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Block 4 > Week 3 > Flashcards

Week 3 Flashcards

1
Q

Where do the coronary arteries arise from?

A 
The aorta (at the aortic sinuses)
\*branch over surface of heart to supply blood flow to myocardium and epicardium
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2
Q

How does blood from right side of heart come back into the heart?

A
  1. Blood from heart returns via small anterior cardiac veins and empty into right atrium
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3
Q

How does blood from left side of heart come back into the heart?

A
  1. Blood from heart returns via coronary sinus and empties into right atrium
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4
Q

What is coronary dominance?

A

Whether a person has a posterior descending artery arising from the RCA or LCA

some people have codominance

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5
Q

Explain how plexus of arteries supply cardiac muscle?

A
  • Coronary arteries lie on surface of the heart
  • Smaller arteries then penetrate the cardiac muscle
  • There are subendocardial arteries lying beneath the endocardium
  • Together they all make a plexus
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6
Q

dWhat are the determinants to regulation of coronary blood flow? (5)

A
  1. Aortic pressure (driving force of blood through sinuses)
  2. Metabolic activity of heart (when heart demands more oxygen during exertion, coronary resistance decreases to allow more blood flow)
  3. Intraluminal physical forces (When increased intraluminal pressure from arriving from small arteries would cause distention of the large vessels, smooth muscle constriction works to decrease diameter → brings back flow back to original level)
  4. Extravascular subendocardial arteries experience more pressure due to being squeezed by myocardium or compressed by ventricular filling
  5. Neural and hormonal factors (sympathetic innervation)
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7
Q

Explain coronary flow reserve

A

The ratio between maximum coronary flow and resting coronary flow

  • The capacity of the coronary circulation to dilate and thus increase flow following an increase in myocardial metabolic demands
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8
Q

What changes can increase resting coronary flow?

A
  • increased resting heart rate
  • increased contractility
  • This increases resting coronary flow but decreases overall coronary flow reserve
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9
Q

What decreases maximum coronary flow?

A
  1. LV hypertrophy
  2. Microvascular disease
  3. This decreases both max coronary flow and coronary flow reserve
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10
Q

Less/more coronary flow reserve makes myocardium more vulnerable to ischemia?

A
  1. Less coronary flow reserve
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11
Q

Why is subendocardium more vulnerable to ischemia?

A

Flow in the subendocardium during exertion is impeded by compressive pressure of the systolic contraction and the flow reserve is sooner exhausted leaving tissue vulnerable to oxygen deficits

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12
Q

Explain the coronary steal syndrome?

A
  • occurs downstream of a stenoic or occluded coronary vessel
  • At baseline, due to occluded vessel - the downstream vessels will be dilated and lead to an increased resting coronary flow. Although little blood is coming through occluded vessels, other contributing vessels can donate blood to dilated vessels downstream
  • When person is given vasodilator therapy, the other contributing vessels and their originating vessels dilate, steal blood that was being “donated”, and lead to the downstream vessels of occluded vessels to go through ischemia
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13
Q

What type of blood is found in pulmonary arteries vs pulmonary veins?

A
  1. pulmonary arteries pump deoxygenated blood to lungs
  2. pulmonary veins bring oxygenated blood back to heart from lungs
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14
Q

What comprises the walls of lymphatic system vessels?

A

Just endothelium. Highly porous to allow fluids, proteins, cells to cross

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15
Q

What helps lymph fluid move in one direction?

A

The valves prevent back flow and contraction of muscles during exercise helps push lymph forward

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16
Q

What is the pathway in systemic circulatory system starting with left ventricle?

A
  1. Left ventricle
  2. aorta
  3. arterial tree
  4. capillaries
  5. venous tree
  6. vena cava
  7. right atrium
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17
Q

What is the pathway in pulmonary circulatory system starting with right ventricle?

A
  1. Right ventricle
  2. pulmonary arteries
  3. capillaries of lungs
  4. pulmonary veins
  5. left atrium
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18
Q

What is portal blood circulatory system?

A

Several capillary beds in series

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19
Q

Everything larger than a capillary has vessel walls with 3 layers.

What are the three layers?

A
  1. Tunica intima (innermost layer touching blood)
  2. Tunica media
  3. Tunica adventitia
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20
Q

What is in the tunica intima?

A
  1. endothelium
  2. basal lamina
  3. connective tissue
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21
Q

What is in the tunica media?

A
  1. smooth muscle cells in circular arrangement
  2. protein fibers like collagen and/or elastin
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22
Q

What is in Tunica adventitia

A
  1. contains connective tissue to attach vessel to body
  2. the large vessels have blood vessels to supply blood vessels
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23
Q

What are pericytes?

A

Wrap around capillary cells to offer support and are possible stem cells to create no blood vessels

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24
Q

Aorta/elastic arteries

  1. size in terms or arteries
  2. Size of tunica media
  3. Size of tunica adventitia
A
  1. largest of arteries
  2. Very thick tunica media
  3. Thinner tunica adventitia
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25
Q

Muscular artery/Artery

  1. size in terms or arteries
  2. Size of tunica media
  3. Special aspect of tunica intima?
A
  1. Medium sized arteries
  2. Tunica media is thinner (less elastin, more smooth muscle)
  3. Tunica intima has a dense layer of elastic fiber known as inner elastic lamina that shows up as a wavy line under microscope
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26
Q

Arterioles

  1. size in terms or arteries
  2. Tunica intima description
  3. Size of tunica media
  4. Tunica adventitia
A
  1. smallest branch of arterial tree
  2. lacks inner elastic lamina
  3. Tunica media is thin (1-3 cells thick)
  4. Tunica adventitia is very thin
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27
Q

Venules

  1. size in terms or venous branch
  2. Size of tunica intima
  3. Size of tunica media
  4. lumen description
A
  1. smallest of venous branch
  2. normal tunica intima
  3. thin tunica media (<2 cells thick) → in post capillary venules though it is absent
  4. lumen is usually flattened
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28
Q

Veins

  1. size in terms or venous branch
  2. Size of tunica intima
  3. Size of tunica media
  4. size of tunica adventitia
A
  1. mediam sized veins
  2. regular tunica intima that contain valves (medium veins contain valves)
  3. Thin tunica media
  4. Tunica adventitia is thicker than tunica media (lots of collagen fibers and elastic fibers)
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29
Q

Large veins/vena cava of venous branch

  1. Size of tunica intima
  2. Size of tunica media
  3. Size of tunica adventitia
A
  1. regular tunica intima with valves
  2. thin tunica media
  3. very thick tunica adventitia ( has smooth muscle in longitudinal arrangement)
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30
Q

What happens during cold temperatures in the capillaries in terms of blood flow and metarterioles?

