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Non-Negotiables > B&B Test 2 > Flashcards

B&B Test 2 Flashcards

1
Q

What is special about alpha-2 receptors?

A

They are presynaptic autoreceptors

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2
Q

What effect do parasympathetics have on most blood vessels?

A

None

exception: M receptors on endothelial cells–>NO release–> vasodilation

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3
Q

What is generally under sympathetic control? (at rest) (2 things)

A

Sweat glands and arterioles

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4
Q

How can we increase outflow of aqueous humor?

A

alpha agonist or muscarinic agonist

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5
Q

How can we decrease secretion of aqueous humor?

A

Beta blocker

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6
Q

What is the principle CNS integration center for the ANS?

A

Hypothalamus

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7
Q

What does the anterior hypothalamus control as far as PNS goes? Posterior?

A

Anterior- Cholinergic (sweat glands + PS)

Posterior- Adrenal (sympathetic)

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8
Q

What type of bladder dysfunction with:

1) Cortex/ hypothalamus lesion
2) Between pons and lumbar SC
3) Sacral SC or cauda equina

A

1) Infantile (uninhibited) bladder
2) UMN- spastic bladder with hyperreflexia, no voluntary control, cystitis due to incomplete empty
3) LMN- flaccid bladder, arreflexic, severe retention that can cause renal damage

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9
Q

Where is COX-1 expressed?

A

Almost all cells

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10
Q

Where is COX-2 expressed

A

Only expressed in inflammation

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11
Q

What does aspirin decrease? What type of cells produce it?

A

TXA2, Platelets

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12
Q

Equilibration time definition

A

Time at which the alveolar concentration equals the inhaled concentration

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13
Q

How do inhaled anesthetics probably work?

A

Ligand gated ion channels (probably GABA?)

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14
Q

MAC definition

A

Equilibrium concentration required to prevent movement to skin incision at 1 ATM in 50% of patients

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15
Q

What do NMBDs cause? What do they not cause?

A

Cause paralysis, not anesthesia

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16
Q

What subunits of nicotinic receptors bind ACh

A

Only alpha subunits

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17
Q

What is the only used depolarizing muscle relaxant?

A

Succinylcholine

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18
Q

What receptors does succinylcholine stimulate?

A

ALL ACh receptors

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19
Q

Who do we not use Sch in? How is it broken down?

A

Pediatrics (undiagnosed myopathies, hyperkalemia)

Pseudocholinesterase in plasma

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20
Q
  • curium (suffix)

- curonium (suffix)

A

Benzylisoquinolines
Steroidal
(Both non-depolarizing NMDB)

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21
Q

What reverses non-depolarizing NMDBs? What do we give with it and why?

A 
AChE inhibitors (neostigmine)
WE give atropine or glycopyrollate to avoid muscarinic side effects
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22
Q

What causes the termination of effects in most IV anesthetics?

A

Distribution (as opposed to metabolism and elimination)

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23
Q

What IV anesthetic is best at protecting the brain from hypoxic/ischemic damage?

A

Thiopental (barbituate)

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24
Q

What are the best amnestic agents?

A

Benzodiazepines

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25
Q

What are opiods good at? What are they bad at?

A

Opiods are analgesics with some hypnotic action, but are not good for amnesia

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26
Q

What is the shortest acting opiod? What is significant about it?

A

Remfentanil, it is terminated by elimination

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27
Q

What can remfentanil cause?

A

Acute tolerance to other opiods

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28
Q

What is the mechanism of ketamine? What is it good at?

A

Non-competitive NMDA antagonist that is very good at analgesia (relatively complete anesthetic agent)

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29
Q

What drug is best when hemodynamic stability is a must?

A

Etomidate

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30
Q

What is the mechanism of dexmedetomidine?

A

Alpha-2 agonist

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31
Q

What is the most common cause of acute liver failure in the US?

A

Acetominophen toxicity

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32
Q

What is the basis of acetaminophen toxicity?

A

Liver metabolism (NAPQI formed when p450 metabolizes it)

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33
Q

What must you do as pretreatment for NAC?

A

Antihistamines and steroids to prevent anaphylaxis

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34
Q

How do you decide who to treat for acetaminophen toxicity? What is it and what are its limitations?

A 
Rumack Nomogram (APAP vs. Time graph)
Limitations include limited to single ingestions within 24 hours of OD and doesn't account for inducing drugs
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35
Q

What does use dependent block describe?

A

Local anesthetics preferably working on active nerves

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36
Q

What does the duration of local anesthetics depend on?

A

potency and lipid solubility

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37
Q

List the absorption spectrum for local anesthetics of the following:
Brachial plexus, Epidural, IV, Intercostal, Paracervical, Sciatic, subcutaneous, tracheal

A

IV>tracheal>Intercostal>paracervical>epidural>brachial plexus> sciatic> subcutaneous

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38
Q

What helps that action of LAs by decreasing absorption and increasing neural uptake?

A

Vasoconstrictors

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39
Q

Result if LA is injected directly into muscle?

A

Myotoxicity

40
Q

Eating nonfood, non-nutritional substances (ex. ice, chalk)

A

Pica

41
Q

Repeated regurgitation of food not due to a medical problem

A

Rumination disorder

42
Q

Lack of interest in food

A

Avoidant food intake

43
Q

Intense fear of gaining weight and behavior that causes it. Can be associated with amenorrhea, lanugo hair, and keratitis

A

Anorexia Nervosa

44
Q

Binge-Purge-Binge-Purge-Binge-Purge

A

Bulimia Nervosa

45
Q

What are symptoms of bulimia?

A

more cavities, acid reflux, Russel’s sign, enlarged salivary glands

46
Q

Lack of control of eating large quantities of food

A

Binge eating disorder

47
Q

What are complications of AN and BN caused by?

A

AN- Starvation and weight loss

BN- Frequency and type of purging

48
Q

Cardiac complications of AN and BN

A

AN: Bradycardia, hypotension, atrophy
BN: Normal HR, arrhythmias secondary to electrolyte imbalances

49
Q

What are two big hints for AN? What is the electrolyte status?

A

Osteoporosis and amenorrhea with normal electrolyte levels

50
Q

Hypokalemia in young, healthy women is a very specific sign for what?

A

Bulimia Nervosa

51
Q

Lateralized pain that is dull and deep, aura, photo/phonophobia?

A

Migraine

52
Q

How do we treat migraines? Prevention?

A

Treat with excedrin or triptans

Prevent with Calcium blockers, beta blockers or TCA

53
Q

Repetitive headache with times of remission described as sharp, stabbing pain. Ipsilateral pain and horner’s like problems, yet patients choose to stay active

A

Cluster headaches

54
Q

How do we treat cluster headaches?

A

100% oxygen

55
Q

What is the DOC for tension headaches?

A

NSAIDs

56
Q

What do you suspect with visual loss, weight loss, jaw/arm claudication? What do you do?

A

Temporal arteritis. Temporal artery biopsy, start steroids

57
Q

What age group is susceptible to temporal arteritis?

A

> 50

58
Q

Otoliths into semicircular canal

A

Benign positional vertigo

59
Q

Describe the path of the vestibule-ocular reflex.

A

Vestibular nucleus–> CN6–> MLF–> CN 3,4

60
Q

How does the direction of endolymph flow relate to tracking direction, nystagmus direction?

A

Tracking direction is the same, nystagmus direction is the opposite

61
Q

What can compress CN7 and CN8 and where?

A

Acoustic neuroma (schwannoma) in the internal auditory meatus

62
Q

When is ADHD diagnosed? More males or females?

A

School-age, more males

63
Q

What is the strongest evidence for the cause of ADHD?

A

NE neurons in locus coeruleus

64
Q

How many sx must be present in people up to 16? After?

A

6, 5

65
Q

What are the four required characteristics of ADHD?

A

1) Sx before age 12
2) Interfere with functioning
3) Occur in more than one setting
4) Does not only occur with other disorders

66
Q

What would you suspect if a child with ADHD becomes irritable or hyperactive all of the sudden?

A

rebound effect as the drugs are wearing off

67
Q

How much louder in decibels is a sound that is 10x louder? 100x?

A

db=20log(x)
10x= 20
100x=40

68
Q

How does a low force sound wave on the tympanic membrane cause a large enough force on the oval window?

A

Impedence matching

69
Q

What are the two muscles that protect from hyperacusis? What innervation?

A

1) Stapedius- CN7

2) Tensor Tympani- CN5

70
Q

What would you suspect with a patient that has ear pain with changes in pressure such as flying or scuba diving?

A

Perilymph fistula (leakage)

71
Q

What two distinguishing factors will you see on brain sections of a patient with prions?

A

1) Amyloid plaques

2) Spongiform changes and neuron loss

72
Q

How can prion be transmitted?

A

Sporadic, mutations, ingestion or inoculation of contaminated material

73
Q

How do you diagnose Prion disease?

A

Western blot of tonsil biopsy, brain biopsy

74
Q

Viral encephalitis characterized by hydrophobia

A

Rabies

75
Q

What would you suspect with Negri bodies?

A

Rabies

76
Q

What is another way to diagnose rabies besides brain biopsy?

A

DFA- Direct fluorescent antibody with the nape of the neck

77
Q

How do we treat rabies?

A

Rabies Ig, Post-exposure vaccination

78
Q

What four families of virus fit in arbovirus? Exceptions?

A

1) Togavirus (rubella)
2) Flavivirus
3) Bunyavirus (not hantavirus)
4) Reovirus (not rotavirus)

79
Q

What causes the sudden fever associated with arboviruses?

A

RNA viruses elicit a massive IFN response

80
Q

Are arboviruses enveloped or non enveloped. Exception?

A

Enveloped with the exception of Colorado Tick Fever

81
Q

Subgenomic RNA

A

Togavirus

82
Q

Polyprotein

A

Flavivirus

83
Q

Transovarial Transmission

A

Bunyavirus

84
Q

Segmented, negative-sense RNA

A

Bunyavirus

85
Q

Are arboviruses seasonal?

A

Yes, summer and early fall

86
Q

What do you do upon suspicion of viral encephalitis?

A

Give acyclovir (in case it is herpes)

87
Q

Will you always see virus in the blood?

A

No, viremia is transient and only at the early stages of the disease

88
Q

What is the most important arboviral concern to human health?

A

Dengue Virus

89
Q

When should you suspect Dengue? Diagnostic test?

A

Anyone with fever who has travelled to the tropics. Tourniquet test

90
Q

What is the significance of multiple serotypes of Dengue? How many?

A

5 serotypes and it is thought that reinfection leads to more severe disease

91
Q

Why would reinfection lead to more severe disease with Dengue?

A

Antibody-Dependednt Enhancement, antibodies that do not neutralize virus just mark it for dendritic cell and macrophage uptake, which is the target of the virus anyway.

92
Q

How do we treat Dengue?

A

We have no treatment. Mosquito eradication

93
Q

How do we treat tetanus?

A

Tetanus booster, DEBRIDEMENT, Toxin Ig, antibiotic

94
Q

Compare the mortality of infant tetanus and botulism.

A

Tetanus ~90%

Botulism ~1-2%

95
Q

What type of nerve infection do we often see in botulism?

A

Cranial Nerves!!!!

96
Q

How do we treat botulism?

A

HBAT (equine heptavalent botulism anti toxin) ALWAYS CHECK FOR ALLERGIES

Non-Negotiables (4 decks)

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