Patho Exam 2: Carol Dobbs

Comprehensive vocabulary flashcards covering pathophysiology, ophthalmology, and ENT concepts from the lecture notes.

Epstein-Barr Virus (EBV) Transmission

Primary mode is saliva/respiratory secretions entering the mouth via sharing food/drinks or kissing. Less common modes include placenta, blood transfusions/organ transplants, sexual contact, and breast milk.

Lytic Cycle

Active EBV infection where phages infect epithelial cells of the oropharynx/tonsils, replicate, and ultimately burst the host cell leading to cell death.

EBV Latent Infection

Viral phase where the virus enters B cells via CD21, drives rapid B cell proliferation, and downregulates antigen loading onto MHC I; viral DNA is retained and replicated without damaging the infected B cells.

NK Cells (in EBV response)

Non-specific innate immune response in which patrolling cells target suspicious B cells for destruction due to the absence of presenting self-antigen (a viral attempt to evade T cell detection).

Cytotoxic T Cells (in EBV response)

Acquired, antigen-specific immune response in which activated cells bind viral antigens displayed on infected B cells, targeting them for destruction to control rates of viral DNA replication and gene expression.

IgM anti-VCA (Viral Capsid Antigen)

Common diagnostic marker that is produced during primary, acute infection.

IgG anti-VCA (Viral Capsid Antigen)

Diagnostic marker that rises during acute infection and persists for life.

IgG anti-EA (Early Antigen)

Diagnostic antibody produced during active viral DNA replication phase (lytic cycle) that provides definitive diagnostic correlation.

IgG anti-EBNA (Epstein Bar Nuclear Antigen)

Antibody produced only weeks to months after acute symptoms have resolved, serving as a definitive marker of past disease.

Mononucleosis (Disseminated EBV)

Condition causing post-cervical lymphadenopathy, hepatomegaly, and splenomegaly (with risk of spleen rupture; contact sports avoided for $3\text{--}4\text{ weeks}$); cytotoxic T cells appear as atypical lymphocytes with megarich cytoplasm molding around RBCs.

Monospot Test

Diagnostic test where heterophile antibodies produced by infected B cells agglutinate horse/sheep RBCs; false negatives occur early in infection or in children $<4\text{ years old}$.

GAS Manifestations

Palatal petechiae, Cervical lymphadenopathy, Pharyngeal edema/exudates, local edema, and Scarlatiniform rash.

Rheumatic Fever

Molecular mimicry where GAS antibodies cross-react with cardiac myosin and tissue, promoting cardiac damage/inflammation via a Type II hypersensitivity reaction (recruits NK cells, releases cytotoxins); occurs after pathogens are cleared.

Post-Streptococcal Glomerulonephritis (PSGN)

Type III hypersensitivity reaction where GAS antigen-IgG immune complexes lodge in the glomerulus (forming a 'starry sky' immunofluorescence pattern), activating complement and damaging podocytes; causes leaky membranes leading to proteinuria, hematuria, and sodium/water retention leading to interstitial edema.

Acute Epiglottitis

Life-threatening inflammation where the epiglottis, aryepiglottic folds, or base of tongue swell, obstructing the airway (mainly affecting adults/immunocompromised or unvaccinated kids with Hib or GAS); manifests with the 3 Ds (Drooling, Dysphagia, Distress), painful swallowing, inspiratory stridor, tachypnea, tachycardia, and tripod positioning.

Fever

Process where exogenous pyrogens trigger endogenous pyrogens (IL, TNF, IFN) to induce PGE2 production in the hypothalamus, raising the temperature set point and triggering shivering, vasoconstriction, piloerection, and epinephrine release.

Hyperthermia

Heat production exceeding heat loss without changing the hypothalamic set point.

Hyperthermic Injury

Spectrum including:
Heat Cramp (salt/water loss raising membrane potential)
Heat Exhaustion (vasodilation, dehydration, hypotension)
Heat Stroke (hypothalamus overload with absence of sweating/vasodilation).

Uvea

Vascular, nutrient-dense structure supplying oxygen, consisting of the iris, ciliary body, and choroid.

Ciliary body

Structure that attaches the choroid to the iris, controls lens shape, and secretes aqueous humor.

Canal of Schlemm

Structure that drains aqueous humor from the anterior chamber into the bloodstream to regulate intraocular pressure (IOP).

Dry age related macular degeneration (DAMD)

Gradual degeneration due to reduced retinal circulation/debris removal and accumulation of drusen (debris) leading to inflammation and slow photoreceptor degeneration.

Wet age related macular degeneration (WAMD)

Rapid degeneration where drusen leads to inflammation and VEGF activation, causing choroid neovascularization; new vessels are leaky, easily hemorrhage, and form scars leading to fast photoreceptor degeneration.

Myopia

Refractive error leading to 'Near Sightedness', in which nearby objects remain clear and far off objects appear fuzzy/blurry.

Hyperopia

Refractive error leading to 'Far Sightedness', in which far off objects remain clear and nearby objects appear fuzzy/blurry.

Presbyopia

Normal, age-related vision changes where the lens becomes stiff and cannot change shape to allow accommodation, resulting in hyperopia or 'far sightedness'.

Central Retinal Artery Occlusion (CRAO)

Ischemic event where the retina cannot receive oxygenated blood, causing sudden, painless, severe vision loss; the retina appears pale typically with a cherry red spot (fovea).

Central Retinal Vein Occlusion (CRVO)

Condition where blood cannot leave the retina, increasing vessel pressure which can burst and leak into the retina, causing sudden, painless, variable vision loss; retina has a 'blood and thunder' appearance (microhemorrhages, cotton wool spots, edema, tortuous veins).

Non proliferative diabetic retinopathy

High blood glucose damages existing retinal blood vessels leading to microaneurysms.

Proliferative diabetic retinopathy

Blood vessels damaged via hyperglycemia suffer decreased retinal perfusion. Characteristic neovascularization (VEGF), hemorrhage, and opacities.

Glaucoma

Increased ocular pressure due to blockage of the canal of Schlemm (drains aqueous humor), resulting in death of retinal ganglion cells and progressive vision loss (peripheral to central).

Open angle glaucoma

Condition where aqueous humor fails to drain through the trabecular meshwork, resulting in a slow, typically painless progression of pressure increase and vision loss.

Closed angle glaucoma

Condition where the canal of Schlemm is physically blocked by the iris, resulting in a rapid, painful increase in IOP and faster vision loss.

Prolonged darkness

Common trigger of acute angle closure glaucoma. Pupil dilation and increased posterior chamber pressure push the iris against the trabecular meshwork and canal of Schlemm, trapping fluid in the anterior chamber and increasing IOP.

Rhegmatogenous retinal detachment

Accumulation of vitreous humor behind the retina due to trauma or posterior vitreous detachment from age-related liquefaction of vitreous humor.

Vitreous traction retinal detachment

Retinal detachment caused by strong vitreoretinal adhesion and contraction of fibrous membrane (formed from microtrauma during aging or disease).

Exudative retinal detachment

Fluid accumulation between the retina and back of the eyeball due to inflammatory conditions or associated tumors.

Cataracts

Bilateral opacification of the lens from protein deposits, causing light to scatter and resulting in blurred vision.

Temporal/ Giant Cell Arteritis (GCA)

Autoimmune vasculitis of the temporal artery involving transmural inflammation of all three blood vessel layers (largely tunica media and interna); characterized by severe unilateral headache, vision changes, jaw claudication, and strong association with polymyalgia rheumatica in white women over $50$.

Temporomandibular joint dysfunction (TMJ)

Disorder presenting with jaw clicking, tinnitus, vertigo, ear pain, jaw clenching, neck pain, headache, and trismus.

Referred otalgia (w TMJ)

Pain mechanism where the V3 branch of CN V (trigeminal) collects sensory info from the TMJ and the front of the EAC; nerve fibers converge before entering the brain, making the source of the pain signal unclear when processed.

Secondary (Referred) otalgia

Pain felt in the ear originating from an outside source such as tooth pain, TMJ (CN V), facial nerve pain (CN VII), posterior pharynx, tonsil, back of tongue (CN IX); laryngitis, neck or occipital pain (spinal nerves C2-3).

Primary otalgia

Process in which the ear is the source of pain, presenting with an abnormal ear exam.

Secondary otalgia

Referred pain beyond the ear, presenting with a normal ear exam.

Retracted tympanic membrane (TM)

The result of negative pressure in the middle ear due to ETD.

Conductive hearing loss

Diminished air sound conduction caused by obstruction or dysfunction in external/middle ear; sound is unable to be conducted through the air, but bone conduction is preserved and it is often reversible.

Sensorineural hearing loss

Permanent hearing loss caused by direct damage to the cochlea or CN VIII (vestibulocochlear), resulting in both air and bone conduction being diminished; causes include age, Meniere's disease, noise exposure, diabetes, hereditary malfunctions, and trauma.

Air-bone gap

Measurement finding where air conduction is diminished while bone conduction is preserved in conductive hearing loss, whereas both air and bone conduction are diminished in sensorineural hearing loss.

Eustachian tube dysfunction (ETD)

Inability to equalize pressure across TM or clear secretions due to URI/allergic swelling, horizontal/short/floppy shape (in children), smoking, or Cystic Fibrosis.

Cholesteatoma

Persistent negative pressure from ET dysfunction forms a retraction pocket lined with keratinized squamous epithelium where desquamated epithelia accumulate into a mass, causing hearing loss via erosion of ossicles and physical obstruction of sound transmission.

Mastoiditis

AOM inflammation causing purulent material accumulation in mastoid air cells, increasing pressure and destroying thin septae to form abscess cavities; complications include osteomyelitis, hearing loss/labyrinthitis, CN VII facial paralysis, meningitis, and Bezold abscess.

Semicircular canals

Vestibular structures detecting head motion: Anterior/Y axis detects vertical movement; Posterior/X axis detects rotation around coronal plane (tilting head side to side); Lateral/Z axis detects rotation around transverse plane (spinning in a circle).

Ampullae

Enlarged portion on the end of the 3 semilunar canals, before the cochlea, containing endolymph, crista ampullaris, hair cells, and cupula.

Utricle

Otolith-containing organ that detects horizontal movement/head tilting.

Saccule

Otolith-containing organ that detects vertical body movement.

Endolymph

Fluid filling semicircular canals, utricle, and saccule that pushes on cupula inside ampullae during head rotation, causing hair cells to bend and polarize to release NTs to CN VIII to signal rotation to the brain.

Otoliths

Calcium carbonate crystals overlying vestibular hair cells whose gravity-induced movement detects horizontal movement in the utricle or vertical movement in the saccule.

Vertigo

Sensation of self-motion when there is no motion or a distorted sense of self-motion due to conflicting visual, proprioceptive, and vestibular info; categorized as central (involving brain structures) or peripheral (involving inner ear and CN VIII).

Vestibular neuronitis/neuritis

Inflammation of the vestibular portion of CN VIII (often post-URI) causing the brain to interpret movement from the unaffected side only; hearing is unaffected.

Benign paroxysmal positional vertigo (BPPV)

Disorder where otoliths dislodge from utricle/saccule, enter semicircular canals, disrupt endolymph flow, and stimulate ampullary hair cells; hearing is unaffected and condition is treated with the Epley maneuver.

Meniere's disease

Excess endolymph accumulation in the inner ear that increases pressure, damaging the cochlea and vestibular apparatus; causes vertigo, sensorineural hearing loss, and tinnitus.

Motion sickness

Sensory mismatch of visual, vestibular, and proprioceptive signals about body movement/position passing through vestibular nuclei in the brainstem, causing nausea, vomiting, sweating, and increased saliva.

Optic Nerve (CN II)

Transmits sensory visual signals and action potentials from the retinal photoreceptors to the brain.

Trigeminal Nerve (CN V)

Carries sensory inputs from the teeth and temporomandibular joint; fiber convergence causes referred otalgia during dental or joint pathology.

Facial Nerve (CN VII)

Can produce referred ear pain and is vulnerable to inflammatory damage or paralysis as an intratemporal complication of mastoiditis.

Vestibulocochlear Nerve (CN VIII)

Structure that transmits auditory inputs from the cochlea and equilibrium inputs from the vestibular apparatus. Injury results in sensorineural hearing loss, and inflammation causes acute vertigo.

Glossopharyngeal Nerve (CN IX)

Supplies sensory innervation to the tonsils, posterior pharynx, and base of the tongue; acute oropharyngeal conditions can trigger referred pain to the ear along this pathway.

Trigeminal Nerve (CN V)

Collects sensory input from the temporomandibular joint and the anterior external auditory canal, leading to referred otalgia when processed by converging neural pathways.

Palatal petechiae

Pyrogenic exotoxins damage submucosal capillaries

Cervical lymphadenopathy

Antigen trapping and lymphocyte proliferation in nodes

Pharyngeal edema/exudates

Hyaluronic acid destruction

Local edema

Neutrophil recruitment

Scarlatiniform rash

Pyrogenic exotoxins trigger inflammation/hemolysis of dermal capillaries