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• Diabetes Mellitus

  Disorder of carbohydrate, protein, and fat metabolism

  Results from an imbalance between insulin availability and insulin need • Can represent:

  • An absolute insulin deficiency

  • Impaired release of insulin by the pancreatic beta cells

  • Inadequate or defective insulin receptors

  • Production of inactive insulin or insulin that is destroyed before it can carry out its action

  • Has a common feature of hyperglycaemia
• type 1 diabetes results from loss of beta cell function

  an absolute insulin deficiency

  Type 1A - immune -mediated diabetes

  Type 1B - idiopathic diabetes
• type 2 diabetes results from impaired ability of the tissues to use insulin

  a relative lack of insulin or impaired release of insulin in relation to blood glucose levels
• prediabetes :

  impaired fasting plasma glucose , FPG : 5.6-6.9 mmol/L

  impaired glucose tolerance , OGTT - 7.8 -11.0 mmol/L

  increased risk of atherosclerotic heart disease and increased risk of progression to type 2 diabetes
• development of type 1A diabetes:

  Genetic predisposition

  • Immunologically mediated beta cell destruction

  • Insulin antibodies or islet antibodies

  • Formerly juvenile diabetes

  • More common in young persons but can occur at any age

  • A hypothetical triggering event involving an environmental agent that incites an immune response

  • Infection, hypersensitivity reaction, prolonged major stressful event

  • Prone to the development of ketoacidosis

  • Insulin inhibits lipolysis and releases free fatty acids

  • Without insulin ketosis develops and are converted to ketones in the liver
• idiopathic type 1B diabetes :

  Those cases of beta cell destruction in which no evidence of autoimmunity is present

  • Only a small number of people with type 1 diabetes fall into this category

  • Strongly inherited.

  • People with the disorder have episodic ketoacidosis due to varying degrees of insulin deficiency with periods of absolute insulin deficiency that may come and go.
• type 2 diabetes :

  Heterogeneous condition that describes the presence of hyperglycemia in association with relative insulin deficiency

  • Peripheral insulin resistance

  • Impaired beta cell function and insulin secretion

  • Increased hepatic glucose production

  • Associated with overweight and obese persons

  • Environmental and genetic origins

  • Could be 20 or more genes responsible
• causes of beta cell dysfunction:

  An initial decrease in the beta cell mass

  • Increased beta cell apoptosis/decreased regeneration

  • Long-standing insulin resistance, leading to beta cell exhaustion

  • Chronic hyperglycemia can induce beta cell desensitisation (“glucotoxicity”).

  • Chronic elevation of free fatty acids can cause toxicity to beta cells

  (“lipotoxicity”).

  • Amyloid deposition in the beta cell can cause dysfunction
• individuals with type 2 can have low to normal to high levels of insulin

  peripheral insulin resistance can result in a feedback mechanism to increase production of insulin

  — hyperinsulinemia

  Increase demands exhaust the beta cell and result in failure or dysfunction

  decrease in glucose removal from the blood
• type 2 also can cause:

  — Hyeprglycaemia develops

  — insulin resistance worsen over time

  — insulin resistance is associated with obesity

  • excess body fat increases availability of free fatty acids

  • increase hepatic glucose production

  • inhibits glucose utilisation and insulin secretion
• metabolic syndrome:

  • Evidence suggests that insulin resistance not only contributes to the hyperglycaemia but may play in a role in other metabolic abnormalities

  — obesity and insulin resistance

  — increased resistance to the action of insulin

  — impaired suppression of glucose production by the liver

  — hyperglycaemia and hyperinsulinemia

  — elevated triglycerides

  — HDL

  — hypertension
• Manifestations of diabetes

  hyperglycaemia exerts a strong influence on blood osmotic pressure

  fluid is drawn out of the interstitial compartment into the blood

  fluid is drawn out of the cell to replace interstitial fluid

  cell dehydration

  cell function compromised ( nervous system dysfunction )
• symptoms of hyperglycaemia:

  • weight loss

  • recurrent blurred vision

  • slurred speech

  • loss of sensory function

  • fatigue

  • seizures

  • skin infections
• three polys of diabetes:

  most commonly identified manifestations are:

  polyuria

  -excessive urination

  polydipsia

  -excessive hunger

  
• acute complications : diabetic ketoacidosis

  in insulin dependent diabetes peripheral cells switch to metabolism of free fatty acids

  free fatty acids breakdown into ketone bodies

  metabolic acidosis

  nervous system impairment

  coma, death
• acute complications: hypoglycaemia

  due to medication , not eating or excessive exercise

  lapses in concentration

  headaches and irritability

  fine tremors

  skin pale and clammy

  changes in heart rate

  seizures , coma , death
• hypersomolar hyperglycaemic (HHS)

  -hyperglycaemia

  -hyperosmolarity

  --dehydration /pulls water out of body cells

  --difficult to maintain adequate fluid intake

  
  

  plasma volume contracts , renal insufficiency develops , increase blood glucose levels

  -depression of sensorium

  -neurological symptoms

  (babinski reflex,aphasia, muscle fasiculation , hyperthermia)
• chronic complications of diabetes :

  disorders of the microvasculature

  • neuropathies , nephropathies , retinopathies

  • distal symmetric neuropathy , foor ulceration

  • macrovascualr complications

  — CAD , cerebral vascular and peripheral vascular disease

  risk of complications decrease with better glycemic control
• chronic complications of diabetes:

  Thickening of the walls of the nutrient vessels that supply the nerve

  —> leading to the assumption that vessel ischaemia plays a major role in the development of neural changes

  • segmental demyelinisation process that affects the Schwann cell

  • accompanied by a slowing of nerve conduction
• diabetic peripheral neuropathies:

  SOMATIC

  • Polyneuropathy (bilateral sensory)

  • Loss of function occurs in a stocking – glove pattern

  • Diminished perception of vibration, pain, temperature

  • Loss of sensory and motor function – increase falls risk

  • Lesions in the peripheral nervous system
• diabetic peripheral neuropathies:

  MONONEUROPATHY :

  • Involvement of a mixed nerve trunk that includes loss of sensation, pain, and motor weakness
• Diabetic peripheral neuropathies :

  AMYOTROPHY :

  Associated with muscle weakness, wasting, and severe pain of muscles in the pelvic girdle and thigh
• Diabetic peripheral neuropathies :

  CRANIAL NERVE INVOLVEMENT ;

  Extraocular nerve paralysis

  • Impaired pupillary responses

  • Impaired special senses
• Diabetic peripheral neuropathies :

  AUTONOMIC :

  • Impaired vasomotor function

  • Postural hypotension

  • Impaired gastrointestinal function

  • Impaired genitourinary function
• diabetes other complications:

  • Bladder control problems

  • Heart disease and stroke

  • Diabetic retinopathy (eye disease)

  • Erectile dysfunction

  • Diabetic nephropathy (kidney disease)

  • Stomach nerve damage (Gastroparesis)

  • Foot ulcers

  • Infection
• DIAGNOSIS AND TREATMENT OF DIABETES :

  BLOOD TESTS

  • patient history

  • fasting blood glucose test

  • casual blood glucose test

  • capillary blood tests and self-monitoring of capillary blood glucose levels

  • glaciated haemoglobin testing
• TREATMENT PLANS FOR DIABETES :

  • nutrition therapy

  — specific nutrition services to treat an illness , injury , or condition and involves both the assessment of the nutrition status and the treatment measure

  — includes counselling and use of supplements

  • exercise

  • anti-diabetic agents

  • surgery
• DISORDER OF ENDOCRINE CONTROL :

  Endocrine system affects all aspects of the body.

  For example:

  • Growth and development

  • Muscle and adipose tissue distribution

  • Sexual development

  • Gastrointestinal and cardiovascular function

  • Body response to stress

  • Nutritional status describes the condition of the body related to the availability and use of nutrients

  • Nutrients are taken into the body and used for important functions

  • The body can also store what is not needed in the form of adipose tissue
• endocrine disorders:

  HYPOFUCNTION

  • underproduction of hormone

  causes :

  congenital defects

  • injury to glandular cells

  — disruption in blood flow , infection , inflammation , autoimmune responses , neoplastic growth or invasive tumour growth

  • decline in function with aging

  • atrophy as the result of drug therapy or unknown reasons

  • receptor defects
• endocrine disorders:

  HYPERFUNCTION:

  • excessive hormone production

  causes :

  excessive stimulation and hyperplasia or hypertrophy of the endocrine gland

  hormone- producing tumour of the gland

  ectopic hormone secretion

  medicatioon

  decrease negative feedback
• HYPOTHALAMUS AND PITUITARY DISORDERS

  —> interface between nervous system and endocrine system

  —> anterior pituitary is controlled by releasing hormones secreted from the hypothalamus

  — travel via a portal vein

  —> result in the release of many hormone that control

  • thyroid

  • adrenal

  • gonads
• pitutary gland: anterior

  • Human growth hormone (hGH)

  • Thyriod stimulating hormone

  (TSH)

  • Follicle stimulating hormone

  (FSH)

  • Lutenizing hormone (LH)

  • Prolactin

  • Adrenocortictropic (ACTH)

  • Melanocyte stimulating hormone

  (MSH)
• pitutary gland : posterior

  • oxytocin ( OT)

  • antidiuretic hormone (ADH) or vasopressin
• causes of multi-hormone pituitary disruptions:

  • Tumours

  • Pituitary surgery or radiation

  • Lesions and head trauma

  • Infection or inflammation

  • Autoimmune disease

  •Malfunctioning target organ

  • Genetic disease

  • Hypothalamic disorders

  • Pituitary infarction

  • Pituitary apoplexy

  • Hypoxic necrosis
• hypopitutarism happens when the pituitary gland is not active enough. It does not make enough hormones. Hypopituitarism can directly affect the pituitary gland.
• hypopituitarism : clinical manifestations

  • usually occur gradually

  • 70-90% destroyed before clinical symptoms

  • can present an acute and life-threatening condition
• hypopituitarism :symptoms

  • Headache

  • Altered mental state

  • Postural hypotension

  • Being chronically unfit

  • Weakness and fatigue

  • Growth failure

  • Loss of appetite

  • Impairment of sexual function

  • Cold intolerance

  •Decrease bone density

  • Morbid obesity
• Single pituitary hormone defects

  —> may only effect the release of one hormone

  most common are

  — growth hormone

  • excess - gigantism ( children) , acromegaly (adults)

  • depletion - dwarfism ( children)

  — ADH

  • excess - SIAHD

  • depletion - diabetes insipidus

  — ACTH

  • excess - cushings

  • depletion - Addisons
• growth hormone hypersection : children

  results in increased linear bone growth (gigantism)

  thickening of fingers , jaw, forehead , hands , feet

  decreased bone density

  delayed puberty

  double vision

  weakness
• growth hormone hypersection -adults

  aka acromegaly

  overgrowth of the cartilaginous parts of the skeleton

  enlargement of the heart and other organs of the body

  metabolic disturbances resulting in altered fat metabolism and impaired glucose tolerance

  goiter and cardiomyopathy

  sleep apnoea