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Block 6 > Week 4 > Flashcards

Week 4 Flashcards

1
Q

NSAID and triptan is a better combo tx than NSAIDs by itself for what condition?

A
  1. migraine - acute treatment
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2
Q

Triptans
1. MOA
2. Uses

A
  1. 5-HT1b and 5-HT1d receptor agonists. These receptors are found on meningeal vessels (induce vasoconstriction and attenuates stretch at pain receptors), trigeminal nerve (to prevent release of vasoactive peptides), brainstem (inhibiting pain pathways)
  2. acute tx of migraines, prophylaxis of migrains, and tx of cluster headaches if combined with inhaled oxygen
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3
Q

Triptans
1. side effects

A
  1. coronary vasospasm (contraindicated in pts with angina)
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4
Q

Migraines can have prophylaxis treatment that is often triptans but also can be…(5)

A
  1. Calcium channel blockers
  2. beta blockers (propanolol, timolol, metoprolol)
  3. Valproid acid (antiepileptic)
  4. Topiramate (antiepileptic)
  5. TCAs
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5
Q

Gepants (ubrogepant, rimegepant)
1. what are these used for?
2. benefits?

A
  1. migraines
  2. these don’t have CV risks and overall less side effects
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6
Q

Ditans (lasmiditan)
1. what are these used for?
2. pros and cons?

A
  1. migraine tx
  2. doenst have CV risks but does have side effects of hallucinations
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7
Q

Ergot alkaloids (ergots)
1. what are these used for?
2. side effects?

A
  1. used only for infrequent, severe migraine attacks bc too much can cause overuse headache (can be sublingual, injected, or nasal spray)
  2. no specific 5-HT agonist so has more side effects -> trigger N/V, vasoconstriction, muscle pain
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8
Q

Tension type headache
1. tx for acute management

A
  1. NSAIDs and acetominophen
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9
Q

Tension type headache
1. tx for chronic headaches

A
  1. may consider amitriptyline (TCAs)
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10
Q

Tension type headache
1. What to avoid as tx?

A
  1. opioids and barbiturates -> can lead to development of tolerance and/or med overuse headaches
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11
Q

Migraine
1. location
2. description
3. duration

A
  1. unilateral (most common)
  2. crescendo, pulsating, aggravated by activity
  3. 4-72 hours
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12
Q

Migraines
1. associated sx
2. pt prefers?

A
  1. N/V, photophobia, phonophobia, aura
  2. prefers rest, dark, quiet

POUND (pulsing, one day, unilateral, Nausea, Disabling)

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13
Q

Tension Headache
1. location
2. description
3. duration

A
  1. bilateral (headband)
  2. pressure, tightness, waxes/wanes
  3. variable but less than 24 hrs ( can last 30min-several hours)
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14
Q

Tension Headaches
1. associated sx
2. pt prefers?

A
  1. muscular pain-neck
  2. can be active or rest
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15
Q

Cluster Headache
1. location
2. description
3. duration

A
  1. unilateral, near eye or temple
  2. starts and peaks in minutes, continuous, excruciation
  3. short duration
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16
Q

Cluster Headache
1. Associated sx
2. pt prefers?

A
  1. ipsilateral lacrimation, eye redness, congestion, rhinorrhea, eyelid edema, forehead and facial sweating, miosis and/or ptosis, restlessness
  2. can remain active
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17
Q

Signs and sx of migraine.
1. area of pain
2. how long does it last
3. worsens or no change with activity, sleep, noise, etc
4. Is there an aura?
5. Other sx

A
  1. unilateral pain that is pulsating - most often
  2. 4-72 hrs
  3. worsens with activity, photophobia, phonophobia
  4. Yes - precedes migraine
  5. Nausea and vomiting
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18
Q

What is cortical spreading depression?

