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Adult Health I - NUR 152 > Test 4 > Flashcards

Test 4 Flashcards

1
Q

What is diabetes mellitus?

A

a metabolic disorder characterized by inappropriate hyperglycemia. resulting from defects in insulin secretion, insulin action, or both.

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2
Q

What are the classifications of diabetes?

A
  1. Type 1 Diabetes
  2. Type 2 Diabetes
  3. Gestational Diabetes
  4. Diabetes associated with other conditions or syndromes
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3
Q

What is Type 1 diabetes?

A

also called juvenile-onset diabetes or insulin-dependent diabetes mellitus. the result of pancreatic islet cell destruction and a total deficit of circulating insulin.

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4
Q

What are the risk factors for Type 1 diabetes?

A

Genetic Disposition.
Genetic Markers - DR3 & DR4 found in 95% of people with Type 1
Environmental Factors- chemical toxins, measles, mumps

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5
Q

What is Type 2 diabetes?

A

also called non-insulin-dependent diabetes or adult-onset diabetes. results from insulin resistance with a defect in compensatory insulin secretion.

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6
Q

What are the risk factors of Type 2 diabetes?

A
  • Obesity- 20% over desired body weight
  • Race- Black, Asian, native American, pacific islander
  • Age- >40 white population, >25 black/Asian population
  • Impaired fasting glucose
  • impaired glucose tolerance test
  • HTN >/= 130/80
  • HDL = 35 or triglycerides >/= 200
  • Hx of gestational diabetes, PCOS, or delivery of babies >9lbs
  • Physical inactivity
  • Metabolic syndrome
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7
Q

When is gestational diabetes noticed?

A

@ 24 weeks. doesn’t have symptoms but is identified by a glucose tolerance test.

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8
Q

What are the risks of gestational diabetes?

A

placenta hormones, obesity, family hx, race, age.

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9
Q

What are the effects of gestational diabetes?

A

High birth weight of baby >9lbs. increases chance of type 2 diabetes.

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10
Q

What is the treatment of gestational diabetes?

A

dietary changes. pregnant women cannot take oral anti-diabetic agents, only insulin.

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11
Q

Characteristics of Type 1 diabetes

A 
age of onset- child
sudden onset of symptoms
body weight - normal to underweight
hereditary influences <20%
autoimmunity
beta cells and insulin decrease or destroyed
ketosis occurs
clinical approach- insulin, diet exercise
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12
Q

Characteristics of Type 2 diabetes

A 
age of onset-adult
gradual onset of symptoms
body weight- overweight or obese
hereditary influences >60%
no autoimmunity
beta cells and insulin is normal
ketosis is rare
clinical approach- diet, exercise, and medication
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13
Q

What type of diabetes exhibits Diabetic Ketoacidosis (DKA)?

A

Primarily type 1

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14
Q

Onset of diabetic ketoacidosis

A

slow, gradual onset

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15
Q

Cause of diabetic ketoacidosis

A

decreased insulin, infection

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16
Q

Risk factors for diabetic ketoacidosis

A

surgery, trauma, illness, omitted insulin, stress

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17
Q

Assessment findings of diabetic ketoacidosis

A

skin-flushed, dry, warm. fruity breath. decreased BP. increased pulse. Kussmaul respirations. confused mental status. increased thirst. increased fluid intake. nausea/vomiting. abdominal pain. moderate fluid loss. decreasing LOC. weak energy level. weight loss. blurred vision.

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18
Q

Lab findings with diabetic ketoacidosis

A 
blood glucose- >300 mg/dL
increased plasma ketones
increased urine glucose
increased urine ketones
abnormal serum potassium
abnormal serum sodium
abnormal serum chloride
plasma pH <7.3
osmolality >340 mOsm/L
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19
Q

What is the treatment of diabetic ketoacidosis?

A

insulin, IV fluids, electrolytes

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20
Q

What type of diabetes exhibits Hyperosmolar hyperglycemic state (HHS)?

A

type 2 diabetes

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21
Q

How is the onset of hyperosmolar hyperglycemic state?

A

slow, gradual onset

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22
Q

What is the cause of hyperosmolar hyperglycemic state?

A

deceased insulin, older age

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23
Q

risk factors of hyperosmolar hyperglycemic state?

A

surgery, trauma, illness, dehydration, medications, dialysis, hyper alimentation.

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24
Q

Assessment findings of hyperosmolar hyperglycemic state?

A

flushed, dry, warm skin. decreased BP. increased pulse. lethargy. increased thirst. increased fluid intake. nausea/vomiting. abdominal pain. profound fluid loss. decreasing LOC. weak energy level. weight loss. malaise. extreme thirst. seizures.

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25
Q

Lab findings of hyperosmolar hyperglycemic state?

A 
blood glucose >600mg/dL
increased urine glucose
abnormal serum potassium
abnormal serum sodium
abnormal serum chloride
osmolality >340 mOsm/L
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26
Q

Treatment of hyperosmolar hyperglycemic state

A

insulin, IV fluids, electrolytes

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27
Q

What type of diabetes exhibits hypoglycemia?

A

both type 1 and type 2 diabetes

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28
Q

What is the onset of hypoglycemia?

A

rapid onset

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29
Q

What is the cause of hypoglycemia?

A

low insulin, omitted meal/snack, error in insulin dose

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30
Q

What is the assessment findings of hypoglycemia?

A

pallid, moist, cool skin. profuse perspiration. decreased BP. increase pulse. anxious/restlessness, hunger. decreasing LOC. fatigue. headache. altered vision. mood changes. seizures.

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31
Q

What is the lab findings for hypoglycemia?

A

<50 mg/dL

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32
Q

What is the treatment of hypoglycemia?

A

glucagon. rapid-acting carbohydrate. IV solution of 50% glucose.

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33
Q

What is hypoglycemia?

A

low blood sugar

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34
Q

What is hyperglycemia?

A

high blood sugar

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35
Q

What is the lab findings for hyperglycemia?

A

> 120 mg/dL

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36
Q

What is the cause of hyperglycemia?

A

too little insulin. excess food.

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37
Q

What is the risk factors of hyperglycemia?

A

illness. surgery. trauma. dehydration. medications.

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38
Q

What is the assessment findings of hyperglycemia?

A

hot, dry, skin. poor skin turgor. increased thirst. decreased BP. change in LOC. increased respirations. nausea/vomiting. abdominal pain.

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39
Q

Clinical manifestations of Type 1 diabetes

A

polyuria. polydipsia. polyphagia. fatigue. weakness. weight loss.

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40
Q

Clinical manifestations of Type 2 diabetes

A

slower onset of symptoms. polydipsia. polyuria. blurred vision. fatigue. paresthesia. slow healing infections. impotence in men.

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41
Q

diagnosis of diabetes

A

fasting glucose. glycosylated hemoglobin (A1C). Symptoms of diabetes plus casual plasma glucose. (PG)
two hours PG during oral glucose tolerance test (OGTT)

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42
Q

What is the goal in managing diabetes?

A

normalize blood glucose

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43
Q

What are the components of managing diabetes?

A

nutrition. exercising. monitoring. medication. education.

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44
Q

What are some precautions taken with a diabetic when exercising?

A

avoid prolonged exercise until glucose control improves. risk for exercise-induced hypoglycemia is lowest before breakfast. low-impact aerobic exercises are encouraged. exercise should be moderate and regular. exercising at a peak insulin action time may lead to hypoglycemia. self-monitoring blood glucose levels is essential before and after exercise. food intake may need to be increased to compensate for activity. fluid intake is essential.

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45
Q

What should you teach diabetics?

A

annual eye exams. annual assessment for albuminuria and renal function. meticulous prevention and control of HTN. monitor for neuropathy, particularly in feet. avoid cigarette smoke. optimal management of cholesterol and triglycerides. EKG and carotid Doppler exams. kidney and urology exams.

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46
Q

What is insulin?

A

hormone produced by the beta cells of the islets of Langerhans in the pancreas. controls blood glucose levels.

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47
Q

What insulin can be given via IV?

A

regular insulin

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48
Q

What is the saying to remember how to draw up insulin?

A

air in cloudy, air in clear. draw up clear, draw up cloudy.

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49
Q

What can effect blood glucose readings?

A

increased hematocrit will give a false low glucose reading.

decreased hematocrit can give a falsely high blood glucose reading.

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50
Q

What are some common insulin injection sites?

A

upper, outer arm. lower abdomen. low back fat pads. upper front of thigh.

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51
Q

What are some things to remember with insulin injections?

A

rotate injection sites. insert needle at a 90 degree angle. wait until alcohol dries on skin. penetrate skin quickly. aspiration not necessary. best place to give insulin in the stomach. do not massage site. if site bleeds, hold pressure.

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52
Q

What is the time for onset of very rapid acting insulin?

A

5-15 min

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53
Q

What is the peak of very rapid acting insulin?

A

30-90 minutes

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54
Q

What is the duration of very rapid acting insulin?

A

3-5 hours

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55
Q

What are some examples of very rapid acting insulin?

A

aspart, lispro

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56
Q

What is the onset for short acting insulin?

A

30 min - one hour

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57
Q

What is the peak of short acting insulin?

A

2-4 hours

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58
Q

What is the duration of short acting insulin?

