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Mind & Motion > Midterm 1: Buzzword Bingo > Flashcards

Midterm 1: Buzzword Bingo Flashcards

1
Q

DSM criteria for diagnosing psychiatric disorders

A

1) symptoms and duration + 2) functional impairment + 3) not due to a medical problem or substances

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2
Q

False, fixed belief

A

Delusion

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3
Q

DSM-V criteria for diagnosis of schizophrenia

A

2+ of the following for >1 month, with at least numbers 1, 2, or 3 included:

1) delusions
2) hallucinations
3) disorganized speech
4) grossly disorganized or catatonic behavior
5) negative symptoms

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4
Q

Disorder characterized by neurofibrillary tangles and beta amyloid deposits/plaques

A

Alzheimer’s Disease

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5
Q

Impairment of the ability to store new memories

A

Anterograde amnesia

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6
Q

Which apoE allele appears to be protective for Alzheimer’s disease?

A

ApoE-e2

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7
Q

How can you test for apraxia at bedside?

A

Ask a patient to demonstrate the use of an object or complete a set of steps (take this paper, fold it in half, place it on the table)

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8
Q

Inability to recognize or identify objects despite intact sensory function

A

Agnosia

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9
Q

What does anosognosia mean?

A

The inability to recognize one’s own condition or impairments

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10
Q

Congo Red stains this extracellular finding in Alzheimer’s disease

A

Amyloid plaques

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11
Q

Amyloid cores surrounded by swollen and degenerated neural processes

A

Senile plaques

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12
Q

Impairment of the ability to recall old memories

A

Retrograde amnesia

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13
Q

Accumulations of paired helical filaments in the cytoplasm of neurons

A

Neurofibrillary tangles

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14
Q

What area of the brain displays the most atrophy in Alzheimer’s disease?

A

Medial temporal, but also inferior temporal and superior and middle frontal gyri

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15
Q

Which of the key microscopic findings in Alzheimer’s is extracellular?

A

Amyloid plaques. Neurofibrillary tangles are intracellular.

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16
Q

Lewy bodies in subcortical regions

A

Parkinson’s disease dementia

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17
Q

Clinical condition due to amyloid deposition in the walls of parenchymal and arachnoid blood vessels

A

Cerebral amyloid angiopathy

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18
Q

What are some of the genes associated with familial Alzheimer’s disease?

A

Presenilin-1 (chromosome 14) and presenilin-2 (chromosome 1), which form the gamma secretin enzyme that cleaves amyloid precursor protein to form beta amyloid.

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19
Q

Carriers of apoE-e4 allele have a ___ incidence of Alzheimer’s

A

Higher incidence, occurrence at earlier age (greater risk if you’re homozygous for it).

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20
Q

What are some anatomical and histological findings characteristic of Alzheimer’s?

A

Neurofibrillary tangles and beta amyloid plaques; brain atrophy in medial temporal lobe; loss of neurons so great that brain weight may be reduced by 300-400 grams

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21
Q

Describe the role of microglia in Alzheimer’s disease.

A

Microglia cannot adequately clear all the plaques and may lead to increased inflammation

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22
Q

Most powerful risk factor for development of dementia

A

Age

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23
Q

Dementia in a patient aged 65-75 with high cholesterol, HTN, history of cardiac disease

A

Vascular dementia

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24
Q

Most common cause of dementia

A

Alzheimer’s disease

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25
Q

Core clinical symptom of Alzheimer’s disease

A

Amnesia

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26
Q

Are patients with mild cognitive impairment likely to develop Alzheimer’s disease?

A

Yes, they can. They convert to AD at a rate of 12% per year.

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27
Q

Common cognitive findings in Alzheimer’s disease

A

Amnesia, aphasia, visuospatial problems, executive dysfunction

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28
Q

What seems to be the anatomical cause of the memory loss in dementia?

A

Degeneration of hippocampus and medial temporal lobe, and associated disruption of cholinergic transmission

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29
Q

Should you be concerned about emotional/psychological disturbances in caregivers of patients with Alzheimer’s disease?

A

Yes!

