Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Surgery Specialities > GI > Flashcards

GI Flashcards

1
Q

How do you take an abdominal pain history?

A

https://geekymedics.com/gi-history/

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Site abdo pain examples

A

Epigastric pain/acute abdo - pancreatitis, gastro duodenal ulcers, perforation
Groin lump - hernias
RIF - appendicitis
LIF - IBD, diverticular disease
RUQ - gallstones
From epigastric to whole of abdomen- peritonitis (if spread to chest then cardiac)
Other - intestinal obstruction, stoma’s

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Onset epigastric pain examples

A

Sudden - perforation of viscus (like ulcer)
Maximal intensity at 10-20 mins - acute pancreatitis or billary colic
Maximal intensity at Hours - cholecystitis, hepatitis, pneumonia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Epigastric pain character examples

A

Crushing or tight - cardiac (spread ro jaw neck and arm)
Sharp/burning - peptic Ucler, gastritis, duodenitis
Deep ‘boring’ - pancreatitis (with spread to back)
Retrosternal - oesophagitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Relieving and aggravating factors epigastric pain examples

A

Sitting forward - acute pancreatitis better
Eating - duodenal better and gastric worse
Movements - peritonitis worse
Deep breathing - pleural inflammation worse
Fatty meals - billary colic worse

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Which epigastric pain conditions are likely to present to hospital?

A

Pancreatitis, perforated peptic ulcer and MI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What other symptoms are common with epigastric pain?

A

Nausea/vomit - acute pancreatitis amd inferior MI(irritation of diaphragm)
After vomit - pain - boerhaave’s syndrome - perforation of oesophagus
Fever - infection - hepatitis or peritonitis
Dyspepsia- heartburn, bitter taste - GORD
Change in stool - pale - bile blocked or if stetorrhea so float, pale and foul smell - pancreatic exocrine insuffiency or billary disease
Cough - basal pneumonia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

How do you perform an abdo exam?

A

https://learn-eu-central-1-prod-fleet01-xythos.content.blackboardcdn.com/5bfe8efc36910/2138481?X-Blackboard-Expiration=1661709600000&X-Blackboard-Signature=KltoaT1A5woXZmZBxdU8wbjCWuyWLnQAwInxlDTlLI4%3D&X-Blackboard-Client-Id=160309&response-cache-control=private%2C%20max-age%3D21600&response-content-disposition=inline%3B%20filename%2A%3DUTF-8%27%27Examination%2520Checklists%2520-%2520Cardiovascular%252C%2520Respiratory%252C%2520GI%252C%2520CNS%2520%2528Cranial%2520and%2520Peripheral%2529%2520%25282%2529.pdf&response-content-type=application%2Fpdf&X-Amz-Security-Token=IQoJb3JpZ2luX2VjEI3%2F%2F%2F%2F%2F%2F%2F%2F%2F%2FwEaDGV1LWNlbnRyYWwtMSJGMEQCIDSmSZ8oiE52YgmYZLM%2FDu6URxmEi%2Fo%2BZ3RmeH6mp%2BXqAiANbVsFDKZMpZgfMpO3Xh2n5edXNmTty4m8KDrq%2B7tncSrcBAgWEAIaDDYzNTU2NzkyNDE4MyIMvkVPrVPr%2FqjIgu2gKrkEKlGdVedOq%2Bh1nhykOXA6EPzl3%2F%2FU5ZCMweyMcfOE2phDzJtQoCGf2CpsIOHKoCrwEq7ON7e%2F%2ButXjYeD61oxEheoXPTe4Jq5glJz3gH177qwiInl6%2B%2Fg9Ys1AMoguPJX%2FoH4UjuhzUQ%2F77p%2Fmn6NbYYjQSSZyCEAEC5ADdd5SFIzc%2FCF58Rfn9kcHQ7JQB66g3K4C%2BfDPJX5MU8ZkYMiueFGsjBmES%2FcAKNjpM5rg3PskqQJtYDWKBMz20C9LE4XK17JWBt3L9qhHs%2FPbFmZpFJ9L2UxC5%2BzbNDh7HybcDJ71VG30e8aaDD7H%2BWiEPjaPYO6M5xKJDJNJyB1hE0WPdDspj4%2FuxCDEbBlfLVHqkE%2FH477ynrVwY37wQjsBWsvKq4bbcpOV1QmChCtYLl%2BbSeBJPaGjnd6d%2FNuLOomTZkjJj5aomMccWP0U45Q7qZDKCwDiXcXFODdiCPBIU5BxgHIwy6rkE0fU2KE%2Bwyu5HS3VEpeEmRxlFmqKdPqOI%2BLctgrh1%2BtWfaRam5r1Di2YhClSaw5Oe%2Bp7aXAvB0rQLv04VETbGXnIBzag7RklokN2whTCc7hWR8l9JSYC3bmvj3Fc0XnBHQPjHUrdOuXB%2B7DlHN3ykRb5G7tNC0CIrPCZphhxJA2FeJ%2FgnujP6ZIM6il05uftcJybUUlE0erFucXcciwxjU6MlNXVt5U7PMcliUL5421%2B2DEqQ9kdleZidkfvmGFhyO%2BgxGxc2OFmU4gdfjRrOPcXzEwxNStmAY6qgFJqtFnWKU3L282Tsyx5A4HOWD9U2MmepYAKxDQ5jGlEPg7lzsiGuNVlYKeoEVVEcdX0s%2BMQVcMEgsxbbK4JRvh5UIwHQcV7haHVxX0yPa7dJkcYG59Qhnov%2BpNklLn4HzSGxhyGNue1VVnxzx5CNBP1osGH8gGE1CF%2F4Jk20r828SPkYMJEMAdreRBk9GkZdVdLAx5%2BWgBBKzWtX8%2FL1BDROLOI0l9e1mpQQ%3D%3D&X-Amz-Algorithm=AWS4-HMAC-SHA256&X-Amz-Date=20220828T120000Z&X-Amz-SignedHeaders=host&X-Amz-Expires=21600&X-Amz-Credential=ASIAZH6WM4PL7LRB5MCL%2F20220828%2Feu-central-1%2Fs3%2Faws4_request&X-Amz-Signature=7b6ab6eb065679004e4923c58c76396ede6f9f1407044089ee918300dfeca4f8

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are common acute surgical conditions?

A

Intestinal obstruction
Rupture AAA
Ruptured ectopic pregnancy
Bleeding gastric ulcer
Peritonitis
Ischaemic bowel

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is the common presentation for intestinal obstruction?

A

Small bowel - peri umbilical pain suddenly, (early) nausea and vomit, abdo tender and distended, more younger
High pitched bowel sounds, absolute constipation
Large bowel - periumbilical pain, abdo tender and distended, N+V, constipation then diarrhoea, older

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

How do you manage an intestinal obstruction?

A

Diagnosed - x ray - distended loops peripherally or centrally
Air enema or surgery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are the causes of an intestinal obstruction?

A

Small bowel - intra abdominal adhesions (fibrous bands between organs or tissues or both), prior surgery, incarcerated hernias, meckels diverticulum, strictures from crohns, tumours, foreign body
Large - colorectal cancer, caecal or sigmoid Volvulus, strictures from diverticulitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What are the common presentations of an upper GI haemorrhage?

A

Haematemesis - coffee ground like as partially digested blood
Altered bowel habits - dark tarry stools (malaena) or haematochezia - fresh blood
Epigastric abdo pain
Syncope due ro hypovolaemia or cerebral hypoperfusion
Tachycardia
Hypotension

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

How do you manage an upper GI haemorrhage?

A

FBC UE
Endosocpy
Prophylactic antibiotics
Medication

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What are the common causes of an upper GI haemorrhage?

A

Peptic ulcer
Mallory-Weiss tears
Varices
Oesophagitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are the common presentations of stomach cancer?

A

Similar pain to peptic ulcer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

How do you manage a patient with stomach cancer?

A

FBC, tumour markers,X ray, CT/MRI, endoscopy/colonscopy, TNM, Duke’s
Surgical resection, chemo, radio, palliative

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What are the causes of stomach cancer?

A

Smoker, high diet, h.pylori, men, FHx

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

How does oesophageal cancer present?

A

Dysphagia
Epigastric pain
Malaena
Haematemesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

How do you manage oesophageal cancer?

A

FBC, tumour markers,X ray, CT/MRI, endoscopy/colonscopy, TNM, Duke’s
Surgical resection, chemo, radio, palliative

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What are the common presentations of HPB?

A

Hepato - hepatomegaly, jaundice, unintentional weight loss, painless, ascites
Pancreatic - jaundice, vague symptoms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What is the management of HPB cancer?

A

FBC, tumour marker (CA19-9 - pancreatic)X ray, CT/MRI, endoscopy/colonscopy, TNM, Duke’s
Surgical resection, chemo, radio, palliative

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What are the causes of HPB cancer?

A

men, fh, smoker! chronic pancreatitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What are the presentations of colorectal cancer?

A

Unintentional weight loss, unexplained abdo pain, PR bleeding,, change in bowel habitn(ride sided - late change, left -early), anaemia, tenesmus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What is the management of colorectal cancer?

A

FBC, tumour marker (CEA), X ray, CT/MRI, endoscopy/colonscopy, TNM, Duke’s
Surgical resection, chemo, radio, palliative

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What are the causes of colorectal cancer?

A

FHx, IBD, polypodies syndrome, diet snd lifestyle (low fibre), coeliac (small)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What is the common presentation of different hernias?

A

Not incarcerated - fullness/swelling, gets larger when intra abdo pain increases, aches
Incarcerated - pain, nor moveable, N+V, symptomatic sx if ischaemic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What is the management of hernias?

A

Reduce it and cut out any ischaemia bowel

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What are the causes of hernias?

A

Weakness in cavity - congenital (if processes vaginalis doesn’t close - connection from peritoneal cavity to scotum), post surgery,
Increases in abdo pressure - obesity, weightlifting, constipation/cough, pregnancy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What is the presentation of gallstones?

A

RUQ - shoulder tip
Complication - billary colic - RUQ pain after eating fatty pain, acute cholecystitis - murphy’s sign, acute ascending cup,angitis - pain, inflammation and jaundice (Charcot)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What is the management of gallstones?

A

USS (radio lucent), analgesia, biliary colic and acute cholecystitis- elective cholecystectomy, ascending cholangitis - Iv antibiotics, fluid amd relieve obstruction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What are the causes of gallstones?

A

High cholesterol, overweight, 40\5., woman, pregnancy,

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What are the common presentations of acute pancreatitis?

A

Epigastric pain radiating to back, vomit, Cullen and Grey turners

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What is the management of acute pancreatitis?

A

CR/MRI to detect necrosis, raised lipases
Fluids and organ support

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What are the causes of acute pancreatitis?

A

Gallstones, alcohol, trauma, steroids, mumps, autoimmune, hyperlipidaemia, drugs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

What are the presentation f intrahafominap/subcutaneous and peri anal abscess or sepsis?

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What is the management of a patient with an abscess/sepsis?

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

What are the causes of abscess/sepsis?

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

What are the common presentations requiring a stoma?

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

What is the initial management with a stoma?

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

How are wounds managed?

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Why might someone require a stoma?

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

What are the causes of oesophageal cancer?

A

Smoker, Barrett’s

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

what is the pathophysiology of a bowel obstruction?

A

mechanical blockage of bowel..gross dilation of proximal limb of bowel…increased peristalysis, secretion of electrolyte rich fluid into bowel

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

what is the most common cause of bowel obstruction
- small bowel
- large bowel?

A

small - adhesions and hernia
large - malignancy, diverticular disease and volvulus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

what are the causes of bowel obstruction
-intraluminal
-mural
-extramural?

A

intraluminal - gallstone ileus, foreign body, faecal impaction
mural - cancer, strictures, intessusception, meckel’s diverticulum,lymphoma
extramural - hernia, adhesion, volvulus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

what are the cardinal features of bowel obstruction?

A

abdo pain -colicky or cramp
vomit - early if proximal and late if distal
constipation - vice versa
distension

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

what may be found on examination of someone with bowel obstruction?

A

distension
cachexia - malignancy
previous surgical scars
hernia
tympanic sound on percussion
tinkling bowel signs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

differentials for bowel obstruction

A

paralytic ileus
toxic megacolon
constipation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

which investigations are required for suspected bowel obstruction?

A

urgent bloods - fbc, ue (lots of third space losses), crp, lfts and group and save
venous blood gas - lactate shows signs of ischaemia
imaging - CT with contrast of abdo and pelvis, may use abdo x ray (>3cm in small, >6cm in large, >9cm in caecum)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

how do small and large bowel look different on x ray?

A

small - central, valvulae conniventes (completely cross bowel )
large - peripheral, haustra (halfway)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

what is the initial management of a patient with bowel obstruction?

A

IV fluid rescusitation (to drip)
urinary catheter
NBM
NG tube (and suck - to decompress bowel)
analgesia and anti emetics

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

what are some red flag sx of bowel obstruction indicative of ischaemia?

A

focal tenderness, pyrexia and pain worse on movement #

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

how is the management of bowel obstruction decided?

A

if previous surgery resulting in adhesion - treated conservatively unless evidence of ischaemia
if not resolves within 24 hrs with conservative management…water soluble contrast…not reach colon by 6 hours..surgery
if not had surgery and has obstruction - usually requires surgery
if needs surgical correction, ie strangular hernia - surgery
fails to improve within 48 hours -surgery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

what are the 3 most common complications of bowel obstruction?

A

bowel ischaemia
bowel perforation
dehydration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

define melena

A

black tarry stools with offensive smell - upper gi bleed..alteration and degradation of blood by digestive ienzymes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

define melena

A

black tarry stools with offensive smell - upper gi bleed..alteration and degradation of blood by digestive ienzymes
- PID, liver disease and gastric cancer…confirmed by DRE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

how can liver cirrhosis result in melena?

A

varices- dilation of the porto-systemic anastomses in oesophagus…due to portal hypertension secondary to liver cirrhosis which can rupture

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

what features are important to ellicit in a patient with melena?

A

colour and tecture
abdo pain, dyspepsia, dysphagia
smoking/alcohol
steroids, nsaids, anticoag

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

which investigations are required for melena?

A

FBC, UE, LFT, clotting - drop in Hb, Liver damage, rise in urea:creatinine ratio
group and save and 4 units cross matched
ABG
OGD or CT abdo with contrast

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

how is melena managed?

A

A to E approach
if PID = injections of adrenaline and cauterisation, high dose PPI IV
if varices - endoscopic banding, prophylactic abx, somatostain analogue (reduce splanchnic blood flow), tube inserted to compress bleeding
if GI malignancy - biopsies, surgical/oncological management
- may require blood transfusion and correction of coagualtion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

what are the causes of Gi perforation?

A

diverticulitis
PUD
Gi malignancy
iatrogenic - endoscopy
trauma
foreign body
appendicits or meckel’s diverticulum
mesenteric ischaemia
toxic mgacolon
excess vomiting

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

what are the clinical features of GI perforation?

A

pain is rapid and sharp
systemically unwell
malaise
vomit
lethargy
features of peritonism - localised, generalised rigid abdomen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

which investigations are required for perforation?

A

FBC, UE, LFT, clotting, G and S
usually raised WCC + CRP
CT scan - free air

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

which investigations are required for perforation?

A

FBC, UE, LFT, clotting, G and S
usually raised WCC + CRP
CT scan - free air

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

which investigations are required for perforation?

A

FBC, UE, LFT, clotting, G and S
usually raised WCC + CRP
CT scan - free air

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

which investigations are required for perforation?

A

FBC, UE, LFT, clotting, G and S
usually raised WCC + CRP
CT scan - free air

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

which investigations are required for perforation?

A

FBC, UE, LFT, clotting, G and S
usually raised WCC + CRP
CT scan - free air

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

which investigations are required for perforation?

A

FBC, UE, LFT, clotting, G and S
usually raised WCC + CRP
CT scan - free air

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

how is gi perforation managed?

A

broad spectum abx
NBM
NG tube
IV fluid resuscitation
analgesia
repair of perforated viscus and washout
localised diverticular perforation and sealed upper gi perforation and elderly patients - conservative

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

what presentations require urgent intervention?

A

bleeding so in hypovolaemic shock- ruptured AAA- refer to vascular team and immediate surgery
- ruptured ectopic pregnancy
- bleeding gastric ulcer
- trauma
perforated viscus = peritonitis
- peptic ulceration
- obstruction
- diverticular disease
- IBD
lay still, tachy and hypo, rigid abdomen, involuntary guarding, reduced bowelsounds
ischaemic bowel - severe out of proportion, raised lactate, diffuse pain,CT with contrast
others which are less acute - colic - can not get comfortable
- peritonism (not peritonitis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

which investigations are required for acute abdo pain?

A

urine dipstick - infection, haematuria, preg
ABG - septic or bledding
routine blood - fbc, ue,lft, crp, amylase,group and save
blood cultures - infection
imaging - erect chest x ray for free air
- USS for KUB - hydronephrosis, nilliary tree and liver for gallstones, transvaginal for tubo-ovarian pathology
- possible CT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

what is the general management of acute abdo pain?

A

IV access - large bore cannulas
NBM
analgesia
anti emetics
imaging
VTE prophylaxis
urine dip
bloods
catheter
NG tube
Iv fluids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

what are the emergency causes of haematemesis?

A

oesophageal varices
gastric ulceration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

what are the non emergency causes of haematemesis?

A

mallory-weiss tear
oesophagitis
gastritis
gastric malignancy
meckel’s diverticulum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

define oesophageal varices

A

porto systemic venous anastomoses in oesophagus
dilated veins prone to rupture
common underlying cause - alcoholic liver disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

what is the first line investigation of a patient with haematemesis and history of alcohol abuse?

A

URGENT OGD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

where can gastric ulceration most commonly occur?

A

blood vessels supplying:
lesser curve of stomach
posterior duodenum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

define mallory weiss tear

A

forceful vomiting causes a tear in epithelial lining of the oesophagus
most cases benign but if prolonged - OGD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

what are the causes of oesophagitis?

A

GORD
infections such as candida albicans
medications - bisphosphonates
radiotherapy
ingestion of toxic substances
crohns disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

what features are important in a history with haematemesis?

A

timing, frequency, volume
history of dyspepsia, dysphagia
past medical hx and smoking and alcohol
use of steroids, nsaids, anticoagulations, bisphosphonates

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

which investigations are required for haematemesis?

A

fbc may not show anaemia
LFT - liver damage
group and save and 4 units cross matched
OGD
chest x ray - pneumoperitoneum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

what system is used to risk stratify patients admitted with upper GI bleed?

A

glasgow-blatchford bleeding score

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

how are patients with haematemesis managed?

A

rapid A->E
-2 large bore Iv cannulas
- fluid resuscitation
- crossmatch blood
- OGD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

how is peptic ulcer managed?

A

injections of adrenaline, cauterisation of bleeding
high dose PPI
H.pylori eradication

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

how is oesophageal varices managed?

A

blood products
prophylactic abx
endoscopic banding
somatostatin analogues or vapressors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

how is an active bleed managed?

A

angio-embolisation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

what are the causes of dysphagia?

A

oesophageal malignancy
benign strictures
extrinsic compression - thyroid
pharngeal pouch
foreign body
post stroke
achalasia
myasthenia gravis
MS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

what is the medical term for pain when swallowing?

A

odynophagia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

what sx do you need to ask about with a patient who has dysphagia?

A

regurgiation
sensation of food getting stuck
hoarse voice
weight loss
referred ear or neck pain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

which investigations are required for dysphagia?

A

endoscopy +- biopsy
FBC, LFT
barium swallow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

define gastric outlet obstruction

A

mechanical obstruction between gastric pyloris and proximal duodeum so stomach can not empty

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

what are some causes of gastric outlet obstruction?

A

peptic ulcer, gastric cancer/small bowel cancer, iatrogenic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

what are the clinical features of a patient presenting with gastric outlet obstruction?

A

epigastric pain
postprandial vomiting
early satiety
dehydrated
hypovolaemic
tachycardic
tender upper abdomen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
90
Q

medical term for delayed gastric empyting

A

gastroparesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
91
Q

which investigations are required for gastric outlet obstruction?

A

fbc, crp, ue, clotting, group and save
abdo x ray or CT with contrast
endoscopy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
92
Q

how is gastric outlet obstruction managed?

A

resuscitation fluids
catheter
NG tube to decompress stomach
IV PPI
endocopy can dilate
surgery if all else fails

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
93
Q

what are some lower GI causes of rectal bleeding?

A

diverticular disease, ischaemic or infective colitis, haemorrhoids, malignancy, crohn’s or UC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
94
Q

define haemorroids

A

engorged vascular cushions in the anal canal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
95
Q

what are important to ask in a hx with per rectal bleeding?

A

duration,frequency, colour, relation to stool and defecation
associated sx
family hx of bowel cancer or IBD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
96
Q

which investigations are required for per rectal bleeding?

A

bloods - fbc, ue, lft, clotting, group and save
stool culture - rule out infective cause
urgent CT angiography if haemodynamically unstable
flexible sigmoidoscopy - left colon malignancy
OGD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
97
Q

how is per rectal bleeding managed?

A

unstable rectal bleeding (less common) - A->E, IV fluids, blood products
any Hb<70 - red cell transfusion
endoscopic haemostasis - injected diluted adrenaline
arterial embolisation
possible surgical tx

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
98
Q

what are the risk fx for GORD

A

age, obesity, male, alcohol, smoking, caffeine/spicy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
99
Q

what are the risk fx for GORD

A

age, obesity, male, alcohol, smoking, caffeine/spicy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
99
Q

what are the risk fx for GORD

A

age, obesity, male, alcohol, smoking, caffeine/spicy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
100
Q

what are the clinical features of GORD

A

chest pain
burning retrosternal sensation
worse after meals, lying or bending over
relieved by antacids
possible - belching, odynophagia, chronic cough

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
101
Q

what are the red flag symptoms for GORD?

A

dysphagia
weight loss
early satiety
malaise
loss of appetite

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
102
Q

what is GORD a risk fx for?

A

barretts oesophagus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
103
Q

what red flag sx required urgent endoscopy?

A

dysphagia
>55 with upper abdo pain, weight loss, dyspepsia,reflux

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
104
Q

what investigations are required for GORD and when would you consider investigating?

A

endoscopy - worsen depsite PPI, new onset and in older pts
24 hr pH monitor is gold standard for GORD + manometry to exclude dysmotility

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
105
Q

how do you manage GORD?

A

conservative - less caffeine, weight loss, smoking cessation, PPI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
106
Q

what are the indications for surgery in GORD?

A

failure to response, patient preference, with complications - recurrent pneumonia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
107
Q

how is GORD handled surgically?

A

fundoplication - fundus wrapped around GOJ

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
108
Q

what are the main complications of GORD?

A

aspirational pneumonia, barrets, strictures, cancer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
109
Q

what are the risk factors for squamous cell carcinoma?

A

middle and upper thirds -
smoking and alcohol
achalasia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
110
Q

what are the risk factors for adenocarcinoma?

A

lower third (usally barretts)
LONG STANDING gord
OBESITY
HIGH FAT INTAKE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
111
Q

what are the clinical features of oesophageal cancer?

A

dysphagia
weight loss
odynophagia
hoarseness
supraclavicular lymphadenipathy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
112
Q

which investigations are required for oesophagus cancer?

A

OGD within 2 week, biopsy
staging - CT CAP, endoscopic USS, staging laproscopy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
113
Q

how is squamous cell v adenocarcinoma treated?

A

scc - chemo - radiation
adeno -neoadjuvant chemo or chemo radiotherapu following resection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
114
Q

what is the main surgical management for oesophageal cancer?

A

oesophagectomy - removes tumour, top of stomach, surrounding lymph nodes
ivor lewis or mckeon procedure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
115
Q

whaat is post op function post oesophagectomy?

A

lose the reservoir function of the stomach. Many centres will routinely insert a feeding tube into the small bowel (a “feeding jejunostomy”) to aid nutrition. However, most patients will need to eat 5-6 small meals per day to meet their nutritional requirements.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
116
Q

whaat is post op function post oesophagectomy?

A

lose the reservoir function of the stomach. Many centres will routinely insert a feeding tube into the small bowel (a “feeding jejunostomy”) to aid nutrition. However, most patients will need to eat 5-6 small meals per day to meet their nutritional requirements.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
117
Q

prognosis of oesophageal cancer

A

poor - 5-10% as late presentation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
118
Q

define oesophageal perforation

A

full thickness rupture
if spontaenous - boerhaave’s syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
119
Q

define oesophageal perforation

A

full thickness rupture
if spontaenous - boerhaave’s syndrome
Perforation will result in leakage of stomach contents into the mediastinum and pleural cavity, which triggers a severe inflammatory response which will rapidly become overwhelming, resulting in a physiological collapse, multi-organ failure, and death.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
120
Q

what are the clinical features of oesophageal perforation?

A

retrosternal chest pain, resp distess, subcutaneous emphysema

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
121
Q

which investigations are required for oesophgeal perforation?

A

routine bloods
chest x ray - pneumoperitoneum
CT chest abdo pelvis with contrast

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
122
Q

what is involved in the initial management of oesophageal perforation?

A

septic and require urgent fluid resus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
123
Q

what are the indications for surgical management of oesophageal perforation and what surgery?

A

spontaneous perforation
thoractomy to control leak and wash out chest

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
124
Q

how is oesophageal perforation managed non surgically and the inidcations?

A

iatrogenic tend to be more stable
or if too frail/co morbidities to undergo surgery
Initial suitable resuscitation and transfer to Intensive Care / High Dependency Unit
Appropriate antibiotic and anti-fungal cover
Nil by mouth for 1-2 weeks, with endoscopic insertion of an NG tube on drainage
Large-bore chest drain insertion
Total Parenteral Nutrition (TPN) or feeding jejunostomy insertion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
125
Q

what is the prognosis of oesophageal perforation?

A

mortality and morbidity high

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
126
Q

define mallory weiss tear

A

lacerations in mucosa usually at GOJ
after profuse vomiting
short period of haemaetemsis
managed conservatively

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
127
Q

the anatomy of the oesophagus

A

The upper oesophageal sphincter is comprised of skeletal muscle, and prevents air from entering the GI tract. The lower oesophageal sphincter (LOS) is composed of smooth muscle, and prevents reflux from the stomach.

Peristaltic waves, controlled by the oesophageal myenteric neurones, propel ingested food down the oesophagus. The primary wave is under control of the swallowing centre and the secondary wave is activated in response to distention.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
128
Q

define achalasia

A

failure of relaxation of LOS and absence of peristalysis along oesophagus
increased risk of cancer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
129
Q

what are the clinical features of achalasia?

A

progressive dysphagia for solids and liquids
regurgitation
resp complications, chest pain, dyspepsia,weight loss

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
130
Q

which investigations are required for suspected achlasia?

A

OGD - cancer
oesophageal menometry - Absence of oesophageal peristalsis
Failure of relaxation of the lower oesophageal sphincter
High resting lower oesophageal sphincter tone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
131
Q

conservatyive management of achalasia

A

sleep with pillows, eating slowly, chewing, fluids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
132
Q

medical management of achalasia

A

calcium channel blockers - inhibit LOS contraction
botox due to LOS via endoscopy

133
Q

surgical management of achalasia

A

Laparoscopic Heller Myotomy* – the division of the specific fibres of the lower oesophageal sphincter which fail to relax (Fig. 4), often seen as the
A long-term improvement in swallowing is seen in ~85% of patients, with lower side-effect profile compared to endoscopic treatment
Per Oral Endoscopic Myotomy (POEM) – a cardiomyotomy at the LOS is performed from the inside of the oesophageal lumen, through a submucosal tunnel
Endoscopic Balloon Dilatation – insertion of a balloon into the lower oesophageal sphincter, which is dilated to stretch the muscle fibres
or well patients with type II pattern by HRM
Those with end-stage refractory achalasia may eventually require an oesophagectomy.

134
Q

define diffuse oesophageal spasm

A

dysfunction of oesophageal inhibitory nerves

135
Q

what are the clinical features of diffuse oesophageal spasm?

A

severe dysphagia to solids and liquids
central chest pain
will respond to nitrates unlike angina pectoris

136
Q

which investigations are required for diffuse oesophageal spasm?

A

manometry - repetitive, simulatenous and ineffective contractions
endoscopy

137
Q

how is DOS managed?

A

relax oesophageal smooth muscle via CCB
pneumatic dilation and heller myotomy - surgery

138
Q

what are some other causes of oesophageal dysmotility?

A

autoimmune
CT disorders

139
Q

how is a hiatus hernia classified?

A

sliding (80%) - GOJ, abdo part of oesophagus and cardia of stomach move upwards through diaphragmatic hiatus into thorax
rolling or para-oesophageal (20%) - upward movement of gastric fundus occurs to lie alongside a normally positioned GOJ..bubble

140
Q

what are the risk fx for developing a hiatus hernia

A

age related loss of diaphragmatic tone, increased abdo pressure, increased size of diaphragmatic hiatus, pregnnacy, obesity, hiatus

141
Q

what are the clinical features of a hiatus hernia?

A

vast are asx
GORD sx, vomit, weight loss, bleeding/anaemia, hiccups, palpitations, swallowing difficulties
bowel sounds may be auscultated within chest

142
Q

which investigations are required for hiatus hernia?

A

OGD
or incidentally on CT/MRI

143
Q

conservative management of hiatus hernia

A

PPI with food
weight loss
alteration of diet
smoking cessation
reduce alcohol

144
Q

how is a hiatus hernia managed surgically>

A

Cruroplasty – The hernia is reduced from the thorax into the abdomen and the hiatus reapproximated to the appropriate size. Any large defects usually require mesh to strengthen the repair.
Fundoplication – The gastric fundus is wrapped around the lower oesophagus and stitched in plac

145
Q

what are the indications for surgery of a ahiatus hernia?

A

Remaining symptomatic, despite maximal medical therapy
Increased risk of strangulation/volvulus* (rolling type or mixed type hernia, or containing other abdominal viscera)
Nutritional failure (due to gastric outlet obstruction)

146
Q

what are some specific complications of a hiatus hernia surgery?

A

recurrence of hernia
bloating
dysphagia if fundoplication too tight
fundal necrosis - blood supply via left gastric artery and short gastric vessels have been disrupted

147
Q

define gastric volvulus and the triad involved

A

stomach twists on itself by 180 degrees, leading to obstruction of gastric passage and tissue necrosis
bouchardt’s triad - severe epigastric pain, retching without vomiting, inability to pass NG

148
Q

where are peptic ulcers most commonly located?

A

lesser curve of stomach or first part of duodenum

149
Q

what are the most common causes of peptic ulcer?

A

H.pylori
NSAIDS
chronic alcohol use
gastric bypass
severe burns
head trauma
zollinger ellison syndrome

150
Q

when should an urgent OGD be done in context of PUD?

A

New-onset dysphagia
Aged >55 years with weight loss and either upper abdominal pain, reflux, or dyspepsia
New onset dyspepsia not responding to PPI treatment

151
Q

which other investigations are required apart from OGD is required for PUD?

A

c-12 breath test, serum antibody to H pylori, stool antigen test

152
Q

how are peptic ulcers managed conservatively?

A

smoking cessation
weight loss
less alcohol
less NSAIDS
PPI or triple therapy if h,pylori

153
Q

why might surgery be required in PUD and why is it indicated?

A

only in emergencies when it perforates or if zollinger ellison syndrome
in severe or relapsing - partial gastrectomy, selective vagotomy

154
Q

what are the risk fx for gastric cancer/

A

male
h.pylori
age
smoking

155
Q

what are the clincial features of gastric cancer?

A

vague
dyspepsia
dysphagia
early satiety
vomit
malaena
non specific cancer sx
epigastric mass
troisier’s sign - palpable left supraclavicular node
hepatomegaly, ascites, jaundice

156
Q

which investigations for gastric cancer?

A

URGENT OGD
for staging - CT TAP and staging laparascopy

157
Q

where should biopsies from a suspected gastric malignancy be sent?

A

histology
CLO test - h.pylori
HER2/neu protein expression - monocloncal therapies

158
Q

how is gastric cancer managed surgically>

A

proximal - total gastrectomy
distal - subtotal gastrectomyy
reconstructed with roue-en-Y

159
Q

what are some gastrectomy complications?

A

death
anastamotic leak
re operation
dumping syndrome
vit B12 defiency

160
Q

what are the main complications of gastric cancer

A

gastric oulet obstruction
iron defiency anaemia
perforation
malnutrition

161
Q

define direct inguinal hernia

A

bowel enters through hesselbach’s triangle
medial to inferior epigastric vessels

162
Q

define indirect inguinal hernia

A

bowel enters the inguinal canal via deep inguinal ring. due to incomplete closure of processus vaginalis
lateral to inferior epigastric vessels

163
Q

risk fx for inguinal hernia

A

Male gender
Increasing age
Raised intra-abdominal pressure, from chronic cough, heavy lifting, or chronic constipation
High BMI

164
Q

what are the clinical fx of inguinal hernia

A

lump in groin..if reducible disappear when lying down
mild discomfort
if incarcerated - painful and non reducible
possible bowel obstruction sx

165
Q

how do you examine any groin lump?

A

Cough impulse – remember that an irreducible hernia may not have a cough impulse
Location – inguinal hernia appear superomedial to the pubic tubercle* (whilst femoral hernia appear inferolateral to the pubic tubercle)
Reducible – On lying down or with gentle pressure
If it enters the scrotum, can you get above it / is it separate from the testis

166
Q

how do you locate the deep inguinal ring?

A

midpoint of inguinal lig

167
Q

what are some differentials for groin lump?

A

femoral hernia, saphena varix, inguinal lymphadenopathy, lipoma, or groin abscess. If the mass extends into the scrotum, consider a hydrocoele, varicocoele, or a testicular malignancy.

168
Q

which investigations are required for groin lump

A

USS
Ct if strangulation/obstruction

169
Q

how is an inguinal managed?

A

symptomatic - surgical
strangulated (pain out of proportion or derranged UE) - surgery
asx - maybe conservative

170
Q

how are inguinal hernias repaired surgically?

A

open repair(lichenstein) or laprascopic
if primary = open mesh
if bilateral or recurret or female/chronic pain = laprascopic

171
Q

what are the main complications following elective inguinal hernia repair?

A

haematoma, seroma, recurrence, chronic pain, damage to vas deferens or testicular vessels

172
Q

define femoral hernia

A

abdominal viscera or hernia pass through femoral ring and into potential space of femoral canal

173
Q

risk fx for femoral hernia

A

Female
Pregnancy (higher incidence in multiparous women)
Raised intra-abdominal pressure (e.g. heavy lifting, chronic constipation)
Increasing age

174
Q

what are the clinical fx of femoral hernia?

A

small lump in groin
usually p[resent as emergency as femoral canal narrow

175
Q

how do you differentiate between a femoral and inguinal hernia?

A

Femoral hernia – found infero-lateral to the pubic tubercle (and medial to the femoral pulse)
Inguinal hernia – found supero-medial to the pubic tubercle
A femoral hernia can roll up superiorly and in front of the inguinal ligament and are often misdiagnosed as inguinal

176
Q

how are femoral hernias managed?

A

all surgically within 2 weeks of presentation
low approach = below inguinal lig
high approach = easy access to small bowel
…reduce hernia and narrow femoral ring

177
Q

define epigastric hernia

A

through upper midline through fibres of linea alba
secondary to raised intra abdo pressure
usually middle aged men

178
Q

define paraumbilical hernia

A

through linea alba around umbilical region
secondary to chronic raised intra abdo pressure
contain usually pre peritoneal fat and bowel
or in children - omphalocele or gastroschsiss

179
Q

define spigelian hernia

A

rare
through semilunar line around level of arcuate line
present as mass in lower lateral edge of rectus abdominus
high risk of strangulation

180
Q

define obtruator hernia

A

hernia of pelvic floor - through obtruator foramen into obtruator canal
more common in women due to wider pelvis
usually elderly
mass in upper medial thigh
features of small bowel obstruction
compression of obtruator nerve - postive howship-romberg sign

181
Q

define littre’s hernia

A

very rare form of abdominal hernia, whereby there is herniation of a Meckel’s diverticulum. This most commonly occurs in the inguinal canal and many will become strangulated.

182
Q

define lumbar hernia

A

rare posterior hernias, that typically occur spontaneously or iatrogenically following surgery (classically following open renal surgery). They present as a posterior mass, often with associated back pain.

183
Q

define richter’s hernia

A

only a partial herniation of bowel, where anti mesenteric border becomes stangulated so only one of lumen of bowel within hernia sac

184
Q

define richter’s hernia

A

any hernia - only a partial herniation of bowel, where anti mesenteric border becomes stangulated so only one of lumen of bowel within hernia sac
tender irreducible mass at orifice

185
Q

define gastroenteritis

A

inflammation of GI tract usually infective(viral)

186
Q

PC of gastroenteritis

A

diarrhoea, vomit,abdo pain
night sweats, weight loss, dehydrated, pyrexia
hx - bowel movements, affected family, recent travel, recent use of abx

187
Q

how do you differentiate between the causative organisms of gastroenteritis?

A

bacterial toxins - hours
bacteria - weeks
viruses - days
parasites - months

188
Q

risk fx for gastroenteritis

A

Poor food preparation, especially in handling and cooking
Immunocompromised
Poor personal hygiene

189
Q

when may an investigations of gastroenteritis be required?

A

stool culture if blood or mucus in stool and if pt is immunocompromised or if severe or persitent

190
Q

how is gastroenteritis managed?

