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Year 3 > General surgery, Gastro and hepatology > Flashcards

General surgery, Gastro and hepatology Flashcards

1
Q

Appendicitis

A

acute inflammation of the vermiform appendix usually due to obstruction of the appendiceal lumen

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2
Q

Epidemiology of appendicitis

A

Most common cause of acute abdomen in children & adults

usually presents age 10-20yrs

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3
Q

Most common cause of acute abdomen

A

Appendicitis

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4
Q

Presentation of appendicitis

A

Abdominal pain (usually severe)

  • starts periumbilical then migrates to RIF due to peritoneal inflammation
  • worse on movement/coughing (i.e. pt lies still)

Nausea & vomiting
mild pyrexia
guarding, rebound tenderness, tenderness

Rovsing’s sign +ve: palpation of LIF leads to pain in RIF
Psoas sign +ve in retrocaecal appendix: pain on hip extension

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5
Q

Investigations for appendicitis

A

essentially a clinical diagnosis

FBC (↑ WCC, neutrophilia)
Pregnancy tests in females
CRP (↑)
USS or CT ± contrast

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6
Q

Management of appendicitis

A

appendectomy
-laparoscopic = 1st line

prophylactic Abx
analgesia

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7
Q

Complications of appendicitis

A 
perforation (~20%)
appendix abscess (after untreated perforation)
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8
Q

Aetiology of acute pancreatitis

A

GET SMASHED
G: gallstones
E: ethanol
T: trauma

S: steroids
M: mumps 
A: autoimmune
S: scorpion stings
H: hypercalcaemia 
E: ERCP
D: drugs e.g. mesalazine
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9
Q

Most common causes of acute pancreatitis

A

biliary pancreatitis (i.e. after gallstones)
alcohol induced
post ERCP, steroids, trauma

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10
Q

Presentation of acute pancreatitis

A 
constant severe epigastric pain radiating to back
 -worse after meals
 -better when leaning forward
N&V
jaundice
shock (hypotension, tachycardia)
dyspnoea
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11
Q

Investigations for acute pancreatitis

A

often a clinical diagnosis

serum amylase (↑, often >3x upper limit of normal)
serum lipase (↑, often >3x upper limit of normal)
FBC (↑WCC)
U&Es
CRP
plain erect AXR

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12
Q

Glasgow score use

A

used for acute pancreatitis as a prognostic tool

alternatives include the RANSON score and the APACHE II score

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13
Q

Glasgow score for acute pancreatitis

A 
Age >55 yrs
WCC >15x10^9/L
Urea >16 mmol/L
glucose >10 mmol/L
pO2 <8 kPa
albumin <32 g/L
Ca2+ <2 mmol/L
LDH >600 units
AST/ALT >200 units
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14
Q

Poor prognostic indicators for acute pancreatitis

A 
age > 55 years
hypocalcaemia
hyperglycaemia
hypoxia
neutrophilia
elevated LDH and AST
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15
Q

Management of acute pancreatitis

A 
aggressive IV fluid therapy
Nil by mouth
NG tube feeding
analgesia
consider Abx if severe
Early cholecystectomy/ERCP if related to gallstones
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16
Q

Chronic pancreatitis

A

caused by progressive inflammation & irreversible damage to the structure and exocrine/endocrine functions of the pancreas

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17
Q

Aetiology of chronic pancreatitis

A

~80% due to long term heavy chronic alcohol misuse

others: cystic fibrosis, heamachromatosis, ductal obstruction

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18
Q

Epidemiology of chronic pancreatitis

A

average pt is aged 40 yrs

4:1 male: female ratio

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19
Q

Presentation of chronic pancreatitis

A 
epigastric pain
 -radiates to back
 -worse after meals (i.e. exacerbated by eating)
 -begins episodic then becomes constant 
weight loss
pancreatic diabetes 
steatorrhoea 
 -cramping/bloating
Vit ADEK deficiency secondary to steatorrhoea
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20
Q

Investigations for chronic pancreatitis

A

AXR (pancreatic calcification)
CT (more sensitive for calcifications)
FBCs/U&Es/creatinine/LFTs/Ca2+/glucose
amylase (is normal)

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21
Q

Management of chronic pancreatitis

A 
analgesia (often requires opioids)
pancreatic enzyme replacement e.g. CREON
abstinence from alcohol/smoking/drugs
supplements such as Vit ADEK
surgery if intractable pain
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22
Q

Diverticular disease

A

a set of colonic pathologies resulting from the abnormal out pouching of the colonic mucosa i.e. diverticula

Includes:
Diverticulosis (non-inflamed diverticuli)
Diverticulitis (inflammed/infected diverticuli)

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23
Q

Aetiology of diverticular disease

A

develop due to chronic elevations of intraluminal pressure e.g. due to constipation & the age related weakening of connective tissue

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24
Q

Risk factors diverticular disease

A

age >50 yrs
low fibre diet
obesity

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25
Q

Presentation of Diverticulosis

A

non specific abdo pain/discomfort
chronic constipation
bloating

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26
Q

Presentation of Diverticulitis

A 
LLQ pain (NB pts of asian pts tend to have right sided diverticuli so present with LRQ pain)
altered bowel habit (diarrhoea/constipation)
localised tenderness on palpation
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27
Q

Presentation of diverticular haemorrhage

A

painless abrupt frank PR bleeding

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28
Q

Investigations for diverticular disease

A

if asymptomatic its usually and incidental finding

colonoscopy (diagnostic modality of choice)
FBCs (↑ WCC)/CRP (↑) in diverticulitis
U&Es
barium enema 
CT cologram
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29
Q

Management of diverticular disease

A

↑ dietary fibre intake & ensure adequate fluid intake
analgesia

ABx for diverticulitis

surgery if perforation/uncontrolled sepsis/fistula

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30
Q

Complications of diverticular disease

A 
fistulas
perforation leading to peritonitis
abscess formation
haemorrhage 
intestinal obstruction
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31
Q

Hepatitis A (Hep A)

A

a viral hepatitis that is not associated with chronic liver disease

Key facts:
most common form of acute viral hepatitis 
NOTIFIABLE disease in UK
DOES NOT CAUSE CHRONIC DISEASE
transmitted faeco-oral route
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32
Q

Hep A risk factors

A

travel to high risk areas e.g. tropics, male homosexuality + multiple partners, IVDU, personal contacts, pts with clotting disorders receiving factor VIII & IX

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33
Q

Presentation of Hep A

A

Flu like prodrome (fevers, malaise, myalgia)
RUQ pain
tender hepatomegaly
jaundice ± pruritus/pale stools/dark urine

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34
Q

Specific investigations for Hep A

A

anti-HAV IgG (↑)
-persist indefinitely=sign of previous infection/vaccination

anti-HAV IgM (↑)
-present in active infection

HAV RNA (+ve)

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35
Q

Investigations for acute viral hepatitis

A 
ALT ↑
AST ↑
ALP ↑ 
gamma-GT ↑
bilirubin ↑
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36
Q

Management of Hep A

A

supportive management
avoid alcohol
avoid food handling
avoid unprotected intercourse

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37
Q

Hep A vaccination

A

not routinely given

consider if high risk pt e.g. MSM, IVDU, sewage workers, pts with chronic liver disease, pts with haemophilia

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38
Q

Hepatitis B (Hep B)

A

most common cause of hepatitis world wide

transmitted sexually, parenterally or perinatally

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39
Q

Acute presentation of Hep B

A

acute illness often sub clinical or presents as flu like illness (similar to Hep A)

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40
Q

Chronic presentation of Hep B

A 
chronic disease (if HbsAg +ve for >6 months)
fatigue, RUQ pain
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41
Q

Hep B investigations

A

LFTs (ALP/AST/ALT/bilirubin ↑)

HBsAg (+ve in acute disease)
HbeAg (+ve implies infectivity, i.e. recent infection)
HbcAg i.e. anti-HBc (+ve implies past infection, if only vaccinated -ve)
HbsAg i.e. anti-HBs (+ve if vaccinated or immunity)

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42
Q

Prevention of Hep B

A

vaccination
on routine childhood immunisation schedule
given at 2,3 and 4 months

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43
Q

Complications of Hep B

A

↑ risk of hepatocellular carcinoma (HCC)

chronic hepatitis

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44
Q

Hepatits C (Hep C)

A

transmitted parenterally e.g. IVDU/needlestick

↑ cases in UK

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45
Q

Presentation of Hep C

A

~80% initially asymptomatic initially, ~20% acute hepatitis (malaise, RUQ pain, tender hepatomegaly, jaundice)

Chronic infection (>6 months HCV RNA +ve)
liver cirrhosis, arthralgia/arthritis, HCC, cryoglobulinaemia, membranoproliferazive glomerulonephritis
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46
Q

Investigations for Hep C

A

LFTs (↑ AST/ALT/ALP/GGT/bilirubin)
Hep C antibodies (+ve in immunocompetent pts)
HCV RNA (+ve)

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47
Q

Treatment for Hep C

A

Acute:
active monitoring or interferon to ↓ risk of chronic HCV

Chronic:
combination of protease inhibitors ± ribavirin

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48
Q

Viral hepatitis unable to vaccinated against

A

Hep C has no vaccine currently available

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49
Q

Hepatitis D (Hep D)

A

Virus requiring Hep B surface antigen to survive, so only develops in pts with HBsAg

i.e. as co-infection or superinfection with HBV

treated with interferon

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50
Q

Cirrhosis

A

a process characterised by diffuse fibrosis & conversion of normal liver architecture to structurally abnormal nodules known as regenerative nodules

the final stage of a variety of liver diseases

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51
Q

Aetiology of cirrhosis

A

Alcoholic liver disease
Hep B & Hep C infections
Non alcoholic fatty liver disease (NAFLD)

Others: haemochromatosis, primary biliary cirrhosis, primary sclerosis cholangitis

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52
Q

Risk factors for liver cirrhosis

A 
excess alcohol consumption
Hep B/C infection
obesity
IVDU
unprotected sexual intercourse
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53
Q

Presentation of cirrhosis

A

often asymptomatic until decompensation

symptoms are generally vague
oedema, ascites, easy bruising, pruritus, jaundice, spider naevi, palamar erythema, leuchonychia, hepatomegaly,, nodular liver

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54
Q

Investigations for cirrhosis

A 
LFTs
  -AST ↑
  -ALT ↑
  -GGT ↑
  -ALP ↑
albumin ↓
FBC (↓Hb, thrombocytopenia)
coagulation screen (↑ prothrombin time)
transient elastography/acoustic radiation impulse imaging

Hep B/C serology, U&Es, ceruplasmin, urinary copper, ferritin, haemateninics

NB if AST > ALT indicates alcoholic liver disease, but ALT > AST suggests other causes

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55
Q

Classification of cirrhosis

A

Child-Pugh-Turcotte system

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56
Q

Management of cirrhosis

A

treat underlying cause
ensure adequate nutrition
stop alcohol intake
Zinc supplements (Zinc deficiency common)
Hep A/influenza/pneumococcal vaccinations
liver transplant (only curative measure)

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57
Q

Compensated vs decompensated cirrhosis

A

compensated = liver still able to function, generally minimal symptoms present

decompensated = liver not properly functioning leading to features such as jaundice, ascites etc

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58
Q

oesophageal varices

A

occur at the junction of the portal & systemic venous circulation usually in the distal oesophagus and/or proximal stomach

due to portal hypertension leading to dilation of the anastomosis of the 2 venous systems

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59
Q

Presentation of oesophageal varices

A 
generally asymptomatic unless haemorrhaging
haematemesis
abdo pain
malaena
dysphagia/odynophagia
pallor
shock (hypotension, tachycardia, ↓ GCS)
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60
Q

Investigations for oesophageal varices

A 
Endoscopy (OGD)
 -shows dilated veins
 -also therapeutic 
U&Es (↑ Urea)
FBC, group & screen, LFTs
U&Es (↑ Urea)
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61
Q

Management of oesophageal varices

A

Resuscitation, IV fluids, blood transfusions

Pre-endoscopy

  • terlipressin or ocreotide
  • prophylactic Abx

Endoscopy
-variceal band ligation (1st line)

uncontrolled haemorrhage
-sengstaken-blakemore tubes

Transjugular intrahepatice portosystemic shunt (TIPSS)
-last resort

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62
Q

Prophylaxis of oesophageal varices

A

Propanolol

endoscopic vatical band ligation + PPI cover

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63
Q

Portalhypertension

A

pathological elevation of portal venous pressure from obstruction of portal blood flow which may be pre-hepatic (portal vein thrombosis), intra-hepatic (cirrhosis) or post-hepatic (right sided HF)

clinically significant if hepatic venous pressure gradient ≥10mmHg

most commonly due to cirrhosis

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64
Q

Presentation of portal hypertension

A

dilated veins at portosystemic anastomosis

  • paraumbilical veins & epigastric veins → caput medusae
  • rectal veins → hemorrhoidal or anorectal varices
  • veins of the gastric fundus & distal 1/3 of the esophagus → gastric/oesophageal varices

Congestive splenomegaly
Transudative ascites
signs of liver failure (jaundice, spider naevi, palmar erythema)
hyper dynamic circulation (bounding pulse, ↓BP, warm peripheries)

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65
Q

Investigations of portal hypertension

A

FBC, U&Es, LFTs, clotting
abdo USS (splenomegaly, portal vein dilation, cavernous transformation of portal vein)
abdo CT
Hepatic venous pressure gradient ( ≥10mmHg)

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66
Q

Management of portal hypertension

A

beta blockers ± nitrates (↓ pressure)
salt restriction & diuretics
Transjugular intrahepatice portosystemic shunt (TIPSS)\

treat underlying cause or liver transplant

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67
Q

complications of Transjugular intrahepatice portosystemic shunt (TIPSS)

A

exacerbation of hepatic encephalopathy is a common complication

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68
Q

Ascites

A

pathological collection of fluid in the peritoneal cavity

on clinical examination ~1500ml detectable
on USS can detect volumes ≤500ml

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69
Q

Aetiology of ascites

A 
~75% = cirrhosis 
~15% = malignancy e.g. meigs syndrome with ovarian cancer or GI tract malignancy

others: Heart failure, nephrotic syndrome

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70
Q

Presentation of ascites

A

progressive abdominal distension
abdominal discomfort (secondary to distension)
↑ weight
early satiety
dyspnoea
shifting dullness on percussion (+ve if ~1500ml fluid)
peripheral/generalised oedema

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71
Q

Investigations for ascites

A

serum-ascites albumin gradient (SAAG)
≥11g/L or ≥1.1g/dL = transudate (portal hypertension)
<11g/L or <1.1g/dL = exudate (hypoalbuniaemia)
FBC, U&Es, LFTs, clotting, TFTs
abdo USS or abdo MRI/CT (may show underlying cause)
ascitic tap
-SAAG
-cell count (neutrophils >250 indicates SBP)
-RBCs (<1000 = normal, ↑ indicates malignancy)

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72
Q

Serum-ascites albumin gradient (SAAG)

A

Helps to determine underlying cause but requires ascitic tap

≥11g/L or ≥1.1g/dL = transudate
indicates portal hypertension
i.e. liver failure/cirrhosis, liver malignancy, right sided HF, constrictive pericarditis etc

<11g/L or <1.1g/dL = exudate
indicates hyporlbuniameia
i.e. nephrotic syndrome, severe malnutrition (e.g. kwashiorkor), infections, pancreatitis

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73
Q

Management of ascites

A

restrict salt intake (especially in cirrhosis)
diuretics
-spironolactone (1st line in cirrhosis), monitor K+
± loop diuretics e.g. furosemide

therapeutic paracentesis
  -give Human albumin solution if removing large volumes
TIPSS
prophylactic ABx (to prevent SBP)
  -ciprofloxacin/norofloxacin
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74
Q

Spontaneous bacterial peritonitis (SBP)

A

a bacterial infection of ascitic fluid in the absence of any identifiable intra-abdominal source of infection
may be due to bacteria spreading across intestinal wall

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75
Q

Aetiology of Spontaneous bacterial peritonitis (SBP)

A

most commonly E. Coli

otherwise Klebsiella

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76
Q

Presentation of Spontaneous bacterial peritonitis (SBP)

A 
fever
ascites
abdo pain
naseau & vomiting 
constipation/diarrhoea
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77
Q

Investigations for Spontaneous bacterial peritonitis (SBP)

A 
ascitic tap
  -neutrophil count >250 cells/mm3
  -ascitic fluid culture
FBC
blood cultures
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78
Q

Management of Spontaneous bacterial peritonitis (SBP)

A

empirical Abx (generally IV)
-1st line: IV cefotaxime
-2nd line: IV ceftriaxone/ciprofloxacin
consider human albumin solution

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79
Q

Hepatorenal syndorme (HRS)

A

development of acute renal failure in pts with severe liver disease, commonly associated with Spontaneous bacterial peritonitis (SBP) or other infections

diagnosis of exclusion generally

can be in acute or chronic liver failure

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80
Q

Presentation of Hepatorenal syndorme (HRS)

A

jaundice
ascites
features of liver failure
peripheral oedema

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81
Q

Diagnostic criteria for Hepatorenal syndorme (HRS)

A

Diagnostic criteria:

  • cirrhosis
  • creatinine >133
  • absence of shock/absence of hypovolaemia
  • no recent treatment with nephrotoxic drugs
  • absence of parenchymal renal disease
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82
Q

Types of Hepatorenal syndorme (HRS)

A 
HRS type 1:
rapidly progressing
associated with precipitant event e.g. infection
creatinine doubles to >221 in <2 weeks 
very poor prognosis

HRS type 2:
gradual decline of renal function
associated with Na+ retention & refractory ascites

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83
Q

Treatment of Hepatorenal syndorme (HRS)

A

splanchnic vasoconstrictors e.g. terlipressin
human album solution
treat precipitating infection
TIPSS

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84
Q

Hepatic encephalopathy

A

a spectrum of neuropsychiatric abnormalities cause by acute/chronic hepatic insufficiency generally related to excess ammonia & glutamine absorption in the brain due to portosystemic shunting

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85
Q

precipitating events for hepatic encephalopathy

A 
transjugular intrahepatic portosystemic shunting (TIPSS)
infections e.g. SBP
renal failure
constipation
GI bleed
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86
Q

Presentation of hepatic encephalopathy

A

confusion & altered level of consciousness
fatigue, lethargy, apathy, irritability
disorientation, memory loss, sleep impairment
socially aberrant behaviour
slurred speech, muscle rigidity, constructional apraxia
asterix (liver flap)
arrhythmic negative myoclonus

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87
Q

Grading of hepatic encephalopathy

A

I: irritability & sleep disturbances
II: confusion & inappropriate behaviour
III: incoherent, restless, somnolent but rousable, amnesia, disorientation
IV: coma

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88
Q

Management of hepatic encephalopathy

A

reducing gut nitrogen load
1st line : lactulose + rifamixin (sedentary prophylaxis)
2nd line enemas

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89
Q

Prophylaxis of hepatic encephalopathy

A

Rifamixin reduces recurrences

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90
Q

Hepatopulmonary syndrome

A

secondary to portal hypertension

triad of hepatic dysfunction, hyperaemia, extreme vasodilation of intrapulmonary vasculature

presents with dyspnoea, platypnoea (SOB better when lying flat), orthodeoxia (↓sats when going from lying to standing)

resolves after liver transplant

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91
Q

Portopulmonary hypertension

A

unexplained pulmonary hypertension in association with portal hypertension

often asymptomatic

requires echo & right heart catheterisation

treatment is liver transplant

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92
Q

Hepatocellular carcinoma (HCC)

A

a malignant usually solitary tumour of the liver often seen in pts with pre-existing cirrhosis or chronic hepatitis

~90% of all liver cancers (most common primary liver tumour)

