Endocrine/Exocrine Flashcards

Question

What does posterior pituitary secrete? ## Footnote x2

Answer 1

secretes antidiuretic hormone (ADH), also known as vasopressin, and oxytocin.

Answer 2

In response to **corticotropin‐releasing hormone (CTRH) from the hypothalamus,** -- the **anterior pituitary gland secretes adrenocorticotropic hormone (ACTH)** which acts on the **cortex of the adrenal gland** to secrete cortisol to the body

Answer 3

* dysfunction of pancreatic beta cells results in an absolute or relative deficiency of insulin * Type 1 or Type 2

Answer 4

Without insulin, glucose is unable to enter the cells, = osmotic diuresis and compensatory polydipsia with the potential for severe dehydration if the patient is unable to keep up with the water requirements

Answer 5

primary insulin‐dependent diabetes mellitus (type 1), resulting from **destruction of insulin‐producing pancreatic beta cells** -- can be congenital, immune mediated, or idiopathic ## Footnote Receptors are functional but there is no insulin production

Answer 6

**non‐insulin‐dependent diabetes mellitus** (type 2), resulting from a combination of insulin resistance, dysfunctioning beta cells (producing less insulin), and increased hepatic gluconeogenesis -- insulin secretion may be high, low, or normal, but is insufficient to overcome the **insulin resistance present in the patient** -- Obesity, genetics, islet amyloidosis, and abnormal insulin response are possible causes ## Footnote Insulin is present but receptors are dysfunctioning

Answer 7

develop carbohydrate intolerance secondary to concurrent insulin‐resistant disease, such as **pregnancy (diestrus)**, **hyperadrenocorticism**, or acromegaly. -- Secondary diabetes mellitus can result in permanent primary insulin‐dependent diabetes mellitus

Answer 8

refers to **beta cell damage caused by persistent hyperglycemia** and is reversible if caught early

Answer 9

Goals: correcting obesity, providing caloric stability, and minimizing postprandial blood glucose fluctuations -- **high in complex carbohydrates (i.e. fiber)**. Fiber helps promote weight loss and slows absorption of glucose from the gastrointestinal tract, which helps reduce the postprandial flux of glucose -- cats with non‐insulin‐dependent diabetes mellitus, benefit from a high‐protein diet

Answer 10

-- Porcine, human, and canine insulin are similar in chemical structure -- bovine and feline insulins are more similar.

Answer 11

also called crystalline zinc, -- short‐acting human insulin with a **duration of approximately six hours.** -- starts working after subcutaneous injection after approximately 30 minutes and **peaks at between two and four hours** -- often given as a constant rate infusion to treat diabetic ketoacidosis. -- Regular insulin is the only type of insulin that is potentially administered intravenously. -- can also be given IM in the intensive care unit after meals to complement another insulin. .

Answer 12

has two peaks of activity following subcutaneous administration I**n Dogs:** -- first peak (amporphous insulin peak) occurring at 2–6 hours -- second (crystalline insulin peak) at 8–14 hours, with a total duration of 10–24 hours. **In cats:** -- peak activity following subcutaneous administration occurs at 1.5–8 hours, and the duration of activity varies between eight and 12 hours.

Answer 13

isophane insulin, which contains protamine, a protein that slows insulin absorption. peaks in 4–6 hours and lasts 14–20 hours.

Answer 14

For use in cats: protamine and zinc buffers create an extremely slow absorption such that PZI **peaks in 16–18 hours** and can **last up to 36 hours** -- long duration can be variable and thus may make tight glycemic control hard to achieve

Answer 15

recombinant human insulin that forms microprecipitates at the injection site that last for 24 hours -- Glargine is commonly used in cats and has a minimal peak but a steady effect that lasts 18–26 hours

Answer 16

blood glucose should remain >80 mg/dL at all times ideally be between 100–300 mg/dL for the diabetic cat 100–250 mg/dL for the diabetic dog

Answer 17

-- Fructosamine is** formed by glycosylation of serum proteins such as albumin.** -- concentrations are directly related to blood glucose concentrations. -- The higher the blood glucose concentrations over the past 2–3 weeks, the higher the fructosamine level will be. -- is not dramatically affected by isolated changes in blood glucose, such as might be seen from stress or excitement ## Footnote Values >500 µmol/L suggest inadequate control of diabetes.

Answer 18

Doses of insulin that are too high may bring about the Somogyi phenomenon = **episodes of hypoglycemia followed by rebound hyperglycemia.** -- asymptomatic hypoglycemia occurs undetected, the rebound release of glucagon, epinephrine, cortisol, and growth hormone can result in insulin resistance and hyperglycemia persisting for 24–72 hours after a hypoglycemic event.

Answer 19

1. alpha cells secrete glucagon, 1. beta cells secrete insulin, 1. delta cells secrete somatostatin 1. F cells secrete pancreatic polypeptide

Answer 20

-- insulin deficiency, -- diabetogenic hormone excess, -- fasting, and dehydration -- ultimately responsible for the **increase in ketogenesis and gluconeogenesis** -- hyperglycemia/glucosuria, ketonemia/ketonuria, and high anion gap metabolic acidosis

Answer 21

-- **cytokine dysregulation** may contribute to ketogenesis, along with **increases in glucagon despite detectable to even normal insulin** levels. -- insufficient insulin action and increased concentrations of counterregulatory hormones and cytokines **contributes to increased lipolysis and decreased fatty acid storage**, resulting in increased circulating concentrations of free fatty acids

Answer 22

1. pancreatitis, 1. bacterial urinary tract infections, 1. neoplasia, 1. hyperadrenocorticism ## Footnote **Any potential to trigger the secretion of insulin counterregulatory hormones** such as glucagon, catecholamines, cortisol, and growth hormone.

Answer 23

1. Beta‐hydroxybutyrate 1. Acetoacetate 1. Acetone → **Acetoacetate** and **β-hydroxybutyrate** are anions of **moderately strong acids** that dissociate to a significant degree at physiologic pH, resulting in a **metabolic acidosis and high Anion Gap**

Answer 24

1. hepatic lipidosis, 1. cholangiohepatitis, 1. pancreatitis, 1. bacterial and viral infections 1. neoplasia ## Footnote **Any potential to trigger the secretion of insulin counterregulatory hormones** such as glucagon, catecholamines, cortisol, and growth hormone.

Answer 25

promotes glycogenolysis, gluconeogenesis, lipolysis, proteolysis, and ketone production (ketogenesis). -- liver is stimulated to produce glucose but cells are **unable to utilize this glucose due to lack of insulin** -- with the lack of insulin, fatty acids are converted to acetyl CoA, → into **beta‐hydroxybutyrate**, → further broken down into **acetoacetate** and **acetone**

Answer 26

-- FFA → mitochondrial beta oxidation → acetyl-coenzyme A (acetyl-CoA), which then enters the **citric acid cycle** to contribute to ATP production -- # of acetyl-CoA carriers in the citric acid cycle is reduced → oxidation of excess acetyl-CoA into ketone bodies = **acetoacetate,** which can then be metabolized to **β-hydroxybutyrate** (the predominant ketone body in dogs and cats suffering from DKA), and **acetone**.

Answer 27

diabetogenic hormone excess (glucagon, cortisol, growth hormone, and catecholamines)

Answer 28

Ketonemia overwhelms the body’s buffering system → increase in H+ concentration, a compensatory decrease in HCO3− and a lowering of the blood pH = acidemia

Answer 29

-- **Glucosuria-induced osmotic diuresis**→ worsens dehydration and electrolyte imbalances. -- Osmotic diuresis and V/D and hyperventilation all contribute to dehydration -- can progress to contraction of the intravascular fluid space, leading to hypovolemia, decreased cardiac output, decreased delivery of oxygen to tissue, and hypotension.

Answer 30

sodium, potassium, phosphorus, and magnesium -- Circulating electrolytes are **lost excessively due to increased osmotic renal secretion.**

Answer 31

-- volume depletion, acidosis progress, decreased renal perfusion, renal excretion, and hypoinsulinemia -- may make extracellular K+, phos-, and mg++ concentrations appear normal in untreated DKA. -- Acidosis can further contribute to normal extracellular potassium concentration due to **shifting of K+ ions to the extracellular space in exchange for H+ ions.**

Answer 32

Kussmaul respiration

Answer 33

unremarkable or exhibit derangements = -- Hemoconcentration -- Leukocytosis, characterized by neutrophilia with a left shift = concurrent systemic infection (e.g. urinary tract infection) or inflammation (e.g. concurrent pancreatitis) -- normochromic-normocytic anemia (approx. 1/2)

Answer 34

-- changes to liver and choleostatic enzymes -- (ALT), total bilirubin, (ALKP), → diabetic hepatopathy, decreased hepatic blood flow, hepatic lipidosis, or pancreatitis -- prerenal azotemia secondary to dehydration and decreased cardiac output -- Hyperlipidemia -- Hypercholesterolemia and increases in ALT are also common features of feline DKA

Answer 35

**Insulin deficiency** prevents activation of lipoprotein lipase → lipemia results

Answer 36

reveal a metabolic acidemia with secondary respiratory alkalosis

Answer 37

frequently a whole‐body depletion of many of these ions (e.g. potassium, magnesium) typicall despite inital normal values. -- Abnormalities often seen as treatment progresses and electrolytes shift between the intracellular and extracellular spaces, revealing an overall depletion of one or all of these electrolytes. ## Footnote Ex: K+ becomes extracellular with acidemia, then with gradual resolution becomes hypoK+ as K+ transistions back intracellularly

Answer 38

-- **Urine dipsticks react with acetoacetate** and to a lesser extent acetone, but **NOT** the predominant ketone body **β-hydroxybutyrate** -- is possible that ketonuria is not yet present in early disease. -- plasma or serum from a microhematocrit tube can be used on urine reagent strips to test for acetoacetate and acetone with better sensitivity -- If ketonemia cannot be confirmed with urine reagent strips, blood should be tested specifically for the presence of **β-hydroxybutyrate** using more sensitive quantitative enzymatic assays or a **portable ketone analyzer.** ## Footnote Concentrations of >3.5 mmol/L in dogs and >2.4 mmol/L in cats are associated with DKA

Answer 39

glucosuria, ketonuria, proteinuria, elevated UPC ratio, hemoglobinuria, and hypersthenuria (due to pronounced glucosuria) are present in a large proportion of dogs. -- Pyuria is rarely reported, and urine cultures are negative in up to 87% of dogs -- if urine culture is positive, the most commonly reported bacterial isolate is Escherichia coli.

Answer 40

--HypoNa+ often occurs in patients due to the hyperglycemia itself. -- increase in osmoles w/i circulation draws fluid into the vascular space = dilution of the patient’s sodium concentration. ## Footnote corrected sodium value should be obtained to assess glucose’s influence in sodium concentration

Answer 41

Metabolic acidosis, lack of insulin, and serum hypertonicity contribute to the shift of potassium from the intracellular to the extracellular space

Answer 42

may benefit from magnesium supplementation ## Footnote Both major intracellular Cations

Answer 43

can result in life‐threatening hemolytic anemia, as well as weakness, ataxia, and seizures

Answer 44

should not be used in conjunction with calcium supplementation. --Overzealous phosphate administration can **result in iatrogenic hypocalcemia** and associated neuromuscular signs, hypernatremia, hypotension, and diffuse tissue calcification

Answer 45

vital to achieve metabolic breakdown of the remaining ketone bodies and resolve acidosis

Answer 46

in order to reverse ketosis and resolve acidosis, insulin is required. -- survey of criticalists (October 2020) described near universal support for starting insulin within 6 hours of admission -- DiFazio and Fletcher found that early insulin administration was associated with more rapid resolution of diabetic ketosis (DK)/DKA without an associated increase in complication rates when evaluated retrospectively ## Footnote DK/DKA took longer to resolve in animals with more severe ketonuria.

Answer 47

concern for **cerebral edema** brought about by **too rapid of a drop of glucose** or the presence of hypokalemia that should be corrected before starting insulin

Answer 48

-- CRI or Intermittent IM injections of regular insulin and is important to give hourly initially until the glucose is less than 250 mg/dl (13.9 mmol/L). -- also acceptable to start with longer acting insulin (e.g., NPH or glargine) for the treatment of DKA and add additional short/rapid acting insulin.

Answer 49

by no more than 50 to 75 mg/dl/hr.

Answer 50

-- IV fluids containing **bicarbonate precursors (such as lactate, acetate, or gluconate;**) aid in faster resolution of metabolic acidosis and decrease the incidence of hyperchloremia -- **hyperchloremia associated with negative effects** such as increased time to DKA resolution, risk of acute kidney injury, and increased hospital length of stay

Answer 51

1. paradoxical cerebral acidosis, 1. increased carbon dioxide production and the potential for hypercapnia, 1. increased sodium and osmole concentration, risk for circulatory system overload, 1. iatrogenic metabolic alkalosis, 1. changes to the oxygen dissociation curve (Bohr effect), 1. hypokalemia

Answer 52

Replacement of bicarbonate may not be appropriate, as the metabolic acidosis in DKA is **associated with an accumulation of organic anions rather than a loss of bicarbonate**.

Answer 53

Due to the **concern for metabolic acidosis-induced insulin resistance**, the American Diabetes Association recommends IV bicarbonate therapy in patients with an **arterial pH of < 7.0 after 1 hour of intravenous fluid therapy.** If bicarbonate therapy is considered in veterinary patients with severe metabolic acidosis, it should be **administered at one-third to one-half of the calculated sodium bicarbonate dose**

Answer 54

a **shortage of glucose in the brain** thereby affecting the function of neurons and altering brain function and behavior. -- Glucose is an obligate energy source for the brain and relies on constant stream for function

Answer 55

-- Neurogenic signs result from **activation of the adrenergic system** in response to the hypoglycemia -- Prolonged neuroglycopenia can lead to **permanent brain injury and neurologic signs,** especially blindness, that persist beyond resolution of the hypoglycemia -- altered mentation or dullness, lack of response to stimuli, sleepiness, weakness or recumbency, ataxia, blindness or altered vision, and seizures

Answer 56

secretion of insulin‐like growth factor‐1 (IGF‐1) and **beta cell neoplasia** (insulinoma)

Answer 57

because of increased cell utilization of glucose

Answer 58

pancreatic beta cell tumors that secrete insulin without regulation, resulting in hypoglycemia -- type of APUDoma which can form from amine precursor uptake and decarboxylation (APUD) cells found in the body ## Footnote typically malignant

Answer 59

somatostatinomas, pheochromocytomas, gastrinomas, glucagonomas, insulinomas.

Answer 60

presence or absence of an insulinoma is confirmed by a serum insulin concentration test taken at the time of hypoglycemia -- **elevated insulin levels in the face of hypoglycemia is diagnostic**

Answer 61

improving blood glucose to abolish clinical signs. Increasing blood glucose beyond the point of abolishing clinical signs may result in further insulin secretion and refractory hypoglycemia

Answer 62

1. frequent small meals are given every 1–4 hours consisting of a diet that is high in fat, fiber, and complex carbohydrates. Simple sugars should be avoided. 1. strenuous exercise should be limited. 1. **glucocorticoids such as prednisone may be beneficial to antagonize effects to insulin**, thereby increasing insulin resistance. ## Footnote Short term! sx ultimately needed

Answer 63

**Diazoxide** -- diuretic that works in cases of insulinoma by **inhibiting insulin secretion,** **inhibiting tissue use of glucose**, and **stimulating hepatic gluconeogenesis and glycogenolysis**

Answer 64

Streptozocin and alloxan are chemotherapeutic drugs often used in cases of human insulinoma, but their use in small animal medicine needs further study

Answer 65

**non-β-cell neoplasms associated with hypoglycemia include:** hepatomas and hepatocellular carcinoma, leiomyomas and leiomyosarcomas, other carcinomas or adenocarcinomas (especially those of pulmonary, mammary, salivary and hepatocellular origin) lymphoma, plasmacytoid tumors, oral melanoma, hemangiosarcoma

Answer 66

can cause hypoglycemia via -- **secretion of insulin or insulin-like peptides** -- accelerated **consumption of glucose by the tumor cells** -- or by failure of glycogenolysis or gluconeogenesis **by the liver**

Answer 67

-- oral glucose - lowering drugs sulfonylurea drugs chlorpropamide and glipizide -- **Xylitol**-sweetened products cause hypoglycemia in dogs via its **stimulation of insulin release from β cells**, and hepatic necrosis and failure, -- **β-Blockers contribute to hypoglycemia via interference with adrenergic counterregulatory** mechanisms -- oleander plant

Answer 68

-- inadequate substrate for glycolysis or gluconeogenesis -- Glycogen stores are small and easily depleted in the face of inadequate food intake -- immature hepatic systems (neonates)

Answer 69

Portosystemic shunt, glycogen storage disease, severe inflammatory or infectious hepatitis, hepatic lipidosis, cirrhosis, hepatic neoplasia, and toxicity -- lead to dysfunctions of glucagon storage, glycogenoysis, and glucogeneosis -- functional until 70% of liver failure occurs

Answer 70

Hypoadrenocorticism, specifically hypocortisolism, may lead to hypoglycemia via **loss of cortisol-induced counterregulatory**

Answer 71

-- Decreased intake -- Decreased hepatic function -- noninsulin-mediated increased consumption play a role in sepsis-induced hypoglycemia -- induced by inflammatory mediators ## Footnote Ex: Canine babesiosis

Answer 72

"hunting dog hypoglycemia" -- lean hunting or working dogs engaging in vigorous exercise -- Glucose utilization by muscle markedly increases during exercise and endogenous glucose production, via glycolysis and gluconeogenesis, increases to meet demand -- occurs secondary to glycogen depletion in the face of increased glucose utilization

Answer 73

-- occurs s**econdary to increased metabolism of glucose by the large red blood cell mass** --- or because of **reduced plasma volume** -- measured reduction in blood glucose **primarily an artifactual change** and does not usually result in clinical signs of hypoglycemia

Answer 74

characterized by hyperglycemia (blood glucose >600 mg/dL), hyperosmolarity (>350 mOsm/L), and dehydration without the presence of ketoacidosis ## Footnote normal osmolarity in dogs is approximately 290–310 mOsm/L and 290–330 mOsm/L in the cat.

Answer 75

-- relative or absolute lack of insulin coupled with increases in circulating levels of counterregulatory hormones including **glucagon, epinephrine, cortisol, and growth hormone** -- counterregulatory hormones elevated from stressor typically from concurrent infection or dz

Answer 76

-- Epinephrine limits insulin secretion, increases glucagon secretion, and reduces the use of glucose by peripheral tissues -- **Epinephrine and glucagon inhibit insulin-mediated glucose** uptake in muscle and **stimulate hepatic glycogenolysis and gluconeogenesis** = increasing circulating glucose concentration.

