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Test reviews DEDICATED > Sun jul 26 > Flashcards

Sun jul 26 Flashcards

1
Q

which receptor causes the rewarding effects of nicotine?

A

The alpha4Beta2 nicotinic receptor in the CNS -leads to release of dopamine

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2
Q

is varenicline a full or partial agonist?

A

Partial

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3
Q

Varenicline MOA for quitting smoking

A

Partial agonist at nicotinic receptors- reduces symptoms of withdrawal and attenuates the rewarding effects of nicotine

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4
Q

why is cranially nerve IV susceptible to injury?

A

it has a long course

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5
Q

what is the function of CN IV?

A

Innervate the Superior Oblique - eye internally rotates and depresses while adducted

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6
Q

when will the gaze be impmaired in someone with a CN IV injury?

A

when they look down and towards the nose (up-close reading, walking downstairs)

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7
Q

are most DNA virus’s ds or ss?

A

DS

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8
Q

which DNA virus is ss?

A

parvovirus

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9
Q

which ds DNA viruses are enveloped?

A
  • Hepadna (hep B)
  • Herpes (VSV, HSV)
  • Poxvirus
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10
Q

which ds DNA viruses are naked?

A

Adenovirus
Papova (HPV)
Polyoma (JC and BK)

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11
Q

S100 is found in which cells?

A

Cells that derived from the neural crest

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12
Q

what type of tumours will stain positive for HMB45?

A

Melanomas- HMB45 is a MAB against melanosomes

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13
Q

what type of inflammatory response is erythema multiforme?

A

cell-mediated - CD8 lymphocytes

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14
Q

which infections is erythema multiforme associated with?

A

HSV and mycoplasma

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15
Q

how does O2 supplementation lead to oxygen-induced hypercapnia?

A

Areas with poor ventilation lead to shunting of blood to other areas. When O2 is given, the shunting is reversed and blood is taken away from the areas that have adequate respiration, leading to increased physiologic daed space and V/Q mismatch

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16
Q

what causes a charcot bouchard aneurysm rupture?

A

chronic hypertension

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17
Q

where are charcot bouchard aneurysms in the brain?

A

Deep brain structures -basal ganglia, cerebellum, pons, etc.

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18
Q

what is the most common cause of spontaneous lobar hemorage?

A

Amyloid angiopathy

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19
Q

explain the pathophys of cerebral amyloid angiopathy?

A

B amyloid deposits in the walls of small and medium sized cerebral arteries, leading to weaking and proness to rupture

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20
Q

Presentation of pancoast tumour

A
  • Horners syndrome
  • shoulder pain
  • upper limb parasthesias
  • arereflix arm weakness (brachial plexus compression)
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21
Q

why does vincristine lead to neurotoxicity and peripheral neuropathy?

A

It interferes wiht microtubule formation in nerve axons

22
Q

MOA of vinca alkaloids?

A

inhibit microtubule polymerization

23
Q

complications of Sjogrens syndrome?

A
  • corneal damage
  • dental carries
  • non-hodgkin lymphoma
24
Q

what should you give to someone who overdose on salicylate (aspirin)?

A

Na bicarb

25
Q

how does Na bicarb treat salicylate overdose?

A
  1. acts as a base and binds free H in the blood, and converts salicylate to the ionized form - preventing it from moving into tissue
  2. alkalinizes the urine, increasing the excretion of salicylate
26
Q

what causes gigantism?

A

oversecretion of IGF-1 from the liver

27
Q

what is dofelitide?

A

a class III antiarythmic

28
Q

MOA of class III antiarhytmics?

A

predominantly block the K channels in non pacemaker cells, inhibiting the outward current during phase III and thus prolonging repolarization

29
Q

which areas are known for chloroquine resistant strains of malaria?

A

Africa and Asia

30
Q

If someone aquires malaria from Africa, what should you treat them with?

A

Atovaquone-proguanil or artemisians (likely chloroquine resistant)

31
Q

which enzyme of the TCA cycle requires FAD?

A

Succinate dehydrogenase

32
Q

What does succinate dehydrogenase do?

A

Converts succinate to fumarate

33
Q

which enzyme of the TCA cyle requires GDP?

A

succinyl-coa synthetase

34
Q

what does succinyl-coa synthetase do?

A

converts succinyl-coa to succinate

35
Q

the conversion of malate to oxaloacete by malate dehydrogenase requires…

A

NADH

36
Q

the conversion of oxaloacete to PEP requires…

A

GTP

37
Q

how do insulin levels normally change in response to exercise?

A

they would decrease during exercise - you begin glucose production

38
Q

what is abruptio placentae?

A

premature placental separation from the uterus

39
Q

risk factors for placental abruption?

A

hypertension, preeclampsia, cocaine or tobacco use, prior abruptio placento, abdomin trauma

40
Q

presentation of abruptio placentae?

A

sudden onset vaginal bleeding

  • abdominal pain
  • high frequency contractions
  • tender, firm uterus
41
Q

what is placenta accreta?

A

attachment of the placental villi onto the myometrium

42
Q

how does placenta accreta present?

A

Usually presents after the delivery of the baby wiht hemorhage and inability to remove the placenta

43
Q

which tracts degenerate in friederachs ataxia?

A
  • spinocerebellar
  • lateral corticospinal
  • dorsal columns
  • dorsal root ganglia
44
Q

inheritance of friedreichs ataxia?

A

autosomal recessive

45
Q

pathophys of friedreichs ataxia?

A

Increased GAA repeats due to a mutation in the frataxin gene which codes for a mitochondrial protein involved in the assembly of iron-sulfur enzymes.
Decreased mitochondrial activity leads to increased oxidative stress, and degeneration of the neural tracts and peripheral nerves

46
Q

what is charcot-marie-tooth disease?

A

AD disorder with dymelination of the peripheral nerves

47
Q

how may damage to the lateral prefrontal cortex present?

A

Difficulties with executive functions -motivation, organization, planning and purposeful action

48
Q

how may damage to the orbitofrontal cortex present?

A

personality changes, disinhibition and irritability

49
Q

how does damage to the subthalamic nucleus present?

A

contralateral hemiballismus

50
Q

what is uniparental disomy?

A

When someone receives two copies of a chromosome (or part of a chromosome) from one parent and none from the other

51
Q

what are cholesteatomas?

A

collections of squamous cell debris that form a round, pearly mass behind the tympanic membrane

52
Q

presentation of cholesteatomas?

A

Most commonly present as painless otorrhea.
Some produce lytic enzymes which damage the ossicles and lead to conductive hearing loss.
If it grows large enough it may erode the vestibular apparatus leading to vertigo, and can cause facial nerve palsies.

Test reviews DEDICATED (70 decks)

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