Environmental Pathology
Learning Objectives
By the end of this topic, you should be able to:
- Describe the major carcinogens and mechanisms of injury in cigarette smoke and their target organs.
- Stage alcoholic liver disease and explain the biochemical basis of each stage.
- Identify the classic vitamin and trace-element deficiency diseases and match each to its clinical picture.
- Explain the pathology of common environmental toxins (lead, mercury, arsenic, carbon monoxide, asbestos).
- Distinguish thermal, electrical, and radiation injury and describe the tissue changes each produces.
- Apply dose-response and latency concepts to predict who is at risk and when disease will manifest.
Quick Answer
Environmental pathology is the study of tissue injury and disease caused by external physical, chemical, and nutritional agents rather than by infection or inherited mutation. It matters because most of the world's chronic disease burden — lung cancer, cirrhosis, ischemic heart disease, most childhood stunting — traces back to a handful of avoidable exposures: tobacco, alcohol, occupational toxins, and poor nutrition. Unlike a genetic disease, environmental disease is preventable once the causal agent is identified, which is why this chapter is as much about mechanism as it is about public health.
Overview
Every organ has a limited number of ways it can respond to injury — necrosis, fibrosis, inflammation, or neoplastic transformation — but the list of things in our environment that can trigger those responses is enormous. Environmental pathology groups these triggers into four broad families that examiners love to test together: tobacco and alcohol (self-administered, dose-dependent, and together responsible for a huge share of adult mortality), environmental and occupational toxins (lead, mercury, arsenic, CO, asbestos, pesticides), nutritional disorders (deficiency and excess), and physical/chemical injury (thermal, electrical, radiation, mechanical trauma).
The unifying idea is dose and duration determine disease. A single cigarette does not cause cancer; forty pack-years does. A single alcoholic binge does not cause cirrhosis; a decade of daily heavy drinking does. This is why toxicology's dose-response curve and the concept of latency (the gap between exposure and clinical disease) run through every section below — and why they are examiner favorites.
Tobacco-Related Pathology
Definition
Tobacco-related pathology is the spectrum of disease caused by inhaling combustion products of tobacco, principally affecting the respiratory, cardiovascular, and urologic systems.
Explanation
Cigarette smoke contains over 4,000 chemicals; roughly 60 are established carcinogens. The three functional groups to remember for exams:
- Initiators/carcinogens — polycyclic aromatic hydrocarbons (benzo[a]pyrene) and nitrosamines (NNK, NNN), which form DNA adducts and cause point mutations, classically in TP53 and KRAS.
- Tumor promoters — phenol derivatives that don't mutate DNA but encourage proliferation of already-initiated cells.
- Ciliotoxic and irritant agents — acrolein and formaldehyde, which paralyze and destroy respiratory cilia, impairing mucociliary clearance.
- Carbon monoxide and nicotine — CO binds hemoglobin with ~200x the affinity of oxygen (forming carboxyhemoglobin), while nicotine causes vasoconstriction and is the addictive driver that sustains exposure.
Loss of ciliary clearance plus chronic irritation drives squamous metaplasia in the bronchial epithelium — the first step toward squamous cell carcinoma of the lung. Chronic irritation and protease-antiprotease imbalance (smoke inactivates alpha-1 antitrypsin and recruits neutrophils that release elastase) destroy alveolar walls, producing centriacinar emphysema.
Example
A 55-year-old with a 40 pack-year history develops a centrally located lung mass. Squamous cell carcinoma is the classic smoking-associated histology because the central airways bear the highest concentration of inhaled carcinogens.
Real-World Example
Smoking is the single largest preventable cause of death worldwide, linked to cancers of the lung, larynx, oral cavity, esophagus, bladder, pancreas, and cervix, as well as COPD, atherosclerosis (via endothelial injury and LDL oxidation), and peptic ulcer disease (impaired mucosal healing).
Why It Matters
Because the mechanism is dose-dependent and reversible in its early stages, smoking cessation is the single highest-yield intervention a physician can offer — cardiovascular risk drops sharply within a year, though cancer risk declines more slowly over a decade or more.
Common Misunderstanding
Students often think "tar" is the sole carcinogenic component. In reality, tar is a residue mixture that carries many separate carcinogens (PAHs, nitrosamines); CO and nicotine cause distinct, non-carcinogenic harm (hypoxia and vasoconstriction/addiction respectively), and all three mechanisms act together.
Alcohol-Related Pathology
Definition
Alcohol-related pathology is liver, pancreatic, neurologic, and cardiac injury caused by chronic or excessive ethanol metabolism.
Explanation
Ethanol is metabolized by alcohol dehydrogenase to acetaldehyde, then by aldehyde dehydrogenase to acetate. This pathway generates excess NADH, which shifts hepatocyte metabolism toward fat synthesis and away from fatty acid oxidation and gluconeogenesis — the direct cause of fatty change. Acetaldehyde itself is directly toxic, forming protein adducts that impair microtubule function and provoke an immune/inflammatory response.
The three sequential (and overlapping) stages of alcoholic liver disease:
- Hepatic steatosis (fatty liver) — reversible with abstinence; hepatocytes become swollen with macrovesicular fat due to the NADH/NAD+ shift.
- Alcoholic hepatitis — hepatocyte swelling and necrosis, neutrophilic infiltrate, and Mallory-Denk bodies (eosinophilic cytokeratin aggregates) on biopsy; presents with fever, tender hepatomegaly, and jaundice. Still partially reversible.
- Alcoholic cirrhosis — irreversible micronodular fibrosis with loss of normal architecture, portal hypertension, and risk of hepatocellular carcinoma.
Beyond the liver: chronic alcohol causes acute and chronic pancreatitis (intraductal protein plugs and direct acinar toxicity), dilated cardiomyopathy, peripheral neuropathy and Wernicke-Korsakoff syndrome (from associated thiamine deficiency), and fetal alcohol syndrome in pregnancy.
Example
A patient presenting with tender hepatomegaly, fever, and an AST:ALT ratio greater than 2:1 after a drinking binge has classic alcoholic hepatitis — AST rises more than ALT because chronic alcohol use depletes hepatic pyridoxal-5-phosphate, needed more for ALT synthesis.
Real-World Example
Alcoholic cirrhosis remains a leading indication for liver transplantation worldwide, and its progression is entirely dose- and duration-dependent, which is why quantifying "units per week" is a standard part of clinical history-taking.
Why It Matters
Recognizing which stage a patient is in changes management: steatosis and early hepatitis are reversible with abstinence, but once cirrhosis and fibrosis are established, damage is permanent and management shifts to preventing complications (variceal bleeding, ascites, hepatocellular carcinoma surveillance).
Common Misunderstanding
Many students assume the three stages are strictly sequential and mutually exclusive. In practice, steatosis, hepatitis, and early fibrosis frequently coexist on the same biopsy — cirrhosis is simply the end-stage once fibrosis has bridged and regenerative nodules have formed.
Environmental and Occupational Toxins
Definition
Toxins are exogenous chemical or physical agents that cause organ injury through defined biochemical mechanisms, often via occupational or environmental exposure.
Explanation
A short list of classic toxin-mechanism-organ triads that appear repeatedly on exams:
| Toxin | Mechanism | Classic Target/Finding |
|---|---|---|
| Lead | Inhibits ferrochelatase and ALA dehydratase in heme synthesis; deposits in bone and CNS | Microcytic anemia with basophilic stippling, lead lines on gingiva/metaphysis, wrist/foot drop, encephalopathy in children |
| Mercury | Binds sulfhydryl groups; crosses blood-brain barrier (organic forms) | Tremor, erethism (mood change), acrodynia in children, "Mad Hatter" syndrome |
| Arsenic | Inhibits pyruvate dehydrogenase and other enzymes needing lipoic acid | Garlic breath, rice-water diarrhea, peripheral neuropathy, Mees' lines on nails, skin hyperpigmentation, angiosarcoma of liver |
| Carbon monoxide | Binds hemoglobin ~200x affinity of O2, shifts oxygen dissociation curve left | Cherry-red skin/blood (postmortem), headache, cognitive impairment, cardiac ischemia |
| Asbestos | Fibers cause chronic inflammation and fibrosis in pleura/lung | Ferruginous bodies, pleural plaques, bronchogenic carcinoma, malignant mesothelioma |
| Organophosphates/pesticides | Irreversible acetylcholinesterase inhibition | SLUDGE syndrome (salivation, lacrimation, urination, diarrhea, GI upset, emesis) |
Example
A shipyard welder with 20 years of asbestos exposure who develops calcified pleural plaques on chest X-ray and later a diffuse pleural malignancy illustrates the classic asbestos-mesothelioma latency, which can be 20-40 years.
Real-World Example
Occupational lead exposure in battery manufacturing and old-house renovation (lead paint) remains a real public-health issue; pediatric lead poisoning is particularly dangerous because the developing brain is exquisitely sensitive even at levels that cause no symptoms in adults.
Why It Matters
Toxin-target relationships are testable both as "given exposure, predict finding" and "given finding, identify exposure" — recognizing the pattern lets you work backward from a clinical vignette to the causative agent.
Common Misunderstanding
Students often conflate asbestos-related bronchogenic carcinoma with mesothelioma. Both occur, but mesothelioma is far more specific to asbestos (rare without exposure), while bronchogenic carcinoma in an asbestos worker who also smokes shows a multiplicative (not merely additive) increase in risk — smoking and asbestos synergize.
Nutritional Disorders
Definition
Nutritional pathology results from either deficiency or excess of essential vitamins, minerals, or macronutrients, producing organ-specific and systemic disease.
Explanation
Fat-soluble vitamin deficiencies and excesses, and water-soluble vitamin deficiencies, are among the highest-yield facts in this chapter because each has one or two unmistakable, testable features:
| Vitamin/Nutrient | Deficiency Disease | Key Features |
|---|---|---|
| Vitamin A | Night blindness, xerophthalmia | Bitot's spots, squamous metaplasia of respiratory/urinary epithelium |
| Vitamin B1 (thiamine) | Beriberi / Wernicke-Korsakoff | Wet beriberi (high-output cardiac failure), dry beriberi (peripheral neuropathy), confusion + ataxia + ophthalmoplegia in Wernicke's |
| Vitamin B3 (niacin) | Pellagra | The 3 D's: dermatitis (sun-exposed areas), diarrhea, dementia |
| Vitamin B9 (folate) | Megaloblastic anemia | No neurologic signs (distinguishes from B12); neural tube defects in pregnancy |
| Vitamin B12 (cobalamin) | Megaloblastic anemia + neurologic disease | Subacute combined degeneration of the spinal cord, glossitis |
| Vitamin C | Scurvy | Impaired collagen cross-linking: bleeding gums, poor wound healing, corkscrew hairs, perifollicular hemorrhages |
| Vitamin D | Rickets (children) / Osteomalacia (adults) | Impaired bone mineralization; bowing of legs, craniotabes, pseudofractures |
| Vitamin K | Bleeding diathesis | Prolonged PT (extrinsic pathway); hemorrhagic disease of the newborn |
| Iron | Microcytic anemia | Koilonychia, pica, fatigue |
| Zinc | Impaired wound healing, dermatitis | Perioral and acral dermatitis, hypogonadism, poor taste (dysgeusia) |
| Protein-energy (severe, edematous) | Kwashiorkor | Edema, hepatomegaly (fatty liver), skin/hair changes despite adequate calories |
| Protein-energy (severe, non-edematous) | Marasmus | Severe muscle wasting, "old man" facies, no edema |
The mechanistic thread: vitamins are cofactors, so their deficiency states map directly onto the enzymatic pathway they support — vitamin C and collagen hydroxylation, B12/folate and DNA synthesis (thymidine), vitamin K and clotting factor carboxylation.
Example
A strict vegan with no B12 supplementation develops a macrocytic anemia plus loss of vibration sense in the feet — the combination of hematologic and neurologic findings points specifically to B12 deficiency, not folate.
Real-World Example
Kwashiorkor classically occurs in a toddler weaned onto a starchy, protein-poor diet after a younger sibling is born, producing the characteristic edematous, potbellied appearance seen in famine and refugee settings.
Why It Matters
Distinguishing deficiency diseases by their specific, non-overlapping features (e.g., neurologic involvement in B12 but not folate deficiency) is exactly the kind of discriminating fact examiners build vignette questions around.
Common Misunderstanding
Students often assume folate and B12 deficiency are interchangeable because both cause megaloblastic anemia. The distinguishing feature is neurologic disease (subacute combined degeneration), which occurs only in B12 deficiency, because folate cannot substitute for B12 in the methylmalonyl-CoA pathway that maintains myelin.
Physical and Chemical Injury
Definition
Physical and chemical injury refers to tissue damage from thermal, electrical, radiation, or mechanical forces rather than biological or nutritional causes.
Explanation
- Thermal burns are classified by depth: superficial (epidermis only, painful, no blisters), partial-thickness (blistering, into dermis, very painful), and full-thickness (through dermis, leathery/insensate because nerve endings are destroyed). Burns over large body surface areas cause massive fluid shifts and are a leading cause of hypovolemic shock and infection risk.
- Electrical injury causes damage through direct tissue heating (Joule heating) and through interference with cardiac and neural electrical conduction; alternating current is more dangerous than direct current because it can trigger tetanic muscle contraction and ventricular fibrillation.
- Ionizing radiation injury damages DNA both directly and via free-radical generation (radiolysis of water). Rapidly dividing tissues — bone marrow, GI epithelium, gonads — are most sensitive; this is the basis of both radiation sickness and the therapeutic index used in radiotherapy.
- Mechanical/traumatic injury produces the basic wound categories (abrasion, contusion, laceration, incised wound) that forensic and surgical pathology build on.
Example
A high-voltage electrical worker sustains a small entry wound but extensive deep muscle necrosis — electrical injury classically causes far more internal damage than the skin surface suggests, because current follows the path of least resistance (nerves and blood vessels) rather than staying superficial.
Real-World Example
Acute radiation syndrome after a reactor accident produces a predictable timeline: bone marrow suppression appears first (within days, since marrow cells divide fastest), followed by GI mucosal sloughing at higher doses, and cerebrovascular collapse only at extremely high, near-uniformly fatal doses.
Why It Matters
Recognizing the depth of a burn or the systemic pattern of radiation injury directly determines triage and management — a full-thickness burn needs surgical grafting because the nerve endings and regenerative epithelium are destroyed, while a superficial burn heals with dressings alone.
Common Misunderstanding
Students often think burn pain correlates with severity. In fact, full-thickness burns are frequently less painful than partial-thickness burns because the nerve endings themselves have been destroyed — pain intensity is not a reliable marker of burn depth.
Visual Learning
Key Terms
| Term | Definition |
|---|---|
| Dose-response relationship | The principle that the severity/probability of toxic effect increases with the amount and duration of exposure; underlies "the dose makes the poison." |
| Latency period | The time gap between exposure to a causative agent and clinical manifestation of disease (e.g., 20-40 years for asbestos-mesothelioma). |
| Carcinogen | An agent capable of causing cancer by damaging DNA (genotoxic) or promoting proliferation of mutated cells (non-genotoxic/promoter). |
| Bioaccumulation | The build-up of a substance in an organism faster than it can be metabolized or excreted (e.g., mercury in fish). |
| Biomagnification | Increasing concentration of a substance at successive levels of a food chain. |
| Mallory-Denk bodies | Eosinophilic cytoplasmic aggregates of damaged cytokeratin filaments seen in hepatocytes in alcoholic hepatitis. |
| Ferruginous body | Asbestos fiber coated with iron-protein complex, seen histologically in asbestos-exposed lung tissue. |
| Carboxyhemoglobin | Hemoglobin bound to carbon monoxide instead of oxygen, impairing oxygen delivery to tissues. |
| Kwashiorkor | Severe protein deficiency with adequate calorie intake, causing edema and fatty liver despite preserved fat stores. |
| Marasmus | Severe combined protein-calorie deficiency causing generalized wasting without edema. |
| Xerophthalmia | Dryness and keratinization of the conjunctiva/cornea from vitamin A deficiency, a leading cause of preventable blindness. |
| Subacute combined degeneration | Demyelination of the dorsal columns and corticospinal tracts caused specifically by vitamin B12 deficiency. |
Common Mistakes
Misconception 1: "Nicotine is the main carcinogen in cigarette smoke." Why it's wrong: Nicotine is the addictive component and a vasoconstrictor, but it is not a major direct carcinogen. Correct understanding: The carcinogenic burden comes mainly from polycyclic aromatic hydrocarbons and nitrosamines in tar; nicotine's harm is cardiovascular and addictive, not primarily genotoxic.
Misconception 2: "Alcoholic cirrhosis develops suddenly after a period of normal-looking liver." Why it's wrong: This ignores the sequential, overlapping continuum of fatty change and hepatitis that precedes fibrosis. Correct understanding: Cirrhosis is the end-stage of a process that usually starts years earlier as reversible steatosis, progresses through recurrent bouts of alcoholic hepatitis, and only becomes irreversible once bridging fibrosis and regenerative nodules form.
Misconception 3: "All vitamin deficiencies that cause anemia present identically." Why it's wrong: This overlooks the distinguishing neurologic component of B12 deficiency. Correct understanding: Folate and B12 deficiency both cause megaloblastic anemia via impaired DNA synthesis, but only B12 deficiency causes subacute combined degeneration, because B12 (not folate) is required for the methylmalonyl-CoA-to-succinyl-CoA reaction that maintains myelin integrity.
Comparison and Connections
| Feature | Alcoholic Hepatitis | Non-Alcoholic Fatty Liver Disease (NAFLD) |
|---|---|---|
| Cause | Chronic ethanol metabolism | Obesity, insulin resistance, metabolic syndrome |
| AST:ALT ratio | Typically > 2:1 | Typically < 1 (ALT > AST) |
| Histology | Mallory-Denk bodies, neutrophilic infiltrate | Macrovesicular steatosis, less neutrophilic infiltrate |
| Reversibility | Reversible with abstinence in early stages | Reversible with weight loss/metabolic control |
| Feature | Kwashiorkor | Marasmus |
|---|---|---|
| Cause | Protein deficiency with adequate calories | Combined protein and calorie deficiency |
| Edema | Present | Absent |
| Muscle wasting | Relatively preserved (fat/water retained) | Severe |
| Liver | Fatty, enlarged | Not typically fatty |
| Feature | Vitamin B12 Deficiency | Folate Deficiency |
|---|---|---|
| Anemia type | Megaloblastic | Megaloblastic |
| Neurologic findings | Yes (subacute combined degeneration) | No |
| Common cause | Pernicious anemia, vegan diet, ileal disease | Poor diet, alcoholism, pregnancy, certain drugs |
Practice Questions
Recall
-
Name three chemical classes of carcinogens found in cigarette smoke. Answer guidance: Polycyclic aromatic hydrocarbons (e.g., benzo[a]pyrene), nitrosamines (NNK, NNN), and phenol-derived tumor promoters.
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What are the three histologic stages of alcoholic liver disease, in order? Answer guidance: Hepatic steatosis, alcoholic hepatitis, alcoholic cirrhosis.
Understanding
-
Explain why carbon monoxide poisoning causes hypoxia even when the lungs and oxygen supply are normal. Answer guidance: CO binds hemoglobin with roughly 200 times the affinity of oxygen, forming carboxyhemoglobin and displacing oxygen; it also shifts the oxygen-hemoglobin dissociation curve left, impairing oxygen release to tissues even from the oxygen that remains bound. The problem is oxygen delivery/unloading, not oxygen intake.
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Why does vitamin B12 deficiency cause neurologic disease while folate deficiency does not, despite both causing the same type of anemia? Answer guidance: Both are needed for DNA synthesis (megaloblastic anemia), but only B12 is a cofactor for the methylmalonyl-CoA mutase reaction, which is necessary to prevent abnormal fatty acid incorporation into neuronal myelin. Folate cannot substitute for this specific reaction.
Application
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A shipyard worker with 25 years of asbestos exposure presents with progressive dyspnea and a chest X-ray showing calcified pleural plaques. Fifteen years later he develops a diffuse pleural mass. What is the likely diagnosis and why does the long delay make sense? Answer guidance: Malignant mesothelioma. Asbestos-related malignancy has a long latency period (often 20-40 years) because chronic fiber-induced inflammation and fibrosis slowly accumulate genetic damage in mesothelial cells before frank malignant transformation occurs.
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A toddler weaned early after a new sibling's birth develops edema, a distended abdomen, and a fatty liver, but calorie intake seems adequate. What is the diagnosis and underlying mechanism? Answer guidance: Kwashiorkor. Adequate calories but inadequate protein intake impairs synthesis of albumin (causing oncotic pressure loss and edema) and apolipoproteins (impairing export of hepatic triglycerides, causing fatty liver).
Analysis
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Compare the mechanism by which smoking and asbestos each independently increase lung cancer risk, and explain why their combined effect is multiplicative rather than additive. Answer guidance: Smoking delivers direct chemical carcinogens (PAHs, nitrosamines) causing DNA mutation, while asbestos causes chronic mechanical/inflammatory irritation and fibrosis that promotes a mutation-prone, proliferative epithelial environment. Because they act through different but complementary mechanisms (initiation plus promotion/inflammation), their combined carcinogenic risk multiplies rather than simply adding together.
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A patient with chronic alcohol use presents with confusion, ataxia, and ophthalmoplegia. Explain the underlying nutritional deficiency and why glucose administration before thiamine could worsen the condition. Answer guidance: This is Wernicke's encephalopathy from thiamine (B1) deficiency, common in alcoholics due to poor diet and impaired absorption. Thiamine is a cofactor for enzymes in glucose metabolism (e.g., transketolase, pyruvate dehydrogenase); giving glucose first consumes remaining thiamine stores rapidly, precipitating or worsening acute Wernicke's encephalopathy — hence the rule to give thiamine before or with glucose.
FAQ
1. Why is squamous cell carcinoma more associated with smoking than adenocarcinoma? Squamous cell carcinoma arises centrally, where inhaled carcinogens concentrate and drive squamous metaplasia of the bronchial lining. Adenocarcinoma tends to be peripheral and is now the most common lung cancer overall, including in non-smokers, but squamous and small cell types remain the most tightly linked to smoking dose.
2. Is fatty liver from alcohol always reversible? Yes, in isolation — pure hepatic steatosis reverses within weeks of abstinence. The danger is that repeated cycles of drinking and steatosis, layered with recurrent hepatitis, eventually cause fibrosis that does not reverse.
3. Why do children get more severe lead toxicity than adults at the same exposure level? Children absorb a higher fraction of ingested lead from the gut, their blood-brain barrier is more permeable, and their brains are actively developing — so lead disrupts neurodevelopment at exposure levels that would cause only mild symptoms in an adult.
4. Can vitamin excess also cause disease, not just deficiency? Yes — hypervitaminosis A causes headache, hepatotoxicity, and teratogenicity (particularly a concern in pregnancy), and hypervitaminosis D causes hypercalcemia. Fat-soluble vitamins (A, D, E, K) are the ones most likely to accumulate to toxic levels since they aren't easily excreted in urine.
5. Why is a burn's pain level not a reliable way to judge severity? Because full-thickness burns destroy the nerve endings in the skin, they can be less painful than a superficial or partial-thickness burn where nerve endings are irritated but intact — clinicians must assess depth by appearance (blistering, color, capillary refill) rather than by pain alone.
Quick Revision
- Cigarette smoke carcinogens: PAHs (benzo[a]pyrene) and nitrosamines (NNK/NNN) cause DNA mutation; CO causes hypoxia via carboxyhemoglobin; nicotine drives addiction and vasoconstriction.
- Bronchial squamous metaplasia from smoking is the precursor lesion for squamous cell lung carcinoma.
- Alcoholic liver disease stages, in order: steatosis (reversible) → alcoholic hepatitis (Mallory-Denk bodies, AST:ALT > 2:1) → cirrhosis (irreversible).
- Lead poisoning: microcytic anemia with basophilic stippling, inhibits heme synthesis enzymes (ferrochelatase, ALA dehydratase).
- Carbon monoxide binds hemoglobin ~200x more avidly than oxygen; classic finding is cherry-red discoloration.
- Asbestos causes ferruginous bodies, pleural plaques, bronchogenic carcinoma, and mesothelioma after decades of latency; smoking + asbestos multiplies cancer risk.
- Vitamin B12 deficiency uniquely causes neurologic disease (subacute combined degeneration); folate deficiency does not.
- Pellagra (niacin deficiency) = the 3 D's: dermatitis, diarrhea, dementia.
- Scurvy (vitamin C deficiency) impairs collagen cross-linking → bleeding gums, poor wound healing.
- Kwashiorkor = protein deficiency with edema and fatty liver; marasmus = combined protein-calorie deficiency with wasting, no edema.
- Give thiamine before/with glucose in suspected Wernicke's to avoid precipitating acute encephalopathy.
- Full-thickness burns can be less painful than partial-thickness burns because nerve endings are destroyed.
Related Topics
Prerequisites
- General principles of cell injury and cell death (necrosis vs. apoptosis)
- Basic biochemistry of vitamins and cofactor enzymes
- Introduction to carcinogenesis and mutation
Related Topics
- Neoplasia and the multistep model of carcinogenesis
- Nutritional and metabolic disorders in systemic pathology
- Occupational and forensic medicine
Next Topics
- Genetic and pediatric pathology
- Systemic pathology of the respiratory and hepatobiliary systems
- Toxicology and clinical pharmacology