General surgery Flashcards
Upper + lower GI
1
Q
Why does SBO present so acutely?
A
Large amounts of gastric + pancreatic-biliary secretions prevented from passing
2
Q
What are the causes of bowel obstruction?
A
- Within wall: tumours, inflammatory strictures, drug-induced strictures, lymphoma, intussusception (segment of SB telescoped into segment distal to it)
- Within lumen: impacted faeces, gallstones, phytobezoar, trichobezoar
- Outside wall: adhesions (surgery/infection), congenital bands, compressing tumours, strangulated hernias
3
Q
Small bowel obstruction?
A
- Main cause is adhesions
- Other causes: hernias, compression by internal/external masses, Crohn’s disease
- Dilatation of SB >3cm in central loops, valvulae conniventes more visible
4
Q
Large bowel obstruction?
A
- Most caused by malignancy, others include diverticular strictures, volvulus and hernias.
- Dilatation of LB >6cm (peripheral not loops), haustral lines visible
5
Q
Bowl obstruction presentation?
A
- Vomiting-earlier when obstruction more proximal, semi-digested suggests gastric outlet obstruction, bile-stained suggests upper SBO, faeculent suggests more distal obstruction (altered SB contents)
- Pain-upper/middle/lower for foregut/midgut/hindgut, colicky as peristalsis tries to overcome obstruction
- Constipation-absolute
- Incomplete obstruction - less distinct features basically. e.g. intermittent vomiting, erratic bowels, chronic incomplete obstruction e.g. from cancer often visible peristalsis in abdomen
6
Q
Why is LBO more gradual onset?
A
Larger capacity
7
Q
What is the relevance of the ileocaecal valve?
A
In LBO, if the valve is competent no retrograde flow occurs so the caecum distends until it ruptures, whereas if valve is incompetent then the SB can dissent to reduce chance of perforation
So incompetent valve is better
8
Q
Incomplete obstruction?
A
Most common cause is colorectal cancer. Less distinct features e.g. intermittent vomiting, erratic bowel habit, if chronic gradual hypertrophy of bowel wall muscle
9
Q
Clinical signs of bowel obstruction?
A
General: abdo distention, anaemia, lymphadenopathy
Groin: look for hernias
Tender when strangulated/perforated, resonant percussion in centre then more dull at periphery (gas rises), high pitched tinkling bowel sounds
10
Q
Complications of bowel obstruction?
A
ischaemia, perforation, peritonitis, dehydration, renal impairment
11
Q
How would you manage a patient with bowel obstruction?
A
- NBM, NG tube, IV fluids, correct electrolytes
- Urinary catheter + fluid balance
- Analgesia + anti-emetics
- Adhesions treat conservatively unless strangulation/ischaemia, if contrast doesn’t reach colon in 6h need surgery
- Surgery (laparotomy) in: suspected ischaemia, closed loop obstruction , virgin abdomen, strangulated hernia, failure to respond to conservative management in 48h (most LBO need surgery) // or emergency hernia repair. Can sometimes try endoscopic stenting (good for left-sided obstruction)
12
Q
Causes of bowel strangulation
A
Partial obstruction: occludes venous return, oedema worsens obstruction, closed loop of bowel dilates with gas as bacteria ferment, inhibits arterial flow, ischaemia, infarction
Commonest cause are strangulated hernias (usually inflamed but femoral often small and non-tender), others include being trapped by adhesions, passing through omental/mesenteric defect, volvulus
13
Q
Signs of bowel strangulation
A
Signs of obstruction
Abdominal tenderness
Rising tachycardia + leukocytosis
Manage w fluids + urgent surgery
14
Q
Causes of peritonitis
A
Localised - transmural inflammation of bowel (e.g. appendicitis, Crohn’s, diverticulitis) or of viscera (e.g. salpingitis, cholecystitis)
Generalised: chemical peritonitis (bile, stomach contents, exudate from pancreatitis) or bacterial (ruptured abscess, faecal contamination from bowel perforation, surgical spillage, anastomotic leak)
15
Q
Clinical features of peritonitis
A
Localised peritonitis-inflammation, pain localises when PP involved, systemic toxicity
Generalised-rapidly v ill, hypovolaemia from exudation of inflammatory fluid into peritoneal cavity, sepsis
16
Q
Intra-abdominal abscess
A
Worsening continuous pain, diarrhoea, adynamic bowel (from local irritation), swinging pyrexia, leucocytosis, palpable mass, PR hot tender mass. Pt often quite well (except post-op abscess)
May occur after bowel perforation (momentum + adjacent bowel wall wall off the defect, e.g. appendiceal abscess), or as a complication of bowel surgery (localised faecal contamination or anastomotic leak)
M: may drain spontaneously into rectum (pass pus + blood PR), or Abx + drainage if unwell
17
Q
What causes abdominal viscus perforation?
A
Stomach and duodenum - PUD Sigmoid colon - diverticular disease, cancer Appendicitis Severe constipation Severe acute cholecystitis
18
Q
How may perforation present?
A
Small perforations - local abscess as perforation walled off by omentum/bowel e.g. appendicitis
Large colonic perforation-sudden overwhelming faecal peritonitis
Peptic ulcer: board-like rigidity, initially little systemic upset as fluid mostly sterile
19
Q
What surgical repair is employed in the common perforations?
A
Duodenal - plug with omentum
LB - Hartmann’s (end colostomy + rectal stump, temporary colostomy, as an anastomosis won’t heal cos of contamination)
Not suitable for surgery - restrict fluids, NG aspiration, acid suppression, ABx (this is only if can’t have GA)
20
Q
What is acute bowel ischaemia?
A
Acute occlusion of SMA - ischaemia of midgut-derived structures (jejunum, ileum, right colon) - infarction of right colon + most of SB - perforation
Caused by embolism (e.g. AF), thrombosis of artery (e.g. low output HF), mesenteric vein thrombosis often patchy inflammation so may be better prognosis
21
Q
What is the presentation + management of acute bowel ischaemia?
A
Severe pain, abdo usually soft without guarding, later CV collapse, metabolic acidosis, raised lactate
Urgent laparotomy (if limited resection may work), often necrosis so severe that care should be palliative
22
Q
Causes of CF of major GI haemorrhage
A
- Gastric/duodenal erosions - haematemesis/melaena. Common
- Colon cancer/polyps-altered blood PR, common
- Diverticular disease-fresh PR bleeding, common
- Rectal cancer/haemorrhoids-fresh PR bleeding usually small amount
- Ischaemic colitis-abdo pain + fairly fresh PR blood. Quite common
- Colonic angiodysplasias-depends on location within colon, quite common
- Oesophageal varices-haematemesis/melaena
- Mallory Weiss tears-haematemesis/altered blood PR
- Stress gastric ulcers-haematemesis/melaena
- Acute UC-bloody diarrhoea
- Malignant SB tumours or angiodysplasias of SB - altered blood PR
23
Q
Dieulafoy lesion?
A
Large tortuous arteriole that bleeds
24
Q
Anatomy of the appendix
A
Blind-ending tube from caecum at meeting of three taenia coli, base is in RIF close to McBurney’s point (2/3 way from umbilicus to ASIS) - suspended by mesentery and floats around - inflammation fixes in a point e.g. over pelvic brim, retroperitoneally
25
Pathophysiology of appendicitis
Faecolith/obstruction - inflamed mucosa - spreads to serosa (VP) - spreads to adjacent structures - gangrene of appendix wall causes perforation. Then there is either a walling off reaction, or not and spreading peritonitis occurs
26
How is the likelihood of appendicitis graded?
Alvarado score: if 4 or less v unlikely to be appendicitis
1 point each for: migration of pain from centre to RIF, anorexia, N/V, rebound tenderness, temp >37.5, neutrophilia >75%
2 points for tenderness in RIF and leucocytosis (>10)
27
How does appendicitis present?
Abdo pain <72h
Migrates from centre (visceral P) to RIF (parietal P, somatic pain)
Local peritonitis: guarding, tender, rebound/percussion tenderness (as by palpation v severe pain), tender in RIF, ask to blow out abdo wall and draw in
Fever 37.3-38.5 (temp over this makes viral/UTI more likely)
No evidence of UTI
Anterior tenderness on DRE
Atypical: urinary symptoms if appendix near bladder, if near rectum diarrhoea, if retrocaecal irritation of psoas muscle (pain on extension, involuntary R hip flexion), high retrocaecal (pain below R costal margin), pelvic pain
In kids peritonitis and perforation more common, in elderly often walled off by loops of SB
28
Differential diagnoses for appendicitis?
UTI - nitrates in dip
Mesenteric adenines - esp in kids after recent sore throat/viral illness, inflammation of LNs, fever higher
Large bowel disorders - constipation, diverticulitis
Gynae issues-mittelschmerz, salpingitis (lower pain, discharge, adnexal tenderness), torsion of cyst, ectopic pregnancy (anaemia, hypotension)
Small bowel: inflamed Meckel's diverticulum (sam presentation), terminal ileitis from CD
Acute pancreatitis (pain also in epigastric)
Gastroenteritis
29
What is a Lily-White appendix?
Appendix actually fine when do surgery but remove it as otherwise in future people may assume its been removed thus miss appendicitis
30
Complications of appendicectomy
Early: appendix stump blow out, generalised peritonitis, abscess, retained faecolith, haematoma, wound infection, dehiscence
Late: obstruction from adhesions, infertility from tubal occlusion if pelvic infection, incisional hernia
31
Acute abdomen causes
Upper GI: acute cholecystitis, acute pancreatitis, PUD, gastroenteritis, GI haemorrhage, hepatitis
Lower GI: acute appendicitis, Meckel's diverticulitis, diverticulitis, intestinal obstruction, acute intestinal ischaemia, GI haemorrhage, mesenteric adenitis, terminal ileitis from CD, strangulated hernia
AAA, vasculitis
Gynae: ectopic pregnancy, PID, tubo-ovarian abscess, salpingitis
Renal: renal colic, acute urinary retention, testicular torsion, pyelonephritis
Non-surgical: pneumonia, MI, pericarditis, sickle cell crisis, DKA, opiate withdrawal, acute intermittent porphyria
32
Common surgical scars
Kocher - inferior + parallel to R costal marching. For open GB surgery
Mercedes Benz modification - cevron + break through xiphisternum.
