Gastroenterology Flashcards
How would you characterise the causes of dysphagia
Extrinsic
Intrinsic
Oesophageal wall
Neurological
Extrinsic causes of dysphagia
Mediastinal mass
Cervical spondylosis
Intrinsic causes of dysphagia
Tumours
Strictures
Oesophageal wall causes of dysphagia
Achalasia
Hypertensive LOS
Neurological causes of dysphagia
Stroke
Parkinsons
Myasthenia gravis
CVA
Achalasia - characteristics
Difficulty swallowing both solids and liquids
Pathgnomenomic sign of achalasia
Barium study - Bird beak appearance of the oesophagus - Dilated proximally and tapers distablly
How to differentiate achalasia and pseudoachalasia (Oesophageal cancr)
red flag symptoms of cancer - specifically rapid weight loss, Anorexia, Vomitting
What is the mechanism of action of achalasia
Impaired relaxation of the lower oesophageal sphincter
What scoring system is used to triage the severity of Acute pancreatitis
Modified Glasgow score
What is the threshold of the Modified Glasgow score to assess the severity of developing a complication in a patient diagnosed with acute pancreatitis
MGS >3 - At risk of a severe complication
What are the components of the Modified glasgow score to deleniate risk of developing severe pancreatitis
Age > 55 - 1
wcc >15
Glucose >10
LDH >600
AST >200
Serum calcium <2
Albumin <32
(Score of >3 - High risk of developing a severe complication)
How would you characterise the complications of Acute pancreatitis
Local vs systemic
Local complications of acute pancreatitis
1) fluid collection arouns the pancreas
2) Pseudocyst - Conservative management
3) Abscess (Infected pseudocyst)
4) Pancreatic necrosis:
- Sterile necrosis - conservative management
- Infected necrosis - Necrosectomy (hight mortality)
5) Haemorrhage - Sign - Grey turner sign due to retroperitoneal haemorrhage
Systemic complications of Acute pancreatitis
ARDS
- Sudden onset central cyanosis, tachypnoea and SOB
How to Diagnose C.DIFF
Stool sample - +ve for C.Diff Toxin (A/B)
NB - C.Diff antigen +ve means previous exposure (Important in Abx mgt)
What is the classification of Mild C.diff
Normal WCC
What is the classification of Moderate C.DIFF
WC >15X10^9
What is the classification of severe C.Diff
WCC >15 + Fever >38.5
What is the classification of Life trheatening C.DIFF
1) Haemodynamic compromise
2) CT Findings of Severe C.DIFF
3) Toxic Megacolon
4) Complete Ileus
What is the most common cause of C.diff
2nd/3rd gen cephalosporins
What are the causes of C.diff
1) 2nd/3rd gen cephalosporins
2) Clindamycin
3) PPI’s
1st line management of C.diff (Mild - Severe)
Oral Vancomycin
Management of C.diff
1st line - Oral Vancomycin
2nd line - Oral fidoxamicin
3rd line Oral van +/- IV Metronidazole
Management of recurrent C.diff
Within 12 weeks - Oral Fidoxamicin
Afer 12 weeks - Oral Vanc or Oral Fidoxamicin
Management of Life threatening C.diff
Oral Vancomycin + IV Metronidazole
What is the mainstay management of Coeliac disease
Gluten free diet
What grains include gluten
Wheat
Barley
Oats
Rye
What grains are gluten free
Rice
Potatoes
Corn
How do you diagnose coleiac Disease
1st line - Anti-Tissue tranglutaminase Ab - aTTG-IGA
If patients have liver disease, or have an IgA deficiency then TTG-IGA will be false -ve hence need to sue:
- TTG-IgG
How is aTTG-IgA used in coeliacs disease
Diagnosis and to ensure compliance with a gluten free diet
Why are patients with Coeliac disease at higher risk of developing infections caused by encapsulated bacteria
Functional Hyposplenism
Four examples of encapsulated bacteria
Nisseria Meningitidis
Haemophilus Influenza Type B
Strep Pneumonia
E.coli
Vaccinations recommended for coeliac patients
Pneumococcal vaccine one off and booster every 5 years
What are the causes of ischaemic hepatitis
Ischaemic event - I.e cardiac arrest
How does Ischaemic hepatitis present
Post hypoperfusion event resulting in ACUTE rise in Liver function tests (ALT)
-Usually seen in conjunction with acute kidney injury (Tubular necrosis) and other end-organ failure
What causes carcinoid syndrome
Neuroendocrine tumour which is either the primary or metastasized to the liver
Pathophysiology of carcinoid syndrome
NET’s secrete horomones - Serotonin, Bradykinin and Histamines
These result in the manifestation of the signs seen in Carcinoid syndrome
What are the characteristics of cacinoid syndrome
Bradykinin/Histamine:
- Hypotension - Vasodilation
- Facial Flushing
-Bronchoconstriction, Wheeze
Serotonin
- Fibrosis - Heart - Right side - Tricuspid regurgitation/Pulmonary stenosis
- Reduces tryptophan levels - resulting in Vitd D3 deficiency - Phallegra - Diarrhoea, Dermatitis and dementia
What can exacerbate carcinoid syndrome
Exercise
Alcohol intake
Emotional distressH
How do you diagnose Carcinoid syndrome
24 hour - Urinary 5-Hydroxyindolacetic acid (5-HIAA) which is a byproduct of metabolised serotonin (Raised)
How to treat carcinoid syndrome (Symptom control VS Curative)
Symptom control - Somatostatin analogue - Ocreotide
Curative - Surgical removal of the neuroendocrine tumour (Increased somatostatin receptors)
What is spontaneous bacterial peritonitis
It is a form of infective peritonitis seen in patients who have ascites secondary to cirrhosis
How would you categorise the different causes of ascites
By quantifying the Serum-Ascites Albumin Gradient.
Cut off is 11g/L
Causes of ascites in patients with a SAAG of >11G/L
Ascites due to portal hypertension:
- Liver:
a) Acute liver failure
b) Decompensated liver cirrhosis
-Cardiac
a) Right heart failure
Other:
a) Portal venous thrombosis
b) Budd chiari malformation
Causes of ascites in patients ith a SAAG of <11g/L
Nephrotic syndrome
Severe malnutrition
Malignancy
Pancreaititis
Bowel obstruction
How does SBP present
Ascites + Abdominal pain + Fever
What is the most common bacteria causing SBP
E.COLI
How to Diagnose SBP
Paracentesis which shows Neutrophil count of >250units/L
How to treat SBP
IV Cefotaxime
Antibiotic prophylaxis of SBP indications
Previous SBP
Ascites with:
- Fluid Protein <15g/l
- Child-Pugh score >9 (Class B/C)
- Hepatorenal syndrome
What is the antibiotic of choice for prophylaxis against SBP
Oral ciprofloxacin
What is hepatorenal syndrome
It is classified as acute renal failure secondary to Hepatic impairmentP
Pathophysiology of Hepatorenal syndrome
Splanchnic vasodilation results in activation of the RAAS sysytem resulting in renal vasoconstriction and subsequent renal hypoperfusion
Categorise hepatorenal syndrome
T1HRS - Acute within 2 weeks the CrCL drops to <20 or the Cr Doubles
T2HRS - Chronic
Characteristics
Signs of hepatic impairment along with rising creatinine levels and oligouria
Treatment of hepatorenal syndrome
1) Volume expansion - HAS
2) Splanchnic vasoconstriction - Terlipressin (1mg IV over 4-6hours)
3) Definitive - Liver transplant
What are anal fissures
Eliptical tears of the anoderm
Where are anal fissures usually found
90% - Posterior Midline of the anus
10% -Else where -Think IBD if else where
Aeitiology of Anal fissures
Main - Idiopathic
RF’s - Contipation/Trauma
Secondary:
-IBD - Crohn’s»_space;> UC
- Malignancy
- Infectious - Syphylli, HIV, HSV
Symptoms of anal fissures
Pain - Pain on defacation is the main debillitating symptom
PR BLeeding - Scanty, Fresh red blood, usually on wipin or in the bowl
Discharge - Pus
Pruritus Ani
Constipation - Pain can result in avoidance of defecation
DDX of anal fissures
Haemerrhoids - Painless unless thrombosed
Anal fistula?
Management of acute (<6weeks) of anal fissure
Diet - High fibre diet
Laxatives:
-1sT Line - Bulk forming laxative (Isphagula Husk - Fybogel)
2nd line - Lactulose
Petroleum jelly prior to defacation as lubricant
Management of chronci (>6weeks) anal fissure
1st line - Topic GTN ointment (Minimum 8 weeks trial)
2nd line - Botulinum toxin vs surgical spyncterectomy
