Dyslipidemia and Cardiac PT Encounters Flashcards by Avid Learner

A patient has chest pain and is not in severe repirtory distress or shock.

The patient has sharp pleuritic pain that radiates to the shoulders and the back.
The patient reports that they learn forward to relieve the pain.

What is your top Ddx?

Pericarditis

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What lipoprotein is this?

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Describe the general mechanism for Familial hypercholesterolemia

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What are the Lipid effects of statins?

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What is Lymphangitis?
- What is seen on the skin?
- What can result from it?

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What are the First drugs of choice to reduce blood-lipid levels? In what order to you give them?

Statins
Least potent first then go down the line
- Simvastatin is least potent so you start them there.
- Pravastatin is MOST potent.

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What is the Primary vs. Secondary Endpoint for cholesterol clinical trials

Primary
- Better Cardiovascular Outcomes
Secondary
- Lower LDL levels

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What are the pros and cons of PCSK9 inhibitors?

Longterm effects are also unknown

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Concerning the 4 main healthy lifestyle changes that people can make to change their lipid profile for the better:
- What are they?
- Which one does not decrease LDL?

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A patient has chest pain and is not in severe repirtory distress or shock.

The patient has atypical angina pain, along with a low risk of coronary artery disase.

What is your top Ddx?

Pulmonary Embolism
Mitral Valve Prolapse
Digestive Pain
MSK Pain
Psychogenic Pain

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What is Mönckeberg medial sclerosis?

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For Thoracic aorta dissection

What are the essentials for dx?
- How do you dx? How do you classify it?
What tests do you run?
What are the associated symptoms?
How do you manage it?
- include drugs

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Describe how size relates to AAA rupture risk

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What are the pathological outcomes of varicose veins?

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Complete each step

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Relate pulmonary embolism and DVT

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What are the Bile-Acid Sequestrants (BAS)?

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What is the channel that Ezetimibe actually blocks?

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Describe the multiplicative effects of RFs for Atherosclerosis

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What are the two common/concerning tyoes of cardiac related dyspenia?

Dyspenia Types

Orthopenia
- shortness of breath (dyspnea) that occurs when lying flat, causing the person to have to sleep propped up in bed or sitting in a chair.
Paroxysmal nocturnal dyspnea
- Attacks of severe shortness of breath and coughing that generally occur at night. It usually awakens the person from sleep, and may be quite frightening.

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What enzyme is described?

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The response-to-injury hypothesis views atherosclerosis as a chronic inflammatory response of the arterial wall to endothelial injury. According to this model, atherosclerosis results from what process? (Describe the EC injury causes, the role of lipoproteins, platelets, monocytes, SMCs, and macrophages)

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Label these

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If a patient is having palpitations, what would make you immediately suspect that there is underlying arrhythmia?

1. If the palpitations occur with syncope or presyncope. 2. Known history of cardiac disease

What is Raynaud Phenomenon?

Which apolipoprotein is associated with these?

* Where do AAA's occur? * What is present in a majority of cases?

What is Niacin used for?

What are the clinical manifestations of an AAA?

What is Trousseau syndrome?

* Venous thrombi also can result from the **elaboration of procoagulant factors from cancers**; the resulting hypercoagulable state can manifest as thromboses in different vascular beds at different times, so-called “**migratory thrombophlebitis” or “Trousseau syndrome.”**

What are the components of Omega-3 Fatty Acids? What is the name of OTC drug?

How does this plaque relate to the thinning of the vessel wall? What part of the vessel is most thinned, and how does this relate to the location of the plaque?

Describe how age relates to when Atherosclerosis and why MI's increase in prevalence as PTs get older

If a cell needs cholesterol, what are the two ways that it can get it?

Make it or increase LDL receptors

What are the most used statins and why?

Top two drugs have the highest half-life and decrease LDL the most compared to others.

* What accounts for \> 90% of cases of thrombophlebitis and phlebothrombosis - venous thrombosis accompanied by inflammation? What other sites of thrombi can cause this? * What can cause portal vein thrombosis?

What is this?

Describe the historical characteristics of Atherosclerotic plaques

What is shown at each of the two arrows?

* Aorta with severe diffuse complicated lesions, including an **ulcerated plaque** (open arrow), and a l**esion with overlying thrombus** (closed arrow).

Which apolipoprotein is associated with chylomicrons and chylomicron remnants?

