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Health and Illness > Exam 3 > Flashcards

Exam 3 Flashcards

1
Q

How is glucose transported into cells? What happens to excess glucose?

A

Insulin will bind to glucose transfer proteins (GLUT4) found along cell membranes and allow for glucose to enter the cell

stored in liver and muscles as glycogen

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2
Q

What are counterregulatory hormones? Examples?

A

hormones that oppose the effects of insulin and increase blood sugar by: stimulating glucose production and release by the liver and by decreasing movement of glucose into the cell

glucagon, epinephrine, growth hormone, cortisol

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3
Q

What is the fasting blood glucose level? 2 hours postprandial?

A

74 to 106

100 to 140

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4
Q

What is the fasting blood glucose level that indicates prediabetes?

A

100 to 125

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5
Q

What is the blood glucose level of hypoglycemia? Severe hypoglycemia?

A

<70

<50

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6
Q

What can cause hyperglycemia?

A

insufficient insulin production or secretion due to damage to beta islet cells either from an autoimmune response or damage to the pancreas (cancer, pancreatitis)

deficient hormone signaling causing insulin resistance due to decrease in insulin receptors, in GLUT4 transporters, or both. the body can compensate for a while by secreting more insulin but it cannot maintain this

excessive counterregulatory hormone secretion leading to gluconeogenesis and insulin resistance. excess cortisol can be due to chronic stress, pain, acute injury, chronic high doses of steroids

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7
Q

What can cause hypoglycemia?

A

malnutrition: the body will start to breakdown glucose stores

medication reactions: too much insulin, the wrong insulin, high doses of sulfonylurea which can increase insulin production by stimulating the pancreas

over exercising

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8
Q

What is the onset of type 1 DM?

A

autoantibodies are present for months to years before symptoms occur

manifestations develop when the pancreas can no longer produce insulin (due to destruction of beta cells of the islet of langerhans)

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9
Q

What are symptoms of type 1 DM?

A

polydipsia, polyuria, polyphagia, can present with ketoacidosis

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10
Q

Why can type 2 DM be treated with oral insulin while type 1 DM cannot?

A

oral medications will: stimulate the body to make more insulin, stimulate the body to use insulin more effectively, or effect how glucose is stored (especially in the liver)

type 1 does not have any endogenous insulin

type 2 has endogenous insulin but the body either does not respond to it effectively or there’s not enough insulin, or both

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11
Q

How is type 2 DM diagnosed?

A

typically a routine lab is done and finds that the HA1C of 6.5%

fasting glucose of greater or equal to 126

oral glucose tolerance test: 2 hrs after ingesting 75 mg of solution glucose is greater than or equal to 200

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12
Q

What is the fasting blood glucose level seen in pre-diabetic people?

A

100-125 mg/dL

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13
Q

What can cause gestational diabetes? How much of an increase of insulin can be found in the pregnant person?

A

fetal nutrient requirements causes the body to eat more

hormones, such as cortisol, is secreted by the placenta

these can cause insulin resistance

3x more than normal

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14
Q

How often is gestational diabetes seen? What does it increase the risk of?

A

9.2% of all pregnancies

developing type 2 later in life

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15
Q

When and how is gestational diabetes screened for?

A

it typically forms in the second trimester so screening happens between 24 and 28 weeks

oral glucose tolerance test:
step 1 - drink 50g of sugary solution and one hour later draw blood, if the BS >130 then it is considered positive and the person proceeds to second step
step 2 - drink 100g of sugary solution and one, two, and three hours later draw blood, if the BS is high again it is positive for gestational diabetes
if the pregnant person is already at risk they will skip to the second step

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16
Q

What happens if a pregnant person has a high HA1C during their first trimester?

A

it is diagnosed as type 2 DM and there’s an increase risk to fetal development

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17
Q

What is the treatment for gestational diabetes?

A

diet, exercise, glucose monitoring (ACHS), pharmacologic is needed

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18
Q

What are considerations to newborns if the pregnant person had gestational diabetes?

A

macrosomia: larger than average fetus, if the pregnant person’s blood sugar is too high the fetus’ pancreas will make more insulin in response and deposit the excess sugar as fat

hypoglycemia at or shortly after birth: infant hasn’t adjusted to not having a high blood sugar and the pancreas is still creating a surplus of insulin

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19
Q

What are the goals for diabetes management?

A

decrease symptoms, promote well-being, prevent acute complications, delay onset and progression of long-term complications

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20
Q

What are the nutritional therapy goals for type 1 DM?

A

meal planning: based on usual food intake and preferences, balanced with insulin and exercise patterns

day to day consistency makes it easier to manage blood glucose levels

more flexibility with rapid-acting insulin, multiple daily injections, and insulin pump

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21
Q

What are the nutritional therapy goals for type 2 DM?

A

emphasis on achieving glucose, lipid, BP goals

moderate weight loss can lead to a lesser dependence on medications and greater glucose control

nutritionally adequate meal plan with less fats and carbohydrates

spacing meals

regular exercise

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22
Q

How often should screening should be done for specific complications to DM?

A

eyes, CV, kidney function should be done yearly

feet should be checked daily

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23
Q

What is the etiology and pathophysiology of diabetic neuropathy?

