Internal Medicine: Endocrinology: Adrenal Endocrinopathies Flashcards
What are the layers of the adrenal gland?
- Capsule
- Glomerulosa- cortex
- Fasiculata- cortex
- Reticularis- cortex
- Medulla
What do the following layers of the adrenal gland show?
1. Glomerulosa
2. Fasiculata
3. Reticularis
4. Medulla
- Mineralocorticoids
- Glucocorticoids
- Androgens
- Adrenaline, nor-adrenaline
What are examples of mineralocorticoids
Aldosterone
* influence salt and water balance
What is an example of glucocorticoids?
- Cortisol
- Corticosterone
What are examples of androgens?
- Testosterone
- DHT
What is ACTH?
Adrenocorticotropic hormone
What is hyperadrenocorticism?
Over production of cortical (cortex) hormones
Cortisols the baddie
What are the different ways hyperadrenocorticism can be caused?
- PDH- pituitary dependent HAC
- ADH- adrenal dependent HAC
- FAT- functioning adrenal tumour
What hormone is required for the production of cortisol and aldosterone?
Pregenalone
What are the effects of cortisol?
- Breakdown of adipose to fatty acids
- Affects hair follicles
- Gluconeogenesis, insulin resistance
- Reduced bone formation
- Reduced calcium absorption in intestine
- Down regulated the synthesis of collagen
- Raises free amino acids in serum
- Inhibits collagen formation
- Decreasing amino acid uptake by muscle
- Inhibits protein synthesis
- Reduction of IgA, IgM IgE
- Delayed wound healing
- Increases water diuresis, GFR, renal plasma flow
- Increases renal sodium retention of potassium excretion
- Increases intestinal sodium and water absorption and potassium excretion
Who gets hyperadrenocorticism?
- Medium to older age dogs
- PDH: more common in small breeds
- ADH: more common in large breeds
What are common clinical signs of cushings?
- Polydipsia
- Polyuria
- Polyphagia
- Panting
- Abdominal distention
- Endocrine alopecia
- Hepatomegaly
- Muscle weakness
- Systemic hypertension
What would haematology, biochemistry and urinalysis show for cushings?
Haematology
* Neutrophilic leukocytosis
* Lymphopenia
* Eosinopenia
* Thrombocytosis
* Mild erythrocytosis
Serum biochemistry
* Increased ALKP
* Increased ALT
* Hypercholesteraemia
* Hypertriglceridaemia
* Hyperglycaemia
Urinalysis
* Specific gravity
* < 1.013- 1.02
* Proteinuria
* Urinary tract infection
Also- reduced T4, Normal TSH
How can cushings be definitively diagnosed?
Low dose dexamethasone supression test
- 0.01mg/kg dexamethaons
- Blood sample at 3 and 8 hours
- Avoid feeding during test
- High sensitivity
- Lower but ok specificity
Best screening test
How is the ACTH stimulation test done?
- 5 ug/kg ACTH
- Blood sample at 0 and 1
- Avoid feeding
- Sensitivity higher for PDH
- Specificity ok
Less effective
How can urine cortisol creatinine ratio be used for diagnosis of cushings?
Random sample- less sensitive/specific
Sampling 2 days after a clinical visit
Increases sensitivity/specificity
How can ACTH assay differentiate between PDH and FAT?
normal 20-100 pg/ml
* PDH >45 pg/ml in 90%
* FAT < 20pg/ml in 70%
Imaging
What is used to treat cushings?
What is the MOA?
Trilostane
Competitively inhibits enzyme in adrenal cortex slowing production of cortisol production
How is cushings treatment monitored?
- Clinical signs
- ACTH stimulation test- 3 months for first year then 6
What are other effects of trilostane?
- Adrenal necrosis
- Hypoadrenocorticism
- Lack of efficacy
- Vomiting and Diarrhoea
What is mitotaine used for in HAC?
Cancer of the adrenal gland
(FAC)
What frequently occurs with treatment of HAC and how it is treated?
Hypertension
Benazepril
When can surgery for HAC be used?
Adrenal tumuors- if not invading renal vein or vena cava
Pituitary tumours- survival improving
- What is macroadenoma?
- How is it diagnosed?
- How is it treated?
- A benign tissue of the pituitary gland
- Patient gets duller when treated but ACTH stimulation and metabolic screens are good
- Hypophysectomy, radiotherapy
What disease can scottish terriers have that presents as HAC?
Hepatopathy
Abnormal dynamic cortisol
Don’t need trilostane
What is addison’s disease?
Hypoadrenocorticism
What is the aetiology of hypoadrenocortism?
Primary
* Destruction of >90% of adrenal cortices
* Multiple autoimmune-associated genes may be involved
Secondary:
* Defecit ACTH leading to atrophy of adrenal cortex
* Primarily cortisol defiency
What is the most common signalment of hypoadrenocorticism?
- Uncommon
- Middle aged female
Breeds
* Standard poodle
* Beardies
* Gt Dane
* Portugese water dog
* WHWT
* St B
* Wheaten
* Rottie
What are the clinical signs of addisons?
Acute or chronic
* Vague malaise
* Vomiting and diarrhoea/Melaena
* Lethargy/weakness
* PUPD
* Abdominal pain
* Hypovolaemic collapse
What may be identified on physical examination of addisons?
- Weak pulses
- Increased CRT
- Dehydration
- Bradycardia
- Abdominal pain
- Collapse/syncope
What can show on haematology and biochemistry for addisons?
- Mild non-regenerative anaemia
- Mild hypercalcaemia
- Pre-renal azotaemia
- Lymphocytosis ± eosinophilia
- Na:K ratio < 27:1
- Hyperkalaemia
- Hyponatraemia
- Isothenuric to hypesthenuric urine
- Acidosis
What is atypical addisons?
- Cortisol defiency
- Normal mineralocorticoids
- Usually progress to mineralocorticoid deficiency
What are differentials for hyperkalaemia, hyponatraemia?
- GI disease
- Renal failure
- Parasitic infection- whipworms
- Urinary obstruction
- Chronic effusion with repeated drainage
- Pregnancy
- CHF
- Diabetes mellitus
- Chronic blood loss
How can hyperkalaemia present on ECG?
With increased hyperkalaemia
* Bradycardia
* Tall narrow T waves
* Prolonged QRS interval
* Decreased P wave
* Prolonged P-R interval
* Absent P wave
* Complete heart block ventricular arrythmias
How can addisons be diagnosed and ruled out?
Endocrine testing
* Single cortisol- addisons ruled out
* < 55nmol will detect 100% addisons
* High false positive
How does primary and atypical addisons differ?
* Electrolytes
* Pre/Post ACTH cortisol
* Endogenous ACTH
* Cortisol: ACTH
* Aldosterone: Renin
Both
* Pre ACTH cortisol- low
* Post ACTH low
* Endogenous ACTH- high
* Cortisol: ACTH- low
* Aldosterone: Renin- low
Primary- electrolytes abnormal
Atypical- electrolytes normal
How does secondary addisons differ to primary:
* Electrolytes
* Pre/Post-ACTH cortisol
* Endogenous ACTH
* Cortisol:ACTH
* Aldosterone:Renin
Electrolytes
* P- abnormal
* S- normal
Pre/Post ACTH cortisol
* Both low
Endogenous ACTH
* P- high
* S- low
Cortisol:ACTH
* P- low
* S- high
Aldosterone:Renin
* P- Low
* S- high
How is addisons disease treated?
Fluid therapy-
* shock rates initially
Hyperkalaemia-
* dextrose saline + insulin,
* calcium gluconate
Steroid
* Dexamethasone sodium phosphate
* Hydrocortisone
* Prednisolone sodium succinate
* Once eating- oral pred, fludrocorstisone
Maintenance therapy
* Oral pred- maybe only when stressed
* Fludrocortisone
* DOCP- desoxycorticosterone privilate
Life long therapy
What are potential problems with addisons treatment?
- Acute renal failure
- Myelinosis
Prevention- raise sodium slowly
- What is phaeochromocytoma?
- What are the clinical signs?
- How is it diagnosed?
- How is it treated?
- Tumour of adrenal medulla secreting catecholamines
- Episodic: Anxiety, tachycardia, tachypnoea, vomiting, diarrhoea, weight loss, hypertension
- Radiography/US
- Radical excision, antihypertensive
- What causes hyperaldosteronism?
- What are the clinical signs?
- How is it treated?
- Adrenal tumour- produces aldosterone
- PUPD, weakness, hypokalaemia, hypotension
- Restrict sodium, supplement potassium, surgical excisoin, spironolactone
