GI Flashcards
What are the causes of hepatomegaly?
…
What are the management plans for Gastro-Oesophageal Reflux Disease (GORD)?
What are the drugs to avoid?
Lifestyle changes
No alcohol
No fizzy drinks, tomatoes, citrus fruits,
- Medications*
1. Antacids: magnesium trisilicate mixture etc. 10ml/8h or Alginates: Gaviscon 10-20ml/8h
2. PPI: Lansoprazole 30mg/24h or Omeprazole
3. If either PPI doesn’t work, swap to the other one. Try not to give dual PPI at this stage
4. If both don’t work, add ranitidine.
Drugs to avoid
Avoid drugs that affect oesophageal motility like anticholinergic drugs, CCB,
Avoid drugs that disturb mucous lining (NSIADS, bisphosphates, K+ drugs)
What is the MOA of omeprazole?
It irreversibly binds (via covalent bonding) to H+/K+ proton pump channels on gastric parietal cells to inhibit H+ release into the stomach. Omeprazole also inhibits both basal and stimulated acid secretion irrespective of the stimulus.
It is completely metabolised by the P450 cytochrome system, mainly in the liver. Main metabolites are sulfone and hydroxy-omeprazole. Both exert no significant impact on acid secretion.
Effects of inhibition start 1h after administration, reaches a maximum after 2h, wear off after 72h.
What is the MOA of Azathioprine?
Inhibits purine synthesis. Purines are needed to produce DNA and RNA. By inhibiting purine synthesis, less DNA and RNA are produced for the synthesis of white blood cells, thus causing immunosuppression.
Azathioprine is in the purine analogue and antimetabolite family of medication. It works via 6-thioguanine to disrupt the making of RNA and DNA by cells.
Azathioprine converted within tissues to 6-mercaptopurine => add amino acid group => thioguanine => 6-MP and 6-thioguanine are conjugated with ribose => phosphorylated to form the nucleotides thioinosinic acid and thioguanylic acid respectively => masquerade, respectively, as inosinic acid (starting point for purine biosynthesis) and guanylic acid (impt for DNA and RNA biosynthesis) => nucleotides are incorporated into newly synthesized but non-functional DNA => inhibition of the glutamine phosphoribosyl pyrophosphate transaminase (GPAT) aka product inhibition (i.e negative feefback)
A portion of the nucleotides is additionally phosphorylated to the triphosphate forms => bind to GTP-binding protein Rac1 +> block synthesis of the protein Bcl-xL => send activated T cells and mononuclear cells into apoptosis. Increased apoptosis of mononuclear cells is seen in IBS patients treated with azathioprine.
What are the effects of anti-cholinergic drugs on oesophagus motility and the lower oesophageal sphincter (LES)?
Oesophageal motility
Anti-cholinergics, in particular anti-muscurinic drugs, reduce oesophageal motility.
In man, atropine sulfate administered intravenously in doses of 6 and 12 µg/kg decreases the amplitude of the peristaltic contraction waves by about 50 p. cent for about one hour. The speed of propagation is slowed at the transition zone between the smooth and striated muscle. The incidence of primary complete peristaltic sequences provoked by swallowing is reduced to only 60 p. cent, compared with a rate of almost 100 p. cent after administration of isotonic saline
LES
Atropine provokes a 42 p. cent fall in basal pressure of the LES over about an hour.
The relaxation, which is the second essential property of the LES, is not affected by atropine during its activation by swallowing or esophageal distension. Indeed, relaxation is under the influence of putative, noncholinergic nonadrenergic neurotransmitter(s).
What is the MOA of ranitidine?
Competitive and reversible blocker of H2 histamine receptors, which are commonly found in gastric parietal cells. This results in decreased gastric acid secretion and gastric volume, and reduced hydrogen ion concentration.
What are the drugs to avoid in patients with GORD?
Drugs that affect oesophageal motility: anticholinergic drugs, CCB, nitrates
Drugs that disturb mucous lining: NSIADS, bisphosphates, K+ drugs
What are the causes of hepatomegaly?
- Chronic parenchymal liver disease (Cirrhosis)
a. Alcoholic liver disease
b. Fatty liver disease
c. Autoimmune hepatitis
d. Viral hepatitis
e. Primary biliary cirrhosis/primary biliary cholangitis - Malignancy (Cancer)
a. Primary Hepatocellular carcinoma
b. Secondary metastatic cancer - Congestion/Cardiac
a. Congestive heart failure
b. Constrictive pericarditis - Haematological disorders
a. Lymphoma
b. Leukaemia
c. Polycythaemia
d. Myelofibrosis - Rare issues
a. Sarcoidosis
b. Amyloidosis
c. Budd-Chiari Syndrome (narrowing and obstruction of the hepatic veins)
d. Glycogen storage disorders
e. Haemochromotosis
What are the causes of splenomegaly?
- Portal Hypertention
- Haematological issues
a. Lymphoma and lymphatic leukaemia
b. Myeloproliferative disorders, myelofibrosis and polycythaemia rubra vera
c. Haemolytic anaemia
d. Congenital spherocytosis - Infections
a. Salmonellosis, tuberculosis, brucellosis
b. Glandular fever
c. Malaria, kala-azar (leishmaniasis)
d. Bacterial endocarditis - Inflammation
a. Amyloidosis
b. Sarcoidosis
c. Glycogen storage disorders - Andersen disease - Rheumatoid issues
a. Rheumatoid arthritis (Felty’s syndrome)
b. SLE
What do the following terms mean?
Cholangitis Cholecystitis Calculous cholecystitis Cholelithiasis Choledocholithiasis Cholestasis
Cholangitis = obstruction of the biliary tree, which may lead to bile stasis and subsequent bacterial infection.
Cholecystitis = Inflammation of the gall bladder
Calculous cholecystitis = inflammation of the gall bladder resulting from gallstones obstructing the cystic duct
Choletithiasis = Gallstones in gall bladder
Choledocholithiasis = Gallstones in common bile duct
Cholestasis = Reduction or stoppage of bile flow
What is the triad of symptoms typical of cholangitis called? What does it consist of?
Charcot’s triad. Abdominal pain, fever, jaundice
If patient has Primary Sclerosing Cholangitis (PSC) and has IBD such as UC, what is he/she at risk of?
Colorectal malignancy
What are the top causes of liver cirrhosis?
Most common causes:
- Alcohol
- Hep B/C
- Non-alcoholic liver disease (NASH)
Genetic:
* Haemochromatosis - Iron dependent
* Wilson’s disease - Copper deposition in the brain which causes extra-pyramidal symptoms
Alpha-1 anti-trypsin deficiency (A1AT deficiency)
Autoimmune hepatitis
Respiratory:
Emphysema of the lung
Inflammatory: * PBC * PSC TB Schistosomiasis
Drugs:
Methotrexate
*Amiodarone
Rare causes:
Andersen Disease - glycogen storage disorder
Lympho-proliferative disease
What are the risk factors of metabolic syndrome? What are the investigations to do next?
Risk factors:
Fatty liver
Hyperlipidaemia
Diabetes
Ix:
LFTs
What is a common cause of deranged LFTs?
Non-alcoholic fatty liver disease (NASH)
When is nortriptyline only given?
When the patient is in pain
What are the only two treatments for liver disease?
Weight loss and liver transplant
What are the blood tests that can be done in a patient with cirrhosis?
Mitochondrial antibody
ANA - Anti nuclear antibody
ANCA - Anti neutrophil cytoplasmic antibody
SMA - Smooth muscle antibody
Liver kidney microsomal antibody - associated with autoimmune hepatitis
Hep B core antibody
Hep B surface antigen
Hep C antibody
Alpha-1 anti trypsin Wilson's screen - ceruloplasmin Copper Ferritin - always done in a liver screen Transferrin saturation Immunoglobulin
Clotting screen
FBC
INR
What is the cremasteric reflex? What does an absent cremateric reflex mean?
Cremasteric reflex = stroking the inner thigh on one side results in the ipsilateral testis contracting as a result of the cremaster muscle
Absent cremasteric reflex may indicate:
- Corticospinal tract lesion above L1
- Multiple Sclerosis (but not always)
- Lesion in reflex arc
- Local surgery
- Testicular torsion
What is CTAP? What is its purpose?
CTAP = Computer Tomography Arterial Portography
Its purpose is to detect liver tumours and parenchymal disorders
What is the Alvarado score for appendicitis?
MANTRELS
Migration Anorexia Nausea and vomiting Tenderness in RIF Rebound tenderness Elevated temperature (>38 degree Celcius) Leukocytosis (WBC>10) Shift to left (neutrophils >75%)
What is ESR? In what conditions are ESR raised? In what other conditions are ESR lowered?
Erythrocyte sedimentation rate (ESR)
Raised ESR
Inflammation (e.g. infection, MI, malignancy, RA)
Anaemia
Macrocytosis
Lowered ESR
Polycythaemia due to increased RBC concentration
Microcytosis
Sickle-cell anaemia
List the definition, aetiology/risk factors, presenting symptoms, signs, investigations, managements, complications, prognosis and epidemiology of this conditions:
Gallstones/Cholangitis
Refer to edited Laz’s notes
What is the Sepsis 6?
3 In:
IV antibiotics
IV fluids
Oxygen
3 Out:
Blood culture
Serum lactases
Urine output
What does MRCP and ERCP stand for?
ERCP = Endoscopic Retrograde Cholangiopancreatography MRCP = Magnetic Resonance Cholangiopancreatography
What are the signs of liver decompensation?
Ascites
Jaundice
GI bleed
Encephalopathy
What are the two most common surgical causes of upper abdominal pain?
gallstone disease and peptic disease.
Others include PUD/GORD, pancreatitis, biliary pathology, abdominal wall,vascular, small bowel and large bowel disease (small and large bowel relatively rare).
What is the most common non-surgical cause of upper abdominal pain?
Cardiac Gastroenterological Musculoskeletal - osteochondritis/costochondritis Diabetes Dermatological
What is the most representative of liver function? Prothrombin Time? Albumin? AST ALT Bilirubin Alkaline phosphatase Gamma GT
If the PT climbs by more than 1 s per hour, must refer for hospital transplant. If the PT is fine, the patient is fine for now.
What is the Antidote for paracetamol overdose?
N-acetyl cysteine
Treatment for Nash?
Stop alcohol
Nutrition
Vitamins (B1, thiamine, pabrinex)
What are the three signs of portal hypertension?
Ascites
Splenomegaly
Visible veins such as caput medusa
What is the immediate treatment for oesophageal varices?
Sengstaken-Blakemore tube => open balloon and stop the bleeding
What is the substance that causes pruritus in obstructive Jaundice?
Bile salts/acids. Add NaOH and bile acid will become bile salt. Therefore, bile acids and salts mean the same thing.
What is IGF-1? Where is it produced? What stimulates it?
Insulin-like Growth Factor 1. Produced in the liver. Growth Hormone stimulates it. IGF-1 is a primary mediator of the effects of growth hormone (GH). Growth hormone is made in the anterior pituitary gland, is released into the blood stream, and then stimulates the liver to produce IGF-1. IGF-1 then stimulates systemic body growth, and has growth-promoting effects on almost every cell in the body, especially skeletal muscle, cartilage, bone, liver, kidney, nerve, skin, hematopoietic, and lung cells. In addition to the insulin-like effects, IGF-1 can also regulate cellular DNA synthesis
What are the causes of portal hypertension?
Pre-hepatic Portal vein thrombosis Splenic vein thrombosis Splenomegaly Arteriovenous fistula
Hepatic
Post-hepatic
What are some drugs that can cause liver damage (drug-induced liver injury and cirrhosis)
Chronic DILI: Methotrexate Atorvastatin Amoxicillin-clavulanic acid Bentazepam hypervitaminosis A, herbal products, dietary supplements vinyl chloride heroin
Cirrhosis: Methotrexate Amiodarone Isoniazid Ticrynafen Enalapril Valproic acid
What are the signs of Klinefelter’s syndrome? What is its chromosomal pattern?
47, XXY.
Baldness, testicular atrophy, female styled pubic hair in pubic region, very tall, breast development, slightly feminised appearance, poor beard growth, osteoporosis, shortened 4th metacarpal, tendency to lose chest hair
What are the signs of Turner’s syndrome? What is its chromosomal pattern?
45, XO
Short stature, shield-shaped thorax, poor breast development, widely spaced nipples, no menstruation, skin fold at neck, low hairline, distinctive facial features, shortened 4th metacarpal, short fingernails, constriction of aorta