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93
Q

Aetiology of Hepatocellular carcinoma (HCC)

A

chronic Hepatitis B or C infections (most common cause)
alcoholic liver disease
others: haemochromatosis, primary biliary cirrhosis

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94
Q

Epidemiology of Hepatocellular carcinoma (HCC)

A

more common in men (~4x)

usually seen age 65-70 yrs

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95
Q

Presentation of Hepatocellular carcinoma (HCC)

A

usually presents with symptoms of cirrhosis/liver failure

pruritus
splenomegaly & hepatomegaly
weight loss
oesophageal varices
jaundice 
hepatic encephalopathy
ascties
RUQ pain/tenderness
spider naevi
caput medusa
flapping tremor
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96
Q

Screening for Hepatocellular carcinoma (HCC)

A

for pts at risk of HCC e.g. HBV/HCV or alcohol related cirrhosis

USS every 6-12 months ± Alpha fetoprotein (AFP)

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97
Q

Investigations for Hepatocellular carcinoma (HCC)

A 
Serum AFP (↑)
LFTs, FBC, Clotting
liver USS (best initial investigation)
contrast enhanced CT/MRI abdo
liver biopsy
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98
Q

Tumour marker for Hepatocellular carcinoma (HCC)

A

Serum Alpha fetoprotein (AFP)

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99
Q

Management of Hepatocellular carcinoma (HCC)

A

tumour resection
-requires good liver function

liver transplant
-only very few pts suitable

Ablative therapy e.g. radio frequency ablation
-treatment fo choice in early stages

systematic chemotherapy

Chemoembolisation
-requires good liver function & no extra hepatic spread vascular invasion

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100
Q

Non alcoholic fatty liver disease (NAFLD)

A

Fatty liver disease developing in patients that do not consume alcohol in amounts considered harmful

most common cause of chronic liver disease in the developed world

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101
Q

Risk factors for Non alcoholic fatty liver disease (NAFLD)

A 
obesity
T2DM
hyperlipidaemia
jejunoileal bypass
sudden weight loss/starvation
metabolic syndrome
HTN
total parenteral nutrition
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102
Q

Presentation of Non alcoholic fatty liver disease (NAFLD)

A 
often asymptomatic 
hepatomegaly
obesity
fatigue 
features of cirrhosis
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103
Q

Investigations for Non alcoholic fatty liver disease (NAFLD)

A

LFTs (all ↑, ALT > AST, i.e. AST:ALT ratio <1 )
-if AST:ALT ratio reverses (>1) may mean progression to cirrhosis
fasting lipids (↑)
liver USS (hyperechogenic)
Liver biopsy (only definitive test)

FBC, viral serology, iron studies, ceruloplasmin

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104
Q

Management of Non alcoholic fatty liver disease (NAFLD)

A

lifestyle changes (diet &exercise)
weight loss
monitoring of disease

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105
Q

Alcoholic related fatty liver disease

A

similar to Non alcoholic fatty liver disease (NAFLD) but in pts consuming harmful amounts of alcohol

Investigations

  • gamma-GT (↑↑)
  • AST:ALT ratio >2 (>3 almost exclusively sent in alcoholic liver disease)

Managed with drinking cessation
glucocorticoids are used in acute episodes of alcoholic hepatitis

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106
Q

Wilson’s disease (hepatolenticular degeneration)

A

autosomal recessive disease of copper accumulation & copper toxicity caused by mutations of ATP7b gene (part of biliary copper pathway)

i.e. disease of hepatic copper deposition

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107
Q

Genetics of wilson’s disease

A

autosomal recessive

mutations of ATP7b gene

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108
Q

Epidemiology of Wilson’s disease

A

RARE condition

onset usually age 10-25yrs

usually goes undiagnosed until combination of hepatitis, dementia & Parkinsonism causes clinical suspicion

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109
Q

Presentation of Wilson’s disease

A

Hepatic features:
-hepatitis, cirrhosis, hepatosplenomegaly, jaundice, portal hypertension, ascites

Neurological features
-basal ganglia degeneration, dysarthria, dystonia, parkinsonism, drooling, ataxia, wing beating tremor, asymmetric tremor (most common early neurological feature)

Psychiatric features:
-depression, behavioural change, irritability, cognitive impairment, psychosis

ophthalmic features:
-Kayser-Fleischer rings (green-brown rings in periphery of iris due to copper deposition)

Renal tubular acidosis (Fanconi syndrome)
blue nails
infertility

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110
Q

Investigations for Wilson’s disease

A

slit lamp examination
-for Kayser-Fleischer rings

Serum caeruloplasmin (↓)
Total serum copper (↓)
LFTs (deranged)
urinary copper excretion (↑)
Liver biopsy (↑parenchymal copper concentration)
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111
Q

Management of Wilson’s disease

A

monitor LFTs, coagulation, FBCs

1st line: Penicillamine (copper chelation)
-trientine hydrochloride (slowly becoming 1st line)
usually combined with Zinc (↓ copper absorption)

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112
Q

Haemochromatosis

A

multisystem disorder of iron absorption & metabolism resulting in iron accumulation
autosomal recessive mutation of the HFE gene

most common genetic disorder in white people

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113
Q

genetics of Haemochromatosis

A

autosomal recessive

mutation of the HFE gene

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114
Q

Presentation of Haemochromatosis

A

Early features:
-fatigue, lethargy, arthralgia, erectile dysfunction

Later features:

  • liver (abdo pain, jaundice, cirrhosis)
  • bronze pigmentation of skin
  • diabetes mellitus
  • cardiac failure (dilated cardiomyopathy)
  • hypogonadism
  • arthritis (especially of hands)
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115
Q

Investigations for Haemochromatosis

A

Joint X-rays (chonedrocalcinosis)

Ferritin (↑)
serum iron (↑)
Total iron binding capacity (TIBC) (↑)
transferrin saturation (↑)
 ->55% in men, >50% in women

LFTs
-↑AST, ↑ALT

MRI (to measure liver iron content)
echocardiogram (dilated cardiomyopathy)

Genetic testing
-for 1st degree relatives of pt with confirmed disease/confirmed iron overload

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116
Q

Management of Haemochromatosis

A

1st line: phlebotomy/venesection
2nd line: desferrioxamine

Liver transplant in end stage liver disease

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117
Q

Autoimmune hepatitis

A

condition of unknown origin generally seen in young females, associated with other autoimmune conditions

presents with signs of chronic.acute liver disease & amenorrhoea

Investigations include LFTs (deranged, ↑ ↑ALT), serum antibodies, IgG (↑) and liver biopsy (key)

Managed with steroids & immunosuppressants e.g. azathioprine

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118
Q

Acute liver failure

A

rapid onset hepatocellular dysfunction

usually due to paracetamol overdose, acute fatty liver disease fo pregnancy, viral hepatitis (Hep A/B) or alcohol

presents with jaundice, coagulopathy (↑ prothrombin time), hypoalbuminaemia, hepatic encephalopathy and hepatorenal syndrome

Mangement is early liver transplant

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119
Q

Gallstones (cholelithiasis)

A

the presence of solid concretions in the gall bladder which may pass into the bile duct and cause obstruction

very common condition

in developed countries 90% of gallstones are made of cholesterol

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120
Q

Risk factors for gallstones

A 
↑age
FH of gallstones
sudden weight loss
diabetes
oral contraception 
pregnancy 
female gender
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121
Q

Presentation of gallstones

A

mostly asymptomatic

biliary colic:
colicky RUQ pain
-worse after easting, worse after fatty food
-pain may radiate to R shoulder/intrascapular region
N&V
bloating

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122
Q

Investigations for gallstones

A

USS of RUQ (demonstrates stones)
-if -ve but high index of suspicion then repeat

ERCP or CT

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123
Q

Management of gallstones

A

expectant management if asymptomatic
ERCP (to remove stones)
elective laparoscopic cholecystectomy

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124
Q

Acute cholecystitis

A

acute gallbladder inflammation

one of the major complications of gallstones, developing in ~10%of symptomatic pts with gallstones

usually due too complete cystic duct obstruction (~90% of cases)

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125
Q

Risk factors for Acute cholecystitis

A 
gallstones 
female gender
↑age
obesity
pregnancy 
Crohns disease
hyperlipidaemia
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126
Q

Presentation of Acute cholecystitis

A

RUQ pain

  • radiating to R shoulder/epigastric region
  • severe & prolonged pain (>6h)
  • worse after eating

Fever, malaise, N&V

Murphys sign +ve

  • press on RUQ and ask pt to breath in
  • +ve if elicits pain leading to arrestor inspiration
  • only +ve if same manoeuvre in LUQ doesn’t cause pain
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127
Q

Investigations for Acute cholecystitis

A

USS (1st line investigation)
-shows thickened gallbladder walls, distended gallbladder and possibly gallstones

FBC (↑ WCC)
CRP (↑)
LFTs (usually normal)

consider MRI/CT/HIDA if USS inconclusive

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128
Q

Management of Acute cholecystitis

A 
IV Abx
analgesia e.g. morphine 
early laparoscopic cholecystectomy 
 -within 1 week of diagnosis
 -gold standard
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129
Q

Acute/ascending cholangitis

A

an infection of the biliary tree typically secondary to biliary obstruction & stasis secondary to gallstones

may also be caused by malignancy affecting the biliary tree

causative organisms is usually E. Coli

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130
Q

Presentation of Acute/ascending cholangitis

A

Charcots triad:

  1. RUQ pain (maybe poorly localised abdo pain in elderly)
  2. Fever
  3. Jaundice

Raynauds pentad

  1. RUQ pain (maybe poorly localised abdo pain in elderly)
  2. Fever
  3. Jaundice
  4. hypotension (septic shock)
  5. confusion
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131
Q

Investigations for Acute/ascending cholangitis

A 
FBC (↑WCC)
ESR/CRP (↑)
LFTs (↑bilirubin, ↑AST, ↑ALT, ↑ALP, ↑GGT)
U&Es (↑creatinine, ↑urea)
blood cultures 
amylase (may be ↑)
USS abdo (dilated bile ducts ±gallstones)
ERCP/CT scan
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132
Q

management of Acute/ascending cholangitis

A

IV ABx & IV fluids
analgesia
endoscopic retrograde cholangipancreatography (ERCP)
-after 24-48h to relieve any obstruction

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133
Q

Primary biliary cholangitis / Primary biliary cirrhosis (PBC)

A

chronic disease of the small intrahepatic bile ducts of autoimmune origin thats is characterised by destruction of interlobular bile ducts due to chronic inflammation

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134
Q

Conditions associated with Primary biliary cholangitis (PBC)

A

Sjogrens syndrome (up to 80% of pts)
Rheumatoid arthritis
systemic sclerosis
thyroid disease

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135
Q

Presentation of Primary biliary cholangitis (PBC)

A 
initially asymptomatic 
fatigue, pruritus
cholestatic jaundice, dark urine, pale stools
hepatomegaly
RUQ discomfort
hyperpigmentation, xanthelasma 
cirrhosis (in advanced disease)
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136
Q

Investigations for Primary biliary cholangitis (PBC)

A 
LFTs (↑ gamma-GT, ↑ALP, ↑bilirubin)
ESR (↑)
IgM (↑)
anti-mitochondrial antibodies (AMA) M2 (+ve)
abdo USS
MRI cholangiopancreatography (MRCP)
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137
Q

Management of Primary biliary cholangitis (PBC)

A

1st line: ursodeoxycholic acid

cholestyramine for prurits
Vit ADEK supplements

138
Q

Antibodies associated with Primary biliary cholangitis (PBC)

A

98% of pts have anti-mitochondrial antibodies (AMA) M2 (+ve)

smooth muscle antibodies (+ve in 30%)
anti-nuclear antibodies

139
Q

Primary sclerosis cholangitis (PSC)

A

a progressive chronic inflammatory disease of the intrahepatic & extra hepatic bile ducts characterised by inflammation & fibrosis resulting in diffuse multi-focal stricture formation

140
Q

Primary sclerosis cholangitis (PSC) associated conditions

A

strongly associated with ulcerative colitis
-~80% of PSC patients have UC

NB only 5% of UC pts have PSC

141
Q

presentation of Primary sclerosis cholangitis (PSC)

A

cholestasis
-jaundice, scleral icterus, pruritus, pale stools, dark urine
-fatigue
-may cause acute cholangitis (fever, RUQ pain, jaundice)
weight loss
hepatomegaly
cirrhosis (in late stage)

142
Q

Investigations for Primary sclerosis cholangitis (PSC)

A 
MRCP (gold standard)
ERCP
LFTS (↑ALP, ↑gamma-GT, ↑bilirubin, AST/ALT slightly ↑)
cholesterol (↑)
IgM (↑)
p-ANCA (may be +ve)
143
Q

Management of Primary sclerosis cholangitis (PSC)

A

ursodeoxycholic acid (1st line)

balloon dilatation of strictures causing recurring cholangitis
cholestyramine for pruritis
Vit ADEK supplements

liver transplant is only curative treatment

144
Q

Crohn’s disease

A

an inflammatory bowel disease (IBD) of unclear aetiology which manifests anywhere in the GI tract characterised by transmural granulomatous inflammation & skip lesions

often affects terminal ileum & colon

145
Q

Risk factors for Crohn’s disease

A

Family history
smoking (smokers tend to have more aggressive disease)
HLA-B27

146
Q

Presentation of Crohn’s disease

A

generally presents with episodes of acute exacerbation interspersed with remission/less active disease

weight loss, fever, anorexia, fatigue

GI symptoms:
chronic diarrhoea, abdo pain/discomfort, perianal disease (ulcers, skin tags), fistulas, features of malabsorption (e.g. anemia)

Extra intestinal symptoms

  • enteropathic arthritis (usually lower body, asymmetrical, or scaroilitis/ankylosing spondylitis)
  • uveitis, episcleritis
  • pyoderma gangrenosum
  • clubbing, erythema nodosum
147
Q

Investigations for Crohn’s disease

A

Diagnostic (1st line)

  • endoscopy (deep ulcers, skip lesions, cobllesotning, oedema)
  • tissue biopsy (transmural inflammation, non-caveating granulomas)
FBC (↓Hb)
CRP (↑ in active disease)
faecal calprotectin (↑ in active disease)
stool MC&S
CT/MRI with oral contrast
148
Q

Investigations for Crohn’s disease

A

Diagnostic (1st line)

  • endoscopy, both colonoscopy & OGD (deep ulcers, skip lesions, cobllesotning, oedema)
  • tissue biopsy (transmural inflammation, non-caveating granulomas)
FBC (↓Hb)
CRP (↑ in active disease)
faecal calprotectin (↑ in active disease)
stool MC&S
CT/MRI with oral contrast
149
Q

Management of Crohn’s disease

A

Inducing remission:
glucocorticoids (1st line), mesalazine (2nd line)

Maintaining remission:
azathioprine/mercaptopurine (1st line), methotrexate (2nd line)

Surgery
~80% of pts will have surgery,
e.g. bowel resection ± stomas, fistula corrections or stricturoplasty

150
Q

Inducing remission in Crohn’s disease

A

1st line: Glucocorticoids IV/PO
2nd line: 5-ASA drugs e.g. mesalazine
±azathioprine/mercaptopurine/methotrexate (never as mono therapy)

infliximab for refractory disease or fistulating crohn’s

151
Q

Maintaining remission in Crohn’s disease

A

1st line: azathioprine/mercaptopurine (assess TPMT activity before starting)
2nd line: methotrexate

152
Q

Ulcerative colitis (UC)

A

an inflammatory bowel disease (IBD) characteristically involving chronic inflammation of the mucosa of the rectum/colon/caecum

NB always starts at the rectum so rectum is most common site

153
Q

Ulcerative colitis (UC) epidemiology

A

most common form of IBD

peak incidence age 15-25 yrs

154
Q

Risk factors for Ulcerative colitis (UC)

A

HLA-B27
white ehtnicity
FH of IBD

155
Q

Presentation of Ulcerative colitis (UC)

A

generally relapsing and remitting course

bloody diarrhoea ± mucous, faecal urgency ,abdo pain (mainly LLQ), cramps, tenesmus, rectal bleeding, constipation, weight loss, malaise

Extra-intestinal disease

  • erythema nodosum & pyoderma gangrenosum
  • primary sclerosis cholangitis (PSC)
  • anterior uveitis
  • sacroilitis, ankylosing spondylitis
156
Q

Investigations for Ulcerative colitis (UC)

A
  • colonoscopy (rectal involvement, continuous uniform involvement, widespread ulceration, red/raw mucosa, normal terminal ileum, friable mucosa)
  • biopsy (mucin depletion, diffuse mucosal atrophy, crypt abscesses, neutrophil infiltration limited to mucosa/submucosa)

FBC (↑WCC, ↓Hb)
ESR/CRP (↑)
faecal calprotectin (↑)
stool analysis

157
Q

Management of Ulcerative colitis (UC)

A

Inducing remission
PO/topical 5-ASA agents e.g. mesalazine
if extensive PO 5-ASA plus steroids

Maintaining remission
1st line 5-ASA agents PO/topical
if severe then azathioprine/mercaptopurine

Biologicals e.g. infliximab/tofacitinib

surgery:
colectomy is curative (~30% of pts have this procedure)

158
Q

Difference for Ulcerative colitis (UC) and Crohn’s

A

Crohn’s can present anywhere in GI tract,
UC always starts at rectum and is limited to large intestines,

Crohn’s has skip lesions
UC is continuous disease with no skip lesions

Crohns has normal diarrhoea
UC may have bloody diarrhoea

Crohns is transmural inflammation in all layers
UC is inflammation limited to mucosa & submucosa

Methotrexate can be used in Crohn’s
Methotrexate is not used in UC

159
Q

Maintaining remission in Ulcerative colitis (UC)

A

1st line: topical/oral aminosalicylates e.g. Sulfasalazine/Mesalazine

if severe flare/>2 flares in past year = azathioprine/mercaptopurine

160
Q

Irritable bowel syndrome (IBS)

A

A chronic condition characterised by abdo pain associated with bowel dysfunction

its defined by a symptom based diagnostic criteria in the absence of a detectable organic cause

161
Q

Epidemiology for Irritable bowel syndrome (IBS)

A

affects 10-20% of population

more common in women

most prevalent in ages 20-30yrs

162
Q

Presentation of Irritable bowel syndrome (IBS)

A

≥ 6 months of either: abdo pain/discomfort, bloating, change in bowel habit

considered +ve if abdo pain received by defecation or associated with altered bowel habit/frequency or stool form

≥2 of the following as well: altered passage of stool (straining/urgency/incomplete evacuation), bloating, distension, symptoms worsened by eating, passage of mucus

other features include lethargy, nausea, backache

163
Q

Investigations for Irritable bowel syndrome (IBS)

A

clinical diagnosis via ROME IV criteria

consider work up including FBC, U&Es, LFTs, CRP, coeliac screen, faecal calprotectin and CA125

164
Q

Management of Irritable bowel syndrome (IBS)

A

Lifestyle e.g. more fibre, exercise etc

Pharmacological:
1st line:
-Pain: give antispasmodics e.g. mebeverine/alverine
-constipation: bulk forming laxatives but avoid lactulose
-diarrhoea: loperamide
NB if no response to conventional laxatives try linaclotide

2nd line:
-TCAs e.g. amitriptyline

165
Q

Gastro-oesophageal reflux disease (GORD)

A

symptoms or complications resulting from the reflux of gastric contents into the oesophagus or beyond into the oral cavity/lungs

166
Q

Epidemiology of Gastro-oesophageal reflux disease (GORD)

A

2-3x more common men

167
Q

Epidemiology of Gastro-oesophageal reflux disease (GORD)

A

2-3x more common men

168
Q

Risk factors for Gastro-oesophageal reflux disease (GORD)

A 
smoking
stress
obesity
pregnancy
hiatus hernia
caffeine
alcohol
169
Q

Presentation of Gastro-oesophageal reflux disease (GORD)

A 
heartburn (retrosternal burning pain)
 -worse after meals, lying down, straining 
regurgitation
dysphagia
odynophagia
bloating
early satiety
non cardiac chest pain
dyspepsia
halitosis
non-productive night time cough
170
Q

Investigations for Gastro-oesophageal reflux disease (GORD)

A

Proton pump inhibitor (PPI) trial
-4 weeks, +ve if symptoms improve

Oesophagogastroduodenoscopy (OGD)
-indicated if alarm symptoms e.g. dysphagia/odynophagia, weight loss

Barium swallow (may show hiatus hernia)

oesophageal pH monitoring
-pH <4 frequently is abnormal

171
Q

Management of Gastro-oesophageal reflux disease (GORD)

A

lifestyle interventions

  • weight loss
  • stop smoking
  • ↓ alcohol intake
  • small regular meals
  • avoid eating/alcohol within 3h of bedtime

PPI trial for 4 weeks e.g. lansoprazole

  • if no response then double dose
  • if effective then continue PPI
  • considering adding H2RA e.g. ranitidine if still symptomatic
172
Q

Barretts oesophagus

A

a change in the normal oesophageal squamous epithelium to the columnar epithelium normally found in the stomach

a metaplastic process

associated with GORD

173
Q

Epidemiology of Barretts oesophagus

A

seen in ~5% of pts with GORD

more common in men

more common in caucasians

174
Q

Presentation of Barretts oesophagus

A

often asymptomatic
usually GORD symptoms i.e. reflux, heartburn etc
symptoms of oesophageal stricture e.g. dysphagia

175
Q

Risk factors for Barretts oesophagus

A 
GORD
male gender
smoking
central obesity
hiatus hernia
176
Q

Investigations for Barretts oesophagus

A

OGD
-visible colonisation, oesophagitis, inflammation

Biopsy (gold standard)
-area of columnar lined epithelium in the oesophagus at a level superior to the gastro-oesophageal junction

177
Q

Management of Barretts oesophagus

A

endoscopic surveillance with biopsy (every 3-5 years)
high dose PPI

if dysplasia identified

  • endoscopic mucosal resection
  • radio frequency ablation
178
Q

Oesophageal cancer

A

cancer of the oesophagus

2 common types

  • adenocarcinoma (most common in developed world)
  • squamous cell carcinoma

more common in men, usually aged >75yrs

generally has poor prognosis

179
Q

Risk factors for oesophageal cancer

A 
smoking
GORD/Barretts oesophagus (for adenocarcinoma)
strictures (for SCC)
obesity (for adenocarcinoma)
Plummer Vinson syndrome (for SCC)
180
Q

Locations of oesophageal cancers

A

adenocarcinoma: tends to be in lower 1/3 of oesophagus, near gastro-oesophageal junction

Squamous cell carcinoma : tends to be in upper 2/3 of oesophagus

181
Q

Presentation of oesophageal cancer

A 
dysphagia
vomiting
weight loss
anorexia
odynophagia
hoarseness 
retrosternal pain
182
Q

2 week wait criteria for suspect oesophageal cancer

A

unexplained dysphagia at any age

age >55 + weight loss and upper abdo pain/reflux/dyspepsia

183
Q

Investigations for oesophageal cancer

A

OGD with biopsy
CT chest/abdo/pelvis
FBC, U&Es, LFTs, CRP

184
Q

Management of oesophageal cancer

A

Curative (depends on staging)

  • neoadjuvant chemo / adjuvant chemo
  • surgical resection (total or subtotal oesophagectomy)

Palliation

  • stent placement
  • chemo
  • endoscopic therapy

NB a complication of surgery includes anastomotic leak leading to mediastinitis

185
Q

Mallory-Weiss tear

A

acute upper GI bleeding secondary to mucous membrane lacerations at the gastro-oesophageal junction usually after forceful/prolonged vomiting

associated with alcoholism/excessive alcohol intake

presents with haematemesis after a bout of vomiting/retching ± signs of shock

Investigated & treated with OGD

186
Q

Plummer Vinson syndrome

A

triad of iron deficiency anaemia, atrophic glossitis and oesophageal webs/strictures usually seen in middle aged women

presents as painless intermittent dysphagia, lethargy, tiredness

investigated with FBC (↓Hb), barium swallow (webs/strictures)

managed with iron supplementation, endoscopic dilation

187
Q

Boerhaaves syndrome

A

spontaneous oesophageal rupture (usually distal) secondary to repeated episodes of vomiting

presents with sudden onset, severe chest pain and vomiting

investigated with CT contrast swallow

managed with thoracotomy & lavage + primary repair if within 12h or T tube insertion if >12h ago

188
Q

Peptic ulcer disease (PUD)

A

the presence of one or more ulcerative lesions in the stomach or duodenum

break in mucosal lining should be >5mm

189
Q

Aetiology of Peptic ulcer disease (PUD)

A

H. Pylori infection (most common cause)
chronic NSAID use
SSRIs/corticosteroids/bisphosphonates
Zollinger-Ellison syndrome (rare, gastrin secreting neuroendocrine tumour)

190
Q

Conditions associated with H. Pylori infection

A

Peptic ulcer disease (PUD)

Gastric MALT lymphoma (good prognosis)

191
Q

Presentation of Peptic ulcer disease (PUD)

A

generally asymptomatic or presenting with complications such as perforation/bleeding

abdo pain (usually epigastric)
-gastric ulcer: aggravated by eating
-duodenal ulcer: received by eating/worse when hungry
indigestion, reflux, bloating, nausea and vomiting
dyspepsia, oral flatulance, intolerance of fatty food

192
Q

Presentation of gastric ulcer

A

epigastric pain aggravated by eating

193
Q

Presentation of duodenal ulcer

A

epigastric pain when hungry

pain is relieved by eating

194
Q

Investigations for Peptic ulcer disease (PUD)

A

H. Pylori
-urea breath test, still antigen test (if +ve then H. Pylori likely to be the cause)

FBC (↓ Hb if bleeding)
OGD* (demonstrates ulcers)
fasting serum gastrin (↑ in Zollinger-Ellison syndrome)

NB OGD is gold standard

195
Q

Management of Peptic ulcer disease (PUD)

A

stop NSAIDs (if suspected cause)

H.Pylori test -ve:

  • PPIs until ulcer healed
  • reevaluate after 4-8 weeks

H.Pylori test +ve:

  • eradication therapy (triple therapy)
  • PPI + amoxicillin + clarithromycin/metronidazole
  • if penicillin allergy then PPI+ clarithromycin+metronidazole
196
Q

Complications of Peptic ulcer disease (PUD)

A

Bleeding (acute)

  • most common complication, especially if posterior ulcers
  • presents with haematemesis, shock, anaemia
  • clinical diagnosis ± OGD
  • managed with IV PPI & endoscopic ligation

Perforation

  • presents with sudden diffuse abdo pain, rigidity, peritonitis and shock
  • consider CXR/AXR to show free air under diaphragm
  • management includes NBM & urgent surgical repair
197
Q

Upper GI bleed

A

refers to a GI bleed whose origin is proximal to the ligament of Treitz at the duodenojejunal junction

more common than lower GI bleed

198
Q

Aetiology of Upper GI bleed

A 
peptic ulcer disease (~25%)
oesophagi's
gastritis/erosions
varices
malignancy
Mallory-weiss tear

~20% no aetiology is found

199
Q

Presentation of Upper GI bleed

A

haematemesis
malaena
signs of shock (hypotension, tachycardia, tachypnoea)

200
Q

Scoring of Upper GI bleed

A

Blatchford score

  • consists of urea, Hb, sBP, HR, malaria, syncope, hepatic disease & HF
  • used pre-endoscopy to assess need for intervention
  • score of 0 = consider discharge
  • score of ≥1 pt at risk fo requiring intervention

Rockall score

  • used post endoscopy
  • identifies risk of adverse outcomes
201
Q

Pre-endoscopic scoring system for Upper GI bleed

A

Blatchford score

  • consists of urea, Hb, sBP, HR, malaria, syncope, hepatic disease & HF
  • used pre-endoscopy to assess need for intervention
  • score of 0 = consider discharge
  • score of ≥1 pt at risk fo requiring intervention
202
Q

Post-endoscopy scoring system for Upper GI bleed

A

Rockall score

  • used post endoscopy
  • identifies risk of adverse outcomes
203
Q

Investigations for Upper GI bleed

A

FBC, group & screen, cross match, coagulation, LFTs
U&Es (↑ urea)
CXR & AXR
endoscopy
-immediately after resuscitation if severe bleed
-within 24h for all pts

204
Q

Management of Upper GI bleed

A

Resuscitation & reversal of anticoagulation

Non variceal bleed:

  • 1st line: endoscopic therapy (thermal coagulation, clips ± adrenaline)
  • endoscopy can be repeated if necessary
  • PPIs post endoscopy
  • 2nd line: interventional radiology + embolisation

Variceal bleeds:

  • terlipressin & prophylactic Abx at presentation
  • 1st line: endoscopic band ligation of oesophageal varices or injections of N-butyl-2-cyanoacrylate for gastric varices
  • Sengstaken-Blakemore tube if uncontrolled haemorrhage
  • transjugular intrahepatic portosystemic shunts (TIPSS) as last resort
205
Q

Feature indicative of Upper GI bleed

A

↑ Urea is indicative of upper GI bleed

this is due to the ‘protein meal’ of blood in the stomach

206
Q

Management of variceal upper GI bleed

A

terlipressin & prophylactic Abx at presentation

1st line:

  • endoscopic band ligation of oesophageal varices
  • injections of N-butyl-2-cyanoacrylate for gastric varices

uncontrollable haemorrhage

  • Sengstaken-Blakemore tube
  • transjugular intrahepatic portosystemic shunts (TIPSS)
207
Q

Management of non variceal upper GI bleed

A

1st line:

  • endoscopic therapy (thermal coagulation, clips ± adrenaline)
  • can be repeated if necessary
  • PPIs post endoscopy

2nd line:
interventional radiology + embolisation

208
Q

Prophylaxis of variceal bleeding

A

Propanolol

Endoscopic band ligation with PPI cover

209
Q

Lower GI bleed

A

a wide clinical spectrum from small bleeding to major haemorrhage

incidence increases with age

210
Q

Aetiology of Lower GI bleed

A 
Diverticular disease (15-40%)
Meckels diverticulum
colonic angiodysplasisa (common in older people)
ischaemic colitis
colonic cancer
haemorrhoidal bleeding
211
Q

Presentation of Lower GI bleed

A

Haematochezia (may be present in massive upper GI bleed)

  • frank passage of blood PR
  • the darker the blood the more distal the bleed from the rectum

malaena is rare
signs of shock (hypotension, tachycardia, tachypnoea)

212
Q

Investigations for Lower GI bleed

A

colonoscopy after bowel prep (OGD if colonoscopy -ve)
PR examination
CT angiography
FBC, coagulation, U&Es

213
Q

Management of Lower GI bleed

A

Resuscitation as necessary
1st line: supportive management
2nd line: endoscopic cauterisation/band ligation/clipping

NB generally no hyper acute management, can often refer to specialist

214
Q

Pancreatic cancer

A

generally refers to primary pancreatic ductal adenocarcinoma which accounts for ~85% of all pancreatic neoplasms

215
Q

Risk factors for pancreatic cancer

A 
smoking 
FH of pancreatic cancer 
obesity
diabetes 
chronic pancreatitis

familial cancer syndromes

  • Peutz -Jeghers syndrome
  • HNPCC (Lynch syndrome)
  • MEN type I
216
Q

pathognomonic presentation of pancreatic cancer

A

Painless jaundice is pancreatic cancer until proven otherwise

217
Q

Epidemiology of pancreatic cancer

A

tends to present late & metastasis early
poor prognosis

only ~25% survive for ≥1 year after diagnosis

usually seen above age 75

218
Q

Presentation of pancreatic cancer

A 
painless jaundice (pathognomonic)
-if painless jaundice + non tender enlarged gallbladder =courvoisiers signs 
poor appetite, weight loss, fatigue 
malabsorption, pursuits, diarrhoea 
steatorrhoea, pale stools
atypical back pain 
abdo pain (like a belt around abdomen)
migratory thrombophlebitis (Trousseau sign)
219
Q

Investigations for pancreatic cancer

A

Abdo USS (pancreatic mass, dilated bile ducts)
pancreatic protocol CT (mass in pancreas & metastasis)
LFTs (↑bilirubin, ↑ALP, ↑GGT, AST/ALT normal)
Ca 19-9 (+ve)
ERCP or MRCP

220
Q

Management of pancreatitis

A

Whipples resection (pancreaticoduodenectomy) + adjuvant chemo

Palliative
chemo & radiotherapy, ERCP + stent placement

NB only ~20% suitable for surgery at diagnosis

221
Q

Tumour marker for pancreatic cancer

A

Ca 19-9

222
Q

Common metastasis sites of pancreatic cancer

A

Liver
Peritoneum
abdominal viscera
lungs

223
Q

Gastric cancer

A

5th most common cancer world wide and 3rd leading cause of cancer death

~95% are adenocarcinomas

more common in men, usually over age 75

224
Q

Risk factors for Gastric cancer

A 
H. Pylori
male gender
smoking 
diet (high in salt)
atrophic gastritis 
FH of gastric cancer
225
Q

Presentation of Gastric cancer

A

often asymptomatic early on

Gastric symtpoms:

  • Nausea, loss of appetite
  • dyspepsia, weight loss, vomiting, early satiety
  • vague abdo pain

Signs of advanced disease

  • virchows node (L supraclavicular lymphadenopathy)
  • Sister Mary joseph node (palpable umbilical nodule)
  • hepatomegaly, ascites
  • acanthosis nigricans (strongly associated with gastric cancer)
226
Q

Investigations for Gastric cancer

A

endoscopy with biopsy
-may show signet ring cells
CT chest/abdo/pelvis
FBC, LFTs, U&Es

227
Q

Management of Gastric cancer

A

Surgical resection:

  • if early: endoscopic mucosal resection
  • otherwise partial or total gastrectomy ± lymphadenectomy

post resection can perform a Roux-en-Y gastric bypass to reconstruct gastric passage

usually also neoadjuvant or adjuvant chemo

228
Q

Colorectal cancer

A

mostly adenocarcinomas that develop from polyps
often locally invasive

4th most common cancer & 2nd most common cause of cancer death

usually diagnosed age 65-75 yrs

229
Q

Most common site of metastasis for colorectal cancer

A

Liver

other sites e.g. brain/lungs/bones are uncommon if liver mets not present

230
Q

Most common site of Colorectal cancer

A

Rectum

231
Q

Risk factors for Colorectal cancer

A 
FH of colorectal neoplasia
IBD
Polyposis syndromes 
HNPCC (lynch syndrome)
obesity
smoking 
alcohol abuse
diabetes
232
Q

Presentation of Colorectal cancer

A

Right sided Cancer:
weight loss, anaemia, occult bleeding, RIF mass, malaena, diarrhoea,
more likely to be advanced disease at presentation

Left sided Cancer:
colicky pain, rectal bleeding, bowel obstruction, tenesmus, LIF mass, early change in bowel habit, blood in stool

General:
weight loss, night sweats, fatigue, abdo discomfort
change in bowel habit

Metastasis:
jaundice, hepatomegaly

Rectal cancer:
haematochezia, ↓ stool caliber (pencil shaped stools), rectal pain, tenesmus, flatulence, faecal incontinence

233
Q

Investigations for Colorectal cancer

A

FBC (↓ Hb), LFTs (abnormal if liver mets), U&Es

colonoscopy (to confirm diagnosis)
CT colonography (alternative to colonoscopy)
CT Chest/Abdo/Pelvis (staging)
carcinoembryonic antigen (CEA)
-throughout treatment & remission to monitor for relapse

234
Q

Screening for Colorectal cancer

A

one off flexible sigmoidoscopy offered to all adults aged 55yrs (NB abandoned due to covid)

Faecal immunochemical test (FIT) screening

  • offered every 2yrs to all men & women aged 60-74 yrs in england
  • if FIT test abnormal offer colonoscopy
235
Q

Referral criteria for suspected colorectal cancer

A

2 week wait:

  • ≥40 y/o with unexplained weight loss & abdo pain
  • ≥50y/o with unexplained rectal bleeding
  • ≥60y/o with Iron deficiency anaemia or a change in bowel habit
  • FIT test showing occult blood
  • consider if pts < 50y/o with rectal bleeding + unexplained abdo pain/change in bowel habit/iron deficiency anaemia or if unexplained rectal mass/ulceration

NB if the criteria is not met then send for FIT test

236
Q

Management of Colorectal cancer

A

Surgical:

  • Right sided hemicolectomy if caecum/proximal transverse colon
  • Left hemicolectomy if distal transverse colon/descending colon
  • sigmoid colectomy if sigmoid colon
  • anterior resection if low sigmoid colon/high rectal
  • abdomino-perineal resection of lowe rectal

often with adjuvant/neoadjuvant chemo

if possible then liver mets can also be surgically removed

237
Q

Presentation of Left sided colorectal cancer

A

colicky pain, rectal bleeding, bowel obstruction, tenesmus, LIF mass, early change in bowel habit, blood in stool

238
Q

Presentation of Rectal cancer

A

haematochezia, ↓ stool caliber (pencil shaped stools), rectal pain, tenesmus, flatulence, faecal incontinence

239
Q

Colonic polyps

A

polyps are abnormal colonic mucosal outgrowths commonly found in people over the age of 50

seen in younger people in hereditary polyposis syndromes

~70% of polyps are adenomas

240
Q

Presentation of colonic polyps

A

mostly asymptomatic (so may present as colon cancer)

if symptomatic:
haematochezia , change in bowel habit, mucous in stool
palpable rectal polyps on PR

241
Q

Investigations for colonic polyps

A

colonoscopy + biopsy
double contrats barium enema
CT colonography
FIT testing, Hb

242
Q

Management of colonic polyps

A

snare polypectomy if ≤5mm in size

endoscopic mucosal resection if large sessile polyps

surgical resection
-if >2cm / suspected malignancy / familial polyposis syndromes

243
Q

Hereditary polyposis syndromes

A 
Familial adenomatous polyposis 
MYH associated polyposis
Peutz-Jeghers syndrome 
Juvenile polyposis 
Cowden sydrome
244
Q

Hereditary polyposis syndromes

A 
Familial adenomatous polyposis 
MYH associated polyposis
Peutz-Jeghers syndrome 
Juvenile polyposis 
Cowden sydrome
245
Q

Familial adenomatous polyposis

A

autosomal dominant mutation in APC gene
typically presents age 10-30yrs
~100% chance of developing cancer

on colonoscopy shows >100 polyps

treated with prophylactic proctocolectomy with ill-pouch-anal anastomosis and 3 yearly endoscopic surveillance

246
Q

MYH associated polyposis

A

autosomal recessive mutation of MUTYH gene

<100 polyps seen on endoscopy

treated with prophylactic proctocolectomy with ill-pouch-anal anastomosis

247
Q

Peutz-Jeghers syndrome

A

autosomal dominant mutation of STK 11 gene

presents with harmatomatous polyposis and the defining feature of mucocutaneous pigmentation of the lips/buccal mucosa/genitlia/palms/soles

often presents with small bowel obstruction

on endoscopy there is multiple harmatomatous polyps throughout entire GI tract

managed with polyp excision & 3 yearly endoscopic surveillance

248
Q

Juvenile polyposis

A

onset within first decade of life

presents with Gi bleeding & anaemia

249
Q

Cowden syndrome

A

autosomal dominant mutation of PTEN gene

presents with multiple GI polyps and skin manifestations (hyperkeratosis & papules)

associated with breast cancer & thyroid disorders

250
Q

Haemorrhoids (piles)

A

Haemorrhoidal cushions are normal anatomical structures within the anal canal, which may enlarge & protrude outdid the anal canal

251
Q

Types of Haemorrhoids

A

internal (originate above dentate line)

external (originate below dentate line)

252
Q

Risk factors for Haemorrhoids

A

excessive straining e.g. chronic constipation
extended periods of sitting
pregnancy
low fibre diet

253
Q

Presentation of Haemorrhoids

A

painless rectal bleeding
-usually bright red bleeding at end of defecation
perianal pain/discomfort

internal haemorrhoids tend to be painless
external haemorrhoids tend to be painful perianal masses

254
Q

Investigation for Haemorrhoids

A

PR examination

shows tenderness, masses and bleeding

255
Q

Management of Haemorrhoids

A 
↑dietary fibre
↑fluid intake 
bulk forming laxatives
simple analgesia for pain 
topical steroids/local anaesthetics from symptom relief

rubber band ligation
haemorhoidectomy
-reserved for large symptomatic haemorrhoids

256
Q

Small bowel obstruction

A

a mechanical disruption of the potency of the GI tract which is a medical emergency requiring early diagnosis & intervention

257
Q

Risk factors for Small bowel obstruction

A

previous abdominal surgery
hernias
foreign body ingestion
intestinal malignancy

258
Q

Aetiology of Small bowel obstruction

A 
intra-abdominal adhesions (most common)
inguinal hernia with incarceration
other incarcerated hernias
merckels diverticulum 
strictures (from Crohns)
gallstone ileus
tumours
appendicits
259
Q

Presentation of Small bowel obstruction

A

diffuse central abdo pain
nausea
bilious vomiting
complete constipation (failure to pass flatulence or stool)
abdo distensions (resonant on percussion)
tinkling bowel sounds

260
Q

Investigations for Small bowel obstruction

A 
Plain AXR (distended loops of bowel with fluid level)
CT abdo/pelvis (definitive diagnosis) 
ABG, CRP, FBC, U&Es, LFTs, group&save
261
Q

Management of Small bowel obstruction

A

DRIP & SUCK

  • NBM (nil by mouth)
  • IV fluids
  • NG tube with free drainage

explorative laparotomy with management of obstruction cause

262
Q

Large bowel obstructions

A

complete or partial mechanical interruption of flow of intestinal contents

surgical emergency

263
Q

Aetiology of Large bowel obstruction

A

~60% colorectal malignancy
~20% diverticular strictures
~5% volvulus

264
Q

Risk factors for Large bowel obstruction

A 
colorectal adenomas/polyps
current/previous malignancy 
IBD
diverticular disease
current/previous hernia
previous abdo surgery
265
Q

Presentation of Large bowel obstruction

A 
intermitten abdo pain
significant abdo distension 
nausea & vomiting 
total constipation 
high pitched bowel sounds
tympanic percussion 
empty rectum
266
Q

Investigations for Large bowel obstruction

A

AXR (1st line)
CT abdo/pelvis (dilation, shows underlying cause)
FBC, U&Es, group & screen

267
Q

Management of Large bowel obstruction

A

Drip & suck

  • NBM
  • IV fluids
  • NG tube with free drainage

explorative laparotomy

NB if surgery not indicated trial drip & suck for 72h

268
Q

Volvulus

A

defined as a twisting of a loop of bowel on its mesentery most commonly affecting the sigmoid colon (~80%), then caecum (~20%)

one of the most common causes of intestinal obstruction

269
Q

Type of volvulus

A

Sigmoid volvulus:
-associated with older pts & chronic constipation

Caecal volvulus:
-tends to be younger pts

270
Q

Presentation fo volvulus

A

episodes of abdo pain relieved by explosive passage of stool/gas

slowly progressing symptoms of bowel obstruction

bowel ischaemia (tachycardia, hypotension, peritonits, haematochezia)

Bowel perforation (loss of dullness on percussion)

271
Q

Investigation for volvulus

A

AXR

  • sigmoid volvulus = coffe bean sign
  • caecal volvulus = kidney bean sign

CT abdo pelvis
-sigmoid volvulus = whirl sign

Barium eneam
-birds beak sign

272
Q

Management of volvulus

A

Sigmoid:
rigid sigmoidoscopy with recatl tube insertion

Caecal:
right hemicolectomy often needed

273
Q

Toxic megacolon

A

toxic colitis with a megacolon (distension >6cm) is often refereed to as a toxic megacolon

usually due to C. diff infection or IBD if non infectious

274
Q

Presentation of Toxic megacolon

A

bloody diarrhoea, vomiting
abdo distension & pain
sepsis (fever, hypotension, tachycardia, dehydration)

275
Q

Investigations for Toxic megacolon

A

FBC (↑WCC) U&Es (↓K+), ESR/CRP (↑)

AXR
-loss of haustration, multiple air fluid levels, dilated colon

contrast CT
-rules out mechanical obstruction

276
Q

Management of Toxic megacolon

A

NBM, NG tube & IV fluids (Drip & suck)
correct electrolyte imbalance
broad spectrum ABx

surgery if no response to medical treatment within 24-72h

277
Q

Abdominal aortic aneurysm (AAA)

A

a focal dilatation of the abdominal aorta by >1.5x its expected diameter (generally >3cm)

originates inferior to renal arteries in 90% of cases

278
Q

Risk factors of Abdominal aortic aneurysm (AAA)

A 
↑age
smoking*
atherosclerosis
hypercholesterolaemia 
FH of AAA
hypertension
279
Q

Presentation of unruptered Abdominal aortic aneurysm (AAA)

A

generally asymptomatic (i.e. incidental finding)
back pain
pulsate abdominal swelling
bruit on auscultation

280
Q

Presentation of ruptured Abdominal aortic aneurysm (AAA)

A 
hypovolaemic shock
sudden onset severe tearing back/abdo pain
painful pulsatile mass
Grey Turner sign (flank ecchymosis)
Cullen sign (periumbilical ecchymosis)
syncope

NB mortality is ~80%

281
Q

Investigations for Abdominal aortic aneurysm (AAA)

A

abdo USS (aorta diamete >3cm)

CT angiography (especially if pt symptomatic)

282
Q

Management of Abdominal aortic aneurysm (AAA)

A

Asymptomatic AAA <5.5cm: monitor with USS

  • 3.0-4.4 cm annually
  • 4.5-5.4cm 3 monthly
283
Q

Management of Abdominal aortic aneurysm (AAA)

A

Asymptomatic AAA <5.5cm: monitor with USS

  • 3.0-4.4 cm annually
  • 4.5-5.4cm 3 monthly

consider elective repair (endoscopic or open) if symptomatic AAA, AAA >5.5cm, AAA >4.0cm & growing >1cm in one year

Manage lifestyle e.g. smoking and HTN

284
Q

Epidemiology of Abdominal aortic aneurysm (AAA)

A

more common elderly men
usually aged >60yrs

NB rupture of AAA is more common in women

285
Q

Management of ruptured Abdominal aortic aneurysm (AAA)

A

resuscitation & blood transfusion

end-vascular aneurysm repair (EVAR) or open surgical repair within 90 min

286
Q

Monitoring for asymptomatic Abdominal aortic aneurysm (AAA)

A

considered if asymptomatic AAA <5.5cm
monitor with USS

  • 3.0-4.4 cm annually
  • 4.5-5.4cm 3 monthly
287
Q

Constipation

A

a ploy somatic heterogenous disorder defined by the infrequent of difficult passage of stool

  • usually defined as ≤3 bowel movements/week
  • or difficult passage of stool e.g. straining/discomfort
288
Q

Aetiology of constipation

A

low fibre diet, immobility, dehydration IBS, old age
anal fissure, rectal prolapse, strictures
hypothyroidism, hypercalcaemia, opioid analgesia
iron supplements
chronic laxative abuse

289
Q

Investigations for constipation

A

consider investigations if >40y/o, recent change of bowel habit, associated symptoms e.g. weight loss, rectal bleeding, mucous discharge or tenesmus

FBC, U&Es, Ca2+, TFTs
colonoscopy, AXR

290
Q

Management of constipation

A

mobilise pt
↑ fluid intake
↑ fibre intake

Pharmacological i.e laxatives (use for short duration if above don’t work)

  • bulk forming e.g. sterculia, ispagula husk
  • stool softeners e.g. archis oil enema (for impaction)
  • stimulants e.g. senna, docusate
  • osmotics e.g. lactulose, macrogol.movicol (can be used long term for chronic constipation)
  • enemas e.g. phosphate enema
291
Q

Abdominal wall hernias

A

protrusion of an organ or the fascia of an organ through the wall of the cavity that normally contains them

associated with obesity, ascites, ↑age, previous surgery

292
Q

Abdominal wall hernias

A

protrusion of an organ or the fascia of an organ through the wall of the cavity that normally contains them

associated with obesity, ascites, ↑age, previous surgery

Most hernias are clinically diagnosed but may be confirmed with USS

293
Q

Inguinal hernia

A

protrusion abdo/pelvic contents into the inguinal canal and out through the external inguinal ring

Types:

  • indirect = protrusion through internal inguinal ring, ~80% of inguinal hernias, more common in children
  • direct = protrusion through weakness in posterior wall of inguinal canal, more common in the elderly
294
Q

Type sof inguinal hernia

A

indirect

  • protrusion through internal inguinal ring
  • ~80% of inguinal hernias
  • more common in children

direct

  • protrusion through weakness in posterior wall of inguinal canal
  • more common in the elderly
295
Q

Presentation of inguinal hernia

A

mass in inguinal region (groin lump)

  • superior & medial to the pubic tuberosity
  • disappears on pressure/when pts lies down

discomfort/ache worse on exercise/activity

296
Q

Management of inguinal hernia

A

surgical repair of hernia

297
Q

Complications of hernias

A

incarceration of hernia

  • irreducible hernia with normal overlying skin
  • associated with bowel obstruction
  • can attempt manual reduction prior to surgery

strangulated hernia

  • sudden severe groin pain due to constriction & ischaemia
  • associated with bowel obstruction
  • overlying skin is warm, erythematous, tender

