NUR 226 Exam 2 Flashcards
1
Q
What is cholesterol
A
A waxy fat like substance that is found in all cells of the body
2
Q
What is the role of cholesterol in the body?
A
In all cell membranes and is an essential part of phospholipid bilayer/ Highly insoluble
It is the building block of:
Estrogen and testosterone
Vitamin D
Cortisol
Bile Acids
3
Q
Exogenous Cholesterol
A
25%
Dietary
Has some effect on the level
“Cholesterol is not a nutrient of concern for over consumption”
4
Q
Endogenous Cholesterol
A
75%
Manufactured by cells- liver
HMG-CoA reductase
Uses saturated fat
5
Q
HDLs
A
High Density lipoproteins
Good Cholesterol
Helps remove other forms of cholesterol from the blood stream
6
Q
HDLs
A
Good Cholesterol
Helps remove other forms of cholesterol from the blood stream and carries it to the liver, this helps prevent bad cholesterol and triglycerides from building up in the arteries
7
Q
LDLs
A
Low density lipoproteins
Bad cholesterol-makes up most of the bodies cholesterol
Moves cholesterol around the body where it is needed for cell repair and deposits it in artery walls
8
Q
How does blood serum appear after a high fat meal
A
It can appear milky/cloudy due to the increase in triglyceride levels
9
Q
What do we want to keep cholesterol at?
A
<200 mg/dl
Range: 100-200
10
Q
What is our goal for HDL and LDL
A
HDL:
Female: >55 mg/dl’
Male: >45 mg/dl
Optimal >60
LDL: <100 mg/dl
11
Q
What is the goal for triglycerides?
A
< 150 mg/dl
Range: 40-150
12
Q
What is Familial hypercholesterolemia?
A
Genetic elevated cholesterol
Defect in LDL receptors in liver cells
Liver cannot efficiently remove LDL from the blood stream
Elevated LDL cholesterol levels in the blood
13
Q
What is atherosclerosis
A
Injuries to the endothelium
plaque formation in coronary+peripheral arteries
Excess lipids and debris accumulate in vessel wall
14
Q
How does atherosclerosis start?
A
Injury to the endothelium such as smoking, hypertension, hyperglycemia, and more.
15
Q
What are a few of the risk factors for atherosclerosis and heart disease?
A
Hypertension
High Cholesterol
Smoking
Diabetes
Sedentary lifestyle
16
Q
How does atherosclerosis develop
A
Injury to the endothelium
Increased permeability
LDL molecules into vessel wall
Oxidized-damage endothelium
Macrophages arrive- engulf lipids-foam cells
Release of inflammatory mediators
Excess lipids and debris accumulate in vessel wall
Plaque with large lipid core prone to rupture
17
Q
Atherosclerotic Cardiovascular disease
A
-Leading cause of death
-Plaque builds up in the walls of arteries limiting the blood flow to the vital organs
-Coronary heart disease, Myocardial infarction, coronary artery stenosis
18
Q
MOA for HMG-CoA Reductase Inhibitors (statins)
A
HMG-CoA competitively inhibits the enzyme HMG-CoA reductase which is the rate-limiting step in cholesterol synthesis within the live, effectively reducing the body’s production of cholesterol by blocking the conversion of HMG-CoA to mevalonate; this leads to increased LDL receptor expression on liver cells, resulting in enhanced clearance of LDL.
19
Q
What are some popular patient populations where statins might not be effective
A
Liver disease
High LDL despite lifestyle changes
20
Q
Which statins are typically prescribed
A
Atorvastatin
Pravastatin
Rosuvastatin
Simvastatin
Pitavastatin
They are all typically taken at night because that is when we have the highest levels in our blood
21
Q
What are the adverse reactions associated with HMG-CoA reductase inhibitors and what kind of clinical monitoring is required
A
Myopathy
Rhabdomyolysis
Hepatotoxicity
Monitor liver function and muscle strength
22
Q
What are the secondary causes of hyperlipidemia that lead to elevated LDL
A
Diet- Saturated/trans fat, weight gain, anorexia
Drugs-diuretics,cyclosporine, glucocorticoids, amiodarone
Diseases-biliary obstruction, nephrotic syndrome
Disorders- hypothyroidism, obesity, pregnancy
23
Q
What are the secondary causes of hyperlipidemia that lead to elevated triglycerides?
A
Diet: weight gain, low-fat diet, high intake refined CHO, excessive ETOH intake
Drugs: oral estrogens, glucocorticoids, bile acid sequestration, protease inhibitors, tamoxifen, beta blockers
Diseases: nephrotic syndrome, chronically renal failure, lipodystrophies
Disorders: Poorly controlled DM, hypothyroidism, obesity, pregnancy
24
Q
What are bile acid seqestrants?
A
-Bile
-Produced in liver
-Only route for body to excrete cholesterol
- medication used to lower high cholesterol levels in the blood by binding to bile acids in the intestines, preventing their reabsorption and forcing the liver to use more cholesterol to produce new bile acids, ultimately lowering LDL levels
25
What are the side effects of Bile acid seqestrants
Constipation, stomach pain, bloating, vomiting, heartburn, loss of appetite, indigestion, and more.
Mix powder forms with water or other fluids, take pill with plenty of water. Take other medications 1 hour before or 4 hours after
26
What are the benefits of niacin combinations
Niacin can increase the effectiveness of some statins to lower LDL while also raising HDL.
Helps with the health of your heart
27
Fabric acid derivatives
Acceleration of clearance of VLDLs, increase breakdown and elimination of triglycerides, facilitate HDL formation
28
Ezetimibe
Blocks absorption of cholesterol in jejunum
Used in combination with statin
Raises HDL and lowers LDL and TG
29
Fish Oil
Omega 3 polyunsaturated fatty acids
High doses lower TG levels
Low doses reduce platelet aggregation, reduce thrombosis, reduce inflammation
30
when a client is diagnosed with atherosclerosis, the nurse is primarily concerned with which vessels?
Coronary arteries and lower extremities arteries
31
The nurse is teaching a client about atherosclerosis. Which statement would be included for teaching?
There is no treatment for this condition
Increased levels of HDLs can lead to this disease
This disease begins with an injury to the endothelial cells
This disease affects arteries and veins
This disease begins with an injury to the endothelial cells
32
A client is diagnosed with atherosclerosis. Which modifiable risk factors does the nurse see in the clients history?
Age 56
Smoking cigarettes
Eating lean meats
Male gender
Smoking cigarettes
33
The nurse understands that foam cells in a fatty streak are what?
Injured neutrophils
Lipid laden mast cells
Macrophages that engulf LDL
Deposited adipose cells
Macrophages that engulf LDL
34
A client is taking an HMG-CoA reductase Inhibitor to lower cholesterol. The nurse knows to monitor the client closely for the development of which problem?
Pulmonary problems
Neutropenia
Vitamin C deficiency
Liver Dysfunction
Liver Dysfunction
35
The leading cause of Coronary artery and cerebrovascular disease is:
Dyslipidemia
Hypertension
Obesity
Atherosclerosis
Atherosclerosis
36
What is the pathophysiology of hypertension?
Cardiac Output x Peripheral Vascular Resistance
37
What regulates blood pressure
RAAS: Renin Angiotensin Aldosterone System regulates long term blood pressure and extracellular volume
38
What happens in response to low blood pressure and changes in blood volume
Angiotensionogen is released by the liver
39
What happens when there is low fluid volume/low B/P
-It stimulate the kidney to release renin which causes the liver to convert angiotensionogen to ANGIOTENSIN 1
-Angiotensin 1 travels to LUNG where it is converted to Angiotensin 2 by ACE(angiotensin converting enzyme)
-Angiotensin II acts on the ADRENAL GLANDS to cause release of ALDOSTERONE(which then causes fluid retention)
Nephron retains fluid and B/P goes up
40
What is angiotensin II
A potent vasoconstrictor
41
How does Arterial Baroreceptors affect B/P
Receptors in the carotid sinus, aorta, and left ventricle
-Receptors sense blood pressure, can alter B/P by altering HR
-Can also impact vasodilation and vasoconstriction
42
How does vascular auto regulation affect B/P
-helps maintain constant levels of tissue perfusion
- regulates based on mean arterial pressure
- alters the resistance in arterioles (diameter)
- This mechanism helps keep consistent blood pressure at the tissue levels despite the changes that are occurring in other mechanisms
43
What are the two main types of hypertension
Primary- 92-95%
Secondary- Has a cause and can be fixed
44
Normal BP category
Less than 120
AND
Less than 80
45
Elevated BP category
120-129
AND
Less than 80
46
High Blood Pressure (Hypertension) Stage 1
130-139
OR
80-89
47
High Blood Pressure (Hypertension) Stage 2
140+
OR
90+
48
Hypertensive Crisis
Higher than 180
AND/OR
Higher than 120
49
Primary Hypertension
-Occurs when there is no known cause of hypertension
50
What are risk factors for primary hypertension?
