MBBS4 😎

Answer the Questions Below

What is atherosclerosis?

What is the primary cause (aetiology) of atherosclerosis?

What are the non-coronary causes of ischemic heart disease (IHD)?

What inflammatory mediators are involved in the formation of unstable plaques?

Which marker is most sensitive for detecting atherosclerosis?

What is the first step in the pathogenesis of atherosclerosis?

Describe the gross and microscopic morphology of hypertension (HTN).

What is the pathophysiology of hypertension on kidney appearance?

What type of hypertension causes this kidney appearance?

What is the colloquial term for a kidney affected by hypertension?

What are the features of each grade of hypertensive retinopathy?

Which of the following is a non-modifiable risk factor for atherosclerosis?

Smoking Diabetes Family History Hypertension High Cholesterol

What is the main complication of chronic ischemic heart disease (IHD)?

Hypertension (HTN) Heart failure (HF) Myocardial infarction (MI) Arrhythmias

At what percentage of blockage in coronary atherosclerosis do symptoms typically appear, and what factors contribute to the symptoms?

50% blockage, due to high blood pressure and blood clotting 60% blockage, due to increased cholesterol levels 70% blockage, due to lactic acid and bradykinin 80% blockage, due to inflammation and oxidative stress

Atherosclerosis is classified as which type of arteriosclerosis?

Microangiopathy Macroangiopathy

Which vessels are most commonly affected by atherosclerosis?

Pulmonary veins Coronary arteries Hepatic veins Lymphatic vessels

Which of the following is a coronary cause of ischemic heart disease (IHD) that accounts for 90% of cases?

Severe anemia Tachycardia Atherosclerosis Aortic stenosis (AS)

Which statement about a stable plaque is true?

Lipid core is larger than the fibrous cap Prone to rupture and cause embolism Fibrous cap is larger than the lipid core No calcification

What is the first macroscopic feature of atherosclerosis?

Central necrotic core Intimal ulceration Fatty streaks Foam cell necrosis

Given a blood pressure of 155/99, what type of hypertension does the patient have?

Normal Grade 1 (mild) Grade 2 (moderate) Grade 3 (severe) Isolated systolic hypertension

What are the causes of right-sided/pulmonary hypertension and their associated complications?

Right-sided hypertrophy (RVH) in chronic lung disorders Chronic: Cor-Pulmonale in chronic lung disorders, Acute: Pulmonary Embolism Acute: Cor-Pulmonale, Chronic: Pulmonary Embolism Right-sided hypertrophy (RVH) due to congestive heart failure

What are the types of arteriolosclerosis and their associated features?

Hyaline Arteriolosclerosis - Protein deposition (typical of DM) Hyaline Arteriolosclerosis - Protein deposition (typical of DM), Hyperplastic Arteriolosclerosis - Smooth muscle hyperplasia & fibrosis (typical of HTN) Hyperplastic Arteriolosclerosis - Protein deposition (typical of DM) Hyaline Arteriolosclerosis - Smooth muscle hyperplasia & fibrosis (typical of HTN)

What is the relationship between STEMI and NSTEMI in terms of infarct location?

STEMI - Subendocardial infarction, NSTEMI - Transmural infarction STEMI - Transmural infarction, NSTEMI - Subendocardial infarction STEMI - Subendocardial infarction, NSTEMI - Myocardial ischemia STEMI - Myocardial ischemia, NSTEMI - Transmural infarction

What are the physiological responses to high blood pressure that help decrease it?

ANP, BNP - diuresis Aldosterone - sodium retention Renin - vasoconstriction ADH - vasodilation

List the other causes of MI that are not atherosclerosis.

Time Period: < 4 hours

MI - GROSS:

Normal
normal w loss of glycogen
Yellow center, red border
Pale grey, thin red border

MI - MICROSCOPY:

loss of glycogen only, appears normal
Necrosis + Macrophages phagocytosing dead cells
Granulation tissue, macrophages, BV fibroblasts, collagen
Dense fibrosis (mature scar)

Time Period: 1-3 days

MI - GROSS:

Normal (loss of glycogen)
Recent dark red area
Yellow center, red border
Pale grey, thin red border

MI - MICROSCOPY:

Coagulative necrosis (normal shape but no nucleus), Hemorrhage, Neutrophils
Necrosis + Macrophages phagocytosing dead cells
Granulation tissue, macrophages, BV fibroblasts, collagen
Dense fibrosis (mature scar)

Time Period: < 2 weeks

MI - GROSS:

Normal (loss of glycogen)
Recent dark red area
Yellow center, red border
Pale grey, thin red border

MI - MICROSCOPY:

Time Period: < 8 weeks

MI - GROSS:

Normal (loss of glycogen)
Recent dark red area
Yellow center, red border
Pale grey, thin red border

MI - MICROSCOPY:

Time Period: > 8 weeks

MI - GROSS:

Normal (loss of glycogen)
Recent dark red area
Yellow center, red border
small white scar

MI - MICROSCOPY:

List 3 chronic complications of MI:

List 3 acute complications of MI:

List 3 causes of Mitral Regurgitation:

2. What is shown?

Unstable Plaque Stable Plaque Fibrous Plaque Calcified Plaque

3. What is shown?

Complex Plaque Atherosclerotic Plaque Stable Plaque Thrombotic Plaque

4. What is shown and what does it tell you about the disease time course?

MI <24 hours old. Red myocytes, pyknotic nucleus, inflammatory cells. Hemorrhage around BV. MI 48-72 hours old. Extensive fibrosis, minimal inflammation. Chronic MI. Dense collagen deposition and no inflammatory cells. Acute MI with coagulative necrosis, but no inflammatory cells or hemorrhage.

5. What is shown and what does it tell you about the disease time course?

Dense collagen bundles. Old MI >8 weeks Acute MI. Evidence of necrosis and hemorrhage. Subacute MI (2-4 weeks). Fibrosis with minimal inflammation. Chronic MI with extensive calcification and fibrosis.

6. What is shown here?

Fatty Streak Fibrous Plaque Stable Plaque Atherosclerotic Plaque with necrosis

7. What is shown here and what are 3 key features?

Stable Plaque. Thick fibrous cap, lipid core, inflammatory cells Unstable Plaque. Thin fibrous cap, lipid core, hemorrhage Complex Plaque. Heavy calcification, minimal inflammatory cells Atherosclerotic Plaque. Thin cap, no lipid core, no inflammatory cells

1. List three indications for Cardiac Rehabilitation:

2. List three absolute contraindications for Cardiac Rehabilitation:

3. List three benefits of Cardiac Rehabilitation:

4. List three components of Cardiac Rehabilitation:

What are the high-risk criteria in the QLD suspected ACS pathway?

Ongoing chest pain, runs of VT/VF, haemodynamically unstable (hypotensive) Previous MI, ATSI, another episode of pain UA with no troponin rise Normal results on ECG and troponin

What actions should be taken for high-risk criteria in the QLD suspected ACS pathway?

Reperfuse, continuous cardiac monitoring, admit to CCU/HDU, refer to interventional cardiology Discharge for GP follow-up, typically for EST Consider PCI, refer to inpatient exercise stress testing No actions necessary, monitor vitals regularly

What are the intermediate-risk criteria in the QLD suspected ACS pathway?

Ongoing chest pain, runs of VT/VF, hypotensive Previous MI, ATSI, another episode of pain UA with no troponin rise Normal results on ECG and troponin

What actions should be taken for intermediate-risk criteria in the QLD suspected ACS pathway?

Reperfuse, continuous cardiac monitoring, admit to CCU/HDU Consider PCI, refer to inpatient exercise stress testing Discharge for GP follow-up No actions necessary, monitor vitals regularly

What are the low-risk criteria in the QLD suspected ACS pathway?

Previous MI, ATSI, another episode of pain UA with no troponin rise Ongoing chest pain, runs of VT/VF, hypotensive Normal results on ECG and troponin

What actions should be taken for low-risk criteria in the QLD suspected ACS pathway?

Reperfuse, continuous cardiac monitoring, admit to CCU/HDU Discharge for GP follow-up → typically for EST with referral to cardiology outpatient for angiogram Consider PCI, refer to inpatient exercise stress testing No actions necessary, monitor vitals regularly

How soon must PCI (Percutaneous Coronary Intervention) be performed after diagnosis?

Within 30 minutes of diagnosis Within 60 minutes of diagnosis Within 90 minutes of diagnosis Within 120 minutes of diagnosis

What are 3 essential criteria for thrombolysis?

Chest pain > 15 minutes and < 24 hours, ST elevation or new LBBB, can be treated with pPCI Chest pain > 30 minutes and < 12 hours, ST depression, MI not likely from history Chest pain > 30 minutes and < 12 hours, ST elevation or new presumed LBBB, MI likely from history, Cannot be treated with pPCI within 90 minutes of first medical contact Chest pain > 10 minutes and < 6 hours, ST elevation, can be treated with pPCI within 90 minutes

What are 2 absolute contraindications to PCI?

Severe hypertension, renal failure High bleeding risk (thrombocytopenia, peptic ulcer, severe coagulopathy), multiple percutaneous coronary intervention restenosis Uncontrolled diabetes, advanced age Active myocardial infarction, severe hypotension

What is the primary difference between hypertensive urgency and hypertensive emergency?

Hypertensive urgency involves a blood pressure increase >180/110 without signs of organ damage, while hypertensive emergency involves a blood pressure increase >220/140 with signs of acute organ damage Hypertensive urgency requires immediate treatment to lower blood pressure, while hypertensive emergency does not require urgent intervention Hypertensive urgency occurs only in individuals over 65, while hypertensive emergency can affect individuals of all ages Hypertensive urgency involves no risk to organs, while hypertensive emergency leads to immediate organ failure if left untreated

Which of the following are first-line pharmacotherapies for hypertension?

ACE inhibitors (ACEI), Angiotensin II receptor blockers (ARB), Dihydropyridine calcium channel blockers (DHP CCB), Thiazide diuretics Beta-blockers, Alpha blockers, Potassium-sparing diuretics Direct vasodilators, Loop diuretics, Spironolactone ACE inhibitors (ACEI), Calcium channel blockers (non-DHP), Loop diuretics

What is the recommended follow-up schedule for individuals with cardiovascular risk?

Close monitoring and follow-up every 6–12 months Follow-up only every 2 years Monthly visits for intensive monitoring Follow-up every 5 years

Which of the following CVD risk factors is most important for monitoring in diabetic patients?

HbA1c and time since diagnosis of diabetes Age and sex Smoking status and family history Atrial fibrillation and BMI

What is the recommended management approach for individuals at high cardiovascular risk (greater than 10%)?

Intensive lifestyle interventions and pharmacological treatment (statins, antihypertensives, aspirin in some cases) Lifestyle changes alone, with no need for pharmacological treatment Close monitoring only every 2 years Immediate surgery for risk reduction

Which of the following is a key lifestyle factor for managing cardiovascular risk?

Physical activity Gender Age Family history of heart disease

Which of the following is a cardiovascular risk factor specifically relevant to people with diabetes?

Ratio of total cholesterol to HDL Chronic kidney disease Family history of CVD Smoking status

Which of the following is **not** an exclusion criterion for cardiovascular risk assessment?

Patients with established CVD (managed differently) Individuals with high cholesterol only Individuals with short life expectancy or severe comorbidities Young adults with no risk factors

Who should undergo cardiovascular risk assessment for individuals without known cardiovascular disease (CVD)?

All people aged 45–79 years, people with diabetes aged 35–79 years, and First Nations people aged 30–79 years People aged 18–45 years, with or without risk factors People aged 25–45 years with family history of CVD Individuals aged 30–50 years without any risk factors

Cholesterol has various roles in the body. Which of the following is a true statement about cholesterol?

Cholesterol is always harmful to the body. Cholesterol is only harmful in excess; HDL is good, while LDL is bad. HDL and LDL are both equally beneficial to health. Cholesterol is essential but doesn't have a role in disease processes.

1. What are cardiac causes of Acute Pulmonary Oedema (APO)?

Myocardial Infarction (MI), Left-Sided Heart Failure (LSHF), Hypertensive emergency Aortic Dissection, Pulmonary Embolism, Myocarditis Arrhythmia, Cardiomyopathy, Valvular heart disease Severe Anemia, Chronic Kidney Disease, Hypervolemia

2. What are respiratory causes of Acute Pulmonary Oedema (APO)?

Acute Respiratory Distress Syndrome (ARDS), Pneumonia Pulmonary Embolism, Chronic Bronchitis Asthma Exacerbation, Cystic Fibrosis Interstitial Lung Disease, Emphysema

3. What's the age of peak incidence for Acute Rheumatic Fever (ARF) in Indigenous Australians?

15-20 years 0-5 years 5-14 years 20-30 years

4. List 4 features that make someone at high risk of contracting Acute Rheumatic Fever (ARF).

5. Describe the pathogenesis of Acute Rheumatic Fever (ARF).

6. Describe the pathophysiology of ARF. Fill in the symptom associated with the condition.

pancarditis → murmur autoimmune-mediated basal ganglia damage → pro-inflammatory cytokines → myocardial ischemia → angina

7. What are 4 specific microscopic features of pericarditis?

Fibrinoid necrosis, Anitschkow/caterpillar cell, Aschoff body, Giant multinucleated cells Granulomas, Eosinophilic infiltration, Macrophage proliferation Fibrosis, Necrotizing vasculitis, Hemorrhagic effusion Fibroblastic growth, Collagen deposition, Hemorrhagic necrosis

8. What is an Aschoff body?

9. Describe the clinical features of Acute Rheumatic Fever (ARF).

10. Describe the diagnostic criteria of definite Rheumatic Fever (ARF).

2 major OR 1 major and 2 minor or 3 minor manifestations (if recurrent) with evidence of preceding GAS infection 3 major manifestations with no evidence of any GAS infection 1 major and 1 minor manifestation with evidence of any previous infection Only lab evidence of streptococcal infection

11. What are the minor manifestations of ARF for a high-risk group individual?

Temp >38.5C, Monoarthralgia, ESR or CRP >30, Prolonged PR interval Rash, Fever, Small joint pain, Tachycardia Joint swelling, Muscle weakness, Fatigue Hypertension, Cheyne-Stokes respiration

12. How do the minor manifestations of ARF compare to the low-risk group?

Must have polyarthralgia or aseptic monoarthritis, ESR >60 Must have polyarthralgia or aseptic monoarthritis, ESR >60 Must have fever with rash and fatigue Must have a history of rheumatic fever only

13. What is the test that can diagnose Rheumatic Heart Disease (RHD)?

14. What is the test that indicates GAS infection?

15. What does a mitral valve with Rheumatic Heart Disease (RHD) look like?

16. What are the 5 steps in management for Rheumatic Heart Disease (RHD)?

17. What are some considerations when planning valve interventions?

18. What are 3 complications of Rheumatic Heart Disease (RHD)?

19. What is primordial, primary, secondary, and tertiary prevention of ARF?

20. Describe the pathogenesis of heart failure.

mechanical dysfunction → systolic dysfunction (impaired ventricular contractility) → HFrEF mechanical dysfunction → systolic dysfunction (impaired ventricular contractility) → HFrEF; diastolic dysfunction (impaired ventricular relaxation) → HFpEF myocyte dysfunction → excess fluid accumulation → heart failure valve dysfunction leading to volume overload → heart failure

21. What are the compensatory mechanisms in heart failure?

22. What happens in decompensation?

SNS stimulation → adrenergic desensitization and ↑ O2 demand; RAAS activation → overwhelm Frank-Starling mechanism The body compensates effectively without any adverse effects Fluid overload leads to pulmonary congestion only No changes occur in decompensation

23. What is the change in the liver in congestive heart failure? Why does it appear this way?

Nutmeg liver due to congestion around central veins of liver lobules Nutmeg liver due to congestion around central veins of liver lobules Liver functions normally without any change Hepatomegaly due to increased fat deposition

24. What is level 2 vs level 3 on the NYHA level of clinical impairment scale?

Level 2: ordinary physical activity results in undue breathlessness; level 3: less than usual activity results in undue breathlessness Level 2: any physical activity results in severe breathlessness Level 3: breathing is normal without any exertion Level 2: no limitations at all in physical activity

25. What is the pharmacological long-term treatment guideline for heart failure?

26. What are 3 mechanisms by which you could get a defective aortic valve?

Calcific from wear and tear, ARF endocardial inflammation, congenital bicuspid valve Calcific from wear and tear, infective endocarditis, Marfan syndrome Structural abnormality, Infective Endocarditis, Myocardial Ischemia All answers are correct

27. What does Aortic stenosis sound like?

High-pitched mid-systolic crescendo-decrescendo murmur with a thrill High-pitched mid-systolic crescendo-decrescendo murmur with an ejection click Low-pitched diastolic murmur Continuous murmur throughout systole and diastole

28. How can you better auscultate Aortic Stenosis and where does it radiate to?

Loudest over the aortic area when sitting forwards on expiration; radiates to the carotid arteries Loudest over the pulmonary area and does not radiate Loudest when lying supine, radiating to the shoulder Loudest over the epigastrum, with radiation to the back

29. What conditions cause pulmonary valve stenosis?

Congenital Tetralogy of Fallot, Rheumatic Heart Disease Congenital Tetralogy of Fallot, Right Heart Failure Pulmonary Hypertension, Left Ventricular Hypertrophy Myocardial Infarction, Coronary Artery Disease

30. What does a pulmonary stenosis sound like?

High-pitched systolic murmur with a thrill High-pitched midsystolic crescendo-decrescendo murmur with an ejection click Low-pitched diastolic murmur Continuous murmur throughout systole

31. What does mitral regurgitation sound like?

High-pitched blowing holosystolic murmur Low-pitched rumbling diastolic murmur Systolic ejection murmur Continuous murmur during diastole

32. What conditions cause MR?

33. What conditions cause AR?

34. What does AR sound like?

High-pitched blowing early diastolic decrescendo murmur High-pitched blowing early diastolic decrescendo murmur Continuous murmur during systole Systolic ejection murmur

35. Where is AR heard the loudest?

Aortic area Left sternal edge Apex of the heart Pulmonary area

36. What are physical signs associated with AR?

Water hammer collapsing pulse, Displaced hyperdynamic apex beat Cyanosis, Clubbing Loud S1, S3 gallop Jugular venous distention

37. What is the pathogenesis of MS?

ARF → turbulent blood flow over inflamed valves → PLT and fibrin deposition (sterile thrombus) → chronic inflammation/scarring → fibrotic mitral valve Infective endocarditis causing valve rupture Ischemia leading to myocardial damage All answers are correct

38. What does MS sound like and where is it best heard?

Low-pitched rumbling mid-diastolic murmur with an opening snap; loudest over the apex in the left lateral decubitus position on expiration High-pitched systolic murmur Continuous murmur throughout the cardiac cycle None, it cannot be auscultated

39. Describe the pathogenesis of Infective Endocarditis (IE).

40. What are the major criteria for the modified Duke criteria for diagnosis of IE?

2 x positive blood cultures 12 hours apart, Echo evidence of endocardial involvement Unexplained fever and anorexia Single positive blood culture with physical examination findings Laboratory evidence of streptococcal infection

41. List the common causes of atrial fibrillation (AF).

42. What does the CHA2DS2VASc score measure?

Risk of thromboembolic event Risk of thromboembolic event Risk of bleeding events Risk of acute coronary syndrome

43. What does HASBLED measure?

Risk of bleeding events Risk of thromboembolic events Risk of acute myocardial infarction Risk of sudden cardiac death

44. What are causes of Aortic Regurgitation (AR) other than Rheumatic Heart Disease (RHD)?

Infective Endocarditis (IE), Syphilis Aortic Dissection, Marfan Syndrome Myocardial Infarction, Familial Hypercholesterolemia Diastolic Heart Failure, Cor pulmonale

45. What is one cause of Mitral Regurgitation (MR) other than RHD?

46. What are the early and late manifestations on auscultation of floppy valve syndrome?

47. What is this murmur? Murmur Image

48. What is this murmur? Murmur Image

49. What is this murmur? Murmur Image

50. What is this murmur? Murmur Image

51. What is shown left, middle and right? Valve Pathology Image

1. Which of the following are characteristics of Dilated Cardiomyopathy?

Commonest, slowly progressive, presents at late stage with flabby 4 chamber dilatation & mural thrombi, systolic dysfunction, and LV ejection fraction <40% Irregular hypertrophy of the left ventricle, autosomal dominant inheritance Normal-sized chambers that are stiff, leading to diastolic dysfunction Thickened myocardium with high stroke volume

2. What percentage of Dilated Cardiomyopathy cases are familial, and what is a common genetic cause?

~30%, β-myosin mutation ~50%, Dystrophin gene mutation ~50%, Dystrophin – cytoskeleton abnormality ~70%, Hypertrophic cardiomyopathy

3. Which of the following can be considered secondary causes of Dilated Cardiomyopathy?

Peripartum, Alcohol, infections (viral), iron overload, Adriamycin, Doxorubicin Genetic mutations only Hypertension and ischemic heart disease Myocarditis due to bacterial infections

4. What is a significant characteristic of Arrhythmogenic Right Ventricular Cardiomyopathy?

LV hypertrophy and systolic dysfunction Thin, dilated right ventricle with myocytes replaced by fibro-fatty tissue Fixed obstruction of the right ventricle Left ventricular dilation with mural thrombi

5. What is the main structural characteristic of Hypertrophic Cardiomyopathy?

Irregular hypertrophy of the left ventricle, particularly the septum, leading to a narrowed "banana" shape lumen Simultaneous contraction of all heart chambers Normal-sized ventricular walls with fibrosis Concentric hypertrophy with no functional impairment

6. What is the genetic inheritance pattern of Hypertrophic Cardiomyopathy?

100% genetic, Autosomal Dominant Multifactorial with environmental triggers X-linked recessive inheritance Sporadic; no family history

7. What type of dysfunction is primarily associated with Hypertrophic Cardiomyopathy?

Systolic dysfunction leading to low LV ejection fraction Diastolic dysfunction resulting in low stroke volume Mixed systolic and diastolic dysfunction Isolated atrial dysfunction

8. What defines Restrictive Cardiomyopathy?

Increased chamber size with systolic dysfunction Normal size but stiff myocardium leading to diastolic dysfunction Significant hypertrophy of the myocardial walls Progressive dilation of both ventricles

9. Which of the following is a cause of Restrictive Cardiomyopathy?

Amyloidosis, Endomyocardial fibrosis, Idiopathic fibrosis Chronic hypertension Dilated cardiomyopathy Aortic stenosis

10. What is a common complication associated with Hypertrophic Cardiomyopathy in young individuals?

Sudden cardiac death Congestive heart failure Peripheral edema Recurrent syncope

### Short Answer Questions (SAs) ```html

11. What are the microscopy findings in Hypertrophic Cardiomyopathy?

12. What is one characteristic of Endocardial Fibrosis in Restrictive Cardiomyopathy?

13. List three causes or types of Restrictive Cardiomyopathy.

14. What are some complications associated with Acute Rheumatic Fever (ARF)?

Cholesterol has various roles in the body. Which of the following is a true statement about cholesterol?

What determines the function of lipoproteins like HDL and LDL?

The size of the lipoprotein molecule. Apolipoproteins. The amount of cholesterol contained in the lipoprotein. The type of fatty acids present in the lipoprotein.

Which apolipoprotein is associated with reverse cholesterol uptake in HDL?

ApoA ApoB ApoC ApoE

In the process of exogenous triglyceride movement, which of the following is the correct sequence?

Chylomicrons lose triglycerides, form remnants, and enter the liver. Dietary fat enters plasma as VLDL. Triglycerides from HDL are transferred to chylomicrons for delivery to tissues. Liver produces VLDL and releases it into plasma for uptake by macrophages.

In endogenous triglyceride movement, what happens after VLDL exchanges triglycerides for apoC from HDL?

VLDL becomes IDL or LDL after losing triglycerides through LPL action. VLDL is transformed into chylomicrons. VLDL exits the bloodstream and enters the liver without modification. VLDL deposits triglycerides into the muscle and adipose tissue.

Which of the following conditions can disrupt normal triglyceride movement in or out of plasma?

Diabetes (insulin resistance impairs LPL function). Healthy kidneys (no effect on triglyceride metabolism). Nephrotic syndrome (proteinuria leads to increased plasma oncotic pressure). All of the above.

How is LDL receptor (LDL-R) expression regulated?

By the amount of cholesterol in the liver; high cholesterol reduces LDL-R expression. By cholesterol homeostasis and the SREBP pathway, where low cholesterol increases LDL-R expression. By the type of dietary fats consumed in the diet. By genetic mutations affecting cholesterol synthesis.

Which three types of lipid abnormalities promote atherogenesis?

Increased LDL, abnormal LDL, decreased HDL. Increased HDL, abnormal HDL, increased triglycerides. Decreased LDL, abnormal triglycerides, decreased HDL. Increased triglycerides, increased VLDL, abnormal HDL.

What factors favor LDL uptake via macrophage scavenger receptors?

Low LDL-R expression and abnormal LDL (oxidized, glycosylated). High HDL levels and normal LDL. Low triglyceride levels in plasma and reduced LDL. Normal HDL and LDL receptors.

What are the steps involved in reverse cholesterol transport?

ApoA1 enables cholesterol uptake from peripheral cells, activates LCAT, and offloads cholesterol to VLDL and LDL for liver excretion. LDL takes cholesterol from VLDL and brings it to peripheral cells. HDL takes cholesterol from the liver and brings it to peripheral cells. Cholesterol is converted into bile and excreted by HDL.

What is the genetic defect associated with Familial Hypercholesterolemia (FH)?

Defective LDL receptor (autosomal dominant). Defective apoA1 (autosomal recessive). Defective HDL (X-linked recessive). Defective LPL (autosomal dominant).

What are the clinical features of Familial Hypercholesterolemia (FH)?

Early atherosclerosis and xanthomas. Statin therapy is initiated by age 10. Early atherosclerosis and xanthomas, statin therapy initiated by age 10. No clinical features unless advanced, statin therapy initiated by age 20. Only xanthomas, no early atherosclerosis.

What are the complications of Familial Hypercholesterolemia (FH)?

Ischemic Heart Disease (IHD). Ischemic Heart Disease (IHD). Stroke. Liver failure.

Who should be screened for cardiovascular disease (CVD) risk?

Individuals ≥45yo (≥35yo if diabetic, ≥30yo if ATSI). Individuals ≥45yo (≥35yo if diabetic, ≥30yo if ATSI). All individuals under 60 years old. Only those who show symptoms of CVD.

Who is considered 'high risk' for cardiovascular disease (CVD)?

Existing CVD, diabetes >60yo, diabetes with microalbuminuria, CKD, FH, BP ≥180/110, total cholesterol >7.5, ATSI >74yo. Existing CVD, diabetes >60yo, diabetes with microalbuminuria, CKD, FH, BP ≥180/110, total cholesterol >7.5, ATSI >74yo. Only people with existing cardiovascular disease. People under 45 with no known risk factors.

What should be the first-line treatment for patients with high cholesterol?

Statins (HMG-CoA reductase inhibitors). Statins (HMG-CoA reductase inhibitors). Ezetimibe. Omega-3 fatty acids.

What is the primary goal of therapy for Familial Hypercholesterolemia (FH)?

Lowering LDL cholesterol levels to reduce cardiovascular risk. Reducing triglycerides. Increasing HDL cholesterol levels. Reducing total cholesterol levels.

What class of drugs is commonly used to lower LDL cholesterol in high-risk individuals?

Statins. Fibrates. Bile acid sequestrants. Niacin.

Which of the following is a potential side effect of statin therapy?

Muscle pain and weakness. Weight gain. Skin rashes. Increased heart rate.

What lifestyle change is recommended for individuals with high cholesterol?

Diet modification, exercise, and weight loss. Only diet modification and exercise. Only weight loss and medication. Only exercise and medication.

What is the recommended screening age for cardiovascular disease (CVD) in individuals with a family history of CVD?

Start screening 10 years earlier than the age of the earliest onset of CVD in the family. Start screening at age 40 for men and 50 for women. Only screen if symptoms appear. Screening is not necessary for individuals with a family history of CVD.

Which of the following is a primary prevention measure for cardiovascular disease?

Reducing smoking, controlling blood pressure, and managing cholesterol levels. Only reducing cholesterol levels. Taking aspirin daily. Increasing physical activity and taking statins.

What is the main function of the apolipoprotein B (apoB) protein?

It is a key component of VLDL, IDL, and LDL particles, helping with lipid transport. It activates lipoprotein lipase (LPL) to hydrolyze triglycerides. It helps in the conversion of HDL to LDL. It facilitates cholesterol uptake by liver cells.

What is the significance of HDL cholesterol in cardiovascular health?

HDL removes excess cholesterol from the bloodstream and is protective against atherosclerosis. HDL removes excess cholesterol from the bloodstream and is protective against atherosclerosis. HDL is harmful and increases the risk of cardiovascular disease. HDL has no impact on cardiovascular health.

What is the role of lipoprotein lipase (LPL) in lipid metabolism?

LPL hydrolyzes triglycerides in chylomicrons and VLDL, enabling their uptake by tissues. LPL facilitates the breakdown of cholesterol in HDL particles. LPL converts LDL into VLDL particles. LPL helps in the synthesis of triglycerides in the liver.

What is the mechanism by which oxidized LDL contributes to the development of atherosclerosis?

Oxidized LDL penetrates the endothelial layer and binds to scavenger receptors on macrophages, leading to foam cell formation. Oxidized LDL penetrates the endothelial layer and binds to scavenger receptors on macrophages, leading to foam cell formation. Oxidized LDL stimulates the release of pro-inflammatory cytokines from endothelial cells. Oxidized LDL promotes the synthesis of HDL, which is protective against atherosclerosis.

Which of the following best describes the relationship between insulin resistance and lipoprotein metabolism in the context of cardiovascular disease?

Insulin resistance increases triglyceride synthesis and decreases lipoprotein lipase (LPL) activity, contributing to elevated VLDL and triglyceride levels. Insulin resistance increases triglyceride synthesis and decreases lipoprotein lipase (LPL) activity, contributing to elevated VLDL and triglyceride levels. Insulin resistance leads to a reduction in cholesterol synthesis and a decrease in LDL receptor activity. Insulin resistance increases HDL levels while decreasing LDL and VLDL levels.

How does nephrotic syndrome lead to lipid abnormalities?

Nephrotic syndrome leads to proteinuria, resulting in reduced plasma oncotic pressure, which triggers compensatory production of VLDL and hyperlipidemia. Nephrotic syndrome leads to proteinuria, resulting in reduced plasma oncotic pressure, which triggers compensatory production of VLDL and hyperlipidemia. Nephrotic syndrome directly increases HDL production due to liver dysfunction. Nephrotic syndrome inhibits cholesterol uptake by the liver, leading to a decrease in circulating LDL.

In the pathophysiology of Familial Hypercholesterolemia (FH), how does a defective LDL receptor affect cholesterol homeostasis?

A defective LDL receptor impairs the liver's ability to clear LDL from the bloodstream, leading to elevated plasma cholesterol levels. A defective LDL receptor impairs the liver's ability to clear LDL from the bloodstream, leading to elevated plasma cholesterol levels. A defective LDL receptor increases cholesterol synthesis in the liver and decreases LDL levels. A defective LDL receptor leads to enhanced HDL cholesterol production.

What is the role of the SREBP pathway in regulating cholesterol levels in the liver?

The SREBP pathway is activated when cellular cholesterol levels are low, leading to increased expression of LDL receptors and increased cholesterol uptake. The SREBP pathway is activated when cellular cholesterol levels are low, leading to increased expression of LDL receptors and increased cholesterol uptake. The SREBP pathway reduces cholesterol synthesis in response to high dietary cholesterol levels. The SREBP pathway inhibits LDL receptor activity to prevent excess cholesterol uptake.

Which of the following is the most likely consequence of high triglyceride levels on HDL function?

Elevated triglycerides reduce HDL functionality by enhancing CETP activity, leading to the transfer of triglycerides to HDL, impairing its protective properties. Elevated triglycerides reduce HDL functionality by enhancing CETP activity, leading to the transfer of triglycerides to HDL, impairing its protective properties. Elevated triglycerides increase HDL functionality by promoting the exchange of cholesterol with VLDL particles. Elevated triglycerides have no effect on HDL functionality.

Which of the following is true regarding the role of apolipoprotein A1 (apoA1) in reverse cholesterol transport?

ApoA1 promotes the transfer of cholesterol from peripheral tissues to HDL and activates LCAT to convert free cholesterol into esterified cholesterol. ApoA1 promotes the transfer of cholesterol from peripheral tissues to HDL and activates LCAT to convert free cholesterol into esterified cholesterol. ApoA1 is responsible for promoting the uptake of cholesterol into peripheral tissues. ApoA1 enhances LDL uptake in the liver by promoting LDL receptor expression.

What is the primary cause of early atherosclerosis in Familial Hypercholesterolemia (FH)?

The defective LDL receptor impairs the liver’s ability to clear LDL, leading to high LDL levels that promote plaque formation in arteries. The defective LDL receptor impairs the liver’s ability to clear LDL, leading to high LDL levels that promote plaque formation in arteries. High HDL levels in FH patients contribute to early atherosclerosis by promoting endothelial dysfunction. The increased production of VLDL in FH patients leads to early atherosclerosis by increasing triglyceride levels.

Which of the following is a consequence of chronic hyperglycemia in individuals with uncontrolled diabetes mellitus on lipid metabolism?

Chronic hyperglycemia decreases the activity of lipoprotein lipase (LPL), leading to the accumulation of triglycerides in peripheral tissues. Chronic hyperglycemia increases hepatic VLDL production and decreases lipoprotein lipase activity, leading to elevated triglycerides in the bloodstream. Chronic hyperglycemia decreases the synthesis of fatty acids in the liver, reducing triglyceride levels in the circulation. Chronic hyperglycemia enhances HDL synthesis, resulting in improved reverse cholesterol transport and lower cardiovascular risk.

What is the mechanism of action of PPAR agonists in cholesterol management?

How do fibrates lower cholesterol levels?

What is the mechanism of action of statins in cholesterol lowering?

How do PCSK9 inhibitors work to lower cholesterol levels?

Which of the following is the primary effect of PPAR agonists on cholesterol?

Increase LDL cholesterol Decrease triglycerides and increase HDL cholesterol Increase HDL and decrease LDL cholesterol Decrease triglycerides and increase HDL cholesterol

Which enzyme do statins inhibit to lower cholesterol levels?

ATP-citrate lyase HMG-CoA reductase HMG-CoA reductase ACAT

What receptor do fibrates primarily activate to help lower cholesterol?

PPARγ PPARα PPARβ RXR

What is the effect of PCSK9 inhibitors on LDL receptors?

Increase degradation of LDL receptors Increase the number of LDL receptors on liver cells Block LDL receptor activity Decrease synthesis of LDL receptors

What are common causes of increased LDL (LDL$^\ast$)?

What are common causes of abnormal LDL (LDL$^\dag$)?

What are common causes of decreased HDL (HDL$^\ddag$)?

1. 16-year-old with episodic palpitations while playing sport and while studying at his desk. ECG shows?

ATRIAL RHYTHM HYPERTROPHIC CARDIOMYOPATHY JUNCTIONAL RHYTHM NORMAL SINUS RHYTHM WPW PATTERN

2. Hypertrophy diagnosis?

RAA LAA RVH LVH Combination HCM

3. 84-year-old woman with recent chest pain after meals relieved by antacids. ECG shows large Q waves in AVR and V1. These Q waves most likely represent:

COPD LEFT VENTRICULAR HYPERTROPHY NORMAL VARIANT PREVIOUS INFERIOR MI PREVIOUS SEPTAL MI

4. Hypertrophy diagnosis?

RAA LAA RVH LVH Combination

5. A 22-year-old woman with COVID complains of anterior chest pain, worse when lying down. ECG shows. The most likely diagnosis is:

ANTERIOR STEMI INFERIOR STEMI LEFT VENTRICULAR HYPERTROPHY PERICARDITIS PERICARDIAL TAMPONADE

6. A 56-year-old woman develops tachycardia, hypotension, and respiratory distress day 1 post mitral valve replacement. ECG shows. The most likely cause of her deterioration is:

