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
Iatrogenic cushings looks like the dog has ______ but will test as _______
Cushing | Addison
26
ACTH stimulation test with a post cortisol value above ____ along with clinical signs is diagnostic for cushings
21
27
A Pituitqru tumor response produces high amounts of ____ thus higher ____ from the adrenal gland
ACTH Cortisol ACTH stim test will have increased cortisol
28
Adrenal tumor response produce ______ which gives a negative feedback to the pituitary thus decreasing _______
Cortisol ACTH ACTH stim test will either be elevated or normal cortisol
29
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
E- pre and post low
30
What are benefits of the low dose dexamethasone suppression test
``` 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) ```
31
How is low dose dex suppression test done
Baseline cortisol Dex 4hr 8hr
32
If the LDDST is above ____ at hour 8 then it is cushings
1.4 | 4 hr is for differentiation
33
LDDST and HDDST can diagnose what type of cushings
PDH not ADH (dex at any dose does not suppress cortisol secretion because adrenal gland don’t respond to negative feedback)
34
With PDH ~70% of dogs will show suppression in LDDST and LDDST. Dogs that have PDH but do not suppress (dex resistant) likely have
Large pituitary tumor
35
Suppression at hour 4 in dex tests with a rebound at hour 8 is called a
Escape pattern
36
In ADH the dexamethasone will
Not be suppressed at any point
37
In a LDDST, PDH is diagnosed if
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
38
ACTH concentrations are expected to be higher with (PDH/ ADH) and suppressed with (PDH/ ADH)
PDH | ADH
39
What is the most accurate stand alone test for differentiation of cushings
Endogenous ACTH
40
In an ultrasound a PDH would show what on the adrenals. An ADH would show what
PDH- bilaterally enlarged or normal adrenal glands- CT recommended AFH- 1 enlarged or mass
41
Endogenous ACTH has significant overlap between normal levels of ACTH and (PDH/ADH)
PDH. ADH = little to no overlap for normal. (Very low)
42
What are some potential complications or infections with cushings
``` Hypertension Pyeloneohritis UTI Pancreatitis Urinary Calculi GB mucocele DM Hypercoaguble (pulmonary thromboembolism) ```
43
Medical is the treatment of choice for (PDH/ADH) while surgery is the treatment of choice for (PDH/ADH)
PDH | ADH
44
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
ABE If sx- hypophysectomy A B also for ADH A- less common for SE but more severe than B Significant monitoring
45
What surgery is preformed for ADH
Adrenalectomy Better chance of survival compared to medical tx
46
Calcitriol is activated by _______ in the ______
Vitamin D | Kidneys
47
The chief cells of the parathyroid glands regulate what 2 elements
Ionized Ca | Phosphorus
48
If serum calcium goes up then _______ will go down
Phosphorus | And PTH
49
PTH (increases/ decreases) resorption (release) of calcium and phosphorus, (increases/ decreases) calcium excretion and (increases/ decreases) phosphorus excretion
Increases Decreases (resorption of Ca) Increases
50
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 ______
``` Vitamin D (calcitriol) Calcium and phosphorus ```
51
Calcitriol acts on the Parathyroids glands via a negative feedback loop to decrease ____
PTH
52
Calcitonin’s primary function is to _____
Decreased serum calcium | Decreases osteoclasts formation
53
When calcium goes down ____ goes up
PTH
54
What are the hypercalcemia differentials
``` Hyperparathyroidism Osteolytic Granulomatous Dz Spurious Idiopathic Neoplasia Young Addisons Renal Dz Vitamin D toxicosis ```
55
PTH will cause (high/low) phosphorus while calcitriol will cause (high/low) phosphorus
Low | High
56
What causes PHP (excessive production of PTH)
Parathyroid adenoma (1) Parathyroid carcinoma Parathyroid hyperplasia
57
What are common signalments for PHP
Middle age or older | Keeshond lab golden GSD
58
T/F unlike other causes of hypercalcemia, dogs with PHP are usually not clinical
True- other causes= very sick dog
59
T/F A dog with PHP usually presents normally with only subtle non specific signs or related to urinary issues
True
60
What are lab findings of a dog with PHP
``` Maybe mild anemia Hypercalcemia Low phosphorus Iso- hyposthenuria UTI Calculi ```
61
A CT of a dog with PHP may show
Metastasis | Thyroid mass- difficult to visualize
62
Elevated or inappropriately normal PTH along with elevated iCa confirms _____
PHP | Elevated PTHrp supports hypercalcemia of malignancy
63
What are some treatments for PHP when there is severe hypercalcemia
``` Fluids Diuretics Glucocorticoids Bisphosphates - prevent bone destruction Calcitonin- short action though Surgical removal Radio frequency heat ablation Ethanol ablation ```
64
What must be done before a PHP surgery
Start on prophylactic calcitriol (vitamin D) then taper over 2-4 months Ca carbonate after sx 2-4 months taper
65
What is seen in hypoparathyroidism
Decreased Ca Increased Ph Decreased PTH= reduced bone resorption, decreased Ca resorption and increased Ph from Kidney
66
What are the 4 causes of HypoPTH
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)
67
What are differentials for hypocalcemia
``` Phosphate enema Eclampsia Albumin decrease CKD Ethylene glycol /AKI PTH deficiency Acute pancreatitis Intestinal malabsorption Nutritional (vitamin D deficiency) ```
68
What is a common signalmen for hypoPTH
``` Dogs>cats Female> male Poodle Schnauzer GSD lab Terrier ```
69
What are signs of HypoPTH
``` Seizure Facial rubbing and biting at paws Tetany Stiff Anorexic Lethargy Pant Cataracts fever CV abnormalities ```
70
A dog with hypoPTH should have low Ca and what else
Increased Ph PTH low (or inappropriately normal) Decreased calcitriol
71
What is a treatment plan for a dog with hypoPTH
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
72
Which thyroid hormone is the most biologically active and is up to 3-4x more potent
T3 enters cell more rapidly | Only 20% made in thyroid remained is by peripheral deionization of T4
73
What are possible etiologies of hypothyroid
Thyroiditis Idiopathic atrophy Bilateral neoplasia (uncommon)
74
What breed tend to be more effected by hypothyroid
``` Borzoi Toy fox terrier Beagle Setter Dave’s Golden Doberman ```
75
What are some metabolic signs seen with hypothyroid
``` Decreased rate Lethargy Weight gain Cold intolerant Dull Unwilling to exercise ```
76
What are some dermatological signs seen with hypothyroid
``` Symmetric alopecia Hyperpigmentation Dry scaly skin Pyoderma Otitis Seborrhea Dry brittle hair coat Myxedema (thickening of skin) ```
77
What are some neurological signs seen with hypothyroid
PNS- weak, exercise intolerant to ataxia or paresis CNS- seizures central vestibule dz and mentation changes CN- facial nerve paralysis vestibule dz
78
What are some cardiovascular signs seen with hypothyroid
``` Bradycardia Low QRS voltage Inverted T Reduced LV pump function Weak heart ```
79
What are some other signs seen with hypothyroid
Reproductive dysfunction Ocular changes Mega esophagus Lar par
80
T/F hypothyroidism can be tested without history clinical signs or physical exams that point to it
False- only test with clinical signs
81
What is seen in blood work of a dog with hypothyroid
Normochromic normocytic non regenerative anemia Fasting hypertriglyceridema Fasting hypercholesterolemia* Increased ALP or other liver enzymes
82
What is the gold standard for hypothyroid testing
TSH stimulation test TRH stimulation test has equivalent results Ultrasound is insensitive
83
What should be ignored when looking at Turpin hormone levels
T3 and fT3 | Fluctuate way too much
84
A total t4 test for hypothyroid is (poorly/ moderately/ highly) sensitive and (poorly/moderately/ highly) specific
Highly | Moderately
85
Euthyroid sick syndrome will show what thyroid levels
Decreased tT4 Normal/ decreased fT4 Normal TSH Do not need supplementation - tx underlying cause
86
Free t4 is the active form of T4 and is more specific How should this test be preformed
Equilibrium dialysis
87
TSH testing is positive in ___% of hypothyroid dogs
70
88
What drugs should be avoided when attempting to test for hypothyroid
Glucocorticoids- decrease T4 and TSH Phenobarbital - decrease t4 and increase TSH TMS- decrease t4 and increase TSH
89
T/F antibodies of TG, T3 and T4 is diagnostic for hypothyroid
False. Only supportive. Only seen in 50 % of hypothyroid dogs
90
A therapeutic trail of ______ which is tested 4-8 weeks later to see improvement of signs can be used to diagnose hypothyroid
Levothyroxine. If signs return then hypothyroid
91
Levi thyroxine is a synthetic form of ___
T4- must be monitored 4-8 weeks after therapy then every 6 months
92
What are some side effects seen with levothyroxine
Hyperthyroid- PUS PD Polyphasia tachycardia nervousness
93
How long does it take to see improvement of hypothyroidism after treatment is started
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
What is the most common endocrine disorder in cats
Hyperthyroid
95
Hyperthyroid is caused by overproduction if t3 and t4 by a thyroid _______
``` Adenoma Benign Bilateral common ~95% of cases Malignant carcinoma = <5% ```
96
What is a common signalmen for a cat with hyperthyroid
Older than 10
97
What are clinical signs of a cat with hyperthyroid
``` Weight loss Polyphagia PU PD Hyperactive Vomiting Anorexic (10%) ```
98
What does a PE of hyperthyroid show
``` 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
What will initial blood work show with hyperthyroid
Increased hematocrit Increased ALT Azotemia Isothenuria
100
How is a difinitibe dx reached with hyperthyroid
Total t4. High sensitivity and specificity
101
Why is free T4 by equilibrium dialysis not the screening test of choice for hyperthyroid
More sensitive but less specific More false positive Mostly useful in cats with clinical support of hyperthyroid but normal t4 values
102
A T3 suppression test may be preformed as a last resort for testing hyperthyroid
Following t3 administration | T4 should be <50% baseline in normal cats while there is little suppression in hyperthyroid
103
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
Iodine Can tell if uni or bilateral (sx) Id ectopic tissue (sx not an option if intrathoracic) Id metastasis (adenoma vs carcinoma)
104
Hyperthyroid can cause organ damage in which organs
Neuro Heart Kidney Ocular- retinal hemorrhages tortuous vessels
105
T/F The changes seen from hyperthyroid involving hypertrophic cardiomyopathy are reversed when treatment is started
True. Is reversible
106
What are some medical treatments for hyperthyroid
Methimazole (Tapazole)
107
How does methimazole work
Blocks thyroid hormone synthesis by inhibiting thyroid peroxidase 2 weeks before improvement Oral or transdermal
108
What are side effects of methimazole
``` Hi upset Neutropenia Thrombocytopenia Facial excoriation Hepatotoxicity Renal decompensation Reversible if caught in time ```
109
Methimazole (tapazole) “plutonic lecithin organogel” (PLO) used transdermally is (more/less) effective than if used orally
Less. But still effective | Less GI signs
110
Symptomatic medical treatments for hyperthyroid need to be given (lifelong/ only until T4 normalizes)
Only until t4 normalizes Hypertension- amlodipine Tachycardia, hyperactivity- b blockers (propranolol atenolol)- but not normally needed
111
``` 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 ```
C- usually inexpensive
112
T/F when using radioactive iodine (I-131) to treat hyperthyroid normal tissue is preserved
True B particles destroy local hyperactive tissue- normal tissue is atrophied and is not taking up iodine
113
How long does it take for T4 to normalize after being treated with radioactive iodine
Weeks but at most 3 months in 95% of cases
114
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 B C Is expensive and may also cause hypothyroid and unmask renal issues. Iso for 10 days
115
What is restricted in dietary management of hyperthyroid
Iodine - inhibits ability to form thyroid hormones
116
T/F cats with hyperthyroidism usually take about 2 weeks to see improvement after starting to eat a thyroid diet
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
What is the prognosis of act with hyperthyroid
Variable but generally good
118
Insulin facilitates the uptake of
Glucose AA FA K Phos Mg
119
Insulin inhibits
``` Gluconeogenesis Glycogenolysis Protein catabolism Lipolysis Ketogenesis ```
120
Diabetes mellitus is defined as insufficient production of insulin by _____ cells of the pancreas and is common in dogs and cats.
Beta
121
DM in dogs almost always sees what type of insulin deficient
Absolute | Insulin dependent
122
DM in cat usually (80%) sees what type of insulin deficient
Relative insulin deficiency Non insulin dependent Dysfunctional B cells (impaired secretion) along with insulin resistance
123
What causes B cell degeneration
Amyloid deposition into pancreas in cats | But is reversible depending on degree of damage
124
Name some predisposing factors that lead to insulin resistance
``` Obesity Pancreatitis Glucocorticoids Progesterone (diestrus. Megestrol acetate) Infection Concurrent dz Stress ```
125
In DM the pathophysilogy that leads to polydipsia is___
Insulin deficiency -> decreased cell glucose and increased hepatic gluconeogenesis -> hyperglycemia -> glucosuria (renal threshold >180) -> polyuria -> polydipsia
126
What is a common signalment of DM in dogs
Females 2x as males Middle aged Terrier schnauzer min poodle
127
What is a common signalment of DM in cats
``` Neutered males Older than 6 Burmese Abyssinian Siamese (DKA) ```
128
Most animals presenting WITH DM present wiTH DKA T/ F
False | Normally a “well diabetic”
129
What are classic signs of DM and what additional signs are seen with DKA
PU PD Polyphagia Weight loss Anorexia Depression Vomiting Dehydration
130
What are some concurrent endocrinopathies seen in dogs
Hyperadrenocorticism | Hyperthyroid acromegaly in cats
131
What are other possible findings in animals with DM
``` Heptatomegaly Dehydration Poor coat Cataracts (dogs) Peripheral Neuropathy (cats) ```
132
The initial diagnoses of DM is usually straight forward. What few things are required to make a diagnoses
``` Clinical sign Hyperglycemia Glucosuria (Maybe ketouria or fructosamine) Cats- other Dif Dx with these is stress ```
133
How high can a stress hyperglycemia go in cats
Up to 400 | No other signs of DM
134
A CBC in a DM animal shows ______
Nothing
135
A chem panel in an animal with DM will show
``` Hyperglycemia Hyper cholesterol Increased ALP ( Dog cholestasis not cats) Increased ALT Amylase increase (dog) Prerenal azotemia ```
136
A UA in an animal with DM with show
Glucosuria May show : Keto Protein Bacteria Pyuria
137
What are some signs of a too high dose of insulin (hypoglycemia)
``` Muscle tremors Weakness Lethargy Head tilt Dull or dazed Disorientation Ataxia Seizure Coma ```
138
``` 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 C D
139
``` 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- only if can’t increase protein B E
140
Risk for antibody formulation is more common in (dog/cats)
Dog
141
What is the only insulin that can go IV for DKA
Humulin R
142
Which insulin’s are used for cats. For dog?
Prozinc (u40) and glargine (u100) | Vetsulin (u40) and Humulin N (u100)
143
What is the gold standard of monitoring insulin
Blood glucose curve
144
Spot checks should only be used to check for
Hypoglycemia
145
In a regulated DM dog urine glucose strips should be (-/+)
+. Renal threshold 180 | Cats less predictable. Can be negative
146
Fructosamine in glycated proteins synthesized during
Insulin independent binding of glucose | Helpful in cats as it is uneffected by stress
147
``` 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 B C Without- D
148
___%of cats with NIDDM go into remission
80 | But 25% relapse back
149
Insulin resistance is seen at was dose
>2 u/kg of insulin per dose
150
Dogs tend to get _____ complication while cats get ______ from DM
Cataracts | Diabetic neuropathy - see weakness glomerular dysfunction and proteinuria
151
What are triggers for DKA
``` Insulin deficiency Infection Pancreatitis Neoplasia Glucocorticoids Progesterone ```
152
Lot one bodies overwhelm the body’s buffering capacity leading to
Acidosis | Accumulate in urine= osmotic diuresis and dehydration
153
What is seen in a CBC if a DKA
``` Non regenerative anemia Left shift NTphilia Thrombocytosis Heinz body (cats) Increased ALP alt cholesterol Azotemia Decreased Mg Ph K Na (pseudo) Cl ```
154
T/F a patient with DKA should first be given insulin
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
Fluids and resolution if ketones should correct acidosis but what can be used to more rapidly correct acidosis
Bicarbonate but is controversial (needed if severe)
156
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
True
157
___% of animals survive to discharge after treatment of DKA
70
158
ADH is produced by the ______ and is released by the _______
Hypothalamus | Posterior pituitary
159
What conditions effect ADH
``` Cushings Primary hyperparatyroidism Pheochromocytoma Hypercalcemia Neoplasia Pyometria Hyperviscosity Polycythemia Hypokalemia ```
160
What is the difference between central DI and nephrogenic DI
ADH is not made in central | Kidney not responding to ADH in nephrogenic
161
``` 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- rare
162
(Primary/Secondary) nephrogenic DI is more common
Secondary (acquired) | Primary- mutation in ADH receptor or aquaporin
163
How is secondary nephrogenic DI caused
Conditions affecting ADH binding and function in renal tubules, loss of medullary gradient, osmotic diuresis
164
When finding a cause of PU PD what tests should be preformed before testing primary DI
``` Ultrasound CBC Chem Culture e Lepto serology ACTH LDDS thyroid levels GFR study ```
165
When assessing for DI what tests can be preformed