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30
Q

Are cognitive enhancers effective in frontotemporal dementia?

A

No they are not - rapid course, death generally within 5 years

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31
Q

Dementia with most patients ages 75-85 years old, relentlessly progressive, course tends to be 6-12 years from diagnosis to death, characterized by amnesia and other cognitive impairment

A

Alzheimer’s disease

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32
Q

MOA of donepezil, galantamine, rivastigmine

A

Cognitive enhancing medications that inhibit acetylcholinesterase, making more ACh available in synapses

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33
Q

NMDA inhibitor that blocks NMDA receptors when there are excessive levels of glutamate, used as a cognitive enhancing medication

A

Memantine

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34
Q

Impaired performance of learned motor movements, despite being physically able and willing to do so

A

Apraxia

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35
Q

Ways to slow progression of vascular dementia

A

Cognitive enhancers (donepezil, galantamine, rivastigmine, memantine) and addressing vascular risk factors

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36
Q

What kind of staining can allow you to easily visualize neurofibrillary tangles?

A

It is birefringent under polarized light, and is easily visualized with silver stains or immunohistochemistry.

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37
Q

Drug for GAD that does not cause sedation, addiction, or tolerance, takes effect within 1-2 weeks, and stimulates 5HT1A receptors

A

Buspirone

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38
Q

Simplified Nernst equation

A

Ex = 60 log10 [Xout]/[Xin]

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39
Q

Long term typical antipsychotic use can cause ___

A

Tardive dyskinesia

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39
Q

Subcortical structure that is key to detection of threats

A

Amygdala

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41
Q

A kind of dementia with specific clinical manifestations that tend to progress in a step-wise course, with sudden changes in cognition and functioning separated by periods of stability

A

Vascular dementia

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43
Q

Treatment of Lewy body disease

A

Antiparkinsonian agents and/or cognitive enhancers, tend to avoid antipsychotics because they exacerbate Parkinsonism

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44
Q

Altered mental status for hours-days, with abrupt onset and waxing/waning symptoms

A

Delirium

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45
Q

Disturbance of reticular activating system causes ___

A

Delirium

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46
Q

Type of dementia characterized by tau+ inclusion bodies, degeneration of frontal and temporal lobe, behavioral disturbance and/or aphasia, and a young age of onset (ages 50-65)

A

Frontotemporal dementia

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47
Q

Symptoms of Dementia with Lewy Bodies (DLB)

A

1) fluctuating symptoms
2) visual hallucinations
3) cognitive impairment
4) less severe Parkinsonian symptoms than in Parkinson’s disease

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47
Q

Lewy bodies in cerebral cortex

A

Dementia with Lewy Bodies

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48
Q

Chord conductance equation

A

Vm = (GNa/Gtot)ENa + (GK/Gtot)EK

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49
Q

Symptoms found among people who do not have the disorder; that is, they are things that are NOT present in people with the disorder

A

Negative symptoms

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51
Q

Fluoxetine, paroxetine, sertraline, citalopram

A

Selective serotonin reuptake inhibitors. Good for depression, GAD, panic disorder, OCD, bulimia, social anxiety disorder, PTSD. Takes 4-8 weeks to have an effect. Acts on SERT transporters. Fewer side effects than TCAs but can cause GI distress, SIADH, sexual dysfunction.

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52
Q

Neuromuscular activity, autonomic stimulation, agitation

A

Serotonin syndrome

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53
Q

Side effects of tricyclic antidepressants

A

Convulsions, coma, cardiotoxicity (arrhythmias from Na channel inhibition)

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54
Q

Uses for SNRIs (venlafaxine, desvenlafaxine, duloxetine, levomilnacipran, milnacipran)

A

Depression, GAD, and use venlafaxine for social anxiety disorder, etc.

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55
Q

Bupropion MOA

A

Increases norepinephrine and dopamine

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56
Q

Anti epileptics used for bipolar disorder

A

Valproate, carbamazepine

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57
Q

MAOIs mechanism of action

A

Nonselective inhibition of monoamine oxidase leads to increased levels of NE, serotonin, dopamine. Good for treating atypical depression and anxiety

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58
Q

Low-tyramine diet: what is it, why do you need it?

A

Tyramine + MAOIs can cause a hypertensive crisis. Tyramine is in the Wisconsin diet - anything fermented or aged

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60
Q

Lithium MOA (Probable)

A

Involves inhibition of phosphoinositol cascade

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61
Q

Atypical antipsychotic with highest risk of metabolic issues

A

Olanzapine

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62
Q

Side effect associated with risperidone

A

Hyperprolactinemia, causing amenorrhea, galactorrhea, gynecomastia

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63
Q

Loss of the ability to comprehend and/or produce language

A

Aphasia

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64
Q

Adverse effects with lithium

A

Tremor, hypothyroid, polyuria/dehydration/nephrogenic diabetes insipidus, teratogen, narrow therapeutic window. Stay well hydrated!

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65
Q

Dementia with onset of memory loss, slowed processing speed, and inattention at least one year after onset of motor symptoms including rigidity, tremor, and bradykinesia

A

Parkinson’s disease dementia, due to development of Lewy bodies in subcortical regions

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66
Q

Side effects associated with clozapine (as opposed to other atypical antipsychotics)

A

Agranulocytosis (measure WBC counts)

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67
Q

Non-benzo hypnotic drugs

A

Zolpidem, zaleplon, eszopiclone

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69
Q

Side effects of all antipsychotics

A

QT prolongation, EPS and anticholinergic side effects (more with typical > atypical)

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72
Q

List social risk factors associated with schizophrenia

A

childhood abuse, immigration, living in an impoverished inner city community

73
Q

Short-term extrapyramidal symptoms with typical antipsychotics

A

Muscle spasm, stiffness, acute dystopia

74
Q

Why do patients tend to be admitted to the hospital in schizophrenia?

A

Cognitive dysfunction makes it impossible to function normally

75
Q

EPS with typical antipsychotics

A

Dystonia, akathisia, Parkinsonism, tardive dyskinesia

76
Q

Fever, encephalopathy, unstable vials, autonomic instability, increased rigidity, myoglobinuria in a patient on typical antipsychotics

A

Neuroleptic malignant syndrome

77
Q

MOA of typical antipsychotics

A

Block dopamine D2 receptors, increasing CAMP

78
Q

Molecule that helps organelles move retrograde along microtubules in the axon

A

Dynactin

79
Q

Describe the behavioral/learning model in PTSD

A

Avoidance maintains anxiety, so facing the anxiety-inducing stimulus allows for habituation to it.

80
Q

MOA of most atypical antipsychotics

A

Most are D2 agonists with varied effects on 5HT2, dopamine, alpha, and H1 receptors

81
Q

Side effects of haloperidol

A

Neuroleptic malignant syndrome, tardive dyskinesia

82
Q

MOA of carbamazepine

A

Inhibitory - blocks Na+ channels

84
Q

Side effects of carbamazepine

A

Agranulocytosis, ataxia, teratogen, risk of Stevens-Johnson syndrome

85
Q

MOA of valproic acid

A

Increases sodium channel inactivation and increases GABA concentration by inhibiting GABA transaminase

86
Q

MOA of benzodiazepines

A

Facilitate GABA-A action by increasing frequency of chlorine channel opening

87
Q

Hand-wringing (midline) and intellectual disability and ataxia, only in girls, seen around ages 1-4

A

Rett Syndrome

88
Q

Hyperactivity, impulsivity, and inattention in multiple settings with normal intelligence, first seen before age 12

A

ADHD

89
Q

Molecule that helps organelles and vesicles move anterograde along microtubules through axons

A

Kinesin

90
Q

Location of the nucleus accumbens

A

Ventral striatum

91
Q

When do you give lamotrigine?

A

Lamotrigine is a mood stabilizer/anti epileptic. It is a good choice for treatment in BPAD II

92
Q

Describe the normal stress response from a physiological perspective.

A

Stress activates the HPA axis, leading to cortisol release in the periphery.

Input from hippocampus, amygdala, PFC, brainstem, lateral hypothalamus, locus coeruleus integrated at PVN -> Paraventricular nucleus of the hypothalamus releases CRF onto anterior pituitary -> Pituitary releases ACTH -> Adrenal glands respond to ACTH and release cortisol into the bloodstream -> cortisol mobilizes a physical response to stress, leading to increased glucose uptake in muscles

93
Q

What would be caused by a lesion in the amygdala?

A

Loss of fear response

94
Q

What is the only sensory signal that doesn’t pass through the thalamus?

A

Sense of smell

95
Q

Function of the locus coeruleus in stress

A

Produce NE in response to amygdala and PVN, as signaled by CRF

96
Q

How long must symptoms last for a patient to meet diagnostic criteria for PTSD?

A

> 1 month with significant distress or impairment

97
Q

Risk factors for PTSD

A

Type of trauma (especially sexual assault or assaultive violence), history of previous trauma, history of depression and anxiety, family psych history, age at trauma occurence (younger - worse outcomes), lack of social support, dissociative reaction, severity and duration of trauma, feelings of anger/shame

98
Q

Structure in the ventral striatum that is important in reward seeking and addiction

A

Nucleus accumbens

99
Q

Treatment of benzodiazepine overdose

A

Flumenazil - competitive antagonist at GABA-A benzo binding site

100
Q

List biological risk factors associated with schizophrenia

A

genetics, virus exposure in utero, birth complications, heavy cannabis use between ages 12-14

101
Q

Describe the stress/diathesis model

A

A biological factor is present, leading to the disease, but social variables also affect whether or not you get it

102
Q

What are the symptoms that are important in schizophrenia diagnosis, and which ones must be present?

A

Must have delusions, hallucinations, or disorganized speech for >1 month. Other symptoms are grossly disorganized or catatonic behavior, or negative symptoms

103
Q

What kinds of symptoms do antipsychotic meds tend to treat in schizophrenia?

A

Mostly positive symptoms - only aripiprazole tends to have an effect on negative symptoms

104
Q

What kinds of non-pharmacological therapy are useful for treating schizophrenia?

A

Family psychoeducation, psychosocial rehabilitation, CBT

105
Q

Symptoms of PTSD but lasting <1 month (more than 3 days)

A

Acute Stress Disorder - these patients may go on to develop PTSD

123
Q

MOA of Aripiprazole

A

D2 partial agonis

125
Q

High-potency typical antipsychotics

A

Haloperidol, trifluoperazine, fluphenazine

127
Q

Side effects of valproic acid

A

GI distress, rare fatal hepatotoxicity, teratogen

131
Q

Low-potency typical antipsychotics

A

Chlorpromazine, thioridazine, they have more anticholinergic and fewer extrapyramidal side effects

132
Q

Severe drowsiness in which a patient can be aroused by a moderate stimulus but then drifts back to sleep

A

Lethargy

133
Q

Mild/moderate reduction in alertness, less interest in environment, slow response to stimulation

A

Obtundation

134
Q

State of deep sleep or similar unresponsiveness in which the person can only be aroused with vigorous, continuous stimuli

A

Stupor

135
Q

State of unresponsiveness, with eyes closed, in which even vigorous stimuli cannot arouse the person

A

Coma

136
Q

Patient is de-efferented, resulting in paralysis of all limbs and lower cranial nerves

A

Locked-in syndrome

137
Q

Severely impaired consciousness but with minimal but definite awareness of self or environment

A

Vegetative state (minimally conscious syndrome)

138
Q

Can unilateral hemispheric lesions without any other pathology cause coma?

A

No

139
Q

Can lesions of the brainstem below the level of the pons, without any other pathology, cause coma?

A

No

140
Q

GCS 13-15 in a patient with head injury

A

mild traumatic brain injury, aka concussion: loss of consciousness <30 min or post-traumatic amnesia less than 24 hours

141
Q

GCS 9-12 in a patient with head injury

A

moderate traumatic brain injury: loss of consciousness >30 minutes or post-traumatic amnesia greater than 24 hours

142
Q

Post-traumatic amnesia

A

interval from injury until patient is oriented and can form/recall new memories

143
Q

GCS 3-8

A

Severe traumatic brain injury

144
Q

Decorticate posturing (flexion) - what level of damage?

A

Red nucleus

145
Q

Decerebrate posturing (extension) - what level is the damage?

A

Upper pons

146
Q

Small, reactive pupils: causes

A

Diencephalic lesion; drugs; metabolic encephalopathy, etc

147
Q

Pupil fixed and very dilated: causes

A

CN III damage - uncal herniation

148
Q

Midsized, fixed pupils: causes

A

Midbrain damage

149
Q

Pinpoint pupils: causes

A

Pons damage

150
Q

Large (but not super dilated), fixed pupils: causes

A

Pretectal damage

151
Q

Cheyne-stokes breathing in coma

A

forebrain impairment; can also be caused by congestive heart failure

152
Q

Hyperventilation in coma

A

metabolic encephalopathies

153
Q

Apneustic breathing (like agonal gasps) in coma

A

Damage to pontine respiratory nuclei

154
Q

Ataxic breathing in coma

A

Damage to pontomedullary region

155
Q

Apnea in coma

A

Damage to ventral lateral medulla

156
Q

Presentation of a patient with early-stage uncal herniation

A

Moderately dilated pupil ipsilateral to primary lesion that constricts sluggishly, doll’s head maneuver and ice water calorics may be normal or dysconjugate, positive Babinski sign

157
Q

Presentation of a patient with late-stage uncal herniation

A

Hyperventilation (or rarely Cheyne-stokes breathing), pupil ipsilateral to primary lesion is dilated and fixed, doll’s head maneuver is dysconjugate, ipsilateral eye doesn’t move medially on ice water calorics, decorticate or decerebrate posturing

158
Q

What artery might be cut off with a subfalcine herniation?

A

Anterior cerebral artery

159
Q

Monro-Kellie hypothesis

A

Sum of volumes of brain, CSF, and intracranial blood are constant. So trauma increases mass due to swelling and bleeding, and at first venous blood and CSF squeezes out to keep the brain at normal ICP, but eventually nothing else can go, leading to increased ICP from normal (5-15). Cerebral perfusion pressure (CPP) = MAP -ICP. Cerebral blood flow (CBF) = CPP/CVR.

160
Q

Presentation of a patient with dorsal midbrain compression

A

Moderately dilated and fixed pupils, loss of upgaze, downward movement on ice water calorics, bilateral Babinski sign

161
Q

Social zeitgebers

A

People/things in life that keep time, maintain daily rhythm

162
Q

Social zeitstorers

A

Disruptions to your daily rhythm, like crossing time zones, etc.

163
Q

Triggers for mania in BPAD I

A

Changes in daylight/sleep, like travel, seasonal change, sleep deprivation

164
Q

BPAD II diagnostic criteria

A

4+ days of hypomanic symptoms without decrease in function AND one episode of major depression

165
Q

Criteria for a manic episode

A

Euphoric or irritable mood AND 3-4 symptoms including increased self esteem, decreased need for sleep, pressured speech, hedonic activity, etc. with negative changes to function for >1 week

166
Q

Does a patient need to experience a depressive episode to be diagnosed with BPAD I?

A

No, 1 manic episode is sufficient for diagnosis

167
Q

List some red flags in depression that might suggest a patient is at higher risk of actually having BPAD

A

Early onset, panic attacks, alcohol use disorder, family history of BPAD (more than 1 raises the risk substantially)

168
Q

RFs for development of bipolar disorder

A

Family history, alcohol use disorder, panic disorder, early onset of MDD, stimulant use, antidepressant use

169
Q

Which psych disorder has the greatest risk of suicide?

A

BPAD I

170
Q

What medication reduces long-term suicide rate in patients with BPAD I?

A

Lithium

171
Q

What is the catecholamine hypothesis of BPAD?

A

Increased dopamine may increase risk of mania, although there is not a clear one-to-one association.

172
Q

Most effective antipsychotic in BPAD:

A

Haloperidol

173
Q

Psychotherapy recommended for treatment of BPAD I

A

Interpersonal Social Rhythm Therapy

174
Q

What meds are contraindicated in a patient taking lithium?

A

Non-aspirin NSAIDs, thiazide diuretics, ACE inhibitors

175
Q

What labs should be checked before starting lithium?

A

Do a BMP and check TSH

176
Q

Which antipsychotics should be given for inpatient therapy in BPAD?

A

High-potency: haloperidol, olanzapine

177
Q

Which antipsychotics should be given for outpatient therapy in BPAD I?

A

Low potency - quetiapine, lurasidone

178
Q

These medications used in BPAD I treatment may interfere with folate, causing a risk of pancytopenia and liver injury.

A

Valproate, carbamazepine

179
Q

This medication is used for preventing bipolar depression, and is a good treatment in BPAD II, but poses a risk of Stevens-Johnson syndrome.

A

Lamotrigine, an anti epileptic and mood stabilizer

180
Q

This anti epileptic can cause PCOS and hair loss, in addition to being a potent teratogen.

A

Valproate

181
Q

What are some objectives of interpersonal social rhythm therapy?

A

Reinforce social zeitgebers, keep a consistent daily rhythm, process grief/other emotions at diagnosis of BPAD, set new goals

182
Q

Summary of diagnostic criteria for anorexia nervosa

A

1) decreased energy intake relative to requirements, leading to a significantly low body weight
2) intense fear of gaining weight or becoming fat
3) disturbance in the way in which one’s body weight or body shape is experienced

183
Q

What are the two major subtypes of anorexia nervosa?

A

Restrictive; binge-purge

184
Q

Diagnostic criteria for bulimia nervosa:

A

1) recurrent episodes of eating more than normal, feeling a lack of control, which may become very routinized
2) recurrent inappropriate behavior to prevent weight gain
3) binges occur once a week for three months on average
4) self-evaluation is unduly influenced by body shape and weight
5) disturbance is not exclusively during episodes of anorexia

185
Q

Definition of binge eating disorder

A

Rapid, uncomfortable binging when not hungry/when alone, once a week for three months on average

186
Q

Peak age of onset of eating disorders

A

15-25 years of age

187
Q

Medical complications of anorexia nervosa

A

Starving on a balanced diet - fatigue, irritability, lanugo, bruise easily, thinning hair, bulging eyes (lagophthalmos)

GI: dysphasia, fullness (due to gastroparesis), superior mesenteric artery syndrome due to loss of abdominal fat pad (leading to GI blockage)

CV: bradycardia, sudden death

Hematologic: normocytic anemia, but normally low WBC that doesn’t increase in infection

Endo: amenorrhea, decreased estrogen, osteopenia

188
Q

Medical complications of bulimia

A

GERD, hematemesis, enamel erosion and dental caries, salivary gland hypertrophy, cheilosis, calluses on knuckles, hypokalemia, hypochloremia, metabolic alkalosis, risk of fatal arrhythmia

189
Q

Potential protective factors against Alzheimer’s

A

APP/BACE1 polymorphism, apoE2, NSAID use/statin exposure before disease course starts, mild alcohol use (J-shaped curve), Mediterranean/DASH Intervention for Neurocognitive Delay, physical exercise, cognitive stimulation

190
Q

Which pathological finding in Alzheimer’s tends to occur in multiple other conditions?

A

Amyloid sheets

191
Q

Amyloid hypothesis of Alzheimer’s pathogenesis

A

Some problem with amyloid, kicked off by APP or PS1, PS2 -> generation of toxic beta amyloid -> oxidative stress, neuron death, aggregation, inflammation, accumulation of tau -> cell death -> cholinergic defect

192
Q

Where does tau first begin to deposit?

A

In areas of the hippocampus responsible for encoding new memories, and linking memory and emotion

193
Q

How effective are Cholinesterase inhibitors used in Alzheimer’s disease?

A

Not very, may delay progression of cognitive delay by 6-12 months

194
Q

What is the NMDA antagonist used in Alzheimer’s disease?

A

Memantine

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