Dogs and Cats 26 Flashcards
Medical therapy for feline hyperthryoidism what are the pros - EXAM
○ Effective and rapid in most cases ○ Generally safe ○ Avoids hospitalisation ○ Readily available ○ Inexpensive in short term ○ Reversible, adjustable ○ Co-morbid disease setting (20% of cases) ○ Short term control setting (prior to definitive Rx) ○ Available, practical
Medical therapy for feline hyperthryoidism what are the cons - EXAM
- Not curative, ongoing Rx required - ONCE STOP WITH START AGAIN
- Small % poor responders -> will need higher doses overtime
- Does not halt the underlying disease
- Less cost effective long term
- Titration can be challenging
- Need for good compliance, ongoing daily tableting
- Drug side effects
Drug side effects of medical therapy for feline hyperthryoidism what are they
○ GI – common, anorexia, V, D, usually mild and self-limiting, give with food, stop if persists OR transdermal
○ Facial pruritus & excoriation – Stop Rx
○ (Rare) BM suppression, IMHA, coagulopathy – Stop Rx
○ Liver (ddx other hepatopathy) – Stop Rx
○ Iatrogenic hypothyroidism (15-37%)
○ Other – lymphadenopathy, myasthenia gravis
○ Client contact allergies (gel, non-coated tablets) - WEAR GLOVES
In terms of feline hyperthyroidism what are the 2 main options and how to adjusty
1) Carbimazole SR 10 mg SID PO (Vidalta, MSD) - most common
○ Don’t crush tablet
- Increase PO methimazole 2.5 mg/day until euthyroid
○ Reduce by 2.5mg/day if low TT4
○ May later be able to go to SID
○ If total dose > 10mg/day need to question compliance
○ Consider with food, or transdermal if GI side effects
○ Stop medical therapy if skin, BM or liver toxicity
2) Methimazole 2.5 mg BID PO (Felimazole, Dechra)
- From 10 days, no change > 5mg
Feline hyperthyroidism medical therapy how to monitor and what looking for afterwards
How do I monitor therapy?
- 2-3 weeks after dose change or adjustment
- 3 months then as required
What to look for after any Rx
- Has the hyperthyroidism resolved
○ TT4
○ Weight, clinical signs
- Is there concurrent renal disease?
○ Urea, creat, alb, electrolytes, P, Ca, PCV, Urinalysis, +/- UPC, BP, SDMA
- Has iatrogenic hypothyroidism developed?
○ CBC, cholesterol, TT4, (+/- TSH, fT4, T3)
§ Anaemic?, TT4 low?
Feline hyperparathyroidism how to judge adequacy of therapy, what else checking, which lives longer between that and other therapies
How do I judge the adequacy of therapy?
- The TT4 needs to be in the LOWER HALF of the reference range for adequate control
What else should I be checking?
- Monitor blood pressure at diagnosis and during/after treatment
○ 13% of 303 untreated hyperthyroid cats were found to be hypertensive at initial diagnosis
○ 23% of initially normotensive hyperthyroid cats BECAME hypertensive following medical and/or surgical therapy of hyperthyroidism
Who lives longer?
- Radioiodine MST 4 years
- Methimazole MST 2 years - medical therapy
Thyroidectomy as a treatment for feline hyperthyroidism what needs to be done first, what effective against but negatives
- Medical stabilise first
- Effective / cure
○ Most bilateral
○ No requirement for radiation / facilities / isolation
○ Available - Negatives
○ GA, surgery (pain)
○ Requires experience
○ Ectopic thyroid tissue common and cannot remove
○ Medium up-front costs
○ High risk of post-operative complications
§ hypothyroidism / hypoparathyroidism) – failure in 1 in 3 cases, 4-(20%) complications
§ 2% mortality rate, 6% risk of hypoparathyroidism
○ Unilateral OR Bilateral? (can’t treat ectopic tissue)
○ Pre-treatment required
Dietary therapy as a treatment for feline hyperthyroidism what need to feed, what does it have and how effective
- Iodine Limited Diet
- Must be fed exclusively
○ Variable efficacy
○ As effective in outdoor cats - Recently available
- Low protein and low phosphate
○ Associated with lower serum [creatinine], possible option CKD cases - NOT CHRONIC
○ Palatability can be a factor, monitor BW, muscle mass
○ Not recommend for lean cats, DM, DM remission - Need greater numbers / long term research
Dietary therapy for treatment of feline hyperthryoidism pros
- No pilling!
- No Sx, GA, special facilities/training or isolation
- Available
- No carbimazole / methimazole side effects
- Reversible
- Cat and client friendly
- Low initial costs
Potential diet for IRIS stage 1-3 CKD
Dietary therapy for treatment of feline hyperthryoidism cons
- Not a cure
- Compliance - BIG ISSUE
- Time to euthyroidism (stable renal state) - takes longer than radioiodine and medical therapy
- Not for cats that eat other food sources
- Iodine levels
Dietary therapy for treatment of feline hyperthryoidism what are the unknowns and would you use it
the unknowns
- Long term effects?
○ On Hyperthyroid and Normal cats
○ Goitre?
○ Immune deficiency? Cancer? Infection?
○ Causing Hyperthyrodisism?
- Wash out times prior to scintigraphy? - at least a week, could be up to a month
- Long term survival times?
- Studies on transition from y/d to medical therapy?
- Long term effects on thyroid pathology?
- Malignant transformation?
would I use it?
- Maybe if I-131 or medical therapy not possible
- Maybe if need short term option needed before do more definitive therapy
Does unmasking CKD by treating hyperthryoidism affect prognosis and what to do once diagnosed
NO - hyperthyroid state is DAMAGING THE KIDNEYS
- Unmasking CKD by obtaining euthyroidism does not worsen prognosis! - It is better as can now treat the kidney disease
- As long as you avoid iatrogenic hypothyroidism
I have just diagnosed CKD and hyperthyroidism
- Expect with treatment of hyperthyroidism, patient to progress one IRIS stage within 1 month, but then not very progressive if maintain euthyroidism - generally quite stable
○ (and avoid hypothyroidism!)
- Mild stable renal disease should not affect the advice to clients - STAY WITH THE SAME DOSE OF HYPERTHRYOID TREATMENT
- Can still treat with I-131 once stable - radioiodine
○ Scintigraphy, low dose I-131, start L-thyroxine at discharge
§ Associated with minimal worsening azotemia (due unmasking hyperthyroidism effect on kidney) and not due to hypothyroidism when managed this way
Do you need to do a treatment trial for hyperthyroidism before a definitive therapy
NO unless
- To establish underlying renal status?
○ Only if you have advanced renal disease (IRIS stage 3-4)
- Perhaps if you suspect other concurrent disease
Tendency is do to I-131 earlier now
When treating feline hyperthyroidism do you need to worry about iatrogenic hypothryoidism
- Iatrogenic hypothyroidism can develop after medical, surgical or radioiodine therapy
○ Diagnosed by low TT4 and high cTSH - 5 – 30% of cases
- Transient or permanent
- Clinical signs are uncommon
- Usually transient and generally not a problem in non-azotaemic cats
- Iatrogenic hypothyroidism and CKD have shorter surival (MST 456 days vs MST 905 days
When to suspect carcinoma causes feline hypothyroidism - IMPORTANT
- Large of multiple thyroid mass - more than 2 cm in size
- High TT4 > 250 nmol/L, 5x10 fold increase
- No response to medical therapy
- Only respond with very high doses
- Long term medication > 2 years
- No response to bilateral thyroidectomy
- No response to standard radio-iodine
- Find metastasis
Cachexia what is it, diagnosis and treatment
- Cachexia ≠ Starvation
○ Inflammation is a consistent feature
» ↑ Acute phase proteins, ↑ excessive production of pro-inflammatory cytokines
○ Rise in resting energy expenditure
» Altered protein, fat and carbohydrate metabolism
» Insulin resistant state may develop - Diagnosis : PE + chronic inflammatory disease