Modified water deprivation test | DDAVP (desmopressin)
166
Serum osmolality testing of 280-320 indicates
CDI high or high normal | Psychogenic- <275
167
Exogenous DDAVP administration test will confirm CDI if by day 5-7 the USG does what
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
When must a water deprivation test be stoped
If 5% dehydration or USG > 1.025
169
How is CDI treated
DDAVP. Desmopressin
170
How is congenital NDI treated
Low Na diet Thiazides diuretics- paradoxical effect to reduce urine volume and decreases PU PD Good progonosis
171
Which endocrine diseases do not cause PU PD
Hypothyroidism Primary Hyperparathyroidism(if not hypercalcemia) Hypoparathyroidism
172
What endocrine dz cause PU PD
DM Hyperthyroid hyperadrenocorticism hypoadrenocorticism hyperaldosteronism Acromegaly DI Hyperparathyroid (if hypercalcemia)
173
Hypersomatotropism (HS) is an overproduction if growth hormone and leads to _____
Acromegaly (syndrome from HS)
174
A functional adenoma in the pars distalis of the anterior pituitary causes excessive GH and causes the liver to produce _______
Somatomedins (AKA insulin like growth factors) most important is IGF-1 which leads to the clinical signs of acromegaly
175
Almost all cats with acromegaly all have ___
DM If not controlled Didn’t go into remission Require high insulin dose of 1.5-2 u/kg
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What is a good clue of acromegaly in a older male cat that has unregulated DM
Weight gain | Should be losing weight with DM
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What are clinical signs of acromegaly
``` 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 ```
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How is acromegaly diagnosed
Most cL signs and hx IGF-1 concentration possible CT or MRI to see tumor if large enough
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Acromegaly is treated by
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
Acromegaly in dogs is uncommon but is usually seen in what kk d of dog
Intact female dogs- excessive progesterone= production of GH from mammary tissue Also see gum growth Adenoma
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Feline cushing’s in uncommon but we tend to see more (PDH/ADH)
PDH - 80% Adenoma in pars intermedia or pars distalis of pituitary gland ADH- 1 gland if benign adenoma
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Most cats with cushings present with what other disease
DM CL s of DM- weight loss, PU PD DM poorly controlled Insulin resistance from cushings
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What signs are seen in a cushings cat
``` 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) ```
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T/F not much is seen in a CBC chem of a Cushing cat
True. Maybe proteinuria
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How is feline cushings diagnosed
LDDST- test of choice ACTH- 2/3 with HAC have normal cortisol UCCR- poor specificity Imaging
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How is feline cushings treated
Medical- trilostane (1), mitotane, metyrapone Sx- hypophysectomy (expensive), adrenalectomy (poor healing) Radiation- unreliable
187
Aldosterone is produced in the zona glomerulosa and is regulated by RAAS and is release in response to what 3 things
Hypovolemia Hyponatremia Hyperkalemia Function- increase Na Cl resorption , increase K H secretion (lose)
188
Conn’s (primary hyperaldosteronism) is a common dz in cats and is often misdiagnosed as ____
CKD | Caused by adrenocortical carcinoma , adenoma or bilateral nodular hyperplasia
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Clinical signs of hyperaldosteronism is mainly from —-
Hypertension (end organ damage) Hypokalemia (not usually hypernatremia) PU PD Atrophy arrhythmia pendulous abdomen Blindness (retinal detachment) weight loss restless Plantjgrade stance Cervical ventroflexion
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Conn’s lab findings:
``` Hypokalemia Metabolism alkalosis Azotemia Increase phosphorus Increase CK Hyperglycemia Hypernatremia Inappropriate kaliuresis Increased aldosterone: creatinine ratio ```
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How is conn diagnosed
US CT MRI Adrenal mass Metastasis Local invasion by adrenal mass
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How is conn treated
Sx- adrenalectomy for unilateral adenoma or carcinoma | Medical- k, spironolactone (aldosterone blocker), amlodipine
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Insulinoma is a tumor of
Pancreatic beta cells | Most common canine islet cell neoplasia (most are carcinoma)
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How is an insulinoma diagnosed
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%)
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How is an insulinoma treated
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
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How is insulinoma medically managed
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
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Insulinoma prognosis
12-14 month survival time Young dog worse prognosis Post op hyperglycemia better than hypo Can become diabetic after Sx