Exam 2 Flashcards
(324 cards)
1
Q
What is hyperthermia?
A
an elevated body temperature greater than 38 degrees celsius with an unchanged hypothalamic set point
2
Q
What causes hyperthermia?
A
excessive heat production, inadequate ability to cool, hypothalamic regulator dysfunction
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)
4
Q
What are heat cramps?
A
usually brief but severe cramps in large muscle groups that are tired from heavy work
5
Q
Who typically gets heat cramps?
A
athletes with inadequate fluid intake
6
Q
What are symptoms of heat cramps?
A
pain, thirst, nausea, tachycardia, pale/pallor, weakness, profuse diaphoresis
7
Q
What are some nursing interventions for heat cramps?
A
rest, elevate, and massage, fluids, education on prevention
8
Q
What is heat exhaustion?
A
prolonged exposure to heat which causes profuse diaphoresis resulting in excess water and electrolyte loss
9
Q
Who typically gets heat exhaustion?
A
people engaged in strenuous activity in hot or humid weather
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
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
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
13
Q
What is heat stroke?
A
failure of hypothalamic thermoregulatory process resulting in a core temperature that is greater than 41C
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
15
Q
What are symptoms of heat stroke?
A
hot, dry skin, altered mental status (hallucinations, loss of muscle coordination, combativeness), hypotension, tachycardia, weakness
16
Q
Can antipyretics be used to treat heat stroke?
A
no, because the increase in temperature is not caused by infection
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
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
19
Q
What are the types of hypothermia?
A
mild: 35 to 33.9C
moderate: 33.9C to 30C
severe <30C
20
Q
What causes hypothermia?
A
accidental: environmental exposure
therapeutic: intentionally induced to reduce metabolism and prevent tissue ischemia
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
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)
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
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
25
What are some nursing interventions for hypothermia?
remove pt from cold environment, rewarm pt, monitor VS, heart rhythm, LOC, electorlytes
26
What are the ways to rewarm someone?
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
27
Why do you need to rewarm the core before extremities?
if rewarm extremities first the cold peripheral blood will return to the central circulation leading to hypotension, dysrhythmias, rewarming shock
28
What is thermoregulation?
process of maintaining core body temperature at a near constant value, balance of heat production and heat loss to maintain body temperature
29
What is the difference between core temperature and surface temperature?
core: more reliable, relatively constant
surface: fluctuates in response to environmental factors
30
What is normothermia?
body temperature is in normal range
31
What does the basal metabolic rate for heat production depend on?
surface area, thyroid hormones, testosterone
32
What controls heat production? How?
posterior hypothalamus; shivering and vasoconstriction
33
What controls heat loss? How?
anterior hypothalamus; sweating, vasodilation, blood redistribution to body surface vessels, inhibition of heat production
34
What are the ways heat is transferred? Example?
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)
35
What factors affect body temperature?
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
36
What is the normal body temperature for infants?
36.5 to 37.5C
37
Why is there an increase risk of heat loss for infants?
thin SQ fat, blood vessels closer to skin, larger body surface area to body weight ratio
38
Given the way heat is transferred how should that be taken into consideration for infants?
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
39
How do infant produce heat?
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
40
Why can acrocyanosis occur in infants?
vasoconstriction to increase body temperature causing low perfusion to extremities and blue discoloration
41
What is the typical range of rectal temperature for children?
37 to 37.5C
42
How does temperature in children differ from temperature in adults?
until puberty, temperature is more variable, some healthy children can have temperatures as high as 41C without difficulty
43
What is the normal temperature range for older adults?
36 to 36.8C
44
Why is there a reduction in ability for older adults to respond to temperature changes?
cannot vasoconstrict easily, decrease in peripheral circulation, decrease in CO, ability to shiver is diminished, reduced muscle mass, reduced SQ tissue, impaired sweating mechanisms
45
At what age do thermoregulation deaths drastically increase?
those older than 70/75
46
What is focused on for health history for thermoregulation?
past medical history related to thermoregulation (thyroid disease, hypothalamic injury, autoimmune disease, traumatic injury), recent injury or illness, environmental exposure, subjective symptoms
47
What are the lifespan considerations for temperature taking?
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
48
What is pyrexia?
temporary elevation in body temperature triggered by an immune response
49
At what temperatures will pyrexia be dangerous for adults and children?
greater than 39C for adults
greater than 40C for children
50
What are the patterns of pyrexia?
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
51
What is the pathophysiology of pyrexia?
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
52
Who are complications of pyrexia typically seen in?
children, older adults, those with multiple co-morbidities
53
What are some complications of pyrexia? Why do they occur?
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
54
What is some education about febrile seizures?
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
55
What is clotting?
physiological process in which blood is converted from a liquid to a semisolid gel
56
How much of blood does RBC, WBC, and platelets consists of?
around 45%
57
What are the types of bone marrow? And their functions?
red: actively produces stem cells that will differentiate to RBC, WBC, or platelets
yellow: stores fat
58
What does the spleen do?
produces RBC during fetal development, filters old RBC and bacteria from blood, stores more than 300mL of RBC and 1/3 volume of platelets
59
What does the lymphatic system do?
carries fluid from interstitial spaces to blood while filtering out pathogens and foreign particles
60
How does the liver work in the hematologic system?
filters and produces pro-coagulants which is essential for hemostasis and coagulation
61
What is hematopoiesis?
blood cell production that occurs in the red bone marrow
62
What is the primary function of RBC? What is it composed of? How much is there in the body? How long do they survive?
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
63
What is a reticulocyte?
immature RBC that will mature within 48 hours
64
How is erythropoiesis controlled?
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
65
What is hematocrit versus hemoglobin?
hematocrit is the percentage of blood that is composed of RBCs
hemoglobin is the capacity of carrying gas
66
What is the normal lab value of hemoglobin for adult males, females, and pregnant people?
females: 12-16 g/dL
males: 14-18 g/dL
pregnant: less than 10 g/dL
67
What is the normal value of hematocrit for adult males, females, and pregnant people?
females: 37-47%
males: 42 to 52%
pregnant: less than 33%
68
What is the primary function of leukocytes? What are the cell types?
phagocytosis, inflammatory, and immune response; granulocytes: neutrophils, acinophils, and basophils
lymphocytes: B and T cells
monocytes
69
What is the normal WBC count?
5,000 to 10,000
70
What is the primary function of thrombocytes? How long do they live?What are they inhibited by?
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
71
What is the normal thrombocyte count?
150,000 to 400,000
72
What are the components of a CBC?
total RBC count, WBC count, hemoglobin, hematocrit, platelet
73
What are the lifespan considerations for infants and the components of a CBC?
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
74
What are the lifespan considerations for pregnant people and their total blood volume? Why does this occur?
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
75
What are the lifespan considerations for pregnant people and their WBC count?
increase in WBC count, increase in granulocytes
76
What are the lifespan considerations for pregnant people and coagulation? Why does this occur?
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
77
What are the lifespan considerations for older adults and their hemoglobin?
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)
78
What are the lifespan considerations for older adults and their WBC?
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
79
What are the lifespan considerations for older adults and their platelets?
the amount is unaffected by aging but there is an increase in platelet adhesion
80
What is focused on for health history and clotting?
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)
81
What are some symptoms of altered clotting?
petechiae, purpura, jaundice
82
What is activated partial thromboplastin time (aPTT)?
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
83
What is prothrombin time (PT)?
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)
84
What is the therapeutic range of INR for those on warfarin?
2 to 3
85
What is d-dimer? What does an increase indicate?
a clotting study that measures fibrin fragments from clot lysis; hypercoagulable state and/or presence of blood clot
86
What is clotting factor 1? What does a decrease/increase indicate?
fibrinogen; increase: hypercoagulable, decrease: increase risk for bleeding
87
What are the two categories of perfusion?
central: blood flow through the heart and inter peripheral vascular vessels
tissue: volume of blood that flows from arteries and capillaries to target tissues
88
What generates central perfusion?
cardiac output
89
What is the cardiac cycle?
how electrical activity in the heart makes the heart fill composed of diastole: filling, rest and systole: pumping, action
90
What is cardiac output? What is the normal amount?
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
91
What is the normal HR?
50 to 180bpm
92
What factors affect SV? How do they affect SV?
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
93
What is the Frank-Starling law?
the more myocardial fibers are stretched (preload) the greater the force of contraction
94
Which disorder can increase preload and afterload?
HTN
95
How does the sympathetic nervous system impact central perfusion?
stimulating beta 1 receptors in the heart which will then increase HR, contractility, and automaticity
96
What is automaticity?
ability of myocardial cells to depolarize spontaneously
97
How does the sympathetic nervous system impact tissue perfusion?
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
98
How does the parasympathetic nervous system impact central perfusion? What is the system called?
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
99
What is the normal HR for infants? What could alterations to HR indicate in infants?
120 to 160BPM; tachycardia could indicate anemia, hypovolemia, hyperthermia, or sepsis
bradycardia could indicate congenital issues or hypoxemia
100
What is the normal BP for infants? Why does this occur?
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
101
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?
heart defect; about 1 in 100; about 25% which will need surgery or procedure shortly after birth or in the first year of life
102
What is the normal HR for pregnant people?
HR: 150 to 200 BPM
103
What is the normal CO for pregnant people? Why does this occur?
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%
104
What are the types of hypertension in pregnant people?
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
105
What are lifespan considerations for older adults' CO, vasculature and HTN?
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
106
What are the types of hypotension seen in older adults?
postural: orthostatic
postprandial: hypotension after eating
107
What is one of the leading causes of hospitalization for older adults?
congestive heart failure as a complciation of HTN/CAD
108
What are some symptoms of poor perfuison?
pain or pressure, dyspnea, diaphoresis, anxiety, edema, dizziness/fainting, nausea, heartburn
109
What physical exam pieces look specifically at central perfusion? at tissue perfusion?
BP, HR, heart sounds, peripheral edema; skin color and temperature, peripheral pulses, cap refill
110
Which cardiac enzymes are used for diagnostic purposes?
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
111
Which cardiac markers are used for diagnostic purposes?
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
112
What is the serum level of triglycerides for females and males?
females: 35 to 135 mg/dL
males: 40 to 160 mg/dL
113
What is the serum level of LDLs?
less than 130 mg/dL
114
What is the serum level of HDLs for females and males?
females >55mg/dL
males >45mg/dL
115
What is the typical creatinine for females and males?
females: 0.5 to 1.1 mg/dL
males: 0.6 to 1.2 mg/dL
116
What is the normal total cholesterol levels?
less than 200 mg/dL
117
What is the fasting glucose range?
74 to 106 mg/dL
118
What tests can be performed for perfusion?
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
119
What is ejection fraction?
amount of blood pumped out of ventricles with every contraction
120
What are some non modifiable risk factors for impaired perfusion?
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
121
What are some modifiable risk factors for impaired perfusion?
medically treatable: HTN, elevated serum lipids, diabetes mellitus
lifestyle: smoking, obesity, diet and nutrition, physical inactivity, stress
122
What is the primary and secondary prevention for hypertension?
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
123
What is the primary and secondary prevention for hyperlipidemia?
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
124
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?
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
125
How does smoking negatively impact cardiovascular health?
damages coronary vessels, increases blood viscosity, increases risk for atherosclerosis and clots, decreases HDL, decreases activity tolerance
126
What are some AHA recommendations for diet and nutrition to maintain good cardiovascular health?
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
127
What are the positive effects of physical activity?
reduces risk for CVD by 30 to 40% and improves quality of life (improves mental health and immunity)
128
What are the aerobic activity recommendations for adults? for children and adolescents?
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
129
What are the muscle-strengthening recommendations?
moderate to vigorous level of activity twice per week
130
How can chronic stress impact perfusion?
damage arterial walls and weaken immune system
131
What are some stress busting activities?
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
What is systemic vascular resistance?
force opposing the movement of blood into the vessels, determined by radius of arteries and arterioles
133
What are the short term regulation of BP?
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
What are the long term regulation of BP?
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
What happens when BP decreases?
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
What are the AHA BP guidelines?
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
What is the etiology of primary and secondary hypertension?
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
What is the pathophysiology of hypertension? What is the hallmark of HTN?
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
What are non-modifiable risk factors for HTN?
age: male<65 and females>65
gender
ethnicity: BIPOC
family hx
socioeconomic status
140
What are modifiable risk factors for HTN?
diabetes mellitus
stress
sedentary lifestyle
elevated serum lipids
excess diatary sodium intake
alcohol
obesity
tobacco use
141
What are some signs and symptoms of HTN?
often will be secondary to target organ disease
fatigue
reduced activity
SOB
angina
changes in vision
headache
142
What are some complications of HTN?
heart: CAD, LVH, HF, heart attack
kidneys: renal disease
brain: stroke, cognition
eyes: retinopathy
PVD: atherosclerosis
143
What lifestyle modifications can be done for HTN?
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
What is the most important educational point for heart medications?
compliance, do not stop suddenly
145
What is hydrochlorothiazide? Class? MOA? Therapeutic/lab monitoring? Indications? Adverse effects? Nursing considerations?
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
What is furosemide? Class? MOA? Therapeutic/lab monitoring? Indications? Adverse effects?
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
What is spironoactone? Class? MOA? Therapeutic/lab monitoring? Indications? Adverse effects?
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
What is clonidine? Class? MOA? Therapeutic/lab monitoring? Indications? Adverse effects?
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
What is metoprolol? Class? MOA? Therapeutic/lab monitoring? Indications? Adverse effects?
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
What is propranolol? Class? MOA? Therapeutic/lab monitoring? Indications? Adverse effects?
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
What is doxazosin? Class? MOA? Therapeutic/lab monitoring? Indications? Adverse effects?
alpha1 adrenergic
blocks alpha1 causing vasodilation in peripheral vasculature
BP, pulse, fluid levels
HTN, symptomatic BPH
1st dose syncope, dizziness, headache, decrease libido
152
What is hydralazine? Class? MOA? Therapeutic/lab monitoring? Indications? Adverse effects?
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
What is nitroglycerin? Class? MOA? Therapeutic/lab monitoring? Indications? Adverse effects?
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
What is sodium nitroprusside? Class? MOA? Therapeutic/lab monitoring? Indications? Adverse effects?
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
What is captopril? Class? MOA? Therapeutic/lab monitoring? Indications? Adverse effects?
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
What is enalapril? Class? MOA? Therapeutic/lab monitoring? Indications? Adverse effects?
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
What is lisinopril? Class? MOA? Therapeutic/lab monitoring? Indications? Adverse effects?
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
What is losartan? Class? MOA? Therapeutic/lab monitoring? Indications? Adverse effects?
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
What is valsartan? Class? MOA? Therapeutic/lab monitoring? Indications? Adverse effects?
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
What is amlodipine? Class? MOA? Therapeutic/lab monitoring? Indications? Adverse effects?
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
What is diltiazem? Class? MOA? Therapeutic/lab monitoring? Indications? Adverse effects?
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
What is a hypertensive crisis?
a sever and abrupt increase in BP, >180/>120
163
What is the difference between the types of hypertensive crisis?
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
What are the causes of a hypertensive emergency?
head injury, preeclampsia, eclampsia, stimulant drugs, abruptly stopping taking a heart medication
165
What are symptoms of a hypertensive emergency?
seizures, encephalopathy, death, acute kidney failure, heart attack
166
What is the treatment plan for a hypertensive emergency?
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
What is the pathophysiology of coronary artery disease?
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
What are some non-modifiable risk factors for coronary artery disease?
age (increasing)
gender (men until 75, then equalize with women)
race (white males, AA, NA)
genetics
169
What are some major modifiable risk factors for coronary artery disease?
elevated serum lipids, HTN, tobacco use, physical inactivity, obesity
170
What could cause an increase in triglycerides?
reflection of how we eat, physical inactivity
171
What is the dangers with LDL?
contains more cholesterol, attracted to arterial walls and can deposit cholesterol onto them
172
What are the benefits of HDL?
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
What happens to the risk of coronary artery disease after smoking cessation?
damage is irreversible but chance of death will decrease to someone who hasn't smoked within a year of smoking cessation
174
What are some contributing modifiable risk factors for coronary artery disease?
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
How can CAD be diagnosed?
medical and family hx, risk factors, physical, EKG, stress test, echo, chest XR, blood tests, coronary angio and cardiac catheterization
176
What are some nursing and collaborative care for CAD?
identify and manage high risk individuals
promote physical activity
promote heart healthy diet
drug therapies
177
What are the guidelines for pharmaceutical treatment of elevated LDL?
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
What is atorvastatin? MOA?
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
What is gemfibrozil? MOA?
decreases synthesis and secretion of VLDL, most effective for lowering triglycerides and increasing HDL, NO EFFECT ON LDL
180
What is niacin? MOA?
vitamin B6, inhibits synthesis of LDL and triglycerides, needs to be used in high dosages which could increase side effects
181
What is colesevelam? MOA?
reduces LDL and cholesterol by converting them into bile acids, not as strong as statins, second line medication
182
What are PCSK9 inhibitors?
inactivates the PCSK9 protein and lowers LDL
183
What is ezetimibe?
inhibits intestinal absorption of cholesterol
184
What is aspirin used for with CVD?
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
Who should be taking low dose aspirin for CVD?
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
What is ischemia?
oxygen supply is inadequate to meet metabolic needs
187
What is chronic stable angina?
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
What is silent ischemia? Who is it commonly seen in? How is it diagnosed?
no subjective symptoms of ischemia
most common in diabetics due to diabetic neuropathy
seen in ECG changes
189
What is prinzmetal's angina? Risk factors? Cause?
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
What is microvascular angina? Who is it most prevalent in?
angina in the absence of significant CAD or coronary spasm rather it is caused by a distant less impactful coronary microvascular disease
women
191
What is the goal for nursing care in those with ischemia?
decrease oxygen demand and/or increase oxygen supply
192
What is the MOA for short-acting nitrates? What are nursing education points?
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
What is isosorbide? Side effects?
long-acting nitrate to reduce angina incidence
headache, orthostatic hypotension
194
What is nitroglycerin ointment? Side effects?
long-acting nitrate to reduce angina incidence
headache, orthostatic hypotension
195
What is transdermal controlled release NTG? Side effects?
long-acting nitrate to reduce angina incidence
headache, orthostatic hypotension
196
What types of drugs can be used for angina?
short-acting nitrates, long-acting nitrates, ACE, ARBs, beta blockers, calcium channel blockers; lipid lowering, sodium current inhibitor
197
What is ranolazine? Side effects?
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
What is a procedural treatment for CVD?
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
What is venous thrombosis? Types?
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
What are the symptoms of SVT? How is it diagnosed? What is the treatment?
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
What is Virchow's triad?
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
What are some major risk factors for VTE? Other precipitating factors?
Virchow's triad, age, prolonged immobilty, chronic HF, stroke, trauma, tobacco use
CVD, surgery, cancer, pregnancy, postpartum, estrogen based BC
203
What is the pathophysiology of VTE?
platelets aggregate, stimulating clotting factors (traps RBC, WBC, and platelets), fibrin production, fibrin entraps blood cells, thrombus formation
204
What causes the symptoms of VTE? What are the symptoms of VTE?
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
What are complications of VTE?
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
How could VTE be diagnosed?
health and physical exam: risk factors, subjective and objective symptoms
diagnostic studies: labs (CBC, clotting studies, D-dimer), tests (ultrasound of extremity)
207
What are some nursing interventions for VTE?
early and aggressive mobilization
compression stockings
sequential compression devices
administer anti-coagulant drugs and monitor for effectiveness
208
What is a vitamin K antagonist used for? Nursing considerations for the drug it's an antagonist for? Education?
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
What is heparin sodium? Nursing considerations?
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
What is enoxaparin? Nursing considerations?
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
What is bilvalirudin?
direct thrombin inhibitors for cardiac patients during percutaneous coronary intervention (PCI) with a hx of HIT
212
What is fondaparinux? Nursing considerations?
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
What is rivaroxaban? Nursing considerations?
actor Xa inhibitor given PO
works quickly for VTE treatment and prophylaxis, monitor anti-Xa
214
What is apixaban? Nursing considerations?
actor Xa inhibitor given PO
works quickly for VTE treatment and prophylaxis, monitor anti-Xa
215
What are medical interventions for VTE?
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
What are the types of infection?
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
What are the types of defenses?
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
How does the body defend from infection?
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
What increases someone's susceptibility to infection?
age (very young/old) and heredity, having: IVs, indwelling catheters, surgical wounds
220
What are some lifespan considerations for infants and infections?
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
What are some lifespan considerations for older adults and infection?
immune responses become weak and have reduced defenses and physiological changes
222
What are the types of microorganisms that can cause infection?
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
What is the process of infection?
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
What are the types of mode of transmission?
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
What diagnostic tests can be done for those with possible infections? What would their results indicate?
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
What is the difference between inflammation and infection?
infection causes inflammatory response but an inflammatory response can occur from various stimulants
227
What is the mechanism of inflammation?
vascular and cellular response (happen simultaneously), formation of exudate, and healing
228
What is the vascular response to inflammation?
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
What is the cellular response to inflammation?
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
What is inflammatory exudate? Types?
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
What are the components of the healing process?
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
What are the cell types of regeneration? Examples?
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
What are the types of repair intentions?
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
What is initial, granulation, and maturation?
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
What are the lifespan considerations for infants and inflammation?
delayed response of WBC, low levels of neutrophils, limited functions of chemotaxis and phagocytosis
236
What are the lifespan considerations for older adults and inflammation?