Smoking
Sedentary lifestyle
Stress
Obesity
Excess sodium intake
Hyperlipidemia
Family history and genetics
Age 60 or older
Men vs Women
High alcohol consumption
African Americans
51
Secondary Hypertension
Hypertension with a KNOWN cause
Related to an underlying disease or disorder
TREAT THE UNDERLYING CAUSE
-Renal Disease
-Adrenocortical tumors
- Adrenomedullary tumors
- Certain drugs
52
What are causes for secondary hypertension
Health conditions
Certain medications
Recreational drugs
Pregnancy
Hormonal therapy
53
What are signs and symptoms of Hypertension
NONE
Silent killer
Must look for signs of end organ damage:
Chest pain->Heart
Headache->Brain
Visual Changes->Eyes
Weakness/pain in the extremities->brain/stroke
54
What are long term outcomes of hypertension
Cardiac: increased left ventricular work
Kidneys: primary cause of end stage renal disease
Brain: higher risk of stroke, aneurysm, hemorrhage
Eyes: retinopathy and blindness
Lower extremities: gangrene, intermittent claudication
55
What are the potential complications of uncontrolled hypertension
TIA
Stroke
Retinopathy
Peripheral Vascular Disease
Renal Failure
LVH: Left Ventricle Hypertrophy
CHD: Coronary Heart Disease
HF: heart failure
56
Cardiac output
Stroke volume x heart rate
57
Hypertensive urgency
No signs or symptoms of end organ damage
BP greater than 180/120
Treat with oral agents and gradually reduce BP
Causes: anxiety, pain, abrupt withdrawal
58
Hypertensive Emergency
Uncontrolled BP that leads to end organ damage
BP greater than 180/120
Symptoms of organ damage: headache, blurry vision
Stroke, brain hemorrhage, chest pain, acute coronary syndrome, heart dysfunction
Aggressively lower BP in minutes to hours (IV MEDS)
59
What are the main classes of medications used to treat hypertension
Diuretics
RAAS (Renin Angiotensin Aldosterone System) blockers
Calcium Channel Blockers
Sympathetic nervous system blockers
Vasodilators
60
The nurse understands in most cases of combined systolic and diastolic hypertension with no known cause would be documented as which type of hypertension?
-Aquired
-Congenitial
-Primary
-Secondary
PRIMARY
61
The nurse is taking an adult clients blood pressure and determines it to be normal. What would the nurse document?
120/80
62
A client is taking anti hypertensive drug for a few months’ states that a new, persistent dry cough is very bothersome. The nurse knows that this cough is an adverse effect of which class of anti hypertensive drugs?
-ACE inhibitors
-Angiotensin II receptor blockers
-Selective Beta Blockers
-Calcium channel blockers
Angiotensin converting enzyme inhibitors
63
The nurse is working in the emergency department when EMS brings in a client with a hypertensive crisis. What finding will lead the nurse to anticipate an order for IV blood pressure medication?
-Diastolic blood pressure of 110
-Confused and Garbled speech
-Nausea
-Acute alcohol withdrawal
Confused and Garbled speech
64
Cardiac Output x Peripheral Vascular Resistance is the formula for what
Blood Pressure BP
65
SBP 120-129 and DBP less than 80 is what?
Elevated Blood Pressure
66
A patient with a hypertensive emergency and chest pain can be suffering from what?
Myocardial infarction (heart attack )
67
These HMG-CoA reductase inhibitors are best taken at night
Statins
68
Smoking is what kind of risk factor
Modifiable risk factor
69
Beta blockers can cause what
Bradycardia
Hypotension
70
Medication side effects and costs can cause a problem with what
Medication adherence
71
These inhibitors inhibit the production of angiotensin 2
Angiotensin converting enzyme inhibitors (ACE)
72
Statins are most effective when taken at this time of day
Bedtime
73
This type of hypertension has an underlying cause such as renal disease
Secondary
74
Age is what type of risk factor
No modifiable
75
Cholestyramine has variable effects on this medication
Warfarin
76
164/88
Hypertension stage 2
77
118/79
Normal
78
130/58
Hypertension stage 1
79
182/90
Hypertensive Crisis
80
What is pain
A complex experience
Dynamic interactions between physical, cognitive, spiritual, emotional, and environmental factors
-Not just a response to an injury
81
What is acute pain?
Protective
Promotes withdrawal from painful stimuli, allows injured parts to heal and teaches avoidance
82
What are the parts of the nervous system that are involved in the sensation, perception, and response to pain
Afferent pathways
Interpretive centers
Efferent pathways
83
What are Nociceptors
Pain receptors
84
What is nociceptive stimuli
Stimuli of a certain intensity that cause, or are close to causing tissue injury
Chemical stimuli
Physical stimuli
85
What are the 4 stages of Nociception
Transduction
Transmission
Perception
Modulation
86
Physiology of transduction
Painful stimuli converted to action potentials at the sensory receptor
Substances/chemical mediators released as a result of DIRECT injury and inflammation
87
What is prostaglandin
Important mediator that create the reactions that cause pain, fever, and inflammation
88
A-delta fibers
Small diameter
Myelinated:rapid transmission of pain
Pain is sharp, stinging, cutting, and pinching is localized
89
C fibers
Small diameter
Unmyelinated: slow transmission of pain
Pain is dull, burning, aching. Poorly localized
90
A-alpha fibers
Large diameter
Do NOT transmit pain signals
91
A-beta fibers
Do NOT transmit pain signals
92
Physiology of Transmission
the smaller A-delta and C fibers transmit pain
93
Physiology of perception
Brain then receives these signals and interprets them as painful
Factors that affect:
Attention
Distraction
Anxiety
Fear
Fatigue
94
Pain tolerance
Greatest intensity of pain a person can handle
Varies greatly overtime
95
Pain threshold
Lowest intensity of pain that a person can recognize
Perceptual dominance occurs
96
Opioid tolerance
Requires larger amounts for the same effect
97
Physiology of modulation
Synaptic transmission of pain signals in altered
98
Gate control theory
Theory that if we can BLOCK the pain BEFORE it gets to the brain we can STOP or lower pain perception
99
Neurotransmitters
Modulate control related to the TRANSMISSION of pain impulse
Excitatory or Inhibitory
More than 50
100
Endorphins
Natural neurochemicals or endogenous opioids that aid in inhibiting the pain response
101
Acute pain
Nociceptive pain
Normal protective mechanism to tissue injury
Transient, can last seconds to months
Often stimulates the ANS to produce physical response to pain
-HR,BP,diaphoresis,dilated pupils
102
Chronic Pain
Lasting for more than 3-6 months
Serves no purpose, often seems out of proportion to observable tissue damage
Can be ongoing or intermittent
Changes in the PNS and CNS cause dysregulation of nociception and pain modulation
Often no ANS response
103
Nociceptive pain
Cutaneous/somatic-involves MS system
Visceral-involves organs and inflammation
104
Neuropathic pain
Involves nerves
105
Somatic pain complaints
Constant and achy
106
Visceral pain complaints
Cramping
Splitting
N/V
Diaphoresis
107
Neuropathic pain complaints
Shooting
Burning
Electric shock
Sharp
Numb
Motor weakness
108
Somatic pain location
Well localized in skin and subcutaneous
Less well localized in bone
Muscle
Blood vessels
Connective tissue
109
Visceral pain location
Originates in internal organs or linings
Poorly localized
Diffuse
Deep
110
Neuropathic pain location
Originates in injury to peripheral nerve
Spinal cord
Brain
Poorly localized
111
Referred pain
Pain is felt at a distance form from the actual pathology
Common in visceral pain
EX: mi felt in chest
112
Phantom pain
Sensations of pain that originates from an amputated part
Constant
Most intense right after the amputation
Generally resolve overtime
113
This type of pain originates in the spinal cord and is typically burning or shooting.