Chevron (rooftop): gastrectomy, b/l adrenalectomy, liver transplant
Loin: renal surgery
Midline laparotomy
Paramedian (sides of umbilicus) : spleen, kidney, adrenal
Lanz: Mcburney's point for appendicectomy (open, not used now), Rutherford-Morrison is extension of this for kidney transplant
Pfannenstiel-along pubic hairline, for C section, pelvic bladder prostate surgeries
33
Oesophageal carcinoma
Adenocarcinoma most (RF-Barrett's oesophagus squamous to columnar metaplasia, survey every 2y, red mucosa w ulceration at GOJ) squamous cell carcinoma (upper 2/3, RF smoking alcohol)
CF: dysphagia solids then liquids, odynophagia, RLN invasion, oesophago-tracheal fistula, wasting, hepatomegaly from mets, L Virchow's node
M: surgery to relieve obstruction + allow swallowing, chemoradiotherpay, palliative
34
Hiatus hernia
Proximal part of stomach goes through diaphragmatic hiatus into stomach
Sliding HH: GOJ drawn up into chest, bit of stomach constricted at hiatus, hernia slides up with each peristaltic contraction, can become v big, often defective LOS - reflux
Para-oesophagela/rolling HH: GOJ remains below, bulge of stomach herniates through hiatus next to oesophagus, usually pain/dysphagia, sphincter is fine
CF: oesophagitis, pain, regurgitation, worse at night -- most asymptomatic
Comps: persistent inflammation from reflux causing fibrosis + strictures, Barrett's oesophagus
M: weight loss, change diet (e.g. alcohol + smoking relax sphincter so reduce), alginates (foam coats surface to protect), pro kinetic dopamine antagonists (e.g. metoclopramide) to increase S emptying, PPI to reduce acid, dilatation of strictures, surgery (dissect GOJ at hiatus, tightens crura, wrap funds around oesophagus to recreate flutter valve - Nissen operation
35
Achalasia
Neuro issue in parasympathetic plexus - disrupts peristalsis - uncoordinated contraction + inadequate relaxation of LoS (so proximal oesophagus dilates w food)
CF: dysphagia, recurrent chest infection, halitosis, WL, reflux, spluttering dysphagia + coughing (fluids spill over into trachea), vomiting, retrosternal CP
Predisposes to SCC of oesophagus (after 15yish)
CXR-widened mediastinal shadow, fluid level behind heart, barium-tapering constrictor at lower end
M - Heller's cardiomyotomy incision to widen, botulinum toxin injections
36
Diffuse oesophageal spasm
Contractions due to dysfunction of inhibitory nerves. Severe dysphagia, central CP which may respond to nitrates.
Endoscopy often normal, may have dysfunction of LoS, barium may show corkscrew appearance
M: relaxation of oesophageal smooth muscle with nitrates/CCBs, myotomy for severe
37
Pharyngeal pouch
Rare cause of dysphagia. Lack of coordination between inferior constrictor muscle + cricopharyngeus - Killian's dehiscence (area of weakness) - mucosal out pouching
Easily perforated in endoscopy
38
Oesophageal web
Dysphagia due to circumferential mucosal folds, predispose to cancer
Dysphagia + anaemia + atrophic glossitis = Plummer-Vinson syndrome
39
Gastro-oesophageal varices
Portal venous hypertension - abnormal connections between portal + systemic venous circulation - shunting - large submucosal veins at lower end of oesophagus + gastric fundus - when pressure rises can cause massive haemorrhage
Not normally treated until bleeds
M: resuscitation (avoid excess Na and water due to ascites, give FFP), endoscopy to source bleeding (may be varices or ulcer or Mallory Weiss), try to band or inject with sclerosant, infusion of vasopressin or octreotide, try tamponade, if continues TIPS (trans jugular intrahepatic portal-systemic shunting-catheter in intrahepatic IJV with a stent to connect portal system to vena cava). There's also emergency surgery but high mortality e.g. trans gastric oesophageal stapling
40
Oesophageal tears
Perforation: Boerhaave's syndrome (transmural perforation, often ass w vomiting or iatrogenic), causes severe inflammatory response
CF: sudden onset retrosternal CP, resp distress, subcutaneous emphysema, pneumomediastinum, intra-thoracic air-fluid levels.
M: resuscitate, ABs, control leak. Mortality 50-80%
Mallory-Weiss tears: non transmural superficial mucosal tears, most common at GOJ, usually after profuse vomiting (short period of haematemesis), usually self-limiting unless on anticoagulants/clotting abnormal. Mostly conservative management
41
Causes of portal venous hypertension?
Cirrhosis from ALD
Portal vein thrombosis
Hepatic vein thrombosis - Budd-Chiari syndrome
Schistosomiasis
42
Causes of peptic ulcer disease
H pylori - colonises mucosa over a long time, stimulates acid + compromises natural defence
Acid-pepsin production by parietal cells. In duodenal main issue is excess acid, in gastric main issue reduced defence
Mucosal resistance reduced by NSAIDs-block prostaglandins so less mucus
Direct AI of mucosa by NSAIDs, alcohol, cigarettes
Zollinger-Ellison syndrome: gastrin-secreting tumour of pancreas
43
How does PUD present?
Epigastric pain
* Dyspepsia - retrosternal pain, bitter regurgitation, N/V, anorexia, abdo bloating, relationship to food (G ass w eating, D relieved by food, this is tenuous tbh)
* Oesophageal disorders: reflux, often HH, transient/reflux oesophagitis, persistent inflammation (sometimes can cause strictures, UGIB etc)
* Stomach disorders: most in antrum and along lesser curve e.g. gastritis (mild inflammation but can bleed), stress ulcers (develop rapidly in v ill people, may perforate or bleed), chronic ulceration (usually worse with food esp acidic/spicy, may have WL + chronic anaemia, sx fluctuate, rarely may perforate into transverse colon causing gastro-colic fistula + faeculent vomiting)
*Duodenal disorders: duodenitis, ulcer, complete pyloric obstruction by scarring
Perforation + peritonitis
44
H pylori eradication?
PPI + 2 antibiotics (clarithromycin + amoxicillin / metronidazole) for 1w
45
Management of PUD
* Control factors like avoid dietary triggers, avoid NSAIDs/add gastroprotection, stop smoking
* H pylori eradication (PPI + 2 Abx for 1w)
* Reduce irritation: antacids (aluminium containing cause constipation and magnesium containing cause diarrhoea)
* Mucosal protection e.g. sucralfate - used in ICU to prevent stress ulcers
* Reduce acid secretion: PPIs first like as more potent, H2RA
* Correct secondary issues e.g. strictures, pyloric stenosis
46
Peptic ulcer perforation
Sudden epigastric pain, brownish/blood fluid, not toxic until later secondary infection as first is chemical peritonitis, board-like rigidity
Free gas + fluid in abdomen
Need resuscitation + laparotomy - peritoneal toilet, close perforation in duodenum or excise it in gastric
47
Pyloric stenosis
Rare. Chronic ulceration - fibrosis - strictures - partial gastric outlet obstruction - acute exacerbation of ulcer causes mucosal swelling + sphincter spasm - complete obstruction
CF: projectile vomiting with semi-digested food, dehydration, hypochloraemic alkalosis
M: resus, acid suppression + eradicate H pylori (this often underlying cause), gastro-jejunostomy
48
Gastric carcinoma
Adenocarcinoma
Intestinal type similar to intestinal epithelium, diffuse type cells have signet ring appearance with single file cells + marked stromal reaction (worse prognosis)
4th commonest cancer worldwide, rare pre 50, M>F, East Asia highest
Causes: atrophic gastritis - dysplasia - neoplasia, H pylori (intestinal type), excess salt
CF: inlet/outlet obstruction symptoms like vomiting and dysphagia, pain, N&V, early satiety, anaemia, LN, faecal vomiting from gastro-colic fistula (with TC), Virchow's node, palpable mass (Troisier's sign), spread to liver/lung/brain/bone
49
Gastric polyps
Mostly benign hyper plastic nodules of mucosa
| Genuine adenomatous polyps rare
50
Gastrointestinal stromal tumours
Rare anywhere in GIT but mostly in stomach, originate from interstitial cells of Cajal (pacemakers of gut activity). Most small, prone to haemorrhage from ulceration, if in SB present with SBO
51
Gastric and SB lymphomas
H pylori an initiator. In stomach most are B cell NHL, in SB occasionally cause intussusception
M: CHOP chemotherapy regimen, excision, subtotal gastrectomy if bleeding,
52
Carcinoid tumours
Arise from APUD cells of GI endocrine system in any tissue derived from GIT (inc pancreas, biliary)
Most common in appendix, others in SB mostly
Secrete catecholamines + serotonin - carcinoid tumour usually when get liver mets - transient hot flushes, hypotension, asthma, diarrhoea. Measure 5-HIAA in urine as a marker (serotonin metabolite)
Symptom control with octreotide and somatostatin analogue, excise primary lesion + Los, metastases is slow but not curable by radio/chemo
53
Pathological consequences of pancreatitis?
Disturbed membrane stability - inappropriate activation of zymogens esp trypsin - interstitial oedema - peritoneal exudation - fat necrosis in mesentery/omentum, calcium sequestration (so hypocalcaemia), enzymes cause local damage + activate complement/cytokines - SIRS and organ failure - pancreatic necrosis from ischaemia + reperfusion injury, which dark bloody inflammatory exudate containing lipid in the peritoneum
54
Causes of pancreatitis?
