UWorld Neuro

Question 1

What is the treatmetn & MOA for status epilepticus?

Answer 1

IV benzodiazepine

enhave the effect of GABA at GABA-A receptor, which causes increased influx of Cl-, leading to hyperpolarization of postsynaptic neuron

Question 2

What is the MOA of lidocaine?

Has the greatest effect on what type of nerve?

Answer 2

blocking sodium channels in the neuronal cell membrane, preventing depolarization

greatest effect on small, myelinated nerves (pain & temp)

Question 3

What condition is expected with elevated AFP is detected in utero?

Answer 3

open neuraltube defect

d/t failure of primary neurulation

Question 4

What are the MC antibodies detected in the serum of a patient with paraneoplastic cerebellar degeneration?

They primarily attack what cell type?

Answer 4

Anti-yo, anti-P/Q, anti-Hu

purkinje cells

Question 5

Mutation seen in myotonic dystrophy type 1?

What cell types are most affected?

Answer 5

CTG repeat - leading to accumulation of hairpin RNAs

accumulates most in non-dividing cells (skeletal & cardiac muscle, brain)

Question 6

What type of drug is chlorpheniramine?

MOA?

Answer 6

first generation anti-histamine

blocks peripheral & central H1 receptors

Question 7

What type of drug is loratadine?

MOA?

Answer 7

second generation anti-histamine

blocks peripheral H1 receptors

Question 8

What is the probable diagnosis of a patient who is slow to wake up after receiving succinylcholine?

Answer 8

pseudocholinesterase deficience

genetic polymorphism in BCHE gene

Question 9

What is the gross appearance of a glioblastoma?

Answer 9

typically located in the cerebral hemisphere

soft, poorly defined, with areas of necrosis & hemorrhage

Question 10

What psychologic adverse effect can be caused by over the counter allergy medications?

Answer 10

delirium

Question 11

What are the findings seen in TB meningitis?

Answer 11

thick, gelatinous exudate most prominent in the basal portion of the brain

vasculitis of the cerebral arteries that can cause multiple bilateral brain infarctions

hydrocephalus d/t obstruction of CSF outflow by tubercular proteins

Question 12

What are the “3 ds” of botulism intoxication?

Answer 12

diplopia, dysphagia, dysphonia

Question 13

What is the key point in determinig decerebate vs decorticate posture?

Answer 13

red nucleus (rostral midbrain)

above the RN: decorticate (flexing)

below the RN: decerebate (extension) - d/t loss of rubrospinal tract- which causes excitation to upper limb flexors & unopposed vestibulospinal tract output, which causes extension

Question 14

What would you expect to see upon histopathological examination of a patient with HIV-associated dementia?

Answer 14

microglial nodules & multinucleated giant cells

Question 15

What are the mutations associated with early-onset Alzheimer’s disease?

Late-onset?

Answer 15

• early-onset
  
  • amyloid precursor protein (APP) chromosome 2
  • presenilin 1 on chromosome 14
  • presenilin 2 on chromosome 1
• late-onset
  
  • epsilon 4 of apolipoprotein A

Question 16

What chromsomal abnormality is most commonly associated with holoprosencephaly?

Answer 16

incomplete separation of the cerebral hemispheres & has one lateral ventricle

trisomy 13 (patau syndrome)

Question 17

Function of the suprachiasmatic nucleus hypothalamic nucleus?

Answer 17

circadian rhythm & pineal gland function

Question 18

Function of the ventromedial nucleus hypothalamic nucleus?

Answer 18

mediates satiety - desrtuction leads to hyperphagia

Question 19

Function of the lateral nucleus hypothalamic nucleus?

Answer 19

mediates hunger- destruction leads to anorexia

Question 20

Function of the anterior nucleus hypothalamic nucleus?

Answer 20

mediates heat dissipation- destruction leads to hyperthermia

Question 21

Function of the posterior nucleus hypothalamic nucleus?

Answer 21

mediates heat conservation - destruction leads to hypothermia

Question 22

Function of the arcuate nucleus hypothalamic nucleus?

Answer 22

secretion of dopamine (inhibits prolactin), GHRH

Question 23

Function of the medial preoptic nucleus hypothalamic nucleus?

Answer 23

secretion GnRH, regulates sexual behavior

Question 24

Function of the paraventricular nucleus hypothalamic nucleus?

Answer 24

secretion of oxytocin, CRH, TRH, small amounts of ADH

Question 25

Function of the supraoptic nucleus hypothalamic nucleus?

Answer 25

secretion of ADH, small amounts of oxytocin

Question 26

What is the role of glutamate in ischemic neuron death?

Answer 26

within minutes of ischemia, neurons depolarize d/t depletion of ATP

this causes exocytosis of glutamate - activating the NMDA-glutamate receptor which causes an influx of calcium into the cell

this overwhelms the cell & causes mitochondrial dysfunction, free radical formation, & calcium dependent protease activation

Question 27

How is diagnosis of cryptococcus meningitis commonly made?

Answer 27

latex agglutination test for soluble polysaccharide antigen

Question 28

AE of succinylcholine?

MOA?

Answer 28

malignant hyperthermia

severe hyperkalemia

bradycardia

MOA: attaches to nicotinic acetylcholine receptor (nAChR) and depolarizes the neuromuscular end plate - resulting in flaccid paralysis

Question 29

What drug can be use to treat spactisity in patients with cerebral palsy?

Answer 29

benzodiazepines & baclofen

b/c it can be caused by white matter necrosis which leads to loss of descending inhibitory control

this can be improved by CNS inhibitory neurotransmitters - GABA A via benzos & GABA B via baclofen

Question 30

How does the solubility of an anesthetic in peripheral tissue influesnce its onset of action?

Answer 30

if tissue solubility is high, then a lot of the drug will be taken up from the arterial blood, creating a large A/V gradient

therefore, saturation of the blood requires more anesthetic, and since blood saturation takes longer, brain saturation is also delayed

so- inhaled anesthetics w/ high a/v gradients have a slower onset of action

Question 31

The musculocutaneous nerve innervates what muscles?

never roots?

It terminates as what arm?

Answer 31

5-7

coracobrachialis

elbow flexors (biceps brachii, bracialis)

continues course as lateral cutaneous nerve of the forearm and provides innervation to the skin of the lateral forearm

Question 32

Presumptive diagnosis of a patient with nonrhythmic eye movements and involuntary jerking movements of the trunk and limbs (opsoclonus-myoclonus syndrome) and a firm abdominal mass under the age of 2?

expected lab results to confirm diagnosis?

Answer 32

neuroblastoma

MC extracranial solid neoplasm of childhood & arises from neural crest cells in the adrenal medulla or sympathetic ganglion

elevated catecholamine metabolites (HVA, VMA), small blue round cells & Horner Wright rosettes & N-myc amlification (poor prognosis)

Question 33

How does the histology of a neuron change in the occurance of acute irreversible injury (ie. ischemia, seere hypoglycemia) compared to extensive axonal damage?

Answer 33

• acute irreversible injury
  
  • 12-24 hrs post event
  • shrunken cells separating from the tissue
  • pyknotic nucleus
  • loss of basophilic Nissl bodies (so, very red staining cytoplasm)
• axonal injury
  
  • cell body swelling
  • movement of the nucleus to the periphery
  • dispersion of Nissl bodies

Question 34

Surgical targets for Parkinson’s treatment?

Answer 34

subthalamic nucleus

globus pallidus interna

Question 35

chronic axonal injury or inflammation (as occurs w/ neuroma) results in upregulation of what type of ion channel?

Answer 35

sodium

increase nociceptive (pain) sensitivty

Question 36

What enzyme is affected in methylmalonic acidemia?

Biochemical results of this mutation?

Symptoms/Presentation?

Answer 36

methylmalonyl-CoA mutase

results in build up of methylmalonic acid & proprionic acid, leading to a metabolic acidosis; the increased metabolic rate leads to hypoglycemia and direct toxic inhibition of gluconeogenesis by the organic acids- this promotes ketone metabolism (increaseing the anion gap acidosis)

The organic acids also inhibit the urea cycle, leading to hyperammonemia

Symptoms: metabolic anion gap acidosis, hypoglycemia, ketosis, hyperammonemia (hypotonia, lethargy, vomiting, respiratory distress in neonatal period)