Question 1

What is the cushing reflex? Whats its purpose?

Accepted Answer

Increased BP decreased HR and irregular breathing in response to increased intracranial pressure. Purpose is to help maintain Blood pressure in the cranial region

Question 2

Define Dysphagia? 5 Q's do ask in dysphagia history? and what do they suggest? And what is a sign of complete obstruction? What should you look out for on examination? and what tests should you do?

Accepted Answer

Dysphagia is a subjective sensation of difficulty or abnormality of swallowing. Dysphagia can refer to the sensation of not being able to swallow, food 'sticking' or not passing, choking episodes, or aspiration of food and/or liquids. STEP 1: The first step in evaluating patients with nonacute dysphagia is to determine if the symptoms are due to oropharyngeal or esophageal dysphagia. Oropharyngeal dysphagia – Oropharyngeal or transfer dysphagia is characterized by these features: Patients have difficulty initiating a swallow. Patients may point toward the cervical region as the site of their symptoms. Swallowing may be accompanied by nasopharyngeal regurgitation, aspiration, and a sensation of residual food remaining in the pharynx. Oral dysfunction can lead to drooling, food spillage, sialorrhea, piecemeal swallows, and dysarthria. Pharyngeal dysfunction can lead to coughing or choking during food consumption, and dysphonia. Esophageal dysphagia – Patients with esophageal dysphagia commonly report the following: Difficulty swallowing several seconds after initiating a swallow, and A sensation that foods and/or liquids are being obstructed in their passage from the upper esophagus to the stomach. STEP 2: characterising the symptoms: Solid, liquid, or both?—A critical component of the medical history is determining the types of food that produce symptoms (ie, solids, liquids, or both). For example, dysphagia to both solids and liquids from the onset of symptoms is probably due to a motility disorder of the esophagus. Dysphagia to solids only is usually present when the esophageal lumen is narrowed to 13 mm or less by a stricture. Progressive or intermittent?—It is important to ask if the symptoms are intermittent or are gradually progressive. Progressive dysphagia, beginning with dysphagia to solids followed by dysphagia to liquids, is usually caused by a peptic stricture or obstructing lesion. Symptoms of peptic stricture are slowly and gradually progressive, whereas those due to a malignancy progress more rapidly. Intermittent dysphagia may be related to a lower esophageal ring or web. Patients with motility disorders may also exhibit progressive dysphagia (eg, achalasia) or may exhibit intermittent or nonprogressive dysphagia (eg, distal esophageal spasm). Associated symptoms — Associated symptoms or findings can help to narrow the differential diagnosis. These may include: Heartburn, Weight loss, Hematemesis, Anemia, Regurgitation of food particles, and Respiratory symptoms. Not swallowing fluids AND solids from the start? Yes: suggests motility disorder (esp if non progressive: achalasia, CNS or pharyngeal causes). No: solids, then liquids suspect a stricture (benign or malignant). Is it difficult to make the swallowing movement? Yes: suspect bulbar palsy, especially if coughs on swallowing. Is it painful to swallow (odynophagia - painful swallowing)? suspect cancer, oesophageal ulcer, candida, or spasm. Is dysphagia intermittent or is it constant and getting worse? Former: Spasm, latter: malignant stricture. Does the neck bulge or gurgle on drinking? Yes: suspect pharyngeal pouch. Do you cough after eating? suggests epiglottis is not working neuro problem. Dribbling = sign of complete obstruction. On examination - look out for cachexia or anaemia, palpate virchows node, look for signs of neuro disease. Investigations: FBC (anaemia), U&E (dehydration), CXR, Barium swallow and/or endoscopy with biopsy should usually be performed. To rule out perforation due to caustic injury, x-ray with Gastrografin is safe, but barium should be avoided, as it can cause mediastinitis if a perforation exists.

Question 3

Describe the Aetiology of Shock? And the different classifications? Name 3 early markers of shock?

Accepted Answer

Shock can be classified into 3 main categories: 1. Hypovolaemic shock: most common cause. May result from: Blood loss (trauma or gastrointestinal bleeding), Fluid loss (diarrhoea or burns), Sequestration of fluid in the third space (obstruction of the bowel or pancreatitis). In patients with hypovolaemia, decreased intravascular volume leads to a reduction in the venous return, stroke volume, and, ultimately, cardiac output and oxygen delivery. Patients can compensate for a reduction of up to 25% of the circulating volume by increasing endogenous catecholamines that cause vasoconstriction of the venous capacitance system and increase venous return. During this compensatory period, patients may display signs of peripheral vasoconstriction and a low output state with cool, clammy, mottled skin, tachycardia, and poor capillary refill. 2. Cardiogenic shock: Results from heart pump dysfunction (more commonly left-sided) causing a decrease in cardiac output in the setting of increased preload. Can usually diagnose it by presence of: A systolic blood pressure of 18 mm Hg) and pulmonary oedema. But the absence of pulmonary congestion and hypotension at initial clinical evaluation does not exclude a diagnosis of cardiogenic shock. Causes of cardiogenic shock: Myocardial disease: MI, cardiomyopathies, myocarditis. Valvular disease: Acute aortic regurgitation, Critical aortic stenosis, Mitral regurgitation caused by rupture of a papillary muscle or chordae tendineae, Ventricular septal defects. Arrthymias. Obstructive: Pulmonary embolism restricts flow. Constrictive pericarditis, Tension pneumothorax and Pericardial tamponade are filling restrictive. The most frequent cause of cardiogenic shock is acute myocardial infarction. Ischaemia can also cause diastolic heart failure with elevated end diastolic pressures and low stroke volume but a normal ejection fraction. Therefore, cardiac failure cannot always be excluded in the presence of a normal left ventricular ejection fraction. cardiogenic shock can also occur in patients with a non-ST elevation acute coronary syndrome. 3. Vasodilatory (distributive) shock: In patients with vasodilatory shock, the tissue hypoxia is caused by an ineffective tissue oxygen extraction and the loss of vasoregulatory control leading to inappropriate vasodilation and maldistribution of blood flow. Cardiac output is typically preserved or increased. Causes: severe sepsis, anaphylaxis, adrenal failure, drug reactions, Neurogenic shock after cerebral or spinal cord injury, leading to loss of vasomotor tone and bradycardia. And rarely conditions associated with the formation of peripheral shunts, such as chronic liver failure and Paget's disease. Increased RR (o2 consumption over delivery), Increase lactate, Decreased urine output. Can obviously get a mixed Shock picture, so be careful.

Question 4

What is the aetiology of dysphagia? Name 3 uncommon causes of dysphagia?

