Atherosclerotic Vascular Disease

Question 1

Q1: What is the definition of aneurysms?

Answer 1

A1: Aneurysms are defined as a permanent dilation of the artery to twice the normal diameter.

Question 2

Q2: What is the threshold diameter for an abdominal aortic aneurysm (AAA)?

Answer 2

A2: The threshold diameter for an AAA is greater than 3cm for the abdominal aorta.

Question 3

Q3: What is the incidence of AAAs in the population over 60 years of age?

Answer 3

A3:
AAAs are present in 5% of the population over 60 years of age.

Question 4

Q4: Do AAAs occur more frequently in men or women?

Answer 4

A4: AAAs occur five times more frequently in men.

Question 5

Q5: What are some risk factors for developing an AAA?

Answer 5

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.

Question 6

Q6: What is the most common cause of AAA formation?

Answer 6

A6: The most common cause of AAA formation is atherosclerosis.

Question 7

Q7: What happens to the arterial wall in the formation of AAAs?

Answer 7

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.

Question 8

Q8: Where do AAAs most commonly occur?

Answer 8

A8: AAAs most commonly occur below the renal arteries (infrarenal) - approximately 80% of cases.

Question 9

Q9: What are the consequences of a ruptured AAA?

Answer 9

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.

Question 10

Q10: What are the clinical presentations of AAA?

Answer 10

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.

Question 11

Q11: What are some other signs that may be observed in patients with AAA?

Answer 11

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.

Question 12

Q12: What imaging modality is used for monitoring AAA?

Answer 12

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.

Question 13

Q13: What is the recommended diameter threshold for elective surgery in asymptomatic AAAs?

Answer 13

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.

Question 14

Q14: How is a ruptured AAA diagnosed?

Answer 14

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.

Question 15

Q15: What are the medical management strategies for AAA?

Answer 15

A15:
involves controlling risk factors.
* This includes prescribing antihypertensive medications,
* promoting smoking cessation, and
* prescribing lipid-lowering medication.

Question 16

Q16: What are the surgical options for AAA management?

Answer 16

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.

Question 17

Q23: At what aortic diameter are patients referred to a vascular team?

Answer 17

A23: Patients with an aortic diameter above 3cm are referred to a vascular team, urgently if the diameter is more than 5.5cm.

Question 18

Q26: What imaging modality provides a more detailed picture of the aneurysm and helps guide elective surgery for AAA?

Answer 18

A26: CT angiogram provides a more detailed picture of the aneurysm and helps guide elective surgery for AAA.

Question 19

Q29: What are the recommendations for follow-up scans in patients with AAA?

Answer 19

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.

Question 20

Q30: What are the criteria for elective repair of AAA according to NICE guidelines?

Answer 20

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

Question 21

What are the two methods for inserting a graft during elective surgical repair of AAA?

Answer 21

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.

Question 22

Q33: What is the risk of rupture for an AAA based on its diameter?

Answer 22

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.

Question 23

Q36: What is the recommended management approach for a ruptured AAA?

Answer 23

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.

Question 24

Q37: What is permissive hypotension?

Answer 24

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.

Question 25

Q38: What should be considered in patients with co-morbidities that make the prognosis with surgery very poor?

Answer 25

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.

Question 26

Q1: What is aortic dissection?

Answer 26

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.

Question 27

Q2: What are the three layers of the aorta?

Answer 27

A2: The three layers of the aorta are the intima, media, and adventitia.

Question 28

Q3: Where does blood enter in aortic dissection?

Answer 28

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.

Question 29

Q4: What does “intramural” mean in the context of aortic dissection?

Answer 29

A4: “Intramural” refers to within the walls of the blood vessel, indicating the location of the dissection.

Question 30

Q5: What is the most common site of a tear in the ascending aorta?

Answer 30

A5: The right lateral area of the ascending aorta

Question 31

Q6: What are the two classification systems for aortic dissection?

Answer 31

A6:
Stanford system and
the DeBakey system.

Question 32

Q7: What is Type A aortic dissection?

Answer 32

A7: Type A aortic dissection affects theascending aorta, before the brachiocephalic artery.

Question 33

Q8: What is Type B aortic dissection?

Answer 33

A8: Type B aortic dissection affects the descending aorta, after the left subclavian artery.

Question 34

Q9: What is Type I aortic dissection according to the DeBakey system?

Answer 34

A9: Type I aortic dissection begins in the ascending aorta and involves at least the aortic arch, if not the whole aorta.

Question 35

Q10: What is Type IIIa aortic dissection according to the DeBakey system?

Answer 35

A10: Type IIIa aortic dissection begins in the descending aorta and involves only the section above the diaphragm.

Question 36

Q11: What is Type IIIb aortic dissection according to the DeBakey system?

Answer 36

A11: Type IIIb aortic dissection begins in the descending aorta and involves the aorta below the diaphragm.

Question 37

Q12: What are some risk factors for aortic dissection?

Answer 37

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).

Question 38

Q13: What are the triggers that can temporarily cause a dramatic increase in blood pressure and potentially trigger aortic dissection?

Answer 38

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

Question 39

Q14: Which condition is characterized by inflammatory granulomas depositing in the vessel walls and increases the risk of aortic dissection?

Answer 39

A14: Takayasu arthritis

is the condition characterized by inflammatory granulomas depositing in the vessel walls and increases the risk of aortic dissection.

Question 40

Q16: What are the conditions or procedures that can increase the risk of aortic dissection?

Answer 40

A16:
* bicuspid aortic valve,
* coarctation of the aorta,
* aortic valve replacement, and
* coronary artery bypass graft (CABG).

Question 41

Q17: What conditions are commonly associated with patients who have coarctation of the aorta? 2

Answer 41

A17: commonly have a history of Turner Syndrome and an associated bicuspid aortic valve.

Question 42

Q18: What are the four possible scenarios that can occur after a tear in the aortic intima?

Answer 42

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.

Question 43

Q19: What is the typical presentation of aortic dissection?

Answer 43

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.

Question 44

Q20: What are some features that may suggest aortic dissection?

Answer 44

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 ).

Question 45

Q21: What diagnostic tests are commonly used for the diagnosis of aortic dissection?

Answer 45

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.

Question 46

Q22: What is the potential risk of treating myocardial infarction (MI) with thrombolysis in the presence of aortic dissection?

Answer 46

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.

Question 47

Q23: What imaging finding is commonly seen on a chest x-ray in cases of aortic dissection?

Answer 47

A23: A widened mediastinum is a common imaging finding on a chest x-ray in cases of aortic dissection.

Question 48

Q24: Which imaging modality is often the initial investigation to confirm the diagnosis of aortic dissection?
.

Answer 48

A24: CT angiogram is the gold standerd

Question 49

Q25: What is the significance of a radio-radial delay but no radio-femoral delay?

Answer 49

A25: A radio-radial delay without a radio-femoral delay is suggestive of aortic dissection, specifically Type A aortic dissection.

Question 50

Q26: What is the immediate management approach for aortic dissection?

Answer 50

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.

Question 51

Q27: How is Type A aortic dissection typically managed?

Answer 51

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 asynthetic graft.
The aortic valve may also need to be replaced during the procedure.

Question 52

Q28: How is Type B aortic dissection managed beyond the left subclavian artery (involving the descending aorta)?

Answer 52

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.

Question 53

what are the two stypes of hypertenison therapy for patients with aortic dissection before rupture ? and why step1 must done before step2

Answer 53

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

Question 54

Q2: What is dyslipidemia?

Answer 54

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).

Question 55

Q3: How is dyslipidemia generally described in terms of cholesterol?

Answer 55

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.

Question 56

Q4: What is hyperlipidemia?

Answer 56

A4: is characterized by an overall increase in the concentration of lipids in the bloodstream, including an increase in LDL and triglycerides.

Question 57

Q5: What is hypercholesterolemia?

Answer 57

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.

Question 58

Q6: What is hypertriglyceridemia?

Answer 58

A6: Hypertriglyceridemia refers to an increase in the total concentration of triglycerides in the blood, typically defined as levels exceeding 150mg/dL.

Question 59

Q1: How do fatty substances, including cholesterol and fats, get absorbed into the bloodstream from the gastrointestinal (GI) tract?

Answer 59

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.

Question 60

Q2: What is the role of lipoprotein lipase in the process of lipid absorption?

Answer 60

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.

Question 61

Q3: How does HDL differ from LDL in terms of their functions?

Answer 61

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.

Question 62

Q4: What is the role of the liver in lipid metabolism?

Answer 62

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.

Question 63

Q1: What are the familial causes of lipid disorders according to the Fredrickson classification?

Answer 63

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.

Question 64

Q2: What are the primary lipid components carried by chylomicrons and VLDL?

Answer 64

A2: Chylomicrons primarily carry triglycerides, while VLDL also contains a significant amount of triglycerides.

Question 65

Q1: How does diabetes contribute to the development of lipid disorders?

Answer 65

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.

Question 66

Q2: How does hypothyroidism contribute to the development of lipid disorders?

Answer 66

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.

Question 67

Question 1: How does diabetes contribute to dyslipidemia?

Answer 67

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.

Question 68

Question 2: What is the effect of hypothyroidism on LDL levels?

Answer 68

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.

Question 69

Question 3: How does nephrotic syndrome affect lipid levels?

Answer 69

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.

Question 70

Question 4: Which medications have been associated with alterations in lipid profiles?

Answer 70

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.

Question 71

Question 5: How does an increase in weight and a high-fat diet contribute to lipid disorders?

Answer 71

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.

Question 72

What are the skin manifestations associated with lipid disorders?

Answer 72

Answer: Xanthomas, which are characterized by cholesterol and triglyceride deposition in the skin tissue.

Question 73

Name the three types of xanthomas.
Answer:

Answer 73

• 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.

Question 74

What is the skin manifestation called when there is fatty plaque development around the nasal portion of the eye?

Answer 74

Answer: Xanthelasma.

Question 75

What is the term for the brown fatty deposition around the edge of the iris?

Answer 75

Answer: Corneal arcus.

Question 76

What is the liver condition associated with lipid disorders?

Answer 76

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.

Question 77

What can hepatic steatosis progress to?

Answer 77

Answer: Cirrhosis of the liver.

Question 78

What is the risk associated with super high triglyceride levels (> 1000 mg/dL) in lipid disorders?

Answer 78

Answer: Pancreatitis, which is the acute inflammation of the pancreas.

Question 79

How does high LDL, triglycerides, and decreased HDL contribute to ASCVD?

Answer 79

Answer: They increase the deposition of cholesterol and fat in the vessel walls, leading to atherosclerosis.

Question 80

What can happen when atherosclerosis affects the vessels supplying different organs?

Answer 80

Answer: Organ dysfunction can occur due to reduced oxygen and nutrient delivery.

Question 81

Which organ is commonly affected by carotid artery stenosis?

Answer 81

Answer: The brain, as the internal carotid artery supplies it.

Question 82

What condition can occur when there is significant carotid artery stenosis (> 70%)?

Answer 82

Answer: Carotid artery stenosis can lead to transient ischemic attack (TIA).

Question 83

What is the term for an infarct in the brain due to insufficient oxygen supply?

Answer 83

Answer: Cerebrovascular accident (CVA), commonly known as a stroke.

Question 84

What can develop in the heart when plaque forms in the coronary vessels?
Answer:

Answer 84

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.

Question 85

Which region of the body is commonly affected by peripheral artery disease?

Answer 85

Answer: The lower extremities, including the arteries from the aorta to the tibial arteries.

Question 86

What is claudication, and what causes it in peripheral artery disease?

Answer 86

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.

Question 87

What can happen if a severe plaque rupture occurs in peripheral artery disease?

Answer 87

Answer: Acute limb ischemia can occur, resulting in the complete loss of blood flow to the limb and potential limb death.

Question 88

What is the purpose of a lipid panel in the diagnosis of lipid disorders?

Answer 88

Answer: A lipid panel helps determine the risk for complications such as atherosclerotic diseases and the need for treatment.

Question 89

What is considered a high total cholesterol level?

Answer 89

Answer:

200 mg/dL: High

240 mg/dL: Very high and concerning

Question 90

What are the threshold values for LDL levels indicating borderline high, high, and very high levels?

Answer 90

Answer:

130 mg/dL: Borderline high

160 mg/dL: High

190 mg/dL: Very high and concerning

Question 91

Why is a higher level of HDL (High-Density Lipoprotein) desirable?

Answer 91

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.

Question 92

What are the threshold values for triglyceride levels indicating high, very high, and at-risk levels?

Answer 92

Answer:

140 mg/dL: High

200 mg/dL: Very high

500 mg/dL: At risk of numerous problems

Question 93

What is the primary target of statins in the body?

Answer 93

Answer: Statins primarily inhibit the enzyme HMG-CoA reductase, which is involved in the synthesis of cholesterol in the liver.

Question 94

How do statins lower cholesterol levels in the body?

Answer 94

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.

Question 95

Name the statin drugs using the mnemonic “Real American Still Loves Playing Football.”

Answer 95

Answer: The statin drugs are:

Rosuvastatin
Atorvastatin
Simvastatin
Lovastatin
Pravastatin
Fluvastatin

Question 96

Which lipid-lowering agents are effective for patients with high triglycerides?

Answer 96

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.

Question 97

How do PCSK9 inhibitors work to lower LDL cholesterol levels?

Answer 97

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.

Question 98

What is the mechanism of action of niacin (Vitamin B3) in lowering lipid levels?

Answer 98

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.

Question 99

How do bile acid sequestrants lower LDL cholesterol levels?

Answer 99

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.

Question 100

What is the role of ezetimibe in lowering LDL cholesterol levels?

Answer 100

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.

Question 101

How does fish oil (Omega-3 fatty acids) supplementation impact lipid levels?

Answer 101

Answer: Fish oil supplementation, containing Omega-3 fatty acids, helps lower triglyceride levels.

Question 102

What are the indications for high-intensity statin therapy?

Answer 102

Answer: High-intensity statin therapy is indicated for patients with clinical atherosclerotic cardiovascular disease (ASCVD) such as TIA, CVA, CAD, MI, and PAD.

Question 103

Which patients should receive moderate-intensity statin therapy?

Answer 103

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.

Question 104

What is the recommended statin therapy for patients with LDL cholesterol levels above 190 mg/dL?

Answer 104

Answer: Patients with LDL cholesterol levels above 190 mg/dL should be treated with high-intensity statin therapy.

Question 105

Name two high-intensity statins.

Answer 105

Answer:

Rosuvastatin (at a dose of 20-40 mg QD) and

Atorvastatin (at a dose of 40-80 mg QD) are high-intensity statins.

Question 106

Name three moderate-intensity statins.

Answer 106

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.

Question 107

What are the common side effects of lipid-lowering agents?

Answer 107

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.

Question 108

What is the treatment of choice for resistant lipid disorders?

Answer 108

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.