Midterm 1: Buzzword Bingo Flashcards
DSM criteria for diagnosing psychiatric disorders
1) symptoms and duration + 2) functional impairment + 3) not due to a medical problem or substances
False, fixed belief
Delusion
DSM-V criteria for diagnosis of schizophrenia
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
Disorder characterized by neurofibrillary tangles and beta amyloid deposits/plaques
Alzheimer’s Disease
Impairment of the ability to store new memories
Anterograde amnesia
Which apoE allele appears to be protective for Alzheimer’s disease?
ApoE-e2
How can you test for apraxia at bedside?
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)
Inability to recognize or identify objects despite intact sensory function
Agnosia
What does anosognosia mean?
The inability to recognize one’s own condition or impairments
Congo Red stains this extracellular finding in Alzheimer’s disease
Amyloid plaques
Amyloid cores surrounded by swollen and degenerated neural processes
Senile plaques
Impairment of the ability to recall old memories
Retrograde amnesia
Accumulations of paired helical filaments in the cytoplasm of neurons
Neurofibrillary tangles
What area of the brain displays the most atrophy in Alzheimer’s disease?
Medial temporal, but also inferior temporal and superior and middle frontal gyri
Which of the key microscopic findings in Alzheimer’s is extracellular?
Amyloid plaques. Neurofibrillary tangles are intracellular.
Lewy bodies in subcortical regions
Parkinson’s disease dementia
Clinical condition due to amyloid deposition in the walls of parenchymal and arachnoid blood vessels
Cerebral amyloid angiopathy
What are some of the genes associated with familial Alzheimer’s disease?
Presenilin-1 (chromosome 14) and presenilin-2 (chromosome 1), which form the gamma secretin enzyme that cleaves amyloid precursor protein to form beta amyloid.
Carriers of apoE-e4 allele have a ___ incidence of Alzheimer’s
Higher incidence, occurrence at earlier age (greater risk if you’re homozygous for it).
What are some anatomical and histological findings characteristic of Alzheimer’s?
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
Describe the role of microglia in Alzheimer’s disease.
Microglia cannot adequately clear all the plaques and may lead to increased inflammation
Most powerful risk factor for development of dementia
Age
Dementia in a patient aged 65-75 with high cholesterol, HTN, history of cardiac disease
Vascular dementia
Most common cause of dementia
Alzheimer’s disease
Core clinical symptom of Alzheimer’s disease
Amnesia
Are patients with mild cognitive impairment likely to develop Alzheimer’s disease?
Yes, they can. They convert to AD at a rate of 12% per year.
Common cognitive findings in Alzheimer’s disease
Amnesia, aphasia, visuospatial problems, executive dysfunction
What seems to be the anatomical cause of the memory loss in dementia?
Degeneration of hippocampus and medial temporal lobe, and associated disruption of cholinergic transmission
Should you be concerned about emotional/psychological disturbances in caregivers of patients with Alzheimer’s disease?
Yes!
Are cognitive enhancers effective in frontotemporal dementia?
No they are not - rapid course, death generally within 5 years
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
Alzheimer’s disease
MOA of donepezil, galantamine, rivastigmine
Cognitive enhancing medications that inhibit acetylcholinesterase, making more ACh available in synapses
NMDA inhibitor that blocks NMDA receptors when there are excessive levels of glutamate, used as a cognitive enhancing medication
Memantine
Impaired performance of learned motor movements, despite being physically able and willing to do so
Apraxia
Ways to slow progression of vascular dementia
Cognitive enhancers (donepezil, galantamine, rivastigmine, memantine) and addressing vascular risk factors
What kind of staining can allow you to easily visualize neurofibrillary tangles?
It is birefringent under polarized light, and is easily visualized with silver stains or immunohistochemistry.