* Top: chylomicron * Bottom: chylomicron remnants

What is shown?

Raynaud Phenomenon

What does this image show?

What lipoprotein is this?

Where do fibrates, niacin, and CEPT inhibitors fit into this figure, and what do they do?

* All increase HDL * CETP inhibitors decrease LDL

What PT history and Symptoms/Signs are associated with Acute arterial occlusion?

What goes on the outer regions of a protein and what goes in the inner regions?

* Outer * Peripheral proteins * Phospholipids * Some nonesterified cholesterol may sick through the phospholipids * Inner * Integral proteins * Cholesteryl-ester * Triglycerides

What are the ADRs and DDIs for Bile-Acid Sequestrants (BAS)? What do you need to monitor because of the ADRs and DDIs?

Need to stagger doses throughout the day of other oral drugs because of DDIs

What are the Bile-Acid Sequestrants drugs?

**COLE**-

* What are the ADRs subsequent monitoring parameters for Niacin? * What conditions are contraindicated for Niacine use?

Atheromatous plaques * What is at the core of these plaques, and what are the covered by? * How does stenosis, thrombosis, and occlusion relate to these plaques?

What are they DDIs for fibrates?

What are the types of acute arterial Occlusions?

For Abdominal aneurysms * What are the measurements for it? * Symptoms? * Risk factors?

* What are the TRIACYLGLYCEROL carriers? * What are the CHOLESTEROL carriers?

What are the main drugs/drug types that are used to lower LDL levels?

What is described here?

Primary Raynaud phenomenon

C (A is for AAA rupture)

What are the tests to confirm an Acute arterial occlusion?

Angiography or want a duplex urltrasound

HDL Mediates the Formation of LDL What is happening from 1 to 4 in this figure?

What is shown in this vessel wall?

* A **Fatty streak**, demonstrating **intimal**, **macrophage-derived foam** cells (arrows).

For fibrates, * What are the Laboratory test reactions? * What are the ADRs? * What are the Monitoring Parameters?

?Which statins are metabolized by CYP450, 3A4?

SAL

* What location in aortic dissection is associated with the most complications? * What are the classifications of aortic dissection?

* What are the main cells that contribute to thrombosis, atherosclerosis, and hypertensive vascular lesions? * What are the main cells that contribute to luminal occlusion?

What is cystic medial degeneration?

\*\*\*Changes related to factors that cause aneurysms/dissections\*\*\*

Define Ascites

Colleciton of fluid in the **peritoneal** cavity

Describe the measurements/locations associated with aortic dissection. What kind of rupture results in massive hemorrhage or cardiac tamponade?

About ____ % of fatty acids are bound to albumin

What are the pre-2013 guidelines for HDL cholesterol levels that are considered "high risk"?

Describe the process in which inflammation contributes to the initiation, progression, and complications of atherosclerotic lesions.

What are the pre-2013 guidelines for HDL cholesterol levels that are considered "low risk"?

What kind of aneurysm is described? Circumferential dilations up to 20 cm in diameter; these most commonly involve the aortic arch, the abdominal aorta, or the iliac arteries.

Fusiform aneurysms

What are the statins we need to remember?

My **sim** got the **flu**, so I gave them **love** **and** **roses**.

What is the difference between lipedema and lymphodema?

* Lipedema * Edema from fluid retained in the **interstital space by lipids in the dermis** * Lymphodema * Edema from **lymphatic drainage obstruction.**

A patient has chest pain and is not in severe repirtory distress or shock. * The patient has atypical angina pain, along with a high risk of coronary artery disase. **What is your top Ddx?**

**Myocardial Infarction or Ischemia** * Also think of pulmonary embolism, digestive pain, psychogenic pain.

What is the MOA for statins?

How does ezetimibe work?

* It Inhibits Uptake of Dietary Cholesterol * Blocks NPC1L1, which is a gut transporter for dietary cholesterol

What is the purpose of the ACAT enzyme?

Convert **intracellular cholesterol** to the cholesteryl ester

Statins have Extensive first-pass metabolism. How do you get around this?

Prodrugs (Simvastatin and Lovastatin)

What is shown?

* Cross-section of aortic media from a patient with **Marfan** syndrome, showing marked **elastin fragmentation and areas devoid of elastin that resembles cystic spaces** (asterisks).

What is shown here?

