Gastrointestinal Conditions Flashcards
cholecystitis: signs and symptoms
murphys sign
vomiting
nausea
SOB
shoulder pain
RUQ abdominal pain
jaundice
cholecystitis: pathophysiology
Bile which is low in salt or high in cholesterol causes inflammation of the bile duct and gall bladder and causes water and salt reabsorption which makes bile less soluble and it forms precipitate. Stones of bile precipitate may block the bile duct and cause increased inflammation and distension. Infection of E.coli may also cause inflammation. Distension can increase pressure on vessels and reduce blood flow leading to ischaemia and fluid back up can cause peritonitis due to perforation.
Cholecystitis: risk factors
High cholesterol
obesity
liver failure/disease
Hypertension
Diabetes
Smoking
Alcohol and drug use
Family history
Cholecystitis: treatment and management
analgesia - no ENTONOX if obstruction suspected
anti-emetics - no Metoclopramide
CABCDE correction and monitoring for signs of sepsis
Ensure patient is NPO
transfer for surgery/reduction and due to risk of peritonitis.
Appendicitis: pathophysiology
Inflammation caused by infection or obstruction due to fecal matter. Ulceration and inflammation block the mucus outflow of the appendix causing distension and fluid back up. Pressure on vessels and nerves around increases causing ischaemia and pain.
Appendicitis: signs and symptoms
Psoas sign, Rovsing sign
nausea, vomiting
LRRQ pain
anorexia
Appendicitis: treatment and management
Analgesia - No Entonox
Anti- emetic - no Metoclopramide
Oxygen if SOB
Monitor ABCDE on route and look for signs of sepsis/peritonitis including increased fever and dropping BP
Urgent transfer due to risk of rupture and peritonitis- golden hour for appendicitis
Ensure patient is NPO
Bowel Obstruction: signs and symptoms
abdominal distension
cramping
faecal vomit
absent bowel sounds
absence of faeces or flatus
bowel obstruction: treatment and management
Paracetamol or morphine IV/IM/PO
NO ENTONOX
Ondansetron anti-emetic
NO METROPLOPRAMIDE
CABCDE care and monitoring
GP referral
Bowel obstruction: pathophysiology
Caused by scar tissue, adhesions, foreign matter, intussusception or tumours, blockage of large intestines occur and faeces cannot pass through to rectum.
Upper GI haemorrhage: causes
Peptic ulcers
gastritis
oesophagitis due to coughing or vomiting
Caustic poison
tumours
tears in oesophagus due to coughing or vomiting
oesophageal varices - enlargement of vessels in oesophagus due to blockage and back up from portal vein.
Upper GI haemorrhage presentation
melaena - digested blood in stool
haematemesis (coffee ground or blood)
Lower GI haemorrhage causes
diverticular disease
IBS
haemorrhoids
tumour
Lower GI presentation
dark red blood per rectum
GI haemorrhage treatment and management
time critical if large volumes of bright red blood.
fluids
TXA never given
if not transferred, always refer to GP
pancreatitis: signs and symptoms
nausea and vomiting
mid-abdominal pain/RUQ pain
radiating pain to back
hyperglycaemia
anorexia
hypovolemia/hypotension
hypoxaemia
tachycardia
Gall stone pancreatitis
Presence of gall stones without gall bladder distension can mean gall stones are causing obstruction further down in the duodenum. this obstructions prevents intestinal flow and can cause the back up of fluid containing activated enzymes into the pancreas which damage both Langerhans and acinar cells.
Alcoholic pancreatitis pathophysiology
Alcohol is a direct toxic insult to acinar cells of the pancreas. this causes inflammation and membrane destruction. Ethanol increases ductal pressures due to increased protein deposition which favours retrograde flow and intra-pancreatic enzyme activation.
Pancreatitis: treatment and management
Analgesia
Treat oedema if pancreatic OEDEMA PRESENT
anti- emetics
monitor BM and correct
fluids to resolve hypovolemia
in hospital - cholecystectomy, catheterise, alcohol withdrawal prophylaxis (lorazepam)
pancreatitis: risk factors
5 Fs (fat, female, fertile, forty, family history)
tumours
high alcohol consumption
hypercalcaemia
appendicitis,cholecystisis,ABO, pancreatitis key issue with increased pressure
increased intraluminal pressure which exceeds venous ad capillary pressure leads to decreased lymphatic drainage and perfusion. This leads to ischaemia and necrosis which increases perforation risk.