A
  1. metarterioles have smooth muscle that can contract (precapillary sphincter) and this causes blood to move directly from arterioles to venules via metarteriole and avoiding capillary
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31
Q

capillaries

  1. what is the wall of capillaries comprised of?
A
  1. single layer of endothelial cells with basal lamina
  2. Only room for one RBC to go through at a time
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32
Q

Differentiate between continuous capillary, fenestrated capillary, and discontinuous/sinusoidal capillary?

A
  1. Continuous capillary: least porous-have numerous tight junctions and continuous basal lamina. Found in brain/NS, muscle, lungs, skin
  2. Fenestrated capillary: endothelial cells have holes and loose connective tissue, continuous basal lamina. Found in kidney, intestines, endocrine glands
  3. Discontinuous/sinusoidal capillary: endothelial cells have large gaps between them, discontinuous basal lamina. Found in spleen, liver, and bone marrow
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33
Q

Differentiated between venous and arterial vessels under microscope

  1. wall to lumen ratio (thick wall,small lumen vs thin wall, large lumen)
  2. Shape of lumen (round vs flattened)
  3. Thickness of tunica adventitia (thick vs thin)
A
  1. Thick wall, small lumen = arterial ;;; thin wall, large lumen = venous
  2. Round = usually arterial ;;; Flattened = venous
  3. Thick = venous; thin = arterial
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34
Q

What growth factors are used in angiogenesis?

A

VEGF and FGF stimulate angiogenesis when there is hypoxia

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35
Q

What 4 things can cholesterol become?

A
  1. steroid hormones
  2. hydroxysteroles
  3. cholesteryl ester
  4. bile acids
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36
Q
  1. What is the difference between cholesterol and cholesteryl ester? (think hydrophobic/hydrophilic)
  2. How does cholesterol become cholesteryl ester?
A
  1. Cholesteryl ester is more hydrophobic than cholesterol
  2. via LCAT enzyme
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37
Q
  1. What is the committed, rate limiting step of cholesterol synthesis?
  2. What kind of drugs inhibit this step?
A
  1. HMG CoA reductase converts HMG-CoA to mevalonate using NADPH
  2. Statins
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38
Q
  1. How is cholesterol synthesis controlled via ATP citrate lyase?
  2. What drug is involved?
A
  1. Acetyl Co-A is substrate to cholesterol synthesis. To make Acetyl Co-A you need ATP citrate lyase. By inhibiting ATP citrate lyase you inhibit Acetyl Co-A production and thus cholesterol synthesis
  2. Bempedoic acid
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39
Q

How do you control cholesterol synthesis via regulation of transcriptional control?

A
  1. Cholesterol in ER membrane is attached to SCAP/SCREBP complex.
  2. When intracellular cholesterol is low, cholesterol detaches and SCAP/SREBP moves to golgi membrane while proteases cleave off DNA binding domain.
  3. DNA binding domain moves to nucleus and encourages transcription of HMG- CoA reductase (promoting cholesterol synthesis)
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40
Q

How does excess cholesterol and bile acids change levels of HMG-CoA reductase?

A

Excess cholesterol and bile acids can induce conformational change in HMG-CoA reductase which leads to degradation of HMG-CoA reductase (less cholesterol)

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41
Q

How does AMP activated protein kinase affect HMG CoA reductase function?

A
  1. In low energy levels - AMP activated protein kinase converts to active form
  2. Activated AMP activated protein kinase can dephosphorylate HMG-CoA reductase leaving it inactivated (less cholesterol synthesis)
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42
Q

How does cholesterol get secreted/leave the liver?

A
  1. Secretion of cholesterol via VLDL
  2. Free cholesterol secreted in bile
  3. Conversion of cholesterol to bile acids/salts
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43
Q

How does free cholesterol get recycled or excreted in bile?

A
  1. Bile ends up in intestines for fat digestion
  2. Then in intestine, bile gets absorbed and returned to liver for recycling of cholesterol but also 5% gets excreted in feces
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44
Q

What do chylomicrons transport?

A

triglycerides from intestines

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45
Q
  1. What markers do chylomicrons have?
  2. And what is their function?
A
  1. ApoB-48 ; chylomicron marker
  2. ApoC-II: activates lipoprotein lipase (lipoprotein lipase is on adipose tissue and allows for delivery of triglycerides)
  3. ApoE: triggers clearance of chylomicrons
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46
Q

What doe VLDL transport and from where to where?

A
  1. endogenous lipids/triglycerides to peripheral tissues from liver
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47
Q

What markers does VLDL carry?

A
  1. ApoB-100: marker for VLDL, IDL, LDL
  2. ApoC-II: activates lipoprotein lipase
  3. ApoE: triggers clearance of VLDL
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48
Q

What is lipoprotein lipase?

A

lipoprotein lipase (lipoprotein lipase is on adipose tissue and allows for delivery of triglycerides)

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49
Q

What does IDL transport?

A

endogenous lipids/triglycerides to peripheral tissues

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50
Q

What does LDL transport from where to where?

A

transports cholesterol from liver to peripheral tissues

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51
Q

what markers are on LDL?

A

Apo100: Binds to LDL receptor found on extrahepatic tissues and liver to be endocytosed

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52
Q
  1. What does HDL transport from where to where?
  2. What transporters does it use?
A
  1. cholesterol - moving excess cholesterol from peripheral tissues to liver
  2. ABC transporters allow HDL to pick up cholesterol
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53
Q

What markers are on HDL? (and their function)

A
  1. ApoE: triggers clearance
  2. Apo-CII - activates lipoprotein lipase
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54
Q

What markers are on IDL? (and what is their function)

A
  1. ApoE -triggers clearance
  2. ApoC-II - activates lipoprotein
  3. ApoB-100 - marker for VLDL, IDL, LDL
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55
Q

What does the CETP enzyme do?

