Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Neuro > Exam 4 > Flashcards

Exam 4 Flashcards

1
Q

Vertigo

A

Symptom of illusionary movement
Caused by asymmetry of the vestibular system

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

Most important part of history is someone who is dizzy

A

Timing
Recurrent/monophonic
Length
Triggers
Associated symptoms

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

Central lesions causing vertigo

A

Cerebellum or brainstem

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

Peripheral lesions causing vertigo

A

Labyrinth or vestibular nerve

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

Vertigo examination

A

Eye movements
HINTS
Dix-Hallpike
Vestibular Ocular Reflex
Hearing- Weber and Rivne, CALFRAST

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

HINTS testing

A

Head Inpulse
Nystagmus
Test of Skew
Used to determine if lesion is central or peripheral

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

An abnormal HITS test indicated _ problem

A

Peripheral

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

Nystagmus in a peripheral problem

A

Unidirectional nystagmus
Typically horizontal with torsional component

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

Nystagmus with a central problem

A

Can reverse direction
Can be in any direction (purely vertical/purely horizontal= central sign)

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

Visual fixation with peripheral problem

A

Suppression

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

Visual fixation with central problem

A

Not suppressed

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

Test of Skew

A

Cover uncover test
Look for skew deviation

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

Central vs peripheral vertigo

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

Central causes of vertigo

A

Acute stoke

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

First step in management of vertigo

A

If central, MRI to localize and determine next steps

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

Acute central vertigo is _ until proven otherwise

A

stroke

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

Abnormal HINTS exam

A

Brain MRI

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

Acute stroke/TIA management

A

Vascular imaging
Thrombolyic therapy, mechanical thrombectomy, antiplatelet
Manage risk factors

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

Benign Paroxysmal positional vertigo

A

Peripheral cause of vertigo
Recurrent brief episodes of vertigo triggered by head movement
May be associated with nausea/vomiting
Caused by otoliths in semicircular canals causing excessive movement of endolymph
Confirm diagnosis with Dix-Hallpike test
Epley maneuver relieves symptoms

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

Vestibular migraine

A

Another cause of central vertigo

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

Did-Hallpike maneuver

A

Used to detect BPPD

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

Interpretation of Dix Hall Pike test

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

Ménière’s disease

A

Peripheral vertigo
Episodic vertigo, tinnitus, and hearing loss
Unilateral sensorineural hearing loss with aural fullness
Commonly idiopathic

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

Vestibular neuritis

A

Peripheral cause of vertigo
Includes vestibular neuronitis and labrynthitis
Sudden onset sever vertigo for 1-2 day follow by gradual resolution
Hearing preserved= vestibular neuronitis
Hearing loss= labrynthitis

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

The NMJ synapse is only

A

Excitatory

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

Process at NMJ

A

Ach is released and binds to the receptor on post synaptic membrane causing Na channels to open
Na influx generates AP if threshold is reached
the AP causes the release on Ca ions
Ca binds to tropinin initiating contraction
Ach is degraded by acetylcholinesterase

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

Pre synaptic NMJ disorders

A

Lambert-Eaton syndrome
Botulism

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

Post synaptic membrane disorders

A

Myasthenia gravis

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

Presentation of NMJ disorders

A

Motor complaints
Pure motor

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

Myasthenia gravis is a _ disease

A

autoimmune

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

Must common antibody in myasthenia gravis

A

AChR

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

Common presentation myasthenia gravis

A

Variable weakness and fatiguability of striated voluntary muscle (ptosis gets worse throughout the day)
Ocular with pupil sparing
Bulbar and respiratory dysfunction
Axial and proximal limbs affected more

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Myasthenia gravis neuro exam

A

Ocular signs: Ptosis/diploplia with upward gaze, Weakness of eyelid closure
Bulbar signs: jaw weakness, facial diplegia, palatial weakness, tongue weakness
Respiratory signs: respiratory rate, use of accessory muscle, ease of speech and neck strength
Limb strength
Deep tendon reflex

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

Most sensitive test for myasthenia gravis diagnosis

A

Single fiber EMG
AChR is most specific

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

Myasthenia gravis diagnosis

A

Ice pack test
ACh receptor antibodies (block active site, damage receptors with help of complement)
MuSK antibodies (IgG4 does not bind complement)

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

End plate potential is generated

A

At the NMJ after a single nerve action potential (NAP)

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

Muscle action potential is

A

The propagated potential of a single muscle fiber

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Compound Muscle Action Potential is

A

The sum of all the MAPs in a muscle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Safety factor

A

Excess Ach is released beyond what is needed to generate an end plate potential

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Myasthenia neurophysiology

A

Some thresholds not met
Slow rate on repetitive nerve stimulation
Jitter and blocking on single fiber EMG

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Myasthenia treatment

A

Pyridostimige (inhibits AChE)
Immunosuppressives
Thymectomy
Plasmapheresis
IVIG

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Myasthenia crisis

A

Respiratory difficulties
Sever bulbar/respiratory weakness and no cardiac involvement
Treat with IVIG

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Myasthenia can be related to which cancer?

