Endocrine pancreas

Exocrine and endocrine functions

Pancreatic acinar cells and duct cells

They serve as a “roadway” to duodenum

<p>It secretes digestive enzymes into the lumen of the duodenum</p> Signup and view all the answers

<p>Islets of Langerhans</p> Signup and view all the answers

<p>Alpha, beta, Delta and F cells</p> Signup and view all the answers

<p>Alpha = Glucagon Beta = Insulin Delta = Somatostatin F = Pancreatic polypeptide</p> Signup and view all the answers

<p>Glucagon, insulin, somatostatin and pancreatic polypeptide</p> Signup and view all the answers

<p>False (B)</p> Signup and view all the answers

<p>Preprohormone in endoplasmic reticulum cleaved by enzymes to prohormone before getting secreted, Prohormone (aka proinsulin) moves into Golgi apparatus where its packaged in secretory vesicles that contain proinsulin and enzymes and further processed into insulin and the connecting C peptide, insulin and c peptide are released by exocytosis into extracellular space, insulin is transported by blood vessels to its target organ</p> Signup and view all the answers

<p>2 chains, alpha and beta</p> Signup and view all the answers

<p>False (B)</p> Signup and view all the answers

<p>Human insulin differs from feline by = 4 aa Porcine insulin differs from human insulin by = 1 aa Bovine insulin differs from feline insulin by = 1 aa Porcine insulin differs from feline insulin by = 3 a</p> Signup and view all the answers

<p>Amino acids (B)</p> Signup and view all the answers

<p>Fatty acids (A)</p> Signup and view all the answers

<p>Glucose (D)</p> Signup and view all the answers

<p>Volatile fatty acids stimulate secretion. (D)</p> Signup and view all the answers

<p>Genetic variables (A)</p> Signup and view all the answers

<p>Growth hormone and glucagon</p> Signup and view all the answers

<p>Glucose, amino acids, fatty acids and ketones</p> Signup and view all the answers

<p>GIP (C)</p> Signup and view all the answers

<p>Adrenocorticosteroids, somatostatin, Adrenalin, noradrenalin</p> Signup and view all the answers

<p>Acute phase releases preformed insulin and the chronic phase synthesis of protein</p> Signup and view all the answers

<p>False (B)</p> Signup and view all the answers

<p>GLUT1 transporter on the membrane surface enters, which causes an increase in ATP production, this blocks the potassium ATP sensitive channel, causes depolarization in the cell which then allows voltage gated calcium channels to open, an increase in Ca activates vesicles to promote exocytosis of stored insulin</p> Signup and view all the answers

<p>It will act directly on ATP production to increase exocytosis of stored insulin</p> Signup and view all the answers

<p>Insulin receptor tyrosine kinase, two</p> Signup and view all the answers

<p>The goal of insulin is to lower the blood concentration of glucose, fatty acids and amino acids. It does this by promoting intracellular conversion of these compounds to their storage forms</p> Signup and view all the answers

<p>Liver, muscle and adipose tissue</p> Signup and view all the answers

<p>Increases the number of GLUT-4 transporters in the cell membrane (C)</p> Signup and view all the answers

<p>GLUT-4 can be stimulated by both insulin and exercise (D)</p> Signup and view all the answers

<p>Stimulation by physical activity (D)</p> Signup and view all the answers

<p>GLUT-4 (D)</p> Signup and view all the answers

<p>Increases basal glucose levels in the bloodstream (C)</p> Signup and view all the answers

<p>Liver (A), Kidneys (B)</p> Signup and view all the answers

<p>True (A)</p> Signup and view all the answers

<p>Cortisol, growth hormone, glucagon, epinephrine/norepinephrine</p> Signup and view all the answers

