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NUR370 Pathophysiology and Pharmacology > Cognitive Disorders > Flashcards

Cognitive Disorders Flashcards

1
Q

3 components of a neuron

A

a. cell body (soma)
b. dentrites (receptive)
c. axon (transmit message)

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2
Q

Nerve impulses

A

neurons generate and conduct electrical and chemical impulses by selectively changing the electrical potential of their plasma membranes and influencing nearby neurons by the release of neurotransmitters

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3
Q

Synapses

A

empty area where information exchange takes place, transmissions by chemical and electrical conduction

presynaptic: proximal to the synapse (delivering)
postsynaptic: distal to the synapse (receiving)

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4
Q

Neurotransmitter

A
  • more than 46 substances
  • excitatory: stimulate action potential
  • inhibitory: reduce probability of action potential
  • some are both
  • manipulated by chemicals

Dopaminergic pathways: specific NTs in discrete groups of neuron and released in specific nerve pathways

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5
Q

NTs and behaviours

A

theorized that certain behaviours are related to NT imbalances

  • excessive NT production/release
  • insufficient NT production/release
  • inadequate or excessive response to NT
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6
Q

NTs related to cognitive disorders

A

a. acetylcholine (ACh)
b. dopamine (DA)
c. serotonin
d. GABA and glutamate (amino acids)
e. norepinephrine (NE)

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7
Q

Acetylcholine (ACh)

A
  • widely distributed
  • triggers muscle contraction
  • has both excitatory and inhibitory effects

= two kinds of receptors
a. nicotinic: neuromuscular junctions, nerve and muscles
(generally excitatory)
b. muscarinic: in the brain, role in memory, arousal and attention
(both excitatory and inhibitory, depending on subtype of receptor)

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8
Q

Clinical significance of ACh

A

Alzheimer’s disease is associated with a decrease in the number of ACh-secreting neurons (cholinergic hypothesis)

too much..muscle contractions
too little..paralysis

associated disorders: Alzheimer’s disease

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9
Q

Dopamine

A
  • located in some areas of the brain and autonomic nervous system
  • generally excitatory
  • involved in voluntary movement, emotional arousal, reward motivation, inhibits unwanted movement

key role: focus and motivation

too much..schizophrenia
too little..parkinson’s, restless leg syndrome (can’t inhibit unwanted movement)

associated disorder: parkinson’s, schizo, drug addiction, depression

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10
Q

Serotonin

A
  • located in many areas of the brain and spinal cord
  • generally inhibitory
  • involved in mood, anxiety, pain perceptions and sleep induction
  • responsible for bowel movements, mood, nausea, sleep, blood clotting, bone health and sexual function

too much..confusion, twitching, dilated pupils, shivering, headache, sweating, diarrhea, irregular and fast heartbeat
too little..depression and sleep disorders, increased pain perception

associated disorders: depression

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11
Q

Norepinephrine

A
  • located in many areas of brain and spinal cord and autonomic nervous system
  • aka noradrenaline
  • can be excitatory or inhibitory
  • involved in learning and memory
  • fight or flight
  • stimulant drugs increase the release and block the reuptake of norepinephrine

associated disorders: depression, stress

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12
Q

Effect of norepinephrine

A

in brain:
increases arousal and alertness, promotes vigilance, enhances formation and retrieval of memory, focuses attention, increases restlessness and anxiety

in body:
increases HR and BP, triggers release of glucose, increases blood flow to skeletal muscle, decreases blood flow to GI system and promotes elimination

too much..over-arousal, aggression, impulsivity, increased SNS activity, cardiac issues
too little..under arousal, depression, cardiac issues

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13
Q

GABA and Glutamate (amino acids)

A
  • GABA (gamma-aminobutyric acid) is the primary inhibitory NT in the CNS
  • most neurons in CNS have GABA receptors
  • glutamate is the primary excitatory NT in the CNS
  • widespread in the brain and spinal cord
  • associated with learning and memory
  • role in schizophrenia
  • drugs that block glutamate used in treatment of ALS
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14
Q

Clinical significance of GABA

A
  • contributes to motor control, vision, regulates anxiety
  • drugs that increase GABA used to treat epilepsy by inhibiting excessive discharge of neurons

too much..over-sedation, over-relaxing of muscles (including heart and respiration)
too little..epilepsy, seizure disorders, anxiety

associated disorders: anxiety, negative symptoms in schizo

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15
Q

Neuroplasticity

A

= long-lasting functional changes that occur when we learn new things causing changes in neural connections
= changes occur over the lifetime and vary across the lifespan

Two primary types of neuroplasticity

a. developmental (expected brain development)
b. adaptive (compensating for lost function and to maximize function following brain injury)

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16
Q

Dementia

A
  • progressive failure of cerebral functions

pathophysiology

  • neurodegeneration
  • atherosclerosis, infarction
  • trauma and lesions
  • compression, increased intracranial pressure, chronic hydrocephalus
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17
Q

Primary vs Secondary dementia

A

Primary

  • progressive, irreversible
  • not secondary to any other disorder

Secondary

  • potentially reversible
  • a result of some other pathological process
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18
Q

Alzheimer’s Disease (AD)

A
  • leading cause of dementia
  • irreversible, no known cause
  • late onset is most common, related to age and family history
  • early onset, related to genetic defects

Stages

a. mild cognitive impairment (mild memory loss)
b. early stage (measurable short-term memory loss)
c. middle stage (significant forgetfulness, iADL dependent)
d. late stage (little cognitive ability, ADL dependent)
e. end stage (no significant cognitive function, non-ambulatory)

19
Q

Symptoms of AD (7As)

A

anosognosia: loss of insight
agnosia: loss of ability to recognize
aphasia: loss of language
apraxia: loss of purposeful motor movement
altered perception: loss of ability to interpret information
amnesia: loss of memory
apathy: loss of drive or interest

20
Q

Amyloid plaques

neuropathophysiological lesion of AD

A

= increased amounts in AD, also called dendritic or senile plaques
= deposits of neuron fragments, formed from the breakdown of a larger protein, surrounding a core of B-amyloid protein fragments
= hard, insoluble accumulation of beta amyloid protein that clump together between neurons

21
Q

Neurofibrillary Tangles

neuropathophysiological lesions of AD

A

= a main component of tangles is a tau protein, which help bind and stabilize the structure of cells
= chemically altered tau twists to form neurofibrillary tangles inside the neuron
= harms synaptic communication between neurons

22
Q

Brain Atrophy in AD

A 
normal brain mass is about 1300-1400g
in AD, brain becomes smaller in size, <1000g
- shrinkage of cerebral cortex
- shrinkage of the hippocampus
- enlarged ventricles in brain
23
Q

Main NT associated wit AD

A

= decreased production of ACh
- affects learning, memory and mood

= excess glutamate from damaged cells cause increased calcium uptake

24
Q

Diagnosis of AD

A
  • confirmed with microscopic examination of tissues
  • often diagnosed by exclusion of other known causes of dementia (hypothyroidism, hypoglycemia, HE)
  • thorough history, clinical examination and cognitive testing (MMSE, MoCA)
25
Q

Management of AD

A

Environmental

  • facilitate and improve home living
  • implement compensation techniques (memory aids)

Health promotion

  • retain/improve general state of health, nutrition hygiene
  • maintaining cognitive functions that are not impaired

Medication

  • cholinesterase inhibitor
  • NMDA receptors
26
Q

Schizophrenia

A

= a persistent psychotic illness characterized by disorder thinking and a reduced ability to comprehend reality

= comorbidities: substance use disorders, depression, anxiety

27
Q

Etiology of Schizophrenia

A

a. biochemical factors
- dopamine theory, excess dopamine
- under-activation of glutamate receptors

b. neuroanatomic alterations (structural changes)
- enlargement of ventricles
- loss of cortical tissue, brain volume in temporal and frontal lobes
- lower rates of blood flow and glucose metabolism in frontal lobe (decision making)

c. genetics

d. prenatal stressors
- infection, poor nutrition, stress

e. environment
- toxins

28
Q

Symptoms of Schizophrenia

A

a. positive symptoms
- hallucinations, delusions, disorganized speech, bizarre behaviour

b. negative symptoms
- blunted affect, avolition, anhedonia

c. cognitive symptoms
- impaired memory, illogical thinking

d. affective symptoms
- dysphoria, suicidality, hopelessness

impairs social functioning, interpersonal relationships, QoL

29
Q

Management of Schizophrenia

A

a. antipsychotics
b. psychosocial therapy
c. cognitive behavioural therapy

30
Q

Depression

A
  1. Unipolar or major depressive disorder
  2. Bipolar disorder
    a. bipolar I: at least one manic episode
    b. bipolar II: at least one hypomanic episode
31
Q

Etiology of MDD

A

a. genetics

b. biochemical
- serotonin and norepinephrine
- glutamate deficits
- dopamine, ACh, and GABA systems

c. hormonal
- hypothalamic-pituitary-adrenal-cortical axis (HPA axis)
- increased urine cortisol and increased corticotropin-releasing hormone

32
Q

HPA Axis

A

= role in our body’s reaction to stress

  1. when we experience stress, hypothalamus releases CRH
  2. CRH signals anterior pituitary to release ACTH
  3. ACTH travels to kidney to reach adrenal cortex
  4. adrenal cortex releases cortisol
  5. cortisol activates fight or flight response
  6. hypothalamus detects high levels of cortisol and responds by stopping the release of CRH, which in turn stops anterior pituitary from releasing ACTH
33
Q

Effects of Cortisol

A
  • deficits in memory and learning
    reduction in development of new neurons
  • depression (chronic activation of HPA)
    prolonged exposure to cortisol depletes NE levels
  • childhood trauma may result in long-term hyperactivity of the CRH and NE systems
    stress pathways become hyperactive
34
Q

Symptoms of MDD

A
  • sadness and despair
  • dysphoric mood
  • insomnia
  • loss of appetite
  • changes in body weight
  • reduced interest in pleasurable activities and relationships
  • suicidal thoughts
35
Q

Treatment of MDD

A

a. antidepressant medication
b. psychotherapy
c. electroconvulsive therapy (ECT)

36
Q

Etiology of Bipolar

A

a. genetics

b. biochemical
- norepinephrine, serotonin, dopamine
- too little = depression, too much = mania
- proportions of NT and receptor site insensitivity

c. neuroendocine
- hypothyroidism
- estrogen

d. neuroanatomic and functional abnormalities
- pre-frontal cortex (executive functioning), hippocampus (memory), amygdala (emotions, decision making)

37
Q

Symptoms of Bipolar I and II

A

= severe shifts in mood, energy and ability to function between depression and mania

mania

  • elevated levels of euphoria, self-esteem, grandiosity, flights of ideas
  • psychotic, hallucinations, delusions, disturbed thoughts

hypomania

  • lower-level mania
  • excessive activity and energy without psychosis
38
Q

Treatment of Bipolar Disorder

A

a. lithium
b. anticonvulsant agents
c. atypical antipsychotic medications
d. ECT
e. psychotherapy

39
Q

Anxiety disorders

A

= characterized by irrational fears that have great potential to cause disability
= many with anxiety disorders develop depression

a. panic disorder
b. generalized anxiety disorder
c. obsessive compulsive disorder
d. post-traumatic stress disorder

40
Q

Etiology of anxiety disorders

A

a. genetics

b. neurobiological
- limbic system (emotions and memory)
- NTs involved: epinephrine, dopamine, serotonin, GABA
- alterations in structure of brain or function can lead to misinterpretations of events

c. psychological theories
- psychodynamic, behavioural, cognitive
- learned response, acquired response

d. environmental
- traumatic events

41
Q

Panic disorder

A

= recurring, severe panic attacks
= sudden onset of apprehension or fear, feelings of impending doom

lightheadedness, racing heart, difficulty breathing, chest discomfort, sweating, trembling, abdominal discomfort, chills or hot flashes

*agoraphobia: avoidance of places or situations where escape is not readily available

8-% respond to CBT and/or antidepressant meds

42
Q

Generalized anxiety disorder

A

= excessive and persistent worrying, lasting longer than 6 months

restlessness, fatigue, poor concentration, sleep disturbance, irritability, tension

norepinephrine and serotonin abnormalities
++ brain glucose metabolism rates in cingulate areas of cortex from worrying and hypervigilance

antidepressants (SNRIs) and behavioural therapy

43
Q

Obsessive-compulsive disorder

A

= repetitive, intrusive thoughts and/or compulsions
= obsessions: preoccupation with an idea, belief that a negative outcome will occur if a specific act is not performed
= compulsions: physical and mental ritualized acts

linked with blocked or damaged serotonin receptors and abnormalities pathways (for flexible thinking) between the frontal cortex and the basal ganglia

antidepressants (SSRIs) and CBT

44
Q

Post-traumatic Stress Disorder (PTSD)

A

= exposure to terrifying, life-threatening trauma
= intrusive flashbacks, nightmares

increased norepinephrine levels
smaller hippocampus (adults)

group or family therapy, CBT, antidepressant (SSRIs)

NUR370 Pathophysiology and Pharmacology (20 decks)

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