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BMS200 final exam > week 12 > Flashcards

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
what is a solvent for tastants
saliva
26
channels/receptors for the 5 tastes
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
27
odorant receptors are
GPCRs --> usually open Ca2+ and Cl- channels
28
olfactory sensory neurons axons synapse on
primary dendrites of mitral cells and tufted cells, forming distinctive olfactory glomeruli
29
olfactory sensory neurons express 1 olfactory gene, odorant's can bind many odorant receptors olfactory sensory neurons project to 1 or 2 glomeruli (specificity)
ok lol
30
otosclerosis
abnormal bone deposition in middle ear hearing loss
31
babesiosis is caused by
parasitic infection from tick
32
what parasite causes most babesiosis
babesia microti
33
what does babesia microti (babesiosis) do to RBCs
increase splenic clearance of RBC hemolytic anemia + splenomegaly
34
what is virchows triad that causes pathological coagulation
1. hyper coagulability 2. abnormal blood flow (i.e. turbulent, stasis) 3. injury to vessel wall/ endothelium
35
abnormal blood flow causes hypercoagulability via
shear stress- incerases NO, prostacyclin and tPA if decrease shear stress (i.e. stagnant flow) or if excessive (can activate platelets)
36
most common inherited hypercoagulable condition
Factor V Leiden – activated protein C resistance
37
symptoms of Factor V Leiden – activated protein C resistance
DVT deep vein thrombosis
38
anti-phospholipid antibody syndrome
hyper coagulable autoantibodies to protein C, S, endothelial damage...
39
thrombocytopenias
low levels of platelets --> deficient clotting
40
causes of thrombocytopenia (deficient clotting)
-hypersplenism -destroy platelets via autoantibodies (drugs, HCV infection, idiopathic) etc
41
most common immune thrombocytopenia is
Isolated = no other underlying disease or substance that can cause thrombocytopenia
42
what is happening to platelets in isolated thrombocytopenia
destroyed in spleen (might be from T cell, Th1, Th17) splenectomy (remove sleep) helps
43
clinical features of isolated thrombocytopenia
purpura, peteciae, menorrhagia, low platelets, mucocutaneous bleeds
44
3 types of von willebrand disease
▪ 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
vWF function
stabilize FVIII for platelet adhesion via GPIb/IX and GPIIb/IIIa bind to vWF
46
what happens to platelets in von willebrand disease
defects in platelet function but normal platelet count
47
symptoms of von willebrand disease
mucosal bleed, bruised, menorrhagia,
48
disseminated intravascular coagulation
activate coagulation system (release tissue factor or thrombopalstic substances into circulation) causes microthrombi formation then hemorrhage
49
symptoms in disseminated intravascular coagualtion
hemolytic anemia, cyanosis, coma, renal fail, etc acute- hemorrhage chronic- thrombosis
50
polycythemia's vera
excess RBC production- myeloproliferative disorder
51
what causes polycythemia's vera
mutation to JAK2 tyrosine kinase part of signaling cascade for EPO and TPO --> excessive RBC
52
symptoms of polycthemia vera
high Hb or hematocrit, neurologic (vertigo, headache), HTN, thrombosis erythomelalgia (burning hands and feet) plethoric-ruddy complexion spleno + hepatomegaly
53
megaloblastic anemia
blood cell bigger (MCV), impaired maturation from impairment of DNA synthesis
54
2 causes of megaloblastic anemia
b12 or folate deficiency
55
pernicious anemia is from
b12 defienciy
56
what are b12 and folate needed to synthesize
thymidine (DNA component)
57
pernicious anemia (b12 deficiency) usually caused by
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
two mechanisms in autoimmune hemolytic anemai
1. innocent bystander damage (antibodies directed to medication or foreign substance attack RBC) 2. true immunohemolytic anemia (warm and cold)
59
warm antibody hemolytic anemia vs cold agglutinin disease (2 types of autoimmune hemolytic anemias) whats the difference
warm- IgG and >37 celcius cold- IgM
60
warm antibody hemolytic anemia vs cold agglutinin disease which is intravascular and which is extravascular
cold- intravascular (complement activation) warm- extravascular (phagocytose - antibody dependent cell mediated cytotoxicity- splenic or hepatic removal)
61
warm antibody hemolytic anemia vs cold agglutinin disease what more severe? symptoms?
warm hemolysis, jaundice, splenomegaly
62
how to diagnose warm antibody hemolytic anemia and cold agglutinin disease (autoimmune hemolytic anemias)
Coombs test
63
MCV is
measurement of RBC size
64
RDW
RBC distribution width- variance in RBC size
65
reticulocyte
immature RBC with no nucleus and residual RNA
66
hematocrit
% of given volume of whole blood occupied by packed RBCs
67
anisocytosis
The higher the RDW, the more variable the size of RBCs i.e. high in iron deficiency anemia
68
reticulocyte count
assess RBC production - immature RBCs in bone marrow
69
which anemias are normocytic and normochromic vs which are microcytic and hypochromic
* 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
macrocytic and normochromic
megaloblastic anemia
71
prolonged prothrombin time (PT) and activated partial thromboplastin time (aPTT)
vitamin K deficiency or warfarin (blood thinner) disseminated intravascular coagualtion
72
PT/iNR vs aPTT evaluate which factors
PT- factors I, II, V, VII and X aPTT- factor I, II, V, VIII, IX, XI, XII
73
d-dimer
fibrin degradation fragment from fibrinolysis
74
test for disseminated intravascular coagulation
d-dimers (fibrin degradation fragment)
75
conductive vs sensorineural hearing loss
conductive- outer or middle ear, impacts all frequencies sensorineural- higher frequency, inner ear (cochlea or auditory nerve), from noise, presbycusis (aging), toxic substances
76
rinne and weber for conductive vs sensorineural
conductive (outer/middle): Rinne: BC > AC, Weber: lateralizes to affected ear sensorineural (inner): Rinne: AC > BC, Weber: lateralizes to unaffected ear
77
causes of otitis externa
bacteria: staphylococcal, pseudomonas aeruginosa, or E. coli
78
risk factors for otitis externa
increased pH (from infection), water/ humid, heat, loss of cerumen
79
3 types of otitis externa
1. furunculosis (from staph) 2. chronic otitis externa 3. malignant/ necrotizing otitis externa (worst) 4. otomycosis - fungal infection (aspergillus)
80
acute otitis media seen in
kids with short and horizontal Eustachian tube , lack of breastfeeding...
81
bacteria and viruses causing acute otitis media
▪ Major bacteria implicated: H. influenzae, S. pneumoniae, M. catarrhalis ▪ Major viruses implicated: RSV, influenza, parainfluenza, adenovirus
82
triad in acute otitis media
Triad of otalgia, fever, and conductive hearing loss otorrhea if TM perforated
83
otits media with effusion (serous otitis media) is from
untreated acute otitis media
84
clinical features of otitis media with effusion
▪ Conductive hearing loss with or without tinnitus ▪ Feeling of fullness in the ear, low-grade fever ▪ May or may not involve otalgia
85
85
tympanic membrane in acute otitis media vs otitis media with effusion
AOM- red building opaque TM OME- translucent/gray TM with fluid and bubbles
86
types of chronic otitis media
▪ Suppurative or serous chronic otitis media – describes character of the drainage through the perforated TM ▪ Benign chronic otitis media – “dry” – no active infection
87
what is a cholesteatoma
non-neoplastic, cystic lesions lined by keratinizing squamous epithelium or metaplastic mucus- secreting epithelium, and filled with debris in the middle ear
88
3 types of cholesteatomas
primary congenital secondary acquired primary acquired
89
what do choleasteatomas cause
conductive hearing loss if cyst invade dura and intracranial then meningitis and death
90
primary acquired cholestetoma
most common chronic inflammation and abnormal tympanic membrane cell migration (inner surface of TM get stuck to incus) --> mucous accumulate --> implant keratin cells
91
secondary acquired choleasteatoma
from trauma, surgery etc keratin cells implant into tympanic membrane or auditory canal
92
2 types of dizziness
vertiginous (vertigo) and non-vertiginous
93
vertigo is caused by
inner ear (peripheral) or brainstem-cerebellar (central) disorders
94
non-vertiginous dizziness causes
organic- i.e. low blood pressure or visual compromise functional- mood disorders
95
bengign paroxysmal positional vertigo is
seconds to minutes of vertigo when head in certain position (i.e. extend neck, get out of bed) and rotatory nystagmus
96
cause of Benign paroxysmal positional vertigo
free-floating otolith (should be attached)
97
how to diagnose Benign paroxysmal positional vertigo
Dix-Hallpike Positional Testing
98
meniere's disease
episodes of tinnitus, hearing loss and vertigo for mins to hours
99
cause of menieres disease
inadequate absorption of endolymph
100
what triggers menieres disease
high salt intake, caffeine, stress, nicotine, and alcohol
101
3 criteria of menieres disease
* Rotational vertigo ≥20 min * Audiometric confirmation of Sensorineural Hearing Loss * Tinnitus and/or aural fullness
102
vestibular neuronitis
vertigo w nausea, vomit, imbalance without hearing loss that lasts for days to weeks
103
causes of vestibular neuronitis
viral, URTI
104
labyrinthitis
acute infection of inner ear causing vertigo and hearing loss serous (viral) or purulent (bacteria)
105
symptoms of labryinthitis (infection of inner ear)
vertigo, N/V, tinnitus, unilateral hearing loss
106
acoustic neruroma
intracranial tumor from Schwann cells that myelinated vestibular + cochlear nerve
107
acoustic neuroma symptoms
hearing loss, vertigo, facial weak/numb, headache

BMS200 final exam (14 decks)

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