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SAM 4 MT 2 > Adrenal Gland Endocrinopathies > Flashcards

Adrenal Gland Endocrinopathies Flashcards

1
Q

What hormones does the different parts of the adrenal gland produce

A 
Medulla: catecholamines
Cortex:
Z. Reticularis (inner)
- GC
Z. Fasciculata
- androgens
Z. Glomerulosa (outer)
- mineralocorticoids (aldosterone fex)
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2
Q

How is cortisol stimulated and inhibited

A

(Part of day feeding?)
Stress ➡️ CRH ➡️ ACTH ➡️ cortisol/corticosterone
- AVP/ADH/vasopressin, angiotensin II also influence ACTH production
The cortisol in the blood acts as negative feedback for all steps.

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3
Q

What stimulates the RAAS

A

Renin angiotensin aldosterone system - activated as a reaction to hypovolemia.

Hypovolemia ➡️ renin ➡️ ang 1 >2 ➡️ aldosterone ➡️ ⬆️Na, ⬇️K

  • incr. K will also stimulate aldosterone production
  • ACTH will minimally stimulate aldosterone
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4
Q

What is Hypoadrenocorticisom

A

Aka addisons disease, lack of adrenocortical hormones (sickness of the adrenal cortex)

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5
Q

Pathogenesis of addisons disease

A

🔺 Primary (if 90% of AC tissue is lost)
– Cortisol ⬇️ and aldosterone ⬇️, ACTH⬆️
– Autoimmune destruction of cortex (➡️ atrophy)
– (bilateral adrenal tumor, amyloidosis, infection) –„Atypical”: only cortisol⬇️ (yet, ald maybe later)
🔺 Secondary
– ACTH ⬇️, cortisol ⬇️, aldosterone no problem!
–Unprofessional glucocorticoid therapy
– (Hypophysis tumor, trauma, inflammation)

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6
Q

What is the major cause of primary addisons

A

Autoimmune distrustion of cortex (lymphocytic adrenalitis and atrophy of AC)

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7
Q

Signalment of addisons

A

~ Rare, but life threatening disease of dogs (but lethal - important ddx)
~ Young and middle-aged animals
~ More frequent in bitches
~ Great Dane, Rottweiler, Poodle, Schnauzer, Westie, Bearded collie, English cocker spaniel (hu!!)
~ (Very rare in cats)

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8
Q

What are the clinical manifestations of addisons

A

🔺
Aldosterone ⬇️
➡️ Dehydration, K⬆️
➡️ Addisonian-crisis Cortisol⬇️
➡️ Lethargy, stress response⬇️
🔺 Periodic improvement and relapse
🔺 Stress might cause a crisis
🔺 cortical deficiancy: Depression, weakness, tremor, weight loss, hypothermia, anorexia
🔺 Vomiting/diarrhea (+/- bloody), abdominal pain, PD/PU
🔺 hypovol. shock, CRT⬆️, bradycardia, weak pulse (Addisonion crisis!! The bradycardia indicates it - normal adrenal would react with incr hr! Or maybe bad heart could be)
🔺 When these signs are present, include Addison’s disease in differential diagnosis !

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9
Q

Lab and instrumental findings in addisons

A

~ Normocytic normochromic anemia (dehydration can mask the anemia!)
~ Lack of „stress leukogram”: Neu/Ly <2,3 eosinophilia, lymphocytosis (Corticol overprod -> leukocytosis with mature neutrophilia = stress leukogram (addison patients cant cause this ever!!) doesnt atter how sick)
~ Hyponatremia(water follow), hyperkalemia(should! activate RAAS), hypochloremia
Na /K <27(<22) (These should be present in typical addisons simultaniously)
~ (Hypoglycemia), albumin ⬇️(vomitus, diarrhoea), prerenal azotemia (Severily hypovol + addisonial crisis –> decr bp -> prerenal azotemia)
~ ECG (incr K): spiked T wave, Q-T distance ⬆️,
QRS complex wide, P wave low, P-R distance ⬆️, bradycardia
~ X-ray: microcardia, v. cava caudalis ⬇️ (connected to hypovol)
~ Abdominal US: „thinner” adrenals if examiner is experienced

