Wade Test 1

Front 1

how long is typical survival after the onset orf dementia?

Back 1

4.5 years

Front 2

3 most popular things when talking about intracranial aneurysms?

Back 2

1. found in circle of willis
2. increase with HTN
3. anterior circulation

Front 3

most common locations for intracranial aneurysms are:

Back 3

1. bifurcation or circle of willis
2. carotid system
3. vertebrobasilar arteries

Front 4

why should you always aviod valsalva?

Back 4

because most symptoms are asymptomatic (5%) have one and dont know about it.

Front 5

what is less commom than aneurysms but more severe?

Back 5

vascular malformations= when an artery feeds directly into a vein. Patients have chronic non discript headhache or migraine.

Front 6

which is more sensitive, brudinskis or kernigs?>

Back 6

brudinskis

Front 7

What is a significant risk for vasular malformation surgery?

Back 7

redbleeding after one month- so monitor neurological status! 70% mortality rate

Front 8

what type of headache should the person avoid alcohol for?

Back 8

cluster/paroxymal hemicranial

Front 9

what catagory of migraines IS associated with an aura?

Back 9

Classic Migraine.

Front 10

normal CSF pressure?

Back 10

10mmhg

Front 11

what causes an aura?

what causes aura pain?

Back 11

expanding area of reduced cortical activity and decreased blood flow

trigeminal nerve

Front 12

cluster headache AKA

describe the pain

Back 12

horton syndrome

severe, unilateral, 30min-2hours, burning, tearing

Front 13

who is most susceptable to tension HA

Back 13

either sex in their second decade

Front 14

describe tension HA pain

how long is a chronic tension headache

are they agrevated by physical activity?

Back 14

mild-mod
BIlateral
gradual onset
hours-days


over 15 days

No

Front 15

Treatment options for tension headcahes

Back 15

ice, NSAIDS, naproxen, tricyclics

(ikeep an eye out for ODing)

Front 16

Primary tumors are usually

primarily more common in what age group

Back 16

Gliomas

kids (infratentorial)
where as peripheral nerve tumors are more common in adults

Front 17

How come primary tumors rarely metastisize?

Back 17

there are no lymphatics in the brain

Front 18

tumors are associated with what three problems?

Back 18

increased ICP
hypoxia
seizures

Front 19

3 tumors are associated with what three problems?

Back 19

increased ICP
hypoxia
seizures

Front 20

what percentage of poepl with cancer have it spread to the brain?

what cancers are more comminly associated with spreading to the brain?

Back 20

only 25%

lung and breast cancer.

Front 21

70% of secondary tumors are found where?

Back 21

vertebral collumn.
causing nerve compression, collapsed vertebras and pain

Front 22

two types of nerve sheath tumors

Back 22

neurfibroma -inhereted
schwanoma- ladies 50 years

Front 23

what are the early and late signs of having a schwanoma?

Back 23

early: teniitis, HA, unsteqady gait, facial pain

late: vertigo, rapid position changes

Front 24

Name four CNS infections

Back 24

meningitis, HIV, abcess, encephalitis

Front 25

what causes meningitis?

signs

Back 25

bacteria, fungi, parasites, toxins

HA, stiuff neck, photophobia, vomiting, confusion

Front 26

what insect carries encephilitis?

Back 26

mesquito

Front 27

S/S of encephiltiis

Back 27

fever, delerium, confusion, LOC, seizures

Front 28

are MMR, DTO vaccines linked to encephalopathy?

Back 28

Noper

Front 29

toxoplasmosis is comon in people who

Back 29

have aids and dont avoid cat liter and raw meat

Front 30

Lymes Disaease effects what systems? even tough half of patients have reoccuring symptoms, what are the acute signs and the chornic signs?

Back 30

CNS and peripheral nerves

acute: heart problems, CNS infections

chronic: 2 years post bite
arthritis and CNS infections

Front 31

Parkinson Disease is a disorder of...

when is this disease seen?

whats the cause

Back 31

corpus stratum in the basal ganglia

- neurons in the dopqamenergic pathway degenerate

- more in men over 40, most prevalent in people over 60.

the cause is either unknown or envirmental toxins

Front 32

what is a great PT intervention for Parkinsons?

Back 32

PNF, trunk rotation (espeically for gait)

Front 33

S/S for parkinsons-


most common cause of death?

Back 33

resting tremor, loss of rotation (cogwheel), Akinesia,
Festinating gait pattern., orthostatic hypotensions, constipation, depression, dementia, invalid state 15-20 years

pneumonia

Front 34

Festinating =

Back 34

start moving slow, then speed is increases and its hard to stop. Loss of postural stability

Front 35

When should you give parkinsons patient a walker?

Back 35

earleir than you think they need it so they can prepare.

change their body position alot to increase lung health.

Front 36

Describe dementia that is associated with parkinsons

Back 36

80% in mental hospitals
bradyphrenia (slow thinking)
Sundowning
less insight

Front 37

two major signs of Huntintons Disease

Back 37

chorea and dementia

(degenerative disorder of basil ganglia cortex)

Front 38

How is huntingtons the opposite of parkinsons?

