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Endocrinology > Lecture 8 - Endocrine pancreas > Flashcards

Lecture 8 - Endocrine pancreas Flashcards

1
Q

In dogs, how do the pancreatic and bile ducts enter the duodenum?

A

they enter separately

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2
Q

In cats, how do the pancreatic and bile ducts enter the duodenum?

A

the common bile duct and the major pancreatic duct (the larger one) are usually fused prior to the entrance to the major duodenal papilla.

because of this, cats are more prone to pancreatic and biliary disease presenting together.

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3
Q

How many pancreatic ducts do dogs have?

A

dogs typically have two, the pancreatic duct and the accessory pancreatic duct, one entering at the major duodenal papilla and the other at the minor duodenal papilla.

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4
Q

How many pancreatic ducts do cats have?

A

Usually one, the pancreatic duct is the main functional duct; the accessory pancreatic duct usually does not persist.

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5
Q

purpose of the acinar cells of the pancreas

A

formation and secretion of digestive enzymes

  • amylase
  • lipases
  • proteases
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6
Q

purpose of the centroacinar cells of the pancreas

A

formation and secretion of bicarbonate rich duodenal secretions

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7
Q

the endocrine portion of the pancrea consists of?

A

the pancreatic islets of langerhans

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8
Q

the islets of langerhans secrete what hormones?

A

α cells secrete glucagon;
β cells secrete insulin & amylin;
δ or D cells secrete somatostatin; the PP cells secrete pancreatic polypeptide.
etc.

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9
Q

Function of amylin?

A

provoked by nutrient influx to the gastrointestinal tract and co-secreted with insulin by pancreatic islet β-cells.

Amylin inhibits food intake, delays gastric emptying, and decreases blood glucose levels, leading to the reduction of body weight.

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10
Q

the Islets of Langerhans’ capillaries have special morphology, name it

A

fenestration, to increase permeability.

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11
Q

what communicates between the
endocrine and exocrine pancreatic
tissues.

A

An islet-acinar portal system

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12
Q

The islets are innervated by

A

sympathetic and parasympathetic
fibers which influence the release
of pancreatic hormones

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13
Q

insulin secreted by what cells.
purpose of insulin.

A

beta cells
anabolism
(increases the cellular uptake of GLU, amino acids and potassium)

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14
Q

amylin secreted by what cells?
Co-secreted with?

A

beta cells
Co-secreted with insulin

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15
Q

glucagon secreted by what cells.
purpose of glucagon.

A

alfa cells
catabolism

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16
Q

somatostatin is also known as what?
is secreted by what cells?
purpose of somatostatin.

A

Growth Hormone Inhibiting Hormone (GHIH)
secreted by delta cells (of islets)
Paracrine inhibitor of insulin and glucagon secretion.

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17
Q

PP cells stands for?
purpose of it?

A

pancreatic polypeptide

The primary role of PP is to modulate digestion of food by inhibition of gastric emptying as well as biliary secretion.

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18
Q

most abundant cell types in the islets of langerhans

A

beta cells

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19
Q

canine insulin is identical to what other species’ insulin?

A

porcine

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20
Q

feline insulin is most similar to what other species’ insulin?

A

bovine

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21
Q

Circulating insulin is almost entirely

A

unbound.

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22
Q

Half life of insulin

A

5-8 min

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23
Q

Insulin is Metabolized mainly in the

A

liver and kidneys

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24
Q

Name 4 hormones that raise blood sugar?

A

glucagon
glucocorticoids
adrenaline
growth hormone

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25
Q

Main function of insulin?

A

allows the cellular uptake of glucose so it lowers blood sugar.

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26
Q

Name The main catabolic hormone and gives its purpose.

A

Glucagon, acts on the liver to mobilize energy stores, increases hepatic glucose output into circulation.

Counteracts the actions of insulin, increases blood sugar conc.

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27
Q

Main secretory stimuli of glucagon.

A

low plasma glucose conc stimulates because it then increases blood sugar.

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28
Q

Glucagon stimulates what to take place in the liver? (2)

A

Glycogenolysis (break down of glycogen)

Gluconeogenesis (generation of glucose from certain non-carbohydrate carbon substrates)

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29
Q

IAPP is

A

Islet Amylin Polypeptide which is another name for amylin

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30
Q

GHIH is

A

Growth Hormone Inhibiting Hormone, just another name for somatostatin

31
Q

somatostatin is secreted at what locations?

A

From the pancreatic delta cells in order to inhibit insulin and glucagon but also into the Intestines: pyloric antrum & duodenum.

In the GI tract somatostatin decreases gut motility, slows the absorption of nutrients and slows digestion.

32
Q

GLP-1* and GIP** stand for

A

*GLP-1 Glucose-dependent insulinotrophic peptide

**GIP Glucagon-like peptiide 1

33
Q

Glucose homeostasis can be divided into two phases

A

Absorptive phase
and Post-absorptive phase

34
Q

explain GLUT-4

A

GLUT4 is an insulin-regulated glucose transporter that is responsible for insulin-regulated glucose uptake into fat and muscle cells.

In the absence of insulin, GLUT4 is mainly found in intracellular vesicles referred to as GLUT4 storage vesicles (GSVs).

Insulin promotes the expression of GLUT4.

35
Q

Main hormone at play during the absorptive phase.

A

insulin

promotes the expression of GLUT4, and the storage of glucose and glycogen.

36
Q

Main stimulus of insulin secretion?

A

increased blood glucose during the absorptive phase.

Other factors also, such as increased incretins (GLP and GIP), amino acids and K+ which increase after eating.

*GLP-1 Glucose-dependent insulinotrophic peptide
**GIP Glucagon-like peptide 1

37
Q

primary stimulants of the gluconeogenic pathways in the liver

A

glucagon and glucocorticoids

38
Q

Decreased glucose uptake and Increased gluconeogenesis cause what? (5)

A

▫ Hyperglycemia
▫ Glucosuria
▫ the above causes Osmotic diuresis with the loss of electrolytes (Na, K, P) (energy is lost)
▫ The above in turn, causes Polydipsia
▫ plus Polyphagia (compensatory mechanism for lost energy through the glucosuria)

39
Q

Increased protein catabolism causes? (3-4)

A

▫ Increased circulating amino acids accelerating
gluconeogenesis
▫ Weakness, weight loss
▫ Poor wound healing

40
Q

Increased lipolysis causes? (5)

A

▫ Increased NEFA
▫ Ketone body production
▫ Hepatic steatosis
▫ Hyperlipidemia
▫ Weight loss

41
Q

what causes insulin resistance

A
  • Obesity
  • Diestrus
  • Pregnancy
  • Altered „metabolites“
  • Hyperglycaemia
  • Elevated plasma fatty acid level
  • Hypercortisolaemia due to
  • Any significant illness or „stress“
  • Hyperadrenocorticism
  • Concurrent endocrinopathies
42
Q

Describe the acute phase of hyperglycemia

A

hyperglycemia reduces neutrophil functions so infection can be a primary consequence of “glucose toxicity”

43
Q

Insulin resistance in Type 2 diabetes is caused by

A

chronically increased free fatty acid concentrations result in lipotoxicity which causes beta-cell mass to decrease (beta cell dysfunction, apoptosis) which in turn decreases insulin secretion and causes type 2 diabetes.

44
Q

Why can cats not tolerate large amounts of simple carbohydrates (3)

A

Their liver does not possess glucokinase.

They do not possess certain disaccharidases.

Their GI tract is not equipped to absorb large amounts of carbs (rudimentary cecum, short colon).

45
Q

It is currently assumed that diabetes in dogs is
usually similar to?

and diabetes in cats closely
resembles?

A

diabetes in dogs is
usually similar to type 1 and diabetes in cats closely
resembles type 2.

46
Q

Diabetes mellitus in vet med means…?

A

Clinically significant deficiency of insulin secreting capacity.

47
Q

Diabetes mellitus can be characterized how in dogs?

A

Absolute and irreversible in dogs

48
Q

Diabetes mellitus can be characterized how in cats?

A

Absolute or relative and…
frequently reversible in cats

49
Q

Differences between type 1 and 2 diabetes mellitus.

A

Type 1 is irreversible.
Type 2 is reversible with therapy.

50
Q

Pathophysiology of canine diabetes mellitus.

A

normal insulin sensitivity and severe loss of islets.

51
Q

Pathophysiology of feline diabetes mellitus.

A

insulin resistance leading to islet hyperactivity which finally leads to islet underactivity.

  • initially a relative insulin deficiency that is variably reversible
  • insulin deficiency is brought about by overproduction and „islet exhaustion“ in predisposed groups of animals
  • islet numbers can be reduced but also can be unchanged.
  • islet amyloid production (rather than deposition) may play a role in the accelerated islet apoptosis.
52
Q

Juvenile diabetes mellitus has been associated with

A

beta cell hypoplasia (hypoinsulinemia)

53
Q

Clinico-pathological findings of Juvenile diabetes mellitus are

A

Retarded growth due to lack of insulin-like growth factor-1 (IGF-1↓).

Can also be accompanied by:
* EPI
* ↓thyroid hormone deficiency
* ↓cortisol deficiency
* ↓growth hormone deficiency

54
Q

Possible complications of diabetes mellitus in dogs

A

cataracts

In almost 60% of cases of DM
50% developed cataracts in 6 months
76% developed cataracts by one year

55
Q

Possible complications of diabetes mellitus in caats

A

Peripheral neuropathy

56
Q

what is the mechanism behind why diabetes causes cataracts

A

high levels of glucose in the bloodstream can lead to a process called glycation. Glycation involves the binding of glucose molecules to proteins, forming advanced glycation end-products (AGEs). This process can occur in the crystalline lens of the eye, causing proteins to become cross-linked, cloudy and less flexible.

also, excess glucose in the lens is converted to sorbitol through the polyol pathway. Sorbitol tends to accumulate in the lens, drawing water into the lens fibers and causing changes in cell structure and function.

etc.

57
Q

Name 3 Pancreatic endocrine tumours

A
  • Insulinoma
  • Glucagonoma
  • Gastrinoma
58
Q

NET

A

neuroendocrine tumor

59
Q

APUDomas =

A

APUDomas, currently known as neuroendocrine tumors (NETs), are a group of heterogeneous tumors that arise from the diffuse neuroendocrine system

They occur mainly in the gastrointestinal tract and lungs. These tumors typically present with organ-specific features.

60
Q

Insulinoma is a

A

Rare endocrine disorder of the dog and cat.

Functional tumors of the β-cells in the islets
of Langerhans and secrete insulin independent of usual feedback mechanisms.

Thus cause profound hypoglycemia.

61
Q

Most common tumor of the pancreas in dogs.

A

functional insulinoma

62
Q

Insulinoma-presentation

A

neuroglycopenia (inadequate glucose in the
nervous system)

  • Weakness (75%)
  • Ataxia* (40%)
  • Collapse (80%)
  • Disorientation and visual disturbances
  • Behavioral changes
  • Seizures (95%) →coma → death

Some signs are associated with high production of catecholamines as counter regulatory hormones.

63
Q

Insulinoma - prognosis

A

Surgical removal offers the best long-term solution unless gross metastases identified.

Median survival surgical cases 12-14 months.
Median survival 6 months medical therapy alone.

64
Q

Pancreatic Glucagonoma

A

neoplasm to excrete Excess circulating glucagon which in turn cause increased

  • Protein/amino acid catabolism
  • Lipolysis
  • Gluconeogenesis
  • Glycogenolysis
65
Q

Gastrinoma

A

(Zollinger-Ellison like syndrome) a neoplasm that produces excess gastrin but is usually in the pancreas.

Gastrin → stimulates gastric HCl secretion.
This leads to ulceration of the stomach, duodenum and esophagus.

66
Q

Gastrinoma – signalment and clinical signs in dogs

A

Most dogs >8 y
* Vomiting ,weight loss, inappetance, diarrhoea
* Melena, hematochezia, hematemesis, pyrexia
* Emaciation, thin body condition, weight loss

The majority of gastrinomas are malignant
Treatment: surgical & palliative (antacids and gastroprotective therapy).

67
Q

Gastrinoma – signalment and clinical signs in cats

A

8 - 12 y

Vomiting, weight loss, thin, poor hair coat, pale mucous membranes, systolic heart murmur.

The majority of gastrinomas are malignant
Treatment: surgical & palliative (antacids and gastroprotective therapy).

68
Q

Paraneoplastic syndrome in cats usually

A

Tumor of the exocrine pancreas (adenocarcinoma) that causes symmetrical alopecia.

69
Q

Glycogenesis

A

is the process of glycogen synthesis, in which glucose molecules are added to chains of glycogen for storage.

70
Q

Glycolysis

A

is the metabolic pathway that converts glucose into two three-carbon molecules called pyruvates thus extracting energy.

71
Q

Glycogenolysis

A

is the breakdown of glycogen to glucose-1-phosphate and glycogen.

72
Q

Gluconeogenesis

A

is the generation of glucose from certain non-carbohydrate carbon substrates.

73
Q

Mechanisms behind insulin resistance.

A

Insulin resistance is a key factor in the development of type 2 diabetes and Several mechanisms contribute to insulin resistance:

Excess FFAs can interfere with insulin signaling pathways and promote inflammation.

And many other mechanisms.

Endocrinology (16 decks)

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