A

5-7 hours

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59
Q

What are some examples of short acting insulin?

A

novolin R, humulin R

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60
Q

What is the onset of intermediate acting insulin?

A

1-2 hours

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61
Q

What is the peak of intermediate acting insulin?

A

6-10 hours

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62
Q

What is the duration of intermediate acting insulin?

A

16-24 hours

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63
Q

What are some examples of intermediate acting insulin?

A

NPH, Lente

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64
Q

What is the onset of long acting insulin?

A

4-6 hours

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65
Q

What is the peak of long acting insulin?

A

no peak

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66
Q

What is the duration of long acting insulin?

A

24 hours

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67
Q

What are some examples of long acting insulin?

A

lantus (glargine), Levemir

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68
Q

What is the onset of mixed insulins?

A

30 minutes

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69
Q

What is the peak of mixed insulins?

A

varies

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70
Q

What is the duration of mixed insulins?

A

10-16 hours

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71
Q

What are some examples of mixed insulin?

A

Novolin 70/30, humulin 70/30, Humalog 75/25

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72
Q

What are some other delivery methods of insulin?

A

insulin pump and inhalation

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73
Q

What are some examples of oral antidiabetic agents?

A

sulfonylureas, biguanides, alpha glucosidase inhibitors, thiazolidinediones, meglitinides, DPP-4 inhibitors, SGLT 2 inhibitors, incretin memetics, and combination drugs.

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74
Q

What is an oral antidiabetic agent?

A

only used for Type 2 diabetes to supplement insulin production and after diet and exercise were not enough to control their diabetes.

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75
Q

What are some sulfonylureas?

A

glyburide, glipizide, & amaryl.

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76
Q

What is the action of sulfonylureas?

A

act by stimulating the pancreas cells to secrete more insulin and by more insulin by increasing sensitivity of peripheral tissue to insulin

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77
Q

What are side effects of sulfonylureas?

A

hypoglycemia and is exacerbated by NPO status

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78
Q

What is a contraindication of sulfonylureas?

A

type 1 diabetes and gestational diabetes

suspended during hospitalization

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79
Q

What is a caution with taking sulfonylureas?

A

if taken with beta blockers, it may mask usual warning signs of hypoglycemia.

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80
Q

What is an example of a biguanides?

A

metformin

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81
Q

How do biguanides work?

A

decreases the overproduction of glucose by liver and makes insulin more effective in peripheral tissues. enhances insulin sensitivity but will not cause hypoglycemia. they preferred treatment for obese patients

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82
Q

What are side effects of biguanides?

A

weight loss and reduced appetite

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83
Q

What is a caution with biguanides?

A

should be stopped 48 hours before and for 48 hours after use of contrast agent or until renal function is evaluated and normal

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84
Q

What are some examples of alpha glucosidase inhibitors?

A

precise & glyset

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85
Q

What is the action of alpha glucosidase?

A

limit the absorption of glucose in the GI tract & slow carb digestion. does not cause hypoglycemia

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86
Q

What is a side effect of alpha glucosidase?

A

side effects similar to lactose intolerance.

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87
Q

What are some examples off thiazolidinediones?

A

Avandia & actos

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88
Q

What is the action of thiazolidinediones?

A

sensitizes peripheral tissue to insulin. can be used in combo with other drugs. they increase intravascular volume.

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89
Q

What are side effects of thiazolidinediones?

A

fluid retention and reversible increases in liver enzymes

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90
Q

What is a contraindication for thiazolidinediones?

A

liver failure and heart failure patients

91
Q

What is an example of meglitinides?

A

starlix & prandin

92
Q

What is the action of meglitinides?

A

they stimulate rapid and short acting insulin secretion from pancreatic beta cells to decrease spikes in glucose. should be taken shortly before meals.

93
Q

What is an example of DPP-4 inhibitors?

A

januvia

94
Q

What is the action of DPP-4 inhibitors?

A

inhibit DPP-3 enzyme causing more stable glucose by decreasing liver release of glucose and increase insulin secretion.

95
Q

What are some side effects of DPP-4 inhibitors?

A

UTIs, rash, hives, headache, and pancreatitis.

96
Q

What is an example of an SGLT 2 inhibitor?

A

canagliflozin

97
Q

What is the action of SGLT 2 inhibitors?

A

helps to reduce renal glucose reabsorption and increasing urinary glucose excretion

98
Q

What is a contraindication for SGLT 2 inhibitors?

A

renal impairment, CFR <30, ESRD, or dialysis patients

99
Q

What are side effects of SGLT 2 inhibitors?

A

hypotension, hyperkalemia, hypersensitivity reactions, increase LDL, and hypoglycemia

100
Q

What are some incretin memetics?

