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1

Amount of pain is related to amount of tissue injury

specificity theory

2

Pain is transmitted to spinal cord along pathways

Theory: painful stimuli prevented from reaching higher level of CNS by stimulation of larger sensory nerves.

Theoretical “gates” in dorsal horn of spinal cord

Small nerve fivers carry pain impulses through “gate”

When larger fibers are stimulated by touch, vibration, or thermal stimulation, causes “gate to close” which diminishes pain perception.

Does not explain chronic pain or phantom limb pain

Gate control theory (1965)

3

Interventions which are effective in pain management explained by the gate control theory:

Acupuncture

TENS units (transcutaneous electrical nerve stimulation)

Heat and cold

Massage

4

process of how pain is recognized consciously

Nociception

5

pain with a cause of normal tissue injury

Nociceptive pain

6

superficial

somatic

7

internal organs, abdomen, or skeleton

visceral

8

Results from abnormal processing of stimuli (sensory function) in central or peripheral nervous system.


Non-nociceptive pain (Neuropathic)

9

pain of skin

cutaneous

10

pain of muscle, tendon, joint, and blood vessel pain.

Deep somatic

11

organ pain. Ex: cramping, aching, & throbbing.

visceral

12

begins suddenly. self-limiting. ends when injured tissue heals.

acute

13

pain that lasts a substantial amount of time.

chronic

14

Special types of pain:

Neuropathic
Neuralgia
Phantom limb pain

15

Present in an area distant from point of origin. Area of referred pain is supplied by same spinal segment as
actual site. Ex: Myocardial infarction pain ----> L arm pain.

referred pain

16

Persistent or intermittent

Pain lasting beyond expected normal healing time -

Normal healing time varies depending on injury

Common chronic pain conditions?

chronic pain

17

Result of trauma or disease of nerves
Originates from pathology of nervous system.
Painful diabetic neuropathy.
Ex: feeling pins & needles poking or shooting pains.

neuropathic pain

18

Intense pain along course of a nerve (spinal or cranial)

neuraglia

19

Etiology of neuraglia

stimulation of cutaneous region supplied by nerve

20

Clinical manifestations of neuraglia

Severe, brief, often repetitive attacks of lightning-like or throbbing pain

21

Cranial nerve 5. Pain in face/mouth area. Even wind could hurt it.

Trigeminal neuralgia (tic douloureux)

22

Occurs in an amputated body part or limb
Possibly caused by spontaneous firing of spinal cord neurons that have lost their normal sensory input

Phantom limb pain

23

what % of adults report recurrent headaches

25%

24

what percent report daily or nearly daily headaches

4%

25

● Migraine
● Cluster
● Tension

primary headaches

26

Headaches secondary to other medical conditions

meningitis

brain tumor

cerebral aneurysm

27

how to diagnose headaches

comprehensive history/physical to exclude secondary causes.

medication history

headache diary

lab and imaging studies

28

caused by genetic and environmental factors
Triggers include: Variations in estrogen level, Chemicals in foods (MSG, aged cheese, chocolate), & Stress
Affect 20 million people in the USA. Result in considerable time lost from work.

migrane headache

29

clinical manifestations for migrane headache

Pulsatile, throbbing, unilateral headache lasting 1 to 2 days
Pain worsens with activity,
moderate or severe pain intensity,
nausea and vomiting,
photophobia- sensitive to light
phonophobia- sensitive to sound

30

2 major types of migraine headaches

1. Migraine with aura 2. Migraine without aura

31

Visual sensory phenomenon that precedes migraine. Lasts from 5 minutes to 1 hour.

