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Biological: Behavioural genetics · Evolutionary psychology · Neuroanatomy · Neurochemistry · Neuroendocrinology · Neuroscience · Psychoneuroimmunology · Physiological Psychology · Psychopharmacology (Index, Outline)
ICD-10 | K318 | |
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ICD-9 | 536.3 | |
OMIM | [4] | |
DiseasesDB | 32575 | |
MedlinePlus | 000297 | |
eMedicine | / | |
MeSH | {{{MeshNumber}}} |
Gastroparesis, also called delayed gastric emptying, is a medical condition consisting of a paresis (partial paralysis) of the stomach, resulting in food remaining in the stomach for a longer period of time than normal. Normally, the stomach contracts to move food down into the small intestine for digestion. The vagus nerve controls these contractions. Gastroparesis may occur when the vagus nerve is damaged and the muscles of the stomach and intestines do not work normally. Food then moves slowly or stops moving through the digestive tract.
Causes[]
Gastroparesis may be chronic or transient; transient gastroparesis may arise in acute illness of any kind, with the use of certain cancer treatments or other drugs which affect digestive action, or due to anorexia nervosa, bulimia and other abnormal eating patterns.
Chronic gastroparesis is frequently due to autonomic neuropathy. This may occur in people with type 1 diabetes or type 2 diabetes. The vagus nerve becomes damaged by years of high blood glucose, resulting in gastroparesis. Gastroparesis has also been associated with various autoimmune diseases and syndromes, such as fibromyalgia and Parkinson's disease, and may occur as part of a mitochondrial disorder.
Chronic gastroparesis can also be caused by other types of damage to the vagus nerve, such as abdominal surgery.[1]
Idiopathic gastroparesis (gastroparesis with no known cause) accounts for a third of all chronic cases; it is thought that many of these cases are due to an autoimmune response triggered by an acute viral infection. "Stomach flu", mononucleosis, and others have been anecdotally linked to the onset of the condition, but no systematic study has proven a link.
Gastroparesis sufferers are disproportionately female. One possible explanation for this finding is that women have an inherently slower stomach emptying time than men.[2] A hormonal link has also been suggested, as gastroparesis symptoms tend to worsen the week before menstruation, when progesterone levels are highest.[3] Neither theory has been proven definitively.
Signs and Symptoms[]
The most common symptoms of gastroparesis are[4]
- Chronic nausea
- Vomiting (especially of undigested food)
- Early satiety
Other symptoms include
- Heartburn
- Weight loss
- Abdominal bloating
- Erratic blood glucose levels
- Lack of appetite
- Gastroesophageal reflux
- Spasms of the stomach wall
Morning nausea may also indicate gastroparesis. It is important to note that vomiting may not occur in all cases, as sufferers may learn to adjust their diets to include only small amounts of food.[5]
Diagnosis and Treatment[]
Gastroparesis can be diagnosed with tests such as x rays, manometry, and gastric emptying scans. The clinical definition for gastroparesis is based solely on the emptying time of the stomach and not on other symptoms, and severity of symptoms does not necessarily correlate with the severity of gastroparesis. Therefore, some patients may have marked gastroparesis with few, if any, serious complications.
Treatment includes dietary changes (low-fiber and low-residue diets, and in some cases, restrictions on fat and/or solids), oral medications such as Metoclopramide (Reglan, Maxolon, Clopra), Cisapride (Propulsid), Erythromycin (E-Mycin, Erythrocin, Ery-Tab, EES) and Domperidone (Motilium); adjustments in insulin dosage for those with diabetes, a jejunostomy tube, parenteral nutrition, implanted gastric neurostimulators ("stomach pacemakers"), or botulinum toxin.
Viagra, which increases blood flow to the genital area, is also being used by some practitioners to stimulate the GI tract in diabetic gastroparesis.
The antidepressant Mirtazapine has also proven effective in the treatment of gastroparesis unresponsive to conventional treatment. This is due to its anti-emetic and appetite stimulant properties. Mirtazapine acts on the same serotonin receptor (5-HT3) as the popular anti-emetic Ondansetron[6].
Complications[]
Primary complications of gastroparesis include:
- Fluctuations in blood glucose due to unpredictable digestion times (in diabetic patients)
- General malnutrition due to the symptoms of the disease (which frequently include vomiting and reduced appetite) as well as the dietary changes necessary to manage it
- Severe fatigue and weight loss due to calorie deficit
- Intestinal obstruction due to the formation of bezoars (solid masses of undigested food)
- Bacterial infection due to overgrowth in undigested food
References[]
External links[]
- G-PACT Gastroparesis Patient Association
- Overview from NIDDK
- Overview at Mayo Clinic
- [5] at Mayo Clinic
- Overview at University of Chicago Hospitals
- Patient Perspective at the icarecafe
- Diabetic Neuropathy (emedicine.com)
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