Pathophysiology Test 4 Material, Neuropathophysiology

Front 1

two main structural divisions of the nervous system

Back 1

central nervous system
peripheral nervous system

Front 2

what are the two main divisions of the peripheral nervous system

Back 2

afferent - to brain from periphery
efferent -= to periphery from brain

Front 3

what are the two main divisions of the efferent nervous system?

Back 3

autonomic - automatic
and
somatic - voluntary

Front 4

what are the two main divisions of the autonomic nervous system

Back 4

parasympathetic - cholinergic/rest & digest

sympathetic - adrenergic/fight or flight

Front 5

what are the protective structures of the CNS?

Back 5

cerebrospinal fluid
bony structures
meninges

Front 6

what are the meninges and their purposes?

Back 6

dura mater: outmost, tough and thick layer
arachnoid space: not true space = potential space - only if pathology does space become evident
pia mater: attached to brain, conforms to every sulcus/gyrus

Front 7

where is the favored place for csf samling?

Back 7

from the large subarachnoid cistern at the end of the spinal cord at L1, L2

Front 8

what structure produces CSF?
How much CSF is produced every day?

Back 8

choroid plexus
500 mL/day

Front 9

describe the arterial blood supply to the cns

Back 9

2 pairs of arteries
• Internal carotids (anterior circulation)
• Vertebral arteries (posterior circulation

Front 10

describe Production of CSF

Back 10

production independent of BP or intraventricular pressure
Will continue to produce even when circulation/absorption blocked
-↑CSF with pathology=hydrocephalus

Front 11

Which cells line the BBB? Which molecules get through

Back 11

*Cells that line CSF spaces: very tight, difficult to penetrate = **Blood Brain Barrier (BBB): astrocytes maintain integrity by extending “feet” to capillaries
Lipid-soluble molecules pass easier than water-soluble ones. Polar/charged molecules
do not pass

Front 12

General functions of:
• Cerebrum
•

Back 12

Example: frontal lobe, motor cortex responsible for complex thought, behavior, morality
o Example: limbic structures: memory, emotion
Broca/Wernicke’s Area: language
Basal ganglia: coordination of movement
• Parkinson’s disease pathology happens here

Front 13

General functions of:
• • Cerebellum
•

Back 13

Execution of movement, moment-to-moment adjustments (proprioception)

Front 14

General functions of:
• • Diencephalon
•

Back 14

Thalamus, hypothalamus, pineal gland, hypothalamic extension to pituitary
• Hypothalamic extension: responsible for ANS functions (sleep, temperature, appetite, sex drive, regulation of BP, somolarity, blood O2 & CO2, pH, temperature

Front 15

general functions of the brainstem

Back 15

“Stalk” between upper spinal cord and diencephalon
• Vital centers for respiratory/CV function

Front 16

what is the vagus nerve significance. Which cranial nerve is it.

Back 16

Cranial nerve X (VAGUS NERVE) is critical to CV, resp, GI function

Front 17

afferent neurons lead from:

efferent neurons take information from to?:

Back 17

to brain from periphery

information away from CNS to periphery
Muscles, glands, postganglionic

Front 18

autonomic nervous sytem does what in general

Back 18

mediate autonomic or involuntary processes

Front 19

nicotinic receptors are part of which division of the nervous system and are located where?

Back 19

the somatic nervous system
skeletal muscle

Front 20

nicotinic receptors receive what neurotransmitter and are excitatory or suppressor in effect?

Back 20

Ach - excitatory

Front 21

muscarinic receptors are part of which divition of the nervous system, and are located where?

Back 21

the parasympathetic ns
the autonomic organs

Front 22

muscarinic receptors receive what nt's and are excitatory or suppressor in effect?

Back 22

Ach - suppressor

Front 23

differentiate between neurons and glial cells

Back 23

Neurons: generate + transmit impulses
• Glial Cells: supportive, don’t transmit impulses

Front 24

what generates membrane potential in the neuron?

Back 24

K+ greater in ICF
• Na+ greater in ECF
o K+ moves to ECF in concentration gradient, generates
Membrane potential (-70mV);

Front 25

what stimulates release of nt's

Back 25

Open voltage-gated Ca+2 channels simulate release of neurotransmitters…they move to next synapse, Na+ then rushes in, impulse moves down dendrite

Front 26

what enzymes break down Ach

Back 26

Acetylcholinesterase (AchE): quickly degrades Ach after release into synapse to limit duration of action. After degradation, immediately resynthesized

Front 27

what enzymes break down dopamine?

Back 27

Degraded by catechol-O-methyltransferase (COMT)

Front 28

what does dopamine affect?

Back 28

the CNS muscle regulation

Front 29

what is an example of abnormal dopamine metabolism

Back 29

parkinson's, schizophrenia

Front 30

what is NE degraded by?

Back 30

Degraded by catechol-O-methyltransferase (COMT)

Front 31

if a amine neutotransmitter is not broken down in ECF, can be broken down in presynaptic nerve by

Back 31

monoamine oxidase (MAO)

Front 32

List the amine neurotransmitters

Back 32

Dopamine (DA): CNS muscle regulation
 Degraded by catechol-O-methyltransferase (COMT)
 Abnormal DA metabolism=pathology
• Example: Parkinson’s, Schizophrenia
o Norepinepherine (NE)
 Degraded by catechol-O-methyltransferase (COMT)
o Epinepherine
o Serotonin (5-hydroxytryptamine, 5-HT)
 Sleep, mood, pain control
o Histamine
o Endorphins

Front 33

Ca++ channels allow:

Back 33

NT into the synaptic cleft

Front 34

define ischemia

Back 34

occurs when the delivery of oxygenated blood is below the level needed to meet the metabolic demands of the tissue "inadequate blood flow"

Front 35

define hypoxia

Back 35

a reduction in oxygen at the cellular level

Front 36

which comes first, ischemia or hypoxia?

Back 36

ischemia leads to hypoxia

Front 37

why is neuronal tissue especially susceptible to hypoxic damage?

Back 37

Has a limited capacity for anaerobic metabolism
during ischemia
 Uses 20% of total body O2 consumption
 Is dependent on glucose for ATP production
 Has little glycogen for storage

Front 38

what is the mechanism of cellular damage from ischemia?

Back 38

ischemia leads to cell hypoxia. O2 is needed to accept electrons in the TCA/Krebs Cycle. with reduced ATP production and glycolysis running out, H+ accumulates and acidosis occurs. Also, mitochondria fail leading to impaired Ca++ pumps, cuasing Ca++ overload, leading to free radical production and cell death

Front 39

define CVA

Back 39

The onset and persistence of neurological
dysfunction lasting longer than 24 hours and
resulting from disruption of blood supply to the brain

Front 40

define hemorrhagic stroke

Back 40

Leakage of blood or blood vessel and hemorrhage into brain
tissue, which causes edema, compression of brain tissue, and
spasm of adjacent blood vessels
 Can occur outside the dura, beneath the dura ( subdural), in
12
, ),
the subarachnoid space, or within the brain substance itself
(intracerebral)

Front 41

define ischemic stroke

Back 41

Partial or complete occlusion of the cerebral blood
flow to an area of the brain

Front 42

what are the two possible causes of ischemic strokes?

Back 42

Thrombus, most common, generally due to an
10
atherosclerotic plaque in a cerebral artery usually at a
point of bifurcation, occurs over several days
 Embolic, a moving clot of cardiac origin, frequently from
a-fib that travels quickly to the brain and lodges in a small
artery, occur suddenly, immediate and maximum deficits

Front 43

which kind of stroke is associated with a greater morbidity and what is it almost always caused by?

Back 43

hemorrhagic

caused by Hypertension

Front 44

clinical manifestations of CVAs

Back 44

Severe HA, paresthesia, weakness, loss of motor
ability on one side of the body, difficulty in
swallowing, aphasia (expressive, receptive, global),
visual difficulties, loss of half of a visual field, double
vision, altered cognitive abilities

Front 45

what is the treatment goal for strokes?

Back 45

save the penumbra (the area of eschemia in which cells are still viable and have the potential to be saved via reperfusion (initiate RX within 3 hours)

Front 46

what is the significance of the optic nerve in a stroke?

Back 46

↑ICP leads to: HA, vomiting, altered LOC, blurry vision, papilledema (optic disc swelling that is caused by increased intracranial pressure), pupil responsiveness
to light

Front 47

what is the cushing reflex

Back 47

last ditch effort of the body to maintain cerebral perfusion through clamped vessels = extreme somatic nervous sytem response which causes systolic blood pressure to rise above 200 mmHg

Front 48

Define TIA

Back 48

A transient ischemic attack (TIA) is an acute episode of
temporary and focal loss of cerebral function of vascular
(occlusive) origin.
 TIAs are rapid in onset; symptoms reach their maximal
manifestation in fewer than 5 minutes (usually <1 min).
M if i f i bl d i d i ll l 2 15
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Manifestations are of variable duration and typically last 2-minutes (rarely as long as 24 h). Most TIA durations are less than
1 hour; median duration is 14 minutes in the carotid distribution
and 8 minutes in vertebrobasilar ischemia.
 Temporary reduction or cessation of cerebral blood flow
adversely affects neuronal function in cortical, subcortical, and
nuclear regions of the CNS.

Front 49

what makes a TIA different than a CVA?

Back 49

Death does not occur directly from a single
episode of TIA. A TIA may be considered a sign
of generalized atherosclerotic disease
 Blood flow is re established before infarction
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re-takes place, “brain angina”
 TIAs are important warning signs of a potential
impending stroke

Front 50

what is meningitis?

Back 50

Meningitis is an infection of the linings of the
brain and ventricles.
 Can be fungal, viral, bacterial

Front 51

what is the mechanism of infection in the meninges?

Back 51

Usually the brain is protected naturally from the
immune system by a barrier created by the meninges,
the blood brain barrier
 Evolutionarily, this was seen as an advantage, since the
barrier prevents the body from attacking itself
b h h h f d h
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 However, bacteria or other organisms that have found their
way into the brain are isolated from the immune system and
can spread quickly.
 Once the body recognizes that there is an infection, as it tries
to fight the infection, the blood vessels become leaky,
and allow fluid, white blood cells, and other infection fighting
particles to enter the meninges and the brain, causing
swelling, decreased blood flow to parts of the brain, and
worsening symptoms of infection

Front 52

what are the routes of infection in meningitis

Back 52

Hematogenous spread
 Nose and throat
 Localized extension otitis media sinusitis mastoiditis
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extension, media, sinusitis,  Bone fracture, head or neck surgery, penetrating bone injury, skull fracture

Front 53

what is the triad of symptoms in meningitis?

Back 53

Meningitis develops quickly with a classic triad:
1. fever
2. headache
3. stiff neck developing over several hours to one to
two days

Front 54

what are other symptoms of meningits?

Back 54

Other symptoms include nausea, vomiting,
photophobia, mental status change, sleepiness
 Petichial, purpuric rash esp with N. menindititis
 Two classic signs: Kernig, Brudzinski

Front 55

describe kernig and brudzinski

Back 55

Kernig's sign is assessed with the patient lying supine, with the hip and knee flexed to 90 degrees. In a patient with a positive Kernig's sign, pain limits passive extension of the knee. A positive Brudzinski's sign occurs when flexion of the neck causes involuntary flexion of the knee and hip

Front 56

what cells would you see increases in a lumbar puncture lab result?

Back 56

↑Neutrophils, ↑protein,(decreased glucose)

Front 57

The principal damage from bacterial meningitis
is caused by the _____________ and not
the ___________________

Back 57

inflammatory reaction

pathogen

Front 58

define parkinson's

Back 58

Parkinson’s disease is a progressive neurodegenerative
disorder associated with loss of dopamine neurons
 Named after James Parkinson, English physician who first
described the shaking palsy in 1817
41
 The underlying etiology is unclear, possible virus
possible genetic susceptibility, possible toxicity from
pesticides, repeated head injury or other unknown
cause
 Idopathic vs. acquired (infection, intoxification, trauma)

Front 59

Two pathways exist within the basal ganglia circuit, one
stimulatory the other inhibitory, which NTs are which?

Back 59

 Stimulatory: Ach
 Inhibitory: DA

Front 60

what area of the brain is affected in Parkinsons'

Back 60

the cerebral cortex

Front 61

signs and symptoms of Parkinson's

Back 61

Tremor
 the tremor he is noticed in the hands, feet, head, face, lips
 The most noticeable tremor he is pill rolling
 Rigidity
 This is the resistance to movement of both flexor and extents muscles through
full range of motion jerky, ratchet like movement of the joints
 Bradykinesia
 slowness in the initiating or performing of conscious movements
45
 Shuffling gait, no swinging of the arms with walking
 The face lacks emotional expression, poor link reflects
 Tongue, palate, and throat muscles become rigid, frequent drooling,
speech becomes slow and poorly articulated
 Autonomic problems
 Orthostatic hypotension
 Excessive sweating, sebaceous gland secretions, salivation
 Swallowing delayed: aspiration risk
 Dementia

Front 62

how is Alzheimer Disease diagnosed?

