Advanced Patho - Neuro Chronic Ii

Front 1

What are the two types of HA and what is the likelihood of each?

Back 1

1) Primary
2) Secondary

1% of HA is r/t serious intracranial disease..but these can be life threatening

Front 2

What are the 3 types of primary HA? what is a commonality among them?

Back 2

1)Migraine - with or without aura
2) tension-type
3) cluster

All 3: involve trigeminal nerve-M/S, 5th, involved in all 3 types of primary HA, this nerve comes to forehead, jawbone, chin-3 branches

Front 3

What are some types of secondary HA?

Back 3

-sinusitis
-TMJ
-medication/substance abuse
-giant cell arteritis
-meningitis
-increased ICP
-tumor/neoplasm/absess
-CVA

Front 4

What is the patho of primary HA-migraine?

Back 4

trigeminal nerve irritation/excitation

increased vasoactive peptides --> inflammation of meningeal vasculature --> pain!!

-have photo/phono phobia-light and sound

Front 5

What is the patho of tension-type HA (primary)?

Back 5

central mechanism is increased sensitivity trigeminal nerve to pain

peripheral mechanism is muscle contraction

-feels like band around head, tight elastic pain, and pain in back of neck

Front 6

patho of primary HA - cluster

Back 6

trigeminal nerve activation/excitation

increased vasoactive peptides --> neurogentic inflammation --> pain

autonomic: lowered sNS and increased PNS activity

stabbing pain in eye

Front 7

************Pediatric HA: of concern..

Back 7

HA following a pattern on increasing frequency and severity

HA + positive neurologic findings may indicate brain tumor

• track severity and frequency-if both increase may not be a primary HA (also true with adults), look for this in adults too, HA journal helpful, may be r/t stress, food

Front 8

*********What is dementia?

Back 8

a syndrome
****progressive failure of cerebral functions that is NOT caused by an impaired level of consciousness

Front 9

******What is normal in dementia? What is abnoral?

Back 9

level of consciousness is normal

**cognition and awareness declines

**Alterations in awareness: lowered:
memory
cognitive function
orientation
language
executive function (ie balancing checkbook, look for those changes)

Front 10

Cause of dementia?

Back 10

unknown, lots of theories

Front 11

What is Alzheimer Disease?

Back 11

associations:
-progressive and fatal brain disease
-most common form of Dementia
-has no cure
-advanced age is greatest risk factor
-diagnosis is made by ruling out other cause of Dementia

Front 12

Alzheimers Disease Risk Factors

Back 12

family history

diet, environment, education

risk factors of heart disease/stroke
HTN
hyperlipidemia

Causes unknown-changes identified
-structural changes
-neurochemical

Front 13

Alzheimer Disease-patho of microscopic changes

normal vs Alzheimers

Back 13

Amyloid Precuror Protein (APP) is normally found in cell membrane. When not broken down --> Amyloid Plaque formation (made up of Amyloid beta proteins)

Front 14

Why might amyloid plaques form?

Back 14

Mutation for coding APP

Mutation on Chromosome 21

Familial history

-mutation causes APP to cleave in a different position in normal, at beta site, leading to Amyloid beta formation
-Amyloid B likes to clump up
-normal substance broken down abnormally, leading to buildup of amyloid B and excess

OR

or plaque is being formed but nor broken down, apoE4 protein involved with cluster transport, on chromosone 19, found in late familial

Front 15

********Regardless of why there is excess, the excess...

Back 15

****clumps

-senile amyloid plaques:
--are neurotoxic: triggers immune response causing further damage

Front 16

*****Alzheimers: what are neurofibrally tangles?

Back 16

Tau protein-normally stabilizes microtubule network in axons
-In Alzheimers: Tau protein is abnormal --> detach and clumb to form tangles
-these tangles cause Alzheimers Disease although we don't know why

Front 17

So what are the two microscopic changes in Alzheimers Disease?

Back 17

Neurofibriallary Tangle
Senile Plaque

Front 18

What are 3 non-microscopic changes seen in Alzheimers?

Back 18

1) Gross: atrophied gyri (gray part of brain) and increased sulci (black)

2) neurohormonal-decreased acetylcholine

3) glucose utilization decreased

Front 19

What are some clinical manifestations of Alzheimers Disease?

Back 19

-progressive forgetfulness, emotional upset, disorientation, confusion, lack of concentration, decline in abstraction, problem solving, and judgment

Front 20

*****What is Parkinson Disease?

Back 20

severe degeneration of the basal ganglion (corpus striatum) involving the dopaminergic nigrostriatal pathway

Front 21

************What is dopamine? What is it r/t Parkinson Disease?

Back 21

dopamine-helps regulate muscle contraction and provides smooth and controlled movement, makes sure you can write, fluid movement not jerky/uncontrolled

Parkinson-not enough dopamine

Front 22

******What is a major structure involved in Parkinson Disease?

Back 22

***basal ganglia

-area where you have changes and decreases in dopamine-substantia nigra of basal ganglia
-dopamine normaly stimulates basal banglia in path to smooth muscle movement

Front 23

******What are clinical manifestations of Parkinson?

Back 23

Parkinsonian tremor
Parkinsonian rigidity
Parkinsonian bradykinesia
Postural abnormalities

Autonomic and neuroendocrine symptoms
-basal ganglia influences the autonomonic nervous system via the HTO:
-can have autonomic sx too: diaphoresis, gastric retention, constipation, urinary retention

Cognitive-affective sx: depression-not secondary- maybe f/ reduced frontal lobe activity or reduced dopamine

Dementia
late manifestation/Lewy Bodies (protein accumulations), occur and lead to Dementia

Front 24

MS-what is it?

Back 24

Multiple Sclerosis
-progressive demyelinating disorder of the CNS
-autoimmune

Front 25

***********Main components of MS?

Back 25

genetic predisposition plus virus

Front 26

What is myelin sheath? And what is it r/t MS?

Back 26

myelin sheath leads to ability to jump or skip signal, so signal can transmit more quick and efficiently, neurons send signals rapidly down axon

MS: myelin sheath destroyed, message has to move down axon directly, which is much slower

Front 27

What is the patho of MS?

Back 27

genetic predisposition + virus
---->
T-cell attack myelin proteins
inflammation
B-cells: increase inflammation, damage myelin, form autoantibodies
--->
Demyelination
---->
slowed nerve signaling
increased Ca into cell
plaques

Front 28

What are clinical manifestations of MS?

Back 28

depend on plaque formation:
changes in hearing, sight, muscle tone, gait, weakness, numbness, stiffing

Immune response leads to generalized weakness

Front 29

What is pain?

Back 29

an unpleasant sensory and emotional experience associated with actual and potential tissue damage, or described in terms of such damage

Front 30

***********What is the pain pathway?

Back 30

****tissue injury ---> release of inflammatory mediators

nocioceptors triggered

pain signal ascends to dorsal horn of spinal cord

signal transmitted to second order neuron

decussates spinal cord --> ascends through spinothalamic tract to RAS --> thalamus

perception of pain processed in the somatosensory corted

ND2RASTS

Front 31

What is the damping effect r/t Parkinson?

Back 31

damping effect is normal process that occurs at basal ganglia during dopamine stimulation

does not occur with Parkinson

Front 32

What are two different types of pain pathways?

Back 32

A-Delta
-fast, myelinated
-sharp, localized pain

C-Fiber
-slow, unmyelinated
-generalized burning/ache

Front 33

What is CP?

Back 33

Cerebral Palsy
-injury to CNS leading to motor dysfunciton

Front 34

What is one cause of CP and its patho?

Back 34

Hypoxia:

hypoxia
-->
increased CO2, increased lactic acid
--> change in osmotic pressure
--> edema
--> CNS damage

Front 35

****What causes Reyes Syndrome?

Back 35

Virus (often Influenza B or varicella) + Salicylates (ASA/aspirin)

Front 36

*****What happens as a result of Reyes Syndrome?
What systems are affectd?

Back 36

Virus + ASA
--->
increased ammonia and short fatty acids in blood and hypoglymenia

Liver-liver deposits, hepatomegaly
Kidneys-fatty degeneration, azotemia
Brain-edema

Front 37

What are the stages of Reye's Syndrome?

Back 37

Stages I-V: starting with N/V, drowsiness progressing to seizures, DTR loss, respiratory arrest, death

Front 38

What is a neural tube defect?

Back 38

neural tube defects are caused by an arrest in development of the brain and spinal cord

Front 39

**********What are examples of neural tube defects?

Back 39

anencephaly-absence of skull and parts of brain, fatal

encephalocele-herniation of brain and meninginges, good prognosis

*******meningocele-the protrusion of meninges thru a vertebral defect; the spinal cord is not involved; present at birth as a protruding sac; abnml neuro function may be present; hydrocephaly common complication; need sx

spina bifida/myomeningocele-hernation of meninges, spinal fluid, and spinal cord, and nerves thru a vertebral defect; myomeningocele is a sac on the back; bowel/bladder dysfunction