Aura

32

Etiology : mostly unknown

Autosomal dominant genes may be involved

primarily men

cluster headache

33

manifestations for cluster headache

unilateral

clusters or bouts of headaches for days followed by long period of spontaneous remission

extreme pain with short duration

redness and tearing of eyes, pupil constriction, ptosis

nasal congestion, runny nose

34

most common type of headache

Exact etiology is unknown,

May be caused by sustained tension of muscles of scalp and neck

Stress, anxiety, or depression

Exact mechanisms are not known

May be a form of migraine headache that transforms gradually into a chronic tension headache

tension headache

35

clinical manifestations for tension headache

bilateral, dull , aching, diffuse(spread throughout)

mild to moderate bilateral headache

sensation of tight band or "hatband" around head

not associated with nausea or vomiting

not worsened by activity

may be infrequent, episodic, or chronic

36

how to diagnosis tension headache

pain history

responsive to OTC drugs

responsive to non-drug techniques

37

Headaches that occur 15 days or more a month

Chronic Daily Headache (CDH)

38

Etiology: imbalance in joint

movement due to:
poor bite
bruxism (teeth grinding)
joint problems

Temporomandibular joint (TMJ) pain

39

manifestation for TMJ

Usually referred pain and commonly presents as facial muscle pain, headache, neck ache, or earache.

Aggravated by jaw function

40

Chronic autoimmune disease

Caused by antibody-mediated destruction of acethylcholine receptors in the neuromuscular junction

Disorder of transmission at neuromuscular junction

Peak incidence 20-30 years of age

3 times more common in women

Fuzzy tuffs

myasthenia gravis

41

manifestations of myasthenia graves

muscle fatigue

progressive weakness

diplopia

ptosis

difficulty chewing, dysphagia

facial muscle weakness

speech impairment

42

Acquired (immune-mediated) inflammatory disease - demyelination of peripheral nerves

Rapidly progressive limb weakness and loss of tendon reflexes

Acute onset, ascending motor paralysis

Usually a medical emergency – life-threatening - may progress to respiratory arrest

Guillain-Barre' syndrome

43

manifestations for Guillain-Barre' Syndrome

Ascending muscle weakness

Paresis of legs to quadriplegia

44

treatment for guillain-barre

Support of vial function

may use plasmapheresis or IV immunoglobulin

Most fully recover spontaneously within 6-12 months

45

Progressive degenerative disorder of basal ganglia function. causes dopamine depletion which causes abnormal movement

Parkinson Disease

46

manifestations for parkinson's disease

tremors at rest - when they sit there at rest the tremors occur. when they move, they stop.

pill rolling,

tremor lessons with purposeful movement

rigidity (muscle stiffness)

bradykinesia – extreme slowness of movement

postural disturbances
-stooped, flexed, leaning
forward

47

Lou Gehrig disease

Etiology unknown (5 to 10% are familial)

Men more than women

Middle to late adulthood

Progressive- mean survival 2-5 years from onset of symptoms

Affects upper and lower motor neurons of cerebral cortex, brain stem, and spinal cord

Leads to progressive weakness leading to respiratory failure and death

Normal intellectual and sensory function until death.


Amyotrophic lateral sclerosis (ALS)

48

manifestations for Amyotrophic lateral sclerosis (ALS)

Slowly progressive weakness and atrophy in distal muscles of one upper extremity followed by regional spread of weakness

Early symptom: muscle cramps in distal legs

Weakness in any or all muscles

Weakness, spasticity, impaired fine motor control

Dysphagia, dysarthria, dysphonia

Muscle atrophy

49

diagnosis for Amyotrophic lateral sclerosis (ALS) is based on?

history and physical

50

treatment for ALS

psychological support of patient and family

51

progressive, autoimmune, inflammatory, demyelinating disorder -

Demyelination and subsequent degeneration of nerve fibers in the CNS

most common non-traumatic cause of neurologic disability among young and middle adults

Age of onset- between 18
and 45 years of age

Incidence double in women

Genetic predisposition suggested

Immune-mediated disorder

Multiple Sclerosis (MS)

52

clinical features of MS

Paresthesias of face, trunk, or limbs (tingling sensation)

Optic neuritis (inflammation of optic nerve)

Diplopia

Pain

Abnormal gait

Bladder/sexual dysfunction

Fatigue – one of the most common problems

53

diagnosis of MS

Clinical Data

MRI,

CT scans

Cerebrospinal fluid

54

treatment for MS

symptom management

anti-inflammatory drugs

55

Most commonly occurs due to vertebral injuries.

