Quiz 3 Flashcards
What are the 5 histories to take of every patient presenting with headaches?
1) Family History
2) Life history
-Car sickness, abdominal pain as child
-Time course
3) Attack history
-Aura
-OLDCAAARS
4) Medical History
5) Medication History
Includes OTC, drug use, and natural products
What are the four general stages of migraine headache episodes?
What acronym is used to screen for secondary headaches?
What are the four pain sensitive and five pain insensitive structures of the head?
What are the three classes of primary headache disorders? What are the five classes of secondary headache disorders?
What are the ICHD criteria for diagnosing migraine?
What three symptoms of migraine were studied and found to be 93% predictive of migraine if 2/3 were met?
How are episodic vs chronic migraines differentiated?
Episodic: <15 days per month
Chronic: >15 days per month
What type of headache (only type) is more common in men than in women?
Cluster headaches
Named for cycling of attacks in spring or fall
What are the diagnostic criteria for an episodic tension-type headache? What differs in chronic presentation?
Chronic presents on more than 15 days per month.
What is the classic presentation of Temporal Arteritis? What labs are expected to be elevated?
Is IIH or pseudotumor cerebri more common in men or women?
6:1 in women compared to men
A sudden onset of the worst headache of someone’s life should always include what pathology near the top of the differential? What imaging should be done?
A presentation of a new, daily, persistent headache, possibly presenting with fever and nuchal rigidity would point to what on the differential? What testing should be done?
Meningeal irritation: Meningitis
Lumbar puncture must be performed
Where is the most common location for pain in trigeminal neuralgia?
The V2 distribution, and is often triggered by light touch
What is the most common cause of trigeminal neuralgia in younger individuals vs older individuals?
What are the genes and their respective channelopathies associated with familial hemiplegic migraines?
What is the current prevailing theory regarding the etilogy of the aura that presents before about 30% of migraines?
That it is caused by a cortical spreading depression of brain activity.
What effect does CGRP have on migraines? Stimulation of what ganglion increases serum CGRP? Is it a vasocontrisctor or vasodilator?
What are the 4 steps in migraine management according to current guidelines?
In what situations may an opiate be indicated for treatment of migraine?
Pregnancy
Elderly patients
Cardiac cases
What is the MoA of Ergotamine and Dihydroergotamine? Which is more commonly used? What are notable SE or CI?
It can cause spontaneous miscarriage in pregnancy.
What are 4 notable CI for triptan class drug use?
What are the 4 elements of the MoA of triptan class drugs?
Which triptan drugs are short acting ? Which are long acting? Include generic and brand names for both.
Which triptan drug has to have its dose reduced when used with Propranolol? How much should the dose be reduced?
Rizatriptan or MAXALT
Which triptan drug cannot be used within 72 hours of a **CYP3A4 inhibitor* (i.e. ketoconazole, clarithromycin)?
Eletriptan or Relpax
What is the SE profile for triptan drugs?
What is the MoA of Lasmiditan? What advantage does it offer over triptan class drugs? What is the major SE?
Which two major drug classes can add to risk of serotonin syndrome?
SSRIs
Triptans
Just one SSRI and one triptan is not enough to cause this syndrome.
What is the MoA of Gepants? What makes them an especially promising new treatment for headaches? Name two Gepants.
What characterizes Medication overuse headaches? What are some drugs that can cause them? What is the two step treatment?
Name examples of preventative medications for migraine that can be used from the following drug classes:
Anticonvulsants (2)
Anti-depressants (2*)
Beta-blockers (3)
CCBs (3)
NSAIDs (1)
5HT antagonists (1)
OTHER (4)
CCBs
DHP- Amlodipine
Non-DHP- Verapimil, Diltiazem
Avoid drugs that worsen a condition (TCAs or AD in overweight individuals, etc)
What 4 CGRP monocloncal antibodies have been approved by the FDA for episodic and chronic migraine treatment? Which of the 4 targets the CGRP receptor as opposed to the peptide?
How long should a preventative medication for migraine headache treatment be tried?
AT LEAST 6-8 weeks, possibly longer
What are the preventative and acute treatments for cluster headaches? Which are approved by the FDA?
Galcanezumab is the only FDA approved for cluster headache prevention, though Verapamil is the most commonly used, and Topiramate is used less often, sometimes as an add-on
What are potential side effects of anticonvulsant therapy such as topiramate?
-Brain fog
-Changes in taste
-Eye pain -> refer to ophtho
When should a patient with suspected cluster headaches get imaging done?
-If they are in their 30’s or older
-If neurological symptoms present
What brain structure is most likely involved in a cluster headache?
The ipsilateral hypothalamus
Why is SC sumatriptan often preferred over PO sumatriptan when treating cluster headaches?
Cluster headaches tend to last 45 minutes to an hour, and PO sumatriptan would take to long to take effect
In a headache with sudden presentation and worry of a stroke, what type of imaging would be best?
CT (better visualization of fluid than a MRI; also faster)
Why is a migraine aura without headache liable to produce an EEG with lateralized slowing in the brain?
A migraine aura can cause cortical depression, which can lead to depressed activity on EEG
When should TIA/stroke be considered in patients with a typical aura without headache?
What are notable differencies in *visual** and sensory symptoms of an aura in Migraine versus in TIA?
What 4 notable MRI with contrast features are associated with IIH? What number out of 4 is considered high specific for IIH?
Are CTs or MRIs generally preferred for sudden onset headaches?
CT is generally done first
What are typical treatments of Primary Thunderclap headaches?
What is the classic presentation of a patient with a cluster headache?
What is the classic presentation of a patient with a brain tumor headache?
What is the classic presentation of trigeminal neuralgia?
Why is a CN VI palsy sometimes referred to as the falsel-localizing-sign-of-6?
CN VI weakness or palsely is often due to elevated ICP and not necessary a lesion to CN VI specifically
Checking CN VII is a good idea to rule out a pontine lesion.
How does a patient noting that headaches are “worse when lying down, and better when standing up” help to support a diagnosis of headache cause?
A patient with new onset headache who also presents with recent weight gain, increased ICP (such as papilledema, CN VI paralysis or diplopia) and unremarkable MRI scans would most likely have what diagnosis to explain their headaches? What is pathognomonic for this disorder?
Idiopathic intracranial hypertension or IIH
Visual dim-outs when arising from recumbency are pathognomonic for IIH.
Note that the falsely localizing sign of CN VI is often seen in IIH.
What diagnostic procedure could confirm suspected IIH?
A spinal tap could document the elevated ICP. This process (measuring pressure) is called manometry.
What is the normal value for CSF pressure?
12-20cm H2O
OR
120-200mm H2O
Which medications are associated with a diagnosis of IIH?
High Vitamin A derivatives
-Pre-natal vitamin or multivitamin
-Acne medications
-cycline antibiotics
-Doxycycline
-Minocycline
-Tetracycline
If a medication is implied to have caused elevated ICP, the diagnosis is now IATROGENIC intracranial hypertension, as it is no longer idiopathic.
What is the difference between addiction and dependence?
Addiction- the psychological changes and behaviors that occur with repeated substance use
Dependence- physiologic changes that occur with repeated substance use
What are the 3 stages in the Three Stage Model of Addiction?
What is the name of this molecule? What drug class does it belong to?
Succinylcholine, which is a Depolarizing Neuromuscular Blocker
What is the MoA of Succinylcholine? How quick is its onset?
It depolarizes Nm receptors, and due to slow removal from the NMJ it induces a flaccid paralysis with fasciculations.
Rapid onset
What are the four main examples of Non-Depolarizing Neuromuscular Blockers? Which are steroid derivatives vs. benzyl isoquinolones? How quick is their onset?
Rocuronium (1-2 min, rapid)
Vecuronium
Cistracurium
Mivacurium
All except rocuronium have an onset of 2-3 min
What characterizes Phase I block with succinylcholine? How long does it typically last?
It hasa duration of 5-10 minutes.
What characterizes Phase II block with succinylcholine? What can initiate phase II and why should it be avoided?
It can occur with large doses of succinylcholine and should be avoided to due unprredictable duration and reversal.
What are the durations of action of the four main Non-Depolarizing Neuromuscular Blockers?
Mivacurium 15-20 min
Cistracurium 40-75 min
Rocuronium 35-75 min
Vecuronium 45-90 min
What endogenous enzyme metabolizes Succinylcholine?
Plasma pseudocholinesterase
What are notable SE of Succinylcholine?
Malignant Hyperthermia trigger- treat with dantrolene
Hyperkalemia
Cardiac arrythmias
Myalgia
Increased ICP, IOP, IGP (intra-gastric pressure)
What are notable SE for the four main Non-Depolarizing Neuromuscular Blockers?
Mivacurium- Histamine release
Rocuronium- mild vagolytic effects
What is the MoA and clinical use of Dantrolene?
It is a skeletal muscle relaxant that inhibits calcium release from the SR by antagonizing the ryanodine receptor.
It is used to treat Malignant Hyperthermia.
What is the clinical use of Sugammadex?
It is a cyclodextrin reversal agent for:
Rocuronium
Vecuronium
What are reversal agents used for Non-Depolarizing Neuromuscular Blockers?
Neostigmine
Edrophonium
WITH:
Glycopyrrolate
Atropine
Note that Sugammadex can be used for reversal of steroid derivative NDNMBs
What characterizes the first stage of the Three Stage Model of Addiction?
VTA = Ventral Tegmental Area
It is responsible for releasing dopamine onto the Nucleus Accumbens.
NAc = Nucleus Accumbens
It is a core area associated with the reward system
What characterizes the second stage of the Three Stage Model of Addiction?
Two main impacts:
1) Baseline dopamine receptor concentration is reduced
2) HPA/Stress Axis is dysregulated
Hypothalamus releases more CRF
Anterior pituitary releases more ACTH
Adrenal cortex releases more Cortisol
In short, more drug is needed to reach “normal” baseline
What characterizes the third stage of the Three Stage Model of Addiction?
The prefrontal cortex contains the systems that provide the capacity for executive functioning, such as impulse control. One of these such areas is the ventromedial prefrontal cortex.
Define pain:
Define transduction as part of the nociceptive response. What are the main two types of nociceptive fibers and their respective roles?
Transduction is conversion of energy to an electrical signal.
Define transmission as part of the nociceptive response. In what lamina do A-delta and C fibers reside, respectively?
What is central sensitization?
What is wind-up as it pertains to nociception?
What is gate theory as it pertains to nociception? Which fibers are involved and what order neurons are affected?
Define modulation as part of the nociceptive response.
Modulation involves change of nociceptive signal.
What is the signifiance of the Periaqueductal gray or PAG and the Rostral ventromedial medulla or RVM in the modulation of pain?
Define perception as part of the nociceptive response. What 6 areas of the brain comprise the pain matrix? What two divisions of the spinothalamic tract are used to transmit nociceptive signals?
Perception involves the interpretation of the nociceptive signals.
What is generally the difference in duration between acute and chronic pain? What type of pain is consistantly nociceptive?
What is nociceptive pain? What are the two subtypes?
What is somatic pain? What is the common etiology?
What is neuropathic pain? How does it differ from nociceptive pain?
It is important to note that it occurs without activation of peripheral nociceptors by actual or potential tissue injury
What are four significant causes of peripheral neuropathy?
Peripheral neuropathy is a subtype of neuropathic pain.
What two notable anticonvulsant medications are used in the treatment of neuropathic pain? What is their MoA?
What are notable SE of Gabapentin and Pregabalin? What is unique about their doseage and frequency?
What in the MoA of TCAs makes them useable for treating neuropathic pain?
They can:
1) Block serotonin and NE reuptake in presynaptic terminals
2) Competitive antagonists on post-synpatic alpha 1 & 2, muscarinic and histaminergic receptors
Which SNRI is commonly used for neuropathic pain, and is FDA approved for diabetic PN and fibromyalgia? What are common SE?
How can ketamine be used to treat neuropathic pain?
It is used clinically as in pain management, and also as an anesthetic.
Note it can be abused for patients to get high
What is the MoA of ziconotide? What is unique about the delivery mechanism for this drug?
It is delivered intra-thecally through a pump, and is commonly a component of palliative care.
What are two notable local anesthetics used to treat neuropathic pain? Which is taken orally? Which is more poorly tolerated? Which is often used for post-herpetic neuralgia?
What are the 5 main NSAIDs to know for Step 1? Which of these is COX-2 selective? What are common SE of these drugs?
What is the MoA of acetaminophen? What clinical uses does it have? What is the antidote for acetaminophen overdose?
What are the three types of opioid receptors in the body? Which receptor binding produces the most significant analgesic effects?
The mu opioid receptor.
Of this list, which opioid side effects tend to be chronic?
Per the CDC guidelines regarding opioid perscription:
-How long should they be prescribed for acute pain?
-What dose should be started?
-What combination is important to avoid?
-What additional Rx should be considered?
Note that tapering needs to be carefully controlled
What are the three main areas that comprise risk factors for chronic pain?
Note that this is called the Biopsychosocial model
What drug is used to reverse an overdose in Alcohol/Sedative-Hypnotic Dependence Disorder? What is the MoA? What is the RoA and setting in which it must be used? What is its BBW?
Flumazenil
What is the main drug used in relapse prevention/maintenance for patients with Alcohol/Sedative-Hypnotic Dependence Disorder? What is the MoA? What is the RoA? What is the BBW? What type of therapy is it considered?
Name the other drug sometimes used for the above treatment. as well as its MoA and SE.
What is the preferred drug to use in event of opioid overdose?
If a patient with an affected Broca’s area also began to have the area anterior to it affected as well, what symptoms could be expected? What area lies anterior to Broca’s?
What part of the brain is lesioned to produce prosopagnosia?
The fusiform gyrus, which affects the medial occipto-temporal lobes (often bilateral).
What characerizes Delirium Tremens? How long after the last dose of alcohol can it take to set in? How long can it last? What is the mortality rate?
It is the most severe stage of Alcohol withdrawal.
What is the Caine Criteria used for? What are the four criteria? What action should be taken at what point?
It is the criteria for diagnosis and treatment of Wernicke Encephalopathy.
How is a Panic Attack defined?
Palpitations
Sweating
Trembling or shaking
SOB
Feeling of choking
Chest pain/discomfort
MANY more
How long a duration must symptoms be present for GAD, Agoraphobia, Specific Phobia, or Social Anxiety Disorder to be diagnosed? How long must symptoms of Panic Disorder present for following a panic attack?
How does the time course for a normal stress response, Acute Stress Disorder, and PTSD differentiate them?
Are compulsions necessary for a diagnosis of OCD?
What are the 4 areas of symptoms required to diagnose PTSD or Acute Stress Disorder? How many symptoms are required in each section? How are these two disorders differentiated?
What is the function of the following areas of the cerebellum:
Vermis
Hemispheres
What artery supplies blood to the anterior lobe and dorsal vermis of the cerebellum?
What artery supplies blood to the posterior lobe, inferior vermis and tonsils of the cerebellum?
What artery supplies blood to the anterior portion of the posterior lobe as well as the flocculus of the cerebellum?
What are the three cellular layers of the cerebellum? What is significant to know about purkinje cells?
Purkinje cells:
-Are the output cell of cerebellar cortex
-Are highly susceptible to insults
Where are the cerebellar deep nuclei found?
They are found beneath the cerebellar cortex in the white matter.
Identify each of the 4 cerebellar deep nuclei:
What is the function of the Fastigial nuclei in the cerebellum? What is the function of the Globose and Emboliform nuclei? What is the function of the Dentate nucleus?
What is the function of the vestibulo-cerebellum?
Which cerebellar peduncle is connected to each part of the brainstem? What arteries supply each of the cerebellar peduncles?
FItB: The Superior peduncle connects the cerebellum to the Rubrospinal system which modulates __________ motor control. The primary neuron arises from _____________ cells, then synapses with the secondary neuron in the ______________ nucleus, which exits the superior peduncle and decussates in the ___________ and synpases with the tertiary neuron in the ________ nucleus. It then descends through the brainstem via the _____________ tract.
In the Cerebellothalamocortical pathway whhere does the primary neuron arise? Where does it synapse with the secondary neuron? Which cerebral peduncle does it exit? Where does it decussate? Where does it synapse with the tertiary neuron? Where does it terminate?
Where is the primary neuron in the Corticopontocerebellar pathway? What is the secondary neuron? Where does it decussate? Which cerebral peduncle does it enter? Where does it end in the cerebellum?
Would a lesion at location A, B, and/or C produce cerebellar signs?
At C, which could be in the cerebellum proper or in the peduncles.
What is connected by the olivocerebellar tract? What process does it facilitate?
Is the vestibulocerebellar pathway afferent or efferent? What does it connect?
What is connected by the spinocerebellar tract?
The proprioceptive neurons and the cerebellar cortex and nuclei.
Recall which of the following are involved in afferent or efferent pathways:
Superior peduncle
Middle peduncle
Inferior peduncle
Injury to what part of the cerebellum is likely to cause truncal ataxia, gait ataxia, and abdnormal saccades?
Inury to what part of the cerebellum could cause ataxia, hypotonia, intention tremor, and dysdiiadochokinesia?
Injury to what part of the cerebellum could cause truncal ataxia and nystagmus?
What are the four core symptoms used for diagnosing Brief Psychotic Disorder? How many symptoms must be present (and which does not count by itself)? How long is the duration of the disorder?
What arre the five core symptoms used for diagnosing Schizophreniform Disorder? How many core symptoms must be present? Which of those 5 must be at least 1 present? How long is the duration of the disorder?
What is the difference between a diagnosis of Schizophreniform Disorder and Schizophrenia?
What is the diagnostic criteria for Schizoaffective Disorder? How does it differ from a diagnosis of Schizophrenia or Schizophreniform Disorder?
What are the criteria for diagnosing Delusional Disorder?
Note that you do not need to memorize the types of delusions.
What is the main difference between MDD as well as BP I&II and Schizoaffective Disorder?
What is the criteria for diagnosing Substance-induced Psychotic Disorder?
Describe where each of the following dopamine pathways begin and end as well as their function.
-Mesocortical
-Mesolimbic
-Nigrostriatal
-Tuberoinfundibular
Name the 6 main typical antipsychotics or FGAs.
also trifluoperazine
What are four notable side effects of antipsychotics as a result of “dirty binding”?
What are the four main Extrapyramidal Side Effects? What is their time course? How are they treated?
Address the rough timeframe for antipsychotic treatment responses in the following areas.
What 5 notable MoAs of General Anesthetics? What are examples of medications used in each MoA?
GABA-A receptor potentiation- Propofol
Glycine receptor agonism & Nicotinic acetylcholine receptors- Inhalational anesthetics
NMDA receptor antagonism- Ketamine and NO
K+ channels- ?
What are the four stages of anesthesia?
What are some expected symptoms that can help to localize a seizure to each cortical lobe of the brain?
Symptoms of truncal ataxia, titubation (a rocking or tremor of head) and dysmetric saccades would indicate a lesion to what specific area of the cerebellum?
The vermis
Where do efferent axons project to from the following:
Globus pallidus
Putamen
Globus pallidus
Thalamus (Pallidothalamic tract)
Subthalamus
Putamen
Globus pallidus (but no afferents)
What part of the internal capsule separates the caudate from the putamen in the striatum?
The anterior limb of the internal capsule
What type of brain waves are observable during waking hours? What about when one is drowsy or very relaxed? List waves seen and/or notable waveforms seen in the following:
NREM 1
NREM 2
NREM 3
REM
Also, note that GAMMA waves are seen during problem solving, and concentration during wake hours.
What are five notable indications for polysomnography?
What acronym describes the main symptoms associated with Narcolepsy?
What criteria are used to diagnose insomnia disorder?
What is Restless leg syndrome? What time of day is it often worse? What is it associated with?
Address the differences between REM (REM sleep behavior, Nightmare disorder) and NREM (Sleepwalking, Sleep terrors) disorders of sleep in the following areas:
Time of night
Sleep stage
Eye position during episode
Sensorium if awakened
Recall after episode
Polysomnography findings
What is the criteria for diagnosing GAD?
What is the diagnostic criteria for agoraphobia?
Which of these symptoms could be better explained by another condition than OCD? What are examples for each?
Obsession with particular aspect of appearance
Hair pulling
Eating patterns
Difficulty parting with objects
Substance obsessions/compulsions
How is trauma defined as used in diagnosis of psychiatric disorders? Would exposure through the media be considered trauma?
No, PTSD criteria would involve witnessing first hand or being directly related or extremely close to a person experiencing the trauma firsthand
How is PTSD diagnosed?
How is Acute Stress Disorder different from PTSD?
What are the signs of Neuroleptic Malignant Syndrome? What causes it? What is the treatment?
It can be caused by antipsychotic medications, oftentimes in overdose
What differentiates left brain and right brain EEG leads?
A seizure characterized by the following would be called what?
Absence seizure
A seizure characterized by the following would be called what?
Clonic seizure
A seizure characterized by the following would be called what?
Automatism (seen in generalized or focal seizures)
A seizure characterized by the following would be called what?
Tonic-clonic seizure (Grand mal), which is a type of generalized seizure
A seizure characterized by the following would be called what?
Myoclonic seizure
A seizure characterized by the following would be called what?
Tonic seizure
