Atherosclerotic Vascular Disease Flashcards
1
Q
Q1: What is the definition of aneurysms?
A
A1: Aneurysms are defined as a permanent dilation of the artery to twice the normal diameter.
2
Q
Q2: What is the threshold diameter for an abdominal aortic aneurysm (AAA)?
A
A2: The threshold diameter for an AAA is greater than 3cm for the abdominal aorta.
3
Q
Q3: What is the incidence of AAAs in the population over 60 years of age?
A
A3:
AAAs are present in 5% of the population over 60 years of age.
4
Q
Q4: Do AAAs occur more frequently in men or women?
A
A4: AAAs occur five times more frequently in men.
5
Q
Q5: What are some risk factors for developing an AAA?
A
A5: include
age,
male gender, and
having a first-degree relative with an AAA. Aneurysms may also occur secondary to atherosclerosis, infection, trauma, or
genetic conditions such as Marfan’s syndrome or Ehlers-Danlos syndrome.
6
Q
Q6: What is the most common cause of AAA formation?
A
A6: The most common cause of AAA formation is atherosclerosis.
7
Q
Q7: What happens to the arterial wall in the formation of AAAs?
A
A7:
1. The degeneration of the media of the arterial wall occurs, most commonly due to atherosclerosis.
2. Macrophages release enzymes that break down the collagen and elastin of the media, leading to its expansion.
8
Q
Q8: Where do AAAs most commonly occur?
A
A8: AAAs most commonly occur below the renal arteries (infrarenal) - approximately 80% of cases.
9
Q
Q9: What are the consequences of a ruptured AAA?
A
A9: In a ruptured AAA, the wall of the aorta completely fails, and blood escapes freely into a body cavity, such as the abdominal cavity.
This is considered an emergency, with a high fatality rate.
The majority of ruptures are retroperitoneal (rupture contained), while intraperitoneal ruptures are rapidly fatal.
10
Q
Q10: What are the clinical presentations of AAA?
A
A10: AAA can be asymptomatic in 75% of cases and may be discovered incidentally.
Symptomatic AAA can present with epigastric/central pain, which is a risk factor for rupture or dissection.
A ruptured AAA presents as sudden onset abdominal pain radiating to the back, accompanied by an expansile abdominal mass.
11
Q
Q11: What are some other signs that may be observed in patients with AAA?
A
A11: Patients with AAA may present with
“trash feet,” which refers to dusky discoloration of the digits secondary to emboli from the aortic thrombus.
Collapse (due to hypotension) and
tachycardia may also be observed.
12
Q
Q12: What imaging modality is used for monitoring AAA?
A
A12: Ultrasound (USS) is used for monitoring AAA. It can show the presence of an AAA, its anteroposterior (AP) diameter, and whether there is iliac involvement.
In the UK, there is a monitoring program for all men over 65 years of age.
13
Q
Q13: What is the recommended diameter threshold for elective surgery in asymptomatic AAAs?
A
A13:
* Elective surgery for asymptomatic AAAs is only performed if the** AAA is greater than 5.5 cm** in diameter.
* Before reaching this size, the risk of surgery outweighs the risk of rupture.
14
Q
Q14: How is a ruptured AAA diagnosed?
A
A14:
* Diagnosis of a ruptured AAA is usually clinical, and it needs to be made quickly.
* The vascular surgeon should be contacted immediately.
* CT (computed tomography) is the only imaging method that can identify a ruptured AAA.
15
Q
Q15: What are the medical management strategies for AAA?
A
A15:
involves controlling risk factors.
* This includes prescribing antihypertensive medications,
* promoting smoking cessation, and
* prescribing lipid-lowering medication.
16
Q
Q16: What are the surgical options for AAA management?
A
A16: The surgical options for AAA management depend on the clinical presentation.
In asymptomatic cases, elective surgery is considered if the AAA reaches a diameter greater than 5.5 cm.
The surgical options include graft procedures such as endovascular aneurysm repair (EVAR)or open laparotomy.
17
Q
Q23: At what aortic diameter are patients referred to a vascular team?
A
A23: Patients with an aortic diameter above 3cm are referred to a vascular team, urgently if the diameter is more than 5.5cm.
18
Q
Q26: What imaging modality provides a more detailed picture of the aneurysm and helps guide elective surgery for AAA?
A
A26: CT angiogram provides a more detailed picture of the aneurysm and helps guide elective surgery for AAA.
19
Q
Q29: What are the recommendations for follow-up scans in patients with AAA?
A
A29:
The Public Health England screening and surveillance program recommends yearly follow-up scans for patients with aneurysms measuring 3-4.4cm and 3-monthly follow-up scans for patients with aneurysms measuring 4.5-5.4cm.
20
Q
Q30: What are the criteria for elective repair of AAA according to NICE guidelines?
A
A30:
elective repair is recommended for patients with any of the following:
Symptomatic aneurysm
Diameter growing more than 1cm per year
Diameter above 5.5cm
21
Q
What are the two methods for inserting a graft during elective surgical repair of AAA?
A
A31: The two methods for inserting a graft during elective surgical repair of AAA are open repair via a laparotomy and
endovascular aneurysm repair (EVAR)
using a stent inserted via the femoral arteries.
22
Q
Q33: What is the risk of rupture for an AAA based on its diameter?
A
A33: The risk of rupture increases with the diameter of the AAA. It is roughly 5% for a 5cm aneurysm and 40% for an 8cm aneurysm.
23
Q
Q36: What is the recommended management approach for a ruptured AAA?
A
A36:
A ruptured AAA is a surgical emergency and requires immediate involvement of experienced seniors, vascular surgeons, anesthetists, and theater teams.
- Haemodynamically unstable patients should be transferred directly to the theater for surgical repair without delay.
- In haemodynamically stable patients, a CT angiogram can be used to diagnose or exclude a ruptured AAA.
24
Q
Q37: What is permissive hypotension?
A
A37:
Permissive hypotension is a strategy in which fluid resuscitation is aimed at maintaining a lower than normal blood pressure.
The theory is that increasing blood pressure may increase blood loss in the context of a ruptured AAA.
25
Q38: What should be considered in patients with co-morbidities that make the prognosis with surgery very poor?
A38:
In patients with co-morbidities that make the prognosis with surgery very poor, a discussion needs to be held with senior doctors, the patient, and their family about palliative care.
26
Q1: What is aortic dissection?
A1: Aortic dissection refers to when a break or tear forms in the inner layer of the aorta, allowing blood to flow between the layers of the wall of the aorta.
27
Q2: What are the three layers of the aorta?
A2: The three layers of the aorta are the intima, media, and adventitia.
28
Q3: Where does blood enter in aortic dissection?
A3: In aortic dissection, blood enters between the intima and media layers of the aorta, forming a false lumen within the wall of the aorta.
29
Q4: What does "intramural" mean in the context of aortic dissection?
A4: "**Intramural" refers to within the walls of the blood vessel, indicating the location of the dissection.**
30
Q5: What is the most common site of a tear in the ascending aorta?
A5: The **right lateral area of the ascending aorta**
31
Q6: What are the two classification systems for aortic dissection?
A6:
Stanford system and
the DeBakey system.
32
Q7: What is Type A aortic dissection?
A7: Type A aortic dissection affects the**ascending aorta**, before the brachiocephalic artery.
33
Q8: What is Type B aortic dissection?
A8: Type B aortic dissection affects the **descending aorta, after the left subclavian artery.**
34
Q9: What is Type I aortic dissection according to the DeBakey system?
A9: Type I aortic dissection begins in the ascending aorta and involves at least the aortic arch, if not the whole aorta.
35
Q10: What is Type IIIa aortic dissection according to the DeBakey system?
A10: Type IIIa aortic dissection begins in the descending aorta and involves only the section above the diaphragm.
36
Q11: What is Type IIIb aortic dissection according to the DeBakey system?
A11: Type IIIb aortic dissection begins in the descending aorta and **involves the aorta below the diaphragm.**
37
Q12: What are some risk factors for aortic dissection?
A12: S
1. Hypertension or hypertension second to the use of cocaine, heavy weightlifting,
2. inflammation of the blood vessel wall (as in **syphilis**),
3. Takayasu arthritis inflmmatory granuluma in less than 50 years old px
4. conditions or procedures that affect the aorta (such as bicuspid aortic valve, coarctation of the aorta, aortic valve replacement, and coronary artery bypass graft),
5. conditions that affect connective tissues (such as Ehlers-Danlos Syndrome and Marfan's Syndrome).
38
Q13: What are the triggers that can temporarily cause a dramatic increase in blood pressure and potentially trigger aortic dissection?
