Hyperthyroidism Flashcards

1
Q

describe hyperthyroidism

A
  1. much MUCH more common in cats than dogs
    -cats (primary hyperthyroidism):
    –bilateral adenomatous hyperplasia (70% of cases
    –carcinoma (<3%)
    –ectopic thyroid tissue: anywhere between base of tongue and base of heart

-dogs:
–iatrogenic (over-supplementation, diet)
-misdiagnosis (thyroid hormone autoantibodies)
–functional thyroid carcinoma: uncommon form of a rare tumor in dogs

  1. spontaneous hyperparathyroidism in dogs:
    -thyroid tumors represent <2% of all tumors in dogs
    -most are non functional, some are destructive and actually result in hypothyroid and a FEW are functional and cause hyperthyroid
    -most will have a palpable cervical mass!
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2
Q

describe clinical presentation of hyperthyroid in cats

A
  1. older cats
    -most >8yr at diagnosis
    -mean age 13 years
  2. protected breeds (at lower risk but can still be affected)
    -siamese
    -himalayan
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3
Q

describe hyperthyroid physiology

A
  1. increased basal metabolic rate
    -increased O2 consumption and heat generation
  2. cardiovascular changes:
    -increased beta adrenergic receptors/catecholamines
    -increase heart rate/strength
    -increased cardiac output
    -increased systolic blood pressure
  3. renal changes:
    -increased renal blood flow
    -increased GFR
    -increased RAAS activity
    -increased renal sodium absorption
    -decreased ability to concentrate urine
  4. hematologic changes: increased erythrocytosis

5 GI changes: increased otility

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4
Q

describe common owner reported clinical signs of hyperthyroid

A
  1. weight loss
  2. ravenous appetite
  3. unkempt dull coats
  4. V/D
  5. behavior change: agitation restlessness, aggressiveness
  6. PU/PD
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5
Q

describe less common owner-reported clinical signs of hyperthyroid

A
  1. apathetic hyperthyroidism
    -opposite signs to standard disease (anorexia, lethargy)
    -more likely in advanced cases or those with severe concomitant diseases like CHF or neoplasia
  2. end-organ injury from systemic arterial hypertension
    -ocular: acute blindness from retinal detachment, hyphema
    -CNS: seizures, acute CNS signs (vestibular, etc.)

HYPERTHYROIDISM IS A LEADING CAUSE OF HYPERTENSION IN CATS

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6
Q

describe physical exam of a hyperthyroid cat

A
  1. hair coat changes
  2. low BCS/MCS
    -some hyperthyroid cats are overweight tho so don’t let BCS rule out!
  3. thyroid slip:
    -thyroid palpation: palpate from larynx to thoracic inlet
    -enlarged gland will sink down the neck
  4. cardiac abnormalities:
    -tachycardia
    -murmur
    -gallop sound
  5. thickened/ropey intestines
  6. hypertensive retinopathy on fundic exam
    -vessel tortuosity, retinal hemorrhage, retinal detachment
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7
Q

describe thyroid storm

A
  1. rare, severe, life-threatening manifestaiton
  2. clinical syndrome: acute, exaggerated manifestations of thyrotoxicosis
  3. precipitated by aggressive thyroid palpation, thyroid surgery, radioactive iodine treatment, stress
  4. signs:
    -hyperthermia (>104)
    -CNS dysfunction: seizures, coma, extreme agitation, altered mentation
    -neuromuscular dysfunction: LMN weakness, cervical ventroflexion
    -cardiovascualr dysfunction: tachycardia, arrhythmias, CHF, systemic arterial hypertension
    -GI dysfunction: V/D
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8
Q

describe clinicopathologic findings of hyperthyroidism

A

CBC: erythrocytosis

biochem!!:
1. ELEVATED ALT
2. elevated ALP
3. azotemia (10-15%)
4. +/- hyperphosphatemia

urinalysis:
1. variable USG
2. +/- proteinuria, ketonuria

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9
Q

describe hyperthyroidism and CKD

A
  1. frequent comorbidities: both are common diseases of older cats
    -CKD can challenge diagnosis of hyperthyroidism in some cats (non-thyroidal illness syndrome can lower TT4 into normal range)
    -hyperthyroidism can challenge diagnosis and staging of CKD
  2. hyperthyroidism masks/hides kidney disease for 2 reasons:
    -muscle wasting: less muscle mass = less creatinine generated so lower blood creatinine concentrations (over-estimation of true GFR); SDMA can be used to circumvent this

-hyperthyroidism increases renal blood flow GFR, which damages nephrons and accelerates progression of CKD

  1. hyperthyroidism harms the kidneys:
    -extra-renal increase in GFR is not a reason to not treat hyperthyroidism in cats with CKD!
    -is just a reason to be careful when you do
    -goal is to achieve euthyroid and avoid hypothyroid status with treatment
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10
Q

describe serum creatinine in hyperthyroid cats

A
  1. serum creatinine will be lower due to increased GFR and decreased muscle mass
    -so is a poor indicator of CKD
  2. if a hyperthyroid cat is persistently azotemic with no extra-renal factors = azotemic CKD (can be quite advanced)
  3. if a hyperthyroid cat is non-azotemic, it may or may not have CKD
    -you are unlikely to unmask severe renal disease after treating hyperthyroidism in these cases
    -unmasking CKD is more likely in cats with low USG (but not perfect predictor)
    -abdominal imaging can also show you kidney changes!!
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11
Q

what to expect after treatment of hyperthyroid in cats with CKD?

A
  1. as we decrease T4:
    -decrease cardiac output
    -normalize systemic vascular resistance
    -decrease RAAS activity
  2. all of which decrease GFR and
    -decrease muscle metabolism and increase muscle mass (over months)
  3. will increase serum creatinine concentration, proportional to increase in T4
  4. but glomerular hypertension and hyperfiltration improve!
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12
Q

what are other diagnostic considerations in hyperthyroidism

A
  1. heart:
    -hyperthyroidism causes thyrotoxic cardiomyopathy (proportional to severity/chronicity)
    -ECG changes: hypertrophic cardiomyopathy-phenotype (reversible with treatment)
    -thoracic rads can rule out CHF
  2. liver:
    -enzyme elevation from hyperthyroidism can be severe
  3. GI:
    -diarrhea and weight loss mimic enteropathy, so rule out hyperthyroidism in cats with these signs!
  4. blood pressure:
    -HYPERTHYROIDISM IS A LEADING CAUSE OF SYSTEMIC ARTERIAL HYPERTENSION IN CATS
    -you should measure BP and do a fundic exam in ALL hyperthyroid cats (treated or untreated)
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13
Q

describe hormone assessment of hyperthyroidism

A
  1. hypothalamus TRH: high
  2. pituitary gland, TSH: low/suppressed
  3. T4 secretion: high
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14
Q

describe diagnosis of hyperthyroid

A
  1. TT4: screening
    -can be used as a diagnostic test
    -if clin signs syggest and TT4 s elevated, hyperthyroidism!
    -if high-normal and clin suspicion is high, pursue confirmatory testing
    -perform annually in older cats
  2. confirmatory testing:
    -TT4: if elevated = hyperthyroid
    -if high-normal and clinical suspicion is high, and since euthyroid sick can suppress TT4 into reference interval, submit TT4 and fT4 and TSH:
    –if high fT4 and low TSH = hyperthyroid likely
    -retesting in a few weeks is also always an option
  3. but remember!
    -fT4 can be elevated in random samples from some healthy cats
    -never use fT4 alone for screening
    -only assess fT4 along with TT4 +/- TSH
    -always look at the whole clinical picture
  4. TSH considerations:
    -historic assay is for canine TSH, meant to detect high TSH in hypothyroidism so is unable to detect TSH in all cats and can give false undetectable result
    -use a feline-optimized assay if you can
  5. a low TSH can suggest early hyperthyroidism; usually develops within 1-2 years
    -normal TT4 + undetected TSH: check if used canine assay, use a feline assay if you can
    -if previously normal TSH now undetectable = developing hyperthyroidism likely
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15
Q

describe hyperthyroid treatment

A

2 choices

  1. medical management (lifelong)
    -methimazole
    -iodine restricted diet
  2. definitive treatment (hopefully one and done)
    -radioactive iodine (I-131)
    -thyroidectomy: less common now, high morbidity
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16
Q

describe an iodine restricted diet

A
  1. ills y/d
    -most diets caontain at least 0.46ppm of iodine, hills contains less than 0.2
    -response rate is greater than 80%
  2. absolutely the ONLY thing the cat can eat!
    -be careful with supplements, meds, water sources
    -not for outdoor cats
    -palatability can limit use in some cats
    -disease control usually within 4-8 weeks (the higher the T4 the longer it can take, up to 6 months)
    -do not use concomitantly with methimazole (higher risk of hyperthyroidism)
17
Q

describe methimazole

A
  1. blocks thyroid peroxidase, inhibiting T3/T4 synthesis
  2. does not destroy abnormal tissue
  3. progressive hyperplasia can require progressive dose increase
  4. adverse reactions:
    -direct GI upset: if see, transition to transdermal/compounded formulation

