1. Differentiate Rickets vs.
Osteomalacia
Feature Rickets Osteomalacia
Affected
Young, growing animals Adult animals (growth plates closed)
Population
Defective mineralization of bone AND Defective mineralization of bone
Primary Defect
cartilage only (osteoid)
Key Gross Thickened growth plates (physes); enlarged Soft, fragile bones prone to fracture; no
Lesion joints (e.g., "rachitic rosary") growth plate changes
Bowed limbs, swollen joints, pain, poor Bone pain, spinal/pelvic deformities,
Other Signs
growth stiffness
2. Parasites of the Muscles (Location/Description)
Parasite Location in Muscle Gross Description
Cysticercus
Costochondral musculature (esp. Large (1-2 cm), fluid-filled cysts with a
spp. (tapeworm
pigs/cattle) single white larval nodule (scolex) inside.
larvae)
Tongue, masseter, diaphragm, Microscopic larvae become encysted in
Trichinella spiralis
intercostal, eye muscles the muscle.
Grossly visible as white nodules due to
Sarcocystis spp. Herbivores & pigs massive numbers of bradyzoites inside
the cyst.
Neospora caninum, Trypanosoma
Other listed (not
cruzi, Hepatozoon americanum, (No gross descriptions provided)
detailed)
nematode larval migrants
3. Differentiate Purpura, Petechiae, Ecchymoses
These are all hemorrhagic discolorations (red-purple-brown-black) in the skin.
Term Size / Description
Petechia Tiny, pinpoint hemorrhages.
Ecchymoses Larger, bruise-like hemorrhages (>1cm).
Purpura A general term encompassing both petechiae and ecchymoses (multiple hemorrhages).
4. Environmental Induced Skin Disease
I. Actinic (Sun) Injury
• Primary Phototoxicity (Sunburn): Direct UV damage. Lesions on non-pigmented, sparsely haired skin
(ears, abdomen). Chronic cases lead to thickening and squamous cell carcinoma.
• Photosensitization: Photodynamic agent + UV light → tissue damage. Four types (Primary, porphyrin
metabolism, hepatogenous, idiopathic). Lesions only on non-pigmented, sun-exposed areas (e.g.,
"swelled head" in sheep).
II. Chemical Injury
• Contact Dermatitis: Non-immunologic. Caused by irritants (acids, soaps, drugs, body secretions).
Lesions on sparsely haired skin (abdomen, flanks, feet).
III. Physical Injury
• Acral Lick Dermatitis (lick granuloma): Psychogenic in dogs. Single lesion on extremity
(carpus/metacarpus).
• Callus/Hygroma: Thickened plaque from friction over pressure points (elbows, sternum), especially in
large breed dogs on hard flooring.
5. Differentiate the Two Forms of Rabies
Feature Furious Rabies Paralytic (Dumb) Rabies
Key Aggressive, irritable, "mad-dog syndrome." Non-aggressive, rarely bites. Ataxia,
Behavior Loses fear, roams, bites at anything. drooping jaw (dogs), inability to swallow.
Other Dilated pupils, may swallow foreign objects, Profuse salivation (drooling), rapid
Signs follows and bites at a moving hand. progression to paralysis, coma, death.
6. Rabies Infection Sequence (Essay Format)
1. Entry: Virus enters the host via a bite wound from a rabid animal, introduced through infected saliva.
2. Local Replication: The virus replicates locally in muscle tissue at the site of inoculation.
3. Neural Entry & Spread: The virus enters peripheral nerves at the neuromuscular junction and travels
via retrograde axonal transport toward the central nervous system (CNS).
4. CNS Infection: Reaches the spinal cord and brain, causing non-suppurative encephalitis, meningitis, and
vasculitis.
5. Centrifugal Spread: From the CNS, the virus travels via peripheral nerves to other tissues, including
the salivary glands, eyes, and kidneys.
7. Diagnosis of Rabies - Negri Bodies
• What they are: Round or oval, eosinophilic (pink-staining), sharply outlined inclusion bodies (2-10 μm in
diameter).
• Location: Found in the cytoplasm (and sometimes processes) of neurons in rabid animals.
• Significance: They are pathognomonic for rabies (definitive for diagnosis when found).
8. Endocrine Diseases - Clinical Signs Table
Disease Key Clinical Signs & Lesions
Addison's Lethargy, bradycardia, hyponatremia & hyperkalemia (hallmark),
(Hypoadrenocorticism) vomiting/diarrhea, dehydration, hypoglycemia.
Cushing's PU/PD, polyphagia, hepatomegaly, pendulous abdomen, skin lesions,
(Hypercortisolism) dystrophic mineralization, lymphopenia, eosinopenia.
Reduced BMR (lethargy, weight gain), bilaterally symmetric alopecia,
Hypothyroidism
hyperpigmentation, myxedema, high cholesterol, atherosclerosis.
PU/PD, restlessness, weight loss with polyphagia, cervical swelling,
Hyperthyroidism (cats)
coughing/dyspnea, hypertrophic cardiomyopathy.
Hyperglycemia, glycosuria, PU/PD, weight loss with increased appetite,
Diabetes Mellitus
weakness, hepatomegaly, bilateral cataracts, plantigrade stance (neuropathy).
Excess PTH → hypercalcemia, PU/PD, weakening of bones (fibrous
Hyperparathyroidism
osteodystrophy, e.g., "rubber jaw").
9. Differentiate Diabetes Mellitus Type 1 vs. Type 2
*Based on slides 34-35 of "ENDOCRINE VPT [Link]"*
Feature Type I Diabetes Type II Diabetes
Primary Destruction of beta cells → complete Insulin resistance (target cells don't respond to
Problem loss of insulin secretion. insulin).
Insulin Level Completely absent or extremely low. Normal or high (due to resistance).
Over time, can develop into insulin-
Progression Immediately insulin-dependent.
dependent DM (beta cells eventually fail).
Most common form in dogs (similar to
In Dogs Characterized by insulin resistance initially.
Type I).