Endocrine Flashcards

1
Q

Important anterior pituitary hormones in veterinary practice include:

A

Thyroid stimulating hormone (TSH)
Adrenocorticotropic hormone (ACTH)
Follicle stimulating hormone (FSH)
Luteinizing hormone (LH)
Growth hormone (GH)

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2
Q

Posterior pituitary hormones used in veterinary practice include:

A

Antidiuretic hormone (ADH)
Oxytocin

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3
Q

What are some common endocrine diseases

A

Hyperthyroidism
Hypothyroidism
Estrogen incontinence in spayed female dogs (covered in the urogenital section)
Hyperadrenocorticism (Cushing’s disease)
Hypoadrenocorticism (Addison’s disease)
Diabetes
Diabetes mellitus and diabetes insipidus
Disease is caused by either excess hormone or hormone deficiency

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4
Q

What are signs of diabetes insipudis

A

Watery/dilute urine
Lack of antidiuretic hormone production by the hypothalamus

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5
Q

What causes diabetes insupidus

A

Idiopathic
Head injury
Pituitary tumor
The body does not produce enough anti- diurectic hormone (ADH/Vasopressin) or receptors in the kidney do not respond to ADH
The body is constantly in a state of diuresis

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6
Q

How do you diagnose diabetes insipudus

A

Diagnosis–modified water deprivation test and administration of vasopressin

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7
Q

What is the treatment of diabetes insipudis

A

Synthetic vasopressin

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8
Q

Why is diabetes mellitus and what are the signs

A

Lack of insulin OR the insulin receptors are less responsive to insulin
High blood glucose = hyperglycemia
Glucose in the urine = glucosuria
Common in dogs and cats

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9
Q

What is the common signalment with diabetes mellitus

A

Obese cats
Middle aged to older dogs

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10
Q

What are some risk factors for diabetes mellitus

A

Genetics
High carb diets in cats
Obesity (cats)

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11
Q

What are the signs of diabetes mellitus

A

If there is a lack of insulin, glucose accumulates in the blood and urine and tissue cells are not able to utilize glucose
Animals may be polyphagic
Weight loss and muscle wasting
Body enters starvation state → glucogenesis/ketosis
If owner is unable/unwilling to treat, euthanasia should be recommended

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12
Q

What are the 4 types of diabetes in order

A

1.Dogs: autoimmune; no insulin
2.Fat cats; insulin resistance
3.Secondary condition
4.Gestational

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13
Q

How does glucose metabolism normally work

A

Insulin is normally produced by beta-islet cells in the pancreas
Eating causes blood glucose levels to rise and this signals the pancreas to release insulin
Insulin tells the body to:
Metabolize the glucose into energy for the cells
Store extra glucose as glycogen in the liver
Facilitates deposition of fat into adipose tissues
The net effect is to decrease blood glucose by moving glucose out the blood and into cells
When blood sugar is low, the body produces glucagon

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14
Q

How does glucagon normally work

A

Stimulates gluconeogenesis in the liver - converts stored glycogen to glucose
Breaks down fat and muscle for energy
The net effect is to increase blood glucose concentrations

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15
Q

What is type 1 DM

A

insulin dependent DM
Dogs
Inherited
Autoimmune destruction of beta-islet cells
Pancreas is unable to produce insulin

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16
Q

What is type 2 DM

A

non-insulin dependent DM
Cats – obese, male
Adult onset
2 problems
Pancreas produces JUST ENOUGH insulin
Obesity or inflammation causes insulin receptors to be less responsive
Insulin resistance

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17
Q

What is type 3 DM

A

Secondary to another condition
Cushings
Pancreatitis
Iatrogenic cushings

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18
Q

Clinical signs and complications of untreated diabetes

A

Dilute urine and UTIs
Cat pee may become sticky
Diabetic cataract
Diabetic neuropahty
Diebetic ketoacidosis