-iatrogenic hypothyroidism: if see, decrease dose +/- drug holiday
–clinical: (low TT4, high TSH, clinical signs) may require supplementation with levothyroxine
–subclinical (normal TT4, high TSH, no clin signs)

-facial excoriations: if see STOP IMMEDIATELY
-hepatotoxicity
-blood dyscrasias: thrombocytopenia, neutropenia
-myasthenia gravis

18
Q

describe methimazole transdermal formulation

A
  1. when to use:
    -fractious cats
    -clients cannot administer oral meds
    -GI upset on oral meds
  2. differences from oral:
    -usually takes higher dose to control disease (but still start as same dose you would use PO)
    -takes longer to gain control
19
Q

describe methimazole monitoring

A
  1. recheck TT4 and TSH
    -oral: 2 weeks after start/changing treatment and periodically
    -transdermal: 3-4 weeks after start/changing treatment and periodically
    -high TSH suggests hypothyroidism (either overt (low TT4) or subclinical (normal T4))
    –iatrogenic hypothyroid worsens azotemia and decreases survival in these cats
  2. therapeutic goal:
    -TT4 mid to low normal with normal TSH
  3. monitoring for adverse effects/changes in clinical abnormalitiers
    -concurrently perform CBC and chem for first 1-2 months
    -always measure BP even after treatment!!
20
Q

describe radioactive iodine (I-131)

A
  1. destroys hyepractive thyroid tissue while sparing suppressed normal tissue
  2. healthy suppressed thyroid cells should not take up I-131
    - a pre treatment undetectable TSH is helpful to confirm this!
  3. hyperfunctional thyroid cells take up I-131
  4. I-131 emits beta radiation, killing cells within 1-2 min
    -should spare most normal cells
    -these normal cells “wake up” to produce T4 in 1-3 months
  5. treatment of choice for most hyperthyroid cats
    -best for physiologically stable that can be safely maintained in isolation for a few days
    -treats: thyroid adenoma, thyroid carcinoma, ectopic thyroid tissue
  6. one-time SQ injection; isolation for approx 5 days
    -$2200-2600: but cheaper than lifelong methimazole and associated monitoring
    -success: 90-95%, less than 5% need a second injection
21
Q

describe pre-referral considerations for radioactive I-131 treatment

A
  1. ideal candidate is systemically stable to enter isolation: we cannot touch them!!
  2. BP, CBC, chem, urinalysis, +/- imaging
  3. high TT4 with undetectable TSH makes it safer
    -normal tissue is less likely to take up I-131
  4. must be off methimazole for 1-2 weeks prior
    -off hill’s y/d for 2-4 weeks prior
  5. methimazole trials are not usually needed before I-131 BUT
    -should be considered in untreated cats with:
    –azotemia in the later IRIS CKD stage 2 or greater; will cat decompensate in isolation?
    –not needed for cats in IRIS stage 1 or early stage 2, azotemia may worsen but will likely not decompensate in isolation
22
Q

describe post I-131 monitoring

A
  1. recheck TT4 and TSH
    -1, 3, 6, 12 months

-most controlled within 1 month but full response can take 3-6 months

  1. <5% will develop clinical hypothyroidism
    -worsens kidney funciton and decreases survival
    -requires T4 supplementation
    -usually resolves within 1-3 months
  2. monitor for changes in clinical abnormalities
    -concurrently perform BP and assess kidney function + any other abnormalities present pre-treatment
23
Q

describe antihypertensive therapy for hyperthyroid

A
  1. persistently hypertensive, hyperthyroid cats need antihypertensive therapy
    -telmisartan or amlodipine
  2. treatment of hypothyroid might not resolve hypertension
  3. hypertensive target organ damage is occurring while you wait for euthyroidism
    -hypertension is a silent killer!