A

Rehydration, encouraging oral fluid intake where possible
If severe dehydration or unable to tolerate oral fluid, the patient may need admission for intravenous fluid rehydration
Education to prevent future episodes
Exclusion from work is usually 48 hours from the last episode of vomiting or diarrhoea
must notify!

191
Q

what are the viral causes of gastroenteritis?

A

Norovirus – single-stranded RNA virus (Fig. 1), the most common form of viral gastroenteritis in adults, presents with abdominal cramps, watery diarrhoea, and vomiting, usually lasting 1-3 days
Rotavirus – double-stranded RNA virus, results in a severe diarrhoea among infants and young children, generally self-resolves in less than a week
Adenovirus – double-stranded DNA virus, also a common cause of diarrhoea in children

192
Q

what are the bacterial causes of gastroenteritis?

A

Campylobacter –ingestion of affected chicken, eggs, or milk), can have a prodrome of fatigue, fever, or myalgia, followed by nausea, abdominal cramps, and diarrhoea
Campylobacter infections can also result in reactive arthritis, Guillan Barre syndrome, haemolytic uraemic syndrome, and thrombotic thrombocytopaenic purpura
E. Coli – contaminated foodstuffs (but can also spread from animals to human or from person to person contact); several forms of the bacteria exist, but Enterotoxigenic E. coli (ETEC) is the most common cause of Travellers’ diarrhoea
E. coli serotype 0157:H7 is associated with causing haemorragic uraemic syndrome
Salmonella – through undercooked poultry or raw eggs; results in fever, vomiting, abdominal cramps, and bloody diarrhoea
Shigella – contaminated dairy products and water; presents with fever, abdominal pain, or bloody diarrhoea

193
Q

what are the bacterial toxins causing gastroenteritis?

A

symptoms tend to last less than 24 hours.

Staphylococcus aureus – typically found in meat or dairy products, even re-heating of the cooked food does not destroy the exotoxin (even if the bacteria are destroyed)
Bacillus cereus – usually found in reheated rice, known to cause rapid-onset vomiting and abdominal cramps
Clostridium perfringes – typically acquired from re-heating meat dishes; causes diarrhoea yet vomiting is less common
Vibrio cholera – acquired most commonly from contaminated water supplies and causes profound watery painless diarrhoea; an oral vaccine is available

194
Q

what are the parasitic causative organisms of gastroenteritis?

A

Cryptosporidium – protozoan that typically causes a self-limiting watery diarrhoea and abdominal cramps (can be life-threatening in those who are immunocompromised); diagnosis is made with stool culture for ova, cysts, and parasites.
Entamoeba histolytica – anaerobic amoebozoan that becomes acquired from the ingestion of food or water contaminated with faeces (Fig. 3), presents with bloody diarrhoea, abdominal pain, and fever (can also result in liver abscess); stool culture for ova, cysts and parasites is required for diagnosis, recommended treatment is metronidazole or tinidazole
Giardia intestinalis – parasite transmitted through direct contact or faeco-oral route, can cause either acute disease (diarrhoea, fever, fatigue, nausea, and bloating) or chronic disease (steatorrhoea, malabsorption, and weight loss); diagnosis made with stool culture for ova, cysts and parasites, recommended treatment is metronidazole or tinidazole
Schistosoma – a fluke, acquired through contaminated water, with acute schistosomiasis developing about a month after the initial infection, presenting with fever, malaise, abdominal pain, bloody diarrhoea, and severe cases even leading to chronic liver disease; eosinophilia may be seen on full blood count and a stool culture for ova, cysts and parasites is required, with treatment via praziquantel

195
Q

what is the main causative organism for hospital acquired gastroenteritis?

A

c.diff…exotoxin A and B

196
Q

what is a complications of hospital acquired gastroenteritis?

A

toxic megacolon

197
Q

how is c.diff gastroenteritis diagnosed?

A

stool culture and c diff toxin testing…requires metronidazole

198
Q

what are the non infective causes of gastroenteritis?

A

Radiation colitis – inflammation of the gastrointestinal tract secondary to radiation therapy
Inflammatory bowel disease, such as Crohn’s Disease or Ulcerative Colitis
Microscopic colitis – a condition where the colon is macroscopically normal on endoscopy however biopsy demonstrates an increase in the number of inflammatory cells present
Chronic ischaemic colitis – caused by a compromise in blood supply to the colon, most commonly affecting the watershed area around the splenic flexure. Diagnosis is confirmed by endoscopy where one might observe ‘blue swollen mucosa’

199
Q

what is angiodysplasia?

A

formation of arteriovenous malformations
very common - rectal bleeding >60

200
Q

what is the pathophysiology of angiodysplasia?

A

Acquired angiodysplasia – begins as reduced submucosal venous drainage in the colon due to chronic and intermittent contraction of the colon, giving rise to dilated and tortuous veins. This results in the loss of pre-capillary sphincter competency and in turn causes the formation of small arterio-venous communications characterized by a small tuft of dilated vessels.
Congenital angiodysplasia – included causes such as hereditary haemorrhagic telangectasia (Rendu-Osler-Weber syndrome)

201
Q

what are the clinical features of angiodysplasia?

A

rectal bleeding and anaemia
either asx, painless occult PR bleeding, acute haemorrhage
haematemesis or malaena

202
Q

what are the ddx for angiodysplasia?

A

oesophageal varices, gi malignancies, diverticular disease

203
Q

which investigations are required for angiodysplasia?

A

FBC, UE, LFTS, clotting, group and save or crossmatch
upper gi for malignancy
wireless capsule endoscopy - small bowel bleeds
mesenteric angiograpjy - overt bleed

204
Q

how is angiodysplasia managed?

A

conservatively - bed rest and IV fluid, tranxamic acid
endoscopy - subjecting vessel to electric current and argon
mesenteric angiography - super selective catheterisation and embolisation of vessel
surgery - resection and anastomosis of affected bowel

205
Q

what are the risk fx with poor outcome for angiodysplasia?

A

age,liver disease, hypovolaemic shock, current inpatients

206
Q

what are the indications of bowel surgery for angiodysplasia?

A

Continuation of severe bleeding despite angiographic and endoscopic management (or such therapies are unavailable)
Severe acute life-threatening GI bleeding
Multiple angiodysplastic lesions that cannot be treated medically

207
Q

how common are small bowel tumours?

A

rare <5%

208
Q

where is the most common location for small bowel tumours?

A

duodenum
jejenum
ileum

209
Q

what are the histology of small bowel tumours>

A

Benign tumours – typically adenomas, subclassified as simple villous, tubular, or Brunner’s gland adenomas; less common types are leiomyomas, lipomas, and desmoid tumours
Malignant tumours – most common types are either adenocarcinomas or neuroendocrine tumours (40% each*); less common types are stromal tumours, sarcomas, and lymphomas

210
Q

what is the pathophysiology of small bowel tumours?

A

re-existing adenomas through a sequential accumulation of genetic abnormalities (in a model similar to that described for the pathogenesis of colorectal cancer), which can occur over several years.

The tumour suppressor gene p53, which maintains DNA integrity, and the oncogene KRAS, which normally functions in cellular signalling and proliferation, have been implicated in over 50% of small bowel adenocarcinoma cases.

211
Q

what are the risk fx for small bowel tumours?

A

age, crohns, coeliac, genetic (familial adenomatous polyposis)
smoking, obesity, low fibre, high red meat, alcohol

212
Q

what are the clinical fx for small bowel cancer?

A

usually asx
small bowel obstruction as increase in size
PR bleeding
abdo mass, cachexia, jaundice, hepatomegaly, ascites

213
Q

which investigations are required for small bowel tumours?

A

elevated CEA
LIVER metastasis - 5-HIAA
upper GI endoscopy
MRI enterography
bowel obstruction - CT

214
Q

how is small bowel cancer managed?

A

local small bowel adenocarcinomas - surgical resection
duodenal tumours - pancreaticoduodenectomy
lymph nodes - adjuvant chemo
mets - chemo

215
Q

define neuroendocrine tumour

A

originating from neuroendocrine cells in the gastrointestinal tract or the pancreas*, all of which have malignant potential; pancreatic neuroendocrine tumours are discussed further here

The incidence of GEP-NETs is between 2-3 per 100 000 persons per year, with slightly higher rates in women, and rates have been increasing in recent years. The majority of GEP-NETs are located in the small intestine, the remainder either in the rectum or the stomach.

216
Q

define neuroendocrine tumour

A

originating from neuroendocrine cells in the gastrointestinal tract or the pancreas*, all of which have malignant potential; pancreatic neuroendocrine tumours are discussed further here

The incidence of GEP-NETs is between 2-3 per 100 000 persons per year, with slightly higher rates in women, and rates have been increasing in recent years. The majority of GEP-NETs are located in the small intestine, the remainder either in the rectum or the stomach.

217
Q

what are the risk fx of neuroendocrine tumour?

A

complex familial endocrine cancer syndromes such as MEN1, MEN2, neurofibromatosis type 1 (NF1), Von Hippel Lindau (VHL), and Carney complex, however the majority of NETs occur are sporadic. Other risk factors include female gender and family history of NETs.

218
Q

what are the clinical fx of neuroendorcrine tumour?

A

non-functioning tumours (the majority), which have no hormone-related clinical features, or functioning tumours, which cause symptoms due to peptide and hormone release.

All GEP-NETs can present with non-specific symptoms, such as vague abdominal pain, nausea and vomiting, and abdominal distension. In less common cases, they may present with features of bowel obstruction (or appendicitis in appendiceal GEP-NETs), requiring urgent intervention

219
Q

which investigations are required for neuroendocrine tumours?

