Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

sys path > endocrine > Flashcards

endocrine Flashcards

1
Q

endocrine

A

– cells respond to
factors (hormones) produced
by distant cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

thyroid anatomy

A

-pared organ, bilateral, connected at bottom
-1/4 width of trachea
-lots of collagen

parathryoid: partially embedded in thyroid gland, parathyroid is ontop of the thyroid gland. esp. cats

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

hormone synthesis in thyroid follicular cells

A

-iodine is being brought across, T3 and T4 are brought back through and released.
-cell needs AA, Carbs, regular amount iodine which are needed to synthesize thyroglobulin.
-T3/T4 have a negative feedback look with the hypothalamus, if you have an adenoma it can disrupt this. have TRH hypothalamus–> TSH anterior pituitary–> T3/T4

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

effects of thyroid hormones

A

 Effect on many tissues
 Normal development (brain) and growth
 Increase metabolic rate
 Increase lipid metabolism (lipylysis)
 Increase glucose metabolism (glycolysis, glucose absorption)
 Heart: Rate, output, vasodilatation
 Brain: Alter mental state
 Reproductive system

-T3/T4 amps up metabolism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

reverse T3

A

-useless T3 (biologically inactive) in the body, converts t4-> T3 in states of
-protein starvation**
-liver and kidney disease
-febrile illness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

congenital thyroid anomaly

A

 Aplasia or Hypoplasia: Rare

 Accessory thyroid tissue or
ectopic thyroid tissue***
 Common in dogs from the Larynx to diaphragm but 50 % around intrapericardial aorta around base of heart, can become neoplastic
 Differential diagnosis aortic base
tumors

 Thyroglossal duct cysts: Ventral neck midline cervical region dog, can become neoplastic

  • Parathyroid cysts: Bilaterally along trachea in cat.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

incidental seline changes of the thyroid

A

-minerlization, lipofuscinosis, copora amyloidosis,
-horses: thyroid cysts normal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

hypothyroidism

A

One of the MOST COMMON endocrinopathies in DOGS, but is rare in cats and uncommon in other species.
 Affected dogs are usually between 4 and 10 years of age.
 Mid to large breeds&raquo_space;» Toy and miniature breeds
 No sex predilection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

thyroid gland lesions with hypothyroidism

A

 Small thyroid gland:
 Gland is destroyed or was never there. So no functional thyrocytes
 Thyroiditis
 Idiopathic follicular atrophy
 Agenesis

 Big:
 Gland is continuously stimulated (hyperplastic and hypertrophic thyrocytes) by TSH because hormones not produced
 Iodine deficiency/excess
 Goitrogenic compounds
 Defect in biosynthesis of hormones
-goiter thyroid in neonate from pregnant mother with low iodine.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

clinical signs of hypothyroidism

A

 Metabolic changes:
- Weight gain
- Cold intolerance**
- Lethargy

 Skin:**
-Bilateral symmetrical thinning of hair
coat
- Scaliness of coat
- Hyperpigmentation of skin
- Secondary pyoderma
- Myxedema
-hair follicles are the targets of T3/T4 hormones

 Reproductive:
- Anestrus**, lack of libido
- Joint Pain

 Hypercholesterolemia:
- Atherosclerosis
- Lipid infiltration in liver, kidney and
cornea

 Anemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

common causes hypothyroidism

A

 Lymphocytic thyroiditis: Inflammatory

 Idiopathic thyroid atrophy: degenerative
-75% tissue lost before clinical signs

 Goiters (rare) from:
 Iodine deficiency
 Iodine excess
 Goitrogenic compounds
 Genetic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

lymphocytic thyroiditis

A

 Seen mostly in dogs
 may or may not develop clinical hypothyroidism.
-antibodies to Thyroglobulin, Thyroperoxidase, TSH receptor
 Similar to Hashimoto’s disease of humans

 Gross appearance:
 Slightly enlarged, normal size or smaller, pale, micro: lymphocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

idiopathic follicular atrophy

A

 Idiopathic: arising spontaneously or from an obscure or unknown cause

 Primary degenerative disease of the thyrocytes
 Replacement of the gland by adipose tissue
 Not associated with inflammation

 Distinct from the follicular atrophy due to decrease in TSH stimulation.
 Thyroid follicles undergo involution

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

hyperplasia= goiter thyroid

A

-most common sheep, goats at birth: abortion with slow growth rate, lethargy and abnormal mentation.

-non neoplastic, non inflammatory enlargement of the thyroid gland due to increased TSH secretion resulting from inadequate thyroxine synthesis and decreased T3/T4.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

hyperplasia= Goiters path causes 4

A

 The four major pathologic mechanisms include:
1.) Iodine deficient diet**
 Feed deficiency less common – born dead or weak
 Can be exacerbated by goitrogenic compounds
 Begins as a hyperplastic goiter -> colloid goiter with correction of diet

 Excess dietary iodine**
 High intake leads to inhibition of thyroid peroxidase -> decreases the
organification of iodine -> decreased thyroixine

 Goitrogenic compounds interfering with thyroxinogenesis: Brassica plants

 Genetic enzyme defects in hormone synthesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

goiter thyroid 3 morphological causes

A

1.) Diffuse Hyperplastic Goiter:
 More common in young animals born to dams on iodine deficient diet or excess iodide or dams fed goitrogenic substances.

2.) Colloid goiter:
 Represents involutionary phase of hyperplastic goiter (recovery following correction of the problem in diffuse hyperplastic goiter).

3.) Congenital dyshormonogenetic goiter (inherited goiter):
 Autosomal recessive disorder in some breeds of sheep, goats and cattle; rare in dogs and cats (more common in children).
 Result of genetic impairment of thyroglobulin synthesis; T4 & T3 levels are low even though iodine uptake and turnover are increased.
-symmetrically enlagred at birth

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

thyroid hyperplasia/ musculoskeletal syndrome in horses

A

 Hyperplastic goiters
 Mandibular prognathia
 Flexural deformity**
 Ruptured tendons of the common
digital extensor muscles
 Delayed ossification of carpal bones

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

hyperthyroidism

A

-most common endocrinopathie in CATS

 DISCRETE ADENOMAS or HYPERPLASTIC NODULES seen grossly
 Follicles (on histo) outside the adenomas or nodular hyperplasia may be atrophied (decreased TSH due to feedback)
 Carcinomas are uncommon in cats

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

clinical signs/ lesions with hyperthyroidism

A

-metabolic changes: hyperactivity, PU/PP/PD **, weight loss

-skin: rough coat, cervical swelling, coughing and dyspenia due to enlarged gland.

-heart: left ventricular hypertrophy in cats if left untreated, can get to HCM
-tachycardia/ murmor
- 10-15% of cats present with overt
congestive heart failure (dyspnea,
muffled heart sounds, ascites

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

multifocal nodular hyperplasia of the thyroid

A

-idiopathic, incidental lesion in old animals exept CATS where it may be functional

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

follicular cell adenoma in thyroid

A

-more common and may be functional in cats
-also in horses(white) dogs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

hyperthyroidism in dogs

A

-rare Occurs in middle aged and older dogs (7-15 years)
 Clinical findings can be similar to cats with hyperthyroidism
 Discrete Adenomas or hyperplastic nodules (not common)
THYROID CARCINOMAS
 Follicular cell adenocarcinoma
 May or may not be functional
 Highly aggressive and invasive, may become fixed or invade lungs, thyroid vein, lymph nodes.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

parafollicular cells

A

 C cells are found between follicles or follicular cells and are derived
from neural crest cells.
 Secretory granules contain calcitonin (CT), an emergency hormone, which protects against hypercalcemia by:
 Inhibiting bone resorption
 Diuresis of Ca2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

parathyroid feedback

A

 PTH and CT act in concert to keep [Ca2+] in the ECF within narrow
limits

 PTH level is controlled by direct feedback control system based on [Ca2+ /P] in the blood
 Protects against hypocalcemia by
 increasing intestinal absorption of calcium (with Vit D3)
 Stimulating bone resorption of calcium
 Enhances renal tubular reabsorption of calcium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

hypoparathyroidism causes

A

 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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

hyperparathyroidism primary vs secondary

A

-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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

hypercalcemia of malignancy

A

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).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

GNRH -> somatotrophin

A

-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

29
Q

pituitary congenital anomalys

A

 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

30
Q

diabetes insipidus

A

 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.

31
Q

inflammation of the adrenal gland

A

 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

32
Q

pituitary hyperplasia

A

 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

33
Q

pituitary hyperplasia and neoplasia

A

-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

34
Q

corticotroph adenoma

A

 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

35
Q

chromophobe adenoma

A

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

36
Q

horses: pituitary pars intermedia dysfunction PPID

A

-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

37
Q

PPID horses clinical signs (equine cushings like) clinical signs

A

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

38
Q

craniopharyngioma

A

-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.

39
Q

adrenal secretions different zones

A

 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

40
Q

HPA axis

A
41
Q

hypoadrenocorticism types

A

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

42
Q

hypoadrenocorticism lesions

A

 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

43
Q

hyperadrenocortiiscm types

A

 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
44
Q

Primary Hypoadrenocorticism

A
  • 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
45
Q

secondary hypoadrenocorticism

A

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

46
Q

lesions of hyperadrenocorticism

A

 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

47
Q

corticotroph adenoma

A

-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

48
Q

iatrogenic cushings

A

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

49
Q

phenochromatocytoma

A

-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

50
Q

main pancreatic outputs

A

 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

51
Q

hypoglycemia

A

 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

52
Q

glucose feedback loop

A

 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

53
Q

beta cells of the islet

A

-60-70%
- Increased Blood glucose -> insulin release, which leads to:
 Increased GLYCOGENESIS
 Increased GLYCOLYSIS
 Increased GLUCOSE TRANSPOR

also AA transport, protein synthesis, LIPOLYSIS, LIPOGENESIS

54
Q

alpha cells of the islet

A

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

also: gluconeogenesis, increasing blood glucose, increased LIPOLYSIS

55
Q

delta cells and PP cells in pancreases

A

 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

56
Q

type 1 diabetes mellitus

A

 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

57
Q

type 2 diabetes mellitus

A

-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.

58
Q

IAPP

A
  • 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
59
Q

secondary diabetes mellitus

A

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)

60
Q

clinical signs of Diabetes mellitus

A

 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

61
Q

adrenal diabetes

A

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

62
Q

steroid hepatopathy

A

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

63
Q

pancreatic islet tumors ( insulinomas)

A

-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.

64
Q

pancreatic islet tumors

A

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

65
Q

pancreatic nodular hyperplasia

A

This is an EXOCRINE hyperplasia
Multifocal and VERY COMMON

-if chronic has fibrinogen and is dense

66
Q

chemodectoma

A

-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.

67
Q

ferret tumors

A

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.

68
Q

ferret GI problems

A

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

sys path (13 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions