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Small Animal Med > Exam 3 (Starts w/ Endocrine) > Flashcards

Exam 3 (Starts w/ Endocrine) Flashcards

1
Q

Adrenal Anatomy

A

Outside
o Zona glomerulosa – salt – ALD
o Zona Fasciculata – sugar – glucocorticoids
o Reticularis – sex – androgens
Medulla

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2
Q

Affects of Cortisol

A

o Gluconeogenesis/Glycogenolysis

o Maintenance of vascular tone

o Stimulation of erythropoiesis
o Anti-inflammatory
o Adaptation to stress

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3
Q

ALD; regulation, release, primary function

A

Regulated by
* Renin-angitotensin aldosterone system

Released due to
* Hypovolemia
* Hyponatremia
* Hyperkalemia

Primary Function
* Increase Na & Cl reabsorption
* Increase K & H+ secretion

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4
Q

Hypoadrenocorticism (Addison’s) Causes

A

Primary
* Immune mediated destruction of adrenal gland
* Iatrogenic destruction

Secondary
* Rare
* Decreased ACTH due to pituitary lesion

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5
Q

Hypoadrenocorticism (Addison’s); Types

A

Typical
* Electrolyte abnormalities
* Supplementation of cortisol (glucocorticoid) & aldosterone (mineralcorticoid) needed

Atypical
* No electrolyte abnormalities
* Signs of cortisol deficiency only
* Supplementation of cortisol only
* May have normal/partial/no ALD production

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6
Q

Hypoadrenocorticism (Addison’s); Signalment

A
  • Young to middle aged females
  • Standard poodles (doodles)
  • Lots of other breeds at risk
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7
Q

Hypoadrenocorticism (Addison’s); Clinical Signs

A

Acute
* Addisonian crisis
* Present recumbent & in shock

Chonic
* Waxing & waning GI signs
* Chronic PU/PD, lethargy, weightloss

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8
Q

Hypoadrenocorticism (Addison’s); Lab Values

A

CBC
* No stress leukogram
* Eosinophilia
* Lymphocytosis
* Non-regenerative anemia

UA
* Isosthenuria even w/ dehydration (can be hidden by dehydration)

Chem
* Hyponatremia, hyperkalemia, azotemia, hyperphosphatemia (common)
* Hypercalcemia
* Hypoalbuminemia
* Hypoglycemia
* Hypocholesterolemia
* Elevated liver enzymes

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9
Q

Cortisol Vs ALD Deficit

A

Cortisol
* V/D
* Hypoglycemia
* Maintenance of vascular tone

ALD
* PU/PD
* Hyperkalemia
* hyponatremia

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10
Q

Hypoadrenocorticism (Addison’s); Diagnosis

A

Na:K ratio
* K<27 w/ typical addison’s
* NOT HELPFUL in atypical Addison’s

Baseline Cortisol
* <2 – need ACTH stim test
* >2 not Addison’s

ACTH Stim
* Give cosyntropin (ACTH) IV ->
* Measure cortisol 1 hr post administration ->
* Normal animals will have elevated cortisol value 

* Post stim cortisol <2 = Addison’s

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11
Q

Hypoadrenocorticism (Addison’s); Treatment

A

Acute
* IV fluids & symptomatic care
* If you don’t have results of stim right away, give dexamethasone
* Once Na levels are steady, give mineralcorticoid

Chonic
* 0.1-.025mg/kg/d Oral prednisone (glucocorticoid)
* DOCP IM or SQ every 25d (mineralcorticoid)
* Daily Oral Florinef (glucocorticoid & mineralcorticoid)

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12
Q

Hypoadrenocorticism (Addison’s); Monitoring & Prognosis

A

Monitoring
* Monitor electrolytes (due to mineralcorticoid)
* Decrease pred dose if seeing PU/PD, polyphagia, elevated liver enzymes
* Increase pred if seeing GI signs

