Neurology Flashcards

(73 cards)

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
Acute Pain
``` 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. ```
26
Chronic Pain
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
27
Headache: Types and Causes
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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Parietal Lobe
Middle of the brain orients body processes sensory input
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Occipital lobe
back of brain | -vision
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Frontal lobe
``` front of brain -personality decision-making movement behavior mood ability to plan ```
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temporal lobe
temple area hearing speech memory
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Brainstem
heartrate respiration alertness
33
Cerebellum
Controls voluntary movement | coordination
34
Cerebral Circulation
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
Cerebral Aneurysms
- localized weakness in the wall of the artery - usually multiple - at points of bifurcation - initially small and asymptomatic
36
Cerebral Aneurysm S&S
``` 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
Cerebral aneurysm Treatment
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
Arteriosclerosis
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
Atherosclerosis
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
Lipids
``` 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
Low density lipoprotein (LDL)
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
High density lipoprotein (HDL)
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
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Lipoprotein transport
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
Triglycerides
high triglycerides are linked to low levels of HDL, excess body weight and poorly controlled diabetes - less than 1.7mmol/L
45
Total Cholesterol / HDL ratio
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
Hypercholesteremia
``` 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
Atherosclerosis risk factors
``` nonmodifiable: - age -gender -genetic or familial Modifiable - obesity - sedentary -cigarette smoking - diabetes mellitus -poorly controlled hypertension - combination of oral contraceptives and smoking ```
48
Atherosclerosis patho
- 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
Cholesterol tests
serum lipid levels: LDL and HDL exercise stress testing: Screening for arterial obstruction nuclear med studies: determine the degree of tissue perfusion
50
Cholesterol treatment
- 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
Cerebrovascular Accidents (CVAs)
- 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
Ischemic CVAs
Thrombotic: occlusion - atheroma, often in large arteries Embolus: sudden obstruction - lodging in a cerebral artery May be transient (TIA)
53
Ischemic patho
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
Ischemic stroke S&S
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
Brain stem ischemia
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
Cerebellum ischemia
less common than in the cerebrum but can cause severe effects including problems with balance and coordination, dizziness, headaches, nasuea and vomiting
57
cerebrum - left hemisphere
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
cerebrum - right hemisphere
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
Spatial-perceptual alterations (rt-sided stroke)
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
Transient Ischemic attacks (TIAs)
may occur singly or in a series | result from temporary localized reduction of blood flow in the brain
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TIA patho
``` partial occlusion of an artery atherosclerosis small embolus: blood clot after rupture vascular spasm local loss of autoregulation ```
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TIA S&S
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
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Hemorrhagic stroke
- 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)
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Hemorrhagic pathophysiology
blood from vessel leaks into surrounding cerebral tissue blood accumulation exerts pressure on surrounding areas macrophages move in: phagocytosis of blood and necrotic tissue
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Intracerebral hemorrhage
bleeding within the brain 10% of all strokes
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subarachnoid hemorrhage
bleeding into the CSF between the arachnoid and the pia mater membranes on the surface of the brain
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Hemorrhagic S&S
``` severe and sudden headache "thunderclap" vomitting nuchal (neck muscles) rigidity stupor, coma seizures ```
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CVA treatment
``` clot busting agents thrombectomy/embolectomy surgical intervention glucocorticoids supportive treatment occupational and physical therapists treat underlying problem rehab ```
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Stroke prevention
stop smoking lose weight and be active control diabetes, HTN, dyslipidemia, Afib modify alcohol use
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Type 1 (familial hyperchylomicronemia)
- 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
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Type IIA (familial hypercholesterolemia)
- 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
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Type IIb (familial combined (mixed) hyperlipidemia)
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
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type iii familial dysbetalipoproteinemia
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