GI Conditions Flashcards
What is acute cholangitis/ Acending cholangitis
A bacterial infection of the biliary tract (usually E.coli)
Predisposing
Biliary obstruction of any cause:
Gallstones is the most common
Billiary strictures (narrowing from ERCP or cancer)
RF:
over 50 years old
Had cholelithasis (gallstones in gallbladder)
Primary/ secondary sclerosing cholangitis (scars of the bile duct - IBS (UC and crohns patients) usually have)
CLINICAL FEATURES
Charcorts triad-
Fever
RUQ pain
Jaundice
Reynolds Pentad-
charcots three + hypotension + confusion from shock
Other: pale stool and dark urine
INVESTIGATIONS
First line- transabdominal US to look for bile duct dilation and stones (if inconclusive then abdo CT with IV contrast)
Others:
LFTs- high conjugated bilirubin (hyperbilirubinaemia), raised GGT and ALP(alkaline phosphotase), ALT may be raised. Abnormal LFT- cholANGITIS rather than cholecystitis as they are markers of liver injury.
Blood cultures- check for sepsis and organism
ERCP- to look at stone (contraindication of pancreatitis)
FBC+ CRP- high WBC and CRP
U&E- high urea and creatinine
ABG- if suspect sepsis
Blood: high WCC and CRP
MANAGEMENT
1st- ADDRESS THE SEPSIS broad spectrum IV AB’s until know organism. Options include piperacillin/tazobactam, and imipenem/cilastatin, cefuroxime plus metronidazole,
Give Iv fluids and analgesia. NBM
2nd ERCP drainage after 24-48 hours to relieve obstruction
Offer elective cholecystectomy to prevent further
Complications:
Acute pancreatitis
Liver abscesses (injury to liver)
Sepsis
Prognosis:
usually rapidly improve.
If delay decompression or have comoribidties then prognosis poor. Depends on the timing of biliary drainage, administration of antibiotics and comorbidities of the patient.
Prognosis worse when- hyperbilirubinaemia, high fever, leukocytosis, older age and hypoalbuminaemia. If have liver cirrhosis, liver abscess, cancer then worse.
What would show up on an ABG if sepsis is present
Low bicarbonate
Metabolic acidosis
Raised lactate
What is acute pancreatitis
Autodigestion of pancreatic tissue by the pancreatic enzymes leading to necrosis
Causes:
I GET SMASHED
I- idiopathic
G- gallstomes (F)
E- ethanol (M)
T- trauma
S- Steroids
M- mumps
A- Autoimmune/ascaris infection
S- scorpion venom
H- high triglycerides, high chylomicrons hyperchylomicronemia, high calcium, low temperature
E- ERCP
D- drugs: BFS DAMP
Furosemide (hypertension and oedema)
Sodium valporate (epilepsy)
Bendoflumethiazide (thiazide diuretic)
Pentamidine (anti parasite)
Didanosine (HIV)
Azathioprine (immunosuppresant)
Mesalazine (crohns aminosalicylic)
BFS DAMP
bendoflumethiazide, furosemide, sodium valporate, didanosine, azathioprone, mesalazine, pentamidine
Three stages:
Milds- no organ failure, no complications
Moderate- no or transient organ failure (less than 48 hours) possible complications
Severe- More than 48 hours of organ failure, possible complications
CLINICAL PRESENTATION
Constant severe epigastric pain that radiates to back, sudden onset and worse with movement but relieved in tripod/leant forward position. Feels like beein stabbed
Nausea and vomiting- can become dehydrated, abnormal electrolytes, hypokalaemic metabolic alkalosis
Signs of shock- Hypovolaemia (dry mucus membrane + decreased skin turgor + sweating), hypotension, tachycardia
Fever
Decreased appetite
Signs of pleural effusion
IF SEVERE- cullens sign (periumbilical bruising) and Grey-turners sign (flank bruising)
ASSESS SEVERITY
GLASGOW score (over 3 means severe)
PANCREAS
pa02 low (thrombin activated causes blood clots and pancreatic gangrene), Age over 55, Neutrophilia, calcium low (Phospholipase A causes fat necrosis the fat then sequesters to calcium), renal function bad (lots of blood breaking down), enzympe- high LDH and AST, Albumin low (PPLA breaks down), Sugar high (islet necrosis)
Over 55 years
Hypocalcaemia- low calcium
Hyperglycaemia- high sugar
Hypoxia- low oxygen/breathless
Neutrophilia
High LDH and AST
INVESTIGATIONS
Blood Test-
- high serum lipase: more specific than serum amulase, serum lipase has longer half life so can be good for presentations over 24h
- FBC- Leukocytosis with left shift (releasing baby ones to try to fight). If elevated haematocrit then increased risk of necrotisisng pancreatitis so poor prognosis
- U&E- urea and creatinie high shows dehydration or hypovolaemia
-LFTs- high ALT means gallstones is the cause
IMAGING
US imaging to assess cause
Contrast enhanced CT
If have characteristic pain and amylase/lipase 3x normal then can diagnose without imaging
MANAGEMENT
- Fluid resuscitation- aggressive early hydration with crystalloids, aim for urine output higher than 0.5 mls per kg per hr. It will reduce lactic acidosis so help with pain too
-Analgesia with IV opioid
- NBM or enteral nutrition offered if they have moderately severe or severe level withn 72 hours. Paraental if this fails
* no ABs as not infected
If gallstones- ERCP
Debridement if patient doesnt recover and has necrosis and worsening organ dysfunction
Infected necrosis- radiological drainage or surgical necrosectomy
Necrosis indicated by : CRP>200 and high Hat
PROGNOSIS
Most improve in 3-7 days of conservative. Mortality higher in severe stages
Complications:
ARDS
Peripancreatic fluid collections
Pseudocysts- 4 weeks after have raised amylase
Pancreatic necrosis
Pancreatic abscess
Haemorrhage
What are the causes of acute pancreatitis
I GET SMASHED
I- idiopathic
G- gallstomes (F)
E- ethanol (M)
T- trauma
S- Steroids
M- mumps
A- Autoimmune/ascaris infection
S- scorpion venom
H- high triglycerides, high chylomicrons hyperchylomicronemia, high calcium, low temperature
E- ERCP
D- drugs
What drugs can cause acute pancreatitis
Furosemide (hypertension and oedema)
Sodium valporate (epilepsy)
Bendoflumethiazide (thiazide diuretic)
Pentamidine (anti parasite)
Didanosine (HIV)
Azathioprine (immunosuppresant)
Mesalazine (crohns aminosalicylic)
BFS DAMP
bendoflumethiazide, furosemide, sodium valporate, didanosine, azathioprone, mesalazine, pentamidine
What factors indicate severe pancreatitis
GLASGOW score (over 3 means severe)
PANCREAS
pa02 low (thrombin activated causes blood clots and pancreatic gangrene), Age over 55, Neutrophilia, calcium low (Phospholipase A causes fat necrosis the fat then sequesters to calcium), renal function bad (lots of blood breaking down), enzympe- high LDH and AST, Albumin low (PPLA breaks down), Sugar high (islet necrosis)
Over 55 years
Hypocalcaemia- low calcium
Hyperglycaemia- high sugar
Hypoxia- low oxygen/breathless
Neutrophilia
High LDH and AST
What factors are indicativeof developing necrotising pancreatitis
CRP over 200
Elevated haematocrit
What investigation of acute pancreatitis can indicate severity
hypocalcaemia
chronic pancreatitis
Usually from alcohol abuse
Pain worse after meals
Steatorrhoea (foul smell and greasy stool), weightloss, pain
Patients with chronic pancreatitis will usually develop Diabetes mellitus (20 years after symptoms begin as loose endocrine function).
Need HbA1c monitoring every 6 months
INVESTIGATE
CT pancreas with IV contrast (looks at pancreatic calcification)
Faecal elastase (will be low)
Normal amylase
MANAGEMENT
Pancreatic enzyme supplements
Analgesia
What is alcoholic hepatitis and its cause
Inflammation of the liver from damage to liver cells
Long term alcohol consumpton in 10-35% of heavy drinkers (15-20 years)
CLINICAL FEATURES
Jaundice
Nausea and vomiting
RUQ pain
Hepatomegaly
Loss of appetite/ weight loss
Fever with tachycardia
If severe: ascites and splenomegaly from portal hypertension
INVESTIGATIONS
Bloods:
- LFTs = 2AST:1ALT, high GGT, high ALP, high bilirubin, less albumin,
-FBC = non-megaloblastic macrocytic anaemia (KEY), thrombocytopaenia (low platelet)
-High PT= significant liver damage- liver makes clotting factors 2,7,9,10
Scan: US to check for other causes
MANAGEMENT
1st- Pabrinex which has Thiamine to stop wernickes encelophalopathy as well as Vitamin C
Chlordiazepoxide- for withdrawal symptoms
Corticosteroids (prednisolone) to reduced mortality. Maddrey’s discriminant function (DF) calculated using prothrombin time and bilirubin concentration to see who needs steroid therapy
4.6x(pts PT- normal PT) + bilirubin
If 32 or over then bad alcoholic hepatitis
stop alcohol use
PROGNOSIS AND COMP
10% die first month
40% in first year
if alcohol continues will become liver cirrhosis in 1-3 years
What are anal fissures
Longitudinal or elliptical tears of the squamous lining of the distal anal canal
If less than 6 weeks then acute. More than 6 then chronic
RF:
common in young adults
Hard stool
Constipation
Opiate analgesia (causes constipation)
IBD
Pregnancy- third trimester (delivery may cause)
STI
Primary- due to local trauma : low fibre intake, chronic constipation, diarrhoea, anal sex
Secondary (due to underlying disease): IBD, infection, anal surgery, malignancy
CLINICAL PRESENTATION
Painful, bright red rectal bleeding
Pain on defecation
Tearing sensation on passing stool
Anal spasm
90% anal fissures on posterior midline- if not then consider Crohns
INVESTIGATIONS
Clinical diagnosis- no tests needed
maybe anal manometry or anal ultrasound
MANAGEMENT
ACUTE
Soften stool- first-line laxative: bulk-forming laxative first-line, such as ispaghula
second-line: osmotic laxative, such as lactulose
Diet advice- high fibre and more fluid
Lubricants- petroleum jelly
Sitz baths
Topical analgesia
Topical glyceryl trinitrate (GTN) or diltiazem if high sphincter tone- to help relax
Chronic
same techniques as acute anal fissures
Topical glyceryl trinitrate (GTN) or diltiazem may be continues but mainly
sphincterotomy or botulinum toxin
PROGNOSIS
60% heal their fissure at 6-8 weeks
20% heal after topical diltiazem
some may relapse and 30% require surgery
What is appendicitis
Acute inflammation of the appendix- due to obstruction of the appendixes lumen from faecolith (faeces), infective agents of lymphoid hyperplasia
Affects Men more and usually 10-19 years old
CLINICAL PRESENTATION
Central (periumbilical pain) that migrated to right lower quadrant. worse when cough or move
Anorexia
Nausea and vomiting
Diarrhoea, Constipation
Mild pyrexia (up to 38.5) if higher then mesenteric adenitis more liekly
RLQ tenderness at McBurney point (1/3 lateral from umbilicus towards right ASIS)
Rovsings sign- palpate LIF, pain in RIF
Psoas sign - pain when extend hip
Obturator sign- pain on internal rotation of flexed thigh
Blumberg sign- rebound tenderness in RLQ
INVESTIGATIONS
BLOODS
neutrophil dominant leukocytosis, high CRP
URINE TEST- to exclude pregnancy, renal colic and UTI. will show mild leukocytosis but no nitrites
PREGNANCY TEST- child bearing age with RIF/LIF pain.
US scan (rule out ovarian pathology) in pregnant women- abdo ultrasound is 1st line
Then contrast enhanced CT if inconclusive
if thin male with high likelihood then no scan
If think perforated- erect chest xray
SCORE FOR LIKELIHOOD
Alvarado score
M1A1N1T2R1E1L2S1
Migration fo pain to RLQ
Anorexia
Nausea/vomiting
Tenderness in RLQ 2
Rebound pain
Elevated temp
Leukocytosis 2
Shift left neutrophils
4 or less is low
5-6 moderate chnace
7 is high
MANAGEMENT
1st laparascopic appendicectomy within 24h. give prohylactic ABs to reduce wound infection rate (cefuroxime and metronidazole), keep NBM, analgesia and fluids
If perforated- Copious abdominal lavage and urgent appendicectomy
if dont have peritonitis but have appendix mass- broad spectrum ABs and interval appendicetomy considered
COMPLICATIONS
1- pelvic abscess after appendicectomy- pain fever sweats, mucus diarrhoea. have to drain it
2- perforation which will lead to peritonitis
Good prognosis if in good time. Lap appendicetomy decreases overall complications
What is ascites
Abnormal accumulation of fluid in the abdomen
What are the two groups of ascites
What gradient distinguishes between these groups and how is it calculated
What is the second way to identify the cause
What are the different causes of each group
Serum-ascites albumin gradient SAAG
(Serum albumin)- (ascites albumin)= SAAG
If SAAG over 11g/L the ascitic fluid is transudative/ low protein (CAUSE MEMORY AID: OVER 11 IS LIVER or PRESSURE)
Causes:
- portal hypertension (Caput medusae, ascites and splenomegaly are signs of) can cause oesophageal varices (give terlipressin and IV ABs maybe TIPS. During endoscopy can do variceal bind ligation - if uncontrolled bleeding need sengstaken-blakemore tube. If large varices then beta blockers)
- cirrhosis
- congestive heart failure
- alcohol related liver disease
- liver failure
- budd chiari syndrome (hepatic vein thrombosis)
if SAAG less than 11g/l ascitic fluid is educative so high protein.
- Hypoalbuminaemia (nephrotic syndrome or severe malnutrition like kwashiorkor)
- intra-abdominal malignancy with peritoneal spread
- infections- tuberculosis
Pancreatitis
bowel obstruction
PLEURAL TAP
Exudate (more than 30g protein)
Infection- Pneumonia, lung emphsema, fungal infection
PE
Trauma
Pancreatitis
Transudate (less than 30g)
Cirrhosis
CCF
Nephrotic syndrome
Myxoedema
Meigs syndrome- right side pleural effusion, ascites, benign ovarian tumour
If pleural to serum protein ratio is more than 0.5 and pleural LDH to serum LDH ratio is greater than 0.6= exudate
What is the clinical presentation of ascites
Progression Abdominal Distension→ associated symptoms include early satiety, weight gain, dyspnoea
Shifting dullness (dull to resonant when move from supine to lateral decubitus)
Signs of underlying disease- chronic liver disease (spider naevi, jaundice, palmar erythema), heart failure (high JVP), upper abdo malignancy (virchows node, weight loss)
What are the investigations for ascites
- Abdominal Ultrasound → inital study of choice if suspicion of new-onset ascites
- Ascitic Fluid Analysis → appearance can provide evidence of underlying cause
- Diagnostic Paracentesis → to detect any peritoneal infections
Describe the management of ascites
- Restrict Dietary Sodium
- Spironolactone (Aldosterone Antagonist)
- Side Effects ⇒ hyperkalaemia and gynaecomastia
- Therapeutic Paracentesis→ drainage in tense ascites
- Give IV Albumin when doing large volume paracentesis
- Antibiotics (SBP Prophylaxis) ⇒ ciprofloxacin or norfloxacin
- Fluid restriction in pt with hyponatraemia less than 125
monitor weight daily
Complications → abdominal hernias (esp umbilical hernias), spontaneous bacterial peritonitis (ascitic fluid infection - abdominal tenderness, fever, altered mental status)
What is cholecystitis and its risk factors
- Inflammation of the gall bladder, usually due to cystic duct obstruction by a gallstone
- F over 50 yrs old
- Risk Factors → Gallstones(90% of patients), TotalParaentalNutrition (fasting = gallbladder hypomotility & stasis), Diabetes
What is the clinical presentation of cholecystitis
Pain and tenderness in RUQ
Fever due to inflammation
Palpable mass- distended, tender gallbladder
Right shoulder pain
nauseas, anorexia
Murphy sign - sudden pause nd pain during deep inspiration when palpating gallbladder.when breathes in and hits hand pain
What are the investigations for cholecystitis
1- Abdominal Ultrasound if sepsis not suspected- should show thick gallbladder wall
If US is unclear then technetium labelled HIDA scan
If sepsis suspected then CT or MRI of abdomen
FBC- high WCC and CRP
NORMAL LFT- to exclude ascending cholangitis or choledocholithiasis. If LFT deranged then Mirizzi syndrome which is where a gallstone impacted in cyctic duct compressses the common bile duct
serum lipase- to exclude pancreatitis
What is the management f cholecystitis
NBM, IV fluids, analgesia and IV antibiotics to support patient until surgery
Laparascopic cholecystectomy within a week of diagnosis
What are the complications and prognosis of cholecystitis
if stone moves can become ascendign cholangitis
prognosis- if gallbladder perforates 30% die
What is cirrhosis
Pathological end stage of chronic liver disease
Fibrosis and conversion of normal liver tissue to abnormal nodules called regenerative nodules
What are the risk factors/common causes of cirrhosis
Male
Viral Hep B&C
Alcohol related liver disease
Non-alcoholic fatty liver disease
What is the clinical presentation of cirrhosis
Abdominal distension - secondary to ascites from portal hypertension also due to reduced hepatic excretion of conjugated bilirubin
Jaundice and pruritis (itchy skin)- reduced hepatic excretion of conjugated bilirubin
Encephalopothy- high levels of ammonia = confusion, altered glasgow coma scale, asterixis/liver flap
Blood in vomit- haematemesis, malaena- GI bleed from varices due to PH caused liver cirrhosis
Hand and Nails- leukonychia (white line on nails) due to hypoalbuminaemia, plamar erythma, clubbing, dupuytren contracture (curled fingers from alcholol related liver disease)
Spider naevi- fill from centre
gynocomastia
Hepatomegaly and splenomegaly
A to J
Abdominal distention/ascites, Bile stasis, Calcium and Vitamin D deficiencies, En- cephalopathy, Factors deficiency, and Gastroesophageal varices,
A to J of Liver Failure ⇒ asterixis, bruising, clubbing, dupuytren’s contracture, erythema (palmar), fetor hepaticus (bad breath), gynaecomastia, hepatomegaly, itching, jaundice
What are the symptoms fo portal hypertension
Ascites
Splenomegaly
Caput medusae
Oesophageal and rectal varices
What are the investigations for cirrhosis
-Transient elastography ‘Fibroscan’ to measure liver stiffness or Acoustic radiation force impulse imaging. AS NON INVASIVE
if non alcoholic fatty liver disease: use liver fibrosis score to screen if need further testing
- Liver Biopsy*→ most specific and sensitive test for diagnosis of cirrhosis
- Upper GI Endoscopy → check for varices (swelling of veins in oesophagus and rectum due to portal hypertension) in patient’s with new diagnosis of cirrhosis
- Liver Ultrasound (and AFP) every 6 months to check for hepatocellular cancer
- Bloods
- LFTs → AST & ALT levels increase with hepatocellular damage. Normally ALT>AST except for alcohol-related liver disease. (AST- a shot too many)
- Serum Albumin → reduced. Marker of hepatic synthetic dysfunction.