Prognosis
* Good
* Need lifelong treatment
* Meds are expensive

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13
Q

Hyperadrenocorticism (Cushing’s); Causes, Clinical Signs

A

Causes
o Pituitary gland tumor (ACTH) (small dogs)
o Adrenal gland tumor (Cortisol) (large dogs)
o Treatment w/ steroids
o Most are PDH

Clinical Signs
o PU/PD
o Polyphagia
o Panting due to weakness of diaphragm
o Alopecia
o Recurrent UTIs
o Weakness & muscle wasting
o Abdominal distension
o Dyspnea due to pulmonary thromboembolism
o Neuro signs due to tumor compression on brain

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14
Q

Hyperadrenocorticism (Cushing’s); Ways to Diagnose

A
  • CBC/Chem
  • UA
  • Imaging
  • Urine cortisol/creatinine ratio
  • ACTH stim test
  • Low Dose Dex Suppression Test
  • Endogenous ACTH
  • Abdominal ultrasound
  • CT/MRI
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15
Q

Hyperadrenocorticism (Cushing’s); Expected CBC/Chem, UA, Imaging

A

CBC/Chem
* Stress leukogram
* Thrombocytosis
* Increased ALP
* Hypercholesterolemia
* May have increased ALT & glucose

UA
* Isosthenuria (1.007 – 1.012)
* Proteinuria
* UTIs

Imaging
* Hepatomegaly
* Mets in lungs from adrenal carcinoma (rare)

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16
Q

Urine cortisol/creatinine ratio

A

Negative rules out Cushing’s
* First pee in the am before any “stress”
* Shows elevated cortisol but not “why”

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17
Q

ACTH Stim test For Cushing’s

A
  • Only test usable for iatrogenic cause of Cushing’s
  • Does not differentiate PDH & ADH
  • Post cortisol value >21ug/dL -> most likely cushings
  • Normal result doesn’t rule out Adrenal dependent
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18
Q

Low Dose Dexamethasone Suppression Test For Cushing’s

A
  • Differentiates between ADH & PDH
  • Does not diagnose iatrogenic
  • cannot suppress ADH

8hr
* >1.4ug/dL = Cushings
* cortisol <50% baseline but greater than lab cut off = PDH

4hr
* if cortisol below lab cut off or <50% baseline = PDH
AND
* >1.4ug/dL at 8hrs = Cushings

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19
Q

High Dose Deamethasone Suppression Test For Cushing’s

A

expect suppression at both 4hr & 8hr OR or suppression at 4hr & rebound at 8hr

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20
Q

Endogenous ACTH Test

A

Adrenal Tumor
* ACTH suppressd by negative feedback -> low ACTH

Pituitary Tumor
* ACTH levels normal or high

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21
Q

Abdominal Ultrasound & CT/MRI for Cushing’s

A

Abdominal Ultrasound
* Look ay adrenal size

CT/MRI
* Evaluate pituitary
* Look for macroedema

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22
Q

Hyperadrenocorticism (Cushing’s); Reasons to treat or not

A

Treat
* Urinary accidents and nighttime urination
* Excessive appetite driving the owners crazy
* Secondary infections/ Complications
* Concurrent disease such as diabetes mellitus

No
* Cost
* Side effects/risks
* May not prevent secondary complications

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23
Q

Hyperadrenocorticism (Cushing’s); Treatment for PDH

A

Mitotane
* Chemotherapeutic agent

* Adrenolytic – destroys adrenal tissue
* Less expensive & less frequent dose
* Monitor with ACTH stim tests

Trilostane
* Synthetic steroid analog -> prevents formation of cortisol 

* Reversible and dose dependent 

* “user friendly”
* Monitor with ACTH stim testing 
& electrolytes 


Radiation
* Expensive
* Effectiveness varies

Surgery
* Hypophysectomy
* Need to supplement pituitary hormones post
* Need highly skilled surgeon
* Expensive

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24
Q

Hyperadrenocorticism (Cushing’s); ADH Treatment

A

Trilostane or Mitotane
* Both control clinical signs

Surgery
* Adrenalectomy
* May be curative (recommended)

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25
Q

Hyperadrenocorticism (Cushing’s); Prognosis

A

o Pituitary microadenoma – good
o Pituitary macroadenoma – poor w/o treatment & fair w/
o Adrenal tumor – good to poor depending on treatment

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26
Q

PTH; Where is it made, function in bone, kidney, small intestine

A

o Made by chief cells in parathyroid glands

Bone
* Increase resorption of Ca & P -> blood

Kidney
* Increases Ca resoprtion
* Increases P excretion
* Stimulates synthesis of Calcitriol

Small intestines
* Calcitrol induced by PTH increases Ca & P absorption in intestines

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27
Q

Calcitriol Function

A

o Increases absorption of Ca & P from intestines
o Increase Ca & P retention in kidneys
o More calcitriol -> decreases PTH

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28
Q

Calcitonin Function

A

o Made in parfollicular cells of thyroid
o Decrease serum Ca
o Opposite effects of PTH

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29
Q

Differentials for Hypercalcemia

A

o HOGS IN YARD

Hyperparathyroidism
o high PTH, high iCa, decreased P

Osteolytic

Granulomatous Dz
o high calcitriol, increased Ca, maybe increased P

Spurious

Idiopathic, Iatrogenic

Neoplasia
o high PTH-rp, high iCa, P & PTH decreased or normal

Young

Addison’s
o high total Ca & P

Renal Dz
o high total Ca & P

Vitamin D Toxicity
o high calcitriol, High Ca & P

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30
Q

Narrow Down Differentials for Hypercalcemia

A

Phosphorous Levels
* PTH causes low – low/normal P
* Calcitriol causes high-high/normal P

PTH Levels
* High Ca -> low PTH
* PTH normal or high -> increased production of PTH

31
Q

Primary Hyperparathyroidism; What is it? Causes, Signalment, Clinical Signs

A

o Excessive production of PTH by parathyroid glans

Causes
* Parathyroid adenoma
* Parathyroid carcinoma
* Parathyroid hyperplasia

Signalment
* Middle age
* Keeshonds, labs, goldens, german shepherds

Clinical Signs
* Usually not clinical (seem healthy)
* If clinical -> PU/PD, lethargy, UTIs,
* Chronic eventually leads to renal failure

32
Q

Primary Hyperparathyroidism; Lab Findings, imaging, Diagnosis

A

Lab Findings
* Hypercalcemia
* Low-low/normal P
* Isosthenuria or hypersthenuria

Imaging
* Nephrolyths/calculi on rads or ultrasound
* Thoracic rads my show mets
* Cervical ultrasound or CT shows mass in area of thyroid gland or visible parathyroid glands

Diagnosis
* Malignancy panel -> elevated PTHrp -> hypercalcemia of malignancy
* Elevated iCa + elevated or normal PTH

33
Q

Primary Hyperparathyroidism; Treatment

A

Treatment
* physiologic saline diuresis
* Furosemide
* Glucocorticoids
* Bisphosphonates
* Cinacalcet
* Surgical removal of affected glands

Surgery
* Prophylactic calcitrol prior to Sx -> taper over 2-4mo
* Ca supplementation post Sx -> taper over 2-4mo
* Must keep Ca high enough until parathyroid gland recovers

34
Q

Hypoparathyroidism; Causes, Signalment, Clinical Signs, Diagnosis, Treatment

A

Causes
* Suppressed secretion of PTH due to trauma surgery etc
* Atrophy due to sudden correction of chronic hypercalcemia
* Iatrogenic due to removal of parathyroid
* Immune mediated destruction of parathyroid gland

Signalment
* Dogs > cats
* Females > males
* Poodles, mini schnauzers, german sheps, labs, terriers

Clinical Signs
* Seizures
* Facial/paw rubbing/licking/biting
* Tetany/muscle spasms
* Stiff gait
* Anorexia
* Lethargy
* V/D
* Cataracts
* Fever
* Cardiac abnormalities

