Diabetes and GIT

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International Diabetes Federation. IDF Homepage. International Diabetes Federation 2011. Available from: http://www.idf.org/.
Every 10 seconds... 2 people develop
DM The number of patients with diabetes worldwide is expected to
increase from 366 million in 2011 to 552 million in 2030
2
Number of patients, millions
North
America
and
Caribbean
South and
Central
America
Europe Africa India China Other
s
2011 2030

 Disease duration
 Degree of glycemic control.

Poor glycemic control
Delayed gastric emptying

EFFECTS
 Peristalsis
 Reflexive relaxation
 Sphincter tone
 Vascular flow
 Intestinal segmentation

MOST COMMON PROBLEMS
 Constipation
 Diarrhea
 Abdominal pain
 Nausea
 Vomiting

ESOPHAGUS
• Abnormal Motility (50-75%)
• Reduced number, amplitude & velocity of
peristalsis
• Increased spontaneous, spastic and repetitive
contractions
• Appearance of multipeaked contractions
•Impaired(prolonged) esophageal transit-
scintigraphy
• Reduced lower esophageal sphincter pressure

 Hyperglycemia impairs neutrophil function and
opsonization.
 Odynophagia
 ® Nystatin 1lakh U-3-5times/dy, Clotrimazole
10mg(troche) 5 times/dy or 500mg VT HS.
 Fluconazole- 200mg loading + 100mg/dy x
21dys

STOMACH
Type 1: Gastritis/Gastric Atrophy (5% to 10%).
Parietal cell antibodies (15% to 25%).
Pernicious Anemia (2.6% to 4%).
Reduced acid hence decreased ulcer incidence.
Increased risk of ulcer bleeding- microcirculatory
changes that impair mucosal integrity.

GASTROPARESIS DIABETICORUM
 Seen in upto 60%
 Insidious nature, Rarely acute- similar to vagotomy
 Nausea, vomiting, pain, bloating, early satiety,
flatulence, anorexia and postprandial regurgitation- 20%
 Changes in drug absorption
 Food retention- increase of bacteria toxins &
fermentation products- hypermotility and diarrhoea
Examination - succussion splash

● Scintigraphy- Solid and liquid emptying assessed.
Gastroparesis->60% @ 2hrs & >10% @ 4hrs.
● Saline loading- 800-1000ml.
● EGG- Increased frequency of antral dysrhythmias.
Phase 3 MMC are absent →bezoars.

Abnormal
Gastroduodenal pressure gradient
Fundal relaxation
Pylorospasm

TREATMENT
Glycemic control- Depo-insulin to prevent hypoglycaemic episodes
 DIET MODIFICATION:
Smaller/liquid meals, low-fat, low-fiber diet
Jejunal tube feeding/ TPN
 MEDICATIONS-
Prokinetics: Metoclopramide10to20mg, Erythromycin 125mgBD or TDS
or IV200mg over5to10minutesTDS, Domperidone 10 to 30 mg.
Antiemetics- (promethazine or prochlorperazine), scopolamine patch.
Low-dose TCA
5-HT3 receptor antagonists- odansetron, dronabinol
Ghrelin- improves gastric emptying

GES
A) Gastric pacing - improves gastric
emptying
B) Neurostimulation - controls
nausea/vomiting
Endoscopic therapy with injection of
botulinum toxin into the pyloric sphincter
Gastric resection (Partial or complete) in
medically refractory cases

GASTRIC ELECTRICAL STIMULATION-10 YEAR DATA
- Greater Symptom Reduction
- Improved Gastric Emptying  normalized in 23%
- Decreased Hb A1C levels  translates to fewer
complications
- Significant Weight Gain
- Reduction in Hospitalization Days
- Reduced Medication Usage (for gastroparesis)
McCallum, et al, Clin. Gastro & Hep. 9(4):314-319

TABETIC PAIN
 sharp, sudden pain
 With nausea, vomiting, anorexia and weight loss-
mimics intra-abdominal malignancy
 Diabetic radiculopathy of thoracic nerve roots
 The diagnosis- abnormal EMG of the anterior
abdominal wall muscles

DIABETIC ACIDOSIS
 Anorexia, nausea and vomiting- 75%
 Gastric dilatation- reduced gastric
motility→vomiting-(ketones and systemic acidosis)
 Abdominal pain-Acute apendicitis, Acute
pancreatitis-should be excluded

DIARRHEA
 Drugs- Metformin, ά-Glucosidase inhibitors
,sugarfree sweeteners.
 SIBO
 Pancreatic insufficiency
 Fast transit (and hyperthyroidism)
 Celiac disease(4%)
 Hormones- glucagon or somatostatin
 Autonomic neuropathy

CHRONIC DIARRHEA WITHOUT
STEATORRHEA
 Occur 5-10 years later, men > women: 22%
 Exact pathogenesis- still undetermined
 In young-long standing and uncontrolled diabetes.
 Diabetic night diarrhoea
 Hyperglycaemia, hypoglycemia and ketoacidosis.
 Barium transit- segmentation with mucous villous
atrophy, irregularity.

DIABETIC DIARRHEA WITH
STEATORRHEA
 Steatorrhea occurs when diarrhoea worsens: 75%
 Shows intermittent flow.
 More frequently, postpardial and they appear at
night
 Rarely fatty, watery and abundant

TREATMENT
 Strict control of blood glucose
 Broad spectrum antibiotics
 Vitamins, folic acid, liver extracts, bismuth, opiates, atropine
 Corticosteroids
 Clonidine (0.1 to 0.6 mg twice daily) stimulate intestinal
absorption
 Octreotide (50 to 100 subcutaneously, BD) in refractory
diabetic diarrhea
 Codeine sulfate (30 mg every six to eight hours),
 Diphenoxylate with atropine (Lomotil),
 Loperamide
 Psyllium hydrophilic mucilloid

DIABETES AND CELIAC
DISEASE
 Coexist (4%)-shared HLA class II genes and non-HLA
loci
 Found within 4 years of DM.
 Short stature, pubertal delay, - signs of vitamin deficit,
anemia, losing weight and pigmentation,osteoporosis,
and/or reproductive disorders
 Have poor glycemic control- hypoglycemic episodes,
and microvascular complications.
 Small intestine which shows villous atrophy and
abnormal superficial epithelium
 Malabsorbtion in diabetes-limited only to fats
 Respond to gluten free diet

LARGE INTESTINE
 Constipation
 Impaired gastrocolic reflex and delayed colonic
transit
 Ischemic colitis - luminal narrowing of
submucosal arterioles.
 Neuropathy damages the motility.
 Equally frequent and severe without
neuropathy
 Obstipation- nausea, vomiting, belching and
bloating.

MEGASIGMOID
SYNDROME
 Colon dilatation- neuropathy and the
paralysis of ganglia.
 Imitates acute intestinal pseudo-
obstruction.
 Obstipation- long standing and refractory.
 X-ray- dilatation of sigmoid colon.
 Mucosa of the large intestine- Normal.
 Bad prognosis.
 Treatment- Laxative (abuse).

FECAL INCONTINENCE
 The total stool volume is normal.
 Steatorrhea in 30%.
 Impaired internal anal sphincter resting tone and
reflexive internal sphincter relaxation.
 Reduced sensitivity of the rectum to distension.
 Management:
Antidiarrheal therapy
Biofeedback training
Sacral nerve stimulation
Surgery
In some patients incontinence remits spontaneously.

DIABETES – LIVER/BILIARY
HIGHER INCIDENCE OF ACUTE HEPATITIS B-1.4 vs 0.7 per 100,000
patients
HCV- patients have an increased risk of type 2 DM.
GALL BLADDER: acute cholecystitis postoperative complications are
higher
GALLSTONES MORE FREQUENT (2X)
lithogenic bile
hypomotility
prophylactic cholecystectomy.- not recommended
SOMATOSTATINOMA Triad- Gallstones, Diabetes,
Diarrhea/Steatorrhea
STEATOSIS in upto 80%
DM is a risk factor for HCC.

DIABETES -NAFLD
Spectrum of disease:
Simple steatosissteatohepatitis(NASH)  cirrhosis(20%).
Increase the risk of acute hepatic failure
Risk Factors: female, diabetes, obesity, hyperlipidemia
Fatty deposition, nuclear vacuolisation, cellular infiltration and
fibriosis
Cryptogenic cirrhosis  70% obese/50% diabetic!!
Cirrhosis of the liver may precede or cause diabetes→ glucose
intolerant & 30%-60% develop DM

TREATMENT
- Slow/gradual weight loss
- Control diabetes/hyperlipidemia
- Pharmacologic treatment: TZD’s, others
- Surgery:
Bariatric - improvement in 90%
Liver transplant(Cirrhotics)

PANCREAS
 DM for more than 5 years
 Pancreatitis can produce diabetes
 Exocrine pancreas secretion- Deteriorates
 Diabetes and pancreatitis:
Causes hyperglycemia
May persist for several months
Pancreatic calcifications
Degenerative complications-less frequent
 Exocrine secretion-reduced volume & enzymes

GALL BLADDER
 Higher incidence- unexplained
 Defect in the cholinergic pathway
 Reduced α-adrenergic tone
 Deficiency of cholecystokinin receptors
 Arteriolar disease impairing muscle contraction
 Hyperglycemia
 Hyperinsulinemia

CARCINOMAS
 Insulin resistance→secondary hyperinsulinemia →
↓IGF-binding proteins → ↑IGF-1 & Growth hormone
→ cancer growth(Pancreas, liver & colon).
 Loss of weight and deteriorated glycoregulation.
 New onset diabetes >50 yrs.
 HbA1c > 7.5% → young age, more advanced tumor
and poorer survival.
 Slow bowel transit time increase carcinogen exposure

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