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With his age, cholesterol:HDL ratio and the BMI the QRISK score is >10% therefore statins are indicated in his case.

Abdominal US is indicated in all cases of abnormal liver blood test.  If proved to have MASLD (Fatty liver on the US) then should be screened for Hb1Ac for type 2 diabetes.

Lifestyle modification is the most important treatment in his case.

Even though doing a FibroScan is never bad practice (it is non invasive and very helpful to estimate the level of liver fibrosis) the fact is that FibroScan would be strictly indicated IF the FIb4-score was > 2 (remember the cutoff in >65 yo is 2 instead of 1.3).

The lower cutoff for FIB 4   >1.3.  Less than 1.3 rules out advanced fibrosis, and >1.3 needs further investigations.

In elderly patients (>65 yo) this threlsholds has low especificity (many false positive patients who do not really have advanced fibrosis) therefore the cutoff proposed in those is 2 (Fib 4 <2 rules out significant fibrosis)

>2.67 is the upper threshold for advanced fibrosis. Patients scoring this have high chance of advance fibrosis and should be referred to liver clinic

This is a case of Clostridioides (Clostridium) difficile colitis with typical pseudomembranes on the colonic mucosa.  Elderly and nursing home patients are risk factors. We should take biopsies and ask for faecal sample (GDH and /or culture for toxigenic C.diff) because pseudomembrane rarely can have other causes (Staphylococcus aureus, CMV, radiation, ischemic, chemotherapy)

Patient does not meet the definition of Severe (>15000 leucocytes or deranged Creatinin) or fulminant (hypotension, septic shock, megacolon)

Most guidelines no longer recommend Metronidazole for C.diff as first line unless no other alternative available.  Despite ACG recommends either Vancomycin or Fidaxomicin as first line, (Fidaxomicin is more expensive) the European guidelines recommend Fidaxomicin over Vancomycin (Vancomycin is a perfect acceptable good choice , however despite both curing the infection in about the same rates (76.2% vs 70.5%),  lower recurrence rates with fidaxomicin are described (8.3% vs 32.6%) which could justify its higher cost.

The majority of pancreatic cancers are due to spontaneous mutations in a complex combination of usually several mutations ((KRAS) mutations are common in 90% of pancreatic cancers, but in combination with different other mutations, DNA damage and usually other risk factors.

There is however a very important percentage (5%-10%) of new PC which associate familial pancreatic cancer (Defined by two first-degree-relatives with pancreatic cancer), There are indeed genes involved such as BRCA2 gene  mutations  ( 3.5-fold increased risk of pancreatic cancer ).  Other inherited mutations in the STK11 gene cause the Peutz-Jeghers syndrome, and individuals with Peutz-Jeghers have a 130-fold increased risk of pancreatic cancer

To put in context,

One degree relative with PC  makes relative having an 80% increased risk of developing pancreatic adenocarcinoma (this is RR: 1.8)

individuals with 2 degree relatives with PC have a nine fold risk , and this rises to thirty-two times greater risk if three or more first degree relatives have been previously diagnosed

We need to differenciate between non dysplastic (the majority of Barrett's do not have any dysplasia, just metaplasia) versus dysplastic changes (proliferative changes that is characterized by a loss in the uniformity of individual cells in a tissue and loss in the architectural orientation )

The overall yearly incidence of  eosphageal adenocarcinoma in non dysplasitc  is 0.3% (. This is approximate and based on a metanalysis, although we know that factors such a age, smoking or obesity increase the overall risk of adenocarcinoma in Barrett's patients, and equally, the risk lowers when short segment (<3cm) - down to 0.19 % per year)

9.1% is the overall incidence of progression (to either HGD or adenoca) in those who already present low grade dysplasia, up to   9.1% per patient/year  with pooled annual incidence of adenocarcinoma of 0.54% per year

Check the guidelines

According to the  2020 BSG  post-polypectomy surveillance guidelines   we recommend no surveillance if life expectancy is less than 10 y or patient older than 75 yo.  However this can be flexible depending on the patient situation. For example, if histology show incomplete resection margins or colonoscopy was suboptimally prepared then it could be reasonable to repeat the test in 1 year.

If this same case was in a fit and younger patient (e.g  65 yo patient ) then given that we removed 5  adenomas (premalignant) - this would be the cutoff to have another colonoscopy in 3 years

In fact, the majority of the guidelines suggest 3 year follow up if 5 or more small(<10mm)  adenomas are removed.  2020 AGA recommend 3 years followup if 5-10 adenomas, 5 years if 3-4 adenomas and up to 7-10 years if only 1-2 adenomas (or SSL).

For example, if a 65 yo patient had only 4 small adenomas with en bloc resection and good bowel cleaning,  no further surveillance and return to bowel screening according to the British guidelines but would need 5 year colonoscopy according to the AGA guidelines. 

Difficult question, but summarizes the (sometimes) difficult scores.
Montreal classification is easy - A for Age  L for location and B for phenotype.  There is ileal and colonic involvement so it is L3 (Ileocolonic) Small p is added when it is perianal disease (abscesses, ulcers or fistulae , but not skin tags or fissures)

The HBI takes into account the general well being , Abdominal pain   Number of liquid stools per day, Abdominal mass and extrainestinal Complications ( arthralgia, uveitis, erythema nodosum, aphthous ulcers, pyoderma gangrenosum ,anal fissure , new fistula or abscess)

<5 Remission   5-7 Mild disease  8-16 Moderate disease  >16 Severe disease

Her score is 9 (Moderate) But this could be guessed based on her level of pain, stools and absence of systemic inflamamtory reponse.

Check the HBI score