2920 Pathophysiology Exam Two Flashcards
(202 cards)
1
Q
what are the four stages of the pain process in the body?
A
transduction
transmission
perception
modulation
2
Q
what happens in the transduction stage of pain?
A
unpleasant stimuli causes cell damage, which causes the release of chemicals like prostaglandins and histamine, activating nociceptors and generating an action potential
3
Q
what do we do as nurses to prevent pain transduction?
A
numb areas where pain could occur
4
Q
what happens in the transmission stage of pain?
A
action potential travels from injury site to spinal cord, and then from the spinal cord to the brain
5
Q
what do we do as nurses to prevent pain transmission?
A
give opioids and other kinds of blockers
6
Q
what happens in perception of pain?
A
the brain processes and consciously experiences the pain
7
Q
T/F: there must be painful stimuli present for the brain to perceive pain
A
False, no painful stimuli is necessary for the brain to still process and feel pain
8
Q
what do we do as nurses to control pain perception?
A
give things like opioids, adjuvants, and antidepressants
9
Q
what happens in the modulation stage of pain?
A
descending neurons release substances like endogenous opioids to inhibit nociceptive impulses
10
Q
what are characteristics specific to acute pain?
A
sudden onset pain occurring with new tissue injury or inflammation
lasts hours to days and usually resolves with the healing of the disorder
lasts less than 3 months
11
Q
what are some signs and symptoms that might accompany acute pain?
A
increased respirations, heart rate, and blood pressure diaphoresis anxiety confusion grimacing, moaning, crying
12
Q
what is nociceptive pain?
A
pain caused by damage to somatic or visceral tissue
13
Q
amount of pain depends on what in nociceptive pain?
A
amount of cell damage
14
Q
what are typical treatment methods for nociceptive pain?
A
opioid and non-opioid medications adjuvant meds nerve blocks neuroablation massage exercise TENs heat/cold accupuncture distraction and relaxation
15
Q
what are the two types of nociceptive pain?
A
somatic (superficial and deep)
visceral
16
Q
what is neuropathic pain?
A
pain caused by injury or malfunction of spinal cord or peripheral nerves. Nerve pain!
17
Q
what are typical characteristics of neuropathic pain?
A
shooting, burning, numb, tingling, electric shock-like, or pins and needles sensations
18
Q
what are common treatment methods for neuropathic pain?
A
TENS units
antidepressants and adjuvant medications
gabapentin
potentially acupuncture
19
Q
what are some common causes of neuropathy?
A
neuralgias, spinal nerve radiopathy, diabetes, postsurgical pain
20
Q
what can cause central neuropathic pain?
A
post stroke pain or MS
21
Q
what can cause peripheral neuropathies?
A
diabetes or alcohol neuropathy
22
Q
what can cause deafferentation neuropathy?
A
phantom limb sensations or post-mastectomy pain
23
Q
what can cause sympathetically maintained neuropathic pain?
A
phantom limb pain
24
Q
what is the definition of hospice?
A
having less than 6 months to live as determined by two physicians
25
what is the goal of hospice pain care?
allowing patients to die with dignity and little to no pain
26
what are the endocrine and metabolic effects of unrelieved pain?
increased cortisol and epinephrine release
| decreased insulin production
27
what are the consequences of increased stress hormones and decreased insulin in acute pain?
```
increased metabolic activity
increased RR and HR
shock
glucose intolerance
hyperglycemia
fluid overload
hypertension
urinary retention
```
28
what are the cardiovascular effects of unrelieved pain?
increased HR, cardiac output, and resistance
| increased coagulation and myocardial oxygen demand
29
what are the consequences of the cardiovascular effects of unrelieved pain?
hypertension
unstable angina
MI
deep vein thrombosis
30
what are the respiratory effects of unrelieved pain?
decreased tidal volume
hypovolemia
decreased coughing
sputum retention
31
what are the consequences of the respiratory effects of unrelieved pain?
atelectasis
| pneumonia/infection
32
what are the renal effects of unrelieved pain?
decreased urine output
urinary retention
increased ADH release
33
what are the consequences of the renal effects of unrelieved pain?
higher infection risk
| fluid and electrolyte imbalances
34
what are the effects and consequences of unrelieved pain on the GI system?
decreased motility, leading to constipation, anorexia, and paralytic ileus
35
what are the musculoskeletal effects and consequences of unrelieved pain?
muscle spasm and impaired muscle function leading to immobility, weakness, and fatigue
36
what are the neurological effects and consequences of unrelieved pain?
impaired cognitive function, leading to confusion and impaired ability to think/reason/make decisions
37
what are the immunologic effects and consequences of unrelieved pain?
decreased immunity, increasing infection risk
38
what are benefits of using nonopioids for pain?
fewer side effects than opioids
39
what are nursing considerations when administering NSAIDs for pain?
NSAIDs have an analgesic ceiling
patients need to be monitored for bleeding/renal failure/tylenol toxicity
use lowest dose for shortest possible time
40
what is an analgesic ceiling?
limit to effectiveness of medication, where taking more than recommended dose does not offer any extra pain relief
41
what are benefits to opioids to control pain?
no analgesic ceiling
| very effective at controlling moderate to severe pain
42
what are drawbacks to administering opioids to control pain?
many side effects, such as respiratory depression/arrest, constipation (most common side effect), toxicity, sedation, N/V
43
what are nursing considerations when administering opioids?
check on patients 15-30 minutes after giving IV opioid or 30 min-1 hour after giving oral opioid
have naloxone on hand
start with a low dose and increase slowly
44
what are adjuvant analgesics and how are they often used?
drugs developed for other purposes that have also been found effective in controlling pain. can be given with opioid/non-opioid drugs or alone
45
what are some examples of adjuvant analgesics?
corticosteroids
antidepressants
antiseizure drugs
anasthetics
46
what is a PCA pump?
patient controlled analgesia pump: a pump which the patient can use to self administer a preset analgesic dose
47
what is the benefit of a PCA pump?
it helps the patient avoid severe fluctuations in pain level and gives the patient an active role in pain management
48
what are nursing considerations when a patient is using a PCA pump?
the patient must be taught how to use it correctly
patient and family must be educated about benefits of the pain pump
educate about side effects
it is illegal for someone else to push the PCA pump button for the patient (including the nurse!)
49
what are nursing considerations when using ice/cold to help with pain?
cover the cold source with a towel or blanket to avoid burns
alternate with cold on and off the site
cold is usually the most effective in reducing inflammation in the first 24 to 48 hours after a trauma
50
what are nursing considerations when using heat to help with pain?
don't use heat on areas with menthol products/muscle relaxant creams
cover heat source with towel
dont put heat on radiation sites, active bleeds, recent injuries, or areas with decreased sensation
51
what is the difference between inflammation and immunity?
inflammation is guaranteed if an injury occurs, and it is non-specific
immunity is not guaranteed, but it has memory and is specific to a certain organism or protein
52
what are the two stages of the vascular response of inflammation?
vasoconstriction (very short time period)
| vasodilation
53
what happens during the cellular response phase of inflammation?
white blood cells move to the site of an injury and begin working
54
what are the first kinds of WBCs on scene when an injury occurs?
neutrophils and monocytes
55
what is exudate comprised of?
fluid and leukocytes
56
what are the two methods of healing and what is the difference between the two?
regeneration: replacement of lost cells and tissues with the same type of cells
repair: lost cells are replaced with connective tissue and scar tissue is formed
57
why was the rule of nines invented?
to easily estimate the extent of damage with burns
58
what burn characteristics make burns especially severe and in need of specialized burn care?
burns over 25% of the body or more
burns on the face or neck
third degree burns anywhere
59
what is the extent of damage for first degree burns?
only the epidermal layer is damaged
60
how long do first degree burns take to heal?
usually only 3-5 days
61
what skin structures are damaged with first degree burns?
none. tactile and pain sensors, plus skin functions, are all still intact
62
what skin layers are damaged in second degree burns? answer for both superficial partial thickness and deep partial thickness
superficial: epidermis and and papillary dermal layer
deep: epidermis + papillary and reticular layer of dermis
63
how long do second degree burns take to heal and what may be some defining characteristics?
can take 3-6 weeks to heal and may need skin grafting
these burns will blister and may scar when they heal
64
what skin structures/functions are damaged in second degree burns?
nerve endings are damaged but patient will probably still have pain
skin functions are absent (no more bacterial barrier or water vapor barrier)
65
what skin layers are damaged in third degree burns?
epidermis, dermis, hair follicles, and all underlying structures are destroyed/damaged
66
what will third degree burns look like?
white, red, black, brown, or red, with lots of edema
67
how long do third degree burns take to heal and what will be required?
take months to heal, and usually dont heal well without surgery or grafts
68
what skin structures/functions are damaged in third degree burns?
skin functions are absent, so no bacterial barrier or water vapor barrier
nerve endings are destroyed, so patient usually doesnt have pain directly at burn site
69
what skin/body layers are involved in a fourth degree burn?
all layers involved in a third degree plus damage to muscle, bone, and/or tendons
70
what are treatment options for fourth degree burns?
surgical intervention or possible amputation
71
what kind of burns make up 90% of burn injuries?
thermal burns
72
characteristics/causes of thermal burns
exposure to fire, hot objects, scalding liquids, heat, or steam. can be caused by temps over 111 degrees
73
what are causes of scald burns?
Exposure to hot liquids or grease, at temps over 158
74
what are characteristics of scald burns?
necrosis and cell death that occurs within minutes
75
what do chemical burns do to the body?
induce protein coagulation in the tissues
76
what will skin look like with chemical burns and what should one do if chemically burned?
skin will have a grey discoloration
| the chemical must be neutralized, and one should take off their clothing and irrigate the area thoroughly
77
what do electrical burns do to the body?
the electrical current damages the body as it passes through, causing intense tissue damage and cell death. damage can continue worsening for many days without outward signs
78
severity of radiation burns is determined by amount of what?
rads
79
what will radiation burns look like outwardly?
usually like a sunburn, but they can do deep damage
80
explain the fluid and electrolyte shifts that happen in severe burns
vascular permeability increases, causing severe edema and third spacing
potassium moves out of the cell, causing hyperkalemia
sodium and water move into the cell, causing cellular swelling
81
what are the primary concerns with fluid/electrolyte changes in burns?
hypovolemic shock and cardiac dysrhythmias
82
what effect do burns have on metabolism?
induce a hypermetabolic state in the body, increasing temperature, calorie use, oxygen consumption, and heat production
83
explain the cardiovascular responses in severe burns
severe dehydration causes hemoconcentration and risk for clots
hemolysis can occur due to changes in blood chemistry
decreased cardiac output due to fluid shifting and peripheral vasoconstriction
84
what is compartment syndrome?
when edema is so severe it puts pressure on vessels and organs (to the point where they may be damaged/obstructed)
85
what is the number one killer in severe burns?
respiratory damage
86
explain the pulmonary response in severe burns
increased respirations from pain and anxiety
airway edema from heat and mucosal damage
inhalation injury causing loss of cilia, decreased surfactant, edema, and release of inflammatory substances
87
what does increased fluid from burns do to the lungs?
decreases lung compliance, and causes atelectasis and hyperoxemia
88
what respiratory issue are burn patients at risk for?
ARDS
89
explain the metabolic/GI effects in severe burns
decreased blood flow to the GI tract causes malabsorption and ischemia
bacterial leaking causes severely decreased immunity
body goes into hypermetabolic state
90
what two GI issues are burn patients specifically at risk for?
stress ulcers
| paralytic ileus
91
explain the renal response in severe burns
decreased blood flow due to hypovolemia activates the RAAS, causing sodium and water retention and electrolyte loss
renal ischemia can lead to acute renal failure
92
what about burns can cause intrarenal renal failure?
breakdown of hemoglobin and myoglobin due to damage can cause these pieces to get lodged in the renal tubules, causing acute tubular necrosis
93
explain the pathophysiology of deep vein thrombosis
thrombus development in deep veins of lower extremities, especially at an area of inflammation
94
what is a DVT comprised of?
fibrin
platelets
RBCs
WBCs
95
what is virchow's triad?
a triad of risk factors for DVT, which includes hypercoagulability, venous stasis, and intravascualar vessel wall damage
96
what test will tell if a patient is at risk for a clot/DVT?
D-dimer
97
what are other risk factors for DVT?
```
history of vein injury/varicose veins
recent surgery
drugs increasing coagulation
smoking/tobacco use
obesity
sitting for long periods of time
```
98
how might patients describe DVT pain?
```
aching
numb
burning
tingling
hot
swollen
```
99
explain the pathophysiology of pulmonary embolism
a venous thrombus or other thrombus goes through the inferior vena cava into the right side of the heart and then enters pulmonary circulation. it will lodge in the lungs and everything distal to it will die
100
where do PE's normally lodge?
lower lobes of the lungs
101
what can PE's be made of?
venous clots, fat, air, or tumor fragments
102
what are risk factors for PE?
```
all the risk factors for DVT, plus
central line placement
ARDS
inhaled toxins
high altitude
```
103
what are some signs and symptoms of PE?
SOB
anxiety
tachypnea
sense of impending doom
104
how quickly can burn shock develop?
within 20 minutes of getting burned
105
what happens to the blood when the vascular system is dehydrated?
hematocrit and viscosity increase, causing potential for clots
106
what are some of the first warning signs after a head injury?
```
changes in LOC
bleeding or drainage from nose
blurred vision
loss of sensation
slurred speech
vomiting
changes in pupil reactivity
```
107
what is the pathophysiology of traumatic brain injury?
either a focal or diffuse injury to the brain causes swelling of neurons and axons, leading to release of chemicals and changes in metabolic activity in the brain
this will result in hypoxemia, ischemia, and edema in the brain
108
what are some clinical manifestations of traumatic brain injury?
```
decreased LOC
vomiting
seizing
posturing
cushings triad
altered pupil response
loss of gag reflex
```
109
what is cushings triad?
increased blood pressure with widened pulse pressure
decreased heart rate
abnormal respirations
110
why might patients with traumatic brain injury experience diabetes insipidus?
swelling around the pituitary might hinder release of ADH, so tons of urine output
111
what drug will be given to correct diabetes insipidus?
vasopressin (artificial ADH)
112
what in the brain controls LOC/wakefulness?
RAS - reticular activating system
113
decorticate posturing
limbs turning in
114
decerebrate posturing
limbs turn out/extend
115
which type of posturing is worse, and why?
decerebrate, because it indicates that blood has progressed closer to the brain
116
what do seizure precautions entail?
```
padded side rails
bed in the lowest position
patent IV site
suction ready to use
keep things out of mouth
dont leave patient alone
low lights and stimuli
```
117
what is the most common TBI?
concussion
118
what will the nurse see in a patient with a concussion?
```
altered LOC
headache
dizziness
balance issues
amnesia
```
119
what are the three types of skull fractures?
linear: does not affect brain tissue
depressed: commonly an open wound and does affect brain tissue
basilar: temporal bone at base of skull
120
what are risks of skull fractures?
infections like meningitis
121
what are signs of CSF leak?
dripping from the nose or ears
| clearing back of throat repeatedly
122
how would one assess for a halo sign and what does it look like?
wipe dripping nose or ears with gauze
| if there is a yellow outer ring to the fluid, it indicates a CSF leak
123
what is a contusion?
a focalized brain bruise
124
what usually causes contusions?
coup-contrecoup injuries or penetrating TBI
125
what are some manifestations of brain contusions?
```
severe headache
dizziness
vomiting
memory loss
sudden weakness in one arm or leg
hypertension
decreased HR/RR
```
126
what is an epidural hematoma?
bleeding in the space between the dura mater and the skull, usually an arterial bleed that develops quickly and has a low survival likelihood
127
what normally causes epidural hematomas?
skull bone fractures
128
what are some manifestations of epidural hematomas?
```
loss of consciousness
severe headache
vomiting
seizures
cushings triad
positive babinski
ipsilateral hemiplagia
```
129
what is a subdural hematoma?
bleeding in the space between the dura mater and above the arachnoid membrane, usually a venous bleed that develops more slowly than an epidural hematoma
130
how long does it normally take for a subdural hematoma to form?
usually begins within 72 hours of a head injury when subdural veins tear
131
what are risk factors for traumatic brain injury?
```
contact sports
driving cars (especially between the ages of 15 and 24)
gunshot wounds
exposure to explosions
children between the ages of 0 and 4
elderly people
falls
being male
```
132
why are elderly people at higher risk for TBI?
the brain starts shrinking, making it easier for it to bounce around in the head
133
what are the different classifications of TBI?
blunt injury
coup-contrecoup (acceleration/deceleration)
penetrating
134
what does the glasgow coma scale measure and what areas does it evaluate?
it measures level of consciousness and it looks at eye, verbal, and motor response
135
pathophysiology of ischemic CVA
obstruction in cerebral blood flow from thrombus or embolus. this ischemia leads to cerebral infarction
136
explain what happens with glutamate and electrolytes when brain ischemia happens
calcium, sodium, and water enter the cells, making them swell
potassium leaves the cell, and glutamate, which is the most important normal neurotransmitter, becomes toxic to brain tissue and extends the area of injury
137
pathophysiology of hemorrhagic CVA
cerebral artery ruptures and can no longer bring blood to the brain. the blood that spills into the brain tissue causes ischemia, cerebral edema, and brain cell death
138
what is the most common cause of hemorrhagic CVA?
hypertension
139
what are manifestations of left sided CVA?
```
awareness of deficits
aphasias
language and math issues
slow, cautious performance
right sided weakness
impaired left/right discrimination
depression and anxiety
```
140
what are manifestations of right sided CVA?
```
paralyzed left side
denial or neglect of deficits
impulsivity
spatial perceptual deficits
rapid actions and short attention span
safety and risk issues
impaired judgement
impaired time concepts
```
141
what are some other general manifestations of CVA?
facial drooping
slurred speech
vision/sensation loss
neurological deficits
142
what is a TIA?
transient ischemic attack
a temporary change in neurological status that resembles a stroke but resolves on its own. usually caused by an embolus that dissolves on its own
143
should TIA patients still be evaluated? why?
yes, because it signals impending stroke in about 1/4 of cases
144
what are the three main risk factors for ischemic strokes?
a fib
cerebral arteriosclerosis
carotid stenosis
145
what two conditions combined put a patient at much higher stroke risk?
diabetes and hypertension
146
what are other major risk factors for stroke?
```
hypertension
high cholesterol
heart disease
diabetes
obesity
smoking
previous stroke or TIA
sickle cell disease or other blood diseases
inactivity
oral contraceptives
family history
age over 65
being male
ethnicity: AA, NA, HA, alaskan
stress
```
147
what are the three components that make up the intracranial space and what percentages are they?
blood: 10-15%
brain tissue: 78-80%
CSF: 10%
148
if the brain swells enough, where will the swelling go?
through the foramen and onto the brainstem, which will lead to brain death
149
what is normal ICP?
7-15 mmHg in a resting adult
150
ICP above what indicates need for immediate intervention?
above 20 mmHg
151
what is the monro-kellie doctrine?
concept of maintaining normal ICP that states that an increase in pressure in one brain compartment is compensated by a decrease or change in the other compartments
152
what are the three ways the body will try to compensate for increased ICP?
CSF changes: moving it or decreasing production
intracranial blood volume changes
brain tissue compression or distension
153
what happens if the body cannot compensate for increased ICP?
brain herniates and the patient dies
154
what are clinical manifestations of increased ICP?
```
headache
vomiting
decreased LOC
altered pupil response to light (late sign)
Cushings triad
posturing
seizing
```
155
what is MAP?
mean arterial pressure, its the amount of pressure needed to perfuse vital organs adequately
156
what MAP number is needed for adequate perfusion?
60 mmHg
157
how is map calculated?
SBP plus 2 times DBP all divided by 3
158
shock happens because cells cant get what two things?
either oxygen or glucose
159
in general, what is shock?
decreased tissue perfusion and impaired cellular metabolism that can be caused by multiple mechanisms
160
what substance is formed in the body when the body cannot get either adequate oxygen or glucose?
lactic acid
161
what are the end results in shock, no matter the mechanism?
decreased cardiac output, decreased tissue perfusion, and impaired cellular metabolism
162
what are cardiac manifestations of shock in most cases?
tachycardia and decreased BP
163
what are metabolic manifestations of shock?
lactic acidosis
| decreased insulin production
164
what are urinary manifestations of shock?
decreased urine output and renal flow
165
decreased urine output and renal flow will activate what?
the RAAS
166
what are GI manifestations of shock?
decreased peristalsis
decreased bowel sounds
leaky gut
167
what are respiratory manifestations of shock?
crackles and tachypnea (because of metabolic acidosis)
168
what are behavioral manifestations of shock?
anxiety, confusion, and agitation
169
what will the skin look like in shock?
pale and clammy
170
which kinds of shock are known as "warm shock" and why?
septic and anaphylactic, because patients will likely have a fever and rosy complexion
171
which kind of shock may have bradycardia as a manifestation?
neurogenic shock
172
what are the four stages of shock?
initial stage
progressive stage
irreversible stage
complete organ failure
173
what happens in the initial stage of shock?
sudden drop in tissue perfusion activates the SNS and RAAS, leading to tachycardia and vasoconstriction
174
will patients in the initial stage of shock be symptomatic?
not necessarily
175
what is a tell-tale sign in the initial stage of shock?
increased lactic acid
176
which stage of shock is the easiest to reverse?
initial stage
177
what happens in the progressive stage of shock?
the lungs, kidneys, gut, pancreas, and liver have decreased perfusion. kidneys may fail, GI and liver may be ischemic, and toxins will accumulate in the body. this is the turning point in shock
178
what happens in the irreversible stage of shock?
decreased cardiac and brain perfusion can cause MI or strokes. lactic acid builds up, and sodium and water enter cells while potassium leaves, causing cell death
179
what are the four priorities for emergency management of shock?
oxygen and ventilation
fluid resuscitation
drug therapy
nutritional therapy
180
why is nutritional therapy crucial in shock?
because if the mucosal lining starts breaking down and leaking bacteria, sepsis will rapidly occur
181
what is cardiogenic shock?
severe hypotension (less than 90 mmHg) for 30 minutes or longer even with adequate fluid resuscutation
182
what are the four types/causes of cardiogenic shock?
```
systolic dysfunction (heart cant pump)
diastolic dysfunction (heart cant fill)
dysrhythmias
structural factors
```
183
what is the main systolic issue that can cause shock?
severe acute MI
184
what are some examples of diastolic dysfunction that can lead to shock?
cardiac tamponade, ventricular hypertrophy, cardiomyopathy
185
why can dysrhythmias cause cardiogenic shock?
because the heart is filling and beating poorly, leading to inadequate perfusion
186
what kind of structural factors can cause cardiogenic shock?
valvular stenosis, ventricular septal rupture, tension pneumothorax
187
what are the two types of hypovolemic shock? describe them
absolute hypovolemia: loss of blood or fluids from the body
| relative hypovolemia: volume is present but in the wrong space in the body
188
what are some causes of absolute hypovolemia?
hemorrhage, diarrhea
189
what are some causes of relative hypovolemia?
burns
sepisis
bowel obstruction
being pinned under a fallen structure
190
what are the three types of distributive shock?
neurogenic shock
septic shock
anaphylactic shock
191
what is neurogenic shock?
shock caused by spinal cord injury or dysfunction (usually at T5 or above) causing bradycardia and major vasodilation because the parasympathetic nervous system takes over
192
what is anaphylactic shock?
massive vasodilation in the body as a hypersensitivity response to an allergen
193
what is septic shock?
massive vasodilation in response to a systemic infection
194
what is obstructive shock?
physical obstruction impeding filling or outflow of blood, causing reduced cardiac output
195
what are some causes of obstructive shock?
```
cardiac tamponade
tension pneumothorax
superior vena cava syndrome
compartment syndrome
PE
```
196
what is SIRS?
sudden inflammatory response syndrome, an overwhelming inflammatory response to infection, ischemia, infarction, or injury
197
list criteria for SIRS diagnosis
```
tachycardia (over 90 BPM)
tachypnea (over 20/min)
hyperthermia (over 100.4)
hypothermia (less than 96.8)
WBCs greater than 12000 or less than 4000 or greater than 10% immature forms
```
198
how many criteria must be present for SIRS diagnosis?
at least two
199
what is the pathophysiology of sepsis?
body-wide infection overwhelms the immune system and compromises multiple organs
200
what do endotoxins cause in the body in sepsis?
vasodilation and release of cytokines
201
what does platelet activating factor released in sepsis lead to?
formation of microthrombi, which can block capillaries
202
what are manifesations of sepsis?
```
SIRS diagnostic criteria
hypotension even with adequate fluid resuscitation
poor perfusion and hypoxia
altered neuro status
decreased urine output
GI dysfunction
increased c-reactive protein
fluid retention
increased coagulation
```