- Not a specific diagnosis. State of disordered metabolism
- Rx: Underlying disorder
○ Hypercaloric feeding
Cancer cachexia how common, most common cancer, what occurs and treatment
- More common people & cats > dogs
○ Most common to cause is lymphoma - Negative impact on survival
- Host vs. tumour competition - tumour generally winning
○ Favours anaerobic metabolism
○ Altered cytokine profiles
○ ↑[lactate]
○ Altered insulin responsiveness - intake reduces and don’t get energy needed out of food - Treat underlying tumour, consider iatrogenic contributors (drugs), appetite stimulants, control nausea / vomiting,
- Diet: high fat (n-3 fatty acids) (hills N/D), low carbohydrates
Hypoadrenocorticism what also called and signalment
(addisons disease) Signalment - Female > Male Dogs ○ Poodles, westies - Young – middle aged (4-5 years) - Rare in cats
Hypoadrenocorticism what are the 4 main causes, what is deficient and what occurs
1) Primary (most common)
○ Usually glucocorticoid and mineralocorticoid deficient
○ Immune mediated adrenal cortex destruction
○ Occasionally glucocorticoid only deficient early = atypical, only zon fasciculata and reticularis affected, may later progress to typical
2) Secondary (rare)
○ Inadequate ACTH production due to abnormality within the brain (adrenal gland normal)
§ EG - sudden cessation of long term glucocorticoids (rare takes a while to produce as cells atrophy), brain tumours, brain trauma, congenital pituitary defects
§ Only glucocorticoid deficient
3) Atypical
○ Only glucocorticoid deficient
4) Iatrogenic
○ Some cases of HAC (cushings) treated with mitotane/trilostane
○ May be reversible
Hypoadrenocortcism history and physical exam what seen with glucocorticoid deficiency
History - Acute, gradual, wax and wane, chronic intermittent progressive signs - Signs often triggered by stressful event / illness - Vague Physical Exam Glucocorticoid deficiency - Anorexia - Vomiting - Regurgitation (megaoesophagus) - Lethargy / depression - Weakness - Weight loss - Diarrhoea, Tremor - Pu / Pd - Abdominal pain - (Melena) - (Hypoglycaemia / seizures) - rare
Hypoadrenocorticism what seen with mineralcorticoid deficiency
- More severe
- Pu / Pd
- Shock : Hypotensive / hypovolaemia
- Weak pulses
- Prolonged CRT
- Collapse
- Dehydration
- Bradycardia
- Hypothermia
Hypoadrenocorticism clinical pathology findings
on-regenerative normocytic normochromic anaemia - DUE TO CHRONIC DISEASE
○ Or dehydration and polycythaemia
- Normal to increase WCC (INAPPROPRAITE RESPONSE)
○ Eosinophilia (20-30% cases) - BIG CLUE
- Lack of stress leukogram (INAPPROPRIATE AS VERY SICK)
- decrease Na, decrease Cl, decrease Alb, decrease Cholesterol, decrease Glucose
- increase K, increase Ca, increase P, increase ALT, increase ALKP
- Na:K < 27:1 (but not if atypical)
- Prerenal azotaemia
- Metabolic acidosis
- USG < 1.030
Hypoadrenocorticism imaging findings
- Generally done due to regurgitation and thinking maybe aspiration pneumonia
- Microcardia
○ Small pulmonary arteries
○ Small vena cava - Microhepatica
- +/- Megaoesophagus (oesophageal dysfunction)
- Small / absent adrenal (supportive, not diagnostic) - if normal could also be that as well
Hypoadrenocorticism ECG findings
- Hyperkalaemia - LIFE THREATENING - bradycardia
○ Peaked T waves
○ Flattened P waves
○ Increased QRS and P-R interval
○ P waves absent
○ Decreased R waves
○ Bradycardia, ventricular fibrillation / asystole