Week 4 Common Conditions Flashcards
What is constipation?
Common problem: affects ~1/3 population
Several definitions exist:
A bowel movement less frequent than three times a week
Production of a stool which is hard, difficult to pass or painful to pass
Consistency more significant than frequency for diagnosis
The Rome III Criteria (Chronic Functional Constipation):
Requires 2 or more of the following features
Must apply to at least 25% of bowel motions, over a 3 month period
Straining or manual manoeuvres required to facilitate evacuation
Lumpy/hard stools or if loose stools rare without laxatives
Sensation of incomplete evacuation or anorectal blockage
< 3 bowel movements each week
What is the aetiology of constipation? (5)
Dietary factors
e.g. diets low in fibre or water
Lifestyle factors
e.g. sedentary lifestyles
Medication side effects
e.g. analgesics, anti-depressants, iron supplements, diuretics
Psychological & neurological factors
e.g. chronic stress, ignoring the urge to defecate
Organic diseases & metabolic problems
e.g. diverticular disease, GIT malignancies, IBD, hypothyroidism
What is the management of constipation?
Features warranting concern & referral:
Onset in middle age or old age
PR bleed, melena or mucous
Weight loss, fever, rectal pain, anorexia, nausea, vomiting
Family history of colorectal cancer
Targeted management:
Increase fibre & water intake*
Introduce gentle exercise
*Implications for Pt education:
Rapid fibre increases can result in diarrhoea & flatulence
Drug regime modification
Address psychological issues e.g. managing stress
Use of biofeedback or neuromuscular retraining
What is the role of osteopathy in constipation?
Visceral techniques
Implications for patient teaching (sitting posture vs squatting posture)
What are the different types of laxatives?
First-line therapy: Bulking agents e.g. psyllium
Mechanism: increase faecal bulk which stimulates peristalsis
First-line therapy: Osmotic laxatives e.g. lactulose, glycerol
Mechanism: exerts osmotic effect which increases intraluminal pressure
Stool softeners e.g. doccusate
Mechanism: promote the retention of water in faecal matter
Bowel stimulants e.g. senna, bisacodyl
Mechanism: direct stimulation of nerve endings in colonic mucosa
Avoid long-term use
Opioid antagonists e.g. naloxone
Mechanism: competitive antagonist at GIT opioid receptors
May encounter these in patients receiving opioid therapy
Combined preparations exist e.g. Targin (oxycodone/naloxone)
What is diarrhoea (acute and chronic)?
Acute diarrhoea
Sudden onset of >3 loose stools/day
Lasts less than 14 days
Chronic diarrhoea
Present for at least four weeks
What are the common aetiologies of acute and chronic diarrhoea?
ACUTE
Infectious gastroenteritis/enteritis
Bacterial: Salmonella, E. coli
Viral: Rotavirus, Norwalk virus
Dietary issues
e.g. food allergies, binge-eating
Adverse drug reactions
e.g. antibiotics
CHRONIC
Chronic infective diarrhoea
Human immunodeficiency virus
Intestinal disorders
e.g. IBS, IBD, Coeliac disease
Adverse drug reactions
e.g. alcohol abuse
What are features of diarrhoea warranting concern & referral?
Severe/worsening diarrhoea in Pts >70 yrs or immunocompromised
Bloody/mucoid/purulent diarrhoea
Diarrhoea accompanied by severe abdominal pain or signs of infection
What is the management of diarrhoea?
Treatment/management of the causative factor (investigate if not known)
Rehydration & electrolyte replacement (IV therapy required in severe cases)
Antibiotics: for proven bacterial infections
Depending on the underlying disorder - anti-diarrhoeal agents
Synthetic Opioids e.g. loperamide
Mechanism: acts of GIT opioid receptors (reduces peristalsis)
Does not cross BBB (low potential for abuse)
What is IBS?
Functional bowel disorder consisting of abdominal discomfort and constipation or diarrhoea (or an alternation between both)
INCIDENCE
Most common bowel disorder in Western countries
Affects ~10% Australians, greater prevalence in women 20-40
What are the proposed mechanisms of IBS?
Hyperexcitability of ENS; disturbed ANS/CNS processing
Abnormal intestinal motility & secretion
In some people there is a correlation between symptoms and:
Certain foods
Recent intestinal infections or intestinal flora overgrowth
Emotional factors e.g. stress
What are the clinical features of IBS?
Abdominal pain or discomfort
Commonly in the Rt or Lt iliac region, or hypogastrium
Usually relieved by defecation
Variable bowel habit
Predominant constipation/diarrhoea
Alternating constipation/diarrhoea
Abdominal distension, excessive flatus & borborygmi
Nausea, cramping, tenesmus
What is the management of IBS?
