trivia/lipoproteins Flashcards
which members of the digestive tract are completely intraperitoneal?
stomach
jejunum
ileum
pleomorphic adenoma
Most common benign salivary gland tumor (65%). (Parotid gland) Characterized by: proliferation of parenchymal cells and myoepithelial cells. The tumor is not enveloped, but it is surrounded by a fibrous pseudocapsule of varying thickness. The tumor extends through normal glandular parenchyma in the form of finger-like pseudopodia, but this is not a sign of malignant transformation.
Symptoms • Slow growing, painless, firm single nodular mass
• Classified as benign, but has the capacity to grow to
large proportions and undergo malignant transformation • Signs of numbness and weakness and pain due to the
nerve involvement • Usually mobile
Treatment
• Full surgical removal recommended due to the high
incidence of recurrence. • Difficult due to anatomical relationship of the facial
nerve, VII cranial nerve, and may cause facial nerve
dysfunction
what are the functional layers of the GI tract from lumen out
(lumen)
-Mucosa
-Submucosa
(contains Meissner’s plexus for mucous secretion)
- Muscularis layer (inner circular layer and outer longitudinal layer)
- in between those two muscle layers is the Auerbach plexus for muscle contraction
-lastly is the serosal layer which is the outer connective tissue
what are some mnemonics for dermatomes?
- thumbs up on left hand looks like number 6, C6 (includes the thumbs)
- T4 at the teat pore (T4 is horizontal section including the nipples)
- T10 at the belly butten (where appendicitis pain is referred early on), umbilicus
- L1 is IL (at the inguinal ligament)
- L4: down on alL4’s. includes the knee caps
- S2,S3,S4 - keep the penis off the floor. (responsible for erection, sensation of penile and anal zones)
What is Zollinger Ellison syndrome?
A G-cell tumor in the wall of the duodenum. Patients will experience peptic ulcer disease and GI bleeding.
Also causes stereorrhea because too much acid will inactivate the enzymes for fat digestion.
What do statins do?
They are the most widely prescribed drug for lowering cholesterol. They inhibit Hmg coA reductase which blocks denovo synthesis of cholesterol.
What is the underlying cause of glucose-galactose malabsorption?
It is a rare metabolic disorder (AR) which is caused by a defect in SGLT-1
(unable to tolerate sucrose, lactose, starches and glucose) only carbohydrate she can tolerate is fructose (GLUT5).
What is Smith-Lemli-Opitz Syndrome
SOLS
SLOSis a metabolic disorder caused by a mutation in the DHCR7 (7-dehydrocholesterol reductase) gene on chromosome 11.
This gene codes for an enzyme that is involved in the production of cholesterol. People who have SLOS are unable to make enough cholesterol to support normal growth and development.
Facial features include microcephaly, ptosis (drooping eyelid), [toh-sis] broad nasal bridge, upturned nose, and micrognathia (jaw is undersized). Cleft palate is also common. Limb anomalies include: Short thumbs, polydactyly [pol-ee-dak-tuh-lee]
Syndactyly of the second and third toes is the most frequently reported clinical finding.
what are the functions of these Apoproteins?
ApoA-I
ApoA-II
ApoB-48
ApoB-100
ApoC-II
ApoC-III
ApoE.
ApoA-1: is the major protein of HDL, it activates LCAT (which on HDL allows for esterification of cholesterol using phospholipid lecthicin in peripheral cells)
ApoA-II: primarily in HDL, it activates hepatic lipase activity
ApoB-48 - derived from ApoB-100 by RNA editing, is found exclusively in chylomicrons and lacks LDLR binding domain that 100.
ApoB-100: major protein of LDL, it binds to LDL receptor
ApoC-II: activates lipoprotein lipase
ApoC-III: inhibits lipoprotein lipase. Also important for uptake of chylomicron remnants of liver.
(lipoprotein lipase is found on walls of blood capillaries, it hydrolyzes TAG into freefatty acids and glycerol), some free fatty acids are then released back into circulation (bound to liver)
ApoE - “receptor mediated endocytosis of IDLs and chylomicron remnants” major protein of remnant lipoproteins, it binds to LRP and LDLR.
What does lipoprotein lipase and hepatic lipase do?
Apolipoprotein C-II on lipoprotein is a cofactor for LPL.
Lipoprotein lipase is on walls of blood capillaries, it will hydrolyze TAG into free fatty acids and glycerol.
Some released fatty acids return to circulation bound by albumin.
80% will be transported into tissue (adipose, heart, and muscle)
20% goes indirectly to liver.
HL: is a phospholipase and triglyceride hydrolase
- it is synthesized in hepatocytes and is present primarily on liver endothelial cells
- it hydrolyzes triglycerides and excess surface phospholipids in the final processing of chylomicron remnants
- it processes IDL into LDL. (intermediate density to low density)
- ApoA-II protein on HDL serves as cofactor for hepatic lipase
- it participates in conversion of HDL3 to HDL2 by removal of triglyceride and phospholipid from HDL3.
Describe the source and function of the lipoproteins as well as the major apoliproteins.
Chylomicrons
- from intestine, transport dietary TAG
- B48, ApoCII, ApoCIII, ApoE
VLDL
- from liver, trasnport endogenously synthesized TAG
- B100, ApoCII, ApoCIII, ApoE
LDL
- formed in circulation by VLDL metabolism, it delivers cholesterol to peripheral tissue
- B100
HDL
- produced from liver and intestine, removes used cholesterol from tissues and takes it to liver
- it is a reservoir for apoproteins that can be donated or received from other lipoproteins.
- ApoAI, ApoAII, ApoCII, ApoCIII, ApoE.
What is PCSK9
PSCK9 is an enzyme secreted by the liver into the blood. It reaches LDL receptors preventing their recycling back to the plasma membrane surface and promoting degradation by lysosomes.
Overactivity is a potential cause for hypercholesterolnemia.
What is SR-A
the infamous scavenger receptor.
It is a broader specificity receptor as opposed to the LDL receptor and binds both normal and damaged LDL particles. Macrophages and some endothelial cell types possess this receptor.
Example where significant LDL uptake is mediated by these receptors are the spleen and intestine.
Endocytosed particles are transported to lysosomes where cholesterol is then released into the cytosol.
SR-A leads to foam cell formation (the cause of artherosclerosis.
What is Lp(a)?
Lp(a) is an abnormal variant of LDL.
It is formed by a disulfide bond formed between apo(a) molecule and apoB-100.
It is an independent causal risk for artherosclerosis and highly heritable.
Describe reverse cholesterol transport
Reverse cholesterol transport is the cholesterol clearing house where excess cholesterol in peripheral tissue is brought back to the liver.
This pathway uses HDL which contain ApoA-I (LCAT), ApoA-II (hepatic lipase), ApoC’s, ApoE (uptake into liver)
- Nascent HDL is formed in liver and intestine by building on apoA-1. When cholesterol is taken up, it immediately esterifiess by LCAT.
- As cholesteryl esters increase in amount, nascent HDL goes from cholesteryl ester poor HDL3 until HDL2 (larger spherical HDL which is cholesteryl ester rich.
- CETP moves some cholesteryl esters from HDL to VLDL in exchange for TAG, relieving product inhibition of LCAT.
- VLDL are catabolized to LDL which are eventually taken up by liver so cholesteryl esters are transferred by CETP to the liver ultimately.
- Uptake of cholesteryl esters by liver is mediated by SRB-1 (scavenger receptor class B type 1) which binds HDL. Selective uptake of cholesteryl ester from HDL. Hepatic lipase degrades both TAG and phospholipids participates in conversion of HDL3 to HDL2.
- The cholesterol is excreted as bile salts or repackaged in VLDL for distribution.