A

Works on HDL and VLDL (VLDL transfers one triglyceride for one cholesterol on HDL)

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56
Q

What does ACAT do?

A
  1. Makes cholesterol inside hepatocyte and enterocytes
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57
Q

What does LCAT do?

A

Converts free cholesterol into cholesterol ester on HDL

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58
Q
  1. What is dyslipidemia?
  2. How many types are there?
A
  1. elevation of cholesterol, triglyceride, or both
  2. 5 types (actually 6 because theres IIa and IIb)
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59
Q

What are the two types of dyslipidemias with elevated TG only?

A
  1. Type I (familial hyperchylomicronemia)
  2. Type IV (Primary hypertriglyceridemia
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60
Q

What are the three types of dyslipidemias with both elevated TG and cholesterol?

A
  1. Type IIB (Familial combined hyperlipoproteinemia)
  2. Type III (Dysbetalipoproteinemia - remnant disease)
  3. Type V (Mixed hypertriglyceridemia)
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61
Q

What is the type of dyslipidemias with elevated cholesterol only?

A
  1. Type IIa (Familial cholesterolemia)
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62
Q

What types of dyslipidemias are associated with pancreatitis?

A

Type I, IV, and V when TGs are greater than 1000 mg/dL

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63
Q

Describe Type I hyperlipoproteinemia (familial hyperchylomicronemia)

A
  1. Individual has increased triglycerides and increased chylomicrons
  2. inability to clear chylomicrons carrying dietary triglycerides due to lipoprotein lipase deficiency - unable to metabolize chylomicrons into remnants.
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64
Q

How does Type I dyslipidemia serum look like?

A

Serum appears turbid and milky with elevated chylomicrons (even when fasting)

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65
Q

Describe Type IIa Hyperlipoproteinemia (familial hypercholesterolemia)

A
  1. Increased cholesterol and increased LDL (carry cholesterol to body)
  2. Inability to clear LDL due to either mutation in LDL receptor, ApoB, or PCSK9
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66
Q

Clinical presentations of Type IIa Hyperlipoproteinemia (familial hypercholesterolemia)

A
  • Tuberous xanthomas (firm, painless, red-yellow nodules that develop over pressure areas such as knees, elbows, heels)
  • Tendon xanthomas (cholesterol deposits in tendons)
  • Xanthelasma palpebrarum (yellow plaques over eyelids)
  • Corneal arcus (white lining around iris)
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67
Q

Describe Type IIb Hyperlipoproteinemia (Familial combined hyperlipoproteinemia)

A
  1. Increased LDL but also increase in VLDL → leads to increased cholesterol and triglycerides
  2. risk of cardiovascular disease
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68
Q
  1. Describe Type III Hyperlipoproteinemia (Dysbetalipoproteinemia) - “remnant disease”
  2. Genetic reason for this?
A
  1. Increased IDL (holds both cholesterol and triglycerides - so increase of both)
  2. ApoE2/E2 (no longer normal ApoE) - causes inability of IDL to be taken up by liver
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69
Q

Clinical findings of Type III Hyperlipoproteinemia (Dysbetalipoproteinemia) - “remnant disease”

A
  1. Serum is turbid/cloudy
  2. Striate palmar xanthomata- orange/yellow discoloration within skin creases of palm.
  3. Tuberoeruptive xanthomata - raised yellow lesions, usually on the elbows and knees
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70
Q

Describe Type IV Hyperlipoproteinemia (Primary hypertriglyceridemia)

A
  1. Increased VLDL and increased triglycerides
  2. Serum is turbid
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71
Q

Describe Type V Hyperlipoproteinemia (Mixed Hypertriglyceridemia)

A
  1. Increased VLDL and chylomicrons (leads to increased cholesterol and triglycerides)
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72
Q

What causes abetalipoproteinemia?

A
  • Loss of function mutation in MTP which means that TAGs are not transferred to chylomicrons or VLDL - nonfunctioning ApoB
  • chylomicrons, VLDL, LDL are all absent
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73
Q

What is the most common dyslipidemia?

A

Type IV

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74
Q

How do PCSK9 inhibitors work to lower LDL levels?

A
  1. PCSK9 decides in the “sorting” process whether LDL-LDLR complex should be recycled or degraded
  2. With PCSK9 inhibitors there is no change for LDLR to be degraded so it continuously is recycled.
  3. With LDLR continuously present then LDL can be picked up more from circulation thus lowering LDL
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75
Q

What is atherosclerosis?

A

Buildup of plaque along arterial walls which compromises blood flow

  • Considered an inflammatory disease
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76
Q

What is the structure of the plaque in atherosclerosis? (2)

A
  1. Fibrous cap: smooth muscle cells, macrophages, foam cells, lymphocytes, collagen, elastin, proteoglycans, neovascularization
  2. Lipid core: cell debris, foam cells, cholesterol, crystals, calcium salts (mineralization)
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77
Q

What are some risk factors for atherosclerosis? (around 7 but more)

A
  1. Hypertension
  2. Diabetes
  3. Increasing age
  4. family history
  5. male gender
  6. Hyperlipidemia
  7. Smoking and more
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78
Q

What is the process of atherosclerosis formation?

A
  1. starts with endothelial injury (endothelial cells are activated)
  2. Inflammatory cells move into intima and secrete cytokines
  3. Lipids are deposited in lesions and macrophages engulf lipids
  4. when macrophages do this they become foam cells
  5. Growth factors stimulate smooth muscle cell proliferation
  6. Results in thickened extracellular matrix (called neo-intima)
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79
Q

What makes plaques in atherosclerosis stable?

A

Thick fibrous cap

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80
Q

What is a complication of atherosclerosis?

A
  • Vulnerable plaques become complicated by rupture
  • results in thrombosis or embolism after rupture of plaque
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81
Q
  1. What is arteriosclerosis?
  2. What are the two types
A
  1. Hardening of the arteries through various forms.
  2. Hyaline arteriosclerosis and hyperplastic arteriosclerosis
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82
Q

What type of hypertension causes hyaline arteriosclerosis vs hyperplastic arteriosclerosis?

