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Krystan: Semester Two Nursing School > 2850 Pathophysiology Exam One > Flashcards

2850 Pathophysiology Exam One Flashcards

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1
Q

What are the possible effects of genetic disorders?

A

Damage or mutation of DNA

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2
Q

What impact does cellular injury often have?

A

Synthesis of abnormal cellular proteins, which can lead to disease

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3
Q

What are the main causes of gene mutation?

A

Inheritance

Environmental influence

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4
Q

Germ cell mutations

A

Mutations on the genes of sex cells (gametes) that can be passed to future generations of offspring

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5
Q

Somatic mutations

A

Mutations on non-gamete body cells that can affect the individuals body but cannot be passed to future generations

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6
Q

A mutated gene can either produce what or what in terms of proteins?

A

Abnormal proteins or no proteins

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7
Q

What are some diseases that are the result of multifactorial influences?

A

Hypertension
Heart disease
Diabetes
Cancer

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8
Q

What are some predictive factors that can contribute to development of a multifactorial disease?

A

Inheritance of one or more predisposing genes
Environmental factors
Diet
Exercise/lack of exercise

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9
Q

What are some environmental factors that can contribute to disease development?

A 
Pollution
Chemicals
Toxins
Smoking
Alcohol
Drugs
Sunlight
Radiation
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10
Q

Explain the “Two Hit” hypothesis

A

Normally, if one allele on an allele pair becomes damaged or mutated, the corresponding normal allele will counteract the effect of the damaged one.
In order for disease to develop, something must happen to the other allele as well.
So someone could inherit one damaged allele, but not develop the disease until an environmental or lifestyle factor damaged the other allele (or disease won’t develop if that allele stays normal)

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11
Q

What is the exception to the “Two Hit” hypothesis?

A

Autosomal dominant diseases

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12
Q

What should be included in a genetic risk assessment?

A

Family health history
Ethnicity and culture
Social practices

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13
Q

Why is it important to include ethnicity in a genetic assessment?

A

Because certain illness patterns are more common in certain ethnic groups

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14
Q

What are the physical responses that occur with any type of stress?

A

Heart rate goes up and myocardial contractility increases
Bronchodilation
Chemical mediators provoke stress hormone release, increasing alertness
Strength and agility increase

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15
Q

What happens when the stressful situation ends?

A

Hormones end the stress response and the body returns to normal

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16
Q

What are the effects of frequent or long term stressors?

A

Stress hormones are always in the tissues and bloodstream, leading to diminished immunity, increased risk of autoimmune disease, cancer, heart disease, and depression

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17
Q

Which theory discusses adaptive ability and coping mechanisms?

A

Selye’s stress response theory

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18
Q

Adaptive ability

A

How an individual manages stress and reduces the effects of stress

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19
Q

Coping mechanisms

A

Emotional and behavioral responses used to manage threats to physical and mental homeostasis (can be healthy or unhealthy)

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20
Q

What are some conditioning factors when it comes to coping with stress?

A 
Support systems
Age 
Gender
Genetic predisposition 
Developmental and educational level
Life experiences
Pre-existing conditions
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21
Q

How do conditioning factors affect how a person reacts to stress?

A

A person’s perspective on a stressful situation, their past experiences, and other listed factors will determine whether they can adapt or not in times of stress

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22
Q

What hormone is released in the alarm stage of the general adaptation syndrome?

A

Norepinephrine

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23
Q

What happens physiologically in response to norepinephrine release in the alarm stage?

A

Vasoconstriction (increased blood to heart/lungs/muscles)
Increased alertness
Increased cardiovascular and respiratory response

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24
Q

A survival oriented, involuntary, neuroendocrine physiological change in response to a severe, acute stressor

A

Fight or flight response

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25
Q

What are the physiological effects of cortisol?

A

Mobilization of glucose, amino acids, and fat for energy production
Increased WBC production and decreased inflammation (for the first 3-5 days of stress response)

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26
Q

What does cortisol cause after sustained presence in the body after 3-5 days?

A

Immunosuppressive

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27
Q

What are the effects of increased WBC production?

A

Less inflammation and increased immunity

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28
Q

What does aldosterone and ADH do during the alarm stage?

A

Increase sodium and water retention to increase blood pressure

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29
Q

How does the body attempt to stave off stress effects during the resistance stage?

A

Continued hormone and catecholamine (norepinephrine) secretion

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30
Q

What does the parasympathetic nervous system do when stress subsides?