Back 38

loss of gaba neruons with the release of dopamenergic neurons resulting in chorea.
- progressive dementia, emotional changes

life span 10 years

Front 39

Common onset of MS

associated with what type of lesion.... resulting in...

Back 39

20-50 years more in females


UPPER motor!!

Spasticity!!!

Front 40

describe the 4 classification systems of MS

Back 40

1. relapse remitting- most common, no progression between exacerbations, some recovery during remission

2. primary progressive- steady decline

3. secondary progressive- starts with the first and moves into the second kind

4. progressive relapsing- the worst kind, steady p[rogressive with acute attacks)

Front 41

What factors indicate a benign disease course of MS

Back 41

-double vision
-long interval between the first two relapses
- disease onset before 25
- few lesions
- lots of remission
- one region affected
- female

Front 42

what MS factors indicate a malignant course

Back 42

- urinary incontinence
- cerebellar ataxia
- onset after 40
- male sex

Front 43

Most common MS symtoms

Back 43

Visual
Paresis (partial mvt loss)
parathesia (tingling, numbing)

Front 44

MS treatment-

common side effects

Back 44

increase remission times, and prevent exacerbations, plasmapharesis

beta infueron injection (blocks T cells from atacking the myelin)

flue symptoms, liver toxicity, depression

Front 45

what would a good PT do for someon who just got MS

Back 45

breathing exercises

dont use heat

use steriods

Front 46

ALS=

Back 46

amyptrophic lateral sclerosis

motor neuron disease both upper and lower
(DIE FAST, FOCUS IN QOL)

Front 47

amyptrophic=


Lateral Sclerosis=

Back 47

muscle wasting seen with LMN disease

scaring in corticospinal tract with UPMN disease

Front 48

Clinical manafestations of ALS

Back 48

- weakness generally begins in one muscle group
- assymentricall.y effected muscle groups in a mottled distrobution (leading to respiratory failure) and no remissions
- mild spasticity

Front 49

Clinical manafestations of ALS

Back 49

- weakness generally begins in one muscle group
- assymentricall.y effected muscle groups in a mottled distrobution (leading to respiratory failure) and no remissions
- mild spasticity

Front 50

Clinical manafestations of ALS

Back 50

- weakness generally begins in one muscle group
- assymentricall.y effected muscle groups in a mottled distrobution (leading to respiratory failure) and no remissions
- mild spasticity

Front 51

ALS therapy-

Back 51

swimming, dont over exercise, when the spasticity gets bad do prolonged stretching, avoid cold temperatures


FYI- the most common als is sporadic and the cuase is known

Front 52

Classic ALS aka-

presentations-

Back 52

Lou Gehrigs Disease

Upper extremity proximal problems
happens more in males when their are 40 and peaks in the 50's.



some exotic tonxins can cause a familia type of ALS

Front 53

ALS is characterized by:

what is the hypotheses of ALS pathogenesis

Back 53

selective degeneration of motor neurons

Front 54

ALS is characterized by:

what is the hypotheses of ALS pathogenesis

Back 54

selective degeneration of motor neurons

Front 55

Current hypothesis for ALS

Back 55

excitatory neuron toxicity
- increased glutamate which may be toxic to motor nerons

Front 56

Medical word for nerve root problems

Back 56

redicularopathy

Front 57

Etiologic Agent of Hansens Disease

Clinical features of Hansens Disease

Back 57

slowly multiplying bacteria that effects the skin, nerves and mucous membranes cured by felidomuyde but it causes birth defects

chronic infectous disease usualy gets skin and nerves, can be spread by respiratory droplets and numbness by skin lesions.

Front 58

The NS in children develope from

Back 58

dorsal thickening of the ectoderm (neural plate)
mesoderm= blood vessle, micro glial cells, nerve things

Front 59

Dytosis

Back 59

premature closure of sutures

Front 60

fontanelles=

wen is cranial bone ossification complete?

When are sutures completely fused?

Back 60

wider spaces of unossified tissues at the junction of sutures.

posterior closed at 3 months
anterior closed at 2 months

8 years of age

12 years of age

Front 61

When is the myelen sheeth formed?

Back 61

first 3 years olf life

Front 62

When is the myelen sheeth formed?

Back 62

first 3 years olf life

Front 63

Name and describe four types of Neural Tube closure defects

Back 63

1) anecephaly= common,m stil born
2) encephiloceole= brain cyst, aterior frontal lobe gets cut off, can be fixed inutero
3) meningocele
4) mylelomeningocele= common, meninges AND spinal cord are effected. Gets chopped off and all below is paralyzed.

Front 64

Name and describe four types of Neural Tube closure defects

Back 64

1) anecephaly= common,m stil born
2) encephiloceole= brain cyst, aterior frontal lobe gets cut off, can be fixed inutero
3) meningocele
4) mylelomeningocele= common, meninges AND spinal cord are effected. Gets chopped off and all below is paralyzed.

Front 65

Name and describe four types of Neural Tube closure defects

Back 65

1) anecephaly= common,m stil born
2) encephiloceole= brain cyst, aterior frontal lobe gets cut off, can be fixed inutero
3) meningocele
4) mylelomeningocele= common, meninges AND spinal cord are effected. Gets chopped off and all below is paralyzed.

Front 66

Name and describe four types of Neural Tube closure defects

Back 66

1) anecephaly= common,m stil born
2) encephiloceole= brain cyst, aterior frontal lobe gets cut off, can be fixed inutero
3) meningocele
4) mylelomeningocele= common, meninges AND spinal cord are effected. Gets chopped off and all below is paralyzed.

Front 67

Name and describe four types of Neural Tube closure defects

Back 67

1) anecephaly= common,m stil born
2) encephiloceole= brain cyst, aterior frontal lobe gets cut off, can be fixed inutero
3) meningocele
4) mylelomeningocele= common, meninges AND spinal cord are effected. Gets chopped off and all below is paralyzed.

Front 68

what is involved with a meningeocele?

- this is sometimes associated with what?

- how do you manage it?

Back 68

meninges and CSF

- club foot
- bladder dysfunction
- weakness
- hydrocephalus

Front 69

what is a heart disease indicator in blood test?

Back 69

homocyystine (folate metabolizes it)

Front 70

80% of mylomeningocele is found where?

85% of these are asocatied with?
when does this defect occur?

Back 70

lumbar or LS region (one of the most common developmental abnormalities of the NS)

hydrocephalis

first 4 weeks of gestation ( so before you know youre pregnant)

Front 71

Arlnod Chiari 1 Malformation=

Arlnod chiari 2 =

Back 71

-associated with mylomeningocele
- strider is common
- caudal displacement of CB


- seen in adults and isnt as severe.

Front 72

Tethered Cord Syndrome is associated with what NS problem?

what is this syndrome about?

Back 72

mylomeningocele

the filum terminlaies is the direct connection from the skin to the spinal corder ad post operative scar (like if there was surgery for spinda bifida) causes scar tissue and that doesnt stretch and tension is produced

Front 73

lipoma =

Back 73

fat tumor

Front 74

Macawen sign=

Back 74

cracked pot sign-
resonance when skull is tapped due to seperation of sutures. (associated with sun setting. )

Front 75

Craniosynostosis=

Back 75

cranial sutures fuse prematurally. More common in femailes, really mnust be cured and with treatment they must wear a helmet for years.

Front 76

Obstructive hydrocephalus is most often caused by

how do you get this?

causes atresia of...

Back 76

aqueductal stenosis

- transmitted as an X linked recessive trait

- foramen of magendie = dandy walker syndrome

Front 77

atresia=

Back 77

inappropriate development

Front 78

What is one of the most common crippling disorders of childhood?

Back 78

static encephalopathies non progressive aka Cerebral palsy


assocaited with seizures, visual impairments, and sometimes congnitive delays

Front 79

Signs of spastic cerebral palsy?

Back 79

increased muscle tone, prolonged primitive reflexes, exagerrated DTR, clonus, scoliosis, contractures.

Front 80

discribe dyskenetic cerebral palsy

this is from injury to the...

Back 80

problems with fine motor coordination, uncontrolled movements

basil ganglia or extrapryimiddal tracts.

Front 81

discribe Ataxis cerebral palsy-

whats a good drug for them?

Back 81

gait disturbances and instability

Baclofen- decreases stability

or botox, and teach them how to use their muscles so when the botox wears off they are ready.

Front 82

what does botox do?

Back 82

paralyzes snaps and snares.

Front 83

encephalopthies-

Back 83

inhereited metabolic disorders.... c`ommonly amino acids and lipid metabolism

Front 84

Defects in amino acid metabolism =

Defects in lipid metabolism =

Back 84

PKU

Tay sachs (lysomal storage disease)

Front 85

____ are discrete, time limited alterations in brain function including vhsnges in motor acitivity, autonomic acitivity ,consciousness or sensation, that resulrs from an abnormal and escessive elecreical discharege oF a GROUP oF nueons WITHIN the brain

Back 85

seizures

Front 86

the clinical manafestations of a seizure reflect-

Back 86

the area focus and the spread of the electrical discharge

Front 87

Epililepsy=

Back 87

a condition characterized by recurrnet seizures unprovoked by any imedialtley indentifiable cause.

Front 88

when do you usually get diagnosed with epilepsy?

Back 88

before 20 years old

Front 89

what is the third most common neurologic disorder?

Back 89

epilepsy.

following stroke and alszheimers.

Front 90

Seizures can be viewed as resulting from an...

Back 90

imbalence between excitatotry and inhibitory processes in the brain
( and decreased gaba)
** most are idiopathic!

Front 91

what kind of seizures are you conscious for?

Back 91

simple partial and complex partial seizures.

Front 92

Todds paralysis=

Back 92

temporary numbness or weakness in the efected body part after a motor patial simple seizure.

Front 93

Complex Partial Seizures=

Back 93

- half conscious
- aura
- confusion
- good prognsosis

** most common in adult**

Front 94

Generalized, tonic/clonic Grand Mal

when does most commonly occur?

Back 94

LOC
epileptic Cry
incontinence
good prognosis
dont put anything in mouth

in second decade of life.
lasting 2-5 minutes

Front 95

Petite Mal-

Back 95

when the kid spaces out, they tend to grow out of them.
- short seizures.

Front 96

Name 3 unclassified epilextic seizures

Back 96

1. infantile spasms
2. lenox-gastout sydrome
3. juvinile myoclonic

Front 97

infantile spasms-

Back 97

sudden extension of head , abduction and extension of arms, flexed knees, cry

** unique- responds to ACTH -so inflammation must be involved.

Front 98

Lennox- Gastout syndrome is characterized by a triad

do they respond to drugs?

Back 98

1. intractable seizures
2. retardation
3. slow spike and wave pattern on the eeg.

NO... why retardation occurs

Front 99

Whats the difference between an absent and a complex seizure in children?

Back 99

Complex are longer, preceeded by an aura, and have a brief period of posticoital comfusion.

Front 100

what does dylantin negativley effect?

Back 100

gums

Front 101

Lennox- Gastaut Syndrome Triad

Back 101

1. intractable seizures
2. mental and developmental retardation
3. slow spike and wave patterns on the EEG.

Front 102

What seizure sydrome dosnt respond to drugs?

Back 102

lennox- gastaut syndrome
( which is why there is a high rate of retardation)

Front 103

what age does lennox-gastout syndrome usually present?

Back 103

1-6

Front 104

What seizures begin shortly or right after pupurty but may first appear in early adulthood (generally with no cognitive delays)?

Back 104

Juvinile Myoclonic Epilepsy

Front 105

In most patientds with juvenile myoclonic epiolepsy , seizures are controled by...

what time of the day are the seizures most common in?

Back 105

valprioc acid (though the actualy disorder requires life long therapy)

- early morning

Front 106

name two types of acute encephalopathies-

Back 106

Reyes Syndrome and Meningitis

Front 107

Give overview of Reyes Disease=

Back 107

it effects all organs of the body, but lethal to the liver and brain. This is a two part illness and can present as a flu although reyes is not contagious.

abnormal amounts of fat accumulate around viscera, and severely increases pressure in brain. Without treatment the person could die in a few days.

Front 108

Discribe the two stages of Reyes Syndrome

Back 108

I. persisant, continuous vomiting, and sign of brain dysfunction.
II. personality changes, disorientation, convolutions, coma.

Front 109

What could possible be the reason to get reyes?

Back 109

maybe taking asprin when you have influenza... so be careful!!!

Front 110

what is the most common type of meningitis and describe

Back 110

bacterial

- death in young children
- otitis media may present

Front 111

Cerebrovascular disease in children differs from adults in three ways-

Back 111

1. absence of predisposing factors
2. differences in the clinical response
3. anatomic site of the pathalogic condition

Front 112

Name the statisticaly common tumors in adults and then children

Back 112

adults= epithelial tumors
kids= leukemia and brain cancer

Front 113

What are the first two most common neoplasms in children?

Back 113

leukemia
brain tumors

Front 114

Name two early on treatable embrypnoal tumors-

Back 114

neuroblastoma
retinoblastoma

Front 115

Define Mature Bone=

A mature bone cell is called-

how is bone broken down?

when does bone formation begin?

Back 115

a rigid CT consisting of cells, fibers, and ground substance, as well as crstylline minerals (mostly calcium).

osteocyte

by the osteoclasts using hydrolic enzymes

fetal life

Front 116

Wolfs LAW =

Does theraputic standing work?

Back 116

the strength of bone is directly proportional to the stresses placed on it

it has been shown to increase bone weight and slow the loss, so this is good for paraplegics

Front 117

the extracellular componenets of bone tissue are 65%..

Back 117

inorganic (calcium and phosphate materials)

Front 118

The most abundant macromolecule in the body is-

Back 118

collagen (which provides the framework for almost all tissues.

Front 119

what does type on collegen do-

Back 119

it is secreted by osteobolasts to help build bone.

Front 120

what are proteoglycans?

Back 120

(aka mucopolysaccharides)
- polysaccharide complexes attach to a protein core- provide strength
- to control transport and distrobution of ions- especially Calcium.

Front 121

What are Gycoprotiens?

Back 121

CHO rich- that control collagen interactions that lead to fibril formation- and has a role in calcification... maintains osmotic pressure in the bone?

Front 122

During bone mineralization, forming the first crystalline deposit - what is a common mineral?

Back 122

hydroxyapatite

Front 123

what type of bone uses the haversian system?

what type of bone is meant for functional ambulation?

Back 123

compact/ cortical bone

spongy bone ( cancellous, trabicular)

Front 124

Haversian Organization

Back 124

contains a canal filled with lymph, blood vessels and nerves.
there are concentric layers of bone matrix (lamellae) which have the ability to resist torision

between each lamelli is a pocket called the lacuna which contains an osteocyte

the channels between the lamellae are canaliculi and are parallel to the horizontal axis of the bone.

Front 125

how is spongy bone organization?

Back 125

lamelae arranges in plates called trabiculae- patterns are formed due to stress and in the spaces there is bone marrow.

Front 126

How does the periosteum connect to bone?

Back 126

sharpies fibers.

Front 127

3 characterisitics of long bone-

Back 127

1. diaphysis ( compact and marrow, yellow color)

2. Metaphysis (spongy bone internally, some marrow- RED)

3. Epyphysis= also sponngy bone internally and some red marrow, but also calcifies during puberty.

Front 128

Name 3 phases of remodeling-

Back 128

1. activation- cells differenciate into osteoclasts

2. resorption- a cavity is created, either by the haversian canal or the trabiculae

3. formation- secondary bone is laid down by osteoblats in lamella layers

Entire process takes 3-4 months

Front 129

List in order the process of Bone repair-

Back 129

1. hematoma formation
2. procallus formation
3. callus formation
4. calus replacement
.5 remodeling

Front 130

hematoma formation-

procallus formation-

Callus formation-

Back 130

brought on by blood containing growth factors and fibrin

fibroblasts, capillary buds and osteoblasts move in to form granslation tissue.

osteoblats in procallus deposit minerals

Front 131

Callus Replacement-

romodeling=

Back 131

replaced by lamina and trabicular bone by the osteoblasts

periosteal and endostial surfaces are remodleed to the size and shape before injury


repairing of the bone is an ongoing process

Front 132

green stick fracutures are commen in ?

Back 132

kids

Front 133

Describe joint capsule of Synovial Joints

Back 133

NOT ELASTIC

- dense fibers, connective tissue attached to bone by sharpys fibers, reinforced byt ligaments nad tendons
- richly innervated

Front 134

discribe the two layers of the synovial membrane-

Back 134

1. vascular (subintima), merges with joint capsule, elastic and fat

2. Celluyar Layer (intima) rows of synovial cells in a fiber FREE matrix. Makes synovial fluid
type a= phagocytosis
Tybe b= secretes HAP and gives synovial fluid its viscosity.

Front 135

why is it bad to have blood in the joint?

Back 135

the blood iron wears down the cartiledge.

Front 136

tidemark=

Back 136

(ossification front)- a boundry point representing a change in catrilage stiffness from trasitional to calcified.

also an area of weakness since tissues are transitioning.

Front 137

breifly describe layers of articular cartliadges.

Back 137

first few are touch and resistance

then are collumns, less resistant

then supportive

that calsified.

Front 138

Synovial Fluid=

Back 138

ultrafiltrate of plasma from vessels in synovial membrane (also contains free flowing leukocyte)

(must be weight bearing?

Front 139

Just list the 5 components to articular cartiledge

Back 139

hyaline
collegon
surface collagen
proliferative zone
hypertrophic zone

Front 140

What is hyline cartidlge maining made out of?

Back 140

water

Front 141

What is hyline cartidlge maining made out of?

Back 141

water

Front 142

Discribe the way coollegen fibers (articular cart) are placed-

Back 142

parallel at the joint surface of the cartilade and form a dense protective mat.

Front 143

Discribe the way coollegen fibers (articular cart) are placed-

Back 143

parallel at the joint surface of the cartilade and form a dense protective mat.

Front 144

Describe middle layer of articular cartilage-

Inner layer?

Back 144

fibers tangible to outerlayer, allowing deformation to absorb WB forces

fibers are now perpendicuar to joint surface and can resist shearing forces. Contain the tidemark- which achors fibers to the underlying bone.

Front 145

macromolecules in catilage consist of

Back 145

proteins
CHO
HAP

Front 146

what is nessescary so weight bearing dones push out all our synovial fluid?

Back 146

proteoglycans

Front 147

is articular cartilage innervated?

Back 147

NO

Front 148

Healing is very limited in articular cartilage. When DO you see some healing occur?

Back 148

lesion breaches the tidemark- then bone bleeds with helps increase healing.

Front 149

Discribe articular cartilage repair-

Back 149

1. this is done by type 1 cartilage = fibrocartilage

- repair takes 6-8 weeks
- weak scar
- passive ROM is a must

Front 150

Osteoarthritis is the single most common....

aka-

common cause?

Back 150

Degenerative joint disease.

wear and tear arthritis

unknown

Front 151

The hallmark of Osteoarthritis (OA) is

List these events in chronological order.

Back 151

the disorganization of the five zones of articular cartilage.

1. loss of proteoglycans and death of chonrocytes

2. fibrillations (surface cracks parallel to the long axis of the particular surface.

3. synovial fluid leaks into the deep cartilage forming cysts

4. fibrochartilage forms plug and trys to minic articulating hylaine catliage.

Front 152

in bone, what area must you be passed to be able to develope bone spurs?

Back 152

past tidemark

Front 153

cpk =

WHERE is this normaly found?

WHEN is it normally seen?

normal and abnormal amounts:

Back 153

creatine phosphokinase

normally found inside muscle cells- but also found in serum if cells have been lysed.

1. olympic atheletes
2. children with MD
3. indicative of heart attack

1- normal
20,000- abnormal

Front 154

Age related changes in joints

Back 154

1. catiledge becomes rigid and frail. less water
2. decreased ROM due to less extensible CTS
3. osteoperosis begins with fewer trabeculae
4. IV disks may compress

Front 155

Age related changes with muscle

Back 155

muscles remain trainable throughout life

- age related sarcopenia (after 70 years)
- specific decrease in type II fibers
- reduced metabolic capacity

Front 156

sarcopenia=

Back 156

loosing muscle tissue

Front 157

Motor Unit=

associated with what horn?

Back 157

muscle fiber
neuromuscular junction
axon
motor neuron


ventral horn

Front 158

What motor Neuron in skeletal muscle always has stimulation?

What about an action potential in an Ia afferent from a single muscle spindle?

Back 158

alpha

that will only slightly depolarize the soma of the alpha motor neuron to that same muscle

Front 159

myasthenia gravis=

Lambert-Eaton=

Botulism=

Tetnus=

Back 159

antibodies to nicotinic ACH receptors

antibodies to voltage gates CA in presynaptic membrane

inhibitory cns neurons- alpha

paralized vesicles in CNS

Front 160

total force of skeletal muscles=

Back 160

sum of force produced by active cells.

Front 161

where do you find involuntary mucles?

what do they have so entire tissue behaves as one cell?

Roles of involuntary muscles:

Back 161

walls of hollow organs

functional synctium

generate force and mvt
maintain organ dimensions against applied loads

Front 162

myoblasts aka

Back 162

satelight cells

Front 163

are skeletal muscle fibers multinucleated?

how does the muscle fiber develope?

Back 163

yes

from the fusion of single nucleated myoblasts

Front 164

what color are type II fibers?

type I?

Back 164

white

red (myogloben, high capillary density)

Front 165

what comprises a muscle membrane?

Back 165

sarcolemma and basememnt membrane

Front 166

the sarcolemma is continuous into a T tubule and organizedinto a triad

Back 166

wow... and muscle fibers are bundled into fascicles that are bundled into skeletal muscle.
yep

Front 167

what comprises thin filaments?

Back 167

actin, tropomyosin, troponin

fyi- troponin is a regulatory protein

Front 168

how do you measure a sarcomere?

what holds actin in place?

what holds myosin to Zline?

what lines move?

what lines never move?

Back 168

Zline to Zline

Zline- but in general Nebulin supports actin

titin

Zlines

Mlines

Front 169

what protein is only in skeletal muscle?

Back 169

nebulin

Front 170

what muscle filament is globular?


what is the name of a class of transmembrane proteins?

Back 170

actin (2 are wrapped together)

Integrins : links muscle together- also very important in cell migration

Front 171

membrane spanning protein=

Back 171

distrophin
(this is a problem in MD)

Front 172

Integrins function as:

Back 172

1. cell-cell receptors
2. migration receprots
3. cell signaling receptors
4. mechanical links

Front 173

Actin filaments are linked to the basal lamina through the sarcolemma by a complex of? (in skeletal muscle)

Back 173

3 things that form distrophin

1. sarcoglycans
2. dystroglycans
3. syntropins

also links structures intra to extracellular that becomes tendons...

Front 174

relate Dystrophin to Duchennes and to Beckers-

Back 174

Duchennes- NO dystrophin
Beckers- diminished dystrophin- muscle weakness because plasma membrane gets damaged

Front 175

isokinetic contraction means-

Back 175

same speed
varing resistance

Front 176

I band=

A bands=


what bands change and what bands dont

Back 176

lite, only thin filaments, changes length

Dark, entire length of thick filament. NO CHANGE

HI- dont
AM- DO change

Front 177

what controls muscle contraction

Back 177

TM and TN

Front 178

what part of myosin acts independantly?

mysin acts as an atpase but is normally inhibited by?

Just read the paragraph

Back 178

the head

MG levels in sarcoplasm

- hydrolysis of atp secondary to actomyopsin complex represents the fundemental chemomechanical transducion process.
the energy released by atp hydrolysis is stored within the myosin molocule in a HIGH energy state

Front 179

Why is myosin ready to go at rest?

Back 179

atp is already hydrolysed

Front 180

The difference between stress length curves for contracting and relaxed muscles is the...

what length do you get the best contraction?

Back 180

Active stress length relationship

80-120% of resting length

Front 181

How does load influence velocity?

Maximal power is obtained with....

Mechanical efficiency=

Back 181

inc Vel, DEC load

a load of about 30% of the maximal force that can be developed

40-45 % tops
(Ineffieceint)

Front 182

what kind of contraction is good for exercise when you have a joint injury?

Back 182

isometric contraction

Front 183

cross bridges are cycling ________ to permit continuous shortening

Back 183

asynchronously

Front 184

velocity of shortening depends on

Back 184

load
number of sarcomeres
kinetic characteristics of the myosin atpase

Front 185

fused temporal summation =

Back 185

tetunus - maximal force generated by a muscle

Front 186

How does tetanic frequency differ between muscles?

Back 186

slow twitch= 100/s
fast twitch= 300/s

Front 187

what structures are in series and what structures are in parallel?

Back 187

series: tendon and muscle

parallel: sarcolemma and muscle fiber

Front 188

name the three dyhydropuritines

Back 188

ditiosin
verapomil
nifetopen

these are CA+ blockers, that block DHP. We dont care in skeletal muscle but in cardiac muscle it slows down the heart rate. so you can use heart rate as an indicator of work load.

Front 189

what does DHP do?

Back 189

it is a voltage gated ca channel in a t-tubule. its attached to sarcoplasmic reticulums receptor RYR. it changes shape so CA can come through.

Front 190

latent period=

Back 190

time lag between stim, ap in muscle, see a contraction

Front 191

quickly give order for cross bridge cycle

Back 191

1. Ap in sarcolemma cause myoplasmic ca to increase
2. CA binds to TN and thin filament changes conformation
3. cycle
4. ca is removed from myoplasm when the stimulus ends, ca dissassociated from tn
5. thin filament returns to original conformation.


CA+ regulates everything!

Front 192

suicide risk increased with ____ medications

Back 192

seizure

Front 193

threshold for opening a SR ca+ channel is

Back 193

-50mV

Front 194

the rate at which a twitch developes is a function of

Back 194

myosin atpase

Front 195

mckartles disease

Back 195

cant generate enough atp

Front 196

myotonia congenita-

Back 196

over time K increases and there will be repolarization troubles. So muscle uses CL- ions to repolarize the membrane

born with muscle tons cnatrelax- problems with cl- channels

Front 197

Twitch=

Back 197

submaximal response of a muscle fiber to a single action potential (all fibers in the motor unit will twitch)

Front 198

Treppe effect=

Back 198

repetitive action potentials can cause summation of twitches

Front 199

what is the result in a sacromere after contraction

Back 199

a. Sarcomere length shortens b. H Zone disappears
c. I Band length shortens
d. A Band length remains same

Front 200

most of the atp used is...

Back 200

to maintain the muscle rest

Front 201

first burst of energy in sports=

Back 201

atp-pc system

Front 202

pagets disease=

Back 202

hypermetabolism of bone by osteoblasts. aka osteotitis deformans- bones get soft

Front 203

fosomax inhibits....

Back 203

osteoclasts

Front 204

hypertrophy=

Back 204

increasing the diameter of a muscle fiber by synthesis of more fibrils

increases amount of force generated

Front 205

lengthening =

Back 205

more sarcomeres in series, more shortening, greater velocity if shortening

Front 206

bone fibers are made of

Back 206

collogen- gives it tensile strength

Front 207

bone formation begins in fetal life as...

Back 207

mesychymal cells differentiate into chondrocytes

Front 208

osteocytes maintain?

what reabsorbs bone?

what does phosphate in the bone do?

Back 208

bone matrix

osteoclasts

regulates vit D, promoting mineralization

Front 209

what kind of collagen do osteoblasts produce?

Back 209

Type I

Front 210

osteoclasts bind to ther bone surface of cell attachment proteins called:

what makes up the major ORganic component of bone matrix?

Back 210

intigrins

collagen

Front 211

fibrils

Back 211

3 chain collegen- have overlapping patterns, then link togther and form fibers

Front 212

articular cartiledge has what type of collagen?

Back 212

type II

Front 213

what strengthens bone by forming compression resistant complexes between the collogen fibrils?

Back 213

proteoglycans (hyaline cartildge component) polysacharides and a protein core

Front 214

what controls collagen interatcions that lead to firbil formmation?

Back 214

glycoprotiens

Front 215

a huge outcome of the final step in bone formation: bone mineralization is

Back 215

formation of HAP

Front 216

what type of bone makes up 85% of skeleton?

Back 216

corticol

Front 217

tha major difference between the two types of bone =

Back 217

organization of elements.
Compact bone is highly organized- haversain system.
Spongy bone is not complex and has loose trabecula things.

Front 218

shaft of the bone aka=

neck of bone=

where is the yellow marrow and where is the red marrow?

Back 218

diaphysis

metaphysis

yellow= diaphysis
red= epiphysis

Front 219

describe remodeling:

Back 219

1. activation= hormones activate bone cell precursers

2. resorption= osteoclasts do their thang

3. formation= secondary bone gets layed down, new haversian canals are formed- new lamena are laid down

takes 3-4 months

Front 220

Bone stages of wound healing:

Back 220

1. hematome formation
2. procallus formation (produce granulation tissue) cartiledge is formed
3. callus formation (via osteobalsts)
4. Callus Replacement
5. Remodeling- to perfect mechanical properties

This process depends on many things- the first step happens within an hour, the next steps happen over weeks and remodeling can take up to 4 years!

Front 221

each skeletal muscle in an organ contained in a 3 part connective tissue called

Back 221

fascia

Front 222

what part of muscle is in contact with the tendon-

what surrounds the smallest unit of muscle fibers?

Back 222

epimysium

endomysium

Front 223

voluntary indicates that the muscle is ...

Back 223

controlled directly by the CNS

Front 224

the motor unit is from which horn

Back 224

anterior horn

Front 225

what receptor lies parallel to muscle fibers?

Back 225

Muscle Spindles

Front 226

white muscle fibers (II) stain_____ while red fibers (I) stain_______

Back 226

dark

light

Front 227

the tubules of the sarcoplasmic reticulum are important for...

Back 227

movement of CA+

Front 228

Within the sacromere is the giant muscle protein called ____. = molecular spring that determines muscle stiffness and elasticity.

Back 228

Titin

Front 229

You can measure muscle mass with-

Back 229

creatine and creatinin

Front 230

activation, the first step of muscular contraction begins with...

Back 230

spread of action potential from the nerve terminal to the nueromuscular junction

Front 231

activity last longer then ____ expends the available stored atp and phospohocreatine

Back 231

5 seconds

Front 232

adding motor unit within the muscle (activating them)_ is called =

Back 232

repetitive discharge

Front 233

which muscle can genereate more force, long ones or short ones?

Back 233

longer ones

Front 234

arthrography=

Back 234

injection of dye into the joint

Front 235

whats a great test for diseased/damaged muscles?

Back 235

serum CK concentration... and myoglobin in urine

Front 236

Aging and Bones

Back 236

1. remodeling takes longer
2. less mineralizzation
3. increased osteoclatic bone resporption

Front 237

age related loss in skeletal muscle=

Back 237

sarcopenia

Front 238

what is the leading cause of death amoung ages 1-44?

Back 238

Trauma

Front 239

regeneration of muscle fibers relies on..

Back 239

- severity
- vascular supply-
- terminal axons for reinnervation

Front 240

incomplete fractures tend to occur in the more...

Back 240

flexible growing bones of children

Front 241

transchondral fractures are most prevelant in ...

Back 241

adolescents

Front 242

incomplete fractures tend to occur in the more...

Back 242

flexible growing bones of children

Front 243

legg-calve- perthes disease =

Back 243

type of osteochondrosis (self limited disease of the hip)
- children
- the femoral head dies and a new one is remodoeled.
- might see trendelenburg gait
-

Front 244

Cerebral Palsy-

treatment:

Back 244

static disorder of muscle tone and balence caused by ischemia to the brain


spasticity reduction.... botox

Front 245

MD is an ___linked inherited

early clinical manafestations

Back 245

X

around age 3 with slow motor development, muscle weakness and wasting..
Muscle weakness always begins in pelvic girdle- waddling gait

Front 246

complete lack of dystrophin =

Back 246

fibers are poorely anchored and are teared apart during contraction. free calcium comes in causeing cell death and fiber necrosis

Front 247

gowers sign

Back 247

md kids get off the floor by climbing up their legs

Front 248

what week does the neural tube form?

Back 248

fourth week of gestation

Front 249

anencephaly

Back 249

- soft bony component on skull and part of brain is missing
- froglike appearance
- still born or die right away

Front 250

encephalocele-

Back 250

herniation or protursion of brain and meninges through a defect in the skull. Surgery can help

(if ONLY memninges then its called a cranial meningocele

Front 251

Meningocele=

Back 251

neural tube fails to close- sac of minenges filled with spinal fluid.
Does NOT involve spinal cord

Front 252

Myelomeningocele-

Back 252

spina bifida
- hernial protrusion including the spinal cord
- without surgery the csf fluid will cause more damage
-

Front 253

Arnold Chiari type II

Back 253

assocaited with myelomeningocele- downward displacement of posterior brain
- causes cranial nerve palsys
- hydrocephalus
- worsens as child grows and cord is tethered: bladder problems!

Front 254

portwine variety may be...

Back 254

a sign of spina bifida occulta

Front 255

dandy walker deformity=

Back 255

defect in midline cerebellar, where hydrocephalis is caused by atresia of foramin of magendi.

Front 256

macewen sign

Back 256

resonate note when the skul is tapped due to seperation of the sutures
aka cracked pot sign- sunsetting too.

Front 257

encephalopathies

Back 257

general diseases involving the brain

Front 258

major types of cerebral palsy are:

Back 258

ataxia
dyskinesia
spasticity

Front 259

spastic cerbral palsy=

Dyskinetic cerebral palsy=

Back 259

increased muscle tone
prolonged primitive stretches
huge dtrs
clonus
rigidity
contractures


poor fine motor cooridnation
and purposeful movements
- jerky, uncontreolled abrubt movements.

Front 260

ataxic cerbreal palsy

Back 260

gait disturbances and instabitlity

Front 261

HPA

Back 261

lesser form of PKU

Front 262

can diet influence epilepsy?

Back 262

some say a ketogenic diet can reduce seizures. really only works with younger ikids and only works for about 1-2 years.

Front 263

hallmark of viral meningitis-

Back 263

mono munclear response in the CSF and presence of normal blood glucose level.