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249 Cards in this Set
- Front
- Back
Generally what are the two main types of hormones
|
Those made up of amino acids and do not enter the cells (attach to receptors i.e. ADH)
Those that enter the cell and have their effect inside the cell (thyroxine) |
|
What are some organs involved in hormone production
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Pituitary
Thyroid Pancreas Parathyroid Adrenals Ovaries Placenta etc... |
|
What hormones are produced by the anterior pituitary gland
|
TSH
GH ACTH FSH LH MSH (melanocyte stimulating hormone) |
|
What hormone controls sodium and potasium regulation
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Aldosterone
|
|
What does cortisol do
|
Regulates cell membrane integrity
|
|
What hormone is responsible for glucose regulation
|
Insulin
|
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What hormone is responsible for growth regulation
|
Growth hormone
|
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What hormone is responsible for water conservation
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ADH
|
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What is responsible for the release of hormones from the anterior pituitary gland
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Releasing factors produced in the hypothalmus
|
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True or False most hormones function on a positive feedback system
|
False most hormones function on a negative feedback system
|
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What hormones are released by the posterior pituitary
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Oxytocin
ADH |
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Where are ther hormones released from the posterior pituitary produced
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Produced in the hypothalmus and transported via neurons to the posterior pituitary gland
|
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True or False the pituitary is an extension of the hypothalmus
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TRUE
|
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What are the characteristics of diabetes insipidous
|
Large volumes of dilute urine
Insipid = tasteless |
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What are the two forms of diabetes insipidous
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Central diabetes insipidous
Primary renal diabetes insipidous |
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Which form of diabetes insipidous is rare
|
Primary renal form of diabetes insipidous is very rare
|
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True or False many times it is impossible to differentiate between central and primary renal diabetes insipidous
|
TRUE
|
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What happens with central diabtetes insipidous
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1. Lack of ability to produce ADH
2. Lack of appropiate response to increased osmolality |
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What is the normal trigger for ADH release
|
Increased serum osmolality
|
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When is there maximal release of ADH
|
Maximal release of ADH occurs at 320 mOsm
|
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True of False ADH release is increased by hypovolemia
|
TRUE why would I trick you
|
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What is meant by nephrogenic diabetes insipidous
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Secondary diabetes insipidous
|
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True or False excess calcium concentration will block or partially block ADH's effect
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TRUE
|
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Where is the thirst center located
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Hypothalmus
|
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What stimulates thirst
|
Increased serum osmolality
sodium is the major substance that stimulates thirst |
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What is the most significant clinical sign of diabetes insipidous
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Polyuria/polydipsia
|
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True or False CBC abd biochem profiles are usually normal and urine specific gravity is > 1.008 with central diabetes insipidous
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FALSE blood is normal, specific gravity is < 1.008
|
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True or Fasle central diabetes insipidous is a common disease but partial or subtle presentations of diabetes insipidous can be challengiing to treat
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FALSE central diabetes insipidous is not a common disease
|
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What is the specific test for diabetes insipidous
|
Water deprivation test
|
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How is the water deprivation test performed
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Patient values are collected for body weight, serum psmolality, urine spec. grav, serum urea concentrations.
