Endocrine System Diseases Flashcards

1
Q

What is the main trigger of the Endocrine System?

A

hypothalamus

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2
Q

What are Endocrine Glands?

A
  • basic units of the endocrine system
  • secrete hormones directly into the bloodstream
  • ductless
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3
Q

What are Exocrine Glands?

A

units that secrete their products onto epithelial surfaces through tiny tubes called ducts

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4
Q

What are Hormones?

A

chemical messengers produced by -endocrine glands and secreted directly into blood vessels
-produce effects when they find their receptors in or on cells

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5
Q

What is Negative Feedback?

A
  • endocrine glands stimulated to produce more hormone when it drops below a certain level
  • if hormone level is adequate, gland either slows or stops production
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6
Q

What is Direct Stimulation of Nervous System?

A

secretion of some hormones is stimulated by sympathetic nerve impulses when an animal feels threatened

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7
Q

What are the 2 diseases of the Thyroid Gland?

A

hyperthyroidism

hypothyroidism

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8
Q

Where is the Thyroid Gland located?

A

ventral cervical region along lateral margins of trachea

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9
Q

What hormones are produced by the Thyroid Gland?

A

T3 (triiodothyronine)
T4 (tetraiodothyronine thyroxine)
Calcitonin

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10
Q

What cells in the Thyroid Gland produce T3 and T4?

A

follicular cells

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11
Q

What cells in the Thyroid Gland produce Calcitonin?

A

parafollicular cells

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12
Q

What are T3 and T4?

A

iodine containing hormones

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13
Q

What is the function of Calcitonin?

A

causes calcium deposition in bone which decreases blood calcium concentration

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14
Q

What is Hypothyroidism?

A

clinical state associated with deficency of T4, which causes low cell metabolism in most tissues of the body

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15
Q

What % of dogs acquire Hypothyroidism?

A

90%

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16
Q

What is Primary Acquired Hypothyroidism caused by?

A

idiopathic follicular atrophy
lymphocytic thyroiditis
iodine deficiency, neoplasia, infection

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17
Q

What is the cause of Secondary Acquired Hypothyroidism?

A

RARE

anterior pituitary dysfunction or destruction from neoplasia

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18
Q

What is the most common Endocrine Disease in Dogs?

A

Hypothyroidism

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19
Q

What breeds does Hypothyroidism commonly affect?

A

golden retrievers, doberman, irish setter, schnauzer, cocker spaniel, dachshund

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20
Q

What is the signalment for Hypothyroidism?

A

4-10 yrs old

females

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21
Q

What are the common c/s of Hypothyroidism?

A
weight gain w/out diet change
skin changes
cold intolerance
lethargy/sleeping
exercise intolerance
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22
Q

What Skin Changes can occur with Hypothyroidism?

A
bilaterally symmetric truncal alopecia
alopecia of tail, neck, axillae and other areas of friction
seborrhea
superficial pyoderma
dry, lustless haircoat
hyperpigmentation
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23
Q

What are less common c/s of Hypothyroidism?

A
neuropathies (generalized weakness, ataxia, facial paralysis/paresis, seizures)
GI (constipation, regurgitation caused by megaesophagus)
bloodwork abnormalities ( hyper lipemia, gross lipemia, hyper cholesterolemia)
eye(hyperlipidemia, corneal lipidosis)
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24
Q

How do you diagnose Hypothyroidism?

A

blood tests

hypothyroid dogs have lowered levels of T4

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25
Q

What are some considerations with Hypothyroidism?

A

sick animals and animals on certain meds may have low T4 levels (euthyroid sick syndrome)

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26
Q

What breed of dog has naturally low T4 levels?

A

greyhound

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27
Q

How do you treat Hypothyroidism?

A
thyroid supplement (l-thyroxine)
oral, synthetic levothyroxine
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28
Q

What is client info for Hypothyroidism?

A

supplement for life
daily dosing required
overdose=hyperthyroidism
reduced fat diet (if overweight)

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29
Q

What is Hyperthyroidism?

A

pathologic, sustained, high overall metabolism caused by high circulating concentrations of thyroid hormone

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30
Q

What is the pathophysiology of Hyperthyroidism?

A

autonomously hyperfunctioning nodules
no physiologic controls (functional thyroid adenoma)
secrete T3 and T4

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31
Q

What are c/s of Hyperthyroidism?

A
weight loss
polyphagia
vomiting/diarrhea
PU/PD
tachypnea/dyspnea
hyperactivity
aggression
tachycardia
hypertension
poor body condition
thickened nails
unkempt appearance
large palpable gland
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32
Q

How do you diagnose Hyperthyroidism?

A

palpate enlarged thyroid gland
elevated T4, FT4
x rays for associated heart disease

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33
Q

How do you treat Hyperthyroidism?

A

methimazole (tapazole)
radioiodine treatment (#1)-emitted radiation destroys functioning follicular cells
surgical removal of gland

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34
Q

What are complications of Hyperthyroidism?

A

renal disease/failure unveiled when thyroid levels controlled (2-3 months after meds)
tapazole may not be effective after 2-3 years of treatment

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35
Q

What is the prognosis for Hyperthyroidism?

A

excellent if uncomplicated

if labs show azotemia prior to treatment, prognosis is guarded

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36
Q

What is client info for Hyperthyroidism?

A

cause is unknown
surgery and radiation only cures
cat may become hypothyroid following Rx
after tapazole, blood pressure and kidneys should be checked

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37
Q

What are the 2 diseases of the Parathyroid Glands?

A

hyperparathyroidism

hypoparathyroidism

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38
Q

What is secreted from the Parathyroid Gland?

A

parathyroid hormone (PTH)

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39
Q

What is the primary cause of Hyperparathyroidism?

A

adenoma or carcinoma

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40
Q

What is the secondary cause of Hyperparathyroidism?

A

poor diet;low Ca intake

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41
Q

What are c/s for Hyperparathyroidism?

A
many animals show no c/s
urinary/renal calculi
cardiac arrhythmias, tremors
anorexia, vomiting, constipation
weakness
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42
Q

How do you diagnose Hyperparathyroidism?

A
chemistry panel (increased blood calcium, decrease phosphorus)
PTH assay (elevated)
ultrasound of neck (enlarged glands, abdomen-uroliths)
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43
Q

How do you treat Hyperparathyroidism?

A

surgical removal of dz parathyroid gland
ultrasound guided chemical (ethanol)
ultrasound guided heat (laser) ablation

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44
Q

What is post op care for Hyperparathyroidism?

A

hospitalize for 1 wk
calcium therapy
vitamin D supplements

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45
Q

What are causes of Hypercalcemia?

A
neoplasia
renal failure
hypoadenocorticism
vitamin D rodenticide poisioning
drugs or artifacts
46
Q

What are c/s of Hypercalcemia?

A
PU/PD
anorexia
lethargy
vomiting
weakness
stupor/coma
uroliths
47
Q

How do you diagnose Hypercalcemia?

A

elevated serum calcium levels

low to low-normal phosphorus concentrations

48
Q

How do you treat Hypercalcemia?

A

fluids (0.9% NaCl)
diuretics (furosemide)
steroids

49
Q

What are complications associated with Hypercalcemia?

A

irreversable renal failure

soft tissue calcifications

50
Q

What are causes of Hypocalcemia?

A
parathyroid disease (removal of parathyroid gland accidentally #1)
chronic renal failure
puerperal tetany (eclampsia)
51
Q

What are c/s of Hypocalcemia?

A
restlessness, muscle tremors, tonic-clonic contractions, seizures
tachycardia with excitement
bradycardia in severe cases
hyperthemia
stiffness, ataxia
52
Q

How do you diagnose Hypocalcemia?

A

total serum <6.5 mg/dl

53
Q

How do you treat Hypocalcemia?

A

iv infusion of 10% Ca gluconate solution
diazepam (iv) to control seizures
oral supplements of Ca
improve nutrition

54
Q

What is the function of Insulin?

A

moves glucose into cells to be used for energy

decreases blood glucose

55
Q

What is the function of Glucagon?

A

raises blood glucose
stimulates liver to release glucose
stimulates gluconeogenesis

56
Q

What is Hyperglycemia?

A

excessively high blood glucose levels

57
Q

What is the normal glucose level in dogs?

A

60-120 mg/dl

58
Q

What is the normal glucise level in cats?

A

70-150 mg/dl

59
Q

What is Diabetes Mellitus?