Traumatic injury of vertebral and neural tissues.

dislocation

spinal cord trauma

56

single break affecting transverse or spinous processes

simple fracture

57

vertebral body compressed

compressed fracture

58

vertebral body shattered into several fragments

comminuted fracture

59

-temporary complete loss of function below the level of injury
-complete loss of reflex function
-paralysis and flaccidity in muscles
-loss of bladder and rectal control
-can last for hours, days, or weeks

spinal shock

60

how is spinal shock diagnosed? (3)

physical exam

CT scan

MRI

61

treatment for spinal shock

immobilization of spine

corticosteroids

surgery may be necessary

lung function, skin integrity, and bladder and bowel function maintenance

62

-may occur after spinal shock resolves
-massive, uncompensated cardiovascular response to stimulation of sympathetic nervous system
stimulation of sensory receptors below level of cord lesion
-often associated with distended bladder or rectum
-bladder or bowel emptying will usually relieve syndrome
-LIFE THREATENING

Autonomic hyperreflexia (dyxreflexia)

63

S/S of autonomic hyperreflexia

-pounding headache
-blurred vision
-sweating above level of lesion (with flushed skin)
-bradycardia (30-40 beats/min)
-increased risk for CVA

64

treatment for autonomic hyperreflexia

-elevate HOB
-remove stimulus
-antihypertensive meds if BP remains high

65

type of injury which has deprivation of oxygen with maintained blood flow

reduced atmospheric pressure

carbon monoxide poisoning

severe anemia

failure of lungs to oxygenate blood

hypoxic injury

66

condition in which not enough hemoglobin to carry oxygen

anemia

67

type of injury which has greatly reduced or interrupted blood flow

ischemic injury

68

stroke. One area of brain affected

focal ischemia

69

cardiac arrest. Heart isn't pumping blood to brain

global ischemia

70

increase in tissue volume in brain (secondary to fluid accumulation)

cerebral edema (brain swelling)

71

2 types of cerebral edema

vasogenic

cytotoxic

72

blood-brain barrier disrupted - allows fluid to escape into the extracellular fluid that surrounds brain cells. (water and proteins transfer from vascular into interstitial space)

hemorrhage, brain injury, infections (meningitis)

vasogenic

73

swelling of brain cells (increase in intracellular fluid)

hypo-osmotic states (water intoxication, severe ischemia)

impair the function of the sodium-potassium membrane pump

cytotoxic

74

IICP

increased intracranial pressure

75

cranial cavity contains

10% blood
80% brain tissue
10% CSF

76

normal ICP is?

0-15 mm Hg

77

causes for IICP

brain tumor
brain edema
hemorrhage
herniation
hydrocephalus

78

develops in a couple of hours from head injury

acute hydrocephalus

79

traumatic injury to the brain. can produce physical, intellectual, emotional, social, and vocational changes

major head trauma

80

most traumatic brain injuries are caused by:

MVA
falls
sports related events
violence

81

head injuries are categorized as either

closed or open

82

blunt, non missile trauma

head strikes hard surface or rapidly moving object strikes head

dura remains in tact and brain tissues not exposed to environment

closed

83

penetrating, missile trauma. injury breaks dura, brain tissues exposed to environment

open

84

two types of injury

primary & secondary

85

damage caused by impact

primary (direct)

86

damage results from brain swelling, infection, hypoxia

secondary

87

direct trauma

coup

88

injury within school on opposite from site of impact, brain rebounds, hits against inner skull surface

countrecoup

89

transient neurogenic dysfunction caused by mechanical force to the brain (there may be a momentary LOC)

concussion

90

temporary disturbance causing attention and memory deficits but no LOC

mild concussion

91

immediate LOC (<6 hours). return of consciousness may be gradual. confusional state lasting hours to days

classic cerebral concussion

92

protective membranes of brain and spinal cord.

meninges

93

(2 layers) outer protective membrane. subdural space

dura mater

94

middle space. subarachnoid space contains CSF

arachnoid mater

95

internal (adheres to contours of brain and spinal cord)

pia mater

96

result from vascular injury and bleeding. usually fixed with surgery!

hematomas

97

between inner bones of skull and dura

epidural hematomas

98

between dura and arachnoid.

usually at top of skull.

acute developed within 24 hours

subacute develops 2-10 days after injury

chronic develops over several weeks

subdural hematomas

99

frontal and temporal lobes

intracerebral hematomas

100

results from shaking.

acceleration/deceleration injury

results in axonal damage.

severity corresponds to amount of shearing force applied to brain and brain stem.

"shaken baby syndrome"

diffuse axonal injury (DAI)

101

state of awareness of self and environment and of being able to become oriented to new stimuli.

2 major components:
-arousal and wakefulness
-content of thought

consciousness

102

descending levels of consciousness

confusion
delirium
obtundation
stupor
coma

103

less than full alertness

obtundation

104

check for what when checking for neurological function

LOC
pattern of breathing
pupillary changes
oculomotor responses
motor responses

105

On the glascow coma scale what score would be totally unresponsive

3

106

best response?

15

107

comatose client

8 or lower

108

2 forms of neurologic death:

brain death & cerebral death

109

body can no longer maintain internal homeostasis

state law: defined as irreversible cessation of function of entire brain.

brain death

110

remain in coma

emerge into vegetative state

progress into a minimal conscious state (MCS)

fully conscious with intact cognitive function

communicates through blinking

"locked in syndrome"

cerebral death

111

-vascular disorder that injuries brain tissue
-leading cause of mortality and morbidity
-high risk: hypertension, diabetes.
-more common in men

stroke (brain attack)

112

thombi cause occlusions in arteries supplying brain or in intracranial vessels

thrombotic stroke (most common)

113

temporary decreases in brain blood flow

brief episode of neurologic dysfunction with symptoms lasting no more than 1 hour

complete recovery

transient ischemic attacks (TIAs)

114

caused by blood clots

fragments that break from thrombus formed outside brain

embolic stroke

115

caused from a leaking or ruptured aneurysm.

common causes:
hypertension
ruptured aneurysms
head trauma
hemorrhage associated with anticoagulants

symptoms include
-severe headache with immediate unresponsive state
-severe headache with consciousness
-sudden unconsciousness

hemorrhagic stroke

116

type of hemorrhage that blood escapes into subarachnoid space. caused by defective or injured vasculature.

subarachnoid hemorrhage

117

lining of brain and spinal cord inflammation.

meningitis

118

infection or direct extension from infected area to subarachnoid space.

otitis or sinusitis- predisposing conditions.

S/S- severe headache, nuchal rigidity (stiff neck). fever, tachycardia, petechial rash.

treatment- antibiotics, supportive measures

bacterial meningitis

119

acute febrile illness. usually of viral origin with nervous system involvement.

most common forms of encephalitis caused by anthropoid-borne (mosquito) viruses and herpes simplex virus.

most cases are self-limiting

encephalitis

120

abrupt and temporary alteration in cerebral activity resulting in changes in electrical discharge from neurons.

causes brief disruption in brain's electrical functions.

will have a temporary alteration in level of arousal

seizure

121

term often applied to seizures.
tonic-clonic movements associated with some seizures.

convulsion

122

excessive muscle tone, stiffening of body

tonic phase

123

jerking of extremities (alternating contraction and relaxation of muscles)

clonic phase

124

condition of having recurrence seizure activity with no known cause

epilepsy

125

most common type of seizure. involve one hemisphere of brain (begins in specific or focal area)

focal seizures

126

type of seizure that involves whole brain; begin simultaneously in both hemispheres

generalized seizures

127

type of seizure that lasts only a few seconds.

blank stare, motionless, unresponsiveness; motion does occur in many cases

typical seizure

128

similar to typical; greater alterations in muscle tone and less-abrupt onset and cessation

atypical

129

two types of generalized seizures

absence (typical & atypical) & tonic-clonic (grand-mal)

130

early manifestations that may occur hours or days before seizure

prodrome

131

immediately precedes onset of generalized seizure; "funny feeling," dizziness, numbness, peculiar sensation

aura

132

sharp contraction of muscles with extension of extremities and immediate LOC

tonic phase

133

rhythmic contraction and relaxation of extremities

clonic phase

134

immediately following seizure (confusion).

lasts 30-90 min

postictal phase

135

continuing or repetitive seizure activity (seizures that do not stop spontaneously or occur in succession w/o recovery.)

medical emergency that requires immediate intervention.

status epilepticus

136

decrease in memory

progressive failure of cerebral functions not caused by impaired LOC.

dementia

137

"the long goodbye"

-most common type of dementia

-progressive disorder begins with memory impairment.

-progresses to inability to recognize family members and loss of control over bodily functions.

-imaging of brain reveals atrophy of cerebral cortex with enlargement of ventricles.

-neurofibrillary tangles

-senile plaques

alzheimer disease (AD)

138

protein in neurons become distorted and twisted

neurofibrillary tangles

139

areas of degeneration in groups of nerve cells have a plaque-like material

senile plaques

140

manifestations of AD

forgetfulness
emotional upset
disorientation
confusion
lack of concentration
decline in abstraction, problem solving, and judgement
loss of ability to respond to environment

141

how is diagnosis made for AD?

diagnosis of exclusion.
made by ruling out other causes of dementia

142

weakness

paresis

143

loss of motor function

-hemiparesis or hemiplegia
-paraparesis or paraplegia
-quadriparesis or quadriplegia

plegia (paralysis)

144

cranial tumors (3)

-primary intracerebral tumors (glicomas)
-primary extracerebral tumors
-metastatic carcinoma

145

you can loose how much of your blood and stay alive?

40%

146

how many L can be lost in women?

2.2 L

147

universal donor

O

148

how much blood in average body?

6 quarts. 5.5 L

149

Hb or Hgb

hemaglobin

150

what gives blood its color

protein substance in RBCs

151

male Hgb

13.5-18 g/dL

152

female Hgb

12-15 g/dL

153

AKA myeloid tissue

bone marrow

154

2 types of bone marrow

red and yellow

155

fat

yellow marrow

156

hemopoetic (hips, shoulders, sternum)

red marrow

157

bone marrow

hemopoietic

158

thymus, lymph nodes, spleen, & lymph tissue

lymphopoietic

159

CFUs turn into?

mature blood cells

160

hormone like growth factor.

control proliferation, differentiation, function of blood cells

cytokines

161

CSFs

colony stimulating factors

162

RBCs creator

Erythropoietin (EPO)

163

plasma creator

thrombopietin

164

leukocytes arrive from ____ _____.

stem cells.

165

leukocytes mature where?

bone marrow

166

Like PAC men and protect against infection.

granulocytes or agranulocytes

leukocytes (WBCs)

167

low WBCs

NEVER NORMAL and not beneficial

leukopenia

168

Low lymphocytes. seen with acute viral infection

causes: drugs, immune deficiencies, viruses, radiation, & AIDS

lymphocytopenia

169

protect against infection.

phagocytotic

live only 4-5 days

neutrophils

170

low neutrophils.

never normal!!!!

drugs, cancer, and & autoimmune disease.

neutropenia (agranulocytosis)

171

immature WBCs released. termed a shift to the left.

granulocytosis (neutrophilia)

172

aplastic anemia

drug related----idiosycratic

chemotherapy

radiation

acquired neutropenia

173

shift the right?

normal mature WBCs again

174

allergic reactions -- release enzymes that limit histamine

protect against parasites -- attach to them and kill them

eosinophils

175

contain heparin (blood thinning), histamines (vasodilators)

involved in allergic and hypersensitivity reactions

similar to mast cells

basophils

176

destroy foreign cells

natural killer cells (NK)

177

in thymus

T lymphocytes

178

in bone marrow

B lymphocytes

179

lymphoid tissue -- contains macrophages.
RBC graveyard
blood storage

spleen

180

B lymphocytes mature in ___ then go to____ ____.

bone marrow; lymph nodes

181

T lymphocytes mature in ___ then go to ____ ____.

thymus; lymph nodes

182

cardinal sign is throat hurting.

B-lymphocytes become infected with Epstein-barr virus.

heterophil antibodies used to diagnose

infects 90%

Tx: rest, fluid, non-steroid anti-inflammatory

transmitted by: saliva through personal contact

"kissing disease"

asymptomatic patients spread EBV

infectious mononucleosis (MONO)

183

S/Sx of MONO

fever malaise
chills
severe pharyngitis
swollen lymph nodes
increased lymphocyte count

184

CA where the patient has no platelets.

excessive immature WBCs (leukocytes)

2 kinds

leukemia

185

starts fast and if not intervened can kill quickly.

undifferentiated or immature cells, usually blast cells (baby cells)

actue

186

cells are mature but do not function normally.

slower acting

chronic.

187

crowd out the bone marrow

malignant leukocytes form

pancytopenia happens

RBCs down....these up....

blast cells

188

adults more than children. acute and chronic.

Dx with blood work, bone marrow.

Philadelphia chromosome?

ALL and CML. chromosome translocation

Leukemia

189

risk factors for leukemia?

cigarette smoke
benzene
radiation
HIV, Hep C

190

type of leukemia in lymph tissue

lymphocytic

191

type of leukemia in bone

myelocytic

192

WBCs last how long?

120 days

193

immature
poorly differentiated
proliferate rapidly
long life span
circulation in blood stream
cross blood-brain barrier
infiltrate many body organs

leukemia cells

194

on top of head. take out 5mL of CSF and put in 5 mL of chemo

omaya reservoir

195

early detection is difficult

related to depressed bone marrow function

sudden onset

acute leukemia

196

S/Sx of acute leukemia

fatigue (not enough RBCs---not enough Oxygen)

low grade fever

night sweats

weight loss

bleeding --- not enough platelets

bone pain

197

ANC

absolute neutrophil count

198

when is an ANC ordered?

when WBCs are low

199

ALL

acute lymphocytic leukemia

200

AML

acute myeloid leukemia

201

most common cancer in children and adults.

ALL

(acute lymphocytic leukemia)

202

myeloid cells are bone marrow.

associated with acquired genetic alterations -- blast cells occur

Sx: anemia, neutropenia, thrombocytopenia

AML

(acute myeloid leukemia)

203

-blast count elevated
-blood viscosity increases
-treatment: lower blast cells quickly by aphaeresis and chemotherapy

leukostasis

204

small vessels in pulmonary and cerebral circulation affected

sudden SOB, dyspnea --- pulmonary sign

HA (headache) ---cerebral sign

Lethargy --- cerebral sign

leukoblastic emboli

205

no active symtoms stage

remission

206

no cells at all in body

survival

207

CLL

chronic lymphocytic leukemia

208

B lymphocytes involved---isolated increase.

most common form in western world

2 types:
no therapy required - die of other dx
others- rapidly fatal in spite of tx

CLL

209

S/Sx of CLL

related for infiltration of bone marrow and lymphoid tissue by neoplastic lymphocytes

immunologic defects noted

lymph nodes involved. hard and not painful.

infections increase ---staph, strep, flu

210

treatment of CLL

aggressive---chemo/radiation
indolent--nothing till sxs (may die of other disease)

211

CML

chronic myeloid leukemia

212

philadelphia chromosome-- affects one stem cell then off it goes.

Dx with BCR-ABL gene product found in blood.

treatment: inhibit of BCR-ABL

CML