- PT → prolonged. Marker of hepatic synthetic dysfunction.
- Serum Sodium → reduced. Common finding in cirrhotic patients with ascites. Hypervolaemic Hyponatraemia.
Diagnose SBP through paracentesis
- Child-Pugh Score (severity of liver cirrhosis)- higher the score the more likely they have portal hypertension, oesophageal varices and haematemisis
based on ABCDE
albumin
bilirubin
clotting PT time
Distension (ascites)
Encephalopothy
How is cirrhosis severity measured
Child-Pugh classification system. based on bilirubin, albumin, PT, encephalopathy and ascites
A= less than 7
B= 7-9
C= higher than 9
MELD (model for end stage liver disease)- higher the score the higher the severity
What is the management of cirrhosis
if from ALD- stop alcohol, no cure for Hep b and c infection
TREAT SYMPTOMS
for encephalopathy- lactulose to reduce ammonia absorption. Rifaximin as secondary prophylaxis as stops recurrence
Ascites- sodium restriction, diuretic terapy with spirinolactone. paracentesis to drain
spontaneous bacterial peritonitis (SBP)- prohylactic ABs ciprofloxacin or norfloxacin
surgical- TIPS (tranjugular intrahepatic portosystemic shunt ) to reduce portal hypertension and reduces oesophageal varices risk.
- if already have oesophageal varisces then give terlipressin and IV antibiotics, propanolol as prophylaxis and blood tranfusion if bleeding severe and Hb below 7
liver transplant - if develop hepatocellular carcinoma
What are the complications and prognosis of cirrhosis
ascites
gastro-oesophageal varices which may rupture
Varices can lead to caput medusae
hepatocellular carcinoma
bleeding and thombosis
spontaneous bacterial peritonitis
prognosis- median survival 10 years, depends on stage tho
What is coeliac disease and the risk factors
-Autoimmune disorder characterized by an intestinal hypersensitivity to gluten, causing chronic intestinal malabsorption
- Triggered by Gliadin (protein in wheat)
- F more, any age
- Other autoimmune disorders
What is the clinical presentation of coeliac disease
Diarrhoea- steatorrhea (pale, greasy floaty, bad smelling) from malabsorption
Sudden weight loss
Bloating
Abdonimal Pain
Anaemia - malabsorption symptoms
IgA delficiency- autoimmune attacks
dermatitis Herpetiformis- really itchy papulovesicular lesions on extensor surfcaes like elbows and knees
FHx- osteopenias/osteoporosis (malabsorption of vit D), Fatigue, failure to thrive (delayed puberty)
What investigations are needed if someone is suspected of coeliac disease
SEROLOGY - IgA-tTG (tissue transglutimase) antibodies - will be elevated
anti-endomysial antibodies (EMA) and anti-gliadin antibodies (DGP deaminated gliadin peptide) also elevated. Do EMA if tTG unavailable and DGP if IgA deficient
FBC- low Hb, mcrocytic hypochromic red cells.
Skin biopsy- if any lesions look like dermatitis herpetiformis.
small bowel endoscopy and histology if biopsy anything- GOLD STANDARD TO CONFIRM. scalloping due to villois atrophy, crypt hyperplasia. Histology will reveal intra epithelil lymphocytes, villous atrophy and crypt hyperplaia - have to be eating a gluten diet at the time
blood smear- look for target cells and howell jolly bodies as coeliac can cause hyposplenism
What is the management plan for coeliac disease
Gluten free diet- abstain from wheat, rye, barley, (oats may grow along side so to avoid)
vitamin and mineral supplements
pneumococcal vaccine- functional hyposplenism so risk of pneumococcal sepsis
What are the possible complications and prognosis of coeliac disease
osteoporosis/osteopenia - lack of vit D
Dermaitits herpetiformis
malignancy- enteropathy-associated T cell lymphoma. interepithelial T lymphocytes become malignant
iron/folate/b12 deficiency
prognosis- gluten free die is resolution for most, less than 1% develop refractory coeliac disease
What is colorectal cancer and what are the risk factors
Cancers- usually adenocarcinoma from epithelium cells. 60% rectum and sigmoid, 30% decending.
Most sporadic 95%, 5% hereditary non-polyposis colorectal carcinoma
65-74 years old
RF- age, FHx, familial adenomatous palyposis, associated conditions- IBD and polyps, Alcohol, T2D, Obesity, Lynch syndrome
What is the clinical features of colorectal cancer
Rectal bleeding- mixed in stool
Change in bowel habit- inc frequency or loose stool
Iron Def Anaemia- (fatigue, SOB, pallor)
Tenesmus- feeling of incomplete emptying
FLAWS: fever, lethargy, anorexia, weight loss, sweats
Hepatomegaly- if liver met
Rectal mass- found on DRE
What symptoms of colorectal cancer are more specific for left sided, right sided and rectal cancers
RIGHT SIDED:malaena, iron deficiency anemia, diarrhoea
LEFT SIDED_ change in bowel habit, blood streaked stool mixed in, colicky abdo pain
RECTAL-hamatochezia (bright red blood in stool), rectal pain, tenesmus, flatulence, fecal incontinence
What investigations are used if colorectal cancer is suspected
Colonoscopy + Biopsy -> to diagnose, must take laxatives day before
FBC- microcytic anaemia, low ferritin, LFTs look for mets
CT CAP- look for mets. Dukes staging- A tumour limited to mucosa), B (tumour invading bowl wall), C (lymph node mets), D (distant mets).
Barium enema- apple core lesion from stricture due to mass lesion.
DRE- all with lower GI bleeding or red flags should have
FIT test-
Tumoru markers- CEA monitor disease progression
Any patient over 60 with iron def anaemia or a bowel havit change should be referred for bowel cancer 2 week wait. If have symptoms of possible bowel caner but dont meet 2WW standard then FIT
What is the management plan for colorectal cancer and the complication of this
Surgical excision + adjuvant or neoadjuvant chemo/radiotherapy
Anastomotic leak- complication of bowel resection surgery 5-7 days post operation.will present as diffuse abdo tenderness, guarding, hypotensive and tachy
What are the complications an prognosis of colorectal cancer
Complications-
bone marrow suppression from chemo
GI toxicity from chemo
side effects of immunotherapy drugs
metastases to liver lung, bone, brain
Prognosis- half have mets at diagnosis
What is constipation
Infrequent passage of stool, 3 or less per week
What is absolute constipation
No faeces or flatus
What are the categories of constipation and who are at risk of constipation
Primary Constipation- due to poor diet- lack of fibre, dehydration and insufficient exercise
Secondary Constipation- colorectal cancer, diveticulosis, haemorrhoids, bowel obtruction, hypothyroidism, IBS, opiods
Risk- females over 65, low fibre intake, sedentary lifestyle, medicines- opiates, CCBs, antipsychotics
What are the clinical features of constipation
infrequent stools less than 3 a week
difficult defecation
exessive straining
Tenesmus- incomplete
hard stools
confusion if impactation
Can cause outflow obstruction and cause episodes of urinary retention in pt with enlarged prostate
Bristol stool chart- goes up to 7
Constipation is typically type 1 or 2
- Type 1 - hard lumps, like nuts
- Type 2 - sausage-shaped, but lumpy
Rome IV Diagnostic Criteria for functional constipation
2 of the symptoms in 25% or more of defecations in the last 12 weeks with symptoms at least 6 months ago
symptoms:
<3 stools a week
hard or lumpy
sensation of anorectal obstruction/block
manual aid to evacuate
straining
tenesmus
What are the investigations for constipation
Anal Manometry- for evaluation of constipation or functional anorectal pain
FBC- if think secondary cause like iron deficiency anaemia
TFT- hypothyroidism
AXR- rectal mass or faecal impactation
What are the red flags of constipation in children and adults
CHildren-
delayed meconium over 48 hours
severe abdominal distension
blood in stool
constipated when less than 1 month old
FHx of constipation related disorders like Hirschsprung
Bilious vomiting
fever
failure to thrive
congenital abnormalities
Adults:
FHx- colorectal cancer, IBD
Iron deficiency anaemia
Blood in stool
significant weight loss
sudden onset of new change in bowel habit
over 50 yrs and no cancer screening
Palpable mass
reduced stool amount
rectal prolapse
persistent constipation
What is the management for constipation
Lifestyle-high fibre diet, increased fluid intake, exercise
Bulk laxatives, stool softeners
Osmotic laxative like lactulose
stimulant laxative like senna if lactulose doesnt work
Prunes
opioid induced- review opioid and give laxative. plus lifestyle and diet
not opioid-
1st - treatment of underlying cause, diet and lifestyle and to consider laxative
2nd- osmotic and or stimulant laxative with diet changes
If faecal impaction- evacuation measures
What are the complications and prognosis of constipation
Complication- anal fissure, haemorrhoids, faecal impaction
Prognosis- medical therapy usually effective
What is diverticular disease and the three clinical states
Any clinical state causd by symptoms pertaining to colonic diverticula which are outpouchings of the colonic mucosa
DiverticuLOSIS- presense of diverticula in colon, no symptoms and dont need treatment. can have blood in stools and can lead to diverticulitis
Diverticular DISEASE- symptomatic diverticulosis associated with complications like hameorrhage or infection
DiverticuLITIS- inflammation in one or more of the diverticula- get fever and malaise
most particular found in sigmoid colon and descending colon
What are the risk factors for diverticular disease
over 50 (decreased mechanical strength)
low dietary fibre
constipation
diet high in salt, meat, sugar
obesity
NSAID
opioid use
smoking
What are the clinical features of diverticular disease
LLQ abdo pain - severe
change in bowel habit- becoming constipated
rectal bleeding
nausea and vomiting
leukocytosis- (acute diverticulitis)
fever- fiverticulitis
guarding and tenderness in LLQ- acute diverticulitis
If diverticular disease is suspected what investigations should be done
Contrast CT of Abdomen- if suspected acute diveticulitis and raised inflam markers
Perforation - erect CXR- pneumoperitoneum (air under diaphragm), riglers sign- (double wall sign air on both sides of bowel wall sign of pneumoperitoneum)
Colonoscopy- visualise diverticula
FBC- diverticulitis - high WCC and CRP
Barium enema- saw tooth appearanceof lumen looks like shell necklace
U&E- assess kidney function to know if CT can be performed
Diverticular disease
1st line- FBC to see if diverticulitis, U&E to see if renal function okay for CT, CRP to check for diverticulitis. If suspect then contrast CT of abdo- do abdo US if kidneys not good.If suspect oerforation - CXR. colonoscopy if diagnosis of diverticular disease unclear
What is the management of diverticular disease and diverticulitis
Asymptomatic Diverticulosis- diet and lifestyle, more fibre and fluids
Symptomatic diverticular disease- diet and lifestyle, high fibre
Acute diverticulitis without complications- analgesia, oral antibiotics, oral antispasmodic. If doesnt fix in 72 hours then IV AB (ceftriaxone and metronidazole)
Acute diverticulitis with complication:
bleeding- manage bleed, analgesia, IV AB. 2nd line surgery
abscess, perforation, fistulae- radiological drainage(abscess)/laparotomy surgery (perforation) with IV AB and analgesia
Recurrent attacks or complictions- surgeyr - Hartmanns procedure
What signs are there that there might be a colovesical fistula or colovaginal fistula
Pneumaturia (air/gas in urine) or faecaluria and recurrent UTIs may suggest a colovesical fistula.
Vaginal passage of faeces or flatus may suggest a colovaginal fistula.
What are the complications and prognosis of diverticular disease
Abscesses
Perforation
Strictures- LBO
Fistula formation
Prognosis- most dont need surgery. recurrs in 1/3, after surgery 1/4 symptomatic
What is biliary colic and the risk factors
pain resulting from obstruction from gallbladder or common bile duct, usually bc of a stone so cholelithiasis or choledocholithiasis
Pain results when biliary tree contracts to try to move obstruction
RF- fair caucasian, fat, fertile, forty, female
Oral contraceptive pill, reapid weight loss, sickle cell anaemia. haemolytic conditions= bilirubin breakdown
What two types of gallstones are there
Cholesterol stones 80%- cholesterol and calcium carbonate
Pigment stones- associated with haemolytic conditions such as sickle cell anemia as there is more haemolyisis and therefore more unconjugated bilirubin, composed of calcium bilirubinate
What are the clinical features of biliary colic
Colicky RUQ pain - usually after ingestion of fatty meal
Nausea and vomiting
Pain may radiate to right scapula
Murphys sign negative - no cholecystitis
What investigations should be done if biliary colic is suspected
US scan- might see thin gallbladder wall
MRCP- very sensitive do if US is negative but LFTs are raised or bile duct dilated
LFTs- look for ALP ALT and bilirubin.. should be no abnormal LFT as thats liver damage and inflammation.
What is the management plan for patients with biliary colic
Asymptomatic stones= no treatment
Analgesia, IV fluid, NBM, elective laparascopic cholecystectomy. ERCP can also be used to remove stones or put a stent in blocked duct if stone in CBD. If stones just in gallbladder then elective lap chole is fine
what are the potential complications of biliary colic
Acute cholecystitis
Ascending cholangitis
Acute pancreatitis
Gallstone ileus (pneumobilia= air in biliary stree on CXR and SBO), gallbladder cancer
What are the risk factors of gastric cancer
5th most common cancer, most in asia
men more, over 50
RF- diets high in nitrates/salts like dried foods, smoked foods. Hy.pylori infection, smoking, pernicious anaemia ( Antibodies against gastric parietal cells leading to less IF ad B12 deficiency- macrocytic anaemia from not being able to absorb B12)
Mostly adenocarcinoma in lesser cuvature
What is the clinical features of gastric cancer
Abdo pain- vague epigastric, may present as dyspepsia (indigestion- heartburn, bloating, sickness)
Weight loss
Lymphadenopathy
-(Virchows Node)- swelling in left supraclavicular area is a sign of metastatic gastric malignancy
Sister Mary Josephs Nodule- metastatic node on the umbilicus
Acathosis Nigracans- symmetrical, brown, velvety plaques found on neck, axilla or grin
Krukenberg tumour- ovarian mass due to mets of gastric tumour
RFs are key diagnostic features
What investigations should be done if gastric cancer is suspected
1st- Upper GI Endoscopy with Biopsy: determens if there is cancer. Signet ring cells may be seen (cells look like rings (pale in middle makes outline of ring then nucleus is the signet)
CT CAP- to stage after endoscopy. Important for treatment
MRI are more accurate at identifying metastatic spread to liver
Endoscopic US with FNA- good for staging
Urgent Referral for OGD 2 week if dysphagia and over 55 with weight loss + upper abdo pain/reflux/dyspepsia
What is the management plan for gastric cancer
Surgery- endoscopic mucosal resection, partial gastrectomy, or total gastrectomy
Chemotherapy - inc survival if have mets
monitor FBC with chemo
careful nutrition- monitor B12 if had gastrectomy as may cause neurological symptoms
What are the possible complications and prognosis of gastric cancer
Complications- malnutrition, paraneoplastic syndrom, mets
Prognosis- poor as present late, if diagnosed early 5 year survival is 95%
What is GORD and the risk factors
A chronic condition where stomach contents flow back into the oesophagus
10-30% of people in developed countried
due to transiet relaxation of the LOS
RF- smoking, alcohol, stress, obesity, pregancny, hiatus hernia, older
What is the clinical presentation of GORD
Heartburn- burning retrosternal pain- burning sensarion in chest after meal, can be worse after lying down or bending over
Acid Regurgitation- acid into mout, sour bitter taste usually after meal
Halitosis- bad smelling breath
Waterbrash- inc salivation
Dysphagia (pain swallowing) and dyspepsia
What are the investigation if GORD is suspected
Resolution of symptoms after 8 week PPI trial is gold standard
further test- if doesnt improve with PPI or alarming symptoms
Upper GI endoscopy- do if 8 week doesnt work but stop PPi 2 weeks before, also do if alarming symptoms such as over 55, symptoms more than 4 weeks, nor responding to treatment, dyphagia, relapsing symptoms, weight loss)
Oesophageal Manometry with pH monitoring - do if endoscopy is negative
Barium swallow
What is the management of GORD
Lifestyle- weight loss, stop smoking, smaller and more regular meals, avoid foods that may exacerbate like coffee, acidic fruits, alcohol
Medical- Continue PPi if working, add H2 blocker like randitine. Antacids may be useful for symptom relief
PPIs can cause hyponatraemia SIADH, increase risk of c.diff infections, hypomagnesaemia, risk of osteoporosis and fracture
Surgery- nissen fundoplication. Surgery to increase LOS pressure
Monitor- routine endoscopy to assess progression
What are the complications and prognosis of GORD
Complication- oesophageal or ulcer perforation, oesophageal stricture, Barrets oesophagus (metaplasia squamous to columnar epithelium - inc risk of oesophageal adnocarcinoma), adenocarcinoma of oesophagus
Prognosis- most respond to PPI treatment and relapse if stop
What is gastrointestinal perforation and what are the causes
Perforation of the wall of the GI tract with spillage of bowel contents
Causes
- Large bowel perforation- diverticulitis, colorectal cancer, appendicitis
- Gastroduodenal- perforated gastric ulcer or duodenal ulcer
Small Bowel- trauma, infection Tb, crohns
Oesophagus- boerhaaves perfroation
What are the two types of oesophageal tearing
Boerhaaves Perforation (complete/transmural rupture of oesophagus after repeated vomiting and chronic alcohol use - get sudden chest pain and subcut emphysema (symptoms similar to pneumonia and respiratory distress), diagnose through CT contrast swallow dont do any sticks or tubes bcs perforation. usually distal 1/3 of oesophagus)
Mallory-weiss Tear- longitudinal mucous membrane tear- only mucosa and submucosa, usually at gastric oesophageal junction, causes haematemesis - vomit blood,
What are the clinical features of different gastrointestinal perforation
Large bowel- peritonitic abdominal pain , rule out AAA
Gastroduodenal- sudden severe epigastric pain
Oesophageal- severe pain after violent vomiting, neck chest pain and dysphagia
all unwell with signs of shock, pyrexia, pallor, dehydration, and have signs of peritonitis (guarding, rigidity, rebound tenderness)
What investigations should be done if a gastrointestinal perforation is suspected
Oesophageal tear: Erect CXR- look for pneumoperitoneum, pleural effusion, pneumothorax
CT with oral contrast to confirm or Gastrograffin test
CT with IV contrast- for bowel perforation
Bloods:
FBC- normocytic anaemia
U&E- high ureas suggests upper GI bleed not lower because lower is past kidneys so would digest blood, higher then kidneys will filter and get damaged
LFT amylase raised in perforation
AXR- abnormal gas shadowning, riglers sign (double wall, gas outlining both sides of wall)
Gastrograffin Swallow- if suspect oesophageal perforation
WHat are the management plans of GI perforations
For all: IV fluids and IV antibiotics
Oesophagus- repair of ruptured oesophagus
Gastroduodenal- laparotomy, perforation closed with omental patch, If was a ruptured ulcer due to H.pyrlori then iradicate
Large bowel- resection of perforated part- hartmanns procedure. Periotneal lavage- to evaluate bleeding in abdo cavity
What are the potential complications and prognosis of GI perforations
Oesophageal- meadistinitis, shock, severe sepsis
Bowel- peritonitis
Prognosis
Gastroduodenal- gastric ulcers have higher morbidity and mortality that duodenal
Large bowel-high risk of faecal peritonitis if untreated, death from septicaemia and multi organ failure
What are haemorrhoids and the risk factors
vascular rich connective tissue cusions/lumps within the anal canal that may abdnormally enlarge or protrude
External- below the dentate line- prone to thrombosis, pain potentially
Internal- originate above the dentate line, normally no pain
Classified in grades 1-4
1- do nor prolapse out of canal
2- prolapse on defecation but reduce on own
3- manually reduced
4- cant be reduced
RF- 45-65 years old
from excessive straining from chronic constipation or diarrhoea. an inc in intra-abdominal pressure from pregnancy or ascites, or presence of space occupting lesions inside the pelvis
What are the clinical features of haemorrhoids
Rectal bleeding - bright red bleeding on tissue paper, painless
Perianal pain/discomfort- accompanied with tenesmus
anal pruritus
Tender palpable perianal lesion
Anal mass
Absence of alarm symtpoms
Thrombosed haemorrhoids- lots of pain and tender lump will be purplish oedematous, tender subcut perianal mass
What investigations should be done if haemorrhoids is suspected
Anoscopic Examinaton (pproctoscopy)- 1st line and diagnosis, specific and conclusive for haemorrhoids
Clonoscopy/ Flexible sigmoidoscopy- to exlude IBD cancer, do if have symptoms of changes to bowel habit, abdo pain, weght loss, iron deficiency anaemia
DRE
how are haemorrhoid managed
1st for all- diet and lifestyle - more fibre and water to soften stools
Grade 1- Topical corticosteroids for pruritus
Garde 2-3- rubber band ligation
Grade 4- surgical haemorrhoidectomy
What are the complications and prognosis of haemorrhoids
Complications- anaemia from bleeding, thrombosis, faecal incontinence
Prognosis- good after treatment, low recurrence.
Surgical haemorrhoidectomy is best long term. less than 20% symptom recurrence
How can you distinguish between the cause of hepatitis from investigations, history
Alcoholic- history of long term alcohol misuse or binge
AST is 2 or more times ALT, GGT also raised. Needs alcohol abstinence, nutrition and steroids
non-alcoholic steatohepatitis (NASH) - persistant inflammation causes scarring. Insulin resistance, diabetes, obesity, dont drink alcohol.
AST less than ALT. Diet exercise and RF control
Viral-
-Hep a+E : travel to endemic area/ faeco-oral contaminated water
- Hep B- blood products unprotected sex, male n male sex,
-hep C- blood products, needle sharing, babies
AST and ALT in 1000’s, have viral serology
Drug- paracetomol can cause acute liver failure.
AST and ALT in 1000’s, serum paracetomol conc. if paracetomol overdose potentially give N-acetyl cysteine and anti emetic
Autoimmune- other autoimmune, more women.
AST and ALT, ANA ASMA.
What is autoimmune hepatitis and the types
Autoimmune Hepatitis- chronic inflam disease of the liver. Usually young females
- Type 1 AIH (80%): antinuclear antibodies (ANA) and anti smooth muscle antibodies (ASMA). children and aldults
- Type 2 AIH - anti-liver-kidney microsomal-1 antibodies (anti-LKM-1). only children
is idiopathic and associated with other autoimmune conditions
HLA gene plays a role
What are the clinical features of hepatitis
Hepatomegaly
Jaundice
Amenorrhoea
Pruritis
Spider Angiomata
Ascites
Splenomegaly
Nausea
Fatigue
Abdominal discumfort
What investigations should be done if hepatitis is suspected
LFT- high ALT adnd AST
Serum antibodies
- type 1: ANA and ASMA
- type 2 : anti-LKM-1
Serum protein electrophoresis- high IgG (hypergammaglobulinaemia
Liver Biopsy - to confirm diagnosis. see inflammation and bridging necrosis
Pt elongated
Increased Bilirubin
Decreased serum albumin
GGT and ALP should not be markedly raised. If 3x higher than ALT consider bile duct cause
If travelled recently test for Hep A:
IgM anti HAV- if positive means currently affected
If risk of blood products being shared:
Tests for Hep B:
HBsAg- to look for current infection
HBsAb- look for previous infection but could just be vaccine
HBcAb- look for previous infection, not vaccine
HBeAg- see how infective as indicates how fast replicating
HBeAb- whether clearing
HBV DNA- see the viral load
Test for Hep C:
HCV Ab enzyme immunoassay- indicates that there is or was an infection
HCV RNA PCR testing- indicates current
If been travelling, undercooked seafood, faecal oral like hep A
Test for Hep E:
IgM anti HEV. Dangerous for pregnent woman as leads to liver failure
What is the management plan of autoimmune hepatitis
Corticosteroids- prednisolone
Immunosuppressants- azathoprine
Liver transplant
What are the complications and prognosis of hepatitis
Complications- treatment side effect
Prognosis- mod to severe respond in 2 weeks and after 12 months ALT and AST are in normal range
What is ischaemic hepatitis and what marker signifies it
Ischaemic Hepatitis- occurs following acute hepatic hypoperfusion. high AST and ALT levels 1-3 days after insult. Very high LDH- usually means hepaitits
What is the treatment for viral hepatitis
if acute normally resolved by itself
Hep B and C may become chronic so would need and antiviral if body cant clear after 6 months
What are hernias and what are the types
Condition in which part of an organ is displaced and protrudes through the wall of the cavity containing it
Inguinal hernia- abdominal or pelvic contents protrudes through the inguinal canal. Most common type
- Direct Inguinal Hernia: protrusion through the posterior wall of the inguinal canal- only through the superficial inguinal ring. Develops over time due to straining and is caused by weakness in abdominal. Usually older men. Medial to inferior epigastric vessels
Within hesselbachs triangle - inferior epigastric artery, rectus border and inguinal ligament
- Indirect Inguinal Hernia: protrusion into the inguinal canal through the deep inguinal ring. caused by defect in abdominal wall that may have been present since birth, an affect infants. Lateral to inferial epigastric vessels
When reduced and pressure is applied to deep inguinal ring, indirect hernia will remain reduces but direct will reappear
- Femoral hernia- inferolateral to pubic tubercle (inguinal are superiomedial to pubic tubercle
-Strangulated hernia: blood supply cut off and hernia contents become ischaemic
What are the risk factors for hernias
Male, age, obesity, reaised intra-abdo pressure(long term cough), chronic constipation, family history, AAA, marfans syndrome, Ehlers Danlos syndrome, prematuriy
femoral hernia more common in women
What is the clinical presentation of hernias
Inguinal Hernias:
dull, heavy, dragging pain in association with a bulging hernia
visible + palpable groin mass (enlarge with standing or coughing)
nausea and vomiting, constipation (strangulated)
Femoral Hernia:
non reducible
cough impulse absent
What investigations are needed when a hernia is suspected
Clinical diagnosis- observe and palpate
Ultrasound scan of groin- if uncertain
Ct scan if obese
Blood test will show leukocytosis and raised lactate if strangulated hernia
What is the management plan for hernias
If small and asymptomatic- watchful waiting
Treat all if fit for surgery- surgical repair with mesh if large/ symptomatic
If unfit for surgery - can leave inguinal hernias and use Truss support belt. Femoral hernias MUST be operated on due to risk of strangulation
If obstructed/strangulated- emergency laparotomy
- Incarceration: where herniated tissue cant be reduced, pain but no systemic features
- Strangulation- blood supply cut of, leads to ischaemia of hernia, usually if femoral. Tender, distended abdomen with absent bowel sounds and systemic features
What are the complications of hernia surgery and the prognosis
Post op complications: urinary retention, wound seroma (fluid collections), inguinal wound haemotoma, wound infection, bowel obstruction, dysejaculation (burning)
Division of the vas deferens, vascular injury.
Mesh infection, groin pain
Prognosis- excellent after surgery
What is a hiatus hernia and the types
Protrusion of abdominal contents into the thorax- usually the stomach
-Sliding Hiatal Hernia: 95% GOJ moves above the diaphragm
-Rolling Hiatal Hernia- GOJ stays under diaphragm but a separate part of the stomach herniates through the oesophageal hiatus (more urgent as volvulus can result in ischaemia and nerosis)
What are the risk factors of hiatus hernias
Obesity, GORD, increased intra abdominal pressure- pregnancy, ascites, chronic cough or constipation
What are the clinical features of hiatus hernias
Heartburn, dysphagia(difficult to swallow), odonophagia(pain swallowing, regurgitation, SOB, chronic cough, chest pain
GORD symptoms- worse when lying flat
Hiccups
What investigations are used when hiatus hernia is suspected
Barium swallow- assesses type and size of hernia- sensitive test
Upper GI endoscopy- due to symptoms most have this first
CXR- retrocardiac bubble
What is the management of hiatus hernia
conservative- weight loss and PPI 4-8weeks
Surgery (rolling)- laparoscopic/open fundoplication (nissen), hiatoplasy if symptoms persist after conservative
What are the complications and prognosis of hiatus hernias
Complications- GORD usually causes sliding complications,
upper GI bleeding, gastric ulcers, gastric volvulus
If just sliding- symptoms better with medical therapy
Hernia repair with anti reflux procedure gives long term cure
What is infectious colitis and the risk factors
Inflammation of the colon due to bacteria, parasites or viruses
RF- lack of sanitation, drinking contaminated water, antibiotic use
What type of infectious colitis is commonly found in hospitals, why its found in hospitals, and what is the danger
C.difficile which causes pseudomembranous colitis. Will find a gram positive rod
RF- antibiotics and PPI
antibiotics like ciprofloxacin, clarithromycin, clindamycin, cephalosporin
Can cause perforation or toxic megacolon (use AXR and CT- see yellow plaques on intraluminal wall of colon on sigmoidoscopy)
What are the symptoms of infectious colitis
Diarrhoea- watery or blood stained
Blood in mucus and stool
Lower abdo pain
Malaise and fever
What organisms cause infectious colitis
CHESS
Campylobacter
Haemorrhagic e.coli
Entamoeba Histolytica
Salmonella
Shigella
What investigations should be used if infectious colitis
Stool culture- c.diff toxin to be identified but c.diff antigen positivity only shows exposure to the bacteria rather than current infection. Check for raised WCC too.
AXR- show toxic megacolon if c.diff severe
Colonoscopy- cisualise inflammation
Ask about travel history
What is the management plan for infectious colitis
Hydration for lost fluids
Loperamide- anti diarrhoea
Antibitics- depending of infectious agent
C.diff= Oral vancomycin for 10 days, if doesnt respond fidaxomicin. If doesnt respond to either then oral vancomycin +/- metronidazole. NO OPIOID as can ic bacterial uptake in gut
What is Inflammatory Bowel Disease
Affects the digestive system inlcludes two issues:
1) Crohns
2) Ulcerative Colitis
What is Crohns disease and the risk factors
Disorder of unknown aetiology caused by transmural (non caeseating) granulomatous inflammation of the GI tract
Any part of GI tract usually terminal ileum and colon
Characterised by skip lesions, cobblestone mucosa (looks like bubbling ulcers whereas UC looks like flat ulcers), string sign on barium swallow
Th1 mediated
RF- white, FH of Crohns, 15-40 years and 60-80, SMOKING
How does crohns disease present
RLQ Abdo pain- defecation makes better
Prolonged diarrhoea (no blood)
Perianal lesions- skin tags, fistulae, abscesses, scaring
Lethary
Malabsorption- weight loss and anemia (affects all layers)
Fatigue, fever, lethargy
Symptoms away from intestinal symptoms: motuh ulcers, arthropathy (joint pain), skin lesions (erythema nodosum- shins) and pyoderma gangrenosum (leg ulcers). Anterior uveitis (painful red eye with loss of vision and photophobia), episcleritis (painless red eye).
What investigations are used if crohns disease is suspected
Colonoscopy + biopsy- deep ulcers, skip lesions and cobblestone appearance
Histology- transmural inflammation with non-caseating granulomas
Barium enema- kantor’s string sign and rose thorn ulcers
Faecal calprotectin- raised in IBD not IBS
FBC_ anaemia from inflammation and chronic blood loss, iron malabsorption, B12/folate malabsorption
Increased CRP and ESR- inflam markers
Stool microscopy and culture - exclude infection
Serum vitamin B12 (absorbed in terminal ileum which crohns affects) and folate- reduced
Plain AXR or Ct abdomen
How is crohns diseases managed
induce remission with corticosteroids: prednisolone or budenoside
Maintain Remission with Immunomodulators- Azathiprine 1st line, IF NOT methotrexate. Stop smoking
Biologics- Infliximab
No surgery as skip lesions
What are the complications and prognosis of crohns disease
Complications- small bowel obstruction (strictures and fistulae formations), anemia (lack B12), malignancy, kidney stones, gallstones, perianal fistula (fistulotomy or draining seton with MRI to visualise and) and abscess (incision and drainage)
Prognosis- chronic disease, relapse and lots of complications
What is ulcerative colitis and the risk factors
A type of IBD that involves the rectum and extends proximally to affect a variable length of the colon.
If affects just rectum- proctitis
Affects part of colon (left sided colitis
Entire colon- pancolitis
Never goes past ileocaecal valver unless its backwash ileus
Only involves colonic mucosa
20-40 years or older than 60
RF- genetic predisposition (HLA-B27), white, FH of IBD.
Smoking is protective effect
What is the clinical presentation of ulcerative colitis
Bloody diarrhoea- episodic or chronic
LLQ pain
weight loss
rectal bleeding- mild disease may have intermittent rectal bleeding associated with mucus.
Abdominal pain and cramps
Extraintestinal symptoms:
Joint- peripheral arthritis and akylosing spondylitis
Skin- erythema nodosum and pyoderma gangrenosum
Occular- episcleritis more common than uveitis (painless red eyes more common than painful)
What investigations are needed for ulcerative colitis
Colonoscopy and biopsy- continuous distal disease, no granulomas, crypt abscesses, depletion fo goblet cells
If severe colitis- flexible sigmoidoscopy may be done as colonoscopy may cause perforation
Faecal calprotectin- high (makes sure not IBS)
Stool Microscopy and culture- rule infection
LFT- primary sclerosing cholangitis
Bloods- high ESR and CRP, anaemia, leukocytosis
AXR- thumbprinting, loss of haustra, toxic megacolon, psudopoyps
Toxic megacolon- massive transverse colon, loss of haustra, NBM IV fluids, NGT, no colonsscopy)
Barium enema- lead pipe appearance
How is the severity of ulcerative colitis classified
Mild <4 bowel movements per day, small amounts o blood, no temp, no change in pulse rate, no anemia, ESR 30 or lower
Moderate 4-6 bowel movments per day, some blood, o temp, no change in pulse rate, no anemia, ESR 30 or lower
Severe 6+ per day plus : visible blood in stool, pyrexia, pulse rate higher than 90bpm, anemia, ESR over 30
How is ulcerative colitis managed
MILD TO MODERATE UC
5-ASA (mesalazine) topical if distal or oral if more severe (topical if proctisis or proctosigmoiditis, topical+ oral if left sided or extensive). If topical mesalazine doesnt induce remission then add oral mesalazine then oral corticosteroid
Maintain with oral/topical mesalazine or with azathioprine if severe relapse or 2 or more exacerbations in one year
ASA can cause agranulocytosis so monitor FBC
SEVER UC
IV corticosteroids (hydrocortisone) or IV ciclosporin if not improving or worsening.
IV fluids
NBM
Infliximab
If doesnt improve then urgent colectomy
Total colectomy= cure
What are the complications and prognosis of ulcerative colitis
Complications:
Colonic Adenocarcinoma
Toxic megacolon
Primary sclerosing cholangitis :inflammation and fibrosis of intra and extra-hepatic bile ducts. UC + Cholestasis (ie. jaundice and pruritus. Raised ALP and GGT). ERCP/MRCP can be used to diagnose, showing ‘beaded’ appearnace of biliary structures. Associated with p-ANCA and ASMA. Can lead to cholangiocarcinoma (PSC is main risk factor for cholangiocarcinoma, raised CA19-9 levels).
Prognosis- same as people without UC
What is IBS and the risk factors
Chronic condition characterised by abdominal pain and associated bowel dysfunction
20-39 Female (over 50 is unusual)
RF: under 50, female, previous enteric infection, history of physical or sexual abuse, FHx, stress
What are the clinical features of IBS
Abdominal Discomfort- cramping in lower abdomen, relieved by defecation
Change in bowel habits associated with pain- defecation relieves
Abdominal Bloating/Distension- improved with defecation or farting
Mucus in stool
Eating makes worse
Alternates between diarrhoea and constipation
ABC (abdo pain, bloating, change in habit) for at least 6 months
no blood( blood in UC and cancer), not more frequent at nigh (crohns), no weight loss (colorectal carcinoma, crohns, UC), no anamia (crohns, severe UC)
What criteria is used to diagnose IBS
Rome IV(4)
Recurrent abdominal pain on average 1 day week at least during last 3 months associated with 2 or more of:
pain on defecation
change in stool frequency
change in stool form or appearance
What investigations should be used if IBS is suspect
FBC- normal, if abnormal then not IBS
Faecal Calprotectin- should be normal, if raised then some sort of bowel inflammation
Faecal occult blood test
Coeliac screen IgA-TTG
CRP, ESR
What is the management of IBS
Lifestyle- fibre, manage stress, educate and reassure
If mostly constipated- laxatives. use bulk-forming laxative like ispaghula, avoid laculose (makes gas worse)
If diarrhoea- antidiarrhoeals like loperamide
Antispasmodics for pain
What are the complications and prognosis of IBS
Complications- diverticulosis, depression, sleep disorders, damage to fam and work relationships
Prognosis- no long term complcations. symptoms tend to recur particularly with stress, emotional difficulty or dietary indiscretions
What is liver failure and the classifications
Severe liver dysfunction leading to jaundice, encephalopathy and coagulopathy
Hyperacute = less than 7 days
Acute= 1-4 weeks
Subacute= 4-12 weeks
Chronic= progressive deterioration of hepatic function over at least 26-28 weeks (6 months)
- Stigmata of Chronic LIver disease= spider naevi, gynaecomastia, dupuytrens contracture, palmar erythema
- Sign of decompensation= ascites, jaundice, encephalopathy
What are the usual causes of liver failure
Viral Hepatitis (a/b)
Paracetomol overdose
Idiopathic
Alcohol excess
Acute fatty liver of pregnancy
What are the clinical features of liver failure
Jaundice- less conjugated bilirubin, causes pruritus
Encephalopathy- ammonia not being removed, so lose consciousness- can lead to cerebral oedema- toxins in brain lead to problems with function so cause asterixis
Coagulopathy- liver (vit K) clotting factors (2,7,9,10). Life threatening bleeds
Nausea and vomiting
Fever lethargy malaise
Acute fatty liver pregnancy- jaundice following abdo pain and pruritis during pregnancy
What investigations should be done if liver failure is suspected
PT- raised= coagulopathy, best indicator of liver function
LFTs- high bilirubin, AST, ALT, ALP, GGT. Low albumin (leukonychia)
Hypoglycaemia
Viral serology, paracetomol levels- look for cause
EEG- monitor encephalopathy
What is the management of liver disease
N-acetylcysteine (for paracetomol overdose)
Encephalopathy- give lactulose. IV mannitol can help to reduce cerebral oedema
Coagulopathy- vitamin K and FFP
Liver transplant- considered for most
What are the complications and prognosis of liver failure
Complications- infection, coagulopathy, cerebral oedema (raised ICP), respiratory failure
Prognosis- depends
What is malabsorption, the types and the difference between malabsorption and maldigestion
Malfunction of the intestinal wall resulting in insufficient absorption of breakdown products (happend in IBD, Coeliac, lactose intolerance)
Global malabsorption- in diseases causing diffuce mucosal damage or reduction in absorptive surface like coeliac disease
Partial malabsorption - localised absorption impairment resulting in deficiencies in specific nutrients (vit B12 in IBD or terminal ileum affected issues)
Maldigestion- insufficient secretion of pancretic enzymes or bile preventing adequate breakdown of food in intestinal lumen (exocrine pancreas insufficiency or cholestasis)
What is the clinical presentation of malabsorption
Diarrhoea
Steatorrhea- floating and foul smelling
Abdominal Distension
Weight loss and fatigue
Partial malabsorption- sympoms specific to nutrient deficiencies
What investigations are used to diagnose malabsorption
Blood tests- anaemia, vitamin deficiencies
D-xylose absorption test- test absorptive function of upper small intestine
What is the management for malabsorption
Oral supplementation of fluid, nutrients and vitamins
Calorie and protein enriched diet
Severe cases- IV nutrition
What is malnutrition and the risk factors
Important concequence of and contributor to chronic disease
1 of the following:
- BMI <18.5
- Unitntentional weight loss more than 10% within last 3-6 months
- BMI less than 20 and unintentional weight loss more than 5% within last 3-6 months
10% of people over 65 are malnourished with most living independently
RF_ crohns, dysphagia, socially isolated, low income
How do patient who are malnourished present
Unintentional weight loss
lack interest in eating and drinking
Feel tired all the time
Feel weak all the time
Getting ill often and taking long to recover
What investigations are used if malnutrition is suspected
MUST- malnutrition universal screen tool
- should be done if admitted to nursing homes or hospital or if concerned
- Used BMI, recent weight change and present of acute disease
- characterises into risk
What is the management plan for malnourished patients
Dietician support
Food first approach with clear instructions (do this before supplements)
Oral Nutritional Supplements- taken between meals - not a replacement
If severe- feeding tube (enteral (food through GI tract) or paraenteral (iv into a central vein)
- enteral feeding can cause diarrhoea
- total paraenteral used in nutritionally compromised surgical patients
What are the complications of a patient being malnourished and treating them and how to prevent this
Refeeding syndrome- metabolic abnormalities which occur after feeding someone after starvation
Hypophosphataemia, hypokalameia, hypomagnesiumaemia (low magnesium= torsades de pontes)
Prevention- if a patient hasnt eaten for more than 5 days, aim to refeed at 50% or less of requirements for first 2 days
What is mesenteric Adenitis, causes and rf
Inflammation of lymph nodes in the intra abdominal mesentery
recent viral intestinal infection like gastroenteritis (MOST COMMON CAUSE)
children and teenagers mostly
mimics appendicitis sometimes
What are the clinical features of mesenteric adenitis
Abdo pain- RLQ but can be widespread
General abdo tenderness
fever
mesenteric lympth node enlargement
Diarrhoea and vomiting sometimes
history of recent viral intestinal infection
What investigations are used if mesenteric adenitis is suspected
Abdominal ultrasound
Bloods
what is the management plan of mesenteric adenitis
Often self limiting- doesnt need treatment
Paracetomol or ibuprofen for pain
Drink lots of fluids
Antibiotics if caused by bacterial infection
What are the types of oesophageal cancer
more common in men 60-70 yrs
Squamous cell carcinoma (upper2/3): RFs alcohol, smoking, diet low in fruit+veg, HPV, Hot beverages
Adenocarcinoma (lower 1/3): Rfs obesity, male, GORD, Barretts oesophagus, hiatus hernia
What is the clinical presentation of oesophageal cancer
Progressive dysphagia- first difficult to swallow solids then liquids too
Odynophagia- pain when swallowing
Rapid Weight loss- stop eating and cancer multiplying
Signs of Advanced disease: hoarseness (recurrent laryngeal nerve pressed means SCC as upper 2/3 affected), Horners syndrome (ptosis, miosis and anhidrosis)
Signs of upper GI bleeding: Haemetemesis, melaena, raised urea (may have anaemic symptoms like fatigue or SOB)
What investigations are used when oesophageal cancer is suspected
Upper GI Endoscopy with biopsy- gold standard for pt with dysphagia odynophagia and weight loss
CT CAP/MRI for staging to treat
What is the management plan for oesophageal cancer
Surgery- oesophagectomy with adjunct chemotherapy
Chemoradiotherapy is better than radiotherapy alone
EITHER: preoperative chemoradiotherapy then surgery OR surgery and then perioperative chemotherapy
What are the complications and prognosis of oesophageal cancers
Complications- postop pneumonia, aspiration pneumonia, post-resection reflux
Prognosis- poor due to aggressive course and late presentations
How can you tell between achalasia and oesophageal cancer.
What is achalasia, the investigations and management
Achalasia is incomplete relaxation of the LOS (inc pressure of LOS)
Dysphagia is not progressive in achalasia unlike oesophageal cancer, will have dysphagia of solid and liquid from the start in achalasia
Investigation: Manometry- finds increased resting pressure on LOS
Barium swallow; birds beak appearance (narrowed at LOS)
CXR- wide mediastinum, fluid level
Management of achalasia: penumatic dilation or hellers cardiomyotomy to relieve pressure on LOS)
What is the most common from of pancreatic cancer and the risk factors
Primary Pancreatic ductal adenocarcinoma
presents at 60-80 yrs
RF_ smoking, FHx, chronic pancreatitis, high alcohol consumption, T2DM, obesity, inherited genetic syndromes
What are the clinical features of pancreatic cancer
Painless jaundice (if painful then usually obstruction)
Palpable mass in RUQ
Pale stools (reduces stercobilinogen)
Dark urine (reduced urobilinogen + increased conjugated bilirubin in urine)
If cancer at head of pancreas then bile flow obstructed- jaundice
Pruritus- may have scratch marks, because of bile salts in circulation
Non specific upper abdo pain or discomfort (if back pain the retroperitoneal metastases)
Weight loss and anorexia
Courvoisers Law = palpable gallbladder in a pt with painless obstructive jaundice is usually malignancy
If pancreatic cancer is suspected what investigations are needed
High red Abdo Ct scan- find mass in pancreas. will have a double duct sign showing dilation of both pancreatic and common bile duct
Abdo US if CT unavailable- detect mass, dilated bile duct and liver mets
LFTs- degree of obstructive jaundice. Bilirubin, ALP, GGT, elevated in obstructive jaundice. ALT may be slightly elevated but thats liver
CA 19-9 biomarker
What is the management plan for pancreatic cancer
Whipple’s resection (pancreaticduodenectomy)- performed for resectable lesions at head of pancreas. May cause dumping syndrome (food from stomach to bowel to fast, can cause tachy and diarrhoea), may also cause peptic ulcer disease
- Give adjuvant chemotherapy after surgery
ERCP with stenting for palliative
What are the complications and prognosis of pancreatic cancer
Complication- surgical comp;ications (pancreatic leaks and fistula), cholangitis, DVT and PE, duodenal obstruction
Prognosis- aggressive treatment and poor prognosis as present late
What is peptic ulcer disease and gastritis and the RFs
PUD= ulceration of the GI tract, due to exposure to gastric acid and pepsin. Peptic ulcers : duodenal ulcer more common than gastric ulcer
Gastritis- histological presence of mucosal inflammation
Duodenal ulcer- 30 yrs old
Gastric ulcer 50yrs old
Common causes; Helicobacter pylori and NSAID use
other RFs: smoking, older, had PUD before, FHx PUD, patient in intensive care
What are the clincial features of peptic ulcer disease
Epigastric pain- gnawing
- Gastric ulcer- pain right after meals (weight loss)
-Duodenal ulcer- pain a few hours after eating (pain may be relieved by eating so weight gain)
-Perforated ulcer- acutely unwell and haemodynamically unstable (arrythmia, consciousness level, peripheral cyanosis)
Epigastric tenderness
What are the clinical features of gastritis
Nausea, vomiting and loss of appetite so may lose weight
What investigations are used if PUD or gastritis is suspected
Upper Gi endoscopy- will show ulcerations and can biopsy for H.pylori. Do this immediately aka same day if have acute GI bleeding and dyspepsia
Helicobactor pyrlori carbon-13 urea breath test or stool antigen test- use if after endoscopy still unsure whether infected with H.pylori. cant have PPI for 2 weeks and ABx for 4 weeks for this test to work
Erect CXR-
-pneumoperitoneum = perforated duodenal ulcer.
- Dome sign= perforated gastric ulcer
Raised urea= upper GI bleed
Faecal Occult Blood test
FBC- only if has Gi bleeding or seems anaemic
What is the management plan of peptic ulcer disease
Lifestyle: less smoking and alcohol intake
H,pyrlori positive: TRIPLE THERAPY (PPI aka omeprazole + ABx amoxiccillin + broad ABx Clarithromycin) - if allergic to penicillin then metrandazole. 1 week course, twice daily
H.pylori negative: atrop drug causing e.g. NSAID, offer ulcer healing therapy which is 4-8 weeks of PPi therapy (omeprazole 20mg)
- For gastric ulcers repeat endoscopy 6-8 weeks later to ensure healing and rule our malignancy
-For duodenal ulcers repeat urea breath test for h.pylori 6-8 weeks later.
What are the complications and prognosis of PUD and gastritis
Complication-
Upper GI Bleeding
- Haemorrhage causes haematemesis, meleana and anaemia
- Perforation- shock and peritonitis
Prognosis- with PPI duodenal heal in 4 weeks and gastric 8 weeks
What is a perianal abscess
A pus collection in the perianal region
Anal abscesses are the acute manifestation of a purulent infection in the perirectal area
30-60% of anal abscesses progress into anal fistulaes
What is a perianal fistulae
An abnormally chronically infected tract communicating between the rectum and the perineum
Anal fistulaes are the chronic manifestation of purulent infections
What are the causes and risk factors of perianal abscess and fistulaes
Men 20-60 years old
Cause: flow obstruction and bacterial infection of the anal crypt glands.
Less common cause: IBD (Crohns> UC), diverticulitis, appendicitis and malignancy
What are the clinical features of perianal abscesses and fistulaes
Perianal abscess- dull perianal discomfort and pruritus. Erythematous, subcutaneous mass near the anus. Purulent discharge, Fever and malaise as its an infection
Perianal fistula- pus drainage (discharge) from anal canal or surrounding perianal skin. Causes pain on defecation. Constant throbbing pain that worsens when sit down. Smelly discharge
ON DRE- fluctuant (pressure to one end of lsion transmits pressure to every other point thats swolln), indurated mass (thick and hard). Pain with pressure
What investigations should be done if anal fistula or abscesses are
Clinical examination first/DRE
then:
CT/MRI or Anal ultrasonography: tests to confirm deeper abscesses
MRI pelvis: best investigation to characterise fistulae course
Further testing with endoscopy, MRI, fistula probe to identify other possible fistulae and comorbidities like cancer or IBD
What is the management plan for anal abscesses and fistulae
SURGERY- surgical incision and drainage of abscess under local anaesthetic (to prevent spread of infection =sepsis risk). After surgery sitz baths, analgesics+ stool softeners, antibiotics (ONLY ABs IF IMMUNOCOMP)
Fistulotomy- cutting alond the length of the fistula to open it in order for it to be drained
IF complex perianal fistulae (e.g. in crohns)= seton placement- a piece of surgical thread run through fistula to allow continuous drainage while the fistula heals- it makes sure fistula doesnt heal with pus still inside.
What are the complications and prognosis of perianal abscesses and fistulae
Complications- recurrence, damage to internal anal sphincter, incontinence, persisting pain
Prognosis- high recurrence rate if not completely excised
What is peritonitis
Inflammation of the peritoneal lining of the abdominal cavity, can be localised to a part of peritoneum or generalised
Localised= appendicits, cholecystitis and diverticulitis
Spontaneous bacterial peritonitis- usually seen in patients with ascites, secondary to liver cirrhosis. Due to infection of the ascitic fluid. Escherichia coli most common
What are the clinical features of peritonitis
Abdo pain/ tenderness
Ascites
Fever
nausea and vomiting, diarrhoea, altered mental status
What investigations are needed if peritonitis is suspected
Paracentesis (ascitic fluid absolute neutrophil count)- >250 cells/mm^2 is diagnstic for sprontaneous bacterial peritonitis
Ascitic fluid culture- determine the causitive organism
What is the management plan of peritonitis
Empirical IV Antibiotics with cefotaxime
IV Albumin
If ascitic fluid protein conc <15g/Lor had a previous episode of SBp then continuous antibiotic prophylaxis (oral ciprofloxacin or norfloxacin)
what are the complications and prognosis or peritonitis
Complications- sepsis, renal failure
Prognosis- 69% recurrence in one year. Renal dysfunction predicts mortality
What is Vitamin B12’s role
Vit B12= Cobalamin
Role in RBC formation and myelination of the nervous system
In animal products
Absorbed in terminal ileum and requires IF
What are some of the causes of B12 deficiency
Pernicious Anaemia- autoantibodies against IF made by gastric parietal cells. Inc risk of gastric cancer, may have other autoimmune discorders
Post gastrectomy (gets rid of gastric parietal cells)
Vegan diet
Terminal ileum affected conditions- crohns disease or ileocaecal resection
What are the clinical features of vitamin B12 deficiency
Anaemia signs- fatigue, pallor, SOB
Peripheral neuropathy- tingling, numbness, paraesthesia
Demantia
Glossitis (may present as sore tongue)
What is folates role
Folate= Vitamin B9
Essential coenzyme that enables critical biochemical reactions for DNA synthesis and amino acid metabolism
From green leafy veg, fruits, liver, bread, cereal
What are some of the causes of folate deficiency
Malabsorption aka in small bowel disease from IBD or coeliac disease
Malnutrition from chronic alcohol use
Increased requirement from pregnancy
Drug related- methotrexate or antiepileptics
What are the clinical features of folate deficiency
Signs of anaemia- fatigue, pallor, SOB
Glossitis
Fetal spina bifida (neural tube defects) if maternal deficiency
NO NEUROLOGICAL SYMPTOMS
What are the investigations if Vit B12 or folate deficiency is suspected
Signs of macrocytic, megaloblastic anaemia: low Hb, high MCV, hyperchromic RBC, hypersegmented neutrophils
Vit B12 pernicious anaemia- test for anti-IF or antiparietal cell (anti-IF is more specific)
Homocysteine- elevated in both deficiencies
Methylmalonic acid (MMA)- elevated in B12 normal in folate
What is the management plan of Vitamin B12 and folate deficiency
Vit B12 def- IM supplementation of Vit B12 (hydroxocobalamin)
Folate- oral folate supplementation, nutritional councelling to inc folate in diet
- folate given to preg women as risk of neural tube defect such as spinal bfida and anencephaly (400mcg folic acid until 12th week of preg)
REPLACE B12 BEFORE FOLATE PROTECTS AGAINST SUBACUTE COMBINED DEGENERATION OF THE CORD
