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VTS ECC 2024 > Endocrine/Exocrine > Flashcards

Endocrine/Exocrine Flashcards

1
Q

Endocrine system

#9

Can’t The Puppies And Goats Eat Krazy Good Pineapples?

A
  1. central nervous system,
  2. thyroid gland,
  3. parathyroid gland,
  4. adrenal glands,
  5. gastrointestinal tract,
  6. endocrine pancreas,
  7. kidney,
  8. gonads,
  9. placenta
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2
Q

Neurotransmitters

where are the released? where does their action take effect?

A

released by axon terminals of neurons into the synaptic clefts and act locally to control nerve cell function

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3
Q

Endocrine hormones

Where do they get released? where is the location they affect?

A

released by glands into the circulating blood and influence the function of target locations at another distant location within the body.

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4
Q

Neuroendocrine hormones

Where are they sereted? and where is their influence?

A

specifically secreted by neurons into the circulation and influence the function of target locations at distant sites within the body

Ex: Epinephrine, Oxytocin, ADH

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5
Q

Paracrine substances

Where are they secreted? and where are the cells they affect?

A

secreted by cells into the extracellular fluid and affect neighboring target cells of a different type.

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6
Q

Autocrine substances

where are they secreted? and where does their affect take place?

A

secreted by cells into the extracellular fluid and affect the function of the same cells that produce them

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7
Q

Cytokines

where are they secreted?
what types of function can they perform?
examples

A

– proteins secreted by cells into ECF that generally affect the immune system and can function as autocrine, paracrine, or endocrine hormones.
– include chemokines, interferons, interleukins, lymphokines, and tumor necrosis factors

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8
Q

Amino acid derivative class hormone examples

#6

Do Not Ever Try To Read

A
  1. Dopamine
  2. Norepinephrine
  3. Epinephrine
  4. Thyroxine
  5. Tri‐iodothyronine
  6. Reverse T3

Monoamine hormones

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9
Q

Small peptides class hormone examples

#7

Very Obvious Stupid Animals Are Still Good

A
  1. Vasopressin
  2. Oxytocin
  3. Somatostatin
  4. Adrenocorticotropic hormone (ACTH)
  5. Angiotensins
  6. Secretin
  7. Glucagon
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10
Q

Protein class hormone examples

#7

A
  1. Calcitonin → lowers Ca++, counter for PTH
  2. Insulin
  3. Growth hormone
  4. Thyroid‐stimulating hormone (TSH)
  5. Prolactin
  6. Parathyroid hormone (PTH)
  7. Erythropoietin (EPO)
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11
Q

Steriod class hormone examples

#5

A
  1. Progesterone
  2. Testosterone
  3. Estrogens
  4. Glucocorticoids
  5. Mineralocorticoids

lipids that are synthesized from cholesterol = hydrophobic

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12
Q

Fatty acid derivative class hormone examples

#3

A
  1. Prostaglandins
  2. Leukotrienes
  3. Thromboxanes
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13
Q

Transport, and Activation of Endocrine Secretions

A

close control is exerted through negative feedback mechanisms that, after release of a chemical messenger, tend to suppress its further release
– Hormone release can also be under cyclical variation, including changes in season, various stages of development and aging, and in sleep and waking life

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14
Q

Water‐soluble (hydrophilic) compounds

examples

A

(e.g. peptides and catecholamines) dissolve in plasma and are transported from their sites of synthesis to target cells

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15
Q

Protein bound hormones

A

– steroid and thyroid hormones circulate in the blood while being bound to plasma proteins.
– Binding of hormones to plasma proteins greatly slows their clearance from the plasma.

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16
Q

How do hormone receptors sites become more or less available?

A

number and sensitivity of hormone receptors are adjustable and can be increased through upregulation or decreased through downregulation.

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17
Q

How does hormone elicit desired effect?

A
  1. hormone’s action is to bind to specific receptors at the target cell
  2. once a hormone binds to a receptor, it activates the receptor and initiates the hormonal effect.
  3. Following these hormone–receptor site interactions, extensive second messenger system mechanisms activate (adenylyl cyclase‐cAMP, cell membrane phospholipids, and calcium‐calmodulin systems)
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18
Q

types of hormone–receptor site complex interactions

#4

examples of each

A
  1. ion channel‐linked receptor interactions, Ex: ligand gated and voltage gated sodium and calcium ion channels
  2. G protein‐linked hormone receptor interactions Ex: beta-adrenergic receptors, which bind epinephrine
  3. enzyme‐linked hormone receptor interactions Ex: growth factors, cytokines
  4. intracellular hormone receptor interactions Ex: steroid hormones
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19
Q

What or how much action a hormone exerts on target cell depends on:

#5

A
  1. rate of hormone production and secretion,
  2. availability of transport plasma proteins,
  3. ability of tissues that are targeted to convert the hormone,
  4. tactivity and availability of receptors specific for the hormone on the targeted cells or tissues, breakdown or degradation of the hormone,
  5. lastly the liver and/or kidney’s ability to excrete the hormone
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20
Q

Hypothalamic Pituitary Axis

A

relationship and interaction between the hypothalamus, the pituitary gland, and peripheral target organs
– delivers precise signals to the pituitary gland which then releases hormones that influence most endocrine systems in the body

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21
Q

Hypothalamus

A

consolidates signals derived from upper cortical inputs, autonomic function, environmental cues such as light and temperature, and peripheral endocrine feedback

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22
Q

Hypothalamus hormones

x6

A

releasing hormones and inhibiting hormones: influence on anterior pituitary hormones
– major hypothalamic hormones include:
1. thyrotropin‐releasing hormone (TRH),
1. gonadotropin‐releasing hormone (GnRH),
1. corticotropin‐releasing hormone (CRG),
1. growth hormone‐releasing hormone (GHRH),
1. growth hormone inhibitory hormone (somatostatin),
1. prolactin‐inhibiting hormone (PIH)

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23
Q

Pituitary gland

A

– small gland within the brain that is connected to the hypothalamus.
– Physiologically, the pituitary is divisible into anterior and posterior portions, referred to as the adenohypophysis and neurohypophysis

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24
Q

5

Anterior pituitary gland

A

in response to input from the hypothalamus, secretes hormones including:
* thyroid‐stimulating hormone (TSH),
* adrenocorticotropic hormone (ACTH),
* growth hormone (GH),
* prolactin, luteinizing hormone (LG),
* follicle‐stimulating hormone (FSH)

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25
Q

What does posterior pituitary secrete?

x2

A

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

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26
Q

How is Cortisol released?

A

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

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27
Q

Diabetes Mellitus

A
  • dysfunction of pancreatic beta cells results in an absolute or relative deficiency of insulin
  • Type 1 or Type 2
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28
Q

How does lack of Insulin cause PU/PD

A

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

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29
Q

Diabetes Mellitus: Type 1

A

primary insulin‐dependent diabetes mellitus (type 1), resulting from destruction of insulin‐producing pancreatic beta cells
– can be congenital, immune mediated, or idiopathic

Receptors are functional but there is no insulin production

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30
Q

Diabetes Mellitus: Type 2

A

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

Insulin is present but receptors are dysfunctioning

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31
Q

Secondary forms of diabetes mellitus

A

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

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32
Q

Glucotoxicity

A

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

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33
Q

Dietary Modification for DM

A

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

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34
Q

Insulin Therapy Type

K9 vs feline

A

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

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35
Q

Regular insulin

type, duration, peak concentration, administration

A

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. .

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36
Q

Porcine zinc insulin: Vetsulin

Peak; Duration Dogs vs Cats

A

has two peaks of activity following subcutaneous administration
In 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.

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37
Q

Porcine zinc insulin: NPH insulin

Peak and duration

A

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

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38
Q

protamine zinc insulin (PZI)

Duration, peak

A

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

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39
Q

Glargine insulin: Lantus

Duration; Peak

A

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

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40
Q

Glycemic control of dogs and cats

Cat vs Dogs

A

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

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41
Q

Fructosamine levels

What is its source?

A

– 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

Values >500 µmol/L suggest inadequate control of diabetes.

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42
Q

Somogyi Phenomenon

A

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.

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43
Q

four cell types in the endocrine pancreas which regulate glucose production and utilization

A
  1. alpha cells secrete glucagon,
  2. beta cells secrete insulin,
  3. delta cells secrete somatostatin
  4. F cells secrete pancreatic polypeptide
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44
Q

Diabetic Ketoacidosis

3 major contributing factors
what acid/base disturbance does this cause?

A

– 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

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45
Q

What has been shown in recent studies to contribute to Ketogenesis in DKA?

A

– 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

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46
Q

Disease processes that predispose diabetics dogs to DKA

x4
what couterregulatory hormones are involved?

A
  1. pancreatitis,
  2. bacterial urinary tract infections,
  3. neoplasia,
  4. hyperadrenocorticism

Any potential to trigger the secretion of insulin counterregulatory hormones such as glucagon, catecholamines, cortisol, and growth hormone.

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47
Q

3 types of Ketones

How do they cause Metabolic acidosis?

A
  1. Beta‐hydroxybutyrate
  2. Acetoacetate
  3. 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
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48
Q

5

Disease processes that predispose diabetics cats to DKA

A
  1. hepatic lipidosis,
  2. cholangiohepatitis,
  3. pancreatitis,
  4. bacterial and viral infections
  5. neoplasia

Any potential to trigger the secretion of insulin counterregulatory hormones such as glucagon, catecholamines, cortisol, and growth hormone.

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49
Q

Insulin deficiency correlation to DKA

x3 mechanisms

A

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

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50
Q

Formation of Ketones

What is the cycle called?
what are they 3 types of ketones?

A

– 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.

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51
Q

What enhances ketogenesis?

x5

A

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

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52
Q

How does Ketosis form?

A

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

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53
Q

DKA

What contributes to dehydration and electrolyte imbalance?

A

– 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.

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54
Q

DKA

Which electrolytes become imbalanced?

A

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

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55
Q

DKA:

Why do electrolytes appear normal on first evaluation?

A

– 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.

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56
Q

DKA

What is a common classic CS specifically seen with metabolic acidosis on presentation?

A

Kussmaul respiration

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57
Q

DKA: CBC findings

#3

A

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)

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58
Q

DKA: Biochemical findings

#3

A

– 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

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59
Q

Why is hyperlipidemia seen with DKA?

A

Insulin deficiency prevents activation of lipoprotein lipase → lipemia results

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60
Q

DKA: Blood gas analysis

A

reveal a metabolic acidemia with secondary respiratory alkalosis

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61
Q

DKA: Electrolye analysis

Example

A

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.

Ex: K+ becomes extracellular with acidemia, then with gradual resolution becomes hypoK+ as K+ transistions back intracellularly

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62
Q

DKA: Ketone detection

A

– 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.

Concentrations of >3.5 mmol/L in dogs and >2.4 mmol/L in cats are associated with DKA

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63
Q

DKA: UA anlaysis

A

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.

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64
Q

DKA

What causes HypoNa+?

A

–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.

corrected sodium value should be obtained to assess glucose’s influence in sodium concentration

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65
Q

DKA

What contributes to shifts in K+?

A

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

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66
Q

DKA

Refractory HypoK+

A

may benefit from magnesium supplementation

Both major intracellular Cations

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67
Q

DKA

Negative Effects of HypoPhos-

x3

A

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

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68
Q

DKA

When should Phos supplmentation be avoided?

A

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

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69
Q

Why is dextrose used with Insulin administration for DKA?

A

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

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70
Q

DKA

Argument for starting insulin quickly

A

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

DK/DKA took longer to resolve in animals with more severe ketonuria.

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71
Q

DKA

Argument against starting Insulin quickly

A

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

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72
Q

DKA

Methods of Insulin administration for DKA tx

A

– 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.

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73
Q

How quickly should blood glucose be dropped when treating DKA?

A

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

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74
Q

DKA: IVF choice

A

– 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

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75
Q

Adverse effects of HCO3- supplementation?

#6

A
  1. paradoxical cerebral acidosis,
  2. increased carbon dioxide production and the potential for hypercapnia,
  3. increased sodium and osmole concentration, risk for circulatory system overload,
  4. iatrogenic metabolic alkalosis,
  5. changes to the oxygen dissociation curve (Bohr effect),
  6. hypokalemia
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76
Q

Why is HCO3- supplementation not always appropriate for metabolic acidosis from DKA?

A

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.

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77
Q

Sooo.. then when is HCO3- reccomended with DKA?

A

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

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78
Q

Neuroglycopenia

A

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

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79
Q

CS of neuroglycopenia

what does it result from?

A

– 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

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80
Q

hypoglycemia due to paraneoplastic

What the most obvious one?

A

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

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81
Q

Marked leukocytosis and polycythemia with hypoglycemia

A

because of increased cell utilization of glucose

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82
Q

Insulinomas

A

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

typically malignant

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83
Q

Types of APUDomas

Aka neuroendocrine tumors
x5

A

somatostatinomas,
pheochromocytomas,
gastrinomas,
glucagonomas,
insulinomas.

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84
Q

What test is done to confirm an insulinoma?

how is it diagnostic?

A

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

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85
Q

Insulinoma initial Tx

A

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

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86
Q

Insulinoma Medical Management

#3

A
  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.
  2. strenuous exercise should be limited.
  3. glucocorticoids such as prednisone may be beneficial to antagonize effects to insulin, thereby increasing insulin resistance.

Short term! sx ultimately needed

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87
Q

Diuretic medication used to medically manage an Insulinoma

A

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

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88
Q

chemotherapeutic agents used to medically manage an Insulinoma

A

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

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89
Q

Types of Paraneoplastic hypoglycemia

A

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

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90
Q

Paraneoplastic hypoglycemia effects

#3

how does it occur?

A

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

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91
Q

Hypoglycemia: Toxin/medication induced

#4

A

– 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

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92
Q

Hypoglycemia of neonates and toy breed dogs

A

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

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93
Q

Hypoglycemia: Hepatic disease

What % of liver failure occurs resulting in total dysfunction?

A

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

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94
Q

Hypoglycemia: Hypocortisolism

A

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

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95
Q

Hypoglycemia: Sepsis

x3

A

– Decreased intake
– Decreased hepatic function
– noninsulin-mediated increased consumption play a role in sepsis-induced hypoglycemia
– induced by inflammatory mediators

Ex: Canine babesiosis

96
Q

Hypoglycemia: Exercise-induced

A

“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

97
Q

Hypoglycemia: Polycythemia and leukocytosis

x3 possible causes

A

– occurs secondary 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

98
Q

Hyperosmolar Hyperglycemic Syndrome

hyperosmolar hyperglycemic non‐ketotic syndrome

A

characterized by hyperglycemia (blood glucose >600 mg/dL), hyperosmolarity (>350 mOsm/L), and dehydration without the presence of ketoacidosis

normal osmolarity in dogs is approximately 290–310 mOsm/L and 290–330 mOsm/L in the cat.

99
Q

HHS: Hormonal alterations

A

– 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

100
Q

HHS

Effects of Epinephrine and Glucagon on insulin and glucose

A

– 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.

101
Q

HHS

Effects of Cortisol and Growth Hormone on insulin and glucose

A

– 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

102
Q

HHS

Diabetogenic hormones contribution to HHS

A

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

103
Q

Difference between HHS and DKA

A

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.

104
Q

HHS

Effects of Hyperglycemia

A

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

105
Q

HHS

Reduction of glomerular filtration rate from HHS

A

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

106
Q

Concurrent disease with HHS

A

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

107
Q

What causes metabolic acidosis in HHS?

A

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

108
Q

Effects of free water on Na+ with HHS

x3 key points

A

Hyperglycemia will cause 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.

109
Q

Ratio of Hyperglycemia to HypoNa+

A

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

110
Q

Rehydration protocol for Hyperosmolar/Hyperglycemia syndrome

A

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

111
Q

Insulin therapy for HHS

A

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

112
Q

Causes of Hypoadrenocorticism

A

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 idiopathicin most cases
– may have an immune‐mediated cause in some cases
– or iatrogenic causes (e.g. mitotane usage) in others

113
Q

Primary Hypoadrenocorticism causes

A

caused by adrenal gland dysfunction
– has both glucocorticoid and mineralocorticoid insufficiency

114
Q

Hypoadrenocorticism results in:

A

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

115
Q

Atypical hypoadrenocorticism

A

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

116
Q

primary mineralocorticoid deficient in hypoadrenocorticism

A

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

117
Q

primary glucocorticoids deficient in hypoadrenocorticism

x2

A

cortisol and corticosterone

118
Q

Poster child for hypoadrenocorticism

A

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

119
Q

Hallmark CS of Addisonian crisis on presentation

A

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

120
Q

Classic biochemical abnormalities associated with hypoadrenocorticism

#6

A
  1. hyPO-Na+
  2. hypER-K+
  3. hyPO-Cl-
  4. Azotemia,
  5. mild to moderate metabolic acidosis
  6. 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
121
Q

UA findings with hypoadrenocorticism

A

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.

122
Q

CBC findings with hypoadrenocorticism

A

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

123
Q

ACTH stim for hypoadrenocorticism

A

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.

124
Q

EKG abnormalities with hypoadrenocorticism

A

– 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

125
Q

Hypoadrenocorticism Tx

A

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

126
Q

Pheochromocytoma

Where are they found?
What effects do they cause?

A

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

127
Q

Pheochromocytoma CS

A

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

128
Q

Pheochromocytoma Clin Path findings

x3

A

– 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

129
Q

Pheochromocytoma Tx

Which type of medications are rx?
What can occur following tx?

A

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

130
Q

Pheochromocytoma Anesthesia risks

A

– 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.

131
Q

Sx complications with Pheochromacytoma removal

A

– 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

132
Q

Critical Illness‐Related Corticosteroid Insufficiency

A

– 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

133
Q

What can cause CIRCI?

3 examples of causes
which does this result in?

A

– 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

134
Q

Critical Illness‐Related Corticosteroid Insufficiency Tx

A

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

135
Q

Medications that can possibly decreased cortisol production

x4

A
  1. ketoconazole,
  2. etomidate,
  3. propofol,
  4. opiates
136
Q

Clinical effects of CIRCI

A

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

137
Q

Thyroid dysfunction in cats vs dogs

A

Cats typically experience hyperthyroidism while dogs get hypothyroidism

138
Q

Parathyroid dysfunction

A

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.

139
Q

Normal glucose homeostasis

#3 sources

A

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.

140
Q

Hormones affecting glucose concentration

#7

A
  1. glucose-lowering hormone,
  2. insulin
  3. glucose-elevating hormones,
  4. primarily glucagon,
  5. epinephrine,
  6. cortisol,
  7. growth hormone (GH)
141
Q

Nonhormonal mechanisms affecting glucose concentration

x3

A

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

142
Q

Normal Insulin secretion

A

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

143
Q

Normal Insulin actions

what doe it inhibit?

A

– 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

144
Q

Glucagon

Where does it come from?
what does it stimulate and inhibit?

A

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

breaks down glycogen, proteins, and triglycerides for energy

145
Q

Gluconeogenesis

what does it result in? which substances does it utilize?
Where does it occur?

A

– 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

146
Q

Glycogenolysis

Where does it occur? What is it stimulated by?

A

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

147
Q

Glycogen

Where is it found?

A

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

148
Q

Glycolysis

A

– 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.

149
Q

General mechanisms (causes) of hypoglycemia

#4

A

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

150
Q

When do CS typically manifest with hypoglycemia?

A

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

151
Q

How is hypoglycemia sensed in the body?

A

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

152
Q

How does the body defend against hypoglycemia?

A

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

153
Q

Defense against hypoglycemia: hepatic glucose autoregulation

A

– 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

154
Q

Defense against hypoglycemia: increased neural efferent signaling

A

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

155
Q

Clinical signs and consequences of hypoglycemia

A

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

156
Q

Pancreatic Endocrine functions

x3

A

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

157
Q

Pancreatic Exocrine functions

#3

A

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

158
Q

EPI

A

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

159
Q

Diabetes insipidus

A

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+)

160
Q

Central DI

A

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

161
Q

DI nephrogenic

A

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

162
Q

DI

Arginine vasopressin

where does it come from? what type of hormone is it? Aka ADH

A

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

163
Q

DI

Primary functions of AVP

A

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

164
Q

DI

organum vasculosum laminae terminalis (OVLT)

A

– 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

165
Q

DI

Effects of AVasopressin on Kidneys

A

– 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

Once osmolality returns to normal, osmoreceptors inhibit ongoing AVP secretion and thirst to prevent hypoosmolality

166
Q

DI

Apelin

A

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.

167
Q

6

Causes of Acquired Central Diabetes Insipidus

A
  1. Brain Trauma
  2. Neoplasia (Pituitary macroadenoma)
  3. Infectious/inflammatory (Meningitis Toxoplasmosis Fungal (cryptococcus))
  4. Vascular (Intracranial hemorrhage Hypothalamic infarction)
  5. Immune-mediated (Lymphocytic neurohypophysis)
  6. Idiopathic
168
Q

5

Causes of Acquired Nephrogenic Diabetes Insipidus

A
  1. Drugs (Vasopressin, Ofloxacin, Aminoglycosides)
  2. Electrolyte abnormalities (HyperCa++ HypoK+)
  3. Bacterial infection (Escherichia coli Streptococcus spp. Leptospira spp.)
  4. Degenerative (CKD)
  5. Paraneoplastic (Intestinal leiomyosarcoma)
169
Q

Central DI management

A

– 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

170
Q

Nephrogenic DI management

A

– 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.

171
Q

suspected acquired DI diagnosis

A

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

172
Q

Syndrome of inappropriate secretion of antidiuretic hormone secretion (SIADH)

A

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

173
Q

Type A – Unregulated secretion of ADH

A

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

174
Q

Type B – Elevated basal levels of ADH

SIADH

A

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.

175
Q

Type C – Reset osmostat

SIADH

A

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.

176
Q

Type D – Undetectable ADH

SIADH

A

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.

177
Q

Causes of SIADH seen in veterinary patients

A
  1. aspiration pneumonia,
  2. meningoencephalitis,
  3. hydrocephalus,
  4. neoplasia,
  5. liver disease,
  6. general anesthesia
  7. pain and nausea following GA
178
Q

Diagnosis SIADH

A

– 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)

179
Q

Tx for SIADH

A

– 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

180
Q

Thyroid storm

A

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

181
Q

Thyrotoxicosis

A

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.

182
Q

Hyperthyroidism

A

thyroid gland hyperfunction

183
Q

Hyperthyroidism in cats vs dogs

A

– 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

184
Q

4

Laboratory Factors involved with Thyroid storms

A
  1. high levels of circulating TH,
  2. rapid increases in circulating TH
  3. hyperactivity of SNS
  4. an increased cellular response to TH
185
Q

Thyroid storm

High levels of circulating thyroid hormones

A

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

186
Q

Thyroid Storm

Rapid, acute increases in circulating thyroid hormones

A

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

187
Q

Thyroid Storm

Hyperactivity of the sympathetic nervous system

A

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

188
Q

main enzymes responsible for converting T4 to active form and back to euthyroid state

A

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

189
Q

Thyroid storm

Increased cellular response to thyroid hormones can result from;

A

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

190
Q

8

Potential Precipitating Events for Feline Thyroid Storm

A
  1. Radioactive iodine therapy
  2. Thyroidal or parathyroidal surgery
  3. Abrupt withdrawal of antithyroid medications
  4. Stress
  5. Nonthyroidal illness
  6. Administration of iodinated contrast dyes
  7. Administration of stable iodine compounds
  8. Vigorous palpation of the thyroid
191
Q

6 categories

Clinical signs associated with Feline Thyroid Storm

A

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

192
Q

Diagnosis of Thyroid Storm

A

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

193
Q

Tx of Thyroid Storm

x4

A

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).

194
Q

Canine myxedema coma

A

life-threatening complication of hypothyroidism

195
Q

Normal Thyroid hormone effects

A

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

196
Q

Thyroid-stimulating hormone (TSH)

A

– 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

197
Q

Adrenocorticotropic hormone (ACTH)

A

– 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

198
Q

ACTH response to stress

A

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

199
Q

Hormones produced by the Thyroid

A
  1. Thyroid hormone, which mainly helps regulate the body’s metabolic rate
  2. Calcitonin, which helps regulate blood calcium levels.
200
Q

Thyroid hormone

A

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

201
Q

Thyroid hormone’s calorigenic effect

A

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

202
Q

TH effect on Young, Growing Animals

A

– 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

203
Q

Calcitonin

Where is it produced? What type of cell produces it? How does it work?

A

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

204
Q

Parathyroid hormone (PTH)

A

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

205
Q

Adrenal Glands

A

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

206
Q

Adrenal Cortex

A

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

207
Q

Glucocorticoid Hormones

A

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.

Ex: hydrocortisone, prednisone, dexamethasone, and triamcinolone

208
Q

Mineralocorticoid Hormones

A

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

209
Q

Cortisol

A

– 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

210
Q

What regulates serum cortisol?

A

– 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.

211
Q

What does cortisol regulate?

x3

A

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

212
Q

Where is Aldosterone produced?

A

– 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.

213
Q

Aldosterone

A

– 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

214
Q

Macula Densa

Where are they located? What is their function? What cells do they utilize?

A

– 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

215
Q

Adrenal Medulla

A

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

216
Q

Pancreatic Endocrine functions

#2

A

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

217
Q

Pancreatic Exocrine functions

#3

Where do they get released into?

A

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

218
Q

Erythropoietin

A

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

219
Q

Thymus

A

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

220
Q

thymosin and thymopoietin hormones

A

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

221
Q

Prostaglandins

What do they influence?

A

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.

222
Q

Growth hormone (GH)

A

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

223
Q

Prolactin

A

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

224
Q

Pathophysiology of altered mental status from Hypothyroidism

A

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

225
Q

Pathophysiology of altered thermoregulation from Hypothyroidism

A

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

226
Q

Hypothyroid cardiomyopathy

A

– 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,

227
Q

4

Clin Path seen with Hypothyroid Crisis

A
  1. mild nonregenerative anemia,
  2. hypercholesterolemia,
  3. lipemia,
  4. increased AlkPhos
228
Q

Why does Hypothyroidism cause nonregen anemia?

A

– 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

229
Q

Hypothyroid diagnosis

A

Thyroid axis testing
low thyroxine and high TSH concentrations,

230
Q

Drug that may cause low thyroxine levels

A

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

231
Q

Tx of Hypothyroid crisis

A

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

232
Q

Pheochromocytoma

Where are they found? What are they made up of?

A

tumor of the chromaffin cells of the adrenal medulla

233
Q

Clinical signs of Pheochromocytoma

A

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

234
Q

Diagnosis of Pheochromocytoma

A

– 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

235
Q

CBC findings with Pheochromocytoma

x3 examples

A

– 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

236
Q

Biochemistry findings from Pheochromocytoma

x3 examples

A

– 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

237
Q

Pheochromocytoma treatment

A

Definitive treatment is surgical excision

VTS ECC 2024 (17 decks)

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