A13: Events that can temporarily cause a dramatic increase in blood pressure and potentially trigger aortic dissection include
1. heavy weightlifting
2. cocaine and
3. amphetamine
39
Q14: Which condition is characterized by inflammatory granulomas depositing in the vessel walls and increases the risk of aortic dissection?
A14: **Takayasu arthritis**
is the condition characterized by inflammatory granulomas depositing in the vessel walls and increases the risk of aortic dissection.
40
Q16: What are the conditions or procedures that can increase the risk of aortic dissection?
A16:
* bicuspid aortic valve,
* coarctation of the aorta,
* aortic valve replacement, and
* coronary artery bypass graft (CABG).
41
Q17: What conditions are commonly associated with patients who have coarctation of the aorta? 2
A17: commonly have a history of Turner Syndrome and an **associated bicuspid aortic valve.**
42
Q18: What are the four possible scenarios that can occur after a tear in the aortic intima?
A18:
1. re-entry of the blood into the true lumen,
2. increased pressure within the aortic wall leading to rupture,
3. narrowing/occlusion of a branching vessel due to forming **hematoma** causing malperfusion syndromes, and
4. intramural (intraluminal) thrombosis resulting in the formation of a hematoma at the tear site.
43
Q19: What is the typical presentation of aortic dissection?
A19:
1. is a sudden onset of severe "ripping" or "tearing" chest pain.
2. The pain may be in the anterior chest if the ascending aorta is affected or
3. in the back if the descending aorta is affected. The pain may also change location (migrate) over time.
It's important to note that some patients with aortic dissection may not experience chest pain.
44
Q20: What are some features that may suggest aortic dissection?
A20:
1. include hypertension, differences in blood pressure between the arms (a significant difference of more than 20mmHg),
2. radial pulse deficit (decreased or absent radial pulse in one arm that doesn't match the apex beat),
3. diastolic murmur, focal neurological deficit (limb weakness or paraesthesia),
4. chest and abdominal pain, collapse (syncope), and
5. hypotension (a late sign rupture dissection ).
45
Q21: What diagnostic tests are commonly used for the diagnosis of aortic dissection?
A21:
**A widened mediastinum** may be seen on a chest x-ray.
**CT angiogram is usually the initial investigation** to confirm the diagnosis and can be performed quickly.
MRI angiogram provides greater detail but may take longer to obtain.
Trans-oesophageal echocardiography (TOE) is **used when hemodynamically unstable patients.**
46
Q22: What is the potential risk of treating myocardial infarction (MI) with thrombolysis in the presence of aortic dissection?
A22:
* Treatment of myocardial infarction (MI) with thrombolysis in the presence of aortic dissection can cause fatal progression of the aortic dissection.
* Therefore, it is important to consider the possibility of aortic dissection in patients with chest pain and to confirm the diagnosis before initiating thrombolytic therapy.
47
Q23: What imaging finding is commonly seen on a chest x-ray in cases of aortic dissection?
A23: A **widened mediastinum** is a common imaging finding on a chest x-ray in cases of aortic dissection.
48
Q24: Which imaging modality is often the initial investigation to confirm the diagnosis of aortic dissection?
.
A24: CT angiogram is the gold standerd
49
Q25: What is the significance of a radio-radial delay but no radio-femoral delay?
A25: A radio-radial delay without a radio-femoral delay is suggestive of aortic dissection, specifically **Type A aortic dissection.**
50
Q26: What is the immediate management approach for aortic dissection?
A26: Aortic dissection is a surgical emergency and requires immediate involvement of experienced seniors, .
Analgesia, such as morphine, is required to manage the pain.
Blood pressure and heart rate need to be well controlled to reduce stress on the aortic walls, typically achieved through the use of beta-blockers, such as IV labetalol.
Surgical intervention from the vascular team will depend on the type of aortic dissection.
51
Q27: How is Type A aortic dissection typically managed?
A27: Type A aortic dissection is managed as an emergency with **open heart surgery,** specifically midline sternotomy.
The section of the aorta with the defect in the wall is removed, and it is replaced with a**synthetic graft.**
The aortic valve may also need to be replaced during the procedure.
52
Q28: How is Type B aortic dissection managed beyond the left subclavian artery (involving the descending aorta)?
A28: Type B aortic dissection beyond the left subclavian artery, involving the descending aorta, is normally managed conservatively with blood pressure control.
If there is evidence of end organ damage, it may be treated with **thoracic endovascular aortic repair (TEVAR).**
This involves inserting a catheter via the femoral artery and placing a stent graft into the affected section of the descending aorta. Complicated cases may require open surgery.
53
what are the two stypes of hypertenison therapy for patients with aortic dissection before rupture ? and why step1 must done before step2
Step1; use beta blockers such as Esmolol and Labetalol
Step2 ; Vasodilatior -> sodium nitroprusside which could causes refelex tachycardia thus B blockers are used first to prevent this reflex
54
Q2: What is dyslipidemia?
A2: Dyslipidemia refers to the abnormal concentration of specific types of cholesterol or lipoprotein molecules, characterized by an increase in LDL (low-density lipoprotein) and a decrease in HDL (high-density lipoprotein).
55
Q3: How is dyslipidemia generally described in terms of cholesterol?
A3: described as an increase in LDL, which is often referred to as the "bad" cholesterol responsible for atherosclerosis,
and a decrease in HDL, which is considered the "good" cholesterol that helps remove cholesterol plaques from vessel walls.
56
Q4: What is hyperlipidemia?
A4: is characterized by an overall increase in the concentration of lipids in the bloodstream, including an increase in LDL and triglycerides.
57
Q5: What is hypercholesterolemia?
A5:
* is a condition where there is an increased total concentration of cholesterol molecules in the blood, usually defined as total cholesterol levels exceeding 200mg/dL.
* It is characterized by an increase in LDL and VLDL (very low-density lipoprotein) and a decrease in HDL.
58
Q6: What is hypertriglyceridemia?
A6: Hypertriglyceridemia refers to an increase in the total concentration of triglycerides in the blood, typically defined as levels exceeding 150mg/dL.
59
Q1: How do fatty substances, including cholesterol and fats, get absorbed into the bloodstream from the gastrointestinal (GI) tract?
A1: Fatty substances are absorbed across the GI tract and eventually into the bloodstream through the following process:
1. The gallbladder produces bile, which contains bile acids.
2. Bile acids bind to free fatty acids and cholesterol, forming micelles.
3. Micelles are absorbed across the GI tract and enter the lymphatic circulation, where they are packed into chylomicrons.
4. Chylomicrons, which are lipoproteins carrying triglycerides and a small amount of cholesterol, make their way into the bloodstream via the thoracic ducts.
5. Lipoprotein lipase, an enzyme in the bloodstream, breaks down triglycerides in chylomicrons into free fatty acids, which are taken up by adipose tissue and muscle tissue.
6. Chylomicrons become chylomicron remnants and are taken up by the liver.
7. The liver uses the cholesterol from chylomicron remnants to produce very low-density lipoproteins (VLDL).
8. VLDL, similar to chylomicrons, carry triglycerides and some cholesterol. They move through the bloodstream, and lipoprotein lipase breaks down triglycerides, releasing free fatty acids to be taken up by muscle and adipose tissues.
9. Some cholesterol from VLDL is taken back up by the liver, while the remaining cholesterol and fewer triglycerides form low-density lipoprotein (LDL).
10. LDL deposits cholesterol into various tissues, including blood vessels, which can lead to atherosclerotic cardiovascular disease (ASCVD).
11. LDL can also return cholesterol to the liver by binding to LDL receptors (LDL-R).
12. High-density lipoprotein (HDL), produced by the liver, removes cholesterol from plaques in the blood vessels and transports it back to the liver. HDL is considered a "good" lipoprotein.
60
Q2: What is the role of lipoprotein lipase in the process of lipid absorption?
A2:
* Lipoprotein lipase is an enzyme present in the bloodstream that plays a crucial role in the breakdown of triglycerides.
* It acts on chylomicrons and very low-density lipoproteins (VLDL), breaking down triglycerides into free fatty acids.
* These free fatty acids are then taken up by adipose tissue and muscle tissue for storage or energy utilization.
61
Q3: How does HDL differ from LDL in terms of their functions?
A3:
* HDL (high-density lipoprotein) and LDL (low-density lipoprotein) have different functions and compositions:
* HDL is considered the "good" cholesterol because it removes cholesterol from plaques in the blood vessels and transports it back to the liver for processing and excretion.
* HDL does not contain much fat but primarily consists of proteins.
* LDL, on the other hand, is often referred to as the "bad" cholesterol as it deposits cholesterol into various tissues, including the blood vessels.
* This can lead to the formation of fatty plaques and contribute to atherosclerotic cardiovascular disease (ASCVD).
