Pathophysiology is the study of functional changes in body systems that result from disease or injury. It bridges the gap between basic science knowledge and clinical practice by explaining HOW diseases develop and WHY specific clinical signs occur.
Overview and Clinical Importance
Pathophysiology is the study of functional changes in body systems that result from disease or injury. It bridges the gap between basic science knowledge and clinical practice by explaining HOW diseases develop and WHY specific clinical signs occur. Understanding pathophysiology is essential for the BCSE because it enables you to predict disease progression, interpret diagnostic findings, and select appropriate treatments based on underlying mechanisms rather than rote memorization.
The BCSE heavily tests your ability to connect pathophysiological mechanisms with clinical presentations. Questions often present clinical scenarios and ask you to identify the underlying mechanism, predict complications, or explain why certain treatments work. This study guide covers the three key areas: mechanisms of disease progression, system-specific pathophysiology, and integration of clinical signs with underlying pathology.
High-YieldPathophysiology questions on the BCSE often present a clinical scenario and ask you to identify the MECHANISM causing the clinical signs. Focus on understanding WHY things happen, not just WHAT happens.
| Category |
Examples |
Mechanism of Injury |
| Hypoxia/Ischemia |
Anemia, respiratory failure, vascular occlusion, shock |
ATP depletion leads to failure of sodium-potassium pump, cellular swelling, and loss of membrane integrity |
| Toxins/Drugs |
Acetaminophen, heavy metals, ethylene glycol, snake venom |
Direct membrane damage, enzyme inhibition, free radical generation, or metabolic interference |
| Infectious Agents |
Bacteria, viruses, fungi, parasites, prions |
Direct cytotoxicity, toxin production, immune-mediated damage, intracellular replication |
| Immune Reactions |
Autoimmune diseases, hypersensitivity reactions, transplant rejection |
Antibody-mediated cytotoxicity, complement activation, T-cell mediated destruction |
| Physical Agents |
Trauma, temperature extremes, radiation, electrical injury |
Direct tissue destruction, protein denaturation, DNA damage, membrane disruption |
| Nutritional Imbalances |
Deficiencies (vitamins, minerals), excesses (copper toxicosis) |
Metabolic dysfunction, oxidative stress, impaired cellular repair mechanisms |
| Genetic Abnormalities |
Inherited enzyme defects, storage diseases, developmental anomalies |
Abnormal protein production, metabolite accumulation, impaired cellular function |
| Adaptation |
Definition |
Clinical Examples |
| Hypertrophy |
Increase in cell SIZE due to increased functional demand or hormonal stimulation |
Cardiac hypertrophy in aortic stenosis or hypertension; skeletal muscle hypertrophy with exercise |
| Hyperplasia |
Increase in cell NUMBER due to growth factors or hormonal stimulation |
Endometrial hyperplasia from estrogen; prostatic hyperplasia; compensatory liver regeneration |
| Atrophy |
Decrease in cell size due to decreased workload, loss of innervation, or decreased blood supply |
Muscle atrophy from disuse or denervation; testicular atrophy from chronic illness; brain atrophy in aging |
| Metaplasia |
Reversible replacement of one mature cell type with another mature cell type |
Squamous metaplasia of respiratory epithelium in smokers; osseous metaplasia in chronic inflammation |
| Dysplasia |
Disordered cellular growth with variation in size, shape, and organization (often pre-neoplastic) |
Cervical dysplasia; dysplastic nevus; often precedes carcinoma development |
| Reversible Injury |
Irreversible Injury |
| Cellular swelling (hydropic change) due to sodium-potassium pump failure |
Severe membrane damage with loss of intracellular contents |
| Fatty change (steatosis) - accumulation of lipid vacuoles |
Mitochondrial dysfunction with inability to generate ATP |
| Endoplasmic reticulum swelling with ribosome detachment |
Calcium influx activating destructive enzymes (phospholipases, proteases, endonucleases) |
| Membrane blebbing (early stage) |
Nuclear changes: pyknosis, karyorrhexis, karyolysis |
| Clumping of nuclear chromatin |
Point of no return - cell death (necrosis or apoptosis) |
| Feature |
Necrosis |
Apoptosis |
| Cause |
Pathologic injury (ischemia, toxins, infection) |
Programmed (physiologic or pathologic triggers) |
| Cell Size |
Enlarged (swelling) |
Reduced (shrinkage) |
| Nucleus |
Pyknosis, karyorrhexis, karyolysis |
Fragmentation into nucleosome-sized pieces |
| Cell Membrane |
Disrupted with leakage of contents |
Intact with phosphatidylserine externalization |
| Cellular Contents |
Released into extracellular space |
Contained in apoptotic bodies |
| Inflammation |
PRESENT - triggered by released contents |
ABSENT - clean removal by phagocytes |
| Energy Requirement |
None (passive process) |
ATP required (active process) |
| Pattern |
Groups of cells affected |
Single cells affected |
Section 1: Mechanisms of Disease Progression
1.1 Cellular Injury and Adaptation
Cellular injury is the fundamental starting point of disease. Cells respond to stress through adaptation, reversible injury, or irreversible injury leading to cell death. Understanding these responses is crucial for predicting disease outcomes and explaining clinical signs.
Causes of Cellular Injury
[Include Image: Figure 1. Diagram showing causes and mechanisms of cellular injury]
MEMORY AID - HIPT-ING Causes of Cell Injury
Remember the causes of cellular injury with 'HIPT-ING': Hypoxia/Ischemia, Immune reactions, Physical agents, Toxins/drugs, Infectious agents, Nutritional imbalances, Genetic abnormalities
Cellular Adaptations to Stress
Before cells are irreversibly injured, they may adapt to stress through several mechanisms. These adaptations are reversible if the stressor is removed.
MEMORY AID - HAMMD for Cellular Adaptations
Think 'HAMMD' for the spectrum of cellular adaptations: Hypertrophy (bigger cells), Atrophy (smaller cells), Metaplasia (different cell type), Hyperplasia (more cells), Dysplasia (disorganized - pre-cancer warning!)
High-YieldHypertrophy occurs in cells that cannot divide (cardiac myocytes, skeletal muscle). Hyperplasia occurs in cells capable of division. Many tissues show BOTH (e.g., pregnant uterus has hypertrophic and hyperplastic smooth muscle).
Reversible vs. Irreversible Injury
The distinction between reversible and irreversible injury is critical in clinical practice. Reversible injury can be corrected if the injurious stimulus is removed quickly enough. Once injury becomes irreversible, cell death is inevitable.
[Include Image: Figure 2. Comparison of reversible and irreversible cellular injury showing cellular swelling, fatty change, and necrotic changes]
MEMORY AID - Point of No Return - 'CAMP' Signs of Irreversible Injury
Remember 'CAMP' for irreversible injury markers: Calcium influx (massive), ATP depletion (severe), Membrane damage (extensive), Pyknosis/karyolysis (nuclear changes)
Cell Death: Necrosis vs. Apoptosis
Cell death occurs through two main pathways: necrosis (pathologic, uncontrolled) and apoptosis (programmed, controlled). Understanding the differences is essential for interpreting tissue damage and predicting inflammatory responses.
High-YieldNECROSIS causes INFLAMMATION because cellular contents leak out. APOPTOSIS does NOT cause inflammation because contents are packaged into apoptotic bodies that are phagocytosed. This is a VERY commonly tested concept!
MEMORY AID - Types of Necrosis - 'CLIFFS'
Remember necrosis types with 'CLIFFS': Coagulative (most organs - ischemia), Liquefactive (brain, bacterial abscess - enzymes digest), Caseous (TB, fungi - cheesy), Fat (pancreas, trauma - saponification), Fibrinoid (blood vessels - immune complexes), Gangrenous (combination - dry or wet)
1.2 The Inflammatory Response
Inflammation is the body's protective response to tissue injury, infection, or foreign substances. While essential for healing, uncontrolled or chronic inflammation can cause significant tissue damage. Understanding the inflammatory cascade explains many clinical signs and guides therapeutic interventions.
Cardinal Signs of Inflammation
The five classical signs of inflammation, first described by Celsus and Galen, remain clinically relevant today. Each sign has a specific pathophysiological mechanism.
MEMORY AID - Cardinal Signs - 'Red Hot Swollen Painful Limping'
Think of an inflamed joint: RED (rubor), HOT (calor), SWOLLEN (tumor), PAINFUL (dolor), and the animal is LIMPING (functio laesa - loss of function)
Acute vs. Chronic Inflammation
[Include Image: Figure 3. Comparison of acute and chronic inflammatory cell infiltrates showing neutrophils vs. mononuclear cells]
High-YieldNEUTROPHILS dominate ACUTE inflammation (think 'N' for New/Neutrophils). MONONUCLEAR cells (Macrophages, Lymphocytes) dominate CHRONIC inflammation (think 'M' for Months/Mononuclear). This pattern is frequently tested!
Key Inflammatory Mediators
MEMORY AID - Arachidonic Acid Pathway - 'COX makes PGs, LOX makes LTs'
Remember: Cyclooxygenase (COX) makes Prostaglandins (PGs) and Thromboxanes - blocked by NSAIDs. Lipoxygenase (LOX) makes Leukotrienes (LTs) - NOT blocked by NSAIDs. Both come from Arachidonic Acid released by phospholipase.
1.3 Tissue Repair and Healing
Following tissue injury, the body initiates repair processes that can result in regeneration (restoration of normal tissue) or scarring (replacement with fibrous tissue). The outcome depends on the type of tissue injured, the extent of damage, and the presence of a supporting framework.
Phases of Wound Healing
[Include Image: Figure 4. Timeline diagram showing the four phases of wound healing with overlapping curves]
MEMORY AID - Wound Healing Phases - 'HIPR'
Remember the phases in order with 'HIPR': Hemostasis (stop bleeding), Inflammation (clean up), Proliferation (rebuild), Remodeling (strengthen). Think of 'Getting HIP with wound healing Rapidly'
High-YieldMACROPHAGES are the MOST CRITICAL cell in wound healing - they orchestrate the entire process by releasing growth factors and transitioning from inflammatory (M1) to reparative (M2) phenotypes. Wounds heal poorly in macrophage-depleted animals.
Factors Affecting Wound Healing
MEMORY AID - Factors Impairing Healing - 'FIND SOME'
Remember factors that impair healing with 'FIND SOME': Foreign body, Infection, Nutrition deficiency, Diabetes, Steroids (corticosteroids), Oxygen deficiency (ischemia), Movement (excessive), Elderly/age
| Sign (Latin) |
Description |
Pathophysiological Mechanism |
| Rubor (Redness) |
Erythema at site of injury |
Vasodilation and increased blood flow mediated by histamine, prostaglandins, and nitric oxide |
| Calor (Heat) |
Warmth at affected area |
Increased blood flow brings warm blood from core; local metabolic activity increases heat production |
| Tumor (Swelling) |
Edema/tissue enlargement |
Increased vascular permeability allows fluid and proteins to leak into interstitial space (exudate) |
| Dolor (Pain) |
Pain/tenderness |
Inflammatory mediators (bradykinin, prostaglandins) sensitize nerve endings; physical pressure from swelling |
| Functio Laesa (Loss of Function) |
Impaired function |
Combination of pain, swelling, and tissue damage impairs normal tissue function |
| Characteristic |
Acute Inflammation |
Chronic Inflammation |
| Duration |
Hours to days |
Weeks to months/years |
| Onset |
Rapid |
Gradual or follows acute phase |
| Primary Cells |
Neutrophils |
Macrophages, lymphocytes, plasma cells |
| Tissue Damage |
Usually mild and self-limited |
Often severe with ongoing destruction |
| Fibrosis |
Minimal or absent |
Prominent - key feature |
| Examples |
Acute bacterial infection, immediate trauma, acute allergic reaction |
IBD, rheumatoid arthritis, chronic hepatitis, tuberculosis |
| Mediator |
Source |
Main Effects |
Clinical Relevance |
| Histamine |
Mast cells, basophils |
Vasodilation, increased permeability, bronchoconstriction |
Target of antihistamines; anaphylaxis |
| Prostaglandins |
All cells via COX |
Vasodilation, pain, fever, platelet function |
Target of NSAIDs; COX-1 vs COX-2 |
| Leukotrienes |
Leukocytes via LOX |
Bronchoconstriction, chemotaxis, increased permeability |
Important in asthma; not blocked by NSAIDs |
| Cytokines (IL-1, TNF-alpha) |
Macrophages, lymphocytes |
Fever, acute phase response, leukocyte activation |
Systemic inflammation; sepsis pathophysiology |
| Complement |
Liver (plasma proteins) |
Opsonization (C3b), chemotaxis (C5a), MAC lysis (C5b-9) |
Bacterial killing; immune complex disease |
| Nitric Oxide |
Endothelium, macrophages |
Vasodilation, microbial killing, neurotransmission |
Septic shock (excessive NO); erectile function |
| Bradykinin |
Kinin system |
Vasodilation, pain, increased permeability |
ACE inhibitor cough; hereditary angioedema |
| Phase |
Timeline |
Key Events |
Key Cells/Factors |
| Hemostasis |
Immediate (minutes) |
Vasoconstriction, platelet plug formation, coagulation cascade activation, fibrin clot formation |
Platelets, coagulation factors, fibrin; PDGF and TGF-beta released |
| Inflammation |
Hours to days (days 1-3) |
Vasodilation, neutrophil then macrophage infiltration, debris removal, wound debridement |
Neutrophils (early), macrophages (critical - orchestrate repair), cytokines, growth factors |
| Proliferation |
Days to weeks (days 3-21) |
Angiogenesis, granulation tissue formation, epithelialization, fibroblast proliferation, collagen synthesis |
Fibroblasts, endothelial cells, keratinocytes; VEGF, FGF, TGF-beta |
| Remodeling |
Weeks to months/years |
Collagen reorganization (type III replaced by type I), wound contraction, scar maturation, tensile strength increases |
Myofibroblasts, MMPs (matrix metalloproteinases); collagen crosslinking |
Section 2: System-Specific Pathophysiology
Each organ system has unique pathophysiological mechanisms that explain disease manifestations. Understanding these system-specific processes enables you to predict clinical signs, interpret diagnostics, and select appropriate treatments.
2.1 Cardiovascular Pathophysiology
Heart Failure Pathophysiology
Heart failure occurs when the heart cannot pump sufficient blood to meet metabolic demands. Understanding the pathophysiology of left-sided vs. right-sided heart failure explains the distinct clinical presentations.
[Include Image: Figure 5. Diagram showing pathophysiology of left-sided vs right-sided heart failure with backward and forward failure effects]
MEMORY AID - Heart Failure - 'Left = Lungs, Right = Rest of body'
Think anatomically: Left heart failure backs up into the LUNGS (pulmonary edema, cough, dyspnea). Right heart failure backs up into the REST of the body (ascites, hepatomegaly, peripheral edema). The LEFT ventricle pumps to the body but BACKS UP into the lungs!
High-YieldIn DOGS, the most common cause of left-sided heart failure is DEGENERATIVE MITRAL VALVE DISEASE (myxomatous degeneration). In CATS, the most common cause is HYPERTROPHIC CARDIOMYOPATHY (HCM). Species-specific cardiac disease is heavily tested!
Shock Pathophysiology
Shock is a state of inadequate tissue perfusion and cellular oxygen delivery. Despite different causes, all types of shock lead to cellular hypoxia, metabolic acidosis, and organ dysfunction if not corrected.
MEMORY AID - Shock Types - 'HCDO'
Remember shock types with 'HCDO' (like 'Heart Can't Deliver Oxygen'): Hypovolemic (volume loss), Cardiogenic (pump failure), Distributive (vessel problem), Obstructive (blockage)
2.2 Respiratory Pathophysiology
Mechanisms of Hypoxemia
Hypoxemia (low blood oxygen) results from four main mechanisms. Understanding these mechanisms guides diagnostic workup and treatment selection.
MEMORY AID - Causes of Hypoxemia - 'Very Sick Hearts Die'
Remember the four mechanisms of hypoxemia: V/Q mismatch (most common), Shunt (right-to-left), Hypoventilation, Diffusion impairment. V/Q mismatch is BY FAR the most common!
High-YieldV/Q MISMATCH is the MOST COMMON cause of hypoxemia in clinical practice. Shunts are identified by POOR RESPONSE to oxygen supplementation. Hypoventilation is identified by ELEVATED PaCO2 (hypercapnia) - the others have normal or low PaCO2.
2.3 Renal Pathophysiology
Acute Kidney Injury vs. Chronic Kidney Disease
MEMORY AID - AKI vs CKD - 'Big Bloody Kidneys vs Small Shriveled Anemic'
AKI = Big (swollen) kidneys, normal Hematocrit (no anemia yet). CKD = Small (shriveled/fibrotic) kidneys, Anemic (low EPO). Also think: AKI = Acute = potentially reversible; CKD = Chronic = irreversible.
High-YieldNON-REGENERATIVE ANEMIA in CKD results from decreased erythropoietin (EPO) production by damaged kidneys. This is a key differentiator from AKI and explains why CKD patients are anemic. Treatment includes EPO supplementation (darbepoetin).
2.4 Gastrointestinal Pathophysiology
Vomiting vs. Regurgitation
Distinguishing vomiting from regurgitation is clinically critical because they indicate different anatomical locations of disease and require different diagnostic and treatment approaches.
MEMORY AID - Vomiting vs Regurgitation - 'Vomiting is Violent, Regurgitation is Relaxed'
Vomiting = Violent active process with retching, nausea, abdominal effort, can occur anytime. Regurgitation = Relaxed passive process, no effort, usually right after eating, tubular undigested food. Regurgitation = higher aspiration Risk!
2.5 Endocrine Pathophysiology
Feedback Loops in Endocrine Disease
Endocrine diseases result from hormone excess or deficiency. Understanding feedback loops explains why clinical signs occur and guides diagnostic testing. The hypothalamic-pituitary axis controls most endocrine glands through negative feedback.
[Include Image: Figure 6. Diagram showing hypothalamic-pituitary-adrenal axis feedback loop in health and Cushing's disease]
MEMORY AID - Cushing's vs Addison's - 'Cushing's = Cortisol Climbing, Addison's = Adrenal Absent'
Cushing's = TOO MUCH cortisol (pot belly, PU/PD, thin skin). Addison's = TOO LITTLE cortisol AND aldosterone (waxing/waning, bradycardia from high K+, hyponatremia). The Na:K ratio less than 27:1 is classic for Addison's!
High-YieldDIABETES in DOGS is usually Type 1 (immune-mediated beta cell destruction) requiring insulin. DIABETES in CATS is usually Type 2 (insulin resistance) and may be managed with diet/oral hypoglycemics initially, though many cats eventually require insulin. Diabetic cataracts are common in DOGS but rare in CATS.
| Factor |
Effect on Healing |
Clinical Considerations |
| Infection |
Prolongs inflammation, delays granulation tissue, may cause wound breakdown |
Wound hygiene, appropriate antibiotic therapy, drainage of abscesses |
| Poor Blood Supply |
Decreases oxygen and nutrient delivery, impairs inflammatory response and collagen synthesis |
Debridement of necrotic tissue, revascularization procedures, hyperbaric oxygen |
| Diabetes Mellitus |
Impairs neutrophil function, decreases growth factor activity, peripheral neuropathy, microangiopathy |
Strict glucose control, protect from pressure, frequent monitoring for complications |
| Corticosteroids |
Inhibit inflammation, decrease collagen synthesis, impair angiogenesis, thin skin |
Minimize dose when possible, consider Vitamin A supplementation (partial reversal) |
| Nutritional Deficiency |
Protein deficiency impairs collagen synthesis; Vitamin C deficiency impairs collagen crosslinking (scurvy); Zinc deficiency impairs epithelialization |
Nutritional support, specific supplementation (protein, Vitamin C, zinc) |
| Foreign Bodies |
Perpetuate inflammation, serve as nidus for infection, physical barrier to healing |
Surgical removal, thorough wound irrigation and exploration |
| Excessive Movement |
Disrupts granulation tissue, delays epithelialization, increases scar formation |
Immobilization, bandaging, exercise restriction |
| Feature |
Left-Sided Heart Failure |
Right-Sided Heart Failure |
| Primary Problem |
Left ventricle cannot adequately pump blood to systemic circulation |
Right ventricle cannot adequately pump blood to pulmonary circulation |
| Backward Effects |
Blood backs up into pulmonary veins leading to PULMONARY EDEMA |
Blood backs up into systemic veins leading to JUGULAR DISTENSION, HEPATOMEGALY, ASCITES, PERIPHERAL EDEMA |
| Forward Effects |
Decreased cardiac output leading to weakness, exercise intolerance, azotemia |
Decreased blood flow to lungs leading to hypoxemia |
| Key Clinical Signs |
Cough (especially at night/recumbent), dyspnea, tachypnea, pulmonary crackles, orthopnea |
Ascites, jugular venous distension/pulsation, hepatomegaly, subcutaneous edema (ventral) |
| Common Causes (Dogs) |
Mitral valve disease (DMVD - most common), dilated cardiomyopathy |
Heartworm disease, pulmonic stenosis, tricuspid dysplasia |
| Common Causes (Cats) |
Hypertrophic cardiomyopathy (HCM - most common) |
HCM with biventricular failure, pericardial disease |
| Shock Type |
Mechanism |
Causes |
Key Features |
| Hypovolemic |
Decreased circulating volume |
Hemorrhage, severe dehydration, burns, GI losses |
Tachycardia, weak pulses, pale mucous membranes, prolonged CRT |
| Cardiogenic |
Pump failure |
Severe heart failure, arrhythmias, cardiac tamponade |
Pulmonary edema, jugular distension, may have arrhythmias |
| Distributive (Vasodilatory) |
Inappropriate vasodilation, maldistribution of blood flow |
Sepsis (most common), anaphylaxis, neurogenic |
Septic: may have hyperdynamic (warm) or hypodynamic (cold) phases |
| Obstructive |
Mechanical obstruction to blood flow |
Pulmonary embolism, tension pneumothorax, GDV, pericardial tamponade |
Depends on cause; may have muffled heart sounds (tamponade) or absent lung sounds (pneumothorax) |
| Mechanism |
Pathophysiology |
Examples |
Response to O2 Supplementation |
| V/Q Mismatch |
Ventilation-perfusion imbalance; areas of lung are perfused but poorly ventilated or vice versa |
Pneumonia, pulmonary thromboembolism, atelectasis, pulmonary edema |
RESPONDS WELL - supplemental O2 helps |
| Right-to-Left Shunt |
Blood bypasses ventilated alveoli completely (true shunt) |
Severe ARDS, cardiac shunts (VSD, PDA with Eisenmenger), pulmonary AV malformations |
POOR RESPONSE - shunted blood never contacts O2 |
| Hypoventilation |
Inadequate alveolar ventilation leading to elevated CO2 and decreased O2 |
CNS depression, neuromuscular disease, airway obstruction, chest wall injury |
RESPONDS - but need to address underlying ventilation problem; elevated PaCO2 is key finding |
| Diffusion Impairment |
Thickened or reduced alveolar-capillary membrane impairs gas exchange |
Pulmonary fibrosis, interstitial lung disease (rare as sole cause) |
RESPONDS to O2 supplementation |
Section 3: Integration of Clinical Signs with Underlying Pathology
The ability to connect clinical signs with their pathophysiological mechanisms is essential for the BCSE. This section provides frameworks for clinical reasoning and demonstrates how to approach case-based questions.
3.1 Common Clinical Signs and Their Mechanisms
MEMORY AID - PU/PD Causes - 'PUSHED'
Remember common causes of PU/PD with 'PUSHED': Pyometra, Urinary tract disease (kidney), Steroids/Cushing's, Hyperthyroidism/Hypercalcemia/Hyperadrenocorticism, Electrolyte abnormalities (hypokalemia), Diabetes mellitus/insipidus
3.2 Laboratory Finding Interpretation
Connecting Lab Values to Pathophysiology
High-YieldThe Na:K ratio is a valuable screening tool. A ratio less than 27:1 is suggestive of HYPOADRENOCORTICISM (Addison's disease) and should prompt an ACTH stimulation test. However, remember that GI disease, urinary obstruction, and other conditions can also cause similar electrolyte patterns.
3.3 Species-Specific Pathophysiology Considerations
MEMORY AID - Cats and Acetaminophen - 'Cats Can't Conjugate'
Cats have deficient GLUCURONIDATION (Phase II conjugation), making them extremely sensitive to acetaminophen. The toxic metabolite causes METHEMOGLOBINEMIA (brown mucous membranes) BEFORE hepatotoxicity. Dogs tolerate higher doses but still get liver damage.
| Feature |
Acute Kidney Injury (AKI) |
Chronic Kidney Disease (CKD) |
| Onset |
Rapid (hours to days) |
Gradual (weeks to months) |
| Kidney Size |
Normal to enlarged (swelling) |
Small, irregular (atrophy/fibrosis) |
| Hematocrit |
Normal (unless hemorrhage) |
Decreased (non-regenerative anemia from decreased EPO) |
| History |
Recent toxin exposure, infection, ischemia, obstruction |
Chronic PU/PD, weight loss, declining appetite over weeks-months |
| Urine Output |
Variable - may be oliguric, anuric, or polyuric |
Usually polyuric (loss of concentrating ability) |
| Prognosis |
Potentially reversible if cause addressed |
Irreversible; progressive - management focused |
| Common Causes |
Ethylene glycol, NSAIDs, aminoglycosides, leptospirosis, pyelonephritis, ureteral obstruction, ischemia |
Idiopathic (most common in cats), glomerulonephropathy, amyloidosis, polycystic kidney disease, chronic pyelonephritis |
| Feature |
Vomiting |
Regurgitation |
| Mechanism |
ACTIVE process - coordinated reflex involving CNS vomiting center, abdominal muscle contraction |
PASSIVE process - simple expulsion without effort |
| Prodromal Signs |
Nausea (lip licking, hypersalivation), retching, abdominal contractions present |
None or minimal - food just 'falls out' |
| Timing |
Variable - may be hours after eating |
Usually immediately to shortly after eating |
| Contents |
Digested or partially digested food, bile-stained, acidic pH |
Undigested, tubular shape (esophageal mold), neutral pH, may be covered in mucus |
| Location of Disease |
Stomach, intestines, OR extra-GI (CNS, metabolic, toxins, vestibular) |
Esophagus (megaesophagus, stricture, FB) or pharynx |
| Aspiration Risk |
Lower (larynx closes during vomiting reflex) |
HIGHER - larynx does not close; aspiration pneumonia common |
| Condition |
Hormone Status |
Pathophysiology |
Key Clinical Signs |
| Hypothyroidism (dogs) |
Low T4, High TSH |
Primary thyroid gland destruction (immune-mediated or idiopathic atrophy); loss of negative feedback increases TSH |
Obesity, lethargy, cold intolerance, symmetric alopecia, 'tragic face', bradycardia |
| Hyperthyroidism (cats) |
High T4, Low TSH |
Autonomous thyroid adenoma produces excess T4 independent of TSH; negative feedback suppresses TSH |
Weight loss despite polyphagia, tachycardia, hyperactivity, vomiting/diarrhea, palpable thyroid nodule |
| Hyperadrenocorticism (Cushing's) |
High cortisol |
Pituitary-dependent (80-85% dogs): ACTH-secreting pituitary tumor. Adrenal-dependent (15-20%): adrenal tumor. Iatrogenic: exogenous steroids |
PU/PD, polyphagia, pot-bellied appearance, alopecia, thin skin, calcinosis cutis, panting |
| Hypoadrenocorticism (Addison's) |
Low cortisol and aldosterone |
Primary adrenal destruction (immune-mediated most common); loss of mineralocorticoids (aldosterone) causes electrolyte abnormalities |
Waxing/waning illness, weakness, vomiting, diarrhea, bradycardia (hyperkalemia), hyponatremia |
| Diabetes Mellitus |
High glucose, low/dysfunctional insulin |
Type 1: immune destruction of beta cells (dogs). Type 2: insulin resistance plus beta cell dysfunction (cats). Glucose cannot enter cells leading to catabolism |
PU/PD, polyphagia, weight loss, cataracts (dogs), plantigrade stance (cats), ketoacidosis risk |
| Clinical Sign |
Pathophysiological Mechanism(s) |
Common Causes |
| Polyuria/Polydipsia (PU/PD) |
Osmotic diuresis (diabetes mellitus, post-obstructive diuresis); Decreased ADH effect (diabetes insipidus, hypercalcemia, pyometra endotoxins, hypokalemia); Increased cortisol (Cushing's - multiple mechanisms); Primary polydipsia; Renal medullary washout |
Diabetes mellitus, CKD, Cushing's, hypercalcemia, pyometra, hyperthyroidism |
| Icterus/Jaundice |
Pre-hepatic: Excessive RBC destruction overwhelms liver (hemolytic anemia, IMHA); Hepatic: Liver dysfunction impairs bilirubin conjugation/excretion (hepatitis, lipidosis); Post-hepatic: Biliary obstruction prevents bilirubin excretion (cholelithiasis, pancreatitis, neoplasia) |
IMHA, liver disease, bile duct obstruction, sepsis |
| Ascites |
Increased hydrostatic pressure (right heart failure, portal hypertension); Decreased oncotic pressure (hypoalbuminemia from liver failure, protein-losing nephropathy/enteropathy); Increased vascular permeability (peritonitis, neoplasia); Lymphatic obstruction |
Right heart failure, liver failure, PLE, neoplasia, FIP |
| Cough |
Airway irritation/inflammation (tracheobronchitis, pneumonia); Airway compression (cardiomegaly, mass); Pulmonary edema (left heart failure - cough often worse at night); Allergic/inflammatory (feline asthma) |
Heart disease, kennel cough, pneumonia, collapsing trachea, feline asthma |
| Pallor (Pale Mucous Membranes) |
Anemia (decreased RBC oxygen-carrying capacity); Vasoconstriction (shock, hypothermia); Poor perfusion (hypovolemia, heart failure) |
Blood loss, hemolysis, bone marrow suppression, shock |
| Seizures |
Abnormal neuronal electrical activity due to: Metabolic (hypoglycemia, hepatic encephalopathy, electrolyte imbalances); Structural (neoplasia, inflammation, trauma); Idiopathic epilepsy; Toxins (many) |
Idiopathic epilepsy, hypoglycemia, toxins, brain tumor, encephalitis |
| Vomiting |
GI causes: Direct irritation, obstruction, inflammation, dysmotility; Extra-GI causes: CNS (vestibular, increased ICP), metabolic (uremia, hypoadrenocorticism, DKA), toxins, pancreatitis, peritonitis |
Dietary indiscretion, GI FB, pancreatitis, kidney disease, Addison's, vestibular |
| Lab Finding |
Pathophysiological Mechanism |
Clinical Interpretation |
| Elevated BUN without elevated Creatinine |
Pre-renal azotemia (dehydration, GI bleeding) or increased protein catabolism; Urea is reabsorbed more than creatinine when tubular flow is slow |
Check hydration status; GI bleeding increases BUN from protein digestion; High-protein meals can increase BUN. Renal azotemia shows proportional BUN:Cr elevation. |
| Hypoglycemia |
Excess insulin (insulinoma, insulin overdose), decreased gluconeogenesis (liver failure, sepsis, neonates), increased glucose utilization (sepsis, neoplasia) |
Insulinoma: hypoglycemia with inappropriately normal/high insulin. Sepsis: often presents with hypoglycemia. Toy breed puppies prone to hypoglycemia from limited glycogen stores. |
| Elevated ALT |
Hepatocyte membrane damage releases cytoplasmic ALT; indicates hepatocellular injury but NOT function; highly liver-specific in dogs/cats |
High ALT = hepatocellular damage. Must assess liver FUNCTION with bilirubin, albumin, glucose, BUN, bile acids. Normal ALT does not rule out chronic liver disease (end-stage may have few hepatocytes left). |
| Elevated ALP |
Induced by corticosteroids (endogenous or exogenous) in dogs; also increased in cholestasis, bone growth/disease, drug induction (phenobarbital) |
In DOGS: often elevated with Cushing's (steroid-induced isoenzyme). In CATS: ALP has short half-life so ANY elevation is significant. Young animals have higher ALP from bone growth. |
| Hypoalbuminemia |
Decreased production (liver failure), increased loss (PLE, PLN, hemorrhage, third-spacing), decreased intake (starvation) |
Assess liver function, check for proteinuria (PLN), consider GI signs (PLE). Hypoalbuminemia leads to edema/ascites when albumin less than 1.5 g/dL. |
| Hyperkalemia |
Decreased excretion (urinary obstruction, anuric renal failure, hypoadrenocorticism), cellular shift (acidosis, tumor lysis, massive tissue damage), pseudohyperkalemia (hemolysis in Akitas) |
EMERGENCY if greater than 6.5-7 mEq/L (risk of cardiac arrest). Classic with Addison's disease (lack of aldosterone). Urinary obstruction is common cause in male cats. |
| Species |
Condition |
Unique Pathophysiology |
Clinical Relevance |
| Dogs |
Acetaminophen Toxicity |
Dogs have some glucuronidation capacity; toxic metabolite causes hepatotoxicity primarily; methemoglobinemia less common than in cats |
Present with hepatic necrosis, elevated liver enzymes; treat with N-acetylcysteine. Dose-dependent toxicity. |
| Cats |
Acetaminophen Toxicity |
Cats have DEFICIENT glucuronidation (Phase II metabolism); toxic metabolite NAPQI accumulates causing methemoglobinemia and Heinz body anemia BEFORE hepatotoxicity |
Present with brown/cyanotic mucous membranes, facial/paw edema, dyspnea; EXTREMELY TOXIC in cats. N-acetylcysteine is antidote. |
| Cats |
Hyperthyroidism |
Autonomous functional thyroid adenoma (benign in greater than 97%); excess T4 increases metabolic rate, cardiac output, GFR; may mask underlying CKD |
Treating hyperthyroidism unmasks CKD as GFR normalizes. Check renal values before and after treatment. Most common endocrinopathy in older cats. |
| Horses |
Colic (large colon volvulus) |
Large colon is minimally attached allowing displacement/volvulus; vascular compromise leads to ischemic necrosis, endotoxemia, DIC; gut barrier breakdown releases bacteria/endotoxins |
Surgical emergency; severe cardiovascular compromise; high mortality without rapid intervention; endotoxemia causes vasodilation, fever, laminitis risk. |
| Horses |
Laminitis |
Laminar inflammation and ischemia; activation of MMPs degrades basement membrane; mechanical failure of laminar attachments leads to distal phalanx rotation/sinking |
Associated with endotoxemia (colic, retained placenta), carbohydrate overload, Cushing's disease. Pain management critical; chronic cases have poor prognosis. |
| Cattle |
Left Displaced Abomasum |
Abomasal hypomotility (often post-calving) allows gas accumulation; abomasum floats to left side; trapped between rumen and body wall; impairs outflow and causes metabolic alkalosis |
Common in high-producing dairy cows post-partum; characteristic 'ping' on left side auscultation-percussion; surgical correction required. |
| Sheep |
Copper Toxicity |
Sheep have LIMITED ability to excrete copper; accumulates in liver during chronic exposure; then sudden release during stress causes massive intravascular hemolysis |
Often see sudden deaths or hemolytic crisis; jaundice, hemoglobinuria, red urine. Avoid copper-supplemented cattle feeds in sheep. |