تصير لما الكالسيوم يتجمع بجدار المرارة. عادةً تكون asymptomatic ونكتشفها بالصدفة، ومرات نكتشفها كـ palpable mass in the RUQ.
بعض الدراسات تكول أنها تزيد خطر الإصابة بسرطان المرارة adenocarcinoma of the gallbladder ولهذا الإجراء الشائع هو إزالتها عند اكتشافها، رغم أنّ نسبة الخطر تختلف حسب الدراسات وتتراوح بين 6% إلى 21%

هاي أعتقد همين porcelain GB، بس ما متأكد

Abdominal Aortic Aneurysm (AAA) is characterized by a triad of Ssx:

- Severe abdominal pain
- pulsatile abdominal mass
- hypotension (especially orthostatic, even when the supine is normal)

It can be misdiagnosed in about 16% of cases (usually diagnosed as a renal colic). But the history (like smoking history, which is the most important risk factor) and physical exam should point you to the right diagnosis.

Here's a practically useless information:

Why paracetamol is not a NSAID?

Cyclooxygenase (COX) enzymes have 2 subunits: a cyclooxygenase subunit, and a peroxidase subunit.

Most NSAIDs work by inhibiting the cyclooxygenase subunit, and therefore, they inhibit the prostaglandin production and produce their anti-inflammatory and analgesic effect.

Acetamenophin on the other hand, works by inhibiting the peroxidase subunit. Therefore, in sites of inflammation, where peroxide is elevated, acetamenophin loses its ability to inhibit COX enzymes, and as a result, fails as an anti-inflammatory agent but not as an analgesic. This is because the drug is still able to inhibit COX enzymes in the pain centers of the CNS to reduce pain.

NSAIDs and hypertension

NSAIDs and acetamenophin are known to have hypertensive effect, possibly because they decrease sodium excretion in the kidneys and cause volume expansion.
They are also known to decrease the efficacy of anti-hypertensive drugs except for calcium-channel blockers (CCPs), and possibly also beta-blockers (BBs). So in patients with chronic NSAIDs use, treat them with CCPs or BBs as a 1st-line therapy for hypertension.

Aortoenteric fistula (AEF)

Basically when your aorta opens up into your duodenum... which, you know, it shouldn't do that...

The ticking bomb that we call "aortic aneurysm"

IBS is mostly a diagnosis of exclusion. This means that you must "exclude" other diseases in order to diagnose someone with IBS

IBS: Irritable Bowel Syndrome

Why anti-depressants are sometimes used to treat IBS?

TCAs are the most widely used anti-depressants to treat IBS. They are usually used in low doses (25-125 mg/day) less than those required to treat psychological symptoms. So the mechanism of action probably involves changing the serotonin secretion in the GIT, rather than reducing anxiety or depression.

SSRIs (and other modern anti-depressants) on the other hand are used in higher doses that make them psychologically active, so their mechanism of action involves reducing the psychological factors like anxiety and depression that exacerbate IBS.

A quick (anatomy of the pharynx) lesson.
Look at how the inferior pharyngeal & the cricopharyngeus muscles are related to one another and to the esophagus