GI

Question 1

What is Crohn’s disease?

Answer 1

form of inflammatory bowel disease. It commonly affects the terminal ileum and colon but may be seen anywhere from the mouth to anus

Healthy tissue destroyed, initially around crypts in ulceration of sup mucosa, involves deeper, non caseating granulomas. All layers of intestinal wall, mesentery, LN.

20-40 peak 20-30 + 60-70

Question 2

RF for Crohn’s disease?

Answer 2

FH, abnormal gut flora, smoking, NSAIDs, pill, diet in refined sugar, nutritional def, acute gastritis, measles, paratuberculosis, pseudomonas, listeria, white, not BF.

Question 3

Sx of Crohn’s disease?

Answer 3

Flares + remission
Abdo pain: RLQ, peri-umbilical, partially relieved by defecation
Diarrhoea ± blood, urgency, mucus + pus.
FTT, weight loss, anorexia
Inflam skin, eye, joint lesions, uveitis, erythema nodosum, pyoderma gangrenosum, arthritis
Episcleritis
Aphthous ulcers, angular stomatitis, glossitis
Clubbing
Fatigue + malaise
Temp

Question 4

Complications of Crohn’s disease?

Answer 4

Strictures
Fistulas 
Adhesions 
Bowel obstruction
Perianal disease: abscess, phlegmon, skin tags
Toxic dilation/ megacolon (rarer than in UC) 
Abscess 
Sepsis, perf 
Cancer: colon, anal SCC, small bowel, lung, lymphoma
Fatty liver 
PSC
Cholangiocarcinoma 
Osteomalacia, osteoporosis (CS), 
Malabsorption, anaemia, vit/ min def, dehydration, steatorrhoea 
Renal stones 
Amyloidosis 
Short bowel syndrome after resection

Question 5

Investigations for Crohn’s?

Answer 5

Colonoscopy: early hyperaemia + oedema, discrete deep ulcers, cobblestone, skip lesions. Thickened bowel wall (fibrosis), all layers, goblet cells, granulomas, fat wrapping

FBC: normochromic normocytic anaemia.
Leukocytosis, thrombocytosis.

Iron studies

B12, folate

↓Mg + P due to diarrhoea.

↑CRP + ESR

↑faecal calprotectin

Histology - inflammation in all layers from mucosa to serosa, goblet cells, granulomas

Small bowel enema: strictures (Kantor’s string sign), proximal bowel dilation, rose thorn ulcers, fistulae

MRI for suspected perianal fistulae

Question 6

Treatment of Crohn’s disease?

Answer 6

Stop smoking
Perianal fistula: metronidazole, infliximab

Inducing remission
1st - Glucocorticoids
2nd - Amino salicylates eg sulfasalazine
Resistant: azathioprine, mercaptopurine, methotrexate, infliximab
Metronidazole: isolated perianal disease

Maintaining

• Azathioprine/ mercaptopurine
• TPMT activity assessed before starting methotrexate 2nd line

Attacks
Mild: oral pred
Severe: admit, IV steroids, NBM. Infliximab, adalimumab.

Surgery
Resection of affected tissues
Stricturing terminal ileal disease → ileocaecal resection
Balloon dilation of stricture
Draining seton for complex fistulae
Perianal fistulae - oral metronidazole, infliximab, draining seton if complex
Perianal abscess: incision + drainage.

Question 7

What is Ulcerative colitis?

Answer 7

is a form of inflammatory bowel disease.

Inflammation always starts at rectum (hence it is the most common site for UC), never spreads beyond ileocaecal valve and is continuous.

The peak incidence of ulcerative colitis is in people aged 15-25 years and in those aged 55-65 years.

CD8 activation, destruction of cells in mucosa/ submucosa

Ulcerated areas covered by granulatuion tissue > inflam pseudopolyps

Protective: smoking, appendectomy

AI reaction against colonic flora, molecular mimicry, XS sulphide producing bacteria, HLA-B27, NSAIDS, F>M

Relapses: stress + diet, infections.

Question 8

Features of UC?

Answer 8

usually following insidious and intermittent symptoms. Features include:
bloody diarrhoea
urgency
tenesmus
abdominal pain, particularly in the left lower quadrant
extra-intestinal features - PSC, uveititis, erythema nodosum pyoderma gangrenous, arthritis

Question 9

Complications of UC?

Answer 9

Arthritis, uveitis, iritis, uveitis, episcleritis
Erythema nodosum 
Pyoderma gangrenosum 
PSC 
Conjunctivitis 
Sacroiliitis, ankylosing spondylitis 
Cholangiocarcinoma 
Toxic megacolon 
VTE
Anal fissures 
Perirectal abscess
Fulmant colitis 
Colonic adenocarcinoma 
Benign stricture 
Osteoporosis 
Flares: stress, NSAIDs Abx, cessation of smoking
Amyloidosis

Question 10

Investigations of UC?

Answer 10

Colonoscopy + biopsy: not in severe attacks as can perf, flexible sigmoidoscopy. Mucosa red + bleeds easily. No inflammation beyond submucosa. Widespread ulceration with appearance of polyps (pseudo polyps). Inflammatory cell infiltrate in lamina propria. Crypt abscesses, branching or sparsity, loss of goblet cells and mucin from gland epithelium. Granulomas are infrequent. Sup ulcer/ inflam, whole lumen, starts in rectum, continuous, bowel wall thin/ normal, oedema, fat accumulation + hypertrophy of muscles. Inflam cells in lamina propria

in patients with severe colitis colonoscopy should be avoided due to the risk of perforation - a flexible sigmoidoscopy is preferred

↑faecal calprotectin, ESR, CRP, pANCA/ ASCA may be pos, leucocytosis, thrombocytosis, anaemia.

AXR: assess colonic dilation = lead piping, thumbprinting (large bowel oedem)

Barium enema: loss of haustra, superficial ulceration, pseudopolyps, drain pipe colon in long standing (narrow + short)

Question 11

Management of UC?

Answer 11

Mild to moderate UC:
Topical amino salicylate (mesalazine), + high dose oral AS if extensive
If remission not in 4 wks add oral AS, if more extensive than proctitis, offer high dose topical/ oral CS.
If still not remission > oral CS

Severe colitis: hosp, IV steroids, if 72hrs no improvement, IV ciclosporin or surgery.
Colectomy: only if localised, curative.

Maintenance
Mild/mod flare: topical AS OR oral AS + topical AS OR oral AS.
Left-sided and extensive UC - low maintenance dose of an oral aminosalicylate

Severe/>2 relapses in yr: oral azathioprine/ mercaptopurine

Methotrexate not recommended for management of UC (in contrast to Crohn’s disease)

Question 12

Severity of UC?

Answer 12

The severity of UC is usually classified as being mild, moderate or severe:

mild: < 4 stools/day, only a small amount of blood
moderate: 4-6 stools/day, varying amounts of blood, no systemic upset
severe: >6 bloody stools per day + features of systemic upset (pyrexia, tachycardia, abdo tenderness, distension, decreased bowel sounds, anaemia, raised inflammatory markers, hypoalbuminaemia)

Question 13

What is microscopic colitis?

Answer 13

an inflammation of the large intestine (colon) that causes persistent watery diarrhea.

Idiopathic chronic inflam of colon.

Associated w: celiac, AI, PPIs, NSAIDs, statins, smoking, infection, bile acid not absorbed + irritating lining of colon

Trigger, abnormal collagen met, epithelium dysfunctional, altered barrier function mucosal inflam > ↓Na absorption, ↑Cl secretion > secretory diarrhoea.

Triggers: damage to gut, genes, smoking, age, F>M. Immune system attack healthy cells lining colon.

Lymphocytic or collagenous

Question 14

Sx of microscopic colitis?

Answer 14

Watery diarrhoea, sudden explosive, urgency, incontinence

Abdo pain

Bloating

Weight loss, nausea, dehydration

Anaemia

Question 15

Investigations for microscopic colitis?

Answer 15

Endoscopy: non-specific, normal mucosa

Biopsy: inflam changes in lamina propria, IE lymphocytic infiltration, dense subepithelial collagenous layer.

↑ESR, myeloperoxidase

Question 16

Management of microscopic colitis?

Answer 16

Avoid NSAIDs

Antidiarrheals: loperamide

CS: budesonide, prednisone

Bile acid sequestrants: cholestyramine, if bile acid malabsorption

PPIs: omeprazole

Surgical resection: ileostomy

Biological: infliximab

IS: azathioprine +
mercaptopurine

Cut down caffeine, cut down alcohol, stop smoking

Question 17

What is ischaemic colitis?

Answer 17

occurs when blood flow to part of the large intestine (colon) is temporarily reduced, usually due to constriction of the blood vessels supplying the colon or lower flow of blood through the vessels due to low pressures.

Large bowel watershed areas eg splenic flexure borders of territory suppled by SMA/IMA

Occlusive (embolic/ thrombotic), ↓mesenteric circulation (↓BP, vasospasm)

RF: ↑age, hypercoag (F5 leiden), vasculopathy drugs eg vasopressors, AF, endocarditis, cocaine, HTN, DM, malignancy

Question 18

Features of ischaemic colitis?

Answer 18

May be self limiting

Localised abdo cramping/ tender (usually L side)

Loose, bloody stool

Haematochezia

↓bowel sounds

Guarding, rebound tenderness

Fever

Hypotension

Transient, less severe Sx

Question 19

Complications of ischaemic colitis?

Answer 19

Perf, peritonitis, septic shock, met acidosis, organ failure
Gangrenous bowel
Stricture
Pancolitis
Reperfusion injury
Fatal
Gangrenous mucosa promotes fluid/ electrolyte loss, dehydration, shock

Question 20

Investigations for ischaemic colitis?

Answer 20

XR/CT: obstruction, perf, pneumonitis, thumb printing, (bowel oedema, thickening), double halo, pneumatosis coli, pneumoperitoneum

Colonoscopy: ischaemia (oedema, erythema, friable mucosa), single stripe line (linear, ulcer longitudinal axis), submucosa haem: bluish nodules.

Biopsy: transmural infllam, mucosal atrophy

↑lactate, CK, amylase

Question 21

Management of ischaemic colitis?

Answer 21

Bowel rest, O2, IV fluids, electrolytes

Most recover

Abx

Gangrenous: resus, resection of affected bowel, stoma formation

Question 22

What is mesenteric ischaemia?

Answer 22

decreased or blocked blood flow to your large or small intestine. It can be chronic, due to plaque buildup over time, or acute, due to a blood clot. It can also happen from certain drugs and cocaine.

Acute: embolism, classically have AF
Chronic: rarely clinical Dx, intestinal angina
Paralytic: if ischaemic continues

RF: AF, ^ age, hypercoag, vasopressors, endocarditis, HTN, DM, malignancy, arrhythmias, cardiac catheterisation, cardiopul bypass, vasoconstrictors

Question 23

Sx of mesenteric ischaemia?

Answer 23

Severe sudden
Abdo pain, out of keeping with PE, often postprandial
Rectal bleeding
Diarrhoea
Fever, N/V
Chronic: colicky intermittent abdo pain, post prandial, weight loss, abdo bruit.
Paralytic: more diffuse abdo pain, tenderness, bowel movements ↓, absent BS.
Distension
Fever, tachycardia, tachypnoea
Feculent breath

Question 24

Complications of mesenteric ischaemia?

Answer 24

High mortality
Peritonitis
Gangrenous bowel promotes fluid/electrolyte loss, dehydration, shock
Sepsis: break in epithelial line, bacteria in lumen to get into BV wall + peritoneal space + lymphatics.
Reperfusion injury: influx of O2 into already damaged cell overwhelming, oxidative stress, worsens cell damage.
Ileus
Shock
Organ failure

Question 25

Investigations for mesenteric ischaemia?

Answer 25

↑WBCC, lactic acidosis CT/MR angiography Metabolic acidosis Abdo XR/CT: dilated bowel loops, bowel wall thickening thumbprinting, pneumatosis free intraperitoneal air Leucocytosis, L shift, ↑ haematocrit (dehydration) ↑WCC, Hb, serum lactate, amylase, ALP Laparotomy: abdo exploration

Question 26

Management for mesenteric ischaemia?

Answer 26

Urgent surgery Abx: gentamicin, metronidazole IV fluids, electrolytes, inotropic meds surgery resection of infarcted tissue pain management, bowel rest with decompression Restabilising blood flow through surgery, thrombolytic if clot suspected

Question 27

Causes of upper GI bleed?

Answer 27

``` Peptic ulcer Dx Oesophageal varices Oesophagitis. Mallory-Weiss tear Gastritis/ gastric erosions Drugs: NSAIDs, aspirin, steroids, thrombolytics, anticaog Boerhaave syndrome Gastric varices AVM Dieulafoy’s lesions Upper GI tumours Aortoenteric fistulae Coagulopathy ```

Question 28

Sx of upper GI bleed?

Answer 28

Haematemesis Melena Unaltered blood per rectum > massive GI bleed Glasgow-Blatchford Bleeding score - UGIB need medical intervention - Hb, BUN, initial systolic BP, sex, HR, melena, recent scope, hepatic disease history, cardiac failure present Rockall score - assesses risk of death in UGIB - age, shock, co-morbidities, diagnosis, major stigmata of recent haemorrhage

Question 29

Investigations for upper GI bleed?

Answer 29

FBC: Hb, LFTs, ↑urea (bleed in upper GIT has gone through whole digestive tract + RBCs broken into urea, protein meal) Clotting: INR, PTT Urgent endoscopy Glasgow Blatchford: >6 need endoscopic intervention + transfusion. Blood urea, Hb↓, SBP ↓ Rockall score: after endoscopy, risk of rebleed, mortality Forest classification: T1 spurting/oozing, 100% chance rebleed if no intervention, T2 visible vessel, adherent clot or black spot 50% chance rebleed with no intervention, T3 clean based lesion, no stigmata of bleeding 5-10% chance rebleed if no intervention

Question 30

What is the management of UGIB?

Answer 30

Head down, prevent aspiration, 100% O2 2 large bore cannulas Hb <80 give packed cells Plt <50 transfusion FFP: fibrinogen <1g/L, prothrombin >1.5X than normal Prothrombin complex if warfarin + actively bleeding Rebleed: ↑HR, falling JVP, ↓UO, haematemesis/ melaena (normal to pass decreasing amount of melaena 24hrs post haemostasis) Ocreotide Pts Blatchford 0 considered for early discharge Endoscopy within 24 hrs PPIs if non-variceal bleed

Question 31

Causes of lower GI bleed?

Answer 31

Common: diverticula, colonic angiodysplasia, ischaemic colitis, IBD, infectious colitis, CRC, internal haemorrhoids, anal fissure, colonic polyps, dysentery Uncommon: Meckel’s, radiation induced telangiectasia, Dieufaloy’s lesion, aorto-enteric fistula, vasculitis, hereditary haemorrhagic telangiectasia, blue rubber bleb nevus, anal cancer, rectal ulcer, rectal varices, post-polypectomy bleed, NSAID

Question 32

What is an Aorto enteric fistulae?

Answer 32

A fistula is an abnormal, tubelike connection between two structures inside the body. When the connection is between the aorta and a loop of bowel that is near the aorta it is known as an aortoenteric fistula (AEF) Hx of vascular graft or aortic aneurysm

Question 33

Sx of aorto enteric fistulae?

Answer 33

``` Herald bleed (self limiting) before massive Haematochezia Haematemesis Abdo/ back pain Fever ``` Can cause septic shock Can hear Abdo bruits/ feel pulsatile masses O/E

Question 34

What is peptic ulcer?

Answer 34

Break in sup epithelial cells, penetrate to muscularis mucosa fibrous base, inflam cells

Question 35

RFs for peptic ulcer?

Answer 35

h pylori, NSAIDs, SSRIs, corticosteroids, bisphosphonates, stress (cushing’s ↑ICP, curling severe burns), hyperchlorhydria, smoking, COPD, chronic gastritis, hypergastrinemia (Zollinger Ellison syndrome, neuroendocrine tumour in duodenal wall/ pancreas)

Question 36

Sx of peptic ulcer?

Answer 36

Small punched out hole in mucosa Asymptomatic 70% Epigastric burning, night worse Radiate to back/ L/RUP Antacids/PPI relieve N/V, coffee ground emesis Bloating, belching ALARM S: anaemia, loss of weight, anorexia, recent onset/ progressive, melaena/ haematemesis, swallowing difficulty Abdo guarding, peritonitis

Question 37

Complications of peptic ulcer?

Answer 37

Bleed if erosion into BVs Perf: DU>GU, peritonitis, irritates phrenic N, referred shoulder pain. Gastric outflow obstruction: active ulcer + surrounding oedema or healing ulcer + scarring, vomiting, ingested fluid + food Fistula formation

Question 38

Investigations for peptic ulcer?

Answer 38

Abdo CT: perf pneumoperitoneum, site of perf (discontinuity of wall) Barium meal: fill crater, oedematous collar of swollen mucosa, radiating folds of mucsoa away from ulcer. Endoscopy: gastric (biopsy, 6 from edge + 1 from removed region for H pylori), CLO test (biopsy mixed with urea + pH indicator = colour change if urease activity), white punched out lesion, surrounding hyperaemic mucosa 13C urea breath test: off PPI 14 days prior, urea labelled with carbon-13, after 13 mins, measure 13-CO2 production (by urea producing bacterium). Stool test. Gasrtrin levels

Question 39

Management of peptic ulcer disease?

Answer 39

Discontinue NSAIDs, avoid smoking, alcohol, caffeine e Loose weight if H. Pylori negative - PPIs under healed > Lansoprazole, 30mg BD, ↑PH, better plt activity, pepsin requires acid to be active ↓chance clots digested H pylori triple eradication: 1PPI, 2 Abx metro, clarithro, amox Endoscopic ligation/ coag of bleeding ulcer, adrenaline injection (around vessel, not into vessel, causes vasoconstriction in vessels, prevent fluid absorbed allow time for clotting), clipping Misoprostol in NSAID induced ulcers Erythromycin: ↑gastric mobility, enhances stomach emptying, get rid of blood/ clot

Question 40

What are duodenal ulcers?

Answer 40

Most in duodenal cap, more common than gastric Brunner gland hypertrophy Major RF: H pylori, NSAIDs, steroids, SSRIs Minor: 🡩gastric secretion + gastric emptying, blood group O, smoking.

Question 41

Sx of duodenal ulcers?

Answer 41

Epigastric pain, before meals, or at night, worse when hungry Relieved by eating/ drinking milk Weight gain Pain 2-3hrs after meals

Question 42

Complications of duodenal ulcers?

Answer 42

Post wall ulcers more common to bleed due to proximity to vessel (gastroduodenal artery) Gastroduodenal a can be source of significant GI bleed

Question 43

Investigation of duodenal ulcer?

Answer 43

Infection of antrum: causes hyper section if gastrin release, damages duoneal mucosa If suspect perf: upright erect CXR Tests for peptic ulcers

Question 44

Causes of gastric ulcer?

Answer 44

Elderly More common lesser curve near incisura RF: h pylori, NSAIDs, reflux of duodenal contents, delayed gastric emptying, stress

Question 45

Sx of gastric ulcer?

Answer 45

Asymptomatic Epigastric pain - worsened by eating Weight loss Whilst eating or shortly after

Question 46

Complications of gastric ulcer?

Answer 46

Infection of body of stomach: release of urea, inflam response, gastritis, cellular apoptosis > loss of parietal cells, decrease acid production > get 2° hypergastrinaemia

Question 47

Summary of peptic ulcer disease perforation?

Answer 47

Sx - epigastric pain, later becomes generalised, patients may describe syncope Ix - largely clinical diagnosis, upright chest x-ray (free air under diaphragm)

Question 48

Management of acute bleeding of peptic ulcer disease?

Answer 48

ABC approach as with any upper gastrointestinal haemorrhage IV proton pump inhibitor the first-line treatment is endoscopic intervention if this fails (approximately 10% of patients) then either: urgent interventional angiography with transarterial embolization or surgery

Question 49

What is gastritis?

Answer 49

Inflammation of the lining of the stomach. Acute: inflam of gastric mucosa. CS, NSAIDs, uraemia, H pylori, alcohol, smoking, caffeine, physiological stress. Atrophic gastritis: chronic inflame of gastric mucosa, epithelial metaplasia, mucosal atrophy, gland loss. infections (80%): h pylori, AI against intrinsic factor, H+/K+ ATPase, inhib gastric acid secretion. Damage limited to fundus. HLA-DR3, B8.

Question 50

Sx of gastritis?

Answer 50

Asymptomatic Epigastric pain N/V Loss of appetite Heartburn Haemorrhage, haematemesis, melena.

Question 51

Complications of gastritis?

Answer 51

AI: iron def anaemia, Pernicious anaemia - gastric parietal cells Bleeding Stomach ulcers Gastric AC Neuroendocrine Ca

Question 52

Investigations for gastritis?

Answer 52

Infection: normal gastrin level, no hypochloridria, no anti-parietal cell/ anti IF Ig AI: hypergastrinemia, hypochloridria, ↓IF Endoscopic biopsy: nonspecific, mucosal erosions, erythema, lack of rugae. Infectious atrophic: multifocal atrophy, ulcers, erythematous, nodular mucosa, thickened rugae early, loss of rugae late damage limited to antrum. AI: diffuse atrophy, absent rugae, mucosal thinning, visible submucosal BVs. H pylori detection: urea breath test, stool antigen test, biopsy

Question 53

Management of gastritis?

Answer 53

Remove offending agents Eradicate H pylori - triple eradication PPIs, antacids, H2 blocker Correct vit def, for AI

Question 54

What is oesophagitis?

Answer 54

is an inflammation of the lining of the gullet (oesophagus). In most people it is caused by the digestive juices from the stomach, repeatedly moving upwards (reflux) into the lower oesophagus producing redness and ulceration. GORD Infection: candida Eosinophilic infiltration: food allergies, Corrosive meds: NSAIDs, tetracycline, doxy, bisphosphonates. Radiotherapy, NG tube

Question 55

Sx of oesophagitis?

Answer 55

Heartburn Lump in throat Hoarseness Chest discomfort Odynophagia Dysphagia N/V abdo pain Associated with haitus hernia, 80% sliding hernias, 20% rolling hernias.

Question 56

Investigations for oesophagitis?

Answer 56

FBC: ↑eosinophils Endoscopy

Question 57

Management of oesophagitis?

Answer 57

PPIs Avoid cause Treat infection

Question 58

What are oesophageal varices?

Answer 58

are enlarged veins in the esophagus. They're often due to obstructed blood flow through the portal vein, which carries blood from the intestine, pancreas and spleen to the liver. Usually a large volume of fresh blood. Swallowed blood may cause melena. Often associated with haemodynamic compromise. May stop spontaneously but re-bleeds are common until appropriately managed. Dilated veins at junction between portal + systemic venous system. Distal oesophagus ± prox stomach, can be distal stomach + S+L intestine. Blocked flow to liver, collat circulation in lower oesophagus to areas of lower pressure, veins distended + thinner walls Portal HTN Prehepatic: portal vein thrombosis/obstruction (atresia/ stenosis), decreased portal blood flow (fistula), decreased splenic flow. Intrahepatic: cirrhosis, idiopathic portal HTN, acute hepatitis, schistomiasis, congen hepatic fibrosis, myelosclerosis Posthepatic: compression Budd-Chiari syndrome, constrictive pericarditis

Question 59

Sx of oesophageal varices?

Answer 59

Haematemesis Melaena Abdo pain Features of LD Dysphagia/ odynophagia Confusion 2° to encephalopathy Pallor ↓BP ↑HR ↓UO ↓GCS

Question 60

Complications of oesophageal varices?

Answer 60

^ risk of bleed: decompensation of LD, malnourishment, alcohol, physical exercise, circadian rhythms, ↑abdo pressure, aspirin, NSAIDs, bacterial infection. Large varices with red spots are at highest risk of rupture. TIPs: exacerbation of hepatic encephalopathy is common complication

Question 61

Investigations of oesophageal varices?

Answer 61

FBC: low Hb + platelets, MCV high, normal or low. WCC low Clotting including INR Renal function, LFTs Endoscopy

Question 62

Management of oesophageal varices?

Answer 62

Prophylaxis of haem: propranolol, endoscopic variceal band ligation at 2 wk intervals until all varices eradicated. Terlipressin Octreotide Prophylactic IV Abx: quinolones Endoscopy: variceal band ligation, Sengstaken-Blakemore tube if uncontrolled haem, TIPS (connects hepatic vein to portal vein), balloon tamponade salvage Tx for uncontrolled haem

Question 63

What is Mallory Weiss tear?

Answer 63

Typically brisk small to moderate volume of bright red blood following a bout of repeated vomiting. Malena rare. Usually ceases spontaneously. Tear of mucosa + submucosa (not muscular), commonly at point where oesophagus + stomach meet. Severe vomiting, straining coughing, seizures, blunt abdo injury, NG tube placement, gastroscopy. RF: alcoholism, bulimia, food poisoning, hiatal hernia, NSAIDs, M>F, hyperemesis gravidarum

Question 64

Sx of Mallory Weiss tear?

Answer 64

Haematemesis after ep of violent retching/ vomiting Bright red Melena Bleeding may cease after 24-48 hrs Epigastric Back pain ↑HR ↓BP (not usually)

Question 65

Investigation of Mallory Weiss tear?

Answer 65

Endoscopy: red longitudinal break in mucosa, may be covered y clot Hb, haematocrit

Question 66

Management of Mallory Weiss tear?

Answer 66

Supportive: IV PPIs, antiemetics Surgery: endoscopy, cauterisation, haemoclips, endoscopic band ligation, arterial embolization

Question 67

What is Boerhaave's syndrome?

Answer 67

a spontaneous rupture of the oesophagus that occurs as a result of repeated episodes of vomiting, ↑ intraoesophageal pressure + neg intrathoracic pressure. The rupture is usually distally sited and on the left side. Causes - Vomiting/ retching, caustic ingestion, infectious ulcers, Barrett’s, eosinophilic oesophagitis, stricture dilation

Question 68

Sx of Boerhaave's syndrome?

Answer 68

Sudden onset of severe chest pain that may complicate severe vomiting. Subcutaneous emphysema may be observed on the chest wall. Retrosternal pain, radiate to L shoulder or abdo Odynophagia Dysphonia Back pain Inability to lie supine Tachypnoea/ dyspnoea Cyanosis, fever Mackler’s triad: CP, vomiting, subcut emphysema Hamman’s sign: crunching/ rasping sound syncronus with HB, heard over precordium

Question 69

Diagnosis of Boerhaave's syndrome?

Answer 69

CXR: free mediastinal air, pleural effusion, pneumothorax, widened mediastinum, SC emphysema CT contrast swallow - oesophageal wall oedema/ thickening, extraoesophageal air, periesophageal fluid, mediastinal widening, pneumothorax. Spillage of barium sulfate contrast leads to inflam + fibrosis. Water soluble contrast Endoscopy avoided Hb, haematocrit

Question 70

Treatment of Boerhaave's syndrome?

Answer 70

thoracotomy and lavage, if less than 12 hours after onset then primary repair is usually feasible, surgery delayed beyond 12 hours is best managed by insertion of a T tube to create a controlled fistula between oesophagus and skin. Supportive care Prophylactic Abx IV PPI

Question 71

Complications of Boerhaave's syndrome?

Answer 71

Delays beyond 24 hours are associated with a very high mortality rate. Chemical mediastinitis Severe sepsis occurs secondary to mediastinitis Pleural effusion

Question 72

Summary of gastric erosions?

Answer 72

Spots of damage on lining of stomach. Mucous membrane inflamed lamina propria. NSAIDs, alcohol, virus, gastritis, radiation, IS Dyspepsia N+V Blood in vomit/ stool Damage limited to mucosa: epithelium, basement membrane Stop causative agent Most erosions heal on their own once cause removed Surgery PPIs to ↓ acid

Question 73

What is angiodysplasia?

Answer 73

a vascular deformity of the gastrointestinal tract which predisposes to bleeding and iron deficiency anaemia. There is thought to be an association with aortic stenosis, although this is debated. Angiodysplasia is generally seen in elderly patients Usually caecum or ascending colon Age + ↑ strain on bowel wall from chronic + intermittent contraction of colon.

Question 74

Sx of angiodysplasia?

Answer 74

Capillaries of mucosa gradually dilate, precapillary sphincter becomes incompetent.

Question 75

Complications of angiodysplasia?

Answer 75

Bleeding, ↑ in coag disorders + prescribed anticoag Iron def anaemia Obstructs venous drainage of mucosa

Question 76

Investigations of angiodysplasia?

Answer 76

Colonoscopy Mesenteric angiography if acutely bleeding

Question 77

Management of angiodysplasia?

Answer 77

Blood transfusions + endoscopic Tx, where cauterisation or argon plasma coag Tx can be used If Tx fails resection of affected bowel antifibrinolytics e.g. Tranexamic acid oestrogens may also be used

Question 78

What is Barrett's oesophagus?

Answer 78

metaplasia of the lower oesophageal mucosa, with the usual squamous epithelium being replaced by columnar epithelium. There is an increased risk of oesophageal adenocarcinoma, estimated at 50-100 fold. There are no screening programs for Barrett's - it's typically identified when patients have an endoscopy for evaluation of upper gastrointestinal symptoms such as dyspepsia. can be subdivided into short (<3cm) and long (>3cm). The length of the affected segment correlates strongly with the chances of identifying metaplasia. The overall prevalence of Barrett's oesophagus is difficult to determine but may be in the region of 1 in 20 and is identified in up to 12% of those undergoing endoscopy for reflux. the columnar epithelium may resemble that of either the cardiac region of the stomach or that of the small intestine (e.g. with goblet cells, brush border)

Question 79

RFs for Barrett's oesophagus?

Answer 79

gastro-oesophageal reflux disease (GORD) is the single strongest risk factor male gender (7:1 ratio) smoking central obesity hiatal hernia previous damage to oesophageal epithelium (e.g., swallowing lye)

Question 80

Management of Barrett's oesophagus?

Answer 80

endoscopic surveillance with biopsies. for patients with metaplasia (but not dysplasia) endoscopy is recommended every 3-5 years high-dose proton pump inhibitor: whilst this is commonly used in patients with Barrett's the evidence base that this reduces the change of progression to dysplasia or induces regression of the lesion is limited If dysplasia of any grade is identified endoscopic intervention is offered. Options include: endoscopic mucosal resection, radiofrequency ablation NSAIDs may prevent progression Avoid chocolate, coffee, tea, peppermint, alcohol, fatty spicy acidic foods.

Question 81

Features of Barrett's oesophagus?

Answer 81

Asymptomatic Frequent, prolonged heart burn, dysphagia, haematemesis, epigastric pain, weight loss Long: more severe reflux, upright/ supine reflux Short: asymptomatic, upright reflux

Question 82

Complications of Barrett's oesophagus?

Answer 82

Oesophageal adenocarcinoma, sig more likely if long

Question 83

Investigation for Barrett's oesophagus?

Answer 83

Oesophagastro duodenoscopy Screening: M>F, >60, long standing reflux, life expectancy >5 yrs Biopsy: goblet cells, intestinal metaplasia.

Question 84

What is refeeding syndrome?

Answer 84

describes the metabolic abnormalities which occur on feeding a person following a period of starvation. It occurs when an extended period of catabolism ends abruptly with switching to carbohydrate metabolism. ``` The metabolic consequences include: hypophosphataemia hypokalaemia hypomagnesaemia: may predispose to torsades de pointes abnormal fluid balance ``` can lead to organ failure ↓ carb intake, ↓ insulin when carb intake ↑, insulin secreted, ↑cellular uptake of electrolytes

Question 85

Who is at risk of refeeding syndrome?

Answer 85

Patients are considered high-risk if one or more of the following: BMI < 16 kg/m2 unintentional weight loss >15% over 3-6 months little nutritional intake > 10 days hypokalaemia, hypophosphataemia or hypomagnesaemia prior to feeding (unless high) If two or more of the following: BMI < 18.5 kg/m2 unintentional weight loss > 10% over 3-6 months little nutritional intake > 5 days history of: alcohol abuse, drug therapy including insulin, chemotherapy, diuretics and antacids NICE recommend that if a patient hasn't eaten for > 5 days, aim to re-feed at no more than 50% of requirements for the first 2 days.

Question 86

Complications of refeeding syndrome?

Answer 86

Abnormal fluid balance | Organ failure

Question 87

Investigations for refeeding syndrome?

Answer 87

Hypophosphatemia: rhabdomyolysis, resp failure, leucocyte dysfunction, coma ↓K: cardiac issues, ↓Mg, TdP

Question 88

Management of refeeding syndrome?

Answer 88

Start at no more than 50% target energy + protein needs Build up to meet full needs over 1st 24-48 hrs Provide full amounts of electrolytes, vits, minerals from outset of feeding.

Question 89

Causes of malabsorption?

Answer 89

``` IBD, lactase def, tropical sprue, Whipple’s disease, giardiasis, pancreatic (chronic pancreatitis, CF, pancreatic cancer) Biliary: obstruction, PBC Bacterial overgrowth Short loop syndrome Lymphoma Bile acid malabsorption Orlistat Thyrotoxicosis Diabetic induced neuropathy Meckel’s diverticulum ```

Question 90

Features of malabsorption?

Answer 90

Fats: steatorrhoea Protein: dry hair, hair loss, fluid retention, oedema Sugars: bloating, gas, explosive diarrhoea Carpopedal spasm: Ca, Mg Glossitis: B12, folate, iron, niacin Diarrhoea Flatulence + abdo distension: bacterial fermentation of unabsorbed foods ↓BS

Question 91

Complications of malabsorption?

Answer 91

Anaemia Bleeding, bruising, petechiae: vit K + C Night blindness: vit A Amenorrhoea Oedema: hypoalbuminaemia, chronic protein malabsorption Orthostatic hypotension Dermatitis herpetiformis, erythema nodosum + pyoderma gangrenosum, pellagra, alopecia, seborrheic dermatitis.

Question 92

What is coeliac disease?

Answer 92

is an autoimmune condition caused by sensitivity to the protein gluten It is thought to affect around 1% of the UK population. Repeated exposure leads to villous atrophy which in turn causes malabsorption. Conditions associated with coeliac disease include dermatitis herpetiformis (a vesicular, pruritic skin eruption) and autoimmune disorders (type 1 diabetes mellitus and autoimmune hepatitis). It is strongly associated with HLA-DQ2 (95% of patients) and HLA-DQ8 (80%).

Question 93

Features of coeliac disease?

Answer 93

Chronic or intermittent diarrhoea Failure to thrive or faltering growth (in children) Persistent or unexplained gastrointestinal symptoms including nausea and vomiting Prolonged fatigue ('tired all the time') Recurrent abdominal pain, cramping or distension Sudden or unexpected weight loss Unexplained iron-deficiency anaemia, or other unspecified anaemia

Question 94

Complications of coeliac disease?

Answer 94

anaemia: iron, folate and vitamin B12 deficiency (folate deficiency is more common than vitamin B12 deficiency in coeliac disease) hyposplenism osteoporosis, osteomalacia lactose intolerance enteropathy-associated T-cell lymphoma of small intestine subfertility, unfavourable pregnancy outcomes rare: oesophageal cancer, other malignancies

Question 95

Investigations for coeliac disease?

Answer 95

Serology - TTG antibodies (IgA) - endomyseal antibody (IgA) Endoscopic intestinal biopsy - traditional duodenum, show villous atrophy, crypt hyperplasia, increase in intraepithelial lymphocytes, lamina propria infiltration with lymphocytes

Question 96

Management of coeliac disease?

Answer 96

Gluten free diet (avoid wheat, barley, rye, oats) Can have rice, potatoes, corn Immunisation - due to functional hyposplenism, pneumococcal infection every 5 years + influenza

Question 97

Summary of coeliac disease in children?

Answer 97

Children normally present before the age of 3 years, following the introduction of cereals into the diet ``` failure to thrive diarrhoea abdominal distension older children may present with anaemia many cases are not diagnosed to adulthood ```

Question 98

What is lactose intolerance?

Answer 98

Lactase def/inactive, ↑undigested lactose > fermentation by colonic flora, gas, osmotically active substances produced, osmotic pressure decreases (water moves into bowels) Most often acquired due to physiological weaning off milk, after weaning lactase levels tend to decrease RF: non-european, congen (autosomal recessive), underlying intestinal disease.

Question 99

Symptoms of lactose intolerance?

Answer 99

Congen: diarrhoea starting from birth as can’t digest breast milk Abdo pain Cramping in lower quadrants Abdo distension Flatulence V/D Those with lactase persistence can develop bouts of lactose intolerance in response to infection. Inflame

Question 100

Diagnosis of lactose intolerance?

Answer 100

↑osmotic stool gap: unabsorbed carbs Bacterial lactose fermentation: acidic stool Hydrogen breath test: drink lactose solution, test every 15 mins. If breath contains low H2 after consuming lactose = LI. Lactose tolerance test: drink lactose solution, blood sugar tested, if LI blood sugar rise slowly or not at all as body can’t break down lactose into glucose.

Question 101

Diagnosis of lactose intolerance?

Answer 101

↑osmotic stool gap: unabsorbed carbs Bacterial lactose fermentation: acidic stool Hydrogen breath test: drink lactose solution, test every 15 mins. If breath contains high H2 after consuming lactose = LI. Lactose tolerance test: drink lactose solution, blood sugar tested, if LI blood sugar rise slowly or not at all as body can’t break down lactose into glucose.

Question 102

Management of lactose intolerance?

Answer 102

Optimise Ca + Vit D intake Lactose free diet Compensate with lactase

Question 103

What is diverticulosis?

Answer 103

common disorder characterised by multiple outpouchings of the bowel wall, most commonly in the sigmoid colon (as has smallest diameter so ^ pressure) True - is all organ layers False - most common in colonic diverticula mucosa and submucosa Abnormal/ exaggerated smooth muscle contraction, unequal intraluminal pressure distribution, ↑pressure pushes wall out. Risk factors increasing age low-fibre diet Can present as painful diverticular disease (altered bowel habit, colicky left sided abdominal pain) and diverticulitis

Question 104

Sx of diverticulitis?

Answer 104

asymptomatic left iliac fossa pain and tenderness anorexia, nausea and vomiting diarrhoea features of infection (pyrexia, raised WBC and CRP) left sided colic relieved by defection rectal bleeding rectal mass tenderness Fever, malaise, tachycardia Urinary urgency, freq, dysuria (inflamed sigmoid colon, bladder irritation) Acute: abdo pain, severe, localising to LLQ, rectal bleed, rectal mucus

Question 105

Management of diverticulitis?

Answer 105

mild attacks can be treated with oral antibiotics. Uncomplicated: co-amox, 2nd cefalexin + metro Liquid diet, analgesia If Sx don’t resolve within 72 hrs or pt present with severe Sx IV Abx (metro + ceftriaxone) more significant episodes are managed in hospital. Patients are made nil by mouth, intravenous fluids and intravenous antibiotics (typical a cephalosporin + metronidazole) are given Surgical resection Avoid NSAIDs/ opiods as can ↑risk of diverticula perf If no improvement with Tx with seemingly uncomplicated diverticulitis may suggest abscess

Question 106

Complications of diverticulitis?

Answer 106

abscess formation peritonitis obstruction perforation - guarding, rebound tenderness sepsis fistula - faecaluria, pneumaturia, vaginal passage of faeces or flatus

Question 107

Complications of diverticulosis?

Answer 107

BV separated from wall lumen by mucosa so vulnerable to injury + rupture Diverticulitis Segmental colitis If diverticula distended enough, can rupture + form fistula Found in R colon in Asian pts

Question 108

Investigations of diverticulosis?

Answer 108

Often found incidentally XR with barium enema: directly shows pouches CT: visualise colonic diverticula bowel wall thickening (>4mm), ^ soft tissue density with pericolonic. Low fibre diet, constipation, fatty food, red meat, inactivity, smoking, ↑age, M>F, FH, obesity. CT disorders (Marfans, EDS, AD polycystic kidneys)

Question 109

Management of diverticulosis?

Answer 109

Resection ↑fibre, avoid constipation, ↑physical activity, smoking cessation Adequate fluid intake Bulk forming laxatives eg isphagula + methylcellulose

Question 110

What is diverticulitis?

Answer 110

Inflamed/ perf of diverticula Lodged fecalith, obstructs neck of diverticula, stagnation + bacterial multiplication. Erosion of diverticula wall from higher luminal pressures, inflam, focal necrosis, perforation

Question 111

Sx of diverticulosis?

Answer 111

Asymptomatic Vague abdo tenderness Bloating Left sided colic relieved by defecation Nausea Flatulence Diarrhoea/ constipation Rectal bleeding Palpable mass tenderness

Question 112

Investigations of diverticulitis?

Answer 112

CT w contrast: inflam hyperdense tissue, thickened bowel wall, abscess, mass, streaky mesenteric fat, gas in bladder in case of fistula AXR: bowel obstruction, perf, pneumoperitoneum, ileus, soft tissue densitieis, dilated bowel loops Avoid colonoscopy initially as may perf Leucocytosis, ↑WCC, CRP + ESR

Question 113

Symptoms of haemorrhoids?

Answer 113

No sensory fibres above dentate line, aren’t painful unless thrombose when protrodue + gripped by anal sphincter, blocking venous return Bright red blood, on toilet paper, dripping into pan Itching Mucous discharge Thrombosed: pain, purplish oedematous tender SC perianal mass Soiling: 3rd/4th deg

Question 114

Complications of haemorrhoids?

Answer 114

Vulnerable to trauma eg hard stools, bleed Prolapse Severe anaemia Incarceration. Strangulation Hygiene difficulties External prone to thrombosis

Question 115

Investigation of haemorrhoids?

Answer 115

Proctoscopy for internal haemorrhoids PR, internal haemorrhoids not palpable ``` Internal 1 - Bleed but no prolapse 2 - Prolapse on straining, reduce spont 3 - Prolapse on straining, manual reduction 4 - Spontaneous irreducible prolapse ```

Question 116

Management of haemorrhoids?

Answer 116

1st deg: 🡩 fluid + fibre. Analgesics, stool softener. Topical anaesthetics + steroids 2nd/3rd deg: rubber band ligation, sclerotherapy, infra-red coag, cryotherapy Excisional haemorrhoidectomy

Question 117

Summary of anal fissure?

Answer 117

Painful tear in squamous lining of lower canal. Hard bowel movement, anal mucosa stretches, acute fissure, internal anal sphincter spasms, blood flow ↓, diff healing chronic fissure Low fibre, C/D, prev anal surgery, anal trauma, anal cancer, psoriasis, abnormalities in internal anal sphincter, STIs, IBD Features: Midline tear Pain during bowel movement, fear of defecation, constipation, harder stool, more pain Blood on toilet paper/ stool Complication: Faecal bacterial infection Investigation: Hx + exam <6wks acute, >6wks chronic 90% on post midline, if fissures found in alternative locations other causes should be considered Management: Stool softeners, fibre, fluid Bulk forming laxatives if not tolerated try lactulose Chronic: topical nitrates (GTN ointment), CCB (diltiazem), lidocaine ointment Referral for botox, if fail internal sphincterotomy Proper anal hygiene, warm sitz bath

Question 118

What is an anal fistula?

Answer 118

Abnormal communication between anal canal + perianal skin Goodsall’s rule: determines path if ant straight line, if post, internal ooening always at 6 o clock, curved Cause: perianal sepsis, abscess, CD, TB, diverticular disease, rectal carcinoma, IC.

Question 119

What is an anal fistula?

Answer 119

Abnormal communication between anal canal + perianal skin Goodsall's rule states that a fistula with the external opening anterior to an imaginary transverse line across the anus has its internal opening at the same radial position and for an external opening posterior to this line, the internal opening is in the midline posteriorly with a horse-shoe track. Cause: perianal sepsis, abscess, CD, TB, diverticular disease, rectal carcinoma, IC.

Question 120

Features of an anal fistula?

Answer 120

Skin excoriations Itching Pus/ serous fluid/ faeces draining from skin opening, pass pus/ blood when poo Pain: constant, throbbing, worse when sit, move, poo or cough Red, swelling

Question 121

Investigation and management of anal fistula?

Answer 121

Anal exam, delineate course of fistula Drain infection, eradicate fistulous tract, preserve anal sphincter function Require seton suture tightened over time to maintain continence

Question 122

Summary of rectal prolapse?

Answer 122

Partial/ total slip of rectal tissue through anal orifice, due to lax sphincter, prolonged straining, chronic neurological + psychological disorders RF: C/D, pregnancy, pelvic floor damage, rectal intussception, child birth ``` Features: Mass protruding through anus after defecation, when sneezing/ coughing Pain Rectal bleeding Incontence ``` Management: High fibre diet, enemas, Kegel exercises Sutures/ slings to anchor rectum to sacrum Proctosigmoidectomy, reanastomosis of remaining rectum to colon, severe prolapse Anal encirclement with Thiersch wire

Question 123

What is Familial adenomatous polyposis?

Answer 123

is a genetic condition. It is diagnosed when a person develops more than 100 adenomatous colon polyps Autosomal dominance, 100% penetrance Classic: most aggressive, >100 polyps at diagnosis, early onset Attenuated: <100 polyps at diagnosis, later onset. Adenomatous polyps, usually pedunculated or sessile, either tubular, villous or tubulovillous APC gene on chromosome 5q. Gardner’s syndrome: variant with extracolonic manifestations. Malig in colon, thyroid, liver, kidney.

Question 124

Features of Familial adenomatous polyposis?

Answer 124

Asymptomatic til malig If big enough to obstruct, intestines abdo pain + constipation Palpable abdo mass, pain Haematochezia Diarrhoea Polyps begin in puberty, by 20 can have 100-1000s, more descending colon + rectum

Question 125

Complications of Familial adenomatous polyposis?

Answer 125

Malig = mean age 35, by age 50 all do Congen hypertrophy of retinal pigment epithelium Fundic gland polyps Duodenal adenomas Abdo mesenchymal desmoid tumour Thyroid, pancreas, brain, liver Cs Sebaceous cysts Osteomas Epidermal cysts Compression of adjacent structures

Question 126

Investigations of Familial adenomatous polyposis?

Answer 126

Endoscopy, colonoscopy, flexible sigmoidoscopy Barium enema: filling defects Abdo CT: hyperdense outpouchings of colonic wall into lumen Fe def anaemia Digital rectal exam: palpable mass Ophthalmic exam: CHRPE Annual flexible sigmoidoscopy from 15, if no polyps found then 5 yrly colonoscopy from 20.

Question 127

Management of Familial adenomatous polyposis?

Answer 127

NAIDs EGFR inhib: erlotinib Sulindac + celecoxib Freq endoscopic check ups every 1-2yrs, if polyps detected > removal Subtotal colectomy with ileorectal anastomosis. Total proctocolectomy with ileoanal anastomosis

Question 128

What is Lynch syndrome?

Answer 128

Hereditary non-polyposis colon Ca a type of inherited cancer syndrome associated with a genetic predisposition to different cancer types. most common cause of hereditary colorectal cancer mostly at younger age (<50), plus other cancers (uterine, ovarian, bladder, stomach, liver, kidney, brain and certain skin cancers) Colonic tumours likely to be R sided + mucinous Autosomal dominant mutation in DNA mismatch repair genes, hMSH2, hPMS1, MSH6, hMLH1, HPMS2

Question 129

Features of Lynch syndrome?

Answer 129

Blood in stool Diarrhoea Long periods in constipation Crampy pain in abdo Persistent ↓in size or calibre of stool Freq feeling of distension in abdo or bowel region (gas pain, bloating, fullness) Vomiting + continual lack of energy

Question 130

Investigations and management of Lynch syndrome?

Answer 130

Amsterdam criteria: typical (R sided, mucinous, dense lymphocytic infiltrate), 3 individuals (1 1st degree/ 2 sucessive generations), 1 must have Ca diagnosed <50 Colonoscopy: every 1-2 yrs starting by age 25 or 5-10 yrs before age of earliest CRC diagnosed in family. At 40 annual colonsocpy Women: yrly pelvic exam, Pap test. Transvaginal USS starting at 25, annually Upper endoscopy in families with gastric Ca Polyp removal Colectomy

Question 131

What is colorectal cancer?

Answer 131

third most common type of cancer in the UK and the second most cause of cancer deaths. Annually there are about 150,000 new cases diagnosed and 50,000 deaths from the disease. ``` Location of cancer (averages) rectal: 40% sigmoid: 30% descending colon: 5% transverse colon: 10% ascending colon and caecum: 15% ``` most cancers (adenocarcinoma) develop from adenomatous polyps. IBD - UC>CD Screening: NHS offers home-based, Faecal Immunochemical Test (FIT) screening to older adults - every 2 years to all men and women aged 60 to 74 years in England. Patients aged over 74 years may request screening. used to detect, and can quantify, the amount of human blood in a single stool sample - detects Hb. Abnormal results > colonoscopy. 3 types: sporadic HNPCC FAP

Question 132

Features of colorectal cancer?

Answer 132

Asymptomatic initially Vague constitutional Sx: fatigue, anorexia, weight loss Change in bowels: narrowing of stool constipation, diarrhoea, looser more freq stools Rectal bleeding: frank/occult Rectal pain N/V: bowel obstruction if advanved Ascending (R): typically grow beyond mucosa, don’t cause bowel obstruction. Vague abdo pain + weight loss. Can grow large without Sx Late diagnosis. Can ulcerate + bleed. Palpable mass. Descending (L): infiltrating masses, ring shaped, whole circumference of colon wall. Lumen narrowing (napkin ring constriction), early bowel obstruction. Colicky abdo pain + haematochezia. Passage of mucus. Rectal tumour: rectal bleeding usually on defecation, mucus tenesmus

Question 133

Diagnosis of colorectal ca?

Answer 133

Staged using CT of chest/abdomen and pelvis Colonoscopy or CT colonography to evaluate entire colon Tumour below peritoneal reflection should have mesorectum evaluated with MRI

Question 134

Management of colorectal Ca?

Answer 134

MDT Surgery - stents

Question 135

Management of colonic Ca?

Answer 135

MDT Surgery - stents, surgical bypass, diversion stomas as palliative adjuncts - resection is only curative - tailored around resection of particular lymphatic chains Chemo - 5FU and oxaliplatin is common

Question 136

Treatment of rectal ca?

Answer 136

MDT Surgical resection - low tumours or involving sphincter require APER (abdomino-perineal excision of the rectum), 2cm distal clearance margin is required, also dissection of mesolectal fat and LNs, Can use radiation (as it is an exztraperitoneal structure) prior to surgery

Question 137

Surgical resections of colorectal ca?

Answer 137

Caecal, ascending or proximal transverse colon ca > right hemicolectomy > ileo-colic anastomosis Distal transverse, descending colon > left hemicolectomy > colo-colon anastomosis Sigmoid colon ca > high anterior resection > colo-rectal anastomosis Upper rectum ca > anterior resection > colo-rectal anastomosis Low rectum ca > anterior resection > colo-rectal (+/- defunctioning stoma) Anal verge > abdomino-perineal excision of rectum > no anastomosis

Question 138

What is Hartmann's procedure?

Answer 138

When resection of the sigmoid colon is performed and an end colostomy is fashioned

Question 139

RFs for colorectal ca?

Answer 139

Hereditary - FAP, Lynch, APD, K-ras IBD - UC>CD Lifestyle: smoking, physical activity, obesity, ↑alcohol, processed red meat, ↓fruits + veg DM, insulin resistance Socioeconomic status Abdo radiation HPV for anal Ca Black people of African descent, M>F. ↑age

Question 140

Protective factors of colorectal ca?

Answer 140

physical activity use of aspirin NAIDs dietary fibre non-starchy veg pulses Ca garlic

Question 141

Complications of colorectal ca?

Answer 141

High metastatic potential after penetrating muscularis mucosa Iron def anaemia Cachexia Bowel perf > peritonitis Hepatomegaly + bone pain

Question 142

Investigations for colorectal ca?

Answer 142

Colonoscopy/ flexible sigmoidoscopy, biopsy colonoscopy requires full bowel prep before + risk of dehydration + AKI CEA PR: palpable mass if distal rectal mass Stool guaiac test, pos FIC Barium enema: apple core sign, constriction of lumen

Question 143

Staging of colorectal ca?

Answer 143

Stage 0: carcinoma in situ, not passed mucosa Stage 1: not grown beyond mucosa, no spread to LN or distant organs 2: invade entire rectal wall, may reach near organs, no spread to LN or distant organs. 3: spread to LN, but hasn’t spread to distant organs 4: metastatic, reach distant organs, if colon often liver, if rectum often lungs. Duke Duke A: tumour not through muscular layer, nodes -ve. 90-95% 5yr survival Duke B: tumour through muscular layer, 60-80% 5yr survival Duke C1: nodes +ve, but highest node -ve. 1-4 LN, 25-30 5yr survival Duke C2: highest node +ve, >4LN Duke D: distant mets, eg liver, lungs. <1% 5yr survival

Question 144

Surveillance of colorectal ca?

Answer 144

regular CEA, CT chest, abdo pelvis. CRC usually recurs within 2-3 yrs so pt followed up for 5 yrs if discharge free, discharged.

Question 145

What are hernias?

Answer 145

Protrusion of viscus through defect of bowel wall. Area of weakness where prev opening has been closed, heavy lifting/ straining may make more obvious but don’t normally cause Cause: ↑intra abdo press

Question 146

Features of hernias?

Answer 146

Reducible: sac return to abdo cavity spont or with manipulation Irreducible: sac can’t be reduced despite pressure or manipulation Incisional: if incision doesn’t close properly

Question 147

Types of hernias?

Answer 147

Strangulated: blood supply compormised, gangrene in 6 hrs Obstructed: results in intestinal obstruction Epigastric: midline between umbilicus + xiphisternum, 20-30 y/o, form through natural small defect, linea alba. High risk incarceration Incarcerated hernia: can block/ obstruct intestine Spigelian: ventral, rare, older pt. between aponeurotic layer between rectus abdominus medially + semilunar line laterally below umbilicus. Obturator: bowel > obturator foramen often presents with obstruction Richter: rare, only antimesenteric border of bowel herniates through gascial defect. Present with strangulation without obstruction.

Question 148

Summary of direct inguinal hernia?

Answer 148

Protrudes through Hesselback triangle Passes medial to the inferior epigastric artery Defect or weakness in the transversalis fascia area of the Hesselbach triangle Low risk of strangulation Seen in adults Much more common in males

Question 149

Summary of indirect inguinal hernia?

Answer 149

Protrudes through the inguinal ring Passes lateral to the inferior epigastric artery Failure of the processus vaginalis to close Low risk of strangulation May occur in infants Much more common in males

Question 150

Summary of femoral hernia?

Answer 150

section of the bowel or any other part of the abdominal viscera pass into the femoral canal. Protrudes below the inguinal ligament, lateral to the pubic tubercle A lump within the groin, that is usually mildly painful inferolateral to the pubic tubercle Typically non-reducible, although can be reducible in a minority of cases Given the small size of the femoral ring, a cough impulse is often absent. High risk of strangulation Seen in adults More common in females

Question 151

Summary of hiatus hernia?

Answer 151

describes the herniation of part of the stomach above the diaphragm. There are two types: > sliding: accounts for 95% of hiatus hernias, the gastroesophageal junction moves above the diaphragm > rolling (paraoesophageal): the gastroesophageal junctions remains below the diaphragm but a separate part of the stomach herniates through the oesophageal hiatus RFs > obesity > increased intraabdominal pressure (e.g. ascites, multiparity) ``` Features: > heartburn > dysphagia > regurgitation > chest pain ``` Ix: > barium swallow is the most sensitive test > given the nature of the symptoms many patients have an endoscopy first-line, with a hiatus hernia being found incidentally Management: > all patients benefit from conservative management e.g. weight loss, stop smoking, > medical management: proton pump inhibitor therapy > surgical management: only really has a role in symptomatic paraesophageal hernias

Question 152

Features of inguinal hernias?

Answer 152

groin lump superior and medial to the pubic tubercle disappears on pressure or when the patient lies down discomfort and ache: often worse with activity, severe pain is uncommon strangulation is rare

Question 153

Management of inguinal hernias?

Answer 153

the clinical consensus is currently to treat medically fit patients even if they are asymptomatic a hernia truss may be an option for patients not fit for surgery but probably has little role in other patients mesh repair is associated with the lowest recurrence rate > unilateral inguinal hernias are generally repaired with an open approach > bilateral and recurrent inguinal hernias are generally repaired laparoscopically

Question 154

Investigation of inguinal hernia?

Answer 154

Reduce hernia, occlude deep ring with 2 fingers. Ask pt to cough/ stand, if hernia restrained indirect, if still protrudes direct. USS: direct (variable echogenicity of tissue, movement of intra-abdo structures in ant direction through Hesselbech triangle). Indirect (visualisation through abdo wall in females). CT: direct (visualisation of protrusion with compressing inguinal canal contents, moon crescent), indirect (occult hernia complications, hernia neck visualised sup lat to inf epigastric vessels) Strangulation: leucocytosis, ↑lactate

Question 155

Summary of umbilical hernia?

Answer 155

Naval bulging out through opening in abdo muscle Bulge fat from greater omentum (common) or SI Often babies + young children because opening for UC BV didn’t fully close. Symmetrical: umbillical Asymmetrical: paraubilical Adults: obesity, pregnancy or XS fluid in abdo RF: Afro-Caribbean infants, Down’s, mucopolysaccharide storage Surgical in adults Newborns can be born with them, resolve spont 2-3y/o

Question 156

Causes of peritonitis?

Answer 156

Spont bacterial:migration from GI lumen, common in ascites/ cirrhosis, e coli, klebsiella, pseudomonas Perf viscera, leakage of GU contents Foreign material: bile, blood, contrast CD/ diverticulitis Endometriosis Peritoneal dialysis

Question 157

Features of peritonitis?

Answer 157

Fever, chills ↑HR Ascites, abdo distension + rigidity Absent BS Pain + tenderness worse on moving Guarding Anorexia, N/V/D Rebound tenderness

Question 158

Complications of peritonitis?

Answer 158

Toxaemia Septicaemia Multiorgan failure Local abscess formation Toxic megacolon Paralytic ileus Hypovolaemia Renal fialure

Question 159

Investigation for peritonitis?

Answer 159

Supine/ upright films: pneumoperitoneum, abscess, CT to identify cause Paracentesis: serum ascites albumin gradient >1.1 in spont bacterial, neutrophil count >250, most common organism found on ascites fluid culture is E. coli Amylase

Question 160

Management of peritonitis?

Answer 160

SBP - IV cefotaxime Abx: oral ciprofloxacin or norfloxacin if cirrhosis and ascites with an ascitic protein of 15 g/litre or less until the ascites has resolved' Metronidazole, levoflaxcin, co-amox Surgery NG tube IV fluids Peritoneal lavage

Question 161

What is appendicitis?

Answer 161

most common acute abdominal condition requiring surgery. It can occur at any age but is most common in young people aged 10-20 years. lymphoid hyperplasia, faecolith, foreign body, pinworm, tumour, infection → obstruction of appendiceal lumen → gut organisms invading the appendix wall → oedema, ischaemia +/- perforation RF: 10-30, FH, M>F, CF

Question 162

Features of appendicitis?

Answer 162

peri-umbilical abdominal pain (visceral stretching of appendix lumen and appendix is midgut structure) radiating to the right iliac fossa (RIF) due to localised parietal peritoneal inflammation. the migration of the pain from the centre to the RIF has been shown to be one of the strongest indicators of appendicitis patients often report the pain being worse on coughing or going over speed bumps. Children typically can't hop on the right leg due to the pain. vomit once or twice but marked and persistent vomiting is unusual diarrhoea is rare. However, pelvic appendicitis may cause localised rectal irritation of some loose stools. A pelvic abscess may also cause diarrhoea mild pyrexia is common - temperature is usually 37.5-38oC. Higher temperatures are more typical of conditions like mesenteric adenitis anorexia is very common. It is very unusual for patients with appendicitis to be hungry around 50% of patients have the typical symptoms of anorexia, peri-umbilical pain and nausea followed by more localised right lower quadrant pain

Question 163

Signs of appendicitis on examination?

Answer 163

generalised peritonitis if perforation has occurred or localised peritonism > rebound and percussion tenderness, guarding and rigidity retrocaecal appendicitis may have relatively few signs digital rectal examination may reveal boggy sensation if pelvic abscess is present, or even right-sided tenderness with a pelvic appendix classical signs > Rovsing's sign (palpation in the LIF causes pain in the RIF) is now thought to be of limited value > psoas sign: pain on extending hip if retrocaecal appendix

Question 164

Diagnosis of appendicitis?

Answer 164

raised inflammatory markers a neutrophil-predominant leucocytosis is seen in 80-90% urine analysis: useful to exclude pregnancy in women, renal colic and urinary tract infection. In patients with appendicitis, urinalysis may show mild leucocytosis but no nitrites thin, male pas - clinically females - USS - free fluid is pathological - visible, dilated noncompressible, appendix, 🡩blood flow in appendix wall, visible appendicolith, RIF fluid collection. CT - not common practice in UK - appendix diameter + wall enhancement. Abscess, pus spillage

Question 165

Management of appendicitis?

Answer 165

appendicectomy - laparoscopic prophylactic IV Abx - metronidazole patients with perforated appendicitis (typical around 15-20%) require copious abdominal lavage. Avoid laxatives/ enema, may cause rupture

Question 166

Complications of appendicitis?

Answer 166

``` Rupture Peritonitis Periappendiceal abscess Subphrenic abscess Pylephlebitis Potal vein thrombosis Sepsis Preschool: perf rapid, omentum thin, <2y/o 80% perf at CP ```

Question 167

What is bowel obstruction?

Answer 167

serious problem that happens when something blocks your bowels, either your large or small intestine Contents distal to obstruction get past, gas + stool proximal accumulate. Bowel dilates abdo cavity distends. Pressure in lumen ^, contents push towards intestinal wall, compress mucosal BV + LV. Pushes fluid into surrounding area, mucosal oedema Acute: torsion, intussusception Chronic: tumour Recurrent: adhesions Partial/complete Intrinsic: inflam stricture, oedema, haem, FB, parasite, biliary calculus Extrinsic: hernia, torsion Strangulated: blood supply cut off, v ill. Simple: no blood supply impairment, 1 obstructing point. Closed loop: obstruction at each end of bowel section, eg volvulus, grossly distended, perf.

Question 168

Features of bowel obstruction

Answer 168

Abdo distension Cramping Colicky pain C/N/V Anorexia Faeculent vomiting Dehydration Partial: milder, abdo discomfort after meals, constipation Complete: sudden obstipation, no stool or gas. Small bowel: vomiting more common billous, periumbilical pain, few mins at a time, less distension. Large bowel: vomiting less common, lower abdo pain, less freq last longer, constant High pitch tinkling BS: acute mechanical Absence of BS: functional obstruction Peristaltic movements may be visible in very slim pt Hyperresonance / tympany

Question 169

Complications of bowel obstruction?

Answer 169

Compression of mucosal arteries = decrease perfusion, ischaemia + hypoxia (production of reactive O2 damages DNA, RNA + proteins), leading to cell death + infarction, necrosis. Peritonitis, sepsis Bacterial overgrowth due to nutrients from stool + blood from ruptured BVs, inflam response, ↑oedema ↓absorption, dehydration, loss of electrolytes Resp distress: abdo distension push diaphragm, SOB, cyanosis, tachyonoea

Question 170

Investigations for bowel obstruction?

Answer 170

XR: small intestine/ colon distension. Mechanical (dilated loops of bowel w multiple air fluid levels), functional (uniform distension of large/ small bowel). Pneumoperitoneal = perf. Small bowel >3cm. caecum >12cm, >8cm ascending colon, >6.5cm for recto-sigmoid leision Abdo CT w contrast: work out cause Abdo USS: if CT CI, pregnant women, contrast allergies ↑amylase + lactase with strangulation/ perf

Question 171

Causes of bowel obstruction?

Answer 171

Mechanical: small bowel (adhesions, hernias), large (volvulus, diverticula tumour), both (IBD, FB, gall stone gall stone, neoplasm stricture haematoma, meconium (CF), PEG tube, TB, radiotherapy, ischaemic colitis. Functional: disrupt peristalsis, intestinal musculature paralysis causes: trauma (surgery, blunt abdo), meds (opiate anticholinergics), post-op ileus (transient paralysis of smooth muscle), appendicitis, peritonitis, hypothyroid, ↓K ↑Ca

Question 172

Management of bowel obstruction?

Answer 172

Can resolve on their own Surgical: release adhesions, complete obstructions, repair bowel. Irrigation of abdo cavity If cause of obstruction doesn’t require surgeyr, manage consertavely for 72 hrs, 75% will eventually need surgery. NBM Analgesia Fluid/ electrolyte replacement NG decompression, NG sunctioning to remove fluid + air to relive abdo pressure IV Abx

Question 173

Summary of intussusception?

Answer 173

Peristalsis causes 1 part of bowel to move ahead of adjacent section. Ileocecal most common. Adults: abnormal growth, polyp, tumour, causes lead point. nfant: post infection lymphoid hyperplasia RF: <24 mnths old, M>F intestinal malrotation Hx, prev intussusception, intussusception in sibling Features: Intermittent abdo pain (worsens with peristalsis, colic), guarding Intermittent inconsolable crying, with drawing legs up Vomiting (billious) Sausage like abdo mass Red current jelly stool ``` Complications: Peritonitis Sepsis Obstruction Volvulus Intestinal tearing ``` Investigations: Dance’s sign: empty RIF USS, XR, CT: telescoped intestine, classic bull’s eye image May be felt during digital rectal exam (children) USS investigation of choice Surgery: free telescoped intestinal portion, clear obstruction, remove necrotic tissue Reduction by air/ hydrostatic contrast material enema e.g. saline, barium IV fluids

Question 174

What is a volvulus?

Answer 174

Intestinal twisting/looping Sigmoid: more common, middle aged/ elderly. Chronic constipation, pregnancy, adhesions, Chagas disease, neurological eg PD, DMD, schizophrenia. 80% Cecal: impaired abdo mesentery development, colon flop around freely in places, pregnancy, constipation. 20% Midgut: infants/ young children, anomalous intestinal development eg intestinal malrotation.

Question 175

Sx of a volvulus?

Answer 175

Abdo tenderness Pain Distension Bloating Bilious vomiting Constipation Bloody stools if infarction Fever Auscultation (abnormal BS, often ↓) Percussion (tympany) Haematochezia (bowel indicate bowel ischaemia, necrosis).

Question 176

Complications of volvulus?

Answer 176

Mesenteric a compression, blood flow cut off, intestinal wall ischaemia, infarction Intestinal wall perf > infection, diffuse peritonitis, sepsis + CV collapse

Question 177

Investigations of volvulus?

Answer 177

X-ray: assess volvulus shape, bent inner tube sign ‘coffee bean’ sign. Large dilated colon, often with air fluid levels. Barium enema: bird beak perf suspected barium contrast CI CT: twisted mesentery, whirlpool sign.

Question 178

Management of volvulus?

Answer 178

Surgery resection, untwisting, colon + attach to abdo wall IV fluid replacement Bowel decompression, sigmoidoscopy, colonscopy Sigmoid: rigid sigmoidoscopy with rectal tube insertion Cecal volvulus: R hemicolectomy is often needed

Question 179

Summary of gastric volvulus?

Answer 179

RF: congen (bands, pyloric stenosis, rolling hernia) Acquired: gastric/ oesophageal surgery, adhesions Vomiting Pain: severe, epigastric Failed attempt to pass NG Gastric dilation on imaging Endoscopic manipulation Emergency laparotomy

Question 180

Summary of pseudo-obstruction?

Answer 180

No mechanical blockage, but Sx of obstruction Interruption of ANS supply to colon, absence of smooth muscle absence in bowel wall. Myopathy or neuropathy intra-abdo trauma, hypothyroid, ↓Mg, SCI, sepsis, pneumonia, DM, PD, ↓Na, K. Uraemia. Opiates, antidepressants Rapid + progressive distension + pain C/V Tympanic Not passing normal stool but may have paradoxical diarrhoea Toxic megacolon Bowel ischaemia Perforation Dilation of colon due to adynamic bowel XR: gas filled large bowel Abdo pelvis CT with IV contrast: dilation of colon + excl mechanical ostruction ``` NBM, NG tube for decompression IV fluids Endoscopic decompression if doesn’t resolve 24-48hrs, if limited resolution use IV neostigmine Nutritional support Surgical resection ```

Question 181

Summary of ruptured viscus?

Answer 181

Cause: Trauma, tumour, bowel obstruction, perf ulcer, ischaemic bowel, infections incl C diff, toxic megacolon, IBD, loss of wall integrity (TLS), appendicitis, diverticulitis ``` Sx: Pain + abdo tenderness Exacerbated by movement Constant N/V, fever, rigors Haematemesis Silent auscultation, distended, pt stops passing flatus + motion ``` Complications - Peritonitis Shock SI/upper GIT: rapid onset LI: slower onset Oesophagus: sudden onset CP Explorative laparotomy Emergency surgery IV fluids + Abx

Question 182

Summary of pneumoperitoneum?

Answer 182

Gas in peritoneal cavity Perf ant duodenal ulcer, iatrogenic (abdo surgery, gas under diaphragm can be detected on CXR 10 days post op. 🡩 thoracic pressure (mechanical ventilation, chest compressions). Abdo pain Rigidity Absent BS Ileus Supine AXR: Righler’s sign (double wall sign, both sides of abdo wall visible), football sign (massive, ellipsoid shape of abdo cavity outlined by gas) CT: small quantities of air Upright AXR: subdiaphragmatic free air, cupola sign (free intraperitoneal air, well defines sup border formed by diaphragm) Lat decubitus XR: gas between liver + abdo wall Exploratory laparotomy Repair ruptured viscus

Question 183

What is a stoma?

Answer 183

Artificial union between 2 conduits or conduit + outside. SI stomas spouted so irritant contents not in contact with skin LI don’t need to be as contents less irritating to skin.

Question 184

Types of stoma?

Answer 184

Gastrostomy: stomach > skin, used for feeding Percut jejunostomy: feeding, usually LUQ Caecostomy; RIF, stroma of last resort. Urostomy: taking small intestine + attaching ureters to it to form passageway for urine. 1 end brought through abdo. R side, small sprout. Ileostomy: SI to abdo surface, pts with skip lesions of CD, normally R sided. Output: looser consistency + require drainage 3-6X per day Loop ileostomy: temp, diverting faeces away from bowel, allowing it to recover following surgery, usually RIF.. End ileostomy: following complete removal of colon, RIF, can be temp eg emergency bowel resection where unsafe to form anastomosis with remaining bowel. Colostomy: part of colon redirected to outside abdo, normally LIF. IBD, output resemble normal stool, 1-3X per day. Permanent end: resection of large rectal Ca + removal of entire rectum. Temp end: rest bowel in diverticulitis or obstruction, 2 stage Hartmann’s, bowel re-anastomosed later. Loop colostomy: protect distal anastomoses after recent surgery, loop of bowel brought to surface + half-opened, allows faecal matter to drain into stroma bag without reaching distal anastomoses

Question 185

Complications of stoma?

Answer 185

``` Early complications Haem at stroma site Stroma ischaemia ↑output, can lead to ↓K Stroma retraction: falls below skin esp when sitting, common, ileostomy > colostomy. Obese pt, more prone to leaks, skin irritation. Obstruction 2° to adheison Herniation: incisional Prolapse: bowel protrudes through stroma, trauma, infections. ``` ``` Delayed Obstruction: narrowing of stroma Dermatitis around site Fistula Psychological probs: no contact sports/ heavy lifting ```

Question 186

What is gastroparesis?

Answer 186

Delayed gastric emptying, no mechan obstruction Nerve injury, incl vagus which contracts stomach. Idiopathic/ DM, iatrogenic post-viral, amyloidosis, scleroderma

Question 187

Features of gastroparesis?

Answer 187

``` Chronic N/V often undigested food Early satiety, bloating, heartburn Poor appetite Weight loss Abdo pain Erratic blood glucose control ``` Food that stays in stomach too long can ferment, growth of bacteria. Food harden into solid mass (bezoar) blockage Dehydration, malnutrition

Question 188

Investigations for gastroparesis?

Answer 188

Gastric emptying scintigraphy: >10% of food still in stomach 4hrs after eating Wireless capsule test: swallow + see how fast moving through GIT. Barium XR Endoscopy/ CT/MRI: excl mechan obstruction

Question 189

Management of gastroparesis?

Answer 189

Metoclopramide Stop meds that delay gastric emptying Exercise, low fat diet, smaller more freq meals, liquid foods, chew well Domperidone: take before eating to contract stomach muscles Erythromycin Anti-emetics

Question 190

Causes of constipation?

Answer 190

Congen: Hirschsprung’s 1°: functional, normal transit, slow transit, pelvic floor dysfunction. No disease/meds. Disordered reg of colonic anorectal NM function, + brain gut neuroenteric function 2°: poor diet, lack of exercise, IBS, old age, post op pain, hosp environment. DM, hypothyroid, ↑Ca, PD, SCC, anti-diarrhoels, anti-muscarinics, CCB, TCAs, iron, codeine, furosemide, aluminium antacids, CRC, IBD, diverticular disease, rectal prolapse, anal outlet obstruction, stricture, AN, depression, pregnancy

Question 191

Features of constipation?

Answer 191

``` Rome 3, diagnosis of functional constipation if 2+ in preceding 3 mnth: Straining >25% time Lumpy/hard stool >25% time Anorectal blockage Sensation of incomplete evac Manual evac <3 stools/wk ``` Associated Sx: headache, malaise, nausea, bad oral taste, abdo bloating/ discomfort, flatulence, abdo pain. ``` Colicky abdo pain High pitched BS Hyperperistalsis Distension Nausea/ emesis ↓ability to pass wind ``` Complications Overflow diarrhoea Acute urinary retention Haemorrhoids

Question 192

Diagnosis of constipation?

Answer 192

Bloods: U+E, glucose, TFT Ca, ESR PR, sigmoidoscopy, colonoscopy Manometry, transit studies, defecating proctogram

Question 193

Management of constipation?

Answer 193

Acute Treat cause, lifestyle advise 1st: bulk forming laxative isppaghula husk, methylcellulose, 2nd: osmotic eg macrogol or lactulose Fecal impaction: macrogols, enema, suppositories, stimulant laxatives, disempaction with sedatives Chronic 1st: treat cause, lifestyle advicse, bulk laxative + stool softener, isphagula husk, methylcellulose, docusate sodium 2nd: osmotic laxatives (lactulose/ macrogols) if no improvement after 6/52 3rd: add stimulant laxatives senna, bisacodyl

Question 194

Causes of diarrhoea?

Answer 194

Osmotic: maldigestion, eg pancreatis, coeliac, bile salt malabsorption Secretory: chlorea, NaCL secreted, ↑water loss Exudative: blood + pus Inflam: Ca. Damage to mucosal/ brush border. Passive loss of fluid, inability to reabsorb Motility: hypothyroid, IBS Dysentery: visible blood as result of gastroenteritis salmonella shighella. Acute: diet, infection, infective enterocolitis, diverticulitis, constipation with overflow, pseudomembranous colitis (C diff). Bloody diarrhoea (CHEESY, campylobacter, haemorrhagic e coli, enteroinvasive e coli, entomoeba histolyica, salmonella, shigella, yersinia). <14 days Chronic: IBD, IBS, Coeliac, colonic + pancreatic Ca, Whipple’s disease, laxative abuse, CF) >14 dys

Question 195

Investigations for diarrhoea?

Answer 195

PR >50 Stool sample for culture + blood 2 week wait pathway if suspicious of CRC. Bloods: FBC, LFTs, U+Es, Ca, B12, ferritin, TSH, ESR, CRP + tissue transglutaminase for CD low MCV> coeliac or tropical sprue. ^ MCV> Crohn’s. Normal> functional. Colonoscopy

Question 196

Management of diarrhoea?

Answer 196

Oral fluid + electrolyte replacement often required Anti-diarrhoeals may impair clearance isolation + inform PHE Loperamide/ Codeine: Mu opioid receptors of neural plexus of intestines Co-phenotrope: opiate + atropine Kaolin: bindign agent, absorbs water Ca carbonate: constipating

Question 197

What is C. difficile?

Answer 197

Gram positive rod often encountered in hospital practice. causes pseudomembranous colitis. develops when the normal gut flora are suppressed by broad-spectrum antibiotics - 4C’s: cephalosporins, clindamycin, ciprofloxacin, co-amox and PPIs ``` causes: Watery diarrhoea, pus/mucus Nausea Fever Abdo cramps, pain, tenderness ``` ``` can lead to: Dehydration Pseudomembranous colitis: exotin damages mucosa, crypts of colon rupture, mucus spills out, forms pseudomembranes on epithelium, absorption harder Dysentery Toxic megacolon Kidney failure ```

Question 198

Investigations and management of C. difficile infection?

Answer 198

Mild: normal WCC Moderate: ↑WCC, <15X109/L. 3-5 loose stools per day. Severe: ↑WCC >15X109/L acutely ↑Cr (>50%). >38.5°C, evidence of severe colitis (abdo or radiologica signs) LT: hypotension, partial or complete ileus. Toxic megacolon or CT evidence of severe disease Detecting C diff toxin in stool, c diff antigen only shows exposure, rather than current infection. Stop Abx LT: oral vancomycin + IV metronidazole Fecal microbiota transplanted 1st ep 1st: oral vancomycin for 10 days 2nd: oral fidaxomicin 3rd: oral vancomycin +/- IV metronidazole Recurrent ep In 20% of pts, ↑ to 50% after their 2nd ep <12 wks of Sx resolution: oral fidaxocin >12wks of Sx resolution: oral vancomycin or fidaxomicin

Question 199

Causes of gastroenteritis?

Answer 199

GIT infection (12hrs-3days). Mostly viral. Oral faecal route Children: rotavirus Adult: norovirus, astrovirus, adenovirus Parasites: giardia, entamoeba, cryptospordium Toxin mediated: cholera, e coli, b cereus (rice lef too long), s aureus (rapid onset, D/V, dairy food) Penetrating: salmonella, listeria monocytogenes Inflam: shigella, salmonella, e coli, campylobacter, cryptosporidium RF: viral contact eg daycare, cruise ship 1-6hrs: s aureus, b cereus 12-48hrs: salmonella, e coli (travellers), cholera 46-72hrs: shigella, campylobacter >7 days: giardiasis, amoebiasis.

Question 200

Features of gastroenteritis?

Answer 200

Watery diarrhoea N/V Fever, malaise Campylobacter: Sx 2-5 days after ingestion. Malaise, bloody diarrhoea. Flu like prodrome, crampy abdo pain, GBS Salmonella: poultry, meat or eggs. V/D, abdo + fever. E coli: travellers diarrhoea, watery stools, abdo cramps, nausea. Blood in stool, fever. HUS Cryptosporidium: spread through infected water, profuse watery diarrhoea, abdo cramps, nausea, Giardiasis: prolonged non bloody diarrhoea Cholera: profuse, watery, diarrhoea, dehydration, WL Shigella: bloody diarrhoea, vomiting, abdo pain S aureus: severe vomiting, short incubation Bacillus cereus: vomiting within 6hrs, diarrhoeal illness after 6hrs. Amoebiasis: gradual onset, bloody diarrhoea, abdo pain, tenderness may last wks

Question 201

Management of gastroenteritis?

Answer 201

Fluid replacement Severe Sx: anti-emetics eg prochlorperazine, antidiarrhoeals (codeine, or loperamide) Abx if systemically unwell, IS or elderly: cholera (tetracycline), salmonealla, shigella (ciprofloxacin), amoebiasis (metronidazole), campylobacter (erythro, clarithro, ciprofloxacin) Rotavirus vaccine Hygiene Isolate pt Advise not to work Outbreak: 2+ people thought to have common exposure. 48hrs off school following last ep.

Question 202

What is IBS?

Answer 202

Chronic functional GI disorder RF: F>M, prev gastroenteritis, stress, 30-40, 20% adults FH Coexist with CFS, fibromyalgia, TMJ dysfunction Visceral hypersensitivity: N strong response to stimuli Faecal flora alterations/ bacterial overgrowth After gastroenteritis Food sensitivity ``` Features: D/C Recurrent abdo pain, bowel movements improve Sx worse after food Bloating Nausea Mucus in stool Distension Lethargy, fatigue Tenesmus XS stomach noises or rumbling Early satiety Dyspepsia ```

Question 203

Investigation of IBS?

Answer 203

Classify whether D/C predominant Organic disease exclusion Colonoscopy, XR, CT FBC, ESR, CRP, antibody testing for coeliac ``` Rome IV diagnostic Abdo pain >1 day wkly in past 3 mnths Defecation lessens pain Change in stool freq Change in stool consistency ```

Question 204

Management of IBS?

Answer 204

Sx guided therapy Probiotics for 4 wks Diarrhoea pred: loperamide Constipation pred: fibre supplement, fluid, movicol Antispasmodics: mebeverine Anticholinergics, TCAs, SSRIs CBT Diet modication: low FODMAP, avoid gas producing foods, caffeine, alcohol, apples, beans + cauliflower, fresh fruit

Question 205

Causes of oesophageal strictures?

Answer 205

Oesophagitis: inflam, fibrosis, permanent structuring of oesophagus Long standing GORD Corrosives, surgery or radiotherapy Achalasia, hiatus hernia, alcohol use Malig eg tumour CREST syndrome: calcinosis, raynaud’s, esophagela dysmotility, sclerodactyly, telangiectasia Congen stenosis

Question 206

Features of oesophageal strictures?

Answer 206

Dysphagia Feeding food stuck in throat Food regurg Dyspepsia Heart burn Freq burping + hiccups Unintentional weight loss Haematemesis

Question 207

Investigation for oesophageal strictures?

Answer 207

Endoscopy pH manometry studies Radiological contrast studies Barium swallow

Question 208

Management of oesophageal strictures?

Answer 208

Manage underlying condition Oesophageal dilation, or stenting endoscopically

Question 209

What is pharyngeal pouch?

Answer 209

Common in elderly, esp males. Failure of cricopharyngeus part of inf constrictor to relax during swallowing, build up of pressure, resulting in herniation. Posteromed diverticulum through killian’s dehiscence.

Question 210

Features of pharyngeal pouch?

Answer 210

Discomfort in throat Intermittent high dysphagia as pouch enlarges Regurg of undigested foods Chronic cough Bad breath If large gurgling on auscultation Can cause - Aspiration pneumonia

Question 211

Investigation and management of pharyngeal pouch?

Answer 211

Barium swallow with dynamic video fluoroscopy Diverticulotomy Cricopharyngeal myotomy

Question 212

Summary of oesophageal web?

Answer 212

Narrowing of oesophagus due to thin membrane of oesophageal tissues typically located in the anterior postcricoid area of the proximal esophagus Plummer vinson syn, dysphagia, Fe def anaemia, glossitis, cheilosis Causes: Dysphagia Odynophagia Retrosternal pain Fluoroscopy/ barium swallow: jet effect of contrast being ejected distally from webs Dilation of webs endoscopically inflated balloon

Question 213

Summary of oesophageal rings?

Answer 213

occur in the lower esophagus. bands of normal esophageal tissue that form constrictions around the inside of the esophagus Narrowing of oesophagus Mucosal: B ring, Schatzki’s ring, squamocolumnar mucosal junction, common, bolus obstruction Muscular: A ring, located proximal to mucosal ring, may cause dysphagia Barium swallow

Question 214

Summary of oesophageal spasm?

Answer 214

Intermittent dysphagia CP Barium swallow: corkscrew oesophagus

Question 215

What is achalasia?

Answer 215

Failure of oesophageal peristalsis and of relaxation of the lower oesophageal sphincter (LOS) due to degenerative loss of ganglia from Auerbach's plexus i.e. LOS contracted, oesophagus above dilated. Achalasia typically presents in middle-age and is equally common in men and women 1°: no cause, failure of oesophageal inhib neuron 2°: oesophageal Ca, Chagas disease, stomach Ca, amyloidosis, neurofibromatosis T1, sarcoidosis.

Question 216

Features of achalasia?

Answer 216

dysphagia of BOTH liquids and solids typically variation in severity of symptoms heartburn regurgitation of food > may lead to cough, aspiration pneumonia etc malignant change in small number of patients

Question 217

Investigation of achalasia?

Answer 217

oesophageal manometry > excessive LOS tone which doesn't relax on swallowing > considered the most important diagnostic test barium swallow > shows grossly expanded oesophagus, fluid level > 'bird's beak' appearance chest x-ray > wide mediastinum > fluid level Endoscopy: > resistance to passage of endoscope through GOJ, retained food. Biopsy: > hypertrophic musculature, absence of specific nerve cells in myenteric plexus

Question 218

Treatment of achalasia?

Answer 218

pneumatic (balloon) dilation is increasingly the preferred first-line option > less invasive and quicker recovery time than surgery > patients should be a low surgical risk as surgery may be required if complications occur surgical intervention with a Heller cardiomyotomy should be considered if recurrent or persistent symptoms intra-sphincteric injection of botulinum toxin is sometimes used in patients who are a high surgical risk drug therapy (e.g. nitrates, calcium channel blockers) has a role but is limited by side-effects

Question 219

Causes of GORD?

Answer 219

Failure of LOS, stomach contents re-enter oesophagus Obesity, pregnancy, smoking, fat rich diet, caffeine, alcohol, chocolate, spicy foods, large meals Meds: antihistamines, CCB, antidepressants, hypnotics, CS Scleroderma/ systemic sclerosis Hiatus hernia Gastric outlet obstruction, slow gastric emptying

Question 220

Features of GORD?

Answer 220

Post prandial N/V Sore throat Sensation of lump in throat Cough, hoarseness Wheezing, belching Halitosis, tooth decay Nocturnal asthma > aspiration of acid

Question 221

Complications of GORD?

Answer 221

``` Oesophagitis, oedema + erosions Oesophageal stenosis + strictures Barrett’s oesophagus Fe def anaemia Oesophageal adenocarcinoma Laryngitis Chronic cough Pul fibrosis Asthma Recurrent pneumonia Ulcers ```

Question 222

Investigations of GORD?

Answer 222

Clinical Sx Endoscopy: poor therapeutic response/ concerning Sx 24hr oesophageal pH monitoring, <4 Oesophageal manometry Short term trial of PPIs Upper GI XR, barium contrast: identify complications Biopsy: oedema, basal hyperplasia, lymphocytic inflam, neutrophilic/ eosinophilicinflam, elongation of papillae in lamina propria + dilation of vascular channels at tip of papillae, goblet intestinal metaplasia, thinning of squamous layer. Barrets.

Question 223

Management of GORD?

Answer 223

PPIs: lansoprazole Antacids: gaviscon, Mg triscilicate H2 receptor blockers: cimetidine, ranitidine Prokinetics: domperidone, metoclopramide Avoid: nitrates, CCB, anticholinergics, NSAIDs, K salts, bisphosphonates Nissen fundoplication LINXt: titanium magnetic beads round sphincter Avoid lying down 3hrs after eating, elevate head, weight loss, avoid coffee, alcohol, chocolate, fatty/ acidic/ spicy foods, onions, fizzy drinks, tea, smoking cessation, exercise

Question 224

Causes of prehepatic jaundice?

Answer 224

Haemolysis Extravascular haemolytic anaemia: hereditary spherocytosis, rh haemolytic disease, G6PD Ineffective haematopoiesis: thalassaemia, haemolysis Gilbert’s syndrome Malaria, sickle cell ↑ levels of UCB, LFT normal, ALT>ALP

Question 225

Causes of intra hepatic jaundice?

Answer 225

``` Hypothyroidism Crigler-Najjer syndrome Physiological jaundice of newborn Hepatocellular dysfunction Hepatitis Cirrhosis Haemochromatosis Wilson’s α-1-antitrypsin def AI hepatitis Budd-Chiari 1° or metastic liver disease. Rubin Johnson/ rotor syndrome ↓bilirubin excretion ```

Question 226

Causes of obstructive jaundice?

Answer 226

``` Stones Pancreatic Ca Biliary stricture PSC Cholangiocarinoma Biliary atresia Hypercholesterolaemia Xanthoma Pruritis Pale stool + dark urine ```

Question 227

Urine and stools to determine cause of jaundice?

Answer 227

Normal urine + stools = pre-hepatic Dark urine + normal stools = hepatic Dark urine + pale stools = post-hepatic

Question 228

Interpretation of LFTs

Answer 228

ALT>ALP hepatocellular ALP>ALT cholestatic AST = liver parenchymal cells, raised in acute liver damage ALT>AST normal ALP = viral hepatitis AST>ALT = chronic liver disease + cirrhosis ↑GGT + ALP = elevated biliary tract disease ↑GGT + nromal ALP = alcohol

Question 229

Tx of gallstones

Answer 229

``` Treat if symptomatic Bile salts: dissolve cholesterol stones Cholecystectomy Shock wave therapy ERCP ```

Question 230

Ix of gallstones

Answer 230

Cholesterol can’t beseen on XR, rarely soley cholesterol, if contain enough CaCO3 visible on XR. USS MRCP LFTs

Question 231

Pathophysiology of acute cholecystitis

Answer 231

Fatty meal, SI CCK signal GB to contract, stone in duct, obstruction causes GB to stretch, irritates nerves, stagnant bile = irritates mucosa, mucosa secretes mucus, distension, pressure Mirrizzi syndrome: stone in distal cystic duct causing extrinsic CBD compression, obstructive jaund Emphysematous cholecystitis: air in GB wall from gas forming bacteria eg clostridium, e coli.

Question 232

Ix of acute cholecystitis

Answer 232

USS: gallstones/ sludge, GB wall thickening, distension. Air in GB wall (gangrenous cholecystitis), GB wall oedema (double wall sign) Cholescintigraphy/ HIDA scan: tracer excreted in nile, locates blockage. GB won’t be visualised due to blockage MRCP: visulaise blockage Lab results: ^ ALP. Bile backs up, pressure in ducts ↑> cells damaged, die > ALP released. Leucocytosis. ↑ ESR, CRP. Blood cultures.

Question 233

Tx of acute cholecystitis

Answer 233

IV Abx: cefuroxime, metro Early laparoscopic cholecystectomy within 1 wk of diagnosis IV fluids Analgesia: diclofenac with pethidine

Question 234

Complication of chronic cholecystitis

Answer 234

Biliary peritonitis, rupture, sepsis Porcelain GB: fibrosis + calcification, bluish discolouration, hard + brittle. Risk of cancer

Question 235

What is primary sclerosis cholangitis

Answer 235

Chronic inflam + stricture of intra + extrahepatic BD Cells die, fibrosis, tightening of ducts in some areas, dilation in others, obstructs bile Cell death allows bile to leak into interstitial space + blood stream > pruritis AI, T cells destroy BD cells in genetically predisposed HLA-B8/DR3/DRw52a. Associated with CD/UC 2° cause: infection, thrombosis, iatrogenic, trauma.

Question 236

Features of primary sclerosis cholangitis

Answer 236

May remit/ recur spontaneously Jaundice, pruritis RUQ pain Fatigue Fever Steatorrhea Sweats LF: ascites, muscle atrophy, spider angiomas, ↑clotting times, dark urine, pale stools

Question 237

Ix of PSC

Answer 237

ERCP/MRCP: beaded appearance, multiple biliary strictures p-ANCA: pos LFTs: ↑CBR, ALP, GGT ↑ serum IgM antibody Serum albumin + PTT normal

Question 238

Tx of PSC

Answer 238

No effective Tx Immunusuppressants: tacrolimus Chelators Steroids Vit supplementation Ursodeoxycholc acid: ↓bodies reabsorption of cholesterol Pruritis: cholestyramine, rifampicin, naltrexone, sertraline Liver transplant Isolated strictures stented ERCP, balloon dilation

Question 239

What is ascending cholangitis?

Answer 239

Gallstones in CBD, bile obstruction, bacteria ascent from duodenum to BD, infection. E coli, klebsiella, Enterobacter, enterococcus RF: gallstones, stenosis of BD (neoplasm, malig, injury from laparoscopic procedure), parasitic infec, acute pancreatitis, periampullary duodenal diverticulum)

Question 240

Sx of ascending cholangitis?

Answer 240

Charcot triad: RUQ colic, obstructive jaundice, fever/ chills Reynold’s pentad: Charcot’s triad, hypotension/ shock, altered consciousness, confusion Pruritis Pale stools, dark urine N/V

Question 241

Ix of ascending cholangitis?

Answer 241

USS, MRCP ^ WBC, CRP, LFTs (ALP, GGT, ALT, AST), bilirubin, urea + creatinine. 🡫platelets. Metabolic acidosis Blood culture, bile cultures. PTT may be raised with sepsis

Question 242

Tx of ascending cholangitis?

Answer 242

IV Abx: cefuroxime + metronidazole ERCP after 24-48hrs to relieve obstruction Cholecystectomy Stent, balloon dilation

Question 243

Causes of acute pancreatitis?

Answer 243

``` idiopathic/infection (coxsackie B) gallstones ethanol trauma steroids mumps AI scorpion sting hypertriglyceridemia/hypercalcemia/ hypothermia ERCP + emboli Drugs (sulfa, reverse transcriptase inhib, protease inhibs, azathioprine, oestrogens, CS, thiazide/loop diuretics gliptins, Na valproate.) ```

Question 244

Features of acute pancreatitis?

Answer 244

``` Epigastric abdo pain Loss of appetite Palpable tender mass Radiates to back Sitting forward relieves Stone: sudden, knife like, after large meal, dark urine/ pale stool. Alcohol: less abrupt, poorly localised N/V, anorexia Cullen’s sign: periumbilical bruising Grey Turner’s: bruising flanks, BV autodigestion + retroperitoneal haem Fox sign: ecchymosis over inguinal ligament Tachycardia, fever, rigors, shock Rigid abdo Hypotension Jaundice Oliguria ↓/absent BS Guarding Distension/ ascites ```

Question 245

Ix for acute pancreatitis?

Answer 245

CT: inflam, necrosis, abscess, pancreatic pseudocyst, indistinct pancreatic margins, surrounding fat stranding MRI: degree of pancreatic damage USS: GS, pancreatic swelling + necrosis MRCP: biliary/ pancreatic obstruction ↑amylase: >1000u/mL, 3X normal. Leverls fall within 1st 24-48 hrs. False pos: cholecystitis, mesenteric infarction, DKA, pancreatic pseudocyst, GI perf, renal failure. Not prognostic ↑Lipase: more sensitive + specific. Longer ½ life Don’t need imaging if characteristic pain + amylase/lipase >3X normal

Question 246

Glasgow criteria for acute pancreatitis

Answer 246

Determines severity of pancreatitis ``` PaO2: <8kPa Age: >55yrs Neutrophilia: WBC >15 Calcium: <2mmol/L Renal: urea >16 Enzymes: LDH >600iu/L, AST >200iu/L Albumin: <32g/L Sugar: blood glucose >10mmol/L 3+ indicate severe pancreatitis ```

Question 247

Tx for acute pancreatitis

Answer 247

Analgesia: pethidine, morphine, tramadol, fentanyl Fluids Blood transfusion if haemorrhagic pancreatitis NG food, bowel rest. Enteral nutrition within 72 hrs if mod/ severe. Parental if enteral failed or CI. NG suction to prevent abdo distension + ↓risk aspiration pneumonia. Abx only if pancreatic necrosis. Hyperbaric O2 therapy Necrosectomy ERCP Ondasteron Ca + Mg replacement therapy Insulin, can get 2° DM

Question 248

Causes of chronic pancreatitis

Answer 248

Early: Langerhans islets not affected Advanced: atrophy, fibrosis of islets. ↑trypsin, precipitation of protein in duct to form plugs, obstruction, pancreatic damage. Fibrosis calcification Alcohol: impairs Ca regulation, promote trypsinogen activation CF, haemochromatosis, tumours, chronic biliary disease. ``` TIGAR-O T: toxins, alcohol, trauma I: idiopathic G: genes, AD, unopposed trypsin A: AI R: recurrent acute pancreatitis O: obstruction, gall stones, pancreatic head tumour. ```

Question 249

Ix for chronic pancreatitis

Answer 249

AXR: pancreatic calcification CT: more sensitive at detcting pancreatic calcification, pancreatic duct dilation, atrophy USS: hyperechogenicity (fibrosis), psuedocyst, pseudoaneurysm, ascites, pancreatic calcification, indistinct margins + enlargement, ductal strictures, dilation or stones MRCP: PDs, chain of lakes pattern, alternating stenosis + dilation of ducts. Mildly ↑amylase, ALP, bilirubin, lipase. May not be enough healthy tissue to make enzymes Fecal elastase: ↓ shows exocrine function

Question 250

Tx for chronic pancreatitis

Answer 250

Analgesia: tramadol, NSAIDs, octreotide, codeine, gabapentin, pregabalin TCAs: amitriptyline for chronic pain Pancreatic enzyme replacement + nutritonal support PPIs: improve fat absorption Alcohol cessation, low fat diet, ↓obesity, smoking cessation Endoscopy: resection/ drainage, stone removal, dilate strictures with stent

Question 251

Summary of AI pancreatitis

Answer 251

Type 1 IgG4 Asymptomatic jaundice, epigastric pain + pancreatic insuff, multiorgan. Type 2 Associated with IBD Obstructive jaundice, epigastric pain, pancreatic inusff Glucocorticoids Azathioprine Rituximab

Question 252

Types of gastric cancer?

Answer 252

``` Diffuse - adenocarcinoma, mutation in CDH1 Intestinal - adenocarcinoma, H. Pylori Lymphomas - MALT Carcinoid - neuroendocrine Leiomyosarcomas - smooth muscle cells ```

Question 253

Sx of gastric cancer?

Answer 253

Asymptomatic initially Early: vague (malaise, loss of appetite, dyspepsia) Epigastric pain N/V Dysphagia Weight loss GI bleed: anaemia, melena, coffee ground, bright red haematemesis Acanthosis nigricans: darkening of skin at axilla + skin folds Sister Mary Joseph sign: enlarged LN Troisier’s sign: hard + enlarged Virchow’s node Protective: fruit, veg, fibre, folate. RF: smoking, alcohol, age atrophic gastritis

Question 254

Mets of gastric cancer?

Answer 254

Mets: liver, peritoneum, LN (umbilicus, Virchow’s), bilat to both ovaries causes Krukenberg tumour

Question 255

Ix for gastric cancer?

Answer 255

Oesophagogastro duodenoscopy: with biopsy, barium studies, signet ring cells. CT

Question 256

Tx of gastric cancer?

Answer 256

Depends on stage Surgery: endoscopic mucosal resection, partial gastectomy, total gastrectomy Chemo Eradication of H pylori

Question 257

Types of oesophageal ca?

Answer 257

Diagnosed late, rapid mets. SCC: upper 2/3rd, cell damaged smoking, coffee, alcohol, cells divide + mutate Adenocarcinoma: lower 1/3rd, GORD, Barrett’s. now most common, obesity

Question 258

Sx of oesophageal ca?

Answer 258

``` Asymptomatic Dysphagia (food, then liquid) Odynophagia Heartburn Retrosternal pain Weight loss Lymphadenopathy Odynophagia Hoarseness Late: coughing, chest discomfort, when swallowing, hiccups Haematemesis, meleana Virchow’s nodes Vomiting ```

Question 259

Ix of oesophageal ca?

Answer 259

Upper GI endoscopy with biopsy for diagnosis Endoscopic US for locoregional staging EUS guided biopsy, CT XR with barium: identify location + complications eg ulcers + stenosis PET: mets

Question 260

Tx of oesophageal ca?

Answer 260

Resection, oesophagetomy, endoscopic tumour, resection, mucosal ablation, associated nodes. Ivor-Lewis oesophagectomy Radiation Oesophageal stenting: palliative Chemo: cisplatin/ oxilplatin, carboplatin, 5-FU, paclitaxel.

Question 261

Summary of hepatitis A?

Answer 261

RNA picornavirus Most common hep worldwide Faecal oral, Africa + S America, travellers Incubation: 2-4 wks, no carrier state. Acute, no chronic, lifelong immunity ↑AST + ALT, return to normal over 5-20 wks. ↑ESR, leucopenia ↑serum bilirubin, urobilinogen IgG detectable for life (recovery/ vaccination) IgA recent infection ``` Tx: Supportive Avoid alcohol Interferon α Vaccine ```

Question 262

Summary of Hepatitis B

Answer 262

DNA hepadna virus. Surface + core, core infectious Incubation: 1-6mnth, LT carrier status. Transmission: blood + semen RF: IVDU, unprotected sex blood transfusion, haemodialysis, health workers, mother > child IU, minor abrasions. Not transmitted via BF Immune complex related complications: cryoglobulinaemia, polyarteritis nodosa, GN. Chronic hepatitis: ground glass hepatocytes HBV virions found in blood serum, proves viral replication ↑ALT, AST, CRP, ESR, WBC HBsAg (surface antigen): acute infection (1-6 mnths) cleared in recovery; >6 mnths chronic HBcAg (core antigen), acute for 6mnths, if longer carrier. Anti-HBs: immunity (exposure or immunisation), neg in chronic disease. Anti-HBc prev/ current infection. IgM acute/ recent 6 mnths, IgG persists, immune. Chronic infection. Ig without antigens non-infectious. Bilirubin normal to increased To diagnose: antibodies against surface + core. Antibodies against surface from vaccine. Immunisation: 2, 3, 4 mnths of age. At risk (HCP, IVDU, sex workers, blood transfusions, CKD, prisoners, CLD). Avoid alcohol Post exposure prophylaxis with HBV immunoglobulins IFNα, NRTI, lamivudine, entecavir

Question 263

Summary of hepatitis C

Answer 263

RNA flavivirus. Incubation 6-9 wks, lifelong carrier status RF: IVDU, sexual contact, mother to child, chronic haemodialysis, blood transfusion, needle stick injury. BF is NOT CI RF for progression: male, older, higher viral load, use of alcohol, HIV, HBV Doesn’t present with normal acute symptomatic phase, remains non symptomatic + develops to chronic disease. ELISA Specific hep C antigens immunoassay, anti-HCV Ig confirms exposure HCV RNA with PCR confirms ongoing/ chronic. >6mnths = chronic. Can be detected 1-8 wks after infection, if levels ↓ pt recovering. Anti-HCV: usually pos 8 wks from infection, can’t distinguish between acute/ chronic. Pegylated IFN α, ribavirin, daclatasvir, sofosbuvir or sofosbuvir, simeprevir (serine protease inhibitors) Screen for HBV, HIV + HAV: vaccinate against HBV + HAV if tests neg No HCV vaccine available Liver transplant in case of liver failure Quit alcohol. Ribavirin: women shouldn’t become pregnant within 6mnths

Question 264

Summary of hepatitis D

Answer 264

``` Incomplete RNA (needs HBV for its assembly) HBV vaccination prevents Hep D. ``` Body fluids Super infection: Hep B surface antigen pos pt develops hep D, high risk of fulminant hep, chronic hep + cirrhosis Anti-HDV antibody, IgM + IgG both indicate active infection, HDV RNA IFNα limited success Liver transplantation may be needed

Question 265

Summary of hepatitis E?

Answer 265

RNA virus hepeviridae Fecal oral Incubation: 3-8 wks RF: contact with farm animals, travelling, blood transfusions, mother to child Anti-HEV IgM assay in acute infection, PCR in chronic cases ELISA for IgG + IgM, HEV RNA can be detected in serum or stools by PCR ↑ALT, CRP, ESR, WBC IgM > active infection. IgG > immunity. Ribavirin in IS Liver transplant

Question 266

Summary of AI hepatitis?

Answer 266

Autoantibodies against hepatocyte surface antigen, necroinflam, cirrhosis + fibrosis RF: F>M, young, HLA-DR3/4 HLAB8, hypergammaglobulinaemia ↑AST, ALT, PTT. ALT elevated > AST. ↓albumin. 1: ANA, ASMA 2: ALKM-1, ALC-1 3: soluble liver antigen pos or liver pancreas antigen. ↑ bilirubin + hypergammaglobulinemia. ↑IgG Biopsy: mononuclear infiltrate of portal + periportal areas + piecemeal necrosis ± fibrosis. IS: CS, azathioprine Liver transplant

Question 267

Summary of neonatal hepatitis?

Answer 267

1-2 mnths after birth Viruses: 20%, infect mother in preg, baby shortly after birth, rubella, CMV, hep A/B/C Idiopathic: 80%, viral, neonatal cholestasis, newborn bile production immature, developing liver more sensitive to injury α 1 antitrypsin def Hepatitis Sx + failure to grow (impaired bile flow, impaired fat digestion, vitamin absorption) USS: check BD for obstruction Biopsy: multinucleated giant cells ↑bilirubin Ursodeoxycholic acid: ↑ bile formation Cirrhotic liver disease/liver failure requires liver transplant Optimise nutrition/ vitamin supplementation Most recover with little/no damage to liver

Question 268

What is primary biliary cholangitis

Answer 268

Chronic, progressive AI t cell intra hepatic BD destruction. Bile + toxin leakage into parenchyma, inflam, fibrosis, cirrhosis Associated with: Sjogren synd, RA, systemic sclerosis, thyroid disease. F>M, 40-50 Failure of immune tolerance against mitochondrial pyruvate dehydrogenase + other hepatic proteins, antibodies made. Environmental damage can trigger.

Question 269

Sx of PBC

Answer 269

``` Fatigue RUQ pain Pruritis Xanthelasmas Xanthoma Jaundice Pigmentation: face, pressure points Pale stools, dark urine, steatorrhea Sicca syndrome: dry eyes/ mouth Joint pain/ arthropathy Ascites, splenomegaly, varices, hepatic encephalopathy Syncopal eps Clubbing ```

Question 270

Ix of PBC

Answer 270

Anti-Mitochondrial IgM (M2 antigen), ↑serum IgM ↑GGT, ALP, bilirubin, PTT, mildly raised AST, ALT. ↓albumin. ↓fat soluble vits due to poor bile secretion AUSS/MRCP/CT: rule out bile obstruction Biopsy: interlobular BD destruction, inflam, periductal epitheliod granulomas.

Question 271

Tx of PBC

Answer 271

Ursodeoxycholic acid Pruritis: cholestyramine Fat soluble vit supplementation Liver transplant: bilirubin > 100. Recurrence in graft can occur, not usually a problem. Bisphosphonates: osteoporosis Cease all alcohol intake Median survival 12 yrs from Sx onset

Question 272

CYP450 inhibitors

Answer 272

INR increase ``` S: sodium valproate I: isoniazid C: cimetidine K: ketoconazole F: fluconazole A: alcohol (binge), amiodarone/ allopurinol C: chloramphenicol E: erythromycin/ clarithro S: sulfonamides, SSRIs C: ciprofloxacin O: omeprazole M: metronidazole ``` Ritonaviir Quinupristin Grapefruit juice Diltiazem

Question 273

CYP450 inhibitors

Answer 273

INR decrease ``` CRAP GP C: carbamazepine R: rifampicin A: alcohol chronic P: phenytoin G: griseofulvin P: phenobarbitone S: sulphonylureas/ St John’s wort ```

Question 274

Liver mets

Answer 274

Eg breast, stomach, colon, lung, uterus, pancreas, leukaemia, lymphoma, carcinoid tumours

Question 275

Summary of hepatoblastoma?

Answer 275

Childhood malig, arise from primitive hepatic cells, usually R lobe. RF: Beckwith Wiedemann syndrome, trisomy 18, 21, FAP, type Ia glycogen storage disease, Li-Fraumeni syndrome, M>F ``` Abdo mass Discomfort Anorexia Weight loss Extramedullary haematopoiesis may occur in sinusoids 1st 2 yrs of life ``` USS, percut biopsy, CT, MRI ↑AFP Chemo Resection

Question 276

Summary of hepatocellulr carcinoma

Answer 276

RF: hep B/C, HPV, alcoholic cirrhosis, NAFLD, smoking, freq alcohol consumption, androgenic steroids, obesity, α1AT def, gallstone aflatoxin, M>F, haemochromatosis, PBC, hereditary tyrosinosis, glycogen storage disease, oral contraceptives, porphyria cutanea tarda, DM, metabolic syndrome Often no Sx aside from chronic liver disease USS with biopsy, CT, MDCT, arteriography, MRI: tumour visualisation, TNM staging MRI angiography: hepatic circulation, show vascularity of tumour Histology: common to see bile inside hepatocytes, small cancer cells invading large normal cells ↑AFP ↑ALP, GGT, EPO, insulin like GF, PTrP ``` Chemo: sorafenib, gemcitabine, oxaliplatin, cisplatin, doxorubicin, 5-FU, capecitabine, Surgery Liver transplant Radiofreq ablation Transarterial chemoembolization Sorafenib: multikinase inhibitor ```

Question 277

Summary of Wilsons disease

Answer 277

Autosomal recessive, ATP7B gene Chr 13 ↓Cu incorporation into apoceruloplasmin, ↓Cu elimination in bile. Copper accumulation in hepatocytes, free radical gen, hepatocyte damage. Spilling free Cu into blood, Cu accumulation in organs + tissues, free rad gen, tissue damage. Kayser-Fleisher ring CNS: Parkinsonian like movement disorders, tremor, rigidity Psychiatric: depression, personality changes, psychosis, cog dysfunction Dysarthria, dysphagia dyskinesia, dystonia, purposeless stereo types movements, microphagia, ataxia / clumsiness. CP at young age, <30. Usually 5-15 Cirrhosis/ portal HTN Signs of renal dysfunction ↓serum ceruloplasmim + total serum copper ↑24hr copper excretion, ↑Cu excreted in urine, ↑free serum Cu Molecular genetic testing Biopsy: ↑hepatic copper, hepatitis, cirrhosis MRI: degen of BG, frontotemporal dementia, cerebellar + brainstem. Slit lamp exam Penicillamine: chelates copper Trientine hydrochloride is an alternative chelating agent Transplant Eliminate cu rich food eg mushrooms, nuts, shellfish

Question 278

Summary of Gilberts syndrome

Answer 278

Benign, inherited metabolic disorder, ↓conjugation of BR, ↓ability of UGT-1 Recurring ↑UBR, jaundice during physiological stress Autosomal recessive Asymptomatic between episodes Recurring ↑UBR, jaundice during physiological stress (illness, dehydration, fasting, overexertion, menses) ↑bilirubin following prolonged fasting or nicotinic acid No Tx required

Question 279

Summary of Crigler Najjar syndrome

Answer 279

Rare, autosomal recessive Non-haemolytic, ↑BR Mutation in UGT, abnormal UGT1A1 enzyme, ↓ conjugation of BR. If haemolysis occurs eg in infection, stress, or starvation, UBR ↑ + overwhelm hepatocytes Persistent jaundice in 1st few days of life T1: severe, jaundice, BR encephalopathy, kernicterus, don’t survive to adulthood T2: lower BR conc, no neurologic impairment UBR: T1 (20-50mg/dL), T2 (<20mg/dL) Stool colour: T1 (pale yellow, faecal urobilinogen), T2 (normal) Phenobarbital: T2, induces residual UGT activity Liver transplant Phototherapy in 1st yrs of life Plasmapheresis + albumin infusions

Question 280

Summary of haemochromatosis

Answer 280

XS iron absorption in intestine, iron deposited in organs + tissues (liver, pancreas, heart, joints, skin, pit gland), fee radical gen, cellular damage, cell death, tissue fibrosis 1°: autosomal recessive, C282Y mutation in HFE gene on Chr 6, erythrocytes aren’t as good at regulating Fe absorption > iron overload. 2°: multiple blood transfusions, chronic haemolytic anaemia, XS iron intake, thalassaemia RF: European descent, CF Tiredness, arthralgia M: Sx around 50 F: Sx appear 10-20 yrs after menopause Hepatomegaly, jaundice Altered glucose homeostasis (hyper/ hypoglycaemia) Fatigue, malaise Neurological signs: impaired memory, mood swings, irritability, depression ↑serum iron ↑ferritin ↑transferrin saturation >55% men, >50% women ↓total iron binding capacity Liver biopsy: iron seen as brown spots inside hepatocytes, becomes blue with Prussian blue stain. Chondrocalcinosis (deposition of CPPD crystals into fibrous or hyaline cartilage.) Liver MRI: Fe overload

Question 281

Summary of Budd-Chiari syndrome

Answer 281

Hepatic vein obstruction by thrombosis or tumour, congestive hepatocyte damage. Ischaemia + centrilobular necrosis, ↑pressure in portal system, portal HTN liver failure or cirrhosis. Hypercoagulable states: pill, pregnant, malig, paroxysmal nocturnal haemoglobinuria, polycythaemia, thrombophilia, TB, liver or adrenal tumour, ``` ender hepatomegaly Ascites Abdo pain Jaundice Fever ``` Doppler USS: thrombus, alteration of hepatic venous outflow, spider web formation around obstruction due to collateral vessel prolif Venography CT/MRI ↑ALT Treat cause Meds: usually insuff, anticaog, diuretics Liver transplant Portosystemic shunt: divert flow away from obstruction Thrombolytic therapy: dissolve clots, balloon angioplasty

Question 282

Summary of Whipple's disease

Answer 282

Rare, malabsorptive infectious disease, caused by Tropheryma Whipplei Subtotal villous atrophy, mimick coeliac. RF: middle aged M, exposure to faeces, HLA-B27 ``` Diarrhoea, weight loss, abdo pain Skin hyperpigmentation Pleural disease Dementia, seizures Ataxia ``` Lamina propria displays numerous macrophages with periodic acid-Schiff pos intracellular material. >2 pos PCR/PAS tests Stunted villi IV: ceftriaxone, pen G Trimethoprim Co-trimoxazole for 1 yr

Question 283

What is PAD?

Answer 283

Narrowing arteries in periph circulation. LL most common. Aorto-iliac + infra inguinal arteires. Atherosclerosis, stenosis, ↓blood flow, arterial insuff tissue ischaemia. Ulcer formation, poor healing. Ischaemic cells release adenosine, sensation of pain. Intermittent claudication: pain caused by poor circulation Occlusive: plaque/emboli Functional: defect in normal mechanisms that dilate + constrict arteries, vasospasms Acute: thrombus completely occluding artery, sudden lack of flow to limb. DIC, clottingng disorders, venous grafts, emboli. Chronic: >70% vessel is usually symptomatic RF: smoking, HTN, DM, hyperlipidemia, met synd, sedentary lifestyle, >60, obesity, African.

Question 284

Sx of PAD?

Answer 284

Claudication distance: cramping pain after walking given distance. Rest pain: burning/ pain when elevated, relieved when lowered, pain at night relieved when hang legs over side of bed. ↓peripheral pulses Ulcers: don’t heal normally, punched out, often toe joint, malleoli, shin, base of heel, pressure points. Painful. Cutaneous colour changes Elevation pallor Dependent rubor: red when lowered, gravity ↑perfusion Skin: cool, dry, shiny, hairless. Nails: brittle, hypertrophic, ridged, thickened. Cap refill >15 secs

Question 285

Ix of PAD?

Answer 285

U+E: renal disease ECG: cardiac ischaemia Anaemia, polycythaemia Doppler USS: ↓blood flow colour duplex (arterial flow + pulse waveform) MR/CT angiography: assess location of stenosis. Auscultation: bruit Percut transluminal angiography/ angioplasty: injection of contrast, gives roadmap of vessels. ABI: BP taken in ankle + arm compared. <0.9 PAD, 0.4-0.9 claudication, 0.2-0.4 rest pain, 0-0.4 tissue loss, ulcers, gangrene. >1.3 abnormally hard arteries, DM/ renovascular disease Buerger’s test: angle at which leg becomes pale when elevate it, lower angle required, more severe ischaemia. Upon lowering foot returns to normal pinkness more slowly, progresses to redness, sunset foot.

Question 286

Tx of PAD?

Answer 286

Anti-plt therapy: clopidogrel. Percut transluminal angioplasty, balloon inflation, stent insertion. Arterial reconstruction with bypass graft. Endarterectomy Amputation Wound care Statin: atorvastatin 80mg Exercise training Naftidrofuryl oxalate: vasodilator, pts with poor quality of life. Cilostazol: phosphodiesterase III inhib with antiplt + vasodilator effects.

Question 287

What is acute limb ischaemia?

Answer 287

Surgical emergency, revascularisation within 4-6hrs to save limb Sudden ↓ in limb perfusion potential threat to limb viability. Emboli, thrombosis, trauma, rupture of atherosclerotic plaque, bypass graft thrombosis, prothrombotic states, shock (states of low flow), vasculitis, popliteal entrapment syndrome (compressed by gastrocnemius, young, man, sporty, pain by exercise). Compartment syndrome. Iatrogenic (injury of common femoral or sup femoral a following catheterisaition), aortic dissection, graft occlusion

Question 288

Sx of acute limb ischaemia?

Answer 288

6 Ps: pale, pulseless, pain, paralysed, paraesthesia, perishingly cold. Fixed mottling: irreversibility Sensation + movement of leg ↓ Deep duskiness of limb. Tender: muscle ischaemia

Question 289

What is reperfusion injury?

Answer 289

ischaemic limb revascularized, sudden improvement in blood flow, release of toxic metabolites into circulation. Release K, CK, myobloin, lactate + O2 free radicals > renal failure, myocardial toxicity + multi organ failure

Question 290

Ix of acute ischaemic limb

Answer 290

Viable: no abnormality A Threatened, cap return intact/ slow. Salvageable if promptly treated. Partial sensory loss (toes). No muscle weakness. Inaudible doppler on arterial, audible on venous. 2. B threatened. Salvageable with immediate reconstructed. Slow/absent cap refill. Partial paralysis. Partial/ complete sensory loss. Inaudible doppler on arterial, audible on venous. 3. Irreversible: major tissue loss, permanent damage. Absent cap return. Profound paralysis. Profound sensory loss. Inaudible doppler signs. Amputation or palliation. ECG: AF, cardiac event > source of emboli. FBC: haem disorders predisposing to thrombosis U+E: dehydrated, ↑k if muscle necrosis occurred. Handheld doppler

Question 291

Tx of acute limb ischaemia

Answer 291

Emergency, may require urgent open or angioplasty. IV unfractionated heparin to prevent thrombus propagation Surgical embolectomy: fogarty catheter for emboli, local thrombolysis eg tissue plasminogen activator eg alteplase. Endartectomy, bypass graft. Analgesia: opioids Amputation Mechanical clot disruption: injected saline. IV fluids Palliation CI to thrombolysis: bleeding/ severe bleeding tendency, pregnancy, CVA/TIA <2mnth ago, IC tumour /AVM, aneurysm, surgery <2 wks ago, prev GI bleed, trauma <10 days ago

Question 292

What is compartment syndrome?

Answer 292

↑pressure in closed space, insuff venous drainage, further pooling, ↑pressure further, compromises blood supply, ischaemia, tissue damage > inflam Acute: # (supracondylar + tibial shaft), haem, crush injuries, vascular puncture, penetrating trauma, severe circumferential burns, IVDU, revascularisation procedures, poor-fitting casts, reperfusion injury. Chronic: repetitive muscle use/ exertion during vigorous exercise.

Question 293

Sx of compartment syndrome?

Answer 293

Acute: rapid, severe pain (burning, constant, poorly localised) exacerbated by movement, not relieved by analgesics (XS use of breakthrough analgesia), swelling, tense muscle compartment, paraesthesia. Pulseless, function loss, paraesthesia Chronic: Sx in physical activity, subside when activity stops. tense muscle compartment, numbness, tingling, cramping, foot drop

Question 294

Complications of compartment syndrome?

Answer 294

Irreversible N damage Infection Ischaemia > necrosis Limb amputation Volkmann’s contracture permanent affected limb flexion, contracture Rhabdomyolysis Kidney failure

Question 295

Ix of compartment syndrome?

Answer 295

Acute: ↑CK, myoglobin. Intercompartmental pressure >25mmHg. Delta pressure <20-30mmHg (delta pressure = DBP – measured compartment pressure) Chronic: prior to exercise >15mmHg, after 1 min of exercise >30mmHg, after 5 mins of exercise >20mmHg, diagnosis of exclusion. Presence of pulse doesn’t rule out compartment syndrome No pathology on XR

Question 296

Tx of compartment syndrome?

Answer 296

Acute: fasciotomy, escharotomy (burns), limb amputation Myoglobinuria can occur following fasciotomy + result in renal failure. Require XS IV fluids. Chronic: ↓exercise volume, physical therapy Death of muscle groups may occur within 4-6 hrs

Question 297

What is aneurysm

Answer 297

Abnormal dilation in BV 1.5 X larger than normal. >3cm in aortic + thoracic. Areas of high press: aorta, femoral, iliac, popliteal, cerebral. Pressure on BV wall ↑ with diameter of vessel lumen (LaPlace law) True: all layers BC dilate, fusiform (symmetrical), saccular/berry (asymmetric ↑press on 1 side, or wall weaker). Pseudo: small hole in BV wall, in all 3 layers, outer layer of CT aneurysms, blood pools.

Question 298

Sx of aneurysm

Answer 298

60% of AA in abdo, 40% in thoracic. Most between renal A branch + aortic bifurcation as less collagen. Severe pain in specific location Pulsating mass Syncope Hypotension Tachycardia AAA: abdo/ epigastric pain, radiates to back, iliac fossa/groins. Thoraco-abdo: severe chest/ back/ abdo pain. Stridor, haemoptysis, hoarseness. Cerebral: meningeal signs, sudden severe headache, can’t flex neck forwards

Question 299

Ix of aneurysm

Answer 299

USS Screening: all men 65y/o Small: 3-4.4. rescan every 12 mnths Med: 4.5-5.4. rescan every 3mnth Large: >5.5 refer within 2 wks to vascular surgery for probable intervention Low rupture risk: asymptomatic, <5.5cm. abdo US surveillance, optimise CV RF High rupture risk: symptomatic, >5.5cm or rapidly enlarging >1cm/yr. Refer within 2wks.

Question 300

Tx of aneurysm?

Answer 300

EVAR: endovascular repair or open if unsuitable. Stent placed via femoral artery. Surgical clipping of aneurysm at base Endovascular coiling: plt wires promote blood clotting, ↓ blood flow through aneurysm Surgical repair with insertion of graft: involves clamping aorta. Treat HTN Rupture: immediate vascular review with emergency surgical repair. If haem unstable take straight to theatre. If haem stable CT angiogram.

Question 301

What is aortic dissection

Answer 301

Tear forms in tunica intima high pressure blood flows between tunica intima/ tunica media. Layer separation. ↑outside diameter of BV. Most develop in 1st 10cm of aorta. Pressure of blood continues to shear intima making tear larger. TA: ascending / aortic arch, sometimes descending TB: descending / aortic arch w/o ascending. Acute <2 wks, subacute 2-8 wks. Chronic > 8 wks.

Question 302

Sx of aortic dissection

Answer 302

Sudden, intense, tearing CP, radiate to back. TA: CP, TB: back pain N/V, diaphoresis Chronic dissection painless Pulse deficit: weak/ absent carotid, brachial or femoral

Question 303

Ix of aortic dissection

Answer 303

CXR: widened mediastinum Transoes echo: clear picture of aorta. Unstable pts too risky to take to CT CT angio: chest, abdo pelvis, investigation of choice. False lumen. MR angiography ST elevation in inf leads

Question 304

Tx of aortic dissection

Answer 304

TA: surgical, BP controlled to target of SBP 100-120 TB: conservative, best rest, IV labetalol for BP

Question 305

Summary of venous ulcers?

Answer 305

Sustained venous HTN in sup veins, incompetent valves or prev DVT. ↑ pressure, extravasation of fibrin through cap walls > fibrosis of interstitial areas, thickening + ↓oxygenation of tissues = can’t repair damage. Over time, pressure in tissues cause tiny capillaries to get pinched shut, tissue ischaemia, breakdown of tissues incl skin. RF: sup venous incompetence (varicose veins), prev DVT, phlebitis, prev #, trauma or surgery to leg. FH of venous disease Lower leg, bony prominences, medial malleolus. Shallow Wet Irregular edges Heavy exudate Pain, not that severe relieved to some extent by elevation Features of CVI Warm skin, normal periph pulses. Varicose veins, leg oedema Doppler studies before bandaging to ensure not arterial ulcer Venous duplex USS to look for venous incompetence High compression bandage, leg raise Skin grafting Vein transplant, vein repair, vein removal Diuretics, Abx for infection.

Question 306

Summary of arterial ulcers?

Answer 306

Lack of perfusion to caps, when get mild damage RF: PAD, CHD, stroke, TIA, DM, obesity + immobility Punched out lesion Painful > intense, worse when elevated Toes + heels Small, deep, sharply defined, often with necrotic base Doppler ABPI Exam: absent pulses, arterial bruits, cold, pale, atrophic, hairless leg, shiny pale skin, gangrene, brittle or ridged nails. Tx depends on keeping ulcer clean. No compression bandaging Analgesia Revascularisation surgery

Question 307

Summary of diabetic/neuropathic ulcers?

Answer 307

Poor small vessel perfusion to feet. Neuropathy. Hyperglycaemia inhibits immune (particularly neutrophil). Infectious element. Pressure areas: metatarsal heads due to repeated trauma, plantar surface of hallux, soles, heels, toes. Punched out, variable size, depth granulating base. Assess sensation, monofilament test. HbA1c Ischaemic: atrophic foot, cold, pulseless, painful. Neuropathic: painless, high arch foot, clawing toes, warm bounding pulses. Keep ulcer clean, remove pressure. Cushioned shoes Abx Vascular referral Improve glycaemic control + foot hygiene.

Question 308

Summary of pressure ulcers?

Answer 308

Bedsores Pressure applied to soft tissue, complete or partial obstruction to blood flow RF: malnourishment, incontinence, lack of mobility, pain. Bony prominence on LL, often heel, as Waterlow score: screen pts at risk of developing pressure area. 1: non-blanchable erythema, intact skin. Discolouration of skin, warmth, oedema, induration or hardness. 2: partial thickness skin loss, epidermis/dermis. Ulcer sup, abrasion/ blister 3: full thickness skin loss, damage to/ necrosis of SC tissue, may extend to, but not through fascia. 4: extensive destruction, tissue necrosis, damage to muscle, bone or supporting structures, without full thickness skin loss. Moist wound environment, promotes healing. Hydrocolloid dressing, hydrogels. Use of soap discouraged to avoid drying wound. Wound swabs not done routinely, vast majority of ulcers colonised with bacteria. Referral to tissue viability nurse Surgical debridement Redistribution of pressure by regular repositioning.

Question 309

Breast screening

Answer 309

Mammography, every 3yrs 50-70. No screening <40 can’t see tumour due to tissue density Extra screening: 1 1st degree relative <40, 1 1st degree male relative any age, 1 1st degree relative bilat <50. 2 1st degree relatives, or 1 1st degree + 1 2nd degree any age, 1 1st degree/ 2nd degree relative any age + 1 1st degree/2nd degree relative with ovarian Ca. If only 1 1st degree or 2nd degree, extra screening if: <40 at diagnosis, bilat breast Ca, male breast Ca, ovarian cancer, Jewish ancestry, sarcoma in relative < 45, glioma or childhood adrenal cortical Ca, multiple Ca at young age. Paternal Hx of breast ca (2+ relatives)

Question 310

Breast cancer RFs

Answer 310

age, FH, BRCA 1+2, HER2. PMH of breast Ca, HRT, early menarche. Late menopause. COCP, nuliparity, 1st viable preg >35. Radiotherapy to chest, no BF. Li-Fraumeni, Peutz-Jeghers, Klinefelters. Protective: physical activity, BF, healthy diet, NSAIDs, aspirin

Question 311

Types of breast ca

Answer 311

Majority arise from lacotocytes. Ductal Ca in situ: precancerous, non invasive. Abnormal clusters of cells lining lactiferous ducts. Lobular Ca in situ: rare, progression uncertain, usually slow. Infiltrating ductal Ca: most common, 90% adenocarcinoma. Medullary: BRCA1, well circumscribed, smooth borders, triple neg. Infiltrating lobular Inflam Ca: dermal lymphatic invasion + angioinvasion, rapid growth. No mass.

Question 312

Sx of breast ca

Answer 312

Infiltrating ductal Ca: hard lump, skin tethering Lump: size, surface, consistency, contour of edge, temp of skin, tethering LN: enlarged, firm, non-tender Malig: painless, irregular, hard mass, fixed, ↑size, drawing of skin near lump. Discharge: blood/ clear worrying Nipple tethering Skin dimpling: orange peel Inflam breast ca: cancerous cells block lymph drainage, inflamed, can be oedematous, or ulcerate. Weight loss, night sweats, loss of appetite. Nottingham prognostic index: tumour size x 0.2 + LN score + grade score.

Question 313

Ix of breast ca

Answer 313

DCIS: calcification on mammogram. High chance of becoming invasive. No penetration of BM, preceded by duct atypia. Central necrosis, enlarged ducts with atypical epithelium. IDC: disorganised, small, duct like glandular tissue, stromal invasion. Fibrosis of surrounding tissue, microcalcifications. Tubular, medullary, papillary, cribiform. ILC: difficult to see on mammogram, often multiple tumours. Malig cells in lobules, monomorphic cells in single file pattern, ↓ E-cadherin expression, absence of new duct formation. Comedocarcinoma: cells with high grade nuclei, extensive central caseous necrosis. Dystrophic calcifications. 2 ww: >30 + unexplained lump, >50 + discharge, retraction of nipple or other worrying Sx. <30: non-urgent referral. Mammography: >3 then carry on with biopsy USS: hypoechoic lesion, calcifications, irregular margins. Core tissue biopsy: prolif index, oes/prog + HER2 receptor status. If don’t express any of these receptors triple neg. Fine needle aspiration cytology or lump/LN. Malig features: cells lose features of tissue origin, abnormal, rapid mitosis, DNA loss, pleomorphism, invasive growth, neoangiogeneiss.

Question 314

Tx of breast cancer

Answer 314

Wide local excision: solitary lesion, periph tumour, small lesion in large breast, DCIS <4cm clear margin of 2mm should be met. Mastectomy: multifocal tumour, central, large lesion in small breast, DCIS > 4cm Women with no palpable LN pre-op axillary USS. If pos have sentinel node biopsy. LN clearance: if any involved remove all. > lymphoedema. Premenopausal: oes pos tamoxifen. SE: menopausal Sx, weight gain, vaginal discharge/ bleeding, thromboembolism, nausea, endometrial hyperplasia + Ca. Postmenopausal: aromatase inhibs anastrozole, letrozole. SE: hot flushes, vaginal dryness, bleeding, arthralgia, arthritis, bone #, skin rask (SJS) osteoporosis, hair thinning, N/V, drowsy HER2 pos: trastuzumab (Herceptin) cardiotoxic Pre-op chemo/ post-op chemo (always after wide local excision), for axillary node disease. FEC-D used Whole breast radiation for high risk + after wide local exicion, ↓risk of 2/3

Question 315

Ix of lymphedema

Answer 315

0: latent, lymphatic vessels, damaged but no oedema 1: spont reversible, tissue pitting, reversed with pressure + elevated. 2: spont irreversible, spongy appearance, bounces back when pressed, non pitting. Fibrosis starts to develop. Limbs harden, ↑in size. 3: lymphoblastic elephantiasis limbs harden, irreversible

Question 316

Tx of lymphedema

Answer 316

Lower risk: exercise, skin care (dry + moisturised), avoid injections, blood tests, BP > use other limb Manual lymphatic massage, compression bandage Intermittent pneumatic compression therapy

Question 317

Summary of breast cyst

Answer 317

Distended + involuted lobules. Very common 40-50, >60 Esp common with HRT ``` Fluctuates with menstrual cycle Painful/tender Flat, smooth, soft fluctuant. Frew multiple/ bilat Well demarcated from surrounding tissue Firm mobile ``` Small ↑ risk of breast ca Halo appearance on mammogram USS: fluid filled Those that aspirate blood or persistently refill should be biopsied or excised. Needle aspiration

Question 318

Summary of fibroadenoma

Answer 318

Benign, oestrogen sensitive prolif breast lesion. Pregnancy, premenstruation. Regress with age. 15-30y/o 2-3cm, firm, well circumscribed, round, palpable, mobile painless Possibly painful around menstruation Size increases: poss infarction/ inflam USS: well defined, solid, hypoechoic lesion Mammogram: circumscribed, dense lesion, clustered calcifications Biopsy: glandular, fibrous tissue (epithelial cells arranged in fibrous stroma). Excl breast cancer <3cm + highly typical watchful wait. Core biopsy if >3cm = to rule out Phyllodes tumour. Therapy rarely required, often regress post menopause Surgical excision > 3cm or rapidly growing Cryoablation

Question 319

Summary of fibroadenosis

Answer 319

Fibrocystic changes Young/ middle aged women. Sclerosing asdenosis: acini, stromal fibrosis, calcifications. Radial scars + complex scarring lesions. Distortion to lobules w/o hyperplasia Epithelial hyperplasia: ↑ cellularity in terminal duct/ lobular epithelium, atypical cells. Fluctuate, more common in pre menstrual period Secretion of non-bloody discharge, green or brown Irregular nodularity, can be rubbery, bilat Bilat breast pain + tenderness. Breast lumpiness Mammogram: dense breasts with cysts USS: fluid-filled cysts Aspiration: if mass present, excl tumour. If clear fluid obtained + mass disappears > fibrocystic breast changes. Biopsy: cysts (blue serous fluid ‘blue dome’ appearance, various sizes, calcifications common). Fibrosis (due to chronic inflam from cyst rupture, material release to stroma). Adenosis (↑acini per lobule) NSAIDs, COCP Surgical intervention often unnecessary, resolves with menopause

Question 320

Summary of Phyllodes tumour

Answer 320

Rare fibroepithelial breast tumour, in stroma of breast. RF: 30-50, acquired chromosomal mutations, gains in Chr1q. Large, palpable, firm mass, multinodular, well-circumscribed, mobile painless Slow growing or develops rapidly over entire breast. Overlying skin shiny, stretched Bloody discharge Bulky tumours that distort breast, may ulcerate through skin due to pressure necrosis. Can become malig sarcoma. Local recurrence after excision Local haem, necrosis. MRI: well circumscribed lesion, ↑intensity on T1 ↓signal intensity on T2 Mammogram: smooth, polylobulated mass, resembles fibroadenoma USS: solid, hypoechoic, well circumscribed lesion, cystic areas, microcalcifications absent. Core needle biopsy: ↑cellularity, mitotic rate, nuclear polymorphism, fibrous stroma overgrowth, leaf like lobulations, cysts. Cellular pleomorphism indicates malignancy Surgical removal, wide local excision Large/ high risk/ recurrent: adjuvant radiotherapy/ chemo

Question 321

Summary of intraductal papilloma?

Answer 321

Rare benign fibroepithelial breast tumour, arising from lactiferous duct epithelium. Central: near nipple, usually solitary, often arise near menopause. Periph: often multiple, usually in younger. RF: 20-30y/u Intermittent bloody /serous nipple discharge Breast feels full, relieved by discharge passage Large may have mass Galactography: contrast enhanced mammogram. Filling lactiferous duct defect. Mammogram: usually too small to detect. USS: projections extending from duct wall within lumen. Used to diagnose/ guide surgical resection Biopsy: fibrovascular intraductal projections lined by myoepithelial, epithelial cells. Small incidental: Tx unnecessary Surgery: breast duct removal

Question 322

Summary of duct ectasia

Answer 322

Dilation/ distension + shortening of terminal breast ducts within 3cm of nipple. Most common in menopausal women. Smokers Cheese like nipple discharge, may be green, bloody discharge Nipple inversion Firm, stable, painful mass under nipple. Ruptures: local inflam, plasma cell mastitis. Mammogram, USS to determine mammary duct diameter Biopsy: central cavity filled with neutrophils + secretion. Pericentral inflam +/or fibrotic breast parenchyma. Obliteration of cuts. No specific management Microdochectomy if young Total duct excision if older

Question 323

Summary of mastitis

Answer 323

Dry, cracked, fissured areola/ nipple complex portal for infection. Infectious: s aureus Non-infectious: milk stasis, prolonged engorgement, infreq/ inefficient feeding, clogged ducts. RF: impaired immunity, DM. ``` Localised firmness, redness, swelling, heat. Palpable lump Breast pain Tender/ enlarged axillary nodes Fever, malaise, myalgias. ``` Lactation abscess: BF women, red, hot, swollen + tender breast lump. Purulent discharge Non-lactation: extension of periductal mastitis, under areola, nipple inversion. Duct ectasia. Smoking/ DM USS: identifies abscess presence Leukocytosis Breast milk culture: identifies causative microorganism Heat, continue BF Abx: fluclox 10-14 days. If systemically unwell, nipple fissure, if Sx don’t improve after 12-24 hrs of effective milk removal Abscess requires incision/ draining

Question 324

Causes of gynaecomastia

Answer 324

Benign growth of glandular tissue of male breast. Oest XS: tesicular seminoma, ectopic hCG eg lung, HCC, adrenocortical tumours, liver cirrhosis, hyperthyroid, refeeding ↓testosterone: klinefelters, CKD, testicular disorders, starvation. Kallman’s. Drugs: finasteride, spironolactone, ketoxonazole, chemo, haemodialysis. Cannabis. Cimetidine, digoxin. GnRH agonists eg goserelin, buserelin. Oestrogens, anabolic steroids. TCAs, CCBs, heroin, isoniazid, busulfan, methyldopa. Serum levels of testosterone, oestrogen, LH + hCG LFTs, renal function tests, TFT Mammography + USS guided biopsy. Appears as normal breast tissue behind nipple on mammography Surgical removal if >17. Treat cause

Question 325

Causes of galactorrhea

Answer 325

Stress, BF, oestrogens, exercise, sleep. Acromegaly, PCOS ↑PRL: prolactinoma, ectopic PRL tumour, CKD, hypothyroidism (TRH stimulating PRL) Drugs: domperidone, metoclopramide, phenothiazines, haloperidol, SSRIs, opioids.

Question 326

Summary of Pagets disease of breast

Answer 326

Epidermotropic theory: underlying Ca > malig cells migrate through ductal system > nipple epidermis. In situ transformation: nipple keratinocyte transformation Unilat, nipple + adjacent areolar skin: scaly, itching, burning, erythema Bloody nipple discharge, nipple inversion, pain. Palpable mass > worse prognosis. Nipple then latterly spreads to areola Mammogram: mass, microcalcifications, tissue distortion US guided mass core biopsy Nipple scrape cytology/ full-thickness wedge/punch biopsy: malig, intraepithelial adenocarcinoma Paget cells (large, round cells clear halo + prominent nuclei) form intraepithelial adenocarcinoma. Mastectomy Breast conserving surgery Whole breast radiotherapy.

Question 327

Summary of breast fat necrosis

Answer 327

Traumatic aetiology, may be trivial or unnoticed Physical features mimic Ca Mass may increase in size. Initial inflam response Firm, round lesion, may develop into hard, irregular breast lump. Imaging + core biopsy