Normal media for comparison, showing the regular layered pattern of elastic tissue

How can the following cause an aneurysm or dissection to form? Excessive connective tissue degradation

* What are the pre-2013 guidelines for LDL cholesterol levels that are considered: * The goal for people with very high attack of heart disease * The goal for people with heart disease or diabetes * The goal for people who are generally healthy

How do PCSK9 Inhibitors work?

HDL Mediates the Formation of LDL What is happening from 5 to 8 in this figure?

What are the PCSK9 Inhibitors ?

O-Cum antibodies

Describe the signs/symptoms of DVT in the legs

A patient has chest pain and is not in severe repirtory distress or shock. * The patient has sharp pleuritic pain, sudden onset dyspnea. * The patient reports that sometimes they cough up blood and have short "black outs". **What is your top Ddx?**

* **Pulmonary Embolism** * Could also be penumothorax, penumonia, or pleutis.

* Describe what the generation of, the TAG composition, the cholesterol composition, and function of: * VLDL * Chylomicrons

What type of dissection is this?

Type A DeBakey I

What are the ADRs for statins?

Describe the general process of how an Abdominal Aortic Aneurysm develops

Define Anasarca

Edema EVERYWHERE in the body

* In DVT of the legs, what is the most important risk factor?

What is this?

* Hyaline arteriolosclerosis. * The arteriolar wall is thickened with the deposition of amorphous proteinaceous material (hyalinized), and the lumen is markedly narrowed.

What are the main takeaways from the Framingham Heart Study?

* HDL * High HDL is good, probably independent of other types of cholesterols * LDL * Low LDL levels with high HDL levels has the lowest risk of cardiovascular disease

D (2nd is left atrium, then ab. aorta )

What is the general process that causes the migration of SMCs into the tunica intima?

What lipoprotein is this?

What inflammation-associated molecule is useful for measuring risk for Atherosclerosis and other conditions such as MI and stroke.

What are the fibrates?

How do you take Bile-Acid Sequestrants (BAS) and what are the lipid effects? What drugs do they have synergistic effects with?

What are the factors related to aneurysm/dissection pathogenesis?

What is this?

How do fibrates work? (MOA) What are they used for?

What are the 5 concerning/common cardiac symptoms?

1. **C**hest ppain 2. **P**alpitations 3. **D**yspenia 4. **E**dema 5. **S**yncope **PC** **DE**m**S**

A patient has chest pain and is not in severe repirtory distress or shock. * The patient has typical angina pain. * Diffuse retrosternal pressure that radiates to the one arm. * Dyspenia, and nausea **What is your top Ddx?**

* **Myocardial Infarction or Ischemia** * Also think of pulmonary embolism, digestive pain, psychogenic pain.

What is described? Pressurized blood gains entry to the arterial wall through a surface defect and then pushes apart the underlying layers.

Arterial dissections

What is this?

* Hyperplastic arteriolosclerosis * (“onion-skinning”) (arrow) causing luminal obliteration (periodic acid–Schiff stain).

What is the purpose of the LCAT enzyme? What additional molecule does it need?

Convert cholesterol bound to HDL into cholesteryl ester using a lecithin molecule

How can the following cause an aneurysm or dissection to form? Loss of smooth muscle cells (SMCs) or change in the SMC synthetic phenotype

What is the critical function for vascular response to injury?

How Bile-Acid Sequestrants (BAS) work? What condition are they especially food for?

* They force bile salts into the excretory pathway. The liver uses cholesterol to make bile salts, so these drugs decrease LDL by increasing cholesterol conversion into bile salts

What are the differences in Type A and Type B dissections for Tx and PT outcome?

What are palpitations? What is it usually due to?

Awareness of heartbeat * **Cardiac** causses * **Sinus Tachycardia** * Heightened **awarness of NORMAL** sinus rhythm.

What is PCSK9?

A regulatory protein in LDL-receptor metabolism

* What kind of vessels are most affected by Atherosclerosis? * What are the general symptoms related to Atherosclerosis? * What are the major pathological outcomes of Atherosclerosis?

Which statins are metabolized by CYP450, 2C9?

fluvastatin

Describe the general differences in walls between veins and arteries

* Describe what the generation of, the TAG composition, the cholesterol composition, and function of: * HDL * LDL

About \_\_\_% of Lipids in the blood is triglycerides and \_\_\_\_% are phospholipids

What is shown in A and B?