Back 62

R i hi l i l fi i l d
48
 Requires histological confirmation, only done
postmortem, but diagnosis can be made with high
certainty based upon a progressive cognitive decline
that is expressed in loss of memory, language skills, and
activities of daily living

Front 63

describe the pathophysiology of AD

Back 63

The classic neuropathological findings include
 amyloid plaque
 neurofibrillary tangles
51
 Tangles~ tau protein/neural thread protein
 Normally neural thread proteins bind/stablize microtubules--
essential for axon growth and development. In AD, tau twists
into paired helical filaments called neurofibrillary tangles
 synaptic and neuronal cell death.
 Brain in AD=ATROPY
 Changes in Cholinergic System
 choline acetylesterase
  Ach synthesis

Front 64

what are the changes you see in the cholinergic system of someone with AD?

Back 64

choline acetylesterase
  Ach synthesis

Front 65

describe the amyloid plaques in AD

Back 65

Beta amyloid protein
thought to cause
O id i f li id
53
 Oxidation of lipids
 Activation of apoptotic
genes
 Disruption of cell
membranes
 Forms insoluble plaques

Front 66

describe the neurofibrillary tangles

Back 66

Neurofibrillary tangles are
deposited in neurons located
in the hippocampus,
temporal lobe, frontal lobe,
leading to cell death

Front 67

signs and symptoms of AD

Back 67

AD is a progressive dementia with memory loss as a major
clinical manifestation
 Language disturbance
 searching for words when naming objects is common and evolves into
communication breakdown as the patient struggles with a very limited
b l i l h i d d f t i l h i
56
vocabulary, nominal aphasia, and defects in language comprehension
 Behavioral problems are common throughout the disease process
 Early-stage disease shows disturbances of mood such as
depression, anxiety
 Late stage and manifest as delusions, hallucinations, psychosis,
aggression, and inappropriate sexual behavior
 End-stage disease has the patient in a vegetative like state, as
cognitive activity ceases

Front 68

cause of death in AD is usually from:

Back 68

accident/infection

Front 69

differentiate btw concussion and contusion

Back 69

Concussion
 A sudden trauma induced alteration of the alert state
 No brain damage
 Contusion
59
 damage the cerebral cortex by bruising
 CT will show necrosis, laceration, bruising
 Cerebral contusions tend to occur at the tip of the frontal and
temporal lobes where they bang up against interior of the skull
 or the deep white matter can suffer diffuse axonal injury,
which can stretch, tear the axonal connection

Front 70

discuss coup and contracoup

Back 70

Contusion from direct
trauma
 Brain shifts side to side
 Shockwaves are sent to the
brain matter
 Even though the skull may
60
not be penetrated or
fractured, the forces imparted
to the brain can cause the
brain to collide against the
inside of the skull, coup, and
against the opposite area of
the brain =countercoup.
 Both areas of the brain will
be contused and subject to hemorrhage

Front 71

define DAI

Back 71

or the deep white matter can suffer diffuse axonal injury,
which can stretch, tear the axonal connection
 Diffuse Axonal Injury (DAI) occurs more towards the center of the
brain, where axons are subjected to maximal stretching, best example
is a whiplash injury

Front 72

describe whiplash and its relationship to shaken baby syndrom

Back 72

Whiplash, DAI
 The brain consists of billions
of nerve cells that
communicate by way of
axons
62
 In a whiplash injury,
stretching, twisting, and
tearing of these axons and
their connections can occur
 Shaken baby syndrome is the
equivalent

Front 73

define epidural hematoma

Back 73

EDH is a collection of blood which
occurs below the skull but above the
dura
 This area of the brain is basically fluid
and acts as a shock absorber
 The veins that feed and drain the brain
which move through this area can be
EDH area, torn, resulting in a bleed

Front 74

s/s and tx of epidural hematoma

Back 74

These patients have a lucid interval
 Patient is struck in the head, short
period of unconsciousness, followed by
wakefulness and seeming normality,
then rapid deterioration
 This is from the gradual accumulation
of blood in this area which presses on
the brain over time, creating a mass
effect
 Surgery is done to relieve the pressure,
if the person has progressed to coma
with GCS <9

Front 75

define subdural hematoma

Back 75

Between dura and outer
arachnoid membrane
 The source of the bleeding can
b f d h b i
SDH
68
be from damage to the brain
itself, damage to a vein,
 More common in elderly
patients after a fall
 The presence of blood directly
under the brain tissue is
thought to be an irritant to the brain, frequently causing a seizure

Front 76

discuss the skull characteristics that make compensation difficult

Back 76

Skull is a closed system
 Finite ability to compensate
 Brain parenchyma has little ability to volume
 CSF can shunt to venous system via arachnoid villi
 Blood vessels can vasoconstrict

Front 77

what the ranges of ICP

Back 77

Normal = 0-15mmHg
 > 20 abnormal
 >40 = neurological impairment ( decreased level of
consciousness, problems with breathing, pupil dilation,
compression of bringing on MRI, abnormal EEG
 >60 = fatal

Front 78

what does high ICP cause?

Back 78

High ICP will
 deform the brain and push tissue in such a way as to
cause herniation, or a shifting of the brain tissue under
pressure, which is tearing and stretching neurons

Front 79

what is herniation in TBI

Back 79

Complication of ↑ICP
 Protrusion through
opening in dura mater

Front 80

Glasgow coma scale ranges

Back 80

GCS =
Eye+Motor+Verbal
 15 = WNL
 Mild head injury = 13-15
76
pp p
 2 incomprehensible sounds
 1 no response
 Moderate head injury =
9-12
 <8 severe head injury

Front 81

which is worse decorticate posturing or decerebrate?

Back 81

decerebrate

Front 82

what is the common denominator with all migraine headaches

Back 82

Common denominator is meningeal instability/hyperexcitability that releases
several neurotransmitters:
 Dopamine
 Serotonin
 Histamine
 Prostaglandin
 All of these mediate the inflammatory response and cause vascular dilation

Front 83

signs and symptoms of migraines

Back 83

85% of migraineurs have HA without aura
 Pulsatile, unilateral (but can be bilat), throbbing, lasts 1-2 days, inc
pain with physical activity, +n/v from pain, photophobia, inc sound
sensitivity
15% f i i h HA i h a ra
79
 of migraineurs have with aura
 All of the above symptoms plus aura
 Spots, flashing lights, zig-zag/wavy lines cutting across
visual field
 Aura lasts < 1 hour

Front 84

what is the significance of vasodilation in migraine?

Back 84

Vasodilation causes more meingeal irritation trigeminal
instability NT release vasodilation… and a vicious
cycle is born which causes a self-sustaining HA that can go
on for days
So, a migraine is a neuro-vascular disorder at heart and is treated
as such

Front 85

define multiple sclerosis

Back 85

Primary demyelinating disease, acquired,
recurrent, multifocal
 often presents with optic neuritis but can present
with any neurologic abnormality
82
 any white matter can be involved, usually
periventricular, brainstem, optic nerve (optic neuritis
 onset at any age, peak 20-50, females 2x times more
likely to get than males

Front 86

3 s/s

Back 86

3 major symptoms: nystagmus, intention tremor,
scanning speech (monotonous or slurred speech

Front 87

describe optic neuritis in MS

Back 87

optic neuritis - papillitis acutely - central scotoma, decreased
visual acuity, Marcus-Gunn pupil, unilateral papilledem

Front 88

what is the significance of placques in MS

Back 88

MRI is diagnostic, looking for placques in the white matter on CNS

Front 89

seizures are

Back 89

Transient neurological events
 Excessive cortical electrical discharges
 Skeletal motor Fx
 Sensation
 Autonomic visceral Fx
 Behavior
 Consciousness
 Idiopathic, or with a known cause
 Environmental/physiologic/psychosocial

Front 90

define epileptogenic focus

Back 90

Neurons form an epileptogenic focus
 Area in brain where seizure begins
 Functions autonomously, emitting ↑↑discharges
 Can recruit neurons from opposite hemisphere
 Partial=focal; part of brain surface affected
 Generalized=entire brain surface affected

Front 91

what happens if seizure is not treated in status epilepticus

Back 91

Continued seizures without recovery period
 Can be life threatening!
 If not treated for 30-40 minutes
 Ischemic brain damage

Front 92

#1 nursing intervention in seizures

Back 92

#1 PROTECT AIRWAY
#2 Protect from injury

Front 93

significance of aura/prodrome in seizures

Back 93

Aura/Prodrome associated with seizures
 Subjective sense of impending seizure
 Prodromal period: HA, myoclonic jerking, lethargy,
mood change, palpitations, epigastric sensations
 Can last several hours
 Aura: odd sensory experience before seizure
 Patient remembers this after recovery