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19
Q

Why do animals with diabetes get UTIS

A

PUPD- glucose draws water into the urine by osmosis
Bacterial UTIs

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20
Q

Why do animals get diabetic cataracts

A

Sugar accumulates in the lens
Occurs in virtually 100% of diabetic dogs
Very uncommon in cats
Can lead to glaucoma

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21
Q

What is diabetic neuropathy

A

Hind end weakness
Plantigrade stance

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22
Q

What is diabetic ketoacidosis caused by

A

Fat and muscle are metabolised → ketones are a byproduct of fat and muscle breakdown → acidosis
Dehydration
Electrolyte imbalances
Can go into shock

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23
Q

What does insulin stop

A

Glucogenesis
Glycogenolysis
Lipolysis
Ketogenesis
Protolysis

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24
Q

What does insulin start

A

Glucose uptake in muscle and adipose tissue
Glycolysis
Glycogen synthesis
Protein synthesis
Uptake of ions (especially K+ and PO4-3)

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25
Q

How do you preform insulin therapy

A

BID after the animal eats
Only given if the animal eats
Cats: glargine (human product) or ProZinc (veterinary product)
Dogs: Caninsulin (veterinary product), maybe ProZinc?

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26
Q

Diet management with diabetes goals and the food includes

A

Goal: ideal BCS
Obesity causes insulin resistance
Warning: weight loss can correct insulin resistance
Diabetic diet:
Low carbohydrates – especially important in cats
Increased protein – easier to digest for diabetics
Soluble fiber – slows down sugar release

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27
Q

Oral hypoglycemic agents are and work by

A

New medications: Bexagliflozin (Bexacat ®) and Velagliflozin (Senvelgo ®)
Once daily dosing
Action: decrease reabsorption of glucose by the kidneys
Increased urinary losses help to reduce blood glucose levels
Give pancreatic beta cells at rest – may start producing insulin again

28
Q

Senvelgo is used in what

A

Cats that are early diabetic are better candidates – more likely to start producing insulin again
Not recommended for sick or geriatric cats, cats with stage 4-4 CRF, pancreatitis, infections, hyperthyroidism, hypertension, or neoplasia
Not increasing glucose movement into cells so still at risk of developing DKA

29
Q

How do human oral hypoglycemic agents work

A

Human medications
Action: work by stimulating pancreatic beta cells to secrete insulin; therefore some pancreatic function is needed
Example: glipizide
Limited success in animals; seldom used
Relatively high potential for undesired side effects

30
Q

Patient management with diabetes

A

If uncomplicated – treated as an outpatient and manage at home
Fluid therapy may be required in some cases
Diet and feeding schedule MUST be consistent
Teach owner how to handle, store and administer insulin

31
Q

What is important to monitor with diabetic dogs

A

Changes in PU/PD
BCS
Strength and mobility
Blood glucose curve (12-24h)
Fructosmaine

32
Q

How to monitor BG

A

Glucurve
Product approved for use in cats and dogs
Glucose curves

33
Q

How do you do a glucose curve and what does it determine

A

Serial blood glucose measurements
Every 1-2h
Usually done from immediately before morning dose of insulin until evening dose of insulin
Determines the effectiveness of insulin and can help to determine if dose needs to be adjusted or insulin needs to be changed
Duration of action
How high and how low blood glucose is going
Difficult to do in clinic in cats due to “stress hyperglycemia”
Seed glucometer home – teach O how to check glucose levels and perform a curve
Continuous glucose monitor

34
Q

Can type 2 DM self resolve

A

remission in type 2 diabetes
Remission rates of 65% or higher have been reported in cats with good diabetic management

35
Q

What is important with surgery and diabetic patients

A

Discuss fasting protocol with vet before going over pre-surgical instructions with the owner
Have the client bring their pets insulin with them when they drop the patient off for surgery
Blood glucose needs to be checked periodically throughout the procedure and once recovered
Feed ASAP once recovered

36
Q

What is hypoglycemia

A

Low blood glucose concentration
Most commonly occurs in diabetic patients
Starvation, seizures, insulinomas, toxins (xylitol)
Can be fatal rapidly

37
Q

How do you recognize hypoglycemia

A

Diabetic patient that is “off”
Neurological signs
Weakness
Lethargy
Disorientation
Restlessness
Ataxia
Tremors, shaking
Collapse
Seizure
Loss of consciousness/coma
IS AN EMERGENCY

38
Q

Response to hypoglycemia

A

Give sugar – rub syrup on gums
Call vet: and bring patient in
Always err of the side of caution if unsure and have the owner treat for insulin shock
HIGH blood glucose is SAFER than LOW blood glucose

39
Q

What is euthyroid

A

NORMALLY FUNCTIONING thyroid gland
Thyroid hormone feedback loops

40
Q

What is hypoT4 common in

A

Dogs
Some breeds are commonly affected
Doberman, golden retriever, irish setter, cocker spaniel

41
Q

What is the pathophysiology of hypoT4

A

Atrophy or auto-immune damage of the thyroid gland
Decreased thyroid hormone production

42
Q

What are the clinical signs and complications of hypo T4

A

Effects of low metabolism
obesity/weight gain
Lack of energy
Heat-seeking behaviour
Alopecia and skin issues
Immunosuppression
Other (reproductive issues, megaesophagus, neuropathies, seizures, ocular disorders)

43
Q

How do you test for hypo T4

A

Screening tests
Total T4, free T4
TSH
Ask the vet which tests they would like to have run
Testing to monitor response to treatment

44
Q

How do you treat hypoT4

A

Levothyroxine – synthetic T4, treatment is lifelong
T4 is converted to T3 in the tissues on an as needed basis
Side effects mostly related to iatrogenic overdose; if not addressed will eventually be fatal
V/D
Rapid weight loss
Hyperactivity
Tachycardia/murmur/arrhythmia (HCM)
Therapeutic monitoring
Recheck T4 in 4-6 weeks:
After treatment is initiated
Every time levothyroxine dosage is adjusted
Performed every 6-12 months
Blood must be collected 4-6 hours post-pill for testing
Ensure that there have been no recent missed doses

45
Q

Euthyroid sick syndrome is

A

Low thyroid function due to ANOTHER underlying illness
Normal function of a normal thyroid gland
Often misdiagnosed as pathological hypothyroidism

46
Q

HyperT4 is and common in

A

Middle age to older cats
Excess production of thyroid hormone
Idiopathic
Neoplastic
Benign
Carcinoma

47
Q

Pathophysiology and clinical signs of hyperT4

A

Excess T4 causes increased metabolic rate
Increased metabolism → Weight loss, wasting, increased physical activity
Increased blood flow → Hypertension
Tachycardia and 2° HCM to meet the increased blood demand
Hypertension → Retinal detachment
Heat intolerance
Ravenous appetite
Diarrhea – increased GI motility
PU/PD

48
Q

What can be the differential diagnoses with hyperT4

A

HyperT4
Neoplasia
Late stage CKD
Diabetes mellitus
FeLV
FIV
Starvation
Chronic infection
Parasitism

49
Q

What are the treatment options for hyerT4

A

Oral meds (Felimazole) – most common
Topical medication - has inconsistent absorption
Hill’s y/d diet – limited iodine content which effectively “starves” the thyroid tumor of iodine needed to produce T3 and T4
Need new bowls and de-ionized drinking water
Surgical resection of the affected gland
Radioactive iodine treatment – destroys thyroid tumor
Methimazole

50
Q

What is mehimazole and what deos it do

A

Anti-thyroid drug
Prevents iodine from being incorporated into T3 and T4
Adverse effects: BM suppression, bleeding issues, GI issues, facial pruritis, unmasking pre-existing renal disease
Oral tablets
Tapazole® (human),Felimazole® (licensed for use in cats)
Compounded fish paste – high palatability
Also available as compounded transdermal gel
Convenient for cats that are difficult to pill
Usually applied to the inside of the pinna (can damage pinna after chronic use)
Must wear gloves when applying
There is an applicator pen available
Questionable efficacy/absorbency
Increased risk of facial pruritis?

51
Q

Adrenal cortex hormones does what and includes

A

The adrenal cortex is the outer part of the adrenal gland
Hormones produced by the adrenal cortex include:
Mineralocorticoids (aldosterone)
Glucocorticoids (cortisol)
Glucocorticoids regulate nutrient levels in blood (increase blood glucose levels)

52
Q

Hyperadrenocorticism is

A

(cushing’s disease)
Excessive production of glucocorticoids
Dogs, horses, ferrets, rare in cats
Middle aged to older animals

53
Q

What causes cushings disease

A

Functional tumor of
Pituitary gland
Adrenal gland

54
Q

What are the common presenting signs of cushings

A

PU/PD
Polyphagia
Panting
Pot-bellied appearance
Thin skin and coat

55
Q

What are the complications with cushings

A

Steroid hepatopathy
Immunosuppression
Seizures (related to high blood pressure)
Other
Type III DM
Tumor compression causes blindness and neuropathy
Clots, hypertension, hypercalcemia

56
Q

How do you test for cushings

A

LDDST
Low dose dexamethasone suppression test
Diagnostic
8hr test
Book appropriately
ACTH stim test
Adrenocorticotropic hormone stimulation test
Used to diagnose cushings and to monitor response to therapy
Cortrosyn injection
Blood collection before cortrosyn and then 2-4 hours later

57
Q

How do you treat cushings

A

Treatment involves destroying part of the adrenal cortex
Trilostane (Vetoryl®) – most common, reversible
Mitotane – older drug, still used but more significant side effects (irreversible damage to the adrenal gland)
Owner monitors at home
How?
Watch for signs of overdose
Could damage adrenal glands to point of causing iatrogenic Addison’s disease

58
Q

How do you treat iatrogenic cushings

A

Identifying there is a problem
Notifying the prescribing DVM
Creating a program to wean off the steroid

59
Q

When does addisons happen

A

hypoadrenocorticism (decreased function of the adrenal glands)
Over 85% gone
Autoimmune
hypothalamus/pituitary damage
Atrophy

60
Q

Lack of corticosteroid and mineralocorticoid can cause

A

Mineralocorticoid
Na+ loss
K+ gain
Loss of body water
Affects function of muscles and nerves
Corticosteroid
Lack cortisol
Devresed BG
Decreased sympathetic tone
GI symptoms
Standard poodles are over represented

61
Q

What are the clinical signs of addisons disease

A

Vague presenting signs – lethargy, weakness, anorexia, vomiting, diarrhoea, PU/PD
Stress component
Related to inability to mount proper sympathetic response
Due to lack of corticosteroid production

62
Q

how do you treat and diagnose addisons

A

Diagnosed by the ACTH stimulation test
For life
Fludrocortisone: both glucocorticoid and mineralocorticoid activity
Desoxycorticosterone pivalate (DOCP): mineralocorticoid that mimics the effects of aldosterone
Prednisone: used with DOCP

63
Q

What is an addisonian crisis

A

Emergency
Acute event
Rapidly fatal
Occurs in patients with addisons disease
Triggered by stress
At risk for shock

64
Q

How does shock occur with an addisionian crisis

A

Hypovolemic + cardiogenic shock
Low Na+ → water follows Na+ into the renal tubules → water loss in the urine
High K+ → bradycardia
Prevent sympathetic response from compensating
Low aldosterone → aldosterone is required for optimal vasoconstriction
Low glucocorticoids → glucocorticoid is required for the optimal sympathetic response

65
Q

How to recognize an addisonian crisis

A

Patient diagnosed with addisions disease
V/D; often bloody
Shiver/shake/lethargy/collapse
Stress event in the history
Signs of shock such as
Decreased CRT
Pale mm
Bradycardia
Weak pulses
Hypothermia

66
Q

ABCs of shock

A

Place IV catheter
IV fluids – at shock rates
Get vet
Emergency steroids
Correct electrolyte imbalances
Protect heart
Remove stress
Increase BP (vasoconstrictors)