Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Y-Patho 3 > Week 9 + 10 Nervous System > Flashcards

Week 9 + 10 Nervous System Flashcards

1
Q

how long does a migraine last

A

4 to 72 hours

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

why do women more often have igraines

A

hormonal differences

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

diagnostic criteria for migraines (need 2)

A

-unilateral head pain
-pulsating pain
-pain worsening with activity
- moderate or severe pain intensity
-and at least one of the following: nausea or vomiting, or both, or photophobia and phonophobia.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

chronic migraine dx, how many days

A

more than 15 days per month for at least 3 months

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

trigeminal autonomic cephalagia

A

cluster headaches

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

which headache occurs primarily warily in men

A

cluster

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

uncommon headaches occur in clusters for a period of days followed by a long period of spontaneous remission
-extreme pain
-short duration

A

cluster headaches

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

headache attack usually begins without warning and is characterized by severe, unilateral tearing; and burning, periorbital, and retrobulbar or temporal pain lasting 30 minutes to 2 hours.

A

cluster headache

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

do cluster headaches usually happen on the same side

A

yes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

mild to moderate bilateral headache with a sensation of a tight band or pressure around the head. The onset of pain is usually gradual

A

tension HA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

sudden, transient disruption in brain electrical function caused by abnormal excessive hypersynchronous discharges of cortical neurons

A

seizure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

the recurrence of seizures and a type of seizure disorder for which no underlying correctable cause for the seizure can be found

A

epilepsy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

involve neurons bilaterally
-originate from a subcortical or deeper brain focus
-result from cellular, biochemical, or structural abnormalities of a widespread nature
-consciousness always impaired/lost

A

generalized seizures

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

seizure with neurons only unilaterally

A

focal seizures

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

involve neurons bilaterally

A

generalized seizures

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

-local (focal) onset, and originate from discrete areas usually associated with structural abnormalities localized to the cortical brain tissue
-consciousness may be maintained

A

focal seizure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

occur when there is disruption in the balance of excitation and inhibition of electrical impulses

A

seizures

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

long-lasting depolarization of the neuron caused by an influx of extracellular calcium that opens the voltage-dependent sodium channel. The influx of sodium generates repetitive action potentials.

A

invitation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

in epilepsy the sodium potassium channels allow for an influx of too much

A

too sodium
potassium takes too long to leace

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

(phase of muscle contraction associated with increased muscle tone)

A

tonic phase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

(phase of alternating contraction and relaxation of muscles)

A

colonic phase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

This inhibition causes an interruption in the seizure discharge, producing an intermittent contract-relax pattern of muscle contractions. The intermittent clonic bursts gradually become more and more infrequent until they finally cease. At this point the epileptogenic neurons are exhausted and the neuronal membranes probably are hyperpolarized.

A

This inhibition causes an interruption in the seizure discharge, producing an intermittent contract-relax pattern of muscle contractions. The intermittent clonic bursts gradually become more and more infrequent until they finally cease. At this point the epileptogenic neurons are exhausted and the neuronal membranes probably are hyperpolarized.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

seizures demand a 250% increase in
and a increase in what

A

ATP
increase cerebral oxygen need

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

severe seizures can lead to deficient in

A

ATP, phosphocreatine, and glucose then occurs,
-lactate accumulates in the brain tissues

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Severe seizures thus may produce

A

secondary hypoxia, acidosis, and lactate accumulation, all of which are imbalances that may result in progressive brain tissue injury and destruction.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

state of continuous seizures lasting more than 5 minutes, or rapidly recurring seizures before the person has fully regained consciousness from the preceding seizure, or a single seizure lasting more than 30 minutes.

A

Status Epilepticus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

postictal state

A

period from when seizure ends and the patient returns to their baseline

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

The person is still in a postictal state

A

Status Epilepticus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Status epilepticus most often results from

A

-abruptly stopping antiseizure medications
-untreated or inadequately treated persons with seizure disorders.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

status epileptics medical emergency

A

-cerebral hypoxia
-Mental retardation, dementia, other brain damage, and even death are serious threats.
-Aspiration risk.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q
A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Two types of symptoms often signal an impending generalized tonic-clonic seizure:

A
  1. an aura- a partial seizure that immediately precedes the onset of a generalized tonic-clonic seizure
    2.prodroma (malaise, headache etc)- an early manifestation that may occur hours to days before a seizure
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Two types of symptoms often signal an impending generalized tonic-clonic seizure:

A
  1. an aura- a partial seizure that immediately precedes the onset of a generalized tonic-clonic seizure
    2.prodroma (malaise, headache etc)- an early manifestation that may occur hours to days before a seizure
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

signs that seizure is coming on

A

sudden uncontrollable jerking movements of one or more extremities or the entire body
-Loss of postural tone
-person falls to the ground and the body stiffens in an opisthotonos position with legs and, usually, arms extended;

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

evaluation for seizures

A

-health history
-bloodwork (glucose, calcium, blood urea nitrogen, urine sodium, and creatinine)
-EEG
-CSF examination

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Of all strokes, 87% are

A

ischemic (thrombotic or embolic)
(obstruction within a blood vessel to the brain)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

greatest risk factor for stroke

A

high BP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

arise from arterial occlusions caused by thrombi formed in the arteries supplying the brain or in the intracranial vessels

A

thrombotic stroke

38
Q

development of a cerebral thrombosis most frequently is attributed to

A

atherosclerosis (thickening, plaque in arteries)
-inflammatory disease processes (arteritis) that damage arterial walls

39
Q

Transient episodes of neurologic dysfunction (weakness, numbness, sudden confusion, loss of balance, loss of vision, sudden severe headache) resulting from focal cerebral ischemia.

A

Transient Ischemic Attacks (TIAs)

40
Q

will people with TIA experience a stroke?

A

likely within the year

41
Q

Involves fragments that break from a thrombus formed outside the brain or in the heart, aorta, or common carotid artery

A

embolic stroke

42
Q

risk factor for stroke

A

atrial fibrillation (a fib)

43
Q

Embolization is usually in the

A

middle cerebral artery (the largest cerebral artery).

44
Q

when an area of the brain loses blood supply and becomes ischemic because of vascular occlusion (embolic or thrombotic).

A

Cerebral Infarction

45
Q

most common cause of brain occlusion (lose of blood supple)

A

-Cerebral thrombi and cerebral emboli

-also hypotension and atherosclerosis

46
Q

when is Thrombolysis given

A

3-4.5 hours of onset of symptoms

47
Q

if it is more than 4.5 hours and thrombolysis can’t be given, what is given

A

antiplatelet agents are administered (Aspirin, clopidogrel, or aspirin plus extended-release dipyridamole)

48
Q

the progressive failure (an acquired deterioration) of many cerebral functions that includes impairment of intellectual function with a decrease in orienting, memory, language, executive attentional functions, and alterations in behavior. The greatest risk factor is age.

A

dimentia

49
Q

mechanisms leading to dementia

A
  1. neurodegeneration
  2. atherosclerosis
  3. trauma, lesions in the cerebral convolutions
  4. increased cranial pressure
50
Q

leading cause of dementia and one of the most common causes of severe cognitive dysfunction in older adults

A

Alzheimer’s Disease (AD)

51
Q

most prevalent Alzheimer’s Disease (AD)

A

Nonhereditary, or sporadic, late-onset AD (70% of cases) is the most prevalent form.

52
Q

Late onset AD may be associated with

A

chromosome 19
-involved with the apolipoprotein E gene-allele 4 (apoE4).

53
Q

in AD formation of neuritic plaques containing a core of amyloid beta protein, the formation of neurofibrillary tangles, and the degeneration of basal forebrain cholinergic neurons with loss of acetylcholine.

A

-plaques int he brain with alzheimers

54
Q

in AD failure to clear plaque in the brain leads to

A

disruption of nerve impulse transmission, and death of neurons.

55
Q

a microtubule binding protein, in neurons detaches and forms an insoluble filament called a neurofibrillary tangle, which contributes to neuronal death.

A

tau protein

56
Q

chemistry behind loss of memory in AD

A

Loss of acetylcholine and other neurotransmitters

57
Q

The specific diagnosis of AD is made by

A

postmortem examination

58
Q

_____________ are used in mild to moderate AD to enhance cholinergic transmission.

A

Cholinesterase inhibitors (ChE-Is)

59
Q

a complex motor disorder accompanied by systemic nonmotor and neurologic symptoms.

A

Parkinson

60
Q

main disease feature Parkinson

A

degeneration of the basal ganglia involving the dopaminergic (dopamine-secreting) nigrostriatal pathway

61
Q

are men or women more likely to have parkinsons

A

men

62
Q

hallmark feature of parkinsons

A

loss of dopaminergic pigmented neurons in the substantia nigra (SN)

63
Q

underactivity of the direct motor pathway (normally facilitates movement) and overactivity of the indirect motor loop (normally inhibits movement).

-bradykinesia (slow movement) and rigidity

A

parkinsons

64
Q

problems associated with parkinson

A

mitochondrial dysfunction
-oxidative stress
-abnormal folding and accumulation of alpha-synuclein
-abnormal phosphorylation-
dysfunction of the ubiquitin proteasome system

65
Q

fibrillar intracellular eosinophilic inclusions,

A

Lewy bodies

66
Q

Norepinephrine is thought to be neuroprotective and loss of LC neurons may be associated with a worsening of disease progression and the behavioral symptoms of PD.

A

Norepinephrine is thought to be neuroprotective and loss of LC neurons may be associated with a worsening of disease progression and the behavioral symptoms of PD.

67
Q

symptoms appear after a 70% to 80% loss of
pigmented nigral neurons and a 60% to 90% loss of striatal dopamine.

A

parkinsons

68
Q

classic motor manifestations of PD

A

-resting tremor
-bradykinesia/akinesia (poverty of movement)
-rigidity (muscle stiffness)
-postural abnormalities

69
Q

is the parkinsons tremor with movement or at restq

A

at rest, tremor stops with mvoement

70
Q

what mauls are affected with parkinsons

A

All striated muscles
-eventually muscles of mastication (chewing), deglutition (swallowing), and articulation

71
Q

Parkinson’s dx symptoms

A

TRAP
(1) resting tremor
(2) cogwheel rigidity
(3) akinesia,
(4) postural instability

72
Q

parkinsons treatment

A

-dopamine agonist
levodopa (l-dopa)
-effective in early PD but can cause motor fluctuations,“off”periods, and dyskinesia in the long term.

73
Q

is a chronic inflammatory disease involving degeneration of CNS myelin, scarring or formation of plaque, and loss of axons.

A

Multiple Sclerosis (MS)

74
Q

genetic link for MS

A

HLA gene

75
Q

MR envrimoentla risk factors

A

Vitamin D deficiency, cigarette smoking, and Epstein-Barr virus infection

76
Q

The first demyelinating event, or“clinically isolated syndrome”(CIS), is a single episode of neurologic dysfunction lasting greater than 24 hours that can be a prelude to MS.

A

The first demyelinating event, or“clinically isolated syndrome”(CIS), is a single episode of neurologic dysfunction lasting greater than 24 hours that can be a prelude to MS.

77
Q

does MS effect white and grey matter

A

yes

78
Q

MS-
Autoreactive T and B cells recognize myelin autoantigens and trigger inflammation in the CNS, leading to the loss of myelin sheaths and nerve conductivity and subsequently to the death of neurons

A

Autoreactive T and B cells recognize myelin autoantigens and trigger inflammation in the CNS, leading to the loss of myelin sheaths and nerve conductivity and subsequently to the death of neurons

79
Q

classifications of MS

A

Relapsing-remitting, primary progressive, secondary progressive, and progressive-relapsing.

80
Q

IN 2/3RDs of MS patients what marker is elevated

A

CSF immunoglobulin G (IgG)

81
Q

MS tx

A

-Acute= corticosteroids.
-oral and injectable disease-modifying drugs are used to decrease the number of relapses
-vitamin D

82
Q

affects peripheral axons and is the generalized peripheral neuropathy commonly seen

A

Distal axonal polyneuropathy
-more sensory than motor

83
Q

cause of peripheral nuropathy

A

diabetes mellitus
alcohol abuse

84
Q

the myelin or Schwann cells are affected; occurs far less frequently. Weakness is the predominant sign with far less sensory impairment

A

Demyelinating polyneuropathy

85
Q

-autoimmune disease triggered by a preceding bacterial or viral infection
-numbness, pain, paresthesias, or weakness in the limbs
-acute or subacute progressive paralysis.

A

Guillain-Barré syndrome (GBS)

86
Q

most common peripheral paralysis of the 7th cranial nerve, the facial nerve, with an onset that is rapid and unilateral

A

Bells Palsy

87
Q

virus associated with Bells Palsy

A

Herpes simplex type 1

88
Q

sudden, severe, brief, stabbing, and recurrent pain within the distribution of one or more branches of the trigeminal nerve that supplies the forehead, cheek, and lower jaw.

A

Trigeminal Neuralgia`

89
Q

is Trigeminal Neuralgia bilateral or unilateral

A

unilateral

90
Q

drug for trigeminal neuralgia

A

anticonvulsant drug carbamazepine.

91
Q

disorders of spinal nerve roots. As the spinal roots emerge from or enter the vertebral canal,they may be injured or damaged by compression, infection, inflammation, ischemia, or direct trauma whereby the roots are stretched or torn.

A

Radiculopathies

92
Q

clinical manifestations of radiculopathies

A

-Tone and deep tendon reflexes are decreased
-local pain

Y-Patho 3 (10 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions