Diabetic counterregulation
Diabetic counterregulation (or rebound) means the increase in blood sugar concentrations (hyperglycaemia) which is caused by hormones (glucagons, adrenalin, cortisol, STH). This is triggered by and tends to counteract the low blood sugar concentrations (hypoglycaemia) caused by insulin. Cf. type 2 diabetes, type 1 diabetes, Somogyi effect.
Diabetic glomerulosclerosis
also known as Kimmelstiel-Wilson glomerulosclerosis or diabetic nephropathy
Damage to the glomerular capillaries (the smallest blood vessels) in the kidney as a result of long term (mostly more than 10 years) type 2 diabetes or type 1 diabetes, particularly when blood sugar is poorly regulated. Diabetic glomerulosclerosis occurs to different degrees in about a third of diabetics, mostly together with retinopathia diabetica.
Symptoms
Initially there is increased fluid perfusion through the glomerular capillaries with increased formation of primary urine and somewhat increased urinary elimination of the protein albumin. At a later stage, there is a marked increase in urinary protein elimination, a decrease in blood protein levels and increases in blood fat concentrations. Kidney function gradually deteriorates. Diabetic glomerulosclerosis is the most frequent reason for kidney dialysis.
Prevention
Diabetic glomerulosclerosis in patients with type 1 or type 2 diabetes is prevented by exact regulation by the physician of blood sugar values.
Digestion of carbohydrates
Carbohydrates are only absorbed in the intestine as monosaccharides. The breakdown of polysaccharides (starch, glycogen) starts with the enzyme alpha-amylase in the saliva, which is then inactivated in the acid environment in the stomach. The resulting mixture is split into disaccharides by the alpha-amylase of the (pancreas). These are then split into monosaccharides by enzymes in the brush border of the intestinal mucous membrane and aborbed into blood in this form. This absorption can be enhanced by thyroid hormones. Cf. digestion,digestion of proteins, digestion of neutral fats).
Digestion of neutral fats
The breakdown of neutral fats (triglycerides) after ingestion in food starts with the enzymes in gastric juice. The fats are emulsified by bile acids and phospholipids and then broken down by enzymes from the pancreas (pancreatic lipases, see lipasen). Free fatty acids and monoacylglycerols (see glycerols) diffuse passively into the cells of the intestinal mucous membrane and are reassembled there to triglycerides. They pass into the lymph in the form of chylomicrons (small lipoprotein particles) and then into venous blood. After very fatty food they can cause serum to appear turbid (hyperlipidaemia.Cf. digestion, digestion of carbohydrates, digestion of proteins.
Direct measurement of blood pressure
also known as invasive measurement of blood pressure
Measurement of blood pressure during major operations or in patients in intensive care with a catheter laid in an artery. Direct measurement of blood pressure is more exact than indirect measurement of blood pressure. Continuous measurement of blood pressure is possible.
Disturbance in cerebral perfusion
Disturbance in the perfusion of the brain. Occurs mostly after age 50 and men are more often affected than women. The most severe complication is stroke. Cf. arterial occlusive diseases.
Causes
Particularly arteriosclerosis of the vessels which serve the brain, constriction of the vessels within or outside the brain (most frequently constriction of the internal jugular artery with the danger that an embolism is released into the brain, also embolisms from the heart, inflammatory vascular disease, abnormal blood flow properties and low arterial pressure. Risk factors include arterial hypertension (hypertension), high blood fat levels, diabetes mellitus (type 2 diabetes, type 1 diabetes) and nicotine abuse.
Diagnosis
Clinical investigation, ECG (cardiac arrythmia?), brain computer tomography (infarct?, bleeding?), ultrasound investigation of the arteries which serve the brain; perhaps further investigation with other methods, such as angiography of the arteries which serve the brain.
Therapy
1. Removal of risk factors or treatment of the underlying disease; 2. To prevent another episode of abnormal cerebral perfusion, e.g. acetylsalicylic acid. If it is suspected that an embolism has come from the heart, use coagulation inhibitors to thin the blood; 3. Operation to remove the blood clot, only if there is symptomatic constriction of the internal jugular (more than 70 %), possibly widening of the artery with the balloon catheter (PTA); 4. Possibly specific treatment for stroke.
Disturbance in vertebrobasilar perfusion
Disturbance in the perfusion of the area served by the spinal artery (Arteria vertebralis) and the connected Arteria basilaris.
Causes
Arteriosclerosis, constriction or occlusion of the Arteria vertebralis, embolism, more rarely inflammation of the blood vessels.
Symptoms
Fleeting symptoms include giddiness, double vision, lack of sensitivity in the skin of the head, pain in the back of the head, confusion and symptoms arising from damage to the brain stem, such as paralysis to the muscles of the eye and face, hoarseness, drooping eyelid, constriction of the pupils. Cf. disturbance in cerebral perfusion
Disturbances in ossification
Disturbances in bone formation, which may either be in-born or acquired. In-born disturbances in ossification are due to damage before the birth, which may either be genetic or due to external factors. A condition which arises after birth is called an acquired disturbance in ossification.
Forms
I. general disturbance in ossification: 1. primary, in-born disturbance in ossification, such as disturbances in cartilage formation, which are marked at birth and which generally do not get worse; disturbances in the activity of the osteoblasts (cf. osteoblasts), which lead to osteoporosis, as a result of reduced or inferior bone generation; disturbances in the activity of the osteoclasts, which lead to reduced bone breakdown; 2. secondary general disturbances in ossification caused by diseases which may be in-born or acquired after birth, e.g. secondary osteoporosis, osteomalacia, secondary osteosclerosis.
II. local disturbances in ossification: for example, germ-free death of bone mass (aseptic bone necrosis); inflammatory bone diseases: bone marrow inflammation (osteomyelitis), tuberculosis (bone tuberculosis, arthritis tuberculosa and other), syphilis, osteodystrophia deformans; bone tumours.