A

over time hyperglycemia will cause a buildup of sorbitol and frutose in the nerves which will damage them

or

damage to blood vessels that supply peripheral nerves causing distal symmetric polyneuropathy

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24
Q

What can cause sorbitol build up?

A

sorbitol can be produced during glucose metabolism/reduction, in people with normal glucose levels they don’t produce a lot of sorbitol because glucose is used efficiently with no excess, those with diabetes up to a third of glucose goes through reduction

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25
Q

How common is diabetic neuropathy? How often should screening be done for it?

A

60 yo 70% of diabetics have it to some degree

start at diagnoses for those with type 2

start 5 years after diagnoses with type 1 (b/c it is caught quicker than type 2)

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26
Q

What are the signs and symptoms of diabetic neuropathy?

A

loss of sensation

abnormal sensations

pain: burning, cramping, crushing, tearing, will worsen at night or may happen only at night

paresthesia: tingling, burning, itching

numbness/loss of feeling especially in feet

loss of sensitivity to touch and temperature

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27
Q

What is the treatment for diabetic neuropathy?

A

managing blood glucose levels

drug therapy for treatment of symptoms, particularly pain

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28
Q

What is capsaicin? MOA? Nursing considerations?

A

moderately effective topical cream for diabetic neuropathy pain

depletes accumulation of pain mediating chemicals in peripheral sensory neurons

apply 3 to 4x/day
do not use bare fingers to apply
avoid touching eyes, mouth, nostrils, genitals, or irritated areas of skin
doesn’t work immediately, may take up to two months

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29
Q

What is amitriptyline? MOA?

A

tricyclic antidepressant for diabetic neuropathy pain

inhibits reuptake of norepinephrine and serotonin which are neurotransmitters believed to play a role in the transmission of pain through the spinal cord

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30
Q

What is duloxetine? MOA?

A

selective serotonin and norepinephrine reuptake inhibitors for diabetic neuropathy pain

increases levels of serotonin and norepinephrine to improve ability to regulate pain

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31
Q

What is gabapentin? MOA?

A

antiseizure medication for diabetic neuropathy pain

decreases release of neurotransmitters that transmit pain

can be an increase in symptoms at the start of therapy but will have relief in 2 to 3 weeks

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32
Q

What are complications for diabetic neuropathy?

A

foot ulcers

lower extremity amputations

atrophy of small muscles of hands and feet

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33
Q

What is the pathophysiology of foot ulcers?

A

sensory neuropathy causing a loss of protective sensation leading to an unawareness of injury both microvascular and macrovascular

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34
Q

What are the risk factors of foot ulcers?

A

sensory neuropathy, peripheral artery disease, clotting abnormality, impaired immune function, autonomic neuropathy

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35
Q

What is monofilament annual screening?

A

application of flexible filament to several spots on the bottom surface of foot and ask the patient if they can feel it

if there’s insensitivity found there’s a large increase risk for foot ulcers

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36
Q

What are major risk factors for having a lower extremity amputation?

A

smoking, sensory neuropathy is a major risk factor in diabetics

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37
Q

What can atrophy of the small muscles of hands and feet lead to?

A

deformities and limit of fine motor of fine movements

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38
Q

What are examples of rapid acting insulin? Onset? Peak? Duration?

A

lispro and aspart

onset: 10 to 30 min
peak: 30 min to 3 hr
duration: 3 to 5 hr

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39
Q

What is an example of short acting insulin? Onset? Peak? Duration?

A

regular

onset: 30 min to 1 hr
peak: 2 to 5 hr
duration: 5 to 8 hr

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40
Q

What is an example of intermediate acting insulin? Onset? Peak? Duration?

A

NPH

onset: 1.5 to 4 hr
peak: 4 to 12 hr
duration: 12 to 18 hr

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41
Q

What is an example of long acting insulin? Onset? Peak? Duration?

A

glargine

onset: 0.8 to 4 hr
peak: less defined or no pronounced peak
duration: 16 to 24 hr

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42
Q

What are the types of insulin regimens?

A

basal-bolus: most closely mimics endogenous insulin production consisting of rapid or short acting before meals and intermediate or long acting background insulin once or twice a day

less intense regimens can be used with those who have difficulties/unable to maintain a tight regulation

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43
Q

What are combination insulin therapies?

A

mixing short or rapid acting insulin with intermediate acting insulin in the same syringe to provide mealtime and basal coverage in one injection

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44
Q

How is insulin stored?

A

do not heat/freeze
do not expose to direct sunlight
insulin pen can be left at room temp for 4 weeks
extra insulin should be refrigerated

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45
Q

What are the nursing considerations for administering insulin?

A

give SQ injection: absorption is fastest in abdomen, followed by arm, thigh, buttock, not given in muscles because it can be unpredictable and absorb rapidly

only regular insulin can be given IV for rapid onset

cannot be taken orally due to break down in stomach

do not inject in site that will be exercised as it could increase speed of absorption

rotate sites within and between sites

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46
Q

What are complications that can occur with insulin pumps?

A

catheter dislodgment, pump failure

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47
Q

What is afrezza?

A

rapid acting inhaled insulin that can be administered at the beginning of each meal or within 20 minutes after starting a meal, not a substitute for long-acting

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48
Q

What are the classes of oral agents for type 2 DM? MOA?

A

biguandies: (Metformin) reduces glucose production by the liver, enhances insulin sensitivity, improves glucose transport, may cause weight loss, need to d/c before imaging with contrast and can continue 48 hrs after

sulfonylureas: increase insulin production from pancreas with a major side effect of hypoglycemia

meglitinides: increase insulin production from the pancreas with a rapid onset (less likely to cause hypoglycemia than sulfonylureas) taken 30 minutes just before each meal

alpha-gluconsidase inhibitors: “starch blockers” slow down absorption of carbs in small intestines, takes with first bite of each meal, lowers post-prandial blood sugar

dipeptidyl peptidase-4 (DDP-4) inhibitor: blocks inactivation of increatin hormone causing an increase in insulin release, decrease in glucagon secretion, decrease in hepatic glucose production

sodium-glucose co-trasporter 2 (SGLT2) inhibitors: blocks the reabsorption of glucose by the kidneys to increase urinary glucose excretion, commonly used, side effects include UTI and yeast infections

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49
Q

What are some concerns with acute illness and surgery for diabetic patients?

A

increase blood glucose levels secondary to counterregulatory hormones therefore Q4H glucose checks

increase insulin for type 1 diabetes: if high BS, ketones should be monitored for DKA, if BS>300 more than once and ketones found in urine insulin may need to be increased

type 2 DM may need insulin therapy if not on it

maintain normal diet if able, if not possible supplement with CHO-containing fluids while continuing medications

increase noncaloric fluids

continue taking antidiabetic medications

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50
Q

What are the early and late common manifestations of hypoglycemia?

A

early: headache, shaky, cold, clammy, irritable

late: altered mental functioning, untreated hypoglycemia can progress to loss of consciousness, seizures, coma, and death, can mimic being intoxicated

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51
Q

How do you treat hypoglycemia?

A

rule of 15: consume 15g of simple carbohydrates (OJ, little glucose tabs, regular soda), recheck glucose in 15 minutes and if the value is still hypoglycemic try 15g of simple carbs again and recheck in 15 minutes
if done a couple of times with no improvement notify provider

avoid foods with fat (cookies), avoid overtreatment, give complex CHO after recovery

in acute care settings: 50% dextrose 20 to 50mL IV push or with no IV access: IV dextrose or glucagon 1mg IM or SQ (glucagon will stimulate liver to release glucose, side effects include vomiting)

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52
Q

What are the functions of bones?

A

support, protection of internal organs and tissues, voluntary movement (acts as a lever for muscles and movement), blood cell production, mineral storage of Ca and P

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53
Q

What are the types of bones? Examples?

A

long: femur, humerus, tibia

short: carpals, tarsals

flat: ribs, skull, scapula, sternum

irregular: sacrum, mandible, ear ossicles

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54
Q

What is the most common type of joint?

A

freely movable diarthrodiol or synovial

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55
Q

What creates a joint cavity?

A

joint inclosed in a capsule of fibrous connective tissue allowing the two bones to come together

it is supported with structures like ligaments and tendons reinforce to provide limits and stability to joint movement

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56
Q

What is the synovial membrane?

A

lines the joint capsule and secretes thick synovial fluid to help lubricate the joints

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57
Q

What are lifespan considerations for older adults and their mobility?

A

functional problems: some changes begin in early adulthood but obvious signs might not appear until later adult years

risk for falls increases: due to loss of strength and change in balance

decreased bone density: bone remodeling is altered causing an increased bone reabsorption and decreased bone formation, osteopenia and osteoporosis, joints are more likely to be affected by osteoarthritis

decreased muscle mass and strength: by age 70 about 30% of muscle mass is lost

decreased flexibility: movement becomes more rigid

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58
Q

What are the functions of the immune system?

A

defense: infection prevention by protecting

homeostasis: digestion and removal of damaged cellular substances

surveillance: foreign cells and mutations that develop within the body are destroyed

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59
Q

What are the types of immunity?

A

innate: immediate response to any invasion to the body (not antigen-specific)

active acquired: prominent invasion into the body by either natural contact with a pathogen

passive acquired: body receives antibodies to an antigen rather than creating the antigen on its own. this can take place naturally (crossing through the placenta or colostrum from the mom to child or artificially through an injection of antigen containing serum (gamma globulin))

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60
Q

What are lines of defense?

A

first: skin boundary (mucus membranes, enzymes, natural body flora, complement proteins)

second: cell: innate immunity (phagocytes, natural killer T lymphocytes, granulocytes, macrophages)

third: antibodies: acquired immunity (antibodies derived from B and T lymphocytes)

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61
Q

What is the difference between indigenous and foreign antigens?

A

indigenous do not activate the immune system because the body becomes tolerant

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62
Q

What are central lymphoid organs?

A

bone marrow: produces lymphocytes

thymus gland: differentiates and matures T lymphocytes (important for cell mediated immune response)

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63
Q

What are the peripheral lymphoid organs?

A

lymphoid tissues: protects body surfaces from external microbes, found in submucosa of bronchi, gut, and genital tract

lymph nodes: circulate lymphocytes, filter foreign material brought to it

spleen: primary site for filtering foreign antigens from the blood

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64
Q

What happens to the immunity of patients who have undergone a splenectomy?

A

reduced number of IgM

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65
Q

What are mononuclear phagocytes?

A

responsible for capturing, digesting, and presenting foreign antigens to lymphocytes to trigger the immune response

includes: monocytes and macrophages

66
Q

What are lymphocytes?

A

produced in the bone marrow where they will differentiate into B lymphocytes (10-20%), T lymphocytes (70-80%), and natural killer cells (<10%)

67
Q

Where do B lymphocytes mature? What causes them to mature? What do they mature into?

A

bone marrow when the immune system is activated

will turn into plasma cells that produce antibodies (immunoglobulins)

68
Q

Where do T lymphocytes mature? What causes them to mature? What do they mature into?

A

thymus, immunity to viruses, tumor cells, and fungi

T cytotoxic cells: attack antigens on the cell membrane of foreign invaders and will release substances to destroy the pathogens, become sensitive to an antigen once exposed and then if the antigen shows up again a stronger attack will be mounted

T helper: divides into subset of cells and those subsets will produce two different types of cytokines: Th1 (stimulate phagocytes to eat foreign invaders) and Th2 (stimulates eosinophil-mediated immunity when there’s a parasite or allergic reaction)

69
Q

What are natural killer cells?

A

large lymphocytes with numerous granules in the cytoplasm

recognizes and kills virus infected cells

destroy tumor cells and transplanted grafts

70
Q

What are dendritic cells?

A

found throughout the body: skin, lining of nose, lungs, stomach, intestines, and blood

role is to capture foreign antigens at the site of contact with the external environment, will transport the antigen until they encounter a T cell that has a specificity for the antigen

71
Q

Which cells are involved in immune response?

A

cytokines, immunoglobulins, B cell, and T cell

72
Q

What are cytokines?

A

secreted primarily by WBC and serve as messengers between cells

73
Q

What happens with tumor necrosis factor in those who are healthy and those with autoimmune diseases such as rheumatoid arthritis?

A

healthy: excess TNF production in the blood is blocked

autoimmune disorder: higher levels of TNF can lead to more inflammation, joint destruction, and persistent symptoms of rheumatoid arthritis

74
Q

What are the types of immunoglobulins and their functions?

A

IgM: primary immunity

IgG: secondary immune response

IgA: protects mucous membranes

IgD: assists with B cell differentiation

IgE: causes allergic reactions

75
Q

How are B cells involved in the immune response?

A

humoral immunity, antibody-mediated immunity: responds when first exposed to antigen and will begin to produce antibodies for the specific antigen

primary immune response: 4 to 8 days after exposure and involves IgM and IgG

secondary immune response: 1 to 3 days after subsequent exposure, stronger and lasts longer, involves IgG

76
Q

How are T cells involved in the immune response?

A

cell-mediated immunity

initiated by T cell antigen recognition of an intracellular pathogen such as a virus, fungus, or transplanted tissues or contact hypersensitivity reactions

77
Q

What are lifespan considerations of infants and immunity?

A

at birth IgG and IgM are present

IgG is the only immunoglobulin that crosses the placenta, maternal IgG disappears by 3 months, child’s IgG increases gradually until 4 to 6 years

IgM is low at birth and increases until age 2

IgA, IgD, and IgE are not present at birth an begins at 2 weeks old until early childhood

78
Q

What are lifespan considerations for older adults and immunity?

A

normal changes associated with aging include a shrinkage of thymus gland causing fewer mature T cells and fewer antibodies leading to a lowered resistance to infection and a diminished hypersensitivity response

poor response to immunizations due to T cells being less responsive to antigens and B cells producing fewer antibodies

79
Q

What are risk factors for altered immune response?

A

age
non-immunized
environmental: pollutants, contaminated food/water, poor nutrition, hand hygiene, environmental or medications, food, drugs, pollen, mold, insect venoms
chronic illnesses that can suppress the immune system (primary: HIV and secondary: diabetes, cancer, COPD)
immunosuppressants
gender, race, ethnicity, genetics
high risk behavior and substance abuse

80
Q

What diagnostic studies can be done to assess for altered immunity?

A

CBC with WBC differential: low lymphocytes indicates immunodeficiency, eosinophil count is high in type I hypersensitivity reactions

CRP and ESR: inflammation, elevated in those with autoimmune diseases

disease specific blood tests: rheumatoid factor for rheumatoid arthritis, western blot or ELISA for HIV, TORCH for pregnant or newborns looking at specific infections

sputum, nasa, and bronchial secretions to assess for eosinophils

pulmonary function test

chest x ray

challenge test for food allergies: to see if patient may no longer have a reaction to some foods

skin testing for allergens: scratch/prick (reaction in 5 to 10 minutes), intradermal (reaction in 5 to 10 minutes), patch test (substance is placed on outside of body and absorbed SQ, wear for 48 to 72 hours before removing patch)

81
Q

What is compartment syndrome? Where does it often occur?

A

injury to the muscle or bone causing an increase in pressure within the muscle compartment due to the inability of the fascia to flex

LE due to compartments being smaller

82
Q

What is the pathophysiology and etiology of compartment syndrome?

A

may occur initially or may be delayed for several days or may be chronic (in those who exercise a lot)

most commonly from a fracture or trauma (crush injuries, burns due to increased edema, snake bites)

can also occur with prolonged decreased circulation

83
Q

What are the signs and symptoms of compartment syndrome?

A

pain (beyond what is expected), paresthesia, pressure (muscle looking/feeling “tense”), pallor, paralysis, pulselesness

84
Q

What are nursing considerations for compartment syndrome?

A

early recognition and treatment are essential as ischemia can occur within 4 to 8 hours after onset

assess urine output: may see dark, reddish, brown urine due to muscle breakdown of myoglobin which can lead to blockage of renal tubules and kidney injury

do not elevate limb above heart (do not want to lower venous pressure or arterial perfusion)

do not ice (do not want vasoconstriction)

surgical decompression (fasciotomy) may occur

severe can lead to amputation

85
Q

What is fat embolism syndrome? Where does it most commonly occur? How does it occur?

A

a rare complication of fractures where fat globules enter into the circulatory system that can happen 24 to 48 hours after injury

long bones, ribs, tibia, pelvis

idiopathic

86
Q

What are signs and symptoms of fat embolism syndrome?

A

similar to adult respiratory distress syndrome (chest pain, tachypnea, cyanosis, dyspnea, apprehension, tachycardia, changes in mental status, elevated temp, headache)

petechia on neck, anterior chest wall, arm pits (seen in 25 to 50%)

87
Q

How can fat embolism syndrome be prevented? What are nursing interventions?

A

immobilization of fracture

manage symptoms, fluid resuscitation, oxygenation, respiratory support if needed

88
Q

What is osteomyelitis?

A

severe infection of bone, bone marrow, and surrounding soft tissue

89
Q

What is the common cause of osteomyelitis? Pathophysiology?

A

staph aureus

microbe grows and increases the pressure in the bone, ischemia and vascular compromise occurs causing bone death (sequestrum), the sequestrum doesn’t allow for antibiotics to enter and treat due to compromise, the infection will then spread through the bone developing cortex devascularization and necrosis

90
Q

What are clinical manifestations of osteomyelitis?

A

local: pain that worsens with activity and is unrelieved by rest, swelling, tenderness, warmth, restricted movement

systemic: fever, night sweats, chills, restlessness, nausea, malaise, drainage (late)

91
Q

How long does an osteomyelitis last to be considered an acute infection?

A

<1 month

92
Q

What are diagnostic studies of osteomyelitis?

A

bone or soft tissue biopsy to identify the microbe

blood and/or wound cultures

WBC count

ESR

CRP

Xray/MRI/CT: won’t see changes in XR until at least 10 days (by the time it is seen the disease is progression), more helpful when trying to assess disease progress and extent of infection

bone scans

93
Q

What is the treatment for acute osteomyelitis?

A

aggressive, prolonged IV antibiotic therapy: via CVAD (may be started in hospital, continued at home/SNF), can last 4-6 weeks or longer (can increase immobilization, increase likelihood of antibiotic resistance, kidney damage)

surgical debridement and decompression: if there’s a delay in diagnosis

94
Q

What are nursing considerations for acute osteomyelitis?

A

immobilization and careful handling of affecting limb, assess and treat pain, dressing care-sterile technique, proper positioning/support of extremity, pt teaching adverse and toxic reactions to antibiotic therapy

95
Q

What is crepitation?

A

audible grating/grinding of bone from fracture

96
Q

What is the immediate treatment for fractures?

A

immobilize in the position it was found and RICE

97
Q

How do fractures heal?

A

bleeding leads to hematoma formation (72h)

granulation: basis for new bone (3-14d)

callus: minerals and bone matrix (14d)

ossification: mineralization (3wks to 6mo)

consolidation: bone fragments unite

remodeling: excess bone reabsorbed

98
Q

What is the treatment for fractures?

A

reduction: realign bone fragments

closed reduction: done manually (w/o surgery), apply traction and counter traction then immobilize, can be done under local anesthesia

open reduction: done with surgery and application of pins, screws, wires, ect

99
Q

What is traction? Types?

A

provides a pulling force to injury to help with pain, reduce spams, immobilize

skin: 2-3 days (used until surgery or skeletal traction is applied), tape, boots, splints applied to skin, weight is 5 to 10 lbs

skeletal: long term pull, pins or wires inserted into bone, increased infection risk, weight is 5 to 45 lbs

100
Q

What are the do’s and don’ts for cast care?

A

do: apply ice over fx for first 24 hours, elevate extremity above heart for first 48 hours, move joints above and below cast, hair dryer on cool setting for itching, watch for swelling and any compromised circulation, skin dammage

don’t: get the cast wet, remove padding, insert objects in cast, bear weight on cast for 48 hours, cover cast with plastic for long periods of time

101
Q

What is external fixation versus internal fixation?

A

external: pins inserted into bone and attached to external rods to immobilize, used for those with soft tissue damage, if fx is not healing, any bony defects, limb lengthening

internal: devices (pins, plates, ect) are surgically inserted to realign and maintain position of bone fragments, devices are biologically inert and made from stainless steel, vitallium, or titianium, proper alignment and bone healing is evaluated regularly through XR

102
Q

What is the neurovascular assessment?

A

circulation, movement, sensation

103
Q

What are complications from immobility?

A

bone loss/weakness

muscle mass loss to affected extremity

joint contracture (permanent shortening of muscle or joint, this is why ROM exercises and immobilization are important) and instability

CV: orthostatic, thromboembolism, workload

psychosensory

GI, urinary: constipation, urinary retention, calculi

respiratory: diminished function, pneumonia, embolism

skin

metabolic (muscle wasting)

104
Q

What are nursing considerations for patients who have undergone a hip replacement?

A

do not: flex hips greater than 90 degrees, abduct hip (hips together at knees), cross legs, put shoes or stockings on without help

105
Q

What are the types of hypersensitivity reactions? How do they all compare?

A

A: anaphylaxis/allergy (type I)

C: cytotoxic (type II)

I: immune complex (type III)

D: delayed hypersensitivity (type IV)

type I, II, III are humoral with immediate response

type IV is cell mediated with delayed response

106
Q

What is the pathophysiology of Type I hypersensitivity?

A

IgE mediated reaction, antigen enters and will be phagocytized by B-cell which will then create IgE antibodies, when the antigen is presented again IgE will recognize it and induce a reaction

107
Q

What is anaphylaxis? What is the leading cause? Symptoms?

A

type I hypersensitivity life threatening systemic release of all cell mediators

drugs and environmental factors

weak/rapid pulse, hypotension, dilated pupils, dyspnea, angioedema, bronchial edema

108
Q

What are examples of atopic type I hypersensitivity reactions? Target? Symptoms?

A

allgergic rhinits: seasonal/environmental allergy that targets eye conjunctiva and mucosa of UR tract. symptoms: nasal discharge, sneezing, mucosal swelling, itchy eyes

asthma: targets bronchial smooth muscles. symptoms: dyspnea, wheezing, coughing, chest tightness, thick sputum

atopic dermatitis: targets skin. symptoms: generalized skin lesions

utricaria: hives that targets the skin, can occur quickly and last minutes to hours, symptoms: transient fluid filled wheals that vary in shape and size

angioedema: targets eyelids, lips, tongue, larynx, hands, feet, GI tract, and genitalia. symptoms: similiar to urticaria but involves deeper layers of the skin

109
Q

What is the pathophysiology of type II hypersensitivity reactions?

A

cytotoxic and cytolytic reaction. IgG or IgM will bind to a cell antigen activating the complement system causing a reaction and cell death by cytosis from activated complement system and/or enhanced phagocytosis

110
Q

What is hemolytic transfusion reaction? Symptoms?

A

a rare type II hypersensitivity reaction caused with incompatible blood is delivered to a patient, the blood cells will coagulate, blood uses all clotting factors, bleeding may occur

general symptoms: chills, fever, aches, hives, itching
hemolysis symptoms: SOB, headache, chest pain, hematuria

111
Q

What is good pasture syndrome? Symptoms?

A

autoimmune disease causing a type II hypersensitivity reaction that targets the lungs and kidneys

hemoptysis, SOB, N/V, hematuria, edema

112
Q

What is the pathophysiology of type III hypersensitivity? Where does it happen? What happens if it becomes severe?

A

immune-complex reaction. immediate or delayed reaction where antigens combine with IgG and IgM to form complexes that cannot be phagocytized by phagocytes and will begin to deposit and build up in tissues and blood vessels

kidneys, skin, joints, blood vessels, lungs

rheumatoid arthritis, lupus, glomerular nephritis

113
Q

What is the pathophysiology of type IV hypersensitivity? Where is it commonly seen in?

A

delayed hypersensitivity reactions, cell mediated. 24 to 48 hours after exposure sensitized T cells attack antigens and release cytokines which will attract macrophages, the macrophages release enzymes that cause tissue destruction

organ transplant

114
Q

What is contact dermatitis? Target? Symptoms?

A

type IV hypersensitivity of the skin after touching an allergen

location specific

red and swollen area with lesions that are papules or vesicles, site may be itchy, burn, or sting

115
Q

What is an example of microbial hypersensitivity reaction? Pathophysiology?

A

tuberculosis

TB enters the lungs, release an antigen that activates T-cells and causes a cell mediated immune response, can develop n=into caseous necrosis, any subsequent exposure will cause a delayed hypersensitivity reaction

116
Q

What are nursing interventions for anaphylaxis?

A

recognize signs and symptoms as speed is critical

maintain a patent airway, intubate if needed

give drugs: epinephrine every 5 to 15 minutes, high flow oxygen (up to 100%), nebulizzed albuterol, diphenhydramine IV for uticaria and itching, cortiocsteroids

treat for shock: elevate legs, fluid bolus, maintain BP with fluids or drugs

117
Q

What drug treatments can be given for allergic rhinitis?

A

antihistamine, phenylephrine or psuedophedrine (sympathomimetic), nasal corticosteroids, mast-cell stabilizing drugs, leukotriene receptor antagonists

118
Q

What drug treatments can be given for urticaria?

A

antihistamine and topical antipruritic

119
Q

What drug treatments can be given for atopic dermatitis?

A

topical antipruritic

120
Q

What is the treatment plan for SQ immunotherapy?

A

build up phase: 3 to 6 months

maintenance phase: 3 to 5 years

121
Q

What is immunotherapy for allergies?

A

long term SQ injections of an allergen to develop an immunity or tolerance of allergy symptoms

122
Q

What is the SL immunotherapy treatment for allergies? Nursing considerations?

A

allergen extracts (5 grass, single grass, and ragweed) placed SL taken daily at home

first dose with medical supervision due to local site reaction that usually subsides after a few days

123
Q

What is the pathophysiology of latex allergies? Symptoms?

A

type I: allergic reaction
cause: natural rubber latex proteins
reaction time: within minutes of contact
symptoms: redness, urticarial, rhinitis, conjunctivitis, asthma, anaphylaxis

type IV: contact dermatitis
cause: chemicals used in latex glove manufacturing
reacting time: 24 to 48hr after exposure
symptoms: dryness, pruritus, fissuring and cracking of skin followed by redness, swelling, crusting

124
Q

What is latex-food syndrome? Food examples?

A

rubber proteins similar to food protein causing an allergic reaction to latex and associated food

bananas (common), avocado, chestnut, kiwi, hazelnut, potato, peach, grape, apricot

125
Q

What is the mechanism of pain perception

A

transduction: noxious stimuli causes tissue damage, the CNS will convert the stimuli into an action potential

transmission: the pain signal is relayed from the periphery to the spinal cord, and then to the brain using primary afferent fibers (ex/ A delta and C fibers)

perception: changes based on past experience, beliefs, attitudes, ect

modulation: endogenous opioids (ie. endorphins and serotonin) are released to try and stop pain transmission

126
Q

How is pain classified?

A

underlying pathology: nociceptive (caused by damage to somatic or visceral tissue) and neuropathic

druation: acute (<3 mo), chronic (>3 mo)

127
Q

What are common causes of neuropathic pain?

A

trauma, infection, metabolic diseases (DM), infection of nervous system, tumors, toxins, neurological diseases (MS)

128
Q

What type of pain assessment tool is for kids younger than 8?

A

Face scale

129
Q

What are nondrug therapy treatments for pain?

A

massage, exercise, TENS or PENS (small pads applied to certain muscle areas and a small electrical current is released), acupuncture, heat or cold therapy

130
Q

What are challenges to effective pain management?

A

tolerance

physical dependence

psuedoaddiction: usually occurs when there’s inadequate treatment of pain and the patient will begin to exhibit behaviors commonly associated to addiction (frequent refill requests, higher dosages) but once there is adequate pain relief the behaviors stop

addiction: complex neurobiological condition characterized by aberrant behaviors arising from need or drive to get and take substances like opioids for reasons other than prescribed therapeutic value

131
Q

What is a tension-type headache pain characteristics?

A

mild to moderate, acute or chronic, constant but dull

bilateral location and pressing/tightening quality: tension in the cervical and neck muscles (increase muscle tone in neck muscles)

felt as band squeezing head with a weight pushing on top

132
Q

What is migraine headache pain characteristics?

A

intense, pounding/throbbing that involves typically one of the temples, typically unilateral but can be bilateral or switch sides

can last 48 to 72 hours and throb almost at the same time as pulse

133
Q

What other characteristics can be seen with tension-type headache?

A

photophobia and/or phonophobia

does not involve nausea or vomiting

does not ome with a warning

134
Q

What diagnostics can be done for tension-type headache?

A

history (best tool)

electromyography (EMG) (best done while person is currently having a tension-headache, some sustained tightening/contracting of neck, face, and/or scalp can be seen)

135
Q

How is migraine headache differentiated as?

A

with aura (classic) or without aura (common)

136
Q

What is the common age of onset for migraine headaches? When it is most common age to have migraine headaches?

A

20 to 30 year old with it most commonly seen in 25 to 55 year old

137
Q

What are some premonitory symptoms to migraine headaches?

A

Sensory changes

food craving

138
Q

What are some triggers for migraine headaches?

A

hormonal (menstrual cycle)

food (chocolate, red wine, spicy foods, oranges, tomatoes, onions, monosodium glutamate (MSG))

physical exertion

medications

weather

139
Q

What is the biggest risk factor for migraines?

A

family hx/genetics

140
Q

What is cluster headaches classified as?

A

trigeminal autonomic cephalagia

141
Q

What are the clinical manifestations of cluster headaches?

A

swelling around the eye, tearing, facial flushing or pallor, nasal congestion, pupil constriction

142
Q

How is the pain for cluster headaches described as?

A

unilateral sharp and stabbing located in the eye but radiates through the face and head

generally occurs at the same time of day or night that can occur in cycles

causes restlessness and agitation

143
Q

What is the etiology and pathophysiology of cluster headaches?

A

dysfunction of circadian rhythm: irregularities in melatonin and cortisol and onset occurring shortly after waking up

hypothalamic activation at onset

144
Q

What are drug therapies for symptomatic tension type headache? What is the concern with them?

A

aspirin, acetaminophen, and/or NSAIDs alone or with caffeine, sedative, muscle relaxant

if used longterm can be significant long term side effects

145
Q

What are drug therapies for prevention of tension headaches?

A

tricyclic antidepressants

anti-seizures

146
Q

What are drug therapies for prevention of tension headaches?

A

tricyclic antidepressants

anti-seizures (gabapentin)

147
Q

What are drug therapies for symptomatic migraines?

A

mild to moderate: NSAID, aspirin, analgesic with caffeine

moderate to severe: triptans (sumatriptan)

148
Q

What is the MOA for triptans, nursing considerations, and when is it taken?

A

will reduce inflammation and vasoconstriction

be aware of those with heart disease and stroke risk

taken on onset or during aura

149
Q

What are drug therapies for prevention of migraines?

A

antiseizure (gabapentin)

beta blockers (olol)

SSRI (prozac)

botox (not first line, certain criteria must be met, effective in 2 to 4 mo with injections given in head and neck every 3 mo)

150
Q

What are drug therapies for symptomatic cluster headaches?

A

triptans (golden standard)

100% O2 at 6 to 8L for 10 min (causes vasoconstriction and increase serotonin synthesis)

151
Q

What are drug therapies for prevention of cluster headaches?

A

high dose verapamil

loperimide

melatonin

lithium

for very severe: invasive nerve blocks, deep brain stimulation, ablative neurosurgical procedures

152
Q

What is acute pancreatitis? Who is it seen in?

A

inflammation of the pancreas due to pancreatic enzymes causing autodigestion

middle-aged people

153
Q

What is the etiology of acute pancreatitis? Who is it typically caused in?

A

gallbladder disease, gallstones (women)

chronic alcohol intake (men)

smoking

hypertriglyceridemia (tris>1000)

154
Q

Which headaches can be associated with males? females?

A

males: cluster headache (3x more likely than females)

females: migraines and tension headaches

155
Q

What is the etiology and pathophysiology of acute pancreatitis?

A

etiology: it is thought that alcohol increases the amount of digestive enzymes in the pancreas
gallstones can cause reflux of bile acids within the ducts and cause increase pancreatic enzymes

pathophysiology: enzymes causing autodigestion (trypsin: should be inactivate in the pancreas and activated in the small intestine, pancreatitis can cause trypsin to become active in the pancreas leading to self digestion

156
Q

What are the clinical manifestations of acute pancreatitis?

A

pain: sudden onset of deep, piercing, continuous or steady pain in the left upper quadrant or midepigastrium that will radiate to the back (due to the location of pancreas) and is aggravated by eating and can cause nausea and vomiting

abdominal tenderness and muscle guarding

decreased/absent bowel sounds

crackles in lungs due to inflammation

abdominal skin discoloration seen in moderate to severe: caused by damage from circulating trypsin causing cyanosis or green/yellowing of abdominal wall and seepage of blood from pancreas (seen as Grey Turner’s spots (found on flank) and Cullen’s sign (found around umbilicus))

157
Q

What complications can be seen with acute pancreatitis? How is it treated? When are they seen?

A

psuedocyst: fluid, enzyme, debris, and exudates surrounded by wall causing nausea, vomiting, and abdominal pain. will typically resolve on own and if it does not can lead to perforation and peritonitis which will need surgical intervention

pancreatic abscess: infected psuedocyst because of extensive necrosis of pancreas and will need to be drained surgically

severe or recurrent cases

158
Q

What diagnostic studies are done for acute pancreatitis?

A

labs (primarily): serum amylase level (will be elevated early and for several days) and serum lipase level (done b/c serum amylase elevation can be attributed to other things), may see decrease in calcium with severe, elevation in liver enzymes, tris, and glucose

radiology: US or CT

159
Q

What are some interprofessional care for acute pancreatitis?

A

prevention/alleviation of shock

decrease pancreatic secretions (NPO)

correction of fluid/electrolyte imbalance

prevention/treatment of ifnections

removal of precipitation cause

160
Q

What is the medication therapy for acute pancreatitis? What is an example? What do they do?

A

IV morphine: for pain

antispasmodics: (dicyclomine) to reduce vagal stimulation, pancreatic enzyme secretion, and motility

carbonic anyhdrase inhibitors: (acetazolamide) to reduce volume and bicarbonate concentration of pancreatic enzymes

antacids: to decrease secretion of pancreatic enzymes and neutralize HCl secretion

proton pump inhibitors: shut down HCl secretion (which stimulates pancreas)

161
Q

What nutritional therapies are done for acute pancreatitis?

A

NPO initially (if severe parenteral nutrition may be needed)

NG suction to reduce vomiting and abdominal distension

small, frequent feedings when able: high carbohydrate foods (pancreatic enzymes focus on digesting proteins and fats), no alcohol, supplemental fat-soluble vitamins

162
Q

Which positions can a patient be placed in to relieve pain with acute pancreatitis?

A

flex trunk and draw knees to abdomen

side-laying with head of bed elevated 45 degrees

Health and Illness (4 decks)

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