A

Thymoma
Need CT/MR chest
Mandatory thymectomy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

MuSk+ MG

A

Young females
Sever bulbar, respiratory
Poor response to pyridostigmine
Normal/atrophic thymus
treat with steroids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

MG in pregnancy

A

Avoid mycophenolate due to malformation risk

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Lambert Eaton myasthenic syndrome

A

Proximal and generalized weakness
Cholinergic dysautonomia
Decreased or absent deep tendon reflexes
50% paraneoplastic
Diagnosis: + P-Q type VGCC and NCS
Treat: 3,4 DAP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Botulism

A

Wound, foot, infantile, inhalational
Degrades proteins necessary for docking/fusion of ACh vesicles preventing release into synaptic cleft
Symptoms: dysphasia, xerostomia, dysarthria, progressive muscle weakness
Tests: look for toxin
EMG/NCS: low compound muscle action potential
Treat: botulism antitoxin, antibiotics

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Infantile botulism can be caused by

A

Honey

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Presynaptic NMJ disorders

A

Decrement
Facilitation with fast stimulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Myasthenia gravis vs LEMS vs Botulism

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q
A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

ALS is characterized by the deterioration

A

of cortical motor neurons, lower brainstem, and the anterior horn cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

Death in people with ALS is caused by

A

Respiratory weakness leading to death

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

ALS risk factors

A

Family history
Male gender

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

Pathophysiology of ALS

A

Oxidative stress
Glutamate excitotoxicity
Mitochondrial dysregulation
Prion-like protein dysregulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

Pathology of ALS

A

TDP-42 inclusions cause frontotemporal lobar degeneration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

ALS symptoms

A

Focal/regional asymmetric limb onset
Bulbar symptoms
Fasciculations of tongue/limb muscles
Cramps
Spasticity
Weight loss
Muscle loss
Fatigue
SOB/dyspnea/othopnea
Cognitive impairment (frontal temporal dementia)
Parkinsonism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

This that do not indicate ALS

A

Pain
Sensory loss
Loss of sphincter tone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

ALS diagnosis is based on

A

UMN and LMN involvement
Progressive weakness
Excision of alternate diagnosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

Familial ALS

A

AD inheritance
C9orf72 expansion
SOD mutation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

ALS management

A

Riluzole
Sodium phenylbutyrate/taurursodiol
Non-invasive ventilation
Peg-tube
Symptom management

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

ALS prognosis

A

3-5 years after symptom onset (death from respiratory failure)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

Primary lateral sclerosis

A

Affects central motor neurons
No atrophy, fasciculations, or EMG abnormalities
Weakness/spasticity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

Progressive muscular atrophy

A

LMN dysfunction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

Progressive Bulbar palsy

A

Symptoms in bulbar muscles (innervated by CN IX-XII) due to bilateral LMN impairment
Dysarthria, dysphasia, weight loss
Napkin/handkerchief sign
Progress to involve limbs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

ALS/parkinsonism-dementia complex

A

Gait disturbances
Hyperreflexia and limb muscle atrophy
Ridgid-akinetic Parkinsonism and severe dementia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

Kennedy disease

A

C-linked trinucleotide CAG repeat (>36) expansion of the androgen receptor gene
Weakness/atrophy affecting facials bulbar, and limb muscles (cramps)
Endocrine disruptions
Female carriers may experience mild symptoms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

Kennedy disease diagnosis

A

High HbA1c, CK mildly elevated
genetic confirmation of AR expansion
Supportive treatment

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

Spinal muscular atrophy

A

Most common fatal genetic disease in infancy
Homozygous deletion or point mutation of SMN1 gene (AR)
Neurodegeneration of anterior horn cell in spinal cord/ brain stem

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

Spinal muscular atrophy manifestations

A

Tongue atrophy with fasciculations
Hypotonia
Fine tremor
Proximal weakness and atrophy
Waddling gait
Impaired swallowing and ventilatory insufficiency
Kyphoscoliosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

Spinal muscular atrophy diagnosis

A

Genetic confirmation
Supportive care: bipap, tracheostomy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

West Nile virus

A

Acute flaccid paralysis
Meningo-encephalitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

West Nile virus diagnosis

A

Regional and asymmetric flaccid paralysis
No pain or sensory deficits
+/- respiratory failure
CSF IgM is diagnostic
EMG: regional/asymmetric MND

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

Acute Flaccid Myelitis

A

Acute focal onset limb weakness
Caused by coxsackievirus/enterovirus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

Mixed UMN/LMN is classic for

A

ALS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

Chronic focal/regional limb onset

A

ALS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

Acute segmental with asymmetry

A

West Nile virus
Acute flaccid myelitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

Chronic symmetric, generalized, proximal>distal

A

Spinal muscular atrophy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

Chronic limb and bulbar LMN weakness

A

Kennedy’s disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

Alzheimer’s disease pathology

A

Brain atrophy (frontal, temporal, parietal)
Narrowing gyri, sulcal widening, atrophic hippocampus, ventricular enlargement

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

Alzheimer’s disease microscopic findings

A

Plaques (B-amyloid in neutrophils)
Neurofibrillary tangles (tau in neurons
Accumulation due to excessive production/defective removal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

Familial Alzheimer’s

A

APP mutation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

What is the initiating event for the development of Alzheimer’s

A

B-amyloid accumulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

Biomarkers for Alzheimer’s disease

A

Fluorine 18-amyloid PET scan
p-tau and reduced AB
Blood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

Alzheimer’s disease treatment

A

Anti-amyloid antibodies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

B. Amyloid inclusions

A

Amyloid plaques

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

Tau inclusions

A

Neurofibrillary tangles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

Cerebral amyloid angiopathy

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

Frontotempotal lobar degeneration

A

Alteration in personality, behavior, language preceding memory loss
Early onset
FTLD-tau, FTLD-TDP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
90
Q

FTLD-tau (Pick’s disease)

A

Only tau
May be caused by mutation in MAPT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
91
Q

FTLD-TDP

A

Frontal and temporal atrophy
Abnormal TDP43 (RNA binding protein)
Mutations in c9orf72 (expansion), TARDBP, GRN

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
92
Q

ALS

A

Degeneration of corticospinal tracts
Loss of UMN and LMN
Mutations in C9orf72, SOD 1, TARDBP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
93
Q

Parkinson’s disease

A

Loss of dopamine producing neurons in substantia nigra
Parkinsonism
Lewy bodies (a-synuclein)
SMCA mutation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
94
Q

Diffuse Lewy body disease

A

Dementia associated with PD
Lewy bodies in cortical neurons

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
95
Q

Myopathy

A

Muscle weakness

May also have:
Myalgias, cramps, stiffness
Rhabdomyolysis/myoglobinuria
Myotonia
Muscle Atrophy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
96
Q

