Upper GI tract Flashcards

1
Q

Define hiatus hernia with regard to anatomical type (sliding and paraoesophageal).

A

Sliding - Cardia and some of the fundus slide superiorly into the thorax.
Paraoesophageal - a pouch of the peritoneum, often containing the fundus of the stomach extends through the oesophageal hiatus (also contains vagus nerve) anterior to the oesophagus.
Bochdalek and Morgagni are congenital hernias due to diaphragmatic malformation.

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2
Q

List the anatomical and physiological factors predisposing to gastrooesophageal disease.

A

Anatomical: Trauma, obesity, pregnancy, diaphragm malformations, poor posture, sphincter dysfunction.
Physiological: Spicy food, NSAIDs, H Pylori, alcohol/smoking, Zollinger-Ellison syndrome.

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3
Q

Name three typical symptoms of gastro-oesophageal reflux disease (GORD).

A

The 3 cardinal symptoms of reflux disease are: Retrosternal burning pain,
Waterbrash/acid regurgitation,
Dysphagia/odynophagia.
Other symptoms include night cough (assoc w/ aspiration), nausea, laryngitis and tooth decay. The pain may be mistaken for angina if it has a spasmodic character to it..

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4
Q

Describe the investigations used to confirm a diagnosis of GORD.

A

Endoscopy used to establish some of the causes: malignancy, Barretts oesophagus, oesophagitis, hiatus hernia.
Barium meal/swallow can diagnose anatomical problems.
Younger patients may be placed on therapy and if the problem subsides, they are diagnosed.
A 24 hour pH test may also be used. If pH drops below 4 for over 6% of the monitored duration, then diagnosis made.

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5
Q

What is the definition of dysphagia?

A

Difficulty or discomfort swallowing.

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6
Q

List the common causes and discuss the main investigations for dysphagia.

A

Intraluminal: Inflammation, malignancy, foreign body, infection.
Intramural: Achalasia, oesophageal spasm, oesophageal web, strictures.
Extramural: Hiatus hernia, malignancy, pharyngeal pouch.
Neuromuscular: Parkinson’s, MG, MS, stroke.

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7
Q

List the symptoms suggestive of an oesophageal malignancy.

A

Progressive dysphagia (first with solids, then liquids).
Weight loss and anorexia (due o increased metabolic demands and dysphagia).
Pain with food impaction.
Lymphadenopathy.
Less common: Early satiety and haematemesis.

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8
Q

Describe the pathology and natural history of a malignant lesion of the oesophagus.

A

Adenocarcinomas - Arise in the lower third of the oesophagus, may be preceded by Barretts oesophagus (metaplasia) caused by chronic acid reflux. They metastasise early to lymph nodes
Squamous cell carcinomas - Arise in the middle section of the oesophagus at the level of the carina (may cause fistulation) or less commonly at the level of the cricoid cartilage (Plumer-Vinson syndrome).
Tumours may narrow the lumen or cause a polypoid mass. In both forms, the tumour grows both proximally and distally in the submucosal lymphatics – meaning the surgeon has to remove the tumour with wide margins.
Risk factors include: Strictures, achalasia, obesity, smoking, alcohol, a diet low in fruit and fish, breast cancer radiotherapy and coeliac disease.

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9
Q

List the main causes of peptic ulcer disease.

A

H.Pylori, Zollinger-Ellison syndrome, NSAIDs, steroids, SSRIs, excess coffee/acid intake, smoking.

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10
Q

Describe the relationship between H.Pylori, smoking and NSAIDs and peptic ulcer disease, and the mechanisms by which they cause peptic ulceration.

A

90% of DU and 70% of GU due to H.Pylori.
H.Pylori may cause gastritis in the antrum by causing a local inflammatory response.
CagA protein inserted into cells causing changes in cell morphology, apoptosis and replication.
VacA causes vacuole formation and suppresses immune function.
This leads to decreased somatostatin release from D cells, decreasing inhibition of gastrin release from G cells. This results in increased acid production by parietal cells.
Smoking decreases mucosal healing.
NSAIDs inhibit COX enzymes, importntly, COX-1 in the stomach, inhibiting prostaglandin synthesis, which decrease acid production and increase bicarbonate and mucus secretion.
Prostaglandins may also increase blood flow to the stomach, increasing healing.

