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Endocrinology > Pancreas and diabetes > Flashcards

Pancreas and diabetes Flashcards

1
Q

What % of the pancreas is endocrine tissue?

A

1%

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2
Q

What are the parts of the pancreas?

A

head
neck
body
tail

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3
Q

What polypeptide hormones are secreted by the pancreas? (7)

A
  1. insulin
  2. glucagon
  3. somatostatin (GHIH)
  4. pancreatic polypeptide
  5. ghrelin
  6. gastrin
  7. vasoactive intestinal protein
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4
Q

What cell types are insulin, glucagon, somatostain, ghrelin gastrin and pancreatic peptide secreted from?

A

insulin: beta cells
glucagon: alpha cells
somatostatin: delta cells
PP: PP cells
ghrelin: e cells
gastrin: G cells

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5
Q

What effects does insulin have?(5)

A
  • in liver stimulates glycogenesis (stimulates glycogen synthase, inhibits glycogen phosphorylase)
  • in adipose and muscle stimulates GLUT4 to open and so glucose can come in so lowers blood glucose
  • in muscles it increases AA uptake for protein synthesis
  • in liver decrease AA breakdown
  • in adipose inhibits hormone sensitive lipase so less lipolysis
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6
Q

What effects does glucagon have? (3)

A
  • glycogenolysis and gluconeogenesis in liver

also lipolysis which leads to ketone production

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7
Q

what is the renal threshold for glucose and what does this mean?

A

> 10 mmol/L
glucose cannot all be reabsobed so some will be lost in urine leading to glycosuria
It can decrease in pregnancy and increase in elderly

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8
Q

What is the normal plasma conc of glucose ?

A

3.3- 6 mmol/L (7-8 after meal)

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9
Q

how long does insulin and glucagon last in blood? (half life)

A

5 mins half life

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10
Q

Describe the creation of insulin

A
  • synthesised into RER as preproinsulin
  • signal sequence cleaved makes it proinsulin
  • taken to golgi where C peptide cleaved, 2 disulfide bonds between A and B peptide
  • insulin and c protein held in vesicles near cell surface ready for release when stimulated
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11
Q

Describe the stimulation of insulin to be released

A
  • high glucose means more into cell via GLUT2
  • means more metabolism and so more ATP
  • ATP inhibits the ATP sensitive K+ channel
  • less K+ efflux
  • membrane depolarises
  • voltage gates Ca2+ channels open
  • Ca 2+ causes insulin release
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12
Q

Describe the structure of the tyrosine kinase insulin receptor

A
  • a dimer
  • 2 identical a and 2 b subunits
  • disulfide bond between each a and B subunit
  • a subunit on exterior of membrane
  • B subunit transmembrane
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13
Q

What is released when amino acid conc in blood goes up?

A

both glucagon and insulin are released

- possibly because body thinks its starving (muscle breakdown) but also eating meat (?)

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14
Q

Describe the structure of glucagon

A

a long peptide of 29 AA with no disulfide bonds

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15
Q

What causes 90% of type 1 diabetes mellitus?

A
  • 90% is auto immune destruction of the B cells by auto antibodies such as (ICAs, IAAs, IA2s and GADs)
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16
Q

What are the common signs and symptoms of type 1 diabetes mellitus?

A
  • polyuria
  • polydipsia (increased thirst)
  • weight loss
  • tiredness
  • acetone on breath
  • sweet smelling wee
  • lethary
17
Q

In what age group does type 1 diabetes present and over what time period do symptoms progress?

A

usually in young pts under age of 30

- symptoms deteriorate over weeks to months before presentation

18
Q

How does type 1 diabetes lead to ketoacidosis and describe and explain the signs and symptoms (6) of ketoacidosis

A
  • glucose cant be utilised as no insulin
  • lipolysis as need energy that can be used + no insulin to stop it
  • fatty acids converted to ketone bodies in liver
  • leads to excretion of ketones in breath and urine
  • also hyperventilation due to acid in blood–> more breathing= more Co2 removal so lower ph
  • Nausia and vomiting to remove acid from GI
  • abdo pain (dunno why)
  • eventually coma
19
Q

What tests can be done to test for diabetes?

A
  • urine dip stick- look for glucose and ketones in urine
  • HbA1c- glycation of Hb due to long term high glucose
  • fasting glucose above 6mmol/L
  • normal glucose on finger prick above 11mmol/l
20
Q

How is type 1 diabetes managed?

A
  • subcutaneous insulin injections after meals
  • education about when and how to inject
  • eduction on hypos when dont eat for long time–> need to carry sweets with them
  • self monitoring of blood glucose
  • check ups on feet, Bp, kidneys and eyes
21
Q

What are the macrovasculature (3) and microvasculature (5) complications of diabetes as a result of high blood glucose causing vasculature damage?

A

Macro:
- risk of stroke
- risk of MI
- poor circulation to feet
Micro:
- diabetic eye disease (changes in lens due to osmotic effect of glucose)- blurred vision
- retinopathy (damage to blood vessles in eye leads to blindness)
- nephropathy (damage to glomeruli)
- neuropathy (peipheral nerve damage, leads to loss of sensation)
- diabetic foot (poor blood supply and nerve supply leads to foot ulcers)

22
Q

What is type 2 diabetes?

A

insuffiecient insulin production due to an aquired insulin resistance (the balance of resistance vs low production may vary person to person)

23
Q

in what age group does type 2 diabetes occur?

A

older (> 30/40)

24
Q

What symptoms differentiate type 1 and type 2 diabetes?

A
  • type 1 has high ketones, type 2 doesnt (type 2 insulin still has some effect to surpress lypolysis)
  • not usually weight loss in type 2
  • older ppl generally get type 2
25
Q

How is type 2 diabetes managed? (5)

A
  • primarily exersize and weightloss as it can be reversed by this to an extent
  • metformin (inhibits gluconeogenesis, so helps reduce blood glucose)
  • sulponylureas sometimes given - inhibits atp sensitive K+ channels so more insulin released
  • inulin - B cells often give up on secreting it towards later stages
  • bariatric surgery
26
Q

What else can cause excessive thirst (polydipsia) and peeing (polyuria)?

A
  • hypercalacaemia
  • diabetes insipidus (increased ADH release)
  • psychotic polydipsia (more than 3L water per day, washes out renal conc mechanism so wee lots)
27
Q

Describe the symptomatic presentation of type 2 diabetes (most found on normal checks)

A
  • overweight/ obese
  • inactive
  • > 40 yrs old
  • irritable
  • tired
  • down
  • thrush infections
  • weight loss (unusual)
  • increased weeing and drinking
28
Q

Whats the difference between glycation and glycosylation?

A

glycation is non enzymatic

29
Q

What are normal and diabetic levels of HbA1c?

A

normal- 4-6%

above 10% is diabetic

30
Q

What receptor type does glucagon act on?

A

GPCRs

- PKA phosphylates target enzymes

31
Q

What can C peptide be used for?

A

measure endogenous insulin secretion levels

32
Q

What causes hypo and hyperglycaemia?

A

hypo- glucose dropping- may be due to insulin given but they miss a meal, exersize ect
hyper- high glucose- may eat high fat meal and not give insulin

33
Q

What are the effects of hyperglycaemia?

A
  • glucosuria
  • polyuria
  • dehydration
  • confusion
  • polydipsia
  • blurred vision
  • headaches
  • fatigue
34
Q

What are the effects of hypoglycaemia?

A
  • shakey
  • confusion
  • sweaty
  • anxious
  • hungry
  • irritable
  • headache
35
Q

What is metabolic syndrome?

A

having a cluster of the biggest risk factors for cardiovascular disease as a result of a sedentary lifestyle

36
Q

What risk factors are included in metabolic syndrome? (4/5)

A
  • diabetes (or raised plasma glucose)
  • abdominal obesity
  • high LDL or low HDL
  • high BP
37
Q

What causes metabolic syndrome?

A
  • insulin resistance
  • central obesity
  • genetics
  • inactivity
  • ageing
38
Q

What causes insulin resistance to develop in type 2 diabetes? (5)

A
  • central obesity
  • muscle and liver fat deposition
  • elevated free circulating fatty acids may antagonise the insulin receptor
  • inactivity
  • genetic influences

Endocrinology (7 decks)

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