Corticosteroids in Dogs: Dosing, Tapering and Clinical Use — GlobalVetCo

Corticosteroids in Dogs: Dosing, Tapering and Clinical Use

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Narration for: Corticosteroids in Dogs: Dosing, Tapering and Clinical Use
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Anti-inflammatory vs immunosuppressive dosing, condition-specific tapering protocols, HPA axis suppression and recovery, monitoring parameters, and the clinical management of iatrogenic hyperadrenocorticism — a complete prescribing guide for canine corticosteroids.

Key takeaways
  • Corticosteroids are categorised by potency, duration of action, and mineralocorticoid activity — prednisolone is the workhorse oral steroid; dexamethasone is reserved for CNS indications due to its potency and long HPA suppression.
  • Anti-inflammatory doses (prednisolone 0.5–1 mg/kg/day) suppress inflammation; immunosuppressive doses (2–4 mg/kg/day) suppress lymphocyte function — they are not interchangeable.
  • Tapering is mandatory after > 7 days of therapy: abrupt cessation after > 2 weeks can cause an Addisonian crisis due to iatrogenic HPA suppression.
  • The Cushingoid patient (iatrogenic hyperadrenocorticism) can develop within 2–4 weeks of high-dose therapy — monitor for PU/PD, polyphagia, panting, pot-belly, and calcinosis cutis.
  • GI protectants (omeprazole, sucralfate) do NOT prevent corticosteroid-induced GI ulceration — the only effective prevention is to avoid concurrent NSAIDs and use the lowest effective steroid dose.
Red flags / do not miss
  • Abrupt cessation after > 2 weeks of daily corticosteroid therapy can cause an acute Addisonian crisis — hyponatraemia, hyperkalaemia, hypotension, collapse. Taper over weeks, not days.
  • Calcinosis cutis is pathognomonic for iatrogenic or naturally occurring hypercortisolism. It appears as firm, white, gritty plaques in the skin — it does not resolve with tapering and requires prolonged management.
  • Corticosteroids can induce parturition in late pregnancy — do not administer steroids to pregnant bitches within 2 weeks of the expected whelping date.
  • GI ulceration from corticosteroids is insidious — the first sign may be perforation. Melena, unexplained anaemia, or a declining PCV in a dog on steroids warrants immediate investigation.
  • Corticosteroids cause insulin resistance — a diabetic dog started on prednisolone will require increased insulin dosing. Monitor blood glucose q2–4h for 24–48 hours after initiating steroids in a diabetic patient.

1. Introduction: The Double-Edged Sword

Corticosteroids are among the most effective and most misused drugs in veterinary medicine. Their potent anti-inflammatory and immunosuppressive effects are unmatched by any other single drug class, but their adverse-effect profile is equally dramatic. A 2019 survey of small-animal practitioners found that 40% of corticosteroid prescriptions did not include a written tapering plan — a practice that exposes patients to unnecessary risk of iatrogenic hypoadrenocorticism.

This guide provides a complete framework for prescribing, dosing, tapering, and monitoring corticosteroids in dogs. It covers the pharmacology of available agents, condition-specific protocols from allergic dermatitis to immune-mediated haemolytic anaemia, the physiology of HPA axis suppression, and the management of the Cushingoid patient.

2. Pharmacology: Potency, Duration, and Receptor Activity

Drug Relative Glucocorticoid Potency (vs Cortisol) Relative Mineralocorticoid Activity Duration of Action (HPA Suppression) Equivalent Anti-inflammatory Dose (Dog) Typical Indications
Cortisol (hydrocortisone) 1 1 Short (< 12 hours) 2.5 mg/kg PO q8h Physiological replacement only (hypoadrenocorticism). Not used for anti-inflammatory effect.
Prednisone / Prednisolone 4 0.8 Intermediate (12–36 hours) 0.5–1 mg/kg/day (anti-inflammatory); 2–4 mg/kg/day (immunosuppressive) First-line oral steroid for most indications. Prednisolone preferred (no hepatic conversion needed).
Methylprednisolone 5 0.5 Intermediate (12–36 hours) 0.4–0.8 mg/kg/day anti-inflammatory; 1.5–3 mg/kg/day immunosuppressive Alternative to prednisolone. Slightly higher glucocorticoid potency, lower mineralocorticoid activity.
Triamcinolone 5 0 Intermediate (12–36 hours) 0.1–0.2 mg/kg PO or IM. Repeat every 7–10 days. Intralesional or repository injection for focal inflammation (feline eosinophilic granuloma complex, localised allergic dermatitis). Do NOT use systemically long-term.
Dexamethasone 30 0 Long (48–72+ hours) 0.05–0.1 mg/kg/day anti-inflammatory; 0.2–0.4 mg/kg/day immunosuppressive CNS inflammation (IVDD, meningitis), anaphylaxis, emergency. Avoid for chronic daily use due to severe HPA suppression.
Fludrocortisone 10 125 Short–Intermediate NOT used for anti-inflammatory effect Mineralocorticoid replacement for hypoadrenocorticism (Addison's disease).
Desoxycorticosterone pivalate (DOCP) 0 High Long (25–30 days) NOT used for anti-inflammatory effect Injectable mineralocorticoid replacement for hypoadrenocorticism. Administered every 25 days.

2.1 Mechanism of Action

Corticosteroids diffuse across the cell membrane and bind to cytoplasmic glucocorticoid receptors (GR). The steroid–GR complex translocates to the nucleus, where it modulates gene transcription through two main mechanisms:

  1. Transactivation: The steroid–GR dimer binds to glucocorticoid response elements (GREs) in promoter regions, increasing transcription of anti-inflammatory proteins (lipocortin-1, IL-10, IκB). This is responsible for most metabolic side effects (gluconeogenesis, lipolysis, protein catabolism).
  2. Transrepression: The steroid–GR monomer interacts with pro-inflammatory transcription factors (NF-κB, AP-1), inhibiting their activity without binding DNA directly. This mediates most anti-inflammatory effects.

The therapeutic goal is to maximise transrepression (anti-inflammatory) while minimising transactivation (metabolic side effects). This is why 'the lowest effective dose for the shortest possible duration' is the universal prescribing principle.

3. Anti-Inflammatory vs Immunosuppressive Dosing

The distinction between anti-inflammatory and immunosuppressive dosing is not merely semantic — it reflects fundamentally different therapeutic goals, receptor occupancy, and adverse-effect profiles.

Parameter Anti-Inflammatory Dosing Immunosuppressive Dosing
Prednisolone dose (dog) 0.5–1 mg/kg/day PO 2–4 mg/kg/day PO (sometimes divided BID)
Receptor occupancy ~50% GR occupancy >90% GR occupancy
Primary effect Inhibition of phospholipase A2, COX-2, and cytokine production in inflamed tissue Suppression of lymphocyte proliferation, induction of lymphocyte apoptosis, inhibition of antigen presentation
Onset of effect Hours (anti-inflammatory) Days (immunosuppression takes 2–5 days for full effect)
Typical course duration Days to weeks Weeks to months (disease-dependent)
Tapering May not be needed if < 7 days. If > 7 days, taper over 1–2 weeks. ALWAYS required. Taper over weeks to months.
Indications Allergic dermatitis, acute urticaria, insect-bite hypersensitivity, acute bronchitis, intervertebral disc disease (acute) Immune-mediated haemolytic anaemia (IMHA), immune-mediated thrombocytopenia (ITP), immune-mediated polyarthritis, pemphigus foliaceus, inflammatory bowel disease (severe), meningitis of unknown aetiology
Adverse effect risk Moderate with short courses High — expect PU/PD, polyphagia, and panting. Cushingoid changes within 2–4 weeks.
Clinical pearl
If you find yourself prescribing > 1 mg/kg/day prednisolone for an 'allergy', you are almost certainly using an immunosuppressive dose. Re-evaluate the diagnosis — true allergic disease should respond to anti-inflammatory doses. If it does not, consider whether the problem is infectious (pyoderma, Malassezia), parasitic (scabies), or behavioural.

