Alimentary tract and pancreatic disease



Alimentary tract and pancreatic disease


I.D. Penman


C.W. Lees



Clinical examination of the gastrointestinal tract


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4   Abdominal examination


possible findings


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6   Rectal examination


common findings


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Diseases of the gastrointestinal tract are a major cause of morbidity and mortality. Approximately 10% of all general practitioner consultations in the United Kingdom are for indigestion, and 1 in 14 is for diarrhoea. Infective diarrhoea and malabsorption are responsible for much ill health and many deaths in the developing world. The gastrointestinal tract is the most common site for cancer development. Colorectal cancer is the second most common cancer in men, and population-based screening programmes exist in many countries. Functional bowel disorders affect up to 10–15% of the population and consume considerable health-care resources. The inflammatory bowel diseases, Crohn’s disease and ulcerative colitis, together affect 1 in 250 people in the Western world, with substantial associated morbidity.



Functional anatomy and physiology




Oesophagus, stomach and duodenum


This muscular tube extends 25 cm from the cricoid cartilage to the cardiac orifice of the stomach. It has an upper and a lower sphincter. A peristaltic swallowing wave propels the food bolus into the stomach (Fig. 22.1).


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Fig. 22.1 The oesophagus: anatomy and function.
The swallowing wave.

The stomach acts as a ‘hopper’, retaining and grinding food, then actively propelling it into the upper small bowel (Fig. 22.2).


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Fig. 22.2 Normal gastric and duodenal anatomy.


Gastric secretion

Gastrin, histamine and acetylcholine are the key stimulants of acid secretion. Hydrogen and chloride ions are secreted from the apical membrane of gastric parietal cells into the lumen of the stomach by a hydrogen–potassium adenosine triphosphatase (ATPase) (‘proton pump’) (Fig. 22.3). The hydrochloric acid sterilises the upper gastrointestinal tract and converts pepsinogen – which is secreted by chief cells – to pepsin. The glycoprotein intrinsic factor, secreted in parallel with acid, is necessary for vitamin B12 absorption.


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Fig. 22.3 Control of acid secretion.
Gastrin released from antral G cells in response to food (protein) binds to cholecystokinin receptors (CCK-2R) on the surface of enterochromaffin-like (ECL) cells, which in turn release histamine. The histamine binds to H2 receptors on parietal cells and this leads to secretion of hydrogen ions, in exchange for potassium ions at the apical membrane. Parietal cells also express CCK-2R and it is thought that activation of these receptors by gastrin is involved in regulatory proliferation of parietal cells. Cholinergic (vagal) activity and gastric distension also stimulate acid secretion; somatostatin, vasoactive intestinal polypeptide (VIP) and gastric inhibitory polypeptide (GIP) may inhibit it. (ACh-R = acetylcholine receptor; ATPase = adenosine triphosphatase)




Small intestine


The small bowel extends from the ligament of Treitz to the ileocaecal valve (Fig. 22.4). During fasting, a wave of peristaltic activity passes down the small bowel every 1–2 hours. Entry of food into the gastrointestinal tract stimulates small bowel peristaltic activity. Functions of the small intestine are:


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Fig. 22.4 Small intestine: anatomy.
Epithelial cells are formed in crypts and differentiate as they migrate to the tip of the villi to form enterocytes (absorptive cells) and goblet cells.



Digestion and absorption


Fat

Dietary lipids comprise long-chain triglycerides, cholesterol esters and lecithin. Lipids are insoluble in water and undergo lipolysis and incorporation into mixed micelles before they can be absorbed into enterocytes along with the fat-soluble vitamins A, D, K and E. The lipids are processed within enterocytes and pass via lymphatics into the systemic circulation. Fat absorption and digestion can be considered as a stepwise process, as outlined in Figure 22.5.


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Fig. 22.5 Fat digestion.
Step 1: Luminal phase. Fatty acids stimulate cholecystokinin (CCK) release from the duodenum and upper jejunum. The CCK stimulates release of amylase, lipase, colipase and proteases from the pancreas, causes gallbladder contraction and relaxes the sphincter of Oddi, leading bile to flow into the intestine. Step 2: Fat solubilisation. Bile acids and salts combine with dietary fat to form mixed micelles, which also contain cholesterol and fat-soluble vitamins. Step 3: Digestion. Pancreatic lipase, in the presence of its co-factor, colipase, cleaves long-chain triglycerides, yielding fatty acids and monoglycerides. Step 4: Absorption. Mixed micelles diffuse to the brush border of the enterocytes. Within the brush border, long-chain fatty acids bind to proteins, which transport the fatty acids into the cell, whereas cholesterol, short-chain fatty acids, phospholipids and fat-soluble vitamins enter the cell directly. The bile salts remain in the small intestinal lumen and are actively transported from the terminal ileum into the portal circulation and returned to the liver (the enterohepatic circulation). Step 5: Re-esterification. Within the enterocyte, fatty acids are re-esterified to form triglycerides. Triglycerides combine with cholesterol ester, fat-soluble vitamins, phospholipids and apoproteins to form chylomicrons. Step 6: Transport. Chylomicrons leave the enterocytes by exocytosis, enter mesenteric lymphatics, pass into the thoracic duct, and eventually reach the systemic circulation.



Protein

The steps involved in protein digestion are shown in Figure 22.6. Intragastric digestion by pepsin is quantitatively modest but important because the resulting polypeptides and amino acids stimulate CCK release from the mucosa of the proximal jejunum, which in turn stimulates release of pancreatic proteases, including trypsinogen, chymotrypsinogen, pro-elastases and procarboxypeptidases, from the pancreas. On exposure to brush border enterokinase, inert trypsinogen is converted to the active proteolytic enzyme trypsin, which activates the other pancreatic proenzymes. Trypsin digests proteins to produce oligopeptides, peptides and amino acids. Oligopeptides are further hydrolysed by brush border enzymes to yield dipeptides, tripeptides and amino acids. These small peptides and the amino acids are actively transported into the enterocytes, where intracellular peptidases further digest peptides to amino acids. Amino acids are then actively transported across the basal cell membrane of the enterocyte into the portal circulation and the liver.


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Fig. 22.6 Protein digestion.




Protective function of the small intestine



Immunological defence mechanisms

Gastrointestinal mucosa-associated lymphoid tissue (MALT) constitutes 25% of the total lymphatic tissue of the body and is at the heart of adaptive immunity. Within Peyer’s patches, B lymphocytes differentiate to plasma cells following exposure to antigens, and these migrate to mesenteric lymph nodes, to enter the blood stream via the thoracic duct. The plasma cells return to the lamina propria of the gut through the circulation and release immunoglobulin A (IgA), which is transported into the lumen of the intestine. Intestinal T lymphocytes help localise plasma cells to the site of antigen exposure, as well as producing inflammatory mediators. Macrophages in the gut phagocytose foreign materials and secrete a range of cytokines, which mediate inflammation. Similarly, activation of mast-cell surface IgE receptors leads to degranulation and release of other molecules involved in inflammation.



Pancreas


The exocrine pancreas (Box 22.1) is necessary for the digestion of fat, protein and carbohydrate. Proenzymes are secreted from pancreatic acinar cells in response to circulating gastrointestinal hormones (Fig. 22.9) and are activated by trypsin. Bicarbonate-rich fluid is secreted from ductular cells to produce an optimum alkaline pH for enzyme activity.



image22.1   Pancreatic enzymes


























Enzyme Substrate Product
Amylase Starch and glycogen Limit dextrans
Maltose
Maltriose
Lipase
Colipase		 Triglycerides Monoglycerides and free fatty acids
Proteolytic enzymes
Trypsinogen
Chymotrypsinogen
Pro-elastase
Pro-carboxypeptidases		 Proteins and polypeptides Short polypeptides


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Fig. 22.9 Pancreatic structure and function.
Ductular cells secrete alkaline fluid in response to secretin. Acinar cells secrete digestive enzymes from zymogen granules in response to a range of secretagogues. The photograph shows a normal pancreatic duct (PD) and side branches, as defined at magnetic resonance cholangiopancreatography (MRCP). Note the incidental calculi in the gallbladder and common bile duct (arrow). (CCK = cholecystokinin; VIP = vasoactive intestinal polypeptide)


Colon


The colon (Fig. 22.10) absorbs water and electrolytes. It also acts as a storage organ and has contractile activity. Two types of contraction occur. The first of these is segmentation (ring contraction), which leads to mixing but not propulsion; this promotes absorption of water and electrolytes. Propulsive (peristaltic contraction) waves occur several times a day and propel faeces to the rectum. All activity is stimulated after meals, probably in response to release of motilin and CCK. Faecal continence depends upon maintenance of the anorectal angle and tonic contraction of the external anal sphincters. On defecation, there is relaxation of the anorectal muscles, increased intra-abdominal pressure from the Valsalva manœuvre and contraction of abdominal muscles, and relaxation of the anal sphincters.


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Fig. 22.10 The normal colon, rectum and anal canal.


Control of gastrointestinal function


Secretion, absorption, motor activity, growth and differentiation of the gut are all modulated by a combination of neuronal and hormonal factors.



The nervous system and gastrointestinal function


The central nervous system (CNS), the autonomic system (ANS) and the enteric nervous system (ENS) interact to regulate gut function. The ANS comprises:




The enteric nervous system

In conjunction with the ANS, the ENS senses gut contents and conditions, and regulates motility, fluid exchange, secretion, blood flow and other key gut functions. It comprises two major networks intrinsic to the gut wall. The myenteric (Auerbach’s) plexus in the smooth muscle layer regulates motor control; and the submucosal (Meissner’s) plexus exerts secretory control over the epithelium, enteroendocrine cells and submucosal vessels. Together, these plexuses form a two-layered neuronal mesh along the length of the gut. Although connected centrally via the ANS, the ENS can function autonomously, using a variety of transmitters, including acetylcholine, noradrenaline (norepinephrine), 5-hydroxytryptamine (5-HT, serotonin), nitric oxide, substance P and calcitonin gene-related peptide (CGRP). There are local reflex loops within the ENS but also loops involving the coeliac and mesenteric ganglia and the paravertebral ganglia. The parasympathetic system generally stimulates motility and secretion, while the sympathetic system generally acts in an inhibitory manner.





Gut hormones


The origin, action and control of the major gut hormones, peptides and non-peptide signalling transmitters are summarised in Box 22.2.



image22.2   Gut hormones and peptides





























































Hormone Origin Stimulus Action
Gastrin Stomach (G cell) Products of protein digestion
Suppressed by acid and somatostatin		 Stimulates gastric acid secretion
Stimulates growth of gastrointestinal mucosa
Somatostatin Throughout GI tract (D cell) Fat ingestion Inhibits gastrin and insulin secretion
Decreases acid secretion
Decreases absorption
Inhibits pancreatic secretion
Cholecystokinin (CCK) Duodenum and jejunum (I cells); also ileal and colonic nerve endings Products of protein digestion
Fat and fatty acids
Suppressed by trypsin		 Stimulates pancreatic enzyme secretion
Gallbladder contraction
Sphincter of Oddi relaxation
Satiety
Decreases gastric acid secretion
Reduces gastric emptying
Regulates pancreatic growth
Secretin Duodenum and jejunum (S cells) Duodenal acid
Fatty acids		 Stimulates pancreatic fluid and bicarbonate secretion
Decreases acid secretion
Reduces gastric emptying
Motilin Duodenum, small intestine and colon (Mo cells) Fasting
Dietary fat		 Regulates peristaltic activity, including migrating motor complexes (MMC)
Gastric inhibitory polypeptide (GIP) Duodenum (K cells) and jejunum Glucose and fat Stimulates insulin release (also known as glucose-dependent insulinotrophic polypeptide)
Inhibits acid secretion
Vasoactive intestinal peptide (VIP) Nerve fibres throughout GI tract Unknown Vasodilator
Smooth muscle relaxation
Water and electrolyte secretion
Ghrelin Stomach Fasting
Inhibited by eating		 Stimulates appetite, acid secretion and gastric emptying
Peptide YY Ileum and colon Feeding Modulates satiety
Amylin Pancreatic islet β-cells Feeding Glycaemic control


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Investigation of gastrointestinal disease


A wide range of tests are available for the investigation of patients with gastrointestinal symptoms. These can be classified broadly into tests of structure, tests for infection and tests of function.




