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pathophysiology > last week lecture before exam > Flashcards

last week lecture before exam Flashcards

1
Q

what are the data processing deficits?

A
  1. agnosia
  2. dysartria
  3. dysphasia or anaphasia
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2
Q

agnosia is—-

A

inability to recognize patterns

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3
Q

dysarthria is —

A

inability to articulate words clearly

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4
Q

dysphasia is

A

impairment of comprehension and production of language

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5
Q

what are the two types of dysphasia

A
  1. expressive aphasia
  2. receptive aphasia
  3. global aphasia
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6
Q

expressive aphasia

A

inability to produce spoken or written language

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7
Q

receptive aphasia

A

inability to understand spoken or written language

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8
Q

global aphasia

A

both receptive and expressive aphasia

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9
Q

what is the similarities between delirium and dementia

A

they are both state of confusion

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10
Q

what are the differences between delirium and dementia

A

derilium: is sudden onset
- short term
- sleep-wake is disturbed
dementia: slow progressive onset
- long term/ permanent
- sleep-wake is normal

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11
Q

What causes dementia

A

failure of cerebral functions, including permanent intellectual processes, neuron degeneration, brain tissue composition

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12
Q

What causes delirium

A

drug intoxication
metabolic disorders
long stay in the hospital
brain trauma and surgery
electrolyte imbalance

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13
Q

what is Alzheimers disease

A

the leading cause for severe progressive cognitive dysfunction

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14
Q

cause for Alzheimers disease

A

Development of amyloplaques and neurofibrillary tangles, which in turn causes neuron death, brain atrophy, and loss of synapse

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15
Q

cause for Alzheimers disease

A

Development of amyloplaques and neurofibrillary tangles, which inturn causes neuron death, brain atrophy, and loss of synapse

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16
Q

clinical manifestations of Alzheimer’s

A

forgetfulness
lack of concentraryion
loss in problem solving abilities
confusion
decline in abstraction

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17
Q

clinical manifestations of dementia

A

memory loss
lack of orientation in language and memory
alteration in behavior

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18
Q

what results increased cranial pressure

A

increased inter-cranial content due to tumor, edema, hemorrhage, excess cerebral spinal fluid

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19
Q

effects of increased cranial pressure

A

causes an equal reduction in volume in other cranial contents
CSF and cerebral blood flow are decreased
changes in the levels of consciousness

20
Q

What are the 4 stages of increased intracranial pressure

A

stage 1: compesnsation
stage 2: Compensation
stage 3: beginning of decompensation
stage 4: decompensation

21
Q

what happens in stage 1 compensation?

A

Vasoconstriction and external compression of the venous system occurs in an attempt to decrease intracranial pressure
- ICP doesn’t change much and show symptoms because the compensation is working

22
Q

what happens in stage 2 compensation?

A

compensation could not keep up with the increasing expansion of intracranial contents
- cause compromised neural oxygenation and systemic arterial vasoconstriction

23
Q

effects of stage 2 compensation

A

restlessness
sluggish pupils
breathing changes
drowsiness
confusion

24
Q

what happnes in stage 3 beginning of decompensation

A

hypercapnia and hypoxia
ICP approaches arterial pressure

effects:-
widened pulse gap, bradycardia, and hypertension

25
Q

what happens in stage 4 decompensation

A

herniation develops
blood supply is compromised, which increases the probability of getting ischemia and hypoxia
eventually, blood flow stops

effects:-
comma, fixed and dilated pupil, Cheyne strokes breathing

26
Q

Cerebral edema is

A

Increase in intracellular or extracellular fluid within the brain

27
Q

Effects of cerebral edema are

A
  • displacement of brain tissue
  • increase in ICP
  • herniation of blood tissue
  • distortion of blood vessels
28
Q

Cerebral edema is classified into three

A
  1. vasogenic ( most important )
  2. cytotoxic ( metabolic)
  3. interstitial
29
Q

What is vasogenic

A
  • specific place
  • increased permeability of the capillary endothelium of the brain after injury

effects
capillaries of the blood-brain barrier are disrupted

30
Q

cytotoxic

A
  • affects everywhere
  • toxic materials that affect the cellular elements of the brain

Effects:
failure of the transport system
cells accumulate Na

31
Q

interstitial

A
  • caused by the movement of CSF from the ventricles in the extracellular spaces of brain tissue
  • often seen in communicating hydrocephalus
32
Q

hydrocephalus

A

excuss fluid within the cerebra ventricles

33
Q

What causes hydrocephalus

A

-decrease in the absorbtion of CSF
- overproduction of fluid
- obstruction within the ventricular system

34
Q

classified into four

A
  1. communicating
  2. non-communicating
  3. acute hydrocephalus
  4. normal pressure hydrocephalus
35
Q

hypertonia

A

Increase in muscle tone

effects?

36
Q

hypotonia

A

decrease in muscle tone
- passive movements occur without resistance

cause
- cerebral damage, stroke, spinal cord injury

effect
weakness
training easily
difficulty rising and sitting down

37
Q

hypokinesis is

A

decrease in movement

38
Q

hypokinesia is classified into

A
  1. akinesia: absence of voluntary movement
  2. bradykinesia: decreased speed movement
39
Q

hyperkinesia is

A

Increase in movement

40
Q

hyperkinesia is classified into

A
  1. paroxysmal dyskinesia: abnormal involuntary movements
  2. tardive dyskinesia : involuntary movement of the lip, face, or tongue…( caused by prolonged antipsychotic drug)
41
Q

parkinston disease is

A

progressive digenerative disorder

42
Q

how is Parkinson disease caused

A
  • a disorder caused in the basal ganglia
  • loss of dopamine-producing neurons
    -excess acetylcholine
43
Q

What are the clinical maniferstation of parkinston disease?

A
  • excess stimulation affects movement and posture
  • decrease in flexibility
  • progressive tremors
  • dysarthria
  • chewing and swallowing difficulty
44
Q

Amyotrophic lateral sclerosis is —-

A

a progressive degenerative disease affecting the upper and lower motor neurons
- cognition is not affected

45
Q

casuse of amyotropic lateral sclerosis is —-

A

no identified cause but it is linked to gene linked disease

46
Q

clinical manifestation of amyotrophic lateral sclerosis

A
  • loss and weakness of muscle atrophy
  • death due to respiratory failure
    -loss of manual dexterity and gait
  • sparsity

pathophysiology (13 decks)

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