NB both these require emergency surgical repair

298
Q

Femoral hernias

A

protrusion of abdominal viscera into the femoral canal
accounts for ~5% of abdominal hernias

more common in women, especially if multiparous

299
Q

Presentation of femoral hernia

A

lump in groin

  • lateral & inferior to pubic tubercle
  • swells on coughing/straining
  • typically non reducible
300
Q

Management of femoral hernia

A

elective surgical repair ASAP due to strangulation risk

DO NOT used hernia trusses

NB risk of strangulation much higher than for inguinal hernias

301
Q

Incisional hernia

A

herniation of abdominal content through and abdominal wall defect created during previous surgery, generally occur within 3 years of surgery
midline laparotomies pose highest risk

presents as mass/protrusion at site of incisional scar

generally managed conservatively unless symptomatic

302
Q

Umbilical hernia

A

very common in infants, but accounts for ~5% of adult abdominal wall hernias

presents adjacent to umbilical orfice, pushing umbilicus into crescent shape

high risk of incarceration/strangulation

surgical repair should be done ASAP

303
Q

Acute abdomen

A

rapid onset of severe symptoms of abdominal pathology e.g. severe abdo pain lasting ≤5 days

304
Q

Commonest causes of acute abdomen

A 
non specific abdo pain
renal colic
biliary colic
cholecystitis 
appendicitis 
diverticulitis
305
Q

Assessment/management of acute abdomen

A 
pt NBM
IV fluids, analgesia and O2 as needed
NG tube
FBC, U&Es, LFTs, ABG, Ca2+, coagulation, amylase, glucose, group&save
pregnancy test
urinalysis 
AXR, CXR, USS & CT

Laparoscopy can be diagnostic & therapeutic

306
Q

Gastrointestinal perforation

A

full thickness loss of bowel wall integrity that results in perforation peritonitis

307
Q

Aetiology of Gastrointestinal perforation

A 
perforated duodenal ulcer (most common)
IBD
diverticulitis
acute appendicitis
toxic megacolon
foreign body ingestion
308
Q

Presentation of Gastrointestinal perforation

A

sudden onset abdo pain (stabbing & intense)
sudden onset abdo distension
nausea, vomiting, constipation
fever, tachycardia, tachypnoea, hypotension
loss of liver dullness on percussion
signs of peritonitis

309
Q

Investigations for Gastrointestinal perforation

A

Its a surgical emergency and investigations should not delay explorative laparotomy if clinic features are present

ABG (lactic acidosis), FBC (↑WCC)
AXR (free air under diaphragm)
USS (enhanced peritoneal stripe sign, air artefacts)

310
Q

Management of Gastrointestinal perforation

A 
NBM (bowel rest)
IV Abx
IV fluids (if needed) 
NG tube with free drainage
urgent explorative laparotomy
311
Q

Peritonitis

A

inflammation of the peritoneum caused by bacterial infection from a surgically treatable intra-abdominal source

312
Q

Aetiology of peritonitis

A
  • perforation of intra-abdominal viscera
  • appendicitis/diverticulitis/pancreatitis (translocation of bacteria from abdominal organs)
  • trauma (penetrating trauma)
  • anastomotic leak
313
Q

Presentation of peritonitis

A

abdo pain & tenderness
peritoneal signs (local/diffuse rigidity, rebound tenderness, guarding)
nausea, vomiting, ileus
shock/sepsis (hypotension, tachycardia tachypnoea, fever)

NB lack of improvement/worsening of symptoms in suspected SBP after ABx indicated peritonitis

314
Q

Investigations for peritonitis

A

peritoneal fluid analysis (↑WCC, culture +ve, protein >1g/dL)
CT contrast of abdo/pelvis
AXR

315
Q

Management of peritonitis

A

IV broad spectrum Abx

surgical consult for possible explorative laparotomy + lavage

316
Q

Stomas

A

bring lumen or visceral contents through an orifice in the skin, most commonly with bowel

317
Q

Features of a healthy stoma

A

should be red & moist
no separation between mucocutaneous edge & skin
no erythema, rash, ulceration or inflammation of surrounding skin

318
Q

Ileostomy

A

Located in RIF
spouted
outputting liquid

319
Q

Colostomy

A

location varies but usually L side of abdomen
flush with skin
outputting solids

320
Q

Urostomy

A

connection between bladder & abdominal wall

output is urine

321
Q

Stoma appearance

A

Small bowel stomas:
tend to be spouted so their irritant contents are not in contact with the skin

Colonic stomas:
can be flush with skin

322
Q

Wernickes encephalopathy & Wernicke-Korsakoff syndrome

A

a spectrum of disease due to thiamine deficiency usually related to alcohol abuse,

increasing incidence recently

alcohol related brain damaged accounts for ~10-25% of all dementia

323
Q

Wernickes encephalopathy

A

an acute but reversible condition

classic triad of Confusion, Ataxia, Opthalmoplegia/nystagmus

other features include perisperhal sensory neuropathy, autonomic dysfunction & ↓GCS

if untreated can progress to Wernicke-Korsakoff syndrome

324
Q

Classic triad of Wernickes encephalopathy

A

Confusion
Ataxia
Opthalmoplegia/nystagmus

325
Q

Wernicke-Korsakoff syndrome

A

chronic condition that is irreversible

presents with features of Wernickes (Confusion, Ataxia, Opthalmoplegia/nystagmus) plus retrograde & anterograde amnesia, personality change, confabulation, disorientation & hallucinations

326
Q

Investigations for Wernickes encephalopathy & Wernicke-Korsakoff syndrome

A

usually clinical diagnosis

Thiamine levels (↓)
FBC (macrocytic anaemia), U&Es, LFTs, glucose, MRI/CT head
327
Q

Management of Wernickes encephalopathy & Wernicke-Korsakoff syndrome

A

IV high dose thiamine/Vit B (Pabrinex) if Wernicke’s suspected

long term oral Vit B/thiamine supplementation
alcohol abstinence

consider supplementing folate, Vit B6, Vit B12 as well

328
Q

Clostridium difficile associated disease

A

infection of the colon by bacteria clostridium difficile (gram +ve bacillus) leading to a syndrome known as pseudomembranous colitis

329
Q

Presentation of C. Diff

A

symptoms start 5-10 days after Abx therapy or during course of Abx

watery diarrhoea ±blood/mucous
abdominal cramps
fever
nausea

330
Q

Investigations of C. Diff

A

FBC (↑WCC often >15x10^9/L)
U&Es (↓K+)
ABG (↓pH, ↑lactate)
Stool MC&S (detecting C. Diff toxin)

NB to diagnose C. diff the C. diff toxin must be present, if C. Diff antigen present this only means there was a past infection

331
Q

Management of 1st episode of C. Diff

A

1st line: oral vancomycin for 10days
2nd line: oral fidaxomicin
3rd line: or vancomycin + IV metronidazole

332
Q

Management of Recurrent episodes of C. Diff

A

if within 12 weeks of symptom resolution of previous c. diff infection = oral fidaxomicin

if >12 weeks after symptom resolution of previous c. diff infection = oral vancomycin/fidaxomicin

333
Q

Aetiology of C. diff infection

A

often associated with Abx use especially clindamycin, cephalosporins and metronidazole

often hospital acquired

334
Q

General C. Diff management

A

Abx (usually vancomycin or fidaxomicin)
report to PHE (if stool C. diff toxin +ve)
stop causative Abx
avoid opiates & loperamide (slow peristalsis and hence toxin is retained)

335
Q

Coeliacs disease

A

a systemic autoimmune disease triggered by dietary gluten peptides

associated with HLA-DQ2 & HLA-DQ8 as well as other autoimmune disease

affects ~1% of population

336
Q

Presentation of coeliacs disease

A

chronic/recurring diarrhoea & bloating
failure to thrive/faltering growth (in children)
persistent/unexplained GI symptoms e.g. N&V
prolonged fatigue
recurrent abdo pain/cramping/distension
malabsorption (e.g. IDA, folate deficiency)
dermatitis herpetiformis (pruritic papulovesicular rash occurring symmetrically over extensor surfaces)
weight loss

337
Q

Investigations for coeliacs disease

A 
Total IgA (if ↓ other tests gives false negative)
Tissue transglutaminase (tTG) antibodies (+ve)
endoscopic biopsy (villous atrophy, crypt hyperplasia, intra-epithelial lymphocytes)

endomysial antibodies & antigladin antibodies (not as common as tTG)

NB if pt is on gluten free diet already they should restart gluten for minimum 6 weeks before investigations

338
Q

Management of coeliacs disease

A

gluten free diet (i.e. avoid barely/wheat/rye/oats)

339
Q

Achalasia

A

failure of lower oesophageal sphincter to relax

usually presents in middle age as dysphagia to both liquids & solids, regurgitation of food, retrosternal pain, heartburn

investigated by oesophageal manometry (↑ sphincter tone), barium swallow (dilated oesophagus & birds beak sign), CXR

Managed with heller cardiomyomotomy or pneumatic balloon dilatation (if not fit for surgery)

340
Q

Oesophageal strictures

A

if benign then usually secondary to persistent GORD or post-op

presents with longstanding history of progressive dysphagia to solid food

diagnosed via barium swallow & endoscopy + biopsy

treated with pneumatic ballon dilatation

NB if malignant structure then needs to be surgically excised

341
Q

Pharyngeal pouch (Zenkers diverticulum)

A

a posteromedial diverticulum through Kilians

5:1 male:female ration, usually seen age >70yrs

presents with dysphagia, halitosis, regurgitation, aspiration, chronic cough, neck lump (gurgles on palpation)

diagnosed with barium swallow

treated with surgery, usually endoscopically

NB endoscopy should be avoided as this can perforate the lesion.

Year 3 (6 decks)

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