* LDL contains higher amounts of cholesterol and relatively fewer triglycerides compared to HDL.
62
Q4: What is the role of the liver in lipid metabolism?
A4:
* The liver plays a significant role in lipid metabolism.
* It produces bile, which contains bile acids that aid in the digestion and absorption of dietary fats.
* The liver also synthesizes lipoproteins such as very low-density lipoproteins (VLDL) and high-density lipoproteins (HDL).
* It takes up chylomicron remnants and uses the cholesterol from them to produce VLDL.
* Additionally, the liver regulates the uptake of LDL through LDL receptors (LDL-R) and participates in the removal and processing of cholesterol from the bloodstream.
63
Q1: What are the familial causes of lipid disorders according to the Fredrickson classification?
A1: The familial causes of lipid disorders according to the Fredrickson classification are as follows:
Type I: This condition is characterized by an increase in chylomicrons due to a **defect in lipoprotein lipase** **or chylomicron receptors,** leading to high levels of triglycerides in the blood.
Type IIa: Individuals with this condition have elevated levels of LDL due to a **defective LDL receptor**, which impairs the uptake of LDL molecules by liver cells, resulting in increased LDL in the bloodstream.
Type IIb: Similar to Type IIa, this condition involves increased levels of LDL and VLDL. **The LDL receptor is either downregulated or less present, causing reduced LDL uptake by the liver**. **As a compensatory response, the liver increases the production of VLDL.**
Type III: This condition is characterized by increased levels of both chylomicrons and VLDL. **The defect lies in a specific protein called ApoE**, which prevents the uptake of chylomicrons and VLDL by the liver. The accumulation of chylomicrons and VLDL leads to elevated triglyceride levels.
Type IV: Individuals with Type IV lipid disorder have increased levels of VLDL primarily because **the liver overproduces VLDL**. The excess VLDL results in high levels of triglycerides in the blood.
64
Q2: What are the primary lipid components carried by chylomicrons and VLDL?
A2: Chylomicrons primarily carry triglycerides, while VLDL also contains a significant amount of triglycerides.
65
Q1: How does diabetes contribute to the development of lipid disorders?
A1:
* In diabetes, there is decreased activity of lipoprotein lipase (LPL) due to insulin resistance.
* Insulin normally stimulates LPL to convert triglycerides from VLDLs into free fatty acids, which can be utilized by muscles for energy or stored in adipose tissue as fat.
* However, in diabetes, LPL is not as responsive to insulin, resulting in reduced conversion of triglycerides.
* As a result, VLDL retains more triglycerides, leading to increased triglyceride levels in the blood.
* VLDL can then be converted into LDL, further contributing to dyslipidemia.
66
Q2: How does hypothyroidism contribute to the development of lipid disorders?
A2:
* Thyroid hormone normally upregulates LDL receptors in the liver, which facilitates the uptake of LDL from the bloodstream.
* However, in hypothyroidism, where levels of T3 and T4 are low, there is downregulation of LDL receptors.
* This leads to impaired clearance of LDL from the blood, causing increased levels of LDL and contributing to the development of lipid disorders.
67
Question 1: How does diabetes contribute to dyslipidemia?
Answer:
* In diabetes, there is insulin resistance and decreased activity of lipoprotein lipase (LPL).
* As a result, there is a decrease in the conversion of triglycerides from VLDL into free fatty acids.
* This leads to increased levels of VLDL and LDL in the blood, contributing to dyslipidemia.
68
Question 2: What is the effect of hypothyroidism on LDL levels?
Answer:
* In hypothyroidism, there is a downregulation of LDL receptors due to low levels of thyroid hormone (T3 and T4).
* This results in reduced uptake of LDL by the liver, leading to increased levels of LDL in the bloodstream.
69
Question 3: How does nephrotic syndrome affect lipid levels?
Answer:
* In nephrotic syndrome, there is excessive loss of albumin in the urine.
* This leads to decreased albumin levels in the blood, which triggers the liver to produce more proteins, including VLDL.
* Consequently, there is an increase in VLDL concentration and triglycerides in the blood.
70
Question 4: Which medications have been associated with alterations in lipid profiles?
Answer:
Beta-blockers,
estrogen, and
thiazides
* are medications that have been shown to potentially increase LDL and VLDL levels and decrease HDL levels, thereby affecting lipid profiles.
