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