Adrenal Gland Endocrinopathies Flashcards by Julie Smith thjømøe

What hormones does the different parts of the adrenal gland produce

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

How well did you know this?

Not at all

Perfectly

How is cortisol stimulated and inhibited

(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.

How well did you know this?

Not at all

Perfectly

What stimulates the RAAS

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

How well did you know this?

Not at all

Perfectly

What is Hypoadrenocorticisom

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

How well did you know this?

Not at all

Perfectly

Pathogenesis of addisons disease

🔺 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)

How well did you know this?

Not at all

Perfectly

What is the major cause of primary addisons

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

How well did you know this?

Not at all

Perfectly

Signalment of addisons

~ 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)

How well did you know this?

Not at all

Perfectly

What are the clinical manifestations of addisons

🔺
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 !

How well did you know this?

Not at all

Perfectly

Lab and instrumental findings in addisons

~ 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

How well did you know this?

Not at all

Perfectly

Addisons ddx

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

How well did you know this?

Not at all

Perfectly

Addisons diagnostics

🔺 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

How well did you know this?

Not at all

Perfectly

Treatment - give an overview

2 phases: first stabilise the addisonian crisis then maintenance therapy

How well did you know this?

Not at all

Perfectly

How would you treat the addisonian crisis?

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)

How well did you know this?

Not at all

Perfectly

Why is hydrocortisone preferred in stabilizing the addisonian crisis?

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

How well did you know this?

Not at all

Perfectly

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

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)

How well did you know this?

Not at all

Perfectly

How would you follow up an addisons patient

Study These Flashcards

~ 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

What treatment option is usually used long term

Study These Flashcards

DOCP very expensive so usually fludrocorticone+prednisolone given

Prognosis of addisons

Study These Flashcards

~ 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

Define hypercortisolism

Study These Flashcards

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

Describe the pathogenesis of cushings syndrome

Study These Flashcards

🔺 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

Describe the pituitary tumors

Study These Flashcards

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!!

Signalment of cushings syndrome

Study These Flashcards

~ 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

Describe the clinical manifestations of cushings

Study These Flashcards

🔺 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.

Lab of cushings syndrome

Study These Flashcards

~ 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 +)

Pituitary tumor - what to do?

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

Diagnosis of cushings

🔺 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?) <26*10-6: - no cushing >161*10-6: + 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

How can you distinguish PDH and AC tumour?

🔺 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

How would you treat cushings syndrome?

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

How do you use mitotane

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.

How would you use trilostane in cushings treatment

– 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

Describe hypophysectomy as a cushings treatment

– 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

Describe adrenalectomy as a cushings treatment

– 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

Describe the prognosis of cushings

``` 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 ```

Cushings in cats - signalment

~ Rare disease | ~ Middle-aged and old animals

Clinical manifestations of feline cushings

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!!)

What is the treatment options in feline cushings

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

What is the prognosis of feline cushings

guarded – poor

Adrenal Gland Endocrinopathies Flashcards

(37 cards)