Gastro Flashcards
Inguinal hernia
Risk factors
Types
Presentation
Obesity, constipation, chronic cough, heavy lifting, male
Direct (20%) - directly through weakness in posterior wall of inguinal canal medially to inferior epigastric vessels - easily reduced
Indirect (80%) - through deep inguinal ring ± superficial associated with patent inguinal canal - more likely to strangulate
A lump ± pain
Indirect may cause pain in scrotum + dragging
Cough impulse - finger through top of scrotum into external ring and palpate for lump when coughing
Dyspepsia
What
Red Flags
Early post prandial vs late
Pain or discomfort in upper epigastric region may be heartburn or acid reflux
ALARMSAnaemia, Loss of wt, Anorexia, Recent onset (if >55), Melaena, Swallowing difficulty
Early post prandial: gastritis, GORD, gastric Ca
Late post prandial: duodenal ulcer
ROME criteria
For functional dyspepsia: 6M Post-prandial fullness, early satiety, epigastric pain/burning + no struc
Drugs causing dyspepsia (4)
Nitrates
Bisphosphonates
Corticosteroids
NSAIDs - Decrease mucus and bicarbonate secretion
N.b. PPI decreases expression of H+/K+ antiporter on luminal membrane of parietal cells
Dyspepsia Mx
> 55 or alarms (Y) Endoscopy 2-week (N) Lifestlye
Lifestlye - stop offending drugs, decrease tobacco, avoid aggravating foods, lose weight+ over the counter antacids
Test for h.pylori (Y) triple therapy 1 week (N) GORD - PPI 4/52 - if no response H2 receptor antagonist (ranitidine) or long term
Areas of the stomach (5)
Cells in the stomach (5)
Acid stimulating hormones
Acid suppressing hormone
Cardia, fundus, body, antrum, pylorus
Chief cells - pepsinogen (to pepsin by HCl)
G-cells - gastrin (antrum)
Parietal cells - intrinsic factor and HCl (fundus + body)
D-cells - somatostatin (antrum)
Goblet cells - mucus + bicarbonate
Gastrin (CCK-2), histamine (H2), ACh (M3)
Somatostatin
H.pylori infection Appearance Mechanism Ix Mx
G- curved bacillus
H.pylori through mucus layer
Urease secretor - urea + water -> ammonia + CO2 -> neutralise acid (for survival) + mucosal cell death, chronic inflammation -> ulceration
C13 urea breath test - may be done in primary care
Stool antigen test + CLO test (pink with h.pylori)
N.b. must stop PPI for 2 weeks before or ABX 4 weeks
TRIPLE THERAPY - PAM/PAC
PPI + amoxicillin + clarithromycin/metronidazole (1 week)
H.pylori anaemia mechanisms
H.pylori uses iron for own growth
Decreases vitamin C
Micro-erosions and chronic bleeding
Peptic ulcer disease
Types
Causes
Presentation
80% duodenal ulcer - Common at duodenal cap, may erode gastroduodenal artery
20% gastric ulcer - Common at lesser curve, may erode L gastric artery
H.pylori (95% DU, 80% GU), NSAIDs, smoking, alcohol, stress, bile acids, pepsin, Zollinger-Ellison syndrome
Epigastric pain point to pain with one finger
-DU - post prandially (1-3 hours), which is relieved by eating
-GU - on eating
Pain radiation to back if posterior duodenal ulcer as related pancreas
Nausea, oral flatulence, bloating, distension
GORD Presentation (5)
Heartburn: burning feeling rising stomach to neck relieved by antacid. Related to meals, posture (lying down), straining
Water brash: excessive salivation
Acid brash: retrosternal discomfort - regurgitation of acid or bile
Odynophagia - painful swallowing related oesophagitis or stricture
Belching
Causes for GORD
Increased intra-abdominal pressure - Obesity, pregnancy
Increased gastric pressure - Large meals, hiatus hernia
Lifestyle factors: smoking, alcohol, fat (*delays gastric emptying), coffee
Decreased oesophageal peristalsis
Systemic sclerosis
Smoking,
Drugs
-Affecting oesophageal motility (nitrates, anticholinergics, TCA)
Damage mucosa (NSAID, bisphosphonates)
GORD Mx
Lifestyle: reduce weight, stop smoking, reduce alcohol, raise bed at night, regular small meals, avoid drugs
OTC: aluminium or magnesium salts (antacids), alginates (protective layer - gaviscon)
Initial nice first line: PPI for one month or H2 antagonist
Step down PPI for long-term suppression
If oesophagitis on endoscopy - PPI 2 months
Hiatus hernia What Causes Types Mx
Herniation of part of abdominal viscera through oesophageal aperture of diaphragm. Mainly gastric cardia
Widening of diaphragmatic hiatus, pulling up of stomach due to oesophageal shortening (e.g. chronic GORD), pushing up of stomach by intra-abdo pressure - Obesity, pregnancy, ascites, advanced age
Sliding (90%) - gastro-oesophago junction slides into thoracic cavity
Rolling (10%) - gastro-oesophago junction remains in place but stomach herniates next to oesophagus
Lifestlye as GORD + PPI longterm + surgery e.g. gastropexy if refractory
Blood supply/muscle/epithelium of the oesophagus
Upper third
Middle third
Lower third
Inferior thyroid/Striated/Stratified squamous
Aortic & Oesophageal/Mixed/Stratified squamous
Left gastric/Smooth/Columnar
Barretts oesophagus What Causes Most common patient Complications Treatment
Any portion of normal distal squamous epithelium is replaced by metaplastic columnar epithelium
Chronic GORD (comp at 5%) ± HH
50M
H.pylori and NSAIDs
5% progress to adenocarcinoma of the oesophagus in 10-20 years
Low grade: Lifestyle as for GORD + long term PPI ± ablation
High grade: oesophagectomy
Oesophagus Ca
Types
Risk factors
Red flags (5)
80% SCC (upper ⅔) or adenocarcinoma (lower ⅓) - both are common and aggressive
Both - smoking (x10 for SCC, x2 for AC), alcohol
AC- Barrett’s, obesity and other GORD things
SCC - chronic inflammation and stasis e.g. achalasia
RED FLAG PRESENTATION:
Dysphagia (solids>liquids)
Vomiting
Anorexia and weight loss
Symptoms of GI related blood loss e.g. melaema
Symptoms of infiltration - intractable hiccups and persistent retrosternal pain
Upper ⅓ specific - hoarseness and cough - less common
Lymphadenopathy
Dysphagia causes
Oesophageal: GORD, oesophagitis, oesophageal cancer (food sticking), pharyngeal cancer
Neurological: CVA, achalasia, diffuse oesophageal spasm, MS, MND
Others: pharyngeal pouch, external compression (mediastinal tumour), CREST or scleroderma
Achalasia What Mechanism Presentation Ix Management
Disorder of motility of lower oesophageal sphincter
Smooth muscle layer has impaired peristalsis and sphincter fails to relax
Often an acquired aganglionic segment
Possible effect of interstitial cells of Cajal (pacemaker cells)
Dysphagia (solids>liquids) DDx: GORD/ stricture
Regurgitation (90%)
Chest pain in 50% - retrosternal and after eating
?Inhalation pneumonias
CXR - vastly dilated oesophagus behind heart
Barium swallow - characteristic bird’s beak dilated oesophagus with distal narrowing
Manometry - gold standard high resting pressure and incomplete relaxation on swallowing
CCB/nitrates - reduce pressure in LOS may lead to GORD
Surgery - endoscopic dilatation may lead to perforation
Upper GI bleed
Causes
Presentation
Peptic ulcer (most common), oesophagitis, gastritis, varices, Mallory-Weiss tear, malignancy, drugs
Haematemesis
-Bright red - fresh - above stomach, active haemorrhage
-Altered - coffee ground - stomach or below
Melaena - black tarry stools usually due to UGIB but occasionally from small bowel
Haematochezia - fresh blood usually due to colonic bleeding
Abdominal pain - ?location
Features of underlying cause - dyspepsia, weight loss, jaundice
High urea levels can indicate an upper GI bleed versus lower GI bleed
Upper GI bleed
Management
Score
If shock = fluid resuscitation + high flow O2
2 wide bore cannula and send bloods (FBC/UE/LFT/crossmatch/coag)
Fluid bolus 500ml over 15 mins (up to 2L) while waiting for bloods
Transfuse with blood, platelets (<50), FFP (INR or APTT >1.5x normal), prothrombin complex (if warfarin) according to major haemorrhage protocol
CXR, ECG, ABG, catheter, regular monitoring
Endoscopy (<24 hours)
Rockall risk score
- Pre endoscopy for mortality
- Post endoscopy for re bleed
Ileus vs paralytic ileus vs pseudoobstruction
- Non-mechanical obstruction
- Absence of normal peristalsis
- Like mechanical but no cause found
Causes of intestinal obstruction
Small
Large
Adhesions (75% - from prior operations), strangulated hernia, malignancy (caecum as small bowel malignancy rare) or volvulus
Colorectal malignancy - patients > 70, increased risk further down bowel as faeces more solid, diverticulum, sigmoid volvulus
Toxic megacolon
What
Features
Causes
Acute form of colonic distension.
It is characterized by a very dilated colon (megacolon), accompanied by abdominal distension (bloating), and sometimes fever, abdominal pain, or shock.
IBD, C.diff, hursprungs,
Bowel obstruction
Presentation (5)
SBO vs LBO (3)
Vomiting (early in SBO, faeculent in low level), Abdominal pain (diffuse, central, abdominal, colicky=SBO, constant=LBO), Constipation (early in low level, late in high-level) Abdominal distension (SBO