IMED3004 Lecture Notes - Lecture 8: Macrophage, Polydipsia, Parathyroid Gland
1 Nov 2020
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L8 ENDOCRINE PANCREAS:
Normal Endocrine Pancreas:
• Islets of Langerhans
o 4 main types of cells
▪ β – Insulin
(regulates glucose
in tissues, reduces
blood glucose)
▪ α - Glucagon
(stimulates
glycogenolysis in the liver, increases blood sugar)
▪ δ – Somatostatin (suppresses both insulin and
glucagon release)
▪ PP – secretes pancreatic polypeptide (stimulates
gastric and intestinal enzymes and inhibits
intestinal motility)
- lso present outside islets
o 2 minor cell types
▪ D1 – Vasoactive intestinal polypeptide (VIP),
induces glycogenolysis and hyperglycaemia
▪ Enterochromaffin cells – Serotonin
Common Pathology of the Endocrine Pancreas:
1. Diabetes (aka Diabetes mellitus)
o Type 1
o Type 2
2. Disordered growth +/- function of islet cells
o Hyperplasia, neoplasia (mass effects, functional effects)
3. Related mass lesions of the ‘dispersed’ neuroendocrine
system
o (i.e. neuroendocrine tumours of other sites)
Diabetes Mellitus:
• Family of metabolic disorders, common feature is
hyperglycaemia
Hyperglycaemia can result in acute and chronic problems
• Common, extremely important
• The Australian Diabetes Society criteria for the diagnosis of
diabetes are:
1. Fasting (>8hr) plasma glucose ≥ 126 mg/dL (7.0mmol/L),
2. Random plasma glucose ≥ 200 mg/dL (≥11.1 mmol/L) (in a
patient with classic hyperglycemic signs)
3. 2-hour plasma glucose ≥ 200 mg/dL (≥11.1 mmol/L) during
an oral glucose tolerance test (OGTT) with a loading dose
of 75g
4. Glycated hemoglobin (HbA1C) level ≥ 6.5%
Classification:
• Type 1
o Autoimmune disease
o β cell destruction → total or near total insulin
deficiency
o 5-10% of all cases, usually aged <20 years at age of
onset
• Type 2
o Peripheral resistance to insulin and subsequent
inadequate insulin secretion
o 90-95% of cases
o Usually adult onset but occasionally seen in younger
people
• (Impaired Glucose Tolerance)
o Precursor to T2DM in many people, may be reversible
with diet/lifestyle change
o Elevated plasma glucose but not in diagnostic range
o 25% develop T2DM within 5 years
• Others- most rare
o Drugs
▪ (glucocorticoids, thyroid hormone, interferon,
thiazides, phenytoin etc)
o Exocrine pancreatic damage
▪ (chronic pancreatitis, pancreatectomy, trauma,
neoplasia, cystic fibrosis, haemochromatosis, etc)
o Gestational DM
o Endocrinopathies
▪ (Acromegaly, Cushing’s, Hyperthyroidism,
Phaechromocytoma, Glucagonoma)
o Genetic defects in β cell function
▪ (including Neonatal diabetes, MODY, Insulin gene
mutations etc)
o Infections
▪ (rubella, CMV, Coxsackie B)
o Genetic syndromes
▪ (Downs, Klinefelters, Turner, Prader- Willi, others)
• (Latent Autoimmune Diabetes in Adults/LADA)
o “Type 1a”, “Type 1.5”, “Maturity-onset diabetes of the
young”
o Up to 10% of adults with T2DM have islet
autoantibodies, particularly if non-obese
o May be a form of DM that is slower onset and
therefore presents insidiously in adulthood (like T2),
but is autoimmune in nature (like T1)
o Not recognised by NIH (USA) or most other consensus
groups (grouped with T1, often initially diagnosed as T2
due to age)
Clinical:
• Presentation:
o T1: Indolent onset (over
years) but sudden
presentation
(decompensation)
▪ polyuria, polydipsia,
polyphagia, subsequently
DKA
o T2: unexplained fatigue,
dizziness, blurred vision.
▪ Often asymptomatic. May
become hyperosmolar non-
ketotic state.
Document Summary
Insulin (regulates glucose in tissues, reduces blood glucose) Glucagon (stimulates glycogenolysis in the liver, increases blood sugar) Somatostatin (suppresses both insulin and glucagon release) Pp secretes pancreatic polypeptide (stimulates gastric and intestinal enzymes and inhibits intestinal motility) lso present outside islets. D1 vasoactive intestinal polypeptide (vip), induces glycogenolysis and hyperglycaemia. Common pathology of the endocrine pancreas: diabetes (aka diabetes mellitus) Type 2: disordered growth +/- function of islet cells, hyperplasia, neoplasia (mass effects, functional effects, related mass lesions of the dispersed" neuroendocrine system (i. e. neuroendocrine tumours of other sites) Family of metabolic disorders, common feature is hyperglycaemia. Hyperglycaemia can result in acute and chronic problems. The australian diabetes society criteria for the diagnosis of diabetes are: Cell destruction total or near total insulin deficiency. 5-10% of all cases, usually aged <20 years at age of onset. Peripheral resistance to insulin and subsequent inadequate insulin secretion. 90-95% of cases: usually adult onset but occasionally seen in younger people (impaired glucose tolerance)