A

Counteracts SNS actions, so HR goes down, pupil dilation decreases, digestion/urinary functions return to relaxed state, all normal parasympathetic responses resume

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31
Q

What are symptoms of the exhaustion stage?

A 
Feeling run down
Inability to cope
Depression
Anxiety
Illness
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32
Q

What are the effects of chronic stress?

A

effect is cumulative, causing Immunosuppression leading to illness and infection
Also has a negative mental and emotional effect

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33
Q

What are some consequences of long term cortisol secretion?

A

Decreased immunity

Less efficient WBC response

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34
Q

Who theorized about allostasis in terms of stress?

A

McEwen (McEwen’s stress response theory)

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35
Q

Allostasis

A

A dynamic state of balance that changes with exposure to stressors

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36
Q

Allostatic load

A

Wear and tear on body systems caused by stress reactions

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37
Q

What are the four mechanisms that cause accumulation of allostatic load?

A

Repeated stressful experiences
Inability to adapt
Prolonged stress reaction
Inadequate response to stressor

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38
Q

What are some factors that influence adaptive ability?

A 
Genetics
Cognitive ability
Developmental level
SES
Lifestyle 
Diet 
Exercise
Past experiences
Support system
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39
Q

Allostatic overload

A

Stress exceeds the body’s ability to adapt, initiating pathophysiological disorders

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40
Q

Allostatic overload corresponds with which stage of the GAS?

A

Exhaustion stage

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41
Q

What are some examples of stress related disorders?

A 
Asthma 
Autoimmune diseases
IBS
Migraines
Peptic ulcer disease
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42
Q

Why do elderly individuals have less resiliency against stress?

A

Body takes longer to recover from a stressful event as it ages

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43
Q

What are some symptoms of stress?

A 
Nervousness
Irritability
Headaches
Inability to concentrate 
Insomnia
Appetite changes
Depression
Panic attacks
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44
Q

Biological, intrinsic phenomena of aging and the gradual loss of function of body systems

A

Senescence

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45
Q

How does senescence relate to gerontology and geriatrics

A

It describes how the cells lose their ability to replicate and repair over time, leading to the loss of function that comes with aging

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46
Q

What is meant by loss of physiologic reserve?

A

Decreased ability to repair damage and adapt to physiologic stressors

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47
Q

What is meant by the multicausality theory of aging?

A

Combination of Internal processes and environmental factors that cause cell changes and aging of the body

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48
Q

What is the single largest cause of death in the United States?

A

Cardiopathologies

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49
Q

Atherosclerosis

A

Development of cholesterol-laden plaques in the endothelial lining of arteries, and increased connective tissues in the walls of the vessels

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50
Q

Arteriosclerosis

A

Thickening of the inner and central walls of arteries

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51
Q

What does free radical damage do to cardiac cells? What does this cause?

A

It causes inappropriate cross linking of the proteins and DNA that accumulates over time. This causes decreased elasticity of the muscle fibers and decreased ability for arteries to vasodilate

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52
Q

How does maximum achievable heart rate change over time?

A

It decreases in a linear fashion over time

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53
Q

What are some changes to the respiratory system as a result of aging?

A

Responding more slowly to hypoxia and hypercapnia
Decrease in aerobic capacity (10% per decade)
Weaker cough reflex
Decrease in diameter of bronchioles and smaller airways

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54
Q

How does exposure to atmospheric air cause respiratory changes?

A

Damaging pollutants and free radical damage cause alveolar surface area loss and narrowing of bronchioles

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55
Q

Weaker cough reflex makes older adults more susceptible to..

A

Pneumonia

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56
Q

What can cause an older adult to NOT exhibit early warning signs of hypoxia?

A

Serious respiratory illness

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57
Q

What causes decreased kidney function in older adults?

A

Loss of nephrons and decreased activity of nephron tubules

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58
Q

How does aging change when the kidneys excrete fluid and electrolytes?

A

Older kidneys excrete more fluid and electrolytes at nighttime as compared to younger kidneys

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59
Q

Before administering a medication, a nurse checks serum creatinine to determine what?

A

Kidney function (and subsequent ability to eliminate medications)

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60
Q

What are some age related changes in the GI system?

A

Decreased strength in lower esophageal sphincter
Decreased production of hydrochloric acid and intrinsic factor
Changes in normal bacterial flora of the GI system

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61
Q

Presbyesophagus and its consequences

A

Age related changes in the esophagus, including weaker lower esophageal sphincter. This allows more acid reflux into the esophagus, leading to esophagitis and GERD

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62
Q

Why are older adults at greater risk for iron deficient anemia?

