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Module 104: Theme 2 > Diabetes > Flashcards

Diabetes Flashcards

1
Q

Classic symptoms of IDDM

A

Thirst (polydipsia)

Tiredness

Weight Loss

Polyuria- with glucose and ketone bodies

Hyperglycaemic coma

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2
Q

Etiology of IDDM

A

Autoimmune destruction of pancreatic beta-cells

Prevents secretion of insulin, hence no feedback mechanism on alpha cells that secrete glucagon- hyperglucagonaemia

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3
Q

Pathophysiology of weight loss/ muscle weakness in IDDM

A

Low insulin:glucagon ratio leads to increased proteolysis.

Amino acid levels in the plasma rises

Causes loss of muscle mass

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4
Q

Hyperglycaemic mechanism in IDDM

A 
Low insulin:glucagon ratio causes:
- Increased
glycogenolysis
- Increased proteolysis
- Decreased uptake of glucose by tissues

High amino acid levels in the blood from proteolysis causes an increased stimulation of gluconeogenesis.

All factors increase glucose levels in the blood.

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5
Q

Mechanism for ketoacidosis in IDDM

A

Low insulin:glucagon ratio increases lipolysis.
- Increases free fatty acids in the plasma

High FAs level stimulates ketogenesis and ketouria

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6
Q

IDDM effects on the liver

  • Metabolic state
  • Glycolysis
  • Gluconeogenesis
  • Glycogenolysis
  • Fatty acids
  • Acetyl CoA
A

Liver remains gluconeogenic due to low insulin:glucagon ratio

Liver takes in substrates to make glucose:

  • Alanine (proteolysis)
  • Glycerol (lipolysis)

Glycogen synthesis and glycolysis are inhibited due to no insulin.

Fatty acids used to provide energy for the liver or converted to TGs and VLDL.

  • Can lead to hypertriglyceridaemia
  • FAs also oxidised to Acetyl CoA

XS Acetyl CoA used to form ketone bodies to provide energy source
- Can lead to ketoacidosis

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7
Q

IDDM effects on the muscle

  • Metabolic state
  • Glycolysis
  • Gluconeogenesis
  • Glycogenolysis
  • Fatty acids
  • Acetyl CoA
A

Due to no insulin, Glucose entry is very low (GLUT-4)
- Intensifies hyperglycemia

Glycolysis and glycogenolysis are inhibited.

Fatty acids from lipolysis used for fuel.

Ketone bodies made from Acetyl CoA also used as a fuel for energy.

Increased proteolysis causes muscle wasting to support gluconeogenesis.

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8
Q

IDDM effects on the adipose tissue

  • Metabolic state
  • Glycolysis
  • Gluconeogenesis
  • Fatty acids
  • Acetyl CoA
A

No insulin= very low glucose entry via GLUT-4

Lipolysis very high to release FAs and glycerol from TGs

  • FAs used as fuel and also released for fuel in other tissues
  • Glycerol released for gluconeogenesis

Glycolysis and glycolysis inhibited

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9
Q

IDDM state in plasma and urine

A

High glucagon levels= hyperglycaemia

Too much glucose for the kidneys to process

  • Excreted in urine glycosuria
  • Water is loss in urine via osmotic uresis = thirst

Lipoprotein lipase activity not regulated due to lack of insulin

  • Fatty acid synthesis inhibited
  • Increased VLDL = hypertrigylceridaemia
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10
Q

Short term life-threatening consequence of IDDM

A

Hyperglycaemia

Ketoacidosis

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11
Q

Short term life-threatening consequence of NIDDM

A

Non-ketoic hyperosmolar coma

- Hyperglycaemia without ketosis

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12
Q

Long term life-threatening consequence diabetes

A

Neuropathies

Nephropathy

Predisposition to CVD and organ damage

Retinopathy

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13
Q

Effects of hyperglycaemia

A

Increases generation of ROS.