A
  1. Hyaline arteriosclerosis: mild or benign hypertension (systolic <200 mmHg and diastolic <120 mmHg)
  2. Hyperplastic arteriosclerosis: bad or malignant hypertension (<200 mmHg and diastolic <120 mmHg)
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83
Q

How does hyaline and hyperplastic arteriosclerosis differ in terms of imaging?

A
  1. Hyperplastic has onion skin pattern. Theres hyperplastic smooth muscle cells, thick and duplicated basement membrane
  2. Hyaline arteriosclerosis has endothelial damage, plasma leakage
  3. image on left is hyaline; right is hypertension
84
Q

What is Mönckeberg’s sclerosis (medial calcific sclerosis)

A
  1. calcification of the tunica media of small sized and medium sized arteries. It DOES NOT affect the lumen.
85
Q
  1. What is angina?
  2. What are the two types?
A

Myocardial pain due to ischemia but insufficient ischemia to cause myocyte necrosis

  • stable and unstable angina
86
Q

Stable vs unstable angina

  1. % obstruction
  2. Pain presentation
A

Stable angina

  1. 70% obstruction of artery. Pain usually only occurs with activity or stress and is relieved with rest
  2. 90% obstruction of artery. Pain can occur with stress and during rest. (due to vulnerable plaque)
87
Q

What microscopic findings after MI are found at

  1. 4-12 hours
  2. 1-3 days
  3. 3-14 days
  4. >2 months
A
  1. No inflammation yet- can’t detect anything until 12 hours or so
  2. starting to see inflammation all around the area of infarction (not area of infarction because blood can’t get there)
  3. Developed granulation tissue. Period of weakness in necrotic myocardial wall - most common time to see ventricular rupture.
  4. Dense fibrous tissue
88
Q

What are some re-profusion injuries that occur after revascularization therapy?

A
  1. Blood flow can cause hemorrhage in vessels already injured during MI
  2. Oxygen can create ROS which injure muscle protein and lipids- making myocytes leaky
  3. Calcium can gain entry to damaged muscle fibers and cause contraction band necrosis (image)
89
Q

What are some possible outcomes after MI event occurs? (6)

A
  1. ventricular dysfunction-heart failure
  2. Wall rupture
  3. Papillary muscle necrosis and rupture
  4. Pericarditis (swelling and irritation of pericardium)
  5. Ventricular aneurysm
  6. Aneurysm + mural thrombosis
90
Q

What is an aneurysm?

A

Localized abnormal dilation of a blood vessel or heart chamber due to weakness in vascular wall

  • vascular walls layers stay together
91
Q

What is Cystic medial necrosis/Erdheim medial degeneration?

A
  1. Loss of structural integrity of elastic tissue in larger arteries (aorta)
  2. This weakening of wall can lead to aneurysm
92
Q

What is a berry aneurysm?

A

Aneurysm of the brain stem

93
Q
  1. What is syphilitic aneurysm?
  2. What causes can be associated with this?
A
  1. located in the ascending aorta
  2. Atherosclerosis, hypertension, tertiary syphilis, and cystic medial necrosis
94
Q

What is mycotic aneurysms?

A

Infections that result in weakening of abdominal aorta (not fungal though)

95
Q
  1. What is aortic dissection?
  2. What population is most likely to show this?
A
  1. Splitting of the layers of the vascular wall by blood under pressure
  2. Caucasian men in their 5th-7th decade of life
96
Q

What is the mechanism of action of statins?

A
  1. HMG-CoA reductase inhibitor - inhibit conversion o f HMG-CoA to mevalonate (a cholesterol precursor)
  2. Statins are anti-inflammatory
97
Q
  1. What CYP metabolizes statins?
  2. What food inhibits the metabolism of statins?
A
  1. CYP3A4 and CYP2D6
  2. grapefruit juice inhibits CYP3A4
98
Q
  1. What is the main adverse effect of statins?
  2. What drug combination may increase risk of adverse effects?
A
  1. myopathy
  2. Azole antifungals, macrolide antibiotics
99
Q

What are some monitoring parameters for statins?

A
  1. No need for routine monitoring of liver enzymes blood test - but this should be done in liver disease patients
  2. Statin meds are generally safe and have low incidence of liver toxicity
100
Q

For what abnormality (in cholesterol) is statins primarily used for?

A
  1. LDL dominant hypercholesterolemia (for dyslipidemia treatment)
101
Q

For what abnormality (in triglycerides) is fibrates primarily used for?

A
  1. VLDL dominant hypertriglyceridemia
102
Q

What are examples of fibrate drugs?

A
  1. Gemfibrozil
  2. Fenofibrate
103
Q

What is the mechanism of action of fibrates? (2)

A
  1. (For dyslipidemia treatment)Activate PPAR alpha receptors which leads to transcription factors inducing increase in synthesis of lioprotein lipase (decrease amount of triglycerides circulating in blood)
  2. Decrease synthesis of VLDL
  3. Both lead to decrease in triglycerides
104
Q

What are some side effects of fibrates? (2)

A
  1. can increase statin concentration → leads to myopathy risk
  2. GI discomfort
105
Q

Contraindications of fibrates?

A
  1. significant liver or kidney disease
106
Q

What is the mechanism of action of icosapent ethyl (purified omega 3 fatty acids)

A
  1. (for dyslipidemia treatment ) reduces VLDL synthesis and/or secretion (decreases TG presence in blood)
  2. Increases beta oxidation which decreases triglyceride levels (breaking down of fatty acids (found in triglycerides) to get acetyl CoA)
  3. Also activates PPAR alpha receptors → increases LPL
107
Q
  1. Examples of bile acid resins?
  2. For what abnormality (in cholesterol) is bile acid resins primarily used for?
  3. Mechanism of action?
A
  1. cholestyramine, colestipol, colesvelam
  2. LDL dominant - hypercholesterolemia
  3. Resins prevent intestinal reabsorption of bile acids; liver then must use cholesterol to make more bile (for dyslipidemia treatment)
108
Q
  1. what is an example of cholesterol absorption blockers?
  2. Mechanism of action
  3. For what abnormality (in lipds) are cholesterol absorption blockers primarily used for?
A
  1. ezetimibe
  2. (for dyslipidemia treatment) Prevent cholesterol absorption at small intestine (targets NPCL1 to inhibit cholesterol absorption, decreases cholesterol incorporation into chylomicrons, lowers cholesterol delivery to liver)
  3. LDL hyperlipidemia
109
Q
  1. What is ezetimibe + statins meant for?
  2. What is ezetimibe + fenofibrate for?
A
  1. elevated LDL and mixed hyperlipidemia
    1. ezetimibe decreases cholesterol delivery to liver + statins inhibit cholesterol production
  2. Mixed hyperlipidemia
110
Q

What is mixed hyperlipidemia?

A

higher than usual levels of cholesterol and triglycerides

111
Q
  1. What are some examples of PCSK9 inhibitor?
  2. Mechanism of action?
A
  1. evolocumab, alirocumab
  2. Antibodiy against PCSK9 so PCSK9 doesn’t chaperone LDL receptor and lead to its destruction. With LDL recycling it allows for continuous “pick up” of LDL in bloodstream (for dyslipidemia treatment)
112
Q

What is the mechanism of action of bempedoic acid?

A
  1. inhibits ATP-citrate lyase (which makes acetyl coA, a precursor to cholesterol) - for dyslipidemias
113
Q

What is mechanism of action of niacin (vitamin B3)/as a treatment of what?

A
  1. Inhibits lipolysis in adipose tissue (decreasing fatty acid mobilization from adipose tissue which leads to inability to make VLDL)
  2. Reduces hepatic VLDL synthesis
  3. For treatment of dyslipidemias
114
Q

What is vasculitis?

A

Inflammation of blood vessels

115
Q

What three things can cause vasculitis?

A
  1. Immune mediated inflammation (indirect effect of infectious disease)
  2. Direct vascular invasion by infectious agents
  3. Physical and chemical injury
116
Q

What antibodies are found in some types of vasculitis? (2 types)

A
  1. PR3-ANCA
  2. MPO-ANCA
  • high titers tend to reflect larger disease severity
117
Q

Giant Cell Arteritis (temporal arteritis)

  1. What size vessel does this effect?
  2. What specific vessels does it effect?
  3. Most common in what populations?
A
  1. Large vessel
  2. Carotid artery and temporal branch in the head
  3. older adults in developed countries
118
Q

Giant Cell Arteritis (temporal arteritis)

  1. What are microscopic findings (3)
A
  1. Granulomatous inflammation with nucleated giant cells. Giant cells embedded in the elastic lamina between tunica intima and tunica media
  2. Infiltration of lymphocytes and macrophages.
  3. Fibrous growth in middle of lumen which leads to less blood flow.
119
Q

Giant Cell Arteritis (temporal arteritis)

  1. Clinical findings/symptoms
  2. Complications
  3. Treatment
A
  1. Headaches, visual disturbances, and pain with chewing. High ESR levels due to inflammation.
  2. Can lead to permanent blindness if not treated
  3. Corticosteroids and anti-TNF therapies
120
Q

Takayasu Arteritis (pulseless disease)

  1. What size vessel does this effect?
  2. What specific vessels does it effect?
  3. Most common in what populations?
A
  1. large vessels
  2. arteries that branch off of the aortic arch- aorta has scarring and thickening;; arch vessels with luminal narrowing;; causes weak/nonexistent pulse unilaterally or bilaterally + neurological symptoms
  3. asian women under 4o years old
121
Q

Takayasu Arteritis (pulseless disease)

  1. What are microscopic findings (2)
A
  1. Granulomatous inflammation with giant cells. Inflammatory cells migrate and cause vessel wall thickening and blood vessels narrowing.
  2. Giant cells are seen in elastic lamina (between intimal and medial layer)
122
Q

Takayasu Arteritis (pulseless disease)

  1. clinical symptoms
A
  1. with progression you can get reduced upper extremity blood pressure and pulse strength
  2. Neuro deficits
  3. Ocular disturbances
123
Q

Polyarteritis Nodosa

  1. What size vessel does this effect?
  2. What specific vessels does it effect?
  3. Most common in what populations?
A
  1. Medium vessel
  2. small and medium sized muscular arteries (spares pulmonary vessels)
  3. Primarily Young Adults
124
Q

Polyarteritis Nodosa

  1. pathogenesis
A
  1. Immune cells directly attack the endothelium, confusing it for Hep B
  2. Leads to necrotizing inflammation and fibrinoid necrosis → This inflammation/damage to lining of vessels leads to formation of blood clots
  3. Very prone to aneurism due to weakened vessel wall
125
Q

Polyarteritis Nodosa

  1. morphology changes
  2. findings in angiogram
A
  1. Pink band is seen on microscope imaging. The band is fibrinoid necrosis and surrounded by inflammatory tissue
  2. Angiogram - looks like a string of beads
126
Q

How is polyarteritis nodosa treated?

A

Immunosuppression

127
Q

Kawasaki disease (mucocutaneous lymph node syndrome)

  1. What size vessel does this effect?
  2. What specific vessels does it effect?
A
  1. Affects large to medium sized arteries
  2. Affects coronary arteries which can lead to aneurysms (aneurysms can rupture or thrombose)
    3.
128
Q

Kawasaki disease (mucocutaneous lymph node syndrome)

  1. Morphologic changes
A
  1. healing may result in obstructive intimal thickening (similar to polyarteritis nodosa)
129
Q

Kawasaki disease (mucocutaneous lymph node syndrome)

  1. What are the symptoms?
  2. How is it treated
A
  1. CRASH and Burn mneumonic
  • Conjunctivitis
  • Rash
  • Adenopathy
  • Strawberry tongue
  • Hand swelling (and feet)
  • “Burn” → fever >5 days
  1. IV immunoglobulin and aspirin
130
Q

Granulomatosis with Polyangiitis (GPA/Wegners granulomatosis)

  1. What antibody is found in this disorder
  2. Pathogenesis
  3. Classic patient
A
  1. PR3-ANCA
  2. Likely initiated as a cell mediated hypersensitivity response to an inhaled infectious or environmental antigens
  3. Middle aged male
131
Q