Accepted Answer

Swallowing is split into 3 distinct physiological parts: the oral phase, the pharyngeal phase, and the oesophageal phase. This is also useful for grouping causes of dysphagia. Problem with the oral phase: get difficulty in initating swallowing. Causes: Hypertrophic tonsils. Lingual tonsils (at the base of the tongue) may be difficult to visualise but may also become hypertrophic and interfere with swallowing. Can be visualised with flexible nasopharyngoscopy or indirect laryngoscopy with a dental mirror. Oral cavity tumours. Dentition may be a problem - poor dentition may have difficulty with chewing food and are unable to form properly sized food to be bolused into the pharynx. Pharyngeal phase problems: this may be manifest by complaints of food sticking in the throat, symptoms of aspiration, hoarseness, cough, pain in the throat, or even referred pain to the ear. Causes: Anatomical problems: Zenckers diverticulum (The incidence increases by age; more frequent in women, Is associated with regurgitation of undigested food, intermittent solid food dysphagia, halitosis, and excessive salivation, Barium swallow is the best diagnostic test, can be missed on endoscopy.) Pharyngeal/laryngeal tumours (Symptoms may include progressive solid food dysphagia, weight loss, and otalgia (referred pain).) Hoarseness, symptoms of aspiration (especially of liquids), and shortness of breath are often associated with laryngeal tumours. Vast majority of malignancies are squamous cell carcinomas, often very aggressive when this is the primary site with frequent metastases. Endoscopy with biopsy is the best diagnostic test. Stenosis: Mostly caused by prior radiation, surgery, or chemical ingestion. Flexible fibre-optic nasopharyngoscopy/laryngoscopy, oesophagogastroduodenoscopy (OGD), and barium swallow are helpful. Extrinsic compression: Cervical lymphadenopathy, cricopharyngeal bar, cervical spine osteophyte, thyromegaly. Neuromuscular problems: Stroke (most common), Parkinsons, vocal cord paralysis, Amyotrophic lateral sclerosis, Multiple sclerosis, Brain and skull base tumours, Myasthenia gravis, Inflammatory myopathies, Wilson's disease, Progressive supranuclear palsy. Oesophageal problems: sensation of food sticking in the lower aspect or the neck or chest, regurgitation of food, chest pain, or heartburn, cause: Structural: stricture: The main symptom is solid food dysphagia. OGD or barium oesophagrams are the best diagnostic test. Pills such as potassium chloride, doxycycline, quinidine, NSAIDs, iron, and alendronic acid may cause strictures. Foreign Body. Oesophageal/cardia carcinomas. Benign tumours: rare; include leiomyoma, granular cell tumours, and papillomas. Metastasis. Extramural lesions (Mediastinal masses, Bronchial carcinoma, Cervical osteoarthritis/cervical osteophytes). Oesophageal ring (Manifest by intermittent solid food dysphagia. Mucosal ring (Schatzki ring, located at GE junction), Muscular rings: located 1.5 cm proximal to the gastro-oesophageal junction. Typically asymptomatic. Oesophageal webs. Hiatus hernia. Oesophageal diverticulum: known as traction diverticulum secondary to pulling of the oesophageal wall. Located in the middle third of the oesophagus. Barium study is the most useful test to identify them. MOTOR: Idiopathic achalasia (Oesophageal motility disease with insufficient lower oesophageal sphincter relaxation and loss of oesophageal peristalsis. Progressive dysphagia to solids followed by liquids. Oesophageal manometry is useful in detecting motility abnormalities of achalasia). Scleroderma (Causes oesophageal hypomotility and incompetence of lower oesophageal sphincter. Can lead to chronic gastro-oesophageal reflux with subsequent stricture formation.) Diffuse oesophageal spasm (Mostly manifest by recurrent chest pains associated with meals. More common with ingestion of very hot or very cold foods. Is diagnosed by manometry, which reveals simultaneous contractions. Finding on barium swallow study is 'corkscrew' oesophageal body from a simultaneous contraction). Oesophageal spasm can be divided into: Diffuse oesophageal spasm (DES)- there are uncoordinated oesophageal contractions. Several sections of the oesophagus can contract at once. Causes intermittent dysphagia and chet pain. Nutcracker oesophagus (NE) - the contractions are co-ordinated but with an excessive amplitude. DES is defined by the presence of at least 20% of swallows showing simultaneous contractions in the distal oesophagus. NE is defined as normal peristalsis of the oesophageal body with an average distal oesophageal amplitude exceeding 180 mm Hg. Diagnosis of oesophageal spasms is made on oesophageal manometry - this is the preferred investigation. Avoiding cold fluids, and taking hot liquids with meals, helps some patients. Surgical BOTOX, or surgical esophageal dilatation may help some patients. Both types of eosphageal spasm show a corkscrew oesophagus or rosary bead on barium swallow. Others: Calcinosis, Raynaud's disease, (o)esophageal dysmotility, sclerodactyly, telangiectasia (CREST) syndrome or scleroderma. Globus hystericus. Infections such as pharyngitis, oesophageal candidiasis, epiglottitis, and retropharyngeal abscess can cause dysphagia, as can radiation- and/or chemotherapy-induced oral mucositis. Esophageal web, schatzki ring and zenckers diverticulum (hypopharyngeal diverticulum =rare)

Question 5

Name the ALARMS symptoms which suggest malignancy?

Accepted Answer

A= anaemia L=Loss of weight A= Anorexia R = Recent onset of progressive symptoms M =Malaena S= Swallowing difficulty

Question 6

Describe the 2 scoring systems used in Upper GI bleeds? When should endoscopy be offered? Whats the NICE guidance with PPIs in Upper GI bleeds?

Accepted Answer

The GBS is calculated using the following parameters: urea, Hb, systolic BP, pulse, melaena, history or evidence of liver disease, and CAD. A score of '0' indicates low risk and potential suitability for outpatient management or deferment of endoscopic treatment. A score of '6 or more' is associated with over 50% risk of needing an intervention. The Rockall scoring system includes clinical criteria (increasing age, presence of comorbidities, shock) as well as endoscopic findings (such as source of bleeding and/or stigmata of recent bleeding) to identify patients at risk of adverse outcome after acute upper GI bleeding. The total score is calculated by simple addition. A score of less than 3 carries a good prognosis, but a total score of 8 or higher carries a high risk of mortality. Offer endoscopy to unstable patients with severe acute upper gastrointestinal bleeding immediately after resuscitation. Offer endoscopy within 24 hours of admission to all other patients with upper gastrointestinal bleeding. Do not offer acid-suppression drugs (proton pump inhibitors or H2-receptor antagonists) before endoscopy to patients with suspected non-variceal upper gastrointestinal bleeding. Offer proton pump inhibitors to patients with non-variceal upper gastrointestinal bleeding and stigmata of recent haemorrhage shown at endoscopy.

Question 7

Define Upper GI bleed? Whats more common upper GI bleed or Lower GI bleed?

Accepted Answer

Upper gastrointestinal bleeding (UGIB) refers to GI blood loss whose origin is proximal to the ligament of Treitz at the duodenojejunal junction. Acute UGIB can manifest in a variety of manners, including haematemesis, coffee-ground emesis, the return of bright red blood through a nasogastric tube, and melaena with or without haemodynamic compromise. Haematochezia (bright red blood per rectum) may rarely occur in patients with an extremely brisk UGIB. Bleeding from the upper gastrointestinal tract (GIT) is about four times as common as bleeding from the lower GIT. Ordinarily, mortality is secondary to hypovolaemic shock. Patients with UGIB can typically be segregated into 2 groups: those with variceal lesions (either oesophageal or gastric) and those with non-variceal lesions (most commonly peptic ulcers). These 2 groups have slightly different treatment strategies.

Question 8

Aetiology of Upper GI bleed? How common is each one?

Accepted Answer

PUD (35% to 50%), Gastroduodenal erosions/gastritis (8% to 15%), Oesophagitis (5% to 15%), Varices (5% to 14%), Mallory-Weiss tears (15%), Vascular malformations, including aortoenteric fistulae, Angiodysplasia and Dieulafoy's lesions (5%). Dieulafoy's lesions are aberrant submucosal vessels, most commonly seen in the stomach or in the small bowel, which erode through the mucosa and cause a brisk bleed in the absence of an ulcer. Other conditions (e.g., Osler-Weber-Rendu syndrome. malignancy, coagulopathy) constitute the remainder. UGIB from malignant lesions is usually low-level and chronic and only infrequently leads to acute bleeding. In most patients, likely causes of the bleeding can be ascertained through a good history and physical examination. Others: Haemobilia (bleeding from gallbladder or biliary tree)

Question 9

Name 3 risk factors for Upper GI bleed?

Accepted Answer

Alcohol, NSAIDs, Age

Question 10

whats the most common cause of upper GI bleed?

Accepted Answer

peptic ulcer

Question 11

Name 4 signs of an upper GI bleed?

Accepted Answer

Haematemesis, Coffee ground vomit (vomit black material implies bleeding has ceased or is relatively modest) Malaena (altered blood), Haematochezia (=profuse upper GI bleed or colonic bleed)

Question 12

What is the approach to the history of a patient with an Upper GI Bleed?

Accepted Answer

First the History. So in The HISTORY: main aim is to identify cause. So 1. Nausea and vomiting - The absence of nausea and vomiting in the setting of melaena or haematochezia thought to be of upper GI origin suggests a bleeding source distal to the pylorus. Lingering of blood in the lumen of the alimentary canal allows for oxidation of the iron component of Hb and has the effect of darkening blood. Coffee-ground emesis is suggestive of a slower, possibly intermittent bleed, and melaena (see below) is overwhelmingly associated with UGIB rather than with lower GI bleeding (LGIB), which is distal to the duodenojejunal junction at the ligament of Treitz. Thus, coffee-ground emesis argues more for PUD and makes a variceal bleed less likely. Conversely, brisk haematemesis is suggestive of an actively bleeding lesion, most often a variceal bleed (especially in patients with signs of liver disease or portal hypertension), an actively bleeding gastroduodenal ulcer, or a duodenal Dieulafoy's lesion. UGIB starting after vomiting or retching is suggestive of a Mallory-Weiss tear, although many patients with a Mallory-Weiss tear have no history of vomiting. A spontaneous tear of the oesophagus from retching (Boerhaave's syndrome) can be associated with significant haematemesis. 2. Malaena is overwhelmingly associated with UGIB. It is important to note that a patient reporting melaena is not the same as the patient actively passing melaenic stools. Both bismuth-containing products (e.g., Pepto-Bismol) and iron supplements can make the appearance of stools dark or black. A digital rectal examination, including a faecal occult blood test, must be conducted. Haematochezia is more often seen in LGIB than in UGIB. However, bright red blood per rectum can be seen in a brisk UGIB where the rapidity of the transit time precludes any digestion. Consequently, assessing the quantity of bleeding is imperative for 2 chief reasons: A large amount of haematochezia with other historical factors suggesting an upper GI source requires rapid diagnosis and treatment by upper GI endoscopy. A smaller amount of haematochezia associated only with bowel movements, or in the absence of other signs suggesting an upper source, points to LGIB. Hence, colonoscopy, not upper GI endoscopy, is indicated. Persistent or intermittent haematochezia renders upper GI bleed less likely. Gastric varices are strongly associated with massive bleeding and rapid haemodynamic compromise. Dieulafoy's lesions often present with rapid blood loss, although bleeding can be intermittent. Aortoenteric fistulae often present with a 'herald bleed' (an episode of self-limiting bleeding before a massive bleed that can result in exsanguinations), in the form of either haematochezia or haematemesis. Diet - check red coloured gelatin and drinks as may misinterpret as haematemesis. CONSTITUTIONAL symptoms - weight loss, loss of appetite for upper GI cancer. MEDICATION = NSAIDS, CORTICOSTEROIDS, ANTICOAGULANTS, ANTIPLATELETS. Any history of chronic and excessive alcohol use, intravenous drug use (or other behaviour that places people at risk of contracting hepatitis), or underlying liver disease strongly suggests a variceal bleed and proper precautions (i.e., intravenous octreotide) are warranted. Of note, compromised liver function leads to coagulopathy; this can be severe and can complicate endoscopic therapy. Oesophagitis is often seen in the context of long-standing heartburn. Patients sometimes mention a globus sensation; hoarseness can also be present. Many patients who present with melaena and who are suspected of PUD will actually be found to have oesophagitis on endoscopy. Any prior history of PUD makes a recurrence more likely. AVMs are associated with cirrhosis, end-stage renal disease, advanced age, and von Willebrand's disease. Dieulafoy's lesions are regarded as congenital vascular aneurysms, yet they are most often symptomatic in men with alcohol histories, cardiovascular disease including hypertension, diabetes, or chronic kidney disease. Also any travel - A possible cause of portal hypertension is schistosomiasis. A history of a vascular graft or aortic aneurysm should markedly heighten clinical suspicion for aortoenteric fistula

Question 13

Describe the Examination done for a patient with an Upper GI bleed?

Accepted Answer

2 primary questions: What is the degree of anaemia/hypovolaemia? Are there signs of chronic liver disease that might suggest bleeding varices? Vital signs can be used to estimate the patient's volume status. If the patient's other comorbidities are not contraindications, tachycardia with hypotension should trigger aggressive volume resuscitation. If the patient is stable, orthostatic BPs should be obtained. Capillary refill, urine output, moisture in the mucous membranes, and absence of pallor can also assist in assessing the degree of anaemia/hypovolaemia. Chronic liver disease causing portal hypertension can present in 1 or more of the following ways: Encephalopathy with or without asterixis, Scleral icterus, Spider telangiectasias, also known as spider angioma, on the face, chest, or abdomen, Gynaecomastia, Hepatomegaly or splenomegaly, Ascites, Caput medusae with or without Cruveilhier-Baumgarten's bruit (ascultation over umbilical and paraumbilical veins produces a humming). Hypogonadism, Terry's nails (white nails), Palmar erythema. Visualising the nares and the oropharynx can sometimes identify a source of bleeding that does not require endoscopic management, as epistaxis or gingival bleeding can sometimes mimic UGIB. A digital rectal examination is mandatory. Visual inspection of the perineum can rule out the presence of external haemorrhoids. Faecal occult blood testing should be conducted. The degree, location, and character of pain and discomfort can be helpful. In PUD, ingestion of food often transiently improves abdominal pain; mid-epigastric tenderness to palpation is common. Bleeding is sometimes accompanied by mid-epigastric pain or retrosternal pain in patients with a Mallory-Weiss tear. Aortoenteric fistulae can present with significant abdominal or back pain and fever. Oesophagitis is sometimes associated with hoarseness. Cachexia should heighten concern for a GI tumour or other type of tumour. In addition, patients with upper GI tumours sometimes have a palpable abdominal mass and/or enlarged liver. Evidence of dehydration (dry mucosa, sunken eyes, skin turgor reduced (skin turgor is the degree of elasticity of the skin. If it is reduced it take longer to spring back once it is pulled).

Question 14

Describe the Investigations done for a patient with an Upper GI bleed?

Accepted Answer

Key blood tests to obtain are FBC, crossmatch blood and Coagulation profile: prothrombin time with activated partial thromboplastin time and an international normalised ratio (INR), fibrinogen level, LFTs to detect underlying liver disease, Renal function tests and electrolytes. There is no standardised threshold of Hb or Hct below which anaemic patients should be transfused. At most facilities, coagulopathies with an INR over 1.4 warrant correction with either vitamin K or fresh frozen plasma, or both. Elevated urea can often be seen in UGIB; as blood passes through the small bowel and is partially digested, it can result in an elevated urea and urea/Cr ratio. Coagulopathy may be a marker also for advanced liver disease. Key Imaging: CXR: may identify aspiration pneumonia; pleural effusion, perforated oesophagus. Erect and supine abdominal X ray to exclude perforated viscus and ileus. CT scan and ultrasound can identify: Liver disease. Cholecystitis with haemorrhage. Pancreatitis with haemorrhage and pseudocyst. Aortoenteric fistulae. CT scan used when source of bleeding is not obvious from history and examination. Endoscopy is highly effective in diagnosing and treating most causes of UGIB.

Question 15

Describe the initial management of an Upper GI bleed?

Accepted Answer

ABC - 2 large bore cannulae, take blood for FBC, U+E, glucose. Nasal specs for oxygen. Crossmatch. Give IV fluids (500ml of normal saline over 30 mins). While being typed and cross-matched for blood transfusion. Patients at risk of fluid overload may require intensive monitoring with a pulmonary artery catheter. If the blood pressure fails to respond to initial resuscitation efforts, the rate of fluid administration should be increased. In some patients, temporary support with vasopressor drugs may be required. The decision to initiate blood transfusions must be individualized. Our approach is to initiate blood transfusions if the hemoglobin is under 7 g/dL in most patients, however under 9 in those with CAD who cannot tolerate the anaemia. It is particularly important to avoid overtransfusion in patients with suspected variceal bleeding, as it can precipitate worsening of the bleeding. Transfusing patients with suspected variceal bleeding to a hemoglobin over 10 g/dL (100 g/L) should be avoided. Patients with active bleeding and a low platelet count (under 50,000/microL) should be transfused with platelets. Patients with a coagulopathy that is not due to cirrhosis and with a prolonged prothrombin time with INR over 1.5 should generally be transfused with fresh frozen plasma (FFP).Insert urinary catheter and monitor urine output. Organize CXR, ECG and ABG. Crystalloid fluids should be infused to maintain adequate BP. Packed RBCs should be transfused in patients with evidence of ongoing active blood loss or in patients who have experienced significant blood loss or cardiac ischaemia. Fresh frozen plasma should be used to correct coagulopathy (as is commonly seen in patients with underlying liver disease). Monitor pulse, BP and CVP at least hourly until stable. PPIs should not be used prior to diagnosis via endoscopy. Arrange an urgent endoscopy (within 24hrs). Inform surgeons of severe bleed, as if endoscopy fails emergency mesenteric embolization/angiography may be needed. Early risk stratification with 2 Scoring systems have been developed in an attempt to stratify patients who present to the emergency department with upper GI bleeding. These include the Glasgow-Blatchford bleeding score (GBS) and the Rockall score. All patients with acute upper gastrointestinal bleeding should be risk-assessed using the GBS at first assessment and the full Rockall score after endoscopy. After endscopy if Non Variceal bleeding: Antisecretory therapy with a proton pump inhibitor (PPI) is warranted, and this can be done intravenously or orally. Once haemodynamically stabilised, patients with non-variceal UGIB can proceed to endoscopy for an endoclip. If low risk from endoscopy (flat, pigmented spot or clean base) there is no need for endoscopic haemostasis and can be discharged with PPI. For variceal UGIB, NICE recommends terlipressin, a vasopressin analogue, given intravenously until bleeding has stopped or for a maximum of 5 days unless otherwise indicated. Alternatively, octreotide (somatostatin) can be infused as an intravenous bolus, followed by continuous IV infusion for 2 to 5 days. Transjugular intrahepatic portosystemic shunting is the treatment of last resort for patients with variceal UGIB irremediable to endoscopy. A Sengstaken-Blakemore (for oesophageal varices) or Linton-Nachlas (for gastric varices) balloon tamponade device can be used to quell the bleeding until the shunt is placed.

Question 16

How can Upper GI bleeding be stopped with endoscopy?

Accepted Answer

For the endoscopic treatment of non-variceal UGIB, one of the following should be used: A mechanical method (eg, clips) with or without adrenaline (epinephrine). Thermal coagulation with adrenaline (epinephrine). Fibrin or thrombin with adrenaline (epinephrine). For variceal UGIB - endoscopic banding (oesophageal varices) or sclerotherapy (if gastric varices). If not controlled then minnesota tube or sengstaken blakemore tube. Then TIPS.

Question 17

Are PPI recommended prior to endoscopy in upper Gi bleeds?

Accepted Answer

No

Question 18

How is intussusception treated?

Accepted Answer

barium enema

Question 19

What is DIC? Prognosis?

Accepted Answer

It is an acquired syndrome with widespread activation of clotting cascade that results in blood clots in small vessels throughout the body. Also consumes clotting factors and therefore severe bleeding can occur to. Generalised bleeding, evidenced by at least 3 unrelated sites, is highly suggestive of DIC. It can be acute or chronic. Acute DIC is more common with rapid-onset underlying conditions such as major trauma, sepsis/severe infection, and massive blood transfusion. Chronic DIC is more common with less acute disorders such as malignancies, paroxysmal nocturnal haemoglobinuria, and Raynaud's disease. Can get localised DIC which can occur in Aortic aneurysms. Overt DIC means it is not compensated. Non overt means it is stressed but compensated. Mortality is high.

Question 20

Describe the aetiology of DIC

Accepted Answer

Sepsis/ severe Infection - septicaemia - E.coli O157 Malignancy (acute myelocytic leukemia or metastatic mucin-secreting adenocarcinoma), Major trauma or burns, Obstetric problems (amniotic fluid embolism, eclampsia, abruptio placentae, retained dead fetus syndrome), Severe organ destruction or failure (severe pancreatitis, acute hepatic failure) Vascular disorders (Kasabach-Merritt syndrome or giant haemangiomas, large aortic aneurysms) Severe toxic or immunological reactions (blood transfusion reaction or haemolytic reactions, organ transplant rejection, snake bite).

Question 21

Describe the pathophysiology in DIC?

Accepted Answer

In DIC, the processes of coagulation and fibrinolysis become abnormally (and often massively) activated within the vasculature, leading to ongoing coagulation and fibrinolysis. TYPICAL SEQUENCE: 1. Procoagulant exposure: Blood is exposed to one or more procoagulants, such as tissue factor (TF), from which it is normally protected. Examples include: Bacterial LPS. In meningococcal sepsis, microparticles containing TF are found in the circulation. In trauma, damage to the vascular endothelium and tissues may cause release of procoagulant enzymes or phospholipids. "Cancer procoagulant" is a proteolytic enzyme produced by some mucinous tumors and placenta that is capable of activating factor X. In severe intravascular haemolysis: coagulation is activated by a combination of processes including TF release (likely by monocytes), generation of cytokines including tumor necrosis factor (TNF) and interleukin 1 (IL-1), and reduced nitric oxide (NO) function. 2. COAGULATION: Activation of the coagulation cascade leads to the production of thrombi consisting of fibrin and platelets. These can occur in the microvasculature and/or larger vessels. Extensive formation of thrombi in turn leads to consumption of endogenous coagulation factors, producing a "consumption coagulopathy"; and of platelets and anticoagulant factors (eg, protein S, protein C, antithrombin). 3. FIBRINOLYSIS: Fibrinolysis is activated at sites of thrombus formation, with generation of fibrin degradation products (FDP) that, when present in significant amounts, interfere with both fibrin clot formation and platelet aggregation. 4. END ORGAN DAMAGE: Tissue or organ damage may result from reduced perfusion, thrombosis, and/or bleeding. Increasing evidence suggests that damage-associated pattern molecules (DAMPs, also called alarmins) including cell-free DNA (cfDNA), extracellular histones, and DNA-binding proteins play a critical role in the pathogenesis of DIC. DAMPs are released from dying cells or secreted from immune cells in response to infection or tissue injury. Neutrophil extracellular traps (NETs). NETs are web-like structures composed of decondensed chromatin coated with a variety of cellular proteins such as myeloperoxidase, neutrophil elastase, histones, and high mobility group box 1 protein (HMGB1) that are released from dead or dying neutrophils. NET formation (NETosis) is highly procoagulant (provides tissue factor, increases platelet aggregation etc).

Question 22

Describe the presentation of DIC? Investigations to order? DD?

