week 12 Flashcards
opening of the external auditory canal
auditory meatus
3 components of cerumen
▪ anti-microbial proteins
▪ saturated fatty acids
▪ sloughed keratinocytes
3 bones of the middle ear
malleus
incus
stapes
malleus and stapes have what muscle and what nerve innervates
malleus - tensor tympani (CN V) (dampens movements)
stapes- stapedius (CN VII) (dampens vibrations)
what does the stapes attach to
oval window (transition between middle and inner ear)
what is the purpose of the bones in middle ear being levers
helps overcome the acoustic impedance mismatch between air and water
parts of the cochlea and what fluid they have
scala vestibuli (connects to oval window) - perilymph
scala tympani (connects to round window)- perilymph
scala media (hair cells) - endolymph
what barrier so that endolymph and perilymph dont mix
Reissner’s membrane
organ of corti is found in
scala media
what has the hair cells in the Scala media
the organ of corti
endolymph vs perilymph
which is high in K+ and in Na+ Cl-
endolymph- K+
perilymph - Na+ Cl- (similar to CSF)
STEPS of hearing wk 12 lec 1 slide 20,,,,
after going from outer to inner hair cell depolarization what gets opens to depolarize afferent neurons (Ear)
VG Ca2+ channels open which then released glutamate
high vs low frequency sounds detected where in the ear
▪ High-frequency sounds are detected closer to the oval window
▪ Low-frequency sounds are detected closer to the helicotrema
loudness of sound encoded by
frequency of action potentials (how much basilar membrane vibrates –> release more glutamate)
2 types of equilibrium in the ear
static and dynamic
static vs dynamic equilibrium
static- when body not moving or in linear acceleration/deceleration
dyanmic- movements of head
vestibular system in the ear
▪ three semicircular canals
▪ two otolithic organs, the utricle and the saccule
semicircular canal vs utricle and saccule for which types of movements
semicircular- oratory acceleration and motion
U and S- linear acceleration and static position
the ampulla in the semicircular canal contains
crista ampullaris (for rotation and movement of head)
anterior
posterior
and lateral semicircular canals for which motions (as a whole does rotation)
anterior- yes nod
posterior- side tilt
lateral- no nod
utricle and saccule are
otolithic organs and are for linear accelerations and decelerations or static equilibrium
macula in the utricle and saccule has otolithic membrane which has what crystals
calcium carbonate crystals, called otoliths
for the linear acceleration/deceleration
papillae types (contain taste buds) - which one doesnt have taste buds?
▪ 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
what is a solvent for tastants
saliva
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
odorant receptors are
GPCRs –> usually open Ca2+ and Cl- channels
olfactory sensory neurons axons synapse on
primary dendrites of mitral cells and tufted cells, forming distinctive olfactory glomeruli
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
otosclerosis
abnormal bone deposition in middle ear
hearing loss
babesiosis is caused by
parasitic infection from tick
what parasite causes most babesiosis
babesia microti
what does babesia microti (babesiosis) do to RBCs
increase splenic clearance of RBC
hemolytic anemia + splenomegaly
what is virchows triad that causes pathological coagulation
- hyper coagulability
- abnormal blood flow (i.e. turbulent, stasis)
- injury to vessel wall/ endothelium
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)
most common inherited hypercoagulable condition
Factor V Leiden – activated protein C resistance
symptoms of Factor V Leiden – activated protein C resistance
DVT deep vein thrombosis
anti-phospholipid antibody syndrome
hyper coagulable
autoantibodies to protein C, S, endothelial damage…
thrombocytopenias
low levels of platelets –> deficient clotting
causes of thrombocytopenia (deficient clotting)
-hypersplenism
-destroy platelets via autoantibodies (drugs, HCV infection, idiopathic)
etc
most common immune thrombocytopenia is
Isolated = no other underlying disease or substance
that can cause thrombocytopenia
what is happening to platelets in isolated thrombocytopenia
destroyed in spleen (might be from T cell, Th1, Th17)
splenectomy (remove sleep) helps
clinical features of isolated thrombocytopenia
purpura, peteciae, menorrhagia, low platelets, mucocutaneous bleeds
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
vWF function
stabilize FVIII
for platelet adhesion via GPIb/IX and GPIIb/IIIa bind to vWF
what happens to platelets in von willebrand disease
defects in platelet function but normal platelet count
symptoms of von willebrand disease
mucosal bleed, bruised, menorrhagia,
disseminated intravascular coagulation
activate coagulation system (release tissue factor or thrombopalstic substances into circulation)
causes microthrombi formation then hemorrhage
symptoms in disseminated intravascular coagualtion
hemolytic anemia, cyanosis, coma, renal fail, etc
acute- hemorrhage
chronic- thrombosis
polycythemia’s vera
excess RBC production- myeloproliferative disorder
what causes polycythemia’s vera
mutation to JAK2 tyrosine kinase
part of signaling cascade for EPO and TPO –> excessive RBC
symptoms of polycthemia vera
high Hb or hematocrit, neurologic (vertigo, headache), HTN, thrombosis
erythomelalgia (burning hands and feet)
plethoric-ruddy complexion
spleno + hepatomegaly
megaloblastic anemia
blood cell bigger (MCV), impaired maturation
from impairment of DNA synthesis
2 causes of megaloblastic anemia
b12 or folate deficiency
pernicious anemia is from
b12 defienciy
what are b12 and folate needed to synthesize
thymidine (DNA component)
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
two mechanisms in autoimmune hemolytic anemai
- innocent bystander damage (antibodies directed to medication or foreign substance attack RBC)
- true immunohemolytic anemia (warm and cold)
warm antibody hemolytic anemia vs cold agglutinin disease (2 types of autoimmune hemolytic anemias)
whats the difference
warm- IgG and >37 celcius
cold- IgM
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)
warm antibody hemolytic anemia vs cold agglutinin disease
what more severe? symptoms?
warm
hemolysis, jaundice, splenomegaly
how to diagnose warm antibody hemolytic anemia and cold agglutinin disease (autoimmune hemolytic anemias)
Coombs test
MCV is
measurement of RBC size
RDW
RBC distribution width- variance in RBC size
reticulocyte
immature RBC with no nucleus and residual RNA
hematocrit
% of given volume of whole blood occupied by packed RBCs
anisocytosis
The higher the RDW, the more variable the size of RBCs
i.e. high in iron deficiency anemia
reticulocyte count
assess RBC production
- immature RBCs in bone marrow
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
macrocytic and normochromic
megaloblastic anemia
prolonged prothrombin time (PT) and activated partial thromboplastin time (aPTT)
vitamin K deficiency or warfarin (blood thinner)
disseminated intravascular coagualtion
PT/iNR vs aPTT evaluate which factors
PT- factors I, II, V, VII and X
aPTT- factor I, II, V, VIII, IX, XI, XII
d-dimer
fibrin degradation fragment from fibrinolysis
test for disseminated intravascular coagulation
d-dimers (fibrin degradation fragment)
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
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
causes of otitis externa
bacteria: staphylococcal, pseudomonas
aeruginosa, or E. coli
risk factors for otitis externa
increased pH (from infection), water/ humid, heat, loss of cerumen
3 types of otitis externa
- furunculosis (from staph)
- chronic otitis externa
- malignant/ necrotizing otitis externa (worst)
- otomycosis - fungal infection (aspergillus)
acute otitis media seen in
kids with short and horizontal Eustachian tube , lack of breastfeeding…
bacteria and viruses causing acute otitis media
▪ Major bacteria implicated: H. influenzae, S. pneumoniae, M. catarrhalis
▪ Major viruses implicated: RSV, influenza, parainfluenza, adenovirus
triad in acute otitis media
Triad of otalgia, fever, and conductive hearing loss
otorrhea if TM perforated
otits media with effusion (serous otitis media) is from
untreated acute otitis media
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
tympanic membrane in acute otitis media vs otitis media with effusion
AOM- red building opaque TM
OME- translucent/gray TM with fluid and bubbles
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
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
3 types of cholesteatomas
primary congenital
secondary acquired
primary acquired
what do choleasteatomas cause
conductive hearing loss
if cyst invade dura and intracranial then meningitis and death
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
secondary acquired choleasteatoma
from trauma, surgery etc
keratin cells implant into tympanic membrane or auditory canal
2 types of dizziness
vertiginous (vertigo) and non-vertiginous
vertigo is caused by
inner ear (peripheral) or brainstem-cerebellar (central) disorders
non-vertiginous dizziness causes
organic- i.e. low blood pressure or visual compromise
functional- mood disorders
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
cause of Benign paroxysmal positional vertigo
free-floating otolith (should be attached)
how to diagnose Benign paroxysmal positional vertigo
Dix-Hallpike Positional Testing
meniere’s disease
episodes of tinnitus, hearing loss and vertigo for mins to hours
cause of menieres disease
inadequate absorption of endolymph
what triggers menieres disease
high salt intake, caffeine, stress, nicotine, and
alcohol
3 criteria of menieres disease
- Rotational vertigo ≥20 min
- Audiometric confirmation of Sensorineural Hearing Loss
- Tinnitus and/or aural fullness
vestibular neuronitis
vertigo w nausea, vomit, imbalance without hearing loss that lasts for days to weeks
causes of vestibular neuronitis
viral, URTI
labyrinthitis
acute infection of inner ear causing vertigo and hearing loss
serous (viral) or purulent (bacteria)
symptoms of labryinthitis (infection of inner ear)
vertigo, N/V, tinnitus, unilateral hearing loss
acoustic neruroma
intracranial tumor from Schwann cells that myelinated vestibular + cochlear nerve
acoustic neuroma symptoms
hearing loss, vertigo, facial weak/numb, headache
