Diabetes Mellitus

Annotations:

• An inability to maintain blood glucose homeostasis. Raised blood glucose levels There is chronic hyperglycaemia which may be caused by a lack of insulin. Alternatively there may be a reduced ability of the body cells to use the insulin which is present in the blood; this is called insulin resistance.

1. Background

   Annotations:

   • Insulin is produced by beta cells in the pancreatic islets of langerhan. It lowers blood glucose levels by convertng glucose into glycogen to be stored in the liver and muscles. Insulin also facilitates the transfer of glucose into cells. As it is transported into the cell, the amount in the blood and tissue fluid falls. Without this action of insulin, glucose would not be able to enter the cell and be used in energy production. In diabetes the blood and tissue fluid have far too much glucose and the mitochondria in the cells do not have enough. 
2. Predisposes to these conditions

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   • Strokes, heart attacks, peripheral vascular disease and amputation, kidney failure and blindness.
3. Normal glucose homeostasis

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   • 4-8mmol/L Normal fluctuations in this range i.e. high after meal - low after waking in the morning.
   1. 4-8mmol/L
4. Type 1

   Annotations:

   • Associated with complete destruction of the beta cells and an absolute insulin deficiency. Type 1 diabetics are always INSULIN -DEPENDENT.
   1. 10%
   2. Autoimmune response triggered by a viral infection
   3. Presentation

      Annotations:

      • Onset is often around puberty. 
      1. Classic triad
         1. Polyuria & glucosuria

            Annotations:

            • Polyuria = excessive amounts of urine production. Glucosuria  = excretion of glucose in the urine.
         2. Weight loss

            Annotations:

            • More protein is broken down. And fatty acids are used as a fuel instead of glucose which depletes fat reserves
         3. Thirst

            Annotations:

            • Can be explained by systemic dehydration caused by the increased urine output.  Polydipsia = excessive thirst
5. Type 2

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   • Reduced level of beta function however the disease process starts with the insulin receptors which are unable to make use of the insulin due to the receptors not working properly or there being fewer of them in number.The situation is described as insulin resistance. These patients can be managed without using insulin however they may progress to become insulin dependent.
   1. 90%
   2. Risk factors

      Annotations:

      • Overweight Being over 40 Having a close relative with diabetes. Poor lifestyle philosophy
6. Normal glucose regulation

   Annotations:

   • Action of glucagon promotes glycogen breakdown and release of into the blood system - raising blood glucose levels Action of insulin promotes 1. Cellular uptake of glucose and 2.  Storage of glucose in the liver as glycogen - lowering blood glucose levels. They interact to maintain blood glucose levels at 4-8mmol/L
7. Roles of insulin

   Annotations:

   • 1. Facilitates cellular uptake of glucose - where it is converted into glycogen for storage. 2. Promotes uptake of amino acids for protein synthesis. 3. Promotes fat storage in adipose tissue and conversion of glucose to fat.
8. Result of ineffective insulin secretion

   Annotations:

   • 1. Inability to control carb metabolism/glucose homeostasis causing hyperglycaemia. 2. Decreased fat storage and increased fat catabolism causing ketosis. 3. Decreased protein synthesis and increased amino-acid catabolism causing sarcopenia (degenerative loss of sk mm)/ weight loss.
9. Consequences of impaired glucose uptake

   Annotations:

   • Since cellular uptake of glucose is impaired ingested sugars remain largely within the blood system. 1. So although blood sugar levels are high the cell cannot access the glucose - effectively cells "starve" - even though blood is glucose rich (hypergycaemia). 2.  Hyperglycaemia leads to cell damage because they are "starved" (aren't able to function normally). Because cells are starving: - A host of hormones are released in an attempt to rectify the situation including adrenaline. This causes glycogenolysis (breakdown of glycogen) resulting in increased glucose release. Also leads to gluconeogenesis (production of glucose) resulting in increased glucose release. This boosts blood glucose levels but its still not accessible to cells.
10. Rising glucose levels

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    • If blood glucose levels raise higher than the renal threshold then the glucose passes into the urine (glycosuria), and there is an increased amount of urine. Increased fluid loss leads to dehydration and thirst (polydipsia).
11. Decompensation

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    • Usually (because of treatment +/- residual function) cells receive enough glucose to function. However in certain situations - e.g. intial presentation, infections etc, cells may not be able to access blood glucose and therefore "starve in the midst of plenty". Therefore switch fuel source to fat leading to fat catabolism. When cells are not getting enough glucose from carbs they start using fats instead.
12. Consequences of lipolysis in instances of severe hyperglycaemia

    Annotations:

    • Since glucose is unavailable as a metabolic fuel, fats are metbolised. The catabolism of fats releases by-products including ketone bodies ++ (organic acids) leading to acidosis. Body's response to metabolic acidosis is kussmaul breathing ( heavy breathing but at high RR)
13. Ketoacidosis

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    • Acetone breathing, kussmaul breathing, nausea, vomiting. Essentially life-threatening. If untreated: - Negative impact on cardiac function - Negative impact on RBC/O2 Tx - Severe CNS depression - Coma and possible death
14. Measuring diabetic control

    Annotations:

    • 1. Glucose levels - hr by hr 2. HBA1c - Glycosylated Hb (Hb + glucose) = a longer term indicator of control. Can help with predictions of morbidity. Decreaing HBA1c by 1% can significantly reduce risk of cateracts, heart failure and amputation or death due to PVD.
15. Hypoglycaemia

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    • Causes: - insulin excess - insufficient glucose (food) intake - vigorous exercise without adequate calculation of the above. Signs: sweating anxiety dizziness cloudy vision coma convulsions hunger confusion headache death What to do if hypoglycaemia occurs: - eat/drink carbs immediately - IV glucose - subcutaneous glucagon injections
16. Diabetic comas

    Annotations:

    • Main types: - keto-acidotic coma - hyperosmolar coma (secondary to polyuria and dehydration) - hypoglycaemic coma (insulin overdose)
17. Long term complications
    1. Macrovascular disease

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       • Affects the large arteries and arterioles. Atherosclerosis develops. And can lead to: - CHD and MI - CVA - HTN - PVD
    2. Microvascular disruption

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       • Affecting arterioles and capillaries. Retinopathy - visual loss/blindness Nephropathy leading to progressive renal failure Peripheral neuropathy - mainly feet and is mainly sensory - neuropathic foot ulceration Endothelium thickens - diffusion distabce increases so tissues don't get the O2 and nutrients they require.
18. Exercise for DM

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    • 30min daily brisk walk significantly reduces risk of DM. Type II DM and diabetes prevention: F - 5 times per week I - mod intensity RPE 12-13. 60-75% HR max, or 40-60% HRR. T - 150 mins per week T - Aerobic/continuousType 2 DM management - no obesity:F - 5 days per weekI - low to mod 50-80% HRR (12-16 RPE)T - 20-60 mins continuous or accumulated to total = 150mins - 300minsT - various - mainly aerobic - some resistanceType 2 DM management with obesity:F - ideally 5 days per weekI - low to mod 40-60% HRR. Progressing to 50-75% HRRT - 3 x 10-15mins intermittent exs - initially buiding up to 60 mins continuous. 150-300 per week.T - various - mainly aerobic - some resistance.
    1. CV benefits

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       • Improves glycaemic control and insulin sensitivity.  Reduced body fat - maintains lean mm mass Atherosclerosis regression Reduces incidence/severity of debilitating complications.
    2. Strength training benefits

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       • Increases the mass of metabolically active tissue. Decreased mass of metabolically inactive tissues. Increased sensitivity in trained mm. F - 2-3 times per week I - 60-80% 1RM i.e. 2-3 sets of 8-12 reps. T - 8-10 exs involving major muscle groups T - minimise grips, static work, valsalva
    3. Special considerations

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       • - Don't exercise if blood glucose levels are >13mmol/L and rising - Do not inject over active mm -per and post exercise glucose monitoring - don't exercise if glucose <5.55mmol/L
19. Management of DM

    Annotations:

    • Good glycaemic control is essential: - use of insulin (maybe) - diet manipulation - exercise - drug therapy
    1. Pharmacology

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       • Insulin - injections - oral  Metformin - increased sensitivity of insulin receptors Sulponylureas - boost insulin secretion Statins - Cholesterol lowering - acknowledges high risk of CVD disease.