Causes osmotic damage to cells.

Glycosylation of proteins (attachment of glucose to proteins) which alters their functions.

Formation of advanced glycation end products (AGE)
- glycated lipids or lipids
= increased ROS and inflammatory proetins

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14
Q

Two major tests in diagnosing diabetes

A

Fasting blood glucose levels

  • Overnight fast
  • When blood glucose levels is 126mgl/dL (7mM) and above on at least 2 ocassion = diabetes

Glucose tolerance test:

  • Morning after overnight fast
  • Fasting blood sampled before giving glucola drink (75g glucose)
  • Blood glucose sampled 20mins, 1 hr and 2 hr after drink
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15
Q

Treating TI diabetes

A

Insulin given to mimic normal daily insulin secretion.

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16
Q

Insulin treatment regimes

A

Premixed insulin

  • Requires less injecting
  • Meal timing has be very meticulous

Insulin and food together

  • Greater flexibility
  • Potential nocturnal hypoglycaemia

Rapid acting insulin:

  • Reduces risk of nocturnal hypoglycaemia due to short half life
  • More expensive
17
Q

Types of insulin

A

Fast acting

Intermediate acting

Long acting

18
Q

Etiology of NIDDM

A

Impaired insulin secretion
- Due to amyloid deposits

Increased peripheral insulin resistance

Increased hepatic glucose output

19
Q

Mechanisms of insulin resistance

A

Could be caused by:

  • Mutation in insulin receptor gene (most rare)

Defects in insulin signalling pathway

  • Defects in cellular translocation of GLUT-4
  • Prevalent in obesity and diabetes

Peripheral insulin reisstance

  • XS fatty acids
  • Inhibits peripheral glucose disposal
  • Enhances hepatic glucose output
20
Q

Features of NIDDM

A

Often prevalent in older and obese population.

Can survive for a long time without insulin

Associated with macrovascular disease, stroke and atherosclerosis

Low ketone bodies

21
Q

Metabolism in NIDDM

A

Some insulin presence so glucagon secretion suppressed to an extent.

Hyperglycaemia due to lack of glucose uptake

VLDL production from liver increases

  • hypertriglyceridaemia
  • macrovascular disease

No uncontrolled lipolysis = no ketone body formation
- Due to some insulin left to suppress glucagon

22
Q

Treatment of NIDDM

A

Diet and exercise- improves translocation of glucose in GLUT 4

Oral hypoglycaemic agents

23
Q

Sulphonylureas

A

Hypoglycaemic agent that stimulates insulin secretion.

Example: Gliclazide

Mechanism, works on pancreatic beta cells:
When glucose is >7mM…
- Drug binds to close ATP-dependant K+ channels.
- This stimulates depolarisation and influx of Ca2+ via voltage gated channels
- Ca2+ influx stimulates insulin secretion.

24
Q

Biguanides

A

Drugs that increases insulin sensitivity of the tissue

Example: Metformin

Supresses appetite.

Only effective when insulin is present as it increases tissue sensitivity.

25
Q

Thiazolidinediones

A

Drug that enhances tissue effectiveness of endogenous insulin

  • Reduces hepatic glucose output
  • Increase glucose uptake in muscle

Mechanism:
Binds to peroxiome proliferator-activated receptor-gamma on the nucleus
- Regulates gene expression

Example
- Pioglitazone

26
Q

GIP and GLP-1

A

Glucose- dependent insulinotropic peptide
- Produced by endocrine cells in the intestines after food ingestion to stimulate insulin release

Very short half life makes it ineffective to use therapeutically

27
Q

Stimulators of GLP-1

A

Extendin-4

Exenatide (Byetta)
- Synthetic extendin-4 with longer half-life

Vildagliptin (Galvus)

  • Inhibits inactivation of GLP-1 and GIP
  • Combined with oral hypoglycaemic agents

Module 104: Theme 2 (18 decks)

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