4. Tapering Protocols by Condition

Tapering is the gradual reduction of corticosteroid dose to allow recovery of the suppressed hypothalamic–pituitary–adrenal (HPA) axis. The taper rate depends on the duration of therapy and the dose used — not the underlying condition. A patient on 2 mg/kg/day for 3 weeks needs a slower taper than a patient on 0.5 mg/kg/day for 5 days.

4.1 General Tapering Principles

  1. If therapy duration is < 7 days (any dose): no taper required — the HPA axis has not been suppressed long enough to cause clinically significant atrophy.
  2. If therapy duration is 7–14 days at anti-inflammatory doses: taper by 25% of the original dose every 3–5 days. Example: prednisolone 1 mg/kg/day × 10 days → 0.75 mg/kg/day × 3 days → 0.5 mg/kg/day × 3 days → 0.25 mg/kg/day × 3 days → stop.
  3. If therapy duration is > 14 days at anti-inflammatory doses, or > 7 days at immunosuppressive doses: taper by 25% every 2–4 weeks. Monitor for recurrence of the underlying disease at each dose reduction.
  4. If the patient has received immunosuppressive doses for > 4 weeks: consider an ACTH stimulation test before the final taper step (when the dose reaches a physiologic replacement level of ~0.2 mg/kg/day) to confirm HPA axis recovery.

4.2 Condition-Specific Protocols

Condition Starting Dose (Prednisolone) Taper Protocol Expected Total Duration Monitoring Parameters
Acute allergic dermatitis 0.5–1 mg/kg/day PO Reduce by 25% every 3–5 days. If pruritus recurs, return to the last effective dose and taper more slowly. 2–3 weeks Pruritus score, skin lesions
IMHA / ITP 2–4 mg/kg/day PO (divided BID for IMHA) Reduce by 25% every 2–4 weeks once PCV/platelets have stabilised in the normal range for ≥ 2 weeks. Goal: alternate-day therapy at the lowest effective dose. 4–6 months minimum PCV (IMHA), platelet count (ITP), reticulocyte count, serum protein. ACTH stim test optional before final discontinuation.
Inflammatory bowel disease (moderate–severe) 2 mg/kg/day PO Taper by 25% every 2 weeks once clinical signs (diarrhoea, vomiting, weight loss) are controlled. Transition to alternate-day therapy if long-term maintenance is required. 3–6 months (may transition to budesonide or dietary management alone) Body weight, faecal consistency, serum albumin, cobalamin/folate
Intervertebral disc disease (acute) 0.5 mg/kg/day PO (or dexamethasone 0.1 mg/kg IV once for acute spinal cord injury) Reduce by 25% every 3–5 days. Total course rarely > 2–3 weeks. Steroids are NOT recommended for chronic IVDD. 2–3 weeks Neurological status (proprioception, motor function, pain perception)
Meningitis/encephalitis of unknown aetiology 1–2 mg/kg/day PO (often combined with cytarabine or cyclosporine as a steroid-sparing agent) Taper by 25% every 2–4 weeks. Very slow taper — premature reduction risks relapse. 6–12 months or lifelong Neurological status, CSF analysis (if repeated), adverse-effect monitoring
Pemphigus foliaceus 2–3 mg/kg/day PO Taper by 25% every 2–3 weeks once lesions are in remission (no new pustules for ≥ 2 weeks). Adjunctive therapy (azathioprine, cyclosporine, oclacitinib) is nearly always required. Lifelong — goal is lowest effective alternate-day dose + adjunctive therapy Skin lesion score, CBC (azathioprine monitoring), chemistry panel

5. HPA Axis Suppression: Physiology and Recovery

The HPA axis is a classic endocrine feedback loop: hypothalamic corticotropin-releasing hormone (CRH) stimulates pituitary adrenocorticotropic hormone (ACTH), which stimulates adrenal cortisol secretion. Cortisol feeds back to inhibit CRH and ACTH. Exogenous corticosteroids suppress this axis at the hypothalamic and pituitary levels. With prolonged suppression, the adrenal cortices atrophy — they literally shrink — and lose the ability to respond to endogenous ACTH even after the exogenous steroid is withdrawn.

