Ex 4 - Pathology of Pit and Adrenal Glands Flashcards
1
Q
Adenohypophyseal aplasia (dogs/cattle)
A
- fetus is unable to produce cortisol –> fetal stress is the signal for parturition to occur
- caused by ingested toxins, e.g. Verratrum californium
- Development/growth ceases in late term pregnancy –> gestation continues well beyond term
2
Q
Hyperadrenocorticism (Cushing’s) - Clinical signs
A
- usually a disease of older dogs
- PU/PD
- alopecia/skin disease
- polyphagia/weight gain
- pot belly
- acute dyspnea –> puimonary thromboembolism
3
Q
Hyperadrenocorticism (Cushing’s) - Clin Path
A
- Stress leukogram
- thrombocytosis
- mild hyperglycemia
- hypercholesterolemia
- marked elevation in ALP
4
Q
Hyperadrenocorticism (Cushing’s) - Gross Pathologic Findings
- Adrenal glands
- Kidneys
- Pit gland
- Vessels (arteries)
- Liver
- Dermal condition
A
- Bilateral enlargement of adrenal glands
- = diffuse adrenocortical hyperplasia
- this means the disease is in the pituitary!
- Kidney capsules may be hemorrhagic, due to thrombotic events
- = acute renal infarction
- Pituitary adenomas are common
- carcinomas are less common
- 85% of dogs with Cushing’s are pituitary-dependent
- 15% of dogs are adrenal dependent –> one gland is hypertrophic, the other is atrophied
- Arterial thrombi
- adhered to vessel wall, granular surface, dull, laminar on cross-section
- cortisol prevents production of antithrombins –> hyper coagulable state
- Hepatomegaly
- Multifocal dermal mineralization (Calcinosis cutis)
5
Q
Hypoadrenocorticism (Addison’s) - Clinical presentation
A
- Intermittent or waxing/waning signs
- Lethargy, collapse
- Commonly young adult dogs
6
Q
Hypoadrenocorticism (Addison’s) - Clin Path
A
- Mild, non-regenerative anemia
- lack of a stress leukogram***
- Hypoglycemia
- Hyperkalemia
- Hyponatremia/hypochloremia
- Azotemia + minimally concentrated urine
- Na:K ratio is < 25:1
7
Q
Hypoadrenocorticism (Addison’s) - Gross pathologic findings
A
Adrenocortical atrophy!
8
Q
Hypoadrenocorticism (Addison’s) - Pathogenesis
A
- Suspected immune-mediated process
- adrenocortical atrophy
- -> loss of aldosterone & cortisol
- -> Na loss and K retention
- Often insidious onset with non-specific clinical signs
- -> acute circulatory collapse may be most obvious sign
- -> CV manifestations due to hyperkalemia and increased water loss
- Glucocorticoid synthesis decreased/lost
- -> Hypoglycemia
- Azotemia due to loss of normal osmotic gradient –> dehydration
- Non-regenerative anemia
- -> cortisol promotes erythropoiesis (no cortisol, no RBC production)
9
Q
What is the key feature of hypoadrenocorticism
A
Lack of stress leukogram
10
Q
Equine PPID - Causes (MD’s)
A
- Diffuse hypertrichosis
- Pituitary adenoma of the pars intermedia
- poorly formed sella turcica bone in the horse –> compression of pit gland - Laminitis
11
Q
Equine PPID - Pathogenesis
A
- Idiopathic, age-related loss of dopamine inhibition
- Increase secretion of POMC derivatives (MSH, and ACTH to a lesser extent)
- Cortisol is a counter-regulatory hormone of insulin
- increased cortisol results in insulin resistance –> hyperglycemia
12
Q
Feline acromegaly
A
- Acquired syndrome - occurs in older cats (usually tumor related)
- Results in widening and/or elongation of bones by appositional growth (physes are closed)
- Severe hyperglycemia
- growth hormone interfere with insulin pathways
- become severely diabetic and ill
13
Q
Feline acromegaly - Clin Path
A
- Hyperglycemia
- Stress leuk + mild erythrocytosis
- Elevated liver enzymes
- Hyperphosphatemia w/out renal azotemia, mild proteinuria
- Marked glucosuria
14
Q
Feline acromegaly - PE findings
A
- Oval shaped eyes
- Broadening of the maxilla
- large paws
15
Q
Feline acromegaly - MD
A
- Pituitary acidophil adenoma –> very treatable with tumor irriadiation
- Diffuse islet cell degeneration with amyloidosis –> hyperglycemia
- Proliferative and sclerosing glomerulonephropathy –> proteinuria