Core conditions Flashcards

Question

H pylori | - 3 mechanisms of injury

Answer 1

Hypergastrinemia - Negative feedback for gastrin is blocked – resulted in uncontrolled excess gastrin → hyperacidity Direct mucosal injury - Cytotoxins cause increased production of ammonia (toxin to epithelial cells) Inflammatory response - Mediated by macrophages, neutrophils, T-cell

Answer 2

Non-invasive testing - Breath test - Antibody measurement (serology) - > Tells you that in some point have been in contact with helicobacter - Stool HP antigen test Invasive - Culture - used if want antibiotic sensitivity - Histology - Urease (CLO) test - >Changes to red (high pH due to ammonia) - >Used bedside at endoscopy

Answer 3

``` 1st line (90% efficacy) Triple therapy for 1 week ``` PPI - Lansoprazole 30mg 2x daily (or omeprazole 20mg BD) Clarithromycin 500mg 2x daily Metronidazole 400mg 2x daily 2nd line (85-90% efficacy) - 1 week - Lansoprazole 30mg 2x daily (or omeprazole 20mg BD) - Clarithromycin 500mg 2x daily - Amoxycillin 1g 2x daily Eradication not always necessary / eradication may cause regression of some gastric lymphomas – MALTomas SE: diarrhoea (30-50% - mild, C difficile colitis can occur), Amoxicillin: penicillin-sensitivity rash, diarrhoea Clarithromycin: GI upset, enzyme inhibitor Metronidazole: metallic taste, flushing/vomiting if taken with alcohol, nausea, vomiting, abdominal cramps, headaches, rash

Answer 4

Tissue injury → release of phospholipids → arachidonic acid - Leukotrienes (bronchoconstriction) - Cox-1 (constitutional) Cytoprotective prostaglandins -> Protective for gastric mucosa lining; Aid platelet aggregation - Cox -2 (inducible) - Recruit inflammatory white cells; Sensitize skin pain receptor; Stimulate hypothalamic fever response All NSAIDs also inhibit COX-1 → increase risk of developing ulcers due to reduced protection from acid Prostaglandins stimulate bicarbonate and mucus secretion and increase mucosal blood flow RF - Age >60 y/o (atrophic gastritis) - Past history of peptic ulcer disease - Past history of adverse events with NSAIDs - Concomitant corticosteroid use - High dose or multiple NSAIDs - Individual NSAID – lower with ibuprofen Treatment - Offending drug should be removed - NSAIDs should be used at lowest effective dose - Co-prescription of a PPI will heal most ulcers - Prescription of a COX-2 specific drug will limit GI toxicity -> Celecoxib

Answer 5

``` colorectal cancer ischaemic colitis appendicitis IBD Infection ```

Answer 6

Exocrine – digestive function – releases juices into ducts - Trypsin & chymotrypsin → proteins - Amylase → carbohydrates - Lipase → fats • Endocrine – releases hormones into blood; regulates blood sugar

Answer 7

Pancreas divisum (a single pancreatic duct has not formed – remain as two distinct: dorsal and ventral) Annular pancreas (ring of pancreatic tissue continuous with head of pancreas surrounds 2nd part of duodenum → constriction)

Answer 8

Acute inflammatory process of the pancreas - variable involvement of other regional tissues/ remote organ systems Epidemiology: 40/100,000; 3% of all admissions with abdominal pain Mild: Minimal organ dysfunction; Uneventful recovery Severe: Organ failure and/or local complication; Necrosis Pathology - Premature intracellular trypsinogen activation → proteases released and digest pancreas - Nuclear factor kappa activated → mitochondrial dysfunction, autophagy, inflammatory response

Answer 9

I Get Smashed I - idiopathic G – gall stones E – ethanol T – trauma ``` S – steroids M – mumps A – Autoimmune S – scorpion bite H – hypoglycaemia, hypocalcaemia E – ERCP D – dehydration; drugs ``` Idiopathic; Gall stones; Ethanol; Trauma; Steroids; Mumps; Autoimmune; Scorpion bite; ERCP; vascular disease hypothermia Hypoglycaemia, hypocalcaemia, hyperparathyrodism Dehydration; drugs - Furosemide; didanosine; oestrogens; azathioprine, thiazide diuretics; sulphonamides; tetracyclines; sulindac; mercaptopurine Malignancy –periampullary cancer

Answer 10

- Variable Severe abdominal pain radiating to back - Relieved when lean forward; worse with movements Associated with vomiting, nausea, fever, tachycardia Organ failure – respiratory, renal; ARDS Jaundice, cholangitis Grey Turner’s sign (bruising of flanks → retroperitoneal bleeding) Cullen’s sign (bruising around umbilicus due to liberated pancreatic enzymes →diffusion of fat necrosis and inflammation with retroperitoneum or intraabdominal bleeding)

Answer 11

bruising of flanks → retroperitoneal bleeding

Answer 12

bruising around umbilicus due to liberated pancreatic enzymes →diffusion of fat necrosis and inflammation with retroperitoneum or intraabdominal bleeding

Answer 13

Age – 40-50 years; Epigastric tenderness Exam (1) In early stages – guarding & rebound tenderness absent as inflammation principally retroperitoneal - -> Opposite to perforated peptic ulcer (2) Bowel sounds may becomes absent → paralytic ileus Determine cause - Gallstones; alcohol; medications; FH; viral illness Initial: - Pancreatic enzymes (amylase, lipase) – 3-4 times elevated serum amylase elevated - Supports but is not pathogonomic - LFTs - US of gallbladder and biliary tree 2nd line - Fasting plasma lipids - Fasting plasma Calcium (after acute episode) - Viral antibody titres - Autoantibody / IgG4 titres - MRCP / CT scan of pancreas 3rd line - Repeat gallbladder US - Endoscopic US - ERCP (bile for crystals) - Sphincter of oddi manometry

Answer 14

Biliary colic perforated peptic ulcer - will have guarding and rebound tenderness Acute mesenteric ischaemia, Acute MI Basal pneumonia

Answer 15

80% resolve spontanously | 20% develop complications

Answer 16

Supportive treatment ``` Fluid resuscitation IV crystalloids (Ringer’s lactate) Analgesia - Morphine sulphate IV; fentanyl; ketorolac Correct electrolyte abnormalities Nutrition Nil by mouth initially if vomiting; Feeding; Dietician Monitor early warning signs Organ dysfunction Critical care support ? antibiotics - not given unless there is actual inflammation of the pancreas due to bacteria!! if cause is gallstones, do not give antibiotics! ```

Answer 17

Surgery - Doubt in diagnosis - Early cholecystectomy if have gallstones - ERCP ``` Acute cholangitis Jaundice dilated bile duct on US Necrosectomy -> MIRP / Open Bleeding Pancreatic abscesses Pancreatic pseudocyst ```

Answer 18

``` Local - Peripancreatic fluid collection - Pancreatic necrosis; abscess - Infected necrosis  → May lead to shock Treatment: carbapanems, quinolones, metronidazole ``` Pseudocyst   - May be caused by inflammation of parenchyma Biliary/gastric obstruction   General - Respiratory failure; Renal failure; Circulatory failure - Malnutrition

Answer 19

Two peaks in death rates – Early death - 1st week / late death - 2nd week Week 1 – Initial attack → SIRS → MODS -Death due to multi-organ system failure Week 2- Pancreatic necrosis → sepsis → MODS - Death due to infected pancreatic necrosis

Answer 20

>3 = severe disease ``` P- PaO2 <8 kPa (60mmHg) A- Age (>55) N- Neutrophils (WCC >15x10^9/L) C- Calcium (decreased Ca = severe/ increased Ca may have caused pancreatitis) R- renal function (urea >16mmol/L) E- enzymes (delayed LFTs) alanine aminotransferase >200U/L A- albumin S – sugar (high BM) >10mmol/L ``` + lactate dehydrogenase

Answer 21

12/100,000 Continuing inflammatory disease of pancreas - irreversible, morphologic change that typically causes pain or permanent loss of function or both Progressive; Inflammatory change, necrosis, fibrosis Symptoms Loss of exocrine and endocrine elements Epigastric pain that bores through to the back Relieved by sitting forward; hot water bottle (epigastrium /back) Bloating; steatorrhoea Reduced weight Symptoms relapse and worsen

Answer 22

TIGARO T= toxic-metabolic - Alcohol; tobacco; hyperCa, chronic kidney disease I = idiopathic - Tropical/ early or late onset types G = genetic - Hereditary pancreatitis (cationic trypsinogen mutation) - SPINK-1 mutatino - Cystic fibrosis - Haemochromatosis (iron builds up in body) A = auto-immune - Consider in older patients R = recurrent and severe acute pancreatitis - Reccurent; post-necrotic O = obstructive - Ductal adenocarcinoma - Intraductal papillary mucinous neoplasia - Pancreas divisum - Sphincter of Oddi stenosis

Answer 23

Nutritional assessment - Clinical; Anthropometry; Biochemistry Morphology of pancreas (1) US + CT scan CT – pancreatic calcifications, enlargement, ductal dilation MRCP/ MRI pancreas; ERCP Pancreatic function tests - Collect pure pancreatic juice after secretin injection – invasive & seldom used - Endocrine - May have elevated blood glucose/ diabetes occurs in advanced cases Exocrine: Direct; Indirect

Answer 24

Secretin stimulation tests

Answer 25

Faecal elastase, pancreolaurlyl

Answer 26

Analgesia - Coeliac-plexus block Lipase (Creon) Insulin needs may be high/variable – beware hypos Identify cause Alcohol counselling Dietician – nutritional supplements Fat soluble vitamins No alcohol; low fat Role - Relieve symptoms – pain - Treat complications – obstruction (biliary/gastric), pseudocyts, pseudo-aneurysm PPI may be given optimise duodenal pH for pancreatic enzyme activity Surgery Decompression of pancreatic/bile duct - Peustow’s lateral pancreatico-jejunostomy - Hepatico-jejunostomy Resectional surgery  - Whipples pancreatico-duodenectomy - Distal pancreatectomy Combined  - Frey’s surgery  - Beger’s procedure

Answer 27

Form of chronic pancreatitis Mimic cancer but responds to glucocorticoids - Some may require azathioprine Abdo pain, weight loss or obstructive jaundice NO acute attacks of pancreatitis Increased serum IgG or IgG4 Diffusely enlarged pancreas, narrowing of pancreatic duct, structuring of lower bile duct

Answer 28

600-700/year in Scotland ``` Late presentation Typically male (2:1) , >70 years old ``` RF: smoking, alcohol, carcinogens, DM, chronic pancreatitis, increased waist circumference Pathology - Mostly ductal adenocarcinoma (metastasize early, present late) - 60% pancreas head; 25% body; 15% tail - 95% mutation in KRAS2 gene ``` Symptoms Non-specific abdominal symptoms Epigastric pain radiating to back Obstructive jaundice Weight loss, anorexia May have diabetes or acute pancreatitis ``` Exam: - May have epigastric mass, hepatomegaly, splenomegaly, lymphadenopathy, ascites Diagnosis - Bloods: Cholestatic jaundice - US / CT Staging – CT abdomen & chest +/- laparoscopy Treatment Resection - Pancreatoduodenectomy/Whipple’s – head of pancreas, duodenum, portion of stomach removed Chemotherapy - Post-op – delays progression Prognosis Dismal – mean survival <6 months; 5 year survival 3%

Answer 29

Pancreas produces 1.5L/day of bicarbonate and enzyme-rich fluid (digestion of fat, protein, carbohydrate) Lipolytic activity declines first so fat absorption mainly affected Steatorrhoea, weight loss, vitamin deficiency (A,D,E,K) Causes: chronic pancreatitis, pancreatic cancer, CF, haemachromatosis, pancreatic resection, gastric resection Treatment: pancreatic enzyme replacement, taken with meals and snacks, gastric acid suppression (supplements work at higher pH), vitamin supplements

Answer 30

Causes (1) Stasis: strictures (Crohns, TB), Hypomotility (Old age, opiate analgesics, diabetes, systemic sclerosis) (2) Blind loops, diverticulae (3) Immunodeficiency Treatment: 2 weeks antibiotics

Answer 31

Bile acids absorbed in ileum → cause secretory diarrhoea in colon Type 1 – ileal disease or resection Type 2 – idiopathic Type 3 – assoc. with cholecystectomy, rapid transit, coeliac, SIBO, chronic pancreatitis Investigation: Serum 7-alpha cholestenone Treatment: cholestyramine, colesevelam

Answer 32

Non-invasive pathogen Malabsorption due to brush border damage; reduction in absorptive surface; bile acid utilization; induction of hypermotility; enterotoxin Treatment: metronidazole

Answer 33

``` Coeliac disease Pancreatic exocrine insufficiency Small bowel overgrowth Bile acid malabsorption Giardia lamblia ```

Answer 34

Chronic dyspepsia in absence of organic disease -May have early satiety, fullness, bloating, nausea Cause poorly understood – probably mucosal, motility, psychiatric disorders Clinical features - Usually young <40 years; W:M, 2:1 - Abdominal discomfort with other dyspeptic symptoms - Nausea, satiety, bloating after meals - Morning symptoms are characteristic, pain, nausea may occur on waking - History - may have symptoms of IBS - Inappropriate tenderness on abdominal pain - NO weight loss - Symptoms may be disproportionate to clinical well-being Must consider: - Peptic ulcer disease - Intra-abdominal malignancy – older people - Depressive illness? - Alcohol misuse – early-morning nausea, retching Investigations - Rule out pregnancy before radiological investigations! - Check for H. pylori infection -> Offer treatment if +ve ; SE: worsening of underlying GORD - >55 years old – endoscopy to exclude mucosal disease Management - Explanation and reassurance - Explore psychological factors - Idiosyncratic and restrictive diets little benefit – but may try smaller portions, fat restriction Drugs - Antacids sometimes helpful - hydrotalcite - Prokinetic drugs Metoclopramide (SE: extrapyramidal – tardive dyskinesia in young patients), domperidone Given before meals if nausea, vomiting, bloating prominent H2 –receptor antagonist - If night pain or heartburn Low dose tricyclic agents

Answer 35

Persistent & unexplained symptoms - no structural abnormality/ pathological process Disordered physiological function - Attributable to mid or lower GI tract Peak in 20-40 year olds Mainly female = 3:1 Coexisting conditions common: non-ulcer dyspepsia, chronic fatigue syndrome, dysmenorrhoea, fibromyalgia

Answer 36

Likely multifactorial: Chemical / stress/ hormonal changes / food / genetic / infection / anxiety / medications / depression / trauma – panic disorder May be state of low-grade gut inflammation/immune activation, not detectable by tests - Raised number of mucosal mast cells that sensitise enteric neurones by releasing histamine and tryptase - Some respond to Ketotifen – mast cell stabiliser Post infective IBS - 6-17% - onset of symptoms attributed to acute gastroenteritis episode - Salmonella; Campylobacter - 25% continue with altered bowel habits (6 months post episode) - Hypotheses: Increased response to inflammatory stimuli Emotional factors - Psychological factor – 80% - Previous depressive illness – 40%; Current psychiatric illness – 70% - Sometimes associated with history of physical/sexual abuse - BENEFIT from psychologically based therapy Physiological factors: Serotoninergic disorder – increased release of 5-HT in D-IBS & deficiency in constipation-predominant diarrhoea Luminal factors - SIBO – gut dysbiosis present in some Respond to probiotics & non-absorbable antibiotic - rifaximin (for C-IBS) - Chemical food intolerance to poorly absorbed, short-chain carbohydrates (lactose, fructose and sorbitol) – fermentation in colon leads to bloating, pain, wind and altered bowel habits. Dysfunction with motor & sensory aspects – altered gut reactivity (motility and secretion) in response to stimuli, may be environmental, or luminal

Answer 37

Controls intestinal motility & secretory functions Semi-autonomous - Parasympathetic (cholinergic) and sympathetic NS (adrenergic) Functions independently Contains many neurotransmitters – including 5-hydroxytryptamine (5-HT) - IBS = 5-HT mediated visceral hypersensitivity and gut motility 5HT - Distribution: CNS – 5% / GI tract 95% - Enterochromaffin cells – contain serotonin - Act as transducers detecting changes in chemical environment intestinal lumen - Releases serotonin → serotonin receptors on sensory nerves → initiate peristalsis - Enterocytes SERT (transporter) - Inactivate response - Stimulation of 5HT receptors on intrinsic sensory neurones → triggers peristaltic reflex and colonic mass movement

Answer 38

THINK ABC A - abdominal pain or discomfort B - bloating C - change in bowel habit Symptoms - Recurrent abdominal discomfort, bloating worsens throughout day, alternate between episodes of diarrhoea and constipation - Good to classify as predominantly diarrhoea or constipation - May pass mucus; rarely have nocturnal symptoms - Abdominal pain may be variable – Cancer would be in one place! - No weight loss; overall appear well - Dyspepsia 87% - Tiredness 97% - Backache 79% - Dyspareunia 69% - Urinary frequency 56% - Headache 50% - Nocturia 48%; Sleep disorder 28% - Fibromyalgia 20% Exam: Usually unremarkable – some tenderness to palpation Diagnosis - No test – diagnosis by exclusion Only do FBC, ESR, CRP, Antibody testing for coeliac - Absence of biological/physiological markers - Symptoms based criteria: Rome IV Abdominal pain and 2 of: - Pain related to defecation - Change in stool frequency - Change in stool form Symptoms over 6 months on average weekly for last 3 months Management Identify Patient’s Concerns Explain nature of the condition Reassure: IBS is a recognised clinical entity Involve patient: - Symptoms can fluctuate - Diet or stress may precipitate symptoms Provide continuity: - ongoing review may be important to patient - Set realistic expectations - Symptom monitoring with diary – may help find precipitating factors Diarrhea - 1st line = loperamide

Answer 39

``` Rectal bleeding Documented weight loss or fever Persistent diarrhoea or vomiting Constant and recent abdominal distension Anaemia &/or GIH  New onset in patients >50 years Family history of bowel cancer, IBD Frequent Nocturnal symptoms Absence of psychological distress Urinary sediment - haematuria ```

Answer 40

Food intolerance Infection: Giardiasis, amoebiasis, TB IBD Bacterial overgrowth Diveritcular disease Colon cancer Bile salt malabsorption CHO malabsorption: Lactose/ fructose/ sucrose Hormonal syndromes: Medullary thyroid cancer; Gastrinoma / Vipoma; Glucagonoma Rarer types of colitis: Gold colitis; Collagenous / lymphocytic Pseudo-obstruction: Myopathy / neuropathy