Animal is deprived of water and the same measurments are taken every two hours |
|
How long is a water deprivation test conducted
|
Until concentration exceeds 1.020 - 1.025
Animal loses more then 5% of its body weight BUN goes above the normal range Serum osmolality exceeds 305 mOsm |
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What does it mean if patients are able to concentrate urine during a water deprivation test
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They don't have diabetic insipidous
|
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If an animal loses 5% bwt, with no concentration what is the problem
|
Problem is with ADH
Not producing ADH or it is not functioning properly |
|
What level of kidney loss is required for BUN to increase
|
75% kidney loss required for BUN to increase
|
|
At what point do you get a loss of concentrating ability with the kidney
|
2/3
|
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What is the risk of performing a water deprivation test
|
Medullary washout
|
|
What is the best test for profound PU/PD
|
Modified water deprivation test
|
|
What is the modified water deprivation test
|
Animals water intake is slowly decreased over several days
|
|
What is DDAVP
|
Endogenous
|
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What is the ADH response test
|
Give ADH to see if the concentrat
|
|
What are the lab findings with central diabetes insipidous
|
Normal CBC biochem
Specific garvity < 1.008 |
|
What are the differential for a urine specific gravity <1.008
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Central diabetes insipidous
Psychogenic polydipsia Nephrogenic diabetes insipidous |
|
How is a water deprivation test performed
|
Measure baseline bodyweight, serum osmolality, urine specific gravity and serum urea concentration
|
|
When is a water deprivation test stopped
|
Urine concentration reaches 1.020-1.025
Animal loses 5% of its body weight BUN goes above normal range Serum osmolality >305 mOsm |
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What does it mean if they can concentrate urine on a water deprivation test
|
It means they do NOT have diabetes insipidous
|
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What can you cay about the water deprivation test when an animal loses 5% of its body weight without concentrating its urine
|
There is something wrong with ADH
Either its not producing ADH or the ADH is not functioning |
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How much kidney loss is required to get an increase in BUN
|
75%
|
|
How much kidney loss is required to get a loss of concentrating ability
|
2/3 of kidney function lost = loss of ability to concentrate urine
|
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What are the risks od a water deprivation test
|
If animal is PU/PD you can get medually washout
If PU/PD use a modified test |
|
What should you do next when you reach the end point of a water deprivation test and still have no concentrated urine
|
Administer ADH and see if the animal responds
may take several days with medually washout |
|
What does it mean if there is a negative water deprivation test followed by a positive ADH test
|
Central diabetes insipidous
|
|
When do you see psychogenic polydipsia
|
Young excitable dogs
May be associated with primary brain disease May be associated with the PU/PD of cushings |
|
True or False animals with psychogenic polydipsia will have a serum osmolality of < 285 mOsm
|
True because they are overhydrated
|
|
What can cause nephrogenic diabetes insipidous
|
Normal ADH release but unable to exert its effects via receptor sites in the kidney
May be due to increased serum calcium and possible Cushings |
|
WHere is growth hormone released from
|
Anterior pituitary from GHRH
Mammary tissue from progesterone |
|
What inhibits the release of growth hormone
|
somatostatin
|
|
Why is GH release due to progesterone important in dogs
|
Because dogs keep their CL even if they are not pregnant and it releases progesterone this stimulates the release of growth hormone
|
|
What is the main catabolic effect of growth hormone
|
Insulin antagonism
Causes lipolysis and gluconeogenisis Decrease glucose transport across cell membranes Net effect is hyperglycemia |
|
What are the slow effects of growth hormone
|
stimulates growth, chondrogenesis and protein synthesis
|
|
What causes acromegaly in dogs
|
Middle aged intact female dogs post estrus
Dogs given progesterone to prevent estrus |
|
What causes acromegaly in cats
|
Pituitary tumor
|
|
What happens with acromegaly
|
Excessive growth hormone results in excessive soft tissue and bony growth
Also leads to insulin resistance |
|
What are clinical signs of acromegaly in dogs
|
Soft tissue proliferation esp with the head
Wide spaces between the teeth, increased pharyngeal tissue Increased and thickened skin folds especially of the neck usually not diabetic but polyuria and polyphagia |
|
what are the clinical signs of acromegaly in the cat
|
Not as pronounced as in the dog
Most common sign is severe insulin resistance -> manifests as difficult to control diabetes melitus |
|
How can you diagnose acromegaly
|
Measure basal GH concentration
Measure IGF-1 concentration |
|
What is the treatment for dogs with acromegaly
|
Spay intact females
Discontinue progesterone administration |
|
What is the treatment for cats with acromegaly
|
Tratement of the pituitary tumor - surgery, radiation therapy, possibly synthetic somatostatin
|
|
Who gets pituitary dwarfism
|
German Shepherd dogs
|
|
What causes pituitary dwarfism
|
Congenital pituiatary disfunction
Lask of TSH production |
|
What are the clinical signs of piituitary dwarfism
|
Failure to grow
Normal conformation Retained puppy haircoat Possible kidney problems |
|
How can you diagnose pituitary dwarfism
|
Stimulation test with GHRH to measure post treatment GH is the most accurate method
|
|
True or False pituitary dwarfism can be treated with canine GH
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FALSE canine GH is not available
|
|
True or False pituitary dwarfism can be treated with human GH
|
FALSE the dog will produce antibodies to human (or synthetic) GH
|
|
True or False pituitary dwarfism can be treated with porcine GH
|
TRUE porcine GH is the same as canine GH
|
|
How does the adrenal look on ultrasound
|
Kind of a penut shape
|
|
What are all steroidal compounds formed from
|
Cholesterol
|
|
Where does the catabolism of most steroids occur
|
In the liver
|
|
What causes the release of cortisol
|
ACTH
(Adrenocorticotropic hormone) |
|
What causes the release of ACTH
(Adrenocorticotropic hormone) |
CRH (corticotropic releasing hormone) from the hypothalmus
|
|
What causes an increase in CRH
|
CRH stimulated by
Decresed serum cortisol Arginine vasopressin (humans) Angiotensin II (humans) |
|
Where is ACTH released from
|
Pituitary
|
|
What decreases CRH release
|
Increased serum cortisol (also has an effect on the pituitary)
ACTH Oxytocin (humans) |
|
What causes aldosterone release
|
Renin from the kidney via serum angiotensin II
Decreased serum sodium |
|
What is Cushing's disease
|
Hyperadrenocorticism
Excess production of cortisol by the adrenal cortex |
|
What are the types of hyperadrenocorticism
|
** Excess production of ACTH by pituitary (PDH - pituitary dependant hyperadrenocorticism)
** Primary adrenal tumor (ADH - Adrenal dependant hyperadrenocorticism) Ectopic ACTH syndrome Ectopic CRH syndrome |
|
True or False Cushing's is rare in cats
|
TRUE
|
|
What is the typical signalment for Cushings
|
Middle aged to older dogs
Females slightly more then males |
|
What has a better prognosis pituitary dependant or adrenal dependant hyperadrenocorticism
|
PDH has a better prognosis
|
|
What are common clinical signs of Cushing's
|
Bilaterally symetrical truncal alopecia
PU/PD Polyphagia Abdominal enlargement Muscle weakness Lethargy Secondary skin problems (seborrhea, pyoderma, hyperpigmentation, calcinosis cutis) Blood vessel fragility Weight gain Panting Signs of lower urinary tract dz (secondary UTI) |
|
What is the most important clinpath abnormality
|
Increased ALP if there is no increased ALP it is not likely Cushing's
|
|
What are the screening tests for hyperadrenocorticism
|
ACTH stimulation test
Low dose dexamethazone suppression test Urine cortisol/creatinine ratio UCCR |
|
How does concurrent disease affect hyperadrenocorticism testing
|
Concurrent disease is a chronic stressor which makes the results of testing more difficult to interpret
|
|
What is atypical hyperadrenocorticism
|
Dogs have clincal signs and typical hematological and biochemical findings consistant with hyperadrenocorticism but normal ACTH and LDDS results
|
|
What are disxcriminatory tests used for with Cushing's
|
To determine where the disorder is
Pituitary dependant hyperadrenocorticism or adrenal tumor |
|
What are the dicriminatory tests for Cushing's
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High dose dexamethasone suppression test
Endogenous Acth concentration Abdominal ultrasound Radioisotope imaging CT or MRI |
|
True or False if an animal doesn't supress with a high dose dexamethosone test you can rule out Cushing's
|
FALSE even if they do not suppress you still can not rule out Cushings with a HDDS test
|
|
What does it mean if you get suppression with a HDDS test
|
you have PDH
|
|
What are good discriminatory results for an endogenoud ACTH test
|
If you get high or low levels of suppression you will have PDH or ADH respectively
|
|
What is radioisotope testing useful for with hyperadrenocorticism
|
Good for distinguishing a unilateral adrenal tumor from PDH
(limited availability) |
|
True or False for hyperadrenocorticism CT/MRI cannot differentiate between bilateral hyperplasia or bilateral neoplasia of adrenals
|
TRUE
|
|
What is CT/MRI useful for with hyperadrenocorticism
|
For differentating unilateral neoplasia from PDH
|
|
True or False most often we treat medically for PDH
|
TRUE
|
|
What drugs are used to treat hyperadrenocorticism
|
o'p'DDD (mitotane)
Ketoconazole Selegiline Trilostane Melatonin Flaxseed oil with lignans |
|
What is the main drug used for Cushing'
|
o'p'DDD
(Mitotane) |
|
Why are people scared of using Mitotane
|
Can make the dog Addisonian
Needs good monitoring |
|
How does Mitotane work
|
Causes selective destruction of zona fasiculata and reticularis
Dogs with PDH show an exaggerqated response to Mitotane may get clinical remission |
|
What is the goal when treating with Mitotane
|
ACTH stimulation tests consistent with hypoadrenocorticism
or ACTH test results in the low normal range |
|
How does ketoconazole work for treating Cushing's
|
Inhibits production of cortisol by the adrenal cortex
Less serious side effects then Mitotane |
|
What are the disadvantages of treating Cushing's with ketoconazole
|
Must treat multiple times a day
Side effects include vomiting and hepatopathy |
|
How does Selegiline (Deprenyl) work for Cushing's
|
Irreversible inhibitor of monamine oxidase type B
Normalizes (increases) dopamine concentrations |
|
What do you need to consider when treating Cushing's with Trilostane
|
Could lead to full blown Addison's need to send home prednisilone just in case cortisol goes too low
|
|
How does Trilostane work for treating Cushing's
|
Trilostane is a steroid analogue that is a competitive inhibitor of 3-beta hydroxysteroid dehydrogenase system
exactly what I was thinking !!!! |
|
What are the surgical options for treating hyperadrenocorticism
|
Adrenalectomy
Unilateral for primary adrenal tumor Bilateral for PDH |
|
How can you get iatrogenic hyperadrenocorticism
|
Exogenous glucocorticoid administration
|
|
How do you treat iatrogenic Cushing's
|
Gradual withdrawl of exogenous glucocorticoids
|
|
True or False small dogs can absorb enough glucocorticoids from topical treatments to display iatrogenic Cushing's
|
TRUE
|
|
Why do you want to do a gradual withdrawl with iatrogenic Cushing's
|
Because the adrenals have been suppressed you want to give them a chance to regain normal adrenal function
|
|
Which is more common Addison's or Cushing's
|
Cushing's
|
|
How does the animal preent with the acute form of Addison's disease
|
Really sick
Addisonian crisis ? |
|
What is Addison's disease
|
Deficient glucocorticoid production (cortisol) and mineralcorticoid (aldosterone) production by the adrenal cortex
|
|
What are the etiologies for Addison's
|
Immune mediated destruction
Granulomatous destruction Iatrogenic Waterhouse Fredrichsen syndrome (associated with sepsis and multi-orgqn failure) |
|
What are etiologies for cortisol only deficiencies
|
Pituitary lack of ACTH
Iatrogenic Early adrenal destruction |
|
What is the pathophysiology of iatrogenic Addison's
|
Glucocorticoids are given for a prolonged period of time then acutely stopped
|
|
What are the clinical signs of Addison's
|
Mainly GI - vomiting and diarrhea
|
|
How long does it take to recover from iatrogenic Addison's
|
Weeks to months to have cortisol production back uo to normal levels
|
|
True or False hypoadrenocorticism can present as just a deficiency in cortisol but not in aldosterone
|
TRUE
|
|
How gets Addison's typically
|
Young adults (males?)
Standard poodles may be at an increased risk |
|
What do you see clinically with cortisol deficiencies
|
GI signs and lethargy
|
|
What do you see clinically with aldosterone deficiency
|
Depressions
Cardiac arrythmias |
|
What is unique with the acute form of Addison's
|
You get bradycardia and shock (a mismatch)
|
|
True or False you will see a stress response and variable PCV on a CBC with Addison's
|
FALSE you will not see a stress response with Addison's
|
|
What should you think if you sodium is low and your potassium is high
|
Addison's
|
|
What Na/K ratio is suggestive of Addison's
|
< 25:1
Suggesstive of Addison's but also GI, renal and hepatic diseases |
|
How can you diagnose Addison's
|
ACTH stimulation test
|
|
What would you expect to see on an ACTH stimulation test with Addison's
|
No increase in glucocorticoids when ACTH is administered
|
|
What is seen on radiographs with Addison's
|
Microcardia
Small caudal vena cave |
|
What is seen on ECG with Addison's
|
Tented T waves with increased amplitude
Lack of P waves Bradycardia Widened QRS complexes |
|
What is the acute treatment for Addison's
|
IV fluids (may require shock doses)
Glucocorticoids If severe hyperkalemia give crystalline insulin and dextrose or calcium gluconate or sodium bicarb |
|
Why would you give crystalline insulin and dextrose or calcium gluconate or sodium bicarb with sever hyperkalemia from acute Addison's
|
Because Insulin drives glucose into cell with K
Glucose goes into cell with K and Bicarb swapd H for K in the cell so they will all reduce serum potassium levels Check the accuracy of this statement with others |
|
Why would you chose to treat Addisons with dexamethasone over prednisone
|
Because prednisone shows up on cortisol assay (inaccurate test results)
|
|
True or False if you are giving insulin for Addison's you should always give dextrose
|
TRUE
|
|
What do you use for chronic treatment of Addison's
|
Fludrocortisone +/- prednisone
Deoxycortiosterone pivilate (lasts a month) + prednisone Prednisone alone if it is jsut a cortisol deficiency |
|
What treatments are given in order for hyperkalemia from Addison's
|
1. Ca gluconate
2. Insulin and dextrose 3. Sodium bicarb (could be problematic) |
|
What can stress do to the cortisol requirement
|
May increase it by 10X or more
|
|
What is the typical presentation of hypothyroidism
|
Middle aged dogs no sex predilection
|
|
True or False spontaneous hypothyroidism is common in the cat
|
False it is rare
|
|
What are clinical signs of hypothyroidism
|
Decreased metabolic rate
Dermatopathies Reproductive dysfunction Neuromuscular dysfunction |
|
What conditions are associated with decreased metabolic rate with hypothyroidism
|
Mild weight gain
Heat seeking Lethargy |
|
What conditionas are associated with reproductive dysfunction with hypothyroidism
|
Prolonged inestrus interval or anestrus
|
|
What are the neuromuscular dysfunctions associated with hypothyroidism
|
Facial nerve paralysis
Constipation |
|
What are the clinical signs of hypothyroidism in cats
|
NOT A TRICK QUESTION
Lethargy Poor hair growth, seborrhea Puffy face Hair loss |
|
What are the clinicopathologic abnormalities associated with hypothyroidism
|
Anemia
Hypecholesteremia Mildly increased liver enzymes Mild hyponatremia |
|
What is the etiology of hypothyroidism
|
Lymphocytic-plasmacytic thyroiditis
Thyroid atrophy Thyroid neoplasia TSH or TRH deficiency Congenital Iodine deficiency |
|
What test would you run to diagnose hypothyroidism
|
Minimum database
Tests of thyroid function Others based on clinical signs |
|
What are the tests of thyroid function
|
Resting T4
Resting FT4 Endogenous TSH concentration TSH or TRH stimulation test Response to therapy Thyroid hormone antibody concentrations Thyroglobulin antibody concentrations Thyroid biopsy Radioisotope uptake |
|
True or False if the TT4 is normal the dog is likely euthyroid
|
TRUE
|
|
What are the advantages and disadvantages of testing the resting total T4 concentrations
|
Advantage: Easy
Disadvantage: Measures both free and protein bound hormone, influenced by non-thyroidal factors, may get false increase with anti T4 antibodies |
|
What are the advantages and disadvantages of testing the resting free T4 concentrations
|
Advantages: easy, measures just the free/active portion of the hormone
Disadvantages: still influenced by non-thyroidal factors (less then TT4) |
|
What are some influencing factors on thyroid hormone concentrations
|
Age
Breed Temperature Time of day Nutrition Surgery Concurrent illness Drugs |
|
What are the advantages and disadvantages of testing the endogenous canine TSH concentrations
|
Advantages: Easy
Disadvantages: Influenced by non-thyroidal factors can be used in conjunction with TT4 or FT4 |
|
What do you need to condsider when test to see if there is a response to treatment for hypothyroidism
|
Clinical signs respond at different rates
If signs resolve you need to stop treatment to see if they recurr If signs do not fully resolve measure TT4 if low up the dose, if normal look for other causes |
|
What is the treatment for hypothyroidism
|
Levothyroxine (synthroid?)
|
|
Who get hyperthyroidism
|
Middle aged to older cats
No sex predilection Usually bilateral thyroid involvement Thyroid changes rarely malignant |
|
What is the etiology of hyperthyroidism
|
Genetic?
Environmental, nutritional, other? (canned food or cat liiter?)\Decreased inhibitory protein |
|
What are the clinical signs of hyperthyroidism
|
PU/PD
Polyphagia Weight loss Vomiting. diarrhea Oily or matted haircoat Behaviour change |
|
What are the signs of apathetic hyperparathyroidism
|
anorexia
weight loss lethargy |
|
What would you expect to see on physical exam with hyperthyroidism
|
Thin/emaciated
OIly/matted haircoat Hyperactivity or aggression Tachycardia Palpable thyroid enlargment Dyspnea Cardiac murmur or gallop rythym |
|
What are the clinicopathologic abnormalities for hyperpthyroidism
|
Stress leuogram
Mile erythrocytosis or anemia Mild hyperphosphatemia Possible azotemia |
|
How can you diagnose hyperthyroidism
|
Minimum data base
Thoracic rads, ECG Resting TT4, FT4 T3 suppression test TRH stimulation test |
|
What can you say about the results of a TT4 and hyperthyroidism
|
If increased it is diagnostic for hyperthyroidism
If normal (esp with concuurrent illness) you can not rule out hyperthyroidism |
|
True or False FT4 is incresed in hyperthyroid and some cats with non-thyroidal illness
|
TRUE
Should not be used as the primary diagnostic test for hyperthyroidism |
|
what can you say with a high normal TT4 and a normal FT4
|
Probably not hyperthyroid
|
|
What can you say with a normal TT4 and increased FT4
|
Likely hyperthyroid
|
|
What would you expect to happen in a normal and a hyperthyroid cat with a T3 supression test
|
Normal cat -> suppression of T4
Hyperthyroid cat -> no suppression of T4 |
|
What are the biggest drawbacks to performing a T3 suppression test
|
Owner has to pill the cat as scheduled and it require two blood samples
|
|
What would you expect with a TRH stimulation test in a normal cat
|
Increased T4
|
|
What would you expect with a TRH stimulation test in a hyperthyroid cat
|
Little or no increase in T4
|
|
What are the advantages and disadvantages of performing a TRH stimulation test
|
Advantages: Done in hospital one day
Disadvantages: Some cats have transient side effects and it is not 100% diagnostic (for thyroid or non-thyroid causes) |
|
What are the advantages and disadvantages to a technesium scan
|
Advantages: useful before a thyroidectomy
Disadvantages: limited availability, may require sedation, Accuracy? |
|
What is the mediacal treatment for hyperthyroidism
|
Methimazole
Propylthiouracil (PTU) |
|
What are the non-mediacal treatment options for hyperthyroid
|
Thyroidectomy
Radioactive iodine Percutaneous ethanol injection for solitary nodule or radiofrequency abalation |
|
True or false hyperthyroidism may mask renal failure
|
TRUE cause increased renal blood flow and GFR
|
|
What are the side effects to medical treatment of hyperthyroidism
|
Anorexia, vomiting
Facial excoriations/pruritis hepatopathy Granulocytopenia Bleeding tendencies |
|
What are the risks of thyroidectomy
|
Requires anesthesia
risk of post op hypocalcemia with bilateral thyroidectomy (from removal of parathyroid gland anyone?) Other surgical complications |
|
What are the advantages of a thyroidectomy for hyperthyroidism
|
Usually curative
|
|
What are the advantages of radioactive iodine treatment for hyperthyroidism
|
Safe
Usually curative Works for ectopic thyroid tissue as well |
|
What are the disadvantages of radioactive iodine therapy
|
Limited availability
Prolonged hospital stay (requires isolation 5-10 days post treatment) May need repeat treatments |
|
What hormones are produced in the pancreatic islet cells
|
Glucagon (alpha cells)
Insulin (beta cells) Somatostatin (delta cells) Pancreatic polypeptide (F cells) |
|
What hormones are primarily involved in the regulation of carbohydrate, fat and protein metabolism
|
Insulin and glucagon
|
|
What does somatostain do
|
Involved in the regulation of insulin and glugagon (and other hormones) secretion
|
|
What does pancreatic polypeptide do
|
Modulates pancreatic secretory response to food
|
|
True or False in a normal animal feeding and strenuous exercise can increase serum glucose appreciably
|
FALSE
Glucose homeostasis is tightly regulated |
|
What counters glucose influx
|
Glucose influx is largely countered by insulin
|
|
What does insulin do
|
Increases protein synthesis and lipogenesis
Decreases fat and protein catabolism Inhibits hepatic gluconeogenisis and ketogenisis |
|
What does glucagon do
|
Increases gluconeogenisis, glycogenolysis and ketogenisis
|
|
What are the hormonal abnormalities with diabetes mellitus
|
Hypoinsulinemia
Hyperglucagonemia |
|
Why is there polyuria associated with Diabetes mellitus
|
Increased glucose spills over into the urine cause an osmotic effect -> polyuria and a compensatory polydipsia
|
|
Why is there weight loss associated with untreated diabetes mellitus
|
The caloric loss of glucose in the urine and decreased peripheral utilization of glucose
|
|
What are the two causes of diabetes mellitus
|
Decreased insulin secretion
Decreased insulin action |
|
What is the most common type od diabetes in the dog
|
Inulin dependent DM with onset in middle to old aged dogs
|
|
True or False Males are more affected 2X as much as females with insulin dependent DM
|
FALSE Females are 2X as likely as males to get this
|
|
What are the etiopathogenic factors for diabetes melitus
|
Genetics
Increased diabetogenic hormones Infection (viral) Obesity Autoimmunity Pancreatitis Diabetogenic medications Stress or other illness |
|
What is the typical presentation of diabetes mellitus in cats
|
Domestic shorthair cats >5 years of age
neutered males > females most have absolute insulin deficiencey |
|
Compare and contrast the insulin characteristics of diabetes mellitus in cats and dogs
|
Dogs juvelile form - normal absolute insulin level - but still needs exogenous insulin
Dogs adult for - absolute insulin level decreased Cats - absolute insulin deficiency |
|
What are the four classic clinical signs of uncomplicated diabetes mellitus
|
polyuria
polydipsia polyphagia weight loss |
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Aside from the classic clinical signs of uncomplicated diabetes mellitus what OTHER signs might be present
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An obese patient may have hepatic lipidosis and hepatomegaly
Cataracts secondary to prolonged hyperglycemia Sudden blindness from cataracts (see above) Plantigrade stance in cats from diabetic neuropathy |
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What can cause a misdiagnosis of diabetes mellitus
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Evaluating only the urine glucose because dogs with FANCONI syndrome will have a persistant glucosuria
Evaluating only the blood glucose in a cat under stress |
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What does it take to make a diagnosis of diabetes mellitus
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Hx of polyuria, polydipsia, polyphagia and weight loss in conjunction with a persistant fasting hyperglycemia and glucosuria
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True or False diabetes in the cat should only be diagnosed if a persistant hyperglycemia and glucosuria are present
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TRUE
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What can be used to diagnose cats where it is difficult to rule out stress hyperglycemia
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Fructosamine concentration can be evaluated
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What additional diagnostics should every potential diabetic have performed
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Serum lipase analasys and a urine culture (prefeably by cystocentesis)
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What abnormal lab results can be seen with diabetic patients
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Leukocytosis
Normal to increased serum alanine aminotransferase Normal to increased ALP Hypercholesteremia Ketonuria Proteinuria Bacteriuria A lot of dogs will have pancreatitis and/or UTI |
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Why is fructosamine a good test in diabetic animals
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It reflects blood glucose over the previous 1-2 weeks
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What are the types of insulin available for the dog and cat
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Based on origin -
Beef Beef-pork Human (synthetic) Based on formulation - Regular (crystalline) NPH insulin Lente Ultralente |
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True or false porcine and human insulin are fairly similar to canine insulin
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TRUE
Feline insulin is more different |
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Who metabolizes insulin faste cats or dogs
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Cats
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What type of insulin would be used to treat an unstable ketoacidotic diabetic
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Regular (crystalline) insulin until they are stabilized
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What are the primary choices of insulin (in Canada) to treat the diabetic patient at home
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NPH
Lente Glargine |
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What is the protocol for the intitial treatment for diabetes
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Insulin is given twice daily
Blood glucose concentrations are measured every 3-4 hours for a 12-24 hour period Feed 1/2 the daily caloric requirement at time of injection Adjust the next days insulin dose based on the glucose determinations if required |
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What should you be aware of when performing an in clinic blood glucose evaluation in cats
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Stress hyperglycemia can sometimes make it dificult or impossible
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What do you need to tell your client about feeding with a diabetic patient
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The diet of a diabetic patient must be consistent as it will be based on the patients weight and activity level
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Does exercise increase or decrease insulin requirements
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It decreases insulin requirements due to increeased blood flow and insulin delivery to working skeletal muscle
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Should diabetic working dogs get increased or decreased insulin under working conditions
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Decreased insulin or insulin will drive glucose into the cells --> excessive exercise may lead to hypoglycemic seizures
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How does the estrus cycle have an effect on diabetes control
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Progesterone stimulates release of growth hormone which is a diabetogenic hormone and diabetic control may be difficult for the next 2 months after an estrus cycle some bitches may die despite all attempt at diabetic control
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What should be done with diabetic bitches
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They should be spayed as soon as their diabetes is under control
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What are the complications of diabetes mellitus
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Cataract formation
Hepatic lipidosis Diabetic retinopathies Nephropathies Neuropathies Atherosclerosis |
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What are acute complications of diabetes mellitus
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Diabetic ketoacidosis
Nonketotic hyperosmolar Infection Hyperlipidemia Hypertension Possibly pancreatitis |
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What might cause insulin therapy to not work properly
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Improper insulin administration by the owner
Inadequate mixing of insulin prior to withdrawal from the syringe Outdated insulin Inactive insulin (from improper storage) Inaccurate or outdated ketodiastix |
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True or False the effects of insulin on a patient can be evaluated after two consecutive blood glucose samples
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FALSE it will take serial blood glucose levels to determine the effectiveness
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What can cause post hypoglycemic hyperglycemia
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Excessive insulin administration
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What is the pathophysiology of post hypoglycemic hyperglycemia
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Excessive insulin administration causes blood glucose to drop below 3.6 mmol/L this causes the release of diabetogenic hormones which cause an increase in blood glucose
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What should be done with patients that have a rapid metabolism of insulin
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Insulin administration must be changed to
A more frequent administration schedule A longer acting insulin |
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What is Somogyi phenomenon
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Post-hypoglycemic hyperglycemia
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What is the issue of patients with somogyi phenomenon
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When you test in the morning the blood glucose is unchecked and too high so the owner increases the insulin dose exacerbating the syndrome
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What happens with insulin antagonism/resistance
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Something is interfering with the action of insulin --> persistant hyperglycemia and blood glucose does not decline significantly with insulin therapy
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What are causes of insulin resistance
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Exogenous glucocorticoid administration
Hyperadrenocortism Acromegaly (mostly cats) Estrus Pregnancy Infections Prolonged stress |
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What can happen with hypoglycemic reactions
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Patient recieves too much insulin or exercises too much hypoglycemia and associated reactions may occur before diabetogenic hormones are released or have an effect
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What types of insulin must be given SQ
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NPH
Lente Ultralente |
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How can regular/crystalline insulin be administered
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IV
IM SQ |
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What is the pathogenisis of diabetic ketoacidosis
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With diabetes mellitus lipase is not inhibited by insulin properly ->excess free fatty acids delivered to the liver -> ultimately converted to beta-hydroxybutyric acid and acetone (ketoacids) ->ketone accumulation and metabolic acidosis -> resultant osmotic diuresis
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What are common presenting complaints for ketoacidosis
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Anorexia
Not drinking Vomiting Diarrhea Severe depression |
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What should you do when preesented with a case of diabetic ketoacidosis
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ALWAYS look for another disease process
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What disease processes are associated with diabetic ketoacidosis
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Pancreatitis
UTI CHF Pyometra |
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What is the prognosis for diabetic ketoacidosis
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Guarded
Requires fast and accurate recognition and agressive therapy even then pronosis is guarded |
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How is a presumptive diagnosis of diabetic ketoacidosis confirmed
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Both ketones and glucose is present in the urine or hyperglycemia and hyperketonemia
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What are the initial goals of therapy for diabetic ketoacidosis
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Provide adequate insulin to reverse hyperglycemia and ketone production
Correct dehydration and electrolyte abnormalities Correct severe metabolic acidosis Identify any precipitaing factors |
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What are the diabetogenic hormones
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Glucagon
Epinephrine Cortisol Growth Hormone |
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What are the causes of decreased glucose production
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Puppy hypoglycemia
Hepatic insufficiency Glycogen storage disease Hypoadrenocorticism Sepsis |
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What are causes of increased glucose utilization
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Beta cell tumor
Extrapancreatic neoplasia Sepsis |