endocrine Flashcards

Question

hypoparathyroidism causes

Answer 1

 Lymphocytic parathyroiditis: Believed to be immune-mediated  Parturient Paresis (Milk Fever): Occurs in cows fed a high calcium diet before parturition  Other causes include:  Destruction of the parathyroids by neoplasms, accidental removal during thyroid surgery or long-term hypercalcemia from ingestion of calcinogenic plants like Cestrum diurnum.

Answer 2

-primary: - parathyroid adenomas usually in older dogs (single, encapsulated, functional tumors produce excess PTH will see atrophy of para gland -secondary: due to nutritional imbalances -excess dietary P, N or low Ca and vitamin D3. -bran diets in horses -meat diets in cats/ dogs renal: response to hypercalcemia and progressive hyperphosphatemia due to decreased GFR, low calcium secondary will lead to prolonged hypocalemia --> hyperplasia of cheif cells --> bilateral enlargement of parathyroid gland -excess PTH can lead to fibrous osteodystrophy from bone resorption, bones become swollen.

Answer 3

Paraneoplastic syndrome: -caused by secretion of PTH-related protein which mimics the action of PTH - cause hypercalcemia and hypophosphatemia. examples: - Adenocarcinoma of apocrine glands of anal sac (mainly in dogs) -Lymphosarcoma (in dogs and cats).

Answer 4

-metabolic actions: -AA transport into cells -stimulation of protein synthesis -cariltage growth -lipid metabolism -increased insulin resistance, leading to increased blood glucose -release of somatotrophin stimulated by: -sleep stages III and IV -stress, exercise, fasting

Answer 5

 Aplasia or Hypoplasia: Rare  Pituitary Cysts: Rathke’s pouch--> Benign if no changes to pituitary function!  German shepherds with pituitary dwarfism*  Stunted puppy growth (decreased somatotropin) leads to endocrine dystfunction due to lack of sygnals  Secondary hypothyroidism or Cushings  Diabetes insipidus if compresses neurohypophysis

Answer 6

 Hypophyseal form (= central diabetes insipidus)  seen with any lesion that interferes with ADH SYNTHESIS or secretion like damage to the pars nervosa or hypothalamus. -administration of exo ADH will increase urine osmolarity only in hypophyseal form  Nephrogenic form:  hereditary defects in the ADH receptor or in the water channels in kidneys, cells dont respond to ADH  Both forms of diabetes insipidus result in:  PU/PD  urine of low osmolality even after water deprivation.

Answer 7

 Associated with meningitis or encephalitis can spread to hypo or pituitary  can have Neutrophils = Abscesses -sporadic in ruminants and pigs - Bacteria causes A. pyogenes - Fungus (pyogranulomatous) -animals will have neuro signs  Lymphoplasmacytic: - Viral or protozoan

Answer 8

 Old sheep/ horses  Hyperlasia of the pars intermedia can be inactive or lead active and ACTH--> cushing disease  Adenoma vs. Hyperplasia hard to tell grossly  Size and number  Presence of a capsule  Compression of the adjacent tissue

Answer 9

-may be functional: overproducing trophic hormone on organ -or nonfenctional but destructive to adjacent structures ± metastatic. * Adenomas and carcinomas are seen more commonly in middle age to older; craniopharyngiomas seen more in young animal

Answer 10

 Pars Distalis (intermedia) -functional tumor - secretes ACTH which leads to bilateral (symmetrical) hypertrophy/hyperplasia of zona fasciculata and zona reticularis (CORTEX) leads to Too much CORTISOL  Cushing’s diseases

Answer 11

-invades tissues, removing pituitary and brain -non functional -usually in dogs

Answer 12

-horses and ponies over 15 years old -Pituitary is large -PI cells produce excess proopiomelanocortin (POMC) derived peptide --> higher levels α-MSH, β-endorphin**  Modest elevations in:  Plasma cortisol  ACTH  Adrenal cortex hyperplasia

Answer 13

 PU/PD/PP  Muscle atrophy, weakness  Laminitis  Hirsutism  Crested Neck – altered fat deposition  Flop sweats – hyperhidrosis  Hyperglycemia or hyper-insulinemia

Answer 14

-seen in younger animals can be large and lead to dwarfism, diabetes insipidus  adenohypophysis and neurohypophysis destroyed (the entire pituitary gland is destroyed)  leads to Atrophy of thyroid and adrenal glands, hypoplastic adrenal cortex - Thyroid appears normal size but is mostly Colloid, not active follicles.

Answer 15

 Adrenal cortex: -Zona Glomerulosa: Mineralocorticoids (Aldosterone) Salt -Zona Fasciculata: Glucocorticoids (Cortisol) Sugar, controlled by ACTH -Zona Reticularis: Adrenal androgens Sex  Adrenal medulla:  Norepinephrine  Epinephrine  Dopamine

Answer 16

Primary Hypoadrenocorticism:  Bilateral idiopathic adrenal cortical atrophy  Destruction of all THREE CORTICAL LAYERS, often with infiltration of mononuclear inflammatory cells  Bilateral destruction of adrenal glands** Secondary Hypoadrenocorticism:  Destructive pituitary lesions  Iatrogenic  MOST COMMON CAUSE  Following the sudden withdrawal of synthetic glucocorticoids treatment after prolonged usage when they are depended on these exo)  Atrophy of only the inner two zones

Answer 17

 Lethargy,  Stress intolerance  Heart: bradycardia -GI: V/ A/ D  SKIN: hyperpigmentation  Chemistry: hyponatremia & hyperkalemia**** hallmark of Addison’s.  Metabolic: Hypoglycemia, hemoconcentration which does not respond to ACTH administration**

Answer 18

 COMMON endocrinopathy in OLDER DOGS, less so in horses but rare in other animals.  Combined gluconeogenic, lipolytic, protein catabolic and immunosuppressive effects of corticosteroids * Primary hyperadrenocorticism (10-15%): functional cortical neoplasm or hyperplasia * Secondary hyperadrenocorticism (80%): PDH or idiopathic, pituitary depended** * Iatrogenic hyperadrenocorticism (5-10%): medication

Answer 19

* Bilateral idiopathic adrenal cortical atrophy o Autoimmune hereditary? o Occurs most frequently in young to middle-age female dogs o Destruction of all three cortical layers**, often with infiltration of mononuclear nflammatory cells o Deficient production of all cortical hormones * Bilateral destruction of adrenal glands o Due to inflammation, infarction, hemorrhage, tumor

Answer 20

Destructive pituitary lesions: o Damage to the pituitary, including corticotrophs, results in deficiency of ACTH. o Atrophy of only the inner two zones; mineralocorticoids are minimally affected and generally no electrolyte imbalances Iatrogenic** o MOST COMMON CAUSE of secondary hypoadrenocorticism o Following the sudden withdrawal of synthetic glucocorticoids treatment after prolonged usage o Atrophy of only the inner two zones; mineralocorticoids are minimally affected and generally no electrolyte imbalances

Answer 21

 Polyuria / polydipsia  Polyphagia  Hepatomegaly  Pendulous abdomen  Skin lesions (90% of cases) DERMAL ATROPHY, alopecia  Dystrophic mineralization:Calcinosis Cutis  Bacterial infections  Clinical pathology tests:  hypercoagulability  Eosinopenia  Lymphopenia

Answer 22

-in pars distalis secretes ACTH  bilateral (symmetrical) hypertrophy/hyperplasia of zona fasciculata and zona reticularis (CORTEX)  Too much CORTISOL  Cushing’s disease -usually small breed, brown belly, scaily skin, thin haircoat

Answer 23

-atrophy of the cotrex not hyperplasia -from long term, daily use of large doses or corticosteroids -decreased ACTH

Answer 24

-in adrenal medulla cells of dog, horses, cattle  Often large and encapsulated  may invade the vena cava ***and metastasize extensively.  Rarely functional, if so:  secrete epinephrine and/or norepinephrine  can cause tachycardia, edema and cardiac hypertrophy  BULLS: pheochromocytoma and C-cell neoplasia often develop concurrently.  Paraganglioma if outside the adrenal gland

Answer 25

 EXOCRINE: ACINAR CELLS compose most of the pancreas (>90%) and these make pancreatic enzymes that aid in digestion.  ENDOCRINE: Insulin (β cells) and Glucagon (α cells), along with delta and PP cells  GLYCOGENESIS (the conversion of glucose to glycogen)  GLUCONEOGENESIS (the conversion of glycogen to glucose).  This is stimulated by GLUCAGON, CATECHOLAMINES and CORTISOL

Answer 26

 A decrease in blood glucose = HYPOGLYCEMIA  Hypoglycemia can impair brain function, potentially causing seizures, coma, and death, common in young animals. -glucose is a very important energy substrate, particularly for the CNS which cannot use fat metabolism

Answer 27

 Increased blood glucose concentration: increased insulin secretion  Decreased blood glucose concentration--> increased secretions of:  Glucagon  Catecholamines  Somatotrophin  Cortisol insulin response to HIGH GLUCOSE glucagon response to LOW GLUCOSE

Answer 28

-60-70% - Increased Blood glucose -> insulin release, which leads to:  Increased GLYCOGENESIS  Increased GLYCOLYSIS  Increased GLUCOSE TRANSPOR also AA transport, protein synthesis, LIPOLYSIS, LIPOGENESIS

Answer 29

-20%  Decreased Blood glucose -> Glucagon release, which leads to:  Increased HEPATIC GLYCOGENOLYSIS -> Increased blood glucose also: gluconeogenesis, increasing blood glucose, increased LIPOLYSIS

Answer 30

 Delta cells  ~5% of the islet  Produce somatostatin which inhibits release of insulin, glucagon and gastro-intestinal peptides.  PP cells  ~10% of the islet  Make pancreatic polypeptide  inhibits intestinal motility & stimulates secretion of gastric/intestinal enzymes

Answer 31

 Also called insulin-dependent diabetes mellitus.  Destruction of beta cells with progressive loss of insulin secretion.  This is usually an abrupt presentation and insulin is required for life after diagnosis.  May present with KETOACIDOSIS.  In humans, this starts with lymphocytes infiltrating the islets and destroying the beta cells. -not very common, most common one in dogs female over male

Answer 32

-old cats 9-10 years +  Develops due to insufficient insulin secretion relative to metabolic demand  This is usually a gradual presentation**  Insulin resistance AND/OR  Dysfunction of the beta cells  Insulin resistance: secondary to obesity or counter regulatory hormones like GH not functioning properly.

Answer 33

* Produced by pancreatic β-cells*** * Called islet amyloid polypeptide (IAPP or amylin) * It is co-processed, packaged and released with insulin in response to glycemia * Apoptosis in the islets can be seen with toxic accumulations * Common in obese cats, but does not necessarily mean they have diabetes

Answer 34

causes: * Dogs and cats with chronic, relapsing pancreatitis, inflammation interferes with function. * HIGH CORTISOL: from Dogs with Cushing’s or Chronic steroid therapy. cortisol raises blood sugar and inhibits insulin. * Cats with growth hormone excess (GH secreting pituitary tumor). * Glucagon (glucagonomas)

Answer 35

 PU/PD/PP  Weight loss and weakness  Hepatic lipidosis may occur: requires that the cat be overweight and anorexic  Increased omental fat deposition and triglyceride formation  Cataracts (DOGS) – lens becomes cloudy due to high blood sugar  Blood vessels in the glomeruli and retina are most susceptible to damage from DM  peripheral demyelinating neuropathies occasionally seen  Clinical pathology:  Hyperglycemia  Glycosuria  ketone bodies in urine

Answer 36

-increased gluconeogenesis and decreased glucose use leads to secretion of insulin --> adrenal diabetes

Answer 37

-cortisol causes: decreased glucose USAGE by cells. INCREASED GLUCONEOGENESIS -INCREASED gluconeogenesis and glycogenesis --> INCREASED GLYCOGEN STORAGE

Answer 38

-beta cell neoplasms= insulinomas  Mostly seen in adult dogs & ferrets  Often functional and producing excess insulin gross: -single discrete tumor  Adenomas are encapsulated  Carcinomas are larger with features of malignancy and may metastasize  Clinical signs of functional tumors are related to severe hypoglycemia  often present clinically with seizures  CLINICAL diagnosis of an insulinoma is established by detecting high serum insulin, low blood glucose and one or more nodules in the pancreas (ultrasound) with biopsy.

Answer 39

Glucagonomas  Rare, but have been reported in dogs  Produce excess glucagon  secondary diabetes mellitus Gastrinomas  Rare, but have been reported in dogs and cats  Produce excess gastrin  Gastric ulcers

Answer 40

This is an EXOCRINE hyperplasia Multifocal and VERY COMMON -if chronic has fibrinogen and is dense

Answer 41

-aortic body adenoma -tumor of chemoreceptors -heart failure due to large space occupying mass in pericardium -does not usually secrete hormones -heart base tumor is differential diagnosis of a ectopic thyroid tumor.

Answer 42

Lymphosarcoma  Any organ can be affected. (spleen and LN usually)  Ferrets may not have symptoms until full of tumors. Adrenal tumors  Tumors excrete excessive ESTROGEN.  The most common symptoms of this disease is hair loss. bald, Pot belly Insulinoma  Insulin-secreting tumor -> serious drops in blood glucose -> brain dysfunction  The most common symptoms of this disease are lethargy, going into trances or experiencing hind end weakness.

Answer 43

Gastric ulcers:  Suspected to be caused by stress. Treated by acid reducers and bland diet. Inflammatory bowel disease:  Autoimmune disease causing lymphocytic enteritis.  Need to biopsy to distinguish from lymphoma chordoma

endocrine Flashcards

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