Front 94

what are the psycotic illnesses

Back 94

schizophrenia
delusional disorder
depression
bipolar disorder

Front 95

what are the non-psycotic illnesses

Back 95

anxiety disorders (panic d.o, ocd)
personality d.o.'s
eating disorders

Front 96

NT comprimised in Schizophrenia

Back 96

dopamine

Front 97

definition of Schizophrenia

Back 97

Disturbance/deterioration of cognitive, social, emotional functioning
More of a syndrome than a single illness

Front 98

Pathophys of schizoprenia

Back 98

Exact cause unknown. Probably presynaptic dysregulation of DA in D1 and D2 receptors. Excessive DA D2 receptor activity produces more noticeable symptoms

Front 99

s/s of schizophrenia

Back 99

Disorganized thinking, unusual speech (invented words), odd behavior, delusions, hallucinations
Delusion=systematic fixed false beliefs. Can be religious, grandiose, and persecutory

Neologisms=invented words with invented special, private meanings

Hallucinations: breakdown of perceptual selectivity, can affect 5 senses
anhedonia absence of pleasure, interest
Self-identity disturbance= lack of identity; cannot tell self from others
Autism=profound detatchment

Front 100

NT comprimised in Delusional D.O.

Back 100

dopamine

Front 101

definition of delusional d.o.

Back 101

Similar to schizophrenia. Systematic false beliefs. Persist despite evidence demonstrating otherwise. Can dramatically reshape personality and character. Person’s life shapes the delusion; life then confirms the delusion. A defense mechanism?

Front 102

s/s of delusional d.o.

Back 102

Systematic delusions/not bizarre
Impaired reality testing

Front 103

NT comprimised in depression

Back 103

serotonin (5-HT)

Front 104

definition of depression

Back 104

A multi-faceted disorder characterized by: Low energy, inability to experience joy, difficulty initiating tasks, reduced decision-making ability, difficulty sleeping, poor appetite, weight loss, and decreased libido. Thoughts may focus on guilt, futility, emptiness, hopelessness, helplessness, and suicide

Front 105

pathophysiology of depression

Back 105

Low CNS 5-HT transmission: brain serotonin activity via excessive pre-synaptic uptake. OR, could be through stress-related down regulation of post-synaptic receptors

Front 106

s/s of depression

Back 106

Sleep disturbance (melatonin from Pineal Gland)
Depressed mood; loss of interest (anhedonia), fatigue not relieved by rest, restless/irritable/agitated/pacing, impaired concentration, low self-esteem, negative thinking, vegetative state, appetite disturbance, psychosis

Front 107

difference btw minor and major depression

Back 107

Minor depression: symptoms usually resolve in 1-2 years. Also known as dysthymia
Major depression: symptoms last for 2+ years

Front 108

NT comprimised in Bipolar d.o.

Back 108

Serotonin, Norepi (NE), Dopamine

Front 109

definition of bipolar d.o.

Back 109

Depression and/or elation (mania), often mistaken as schizophrenia. A mood disorder connected to diencephalon dysfunction.

Front 110

pathophysiology of bipoloar d.o.

Back 110

Neurotransmitter deficit~depression
Neurotransmitter overactive~mania

Front 111

s/s of bipolar

Back 111

Mania, or hypomania. Depression, or euphoria
Seemingly limitless energy level, impervious to fatigue
Speech disturbances, hallucinations/delusions, impulsive action, impaired judgment, sleep disturbance, hypersexuality. Appetite decreased because they are too distracted to eat

Front 112

NT comprimised in anxiety do's

Back 112

5HT primarily

Front 113

s/s of anxiety do's

Back 113

Panic 5HT Physical (resp. distress, palpitations, choking); Fearful; exaggerated startle response
Generalized GABA, NE, 5HT Muscle tension, sweating, palpitations, Uncontrollable worry
OCD 5HT, DA Compulsions (repetitive rituals), Obsessions (uncontrollable)

Front 114

NT compromised in personality do's

Back 114

HPA axis, 5HT

Front 115

s/s of personality do's

Back 115

borderline = Combination of psychosis/neurosis, alienation, impulsiveness; Manipulation, self-harm, Devalues others (splitting)
Antisocial = “psychopath”, “sociopath”, disregard for others

Front 116

NT compromised in Eating do's

Back 116

NE, 5HT, DA
Related to depression

Front 117

s/s of anorexia

Back 117

Severe ritualistic restriction of caloric intake, binging/purging, body dysmorphia; cardiac arrhythmias, K+

Front 118

s/s of bulimia

Back 118

Binging/purging