Clinical Pathophysiology I · Exam 1 · Class of 2028

Clinical Pathophysiology I Exam 1 Cram Sheet

Lecture 1 Inflammation and Lecture 2 Dermatology — mechanism only. Diagnosis and management belong to Clinical Medicine and Surgery I.

Definitions & Mechanisms Acute vs Chronic Patterns (8) White Blood Cells Sequence of Acute Inflammation Mediators & Opsonins Integument — Anatomy Primary Lesions Secondary Lesions & Healing Mechanisms of Common Conditions Skin Cancers & Nails Non-Neoplastic Abnormalities of Growth Neoplasia, Grading & Benign vs Malignant Routes of Spread & Classification by Origin Gene Alterations, Chemicals, Microbes & Heredity Cancer Staging & TNM From the Lecture Recording ★ KNOW FOR EXAM — HE STATED THESE Eye Anatomy & Vision Physiology Globe Shape & Age-Related Cataract & Glaucoma Retina, Macula & Diabetic Cascade Visual Field Deficits by Lesion Site ★ VERTIGO — HE WEIGHTED THIS ONE Hearing Loss — Conductive vs Sensorineural Otosclerosis, Ototoxicity & Noise Otitis Media & Externa Rhinology Larynx & Neck

How to use this: this is a condensed, night-before-the-exam reference, not a replacement for the full study guide — it assumes you've already learned the material and just need the highest-yield facts at a glance. If a term feels unfamiliar, go back to the full guide for the explanation.

Definitions & Mechanisms

Term	What you need to know
Term	What you need to know
Inflammation	The reaction of VASCULARIZED living tissue to injury. Avascular tissue cannot mount one.
Two healing routes	New tissue from native parenchymal cells, OR fibroblastic scar tissue.
Five main processes	Increased blood flow → increased permeability → migration of neutrophils → chemotaxis → leukocyte recruitment and activation.
The vascular causal chain	Vasodilation of arterioles (more flow) → endothelial contraction (more permeability) → exudation (fluid + blood proteins into interstitium). Each step enables the next.

Acute vs Chronic

Term	What you need to know
Term	What you need to know
Acute	Seconds/minutes/hours/days. Begins WITHIN SECONDS of injury. Damage may be purely physical or involve immune activation (trauma vs bee sting).
Chronic	Days/weeks/months. Histology: lymphocytes and macrophages, proliferation of blood vessels, fibrosis, tissue necrosis.
3 causes of chronic	Persistent infection · prolonged toxic agents · autoimmunity.
Toxic agents	ENDOgenous = atherosclerosis. EXOgenous = particulates such as silica.
Autoimmune examples	Rheumatoid arthritis, lupus.
Chronic cell roles	Lymphocytes + plasma cells mediate ANTIBODY production. Macrophages PROCESS and DELIVER antigen to immunocompetent cells.

Patterns (8)

Term	What you need to know
Term	What you need to know
Serous	Largely plasma, LOW protein. Early or mild.
Fibrinous	Lots of fibrinogen → thick meshwork. Removable ONLY by fibrolytic enzymes; failure → scar tissue.
Suppurative / purulent	Remnants of WBCs, protein, tissue debris = pus.
Hemorrhagic	Damage to blood vessels; occurs WITH other exudates.
Catarrhal	Mucus hypersecretion on a mucous membrane.
Ulcerative	Necrosis + sloughing of surface epithelium → EXPOSES connective tissue beneath (removes a layer).
Pseudomembranous	Superficial necrotic layer of fibrin/inflammatory cells/debris → membrane-like covering OVER mucosa (adds a layer).
Gangrenous	Severe necrosis ± bacterial infection. DRY = coagulative. WET = liquefactive, from infection.

White Blood Cells

Term	What you need to know
Term	What you need to know
Granulocytes (PMN)	Neutrophils, basophils, eosinophils. Granules = membrane-bound enzymes digesting phagocytized particles. PMN = ALL granulocytes, not just neutrophils.
Agranulocytes	Lymphocytes (B, T), monocytes, macrophages. Do contain non-specific azurophilic granules (lysosomes) despite the name.
Neutrophil	First responder to microbial infection; bacterial + fungal. Multilobed nucleus, fine pale lilac granules. CANNOT renew lysosomes → dies after a few pathogens → forms pus.
Basophil	Bi-/tri-lobed nucleus, coarse granules. Allergic and antigen response via HISTAMINE.
Eosinophil	Bi-lobed nucleus, PINK-ORANGE granules. Parasites; predominant cell in allergy (asthma, hay fever, hives).
B lymphocyte	Humoral. Makes antibody, acts as antigen-presenting cell, becomes memory B cell.
T lymphocyte	Matures in Thymus; carries T cell receptors. Helper = activate/regulate T and B. CD8+ cytotoxic and NK = virus-infected and tumor cells. Regulatory = restore normal function, prevent autoimmunity.
Monocyte	Kidney-shaped nucleus, abundant agranulated cytoplasm. Phagocytoses then presents to T cells; becomes tissue macrophage. CAN replace lysosomal contents.

Sequence of Acute Inflammation

Term	What you need to know
Term	What you need to know
Vascular (1–4)	Vasoconstriction → vasodilation → increased vascular permeability → hemoconcentration and stasis.
Cellular (5–9)	Leukocyte adhesion → transmigration → chemotaxis → aggregation → phagocytosis.
Why stasis matters	Slowed flow is the hinge — it lets leukocytes reach and hold against the endothelium, so adhesion can begin.
Digestion of foreign material	Recognition → attachment → engulfment → degradation. Recognition and attachment are enhanced by opsonins.
Acute in review	Short term (minutes–days). Exudation of fluid, plasma, proteins, leukocytes (neutrophils); phagocytosis and enzymatic release.

Mediators & Opsonins

Term	What you need to know
Term	What you need to know
Histamine	FIRST mediator of the initial response. Dilates arterioles; increases permeability of capillaries and venules.
Serotonin	Vasodilation and increased vascular permeability.
Bradykinin	Increases capillary permeability, CAUSES PAIN, may increase leukocyte chemotaxis. Pain is the discriminator.
Complement	10% of circulating serum proteins. Chemotactic to neutrophils and monocytes; cascade may damage bacteria.
Coagulation system	Fibrous network traps exudate, microorganisms, foreign bodies; stops bleeding so repair can begin.
Opsonin	Protein adhering to foreign material, making it easier for immune cells to recognize and attach.
IgG vs C3b	IgG = antibody, read by Fc RECEPTORS on macrophages/neutrophils. C3b = complement fragment, read by COMPLEMENT RECEPTORS.
Biomaterial pearl	Anything not human put into a human gets coated with IgG and C3b → immune cells attach. An implanted device can inflame even when STERILE.

Integument — Anatomy

Term	What you need to know
Three layers	Epidermis · dermis · subcutaneous (hypodermis). Nerves and vasculature sit in the DERMIS — the epidermis has no blood supply of its own.
Epidermal cell types	Keratinocytes (~90%), melanocytes, Merkel cells, Langerhans cells. Turnover every 30–60 days, faster in younger patients.
Strata, deep → superficial	Basale (the only dividing layer) · spinosum (desmosomes = prickle cells; Langerhans) · granulosum (keratohyalin) · lucidum · corneum (20–30 dead layers = the barrier).
Dermis	Papillary (thin, superficial) and reticular (dense, deep). Collagen from fibroblasts = tensile strength; elastin + fibrillin = recoil. Mast cells mediate immunoglobulin E inflammation.
Vitamin D chain	Cholecalciferol made in SKIN under ultraviolet B → hydroxylated in LIVER → then KIDNEY → calcitriol. Three organs.
Sweat glands	Eccrine: onto the surface, water and electrolytes, cooling. Apocrine: axilla/anogenital, protein and lipids, scent — odor comes from bacterial degradation.
Hair	Terminal (thick, androgen-regulated) · lanugo (newborn) · vellus (fine, androgen-independent).

Primary Lesions

Term	What you need to know
NOT palpable	Macule (≤5 mm) and patch (>5 mm). Hyperpigmented = more melanin in basal layer; hypopigmented = LOSS of melanocytes (vitiligo).
Palpable and solid	Papule (<5 mm, epidermal hyperplasia + hyperkeratosis) · nodule (>5 mm, dermal, dense collagen) · plaque (>1 cm, confluence of papules).
Vesicle vs bulla	Vesicle ≤5 mm, fluid within or just beneath epidermis. Bulla >5 mm, SEPARATION of epidermis from dermis — a deeper plane, not just bigger.
Wheal	Mast cell histamine → vasodilation + permeability → plasma into dermis; histamine also hits nerve endings → pruritus. Transient.
Pustule	Purulent: leukocytes, debris, serous fluid, ± organisms. Usually Staphylococcus aureus or Streptococcus pyogenes — but MAY BE STERILE (rosacea).
Cyst vs tumor	Epidermal inclusion cyst: from a hair follicle, keratin-filled. Tumor >2 cm, rapid growth, benign or malignant. Dermatofibroma = fibrous; lipoma = adipocytes.

Secondary Lesions & Healing

Term	What you need to know
Scale vs crust	Scale = desquamating stratum corneum (psoriasis). Crust = dried sebum, debris, blood or necrotic skin (impetigo).
Lichenification	Itch-scratch cycle → hyperplasia and hyperkeratosis. Thick plaques WITHOUT scaling (lichen simplex chronicus).
Erosion vs ulcer	Erosion stays ABOVE the dermal-epidermal junction. Ulcer crosses it into dermis, destroying collagen — which is why an ulcer scars and an erosion does not.
Fissure	Linear ulcer, a crack, from lost elasticity, dryness and mechanical tension, with hyperkeratosis.
Atrophy	Keratinocyte division slows + collagen synthesis slows + elastin degrades.
Healing, 3 phases	Inflammatory d1–3 (fibrin plug, neutrophils/macrophages, growth factors) · Proliferative d4–21 (granulation = macrophages + fibroblasts + endothelial cells) · Remodelling d21–1 yr.
Remodelling	Type III collagen replaced by stronger type I, in small PARALLEL bundles — normal dermis is BASKET-WEAVE. That difference is why a scar never matches.
Keloid	Fibroblast dysregulation prolongs the proliferative phase + deposition/degradation imbalance in remodelling → haphazard bundles that EXCEED the original wound boundary.

Mechanisms of Common Conditions

Term	What you need to know
Petechiae / purpura / ecchymoses	One process at three sizes: ≤1–2 mm / 3–10 mm / >10 mm. Bleeding into dermis, non-blanchable. Henoch-Schonlein = immunoglobulin A vasculitis, skin/joints/kidneys/intestines, ages 3–10.
Telangiectasia	Permanent dilatation and endothelial thinning of superficial dermal vessels — NO inflammatory infiltrate. That absence is the discriminator.
Urticaria	Mast cell degranulation → histamine → wheals.
Allergic vs irritant contact	Allergic = delayed hypersensitivity 48–72 h; sensitization (Langerhans present haptens to T cells) then elicitation. Irritant = direct chemical injury, NO prior exposure needed.
Eczema	T cell-mediated + insufficient FILAGGRIN (barrier defect). “The itch that rashes.”
Psoriasis	Autoimmune; cells multiply up to 10× faster. T cells → keratinocyte proliferation + tumor necrosis factor alpha, interferon gamma, interleukin-12. Epidermal hyperplasia, LOSS OF STRATUM GRANULOSUM, no lipid secretion (xeroderma).
Seborrheic keratosis vs actinic keratosis	SK = BENIGN immature keratinocyte proliferation, ?fibroblast growth factor receptor-3. AK = ultraviolet damage → DYSPLASTIC keratinocytes; most common precancer, risk of squamous cell carcinoma.
Verrucae	Human papillomavirus enters epidermal BASAL cells through microabrasions → epidermal proliferation.
Dermatophytes	Trichophyton, Microsporum, Epidermophyton. Keratinases and proteases digest keratin in the STRATUM CORNEUM → annular patch with central clearing.

Skin Cancers & Nails

Term	What you need to know
Basal cell carcinoma	Most common skin cancer AND most common malignancy in humans. Ultraviolet mutation of basal keratinocytes → HEDGEHOG pathway overactivation. Head/neck, slow, rarely metastasises.
Squamous cell carcinoma	Second most common. Ultraviolet DNA damage + tp53 mutation, from keratinocytes. KERATIN PEARLS are pathognomonic. Immunosuppression is a notable risk.
Melanoma	From melanocytes at the dermal-epidermal junction. Ultraviolet + oxidative stress. Risk inherited autosomal dominant with variable penetrance.
Melanoma growth order	Radial (within epidermis) → vertical (into dermis) → thickness → metastatic. The radial-to-vertical shift is when depth starts to matter.
Nails	Leukonychia = incomplete keratinization (± heavy metals) · koilonychia = impaired keratin synthesis, deficiency anemia · Beau's lines = HALT of keratin production · Terry's = connective tissue overgrowth · clubbing = increased capillary density via vascular endothelial growth factor.

Non-Neoplastic Abnormalities of Growth

Term	What you need to know
Sort the seven into three groups	FAILED TO DEVELOP: agenesis, aplasia, hypoplasia. CHANGED SIZE: atrophy, hypertrophy. CHANGED KIND: metaplasia, dysplasia.
Agenesis vs aplasia	AGENESIS = complete absence, the PRIMORDIAL TISSUE NEVER FORMED. APLASIA = the primordial tissue EXISTS but fails to develop into the mature organ. A timing question.
Hypoplasia vs atrophy	HYPOPLASIA = PARTIAL development, resulting in a FUNCTIONAL DEFICIENCY — it never got there. ATROPHY = shrinkage of a tissue or organ THAT HAD FORMED AND MATURED NORMALLY — it got there and shrank back.
Hypertrophy	Enlargement due to enlargement of INDIVIDUAL CELLS. Especially important in PERMANENT TISSUES — skeletal and cardiac muscle — but may occur elsewhere as adaptive growth. Contrast hyperplasia: MORE cells, not BIGGER cells.
Metaplasia	Change of ONE CELL TYPE TO ANOTHER in response to a CHRONICALLY IRRITATING OR INJURIOUS stimulus; involves a change in DIFFERENTIATION. The slide's example: bladder TRANSITIONAL epithelium → SQUAMOUS. Still orderly, still mature, NOT precancerous.
Dysplasia — four features	DISORDERED GROWTH, typically EPITHELIAL. (1) variation in cellular SIZE AND SHAPE, (2) LOSS OF ARCHITECTURAL ORIENTATION, (3) nuclei may be DARKER AND LARGER, (4) MAY PROGRESS TO CANCER — PRECANCEROUS.
The line that matters	Normal → mild → moderate → severe dysplasia → CARCINOMA IN SITU → INVASIVE CANCER. The BASEMENT MEMBRANE stays intact until the last panel. Everything up to and including carcinoma in situ is still above it — which is exactly what Tis means.

Neoplasia, Grading & Benign vs Malignant

Term	What you need to know
Neoplasm — the defining word	An abnormal mass growing AUTONOMOUSLY — self-perpetuating WITHOUT PHYSIOLOGIC GROWTH STIMULI. That is what separates it from hyperplasia, which stops when the stimulus stops. Interchangeable with TUMOR.
Clonal origin	The ENTIRE proliferating population is derived from ONE CELL that underwent a genetic alteration.
Two components	PARENCHYMA = the proliferating neoplastic cells. STROMA = connective tissue and blood vessels. The stroma is host tissue, not part of the clone.
Cancer & metastasis	CANCER = a MALIGNANT neoplasm. From the Latin for CRAB — 'adheres to any tissue it seizes upon', reaches out with claws. METASTASIS = the portion that has MIGRATED from the primary site.
Histological GRADING (objective k)	Measures how closely the neoplasm RESEMBLES comparable normal cells in appearance and function. WELL differentiated (close) → MODERATELY → POORLY → ANAPLASIA (LACK of differentiation).
GRADING vs STAGING	GRADING asks WHAT DOES IT LOOK LIKE. STAGING asks HOW FAR HAS IT GOT. Different questions, both still used.
Benign vs malignant	BENIGN: well circumscribed border · COMPRESSES surrounding tissue · often a FIBROUS CAPSULE · usually WELL differentiated · does NOT metastasize · SLOW growing. MALIGNANT: RAGGED border · INFILTRATES AND INVADES · VARIOUS degrees of differentiation · MAY metastasize · grows RAPIDLY.
Four histological features of malignancy	PLEOMORPHISM · ABNORMAL NUCLEI · MITOSES · ABNORMAL DIFFERENTIATION.
Stem cell kinetics — why tumors outgrow tissue	A stem cell has UNLIMITED SELF-RENEWAL and CELLULAR IMMORTALITY but a RELATIVELY LOW rate of proliferation; committed progeny proliferate dramatically but have a LIMITED LIFE-SPAN. In cancer, abnormal differentiation puts MORE cells in the PROLIFERATIVE pool at the expense of the MATURATION pool. Growth exceeds normal via a HIGHER PROLIFERATIVE FRACTION AND A LOWER RATE OF CELL LOSS — both halves.

Routes of Spread & Classification by Origin

Term	What you need to know
Hematogenous spread	Typically through VEINS — especially the PORTAL VEIN and INFERIOR VENA CAVA, so cancers often spread to LIVER and LUNGS respectively. Mechanism: cells SEPARATE from each other and DEGRADE INTERCELLULAR TISSUE WITH ENZYMES → invade the vessel → MULTIPLE fragments travel. One organ may carry several nodules.
Lymphatic spread	Cancer spreads into lymphatic vessels AT THE TUMOR MARGIN and follows the NATURAL ROUTE OF LYMPHATIC DRAINAGE. That predictability is what makes nodal staging meaningful.
Seeding	Invasion of tumor THROUGH AN ORGAN SURFACE into a cavity. PERICARDIAL, PLEURAL, PERITONEAL cavities; JOINT cavities; SUBARACHNOID space. MOST COMMONLY THE PERITONEAL CAVITY. A cavity is defined by the membrane covering the organs plus the membrane covering the cavity wall.
Metastasis is NOT random	Determined by: PATTERN OF VENOUS BLOOD FLOW · SPECIFIC RECEPTORS on tumor and endothelial cells · METASTATIC 'FITNESS' IS GENETICALLY DETERMINED.
The three hurdles after invasion	PENETRATION OF VASCULATURE → SURVIVAL IN CIRCULATION → SURVIVAL IN A NEW ORGAN. Reaching the bloodstream is only the first.
THE NAMING RULE	MESENCHYMAL (supportive tissue: connective tissue, adipose, cartilage, smooth and striated muscle, bone) → malignant = SARCOMA. EPITHELIAL → malignant = CARCINOMA.
Benign epithelial names	ADENOMA = benign epithelial tumor with a GLANDULAR pattern or from a gland; sometimes SECRETES the hormone of its gland of origin. PAPILLOMA = visible FINGER-LIKE or WARTY projections from an epithelial surface.
Malignant epithelial names	CARCINOMA. With glandular growth pattern = ADENOCARCINOMA. With squamous cell differentiation = SQUAMOUS CELL CARCINOMA.

Gene Alterations, Chemicals, Microbes & Heredity

Term	What you need to know
Carcinogenesis in one line	A MULTISTEP process resulting from damage to MULTIPLE normal regulatory genes. Damage may be INHERITED and/or from CHEMICAL CARCINOGENS, ULTRAVIOLET AND IONIZING RADIATION, or MICROBIAL ORGANISMS (viruses and a bacterium).
FOUR categories of gene alteration	(1) PROTOONCOGENES — promote REGULATED growth (growth factors, their receptors, nuclear regulatory proteins, signal transduction proteins); mutation → ONCOGENES → ONCOPROTEINS → UNCONTROLLED growth. (2) TUMOR SUPPRESSOR GENES — INHIBIT growth; NF-1, NF-2, RB, APC. (3) DNA REPAIR GENES — BRCA-1, BRCA-2. (4) APOPTOSIS GENES — make damaged cells self destruct, PREVENTING damage becoming permanent in dividing cells.
Chemical carcinogenesis — two steps	INITIATION (initiators): chemicals cause PERMANENT DAMAGE TO DNA. PROMOTION (promoters): SUSTAINED OR ENHANCED PROLIFERATION of cells ALREADY DAMAGED, increasing the risk of successive mutations.
The two named chemicals	POLYCYCLIC AROMATIC HYDROCARBONS — from COMBUSTION OF TOBACCO — bladder and lung cancer; among the MOST POWERFUL CARCINOGENS KNOWN. AROMATIC AMINES — classically emphasized in OCCUPATIONAL BLADDER CANCER.
HPV	Types 16 AND 18 cause most CERVICAL cancer. INTEGRATES viral DNA into the host genome → excess E6 and E7. E6 BLOCKS p53 (needed for self destruction of mutated cells); E7 BLOCKS RB (needed to inhibit cell growth). Also anal, vulvar, vaginal, penile, and OROPHARYNGEAL squamous cell carcinoma.
Epstein Barr virus	Certain B CELL LYMPHOMAS and NASOPHARYNGEAL CARCINOMA. Infects B lymphocytes and IMMORTALIZES them; also infects oropharyngeal epithelium. With NORMAL IMMUNE FUNCTION there is no immortalization → asymptomatic or SELF-LIMITED INFECTIOUS MONONUCLEOSIS.
Hepatitis B	HEPATOCELLULAR CARCINOMA. Chronic infection and injury → CONTINUOUS REGENERATIVE ATTEMPTS → cells at risk of mutation. ALSO encodes a protein that BINDS p53. Emphasizes: CHRONIC INFLAMMATION · REGENERATIVE HYPERPLASIA · GENOMIC INSTABILITY.
Hepatitis C	HEPATOCELLULAR CARCINOMA via chronic hepatitis → repeated cycles of CELL DEATH AND PROLIFERATION. MOST develops in patients with CIRRHOSIS, although cancer can OCCASIONALLY OCCUR WITHOUT cirrhosis.
Helicobacter pylori — the one BACTERIUM	GRAM-NEGATIVE, colonizes the stomach → CHRONIC GASTRITIS → may lead to ATROPHIC GASTRITIS and INTESTINAL METAPLASIA. Associated with GASTRIC ADENOCARCINOMA and MALT LYMPHOMA. ERADICATION can REDUCE gastric cancer risk and may INDUCE REGRESSION of some early MALT lymphomas.
Radiation	ULTRAVIOLET — UVB. And IONIZING radiation.
Heredity — tumor suppressors	Rb protein → RETINOBLASTOMA (rare childhood eye tumor) AND OSTEOSARCOMA. NF-1 and NF-2 → NEUROFIBROMATOSIS types 1 and 2, central and peripheral nervous system tumors. p16 (INK4a) → MALIGNANT MELANOMA. APC → FAMILIAL ADENOMATOSIS POLYPOSIS: 500–2500 premalignant adenomatous polyps in the TEENS AND TWENTIES, COLON CANCER BY AGE 50.
Heredity — repair genes	BRCA-1 and BRCA-2: a MINORITY of breast cancer patients have an inherited mutation. XERODERMA PIGMENTOSUM: inherited DEFECTIVE DNA REPAIR GENES, cannot repair mutations caused by UVB → increased skin cancer in SUN-EXPOSED areas.

Cancer Staging & TNM

Term	What you need to know
Three purposes of staging	INDICATES EXTENT OF SPREAD within the patient · DETERMINES PROGNOSIS · GUIDES MANAGEMENT.
Staging is based on three things	SIZE OF PRIMARY LESION · EXTENT OF SPREAD TO REGIONAL LYMPH NODES · PRESENCE OR ABSENCE OF BLOOD-BORNE METASTASES. Which is exactly T, N and M.
T — primary lesion	Tis = lesion HAS NOT INVADED THROUGH THE TISSUE BASEMENT MEMBRANE ('is' = IN SITU). T1–T3 or higher = increasing SIZE and increasing DEPTH OF INVASION.
N — regional lymph nodes	Nx = nodes CANNOT BE ASSESSED. N0 = NO regional nodal metastasis. N1, N2 or higher = increasing NUMBER AND RANGE of nodes involved.
M — metastasis	Mx = distant metastasis CANNOT BE ASSESSED. M0 = NO distant metastasis. M1 = DISTANT METASTASIS.
The convention, and the caveat	x ALWAYS means cannot be assessed; 0 ALWAYS means none found. And: TNM DEFINITIONS ARE CANCER-SPECIFIC — for some cancers DEPTH OF INVASION IS MORE IMPORTANT THAN SIZE.

From the Abnormal Cell Growth Lecture Recording

Term	What you need to know
HE SIGNPOSTS NOTHING	84 minutes, two independent transcriptions, and NO statement about what is or is not on the exam. Nothing was flagged and nothing was excluded. Study the twelve objectives evenly.
Metaplasia, his example	CHRONIC GERD. The lower esophagus is SQUAMOUS and cannot resist acid → metaplasia to COLUMNAR = BARRETT'S ESOPHAGUS → increased risk of esophageal carcinoma. His corollary: in esophageal carcinoma, SQUAMOUS cells on the sample = a PRIMARY cancer; COLUMNAR cells = SECONDARY TO REFLUX.
Dysplasia, his example	CERVICAL DYSPLASIA, usually caused by HPV — which ties straight back to E6/E7, p53 and RB in the carcinogenesis section. “Might be archival one day because of the vaccine.”
Hypertrophy, his example	WEIGHT TRAINING. Striated muscle cells DO NOT DIVIDE. Protein + resistance → more ACTIN AND MYOSIN → each FIBER gets bigger → the organ gets bigger. BIGGER FIBERS, NOT MORE FIBERS — that is the whole distinction from hyperplasia.
Why 'permanent tissues' matters	“THE MORE SPECIALIZED THE TISSUE IS, THE LESS IT CAN PROLIFERATE.” Skeletal muscle and NEURONS are the two he named. Which is why hypertrophy is the only growth response available to them.
A LINK THE SLIDES DO NOT MAKE	“As the degree of differentiation goes from well to anaplasia, THE TUMOR BECOMES MORE AGGRESSIVE.” The deck gives grading as a scale of resemblance and stops. He attaches the prognosis. Also: ANAPLASIA = ATYPIA, and differentiation is always judged against THE PARENT CELL.
Who diagnoses cancer	THE PATHOLOGIST — “the only one that can diagnose cancer”. Said twice. Grading is a histological judgment made on tissue.
How to PREDICT where mets go	REASON FROM THE VESSELS. GI primary drains by the PORTAL VEIN → LIVER. LUNG cancer sits downstream of the pulmonary circulation, so its cells enter the LEFT HEART and go out the CAROTIDS → BRAIN. “Knowing the vasculature will tell you where there's possibly mets forming.”
His carcinoma in situ mnemonic	“Carcinoma in SIGHT.” The cancerous cells are THERE, but have NOT broken through the BASEMENT MEMBRANE. Once they do, it is an INVASIVE carcinoma.
Nomenclature down to the morphemes	-OMA = tumor (plural CARCINOMATA, not carcinomas). ADENO- = glandular. LEIO- = smooth muscle (leiomyosarcoma). RHABDO- = skeletal muscle (rhabdomyosarcoma). Full nomenclature comes later in the course.
Why epithelium sloughs	EPITHELIAL TISSUE IS AVASCULAR, so the outermost layers are furthest from the nutrient supply and slough off. That is what a NORMAL epithelium looks like, before you compare it with a dysplastic one.

★ KNOW FOR EXAM — HE STATED THESE

Term	What you need to know
He opened with “This is for the test”	CATARACTS · MACULAR DEGENERATION · THE VISUAL PATHWAY · REFRACTION ERRORS · RETINAL DETACHMENT CAUSES · GLAUCOMA · PRESBYOPIA (added after he said “that’s it”).
Glaucoma — what exactly he asked	“What’s the PATHOPHYSIOLOGICAL EXPLANATION for vision loss there?” Answer: raised pressure compresses GANGLION CELL AXONS → APOPTOSIS → DISC CUPPING. It is NERVE loss, not media opacity.
Visual pathway — SCOPED	KNOW A, B, C: optic NERVE, optic CHIASM, optic TRACT. D (optic radiation) and E (occipital cortex) he DEFERRED TO NEUROLOGY — “you can know that if you want.” He also said “MEMORIZE THIS: optic nerve, optic chiasm, optic tract.”
Refraction errors — what he wants	GLOBE GEOMETRY, not lens prescriptions. “Not that important, concave and convex for my purposes. MORE IMPORTANT is knowing the difference between MYOPIA, HYPEROPIA, and the GLOBE SHAPE.” He then contradicted himself on the lenses and corrected mid-sentence — trust the slide, expect the geometry.
Retinal detachment — what he wants	“The DIFFERENT THINGS that can cause retinal detachment.” Three mechanisms, not one presentation.
Presbyopia — the one he came back for	The lens is normally ELASTIC; with age it HARDENS, so it can no longer change shape → CANNOT ACCOMMODATE. Tied to the A in PERRLA (Pupils Equal, Round, Reactive to Light, ACCOMMODATION).

