Settles Endocrine Flashcards
1
Q
What is the MOST active form of the thyroid hormone in a cell?
A
FREE T3! It is free because it is not attached to a protein. Do NOT confuse this with rT3. rT3 is the result of deiodination of T4 to inactive
2
Q
What test is used to dx hypoadrenocorticsm?
A
ATCH stim
3
Q
Is diabetes mellitus ever reversible?
A
Yes
4
Q
What are common clinical signs of hypercalcemia?
A
seizures! weird ECGs
5
Q
What is your T4 level if you have primary hypothyroidism?
A
LOW
6
Q
What are some additional causes of low T4?
A
iatrogenic (if P had I131 tx), euthyroid sick syndrome, drug therapy
7
Q
What is the typical hypothyroid signalment
A
middle age, medium to large breed
8
Q
What are your typical hypothyroid CSs?
A
Generalize weight gain, slow/”old”, lethargic, alopecia (truncal), hyperpigmentation, rat tail, seborrhea
9
Q
What is a specific accompanying condition with hypothyroid patients?
A
hypothyroid myxedema. Occurs around peripheral nerves. It is the deposition of mucopolysaccharides in the dermis
10
Q
If you have hypothyroid as a Ddx, what steps are you going to take next?
A
- CBC, chem, U/A.
11
Q
What will you see on your CBC if your patient is hypothyroid?
A
mild anemia, HYPERCHOLESTEROLEMIA!!!
12
Q
If you submit a T4, what would rule out hypothyroidism?
A
Normal T4 level
13
Q
What do low levels of T4 indicate?
A
hypothyroidsim or ESS
14
Q
If you have low T4 and HIGH TSH, what is this supportive of?
A
Hypothyroid dz!
15
Q
What do you treat hypothyroidism with?
A
Levothyroxine
16
Q
Monitoring therapy: what will you see in 1-2 weeks
A
attitude improvement
17
Q
Monitoring therapy: what will you see in 4-6 weeks
A
improvement in derm signs
18
Q
Monitoring therapy: what will you see in 2-4 months?
A
hair regrowth!
19
Q
When I say hyperthyroidism, you say?
A
CATS
20
Q
What is the etiology of hyperthyroidism?
A
excessive production of T4 and T3
21
Q
What is the most common cause of hyperthyroidism?
A
functional adenoma (70% of cats have this bilaterally)
22
Q
What does the thyroid hormone do to glucose?
A
Increases it!!!! it increases gluconeogenic enzymes
23
Q
What happens to muscles with excess thyroid hormone?
A
thinner muscles due to myosin heavy chain destruction
24
Q
What does your typical hyperthyroid patient look like?
A
skinny (weight loss), unkempt, scraggly coat, PU/PD, GI signs (THEY ARE EATING BUT THEY ARE STILL LOSING WEIGHT!)
25
What are you going to find on PE on a hyperthyroid patient?
goiter, "thyroid slip", tachycardia, murmur/gallop
26
What indicates a thyroid storm?
HR >220, hypertensive, blown retinas
27
What are you going to see on your lab work of a hyperthyroid patient?
CBC: stress leukogram (increased WBC, increased neutrophils, decreased lymphocytes)
Chem: INCREASED ALT!!!
U/A: +/- dilute
28
What are your four treatments available for hyperthyroid patients?
1. medical
2. dietary
3. surgical
4. radioactive
29
What is your number one drug for hyperthyroid patients
methimazole
30
How does methimazole work?
inhibits thyroid hormone synthesis by blocking incorporation of iodine
31
What kind of diet should you place a hyperthyroid patient on?
low iodine
32
What is the surgical tx for hyperthyroidism?
thyroidectomy
33
What type of radiation tx are you going to do on your hyperthyroid patient?
I131
34
What is hyperadrenocorticism?
excessive production of glucocorticoids by the adrenal glands
35
How many forms of hyperadrenocorticism are there?