I GET SMASHED
Commonest are alcohol, gallstones, ERCP and idiopathic
Idiopathic
Gallstones - blockage of PD by large stones/smaller stones transiently obstructing as pass through ampulla
Ethanol - longstanding high intake, or binge
Trauma - ERCP, cardiopulmonary bypass
Steroids
Mumps
Autoimmune
Scorpion/snake venom
Hypercalcaemia/hyperlipidaemia/hypothermia
ERCP
Drugs -- SAND. Steroids/sulfonamides, azathioprine, NSAIDs, diuretics (also AB like metronidazole and H2RA)
55
Clinical features of acute pancreatitis
```
Pain-sudden, continuous, epigastrium, to back, pancreatic position is better, movement makes worse
Vomiting
Systemic illness
Jaundice
Reduced or absent bowel sounds
```
56
Presentation of chronic pancreatitis
Persistent severe upper pain, without the other features, amylase may not be raised/only slightly raised, may see fibrosis on ERCP
57
What investigation results suggest pancreatitis?
Amylase - usually >1000, though often lower in alcoholics. >300 is high, but usually pancreatitis is very high and other causes for moderately raised include pancreatic pseudocyst, mesenteric infarcts, cholecystitis, DKA, perforation
LFTs: ALT high in gallstone
USS of biliary tree 48-72h after onset, ERCP for gallstones
58
What is severe pancreatitis (Glasgow Ranson criteria)?
```
3 features out of:
P - PaO2 <8kPa
A - age >55
N - neutrophils >15
C - calcium <2
R - raised plasma urea >16
E - enzyme, plasma LDH >600
A - albumin <32g/L
S - sugar, glucose >10 mmol/L
```
Meaning high risk of major complications
59
Management of acute pancreatitis
Mild - fluids, analgesia, treat cause
Severe - supportive (oxygen, fluids, NG tube), TPN may be necessary, manage electrolytes, analgesia
60
Complications of pancreatitis?
Death - ARDS, RF, multiple organ dysfunction (e.g. CV collapse, renal insufficiency, DIC)
Pancreatic/peripancreatic necrosis
Fluid collections
Pancreatic pseudocysts (fluid with enzymes + necrotic debris lasting for >6w, pseudo as no epithelial cells)
Pancreatic abscess (swinging fever)
Portal vein thrombosis
Bowel ischaemia esp transverse colon due to position of middle colic artery
Pseudoaneurysms
Diabetes mellitus
Intestinal malabsorption
61
Pancreatic exocrine cancer
Most ductal adenocarcinoma, a few acinar, most in head, 1/5 in body/tail, often well-diff but met to LN, peritoneum + liver (HPV) so at presentation few are resectable
RF: >50y, smoking, chronic pancreatitis, hereditary, obesity/T2DM
CF: weight loss, abdo pain (in more advanced, deep and knawing, nocturnal, hard to control, better leaning forwards, often from retroperitoneal nerve invasion), obstructive jaundice (in 50%, initially painless, CBD compression in pancreatic head - proximal BD dilates - GB may become palpable (Classically Courvoisier's law of palpable gallbladder + painless jaundice is pancreatic cancer not gallstones as in gallstones GB wall is thick so not painful; and in GS jaundice is fluctuating, but this is not always the case), dyspeptic symptoms and N&V, ascites, abdo masses, acute pancreatitis, DM (preceding/following diagnosis), gastric outlet obstruction, thrombophlebitis migrans
Ix: CT CAP can show tumour extent + liver + vascular invasion (SMA/V, coeliac artery - these lessen surgical feasibility).
M:
* ERCP may be done to relieve jaundice with stenting
* Whipple's: pancreatico-duodenectomy. High morbidity + mortality. Post-op chemo with 5-FU or gemcitabine
* Poor prognosis
* Palliation: good analgesia e.g. permanent coeliac ganglion blockade, biliary stent via ERCP for jaundice, surgical bypass to help relieve duodenal obstruction
62
Pancreatic endocrine tumours
*Neuroendocrine tumours in islets of Langerhans
Insulinomas: beta cells, most benign, cause hypoglycaemia
*Glucagonomas: alpha cells, v rare, DM and migratory necrolytic erythema rash
*Gastrinomas: secrete gastrin, from islets/ectopic cells in duodenum, ass w MEN 1. Zollinger-Ellison when cause peptic ulcers + diarrhoea. Most malignant but slowish to grow
*Multiple endocrine neoplasia syndromes - tumours, autosomal dominant inheritance
63
MEN 1, 2a and 2b?
1 - islet cell tumours, pituitary adenoma, parathyroid hyperplasia
2a - medullary thyroid carcinoma, pheochromocytoma, parathyroid adenoma/hyperplasia
2b - medullary thyroid carcinoma, pheochromocytoma, neurofibromas, Marfanoid habitus
64
Pancreatic cyst types
Fluids within pancreas, non-inflammatory (cf pseudocysts)
High risks: mucinous cysts like indraductal papillary neoplasm (ass w PD cancer), mucinous cystic neoplasm (cancer/pre cancer), solid pseudo papillary neoplasm (rare), cystic pancreatic neuroendocrine tumour (MEN1)
Low risk: serous cysts e.g. serous cystic adenoma (honeycomb appearance), simple cyst (always benign), mucinous non-neoplastic, lymphoepithelial
Most asymptomatic, may cause abdo or back pain from compression, post-obstructive jaundice + vomiting, may become infected
Discussed at MDT for resection vs surveillance
65
Biliary tumours
Cholangiocarcinoma - adenocarcinoma of biliary epithelium (in or out liver), ass w PSC, most extra-hepatic + compress bile drainage causing jaundice, LN + vascular often involved so hard to operate
Periampullary carcinoma - adenocarcinoma of AoV, enters duodenum, friable
Gallbladder carcinoma - old age, most from CI of GI
66
Gallstone composition?
Mixed with most cholesterol - abnormal bile e.g. removal of terminal ileum so less bile salts reabsorbed, biliary stasis. Multiple
Cholesterol stones
Pigment stones - excess bilirubin excretion due to haemolytic disorders like infection, malaria, leukaemia
Calcium carbonate stones - excess calcium in bile
67
Mucocele?
GB distended with mucus due to obstruction
68
Biliary colic
Intermittent CD obstruction by stone
Severe pain rises to a plateau then continues unrelentingly (not true colic), afebrile, often V, some local tenderness
Manage with injection of opiate, USS to find location, cholecystectomy definitive, ?low fat diet beforehand as less stimulus to GB.
69
Acute cholecystitis
Physical/chemical/bacterial irritation
Pain RUQ, pain that arrests on inspiration (Murphy's sign), systemically unwell with fever + tachycardia
USS - GS, thickened GB wall
Most dont need ABs as inflammation usually but need cholecystectomy soonish (if done acutely GB may be obstructed + tense etc)
70
Empyema of gallbladder
Pus fills GB
| Swinging pyrexia, may become necrotic + perforate - subphrenic abscess or generalised peritonitis
71
Cholecysto-duodenal fistula
Uncommon, inflamed GB adheres to duodenum and stone ulcerates forming fistula
72
Gallstone ileus
Uncommon, cholesterol stone passes into terminal ileum (narrow) + impacts - gallstone ileus / May present as intermittent SBO
passes through a fistula, not through the bile ducts
73
Stones in bile duct + ascending cholangitis
Most pass into duodenum but may lodge at end of CBD - obstructive jaundice - acute pancreatitis or AC
AC: chronic obstruction + dilatation - bile stasis - bacterial infection. RUQ pain, swinging pyrexia, jaundice (Charcot's triad - not all have), weight loss, rigors (gram negs release endotoxin). Need AB + drain bile duct, remove stone w ERCP
-Raynaud's pentad: the addition of hypotension + altered mental status.
74
Management of gallstone problems
* Chenodeoxycholic acid e.g. if not fit for surgery - bile acid to increase bile salt pool, lots of s/e and takes ages to work
* Bile duct problem: MRCP to diagnose + ERCP to extract stones
* Gallbladder problem: most laparoscopic cholecystectomy. Ligate cystic artery, define junction between CD and CBD, CD ligated near GB, small incision made in CD see flow during op, CD divided and GB dissected out of liver bed
75
Complications of cholecystectomy
General: stone retention, biliary peritonitis, BD damage, haemorrhage, ascending cholangitis, subphrenic abscess
Instrumental: injured bowel, BV injury, tension pneumothorax, bleeding, subcutaneous emphysema, herniation, trauma to biliary system
76
Primary sclerosing cholangitis
Progressive fibrosis + biliary strictures - narrows lumen - obstructive jaundice - cirrhosis
Often in long-term UC
Risk of cholangiocarcinoma
77
Liver abscess
Usually pyrexia, malaise, upper abdo pain. Worldwide amoebiasis commonest
78
Liver tumours
Primary malignant- uncommon, some angiosarcoma, most HCC. HCC is slow growing, often multi centrical, most have a cause like hepatitis C/B, alcohol, haemochromatosis, NAFLD, aflatoxins. Anorexia, WL, abdo pain, jaundice, ascites, stigmata of CLD, palpable mass
Liver mets - v common from many tumours, causes anorexia + WL as parenchyma destroyed, jaundice when terminal. Colorectal mets sometimes chance of cure
79
Liver cysts
Simple cysts: most just leave, thought to be malformed BDs so local dilatation. Most no symptoms, may get abdo pain, nausea, early satiety
Polycystic liver disease: ADPKD or ADPLD, 20 or more cysts, most no symptoms but may get abdo pain hepatomegaly + renal disease.
Cystic neoplasms: asymptomatic usually (or abdo pain anorexia nausea etc), cystoadenomas, pre-malignant so monitor for cancer (suspicious is like septations, wall enhancement, modularity, abscess-like debris)
Hydatid cysts - Echinococcal granulosis tapeworm infection (faeco-oral), zoonosis, goes through HPV. Asymptomatic for years then abdo pain, may cause jaundice or cholangitis, vomiting, dyspepsia, early satiety. DOn't aspirate as contents disseminate causing anaphylaxis so re-roof + anti-helminth agents
80
Indications for splenectomy?
ITP, haemolytic anaemias, sickle cell anaemia, splenic infarct, abscess, haemangiomas
81
Precautions post-splenectomy?
Immunisation Pneumococcus, Haemophilus influenza type B, Meningococcus and lifelong AB prophylaxis
This is because spleen is v important for defence against encapsulated organisms
82
Splenic infarct
Causes: occlusion of splenic artery causing tissue necrosis. Often not complete due to collaterals (the L gastroepiploic a -- short gastric arteries)
This may be due to haemotological things like CML, sickle cell, polycythaemia rubra vera, myelofibrosis, or embolic things like AF
CF: LUQ pain, radiation to L shoulder (Kehr's sign), fever, N&V
M: avoid splenectomy due to risk of infection unless v v bad
Comps: abscess, autosplenectomy due to repeated infarctions causing fibrosis + atrophy (esp in SCA)
83
Splenic rupture
Causes: abdo trauma e.g. seat beat injuries, iatrogenic, underlying splenomegaly causing capsule to thin as spleen grows
CF: abdo pain, hypovolaemia, LUQ tenderness, peritonism, Kehr's sign
M: grade 1-3 conservative, grade 4-5 (more than 25% devascularised/completely shattered) need urgent laparotomy
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SBO
Causes: intra-abdo adhesions, herniae, Crohn's, malignancy, volvulus, TB, parasitic infection
CF: N/V (often bilious), constipation/absolute, abdo distention, pain, fever + tachycardia (ind more strangulation)
Ix: U&;E normal unless dehydration, lactate raised-dehydration or hypo perfusion, do G&S and XM, exclude upper causes, CT, AXR
M: covered earlier but drip and suck, wait 48h if adhesions cause as most recover, if over 48h/virgin abdomen/rupture suspected do laparotomy
Comps: sepsis, abscess, wound dehiscence, aspiration, short-bowel syndrome from multiple surgeries, disability and death, hospital things like HAP, AKI, C diff
85
Risk factors for neuroendocrine tumours?
MEN1, von Hippel-Lindau disease, neurofibromatosis 1, tuberous sclerosis complex
86
Gastroenteritis
Transient D (3 or more loose stools), V, abdo pain, dysentery (blood + mucus)
Causes:
* Viral - symptoms within days. E.g. provirus (cramps, watery D, vomiting), rotavirus (most in kids, infection in childhood=lifelong immunity)
* Bacteria - toxins cause symptoms in hours, or actual bacteria in weeks. Campylobacter jejuni (from chicken/eggs/milk, may have prodrome, if severe give IV erythromycin, can cause reactive arthritis, GBS, haemolytic uraemia syndrome and TTP), E coli (from food or person, can cause uraemia syndrome), bacterial toxins (last <24h, e.g. S aureus from meat and cream, B cereus from reheated rice, C perfringens from meat usually just D, V cholera from water profound rice-water)
* Parasites - symptoms sometimes take months. E.g. Cryptosporidium, Entamoeba histolycitca (may cause liver abscess, bloody diarrhoea), Giardia (acute or chronic w steatorrhoea), Schistosomiasis (~1m after exposure, blood, hepatosplenomegaly)
* Hospital-Acquired: C difficile. After cephalosporins esp. Bacteria produces endotoxins A and B - inflammation - exudate in mucosa of colon - severe bloody diarrhoea + toxic megacolon. Give metronidazole, or vancomycin if severe/not improving
* Non-infective: radiation colitis, IBD, microscopic colitis (chronic watery diarrhoea), chronic ischaemic colitis
M:
* stool culture if suspecting C diff/blood + mucus/severe
* oral rehydration (or IV if not possible)
* stop work/school for 48hr from last episode
* food poisoning is a notifiable disease
87
Groin lump differentials?
Femoral hernia
Inguinal hernia
Saphena varix (dilatation of long saphenous v at SFJ, empties on pressure + goes when lie down, cough impulse)
Inguinal lymphadenopathy
Lipoma
Groin abscess
Psoas abscess
Femoral artery aneurysm (dilatation of CFA just below inguinal lig)
Athletic pubalgia (small tear in rectus sheath in athletes)
Hydrocele, varicocele, testicular mass - can 'get above it'
88
Layers of abdo wall superficial to deep
```
Skin
Camper's fascia (fatty)
Scarpa's fascia (membranous)
External oblique
Internal oblique
Transversus abdominis
Transversalis fascia
Peritoneum
```
89
Borders of the inguinal canal
Roof: TF, IO, transversus abdominis
Floor: inguinal lig, lacunar lig medially
Anterior: EO, IO
Post: TF
Runs from deep inguinal ring (just above midpoint of inguinal ligament so just lateral to the pulse) to superficial ring (more medial + inferior, just above and medial to tubercle)
90
Purpose of inguinal canal?
Contains spermatic cord/round ligament
| Purpose is embryological descent of the testes
91
Borders of the femoral canal
Superior - inguinal ligament
Lateral - medial border of sartorius
Medial - medial border of adductor longus
92
Hernia definition
The protrusion of part/whole of an organ/tissue through the wall of the cavity that normally contains it
93
Types of inguinal hernia
Direct - peritoneal sac (usually fat/tissues) enters through Hesselbach's triangle (weakness in the TF). Usually acquired. Low risk of strangulation. Medial to IEVs
Indirect - peritoneal sac enters via deep inguinal ring due to incomplete closure of processus vaginalis, more likely to get comps, lateral to IEVs
Pantaloon - direct + indirect on same side
Sliding - retroperitoneal viscus slides down the posterior abdo wall and gets into IC
94
Presentation, management and complications of inguinal hernias?
Groin lump: initially reducible esp when lie down, may cause discomfort, may be in scrotum or labia majora, or with comps
M: if symptomatic offer surgery, open preferred for primaries, laparoscopic take longer but better for relapses/risk of chronic pain. In infants always refer for surgery
Comps: irreducible/incarcerated (contents can't return to original cavity), obstruction (bowel lumen obstructed), strangulation (compression of blood supply causing ischaemia - necrosis - perforation)
Post-op comps: pain, haematoma, infection, urinary retention, recurrence, chronic pain, damage to vas deferens
95
Femoral hernias
More common in women, usually asymptomatic except for lump (inferno-lateral to pubic tubercle + medial to femoral pulse). Unlikely to reduce because of tight femoral ring - so need surgery because v high rate of strangulation. Strangulation often has no obvious localising features, classically p/w distal SBO
they can migrate superiorly to the inguinal ligament
96
Ventral hernias
* Incisional - if long time like abdo displaced out then can be dangerous to put back in because of effect on diaphragm
* Epigastric - defect in line alba (between XP + U, usually no symptoms, diff to divarication of recti)
* Umbilical - through cicatrix, more in females + obese, in children v common and usually resolve by age 2
* Paraumbilical - acquired, defect in line elbow, umbilicus pushed to side
* Spigelian - lower lateral edge of rectus abdominis
* Obturator - of pelvic floor t obturator foramen, more in women, rapid weight loss, mass in upper medial thigh
* Littre's hernia - of Meckel's diverticulum
* Lumbar - posterior, weakness after surgery, mass + back pain
* Richter's hernia - partial herniation of SB
97
What is diverticular disease?
Local outpouchings of mucosa through muscle in the bowel wall. Usual site is between the taenia coli (vessels pierce muscle to supply mucosa), rectum lacks these so often spared. Caused by thickened circular muscle due to hyper segmentation which increases pressure and forces mucosa to herniate - sigmoid colon most commonly affected + extends proximally
Diverticulum=singular, diverticula=plural, diverticular=adjective, diverticulosis=asymptomatic, diverticulitis=inflammation due to narrow outlet
98
Presentation of diverticular disease
* Diverticulosis=asymptomatic, v common
* Chronic grumbling pain from low-grade inflammation with erratic bowels, faecal loading. Most managed w high fibre diet + bulking agents
* Acute diverticulitis: spreading pericolic inflammation, continuous LIF pain, pyrexia, tachycardia, give ABs + bowel rest
* Pericolic abscess: extension of inflammation, swinging pyrexia, incomplete obstruction , drain and ABs (Hartmann's safest option as anastomosis won't heal well in infection)
* Free perforation
* Acute rectal haemorrhage: not from inflammation, stops spontaneously, usually fairly fresh blood, usually conservative
* Fistula: into bladder/uterus. E.g. vesico-colic=pneumaturia + UTIs, LB + SB=diarrhoea
* Intestinal obstruction from stricture and inflammation: esp LBO
99
Hinchey classification?
```
Of abscesses and perforation in diverticular disease
1-small pericolic/mesenteric <4cm
2-large, often pelvic
3-small perforation
4-free rupture + faecal peritonitis
```
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Complications of diverticular disease
```
Spreading pericolic inflammation
Pericolic abscess
Intraperitoneal perforation
Fistula to abdo/pelvic viscera
Bowel-bowel adhesions
Fibrous strictures
Acute haemorrhage
```
101
Meckel's diverticulum
Embryological remnant of vitello-intestinal duct, on distal ileum about 60cm from ileocaecal junction. Often has gut-related tissues like ectopic acid-secreting gastric mucosa
CF: usually asymptomatic, in children <2 can cause PR bleeding, in older more occult blood loss, may become inflamed like appendicitis
102
Irritable bowel syndrome #triggered
Disordered peristalsis with segmenting, non-propulsive contractions, small volume of faeces becomes excessively dehydrated.
