Gastro Flashcards
(41 cards)
Summarise bowel obstruction
BOWEL OBSTRUCTION
Can be caused by volvulus, strictures from crohns, intussusception and Hirschprungs in children, diverticular disease, adhesions, hernias (SBO), malignancy (LBO) (BIG THREE!!!). It is an emergency. SBO is more common.
Sx: Constipated, distended, no wind passed, diffuse colicky abdo pain, green bilous vomit (early SBO, late LBO), shock as fluid cannot be reabsorbed in the colon, tinkling bowel sounds heard early on.
THINK ABOUT THE BIG 3: Any hernias, wt loss/ PR bleed for cancer, any previous surgery for adhesions
Ix: XR abdo for distended bowel if unsure. >3cm in SB; >6cm in colon; >9cm in caecum. SB contains valvulae which extend across the WHOLE bowel. LB have haustra which do NOT extend across the full bowel. Definitive imaging is CT with contrast.
U+Es, VBG: Metabolic alkalosis due to vomit, lactate raised due to ischaemia
Mx: ABCDE. NBM. IV fluids resuc for vomit, NGT with drainage “drip and suck”. Conservative may be used if stable otherwise surgery.
Closed loop bowel eg in volvulus= two points of obstruction → so continues to expand before perforating + necrosis:
Summarise alcoholic liver disease
Alcoholic fatty liver (reversible)
Alcoholic hepatitis (reversible with abstinence)
Cirrhosis (irreversible)
Questionnaires: CAGE; AUDIT
Complications: ALD; alcohol dependence and withdrawal; wernicke’s/ korsakoffs, pancreatitis, alcoholic cardiomyopathy
Signs: jaundice, encephalopathy, bruising, spider naevi, palmar erythema, gynecomastia, ascites, caput medusae, asterixe (flapping tremor)
Ix: Raised MCV; Elevated ALT and AST (transaminases) + raised gamma-GT (specific to alcohol). Low albumin can’t be made as normal. Elevated bilirubin in cirrhosis when you get jaundice. Clottings and U+E off.
U/s or fibroscan (good for cirrhosis)
Endoscopy for varices
Liver biopsy confirms, rec if considering steroids
Mx: thiamine, stop alcool, steroids in short-term, treat complications, refer for liver transplant BUT must stop drinking for 3 months before
Delirium tremens: sweaty/ tremor/ headache/ anxious → hallucinations → seizures —> delirium tremens.
Delirium tremens = emergency - caused by the GABA receptors of the brain being unstimulated and having excess adrenergic activity. Mx with chlordiazepoxide, pabrinex
Wernickes: confused, oculomotor issues, ataxia
Korsokoffs: retrograde + anterograde memory loss, behavioural change
Summarise Cirrhosis
Pathophysiology: Cirrhosis is inflammation of the liver which causes scarring and nodules
Causes: Autoimmune, hepatitis B/C, ALD, NAFLD, drugs, CF
Signs: Jaundice, hepatomegaly, splenomegaly, palmar erythema, spider naevi, gynaecomastia (endocrine dysfunction causing less testosterone), ascites, bruising, caput medusae, asterix
Ix: Decompensated - all LFTs derange. Albumin and PT are useful markers of functioning of liver. Hyponatraemia is a bad sign. Alpha feto-protein screening for cancer + u/s every 6 months for ca screening
FIRST LINE Ix in NAFLD: enhancer liver fibrosis test!!!
U/S shows nodules, corkscrew arteries, enlarged portal vein with reduced flow, ascites + shows cancer
Fibroscan - check elasticity of the liver - every 2 yrs in Hepc, alcoholics, ALD, NAFLD, Hep B - hep b yearly
Biopsy confirms
Mx: hepatocellular carcinoma screening; endoscopy every 3 yrs for varices, high protein and low sodium diet, consider liver transplant, manage complications:
Summarise the complications of cirrhosis
Malnutrition - liver uses protein as nutrition as body canr store glycogen in liver
Portal htn and varices: Portal vein comes from superior mesenteric vein + splenic vein - cirrhosis increases resistance of blood flow so things back up → anastomas with the systemic venous system become swollen and torturous (varices) - occur at gastro-oesephageal junction; ileocaecal junction, rectum, anterior abdo wall (results in caput medusae) → mx with propranolol, co-amoxiclav, elastic band ligation. IN emergency give vasopressin analogues, give FFP, abx, urgent endoscopy
Ascites: Fluid leaks out of the capillaries due to the high pressure in the portal veins and into the peritoneum, this causes a drop in circulating BP → RAAS raises overall BP —> Mx with spironolactone (interferes with RAAS), ascitic tap, abx to protect against SBP (quinolones), TIPS shunt
SBP: Happens in 10% of ascites → presents like infection, commonly e.coli, mx with cefotaxime + ascitic culture
Hepatic encephalopathy: build up of toxins that affect the brain such as ammonia. Mx with laxatives (lactulose) to clear from gut before absorption + abx - presents with confusion, lower GCS and changes to memory/ mood
Childs Pugh score for severity: Bilirubin; albumin; PT time; encephalopathy; ascites
Summarise Hepatitis
Pathophysiology: Hepatitis can be due to infection, NAFLD, alcohol, autoimmune, drugs
HEP A + E = foecal oral
HEP B+C+D= sexual/ blood (D piggybacks onto B) —> all public health notifiable
Presentation: Jaundice, RUQ pain, fever, systemically unwell, fatigue, pruritius, myalgia, N+V
Ix: AST/ ALT HIGH (transaminases) + higher bilirubin
Hep A: MOST COMMON around world; can cause cholestasis, can be vaccinated,
Hep B RF - IVDU, more sexual partners, vertical transmission, certain countries, needle stick injury, blood transfusion. DNA virus. In 10% becomes chronic bc the dna becomes part of your own dna.
Hep B viral markers: Surface antigen = active infection.
Core antibodies = past OR current infection (IgM = current, IgG - past).
Surface antibody = vaccinated or past or current infection.
E antigen = how infective you are.
Summarise haemochromatosis
Pathophysiology: High iron. AR inherited on chromosome 6
Presentation: fatigue, arthalgia, pigmented bronze/ grey, hair loss, ED, amenorrhoea, cognitive sx
Also effects thyroid, heart, joints (gout), pituitary, pancreas
Ix: ferritin, transferrin (up in haemochromatosis - differentiates it from raised ferritin in inflammation), genetic testing, liver biopsy with perl’s stain
Mx: venesection first line
Summarise Wilson’s disease
Pathophysiology: High cu deposits, AR inherited
Presentation: hepatic, neuro, psychiatric issues. Keyser fleisher rings on slit lamp, parkinsonisms, dystonia, dysarthria
Other organs: anaemia, osteopenia, renal damage
Ix: Initial = low serum ceruloplasmin though not specific, liver biopsy, 24 hr urine Cu assay
Mx: penicillamine, trientine (chelation agents)
Summarise Primary Biliary Cirrhosis
Pathophysiology: Autoimmune condition which attacks the small bile ducts of the liver - usually bile ducts take bilirubin, cholesterol and bile salts to the intestine so when the bile duct is blocked they go into the blood causing the sx
Presentation: pruritus, fatty stools (lack of bile salts); jaundice, pale stools (lack of bilirubin), xanthoma and CVD (high chol in bld) also get RUG pain + fatigue
Associated with: middle aged women + autoimmune issues
Ix: Raised ALP (as often is case in cholestatic problem), other LFTs rise later, anti-mitochondrial Ab = MOST specific, ANA, ESR raised, biopsy
Mx: Ursodeoxycholic acid, Cholestyramine, liver transplant, immunosuppression
Summarise hepatobiliary cancers
Primary: hepatocellular carcinoma 80% and cholangiocarcinoma are 20%
Secondary: mets to liver are common
RF: alcohol, cirrhosis, PSC for cholangiocarcinoma
Sx: RUQ pain, jaundice, bruising, b sx, pruritus. Cholangiocarcinoma is PAINLESS jaundice
Ix: biopsy, alpha fetoprotein for HCC and CA19-9 for cholangiocarcinoma. US, CT/ MRI to stage.
Mx: Very poor prognosis unless catch early. sorafenib, regorafenib and lenvatinib. Palliative. Transplant in HCC and surgery in cholangiocarcinoma if is early.
Summarise GORD
Where acid from stomach comes back up into the oesophagus through the sphincter
RF: alcohol, stress, lying down, obesity, pregnant, smoking, heavy meals, caffeine
Sx: burning sensation in epigastric region/ CP, bloating, hoarse voice (dyspepsia generally describes indigestion)
Ix: OGD if red flags 2WW.
Mx: avoid RF —> Gaviscon → PPI —> ranitidine (H2 antagonist) → fundoplication
RED FLAGS: anaemia, >55, wt loss, dysphagia, treatment resistant, raised platelets
Barrett’s = squamous in esophagus → columnar. Pre-malignant.
Summarise stomach ulcers
Pathophysiology: Ulcers due to the breakdown of stomach/ duodenal mucosa
RF: NSAIDs, H.pylori break down. Acid increasion can also break down stomach due to stress, alcohol, caffeine, smoking or spicy foods.
Zollinger-Ellison syndrome: rare cause characterised by excessive levels of gastrin, usually from a gastrin secreting tumour.
Ix: Test with urea breath test/ stool antigen test for H.pylori
Sx: Epigastric pain, N+V, dyspepsia, UGI bleed, eating typically worsens the pain of gastric ulcers and improves the pain of duodenal ulcers.
Mx: Endoscopy to monitor, PPI to treat
Mx with PPI + 2 x abx - amoxicillin + clarithromycin/ metronidazole for h.pylori
Complications: UGI bleed, perforating to cause peritonitis, scarring → pyloric stenosis
Summarise UGI Bleed
Causes → varices, mallory weiss tear, ulcers, cancer
Presentation: In shock, melaena, haematemesis (coffee ground vomit), gastritis/ liver disease sx depending on underlying cause
Ix: Glasgow-Blatchford score is used to establish risk of UGI bleed → features urea rise, drop Hb, drop BP, Lower HR, melaena, syncopy
Want U+Es (urea), FBC (Hb), clotting, LFTs, crossmatch
Mx: ABCDE; access, transfuse, endoscopy is definitive mx, stop any anti-coagulants/ NSAIDs
Mx esophageal varices with IV terlipressin (vasoconstriction) and co-amoxiclav. Prevent future varices with propranolol.
Summarise Inflammatory Bowel Disease
Ulcerative colitis: continuous, only colon and superficial mucosa, smoking helps, blood and mucus, PSC association
Crohns: Can use mnemonic Crows NEST: No bld/ mucus, Entire GI tract, Skip lesions, Terminal ileum most affected + Transmural, Smoking is bad/ don’t set the nest on fire) + also get strictures and fistulas
Sx: Abdo pain, mucus and blood in stool, in crohn’s get
Associations: clubbing, erythema nodosum, episcleritis, uveitis, inflammatory arthiritis, PSC in UC
Ix: Colonoscopy and biopsy is diagnostic, FBC, ESR, TFT, U+E, LFT, CRP, fecal calprotectin is very sensitive and specific
Mx:
Crohn’s → active episode: → steroids —> immunosuppressants e.g. azathioprine, methotrexate, infliximab. Remission: azathioprine first line
UC → Active episode: aminosalicylates (skip if v bad)—> steroids —> cyclosporin. Remission: aminosalicylate → azathioprine. Can try surgery and a stoma
Summarise IBS
Cause unknown, functional issue
Sx: abdo pain, diarrhoea, constipation, fluctuating bowels, bloating, worse with food and improved by BO, PR mucus
Ix: Normal blds (coeliacs, FBC, ESR, CRP, calprotectin)
Mx: FODMAP, probiotics trial, reduce processed food, caffeine and alcohol.
1) Loperamide for diarrhoea, laxatives for constipation and antispasmodics for cramps.
2) TCA.
3) SSRIs
Summarise Coeliac’s
Pathophysiology: Gluten damages small bowels by creating an autoimmune reaction → atrophy of villi and crypt hypertrophy
Sx: diarrhoea, wt loss, fatigue, FTT, mouth ulcers, anaemia, dermatitis herpetiformis, rarely neuro stuff eg ataxia.
Associated with T1DM, thyroid issues, PBC and PSC.
Ix: Anti-Tissue transglutaminase and anti-endomysial antibodies + IgA (as may be false neg is IgA deficient), gold standard is colonoscopy and biopsy showing the atrophy and hypertrophy. All tests done whilst still taking gluten.
Complications: vitamin deficiencies, lymphoma
Mx: No gluten!
Summarise appendicitis
Pathophysiology: Inflammation of appendix (which comes off the caecum) secondary to infection which may result in gangrene and rupture → peritonitis
Sx: general abdo pain that localises to RIF pain within 24 hrs (mcburney’s point- 1/3rd from ASIS to umbilicus ), low grade fever, rebound tenderness in RIF, LIF generate pains in RIF (rovsing’s sign), anorexia, guarding, N+V, percussion tenderness
Ix: CRP, U/S to rule out ovarian torsion in women, FBC, hcg in women
Mx: Laparoscopic surgery
Summarise Paralytic Ileus
Peristalsis in the SB stops leading to obstruction. Presents the same as obstruction. Treat with supportive aspects of obstruction until get better e.g. NBM, NGT, fluids.
Summarise volvulus
Bowel + mesentery twist around itself. Since blood supply comes from mesentery and mesenteric arteries in that = ischaemia. Closed loop obstruction.
Sigmoid: more common, older pts, often caused by chronic constipation/ excess laxatives
Caecal: less common, younger pts.
RF: neuropsych disorder, nursing home, high fibre diet, pregnancy, chronic constipation
Presentation: Like bowel obstruct - general abdo pain; bilious vom; tinkling bowel sounds; shock; distension; constipation and no wind
Ix: XR shows COFFEE BEAN SIGN. CT confirms.
Mx: same as BO - NBM, NGT, IV fluids. Can do endoscopic decompression in sigmoid. If need surgery is called a hartmanns in sigmoid and a right hemicolectomy in coecal - cut out the affected portion.
Summarise hernias
Pathophysiology: Weakness in fascia/ muscle allows body organ to pass through wall
Sx: Soft lump that appears with coughing + standing/ disappears when lie down (reducible), ache/ drag
Mx: Conservative if has a wide neck so can be easily pushed back in; Surgery: usually do a tension free repair (use mesh to cover defect in abdo wall) other option tension repair (suture muscles back together)
Complications: Obstruction and strangulation (ischaemia) if non-deductible
TYPES:
Indirect inguinal: where bowel herniates through inguinal canal (contains spermatic cord in males and the round ligament in women) → on examination will be reduced at the deep inguinal ring (half way between ASIS and pubic tubercle) unlike direct hernia
Direct inguinal: bowel comes through abdo wall in Hasselbachs triangle (Rectus abdominis, inferior epigastric vessels, poupart’s ligament)
Femoral hernia: Femoral canal - below inguinal ligament, at top of thigh. Big risk of strangulation.
Incisional: prev surgery
Hiatus hernia: stomach through diaphragm via the esophageal opening → reflux
Summarise Haemorrhoids
Pathophysiology: Enlarged anal cushions (submucosal tissue that connect arteries and veins in the anus, surround the internal and external anal sphincters)
Types: Describe haemorrhoids via clock face where 12 is towards genitals and 6 if towards back. Also classify by whether they are prolapsed permanently, with straining or not at all.
RF: birth, constipation, obesity, age, wt lifting
Sx: PR bleed - fresh, when wipe, sore/ itchy anus. Can see or feel or PR. Ask them to bear down to try make them prolapse.
Differentials for PR bleed: anal fissure, divertulosis, IBD, cancer
Ix: proctoscopy to properly visualise
Mx: laxatives, fluids, better diet, creams (anusol, lidocaine), rubber band ligation, coagulation, surgery.
Thrombosed haemorrhoids are very painful, purple and swollen due to a clot in there.
Summarise Anal disorders
ANAL FISSURE
presents with bright red bleed
Mx first line with topical diltiazem, second line botox, definitive mx is surgery
ANAL FISTULA
May first present with an abscess then discharge from site that isnt the anus. Mx with surgery.
ANAL ABSCESS
Anal swelling and erythema
Incision and drainage.
Summarise Diverticular Disease
Diverticulosis = outpouching in bowel;
diverticular disease = give you sx;
diverticulitis = inflammation and infection. Most commonly affects sigmoid but can affect all of LB.
RF: low fibre, constipation, age, NSAID use
Diverticulosis:
Sx: LIF pain, constipation, PR bleed
Mx: conservative (diet + bulk forming laxatives eg isphagula husk NOT stimulant lax), surgery, beware obstruction
Diverticulitis:
Sx: LIF pain, fever, diarrhoea, N+V, PR bleed, abdo mass if abscess
Ix: raised inflammatory marker,
Mx: If uncomplicated, manage in community with analgesia, clear liquids, co-amox. If complicated do NMB, IV abx, IV fluids, CT and potentially surgery for obstruction.
Summarise Mesenteric Ischaemia
Pathophysiology: Clot in: coeliac artery (foregut), superior mesenteric (midgut) or inferior mesenteric (hindgut)
In chronic mesenteric ischaemia: like angina in the gut. In acute is a sudden clot: like heart attack of the gut.
RF: same as CVD for chronic, AF in acute
Sx: Chronic → colicky abdo pain after eating, wt loss, bruit (TRIAD);
Acute → acute, non-specific abdominal pain, disproportionate to exam, shock
Ix: CT angio - chronic
acute - contrast CT + ABG shows metabolic acidosis and raised lactate
Mx: chronic - address RF and revascularization
acute - surgery to remove necrotic bowel and thrombus - mortality high
Summarise Bowel Cancer
Pathophysiology: Usually affects colon or rectum not anal or SB.
RF: alcohol, red meat, Fhx, FAP (Familial adenomatous polyposis ), Lynch syndrome, IBD, age, smoking, obesity
Screening: 60-74 yrs every 2 yrs do a FIT (fecal immunochemical test) for human Hb in stool. Colonoscopy if +ve.
Sx: change in bowel habits, abdo/ rectal mass, PR bleed, wt loss, microcytic anaemia, abdo pain, obstruction is far along
2 WW Referral: >40 + abdo pain + wt loss.
>50 + PR bleed.
>60 + change bowels/ iron def anaemia. (without other explanation for these things)
Ix: Do FIT test if don’t fit 2WW and have suspicious wt loss or change in bowels.
Colonoscopy gold standard. CT to stage. CEA (serum carcinoembryonic antigen) as a tumour marker.
Duke’s classification for staging.
Mx: MDT etc.