Granulomatosis with Polyangiitis (GPA/Wegners granulomatosis)

  1. Tissue biopsy results
A
  1. GPA triad
  • Necrotizing tissue granulomas (upper respiratory tract, lower respiratory tract, or both)
  • Necrotizing granulomatous vasculitis (affect small to medium sized vessels - most often in lungs and upper airways)
  • Focal necrotizing glomerulonephritis (inflammation/damage to filtering part of kidneys/glomerulus)
132
Q

Granulomatosis with Polyangiitis (GPA/Wegners granulomatosis)

  1. Clinical symptoms
A
  1. bilateral pneumonitis w/nodules and cavitary lesions
  2. Chronic sinusitis (inflammation of tissue lining in the sinuses)
  3. Rash, myalgias, arthralgias, etc
133
Q

Granulomatosis with Polyangiitis (GPA/Wegners granulomatosis)

  1. How is it treated?
A
  1. steroids
  2. cyclophosphamide
  3. TNF inhibitors
  4. Anti-B cell antibodies
134
Q

Microscopic Polyangiitis (hypersensitivity vasculitis or leukocytoclastic vasculitis)

  1. What antibody is found in this disorder
  2. What size vessels does this effect?
  3. Pathogenesis
  4. How is it treated?
A
  1. MPO-ANCA
  2. small vessels
  3. Can be caused by drugs, microorganisms, etc - MPO-ANCA antibody is responsible for activation and recruitment of neutrophils within vascular beds (capillaries, arterioles, and venules) causing the disease.
  4. immunosuppression and removal of offending agent
135
Q

Microscopic Polyangiitis (hypersensitivity vasculitis or leukocytoclastic vasculitis)

  1. Morphologic changes
A
  1. Necrotizing vasculitis.
  2. Fibrinoid necrosis (irreversible, uncontrolled cell death that occurs when antigen-Ab complexes are deposited in the walls of blood vessels along with fibrin)
  3. NO GRANULOMAS PRESENT
  4. Little black dots are fragment neutrophils around lesions (bright pink spot) → multiple lesions show same level of healing
136
Q

Churg-Strauss Syndrome (eosinophilic granulomatosis with polyangiitis)

  1. What antibody is found in this disorder
  2. What size vessels does this effect?
  3. Pathogenesis
A
  1. MPO-ANCA (in 30-40% of cases)
  2. Small vessels
  3. Hyper-responsiveness to some normally innocuous allergic stimulus
137
Q

Churg-Strauss Syndrome (eosinophilic granulomatosis with polyangiitis)

  1. Morphologic changes
A
  1. Lesions have granulomas and eosinophils
  2. Red dots on images are eosinophils
138
Q

Buerger’s disease (thromboangiitis obliterans)

  1. What size vessels does this effect? (also what vessels were affected)
  2. Pathogenesis
  3. Typical patient
A
  1. small vessels;; tibial and radial arteries
  2. Acute+chronic inflammation of small sized arteries. → direct endothelial cell toxicity caused by some component of tobacco;;; inflammation can extend into adjacent veins and nerves
  3. men between 20-40 years old (biggest risk factor is smoking)
139
Q

Buerger’s disease (thromboangiitis obliterans)

  1. morphology changes
  2. Symptoms
A
  1. Veins have been seen to thrombose off in angiogram
  2. Raynaud phenomenon, foot pain induced by exercise, chronic extremity ulcers
140
Q

Henoch-Schonlein Purpura

  1. pathogenesis
  2. Antibody
A
  1. abnormal immune response in small vessels → IgA antibody immune complexes caused by antigenic exposure from an infection or medication deposit in small vessels.
  2. IgA
141
Q

What causes varicose veins?

A
  1. abnormally dilated veins produced by chronically increased blood pressure and weakened vessel walls
  2. Incompetence of the valves in the veins can leads to stasis, edema, pain, thrombosis
142
Q
  1. What is thrombophlebitis?
  2. What are two types?
A
  1. Inflammation of the wall of a vein that causes a blood clot/thrombosis to form.
  2. DVT (deep vein thrombosis) and superficial thrombophlebitis
143
Q
  1. What is phlebothrombosis?
A
  1. presence of a clot within a vein, unassociated with inflammation of the wall of the vein
144
Q
  1. What is superior and inferior vena cava syndrome?
  2. What are the symptoms
A
  1. Blockage of the respective vena cava. Usually caused by a neoplasm that compresses or invades the vena cava.
  2. Edema and cyanosis of the upper and lower body respectively can occur. Pulmonary vessels can be compressed leading to a respiratory distress.
145
Q
  1. What is a hemangioma?
  2. Where are they often found?
  3. What are the three types
  4. Which type is most common
A
  1. benign tumor of blood vessels, very common
  2. typically localized to the head and neck
  3. Capillary, Juvenile, and cavernous
  4. Capillary hemangioma
146
Q
  1. Describe structure of Capillary Hemangioma? (most common)
A
  1. occurs in thin walled capillaries with scant stroma (connective tissue cells)
147
Q
  1. Describe Juvenile (strawberry) hemangioma presentation
  2. microscopic imaging description
A
  1. There can be multiple juvenile hemangiomas and involves the skin (skin lesions regress by age 7) —a common type of birthmark, occurring in about 4 percent of infants. They are made up of collections of immature blood vessels that often grow rapidly, sometimes dramatically, during infancy.
  2. Has lobular architecture
148
Q
  1. Describe Pyogenic granuloma presentation
A
  1. This is a rapidly growing red pedunculated lesion on the skin, gingiva, or oral mucosa.
  2. It can bleed or ulcerate and is associated with trauma
149
Q
  1. Describe Cavernous hemangioma microscopic description
A
  1. large dilated areas/vascular channels that are blood filled;;; do not spontaneously regress
  2. Have a tendency to thrombose and often calcify
150
Q
  1. What is kaposi sarcoma?
  2. What is it caused by
A
  1. Vascular neoplasm - causes lytic and latent infection of endothelial cells
  2. HHV-8
151
Q

What are the 4 types of kaposi sarcoma?

A
  1. Classic kaposi sarcoma
  2. Endemic african KS
  3. Transplant associated KS
  4. AIDS associated KS
152
Q

Classic Kaposi Sarcoma

  1. Clinical features
  2. HIV status
  3. Risk factors?
  4. Morphology
A
  1. Classic KS causes red and purple plaques on distal lower extremities. Associated with malignancy or altered immunity.
  2. NOT ASSOCIATED WITH HIV
  3. Older men of mediterranean and Ashkenazi jewish descent
  4. Three stages: patches, plaques, nodules
153
Q

Endemic African Kaposi Sarcoma

  1. Clinical features
  2. Risk factors
  3. HIV status
A
  1. Chronic, nodular condition predominantly affecting feet and legs.
  2. Younger people, usually. Can have indolent or aggressive course.
  3. HIV negative.
154
Q

Transplant associated Kaposi Sarcoma

  1. Clinical features
  2. Risk factors
A
  1. Usually aggressive. Often involves LNs, mucosa, and viscera
  2. Occurs in organ transplant with T-cell immunosuppression.
155
Q

AIDS associated kaposi sarcoma

  1. Clinical features
  2. HIV status
A
  1. Involves LNs and viscera early in course
  2. HIV positive; Most common HIV related malignancy
156
Q

Angiosarcoma

  1. Pathology
  2. Where is it most often found?
  3. Common patient?
  4. Clinical features
A
  1. Rare cancer that develops in the inner lining of blood vessels and lymph vessels.
  2. skin, soft tissue, breast, liver
  3. older adults
  4. Red nodules to large fleshy red/gray white masses with ill defined margins
157
Q

Angiosarcoma

  1. what do malignant cells stain positive for?
A
  1. CD31 and von willebrand factor
158
Q

Myxoma

  1. Description
  2. Microscopic imaging description
A
  1. Typically arise in the atria and Pedunculated forms swing around causing a wrecking ball- can obstruct and damage valves
  2. Stellate (star form cells), sometimes multinucleated cells
159
Q

Rhabdomyoma

  1. Pathology
  2. Genetic Mutations
  3. Morphology
A
  1. noncancerous tumor that typically grows in clusters in the heart. Usually grow in the muscles of the left and right ventricles. → removal is necessary if restricts flow
  2. TSC1 or TCS2 tumor suppressor genes
  3. image
160
Q

Nitrates

  1. Purpose/Mechanism of action
  2. drug names (3)
  3. Effects on baroreflex?
A
  1. For arterial disease- serves as vasodilators to alleviate symptoms
    1. NO donors activate guanylate cyclase that dephosphorylates myosin light chains and leads to vascular relaxation
  2. Nitroglycerine, nitroprusside, isosorbide dinitrate
  3. Stays intact so when dilation occurs; blood pressure drops, adrenergic push leads to incrase HR and contractility
161
Q

Nitroglycerine (type of nitrate)

  1. What special steps does this drug require when metabolized?
  2. What happens with continuous use of nitroglycerine?
A
  1. requires activation by aldehyde dehydrogenase (which is more prevalent in veins) → thus more effective on veins
  2. Can lead to tolerance
162
Q

Main side effects of nitrates?

A
  1. tachycardia
  2. throbbing headache
  3. orthostatic hypertension
163
Q

Contraindications of nitrates?

A
  1. Don’t use with erectile dysfunction meds
  2. Do not use with patients that have intracranial pressure
  3. Don’t use with patients that have left ventricular outflow obstruction
164
Q

Beta blockers

  1. Purpose
  2. Mechanism of action
  3. Examples
A
  1. Treatment of arterial disease
  2. Decrease beta adrenergic (epinephrine) input in the heart; leads to lower heart rate, reduced contractility, reduces BP
  3. Metropolol, propanolol
165
Q

Side effects of beta blockers? (5)

A
  1. Asthma exacerbation (with B2 antagonists) → for this reason avoid with asthma patients
  2. Decrease in glycogenolysis and then eventually hypoglycemia (beta 2 beta blockers) → avoid in insulin dependent diabetics
  3. Bradycardia → avoid in patients with AV disturbances
  4. Cold extremities → don’t use in reynaud’s
  5. Nightmares
166
Q

Calcium channel blockers

  1. purpose
  2. mechanism of action
  3. two types
A
  1. treatment for arterial disease
  2. Blocks L type calcium channels in heart, slowing contraction, decreasing arterial pressure, contractility, and heart rate
  3. Dihydropyridines and non-dihydropyridines
167
Q

Calcium channel blockers (dihydropyridines)

  1. Where are these most active
  2. What type of channels does this bind to?
  3. What do these drugs end in?
  4. What type of angina is this best used for?
  5. How is it excreted?
A
  1. More active in blood vessels
  2. tends to bind inactive channels
  3. -dipine
  4. Prinzmetal angina (spastic)
  5. by kidney
168
Q

Calcium channel blockers (non-dihydropyridines)

  1. Where are these most active
  2. What type of channels does this bind to?
  3. Two drug names to know
  4. How is each drug excreted?
A
  1. more active in heart
  2. tend to bind to open active calcium channels
  3. Verapamil and diltiazem
  4. Verapamil excreted via kidney; diltiazem excreted via liver
169
Q

Side effects of verapamil?

A
  1. drug induced heart block
  2. verapamil+statins - myopathy
  3. Hypotensive if mixed with erectile dysfunction drugs
  4. Constipation
170
Q

Side effects of diltiazem?

A
  1. drug induced heart block
171
Q
  1. What drug(s) do you use for immediate relief of arterial disease?
  2. What about for long term prevention of arterial disease
A
  1. nitrates
  2. beta blockers (if ineffective use calcium channel blockers)
172
Q

What is the purpose of combining nitrates and beta blockers?

A

the beta blockers block baroreflexes still active in nitrates

173
Q
  1. What is the purpose/mechanism of action of ranolazine?
  2. side effects?
A
  1. (to treat arterial disease) selective inhibitor of late inward sodium current….leads to decrease in myocardial contractility and decreased oxygen demand
  2. Prolonged QT interval, headache, dizziness, constipation
174
Q
  1. What is the purpose/mechanism of action of ivabradine?
  2. side effects?
A
  1. inhibits funny current in SA node to decreases heart rate
  2. Bradycardia
175
Q

What is peripheral artery disease?

A
  1. narrowed arteries reduce blood flow to your limbs
176
Q
  1. Purpose of cilostazol?
  2. What is mechanism of action of cilostazol
A
  1. for management of peripheral artery disease
  2. inhibits phosphodiesterase activity and results in vasodilation. Inhibits platelet aggregation
177
Q
  1. Purpose of pentoxifylline?
  2. What is mechanism of action of pentoxifylline
A
  1. management of peripheral artery disease
  2. inhibits phosphodiesterase activity and results in vasodilation. Inhibit TNF and leukotriene synthesis.
178
Q

On an EKG showing STEMI

  1. What three things should be seen?
A
  1. ST elevation <1 mm (one little box)
  2. ST elevation must be in two contiguous leads for MI diagnosis
  3. Reciprocal changes in another zone
179
Q

What are two patterns showing pathological Q waves?

A
  1. Q waves start getting wider (>1 little box wide)
  2. Q wave is about same size or bigger than QRS complex
  • means patient had a heart attack and heart is trying to figure out how to move electrical signal through the damaged heart tissue
180
Q
  1. changes in ST elevation in V1-V4 indicate what position of heart was affected?
  2. What about V5, V6, I, and aVL
  3. What about leads II, III, and aVF
A
  1. Anterior
  2. lateral
  3. inferior
181
Q

Subendocardial infarction with show ST elevation or depression?

A
  1. ST depression
  • subendocardial means innermost aspect of the myocardium
  • But if its a very large ST depression then it might be a STEMI on the posterior side of heart→ need new EKG
182
Q

What does T wave inversion or flattening mean?

A
  1. heart is most likely struggling and needs to be looked into more
183
Q

Where should Q waves not be seen?

A

V1-V3

184
Q

What is structural, process, and outcome measures?

A
  • Structural measure gives consumers a sense of a health care provider’s capacity, systems, and processes to provide high quality care (like using electronic medical records, number of board certified physicians, etc)
  • Process measures indicate what the provider does to maintain or improve health (like % of preventative services)
  • Outcome measures reflect the impact of the health care service or intervention on the health status of the patient (like % of patients who died as a result of surgery, rate of complications)
185
Q

The heart develops from the (BLANK) layer of the lateral plate of mesoderm.

A
  1. splanchnic layer
186
Q
  1. Identify the myocardium, cardiac jelly, and endocardial tube
A

image

187
Q

Explain how the transverse pericardial sinus appears?

  • Starting with heart as a single midline tube
A
  • as the heart tube loops, the venous and arterial poles approach one another, and the segment of dorsal mesentery between the poles disappears, creating the transverse pericardial sinus
188
Q

Identify the layers to the heart tube

A
  1. sinus venosus (right horn and left horn)
  2. Primitive atrium
  3. Primitive ventricle
  4. Bulbus cordis (proximal part)
  5. Bulbus cordis (middle part)
  6. Bulbus cordis (distal part -arterial end)
189
Q

What does the Right horn of the sinus venosus become?

A

Right atrium

190
Q

What does the left horn of the sinus venosus become?

A

coronary sinus

191
Q

What does the primitive atrium become?

A

right and left atria

192
Q

What does the primitive ventricle become?

A

left ventricle

193
Q

What does the bulbus cordis (proximal part) become?

A

Right ventricle

194
Q

What does the bulbus cordis (middle part) become?

A
  1. conus arteriosus (in right ventricle)
  2. Aortic vestibule (in left ventricle)
195
Q

What does the bulbus cordis (distal part) become?

A
  1. Pulmonary trunk
  2. Aorta
196
Q

Identify

  • Septum primum
  • Foramen primum
A

image

*oxygenated blood comes into RA from placenta

  • foramen primum allows blood from RA to LA
197
Q

Identify

  1. Foramen secundum
  2. Foramen primum
  3. Septum primum
A
  • Foramen secundum binds to endocardial cushions (at bottom of image) but opening forms at top to continue to allow blood flow from RA to LA
198
Q

Identify

  1. Septum secundum
  2. Septum primum
  3. Foramen ovale
A

In top left image

  • allows for blood flow from RA to LA
  • Foramen ovale closes after birth
199
Q

Through foramen ovale opening → how does blood move from RA to LA

A

RA has higher pressure than left atrium (lower pressure)

  • After birth left atrium gains more pressure so septum primum doesn’t allow shunt
200
Q

What is the ductus arteriosus?

A
  1. connection between pulmonary trunk and arch of aorta
  2. Blood that is supposed to go into lungs (doesn’t because baby is in vitro) instead gets dumps blood into aortic arch and eventually to placenta → via ductus arteriosus
201
Q

Aortic arch arteries (coming from truncus arteriosus) → arises from right and left horns

  • each horn is continuous (Blank A) arch arteries
A
  1. 6 arch arteries
202
Q

In embryologic structures

  1. What does the 1st arch artery derive into
  2. 2nd arch artery
  3. 3rd arch artery
  4. 4th arch artery (left and right)
  5. 5th arch artery
  6. 6th arch artery (left and right)
A
  1. mostly disappears but also maxillary artery in head
  2. mostly disappears but also Hyoid and stapedial arteries
  3. common carotid artery
  4. Right (right subclavian artery- proximal portion); left (distal portion of the aortic arch)
  5. disappears
  6. Right (right pulmonary artery); Left (left pulmonary artery +ductus arteriosus)
203
Q

What is door to balloon time?

A

the time between the arrival of a patient with STEMI in the emergency room until the time that a balloon is inflated in the occluded, culprit coronary artery.

204
Q

What is the ideal door to balloon time?

A

90 minutes

205
Q

What is cardiac tamponade?

A

compression of the heart by an accumulation of fluid in the pericardial sac.

206
Q

giant cell arteritis vs takayasu arteritis

  1. age
  2. symptoms
  3. mostly affects what vessels
  4. treatment
A

image

207
Q

Aortic dissection key clinical findings

  1. symptoms
  2. BP
  3. Mediastinum in X-ray
A
  1. Ripping chest pain
  2. pulse/BP changes between arms
  3. Widened mediastinum

Block 4 (8 decks)

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