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54 Cards in this Set

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Which apoprotein serves as a ligand for LDL?
Apo-B100
Which apoprotein serves as a ligand for remnant receptors in the liver?
Apo-E
Which apoprotein serves as a co-factor for LCAT?
Apo-A-I
Which apoprotein serves as a co-factor for LPL??
Apo-C-II
What is the majority of CM, TG or CE?
TGs
What fx does the LPL cofactor serve with Apo C-II?
LPL is a lipase that sits on the endothelium of bv in muscles and fat and serves to liberate TG --> C-II was received from HDL
give the % of CE vs TG in the following: VLDL, IDL, LDL
VLDL=80% TG... IDL 50:50 CE:TG… LDL= mainly CE
What is the functional difference between B100 and B48?
What is the functional difference between B100= 50% bind to the liver 50% have an extended life as a LDL.. and B48, all bind to the liver and are taken up (chylomicrons)?
What does the LDL lack?
What does the LDL lack? Apo E --> which binds to the remnant receptor on the liver
A patient's lab reports show an increased number of VLDL (or LDLs) of a smaller size and also shows signs of metabolic syndrome, what is the diagnosis?
A patient's lab reports show an increased number of VLDL (or LDLs) of a smaller size and also shows signs of metabolic syndrome, what is the diagnosis? Familial combined hyperlipidemia
A patient has a deficiency in fat soluble vitamins, what do you think his Apo-B levels will be? Diagnosis?
A patient has a deficiency in fat soluble vitamins, what do you think his Apo-B levels will be? Decreased… Diagnosis? Hypobetaliproteinemia or abetaliproteinemia
A patient has an excessive input of VLDL (acquired or inherited) plus his genetic test shows that he is homozygous for E2 (two are required for expresion). What do you think his lipid panel will show? Diagnosis?
A patient has an excessive input of VLDL (acquired or inherited) plus his genetic test shows that he is homozygous for E2. What do you think his lipid panel will show? Hyperlipidemia and hypertrigliceridemia;both are elevated because remnants (IDL) have 50:50 of TG:CE… Diagnosis: Remnant removal disease (III)
An infant presents with hypertrigliceridemia, what do you suspect? what genetic tests would you want to perform to confirm your suspicion?
An infant presents with hypertrigliceridemia, what do you suspect? LPL mediated triglyceride removal disorder… what genetic tests would you want to perform to confirm your suspicion? Check for defects in LPL and apo-CII
A patient who has healthy eating habits is found to have have hypercholesterolemia. He has tenon xanthomas, and you find that he is producing excess HMG CoA reductase. What two genetic defects might you check for? What is the reason for excess HMG CoA reductase?
A patient who has healthy eating habits is found to have have hypercholesterolemia. He has tenon xanthomas. What two genetic defects might you check for? LDL-® defect and Apo-B-100 defect. Diagnosis= familial hypercholesterolemia… What is the reason for excess HMG CoA reductase? with no IDL (LDL endocytosis, etc) there is no no cholesterol being taken up by the liver --> no down regulation of HMG CoA reductase
A patient consistently eats food high in cholesterol and high in saturated fats. What do you expect to find? Why?
A patient consistently eats a high cholesterol and high saturated fats diet. What do you expect to find? Acquired hypercholesterolemia...Why? ↑ cholesterol --> ↓ LDL-®… ↑ saturated fats --> ↓ LDL-® and ↑
VLDL production
A person with hypothyroidism presents with hypercholesterolemia… what do you suspect is the reason for this?
A person with hypothyroidism presents with hypercholesterolemia… what do you suspect is the reason for this? Defective LDL-®, which is associated with hypothyroidism
A thin female patient, who eats a low TG diet, doesn't smoke, exercises regularly, and does not drink alcohol presents with ↓HDL, what are the differential diagnoses?
A thin female patient, who eats a low TG diet, doesn't smoke, exercises regularly, and does not drink alcohol presents with ↓HDL… what are the differential diagnoses: Acquired: low fat diet, anti HTN drugs, uremia... diseases: Apo-1 deficiency, LCAT deficiency, Tangier's dz, Fish eye dz
What mutation leats to familial HDL deficiency?
What mutation leats to familial HDL deficiency? ABC1 mutations
Are the following causes of acquired combined hyperlipidemia or hyperTG? Hypothyroidism, nephrotic syndrome, cushing's, acromegaly, diuretics, transplant medications
Are the following causes of acquired combined hyperlipidemia or hyperTG? Hypothyroidism, nephrotic syndrome, cushing's, acromegaly, diuretics, transplant medications --> combined
How are HMG CoA reductase, ACAT and LDL-® affected by the internalization of an LDL via the LDL-®?
↓HMG CoA reductase, ↑ACAT and ↓LDL-®
A patient who previously had familial hypertriglyceridemia and who tests negative for LPL and ApoCII defects presents with a marked increase in his triglyceridemia. What is the likely etiology?
A patient who previously had familial hypertriglyceridemia and who tests negative for LPL and ApoCII defects presents with a marked increase in his triglyceridemia. What is the likely etiology? LPL is saturated due to an existing triglyceride excess disorder PLUS, an acquired disease that independently increases his TGs, e.g., diabetes, hypothyroidism or a nephrotic syndrome
A patient who has pancreatitis is found to have an excess of TGs. You are trying to determine the etiology of the disease. You run a series of lab test and find the following? Low arterial O2, a falsely normal amylase for someone with pancreatitis, low hemaglobin, low serum sodium and an abnormal thyroid fx tes. What is you diagnosis?
A patient who has pancreatitis is found to have an excess of TGs. You are trying to determine the etiology of the disease. You run a series of lab test and find the following? Low arterial O2, a falsely normal amylase for someone with pancreatitis, low hemaglobin, low serum sodium and an abnormal thyroid fx tes. What is you diagnosis? Chylomicroniemia syndrome
What is the role of LCAT?
What is the role of LCAT? Esterfies cholesterol in HDL --> leading to spherical shape of HDLs
A patient is not producing excess numbers of VLDL, yet his TGs are elevated? What would be the cause of this… Diagnosis?
A patient is not producing excess numbers of VLDL (on excess B100), yet his TGs are elevated. What would be the cause of this… excess TG but normal number of VLDL… Diagnosis? Familial hypertriglyceridemia
Are the following causes of hyperTG or combined hyperlipidemia (TG and CE)? DM, obesity, alcohol, ß blockers, E, resins, retinoids.
Are the following causes of hyperTG or combined hyperlipidemia (TG and CE)? DM, obesity, alcohol, ß blockers, E, resins, retinoids. --> hyperTG
A patient has had 7 thrombus events in the last year, he is shown to have an increase in athersclerotic placques, and you suspect a lipid metabolic disorder… what increased level would confirm your suspicions? What are they made from?
A patient has had 7 thrombus events in the last year, he is shown to have an increase in athersclerotic placques, and you suspect a lipid metabolic disorder… what increased level would confirm your suspicions? Increased Lp(a), which interferes with fibrinolysis by competing w/ plasminogen... What are they made from? they're made from an LDL linked to a plasminogen-like moiety
What are the Metabolic syndrome and it manifestation the result of?
What are the Metabolic syndrome and it manifestation the result of? Insulin insensitivity
What is the major contributor to insulin insensitivity?
What is the major contributor to insulin insensitivity? Excess FFA
In terms of the Metabolic Syndrome, what is the difference between visceral fat and subcutaneous fat?
In terms of the Metabolic Syndrome, what is the difference between visceral fat and subcutaneous fat? Visceral --> FFA--> liver (↑ Apo B lipoproteins, ↑ TGemia, ↓HDL, ↑ in smaller denser LDLs)… Subcutaneous FFA--> systemic circulation
What are the 3 consequences of hyperlipidemia?
What are the 3 consequences of hyperlipidemia? Chylomicronemia, atherosclerosis, and cutaneous manifestation (xanthomas)
How is inflammation related to the Metabolic syndrome?
How is inflammation related to the Metabolic syndrome? Inflammation --> ↑ cytokines (IL6, TNF-∂, C reactive protein) --> insulin resistance --> metabolic syndrome
What 4 signs and symptoms are related to chylomicronemia syndrom?
What 4 signs and symptoms are related to chylomicronemia syndrom? Abdominal pain (often due to pancreatitis), eruptive xanthomas, milky plasma, TG> 2000 mg/dl (normal is 200 mg/dl)
What is the etiology of chylomicronemia?
usually the result of genetic and acquired factors
Name 3 primary genetic defects found in patients presenting with chylomicronemia.
Name 3 primary genetic defects found in patients presenting with chylomicronemia. Familial combined hypercholesterolemia ( ↑ Apo B-100), Familial hyperTGemia (↑TG production), Remnant removal dz ( ↓ remnant removal and ↑ lipid production)
What does this define? Change in size and density of lipoprotein w/o hyperlipidemia.
What does this define? Change in size and density of lipoprotein w/o hyperlipidemia = Dyslipidemia
Why are smaller denser LDLs likely to lead to increased risk of atherosclerosis?
Why are smaller denser LDLs likely to lead to increased risk of atherosclerosis? Smaller denser LDLs are susceptible to oxidation
Why is oxidation so critical in atherosclerosis?
Why is oxidation so critical in atherosclerosis? Oxidation is required for macrophage uptake of LDLs --> which leads to foam cell formation
A patient presents with eruptive xanthomas, what is your diagnosis?
A patient presents with eruptive xanthomas, what is your diagnosis? Chronic Chylomicronemia
A patient presents with tendon xanthomas, what is you diagnosis?
A patient presents with tendon xanthomas, what is you diagnosis? LDL-® or Apo B interactin defects.