Diagnosis
* Decreased iCa + increased P
* Low-low/normal PTH
* Decreased calcitriol

Treatment
* IV Ca gluconate (in emergency)
* Calcitriol for life
* Oral Ca carbonate until dz is stable

35
Q

Hypocalcemia; Differentials

A

PEACE PAIN
* Phosphate enemas
* Eclampsia
* Albumin decrease
* Chronic renal dz
* Ethylene glycol toxicity
* PTH deficiency
* Acute pancreatitis
* Intestinal malabsorption
* Nutritional Vit D deficiency

36
Q

T3

A

o Most biologically active
o Enters cell more rapidly
o 3-5 times more potent than T4
o most produced by deiodination of T4

37
Q

Thyroid Hormone Production

A

o Thyroid peroxidase binds tyrosine on thyroglobulins + oxidized iodide ->
o iodinated tyrosine ->
o T 3 & T4 bind to TG & secreted

38
Q

Primary Hypothyroidism; What is it? Causes, Signalment, Clinical SIgns

A

o Decreased T3 & 4

Causes
* Thyroiditis
* Idiopathic thyroid atrophy
* Bilateral thyroid neoplasia (rare)

Signalment
* Borzoi, toy fox terrier, beagle

Clinical Signs
* Lethargy
* Weight gain
* Cold intolerance
* Symmetric alopecia
* Seborrhea
* Hyperpigmentation
* Rat tail
* “sad” expression
* weakness / ataxia
* seizures / mentation changes
* facial nerve paralysis / vestibular dz
* bradycardia

39
Q

Hypothyroidism; Diagnosis

A
  • Normocytic, normochromic, non-regenerative anemia
  • Fasting hypertriglyceridemia & hypercholesterolemia
  • Increased ALP
  • Total T4 for screening (can have false +)

Diagnostic
* Low Free T4 by equilibrium dialysis
* High TSH (normal does not rule out)

40
Q

Euthyroid Sick Syndrome

A
  • Underlying illness suppressing thyroid hormone
  • Decreased total T4
  • Normal TSH
41
Q

Effect of Drugs on Thyroid Testing

A
  • Glucocorticoids can decreas TT4, FT4, & TSH
  • Phenobarbital & TMS can decrease TT4, FT4 & increase TSH
42
Q

Hypothyroidism Therapeutic Trial

A
  • Treat w/ Levothyroxine ->
  • Wait 4-8wks ->
  • Assess for improvements of clinical signs ->
  • Stop supplementation if response seen ->
  • Return of signs = most likely hypothyroid
43
Q

Treatment for Hypothyroidism

A
  • Levothyroxine (synthetic T4)
  • Improve activity first 1-2 wks
  • Weightloss seen in 8 wks
  • Normal haircoat may take months
  • Neuro signs improve rapidly but may take 8-12 wks for full recovery
44
Q

Feline Hyperthyroidism; Causes, Clinical Signs

A

Causes
* Overproduction of hormone from thyroid benign adenoma
* Malignant carcinoma (rare)
* Genetic
* Too much idodine
* Too little selenium consumption
* Toxins in environement
* Immune mediated
* Infectious

Clinical Signs
* Weight loss
* Polyphagia
* PU/PD
* Hyperactivity
* Vomiting
* Anorexia, depression (less common)
* May have palpable thyroid mass (thyroid slip)
* Poor hair coat
* Dehydration
* Maybe cervical ventroflexion (weakness)
* Cardiac issues
* Hypertension & fundic abnormalities

45
Q

Feline Hyperthyroidism; Diagnosis, Treatment, Prognosis

A

Diagnosis
* Increased PCV
* Increased ALT
* May have azotemia
* Isosthenuria
* Increased total T4 (definitive) ->
* Repeat Total T4 ->
* Measure free T4 ->
* T3 suppression test ->
* Nuclear scintigraphy

Treatment
* Methimazole (blocks hormone synthesis = significant side effects but reversible unlike other treatment)
* Amlodipine for hypertension
* Propanolol or Atenolol to reduce tachycardia, arrhythmias, hyperactivity
* Surgery
* Radioactive iodine
* Iodine restricted diet

Prognosis
* Generally good

46
Q

T3 Suppression Test

A
  • Last resort
  • T3 should inhibit TSH
  • Decreased TSH = decreased T4
  • After T3 administrtaion -> T4 should decrease 50% -> Hyperthryoid cats don’t really suppress
47
Q

Nuclear Scintigraphy

A
  • Administer radioactive isotope ->
  • Hyperthyroid have increased uptale ->
  • Quantify gamma emission
  • Helps differentiate adenoma from carcinoma
48
Q

Insulin Dependent Vs Non-insulin Dependent Diabetes Mellitus

A

Insulin Dependent
o Autoimmune damage ->
o beta cells can’t produce insulin ->
o not reversible
o dogs
o 20% of cats

Non-insulin Dependent
o Insulin resistance
o Beta cell dysfunction
o 80% of cats
o potentially reversible

49
Q

Diabetes Mellitus; Signalment

A

Dogs
* Females > males
* Middle aged
* Small breeds & samoyeds

Cats
* Neutered males
* >6yo
* Burmese, abssynians, Siamese

50
Q

Diabetes Mellitus; Clinical Signs

A

o PU/PD
o Polyphagia
o Weight loss
o Many are “well”

Diabetic ketoacidosis or
Hyperglycemic/hyperosmolar syndrome (rare)
* Anorexia
* Dehydration
* Vomiting
* Lethargy

51
Q

Diabetes Mellitus; Diagnosis, Treatment

A

Diagnosis
o Hyperglycemia (don’t confuse w/ stress)
o Glucosuria
o Elevated ALP (dogs)
o hypercholesterolemia
o Maybe ketonuria & proteinuria
o Maybe elevated fructosamine
o Rads & ultrasound to look for underlying cause

Treatment
o Insulin BID following meal
o Oral hypoglycemic agents (not recommended)
o Maintain ideal BCS w/ exercise in diets
o Increase fiber & decrease sugar & fat for dogs
o Increase protein and decrease carbs for cats

52
Q

Diabetes Mellitus; Concurrent Disease & Wether to Test

A

o Pancreatitis
o Exocrine pancreatic insufficiency
o Hypothyroid in dogs (wait to test)
o Hyperthyroid in cats (assess w/ diabetes diagnosis)
o Hyperadrenocorticism (wait to test)

53
Q

Diabetes Mellitus Remission

A

o Possible w/ insulin, diet, & treatment of concurrent dz
o More likely when caught early, older cats, cats w/o peripheral neuropathy
o Risk of hypoglycemia if insulin becomes unnecessary
o After remission continue low carb diet & weight monitoring

54
Q

Blood Glucose Curve; Basics, Nadir, Duration, Affects on Results

A

o 7 days after starting insulin for first time, changing dose, or changing type
o feed & give insulin as normal -> check BG every 2hrs for 12 hrs

Nadir
* time & value when BG is lowest (should happen at 6hrs)
* want to shift up or down – change dose
* if nadir not at 6hrs, change insulin
* Target BG is 100-250

Duration
* amount of time following insulin where BG<250

Affects Results
* Forgetting insulin
* Inappetence
* Vomiting
* Stress hyperglycemia
* Somogyi effect

55
Q

Somogyi Effect

A

o Too much insulin ->
o hypoglycemia (<65 or rapid drop) ->
o diabetogenic hormones take over ->
o rebound hyperglycemia (>300)
o misinterpretation

56
Q

Continuous Glucose Mnitoring

A

o FreeStyle Libre
o Button on skin
o Lasts up to 14 days
o At home use
o Measure interstitial BG
o Values may be lower than curve -> look at trends
o May be hard to keep on patient

57
Q

Amount to Adjust Insulin Dose

A

Dogs
* 10-25% each dose

Cats
* ½ unit per dose

58
Q

Chronic Monitoring for Diabetes Mellitus

A

o Repeat BG curve every 7 days until regulated ->
o Then in 1 month ->
o Then every 3-6mo or clinical signs present
o Repeat urine culture every 6mo

59
Q

Serum Fructosamine

A

o Glucose bound (glycated) proteins made independent of insulin concentrations 

o Marker of BG concentration over the past 2-3 wks 

o Trends most useful 

o Measure when 1st regulated then every 3-6 months 

o Not affected by stress so helpful in cats especially 

o Used for fractious or difficult and well-regulated patients

60
Q

Complications of Diabetes Mellitus

A

Hypoglycemia
* Neuro signs
* Keep karo syrup on hand to rub on gums
* IV dextrose may be needed

Cataracts
* Dogs
* Secondary lens induced uveitis
* Can treat w/ surgery

Diabetic Neuropathy
* Cats
* Rear limb weakness
* Plantigrade stance
* Treat by improving regulation

Diabetic Ketoacidosis

61
Q

Diabetic Ketoacidosis; Triggers, Pathophysiology, Lab Values

A

Trigger
* Marked insulin deficiency
* Concurrent dz that causes insulin resistance

Pathophysiology
* Insulin does not help glucose uptake ->
* Cells starved and start to use free fatty acids & ketone bodies ->
* Ketone bodies overwhelm body’s buffering capacity ->
* Acidosis, osmotic diuresis, dehydration

Lab Signs
* Non-regenerative anemia
* Neutrophilia & Heinz bodies
* Increased ALP, ALT, cholesterol
* Azotemia
* Hypokalemia
* Hypophosphatemia

* Hypomagnesemia
* Hyponatremia (pseudo)
* Hypochloremia

62
Q

Diabetic Ketoacidosis; Treatment, Monitoring, Prognosis

A

Treatment
* Rehydrate w/ isotonic fluids over 24hrs
* IV CRI or IM insulin
* Monitor BG every 1-2hrs
* Monitor K, P, elctrolytes
* Check urine ketones every 24hrs

Monitoring
* BG every 1-2hrs
* K, P, electrolytes every 4-6hrs
* Urine ketones every 24hrs

Prognosis
* 70% survive to discharge

63
Q

Central Diabetes Insipidus

A
  • rare
  • Partial or complete ADH deficiency
  • decreased ability/inability of the kidneys to conserve water and concentrate urine in response to increases in plasma osmolality ->
  • Increased plasma osmolality because fluid is lost in excess of solute ->
  • stimulates thirst
  • usually hyposthenuric but partial can be isosthenuric
64
Q

Nephrogenic Diabetes Insipidus

A
  • Kidneys not responding to ADH
  • Receptors not present or not responsive

Primary
* Congenital defect
* Mutation in ADH receptor or aquaporin
* hyposthenuria

Secondary
* Most common
* Conditions affecting ADH binding and function in the renal tubules, loss of medullary gradient, or osmotic diuresis

65
Q

Testing for Primary Diabetes Insipidus

A

Modified water deprivation test
* Dangerous & time consuming
* Gradually limit water over 3-5d ->
* Remove water and monitor weight, PCV, TP, BUN, Na every 1-2hrs ->
* Look for 5% dehydration or >1.025 USG
* No concentration of urine ->
* Try DDAVP administration test

Serum Osmolality Testing
* Central diabetes insipidus = high-normal
* Psychogenic = low-normal

Exogenous DDAVP Administration
* Increase in USG by 50% Or >1.030 in day 5-7
* = central DI, psyochogenic, or hyperadrenocorticsim

66
Q

Diabetes Insipidus Treatment

A

Acquired Nephrogenic
* Address underlying cause

Central
* DDAVP lifelong

Congenital nephrogenic
* low Na diet
* thiazide diuretics
OR
* Allow constant access to water

67
Q

Diabetes Insipidus Prognosis

A

Acquired Nephrogenic
* Dependent on underlying dz

Congenital Nephrogenic
* Good w/ constant water

Central
* Dependent on lesion

68
Q

Acromegaly; Cause, Signalment, Clinical SIgns, Diagnosis, Treatment

A

Cause
* Functional adenoma in pars distalis of anterior pituitary ->
* Excessive growth hormone ->
* Liver produces insulin-like growth factors

Signalment
* Older
* Males > females
* Uncontrolled DM w/ weight gain

Clinical Signs
* Enlargement of extremities, jaw, tongue, forehead
* Clubbing of paws
* Organ enlargement
* Stridor due to growth of soft tissue in mouth and pharyngeal region
* Degenerative joint disease
* Cardiac signs leading to CHF
* Hypertension
* CNS signs
* Thickening of skin
* Renal signs leading to CRF

Diagnosis
* Test IGF-1 levels (false negatives or positives w/ diabetes)
* CT or MRI of pituitary gland

Treatment
* Sx – Transsphenoidal hypophysectomy
* Radiation (long time)
* Somatostatin anologs (need more research)
* Palliative – high dose insulin & diabetic diet (poor prognosis)

69
Q

Acromegaly in dogs

A

o RARE
o Excessive exogenous progesterone
o OR
o Excessive endogenous progesterone in cycling older intact females

70
Q

Feline Cushing’s; Cause, Signalment, Clinical SIgns, Diagnosis, Treatment

A

Cause
* Rare
* Adenoma in pituitary (most common)
* Benign functional adenoma in adrenal gland (less likely)

Clinical Signs
* Clinical signs of diabetes mellitus
* Weight loss > weight gain
* PU/PD
* Polyphagia
* Pot belly
* Muscle atrophy
* Bilateral symmetric alopecia
* Predisposed to infections
* Fragile skin
* Blindness, abnormal behavior (pituitary)
* Spines on castrated males (adrenal)

Diagnosis
* Stress leukogram
* Lack of effect of cortisol on ADH secretion/sensitivity
* May be Glucosuria
* Maybe proteinuria
* Low dose dex suppression test is test of choice
* High dose to differentiate pituitary from adrenal

Treatment
* Trilostane (preferred)
* Mitotane
* Metyrapone
* Radiation
* Hypophysectomy
* Adrenalectomy

71
Q

Primary Hyperaldoseronism (Conn’s); Signalment, Cause, Clinical Signs

A

Signalment
* Cats > dogs
* older

Cause
* Adrenocortical carcinoma

* Adenoma (unilateral or bilateral)
* Bilateral nodular hyperplasia

Clinical Signs
* Hypertension -> organ damage
* PU/PD
* Muscle atrophy
* Arrhythmia
* Pendulous abdomen/mass
* Blindness (retinal detachment)
* Plantigrade stance
* Cervical ventroflexion

72
Q

Primary Hyperaldoseronism (Conn’s); Lab Findings, Diagnosis, Treatment

A

Lab
* Hypokalemia
* Metabolic alkalosis
* Azotemia
* Increased phosphorus
* Increased CK
* Hyperglycemia
* Hypernatremia

Diagnosis
* Imaging looking for adrenal mass, metastatis

Treatment
* Adrenalectomy (complications_
* K supplementation
* Spironolactone (blocks ALD)
* Amlodipine (hypertension)

73
Q

Insulinoma; Cause, Signalment, Clinical Signs, Diagnosis, Treatment, Prognosis

A

Cause
* Pancreatic beta cell tumors

Signalment
* Older
* Medium-large dogs
* Ferrets > dogs > cats

Clinical Signs
* Hypoglycemia
* Overweight
* +/- mild hypokalemia
* +/- elevated ALP/ALT

Diagnosis
* Paired insulin & BG levels
* Increased insulin despite low BG
* Imaging to find mass

Treatment
* Surgery (difficult to find tumor)
* Steptozotocin chemo
* Frequent small meals, high protein & fat
* Glucocorticoids
* Diazoxide
* Somatostatin
* Glucagon

Prognosis
* poor

Small Animal Med (10 decks)

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