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Phase 1 Exam > GI > Flashcards

GI Flashcards

1
Q

Definition of pancreatitis

A
  • Acute: Acute inflammation of the pancreas, usually occurs over days/weeks and can be mild and self limiting but sometimes severe. It can be recurrent but isn’t common.
  • Chronic: Chronic inflammation leads to the irreversible loss of pancreatic function, usually occurs over years (With recurrent acute episodes).
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2
Q

Aetiology of pancreatitis

A
  • Acute: Gall stones, alcohol, trauma, steroids, mumps, autoimmune conditions, scorpion venom, hyperlipidaemia, ECRP and drugs.
  • Chronic: Most commonly due to alcohol abuse but can be autoimmune. Usually presents in 30’s/40’s.
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3
Q

Pathophysiology of pancreatitis

A
  • Acute: premature activation of pancreatic enzymes due to injury leading to autodigestion and necrotic tissue.
  • Chronic: Replacement of functional pancreatic tissue with fibrous scar tissue over time.
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4
Q

Presentation of pancreatitis

A
  • Acute: Severe upper abdo pain radiating into the back, with nausea/vomiting/fever. Can have be hypotensive, tachycardia and show jaundice. Also possible for abdo distention with/without reduced bowel sounds.
  • Chronic: Persistent severe abdo pain with dull pain in between severe episodes, with weight loss. Also sterrhoea and diabetes when most of the gland is destroyed.
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5
Q

Investigations of pancreatitis

A
  • Increased serum amylase levels are diagnostic for pancreatitis.
  • Abdo exam, LFTs
  • MRI/CT/US of pancreas
  • Biopsy
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6
Q

Mangement of pancreatitis

A
  • Acute: Analgesics, oxygen, fluids, treat gallstones, drain cysts or surgery to remove necrotic tissue.
  • Chronic: Supportive - use of replacement pancreatic enzymes, analgesics, antibiotics, screen for diabetes and potential to remove pancreas.
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7
Q

Definition of pancreatic cancer

A
  • Usually primary pancreatic ductal adenocarcinoma.
  • 5th most common cancer, higher incidence in men than women, increases with age, with patients usually presenting over the age of 60.
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8
Q

Aetiology of pancreatic cancer

A
  • Hereditary or environmental (smoking/obesity).

- Link with chronic pancreatitis due to pre malignant nature.

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9
Q

Pathophysiology of pancreatic cancer

A
  • 65% in head of pancreas, 15% in body, 10% in tail and 10% multifocal.
  • Usually has lymph node metastases, potential to invade vasculature and periureal.
  • Mets usually liver, lungs, brain and skin.
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10
Q

Presentation of pancreatic cancer

A
  • In the head: painless jaundice due to common duct obstruction and weight loss.
  • In the tail/body: Weight loss, abdo pain and anorexia.
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11
Q

Investigation of pancreatic cancer

A
  • US with/without spiral contrast CT.
  • ERCP can be used for palliative care.
  • CA19 - 9 marker is sensitive but not specific.
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12
Q

Management of pancreatic cancer

A
  • Prognosis is poor with local invasion (8 - 12 month) or mets (3 - 6 months).
  • MDT for palliative care - chemo/radiotherapy.
  • Surgical resection is the only curative way.
  • ERCP can be used for jaundice relief.
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13
Q

Risk factors of pancreatic cancer

A
  • Smoking, obesity, family history, diabetes and certain dietary factors.
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14
Q

Definition of oesophageal cancer

A
  • Mucosal lesions in the epithelial cells lining the oesophagus.
  • Usually seen in men more than women.
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15
Q

Aetiology of oesophageal cancer

A
  • Squamous cell carcinoma - linked with increased consumption of salted fish, pickled veg, v hot liquids and food.
  • Adenocarcinoma - linked with Barret’s metaplasia, linked with smoking and obesity.
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16
Q

Pathophysiology of oesophageal cancer

A
  • Barrett’s oesophagus is caused by acid causing metaplasia to the epithelial cells in the oesophagus.
  • Comparison between junction cells - epithelial and glandular.
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17
Q

Presentation of oesophageal cancer

A
  • Progressive dysphagia and weight loss.

- Bolus food impaction or local invasion can lead to chest pain.