Answer 77

-- **inhibit insulin activity and potentiate the effects of glucagon and epinephrine on hepatic glycogenolysis and gluconeogenesis.** -- Cortisol increases glucose-facilitating lipolysis and the release of amino acids from muscle for gluconeogenesis in the liver -- **GH antagonizes the effects of insulin by decreasing peripheral glucose utilization and promoting lipolysis**

Answer 78

increases in the diabetogenic hormones **increase protein catabolism, which in turn impairs insulin activity in muscle and provides amino acids for hepatic gluconeogenesis.**

Answer 79

HHS is very similar to DKA except that, in HHS, the hyperosmolar state → **hepatic glucagon resistance; and small amounts of circulating insulin → inhibits lipolysis at a fraction of the dose needed for glucose uptake** = **all inhibit lipolysis and ketosis and instead promote HHS.**

Answer 80

It promotes osmotic diuresis = increases the magnitude of the hyperglycemia, thus leading to a **vicious circle of progressive diuresis, dehydration, and hyperosmolality.**

Answer 81

Osmotic diuresis + additional losses (v/d) + decreased water intake = **progressive dehydration, hypovolemia, and ultimately a reduction in the GFR** as the syndrome progresses. -- Reductions in GFR increase the magnitude of hyperglycemia, which exacerbates glucosuria and osmotic diuresis -- all glucose that enters the kidney in excess of the renal threshold will be excreted in the urine

Answer 82

Renal failure and CHF also exacerbate the hyperglycemia associated with HHS because of their effects on GFR -- Myocardial failure, diuretic use, and third spacing of fluids associated with CHF may decrease GFR

Answer 83

metabolic acidosis is caused by **accumulation of uremic acids and lactic acid,** rather than large quantities of ketones

Answer 84

Hyperglycemia will c**ause free water movement into the ECF compartment via osmosis** = “dilute” the serum sodium concentration proportionally → **masking an underlying hypernatremia.** -- HHS patient suffers **significant free water loss secondary to osmotic diuresis** -- **resulting hypernatremia** may be difficult to appreciate due to the **dilutional effect of the concurrent hyperglycemia**.

Answer 85

for every **100 mg/dl increase in glucose above normal (100 mg/dl), the measured serum sodium decreases by 1.6 mEq/dl**

Answer 86

Sodium concentration should be reduced at a rate **no greater than 0.5 mEq/L/h** to avoid cerebral edema and worsening of neurological status

Answer 87

insulin therapy is not as critical for reversal of HHS because much of the syndrome **can be improved just by correcting fluid deficit and GFR.** -- In the **nonketotic HHS patient, insulin should not be given until the hypovolemia has resolved**, dehydration improved, and glucose concentrations are no longer adequately declining (< 50 mg/dl/hr) with appropriate fluid therapy alone

Answer 88

Addison’s disease -- **Primary = adrenal gland failure** -- **Secondary = due to pituitary or hypothalamic dysfunction.** -- generally the result of **bilateral adrenal atrophy with fibrosis that is thought to be idiopathic**in most cases -- **may have an immune‐mediated cause** in some cases -- or iatrogenic causes (e.g. mitotane usage) in others

Answer 89

caused by adrenal gland dysfunction -- has **both glucocorticoid and mineralocorticoid insufficiency**

Answer 90

**Inadequate secretion of glucocorticoids and mineralocorticoids** by the adrenal cortex is responsible for signs and symptoms of hypoadrenocorticism

Answer 91

**inadequate secretion of glucocorticoids only** and does not cause the same classic laboratory signs as traditional hypoadrenocorticism

Answer 92

aldosterone, → normally **promotes renal resorption of sodium and water and excretion of potassium and hydrogen ions.**

Answer 93

cortisol and corticosterone

Answer 94

most often develops in young to middle‐aged female dogs. Breeds that seem to have a higher risk are standard poodles, Portuguese water dogs, Great Danes, Labrador retrievers, rottweilers, West Highland white terriers, and wheaten terriers

Answer 95

Approximately one‐third of dogs in crisis will have **bradycardia** **instead of the normal tachycardia associated with hypovolemia**

Answer 96

1. hyPO-Na+ 2. hypER-K+ 1. hyPO-Cl- 1. Azotemia, 1. mild to moderate metabolic acidosis 1. serum sodium to potassium ratio will be low (< 27:1) -- hypoadrenocorticism have **inappropriately low urine specific gravity** (i.e., < 1.030) -- → attributed to **lack of sodium retention and resultant renal medullary washout** --- Renal concentrating ability returns with mineralocorticoid supplementation

Answer 97

inability to appropriately concentrate urine has been attributed to **lack of sodium retention and resultant renal medullary washout**. -- Renal concentrating ability returns with mineralocorticoid supplementation.

Answer 98

**eosinophilia and the absence of a stress leukogram** -- mild to moderate **anemia that is usually nonregenerative due to lack of cortisol’s tropism on the bone marrow** -- significant **concomitant GI bleeding** can have severe anemia that may be nonregenerative -- normal leukogram or the “reverse stress leukogram” in a sick animal raises suspicion for hypoadrenocorticism

Answer 99

ACTH stimulation test should be performed in patients with serum cortisol ≤2 µg/dL for confirmation -- post stimulation values are consistently less than 5.0 µg/mL.

Answer 100

-- Hypoadrenal patients may have bradycardia whether or not they have hyperkalemia -- bradycardia, diminished or absent P waves, “tented” T waves, wide or bizarre QRS complexes, ventricular fibrillation, or asystole. Other cardiac arrhythmias have also been reported in association with hypoadrenocorticism

Answer 101

-- DexSP emergently then after ACTH test hydrocortisone prednisolone, or methylprednisolone can be used -- HyperK+ treatment

Answer 102

neuroendocrine tumors from the **chromaffin cells of the adrenal medulla** -- high potential to invade the caudal vena cava or blood supply to the kidney -- release catecholamines that lead to **systemic hypertension, tachycardia, increased myocardial oxygen demand**, and cardiac arrhythmias -- may be both locally invasive and metastatic

Answer 103

vague and non‐specific signs -- may occur intermittently or continuously due to the episodic nature of catecholamine release -- diagnosis is usually incidental

Answer 104

-- **mild non-regenerative anemia** possible secondary to chronic disease or an increased mean cell volume or packed cell volume may be seen as a **result of catecholamine or erythropoietin-like stimulation of the bone marrow** -- regenerative anemia may reflect hemorrhage from the tumor --- **Leukocytosis or a stress leukogram may be found secondary to catecholamine release** or inflammatory changes associated with the tumor -- **hyperglycemic from catecholamine stimulation** of hepatic gluconeogenesis

Answer 105

Surgical removal of tumor non‐selective adrenergic alpha antagonist (blocks both alpha‐1 and alpha‐2) **phenoxybenzamine** for approximately two weeks prior to surgery → **help to blunt hypertensive episodes during anesthesia** -- Beta‐adrenergic antagonists such as propranolol or atenolol may also be used to control tachycardia and cardiac arrhythmia -- Following adrenal gland removal, hypotension may occur as well as hypoadrenocorticism. -- Glucocorticoid supplementation may be required

Answer 106

-- Marked changes to blood pressure, heart rate, and cardiac rhythm are not uncommon, along with perioperative blood loss, and some have described the process as a roller coaster ride. Direct arterial blood pressure monitoring is considered mandatory. -- Hypertensive crisis is often treated with medication such as nitroprusside, hydralazine, phentolamine, or clevidipine. -- Tachycardia is often treated with esmolol.

Answer 107

-- manipulation of the tumor may cause catecholamine release. --Alternatively, removal of the tumor may result in cardiovascular collapse from lack of catecholamines, requiring **supplementation with sympathomimetic drugs such as phenylephrine or norepinephrine**

Answer 108

-- inadequate cellular corticosteroid activity for the severity of the patient’s disease; pressor-resistant hypotension is the most commonly reported clinical manifestation -- failure of the adrenal glands to secrete adequate cortisol seems to occur → refractory hypotension and shock occur unless corticosteroids are administered -- dissociation between ACTH and cortisol concentrations in critical illness (high cortisol concentration in the presence of low ACTH concentration

Answer 109

-- Direct trauma, infarction or hemorrhage, or cytokine influence may impair HPA axis function and thereby decrease circulating cortisol. -- complex combination of alterations in the production, plasma carriage, metabolism of, and tissue responsiveness to cortisol

Answer 110

replacing physiological “low doses” of glucocorticoids with hydrocortisone or DexSP

Answer 111

1. ketoconazole, 1. etomidate, 1. propofol, 1. opiates

Answer 112

pressor-resistant hypotension, which is logical since glucocorticoids influence adrenergic receptor function

Answer 113

Cats typically experience hyperthyroidism while dogs get hypothyroidism

Answer 114

less common source of endocrine disease in dogs and cats -- commonly manifests as hyperparathyroidism but hypoparathyroidism can also occur -- common cause of hypercalcemia = CS polyuria and polydipsia.

Answer 115

Glucose comes from three sources: (1) intestinal absorption of glucose from **digestion of carbohydrates**; (2) breakdown of the **storage form of glucose (glycogen) via glycogenolysis** (3) production of glucose **from precursors lactate, pyruvate, amino acids, and glycerol via gluconeogenesis.**

Answer 116

1. glucose-lowering hormone, 1. insulin 1. glucose-elevating hormones, 1. primarily glucagon, 1. epinephrine, 1. cortisol, 1. growth hormone (GH)

Answer 117

complex interactions involving the autonomic nervous system and input from many other organ systems including the gastrointestinal tract, brain, and liver.

Answer 118

secreted by β cells of the pancreas in response to of glucose, amino acids, and **gastrointestinal hormones** (gastrin, secretin, cholecystokinin, glucagon-like peptide-1, and gastric inhibitory peptide) present after a meal

Answer 119

-- Insulin **inhibits gluconeogenesis and glycogenolysis, promotes glycogen storage,** -- **stimulates glucose uptake and utilization by insulin-sensitive cells,** and decreases glucagon secretion. -- also promotes triglyceride formation in adipose tissue and the synthesis of protein and glycogen in muscle. -- **decreasing levels of insulin stimulate gluconeogenesis,** reduce glucose used by peripheral tissues, and stimulate hepatic glucose production via glycogenolysis

Answer 120

a **peptide hormone secreted** from the **alpha cells** of the pancreatic islets of Langerhans -- **counteracts the actions of insulin** by stimulating hepatic glucose production and thereby increases blood glucose levels -- **directly stimulates hepatic glycogenolysis and gluconeogenesis,** mobilizes gluconeogenic precursors, and reduces peripheral glucose utilization ## Footnote breaks down glycogen, proteins, and triglycerides for energy

Answer 121

-- metabolic pathway that results in the **generation of glucose from non-carbohydrate carbon substrates** -- **lactate, glycerol and glucogenic amino acids**. -- occurs mainly in the liver and kidney cortex and to a lesser extent in the small intestine

Answer 122

process by which **glycogen, the primary carbohydrate stored in the liver** and muscle cells of animals, **is broken down into glucose** to provide immediate energy and to maintain blood glucose levels during fasting -- occurs in liver and kidneys -- results in nutrition of the skeletal muscle cells and maintenance of blood glucose -- **Stimulated by Glucagon and Epinephrine**

Answer 123

the stored form of glucose -- Found primarily in the liver but also in skeletal muscles

Answer 124

-- metabolic pathway that **converts glucose into pyruvate** and, in most organisms, occurs in the liquid part of cells (the cytosol) -- **does not require oxygen** -- produces **2 molecules of ATP** -- most important enzyme for regulation of glycolysis is **phosphofructokinase** → speeds up or slows down glycolysis in response to the energy needs of the cell.

Answer 125

(1) inadequate dietary intake (2) excessive glucose utilization (3) dysfunctional glycogenolytic or gluconeogenic pathways or inadequate precursors for these pathways (4) endocrine abnormalities.

Answer 126

clinical signs often do not develop until the level is less than 50 mg/dl.

Answer 127

**Receptors w/i portal vein** are essential for detecting and relaying hypoglycemia in the central nervous system → **stimulates both epinephrine and cortisol responses** -- **glucagon and epinephrine levels rise** within minutes of hypoglycemia and have a transient effect on increasing glucose production

Answer 128

-- using hepatic glucose autoregulation and increased neural efferent signaling -- both stimulate hepatic glucose production and limit glucose utilization. --

Answer 129

-- Hepatic glucose autoregulation is a process by which glucose concentration alters the activity of hepatic enzymes such as **glucokinase, glycogen synthase, and glycogen phosphorylase**, as needed, to maintain glucose concentration

Answer 130

Additional neural efferent signaling occurs via the release of **norepinephrine, which increases gluconeogenesis** via enhanced lipolysis and glycogenolysis, **primarily in muscle**

Answer 131

Glucose is an obligate energy source for the brain -- Adequate arterial glucose concentration is essential to maintaining a diffusion gradient -- hypoglycemia results in neuroglycopenia

Answer 132

Islets = secrete different hormones -- Beta cells = insulin --Alpha cells = glucagon (increase BG via glucogenesis) -- S cells = Somatostatin (inhibits EVERYTHING)

Answer 133

**Acini groups** = release secretions into lumen → duodenum --Lipase = breaks down lipids into FFA and monoglycerides -- Proteases = breaks down proteins into AA -- Amylase = breaks down starches into maltose

Answer 134

Exocrine pancreatic Insufficiency --Results from diminshed/reduced production of exocrine proteolytic enzymes --Pancreatic atrophy/chronic pancreatitis

Answer 135

DI results when the **quantity or function of AVP is compromised** excessive urinary electrolyte-free water (free water) loss -- marked dilute polyuria of >50 ml/kg/day and an obligate polydipsia to replete the excreted volume -- central vs nephrogenic -- rapid and life-threatening oscillations in plasma osmolality, (hyperosmolality and hyperNa+)

Answer 136

insufficient or absent circulating arginine vasopressin (AVP) -- hereditary (rare) or acquired

Answer 137

reduced or absent receptor response to circulating AVP -- circulating AVP may be unable to elicit a normal receptor response in the kidney due to **defects in the V2 receptor or abnormal AQP-2 trafficking or composition** -- hereditary (rare) or acquired

Answer 138

**peptide hormone** that is produced within the magnocellular neurons in the supraoptic and paraventricular nuclei of the **hypothalamus** -- stored in axon terminals in the posterior pituitary until triggered for release

Answer 139

**homeostatic control of plasma osmolality** -- triggered by minute elevations in plasma osmolality sensed by **osmoreceptors** located in the organum vasculosum laminae terminalis (OVLT) -- quantity of AVP released parallels the degree of rise in plasma osmolality -- increase of as little as 1% in plasma osmolality will stimulate ADH release

Answer 140

-- OVLT = organ within the **rostral portion of the hypothalamus** that lacks a blood–brain barrier -- Separate osmoreceptors located near the OVL simultaneously **trigger the thirst sensation** -- osmotic threshold for the stimulation of thirst is higher than plasma for ADH release

Answer 141

-- AVP binds Gs protein-coupled **V2 receptors** on the basolateral membrane of principal cells in the **renal collecting ducts**. --lead to fusion of **aquaporin-2 (AQP-2)** water channel-laden cytoplasmic vesicles -- AQP-2 channels provide a pathway for the movement of solute-free water down its concentration gradient from the tubule lumen into the hypertonic renal medulla = prevent urine loss -- **Renal reabsorption of free water coupled with increased water intake promoted by thirst quickly brings the plasma osmolality back into the normal range** ## Footnote Once osmolality returns to normal, osmoreceptors inhibit ongoing AVP secretion and thirst to prevent hypoosmolality

Answer 142

**neuro-vasopeptide** that plays a reciprocal role to AVP in body water homeostasis and may contribute to DI -- decreasing AVP release by the posterior pituitary and interfering with AQP-2 insertion in the renal collecting tubule, **both of which increase free water excretion** -- apelin concentrations were increased in people with nephrogenic DI and contributed to their marked urinary free water loss.

Answer 143

1. **Brain Trauma** 1. **Neoplasia** (Pituitary macroadenoma) 1. **Infectious/inflammatory** (Meningitis Toxoplasmosis Fungal (cryptococcus)) 1. **Vascular** (Intracranial hemorrhage Hypothalamic infarction) 1. **Immune-mediated** (Lymphocytic neurohypophysis) 1. **Idiopathic**

Answer 144

1. **Drugs** (Vasopressin, Ofloxacin, Aminoglycosides) 1. **Electrolyte abnormalities** (HyperCa++ HypoK+) 1. **Bacterial infection** (Escherichia coli Streptococcus spp. Leptospira spp.) 1. **Degenerative** (CKD) 1. **Paraneoplastic** (Intestinal leiomyosarcoma)

Answer 145

-- desmopressin (DDAVP), a pure-V2 receptor agonist -- meticulous free water balance management should be a top priority in hospitalized DI patients, with a goal to carefully monitor plasma sodium levels and tailor medical management accordingly to prevent significant fluctuations in sodium concentration -- monitoring for hypoNa+ following start of tx

Answer 146

-- **thiazide diuretics**, paradoxically decrease total daily urine output in patients with DI. -- decreases total ECF volume, which serves to decrease GFR -- in critically ill pts this can exacerbate existing problems in fluid balance -- free water loss should be replaced enterally or parenterally.

Answer 147

positive urinary free water clearance with concurrent hypernatremia have either central or nephrogenic DI -- DDAVP trial may be used to help distinguish between the two -- Urine osmolarity sampled at 2 to 4 hours following DDAVP administration should increase by 50% or more from baseline in patients with complete central DI or between 9% and 50% from baseline with partial central or nephrogenic DI

Answer 148

release of ADH in the absence of increases in osmolality or decreased ECV -- commonly manifests as euvolemic hyponatremia in conjunction with concentrated urine -- 4 types: Type A, B, C, D

Answer 149

No relationship between plasma ADH concentration and plasma osmolality; **can lead to significant hyponatremia**; reported to be the most common type in human patients

Answer 150

Lower osmotic threshold for ADH release, but the relationship between plasma ADH concentration and plasma osmolality is normal above this threshold. -- result is a relatively stable plasma sodium concentration at a lower than normal level. -- considered an uncommon type of SIADH.

Answer 151

plasma osmolalities above normal, the relationship between plasma ADH concentration and plasma osmolality is normal. At lower osmolality, the basal concentration of ADH is higher than normal. Considered a rare form of SIADH.

Answer 152

Cases fulfill the clinical criteria for SIADH, but plasma ADH concentrations are undetectable; may be due to tumor secretion of an ADH-like substance or mutations in the V2 receptor; considered very rare.

Answer 153

1. aspiration pneumonia, 1. meningoencephalitis, 1. hydrocephalus, 1. neoplasia, 1. liver disease, 1. general anesthesia 1. pain and nausea following GA

Answer 154

-- diagnosis of exclusion: 1. Hypoosmolar hyponatremia 2. Euvolemia 3. Inappropriately concentrated urine – urine osmolality > 100 mOsm/L 4. Urine sodium concentration > 30 mmol/L 5. Hypoadrenocorticism excluded clinical consequence of SIADH is **hypoosmolar hyponatremia in conjunction with urine hyperosmolality **(> 100 mOsm/L)

Answer 155

-- potential causes of SIADH should be removed when possible; in many cases the abnormality will be transient and quickly resolve -- careful fluid restriction and/or loop diuretic administration -- limit water intake

Answer 156

-- syndrome of multiorgan disorder resulting from excessive amounts of circulating thyroid hormone -- acute thyrotoxicosis

Answer 157

any condition in which there is a marked increase of circulating thyroid hormone, whether from excess production and secretion from an overactive thyroid gland, because of leakage from a damaged thyroid gland, or from an exogenous source.

Answer 158

thyroid gland hyperfunction

Answer 159

-- hyperthyroidism common in older female cats; cats that experience an acute accentuation of thyrotoxicosis may be diagnosed with thyroid storm. -- seen rarely in **dogs with a functional thyroid carcinoma**, following oversupplementation of thyroid replacement hormone to hypothyroid dogs, or when uncooked organ meat is fed to dogs

Answer 160

1. high levels of circulating TH, 2. rapid increases in circulating TH 3. hyperactivity of SNS 1. an increased cellular response to TH

Answer 161

there is no difference between serum TH levels in human patients and in more stable hyperthyroid patients. The diagnosis therefore is made primarily based on clinical signs

Answer 162

The rate of change in serum TH levels may be more important than the actual levels themselves -- would explain the occurrence of thyroid storm after radioactive iodine therapy and thyroid surgery -- **damages to the thyroid gland causes release of hormone or after abrupt cessation of antithyroid medication** resulting in a rapid rise in serum TH levels

Answer 163

Activation of the SNS has been implicated in the onset of thyroid storm -- physiologic signs are similar to those seen during **catecholamine excess** (e.g., pheochromocytoma) -- TH can **alter tissue sensitivity to catecholamines** at the cell surface receptor as well as the intracellular signaling levels = increased sensitivity may result in the clinical signs seen during thyroid storm -- D1 enzyme may be a target of the sympathetic nervous system as it is **inhibited by β-adrenergic receptor agonist medications**

Answer 164

**deiodinase D1** is the main enzyme converting T4 to the more cellularly-active T3 in the hyperthyroid state, versus the **deiodinase D2** in the euthyroid state. -- **D1 enzyme may be a target of the sympathetic nervous system as it is inhibited by β-adrenergic receptor agonist medications** → Thyroid storm treatment

Answer 165

Hyperresponsiveness of cells to thyroid hormones has been implicated in cases of thyroid storm resulting from: infection, sepsis, hypoxemia, hypovolemia, lactic acidosis, or ketoacidosis.

Answer 166

1. Radioactive iodine therapy 1. Thyroidal or parathyroidal surgery 1. Abrupt withdrawal of antithyroid medications 1. Stress 1. Nonthyroidal illness 1. Administration of iodinated contrast dyes 1. Administration of stable iodine compounds 1. Vigorous palpation of the thyroid

Answer 167

**Constitutional signs** Hyperthermia, Dehydration **Cardiovascular signs** Arrhythmias Atrial fibrillation, ventricular tachycardia Gallop rhythm Sinus tachycardia CHF, Cardiomegaly, Pleural effusion, Pulmonary edema, Hypertension, Thromboembolic disease **Respiratory signs** Tachypnea **Neuromuscular signs** Behavior changes, Mental dullness/obtundation, Seizures, Muscle weakness, Cervical ventroflexion **Gastrointestinal and hepatic signs** Abdominal discomfort or pain V/D, Icterus **Ocular signs** Hyphema, Retinal lesions Retinal detachment

Answer 168

identification of thyrotoxicosis, clinical signs, and evidence of a precipitating event. -- elevated total thyroxine (T4) level, or a total T4 level in the high-normal range combined with an elevated free T4 level

Answer 169

controlling the four major problematic areas: (1) to reduce the production and/or secretion of thyroid hormones, **(Methimazole)** (2) to counteract the peripheral effects of thyroid hormones, **(medications that block the β-adrenergic receptors)** (3) to provide systemic support **(Cardiac disturbances are common, antihypertensive therapy)** (4) to identify and eliminate the precipitating factor(s).

Answer 170

life-threatening complication of hypothyroidism

Answer 171

TH exert chronotropic and inotropic effects in the heart, as well as catabolic, metabolic, calorigenic, and developmental effects in other organs.

Answer 172

-- stimulates the growth and development of the thyroid gland and causes it to produce its hormones -- TSH secretion is regulated by feedback from its target organ—the thyroid gland -- Homeostasis of thyroid hormone production is maintained through this interaction among the hypothalamus, anterior pituitary gland, and thyroid gland

Answer 173

-- stimulates the growth and development of the cortex (outer portion) of the adrenal gland and the release of some of its hormones. --regulated by feedback from the hormones of the adrenal cortex in much the same manner as TSH production is regulated by feedback from thyroid hormone

Answer 174

sudden stress = ACTH can be released quickly as a result of stimulation by the hypothalamus → sends a burst of ACTH-releasing factor down to the anterior pituitary through the portal system of blood vessels that links them

Answer 175

1. **Thyroid hormone**, which mainly helps regulate the body’s metabolic rate 1. **Calcitonin**, which helps regulate blood calcium levels.

Answer 176

produced when TSH from the anterior pituitary gland stimulates the thyroid gland -- Divided into 2 hormones: 1. T4 (tetraiodothyronine, or thyroxine) = considered a prohormone 2. T3 (triiodothyronine) = the active hormone

Answer 177

helps heat the body -- regulates the metabolic rate of all the body’s cells: the rate at which they burn nutrients to produce energy -- also affects the metabolism of proteins, carbohydrates, and lipids, much like GH does

Answer 178

-- necessary for normal growth and development in young animals. -- it influences the development and **maturation of the CNS and the growth and development of muscles and bones**

Answer 179

the other hormone produced by the thyroid gland -- produced by C cells located between the thyroid follicles -- one of two hormones involved in maintaining homeostasis of blood calcium levels (the other is parathyroid hormone) -- help prevent hypercalcemia -- decreases blood calcium level if it gets too high, mainly by encouraging the excess calcium to be deposited in the bones

Answer 180

helps maintain blood calcium homeostasis -- helps prevent hypocalcemia by increasing the blood calcium level if it should fall -- effects on the kidneys, the intestine, and the bones -- tells kidneys retain calcium, intestines to absorb calcium from food, and it withdraws calcium from bones

Answer 181

two adrenal glands are located near the cranial ends of the kidneys -- each one has 2 parts: **adrenal cortex** and the **inner adrenal medulla**

Answer 182

adrenal cortex produces 1. glucocorticoid hormones, 1. mineralocorticoid hormones 1. sex hormones

Answer 183

comes from its effect on the blood glucose levels -- **cortisol, cortisone, and corticosterone** among them—have a general hyperglycemic effect -- Other effects include helping to **maintain blood pressure anthe body resist the effects of stress.** ## Footnote Ex: hydrocortisone, prednisone, dexamethasone, and triamcinolone

Answer 184

Regulate the levels of some important electrolytes (mineral salts) in the body -- aldosterone is the principal mineralocorticoid

Answer 185

-- hormone released by the adrenal glands in small amounts in a circadian rhythm and in larger amounts during times of physiologic stress -- hypothalamus produces corticotropin-releasing hormone (CRH), which stimulates adrenocorticotropic hormone (ACTH) release from the anterior pituitary -- -- ACTH stimulates the zona fasciculata and zona reticularis of the adrenal cortex to produce and release cortisol

Answer 186

-- determined by the hormonal cascade and negative feedback mechanisms of the **hypothalamic-pituitary-adrenal (HPA) axis** -- when serum cortisol concentration is low, serum CRH and ACTH concentrations increase, stimulating the adrenals to produce more cortisol -- Increased serum cortisol concentration then inhibits further CRH and ACTH release.

Answer 187

-- regulation of carbohydrate, lipid, and protein metabolism; -- immune system modulation; ensuring proper production of catecholamines -- and function of adrenergic receptors; and stabilizing cell membranes

Answer 188

-- is a mineralocorticoid released from the zona glomerulosa of the adrenal cortex under the influence of a complex hormonal cascade that starts in the kidney.

Answer 189

-- maintains normovolemia -- affects the levels of sodium, potassium, and hydrogen ions -- Its target is the kidney, where it causes **sodium ions to be reabsorbed** from the urine back into the bloodstream **in exchange for potassium and hydrogen ions,** which pass out of the body in the urine

Answer 190

-- group of specialized cells in the **distal portion of the thick ascending loop of Henle**, **senses decreased filtrate (specifically chloride) delivery** -- **induces renin release** from the nearby **juxtaglomerular cells of the afferent arteriole** serving that nephron

Answer 191

the inner gland, develops from nervous tissue -- its hormone-secreting cells are modified neurons that secrete directly into the bloodstream -- **epinephrine and norepinephrine.** -- under the control of the sympathetic nervous system

Answer 192

Islets = secrete different hormones -- **Beta cells** = insulin --**Alpha cells** = glucagon (increase BG via glucogenesis) -- **Delta cells** = somatostatin inhibits the secretion of insulin and glucagon, as well as GH, and diminishes the activity of the GIT

Answer 193

Acini groups = **release secretions into lumen → duodenum** -- **Lipase** = breaks down lipids into FFA and monoglycerides -- **Proteases** = breaks down proteins into AA -- **Amylase** = breaks down starches into maltose

Answer 194

produced by the kidneys = stimulates red bone marrow to increase production of oxygen-carrying RBCs -- **stimulated by hypoxia** -- helps maintain the long-term homeostasis of the blood’s oxygen-carrying ability

Answer 195

an organ that is important for the development of a young animal's immune system -- extends cranially from the level of the heart in the thorax up into the neck region along both sides of the trachea, often to the level of the larynx -- After puberty the thymus begins to atrophy -- function involved thymosin and thymopoietin hormones

Answer 196

cause primitive cells in the thymus and other lymphoid organs to be transformed into T (for “thymus-derived”) lymphocytes

Answer 197

hormonelike substances that are derived from unsaturated fatty acids -- produced in a variety of body tissues -- regulate the activities of neighboring cells -- E group of prostaglandins (PGEs) is known to play a role in the initiation of inflammation in the body -- influences on BP, GIT function, respiratory function, kidney function, blood clotting, inflammation, and reproductive functions.

Answer 198

aka somatotropic hormone -- helps regulate the metabolism of proteins, carbohydrates, and lipids in all of the body’s cells -- it encourages the anabolism, or synthesis, of proteins by body cells

Answer 199

helps trigger and maintain lactation --Once lactation has begun, prolactin production and release by the anterior pituitary gland continue as long as the teat or nipple continues to be stimulated by nursing or milking. -- milking ceases, the production of prolactin will cease as well

Answer 200

mental dullness -- may be a result of **decreased blood flow and oxygen delivery to the brain, hyponatremia,** lack of a direct effect of thyroid hormone on the brain, or disruption of the integrity of the blood–brain barrier

Answer 201

Inadequate thyroid hormone function in the hypothalamus may result in the inability to regulate body temperature

Answer 202

-- In the heart, **thyroid hormones increase the number of β-adrenergic receptors** and their affinity to catecholamines, thereby **increasing the inotropic and chronotropic effects of catecholamines** --caused by an increase in α-myosin heavy chains (MHC), which have decreased ATPase activity, and a decrease in β-MHCs, which have more ATP activity -- **in crisis cardiovascular dysfunction is characterized by bradycardia,** -- **decreased cardiac contractility, cardiac enlargement, and hypotension**,

Answer 203

1. mild nonregenerative anemia, 2. hypercholesterolemia, 1. lipemia, 1. increased AlkPhos

Answer 204

-- Thyroid hormones bind thyroid hormone receptors on erythroid progenitors (precursor to RBCs) and act directly to increase erythroid proliferation. -- also increases expression of the erythropoietin gene, further contributing to red blood cell formation

Answer 205

Thyroid axis testing low thyroxine and high TSH concentrations,

Answer 206

**glucocorticoids, NSAIDS, TMS, anticonvulsants** (carbamazepine, valproate, phenobarbital, and potassium bromide), -- antituberculosis drugs (paraaminosalicylic acid, ethionamide, and prothionamide), propranolol, and lithium.

Answer 207

Intravenous levothyroxine at a dosage of 5 mcg/kg administered q12h -- supportive care, thyroid hormone supplementation, and treatment of concurrent conditions.

Answer 208

tumor of the chromaffin cells of the adrenal medulla

Answer 209

-- unclear what stimuli cause secretion of catecholamines from the tumor -- hypertension manifestations = retinal detachment -- tachyarrhythmias, bradyarrhythmias, abdominal distension/pain -- Associated cardiomyopathies

Answer 210

-- most pheochromocytomas in small animals are incidental findings -- may show mineralization in the area of the adrenal glands or may demonstrate retroperitoneal effusion or an abdominal mass effect associated with the tumor

Answer 211

-- **mild nonregenerative anemia** may be present secondary to chronic disease or an increased MCV or PCV as a result of **catecholamine or erythropoietin-like stimulation** of the bone marrow. -- **regenerative anemia may reflect hemorrhage** from the tumor -- **Leukocytosis or a stress leukogram** may be found secondary to catecholamine release or inflammatory changes associated with the tumor

Answer 212

-- **hyperglycemic from catecholamine stimulation** of hepatic gluconeogenesis, refractory catecholamine-induced insulin receptors, and decreased insulin release from α-receptor stimulation. -- **hypercholesterolemia** was present in 25% of dogs, possibly secondary to **increased fat mobilization** from catecholamine secretion or because of concurrent hyperadrenocorticism -- 50% showed **proteinuria, likely caused by a hypertensive** glomerulopathy

Answer 213

Definitive treatment is surgical excision

Endocrine/Exocrine Flashcards

(237 cards)