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CP1 > GI > Flashcards

GI Flashcards

1
Q

What is the acute abdomen?

A

= sudden onset, severe abdominal pain which may indicate potentially life-threatening intra-abdominal pathology that requires urgent surgical intervention.

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2
Q

when can a pain free acute abdomen occur?

A

particularly in older people, in children, in the immunocompromised, and in the last trimester of pregnancy.

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3
Q

potential conditions causing pain in the right hypochondriac region

A 
Gallstones
Cholangitis
Hepatitis
Liver abscess
Cardiac causes
Lower lobe pneumonia
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4
Q

potential conditions causing pain in the epigastric region

A 
Oesophagitis
Peptic Ulcer
Perforated Ulcer
Pancreatitis
MI
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5
Q

potential conditions causing pain in the left hypochondriac region

A

Spleen Abscess
Acute splenomegaly
Spleen rupture
Lower lobe pneumonia

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6
Q

potential conditions causing pain in the right lumbar region

A

Renal stones

Pyelonephritis

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7
Q

potential conditions causing pain in the umbilical region

A 
AAA rupture
Appendicitis (early)
Meckel’s diverticulitis
Small bowel obstruction
Ischaemic bowel
Peritonitis
DKA
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8
Q

potential conditions causing pain in the left lumbar region

A

Renal stones

Pyelonephritis

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9
Q

potential conditions causing pain in the right iliac region

A 
Appendicitis
IBD
Caecum obstruction
Ovarian cyst/torsion
Ectopic pregnancy
Hernias
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10
Q

potential conditions causing pain in the hypogastric/suprapubic region

A 
Testicular Torsion
Urinary retention
Cystitis
Placental Abruption
Large bowel obstruction
PID
Endometriosis
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11
Q

potential conditions causing pain in the left iliac region

A 
Diverticilitis
IBD
Constipation
Ovarian Cyst
Hernias
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12
Q

Acute abdomen - BLEEDING

A

AAA rupture – most serious cause, requires immediate surgical intervention.

Ruptured ectopic pregnancy

Bleeding

Gastric ulcer

Trauma

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13
Q

What is there a risk of in an acutely bleeding patient?

A

Hypovolaemic shock:

  • Hypotension
  • Tachycardia
  • Pale and clammy
  • Cool to touch
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14
Q

Acute abdomen - PERITONITIS

A

Localised or generalised inflammation of the peritoneum

Patients lay completely still, with shallow breathing (pain made worse by movement/coughing/breathing).

Tachycardia and potential hypotension/pyrexia

Percussion/rebound tenderness

Involuntary guarding

Reduced or absent bowel sounds (paralytic ileus)

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15
Q

Localised peritonitis

A

when the inflammation is in a limited area (e.g. adjacent to inflamed appendix/diverticulum prior to rupture).

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16
Q

Generalised peritonitis

A

when the inflammation is widespread (e.g. after the rupture of an abdominal organ)

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17
Q

Why is there rebound tenderness in peritonitis?

A

movement of the peritoneum upon the removal of the palpating hand causes intense pain

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18
Q

Acute abdomen - ISCHAEMIC BOWEL

A

Any patient who has severe pain out of proportion to the clinical signs (i.e. the examination is unremarkable) has ischaemic bowel until proven otherwise

May have acidaemia with raised lactate on blood gases.
=> Due to impaired blood supply resulting in anaerobic respiration of the tissues

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19
Q

How do you diagnose ischaemic bowel?

A

CT scan with IV contrast

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20
Q

Inflammatory abdominal pain

A

Constant pain, supported by a raised temperature, pulse and leucocytosis.

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21
Q

Obstructive abdominal pain

A

COLICKY PAIN

Crescendos to become very severe and then completely goes away

Patients often agitated.

Pain may become constant with superimposed inflammation

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22
Q

Why is biliary colic not “true” colic?

A

the pain never goes away completely

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23
Q

Referred Visceral Pain in the abdomen

A
  • Foregut pain is referred to the upper abdomen.
  • Midgut pain is referred to the middle abdomen
  • Hindgut pain is referred to the lower abdomen
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24
Q

Acute abdomen - bedside tests

A

Basic observations (NEWS2 score)

ECG
=> exclude MI

Urine dip

Pregnancy test
=> all women of reproductive age

BM
=> DKA can present as abdominal pain

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25
Q

Acute abdomen - bloods

A 
FBC
U&E
LFTs and amylase/lipase
CRP
Coagulation
G&S / XM
?Blood cultures
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26
Q

Acute abdomen - Imaging (basic and specialist)

A

?Erect CXR
?AXR
?USS

?CT scan

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27
Q

Amylase levels

A

Amylase 3x higher than upper limit to be diagnostic of pancreatitis

Values lower than this suggests other pathology – e.g. perforated bowel, ectopic pregnancy, DKA

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28
Q

Abdo imaging - use of erect CXR

A

will show bowel perforation (free air under the diaphragm)

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29
Q

Abdo imaging - use of AXR

A

Bowel obstruction
Toxic megacolon
Foreign body ingestion (if radio-opaque)

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30
Q

Abdo imaging - use of USS

A

Biliary pathologies
Kidneys, ureter and bladders
Gynae pathologies
Appendix

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31
Q

Appendicitis

A

= most common cause of an acute abdomen

inflammation of the appendix, usually caused by blockage within the lumen

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32
Q

Causes of appendicitis

A

Faecolith (a stone made of faeces) – most common.

Swollen lymphoid tissue in the wall – common in adolescence

Parasites

Tumours

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33
Q

Pathophysiology of appendicitis

A

Lumen is blocked => bacteria multiply

Appendix swells => blood supply becomes impaired.

ischaemia and necrosis

appendix can eventually perforate due to the raised intraluminal pressure, releasing bacteria into the abdominal cavity, leading to abscess, peritonitis and sepsis

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34
Q

Appendix mass

A

inflamed appendix with an adherent covering of omentum and small bowel

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35
Q

Appendicitis - Differential diagnoses

A

Gynae – ovarian cyst rupture, ectopic pregnancy, PID

Renal – UTI, pyelonephritis, ureteric stones

GI – mesenteric adenitis, diverticular disease, IBD

Urological – testicular torsion, epididymo-orchitis

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36
Q

Appendicitis - Symptoms

A

Abdominal pain
=> Starts dull and central
=> Then becomes localised and sharp in the RIF at McBurney’s point
=> Pain may not be severe until the appendix has ruptured!

Constipation (or sometimes diarrhoea).
Anorexia
Nausea and vomiting (after the pain starts).

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37
Q

Where is McBurney’s point?

A

1/3 of the way between the ASIS and the umbilicus

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38
Q

Appendicitis - Signs

A

Rebound and percussion tenderness in RIF (maximum at McBurney’s point)

Guarding (especially if perforated)

Rovsing’s Sign

Tachycardia, tachypnoea

Mild pyrexia

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39
Q

Rovsing’s sign

A

Pain in the RIF when the LIF is pressed

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40
Q

Appendicitis - investigations

A

Abdominal exam
PR

Pelvic examination in females
Pregnancy test

Bloods – FBC, U&E, CRP/ESR
Urinalysis

USS/CT – if diagnostic uncertainty
AXR/erect CXR – if questioning perforation

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41
Q

Appendicitis - management

A

Nil by mouth ready for appendectomy.

Resuscitation – IV fluids.

Appendectomy (laparoscopic is gold standard)
+ Wash out if ruptured

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42
Q

What are the complications of an appendectomy?

A

Early complications – haematoma, wound infections

Late complications – small bowel obstruction (adhesions) or incisional hernia.

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43
Q

Complications of appendicitis

A

Perforation – if left untreated, causes peritoneal contamination (peritonitis and sepsis).

Surgical site infection

Appendix mass – omentum and small bowel adhere to the appendix.

Pelvic abscess – fever with a palpable RIF mass, CT for confirmation

Adhesions – small bowel obstruction due to scarring.

Universal post-op complications – DVT/PE, bleeding, ileus, surgical damage to other organs, etc.

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44
Q

What is colorectal cancer?

A

a malignant neoplasm of epithelium in the large bowel, excluding the appendix and the anus

Most common variant is Adenocarcinoma
=> Squamous and adeno-squamous variants can be found in the distal rectum

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45
Q

Aetiology of colorectal cancer

A

Colon cancer: Male = Female
Rectal cancer: Male > Female

Age >50 years

3rd most common cancer in the UK

More common in the western world

Global mortality is 50%

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46
Q

non-modifiable risk factors for colorectal cancer

A 
Ethnicity
Age
Sex
T2DM
IBD – Chron’s Disease, UC
Family History
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47
Q

modifiable risk factors for colorectal cancer

A 
Diet rich in red and processed meats
Obesity
Physical inactivity
Smoking tobacco
Heavy alcohol consumption
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48
Q

factors protective against colorectal cancer

A

diet rich in high fibre (and F&V),
exercise,
hormone replacement therapy,
aspirin/NSAIDs

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49
Q

HNPCC/Lynch syndrome

A

Autosomal dominant mutation affecting various mismatch repair genes

Responsible for ~3% of colorectal cancers

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50
Q

Familial Adenomatous Polyposis (FAP)

A

Autosomal dominant defect in tumour-suppressor APC gene.

Causes numerous colonic polyps to develop, with an increased chance of malignancy

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51
Q

MUTYH-associated polyposis

A

Autosomal recessive

Causes polyposis with increased risk of malignancy

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52
Q

Presentation of right-sided colon tumours

A

often asymptomatic;

may present with weight loss/iron-deficiency anaemia;

can present with abdominal discomfort and change in bowel habit

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53
Q

Presentation of left-sided colon tumours

A

PR bleeding/mucous,
altered bowel habit,
tenesmus,
obstruction,

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54
Q

Presentation of rectal tumours

A

PR bleeding,
pain,
changes in bowel habit,
masses/stricture

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55
Q

What signs/symptoms are common to all colorectal tumours (regardless of location)?

A

Weight loss, loss of appetite, N&V

abdominal mass, abdominal pain/discomfort,

Altered bowel habits/constipation/diarrhoea

haemorrhage, perforation, fistula

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56
Q

Where are colorectal tumours most commonly located?

A
  1. Sigmoid colon
  2. Rectum
  3. Ascending colon
  4. Descending/transverse colon
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57
Q

Complications of CRC

A
  • Bowel Obstruction
  • Bowel Perforation
  • Iron Deficiency Anaemia
  • Hepatic and Peritoneal Metastasis
  • Bone and Lung Metastases
  • Colo-vesical fistula
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58
Q

What symptoms can occur from the spread of CRC?

A

Hepatic Metastases: Jaundice, RUQ pain, early satiety

Peritoneal Metastases: Ascites or pain

Colo-vesical fistula: Pneumaturia or recurrent UTI

Weight loss

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59
Q

Screening for CRC in the UK

A

Routine regular colonoscopy – in high-risk groups (positive family history)

average-risk population => colonoscopy, CT colonography, and faecal occult blood (FOB) testing are conducted

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60
Q

CRC - investigations

A

BLOODS

  • FBC, U&E, LFT, Magnesium, Calcium
  • Carcinoembryonic antigen – tumour marker, can be used to monitor disease.
  • Coagulation, G&S/XM

Colonoscopy to identify and obtain tissue for histology
=> For palliative patients – stent insertion.

Imaging for staging
=> CT abdomen-pelvis
=> CT chest

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61
Q

CRC TNM staging

A

T1-T4 = tumour spread
N0-N2 = nodal status
M0 - M1 = metastatic status

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62
Q

Stage I CRC

A

Grown through the inner lining of the bowel, or into the muscle wall. It has not spread to lymph nodes or distant body parts

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63
Q

Stage II CRC

A

Spread into the outer wall of the bowel or into tissue or organs next to the bowel. It has not spread to the lymph nodes or distant parts of the body

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64
Q

Stage III CRC

A

Spread to nearby lymph nodes, but hasn’t spread to distant body parts

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65
Q

Stage IV CRC

A

Spread to distant body parts, such as the liver or lungs

= advanced bowel cancer

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66
Q

Grading of CRC

A

The grades of bowel cancer cells are from 1 to 4 depending on histology:

  1. (Low grade) look most like normal cells
  2. Look a bit like normal cells
  3. Look very abnormal and not like normal cells
  4. (High grade) grade 4 looks completely different from normal cells
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67
Q

Treatment of CRC

A

wide resection of the growth and regional lymphatics
=> e.g. right/left hemicolectomy, sigmoid colectomy, high anterior resection

Total colectomy in FAP, HNPCC and synchronous cancers.

Dysplastic polyps and carcinoma in situ can be removed via colonoscopic excision

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68
Q

What is anal cancer?

A

mainly squamous cell carcinoma of the epithelium of the anus

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69
Q

Risk factors for anal cancer?

A

Ano-receptive sex
Syphilis infection
Anal warts/cervical cancer (HPV)
Immunosuppression

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70
Q

pectinate line

A

an embryological division between the upper 2/3rds and the lower 1/3rd of the anal canal

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71
Q

Anal cancer above the pectinate line

A

Columnar epithelium

Lymph draining to internal iliac nodes

Portal venous drainage (thus hepatic metastases).

More common in women, worse prognosis

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72
Q

Anal cancer below the pectinate line:

  • type of epithelium
  • lymph and venous drainage
  • prognosis
A

Squamous epithelium

Lymph drainage to superficial inguinal nodes.

Caval venous drainage (thus pulmonary metastases)

More common in men, better prognosis

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73
Q

Mechanical vs functional bowel obstruction

A

mechanical - physical blockage of the passage of intestinal contents

functional - decreased bowel motility

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74
Q

What is bowel obstruction?

A

the mechanical of functional blockage of the bowel, resulting in absolute constipation. There will be dilatation of proximal bowel with sequestration of fluid into the intestinal lumen.

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75
Q

Absolute constipation

A

when the patient is not passing any flatus or faeces rectally

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76
Q

Differentials for bowel obstruction

A

Constipation
Paralytic ileus
Toxic megacolon

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77
Q

How does bowel obstruction typically present?

A

Abdominal pain (colicky in early obstruction, constant in perforation)

Vomiting
=> bilous - upper SBO
=> faeculent - lower SBO
=> Undigested food - suggests gastric outlet obstruction

Absolute constipation

Abdominal distension

Dehydration

Tinkling bowel sounds

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78
Q

Why does bowel obstruction cause dehydration?

How can you identify dehydration?

A
  1. Vomiting,
  2. Lack of fluid intake
  3. Fluid sequestration to the bowel/ “Third spacing”

Sleepiness, thirst, muscle weakness, headache, dizziness, dark urine, dry mouth, decreased JVP, low BP, tachycardia, sunken eyes, loss of skin turgor

Fluid sequestered to the bowel tends to be electrolyte rich, so the patient may be hypokalaemic and have an AKI.

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79
Q

How do LBO and SBO present differently?

A

LBO – absolute constipation and pain are more prominent early, vomiting often late
=> Symptoms are generally more gradual due to the large volume of colon.
=> Pain tends to be lower (suprapubic)

SBO – vomiting is the predominant early feature, constipation often late.
=> Pain tends to be peri-umbilical

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80
Q

Strangulating obstructions

A

interruption of the intestinal blood supply with simultaneous blockage of the intestinal lumen

Compromised blood supply may lead to infarction, perforation and peritonitis

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81
Q

Closed loop obstruction

A

an obstruction of two points in the bowel, causing a grossly distended loop of bowel in between those points.

This can grow until it becomes ischaemic and ultimately perforates. This is therefore a SURGICAL EMERGENCY

If the ileocaecal valve is competent, closed-loop obstruction forms with LBO.

If the ileocaecal valve is incompetent bowel content flows from large to small bowel

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82
Q

Volvulus

A

a twisting of a loop of bowel around its mesenteric axis, resulting in obstruction together with venous occlusion at the base of the mesentery

The bowel stretches, becomes ischaemic and is more likely to perforate

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83
Q

Sigmoid volvulus

A

Most common in elderly, constipated patients.
More common in men.

Classic “coffee bean” appearance on X-ray.

Treatment is insertion of a long flatus tube advanced into the sigmoid, which often untwists the volvulus (releases large amounts of faeces/gas).

If this is unsuccessful, there will be an emergency laparotomy

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84
Q

Caecal volvulus

A

Due to congenital malrotation, gives the classic “embryo” appearance of an ectopically placed caecum on AXR.

Treatment is untwisting during laparotomy

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85
Q

Causes of bowel obstruction

A 
SBO (80%)
Adhesions (~80%)
Hernias
Crohn’s disease
Intussusception
LBO (20%)
Carcinoma of the colon - considered til proven otherwise
Diverticular disease
Sigmoid volvulus 
Constipation
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86
Q

Bowel obstruction - bedside tests

A

Basic observations (NEWS2)
Abdominal Exam
Hernial Orifices
PR

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87
Q

Bowel obstruction - bloods

A 
FBC
U&E
LFTs and Amylase
CRP
ABG/VBG
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88
Q

Bowel obstruction - Imaging

A 
AXR
Erect CXR (if perforation suspected)

CT scan (CAP)

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89
Q

Why would you do a blood gas in ?bowel obstruction ?

A

to look for metabolic derangement secondary to dehydration/excess vomiting,

or raised lactate in ?ischaemia

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90
Q

SBO on AXR

A

Dilated loops of bowel are >3cm in diameter.

Dilated loops of bowel are more central in the abdomen.

Valvulae conniventes/plicae circulares present (full crossings).

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91
Q

LBO on AXR

A

Dilated loops of bowel are >6cm in diameter (>9cm at caecum).

Dilated loops are more peripheral.

Haustra present (incomplete crossings).

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92
Q

Management of bowel obstruction

A

NBM, IV fluids, fluid balance, catheter
Analgesia, Antiemetics

SBO - usually drip and suck, hernias need surgery

LBO - usually requires surgery

Volvulus - initially flatus tube, may need surgery

ischaemia - urgent surgery

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93
Q

Red Flag Abdominal Symptoms suggesting upper GI malignancy

A

Dysphagia
Treatment resistant dyspepsia
Loss of appetite
Unintentional weight loss

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94
Q

Red Flag Abdominal Symptoms suggesting lower GI malignancy

A 
Loss of appetite
Unintentional weight loss
Haematemesis
Change in bowel habit
Iron-deficiency anaemia
Unexplained rectal bleeding
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95
Q

What is coeliac disease?

A

a gluten-sensitive enteropathy

involves inflammation of the jejunal mucosa in response to gluten

This ultimately results in decreased surface area for absorption, resulting in malabsorption

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96
Q

What is the pathophysiology of coeliac disease?

A

Alpha-gliandin (protein from gluten) is modified by tissue transglutaminase enzymes (TTG)

activates a T-cell mediated autoimmune reaction against the mucosa of the jejunum

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97
Q

How will a biopsy of duodenal mucosa appear in coeliac disease?

A

Biopsy of the duodenal mucosa will show flattened mucosa due to villous atrophy

There is hyperplasia of the crypts to compensate.

There will also be chronic inflammatory cells (lymphocytes) in the lamina propria

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98
Q

How many people are affected by coeliac disease in the UK?

A

~1 in 100

But only 10-20% of these people have a confirmed diagnosis

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99
Q

Peak age of incidence of coeliac disease

A

can be any age, but peak incidence is age 50-60

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100
Q

Risk factors for coeliac disease

A

Close association with human leucocyte antigens – 90% are positive for HLA DQ2

Family history

Increased risk if concurrent autoimmune illness (e.g. thyroid disorders, T1DM, etc.)

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101
Q

Symptoms/signs of coeliac disease

A

~1/3 are asymptomatic

Dermatitis herpetiformis is a recognised skin manifestation of coeliac disease

Non-specific: iron-deficient anaemia, weight loss, fatigue, aphthous ulcers.

Diarrhoea, steatorrhea, bloating, abdominal pain, N&V.

Failure to thrive in a child

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102
Q

Complications of coeliac disease

A 
Malabsorption
Anaemia
Increased risk of GI malignancy and T-cell lymphoma
Osteoporosis
Hyposplenism
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103
Q

Investigations for coeliac disease

A

BLOODS
FBCs, LFTs, U&Es, bone profile, vitamin D, vitamin B12, haematinics and albumin

Serological blood sample
=> 1st line: total immunoglobulin A (IgA) and IgA tissue transglutaminase (tTG)

=> 2nd line: IgA endomysial antibody (EMA) can be used if IgA tTGA is unavailable, or in cases where it is weakly positive

Definitive diagnosis is made via upper GI endoscopy and biopsy of small bowel tissue

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104
Q

Management of coeliac disease

A

LIFELONG GLUTEN FREE DIET

Correct nutritional deficiency if indicated.

Verify that gluten-free diet is working by using endomysial antibody (EMA) tests

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105
Q

What is IBS?

A

a relapsing functional bowel disorder, with no discernible structural or biochemical cause.

It is shown to have a negative impact on quality of life, but it is not associated with the development of serious pathology

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106
Q

Suggested mechanisms of IBS?

A

Differences in the “brain-gut axis”, leading to increased visceral perception and decreased visceral pain threshold.

Abnormal GI motility

Changes in colonic microbiota

Abnormal GI immune function

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107
Q

Risk factors for IBS

A

Stress and other psychological factors
Dietary triggers (alcohol, caffeine, spicy foods)
Enteric infection

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108
Q

Diagnostic criteria for IBS

A

Consider the diagnosis if any of the following symptoms for at least 6 months:
=> Abdominal pain, or
=> Bloating, or
=> Change in bowel habit.

Make a diagnosis of IBS if a person has abdominal pain which is either:
=> Related to defecation, and/or
=> Associated with altered stool frequency (increased or decreased), and/or
=> Associated with altered stool form or appearance (hard, lumpy, loose, or watery)

AND at least 2 from the following:
=> Altered passage of stool (straining, urgency, tenesmus)
=> Abdominal bloating/ distension/ hardness
=> Symptoms aggravated by eating
=> Passage of rectal mucus
=> Associated gynaecological, urinary symptoms, or back pain.

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109
Q

Investigation and Diagnosis of IBS

A

History - ensure no red flag symptoms

Examination - signs of anaemia/masses?

Investigations:
=> CRP/ESR, faecal calprotectin to exclude IBD.
=> TTG/EMA antibodies to exclude coeliac disease
=> FBC for anaemia

In cases which meet the diagnostic criteria, no further investigations are required

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110
Q

Management of IBS - self-management/lifestyle

A

Advice on avoiding diet triggers, regular exercise, weight loss, stress management, regular meals and plenty of fluids.

Potentially low FODMAP diet

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111
Q

Management of IBS - Pharmacological

A

to target specific symptoms

Loperamide – 1st line for diarrhoea.
=> 2nd line – low-dose TCAs.
=> 3rd line – SSRI

Antispasmodics – abdominal pain/cramping.

Laxatives – constipation (but avoid lactulose as it cases bloating).

Peppermint oil.

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112
Q

Diverticulum

A

= an outpouching of the bowel wall

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113
Q

Diverticulosis

A

= presence of diverticula

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114
Q

Diverticular Disease

A

= Presence of diverticula + symptomatic

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115
Q

Where do diverticula occur?

A

anywhere in the GI tract but are more common in the sigmoid (95% of cases) and descending colon

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116
Q

Why is the sigmoid colon more prone to diverticula formation?

A

has smallest lumen and highest pressures, therefore more prone to diverticulum formation

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117
Q

True diverticulum

A

involving all layers of the intestine – serosa, muscle, submucosa, mucosa

e.g. Meckel’s diverticulum, the appendix

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118
Q

False/pseudo diverticulum

A

does not contain all layers – often mucosa pushed through muscle defect

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119
Q

Prevalence of diverticulosis

A

highest prevalence in Europe and the USA;
rare in Africa and Asia

occurs in 50% of over 50s and 80% of over 80s in the UK.

The majority of patients with diverticula are asymptomatic

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120
Q

Pathophysiology of diverticulosis

A
  1. Weakened bowel
  2. stool movement increases intraluminal pressure
  3. outpouching of the bowel wall
    => mucosa herniates through muscle layers, particularly at weak points close to penetrating vessels
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121
Q

Risk factors for diverticulosis

A

Western/low fibre diet

Age >50 years

Male

Obesity

Connective tissue disorders – e.g Marfans, Ehler-danlos; predisposition to weakened GI wall.

Smoking

Family history

NSAID use

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122
Q

Meckel’s Diverticulum

A

Congenital abnormality - an outpouching in the lower part of the small intestine (a remnant of the vitello-intestinal duct)

Most commonly presents in young (<2 years old) children with painless melaena, then followed by obstruction / intussusception

Can mimic appendicitis

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123
Q

Meckel’s Rule of 2s

A 
Affects 2% of population
2 years old
2:1 M:F ratio
2 inches long
2 feet proximal to ileocaecal valve
2 types of ectopic tissue (gastric/pancreatic)
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124
Q

Diverticulitis

A

bacterial overgrowth within the gut causes inflammation of the diverticula

increased risk of complications such as perforation of the bowel and fistula formation

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125
Q

Presentation of diverticulitis

A

systemically unwell (N&V, pyrexia, tachycardia)

acute onset LIF pain

sometimes also loose stools

If perfortated - localised/generalised peritonitis

126
Q

What can mask symptoms of diverticulitis?

A

if a patient is taking corticosteroids or immunosuppressants

127
Q

Simple vs. complicated diverticulitis

A

Complicated – presence of abscess, formation of fistula, stricture, free perforation.

Simple – inflammation without any of these features

128
Q

Diverticular bleed

A

when the diverticulum erodes into a submucosal blood vessel.

This causes haematochezia (the passage of bright red blood in the stool) but is generally painless.

Severe haemorrhage occurs in ~3-5% of patients with diverticulosis

129
Q

Diverticular Disease - bedside tests

A 
Basic observations (NEWS2)
Abdominal Exam
Urine Drip
PR
\+/- Faecal Calprotectin
130
Q

Diverticular Disease - bloods

A

FBC
U&E
LFTs
CRP

All bloods should be normal in diverticular disease - but it is important to rule out other conditions

131
Q

Diverticular Disease - imaging

A

Routine flexible sigmoidoscopy or colonoscopy

or CT colonogram if not fit

132
Q

Faecal Calprotectin

A

used as a direct measure of bowel inflammation but is non-specific.

Raised in IBS, diverticular disease and IBD.

133
Q

flexible sigmoidoscopy

A

involves using a fibre-optic endoscope to visualise the rectum, sigmoid and some parts of the descending colon

134
Q

colonoscopy

A

involves using an endoscope to visualise the entire large bowel

135
Q

Risks of colonoscopy/sigmoidoscopy in diverticular disease

A 
perforation, 
haemorrhage, 
infection, 
diagnostic failure
need to repeat procedure
136
Q

Diverticulitis - bedside tests

A

Basic observations
=> tachycardia, pyrexia, hypotension

Abdominal Exam
=> palpable mass +/- localised peritonism

Urine dip
PR
+/- faecal calprotectin

137
Q

Diverticulitis - bloods

A 
FBC
U&E
LFTs 
CRP
ABG/VBG
Blood cultures

=> raised WBCs and CRP, and VBG/ABG may show raised lactate

138
Q

Diverticulitis - imaging

A

AXR – ?bowel obstruction
Erect CXR – ?perforation

CT abdomen/pelvis
USS Abdomen/pelvis

139
Q

What imaging is best to AVOID in diverticulitis?

A

endoscopic procedures - risk of perforation

plan these for after the acute episode

140
Q

Diverticular bleed - bedside tests

A

Basic observations
=> tachycardia, increased RR, hypotension

Abdominal Exam
=> palpable mass +/- peritonitic abdomen

Urine dip
PR
+/- faecal calprotectin

141
Q

Diverticular bleed - bloods

A 
FBC
U&E
CRP
ABG/VBG
G&S/XM - for potential blood transfusion
Blood cultures
142
Q

Diverticular bleed - imaging

A

AXR – ?bowel obstruction
Erect CXR – ?perforation

CT abdomen/pelvis

Urgent colonoscopy to find source of bleeding and treat if indicated

143
Q

Diverticulosis - management

A

no management needed

Prophylactic benefit of high fibre diet

144
Q

Diverticulitis - management

A

Most patients will require hospital admission.

Encourage PO fluids (clear fluids only), reintroduce solids slowly.

Paracetamol for analgesia

Broad spectrum antibiotics (IV) and IV fluids.

Blood transfusion if haemorrhage.

Surgical management may be indicated in acute complicated diverticulitis.
=> Hartmann’s procedure or sigmoid resection with primary anastomoses are most likely.

145
Q

What are the complications of diverticulitis?

A

Pericolic abscess - collection of pus within bowel wall
Fistulas (colovesical/colovaginal)
Perforation
Bowel obstruction

146
Q

Which muscles maintain anal continence?

A

Levator Ani

Internal anal sphincter

External anal sphincter

147
Q

What is the dentate line?

A

Divides the anal canal into two parts

Mucosa gathers into longitudinal folds containing the anal glands.

148
Q

Anal canal above the dentate line - origin, epithelium, blood supply and drainage and innervation

A

from embryological hindgut.

Columnar epithelium.

Blood supply from superior rectal artery (from inferior mesenteric artery).

Venous drainage by superior rectal vein (branch of inferior mesenteric vein).

Internal iliac lymph nodes

Innervated by inferior hypogastric plexus – sensitive to stretch only.

149
Q

Anal canal below the dentate line - origin, epithelium, blood supply and drainage and innervation

A

from ectoderm.

Non-keratinising stratified squamous epithelium.

Blood supply from the inferior rectal artery (from pudendal a., a branch of internal iliac a.)

Venous drainage by inferior rectal vein (branch of internal pudendal vein).

Superficial inguinal lymph nodes.

Innervated by pudendal nerve – sensitive to pain, temperature, touch and pressure.

150
Q

What bedside test should anyone with palpable inguinal lymph nodes get?

A

PR exam - ?anal cancer.

151
Q

What happens to the epithelium at the anal verge?

A

the epithelial cells become keratinised squamous (i.e. “true skin”)

152
Q

What is Anal Fissure/ fissure-in-ano?

A

A longitudinal tear in the anal canal mucosa, distal to the dentate line

More common on males
Usually at 6 o’clock (90%) or 12 o’clock (10%)
Can be acute (present <6 weeks) or chronic (present >6 weeks)

153
Q

What are the main causes of fissure-in-ano?

A

Mainly constipation.

Infections (syphilis/herpes)
Trauma
Crohn’s
Anal cancer
Psoriasis

Parturition – causes anterior/12 o’clock tears.

154
Q

Clinical presentation of fissure-in-ano

A

Symptoms:
Severe pain post defecation
Fresh red PR bleeding
Itching

OE:

  • Upon spreading the skin, can see breaks/ulcers in the mucosa.
  • PR exam will be found very painful by the patient.
155
Q

Management of fissure-in-ano

A

Conservative – dietary modification

Medical – laxatives, instillagel, topical diltiazem/GTN cream

Injection of botox sometimes used to relax the anal sphincter and allow healing.

May need examination under general anaesthesia if chronic.

156
Q

What is a drawback of botox in management of anal fissure?

A

Injection of botox can cause transient incontinence (especially flatus) after the procedure

157
Q

How does a perianal abscess occur?

A

= a collection of pus in the anal region

Plugging of the anal ducts (cryptoglandular plugging) causes bacteria overgrowth and cryptoglandular infection. Pus builds up and causes an abscess.

158
Q

What pathogens are normally involved in a perianal abscess?

A

usually gut organisms – E. coli, bacteriodes spp., and enterococcus spp

159
Q

Perianal abscess - presentation

A

Painful, hot, red lump in the perianal region

Discharging of pus

Maybe “fluctuance” in the area of abscess.

Sepsis – diabetic patients in particular can become septic very quickly from anal abscesses

160
Q

Perianal abscess - management

A

Complicated patients might need a CT/MRI to delineate where the abscess is.