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18
Q

Investigations of oesophageal cancer

A
  • OGD and tumour biopsy.

- CT abdo/chest for staging and looking for mets.

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19
Q

Management of oesophageal cancer

A
  • Poor prognosis: surgical resection with pre op chemo with/without radiotherapy.
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20
Q

Definition of gastric cancer

A
  • Stomach cancer is a neoplasm that occurs anywhere in the stomach, usually adenocarcinoma and can invade the lymph nodes and other organs.
  • Increase incidence in age and affects men more than women.
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21
Q

Aetiology of gastric cancer

A
  • Unknown, could be associated with H.pylori.
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22
Q

Risk factors of gastric cancer

A
  • Lifestyle (smoking, diets low in fruit/veg, high in salts, smoked foods), pericineous anaemia, family history and partial gastrectomy.
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23
Q

Pathophysiology of gastric cancer

A
  • H pylori long term infection can cause intestinal metaplasia.
  • Tumour usually starts in situ in the mucosa - if pre mucosa then early and invading the muscle wall is late.
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24
Q

Presentations of gastric cancer

A
  • Pain similar to peptic ulcer, with nausea, weight loss and anorexia.
  • If the tumour is near the pylorus it can lead to outflow obstruction, causing dysphagia and vomiting.
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25
Q

Investigations of gastric cancer

A
  • Gastroscopy and biopsy for diagnosis.

- Laproscopy and CT for staging.

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26
Q

Management of gastric cancer

A
  • Surgical resection with chemo.

- Poor prognosis

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27
Q

Definition of acute appendicitis

A
  • Caused by an obstruction of the appendix lumen due to faecloth.
  • Can occur at any age but quite rare in the very young and very old.
  • Peak incidence is between 5 to 15.
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28
Q

Aetiology of acute appendicitis

A
  • Obstruction caused by the faecloth, undigested food or enlarged lymphoid tissue.
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29
Q

Risk factors of acute appendicitis

A
  • Smoking, low fibre diet, breastfeeding for less than 6 months or improved personal hygiene.
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30
Q

Pathophysiology of acute appendicitis

A
  • The obstruction by the faecloth or undigested food leads to superimposed infection in the mucosa that then spreads through the rest of the appendix.
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31
Q

Presentation of acute appendicitis

A
  • Central abdo pain in the umbilical region then spread to the right iliac fossa.
  • This is combined with potential anorexia, diarrhoea and vomiting.
  • The patient is usually pyrexic with tenderness and guarding of the right iliac fossa due to localised peritonitis.
  • If appendix abscess is present then there would be a large palpable mass.
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32
Q

Investigations of acute appendicitis

A
  • C reactive protein, ESR and white cell count would be raised to indicate infection.
  • Ultrasonography shows inflamed appendix.
  • CT = both highly sensitive and specific.
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33
Q

Mangement of acute appendicitis

A
  • Removal with open surgery/laparoscopy.

- If mass present then treat conservatively with IV fluids/antibiotics then remove.

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34
Q

What is the portal vein formed from?

A
  • Superior mesenteric vein and the splenic vein, and carries blood to the liver.
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35
Q

What is the normal portal vein pressure?

A
  • Between 5 and 8 mmHg.
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36
Q

What types of obstructions lead to portal hypertension?

A
  • Prehepatic ( block to the portal vein before the liver) , intrahepatic (leading to distortion of the liver architecture) and posthepatic (blockage of the venous drainage after the liver).
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37
Q

What causes portal hypertension?

A
  • Most commonly caused by cirrhosis.
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38
Q

How does portal hypertension present?

A
  • Splenomegaly, GI bleed, ascites or hepatic encephalopathy.
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39
Q

Definition of Hepatocellular carcinoma

A
  • 5th most common cancer.

- Geographical difference due to exposure to Hep B/C.

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40
Q

Aetiology of Hepatocellular carcinoma

A
  • Usually seen in patients with chronic liver disease, cirrhosis or those with viral hep.
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41
Q

Presentation of Hepatocellular carcinoma

A
  • Weight loss, abdo pain, ascites, anorexia, fever.

- Rapid development is indicative of HCC.

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42
Q

Investigations of Hepatocellular carcinoma

A
  • Serum bloods could indicate AFP.
  • US/CT imaging.
  • Biopsy.
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43
Q

Management of Hepatocellular carcinoma

A
  • Surgical resection or liver biopsy.
  • Percutaneous catheter ablation to necrosis of the tumour.
  • Chemo
  • Poor prognosis
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44
Q

Definition of bowel cancer

A
  • Malignant tumours affecting the colon and rectum.
  • Classed as malignant when it penetrates the mucosal layer and becomes part of the sub mucosa.
  • 3rd most common type of cancer.
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45
Q

Aetiology of bowel cancer

A
  • Risk factors include diets high in animal fat and low in fibre with sedentary lifestyles, also IBD, genetic predisposition and excess alcohol.
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46
Q

Carcinogenesis of bowel cancer

A
  • Found in large bowel.
  • Usually on the left hand side.
  • Comes from precancerous polyps.
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47
Q

Presentation of bowel cancer

A
  • Left side - blood/mucosa in the stool, altered or obstruct bowel habits, difficulty completing stools and mass.
  • Right side: weight loss, iron deficiency anaemia, abdo pain.
  • Fistulas, perforation, haemorrhage and abdo mass.
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48
Q

Management of bowel cancer

A
  • Primary care: DRE, Bloods.
  • Secondary care: flexible sigmoidscopy, colonoscopy, CT.
  • Treatment: Surgery, chemo and radiotherapy.
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49
Q

Red Flags of bowel cancer

A
  • Unexplained weight loss
  • Blood in stool
  • Rectal bleeding
  • Abdo pain
  • Altered bowel habits
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50
Q

Definition of peritonitis

A
  • Inflammation of the peritoneum.
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51
Q

Aetiology of peritonitis

A
  • GI perforation (appendicitis and perforated ulcer)
  • Transmural translocation (pancreatitis or ischaemic bowel)
  • Exogenous spread (drains or open surgery)
  • Female genital tract infections (Pelvic inflammatory disease)
  • Haematogenous spread (Septicaemia)
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52
Q

Presentation of peritonitis

A
  • Localised - usually signs and symptoms of the actual cause, pain that gradually gets worse and rising temperature. Patient usually has localised guarding, positive relief signs and rigidity.
  • Early diffuse - usually pain that is worse when moving, it starts in one area and then spreads out.
  • Diffuse - usually distended bowel with rigidity and reduced bowel sounds.
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53
Q

Investigations of peritonitis

A
  • Urine dipstick, bloods and imaging of the abdomen.
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54
Q

Management of peritonitis

A
  • Correct fluid volume and circulating volume.
  • Analgesics and antibiotics.
  • Catheterisation.
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55
Q

Definition of IBS

A
  • A chronic condition characterised by abdo pain associated with bowel dysfunction such as intestinal motility, enhanced visceral perception or microbial dysbiosis.
  • Pain is relieved by defecation and sometimes accompanied by abdo bloating.
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56
Q

Types of IBS

A
  • With constipation, bloating, mixed bowel habits and unspecified.
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57
Q

Aetiology of IBS

A
  • Uncommon.
  • Can be due to inflammatory or immune response with normal mucosal biopsies.
  • Can triggered by stress or emotional tension.
58
Q

Pathophysiology of IBS

A
  • Dysfunction with motor and sensory aspects of the digestive tract.
  • Altered gut reactivity due to emotional or immune triggers leading to pain and constipation/diarrhoea.
59
Q

Risk factors of IBS

A
  • Female, Less than 50, previous enteric infection or physical or sexual abuse.
60
Q

Presentation of IBS

A
  • Presence of risk factors, abdo discomfort, pain associated with altered bowel habits, abdo distention or bloating and normal abdo exam.
61
Q

Management of IBS

A
  • Positive diagnosis using history.
  • Rule out coeliac with serology and bloods to rule out infection.
  • Refer for colonosopy if over 60 or family history of bowel cancer/ovarian cancer with red flags.
  • Treatment about managing symptoms, avoiding triggers, psychological assessment.
62
Q

Definition of Coeliac disease

A
  • An autoimmune condition characterised by abnormal jejunal mucosa, improved by withdraw of gluten.
  • Women over men.
  • Around 1 in 100 patients.
  • Peak incidence between 8m to 12m and 40 to 60.
63
Q

