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Flashcards in GI Deck (22)
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1
Q

Indications of splenomegaly

A

Splenomegaly ∆∆
Massive spleen (>8cm):
CML (most common).
Myelofibrosis.

Infections: painful nodes
Infectious mononucleosis.
Viral hepatitis (large liver).
Malaria (recent travel).
Haemolytic anaemia (↓Hb).
Portal hypertension:
Cirrhosis (alcohol; ↑liver initially).
Schistosomiasis (travel).
Sarcoidosis. Amyloidosis.
Rheumatoid arthritis.
Renal or colonic mass?
Mild spleen (2-4cm):
Lymphoma:
NHL (extra-nodal disease).
HL (20s & old, alcohol pain).
Leukaemia:
CML (most common; ↑WCC).
CLL (chronic, older).
ALL (acute, children).
AML (acute, gum hypertrophy).
Myeloproliferative:
Myelofibrosis (large liver).
Polycythaemia rubra vera (↑Hb).
Essential thrombocythaemia (↑platelets).
2
Q

Indications of lymphadenopathy

A
Lymphadenopathy ∆∆
Leukaemia
Lymphoma
Metastasis (firm, painless).
Infectious mononucleosis.
Mumps (parotids).
Reactive lymphadenitis (soft, mobile, tender. TB, inf. mono., local inf’n).
SLE (generalised lymphadenopathy).
Sarcoidosis.
3
Q

Gut nervous system

A

Enteric Nervous System
“The brain of the gut”: 100 million neurons stretching from oesophagus to the anus. Can function independently.
Myenteric plexus: mainly controls GI tract motility (frequency and strength of contraction) of muscularis.
Submucosal plexus: controls secretory cells of mucosal epithelium; chemoreceptors (chemicals within foods) and stretch receptors (food dispending wall).
Autonomic Nervous System
Vagus (X): supply parasympathetic fibers to most part of the GI tract, except last half of large intestine.
Pelvic Splanchnic: supply parasympathetic fibers to last half of large intestine.
Parasympathetic: parasympathetic nerves form neural connections with ENS. Parasympathetic stimulation cause increase in GI secretion and motility (by increasing activity of ENS neurons).
Sympathetic: form neural connections with ENS. Stimulation decrease GI secretion and motility.
Gastrointestinal Reflex Pathways
Regulate GI secretions and motility in response to GI tract stimuli. Sensory receptors (chemo and stretch) synapse with ENS, CNS and ANS neurons causing response.
Types
Colic, endoderm, vague pain.
Foregut: pharynx – ampulla of Vater. Referred to epigastric region.
Midgut: ampulla of Vater – 2/3 across transverse colon. Referred to umbilical region.
Hindgut: 2/3 across transverse colon – upper part of anus. Referred to hypogastric (pubic) region.
Constant, ectoderm, localized – includes parietal peritoneum.

4
Q

Signs of gut ischaemia

A

Arterial, sudden, acidosis, bacteraemia, distention, colicky pain, septic pain out of proportion to physical signs (e.g., ischaemia bowel).

5
Q

Oesophageal dysmobility

A
Achalasia: malfunction of myenteric plexus; lower oesophageal sphincter fails to relax as food approaches (dysphagia, regurgitation). Oesophageal distension causes chest pain (often confused with heart origin). Managed by endoscopic dilatation (weakening the sphincter).
Bulbar palsy (e.g., motor neurone disease), diabetes mellitus.
Oesophageal Diverticula: epithelial pouch causing dysphagia and regurgitation. Usually asymptomatic. Surgically repaired if severe symptoms.
Benign Oesophageal Stricture: Peptic stricture (with smooth epithelial wall) secondary to reflux, corrosive ingestion, radiotherapy, varices sclerosis, prolonged NG intubation. Managed by dilatation (occasionally surgery).
6
Q

Oesophageal carcinoma

A

Oesophageal Carcinoma
Aetiology: Adenocarcinoma (more common, related to Barrett’s oesophagus), squamous cell carcinoma (becoming more rare). Peaks in 60s. Usually ulcerative lesion, extending around oesophagus, causing stricture.
Clinical features: dysphagia (progressive, unrelenting), pain, weight loss, anorexia, aspiration (late).
Investigations: endoscopy, barium swallow, CT (staging).
Management: surgery (if within oesophagus wall), radio and chemo therapy (adenocarcinoma is radio-insensitive), stenting, brachytherapy.
History and interpretation
Difficult swallowing solids and liquids from the start? Yes: motility disorder (achalasia, neurological) or pharyngeal causes. No: solids then fluids: suspect stricture.
Difficulty initiating swallowing: bulbar palsy (especially if coughs on swallowing).

Painful swallowing (odynophagia): cancer, oesophagitis, achalasia, oesophageal spasm.
Intermittent dysphagia: oesophageal spasm. Worsening: malignant stricture.
Burge or gurgle on drinking: pharyngeal pouch.

7
Q

Mallory-weiss tear

A

Linear mucosal tear at oesophagogastric junction due to intra-abdominal pressure (after coughing, retching, or alcohol binge). Presents with haemorrhage, which usually spontaneously stops (occasionally requires surgery).

8
Q

Pyloric stenosis

A

Failure of the pyloric sphincter to relax produces hypertrophy of the adjacent pyloric muscle. Associations with Turner’s syndrome, oesophageal atresia and phenylketonuria. Occurs in 1 in 400, 4 males to 1 female, genetic component (polygenic, 5% risk of passing on).
Clinical features
Develops in first 3 to 6 weeks of life. Projectile vomiting, no bile, child hungry and will re-feed. Failure to gain weight (failure to thrive). Constipation (due to dehydration). 95% have a palpable RUQ pyloric mass (shape and size of an olive). Occasionally haematemesis.
Investigations
Barium meal (delayed gastric emptying, a dilated stomach and a narrowed and attenuated pyloric canal - the ‘string sign’), U&E (hypokalaemia, hypochloraemic), ABG (metabolic alkalosis).
Management
Stabilize electrolytes, Ramstedt’s operation (longitudinal incision is made through the hypertrophied muscle as far as the mucosa; the mucosa is left intact and is seen bulging into the incision the cut edges are separated), restart feeding after 3 hours (initially glucose, then milk).

9
Q

Causes of Jaundice

A

Pre-hepatic
Excess production of bilirubin: high serum bilirubin with normal LFTs suggests non-liver cause (Gilbert’s syndrome, haemolysis, ineffective erythropoiesis, rifampicin).
Hepatocellular

High serum bilirubin, abnormal LFTs (congenital liver disease, cirrhosis or hepatitis, inflammatory cholestasis, paracetamol, methyldopa Pre-hepatic
Excess production of bilirubin: high serum bilirubin with normal LFTs suggests, barbiturates).
Obstructive (cholestatic)
Blockage of bile drainage, very high serum bilirubin, abnormal LFTs (gallstones / cholangitis, pancreatitis, duodenum or pancreatic Ca, isoniazid, chlorpromazine).

Neonatal jaundice
<24hr of birth: always abnormal. Sepsis, Rhesus haemolytic disease, ABO incompatibility, glucose-6-phosphate dehydrogenase deficiency.
>24hr after birth: common and usually physiological.
Prolonged jaundice (more than 14 days): breast-feeding, sepsis, hypothyroidism, CF, biliary atresia if conjugated and pale stools.
Managed by phototherapy; exchange transfusion.

Gilberts syndrome
Common (3-5% of population) prehepatic jaundice: jaundice,  bilirubin (mainly unconjugated), normal urine, no risk factors, normal LFTs, no signs of haemolysis.
Caused by defect in glucuronyl transferase which conjugates bilirubin with glucuronic acid in liver.

10
Q

Signs of hepatic cirrhosis

A

Jaundice (above), fever, spider naevi (in superior vena cava distribution, secondary to hyperoestrogenism, pressure on center blanches legs, >2 abnormal), palmar erythema, xanthomas (cholesterol deposits, palmar creases, above eyes; hypercholesterolaemia in chronic biliary obstruction), hepatomegaly (although ends up being small with chronic cirrhosis), splenomegaly (portal hypertension), gynaecomastia and testicular atrophy (oestrogen not being converted to testosterone), caput medusa (see portal hypertension), haematemesis (oesophageal varices: see portal hypertension), ascites (distended abdomen) and peripheral oedema (low albumin in blood), bleeding / bruising (reduced clotting factors), confusion (encephalopathy), liver flap, leukonychia, clubbing, sepsis (bacteria peritonitis), melaena (black tarry faeces, of partially digested blood, from 500mL+ upper GI bleed / haematemesis), dark urine (conjugated hyperbilirubinaemia), pale stools (lack of bile in stools), steatorrhoea (malabsorption of fat due to bile obstruction), pruritus (itching due to biliary obstruction resulting in bile salt accumulation).

11
Q

Managing portal hypertension

A

Portal hypertension
Aetiology:  portal vascular resistance due to chronic liver disease.
Prehepatic: portal vein thrombosis (esp children).
Intrahepatic: cirrhosis, schistosomiasis, fibrosis.
Posthepatic: heart failure, constrictive pericarditis.
Clinical features: haematemesis, melaena, oesophageal varices, ascites, encephalopathy.
Collateral circulation at portal-systemic anastomoses: oesophageal varices, haemorrhoids (rectum), caput medusa (systemic superficial epigastric veins communicate with paraumbilical veins), colon anastomoses (systemic retroperitoneal veins communicate with colic vein twigs).
Management: TIPS (transjugular portosystemic shunt (portal vein to hepatic vein)).

12
Q

Managing liver failure

A

10% dextrose IV (avoiding hypoglycaemia), vitamin K and clotting agents, treat infections (not gentamicin -  risk of renal failure), manage any ascites ( Na+ and water intake), haemofiltration and albumin IV (if renal failure develops), avoid drugs with hepatic metabolism, consult with transplant center for assessment

13
Q

Coeliacs

A

Coeliac disease
Aetiology
Digestive disease that damages small intestine. Caused by protein called Gliadin (constituent of gluten) found in wheat, rye and barley. If eaten causes damaging immune response. Loss of villi occurs. Associated with lymphoma.

Clinical features
Chronic diarrhoea, steatorrhoea, abdominal distension, failure to thrive. Skin vesicles: Dermatitis herpetiformis.
Investigations
Gold standard blood test is endomysial antibodies, duodenal biopsy (flat mucosa), then gluten free diet, finally 9 months later another biopsy (normal mucosa).
Management
Gluten free diet.

14
Q

Types of hernias

A

Reducible (hernia can be completely replaced into peritoneal cavity). May disappear on lying down, usually painless, reducible with cough impulse (a palpable impulse when the patient coughs).
Irreducible (cannot be reduced due to adhesion or contents being larger than sac neck). Does not reduce, usually painless, cough impulse.
Strangulated (contents of hernia constrict sac neck cutting off circulation). Severe hernia pain and colicky abdominal pain, obstruction signs (vomiting, distension, constipation). Cannot be reduced, no cough impulse.

Umbilical hernia: congenital failure of complete closure of umbilical cicatrix. Common in black children. Vast majority close spontaneously. Surgical repair only if hernia persists after 2 years old.
Para-umbilical hernia: acquired hernia occurring just above or below umbilicus. Common in obese, multiparous, middle-aged ♀. Narrow neck makes irreducibility and strangulation likely. Mayo’s operation overlaps rectus sheath above and below hernia.
Ventral hernia: upper midline ventral hernia. Gap between recti. Most require no treatment.
Epigastric hernia: form of ventral hernia, protruding through linea alba. Painful, requiring suturing of defect.
Incisional hernia: through defect in scar. Usually wide neck, so strangulation if rare. Surgically dissect out and re-suture; or mesh if large.
Congenital diaphragmatic hernia: through foramen of Morgagni: small and unimportant. Foramen of Bochdalek or central tendon are large, presenting as respiratory distress shortly after birth; urgent surgical repair is required. Congenital hiatus hernia presents with regurgitation, vomiting, dysphagia, progressive weight loss in small children; usually respond to feeding in sitting position, otherwise surgery.
Traumatic diaphragmatic hernia: rare. L>R sided. Herniation of stomach or spleen into thoracic cavity (gas filled stomach can be mistaken for pneumothorax). Urgent surgical repair.
Hiatus hernia: Sliding (90%): stomach slides though hiatus, producing effects of space-occupying lesion in chest and disturbance of cardio-oesophageal sphincter. Rolling (10%): produces partial volvulus (twisting of GIT). Most hiatus hernias are asymptomatic, others fall into 3 groups: mechanical (cough, dyspnoea, palpitations, hiccough), reflux (burning retrosternal or epigastric pain, aggravated by lying down or stooping), oesophagitis (dysphagia, bleeding). Sliding treated symptomatically. Rolling are often asymptomatic, but are more serious with risk of complete gastric volvulus – surgical repair indicated.

15
Q

Intussusception

A

spasms occurring every 10-15 minutes, lasting 2-3 minutes, passage of blood and/or slime per rectum (late; red current jelly on examining finger), sausage-shaped mass usually palpable (often RUQ).
In <24 hours child can become intensely toxic, have a distended abdomen, and exhibit faeculent vomiting. Chronic intussusception is rare, presenting with milder features. It may cause failure to thrive.
Investigations
Assess hydration status, AXR (obstruction), US (Swiss-roll appearance), barium enema (stack of coins sign).
Management
Rehydrate if necessary.
Reduction by barium enema under radiological control (increase air pressure in bowel; contraindicated if features of perforation or peritonitis).
Surgical indications include: child under 3 months or over 2 years, clinical signs of peritonitis, gross dehydration, failure of medical treatment, or recurrence after medical treatment.

16
Q

Colorectal cancer

A

Pathology: most tumours arise from malignant transformation (accumulation of gene mutations) of benign adenomatous polyp (65% rectosigmoid). Polypoid mass with ulceration, spreading by direct infiltration through bowel wall. Involves lymphatics and blood vessels, subsequently spreading to liver.

Histology: “Signet ring” cells in which mucin (glycoprotein – main constituent of mucous) displaces the nucleus to the side of the cell.
Clinical features
Altered bowel habit, rectal bleeding (or mixed with stools), anaemia, weight loss, tenesmus (desire to defecate), passing mucous.
Investigations
Digital exam, colonoscopy is gold standard (visual and biopsy), CT (staging), MRI (better view through pelvis than CT).
Dukes staging of colorectal cancer:
A: tumour confined within bowel wall.
B: tumour extended through bowel wall.
C1: tumour involving proximal lymph nodes.
C2: tumour involving distal lymph nodes.
D: distant metastases.
Management
Surgical removal.
Preoperative chemo-radiotherapy if lesion needs shrinking.

17
Q

IBS

A

Irritable Bowel Syndrome is the most common cause of diarrhoea in adults and abdominal pain in children. UK prevalence 10%, 2♀:1♂. IBS is a functional disorder of the bowel, characterized by a hypersensitivity to normal stimuli.
Clinical features
NICE suggest positive diagnosis of IBS, in the absence of “red-flags”, when the following symptoms recur for six months:
Abdominal discomfort:
relieved by defaecation or
associated with altered bowel habit (frequency or form).
and two from:
altered stool passage (straining, urgency, incomplete evacuation),
abdominal bloating or distension,
symptoms made worse by eating,
passage of mucus.
Lethargy, nausea, lower backache, and increased urinary frequency support the diagnosis.
Investigations
Full blood count (anaemia), erythrocyte sedimentation rate or c-reactive protein (inflammation), endomysial antibodies or tissue transglutaminase (coeliac disease).
Management
Immediate referral to secondary care for “red-flags”: unexplained weight loss, rectal bleeding, family history of ovarian or bowel cancer, anaemia, abdominal or rectal masses, inflammatory markers, or six week history of increased stool frequency in person aged over 60 years.
Diet: limit fibre intake (soluble preferable to insoluble), reduce digestion-resistant starches (common in processed foods), restrict fresh fruit to three portions per day, encourage non-caffeinated fluids (especially water), any use of probiotics should be given 4 weeks to provide benefit. Refer to dietitian for food avoidance or exclusion diet, when food considered to be a major factor.
Lifestyle: explain the benefits of higher activity levels, making the most of leisure time, and protecting relaxation time.
1st line medication: antispasmodics (hyoscine, mebeverine), laxatives for constipation, and antimotility agents (loperamide) for diarrhoea. Doses should be titrated to provide a soft well-formed stool, and balanced with patient tolerance of IBS symptoms and medication side-effects.
2nd line medication: low dose tricyclic antidepressant (amitriptyline). Selective serotonin reuptake inhibitor if tricyclic ineffective

18
Q

Peritonitis

A

Infected peritonitis
Perforation of hollow viscus (common): peptic ulcer, gastric carcinoma, appendicitis, diverticulitis, Meckel diverticulum, inflammatory bowel disease, intestinal infarction, intestinal strangulation, colorectal carcinoma, cholecystitis, trauma, ingestion of a sharp foreign body, perforation by endoscope or catheter, and anastomotic leakage. Agents: gram -ve (e.g. Escherichia coli) and anaerobic bacteria (e.g. Bacteroides fragilis).
Disruption of the peritoneum: trauma, surgical wound, continuous ambulatory peritoneal dialysis, intra-peritoneal chemotherapy. Agents: staphylococcus aureus, staphylococci.
Spontaneous bacterial peritonitis: absence of obvious source. Occurs in children, or in patients with ascites.
Systemic infections (such as tuberculosis) may rarely have a peritoneal localization.
Non-infected peritonitis
Leakage of sterile body fluids into the peritoneum, such as blood (e.g. endometriosis, blunt abdominal trauma), gastric juice (e.g. peptic ulcer, gastric carcinoma), bile (e.g. liver biopsy), urine (pelvic trauma), menstruum (e.g. salpingitis), pancreatic juice (pancreatitis). While these body fluids are sterile at first, they frequently become infected once they leak out of their organ, leading to infectious peritonitis within 24-48h.
Sterile abdominal surgery normally causes localized or minimal generalized peritonitis, which may leave behind a foreign body reaction and/or fibrotic adhesions. May also be caused by sterile foreign body left in the abdomen after surgery.
Rare: familial Mediterranean fever, porphyria, and systemic lupus erythematosus.

Symptoms
Abdominal pain, tenderness, guarding, rebound tenderness, lying still. Generalized peritonitis often causes a “washboard” diffuse abdominal rigidity. Other: ileus (absence of bowel sounds; causes nausea and vomiting), fever, tachycardia.
Complications
Sequestration of fluid and electrolytes (electrolyte disturbances, hypovolaemia, shock, acute renal failure), peritoneal abscess, sepsis, breathing difficulties (fluid pushing on diaphragm).
Diagnosis
Clinical picture (above), leukocytosis and acidosis may be present, erect CXR (gas under diaphragm), exploratory peritoneal lavage (e.g. in cases of trauma, looking for WBC, RBC or bacteria).
Management
IV rehydration, IV antibiotics, laparotomy to explore and lavage.

19
Q

Causes of peripheral neuropathy

A

Diabetes - this is the most common cause of chronic peripheral neuropathy in Europe. The high blood sugar (glucose) levels in people with poorly controlled diabetes can lead to the nerve damage.

Dietary deficiencies - B12 or folate vitamin deficiencies can cause nerve damage and peripheral neuropathy.
Medicines - certain medicines such as some chemotherapy medication and medicines used to treat HIV can cause damage to peripheral nerves.

Poisons (toxins) - some toxins, such as insecticides or solvents (a problem for people who sniff glue), can cause peripheral nerve damage.

Cancers - if you have certain cancers, you can develop peripheral neuropathy.

Alcohol excess - alcoholic neuropathy is the name given to peripheral neuropathy that affects some people who drink large amounts of alcohol. The high alcohol levels in the body cause the nerve damage.

Chronic kidney disease - if your kidneys are not functioning normally, this can lead to an imbalance of salts and chemicals in the bloodstream and can cause peripheral neuropathy.

Injuries - these can put pressure directly on the nerves. Injuries can include broken bones and nerve compression injuries (for example, pressure placed on nerves by plaster casts, splints, braces).

Infections - damage can be caused to peripheral nerves by some infections, including shingles, HIV infection and Lyme disease (an infection caused after you are bitten by a tick infected with a specific germ (bacterium)). Guillain-Barré syndrome is the name given to a specific type of peripheral neuropathy that is usually triggered by an infection.

Connective tissue diseases - conditions including rheumatoid arthritis, Sjögren’s syndrome and systemic lupus erythematosus can all lead to peripheral neuropathy in some people.

Certain inflammatory conditions - conditions including sarcoidosis and coeliac disease can also cause peripheral neuropathy.

Hereditary diseases - certain diseases that you can inherit from your parents can cause peripheral neuropathy. Two of the most common of these are Charcot-Marie-Tooth syndrome and Friedreich’s ataxia.

20
Q

Lactose intolerance

A

Congenital lactase deficiency is a disorder in which infants are unable to break down lactose in breast milk or formula. This form of lactose intolerance results in severe diarrhoea. If affected infants are not given a lactose-free infant formula, they may develop severe dehydration and weight loss.

Lactose intolerance in adulthood is caused by reduced production of lactase after infancy (lactase nonpersistence). If individuals with lactose intolerance consume lactose-containing dairy products, they may experience abdominal pain, bloating, flatulence, nausea, and diarrhoea beginning 30 minutes to 2 hours later.

Lactose intolerance in infants (congenital lactase deficiency) is caused by mutations in the LCT gene. The LCT gene provides instructions for making the lactase enzyme. Mutations that cause congenital lactase deficiency are believed to interfere with the function of lactase, causing affected infants to have a severely impaired ability to digest lactose in breast milk or formula.

Lactose intolerance in adulthood is caused by gradually decreasing activity (expression) of the LCT gene after infancy, which occurs in most humans. The type of lactose intolerance that occurs in infants (congenital lactase deficiency) is inherited in an autosomal recessive pattern.

21
Q

Pin rolling tremor

A

If you have a pill rolling tremor, it looks like you are trying to roll a pill or another small object between your thumb and index finger. It’s a resting tremor, which means that it’s most likely to happen when your body is relaxed rather than when you’re using your hands. Associated with Parkinsons.

22
Q

Causes of yellow stool

A

Diarrhoea, coeliac, giardiasis, gilberts syndrome,

GERD, cholestasis, pancreatic, liver, or gallbladder disease, abdominal tumour, cirrhosis, hepatitis.