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11
Q

List the symptoms of peptic ulcer disease and discuss differences between gastric and duodenal ulcer.

A

Peptic ulceration causes a localised burning epigastric pain which may radiate to the back. The pain may be worse (GU) or better (DU) upon eating and is most likely worse/only at night. Weight loss/anorexia may accompany this pain. Bleeding/perforation may occur which may be noticed in vomit/faeces, although vomiting is not always present. Perforation into adjacent structures such as the transverse colon may cause fistulation.
The natural history of the disease may take 2 paths.
1 Relapse and remittance over a number of years due to atrophic gastritis and decreased acid secretion.
2 Acutely via anaemia, haematemesis or acute perforation.
DUs tend to occur in a younger demographic, in patients between 45-55 years old, with GUs occurring in 55-65 year olds. DUs are 2-3 times more common than GUs.

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12
Q

Discuss the investigation of peptic ulcer disease and the role of endoscopy.

A

Endoscopy is capable of visualising ulceration and should be given to patients displaying ALARMS<55 symptoms (Anaemia, loss of weight, anorexia, rapid onset, melaena/haematemesis, swallowing problems, age<55).
All ulcers should be biopsied to rule out cancer.
Urea breath test is also used where patients ingest 13C urea and breath out 13C02. Over 96% sensitive and specific for identification of H.Pylori.

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13
Q

List the symptoms, signs of acute upper and lower gastrointestinal bleeding.

A

Cardinal symptoms: Malaena and haematemesis (appear due to a bleed proximal to the caecum).
Haematechezia in haemorrhage or shock may also occur.
In severe intravascular volume depletion postural hypotension may occur.The Rockall and Blatchford scores assess risk of rebleed and mortality on the following criteria: age, co-morbidity, shock, endoscopic Dx, ulcer, chronic liver disease.
Pain may be present.
Signs include pallor and sweating.

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14
Q

Outline conditions where such upper GI haemorrhage can occur

A

 Chronic peptic ulcer (50%) – need to eradicate H. Pylori. If bleeding not controlled, surgical ligation. Adrenaline injection, thermal coagulation and PPI may be indicated.
 Gastric Ca – oozing is difficult to control endoscopically, but not usually large bleeds
 Oesophageal varices (10-20%) should be banded.
 Mallory-Weiss tear (5-10%) – tear at GOJ after sudden IAP increase. Classically seen after
alcoholic “dry heaves”. Most bleeds are minor and discharge w/in 24hrs.
 Bleeding after PCI – 2% of patients undergoing PCI, mortality rate 5-10%. PPI should be given
IV. Difficult to manage, as prevalence of concurrent anti-platelet treatment is high. High
Rockall scores would suggest risk:benefit ratio in favour of stopping anti-platelets.
 Reflux oesophagitis (2-5%)
 Haemorrhagic erosion and gastropathy (15-20%) (rebleed).

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15
Q

Outline the causes of lower GI bleeding.

A

Crohn’s ulcers, diverticula, colon cancer, anal fissures, haemorrhoids, ischaemic colitis, angiodysplasia, polyps.

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16
Q

Risk factors for gastric neoplasm

A
2:1 ratio men:women. 
H. Pylori
Smoking
Pernicious anaemia
High salt diet
Pickled foods
Family history
Blood group A
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17
Q

List the symptoms and signs that would suggest gastric cancer.

A

Nausea and vomiting (severe and frequent)
Epigastric pain (constant and severe, relieved by antacids)
Weight loss
Anaemia via occult blood loss
Palpable Virchow’s lymph node
Palpable epigastric mass
Other symptoms are due to metastasis: Jaundice, ascites, bone pain, epilepsy, SOB.

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18
Q

Describe the classification and morphology of gastric cancers.

A

Majority of gastric cancers are adenocarcinomas (90%) with most of them arising in the antrum.
Type 1 Intestinal- Tubular structures where H.Pylori infection is common.
May have multiple lumens.
Ulcerative or polypoid

Type 2 Diffuse- Signet ring shaped cells which cause linitus plastica and infiltration.
Tightening and thickening of mucosa causes a decrease in stomach capacity.

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19
Q

Describe the natural history of gastric cancers.

A

Gastric cancers may infiltrate through the peritoneum to cause malignant ascites.
Metastasis may occur to the ovary to give “Krukenberg” tumour, or to the umbilicus to give “Sister Mary Joseph’s nodule”.
Other tumours include GIST (GI stromal tumours) primary gastric lymphoma and gastric polyps.

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20
Q

List diagnostic methods used to investigate patients with suspected gastric neoplasia.

A

Gastroscopy and biopsy are used to make diagnosis.

CT used to stage cancer.

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21
Q

Specify a definition of the term “the acute abdomen”.

A

“An acute abdominal condition that causes the patient to be hospitalised within a few hours of the onset of pain.”.

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22
Q

Identify the cardinal symptoms of the acute abdomen.

A

Inflammation - Nausea, Pain
Obstruction - Pain, nausea and vomiting, absolute constipation.
Perforation - Bleeding, peritonitis, pain, hypotension.
Organic pathology - specific signs, referred pain.

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23
Q

List differential diagnoses for Acute RUQ pain

A

Cholecysitis, ascending cholangitis, acute hepatitis, pancreatitis, pleural rub.

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24
Q

List DDx for acute Epigastric pain.

A

GORD, peptic ulcer, MI.

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25
Q

List DDx for acute LIF pain.

A

Diverticulitis, bowel obstruction, gynaecological problems (ruptured/torted ovarian cysts, salpingitis).

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26
Q

List DDx for acute RIF pain.

A

Appendicitis, pyelonephritis, renal colick.

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27
Q

Identify and define the physical findings associated with the acute abdomen and relate these to the basic underlying pathology.

A

Patient may look ill, pale, sweaty, tachycardic with a weak pulse.
Guarding and rigidity suggest peritonitis.
High pitched tinkling sounds suggest fluid obstruction.
Distention suggests obstruction.
Fever may be present.

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28
Q

Select appropriate laboratory and ancillary studies to further define a cause for an acute abdomen.

A

FBC (Hb + WBC), CRP + ESR, lactate, U+Es, serum amylase, pregnancy test.
Erect CXR, Supine AXR, USS, CT, E/MRCP.
Laparoscopy.

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29
Q

Outline the appropriate initial management of a patient with an acute abdomen.

A

ABCDE: IV Fluids, Oxygen, Analgesia.
Insert catheter for fluid balance, NG tube for drain/feeding (patient should be kept NBM).
History and examination should be undertaken and the necessity of theatre assessed.

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30
Q

List the symptoms and signs of acute appendicitis.

A

Dull ache in umbilical region progressing to a sharper pain in the RIF.
Associated N/V
Rebound tenderness at McBurneys point
In perforation - pyrexia, tachycardia, tachypnoea.

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31
Q

Where is McBurney’s point?

A

1/3 way between ASIS and umbilicus.

32
Q

Formulate a differential diagnosis of the conditions that commonly mimic acute appendicitis.

A
Mesenteric lymphadenitis, 
Ovarian cyst rupture, 
Caecal volvulus,
Psoas abscess, 
Diverticulitis,
IBD,
Cancer, 
Pyelonephritis, 
Meckel’s Diverticulum.
33
Q

Outline the diagnostic workup in a patient with suspected appendicitis.

A

WBC, CRP, urine dip.
USS to rule out other diagnoses (esp Gynae)
CT may be used if in real doubt
Diagnosis mainly made clinically.

34
Q

List the laboratory findings that would tend to confirm the diagnosis of appendicitis.

A

Raised CRP and WCC

35
Q

List the complications of a perforated appendix.

A
Abscess (all along paracolic gutter).
Peritonitis
Pyaemia
Sepsis
Death
Peritonitis
Adhesions
Fistula (bladder/rectum).
36
Q

List and discuss the common complications following appendicectomy and explain how each can be prevented.

A
Wound infection
Dehiscence
portal site hernia
Abscess
Adhesions
Death
Stump appendicitis
Haematoma
37
Q

Discuss the pathology of causes of a mass in the right iliac fossa and outline the assessment, investigation and management.

A
Cancer
Psoas abcess
Appendicitis
Pelvic kidney
Crohns
TB/yersinia (Infective pathogens may cause an abscess and or inflammatory granulomatous mass.)
38
Q

Describe the nature of a Meckel’s diverticulum and its possible pathological effects.

A

Most common GI congenital abnormality (affects 2-3% population).
Diverticulum projects from anti-mesenteric border of ileum 60cm from the ileocaecal valve.
May contain gastric mucosa which may secrete HCl, causing peptic ulceration.
Acute inflammation is clinically indistinguishable from appendicitis.
May be visualised with gamma camera scan.
Can be surgically removed via laparoscopy.

39
Q

What is the rule of 2’s applied to Meckle’s diverticulum?

A
2% of the population, 
within 2 feet of the ileocecal valve, 
2 inches in length, 
2 types of heterotopic Mucosa, 
presentation before the age of two.
40
Q

Describe the symptoms in a patient with intestinal obstruction.

A

Abdominal colic
Constipation without passing wind
Vomiting

41
Q

Describe the signs in a patient with intestinal obstruction.

A

Tinkling bowel sounds
Distention
Marked tenderness (strangulation)

42
Q

List the common causes of intestinal obstruction.

A

Intraluminal: Gallstone ileus, faecal impaction, foreign body.
Intramural: Malignancy, IBD, strictures (Crohns), neuromuscular ileus, intussusception (hot dog), diverticular disease.
Extramural: Adhesions, malignancy, volvulus, herniation.

43
Q

Describe the pathology of intestinal obstruction.

A

In acute obstruction, there is good peristalsis followed immediately by immobility and distension. Secretions increase, and absorption decreases – bacteria tend to flourish. Stagnation of the bowel distal to the obstruction (not being flushed out) means bacteria can multiply freely.
In subacute obstruction, there is time for the proximal smooth muscle to hypertrophy and overcome the blockage. Eventually, muscle hypertrophy cannot compensate. Dilation of the bowel follows, with accumulation of swallowed gas and secretions.

44
Q

Discuss the complications of small bowel obstruction including fluid and electrolyte shifts, vascular compromise of the intestine and sepsis.

A

Retroperistalsis - Fluid passes to the stomach where some faecal vomiting occurs. Fluid is alkali causing an acidosis and dehydration.
Pressure - Blood supply to gut is compromised causing ischaemia and release of toxins into peritoneal cavity.
Bacterial proliferation - Bacteria proliferate proximal and distal to the obstruction and cause inflammation to the walls of the bowel eventually causing ulceration - may perforate - peritonitis
Fluid and electrolytes pool in the wall of the oedematous bowel.

45
Q

List the appropriate laboratory and X-ray tests to be employed in a patient with suspected small intestinal obstruction.

A

FBC, U+Es, CRP.
Small bowel - >3cm = dilated. The valvulae conniventes run the whole way across the small bowel. Large bowel - >5cm = dilated. The haustra do not run the whole way across the large bowel.
A barium enema may reveal the site of obstruction if in the large bowel.
A CT or barium follow through may reveal site or cause of small bowel obstruction.

46
Q

In a patient with suspected intestinal obstruction, examine the abdomen and demonstrate clinical findings suggestive of obstruction.

A

Distension; tinkling, hyperactive bowel sounds; tenderness (suggestive of strangulation). The rectum will be devoid of faecal matter.

47
Q

Describe symptoms that may suggest a diagnosis of IBS.

A

Abdomen pain, diarrhoea/constipation, bloating.
May be associated with non-intestinal symptoms such as:
Headache
Fatigue
Pain during sex
Urological (frequency, urgency, incomplete emptying, nocturia.)
Back pain
Halitosis

48
Q

Describe the pathology of Crohn’s

A

Can affect mouth to anus.
May contain skip lesions where some areas affected and others not - Cobblestone appearance.
Lesions are transmural, affecting the whole way to the serosa.
When the terminal ileum is involved - it becomes inflammed and thickens and narrows.
Mesentary is oedematous and thick and lymph nodes enlarge.

49
Q

Describe the local consequences of Crohn’s

A

(a) transmural inflammation – adhesions, fistulae.
(b) luminal narrowing – intestinal obstruction.
(c) ileal involvement – malabsorption, especially of B12.
(d) cancer – risk of colonic and small intestinal cancer, but not as high as with UC.

50
Q

Describe the pathology of UC.

A

Begins in the rectum and progresses proximally (20% whole colon affected.)
Rarely appears in perianal region.
Area which is not affected is associated with pseudo-polyps.
Inflammation confined to mucosa, doesn’t penetrate through muscularis mucosae.
Remission periods may occur where ulcers partially heal.

51
Q

Describe the local consequences of UC.

A

(a) toxic megacolon – inflammation becomes very severe and colon thins and dilates greatly. (b) dysplasia and colonic cancer – risk greatly increased, even more so with increased colonic involvement, early onset, and chronic disease.

52
Q

Describe common presenting symptoms of Crohn’s disease.

A

Young adults
Diarrhoea
Abdominal pain
Weight loss

53
Q

Describe common presenting symptoms of ulcerative colitis.

A

Young patients
Bloody diarrhoea
In severe cases: Weight loss and anaemia
Course has remitting and relapsing phases

54
Q

List the extra-colonic manifestations of inflammatory bowel disease.
2 for UC
4 for both

A

UC associated with: Primary sclerosing cholangitis and cholangiocarcinoma.
Both associated with:
Seronegative arthritis of spine and peripheral joints
Eye conditions (conjunctivis, uvetis)
Erythema nodosum
pyoderma gangrenosum

55
Q

List the investigation of a patient with suspected inflammatory bowel disease.
2 bloods
2 other tests

A

FBC (anaemia caused by malabsorption or bleeding.)
CRP inflammation, track progress.
Colonoscopy or sigmoidoscopy to visualise lesions + biopsy.
AXR may show rose thorn lesions (deep linear lesions Crohn’s) and thumb prints (UC).

56
Q

Understand the principle and range of operative procedures used to treat IBD.

A

UC: Operate if toxic megacolon, perforation or increased length increasing cancer risk.
panproctocolectomy and ileostomy
Crohn’s: Surgery to remove complications: strictures, adhesions, obstruction and fissures, abscesses and fistulas.

57
Q

Outline the theories on the aetiology of diverticulosis of the colon.

A

Thickened muscle wall of colon and increased intraluminal pressure results in outpouches of colonic wall.
Diets lacking in fibre and cholonergic denervation may lead to hypertrophy of the muscle and hypersensitivity respectively.

58
Q

Describe the morphology and pathological consequences of diverticulosis of the colon.

A

Weak outpouchings of mucosa surrounded by peritoneum.
If pouch is blocked by faecal matter, diverticulitis occurs.
Inflammation of the pouch may cause, ulceration, perforation, fistulae, abscess, haemorrhage and carcinoma.
Repeated attacks may result in muscle thickening and stenosis.

59
Q

Describe the clinical features of diverticulosis of the colon, differentiating the symptoms and signs from diverticulitis.

A

Diverticulosis is asymptomatic in 95% of cases and picked up on barium meal.
Diverticulitis presents with LIF colicky pain, irratic bowel habits (constipation). Upon examination there will be LIF tenderness and guarding. Fever may also be present.

60
Q

Outline the complications of diverticulosis.

A

Fistulae may form with vagina or bladder, perforation, constipation, bleeding with mucosal inflammation.

61
Q

List environmental risk factors for carcinoma of the large bowel.

A

Diets low in fibre and high animal protein and fat.
Obesity.
Pre existing lesions e.g. IBD

62
Q

List genetic risk factors for carcinoma of the large bowel.

A

FAP - mutation in tumour suppressor gene. Patient develops 1000’s of polyps and develops carcinoma between the age of 30-40.
HNPCC - mutation to mismatch repair genes. Develop carcinoma early and are predisposed to carcinoma of the endometrium, ovary and stomach.

Both are autosomal dominant diseases.

63
Q

What is the most common type of carcinoma of the large bowel and where does it occur?

A

Tubular adenoma 90%
Most commonly occur in the sigmoid colon and rectum.
Start off as benign polyps.

64
Q

Apart from tubular adenomas what other types of colonic carcinoma are there and where do they occur?

A

Mixed tubulovillous polyps occur in 9% of cases and often progress into carcinomas.
Villous adenomas 1%
Occur in the rectum, frond like structure.

65
Q

What do Tubular adenomas look like?

A

Peduncled structures

66
Q

Describe features common in caecal tumours.

A
20% or colorectal cancers
Ulcerating central growth
polypoid, everted edge
Lumen is wide
obstruction uncoomon
Liquid feces
Present late with anaemia, abdominal mass, liver mets.
67
Q

Describe features of recto-sigmoid tumours.

A

50% of tumours.
Stenosing
Narrow lumen
Solid feces
Obstruction is common
Hypertrophy and dilation of proximal bowel.
Present with, altered bowel habits, obstruction, PR bleeding.

68
Q

List the common symptoms suggestive of carcinoma of the colon, rectum and anus.

A
Anaemia
PR bleeding
Weight loss
Abdominal mass
Colicky pain
Obstruction
Tenesmus (constant need to open bowels)
Need to open bowels at night
30% of patients present in an emergency with - Obstruction (80%), perforation (15%) and haemorrhage (5%).
69
Q

Outline the TNM staging system and be able to relate this to possible associated findings on clinical examination.

A

Size of tumour (0-4), number of nodes involved (0-3), yes/no metastases (0-1).

70
Q

Discuss the anatomy of haemorrhoids.

A

The anal canal consists of 3 anal cushions.
They are weakened and sheared by age and the passage of hard stool respectively.
This may cause them to prolapse and due to impaired venous return, become engorged.
They may become further engorged by straining, pregnancy and low-fibre diets.

71
Q

Differentiate internal from external haemorrhoids.

A
Internal: 
Above dentate line
Non painful
Drain to superior rectal artery into venous portal system.
Anal cushions

External
Below dentate line
Painful
Drain to middle and inferior rectal veins into systemic circulation
Innervated by cutaneous branches of pudendal nerve.

72
Q

Describe the symptoms and complications of haemorrhoids.

A

PR bleeding (small amounts of blood on toilet tissue or in bowel)
discomfort
pruritis ani
Pain may occur due to strangulation or thrombosis

73
Q

Describe the physical examination of a patient with haemorrhoids, including proctoscopy.

A

Inspection of the perineum may show large external haemorrhoids at 3, 7 and 11 (left lateral, right posterior, right anterior).

74
Q

Outline the symptoms of patients with perianal infections.

A
Fever
Pain
Swelling
Mass (Abscess)
Discharge
75
Q

Describe the findings on physical examination of patients with perianal infections.

A

If abscess present, a mass may be palpated.

76
Q

Define fissure in ano.

A

A tear to the sensitive skin lining the lower anal canal, below the dentate line.
Most commonly found at 6 o’clock but may occur t 3 o’clock in multi-paritous women.

77
Q

Describe the symptoms and signs of patients with fissure-in-ano.

A

May occur in association with IBD in young patients.
Rectal examination is usually not possible due to pain and rectal spasm (causing pain and preventing healing).
Perianal abscesses and fistulae may be present
Patient may notice small discharging sinus.