PathoMed Exam 1: my notes

Basic elements of a clinical note (in order)

Intro/chief complaint, HPI, MedHx, Meds, Allergies, SocHx, physical exam, regional head and neck exam (extraoral exam EOE, intraoral exam IOE), radiograph exam, clinical impression (diagnosis), Tx, Rx, NV (next visit)

SOAP: Subjective

Intro/CC, HPI, MedHx, Meds, Allergies, SocHx. What the patient has experienced and describes.

SOAP: Objective

Physical exam, H&N exam, EOE, IOE, radiographs. Facts based on data the clinician collects.

SOAP: Assessment

Clinical impression/diagnosis. The doctor's critical thinking and judgment drawn from biomedical + clinical knowledge. Appropriate plans flow from a solid assessment. Reasoning runs clinical → microscopic → molecular.

SOAP: Plan

Tx (treatment), Rx (prescription), NV (next visit). Next steps taken to address the chief complaint.

Purpose of a medical consult

Screens medically complex patients BEFORE treatment; protects patient and provider; translates pathology knowledge into real clinical decisions. Required before managing many cardiovascular, endocrine, and immunocompromised patients.

Why is a thorough medical history more than "just a form"?

It is where the diagnosis lives. The form is a starting point, not the whole history.

ASA I

Normal, healthy patient (e.g., non-smoker, no/minimal alcohol). Dental implication: routine care.

ASA II

Mild systemic disease WITHOUT substantive functional limitation. Examples: well-controlled HTN/DM, current smoker, pregnancy, obesity (BMI 30-40). Routine care with minor modifications.

ASA III

Severe systemic disease WITH substantive functional limitation. Examples: poorly controlled HTN/DM, BMI ≥40, ESRD on dialysis, pacemaker, MI or CVA more than 3 months ago. Treatment modification; consultation often indicated.

ASA IV

Severe systemic disease that is a CONSTANT THREAT TO LIFE. Examples: MI, CVA, TIA or coronary stent within 3 months, ongoing ischemia, severe valve dysfunction, sepsis, ESRD not dialysed. Defer elective care; emergency care only, in an appropriate setting.

ASA V / VI

V = moribund; VI = declared brain-dead. Not treated in a dental office.

ASA class: recent MI or stroke (

Functional capacity screening question

"Can you climb one flight of stairs without stopping?" ≈ 4 METs, the practical threshold in perioperative risk assessment. Cannot do it = limited cardiopulmonary reserve.

Why is the timing of a patient's "heart attack in March" important?

Diagnosis was made on troponin; the timing of the event drives your ASA class AND your epinephrine decision.

High-yield history question: hospitalization

"Have you been hospitalized in the past year? What for?"

High-yield history question: last physician visit

"When did you last see your physician, and what did they say?"

High-yield history question: changes since form

"Has anything changed since you filled this form out?" Ask at EVERY visit, not just the first.

High-yield history question: non-pharmacy products

"Are you taking anything that did not come from a pharmacy?" Supplements, peptides, imported meds. Often yes, and NOT on the form.

Consultation = ?

A request for SPECIFIC INFORMATION, not a request for permission. The physician advises on the medical condition; the dental decision is yours.

Why does the consult form ask about epinephrine?

Because of cell injury: epinephrine (and local anesthetic) raises HR and contractility → increases myocardial O2 demand in patients whose coronary supply may be fixed.

Consult checkbox: General status — check when…

Recent hospitalization, unstable medical condition, implanted cardiac device, or poor exercise tolerance (can't climb one flight). Asks: is it safe to treat now, or does medical stabilization come first?

Consult checkbox: Hemostasis — check when…

Any anticoagulant/antiplatelet (warfarin, apixaban, rivaroxaban, dabigatran, aspirin, NSAIDs, clopidogrel), liver disease, or history of abnormal bleeding/bruising. Asks for: PT, INR, aPTT, platelet count, and guidance on medication timing/dosage.

Consult checkbox: Antibiotic prophylaxis — check when…

Prosthetic heart valve, prior infective endocarditis, certain congenital heart defects, or heart transplant with valvulopathy. Asks: is prophylaxis indicated before procedures involving gingival manipulation or mucosal incision?

Consult checkbox: Local anesthesia/epinephrine — check when…

Severe or unstable heart disease, significant arrhythmia, recent MI, hyperthyroidism, non-selective beta blockers, cocaine or methamphetamine use. Asks: is epi-containing anesthetic safe, limited, or avoided entirely?

Consult checkbox: Other — check when…

Head & neck radiation, bisphosphonate/denosumab, immunosuppression (chemo, biologics, corticosteroids), pregnancy, OSA, kidney or liver failure, poorly controlled diabetes. Anything that alters healing, infection risk, or anesthetic choice.

5 components of a faxed physician response

1) Recommendation ("may be performed"/"do not perform" + reason)

2) Epinephrine plan (with / limit / no epi)

3) Hemostasis (labs)

4) Antibiotic prophylaxis ("not indicated" or "indicated due to ___")

5) Other notes (avoid NSAIDs, steroid supplementation, avoid electrocautery with implanted defibrillator).

Hemostasis thresholds for routine dental care

INR ≤ 3.0 → routine care usually acceptable. Platelets ≥ 100,000 → adequate for minor surgery. Below either threshold → delay and coordinate with the physician.

Sample reply: "Stable for extraction. Limit epinephrine. Continue apixaban. No antibiotic prophylaxis." — your dental plan?

Max 2 cartridges of 1:100,000 epinephrine; local hemostatic measures (sutures, pressure, tranexamic acid if available); no premedication; do NOT stop apixaban; document every physician instruction in the chart.

Cause vs mechanism of cell injury

Cause = the bad thing (mostly environmental). Mechanism = what that cause does biochemically to mediate damage. Many causes converge on the same few mechanisms (why one framework covers ischemia, toxins, radiation, infection).

Causes of cell injury

O2 deprivation, chemical agents, infectious agents, immunologic reactions, genetic defects, nutritional deficiencies, physical agents, aging.

Mechanisms of cell injury

ATP depletion, mitochondrial damage, calcium influx, reactive oxygen species accumulation, increased membrane permeability, accumulation of damaged DNA and misfolded proteins.

Hypoxia

Deficient O2 reaching tissue; can occur with NORMAL blood flow (high altitude, severe anemia, carbon monoxide).

Ischemia

Inadequate arterial blood flow/perfusion (e.g., thrombus or embolus). Worse than hypoxia alone: withholds O2 AND substrates and lets metabolites accumulate.

Why does ischemic tissue injure faster/more severely than hypoxic tissue?

Glycolysis can't be sustained without delivered glucose, and metabolites accumulate.

Chain of events after coronary artery occlusion

1) O2 blood delivery to myocardium stops

2) mechanisms of injury start; ATP depletion first

3) within ~60 seconds muscle stops contracting (loss of function precedes loss of viability)

4) diminished contraction = diminished cardiac output

5) diminished systemic perfusion → every tissue/organ on the receiving end.

Does cardiac muscle die within 60 seconds of ischemia?

No — it stops WORKING (stops contracting), it doesn't die yet. Loss of function precedes loss of viability.

3 factors determining impact of injury

1) Duration & severity (completeness of occlusion, time-to-reperfusion)

2) Metabolic rate of tissue (brain and heart high; fibroblasts and skeletal muscle tolerate far more)

3) History of prior injury (less reserve, lower threshold).

Prior injury examples that lower threshold for next insult

Previous MI, irradiated jaw, previous infected socket, previous scarred kidney.

2 routes by which dental care raises myocardial O2 demand

Exogenous: epinephrine and local anesthetics (systemic absorption ↑ HR and contractility). Endogenous: pain, anxiety, long stressful appointments release the patient's own catecholamines.

How to mitigate cardiac risk at the chair

Profound local anesthesia (inadequate anesthesia releases MORE catecholamine than the cartridge you feared); limit epi dose and aspirate to avoid IV injection; short morning appointments, stress reduction, patient's own nitroglycerin; ask when last cardiac event was and consult if recent.

Cell response spectrum

Normal (homeostasis) → Adapted (new steady state, function preserved, REVERSIBLE) → Reversible injury (adaptive capacity exceeded) → Irreversible injury (point of no return) → Cell death (necrosis or apoptosis).

Hypertrophy

↑ cell SIZE, no new cells; occurs in permanent tissue that can't divide. Physiologic: skeletal muscle w/ exercise, uterus in pregnancy. Oral: masseter hypertrophy in chronic bruxism.

Hyperplasia

↑ cell NUMBER; requires tissue capable of division. Physiologic: breast at puberty, liver after partial resection. Oral: drug-related gingival overgrowth, inflammatory fibrous hyperplasia.

Atrophy

↓ cell size AND number; reduced metabolic demand. Examples: uterus after childbirth, thymus with age. Oral: alveolar ridge resorption after extraction, disuse atrophy.

Metaplasia

One differentiated cell type replaced by another better suited to the stress. Barrett esophagus (squamous → columnar). Oral: squamous metaplasia in smokers, nicotinic stomatitis.

Physiologic vs pathologic adaptation: how do you tell?

The MECHANISM doesn't tell you — context does. Example hypertrophy: athlete's LV (physiologic) vs hypertensive LV (pathologic). Hyperplasia: hormonal/compensatory (physiologic) vs endometrial hyperplasia, drug gingival overgrowth (pathologic).

Metaplasia: the trade-off

Always a response to chronic stress; new epithelium survives insult better but gives up function of the original (e.g., ciliated respiratory epithelium → squamous survives smoke but can't clear mucus). A population dividing to make a new phenotype under chronic stress is the population in which DYSPLASIA arises.

Drug-related gingival overgrowth: mechanism

Hyperplasia: ↑ fibroblast and matrix production driven by the drug in the presence of plaque-induced inflammation. Target is the fibroblast, not the drug.

Drugs causing gingival overgrowth

Cyclosporine (immunosuppressant), nifedipine (calcium channel blocker), phenytoin (anticonvulsant). Three unrelated classes → one tissue response.

Management of drug-related gingival overgrowth

Address stimulus first (med stop/substitution in consultation with prescriber); meticulous plaque control and frequent maintenance (inflammatory component is your control); gingivectomy where overgrowth is established. Surgery without addressing the drug → recurrence.

Adaptation vs neoplasia

Adaptation is stimulus-dependent: remove stimulus and it reverses. Growth that persists after the stimulus is gone = autonomous = neoplasia.

Reversible vs irreversible injury: diff slope or threshold?

Threshold, not slope.

Reversible injury hallmarks

Cellular swelling (first and most common):

ATP depletion → Na+/K+ ATPase fails → Na+ and water enter.

Fatty change (lipid vacuoles; hypoxic/toxic injury, esp. liver and heart).

Ultrastructure: blebbing, blunted microvilli, mitochondrial swelling, ER dilation, chromatin clumping. All reverses if stress removed.

Gross appearance of cellular swelling

Organ pallor, increased turgor and weight.

Irreversible injury hallmarks

Irreversible mitochondrial dysfunction (no ATP recovery even after reperfusion)

profound membrane failure incl. lysosomal membrane → hydrolytic enzymes digest the cell;

nuclear changes: pyknosis → karyorrhexis → karyolysis

protein leakage across failed membrane enables serum biomarkers.

Nuclear changes of necrosis in order

Pyknosis (shrinkage/condensation) → karyorrhexis (fragmentation) → karyolysis (dissolution).

Coagulative necrosis

Firm. Cell death with preserved tissue architecture (enzymes denatured before they can digest). Infarction of any solid organ EXCEPT CNS.

Liquefactive necrosis

Liquid. Digestion of dead cells into viscous mass. CNS infarction; bacterial/fungal infection producing pus (abscess).

Gangrenous necrosis

A CLINICAL term, not a histologic pattern: layers of coagulative necrosis in a limb. "Wet" gangrene = bacterial superinfection. Lower limb ischemia, often diabetes.

Caseous necrosis

"Cheese-like." Granulomatous inflammation; architecture NOT preserved. Tuberculosis; certain fungal infections.

Fat necrosis

Chalky. Enzymatic digestion of fat with saponification by released lipases. Acute pancreatitis; traumatic fat necrosis.

Fibrinoid necrosis

No gross change; immune complexes in vessel walls with pink fibrin-like material on microscopy. Immune-mediated vasculitis, e.g., polyarteritis nodosa.

Why does the brain undergo liquefactive necrosis?

Very high lipid content, little supporting fibrous stroma, abundant lysosomal enzymes from resident microglia → dissolution instead of preservation; infarct becomes a fluid-filled cavity. Brain also has the highest metabolic rate and tolerates diminished perfusion worst. "The way a tissue lives determines the way it dies."

Best biomarker for cardiac myocyte necrosis

High-sensitivity cardiac troponin I or T (far more cardiac-specific than CK; detectable within 1-3 hours). Serial measurements and the CHANGE between draws matter. CK/CK-MB no longer recommended for routine MI diagnosis.

Tissue-specific necrosis biomarkers

Cardiac myocyte: troponin I/T. Hepatocyte: ALT and AST. Pancreatic acinar: lipase. Skeletal muscle: creatine kinase.

Necrosis vs apoptosis: nature and trigger

Necrosis: always pathologic; overwhelming external injury.

Apoptosis: physiologic OR pathologic; regulated internal program.

Necrosis vs apoptosis: cell size, membrane, contents

Necrosis: swollen; membrane disrupted; contents leak and digest surrounding tissue.

Apoptosis: shrunken; membrane intact with phosphatidylserine flipped outward; packaged into apoptotic bodies and phagocytosed.

Necrosis vs apoptosis: host response and enzymes

Necrosis: inflammation; lysosomal hydrolases.

Apoptosis: no inflammation (cleared before secondary necrosis); caspases.

Dystrophic calcification

Calcium in DEAD or DYING tissue; serum calcium NORMAL (tissue abnormal, blood normal). Atherosclerotic plaque, damaged valves, old necrosis, tuberculous nodes. Oral: pulp stones (denticles), calcified lymph nodes, tonsilloliths, sialoliths.

Metastatic calcification

Calcium in NORMAL tissue on a background of HYPERCALCEMIA (blood abnormal, tissue normal).

4 causes of hypercalcemia (metastatic calcification)

1) ↑ PTH (primary hyperparathyroidism or PTHrP from a tumor) 2) Bone destruction (metastases, myeloma, Paget disease) 3) Vitamin D disorders (intoxication, sarcoidosis) 4) Renal failure with secondary hyperparathyroidism.

Dystrophic vs metastatic: one test

Serum calcium. Normal = dystrophic; high = metastatic. They look identical under the microscope, so work-up is needed.

Acute inflammation

Fast, loud; minutes to days; neutrophils first and in numbers; usually resolves completely.

Chronic inflammation

Slow; weeks to years; macrophages and lymphocytes; tissue destruction, fibrosis, remodeling.

Cardinal signs of inflammation and mechanisms

Calor + rubor (arteriolar vasodilation → hyperemia); tumor (↑ vascular permeability, protein-rich fluid into interstitium); dolor (pressure on nerve endings + bradykinin and prostaglandins lowering threshold); functio laesa (loss of function; consequence of swelling + pain).

Vascular changes of acute inflammation in order

1) Transient vasoconstriction (seconds) 2) Vasodilation (calor, rubor) 3) Increased permeability (endothelial gaps open; plasma proteins and WBCs leak; = tumor) 4) Stasis (fluid loss concentrates blood, flow slows, leukocytes move to vessel periphery).

Transudate

Driven by ↑ hydrostatic pressure or ↓ oncotic pressure; vessel wall INTACT. Low protein, few cells, clear. Usually non-inflammatory (heart failure, venous obstruction, hypoalbuminemia).

Exudate

Driven by ↑ vascular PERMEABILITY. High protein, cell-rich, cloudy. Raises interstitial osmotic pressure → pulls in more fluid.

Clinical contrast: transudate vs exudate swelling

Soft, pitting, bilateral, painless = transudate (systemic problem; not yours to treat). Firm, warm, tender, unilateral = exudate/inflammation (yours to treat).

Leukocyte recruitment: 5 steps (MR. FTC)

Margination, Rolling, Firm adhesion, Transmigration, Chemotaxis.

Leukocyte recruitment: margination

Stasis pushes red cells centrally; leukocytes move to vessel periphery. No specific molecule.

Leukocyte recruitment: rolling

Transient, low-affinity contact with endothelium. Mediated by SELECTINS (E, P, L).

Leukocyte recruitment: firm adhesion

Integrins shift to high-affinity conformation and lock on to ICAM-1 and VCAM-1.

Leukocyte recruitment: transmigration

Diapedesis between endothelial cells; collagenases breach basement membrane. Molecule: PECAM-1 (CD31).

Leukocyte recruitment: chemotaxis

Migration up a chemoattractant gradient to the offending agent. Chemoattractants: IL-8, C5a, LTB4.

Neutrophils: timing and traits

Arrive 0-24 hrs; most numerous, fastest, most adherent to selectins; short-lived (apoptosis at 24-48 hrs).

Monocytes/macrophages: timing and traits

Arrive 24-48 hrs; longer-lived; greater phagocytic capacity.

Exceptions to the usual leukocyte sequence

Pseudomonas: neutrophils persist for days. Viral infection: lymphocytes may arrive first. Hypersensitivity: eosinophils arrive first. The cell tells you the cause.

Pathology report says "acute and chronic inflammation" — meaning?

A lesion old enough to have recruited both cell populations and still being provoked.

Toll-like receptors (TLRs)

10 mammalian TLRs on phagocytes, dendritic (Langerhans) cells, and epithelium. Plasma membrane TLRs detect extracellular bacteria; endosomal TLRs detect ingested material (e.g., viral dsRNA, bacterial DNA). Recognize endotoxin. Activate transcription of inflammatory mediators and interferons.

Inflammasome

Multiprotein complex that recognizes products of dead cells (uric acid, extracellular ATP). Activates caspase-1 → cleaves pro-IL-1β into active IL-1. Also triggered by urate crystals (gout), cholesterol crystals (atherosclerosis), fatty acids (obesity-associated diabetes).

Sterile inflammation

Inflammation with no infection, driven by inflammasome activation by dead-cell products/crystals (gout, atherosclerosis, diabetes).

3 steps of phagocytosis

Recognition and attachment → engulfment → killing and degradation.

Opsonins

Make microbe easier to grip: IgG (Fc-gamma receptor), C3b (complement receptors CR1, CR3), collectins (C1q). Two of three depend on adaptive immunity/complement → immunocompromised pts phagocytose poorly.

Oxidative burst: 3 enzymatic steps

1) NADPH oxidase makes superoxide 2) Superoxide dismutase converts superoxide → H2O2 3) Myeloperoxidase: H2O2 + Cl- → HOCl (hypochlorous acid).

Clinical link of neutrophil oxidative burst to endodontics

HOCl is the active species in sodium hypochlorite — the neutrophil in a periapical lesion makes the same molecule you place in a root canal.

Histamine

Preformed in mast cell granules → acts within seconds. Immediate ↑ vascular permeability and vasodilation.

Prostaglandins

Pain sensitization (lower nociceptor threshold), fever, vasodilation. What NSAIDs block.

Leukotriene B4

Neutrophil chemotaxis (amplifies acute inflammation).