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
What are some risk factors for altered inflammation?
autoimmune disease
compromised immune system
238
What are some systemic assessment pieces found with inflammation?
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
What are some diagnostic tests for inflammation? What do they determine?
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
What are some diagnostic tests for inflammation? What do they determine?
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
What is an acute inflammation?
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
What are some nursing managements for acute inflammation?
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
What types of pharmaceuticals can be used for acute inflammation? MOA?
saliclates (aspirin)
corticosteroids (prednisode)
NSAIDs (ibuprofen)
inhibits synthesis of prostaglandins
244
What are the predominant cells seen in chronic inflammation?
lymphocytes and macrophages
245
When does inflammatory bowel disease peak?
15 to 30 of age
246
What is the etiology of inflammatory bowel disease?
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
What is the prevalence of inflammatory bowel disease?
1.3 million americans, UC is more common than Chron's
248
Where does Chron's disease effect?
anywhere in the GI from mouth to anus, typically seen in descending colon and terminating ilieus
249
Where does ulcerative colitis disease effect?
mucosa and submucosa of rectum and colon, seen more in superficial mucosa, a crypt abscess can form and penetrate superficial mucosa
250
How does the inflammation progress in Chron's?
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
What is the inflammation process of ulcerative colitis?
over time the colon begins to narrow and shorten
252
What are the clinical manifestations of Chron's?
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
What are the clinical manifestations of ulcerative colitis?
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
What is the stool frequency for the degrees of ulcerative colitis?
mild: up to 4x/day
moderate: up to 10x/day
severe: greater than 10-20x/day
255
What are complications of Chron's?
intestinal obstruction
abscess and fistula
hemorrhage leading to anemia
perforation of bowel
malnutrition and nutritional deficiencies
increase risk of small intestinal cancer
256
What are complications of ulcerative colitis?
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
Which diagnostic tests can be done for inflammatory bowel diseases?
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
What is the focus of treatment for inflammatory bowel disorders?
relief of symptoms, correcting malnutrition, addressing stress and quality of life
259
What is the goal of pharmacological treatments for inflammatory bowel disease?
terminate acute attacks quickly and reduce incidence of relapse
260
What is the step up approach?
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
What is mesalamine?
5-ASA that can prevent flareups of both inflammatory bowel diseases and treat mild symptoms
262
What is the step-down approach
for severe cases of inflammatory bowel disease begin with immunosuppressants
263
What is mercaptopurine?
immunosuppressant used for inflammatory bowel disease
264
What is azathioprine?
immunosuppressant used for inflammatory bowel disease
265
What is infiximab?
immune response modifier/biologic that will reduce inflammation by blocking proteins that cause inflammation, used in inflammatory bowel disease
266
What are some nonpharmacological therapies for inflammatory bowel disease?
replacing fluids and electrolytes
trying to reduce weight loss
increased dietary fiber to reduce diarrhea but could cause blockages if colon is narrowed
267
When is surgery used for inflammatory bowel disease?
complications occur: bowel obstruction, perforation, internal or external fistula, abscess, perineal complications, cancer
268
Which assessments will nurses do for inflammatory bowel disease?
stool frequency, amount, and characteristics
fluid and electrolytes
skin
269
What are the layers of the skin?
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
What are the types of glands found in the skin?
apocrine: secretes odorless substances (produce odor when mixes with bacteria), enlarges during puberty
eccrine: cools the body via evaporation, excretes waste products
271
What are lifespan considerations for infants and integumentary system?
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
What are normal common alterations to infants' integumentary system?
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
What are lifespan considerations for pregnant people's integumentary?
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
What are lifespan considerations of older adults' integumentary?
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
What diagnostic tests can be done for tissue integrity?
biopsy
culture
patch test
woods lamp (UV light to see fluorescent substances)
276
What defines a chronic alteration of tissue?
not healed within 3 months
277
How do you classify wounds?
etiology, actue/chronic, depth of tissue involvement
278
What can the wound base be made of?
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
What are the goals of wound management?
promote healing, protect from further trauma, prevent/treat infection
280
What is the process of wound management for clean wounds?
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
What is the process of wound management for contaminated wounds?
debridement needs to occur before healing can begin
282
How can debridement occur?
surgical
mechanical (wet to dry dressing, wound irrigation)
autolytic (dressings soften dry eschar)
enzymatic (drugs dissolve necrotic tissue)
absorption dressing
283
What type of patient education is needed with wound management and drain care?
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
What is negative-pressure wound therapy?
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
What is monitored when using negative-pressure wound therapy?
drainage, healing process, serum protein and electrolyte levels, coagulation studies
286
What is hyperbaric oxygen therapy? What is the physiology?
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
What is becaplermin?
platelet-derived growth factor gel that will stimulate cell proliferation and migration, can only be used for clean wounds ex/ diabetic foot ulcer
288
What are pressure injuries? Where are they commonly found?
localized injury to skin and/or underlying tissue over bony prominence
sacrum and heels
289
What is the etiology of pressure injuries?
intensity and duration of pressure
tissue tolerance
sheering forces
excessive moisture
290
What are risk factors for pressure injuries?
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
What is the pathophysiology of pressure injuries?
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
What are the stages of pressure injuries?
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
What are the top 10 tips for assessing darkly pigmented skin pressure ulcers?
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
What are complications of pressure injuries?
recurrence (most common)
infection: cellulitis, osteomyelitis, sepsis
loss of function and death
295
What does the braden scale assess? What are the categories of the scale?
pressure injury risk
sensory perception, moisture, activity, mobility, nutrition, friction and sheer
296
What braden scale score would indicate at risk?
18 or less
297
What medical treatments can be done for pressure injuries?
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
What are physiologic mechanisms to prevent UTIs?
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
What is the most common bacterial infection in women? What is the most common bacteria that causes it?
UTIs, E. coli
300
What is pyelonephritis?
upper urinary tract infection of renal parenchyma, pelvis, and/or ureters
301
What is cystitis or urethritis?
lower urinary tract infection of bladder or urethra
302
What is urosepsis?
sepsis caused by UTI
303
What is an uncomplicated UTI?
typically just involves bladder
304
What is a complicated UTI?
coexisting obstruction, stones, or catheters, abnormal GU tract, antibiotic resistance, recurrent infections, those susceptible to UTIs
305
What are risk factors for UTIs?
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
What are the signs and symptoms of lower UTIs?
emptying: hesitancy, incomplete emptying, retention, dysuria, hematuria/cloudy urine
storage: urinary frequency, urgency, incontinence, nocturia
307
What are signs and symptoms of upper UTIs?
flank pain, fever, chills
308
What are signs and symptoms of a UTI in older adults?
non-localized abdominal discomfort
cognitive impairment
unlikely to have a fever until septic
309
What diagnostic studies can be done for UTIs?
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
What is the treatment for uncomplicated UTIs?
3 day treatment of: TMP/sulfa (empiric treatment), nitrofurantonin, ampicillin, amoxicillin
311
What is the treatment for complicated UTIs? Nursing considerations?
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
What are the phenazopyridine? Side effects?
localized analgesic effect to relieve dysuria and urgency
orange urine
313
Why can cranberry juice help with UTIs?
there're enzymes to inhibit bacteria from attaching to epithelium of bladder
314
What is acute pyelonephritis?
inflammation of renal parenchyma and collecting system (including the renal pelvis), chronic can lead to kidney disease
315
How does the pathophysiology of acute pyelonephritis begin? What are the most common cause?
coloniation and infection of lower tract via ascending urethral route
E.coli, klebsiella, enterobacter
316
What are the clinical manifestations of acute pyelonephritis?
mild fatigue
chills
fever
vomiting
malaise
flank pain
characteristics of cystits
costoveterbral (CVA) tenderness to percussion present on affected side
317
What diagnostic studies can be done for acute pyelonephritis?
UA, culture and sensitivity, blood culture (if suspected bactermia), ultrasound for anatomic abnormalities
318
Who is typically hospitalized for acute pyelonephritis?
those with severe infections and complications such as nausea and vomiting with dehydration
319
What is the treatment for acute pyelonephritis? How quickly will symptoms improve after the start of treatment?
antibiotics: ciprofloxacin, levofloxacin (parenteral administration in hospital to rapidly establish high drug levels), NSAIDs, antipyretic drugs, urinary analgesics
48 to 72 hours
320
What is respiratory syncytial virus? Who typically gets it? When do they typically get it?
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
What are the clinical manifestations for RSV initially and later stages?
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
What diagnostic test is done for RSV?
nose swab, chest XR
323
What is the treatment for RSV? How long does it take for RSV to resolve?
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
What is palivizumab? What are the nursing considerations?
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
