Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
138 Cards in this Set
- Front
- Back
|
Benzodiazapines are used to treat anxiety. Please answer the following questions:
Why are they used over barbituates? What is their proposed mechanism of action? What are the benzodiazepines not metabolized by the liver (aka, you would give them to old people or people with liver failure)? |
Benzodiazepines are safer to use than barbituates because their affect will saturate out at a certain amount (before coma!) Barbituates can directly affect the chloride channels.
The MOA of benzodiazepines is stimulation of GABA receptors, leading to increased Cl permeability and increased inhibition. **location of action specific to the limbic system (this is where emotional behavior is controlled** Oxalzepam, temazepam and lorazepam (OTL- outside the liver) |
|
|
Benzodiazepines can be used in the treatment of anxiety. Please answer the following questions:
What can they also be used to treat? What drugs will increase their effect? What drugs will decrease their effect? |
Benzodiazepines can also be used to treat: alcohol withdrawal (remember disulfram is CONTRAINDICATED in acute OH tox), insomnia, preanesthetic meds, neuromuscular disorders, anticonvulsants, PMDD
Benzo action is enhanced by: other CNS depressants like OH; grapefruit juice is a CYP3A4 inhibitor, thus increasing BZD levels Smoking and caffiene (CNS stimulatnds) increase the effects of benzos |
|
|
What is buspirone?
How does it work? |
Buspirone is an anxiolytic
It acts as a parital 5HT agonist... it differs from benxos because there is a delayed onset of activity, less sedation, no anticonvulsant activity, no muscle relaxation and no potential for abuse. It does NOT interact with OH. Buspirone --> people get anxious about missing the BUS |
|
|
Sara's mother brings her in because she states that Sara washes her hands 17 times before she can come downstairs to eat dinner. What is going on? How do we pharmacologically treat it?
|
Obsessive Compulsive Disorder
Treat with Clomipramine --> tricyclic 5HT reuptake blocker |
|
|
What pharmacological treatments are available for GAD?
PTSD? |
GAD: SSRI > buspirone > benzidoazepines
PTSD: cognitive behavioral therapy > SSRI |
|
|
Spasmolytic agents are often necessary in stroke, MS, CP, or spinal injury. What is their intended area of pharmacological treatment? Please give some examples?
|
Intended to decrease activity of Ia neurons activating primary motor neurons or increase the activity of inhibitor internencial neurons.
Diazepam -- GABA(a) Baclofen -- GABA(b) Dantrolene -- block ryanodine receptors |
|
|
Some of the major hypnotics are the BZD1 receptor agonists. What are they, how do they act, and when would they be prescribed?
|
BZD1 receptor agonists are not benzodiazepines, but bind to the receptor and only produce the hypnotic affects (not the anticonvulsant or muscle relaxing effects)
Zolpidem- onset in 30 minutes, last 6-8 hours (give to people who have trouble staying asleep) Zaleplon- onset 20 minuts, last 4 hours (give to people who have trouble falling asleep, but can stay asleep) Eszopiclone- onset 30 minuts, last 8 hours (give to people who have trouble staying asleep); approved for CHRONIC use remember, these are sweet because they don't really alter the normal sleep structure! |
|
|
Which melatonin receptor is effective as a hypnotic? How does it work?
|
Ramelteon! MT receptor agonist. Small decreases in stage 3 and 4 sleep.
Helps patients fall asleep, but doens't help them stay asleep. Effective for chronic use. |
|
|
What hypnotic drug is contraindicated in a patient with obstructive sleep apnea?
How does this drug work? |
Benzodiazepines!
GABA agonists. Alter normal sleep structure by increasing the stages 1 and 2 and decreasing stages 3, 4 and REM. Altern normal sleep patterns. Can worsen OSA because they are muscle relaxants! |
|
|
How are barbituates affective as hypnotics?
Why are these more dangerous to use than barbituates? |
Enhance GABA effects. Induce hypnosis by decreasing REM and increasing stage 2 (NREM) --> REM rebound.
Higher risk of drug tolerance, phychological and physical dependence can occur |
|
|
Using barbituates as a sleep aid can result in fatality on abrupt withdrawal. What are the symptoms?
|
CV collapse --> vasomotor depression may cause CHF, hypovolemic shock and cardiac arrest
Respiratory depression at the medullary respiratory center |
|
|
What precipitates acute intermittent porphyria?
|
Barbituates
|
|
|
What is REM rebound? How can you get it? How is it treated?
|
Not getting sufficient REM sleep, due to alteration of normal sleep pattern.
Get it from use of benzodiazepine or barbituate. Reversible with Ramelteon or BZD1 receptor agonists (zolpidem, saleplon, eszopiclone) |
|
|
What is sodium oxybate?
|
Sodium Oxybate (GHB) can be used to treat cataplexy associated with narcoplexy
|
|
|
How does opioid receptor activation decrease pain?
|
Opioid receptors are linked to G proteins --> Gi --> decrease cAMP --> closure of voltage gated Ca channels (decreased release of ACh, NE, glutamate, serotonin and substance P) and opening of K channels causing hyperpolarization
|
|
|
What is used to treat breakthrough pain associated with morphine use?
|
Fentynl patch!
Fentynl is another full opioid agonist; it must be a full agonist for breathrough pain because mixed agonists can actually increase the pain. |
|
|
Which opioid receptors are associated with:
Analgesia Respiratory depression Dysphoria Physical dependence |
Analgesia- mu
Respiratory depression- mu Dysphoria- kappa Physical dependence- mu |
|
|
What is the most common cause of over dose death in patients on opioids?
|
Respiratory depression --> decreased sensitivity of respiratory center to CO2 drive
|
|
|
A patient on chronic opioid use should be placed on a laxative. Why?
|
Opioids increase gastric tone and decrease peristalsis --> constipation
No tolerance to the stimulating effects of opioids (ie the miosis, constipation) |
|
|
What pharmocokinetics are associated with opioid use?
Why is oral morphine only used in patients with cancer? |
Opioids have a rapid first pass effect --> 90% may be metabolized
Morphine (active) ingested --> 90% metabolized into M3G (inactive) and 10% metabolized into M6G (active) Be careful giving this to patients in renal failure because if they can't excrete metabolites well, M3G can build up and cause seizures. Reserved for patients with cancer because the first pass effect is different for everyone |
|
|
What signs in the ER would tip a physician off that the person has acute heroin toxicity?
Treatment? |
Acute opioid toxicity has triad of: coma, pinpoint pupils and respiratory depression
Tx: maintain respiration, naloxone |
|
|
What are some contraindications to opioid use?
|
Bronchial asthma, emphysema (it suppresses respiration), liver damage, closed head injury, OH intoxication
|
|
|
A patient on codiene comes back because they say that their pain in not relieved and they need a larger prescription. How do you respond?
|
Well, they could be a druggie.
OR They could be in the 7% of people who don't have CYP2D6 to metabolize it to active morphine (codiene is a prodrug) |
|
|
Which opioid is safer to use in pregnant women?
Why would you not want to give an opioid at all to a pregnant women at term? |
Meperidine --> lesser degree of respiraoty depression in fetus and does not inhibit uterine contraction
Giving it to preggos at the beginning can cause cardiac defects. Giving it to preggos during pregnancy can result in fetal dependence. Giving it to them term can have an increased risk of respiratory depression |
|
|
In order to prevent the constipation effects in a patient with cancer on a chronic dose of opioids, which additional drug should you use?
|
Methylnaltrexone!
It is a pure opioid antagonist that reverses opioid induced constipation without reducing the analgesic therapy. |
|
|
What is keterolac? What is its MOA?
|
Keterolac is a long acting NSAID
NSAIDs block COX --> no production of PG --> PG are what sensitize the pain receptors --> NO PAIN |
|
|
Compare COX1 and COX2
|
COX1 is a constitutive enzyme (inhibition of this leads to gastric ulcer)
COX2 is an inducible enzyme (induced by inflammation, inhibition of this leads to beneficial effects) |
|
|
Which drugs can be given as preanesthetic agents?
|
Benzodiazepines, opioids, antocholinergics
|
|
|
What is the blood/gas coefficient?
How does it relate to different anesthetics? |
Blood/gas coefficient (lambda) is a measure of the solubility of an anesthetic gas in the blood
If the blood/gas coefficient is elevated, that means that tons is dissolved in the blood, and so it does not get into the brain very well --> slower onset INCREASED LAMBDA, SLOW ONSET ex.) N2O has lower lambda than halothane, so N2O has a faster onset |
|
|
What is MAC?
How does it relate to different anesthetics? |
MAC is the mean alveolar concentration that will block movement in 50% of patients.
If MAC is high, the lipid gas coefficient is low, that means that more of the anesthetic is needed to sedate patients, ie is it not very potent ex.) N2O has a MAC of 105, halothane has a MAC of 0.76 --> lower doses of halothane will be effecting in putting a patient to sleep |
|
|
When administering anesthetic, what areas of the CNS are most sensitive?
|
Most sensitive to least sensitive: RAS and cortex > hippocampus > basal ganglia > cerebellum > spinal cord > medulla
|
|
|
Which anesthetic can cause hepatits on subsequent administrations?
|
HALOTHANE HEPATITIS
|
|
|
Read this.
|
1. patients who have had ketamine anesthesia should be protected from unnecessary visual, tactile, and auditory stimuli to prevent excitedment and psychic reactions during emergence from anesthesia.
2. Succinylcholine can cause poste operative muslce pains. |
|
|
What is dissociative anesthesia? What is used to produce it?
|
KETAMINE
|
|
|
What is the proposed mechanism of action of the general anesthetics?
|
Direct interactions with GABA and glycine --> inhibitors
Also inhibit the activity of excitatory transmitters acetylcholine and serotonin Ketamine and N2O also inhibit glutamate activity |
|
|
Which local anesthetic is most cardiotoxic?
Most widely used clinically? Most likely to cause CNS sedation? Limited to surface/topical anesthesia? Most likely to produce vasoconstrictor effects? Used in opthamological anesthesia? |
Most likey cardiotoxic- BUPIVICAINE
Most widely used- LIDOCAINE Causes CNS sedation- LIDOCAINE Limited to topical- COCAINE Produces vasoconstrictor effects- COCAINE Ophthalmological- TETRACAINE |
|
|
Why is used in many OTC preparations as a surface anesthetic?
|
BENZOCAINE- it is almost 100% uncharged at physiological pH --> it can get to where it needs to go!
It's pKa is 3 --> essentially unionized (can cross, but weak action) |
|
|
What is the proposed mechanism of local anesthetics?
|
Block activation of voltage gated sodium chanels in neuronal membranes --> have greatest affinity for sodium channels in inactivated state and interefere with its reversion to the resting state --> shut down for a prolonged period of time
Also have higher affinity for Na chanes that are in neurons that are fired more frequently |
|
|
Local anesthetics are...
weak acid weak base How does this interfere with their action? How does inflammation change this? |
LA are weak bases and are limited by their pKa (8-9), lipid solubility and molecular size.
LA are active in their charged form, but in order to enter the cell membrane, must be uncharged. At pH 7.4 (physiologic), 80-90% is unionized and can't enter cells --> rate of onse tis related to pKa --> LOWER pKa, FASTER ONSET) Inflammation produces lower pH in tissues --> LA are more ionized, so doesn't penetrate very well and decreased ability of LA to produce effects |
|
|
There are two chemical classes of local anesthetics. What are they? How do their effects differ?
|
Amides- two 'i's' in the name- lidocaine, bupivacaine, ripivacaine; more slowly destroyed by liver microsomal P450 enzymes --> more systemic effects
Ester- only one 'i'- procaine, tetracaine, benxocaine, cocaine; rapidly metabolized to PABA in plamsa by a cholinesterase, so don't cause systemic tox; since they are metabolized by a cholinesterase, remember that if a patient is on a cholinesterase inhibitor (ie physostigmine, they will have a more toxic buildup!!!) Cross sensitivity between classes |
|
|
How do vasoconstrictors affect local anesthetics?
When would you not use a vasoconstrictor? |
Decrease teh rate of systemic absorption and decrease systemic toxicity. Increase local drug concentration and increase neuronal uptake of LA. increase local duraiton of action. Use vasoconstrictors except fingers, nose, toes and hose
|
|
|
What is Strychnine? What are the symptoms of it's toxicity? How do you treat an overdose?
|
Strychnine is a disinhibiting analeptic found in rat poison
After ingesting, will see a gradual increase in muscle activity including tightness of neck and jaw, hyperreflexia, tonic extensor thrusts, tetanic symmetrical convulsions (opisthotonus), respiratory arrest Treatment includes: IV diazepam, lorazepam, respiratory support, quiet surroundings, gastric lavage |
|
|
What is the mechanism of action of caffeine? What effects does it have?
|
antagonist at adenosine receptors (adenosine receptors block NE release) to increase NE
causes diuresis, stimulation of carcdiac muscle, smooth muscle relaxation, secretion At 1g --> insomnia, excitement, increased HR and respiration At 10g --> convulsions and death |
|
|
How are amphetamines affective in treating ADHD?
|
Release NE, DA and 5HT to respectively increase alertness, euphoria and mood
|
|
|
A side effect of this drug is synesthesia.
|
LSD- heightened awareness of sensory input; see sounds and hear colors
|
|
|
First time use of this CNS stimulant can impair the ability of the body to regulate temperature, resulting in overheating and dehydration.
|
3,4 METHYLENEDIOXYMETHAMPHETAMINE
kids do this drug in clubs these days |
|
|
What is the methadone maintenance program and the methadone detox program?
|
Methadone detox- substitute and withdraw over next three weekd (synthetic opioid)
Methadone maintenance- substitute and maintain |
|
|
Define:
Drug Abuse Tolerance Psychological Dependence Abstinence Syndrome Addiction |
Drug Abuse- use of drugs in a manner which cause major and continuing problems in life
Tolerance- decreased response to a given dose of drug after repeated doses Psychological Dependence- drug needed for optimal state of mental well being Abstinence Syndrome- physiological reaction to the absence of a drug to which a person is physically dependent Addiction- extreme pattern of compulsive drug use with a high possibility of relapse after withdrawal |
|
|
Recent studies have shown that damage to this area of the brain can relieve patients of their addictive behaviors.
|
Insular cortex
|
|
|
When do withdrawal symptoms of heroin start to occur? What are they?
|
Symptoms start 6-12 hours after the last dose and include restlessness, lacrimation, rhinorrhea, sweating
In 24 hours, restless sleep, dilated pupils, anorexia, piloerection, irribability |
|
A sweet babe comes in with teeth like this. What drug is she on?
|
METH :)
|
|
|
What is the emergency treatment for benzodiazapine intoxication?
Amphetamine intoxication? Barbituate intoxication? Opioid intoxication? |
Benzodiazepine --> flumazenil
Amphetamine --> lorazepam Barbituate --> none Opioid --> naloxone |
|
|
What is the treatment for acute alcohol intoxication?
Chronic alcoholism? |
Acute- Symptomatic support or benzodiazepines (for DT)
hangover? ibuprofen Chronic- vit B replenishment, diazepam, disulfiram |
|
|
What is delirium tremens? What is the treatment?
|
Life treatening alcohol withdrawal syndrome that peak 2-5 days after last drink
Autonomic system hyperactivity (tachy, tremors, anxiety), psychotic symptoms (hallucinations), confusion Tx: benzodiazepines |
|
|
How does the metabolism of ethanol differ from methanol?
|
Methanol is oxidized in the body by ADH to formic acid and formaldehyde
Ethanol competes with methanol for alcohol dehydrogenase, thereby decreasing the rate of methanol oxidation --> this competition forms the basis of ethanol's use in the treatment of methanol intoxication |
|
|
What are the potential drug interactions with alcohol and...
1. CNS depressants 2. oral hypoglycemics 3. anticoagulants 4. salicylates 5. acetaminophen 6. anticonvulsants 7. antimicrobial agents |
1. CNS depressants- increase effect
2. oral hypoglycemics- potentiation of hypoglycemic effect 3. anticoagulants- half life of warfarin is decreased 4. salicylates- increased risk of hemorrhage 5. acetaminophen- increased risk of gastric hemorrhage 6. anticonvulsants- half life of phenytoin decreased 7. antimicrobial agents- disulfiram like actions |
|
|
What is the proposed mechanism of alhocol action?
|
Action on GABA receptor --> inhibition
May also inhibit NMDA --> blackouts |
|
|
Why don't drunk people get cold?
|
Alcohol causes depression of the hypothalamus, resulting in hypothermia
But guess what, they can't feel it! That's why Alaska drinking is so dangerous |
|
|
Why is drinking when you are preggo not a sweet idea?
|
Chronic ingestion will lead to decreased absorption of folic acid
|
|
|
How is alcohol metabolized?
|
zero order kinetics
Ethanol --> (alcohol dehydrogenase) --> acetalaldehyde --> (acetaladehyde dehydrogenase) --> acetic acid --> acetyl CoA --> CO2 + H2O The rate limiting state is alcohol dehydrogenase |
|
|
A 31 year old woman presents to the ER in a seemingly confused and combative state. Her husband says that she was fine, until about 7 hours ago, when she began babbling about Star Wars and Siths and 5th Elements and Angry Birds and Doxycycline concentration in prostatic fluid. Is this Dementia or Delirium?
|
This is delirium!! --> acute onset, fluctuation throughout the day, language impairment, perceptual disturbance, delusions, agitation, intense moods
Subtype is hyperactive delirium (she is combative) |
|
|
What vulnerabilities predispose a person to a delirious episode?
|
Advance age
Dementia or a cognitive impairment Brain disease or injury OH abuse Sensory impairment |
|
|
What insults can precipitate delirium?
|
TONS OF THINGS
acute cardiac events, infection, medication, malnutiriton, fecal impaction, indwelling devices, hypoglycemia, hypoperfusion, poisons, toxins, polypharmacy RE-READ THIS SLIDE |
|
|
What are the keys to effective management of a delirious patient?
|
provide social restraints, avoid physical restraints, let family stay in the room, monitor them all the time
The best treatment if prevention |
|
|
What lobe controls personality?
What is a personality disorder? How do defense mechanisms come about? |
FRONTAL lobe controls personality. A personality disorder is a behavior that deviates markedly from the expectations of the culture, is inflexible, is maladaptive and affects multiple areas of functioning.
Defense mechanisms arise about of the Ego not being able to balance the SuperEgo and Id --> anxiety --> defense mechanism |
|
|
Stan doesn't have friends and he doesn't want them. Personality disorder?
|
Schizoid (A)
|
|
|
Stan doesn't have friends because he spends all of his time playing his favorite video game-- Siths vs. Sharks: Oblivion City
But he really wants to have friends. Personality disorder? |
Schizotypal (A)
|
|
|
Kyle has broken the law multiple times. He really doesn't care about what happens to anyone else. He has a temper, is impulsive and remorseless. Personality Disorder?
|
Antisocial Personality Disorder (B)
|
|
|
Unstable and intense. Anger issues. Abandonment issues. Mood instability. Impulsive. Personality disorder?
|
Borderline (B)
|
|
|
Name someone with Histrionic Personality Disorder.
Name someone with Narcissistic Personality Disorder. |
Histrionic- Praise me
Narcissistic- Special |
|
|
Sally feels inadequate, is super sensitive to criticism and never wants to try anything new because she is afraid she will fail and embarass herself. Personality disorder?
|
Avoidant (C)
|
|
|
Describe Dependent Personality Disorder?
Describe OCD Personality Disorder? |
Dependent- submissive and clinging behavior and fears of seperation
OCD- obsessed with orderliness, perfectionism and control |
|
|
Some anxiety is good to have, it allows us to reach our peak performance. When does anxiety become a problem?
|
Anxiety disorders tend to be chronic or recurrent and impair social and occupational functioning
|
|
|
Grandma won't leave the house. What's wrong?
Susan is worried her dog will die, she will lose her job and the world will explode. What's wrong? |
Grandma has agoraphobia
Susan has GAD |
|
|
To diagnose a panic attack...
When do panic attacks become panic disorder? |
Period of intense fear or discomfort that peaks within 10 minutes and manifests as: palpitation, sweating, trembling, chest pain, SOB, NV, derealization, depersonalization
Panic disorder is when patient worries about having another panic attack and avoids places/situations for fear of having a panic attack |
|
|
What is the difference between PTSD and ASD?
|
Post traumatic stress disorder- symptoms last longer than one month; can occur any time after the event
Acute stress disorder- symptoms last from 2 days to 4 weeks; occurs within 4 weeks of the event |
|
|
What is the difference between somatization disorder and malingering?
|
Somatization disorder has no conscious effort to decieve the physician, these people actually believe something is wrong with them
In malingering, the person is trying to decieve the physician, for some secondary gain, like missing work |
|
|
Betty comes into the ER for the 4th time this month, complaining of a headache. She requests a CT of her head, just to make sure she doesn't have a brain tumor and recommends that she stay overnight in the hospital because she is so worried. What is going on?
|
She has a factitious disorder. Signs and symptoms are consciously produced by the patient to assume the 'sick role'. They want to have tests run and can sometimes even demand to be hospitalized.
This is NOT hypochondriasis- the symptoms would have to be evident for at least 6 months for that diagnosis |
|
|
What are the somatoform disorders?
|
Somatization disorder- multiple unexplained somatic symptoms NOT intentionally produced
Hypochondriasis- preoccupation with fears of having a serious disease for at least 6 months Conversion disorder- one or more neurologic symptoms that are unexplained by a medical disorder that is associated with an specific conflict or stressor (ie. watch someone get murdered and now you don't talk) Pain disorder- significant pain not fully explained by a medical condition Body dysmorphic disorder- preoccupation with an imagined deficit |
|
|
What are the most likely causative agents of viral meningitis?
Viral encephalitis? |
Viral Meningitis- Enterovirus (coxsackie) > Arbovirus (west nile) > HSV > mumps
Viral Encephalitis- Arbovirus (west nile, la crosse) > HSV > rabies |
|
|
If a patient comes into the ER with a stiff neck, fever, chills, vertigo, headache and you suspect either meningitis or encephalitis, what is your first action?
|
Start them on Acyclovir (anti HSV) and on an antibiotic.
These are probably not the cause of the meningitis or encephalitis, but if they are, they are fatal and treatable, so CYA!!! |
|
|
La Crosse Virus is what type of virus? Please give me deets about how you get it (vector, host)
|
La Cross Virus is an Arbovirus (arthropod bourne).
Vector is woodland mosquito, breeds in treeholes Natural host is chipmunk/squirrel |
|
|
18 year old male comes in with a stiff neck, fever and seizures. You suspect viral encephalitis. Causative agent? How did he get it?
How do you confirm this? |
CAMPING --> ARBOVIRUS, this is the average case presentation for LaCrosse virus
He got that **** by a squito! Diagnosis confirmed by increase IgM in CSF and elevated antibody titre to arbovirus |
|
|
Rabies can cause FATAL encephalitis.
How do humans get infected and what can we do about it? How can we recognize a rabid human? |
Rabies virus is found in BATS as a natural host. Most human in the US are infected by bats, skunks, raccoons and cyotes (world wide is wild dogs)
Virus multiplies locally and enters the nervous system at the NMJ --> incubation period several days depending on site of bite (this allows for post infection vaccination!) Death 3-5 days after onset of symptoms (excitation, convulsions, hydrophobia, respiratory paralysis) |
|
|
Smear shows Negri Bodies.
|
RABIES
|
|
|
A person is bit by a dog, but the dog looks fine. Recommend they just ice it?
|
NO
They need a rabies vaccine. The rabies virus can sit in the saliva of an animal for 3-5 days before the animal starts to act weird. Depending on the bite location, it can incubate for several days before the virus actually starts to multiply |
|
|
What is the typical cause of viral meningitis? How is it transmitted?
|
Coxsackie A and B Echoviruses
Fecal oral transmission primarily in infants and children in the late summer or early fall |
|
|
How can we differentiate between virally induced and bacterially induced meningitis?
|
CSF!
Bacteria- tons of WBC, increase PMN, decrease glucose, increase protein Viral- normal WBC, increase lymphocytes, normal protein, normal glucose |
|
|
Meningitis may present with a postitive Kernig or Brudzinski sign. What are these?
|
Kernig- bending leg up --> irritation
Brudzinski- chin to chest --> irritation |
|
|
What is the number one cause of fungal meningitis? What are it's pathogenic factors? How are humans exposed?
|
Cryptococcus neoformans
Negatively charged capsule inhibits phagocytosis, melanin production protects it from oxidative compounds and causes chemoattraction of nutrients Humans are infected by inhaling the yeast form from dried pigeon **** |
|
|
A patients with AIDS comes in with meningitis. What probably caused it? How do we confirm the diagnosis? How do we treat it?
|
Cryptococcus neoformans
India ink stain of CSF Tx- amphotericin B (plus flucytosine-- which must be activated by fungal cytosine deaminase to form what?), fluconazole, or itraconazole |
|
|
Of people infected with poliovirus, how many are asymptomatic? Of the symptomatic patients, what are their symptoms?
|
95% are asymptomatic (but can still spread the virus)
5% are symptomatic and symptoms range from mild fever, NV, viral meningitis and paralytic poliomyelitis (muscle wasting) |
|
|
Where does the poliovirus attack?
|
Introduced via fecal-oral route --> GI infection spreads via blood to peripheral nerves --> can attack anterior horn cells (spinal polio, motor), brain stem (bulbar polio), or both
|
|
|
What vaccines are used to prevent polio? Which one do we use to eradicate the wild type?
|
Salk (killed)
- given to countries where the virus has been eradicated Sabin (live attenuated)- prevents fecal oral spread of wild type; give to countries with continuing disease prevalence both- give to countries w/o polio, but with continued environmental presence of wild type virus |
|
|
What is a 'transmissible spongiform encephalopathy'?
|
Encephalopathy caused by an abberant form of a normally expressed neuronal protein (prion) --> the proteins have moved from an alpha helix conformation to a beta sheet conformation --> body cannot clear them appropriately because they are resistant to degradation and non immunogenic --> these prions build up in the brain and cause disease
|
|
|
What is Creutzfeld-Jakob Disease? Breakdown of familial and sporadic? Symptoms of the disease?
|
85% is sporadic (codon 129, normal)
15% is familial (codon 200, changing base from glu to lys) Average age of onset is 60-65 y/o, progressive degeneration of brain wtih rapidly progressive dementia and myoclonus --> death within one year |
|
|
Creutzfeld-Jakob Disease is associated what CSF finding? What histopathology finding?
|
Protein 14-3-3 and elevated tau in CSF
Florid plaques in brain tissue |
|
|
If a physican saw the thalamus light up on an MRI, what would be the first thought?
|
Pulvinar sign --> Creutzfeld-Jakob Disease
|
|
|
26 year old patient presents with a change in behavior, painful sensation and fever. On MRI, a pulvinar sign is noted. After being hospitalized for several days, the patient dies. What is going on?
|
VARIANT CREUTZFELD-JAKOB DISEASE
vCJD median age of death is 28 years, prominent psychiatric/behavioral symptoms, painful dyesthesiasis, delayed neurologic signs, pulvinar sign present, lots of florid plaques Classic CJD- average age of death is 68, dementia, no pulvinar sign reported, no florid plaques |
|
|
What would be warning flags that your patient may be anorexic?
|
Refusal to maintain body weight at or above a minimally normal weight for age and height.