Reassurance that there is no serious underlying pathology
Appropriate strategies to manage the constipation & diarrhoea
Food elimination approaches are helpful in some cases
Pharmacological agents
In addition to the aperients & anti-diarrhoeal agents previously mentioned
Serotonin-receptor modulators
5HT4 receptor agonists (severe constipation)
5HT3 receptor antagonists (severe diarrhoea)
Anti-spasmodics
Hyoscine butylbromide
Mechanism: muscarinic receptor antagonist
Meberverine
Mechanism: direct relaxing effect on GIT smooth m. (anaesthetic properties)
Also has weak anti-muscarinic action
What is diverticular disease?
DEFINITION: Presence of saccular outpouching in the wall of the colon, synonymous with diverticulosis
If the pouches become inflamed the process is called diverticulitis
INCIDENCE:
5-10% across all ages, 30 - 50% in those aged over 60
Lower in non-Western countries (? dietary differences)
What is the aetiology of diverticular disease?
A diet low in roughage (higher intraluminal pressures required to move stool)
Vegetarians have a threefold less chance of developing diverticula
What is the pathophysiology of diverticular disease?
Recall the longitudinal muscle layer of the colonic wall
The thickness of this layer is not uniform around its circumference (teniae coli)
Weaker areas of the wall exist where arteries penetrate the circular muscles to nourish the mucosal layer
These areas are the characteristic sites for outpouching
Diverticula are most are often are found in parallel rows (however, a single diverticulum can exist)
Most common site is the sigmoid colon
What are the complications of diverticular disease?
Diverticulitis
Acute inflammation of the diverticula (? due to faecal retention)
Abscess formation
Abscess: collection of pus
Can perforate the bowel wall leading to peritonitis
Fistula formation
Fistula: abnormal connection between two hollow structures
Occurs when the abscess penetrates neighbouring organs
Potential fistulae: colovesical, colovaginal, coloenteric
Fibrosis
Can result in bowel obstruction
Haemorrhage
What are the clinical features of diverticular disease?
Most cases of diverticulosis are asymptomatic
Pain & tenderness: left iliac fossa
Change of bowel habit:
Constipation alternating with diarrhoea
Increasing constipation
Acute diverticulitis: severe pain, guarding, rigidity
Abscess formation: palpable mass
What is the management of diverticular disease?
Asymptomatic diverticulosis
High-fibre diet & increased H2O to bulk up stool
Acute diverticulitis
Antibiotics, analgesia & anti-inflammatories
I.V. fluids, possibly naso-gastric suction
Usually the inflammation resolves
SURGERY
Sometimes a temporary colostomy is required to rest the bowel
Also indicated to treat fistulae or bowel obstructions
What are haemorrhoids?
Internal haemorrhoid: varicosity of the superior rectal vein (proximal to pectinate line)
External haemorrhoid: varicosity affecting the perianal venous plexus (distal to pectinate line)
What are the classifications of haemorrhoids?
First degree
Vein is distended and may bleed, but remains internal
Second-degree
Prolapse during defecation, but spontaneously reduce
Third-degree & fourth-degree
Remain protruding after defecation
What is the aetiology of haemorrhoids?
Any factor that increases venous pressure can cause the vein wall to become distended
Low-fibre diet (most common cause)
Increased intraluminal pressure req’d to evacuate stool
Chronic cough, obesity, pregnancy, obstruction e.g. neoplasia
Inherited valve incompetence
INCIDENCE
Very common disorder – the incidence increases with age
UK: 50% of adults > 50 years
~300,000 Australians receive treatment for haemorrhoids/year
What are the clinical features of haemorrhoids?
Bright red bleeding common (noted around the stool/toilet paper)
Prolapse may be described
Pain: quality varies depending on location.. recall the n. supply of the anal canal
Dull vs. sharp
What are the complications of haemorrhoids?
Strangulation
Irreducible haemorrhoids compressed by anal sphincter
Patients with acute pain
Thrombosis: acute pain, tender swelling +/- infection, ulceration, gangrene
Healing with fibrosis: can result in skin tags and an increased risk for anal fissures
Persistent blood loss: iron deficiency anaemia
What is the management of haemorrhoids?
Rectal examination
Sigmoidoscopy/colonoscopy to exclude other causes of bleeding
Symptom relief
Oral or topical preparations (ointments, suppositories) to reduce pain &/or inflammation
Hydrocortisone/Cinchocaine Ointment
Corticosteroid combined with local anaesthetic
Increasing dietary fibre: reduces the need for surgical intervention
What is appendicitis?
DEFINITION: Inflammation of the appendix
INCIDENCE
Most common surgical emergency of the abdomen
Affects 7-12% of the population
Can develop at any age, peak age for diagnosis 20-30 years
What is the aetiology of appendicitis?
? Exact causative mechanism
Most common theory relates to obstruction of the lumen and consequent bacterial infection
Obstruction due to stool (faecolith), tumour or foreign body
What is the pathophysiology of appendicitis?
Obstruction of the lumen prevents proper drainage
As mucosal secretions continue, intraluminal pressure increases (decreases mucosal blood flow)
Hypoxia-induced ulceration promotes bacterial invasion & inflammation
Gangrene develops from thrombosis of the luminal blood vessels, followed by perforation of the appendix
Complications: Peritonitis, abscess formation
What are the clinical feature of appendicitis?
Abdominal pain
Initially vague, constant and felt in the gastric or peri-umbilical region
Increases over 3-4 hours
Visceral pain is replaced by intense somatic pain in the RLQ
Mediated by a different neural pathway (thoracoabdominal nerves)
Indicates extension of inflammation to parietal peritoneum
The somatic pain is sharp, well-localised and sensitive to stretch
e.g. inspiration, rebound tenderness
Common: Nausea, vomiting, anorexia and fever
Bowel habit can vary from diarrhoea to a sensation of constipation
What is the management of appendicitis?
Appendectomy
For simple or perforated appendicitis
Laparoscopic or open
Antibiotic therapy
Alternative to surgery
Some evidence: resolution of mild-moderate appendicitis with antibiotics alone
However, it carries a risk of recurrence and the factors leading to the failure of antibiotic therapy are not well known
Usually reserved for patients too frail to undergo surgery
What is inflammatory bowel disease?
Ulcerative colitis & Crohn’s disease are referred to as the inflammatory bowel diseases
Affect > 75, 000 Australians
Common to both diseases:
Genetic predisposition
Autoimmune dysfunction
Abnormal gut microflora
10-20% of cases – not possible to distinguish which disease is involved
What is ulcerative colitis?
A chronic inflammatory disease that causes ulceration of the colonic mucosa, usually in the rectum & sigmoid colon
INCIDENCE:
Affects ~33,000 Australians
Peak age for diagnosis 20-40 years
What is the aetiology of ulcerative colitis?
Exact cause is undetermined
Genetic, immunological & infectious factors are usually involved
Autoimmune dysfunction:
Anti-colon antibodies
Increased levels of inflammatory cytokines: TNF-α, Interleukins
What is the pathophysiology of ulcerative colitis?
Inflammation begins at the crypts of large intestine, but does not usually spread beyond the submucosa
Most severe at rectum & sigmoid colon (40% of cases spread to the appendix, terminal ileum rarely affected)
Mucosa becomes swollen & hyperaemic (contains excess blood and readily bleeds)
Small erosions form and develop into ulcers (mucosa adopts a ragged appearance)
Healing with fibrosis leads to pseudopolyp formation (clumps of granulation tissue)
Oedema & thickening of the muscularis narrows the lumen
What are the clinical features of ulcerative colitis?
Initial attack is most severe
Subsequent course involves remissions & exacerbations (vary in intensity)
Large volumes of watery diarrhoea +/- blood, mucous, pus
Paradoxically, there may be constipation (due to strictures or reflex bowel spasm)
Lower abdominal pain, tenderness or cramping
Proctitis leads to tenesmus
Severe episodes > 20 bowel motions/day Dehydration, tachycardia Fever (interleukin = endogenous pyrogen) Anaemia
What is Chron’s disease?
A chronic inflammatory disorder that can affect any part of the GIT from the mouth to the anus
INCIDENCE
Affects 28,000 Australians (lower incidence than UC)
Peak age for diagnosis 20 – 40 years
What is the aetiology of Chron’s disease?
As for UC, there is strong evidence of autoimmune involvement
Dysregulation of humoral & cell mediated immunity
Bacterial flora
Susceptibility genes
What is the pathophysiology of Chron’s disease?
Inflammation begins in the submucosa and spreads to involve the entire thickness of the intestinal wall
Most common sites: terminal ileum, ascending colon & transverse colon
Skip lesions: inflammation can affect some regions of the GIT but not others (rectum is seldom involved)
Chronic inflammation leads to the development of granulomas (clusters of modified macrophages)
These occur in the gut wall, mesentery & mesenteric lymph nodes
The intestinal wall adopts a cobblestone appearance, due to lines of ulceration surrounding areas of mucosal swelling
What are the clinical features of Chron’s disease?
Will vary - depending on site affected, extent and duration of disease
Early stages may mimic irritable bowel, or even a peptic ulcer
Diarrhoea: most common symptom
If colon affected: blood, pus, mucous
Weight loss and abdominal pain
If small bowel affected: issues related to malabsorption
Steatorrhoea
Hypoalbuminaemia
Vitamin D
Vitamin B12
Iron
What are the extra-intestinal manifestations of IBD?
Ankylosing spondylitis Biliary Tree Disorders (cirrhosis, stones) Eye Disorders (conjunctivitis) Renal Disorders (stones) Skin Disorders (erythema nodosum)
What are the complications of IBD?
Risk for colorectal cancer: increased in both UC & CD
Bowel obstruction
Repeated inflammation fibrosis
Features of acute obstruction: colicky pain, vomiting, nausea, excessive borborygmi
UC - Toxic megacolon
If ulceration is severe enough to affect muscularis
Results in dilated, atonic section of bowel
CD - Chronic anal fissures, fistula development
Coloenteric, colovesical, colovaginal
What are the medications for IBD?
Anti-inflammatory agents
Corticosteroids e.g. prednisolone, budesonide, hydrocortisone
Oral: enteric-coated, sustained-release tables
Suppository/enema
5-Aminosalicylic Acid (5-ASA)
Sulphasalazine (prodrug) is hydrolysed to 5-ASA in the colon
Mechanism: prostaglandin synthesis inhibitor
Biological agents
Anti-TNFa antibodies e.g. infliximab (chimeric Ab), adalimumab (human Ab)
Mechanism: targets & reduces levels of the cytokine TNFa.
Immunosuppressants
e.g. methotrexate, cyclosporin, azathioprine
Anti-diarrhoeal agents
What is the management of IBD?
Regular endoscopic surveillance
CD: dietary management for malabsorption
High protein, high energy diet recommended
Supplementation for specific deficiencies
Severe Exacerbations:
Hospitalisation required
Rehydration, plasma or blood transfusions
Exclusive enteral nutrition: useful in achieving remission
Sometimes total parenteral nutrition may be necessary
What are intestinal malignancies?
Despite its length, cancer affecting the small bowel is rare (difference due to transit times?)
Large bowel: slow transit rate (greater exposure of mucosa to potential carcinogens)
Describe colorectal carcinoma
Accounts for > 90% of intestinal malignancies
2nd most common malignancy overall & 2nd highest cause of cancer-related deaths
Overall risk: 1 in 11 (M) and 1 in 16 (W)
Peak age for diagnosis: late 60s
Incidence is dropping in women, but still rising in men
Failure of men to change their diets?
What is the aetiology of colorectal carcinoma? (4)
Like most cancers, CRC arises from complex interplay between environmental & genetic factors
Dietary factors: Low-fibre diets, high-fat diets, diets high in charred red meats
Smoking
Inflammatory bowel disease
Familial component
Increased risk if a first-degree relative has had CRC
Familial adenomatous polyposis
Polyp: benign, finger-like projection of mucosal epithelium
What is familial adenomatous polyposis?
Uncommon autosomal dominant disorder (1/8,000) that results in numerous polyps throughout the bowel
In FAP, polyps undergo malignant change in ~15 yrs
What is the risk of familial adenomatous polyposis?
The general population has a 1 in 10 -15 risk for CRC
Those with a first-degree relative have a 1 in 3 risk
100% of those with FAP will develop CRC by age 40-50
What is the pathophysiology of familial adenomatous polyposis?
Most tumours develop in pre-existing adenomatous polyps
Risk of malignancy increases with polyp size
50% chance of finding neoplastic cells in polyps >4cm
Most common sites: rectum (M), sigmoid colon (F)
Caecum & ascending colon next most common for both sexes.
What are the clinical features of familial adenomatous polyposis?
Malignant polyps can ulcerate: bloody or mucoid diarrhoea
Distal bowel - frank blood
Proximal bowel – occult blood
Caecal tumours – asymptomatic until large
Alternatively, a large polyp can restrict the bowel lumen: constipation
Lower abdominal pain: can vary from vague discomfort to colic
Palpable mass
Non-specific features
Features of metastasis (direct spread, lymphatics, blood)
Liver mets are especially common
What is the management of familial adenomatous polyposis?
Diagnosis: colonoscopy with biopsy
Surgical resection is the only definitive treatment.
Polyp – endoscopic mucosal resection
Simple resection w. end-to-end anastomosis
Temporary/permanent colostomy
Radiotherapy & chemotherapy: adjuncts to surgery or palliation
SCREENING
Faecal occult blood test & endoscopy
FAP: regular endoscopy starting age 10
If first-degree relative has had CRC – from age 25
General population: routine endoscopy every 5 years after age of 40