Myopathies can be

A

Hereditary (muscular dystrophies, congenital myopathies, myotonies, channelopathies, metabolic myopathies, mitochondrial myopathies)
Or
Acquired (inflammatory, endocrine, drug induced/toxic, associated with systemic illness)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
97
Q

Labs for myopathy

A

CK
Aldolase
AST, ALT
Gamma GT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
98
Q

Inflammatory myopathies

A

Dermatomyositis
Inclusion body myositis
Polymyositis
Overlap syndrome
Necrotizing autoimmune myopathy
Infectious

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
99
Q
A

Dermatomyositis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
100
Q
A

Inclusion body myositis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
101
Q

Muscle weakness pattern in inflammatory myopathies

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
102
Q

Most common myopathy after 50

A

Inclusion body myositis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
103
Q

Proximal muscle weakness of forearm and thigh atrophy

A

Inclusion body myositis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
104
Q

Polymyositis vs Dermatomyositis vs inclusion body myositis

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
105
Q

Necrotizing autoimmune myopathy

A

Subacute severe progressive proximal weakness
Very high CK
Anti-SRP, anti-HMGCoA, connective tissue disease and paraneoplastic
induced by statins
Early aggressive dual immunotherapy improves prognosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
106
Q

Steroid myopathy

A

Endocrine myopathy
Due to prednisone >30 mg/day
Fluoridated steroids are worse
Proximal muscle weakness
Normal CK, myopathies EMG without active denervation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
107
Q

Hyperthyroidism and hypothyroidism can both cause

A

Endocrine myopathies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
108
Q

Hyperthyroidism myopathy

A

CPK normal
Proximal weakness, periodic paralysis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
109
Q

Hypothyroidism

A

Endocrine myopathy
Proximal weakness, muscle hypertrophy
Ankle jerks=delayed relaxation
Myoedema

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
110
Q

Vitamin D deficiency may cause

A

Endocrine myopathy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
111
Q

Critical illness myopathy

A

Associated with sepsis, organ failure, systemic inflammation
Systemic flaccid limb weakness (proximal>distal)
Failure to extubate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
112
Q

Muscle dystrophy

A

Progressive weakness and wasting
Fiber size variation, fibular necrosis and regeneration
Fibrosis and fatty replacement

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
113
Q

Muscular dystrophies

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
114
Q

Age of onset muscular dystrophy

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
115
Q

Largest protein in the human body

A

Dystrophin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
116
Q

Dystrophinopathies

A

Proximal weakness, neck extensor weakness, calf hypertrophy, lordotic posture, toe walking, waddling gate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
117
Q

Duchenne vs Becker

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
118
Q
A

Dermatomyositis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
119
Q
A

Dystrophinopathies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
120
Q

Steroids are used in which muscular dystrophy?

A

Duchenne

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
121
Q

Most common dystrophy in adults

A

Myotonic dystrophy
-difficulty releasing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
122
Q
A

Myotonic dystrophy: distal pattern with facial weakness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
123
Q

Myotonic dystrophy diagnosis

A

CK normal-mildly elevated
EMG
Muscle biopsy
Genetic testing: >50 CTG repeats C19

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
124
Q

Myotonic dystrophy treatment

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
125
Q

Rhabdomyolysis

A

Acute muscle necrosis and release of intracellular muscle constituents
Triad muscle pain, weakness, dark urine
CK 1500-100,000, myoglobinuria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
126
Q

Rhabdomyolysis treatment

A

Stop offending agent
Hydration, monitor kidney function

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
127
Q

Recurrent Rhabdomyolysis can be caused bt

A

CPTII deficiency

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
128
Q

Metabolic myopathies

A

Dynamic symptoms: exercise intolerance with muscle pain and cramps
Worsen due to increased physiologic stress
Disorders of glycogen,, lipids, mitochondrial muscle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
129
Q

Glycogen vs lipid storage Rhabdomyolysis

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
130
Q

Mitochondrial myopathy

A

Hearing loss, short stature, myopathy and peripheral neuropathy
Can be:
Isolated myopathy
Chronic progressive external ophthalmoplegia or Kearns-Sayre syndrome
Encephalopathy of infancy and childhood
Multisystem disease with myopathy (MELAS, MERRF)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
131
Q

Acute weakness with CK >5-10K

A

Rhabdomyolysis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
132
Q

Subacute-chronic with rapid progression and high CK

A

Auto-immune myositis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
133
Q

Peripheral nerve disorders affect

A

Root
Plexus
Nerve

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
134
Q

Monomelic conditions

A

Mononeurophathy
Plexopathy
Radiculopathy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
135
Q

Polymelic

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
136
Q

Radiculopathy

A

Degenerative disease of spine or disc herniation
Pain and mild sensory loss in root distribution
Inflammatory/infectious/neoplastic
Commonly C7, L5
Exam: reflex abnormalities

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
137
Q

Plexopathy

A

Single limb with motor, sensory, reflexes impaired
Due to trauma (MVA, penetrating injuries, contact sports, birth trauma), tumor (pancoast), delayed radiation injury, plexitis, Parsonage-Turner syndrome
Can be painful or painless

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
138
Q

Birth trauma may cause which Plexopathy condition

A

Erb’s palsy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
139
Q

Mononeuropathy

A

Diabetes, amyloidosis, peripheral neuropathy, hypothyroidism, HNPP
Can cause sensory or motor symptoms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
140
Q

Mononeuropathy vs Radiculopathy

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
141
Q

Most common cause of peripheral neuropathy

A

Diabetes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
142
Q

Approach to polyneuropathy

A

What: fibers affected/loss of function
When: onset and temporal evolution
Where: length dependent vs non-length dependent
What setting: young- genetic, elderly-idiopathic, middle age-acquired

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
143
Q

Small fiber vs large fiber neuropathy

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
144
Q

Painful polyneuropathy with Mee’s lines

A

Chronic arsenic or thallium poisoning

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
145
Q

Asymmetric sensory neuropathy with predilection to could skin areas and skin ulceration

A

Leprous neuropathy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
146
Q
A

Vitamin B12 deficiency and pernicious anemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
147
Q
A

POEMS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
148
Q

Axonal neuropathies

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
149
Q

Demyelinating neuropathies

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
150
Q

Polyneuropathy labs

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
151
Q

Diabetic neuropathy is usually

A

Distal symmetric large fiber sensorimotor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
152
Q

Polyneuropathy treatment

A

Foot inspections
Medications: Gabapentin, Pregambalin
B12 replacement, diabetes control, alcohol reduction, immunotherapy, infection treatment, cancer or blood dyscrasia treatment

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
153
Q

Toxic neuropathy

A

Painful axonal peripheral neuropathy
Timely linked to exposure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
154
Q

Most common inherited neuropathies

A

Charcot-Marie-Tooth type 1a
Distal sensory is predominant phenotype

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
155
Q
A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
156
Q
A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
157
Q

Polyradiculoneuropathy vs Polyneuropathy

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
158
Q

Most common cause of acute generalized paralysis

A

GBS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
159
Q

GBS is caused by

A

Molecular mimicry due to preceding infection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
160
Q

GBS presentation

A

Weakness, Paresthesia, areflexia
Symmetric weakness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
161
Q

GBS diagnosis

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
162
Q

Ganglionopatheis

A

Asymmetric, non length dependent sensory impairment
Rapid onset, subacute progression
Sensory ataxia
Autoimmune, toxic, infectious, paraneoplastic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
163
Q

GBS treatment

A

Plasma exchange
IVIG

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
164
Q

Multiple mononeuropathies

A

Abrupt onset and painful, step-wise subacute progression
Asymmetric
Weakness and sensory loss mapped to multiple nerve territories
Commonly caused by Vasculitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
165
Q

_ is an enduring emotional tone

A

Mood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
166
Q

_ is the physical expression of a person’s immediate felling state, typically focusing on facial expression

A

Affect

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
167
Q

Euthymic

A

Normal mood

168
Q

How thoughts are put together-structure

A

Thought process

169
Q

Circumstantial thought process

A

Coherent but over inclusive

170
Q

Tangential structure

A

Coherent but drifts away from topic

171
Q

Flight of ideas

A

Rapidly shifting from one idea to another

172
Q

Loose associations

A

Incoherence

173
Q

Insight

A

Ability to understand the current situation and implications of various choices

174
Q

Judgement

A

Decision making

175
Q

Depression diagnosis

A

depressed mood or anhedonia
plus 4 of the following: SIGECAPS

176
Q

Which health condition can present like major depressive disorder

A

Hypothyroidism

177
Q

Major depressive disorder diagnosis

A

At last 1 major depressive episode
No history of mania or hypomania

Use screening tools: PHQ-2,9, Edinburgh depression scale

178
Q

Major depressive disorder specifiers

A

Psychotic features (in severe depression)

179
Q

Pathophysiology of major depressive disorder

A

Increased blood flow/decreased volume to prefrontal cortex
Decreased slow wave sleep, decreased REM latency, increased REM sleep
Abnormal variation in cortisol production and non-suppression of cortisol production
Decreased serotonin

180
Q

Natural course of major depressive episode

A

Resolves in 6 months
50% chance of recurrence
75% risk of recurrence
>95% risk

181
Q

Persistent Depressive Didorder

A

Depressed mood for majority of 2 years
2 SIGECAPS symptoms
Cannot be symptom free for more than 2 months
Never experiences a manic or hypomanic episode

182
Q

Substance/medication induced depressive disorders

A

Major depressive episode which starts during or soon after intoxication or withdrawal of a substance

183
Q

Premenstrual Dysphoric Disorder

A

1 of the following symptoms: lability, anger, depressed mood, anxiety
1 of the following: anhedonia, problems concentrating, low energy, appetite changes, sleep changes, physical symptoms
Most have 5 total symptoms combined

184
Q

Depressive disorder due to another medical condition

A

Depressed mood/anhedonia

185
Q

Adjustment disorder

A

Development of emotional/behavior dysfunction in response to a stressor which starts within 3 months of the onset of the stressor

186
Q

Bereavement

A

Normal low mood in response to an acute loss

187
Q

Treatment of mild depression

A

Psychotherapy
Exercise

188
Q

Treatment of moderate and serve depression

A

Medications
Therapy

189
Q

Treatment resistant depression

A

Electroconvulsive treatment (ECT)

190
Q

SSRI side effects

A

GI side effects
Bleeding
Hypotnatremia
Sexual side effects
Increased suicide risk

191
Q

SNRIS can also cause

A

Excessive sweating
Dry mouth
Insomnia

192
Q

NDRI

A

Can increase anxiety or cause weight loss

193
Q

TCA side effects

A

Anticholinergic effects
Bleeding risk
QT prolongation and arrhythmias
Sedation
Suicidal thoughts
Lethal in overdone

194
Q

MAOIs

A

Can cause hypertensive crisis
Must eat low tyramine diet

195
Q

To have a bipolar disorder there must be

A

A manic or hypomanic episode

196
Q

Major depressive disorder in adolescents

A

Do not have to be depressed- may be irritable
Do not have to loos/gain weight- consider failure to make expected weight gain

197
Q

Empirical treatments for depression in adolescents

A

SSRI (fluoxetine-Prozac)
CBT
interpersonal therapy for adolescents

198
Q

Gold standard medication for pediatric population

A

Fluoxetine (Prozac)

199
Q

Atypical/non-SSRI antidepressant efficacy in adolescents

A

No better than placebo

200
Q

Optimal treatment for adolescent depression

A

Combination treatment

201
Q

Mania vs hypomania

A

Mania- more than 1 week, or any duration if hospitalization is necessary
Hypomania- lasts at least 4 consecutive days