Imaging




Contrast studies

X-rays with contrast medium are usually performed to assess not only anatomical abnormalities but also motility. Barium sulphate provides good mucosal coating and excellent opacification but can precipitate impaction proximal to an obstructive lesion. Water-soluble contrast is used to opacify bowel prior to abdominal computed tomography and in cases of suspected perforation. The double contrast technique improves mucosal visualisation by using gas to distend the barium-coated intestinal surface. Contrast studies are useful for detecting filling defects, such as tumours, strictures, ulcers and motility disorders, but are inferior to endoscopic procedures and more sophisticated cross-sectional imaging techniques, such as computed tomography and magnetic resonance imaging. The major uses and limitations of various contrast studies are shown in Box 22.3 and Figure 22.11.



image22.3   Contrast radiology in the investigation of gastrointestinal disease





















  Barium swallow/meal Barium follow-through Barium enema
Indications and major uses Motility disorders (achalasia and gastroparesis)
Perforation or fistula (non-ionic contrast)		 Diarrhoea and abdominal pain of small bowel origin
Possible obstruction by strictures
Suspected malabsorption
Crohn’s disease assessment		 Altered bowel habit
Evaluation of strictures or diverticular disease
Megacolon
Chronic constipation
Limitations Risk of aspiration
Poor mucosal detail
Low sensitivity for early cancer
Inability to biopsy		 Time-consuming
Radiation exposure
Relative insensitivity		 Difficult in frail or incontinent patients
Sigmoidoscopy needed to see rectum
Low sensitivity for lesions < 1 cm


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Fig. 22.11 Examples of contrast radiology.
A Non-ionic contrast swallow shows leakage of contrast (arrow) into the mediastinum following stricture dilatation. B Barium follow-through. There are multiple diverticula (arrows) in this patient with jejunal diverticulosis. C Barium enema showing severe diverticular disease. There is tortuosity and narrowing of the sigmoid colon with multiple diverticula (arrows).


Ultrasound, computed tomography and magnetic resonance imaging

Ultrasound (US), computed tomography (CT) and magnetic resonance imaging (MRI) are key tests in the evaluation of intra-abdominal disease. They are non-invasive and offer detailed images of the abdominal contents. Their main applications are summarised in Box 22.4 and Figure 22.12.



image22.4   Imaging in gastroenterology
























  Ultrasound CT MRI CT-PET
Indications and major uses Abdominal masses
Organomegaly
Ascites
Biliary tract dilatation
Gallstones
Guided biopsy of lesions
Small bowel imaging		 Assess pancreatic disease
Hepatic tumour deposits
CT colonography (‘virtual colonoscopy’)
Tumour staging
Assess lesion vascularity
Abscesses and collections		 Hepatic tumour staging
MRCP
Pelvic/perianal disease
Crohn’s fistulae
Small bowel visualisation		 Detection of metastases not seen on ultrasound or CT
Images can be fused with CT to form composite image
Limitations Low sensitivity for small lesions
Little functional information
Operator-dependent
Gas and obesity may obscure view		 Cost
Radiation dose		 Claustrophobic patients
Contraindicated in presence of metallic prostheses, cardiac pacemaker, cochlear implants		 Signal detection depends on metabolic activity within tumour – not all are metabolically active


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Fig. 22.12 Examples of ultrasound, CT and MRI.
A Ultrasound showing large gallstone (arrow) with acoustic shadowing. B Multidetector coronal CT showing large solid and cystic malignant tumour in the pancreatic tail (arrow). (PV = portal vein; L = liver) C Pelvic MRI showing large pelvic abscess (arrow) posterior to the rectum in a patient with Crohn’s disease. D Fused CT-PET image showing two liver metastases (arrows).


Endoscopy

Videoendoscopes provide high-definition imaging and accessories can be passed down the endoscope to allow both diagnostic and therapeutic procedures, some of which are illustrated in Figure 22.13. Endoscopes with magnifying lenses allow almost microscopic detail to be observed, and imaging modalities, such as confocal endomicroscopy, autofluorescence and ‘narrow band imaging’, are increasingly used to detect subtle abnormalities not visible by standard ‘white light’ endoscopy.


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Fig. 22.13 Examples of therapeutic techniques in endoscopy.


Upper gastrointestinal endoscopy

This is performed under light intravenous benzodiazepine sedation, or using only local anaesthetic throat spray after the patient has fasted for at least 4 hours. With the patient in the left lateral position, the entire oesophagus (excluding pharynx), stomach and first two parts of duodenum can be seen. Indications, contraindications and complications are given in Box 22.5.



image22.5   Upper gastrointestinal endoscopy



Indications






Capsule endoscopy

Capsule endoscopy (Fig. 22.14) uses a capsule containing an imaging device, battery, transmitter and antenna; as it traverses the small intestine, it transmits images to a battery-powered recorder worn on a belt round the patient’s waist. After approximately 8 hours, the capsule is excreted. Images from the capsule are analysed as a video sequence and it is usually possible to localise the segment of small bowel in which lesions are seen. Abnormalities detected usually require enteroscopy for confirmation and therapy. Indications, contraindications and complications are listed in Box 22.6.



image22.6   Wireless capsule endoscopy





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Fig. 22.14 Wireless capsule endoscopy.
A Examples of capsules. B Capsule endoscopy image of bleeding jejunal vascular malformation.


Double balloon enteroscopy

While endoscopy can reach the proximal small intestine in most patients, a newer technique called double balloon enteroscopy is also available, which uses a long endoscope with a flexible overtube. Sequential and repeated inflation and deflation of balloons on the tip of the overtube and enteroscope allow the operator to push and pull along the entire length of the small intestine to the terminal ileum, in order to diagnose or treat small bowel lesions detected by capsule endoscopy or other imaging modalities. Indications, contraindications and complications are listed in Box 22.7.



image22.7   Double balloon enteroscopy







Sigmoidoscopy and colonoscopy

Sigmoidoscopy can be carried out either in the outpatient clinic using a 20 cm rigid plastic sigmoidoscope or in the endoscopy suite using a 60 cm flexible colonoscope following bowel preparation. When sigmoidoscopy is combined with proctoscopy, accurate detection of haemorrhoids, ulcerative colitis and distal colorectal neoplasia is possible. After full bowel cleansing, it is possible to examine the entire colon and the terminal ileum using a longer colonoscope. Indications, contraindications and complications of colonoscopy are listed in Box 22.8.



image22.8   Colonoscopy





*Colonoscopy is not useful in the investigation of constipation.




Endoscopic retrograde cholangiopancreatography

Using a side-viewing duodenoscope, it is possible to cannulate the main pancreatic duct and common bile duct. Nowadays, ERCP is mainly used in the treatment of a range of biliary and pancreatic diseases that have been identified by other imaging techniques such as MRCP, EUS and CT. Indications for and risks of ERCP are listed in Box 22.9.



image22.9   Endoscopic retrograde cholangiopancreatography (ERCP)





*Laparoscopic surgery is preferred in fit individuals who also require cholecystectomy.



image22.10   Endoscopy in old age







Tests of function


A number of dynamic tests can be used to investigate aspects of gut function, including digestion, absorption, inflammation and epithelial permeability. Some of the more commonly used ones are listed in Box 22.12. In the assessment of suspected malabsorption, blood tests (full blood count, erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), folate, vitamin B12, iron status, albumin, calcium and phosphate) are essential, and endoscopy is undertaken to obtain mucosal biopsies. Faecal calprotectin is very sensitive at detecting mucosal inflammation.



image22.12   Dynamic tests of gastrointestinal function








































Process Test Principle Comments
Absorption      
Lactose Lactose H2 breath test Measurement of breath H2 content after 50 g oral lactose. Undigested sugar is metabolised by colonic bacteria in hypolactasia, and expired hydrogen is measured Non-invasive and accurate. May provoke pain and diarrhoea in sufferers
Bile acids 75SeHCAT test Isotopic quantification of 7-day whole-body retention of oral dose 75Se-labelled homocholyltaurine (> 15% = normal, 5–15% borderline, < 5% = abnormal) Accurate and specific but requires two visits and involves radiation. Results can be equivocal. Serum 7α-hydroxycholestenone is as sensitive and specific
Pancreatic exocrine function Pancreolauryl test Pancreatic esterases cleave fluoroscein dilaurate after oral ingestion. Fluoroscein is absorbed and quantified in urine Accurate and avoids duodenal intubation Takes 2 days. Accurate urine collection essential. Rarely performed
Faecal elastase Immunoassay of pancreatic enzymes on stool sample Simple, quick and avoids urine collection. Does not detect mild disease
Mucosal inflammation/ permeability Faecal calprotectin A protein secreted non-specifically by neutrophils into the colon in response to inflammation or neoplasia Useful screening test for gastrointestinal inflammation and for monitoring patients with Crohn’s disease and ulcerative colitis. Poor sensitivity for cancer


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Oesophageal motility

A barium swallow can give useful information about oesophageal motility. Videofluoroscopy, with joint assessment by a speech and language therapist and a radiologist, may be necessary in difficult cases. Oesophageal manometry (see Fig. 22.1, p. 840), often in conjunction with 24-hour pH measurements, is of value in diagnosing cases of refractory gastro-oesophageal reflux, achalasia and non-cardiac chest pain. Oesophageal impedance testing is useful for detecting non-acid or gas reflux events, especially in patients with atypical symptoms or those who respond poorly to acid suppression.



Gastric emptying

This involves administering a test meal containing solids and liquids labelled with different radioisotopes and measuring the amount retained in the stomach afterwards (Box 22.13). It is useful in the investigation of suspected delayed gastric emptying (gastroparesis) when other studies are normal.



image22.13   Commonly used radioisotope tests in gastroenterology

























Test Isotope Major uses and principle of test
Gastric emptying study 99mTc-sulphur
111In-DTPA		 Used in assessment of gastric emptying, particularly for possible gastroparesis
Urea breath test 13C-urea Used in non-invasive diagnosis of H. pylori. Bacterial urease enzyme splits urea to ammonia and CO2, which is detected in expired air
Meckel’s scan 99mTc-pertechnate Diagnosis of Meckel’s diverticulum in cases of obscure gastrointestinal bleeding. Isotope is injected IV and localises in ectopic parietal mucosa within diverticulum
Somatostatin receptor scan (SRS) 111In-DTPA-DPheoctreotide Labelled somatostatin analogue binds to cell surface somatostatin receptors on pancreatic neuro-endocrine tumours





Presenting problems in gastrointestinal disease


Dysphagia


Dysphagia is defined as difficulty in swallowing. It may coexist with heartburn or vomiting but should be distinguished from both globus sensation (in which anxious people feel a lump in the throat without organic cause) and odynophagia (pain during swallowing, usually from gastro-oesophageal reflux or candidiasis).


Dysphagia can occur due to problems in the oropharynx or oesophagus (Fig. 22.15). Oropharyngeal disorders affect the initiation of swallowing at the pharynx and upper oesophageal sphincter. The patient has difficulty initiating swallowing and complains of choking, nasal regurgitation or tracheal aspiration. Drooling, dysarthria, hoarseness and cranial nerve or other neurological signs may be present. Oesophageal disorders cause dysphagia by obstructing the lumen or by affecting motility. Patients with oesophageal disease complain of food ‘sticking’ after swallowing, although the level at which this is felt correlates poorly with the true site of obstruction. Swallowing of liquids is normal until strictures become extreme.


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Fig. 22.15 Investigation of dysphagia.



Dyspepsia


Dyspepsia describes symptoms such as discomfort, bloating and nausea, which are thought to originate from the upper gastrointestinal tract. There are many causes (Box 22.14), including some arising outside the digestive system. Heartburn and other ‘reflux’ symptoms are separate entities and are considered elsewhere. Although symptoms often correlate poorly with the underlying diagnosis, a careful history is important to detect ‘alarm’ features requiring urgent investigation (Box 22.15) and to detect atypical symptoms which might be due to problems outside the gastrointestinal tract.



image22.14   Causes of dyspepsia





image22.15   Alarm features in dyspepsia




Dyspepsia affects up to 80% of the population at some time in life and most patients have no serious underlying disease. Patients who present with new dyspepsia at an age of more than 55 years and younger patients unresponsive to empirical treatment require investigation to exclude serious disease. An algorithm for the investigation of dyspepsia is outlined in Figure 22.16.


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Fig. 22.16 Investigation of dyspepsia.



Vomiting


Vomiting is a complex reflex involving both autonomic and somatic neural pathways. Synchronous contraction of the diaphragm, intercostal muscles and abdominal muscles raises intra-abdominal pressure and, combined with relaxation of the lower oesophageal sphincter, results in forcible ejection of gastric contents. It is important to distinguish true vomiting from regurgitation and to elicit whether the vomiting is acute or chronic (recurrent), as the underlying causes may differ. The major causes are shown in Figure 22.17.


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Fig. 22.17 Causes of vomiting.

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