A

Decreased HCl production in the stomach leads to less iron and calcium absorption

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63
Q

Why are older adults at higher risk for pernicious anemia?

A

Decreased intrinsic factor causes decreased absorption of vitamin B12

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64
Q

Pernicious anemia causes..

A

Decreased red blood cell production in the bone marrow

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65
Q

What predisposes older adults to GI infections?

A

Changes in GI flora, leading to decreased GI immunity

66
Q

Why does BMR decrease with age?

A

Less thyroid action/secretion of thyroid hormones

67
Q

What causes thin skin in older adults?

A

Slower replacement of epidermal cells

68
Q

Why do older adults have difficulty with thermoregulation?

A

Decrease in subdermal fat, sweat glands, hair follicles, and sensory end organs

69
Q

What are the most common areas of bone loss in older adults?

A

Trabecular bones of vertebrae, hips, and wrists

70
Q

Why are women at greater risk for bone loss than men?

A

Decreased estrogen levels after menopause (estrogen helps keep osteoblasts viable)

71
Q

What are the neurological consequences of vitamin B12 deficiency?

A

Demyelination of dorsal columns of spinal cord, which can cause gait issues, tremors, and confusion

72
Q

What are some possible outcomes of the higher pain threshold of older adults?

A

Mechanical and thermal injury due to less protective actions being taken

73
Q

How does aging change hearing and vision?

A

Both decline, especially hearing high pitched noises and seeing things close to the face

74
Q

What is meant by frailty in older adults/How does it manifest?

A 
Fatigue
Cognitive impairment
Weakness
Weight loss
Decreased balance and activity 
Slowness
Social withdrawal
75
Q

What are some factors that contribute to frailty?

A 
Normal aging changes 
Common diseases 
Musculoskeletal changes 
Neurological changes
Immune system changes
76
Q

Atrophy

A

Cells reverting to smaller size in response to metabolic or environmental changes

77
Q

What are some causes of cellular atrophy?

A 
Paralysis
Loss of hormone stimulation to cells 
Aging
Malnutrition 
Disuse 
Ischemia
78
Q

Hypertrophy

A

Cellular adaptation in which individual cell size and functional tissue mass increases, stimulating angiogenesis

79
Q

Describe the difference between physiologic hypertrophy and pathological hypertrophy

A

Physiologic: enlarged muscles have adequate blood supply, oxygen, and nutrients
Pathologic: increase in cellular size without an increase in necessary supportive structures for increased metabolic needs

80
Q

Example of physiologic hypertrophy

A

Muscles of athletes

81
Q

Example of pathologic hypertrophy

A

Left ventricular hypertrophy

82
Q

Hyperplasia

A

Cellular adaptation in which number of cells in a tissue or organ increase

83
Q

What is an example of hyperplasia?

A

Benign prostatic hyperplasia

84
Q

What are two conditions of hyperplasia that are caused by hormone stimulation?

A

Breast gland cells in pregnancy and keloid development in wound healing

85
Q

Metaplasia

A

Cellular adaptation in which cells of one type are replaced by cells of another type

86
Q

What is metaplasia normally caused by?

A

Chronic inflammation

87
Q

Give an example of metaplasia

A

Acid reflux causing the squamous cells of the esophagus to change to columnar cells that are more similar to stomach cells

88
Q

Dysplasia

A

Cellular adaptation that is deranged cellular growth within a specific tissue, often due to chronic inflammation or a precancerous condition

89
Q

Give an example of dysplasia

A

Cervical dysplasia (detected by Pap test)

90
Q

How do dysplastic cells differ from healthy cells?

A

They vary in size, shape, and architectural arrangement compared to healthy cells

91
Q

What alteration occurs when the active transport system (sodium potassium pump) is not occuring?

A

Osmotic balance altered, leading the cellular swelling

92
Q

What effect does a defective sodium potassium pump have on calcium?

A

Calcium pump also becomes deficient, leading to calcium accumulation in the cell and altered biochemical processes

93
Q

What factors contribute to accumulation of substances inside cells?

A

Abnormal metabolic function
Aging
Exposure to high amounts of environmental materials

94
Q

What are the consequences of intracellular accumulation?

A

Cell injury

95
Q

Give two examples of conditions associated with continual accumulation of substances within cells

A 
Alcoholism causing hepatocyte accumulation, leading to fatty liver 
Familial hypercholesterolemia (defective cholesterol metabolism)
96
Q

What is the most common cause of hypoxia?

A

Diminished circulation (ischemia)

97
Q

What are some additional causes of ischemia?

A 
Anemia
Low environmental oxygen
Inadequate diffusion at alveoli 
Suffocation injury 
Airway obstruction
98
Q

Describe ischemic reperfusion injury

A

When a tissue experiences transient ischemia and then circulation resumes, leading to oxidative stress and activation of damaging forces by free radicals, causing death to cells that might have otherwise recovered

99
Q

Free radicals

A

Reactive oxygen molecules caused as a byproduct of cellular energy production

100
Q

A potential consequence of free radicals is

A

Oxidative stress

101
Q

Oxidative stress

A

A form of cell injury in which free radical removal mechanisms are overwhelmed

102
Q

What is a disease that involves ischemic-reperfusion injury?

A

Heart disease

103
Q

What is the difference between endogenous and exogenous substances?

A

Endogenous: biological substances
Exogenous: synthetic substances

104
Q

How does hypernatremia cause cellular injury?

A

It causes cell dehydration and shrinkage

105
Q

What are some symptoms of hypernatremia?

A

Lethargy
Weakness
Irritability
Confusion

106
Q

How does hyperglycemia cause cellular injury?

A

High blood glucose reacts with endothelial membrane to produce advanced glycation end products that can damage arteries, kidneys, nerves, and retina of eyes

107
Q

What is VEGF?

A

Vascular endothelial growth factor

108
Q

What does VEGF do?

A

Stimulates the synthesis of collateral blood vessel branches

109
Q

What will endothelial damage do to blood flow?

A

Decrease it, because there will be less VEGF to stimulate blood vessel formation

110
Q

What does endothelial cell injury initiate?

A

Arteriosclerosis leading to cardiovascular disease

111
Q

Apoptosis

A

Genetically programmed degenerative changes leading to cell death

112
Q

Physiologic apoptosis example

A

Development of individual fingers from web-like structure in embryos

113
Q

Dysfunctional apoptosis example

A

Cells no longer doing apoptosis, giving rise to certain cancers

114
Q

What are the benefits of normal apoptosis?

A

Elimination of damaged or unwanted cells without inflammation or injury to surrounding tissue

115
Q

Cell necrosis

A

Cell death due to stressors that overwhelm the cells survival ability

116
Q

Infarction

A

Ischemic necrosis (death due to prolonged ischemia)

117
Q

Osteoblasts

A

Bone building cells that secrete osteoid to form bone matrix

118
Q

Osteocytes

A

Mature osteoblasts trapped in bony matrix. Help maintain metabolism and nutrient and waste exchange

119
Q

Osteoclasts

A

Bone breakdown cells. reabsorption and degradation of existing bones

120
Q

Bone modeling

A

Period in which osteoblast activity dominates and bone mass increases

121
Q

Bone remodeling

A

Mature bone breaking down and being renewed by osteoclasts activity

122
Q

What leads to hypertrophy of skeletal muscle?

A

Working it against high resistance

123
Q

Causes of atrophy

A

Long periods of immobility

124
Q

Function of tendons

A

Attach muscles to bones and transmit load from muscle to bone. Causes joint motion

125
Q

Example of well-known tendon

A

Achilles’ tendon

126
Q

Function of ligaments

A

Attaching bone to bone and creating joint stability

127
Q

Example of well-known ligament

A

ACL

128
Q

What is the impact of injury to tendons?

A 
Inflammation
Tendon weakening
Tendon rupture (prolonged healing process)
129
Q

Impact of injury to ligaments

A

Inability to return to normal shape —> rupture

Healing process replaces ligament with hypertrophic mass which provides less joint stability

130
Q

Muscular dystrophy

A

Progressively degenerative non-inflammatory muscle disorder

131
Q

Etiology of dúchenne muscular dystrophy

A

X-linked recessive genetic disorder

Half of cases arise from hereditary mutation, the other half arise from sporadic mutation

132
Q

Pathophysiology of muscular dystrophy

A

Defects in the genetic code for dystrophin (which is found in all muscle as well as brain tissue) causes T cells to attack the muscles. The dead muscle is then replaced with a fibrous fatty infiltrate

133
Q

The changes that occur due to muscle being replaced with fatty fibrous infiltrate in muscular dystrophy is called

A

Pseudo hypertrophy

134
Q

What are the initial clinical manifestations of muscular dystrophy?

A

Progressive muscle weakness without obvious cause

135
Q

What are additional clinical findings with muscular dystrophy?

A 
Waddling, wide based gait
Children not walking until 18 months or after 
Hyperlordosis of spine
Toe walking
Growers sign
Weakness
Poor posture
Pain and pseudohypertrophy in calves
136
Q

Describe multiple sclerosis

A

Progressive, demyelinating autoimmune disorder that causes inflammation and damage to nerve cells in the CNS and peripheral nerves

137
Q

Etiology of multiple sclerosis

A

Unknown, but is thought to be autoimmune and inflammatory

138
Q

What is the role of T cells in the development of MS?

A

It is theorized that they become abnormally sensitized to attack myelin, but exact role is unknown

139
Q

What are some risk factors for MS development?

A 
Being a woman
Heavy metal exposure 
Genetics
Virus/infection
Trauma
140
Q

Describe what happens in MS remission

A

Inflammation periodically resolves, allowing the demyelination to heal

141
Q

What happens when MS fails to go into remission?

A

There is no time for damage to heal, so demyelinated areas turn into fibrotic scar tissue, permanently disrupting/altering nerve impulse conduction

142
Q

What are common symptoms of MS?

A 
Weakness
Numbness
Tingling
Balance problems 
Blurred vision
Fatigue
143
Q

Describe how to remitting-relapsing form of MS works

A

Brief episodes that can last for a couple weeks to three months and occur every 1-3 years. Each episode is followed by a near complete return to normal

144
Q

What causes the vision problems that occur with MS?

A

Optic nerves are highly myelinated, so them being attacked can cause vision issues

145
Q

What kind of vision issues can be caused by MS?

A

Vision loss
Changed color perception
Pain with eye movement

146
Q

What are some symptoms of motor nerve damage with MS?

A 
Hemiparesis
Paraparesis
Quadriparesis 
Problems with walking and coordination 
Incontinence and sexual dysfunction
147
Q

Why are MS patients in late stages at higher risk for aspiration pneumonia?

A

Weakened esophageal muscles

148
Q

What are some risk factors for osteoarthritis?

A 
Aging
Obesity
Team sports participation
Joint trauma and overuse
Heavy occupational work
149
Q

Describe the etiology of osteoarthritis

A

Stress on the joints leads to degenerative alteration of articular cartilage, which leads to breakdown of chondrocytes and subchondral bone

150
Q

What is the impact of excessive pressure on a joint?

A

It wears away cartilage and exposes subchondral bone, leading to inflammation and swelling

151
Q

What is the role of proteoglycans in the progression of osteoarthritis?

A

Fluid substance secreted by chondrocytes to try to repair cartilage, but levels decrease as OA progresses, causing cartilage to lose elasticity and crack

152
Q

What are the consequences of damaged cartilage in osteoarthritis?

A

Bone is exposed, and the increasing stress on the bone exceeds the strength of the bone, increasing inflammation. The joint then thickens

153
Q

What are some presenting symptoms of osteoarthritis?

A 
Deep and aching joint pain
Swelling
Pain in cold or after activity 
Limited ROM
Fluid buildup
Does not have to be symmetrical
154
Q

What are herberden’s nodes and Bouchards nodes?

A

Swelling at interphalangeal joints in the hands

155
Q

Describe rheumatoid arthritis

A

Systemic, inflammatory autoimmune disorder affecting joints and other organs as well (heart, lungs, etc)

156
Q

What are factors that may play a significant role in development of RA?

A 
Age
Genetics
Being female
Past infections
Immunological factors
157
Q

What is the pathophysiology of RA?

A

The immune system attacks synovial tissues

158
Q

What are the consequences of the inflammatory process of RA?

A

Destruction of cartilage, bones, tendons, and ligaments

Damage to heart, lungs, etc

159
Q

What is the role of activated T cells in the progression of RA?

A

They secrete cytokines, which bring white blood cells to the area, which escalates inflammation

160
Q

What is the result of continual inflammation of the synovial membrane?

A

Hypertrophy in pannus of the joint and loss of cartilage

161
Q

What are the classic symptoms of RA?

A

Symmetrical, tender, swollen joints
Fever
Fatigue
Malaise

162
Q

What are the consequences of chronic joint inflammation associated with RA?

A

Permanent damage to surface of joints and mobility limitations

Krystan: Semester Two Nursing School (13 decks)

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