Incision and drainage of the abscess under spinal/general anaesthetic
=> to prevent rupture/possible formation of fistula.

161
Q

Fistula-in-ano

A

= an abnormal connection between the anal canal and peri-anal skin.

This is commonly associated with peri-anal abscesses
(~1 in 3 abscess patients have a fistula).

162
Q

Risk factors for fistula-in-ano

A 
Peri-anal abscess
IBD
Systemic disease – HIV, TB, diabetes
Trauma
Pelvic radiation
163
Q

Goodsall’s Rule

A

= the position of the external opening can give you clues as to the tract of the fistula

Anterior to transverse line – short, direct radicular tract to the interior opening.

Posterior to transverse line – curved/horseshoe tract to the interior opening

164
Q

Presentation of fistula-in-ano

A

Maybe peri-anal abscess

Intermittent or continuous discharge of pus/blood/mucous from the perineum

165
Q

Investigation of fistula-in-ano

A

PR exam
Proctoscopy under anaesthesia
(Complex cases – pelvic MRI)

166
Q

Management of fistula-in-ano

A

Drain abscess in acute setting.

Seton-suture – an elastic band slung through the external opening into the internal opening in the anal canal and tied to make a loop that allows sepsis to drain, preventing abscess.

Fistulotomy – laying open of the tract, including the overlying skin and/or muscle.

167
Q

Odynophagia vs dysphagia

A
  • Dysphagia – swallowing difficulties

* Odynophagia – painful swallow

168
Q

GI history - difficulty swallowing

A

Any pain?

Onset – how quickly did they start and how have they progressed?

Solids and liquids – difficulty with one or the other/both?

Progression – intermittent? Constant? Worsening?

169
Q

GI history - N+V

A

Frequency and volume

Appearance - e.g. undigested, fresh bleed, coffee ground, bilous, faecal matter?

170
Q

What would cause vomiting with fresh blood?

A

Mallory Weiss tear,

oesophageal variceal rupture

171
Q

What would cause vomiting with “coffee ground” appearance?

A

peptic/duodenal ulcer

172
Q

GI history - Weight loss

A 
How much?
Over how long?
Intentional or unintentional?
Anorexia? 
Dysphagia? 
Life stressors?
173
Q

GI history - Dysuria

A 
Urgency and frequency?
Volume?
Nocturia?
Appearance? (haematuria/cloudy)
Abdominal pain?
Temperature?
174
Q

GI history - Haematuria

A 
Quantity?
Thick blood or discoloured urine?
Recent catheter?
Anaemia symptoms?
Occupation?
Trauma?
175
Q

GI history - abdominal distension

A

Any weight gain – eating more/decreased exercise/stress eating?

Alcohol intake?

Any systemic features of malignancy?

Bowel habits?

Any chance of pregnancy?

176
Q

GI history - altered bowel habits

A

What is normal for the patient?

How often? Any urgency?

How long has this been happening?

Appearance – consistency, mucous, blood, melaena, pale?

Any recent antibiotics? Laxatives?

Recent suspicious food?

177
Q

GI history - jaundice

A

Any dark urine/pale stools?
Any pain?
Itching? (Pruritis)

178
Q

GI History - PMH

A

Previous medical conditions etc.

BUT ALSO
any pervious surgery?
previous colonoscopy/endoscopy?

179
Q

GI History - FH

A

specifically history of polyps or bowel cancer?

180
Q

what are the anal vascular cushions ?

A

highly vascular areas, formed of smooth muscle with subepithelial anastomoses of the rectal arteries/veins.

The 3 cushions act to assist the anal sphincter in maintaining continence

181
Q

Where are the 3 anal cushions located?

A

positioned at the 3-, 7- and 11 o’clock positions when viewed from the lithotomy position

182
Q

What are haemorrhoids?

A

disrupted/dilated anal vascular cushions

183
Q

1st Degree Haemorrhoids

A

Remain in the rectum

184
Q

2nd Degree Haemorrhoids

A

Prolapse through the anus on defecation but spontaneously reduce

185
Q

3rd Degree Haemorrhoids

A

Prolapse through the anus on defecation but require digital reduction

186
Q

4th Degree Haemorrhoids

A

Remain persistently prolapsed

187
Q

Causes/risk factors for haemorrhoids

A

Idiopathic

Excessive straining/increased anal tone – chronic constipation, low-fibre diet.

Increasing age

Raised intra-abdominal pressure – pregnancy, chronic cough, or ascites.

Congestion of superior rectal veins – cardiac failure, rectal carcinoma, portal hypertension

188
Q

Symptoms of haemorrhoids

A

Often asymptomatic

Painless rectal bleeding - on SURFACE of stool

Prolapse

Mucous discharge – pruritis ani due to chronic irritation.

Impaired continence

Rectal fullness/anal lump

Pain if the haemorrhoids are thrombosed.

189
Q

Complications of haemorrhoids

A

Anaemia – if severe/continuous bleed.
Thrombosis
Ulceration/gangrene (secondary to thrombosis).
Perianal sepsis.

190
Q

Thrombosis of haemorrhoids

A

When prolapsing haemorrhoids are gripped by the anal sphincter (“strangulated”).

Venous return is occluded, leading to thrombosis.

Haemorrhoids swell, become purple/blue and tense, cause significant pain/distress.

Often fibrose within 2-3 weeks, giving spontaneous cure.

Management is conservative – cold compresses, opioids and rest.

191
Q

DDx for haemorrhoids

A

exclude other causes of rectal bleeding – malignancy, IBD, diverticular disease.

Other perianal DDx – fissure-in-ano, perianal abscess, fistula-in-ano

192
Q

Haemorrhoids - investigations

A

PR exam – prolapsing haemorrhoids are obvious.
Protoscopy – can visualise the haemorrhoids and assess for any lesion higher in the rectum.

Abdominal exam – palpable mass, enlarged liver.

Colonoscopy/flexi-sigmoidoscopy – if symptoms suggest a different pathology (e.g. malignancy).

If significant/prolonged bleeding – FBC and coagulation screen.

193
Q

Haemorrhoids - management

A

Normally always conservative/medical management:

  • plenty of fluids, lots of fibre, try not to strain.
  • ice packs
  • Topical analgesia (e.g. instillagel)
  • Bulk forming laxative.

Sometimes surgical management, particularly if bleeding:

  • Banding
  • Sclerotherapy
  • Haemorrhoid artery ligation operation (HALO)
  • Surgical haemorrhoidectomy
194
Q

“Heartburn”

A

epigastric discomfort following a meal

Central, no radiation.

Worse with bending/lying down and when drinking hot liquids/alcohol.

Improves with sitting upright and Gaviscon

195
Q

GORD

A

= Gastro-oesophageal Reflux Disease

A long-term condition where stomach contents rise up into the oesophagus - prolonged contact of the gastric contents with the oesophageal mucosa, leading to oesophagitis.

Results in either symptoms or complications.

196
Q

Lower oesophageal sphincter - components and purpose

A

helps to prevent gastric contents reflux

Two muscular components – external and internal.
One physiological sphincter – angle of His

197
Q

Symptoms of GORD

A 
Heartburn.
Acid reflux
Oesophagitis – sore, inflamed oesophagus. 
Halitosis – bad breath
Bloating and belching
Nausea and/or vomiting
Odynophagia and/or dysphagia
198
Q

Risk factors for GORD

A 
Obesity
Hiatus hernia 
Pregnancy
Connective tissue disorders
Delayed stomach emptying
199
Q

What can aggravate acid reflux?

A

Smoking

Eating large meals/late at night

Certain foods/drinks – e.g. fatty/fried foods, alcohol, coffee.

Certain medications, such as aspirin.

200
Q

Complications of GORD

A

Oesophageal ulcers

Oesophageal strictures
=> Caused by repeated ulcers/inflammation

Barrett’s Oesophagus
Oesophageal Cancer

201
Q

What are the Red Flag upper GI symptoms ?

A 
ALARM55:
Anaemia (iron deficient)
Loss of weight
Anorexia
Recent onset, progressive symptoms
Melaena or haematemesis
Swallowing difficulties.
>55 years of age
202
Q

Diagnosis of GORD

A

Diagnosis is usually based on symptoms and treated empirically.

referral for endoscopy if red flag symptoms or symptoms are persistent/not controlled by medication.

Specialist investigations -

  1. Oesophageal manometry and ambulatory 24-hour oesophageal pH monitoring
  2. Barium swallow to rule out structural disorders
203
Q

Management of GORD

A

LIFESTYLE
Weight loss and smoking cessation
Eat small and regular meals, >3h before bed.
Avoid hot drinks/alcohol.
Avoid drugs that exacerbate the condition/damage the mucosa (e.g. NSAIDs)

MEDICAL
Antacids +/- alginates
H2RAs/PPIs
Full-dose PPI for 8-weeks to heal severe oesophagitis.

204
Q

What is Barrett’s oesophagus

A

= A pre-cancerous condition involving metaplasia in the mucosal cells lining the lower portion of the oesophagus.

occurs due to long-standing reflux

Cells transform from normal stratified squamous epithelium to gastric glandular columnar

Continued inflammation can lead to dysplasia and malignant changes

205
Q

Diagnosis of Barrett’s Oesophagus

A

Diagnosis is with upper GI endoscopy

if present it will be visible and biopsies can be taken to confirm disease

206
Q

Management of Barrett’s Oesophagus

A

Regular endoscopic surveillance

Biopsies to look for dysplasia/carcinoma in situ.

207
Q

At what vertebral level is the oesophageal hiatus?

A

T10

208
Q

Hiatus hernia

A

the protrusion of an organ (typically the stomach) through the oesophageal opening in the diaphragm, into the thoracic cavity.

209
Q

What are the two types of hiatus hernia

A

Sliding

Rolling (para-oesophageal)

210
Q

Sliding hiatus hernia

A

G-O junction slides through the hiatus to lie above the diaphragm.

Occurs in 30% of adults >50.

Usually of no significance, but symptoms may occur due to associated reflux.

211
Q

Rolling hiatus hernia

A

A small part of the fundus rolls up through the hernia alongside the oesophagus, but the sphincter remains competent below the diaphragm.

Very occasionally can present with severe pain, requiring surgical intervention for gastric volvulus/ strangulation

212
Q

What is a peptic ulcer?

A

a defect in the gastric or duodenal mucosa that extends through the muscularis mucosa

213
Q

Gastric ulcers

A

Occur in older patients (>55)

Mainly on the lesser curve of the stomach

Pain is worse on eating
Relieved by antacids

May present with small bleed (iron deficiency anaemia) or major haemorrhage (haematemesis)

214
Q

Peptic Ulcers

A

4x more common than gastric ulcers

90% located within 2cm of the pylorus.

Pain is at night and before meals.
Relieved by eating food/drinking milk.

May present with bleeding or perforation

215
Q

Risk Factors/Causes of peptic ulcers

A

H. pylori infection

Long-term NSAIDs
Long-term/high-dose corticosteroids

Zollinger-Ellison Syndrome

Increased ICP (Cushing ulcers)
Post severe burns (Curling ulcer)

Hepatic/renal failure

216
Q

Zollinger-Ellison Syndrome

A

Excessive acid secretion due to a non-insulin secreting islet cell tumour of the pancreas which secreting gastrin-like hormone.

217
Q

What can make peptic ulcers worse?

A 
Smoking
Alcohol 
Coffee consumption
Stress
Spicy foods
218
Q

How does smoking impact peptic ulceration?

A

Smoking impairs gastric mucosal healing, and nicotine increases acid secretion.

219
Q

How do NSAIDs impact peptic ulceration?

A

NSAIDs inhibit COX enzymes – inhibition of COX-1 in the stomach means that there is less production of prostaglandins which normally inhibit acid secretion and protect the mucosa.

220
Q

Peptic Ulcers - Clinical Presentation

A

Nearly 75% of patients are asymptomatic

Symptoms can be:

  • Burning epigastric pain, related to food intake.
  • Feeling of fullness, bloating or belching.
  • Appetite changes
  • Unexplained weight loss
  • Haematemesis/melaena
  • Nausea
  • Severe abdominal pain (?perforation)
221
Q

Peptic Ulcers - management

A

If ALARMS55 symptoms – urgent referral for OGD (to be performed within 2 weeks).

If ALARMS symptoms not present:
1. Lifestyle measures – avoid food triggers, stop smoking.

  1. Medications
    => PPIs/H2Ras to reduce acid secretion
    => Stop NSAIDs if possible.
222
Q

H. Pylori bacteria

A

Gram-negative, helical shaped rod bacteria

Produce a urease enzyme that will hydrolyse urea to form ammonium.

Ammonium neutralises the gastric acid in the surrounding environment to aid survival

223
Q

What does H. Pylori infection cause?

A
  1. Direct mucosal injury via cytotoxins => mucosal damage.
  2. Increased gastrin release to make up for the neutralised environment => increased acidity.

This normally occurs in the antrum of the stomach and ulcer forms.
Also associated with duodenal ulcers

224
Q

Management of H. Pylori infection

A

Eradication involves triple therapy:

= PPI + 2 antibiotics for 7 days.

Normally Omeprazole + 2 of clarithromycin/amoxicillin/metronidazole

225
Q

Investigation of H. Pylori infection

A

Carbon-13 urea breath test

Stool antigen test

Laboratory-based serology (where its performance has been locally validated)

Biopsy of antral mucosa

226
Q

Follow-up for peptic ulcers/H.pylori infection

A

Offer people with gastric ulcer and H. pylori repeat endoscopy 6 to 8 weeks after beginning treatment, depending on the size of the lesion

Perform re-testing for H. pylori using a carbon-13 urea breath test.

227
Q

Globus

A

= a sensation of a lump/foreign body in the throat.

228
Q

Dyspepsia

A

= a complex of upper GI tract symptoms, which are typically present for >4 weeks. Includes upper abdominal pain/discomfort, heartburn, acid reflux, nausea and/or vomiting.

229
Q

Physical/obstructive causes of dysphagia

A 
Foreign body (mainly in children)
Tonsilitis
Stricture
Pharyngeal pouch
Oesophagitis (GORD, infection, eosinophilic)
Oesophageal malignancy
Gastric malignancy
Extrinsic pressure (lymph nodes, goitre, bronchial ca.)
230
Q

Functional/neurological causes of dysphagia

A

CNS – Brain injury, Parkinson’s, MS, dementia

PNS – motor neurone disease, myasthenia gravis

Muscle – CREST syndrome, oesophageal spasm, achalasia

Functional – globus sensation

231
Q

What infections can cause oesophagitis?

A

Bacteria

Candida (immunocompromised, poor steroid inhaler technique)

232
Q

Dysphagia - duration of symptoms

A

Sudden – stroke

Rapidly progressive – cancer

Insidious – MND/MG

Longstanding – oesophageal spasm/achalasia.

233
Q

Dysphagia - progressive vs. intermittent

A

Progressive – suspect benign/malignant stricture

Intermittent – motility disorders, spasms, achalasia

234
Q

Dysphagia - solids/fluids/both?

A

Solids – suspect mechanical obstruction (benign/malignant stricture)

Fluids – suspect motility disorder (e.g. neuromuscular disease)

235
Q

Dysphagia - is it difficult to make the swallowing movement?

A

If yes, suspect neurological cause.

236
Q

Dysphagia - is swallowing painful?

A

If yes, suspect cancer, oesophageal ulcer, candida or spasm.

237
Q

Dysphagia - associated symptoms

A 
Gurgling
Cough
Hoarse voice
Halitosis
Weight loss (= red flag)
Neurological symptoms
238
Q

What is important PMHx in a history for dysphagia?

A

GORD – predisposes to oesophageal adenocarcinoma and also non-malignant strictures.

Peptic ulcers – scarring and strictures

Neurological condition

239
Q

What is important DHx and SHx in a history for dysphagia?

A

any medications which increase the risk of GORD (e.g. NSAIDs, steroids, bisphosphonates)

Allergies

excess smoking and alcohol causes increased risk of gastric/oesophageal malignancy

240
Q

Investigation of dyspepsia - Bedside tests

A 
Basic observations
Fluid status assessment
Palpate neck
Palpate abdomen 
Examine for Virchow’s node
Examine for cachexia & anaemia
Cranial nerves
241
Q

Investigation of dyspepsia - Bloods

A

FBC
U&E
LFTs

242
Q

Investigation of dyspepsia - Imaging

A

Key imaging = OGD +/- Biopsy

(CXR)
Barium swallow
Manometry

Staging CT if malignancy

243
Q

What could be the cause of cachexia in dysphagia?

A

Weight loss due to inability to swallow

Weight loss due to malignancy

244
Q

What could a CXR show in dysphagia ?cause ?

A 
?gross dilatation of achalasia
?bronchial carcinoma
?hiatus hernia
?aspiration pneumonia
?mass impinging on oesophagus
?foreign body
245
Q

Oesophageal malignancy - presentation

A

Initially asymptomatic – patients tend to present late

Progressive dysphagia
=> Starting with solids, then liquids and eventually difficulty swallowing saliva

Odynophagia
Weight loss and anorexia.
Retrosternal chest pain
Coughing
Hoarse voice
Haemoptysis
Vomiting
Occasional lymphadenopathy.
246
Q

Incidence of oesophageal cancer

What type of tumour is it normally?

A

3x more common in men than women

More common in age >55, but increasingly common in younger groups.

Mainly adenocarcinomas, with the remainder being mostly SCC

247
Q

Oesophageal malignancy - adenocarcinoma

A

More common in UK and western Europe

Typically lower 1/3 of oesophagus

Risk factors:
• GORD – obesity/alcohol/medications
• Barrett’s Oesophagus
• Smoking

Metastasise earlier via lymphatics

248
Q

Oesophageal malignancy - squamous cell carcinoma

A

More common worldwide

Typically middle and upper 1/3 oesophagus

Risk factors:
•	Alcohol
•	Smoking
•	Diet – high nitrates/nitrosamines
•	Chronic inflammation (e.g. Achalasia)

Regional lymph node spread.

249
Q

Oesophageal malignancy - diagnosis

A

If suspected oesophageal malignancy – urgent OGD.

Staging CT CAP and PET-CT scan

Metastases are common at diagnosis (25%) in the liver/lungs/bones.

250
Q

Oesophageal malignancy - management and prognosis

A

MDT management

Curative treatment = typically surgery +/- neoadjuvant chemotherapy or chemo-radiotherapy.

70% treated as palliative as the majority have advanced disease

Prognosis for both is poor (<10% 5-year survival), with SCC having a slightly better prognosis as it is more responsive to radiotherapy.

251
Q

Incidence of gastric cancer

A

Falling incidence in the UK, but poor prognosis

75% of cases are in men

Most common in >55s

252
Q

Risk factors for gastric cancer

A
  • Hypochlorhydria
  • H. pylori infection leading to metaplasia
  • High salt/nitrate diet
  • Smoking
  • Genetic factors – blood group A, HNPCC, Japanese heritage
  • Pernicious anaemia
  • Adenomatous polyps
  • Low socio-economic status.
253
Q

Pathophysiology of gastric cancer and its spread

A

Most are adenocarcinomas, occurring in the antrum.

Metastases are local by direct invasion of abdominal viscera, lymphatic and then to the liver by portal dissemination.

Transcoelomic spread may cause peritoneal mets, including ovarian tumours.

More rare forms of cancer are stromal tumours (leiomyomas/leiomyosarcomas) arising from the interstitial cells of Cajal.
=> These are usually more slow-growing/benign.

254
Q

Gastric cancer - clinical presentation

A

SYMPTOMS are frequently vague/non-specific symptoms.

Dyspepsia/epigastric pain
Dysphagia
Early satiety
Nausea and Vomiting
Anorexia, weight loss, anaemia, fatigue – late-stage symptoms

SIGNS are usually completely absent (esp. in early stages)
Anaemia
Jaundice
Hepatomegaly/jaundice/ascites – if liver metastases
Virchow’s node
Acanthosis nigricans
Palpable epigastric mass

255
Q

Troisier Sign

A

Enlarged/hard left supraclavicular node (Virchow’s node)

This indicates intra-abdominal malignancy

256
Q

Investigation of gastric cancer - bedside tests

A

Basic observations
Abdominal Exam
Lymph nodes

257
Q

Investigation of gastric cancer - bloods

A

FBC - ?anaemia, ?raised platelet count
U&E
LFTs

258
Q

Investigation of gastric cancer - imaging

A

OGD
=> Biopsies from suspected malignancy sent for histology, CLO testing and HER2

Staging CT CAP
Laparoscopy for peritoneal mets

259
Q

Gastric cancer - management

A

Only ~1/3 have curable disease at presentation, the remainder are treated palliatively.

Treatment tends to be radical surgery, sandwiched between chemotherapy (neoadjuvant and adjunct).

260
Q

Achalasia

A

= Failure of the lower oesophageal sphincter to relax during peristalsis (due to loss of ganglion cells).

Causes retention of a food bolus in the oesophagus.

There is consequential proximal inflammation, dilatation and muscle hypertrophy.

Chronic inflammation leads to a malignancy risk, particularly SCCs.

261
Q

Achalasia - Clinical Features

A

Progressive, variable dysphagia on ingestion of both solids and liquids.

Regurgitation/vomiting

Nocturnal cough

Retrosternal discomfort – due to oesophageal inflammation

Weight loss

262
Q

Achalasia - Investigations

A

OGD
=> rule out oesophageal malignancy

Mannometry (gold-standard diagnosis)
=> High resting pressure in the lower oesophageal sphincter
=> Incomplete relaxation on swallowing
=> Absent peristalsis

Barium swallow
=> Dilated tapering of oesophagus

263
Q

Achalasia - Management

A

Conservative/lifestyle measures
=> Eat slowly, chew food well, always eat upright, drink lots with meals, etc.

Botulinum toxin injection (Temporary relief)

Endoscopic balloon dilation
Heller’s myotomy - Muscles of the cardia are divided.

264
Q

Pharyngeal Pouch

A

an outpouching of posterior pharyngeal wall

typically at level C5-6

265
Q

Incidence of pharyngeal pouch

A

Seen mostly in 60-80 year olds

more common in males (5:1)

266
Q

Pharyngeal Pouch - Clinical Features

A
  • Dysphagia - Solids AND liquids
  • Regurgitation
  • Chronic cough
  • Gurgling on drinking
  • Halitosis
  • Globus
267
Q

what is inflammatory Bowel Disease ?

A

= chronic, relapsing and remitting condition

Mainly due to an inappropriate immune activation in the mucosa.

Patients will have flare ups of symptoms and periods where they are completely symptom-free.

Mainly seen in teenagers/young adults.

More common in Caucasians, and Ashkenazi Jews

268
Q

What are the types of IBD?

A
  1. Ulcerative colitis
  2. Crohn’s disease
  3. Indeterminate colitis (when it is not possible to distinguish between UC and Crohn’s)
269
Q

What is Crohn’s disease?

A

Inflammation affects any part of the GI tract (mouth to anus).

Most commonly terminal ileum and proximal ascending colon.

Can affect just one area, or multiple areas leaving normal bowel in between (“skip lesions”).

270
Q

pathophysiology of Crohn’s disease

A

The involved bowel is narrowed due to thickened wall, with deep ulcers.

“Rose thorn ulcers”
“Cobblestone” appearance on CT (specific to crohn’s, not seen on XR).

Due to inflammation, a lot of fat wrapping/stranding is seen around the intestine.

Inflammation extends through all layers of the bowel, so fistulas and strictures are common

271
Q

Crohn’s disease - clinical presentation

A

Abdominal pain (varying in character)

Diarrhoea
=> Steatorrhoea in ileal disease
=> Bloody in colonic disease

Weight loss (or failure to thrive) – due to malnutrition

Severe apthous ulceration of the mouth (early sign)

Anal complications – fissure, fistula, haemorrhoids, skin tags, abscesses

Extra-GI manifestations of IBD

Can present with RIF pain/mass

272
Q

Ileocolitis

A

inflammation of the terminal ileum and proximal ascending colon

273
Q

pathophysiology of Ulcerative colitis

A

the inflammatory process is thought to be autoimmune in nature.

Inflammation that starts at the rectum, extending proximally along the colon

The inflammation only affects the mucosa (i.e. superficial ulceration). Ulceration is extensive and continuous, with only very small portions of normal mucosa.

Mucosa is reddened, inflamed and bleeds easily.

Inflammation leads to loss of the colonic haustra.

Gives the adjacent mucosa the appearance of inflammatory polyps.

274
Q

what is a protective factor in UC?

A

smoking!

275
Q

Backwash ileitis

A

when UC also causes inflammation of the distal terminal ileum

276
Q

The extent of UC in the colon

A 
Proctitis – affects the rectum alone
Proctosigmoiditis 
Distal colitis
Extensive colitis
Pancolitis – whole colon is affected
277
Q

UC - clinical presentation

A

Crampy lower abdominal discomfort

Gradual onset diarrhoea (often bloody)
Urgency and tenesmus if disease confined to rectum

Extra-GI manifestations of IBD

278
Q

What are the extra-GI manifestations of IBD?

A

Can be:

Skin disorders
Joint pain
Eye manifestations – conjunctivitis/episcleritis/iritis
Venous thrombosis
Fatty liver
279
Q

What might appear on an AXR in UC?

A

may show dilated colon, with some thumb-printing of the bowel wall.
=> Indicates inflammation and thickening

280
Q

Histological differentiation of Crohn’s and UC

A

Crohn’s – transmural inflammation, lymphoid hyperplasia, granulomas.

UC – mucosal inflammation, crypt abscesses, goblet cell depletion

281
Q

Investigating IBD - bloods

A

FBC, U&E, LFT, CRP/ESR
Serum iron, B12, folate

Might see raised systemic inflammatory markers,
Anaemia, raised WCC, raised platelets

282
Q

Investigations IBD - stool studies

A

Stool chart
MCS x3 to exclude infective causes
Calprotectin

283
Q

Investigations IBD - radiology/endoscopy

A

AXR/CXR
Potentially CT in Crohn’s

Rigid/flexi-sigmoidoscopy
Colonoscopy
Endoscopic rectal biopsy

284
Q

What are complications of IBD?

A

Bowel perforation
Lower GI haemorrhage
Toxic dilatation (more common in UC)
Colonic carcinoma (Higher risk in Crohn’s than UC)

285
Q

Toxic dilatation of the colon

A

Features – persistent fever, tachycardia, loose blood-stained stools.

Investigations – falling albumin/potassium.

AXR – dilated (>6cm) colon with mucosal islands.

Perforation is imminent

Surgery often required

286
Q

Management of IBD

A

Aim of treatment is to prolong the remission phase and prevent relapses with maintenance therapy.

The type of treatment used depends on the severity of the disease and the responsiveness to therapy

Options are:

  • surgery
  • biologics
  • immunomodulators
  • antibiotics
  • corticosteroids
  • aminosalcylates
287
Q

The use of surgery in IBD

A

Surgery tends to only be effective in UC – colectomy provides cure.

In Crohn’s, surgery is never curative and patients still tend to develop recurrent disease

288
Q

How does malnutrition impact hospital patients?

A

Increases length of stay
Impairs wound healing
Leads to a longer and more difficult recovery
Increases risk of poor outcome and reduced functioning after admission.

289
Q

In which patients is malnutrition more common?

A

Long-term health conditions – particularly those that affect the gut such as Crohn’s disease

Swallowing difficulties

Social isolation

Recovery from injuries or burns.

290
Q

How do you work out daily calorie requirements?

A

BMR x Activity level

Varies depending on age, weight, gender, activity, and medical conditions

291
Q

What are the fat soluble vitamins?

A

A, D, E, K

292
Q

What are the water soluble vitamins?

A

B, C

293
Q

What is the issue with BMI?

A

Not accurate for patients of extreme sizes, amputees, etc.

294
Q

What are the indications for NG tube insertion?

A

Unsafe swallow (e.g. result of stroke, motor neuron disease, head injury)

Altered level of consciousness (e.g. ventilated patients)

Supplement oral intake

Upper GI strictures (e.g. possible bowel obstruction)

295
Q

How do you check the placement of an NG tube?

A

pH aspirate - pH >5.5 suggests presence of gastric acid

CXR if unsure

296
Q

What is the issue with obesity?

A 
Increases the risk of many conditions including:
T2DM, 
HTN, 
CVA, 
Hyperlipidemia, 
Some cancers.
OA
297
Q

Obestity - conservative management

A

Diet - aim to be mildly hypocaloric.

Minimise alcohol.

Exercise

298
Q

Obesity - pharmacological management

A

Orlistat - Pancreatic lipase inhibitor
Liraglutide - GLP-1 agonist

Very low calorie diet (<800 kcal/day)

299
Q

What are some of the side effects of orlistat?

A

Can cause abdominal pain, diarrhoea and anal leakage

300
Q

Obesity - surgical management

A

recommended in those who have a BMI >40, or >35 with complications (e.g. T2DM) after appropriate nonsurgical measures have been tried.

or option of choice for those with a BMI >50.

Broadly 2 types:

  1. Restrictive types – such as gastric bands and sleeve gastrectomy.
  2. Malabsorptive types – such as gastric bypass
301
Q

Travel History

A

When and where did they travel?
Other relevant travel history in the last few years?

What did they do when they were there?

Personal questions - IV drug use, sex, tattoos

Timeline and location of when symptoms began.

Any hospital/doctor visits abroad?

pre-trip immunisations / malaria prophylaxis ?

302
Q

What are the 4 main species causing malaria?

A

Plasmodium falciparum – more dangerous infection
P. vivax
P. ovale
P. malariae

303
Q

Process of malaria infection

A

Infection is transmitted by mosquitos – their saliva can contain the sporozoite of the parasite.

After a period of infection in the liver, the parasite emerges into the bloodstream and infects the red blood cells.

Blood cells become increasingly infected and the parasitic burden increases.

In P. falciparum this tends to happen more in the microvasculature in organs (e.g. brain and kidneys).
=> This makes it harder for the spleen to remove parasites and makes the disease more severe.

304
Q

Clinical Features of Malaria

A 
Often non-specific symptoms:
Fevers and rigors
Malaise
Headache
GI upset
If severe:
Reduced GCS
Seizures
ARDS
Shock
Jaundice
Anuria/oliguria – due to severe AKI/renal failure. 
Severe anaemia (Hb <50)
Acidosis 
DIC or spontaneous bleeding due to low platelets
305
Q

Diagnosis of malaria

A

Diagnosis is via a blood film looking for parasites or a rapid diagnostic test.

Should also get parasite load (%) as higher percentage of parasitaemia is associated with risk of more severe illness (falciparum)

Important to also look for complications of severe disease with other investigations

306
Q

Timings of infectious gastroenteritis

A

Bacterial and viral gastroenteritis - Onset tends to be acute.

Protozoal - often a more chronic onset.

Typhoid/paratyphoid – diarrhoea starts around week 3 of illness

307
Q

Questions to ask about the appearance of traveller’s diarrhoea

A

Blood?
=> Dysentery is bloody diarrhoea and may be due to E. coli, campylobacter, shigella or amoebiasis.

Mucous?
=> Mucous is suggestive of large bowel pathology
=> Mucous + blood common in dysentery

Pus?
=> Increases likelihood of a bacterial cause

Is it watery?
=> E.g. cholera is classically a ‘rice water diarrhoea’

Colour?
=> C. diff often has a green tinge.

308
Q

Diagnosis of traveller’s diarrhoea

A

Physical examination

Stool sample – may need more than one!

Blood cultures and malaria investigations if pyrexic

309
Q

Causes of traveller’s diarrhoea

A

Normal causes - noro/rotavirus

Shigellosis
Campylobacter
E. coli
Enteric fever/typhoid
Parasitic causes
310
Q

Potential causes of Jaundice in the returned traveller

A

Hepatitis A
Yellow Fever
Leptospirosis

CP1 (12 decks)

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