CVS

To what are the Atrial and venticular myocardial fibers attatched to?To the fibrous skeleton of the heart CVS, CVS_physiology CVS_physiology_1 what is the fibrous skeleton made of?"the union of four fibrous rings <div><br></div><div><img src=""fIIKks04522cSyM1uthdg_Anulus_fibrosus_dextra__Valva_atrioventricularius_dextra__02.png""><br></div>"CVS, CVS_physiology CVS_physiology_1 what are each of the fibrous skeleton rings attatched to?attatched to the four cardiac valves - tricuspid, mitral, aortic, pulmonaryCVS, CVS_physiology CVS_physiology_1 There is no {{c1::muscular}} communication between the atria and the ventricles CVS, CVS_physiology CVS_physiology_1 Cardiac muscle is {{c1::red and stirated}}, as in skeletal muscle (appearance), however cardiac muscle behaves like {{c2::smooth muscle }}CVS, CVS_physiology CVS_physiology_1 the myocardium is {{c1::regulated}} by nerves, not {{c2::operated}}CVS, CVS_physiology CVS_physiology_1 in relation to nuclei, the cardiac muscle is a {{c1::syncyitum }}CVS, CVS_physiology CVS_physiology_1 Individual myocardial cells are connected in series and in parallel with one another by the {{c1::intercalated discs}}.CVS, CVS_physiology CVS_physiology_1 intercalated discs have what type of junctions?Gap junctionsCVS, CVS_physiology CVS_physiology_1 intercalated discs have gap junctions that allow {{c1::rapid diffusion of ions and action potential}}.CVS, CVS_physiology CVS_physiology_1 The heart actually is composed of two syncytiums: {{c1::the atrial syncytium}}, and {{c2::the ventricular syncytium}}. why is the heart divided into two different functional syncytiums?To allow the atria to contract a short time ahead of ventricular contraction, which is important for the effectiveness of heart pumping.CVS, CVS_physiology CVS_physiology_1 can contraction be graded when it comes to the myocardium?Yes.CVS, CVS_physiology CVS_physiology_1 in the myocardium, {{c1::Initial length}} is not fixedDifferences Between Myocardium and Skeletal MuscleCVS, CVS_physiology CVS_physiology_1 the myocardium requires {{c1::extracellular Ca2+}} for its contractionDifferences Between Myocardium and Skeletal MuscleCVS, CVS_physiology CVS_physiology_1 Can the myocardium be tetanized? if not, then how does it act?Cannot be tetanized, acts as repeated simple muscle twitches.CVS, CVS_physiology CVS_physiology_1 which is more powerful: the myocardium or skeletal muslcesskeletal muscles are more powerful.<div><br></div>CVS, CVS_physiology CVS_physiology_1 {{c1::The myocardium}} cannot be fatigued practically CVS, CVS_physiology CVS_physiology_1 which can be stretched more: the myocardium or skeletal muscles?the myocardium, 4-6x that of skeletal muscle CVS, CVS_physiology CVS_physiology_1 The mode of contraction in the myocardium is {{c1::isotonic}} and {{c1::auxotonic}}isotonic = changes in length, movement occurs<div><br></div><div>auxotonic - ask about this </div>CVS, CVS_physiology CVS_physiology_1 Mention the 2 types of cardiac valves atrioventricular (AV) --> mitral & tricuspid <div><br></div><div>semilunar --> pulmonic and aortic</div>CVS, CVS_physiology CVS_physiology_1 "Cardiac valves' leaflets consist of?"Thin flaps of <b>flexible</b>, <b>tough</b>, <b>endothelium-covered</b> fibrous tissue. CVS, CVS_physiology CVS_physiology_1 what do cardiac valves attach to?"they are firmly attatched at the base to the fibrous skeleton rings<div><br><img src=""The-Four-Valves-of-the-Heart.jpg""><br></div>"CVS, CVS_physiology CVS_physiology_1 Movement of the valve leaflets is essentially {{c1::passive}}<br><br><br><div>because it depends on pressure. If pressure is too high it will automatically close, if its too low it will close!<div><br></div></div>CVS, CVS_physiology CVS_physiology_1 the {{c1::orientation of the cardiac valves}} is responsible for the unidirectional flow of blood through the heart.CVS, CVS_physiology CVS_physiology_1 location of the tricuspid valvelocated between the <b>right atrium</b> and the <b>right ventricle</b><div><div><div><b><br></b></div></div></div>CVS, CVS_physiology CVS_physiology_1 location of mitral valvelies between the<b> left atrium</b> and the <b>left ventricle</b>CVS, CVS_physiology CVS_physiology_1 mitral valve has {{c1::two}} cuspsCVS, CVS_physiology CVS_physiology_1 "AV valves' shape?"funnel CVS, CVS_physiology CVS_physiology_1 what is attatched to the free edges of AV valves?chordae tendineaeCVS, CVS_physiology CVS_physiology_1 {{c1::chordae tendineae}} are fine, strong ligaments that arise from the powerful {{c2::papillary muscles}} of the respective ventricles.CVS, CVS_physiology CVS_physiology_1 {{c2::The chordae tendineae}} prevent the valves from becoming {{c1::everted}} during ventricular systole<br><br><div><br></div><div>stops them from opening during vent. contraction </div>CVS, CVS_physiology CVS_physiology_1 what are the semilunar/outlet valves?pulmonic and aortic valvesCVS, CVS_physiology CVS_physiology_1 pulmonic valve is located between the {{c1::right ventricle}} and the {{c1::pulmonary artery}}CVS, CVS_physiology CVS_physiology_1 aortic valve is located between {{c1::the left ventricle}} and {{c1::the aorta}}.CVS, CVS_physiology CVS_physiology_1 {{c1::Four}} sounds are usually generated by the heart, but only <div>{{c1:: two}} are ordinarily audible through a stethoscope.</div><div><br></div><div><br></div>CVS, CVS_physiology CVS_physiology_1 The first heart sound is initiated at the onset of {{c1::ventricular systole}} and reflects {{c1::closure of the AV valves}}CVS, CVS_physiology CVS_physiology_1 The second heart sound occurs with {{c1::the abrupt closure of the semilunar valves.}}<div><br></div><div><br></div>CVS, CVS_physiology CVS_physiology_1 Valvular lesions (such as stenosis or incompetence) are usually associated with {{c1::heart murmurs}}CVS, CVS_physiology CVS_physiology_1 The fibrous pericardium is connected to the posterior surface of the sternum by the {{c1::sternopericardial ligaments}}(you should already know this :p) CVS, The serous pericardium is reflected at the {{c1::roots of the great vessels}} to form 2 layers: {{c1::parietal and visceral }}"<img src=""pericardium.gif"">"CVS, Parietal Serous Pericardium lines the {{c1::fibrous pericardium}}"<img src=""pericardium.gif"">"CVS, the visceral serous pericardium is often called the {{c1::epicardium}}CVS, Visceral Serous Pericardium covers the {{c1::entire surface of the heart}}CVS, The space between the parietal and visceral layers is called the {{c1::pericardial cavity.}}"<img src=""pericardium.gif"">"CVS, what does the pericardial cavity normally contain?a thin film of fluid, the pericardial fluid.CVS,  the pericardial fluid functionacts as a lubricant to facilitate the movements of the heart within the pericardiumCVS, The transverse sinus location "It is situated above the heart, between the ascending aorta and pulmonary trunk in front, and the superior vena cava, left atrium and pulmonary veins behind<br><br><img src=""paste-373e21ec17c0ca44381d74d29c8086d932c5ef76.jpg""><br><br><img src=""060717_0916_SINUSESOFPE1.jpg""><img src=""echo14211-fig-0003-m.jpg""><br>"CVS, {{c1::The Transverse Sinus}} connects the two sides of the pericardial cavity"<br><div><br><br></div><div><br></div><div>""The Transverse Sinus is the <b>transverse communication</b> between the left and right parts of the pericardial space""<br></div>"CVS, why is the transverse sinus called so?"because it is a <b>transverse </b>passage between parietal and visceral layers of the serous membrane. <img src=""paste-cb937109b1eed5e7697c0d2f551a986b34cdee14.jpg"">"CVS, the transverse sinus is is the remnant of an aperture in {{c1::the dorsal mesocardium}}CVS, oblique sinus is called so because?"It is an oblique passage between the parietal and visceral layers of the serous pericardium<div><br></div><div><img src=""fractures1.gif""><br></div><div><br></div><div><img src=""echo14211-fig-0003-m.jpg""><br></div>"CVS, oblique sinus location "behind the heart, between the left atrium,<div>in front and the fibrous pericardium behind, </div><div><br></div><div>posterior to which the esophagus descends.<br><br><div><img src=""echo14211-fig-0003-m.jpg""> <br></div></div>"CVS, SA node is responsible for {{c1::autorhythmicity}} in the heart CVS, CVS_physiology CVS_physiology_2 SA node is the {{c1::pacemaker}} of the heart CVS, CVS_physiology CVS_physiology_2 The normal rate of the SA node is {{c1::70 to 80 times}} per minuteCVS, CVS_physiology CVS_physiology_2 the internodal and interatrial bands are responsible for {{c1::conduction}} in the heartCVS, CVS_physiology CVS_physiology_2 where is the AV node located?posterior wall of the right atriumCVS, CVS_physiology CVS_physiology_2 Function of the AV nodedelay conductionCVS, CVS_physiology CVS_physiology_2 (heart) The parasympathetic fibers are derived from the {{c1::Vagus nerve}} Stimulation of the sympathetic produces {{c1::acceleration}} of the heart, whereas vagal stimulation results in {{c1::slowing}} of the heart efferent or afferent fibers in the heart?both - vagus and sympathetic lipoprotein particles include (1) {{c1::Chylomicrons}}, (2) {{c1::Very-low-density lipoproteins (VLDLs)}}, (3) {{c1::Low-density lipoproteins (LDLs)}}, (4) {{c1::High-density lipoproteins (HDLs)}}.<br><br>1 CVS_biochemistry CVS_biochemistry_1 Lipoproteins differ from each other in {{c1::lipid and protein composition}}, {{c1::size}}, {{c1::density}}, and {{c1::site of origin}}.1 CVS_biochemistry CVS_biochemistry_1 We always measure the plasma lipids concentration in the {{c1::fasting state}}1 CVS_biochemistry CVS_biochemistry_1 Why do we measure plasma lipids in the fasting state?because we don’t want the lipids gained from food to influence the real value of each type of lipids1 CVS_biochemistry CVS_biochemistry_1 Lipoproteins are composed of a {{c1::non-polar lipid }} core, containing {{c1::Triacylglycerol (TAG) and cholesteryl esters (CE).<div></div>}}<div><br></div><div>Surrounded by a shell of amphipathic {{c1:: apolipoproteins}}, {{c1::phospholipid (PL)}}, and {{c1::non-esterified cholesterol}}.</div><div><br></div><div><br></div><br><div>lipoproteins: Nonpolar core surronded by a amphipathic core </div><div><br>*Amphipathic: Chemical compound possessing both hydrophilic (water-loving, polar) and lipophilic (fat-loving) properties. Free cholesterol, PL, apo. <br></div><div><br></div><div><br></div>1 CVS_biochemistry CVS_biochemistry_1 how are lipoproteins soluble in water?amphipathic compounds are oriented such that their polar portions are exposed on the surface of the lipoprotein, thereby rendering the particle soluble in an aqueous solution.1 CVS_biochemistry CVS_biochemistry_1 "how did the human body ""solve"" the problem of transporting lipids in blood?"the neutral non-polar lipid core (TAG, CE)<div><br></div><div><br></div><div>is covered by the shell of the soluble, amphipathic PL, Cholesterol, apo.<br></div><div><br></div><div><br></div><div>To form a hydrophilic lipoprotein complex.</div>1 CVS_biochemistry CVS_biochemistry_1 Apolipoproteins are either: <br><br>1. {{c1::Peripheral}} ({{c2::Can be transferred}}). <div><br></div><div>2. {{c1::Integral}} ({{c2::Can’t be transferred}}).</div>1 CVS_biochemistry CVS_biochemistry_1 apolipoproteins associated with lipoproteins have a number of functions,<div><br>such as <br><br></div><div>1. {{c1::providing recognition sites for cell surface receptors }}</div><div><br></div><div>2. {{c1::serving as activators or coenzymes for enzymes involved in lipoprotein metabolism}}</div>"<img src=""paste-be94b21ee9b92619cbc8f241e95210a0dec2e9fe.jpg"">"1 CVS_biochemistry CVS_biochemistry_1 mention an example on apolipoproteins working as activators for enzymes "<b>apo C II </b>activator for<b> ""lipoprotein lipase""</b>"1 CVS_biochemistry CVS_biochemistry_1 mention an example on apolipoproteins working as recognition sites for cell surface receptors<div><br></div><div>(receptor-mediated uptake of plasma lipoproteins)</div>"There are receptors for the apolipoprotein E (ApoE) in liver cells for the uptake of chylomicrons (lipoprotein)<div><br></div><div><img src=""images.jpg""><br></div>"1 CVS_biochemistry CVS_biochemistry_1 mention the 5 major groups of lipoproteins "1. Chylomicrons (CM)<div><br></div><div>2. Very low-density lipoproteins (VLDL, or pre-β-lipoproteins)</div><div><br></div><div>3. Low-density lipoproteins (LDL or β-lipoprotein): - BAD</div><div><br></div><div>4. High-density lipoproteins (HDL or α-lipoprotein) - GOOD</div><div><br></div><div>5. Albumin + FFA (NEFA)</div><div><br></div><div><img src=""paste-1ceb3733b763a1b4b2396aa611c57ea3d64dbc77.jpg""><br></div>"1 CVS_biochemistry CVS_biochemistry_1 <b>Chylomicrons (CM) </b>are derived from {{c1::intestinal absorption of triacylglycerols and other lipids}}1 CVS_biochemistry CVS_biochemistry_1 <b>Chylomicrons (CM) </b>are mainly formed of {{c1::TAG (98% lipids, 2% protein)}}. It "<br><div><br></div><div><br></div><div>remember, lipoproteins made of a nonpolar core of <b>TAG</b> and CE (lipids)</div><div><br></div><div>surronded by a shell of apolipoproteins, phospholipids, free cholesterol</div><div><br></div><div><img src=""Figure1.png""> </div>"1 CVS_biochemistry CVS_biochemistry_1 {{c2::chylomicrons}} are the form of {{c1::absorbed fat.}}"<div><br></div><div><br></div><div>""The intestinal cells absorb the fats. Long-chain fatty acids form a large lipoprotein structure called a chylomicron that transports fats.""</div>"1 CVS_biochemistry CVS_biochemistry_1 VLDL - pre-B-lipoprotein are derived from the {{c1::liver}} for the export of {{c2::triacylglycerols}} to different cells. "<br><br>""<span style=""color: rgb(33, 33, 33);"">VLDL is made in the liver and is responsible for delivering TAGs to cells in the body, which is needed for cellular processes.""</span><div><span style=""color: rgb(33, 33, 33);""><br></span></div><div>triacylglycerols = TG, TAG, triglycerides<br></div>"1 CVS_biochemistry CVS_biochemistry_1 TAG is exported from the liver by VLDL. If VLDL is absent, {{c1::fatty change}} will occur.1 CVS_biochemistry CVS_biochemistry_1 LDL - B-lipoprotein - represent a {{c1::final stage for catabolism of VLDL.}}"<br><div><br><img src=""paste-1ceb3733b763a1b4b2396aa611c57ea3d64dbc77.jpg""><br></div><div><br></div><div>VLDL (mostly TAGs, made by liver) --> cells take up TAGs --> TAGs gone, shell (high in protein, cholestrol) remains --> LDL</div>"1 CVS_biochemistry CVS_biochemistry_1 We prefer {{c1::LDL, B-lipoprotein}} in low amounts because it is {{c1::Bad Cholesterol}}(mostly free cholesterol) 1 CVS_biochemistry CVS_biochemistry_1 High-density lipoproteins (HDL or α-lipoprotein) are involved in {{c1::chylomicrons and VLDL metabolism}} as well as {{c1::cholesterol transport.}}"<span style=""background-color: rgb(255, 255, 255);""><font color=""#0000ff"">HDL helps rid your body of excess cholesterol (""cholesterol transport"")</font></span><br><div><span style=""background-color: rgb(255, 255, 255);""><font color=""#0000ff""><br></font></span></div>" Why do we prefer HDL in high concentrations? because it is Good Cholesterol. (takes away cholesterol in its structure) rank lipoproteins in size and density (protein content)"<div><br></div>Chylomicrons --> VLDL --> LDL --> HDL<div><br></div><div><img src=""paste-1ceb3733b763a1b4b2396aa611c57ea3d64dbc77.jpg""><br></div>" Plasma lipoproteins are separated into different fractions by two methods:Electrophoresis, Ultracentrifugation how do we use Electrophoresis in classifying lipoproteins?"According to their <b>mobility</b> in the electric field. The particles are distributed according to their <b>charge, weight, size & shape.</b> <div><br></div><div>all lipoproteins are put in a gel and move toward + pole</div><div><br></div><div>farthest from (+) --> biggest, but not necessarily (depends on size, shape and charge too)</div><div><br></div><div><img src=""paste-d4b1b0c5b8d39e6ee5bf087da8752219f28c3e66.jpg""><br></div><div><img src=""paste-028ffa0ab59b8bea6a134bd3c620e1cd63f84536.jpg""><br></div><div><br></div><div><br></div><div><br></div>"1 CVS_biochemistry CVS_biochemistry_1 mention the order of lipoproteins in  electrophoresis(-) Chylomicron --> LDL --> VLDL --> HDL --> Albumin/FFA (+)                                                          1 CVS_biochemistry CVS_biochemistry_1 how do we use ultracentrifugation in lipoprotein classification?They are separated according to their density. The higher the protein content the higher the density of the particles.<div><br>FFA/Albumin --> HDL --> LDL --> VLDL --> chylomicron</div>1 CVS_biochemistry CVS_biochemistry_1 Chylomicrons are assembled in {{c1::intestinal mucosal cells}}  1 CVS_biochemistry CVS_biochemistry_1 Chylomicrons carry dietary (exogenous) {{c1::TAG}}, {{c1::cholesterol}}, {{c1::fat-soluble vitamins}}, and {{c1::cholesteryl esters}} to the peripheral tissues1 CVS_biochemistry CVS_biochemistry_1 Chylomicrons are chiefly composed of the {{c1::absorbed TAG (Major fat in our body)}} which are added with smaller amounts of {{c1::CE}}, {{c1::C}}, {{c1::PL}}, and {{c1::proteins.}}98% lipids, 2% protein<div><br>CE = cholestreyl ester, center </div><div>C = cholesterol, shell</div><div>PL = phosopholipid, shell</div><div><br></div>1 CVS_biochemistry CVS_biochemistry_1 Main function of chylomicrons transport TAGs to various tissues and cholesterol to the liver.1 CVS_biochemistry CVS_biochemistry_1 Nascent chylomicron (<b>Premature</b> Chylomicron) principally contains 2 types of proteins, {{c1::apo A}} and {{c1::apo B-48}}"<img src=""paste-18fbb57bba7e64ec5432817222a167fd4bf9b784.jpg""><br>NOTE: picture is <b>mature </b>chylomicron, no pic for premature:("1 CVS_biochemistry CVS_biochemistry_1 The nascent chylomicron is transported to the plasma via {{c1::lymphatics}} <div><br></div><div>where it is rapidly modified (converted to mature chylomicron) by receiving {{c1::apo E}} and {{c1::apo C}} from {{c1::HDL.}}</div>"<img src=""paste-18fbb57bba7e64ec5432817222a167fd4bf9b784.jpg"">"1 CVS_biochemistry CVS_biochemistry_1 Chylomicron: apo C contains {{c1::apo C-II}} which is an activator for {{c1::lipoprotein lipase (LPL).}}1 CVS_biochemistry CVS_biochemistry_1 """lipoprotein lipase LPL"" presents extracellularly anchored by {{c1::heparan sulfate}}"it is activated by Apo-C-II on chlyomicrons 1 CVS_biochemistry CVS_biochemistry_1 where is lipoprotein lipase mainly found?anchored by heparan sulfate to the<b> capillary walls of most tissue</b>, but predominates in <b>adipose tissues, cardiac and skeletal muscles</b>1 CVS_biochemistry CVS_biochemistry_1 lipoprotein lipase function hydrolyze triacylglycerol present in CM to <b>glycerol & FFA.</b>1 CVS_biochemistry CVS_biochemistry_1 from where do we get FFA (fatty acids) & glycerol?Stored in lipoproteins, as TAG, lipoprotien lipase (LPL) hydrolyzes TAGs to release FFA, glycerol. <br><br><div>LPL is activated by apo-C-II </div>1 CVS_biochemistry CVS_biochemistry_1 Fatty acids are stored by {{c1::adipose tissues}} or used {{c1::for energy}} by the muscle1 CVS_biochemistry CVS_biochemistry_1 Most of the FFA, about 90%, are taken up by the {{c1::extrahepatic tissue}} where hydrolysis occurs.1 CVS_biochemistry CVS_biochemistry_1 10% of FFA , remains in the {{c1::circulation}} bound to {{c1::albumin}} & is taken by {{c1::the liver}} <br><br><br>FFA = fatty acids1 CVS_biochemistry CVS_biochemistry_1 Glycerol is used mainly by {{c1::liver cells}}, due to the high activity of {{c1::glycerol kinase}}Glycerol kinase is an enzyme that catalyzes the conversion of glycerol to glycerol 3-phosphate<br>1 CVS_biochemistry CVS_biochemistry_1 All glycerol resulting from hydrolysis of TAG remains in the circulation & is mostly taken up by the liver. <div><br></div><div><br></div><div>It is not taken by other tissues due to the {{c1::absence of the glycerol kinase enzyme required for its utilization.}}</div>1 CVS_biochemistry CVS_biochemistry_1 After triacylglycerol hydrolysis (into FFA, glycerin), the remaining part of CM is called {{c1::CM remnant}}1 CVS_biochemistry CVS_biochemistry_1 Hydrolysis of TAG is associated with loss of {{c1::apo A & apo C}} to plasma HDL, leaving a CM remnant1 CVS_biochemistry CVS_biochemistry_1 Cholesterol ester transfer protein (CETP) helps in the transfer of {{c1::cholesteryl esters CE}} from {{c2::HDL}} to {{c2::chylomicron remnants}} in exchange with TAG.1 CVS_biochemistry CVS_biochemistry_1 remnant CM is rich in {{c1::CE}} and poor in {{c1::TAG}}1 CVS_biochemistry CVS_biochemistry_1 remnant CM is very rich in CE and poor in TAG. Why?because Cholesterol ester transfer protein (CETP) <div><br></div><div>transfers TAG from CM to HDL</div><div><br></div><div>and takes in CE from the HDL instead</div>1 CVS_biochemistry CVS_biochemistry_1 The CM remnants are taken up by {{c1::endocytosis}} by {{c1::liver}} cells where their components are hydrolyzed by lysosomes.1 CVS_biochemistry CVS_biochemistry_1 CM remnant uptake is mediated by {{c1::specific remnant (Apo E) receptors}}1 CVS_biochemistry CVS_biochemistry_1 mention microvessles Arterioles.<div><br></div><div>Capillaries. </div><div><br></div><div>Post-capillary venules.</div> What is arteriosclerosis?hardening and narrowing of the arterial wall, leading to poor circulation throughout the bodyCVS_pathology CVS_pathology_1 Mention the three patterns of arteriosclerosis?1. Atherosclerosis - medium + large <br>2. Arteriolosclerosis - small<br>3. Monckeberg medial sclerosisCVS_pathology CVS_pathology_1 Layers of the normal human arteryTunica externa - tunica media - tunica intimaCVS_pathology CVS_pathology_1 What does the tunica media consist of?smooth muscle, collagen, and elastic tissueCVS_pathology CVS_pathology_1 Where does the plaque of atherosclerosis form?In the tunica INTIMA layer of the arteryCVS_pathology CVS_pathology_1 What is an atheroma?A fatty plaque seen in blood vessel walls...CVS_pathology CVS_pathology_1 Appearance of atheromasoft yellow core of lipid (mainly cholesterol & cholesterol esters) covered by a firm, white fibrous capCVS_pathology CVS_pathology_1 Atheromas cause up to —- of all deaths50%CVS_pathology CVS_pathology_1 Mention modifiable atherosclerosis risk factorsHypertension <br><br>Hypercholesteremia (LDL)<br><br>Smoking<br><br>DiabetesCVS_pathology CVS_pathology_1 Mention nonmodifible risk factors for atherosclerosisAge, sex (estrogen ⬇️ lowers risk), geneticsCVS_pathology CVS_pathology_1 Estrogen effect on atherosclerosisLowers the risk. Post menopausal women stop reaping this benefitCVS_pathology CVS_pathology_1 higher levels of HDL correlate with (——-) risk of atherosclerosis.Reduced ⬇️CVS_pathology CVS_pathology_1 diet and drugs (ex: ——-?) that lower LDL or total serum cholesterol and raises serum HDL are valuableStatinsCVS_pathology CVS_pathology_1 Hypertension increases risk of?Ischemic heart disease - caused by atherosclerosis/narrowed arteries of the heart.CVS_pathology CVS_pathology_1 Hypertension increase the risk for Ischemic Heart disease (IHD) by (?) compared with normotensive60%CVS_pathology CVS_pathology_1 Without treatment, ( ?) of hypertensive patients will die of IHD.50%CVS_pathology CVS_pathology_1 Smoking increases the risk of?"Ischemic heart disease (caused by atherosclerosis in the heart's arteries)"CVS_pathology CVS_pathology_1 Prolonged (years) smoking of one pack of cigarettes or more daily increases the death rate from IHD by ?%.200%CVS_pathology CVS_pathology_1 diabetes mellitus increases the risk of?hypercholesterolemia ⬆️ LDL —-> atherosclerosisCVS_pathology CVS_pathology_1 The incidence of IHD is (?) as high in diabetic as in non-diabeticTwiceCVS_pathology CVS_pathology_1 DM and hypercholesterolemia lead to?Ischemic heart disease <br><br>Strokes (brain) <br><br>Gangrene (feet, hands)CVS_pathology CVS_pathology_1 Additional Risk Factors of atherosclerosis x4Inflammation <br><br>⬆️ homocysteine -Hyperhomocysteinemia<br><br>⬆️ Lipoprotein A levels (like LDL)<br><br>StressCVS_pathology CVS_pathology_1 Why does inflammation lead to an increased risk of atherosclerosisBecause Inflammation is present during all stages of atheroma plaque formation & ruptureCVS_pathology CVS_pathology_1 Age: incidence of IHD increases (?)-fold between 40 and 60 years of age5 foldCVS_pathology CVS_pathology_1 Does giving postmenopausal women estrogen work in lowering risk of IHD/atherosclerosis?NoCVS_pathology CVS_pathology_1 Pathogensis of atherosclerosis (direct cause)Arterial wall endothelial cell injury in the intima layer - and the subsequent CHRONIC inflammationCVS_pathology CVS_pathology_1 Steps of atherosclerosis (in detail)1. Endothelial cell injury (by toxins, high blood pressure, sugar...etc) —> increased endothelial permeability <br><br>2. LDL and oxidized LDL enter intima <br><br><br>2. Adhesions of monocytes, T-cells (from blood stream) by VCAM to endothelial cells and enter the intima layer. <br><br>2B. Monocytes become macrophages and foam cells.<br><br>3. Smooth muscles also enter intima from the media layer<br><br>5. Smooth muscle cells and macrophages both take up LDL - accumulation - FATTY STREAK<br><br>6. Some smooth muscle cells and foam cells die - release necrotic debris and lipid<br><br>7. Active Macrophages release toxins - EC injury all over again <br><br><br>8. Active t-cells - INF-Y - ⬆️ growth factors to ECs and smooth muscle - fibrous cap<br><br>9. Rupture of the fibrous cap → superimposed thrombusCVS_pathology CVS_pathology_1 Types of arteriolosclerosisHyaline and hyperplasticCVS_pathology Hyaline arteriolosclerosis seen in?DM patients and benign hypertensionCVS_pathology Hyaline arteriolosclerosis appearancePink hyaline thickening of arteriolar walls <br><br>Luminal narrowing <br><br>caused by proteins leaking into the vessel wallCVS_pathology Hyaline arteriolosclerosis in the kidneys causes?nephrosclerosis (glomerular scarring) - <br><br>slowly progresses to chronic renal failureCVS_pathology Hyaline arteriolosclerosis most common pts x31 - diabetic microangiopathy<br><br>2 - elderly (normon or hypertensive)<br><br>3 - benign hypertensionCVS_pathology Hyperplastic arteriolosclerosis most common ptsMalignant hypertensionCVS_pathology Hyperplastic arteriolosclerosis appearanceHyperplasia of the smooth muscle<br><br>Onion skin appearance<br><br>Accompanied by fibroid deposits and vessel wall necrosisCVS_pathology What is monckeberg medial sclerosis?Calcified deposits in muscular arteriesCVS_pathology Where is monckeberg most seen?In adults over 50CVS_pathology Most vessels involved with atherosclerosis and its resulting disease x5Coronary arteries - IHD<br><br>infrarenal abdominal aorta - aneurysms <br><br>Popliteal arteries - gangrene <br><br>Internal carotid arteries (neck) - stroke<br><br>Vessels of the circle of willis (brain) - strokeCVS_pathology Types of atheromas/plaquesVulnerable and stableCVS_pathology The three characteristics of vulnerable plaques1. Large number of foam cells and abundant extracellular lipid<br><br>2. Thin fibrous caps <br><br>3. Clusters of inflammatory cells.CVS_pathology The three characteristics of stable plaquesMinimal lipid accumulation <br><br>Thicc fibrous cap<br><br>Minimal inflammationCVS_pathology What is the effect of an atheroma? (detailed)1. Narrowing or even complete occlusion of the lumen of the artery - ischemia (stenosis)<br><br>2. Ulceration, fissuring, erosion or rupture of the fibrous cap —> thrombogenic substances spill into the blood —> thrombus formation<br><br>This thrombus can occlude the lumen fully or partially<br><br>The thrombus can also embolize. <br><br>The thrombus can also organize and regress in the atheroma and become part of it <br><br>3. A hemorrhage inside the atheroma itself - intra-plaque hemorrhage <br><br>4. Aneurysm - the atheroma blocks blood (& oxygen) from the media layer - ischemic atrophy of the tunica media layer - loses elasticity - weaknessCVS_pathology Clinical Consequences of Atherosclerotic DiseaseIschemia in the heart , brain , kidney, lower extremities ✋ - think stenosis <br><br>MI, cerebral infarction (stroke), aortic aneurysms, peripheral vascular disease (gangrene of the extremities).<br><br>AtheroembolismCVS_pathology Outcome of atherosclerosis depends on?Size of affected vessel<br><br>Size and stability of plaquesCVS_pathology Stenosis at early stages ?Remodels the media to preserve luminal diameter and increase circumfrenceCVS_pathology Stenosis at critical stages ?Chronic occlusion limits flow —> demand exceeds supply :(CVS_pathology Primary prevention of stenosis - whenAim to delay plaque formation in pts who have not yet suffered a serious complicationCVS_pathology Primary prevention of stenosis - what? x5Cessation of cigarettes smoking<br><br>Control hypertension <br><br>Weight loss<br><br>Exercise <br><br>Lower LDL, increase HDLCVS_pathology Secondary prevention of stenosis - when?Prevent RECURRENCE of ihd, strokeCVS_pathology Secondary prevention of stenosis - what? x3Aspirin - anti-platelet<br><br>Statins <br><br>Beta blockers - ⬇️ heart demandCVS_pathology The main protein of nascent VLDL is {{c1::apo B-100}} After release of nascent VLDL into the circulation, {{c1::apo C-II}} & {{c1::apo E}} are transferred from {{c1::HDL}} to it. About 50% of the TAG in VLDL are hydrolized by {{c1::LPL}}. This is associated with loss of {{c1::apo C}}, which goes to HDL {{c1::CETP}} helps transfer of CE from HDL to VLDL in exchange with TAGCVS_biochemistry intermediate density lipoprotein (IDL), also known as VLDL remnant has apoproteins: apo B-100 and apo E.CVS_biochemistry Most of IDL (remnant vldl) undergoes further catabolism by {{c1::hepatic lipase}}CVS_biochemistry Most of IDL undergoes further catabolism by hepatic lipase, which hydrolyzes most of its TAG, a process associated with loss of {{c1::apoE}} to HDLCVS_biochemistry after formation of IDL, and it undergoing catabolism by hepatic lipase and loss of ApoE <br><br>This results in the formation of a lipoprotein particle poor in TAG, very rich in CE, and containing mainly the protein apo B-100, called {{c1::LDL}}CVS_biochemistry LDL only has apolipoprotein {{c1::<b>B-100</b>}}CVS_biochemistry {{c1::LDL}} is formed from VLDL as described before. It may also be directly formed by the liverCVS_biochemistry the main function of ldl is to {{c1::transport cholestrol}}CVS_biochemistry The main protein protein of LDL is {{c1::apo B -100}} , and the main lipid is {{c1::CE}}CVS_biochemistry LDL bind to specific apo B-100 receptors, in both extrahepatic tissues ({{c1::30%}}) and liver ({{c1::70%}})CVS_biochemistry LDL bind to specific apo B-100 receptors, in both extrahepatic tissues (30%) and liver (70%) where they are {{c1::endocytosed and metabolized}} by {{c1::lysosomes}}, liberating free C.CVS_biochemistry what does librated, free C do to the cell? x31. decreases the synthesis of C (by inhibiting the enzyme HMG-CoA reductase)<br><br>2. increases the esterification of C (helping its storage, by increasing the activity of the enzyme acyl-CoA<br><br>3. Downregulates the LDL receptor (to decrease LDL uptake by the cell)CVS_biochemistry Deficiency of apolipoprotein B-100 receptors for the uptake of LDL leads to?type II hyperlipoproteinemia, a very sever type of hypercholestrolemiaCVS_biochemistry Most of plasma LDL is taken up by apolipoprotein B-100 receptors, but it can also be taken up by?<br><br>Some LDL is also taken by the <b>macrophages</b> and <b>arterial smooth muscles</b> by a <i>non- receptor</i>, or a receptor called <b>scavenger receptor</b>, mediated mechanismCVS_biochemistry when does the scavenger/non-recpetor/macrophage uptake of LDL become more significant?if plasma LDL level is elevated or if LDL is modifiedCVS_biochemistry how can LDL be modified? (and then later taken up by macrophages)as a result of <br><br><b>peroxidation of FA </b>or <br><br><b>glycation of proteins (as in diabetes mellitus).</b>CVS_biochemistry LDL uptake by scavenger receptors is NOT {{c1::regulated}} savenger LDL uptake effect on macrophages?The macrophages become overloaded with C and are transformed into foam cells. These cells die under the intima of arteries, causing deposition of CE, leading to atherosclerosis The incidence of cronary atherosclerosis is directly related to the concentration of {{c1::LDL}} in the blood plasma what decreases the incidence of atherosclerosis?vitamin C and E (antioxidants) , HDL why does ischemic heart disease <u>happen</u>?due to an imbalance between <b>cardiac blood supply (perfusion)</b> & <b>myocardial oxygen demand</b>CVS_pathology IHD is synonymous with {{c1::coronary artery disease (CAD).}}CVS_pathology more than 90% of cases of ischemic heart disease are due to ?<br>obstructive atherosclerotic vascular disease (atheroma)CVS_pathology other cause for IHD (other than atherosclerotic disease) x4<br>1. Increased demand (e.g., with increased heart rate or hypertension) - heart wants more<br><br>2. Diminished blood volume (e.g., with hypotension or shock) - not enough blood<br><br>3. Diminished oxygenation (e.g., due to pneumonia or congestive heart failure) - not enough O2<br><br>4. Diminished oxygen-carrying capacity (e.g., due to anemia or carbon monoxide poisoning) - not enough O2 carrying CVS_pathology "what ischemic heart disease causes cardiomyocyte death and what doesn't?<br><br>cardiomyocyte death = irreversible injury""Angina pectoris - ischemia <b>insufficient </b>to cause cardiomyocyte death. - causes pain<br><br>Acute myocardial infarction (MI): Ischemia <b>sufficient</b> to cause cardiomyocyte death.<br><br><img src=""images-48b62ec580f110f088acfac6f00f7c6a38bafa46.jpg"">"CVS_pathology what is <b>chronic</b> ischemic heart disease IHD?<b>Progressive</b> cardiac heart <b>failure</b> following MI.CVS_pathology what is <b>sudden cardiac death SCD</b>? - cardiac arrestlethal <b>arrhythmia</b> after MICVS_pathology what are the possibilities following an MI?chronic IHD - Progressive cardiac heart failure following MI.<br><br>OR<br><br>Sudden cardiac death (SCD): can occur due to lethal <b>arrhythmia</b> after MICVS_pathology Acute coronary syndrome is a term is applied to the three catastrophic manifestations of IHD: {{c1::unstable angina}}, {{c1::acute MI}}, and {{c1::SCD}}CVS_pathology Critical stenosis occurs when the lesion is obstructing {{c1::70% to 75%}} or more of a single vessel lumen (%)CVS_pathology Critical stenosis occurs when the lesion is obstructing 70% to 75% or more of a single vessel lumen, <br><br>generally causing {{c1::stable angina}} "<img src=""paste-943c408c368082740b237fe59f7e978155c77ea7.jpg"">"CVS_pathology stable angina is relieved by?Rest - ⬇️ heart demand <br><br>nitroglycerin - vasodilator CVS_pathology A fixed 90% stenosis can lead to inadequate coronary blood flow even {{c1::at rest}}CVS_pathology Slow rate atherosclerosis, over the years, can lead to {{c1::collateral perfusion}}"<img src=""paste-17a7a30ac4c31e477ad0be82a60ffd7abea3b7c9.jpg""><br><font color=""#0000ff""><br>""Collateral circulation is a network of tiny blood vessels, under normal conditions, not open.<br><br> When the coronary arteries narrow to the point that blood flow to the heart muscle is limited (coronary artery disease), collateral vessels may enlarge and become active""<br><br>لما القلب يقل كمية الدم الي جاي إله من الشرايين الرئيسية, يفتح شرايين صغيرة تعوض</font>"CVS_pathology collateral perfusion can subsequently {{c1::protect against MI}} even if the vessel eventually becomes completely occluded"<img src=""paste-17a7a30ac4c31e477ad0be82a60ffd7abea3b7c9.jpg"">"CVS_pathology when does the heart have NO TIME for collateral flow to develop?in ACUTE coronary blockage. - infarction results.CVS_pathology Angina pectoris is intermittent chest pain caused by {{c1::transient}}, {{c1::reversible}} myocardial ischemia."<img src=""paste-53c721b2abaf951658c8b76ef7dd5e84332e213e.jpg"">"CVS_pathology mention the 3 variants of angina ➢Typical or stable angina <br>➢Unstable angina (crescendo angina) <br>➢Prinzmetal or variant anginaCVS_pathology cause of chronic, stable angina?atherosclerosis, leads to a fixed narrowing of blood vessels -<br><br>(70-75)% stenosis and blockCVS_pathology cause of variant Prinzmetal angina?"coronary vasospasm - (vessels can look normal)<br><br><img src=""coronaryarteryspasm.gif"">"CVS_pathology cause of unstable angina?"THROMBOSIS - formation and breakdown of clots <img src=""paste-53c721b2abaf951658c8b76ef7dd5e84332e213e.jpg"">"CVS_pathology stable angina: Episodic chest pain associated with {{c1::particular levels of exertion}}CVS_pathology what can kind of exeretion can trigger stable angina? x4tachycardia <br><br>hypertension<br><br>fever<br><br>anxiety, fearCVS_pathology stable angina clinical presentation - character, radiation<b>Crushing</b> or <b>squeezing</b> substernal sensation that can <b>radiate</b> down the left arm or to the left jaw (referred pain)CVS_pathology Unstable angina (crescendo angina) clinical presentation Increasingly <b>frequent</b> pain, precipitated by progressively <b>less exertion</b> or even occurring <b>at rest</b>.<br><br>CVS_pathology Unstable angina (crescendo angina) causeplaque disruption and superimposed <b>thrombosis</b>, and/or vasospasm.CVS_pathology Unstable angina (crescendo angina) is a risk for?carries a risk for potentially<b> irreversible ischemia</b> (due to <b>complete</b> luminal occlusion by thrombus) & is therefore sometimes called pre-infarction anginaCVS_pathology Unstable angina (crescendo angina) sometimes called?pre-infarction anginaCVS_pathology can prinzmetal angina occur at rest?yesCVS_pathology Prinzmetal or variant angina caused by?coronary artery spasm.CVS_pathology Prinzmetal or variant angina can occur in the coronaries, but can also occur in?Completely normal vessel can be affectedCVS_pathology what does Prinzmetal or variant angina respond to ?Responds to vasodilators such as nitroglycerin and <b>calcium channel blockers!</b>. <b>✅</b>CVS_pathology what ischemic heart diseases cause reversible, temporary injury to cardiac myocytes?chronic stable angina<br><br>Prinzmetal<br><br>unstable angina CVS_pathology what is a heart attack?a myocardial infarctionCVS_pathology what happens to tissue during MI?necrosis of heart muscle due to ischemia.CVS_pathology Vast majority of MIs are caused by {{c1::acute coronary artery thrombosis}}CVS_pathology 10% of MIs occurs in the absence of occlusive atherosclerosis --> but due to {{c1::embolization from mural thrombi}}CVS_pathology most involved vessles in MI?Left anterior descending artery (40% to 50%)  - interventricular <br><br>Left circumflex artery (15% to 20%):<br><br>Right coronary artery (30% to 40%)CVS_pathology if MI happens in left interventricular artery, what parts of the heart would be involved?anterior LV, anterior interventricualr septum, & apex circumferentially.CVS_pathology if MI happens in RCA, what parts of the heart would be involved?MI involves posterior LV, posterior Interventricular Septum, &<br><br>RV free wall in some cases.CVS_pathology if MI happens in Left circumflex artery, what parts of the heart would be involved?MI involves lateral LV, except the apex.CVS_pathology What happens within seconds of vascular obstruction? (cell level)-> aerobic glycolysis <b>ceases<br></b><br>-> drop in ATP<br>  <br>-> accumulation of potentially noxious metabolites (e.g., lactic acid) in the cardiac myocytes.CVS_pathology Within a minute of the onset of ischemia and obstruction, what happens?Rapid loss of contractilityCVS_pathology Within few minutes of ischemia and obstruction, what happens? <b>Ultrastructural</b> changes: myofibrillar relaxation, glycogen depletion, cell and mitochondrial swellingCVS_pathology early changes of ischemia are {{c1::reversible}} (seconds, minute, minutes)CVS_pathology Severe ischemia lasting 20 to 40 minutes causes {{c1::irreversible damage}} and {{c1::coagulative necrosis}}.CVS_pathology what is the rationale for quick, prompt intervention by thrombolysis or angioplasty for ischemia?If myocardial blood flow is restored before irreversible injury occurs, cell viability can be preservedCVS_pathology Irreversible injury of ischemic myocytes first occurs in the {{c1::subendocardial zone }}"between endocardium and myocardium <br><br><img src=""paste-698be7023533eff7d2f1702c6a7efdfe5add7f1b.jpg""><br><img src=""paste-ea45649517165a4291a2f6c956343a26e7571ea1.jpg"">"CVS_pathology why are the myocytes in the subendocardial zone first to get irreversibly injured?"(because sub endocardium is the last area to receive blood delivered by the epicardial vessels)<br><br>+ sub endocardium is exposed to relatively high <b>intramural pressures</b>, which act to impede the inflow of blood.<br><br><img src=""paste-9fe7ab87cc08b7f3749a3a1154b327d766c1c9b1.jpg"">"CVS_pathology With more prolonged ischemia, a wave front of cell death moves, with the infarct usually achieving its <b>full</b> extent within {{c1::3 to 6 hours}}"<img src=""paste-d9993f040b6b6176f9cb8e4f51582d519075df21.jpg"">"CVS_pathology The location, size, and morphologic features of an acute MI depend on? x4✓The <b>size</b> and distribution of the involved vessel <br><br>✓The rate of development and the <b>duration</b> of the occlusion <br><br>✓<b><u>Metabolic</u></b> demands of the myocardium<br><br>✓Extent of <b>collateral</b> supplyCVS_pathology Transmural infarctions involves what part?"full thickness of the ventricle<br><br><img src=""paste-c8f5177844fddf5204cde2548a68136eb78cd01a.jpg"">"CVS_pathology Subendocardial infarctions involve "Limited to the inner third of the myocardium<img src=""paste-dd0066a2f94bd5e4f3de723402be6f92eafd7696.jpg"">"CVS_pathology which infarction are st segment elevated (STEMI) and which arent (NSTEMI)?"STEMI - transmural<br><br>NSTEMI - subendo<br><br><img src=""paste-dd0066a2f94bd5e4f3de723402be6f92eafd7696.jpg"">"CVS_pathology The gross and microscopic appearance depends on the {{c1::age}} of the MICVS_pathology Infarcts more than<b> 3 hours old</b> can be <u>visualized</u> by exposing myocardium to {{c1::triphenyltetrazolium chloride}}, a substrate for lactate dehydrogenase."<br><br>(TTC)<br><br><img src=""paste-6c699a44542cc1341d0ac4683d3628bfe8eec307.jpg"">"CVS_pathology TTC is an enzyme that is {{c1::depleted}} in the area of ischemic necrosis (it leaks out of the damaged cells), and the infarcted area is {{c1::unstained (pale)}}"<img src=""paste-a0e42d022326a423bb3bf2534b9b54c92858db9c.jpg"">"CVS_pathology GROSS appearance 12 - 24 hours after MI?"red-blue discoloration caused by stagnated, trapped blood.<br><br><img src=""paste-6a24ba1beb61ffdef5910f6fa33432db78708d92.jpg"">"CVS_pathology GROSS apperance of MI after 10-14 days?"infarcts are rimmed by hyperemic (highly vascularized) granulation tissue.<br><br><img src=""paste-3359f4b0794ef03d1573930ac615f54041508135.jpg""><br>"CVS_pathology GROSS MI after 2+ weeks?fibrous scarCVS_pathology 0-12 hours apperance after MI?no morphological changes yetCVS_pathology when does coagulative necrosis begin following MI?one slide says 12-18 hrs in<br><br>another says 4-12 hrs inCVS_pathology when does the cytoplasm of necrotic myocytes become eosinphilic (pink)?12-18 hours after MICVS_pathology "when does <span style=""color: rgb(34, 34, 34);"">loss of cross striations, pyknosis and karyorrhexis happen after MI?</span>"12-18 hoursCVS_pathology """Wavy fiber change at the periphery of the infarct."" after how many hours of MI?"12-18 hrsCVS_pathology """<span style=""color: rgb(34, 34, 34);"">The area shows a slight pallor"" </span> after how many hours of MI?"18-72 hours CVS_pathology when does inflammation in general occur after MI?18-72 hrsCVS_pathology """Neutrophils begin to show up and subsequently diminish""  after how many hours of MI?"18-72 hoursCVS_pathology """contraction bands at the periphery of the infarct produced by hypercontraction of myofibrils in dying cells""  after how many hours of MI?"18-72 hrsCVS_pathology neutrophils after how many hours of MI? macrophages?neutrophils --> 18-72 hrs<br><br>macrophages --> 4-7 daysCVS_pathology when does the infarct appear fully pale? not slight4-7 days after MICVS_pathology """ Macrophages, fibroblasts and capillaries first appear at the margins then begin to migrate into center""   after how many hours of MI?"4-7 daysCVS_pathology """<span style=""color: rgb(34, 34, 34);"">Macrophages begin to phagocytoze the necrotic myocytes."" after how much time following MI?</span>"4-7 daysCVS_pathology """<span style=""color: rgb(34, 34, 34);"">The necrotic area is yellow, soft"" </span><span style=""color: rgb(34, 34, 34);"">after how much time following MI?</span>"10 daysCVS_pathology """the granulation tissue is visible grossly at the edge of the infarct as a red-purple zone"" <span style=""color: rgb(34, 34, 34);"">after how much time following MI?</span>"10 daysCVS_pathology general events after MI:<br><br>0-12 hrs: {{c1::nothing}} <br><br>12-18 hours: {{c1::coagulative necrosis}} <br><br>18-72 hours: {{c1::neutrophil inflammation }}<br><br>4-7 days: {{c1::macrophage inflammation }}<br><br>10 days: {{c1::granulation <br>}}<br>4-8 weeks: {{c1::dense scar tissue}} CVS_pathology primary HTN causeunknownCVS_pharm Primary HTN mechanism<b>hypertrophy</b> & <b>proliferation</b> of smooth muscles in arterioles → VC &↑ peripheral resistance. <br><br>Gq- link.CVS_pharm why is Gq involved in HTN?Because in case of Gq stimulation there’ll be an increase in free Ca +2 which causes the constriction of arteriolesCVS_pharm Primary, 2ndary HTN usual age range1ary --> middle age<br><br>2ndary --> age extremesCVS_pharm 2ndary HTN causerenal or endocrine dysfunction<br><br>congenital or acquiredCVS_pharm BP target in HTN patient with n target organ damage & comorbidities<br><130/80CVS_pharm mild diastolic HTN?