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10
Q

Addisons ddx

A

– Renal failure (Na/K may be low)
– Gastroenteritis (Na/K may be low eg if vomitus dominating)
– Acute pancreatitis, (Ileus)

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11
Q

Addisons diagnostics

A

🔺 ACTH-stimulation test
– 5 μg/kg tetracosactide IV (Synacthen inj.)
– Blood sampling: t0, t1
– Positive: t0 cortisol <28nmol/l, t1 cortisol <100 nmol/l
– On the morning of the test the hydrocortisone injection should be postponed (it would incr cortisone)
🔺 Single cortisol >55 nmol/l: Addison’s unlikely (if a single measurement is above this we can rule out - if not need acth stim test!) this is good to try first esp if cant get hold of tetracosactide

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12
Q

Treatment - give an overview

A

2 phases: first stabilise the addisonian crisis then maintenance therapy

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13
Q

How would you treat the addisonian crisis?

A

Hypovolemia + hormone repl. Treatment!
– 20-50 ml/kg/h normal saline for 2 hours (0.9%saline, no K so dilutes hyperkal!)
– Thereafter: 100 ml/kg/24h normal saline
– 5 mg/kg hydrocortisone with the first infusion (Solu-Cortef inj.)
– Thereafter: 1 mg/kg/6h hydrocortisone SC

Should feel better after some days (no vomitus, diarrh, hypovol, incr appatite)

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14
Q

Why is hydrocortisone preferred in stabilizing the addisonian crisis?

A

An “old” GC, has mineralocorticoid effect too - aldosterone effect aswell as incr cortisol.
–> help hypovolemia aswell (Na⬆️K⬇️)

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15
Q

How would you treat the patient after stabilizing the addisonian crisis?

A

Maintenance therapy - long term treatment!
➡️ we treat lacking GC+MC!

– Fludrocortisone (tablet BID, Mineralocorticoid, some GC activity aswell!)
or
DOCP IM/SC (Desoxycorticosterone-pivalate) Long acting inj., lasting 25-28d. Strictly mineralocort so we prescribe together with prednisolone aswell. Life long treamtent.
– Prednisolone (tabl BID.; in stress 2-4x dose!)
– Sodium chloride BID mixed with food (hyponatremia)

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16
Q

How would you follow up an addisons patient

A

~ Controls: 2-3 weeks later, then every 6 months to set the proper concentration of treatment.
~ If K ↔️ and Na ⬆️⬇️: sodium chloride dose ⬆️⬇️
~ If K⬆️ and Na ⬇️, or K ⬇️and Na ⬆️: fludrocortisone dose⬆️⬇️
~ If Na ↔️ and K ⬆️⬇️: fludrocortisone dose ⬆️⬇️

PD/PU, incr …, weight gain - GC (predisolone) too high, may have to skip the prednisolone completely - the fludro has some effect on GC

17
Q

What treatment option is usually used long term

A

DOCP very expensive so usually fludrocorticone+prednisolone given

18
Q

Prognosis of addisons

A

~ Generally good, if the patient survives the crisis
(Relapse into cristis if cant admin the fludrocortisone tablet - the DOCP has advantage here: injection!! Eg poor apatite, anorexia..)Even if fludro+pred - should have a DOCP at home in case for some reason cannot admin, to avoid addsonion crisis relapse (storage for some years)
~ In the secondary form due to hypophyseal disease it is determined by the primary lesion

19
Q

Define hypercortisolism

A

Aka Cushing’s syndrome
~ Cortisol high
~ (Hyperaldosteronism is rare) so we dont call it hyperadrenocorticism

20
Q

Describe the pathogenesis of cushings syndrome

A

🔺 Pituitary-dependent (PDH; 85%)
- ACTH ⬆️, cortisol ⬆️
- Hypophysis (A.L.) hyperplasia, adenoma
🔺 Adrenocortical tumors (ADH; 15%) (=adrenal dependant)
- Cortisol ⬆️, ACTH ⬇️ - Strong feedback on pituitary so very low acth - below detection rate
- AC adenoma or carcinoma (usually unilateral)
50-50 benign malignant. Only seen after HP! US findings may be suggestive, locally invasive, maybe distant metastasis in liver in lung - then we know its carcinoma
🔺 Iatrogenic form: long-lasting glucocorticoid therapy
- ACTH ⬇️(neg feedback), cortisol ⬇️(downreg) !!! (AC atrophy as result) Always stop gradual admin if longer than 2-3w, longer therapy slower decr dose

21
Q

Describe the pituitary tumors

A

Pituitary dep cutshings
Pituitary tumour: almost always benign, small=microadenoma, may grow big, bigger than 1cm = macroadenoma, may compress sorrunding structures (optic chiasm - blind, seizures, hydrocephalus
So remember neurological symptoms!!

22
Q

Signalment of cushings syndrome

A 
~ Common endocrinopathy
~ Middle-aged and old dogs
~ Poodle, Dachshund, Yorkshire terrier, Hungarian vizsla, Boxer
~ (any form in any dog may arise)
PDH: small dogs
AC tumors: large dogs
23
Q

Describe the clinical manifestations of cushings

A

🔺 Glucocorticoids ⬆️
➡️ proteolysis ⬆️ (ig, decr immunity)
➡️ GNG ⬆️, lipogenesis ⬆️ (fat deposition in subcut, mesenterium, mostly abdomen)
🔺 PD/PU initial sign
🔺 polyphagia, centripetal obesity, abdominal enlargement/pot belly, muscle wasting (mast. Mm!)
🔺 after months: Thin, atrophic skin, keratin plugs, alopecia, hyperpigmentation, calcinosis cutis (Ca dep. Like coin in skin, pathognomonic but not always present.
🔺 Hepatomegaly
🔺 Testicular atrophy, anestrus
🔺 Secondary infections (skin, urinary tract) typical old age demodicosis!
🔺 (Cerebral signs) pit. Macroadenoma see before.

24
Q

Lab of cushings syndrome

A

~ Leukocytosis, neutrophilia
~ AP⬆️(SIAP⬆️) very high!
~ Cholesterol ⬆️, lipemia, blood glucose ⬆️ 10% become severily diabetic!
~ Low specific gravity of urine (except if also dm) - PU/PD!, UTI may find as complication common
~ Ultrasound very useful!: enlargement of adrenal gland(s), metastases (liver, vessels) - into v. Cava caud, hypogastric - info to surgeon! Thromboembolism.
~ X-ray: hepatomegaly, osteoporosis, calcinosis cutis, lung metastasis
~ CT: pituitary tumor
~ Blood pressure measurement: hypertension +/- (treatment may be required if +)

25
Q

Pituitary tumor - what to do?

A

Macroadenoma, signs - hypophysectomy through os sphenoidale? - remove the tumor and pituitary too

26
Q

Diagnosis of cushings

A

🔺 Measurement of urinary corticoid/creatinine ratios (3 urine samples in morning for 3 days
At home - stress free sample)
– Not specific; screening test - Ruling out cushings: if very low ratio you can rule out cushings (proteolysis?)
<2610-6: - no cushing
>16110-6: + might have cushing
🔺 LDDSupression test - done if doubtful ratio from screening test^
– In the morning: 0,01 mg/kg dexamethasone IV (Dexadreson inj.)
– Blood sampling: t0, t4, t8
– Positive: t8 cortisol >40 nmol/l (Not adequate suppr. in 8h sample then cushings)
– If t4 cortisol <0,5 X t0: PDH (if half the t0 value or less?) fast suppression PDH - no transient suppression in tumor?
🔺 ACTH-stimulation test: if iatrogenic is suspected

27
Q

How can you distinguish PDH and AC tumour?

A

🔺 Abdominal US gives us a typical picture:
- PDH: Bilat, symmetrical bc same stimulation
- ADH: Asymmetric, one has a tumor, abn structure. The other one hard to find, atrophic, smaller than physiological. Negative feedback on pit - low acth - non ADH adrenal atrophies.
🔺 HDDS test
– in a normal dog the dex would suppr ACTH and therefore cortisol
- in ADH any dose would NOT suppress cortisol as neg feedback not working (low acth anyways)
- in PDH 75% of dogs the cortisol level will decrease with high dose dex, for 25% it will not. (ACTH and then cortisol would decrease)
- 25%: probably a macroadenoma since no response.
-
– If t4 or t8 cortisol <0,5 X t0: PDH If t4 or t8 cortisol <40 nmol/l: PDH
🔺 Measurement of endogenous ACTH - we do this one mostly
- Frozen sample!! ACTH is polypeptic? - quick degr in blood
- ADH: Low ACTH bc neg feedback on pit!
- PDH: high ACTH, or just high physiological

28
Q

How would you treat cushings syndrome?

A 
🔺 Mitotane (tabl.)
– Selective destruction of AC
🔺 Trilostane (caps.)
- reduce cortisol synthesis
🔺 Hypophysectomy
🔺 Adrenalectomy
29
Q

How do you use mitotane

A

Mitotane (tabl.)
– Selective destruction of AC
🔺 „DUTCH PROTOCOL”
– 50-75 mg/kg/24h for 25 days
(iatrogenic Addison’s disease is induced)
– From the 3rd day replacement therapy is started (prednisolone, fludrocortisone, sodium chloride)
– About 25% of patients relapse within one year
- Risk! addisonian crisis if not given fludrocort.!
🔺 „AMERICAN PROTOCOL”
– 25 mg/kg/12h on first 3-4 days
– Maintenance: 12,5 mg/kg/12h on Wednesday and Sunday
– Control: ACTH-stimulation test
- Less risky, just partly destroy - smaller dose of mitotane. Somewhere btw cushing and addisons.

30
Q

How would you use trilostane in cushings treatment

A

– Competitive inhibitor of 3-β-hydroxisteroid- dehydrogenase enzyme; effectively reduces cortisol synthesis at adrenal level.
–Reversible action
– Must be given continuously
– (1)2…10 mg/kg/day, divided into 2 portions, with food
– Control: ACTH-stimulation test
– Rarely: adrenocortical necrosis - Prob due to very high acth secr in PDH treated cases
-> pit tumor goes wild with acth prod

31
Q

Describe hypophysectomy as a cushings treatment

A

– Therapy for PDH: Removal of hypophysis. Tricky surgery, expensive, not all countries
– Good results - iatrogenic addisons
– The patient recquires replacement therapy for life: thyroxine + cortisone or prednisolone

32
Q

Describe adrenalectomy as a cushings treatment

A

– Unilateral AC tumor: intra- and postoperative hydrocortisone/cortisone/prednisolone for 6-8 weeks (other one is atrophic - drug with decr dose? Takes time for to go back to normal?)
– Left: laparoscopic technique - Minimally invasive surgery, less pain and trauma

33
Q

Describe the prognosis of cushings

A 
Good --> Poor prognosis order:
🔺Good:
- Iatrogenic Cushing’s syndrome
- Unilateral AC tumor without metastasis 
🔺Less favorable:
- PDH without cerebral signs
- PDH or AC tumor + diabetes mellitus
- PDH with cerebral signs
- Unilateral AC tumor + liver / lung metastasis
34
Q

Cushings in cats - signalment

A

~ Rare disease

~ Middle-aged and old animals

35
Q

Clinical manifestations of feline cushings

A

Like the dog, but:
~ Alopecia, hyperpigmentation and keratin plugs are less pronounced!! (Bilat, symmetrical alopecia in cat yes, not in every cat. Skin atrophy under normal fur - can make wounds if hold cat in a rough way…)
~ The skin is very fragile (full thickness skin defect), unkempt hair coat
~ (Insulin resistant) diabetes mellitus is common (so typical case poorly kept diabetic cat ddx cushings imp!!)

36
Q

What is the treatment options in feline cushings

A

~ Trilostane (Vetoryl A.U.V.): 10-30 mg/cat/12-24h PO - like dog!
~ Hypophysectomy is promising
~ Bilateral adrenalectomy (mitotane is not useful)

37
Q

What is the prognosis of feline cushings

A

guarded – poor

SAM 4 MT 2 (12 decks)

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