A

CgA - high in functional and non functional
PP high when CgA and CgB are normal
urinary 5-HIAA
CT enteroclysis
endoscopy
whole body somatostatin receptor schintigraphy

220
Q

how is neuroendocrine tumours managed?

A

. Surgery is the only curative treatment for GEP-NETs*, however nodal or liver metastases are found at presentation in 40–70% of patients.

Well-differentiated GEP-NETs are managed according to site, staging, and functionality. Localised disease should be resected; any liver metastases present should also be resected where feasible, along with the primary tumour, as this has been shown to improve survival rates.

Poorly-differentiated GEP-NETs have a poor prognosis; if the disease is localised, then treatment is often surgical resection followed by chemotherapy, whilst in metastatic disease, palliative chemotherapy alone is typically advised.
surgery -

221
Q

surgery for neuroendocrine tumour

A

Gastric NETs management grade, as the lower subtypes often have a very low metastatic potential, therefore can usually be treated with endoscopic resection and annual surveillance. However, the more aggressive lesions should be treated more aggressively, requiring gastrectomy with regional lymph node clearance.

Small intestinal NETs are almost always malignant. Resection of the tumour with mesenteric lymph node clearance is nearly always performed, regardless of the presence of liver metastases.

Appendiceal NETs are often identified incidentally following appendicectomy. A completion right hemicolectomy will be required for tumours >2cm in size, with a serosal breach, cellular atypia, invasion of mesoappendix (by more than 3 mm), or involvement of the base of the appendix

Colonic NETs have the worst prognosis of any gastrointestinal NET, with their treatment often requiring a segmental colectomy with regional lymph node clearance. Rectal NETs have a more benign character, with smaller tumours treated with endoscopic resection and larger tumours requiring either AP resection or low anterior resection.

222
Q

prognosis for neuroendocrine tumour

A

slow growing
rectal - highest sruvical rates

223
Q

what is the pathophysiology behind an acute appendicitis?

A

caused by direct luminal obstruction, usually secondary to a faecolith (Fig. 1) or lymphoid hyperplasia, impacted stool or, rarely, an appendiceal or caecal tumour.

When obstructed, commensal bacteria in the appendix can multiply, resulting in acute inflammation. Reduced venous drainage and localised inflammation can result in increased pressure within the appendix, in turn can result in ischaemia.

If left untreated, ischaemia within the appendiceal wall can result in necrosis, which in turn can cause the appendix to perforate.

224
Q

risk fx for appendicitis

A

family history
caucasians
summer

225
Q

sx of appendicitis

A

abdo pain - peri umbilical from visceral perioteneum inflammation and migrates to RIF when parietal peritoneum is inflammed
vomit
anorexia
nasua
diarrhoea
constipation
rebound tenderness and percussion pain over mcburneys point
appendiceal abscess may be able to be palpated
tachycardic and hypotensive
guarding if peritonitic

226
Q

which clinical signs can be illicited in an acute appendicitis?

A

Rovsing’s sign: RIF fossa pain on palpation of the LIF
Psoas sign: RIF pain with extension of the right hip
Specifically suggests an inflamed appendix abutting psoas major muscle in a retrocaecal position

227
Q

how might an acute appendicitis present in children?

A

diarrhoea, urinary symptoms, or even left sided pain

228
Q

ddx for appendicitis

A

Gynaecological: ovarian cyst rupture, ectopic pregnancy, pelvic inflammatory disease
Renal: ureteric stones, urinary tract infection, pyelonephritis
Gastrointestinal: inflammatory bowel disease, Meckel’s diverticulum, or diverticular disease*
Urological: testicular torsion, epididymo-orchitis
Specifically in children, differentials to consider include acute mesenteric adenitis, gastroenteritis, constipation, intussusception, or urinary tract infection.

229
Q

which investigations are required for an eppendicitis?

A

urinalysis
preg test
FBC, CRP, UE, seum beta HCG
men - CT, women -USS then CT

230
Q

how is an appendictis managed?

A

laprascopic appendicectomy
abx
appendix then sent to histology for malignancy

231
Q

give some complications of appendicitis

A

Perforation, if left untreated the appendix can perforate and cause peritoneal contamination
This is particular note in children who may have a delayed presentation
Surgical site infection
Rates vary depending on simple or complicated appendicitis (ranging 3.3-10.3 %)
Appendix mass, where omentum and small bowel adhere to the appendix
Pelvic abscess
Presents as fever with a palpable RIF mass, can be confirmed CT scan for confirmation; management is usually with antibiotics and percutaneous drainage of abscess

232
Q

how common colorectal cancer

A

second highest mortality
4th most common
20 yr -40 yrs old

233
Q

how do colorectal cancers develop?

A

via a progression of normal mucosa to colonic adenoma (colorectal ‘polyps’) to invasive adenocarcinoma (termed the “adenoma-carcinoma sequence”). Adenomas may be present for 10 years or more before becoming malignant; progression to adenocarcinoma

234
Q

which genetic mutations are mostly associated with colorectal cancer?

A

APC, HNPCC

235
Q

what are the risk fx of colorectal cancer?

A

increasing age,male, family hx, IBD, low fibre diet, high processed meat, smoking, excess alcohol

236
Q

what are the clinical features of colorectal cancer?

A

change in bowel habit
rectal bleeding
weight loss
abdo pain
iron def anaemia
vary on position -Right-sided colon cancers – abdominal pain, iron-deficiency anaemia, palpable mass in right iliac fossa, often present late
Left-sided colon cancers – rectal bleeding, change in bowel habit, tenesmus, palpable mass in left iliac fossa or on PR exam

237
Q

what’s the criteria for referralof urgent investigations of suspected bowel cancer?

A

≥40yrs with unexplained weight loss and abdominal pain
≥50yrs with unexplained rectal bleeding
≥60yrs with iron‑deficiency anaemia or change in bowel habit
Positive occult blood screening test

238
Q

ddx for colorectal cancer

A

IBD, haemorrhoids

239
Q

how does colorectal cancer screening work?

A

every 2 yrs for men and women 60-75yrs
FIT test
if positive - colonoscopy

240
Q

which investigations are required for colorectal cancer?

A

FBC - microcytic anaemia
LFT
clotting
CEA - monitor disease progression
colonoscopy with biopsy
staging process - CT TAP, MRI rectum, endo anal USS

241
Q

how is colorectal cancer staged?

A

dukes
Stage Description 5 Year Survival
A Confined beneath the muscularis propria 90%
B Extension through the muscularis propria 65%
C Involvement of regional lymph nodes 30%
D Distant metastasis <10%

242
Q

how is colorectal managed

A

MDT
asurgery and chemo and radio - chemotherapy regime for patients with metastatic colorectal cancer is FOLFOX, comprised of Folinic acid, Fluorouracil (5-FU), and Oxaliplatin
regional colectomy
radio - rectal cancer

243
Q

right hemicolectomy

A

The surgical approach for caecal tumours or ascending colon tumours, with the extended option performed for any transverse colon tumours. During the procedure the ileocolic, right colic, and right branch of the middle colic vessels (branches of the SMA) are divided and removed with their mesenteries

244
Q

left hemicolectomy

A

The surgical approach for descending colon tumours. Similar to the right hemicolectomy, the left branch of the middle colic vessels (branch of SMA/SMV), the inferior mesenteric vein, and the left colic vessels (branches of the IMA/IMV) are divided and removed with their mesenteries

245
Q

sigmoidectomy

A

The surgical approach for sigmoid colon tumours. In this instance, the IMA is fully dissected out with the tumour in order to ensure adequate margins are obtained.

246
Q

anterior resection

A

The surgical approach for high rectal tumours, typically if >5cm from the anus. This approach is favoured as leaves the rectal sphincter intact if an anastomosis is performed (unlike AP resections). Often a defunctioning loop ileostomy is performed to protect the anastomosis and reduce complications in the event of an anastomotic leak, which can then be reversed electively four to six months later

247
Q

AP resection

A

The surgical approach for low rectal tumours, typically <5cm from the anus. This technique involves excision of the distal colon, rectum and anal sphincters, resulting in a permanent colostomy

248
Q

hartmanns procedure

A

used in emergency bowel surgery, such as bowel obstruction or perforation. This involves a complete resection of the recto-sigmoid colon with the formation of an end colostomy and the closure of the rectal stump

249
Q

define diverticulitis/diverticular disease

A

Diverticulosis – the presence of diverticula (asymptomatic, incidental on imaging)
Diverticular disease – symptoms arising from the diverticula
Diverticulitis – inflammation of the diverticula
Diverticular bleed – where the diverticulum erodes into a vessel and causes a large volume painless bleed

250
Q

what is the pathophysiology behind diverticular disease?

A

aging bowel becomes weakened over time, movement fo stool causes increased intraluminal pressure…outpouchings of musosa through weaker areas of bowel wall…bactera can overgrow…inflammation which can perforate..peritonitis and death
fistula can form - colovesicular or colovaginal

251
Q

simple v chronic diverticulitis

A

complicated - abscess or free perforation
simple - inflammation without these features

252
Q

risk fx for diverticular disease

A

age, low dietary fibre intake, obesity, smoking, family history, and NSAID use.

253
Q

what are the clinical fx of diverticulosis etc?

A

diverticulosis - asx
diverticular disease - intermittent lower abdo pain, relieved by defecation, altered bowel habit, nausea, flatulence
acute diverticulitis - acute abdo pain LIF, tenderness, decreased appetite, pyrexia, nausea
perforated - peritonism

254
Q

which investigations are required for diverticulitis?

A

FBC, CRP, UE, faecal calprotectin
group and save
venous blood gas
urine dipstick
CT abdo plevis - thicekning colonic wall, pericolonic fat stranding, abscesses, localised air bubbles, free air
flexy sig if uncomplicated
CT colonoscopy if complicated

255
Q

how is diverticulitis staged?

A

hinchey classification - CT findings
Stage 1 Phlegmon (1a) or diverticulitis with pericolic or mesenteric abscess (1b)
Stage 2 Diverticulitis with walled off pelvic abscess
Stage 3 Diverticulitis with generalised purulent peritonitis
Stage 4 Diverticulitis with generalised faecal peritonitis

256
Q

how is diverticular disease managed?

A

uncomplicated - analgesia, fluid, outpatient colonoscopy to exclude malignancies
diverticular bleeds - as above, blood products too
if not respond - embolisation or surgical resection
acute diverticulitis - abx, IV fluids, analgesia,
surgery - if perforated with faecal peironitis/sepsis …hartmann’s

257
Q

give some complications of diverticulitis

A

recurrence, stricture causing large bowel obstruction or fistula formation (colovesical - recurrent UTI, pneumoturia - gas bubbles in urine, colovaginal - vaginal discharge)

258
Q

crohns age distribution

A

bimodal

259
Q

define crohns disease

A

affects any part of GI tract - distal ileum or proximal colon
familial link
smoking increases risk
transmural inflammation
deep ulcers and fissures
skip lesions
non caseating granulomatous
fistula can form - usually perianal

260
Q

differences between crohns and uc

A

Ulcerative Colitis Crohn’s Disease
Site Involvement Large bowel Entire GI tract
Inflammation Mucosa only Transmural
Microscopic Changes Crypt abscess formation
Reduced goblet cells
Non-granulomatous Granulomatous (non-caseating)
Macroscopic Changes Continuous inflammation (proximal from rectum) Pseudopolyps and ulcers may form vs Discontinuous inflammation (‘skip lesions’)Fissures and deep ulcers (‘cobblestone appearance’)
Fistula formation

261
Q

risk fx of crohns

A

family history
smoking

262
Q

what are the clinical features of crohns disease

A

colicky pain, diarrhoea, can contain blood or mucus, malaise, anorexia, low grade fever, perianal disease like abscess, oral apthous ulcers

263
Q

what are the extra intestinal mainfestations of crohns?

A

Musculoskeletal, such as Enteropathic arthritis (typically affecting sacroiliac and other large joints), nail clubbing, or with metabolic bone disease (secondary to malabsorption)
Skin, either as erythema nodosum (tender red/purple subcutaneous nodules, typically on the shins or pyoderma gangrenosum (erythematous papules/pustules that develop into deep ulcers
Eyes – Episcleritis, anterior uvetitis, or iritis
Hepatobiliary – Primary sclerosing cholangitis (more associated with UC), cholangiocarcinoma (due to association with primary sclerosing cholangitis), or gallstones
Renal – Renal stones

264
Q

which investgiations are required for crohns disease?

A

routine bloods - anaemia, low albumen, evidence of inflammation
faecal calprotectin test
stool sample for infective causes
colonoscopy with biopsies
CT abdo pelvis - bowel obstruction, perforation, intra abdominal collections,
MRI - fistula, peri anal disease or EUA for perianal

265
Q

how is crohns disease managed

A

referred to gastroenterologist
loperamide - in acute attacks
inducing remission - fluids, heparin and anti-embolic stockings (due to the prothrombotic state of IBD flares). corticosteroid therapy, immunosuppresive agents, such as mesalazine or azathioprine, or biological agents, such as infliximab or adalimumab
maintaining remission - azathioprine, colonoscopic surveillance as risk of malignancy, enteral nutritional support
surgical - Ileocaecal resection (removal of terminal ileum and caecum with primary anastomosis)
Small bowel resection or large bowel resection
Surgery for peri-anal disease (e.g. abscess drainage, seton insertion, or laying open of fistulae)
Stricturoplasty (division of a stricture that is causing bowel obstruction)

266
Q

give some complications of crohns disease

A

Fistula, including enterovesical, enterocutaneous, or rectovaginal fistula
Stricture formation
Recurrent perianal fistulae
GI malignancy

267
Q

give some extraintestinal complications of crohns

A

Malabsorption, including growth delay in children
Osteoporosis, secondary to malabsorption or long-term steroid use
Increased risk of gallstones, due to reduced reabsorption of bile salts at the terminal ileum
Increased risk of renal stones – Due to malabsorption of fats in the small bowel which causes calcium to remain in the lumen; oxalate is then absorbed freely (as normally bound to calcium and excreted in stool), resulting in hyperoxaluria and formation of oxalate stones in the renal trac

268
Q

distibution of UC

A

bimodal

269
Q

aetiology of UC

A

unknown

270
Q

pathophysiology behind UC

A

diffuse continual mucosal inflammation of large bowel beginning in rectum spreading proxiamlly but only to large bowel
non granuloamatous inflammation, crypt abscesses, goblet cell hypoplasia, psuedopolyps

271
Q

what are the clinical features of UC?

A

blood diarrhoea
proctitis - inflammation confined to rectum
PR bleeding and mucus discharge
increased frequency and urgency of defecation and tenesmus
dehydration
electrolyte imbalance
malaise
anorexia
low grade pyrexia
if severe abdo pain - toxic megacolon or colonic perforation

272
Q

ddx what are some extra intestinal manifestations of UC?

A

Musculoskeletal – enteropathic arthritis (typically affecting sacroiliac and other large joints) or nail clubbing
Skin – Erythema nodosum (tender red/purple subcutaneous nodules, typically on the shins, Fig. 2)
Eyes – Episcleritis, anterior uveitis, or iritis
Hepatobiliary – Primary sclerosing cholangitis* (chronic inflammation and fibrosis of the bile ducts)

273
Q

ddx for UC

A

crohns
schistosomiasis
mesenrteric ischaemia
radiation colitis
IBS
coeliac

274
Q

which investigations are required for UC?

A

FBC, UE, CRP, LFT, clotting - anaemia, low albumin, inflammation
faecal calprotectin - raised in IBD, unchanged in IBS
stool sample
colonoscopy with biopsy
plain film radiographs or CT for toxic megacolon and bowel perforation, mural thickening, thumbprinting, lead pipe colon in chronic cases

275
Q

how is UC managed?

A

sameas crohns
medical management to induce remission in UC typically requires use of intravenous corticosteroid therapy and immunosuppresive agents, such as ciclosporin or 5-ASA suppositories. Biological agents, such as infliximab, can be trialled as rescue therapy if then needed.
surgery - segemenratl bowel resection, for elective - total proctocolectomy is curative

276
Q

give some complications of UC

A

toxic megacolon, colorectal carcinoma, osteoporosis, pouchitis

277
Q

define pseudo obstruction

A

dilation of colon due to an adynamic bowel in the abasence of mechanical obstruction
affects mainly caecum and ascending colon
due to interruption of the autonomic nervous supply to the bowel leading to increased risk of toxic megacolon, bowel ischameia and perforation

278
Q

give some causes of pseudo obstruction

A

Electrolyte imbalance or endocrine disorders
Including hypercalcaemia, hypothyroidism, or hypomagnesaemia
Medication
Including opioids, calcium channel blockers, or anti-depressants
Recent surgery, severe illness, or trauma
Includes cardiac ischaemia
Neurological disease
Includes Parkinson’s disease, Multiple Sclerosis, and Hirschsprung’s disease

279
Q

what are the clinical fx of pseudo obstruction?

A

abdo pain, distention, constipation, vomit, typanic on exam, non tender

280
Q

what are the ddx for pseudo-obstruction?

A

Mechanical obstruction
Paralytic ileus
Toxic megacolon

281
Q

which investigations are required for pseudo-obstruction?

A

FBC, UE, calcium,magnesium,TFTs,
plain film radiographs - bowel distention
abdo pelvis CT with IV - dilation of colon

282
Q

how is pseudoobstruction managed?

A

NBM
IV fluids
NG
endoscopic decompression
nutrition
if perforates or ischaemia - segmental resection or caecostomy or ileostomy

283
Q

risk fx of volvulus

A

Increasing age
Neuropsychiatric disorders
Resident in a nursing home
Chronic constipation or laxative use
Male gender
Previous abdominal operation

284
Q

what are teh clinical fx of volvulus?

A

bowel obstruction -
colicky pain, distention, absolute constripation, rapid onset, tympanic to percussion

285
Q

what are the ddx of volvvulus?

A

severe constipation, pseudo-obstruction, sigmoid diverticular disease

286
Q

which investigations are required for volvulus?

A

routine bloods - calcium, TFT to exclude pseudo-obstruction
CT abdo pelvis - very dilated sigmoid colon with a whirl sign from twisting mesentery
abdo x ray - coffe bean from left iliac

287
Q

how is a volvulus managed?

A

fluid resuscitation
decompression by signmoidoscope and insertion of flatus tube through rectum
surgery - laparotomy for hartmanns

288
Q

what are the indications for surgery of a volvulus?

A

Colonic ischaemia or perforation
Repeated failed attempts at decompression
Necrotic bowel noted at endoscopy

289
Q

what are the main complications of a sigmoid volvulus?

A

bowel ischaemia and perforation
risk of recurrence

290
Q

what is the age distribution of a caecal volvulus?

A

bimodal
younger -intestinal malformations or excessive exercise which predisposes them
older - chronic constripation, distal obstruction, dementia

291
Q

how does a caecal volvulus appear on CT?

A

swirl in RIF

292
Q

how is a caecal volvulus managed?

A

lapratomy and ileocaecal resection

293
Q

define haemorrhoids

A

abnormal swelling or enlargement of the anal vascular cushions.

294
Q

how are haemorrhoids classified?

A

1st Degree Remain in the rectum
2nd Degree Prolapse through the anus on defecation but spontaneously reduce
3rd Degree Prolapse through the anus on defecation but require digital reduction
4th Degree Remain persistently prolapsed

295
Q

what are the risk fx of haemorroids?

A

excessive straining, increased age, raised intra abdo pressure

296
Q

what are the clinical fx of haemorrhoids?

A

painless bright red rectal bleeding
pruritus
rectal fullness
soiling
can thrombose which is painful - purple oedematous tense and tender peianal mass

297
Q

what are the ddx for haemorrhoids?

A

malignancy, IBD, diverticular disease, fissure in ano, perianal abscess, fistula in ano

298
Q

which investigations are required for haemorrhoids?

A

proctoscopy
fbc - prolonged bleeding
colonosocpy - other anorectal pathology

299
Q

how are haemorrhoids managed?

A

usually conservatively - more fibre, fluid, laxative, topical lignocaine, oral opioids avoided,
1st and 2nd degree - rubber band ligation
surgery - haemorrhoidal artery ligation - blood supply identified through doppler and tiesdoff
or haemorrhoidectomy but leave internal sphincter muscle…can result in incontinence

300
Q

define pilonidal sinus disease

A

disease of the inter-gluteal region*, characterised by the formation of a sinus in the cleft of the buttocks. It most commonly affects males aged 16-30 years .

*The term pilonidal is derived from the Latin pilus (hair) and nidus (nest).

301
Q

what is the pathophysiology of pinodial sinus disease?

A

starts from hair follicle which extends inwards forming a pit…foreign body reaction leads to formation of cavity

302
Q

what are the risk factorsfor pilonidal sinus disease?

A

caucasian male
coarse dark hair
sit for long periods
increased sweating
buttock friction
obesity
poor hygeien
local trauma

303
Q

what are the clinical fx for pilionidal sinus disease?

A

discharging and intermittently painful sinus in sacrococcygeal region
…can form an abscess
does nto communicate with anal canal - rigid sigmoidoscopy or MRI to compare with fistula

304
Q

how is pilonidal sinus disease managed?

A

shaving affected region and pluck sinus
washed out
abx in septic/abscess
surgery - incision and drainage
if chronic - removal of pinonidal sinus tract

305
Q

define perianal fistula

A

an abnormal connection between the anal canal and the perianal skin.abscess becomes fistula

306
Q

how are perianal fistulas clasified?

A

Park’s Classification System divides anal fistulae into four distinct types; inter-sphincteric fistula (most common), trans-sphincteric fistula, supra-sphincteric fistula (least common), and extra-sphincteric fistula

307
Q

what are teh causes of perianal fistula?

A

from abscess -
Inflammatory bowel disease, mainly perianal Crohn’s Disease
Systemic diseases, typically Diabetes Mellitus
History of trauma to the anal region
Previous radiation therapy to the anal region

308
Q

what are the clinical fx of fistula?

A

recurrnet perianal abscess, intermittent or continuous discharge onto perineum - mucus, blood, pus, faeces
examination - an external opening on the perineum
DRE - fibrous tract felt underneath skin

309
Q

define goodsall rule

A

predicts trajectory of fistula tract depending on location of external opening
External opening posterior to the transverse anal line – fistula tract will follow a curved course to the posterior midline
External opening anterior to the transverse anal line – fistula tract will follow a straight radial course to the dentate line

310
Q

which investigations are required for perianal fistula?

A

MRI

311
Q

how is a perianal fistula managed?

A

For those due to perianal Crohn’s disease (following drainage of any perianal abscess present), medical management of the Crohn’s disease is often started first prior to further surgical intervention
surgery - fistulotomy -lays tract open and cuts skin and tissues, placement of a seton - bring together and closes the tract…if low track coruse - faceal incontinence is rarely impaired versus high track

312
Q

define anorectal abscess

A

collection of pus in the anal or rectal region. They are more common in men than in women and have high rates of recurrence. One third of patients with an anorectal abscess have an associated perianal fistula at the time of presentation.

313
Q

what is the pathophysiology behind anorectal abscess?

A

plugging of the anal ducts which drain the anal glands in the anal wall….fluid stasis and infection
usually due to e.coli or enterococcus

314
Q

how can anorectal abscesses be categroised?

A

(1) Perianal* (2) Ischiorectal (3) Intersphincteric (4) Supralevator

315
Q

what are the clinical fx of anorectal abscesses?

A

evere pain in the perianal region, worse with direct pressure (i.e. when sat down), alongside potential perianal discharge or bleeding. Severe abscesses may present with systemic features* such as fever or rigors, general malaise, or clinical features of sepsis.

On examination, there will be a erythematous, fluctuant, tender perianal mass (Fig. 1), which may be discharging pus or have surrounding erythema and induration. Deeper abscesses may not have any obvious external signs, however produce severe tenderness on PR examination.

316
Q

which investigations are required for perianal abscesses?

A

FBC, UE, clotting, Group and save for surgery
HbA1C if no fistula to check if diabetic
if atypical or complex - MRI

317
Q

how are perianal abscesses managed?

A

abx
analgesia
EUA rectum and incision and drainage and left heal by secondary intention
intra op proctoosocpy to check for fistula and then inserted seton
post op abx

318
Q

define anal fissure

A

tear in the mucosal lining of the anal canal, most commonly due to trauma from defecation of hard stool

319
Q

how can anal fissures be classified?

A

Acute – present for <6 weeks
Chronic – present for >6 weeks
or primary versus secondary from IBD

320
Q

what are the risk fx of an anal fissure?

A

constipation
dehydration
IBC
chronic diarrhoea

321
Q

what are the clinical fx of fissure?

A

intense pain post-defecation
Pain can be far out of proportion to the size of the fissure. Other associated symptoms may include bleeding (commonly bright red blood on wiping) or itching, both typically post-defecation
fissure scna be visible
most common - usually in posterior midline
dre - exmaination under anaesteheisa
or prcotsopcy but may be too painful

322
Q

how is anal fissure managed?

A

reduce risk fx
analgesua
fibre and fluid intake increase
stool softener laxative
topical lidocaine
GTN cream
if chronic = botox injections or lateral sphincterotomy

323
Q

define rectal prolapse

A

protrusion of mucosal or full-thickness layer of rectal tissue out of the anus. - mianly older women

324
Q

give 2 types of rectal prolapse

A

Partial thickness – the rectal mucosa protrudes out of the anus
Full thickness – the rectal wall protrudes out the anus

325
Q

what are the pathophysiologies behind anal; prolapse

A

full prolapse suggest that is a form of sliding hernia, through a defect of the fascia of the pelvic region. This may be caused by chronic straining secondary to constipation, a chronic cough, or from multiple vaginal deliveries.

In contrast, partial thickness prolapses are associated with the loosening and stretching of the connective tissue that attaches the rectal mucosa to the remainder of the rectal wall. This often occurs in conjunction with long standing haemorrhoidal disease.

326
Q

what are the risk fx for rectal prolapse?

A

increasing age, female gender, multiple deliveries, straining, anorexia, and previous traumatic vaginal delivery

327
Q

what are the clinical fx of rectal prolpase?

A

rectal mucus discharge, faecal incontinence, per rectum bleeding, or with visible ulceration.

Full thickness prolapses will begin internally and thus can initially present with a sensation of rectal fullness, tenesmus, or repeated defecation.
prolpase seen when straining
For a suspected internal prolapse, defecating proctography and examination under anaesthesia

328
Q

how is an anal prolpase managed?

A

dietary fibre, fluid increase
banded in clinic
surgery - abdo and perineal approach

329
Q

what are the types of anal cancer?

A

squamous cell - above dentate line - majority (can be anal intraepithelial neoplasia before and is strongly linked to HPV)
adenocarcinoma
melanomas and anal skin cancers

330
Q

what are the risk fx for anal cancer?

A

HPV infection (accounts for 80-90% of cases, especially HPV-16 and HPV-18), HIV infection, increasing age, smoking, immunosuppression, or Crohn’s disease.

331
Q

what are the clinical fx of anal cancer?

A

rectal pain and bleeding
anal discharge
pruritus
palpable mass
infection and fistula
faecal incontinence if sphinctersinvolved
ulceration or wart like lesions
lymphadenopathy

332
Q

where does lymph drain in the rectal region?

A

*Lymph from the area below the dentate line drains to the superficial inguinal nodes, whereas the anal canal and rectum above the dentate line drain into the mesorectal, para-aortic, and paravertebral nodes.

333
Q

which investigations are required for anal cancer?

A

proctosocopy
EUA
smear test - CIN or VIN
HIV test
USS guided fine needle aspiration
CT TAP
MRI pelvishow

334
Q

how is an anal cancer managed?

A

MDT
chemo-radiation via external beam
surgical excision if advanced - AP resection

335
Q

what is the complication of tx for anal cancer?

A

Chemoradiation-related pelvic toxicity is the most common short term complication, which can present with dermatitis, diarrhoea, proctitis, and/or cystitis.

Longer term, patients may develop fertility issues, faecal incontinence, vaginal dryness, erectile dysfunction, and rectovaginal fistula.

336
Q

what is the prognosis of anal cancer?

A

stage versus 5 yr survival rate
I 69.5
II 61.8
IIIa 45.6
IIIb 39.6
IV 15.3

337
Q

what is the biggest risk factor for anal cancer?

A

HPV infection

Surgery Specialities (7 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions