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Yr 3 Sem 1 > Week 4 Common Conditions > Flashcards

Week 4 Common Conditions Flashcards

1
Q

What is constipation?

A

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

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2
Q

What is the aetiology of constipation? (5)

A

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

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3
Q

What is the management of constipation?

A

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

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4
Q

What is the role of osteopathy in constipation?

A

Visceral techniques

Implications for patient teaching (sitting posture vs squatting posture)

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5
Q

What are the different types of laxatives?

A

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)

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6
Q

What is diarrhoea (acute and chronic)?

A

Acute diarrhoea
Sudden onset of >3 loose stools/day
Lasts less than 14 days

Chronic diarrhoea
Present for at least four weeks

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7
Q

What are the common aetiologies of acute and chronic diarrhoea?

A

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

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8
Q

What are features of diarrhoea warranting concern & referral?

A

Severe/worsening diarrhoea in Pts >70 yrs or immunocompromised
Bloody/mucoid/purulent diarrhoea
Diarrhoea accompanied by severe abdominal pain or signs of infection

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9
Q

What is the management of diarrhoea?

A

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)

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10
Q

What is IBS?

A

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

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11
Q

What are the proposed mechanisms of IBS?

A

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

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12
Q

What are the clinical features of IBS?

A

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

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13
Q

What is the management of IBS?

A

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

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14
Q

What is diverticular disease?

A

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)

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15
Q

What is the aetiology of diverticular disease?

A

A diet low in roughage (higher intraluminal pressures required to move stool)
Vegetarians have a threefold less chance of developing diverticula

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16
Q

What is the pathophysiology of diverticular disease?

A

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

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17
Q

What are the complications of diverticular disease?

A

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

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18
Q

What are the clinical features of diverticular disease?

A

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

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19
Q

What is the management of diverticular disease?

A

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

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20
Q

What are haemorrhoids?

A

Internal haemorrhoid: varicosity of the superior rectal vein (proximal to pectinate line)

External haemorrhoid: varicosity affecting the perianal venous plexus (distal to pectinate line)

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21
Q

What are the classifications of haemorrhoids?

A

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

22
Q

What is the aetiology of haemorrhoids?

A

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

23
Q

What are the clinical features of haemorrhoids?

A

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

24
Q

What are the complications of haemorrhoids?

A

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

25
Q

What is the management of haemorrhoids?

A

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

26
Q

What is appendicitis?

A

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

27
Q

What is the aetiology of appendicitis?

A

? 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

28
Q

What is the pathophysiology of appendicitis?

A

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

29
Q

What are the clinical feature of appendicitis?

A

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

30
Q

What is the management of appendicitis?

A

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

31
Q

What is inflammatory bowel disease?

A

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

32
Q

What is ulcerative colitis?

A

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

33
Q

What is the aetiology of ulcerative colitis?

A

Exact cause is undetermined
Genetic, immunological & infectious factors are usually involved

Autoimmune dysfunction:
Anti-colon antibodies
Increased levels of inflammatory cytokines: TNF-α, Interleukins

34
Q

What is the pathophysiology of ulcerative colitis?

A

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

35
Q

What are the clinical features of ulcerative colitis?

A

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
36
Q

What is Chron’s disease?

A

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

37
Q

What is the aetiology of Chron’s disease?

A

As for UC, there is strong evidence of autoimmune involvement
Dysregulation of humoral & cell mediated immunity

Bacterial flora
Susceptibility genes

38
Q

What is the pathophysiology of Chron’s disease?

A

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

39
Q

What are the clinical features of Chron’s disease?

A

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

40
Q

What are the extra-intestinal manifestations of IBD?

A 
Ankylosing spondylitis
Biliary Tree Disorders (cirrhosis, stones)
Eye Disorders (conjunctivitis)
Renal Disorders (stones)
Skin Disorders (erythema nodosum)
41
Q

What are the complications of IBD?

A

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

42
Q

What are the medications for IBD?

A

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

43
Q

What is the management of IBD?

A

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

44
Q

What are intestinal malignancies?

A

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)

45
Q

Describe colorectal carcinoma

A

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?

46
Q

What is the aetiology of colorectal carcinoma? (4)

A

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

47
Q

What is familial adenomatous polyposis?

A

Uncommon autosomal dominant disorder (1/8,000) that results in numerous polyps throughout the bowel

In FAP, polyps undergo malignant change in ~15 yrs

48
Q

What is the risk of familial adenomatous polyposis?

A

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

49
Q

What is the pathophysiology of familial adenomatous polyposis?

A

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.

50
Q

What are the clinical features of familial adenomatous polyposis?

A

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

51
Q

What is the management of familial adenomatous polyposis?

A

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

Yr 3 Sem 1 (7 decks)

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