A

disorder of carbs, fats and protein metabolism caused by an absolute or relative insulin deficiency

60
Q

What is Type 1 DM?

A

insulin dependent

very low or absent insulin secretory ability

61
Q

What is Type 2 DM?

A

non insulin dependent

inadequate or delayed insulin secretion relative to the needs of the patient

62
Q

What are the causes of DM?

A

chronic pancreatitis

immune mediated diseases (beta cell destruction)

63
Q

What are predisposing/risk factors of DM?

A
cushing's
acromegaly
obesity
genetic predisposition
drugs (steroids)
64
Q

What age/sex does DM affect most?

A

dogs: 4-14, females 2x more likely
cats: all ages, but 75% are 8-13yrs, neutered males

65
Q

What breeds does DM affect most?

A

poodles, schnauzers, keeshonds, cairn terriers, dachshunds, cockers, beagles

66
Q

When do c/s of DM develop?

A

exceeds capacity of renal tubular cells to reabsorb

dogs: BG > 180-220 mg/dl
cats: BG >200-280 mg/dl

67
Q

What systems does DM affect?

A
endocrine/metabolic
hepatic
opthalamic
renal/urologic
nervous
musculoskeletal
68
Q

What are c/s of DM?

A
polyuria
polydipsia
polyphagia
weight loss
dehydration
cataract formation (dogs)
plantigrade stance (cats)
69
Q

What is Diabetic Ketoacidosis?

A

true medical emergency secondary to absolute or relative insulin deficiency causing hyperglycemia, ketoemia, metabolic acidosis, dehydration and electrolyte depletion

70
Q

How is Diabetic Ketoacidosis diagnosed?

A

ketones in urine or in blood

71
Q

What are c/s of Diabetic Ketoacidosis?

A
all of the DM signs
depression
weakness
tachypnea
vomiting
odor of acetone on breath
72
Q

How do you treat Diabetic Ketoacidosis?

A

IV fluids 0.9% NaCl
regular insulin to decrease BG
monitor BG q 2-3hrs
when BG is normal, switch to long acting insulin

73
Q

How do you diagnose Diabetic Ketoacidosis?

A
CBC
biochem panel 
UA
low electrolytes
blood gases
fructosamine levels
74
Q

What diet should a dog with DM be placed on?

A

high fiber, complex carbs

slows digestion, reduces post prandial glucose spike, promotes weight loss, reduces risk of pancreatitis

75
Q

What diet should a cat with DM be placed on?

A

high protein, low carbs

76
Q

What oral hypoglycemics should be used in treatment of DM?

A

sulfonylureas-glipizide (cats)

alpha glucosidase inhibitors (dogs)

77
Q

What is client info for DM?

A

lifelong insulin replacement therapy
refridgerate insulin, mix gently
if animal doesn’t eat - no insulin

78
Q

What is Hypoglycemia?

A

low blood glucose levels

79
Q

What are causes of Hypoglycemia?

A
neonatal and juvenile
septicemia
neoplasia
starvation
iatrogenic - insulin overdose
portosystemic shunt
80
Q

What are causes of Insulin Shock?

A

insulin overdose
too much exercise
anorexia

81
Q

What are c/s of Insulin Shock?

A

weakness
incoordination
seizures
coma

82
Q

How do you prevent Insulin Shock?

A

consistant diet/consistent exercise
monitor urine/blood glucose at same time each day
feed 1/3 insulin, the rest 8-10hrs later
have sugar supply handy

83
Q

What is the cause of Insulinoma?

A

tumor of beta cells, secreting excess insulin

84
Q

What are c/s of Insulinoma?

A
prolonged hypoglycemia
weakness
ataxia
muscle fasiculations
posterior paresis
brain damage
seizures
coma
death
85
Q

How do you diagnose Insulinoma?

A
chem panel (low glucose, high insulin)
observations (symptoms occur after fasting or exercise)
86
Q

How do you treat Insulinoma?

A

removal of tumor
acute at home (administer glucose)
acute at hosp ( adm. glucose 50% dextrose)
chronic care (3-6 small meals/day, glucocorticoid therapy, diazoxide, octreotide injections)

87
Q

What is EPI?

A

exocrine pancreas insufficiency

inability to process nutrients efficiently due to lack of production of enzymes from pancreas

88
Q

What breeds is EPI most commonly found?

A

german shepherds

rough collies

89
Q

Where is EPI most commonly a result of in cats?

A

chronic pancreatitis

90
Q

When is EPI usually evident?

A

when 85%-90% of pancreas is unable to secrete enzymes

91
Q

What are c/s of EPI?

A

weight loss, no change in diet or appetite
persistant tarry diarrhea
flatulence
poor haircoat

92
Q

How do you test for EPI?

A

TLI ( trypsin-like immunoreactivity)

detects trypsin and trypsinogen

93
Q

How do you treat EPI?

A

enzymatic supplements

viokase powder

94
Q

What is client info for EPI?

A

life long treatment
expensive
can be well controlled
should not be bred

95
Q

What are the 2 diseases of the Adrenal Glands?

A

cushing’s (hyperadrenocorticism)

addison’s (hypoadrenocorticism)

96
Q

What is Cushing’s Disease?

A

hyperadrenocorticism

disorder caused by deleterious effects of high circulation cortisol concentrations on multiple organ systems

97
Q

What organ systems are affected by Cushing’s?

A
renal
skin
cardiovascular
respiratory
endocrine/metabolic
musculoskeletal
nervous
reproductive
98
Q

What are the effects of excess glucocorticoids?

A

suppress inflammation
suppress immune system
inhibit cartilage growth, development and repair

99
Q

What are c/s of Cushing’s?

A
bilaterally symmetrical alopecia
pot belly
pyoderma
PU/PD
muscle wasting
thin coat
calcinosis cutis
abnormal gonadal function
100
Q

Where is Calcinosis Cutis usually seen?

A

dorsal midline
ventral abdomen
inguinal region
skin is usually thin and atrophic

101
Q

How do you diagnose Cushing’s?

A
chem panel ( increased ALP, ALT, CHOL, BG, decreased BUN, lipemia, low USG)
urine cortisol/creatinine ratio (normal = no cushings, elevated = cushings)
102
Q

What are the 3 tests to diagnose Cushing’s?

A

ACTH stimulation test
low dose dexamethason suppression test
high dose dexamethasone suppression test

103
Q

What is the ACTH stimulation test?

A

normal pt. show increase of plasma cortisol
pituitary dependant diseases : excess ACTH release
adrenal tumors (exaggerated cortisol response)
doesn’t differentiate between pit disease and adrenal tumor

104
Q

What is the Low Dose Dexamethasone Suppression Test?

A

inject low dose of steroid
measure plasma cortisol at 0, 4, 8 hrs
Interpretation: normal= decrease, pit and adrenal tumors = no affect @ 8hrs

105
Q

What is the High Dose Dexamethasone Suppression Test?

A

0.1 mg/kg IV
collect plasma cortisol at 0,4,8 hrs
Interpretation: pit. disease= 70-75% show decrease at 4 or 8hr, adrenal tumor=no change

106
Q

How do you treat Cushing’s?

A
sugical removal (not pituitary)
medical treatment: lysodren (necrosis of z fasiculata, z reticularis)
107
Q

What is an alternative to Lysodren?

A

trilostane

less side effects

108
Q

What is Addison’s Disease?

A

hypoadrenocorticism
disorder caused by deficient production of glucocorticoids (cortisol) or mineralocorticoids (aldosterone) or both
secondary disease caused by chronic admin of corticosteroids

109
Q

What are c/s of Addison’s?

A
due to mineralcorticoid (aldosterone) deficiency
lethargy, weakness, anorexia, wt. loss
vomiting/diarrhea
PU/PD, dehydration
bradycardia
110
Q

How do you diagnose Addison’s?

A

Na:K ratio
increased BUN, CREA and Ca++
decreased blood glucose and albumin
ACTH stimulation (normal = increase cortisol, abnormal= low, unchanged cortisol levels)

111
Q

How do you treat Addison’s?

A

acute crisis ( normal saline, glucorticoid replacement: dexamethasone or prednisone, mineralocorticoid replacement: florinef, percortin)

112
Q

How do you treat chronic Addison’s?

A

glucocorticoid replacement : prednisone, predisolone
mineralocorticoid replacement : florinef, percortin V
monitor electrolytes, BUN/CREA, c/s