71
Question 5: How does an increase in weight and a high-fat diet contribute to lipid disorders?
Answer:
* An increase in weight and a diet high in cholesterol and triglycerides can lead to increased absorption of fats into the bloodstream via chylomicrons.
* This increases the production of VLDL and LDL by the liver, resulting in elevated levels of these lipoproteins.
* Additionally, excess weight and a sedentary lifestyle can decrease the production of HDL, which impairs the removal of cholesterol from plaque in the vessel walls, increasing the risk of atherosclerosis and lipid disorders.
72
What are the skin manifestations associated with lipid disorders?
Answer: **Xanthomas**, which are characterized by cholesterol and triglyceride deposition in the skin tissue.
73
Name the three types of xanthomas.
Answer:
* Eruptive xanthomas: Yellowish papules with an erythematous border seen on the buttocks, back, and extensor surfaces.
* Tendinous xanthomas: Firm, nodular appearance on tendons, commonly found on the extensor tendons of the hand and the Achilles tendon.
* Tuberous xanthomas: Yellowish nodules with an erythematous border that usually appear across joints, especially in the elbow and knees.
74
What is the skin manifestation called when there is fatty plaque development around the nasal portion of the eye?
Answer: Xanthelasma.
75
What is the term for the brown fatty deposition around the edge of the iris?
Answer: Corneal arcus.
76
What is the liver condition associated with lipid disorders?
Answer: Hepatic steatosis or non-alcoholic fatty liver disease (NAFLD), characterized by the deposition of triglycerides and cholesterol in the liver, leading to its fatty appearance.
77
What can hepatic steatosis progress to?
Answer: Cirrhosis of the liver.
78
What is the risk associated with super high triglyceride levels (> 1000 mg/dL) in lipid disorders?
Answer: Pancreatitis, which is the acute inflammation of the pancreas.
79
How does high LDL, triglycerides, and decreased HDL contribute to ASCVD?
Answer: They increase the deposition of cholesterol and fat in the vessel walls, leading to atherosclerosis.
80
What can happen when atherosclerosis affects the vessels supplying different organs?
Answer: Organ dysfunction can occur due to reduced oxygen and nutrient delivery.
81
Which organ is commonly affected by carotid artery stenosis?
Answer: The brain, as the internal carotid artery supplies it.
82
What condition can occur when there is significant carotid artery stenosis (> 70%)?
Answer: Carotid artery stenosis can lead to transient ischemic attack (TIA).
83
What is the term for an infarct in the brain due to insufficient oxygen supply?
Answer: Cerebrovascular accident (CVA), commonly known as a stroke.
84
What can develop in the heart when plaque forms in the coronary vessels?
Answer:
Myocardial infarction:
* Insufficient oxygen supply to the myocardial tissue, resulting in tissue death.
* Coronary artery disease: Reduced oxygen supply to the heart tissue without tissue death, often causing anginal chest pain.
85
Which region of the body is commonly affected by peripheral artery disease?
Answer: The lower extremities, including the arteries from the aorta to the tibial arteries.
86
What is claudication, and what causes it in peripheral artery disease?
Answer: Claudication is pain in the muscles of the lower extremities that occurs during exertion due to inadequate oxygen and nutrient supply caused by plaques in the arteries.
87
What can happen if a severe plaque rupture occurs in peripheral artery disease?
Answer: Acute limb ischemia can occur, resulting in the complete loss of blood flow to the limb and potential limb death.
88
What is the purpose of a lipid panel in the diagnosis of lipid disorders?
Answer: A lipid panel helps determine the risk for complications such as atherosclerotic diseases and the need for treatment.
89
What is considered a high total cholesterol level?
Answer:
200 mg/dL: High
240 mg/dL: Very high and concerning
90
What are the threshold values for LDL levels indicating borderline high, high, and very high levels?
Answer:
130 mg/dL: Borderline high
160 mg/dL: High
190 mg/dL: Very high and concerning
91
Why is a higher level of HDL (High-Density Lipoprotein) desirable?
Answer: HDL helps remove cholesterol from the vessels, reducing the risk of plaque formation. A low HDL level (<60 mg/dL) can increase the risk of plaques.
92
What are the threshold values for triglyceride levels indicating high, very high, and at-risk levels?
Answer:
140 mg/dL: High
200 mg/dL: Very high
500 mg/dL: At risk of numerous problems
93
What is the primary target of statins in the body?