ANTERIOR STEMI INFERIOR STEMI LEFT HEART FAILURE PERICARDIAL TAMPONADE RIGHT HEART FAILURE

7. Hypertrophy diagnosis?

RAA LAA RVH LVH Combination

8. Hypertrophy diagnosis?

RAA LAA RVH LVH HCM

9. An 86-year-old woman presents to her GP for a repeat script of ramipril. A routine ECG is performed. The appearance of her ECG is consistent with:

ACUTE PERICARDITIS ANTERIOR STEMI LEFT VENTRICULAR HYPERTROPHY NSTEMI RIGHT VENTRICULAR HYPERTROPHY

10. Hypertrophy diagnosis?

RAA LAA RVH LVH RVH

1. WHICH OF THE FOLLOWING ECG FEATURES IS MOST CONSISTENT WITH HYPERCALCAEMIA?

PROLONGED PR INTERVAL ST SEGMENT DEPRESSION SHORTENED QT INTERVAL TALL, PEAKED T WAVES WIDE QRS COMPLEX

2. WHICH OF THESE IS A CAUSE OF ST SEGMENT DEPRESSION?

ACUTE MYOCARDITIS ACUTE PERICARDITIS HYPERCALCAEMIA MYOCARDIAL ISCHAEMIA VENTRICULAR ANEURYSM

3. 84-YEAR-OLD WOMAN COMPLAINS OF EIGHT HOURS OF CHEST HEAVINESS AND WORSENING SHORTNESS OF BREATH. SHE HAS A BACKGROUND HISTORY OF DIABETES, HYPERTENSION, AND SLE. AN ECG IS PERFORMED AND IS SHOWN IN IMAGE 1. THE MOST LIKELY DIAGNOSIS IS:

ANTEROLATERAL STEMI HYPERKALAEMIA INFEROLATERAL STEMI PERICARDITIS POSTERIOR STEMI

4. A 68-YEAR-OLD MAN IS BROUGHT IN BY HIS FAMILY TEN WEEKS POST ANTERIOR STEMI. HE IS COMPLAINING OF GRADUALLY WORSENING EXERCISE TOLERANCE, PALPITATIONS AND SHORTNESS OF BREATH. AN ECG IS PERFORMED AND IS SHOWN IN IMAGE 2. THE MOST LIKELY DIAGNOSIS IS:

ACUTE CORONARY SYNDROME DRESSLER SYNDROME HYPERCALCAEMIA PERICARDIAL TAMPONADE VENTRICULAR ANEURYSM

5. WHICH ONE OF THE FOLLOWING ECG FEATURES WOULD BE SUPPORTIVE OF A DIAGNOSIS OF AN INFERIOR STEMI?

A NEW LEFT BUNDLE BRANCH BLOCK ST DEPRESSION IN II, III AND AVF ST DEPRESSION IN I, AVL AND V2 ST ELEVATION IN V5, V6, I AND AVL TALL R WAVES IN V1-V3

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1. Which of these are causes of Tall T waves (>5mm in Limb leads, >10mm in chest leads)?

Hypokalemia, Acute pericarditis Hyperkalaemia, Acute transmural MI Left ventricular hypertrophy, Aortic stenosis Myocardial ischemia, Atrial fibrillation

2. What are prominent U waves a sign of?

Hypercalcemia Myocarditis Hypokalemia Hyperkalemia

3. What do inverted U waves represent?

Left bundle branch block Hypotension Hyperkalemia Myocardial ischemia

4. What is the commonest form of atrial flutter?

Clockwise reentry producing positive flutter waves in leads II, III, aVF Anticlockwise reentry producing positive flutter waves in leads II, III, aVF Multifocal reentry producing chaotic flutter waves in leads I, II, III Anticlockwise reentry producing negative flutter waves in leads II, III, aVF

5. What is the average lifetime risk over age 40 of AF?

1 in 10 1 in 5 1 in 4 1 in 2

5. A man has AF for 30 hours which spontaneously reverts, what is this called?

Persistent AF Paroxysmal AF Long-standing AF Permanent AF

6. A woman has AF >1 year, they are planning to try an ablation on Tuesday. Classify her AF?

Paroxysmal AF Long-standing persistent Long-standing persistent Persistent AF

7. A man has had AF for 8 days, what is this classified as?

Paroxysmal AF Persistent AF Long-standing AF Permanent AF

8. What are the criteria for AV nodal (Junctional) Ectopic beats?

Wide QRS, No P wave, followed by compensatory pause Narrow QRS, either 1. No p-wave or 2. retrograde p wave, occurring before, during, or after QRS, occurs sooner than would be expected for next sinus impulse, followed by compensatory pause Narrow QRS, with P wave after QRS complex, occurs with a longer than expected interval Wide QRS, retrograde P waves, followed by compensatory pause

9. How can you tell if it is junctional tachycardia rather than something else?

Sudden onset, narrow complex, absent or retrograde P waves, 100-140 BPM Gradual onset, broad complex, absent or retrograde P waves, 100-140 BPM Gradual onset, absent or retrograde P waves, narrow complex, 100-140 BPM Sudden onset, wide complex, retrograde P waves, 140-160 BPM

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