Please read and agree to the disclaimer before watching this video.
. Gallbladder Stones and Flareups

95% of the gallbladder diseases are cholelithiasis (gallstones.)

About 2% of the US health budget goes towards the management of cholelithiasis and its complications.

10%-20% of the population in the western hemisphere has gallstones.
25-50 tons of the gallstones are carried by more than 20 million Americans.

In the US about 1 million new cases are diagnosed annually, out of these, 2/3 will undergo surgery for the gallstones.

Gallstones are of two main types. 80% are cholesterol stones. Consisting of crystalline cholesterol monohydrate. The remainder are mainly bilirubin calcium salts and are called pigment stones.

High-Level Pathophysiology
The basic reason for the formation of the cholesterol stones is the following:
They only path for the cholesterol removal from the body is via the bile system. Cholesterol is not water soluble. We need to make it water soluble to traverse this path. To solve this, our body forms bile salts and lecithins. These bind with cholesterol and allow the passage through the bile system. These salts and lecithins are like boats on the water to which cholesterol is bound. If the quantity of the cholesterol is more than the binding capacity of these salts, then the unbound cholesterol forms cholesterol monohydrate crystals. These crystals precipitate in solid form. These precipitations irritate the gallbladder layers that in turn release mucus which traps these solid structures in the gallbladder resulting in the stone formation.
In summary, the following four events occur simultaneously for the formation of a gallstone:
1. Amount of cholesterol more than the binding capacity of the bile salts (supersaturation.)
2. Formation of the cholesterol monohydrate crystals.
3. Precipitation and aggregation of these crystals forming solid stone particles.
4. Mucus secretion by the gallbladder’s inner surface resulting in the entrapment of these solid particles in the gallbladder.

.
.
.
.
.
#DrBeen #Medicine #cholelithiasis #pathophysiology #gallbladder #gallstones #cholesterol_stones #pigment_stones #cholesterol_mono_hydrate #MedLife #nursing #nursingLife #MedSchool #NursingSchool #NursePractitioners #physicianassistants #usmle #Step2 #step1 #nclex #mbbs #comlex #DrMobeenSyed …

Disclaimer:
This video is not intended to provide assessment, diagnosis, treatment, or medical advice; it also does not constitute provision of healthcare services. The content provided in this video is for informational and educational purposes only.
Please consult with a physician or healthcare professional regarding any medical or mental health related diagnosis or treatment. No information in this video should ever be considered as a substitute for advice from a healthcare professional. …
Disclaimer:
This video is not intended to provide assessment, diagnosis, treatment, or medical advice; it also does not constitute provision of healthcare services. The content provided in this video is for informational and educational purposes only.
Please consult with a physician or healthcare professional regarding any medical or mental health related diagnosis or treatment. No information in this video should ever be considered as a substitute for advice from a healthcare professional.
Video Rating: / 5

Normally, the walls of an artery are smooth, allowing blood to flow unimpeded. Atherosclerosis is when harmful material collects on the wall of an artery. This material includes fat, cholesterol, and other substances.

Eventually, the material builds up and a plaque is formed, narrowing the artery. When the build-up is severe, a clot could block the vessel completely.

—–

Mechanism

Atherogenesis is the developmental process of atheromatous plaques. It is characterized by a remodeling of arteries leading to subendothelial accumulation of fatty substances called plaques. The buildup of an atheromatous plaque is a slow process, developed over a period of several years through a complex series of cellular events occurring within the arterial wall, and in response to a variety of local vascular circulating factors. One recent hypothesis suggests that, for unknown reasons, leukocytes, such as monocytes or basophils, begin to attack the endothelium of the artery lumen in cardiac muscle. The ensuing inflammation leads to formation of atheromatous plaques in the arterial tunica intima, a region of the vessel wall located between the endothelium and the tunica media. The bulk of these lesions is made of excess fat, collagen, and elastin. At first, as the plaques grow, only wall thickening occurs without any narrowing. Stenosis is a late event, which may never occur and is often the result of repeated plaque rupture and healing responses, not just the atherosclerotic process by itself.

Atherosclerosis (also known as arteriosclerotic vascular disease or ASVD) is a specific form of arteriosclerosis in which an artery wall thickens as a result of invasion and accumulation of white blood cells (WBCs).

The accumulation of the WBCs is termed “fatty streaks” early on because of appearance being similar to that of marbled steak. These accumulations contain both living, active WBCs (producing inflammation) and remnants of dead cells, including cholesterol and triglycerides. The remnants eventually include calcium and other crystallized materials, within the outer-most and oldest plaque. The “fatty streaks” reduce the elasticity of the artery walls. However, they do not affect blood flow for decades, because the artery muscular wall enlarges at the locations of plaque. The wall stiffening may eventually increase pulse pressure; widened pulse pressure is one possible result of advanced disease within the major arteries.

Atherosclerosis is therefore a syndrome affecting arterial blood vessels due to a chronic inflammatory response of WBCs in the walls of arteries. This is promoted by low-density lipoproteins (LDL, plasma proteins that carry cholesterol and triglycerides) without adequate removal of fats and cholesterol from the macrophages by functional high-density lipoproteins (HDL). It is commonly referred to as a “hardening” or furring of the arteries. It is caused by the formation of multiple atheromatous plaques within the arteries.[1][2]

The plaque is divided into three distinct components:

The atheroma (“lump of gruel”, from Greek ἀθήρα (athera), meaning “gruel”), which is the nodular accumulation of a soft, flaky, yellowish material at the center of large plaques, composed of macrophages nearest the lumen of the artery
Underlying areas of cholesterol crystals
Calcification at the outer base of older or more advanced lesions.

Atherosclerosis is a chronic disease that remains asymptomatic for decades.[3] Atherosclerotic lesions, or atherosclerotic plaques, are separated into two broad categories: Stable and unstable (also called vulnerable).[4] The pathobiology of atherosclerotic lesions is very complicated but generally, stable atherosclerotic plaques, which tend to be asymptomatic, are rich in extracellular matrix and smooth muscle cells, while, unstable plaques are rich in macrophages and foam cells and the extracellular matrix separating the lesion from the arterial lumen (also known as the fibrous cap) is usually weak and prone to rupture.[5] Ruptures of the fibrous cap expose thrombogenic material, such as collagen,[6] to the circulation and eventually induce thrombus formation in the lumen. Upon formation, intraluminal thrombi can occlude arteries outright (e.g. coronary occlusion), but more often they detach, move into the circulation and eventually occluding smaller downstream branches causing thromboembolism. Apart from thromboembolism, chronically expanding atherosclerotic lesions can cause complete closure of the lumen. Chronically expanding lesions are often asymptomatic until lumen stenosis is so severe (usually over 80%) that blood supply to downstream tissue(s) is insufficient, resulting in ischemia.
Video Rating: / 5

Share this page: