Abdominal Flashcards
Definition of Gastro-esophageal reflux disease (GERD)
Condition in which stomach contents flow back into the esophagus, causing irritation to the mucosa. Reflux is primarily caused by an inappropriate, transient relaxation of the lower esophageal sphincter.
Gastro-esophageal reflux disease (GERD) presentation, investigations and treatment
Presn: retrosternal burning pain (heartburn) and regurgitation, presentation is variable and may also include chest pain and dysphagia.
Ix: esophagogastoduodenoscopy and/or 24hr pH test.
Rx: PPIs (e.g. pantoprazole), lifestyle modifications, medication, in some cases surgery.
GERD complications
Complications: esophagitis and chronic mucosal damage can cause barretts esophagus, a premalignant condition that can progress to adenocarcinoma.
Peptic ulcer disease etiology
Presence of one or more ulcerative lesions in the stomach or duodenum. Etiologies include infection with H pylori (most common), prolonged NSAID use, condition associated with overproduction of stomach acid (hypersecretory states) and stress.
Peptic ulcer disease treatment
Rx: Symptom control (e.g. acid lowering medication - antacids), H pylori eradication therapy (clarithromycin + amoxicillin + PPI) and withdrawal of causative agents. Antisecretory drugs (eg PPIs) which reduce stomach acid production, are continued for 4-8 weeks after eradication therapy and may be considered for maintenance therapy.
Coeliac disease pathophysiology
Maladaptive immune response to gluten, a protein found in many grains.
Often occurs in patients with other autoimmune illnesses, associated with HLA variants.
Gluten intolerance triggers an autoimmune reaction and production of autoantibodies that target tissue transglutaminase, specifically within the proximal small intestine.
Coeliac disease presentation, investigations, treatment
Presn: change in bowel habits and symptoms assoc w malabsorption (e.g. fatigue, weight loss, vitamin deficiency).
Ix: diagnostic tests include the detection of various antibodies, to confirm the diagnosis, an endoscopic biopsy from the small intestine is needed. Histopathological changes include villous atrophy and crypt hyperplasia.
Rx: Gluten free diet, if adhered to, increased risk of celiac-associated malignancies (e.g. intestinal lymphoma) is mitigated.
Hepatitis A transmission
Faecal-oral, endemic in tropical, subtropical regions
Hep A disease course and symptoms
Acute viral hepatitis, initial prodromal symptoms (fever and malaise) followed by jaundice. Self-limited, acute liver failure rarely occurs.
Prodromal symptoms resolve within 1-2 wks, jaundice can persist for 1-3 months.
Hep A diagnosis
Lab findings include high serum transaminase levels and mixed hyperbilirubinemia. Serological detection of anti-HAV IgM antibodies confirms diagnosis.
Hepatitis B transmission
Transmitted sexually, parenterally or vertically. After an intubation period of 1-6 months, most patients develop asymptomatic or mild inflammation of the liver, which resolves spontaneously within a few weeks to months. However, 5% of adult patients and 90% of infants infected perinatally develop chronic hep B.
Hepatitis B treatment
Supportive measures. For chronic active Hep B, nucleoside or nucleoside analogs (e.g. tenofovir) are the preferred agents for reducing viral replication and infectivity.
Hepatitis B Investigations
Serological testing initially includes measurement of Hep B surface antigen (HBsAg), hepatitis B surface antibody (anti-HBs) and hepatitis B core antibody (anti-HBc). A detectable serum anti-HBs (indicating seroconversion) is a sign of recovery or successful immunization.
Hepatitis C transmission
A bloodborne pathogen commonly transmitted through needlestick injuries in health care settings or through shared injection needles.
Hepatitis C disease course and presentation
Attacks liver cells and causes liver inflammation.
2wk to 6month incubation period. Malaise, fever, myalgias, arthralgias, RUQ pain, tender hepatomegaly, nausea, vomiting, diarrhea, jaundice, pruritus.
Screening plays a role in detecting HCV infection because most infected individuals are asymptomatic or mildly symptomatic.
Approx 85% of individuals with an acute infection that is not recognised and treated will develop chronic Hep C, which is associated with cirrhosis, hepatocellular carcinoma and increased mortality. Mixed cryoglobulinemia, lymphoma (esp B cell non-Hodgkin lymphoma), membranoproliferative glomerulonephritis + many more
Hepatitis C investigations
Presence of HCV antibodies and HCV RNA confirm the diagnosis. HCV infection can be safely and effectively treated with direct acting antivirals which have cure rates of over 95%
Alcohol related fatty liver disease investigation results
AST>ALT (both elevated). Elevated GGT, elevated serum ferritin, macrocytic anemia, elevated CDT. US; mild hepatomegaly, blood vessels cannot be visualized, increased liver echogenicity because of steatosis. CT; decreased liver attenuation. Transaminase levels, imaging studies
Non-alcoholic fatty liver disease pathophysiology
Excess energy supply -> insulin resistance -> increased circulating dietary sugars and FFAs -> hepatic FFAs -> triglyceride synthesis -> hepatic steatosis. MASH cirrhosis; oxidative stress, ER stress and inflammasome activation -> inflammation and hepatocyte stress and/or death -> fibrogenesis -> cirrhosis
Non-alcoholic fatty liver disease investigation results
Normal or increased AST and/or ALT. AST/ALT ratio usually <1, AST/ALT ratio of >1 may indicate progression to cirrhosis. Normal or decreased serum albumin. CBC: normal or decreased platelet count
Non-alcoholic fatty liver disease definition
Accumulation of excess fat in hepatocytes in individuals with at least one cardiometabolic RG (e.g. HTN, impaired glucose tolerance) in the absence of an alternative cause (e.g. heavy alcohol uses, drug induced liver injury). MASH(NASH); chronic hepatocellular inflammation and damage.
Cirrhosis clinical findings (5)
Jaundice
Hepatosplenomegaly
Ascites
Skin changes (spider angiomata, palmar erythema, caput medusae)
Hormonal changes (gynecomastia, hypogonadism, sexual dysfunction)
Abdominal distension.
Hepatocyte damage investigation findings (2)
Elevated liver enzymes
Hyperbilirubinemia
Impaired hepatic synthetic function investigation findings (2)
Prolonged prothrombin time
Low albumin
Cirrhosis diagnosis confirmation
Abdominal ultrasound - shrunken heterogenous liver parenchyma with a nodular surface.
Liver biopsy if results from other diagnostic modalities are inconclusive
Primary hepatocellular malignancy presentation
HCC usually asymptomatic in early stage, ascites, jaundice
Advanced HCC; abdominal pain, weight loss, anorexia
Most common malignant liver lesion
Metastatic liver disease
Typical primary tumor sites for metastatic liver disease (3)
GI tract (colon, stomach, pancreas)
Lung
Breast
Metastatic liver disease abdominal ultrasound findings
’Bullseye’ with a hyperechoic center and hypoechoic periphery.
Metastatic liver disease CT abdomen findings
Recommended imaging modality for suspected liver metastases, multiple hypodense lesions (rarely; solitary metastases)
Is viral or bacterial leading cause of infective gastroenteritis? and what are the most common pathogens? (4)
Viral - Norovirus, rotavirus, enteric adenovirus, CMV.
Infective gastroenteritis bacterial pathogens (7)
Campylobacter
Salmonella
Shigella
Yersinia
Vibrio cholerae
E coli
Clostridioides difficile
Infective gastroenteritis alarm symptoms & criteria (9)
Sepsis,
Intense abdominal pain
Severe dehydration
Electrolyte abnormalities
Age >65
Pregnancy
Weight loss
Bloody stool/rectal bleeding
Abnormal renal function.
Infective gastroenteritis investigations in severe or immunocompromised
Stool cultures followed by empiric Abx therapy may be considered
Crohn’s disease gene association
HLA-B27 association
Crohn’s disease basic pathophysiology
Unrestrained Th17 cell function leading to inflammation, tissue damage, obstruction, fibrotic scarring, stricture and strangulation of bowel
Ulcerative colitis definition
Inflammatory bowel disease characterised by chronic mucosal inflammation of the rectum, colon and cecum.
15-35yo and >55yo M=F.
HLA-B27 association.
Smoking ad appendectomy are protective factors.
Ulcerative colitis location and disease spread
Ascending inflammation beginning in rectum and spreads continuously proximally. Inflammation limited to mucosa and submucosa.
Ulcerative colitis common symptoms (4)
Bloody diarrhea
Abdominal pain
Tenesmus
Fecal urgency
Ulcerative colitis treatment
5-aminosalicylic acids (e.g. mesalamine) are the mainstay of Rx for mild to moderate disease. Severe; corticosteroids or other immunosuppressants.
Proctocolectomy is curative and indicated in patients with complicated UC or dysplasia.
Irritable bowel syndrome symptoms
Chronic abdominal pain - cramping sensation, periodic exacerbations, pain freq related to defacation, either relieved or worsened, altered bowel habits - diarrhea, constipation or mixed. Bloating, abdo distension and flatulence. Diarrhea - loose stools, small to mod volume, urgency after meals, sometimes tenesmus.
IBS rome III criteria
(I) improvement after defacation, (II) onset of symptoms asssoc w bowel freq. (III) onset of symp. Assoc. w change in stool appearance
IBS treatment
Low FODMAP diet, adequate fibre intake, Gentle laxatives (constipation pred.) vs loperamide (diorrhea pred.), Peppermint oil, hyoscine butylbromide (buscapan), mebeverine, Psychological therapies. Modification of gut microbiota
Risk factors for GERD (4)
Obesity, stress, eating habits (e.g. heavy meals, lying down shortly after eating), changes in anatomy of the esophagogastric junction (e.g. hiatal hernia).