Eye Anatomy & Vision Physiology

Term	What you need to know
The three tunics	FIBROUS (outer): sclera + cornea. UVEA (vascular, middle): choroid + ciliary body + iris. RETINA (neurosensory, inner).
Five unique features	CORNEA AVASCULAR — oxygenated by AIR AND TEARS, ~70% OF REFRACTION. RETINA has the HIGHEST OXYGEN CONSUMPTION of any tissue, higher than cortex. Only place to see LIVE NEURAL TISSUE and NATIVE MICROCIRCULATION directly. ~83% of knowledge acquisition.
Three requirements for vision	IMAGE FORMATION (cornea + lens onto retina) · PHOTORECEPTOR EXCITATION (photons → HYPERPOLARIZING potentials) · NEURAL TRANSMISSION (optic nerve → occipital cortex).
Rods vs cones	RODS ~120 MILLION — dim light, PERIPHERAL retina. CONES ~6 MILLION — color + sharp acuity, concentrated in the FOVEA CENTRALIS within the macula.
Retinal pigment epithelium — 3 jobs	ABSORBS SCATTERED LIGHT · PHAGOCYTOSES outer photoreceptor segments · maintains the BLOOD-RETINAL BARRIER.
Retinal interneurons	BIPOLAR, HORIZONTAL, AMACRINE modulate the signal → GANGLION CELLS, whose axons form the OPTIC NERVE.
Optic disc	THE BLIND SPOT — no rods or cones.
Aqueous: made where, drains where	MADE by the NON-PIGMENTED EPITHELIUM OF THE CILIARY BODY into the POSTERIOR chamber → through the pupil → ANTERIOR chamber (nourishes avascular LENS and CORNEA) → TRABECULAR MESHWORK → CANAL OF SCHLEMM → EPISCLERAL VEINS. That route is all of glaucoma.
Vitreous	WATER + TYPE II COLLAGEN + HYALURONIC ACID. Shock absorber pressing retina onto RPE. Its age LIQUEFACTION is all of rhegmatogenous detachment.

Globe Shape & Age-Related

Term	What you need to know
MYOPIA	Axial globe TOO LONG → focal point IN FRONT of the retina. Near vision preserved.
HYPEROPIA	Axial globe TOO SHORT → focal point BEHIND the retina. Distance vision preserved.
ASTIGMATISM	IRREGULAR CORNEAL OR LENS CURVATURE → non-spherical focal points, so NOTHING focuses properly anywhere. Can STACK on myopia or hyperopia.
PRESBYOPIA	LENS SCLEROSIS, loss of elasticity + loss of ciliary accommodation → cannot focus NEAR. “Readers”/bifocals.
STRABISMUS = MECHANICAL	Visual axes fail to land on corresponding retinal points. ESOtropia in · EXOtropia out · HYPERtropia up · HYPOtropia down. From EOM IMBALANCE or CN III/IV/VI PALSY.
AMBLYOPIA = VISUAL DEFICIT	Reduced BEST-CORRECTED acuity from abnormal visual processing in the CRITICAL DEVELOPMENTAL PERIOD. Causes: uncorrected strabismus, severe refractive error, DEPRIVATION (congenital cataract, ptosis).
Amblyopia treatment window	BEFORE AGE 7–8 — because that is when the visual system stops being plastic.

Cataract & Glaucoma

Term	What you need to know
CATARACT — four mechanisms	SENILE: insoluble aggregation of LENS CRYSTALLIN PROTEINS. DIABETES: glucose → SORBITOL → OSMOTIC SWELLING. DRUGS/TRAUMA: chronic CORTICOSTEROIDS, capsule rupture. CONGENITAL/ENVIRONMENTAL: DOWN SYNDROME, UV, oxidative damage.
Cataract presentation	GRADUAL, PAINLESS, BILATERAL blurring · GLARE AROUND HEADLIGHTS AT NIGHT · MONOCULAR DIPLOPIA · altered color. EXAM: LOSS OF THE RED REFLEX, leukocoria if severe. Usually PERIPHERAL in the lens; NUCLEAR is often post-TRAUMATIC.
GLAUCOMA — the hallmark (he asked for this)	Raised IOP compresses RETINAL GANGLION CELL AXONS → GANGLION CELL APOPTOSIS → progressive OPTIC DISC CUPPING, cup-to-disc ratio > 0.5.
OPEN-ANGLE	Angle stays OPEN; MICROSCOPIC RESISTANCE in the TRABECULAR MESHWORK impairs outflow → gradual rise. INSIDIOUS, PAINLESS, BILATERAL. PITFALL: ASYMPTOMATIC until severe PERIPHERAL loss (“tunnel vision”).
ANGLE-CLOSURE	MYDRIASIS displaces iris forward against cornea (IRIS BOMBÉ) → total outflow blockage → spike ABOVE 50 mmHg. SEVERE PAIN, HEADACHE, HALOS, CLOUDY CORNEA, FIXED MID-DILATED PUPIL, NAUSEA/VOMITING.
The deck contradicts itself on normal IOP	Slide 24 says 10–21 mmHg; slide 25 says “about 6–19.” PD2’s deck independently says 10–21. NOTHING IS GRADED ON THIS. What is NOT disputed: the acute spike ABOVE 50.

Retina, Macula & Diabetic Cascade

Term	What you need to know
Why age matters first	The VITREOUS LIQUEFIES with age. Liquefied vitreous is what can pass through a break.
RHEGMATOGENOUS	FULL-THICKNESS TEAR → liquefied vitreous enters the SUBRETINAL SPACE and PEELS the retina off the RPE. Risks: PVD, AGE, SEVERE MYOPIA, TRAUMA, LATTICE DEGENERATION. Symptoms: PHOTOPSIA · SHOWER OF FLOATERS · CURTAIN FALLING.
TRACTIONAL	Proliferative FIBROVASCULAR MEMBRANES on the retinal surface PHYSICALLY PULL the retina off. Chiefly PROLIFERATIVE DIABETIC RETINOPATHY; also prior trauma/surgery/vitrectomy scarring.
EXUDATIVE (SEROUS)	Subretinal fluid with NO TEAR AND NO TRACTION — BLOOD-RETINAL BARRIER BREAKDOWN. Causes: SEVERE MALIGNANT HYPERTENSION, SARCOIDOSIS, CHOROIDAL MELANOMA.
DRY (ATROPHIC) AMD	Slow bilateral degeneration of photoreceptors, RPE and choroid. HALLMARK: DRUSEN — yellow extracellular debris (LIPOFUSCIN, APOLIPOPROTEINS) beneath the RPE and BRUCH MEMBRANE. Slow central loss, METAMORPHOPSIA, SCOTOMA.
WET (NEOVASCULAR) AMD	HYPOXIA + INFLAMMATION → CHOROIDAL NEOVASCULARIZATION beneath the RPE into the subretinal space. Leak → RAPID central loss, DISCIFORM SCARRING, detachment. ~90% OF SEVERE AMD BLINDNESS.
Pathogenesis of AMD	UNKNOWN — the deck says so for both forms.
Two blindness statistics — do not swap them	DIABETIC RETINOPATHY: leading cause of new-onset blindness in US adults 20–74. MACULAR DEGENERATION: leading cause in US adults OVER 75.
Diabetic retinopathy cascade	CHRONIC HYPERGLYCEMIA damages capillaries + endothelial basement membranes → OCCLUSION + HYPOXIA. NON-PROLIFERATIVE: dilated veins, MICROANEURYSMS, dot/blot hemorrhages, HARD EXUDATES (lipid, OUTER PLEXIFORM layer), COTTON-WOOL SPOTS (NERVE FIBER layer ischemia), macular edema. PROLIFERATIVE: ischemia → VEGF → NEOVASCULARIZATION → vitreous hemorrhage, traction, detachment.

Visual Field Deficits by Lesion Site

Term	What you need to know
THE ONE FACT EVERYTHING FOLLOWS FROM	NASAL retinal fibers — which carry the TEMPORAL visual fields — CROSS at the chiasm. TEMPORAL retinal fibers stay IPSILATERAL.
The pathway	OPTIC DISC → OPTIC NERVE → CHIASM → OPTIC TRACT → LATERAL GENICULATE NUCLEUS → OPTIC RADIATION → OCCIPITAL CORTEX.
A — ipsilateral OPTIC NERVE	MONOCULAR BLINDNESS. Causes: trauma, optic neuritis, ischemic optic neuropathy.
B — OPTIC CHIASM (center)	BITEMPORAL HEMIANOPSIA — only the crossing NASAL fibers are cut, and they carry the TEMPORAL fields. Commonest cause: PITUITARY ADENOMA.
C — OPTIC TRACT / LGN	CONTRALATERAL HOMONYMOUS HEMIANOPSIA. Stroke, tumor, demyelination.
D and E — HE DEFERRED THESE	D temporal optic radiation → contralateral SUPERIOR quadrantanopsia (“pie in the sky”). E occipital cortex, PCA occlusion → contralateral homonymous hemianopsia WITH MACULAR SPARING (dual supply). “You can know that if you want.”
Losing one eye	Loses the BINOCULAR OVERLAP and therefore DEPTH PERCEPTION. Everything becomes flat.

★ VERTIGO — HE WEIGHTED THIS ONE

Term	What you need to know
Why it leads	“On my board exams, A THIRD OF MY NEUROLOGY QUESTIONS WERE VERTIGO RELATED. So know this, know these things.” He also narrowed it: “we are more interested for this lecture on PERIPHERAL vertigo.”
VERTIGO vs DIZZINESS — one line	VERTIGO = HALLUCINATION OF MOTION from ASYMMETRICAL VESTIBULAR INPUT. Nystagmus + ataxia. NO SYNCOPE. DIZZINESS = non-vestibular impending faint, from CEREBRAL HYPOPERFUSION, ORTHOSTATIC HYPOTENSION or METABOLIC IMBALANCE — fainting IS on the table.
Why “no syncope” works	Vertigo is a FALSE MOTION SIGNAL with NORMAL perfusion, so the patient does not faint. Dizziness IS the perfusion/metabolic problem. The patient says “dizzy” for both — the word tells you nothing.
PERIPHERAL vertigo	Inner ear or CN VIII. SUDDEN onset · HORIZONTAL/ROTATIONAL nystagmus · FATIGABLE · SUPPRESSED BY VISUAL FIXATION. Causes: BPPV, MÉNIÈRE, LABYRINTHITIS, VESTIBULAR NEURITIS.
CENTRAL vertigo	Brainstem/cerebellum. GRADUAL onset · VERTICAL or NON-SUPPRESSIBLE nystagmus · NEUROLOGICAL DEFICITS PRESENT. Causes: BRAINSTEM STROKE, MULTIPLE SCLEROSIS, CEREBELLAR TUMOR.
Visual fixation — why it splits them	Fixing the gaze lets VISION OVERRIDE the false vestibular signal. Works in PERIPHERAL. “You CANNOT do that with central” — central has broken the machinery that does the overriding.
THE FOUR PERIPHERAL — read DURATION first	BPPV: UNDER 1 MINUTE, positional, NO hearing loss. MÉNIÈRE: HOURS, low-tone loss + aural fullness. LABYRINTHITIS: DAYS (improving over weeks), unilateral SNHL, AFTER A VIRAL URI. VESTIBULAR NEURITIS: days, NO hearing loss — nerve only.
BPPV mechanism	CANALITHIASIS = OTOCONIA dislodged from the UTRICLE, floating FREE in the SEMICIRCULAR CANALS. “What you need to know for pathophysiology is that THEY CAN BECOME LOOSE” and hit structures, causing a false sensation of motion. Explains all three features: brief, positional, no hearing loss.
MÉNIÈRE mechanism	ENDOLYMPHATIC HYDROPS — DEFECTIVE ENDOLYMPH RESORPTION (production is normal, DRAINAGE is not) → fluid accumulates in the membranous labyrinth, BALLOONING THE SCALA MEDIA until MICRO-RUPTURES occur. The ruptures are why it is episodic.
MÉNIÈRE — the classic TETRAD	He said “classic symptom, TETRAD”: (1) EPISODIC VERTIGO, sudden, HOURS · (2) LOW-FREQUENCY FLUCTUATING TINNITUS · (3) PROGRESSIVE LOW-TONE SNHL · (4) AURAL FULLNESS/pressure.
MÉNIÈRE takes the LOW tones	The only sensorineural loss here that starts LOW. Presbycusis and aminoglycosides take the HIGH ones. That contrast alone separates hydrops from the rest.
LABYRINTHITIS mechanism	INFLAMMATORY SWELLING, VASCULAR CONGESTION and ENDOLYMPHATIC DISRUPTION across the SEMICIRCULAR CANALS AND THE COCHLEA. One continuous fluid space serves both, so BALANCE AND HEARING FAIL TOGETHER. Cause: VIRAL infection, recent viral URI.
★ SLIDE 17 IS WRONG — he corrected it TWICE	The slide says labyrinthitis gives “EPISODIC” vertigo. IT IS CONTINUOUS. “This is not episodic. This is CONTINUOUS vertigo… classic symptoms is continuous, not episodic vertigo.” ANSWER CONTINUOUS — lasting DAYS, improving over WEEKS. If it were episodic it would be indistinguishable from Ménière.
LABYRINTHITIS nystagmus	HORIZONTAL-ROTARY, fast phase beating AWAY from the affected side. Plus severe postural instability, gait ataxia, nausea.
VESTIBULAR NEURITIS	Not on a slide of its own. “That’s just the same thing, but just INFLAMMATION OF THE NERVE FIBERS. That’s the only difference.” Whole labyrinth → hearing goes too; NERVE ALONE → only balance.
The balance organs	SEMICIRCULAR CANALS (3 loops: sagittal, coronal, transverse) detect ROTATIONAL acceleration — ENDOLYMPH INERTIA bends the CUPULA in the AMPULLA. OTOLITH ORGANS — UTRICLE (horizontal), SACCULE (vertical) — detect LINEAR acceleration and GRAVITATIONAL POSITION.
Canals vs otoliths, in one line	Canals answer “AM I TURNING?” Otoliths answer “WHICH WAY IS DOWN?” BPPV is an OTOLITH failure producing a CANAL symptom.

Hearing Loss — Conductive vs Sensorineural

Term	What you need to know
CONDUCTIVE — site & mechanism	EXTERNAL or MIDDLE ear. DEFECTIVE SOUND WAVE TRANSMISSION to the oval window.
SENSORINEURAL — site & mechanism	INNER EAR (cochlea) or CN VIII / central pathways. DESTRUCTION OF HAIR CELLS or AUDITORY NERVE FIBERS.
WEBER — the one people invert	CONDUCTIVE: lateralizes to the AFFECTED ear. SENSORINEURAL: lateralizes to the UNAFFECTED ear. Why: a blockage stops competing room noise reaching that cochlea, so the bone-conducted tone has that ear to itself.
RINNE	CONDUCTIVE: BONE > AIR (abnormal). SENSORINEURAL: AIR > BONE (normal ratio).
Causes — conductive	CERUMEN IMPACTION · OTOSCLEROSIS · OTITIS MEDIA · TYMPANIC MEMBRANE PERFORATION.
Causes — sensorineural	PRESBYCUSIS · OTOTOXIC DRUGS · NOISE TRAUMA · ACOUSTIC NEUROMA.
CONDUCTIVE — the 4 core mechanisms	(1) OBSTRUCTION — impacted cerumen, foreign bodies, canal exostoses. (2) MASS LOADING — middle ear effusion, cholesteatoma. (3) STIFFNESS — otosclerosis (stapes footplate fixation). (4) DISCONTINUITY — temporal bone fracture, ossicular necrosis.
Mass loading vs stiffness — the confusable pair	MASS LOADING ADDS WEIGHT to a chain that CAN STILL MOVE (effusion DAMPS). STIFFNESS STOPS THE CHAIN MOVING AT ALL (otosclerosis FIXES).
CHOLESTEATOMA — he said know it	A MASS LOADING cause: added TISSUE weight damps tympanic membrane and ossicular movement. KERATINIZED SQUAMOUS EPITHELIUM, NOT cholesterol and not a neoplasm (CMS ear deck); usually needs SURGICAL removal.
Transduction chain — memorize the order	STAPES at OVAL WINDOW → pressure waves in SCALA VESTIBULI → displaces ENDOLYMPH → BASILAR MEMBRANE displacement SHEARS STEREOCILIA against the RIGID TECTORIAL MEMBRANE → opens TIP-LINK CHANNELS → rapid ION INFLUX FROM ENDOLYMPH → voltage-gated channels → GLUTAMATE onto CN VIII.
Read the chain backwards	Break STEP 1 → CONDUCTIVE. Break STEPS 2–4 → SENSORINEURAL. Nothing in this lecture changes that division.

Otosclerosis, Ototoxicity & Noise

Term	What you need to know
OTOSCLEROSIS — pathogenesis	ABNORMAL OSTEOCLASTIC BONE RESORPTION followed by HYPERVASCULAR SPONGY OSTEOID REPLACEMENT around the OTIC CAPSULE and STAPES FOOTPLATE. Resorption FIRST, then the wrong bone grows back.
OTOSCLEROSIS — the one event	ANKYLOSIS OF THE STAPES FOOTPLATE IN THE OVAL WINDOW halts vibration transfer → progressive CONDUCTIVE loss. The cochlea is untouched — mechanism 3, STIFFNESS.
OTOSCLEROSIS — demographics (he flagged it)	Commonest in YOUNG-TO-MIDDLE-AGED FEMALES · ACCELERATED BY PREGNANCY · 50% AUTOSOMAL DOMINANT with VARIABLE PENETRANCE.
The sorting rule for ototoxicity	“Ototoxic medications, ALMOST ALWAYS REVERSIBLE, EXCEPT FOR SOME LIKE PLATINUM CHEMOTHERAPY.”
AMINOGLYCOSIDES — gentamicin, tobramycin	Induce REACTIVE OXYGEN SPECIES that selectively destroy OUTER HAIR CELLS starting at the COCHLEAR BASE → HIGH PITCH LOST FIRST. Permanent.
PLATINUM — cisplatin, carboplatin	CROSS-LINKS DNA IN STRIA VASCULARIS CELLS → compromises ENDOLYMPH ION HOMEOSTASIS → BILATERAL PERMANENT sensorineural loss.
FUROSEMIDE	Alters the STRIA VASCULARIS POTENTIAL → REVERSIBLE conductive/sensorineural loss.
SALICYLATES	Inhibit the PRESTIN motor protein in OUTER HAIR CELLS → TINNITUS.
Cisplatin vs furosemide — same target	BOTH hit the STRIA VASCULARIS. Cisplatin CROSS-LINKS ITS DNA and kills it (PERMANENT); furosemide only SHIFTS ITS POTENTIAL (REVERSIBLE). That is the whole difference.
Why high frequencies go first	ANATOMICAL, not chemical: the COCHLEAR BASE encodes HIGH pitch, and the base is where the damage starts. Same geometry drives presbycusis.
NOISE — the number	Long-term chronic exposure ABOVE 85 dB → IRREVERSIBLE STEREOCILIA DEGENERATION and HAIR CELL APOPTOSIS. 85 dB = occupational limit · 90 lawnmower/traffic · 120 ambulance siren = ACOUSTIC TRAUMA · 140 jet engine/blast = IMMEDIATE DAMAGE.
PRESBYCUSIS	GRADUAL, SYMMETRICAL, BILATERAL sensorineural loss in older adults. Begins with HIGH-FREQUENCY tones — the speech CONSONANTS /s/, /f/, /t/. Complaint is never “I can’t hear”, it is “I CAN’T FOLLOW CONVERSATION IN A NOISY ROOM”: vowels carry volume, CONSONANTS CARRY MEANING.

Otitis Media & Externa

Term	What you need to know
Eustachian tube dysfunction — the sequence	TUBE FAILS TO OPEN PERIODICALLY → OXYGEN AND NITROGEN ABSORBED INTO THE MIDDLE EAR MUCOSA → NEGATIVE MIDDLE EAR PRESSURE. The middle ear is a SEALED AIR-FILLED BOX whose only vent stopped working.
OTITIS MEDIA — bacterial	STREPTOCOCCUS PNEUMONIAE · HAEMOPHILUS INFLUENZAE · MORAXELLA CATARRHALIS. He scoped these: “not really for my exam, BUT LIKE BOARD EXAMS.”
OTITIS MEDIA — viral	RESPIRATORY SYNCYTIAL VIRUS · RHINOVIRUS · INFLUENZA · ADENOVIRUS. Typically after a URI.
OTITIS EXTERNA — bacterial (80–90%)	PSEUDOMONAS AERUGINOSA and STAPHYLOCOCCUS AUREUS. “Swimmer’s ear”.
OTITIS EXTERNA — fungal	ASPERGILLUS NIGER or CANDIDA ALBICANS, secondary to PROLONGED ANTIBIOTIC USE or HYPERHUMID CONDITIONS. Same logic as thrush: remove the competition or keep it wet.

Rhinology

Term	What you need to know
Rhinitis vs rhinosinusitis	RHINITIS = NOSE. RHINOSINUSITIS = NOSE AND SINUSES — which is why FACIAL PAIN belongs to rhinosinusitis.
ACUTE rhinosinusitis	UNDER 4 WEEKS. Usually VIRAL (rhinovirus, influenza); secondary bacterial = STREP PNEUMONIAE or H. INFLUENZAE. PURULENT rhinorrhea, facial pain, nasal congestion.
CHRONIC rhinosinusitis	BEYOND 12 WEEKS DESPITE THERAPY, often WITH NASAL POLYPS. Usually a secondary infection layered on an allergic process.
ALLERGIC RHINITIS	IgE-MEDIATED TYPE 1 HYPERSENSITIVITY of nasal mucosa to inhaled allergens. CLEAR rhinorrhea, nasal itching, sneezing, BOGGY TURBINATES, allergic “shiners”. (He de-scoped it: “plain vanilla… I don’t wanna ask about this.”)
Discharge color — fastest discriminator	ALLERGIC = CLEAR. ACUTE BACTERIAL SINUSITIS = PURULENT.
NASAL POLYPS	NON-NEOPLASTIC, benign EDEMATOUS masses from mucous membranes of the SINUS OSTIA or ETHMOID AIR CELLS. Not new tissue — existing mucosa waterlogged.
POLYPS — molecular pathway	Chronic TYPE 2 allergic response · cytokines IL-4, IL-5, IL-13 · TISSUE EOSINOPHIL INFLUX.
★ SLIDE 21 — he corrected the heading	The slide says “Type 2 Inflammation”. He stopped to fix it: “I meant to put T HELPER CELL TYPE 2 allergic inflammation. VERY IMPORTANT.” Then: “I’m not gonna ask you about that, but just so you know.” Know what it means; don’t expect to be asked.
TURBINATE HYPERTROPHY	Enlargement of the INFERIOR turbinates from VENOUS SINUSOID ENGORGEMENT, MUCOSAL EDEMA or BONY HYPERTROPHY. Triggers: allergic rhinitis, vasomotor instability, and REBOUND HYPEREMIA from topical decongestants.
RHINITIS MEDICAMENTOSA	REBOUND HYPEREMIA from OVERUSE OF TOPICAL DECONGESTANT SPRAYS — the spray produces the congestion it was bought to relieve.
DEVIATED SEPTUM — the physics	POISEUILLE’S LAW — even small airway narrowing DRAMATICALLY increases resistance. He put the split at “97% of all air going through one side.”
DEVIATED SEPTUM — consequences	CHRONIC OBSTRUCTION → mouth-breathing, aggravates SLEEP APNEA · MUCOSAL DRYING + EPISTAXIS from TURBULENT airflow · OLFACTORY DYSFUNCTION because air FAILS TO REACH THE CRIBRIFORM PLATE · SINUS OSTIA BLOCKAGE → mucus stasis, hypoxia, secondary bacterial rhinosinusitis.
★ The compensation is CONTRALATERAL	The WIDE cavity undergoes INFERIOR TURBINATE HYPERTROPHY to humidify the increased air volume — the hypertrophied turbinate is on the OPEN side, NOT the blocked one. So a ONE-SIDED deviation can obstruct BOTH sides. Reverse the inference: find big inferior turbinates → go looking for the deviation.
EPISTAXIS — ANTERIOR (90%)	Source: KIESSELBACH’S PLEXUS, anterior septum. Etiology all LOCAL: digital trauma, LOW HUMIDITY, localized mucosal erosion, mild rhinitis. Unilateral anterior bleeding.
EPISTAXIS — POSTERIOR (10%)	Source: WOODRUFF’S PLEXUS, posterolateral wall. Etiology all SYSTEMIC: HYPERTENSION, ATHEROSCLEROSIS, ANTICOAGULANT THERAPY, COAGULOPATHY. PROFUSE bleeding down the posterior pharynx, AIRWAY RISK.
Why posterior is the dangerous one	WOODRUFF’S carries FAR MORE ARTERIAL SUPPLY than Kiesselbach’s, and it sits where you cannot compress. “That thing may not stop bleeding.” But “you will usually only see ANTERIOR epistaxis.”

Larynx & Neck

Term	What you need to know
VOCAL CORD NODULES	BILATERAL, SYMMETRICAL fibrous CALLUSES at the junction of the ANTERIOR 1/3 and POSTERIOR 2/3. From CHRONIC mechanical PHONOTRAUMA (yelling, cheering) → BASEMENT MEMBRANE HYALINISATION. “Singer’s nodes”.
VOCAL CORD POLYPS	UNILATERAL, soft/fluid-filled or vascular, PEDUNCULATED, on the MIDDLE THIRD of the true cord. From ACUTE SEVERE voice strain or VOCAL CORD HEMORRHAGE → localized inflammatory healing response.
Nodules vs polyps, in one line	CHRONIC + BILATERAL vs ACUTE + UNILATERAL. Repeated impact damages BOTH cords at the SAME POINT; one violent strain or bleed damages ONE. (He misspoke “bilateral” for polyps and corrected himself — the slide and its picture both say UNILATERAL.)
Hyalinisation vs callus	“HYALINISATION IS NOT THE SAME AS CALLUS FORMATION. Hyalinisation is a PINK, EXCESSIVE MEMBRANE GROWTH. Callus is a FIBROUS MATERIAL FORMATION — but it can be EITHER OR in the nodules.”
TONSILLITIS	Acute VIRAL or BACTERIAL inflammation of the PALATINE TONSILS and pharyngeal mucosa. Bacterial is usually GROUP A STREPTOCOCCUS.
TONSILLITIS — symptoms	Sore throat · ODYNOPHAGIA (pain on swallowing) · fever · TONSILLAR EXUDATES · TRISMUS · ASYMMETRIC TONSILLAR DEVIATION IF COMPLICATED BY ABSCESS.
Asymmetry is the alarm	Tonsillitis is SYMMETRICAL. An ABSCESS pushes ONE tonsil across the midline and CLAMPS THE JAW. Chronic swollen tonsils that OBSTRUCT THE AIRWAY are an emergency. Epiglottitis sits “a little inferior to the tonsillitis”.
Bacterial vs viral tonsils (from the picture)	WHITE PATCHES or NODULES on red swollen tonsils → BACTERIAL. RED AND SWOLLEN WITH NO EXUDATE → VIRAL.
CERVICAL LYMPHADENOPATHY — reactive	Usually BENIGN enlargement responding to regional head/neck infection (viral URI, OTITIS MEDIA, DENTAL DISEASE) or systemic inflammatory conditions. PALPABLE AND TENDER.
★ The red-flag COMBINATION	PERSISTENT + RUBBERY OR MATTED + SUPRACLAVICULAR OR CERVICAL + OLDER ADULT → immediate assessment to rule out LYMPHOMA. Not any large node — the combination.
Tender vs matted	TENDER AND SOFT = REACTIVE. PAINLESS, RUBBERY, MATTED = not. MATTED means the nodes have LOST THEIR INDIVIDUAL CAPSULES and move as one mass.