3! pituitary dependent, adrenocortical neoplasia, iatrogenic
36
what percentage of cases does pituitary dependent cushing's account for?
80-85%.
37
What determines a pituitary dependent cushing's patient
functional ACTH secreting pituitary tumor! It will cause bilateral adrenocortical HYPERplasia
38
Why would you classify a chushing's patient, as iatrogenic cushing's?
excessive exogenous steroids; bilateral adrenal atrophy
39
What classifies an adrenal dependent cushing's patient?
adrenocoritcal tumors! usually atrophy of the contralateral gland
40
What is your typical signalment of a cushing's patient?
poodles, boxers, dachshunds, schnauzers, boston terriers, GSDs; Middle aged-old; RARE in cats!
41
What is your typical hx and CSs in a cushing's patient?
PU/PD; polyphagia; pendulous abdomen; panting; thin skin; muscle/ligament weakness and atrophy; calcinosis cutis!!!; hyperpigmentation; CNS signs
42
How are you going to dx cushings?
Hx and CSs usually!
43
But because this is Settles, how are you REALLY going to dx cushings?
With ultrasound, duhhhh
44
What are you going to see on a CBC of a cushings patient?
polycythemia, stress leukogram
45
What are you going to see on a chem of a cushings patient?
HYPERCHOLESTEROLEMIA!
| INCREASED ALP!
46
what other dx test are you going to perform on a cushings patient other than a CBC and chem?
UA! specifically a urine culture and UPC
47
What is important about a UPC in a cushings patient?
a negative UPC will make cushings unlikely. a positive test WILL make cushings likely but it is NOT diagnostic!
48
Is LDDST a diagnostic test?
yes! 95% dx with PDH, 100% dx with AT. Cushingoid dogs do NOT supress
49
What is the test of choice for addisons dz (hypoadrenocorticisim?)
ATCH stim
50
Are you going to use HDDST to diagnose cushings?
Nope!! but if you note suppression, chances are it's a PDH
51
When are you going to use ACTH stim?
with a mild CS/lab abnorm.
patients with concurrent non-adrenal dz
patients with suspected IATROGENIC cushing's dz
patients on phenobarb
52
When are you going to use LDDST?
patients with severe CSs and no evidence of non-adrenal dz
| patients with suspected AT
53
What are your tx options for hyperadrenocorticism?
Mitotane, selegiline, Trilostane, ketoconazole, surgical, radiation
54
What does mitotane do?
it is an adrenal cytoTOXIC agent used to treat PDH
- causes severe, progressive necrosis of the zona fasciculata and zona reticularis
- PERMANENT adrenal atrophy
55
What does selegiline do?
MAO-B inhibitor that may be useful for cognitive dysfunction syndrome in dogs/cats/or PDH patients
- cheap tx
- use on Ps that are negative on labwork but have mild CSs of cushings
56
What does trilostane do?
competitive inhibitor of 3-beta hydroxysteroid dehydrogenase
- reduces the synthesis of cortisol, aldosterone, and adrenal adrogens
- inhibition is REVERSIBLE
- can cause hyperkalemia
57
What does ketoconazole do?
palliative tx in dogs with large, malignant, or invasive AT.
| - reversible inhibitor of steroidogenesis
58
Prognosis of cushing's patients?
PDH - good
malignant AT - POOR
good prognosis if ZERO evidence of local invasion/benign AT
59
What are the two hormones made in the posterior pituitary?
ADH/vasopressin and oxytocin
60
What is the function of ADH/vasopressin?
promotes the reabsorption of water int he CT of the kidneys
61
How does aldosterone work?
promotes Na, Cl reabsorption, K excretion
62
What are the major regulators of aldosterone secretion?
Plasma K+ levels and RAS
63
Where is ADH made?
in the hypothalamus. The nerve cells transport ADH to the pituitary gland where it is released into the blood stream
64
What does ADH do?
decreases urine production, decreases sweating, increased BP
65
If patient is dehydrated?
ADH is released! It wants to conserve water!
66
If patient is overhydrated?
ADH is inhibited! It wants to get rid of excess water!
67
What is aldosterone?
a hormone that affects Na reabsorption. It gets released if blood is diluted and low in volume. It causes more sodium to be reabsorbed
68
is ACTH needed for aldosterone release?
NO!
69
What are your main indicators for an addisonian patient?
dogs, young-middle aged, females >males, ADR, anorexia, lethargy, dehydration, weakness, polyuria
70
What is the definition of "typical" hypoadrenocorticism?
deficient in mineralocorticoids and glucocorticoids due to primary lesions
71
What is something you will not see on the CBC of an addisonian patient
you will NOT see a stress leukogram!!!!
72
What are some clinpath abnormalities you'll see in an addisonian patient?
hyponatremia, hyperkalemia, USG will be isosthenuric, mild hypoglycemia
73
What is going to be your typical maintenance therapy for your addisonian patients?
percorten injections. DOCP injections do NOT possess any glucocorticoid activity; florinef - has some glucocorticoid activity
74
What is the definition of Type I DM
failure of pancreatic beta cells, immune cells destroy beta cells in the pancreas
75
What is the definition of Type II DM
insulin resistance and beta cell burnout with time
- pancreas produces less insulin
- more glucose is in the blood
- insulin moves less glucose into the bells
76
Which diabetes is most common in cats?
Type II DM
77
Which diabetes is most common in dogs
Type I DM
78
What are CSs of diabetes in dogs?
PU/PD/polyphagia
| weightgain leading to weight loss
79
what are some diabetic neuropathies?
pantigrade posture; sensorimotor neuropathy in BOTH pelvic and thoracic limbs
80
Why do you get nerve structural abnormalities with diabetes?
increases in fructose and sorbitol
81
What are CSs of a healthy diabetic?
PU/PD, +/- weightloss, polyphagia, dry/flaky skin, plantigrade stance
82
What are the 3 types of insulin?
short, intermediate, and long
83
What is short insulin?
Ex: regular (glargine, R-insulin)
15 min onset
5-6h duration
84
What is intermediate insulin?
Ex: NPH, lente (vetsulin)
15 min onset
6-12h duration
85
What is long insulin?
Ex: PZI, ultralente
1-2h onset
8-24h duration
86
What kind of dietary therapy are you going to place a diabetic pet on?
high protein, low carb
87
What is weird about fructosamine levels in cats?
Fructosamine levels will be falsely lowered in cats with hypoproteinemia and hyperthyroidism
88
What is total calcium made up of?
iCa - 50%
chelated Ca - 10%
protein bound - 40%
89
What are some sources of active vitamin D?
Fortified food!
fish
dairy
90
What does calcitonin do?
Tones down the Ca! It increases Ca deposition in bones, decreases Ca uptake in intestines, and decreases Ca reabsorption from urine
91
What does the PTH do?
increases Ca release from the bones, increases Ca uptake in intestines, and increases Ca reabsorption from urine
92
What are the CSs of hypercalcemia?
PU/PD, weakness lethargy, inappetence, V+/d+
93
The important Ddx of hypercalcemia
DRAGONSHIT
D= hypervitaminosis D
A= addisons
H= hyperparathyroidism
94
Calcium and phosphorus have what kind of relationship?
INVERSE! Also if the product of [Ca][P] = >70, you will have mineralization of soft tissues!!!
95
Hypocalcemia will result in what?
minor drop in Ca = increase in PTH
| major drop in Ca = increase in PTH and Vitamin D3
96
Etiologies of hypocalcemia
1. primary hypoparathyroidism
| 2. eclampsia
97
How do you dx hypocalcemia?
serum iCa, PTH levels, ECG
98
Calcitriol is:
- manmade
- 1,25-dihydroxycholecalciferol
- Vitamin D3
99
Calciferol is:
ergocalciferol --> 25 hydroxyvitamin D --> 1,25 dihydroxyvitamin D (ACTIVE FORM!)