A patient presents with palmar and tubo eruptive xanthomas, what is your diagnosis?
A patient presents with palmar and tubo eruptive xanthomas, what is your diagnosis? Remnant accumulation and removal disease
Match the drug with the mechanism of action (Niacin, bile acid sequestrants, cholesterol absorption inhibitor, fibrates, statins) HMG CoA reductase inhibitor.
Match the drug with the mechanism of action (Niacin, bile acid sequestrants, cholesterol absorption inhibitor, fibrates, statins): HMG CoA reductase inhibitor = Statin
Match the drug with the mechanism of action (Niacin, bile acid sequestrants, cholesterol absorption inhibitor, fibrates, statins): reduction of hepatic secretion of VLDL and stimulation of LpL activity.
Match the drug with the mechanism of action (Niacin, bile acid sequestrants, cholesterol absorption inhibitor, fibrates, statins): reduction of hepatic secretion of VLDL and stimulation of LpL activity = Fibrates
Match the drug with the mechanism of action (Niacin, bile acid sequestrants, cholesterol absorption inhibitor, fibrates, statins): inhibits VLDL production and delays HDL clearance
Match the drug with the mechanism of action (Niacin, bile acid sequestrants, cholesterol absorption inhibitor, fibrates, statins): inhibits VLDL production and delays HDL clearance = Niacin
Match the drug with the mechanism of action (Niacin, bile acid sequestrants, cholesterol absorption inhibitor, fibrates, statins): prevent enterohepatic absorption of ______?
Match the drug with the mechanism of action (Niacin, bile acid sequestrants, cholesterol absorption inhibitor, fibrates, statins): prevent enterohepatic absorption of Bile? Bile sequestrants bind bile and prevent enterohepatic absorption
Match the drug with the lipid lowering effects (Niacin, bile acid sequestrants, cholesterol absorption inhibitor, fibrates, statins): Most effective for lowering LDLs, raises HDLs, causes non specific myalgias, may reduce inflammation
Match the drug with the lipid lowering effects (Niacin, bile acid sequestrants, cholesterol absorption inhibitor, fibrates, statins): Most effective for lowering LDLs, raises HDLs, causes non specific myalgias, may reduce inflammation= Statins… may reduce TG
Match the drug with the lipid lowering effects (Niacin, bile acid sequestrants, cholesterol absorption inhibitor, fibrates, statins): loweres TG, increase HDL, may increase or decrease LDLs
Match the drug with the lipid lowering effects (Niacin, bile acid sequestrants, cholesterol absorption inhibitor, fibrates, statins): loweres TG, increase HDL, may increase or decrease LDLs = Fibrates
Match the drug with the lipid lowering effects (Niacin, bile acid sequestrants, cholesterol absorption inhibitor, fibrates, statins): ↓ LDL, ↑HDL, ↓ TG, ↓ Lp(a), may cause flushing, puritis, Gi problems.
Match the drug with the lipid lowering effects (Niacin, bile acid sequestrants, cholesterol absorption inhibitor, fibrates, statins): ↓ LDL, ↑HDL, ↓ TG, ↓ Lp(a), may cause flushing, puritis, Gi problems = Niacin
Match the drug with the lipid lowering effects (Niacin, bile acid sequestrants, cholesterol absorption inhibitor, fibrates, statins): ↓ LDL and ↑ HDL, with an adverse INCREASE in TGs
Match the drug with the lipid lowering effects (Niacin, bile acid sequestrants, cholesterol absorption inhibitor, fibrates, statins): ↓ LDL and ↑ HDL, with an adverse INCREASE in TGs = biles sequestrants
Match the drug with the lipid lowering effects (Niacin, bile acid sequestrants, cholesterol absorption inhibitor, fibrates, statins): ↓ LDL, but works well with Statins.
Match the drug with the lipid lowering effects (Niacin, bile acid sequestrants, cholesterol absorption inhibitor, fibrates, statins): ↓ LDL, but works well with Statins = cholesterol absorption inhibitors "ezetimide"
Which drug is contraindicated for gout and DM?
Niacin: ↑ hyperglycemia, ↑uric acid
What is a good marker for demonstrating risk for inflammatory risk?
What is a good marker for demonstrating risk for inflammatory risk? C-reactive protein
What do modified (oxidized) LDL cause endothelial cells to express that serves as a monocyte recruiter?
What do modified (oxidized) LDL cause endothelial cells to express that serves as a monocyte recruiter? MCP-1
What do macrophages secrete which stimulates endothelial cells to secrete vascular cell adhesion molecule (VCAM)?
TNF-∂ and IL-1… thus MCP-1=VCAM… attracts and monocytes --> foam cells
What factor is produced by macrophages and foam cells in more advanced atherosclerotic lesions that cause cell proliferation and matrix degeneration?
What factor is produced by macrophages and foam cells in more advanced atherosclerotic lesions that cause cell proliferation and matrix degeneration?Metalloproteinases