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Equine > SA 3 > Flashcards

SA 3 Flashcards

1
Q

Zona glomerulosa makes______ zona fasiciculata makes________

Zona reticularis makes_____

A

Salt- aldosterone
Sugar- glucocorticoid
Sex- androgens

Medulla- catecholamines (epi norepi)

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2
Q

Aldosterone is regulated by renin- angiotensin- aldosterone system (RAAS) and is released in response to

A

Hypovolemia
Hyponatremia
Hyperkalemia

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3
Q

Primary (adrenal gland lesion) hypoadrenocorticism (addisons) is caused by what

A

Immune mediated destruction of adrenal cortex
Iatrogenic destruction by drugs or surgery
Exogenous steroids
Neoplasia
Granulomatous disease

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4
Q

Where is the lesion of a secondary addisons

A

Pituitary gland lesion
Rare
Decreased ACTH

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5
Q

What is the difference between typical and atypical addisons

A

Electrolyte abnormalities
No aldosterone
Supplementation of cortisol and aldosterone

Atypical
No electrolyte abnormalities
Cortisol deficiency signs (cortisol supplement only)
Normal partial or no aldosterone production but elctrolytes not effected by aldosterone

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6
Q

What are breeds and gender predisposed to addisons

A 
Poodle
Water dog
NSDTR
bearded collie
Young middle aged females
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7
Q

What is Addison also known as

A

The great pretender because signs are variable and resemble other diseases

  • waxing and waning GI signs
  • PU/PD, weakness, weight loss
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8
Q

What are signs of a crisis addisons

A 
Weakness
Dehydration 
Pale MM
Decreased pulse strength 
Bradycardia
Hypothermia
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9
Q

What are some lab abnormalities of a addisons dog

A 
No stress luekogram 
Non-regenerative anemia 
Isosthenuria 
Medullary washout due to low sodium
Renal injury from hypovolemia (azotemia)
Low Na, high K, high Ph
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10
Q 
Atypical addisons only show which of these signs from a addisons cL signs list.
A. Vomiting diarrhea
B. Hypoglycemia
C. PU/PD
D. Low Na
E. High K
A

A and B. Typical is all

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11
Q

How is addisons Dx

A

Na:K ratio
Baseline cortisol
ACTH stimulation test- gold standard (won’t increase cortisol after administration)

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12
Q

If cortisol is >2 then

A

It’s not addisons

If below 2 then need more tests

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13
Q

What is the treatment for crisis addisonian

A

Fluids
Supportive care
Symptomatic care
ACTH stim
Glucocorticoids if unstable (1 time dexamethasone not pred)
Once electrolytes stable then mineralcorticoids

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14
Q

What is the treatment of chronic addisons

A

Glucocorticoids- prednisone daily
Mineralcorticoid - DOCP (percortin/ zycortal) IM or SQ Injection- 1 per month
Florinef (fludrocortisone)

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15
Q

When may pred dose need to be decreased

A 
PU PD
Polyphagia
ALP> ALT
GI signs then too low
Good prognosis
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16
Q

Hyperadrenocorticism is due to a tumor in the ______ or the _____

A

Pituitary gland 80%
adrenal gland 20%
Dog

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17
Q

What are common signalments for dogs with hyperadrenoacorticism

A

Middle to older age
Toy breeds (but any breed can be affected)
Females

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18
Q

What are presenting signs for hyperadrenocortism

A 
PU PD- blocked ADH
Polyphagia
Panting
Thin skin Truncal alopecia- symmetrical 
Secondary infections 
Adult onset demodicosis
Calcinosis cutis (decreased Ca under skin)
Hyperpigmentation 
Dilute urine
Weakness
Muscle wasting 
Potbelly
Hepatomegaly
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19
Q

Why does a macro adenoma cause CNS signs

A 
Compression in the brain 
Inappetance 
Dullness
Circling
Ataxia
Behavior changes
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20
Q

What lab work changes will you see with hyperadrenocorticism

A 
Stress leukogram
Thrombocytosis
Increased ALP
Increased cholesterol 
Increased alt (mild) swollen cells
Elevated fasting blood glucose
Isosthenuria 
Proteinuria 
UTI
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21
Q

What can be seen on an X-ray of a dog with hyperadrenocorticism

A

Hepatomegaly

Rarely- metastasis from adrenal carcinoma

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22
Q

If cushings is suspected what are the first diagnostic tests

A

Urine cortisol creatinine ratio
ACTH stimulation test (high)
Low dose dexamethasone suppression test

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23
Q 
What are benefits of urine cortisol creatinine ratio test for cushings
A. Easy
B. Cheap
C. Specific
D. Sensitive 
E. Preformed at hospital visit
A

A B D

Not specific. Not at hospital (owner brings it)
Rules out cushings but doesn’t diagnose it

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24
Q

T/F ACTH stimulation testing determines the difference between PDH and ADH

A

False. Only test for iatrogenic cushings
Cannot differential between ADH PDH
Is fast with good specificity and sensitivity

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25
Q

Iatrogenic cushings looks like the dog has ______ but will test as _______

A

Cushing

Addison

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26
Q

ACTH stimulation test with a post cortisol value above ____ along with clinical signs is diagnostic for cushings

A

21

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27
Q

A Pituitqru tumor response produces high amounts of ____ thus higher ____ from the adrenal gland

A

ACTH
Cortisol
ACTH stim test will have increased cortisol

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28
Q

Adrenal tumor response produce ______ which gives a negative feedback to the pituitary thus decreasing _______

A

Cortisol
ACTH
ACTH stim test will either be elevated or normal cortisol

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29
Q

Which is false regarding iatrogenic cushings
A. Cushings signs
B. Cushings blood abnormalities
C. Atrophy of adrenal glands= lack of steroid production
D. Inability of adrenal gland to respond to ACTH or produce cortisol
E. ACTH stim test shows normal cortisol pre and post

A

E- pre and post low

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30
Q

What are benefits of the low dose dexamethasone suppression test

A 
Less expensive than ACTH stim
Good sensitivity 
Fair specificity 
Differentiate between PDH and ADH
(Is time consuming and is more effected by non adrenal illnesses)
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31
Q

How is low dose dex suppression test done

A

Baseline cortisol
Dex
4hr
8hr

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32
Q

If the LDDST is above ____ at hour 8 then it is cushings

A

1.4

4 hr is for differentiation

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33
Q

LDDST and HDDST can diagnose what type of cushings

A

PDH not ADH (dex at any dose does not suppress cortisol secretion because adrenal gland don’t respond to negative feedback)

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34
Q

With PDH ~70% of dogs will show suppression in LDDST and LDDST. Dogs that have PDH but do not suppress (dex resistant) likely have

A

Large pituitary tumor

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35
Q

Suppression at hour 4 in dex tests with a rebound at hour 8 is called a

A

Escape pattern

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36
Q

In ADH the dexamethasone will

A

Not be suppressed at any point

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37
Q

In a LDDST, PDH is diagnosed if

A

At hour 4 the cortisol is below lab cutoff or <50% of baseline
Or
At hour 8 the cortisol is <50% baseline but greater than the lab cut off

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38
Q

ACTH concentrations are expected to be higher with (PDH/ ADH) and suppressed with (PDH/ ADH)

A

PDH

ADH

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39
Q

What is the most accurate stand alone test for differentiation of cushings

A

Endogenous ACTH

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40
Q

In an ultrasound a PDH would show what on the adrenals. An ADH would show what

A

PDH- bilaterally enlarged or normal adrenal glands- CT recommended
AFH- 1 enlarged or mass

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41
Q

Endogenous ACTH has significant overlap between normal levels of ACTH and (PDH/ADH)

A

PDH. ADH = little to no overlap for normal. (Very low)

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42
Q

What are some potential complications or infections with cushings

A 
Hypertension
Pyeloneohritis UTI
Pancreatitis 
Urinary Calculi
GB mucocele
DM
Hypercoaguble (pulmonary thromboembolism)
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43
Q

Medical is the treatment of choice for (PDH/ADH) while surgery is the treatment of choice for (PDH/ADH)

A

PDH

ADH

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44
Q

Which of the following drugs that are recommended for PDH treatment
A. Mitotane- chemo
B. Trilostane- steroid that prevents cortisol
C. L- Deprenyl
D. Ketoconazole
E. Radiation

A

ABE

If sx- hypophysectomy
A B also for ADH
A- less common for SE but more severe than B
Significant monitoring

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45
Q

What surgery is preformed for ADH

A

Adrenalectomy

Better chance of survival compared to medical tx

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46
Q

Calcitriol is activated by _______ in the ______

A

Vitamin D

Kidneys

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47
Q

The chief cells of the parathyroid glands regulate what 2 elements

A

Ionized Ca

Phosphorus

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48
Q

If serum calcium goes up then _______ will go down

A

Phosphorus

And PTH

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49
Q

PTH (increases/ decreases) resorption (release) of calcium and phosphorus, (increases/ decreases) calcium excretion and (increases/ decreases) phosphorus excretion

A

Increases
Decreases (resorption of Ca)
Increases

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50
Q

PTH acts on the kidney to stimulate _____ activation via increased activity of 1-a-hydroxylase. This then acts on the SI to increases absorption of _______ and ______

A 
Vitamin D (calcitriol)
Calcium and phosphorus
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51
Q

Calcitriol acts on the Parathyroids glands via a negative feedback loop to decrease ____

A

PTH

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52
Q

Calcitonin’s primary function is to _____

A

Decreased serum calcium

Decreases osteoclasts formation

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53
Q

When calcium goes down ____ goes up

A

PTH

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54
Q

What are the hypercalcemia differentials

A 
Hyperparathyroidism
Osteolytic
Granulomatous Dz
Spurious
Idiopathic 
Neoplasia 
Young
Addisons
Renal Dz
Vitamin D toxicosis
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55
Q

PTH will cause (high/low) phosphorus while calcitriol will cause (high/low) phosphorus

A

Low

High

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56
Q

What causes PHP (excessive production of PTH)

A

Parathyroid adenoma (1)
Parathyroid carcinoma
Parathyroid hyperplasia

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57
Q

What are common signalments for PHP

A

Middle age or older

Keeshond lab golden GSD

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58
Q

T/F unlike other causes of hypercalcemia, dogs with PHP are usually not clinical

A

True- other causes= very sick dog

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59
Q

T/F A dog with PHP usually presents normally with only subtle non specific signs or related to urinary issues

A

True

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60
Q

What are lab findings of a dog with PHP

A 
Maybe mild anemia
Hypercalcemia
Low phosphorus 
Iso- hyposthenuria
UTI
Calculi
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61
Q

A CT of a dog with PHP may show

A

Metastasis

Thyroid mass- difficult to visualize

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62
Q

Elevated or inappropriately normal PTH along with elevated iCa confirms _____

A

PHP

Elevated PTHrp supports hypercalcemia of malignancy

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63
Q

What are some treatments for PHP when there is severe hypercalcemia

A 
Fluids
Diuretics 
Glucocorticoids 
Bisphosphates - prevent bone destruction 
Calcitonin- short action though
Surgical removal
Radio frequency heat ablation 
Ethanol ablation
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64
Q

What must be done before a PHP surgery

A

Start on prophylactic calcitriol (vitamin D) then taper over 2-4 months
Ca carbonate after sx 2-4 months taper

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65
Q

What is seen in hypoparathyroidism

A

Decreased Ca
Increased Ph
Decreased PTH= reduced bone resorption, decreased Ca resorption and increased Ph from Kidney

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66
Q

What are the 4 causes of HypoPTH

A
  1. Suppressed secretion of PTH w/o destruction (Trauma)
  2. Atrophy (post op PHP Sx)
  3. Iatrogenic (removal of thyroid glands)
  4. Idiopathic -primary (immune mediated)
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67
Q

What are differentials for hypocalcemia

A 
Phosphate enema
Eclampsia 
Albumin decrease
CKD
Ethylene glycol /AKI
PTH deficiency 
Acute pancreatitis 
Intestinal malabsorption 
Nutritional (vitamin D deficiency)
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68
Q

What is a common signalmen for hypoPTH

A 
Dogs>cats
Female> male
Poodle
Schnauzer
GSD
lab
Terrier
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69
Q

What are signs of HypoPTH

A 
Seizure
Facial rubbing and biting at paws
Tetany
Stiff
Anorexic
Lethargy 
Pant
Cataracts fever 
CV abnormalities
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70
Q

A dog with hypoPTH should have low Ca and what else

A

Increased Ph
PTH low (or inappropriately normal)
Decreased calcitriol

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71
Q

What is a treatment plan for a dog with hypoPTH

A

Emergency :Calcium gluconate (IV) over 10-30 min
SQ- skin sloughing or inflammation possible
Chronic: calcitriol (lifelong) Ca carbonate oral (tums) that can be tapered once stable

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72
Q

Which thyroid hormone is the most biologically active and is up to 3-4x more potent

A

T3 enters cell more rapidly

Only 20% made in thyroid remained is by peripheral deionization of T4

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73
Q

What are possible etiologies of hypothyroid

A

Thyroiditis
Idiopathic atrophy
Bilateral neoplasia (uncommon)

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74
Q

What breed tend to be more effected by hypothyroid

A 
Borzoi
Toy fox terrier
Beagle
Setter
Dave’s 
Golden 
Doberman
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75
Q

What are some metabolic signs seen with hypothyroid

A 
Decreased rate
Lethargy 
Weight gain
Cold intolerant 
Dull
Unwilling to exercise
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76
Q

What are some dermatological signs seen with hypothyroid

A 
Symmetric alopecia
Hyperpigmentation 
Dry scaly skin
Pyoderma
Otitis
Seborrhea
Dry brittle hair coat
Myxedema (thickening of skin)
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77
Q

What are some neurological signs seen with hypothyroid

A

PNS- weak, exercise intolerant to ataxia or paresis
CNS- seizures central vestibule dz and mentation changes
CN- facial nerve paralysis vestibule dz

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78
Q

What are some cardiovascular signs seen with hypothyroid

A 
Bradycardia
Low QRS voltage
Inverted T
Reduced LV pump function 
Weak heart
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79
Q

What are some other signs seen with hypothyroid

A

Reproductive dysfunction
Ocular changes
Mega esophagus
Lar par

80
Q

T/F hypothyroidism can be tested without history clinical signs or physical exams that point to it

A

False- only test with clinical signs

81
Q

What is seen in blood work of a dog with hypothyroid

A

Normochromic normocytic non regenerative anemia
Fasting hypertriglyceridema
Fasting hypercholesterolemia*
Increased ALP or other liver enzymes

82
Q

What is the gold standard for hypothyroid testing

A

TSH stimulation test

TRH stimulation test has equivalent results
Ultrasound is insensitive

83
Q

What should be ignored when looking at Turpin hormone levels

A

T3 and fT3

Fluctuate way too much

84
Q

A total t4 test for hypothyroid is (poorly/ moderately/ highly) sensitive and (poorly/moderately/ highly) specific

A

Highly

Moderately

85
Q

Euthyroid sick syndrome will show what thyroid levels

A

Decreased tT4
Normal/ decreased fT4
Normal TSH
Do not need supplementation - tx underlying cause

86
Q

Free t4 is the active form of T4 and is more specific How should this test be preformed

A

Equilibrium dialysis

87
Q

TSH testing is positive in ___% of hypothyroid dogs

A

70

88
Q

What drugs should be avoided when attempting to test for hypothyroid

A

Glucocorticoids- decrease T4 and TSH
Phenobarbital - decrease t4 and increase TSH
TMS- decrease t4 and increase TSH

89
Q

T/F antibodies of TG, T3 and T4 is diagnostic for hypothyroid

A

False. Only supportive. Only seen in 50 % of hypothyroid dogs

90
Q

A therapeutic trail of ______ which is tested 4-8 weeks later to see improvement of signs can be used to diagnose hypothyroid

A

Levothyroxine. If signs return then hypothyroid

91
Q

Levi thyroxine is a synthetic form of ___

A

T4- must be monitored 4-8 weeks after therapy then every 6 months

92
Q

What are some side effects seen with levothyroxine

A

Hyperthyroid- PUS PD Polyphasia tachycardia nervousness

93
Q

How long does it take to see improvement of hypothyroidism after treatment is started

A

Increased activity 1-2 weeks
Weight loss - 8 weeks
Hair coat- months (worse before better)
CNS- rapidly but 8-12 weeks before complete resolution

94
Q

What is the most common endocrine disorder in cats

A

Hyperthyroid

95
Q

Hyperthyroid is caused by overproduction if t3 and t4 by a thyroid _______

A 
Adenoma
Benign 
Bilateral common 
~95% of cases
Malignant carcinoma = <5%
96
Q

What is a common signalmen for a cat with hyperthyroid

A

Older than 10

97
Q

What are clinical signs of a cat with hyperthyroid

A 
Weight loss
Polyphagia
PU PD
Hyperactive 
Vomiting 
Anorexic (10%)
98
Q

What does a PE of hyperthyroid show

A 
Underweight
Palpable thyroid slip
Hyperactive and grumpy
Poor hair coat
Dehydration
Poorly behaved
Cervical ventroflexion
Cardiac (50%)- increased B receptor, tachy, gallop, thick cardiac wall
Hypertension and funding abnormalities
99
Q

What will initial blood work show with hyperthyroid

A

Increased hematocrit
Increased ALT
Azotemia
Isothenuria

100
Q

How is a difinitibe dx reached with hyperthyroid

A

Total t4. High sensitivity and specificity

101
Q

Why is free T4 by equilibrium dialysis not the screening test of choice for hyperthyroid

A

More sensitive but less specific
More false positive
Mostly useful in cats with clinical support of hyperthyroid but normal t4 values

102
Q

A T3 suppression test may be preformed as a last resort for testing hyperthyroid

A

Following t3 administration

T4 should be <50% baseline in normal cats while there is little suppression in hyperthyroid

103
Q

Nuclear scintigraphy uses radioactive isotope that is taken up similarly to ______ as this is used to make thyroid hormones The gamma emission is then quantified

A

Iodine
Can tell if uni or bilateral (sx)
Id ectopic tissue (sx not an option if intrathoracic)
Id metastasis (adenoma vs carcinoma)

104
Q

Hyperthyroid can cause organ damage in which organs

A

Neuro
Heart
Kidney
Ocular- retinal hemorrhages tortuous vessels

105
Q

T/F The changes seen from hyperthyroid involving hypertrophic cardiomyopathy are reversed when treatment is started

A

True. Is reversible

106
Q

What are some medical treatments for hyperthyroid

A

Methimazole (Tapazole)

107
Q

How does methimazole work

A

Blocks thyroid hormone synthesis by inhibiting thyroid peroxidase
2 weeks before improvement
Oral or transdermal

108
Q

What are side effects of methimazole

A 
Hi upset 
Neutropenia
Thrombocytopenia 
Facial excoriation
Hepatotoxicity
Renal decompensation
Reversible if caught in time
109
Q

Methimazole (tapazole) “plutonic lecithin organogel” (PLO) used transdermally is (more/less) effective than if used orally

A

Less. But still effective

Less GI signs

110
Q

Symptomatic medical treatments for hyperthyroid need to be given (lifelong/ only until T4 normalizes)

A

Only until t4 normalizes
Hypertension- amlodipine
Tachycardia, hyperactivity- b blockers (propranolol atenolol)- but not normally needed

111
Q 
Which is not a disadvantage/ possible outcome of surgical treatment for hyperthyroidism
A. Hypoparathyroidism 
B. Missed ectopic tissue
C. Relatively expensive
D. Recurrent laryngeal nerve damage
E. Hypothyroism
A

C- usually inexpensive

112
Q

T/F when using radioactive iodine (I-131) to treat hyperthyroid normal tissue is preserved

A

True B particles destroy local hyperactive tissue- normal tissue is atrophied and is not taking up iodine

113
Q

How long does it take for T4 to normalize after being treated with radioactive iodine

A

Weeks but at most 3 months in 95% of cases

114
Q

What are all of the advantages of radioactive iodine treatment in hyperthyroid
A. Effective
B. Rapid
C. Treats both ectopic tissue and carcinoma
D. Low cost

A

A B C

Is expensive and may also cause hypothyroid and unmask renal issues. Iso for 10 days

115
Q

What is restricted in dietary management of hyperthyroid

A

Iodine - inhibits ability to form thyroid hormones

116
Q

T/F cats with hyperthyroidism usually take about 2 weeks to see improvement after starting to eat a thyroid diet

A

False. Up to 6 months or longer

But is safe with cats with kidney disease. No SE. but may not normalize severe T4 elevations

117
Q

What is the prognosis of act with hyperthyroid

A

Variable but generally good

118
Q

Insulin facilitates the uptake of

A

Glucose
AA
FA
K Phos Mg

119
Q

Insulin inhibits

A 
Gluconeogenesis
Glycogenolysis
Protein catabolism
Lipolysis
Ketogenesis
120
Q

Diabetes mellitus is defined as insufficient production of insulin by _____ cells of the pancreas and is common in dogs and cats.

A

Beta

121
Q

DM in dogs almost always sees what type of insulin deficient

A

Absolute

Insulin dependent

122
Q

DM in cat usually (80%) sees what type of insulin deficient

A

Relative insulin deficiency
Non insulin dependent
Dysfunctional B cells (impaired secretion) along with insulin resistance

123
Q

What causes B cell degeneration

A

Amyloid deposition into pancreas in cats

But is reversible depending on degree of damage

124
Q

Name some predisposing factors that lead to insulin resistance

A 
Obesity
Pancreatitis
Glucocorticoids
Progesterone (diestrus. Megestrol acetate)
Infection 
Concurrent dz
Stress
125
Q

In DM the pathophysilogy that leads to polydipsia is___

A

Insulin deficiency -> decreased cell glucose and increased hepatic gluconeogenesis -> hyperglycemia -> glucosuria (renal threshold >180) -> polyuria -> polydipsia

126
Q

What is a common signalment of DM in dogs

A

Females 2x as males
Middle aged
Terrier schnauzer min poodle

127
Q

What is a common signalment of DM in cats

A 
Neutered males
Older than 6
Burmese
Abyssinian 
Siamese (DKA)
128
Q

Most animals presenting WITH DM present wiTH DKA

T/ F

A

False

Normally a “well diabetic”

129
Q

What are classic signs of DM and what additional signs are seen with DKA

A

PU PD
Polyphagia
Weight loss

Anorexia
Depression
Vomiting
Dehydration

130
Q

What are some concurrent endocrinopathies seen in dogs

A

Hyperadrenocorticism

Hyperthyroid acromegaly in cats

131
Q

What are other possible findings in animals with DM

A 
Heptatomegaly
Dehydration 
Poor coat
Cataracts (dogs)
Peripheral Neuropathy (cats)
132
Q

The initial diagnoses of DM is usually straight forward. What few things are required to make a diagnoses

A 
Clinical sign 
Hyperglycemia 
Glucosuria
(Maybe ketouria or fructosamine) 
Cats- other Dif Dx with these is stress
133
Q

How high can a stress hyperglycemia go in cats

A

Up to 400

No other signs of DM

134
Q

A CBC in a DM animal shows ______

A

Nothing

135
Q

A chem panel in an animal with DM will show

A 
Hyperglycemia 
Hyper cholesterol
Increased ALP ( Dog cholestasis not cats)
Increased ALT
Amylase increase (dog)
Prerenal azotemia
136
Q

A UA in an animal with DM with show

A

Glucosuria

May show : Keto
Protein
Bacteria
Pyuria

137
Q

What are some signs of a too high dose of insulin (hypoglycemia)

A 
Muscle tremors
Weakness
Lethargy 
Head tilt
Dull or dazed
Disorientation 
Ataxia 
Seizure 
Coma
138
Q 
Which of the following are recommended for dietary management of dogs with DM
A. Increase Fiber
B. Increase Protein 
C. Decrease simple sugars
D. Decrease fat
E. Decrease Carb
A

A
C
D

139
Q 
Which of the following are recommended for dietary management of dogs with DM
A. Increase Fiber
B. Increase Protein 
C. Decrease simple sugars
D. Decrease fat
E. Decrease Carb
A

A- only if can’t increase protein
B
E

140
Q

Risk for antibody formulation is more common in (dog/cats)

A

Dog

141
Q

What is the only insulin that can go IV for DKA

A

Humulin R

142
Q

Which insulin’s are used for cats. For dog?

A

Prozinc (u40) and glargine (u100)

Vetsulin (u40) and Humulin N (u100)

143
Q

What is the gold standard of monitoring insulin

A

Blood glucose curve

144
Q

Spot checks should only be used to check for

A

Hypoglycemia

145
Q

In a regulated DM dog urine glucose strips should be (-/+)

A

+. Renal threshold 180

Cats less predictable. Can be negative

146
Q

Fructosamine in glycated proteins synthesized during

A

Insulin independent binding of glucose

Helpful in cats as it is uneffected by stress

147
Q 
Which of the following cats are likely to go into DM remission
A. Treated right after Dx
B. Recently received glucocorticoids 
C. Older cats
D. Cats with peripheral neuropathy
A

A
B
C
Without- D

148
Q

___%of cats with NIDDM go into remission

A

80

But 25% relapse back

149
Q

Insulin resistance is seen at was dose

A

> 2 u/kg of insulin per dose

150
Q

Dogs tend to get _____ complication while cats get ______ from DM

A

Cataracts

Diabetic neuropathy - see weakness glomerular dysfunction and proteinuria

151
Q

What are triggers for DKA

A 
Insulin deficiency 
Infection 
Pancreatitis
Neoplasia 
Glucocorticoids
Progesterone
152
Q

Lot one bodies overwhelm the body’s buffering capacity leading to

A

Acidosis

Accumulate in urine= osmotic diuresis and dehydration

153
Q

What is seen in a CBC if a DKA

A 
Non regenerative anemia
Left shift NTphilia
Thrombocytosis 
Heinz body (cats)
Increased ALP alt cholesterol 
Azotemia
Decreased Mg Ph K Na (pseudo) Cl
154
Q

T/F a patient with DKA should first be given insulin

A

False. 1st fluids. Insulin 1-2 hours later (regular insulin for short duration )
Isotonic fluids over 24 hrs
Dextrose to fluids to maintain BG and allow insulin administration

155
Q

Fluids and resolution if ketones should correct acidosis but what can be used to more rapidly correct acidosis

A

Bicarbonate but is controversial (needed if severe)

156
Q

T/F insulin will drive K and phosphorus into cells so even if normal initially can plummet dramatically with treatment and may need to be supplemented in DKA

A

True

157
Q

___% of animals survive to discharge after treatment of DKA

A

70

158
Q

ADH is produced by the ______ and is released by the _______

A

Hypothalamus

Posterior pituitary

159
Q

What conditions effect ADH

A 
Cushings 
Primary hyperparatyroidism
Pheochromocytoma
Hypercalcemia 
Neoplasia
Pyometria
Hyperviscosity
Polycythemia 
Hypokalemia
160
Q

What is the difference between central DI and nephrogenic DI

A

ADH is not made in central

Kidney not responding to ADH in nephrogenic

161
Q 
Which is false about central DI?
A. Common form
B. USG <1.006
C. Can be congenital or acquired
D. A partial central DI may lead to Isosthenuria
A

A- rare

162
Q

(Primary/Secondary) nephrogenic DI is more common

A

Secondary (acquired)

Primary- mutation in ADH receptor or aquaporin

163
Q

How is secondary nephrogenic DI caused

A

Conditions affecting ADH binding and function in renal tubules, loss of medullary gradient, osmotic diuresis

164
Q

When finding a cause of PU PD what tests should be preformed before testing primary DI

A 
Ultrasound
CBC
Chem
Culture e
Lepto serology
ACTH LDDS thyroid levels
GFR study
165
Q

When assessing for DI what tests can be preformed

A

Modified water deprivation test

DDAVP (desmopressin)

166
Q

Serum osmolality testing of 280-320 indicates

A

CDI high or high normal

Psychogenic- <275

167
Q

Exogenous DDAVP administration test will confirm CDI if by day 5-7 the USG does what

A

Increase of USG by at least 50% compared with pretreatment or USG increases to >1.030
Results like this also include psychogenic and cushings

168
Q

When must a water deprivation test be stoped

A

If 5% dehydration or USG > 1.025

169
Q

How is CDI treated

A

DDAVP. Desmopressin

170
Q

How is congenital NDI treated

A

Low Na diet
Thiazides diuretics- paradoxical effect to reduce urine volume and decreases PU PD
Good progonosis

171
Q

Which endocrine diseases do not cause PU PD

A

Hypothyroidism
Primary Hyperparathyroidism(if not hypercalcemia)
Hypoparathyroidism

172
Q

What endocrine dz cause PU PD

A

DM Hyperthyroid hyperadrenocorticism hypoadrenocorticism hyperaldosteronism
Acromegaly
DI
Hyperparathyroid (if hypercalcemia)

173
Q

Hypersomatotropism (HS) is an overproduction if growth hormone and leads to _____

A

Acromegaly (syndrome from HS)

174
Q

A functional adenoma in the pars distalis of the anterior pituitary causes excessive GH and causes the liver to produce _______

A

Somatomedins (AKA insulin like growth factors) most important is IGF-1 which leads to the clinical signs of acromegaly

175
Q

Almost all cats with acromegaly all have ___

A

DM
If not controlled
Didn’t go into remission
Require high insulin dose of 1.5-2 u/kg

176
Q

What is a good clue of acromegaly in a older male cat that has unregulated DM

A

Weight gain

Should be losing weight with DM

177
Q

What are clinical signs of acromegaly

A 
Enlarged extremities jaw tongue and forehead
Clubbing of paws
Organ enlargement 
Stridor (growth of soft tissue)
Degenerative joint dz
Systolic murmur- thickened heart and CHF
Hypertension 
CNS or diabetic neuropathy 
Proteinuria
Thickened skin
178
Q

How is acromegaly diagnosed

A

Most cL signs and hx
IGF-1 concentration possible
CT or MRI to see tumor if large enough

179
Q

Acromegaly is treated by

A

Sx- transsphenoidal hypophysectomy ( remission within 4 weeks)
Radiation- variable response -up to year
Medical therapy - somatostatin analogs (still being tested)
Palliative- 20x dose of insulin- poor long term prognosis (organ failure, CNS signs)

180
Q

Acromegaly in dogs is uncommon but is usually seen in what kk d of dog

A

Intact female dogs- excessive progesterone= production of GH from mammary tissue
Also see gum growth
Adenoma

181
Q

Feline cushing’s in uncommon but we tend to see more (PDH/ADH)

A

PDH - 80%
Adenoma in pars intermedia or pars distalis of pituitary gland
ADH- 1 gland if benign adenoma

182
Q

Most cats with cushings present with what other disease

A

DM
CL s of DM- weight loss, PU PD
DM poorly controlled
Insulin resistance from cushings

183
Q

What signs are seen in a cushings cat

A 
Abdominal distention- pot belly
Panting
Atrophy 
Unkempt hair coat
Bilateral symmetric alopecia
2 infections
Blindness abnormal behavior
Sex hormones causing spines on castrated males
Fragile skin syndrome 
NOT calcinosis (dog only)
184
Q

T/F not much is seen in a CBC chem of a Cushing cat

A

True. Maybe proteinuria

185
Q

How is feline cushings diagnosed

A

LDDST- test of choice
ACTH- 2/3 with HAC have normal cortisol
UCCR- poor specificity
Imaging

186
Q

How is feline cushings treated

A

Medical- trilostane (1), mitotane, metyrapone
Sx- hypophysectomy (expensive), adrenalectomy (poor healing)
Radiation- unreliable

187
Q

Aldosterone is produced in the zona glomerulosa and is regulated by RAAS and is release in response to what 3 things

A

Hypovolemia
Hyponatremia
Hyperkalemia

Function- increase Na Cl resorption , increase K H secretion (lose)

188
Q

Conn’s (primary hyperaldosteronism) is a common dz in cats and is often misdiagnosed as ____

A

CKD

Caused by adrenocortical carcinoma , adenoma or bilateral nodular hyperplasia

189
Q

Clinical signs of hyperaldosteronism is mainly from —-

A

Hypertension (end organ damage)
Hypokalemia (not usually hypernatremia)

PU PD Atrophy arrhythmia pendulous abdomen
Blindness (retinal detachment) weight loss restless
Plantjgrade stance
Cervical ventroflexion

190
Q

Conn’s lab findings:

A 
Hypokalemia
Metabolism alkalosis
Azotemia
Increase phosphorus
Increase CK
Hyperglycemia 
Hypernatremia
Inappropriate kaliuresis
Increased aldosterone: creatinine ratio
191
Q

How is conn diagnosed

A

US CT MRI
Adrenal mass
Metastasis
Local invasion by adrenal mass

192
Q

How is conn treated

A

Sx- adrenalectomy for unilateral adenoma or carcinoma

Medical- k, spironolactone (aldosterone blocker), amlodipine

193
Q

Insulinoma is a tumor of

A

Pancreatic beta cells

Most common canine islet cell neoplasia (most are carcinoma)

194
Q

How is an insulinoma diagnosed

A

Normal CBC
CHEM- hypoglycemia, hypokalemia, increased ALP or ALT
Urinalysis is unremarkable
High insulin with low glucose (insulin should be inhibited at a BG of 65-80)
US (seen in 50%)

195
Q

How is an insulinoma treated

A

Sx- to of choice by often has metastasized and hard to find tumor (left side?)
Chemo- destroys B cells in pancreas and metastatic sites Neohrotoxic. Similar prognosis to Sx

196
Q

How is insulinoma medically managed

A

Frequent small meals (4-6)
High pt fat and complex carb
Avoid simple sugar
Glucocorticoids (increases gluconeogenesis)
Diazoxide (inhibits insulin release)
Somatostatin (octeotide)- insulin antagonist
Glucagon- increased gluconeogenesis

197
Q

Insulinoma prognosis

A

12-14 month survival time
Young dog worse prognosis
Post op hyperglycemia better than hypo
Can become diabetic after Sx

Equine (10 decks)

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