<p>Glucagon (A), Epinephrine (C)</p> Signup and view all the answers

<p>Increases lipolysis (C)</p> Signup and view all the answers

<p>Epinephrine (C)</p> Signup and view all the answers

<p>Epinephrine (B)</p> Signup and view all the answers

<p>True (A)</p> Signup and view all the answers

<p>Hypoglycemia</p> Signup and view all the answers

<p>Glucose enters cells via GLUT transporter, Glucose is used to generate ATP, Low glucose results in low intracellular ATP, low ATP levels close ATP-sensitive potassium channels, effluent of potassium is reduced and causes the cell membrane to change, it in turn opens voltage dependent calcium channels and causes an influx of Ca to trigger exocytosis of glucagon.</p> Signup and view all the answers

<p>It opposes most insulin actions, maintain blood glucose concentration</p> Signup and view all the answers

<p>False (B)</p> Signup and view all the answers

<p>Enhances glucose availability to other cells (D)</p> Signup and view all the answers

<p>Alanine and Arginine (B)</p> Signup and view all the answers

<p>Promotes lipolysis (D)</p> Signup and view all the answers

<p>Stimulates insulin release (D)</p> Signup and view all the answers

<p>Inhibits secretion from Islet of Langerhans cells (D)</p> Signup and view all the answers

<p>F or PP cells (B)</p> Signup and view all the answers

<p>Inhibits its secretion (C)</p> Signup and view all the answers

<p>Decreases gastric emptying (A)</p> Signup and view all the answers

<p>It decreases motility of the gastrointestinal tract. (A)</p> Signup and view all the answers

<p>Absolute insulin deficiency is the complete absence of insulin, characteristic of type 1 diabetes, while relative insulin deficiency refers to insulin that is not functioning properly, as seen in type 2 diabetes.</p> Signup and view all the answers

<p>Two primary clinical signs are polyuria (increased urination) and polydipsia (increased thirst).</p> Signup and view all the answers

<p>Insulin deficiency leads to increased glucagon production due to the loss of inhibition, causing hyperglucagonemia and disrupting the regulation of glucagon secretion.</p> Signup and view all the answers

<p>Hormone-sensitive lipase is activated by insulin deficiency, leading to lipolysis of stored fat and increased free fatty acids in the blood.</p> Signup and view all the answers

<p>Insulin deficiency results in protein depletion and increased plasma amino acids due to increased protein catabolism and halted protein synthesis.</p> Signup and view all the answers

<p>Glucagon stimulates gluconeogenesis by promoting the conversion of amino acids and glycerol to glucose in the liver, especially when insulin levels are low.</p> Signup and view all the answers

<p>Excess FFA can lead to increased liver production of triglycerides and cholesterol, contributing to hyperlipidemia.</p> Signup and view all the answers

<p>Paradoxical hyperglucagonemia indicates a loss of regulatory control over glucagon secretion due to beta cell deficiency and insulin resistance, exacerbating hyperglycemia.</p> Signup and view all the answers

<p>Autoimmune destruction of beta cells (B)</p> Signup and view all the answers

<p>Accumulation of sorbitol and galactitol (D)</p> Signup and view all the answers

<p>It results from relative insulin deficiency and insulin resistance. (A)</p> Signup and view all the answers

<p>Islet amyloidosis (A)</p> Signup and view all the answers

<p>It causes aggregation leading to amyloid deposition in pancreatic islets. (C)</p> Signup and view all the answers

<p>Healthy beta cells can adapt to obesity and insulin resistance. (A)</p> Signup and view all the answers

<p>It converts glucose into sorbitol and galactitol. (D)</p> Signup and view all the answers

<p>Increased glucose utilization (B)</p> Signup and view all the answers

<p>Obesity.</p> Signup and view all the answers

<p>Clinical signs disappear and blood glucose levels normalize, allowing for the discontinuation of insulin treatment.</p> Signup and view all the answers

<p>Diabetic neuropathy, primarily caused by hyperglycemia leading to nerve injury.</p> Signup and view all the answers

<p>Glucotoxicity is a reversible condition affecting beta cell function, which can lead to complications in diabetes.</p> Signup and view all the answers