Intense fear of gaining weight or becoming fat Amenorrhea, the absence of at least three consecutive cycles Physical findings: brittle hair, dry skin, cachexia, lanugo, hypoactive bowel sounds, cognitive impairment, dehydration, hypothermia, hypotension |
|
|
What would be warning flags that your patient is bulimic?
|
Recurrent episodes of binge eating
Recurrent inappripriate compensatory behavior in order to prevent weight gain (exercising too much) The binge eating and compensatory behavior occurs on average at least twice/week for 3 months Physical findings: eroded dental enamel, painless parotid gland enlargement, Russell's sign, hypoactive bowel sounds, peripheral edema (d/t laxative use) |
|
|
When is the usual onset of anorexia? Bulemia?
|
Anorexia- adolescence (14-18)
Bulimia- late adolescence through early adulthood (college) |
|
|
What is the female athlete triad?
|
Disordered eating
amenorrhea (absence of at least three consecutive cycles) osteoporosis |
|
|
Why is diabetes a risk factors for an eating disorder?
|
diabetes management can exacerbate an eating disorder
INSULIN RESTRICTION is a purge equivalent Adolescent with DM --> anorexia Adult with DM --> bulimia |
|
|
How does serotonin affect feelings of hunger or satiety? Where does serotonin act to accomplish this?
|
Serotonin triggers sensations fo satiety and inhibits feeding by triggering 5HT receptors in the ventromedial hypothalamus
Serotonin also mediates temperament, impulse control, mood and anxiety In dieting, low 5HT induces hunger |
|
|
What physical findings are associated with binge eating disorder?
|
obesity, pressure sores, back pain, obesity related physical complications
|
|
|
Malnutrition, loss of bone density, secondary amenorrhea and dermatologic effects are the main medical complications of what eating disorder?
|
Anorexia
|
|
|
Mallory Weiss tears, Boerhaave ruptures, depression, chronic constipation and toxic megacolon are the main medical complications of what eating disorder?
|
Bulemia
|
|
|
Treatment of Anorexia consists of:
|
Full weight restoration
Cognitive Behavioral Therapy |
|
|
Treatment of Bulimia consists of:
|
normalization of eating behavior, CBT, fluoxetine for weight restored bulimics (high dose SSRI if present with OCD)
|
|
|
A complication of weight restoration is refeeding syndrome. What is this?
|
Develops on day 4 of rapid refeeding from any malnourished state.
HYPOPHOSPHATEMIA followed by fluid shifts and other electrolyte deficiencies --> mortality due to heart failure or pulmonary edema |
|
|
Patients with eating disorders are at a higher rik of osteopenia and osteoporosis. How do we deal with this?
|
Malnutrition, low estrogen, progesterone and IGF can increase risk.
We want to restore weight, stop smoking, add calcium and vitamin D supplements, add alendronate (bisphosphonate that inhibits osteoclast mediated bone resorbtion), DEXA scan at one year from diagnosis |
|
|
When is fluoxetine recommended for an eating disorder?
|
Evidence supports using fluoxetine for weight restored bulimics
Will improve mood and anxiety in any eating disorder |
|
|
Bulemic patient has OCD. What pharmacologically do you prescribe?
|
HIGH DOSE SSRI
|
|
|
The following medications are CONTRAINDICATED or use with caution only, for the treatment of eating disorders:
|
Bupropion (wellbutrin) is contraindicated in any patient with a history of an eating disorder
Mirtazepine (tetracyclic antidepressant, anorexia is a SE), TCA (but they are indicated for it...), benzodiazepines and topiramate (causes wt loss) are use with caution drugs |
|
|
How do you spell the specialty of medicine dealing with diseases and surgery of the eye?
|
OPHTHALMOLOGY
|
|
|
The mean onset of diabetic retinopathy in Type II diabetes is:
|
20 years old
|
|
|
A patient presents with red eye. Exam shows mucopurulent discharge, papillary conjunctival response and no palpable preauricular lymph nodes. The most likely diagnosis is:
|
bacterial conjunctivitis
|
|
|
Most common cause of untreatable legal blindness in patients over 55 is:
|
Age related macular degeneration
|
|
|
Inflammatory eye disease has been associated with:
|
ALL
ankylosing spondylitis, crohn's disease, RA |
|
|
What are the first, second and third leading causes of death in persons age 15-24?
|
Leading cause of death is INJURY
Second leading cause of death is HOMICIDE Third leading cause of death is SUICIDE |
|
|
Describe the general demographics of suicide.
Age Gender Race Marital Status Religion Occupation |
Suicide is a phenomenon of adolescents and the elderly, with elderly white males being at the highest risk.
Elderly Male White Single, widowed, divorced Protestant, Jewish Professionals- physicians and unemployed |
|
|
How do suicide and psychiatric illness relate?
|
90% of completed suicides are associated with a psychiatric illness at the time. (usually MDD or substance abuse)
|
|
|
What is the number one risk factor for suicide?
|
PREVIOUS ATTEMPT
|
|
|
Mollie starts to cut herself to get attention. What is this called?
|
Parasuicidal behavior- person who engages in self harm without the expectation of dying --> want attention or hospital admission
|
|
|
What are some static risk factors for violence?
Age Gender SES Psychiatric Dx What is the best predictor of future violence? |
Increased risk in teens to early 20s and over 70
Men 3x more likely than women low SES Mental illness or substance abuse at increased risk the best predictor of future violence is PAST HISTORY |
|
|
Patient is depressed and a smoker?
|
Wellbutrin (bupropion)
|
|
|
A pregnant woman comes in with severe depression. What should you do?
|
All psychotropic medications cross the placenta and are contraindicated in pregnancy
Electroconvulsive therapy can be used |
|
|
Just read this
Key points from Dr. Comeaux's OPP lecture |
Body state, mental state and perception all play a role in how a patient percieves their health
Axis I- mental disorders, learning disorders Axis II- personality disorders, MR Axis III- medical disorders Axis IV- environmental factors Be on the look out for patients with mental issues --> they will give you a ton of symptoms that don't add up to an organic cause Use palpation to narrow your diagnosis. It can help discriminate between somatic (organic) issues and somatizing (somatoform) issues. Tx of depression- sympathetic correlations (ie thoracic) Treat thoracic for sympathetic relief, treat cranial for parasympathetic relief Anxiety/Panic disorder --> dissociated sympathetic hyperarousal --> want to treat sympathetics, so work in thoracic area! Use primary care and OPP together: explain that the patient is not crazy, condition is self limiting, identify treatment and coping strategies, OMT to thoracic region as you talk to them |
|
|
Which analgesics are associated with serotonin syndrome?
What physical findings are pathomneumonic or serotonin syndrome? |
Meperidine, fentanyl, tramadol and pentazocine *** TQ***
Mydriasis and clonal jerking |
|
|
How can you differentiate between serotonin syndrome and neuroleptic malignant syndrome? What causes each? What is used to treat each?
|
Serotonin syndrome will have mydriasis, neuroleptic malignant will NOT
Serotonin syndrome- caused by SSRI, MAOi, Tramadol; treatment includes stop offending agent, benxzo, 5HT antagonists (cyproheptadine) Neuroleptic Malignant- cause by neuroleptic (antipsychotic), typicals>atypicals, clozapine, lithium; treatment includes: stop medication, antipyretic, lorazepam, dantrolene |
|
|
A physician can terminate a patient case under what circumstances?
|
Must be at least 30 days of notice
Letter of termination must be sent via certified mail Provide the patient with contact information for other physicians |
|
|
What is the criteria for mental retardation?
What is the number one case? |
Global delay in development
Social behaviors normal for their developmental age IQ<70 (this is 2SD below the mean) Adaptive behavior skills<70 Patient must be diagnosed before age 18 Etiology unclear most of the time |
|
|
Describe mild, moderate, severe and profound mental retardation.
|
Mild- 50-70; most common, usually work and live semi-independently
Moderate- 35-50; moderate supervision for personal care, live in community or supervised settings Severe- 20-35; little communication, live with family, can recognize alphabet Profound- below 20; motor and sensory impairments |
|
|
How does mental retardation severity affect the incidence, age of diagnosis, comorbity and mortality?
|
As severity increases, incident increases, age of diagnosis decreases, comorbidity increases, mortality increases
|
|
|
How are learning disabilities diagnosed?
|
A classic learning disability shows academic skill significantly below IQ --> look to see if there is at least a 15 point discrepancy between IQ and individual scores in the ability-acheivement discrepancy analysis
|
|
|
Autistic disorder manifests abnormalities in what areas?
|
Socialization
Communication Play Abnormal development as opposed to global delay; child's behavior is not 'normal' for any age |
|
|
ADHD diagnosis requires what?
How does this differ from oppositional defiant disorder? |
Symptomatology before the age of 7 in two or more social settings (ie. school or home)
Symptoms include: inattention, hyperactivity, impulsivity Oppositional defiant disorder is a recurrent pattern of negativistic, defiant, disobedient and hostile behavior toward authority figures that persists for at least 6 months |