Accepted Answer

There is no single diagnostic test for DIC. Risk factors, clinical manifestations, and all available laboratory results must be considered to make the diagnosis. Signs - Bleeding from at least 3 unrelated sites, Fever, Petechiae, signs of ARDS, signs of haemorrhage, Acral cyanosis (blue discolouration of extremities). Microvascular thrombosis often results in multi-organ ischaemia and failure. Ischaemic findings include purpura fulminans/gangrene/acrocyanosis, delirium/coma, oliguria/azotaemia, hypotension/tachycardia/circulatory collapse, dyspnoea/hypoxia, GI ulcers, and adrenal dysfunction. Haemorrhagic findings include petechiae/ecchymosis, oozing, intracranial bleeding, haematuria, and massive GI bleeding. In general, ischaemic findings are considered earlier signs of DIC, while bleeding findings are late but overt signs. Initial laboratory investigations to order in all patients are: Platelet count: shows thrombocytopenia, Prothrombin time: prolonged, Fibrinogen: low levels, D-dimer/fibrin degradation products: elevated. Additional investigations should be ordered to assist in diagnosis of the underlying disorder. The initial tests are used to generate a score. A total score over or equal to 5 is compatible with overt DIC. DD: Severe Liver failure, Heparin-induced thrombocytopenia, Vitamin K deficiency, HELLP syndrome.

Question 23

Tx for DIC? 2 things

Accepted Answer

Treat cause, Replace platelets, fibrinogen and clotting factors if not bleeding if platelets are less than 10,000 /microL. If they are equal or over then do not replace. Patients with serious bleeding or need for urgent/emergent surgery and a platelet count under 50,000/microL should be given platelet transfusions.Typically, we give one to two units of random donor platelets per 10 kg of body weight. Patients with a platelet count under 10,000/microL should be given platelet transfusions due to the increased risk of spontaneous bleeding. Patients with serious bleeding and a significantly prolonged prothrombin time (PT) or activated partial thromboplastin time (aPTT), or a fibrinogen level under 50 mg/dL and serious bleeding, should receive coagulation factor replacement. Options include Fresh Frozen Plasma (FFP), related plasma products such as Plasma Frozen Within 24 Hours After Phlebotomy (PF24), or cryoprecipitate. Cryoprecipitate provides a good source of fibrinogen with significantly less volume load than FFP or PF24. Of note, the administration of antifibrinolytic agents such as tranexamic acid (TXA), epsilon-aminocaproic acid (EACA) or aprotinin is generally contraindicated since blockade of the fibrinolytic system may increase the risk of thrombotic complications.

Question 24

What is Zollinger Ellison syndrome? Name 4 signs. Name 4 Tx options. Where are the 3 common sites.

Accepted Answer

It is a gastrin secreting tumour, causes multiple, refractory and recurrent peptic ulcers. It is believed to be responsible for up to 1% of duodenal ulcers. Diagnosis typically occurs between the ages of 20 to 50 years but has occurred as young as age 9 years and as old as 90 years. There is equal distribution among men and women. About 20% of patients with ZES have multiple endocrine neoplasia (MEN) type I; the remaining cases are sporadic. The tumour (gastrinoma) is usually in the duodenum (60-65%) or the pancreas (30%). Progression to metastastic gastrinoma is the most common cause of mortality. Delta cells in the pancreas and enteroendocrine cells in the small intestine. Gastrinomas located in the duodenum are usually multiple and small in size, and are less likely to become malignant than the solitary, sporadic pancreatic gastrinomas. About 55% to 90% of gastrinomas are malignant and usually will metastasise to the lymph nodes and liver. Gastrin not only directly stimulates parietal cell secretion but also causes expansion of the mass of parietal cells. The increase in parietal cells results in an increase in basal acid output and maximal acid output. This substantial secretion of acid results in gastro-oesophageal reflux disease (GORD) symptoms and damage to the mucosal lining of the GI tract, causing peptic ulcers. In addition, the acid inactivates pancreatic enzymes, which contributes to the diarrhoea, steatorrhoea, and malabsorption of lipid-soluble nutrients. So 2 types: sporadic, and genetic form (MEN1). Signs - epigastric pain, diarrhoea, nausea, vomiting. TESTS: fasting serum gastrin (over 1000 picograms/mL), if gastrin is elevated acid output (basal and maximal) should be measured (to exclude the presence of achlorhydria secondary to chronic atrophic gastritis). If the BAO is elevated and the serum gastrin is between 48 to 481 picomols/L (100 to 1000 picograms/mL), a secretin provocation test should be done to confirm diagnosis. A calcium infusion test can be used for diagnosis because gastrin-secreting tumours express receptors for calcium. Less sensitive than the secretin test. Others: upper GI endoscopy - get prominent Gastric folds. MRI or spiral CT liver for metastases. DD: Atrophic gastritis, H pylori peptic ulcer disease, PPI use can cause an appropriate fasting hypergastrinaemia. To diagnose ZES in patients on PPI therapy, a fasting serum gastrin level can be repeated 1 week following discontinuation of PPI. Pernicious anaemia, gastric outlet obstruction. TREATMENT - PPIs H2RA, chemo or surgery. pyloric antrum, duodenum and pancreas. The liver is the most common metastatic site for gastrinomas. The second most common site is the bone. Due to advanced disease, patients are not candidates for surgical therapy. Inhibition of tumour growth and symptoms can be achieved with somatostatin analogues, Complications: anaemia (from chronic GI bleeding from peptic ulcers), nephrolithiasis (Common in patients with multiple endocrine neoplasia (MEN) type 1.)

Question 25

Name the order of ABO groups in terms of their prevalence with most common one 1st

Accepted Answer

O+ A+ O- B+ A- AB+ B- AB-

Question 26

Whats binge drinking in men and women? What is problematic alcohol use called? Define? Aetiology? Pathophysiology? What is hazardous drinking?

Accepted Answer

Alcohol use disorder. Alcohol-use disorder is a chronic, relapsing disorder that results from a variety of genetic, psychosocial, and environmental factors. It is characterised by increased tolerance to the effects of alcohol, the presence of characteristic withdrawal signs and symptoms, and impaired control over the quantity and frequency of drinking. PATHOPHYSIOLOGY: The pleasurable and stimulant effects of alcohol are mediated by a dopaminergic pathway projecting from the ventral tegmental area to the nucleus accumbens. Repeated, excessive alcohol ingestion sensitises this pathway and leads to the development of dependence. Long-term exposure to alcohol causes adaptive changes in several neurotransmitter systems, including down-regulation of inhibitory neuronal gamma-aminobutyric acid receptors, up-regulation of excitatory glutamate receptors, and increased central norepinephrine (noradrenaline) activity. Discontinuation of alcohol ingestion leaves this excitatory state unopposed, resulting in the nervous system hyperactivity and dysfunction that characterise alcohol withdrawal. It has also been suggested that withdrawal symptoms intensify as withdrawal episodes grow in number, a phenomenon called 'kindling'. Patients with alcohol-use disorder often experience craving, defined as the conscious desire or urge to drink alcohol. Craving has been linked to dopaminergic, serotonergic, and opioid systems that mediate positive reinforcement, and to the gamma-aminobutyric acid, glutamatergic, and noradrenergic systems that mediate withdrawal. 'Hazardous drinking' is another designation used to describe non-dependent problem use of alcohol. 8 units men. 6 units women

Question 27

Where is aspirin mostly absorbed? Name 2 side effects. Name 1 condition that it should not be used in. Whats its active metabolite?

Accepted Answer

Ileum. SE - salicyclism - tinnitus vertigo loss of hearing - reyes syndrome - causes hepatic encephalopathy Gout Salicylate

Question 28

Name 3 stages of shock. What plasma lactate threshold = shock? What % of blood loss can the baroreceptor reflex compensate for?

Accepted Answer

pre shock, shock, system failure. over 4 mmol/L. 10%

Question 29

Name 5 signs of septic shock

Accepted Answer

Pyrexia Warm peripheries Bounding Pulse Rapid capillary refill Nausea vomiting

Question 30

Name 6 signs of an anaphylactic shock

Accepted Answer

Warm peripheries Tachycardia Angiooedema Bronchospasm oedema of face, pharnyx, larnyx Urticaria

Question 31

Name 4 features which would suggest cardiogenic shock

Accepted Answer

Raised JVP pulsus alternans - pulse with strong and weak beats Pulmonary oedema gallop rhythm

Question 32

Name 6 signs of hypovolemic shock

Accepted Answer

Slow capillary refill Clammy Oliguria Tachycardic Low BP Pale skin

Question 33

What are the most common sites of infection in sepsis? Pathophysiology in sepsis?

Accepted Answer

The pulmonary tract (35%), digestive tract (11%), and urinary tract (7%) are the most common sites. The innate immune system is activated by bacterial cell wall products, such as lipopolysaccharide, binding to host receptors, including Toll-like receptors (TLRs). Pro-inflammatory cytokines such as tumour necrosis factor (TNF)-alpha and interleukins 1 and 6 are released, which in turn activate immune cells. Reactive oxygen species, nitric oxide (NO), proteases, and pore-forming molecules are released, which bring about bacterial killing. NO is responsible for vasodilatation and increased capillary permeability, and has been implicated in sepsis-induced mitochondrial dysfunction. The complement system is activated, Activated endothelium not only allows the adhesion and migration of stimulated immune cells, but becomes porous to large molecules such as proteins, resulting in the tissue oedema. Alterations in the coagulation systems include an increase in procoagulant factors, such as plasminogen activator inhibitor type I and tissue factor, and reduced circulating levels of natural anticoagulants, including antithrombin III and activated protein C (APC). Impaired tissue oxygen delivery is exacerbated by pericapillary oedema. This means that oxygen has to diffuse a greater distance to reach target cells. There is a reduction of capillary diameter due to mural oedema and the pro-coagulant state results in capillary microthrombus formation. Additional contributing factors include disordered blood flow through capillary beds, resulting from a combination of shunting of blood through collateral channels and an increase in blood viscosity secondary to loss of red cell flexibility. As a result, organs may become hypoxic, even though gross blood flow to an organ may increase. These abnormalities may lead to lactic acidosis, cellular dysfunction, and multi-organ failure.

Question 34

Name the 4 causes of cardiogenic shock?

Accepted Answer

Dysrhythmia, mechanical (heart valves) , cardiomyopathy (MI) Extracardiac (PE, Pulmonary HTN, tamponade, constrictive pericarditis)

Question 35

2 types of hypovolemic shock? 2 types of distributive or vasodilatory shock?

Accepted Answer

fluid loss, and haemorrhagic sepsis anaphylaxis

Question 36

Name 4 common bacterial causes of sepsis

Accepted Answer

E.coli, P. aueruginosa, S.aureus, Haemophilius influenzae

Question 37

What are the 3 elimination pathways for alcohol? and where are they found?

Accepted Answer

Microsomal ethanol oxidizing system (MEOS) and SER ADH pathway - cystol Catalase - peroxisome

Question 38

Why are orientals shit drinkers? and what is ethanol converted into and then what is that converted into?

Accepted Answer

Ethanol - acetaldehyde - acetate Orientals have mutant ALDH 2 therefore decreased capacity to metabolize acetaldehyde and circulating concn increases producing facial flushing response

Question 39

Whats the units equation?

Accepted Answer

units = ABV x vol / 1000

Question 40

Why are women shit drinkers?

Accepted Answer

Because body water and hence compartment in which the ethanol distributes is significantly smaller than in men.

Question 41

What is ethanols effect on heart? BP? NS? skeletal muscle? Skin? sexual function?

Accepted Answer

Heart - depression of LV function BP - increased Alcholic cardiomyopathy Alcoholic dementia - shrinkage of cortex - reversible to an extent Wenicke encephalopathy Korsakoffs psychosis cerebellar degeneration Marchiafara bignami syndrome - demyelination of corpus callosum Peripheral neuropathy Acute myopathy - rhabdomyolysis chronic myopathy Discoid eczema - circular patches of eczema with well defined edges Acne rosacea - redness to face Linear telangiectasia - dilated blood vessels in outer layer of skin decreased sperm count

Question 42

Name 6 signs of wernickes encephalopathy? Where does it affect and whats it due to?

Accepted Answer

Global confusion Apathy disorientation Nystagmus ataxia disturbed memory structures around the 3rd V and mamillary body and due to thiamine deficiency

Question 43

What is korsakoffs psychosis? and where have changes taken place?

Accepted Answer

amnesic state. Changes in dorsomedial thalamus

Question 44

Name some medications that help prevent alcohol relapses in previous alcohol dependents?

Accepted Answer

Calcium acetyl-homotaurinate (acamprosate) This blocks gamma-aminobutyric acid (GABA) and reduces N-methyl-D-aspartate (NMDA) receptor glutamate-related excitation. Reduces cravings. Naltrexone: Alcohol causes pleasure by release of endogenous opioids. Naltrexone is a competitive antagonist of the opioid receptor which prevents the endogenous opioid from binding to the receptor, therefore giving reduction in the pleasurable effects from alcohol.

Question 45

What questionnaire is used to assess drinking? what are the questions? what is hazardous drinking from this tool? Name another one.

Accepted Answer

CAGE questionnaire felt ought to Cut down? Ever felt Annoyed when asked about your drinking? Ever felt Guilty about your drinking? Ever had an Eye opener (drink 1st thing in the morning) ? 2 or more. Alcohol Use Disorders Identification Test (AUDIT) is another one. Specialist advice should be sought if they score more than 15 on AUDIT assessment.

Question 46

Why does alcohol make you piss more?

Accepted Answer

Inhibits Adh and osmotic effect in kidneys

Question 47

Describe effects of alcohol on metabolism?

Accepted Answer

Leads to excess Nadh production - which inhibits gluconeogenesis and so hypoglycaemia and lactic acidosis. Also inhibits lipolysis - excess fat

Question 48

Name drug used to stop alcohol abuse?

Accepted Answer

disulfiram

Question 49

What is complete rupture of the oesophagus called?

Accepted Answer

Boerhaave syndrome

Question 50

What is the main type of stomach cancer? Epideems? Aetiology of gastric cancer? risk factors?

Accepted Answer

Most are adenocarcinomas. Other histological types include lymphoma, leiomyosarcoma, neuroendocrine tumours, and squamous cell carcinomas, but these are uncommon. Especially common in Japan, China and parts of South America. More common in Males. RISK FACTORS: H pylori has been associated with molecular events that could lead to gastric cancer, such as an increase in p53 mutations. smoking, male, Diet (low vit C high in salt), H pylori, pernicious anaemia. Consumption of smoked and salted foods. Mass screening programmes for gastric cancer have been implemented in countries with a high incidence of the disease, such as Japan and Chile. 1% to 3% of gastric cancers may be linked to genetic factors.

Question 51

PRESENTATION OF GASTRIC CANCER? What are the 1st symptoms of gastric cancer? what are the later symptoms?

Accepted Answer

Weight loss and persistent abdominal pain are the most common presenting symptoms in patients with gastric cancer, although dysphagia is common in cancers of the proximal stomach or gastro-oesophageal junction. Patients may present with melaena. 1st = dyspepsia, 2nd = epigastric pain weight loss and anaemia. EXAMINATION: Abdominal tenderness may be noted on examination; this tends to be epigastric and vague in early-stage disease. An abdominal mass may be present in patients with advanced disease. Lymphadenopathy may also be present, and the presence of a left supraclavicular node (Virchow's node), periumbilical nodule (Sister Mary Joseph's nodule), or left axillary node (Irish node) may indicate advanced disease. Early gastric cancer often has symptoms suggesting a benign aetiology. 70% of patients with early gastric cancer only have symptoms of uncomplicated dyspepsia and are not complicated by anaemia, dysphagia, or weight loss.

Question 52

Investigations for gastric cancer? DD?

Accepted Answer

OGD, CT, US. Upper GI endoscopy with biopsy is the initial diagnostic procedure of choice. Once the diagnosis is established, patients should undergo further staging to determine the extent of their disease. Endoscopic ultrasound has become an important modality because of its accuracy for tumour and node staging. A CXR should be obtained, with strong consideration given to a chest CT scan in patients with proximal lesions. A CT scan of the abdomen and pelvis should be performed to look for metastatic disease. PET/CT should be considered to rule out distant metastases, which would make the patient ineligible for definitive therapy. However, the effectiveness of PET is uncertain, because 50% of gastric tumours are fluorodeoxyglucose (FDG)-negative. [20] Staging laparoscopy should be considered, as peritoneal and metastatic disease

Question 53

Management of Gastric cancer? Prognosis for gastric cancer?

Accepted Answer

If medically fit, surgical resection should be the primary treatment for early localised disease. Extent of surgical resection depends on the location of the tumour. Total gastrectomy is usually recommended for proximal tumours. Patients with distal gastric cancers have had no survival benefit for total gastrectomy compared with subtotal gastrectomy. Patients with superficial early gastric cancer (T1a) can be treated with endoscopic mucosal resection (EMR). Plus periop chemo, or post op chemoradiotherapy. Patients with localised disease who are not surgical candidates should be offered chemoradiation. If metastasised then chemo. Then palliative gastrectomy to help relieve symptoms of bleeding and obstruction. In UK, Overall survival rate is 15%. 11% of people live for at least ten years.

Question 54

What are leiomyomas?

Accepted Answer

benign tumours that can occur anywhere in the GI tract

Question 55

What are 2 main types of oesophageal cancer and where do they arise? AETIOLOGY. Pathophysiology of GORD and alcohol.

Accepted Answer

squamous cell carcinoma upper, middle oesohagus adenocarcinoma lower oesophagus. adenocarcinomas are now more prevalent than squamous cell carcinomas overall in the US and Western Europe. AETIOLOGY: FACTORS IMPLICATED IN ADENOCARCINOMA: Gastro-oesophageal reflux and Barrett's oesophagus. It has been found that any increase in body mass seems to increase the risk of oesophageal adenocarcinoma. here is a strong male predominance over females, of the order of 7:1. Diets high in total fat, saturated fat, and cholesterol seem associated with an increased risk of this cancer. FACTORS IMPLICATED IN SQUAMOUS CELL CARCINOMA: Tobacco use is more strongly associated with oesophageal squamous cell carcinoma (a 3-fold to 7-fold increase in risk) than it is with oesophageal adenocarcinoma (a 2-fold increase. Excessive alcohol consumption (3 or more drinks per day) is one of the strongest predisposing factors to developing oesophageal squamous cell carcinoma. HPV virus. Metastasis typically occurs to the peri-oesophageal lymph nodes, liver, and lungs. PATHOPHYSIOLOGY: Alcohol doesn't cause cancer it is the breakdown product acetaldehyde that does. Chronic GORD causes metaplasia (Barrett's oesophagus) in which the stratified squamous epithelium that normally lines the distal oesophagus is replaced by abnormal columnar epithelium. Although this might seem a favourable adaptation to chronic reflux (because columnar epithelium appears more resistant to reflux-induced injury), these metaplastic cells may become dysplastic, and ultimately malignant.

Question 56

PRESENTATION OF OESOPHAGEAL CARCINOMA? Investigations for oesophageal cancer name 3

Accepted Answer

Often presents late hence poor prognosis. OGD with biopsy. The most common presenting signs of squamous cell carcinoma or locally advanced adenocarcinoma are dysphagia and odynophagia. For patients with Barrett's oesophagus and early stage adenocarcinoma of the oesophagus and gastro-oesophageal junction, reflux is the most common presenting sign. Severe weight loss usually occurs after swallowing difficulties begin. Upper oesophageal tumours can involve the recurrent laryngeal nerve, causing the patient to have a hoarse voice. Phrenic nerve involvement can trigger hiccups. A postprandial or paroxysmal cough may indicate the presence of an oesophago-tracheal or oesophago-bronchial fistula resulting from local invasion by a tumour. INVESTIGATIONS: first investigation is usually an upper GI endoscopy. Barium swallow sometimes done before to confirm obstruction but not routine. Serum electrolytes and renal function testing should be performed in advanced cases with near or complete oesophageal obstruction, as patients may become severely volume-depleted and hypokalaemic because of their inability to swallow fluids and their own potassium-rich saliva. CT thorax and abdomen (indicates size of primary tumour, local invasion, and presence or absence of metastases). MRI is an alternative to CT. (18F)-fluoro-2-deoxy-D-glucose positron emission tomography (FDG-PET) is now a routine investigation before initiating therapy. (hyperactivity (hot spot) at primary tumour site and locoregional disease). Endoscopic ultrasound (EUS) is now a standard pre-treatment test. It can identify all the histological layers of the oesophagus and thereby confirm the T-stage with 90% accuracy. Bronchoscopy with fine needle aspiration if middle or upper 1/3s. DD: Barretts esophagus, achalasia benign stricture.

Question 57

TX for oesophageal cancer? Complications? 5 year survival? PROGNOSIS?

Accepted Answer

Treatment options: oesophagectomy. Endoscopic resection. chemoradiotherapy. Radiotherapy. Metal stenting and brachytherapy for symptom relief. only 40% resectable. Complications: postoperative pneumonia, aspiration pneumonia, post-resection oesophageal reflux, oesophago-aortic fistula, tracheo-oesophageal fistula. 5yr survival = 10%. Survival depends on stage of disease and treatment. With aggressive therapy involving surgery and chemoradiotherapy , 5-year survival for stage 1 disease approaches 80%; for stage 2 disease, it approaches 60%; for stage 3 disease, it ranges between 30% and 50%. With surgery alone, the results are worse. Overall, 5-year survival after tumour resection is about 20% to 35%. For patients with early tumours limited to the mucosa, 5-year survival rates can exceed 80%. Lymph node involvement is an important determinant of survival; patients free of lymph node metastases have 5-year survival of 60%, whereas survival decreases to 10% to 20% in lymph node-positive patients.

Question 58

What is Achalasia? Name 3 investigations? Name 3 Tx options?

Accepted Answer

failure of relaxation of lower oesophageal sphincter Barium swallow, oesophageal manometry, OGD botox injection, Hellers cardiomyotomy, balloon dilatation

Question 59

Name 3 causes of oesophageal strictures? and Tx

Accepted Answer

Gord, cancer and collagen disorders (SLE, scleroderma) balloon dilatation and oesophageal replacement surgery

Question 60

What 2 lab tests suggest Gi bleed?

Accepted Answer

urea increase and haemoglobin decrease

Question 61

Hiatus hernia - epidemiology? Aetiology? Pathophysiology? diagnosis 2 things? 2 types? whats the most common? Tx?

Accepted Answer

Hiatal hernia is the protrusion of intra-abdominal contents through an enlarged oesophageal hiatus of the diaphragm. A hiatal hernia most commonly contains a variable portion of the stomach; less commonly, it may contain transverse colon, omentum, small bowel, or spleen, or some combination of these organs. The herniated contents are usually contained within a sac of peritoneum. 50% people over 50. Among all hiatal hernias, the sliding (type I) hernia is by far the most common, accounting for 90% to 95% of cases. During normal swallowing, the oesophagus shortens several centimetres secondary to contraction of its longitudinal muscular layer. This action, in combination with elevations in intra-abdominal pressure such as from coughing, sneezing, straining, and strenuous exercise, produces physiological movement of the distal oesophagus and possibly the gastro-oesophageal junction through the oesophageal hiatus and into the posterior mediastinum. This movement is countered by the resistance of the phreno-oesophageal ligaments, which run between the diaphragm and the gastro-oesophageal junction. These ligaments are somewhat elastic in terms of their stretch and recoil. At some point, however, the physiolgical movement and stretching may enlarge the hiatus, leading to permanent residence of a portion of the stomach above the diaphragm. Although a number of risk factors predispose a patient to hiatal hernia, the precise cause of hiatal hernia is difficult to know with certainty in most patients. In sliding hiatal hernia, the displacement of the gastro-oesophageal junction above the diaphragm decreases the lower oesophageal sphincter (LOS) pressure. Because the LOS is the primary determinant of the anti-reflux valve, a decrease in LOS pressure predisposes the patient to gastro-oesophageal reflux. Thus, the most common symptom of a symptomatic sliding hiatal hernia is reflux-associated heartburn, or pyrosis. It follows that the mainstay of treatment for a symptomatic sliding hiatal hernia is very similar to that for GORD. The situation for the relatively uncommon para-oesophageal hernia differs in that the rotation and twisting of the stomach as it migrates into the chest can produce intermittent strangulation with obstruction and ischaemia. This can result in pain, vomiting, ulcers, and necrosis. Pain from a para-oesophageal hernia can easily be mistaken for angina pectoris. Ischaemic ulcers can produce upper GI haemorrhage with haematemesis. Ischaemic necrosis of the stomach is one of the most feared complications of para-oesophageal hernia. Such an event typically progresses rapidly to mediastinitis and death if left untreated. Strong risk factor: obesity. PRESENTATION: Bowel sounds in chest. Patients with sliding type I hiatal hernias always have associated GORD. Type II and III (paraesophageal) hiatal hernias may or may not have associated GORD. heartburn, reflux of sour liquid material (water brash), dull retrosternal chest pain (especially associated with swallowing), dysphagia, crampy pain associated with swallowing (odynophagia), vomiting undigested food, haematemesis, early satiety, bloating, hoarseness, and wheezing/dyspnoea. None of these features are pathogonomic for hiatal hernias. Some of these symptoms may be made worse by positions that increase intra abdominal pressure. The patient presenting with a complicated hiatal hernia (involving obstruction, bleeding, and/or ischaemia) may have the following symptoms: severe chest pain, non-bilious vomiting, haematemesis (over 50 cc), dyspnoea, fevers and chills, confusion. Signs on examination: oropharyngitis (secondary to reflux of gastric contents) wheezing (secondary to aspiration of refluxate) decreased left chest breath sounds, dullness to thoracic percussion, presence of bowel sounds in the left chest. INVESTIGATIONS: A CXR is a simple and inexpensive test and is indicated as the first test in all symptomatic patients. Patients with hiatal hernia may have a retrocardiac air bubble in the intrathoracic portion of the stomach. The diagnosis of hiatal hernia primarily is established through the use of diagnostic testing, including: CXR, contrast upper GI series, oesophago-gastro-duodenoscopy (OGD) (For eosphagitis), CT scan or MRI. barium swallow and endoscopy. Sliding - whole G-E junction into chest (80%). Rolling - bulge of stomach (20%). sliding - conservative Tx. Rolling - fundoplication. Lifestyle modifications such as losing weight, elevating the head of the bed, and avoiding large meals, meals just before bedtime, alcohol, and acidic foods. If conservative treatment fails, and PPIs not helpful or poor compliance to it then surgery is indicated. A loose Nissen's fundoplication (i.e., 360° wrap) should generally be used whenever feasible, even in patients without GORD.

Question 62

Define peptic ulcer disease? Aetiology? Presentation? Name 3 complications?

Accepted Answer

A break in the mucosal lining of the stomach or duodenum more than 5 mm in diameter, with depth to the submucosa. Ulcers smaller than this or without obvious depth are called erosions. Peptic ulcers result from an imbalance between factors promoting mucosal damage (gastric acid, pepsin, Helicobacter pylori infection, non-steroidal anti-inflammatory drug use) and those mechanisms promoting gastroduodenal defense (prostaglandins, mucus, bicarbonate, mucosal blood flow). AETIOLOGY:- smoking, alcohol, NSAiDs (most of gastric ulcers), zollinger-ellison syndrome, H.pylori (90% of duodenal ulcers) gastric ischaemia (responsible for the 'stress ulcers' that occur commonly in patients with multiple organ failure in intensive care units). certain medications (e.g., potassium chloride, bisphosphonates), crohns. PRESENTATION: GI bleeding (uncommon), Epigastric pain, epigastric tenderness, heartburn, bloating, nausea, vomiting. RISK FACTORS: Smoking, H pylori, ITU, NSAIDS, family history or previous history of ulcers. INVESTIGATIONS: Helicobacter pylori breath test or stool antigen test (Ordered in patients 55 years or younger without alarm features.), upper gastrointestinal endoscopy (The most specific and sensitive test. Initially ordered if patient has any 'alarm symptoms' or is over 55 years of age, and subsequently if patient does not respond to treatment, If an ulcer is present, H pylori testing should always be performed. Endoscopy should be repeated after 6 to 8 weeks in patients with gastric ulcer to ensure ulcer healing and to rule out malignancy, unless ruled out at first endoscopy.)., FBC (if has evidence of GI bleeding), stool heme test. Other tests: fasting serum gastrin levels: hypergastrinaemia in Zollinger-Ellison syndrome. Treatment: Acute active bleeding ulcer: NSAIDS discontinued, transfusion if needed, endoscopy, H pylori testing. PPI IV (After 72 hours, patient should be switched to oral dosing and continue for 4 to 8 weeks after discharge.) Surgery if perforated Ulcer. No bleeding: H pylori negative: NSAIDS discontinued. Try find underlying cause. 1st line: PPIs. 2nd Line: H2RA or sucralfate or sucralfate or misoprostol (can be used if NSAIDS need to be continued). No bleeding: H pylori positive: H pylori eradication therapy (shouldn't be started without documented infection): 7 days (quadruple therapy: bismuth, 2 antiBs, PPI), 10 days (sequential therapy: PPI and 1 antibiotic for 5 days, then another 2 for the rest), or 14 days (triple therapy). Ideally, treatment with triple therapy is recommended for 14 days. If the first treatment does not eradicate H pylori, at least 1 alternative out of the sequential, quadruple, or triple therapy regimens should be tried. If the organism cannot be eradicated despite repeated attempts, long-term acid suppression therapy may be necessary to control symptoms. Check for eradication of H pylori 1 month after the end of therapy. If it is eradicated acid suppression is not needed. If ONGOING: Acid supression therapy (PPI, or H2RA). Misoprostol (Specifically indicated for non-steroidal anti-inflammatory drug (NSAID)-associated ulcers only.).

Question 63

Name 3 symptoms of peptic ulcer disease ?

Accepted Answer

Epigastric pain, dyspepsia, heart burn

Question 64

6 DD for peptic ulcer?

Accepted Answer

Gord, Gastroparesis (Early satiety prominent. Usually a history of longstanding diabetes with evidence of peripheral neuropathy and other end-organ damage.) Gastric cancer. gallstones. Crohns . chronic pancreatitis. Hepatitis. FUnctional dyspepsia. Oesophageal cancer.

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2.03 Brown vomit: UGIB, Alcoholism, GORD, Dyspepsia, Dysphagia, PUD, Achalasia, Zollinger Ellison syndrome, Stomach cancer, Shock, Sepsis, Anaphylaxis, DIC, Hiatus Hernia, Eosphageal cancer, Gastroenteritis. Diarrhoea. Constipation. Nausea and vomiting. Oesophageal perforation. Flashcards

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