week 12 Flashcards

1
Q

opening of the external auditory canal

A

auditory meatus

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2
Q

3 components of cerumen

A

▪ anti-microbial proteins
▪ saturated fatty acids
▪ sloughed keratinocytes

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3
Q

3 bones of the middle ear

A

malleus
incus
stapes

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4
Q

malleus and stapes have what muscle and what nerve innervates

A

malleus - tensor tympani (CN V) (dampens movements)

stapes- stapedius (CN VII) (dampens vibrations)

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5
Q

what does the stapes attach to

A

oval window (transition between middle and inner ear)

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6
Q

what is the purpose of the bones in middle ear being levers

A

helps overcome the acoustic impedance mismatch between air and water

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7
Q

parts of the cochlea and what fluid they have

A

scala vestibuli (connects to oval window) - perilymph

scala tympani (connects to round window)- perilymph

scala media (hair cells) - endolymph

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8
Q

what barrier so that endolymph and perilymph dont mix

A

Reissner’s membrane

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9
Q

organ of corti is found in

A

scala media

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10
Q

what has the hair cells in the Scala media

A

the organ of corti

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11
Q

endolymph vs perilymph

which is high in K+ and in Na+ Cl-

A

endolymph- K+

perilymph - Na+ Cl- (similar to CSF)

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12
Q

STEPS of hearing wk 12 lec 1 slide 20,,,,

A
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13
Q

after going from outer to inner hair cell depolarization what gets opens to depolarize afferent neurons (Ear)

A

VG Ca2+ channels open which then released glutamate

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14
Q

high vs low frequency sounds detected where in the ear

A

▪ High-frequency sounds are detected closer to the oval window
▪ Low-frequency sounds are detected closer to the helicotrema

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15
Q

loudness of sound encoded by

A

frequency of action potentials (how much basilar membrane vibrates –> release more glutamate)

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16
Q

2 types of equilibrium in the ear

A

static and dynamic

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17
Q

static vs dynamic equilibrium

A

static- when body not moving or in linear acceleration/deceleration

dyanmic- movements of head

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18
Q

vestibular system in the ear

A

▪ three semicircular canals
▪ two otolithic organs, the utricle and the saccule

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19
Q

semicircular canal vs utricle and saccule for which types of movements

A

semicircular- oratory acceleration and motion

U and S- linear acceleration and static position

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20
Q

the ampulla in the semicircular canal contains

A

crista ampullaris (for rotation and movement of head)

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21
Q

anterior
posterior
and lateral semicircular canals for which motions (as a whole does rotation)

A

anterior- yes nod
posterior- side tilt
lateral- no nod

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22
Q

utricle and saccule are

A

otolithic organs and are for linear accelerations and decelerations or static equilibrium

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23
Q

macula in the utricle and saccule has otolithic membrane which has what crystals

A

calcium carbonate crystals, called otoliths

for the linear acceleration/deceleration

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24
Q

papillae types (contain taste buds) - which one doesnt have taste buds?

A

▪ Fungiform papillae - near
the tongue’s tip
▪ Circumvallate papillae,
forming a V-shape on the
back of the tongue
▪ foliate papillae, located on
the posterior edge

  • filiform papillae – lack taste buds
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25
Q

what is a solvent for tastants

A

saliva

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26
Q

channels/receptors for the 5 tastes

A

salt- ENaC (epithelial sodium channels)

sour- H+/ proton via ENaC and cyclic nucleotide-gated cation channels (HCN)

sweet- GPCRs; T1R2 and T1R3

bitter- GPCRs; T2R family

umami- T1R1 and T1R3 and truncated metabotropic glutamate receptor, mGluR4

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27
Q

odorant receptors are

A

GPCRs –> usually open Ca2+ and Cl- channels

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28
Q

olfactory sensory neurons axons synapse on

A

primary dendrites of mitral cells and tufted cells, forming distinctive olfactory glomeruli

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29
Q

olfactory sensory neurons express 1 olfactory gene, odorant’s can bind many odorant receptors

olfactory sensory neurons project to 1 or 2 glomeruli (specificity)

A

ok lol

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30
Q

otosclerosis

A

abnormal bone deposition in middle ear

hearing loss

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31
Q

babesiosis is caused by

A

parasitic infection from tick

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32
Q

what parasite causes most babesiosis

A

babesia microti

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33
Q

what does babesia microti (babesiosis) do to RBCs

A

increase splenic clearance of RBC

hemolytic anemia + splenomegaly

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34
Q

what is virchows triad that causes pathological coagulation

A
  1. hyper coagulability
  2. abnormal blood flow (i.e. turbulent, stasis)
  3. injury to vessel wall/ endothelium
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35
Q

abnormal blood flow causes hypercoagulability via

A

shear stress- incerases NO, prostacyclin and tPA

if decrease shear stress (i.e. stagnant flow) or if excessive (can activate platelets)

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36
Q

most common inherited hypercoagulable condition

A

Factor V Leiden – activated protein C resistance

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37
Q

symptoms of Factor V Leiden – activated protein C resistance

A

DVT deep vein thrombosis

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38
Q

anti-phospholipid antibody syndrome

A

hyper coagulable

autoantibodies to protein C, S, endothelial damage…

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39
Q

thrombocytopenias

A

low levels of platelets –> deficient clotting

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40
Q

causes of thrombocytopenia (deficient clotting)

A

-hypersplenism
-destroy platelets via autoantibodies (drugs, HCV infection, idiopathic)
etc

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41
Q

most common immune thrombocytopenia is

A

Isolated = no other underlying disease or substance
that can cause thrombocytopenia

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42
Q

what is happening to platelets in isolated thrombocytopenia

A

destroyed in spleen (might be from T cell, Th1, Th17)

splenectomy (remove sleep) helps

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43
Q

clinical features of isolated thrombocytopenia

A

purpura, peteciae, menorrhagia, low platelets, mucocutaneous bleeds

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44
Q

3 types of von willebrand disease

A

▪ Type 1 vWD: mild disease, autosomal dominant,
results in deficiency of vWF

▪ Type 2 vWD: autosomal dominant, variable disease severity (mild-moderate), lots of vWF in circulation but it does not function effectively

▪ Type 3 vWD: more severe disease, autosomal recessive, severe deficiency of vWF

45
Q

vWF function

A

stabilize FVIII

for platelet adhesion via GPIb/IX and GPIIb/IIIa bind to vWF

46
Q

what happens to platelets in von willebrand disease

A

defects in platelet function but normal platelet count

47
Q

symptoms of von willebrand disease

A

mucosal bleed, bruised, menorrhagia,

48
Q

disseminated intravascular coagulation

A

activate coagulation system (release tissue factor or thrombopalstic substances into circulation)

causes microthrombi formation then hemorrhage

49
Q

symptoms in disseminated intravascular coagualtion

A

hemolytic anemia, cyanosis, coma, renal fail, etc

acute- hemorrhage
chronic- thrombosis

50
Q

polycythemia’s vera

A

excess RBC production- myeloproliferative disorder

51
Q

what causes polycythemia’s vera

A

mutation to JAK2 tyrosine kinase

part of signaling cascade for EPO and TPO –> excessive RBC

52
Q

symptoms of polycthemia vera

A

high Hb or hematocrit, neurologic (vertigo, headache), HTN, thrombosis

erythomelalgia (burning hands and feet)

plethoric-ruddy complexion

spleno + hepatomegaly

53
Q

megaloblastic anemia

A

blood cell bigger (MCV), impaired maturation

from impairment of DNA synthesis

54
Q

2 causes of megaloblastic anemia

A

b12 or folate deficiency

55
Q

pernicious anemia is from

A

b12 defienciy

56
Q

what are b12 and folate needed to synthesize

A

thymidine (DNA component)

57
Q

pernicious anemia (b12 deficiency) usually caused by

A

autoimmune attack of parietal cells

Cells in the stomach that secrete gastric acid and intrinsic factor, which is necessary for the absorption of vitamin B12

58
Q

two mechanisms in autoimmune hemolytic anemai

A
  1. innocent bystander damage (antibodies directed to medication or foreign substance attack RBC)
  2. true immunohemolytic anemia (warm and cold)
59
Q

warm antibody hemolytic anemia vs cold agglutinin disease (2 types of autoimmune hemolytic anemias)

whats the difference

A

warm- IgG and >37 celcius

cold- IgM

60
Q

warm antibody hemolytic anemia vs cold agglutinin disease

which is intravascular and which is extravascular

A

cold- intravascular (complement activation)

warm- extravascular (phagocytose - antibody dependent cell mediated cytotoxicity- splenic or hepatic removal)

61
Q

warm antibody hemolytic anemia vs cold agglutinin disease

what more severe? symptoms?

A

warm

hemolysis, jaundice, splenomegaly

62
Q

how to diagnose warm antibody hemolytic anemia and cold agglutinin disease (autoimmune hemolytic anemias)

A

Coombs test

63
Q

MCV is

A

measurement of RBC size

64
Q

RDW

A

RBC distribution width- variance in RBC size

65
Q

reticulocyte

A

immature RBC with no nucleus and residual RNA

66
Q

hematocrit

A

% of given volume of whole blood occupied by packed RBCs

67
Q

anisocytosis

A

The higher the RDW, the more variable the size of RBCs

i.e. high in iron deficiency anemia

68
Q

reticulocyte count

A

assess RBC production
- immature RBCs in bone marrow

69
Q

which anemias are normocytic and normochromic

vs

which are microcytic and hypochromic

A
  • Normocytic, normochromic anemia
    ▪ Early iron deficiency
    ▪ Anemia of chronic illness/disease (ACD)
    ▪ Acute blood loss
    ▪ Aplastic anemia or other types of marrow failure
    ▪ Hemolytic anemias
  • Microcytic, hypochromic anemia
    ▪ Late iron deficiency
    ▪ Thalassemia
    ▪ Lead poisoning
    ▪ Sideroblastic anemia
    ▪ ACD can also be mildly microcytic, hypochromic
    ▪ Mnemonic - TAILS
70
Q

macrocytic and normochromic

A

megaloblastic anemia

71
Q

prolonged prothrombin time (PT) and activated partial thromboplastin time (aPTT)

A

vitamin K deficiency or warfarin (blood thinner)

disseminated intravascular coagualtion

72
Q

PT/iNR vs aPTT evaluate which factors

A

PT- factors I, II, V, VII and X

aPTT- factor I, II, V, VIII, IX, XI, XII

73
Q

d-dimer

A

fibrin degradation fragment from fibrinolysis

74
Q

test for disseminated intravascular coagulation

A

d-dimers (fibrin degradation fragment)

75
Q

conductive vs sensorineural hearing loss

A

conductive- outer or middle ear, impacts all frequencies

sensorineural- higher frequency, inner ear (cochlea or auditory nerve), from noise, presbycusis (aging), toxic substances

76
Q

rinne and weber for conductive vs sensorineural

A

conductive (outer/middle):
Rinne: BC > AC,
Weber: lateralizes to affected ear

sensorineural (inner):
Rinne: AC > BC,
Weber: lateralizes to unaffected ear

77
Q

causes of otitis externa

A

bacteria: staphylococcal, pseudomonas
aeruginosa, or E. coli

78
Q

risk factors for otitis externa

A

increased pH (from infection), water/ humid, heat, loss of cerumen

79
Q

3 types of otitis externa

A
  1. furunculosis (from staph)
  2. chronic otitis externa
  3. malignant/ necrotizing otitis externa (worst)
  4. otomycosis - fungal infection (aspergillus)
80
Q

acute otitis media seen in

A

kids with short and horizontal Eustachian tube , lack of breastfeeding…

81
Q

bacteria and viruses causing acute otitis media

A

▪ Major bacteria implicated: H. influenzae, S. pneumoniae, M. catarrhalis

▪ Major viruses implicated: RSV, influenza, parainfluenza, adenovirus

82
Q

triad in acute otitis media

A

Triad of otalgia, fever, and conductive hearing loss

otorrhea if TM perforated

83
Q

otits media with effusion (serous otitis media) is from

A

untreated acute otitis media

84
Q

clinical features of otitis media with effusion

A

▪ Conductive hearing loss with or without tinnitus
▪ Feeling of fullness in the ear, low-grade fever
▪ May or may not involve otalgia

85
Q
A
85
Q

tympanic membrane in acute otitis media vs otitis media with effusion

A

AOM- red building opaque TM

OME- translucent/gray TM with fluid and bubbles

86
Q

types of chronic otitis media

A

▪ Suppurative or serous chronic otitis media – describes
character of the drainage through the perforated TM

▪ Benign chronic otitis media – “dry” – no active infection

87
Q

what is a cholesteatoma

A

non-neoplastic, cystic lesions lined by keratinizing squamous epithelium or metaplastic mucus- secreting epithelium, and filled with debris in the middle ear

88
Q

3 types of cholesteatomas

A

primary congenital

secondary acquired

primary acquired

89
Q

what do choleasteatomas cause

A

conductive hearing loss

if cyst invade dura and intracranial then meningitis and death

90
Q

primary acquired cholestetoma

A

most common

chronic inflammation and abnormal tympanic membrane cell migration (inner surface of TM get stuck to incus) –> mucous accumulate –> implant keratin cells

91
Q

secondary acquired choleasteatoma

A

from trauma, surgery etc

keratin cells implant into tympanic membrane or auditory canal

92
Q

2 types of dizziness

A

vertiginous (vertigo) and non-vertiginous

93
Q

vertigo is caused by

A

inner ear (peripheral) or brainstem-cerebellar (central) disorders

94
Q

non-vertiginous dizziness causes

A

organic- i.e. low blood pressure or visual compromise

functional- mood disorders

95
Q

bengign paroxysmal positional vertigo is

A

seconds to minutes of vertigo when head in certain position (i.e. extend neck, get out of bed)

and rotatory nystagmus

96
Q

cause of Benign paroxysmal positional vertigo

A

free-floating otolith (should be attached)

97
Q

how to diagnose Benign paroxysmal positional vertigo

A

Dix-Hallpike Positional Testing

98
Q

meniere’s disease

A

episodes of tinnitus, hearing loss and vertigo for mins to hours

99
Q

cause of menieres disease

A

inadequate absorption of endolymph

100
Q

what triggers menieres disease

A

high salt intake, caffeine, stress, nicotine, and
alcohol

101
Q

3 criteria of menieres disease

A
  • Rotational vertigo ≥20 min
  • Audiometric confirmation of Sensorineural Hearing Loss
  • Tinnitus and/or aural fullness
102
Q

vestibular neuronitis

A

vertigo w nausea, vomit, imbalance without hearing loss that lasts for days to weeks

103
Q

causes of vestibular neuronitis

A

viral, URTI

104
Q

labyrinthitis

A

acute infection of inner ear causing vertigo and hearing loss

serous (viral) or purulent (bacteria)

105
Q

symptoms of labryinthitis (infection of inner ear)

A

vertigo, N/V, tinnitus, unilateral hearing loss

106
Q

acoustic neruroma

A

intracranial tumor from Schwann cells that myelinated vestibular + cochlear nerve

107
Q

acoustic neuroma symptoms

A

hearing loss, vertigo, facial weak/numb, headache