Type I diabetes description
You should inc:
– Aetiology (causes) & pathogenesis (how the disease develops).
– Describe the typical initial clinical presentation (prior to diagnosis/treatment).
– List some (at least 4 of the possible long-term consequences.
Anthology:
- Type I is an autoimmune disease,
patients are born with normal beta cells but a trigger in childhood sets up an autoimmune disease which targets their beta cells. The patient’s beta cells are destroyed by their immune system so the patient has no beta cells and
therefore no insulin production
- Target tissues (liver, fat and skeletal
muscle) can’t take up blood glucose
without insulin so are starving and must use alternate fuel sources (fatty acids & ketones) - Meanwhile the patient’s blood glucose is severely high as the liver, fat and skeletal muscle is not able to remove it from the blood and use/store it.
Pathogenisis and clinical presentation:
- People usually present in childhood and are normal weight or underweight because their target tissues can’t take up and use glucose.
- Type I frequently presents in an acute emergency situation associated with severe hyperglycaemia; ketoacidosis and volume depletion that can result in
altered consciousness and coma.
Long-term consequences:
- more at risk for developing,
atherosclerosis and arteriosclerosis which predisposes the sufferer to ischaemic heart disease,
cerebrovascular disease, peripheral vascular disease, neuropathy, nephropathy, retinopathy, glaucoma,
cataracts and infections.
Type II diabetes description
You should inc:
– Aetiology (causes) & pathogenesis (how the disease develops).
– Describe the typical initial clinical presentation (prior to diagnosis/treatment).
– List some (at least 4 of the possible long-term consequences.
Anthology:
- Type II diabetes has a strong genetic component but this can usually be overcome with environmental interventions.
- Typically, in type II diabetes people are overweight or have a lot of truncal/central adiposity. They are inactive/sedentary and present with vague/chronic symptoms.
- Type II diabetics have insulin insensitivity, the target tissues
(liver, skeletal muscle & fat) takes up enough blood glucose to sustain themselves (so there is no weight loss or ketoacidosis) but they do not take up enough glucose to reduce the serum levels to within a physiological range. - During this phase of the disease, weight loss can halt the condition and even reverse it (not the neuropathies if present). However, if blood glucose is not controlled, beta cells will eventually “burn out” and the individual will have an irreversible condition.
Pathogenisis and clinical presentation:
- Type II patients present with vague
symptoms which often include polyphagia, polydipsia & polyuria. They may feel lethargic and are usually overweight and sedentary. They may have some signs of neuropathy including loss of sensation, chronic pain or pins and needles.
Long-term consequences:
- more at risk for developing,
atherosclerosis and arteriosclerosis which predisposes the sufferer to ischaemic heart disease,
cerebrovascular disease, peripheral vascular disease, neuropathy, nephropathy, retinopathy, glaucoma,
cataracts and infections.
Compare & contrast type I & II diabetes. You should inc:
– Aetiology (causes) & pathogenesis (how the disease develops).
– Describe the typical initial clinical presentation (prior to diagnosis/treatment).
– List some (at least 4 of the possible long-term consequences.
Understand what is meant by ‘functional’ tumour & the possible implications for hormone levels.
What is the most common cause of hyperthyroidism & the symptoms associated with the condition?
Causes:
Grave’s disease - hyperthyroidism caused by an immune disorder in which B cells produce antibodies that mimic TSH. Ordinarily TSH is released from the anterior pituitary in response to TRH from the hypothalamus. TSH
induces growth of the thyroid gland and the synthesis and release of T3 and T4 which negatively feedback to decrease the signals of TRH and TSH. The TSH mimicking antibodies are continually produced but not subject to negative feedback regulation so TRH and TSH are low but T3/T4 and the
antibody levels are high
Symptoms:
- Increased metabolic rate, heat intolerance, weight loss, anxiety and agitation, fine tremor, proptosis/exophthalmos. The weight loss includes fat, muscle and bone increasing the risk of sarcopenia
and osteoporosis
Based on the above, what are the effects of hypothyroidism?
Reduced metabolic rate, weight gain, muscle weakness, poor concentration, depression, dry cold skin prone to hypothermia
List the diseases associated with GH excess pre/post puberty?
In an adult it results in acromegaly typified by growth of bones in the skull, hands and feet and thickening of connective tissue leading to a
coarsening of appearance.
In children the growth plates have yet to fuse so we will see gigantism.
What is the result of GH deficiency in embryogenesis?
What is Cushing’s syndrome & how may it be caused?
What it is:
- A constellation of effects caused by excess cortisol or prolonged use of corticosteroids, it includes increased fat deposition in the trunk & face (moon face); the development of a buffalo hump, muscle atrophy & weakness, osteoporosis, thinning skin & the formation of striae (stretch marks); poor wound healing & increased risk of nfections; hyperglycaemia & hypertension; mood changes & depression
Causes:
- It may be caused by a cortisol or ACTH secreting tumor, chronic stress or inappropriate &/or excessive use of
corticosteroids/glucocorticoids
Time permitting: What are the endocrine functions of the kidney
and how are they altered in renal failure?
