endocrine pancreas

Question 1

4 main types of islands of langerhans cells

Answer 1

Beta cells - insulin
alpha cells - glucagon
delta cells - somatostatin
PP cells - secretes pancreatic polypeptide

Question 2

2 minor cell types of the normal endocrine pancreas

Answer 2

D1 - vasoactive intestinal polypeptide (VIP), induces glycogenolyss and hyperglycaemia
enterochromaffin cells - serotonin

Question 3

types of diabetes

Answer 3

dibetes type 1
diabetes type 2
hypoglycaemia 
diabetic ketaacidosis 
hyperglycaemic hyperosmolar state

Question 4

diabetes mellitus

Answer 4

common disease

family of metabolic disease - common feature is hyperglycaemia

Question 5

type 1 diabetets

Answer 5

autoimmune
B cell destruction - total or near insulin deficiency
usually ages <20 at onset

Question 6

type 2 diabetes

Answer 6

peripheral resistance to insulin and subsequent inadequate insulin secretion
90-95% of cases
usually adult onset but occasionally seen in younger people

Question 7

impaired glucose tolerance

Answer 7

precursor to T2DM
may be reversible with diet/lifestyle change
elevated plasma glucose but not in diagnostic range
25% develop T2DM within 5 years

Question 8

other causes of diabetes

Answer 8

• drugs - glucoocorticoids, thyroid hormone, interferon, pancreatitis, pancreatomy, trauma, neoplasia, cystic fibrosis, haemochromatosis
• gestational DM
• endocrinopathies - acromegaly, cushings, hyperthyroidism, phaeochromocytoma, glucagonoma
• genetic defects in B cell function
• infections - rubella, CMV, coxsackie B
• genetic syndromes - downs, klinefelters, turner, prayer willi, others

Question 9

latent autoimmune diabetes

Answer 9

maturity onset diabetes of the young

have islet autoantibodies

Question 10

clinical presentation of type 1

Answer 10

indolent but silent onset over years, often sudden presentation with acute severe hyperglycaemia (decompensation)
- polyuria, polydipsia, polyphagia, subsequently DKA

Question 10

clinical presentation of type 1

Answer 10

indolent but silent onset over years, often sudden presentation with acute severe hyperglycaemia (decompensation)
- polyuria, polydipsia, polyphagia, subsequently DKA

Question 10

clinical presentation of type 1

Answer 10

indolent but silent onset over years, often sudden presentation with acute severe hyperglycaemia (decompensation)
- polyuria, polydipsia, polyphagia, subsequently DKA

Question 10

clinical presentation of type 1

Answer 10

indolent but silent onset over years, often sudden presentation with acute severe hyperglycaemia (decompensation)
- polyuria, polydipsia, polyphagia, subsequently DKA

Question 11

clinical presentation of type 2

Answer 11

unexplained fatigue, dizziness, blurred vision, symptoms often mild and come/go depending on BSL
often asymptomatic. may becomes hyperosmolar non-ketonic state if BSL very high

Question 12

pathogenesis of type 1

Answer 12

develops in childhood and manifest around puberty
without exogenous insulin they becomes ketotic causing coma and death
interplay of genetics and environment
B cell destruction follows loss of self tolerance for T cells specific islet antigens - insulin receptor, GAD, others - auto active T cells are not removed, are able to attack islets

Question 13

pathogenesis of type 2

Answer 13

interplay of genetics and environment
develops in adulthood, slow progression initially high insulin but peripheral insulin resistance, later low insulin due to B cell dysfunction

Question 14

insulin sensitivity decreases in T2DM because

Answer 14

free fatty acids
adipokines - secreted by adipocytes
inflammation (pro-inflammatory cytokines secreted in response to nutrient excess)

Question 15

gestational diabetes pathogenesis

Answer 15

• patients with pre existing DM
• pregnancy may result in impaired glucose tolerance
• higher rates in obese women
• associated with increased risk of stillbirth, congenital malformations in the foetus, especially macrosomia (high birth weight)
• laos associated with increased risk of obesity and diabetes later in life (for mother and baby)
• typically resolves following delivery

Question 16

acute diabetic ketacidosis

Answer 16

usually T1DM
insufficient insulin - initial presentation or under administration of exogenous insulin (ie. patient not taking enough insulin)
- increased needs due to infection, illness, drugs etc. increased adrenaline secretion blocks insulin and stimulates glucagon

Question 17

acute ketoacidosis causes

Answer 17

hyperglycaemia
osmotic diuresis and dehydration
activates ketogenic pathway, increased fat breakdown, which leads to increase ketone bodies as a byproduct
if urinary excretion is composed, systemic ketoacidosis

Question 18

symptoms of acute diabetic ketoacidosis

Answer 18

fatigue, nausea, vomiting, abdominal pain, ketotic breath, laboured breathing (kussmaul), eventually loss of consciousness and coma

Question 19

treating acute diabetic ketoacidosis

Answer 19

correct insulin deficiency, correct metabolic acidosis and treat precipitating factors
rare in T2DM

Question 20

cosequences of acute diabetic ketoacidosis

Answer 20

hyperosmolar hyper osmotic state
usually in T2DM
severe dehydration due to severe osmotic diuresis due to hyperglycaemia
absence of ketosis, mild or no metabolic acidosis

hypoglycaemia

• over treatment of hyperglycaemia
• dizziness, tachycardia, confusion, palpitations, potentially loss of consciousness and death
• always consider hypo and hyperglycaemia in an unconscious or drowsy patient

Question 21

chronic consequences of diabetes

Answer 21

• impaired immunity
• CVD
• cerebrovascular disease
• eye issues
• peripheral nervous system neuropathy
• diabetic nephropathy, glomerulosclerosis, pyelonephritis and papillary necrosis, arteriosclerosis, nephrosclerosis
• gangrene and ulceration

Question 22

macroangiopathy

Answer 22

atherosclerosis
ischaemic heart disease
cerebrovascular disease
peripheral vascular disease (esp. lower limb ischaemia)

Question 23

microangiopathy

Answer 23

retinopathy, nephropathy and neuropathy

diffuse thickening of basement membranes of capillaries
- skin, muscle, retina, renal glomeruli and medullar as well as non-vascular structures and nerves
- vessels are leaky, plasma proteins escape
microangiopathy underlies many of more serious complications including diabetic neuropathy, retinopathy and some neuropathies
poor wound healing

Question 24

predisposition to infection in diabetes

Answer 24

bacterial and fungal infections of skin, mucosal surfaces and urinary tract most common
impaired neutrophil function
abnormalities in chemotaxis, adhesion to endothelium , phagocytic capacity and microbicidal activity
impaired cytokine production by macrophages
impaired blood supply

Question 25

glomerular leions in diabetic nephropathy

Answer 25

nodular glomerulosclerosis, diffused mesangial sclerosis, glomerular capillary basement membrane thickening

Question 26

renal vascular lesions in diabetic nephropathy

Answer 26

diabetic microanggiopathy

renal artery atherosclerosis

Question 27

tubular/parenchymal lesions in diabetic nephropathy

Answer 27

pyelonephritis and necrotising papillitis

glycogen/lipid vacuoles in tubules