A

waves of neuronal discharge (depolarization) move slowly along the brain cortex surface causing temporary impairment behind the spreading wave - this is what happens in migraine

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19
Q

What leads to pain in migraines? (pathophysiology)

A
  1. dura meningeal blood vessels dilate and activates perivascular sensory trigeminal afferents
  2. then sends impulses to the brain stem trigeminal caudalis nucleus
  3. vasoactive peptides are released which cause further vasodilation and neurogenic inflammation
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20
Q

How does acronym PIN help with dx of migraine

A
  1. Photophobia
  2. Impairment - interference with activity
  3. Nausea

2/3 = 81% prob but 3/3 is 93% prob

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21
Q

Trigeminal Autonomic Cephalalgias
1. What are the types? (5)

A
  1. Cluster Headache
  2. Paroxysmal Hemicrania
  3. Hemicrania Continua
  4. SUNCT and SUNA
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22
Q
  1. What medication is used to prevent cluster headaches?
  2. What about for acute treatment
A
  1. verapamil - Calcium channel blocker
  2. high rate of oxygen
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23
Q

Paroxysmal Hemicrania
1. location
2. duration

A
  1. severe unilateral orbital, supraorbital, and/or temporal pain
  2. 2-30 min (at least 20 attacks)
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24
Q

Paroxysmal Hemicrania and Hemicrania Continua
1. prevention medication

A
  1. indomethacin (NSAID)
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25
Q

Hemicrania continua
1. location
2. duration

A
  1. unilateral headache
  2. chronic and persistent
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26
Q

Trigeminal Neuralgia
1. What is it
2. what induces it
3. types

A
  1. recurrent violent attacks of unilateral facial pain in the distributions of the CN V (v2, v3 usually) - typically lasts 2 minutes
  2. stimuli like face washing, brushing teeth, shaving, etc
  3. classical (microvascular compression with changes in the nerve root), secondary (caused by underlying disease like tumor), idiopathic
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27
Q

Trigeminal Neuralgia
1. Med tx (4 but one general med type)

A
  1. carbamazepine or oxcarbezipine (anticonvulsant)
  2. Gabapentin (anticonvulsant)
  3. Lamotrigine (anticonvulsant)
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28
Q
  1. sudden onset of thunderclap type of headache and stiff neck can indicate what condition?
A
  1. subarachnoid hemorrhage
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29
Q
  1. acute headache with stiff neck, nausea, fever, and maybe thunderclap headache that goes down neck can be what condition?
A
  1. meningitis
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30
Q

Cell count in lumbar puncture
1. 10-10,000 WBC/hpf mostly PMNs -> what is most likely cause of meningitis (+ low glucose <40 mg/dl)
2. <200 cells mostly lymphocytes and RBCs -> what is most likely cause of meningitis (normal glucose levels)

A
  1. bacterial
  2. viral
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31
Q

Idiopathic intracranial hypertension
1. what is this
2. what causes this
3. tx with what
4. Commonly found in

A
  1. headache, blurry vision, pulsatile tinnitus, papilledema in eye
  2. CSF fluid pressure increases but normal composition
  3. Acetazolamide (diuretic and CA inhibitor)
  4. obese females of childbearing age
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32
Q

Benign Positional Paroxysmal Vertigo
1. pathophysiology
2. dx with
3. sx

A
  1. calcium debris in semicircular canals usually found in utricle and saccule are dislocated and found in the canals
  2. Dix Hallpike Maneuver (epley maneuver is what repositions the stones)
  3. vertigo with head turning or head position
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33
Q

What is the most common cause of vertigo

A

benign positional paroxysmal vertigo

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34
Q
  1. How to do the dix hallpike maneuver
  2. What is a positive or negative result
A
  1. Positive: nystagmus (horizontal and rotational go togehter and then there is also vertical)
  2. negative - no nystagmus
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35
Q

Vestibular Neuritis
1. What does this cause
2. pathophysiology
3. tx with

A
  1. prolonged vertigo
  2. inflammation of vestibular portion of CN VIII -> usually after viral or post inflammatory infection
  3. corticosteroids
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36
Q

Meniere’s Disease
1. Pathophysiology
2. sx
3. Tx

A
  1. excess fluid/endolymph accumulation and swelling of labyrinthe system
  2. tinnitus, sensorineural hearing loss, vertigo
  3. avoid high salt, avoid caffeine, diuretics
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37
Q

Acoustic neuroma- schwannoma
1. pathophysiology
2. What other disorder is it associated with?

A
  1. slow growing and benign tumor on CN VIII
  2. Neurofibromatosis type 2
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38
Q

What type of nystagmus is seen with peripheral vs central causes of vertigo

A
  1. Peripheral - horizontal/torsional
  2. Central - vertical nystagmus
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39
Q

In peripheral vs central causes of vertigo
1. which causes immediate vs delayed nystagmus while doing positional testing

A
  1. peripheral causes delayed nystagmus, nystagmus may fatigue with time + no other sx
  2. central causes immediate nystagmus + other sx include diplopia, skew deviation, ataxia, other CNS sx
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40
Q

Labyrinthitis
1. pathophysiology
2. is hearing loss involved?
3. tx?