A

victoza, liraglutide, exenatide, byetta, bydureon

101
Q

What is the action of incretin memetics?

A

improves blood sugar by allowing insulin to work more effectively, mimics the action of the hormone called glucagon-like peptide., which are released into the blood by the intestine and increases secretion of insulin from pancreas, slows absorption of glucose from gut, and reduces action of glucagon.

102
Q

What are side effects of incretin memetics?

A

nausea, headache, diarrhea, pancreatitis.

103
Q

What is a contraindication of incretin memetics?

A

hx of medullary thyroid cancer and multiple endocrine neoplasia.

104
Q

What are some sick-day teaching with diabetes?

A

monitor blood glucose atleast 4x day throughout illness. test urine for ketones if blood glucose is greater than 240. continue taking insulin or oral antidiabetic meds. sipping 8-12 oz of water an hour. substituting easily digested liquids or soft foods if solid foods are not tolerated. call health care provider if unable to eat for more than 24 hours or vomiting or diarrhea lasting longer than 6 hours.

105
Q

What is diabetic ketoacidosis?

A

untreated type 1 diabetes mellitus, the insulin deficit causes fat stores to break down, the result is continued hyperglycemia and mobilization of fatty acids with subsequent ketosis. a blood glucose level greater than 250.

106
Q

What are risk factors of diabetic ketoacidosis?

A

untreated type 1 diabetes mellitus.

an individual with diagnosed diabetes who is sick, has an infection, or who decreases or omits insulin doses.

107
Q

Diabetic ketoacidosis includes what four metabolic problems?

A

hyperosmolarity from hyperglycemia and dehydration.
metabolic acidosis from an accumulation of ketoacids.
extracellular volume depletion from osmotic diuresis.
electrolyte imbalances from osmotic diuresis

108
Q

What are clinical manifestations of diabetic ketoacidosis?

A

thirst. warm, dry skin w/poor turgor. weakness, malaise. rapid, weak pulse. HTN. Nausea, vomiting. fruity breath. Lethargy, coma. abdominal pain. kussmauls respirations.

109
Q

What is the treatment for DKA?

A

NS for 2-3 hours, then 1/2 NS till blood glucose is 250, then D5W. along with fluid replacement, insulin is used.

110
Q

What are precipitating factors in DKA?

A

infection, ischemia, infarction, intoxication, insulin missed, and illness.

111
Q

What is hyperosmolar hyperglycemic state?

A

characterized by plasma osmolarity of 340 or greater, blood glucose greater than 600, and altered level of consciousness.

112
Q

What are the precipitating factors of hyperosmolar hyperglycemic state?

A

infection, therapeutic agents, therapeutic procedures, acute illness, and chronic illness.

113
Q

What are clinical manifestations of hyperosmolar hyperglycemic state?

A

slow to appear, onset of 24 hours to two weeks. hyperglycemia. increased urinary output. decreased plasma volume and GFR.
increased pH. positive babinskis. leg cramps. sunken eyes. rapid, thread pulse. constipation. anorexia. seizures.

114
Q

What is the treatment of HHS?

A

IV fluid replacement. and insulin.

115
Q

What is hypoglycemia?

A

also known as insulin shock. occurs when blood glucose is less than 60.

116
Q

What are clinical manifestations of hypoglycemia?

A

tachycardia. irritability. restless. excessive hunger. diaphoresis.

117
Q

How do you treat hypoglycemia?

A

conscious patient: rule of 15. 4oz (15ml) of orange/apple juice. 2-3 tsp sugar/honey. 5-10 hard candy. commercially prepared tablet/gel. D5W.
unconscious patient: glucagon 1 mg IM or SQ. 50% dextrose IV 10 mL/min

118
Q

What are some long term complications of diabetes?

A

CAD, HTN, CVA, PVD. Retinopathy. Neuropathy. Nephropathy.

119
Q

What is diabetic neuropathy?

A

thickening of blood vessel walls. demyleinization of the schwann cells slow nerve conduction. formation of sorbitol w/the schwann cells cause impaired nerve conduction.

120
Q

What are clinical manifestations of neuropathy?

A

distal paresthesias (numbness, tingling) aching burning feet. cold feet. impaired sensation of touch.

121
Q

What is nursing care for diabetes?

A

educate on S/S of hypoglycemia.
educate on effects of hyperglycemia.
prevent skin breakdown.
education on importance of smoking cessation.
educate on proper diet, exercise, & meds
importance of good dental hygiene.
educate on complications & sick day management

122
Q

What are special issues for diabetic foot care?

A

foot care is very important. check feet daily for numbness, tingling, redness. never go barefoot. do not use commercial or OTC meds on feet. do not allow feet to become sunburnt. do not sit with legs crossed. no open-toed shoes, sandals, or high heels. wear socks made of wool or cotton. see podiatrist for care of toenails.

123
Q

What is osteoporosis?

A

exact patho unknown. involves imbalance in the activity of osteoblasts that form new bone and osteoclasts that reabsorb bone. when the creation of new bone cannot keep up with the removal of old bone.

124
Q

What are some unmodifiable risk factors for osteoporosis?

A

being female, thin, and having small frame. history of fractures. family history. age. ethnicity (Caucasian and Asians). chronic diseases (hyperthyroidism. parathyroidism. DM. RA. and lupus). current low bone mass (spina bifida or cerebal palsy)

125
Q

What are some modifiable risk factors for osteoporosis?

A

estrogen. diet soda. GI surgery. sedentary lifestyle. medications that increase Ca excretion. substance abuse. acidosis. calcium deficiency. menopause (can take replacement therapy). female athletes.

126
Q

What are some clinical manifestations of osteoporosis?

A

no symptoms in early stages of bone loss.
eventually, loss of height, progressive curvature of spine. low back pain. fracture of forearm, spine, or hip. bones so brittle that even a cough or bending over can cause a fracture. limits mobility. get a “dowagers hump”

127
Q

How is osteoporosis diagnosed?

A

medical and physical history. clients height. FRAX tool. DEXA. bone densitometry. ultrasound. alkaline phosphatase is elevated. serum bone Gla protein.

128
Q

What is a FRAX tool?

A

developed by the world health organization, assesses an individuals risk for developing fractures.

129
Q

What does the FRAX tool include questions about?

A

age, smoking, family hx of hip fractures. glucocorticoid use. arthritis. femoral neck bone mineral density.

130
Q

What is a dual energy x-ray absorptiometry (DEXA)?

A

measures bone density in lumbar spine or hip and is considered highly accurate. radiation exposure is low.

131
Q

What is bone densitometry?

A

test like an xray that quickly and accurately measures the density of the bone.

132
Q

What is the treatment of osteoporosis?

A

Physical therapy.
diet high in Ca - dairy, veggies, broccoli, yellow peppers, dark, green leafy veggies, and beans.
supplemented Ca rich foods - OJ breakfast cereals, breads
Vit D rich foods - fish, beef liver, cheese, egg yolks, milk, breads, sunshine
Meds - Ca gluconate. Vit D, bisphosphonates.

133
Q

What are some meds used for treatment of osteoporosis?

A

hormonal agents- Calcitonin (calciman, miacalcin), Raloxifene hydrochloride (evista), teriparatide (forteo)

bisphosphonates- alendronate sodium (Fosamax), etidronate disodium (didronel), ibandronate (Boniva), pamidronate disodium (aredia), risedronate sodium (Actonel), tilundronate disodium (skelid)

134
Q

What is the action of biophosphonates?

A

inhibits bone reabsorption by suppressing osteoclast activity

135
Q

What to remember with biophosphonates?

A

take these on an empty stomach related to poor absorption. side effects include GI problems.

136
Q

What are some nursing diagnoses related to osteoporosis?

A

risk for injury.
imbalanced nutrition: less than body requirements
acute pain

137
Q

What is appropriate planning with a patient with osteoporosis?

A

the client will participate in weight-bearing exercises for 30 min 4x a week.
the client will get sufficient nutrition, particularly calcium and vit D.
the client’s bone density is evaluated every other year.
the client will be able to discuss risk factors for osteoporosis and how to prevent or minimize them.
the client with high risk for injury will modify their environment to minimize risk of falls.

138
Q

What should you teach a patient about osteoporosis?

A

about the disease process. how to maintain physical mobility. implement safety precautions. avoid restraints. use assistive devices. encourage post menopausal woman should maintain Ca intake of 1,000 to 1,500 mg/day

139
Q

What are the different types of hearing impairment?

A

partial or total
congenital or acquired
one ear or both

140
Q

What is slight/mild hearing loss?

A

26-40 DB

141
Q

What is moderate hearing loss?

A

41-60 DB

142
Q

What is severe hearing loss?

A

61-80 DB

143
Q

What is profound hearing loss?

A

81-90 DB

144
Q

What is considered deaf?

A

> 90 DB

145
Q

What are the types of hearing loss?

A

conductive hearing loss, sensorineural hearing loss, and presbycusis.

146
Q

What is conductive hearing loss?

A

disruption in transmission of sound. obstruction. often built up earwax.

147
Q

What is sensorineural hearing loss?

A

affects inner ear, auditory nerve pathway. noise exposure. ototoxic drugs. tumors, vascular disorders, degenerative diseases.

148
Q

What is presbycusis?

A

hair cells of cochlea degenerate with aging. higher pitched tones, conversational speech lost initially.

149
Q

What are risk factors for hearing loss?

A 
50% of hearing loss in children is genetic.
25% of hearing loss in children is environmental around the time of birth
positive titer for TORCH infections
craniofacial abnormalities
very low birth weight
bilirubin >16
aminoglycoside medication administration
low apgar score
bacterial meningitis
mechanical ventilation for over 5 days
syndromes associated with hearing loss
150
Q

What is an example of ototoxic medications?

A

aminioglycosides - tobramycin, gentamicin, amikacin
loop diuretics - bumex, lasik
NSAIDs - ibuprofen, naproxen, salicylates

151
Q

How to prevent hearing loss?

A

avoid loud noises for long periods of time.

avoid ear bunds and headphones, if using keep volume levels down.

152
Q

What is a warning sign of auditory damage causing hearing loss?

A

the inability to hear another individual’s voice from a distance of 3 feet away.

153
Q

What is a clinical manifestation of conductive hearing loss?

A

loss of hearing at all sound frequencies

154
Q

What is a clinical manifestation of sensorineural hearing loss?

A

loss of high-frequency tones

speech discrimination is difficult

155
Q

What is tinnitus?

A

buzzing, ringing, roaring in ears

156
Q

How do you diagnosis hearing loss?

A

whisper test, otoscope exam, tympanogram, tuning fork.

157
Q

What surgeries help with hearing loss?

A

reconstructive surgeries of middle ear - stapedectomy, tympanoplasty.
Cochlear Implant

158
Q

What is a cochlear implant?

A

microphone, speech transmitter. receiver/stimulator, electrodes. function similar to way ear normally processes sounds. provides sound perception, not normal hearing.

159
Q

How do hearing aids help with hearing loss?

A

they amplify sounds. makes distorted sounds louder NOT clearer

160
Q

What are some medications to help temporary hearing loss?

A

decongestants for hearing loss caused by upper respiratory infections.
steroids for sudden sensorineural hearing loss.
antibiotics for hearing loss caused by otitis media.

161
Q

What do you need to remember when taken steroids, antibiotics, and statins?

A

do not drink grapefruit juice while taking.

162
Q

What are nursing diagnoses of clients with hearing loss?

A

risk for injury
impaired verbal communication
social isolation

163
Q

What is cataracts?

A

opacification of the lens of the eye. (cloudy lens) can significantly interfere with light transmission to the retina and ability to perceive images, causing visual deficits.

164
Q

What results in cataracts?

A

the aging process. lens ages, fibers and proteins change and degenerate. proteins clump, clouding the lens, and reducing light transmission.

165
Q

What are the four types of cataracts that occur independent of the aging process?

A

secondary- occurs after another eye disorder
traumatic- trauma, diabetes
radiation- exposure to radiation
congenital- childhood, often both eyes

166
Q

What are some risk factors of cataracts?

A 
age
genetics
environmental and lifestyle factors- long term sun exposure, cigarette smoking, heavy alcohol consumption, eye trauma.
diabetes mellitus
drugs
167
Q

What are clinical manifestations of cataracts?

A

tend to occur bilaterally, at different rates.
may say “things seem dimmer”
hard to distinguish blues and purples
poor night vision
visual acuity decreases, affecting both close and distance vision

168
Q

What diagnostic test are used for cataracts?

A

visual acuity tests
Snellen and rosenbaum charts
dilated eye exam
slit-lamp exam

169
Q

What is the treatment for cataracts?

A

surgical removal is the only treatment

170
Q

When is surgery for cataracts necessary?

A

when vision and ADLs are affected

171
Q

What is the surgery for cataracts?

A

an outpatient surgery. extracapsular extraction of lens, with an intraocular lens implanted. one eye done at a time, with weeks to months apart.

172
Q

What are nursing diagnoses related to cataracts?

A

risk for injury related to visual impairment
decisional conflict related to cataract removal
risk for ineffective health maintenance

173
Q

How do you prevent injury with cataracts?

A

wear sunglasses when outdoors
use reading or prescription glasses/contacts as necessary
maximize lighting for reading, cooking, and indoor activities
limit or discontinue nighttime driving

174
Q

How do you promote wellness with cataracts?

A

ophthalmologist every 2 years
smoking cessation
appropriate eye protection with tools, sun
eye, vision assessment at each visit - >65 y/o

175
Q

What are some post op teaching for cataract surgery?

A

for four weeks:
eye shield at night, sunglasses, no bending over, no reading, eye straining. no cough, sneeze, blow nose. take analgesics.
report:
floaters, decreased vision, pain

176
Q

What is a detached retina?

A

a medical emergency!
separation of retina from choroid. may be precipitated by trauma, aging, myopia, aphakia. may tear and fold back on itself.

177
Q

What are clinical manifestations of retinal detachment?

A 
does not have pain!
cobwebs
flashes of light
sudden increase of floaters
curtain coming across vision
detached retina
178
Q

What are diagnostic tests for retinal detachment?

A

facial xrays, CT scans, ultrasonography.

179
Q

How is retinal detachment treated?

A

surgery - scleral buckling, pneumatic retinopexy
medical emergency that can lead to permanent blindness if not treated.
if ophthalmologist unavailable, position head so gravity pulls retina closer to choroid

180
Q

What are nursing diagnoses are used for retinal detachment?

A

impaired tissue integrity: ocular
acute pain
anxiety
ineffective tissue perfusion: retinal

181
Q

What is glaucoma?

A

condition characterized by optic neuropathy with gradual loss of peripheral vision, usually increased intraocular pressure of eye

182
Q

What is acute-closure glaucoma?

A

an ocular emergency. severe eye pain. face pain. N/V. colored halos. sudden decreased acuity. can cause blindness. caused by antihistamines or decongestants intraocular pressure rises abruptly. typically unilateral. pupil dilation blocks aqueous outflow.

183
Q

What is open-angle glaucoma?

A

painless, gradual loss of peripheral vision. chronic, gradually progressive. typically affects both eyes but may not be symmetric. anterior chamber angle between iris and cornea is normal, but flow of aqueous humor is obstructed.

184
Q

What are risk factors for glaucoma?

A

age, over 40. most common over 60.
race - African americans, Mexican americans, Asian.
family history

185
Q

What are diagnostic tests for glaucoma?

A

eye exams every 2-4 hours, over age 40 yearly.
tonometry- measures eye pressure
funduscopy- visual inspection of optic fundus
gonioscopy- measures depth of the anterior chamber
visual field testing- identifies central visual field narrowing and peripheral vision loss

186
Q

What surgical interventions are for glaucoma?

A

laser tabeculoplasty - burns holes in trabecular meshwork
trabeculectomy- removes trabecular meshwork
photocoagulation- freezes and destroys portions of ciliary body

acute angle closure glaucoma:
gonioplasty
laser iridotomy- hole in iris

187
Q

What are the bottle top colors for glaucoma eye drops?

A 
beta-blockers = yellow or light blue
prostaglandin analogs = light green or teal
alpha-adrenergic agents = purple
carbonic anhydrase inhibitors = orange
miotics = dark green
combination drops = dark blue
188
Q

What is the action of beta-adrenergic blockers for glaucoma?

A

decrease the production of aqueous humor in the eye, thus decreases intraocular pressure.

189
Q

What are examples of beta-adrenergic blockers for glaucoma?

A

timolol (timoptic)
levobunolol (betagan)
carteolol (ocupress)
metipranolol (optipranolol)

190
Q

What is the action of prostaglandin analogs for glaucoma?

A

increase drainage of aqueous humor through uveoscleral pathway. reduce intraocular pressure by about 30%

191
Q

What are examples of prostaglandin analogs for glaucoma?

A

latanoprost (xalatan)
bimatoprost (lumigan)
travoprost (travatan)

192
Q

What is the action of alpha2-adrenergic agonists for glaucoma?

A

decrease production of aqueous humor in the eye and increase the drainage of aqueous humor through the uveoscleral pathway

193
Q

What are examples of alpha2-adrenergic agonists for glaucoma?

A 
brimonidine tartrate (alphagan)
apraclonidine (iopidine)
194
Q

What is the action of carbonic anhydrase inhibitors for glaucoma?

A

decrease production of aqueous humor into the eye. related to sulfa drugs.

195
Q

What are examples of carbonic anhydrase inhibitors for glaucoma?

A

acetazolamide (Diamox)
methazolamide (neptazane)
brinzolamide (azopt)
dorzolamide (trusopt)

196
Q

What are examples of combination drugs for glaucoma?

A

cospot (beta-blocker plus carbonic anhydrase inhibitor)

combigan (beta-blocker plus alpha2-adrenergic agonist

197
Q

What is the action of miotics for glaucoma?

A

increase drainage of aqueous humor through the trabecular meshwork via pupillary constriction

198
Q

What are examples of miotics for glaucoma?

A

pilocarpine (Isopto, carpine, pilopine, pilostat)

carbachol (Isopto, carbachol)

199
Q

What are some nursing diagnoses for glaucoma?

A

risk for ineffective self-health management
risk for injury
anxiety

200
Q

What teaching is needed for those with glaucoma?

A

vision loss will never improve. need to take medications for life. screening is important. eyedrops will be taken 3x day. drops may sting.

201
Q

What is macular degeneration?

A

gradual process of degeneration in the macular area of the retina. leading cause of blindness over age 60. loss of central vision.

202
Q

What are the two types of macular degeneration?

A

nonexudative (dry) and exudative (wet)

203
Q

What is nonexudative macular degeneration?

A

gradual accumulation of deposits. pigment epithelium detaches in small areas. typically vision loss not significant, progresses slowly. risk that disorder will progress to exudative stage.

204
Q

What is exudative macular degeneration?

A

formation of new, weak blood vessels. new vessels prone to leak. elevate retina from choroid. bleeding can occur. acute vision loss.

205
Q

What is the treatment for wet or exudative macular degeneration?

A

injection of meds into eye. slow/stop growth of vessels.

206
Q

What are risk factors of macular degeneration?

A 
low risk for those with darker pigmentation.
aging. 
smoking.
race- whites higher risks
cardiovascular health
possibly genetic factors
207
Q

What are some clinical manifestations of macular degeneration?

A

blind or blurry spots in central vision.
require brighter light; difficulty adjusting between bright and lower light.
peripheral vision intact
difficulty recognizing faces.
Wet AMD: straight lines appear crooked or wavy.
objects appear different sizes between eyes

208
Q

What are diagnostic tests for macular degeneration?

A

vision and retinal exam
amsler grid
fluorescein angiogram
optical coherence tomography

209
Q

What is used in the treatment of macular degeneration?

A

verteporin-injection
laser surgery
photodynamic therapy
antiangiogenic drugs

210
Q

What are some antiangiogenic drugs used with macular degeneration?

A

ranibizumab (lucent)
bevacizumab (avastin)
pegaptanib (macugen)

211
Q

What are some nursing diagnoses with macular degeneration?

A

risk for injury
risk for ineffective self-health management
fear

212
Q

What is peripheral neuropathy?

A

results when trauma or a disease process interferes with innervation of peripheral nerves. effectiveness of blood vessels decreases. superficial blood vessels constrict to divert blood to larger vessels. peripheral nerve endings suffer from decreased blood flow. neuropathy develops.

213
Q

What is polyneuropathies?

A

bilateral sensory disorders often associated with diabetes

214
Q

What is mononeuropathies?

A

isolated, affect a single nerve. caused by injury, trauma, or repetitive motions.

215
Q

Neuropathies can be

A

acquired - injury, trauma
hereditary
idiopathic - caused by disease processes

216
Q

Polyneuropathy is a complication of …

A

gulliain barre syndrome
systemic diseases
prognosis ranges
alcoholism, cancer, carpal tunnel syndrome.

217
Q

What are risk factors for peripheral neuropathy?

A 
diabetes
alcohol abuse
vitamin deficiencies, particularly B vitamins
immune system suppression
autoimmune diseases
kidney, liver, thyroid diseases
exposure to toxins
age
218
Q

How do you prevent peripheral neuropathies?

A

controlling medical conditions
healthy diet of vegetables, fruits, and whole grains
intake of vitamin B 12
avoid triggers such as repetitive motions, smoking, toxic chemicals, and cramped positions.

219
Q

What are some clinical manifestations of peripheral neuropathy?

A 
depends on nerves affected.
commonly distal paresthesias.
guillian barre syndrome.
stocking-glove pattern- feels like they have socks or gloves on
weakness in arms or legs
pain
220
Q

What are some diagnostic tests for peripheral neuropathy?

A 
electromyography (EMG).
CBC
thyroid function tests
serum levels for B12 and thiamine
metabolic panel
urine screening
nerve biopsy
221
Q

What surgical interventions are done for peripheral neuropathy?

A

appropriate for peripheral neruopathies caused by compression.
ex. nerve tumors or carpal tunnel syndrome

222
Q

What are medications used to treat pain of peripheral neuropathy?

A

pain relievers
anticonvulsants- gabapentin (Neurontin), carbamazepine (carbatrol, tegretol), pregabalin (lyrica), topiramate (Topamax).
tricyclic antidepressants- amitriptyline (Elavil), nortriptyline (pamelor)
serotonin-norepinephrine reuptake inhibitors (antidepressants)- duloxetine (Cymbalta)

223
Q

What are some nonpharmacologic therapies for peripheral neuropathy?

A 
physical and occupational therapy.
compliance with therapeutic regimen
healthy, well-balanced diet
limit alcohol
optimal weight
regular exercise 
smoking cessation
daily foot care
acupuncture
biofeedback
TENS
massage
224
Q

What are nursing diagnoses with peripheral neuropathy?

A

risk for injury
ineffective peripheral tissue perfusion
pain
anxiety

Adult Health I - NUR 152 (2 decks)

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