What are the constitutional risk factors for Atherosclerosis?

This is an image of an Aorta. What is being shown at the arrows?

(A) Aorta with **fatty streaks (arrows),** mainly near the ostia of branch vessels.

What type of dissection is this?

Type B DeBakey III

What is the difference in vulnerable plaques and stable plaques?

Describe the general morphology of an Atherosclerotic plaque, keeping in mind the 3 basic components of Atherosclerotic Plaques.

What is the classic clinical symptom of aortic dissection? What is the most common cause of death?

What enzyme is described?

* Concerning genetics * What is the most independent risk factor for Atherosclerosis? * What are some other genetic RFs?

Why do you give some statins at night? What are the statins that this is important to remember?

Why is atherosclerosis-related mortality typically reflective deaths by ischemic heart disease?

What planes are disrupted in an aortic dissection? What groups does this occur at higher rates?

What is this?

Concerning gender, what group of people seem to be protected against Atherosclerosis?

What type of Arteriosclerosis is associated with malignant HTN?

hyperplastic arteriolosclerosis

Concerning algorithms for calculating statin use, * What alarming pattern is seen in older patients? * What measurement is being considered as an addition to the algorithms? * Why should the outcome of an algorithm be taken with a grain of salt?

* Healthy old people are recommended to be on statins * Coronary artery calcium levels * Many different algorithms. Some may say a PT needs to be on statins and others say they do not need a statin.

What is shown in this Aorta at the arrow?

Aorta with **mild atherosclerosi**s composed of **fibrous** **plaques**, one denoted by the arrow.

What are the two variants of Arteriosclerosis?

* What is Prinzmetal angina? * What can occur if it lasts 20-30 minutes? * What can it do vessels and how? * What weird ass cardiac condition can result from it?

What are the Fibrates?

A **fe**minine **gem**ini

* Give the order of descending severity for atherosclerosis in the following structures * Popliteal Arteries * Vessells of the Circle of Willis * Coronary Arteries * Abdominal Aorta * Internal Carotid Arteries

For PCSK9 Inhibitors, list the * Lipid Effects * PKs * ADRs

What are the three concentric layers of the walls of large vessels?

* Describe how hyperlipidemia relates to Atherosclerosis * What is the main lipid-carrier associated with increased risk for Atherosclerosis? * What does each of those lipid-carrier do?

* For Omacor * What are its components? * What are its effects on lipids? * When do you use it? * What its PKs?

What is the difference in true and false aneurysms?

This is Atherosclerotic plaque in a coronary artery. What does each letter stand for?

Describe the Management of Acute arterial occlusion

What type of dissection is this?

Type A DeBakey II

What occurs when a rupture, ulceration, or erosion of the surface of atheromatous plaques?

What are the general ADRs for statins?

What is Ezetimibe used for, and what is are its DDIs/ADRs?

What kind of drugs are the current PCSK9 inhibitors? What are their names?

What does this show?

Acute coronary thrombosis superimposed on an atherosclerotic plaque with focal disruption of the fibrous cap, triggering fatal myocardial infarction

What kind of aneurysm is described? Discrete outpouchings ranging from 5 to 20 cm in diameter, often with a contained thrombus.

Saccular aneurysms

What lipoprotein is this?

Describe the two general ways that serum levels of LDL is altered

* Cholesterol sources for cells * Importing LDL into cells * Synthesizing of cholesterol by cell * LDL receptors * Degrading after use * Recycling after use

Are the essentials to diagnose blue toe syndrome?

Describe the types of Peripheral Arterial Aneurysms

What can chronic edema lead to?

What are the main drugs/drug types that are used to increase HDL levels?

How does Niacin work, and what are the PKs for it? When do you use niacin for hyperlipidemia?

Decrease of hormone-sensitive lipase in adipose tissue

What are the modifiable risk factors for Atherosclerosis?

Describe the management for a AAA and complications for ruptured AAA

All of the above

Describe how LDL receptors are activated and what happens once they are activated

* Decreases in cholesterol induces an increase in LDL-receptors * This causes endocytosis of LDL and thus a decrease in serum LDL. * LDL will donate cholesterol to cells

What does this show?

Plaque rupture with superimposed thrombus

Does the use of Ezetimibe and Simvastatin as combo-therapy cause a decrease in LDL? What about a decrease in cardiovascular disease?

* Does the use of Ezetimibe and Simvastatin as combo-therapy cause a decrease in LDL? * Yes * What about a decrease in cardiovascular disease? * No

Concerning Varicose Veins of the Extremities * What exactly are they? * What part of the body do they normally affect? * Who gets it more often, and why? * What are the clinical manifestations of it?

A patient has chest pain and is not in severe repirtory distress or shock. * The patient reports that the pain feels like a ripping or tearing senstion. * The pain radiates to the back. * The patient also has a history of hypertension.

Aortic Disection

What is the difference between myxedema and pretibial myxedema?

* Myxedema * Edma from **HYPOthyroidusm** * Pretibial myxedema * **Swelling of the shin**s due subcuntaneas plaques form **Graves Disease**

What are the three principal components of Atherosclerotic plaques?

About \_\_\_% of Lipids in the blood is cholesterol, with ____ being actual cholesterol and _____ being esterified cholesterol

For Ezetimibe, what is the MOA and what are the lipid effects?

What are the 4 causes of chest pain?

1. **Ischemic** Cardiac 2. **Non-ischemic** Cardiac 3. **Non**Cardiac 4. **Psycho**

What is Milroy disease and how does it relate to edema?

What are the PCSK9 Inhibitors?

**O**-**Cum** **A**nti**b**odies

Atherosclerosis * What is an atheroma? * What conditions can Atherosclerosis be the outcome of? * Why is this disease so significant to the world?

Intimal lesions * How do these lesions weaken the tunica media? * What is a major/deadly outcome of this weakness?

Ischemic tunica media + ECM changes by inflammation can lead to **aneurysm**

What is a fatty streak?

* What will eventually happen to an expanding atheroma? * How is the above outcome represented in patient activity? * Describe how chronic arterial hypoperfusion is related to Atherosclerosis. * What can Acute Plaque Change (plaque erosion or rupture) trigger?

1. What is the regulatory step in cholesterol synthase? 2. What kind of regulation does this enzyme have? 3. How do statins affect this mechanism?

1. **HMG-CoA Reductase** 2. **Feedback inhibition** * Cholesterol, the product, will inhibit the enzyme, HMG-CoA Reductase 3. Bind to **HMG-CoA Reductase as competitive inhibitors, inhibiting cholesterol synthase.** The cell then uses the mechanism of increasing LDL receptors to get cholesterol instead of synthesizing it on its own.

What are the different types of edema?

* **A**nasarca * **A**scites * **L**ipedema * **L**ymphedema * **M**yexedma * Pretibial **M**yexedma Llama

What are the Pleiotropic Effects of Statins?

* What are the most important predisposing conditions for aortic aneurysms? * What kind of aneurysms are they associated with?

What is CETP?

Atherosclerotic Plaque * What are the key features of this? * How big are they? * What color are they, and what could be the reason why they have color changes? * What do some vessels have an increased incidence of having Atherosclerotic Plaques compared to others?

What are the "random" risk factors for Atherosclerosis?

What is Familial Hypercholesterolemia?

* Familial hypercholesterolemia is a genetic disorder. * Caused by one of 2 mechanisms * The LDL-receptors become are defected in these PTs. * *OR** * The APO B-100 on LDL is defective * The defect makes the body unable to remove LDL cholesterol from the blood, and this serum LDL increases. * PTs have an increase in risk cardiovascular disease

What are the two receptors in the liver that are able to bind chylomicron-remnants?

What is the function of Hepatic Lipase?

* What must occur before Triglycerides can enter a cell? * What is the exception to this?

What statistic is important in remembering the relation to lipid profiles and MIs?

Only 50% of PTs who suffer from an MI have bad lipid profiles

What structure narrows and causes an aortic dissection? What condition(s) are associated with aortic dissection?

What conditions are associated with Thoracic Aortic Aneurysm?

How do PCSK9 inhibitors work?

In the liver... * Normally PCSK9 is secreted into the ECF, which then binds to the LDL-receptor on the cell surface. * The receptor is endocytosed by the cell and the PCSK9/LDL-receptor complex forces the LDL-receptor into the lysosome degradation pathway rather than the recycling pathway. * Binding to PCSK9 by PCSK9-inhibitors, therefore, increases the likelihood that LDL-receptors will be recycled, thus decreasing LDL serum concetrations.