Diabetes Type 2 Flashcards
Vascular Effects of diabetes? Atherosclerosis is
The main reason for impaired life expectancy in patients with diabetes whereas diabetic nephropathy and retinopathy are the largest contributors to end-stage renal disease and blindness, respectively.
Some symptoms of diabetes-related vascular problems include:
Blurred vision
Floating spots in vision
Unexpected weight gain or swelling in your face or limbs
Foamy looking urine
Sores on your feet
Loss of feeling in your hands or feet
Burning feeling in your hands or feet
Pain in your legs when walking
High blood pressure
Chest pain
Overweight people with either pre-diabetes or type 2 diabetes most typically produce
most typically produce significantly more insulin than non-diabetic people resulting from a higher ratio of body fat to muscle.
The reason for this is insulin resistance, which means that the body can’t use its insulin effectively enough.
The reason for this is insulin resistance, which means that the body can’t use its insulin effectively enough.
Therefore, it makes sense that the body should produce more insulin to compensate.
However, the strain of producing all this extra insulin means that the beta cells become over worked and over time will start to fail.
The most important
regulator of glucose uptake from the blood is the hormone
insulin, which is produced by islet beta cells and
acts on insulin receptors to promote nutrient uptake and
processing.
Exposure to prolonged hyperglycaemia causes reversible and then irreversible
changes to tissue metabolism and structure
, in one study an average blood glucose more
than 50% above the normal range was associated with
a
40% risk of developing severe retinopathy at 14 years: in
contrast, this risk was only 5% in those patients with blood
glucose levels close to the normal range.
This process of glycation can alter the structure and function of the protein. Further changes can lead to
glycation
products with extensive cross-linkage called advanced
glycation end products - an irreversible change. These
molecules may lead to the production of free oxygen radicals which could themselves cause tissue damage.
The
second mechanism is the production of excess sorbitol
though a
normally redundant pathway involving the
enzyme aldose reductase. Sorbitol cannot readily leave a
cell and accumulation of the alcohol sugar could lead to
osmotically driven overhydration of the tissue and damage.
The third mechanism involves the direct competition
between glucose and myoinositol.
Myoinositol is an
important substrate in cellular energy production, and its
structure is very similar to that of glucose. Excess glucose
can therefore compete for myoinositol uptake by a cell,
leading to myoinositol depletion.
Inositol might balance certain chemicals in the body to possibly help with mental conditions such as panic disorder, depression, and obsessive-compulsive disorder. It might also help insulin work better.
hepatic rather than muscle insulin resistance is
involved in the occurrence of hyperglycemia and overt diabetes . The pre-existing muscle
insulin resistance caused by inherited and environmental factors leads to
raised plasma insulin
levels, which, together with an increased caloric overload, will exert accumulation of fat in the liver. In turn, liver fat accumulation causes hepatic insulin resistance, hence the failure of
insulin to suppress liver glucose production
Adipose tissue may become a source of
inflammation as well, as adipocyte hypertrophy is associated with
increased macrophage accumulation, which
produce proinflammatory mediators such as TNFα and
IL-6, in obese individuals
The progression of T2D has been causally linked to various types of immune cells but the primary sources of inflammatory effectors contributing to insulin resistance are
Macrophages
In patients with diabetes,
atherosclerosis is the main reason for impaired life expectancy, and diabetic nephropathy and retinopathy are the largest contributors to end-stage renal disease and blindness, respectively.
Apolipoprotein B-containing and modified LDL retained in the arterial intima recruits
monocyte-derived macrophages, which take up lipoproteins and differentiate into foam cells (fig. 2). Cytokines and chemokines released from macrophage foam cells and other immune cells recruit additional immune cells. Overproduction of reactive oxygen species (ROS) as a result of altered glucose metabolism and formation of advanced glycation end-products (AGE) further amplifies this process by activating nuclear factor κB (NFκB) and other proinflammatory pathways.
In combination with endothelial cell insulin resistance, these changes cause endothelial dysfunction manifesting itself by increased expression of adhesion molecules and other changes
The most important early clinical risk factor for diabetic nephropathy is
`which is caused by hemodynamic changes and by impairment of the glomerular filtration barrier
Patients with hypothyroidism often complain of
muscular pain
and stiffness of extremities .
Pain and
paraesthesiae in the fingers, sometimes secondary to tenosynovitis, but mostly to CTS, is a frequently observed complaint
in hypothyroidism. It has been suggested that a combination of
mild compression within the carpal tunnel and neuropathy due
to hypothyroidism-induced demyelinization may occur in the
affected nerve
What is Reflex sympathetic dystrophy?
Reflex sympathetic dystrophy is also known as algodystrophy, Sudeck’s atrophy, and chronic regional pain syndrome type 1. It is characterised by localised or diffuse pain, usually with associated swelling, trophic changes, and vasomotor disturbances,31 with impaired mobility of the affected region
What is Flexor tenosynovitis?
Flexor tenosynovitis (trigger finger or stenosing tenovaginitis) is caused by fibrous tissue proliferation in the tendon sheath leading to limitation of the normal movement of the tendon.
The prevalence of flexor tenosynovitis is estimated at 11% in diabetic patients, compared with <1% in non-diabetics.
What is DIFFUSE IDIOPATHIC SKELETAL HYPEROSTOSIS?
Diffuse idiopathic skeletal hyperostosis, also known as ankylosing hyperostosis or Forestier’s disease, is characterised by new bone formation, particularly in the thoracolumbar spine (figs 6 and 7). New bone appears to “flow” from one vertebra to the next, and is more prominent on the right side of the thoracic vertebra.33 Ossification of ligaments and tendons elsewhere may occur, such as the skull, pelvis, heels, or elbows
A proposed mechanism of causation is the prolonged and high levels of insulin or insulin-like growth factors occurring in diabetic patients, stimulating new bone growth, and may explain the higher prevalence in type 1 compared with type 2 diabetes
Diabetic amyotrophy is a type of
diabetic neuropathy that
affects proximal segments of nerves
It is more frequent in patients with type 2 diabetes aged
50-60 years and presents with severe pain and uni- or
bilateral subacute muscle weakness and atrophy, especially
in the proximal thigh muscles. Less frequently there may be
involvement of the shoulder girdle [54, 55] and, in rare
cases; the compromise of the upper and lower limbs may
result in quadriparesis
Calcific Periarthritis of the Shoulder
Inflammatory processes of the structures surrounding the
shoulder joint (tendons, capsule, bursas, etc.) are known as
periarthritis. In diabetic patients, these disorders are three
times more frequent than in general population
While etiology of calcific periarthritis of the shoulder is
unclear, degeneration of tendinous tissues (usually of supraspinatus muscle) by ischemia and mechanical strain may
result in breakdown of fibrils leading to a cell-mediated reaction. This process is followed by further deposit of calcium
and collagenous fibers on adjacent tissues and compromise
of the subacromial/subdeltoid bursa, the joint capsule and the
bicipital tendon [