<p>Clinical signs can range from very mild to severe, affecting mobility and overall nerve function.</p> Signup and view all the answers

<p>False (B)</p> Signup and view all the answers

<p>Glucagon (B)</p> Signup and view all the answers

<p>Na, K and Phosphate</p> Signup and view all the answers

<p>Increase in [H+] (C)</p> Signup and view all the answers

<p>Physiochemical properties of ketone bodies (A)</p> Signup and view all the answers

<p>Inability to maintain stable pH (B)</p> Signup and view all the answers

<p>Beta hydroxybutyrate (C)</p> Signup and view all the answers

<p>Impairment of metabolic processes (A)</p> Signup and view all the answers

<p>Insulinoma (B)</p> Signup and view all the answers

<p>Superficial necrolytic dermatitis (B)</p> Signup and view all the answers

<p>Cats (A)</p> Signup and view all the answers

<p>Alpha cells (A)</p> Signup and view all the answers

<p>They produce insulin regardless of blood glucose levels. (D)</p> Signup and view all the answers

Insulin release is regulated by several factors including nutrition, nerves, hormones, and local signaling molecules.

In omnivores, glucose is the primary stimulus for insulin secretion.

In carnivores, amino acids are the primary stimulus for insulin secretion.

Fatty acids stimulate insulin release in humans.

Volatile fatty acids stimulate insulin secretion in ruminants.

A type of glucose transporter protein that's sensitive to insulin and exercise. It helps move glucose from the bloodstream into cells.

Insulin increases the number of GLUT-4 transporters on the cell membrane, allowing more glucose to enter the cells.

Physical activity can stimulate GLUT-4 translocation to the cell membrane, independent of insulin.

This refers to the increase in GLUT-4 transporters on the cell membrane due to exercise.

GLUT-4 is crucial for regulating blood sugar levels by facilitating glucose uptake into muscle and fat cells.

Hormones that oppose the effects of insulin, raising blood glucose levels during hypoglycemia. These include cortisol, epinephrine/norepinephrine, glucagon, and growth hormone.

The immediate reaction to low blood sugar, primarily driven by glucagon and epinephrine, increasing glucose production and release.

The longer-term response to prolonged low blood sugar, mediated by cortisol and growth hormone, promoting glucose production and reducing glucose uptake.

Counter-regulatory hormones stimulate the liver to produce more glucose through glycogenolysis (breaking down stored glycogen) and gluconeogenesis (producing glucose from other sources).

These hormones increase lipolysis in adipose tissue, releasing fatty acids into the bloodstream to be used as alternative energy sources by cells.

The liver is the primary target tissue for glucagon, where it plays a crucial role in regulating glucose availability for the entire body.

Glucagon promotes lipolysis, the breakdown of stored fat, increasing the availability of free fatty acids for energy.

Glucagon stimulates the conversion of amino acids into glucose, particularly in carnivores, where it aids in maintaining blood sugar levels.

Glucagon activates HSL, an enzyme that breaks down stored triglycerides in adipose tissue, releasing fatty acids.

Glucagon's role as a counter-regulatory hormone is crucial for maintaining blood glucose levels, especially during fasting or periods of low glucose.

Somatostatin, produced by delta cells in the pancreas, acts as an inhibitor, slowing down the activity of the digestive system and suppressing the release of hormones from other pancreatic cells.

Somatostatin primarily impacts the digestive tract, reducing its motility and secretion, and also affects the release of hormones from the pancreatic islets, particularly glucagon.

Pancreatic polypeptide is secreted by F or PP cells in the pancreas. Its release is triggered by various stimuli including gastrointestinal hormones, vagal nerve stimulation, and protein intake.

Pancreatic polypeptide primarily targets the digestive system, regulating motility and emptying of the stomach, as well as the release of digestive enzymes from the pancreas.

Somatostatin inhibits the release of pancreatic polypeptide, providing an important regulatory mechanism in the digestive system.

A condition characterized by an absolute or relative deficiency of insulin, leading to hyperglycemia.

Caused by an absence of insulin production due to immune system destruction of pancreatic beta cells.

Caused by insulin resistance, where the body's cells don't respond properly to insulin.

High blood sugar levels, a hallmark of diabetes mellitus.

Excessive urination, thirst, and hunger, common signs of diabetes mellitus.

Increased glucagon secretion in diabetes, despite high blood sugar levels, due to beta cell deficiency and alpha cell resistance.

Insulin deficiency causes lipolysis, releasing free fatty acids (FFA) from adipose tissue.

Insulin deficiency leads to protein breakdown (catabolism) in muscle tissue.

The accumulation of sorbitol and galactitol in the lens of the eye due to altered osmotic pressure. These sugar alcohols are byproducts of glucose and galactose reduction by the enzyme aldose reductase.

A condition in which amyloid deposits accumulate in the islets of Langerhans, damaging beta cells and contributing to insulin deficiency in cats.

A polypeptide hormone produced by beta cells alongside insulin. It plays a role in regulating appetite and blood sugar.

Healthy beta cells in obese cats can adapt by producing more insulin to compensate for insulin resistance. However, once beta cell function is compromised, diabetes develops.

When amylin aggregates, it forms amyloid deposits within the islets. This is particularly common in cats, humans, and primates.

Amyloid deposition within the islets disrupts normal beta cell function, impairing their ability to produce and release insulin.

A condition where the body produces very little or no insulin, leading to elevated blood sugar levels.

Obesity, Cushing's disease, acromegaly, glucocorticoid use, infections, pancreatitis, gingivitis, hyperthyroidism, renal failure, and inflammatory bowel disease can all contribute to insulin resistance in cats.

Clinical signs of type 2 diabetes in cats can disappear, blood glucose levels normalize, and insulin or other antidiabetic medications can be discontinued. However, remission depends on the level of beta cell dysfunction.

Amyloidosis, the accumulation of amyloid protein in the pancreas, is irreversible. This can damage beta cells and make insulin production less effective.

A common complication of diabetes in cats, diabetic neuropathy occurs due to nerve damage caused by high blood glucose levels. It can range from mild to severe.

High blood sugar levels damage Schwann cells and axons of myelinated fibers, leading to impaired nerve function. Microvascular abnormalities also contribute to nerve damage.

An excess of ketones in the blood causes acidosis. Ketones are produced when the body breaks down fat for energy instead of glucose.

These are two major ketones produced during fat breakdown. Their chemical properties make it difficult for the kidneys to remove them efficiently, contributing to acidosis.

During diabetic ketoacidosis (DKA), the kidneys struggle to compensate due to the build-up of ketones, leading to a dangerously acidic blood pH.

A combination of excess ketone production and the kidneys' inability to remove them effectively leads to acidosis in DKA.

The build-up of acidic ketones in the blood puts a strain on the kidneys, interfering with their ability to filter waste and regulate pH balance.

Acidosis develops in diabetic ketoacidosis (DKA) because the body produces excessive ketones (beta-hydroxybutyrate and acetoacetate), which the kidneys struggle to remove.

The kidneys' failure to compensate for the excessive ketones in DKA partly stems from the unique chemical properties of beta-hydroxybutyrate and acetoacetate, making them hard to eliminate.

A tumor in the pancreas that produces too much insulin, causing low blood sugar even when glucose levels are high. This occurs due to beta cells producing insulin regardless of blood glucose levels.

A tumor of the alpha cells in the pancreas that produces too much glucagon, leading to weight loss and skin problems.

These cells in the pancreas produce insulin, but in insulinoma they keep producing it even when blood sugar is low, causing hypoglycemia.

These cells in the pancreas produce glucagon, but in glucagonoma they overproduce it, leading to weight loss, skin issues, and hyperglycemia.

This tumor is primarily seen in dogs and ferrets, and it is rare in cats.