrin clot formation and blood coagulation |
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Hematology
Blood Clotting Blood clotting cascade |
Triggered by the formation of the platelet plug
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Hematology
Blood clotting cascade Intrinsic Factors |
Intrinsic Factors:
• Problems or substances directly in the blood itself that first make platelets clump and then activate the blood clotting cascade • Produced by the parietal cells of the stomach • Necessary for the absorption of vitamin B12 |
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Hematology
Blood clotting cascade Extrinsic Factors |
Extrinsic Factors:
• Changes or events outside of the blood, in the blood vessels, that cause platelet plugs to form • The most common extrinsic event is trauma • The platelet plug is formed within seconds of the trauma • The blood clotting cascade is activated faster by the extrinsic pathway because it bypasses steps of the intrinsic pathway |
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Hematology
Blood clotting cascade Clotting factors |
Clotting factors:
• Inactive enzymes that become activated in a sequence • Each activated enzyme from the previous step activates the next enzyme in the sequence • The last part of the sequence is activation of fibrinogen into fibrin |
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Hematology
Blood clotting Fibrin clot formation |
• The fibrin threads (made from fibrinogen in the liver) make a netlike meshwork that forms the base of a blood clot
• After the fibrin mesh is formed, clotting factor XIII tightens up the mesh, making it more dense and stable |
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Hematology
Blood clotting Fibrinolysis |
• Whenever the blood clotting cascade is started, counterclotting or anticoagulant forces are also started
• These forces limit clot formation to damaged areas only so that normal blood flow is maintained everywhere else • In D.I.C. this system does not work correctly (pathological coagulation uses up all the clotting factors) |
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Hematology
Platelet Inhibitors Salicylates (Aspirin) |
• Inhibits production of substances that trigger platelet activation, such as thromboxane
• Prevents platelets from becoming active • Most widely used drug for this effect • Platelet aggregation is affected for up to 10 days after a single dose |
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Hematology
Platelet Inhibitors RePro |
• Changes the platelet membrane, reducing its “stickiness”
• Prevents activators from binding to platelet receptors • Prevents activated platelets from clumping • Contains human and mouse proteins that may induce allergic reaction |
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Hematology
Anticoagulants Action |
• Interfere with one or more steps of the blood clotting cascade
• Prevent new clots from forming and limit or prevent extension of formed clots • Do NOT dissolve existing clots |
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Hematology
Anticoagulants Heparin (Calciparin) |
• Prevents clot formation
• Interferes with thrombin formation and prevents conversion of fibrinogen to fibrin • Must be given parenterally • Half-life is 1-6 hours • Antidote is protamine sulfate |
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Hematology
Anticoagulants Low-Molecular-Weight Heparin (Lovenox) |
• Prevents clot formation
• Interferes with thrombin formation and prevents conversion of fibrinogen to fibrin • Must be given parenterally • Half-life is 1-6 hours • Antidote is protamine sulfate • Does NOT require monitoring of lab values (aPTT) |
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Hematology
Anticoagulants Vitamin K Antagonist (Coumadin) |
• Disrupts liver synthesis of vitamin K-dependent clotting factors
• Requires 48-96 hours to reach peak effect • Requires 1 week to clear after discontinued • May be started while still on heparin • Do not take with aspirin or other platelet inhibitors • Labs important to check drug serum levels • Antidote is vitamin K |
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Hematology
Reticulocytes |
• Immature RBC that still has its nucleus
• Count = Test to determine bone marrow function • Elevated if increased RBC production by the bone marrow --- Because of anemia=good --- After hemorrhage=good --- Without precipitating cause=bad=PV • Normally 2% of circulating RBCs are reticulocytes --- Range = 0.5% - 2% of RBCs |
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Hematology
Bone Marrow Aspiration |
1. Done when other hematologic tests show persistent abnormal results
2. Aspiration = cells and fluid are suctioned from the bone marrow 3. Biopsy = solid tissue and cells are obtained by coring out an area of bone marrow with a large bore needle 4. Doctor’s order and signed consent are required 5. Most common site is iliac crest with client in prone or side-lying position 6. If more marrow is needed, the sternum can be used 7. Apply external pressure to site until hemostasis ensured 8. Pressure dressings or sandbags may be applied to reduce bleeding at site 9. Cover site with dressing after bleeding is controlled and observe for 24 hrs for s/s of bleeding or infection 10. Ice packs may be placed over the site to reduce bruising 11. Aspirin free analgesic used for discomfort |
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Hematology
PT and INR Coumadin |
PT measures how long blood takes to clot
--normal is between 11 and 13 seconds INR measures the same process as PT in a slightly different way: by establishing a mean or PT --normal is between 0.7 and 1.8 PT is prolonged when one or more clotting factors (II, V, VII, or X) is deficient, such as when liver disease is present Coumadin therapy is considered normal when the PT is prolonged by 1 ½ times to 2 times the client’s normal PT or when INR is between 2 and 3 regardless of the actual PT in seconds. |
