Endocrine Flashcards

(67 cards)

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
How do you preform insulin therapy
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?
26
Diet management with diabetes goals and the food includes
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
27
Oral hypoglycemic agents are and work by
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
Senvelgo is used in what
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
How do human oral hypoglycemic agents work
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
Patient management with diabetes
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
What is important to monitor with diabetic dogs
Changes in PU/PD BCS Strength and mobility Blood glucose curve (12-24h) Fructosmaine
32
How to monitor BG
Glucurve Product approved for use in cats and dogs Glucose curves
33
How do you do a glucose curve and what does it determine
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
Can type 2 DM self resolve
remission in type 2 diabetes Remission rates of 65% or higher have been reported in cats with good diabetic management
35
What is important with surgery and diabetic patients
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
What is hypoglycemia
Low blood glucose concentration Most commonly occurs in diabetic patients Starvation, seizures, insulinomas, toxins (xylitol) Can be fatal rapidly
37
How do you recognize hypoglycemia
Diabetic patient that is “off” Neurological signs Weakness Lethargy Disorientation Restlessness Ataxia Tremors, shaking Collapse Seizure Loss of consciousness/coma IS AN EMERGENCY
38
Response to hypoglycemia
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
What is euthyroid
NORMALLY FUNCTIONING thyroid gland Thyroid hormone feedback loops
40
What is hypoT4 common in
Dogs Some breeds are commonly affected Doberman, golden retriever, irish setter, cocker spaniel
41
What is the pathophysiology of hypoT4
Atrophy or auto-immune damage of the thyroid gland Decreased thyroid hormone production
42
What are the clinical signs and complications of hypo T4
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
How do you test for hypo T4
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
How do you treat hypoT4
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
Euthyroid sick syndrome is
Low thyroid function due to ANOTHER underlying illness Normal function of a normal thyroid gland Often misdiagnosed as pathological hypothyroidism
46
HyperT4 is and common in
Middle age to older cats Excess production of thyroid hormone Idiopathic Neoplastic Benign Carcinoma
47
Pathophysiology and clinical signs of hyperT4
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
What can be the differential diagnoses with hyperT4
HyperT4 Neoplasia Late stage CKD Diabetes mellitus FeLV FIV Starvation Chronic infection Parasitism
49
What are the treatment options for hyerT4
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
What is mehimazole and what deos it do
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
Adrenal cortex hormones does what and includes
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
Hyperadrenocorticism is
(cushing's disease) Excessive production of glucocorticoids Dogs, horses, ferrets, rare in cats Middle aged to older animals
53
What causes cushings disease
Functional tumor of Pituitary gland Adrenal gland
54
What are the common presenting signs of cushings
PU/PD Polyphagia Panting Pot-bellied appearance Thin skin and coat
55
What are the complications with cushings
Steroid hepatopathy Immunosuppression Seizures (related to high blood pressure) Other Type III DM Tumor compression causes blindness and neuropathy Clots, hypertension, hypercalcemia
56
How do you test for cushings
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
How do you treat cushings
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
How do you treat iatrogenic cushings
Identifying there is a problem Notifying the prescribing DVM Creating a program to wean off the steroid
59
When does addisons happen
hypoadrenocorticism (decreased function of the adrenal glands) Over 85% gone Autoimmune hypothalamus/pituitary damage Atrophy
60
Lack of corticosteroid and mineralocorticoid can cause
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
What are the clinical signs of addisons disease
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
how do you treat and diagnose addisons
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
What is an addisonian crisis
Emergency Acute event Rapidly fatal Occurs in patients with addisons disease Triggered by stress At risk for shock
64
How does shock occur with an addisionian crisis
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
How to recognize an addisonian crisis
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
ABCs of shock
Place IV catheter IV fluids – at shock rates Get vet Emergency steroids Correct electrolyte imbalances Protect heart Remove stress Increase BP (vasoconstrictors)
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