Aetiology of Coeliac disease

A
  • Association between Coeliac disease and 2 antigen class II molecules.
64
Q

Pathophysiology of Coeliac disease

A
  • Gluten contains a toxic peptide called alpha gliadin.
  • The gliadin isn’t broken down by the protease in the small intestine lumen and therefore it is allowed to pass through the already damaged epithelium.
  • This leads to an inflammatory cascade that causes vilious atrophy and crypt hyperplasia.
65
Q

Risk factors of Coeliac disease

A
  • Type 1 diabetes, those with autoimmune conditions, Turners syndrome, Down’s syndrome, family history and IBD.
66
Q

Presentation of Coeliac disease

A
  • Caused by eating gluten leading to diarrhoea, flactulance, bloating and abdo pain.
  • Screen those with unexplained osteoporosis, issues with conceiving or miscarriage or failure to thrive in babies.
67
Q

Investigations of Coeliac disease

A
  • Serum IgA tissue transglutimase.
  • Distal duodenal biopsies.
  • Bloods to identify deficiencies and blood count.
68
Q

Management of Coeliac disease

A
  • Lifelong gluten free diet and correction of any deficiencies.
  • Pneumococcal vaccine.
69
Q

Definition of autoimmune hepatitis

A
  • Progressive inflammatory condition of the liver.
  • Common in women.
  • 40% have history of autoimmune condition and 20% present with accompanying autoimmune condition.
70
Q

Aetiology of autoimmune hepatitis

A
  • Genetic susceptibility.
71
Q

Presentation of autoimmune hepatitis

A
  • Insidious: nausea, anorexia, fatigue and malaise.
  • Can present as acute hepatitis progressing in liver disease.
  • Chronic liver disease presents as spider naevia, palmer erythema, jaundice and hepatosplenomegaly.
72
Q

Investigations of autoimmune hepatitis

A
  • Circulating autoantibodies.
  • Hypergammaglutanemia.
  • Raised serum bilirubin and aminotransferase.
  • Liver biopsy would show non specific chronic hep.
73
Q

Management of autoimmune hepatitis

A
  • Predisolone 30mg for 2 weeks then reduce dose.
  • Azathropine also.
  • Remission induced in 80% of patients and life long treatment needed.
74
Q

Definition of ascites

A
  • Fluid build up in the peritoneal cavity.

- In healthy men there is no fluid normally and around 20ml in women.

75
Q

Aetiology of ascites

A
  • Cirrhosis
  • Portal hypertension
  • Hepatic outflow obstruction
  • Pancreatitis
76
Q

Presentations of ascites

A
  • Fullness in the flank with alternating dullness.
  • Uncomfortable.
  • Respiratory distress.
  • Nausea/ lack of appeptide.
  • Pain
  • Constipation.
  • Abdo distension.
77
Q

Investigations of ascites

A
  • Diagnostic aspiration of 10 - 20ml to look for:
  • albumin
  • amylase
  • cytology
  • culture and stain
  • neutrophil
78
Q

Management of ascites

A
  • Treat cause.

- Restrict sodium, diuretics, paracentitis, indwelling drain and shunt.

79
Q

Definition of NAFLD

A
  • The most common type of chronic liver disease in the developed world.
  • Mostly picked up on routine abdo ultrasound showing steatosis.
  • Term for a group of different conditions.
  • Hepatic manifestation of metabolic syndrome - central obesity, hyperlipidaemia and intolerance to glucose.
80
Q

Risk factors of NAFLD

A
  • Type 2 diabetes, obesity, hyperlipidaemia, certain medications.
81
Q

Pathophysiology of NAFLD

A
  • Thought to be due to insulin resistance leading to an excess accumulation of triglycerides in the liver eventually causing steatosis.
82
Q

Presentation of NAFLD

A
  • Asymptomatic but can see hepatosplenomegaly.
  • Possible generalised fatigue and malaise.
  • History suggests absence of excess alcohol intake.
  • Possible pain/discomfort in the right upper abdo cavity.
83
Q

Investigations of NAFLD

A
  • Mild increase in serum aminotransferase and y - GT.
  • Elastiography shows degree of fibrosis.
  • Potential CT/MRI/biopsy.
84
Q

Management of NAFLD

A
  • Lifelong risk factor co rrection - loss of weight, increased exercise and attention to CVD risk.
  • Potential bariatric surgery can reduce steatosis, steatohepatitis and fibrosis.
85
Q

Definition of alcoholic liver disease

A
  • 3 stages:
  • Steatosis (Fatty liver)
  • Alcoholic hepatitis (necrosis and inflammation)
  • Alcoholic liver cirrhosis
86
Q

Aetiology of alcoholic liver disease

A
  • Chronic long term alcohol use - alcoholics.
  • Levels needed unknown but lower in Hep C and obese patients.
  • Risk factors - obesity and smoking.
87
Q

Pathophysiology of alcoholic liver disease

A
  • The two pathways that process alcohol through the liver.
  • Alcohol dehydrogenase: leads to fatty acid oxidation and fatty infiltrate.
  • Cytochrome P450: leads to production of free radicals.
88
Q

Presentation of alcoholic liver disease

A
  • Usually history of longterm alcohol use, usually seen common in Hep C and women.
  • Jaundice, asictes, hepatosplenomegaly, abdo pain, weight loss/gain, wasting, malnutrition.
89
Q

Management of alcoholic liver disease

A
  • Reduced drug injury
  • Alcohol abstinence/withdrawal.
  • Weight loss and smoking cessation.
  • Vaccinations
  • Corticosteroids
  • Liver transplant
90
Q

Definition of Cirrhosis

A
  • Irreversible replacement of normal liver architecture with bands of fibrous tissue that separates nodules of regenerating hepatocytes.
  • The pathological end stage of many chronic liver diseases include Hep B/C, NAFLD and ALD.
  • Common and increasing in incidence due to increase in alcohol consumption and obesity.
91
Q

Aetiology of Cirrhosis

A
  • Alcohol, hep B and C and NAFLD.

- RF: unprotected sex, IVDU’s and obesity.

92
Q

Presentation of Cirrhosis

A
  • Spider naevia, palmer erytherma, hepatosplenomegaly, jaundice, ascites, abdo distention, black stool and vomiting blood.
93
Q

Investigations of Cirrhosis

A
  • Raised ALP and ALT
  • Screen LFT’s - albumin and prothrombin time.
  • Thrombocytopenia
  • Low sodium and creatinine.
94
Q

Management of Cirrhosis

A
  • Irreversible and progressive.
  • Management of complications
  • Flu vaccination.
  • Liver transplant.
  • Screen for HCC every 6 months.
95
Q

Complications of Cirrhosis

A
  • Portal hypertension, acites, portosystemic encephalopathy, variceal haemorrhage
96
Q

Definition of primary biliary cholangitis

A
  • Chronic disorder in which there is progressive destruction of intrahepatic bile ducts leading to cholesistits and cirrhosis.
97
Q

Aetiology of primary biliary cholangitis

A
  • Inherited abnormality of immune regulation causing T cell mediated attacks on the bile duct.
  • Environmental factors.
98
Q

Presentation of primary biliary cholangitis

A
  • Piuritis with/without jaundice.

- Hepatosplenomegaly and xathelasma.

99
Q

Investigations of primary biliary cholangitis

A
  • Raised alkaline phosphatase
  • Serum autoimmune antibodies
  • Liver biopsy - shows bile duct loss
100
Q

Management of primary biliary cholangitis

A
  • Ursodeoxycholic acid for life - this reduces the progressive of the disease and the need for transport.
  • Asymptomatic patients have a better prognosis than symptomatic patients, who may required liver transplants within 5 years.
101
Q

Definition of obstruction

A
  • Mechanical/functional blockage of the bowel that can either be classified as partial/complete or small/large.
  • Classified depending on site, extent of lumen blockage, mechanism and pathology of the blockage.
102
Q

Aetiology of obstruction

A
  • Small bowel: adhesions, hernias, interussuception, Chron’s and malignancy
  • Large bowel: tumours, diverticular structures and sigmoid volvulus.
103
Q

Risk Factors of obstruction

A
  • Large bowels: history of radiotherapy, gynae problems, females, increasing in age, mental health issues and institutionalisation.
104
Q

Pathogenesis of obstruction

A
  • Mechanical blockage to the bowel prevents normal peristaltic movements.
105
Q

Presentation of obstruction

A
  • Small bowel: acute colicky abdo pain, abdo distension, early onset vomiting and late onset constipation
  • Large bowel: acute colicky abdo pain, abdo distension, altered bowel movement, early onset constipation and late onset vomiting.
106
Q

Management of obstruction

A
  • Pain relief
  • Bloods
  • Fluids
  • Drip and suck
  • Abdo and chest XR
  • CT
  • Surgery
107
Q

What is C. diff?

A
  • Responsible for some cases of antibiotic related diarrhoea - especially broad spectrum antibiotics and nearly all cases of pseudomembranous colitis.
  • Spread through faeco - oral route or through spores.
  • Usually seen in the symptomatic in over 65’s, hospitalisation and patients on recent antibiotics.
108
Q

Pathophysiology of C. diff

A
  • Disease occurs when the normal colonic microbiotic is altered, usually by antibiotics and creates an environment which favours the proliferation of c. diff.
109
Q

Presentation of C. diff

A
  • Varies from mild diarrhoea to threatening disease with profuse diarrhoea, abdo pain and toxic megacolon.
110
Q

Investigations of C. diff

A
  • Testing for toxin using an EIA or NAAT.
  • Culture to identify strain.
  • Sigmoidoscopy to obtain histology.
111
Q

Management of C. diff

A
  • Isolation with barrier nursing - fluid management.

- Control antibiotic usage.

112
Q

Definition of IBD

A
  • Inflammatory bowel disease are a group of chronic system disease involving the inflammation of the intestine and includes ulcerative colitis and chron’s disease.
  • Usually presents in late teens or twenties.
113
Q

Aetiology of IBD

A
  • Genetic predisposition = Chron’s more than UC.
  • Environmental = smoking increases risk of Chron’s but protects against UC.
  • Host immune response = patients with IBD have a defective mucosal immune response allowing luminal antigens, creating a leaky epithelium.
114
Q

Pathology of IBD

A
  • Chron’s - any part of the GI tract, skip lesions, oral/perianal spread, transmural inflammation and sometimes granulomas.
  • UC - affects only the colon and usually starts in the rectum and then spreads proximally, continuous involvement, ulcers and pseudopolyps and no granulomas.
115
Q

Presentation of IBD

A
  • Chron’s - depends on region affected, could be abdo pain, weight loss, diarrhoea with bleeding and pain related to defecation.
  • UC - diarrhoea with blood and mucus and either persistent diarrhoea, relapses or remission.
116
Q

Investigations of IBD

A
  • Bloods to identify potential anaemias and also raised CRP and ESR in patients with Chron’s.
  • Radiology/imaging - rigid or flexible sigmoidscopy.
117
Q

Management of IBD

A
  • Need to induce and maintain remission.
  • Steroids such as oral predinisolone, potential such thiopirine drugs such as azathioprine or anti TNF antibodies if patients are steroid resistant - such as Rituximab
  • Surgery
118
Q

What are the key characteristics of hepatitis?

A
  • Liver necrosis and inflammatory cell infiltration.
119
Q

What the differences between chronic and acute hep?

A
  • Acute = self limiting, the liver returns to normal structure and function, usually presents with jaundice and enlarged/tender liver and raised ALT. Can be monitored through prothrombin time and levels of bilirubin.
  • Chronic = characterised as inflammation of the liver for than 6 weeks - can lead to cirrhosis, chronic liver disease and hepatocellular carcinoma.
120
Q

Hep A

A
  • Most common, usually spread through faecal oral route or through contaminated water and shellfish.
  • Most commonly seen in travellers from South America and Africa.
  • Most infectious pre jaundice, shed in diarrhoea 2 weeks prior to symptoms and for 7 days after.
  • Incubation period 2 to 6 weeks but usually present around 28 days.
  • Present with nausea, anorexia and distaste for cigarettes before moving to jaundice with pale stool and dark urine with subsiding of other symptoms.
  • Investigations would show raised ALT and bilirubin as well as the presence of IgM anti Hep A antibodies for active disease or IgG anti Hep A antibodies for previous infection.
  • Management is supportive and important to vaccinate to avoid.
121
Q

Hep B

A
  • Can be either acute or chronic.
  • Can be spread through vertical or horizontal transmission, MSM and needle stick injuries.
  • Asymptomatic or like Hep A and occurs around day 75.
  • Acute investigations show core anti Hep B IgM antibodies or core anti Hep B IgG antibodies with anti hep B surface antibodies.
  • Chronic = presence of core anti Hep B IgM antibodies for more than 6 months, leading to fibrosis.
  • Treatment is either supportive or anti virals such as pegylated interferon - a 2a or oral necleoside analogues.
  • Immunisation required.
122
Q

Hep D

A
  • Usually through blood or body fluids.

- Can occur with Hep B and be acute or chronic.

123
Q

Hep C-

A
  • Spread through blood or blood products, common in haemophilics and IVDU.
  • Mostly asymptomatic.
  • Chronic leads to the formation of cirrhosis.
  • Treatment is with direct acting antivirals.
  • Screening of UK blood products.
124
Q

Hep E

A
  • Spread through undercooked meat.
  • Either shows IgM/IgG anti Hep E antibodies.
  • Treatment is either supportive or with rivarbin or reverse immunosuppressants.
125
Q

What is gastroenteritis?

A
  • Can be caused through bacterial, viral or parasitic infections.
126
Q

What is diarrhoea?

A
  • 3 or more episodes of partially formed or water stools within a day.
  • Acute < 14 days
  • Persistant > 14 days.
127
Q

What is dysentry?

A
  • Infectious bloody diarrhoea.
128
Q

What are viral causes of diarrhoea?

A
  • Rotavirus (most commonly seen in immunocompromised adults or nursery age children, presents with nausea, fever and watery diarrhoea)
  • Noravirus (extremely infectious - can spread through clusters so hospitals, carehomes, schools, cruise ships, presents with nausea, vomiting, abdo pain, watery diarrhoea)
129
Q

What are bacterial causes of diarrhoea?

A
  • Cholera = gram negative bacillus
  • E.coli = gram negative rod shaped.
  • Shigella = bloody diarrhoea
  • Camplyobacter = most common
130
Q

Definition of gallstones

A
  • Caused by bile concentrations –> cholesterol, bile pigment and phospholipid.
131
Q

Pathology of gallstones

A
  • Imbalance in chemical composition where increased cholesterol in gall bladder or increased bilirubin levels.
132
Q

Risk factors of gallstones

A
  • Fat, female, fertile and 40

- Use of OCP and HRT

133
Q

Presentation of gallstones

A
  • Asymptomatic if free floating
  • Lead to biliary colic becoming suddenly severe and last 1 to 5 years.
  • Umbilical/ right hypochondriac region or in the shoulder.
  • Bile duct –> high temp, more persistent pain, tachycardia, jaundice, itchy skin and diarrhoea.
134
Q

Investigations of gallstones

A
  • Murphy’s skin - finger or hand on the right upper abdo cavity and asking the patient to breathe in if pain then suggests gallbladder.
  • Ultrasound/ choligography.
135
Q

Management of gallstones

A
  • Active management if no symptoms.
  • Ursodeoxycholic acid if small
  • Surgery - laproscopic/open cholecystectomy and ERCP
136
Q

What is jaundice?

A
  • Yellow discolouration of the sclerae and skin due to the increase in bilirubin levels.
  • It is usually when bilirubin levels are more than 50.
137
Q

How is bilirubin formed?

A
  • Bilirubin is from breakdown of haemaglobin within the spleen and is carried to the blood bound to albumin.
  • It becomes conjugated in the liver and is then secreted by the bile duct and is unconjugated again in the terminal ileum and excereted in the faeces or reabsorbed and excreted in the kidneys.
138
Q

What is haemolytic jaundice?

A
  • Increased breakdown of red bloods cell leading to increased bilirubin levels.
  • Mostly common caused by sickle cell disease.
  • Investigations of features of haemolysis and increased serum unconjugated bilirubin.
139
Q

What is congenital hyperbilirubinaemia?

A
  • Gilbert’s syndrome

- Asymptomatic

140
Q

What is cholestatic?

A
  • Pale stools and dark urine as the bilirubin is conjugated.

Phase 1 Exam (25 decks)

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