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Flashcards in Psych and substance abuse Deck (61)
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1
Q

Patient with liver dysfunction has alcohol withdrawl symptoms.. which benzo do we use?

A

Outside The Liver

Oxazepam
Tenazepam
Lorazepam

2
Q

Somatic symptom vs illness anxiety disorder

A

Somatic symptom - excessive anxiety over 1 or more unexplained symptoms.

Illness anxiety disorder - Fear of having a serious ilness despite few or NO symptoms and consistently negative evaluations.

3
Q

what is the normal age range for stranger anxiety?

A

6 months to 2 years

4
Q

Normal child at birth.. then develops LOSS of ability to speak, feed. + abnormal gait and hand rubbing is seen in what syndrome?

A

RETT syndrome.

mainly seen in girls due to mutations in x-linked MECP2 Gene.

They often get numerous SEIZURES and get worse with age.

5
Q

Angelman syndrome features

A

developmental delay FROM BIRTH.

Happy disposition + Jerky Gait + Hand Flapping.

6
Q

Delayed Sleep wake disorder

A

Sleeping late.. and not able to get up early

7
Q

Advanced sleep wake disorder

A

Cant stay awake in evenings (after 7pm).. and wake up early in the mornings

8
Q

Shift work disroder

A

Shift work making it difficult to form a good sleep pattern. Leads to day time sleepiness.

9
Q

Delerium tremens does not only present with psych findings.. what are some of the physical symptoms?

A

FEVER, TACHYCARDIA, HYPERTENSION, diaphoresis, hallucinations, confusion, agitation

10
Q

HIV associated neurocog disorder

A

Occurs after long standing HIV disease and CD4 below 200.

Results in Impaired Memory, Attention, Personality and behavioral changes, And Motor symptoms (ataxia, slowed movement).

Diagnosis - clinical presentation, neuropsych testing.

MRI will show DIFFUSE increase in INTENSITY in the WHITE MATTER

11
Q

Children with a history of ABUSE, NEGLECT, prolonged institutionalization.. inconsistent care (multiple foster homes) are predisposed to having what pscyh disorder?

A

Reactive Attachment disorder.

These patients seldom seek comfort, and do not respond to attempts to comfort them.

Other symptoms include LACK of SOCIAL RESPONSIVENESS, lack of emotions, and episodes of unexpected irritability or sadness in response to nonthreatening encounters.

12
Q

Prenatal exposure to Opiates vs Cocaine symptoms

A

Opiates including Methadone and Heroin - INTRAUTERINE GROWTH RESTRICTION, SIDS and Neonatal Abstinence Syndrome ( Irritablity, HIGH PITCHED CRY, sleeping and feeding difficulties, tremors, seizures, SWEATING and SNEEZING, tachypnea, vomiting.

Cociane exposure: Jitteriness, Excessive sucking, and Hyperactive MORO REFLEX.

13
Q

what is a bipolar med that is safe in pregnancy?

A

Lamotrigrine.

anytime you switch from one med to another, pregnancy should be DELAYED by 3-6 months to assess the EFFICACY of the med. If its effective and stable.. then get prego.

14
Q

Acute Dystonia (an extra pyramidal symptom) can occur with antipsychotics and what other drugs?

A

AntiEMETICS –> Metoclopramide and Prochlorperazine (anti emetic but also antipsychotic).

15
Q

Language disorder

A

Persistent difficulties in COMPREHENSION (receptive) and / or PRODUCTION (expression) of written language.

May involve any part of language (grammar, syntax, vocabulary, functional use of language etc).

16
Q

OCD therapy

A

SSRI + CBT (exposure and response prevention therapy)

17
Q

McCune-Albright Syndrome features

A
  1. Precocious puberty –> onset of secondary sexual characteristics in girls before 8 or in boys before 9.
  2. Irregular Cafe-au-lait macules on ONE SIDE of the body
  3. Polyostoic Fibrous Dysplasia

Caused by Mutation in GNAS gene resulting in constant activation and OVERPRODUCTION of pituitary hormones.

Peripheral precocious puberty (GNRH independent!!!.. caused by release of LH and FSH). and also TSH (thyrotoxicosis) + Acromegaly (GH) + ACTH (Cushing)

18
Q

Central vs peripheral precocious puberty

A

Central Precocious puberty - Caused by EARLY INACTIVATION of the hypothalamic-pituitary-gonadal axis –> release of GnRH

Peripheral Precocious Puberty –> caused by premature secretion of sex horomones INDEPENDENT of GnRH

19
Q

how does an adreanl tumor cause premature adrenarche?

A

It causes ISOLATED premature adrenarche and specifically Pubic, axillary hair, acne, body odor.. but not other sexual characteristics like Breast development.

20
Q

Sturge Weber syndrome findings

A

Intellectual disability, seizures and visual impairment due to capillary-venous malformations.

Skin lesions - Port Wine stain over the territory of the Trigeminal Nerve.

21
Q

Marfans syndrome findings

A

JOINT HYPERMOBILITY, skin hyperELASTICITY, Long fingers, PECTUS EXCAVATUM, SOLIOSIS / KYPHOSIS.

Face is LONG
Plate is ARCHED
teeth are CROWDED
Lens DISLOCATION
FEET are flat
AORTIC ROOT DILATION - most life threatening finding. can result in ANEURYSMS and AORTIC ARCH DISSECTION.

MVP is also a common finding in these patients –> misystolic click and late systolic murmur.

First degree relatives should undergo genetic testing.

22
Q

Homocystinuria vs marfans

A

Patients look very similar to marfans (Pectus deformity, tall stature, arachnodactyly)

however Homocystinuria has FAIR complexion, THRomboemboic events, and intellectual disablity.

Also LENS dislocation in Homocystinuria is DOWN wards (bend down like homo)

and UPWARDS in marfans.

23
Q

why do you get swelling in turners syndrome?

A

lymphatic network dysgenesis.

NON pitting EdemA.

Protein rich interstitial fluid accumulates in the hands, feet and neck. Severe obstruction of lymphatic vessesl can result in a CYSTIC HYGROMA of the neck and fetal hydrops.

24
Q

Turner Syndrome Findings

A

Webbed neck, carpal and pedal edema, nail DYSPLASIA, HORSESHOE KINDEY

Increased risk of osteoperotic fracture. The OVARIAN DYSGENESIS leads to STREAK OVARIES –> estrogen deficient and thus amenorrhea with mininal or no breast development.

Estrogen normally inhibits osteoclastic bone resorption. Since there is no estrogen in Turners.. they have increased bone resorption –> decreased bone mineral density –> increased risk for osteoporotic fracture.

25
Q

What are indications for Chlamydia and Gonorrhea screenign?

A

ALL SExually active women under 24

Anyone with a new partner withing the past 2 months

Multiple partners

History of STDs

Illicit drug use

Incarceration

Prostitutes.

Best Screening test = NUCLEIC ACID AMPLIFICATioN test.

26
Q

when should you do universal screening for dyslipdemia in kids?

A

between ages 9-11 and at ages 17-21.

Lipid levels are relatively stable before and after puberty.

Screening outside of this should be done on people with CAD risk factors ( OBesity, DM, SMokin, Fam history)

and ALL MEN ABOVE 35

27
Q

Duchennes vs Beckers Muscular Dystrophy

A

Duchenees and Beckers are both X-linked RECESSIVE deletions of the DYSTROPHIN GENE on chromosome Xp21.

Duchennes: (COMPLETE LACK of dystrophin) presents at 2-3 years old Progressive weakness, GOWER MANUVER, calf PSEUDOHYPERTROPHY. Scoliosis and CARDIOMYOPATHY.
These patients are usually WHEELCHAIR bound by Adolecence. DEATH by age 20-30 from RESP or Heart failure.

Beckers: milder weakness (REDUCED dystrophin). Onset age 5-15 years old. Milder weakness. CARDIOMYOPATHY. Death by age 40-50 from HEART FAILURE

28
Q

Myotonic Dystrophy

A

Autosomal DOminant expansion of a CTG trinucleotide repeat in DMPK gene.

Onset age = 12-30 years old

Facil weakness, Hand grip myotonia, Dysphagia.

Comorbidities = Arrhythmias, Cataracts, BALDING, Testicular ATROPHY / infertility.

Death from resp or heart failure.. depends on age of onset.

29
Q

What is the GOLD STANDARD for confirming the diagnosis of duchennes or beckers muscular dystrophy?

A

GENETIC TESTING to see a deletion of the dystrophin gene or Xp21.

NOT biopsy.

30
Q

Intrauterine growth restriction + Microcephaly + CLOSED FISTS WITH OVERLAPPING FINGERS + MICROGNATHIA + rocker bottom feet and severe intellectual disability

A

TRISOMY 18 = EDWARDS syndrome

after trisomy 21 this is the most common autosomal trisomy of live births.

31
Q

What is the most common cause of death in Friedreich Ataxia?

A

Cardiac Dysfunction

Progressive gait ataxia and dysarthria in adolescents or young adults.

Caused by a trinucleotide repeat GAA which results in a mutation in the FRATAXIN gene.

Neuro mangifestations –> ataxia, DYSARTHRIA, loss of Vibration and position sense (caused by DEGENERATION of the spinal tracts.. Posterior colunns).

Other clinical features include HYPERTROPHIC CARDIOMYOPATHY –> cardiac dysfunction –> fatal arrhythmia –> death.

32
Q

Hypotonia + WEAK SUCK reflex in infants + HYPERPHAGIA and OBESity + HYPOGONADISM + Retardation + narrow forehaead, ALMOND SHAPED EYES and downturned mouht

A

PRADER WILLI SYNDROME

deletions of PATERNAL 15q11-q13

Patients will have sleep apnea and Type 2 DM.. they should be screened for both!

33
Q

How do you diagnose and treat compartment syndrome?

A

Serial COMPARTMENT PRESSURE monitoring. If its high do a compartment decompression by FASCIOTOMY.. or in the case of circumferential burns ESCHAROTOMY.

34
Q

Subcutaneous bacterial invasion can lead to cellulitis or gas gangrene (c. perferingens).. how can u tell th edifference on physical?

A

Cellulitis = warmth

Gas gangrene = crepitus.

35
Q

child takes pills. VOmiting + Abdominal pain + COFFEE GROUND emesis + irritable and lethargic. Abdominal imaging shows RADIO OPAQUE tablets. what is the diagnosis and what is the treatment?

A

Diagnosis = Iron poisoning

Treatment = DEFEROXAMINE

Iron damages tissues by creation of FREE RADICALS and LIPID PEROXIDATION –> Impairs various cell processes, leading to systemic manifestations –> HEMATEMESIS, HYPOVOLEMIC SHOCK, METABOLIC ACIDOSIS.

36
Q

What is the treatment for TCA and Aspirin overdose?

A

Sodium Bicarb

Works because the SODIUM LOAD will alleviate depressant action on MYOCARDIAL SODIUM CHANNELS.

GIVE sodium bicarb when the QRS > 100msec! in the setting of TCA overdose.

37
Q

What is given to someone with prolonged QT?

A

Mag Sulfate

38
Q

What is the treatment for lithium toxicity?

A

Hemodialysis.

It is the most dialyzable toxin.

39
Q

Lead poisoning treatment options

A

Oral Succimer - mild to moderate late poisoning

Calcium EDTA - Moderate to SEVERE lead poisoning

Dimercaperol –> used to increase the urinary and FECAL excretion of lead

40
Q

What is used for acetaminophen toxicity?

A

N-Acetylcysteine.

Works by restoring GLUTATHIONE.. which then metabolizes acetaminophens toxic metaboline, N-acetyl-p-benzoquine imine (NAPQI) to nontoxic metabolites.

41
Q

Methanol poisoning symptoms?

A

Same as alcohol at first.. then 24 hours later –>

  1. headache / nausea / vomiting
  2. epigastric pain
  3. VISION LOSS –> seen as OPTIC DISC HYPEREMIA at first
  4. COMA

ANION GAP METABOLIC ACIDOSIS

42
Q

Methemoglobinemia can occur from exposure to what substances?

A

Oxidizing substances ( DAPSONE, NITRITES, Local / topical ANESTHETICS)

Clinical exam:

  1. Cyanosis
  2. Pulse ox around 85%
  3. Dark Choclate colored blood

Lab findings:
Saturation gap –> 5% difference between oxygne saturation on pulse ox and ABG.

NORMAL PaO2!!

can cause seizures, respiratory depression and death.

Iron goes from (normal) Ferrous (Fe2+) —> Oxidized FERRIC (Fe3+) –> Acute Methemoglobinemia.

Ferric iron CANNOT bind oxygen –> increased oxygne afinity in ferrous sites –> PREVENTS O2 release to PERIPHEAL TISSUES (DECREASED OXYGEN DELIVERY)… LEFT SHIFT

on labs they will show PULSE OX of 85.. because the METHEMOGLOBIN aborbs light at a DIFFERENT WAVELENGHT.. thus regardless of the actual saturation it will alwasy show 85%.

conversly.. ABG only analyzes UNBOUND O2.. and thus shows a falesly elevated O2 (normal PaO2).. even though it shouldnt.

Co-Oximetry test –> can distinguish between Hemoglobin, Methemogloin and Carboxyhemoglobin. it can be used to confirm the diagnosis.

43
Q

What is the treatment for Methemoglobinemia and how does it work?

A

Methylene BLUE.

Methylene Blue is an ELECTRON ACCEPTOR for NADPH –> this is then turned into LEUCOmethylene blue which then REDUCES METHEMOGLOBIN TO HEMOGLOBIN.

High Dose VItamin C (ascorbic acid) can be used as a reducing agent when methylene blue is unavailable or contraindicated (G6PD deficiency)

44
Q

what do you give someone who overdoses on BB or CCBs?

A

GLUCAGON!

Activates Adenylate Cyclase –> increases INTRACELLULAR CALCIUM and improves CARDIAC contractility.

45
Q

organophosphate toxicity is caused by blockage of Achesterase inhibitors and thus lots of Ach.

What is given to stop this?

A

Pralidoxime + Atropine.

Pralidoxime reactiveates the CHOLINESTERASE ENzyme.

46
Q

Caustic ingestion.. what are the next steps?

A
  1. Secure Airway, Breathing, Circulation
  2. Decontamination - remove containated clothing and visible chemicals. Irrigate exposed skin
  3. CXR if resp symptoms
  4. ENDOSCOPY within 24 hrs!
47
Q

What is the pathophys of fever vs heat stroke?

A

Fever - Cytokine activation during inflammation. Temps usually under 104. Fever results from the thermoregulatorsy centers temporary upregulation of body temp (regulated in The HYPOTHALAMUS)

Heat stroke - failure of the body to THERMOREGULATE.. cannot DISSIPATE HEAT when the humidity is over 75% and temp is elevated Temp above 104. RHABDO –> end organ damage.
Blood but no RBCs on urine dipstick.

48
Q

what are the features of hypothermia and what is the treatment?

A

Mild –> Tachycardia and Tachypnea, ATAXIA, INCRASED SHIVERING.

Moderate –> BRADYCARDIA, lethargy, HYPOVENTILATION, DECREASED shivering.

SEVERE (below 82F) –> COMA, CARDIOVASCULAR COLLAPSE, vetricular ARRHYTMIAS

Moderate hypothermia treatment –> active EXTERNAL REwarming (warm blankets / heating pads / warm bath)

SEVER hypothermia treatment –> Active INTERNAL rewarming (warmed pleural or peritoneal irrigation, warmed humidified oxygen)

Atropine and Pacers will not help the bradycardia in hypothermia. THe bradycardia will improve when you treat the hypothermia.

49
Q

Carbon monoxide poisoning symptoms and treatment

A

Symptoms - headaches, nausea, vomiting, abdominal discomfort, confusion and coma.

PINKISH RED SKIN HUE.

Diagnosis is established by obtaining CARBOXYHEMOGLOBIN levels.

Treatment - HYPERBARAIC oxygen

50
Q

Arsenic poisoning symptoms?

A

GARLIC breath, vomiting, diarrhea, QTc Prolongation

HYPO/HPERpigmentation, HYPERKERATOSIS, STOCKING - GLOVE pattern neuropathy.

Treatment = DIMERCAPEROL (British anti-lewisite).

DMSA (Meso-2,3-dimercaptosuccinic acid, succimer).

found in PRESSURE TREATED WOOD, Pesticides, contaminated water (often from wells)

DISRUPTS CELLULAR RESPIRATION and GLUCONEOGENESIS.

Severe toxicity –> PANCYTOPENIA and HEPATITIS

51
Q

Slurred speech + Unsteady gait + Drowziness + NORMAL VITALS + NORMAL PUPILLARY SIZE (2-4mm in bright light) suggests what?

A

BENZO OVERDOSE!!!

they will NOT have resp depression or hypotension or any of that.

52
Q

Tremor + Hyperreflexia + ataxia + Seizures + Vomiting + Diarrhea

A

LITHIUM TOX

53
Q

Can you confirm the diagnosis of lead poisoning with Capillary (fingerstick) blood specimens?

A

NO.

These have very high false postive rates.

If capillary led level is elevated (>5 micrograms / dl) then MUST CONFIRM with VENOUS LEAD measurment.

54
Q

what shold patients with confirme lead poisoning be screened for ?

A

Iron Deficiency.

Give them ORAL FERROUS SULFATE if they have a deficiency.

Co-morbid iron deficiency can increase GI absorption of lead.

55
Q

what is seen on peripheral smear of patients with lead poisoning?

A

BASOPHILIC STIPPLING.

will also see HYPERURICEMIA (due to impaired purine metabolism)

56
Q

what is the treatment for Acetaminophen Intoxication?

A

Can be ASYMPTOMATIC the first 24 hrs.. and then turn into SEVERE liver injury.

Initial Management –> gastric DECONTAMINATION with ACTIVATED CHARCOAL if the patient presents WITHIN 4 hours of ingestion.

OBtain ACETAMINOPHEN levels at the same time.

After this use the NOMOGRAM to dictate N-ACETYLCYSTINE administration.

57
Q

what are the two products of combustion in enclosed spaces?

A

Carbon Monoxide

and

hydrogne CYANIDE (when foam, cotton paint, silk burn)

There is no rapid test for Cyanide toxicity.. so all patients should be treated EMPERICALLY with the antidotes –> HYDROXOCOBALAMIN or SODIUM THIOSULFATE or with Nitrites (to induce methemoglobinemia.. giving cyanide somethine else to bind to other than Hb)

Patients will develop cardiorespiratory arrest and PERMANENT neuro disability if not treated quickly.

58
Q

what is the most reliable and predictive sign of Opioid Intoxication?

A

Decreased Resp Rate

59
Q

Dry Mouth / Skin + Blurry vision / Mydriasis + Hyperthermia + RED skin + Urinary Retention + Decreased bowel sounds.

what is diagnosis and what is treatment?

A

Anticholinergic toxicity.

Treatment = PHYSOSTIGMINE (cholinesterase inhibitor)

60
Q

What kind of stones do you see in ethylene glycol poisoning?

A

Calcium oxalate crystals

Ethylene glycol –> oxalic acid and glycolic acid. Glycolic acid damages kidney tubules.. and oxalic acid binds calicum and forms stones.

61
Q

Visual blurring, central scotoma, afferent pupillary defect, altered mentation are all seen in intoxication with what substance?

A

Methanol