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Health and Illness > Exam 2 > Flashcards

Exam 2 Flashcards

1
Q

What is hyperthermia?

A

an elevated body temperature greater than 38 degrees celsius with an unchanged hypothalamic set point

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2
Q

What causes hyperthermia?

A

excessive heat production, inadequate ability to cool, hypothalamic regulator dysfunction

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3
Q

What are some risk factors for hyperthermia

A

very young or very old

preexisiting conditions (CVD, hypothyroidism, diabetes, alcoholism)

medications that decrease the body’s ability to lose heat (phenothiazianes (thorazine), anticholinergics, diuretics, amphetamines, beta-adrenergic receptor agonsits)

prolonged environmental exposure (outdoor workers, athletes, homeless)

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4
Q

What are heat cramps?

A

usually brief but severe cramps in large muscle groups that are tired from heavy work

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5
Q

Who typically gets heat cramps?

A

athletes with inadequate fluid intake

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6
Q

What are symptoms of heat cramps?

A

pain, thirst, nausea, tachycardia, pale/pallor, weakness, profuse diaphoresis

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7
Q

What are some nursing interventions for heat cramps?

A

rest, elevate, and massage, fluids, education on prevention

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8
Q

What is heat exhaustion?

A

prolonged exposure to heat which causes profuse diaphoresis resulting in excess water and electrolyte loss

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9
Q

Who typically gets heat exhaustion?

A

people engaged in strenuous activity in hot or humid weather

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10
Q

What are symptoms of heat exhaustion?

A

cold, clammy, pale skin, fatigue and weakness, profuse sweating and extreme thirst, altered mental status, hypotension, tachycardia, weak pulse, tempeature of 37.5C-41C

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11
Q

What are some nursing interventions for heat exhaustion?

A

remove from environment, remove constrictive clothing, monitor ABC’s and cardiac rhythm, fluids, moist sheet

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12
Q

Who is typically hospitalized for heat exhaustion?

A

very young, very old, those with chronic conditions, someone who hasn’t improved in the first 3 to 4 hours after initiating treatment

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13
Q

What is heat stroke?

A

failure of hypothalamic thermoregulatory process resulting in a core temperature that is greater than 41C

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14
Q

What is the pathophysiology of heat stroke?

A

increased sweating, vasodilation, and respiratory rate

fluid and electrolyte depletion

sweat glands stop functioning

core temperature rapidly rises within 10 to 15 minutes

circulatory collapses

decreased cerebral blood flow, neurological symptoms begin

decreased systemic blood flow

cerebral edema and hemorrhage

rhabdomyolysis leading to myoglobinuria (causing kidney damage)

permanent neurological damage

acute kidney injury

death

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15
Q

What are symptoms of heat stroke?

A

hot, dry skin, altered mental status (hallucinations, loss of muscle coordination, combativeness), hypotension, tachycardia, weakness

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16
Q

Can antipyretics be used to treat heat stroke?

A

no, because the increase in temperature is not caused by infection

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17
Q

What are some nursing interventions for heat stroke?

A

rapid cooling methods, monitor and treat shivering, monitor for symptoms of rhabdomyolysis, may give 100% oxygen due to hypermetabolic state

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18
Q

What can IV chlorpromazine be used for?

A

control shivering, if the patient shivers while being treated for hyperthermia it will work against them

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19
Q

What are the types of hypothermia?

A

mild: 35 to 33.9C
moderate: 33.9C to 30C
severe <30C

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20
Q

What causes hypothermia?

A

accidental: environmental exposure

therapeutic: intentionally induced to reduce metabolism and prevent tissue ischemia

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21
Q

What are some risk factors for hypothermia?

A

very young or very old

prolonged environmental exposure: wet clothing (increases evaporation loss 5x), immersion (increased evaporation loss 25x)

metabolic: hypoglycemia, hypothyroidism

healthcare associated: neuromuscular blockage, blood administration, cold IV fluids, inadequate warming in OR

alcohol (vasodilation)
phenothiazines (thorazine)
barbiturates
homeless

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22
Q

What is the pathophysiology of hypothermia?

A

drop in core temperature

drop in metabolic rate causing:
irritable myocardia (causing dysrhythmias), decreased systemic perfusion (causing hypoxia), and decreased renal blood flow (decrease GFR, impaired water reabsorption, dehydration (increased HCT, increased risk for stroke, MI, and PE)

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23
Q

What are the symptoms for each type of hypothermia?

A

mild: shivering, lethargy, confusion, some irrational behavior, mild changes in HR

moderate: muscle rigidity, bradycardia, bradyapnea, weak pulses, BP hard to ascertain (need doppelr), hypovolemia

severe: (person looks dead) absent reflexes, pupils fixed and dilated, bradycardia, arrhythmia, ventricular fibrillation, bradyapnea

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24
Q

When is someone pronounced dead from hypothermia? What usually causes the death?

A

every effort is made to rewarm the person to at least 86F or 30C; fatal arrhythmia or ventricular fibrillation

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25
Q

What are some nursing interventions for hypothermia?

A

remove pt from cold environment, rewarm pt, monitor VS, heart rhythm, LOC, electorlytes

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26
Q

What are the ways to rewarm someone?

A

passive: move to warm, dry place, remove wet clothing, use radiant lights, warm blankets

active external: fluid or air-filled warming blankets (bear hugger), warm water immersion (98.6 to 104F water)

active internal: (for moderate to severe) application of heat to core through warm IV fluids, peritoneal lavage, heated and humidified oxygen

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27
Q

Why do you need to rewarm the core before extremities?

A

if rewarm extremities first the cold peripheral blood will return to the central circulation leading to hypotension, dysrhythmias, rewarming shock

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28
Q

What is thermoregulation?

A

process of maintaining core body temperature at a near constant value, balance of heat production and heat loss to maintain body temperature

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29
Q

What is the difference between core temperature and surface temperature?

A

core: more reliable, relatively constant

surface: fluctuates in response to environmental factors

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30
Q

What is normothermia?

A

body temperature is in normal range

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31
Q

What does the basal metabolic rate for heat production depend on?

A

surface area, thyroid hormones, testosterone

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32
Q

What controls heat production? How?

A

posterior hypothalamus; shivering and vasoconstriction

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33
Q

What controls heat loss? How?

A

anterior hypothalamus; sweating, vasodilation, blood redistribution to body surface vessels, inhibition of heat production

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34
Q

What are the ways heat is transferred? Example?

A

convection: flow of body heat to cooler air (fan)

evaporation: loss of heat when liquid is converted to vapor (sweating)

radiation: indirect loss of body heat from a cold surface that is within proximity (bed near window or a/c)

conduction: direct loss of body heat from contact with cold surface (ice packs)

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35
Q

What factors affect body temperature?

A

age, exercise (metabolism and heat production), hormone levels (female’s menstrual cycle and menopause), circadian rhythm (steadily rises through day and falls during night, lowest between 1a and 4a), stress (increase heat production), environment

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36
Q

What is the normal body temperature for infants?

A

36.5 to 37.5C

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37
Q

Why is there an increase risk of heat loss for infants?

A

thin SQ fat, blood vessels closer to skin, larger body surface area to body weight ratio

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38
Q

Given the way heat is transferred how should that be taken into consideration for infants?

A

convection: try to keep room temperature between 72 and 78

evaporation: should be dried thoroughly after bathing, one of most significant losses of heat for infants

radiation: don’t put crib next to window or a/c

conduction: infant warmers, skin-to-skin contact with caregiver

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39
Q

How do infant produce heat?

A

they are unable to shiver therefore they rely on:

metabolism of brown fat to increase heat production by 100% but will be depleated quickly with cold stress

muscle activity and vasoconstriction

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40
Q

Why can acrocyanosis occur in infants?

A

vasoconstriction to increase body temperature causing low perfusion to extremities and blue discoloration

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41
Q

What is the typical range of rectal temperature for children?

A

37 to 37.5C

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42
Q

How does temperature in children differ from temperature in adults?

A

until puberty, temperature is more variable, some healthy children can have temperatures as high as 41C without difficulty

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43
Q

What is the normal temperature range for older adults?

A

36 to 36.8C

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44
Q

Why is there a reduction in ability for older adults to respond to temperature changes?

A

cannot vasoconstrict easily, decrease in peripheral circulation, decrease in CO, ability to shiver is diminished, reduced muscle mass, reduced SQ tissue, impaired sweating mechanisms

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45
Q

At what age do thermoregulation deaths drastically increase?

A

those older than 70/75

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46
Q

What is focused on for health history for thermoregulation?

A

past medical history related to thermoregulation (thyroid disease, hypothalamic injury, autoimmune disease, traumatic injury), recent injury or illness, environmental exposure, subjective symptoms

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47
Q

What are the lifespan considerations for temperature taking?

A

birth to 2 years: axillary, rectal if definitive temperature reading is needed for infants older than 1 month

2 to 5 years: axillary, tympanic, oral when child can hold thermometer under tongue, rectal if definitive temperature is needed

older than 5: oral, axillary, tympanic

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48
Q

What is pyrexia?

A

temporary elevation in body temperature triggered by an immune response

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49
Q

At what temperatures will pyrexia be dangerous for adults and children?

A

greater than 39C for adults

greater than 40C for children

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50
Q

What are the patterns of pyrexia?

A

sustained: constant temperature with little fluctuation

intermittent: cycles of fever spikes and return to normal

remittent: fever spikes and falls but does not return to normal

relapsing: periods of febrile episodes and periods of acceptable temperature range

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51
Q

What is the pathophysiology of pyrexia?

A

pathogens (bacteria or virus) enter the body

they trigger an immune response

hypothalamus reacts by increasing body’s set point

body temperature begins to rise inducing chills, shivers, feeling of cold

the pathogen is destroyed and the hypothalamus drops the set point

vasodilation occurs to promote heat loss inducing diaphoresis and the feeling of warm

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52
Q

Who are complications of pyrexia typically seen in?

A

children, older adults, those with multiple co-morbidities

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53
Q

What are some complications of pyrexia? Why do they occur?

A

hypoxia: increase cellular metabolism leading to increase oxygen use and depletion of nutrient stores, the inability to compensate to change in thermoregulation causing myocardial hypoxia (seen as angina) and cerebral hypoxia (seen as confusion)

dehydration: increase in insensible water loss due to elevated RR and diaphoresis causing a fluid volume deficit

febrile seizures: common for children 6 months to 5 years, occurs during the rise in temperature (the higher the temperature change, the more likely to occur), generalized tonic-clonic that is over before EMS arrives and there is not much treatment for it unless it’s repetitive or something else occurs during the seizure

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54
Q

What is some education about febrile seizures?

A

seek emergency medical care if the child: has a febrile seizure that lasts more than 10 minutes, turns blue, and/or vomits during febrile seizure

do not put anything in their mouth or hold them down

prevention: if the child is uncomfortable due to fever give acetaminophen or ibuprofen as directed, no one knows why the seizures happen, call provider of ran evaluation after the seizure

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55
Q

What is clotting?

A

physiological process in which blood is converted from a liquid to a semisolid gel

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56
Q

How much of blood does RBC, WBC, and platelets consists of?

A

around 45%

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57
Q

What are the types of bone marrow? And their functions?

A

red: actively produces stem cells that will differentiate to RBC, WBC, or platelets

yellow: stores fat

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58
Q

What does the spleen do?

A

produces RBC during fetal development, filters old RBC and bacteria from blood, stores more than 300mL of RBC and 1/3 volume of platelets

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59
Q

What does the lymphatic system do?

A

carries fluid from interstitial spaces to blood while filtering out pathogens and foreign particles

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60
Q

How does the liver work in the hematologic system?

A

filters and produces pro-coagulants which is essential for hemostasis and coagulation

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61
Q

What is hematopoiesis?

A

blood cell production that occurs in the red bone marrow

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62
Q

What is the primary function of RBC? What is it composed of? How much is there in the body? How long do they survive?

A

transport gases to tissues, maintain acid-base balance; hemoglobin to bind with O2 and CO2; 3.8 to 5.7 million per mm/uL; 90 to 120 days

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63
Q

What is a reticulocyte?

A

immature RBC that will mature within 48 hours

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64
Q

How is erythropoiesis controlled?

A

hypoxia, the kidneys monitor the level of oxygen in the blood, if it’s low they will secrete erythropoietin which will stimulate bone marrow to produce RBCs

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65
Q

What is hematocrit versus hemoglobin?

A

hematocrit is the percentage of blood that is composed of RBCs

hemoglobin is the capacity of carrying gas

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66
Q

What is the normal lab value of hemoglobin for adult males, females, and pregnant people?

A

females: 12-16 g/dL

males: 14-18 g/dL

pregnant: less than 10 g/dL

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67
Q

What is the normal value of hematocrit for adult males, females, and pregnant people?

A

females: 37-47%

males: 42 to 52%

pregnant: less than 33%

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68
Q

What is the primary function of leukocytes? What are the cell types?

A

phagocytosis, inflammatory, and immune response; granulocytes: neutrophils, acinophils, and basophils

lymphocytes: B and T cells

monocytes

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69
Q

What is the normal WBC count?

A

5,000 to 10,000

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70
Q

What is the primary function of thrombocytes? How long do they live?What are they inhibited by?

A

initiate clotting cascade (creates initial platelet plug at site of injury) and maintains integrity of cell walls; 8 to 10 days; aspirin, NSAIDs, platelet disorderes

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71
Q

What is the normal thrombocyte count?

A

150,000 to 400,000

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72
Q

What are the components of a CBC?

A

total RBC count, WBC count, hemoglobin, hematocrit, platelet

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73
Q

What are the lifespan considerations for infants and the components of a CBC?

A

high RBC, Hgb, and Hct at birth that will fall slowly over the first month (indicating less efficient gas exchange)

high WBC that will rapidly decrease (high risk for infection, neutrophils are unable to recognize foreign substances and mount a defense)

platelets: active at birth and the same amount as adults

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74
Q

What are the lifespan considerations for pregnant people and their total blood volume? Why does this occur?

A

increase in total blood volume by 40 to 50%, an increase in plasma volume leading to more plasma volume than RBC causing a low Hgb and Hct which results in physiologic anemia due to dilution of blood; protective mechanisms: perfuse uterus, hydrate fetal and maternal tissues, fluid reserve for blood loss at birth and post-partum

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75
Q

What are the lifespan considerations for pregnant people and their WBC count?

A

increase in WBC count, increase in granulocytes

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76
Q

What are the lifespan considerations for pregnant people and coagulation? Why does this occur?

A

increase in clotting factors and a decrease in coagulation inhibiting factors lead to a hypercoagulability state; protective mechanism: decrease fibrinolytic activity to decrease risk of bleeding but there is an increase risk of thrombus

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77
Q

What are the lifespan considerations for older adults and their hemoglobin?

A

decreased hemoglobin which increases the rate of iron deficiency (also impacted by decrease in iron absorption and serum iron biding capacity) causing a reduced cellular response to hemorrhage or hypoxemia (due to decrease reticulocyte production)

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78
Q

What are the lifespan considerations for older adults and their WBC?

A

while the count is unaffected by aging there is a decrease in lymphocyte function causing a lower increase in WBCs during infection this will put them at a greater risk for infection and a diminished ability to compensate for acute or chronic illness

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79
Q

What are the lifespan considerations for older adults and their platelets?

A

the amount is unaffected by aging but there is an increase in platelet adhesion

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80
Q

What is focused on for health history and clotting?

A

pmh of clotting issues, medications (including herbs/supplements, esp garlic and ginko), surgery (post-op bleeding, problems with wound healing, blood transfusion hx), nutrition, elimination (black/tarry stools, tea-colored urine), activity (SOB or DOE, frequent falls, bruising), sexuality (menstrual cycle/menopasue, impotence)

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81
Q

What are some symptoms of altered clotting?

A

petechiae, purpura, jaundice

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82
Q

What is activated partial thromboplastin time (aPTT)?

A

a clotting study that looks at the intrinsic clotting from multiple factors, measured in seconds, used to look at coagulation rates on those on heparin to help titrate drop rates

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83
Q

What is prothrombin time (PT)?

A

a clotting study that measures how thin the blood is and extrinsic coagulation from multiple factors, measured in seconds, recorded as international normalized ratio (INR)

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84
Q

What is the therapeutic range of INR for those on warfarin?

A

2 to 3

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85
Q

What is d-dimer? What does an increase indicate?

A

a clotting study that measures fibrin fragments from clot lysis; hypercoagulable state and/or presence of blood clot

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86
Q

What is clotting factor 1? What does a decrease/increase indicate?

A

fibrinogen; increase: hypercoagulable, decrease: increase risk for bleeding

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87
Q

What are the two categories of perfusion?

A

central: blood flow through the heart and inter peripheral vascular vessels

tissue: volume of blood that flows from arteries and capillaries to target tissues

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88
Q

What generates central perfusion?

A

cardiac output

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89
Q

What is the cardiac cycle?

A

how electrical activity in the heart makes the heart fill composed of diastole: filling, rest and systole: pumping, action

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90
Q

What is cardiac output? What is the normal amount?

A

HRxSV = how much blood is pumped by the heart (L/min) as a result of the cardiac cycle, indicates how well the heart is doing; 4 to 8L/min

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91
Q

What is the normal HR?

A

50 to 180bpm

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92
Q

What factors affect SV? How do they affect SV?

A

preload: volume in ventricles at the end of diastole, determines the amount of stretch placed on myocardial fibers

afterload: pressure the ventricles have to overcome to eject blood, affected by size of ventricles and arteriole BP

contractility: ability of myocardial cells to shorten their fibers

an increase in all/any of these will increase workload of heart and increase demand for oxygen

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93
Q

What is the Frank-Starling law?

A

the more myocardial fibers are stretched (preload) the greater the force of contraction

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94
Q

Which disorder can increase preload and afterload?

A

HTN

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95
Q

How does the sympathetic nervous system impact central perfusion?

A

stimulating beta 1 receptors in the heart which will then increase HR, contractility, and automaticity

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96
Q

What is automaticity?

A

ability of myocardial cells to depolarize spontaneously

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97
Q

How does the sympathetic nervous system impact tissue perfusion?

A

stimulating alpha and beta 2 receptors in the lungs, veins, and arteries

alpha receptor stimulation causes vasoconstriction

beta 2 receptor stimulation causes vasodilation and bronchodilation

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98
Q

How does the parasympathetic nervous system impact central perfusion? What is the system called?

A

innervates at the SA and AV node and atrial muscle via the vagus nerve to decrease HR and contractility; this is called the vasovagal response

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99
Q

What is the normal HR for infants? What could alterations to HR indicate in infants?

A

120 to 160BPM; tachycardia could indicate anemia, hypovolemia, hyperthermia, or sepsis
bradycardia could indicate congenital issues or hypoxemia

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100
Q

What is the normal BP for infants? Why does this occur?

A

60 to 80/40 to 50 mmHg; low systolic bp due to weaker left ventricle, left ventricle will strengthen during first 6 weeks and after puberty the systolic pressure will rise to adult levels

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101
Q

What are the most common congenital malformations? What are the chances they occur? Of those chances what are the chances of a critical congenital malformation?

A

heart defect; about 1 in 100; about 25% which will need surgery or procedure shortly after birth or in the first year of life

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102
Q

What is the normal HR for pregnant people?

A

HR: 150 to 200 BPM

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103
Q

What is the normal CO for pregnant people? Why does this occur?

A

increases 30 to 50% due to increase tissue demands for oxygen, in the second half of pregnancy compression of the vena cava can occur and when the pregnant person is supine CO can decrease by 25 to 30%

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104
Q

What are the types of hypertension in pregnant people?

A

gestational: after week 20 of pregnancy without proteinuria

preeclampsia: after week 20 of pregnancy with proteinuria, can also have oliguria and presence of inner uterine growth restriction

eclampsia: emergency, seizure activity or coma in a pregnant person with preeclampsia when they have had no hx of seizures

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105
Q

What are lifespan considerations for older adults’ CO, vasculature and HTN?

A

CO decreases due to less efficient and strength of heart, time for diastole increases, heart valves thicken and become less elastic

vasculature becomes less elastic causing perfusion issues

HTN is most common and prevalent CVD in older adults that is mostly due to age-related changes but compounded with lifestyle factors

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106
Q

What are the types of hypotension seen in older adults?

A

postural: orthostatic

postprandial: hypotension after eating

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107
Q

What is one of the leading causes of hospitalization for older adults?

A

congestive heart failure as a complciation of HTN/CAD

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108
Q

What are some symptoms of poor perfuison?

A

pain or pressure, dyspnea, diaphoresis, anxiety, edema, dizziness/fainting, nausea, heartburn

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109
Q

What physical exam pieces look specifically at central perfusion? at tissue perfusion?

A

BP, HR, heart sounds, peripheral edema; skin color and temperature, peripheral pulses, cap refill

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110
Q

Which cardiac enzymes are used for diagnostic purposes?

A

troponin: myocardial protein released after injury to the heart, if suspected MI draw this erially

creatinine kinase in myocardium (CK-MB): enzyme in myocardium that will be elevated after injury to the heart

brain natriuretic peptide (BNP): hormone secreted from myocardial cells during high BP, used to detect HF

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111
Q

Which cardiac markers are used for diagnostic purposes?

A

homocysteine: amino acid produced during metabolism of proteins, elevated levels can predict: CVD, CAD, stroke, peripheral artery disease, venous thrombosis

C-reactive protein (CRP): produced during any inflammatory process but especially the heart, evaluates risk for developing CAD

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112
Q

What is the serum level of triglycerides for females and males?

A

females: 35 to 135 mg/dL
males: 40 to 160 mg/dL

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113
Q

What is the serum level of LDLs?

A

less than 130 mg/dL

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114
Q

What is the serum level of HDLs for females and males?

A

females >55mg/dL
males >45mg/dL

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115
Q

What is the typical creatinine for females and males?

A

females: 0.5 to 1.1 mg/dL

males: 0.6 to 1.2 mg/dL

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116
Q

What is the normal total cholesterol levels?

A

less than 200 mg/dL

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117
Q

What is the fasting glucose range?

A

74 to 106 mg/dL

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118
Q

What tests can be performed for perfusion?

A

12 lead ECG to look at electrical impulses of heart

cardiac stress test including an exercise cardiac stress test and pharmacologic stress test (if there’s mobility issues)

radiographic studies: chest XR, echocardiogram (estimates ejection factor to indicate how well the heart is functioning, looks at flow of blood), ultrasound, arteriogram/angiogram

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119
Q

What is ejection fraction?

A

amount of blood pumped out of ventricles with every contraction

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120
Q

What are some non modifiable risk factors for impaired perfusion?

A

increasing age, gender (men over 45 and women over 55), genetics (family hx of: hypercholesterolemia, hemoglobinopathies (sickle cell), bleeding disorders (hemophilia and Von willebrand disease)), ethnicity, socioeconomic status

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121
Q

What are some modifiable risk factors for impaired perfusion?

A

medically treatable: HTN, elevated serum lipids, diabetes mellitus

lifestyle: smoking, obesity, diet and nutrition, physical inactivity, stress

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122
Q

What is the primary and secondary prevention for hypertension?

A

primary: maintain BP, age 13 and older BP<120/80, children 1 to 13<90th percentile

secondary: annual BP screening across lifespan, includes those being treated for HTN

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123
Q

What is the primary and secondary prevention for hyperlipidemia?

A

primary: maintain total cholesterol, adults over 20 <200, children and adolescents <170

secondary: cholesterol screening for men 20-35 for increased risk and those over 35, women 20 to 45 for increased risk and those over 45, children and adolescents age 9 to 11 for baseline and high risk screening by age 10

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124
Q

What are the chances of developing CVD for those who smoke? for having an MI? What happens to the chance of CVD after 1 year of not smoking?

A

2 to 4x greater than a nonsmoker; those who smoke a pack of cigarettes a day have more than 2x risk for MI; risk is equalized

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125
Q

How does smoking negatively impact cardiovascular health?

A

damages coronary vessels, increases blood viscosity, increases risk for atherosclerosis and clots, decreases HDL, decreases activity tolerance

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126
Q

What are some AHA recommendations for diet and nutrition to maintain good cardiovascular health?

A

fruits and veggies (make up half of the plate), whole grains, nuts and legumes, skinless poultry and fish, low-fat dairy products (should be limited to once or twice a day), non-tropical vegetable oils

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127
Q

What are the positive effects of physical activity?

A

reduces risk for CVD by 30 to 40% and improves quality of life (improves mental health and immunity)

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128
Q

What are the aerobic activity recommendations for adults? for children and adolescents?

A

150 min of moderate-intensity (talk but cannot sing) or 75 minutes of vigorous intensity (breathing hard and fast, but cannot say more than a few words) per week; 60 minutes of moderate-intensity per day

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129
Q

What are the muscle-strengthening recommendations?

A

moderate to vigorous level of activity twice per week

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130
Q

How can chronic stress impact perfusion?

A

damage arterial walls and weaken immune system

131
Q

What are some stress busting activities?

A

engaging in regular physical activity, giving up bad habits (excessive drinking or smoking), talk with family and friends, laugh, take time for yourself, get enough sleep

132
Q

What is systemic vascular resistance?

A

force opposing the movement of blood into the vessels, determined by radius of arteries and arterioles

133
Q

What are the short term regulation of BP?

A

baroreceptors found in the carotid artery and aortic arch will detect a change in BP and activate the SNS

vascular endothelium will regulate substances that cause vasodilation (NO) and vasoconstriction (endothelin)

134
Q

What are the long term regulation of BP?

A

renal system will release renin and activate the RAAS system in response to decrease BP, endocrine system will have the pituitary release ADH in response to a decrease BP

135
Q

What happens when BP decreases?

A

baroreceptors activate the SNS

SNS causes systemic vasoconstriction and an increase in HR and contractility will occur

a decrease in BP will decrease renal artery pressure

renin secretion will be increased and converted into angiotensin I via angiotensinogen

angiotensin I will be converted to angiotensin II via ACE

angiotensin II will increase systemic vasoconstriction and activate the pituitary to release ADH

ADH will increase water and sodium reabsorption

angiotensin II will increase secretion of aldosterone which will increase water and sodium reabsorption

136
Q

What are the AHA BP guidelines?

A

normal: <120 and <80

elevated: 120-129 and <80

HTN 1: 130-139 or 80-89

HTN2: >140 or >90

Hypertensive crisis: >180 and/or >120

137
Q

What is the etiology of primary and secondary hypertension?

A

primary (essential or idiopathic) HTN, makes up most of the cases

secondary HTN: sudden development with an underlying cause, once underlying cause is treated the HTN is typically cured (ex/pregnancy)

138
Q

What is the pathophysiology of hypertension? What is the hallmark of HTN?

A

angiotension II will cause vasoconstriction and tissue growth which will lead to vessel wall remodeling (hardening of vessel walls) resulting in primary HTN and atheroscloerosis, primary hallmark is increased SVR

139
Q

What are non-modifiable risk factors for HTN?

A

age: male<65 and females>65
gender
ethnicity: BIPOC
family hx
socioeconomic status

140
Q

What are modifiable risk factors for HTN?

A

diabetes mellitus
stress
sedentary lifestyle
elevated serum lipids
excess diatary sodium intake
alcohol
obesity
tobacco use

141
Q

What are some signs and symptoms of HTN?

A

often will be secondary to target organ disease

fatigue
reduced activity
SOB
angina
changes in vision
headache

142
Q

What are some complications of HTN?

A

heart: CAD, LVH, HF, heart attack

kidneys: renal disease

brain: stroke, cognition

eyes: retinopathy

PVD: atherosclerosis

143
Q

What lifestyle modifications can be done for HTN?

A

weight reduction
diet rich in fruits, vegetables, low fat with reduced saturated and total fat
sodium reduction
physical activity
moderation of alcohol consumption
omega-3 fatty acids
smoking cessation
stress management

144
Q

What is the most important educational point for heart medications?

A

compliance, do not stop suddenly

145
Q

What is hydrochlorothiazide? Class? MOA? Therapeutic/lab monitoring? Indications? Adverse effects? Nursing considerations?

A

thiazide diuretic

increase excretion of Na and water by inhibiting Na reabsorption in distal tubule

monitor electrolytes (K), BG, kidney function, uric acid levels

mild to moderate HTN (first choice drug)

hypokalemia, pancreatitis, lethargy, dehydration

take in morning with food or milk

146
Q

What is furosemide? Class? MOA? Therapeutic/lab monitoring? Indications? Adverse effects?

A

loop diuretic

inhibits reabsorption of Na and Cl promoting excretion of water and electrolytes

assess fluid status, digoxin toxicity, renal and hepatic function, serum glucose, uric acid levels

edema due to HF, hepatic impairment, renal disease, HTN

erythema multiforme, dehydration, aplastic anemia, agranulocytosis, tinnitus

147
Q

What is spironoactone? Class? MOA? Therapeutic/lab monitoring? Indications? Adverse effects?

A

potassium-sparing diuretic

interferes with Na/K pump in tubules and binds competitively to aldosterone receptors to promote excretion

assess fluid and electrolytes, ECGs

HTN, edema

hyperkalemia, amenorrhea, gynecomastia (male), hair growth (female), ED, muscle cramps

148
Q

What is clonidine? Class? MOA? Therapeutic/lab monitoring? Indications? Adverse effects?

A

alpha2 adrenergic receptor stimulator

reduces SNS response to baroreceptors leading to vasodilation

assess fluid levels, signs for opioid withdrawal, BG

mild to moderate HTN

dry mouth, ED, weight gain, drowsiness, hallucinations, paresthesia, withdrawal phenomenon

149
Q

What is metoprolol? Class? MOA? Therapeutic/lab monitoring? Indications? Adverse effects?

A

cardio selective beta blocker

blocks beta 1 adrenergic receptors in heart

ECG, fluid levels, angina, kidney function, K, triglycerides, uric acid

HTN, angina pectoris, prevention of MI

bradycardia, HF, pulmonary edema, hyperglycemia, ED, decrease libido, fatigue, weakness, depression, withdrawal phenomenon

150
Q

What is propranolol? Class? MOA? Therapeutic/lab monitoring? Indications? Adverse effects?

A

nonselective beta blocker

blocks beta1 and beta2 adrenergic receptors in lungs and heart

ECG, fluid levels, SJS, angina, renal function, K, triglycerides, uric acid

HTN, angina, arrhythmia, hypertrophic cardiomyopathy, prevention and management of MI

arrhythmia, bradycardia, HF, pulmonary edema, blurred vision, ED, wheezing, fatigue, withdrawal phenomenon, do not take with albuterol

151
Q

What is doxazosin? Class? MOA? Therapeutic/lab monitoring? Indications? Adverse effects?

A

alpha1 adrenergic

blocks alpha1 causing vasodilation in peripheral vasculature

BP, pulse, fluid levels

HTN, symptomatic BPH

1st dose syncope, dizziness, headache, decrease libido

152
Q

What is hydralazine? Class? MOA? Therapeutic/lab monitoring? Indications? Adverse effects?

A

vasodilator

acts directly in peripheral vasculature to vasodilate and reduce SVR

BP, pulse, CBC, electrolytes

HTN

tachycardia, angina, drug induced lupus syndrome, drowsiness, dizziness, tachycardia, headache, edema

153
Q

What is nitroglycerin? Class? MOA? Therapeutic/lab monitoring? Indications? Adverse effects?

A

nitrate

vasodilates and reduces myocardial oxygen consumption to reduce preload and SVR; in low doses causes venous dilation, in high doses causes atrial dilation

pain, BP, pulse, ECT (if IV)

chronic stable angina, acute and long-term prophylactic for angina, HTN

hypotension, tachycardia, blurred vision, dizziness (take sitting down), headache

154
Q

What is sodium nitroprusside? Class? MOA? Therapeutic/lab monitoring? Indications? Adverse effects?

A

vasodilator

direct arterial vasodilator, reduces SVR

BP, HR, ECG

HTN, cardiogenic shock/cardiac pump failure

blurred vision, tinnitus, acidosis, abdominal pain, nausea, dizziness, headache, cyanide toxicity, possible fetal harm

155
Q

What is captopril? Class? MOA? Therapeutic/lab monitoring? Indications? Adverse effects?

A

ACE inhibitor

blocks conversion of angiotensin I to II

BP, pulse, signs of angioedema, fluid levels, kidney function

HTN, HF, diabetic nephropathy

dry persistent cough, angioedema, hypotension, taste disturbances, agranulocytosis, hyperkalemia

156
Q

What is enalapril? Class? MOA? Therapeutic/lab monitoring? Indications? Adverse effects?

A

ACE inhibitor

blocks conversion of angiotensin I to II

BP, pulse, signs of angioedema, fluid levels

HTN, symptomatic HF

dry persistent cough, angioedema, hyperkalemia, proteinuria, teratogenic

157
Q

What is lisinopril? Class? MOA? Therapeutic/lab monitoring? Indications? Adverse effects?

A

ACE inhibitor

blocks conversion of angiotensin I to II

BP, pulse, signs of angioedema, fluid levels

HTN, symptomatic HF

dry persistent cough, angioedema, hyperkalemia, proteinuria, teratogenic

158
Q

What is losartan? Class? MOA? Therapeutic/lab monitoring? Indications? Adverse effects?

A

angiotensin II receptor blocker

blocks angiotensin II at receptor to inhibit vasoconstriction

orthostatic BP, pulse, angioedema, kidney function

HTN, diabetic nephropathy, stroke prophylactic

(side effects less than ACE inhibitors) teratogenic, diarrhea, angioedema, hyperkalemia, dizziness, angina

159
Q

What is valsartan? Class? MOA? Therapeutic/lab monitoring? Indications? Adverse effects?

A

angiotensin II receptor blocker

blocks angiotensin II at receptor to inhibit vasoconstriction

orthostatic BP, pulse, angioedema, kidney function

HTN, HF

(side effects less than ACE inhibitors) teratogenic, diarrhea, angioedema, hyperkalemia, dizziness, angina

160
Q

What is amlodipine? Class? MOA? Therapeutic/lab monitoring? Indications? Adverse effects?

A

dihydropyridine Ca channel blocker

inhibits movement of calcium into vascular smooth muscle to relax vascular smooth muscle to decrease SVR and arterial BP

BP, pulse, ECG, angina

HTN, chronic stable angina, vasopastic (Prinzmetal’s) angina

peripheral edema, hypotension, palpations, careful use in those with HF

161
Q

What is diltiazem? Class? MOA? Therapeutic/lab monitoring? Indications? Adverse effects?

A

non-dihydropyridine ca channel blocker

inhibits movement of ca across cell membranes causing vasodilation

hemodynamic monitoring, kdiney function, neurological changes, ECG, signs of HF

HTN, chronic stable angina, vasopastic (Prinzmetal’s) angina

arrhythmia, HF, peripheral edema, cough, constipation, gynecomastia (male), hyperglycemia, weight gain, tremor, headache, paresthesia, digoxin toxicity

162
Q

What is a hypertensive crisis?

A

a sever and abrupt increase in BP, >180/>120

163
Q

What is the difference between the types of hypertensive crisis?

A

the rate of increase in BP is more important than the absolute value in determining the need for emergent treatment

hypertensive urgency: elevation onset is days to weeks, no target organ damage, often hospitalization is not required will be prescribed oral medications and will be outpatient with a followup within 24 hours

hypertensive emergency: elevation onset is hours to days, there is target organ damage (this condition typically is due to a secondary condition), hospitalization is required and IV medications will be administered with intensive hemodynamic monitoring

164
Q

What are the causes of a hypertensive emergency?

A

head injury, preeclampsia, eclampsia, stimulant drugs, abruptly stopping taking a heart medication

165
Q

What are symptoms of a hypertensive emergency?

A

seizures, encephalopathy, death, acute kidney failure, heart attack

166
Q

What is the treatment plan for a hypertensive emergency?

A

IV anti-hypertensive medications (sodium nitroprusside), slowly titrate the medication, want to slowly decrease MAP by 30-35% to avoid decreased perfusion to major organs, monitor renal labs

167
Q

What is the pathophysiology of coronary artery disease?

A

chronic endothelial injury (due to: diabetes, smoking, HTN)

creation of a fatty streak (earliest lesion, lipids start to accumulate, can start in teenage years or age 20)

collagen covers the fatty streak to create the fibrous plaque (can start by age 30)

becomes a complicated lesion as the inflammation and narrowing increases (could lead to total occlusion of artery and/or the lesion will rupture

all resulting in impaired blood flow to myocardium

168
Q

What are some non-modifiable risk factors for coronary artery disease?

A

age (increasing)
gender (men until 75, then equalize with women)
race (white males, AA, NA)
genetics

169
Q

What are some major modifiable risk factors for coronary artery disease?

A

elevated serum lipids, HTN, tobacco use, physical inactivity, obesity

170
Q

What could cause an increase in triglycerides?

A

reflection of how we eat, physical inactivity

171
Q

What is the dangers with LDL?

A

contains more cholesterol, attracted to arterial walls and can deposit cholesterol onto them

172
Q

What are the benefits of HDL?

A

has more proteins than cholesterol, carries lipids away from arteries so they can be metabolized, can be increased with physical activity (females have higher HDL until menopause)

173
Q

What happens to the risk of coronary artery disease after smoking cessation?

A

damage is irreversible but chance of death will decrease to someone who hasn’t smoked within a year of smoking cessation

174
Q

What are some contributing modifiable risk factors for coronary artery disease?

A

increase fasting blood glucose (diabetes (even with good control) and metabolic syndrome)

increase homocysteine levels (promotes plaque build up, damages lining of blood vessels, alters clotting mechanism)

substance abuse (causes spasms to coronary arteries)

psychosocial (type A personality, acute and chronic stress, anxiety, hostility and anger, lack of social support, depression (increases catecholamine levels which will increase damage)

175
Q

How can CAD be diagnosed?

A

medical and family hx, risk factors, physical, EKG, stress test, echo, chest XR, blood tests, coronary angio and cardiac catheterization

176
Q

What are some nursing and collaborative care for CAD?

A

identify and manage high risk individuals
promote physical activity
promote heart healthy diet
drug therapies

177
Q

What are the guidelines for pharmaceutical treatment of elevated LDL?

A

known CVD
LDL>/=190
pt’s 40-75 with LDL=70-189 and/or diabetes and/or 10 yr risk of CVD of at least 7.5%

178
Q

What is atorvastatin? MOA?

A

first line medication for restricting lipoprotein production, blocks synthesis of cholesterol and can aid liver to filter out LDL from blood, there will be a small increase in HDL

179
Q

What is gemfibrozil? MOA?

A

decreases synthesis and secretion of VLDL, most effective for lowering triglycerides and increasing HDL, NO EFFECT ON LDL

180
Q

What is niacin? MOA?

A

vitamin B6, inhibits synthesis of LDL and triglycerides, needs to be used in high dosages which could increase side effects

181
Q

What is colesevelam? MOA?

A

reduces LDL and cholesterol by converting them into bile acids, not as strong as statins, second line medication

182
Q

What are PCSK9 inhibitors?

A

inactivates the PCSK9 protein and lowers LDL

183
Q

What is ezetimibe?

A

inhibits intestinal absorption of cholesterol

184
Q

What is aspirin used for with CVD?

A

decreases platelet aggregation and clot formation, need to take chronically (at least 10 years) therefore pt needs to have a life expectancy of 10 eyars

185
Q

Who should be taking low dose aspirin for CVD?

A

adults 50-59 with a CVD risk >/=10, there’s no evidence those under 50 or over 70 should take daily to prevent CVD

186
Q

What is ischemia?

A

oxygen supply is inadequate to meet metabolic needs

187
Q

What is chronic stable angina?

A

narrowing of coronary arteries causing a limited supply of oxygen when the demand is high causing a pattern of pain during activity and relief during rest

188
Q

What is silent ischemia? Who is it commonly seen in? How is it diagnosed?

A

no subjective symptoms of ischemia

most common in diabetics due to diabetic neuropathy

seen in ECG changes

189
Q

What is prinzmetal’s angina? Risk factors? Cause?

A

angina that occurs at rest and not with increased physical demand

hx of migraines, raynauds (vasopastic disease), smoking

spasm of coronary artery, increased O2 demand (trigger substances, medications that vasodilate, exposure to cold, REM sleep)

190
Q

What is microvascular angina? Who is it most prevalent in?

A

angina in the absence of significant CAD or coronary spasm rather it is caused by a distant less impactful coronary microvascular disease

women

191
Q

What is the goal for nursing care in those with ischemia?

A

decrease oxygen demand and/or increase oxygen supply

192
Q

What is the MOA for short-acting nitrates? What are nursing education points?

A

dilate peripheral and coronary blood vessels that works in 1 to 5 minutes; maximum of 3 doses in a row with 5 minutes in between, sit/lay while taking, do not chew tab

193
Q

What is isosorbide? Side effects?

A

long-acting nitrate to reduce angina incidence

headache, orthostatic hypotension

194
Q

What is nitroglycerin ointment? Side effects?

A

long-acting nitrate to reduce angina incidence

headache, orthostatic hypotension

195
Q

What is transdermal controlled release NTG? Side effects?

A

long-acting nitrate to reduce angina incidence

headache, orthostatic hypotension

196
Q

What types of drugs can be used for angina?

A

short-acting nitrates, long-acting nitrates, ACE, ARBs, beta blockers, calcium channel blockers; lipid lowering, sodium current inhibitor

197
Q

What is ranolazine? Side effects?

A

sodium current inhibitor for chronic stable angina in those who have no response to other medications

cause EKG changes (QT interval), dizziness, nausea, headache, no fluoxetine or prozac

198
Q

What is a procedural treatment for CVD?

A

cardiac catheterization/coronary angiography to visualize blockages of major vessels and possibly open the blockages if symptomatic with percutaneous coronary interventions, balloon angioplasty, or stent

199
Q

What is venous thrombosis? Types?

A

clot formation in a vein, the most common disorder of veins

DVT found in deep veins like femoral or common iliac

SVT found in superficial veins like great saphenous

200
Q

What are the symptoms of SVT? How is it diagnosed? What is the treatment?

A

firm, cordlike vein that can be palpated, red, itchy, painful, warm, edematous

diagnosed with ultrasound

NSAIDs for symptom management, warm compresses, compression, elevate or mild exercise

201
Q

What is Virchow’s triad?

A

Risk factors for VTE
venous stasis: alterations in blood flow, stasis of blood (varicose veins, turbulence of blood)

hypercoagulability: alterations in blood to make it more susceptible to clotting (smoking, genetics)

vascular wall damage (sheer, stress, HTN)

202
Q

What are some major risk factors for VTE? Other precipitating factors?

A

Virchow’s triad, age, prolonged immobilty, chronic HF, stroke, trauma, tobacco use

CVD, surgery, cancer, pregnancy, postpartum, estrogen based BC

203
Q

What is the pathophysiology of VTE?

A

platelets aggregate, stimulating clotting factors (traps RBC, WBC, and platelets), fibrin production, fibrin entraps blood cells, thrombus formation

204
Q

What causes the symptoms of VTE? What are the symptoms of VTE?

A

pressure build up from reflux of blood flow and veins cannot expand in response to activity

pain, edema, tenderness with palpation, sense of fullness in thigh or calf, warm skin, fever, paresthesia, poor wound healing to area

205
Q

What are complications of VTE?

A

PE

post-thrombotic syndrome: chronic inflammation, venous HTN, happens to 20-50% of people (even with adequate anticoagulant therapy)

redness, swelling ,ulcers, and leg pain

phlegmasia cerulea dolens: rare, near total occlusion of venous blood flow, can lead quickly to amputation, swollen, blue, painful leg

206
Q

How could VTE be diagnosed?

A

health and physical exam: risk factors, subjective and objective symptoms

diagnostic studies: labs (CBC, clotting studies, D-dimer), tests (ultrasound of extremity)

207
Q

What are some nursing interventions for VTE?

A

early and aggressive mobilization

compression stockings

sequential compression devices

administer anti-coagulant drugs and monitor for effectiveness

208
Q

What is a vitamin K antagonist used for? Nursing considerations for the drug it’s an antagonist for? Education?

A

warfarin, anti-coagulant

PO, should be given at the same time every day, monitor INR for therapeutic range (2-3), takes a few days to weeks for therapeutic levels to be reached therefore bridging with LMWH or UH is necessary

risk of bleeding, do not increase vitamin K intake (green leafy veggie), interactions with herbals, NSAIDs, grapefruit juice, antidte is vitamin K (if given, need to bridge with heparin for a couple of days to return warfarin levels to therapeutic)

209
Q

What is heparin sodium? Nursing considerations?

A

unfractionated heparin, indirect thrombin inhibitors

administered via IV infusion for VTE: has short half-life, if stop infusion it will stop working within about a half an hour, APTT is calculated to find therapeutic levels
administered SQ for prophylaxis or bridging (due to risk of HIT, not usually given SQ)
monitor for HIT

210
Q

What is enoxaparin? Nursing considerations?

A

low-molecular-weight heparin, indirect thrombin inhibitor

most commonly given for bridge therapy, longer half-lfie than heparin, fewer complications (no HIT, no need for ongoing lab monitoring)

211
Q

What is bilvalirudin?

A

direct thrombin inhibitors for cardiac patients during percutaneous coronary intervention (PCI) with a hx of HIT

212
Q

What is fondaparinux? Nursing considerations?

A

factor Xa inhibitor given SQ

works quickly for VTE treatment and prophylaxis, do labs for CBC (threat of thrombocytopenia) and creatinine (kidney damage), monitor anti-Xa

213
Q

What is rivaroxaban? Nursing considerations?

A

actor Xa inhibitor given PO

works quickly for VTE treatment and prophylaxis, monitor anti-Xa

214
Q

What is apixaban? Nursing considerations?

A

actor Xa inhibitor given PO

works quickly for VTE treatment and prophylaxis, monitor anti-Xa

215
Q

What are medical interventions for VTE?

A

thrombolytic infusion with a tissue plasminogen activator (alteplase) given at the site of the clot

thrombectomy: surgical removal of clot

inferior vena cava filter placement to prevent embolism

216
Q

What are the types of infection?

A

acute: resolves in a few days or a week

chronic: lasts longer than 12 weeks, may or may not be curable

localized: limited to a specific body area

disseminated: infection will spread from initial site to other areas of the body

sepsis: systemic infection where the pathogens are in teh blood or other tissues

217
Q

What are the types of defenses?

A

nonspecific: anatomical physiological barrier and inflammatory response

specific: involve immune system, when an antigen induces a state of sensitivity and antibodies respond to contain or destroy antigen

218
Q

How does the body defend from infection?

A

intact skin and mucous membranes are the first line of defense

nasal passages: cilia and moist mucous membranes to trap

oral cavity: frequently sheds mucosal epithelium and the flow of saliva

eyes: constant producing tears

GI: high acidity, resident flora in large intestines, peristalsis to move microbes out of the body

vagina: normal pH will inhibit growth

urine flow: flushing and bacteriostatic

219
Q

What increases someone’s susceptibility to infection?

A

age (very young/old) and heredity, having: IVs, indwelling catheters, surgical wounds

220
Q

What are some lifespan considerations for infants and infections?

A

infections are the major cause of death

protected by immunoglobulins from mother for first 2 to 3 months and begin to synthesize their own between 1 and 3 months of age

due to being nose breathers for first few months of life they have a tough time fighting off respiratory infections

221
Q

What are some lifespan considerations for older adults and infection?

A

immune responses become weak and have reduced defenses and physiological changes

222
Q

What are the types of microorganisms that can cause infection?

A

bacteria: most commonly cause of infections, can cause disease by growing inside cells (TB) or secreting toxins (Staph)

viruses: consist primarily of nucleic acid and must enter living cells in order to multiply

fungi: yeasts and molds

parasites

223
Q

What is the process of infection?

A

pathogen, susceptible host, reservoir (anywhere the pathogen can live and multiply), portal of exit (from reservoir), mode of transmission, portal of entry (to susceptible host)

224
Q

What are the types of mode of transmission?

A

direct: immediate in direct transfer of the microorganism from one individual to another

droplet: within 3 feet sneezing, spitting, singing, or talking

indirect: vesicle (substances serve as an intermediate means to transport (fomites (inanimate objects that aren’t clean or sterile)) or vector borne (transmission through injection of salivary fluid during biting, depositing feces, or other material on skin through the bite wound or an area of the skin that’s traumatized)

airborne: droplets or dust residual or evaporated droplets are emitted by infected host and that can last in the air for long periods of time

225
Q

What diagnostic tests can be done for those with possible infections? What would their results indicate?

A

CBC with WBC differential count: elevated B and T lymphocytes, neutrophils, and monocytes indicative of infection (bacterial or viral), elevated neutrophils for bacterial infections, elevated basophils and eosinophils for parasitic infections

culture and sensitivity

serological testing for presence of virus or if the body has antibodies against the pathogen

Xray of chest, abdomen, or urinary systems to assess for organ abnormalities that indicates inflammatory response or tissue damage

ultrasound: echo or renal US to evaluate organ function

226
Q

What is the difference between inflammation and infection?

A

infection causes inflammatory response but an inflammatory response can occur from various stimulants

227
Q

What is the mechanism of inflammation?

A

vascular and cellular response (happen simultaneously), formation of exudate, and healing

228
Q

What is the vascular response to inflammation?

A

cellular injury/death causes brief vasoconstriction and the release of chemical mediators (histamine, bradykinin, and prostaglandins)

this causes increased capillary permeability causing edema

the edema will isolate the foreign substance from any further contact with body tissues

fibrinogen will strengthen a clot that will trap bacteria if present and begin wound healing

229
Q

What is the cellular response to inflammation?

A

movement of leukocytes towards the site of tissue damage or infection (chemotaxis) and the outward passage of blood cells through intact vessel walls (diapedesis) stimulated by chemical mediators released

neutrophils will arrive in 6 to 12 hours and turn into phagocytes, their lifespan is 24 to 48 hours and when they die they will form with a collection of dead tissue, dead bacteria, and live phagocytes to form pus

monocytes will arrive in 3 to 7 days and turn into macrophages along with the tissue macrophages and assist with phagocytosis which is important to clean up the are before healing process can take effect

lymphocyte is a much later immune response and has a primary role in humoral and cellular immunity

230
Q

What is inflammatory exudate? Types?

A

result from vascular and cellular response

serous: outpouring of fluid seen in early stages of inflammation with mild injuries (skin blisters, pleural fluid, pleural effusion)

serosanguinous: RBC and serous fluid, the typical look of surgical wound fluid

fibrinous: caused by increased vascular permeability which causes fibrinogen leakage into interstitial spaces, commonly seen with surgical drains

hemorrhagic: bright red blood from a fresh injury or hematoma caused by rupture or necrosis of blood vessel walls

purulent: consists of WBC, dead and alive microorganisms, and other debris, typically seen in cellulitis or in vascular wounds

catarrhal: greek for flow down, mucus whose production is accelerated by the inflammatory process

231
Q

What are the components of the healing process?

A

regeneration (replacement of lost cells and tissues of the same type) and repair (lost cells are replaced with connective tissue, this is how most injuries heal)

232
Q

What are the cell types of regeneration? Examples?

A

labile cells rapidly regenerate (skin, lymph organs, bone marrow, mucous membranes)

stable cells slowly regenerate (liver, pancreas, kidney, bone cells)

permanent cells cannot regenerate and will be replaced with scar tissue (neurons, skeletal, and cardiac muscle cells)

233
Q

What are the types of repair intentions?

A

primary: healing of well-approximated wound margins (surgical incisions or paper cuts), there are three phases (initial, granulation, maturation and scar contraction)

secondary: healing of traumatic wounds, ulcers, or infected wounds that has a significant amount of exudate and tissue loss, debridement may need to occur before healing can begin, the healing process is similar to primary but the wound is bigger with gaping edges, healing will occur from edges inward and then bottom up, it will take longer to heal and there’s a scar

tertiary: delayed primary intention due to wound infection that will occur when you have to re-open a wound due to infection or there’s a delay in suturing of a wound due to contamination, more likely to have a larger and deeper scar than a wound healed with primary or secondary

234
Q

What is initial, granulation, and maturation?

A

the three phases of primary intention

initial: occurs 3 to 5 days, edges align and close (via sutures or staples), an acute inflammatory response occurs (clotting process and platelets release chemotaxis chemicals, the debris and fibrin clot serves as the area of growth

granulation: 5 days to 4 weeks, proliferative, migration of fibroblasts which secrete collagen to form scar tissue, abundance of capillary buds, wound is fragile and vulnerable to dehiscence (wound reopening)

maturation and scar contraction: 7 days to several months, collagen is remodeled and scar is strengthened, overlaps with granulation phase

235
Q

What are the lifespan considerations for infants and inflammation?

A

delayed response of WBC, low levels of neutrophils, limited functions of chemotaxis and phagocytosis

236
Q

What are the lifespan considerations for older adults and inflammation?

A

decline in inflammatory defenses and will present atypically

increase in pro-inflammatory cytokines causing an increase in prevalence of pro-inflammatory diseases (atherosclerosis, diabetes, and osteoporosis)

237
Q

What are some risk factors for altered inflammation?

A

autoimmune disease

compromised immune system

238
Q

What are some systemic assessment pieces found with inflammation?

A

left shift (increase WBC count with elevated band neutrophils)

leukocytosis (with a suspected bacterial infection): malaise, nausea, anorexia

fever, increased pulse, and respiratory rate (due to prostaglandins)

239
Q

What are some diagnostic tests for inflammation? What do they determine?

A

WBC with differential to see the cellular response and determine if bacterial or viral and if acute or chronic

blood test for generalized inflammatory response: CPR, ESR (measures how quickly RBC settle at teh bo

240
Q

What are some diagnostic tests for inflammation? What do they determine?

A

WBC with differential to see the cellular response and determine if bacterial or viral and if acute or chronic

blood test for generalized inflammatory response: CPR, ESR (measures how quickly RBC settle at the bottom of the test tube, if it is quick it could indicate inflammation)

241
Q

What is an acute inflammation?

A

caused by an injury or trauma to the body and will heal in 2 to 3 weeks leaving no residual damage

the predominant cell present: neutrophils

242
Q

What are some nursing managements for acute inflammation?

A

promote adequate nutrition and fluid intake to promote healing

RICE: rest (repair), ice (vasoconstriction to reduce swelling and pain), compression (to stop bleeding and support but check for color, movement, sensation, and temperature (CMST)), elevation (above heart to reduce edema

243
Q

What types of pharmaceuticals can be used for acute inflammation? MOA?

A

saliclates (aspirin)

corticosteroids (prednisode)

NSAIDs (ibuprofen)

inhibits synthesis of prostaglandins

244
Q

What are the predominant cells seen in chronic inflammation?

A

lymphocytes and macrophages

245
Q

When does inflammatory bowel disease peak?

A

15 to 30 of age

246
Q

What is the etiology of inflammatory bowel disease?

A

idiopathic

autoimmunity of GI

genetic (strongest predictor)

environmental: chronic stress, air pollutants, some medications (NSAIDs, antibiotics)

lifestyle factors: smoking, diets high in fat, refined sugar, and beef

equal in sex

247
Q

What is the prevalence of inflammatory bowel disease?

A

1.3 million americans, UC is more common than Chron’s

248
Q

Where does Chron’s disease effect?

A

anywhere in the GI from mouth to anus, typically seen in descending colon and terminating ilieus

249
Q

Where does ulcerative colitis disease effect?

A

mucosa and submucosa of rectum and colon, seen more in superficial mucosa, a crypt abscess can form and penetrate superficial mucosa

250
Q

How does the inflammation progress in Chron’s?

A

begin as shallow lesions

they develop into skip lesions: areas of normal healthy bowel followed by areas of inflammed bowel, cobble stone appearance

some skip lesions can become deeper and become fissures

small leaks can develop and bowel contents will leak into peritoneum and cause peritonitis

251
Q

What is the inflammation process of ulcerative colitis?

A

over time the colon begins to narrow and shorten

252
Q

What are the clinical manifestations of Chron’s?

A

GI symptoms: persistent diarrhea (cramping, ab pain and tenderness), pain in RLQ that can be relieved with defecation, palpable mass in RLQ

systemic symptoms: fever, fatigue, weight loss

253
Q

What are the clinical manifestations of ulcerative colitis?

A

GI symptoms: diarrhea (predominant symptom, that contains blood and mucus), urgency, frequency, tenesmus (feeling of haven’t completly defecated even after just going), LLQ cramping relieved by defecation

Systemic symptoms: fatigue, rapid weight loss, dehydration, tachycardia, anemia

254
Q

What is the stool frequency for the degrees of ulcerative colitis?

A

mild: up to 4x/day
moderate: up to 10x/day
severe: greater than 10-20x/day

255
Q

What are complications of Chron’s?

A

intestinal obstruction
abscess and fistula
hemorrhage leading to anemia
perforation of bowel
malnutrition and nutritional deficiencies
increase risk of small intestinal cancer

256
Q

What are complications of ulcerative colitis?

A

hemorrhage
colon perforation
toxic megacolon: dilated and inflamed colon leading to paralysis or perforation which could lead to sepsis or hemorrhage (treated with decompression or colectomy)
after 10 years of disease there’s an increase in colon cancer

257
Q

Which diagnostic tests can be done for inflammatory bowel diseases?

A

imaging: sigmoidoscopy, colonoscopy, barium upper/lower XR

biopsy for definitive diagnosiss

laboratory: CBC, ESR, CPR, serum levels of electrolytes

stool tests to rule out C.diff

258
Q

What is the focus of treatment for inflammatory bowel disorders?

A

relief of symptoms, correcting malnutrition, addressing stress and quality of life

259
Q

What is the goal of pharmacological treatments for inflammatory bowel disease?

A

terminate acute attacks quickly and reduce incidence of relapse

260
Q

What is the step up approach?

A

for mild to moderate inflammatory bowel disease, locally acting and systemic anti-inflammatory drugs

start with least powerful drugs: 5-ASA and corticosteroids

if it doesn’t work then use immunosuppressants

261
Q

What is mesalamine?

A

5-ASA that can prevent flareups of both inflammatory bowel diseases and treat mild symptoms

262
Q

What is the step-down approach

A

for severe cases of inflammatory bowel disease begin with immunosuppressants

263
Q

What is mercaptopurine?

A

immunosuppressant used for inflammatory bowel disease

264
Q

What is azathioprine?

A

immunosuppressant used for inflammatory bowel disease

265
Q

What is infiximab?

A

immune response modifier/biologic that will reduce inflammation by blocking proteins that cause inflammation, used in inflammatory bowel disease

266
Q

What are some nonpharmacological therapies for inflammatory bowel disease?

A

replacing fluids and electrolytes
trying to reduce weight loss
increased dietary fiber to reduce diarrhea but could cause blockages if colon is narrowed

267
Q

When is surgery used for inflammatory bowel disease?

A

complications occur: bowel obstruction, perforation, internal or external fistula, abscess, perineal complications, cancer

268
Q

Which assessments will nurses do for inflammatory bowel disease?

A

stool frequency, amount, and characteristics
fluid and electrolytes
skin

269
Q

What are the layers of the skin?

A

epidermis: outer most, contains 5 interrelated layers, major cells: keratinocytes and melanocytes (gives pigmentation and protects from UV)

dermis: three layers of connective tissue (collagen, elastic fibers, and reticular fibers), contains blood vessels, nerves, lymphatics, hair follicles, and sabaceous glands, major cell: fibroblast (produces collagen and elastin)

subcutaneous tissue: loose connective tissue and fat cells, helps with insulation, attaches skin to muscles and bones

270
Q

What are the types of glands found in the skin?

A

apocrine: secretes odorless substances (produce odor when mixes with bacteria), enlarges during puberty

eccrine: cools the body via evaporation, excretes waste products

271
Q

What are lifespan considerations for infants and integumentary system?

A

skin: 40-50% thinner than adults, erythematous at birth that will fade, acrocyanosis

glands: sabacceous glands on face, no sweating for the first 24 hours

272
Q

What are normal common alterations to infants’ integumentary system?

A

mongolian spots: birthmark, bruise spot on coccyx and back

nevi: birthmark, salmon patches found at the base of the neck, face, and lower back, easily blanchable, the skin will thicken over them but they will always be present

erythema toxicum: rash due to inflammatory response that can happen 1 to 3 days and up to 3 weeks after birth

acrocyanosis: bluish tone to extremities

milia: bumps on face and chin from when the skin flakes and gets trapped

273
Q

What are lifespan considerations for pregnant people’s integumentary?

A

increase in melanotropin hormone causes hyperpigmentation which can be seen as: melasma (blotchy appearance that shows more in the sun) and linea nigra (dark midline that runs from the naval area and down

increase in estrogen hormone causes an increase in blood flow to the skin which can be seen as: angiomatas (lines on the face, arms, thorax, and neck seen around late 1st trimester and post-partum) and palmar erythema (blotchy appearance to palms)

mechanical stretching of skin can lead to striae gravidarum (stretch marks)

there is accelerated growth of hair and nails (hirsutism)

274
Q

What are lifespan considerations of older adults’ integumentary?

A

dermis thins
decrease in elasticity
loss of SQ causing wrinkles, lines, and sagging
At age 30 and every decade after: melanocytes decrease by 10 to 20%

by age 50 the hair will thin and lose pigment, thickening of hair in the nose and ears

nails become brittle and grow slowly

there’re fewer sweat glands and lowered function

275
Q

What diagnostic tests can be done for tissue integrity?

A

biopsy
culture
patch test
woods lamp (UV light to see fluorescent substances)

276
Q

What defines a chronic alteration of tissue?

A

not healed within 3 months

277
Q

How do you classify wounds?

A

etiology, actue/chronic, depth of tissue involvement

278
Q

What can the wound base be made of?

A

eschar: dry, leathery, thick tissue that is a bit dark (brown, black); seen in late stage pressure injuries

slough: yellow, tan, green, moist, stringy

279
Q

What are the goals of wound management?

A

promote healing, protect from further trauma, prevent/treat infection

280
Q

What is the process of wound management for clean wounds?

A

cleaning
dressing change (leave superficial wound closures in place (steri-strips, sutures, dermabond), schedule varies on wound and dressing type)
maintain moist environment for healing
topical antimicrobials/bacterials
drains

281
Q

What is the process of wound management for contaminated wounds?

A

debridement needs to occur before healing can begin

282
Q

How can debridement occur?

A

surgical
mechanical (wet to dry dressing, wound irrigation)
autolytic (dressings soften dry eschar)
enzymatic (drugs dissolve necrotic tissue)
absorption dressing

283
Q

What type of patient education is needed with wound management and drain care?

A

wound management: promote wound healing with adequate nutrition and rest, monitor for symptoms of infection

drain: how to empty, what to record (color, clarity, output), cleaning

284
Q

What is negative-pressure wound therapy?

A

for acute and chronic wounds, continuous or intermittent negative pressure in wound bed to: remove excess fluid and exudate, reduce bacterial load, encourage blood flow

285
Q

What is monitored when using negative-pressure wound therapy?

A

drainage, healing process, serum protein and electrolyte levels, coagulation studies

286
Q

What is hyperbaric oxygen therapy? What is the physiology?

A

topical or systemic delivery of 100% oxygen at 1.5 to 3x the normal atmospheric pressure

oxygen diffuses into serum and tissues, moving through areas that RBC cannot go, stimulates angiogenesis, kills anerobic bacteria, accelerates granulation of tissue and wound healing

287
Q

What is becaplermin?

A

platelet-derived growth factor gel that will stimulate cell proliferation and migration, can only be used for clean wounds ex/ diabetic foot ulcer

288
Q

What are pressure injuries? Where are they commonly found?

A

localized injury to skin and/or underlying tissue over bony prominence

sacrum and heels

289
Q

What is the etiology of pressure injuries?

A

intensity and duration of pressure
tissue tolerance
sheering forces
excessive moisture

290
Q

What are risk factors for pressure injuries?

A

immobility, inadequate nutrition, fecal and urinary incontinence, decreased mental status, diminished sensation, excessive body heat, advanced age, chronic medical conditions, poor lifting and transferring techniques, incorrect application of pressure-relieving devices

291
Q

What is the pathophysiology of pressure injuries?

A

various risk factors act on areas of soft tissue overlaying bony prominence
pressure exceeds normal capillary pressure
occlusion and tearing of capillaries
reduced tissue perfusion
ischemic necrosis
pressure injury

292
Q

What are the stages of pressure injuries?

A

1: nonblanchable erythema of intact skin
2: partial-thickness skin loss involving dermis
3: full-thickness skin loss involving damage or necrosis of SQ tissue. bone, tendon, and muscle are not exposed
4: full thickness skin loss with extensive tissue damage and necrosis. muscle, tendon, and bone exposed and directly palpable (slough or eschar may be present)
unstageable: eschar or slough present, unable to assess depth, undermining
suspected deep tissue injury: skin with purple discoloration or blood filled blister

293
Q

What are the top 10 tips for assessing darkly pigmented skin pressure ulcers?

A

1: early signs of skin color change are blunted therefore a thorough risk assessment should be done
2: good lighting
3: compare color of skin subjected to pressure to skin around area
4: describe variations in skin color using objective system such as a skin tone chart
5: moisten skin
6: palpate skin in areas that may have been exposed to pressure or shear
7: anticipate variation in presentation of deep tissue pressure injury
8: use technology designed to assess perfusion or subepidermal moisture changes (ex/ infrared thermography)
9: superficial wounds are more easily identified and open blisters often retain the epidermis
10: healing wounds can lead to changes in pigmentation

294
Q

What are complications of pressure injuries?

A

recurrence (most common)

infection: cellulitis, osteomyelitis, sepsis

loss of function and death

295
Q

What does the braden scale assess? What are the categories of the scale?

A

pressure injury risk

sensory perception, moisture, activity, mobility, nutrition, friction and sheer

296
Q

What braden scale score would indicate at risk?

A

18 or less

297
Q

What medical treatments can be done for pressure injuries?

A

debridement

skin grafts (section of skin is transplanted that does not include muscle or vessels)

skin flaps (sections of skin and vessels transplanted)

musculocutaneous flap (section of skin, muscle, and vessels transplanted)

298
Q

What are physiologic mechanisms to prevent UTIs?

A

uretrovesical junction competence: ureter connects to bladder and the junction should act as a one-way valve to only allow urine to go down

minor amount of peristaltic activity

urine is acidic

299
Q

What is the most common bacterial infection in women? What is the most common bacteria that causes it?

A

UTIs, E. coli

300
Q

What is pyelonephritis?

A

upper urinary tract infection of renal parenchyma, pelvis, and/or ureters

301
Q

What is cystitis or urethritis?

A

lower urinary tract infection of bladder or urethra

302
Q

What is urosepsis?

A

sepsis caused by UTI

303
Q

What is an uncomplicated UTI?

A

typically just involves bladder

304
Q

What is a complicated UTI?

A

coexisting obstruction, stones, or catheters, abnormal GU tract, antibiotic resistance, recurrent infections, those susceptible to UTIs

305
Q

What are risk factors for UTIs?

A

foreign bodies: catheters or cytoscopy

anatomic: fistula or congenital defect

frequent delaying of urination causing backflow

poor hygiene

diabetics, sugar is a good food for bacteria

person on multiple antibiotics (esp fungal UTIs)

306
Q

What are the signs and symptoms of lower UTIs?

A

emptying: hesitancy, incomplete emptying, retention, dysuria, hematuria/cloudy urine

storage: urinary frequency, urgency, incontinence, nocturia

307
Q

What are signs and symptoms of upper UTIs?

A

flank pain, fever, chills

308
Q

What are signs and symptoms of a UTI in older adults?

A

non-localized abdominal discomfort
cognitive impairment
unlikely to have a fever until septic

309
Q

What diagnostic studies can be done for UTIs?

A

dipstick urinalysis to identify presence of nitrites and WBCs

UA for culture and sensitivity: clean-catchy sample perferred, specimen by cathertization or suptrapubic needle aspiration more accurate

310
Q

What is the treatment for uncomplicated UTIs?

A

3 day treatment of: TMP/sulfa (empiric treatment), nitrofurantonin, ampicillin, amoxicillin

311
Q

What is the treatment for complicated UTIs? Nursing considerations?

A

7 to 14 day treatment of: ciprofloxacin, levofloxacin

antacids will reduce oral absorption, at increased risk for tendon rupture in older adults, black box warning

312
Q

What are the phenazopyridine? Side effects?

A

localized analgesic effect to relieve dysuria and urgency

orange urine

313
Q

Why can cranberry juice help with UTIs?

A

there’re enzymes to inhibit bacteria from attaching to epithelium of bladder

314
Q

What is acute pyelonephritis?

A

inflammation of renal parenchyma and collecting system (including the renal pelvis), chronic can lead to kidney disease

315
Q

How does the pathophysiology of acute pyelonephritis begin? What are the most common cause?

A

coloniation and infection of lower tract via ascending urethral route

E.coli, klebsiella, enterobacter

316
Q

What are the clinical manifestations of acute pyelonephritis?

A

mild fatigue
chills
fever
vomiting
malaise
flank pain
characteristics of cystits
costoveterbral (CVA) tenderness to percussion present on affected side

317
Q

What diagnostic studies can be done for acute pyelonephritis?

A

UA, culture and sensitivity, blood culture (if suspected bactermia), ultrasound for anatomic abnormalities

318
Q

Who is typically hospitalized for acute pyelonephritis?

A

those with severe infections and complications such as nausea and vomiting with dehydration

319
Q

What is the treatment for acute pyelonephritis? How quickly will symptoms improve after the start of treatment?

A

antibiotics: ciprofloxacin, levofloxacin (parenteral administration in hospital to rapidly establish high drug levels), NSAIDs, antipyretic drugs, urinary analgesics

48 to 72 hours

320
Q

What is respiratory syncytial virus? Who typically gets it? When do they typically get it?

A

very common respiratory infection that is the major cause of bronchiolitis

peaks at 6 months, most have been infected by age 3 at least once

winter and spring

321
Q

What are the clinical manifestations for RSV initially and later stages?

A

initial: rhinorrhea, cough, low grade fever, otitis, conjunctivitis, pharyngitis, wheezing

later: increase wheeze and cough, air hunger, tachypnea, retractions, cyanosis, crackles, decreased breath sounds

322
Q

What diagnostic test is done for RSV?

A

nose swab, chest XR

323
Q

What is the treatment for RSV? How long does it take for RSV to resolve?

A

symptomatic and supportive care: hydration (IV fluids if unable to take PO), nutritional support, oxygen, frequent respiratory assessment

ribavarin (RBV): antiviral, only for severe RSV (those at high risk of death), given PO or inhaled

resolve within 1 to 2 weeks

324
Q

What is palivizumab? What are the nursing considerations?

A

very expensive monthly IM monoclonal antibody to boost the immune system to avoid RSV complications (NOT A VACCINE)

need to meet at least one criteria for receiving in first year of life: born before 29 weeks, chronic lung disease of prematurity (born<32 weeks) and needed oxygen for at least 28 days after birth, certain heart defects

Health and Illness (4 decks)

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