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MEH Sem 1 > Lecture 10 - Diabetes & Pancreas > Flashcards

Lecture 10 - Diabetes & Pancreas Flashcards

1
Q

What cells in the pancreas have exocrine functions and which cells have endocrine functions?

A
  • Exo: Acinar cells (arranged in clusters) (98%)

- Endo: Islets of Langerhans (2%)

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2
Q

What do acinar cells secrete? (exo func)

A

Digestive enzymes and bicarbonate ions (buffers the gastric acid released from the stomach creating appt. pH for digestion)

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3
Q

List 3 types of digestive enzymes secreted by acinar cells in pancreas

A
  • Proteases: Trypsin & Chymotrypsin (stored as pro-enzymes to prevent digestion of pancreas)
  • Lipase
  • Amylase
    (LAP)
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4
Q

List 3 cell types in Islets of Langerhans

A
  • α cell: secrete glucagon
  • β cell: secrete insulin
  • δ cell: secrete somatostatin (inhibit GH secretion from A.P)
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5
Q

Compare & contrast insulin and glucagon

A

Similarities

  • Both peptide hormones + water sol.
  • Both have short half life (~5 mins)

Differences

  • Insulin receptor: Tyrosine Kinase
  • Glucagon receptor: G-protein coupled receptor
  • B.G: Insulin ⬇️, Glucagon ⬆️
  • Insulin stimulates glycogenesis, glucose oxidation/uptake, ⬆️lipogenesis/protein synthesis
  • Insulin promotes GLUT 4 translocation in muscle, glucagon X effect (no receptors in muscle)
  • Insulin acts on liver, adipose & muscle, glucagon acts on liver & adipose
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6
Q

Desc. structure of insulin

A
  • Made of 2 chains: α & β chain
  • Held together by 2 disulphide bonds, 3rd intra-chain bond
  • Peptide hormone, water sol
  • Stored as pro-insulin (highly stable)
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7
Q

Desc. steps of insulin synthesis

A

DNA in β cell (transcription) —> mRNA (translation) –> Preproinsulin (signal peptide cleavage) –> Proinsulin (proteolysis) –> Insulin & C peptide (marker for endogenous insulin secretion)

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8
Q

Describe how the ultrastructure of B cells relate to synthesis of insulin

A
  1. mRNA on ribosomes of ER undergo transcription and translation to form preproinsulin
  2. Enzymes in ER cleave signal peptide –> proinsulin
  3. Travel to Golgi
  4. Secretory vesicles leave Golgi. Enzymes proteolyse proinsulin –> insulin + C peptide
  5. Exocytosis
  6. Hormone travel to target
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9
Q

How is C-peptide removed from proinsulin?

A

Trimmed off by carboxypeptidase H

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10
Q

What are some stimulators and inhibitors of insulin?

A

Stimulators (Parasympathetic N.S)

  • Glucose/F.A/a.a⬆️
  • Gastrin, adrenaline at B receptor

Inhibitors (Sympathetic N.S)

  • Somatostatin
  • Leptin
  • Adrenaline at α receptor
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11
Q

Desc phases of insulin secretion

A
  1. Initial burst
  2. Second phase of gradual increment
  3. No insulin produced when B.G <2.8mmol/L
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12
Q

How does insulin exert its effects on cells?

A
  1. Insulin binds to tyrosine kinase receptor
  2. Receptor auto-phosphorylates
  3. Activation of signalling cascade
  4. ⬆️glucose uptake, glycogenesis, glycolysis (oxidation to energy)
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13
Q

Desc insulin effects on cells

A
  1. Liver: ⬆️ Glycogenesis, Glycolysis, Lipogenesis, ❌Glycogenolysis, gluconeogenesis, lipolysis
  2. Muscle: ⬆️ Glucose uptake (GLUT 4), Lipogenesis, Glycogenesis, Glycolysis, Protein Synthesis,a/a transport ❌Lipolysis, Proteolysis
  3. Adipose: ⬆️ Glucose uptake (GLUT 4), Lipogenesis, Glycolysis, ❌Lipolysis
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14
Q

Desc. structure of glucagon

A
  • Peptide hormone, water sol.
  • No disulphide bonds
  • Forms preproglucagon(cleaved) –> proglucagon (proteolysis)–> glucagon
  • proglucagon is more complex than insulin, contains more peptide hormones
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15
Q

What are the effects of glucagon on the body?

A
  • Major target is liver: ⬆️Glycogenolysis, Gluconeogenesis, Release of glucose into bloodstream
  • Adipose: Lipolysis
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16
Q

How does glucagon exert its effects on cells?

A
  1. Binds to glucagon receptor (GPCR)
  2. G-protein activation
  3. Effector protein activation
  4. 2nd messenger formed
  5. ⬆️Glycogenolysis, Gluconeogenesis, Lipolysis
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17
Q

How is diabetes mellitus characterised?

A
  • Chronic hyperglycemia that leads to long-term clinical complications
  • Renal threshold for glucose is exceeded (glucosuria)
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18
Q

What is the difference between Type 1 and Type 2 diabetes?

A
  • Type 1: Absolute insulin deficiency caused by autoimmune destruction of pancreatic β cells
  • Type 2: Relative insulin deficiency caused by insulin resistance. β-cells eventually wear off from overproduction
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19
Q

Define the condition Diabetes Mellitus

A

A group of metabolic disorders characterised by chronic hyperglycaemia due to insulin deficiency or resistance or both.

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20
Q

How does type 2 diabetes present?

A
  • Typical symptoms of hyperglycaemia: Polyuria, polydipsia, blurring of vision
  • Symptoms of inadequate energy utilisation: Tiredness, weakness, lethargy + weight loss
21
Q

How does a clinician distinguish between type 1 & type 2 diabetes?

A

Type 1:

  1. Common in young
  2. Due to progressive loss of β cell
  3. Rapid onset + fatal
  4. Must be treated with insulin
  5. Diabetic Ketoacidosis (DKA)

Type 2:

  1. Usually older/obese patients
  2. Slow progressive loss of β-cells + insulin resistance
  3. May be present for a long time before diagnosed
  4. May not initially need treatment w insulin
22
Q

How is diabetes diagnosed?

A
  1. Test fasting glucose level ( ≥ 7.0mmol/L/ ≥6.1 for whole blood)
  2. Oral Glucose Tolerance Test
  3. Venous plasma glucose conc (≥11.0mmol/L)
  4. HbA1c (10% diabetic)
    * do more than one test to confirm. X use glucosuria/finger prick to confirm
23
Q

How is type 1 diabetes presented in clinic?

A
  • Rapid onset of symptoms (weight loss, polyuria, polydipsia)
  • Vomitting due to ketoacidosis
  • Young
  • Elevated venous plasma glucose conc
  • Presence of ketones (breakdown products of fats)
24
Q

How is Type 1 diabetes treated?

A
  • Exogenous insulin given subcutaneously several times per day
  • Diet/Exercise
  • Constant monitoring of blood glucose through finger prick test
  • Regular check-ups
25
Q

Define ketoacidosis

A
  • Hyperglycaemia
  • Ketonemia
  • Acidosis
26
Q

Why is the presence of ketones is an indication for immediate insulin therapy?

N.B
- Measure using ketone meter

A
  • Prevent DKA

- Life threatening condition: nausea, vomiting, hyperventilation, extreme muscle weakness (prostration)

27
Q

Why does DKA occur in type 1 diabetes?

A
  • Insulin suppresses ketone production. Due to autoimmune destruction of β-cells, X insulin secreted
  • Leads to enhanced lipolysis –> increase ketones (acetoacetate, acetone, 3-β- hydroxybutyrate)
  • Activation of the ketogenic enzymes in the liver.
28
Q

What is the diagnosis of DKA?

A
  • Ketonaemia (≥ 3.0mmol/L) or sig. ketonuria (more than 2+ standard urine sticks)
  • Blood glucose (≥11.0mmol/L)
  • Bicarbonate (<15.0) and/or venous pH (<7.3) or Arterial pH 6.9
29
Q

What causes insulin resistance to develop in type 2 diabetes?

A
  • Obesity (particularly central obesity)
  • Muscle and liver fat deposition
  • Physical inactivity
  • Genetic influence
30
Q

Treatment for type 2 diabetes

A
  1. Lifestyle:
    - Low calorie diet (liver fat content decreases)
    - Non-insulin therapies: Sulphonylureas (increase insulin production), Metformin (decrease gluconeogenesis)
    - Insulin
  2. Education + regular monitoring of B.G (finger prick)
  3. Treat other vascular risk factors (BP, lipids, smoking)
  4. Exercise
  5. Regular check ups

Bariatric surgery (weight loss surgery)

31
Q

What are some symptoms of type 2 diabetes?

N.B Symptoms variable due to slower rise of blood glucose

A
  • Polyuria, Polydipsia, Weight loss
  • No DKA
  • May be asymptomatic (diagnosed during routine screening)
  • Usually old/obese
32
Q

How can monitoring BG be carried out by patients?

A
  • Capillary testing (rapid test used for assessing the blood flow through peripheral tissues) for type 1 and more complex type 2
  • Ketone testing (urine/plasma) for type 1
  • Flash continuous glucose monitoring
33
Q

What are some ACUTE complications of diabetes?

A
  1. Complications of hyperglycaemia: [due to dehydration, renal failure]
    - Metabolic decompensation (DKA in type 1)
  2. Complications of hypoglycaemia: [due to drugs (iatrogenic)]
    - Coma (brain has absolute requirement for glucose)
34
Q

What are some CHRONIC complications of diabetes?

A
  1. Macrovascular:
    - Myocardial infarction
    - Stroke
    - Peripheral vascular disease (gangrene due to less blood flow)
    - Intermittent claudication (pain to calves/thigh/buttock)
  2. Microvascular: (F.E.K.S)
    - Diabetic feet: Gangrene due to poor blood supply/increased risk of infection
    - Retinopathy: Damage to blood vessels –> burst –> proliferative retinopathy or protein exudates (leak) or blindness OR cataracts
    - Nephropathy: Damage to glomeruli/poor blood supply/infection –> microalbuminuria
    - Neuropathy: Damage to peripheral nerves –> loss of sensation
35
Q

What is metabolic syndrome?

A

A cluster of risk factors associated w cardiovascular disease (diabetes, abdominal obesity, high BP/cholesterol)

36
Q

How to determine if an individual suffers from metabolic syndrome?

A
  • Waist measurement: >94cm for men, >80cm for women
    Plus 2:
  • Raised triglyceride: >1.7mmol
  • Reduced HDL cholesterol: <1.0 for men, <1.2 for women
  • Raised BP: >135/85 (normal is less than 120/80 mmHg)
  • Raised fasting blood glucose (>5.6 or diabetes)
37
Q

What causes metabolic syndrome?

A
  • Insulin resistance
  • Central obesity
  • Genetics
  • Sedentary lifestyle
  • Ageing
38
Q

How common is polydipsia and polyuria in the general population?

A
  • Polydipsia is 30%, Polyuria is 25%
39
Q

What is the primary transporter of glucose in pancreatic β cells?

A

GLUT 2 (bidirectional)

40
Q

The ATP sensitive potassium channel KATP plays a key role in regulating insulin secretion by pancreatic β cells.
What effect would a decrease in the intracellular concentration of ATP have on these channels?

A
  • More KATP channels would be in the open state. ⬆️K+ leaving cell –> more negative membrane –> less calcium channels open (Ca2+ ions stimulate fusion of vesicles and release of insulin) –> less insulin
  • KATP are inhibited by ATP.
41
Q

A 41 year old man eats a meal. Shortly afterwards the concentration of the hormone insulin rapidly increases in his blood.
What has occurred in the man’s pancreatic beta cells to initiate this rise in hormone concentration?

A
  • Plasma membrane depolarised
  • More glucose= more ATP –> Katp X open –> Less K+ leave –> depolarisation –> Ca2+ channels open –> insulin secreted
42
Q

From where does the pancreas emerge as an outgrowth during embryonic development?

A

Foregut

43
Q

Mutations in the gene coding for which protein could have resulted in neonatal diabetes mellitus?

A
  • Kir6.2

- Pore forming subunit of the ATP-sensitive potassium channels (KATP) expressed in pancreatic β cells(inhibited by ATP)

44
Q

A 17 year old girl with type 1 diabetes mellitus self administers a subcutaneous injection of the hormone insulin in order to control her plasma glucose level.
What would be the result of this injection? (In terms of C-peptide)

A
  • Plasma C-peptide concentration would remain the same.

- Commercial insulin preparations for injection just contain insulin (no C-peptide is added to the preparation)

45
Q

State the normal plasma concentration for glucose.

**sometimes question will trick you with diff. units

A
  • 3.3 to 6.0 mmol/litre
46
Q

What process is HbA1c formed?

A

Glycation: non-enzymatic process that adds glucose to proteins

47
Q

Major structural features of pancreatic B-cell for insulin secretion?

A
  1. ⬆️mitochondria: exocytosis of insulin
  2. ⬆️RER: site of synthesis of preproinsulin
  3. ⬆️Golgi: Formation of hormone storage vesicles
  4. ⬆️Storage vesicles: Contain active insulin + C-peptide
  5. ⬆️microtubules + microfilaments: for exocytosis
48
Q

List the factors that affect insulin secretion and explain their physiological significance.

A
  1. ⬆️Glucose, F.A, A. A = ⬆️insulin when the nutrients exceed fasting values –> insulin interacts with target tissues (liver & S.M) –> ⬆️uptake/storage/utilisation of glucose
  2. Catecholamines (adrenaline & noradrenaline) inhibit insulin secretion –> ⬆️B.G stress response
  3. Gut hormones = ⬆️ insulin –> part of digestion process –> prevent major increase in B.G

MEH Sem 1 (18 decks)

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