5.1 Timeline of HPA Suppression

  • Single dose: Transient suppression for 24–48 hours. The axis recovers spontaneously.
  • Daily therapy, < 7 days: Mild, reversible suppression. Recovery within 3–7 days of cessation — tapering optional but conservative.
  • Daily therapy, 7–14 days: Moderate suppression. Recovery within 1–2 weeks with tapering. Abrupt cessation can cause transient hypoadrenocorticism (lethargy, anorexia, GI signs).
  • Daily therapy, > 2 weeks: Significant suppression with likely adrenal atrophy. Recovery may take 4–8 weeks or longer. Tapering is mandatory. An ACTH stimulation test should confirm recovery before final discontinuation.
  • Daily therapy, > 4 weeks at immunosuppressive doses: Severe, prolonged suppression. Adrenal atrophy is substantial. Recovery may take months. Some patients never fully recover their stress-appropriate cortisol response.

5.2 The ACTH Stimulation Test for Monitoring Recovery

When tapering off long-term steroids, an ACTH stimulation test is performed to assess whether the adrenal glands are capable of producing cortisol. The test is performed when the prednisolone dose has been tapered to ≤ 0.2 mg/kg/day or to alternate-day therapy.

  • Administer synthetic ACTH (cosyntropin, 5 μg/kg IV or IM, maximum 250 μg/dog).
  • Measure cortisol at 0 and 60 minutes post-ACTH.
  • A post-ACTH cortisol > 5.5 μg/dL (150 nmol/L) indicates adequate adrenal reserve — tapering can continue.
  • A post-ACTH cortisol < 2 μg/dL (55 nmol/L) indicates adrenal atrophy — the taper should be paused or the dose increased slightly until recovery occurs.

6. Managing the Cushingoid Patient (Iatrogenic Hyperadrenocorticism)

Iatrogenic hyperadrenocorticism (IHC) is the clinical syndrome caused by chronic exogenous corticosteroid excess. It is clinically indistinguishable from naturally occurring (pituitary-dependent or adrenal-tumour) hyperadrenocorticism, with one exception: cortisol levels are low (suppressed) rather than high, because the exogenous steroid suppresses endogenous cortisol production.

Clinical Sign Frequency in IHC Mechanism Reversibility
PU/PD (polyuria/polydipsia) 80–95% Steroid antagonism of ADH at the renal collecting duct, plus osmotic diuresis from hyperglycaemia Reverses within days of dose reduction
Polyphagia 80–90% Direct central effect of glucocorticoids on appetite centres Reverses within days of dose reduction
Panting 60–80% Respiratory muscle wasting, increased diaphragmatic work of breathing, direct central stimulation of respiratory centres Reverses over weeks as muscle mass recovers
Pot-belly / abdominal distension 50–70% Hepatomegaly (glycogen deposition), abdominal muscle wasting, redistribution of body fat Reverses over months; muscle reconditioning required
Calcinosis cutis 10–30% (pathognomonic) Dystrophic mineralisation of dermal collagen and elastin fibres — calcium and phosphate deposition in degenerate connective tissue POORLY REVERSIBLE — lesions may persist for months after steroid cessation. No specific treatment; control secondary infection (often requires long-term antibiotics).
Alopecia (truncal, bilaterally symmetrical) 50–70% Telogen arrest of hair follicles — hair stops growing and existing hairs are retained until shed normally Reverses over months — hair regrowth begins 4–8 weeks after steroid cessation
Muscle wasting (temporal, epaxial, abdominal) 50–60% Protein catabolism: glucocorticoids promote proteolysis and inhibit protein synthesis in skeletal muscle Reverses over weeks to months with dose reduction and exercise
Hepatomegaly 50–70% Steroid-induced glycogen deposition and hepatocellular swelling (steroid hepatopathy — ALP elevation is the hallmark laboratory finding) Reverses over weeks

6.1 Laboratory Findings in IHC

  • ALP (alkaline phosphatase): Elevated in 85–95% of dogs with IHC. The corticosteroid-induced isoenzyme of ALP (CALP) is produced by hepatocytes in response to glucocorticoid exposure. ALP can exceed 10× the upper reference limit.
  • ALT: Mild to moderate elevation (hepatocellular swelling, not necrosis).
  • Hyperglycaemia: Steroid-induced insulin resistance — fasting glucose > 6.5 mmol/L (> 117 mg/dL) in 30–50% of cases. May progress to overt diabetes mellitus if steroids are continued.
  • Lipidaemia: Visible lipaemia in a fasting sample.
  • Low cortisol: A low baseline cortisol (< 1 μg/dL or < 28 nmol/L) in a dog with clinical signs of Cushing's is highly suggestive of IHC rather than naturally occurring disease. However, exogenous steroids cross-react variably with cortisol assays — always ask the laboratory which steroids interfere.

7. Clinical Pearls and Prescribing Safeguards

  • Always write the taper on the prescription label: 'Give 1 tablet twice daily for 5 days, then 1 tablet once daily for 5 days, then ½ tablet once daily for 5 days, then stop.' An oral taper plan prevents the owner from continuing the starting dose indefinitely.
  • Alternate-day therapy: Giving the total 48-hour dose as a single morning dose every other day reduces HPA suppression. The HPA axis has ~24 hours to recover between doses. This is only appropriate for maintenance therapy — not for initial disease control.
  • Morning dosing: Administer the daily dose in the morning to mimic the natural diurnal cortisol rhythm. Evening dosing suppresses the normal early-morning ACTH surge and may exacerbate HPA suppression.
  • Steroid-sparing agents: For conditions requiring long-term immunosuppression (IMHA, pemphigus, IBD), add a steroid-sparing agent early — azathioprine (dogs only, 2 mg/kg PO q24–48h), cyclosporine (5 mg/kg PO q12–24h), mycophenolate (10–20 mg/kg PO q12h), or oclacitinib (for atopic dermatitis). This allows a lower prednisolone dose and faster taper.
  • GI protectants: Omeprazole and sucralfate do NOT prevent steroid-induced GI ulceration. Corticosteroid-induced ulcers result from inhibition of prostaglandin synthesis and impaired mucosal repair — neither of which is addressed by acid suppression or mucosal coating. The only effective prevention is to use the lowest effective steroid dose and never combine with NSAIDs.

8. Contraindications and Cautions

  • Absolute contraindications: Systemic fungal infection (blastomycosis, histoplasmosis — steroids promote dissemination), corneal ulcer (steroids inhibit corneal epithelial migration and collagenase production), concurrent NSAID therapy, and late pregnancy (steroids induce parturition).
  • Relative contraindications / use with caution: Diabetes mellitus (steroids cause insulin resistance), congestive heart failure (mineralocorticoid activity causes sodium and water retention), hypertension, and renal insufficiency (steroids increase protein catabolism and BUN).
  • Vaccination: Do not administer modified-live vaccines to a dog on immunosuppressive doses of corticosteroids. Killed vaccines may have reduced efficacy. Ideally, vaccinate before initiating immunosuppressive therapy.
Clinical pearls
  • Prednisone is a prodrug — it requires hepatic conversion to prednisolone for activity. In patients with hepatic insufficiency, use prednisolone directly. The conversion may also be impaired in very young animals.
  • Dexamethasone has essentially zero mineralocorticoid activity — this makes it unsuitable for treating hypoadrenocorticism (Addison's disease), which requires both glucocorticoid and mineralocorticoid replacement.
  • A single dose of dexamethasone (even 0.1 mg/kg IV) suppresses the HPA axis for 24–48 hours — do not perform an ACTH stimulation test within 48 hours of any steroid administration.
  • Topical otic steroids (in ear medications) can be absorbed systemically and suppress the HPA axis in small dogs — this is an under-recognised cause of iatrogenic Cushing's.
  • Alternate-day therapy (giving the total 48-hour dose every other morning) reduces HPA suppression compared to daily dosing while maintaining comparable anti-inflammatory efficacy for many conditions.

Frequently asked questions

What is the difference between prednisone and prednisolone?
Prednisone is a prodrug — it is inactive until the liver converts it to prednisolone via 11β-hydroxysteroid dehydrogenase. Prednisolone is the active drug. In dogs with hepatic insufficiency, very young animals, or patients on drugs that inhibit hepatic enzymes, prednisolone is preferred because it does not require hepatic activation. In practice, the two are often used interchangeably at the same doses in dogs with normal hepatic function.
How fast can I taper steroids?
The taper speed is determined by the duration of therapy, not the underlying disease. Therapy < 7 days: no taper needed. 7–14 days: taper by 25% every 3–5 days. > 14 days: taper by 25% every 2–4 weeks. Immune-mediated diseases are tapered slowly not because of HPA-axis concerns, but because rapid taper risks disease relapse.
Can I use dexamethasone instead of prednisolone?
Dexamethasone is 30× more potent than cortisol (7.5× more than prednisolone) and has a duration of HPA suppression of 48–72+ hours. It is appropriate for acute CNS inflammation (IVDD, head trauma, meningitis), anaphylaxis, and emergency use. It is NOT appropriate for chronic daily therapy of allergic or immune-mediated disease — prednisolone allows finer dose adjustment, has a shorter duration of HPA suppression, and has a better safety profile for long-term use.
Do topical steroids (ear drops, eye drops, skin creams) cause HPA suppression?
Yes — especially in small dogs. Otic preparations containing potent steroids (betamethasone, dexamethasone, mometasone) applied to inflamed ear canals can be absorbed systemically. A 5 kg dog receiving twice-daily otic dexamethasone can absorb a systemic dose equivalent to 0.05 mg/kg/day — enough to suppress the HPA axis after 2–3 weeks. Similarly, ophthalmic prednisolone acetate 1% applied q6h can suppress the HPA axis in dogs < 10 kg.
What is an 'Addisonian crisis' from steroid withdrawal?
Iatrogenic hypoadrenocorticism (secondary Addison's) occurs when exogenous steroids are abruptly withdrawn after prolonged use. The atrophied adrenal glands cannot produce cortisol (and, to a lesser degree, aldosterone). Clinical signs: acute collapse, bradycardia, hypotension, hyponatraemia, and hyperkalaemia — identical to a primary Addisonian crisis. Treatment: IV fluids (0.9% NaCl), dexamethasone IV (does not interfere with subsequent ACTH stimulation testing), and supportive care. The crisis is entirely preventable by appropriate tapering.
Should I give gastroprotectants with steroids?
The evidence does not support the routine use of gastroprotectants (omeprazole, sucralfate, misoprostol) to prevent corticosteroid-induced GI ulceration in dogs. Steroid ulcers result from impaired mucosal prostaglandin synthesis and reduced epithelial repair — mechanisms not addressed by acid suppression. The best prevention is to use the lowest effective dose, avoid concurrent NSAIDs, and monitor for melena or unexplained anaemia.
Can I use budesonide instead of prednisolone for inflammatory bowel disease?
Budesonide is a locally acting corticosteroid with high first-pass hepatic metabolism — it is designed to act on the intestinal mucosa with minimal systemic absorption. In dogs, however, the first-pass metabolism is less complete than in humans, and systemic effects (HPA suppression, Cushingoid signs) still occur at high doses. Budesonide (1–3 mg/m² PO q24h) is a reasonable option for IBD as a steroid-sparing strategy, but it is not free of systemic effects and should also be tapered.
How do I manage a dog that relapses every time I taper the prednisolone?
This indicates the underlying disease is not in remission — the steroids were suppressing but not resolving the disease process. Options: (1) increase the steroid dose back to the last effective level and taper more slowly (half the increment, twice the interval), (2) add a steroid-sparing immunosuppressive agent (azathioprine, cyclosporine, mycophenolate) to allow a lower steroid dose, or (3) reconsider the diagnosis — has an infectious, neoplastic, or dietary trigger been missed?

Self-check quiz

Test yourself. Answers are below each question — cover them first if you are studying.