Functional disorder of abdo pain relieved by defecation + a change in stool frequency and consistency (can be D or C, usually alternates but one predominates). Other features: flatus, bloating, mucorrhoea. Worse in stress.
M: exclude other diagnoses like cancer and IBD. Adjust diet if they can find triggers. Antispasmodics e.g. mebeverine, hyoscine butylbromide (Buscopan), anti-diarrhoea e.g. loperamide
Lactulose not used in IBS even tho helps constipation
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Constipation?
Slow transit
Evacuation disorder
Low fibre/fluid/inactivity. In infants ultra-short segment Hirschsprung's disease
Can be really bad causing impaction + obstruction. predisposes to urinary retention, UTI and incontinence
Stop constipating meds, increase fluid + fibre (but sometimes fibre is worse), oral maintenance (lactulose, fybogel, sodium decussate-softens), rectal (glycerine suppositories, phosphate/arachis oil enemas, strong laxatives for v severe e.g. sodium picosulfate (stimulant)
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Sigmoid volvulus
Twisting of loop of bowel around mesentery - closed loop obstruction - ischaemia - necrosis - perforation.
RF: psych disorder, nursing home, chronic constipation/laxative, previous surgery to abdomen, DM
Chronic constipation - big colon, heavy easier to twist
CF: abdo pain + distention, absolute constipation, rectum empty but big, tympanic percussion, if perforation peritonism.
AXR: coffee bean sign arising from LIF, if ileocaecal valve incompetent also SB dilatation
CT: whirl sign from twisting mesentery
M: rigid sigmoidoscope and insert flatus tube pass into the loop to relieve obstruction, leave for 24h, if doesn't work need sigmoid colectomy with Hartmann's or primary anastomosis
C: ischaemia, perforation, recurrence, stoma complications
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Caecal volvulus
Peaks in 10-29y (intestinal malformation, excessive exercise) and 60-79y (constipation, distal obstruction)
May have coffee bean sign arising from RLQ
Manage with decompression or surgery, surgery probs better
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Colonic angiodysplasia
Common cause of acute and chronic PR bleeding. Tiny hamartomatous vascular lesions (AV malformations), usually AC + colon (or stomach + SB possible), bleed out of proportion to their size, occur in later life.
Causes: acquired from reduced submucosal venous drainage, or congenital e.g. hereditary haemorrhage telangiectasia
CF: acute rapid bleeding (do mesenteric angiography for source), chronic (LB lesions on colonoscopy, painless occult PR bleed, iron def anaemia). Upper-haematemesis/melaena, lower-haematochezia (fresh blood)
M: conservative, endoscopy + coagulation, mesenteric angiography (SB as can't reach w endoscope), minority need surgery with resection + anastomosis (high mortality)
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Ischaemic colitis
Elderly, PR bleed. Cramping abdo pain for a few hours, then dark red blood without faeces about 1-3 times over 12h, stops spontaneosly
Transient ischaemia of a LB segment - mucosa sloughs - esp in splenic flexure
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Colorectal polyps
Localised lesion protruding from bowel mucosa into lumen, v common in LB
Adenomas: all have malignant potential, tubular (least MP), villous (secrete mucus) and tubule-villous types
Lymphomas, leiomyomas/sarcomas, lipoma/sarcoma etc - rare
Hyperplasia e.g. metaplastic mucosal polyps (v common), lymphoid aggregations (common in young children)
Hamartomas e.g. angiomas (uncommon), Peutz-Jghers polyps (small MP, uncommon)
Inflammatory e.g. pseudo polyps in UC
Most in rectum + sigmoid. Adenomas often transform to adenocarcinoma but over like 10y
CF: most asymptomatic, if symptoms may be bleeding, mucus, tenesmus in distal lesions
Ix: rigid sigmoidoscopy, flexisig reaches splenic flexure so not full but approx 75% (give phosphate enema first), colonoscopy best
M: remove polyps, faecal occult blood screening age 60-74 every 2y, if over 75 can request, at 55 invited for a one off flexi sig
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Inherited causes of colorectal cancer
Hereditary non-polyposis colorectal cancer (HNPCC / Lynch syndrome): high risk of colorectal, and also risk of endometrium/ovary/urothelium/SB/brain cancer
Polyposis syndromes:
- Familial adenomatous polyposis (FAP): LB cancer inevitable if not treated, AD defect in APC gene, adenomatous polyps in teenage so need prophylactic surgery e.g. subtotal colectomy + ileorectal anastmosis
- Peutz-Jeghers syndrome: hamartomatous polyps throughout GIT, often freckles, half die by age 50 due to bowel intussusception/LB SB stomach pancreas testis breast cancer
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Risk factors for colorectal cancer
Low fibre, high fat diet
Age >60
Ulcerative colitis
Inherited conditions like HNPCC, FAP
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Pathophysiology of colon cancer
Exophytic (protrude into lumen) - ulcerate - invade muscular wall causing fibrosis and LBO - serosa - surrounding structures - met via lymph
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Presentation of colorectal carcinoma
Anaemia
Palpable mass often RIF
Change of bowel habit (diarrhoea more likely due to mucus + blood from cancer)
LBO (more common in left-sided cancers)
Partial LBO (often constipation w overflow diarrhoea cf)
PR bleed (distal to splenic flexure)
Tenesmus (in rectum)
Perforation (pericolic abscess ruptures)
Fistulation
Secondary effects: obstructive compression in portal hepatis, retroperitoneal LN involvement, systemic
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What are the likely symptoms from colorectal cancer of different parts of the colon?
Caecal area: painless, iron-def anaemia, mass in RIF, diarrhoea
Descending: PR blood loss, changed bowel habit, colicky pain, obstruction, mucus, fistula, perforation
Rectum: tenesmus, bleeding, mucus, diarrhoea, hypokalaemia, local pain from infiltration into sacral plexus
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What marker is used to monitor colorectal cancer recurrence?
CEA - carcino-embryonic antigen
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Staging for colorectal cancer
Modified Dukes' staging:
A - T1/2 (submucosa/muscularis propria), no LN mets
B - T3/4 (beyond MP/to other organs), no LN
C - any T, N1 or 2 (up to 3/more than 3), no distant mets
D - distant mets
Also UICC stage and TNM staging
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Management of colorectal cancer
Surgical excision: right hemicolectomy, transverse colectomy, left hemicolectomy or sigmoid colectomy. Remove affected segment with a margin either side of tumour, determined by distribution of the BVs
Adjuvant radio/chemo given to Dukes' C patients (5-FU main agent)
Advanced: often resect to relieve local effects, if mets only in liver can remove and improve survival
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Pseudo-obstruction
Aka Oglivie's syndrome. Dilatation of colon due to dynamic bowel in absence of mechanical obstruction. Most occur in caecum and AC
Caused by interruption to the ANS of the colon which stops smooth muscle action - increases colon diameter - increased risk of toxic megacolon, ischaemia and perforation. E.g. hypercalcaemia, low thyroid, opioids, CCBs, recent surgery/trauma/illness, Parkinson's, Hirschsprung's disease
CF: abdo pain, distention, constipation/overflow diarrhoea, vomiting, bowel sounds often present, tympanic percussion, focal tenderness=ischaemia
AXR looks same as mechanical so need CT AP w contrast
M: make NBM + fluids, NG if vomiting, endoscopic decompression, nutritional support, surgery if perforated/ischaemic obv
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What are the indications for stomas?
Permanent: no distal bowel segment/bowel can't be rejoined. E.g. after abdomino-perineal excision of rectum (colostomy), or panproctocolectomy (ileostomy)
Temporary in emergencies to relieve distal LBO when competent ileocaecal valve
De-functioning stoma: temporary, to protect a more distal anastomosis by reducing pressure, reverse after ~3m
Bowel rest: 'rest' a more distal segment involved in inflammation e.g. pericolic abscess, complex fistulae
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Colostomy?
USUALLY in LIF. Contents more solid as water has been absorbed, flush to the skin, works intermittently
Types: permanent end (often in abdominoperineal resections), temporary end (e.g. diverticulitis, in Hartmann's procedure), loop (protects distal anastomosis after surgery, loop of bowel brought to surface and half opened to drain into stoma bag)
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Ileostomy?
USUALLY in RIF, contents lighter + liquid, enzymes toxic to skin so has spout sticking out, work continuously throughout day
Types: permanent (after panproctocolectomy), temporary end (emergencies e.g. bleeding, sepsis), loop (2 openings like in loop colostomies, connected and used to protect distal anastomoses)
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Urostomy?
In RIF, after cystectomy, contains urine not faeces, ill conduit used to route urine into bag, ureters attached to other end of conduit so the urine drains through a section of bowel
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Hartmann's procedure?
End colostomy + rectal stump
Safe after emergency resections of rectosigmoid lesions where primary anastomosis not suitable
May reconnect to bowel after a few months
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Complications of stomas
Early: mucosal sloughing, necrosis of terminal bowel from ischaemia, obstruction wit oedema/faeces, persistent leakage from inappropriate siting
Late: parastomal hernia, prolapsed bowel, parastomal fistula, retraction of spout ileostomy, stenosis, perforation, psychological
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types of bowel surgeries
low anterior resection = remove sigmoid, rectum
high anterior resection = remove sigmoid + upper rectum (less removed than low)
abdomino-perineal section = remove sigmoid, rectum + anus (permanent end colostomy)
sigmoid colectomy = remove sigmoid
left hemicolectomy = remove descending colon + bit of transverse colon
right hemicolectomy = remove ascending colon + small bit of TC
extended right hemicolectomy = remove AC + most of TC
subtotal colectomy = remove AC, TC and DC (not sigmoid)
total abdominal colectomy = remove whole colon
total proctocolectomy = remove whole colon + rectum + anus
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Lymphatic drainage of the anus
Upper part - abdominal + pelvic LN chain
| Lower part - inguinal LNs
126
Haemorrhoids definition
Abnormal swelling of anal vascular cushions (vessels in folds of left lateral, right posterior + right anterior sections)
127
Haemorrhoid classification
1st degree: remain in rectum
2nd degree: prolapse through anus on defecation + spontaneously reduce
3rd degree: prolapse on defecation + require manual reduction
4th regret: persistently prolapsed
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Haemorrhoid causes
Constipation - straining raises IAP, obstructs venous return, venous plexuses engorge, bulging mucosa dragged down by hard stool; also causes pelvic floor to sag down
Pregnancy - venous engorgement, mucosal prolapse, progesterone mediates venous dilatation
Also increased age, other causes of raised IAP, pelvic/abdo masses, portal HTN, FH
129
Where are haemorrhoids usually found?
3, 7 and 11 o'clock positions
| Matches anatomical positions of anal cushions
130
Haemorrhoids presentation
Often intermittent attacks precipitated by constipaiton. Painless bright red bleeding (on paper or in pan, blood on surface not mixed in), pruritis ani (chronic irritation), mucus leakage from imperfect closure, prolapse (rectal fullness/anal lump), mild incontinence of flatus due to incomplete closure
E: often normal, 'external piles' often simple skin tags or 'sentinel piles' from a fissure
Acute: can thrombose or strangulate, become v painful, purple/blue, oedematous, tense, spasm of anal sphincter, may ulcerate/necrose
Complications: ulceration, skin tags, ischaemia/gangrene, perianal sepsis
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Haemorrhoids management
Majority conservative: increase fibre + fluid, laxatives, topical analgesia e.g. lignocaine gel, rubber band ligation (place above dentate line to avoid pain), infrared coagulation
Surgical - haemorrhoidectomy
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Anal fissure
Longitudinal tear in mucosal lining of anal canal, often from defecation of hard stool or inflammation. RF: constipation, dehydration, IBD, chronic diarrhoea.
CF: intense pain, sphincter spasm post-defecation, out of proportion to size of fissure, fear of defecation which worsens constipation, bleeding bright red on paper, itching post-defecatiion, patients often refuse DRE, may see small skin tag (Sentinel pile) at superficial end
M: diet, stool softeners e.g. lactulose or movicol, GTN or diltiazem cream to increase blood to region (relaxes internal sphincter so less pressure to promote healing), surgical for chronic (sphincterectomy)
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Anal fistula
Abnormal communication between two epithelial surfaces (anal canal + peri-anal skin)
Main cause is after an anal abscess, occasionally caused by cancer, more risk in IBD, immunosuppression, anal trauma
CF: most superficial, causes discharge onto perineum (blood/mucus/pus/faeces), may see external opening onto perineum with granulation tissue, may feel fibrous tract underneath skin, Goodsall rule to predict trajectory (if ext opening posterior to transverse anal line the tract is curved to inferior opening in post midline; if opening is anterior to that line the tract follows a straight line to the dentate line)
M: conservative if no symptoms, need to identify internal + external openings, fistulotomy (divide skin etc of tract and allow to heal by secondary intention)
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Anorectal abscess
Anal ducts get blocked- stasis - bacterial overgrowth - spreads to adjacent areas (peri-anal abscess, ischiorectal, intersphincteric, supralevator)
CF: systemic infection (esp in ischiorectal), rectal pain worse when sit, localised swelling, itching, discharge, difficulty in micturition, palpate tender mass on DRE. often intermittent sx
M: high rate of recurrence + fistulae (50%) so do surgical drainage if big (if v early presentation oral ABs from GP may work), heal by secondary intention, differentiate if infection from skin or bowel, ABs if acute infection
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Pilonidal disease
Sinus/cyst/abscess of the skin of anorectal region rather than anus itself. They contain a nest of hairs
RF: young adults, hirsute men, sitting for a long time, sweat, buttock friction, poor hygiene, local trauma
C: hair follicle in interglutela cleft gets inflamed - obstructs opening to follicles so extends inwards forming a pit - foreign body type reaction causes a cavity connected to skin surface by epithelialise sinus tract
Sinuses: long course with intermittent/chronic purulent discharge, exacerbations may cause abscess
Pilonidal abscess: mass of hair + skin debris in a sinus cause reaction - secondary infection causes abscess
CF: red, painful swollen mass in sacrococcygeal region, often with discharge, may have systemic infection, opens onto the skin but doesn't continue into anal canal
M: non surgical like plucking away hair, washing out, ABs in infection, but tbh surgery needed - acutely drain + washout abscess, later remove sinus tract (secondary intention by opening it or excising tract + closing wound). They commonly recur
136
Rectal prolapse
Herniation of rectum through pelvic floor. Partial (rectal mucosa) or full thickness (rectal wall).
Causes include long-standing haemorrhoids, chronic straining from cough/constipation, PV deliveries
CF: rectal mucus discharge, faecal soiling, bright red blood on wiping, ulceration, rectal fullness, tenesmus, repeated defecatin
M: surgical is only definitive management (but obv improve constipation etc)
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Faecal incontinence
Of flatus, then fluid and then solids as control is lost
Causes include pudendal neuropathy causing anorectal incompetence of sphincter (e.g. weak pelvic floor), colorectal disease like IBD, diarrhoea, rectal reservoir, higher cerebral e.g. dementias, sensorimotor issues e.g. spinal issues, mobility loss
138
What is Condylomata accuminata?
Anal warts
| Caused by HPV in UK mostly
139
SCC of anus
RFs: HPV 16 + 18, age, smoking, immunosuppressed, CD
Arise from below the dentate line. CF include pain, rectal bleeding, anal discharge, pruritis, palpable mass, infection/fistula from local invasion, incontinence/tenesmus from sphincter involvement
140
Pathology in UC vs CD
UC: recurrent acute inflammation, continuous involvement of affected part of colon, always affects rectum, limited to mucosa, ulceration, pseudopolyps, no granuloma, minimal wall fibrosis
CD: chronic relapsing inflammation, skip lesions along any part of GIT, ileum involved in most, transmural inflammation (including sera), fissured ulceration causing cobblestone appearance, may have granulomas, marked wall fibrosis
141
Clinical features of IBD
UC: severe diarrhoea during acute attacks, often incontinence, PR bleeding, abdo pain pre-defecation, no abdo mass
CD: diarrhoea + PR bleeding less prominent, abdo pain dominant feature, abdo mass quite common, general debility
142
Complications of IBD
UC: toxic megacolon in fulminant attacks - perforation, massive haemorrhage, high risk of malignant change, PSC. Strictures etc are rare in UC
CD: strictures, fistulae, anal lesions, incomplete obstruction are common, rarer are massive haemorrhage and free perforation, low risk of malignant change
143
RF for IBD
Smoking for CD (non-smoking is RF for UC)
Familial - polygenic
Late teens-twenties
Initiating attack of gastroenteritis
Other autoimmune disorders e.g. ankylosing spondylitis
144
Features of UC?
Mucosa of LB only, starts in rectum goes proximally.
P: AI of mucosa, neutrophils in LP + tubular glands form crypt abscesses - mucosa sloughs making ulcers. Persistent inflammation - ulcers coalesce, islands of intact mucosa project into lumen (pseudo polyps), when not in attacks AI the LP remains swollen by CI, dysplasia predisposes to adenocarcinoma. Later feature is fibrosis - smooths out haustrations - lead pipe colon
CF: acutely loose bloody stools with mucus, cramping abdo pain, incontinence; fulminant v severe and may lead to toxic megacolon + systemically unwell; proctitis - inflammation in lower rectum of unknown cause and is more self-limiting
145
Backwash ileitis?
In people with pan colitis UC, distal end of ileum becomes affected
146
Extra-intestinal manifestations of IBD
Weight loss
Anaemia - normochormic normocytic, or microcytic
Arthropathy: sacroiliitis, ankylosing spondylitis, rheumatoid-like arthritis
Uveitis + iritis
Skin lesions: erythema nodosum (uncommon tender red nodules on shins), pyoderma gangrenosum (rare, purulent skin ulcers)
Sclerosing cholangitis: ass w UC, progressive fibrosis of intrahepatic biliary system
147
Investigations in UC
Contrast radiology e.g. barium enema - loss of haustrations, pseudopolyps
Endoscopy - colonoscopy in non-acute
Fulminant UC risk of TM so monitor with AXR - dilated colon, loss of normal convex outward pattern, thick folds crossing lumen, usually TC
Stool analysis for bacteria/parasites/CMV
148
Management of UC
Aminosalicylate suppositories or oral e.g. sulfasalazine, mesalazine - for mild attacks or maintenance
Avoid NSAIDs made it worse
Corticosteroids - suppositories for rectal inflammation, short course for severe exacerbations
Immunosuppressants e.g. cyclosporin, azathioprine (steroid-sparing)
Avoid codeine + loperamide as cause toxic megacolon
Surgery: needed in about 20%, is curative if remove whole colon)
Options are subtotal colectomy with ileostomy (safest in emergency, most colon removed and left with inflamed rectal stump which can be dealt with later), proctocolectomy with permanent ileostomy (rectum removed, for elderly people) and restorative proctocolectomy/ileo-anal pouch (sphincter-preserving, avoids permanent ileostomy, entire colon and rectal mucosa excised and pouch made from a loop of terminal ileum, brought into pelvis and anastomosed to upper anal canal, temporary ileostomy for a few months to allow healing)
149
Features of Crohn's disease
Chronic relapsing inflammation of any part of GIT, most involve bowels, mostly starts in younger.
Transmural inflammation + oedema, epithelium mostly intact but with deep fissured ulcers, intervening areas of thickened mucosa-cobblestone appearance, granuloma (multinucleate giant cells in bowel + LNs, non-caseating [rarer in UC from ruptured crypt abscesses]), fibrosis from long term causing strictures, skip lesions (discrete segments of bowel affected with intervening parts healthy)
CF: diarrhoea (less than UC, only bloody/mucus if in colon), obstruction from narrowed lumen (grumbling colicky abdo pain), weight loss, general malaise, reduced absorption in SB (iron, folate, protein, growth issues, gallstones as less bile salts reabsorbed), apthous ulcers, non-GI things like in UC, usually feel ill during acute attacl
150
Complications of CD
Terminal ileitis: inflammation affects parietal peritoneum, mimics appendicitis
Adhesions: post-inflammatory
Perforation: contained perforation causing pericolic/pelvic abscess
Fistulae: between diseased bowel and hollow viscera e.g. gastro colic (true faecal vomiting), ileo-rectal (more diarrhoea), entero-vesical (severe UTI, pneumaturia), perianal inflammation (abscess, bluish 'piles', fissures, fistulae, sometimes so many 'pepper pot perineum')
151
Management of CD
Aim is to cause + maintain remission
5-ASA: act locally, corticosteroids for flare ups
Immunomodulators: azathioprine, 6-mercaptopurine, methotrexate, infliximab
Supportive: antidiarrhoeals e.g. loperamide, anti-spasmodics, diet modification (e.g. low fibre in obstructions, supplementary calories/iron etc)
--> in kids sometimes they do bowel rest with fortisip type things for a few weeks but needs cooperation
Surgery: not curative but most eventually need some form, if have complications or intolerable long-term obstruction etc.
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Other causes of IBD except UC + CD
Pseudomembranous colitis
Amoebic colitis: Entamoeba histolytic. Invades LB mucosa causing chronic relapsing symptoms like UC, may pass to liver in HPV causing abscesses. Usually in proximal colon causing colicky pain, erratic bowel habit, some blood-stained stools etc. Metronidazole
Microscopic colitis: histology abnormal but macroscopic normal. Chromic watery diarrhoea
153
What surgeries are used for cancer of colon?
Caecal/AC/prox TC - right hemicolectomy with ileo-colic anastomosis
Distal TC/DC - left hemicolectomy with colo-colon anastomosis
Sigmoid - high anterior resection with colo-rectal anastomosis
Upper rectum - anterior resection with colo-rectal anastomosis
Low rectum - anterior resection with colorectal anastomosis +/- defunctioning stoma
Anal verge - abdomino-perineal excision of rectum (no anastomosis)
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Pathophysiology of bowel obstruction
bowel segment occluded - gross dilatation of proximal part of bowel - increased peristalsis - large volumes of electrolyte rich fluid secreted into bowel (third spacing) -- why they get dehydrated. If there’s a§ second obstruction proximally is a closed-loop obstruction (if obstruction due to a volvulus or in LBO if ileocaecal valve is competent) surgical emergency as bowel will continue to distend until it perforates.
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Presentation of neuroendocrine tumours
- Non specific symptoms like abdo pain, N&V, abdo distension, may have features of obstruction
- Unintentional weight loss, palpable mass
- Majority are non-functioning (no hormone hypersecretion) but may be functioning
- Carcinoid syndrome: well-differentiated midgut NETs can present with this, occurring after metastasis of a carcinoid tumour causing cells to oversecrete bioactive mediators like serotonin, prostaglandins and gastrin -- symptoms of flushing, abdo pain, diarrhoea, wheezing and palpitations
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How do you do a groin examination?
• Examine standing up first if poss, ask them to lower their underwear
• Inspection: obvious lumps, asymmetry, scrotal swelling, scars, ask to cough to accentuate any hernia
• Lump palpation: if obvious examine that side first. Assess number (e.g. multiple more likely LNs or superficial lesions), consistency (soft or hard), cough impulse (incarcerated most likely don’t have a cough impulse as hernia is trapped), reducible?, pulsatile?, can you get below it, does it extend into scrotum?
• Hernia palpation:
o What is relation to pubic tubercle: above + medial=inguinal, below + lateral = femoral
o Reducing it: push it from the superficial along to the deep ring (try to get all in)
o Femoral more likely a ‘pea sized’ lump so harder to find but higher rates of obstruction, often incarcerated so rarely have a cough impulse
o Repeat for other side as 20% of inguinal hernias are bilateral
o Ask to lie down – if lump reduces spontaneously it indicates a hernia
o If lump is already reduced, ask patient to sit up/stand up/bring head up to tense abdo muscles
• Clinically use cough impulse to see direct/indirect (but actually v unreliable so do at surgery as indirect are lateral and direct are medial to inferior epigastric vessels).
o You do this by pressing over the deep ring (just above the midpoint of the inguinal ligament) whilst you have the hernia reduced, ask patient to cough
o If it protrudes when deep ring is occluded then it is a direct hernia (indirect you can still feel it but it doesn’t protrude), have to be pressing quite firmly. This is because in indirect you push it back into the canal and through the deep ring into abdomen, which you are occluding so it can’t get out, whereas in a direct inguinal hernia the weakness is in the posterior wall (Hesselbach’s triangle) which you can’t occlude so when cough (increased intra-abdominal pressure) the hernia comes back out
o Irreducible hernia may not have a cough impulse!!
• If irreducible/incarcerated may be painful, tender, erythematous
• If obstructed may have abdo distention, vomiting, absolyte constipation
• Completion: state you would examine external genitalia. This assesses for scrotal extension of hernia and genital lesions that may have spread to inguinal LNs (testicular lesions drain to iliac nodes so not palpable)
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How are refined diets causing disease?
* Slow GI transit – more contact of stool with bowel – more contact with carcinogens
* Raised intra-abdo pressure due to straining at stool – obstructs venous return (haemorrhoids, varicose veins) and predisposes to HH, IH and rectal prolapse
* Reduced bulk + more solid faeces – less effective peristalsis, intracreased intraluminal pressure, more friction (anal fissure), small stool bulk increases concentration of carcinogens
* Less bile salts lost in faeces due to more fat – increased bile salt pool so gallstones and may form carcinogens
* Changed bacterial flora – carcinogens, appendicitis
* More refined carbs – predisposes to diabetes and excess calorie intake
* Increased fat esp sat animal fats, and increased absorption as less binding to fibre – atherosclerosis, gallstones, obesity
* Obesity weakens abdo wall muscles (hernias, vaginal prolapse), thromboembolism, MSK disorders
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Typical non-acute abdo disease presentations
• GB dysfunction-biliary colic irregularly recurrent bouts of severe pain that aren’t true colic as last continuously for 1-12h, most often on right, may radiate to the right and be precipitated with rich foods and cause vomiting
• PUD-intermittent boring epigastric pain, not as severe as BC unless perforation, retrosternal burning in oesophagitis, classically duodenal better with food and gastric worse
• Pancreas Ca/chronic pancreatitis-severe gnawing poorly localised central pain, radiates to back, associated with anorexia and weight loss, may be better leaning forward
• IBS and constipation-poorly localised, bloating pain, post-prandially common, intensity varies, transient disturbed bowel function, often relieved by flatus or stool passage
• Diverticular and Crohn’s-partial bowel obstruction, more low key symptoms
• Hydronephrosis-dull poorly defined fairly constant loin pain, may radiate to groin or genitalia, urinary symptoms, often made worse by fluids
• Gynae-may be poorly defined lower abdo pain
• ‘Medical’ disorders-liver congestion in HF (common), splenic infarcts or diabetes (uncommon), acute intermittent porphyria, SCA, tertiary syphilis (v rare)
• Children:
o Infantile colic – sometimes due to cow’s milk allergy
o IBS
o Chronic IBD
o Recurrent streptococcal infections
o Periodic syndrome: episodes of poorly defined inconsistent pain and/or vomiting
o Abdominal migraine: may have nausea, pallor, photophobia, most common pre puberty
o Psychosomatic
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Typical locations for pathology in non-acute abdomens
* Epigastrium: foregut structures so lower oesophagus, stomach/duodenum, biliary tract, pancreas. Can also be cardiac
* RUQ: biliary tract, liver, basal pleura
* LUQ: rarely directly related to anatomical structures. Sometimes spleen or stomach
* Right or left loin: kidneys, ureters, spinal nerve roots
* Central abdomen: midgut structures so SB, LB, pancreas (deep pain radiating to the back)
* RIF: caecum, appendix, ovary/Fallopian tube, kidney/ureter, mesenteric LN, abdominal wall
* LIF: sigmoid colon, ovary/Fallopian tube, kidney/ureter, abdo wall
* Suprapubic: bladder, uterus and adnexae
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Dysphagia
Usually always oesophagus issues but occasionally pharynx or stomach. Initially solids then liquids with more narrowing, except achalasia which is fluids worse than solids (spluttering dysphagia). Bolus obstruction-acute dysphagia where lump of food sticks at narrowed part, completely obstructing oesophagus.
Causes:
*Obstruction in wall
o Common: peptic oesophagitis (sometimes causing stricture), carcinoma of oesophagus or cardia
o Uncommon: candida oesophagitis (esp after major surger)
o V rare: pharyngeal pouch, oesophageal web, oesophageal apoplexy from haematoma in wall, leiomyoma of oesophageal muscle
*Neuromuscular issues: achalasia (uncommon), bulbar or pseudobulbar palsy and myasthenia gravis (rare)
*External compression of oesophagus
o Subcarinal LN secondaries from Ca bronchus (quite common)
o Left atrial dilatation in mitral stenosis (rare)
o Dysphagia lusoria-compression from abnormally placed great arteries (v rare)
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Causes of weight loss + anorexia
* Intra-abdominal malignancies: Ca stomach/pancreas, metastatic disease in liver/widespread across peritoneal cavity (esp from stomach, LB, ovary, breast or bronchus), bowel lymphomas
* Medical conditions: alcoholism, cirrhosis, viral diseases (e.g. hepatitis, infectious mononucleosis), uncontrolled diabete or thyrotoxicosis, malabsorption, renal failure, cardiac cachexia
* Psychological
* Chronic visceral ischaemia: v uncommon, atherosclerotic narrowing of at least two of the coeliac axis/SMA/IMA causing ‘fear of food’ and massive weight loss
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Causes of anal problems
* Bleeding: fresh (haemorrhoids, rectum/sigmoid/anal canal cancer)
* Pain and discomfort: haemorrhoids (main, intermittent), anal carcinoma (usually painless tho), fissure in ano (severe pain after defecation), intersphincteric abscess (rare), perianal haematoma (acute onset, strangulated/thrombosed haemorrhoids or an abscess), proctalgia fugax (recurrent shooting pain)
* Perianal itching and irritation: most common inadequate hygiene causing skin issues, discharge from haemorrhoids/fistulae/tumours (low grade infections), threadworm in children
* ‘Something coming down’: haemorrhoids, skin tags, mucosal/rectal prolapse. Worse by defecation
* Perianal discharge: leakage of pus/inflammatory exudate/mucus e.g. pilonidal sinus, anal fistula, haemorrhoids, proctitis, adenoma or ulcerating carcinoma
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Change in bowel habit
*Constipation:
o Incomplete bowel obstruction-faecal impaction, obstructing Ca or stricture, extrinsic lesion e.g. ovarian Ca
o Loss of peristalsis-acutely from narcotics/antidepressants/iron, chronic diverticular disease or laxative abuse
o Inadequate fibre or fluid-less faecal volume and more transit time
o Bed-bound-immobility, diet, fluid, drugs
*Diarrhoea:
o Irriation or inflammation of SB or LB: IBD, chronic parasitic infections, following acute bacterial colitis e.g. Salmonella
o Blind loop syndrome: blind loop of SB after bypass surgery colonised with bacteria
o Malabsorption syndromes: e.g. after distal SB resection, as defective bile salt resorption causing irritation
o Laxative abuse, anxiety state
*Erratic bowel habit: IBS, diverticular disease, antibiotic-associated C diff causes psueodmembranous colitis
*Changes in nature of stool:
o Jaundice – clay coloured as bilirubin doesn’t reach gut
o Steatorrhoea – more fat due to malabsorption e.g. coeliac
o Undigested food in stool – malabsorption or a ‘short circuit’
* Frank rectal bleeding: bright red-lesion in rectum or anus. If clearly separate from stool suggests anal issue, if on surface suggests an adenoma or carcinoma of rectum/DC, if dark blood mixed with stool indicates more proximal disease (DC or TC, often Ca or IBD), if shiny black/plum coloured and tarry – melaena (may not be recognised as blood by pt, more proximal e.g. peptic ulcer), iron therapy have greenish-black formed stools
* Occult faecal blood loss: may not alter stool appearance but can cause anaemia
* Rectal passage of mucus or pus-most likely IBS, villous adenomas often secrete copious mucus, may be in haemorrhoids
* Tenesmus: unpleasant sensation of incomplete evacuation of the rectum. Most common causes are IBS and abnormal masses in rectum or anal canal, occ a prostatic carcinoma may invade around lower rectum
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Iron deficiency anaemia
*Inadequate dietary iron intake
*Lesions in GIT
o Ulcerating tumours/polyps: caecum, stomach, rest of LB, (rare) stromal tumours of SB
o Chronic peptic ulceration
o Other ulcerating lesions like haemorrhoids, angiodysplasias
o Chronic parasitic infection e.g. hookworm (developing countries)
*Lesions in female genital tract
o Menorrhagia
o Ca of uterus or cervix – usually abnormal PV bleeding tho
*Lesions in urinary tract – rarely cause anaemia
o TCC of bladder, pelvicalyceal system or ureter
o RCC-may cause hameturia, rarely anaema
o Chronic parasitic infestation e.g. schistosomiasis
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Causes of obstructive jaundice
* Stones in CBD – v common. Hx typical of biliary colic, jaundice may be progressive (stone firmly impacted), fluctuant (stone impacts and disimpacts alternately without actually going away) or intermittently (multiple small stones impact then pass through)
* Carcinoma of head of pancreas – common. May also compress 2nd part of duodenum. Typically painless persistent/progressive jaundice, may palpate GB
* Pancreatitis – uncommon. CBD obstructed by inflammatory swelling (acute) or scarring (chronic)
* Mirizzi’s syndrome – rare. In 1% of cholecystectomy patients, gallstones impacted in Hartmann’s pouch cause inflammation of GB – fuses w CHD – secondary stenosis, large stones sometimes cause pressure necrosis *Periampullary malignant tumours – uncommon
* Benign strictures of CBD – uncommon
* Other malignant tumours – rare. E.g. LN mets in porta hepatis, primary cholangiocarcinoma, Ca GB
* Intrahepatic or hilar BD obstruction – primary cholangiocarcinoma, sclerosing cholangitis (hepatic mets rarely cause obstructive jaundice)
* Intrahepatic cholestasis – common. E.g. viral hepatitis, systemic sepsis (due to liver dysfunction, idiosyncrasy to some drugs, oral contraceptives interferes w bile excretion from hepatocytes, widespread hepatic lymphoma (rare)
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Causes of hepatomegaly
o Physiological-Riedel’s lobe
o Malignant tumours-HCC, mets
o Infective-viral (hep, EBV, CMV), bacterial (TB, leptospirosis, liver abscess), protozoal (malaria, schistosomiasis, amoebiasis, histoplasmosis, hydatid disease)
o Alcoholic-fatty liver, early cirrhosis
o Systemic disease-Wilson’s disease, haemochromatosis, cellular infiltration like amyloid or sarcoid
o Hepatic adenomas
o Congestive cardiac failure-RHF, TR, Budd-Chiari syndrome
o Lymphoma, leukaemia, myeloproliferative disorders
o Anaemia
o Misc: PBC, polycystic liver disease
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Causes of splenomegaly
o Infective-viral (hep, EBV, CMV), bacterial (subacute endocarditis, typhoid, TB, leptospirosis), protozoal (malaria, toxoplasmosis, brucellosis, schistosomiasis, leishmaniasis)
o Systemic-sarcoid, amyloid, RA (Felty’s syndrome), storage diseases (e.g. Gaucher’s)
o Congestive splenomegaly-hepatic vein thrombosis, portal vein thrombosis, splenic vein thrombosis, cirrhosis w portal HTN
o Lymphoma, leukaemias, CML, myelofibrosis
o Anaemia-haemolytic, megaloblastic
o Thyrotoxicosis
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Causes of hepatosplenomegaly
o Infective-viral (hep, CMV), bacterial (TB, leptospirosis), protozoal (malaria, toxoplasmosis, brucellosis, schistosomiasis, leishmaniasis)
o Amyloid, storage diseases e.g. Gaucher;s
o Congestive hepatosplenomegaly- hepatic vein thrombosis, portal vein thrombosis, splenic vein thrombosis, cirrhosis w portal HTN, Budd-Chiari syndrome
o Lymphoma, leukaemia, CML, myelofibrosis, polycythaemia rubra vera, essential thrombocytopenia
o Megaloblastic anaemia
o Infantile polycystic disease
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Causes of RUQ mass
usually hepatobiliary origin so will continuous with main builk of liver on palpation and percussion
o If diffusely enlargd inferior margin is regular and well-defined, if cancerous may be hard/irregular or may be diffusely enlarged
o Riedel’s lobe-rare congenitally enlarged right lobe, soft and mobile
o Less common-diseased GB, continuous w liver above and having pear-shaped rounded outline likely mucocele, if painful may be empyema
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Causes of epigastric mass
usually cancer of stomach or TC, or omental secondaries from ovaries, or cancer of left liver lobe. Occ due to massive para-aortic LNs from lymphoma or testicular secondaries. Pulsatile-AAA
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Causes of a LUQ mass
Ca of stomach or splenic flexure, not having a discrete edge unlike splenomegaly
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Causes of iliac fossa masses
* LIF: sigmoid colon tumour or diverticular inflammatory mass
* RIF: unresolved appendix inflammation, Ca caecum, CD of terminal ileum
* Either: ovary, bladder lesions or hernia
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Causes of a central abdominal mass
o Malignancy: greater omentum, LN, pancreas, aorta
o AAA-expansile pulsation
o Hernias-incisional (most common, due to poor closure or infection), paraumbilical/umbilical (common in obese), divarication of the recti (rectus abdominus muscles, not a true hernia. Recti splayed apart due to pregnancy or obesity)
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Ascites
chronic accumulation of fluid within abdo cavity, can usually only b detected clinically when >2L. Dullness to percussion in flanks and suprapubic region with central resonance is suspicious, attempt to elicit fluid thrill or shifting dullness
causes:
o Malignant ascites: cells from tumour deposited in peritoneum which secrete a protein-rich fluid containing malignant cells
o Lymphatic obstruction: rare, major obstruction of lymphatic drainage – involvement of para aortic notes with lymphoma or metastatic testicular cancer most common. Chylous ascites-milky white ascitic fluid, rare, from proximal lymph obstruction so chylomicrons in the fluid
o TB: uncommon in developed, due to peritoneal tubercles
o Non-surgical: gross CCF, constrictive pericarditis, severe hypoalbuminaemia, portal venous obstruction
o Diffuse abdominal distension w/o palpable mass: exclude sinister causes. Gas within bowel common (e.g. IBS, aerophagia), chronic gaseous abdo distention from partial sigmoid volvulus, gross faecal loading