-visceral
-nociceptive
-somatic
-neuropathic
Neuropathic
114
A nursing intervention to relieve pain by “closing the gate” would focus on stimulation of what?
-peripheral nervous system
-A-delta and c nerve fibers
-large diameter nerve fibers
-small diameter nerve fibers
Large diameter nerve fibers
115
Acetaminophen has dose restrictions. The maximum dose for this drug in 24 hours for most adults is?
4 grams
116
Pain that is felt at a distance from the injury is known as ______ pain.
Referred
117
The mechanism of action for morphine (and all opioids) is binding to mu receptors, similar to endorphins, creating a response.
True
118
Neurotransmitters modulate control of the transmission of the pain impulse. Of the neurotransmitters we discussed, which are inhibitors of pain transmission?
-Acetylcholine
-Norepinephrine
-Gamma Aminobutyric Acid
-Dopamine
Gamma Aminobutyric Acid (GABA)
119
Nociceptors are NOT found in which area of the body
BRAIN
120
Which of the following is a characteristic of C-fibers?
-large diameter
-myelinated
-slow transmission
-rapid transmission
Slow transmission
121
A client is taking oxymorons and acetaminophen for pain control after surgery the previous day. The nurse is reviewing the clients medication what other medications would the Brüste expect to find on the MAR? SATA
-stool softener
-fever reducer
-duragesic
-anti-emetic
Stool softener
Anti-emetic
122
Classification of an esthetics that block nerve conduction
Local
123
A commonly used local anesthetic
Lidocaine
124
Older adults are also at an increased risk for induced GI toxicity related to this drug classification
NSAIDS
125
Most common reason people seek healthcare
Pain
126
Most reliable source of pain description
Patient
127
Pain related to abnormal processing of sensory input
Neuropathic
128
Classification of pain can be characterized as cancer or no cancer pain
Chronic
129
Allows patients to self administer doses of pain meds
PCA
130
An anticonvulsant used for pain
Gabapentin
131
Normal pain reception
Nociceptors
132
Processes by which noxious stimuli, such as a surgical incision or burn, active Nociceptors
Transduction
133
What is a bowel complication of analgesics
Constipation
134
Type of pain where patient has continuous chronic pain and also experiences acute exacerbations
Breakthrough
135
A decrease in one or more effects of an opioid; occurs with regular use
Tolerance
136
This is a chronic, relapsing, treatable neurological disease, craving opioids
Addiction
137
A dissociative anesthetic with dose dependent analgesic, sedative, and Amnestie properties
Ketamine
138
What are the 6 types of cellular adaptation
Atrophy
Hypertrophy
Hyperplasia
Metaplasia
Dysplasia
Anaplasia
139
Atrophy
Cells decrease in size
Decrease in size of an organ
Can be normal physiologic process
Results in decreased: workload/function, use, blood supply, nutrition, hormonal stimulation, nervous stimulation, etc
140
Hypertrophy
Increases in size of cells
Increase in size of organ: increased hormonal stimulation and functional demand
Physiologic: increased metabolic demand, striated muscle, triggered by stretch and growth factors
INCREASE IN PROTEIN NOT FLUID
Pathologic: hypertension and valve abnormalities
141
Hyperplasia
Increase in number of cells
Increased rate of division
Response to injury: loss of epithelial, liver, kidney cells
Normal:compensatory/regeneration/hormonal
Pathologic: abnormal proliferation of cells, excessive hormonal stimulation or growth factors
Endometrium: imbalance of estrogen and progesterone, excessive uterine bleeding
142
Metaplasia
Change from 1 cell type to another
New cells better able to tolerate adverse conditions
Can protect the organ
*can be reversible
143
Dysplasia
Abnormal size and shape of mature cells
Chronic inflammation
Precancerous condition
Frequent monitoring
Evaluate for the development of neoplasia
144
Anaplasia (Neoplasia)
Abnormal,new,cellular growth: disorganized, uncoordinated, uncontrolled growth rate
Benign or Malignant: differentiation of the cells, malignant cells are less differentiated
145
Cellular injury causes
Chemical agents
Hypoxia (ischemia)
Infectious agents
Physical/mechanical factors
Nutritional imbalances
146
Chemical injury
Heavy metals (lead)- inhibits enzymes for HGB synthesis
Carbon monoxide-oxygen
Alcohol
Street drugs
Direct or indirect
Deliberate, unintentional or consequence
147
Hypoxia or ischemic injury
Components of tissue oxygenation: oxygen content, hemoglobin, cardiac output
Cell reverts to anaerobic metabolism: fall in pH, lactic acid accumulates in cell
148
Infectious agents damaging cellular components
Damage can be caused by the infection itself……. Bacteria, viruses, parasites
Exotoxins: disrupts specific cellular functions
Endotoxins: gram negative bacteria
149
Physical or mechanical injury
Blunt force injury: contusion, abrasion, laceration, or fractures
Sharp force injury: incised, stabs, puncture, chopping
Gunshot injury: entrance wound, exit wound
Asphyxia: suffocation, strangulation, drowning
Temperature: hyperthermia, hypothermia
Electrical
Radiation: Ionizing
150
Nutritional injury
Malnutrition: poverty, chronic alcoholism, acute and chronic illness, self imposed dietary restrictions, malnutrition-absorption syndromes
Excess
151
Accumulation
A build-up of stuff:
-normal intrazellular components
-abnormal substances
-faulty metabolism
-faulty synthesis
Pigments or particles that can not be digested by the cell
In born errors of metabolism
Melanin-tanned skin
Hemosiderin and bilirubin
Mineral dusts
Fatty liver
Familial hypercholestolemia
152
Necrosis
Irreversible: leads to swelling, bursting of cell, inflammation
Ischemic necrosis: infarction, prolonged ischemia
Can lead to gangrene: dead tissue is breeding ground for bacteria
153
Liquefactive necrosis
In tissues with a lot of lipids (brain) or where there are numerous inflammatory cells-release of proteolytic enzymes which destroy tissue
154
Caseous necrosis
Occurs when the necrotic cells disintegrate but the cellular debris remains in the area for months or years
155
Dry Gangrene
Blackened, dry, wrinkled
Occurs due to reduced blood flow, leading to tissue drying and shrinkage, often without infection
156
Wet gangrene
Liquefaction
Foul smelling
Rapid spread
Can be systemic
Involves infection, characterized by swelling, blistering, and a wet appearance due to fluid buildup
157
Gas gangrene
Clostridium perfringens
Gaseous bubbles
Caused be bacterial infection, particularly by clostridium species, leading to the production of gas within tissue
158
Apoptosis
Pre-programmed cell death cellular suicide
There is digestion of cell and contents by neighboring cells
Very little, if any inflammation
159
Kate is a 13 year old female who has come to the clinic to have a left arm cast removed. She has had the cast on for 6 weeks. After the cast is removed, Kate expresses concern about the size of of her left arm, stating that it appears much thinner than her right arm. You tell her that this most likely due to the following:
Atrophy
Dystrophy
Anaplasia
Dysplasia
Atrophy
160
Characteristics of apoptosis include all of the following except:
Cellular suicide
Both a physiologic and pathologic cell response
A response to the removal of hormonal signals
Inflammation
Inflammation
161
Stephen a 65 year old male suffered a MI. During a MI the heart is deprived of oxygen and cardiac cells suffer from ischemia. Cardiac cells that cannot adapt to the ischemia will suffer irreversible damage and die. This type of cell death is:
Necrosis
Apoptosis
Serotonin
Cellular absorption
Necrosis
162
Caryn is a smoker with a 12 year history of smoking a half pack of cigarettes daily. She states that she feels find and wonders why you suggest smoking cessation. You tell Caryn that cells respond to their environment. If the cell is exposed to a chronic irritation such as smoke or pollution, the cells in the airways will adapt. This change is related to adaptation in the cells is called__________, which can lead to cancer.
Hyperplasia
Metaplasia
Hypoplasia
Dysplasia
Metaplasia
163
The most significant change the pathologist will look for in the cells is:
Dysplasia
Hypertrophy
Atrophy
Metaplasia
Dysplasia
164
Obstructive Disease
Resistance to air flow
Reduced air flow
Obstruction in the wall of the lumen: Asthma, COPD, Bronchitis
Obstruction from increased pressure around the lumen: tumor, COPD, Emphysema
Obstruction of the airway: foreign body
165
Restrictive Disease
Decreased lung volume
Decreased expansion of lung-hard to inhale
-EX: Atelectasis, pulmonary fibrosis, pulmonary edema, ARDS
There is a reaction to the alveoli: they can’t expand
The alveolar wall is thick and stiff
The chest wall is stiff and can’t expand
Muscles of respiration don’t work
166
COPD
A common preventable and treatable disease characterized by persistent respiratory airflow limitation that is usually progressive and associated with an enhanced chronic inflammatory response in the airways and lungs to noxious particles or gases
Alpha-1 antitrypsin deficiency
167
Alpha-1 antitrypsin
Protein that protects the lung
Produced in the liver
Deficiency increases risk of lung and liver disease
168
Chronic bronchitis
Presence of chronic productive cough for 3 months in each of 2 consecutive years in a patient in whom other causes of chronic cough have been excluded
169
Emphysema
Abnormal permanent enlargement of the air spaces distal to the terminal bronchioles, accompanied by destruction of their walls and without obvious fibrosis
170
Pathophysiology of COPD
Airflow limitation is progressive, associated with abnormal inflammatory response
Chronic inflammation damages tissue
Scar tissue in airways results in narrowing
Scar tissue in the parenchyma decreases elastic recoil
Scar tissue in pulmonary vasculature causes thickened vessel lining and Hypertrophy of smooth muscle
Surface area for diffusion of O2 decrease
171
Defining characteristics of COPD
Forced exhalation due to loss of elastic recoil
Airflow obstruction due to mucous hyper secretion, mucosal edema, and bronchospasm
Hyperinflation of lungs
172
Chronic Bronchitis
Cough and sputum production for at least 3 months in each of 2 consecutive years
Ciliary function is reduced, bronchial walls thicken, bronchial airways narrow, and mucous may plug airways
Alveoli become damaged, fibroses, and alveolar macrophage function diminishes
The patient is more susceptible to respiratory infections
173
Emphysema
Abnormal dissension of air spaces beyond the terminal bronchioles with destruction of the walls of the alveoli
Decreased alveolar surface area increases in “dead space” impaired oxygen diffusion
Hypoxemia
Increased pulmonary artery pressure may cause right sided heart failure
174
Clinical Manifestations of COPD
Chronic cough
Sputum production
Dyspnea
Barrel chest
Weight loss due to dyspnea
175
COPD-Cigarette Smoking
Smoking cessation:
Biggest impact in reducing risk of developing COPD
Accelerated decline in pulmonary function slows to almost nonsmoking levels
176
COPD-Cigarette smoking carbon monoxide
Decreased o2 carrying capacity
Increased heart rate
Impaired psychomotor performance and judgement
177
Complications of COPD
Respiratory insufficiency and failure
Pneumonia
Chronic atelectasis
Pneumothorax
COR pulmonale
178
Pulmonary function tests
Tidal volume
residual volume
Vital capacity
Functional residual capacity
Peak expiratory flow rate
179
Tidal volume
Air inspired and expired normal breath
180
Residual volume
Gas in lung after max expiration
181
Vial capacity
Max air expired after max air inspired
182
Functional residual capacity
Air in lung after normal expiration
183
FEFR
Volume of air forcible exhaled in a unit of time
184
Peak expiratory flow rate
Highest rate of flow sustained for 10 seconds or more at which air can be expelled from the lungs
