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
