Exam 5 Flashcards
(120 cards)
1
Q
primary headaches
A
not caused by disease or another medical condition
2
Q
secondary headaches
A
caused by another condition or disorder (sinus infection, neck injury, or stroke)
3
Q
primary classifications of headaches
A
- tension-type
- migraine
- cluster
4
Q
tension-type headaches
A
- characterized by bilateral location and pressing/tightening quality
- usually of mild or moderate intensity
5
Q
most common type of headache
A
tension-type
6
Q
migraine headache
A
- recurring headaches
- unilateral or bilateral throbbing pain
- a triggering event or factor
- manifestations associated with neurologic and ANS dysfunction
7
Q
categories of migraine headache
A
- migraine without aura (most common)
- migraine with aura
8
Q
cluster headache
A
- rare form of headache
- sharp, stabbing pain
- can occur repeatedly for weeks to months at a time, followed by periods of remission
- one of the most severe forms of head pain
- all over the face
9
Q
what can occur with a pts. mood if they have a cluster headache?
A
they can become agitated and restless
10
Q
acute treatment for a cluster headache
A
inhalation of 100% oxygen at 6-8 L/min for 10-20 min
11
Q
PAD
A
involves progressive narrowing and degeneration of arteries of upper and lower extremities
12
Q
leading cause of PAD
A
atherosclerosis
13
Q
intermittent claudication
A
- ischemic muscle pain that is caused by a constant level of exercise
- caused by buildup of lactic acid resulting from anaerobic metabolism
- resolves within 10 minutes
- reproducible
14
Q
what should you do if you have intermittent claudication?
A
sit down until it stops
15
Q
clinical manifestations of PAD
A
- intermittent claudication
- paresthesia
- thin, shiny, taut skin
- loss of hair on lower legs
- diminished or absent pedal, popliteal, or femoral pulses
- pallor of foot with leg elevation
- reactive hyperemia of foot with dependent position
- pain at rest (mostly at night)
16
Q
complications of PAD
A
- atrophy of skin and underlying muscles
- delayed healing
- wound infection
- tissue necrosis
- arterial ulcers
- nonhealing arterial ulcers and gangrene are most serious complications
- may result in amputation
17
Q
risk factor modification for PAD
A
- tobacco cessation
- aggressive treatment of hyperlipidemia (dec. LDL and triglycerides, inc. HDL)
- BP <140/90
- A1C < 7.0% for diabetes`
18
Q
what does exercise do in PAD?
A
improves oxygen extraction in the legs and skeletal metabolism
19
Q
ideal waist circumference
A
men: < 40 inches
women: < 35 inches
20
Q
percutaneous transluminal balloon angioplasty (PTA)
A
- used for PAD
- involves the insertion of a catheter through the femoral artery
- balloon is inflated dilating the vessel by compressing atherosclerotic intimal lining
- stent is places
21
Q
atherectomy
A
- removal of the obstructing plaque
- can lead to clot floating around in circulation
22
Q
cryoplasty
A
- combines percutaneous transluminal angioplasty and cold therapy
- liquid nitrous oxide - the cold limits restenosis by reducing smooth muscle cell activity
- freeze it
23
Q
what should we monitor for after a surgery with PAD?
A
- skin color and temperature
- capillary refill
- presence of peripheral pulses distal to the operative site
- sensation and movement of extremity
24
Q
what position should be avoided after PAD surgery?
A
knee-flexed except for exercise
25
what do we want to tell someone for home care after surgery with PAD?
- manage risk factors
- long-term aspirin therapy
- gradual physical activity
- meticulous foot care
- inspection of the feet
- comfortable shoes with rounded toes and soft insoles
- shoes lightly laced
26
acute arterial ischemic disorders
- sudden interruption of arterial blood supply
- if persists can cause tissue death
27
clinical manifestations of acute arterial ischemic disorders
SIX Ps
- Pain
- Pallor
- Pulselessness
- Paresthesias
- Paralysis
- Poikilothermia (adaptation of the limp to environmental temperature)
28
how do we treat raynaud's?
- teach to avoid temperature extremes-wear gloves
- immerse hands in warm water
- stop all tobacco, caffeine, or any vasoconstricting drugs
- debridement or sympathectomy (cut nerves)
29
how do we treat phlebitis?
- remove IV
- warm moist heat and elevation
- NSAIDs
30
virchow's triad
- venous stasis
- endothelial damage
- hypercoagulability of blood
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clinical manifestations of VTE
- superficial: palpable cord, warm, tender, reddened area around the affected vein
- deep: unilateral leg pain, tenderness, warm skin, erythema, leg edema
32
complications of VTE
- PE
- post thrombotic syndrome: persistent edema, pigmentations, varicosities, lipodermatosis
33
nursing care when giving anti-thrombolytics
- monitor VS
- examine for signs of bleeding
- evaluate labs
- avoid IM injections, use small calibers needles, hold pressure
34
clinical manifestations of varicose veins
- heavy achy feeling after prolonged standing
- relieved by walking or elevation of limb
35
treatment of chronic venous insufficiency and venous leg ulcers
- compression
- wound care
- nutrition
- position changes
- walking
36
modifiable risk factors for CVA
- HTN
- a fib
- DM II
- serum cholesterol
- smoking
- alcohol consumption
- sedentary lifestyle
- hypercoagulable state
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non-modifiable risk factors for CVA
- age >65
- women increased risk due to increased estrogen
- blacks
- family history
38
normal LDL levels
< 100
39
normal triglyceride levels
< 150
40
normal HDL levels
> 40
41
BEFAST of stroke
Balance off
Eyes - unclear vision
Face/facial droop
Arms/legs weak
Speech slurred, confused
Time lost is brain lost
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ischemic stroke
lack of blood flow, lack of O2 to brain
43
hemorrhagic stroke
something bleeding into brain
44
prehospital principles to help with a stroke
- keep airway safe
- O2 if sat <90%
- check BG, treat less than 60
- avoid treating HTN: permissive HTN for 24 hours, post tPA >180/105, no tPA >220/120
- report to ED
45
eligibility criteria for tPA
- ischemic stroke causing measurable neurologic deficit
- time from onset of stroke symptoms less than 4.5 hours before tPA administration
- NIHSS >5
46
what is the relationship between HTN and cardiovascular disease?
direct
47
BP =
CO x SVR
48
definition of HTN
- sys. BP >=140 mm Hg
- dia. BP >=90 mm Hg
- current use of antihypertensive drugs
49
definition of prehypertension
- sys. BP 120-139 mm Hg
- dia. BP 80-89 mm Hg
50
primary HTN
- elevated BP without an identified cause
- 90-95% of all cases
51
secondary HTN
elevated BP with a specific cause
52
epilepsy
- condition in which a person has spontaneously recurring seizures caused by underlying chronic condition
- in US, 3 million people have epilepsy
53
what is the main goal in a tonic-clonic seizure?
SAFETY
54
how are focal seizures divided?
- simple focal seizures
- complex focal seizures
55
simple focal seizures
person remains conscious
56
complex focal seizures
- person has change or loss of consciousness
- produces a dreamlike experience
57
complications of epilepsy
- status epilepticus
- tonic-clonic status epilepticus
- severe injury and death from trauma during a seizure
- effect on lifestyle
58
status epilepticus
- a state of constant seizure or condition when seizures recur in rapid succession with out return to consciousness between seizures
- most serious complication
- neurologic emergency
- can involve any type of seizure
- causes the brain to use more energy than is supplied
- neurons become exhausted and cease to function
- permanent brain damage can result
59
tonic-clonic status epilepticus
- most dangerous
- can cause ventilatory insufficiency, hypoxemia, cardiac arrhythmias, hyperthermia, systemic acidosis
- can be fatal
- ask them if they breathe in post-ictal state!!!!
60
mortality rate with epilepsy
2-3 times the rate of the general population
61
when should we seek immediate medical care in a seizure?
- status epilepticus occurs
- significant bodily harm occurs
- the event is a first- time seizure
62
what do we give initially in status epilepticus?
rapid-acting IV lorazepam (Ativan) or diazepam (Valium) followed by long-acting drugs
63
what do neurologic assessment test for in seizures?
- testing for toxicity
- nystagmus
- hand and gait coordination
- cognitive functioning
- general alertness
64
gerontologic considerations in seizures
- consider liver function (can become toxic)
65
health promotion for seizures
- promote safety measures
- wear helmet if risk for head injury
- general health habit (diet, exercise)
- assist to identify events or situations precipitating seizures and avoid if possible
- instruct to avoid excessive alcohol, fatigue, and loss of sleep
66
acute intervention for seizures
- maintain patent airway, support head, turn to side, loosen constrictive clothing, ease to floor
- do not restrain
67
classic triad of PD
- tremor
- rigidity
- bradykinesia
68
tremor
- so minimal initially that only the patient notices
- more prominent at rest and is aggravated by emotional stress or increased concentration
- describe as pill rolling
69
rigidity
- increased resistance to passive motion when limbs are moved through ROM
- typified by a jerky quality when joint moved
- similar to intermittent catches in the movement of a cogwheel
- complaint of soreness, feeling tired and achy, pain in the head, upper body, spine or legs
70
bradykinesia
- slowing down in initiation and execution of movement
- evident in loss of autonomic movements: blinking, swinging of arms while walking, swallowing, self-expression with facial movement
71
what do we want to ensure with PD when they are eating?
can cause dysphagia, so food needs to be easily chewed and swallowed
72
what can we do to help PD when they are discharged home?
- remove rugs and excess furniture
- simplify clothing from buttons and hooks
- use elevated toilet seats
- use ottoman to elevate legs
73
myasthnia gravis
mouth to ground; muscles
74
GB syndrome
ground to brain; worried about when it gets to diaphragm controlled by brain
75
ALS (Lou Gehrig)
froze, loss of function in muscles everywhere except face; "frozen in own body"
76
huntington's
genetic, "sneaky movement"
77
multiple sclerosis
- chronic, progressive, degenerative disorder of the CNS
- characterized by segmental demyelination of nerve fibers of the brain and spinal cord
78
when is the onset of MS
20-50 years of age
79
who is affected more with MS?
- women are affected 2-3 times more than men
- 5x more prevalent in temperate climates (don't get a lot of vitamin D)
80
how do researchers believe MS develops?
in genetically susceptible person as a result of environmental exposure, infection, smoking, physical injury, emotional stress, excessive fatigue, pregnancy, and a poorer state of health
81
is MS autoimmune?
yes, it is orchestrated by activated T cells
82
what happens with the T cells in MS?
they migrate to the CNS, cause blood-brain disruption. subsequent antigen-antibody reaction leads to demyelination of axons
83
what does pregnancy do with autoimmune disease?
it makes them better
84
most common classification of MS
relapsing-remitting: it is the most manageable too
85
are there any diagnostic tests for MS?
- no definitive
- based on history, manifestations, diagnostic tests
- MRI of brain and spinal cord may show the presence of plaques, inflammation, atrophy, and tissue breakdown and destruction
- CSF increased in IgG and presence of oligoclonal banding
86
for a diagnosis of MS, what must happen?
- evidence of at least 2 inflammatory demyelinating lesions in at least 2 different locations within the CNS
- damage or an attack occurring at different times (usually >= 1 month apart)
- all other possible diagnoses must have been ruled out
87
is there a cure for MS?
- no cure; collaborative care is aimed at slowing disease process and symptomatic relief
- risk of side effects and end organ damage versus rate of progression and severity of attacks
88
planning for MS
- maximise NM function
- maintain independence
- manage disabling fatigue
- optimize psychosocial well-bring
- adjust to illness
- decrease factors that precipitate exacerbations
- teah patient
89
vascular dementia
- loss of cognitive function due to brain lesions cause by CV disease
- result of decreased blood supply from narrowing and blocking of arteries that supply brain
- can be caused by a single stroke or multiple strokes
- can be prevented through treatment of risk factors: HTN, diabetes, smoking, hypercholesterolemia, dysrhythmias
90
what is the greatest risk factor for dementia?
aging; not a normal part of aging
91
what does family history have to do with dementia?
those with a 1st degree relative at higher risk
92
other predisposed risks of dementia
- diabetes mellitus
- head trauma
- obesity
- smoking
- cardiac dysrhythmias
- HTN
- hypercholesterolemia
- CAD
93
acute or subacute pattern of change may be more indicative of what?
an infectious or metabolic change
94
how is dementia diagnosed?
- through determining the cause
- ruling out other conditions
- MRI and CT to identify cognitive loss and brain lesions
95
alzheimer's disease
chronic, progressive, degenerative disease of the brain; most common form of dementia
96
cause of alzheimer's
exact cause is unknown; likely a combination of genetic and environmental factors
97
most important risk factor of alzheimer's
age
98
what is the main thing that happens in alzheimer's?
brain atrophy
99
in alzheimer's, pathologic changes precede clinical manifestions...
by 5-20 years
100
early signs of alzheimer's
1. memory loss that affects job skills
2. difficulty performing familiar tasks
3. problems with language
4. disorientation to time and place
5. poor or decreased judgement
6. problems with abstract thinking
7. misplacing things
8. changes in mood or behavior
9. changes in personality
10. loss of initiative
101
initial manifestations of AD
- memory loss
- mild disorientation
- trouble with words and numbers
102
what is the goal of AD?
early intervention
103
MCI
- does not yet meet criteria for dementia
- is within 2nd stage in AD spectrum
- is below defined norms
104
causes of MCI
stress, anxiety, depression, physical illness
105
primary treatment of MCI
based on careful monitoring - watch for 10 signs of AD
106
how is AD diagnosed?
by exclusion
107
what does a definitive diagnosis of AD require?
an autopsy
108
collaborative management of AD
- controlling undesirable behavior manifestations
- providing support for the family caregiver
109
what does drug therapy do for AD?
- some modest decrease in rate of decline of cognitive function
- treating associated depression
110
overall goals of AD
- maintain functional ability as long as possible
- be maintained in a safe environment with a minimum of injuries
- have person care needs met
- have dignity maintained
- reduce caregiver stress
- maintain personal, emotional, and physical health
- cope with long-term effects associated with caregiving
111
what are some big problems for those with AD?
- inability to communicate other healthcare problems
- hospitalization can precipitate a worsening of disease or delirium
112
what might family need when dealing with a family member with AD?
resources for respite
113
what is sundowning and who experiences it?
AD patients can experience; patient becomes more confused and agitated late in afternoon or evening
114
ultimate cause of death in many AD patients
pneumonia
115
who might need to be consulted with help eating for AD patients?
OT
116
delirium
- state of temporary but acute mental confusion
- common problem
- life-threatening
- possibly preventable syndrome
117
main hypothesis of delirium
reversible impairment of cerebral oxidative metabolism and multiple neurotransmitter abnormalities
118
precipitating factors for delirium
- admission to ICU
- use of physical restraints
- pain (especially untreated)
- emotional stress
- prolonged sleep depreivations
- dehydration
- malnutrition
- drugs
119
acute delirium clinical manifestations
- lasts from 1-7 days
- may persists up to and after discharge
- patient at increased risk for falls
- manifestations are sometimes confused with dementia and dpression
120
acute delirium clinical manifestations
- lasts from 1-7 days
- may persists up to and after discharge
- patient at increased risk for falls
- manifestations are sometimes confused with dementia and depression