Answer: Statins primarily inhibit the enzyme HMG-CoA reductase, which is involved in the synthesis of cholesterol in the liver.
94
How do statins lower cholesterol levels in the body?
Answer: By inhibiting HMG-CoA reductase, statins reduce the production of cholesterol, resulting in decreased levels of VLDL (very-low-density lipoprotein) and LDL (low-density lipoprotein) cholesterol.
95
Name the statin drugs using the mnemonic "Real American Still Loves Playing Football."
Answer: The statin drugs are:
Rosuvastatin
Atorvastatin
Simvastatin
Lovastatin
Pravastatin
Fluvastatin
96
Which lipid-lowering agents are effective for patients with high triglycerides?
Answer:
Fibrates, such as fenofibrate and gemfibrozil, are effective for patients with high triglycerides as they increase lipoprotein lipase activity and promote the breakdown of VLDL and chylomicrons, leading to decreased serum triglyceride levels.
97
How do PCSK9 inhibitors work to lower LDL cholesterol levels?
Answer:
* PCSK9 inhibitors (PCSK9-I) inhibit the degradation of LDL receptors or increase LDL receptors on the liver, resulting in increased uptake of LDL by the liver and decreased serum LDL levels.
* Evolocumab is an example of a PCSK9 inhibitor.
98
What is the mechanism of action of niacin (Vitamin B3) in lowering lipid levels?
Answer:
* Niacin inhibits the synthesis of VLDLs and lipolysis from fat tissue.
* It decreases the incorporation of triglycerides, cholesterol, and protein into VLDL and reduces lipolysis, leading to decreased VLDL synthesis and lower free fatty acid levels in the bloodstream.
99
How do bile acid sequestrants lower LDL cholesterol levels?
Answer:
* Bile acid sequestrants, such as cholestyramine and colestipol, inhibit the incorporation of bile acids with fatty acids and cholesterol.
* This reduces the formation of micelles and decreases the absorption of cholesterol, leading to decreased VLDL formation in the liver and lower LDL levels.
100
What is the role of ezetimibe in lowering LDL cholesterol levels?
Answer:
Ezetimibe inhibits the incorporation of cholesterol with fatty acids and bile acids, resulting in decreased micelle formation, reduced chylomicron production, and decreased LDL levels.
101
How does fish oil (Omega-3 fatty acids) supplementation impact lipid levels?
Answer: Fish oil supplementation, containing Omega-3 fatty acids, helps lower triglyceride levels.
102
What are the indications for high-intensity statin therapy?
Answer: High-intensity statin therapy is indicated for patients with clinical atherosclerotic cardiovascular disease (ASCVD) such as TIA, CVA, CAD, MI, and PAD.
103
Which patients should receive moderate-intensity statin therapy?
Answer: Patients aged 40-75 years with ASCVD greater than 75% or those aged 40-75 years with diabetes (DM) and ASCVD less than 75% should receive moderate-intensity statin therapy.
104
What is the recommended statin therapy for patients with LDL cholesterol levels above 190 mg/dL?
Answer: Patients with LDL cholesterol levels above 190 mg/dL should be treated with high-intensity statin therapy.
105
Name two high-intensity statins.
Answer:
Rosuvastatin (at a dose of 20-40 mg QD) and
Atorvastatin (at a dose of 40-80 mg QD) are high-intensity statins.
106
Name three moderate-intensity statins.
Answer:
Rosuvastatin (at a dose of 5-10 mg QD),
Atorvastatin (at a dose of 10-20 mg QD), and
Simvastatin (at a dose of 20-40 mg QD) are moderate-intensity statins.
107
What are the common side effects of lipid-lowering agents?
Answer:
Common side effects of lipid-lowering agents include CYP450 interactions, hepatotoxicity (seen with statins and fibrates), myopathy (myalgia and rhabdomyolysis, associated with statins and fibrates), diarrhea (seen with cholesterol inhibitors like ezetimibe and bile acid sequestrants), and niacin side effects such as increased blood glucose, increased uric acid, and skin manifestations like redness and itchiness due to increased prostaglandins.
108
What is the treatment of choice for resistant lipid disorders?
Answer: For resistant lipid disorders, particularly hypertriglyceridemia (TG > 1000 resistant to medications) or familial hypercholesterolemia, treatment options include LDL apheresis, where LDL is filtered through a column, and liver transplant for patients with liver dysfunction who lack healthy LDL receptors.
