Clinical Pathophysiology I · Exam 1 — Study Guide

1 · Inflammation

1.1 · Objective a — Molecular mechanisms of inflammatory processes

Inflammation is the reaction of vascularized living tissue to injury. The word vascularized is doing real work in that definition — tissue without a blood supply cannot mount the response at all. The process is a sequence of events that heals the injury or implant site, either by generating new tissue from native parenchymal cells or by forming fibroblastic scar tissue.

The five main processes, in order:

1.2 · Objective b — Types and etiologies of inflammation

The three causes of chronic inflammation, each with the lecture's own examples:

1.3 · Objective b — Patterns of inflammation

Chronicity and pattern are two independent axes. A process is acute or chronic, and separately shows one of these patterns:

1.4 · Objective c — Mechanism of white blood cells

Note the terminology trap: PMN refers to all granulocytes, not to neutrophils alone, even though neutrophils are the ones usually meant in conversation.

1.5 · Objective d — Vascular changes in acute inflammation

The reviewed sequence opens with four vascular events, in this order:

1.6 · Objective e — Cellular changes in acute inflammation

The sequence continues with five cellular events:

Acute inflammation in review: short term (minutes to days), with exudation of fluid, plasma, proteins and leukocytes (neutrophils), then phagocytosis and enzymatic release. Activated neutrophils and macrophages digest foreign material through four steps — recognition, attachment, engulfment, degradation — and recognition and attachment are enhanced when serum factors (opsonins) are present.

Chronic inflammation in review: long term (at least days), characterized by macrophages, monocytes and mononuclear cells including lymphocytes and plasma cells, accompanied by proliferation of blood vessels and connective tissue. Lymphocytes and plasma cells mediate antibody production; macrophages process and deliver antigen to immunocompetent cells.

1.7 · Objective f — Mediators of inflammation and their functions

Opsonins are proteins that adhere to foreign material and make it easier for immune cells to recognize and attach to it.

Source: 1. Inflammation.pptx (Professor Lauren Reynolds), Slides 1–35, and the PAJ 5101 syllabus instructional objectives. Course text: Robbins & Cotran Pathologic Basis of Disease, 10th edition — Chapter 3, “Inflammation and Repair”.

2 · Dermatology: Pathophysiology of the Skin

Stacie Gopal, DMS, PA-C

2.1 · Objective a — Anatomy of the integumentary system

Skin is the largest organ in the body, with hair, nails and glands as accessory structures. Its functions are a physical barrier against pathogens, ultraviolet light, fluid loss and trauma; thermoregulation; sensation; and an endocrine role.

Three layers: epidermis, dermis and subcutaneous (hypodermis). The dermis is where the nerves and vasculature sit.

The epidermis

Stratified squamous epithelium, 0.05 to 1.5 mm, with four cell types — keratinocytes (about 90%), melanocytes, Merkel cells and Langerhans cells. Turnover is every 30 to 60 days and is more rapid in younger patients.

The dermis and the appendages

Two connective tissue layers: papillary (thin, superficial) and reticular (dense, deeper). Collagen is the primary component, produced by fibroblasts, giving tensile strength; elastic fibers of elastin and fibrillin give recoil. Cells include fibroblasts, macrophages, histiocytes, adipocytes and mast cells, which mediate immunoglobulin E-driven inflammation.

Hair comes in three types: terminal (thick, androgen-regulated), lanugo (fine, newborn) and vellus (fine, short, growth independent of androgens).

2.2 · Objective b — Primary skin lesions

A primary lesion is the direct result of the underlying disease and retains its original, unmodified appearance. Read the table by mechanism rather than by name — the size cut-offs are arbitrary, but what is happening in the tissue is not.

2.3 · Objective c — Secondary skin lesions

A secondary lesion is a primary lesion modified over time by infection, trauma or other factors, and it may or may not still resemble what it came from.

2.4 · Objective c — Wound healing and scar

The lecture marks remodelling as the important phase, and the collagen swap is why: the scar ends up strong but architecturally different from the skin around it, which is why it never quite matches.

2.5 · Objective d — Molecular mechanisms of common conditions

Nails

2.6 · Objective d — Skin cancers

Lecture references include Fitzpatrick’s Color Atlas and Synopsis of Clinical Dermatology (9th edition) and several StatPearls chapters; the course text is Banasik, Pathophysiology.

3 · Abnormal Cell Growth and Differentiation

3.1 · Objective b — Non-neoplastic abnormalities of cell growth

Seven terms, and they sort cleanly into three that are developmental failures, two that are changes in size, and two that are changes in kind. Learning them in those groups is far easier than as a list.

3.2 · Objectives a & b — Metaplasia, dysplasia, and the line that matters

Metaplasia and dysplasia are the two that carry towards cancer, and they are not the same thing. Metaplasia swaps one orderly tissue for another orderly tissue. Dysplasia keeps the tissue type and loses the order. Only the second is precancerous.

3.3 · Objectives c & k — Neoplasia and histological grading

A neoplasm is an abnormal mass of tissue growing autonomously — self-perpetuating without physiologic growth stimuli. That single word is what separates it from hyperplasia, which stops when the stimulus stops. The entire proliferating population is derived from one cell that underwent a genetic alteration, so a tumor is a clone. It has two components: parenchyma, the proliferating neoplastic cells, and stroma, the connective tissue and blood vessels supporting them. Neoplasm and tumor are interchangeable.

Cancer is a malignant neoplasm. The word comes from the Latin for crab, because it “adheres to any tissue that it seizes upon” and reaches out with claws into surrounding tissue. A metastasis is the portion of a cancer that has migrated from the primary site to other sites.

Histologically, four features move a tumor along that spectrum: pleomorphism, abnormal nuclei, mitoses, and abnormal differentiation.

Why does a tumor outgrow normal tissue? The deck answers it from stem cell kinetics. A stem cell has unlimited self-renewal and cellular immortality but a relatively low rate of proliferation; once a cell commits to differentiation, proliferation can be dramatic, but those differentiated cells have a limited life-span. Abnormal differentiation in cancer puts a greater percentage of cells in the proliferative pool at the expense of the maturation pool, so the mass grows through a higher proliferative fraction AND a lower rate of cell loss — both halves, not just faster division. The deck is careful to call the cancer stem cell idea a conceptual framework rather than an absolute explanation.

3.4 · Objective d — Routes of tumor spread

A cavity here is defined by the membrane covering the organs in it and the membrane covering the cavity wall — pericardium, pleura and peritoneum over heart, lungs and abdominal organs respectively.

3.5 · Objectives e & f — Classifying tumors by origin

This is a naming rule, and once you have it, every tumor name in medicine decodes. Two origins, and a suffix for each.

3.6 · Objectives g & h — Gene alterations and chemical carcinogenesis

Carcinogenesis is a multistep process resulting from damage to multiple normal regulatory genes. Those genes may be inherited and/or damaged by chemical carcinogens, ultraviolet and ionizing radiation, or microbial organisms — viruses and a bacterium.

Chemical carcinogenesis has two named steps. Initiation, caused by initiators: chemicals cause permanent damage to deoxyribonucleic acid. Promotion, caused by promoters: sustained or enhanced proliferation of cells already damaged by an initiating agent, raising the risk of successive mutations.

3.7 · Objective i — Microorganisms and carcinogenesis

Five organisms, and they divide into two mechanisms. Either the microbe directly disables a tumor suppressor, or it causes chronic inflammation with repeated regeneration and lets mutations accumulate. Sorting them that way turns five facts into two ideas.

And the inflammatory mechanism has a testable consequence: eradicating Helicobacter pylori can reduce the risk of gastric cancer and may induce regression of some early MALT lymphomas. That is the cleanest evidence in the lecture that the chronic inflammation is doing the carcinogenic work.

Radiation gets its own short slide: ultraviolet radiation — UVB — and ionizing radiation.

3.8 · Objective j — Heredity and carcinogenesis

Inherited cancer risk comes through the same gene categories, just present from birth.

3.9 · Objective l — TNM staging

Staging has three purposes: it indicates the extent of spread within the patient, it determines prognosis, and it guides management. It is based on three things, which are exactly the three letters: the size of the primary lesion, the extent of spread to regional lymph nodes, and the presence or absence of blood-borne metastases.

4 · Ophthalmic Pathophysiology

4.1 · Objectives a & b — Anatomy and the physiology of vision

Five things make the eye unusual, and each one explains a disease later in this lecture. The cornea is avascular, oxygenated by direct contact with air and tears, and about seventy percent of refraction depends on it — which is why corneal disease blurs vision so completely. The retina has the highest oxygen consumption and metabolic rate of any tissue, higher than cerebral cortex, which is why it tolerates ischemia so badly. And the eye is the only place in the body where live neural tissue and native microcirculation can be seen directly, without cutting anything.

The three tunics, outside in:

Vision needs three things and will fail if any one is lost: image formation (light refracted by cornea and lens onto the retina), photoreceptor excitation (photons make rods and cones fire hyperpolarizing potentials), and neural transmission (optic nerve to occipital cortex).

Rods, about 120 million, are high-sensitivity, for dim light and the peripheral retina. Cones, about 6 million, carry color and sharp acuity and are concentrated in the fovea centralis within the macula. Beneath them the retinal pigment epithelium does three jobs — absorbs scattered light, phagocytoses spent photoreceptor outer segments, and maintains the blood-retinal barrier. Signals pass through bipolar, horizontal and amacrine interneurons to the ganglion cells, whose axons become the optic nerve. The optic disc is the blind spot because it has no rods or cones.

Fluid mechanics. Aqueous humor is made continuously by the non-pigmented epithelium of the ciliary body into the posterior chamber, flows through the pupil into the anterior chamber nourishing the avascular lens and cornea, and drains trabecular meshwork → canal of Schlemm → episcleral veins. That drainage route is the whole of glaucoma. Behind the lens, vitreous humor — water, type two collagen, hyaluronic acid — acts as a shock absorber pressing the retina against the pigment epithelium. Its age-related liquefaction is the whole of rhegmatogenous detachment.

4.2 · Objectives d & e — Globe shape, and the age-related conditions

Astigmatism can stack on top of myopia or hyperopia, adding an axis error to a focal-length error, which is why it blurs the whole field rather than one distance.

Presbyopia is the one he came back for. The lens is normally elastic; with age it hardens, so the ciliary muscle can no longer change its shape — that is what “cannot accommodate” means. He tied it to the A in PERRLA — Pupils Equal, Round, Reactive to Light and Accommodation — and quizzed the room on what the A stands for.

Strabismus versus amblyopia is a mechanical problem against a developmental one. Strabismus is misalignment — the visual axes fail to land on corresponding retinal points — from extraocular muscle imbalance or a third, fourth or sixth nerve palsy; subtypes are esotropia (in), exotropia (out), hypertropia (up), hypotropia (down). Amblyopia is reduced best-corrected acuity from abnormal visual processing during the critical developmental period, caused by uncorrected strabismus, severe refractive error, or deprivation from congenital cataract or ptosis. The treatment window closes at seven to eight years because that is when the visual system stops being plastic.

4.3 · Objective g — Cataract

A cataract is opacification of the crystalline lens. Four routes to it:

Presentation: gradual, painless, bilateral blurring; glare around headlights at night; monocular diplopia; altered color perception. On examination: loss of the normal red reflex, with a white opacity through the pupil (leukocoria) when severe. Usually peripheral in the lens, but a nuclear cataract is often post-traumatic.

4.4 · Objective f — Glaucoma

The hallmark: raised intraocular pressure compresses retinal ganglion cell axons at the disc → ganglion cell apoptosis → progressive optic disc cupping, an increased cup-to-disc ratio above 0.5. The vision loss is nerve loss, not media opacity — that is the whole answer to his question.

4.5 · Objectives h & i — Retinal detachment and macular degeneration

Why age matters first: the vitreous is gel-like in youth and liquefies with age — the lecturer's analogy was jelly left in the fridge, separating into a liquid layer over a solid one. Liquefied vitreous is what can pass through a break.

Rhegmatogenous symptoms: flashing lights (photopsia), a shower of floaters, then a curtain falling across the field.

Macular degeneration is the leading cause of new-onset blindness in United States adults over 75. The deck is explicit that the pathogenesis is unknown for both forms.

Diabetic retinopathy is the leading cause of new-onset blindness in United States adults 20 to 74 — a different age band from macular degeneration, and an easy pair to swap. Chronic hyperglycemia damages capillaries and endothelial basement membranes → capillary occlusion and hypoxia. Non-proliferative: dilated veins, microaneurysms, dot and blot hemorrhages, hard exudates (lipid in the outer plexiform layer), cotton-wool spots (nerve fiber layer ischemia), macular edema. Proliferative: severe ischemia upregulates vascular endothelial growth factor → neovascularization on disc and retina → vitreous hemorrhage, fibrotic traction, tractional detachment.

4.6 · Objective j — Visual field deficits by lesion site

The decussation is the key. Nasal retinal fibers — which carry the temporal visual fields — cross at the chiasm. Temporal retinal fibers stay ipsilateral. Everything below follows from that one fact. The pathway runs optic disc → optic nerve → chiasm → optic tract → lateral geniculate nucleus → optic radiation → occipital cortex.

D and E are grayed because he deferred them to neurology. They are on the slide, so they are here — but A, B and C carry the weight.

One more consequence he drew out: losing vision in one eye costs the binocular overlap, and with it depth perception. Everything becomes flat.

5 · ENT Pathophysiology

5.1 · Objectives 1 & 3 — Anatomy and auditory transduction

The ear is three compartments with three different jobs, and almost every disease in this lecture is a failure of one of them. The external ear — auricle and canal — captures and concentrates acoustic waves and localizes sound; ceruminous glands line it and the outer third carries protective hair follicles. The middle ear is air-filled, which is the single fact that makes otitis media and Eustachian tube dysfunction make sense: the tympanic membrane vibrates, the malleus, incus and stapes amplify, and the Eustachian tube equalizes pressure. The inner ear holds the cochlea, which converts fluid displacement into neural signal at the organ of Corti, and the vestibule and semicircular canals, which hold dynamic rotational equilibrium.

The transduction chain, in the order the slide gives it. Follow it once and four later diseases become obvious:

1. Stapes vibration at the oval window generates pressure waves in the fluid-filled scala vestibuli, displacing endolymph in the cochlear duct.
2. Shearing force. Basilar membrane displacement bends the stereocilia against the rigid tectorial membrane. The rigidity is the point — the cilia are bent because one end moves and the other does not.
3. Ion depolarization. That mechanical deflection opens tip-link channels, permitting rapid influx from endolymph into the hair cells.
4. Neurotransmission. Depolarization triggers voltage-gated channels, releasing glutamate onto cranial nerve VIII fibers.

Read that chain backwards and you have the map of hearing loss. Break step 1 and you get conductive loss. Break steps 2 to 4 and you get sensorineural loss. Nothing else in this lecture changes that division.

5.2 · Objective 5 — Conductive against sensorineural loss

The Weber result is the one people invert. It goes to the bad ear in conductive loss, which feels wrong until you see why: the blockage stops competing room noise from reaching that cochlea, so the bone-conducted tone has the ear to itself and sounds louder there. In sensorineural loss the cochlea itself is damaged, so the tone is simply heard better on the side that still works. He walked the class through both tests live [5:02–6:48]: Weber on top of the head, Rinne first at the ear and then on the mastoid.

Conductive loss has exactly four core mechanisms, and every cause on the slide is one of them. Learn the mechanism and the examples come free:

Two and three are the pair that get confused. Mass loading adds weight to a chain that can still move; stiffness stops the chain moving at all. Effusion damps; otosclerosis fixes.

Cholesteatoma is on the slide as a mass-loading example: added tissue weight that damps tympanic membrane and ossicular movement, the same way an effusion adds fluid weight. He flagged it at [12:17] as one to know (“you should know about it”) and said it usually needs surgical removal. Despite the name it is not a cholesterol mass: the CMS External and Middle Ear deck defines it as a collection of keratinized squamous epithelium in the middle ear or mastoid, with no cholesterol components and not a neoplasm.

5.3 · Otosclerosis

Pathogenesis: abnormal osteoclastic bone resorption followed by hypervascular spongy osteoid replacement around the otic capsule and the stapes footplate. Resorption first, then the wrong bone grows back in its place.

The clinical pearl is one event: ankylosis of the stapes footplate in the oval window halts mechanical vibration transfer, giving progressive conductive loss. The cochlea is untouched, which is why this is conductive rather than sensorineural — it is mechanism 3, stiffness.

Demographics and inheritance, which he flagged at [16:16] as the thing to remember: commonest in young-to-middle-aged females, accelerated by pregnancy, and 50% autosomal dominant with variable penetrance.

5.4 · Ototoxicity and noise

He gave the organizing rule before the detail [16:34]: “Ototoxic medications, almost always reversible, except for some like platinum chemotherapy.” Sort the four drug groups by whether the damage stays.

Why high frequencies go first is anatomical, not chemical. The base of the cochlea encodes high pitch, and the base is where the aminoglycoside damage starts. The same geometry explains presbycusis, which is why the two sound alike on an audiogram.

Two drugs hit the same structure with opposite outcomes. Cisplatin and furosemide both act on the stria vascularis — the strip of tissue that maintains endolymph. One cross-links its DNA and kills it; the other only shifts its electrical potential. That is the whole of why one is permanent and one is not.

Noise. Long-term chronic exposure above 85 decibels induces irreversible stereocilia degeneration and acoustic hair cell apoptosis. The deck's ladder, with what he added aloud at [9:01]:

Presbycusis is gradual, symmetrical, bilateral sensorineural loss in older adults. Its frequency curve begins with high-frequency tones — the speech consonants /s/, /f/, /t/ — which is why the complaint is never “I cannot hear” but “I cannot follow conversation in a noisy room”. Vowels carry the volume; consonants carry the meaning, and it is the consonants that go.

5.5 · Otitis media and otitis externa

Otitis media usually begins with Eustachian tube dysfunction, and the sequence is mechanical: failure of the tube to open periodically → absorption of oxygen and nitrogen into the middle ear mucosa → negative middle ear pressure. The air-filled middle ear is a sealed box whose only vent has stopped working; the mucosa takes up the gas and the pressure drops. Effusion follows, and the membrane bulges once fluid accumulates [23:06].

The fungal trigger is worth a second look, because it is the same logic as thrush: clear the bacteria with a long antibiotic course, or keep the canal permanently wet, and the fungus has no competition.

5.6 · Objective 4 — Equilibrium, and vertigo against dizziness

Two separate detectors, and they answer different questions:

Canals answer “am I turning?”; otoliths answer “which way is down?” Keep them apart, because benign paroxysmal positional vertigo is precisely a failure of the otolith organs that produces a canal symptom.

Now the distinction the objective actually asks for:

“NO syncope” is the discriminator the deck puts in capitals, and it is the cleanest one you have. Vertigo is a false signal of motion; the brain is perfused normally, so the patient does not faint. Dizziness is a perfusion or metabolic problem, so fainting is exactly what is threatened. The word the patient uses tells you nothing — both arrive as “dizzy”.

Visual fixation is the bedside test and he explained why it works [29:38]: “by fixing view … you’re overriding the vestibular function telling you that things are moving. You’re actually helping a person to kind of calm the vertigo down. You can do that with peripheral vertigo. You cannot do that with central.” A peripheral lesion sends a false signal that vision can outvote; a central lesion has broken the machinery that does the voting.

5.7 · The four peripheral vertigos

This is the highest-yield table in the lecture. Read down the duration column first — seconds, hours, days — then check hearing.

Vestibular neuritis is not on a slide of its own and he explained why [32:32]: “Labyrinthitis … is just an inflammation of the entire inner ear. Remember I said there’s another thing called vestibular neuritis? That’s just the same thing, but just inflammation of the nerve fibers. That’s the only difference.” One lesion in two places: hit the whole labyrinth and hearing goes with balance; hit the nerve alone and only balance goes.

Ménière disease — endolymphatic hydrops. Defective endolymph resorption leads to excessive fluid accumulating in the membranous labyrinth, ballooning the scala media until micro-ruptures occur. Production is normal; drainage is not. The episodic pattern follows directly from the micro-ruptures — pressure builds, the membrane gives way, symptoms fire, pressure re-equilibrates, and the cycle restarts.

Labyrinthitis — otitis interna. Inflammatory swelling, vascular congestion and endolymphatic disruption within the semicircular canals and the cochlea produce a sudden, concurrent impairment of both balance and hearing. Cause: viral infection, recent viral upper respiratory infection. Hearing and balance fail together for a purely anatomical reason — one continuous fluid space serves both organs, so inflammation anywhere in it disturbs both.

Its features: unilateral tinnitus in the affected ear, unilateral sensorineural hearing loss, and horizontal-rotary nystagmus with the fast phase beating AWAY from the affected side, with severe postural instability, gait ataxia and nausea.

Benign paroxysmal positional vertigo — canalithiasis. Otoconia, the crystals that normally sit in the utricle, become dislodged into the semicircular canals. Asked in the room how that happens, he scoped the answer for this course [36:43–37:16]: aging, “no one really knows exactly … but what you need to know for pathophysiology is that they can become loose. And when they come loose and they’re floating around in the endolymph, they can hit structures and cause the sensation of movement, of motion.”

Which explains all three of its features at once: episodes under a minute (the crystals settle), triggered by positional change of the head (they only move when gravity moves them), and NO hearing loss (the cochlea is nowhere near this). No hearing loss is the discriminator — it is the one peripheral vertigo that leaves hearing alone, apart from vestibular neuritis.

5.8 · Rhinology

Rhinitis is the nose; rhinosinusitis is the nose and the sinuses [37:39]. Duration then splits it:

Discharge color is the fastest discriminator and he opened the section with it [37:26]: allergic rhinitis gives clear discharge, acute bacterial sinusitis gives purulent discharge. Facial pain localizes to the sinuses, which is why it belongs to rhinosinusitis and not to rhinitis.

He was also honest about the gap in the definitions [37:54]: “I always wonder, so what’s the in-between? … What if it’s seven weeks?” Four to twelve weeks is unclassified, and in practice means either a second acute episode or an untreated allergy underneath.

Nasal polyps. Non-neoplastic, benign edematous masses arising from the mucous membranes of the sinus ostia or ethmoid air cells. Molecular pathway: chronic type 2 allergic responses, diffuse cytokine release — interleukins 4, 5 and 13 — and tissue eosinophil influx. Not neoplastic is the word that matters: no new tissue is being grown, the existing mucosa is waterlogged [40:28].

Turbinate hypertrophy is enlargement of the inferior nasal turbinates from venous sinusoid engorgement, mucosal edema, or bony hypertrophy. Triggers: allergic rhinitis, vasomotor instability, and rebound hyperemia from topical decongestants — rhinitis medicamentosa. Overuse of a decongestant spray produces the congestion it was bought to relieve [42:44].

Deviated septum. Displacement of nasal cartilage or bone off the midline divides the cavities into asymmetric flow channels, and the consequences all follow from airflow physics rather than from the deviation itself:

The compensation is the part that gets missed. The turbinate that hypertrophies is on the open side, not the blocked one — it is working harder, humidifying air the narrow side can no longer carry. So a patient can be obstructed on both sides from a one-sided deviation. He put the airflow split at “97% of all air coming into the nose going through one side” [45:23], and told the class to reverse the inference: when you find enlarged inferior turbinates, go looking for the septal deviation that caused them [42:22].

Epistaxis. Two bleeds, two vessels, two risk profiles. The management column on the slide belongs to Clinical Medicine and Surgery; what this course asks for is the vascular source and the etiology.

The etiology columns are the tell. Anterior causes are all local — something hit or dried the mucosa. Posterior causes are all systemic — vessel pressure and clotting. That is also why posterior bleeds are dangerous: he explained at [44:49] that Woodruff’s plexus carries far more arterial supply than Kiesselbach’s, so an arterial bleed sits behind a space you cannot compress. “You get a posterior bleed, that thing may not stop bleeding” [44:30] — but “you will usually only see anterior epistaxis” [45:06].

5.9 · Larynx and neck

Nodules against polyps. Everything separates on laterality, site and the kind of trauma:

Chronic and bilateral against acute and unilateral. Repeated impact damages both cords at the same point, because both cords take the same blow; a single violent strain or a bleed damages one. He drew the same line on the tissue at [46:04]: “hyalinisation is not the same as callus formation. Hyalinisation is kind of like a pink, excessive membrane growth. Callus is obviously like a fibrous material formation, but it can be either or in the nodules.”

Where the audio and the slide disagree, the slide wins here. At [46:38] he began “Polyps, however … these are usually bilateral” and corrected himself inside the same sentence to “Unilateral lesions in the polyps”. The slide says unilateral, and the slide's own picture shows one lesion on one cord. Polyps are unilateral.

Tonsillitis. Acute viral or bacterial inflammation of the palatine tonsils and pharyngeal mucosa, usually Group A Streptococcus when bacterial. Symptoms: sore throat, odynophagia (pain on swallowing), fever, tonsillar exudates, trismus, and asymmetric tonsillar deviation if complicated by a tonsillar abscess.

Asymmetry is the alarm. Tonsillitis is symmetrical; an abscess pushes one tonsil across the midline and clamps the jaw. He added the airway point at [47:18]: chronic swollen tonsils that obstruct the airway are an emergency. And epiglottitis sits just below, “a little inferior to the tonsillitis”.

The slide’s picture carries a distinction its text does not: white patches or nodules on red swollen tonsils point bacterial; redness and swelling with no exudate points viral — which is how he read it aloud at [47:31].

Cervical lymphadenopathy. Usually benign enlargement of cervical nodes responding to regional head and neck infection — viral upper respiratory infection, otitis media, dental disease — or to systemic inflammatory conditions. The reactive node is palpable and tender.