202
Q

Mania criteria

203
Q

Bipolar disorder onset

A

Most between 15-19 years
Prepubertal onset should be considered unlikely

204
Q

Bipolar disorder treatment

A

Medications (atypical antipsychotics)

205
Q

Elements of consciousness

A

Reactivity (arousal) and content (awareness)

206
Q

Disorders of reactivity

A

Somnolence
Stupor
Coma

207
Q

Disorders of content

208
Q

Structural causes of coma

A

Brainstem or diffuse cortical damage

209
Q

Non-structural causes of coma

A

Toxic
Metabolic
Electrical

210
Q

Next step for patient in coma

A

Semiology and imaging (CT)

211
Q

Semiology

212
Q

Oculi-Cephalic reflex

A

Tests connection between midbrain and pons

213
Q

Bilateral damage between cortex and red nucleus

A

Decorticate posturing

214
Q

Bilateral damage below the red nucleus

A

Decerebrate posturing

215
Q

Coma mimics

A

Locked-in state
fulminant Guillain-Barré syndrome
Akinetic mutism
Catatonia
Psychogenic come

216
Q

Delirium

A

Deficits in attention
Altered arousal
Symptoms of psychosis
Fluctuate in presence and severity
Medical/surgical triggers
Predisposing factors

217
Q

Brain death

A

Complete absense of brain function
Irreversible damage of brainstem
Must do imaging to find clear cause (ICH, malignant MCA infarct, DAH, severe TBI, Cardiac arrest)
Absence of confounders

218
Q

Testing for brain death

A

Apnea test
Nuclear medicine
TCB
EEG vascular studies

219
Q

Aphasia

A

Impairment of language

220
Q

Dysarthria

A

Disorder of speech production

221
Q

Leading cause of aphasia

222
Q

Dysarthria is common in

A

Neurologic conditions

223
Q

Developmental langue disorder

A

Problems in children that impact language production or understanding

224
Q

Speech sound disorder

A

Speech disorder (ex. Stuttering)

225
Q

Occlusion of a branch of the middle cerebral artery in the inferior lateral frontal lobe

A

Broca’s area

226
Q

Non fluent aphasia

A

Broca’s aphasia

227
Q

Wernicke’s aphasia

A

Fluent aphasia

228
Q

Watershed infarcts

A

TCM, TCS Aphasia

229
Q

Damage to the accurate fasciculus

A

Inability to repeat

230
Q

Dorsal streams

A

Sensorimotor integration

231
Q

Ventral steam

A

Speech comprehension

232
Q

Global aphasia

A

Inability to understand and produce words

233
Q

Aprosodias

A

Right hemisphere, non-verbal aspects of speech and language

234
Q
A

Alecia without a graphic
Right homonymous hemianopia

235
Q

Dysarthria

A

Motor speech disorder due to breakdowns in muscle groups used for respiration, phonation, articulation, resonation, or prosody

236
Q

Spastic dysarthria

A

Strained, strangles, slurred and slow speech, monotone
UMN lesion

237
Q

Flaccid dysarthria

A

Poor articulation
LMN

238
Q

Ataxic dysarthria

A

Irregular articulation, variable duration, poor voice and volume control, drunk speech
Dysfunction of cerebellum

239
Q

Hypokinetic dysarthria

A

Hypophonia, decreased articulation, mono pitch
Basal ganglia dysfunction

240
Q

Aphasia treatment

A

Speech and language therapy
Compensatory approaches
Early identification and intervention
Lee Silverman voice treatment

241
Q

Dementia

A

Decline in cognitive abilities leafing to impairment of functional abilities
Chronic

242
Q

Causes of delirium

A

Metabolic, toxic, sepsis, ICP

243
Q

Dementia types

A

Alzheimer’s
Vascular
Lewy body
Frontotemporal

244
Q

Dementia staging

245
Q

Amyloid plaques and Neurofibrillary changes

A

Alzheimer’s

246
Q

Alzheimer’s disease

A

Gradual onset/progression
No weakness or sensory loss

247
Q

Vascular dementia

A

Sudden onset, step-wise decline
Focal motor, sensory, reflex changes
Focal cognitive impairment
Vascular disease on brain imaging
Prevention: stroke treatment

248
Q

Vascular dementia subtypes

A

Small vessel
Large vessel
Mixed

249
Q

Subcortical dementia

A

Impaired executive cognitive function, visual spatial abilities, memory retrieval
Two core features: extrapyramidal features, fluctuating cognition, visual hallucinations, REM sleep behavior disorder
Faster progression, restless leg syndrome

250
Q

Frontotemporal dementia

A

Behavioral changes
Diagnosis supported by neuropsychological testing and structural/functional brain imaging
Caused by tau or TDP-43

251
Q

Pick’s disease

252
Q

FTD imaging findings

A

Atrophy of frontal lobes
Decreased glucose metabolism in frontal lobes

253
Q

Normal pressure hydrocephalus

A

Gait apraxia
Cognitive impairment
Incontinence
Tap test diagnosis
Treat with VP shunt
Must have evidence of hydrocephalus

254
Q

CJD

A

Rapidly progressive dementia
Movement disorder
Prion disorder

255
Q

Dementia workup

A

H&P
Lab tests
Brain imaging
MoCA

256
Q

Lewy bodies

A

Parkinson’s
Lewy body dementia

258
Q

Alzheimer’s biomarkers in CSF

A

Low amyloid beta
High tau

259
Q

Alzheimer’s risk factors

A

Age
Genetics- PSEN1/2, APP, APOE4
Lifestyle

260
Q

Cholinesterase inhibitors

A

Increase Ach by inhibiting acetylcholinesterase
First approved drug for Alzheimer’s
For mild-moderate dementia
Do not prevent progression (moderate improvement)
Side effects: bradycardia, avoid in peptic ulcer disease)

261
Q

Memantine

A

Moderate-severe AD
NMDA receptor antagonist
Inhibits glutamate

262
Q

Aducanumab

A

Not very effective
Can cause microhemorrhages, edema

263
Q

Medication approved for Parkinson’s disease dementia

A

Rivastigmine

264
Q

Mild cognitive impairment medication

265
Q

Behavior and psychological symptoms of dementia

A

Aggression
Agitation
Apathy
Depression
Psychosis

266
Q

The DICE approach

A

Describe
Investigate
Create
Evaluate
Non-pharmacologic strategies for dementia

267
Q

Antipsychotics are best reserved for

A

Troubling psychotic symptoms

268
Q

Non-pharmacological strategies for Alzheimer’s

A

Structure
Children
Pets
Music
Aromatherapy
Snoezelen
Reminiscence therapy

269
Q

Top 3 things leading to nursing home placement

A

Wandering
***Insomnia
Incontinence

270
Q

Pathological anxiety

A

Excessive fear/anxiety response that is impairing or distressing rather than helpful or manageable
Occurs in context or with response to cues where there is no real threat

271
Q

Having an anxiety disorder increased your risk of

A

Developing a chronic medical condition

272
Q

Fear conditioning

273
Q

Neurobiology of mood and anxiety disorders

A

The limbic system
The prefrontal cortex

274
Q

Amygdala

A

Processes emotionally salient stimulant initiates the behavior response (accelerates fear response)
prefrontal cortex performs execute function, planning, decision making (shuts fear response down)

275
Q

Hypothalamic-pituitary adrenal axis

A

Endocrine- slow response
Sympathetic nervous system- fast response

276
Q

Fear extinction

A

Cognitive behavioral therapy
Graduated exposure

277
Q

Main brain structure involved in fear and emotional processing

278
Q

Diagnosis of a specific phobia

A

Fear/anxiety about object/situation
Persists for at least 6 months

279
Q

Agoraphobia

A

Fear of being outside, around other people
Lasts more than 6 months

280
Q

Clinical management of agoraphobia

A

Exposure therapy

281
Q

Social anxiety disorder

A

Fear of social situations and scrutiny from others
Fear of acting in a way that will be humiliating or embarrassing
Lasts for at least 6 months

282
Q

Generalized anxiety disorder

A

Excessive anxiety and worry for more than 6 months
Worry is difficult to control

283
Q

Obsessive compulsive disorder

A

Presence of obsessions, compulsions or both
Obsessions-persistent thoughts
Compulsions- repetitive behaviors

284
Q

Neurobiology of OCD

A

Cortico-striato-thalamo-cortical loop

285
Q

What can cause the onset of OCD in children

A

PANDAS: loop for anti-streptolysin O tiger or DNase B antibodies

286
Q

OCD management

A

Exposure and response prevention
SSRIs
Clomipramine

287
Q

Management of anxiety disorders

288
Q

Adjustment disorder

A

Emotional or behavioral symptoms in response to identifiable stresses occurring within 3 months of onset of stressor
Symptoms are over within 6 moths characterized by depressed mood, anxious mood, mixed anxiety/depression, disturbance of conduct

289
Q

PTSD

A

Severe trauma the constitutes a threat to the physical integration or life of the individual or another person
(Onset 1-3 months after trauma)
If <1 month it is acute stress disorder

290
Q

Diagnostic criteria for PTSD

A

Exposure
Intrusion
Avoidance
Negative alterations in cognition or mood
Arousal and reactivity
Symptoms for more than a moths
Significant distress or impairment

291
Q

PTSD can cause

A

Dissociative symptoms
Delayed expression

292
Q

Acute stress disorder

A

3 days-1 moths after trauma exposure

293
Q

PTSD treatment

A

SSRI Or SNRI
Psychotherapy (prolonged exposure therapy

294
Q

Major depression vs demoralization

295
Q

ODD

A

Angry
Defiant
Vindictiveness
Lasts at least 6 months

296
Q

ODD is associate with

297
Q

Conduct disorder

A

Aggression
Destruction
Deceitfulness
Serious violation of rules
Longer than 6 months

Lack of remorse or guilt
Callous-lack of empathy
Unconcearned about performance
Shallow or deficient affect

298
Q

ODD and conduct disorder treatment

A

NO medication
Behavioral management training

299
Q

ADHD

A

Neurodevelopmental disorder with core characteristics of behavior and response inhibition

Can be inattentive, hyperactive/impulse presentation, combined presentation

300
Q

ADHD diagnostic criteria

A

Careless mistakes
Difficulty sustaining attention
Does not listen
Does not follow through
Difficulty organizing
Avoids tasks that require sustained mental effort
Loses things
Easily distracted
Often forgetful
Prior to age 12
Two or more settings
Reduced functioning

301
Q

ADHD diagnosis

A

Clinical interview and history
Collateral information

302
Q

Neuropsychological testing

A

Used for ADHD
Used to establish IQ, underlying learning disorders

303
Q

Most common comorbidity of someone with ADHD

304
Q

ADHD maturation delay

A

Right frontal side

305
Q

ADHD treatment

A

Medication treatment (stimulants-amphetamines, methylphenidate) if active use disorder use atomoxetine
Behavioral therapy

306
Q

Autism diagnosis

A

Deficits in social communication and interaction across multiple contexts
Restricted, repetitive patterns of behavior, interests, or activities
Must been in early development, cause impairment of functions

307
Q

Autism specifiers

A

With or without intellectual impairment
With or without language impairment

308
Q

Syndromes associated with autism

A

Fragile X
Tuberous sclerosis
Rett syndrome

309
Q

Intellectual disability

A

Inherited- fragile X
Genetic- trisomy 21
Preventable- fetal alcohol disorder

310
Q

Things that are not evidence based psychotherapy

311
Q

Cognitive behavioral therapy has evidence for

A

Depression
Generalized anxiety disorder
Schizophrenia
ADHD
Bulima
Insomnia

312
Q

Behavioral therapy has evidence for

A

ADHD
Obesity
Alcohol use disorder
Autism spectrum disorder

313
Q

Parent management has evidence for

A

Disruptive behavior/ noncompliance
ODD
ADHD

314
Q

Exposure therapy has strong evidence for

A

Specific phobias
OCD
Panic disorder

315
Q

Prolonged exposure is

A

Modified for PTSD

316
Q

When does therapy come first

A

Pediatric populations
Tics
Trichotillomania
Behavioral sleep disorders
Enuresis/encopresis
When a patient wants it

317
Q

Piagets theory of cognitive development

318
Q

Stages of cognitive development

319
Q

Vygotsky sociocultural theory

A

Cognition is dependent on the social, cultural, and historical context
Culture defines what knowledge and skills a child needs to acquire and gives them the tools
The intermental constructs the intramental
All of this has to occur in zone of proximal development (what I can do with help)

320
Q

Erik Eriksons psychological stages

A

Personality develops in predetermined order
Each stage has a crisis that must be resolved to move onto next stage
Failure to resolve a crisis results in stagnancy

321
Q

Attachment theory

A

Stages:
Pre-attachment
Attachment in the making (3-6 months)
True (7-18 months)

assess using strange situation procedure

322
Q

Strange situation response patterns

323
Q

When are basic emotions developed

A

By 6 moths

324
Q

When are complex emotions developed

A

18-24 months

325
Q

Self concept evolution

326
Q

Two general dimensions of parenting

A

Parental warmth and responsiveness
Parental control

327
Q

Delirium

A

An acute mental disturbance caused by another medical condition characterized by confused thinking and disrupted attention
Disturbance in attention and awareness
Fluctuates throughout the day
Disturbance in cognition
Caused by another general medical condition

328
Q

Delirium prevention and treatment

A

Re-orientation
Prevent dehydration and constipation
Access hypoxia
Encourage mobility
Medication review
Look for and treat medication
Treat pain
Good nutrition
Prevent sensory impairment
Avoid sleep disturbance

329
Q

Medication treatment for delirium

A

No medications indicated

330
Q

Testing for patients with delirium

331
Q

Delirium risk factors

332
Q

Delirium take home points

333
Q

Somatic Symptoms Disorders are marked by

A

Cognitive distortions
“Being healthy means being symptom free”
“I have a symptom therefor it must be a disease”
Disproportionate and persistent thoughts about the seriousness of symptoms
Persistently high level of anxiety about health or symptoms
Excessive time and energy devoted to these concerns or health symptoms

334
Q

Fictitious disorder

A

Falsification of symptoms associated with deception
Deception
Patient commonly causes symptoms
Inconsistent response to treatments
Common for people who wants attention
Seeking sick role and attention that comes with it

335
Q

Functional Neurological Symptom disorder

A

Impaired coordination/balance
Paralysis/weakness
Inability to swallow
Loss of touch/pain
Blindness
Deafness
Mutism
Nonepileptic spells

336
Q

Refeeding syndrome

A

Life threatening shifts of electrolytes that can be associated with anorexia
Must monitor phosphorous

337
Q

Russells sign

A

Calluses on back of dominant hand associated with bulimia

338
Q

Complications of bulimia

A

Esophageal rupture

339
Q

Binge eating disorder

A

Binge eating without inappropriate compensatory behaviors

340
Q

Personality disorder characteristics

A

Ego syntonic-limited insight
Don’t seek help
Do not have frank psychosis

341
Q

What is a personality disorder

A

Enduring pattern that deviates marked
Pervasive and inflexible
Onset in adolescence
Stable over time
Leads to distress or impairment

342
Q

Manifestations of personality disorders

A

Cognition
Emotional response
Interpersonal functioning
Impulse control

343
Q

Cluster A personality disorders

A

Paranoid
Schizoid
Schizotypal
Odd and eccentric behaviors

344
Q

Cluster B personality disorders

A

Antisocial
Borderline
Narcissistic
Histrionic

345
Q

Cluster C personality disorders

A

Avoidant
Dependent
Obsessive-compulsive

346
Q

Paranoid personality disorder

A

Mistrust in people

347
Q

Schizoid personality disorder

A

Lifelong social withdrawal

348
Q

Schizotypal personality disorder

A

Bizarre dress and speech

349
Q

Narcissistic personality disorder

A

Heightened sense of self importance
Unempithetic, entitled

350
Q

Histrionic Personality Disorder

A

Theatrical
Extroverted
Emotional
Sexually provocative
“Life of the party”
Connot maintain intimate relationships

351
Q

Antisocial personality disorder

A

Refuses to confirm to social norms
No concearn for others
Does not learn from expense
Psychopath, sociopath
Continual criminal acts
Lacks a conscience
Cons others
Must have prior diagnosis of a conduct disorder before the age of 15

352
Q

Borderline personality disorder

A

Erratic unstable behavior and mood
Borden
Feelings of aloneness
Impulsiveness
Suicide attempts
Mini psychotic episodes

353
Q

Avoidant personality disorder

A

Timid
Sensitive to rejection
Socially withdrawn
Feelings of inferiority
Fearful of embarrassment and rejection

354
Q

Dependent personality disorder

A

Get others to assume responsibility for their actions
Intense discomfort when being alone
Exaggerated fears of being helpless when alone

355
Q

Obsessive compulsive personality disorder

A

Perfectionist
Orderly
Stubborn
Indecisive
Feelings of imperfection

356
Q

OCPD

A

Limited insight
May think others cause their problems
Generally don’t seek help unless compelled by others
Ego dystonic

357
Q

Personality disorder treatment

358
Q

Psychosis

A

Symptom not diagnosis
Distorted perception of reality
Positive symptoms: Delusion, hallucinations/illusions, disorganized thinking/behavior

359
Q

Delusions

A

Fixed false belief which is not in line with the beliefs of others in the patient’s culture

360
Q

Perceptual disturbance

A

Hallucination: a sensory experience with no corresponding stimulus (auditory, visual, tactile, olfactory, gustatory)

361
Q

Disorganized speech is indicative of

A

Disorganized thoughts

362
Q

Negative symptoms of psychosis

A

Affective blunting- decreased emotional expression
Avolition- lack of motivation to engage in social activities
Apathy- lack of interest in engaging in social activities s
Anhedonia- lack of pleasure in activities
Alogia- decreased speech output, “poverty of speech”

363
Q

Cognitive symptoms of psychosis

A

Problems with executive functioning
Deficits in working memory
Deficits in attention and focus

364
Q

Criteria for schizophrenia

A

2 or more:
Delusions
Hallucinations
Disorganized speech
Grossly disorganized or catatonic behavior
Negative symptoms
Lasts more than 6 months

365
Q

Brief psychotic disorder

A

One or more symptoms of schizophrenia
Lasting longer than 1 day but less than 1 moths
People return to premorbid level of function

366
Q

Schizophreniform disorder

A

Meet criteria for schizophrenia except for the time requirement
Lasts longer than 1 month but less than 6 months

367
Q

Schizoaffective disorder

368
Q

Delusional disorder

369
Q

Catatonia

370
Q

Most effective treatment for schizophrenia

371
Q

Dopamine blocking-related side effects
IMPORTANT

372
Q

Bipolar disorder diagnosis s

A

Must have a manic episode

373
Q

Bipolar disorder type 2

A

Recurrent depressive episodes and hypomanic episode
Must last at lease for days

374
Q

Bipolar disorder type 1

A

At least one manic episode with recurrent depressive episodes

375
Q

Environmental triggers for bipolar disorder

A

Sleep deprivation or disruption
Time changes
Season changes
Alcohol use
Drug use
Stress

376
Q

Psychiatric emergency

A

Acute disturbance of thought, mood, behavior, or social relationship
Required immediate intervention
Has potential to rapidly become catastrophic outcome
Resources to handle situation are not currently available

377
Q

Examples of psychiatric emergencies

A

Homicidal ideation
Auditory hallucinations commanding violence
Suicidal ideation
Underlying causes: substance intoxication/withdrawal, sever depression, psychosis, bipolar mania, antisocial personality disorder, adjustment disorder, personality disorder

378
Q

Psychedelic

A

Used interchangeably with hallucinogen
Psilocybin
MDMA
Ketamine
THC

379
Q

Psilocybin

A

Found in mushrooms
Increase self compassion, love, acceptance of death
Mystical experience
May cause hallucinations after withdrawal

380
Q

MDMA

A

Releases supraphysiological levels of serotonin, dopamine, norepinephrine
Stimulates release of hormones like oxytocin
Enhance feelings of trust, openness, and connection to other people
Benefits more likely in conjunction with psychotherapy
May cause neurotoxicity

381
Q

Ketamine

A

Used for treatment resistant depression (rapid reductions in suicidality)
NMDA receptor antagonism

382
Q

CBD

A

Not related to misuse, abuse, or dependence
general anti-inflammatory and antioxidant properties
Used for chronic pain, mental health, psychosis, PTSD

383
Q

Addiction

A

Treatable
Chronic medical disease involving complex interactions between brain circuits, genetics, the environment, and the individuals life experiences
Addictive behavior leads to compulsions and continued substance use despite harmful consequences
Prevention and treatment are generally successful

384
Q

Substance use disorder criteria

A

A problematic pattern leading to clinically significant impairment or distress

385
Q

Uppers substances

A

Stimulants

386
Q

Downers substances

A

Alcohol
Sedative-hypnotic-anxiolytics
Opioids
Cannabis

387
Q

Sideways substances

A

Hallucinogens
Dissociatives

388
Q

Other substances

A

Nicotine/tabacco
Caffeine
Inhalants
Synthetic Cathinones
Steroids

389
Q

Intoxication and withdrawal care

A

Supportive care
Monitor ABCs
Protect from self harm
Manage fluid/electrolyte balances
Symptomatic treatment

390
Q

Stimulants

391
Q

Downers

392
Q

CIWA-Ar

A

Alcohol withdrawal state

393
Q

Alcohol withdrawal treatment

A

Benzodiazepines
Anticonvulsants
Vitamin and electrolyte replacement

394
Q

Wernicke encephalopathy’s

A

confusion, ataxia, ocular changes
IV thiamine followed by glucose

395
Q

Korsakoff syndrome

A

Untreated wernicke
Chronic and irreversible
Anteriograde amnesia, confabulation, personality changes

396
Q

Downers

397
Q

Opioid overdose reversal

398
Q

Opioid withdrawal

399
Q

Downers

400
Q

Cannabis use

401
Q

Sideways

402
Q

Stage 1 sleep (NREM1-N1)

A

Transition from wake to sleep
Hypnic jerks
Slow, rolling eye movements

403
Q

Stage 2 sleep (NREM 2-N2)

A

Most common stage of sleep
No eye movement
Sleep spindles generated in thalamus
K-Complexes

404
Q

Stage 3 sleep (NREM 3-N3)

A

Delta waves (0.5-2 Hz)
Dreaming can occur
Parasomnias
More during the first half of the night

405
Q

REM sleep

A

More in latter half of the night
Relative paralysis

406
Q

Sleep stage time length

A

90 minutes

407
Q

the timing of _ is linked to body temp

408
Q

NREM accounts for _ of total sleep time

409
Q

Wakefulness

A

Coordinated activity of interconnected ascending arousal systems

410
Q

Primary inhibitory neurotransmitter

A

GABA (sleep promoting)
Located in VLPO

411
Q

Hypocretin (orexin)

A

Wake promoting (lateral and posterior hypothalamus)
Stabilizing neuromodulator

412
Q

Wake activating neurotransmitters

A

Ach
Dopamine
Histamine
NE
Serotonin

413
Q

Primary REM on neurotransmitter

414
Q

Adenosine (sleep promoting) is inhibited by

A

Caffeine (adenosine receptor agonist)

415
Q

Humanities context

A

Transdisciplinary

Neuro (5 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions