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NURS2750 > Neurology > Flashcards

Neurology Flashcards

1
Q

Causes of Pain

A 
Inflammation
Infection
Ischemia and tissue necrosis
Stretching of tissue
Stretching of tendons, ligaments, joint capsule
Chemicals
Burns
Muscle spasm
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2
Q

Somatic Pain

A

From Skin
Bone, muscle
conducted by sensory fibers

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3
Q

Visceral Pain

A

from organs
conducted by sympathetic fibers
can be acute or chronic

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4
Q

Sensory Dimensions:

A 
The perception of pain by the individual including:
•location
•Intensity
•Pattern
•quality
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5
Q

Pain threshold:

A

the point at which stimulus is perceived as painful

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6
Q

Pain tolerance:

A

the maximum intensity or duration of pain that a person is willing to endure before doing something about it

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7
Q

Pain reaction:Autonomic responses

A

•Automatic response to protect the individual (eg. moving your hand from a hot stove)

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8
Q

Pain reaction:Behavioral responses:

A

•Learned behaviors as a method to coping with the pain (eg. rubbing a sore leg)

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9
Q

Hyperalgesia:

A

an increased sensitivity to pain, which may be the result of damage to nociceptors or peripheral nerves (eg. shingles)

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10
Q

nociception

A 
The neural mechanisms by which pain is perceived consists of 4 major processes:
I.Transduction
II.Transmission
III.Perception
IV.Modulation
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11
Q

Transduction

A

The conversion of a mechanical, thermal or chemical stimulus into a neuronal action potential
Mechanical: trauma, surgery, muscle spasm
Thermal: extreme heat or cold
Chemical: lactic acid, bradykinins, enzymes
occurs at free nerve endings, action potential moves from periphery to spinal cord

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12
Q

Transmission

A

The movement of pain impulses from the site of transduction to the brain
3 segments involved in nociception signal transmission:
Segment 1: Transmission along nociceptor fibers to the spinal cord
Segment 2: Dorsal Horn Processing
Segment 3: Transmission to the thalamus and cortex

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13
Q

A Fibers (beta and delta):

A

peripheral nerve fiber small, myelinated

•Transmit signals rapidly. Produce sharp, localized pain

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14
Q

C Fibers:

A

peripheral nerve fiber large, unmyelinated

•Transmit signals slowly. Produce dull, achy pain in deeper structures

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15
Q

Dorsal Horn Processing

A

Once the nociceptor signal arrives in the central nervous system it is processed within the dorsal horn of the spinal column
Processing includes the release of neurotransmitters (eg. substance P) which may either excite or inhibit the cell

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16
Q

Pain Pathways

A

Somatic sensory area in the cerebral cortex located in the parietal lobe
- Perception and localization of sensation
Hypothalamus and limbic system
- Emotional factors (crying when something hurts)
Communication with other regions of the brain to integrate responses
Reticular activating system (RAS)
-Reticular formation in the pons and medulla
-Awareness of incoming brain stimuli
Cortical Structures:
-Meaning of pain

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17
Q

Perception

A

Occurs when pain is recognized, defined and responded to
Conscious awareness of the pain
Subjective interpretation

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18
Q

Modulation

A

neurons from the brain descend the spinal column and release substances to inhibit nociception

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19
Q

Gate control theory

A

Control systems, “gates” built into normal pain pathways

Can modify pain stimuli conduction and transmission in the spinal cord and brain.
Gates open: Pain impulses transmitted from periphery to brain
Gates closed: Reduces or modifies the passage of pain impulses

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20
Q

Pain Control

A

Application of ice: Impulses from temperature receptors close gates.
Transcutaneous electrical nerve stimulation (TENS): Increases sensory stimulation at site, blocking pain transmission.
Opiate-like chemicals (opioids):
-Secreted by interneurons of the CNS (endogenous).
-Block conduction of pain impulses to the CNS
-Resemble morphine: Enkephalins, dynorphins, beta-lipoproteins

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21
Q

Pain - S&S, diagnosis

A

Location of pain
Descriptive terms: Aching, burning, sharp, throbbing, widespread, cramping, constant, periodic, unbearable, moderate
Timing of pain
Association with an activity
Physical evidence of pain: Pallor and sweating, High blood pressure, tachycardia
Nausea and vomiting: May occur with acute pain.
Fainting and dizziness: May occur with acute pain.
Anxiety and fear: Frequently evident in people with chest pain or trauma
Clenched fists or rigid faces
Restlessness or constant motion
Guarding area to prevent stimulation of receptors

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22
Q

Young Children and Pain

A

Infants respond physiologically Examples: tachycardia, increased blood pressure, facial expressions
Great variations in different developmental stages:
-Different coping mechanisms
-Range of behavior
-Often have difficulty describing the pain
-Withdrawal and lack of communication in older children

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23
Q

Referred Pain

A

Source may be difficult to determine.
Pain may be perceived at site distant from source.
-Characteristic of visceral damage in the abdominal organs
-Heart attack or ischemia in the heart

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24
Q

Phantom Pain

A

Usually in adults
More common if chronic pain has occurred.
Can follow an amputation
Pain, itching, tingling
Usually does not respond to common pain therapies.
May resolve within weeks to months.
Phenomenon not fully understood

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25
Q

Acute Pain

A 
Usually sudden and severe, short term
Indicates tissue damage.
May be localized or generalized.
Initiates physiologic stress response.
Increase blood pressure and heart rate; cool, pale, moist skin; increase respiratory rate; increase skeletal muscle tension 
Vomiting may occur.
Strong emotional response may occur.
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26
Q

Chronic Pain

A

Occurs over extended time; may be recurrent.
Usually more difficult to treat than acute pain
Often perceived to be generalized.
Individual may be fatigued, irritable, depressed.
Sleep disturbances common
Specific cause may be less apparent.
Appetite may be affected.
Can lead to weight gain or loss

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27
Q

Headache: Types and Causes

A

Congested sinuses, nasal congestion, eye strain
Muscle spasm and tension: From emotional stress
In temporal area: Temporomandibular joint syndrome
Migraine: Abnormal blood flow and metabolism in the brain
Intracranial: Increased pressure inside the skull
Central pain: Caused by dysfunction or damage to the brain or spinal cord
Neuropathic pain: Caused by trauma or disease involving the peripheral nerves
Ischemic pain: Results from a profound, sudden loss of blood flow to an organ or tissue
Cancer-related pain: caused by advance of the disease; pain associated with treatment; result of coexisting disease

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28
Q

Parietal Lobe

A

Middle of the brain
orients body
processes sensory input

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29
Q

Occipital lobe

A

back of brain

-vision

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30
Q

Frontal lobe

A 
front of brain
-personality
decision-making
movement
behavior
mood
ability to plan
31
Q

temporal lobe

A

temple area
hearing
speech
memory

32
Q

Brainstem

A

heartrate
respiration
alertness

33
Q

Cerebellum

A

Controls voluntary movement

coordination

34
Q

Cerebral Circulation

A

Anterior: carotids
- at the circle of willis divides into middle cerebral artery (MCA) and anterior cerebral artery (ACA)
Posterior: Vertebrals
- converge to form the basilar artery
- terminates into the L&R posterior cerebral arteries

35
Q

Cerebral Aneurysms

A
  • localized weakness in the wall of the artery
  • usually multiple
  • at points of bifurcation
  • initially small and asymptomatic
36
Q

Cerebral Aneurysm S&S

A 
Enlarging aneurysm
- pressure on surrounding structures or nerves 
- loss of visual field or visual disturbance
- headache
A small leak: 
- headache
- photophobia
- intermittent periods of dysfunction (confusion. slurred speech, weakness)
- nuchal rigidity or neck stiffness
Massive rupture:
- immediate severe blinding headache
- vomiting
-photophobia
-seizures and LOC
-leading to death
37
Q

Cerebral aneurysm Treatment

A

surgical treatment
- if diagnosed before rupture: clipping and tying off
- clipping may be done after rupture: reduce rebleeding
focused on reducing increased ICP and cerebral vasospasm

38
Q

Arteriosclerosis

A

General term for all types of arterial changes

  • degenerative changes in small arteries and arterioles
  • loss of elasticity, walls thick and hard
  • lumen gradually narrows and may become obstructed
  • leading to ischemia and necrosis in tissues as kidney
  • cause of increased BP
39
Q

Atherosclerosis

A

Large and medium sized arteries
- presence of atheroma: plaques consisting of lipis, calcium, and possible clots
- related to diet, exercise and stress
formation of fibro fatty lesions in initmal lining of arteries
- vessel narrowing and ischemia
- may occlude the vessel and predispose the formation of a thrombus
- leading cause of CAD and CVD

40
Q

Lipids

A 
essential element
synthesized in liver
transported in combination with proteins as
Very low density lipoprotein (VLDL)
low density lipoprotein (LDL)
high density lipoprotein (HDL)
41
Q

Low density lipoprotein (LDL)

A

has higher cholesterol component than proteins
transports cholesterol from liver to cells
major factor contributing to atheroma formation
“Bad” lipoprotein
less than 3.5mmol/L is good unless high risk than 2.0mmol/L is target

42
Q

High density lipoprotein (HDL)

A

has more protein than cholesterol
transports chloesterol away from peripheral cells to liver
catabolism in liver and excretion
higher than 1.0 mmol/L for men and 1.3 for women

43
Q

Lipoprotein transport

A
  1. intake of cholesterol and triglycerides
  2. Chylomicrons absorbed into blood and lymph
  3. Lipid uptake by adipose and skeletal muscle cells
  4. Remnants to liver
  5. Liver synthesizes lipoproteins
  6. LDL transports cholesterol to the cells
  7. LDL attaches to LDL receptor in smooth muscle and endothelial tissue
  8. HDL transports cholesterol from cells to liver
44
Q

Triglycerides

A

high triglycerides are linked to low levels of HDL, excess body weight and poorly controlled diabetes
- less than 1.7mmol/L

45
Q

Total Cholesterol / HDL ratio

A

rate shows how high HDL is relative to the overall levels
a lower number is associated with decreased risk of heart disease
less than 5.0mmol/L is target

46
Q

Hypercholesteremia

A 
affected by:
excess caloric intake (Lower HDL, Raise LDL)
saturated fats (raises VLDL and LDL)
Cholesterol (increase LDL)
Primary = familial
Secondary = obesity, diabetes mellitus
47
Q

Atherosclerosis risk factors

A 
nonmodifiable:
- age
-gender
-genetic or familial
Modifiable
- obesity
- sedentary
-cigarette smoking
- diabetes mellitus
-poorly controlled hypertension
- combination of oral contraceptives and smoking
48
Q

Atherosclerosis patho

A
  • there is damage to the endothelium
  • cholesterol collects under damage and endothelium is oxidized
  • inflammatory response happens and brings monocytes
  • monocyte converts to macrophage and becomes engorged with cholesterol, becomes foamy and dies
  • foamy cells accumulate and pile, release cytokines which brings more monocytes etc
  • LDL is still being deposited forming a fatty streak
  • smooth muscle cells proliferate, multiply and move into the tunica intima
  • muscle cells cover the plaque by producing a fibrous cap of collagen and elastin. Calcium is deposited
  • platelets adhere to cap forming thrombus and release prostagladins which precipitate inflammation and vasospasm, drawing more platelets
49
Q

Cholesterol tests

A

serum lipid levels: LDL and HDL
exercise stress testing: Screening for arterial obstruction
nuclear med studies: determine the degree of tissue perfusion

50
Q

Cholesterol treatment

A
  • weight loss
  • increase exercise
  • dietary modification
  • reduction of sodium intake
  • control hypertension
  • control of primary disorder
  • cessation of smoking
  • antilipidemic drugs
  • surgical intervention: CABG
51
Q

Cerebrovascular Accidents (CVAs)

A
  • an infarction of brain tissue that results from lack of blood
  • 5 minutes of ischemia causes irreversible nerve cell damage
    - central area of necrosis develops
    - all function lost
    - surrounded by an area of inflammation. this zone
    will regain function following healing
    Types: Ischemic, hemorrhagic
52
Q

Ischemic CVAs

A

Thrombotic: occlusion - atheroma, often in large arteries
Embolus: sudden obstruction - lodging in a cerebral artery
May be transient (TIA)

53
Q

Ischemic patho

A

Atherosclerosis happens
Cerebral edema and area of infarction keep increasing in the first 48-72 hrs.
with gradual obstruction, collaterals tend to enlarge or extend into adjacent tissue
Neurons do not regenerate: area of scar tissue with perm loss of neurons
Recovery of some loss of function is possible
-

54
Q

Ischemic stroke S&S

A

come on suddenly and include one or more of the following

  • face may droop
  • may not be able to raise arm on one side
  • may feel confused and have trouble understanding what people are saying
  • speech may sound slurred and jumbled when you talk (aphasia)
  • may have difficulty seeing with one or both eyes
  • S&S develop depending on where the damage is done
55
Q

Brain stem ischemia

A

uncommon but often fatal
- problems with breathing, heart function, balance and coordination, chewing, swallowing, speaking, and seeing as well as weakness and paralysis on both sides of body

56
Q

Cerebellum ischemia

A

less common than in the cerebrum but can cause severe effects including problems with balance and coordination, dizziness, headaches, nasuea and vomiting

57
Q

cerebrum - left hemisphere

A

cause weakness or paralysis on the right side of your body, and cognitive problems including difficulties with reading talking and thinking and learning and remembering new information

58
Q

cerebrum - right hemisphere

A

cause problems with vision, depth perception, short-term memory loss, and judgement, as well as weakness or paralysis on the left side, and a tendency to ignore things on your left side including your own left arm and leg

59
Q

Spatial-perceptual alterations (rt-sided stroke)

A

Anosognosia: incorrect perception of self and illness, secondary to loss of parietal lobes
Erroneous perception of self in space, may neglect all input from the affected side
Homonymous hemianopia: blindness occurs in same half of visual fields of both eyes
agnosia: inability to recognize an object by sight, touch or hearing
apraxia: inability to carry out learned sequential movements on command

60
Q

Transient Ischemic attacks (TIAs)

A

may occur singly or in a series

result from temporary localized reduction of blood flow in the brain

61
Q

TIA patho

A 
partial occlusion of an artery
atherosclerosis
small embolus: blood clot after rupture 
vascular spasm
local loss of autoregulation
62
Q

TIA S&S

A

directly related to location of ischemia
intermittent short episodes of impaired function: muscle weakness in arm and leg
Visual disturbances
numbness and paresthesia in face
transient aphasia or confusion may develop
repeated attacks may be a warning sign for obstruction

63
Q

Hemorrhagic stroke

A
  • caused by rupture of a cerebral artery in patient with severe hypertension and aneurysm
    - effects are evident in both hemispheres
    - complicated by secondary effects of bleeding
    Usually abrupt onset
    -10-20% of all strokes
    -HTN, ruptured aneurysm, trauma
  • 50% mortality rate
  • +++++ disability (mortality)
64
Q

Hemorrhagic pathophysiology

A

blood from vessel leaks into surrounding cerebral tissue
blood accumulation exerts pressure on surrounding areas
macrophages move in: phagocytosis of blood and necrotic tissue

65
Q

Intracerebral hemorrhage

A

bleeding within the brain 10% of all strokes

66
Q

subarachnoid hemorrhage

A

bleeding into the CSF between the arachnoid and the pia mater membranes on the surface of the brain

67
Q

Hemorrhagic S&S

A 
severe and sudden headache "thunderclap"
vomitting
nuchal (neck muscles) rigidity
stupor, coma
seizures
68
Q

CVA treatment

A 
clot busting agents
thrombectomy/embolectomy
surgical intervention
glucocorticoids
supportive treatment
occupational and physical therapists
treat underlying problem
rehab
69
Q

Stroke prevention

A

stop smoking
lose weight and be active
control diabetes, HTN, dyslipidemia, Afib
modify alcohol use

70
Q

Type 1 (familial hyperchylomicronemia)

A
  • massive fasting hyperchylomicronemia even following normal dietary intake resulting in high TG
  • deficiency of lipoprotein lipase or normal apoliprotein CII (rare)
  • not associated with increase CAD
  • treat: low fat diet, no drug therapy
71
Q

Type IIA (familial hypercholesterolemia)

A
  • elevated LDL with normal VLDL due to a block in LDL degradation. result = increased serum cholesterol but normal TG levels
  • caused by defects in the synthesis or processing of LDL receptors
  • ischemic heart disease is greatly accelerated
  • treat: diet, heterozygotes: Cholestyramine and niacin or a statin
72
Q

Type IIb (familial combined (mixed) hyperlipidemia)

A

similar to type IIA except VLDL is also increased
- elevated serum TG and cholesterol levels
caused by overproduction of VLDL by the liver
relatively common
treatment: diet, drug therapy similar to type iia

73
Q

type iii familial dysbetalipoproteinemia

A

serum LDL increased -> increased TG and cholesterol
cause is either overproduction or underutilization of LDL due to mutant apolipoprotein E
Xanthomas and accelerated vascular disease develops in patients by middle age
treat: diet, niacin and fenofibrate or statin

NURS2750 (3 decks)

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