Endocrine Diseases Flashcards
(97 cards)
1
Q
Hyperadrenocorticism is also know by two other names
A
- Cushing’s disease
- Cushing’s syndrome
2
Q
Cushing’s disease is ______ to pituitary release of excess ACTH
A
secondary
C’s d AKA pituitary-dependent hyperadrenocorticism (PDH)
3
Q
Cushing’s __________ in primary hyperadrenocorticism is d/t what?
A
syndrome; d/t adrenal tumor that increases cortisol
C’s s AKA adrenal-dependent dyperadrenocorticism (ADH)
4
Q
___% of hyperadrenocorticism are due to anterior pituitary adenomas and are called PDH
A
80%
5
Q
Classic signs of hyperadrenocorticism in dogs
A
- PU/PD
- Pendulous abdomen
- bilateral alopecia
6
Q
Thin skin is the hallmark sign of hyperadrenocorticism in what species?
A
cats
7
Q
Signs of hyperadrenocorticism in horses
A
- long hair coat out of season
- broodmares with recent history of infertility
- laminitis, weight loss, PD, inability to masticate properly
- muscle wasting
8
Q
Challenges of diagnosing Cushings in dogs (4)
A
- incr serum enzymes
- plasma [glucose] can be increased
- plasma [total T4] can be decreased
- hypercholesterolemia, decrease BUN
9
Q
How is a low-dose dexamethasone suppression test used for Cushing’s testing?
A
- should lead to a dec in plasma [cortisol] in NORMAL animals
- No change = indicative of hyperadrenocorticism
10
Q
How is a corticotropin stimulation test used for Cushing’s testing?
A
- diagnostic for enlarged adrenal glands
- chronic pit. stimulation causes exaggerated corticotropin response
11
Q
What can an abdominal ultrasound tell you for Cushing’s?
A
Both adrenals of same size = secondary locus
One adrenal enlarged relative to other = primary locus (the enlarged one is the diseased one)
12
Q
4 common drugs in the medical management of ADH or PDH
A
- mitotane
- ketoconazole
- L-deprenyl
- trilostane
13
Q
Beyond medical management, what else can be done for adrenal neoplasm?
A
surgery (adrenalectomy)
14
Q
This disease is also called Addison’s-like syndrome
A
Hypoadrenocorticism
15
Q
What is wrong endocrinologically with hypoadrenocorticism?
A
- deficient glucocorticoid and mineralocorticoid synthesis
* increase in ACTH, renin, Angiotensin
16
Q
Causes of Addison’s
A
- usually primary, d/t lymphocytic infiltration of adrenal cortex
- iatrogenic Addison’s = secondary to mitotane treatment for Cushing’s
- autoimmune, opportunistic infections in AIDs destroy adrenal cortex
17
Q
Common patients for Addison’s?
A
middle-aged dogs
18
Q
Signs of Hypoadrenocorticism
A
- hyperkalemia (arrhythmias)
- hyponatremia (dec blood vol)
- muscle atrophy, depression, weight loss
- bradycardia/ widened QRS complex
- hypotension
- salt craving!
19
Q
KEY sign of hypoadrenocorticism
A
bracycardia/widened QRS complex
20
Q
Treatment of hypoadrenocoricism
A
Replacement therapy
- mineralocorticoids
- glucocorticoids
- Deoxycorticosterone pivalate (DOCP) has both properties
21
Q
Induced hyperadrenocorticism (Cushing’s syndrome)
A
- iatrogenic
- overuse of glucocorticoids
22
Q
Induced hypoadrenocorticism
A
- iatrogenic
- adrenalectomy
23
Q
Induced hypothroidism
A
- iatrogenic
- treatment of goiter
24
Q
What hormone is related to Diabetes Insipidus?
A
Vasopressin -specifically a loss of vasopressin action
25
DI can have two forms. What are they?
- hypothalamic form - lesion in area where vasopressin is formed
- nephrogenic insensitivity of vasopressin
26
Signs of DI
- PU/PD
- urine with a low specific gravity
- dehydration
27
Differentials for DI
- PD animals with overhydration
| - dehydration via water restriction
28
Pathognomonic sign of DI
dilute urine
29
If the problem originates in the hypothalamus, what type of DI is it?
Central DI
30
If the problem is in the nephron, what type of DI is it?
Nephrogenic DI
31
Modified H2O deprivation test for DI
- Determine if endogenous ADH release can occur = IF inc. ADH release and [ ] of urine, THEN NOT central DI
- Confirm via response to exogenous ADH = IF response to exogenous ADH, THEN NOT nephrogenic
32
Why is it important to recognize renal failure prior to a water deprivation test?
failure may lead to incorrect/inconclusive diagnosis or morbidity in patients
33
Treatment for Hypothalamic DI
Rx vasopressin IM every 1-3 days
34
Treatment for Nephrogenic DI
-thiazide diurectics - have paradoxical effect on PU/PD
35
Pit. Dwarfism
- fairly rare
- deficiency in GH
- commonly seen in German Shepherd 2-6 months old
* autosomal defect in German Shepherds d/t cystic Rathke's pouch
36
Clinical Signs of Pit. Dwarfism in young animals
- proportional dwarfism
- delayed dentition
- delayed closure of growth plates
- hair coat abnormalities (retention of puppy coat, no primary guard hairs)
- Behavioral abnorms
* reduced exercise performance
* retain puppy-like behavior
37
Clinical Signs of Pit. Dwarfism in adult animals
- abnorm. weight gain
- reduced lean mass
- reduced exercise performance
- osteopenia
38
Differential Diagnosis for Pit. Dwarfism
- hypothyroid dwarfism
- portosystemic shunt
- diabetes mellitus
- hyperadrenocorticism
- malnutrition
- parasitism
39
Acromegaly (AKA hypersomatotropism)
- excess GH, post-puberty
| - d/t: pit. adenomas or pit. hyperplasia
40
Clinical Signs of Acromegaly
- KEY: net weight gain lean body mass in animals w/ Diabetes Mellitus
- enlarged jaw, tongue, forehead, and extremities
- striking hirsutism (excessive hair growth), failure to shed
41
Diagnosis of Acromegaly
plasma [GH] and/or glucose suppression test
42
Differential diagnosis for Acromegaly
-Cushing's syndrome (hyperadrenocorticism
43
Treatment of Acromegaly
radiation therapy
44
Diabetes Mellitus
- "sweet diuresis"
| - absolute or relative deficiency of insulin
45
Clinical Types of Diabetes Mellitus (3- this is not Type I/II)
- nonketotic
- ketoacidotic
- nonketotic hyperosmolar syndrome
46
Signs of DM
- PU (and urinary tract infections)
- PD
- bacterial cystitis in females (glucose in urine)
- cataracts
- most patients are obese, but w/ recent weight loss and polyphagia
- hepatomegaly (enlarged liver)
- acetone breath (ketones)
47
Why do cataracts form in relation to DM?
sorbitol or fructose trapped in lens
48
Diagnosis of DM
- persistent fasting hyperglycemia
| - evidence of chronic hyperglycemia
49
Control of DM
Goals
- normal bodyweight
- normal physical activity
- normal water comsumption/urine output
Insulin therapy
50
Type I DM
- insulin-dependent diabetes
| - inadequate insulin production in pancreas
51
Type II DM
- insulin-independent diabetes
- more likely inherited
- adequate/nearly adequate insulin production by pancreas
52
As there is adeqaute/nearly adequate insulin production in Type II DM, why are there problems?
- peripheral insulin resistance = dec GLUT4 transporters
| - excessive glucose production by the liver
53
Type ___ DM is also assoc. with obesity
II
54
T/F: Insulin therapy is often part of treatment for both types of DM in companion animals
True
55
T/F: Zinc complexes slow release of insulin
True
56
Insulinoma
- tumors of pancreas that secrete insulin
- more common in ferrets than any other pet = ferrets older than 5 yrs are susceptible
- can be small multiples or a single nodule
57
Symptoms of Insulinoma
- detached, unengaged mood, trance
- lethargy, depression
- weight loss
- difficulty with rear legs
- seizures, fainting (advanced cases)
58
Diagnosis of Insulinoma
hypoglycemia after 4 hour fast
59
Treatment of Insulinoma
best option = surgery
60
What is the largest purely endocrine gland?
Thyroid
61
Is the thymus normally palpable?
NO!
62
What is a palpable enlargement of the thymus called?
goiter
63
Job of follicular cells/ follicles of the thymus? (3)
- collect and transport iodine
- synthesize and secrete thyroglobulin
- remove and secrete T3 and thyroxine (T4)
64
Job of parafollicular cells of the thymus? (2)
- secrete calcitonin
| - calcium and phosphorus metabolism
65
How do the parafollicular cells help with calcium metabolism?
- decrease blood Ca2+
| - increase urinary loss of Ca2+
66
In regards to T3/T4, is the thymus pit. dependent or independent?
Pit. Dependent
67
The thymus is pit. independent for parafollicular cells. What regulates their actions?
[Ca2+] in the blood
68
T4 is a __________ for T3
prohormone
69
Actions of calcitonin
- lower blood Ca2+ and phosphorus
| - antagonistic action to parathyroid hormone
70
How does calcitonin lower blood Ca2+ and phosphorus? (2)
- blocks osteoclasts action (inhibits bone resorption) = Ca2+ deposition
- blocks renal reabsorption of calcium and phosphorus = Ca2+ excretion
71
A non-neoplastic, non-inflammatory enlargement of the thyroid is a ____________
goiter
72
Causes of Goiter (3)
- iodine-deficient diet = 90%
- goiterogenic compounds
- genetic defects of thyroid hormone synthesis
There are other things as well.
73
What can cause an excess of thyroid follicular hormone?
- usually primary hyperthyroidism
| - thyroid adenoma
74
Clinical Signs/ Lab Findings of Hyperthyroidism
- increased metabolic rate
- goiter - 90%
- weight loss
- Polyphagia
- PU/PD
- hyperactivity, nernousness, insomnia
- tachycardia
- cardiac murur
- diarrhe and increased fecal volume
- serum enzymes may be elevated = stress leukogram
75
Beyond clinical signs, what are some other things that might be seen with hyperthyroidism? (3)
- heat insensitivity = feel hot, so will seek cold
- unkempt coat
- protuding eyes (more in human med)
76
Diagnosis of hyperthyroidism
- serum total T4 > 4 microgram/ decaliter
- borderline cases differentiated by TSH stimulation test
- thyroid scan - only necessary if no goiter
77
Why are borderline cases of hyperthyroidism differentiated by TSH stimulation test?
tumors are not stimulated by TSH
78
Treatment of Hyperthyroidism
- antithyroid drugs
- radioactive iodine
- surgery = partial/complete thyroidectomy
- propanolol for tachycardia and excess adrenergic effects
79
Antithyroid drug can be used in the treatment of hyperthyroidism. Two examples methimazole and propylthiouracil. Why are they used?
methimazole = inhibits thyroperoxidase
propylthiouracil = goiterogenic compound
80
Hypothroidism Signs (5)
- cretinism
- myxedema
- lymphocytic thyroiditis
- iodine deficiency
- heat seeking
81
How much of the thyroid may be non-functional before clinical hypothyroidism is apparent?
>75%
82
Additional signs of hypothyroidism
- poor response to TSH stimulation
- alopecia on dorsal proximal tail
- lethargy
- infertility
- weight gain
- hyperpigmentation of skin and thickening of skin
- bracycardia, cardiac arrhythmias, hyperlipidemia
83
Diagnosis of Hypothyroidism
- hypercholesterolemia couple with other clinical signs
- serum total T4 (and TSH)
- biopsy of thyroid
84
Treatment of Hypothroidism
- Administer synthetic T4 (levothyroxine)
| - Allow 6 weeks for improvement
85
Hyperparathyroidism
- excess PTH
- results in disturbances of serum levels of Ca2+ (increases serum Ca2+)
- affects metabolism of bone
86
How is the metabolism of bone affected by hyperparathyroidism?
- increased bone resorption
- decreased radiographic density
- incomplete fractures
87
Signs of hyperparathyroidism
- depressed mentation
- muscular weakness
- peptic ulcers
- lethargy
- renal failure
88
Primary hyperparathyroidism
- pit. independent
- less common than secondary hyperparathyroidism
- adenoma of chief cells
89
Signs of primary hyperparathyroidism
- calcification of soft tissues
- loss of lamina dura of teeth
- subperiosteal cortical resorption
- mineralization of CT = relatedly, secondary renal probs
- hypercalciuria, hypercalcemia
- hyperphosphaturia, HYPOphosphatemia
90
Secondary hyperparathyroidism (RENAL)
- RENAL hyperparathyroidism (secondary) = caused by chronic renal failure
- renal damage reduces 1,25-Vit. D synthesis
As [phosphate] increases, [Ca2+] decreases
- hyperphosphatemia
- NORMOcalcemia, HYPOcalciuria
- rubber-jaw disease, loose teeth
91
Secondary hyperparathyroidism (NUTRITIONAL)
-caused by nutritional deficiencies, mineral imbalances
ETIOLOGY
- low calcium content of foods
- excess phosphorus content of food
- ratio: low Calcium, high phosphorus
- inadequate Vit. D
- hyperphosphaturia
- mild hypocalcemia, hypocalciuria
- vertebral fractures, lameness, reluctance to move
92
Hypoparathyroidism
hyposecretion of PTH due to:
- lymphocytic parathyroiditis
- surgery for hyperthyroidism
93
Clinical Signs of hypoparathyroidism
-serum calcium must be
94
Lab findings/ diagnosis of hypoparathyroidism
-serum calcium 5.0 mg/dl
95
Other causes of hypocalcemia
- hypoalbuminemia
| - hypercalcitonism
96
Treatment of Hypoparathyroidism, acute hypocalcemia
IV calcium gluconate
97
Treatment of Hypoparathyroidism, chronic hypocalcemia
- oral calcium carbonate
- oral Vit. D
- low phosphorus diet