Drug for GAD that does not cause sedation, addiction, or tolerance, takes effect within 1-2 weeks, and stimulates 5HT1A receptors
Buspirone
Simplified Nernst equation
Ex = 60 log10 [Xout]/[Xin]
Long term typical antipsychotic use can cause ___
Tardive dyskinesia
Subcortical structure that is key to detection of threats
Amygdala
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
Vascular dementia
Treatment of Lewy body disease
Antiparkinsonian agents and/or cognitive enhancers, tend to avoid antipsychotics because they exacerbate Parkinsonism
Altered mental status for hours-days, with abrupt onset and waxing/waning symptoms
Delirium
Disturbance of reticular activating system causes ___
Delirium
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)
Frontotemporal dementia
Symptoms of Dementia with Lewy Bodies (DLB)
1) fluctuating symptoms
2) visual hallucinations
3) cognitive impairment
4) less severe Parkinsonian symptoms than in Parkinson’s disease
Lewy bodies in cerebral cortex
Dementia with Lewy Bodies
Chord conductance equation
Vm = (GNa/Gtot)ENa + (GK/Gtot)EK
Symptoms found among people who do not have the disorder; that is, they are things that are NOT present in people with the disorder
Negative symptoms
Fluoxetine, paroxetine, sertraline, citalopram
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.
Neuromuscular activity, autonomic stimulation, agitation
Serotonin syndrome
Side effects of tricyclic antidepressants
Convulsions, coma, cardiotoxicity (arrhythmias from Na channel inhibition)
Uses for SNRIs (venlafaxine, desvenlafaxine, duloxetine, levomilnacipran, milnacipran)
Depression, GAD, and use venlafaxine for social anxiety disorder, etc.
Bupropion MOA
Increases norepinephrine and dopamine
Anti epileptics used for bipolar disorder
Valproate, carbamazepine
MAOIs mechanism of action
Nonselective inhibition of monoamine oxidase leads to increased levels of NE, serotonin, dopamine. Good for treating atypical depression and anxiety
Low-tyramine diet: what is it, why do you need it?
Tyramine + MAOIs can cause a hypertensive crisis. Tyramine is in the Wisconsin diet - anything fermented or aged
Lithium MOA (Probable)
Involves inhibition of phosphoinositol cascade
Atypical antipsychotic with highest risk of metabolic issues
Olanzapine
Side effect associated with risperidone
Hyperprolactinemia, causing amenorrhea, galactorrhea, gynecomastia
Loss of the ability to comprehend and/or produce language
Aphasia
Adverse effects with lithium
Tremor, hypothyroid, polyuria/dehydration/nephrogenic diabetes insipidus, teratogen, narrow therapeutic window. Stay well hydrated!
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
Parkinson’s disease dementia, due to development of Lewy bodies in subcortical regions
Side effects associated with clozapine (as opposed to other atypical antipsychotics)
Agranulocytosis (measure WBC counts)
Non-benzo hypnotic drugs
Zolpidem, zaleplon, eszopiclone
Side effects of all antipsychotics
QT prolongation, EPS and anticholinergic side effects (more with typical > atypical)
List social risk factors associated with schizophrenia
childhood abuse, immigration, living in an impoverished inner city community
Short-term extrapyramidal symptoms with typical antipsychotics
Muscle spasm, stiffness, acute dystopia
Why do patients tend to be admitted to the hospital in schizophrenia?
Cognitive dysfunction makes it impossible to function normally
EPS with typical antipsychotics
Dystonia, akathisia, Parkinsonism, tardive dyskinesia
Fever, encephalopathy, unstable vials, autonomic instability, increased rigidity, myoglobinuria in a patient on typical antipsychotics
Neuroleptic malignant syndrome
MOA of typical antipsychotics
Block dopamine D2 receptors, increasing CAMP
Molecule that helps organelles move retrograde along microtubules in the axon
Dynactin
Describe the behavioral/learning model in PTSD
Avoidance maintains anxiety, so facing the anxiety-inducing stimulus allows for habituation to it.
MOA of most atypical antipsychotics
Most are D2 agonists with varied effects on 5HT2, dopamine, alpha, and H1 receptors
Side effects of haloperidol
Neuroleptic malignant syndrome, tardive dyskinesia
MOA of carbamazepine
Inhibitory - blocks Na+ channels
Side effects of carbamazepine
Agranulocytosis, ataxia, teratogen, risk of Stevens-Johnson syndrome
MOA of valproic acid
Increases sodium channel inactivation and increases GABA concentration by inhibiting GABA transaminase
MOA of benzodiazepines
Facilitate GABA-A action by increasing frequency of chlorine channel opening
Hand-wringing (midline) and intellectual disability and ataxia, only in girls, seen around ages 1-4
Rett Syndrome
Hyperactivity, impulsivity, and inattention in multiple settings with normal intelligence, first seen before age 12
ADHD
Molecule that helps organelles and vesicles move anterograde along microtubules through axons
Kinesin
Location of the nucleus accumbens
Ventral striatum
When do you give lamotrigine?
Lamotrigine is a mood stabilizer/anti epileptic. It is a good choice for treatment in BPAD II
Describe the normal stress response from a physiological perspective.
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
What would be caused by a lesion in the amygdala?
Loss of fear response
What is the only sensory signal that doesn’t pass through the thalamus?
Sense of smell
Function of the locus coeruleus in stress
Produce NE in response to amygdala and PVN, as signaled by CRF
How long must symptoms last for a patient to meet diagnostic criteria for PTSD?
> 1 month with significant distress or impairment
Risk factors for PTSD
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
Structure in the ventral striatum that is important in reward seeking and addiction
Nucleus accumbens
Treatment of benzodiazepine overdose
Flumenazil - competitive antagonist at GABA-A benzo binding site
List biological risk factors associated with schizophrenia
genetics, virus exposure in utero, birth complications, heavy cannabis use between ages 12-14
Describe the stress/diathesis model
A biological factor is present, leading to the disease, but social variables also affect whether or not you get it
What are the symptoms that are important in schizophrenia diagnosis, and which ones must be present?
Must have delusions, hallucinations, or disorganized speech for >1 month. Other symptoms are grossly disorganized or catatonic behavior, or negative symptoms
What kinds of symptoms do antipsychotic meds tend to treat in schizophrenia?
Mostly positive symptoms - only aripiprazole tends to have an effect on negative symptoms
What kinds of non-pharmacological therapy are useful for treating schizophrenia?
Family psychoeducation, psychosocial rehabilitation, CBT
Symptoms of PTSD but lasting <1 month (more than 3 days)
Acute Stress Disorder - these patients may go on to develop PTSD
MOA of Aripiprazole
D2 partial agonis
High-potency typical antipsychotics
Haloperidol, trifluoperazine, fluphenazine
Side effects of valproic acid
GI distress, rare fatal hepatotoxicity, teratogen
Low-potency typical antipsychotics
Chlorpromazine, thioridazine, they have more anticholinergic and fewer extrapyramidal side effects
Severe drowsiness in which a patient can be aroused by a moderate stimulus but then drifts back to sleep
Lethargy
Mild/moderate reduction in alertness, less interest in environment, slow response to stimulation
Obtundation
State of deep sleep or similar unresponsiveness in which the person can only be aroused with vigorous, continuous stimuli
Stupor
State of unresponsiveness, with eyes closed, in which even vigorous stimuli cannot arouse the person
Coma
Patient is de-efferented, resulting in paralysis of all limbs and lower cranial nerves
Locked-in syndrome
Severely impaired consciousness but with minimal but definite awareness of self or environment
Vegetative state (minimally conscious syndrome)
Can unilateral hemispheric lesions without any other pathology cause coma?
No
Can lesions of the brainstem below the level of the pons, without any other pathology, cause coma?
No
GCS 13-15 in a patient with head injury
mild traumatic brain injury, aka concussion: loss of consciousness <30 min or post-traumatic amnesia less than 24 hours
GCS 9-12 in a patient with head injury
moderate traumatic brain injury: loss of consciousness >30 minutes or post-traumatic amnesia greater than 24 hours
Post-traumatic amnesia
interval from injury until patient is oriented and can form/recall new memories
GCS 3-8
Severe traumatic brain injury
Decorticate posturing (flexion) - what level of damage?
Red nucleus
Decerebrate posturing (extension) - what level is the damage?
Upper pons
Small, reactive pupils: causes
Diencephalic lesion; drugs; metabolic encephalopathy, etc
Pupil fixed and very dilated: causes
CN III damage - uncal herniation
Midsized, fixed pupils: causes
Midbrain damage
Pinpoint pupils: causes
Pons damage
Large (but not super dilated), fixed pupils: causes
Pretectal damage
Cheyne-stokes breathing in coma
forebrain impairment; can also be caused by congestive heart failure
Hyperventilation in coma
metabolic encephalopathies
Apneustic breathing (like agonal gasps) in coma
Damage to pontine respiratory nuclei
Ataxic breathing in coma
Damage to pontomedullary region
Apnea in coma
Damage to ventral lateral medulla
Presentation of a patient with early-stage uncal herniation
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
Presentation of a patient with late-stage uncal herniation
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
What artery might be cut off with a subfalcine herniation?
Anterior cerebral artery
Monro-Kellie hypothesis
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.
Presentation of a patient with dorsal midbrain compression
Moderately dilated and fixed pupils, loss of upgaze, downward movement on ice water calorics, bilateral Babinski sign
Social zeitgebers
People/things in life that keep time, maintain daily rhythm
Social zeitstorers
Disruptions to your daily rhythm, like crossing time zones, etc.
Triggers for mania in BPAD I
Changes in daylight/sleep, like travel, seasonal change, sleep deprivation
BPAD II diagnostic criteria
4+ days of hypomanic symptoms without decrease in function AND one episode of major depression
Criteria for a manic episode
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
Does a patient need to experience a depressive episode to be diagnosed with BPAD I?
No, 1 manic episode is sufficient for diagnosis
List some red flags in depression that might suggest a patient is at higher risk of actually having BPAD
Early onset, panic attacks, alcohol use disorder, family history of BPAD (more than 1 raises the risk substantially)
RFs for development of bipolar disorder
Family history, alcohol use disorder, panic disorder, early onset of MDD, stimulant use, antidepressant use
Which psych disorder has the greatest risk of suicide?
BPAD I
What medication reduces long-term suicide rate in patients with BPAD I?
Lithium
What is the catecholamine hypothesis of BPAD?
Increased dopamine may increase risk of mania, although there is not a clear one-to-one association.
Most effective antipsychotic in BPAD:
Haloperidol
Psychotherapy recommended for treatment of BPAD I
Interpersonal Social Rhythm Therapy
What meds are contraindicated in a patient taking lithium?
Non-aspirin NSAIDs, thiazide diuretics, ACE inhibitors
What labs should be checked before starting lithium?
Do a BMP and check TSH
Which antipsychotics should be given for inpatient therapy in BPAD?
High-potency: haloperidol, olanzapine
Which antipsychotics should be given for outpatient therapy in BPAD I?
Low potency - quetiapine, lurasidone
These medications used in BPAD I treatment may interfere with folate, causing a risk of pancytopenia and liver injury.
Valproate, carbamazepine
This medication is used for preventing bipolar depression, and is a good treatment in BPAD II, but poses a risk of Stevens-Johnson syndrome.
Lamotrigine, an anti epileptic and mood stabilizer
This anti epileptic can cause PCOS and hair loss, in addition to being a potent teratogen.
Valproate
What are some objectives of interpersonal social rhythm therapy?
Reinforce social zeitgebers, keep a consistent daily rhythm, process grief/other emotions at diagnosis of BPAD, set new goals
Summary of diagnostic criteria for anorexia nervosa
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
What are the two major subtypes of anorexia nervosa?
Restrictive; binge-purge
Diagnostic criteria for bulimia nervosa:
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
Definition of binge eating disorder
Rapid, uncomfortable binging when not hungry/when alone, once a week for three months on average
Peak age of onset of eating disorders
15-25 years of age
Medical complications of anorexia nervosa
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
Medical complications of bulimia
GERD, hematemesis, enamel erosion and dental caries, salivary gland hypertrophy, cheilosis, calluses on knuckles, hypokalemia, hypochloremia, metabolic alkalosis, risk of fatal arrhythmia
Potential protective factors against Alzheimer’s
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
Which pathological finding in Alzheimer’s tends to occur in multiple other conditions?
Amyloid sheets
Amyloid hypothesis of Alzheimer’s pathogenesis
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
Where does tau first begin to deposit?
In areas of the hippocampus responsible for encoding new memories, and linking memory and emotion
How effective are Cholinesterase inhibitors used in Alzheimer’s disease?
Not very, may delay progression of cognitive delay by 6-12 months
What is the NMDA antagonist used in Alzheimer’s disease?
Memantine
