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KCSU17 Patho/Pharm Submodule 1 > Neuro Abnormal Physiology > Flashcards

Neuro Abnormal Physiology Flashcards

1
Q

types of primary headaches

A

tension

migrane

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2
Q

tension headache

A

mild-moderate

bilateral

band-like

associated with pericardial muscle tenderness (sore neck)

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3
Q

tension headache

pathophysiology

A

not well understoon

overstimulation of nociceptive (pain) receptors from sustained tension in scalp and neck muscles

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4
Q

tension headache

treatment

A

OTC meds (decrease sensitivity)

NSAIDS, acetaminophen PRN

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5
Q

Migrane

A

recurrent

unilateral

throbbing HA that occurs with associated SXS

may be preceded by aura (classic) or no (common)

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6
Q

migrane pathophysiology

A

cortical spreading depression

flow of neuronal activity spreading across cerebral cortex chasing the meninges (dura) to cause headache

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7
Q

migrane treatment

A

depends on acuity v. chronicity

abortive (stop the headache)

may try to go for symptoms

not much

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8
Q

most common reason for malignancy in brain

A

metastases from other cancer sites that travel to brain

mostly secondary metastases

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9
Q

primary brain tumors

A

benign or malignant (both have serious consequences bc major impact on basic fx)

grow and develop in the brain

seldom metastasize outside CNS

able to grow for a while unnoticed bc the brain is pain free so won’t give symptoms

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10
Q

types of primary brain tumors

A

neuroglial tumors

  1. astrocytomas as
  2. oligodendrogliomas
  3. ependyomas
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11
Q

astrocytomas

A

infiltrating or non infiltration

MC in 40s-60s

most agressive: Glioblastoma

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12
Q

oligodendrogliomas

A

MC 40s-50s

MC in white matter of cerebral hemisphere

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13
Q

ependyomas

A

MC in first two decades
pediatric/adolescent cancer

MC in 4th ventricle or spinal cord

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14
Q

Intracranial pressure

A

fixed amount of space in head due to skull

increase in cerebral volume (i.e. growth of abnormal cancer tumor) will increase the ICP

for a while the ventricles can compensate but after a while it is too much

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15
Q

s/s of intracranial pressure

A

HA
vision changes
N/v
papilledema (swelling of optic disk)

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16
Q

Headaches and brain tumors

A

caused by eventual compression of dura mater or vascular structures

diffuse by may be ipsilateral to tumor

early stages: only in morning, improves with head elevation

later: more constant, exacerbated by anything to increase cranial pressure

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17
Q

meningitis

pathophysiology

A

acquisition of a pathogen via ear infection or sore threat, etc. that then invades and survives in blood and cross BBB to get into CSF

eventually Cytokines are relied in CSF and inflammation results to cause damage to CSF (edema of brain, loss of cerebrovascular auto regulation and increase ICP

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18
Q

swelling in meningitis caused by

A

immune response to presence of pathogen in CSF

BBB is loosened so it is permeable to fluid without being able to relieve pressure

also lets in WBCs and medications to fight infection

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19
Q

how is meningitis diagnosed?

A

lumbar puncture

puncture occurs b/t L4 and L5

check for increased pressure and color

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20
Q

meningitis treatment

A

can use stereos (dexamethasone) where inflammation is more significant than worsening outcome

steroids decrease inflammation, so controversial bc inflammation is also what heals it but can be dangerous

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21
Q

normal lumbar puncture/csf analysis:

pressure

A

50-200 mmHg

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22
Q

normal lumbar puncture/csf analysis:

appearance

A

clear, colorless

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23
Q

normal lumbar puncture/csf analysis:

protein

A

10-50 mg/dL

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24
Q

normal lumbar puncture/csf analysis:

glucose

A

50-80

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25
Q

normal lumbar puncture/csf analysis:

gram stain

A

negative/normal

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26
Q

normal lumbar puncture/csf analysis:

glucose csf:serum ratio

A

0.6

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27
Q

normal lumbar puncture/csf analysis:

WBC

A

<5 - all mononuclear

28
Q

normal lumbar puncture/csf analysis:

other

A

no RBCs unless you have a traumatic tap

usually appear in first vile but not 4th

29
Q

infection and inflammation of the brain parenchyma

A

encephalitis

can co-occur with meningitis

30
Q

encephalitis is caused by

A

most often caused by virus

ex. HSV, West Nile, HIV, Arbovirus, Polio, Rabies

31
Q

encephalitis

A

local necrotizing hemorrhage and prominent cerebral edema

caused by virus, treat with acyclovir (antiviral medications)

32
Q

encephalitis treatment

A

antiviral medication like acyclovir

sometimes also put in antibiotics, bc it can be meningitis too

33
Q

epilepsy

A

disordered characterized by recurrent seizures that are not provoked by anything else

display a known pattern

34
Q

seizure

A

discharge of neurons in an abnormal way

abrupt, excitatory, lasts about 1 minute

not a disease itself but a symptom of some other complication

could be motor, sensory, autonomic or psychic

35
Q

types of seizures

A

partial/focal

generalized

36
Q

partial seizures

A

originate in small collection of neurons in one hemisphere and spread elsewhere

either simple or complex

37
Q

complex partial sezires

A

seizure beings in a localized area and then spreads to both hemispheres

involves loss of conciousness

38
Q

simple partial sizures

A

seizures that are confined to one hemisphere

don’t involve loss of consciousness

39
Q

generalized sizures

A

abnormal discharge of widespread electrical activity across both hemispheres

impaired consciousness (generally)

may or may not b`e convulsive – must be bilateral for motor

40
Q

how are seizures diagnosed?

A

use of EEG

evaluates electrical activity of the brain

even if normal, doesn’t rule out epilepsy

41
Q

dementia

A

progressive deterioration of cognitive function

interferes with social performance

many forms

42
Q

forms of dementia (6)

A
  1. alzheimers disease
  2. vascular (ischemic or hemorrhagic damage)
  3. frontotemporal
  4. CJD
  5. Wernicke-korsakoff syndrome (liver toxicity)
  6. huntington disease
43
Q

alzheimer’s disease

A

atrophy of cerebral cortex with subsequent enlargement of ventricles

neurotic plaques and neurofibrillary tangles

due to inability to synthesize acetylcholine

follows predictable course

44
Q

neurotic plaques

A

areas of degenerated nerve terminals around an amyloid core

45
Q

neurofibrillary tangles

A

abnormally found in cytoplasm of neurons

resist breakdown, even if neuron dies

46
Q

how is Alzheimer’s diagnosed?

A

very extensive process that is a diagnosis of exclusion

can’t diagnose directly, just make sure it isn’t anything else

47
Q

management/treatment of Alzheimer’s

A

no cure, treat both patient and family with support groups and respite care

prescribe medication that slows the progression of the disease (cholinesterase inhibitors and memantine)

48
Q

medications prescribed for Alzheimer’s and their function

A

cholinesterase inhibitors (good for mild, allows for more acetylcholine to be available)

memantine :works with cholinesterase inhibitors to modify the glutamate receptor (NMDA)

49
Q

common age of presentation of Huntington disease

A

typically appears in the 4th-5th decade (40s-50s) – after people have had children, so it gets passed on (autosomal dominant)

50
Q

pathophysiology of Huntington disease

A

causes neuronal death

starts in Basal ganglia (coordinate motor output)

no cure

51
Q

symptoms of Huntington disease

A

choreiform movements

memory loss

results in personality changes: depression, impulse behavior, mood lability (swings)

52
Q

Parkinson disease

A

progressive degenerative disorder of the basal ganglia

specifically degeneration of substantial nigra – dopamine degeneration

53
Q

neurotransmitter associated with Parkinson disease

A

dopamine

54
Q

symptoms of Parkinson disease

A

results in tremor (esp. in fine movements such as writing), rigidity, bradykinesia (slow movements)

55
Q

medication management of Parkinson disease

3 medications used and their fxn

A

typically prescriptions are focused on improving dopamine system and levels

to increase levels: Levodopa + Cardopa

agonist of dopamine receptors: Bromocriptine

inhibit the breakdown of dopamine: Selegine

56
Q

medical term for a stroke

A

cerebrovascular accident (CVA)

57
Q

stroke

A

acute, focal loss of oxygenated blood in the brain that leads to neuronal death

two main types: ischemic stroke, hemorrhagic stroke

also transient ischemic attacks

58
Q

transient ischemic attacks (TIA)

A

mild, self limited episodes of neurologic dysfunction without acute infarction (no death of nerve cells)

symptoms typically resolve in 24hrs so often not diagnosed

59
Q

most common type of stroke?

A

ischemic stroke

60
Q

ischemic CVA

A

caused by thrombi or emboli

characterized by a prenumbra

goal of treatment is to restore blood flow to area (try to get it quickly and minimized long term sequelae)

use thrombolytics to restore blood flow

61
Q

Hemorrhagic CVA

A

less common, higher mortality

spontaneous intracerebral hemorrhage usually due to rupture of a blood vessel or an existing aneurysm

62
Q

increased risk for hemorrhagic CVA: (why)

A

hypertension (thins the walls of the blood vessels so more likely to rupture)

anticoagulation (slightest trauma will cause a major blood rush to the head)

63
Q

hemorrhagic cva work up

A

preform non contrast CT first
blood will appear bright white

(if you use contrast you won’t see the blood – obscured blood)

64
Q

treatment of hemorrhagic cva

A

management fr pressure, blood pressure, and mechanical ventilation

neurosurgical team consult to get in and stop the bleeding/repair the vessel

65
Q

prenumbra

A

ischemic cva

central core of dead cells that are surrounded by cells that are minimally perfused/ischemic

KCSU17 Patho/Pharm Submodule 1 (12 decks)

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