Q1. A 4-year-old dog has been on prednisolone 2 mg/kg/day for IMHA for 6 weeks. The PCV has been stable in the normal range for 3 weeks. You decide to begin tapering. What is the most appropriate first taper step?
  1. Stop prednisolone immediately — the disease is in remission
  2. Reduce to 1.5 mg/kg/day (25% reduction) and recheck PCV in 2 weeks
  3. Reduce to 1 mg/kg/day (50% reduction) and recheck PCV in 1 week
  4. Switch to dexamethasone for faster taper
  5. Add azathioprine and stop prednisolone immediately
Show answer

Answer: Reduce to 1.5 mg/kg/day (25% reduction) and recheck PCV in 2 weeks

After > 4 weeks of immunosuppressive therapy, taper by 25% of the current dose every 2–4 weeks. Reducing by 50% risks disease relapse. Stopping abruptly risks both disease relapse and an Addisonian crisis. Azathioprine takes 2–4 weeks for full effect — it should be started before or at the beginning of the taper, not used to replace steroids abruptly.

Q2. Which corticosteroid is specifically contraindicated for chronic daily therapy due to its prolonged HPA suppression?
  1. Prednisolone
  2. Methylprednisolone
  3. Dexamethasone
  4. Cortisol (hydrocortisone)
  5. Fludrocortisone
Show answer

Answer: Dexamethasone

Dexamethasone has a biological half-life of 36–54 hours and suppresses the HPA axis for 48–72+ hours after a single dose. Chronic daily use produces profound, prolonged HPA suppression that is very difficult to reverse. It is reserved for acute CNS conditions and emergency use. Prednisolone (intermediate-acting) is the drug of choice for chronic oral therapy.

Q3. A 10-year-old diabetic dog develops acute allergic dermatitis. The pruritus is severe and requires corticosteroid therapy. What is the most important clinical consideration?
  1. Steroids are contraindicated in diabetics — use antihistamines only
  2. Start prednisolone at 2 mg/kg/day to rapidly control pruritus
  3. Expect insulin requirements to INCREASE and monitor blood glucose closely
  4. Expect insulin requirements to DECREASE and reduce the insulin dose pre-emptively
  5. Use dexamethasone — it has less effect on glucose metabolism than prednisolone
Show answer

Answer: Expect insulin requirements to INCREASE and monitor blood glucose closely

Corticosteroids cause insulin resistance through multiple mechanisms (increased hepatic gluconeogenesis, reduced peripheral glucose uptake). In a diabetic dog, starting prednisolone will predictably cause hyperglycaemia, and the insulin dose will need to be increased — often by 25–50%. Monitor blood glucose q2–4h for the first 24–48 hours and adjust insulin accordingly. Steroids are not absolutely contraindicated in diabetics but must be used with caution.

Q4. Which clinical sign is PATHOGNOMONIC for iatrogenic (or naturally occurring) hypercortisolism in dogs?
  1. Polyuria and polydipsia
  2. Bilateral truncal alopecia
  3. Calcinosis cutis
  4. Hepatomegaly
  5. Muscle wasting
Show answer

Answer: Calcinosis cutis

Calcinosis cutis — firm, white, gritty, often erythematous plaques in the skin — is pathognomonic for hypercortisolism. No other canine disease produces this lesion. It results from dystrophic mineralisation of dermal collagen and elastin fibres. All other signs (PU/PD, alopecia, hepatomegaly, muscle wasting) can occur with other endocrine, metabolic, or nutritional disorders.

Q5. A dog has been on prednisolone 0.5 mg/kg/day for acute bronchitis for 5 days. The cough is resolved. What is the appropriate discontinuation plan?
  1. Taper by 25% every 3–5 days for 2 weeks
  2. Taper by 50% every 7 days for 3 weeks
  3. Stop immediately — no taper needed
  4. Switch to alternate-day therapy for 2 weeks, then stop
  5. Perform an ACTH stimulation test before stopping
Show answer

Answer: Stop immediately — no taper needed

Corticosteroid therapy of less than 7 days duration at anti-inflammatory doses does not cause clinically significant HPA suppression and does not require tapering. An ACTH stimulation test is unnecessary for such a short course. Alternate-day therapy is used for maintenance, not for short-course discontinuation.

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Educational disclaimer: This article is for veterinary students and licensed professionals. It is not a substitute for case-specific clinical judgment, local formulary rules, or current drug labels. Always verify doses, legality, and species contraindications before treating.
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