A
  1. entire labyrinth is inflammed - canals, otoliths, and cochlear
  2. presents same ways as vestibular neuritis but WITH HEARING LOSS
  3. steroids
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41
Q

Vestibular neuritis
1. sx
2. hearing loss involved?
3. What can develop after?

A
  1. one severe prolonged episode of vertigo with n/v, no reoccurrence of vertigo
  2. no hearing loss
  3. can develop BPPV
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42
Q

BPPV, Vestibular Neuritis, Labyrinthitis, Meniere’s disease
1. which have hearing loss
2. Which have persistent vertigo

A
  1. Meniere’s and Labyrinthitis
  2. Vestibular neuritis, Labyrinthitis

BPPV has no hearing loss and is episodic

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43
Q

What are some causes to central vertigo?

A
  1. brainstem or cerebellar lesion
  2. Stroke/TIA
  3. cerebellar infarction/hemorrhage
  4. Tumors
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44
Q

Vestibulo-spinal reflex
1. What is it?
2. basic pathway starting with utricle and saccule (3)

A
  1. relays changes in gravity and linear forces to muscles of neck, thorax, and lower limbs (bracing for fall)
  2. Utricle/saccule send signals of linear accel and gravity to CN VIII
    -> send info to medial and lateral vestibular nuclei
    -> then send 2nd order neurons to anterior horn cells of cervical cord and entire spinal cord (for control of postural muscles)
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45
Q

Stroke involving what arteries would affect the cerebellum and its function in balance and avoiding vertigo

A
  1. PICA and AICA
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46
Q

What is the sunshine act?

A

Requires medical product manufaturers to disclose any payments or other transfers of value made to physicians or teaching hospitals

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47
Q

What is the stark laws?

A

Prohibit physicians from referring Medicare patients to clinical labs in which the physician had some financial relationship, including an ownership interest.

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48
Q

Aphthous ulcer (canker sore)
1. what age does it first start?
2. description
3. when do they arise?

A
  1. as a child <10 years old
  2. painful ulcer of oral mucosa + grayish base (granlulation tissue) surrounded by erythema
  3. in relation to stress and resolves spontaneously but often recurs
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49
Q

Oral Herpes
1. pathophysiology
2. at what age does infection first begin
3. description

A
  1. Usually due to HSV-1 infection - infection in childhood but then lesion heals but virus remains dormant in GANGLIA OF TRIGEMINAL NERVE
  2. 2-4 years old
  3. vesicles involving oral mucosa (usually lips-cold sore) that can rupture and cause a shallow, painful, red ulcer
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50
Q

Koplik Spots
1. description
2. what disease causes this?

A
  1. small red, irregular shaped lesions with blue-white centers
  2. measles (rubeiola)
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51
Q

Dental Caries
1. what bacteria causes caries?

A
  1. s. mutans, s. sobrinus, lactobacillus, etc
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52
Q

What is the difference between gingivitis and periodontitis?

A
  1. gingivitis - inflammation of the oral mucosa around teeth
  2. periodontitis - inflammation of tooth support structure
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53
Q

Irritation Fibroma
1. What is it?
2. Where is often found?

A
  1. soft tissue mass in the oral mucosa - inflammatory lesion covered by squamous epithelium
  2. buccal mucosa or lateral border of the tongue
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54
Q

Pyogenic Granuloma
1. What is it
2. What type of patients is it seen in?

A
  1. A nodular lesion caused by highly vascularized granulation tissue
  2. pregnant patients
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55
Q

Peripheral Ossifying Fibroma
1. what is it?

A
  1. What fibrous tissue with bone matrix or cementum
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56
Q

Peripheral Odontogenic Fibroma
1. What is it

A
  1. Gingival nodular mass that is collagen rich but does not involve bone although it can have dental lamina (remnants of tooth forming epithelium)
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57
Q

Periapical cyst
1. what is it?

A
  1. cyst around the root of a tooth - at times tx with a root canal
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58
Q

Odontogenic keratocyst
1. What is it and the location?

A
  1. cystic lesion usually located at the posterior jaw
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59
Q

Dentigerous cyst
1. What is it and where is it often found?

A
  1. cyst around the crown of usually 3rd premolar (wisdom tooth)
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60
Q

Ameloblastoma
1. what is it?
2. What does it look like on imaging?

A
  1. tumor of odontogenic epithelium
  2. soap bubble appearance
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61
Q

Odontoma
1. What is it?

A
  1. slow-growing, asymptomatic neoplasms found in jaws -> associated with impacted or unerupted teeth
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62
Q

Leukoplakia vs Erythroplakia
1. What do they look like
2. Risk or considerations for cancer

A
  1. Leukoplakia - white patches inside mouth that cannot be scraped away. They are considered pre-malignant so a bx is needed to rule out malignancy.
  2. Erythroplakia - red plaque (vascularized) that suggests new blood vessel growth -> highly suggestive of squamous dysplasia (SCC)
63
Q
  1. What is the most common form of oral cancer?
  2. What two things is it linked to?
A
  1. SCC
  2. abuse of tobacco and alochol but also linked to HPV
64
Q

Laryngeal papilloma
1. what is it
2. Risk factors
3. course

A
  1. benign papillary tumor of vocal cords
  2. HPV 6 and 11 (low risk for carcinoma)
  3. usually one single lesion in adults (multiple in children) - presents with hoarseness
65
Q

When do nasal polyps or vocal cord nodules occur?

A
  1. Nasal polyps- repeated bouts of rhinitis
  2. Vocal cord nodules - excessive use of vocal cords
66
Q

Nasopharyngeal Carcinoma (NK T cell lymphoma)
1. malignant or benign?
2. Risk factors
3. What location does it affect?
4. What markers are expressed?

A
  1. malignant
  2. EBV, african children and chinese adults
  3. Nasal passages
  4. The tumor harbors Epstein Barr virus (EBV) and shows expression of LMP-1 and EBNA-1, but lacks EBNA-2.
67
Q

Laryngeal Carcinoma
1. Type of cancer
2. risk factors
3. arises from

A
  1. SCC
  2. alcohol and tobacco
  3. arising from squamous epithelial lining of vocal cord
68
Q

Angiofibroma
1. benign or malignant?
2. what type of patient is this seen in?
3. Morphology
4. sx

A
  1. benign tumor nasal mucosa
  2. adolescent males
  3. large blood vessels and fibrous tissue
  4. profuse epistaxis
69
Q

Squamous papilloma
1. Risk factor (associated with)
2. type of patient this is seen in?

A
  1. HPV 6 and 11
  2. adults
70
Q

Ottitis Media
1. What can commonly cause this
2. What organisms can cause Chronic ottitis?

A
  1. most commonly viral (with serous exudate) but can have superimposed bacterial infections
  2. pseudomonas, staph aureus, fungus
71
Q

What is a cholesteatoma?

A
  1. abnormal collection of skin cells deep inside your ear - commonly associated with ottitis media
72
Q
  1. What is the common tumor of the ear
  2. where does it most often occur
A
  1. BCC
  2. pina of ear
73
Q

Branchial Cysti
1. where are they located
2. derived from what branchial arches

A
  1. neck regions - laterally
  2. 2nd and 3rd branchial arches
74
Q

Paragangliomas
1. What are they derived from?
2. where are they found
3. Structure in histology?

A
  1. Neuroendocrine tumors
  2. head and neck sites - most commonly the carotid body tumor
  3. Zellballen structure
75
Q

Xerostomia
1. sx
2. pathophysiology

A
  1. dry mouth
  2. due to failure of salivary secretion
  3. drug therapy is #1 cause but can be due to other things too
76
Q

Sialadenitis
1. what is it?

A
  1. inflammation of the salivary glands
77
Q

Sialolithiasis
1. What is it?
2. Can lead to infection with what

A
  1. obstruction of salivary glands due to stone formation
  2. Staph aureus
78
Q

Mucocele
1. What causes this?
2. How is ranula related to this?

A
  1. Blockage or rupture of salivary gland duct resulting in ductal dilation and mucous accumulation
  2. Ranula is a type of mucocele - blockage specifically of sublingual gland
79
Q
  1. What is the most common salivary gland neoplasm
  2. Histology: what does it contain?
A
  1. pleomorphic adenoma (generally a mixed tumor and is benign)
  2. contains both epithelial and mesenchymal elements. The mesenchyme-like background is usually loose myxoid tissue containing islands of cartilage and rarely, foci of bone.
80
Q

Pleomorphic adenoma
1. Common location
2. is it stationary or mobile
3. risk of turning malignant

A
  1. most commonly in parotid gland
  2. mobile
  3. rarely does - hint of its progression is signs of facial nerve damage
81
Q

Warthrin tumor
1. malignant or benign
2. common location
3. what is found in this tumor (cell makeup)

A
  1. benign
  2. 2nd most common tumor of salivary gland - almost always in parotid
  3. cystic tumor with lymph node tissue
82
Q

Mucoepidermoid Carcinoma
1. benign or malignant
2. common location
3. cell makeup

A
  1. malignant
  2. parotid (salivary gland) and involves the facial nerve often
  3. mucinous (low grade) and squamous cells (high grade)
83
Q

Adenoid cystic carcinoma
1. benign or malignat
2. where does it affect

A
  1. malignant
  2. can affect major and minor salivary glands
84
Q

What does the superior olivary complex do for hearing?

A
  1. Where brain localizes sound
85
Q

The superior olivary complex for hearing has two parts (medial and lateral superior olive)
1. What is the purpose of each one

A
  1. MSO – determines where the noise is coming from
  2. LSO (excitatory) - (along with MNTB - inhibitory) are essential for determining sound intensity
86
Q

Human ear can detect frequencies from what Hz range?

A
  1. 20-20,000 Hz
87
Q

What is conductive vs sensorineural loss?

A
  1. conductive - when sounds cannot get through the outer and middler ear
  2. sensorineural - when there is damage to the inner ear (the structures of your inner ear or auditory nerve)
88
Q

Sudden Sensorineural Hearing Loss (SSHL)
1. what does it present as
2. Causes?

A
  1. sudden loss over a 3 day period of at least 30 dB, and 3 contiguous frequencies
  2. idiopathic, vascular, infections, neoplasm, ototoxic, trauma
89
Q
  1. What are the three common causes of hearing loss in pediatrics?
  2. For adults - 2 main ones but there can be more
A
  1. infections, neonatal expsoure (premature, intubation, etc), genetics
  2. Presbycusis (degeneration of inner ear structures over time), Loud noise/trauma (exposure to loud sounds or from short blast of loud noise)

adults: familial, autoimmune, toxicity, tumor, infection, ostosclerosis

90
Q

When the sound vibrations move the stapes onto the oval window what happens next?

A
  1. pushes on fluid in cochlea which moves to the end of the cochlea and comes back to be disseminated via the round window
  2. movement of fluid causes deflection of basilar membrane
91
Q

Basilar membrane is tonotopically organized
1. highest frequences are detected near [oval window or helicotrema/end of cochlea]
2. lowest frequencies are detected near [oval window or helicotrema/end of cochlea]

A
  1. oval window
  2. helicotrema
92
Q

What part of auditory pathway participate in sound localization?

A
  1. superior olivary nucleus
93
Q

What is the function of the maculas in the vestibular system

A

There are two (one of the utricle and one of the saccule)
1. Macula of utricle - detects horizontal acceleration
2. Macula of saccule - detects vertical acceleration

94
Q
  1. What is the function of the semicircular ducts
  2. What are they filled with
A
  1. detect rotational movement in the x, y, and z planes of motion
  2. endolymph
95
Q
  1. Where are ampulla of vestibular system found?
A
  1. bulges at the base of the semicricular ducts
96
Q

Otolith organs are made up of what two structures?

A
  1. Utricle and Saccule
97
Q

Neurofibromatosis Type I
1. Genetic mutation/inheritance pattern
2. What presentations can occur (7)
3. How many are needed for dx

A
  1. ## Autosomal dominant mutation in NF1 gene on chromosome 17 (or sporadic)
  2. Cafe au lait spots >= 6
  3. Neurofibromas >= 2 (benign tumors on cutaneous nerves)
  4. Axillary or inguinal freckles
  5. Optic gliomas
  6. Lisch Nodules >= 2
  7. Bone abnormalities
  8. ## First degree relative with NF1 mutation
  9. 2 out of 7
98
Q

Neurofibromatosis Type 1
1. What neurological manifestations can occur? (5)

A
  1. Learning disability
  2. Seizures
  3. Increased risk of CNS tumors
  4. Increase risk of rhabdomyosarcoma
  5. Vascular abnormalities
99
Q

Which is more common Neurofibromatosis Type 1 or Type 2?

A
  1. Type 1
100
Q

Neurofibromatosis Type 2
1. Genetic mutation/inheritance pattern
2. What manifestations occur? (3 general)

A
  1. ## Autosomal dominant mutation on NF2 gene on chrom 22
  2. Neurologic Lesions (benign nerve sheath tumors, spinal cord tumors, meningiomas bilateral schwannomas)
  3. Eye lesions (cataracts, retinal hamartomas, etc)
  4. Skin lesions (cutaneous tumors, skin plaques, subcut. tumors)
101
Q

Tuberous Sclerosis
1. Genetic mutation/inheritance pattern
2. What presentations can occur (4)

A
  1. ## Autosomal dominant mutation in TSC1 or TSC2 on chrom 9
  2. Ash leaf spots
  3. Angiofibroma (facial rash of small pink to hyperpigmented papules with malar or perioral distribution)
  4. Ungual fibromas (lumps that emerge from the nail folds, more common on feet than hands)
  5. Shagreen patch (flesh colored, flat to slightly elevated lesion with “pig skin” or “orange peel”)
102
Q

Tuberous Sclerosis
1. Neurological manifestations (2)

A
  1. CNS hamartomas -> lead to seizures
  2. Widespread tumor (cortex, lining of ventricles/ependyma, inter-ventricular foramen)
103
Q

Sturge Weber Syndrome
1. Genetic mutation/inheritance pattern
2. What presentations can occur (3)

A
  1. ## not inherited - mutation in GNAQ
  2. facial port wine stain
  3. Eye abnormalities (glaucoma)
  4. Leptomeningeal (pia and arachnoid) vascular malformation - capillary venous malformation on same side as port wine stain
104
Q

what is the difference between Type 1, Type 2, and Type 3 - Sturge-Weber Syndrome?

A
  1. Type 1 - angiomas present in skin of face and meninges
  2. Type 2 - only facial angioma
  3. Type 3 - only leptomeningeal angioma
105
Q

Von Hippel - Lindau Syndrome
1. Genetic mutation/inheritance pattern
2. What types of tumors can occur (4)

A
  1. ## Autosomal Dominant mutation in VHL gene on chromosome 3 + requires two hits
  2. Hemangioblastoma of the brain and spine
  3. Retinal capillary hemangioblastoma
  4. Clear cell renal cell carcinoma
  5. Pheochromocytomas
106
Q

Ataxia Telangiectasia
1. Genetic mutation/inheritance pattern
2. What presentations can occur (6)

A
  1. ## Autosomal recessive - deffective DNA repair mechanism (ATM genetic mutation)
  2. progressive cerebellar ataxia
  3. abnormal eye movements
  4. oculomotor apraxia (problems with voluntary horizontal eye movement)
  5. Cognitive impairment
  6. Telangiectasia of blood vessel on bulbar conjuctiva
  7. Telangiectasia on nose, face, and neck
107
Q

Primary CNS brain tumors are not that common but are more significant in…. (Blank)

A

Children <15 years old

108
Q
  1. [infratentorial/supratentorial] tumors are more common in children
  2. [infratentorial/supratentorial] tumors are more common in adults
A
  1. infratentorial
  2. supratentorial
109
Q

Why are CNS primary tumors not staged?

A

Because CNS tumors typically don’t spread beyond the brain

110
Q

Gliomas (tumors)
1. What are they derived from?
2. Diffuse types (4)
3. Localized types (2)

A
  1. glial cells
  2. Oligodendroglioma, Diffuse astrocytoma, Anaplastic astrocytoma, Glioblastoma
  3. Pilocytic astrocytoma, ependymoma,
111
Q

Oligodendroglioma
1. more common in which sex
2. diffuse or localized glioma
3. Where is it typically located?

A
  1. male adults
  2. diffuse
  3. Frontal lobe - tumor of white matter
112
Q

Oligodendroglioma
1. molecular markers that dx this? (2)
2. What does it look like microscopically (2)

A
  1. 1p/19Q co-deletion and IDH mutation
  2. round “fried egg” cells + chicken wire vasculature

extra: can also have cystic spaces and calcifications

113
Q

Diffuse Astrocytoma
1. diffuse or localized glioma
2. Where is it typically located?

A
  1. Diffused
  2. cerebral hemispheres, but also brainstem, spinal cord, and rarely in cerebellum
114
Q

Diffuse Astrocytoma
1. molecular markers
2. Histology shows what changes

A
  1. IDH mutations only
  2. Mild increase in cellulary + mild nuclear pleomorphism (diff sizes and shapes of tumor cells)
115
Q

Anaplastic Astrocytoma
1. diffuse or localized glioma
2. What histology changes are seen? (3)

A
  1. diffuse
  2. increased cellularity, pleomorphism, mitotic figures
116
Q

Glioblastoma
1. diffuse or localized gliomas
2. most common brain tumor in (Blank)
3. Where does it most often occur?

A
  1. diffuse
  2. adults
  3. cerebral cortex, often crossing corpus callosum (butterfly glioma)
117
Q

Glioblastoma
1. Histology changes (2)

A
  1. Necrosis (can cause pseudopalisading)
  2. vascular endothelial proliferation
118
Q

Pilocytic Astrocytoma
1. most common brain tumor in (Blank)
2. diffuse or localized
3. where is it usually localized
4. What glial cell is it derived from?

A
  1. children
  2. localized
  3. posterior fossa of cerebellum - well circumscribed, cystic, or solid (but can occur in the third ventricle, the optic nerves, and occasionally in the cerebral hemospheres.)
  4. astrocyte (present as cystic lesions)
119
Q

Pilocytic Astrocytoma
1. Histology change can occur?
2. What does this tumor stain for?
3. What molecular markers are found?
4. Prognosis?

A
  1. Rosenthal fibers (circled in image)
  2. GFAP
  3. BRAF mutation
  4. very good with resection
120
Q

Ependymoma
1. more common in adult or children?
2. localized or diffuse gliomas?
3. What glial cells is it derived from?
4. Where is it found?

A
  1. children
  2. localized
  3. ependymal
  4. lining of ventricles (often 4th ventricles) since ependymal cells make CSF
121
Q

Ependymoma
1. What histology changes are found?

A
  1. pseudorosette - cells surrounding central core which is usually blood vessel
  2. true ependymal rosettes - no blood vessel in center just a lumen
122
Q

Medulloblastoma
1. most common in (Blank)
2. Location it is usually found?

A
  1. children
  2. cerebellum
123
Q

Medulloblastoma
1. Histology changes (2)

A
  1. small round blue cell tumor, numerous mitosis/apoptosis
  2. Homer-wrights rosettes - differentiated tumor cells grouped around a central region containing neuropil (image)
124
Q

Choroid Plexus Tumors
1. most common in (Blank)
2. Where is it located?

A
  1. children
  2. lateral ventricles -> leads to hydrocephalus
125
Q

Choroid Plexus Tumors
1. Histology changes

A
  1. a finger like projection with middle vasculature structure and tumor cells on the exterior
126
Q

Meningioma
1. 2nd most common tumor in (Blank)
2. How does it present on scan?
3. Arises from what type of cells?

A
  1. adults
  2. occurs near surfaces of brain since they arise from arachnoid capillary cells - compress the brain without invading it
  3. arachnoid cells
127
Q

Meningioma
1. Histology changes (2)

A
  1. Whorls
  2. Psammoma bodies (little collections of calcium)
128
Q

Hemangioblastoma
1. more common in (Blank)
2. Where is it often located?
3. description of tumor

A
  1. adults
  2. cerebellum, but also brainstem and spinal cord
  3. well circumscribed and highly vascularized
129
Q

CNS Lymphoma
1. Most common CNS tumor in (Blank) patient
2. What lymphocyte is predominant
3. Histology changes (2)

A
  1. immunocompromised
  2. B cell lymphoma (CD20 is a marker for this)
  3. small round blue cell tumor + angiocentric growth pattern (growth around vessels)
130
Q
  1. What are the tumors that most commonly metastasize to the brain?
  2. where do they typically metastasize
A
  1. lung, breast, melanoma, kidney, GI
  2. grey-white matter junction
131
Q

Schwannoma
1. Where is it located
2. benign or malignant
3. peripheral or CNS

A
  1. arises from schwann cells around the CN VIII (in cerebellopontine angle)
  2. benign but does cause sx
  3. peripheral
132
Q

Schwannoma
1. Histology changes (2)

A
  1. Biphasic appearance
  2. Verocay bodies (dense areas located between palisading spindle cells)
133
Q

Neurofibroma
1. Where is it located
2. benign or malignant
3. gross anatomy description

A
  1. grows within the nerve (collection of axons) and between axons
  2. benign
  3. for plexiform neurofibroma (advanced form) - bag of worms description - image
134
Q

Neurofibroma
1. Histology features

A
  1. “dolphins” wavy spindle cells in background of wispy collage and myxoid material
135
Q

What brain/nervous system tumor is associated with NF1

A
  1. plexiform neurofibromas
136
Q

What brain/nervous system tumors are associated with NF2

A
  1. bilateral vestibular schwannomas
  2. multiple meningiomas
  3. ependymomas in spinal cord
137
Q
  1. What are paraneoplastic syndromes?
A
  1. non-metastatic complications of malignancy due to immune-mediated neuronal dysfunction or death
138
Q

Cortical tubers
1. what are they
2. what phakomatose disease are they seen with?

A
  1. firm areas in cortex composed of haphazardly arranged neurons that lack the normal organization of neocortex - blurrs gray-white matter junction
  2. Tuberous sclerosis
139
Q

Subependymal Giant Cell Astrocytoma (SEGA)
1. what are they
2. what phakomatose disease are they seen with?

A
  1. slow growing tumor, typically in wall of lateral ventricles and composed of large ganglioid astrocytes
  2. tuberous sclerosis
140
Q

Von Hippel Lindau Syndrome
1. Mutation in what gene?
2. What tumor does it lead to?
3. Where is this tumor typically?

A
  1. VHL gene in chrom 3
  2. hemangioblastomas (highly vascularized)
  3. cerebellum
141
Q

The pharynx is made up of what three structures?

A
  1. Nasopharynx (behind nasal cavities and above soft palate)
  2. Oropharnyx (behind oral cavity- from soft palate and epiglottis)
  3. Laryngopharynx (from epiglottis to esophagus)
142
Q

What CN is vulnerable to injury during removal of palatine tonsil?

A
  1. The CN IX (glossopharyngeal)
143
Q
  1. What is the sensory supply of the nasopharynx?
  2. What about the oropaharynx
  3. What about the larygnopharynx?
A
  1. Maxillary nerve (V2)
  2. CN IX
  3. CN X
144
Q

What is the arterial supply (upper and lower part) of the pharynx?

A
  1. upper - branches of external carotid artery
  2. branches of subclavian artery
145
Q

What is the arterial supply of the palatine tonsils?

A

Branch of the facial artery

146
Q

Waldeyer’s Ring
1. What is it?
2. In communication with?

A
  1. Ring of mucosa-associated lymphoid tissue which surrounds the openings of the digestive and respiratory tracts
  2. Lymp drainage of pharyngeal tonsils, tubal tonsils, palatine tonsils, lingual tonsils (overall pharnx)
147
Q

Lymphatic drainage of palatine tonsils is via what nodes?

A
  1. Jugulodigastric node
148
Q
  1. What is the motor supply to all muscles of pharynx except stylopharyngeus?
  2. What about stylopharyngeus
A
  1. Vagus nerve (CN X)
  2. CN IX
149
Q
  1. What is the arterial supply to the area above the vocal folds (in pharynx)
  2. What is the arterial supply to the area below the vocal folds (in pharynx)
A
  1. Superior laryngeal artery (from ECA)
  2. inferior laryngeal artery (from Subclavian artery)
150
Q
  1. What is the lympathic drainage of the area above the vocal folds (in pharynx)
  2. What is the lymphatic drainage of the area below the vocal folds (in pharynx)
A
  1. Deep cervical LN
  2. Upper tracheal LN
151
Q

What is best prophylaxis for migraines in apatient with high BMI, hypertension, and stable angina

A
  1. propanolol
  2. others can increases the weight
152
Q

Metoclopramide
1. function
2. MOA

A
  1. Metoclopramide (Reglan) is a dopamine and serotonin antagonist that is used off-label to treat migraine headaches in the emergency department (ED). Because metoclopramide is an antiemetic, it makes sense that this drug can be effective for nausea and vomiting associated with certain types of headaches.
153
Q

What is central sensitization in migraines?

A
  1. Phenomenon where neurons become more and more sensitve to weaker stimuli as the migraine duration increases

Block 6 (9 decks)

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