185
More emphysema PINK PUFFER
Lower BMI
Fewer cardiovascular co-morbidities
Fewer metabolic co-morbidities
Less muscle mass
Hyperinflation
Low diffusion capacity for CO
More dyspnea
Decreased exercise capacity
Worst health status
Lower serum levels of sRAGEs
186
Less emphysema BLUE BLOATER
Higher BMI
More metabolic co-morbidities
Cardiac compromise
OSA-COPD overlap
Less hyperinflation
More chronic bronchitis
Increased exacerbations
More normal diffusion capacity
Higher serum levels of inflammatory markers
187
Flutter mucous clearance device for COPD
Flutter has a mouthpiece, a high density stainless steel ball, and a cone that holds the ball. When the patient exhales through the flutter, the steel ball moves which causes vibrations in the airways and loosens mucus
Patient must be upright
Provides positive expiratory pressure
188
Asthma
-Chronic inflammatory disease of the airways that causes hyper responsiveness mucosal edema and mucus production
-Inflammation leads to cough, chest tightness, wheezing, and dyspnea
-Asthma is largely reversible; spontaneously or with treatment
-Allergy is the strongest predisposing factor
189
Characteristics of Asthma
Bronchoconstriction, inflammation
Hyperactivity to stimuli
190
Symptoms of asthma
Dyspnea, wheezing, chest tightness
Cough, sputum production
191
Asthma pathophysiology
Bronchoconstriction narrows airways
-sphincter action can completely occupied airways
-Aggravated by inflammation, mucosal edema, excessive mucus
-Mast cells release substances in response to causative stimuli—->bronchoconstriction and inflammation
192
Asthma risk factors
Atopy:
Genetic tendency to develop allergies
Heightened immune response to common allergens
Obesity:
Adults-highest risk
Children-what came first: obesity or asthma
Increase GERD-worsening asthma
193
Highest risk for asthma
Women>men
Boys>girls
18-24 higher risk than older adults
Multi-race and black adults
Less than high school graduate
<75,000 annual income
194
What are symptoms of asthma
Wheezing
Dyspnea
SOA
Cough
Chest tightness
Tachycardia
195
Agonist
Chemical that binds to a receptor to produce a biological response
Produces an effect
196
Antagonist
Chemical that may bind to a receptor,but does not produce a response, instead it blocks that receptor to a natural agonist
197
Adrenergic amines
Drugs that stimulate the sympathetic nervous system
198
Alpha-1 + Alpha-2
Vascular smooth muscle
199
Beta-1
Located in heart
200
Beta-2
Located in the bronchioles of the lungs and arteries of skeletal muscles
201
Muscarinic
Parasympathetic nervous system and acetylcholine receptors
202
Cholinergic
Mimic the action of the neurotransmitter acetylcholine, the primary transmitter of nerve impulses within the parasympathetic nervous system
203
A client newly diagnosed with asthma is preparing for discharge. Which point should the nurse emphasize during the clients teaching?
-Contact the HCP if nighttime wheezing becomes a concern
-Limit exposure to sources that trigger an asthma attack
-Use the peak flow meter only if symptoms are worsening
-Use inhaled steroid medication as the rescue/reliever inhales
Limit exposure to sources that trigger an asthma attack
204
Chronic hyperinflation of the lungs in the COPD patient leads to:
-barrel chest
-bottle chest
-depression
-musculoskeletal wasting
Barrel chest
205
The strongest predisposing factor for asthma is:
-smoking
-genetics
-allergens
-gender
Genetics
206
Education by the nurse that could reduce the risk of chronic obstructive pulmonary disease in healthy individuals would include?
-Participation in regular aerobic exercise
-Consumption of a high protein diet
-Abstention from cigarette smoking
-Avoidance of persons with known respiratory infections
Abstention from cigarette smoking