>85CVS_pharm moderate diastolic HTN?>100CVS_pharm severe malignant diastolic HTN?>115CVS_pharm 60% of deaths due to hypertension are {{c1::cardiac}} <br><br>what do they include?heart failure, IHD, arrhythmias & sudden deathCVS_pharm 30% of HTN deaths are due to {{c1::renal failure}}.CVS_pharm 10% of HTN deaths are attributed to?<b>hypertensive emergencies:<br></b><br>-hypertensive crisis & hypertensive encephalopathy.<br><br>10% of deaths due to hypertension are due to <b>epistaxis</b> and <b>cerebral hemorrhage</b>CVS_pharm what angina responds to Ca++ channel blockers?prinzmetal, variant anginaCVS_pathology describe an aneryusm  atheroma blocks blood (& oxygen) from the media layer - ischemic atrophy of the tunica media layer - loses elasticity - weaknessCVS_pathology the <u>mechanical properties of the heart </u>are studied through the {{c1::cardiac cycle}}CVS_physiology what is the cardiac cycle?The cardiac events that occur from the beginning of one heart beat to the beginning of the nextCVS_physiology time of cardiac cycle depends on?Heart rateCVS_physiology If heart rate is 72 beats/min, the duration of the cardiac cycle is about {{c1::0.8 second}} per beatCVS_physiology If heart rate is 72 beats/min, the duration of the cardiac cycle is about 0.8 second per beat<br><br>Of which {{c1::0.3 second}} is for systole and {{c1::0.5 second}} is for diastole CVS_physiology {{c1::80%}} of the ventricular filling is achieved even <b>before</b> the onset of atrial contractCVS_physiology when heart rate is up, cardiac cycle is {{c1::faster}}CVS_physiology heart rate is faster --> cardiac cycle is faster --> {{c1::systole}} takes up more time rather than {{c1::diastole}}CVS_physiology Atrial contraction has {{c1::secondary}} function during cardiac cycleCVS_physiology how much of the ventricle does the atria fill up?20%CVS_physiology if atria stops contraction, what is noticed?not a massive problem, only seen during exercise<br><br>--> dyspnea, hunger for airCVS_physiology Systole phasesIsovolumeic --> no blood leaves or enters<br><br>Ejection CVS_physiology Diastole phases isovolumeic, rapid inflow, diastasis, atrial contraction CVS_physiology how much of the blood is ejected during the first 1/3 of the ejection phase ?70%CVS_physiology what is the End Diastolic Volume EDV?the amount of blood that enters the ventricle during diastole (filling)<br><br>--> max. amount of blood the ventricle contains during the cycle.<br><br>CVS_physiology EDV is an index of the {{c1::preload}}CVS_physiology how much is the EDV usually? how much can it reach?110-120 ml<br><br>can be as high as 150-180 mlCVS_physiology what tells me how much the sacromere stretched to accomdate blood?Preload, EDVCVS_physiology what is the End Systolic Volume?"blood <b>left behind</b> during vent. systole (blood the ventricle couldn't eject)<br><br>--> least amount of the blood"CVS_physiology how much is the ESV? how low can it reach?40-50 ml<br><br>can be as low as 10-20 ml (vent. pumped very hard)CVS_physiology when can ESV be very low?if ventricle myocardial contractility was very highCVS_physiology The higher the {{c1::myocardial contractility}} the lower is the ESVCVS_physiology what is Stroke Volume SV?the amount of blood that was pumped out of each ventricle <br><br>EDV - ESVCVS_physiology what is the ejection fraction EF?the fraction of the EDV that was ultimately pumped <br><br>(Stroke volume / EDV) 100%CVS_physiology how much is the ejection fraction usually?60%CVS_physiology how much is the stroke volume usually?120-50= 70 mlCVS_physiology beginning of vent. systole - isovolumetric phase, what valves close, open? --> AV valve close - #1st 💗sound<br><br>--> semilunar valve closedCVS_physiology beginning of vent. systole - isovolumetric phase - pressure in aorta, ventricle, atriumaorta > ventricle > atriumCVS_physiology what is a-wave of the atira caused by?due to atrial <b>contraction </b>CVS_physiology Isovolumic contraction, what valves are open, closed? and why?both (AV, semilunar) closed.<br><br>Semilunar --> pressure in aorta/pul is higher than ventricle<br><br>AV ---> pressure in ventricle is higher than atriumCVS_physiology Isovolumic contraction phase, ventricle pressure goes from {{c1::zero}} to {{c1::80}}CVS_physiology once pressure reaches 80 in ventricle, what opens?the semilunar (aortic) valveCVS_physiology what causes 1st heart sound?AV valve closing at beginning of systole, isovolumeic contraction CVS_physiology "<img src=""paste-75b9e8d494ee72241de1638f780e9999f9c0aa23.jpg""><br>point out vent systole""<img src=""paste-2a80db400d20cccaf37e657087680caffd932012.jpg"">"CVS_physiology when does aortic (semilunar valve) open?when ventricular pressure bypasses aortic pressure and forces its valve openCVS_physiology during {{c1::ejection phase}} aorta/pul and ventricle contract as oneCVS_physiology Dicrotic notch cause <br><br><b>closure of the aortic valve</b> and elastic recoil of the aortic wallCVS_physiology dicrotic notch, when?end of systole, 2nd heart sound, closure of aortic valve.<br><br>blood backs upCVS_physiology in isovolumeic relaxation, ventricle pressure goes down below {{c1::80}} to {{c1::zero}}below aortic pressure CVS_physiology when does the AV valve open during cardiac cycle?when vent. pressure is below atrial pressure<br><br>--> beginning of ventricle filling phaseCVS_physiology Rapid filling inflow phase happens because of?"AV valve opening --> dumping all its passive venous blood from the lungs in the ventricle --> <b>Rapid filling<br><br></b><img src=""HD002f heart 2007.gif""><b><br></b>"CVS_physiology what is Diastasis? a phase during vent. filling where there is <b>slow filling </b>of the ventricle. it follows rapid inflow.CVS_physiology Atrial systole follows?diastasisCVS_physiology "label these phases<img src=""paste-8d9976abbf81bb15fa2ade3b7f7ed5daa9344ad9.jpg"">"from left to right:<br><br>Isovolumic contraction<br><br>ejection<br><br>isovolumic relaxation<br><br>Rapid inflow<br><br>Diastasis<br><br>atrial systoleCVS_physiology "<img src=""paste-4bd2ab2eb6204f874df105836d961b105ae7fa6f.jpg"">which valves open and which close?""1 --> AV valves close<br><br>2--> Aortic valve opens<br><br>3 --> aortic valve closes<br><br>4 --> AV valves open<br><br><img src=""paste-99e565550458fc9723c174de2083cf45e70d0fa4.jpg"">"CVS_physiology "<img src=""paste-ac045a07209da62193df46f6442c2ca7e215d7bf.jpg""><br><br>label atrial pressure waves?"left to right <br><br>a-wave, c-wave, v-waveCVS_physiology The a wave is due to {{c1::atrial systole}}CVS_physiology Factors that impede the flow of blood from the atria to the ventricles, such as {{c1::tricuspid valve stenosis}}, increase the amplitude of the a-wave.<br>atria needs more force to bypass stenosisCVS_physiology Factors that impede the flow of blood from the atria to the ventricles, such as tricuspid valve stenosis, {{c1::increase}} the amplitude of the a-wave.<br>atria needs more force to bypass stenosisCVS_physiology The c wave is produced by the {{c1::bulging of the tricuspid valve}} into the atria during {{c1::isovolumetric ventricular contraction}}<br>pressure building up in ventricle = c-waveCVS_physiology Tricuspid valve incompetence results in a high amplitude c-wave<br><br>why?because it leads to blood leaking back in the atria --> more pressure CVS_physiology Tricuspid valve incompetence results in a {{c1::higher amplitude c-wave}}because it leads to blood leaking back in the atria --> more pressure CVS_physiology The v wave mirrors the rise in {{c1::atrial pressure}} before the tricuspid valve opens during diastoleCVS_physiology The v wave mirrors the rise in atrial pressure before the tricuspid valve opens during diastole.<br><br>why does atrial pressure increase?taking in blood from the lungsCVS_physiology {{c1::Tricuspid valve stenosis}} results in a {{c2::weakning}} of the descending phase of the v-waveCVS_physiology what signifies the start of systole?first heart sound - AV valve closingCVS_physiology The intensity of the first heart sound is proportional to the strength of {{c1::myocardial contraction}}CVS_physiology only the {{c1::1st}} heart sound is proportional to the strength of myocardial contractionCVS_physiology what accompanies the 2nd heart sound?the dicrotic notchCVS_physiology {{c1::2nd heart sound}} signifies the end of systole and the start of diastoleCVS_physiology Splitting of S2, also known as {{c1::physiological split}}, normally occurs during {{c2::deep inhalation}}CVS_physiology Splitting of S2, also known as physiological split, normally occurs during deep inhalation<br><br>why?S2 occurs when semilunar valves close. (Pul, aorta<br><br>Deep inhalation --> closure of the aortic valve and the closure of the pulmonary valve are<b> not synchronized</b> during inspirationCVS_physiology A widely split S2 can be associated with several different cardiovascular conditions, including {{c1::Right bundle branch block}} and {{c1::atrial septal defect}}CVS_physiology The Third Heart Sound is {{c1::not normally heard in}} healthy people.CVS_physiology The Third Heart Sound is due to abrupt cessation of ventricular distention and the deceleration of blood flow just before {{c1::diastasis}}.<br><br>الترجمة--> the blood stopping from rapid inflow suddenly and going in the ventricle more slowlyCVS_physiology The third heart sound is amplified in abnormally stiff or distended ventricles, such as that associated with {{c1::heart failure}}CVS_physiology S3 presence over the age of {{c1::40}} is considered a serious sign of underlying cardiac abnormalitiesCVS_physiology at the height of the ejection phase, vent. pressure reaches {{c1::120}}CVS_physiology The CO is the volume of blood pumped by {{c1::each ventricle}} per {{c2::minute}}. <br><br>It is not the total amount of blood pumped by the heart.CVS_physiology the CO is {{c1::equal }} to how much blood is in our bodyCVS_physiology During exercise the CO can {{c1::increase}}CVS_physiology The CO is equal to (x3) {{c1::aortic blood flow, venous return, or pulmonary blood flow.}}CVS_physiology CO = {{c1::SV X HR}}<br><br>math lawCVS_physiology The Stroke Volume (SV): the amount of blood pumped out of {{c1::each ventricle}} per {{c2::beat.}}<br><br>(CO is per minute)CVS_physiology The Cardiac Reserve: the difference between the cardiac output {{c1::at rest}} and the {{c1::maximal volume of blood the heart is capable of pumping per minute}}"<br><br>CO at rest vs when you're at your max"CVS_physiology The Cardiac Index (CI): It is the output per {{c1::minute}} per {{c1::square meter}} of body surface area<br><br>we use this to figure out CO of a patient depending on their sizeCVS_physiology EF is an index for? how much is it?myocardial contractility <br><br>about 65%CVS_physiology what is heart failure?"heart's loss of contractility<br><br>ejection fraction is an index for contractility <br><br>if EF drops below 50% --> failure"CVS_physiology ejection fraction EF and heart failure?ejection fraction is an index for contractility <br><br>if EF drops below 50% --> failureCVS_physiology when does cardiac output increase? (general concept)when venous return increaseCVS_physiology What is the primary hypertension caused by?Unknown What is the mechanism of primary hypertension?Either by increased sympathetic activity, or renin angiotensin activity why does Na+ increase BP?Increases basal tone of smooth muscle is vessels<br><br>Increases release and response to NE<br><br>Increases response to A2<br><br>Fluid retention What causes iatrogenic HTN? x8—> sympathomimetics (Epi, NE...etc) <br><br>—> sudden withdrawal of beta blockers <br><br>—> caffeine, nicotine, alcoholism<br><br>—> herbs <br><br>—> corticosteroids <br><br>—> NSAIDs <br><br>—> sex hormones + contraceptives <br><br>—> NaHCO3 Why does caffeine increase HTN?Adenosine (VD) antagonist ⬇️ Target end damage HTN causes? x51. IHD <br><br>2. Renal dysfunction 🚽<br><br>3. Stroke, transient ischemic attacks, dementia <br><br>4. Peripheral artery disease <br><br>5. Retinopathy 👀 ttt of HTN?Life style<br><br>Drugs For HTN (——) is better than increasing dosageCombination therapy Why must htn exercise be mild?To avoid overworking the heart and causing lethal arrhythmia Types of antihypertensive drugs x91. Central-acting <br><br>2. Beta blockers<br><br>3. Alpha1 blockers (prazosin)<br><br>4. Adrenergic neuronal blockers<br><br>5. Slow Ca++ channel blockers <br><br>6. ACEIs <br><br>7. Angiotensin II blockers + renin inhibitors <br><br>8. Diuretics<br><br>9. Vasodilators metabolic syndrome includes? x10 1.↑body wt.<br>2. ↑BP. <br>3. ↑plasma lipids. <br>4. ↑plasma insulin then glucose. <br>5. ↑prothrombotic & proinflammatory state, thrombophilia & oxidative stress, atherosclerosis. CRP.<br>6. ↑uric acid..., gout. <br>7. Fatty liver. NAFLD is better predictor of cardiovascular disease & mortality. <br>8. Polycystic ovary syndrome. • <br>9. Rheumatoid arthritis. •CVS_pharm types of central acting drugs that lower HTN<b>Psychotropic drugs</b> (benzos + antidepressants)<br><br><b>Central sympathetic blockers</b>: lipophilic β blockers<br><br><b>α2 agonists</b> (increase VD) as clonidine & α methyl dopa.CVS_pharm General adverse effects of central HTN drugs (except antidepressants) are {{c1::sedation}} or {{c1::depression}}CVS_pharm Psychotropic drugs that lower HTN?benzos + anti-depressants CVS_pharm Central sympathetic blockers: {{c1::lipophilic β blockers}} (ex)CVS_pharm α2 agonists as {{c1::clonidine}} & {{c2::α methyl dopa}}CVS_pharm Prazosin (a1 blocker) adverse effect;<b>1st dose phenomnon </b><br>1st dose causes <b>Postural hypotension</b> (when pt stands up, they get hypotension)<br><br>2.<b> reflex tachycardia</b> (less Venous return, increased HR ~ CO = HR * SV)<br><br>3. <b>salt + water retention, edema, wt gain</b><br><br>4. <b>less ejaculation </b><br><br><br>Prazosin --> VD, peripheral effect<br>increase in peripheral resistance, less venous return, less BP, <br><br>VD --> less SV, more HRCVS_pharm prazosin works on both {{c1::veins and arteries}}CVS_pharm how do we minimize 1st dose phenomenon (caused by prazosin a1 blocker)? X3a. Start with minimal dose. <br>b. Given at bed time. <br>c. No <b>diuretics</b> in the 1st few daysCVS_pharm Prazosin is commonly combined with {{c1::B-blockers}} & {{c1::diuretics}}CVS_pharm Prazosin (a1 blocker) commonly combined with β blockers & diuretics <br><br>why?B-blocker - to bypass increased HR<br><br>Diuretics - to bypass water/salt retention CVS_pharm compelling use of prazosin (a1 blocker)old pts. with prostatic enlargement. Good lipid profile.CVS_pharm Adrenergic neuronal blockers for HTN exampleLow dose of <b>reserpine</b> + <b>diuretics<br></b><br>effective, with low adverse effects.CVS_pharm explain mechanism of cardiac remodeling stress on the heart --> hypertrophy (<b>remodeling)</b> --> not enough O2 for hypertrophied heart --> ischemia --> IHD --> necrosis <br><br>OR<br><br>hyperytophy --> fibrosis, stifness --> heart failureCVS_pharm what causes cardiac remodeling?anything that increases stress --> catecholamines : E, NE..etcCVS_pharm mention drugs that treat cardiac remodeling?anything that <b>lowers </b>stress (HTN is stress)<br><br>B-blockers<br><br>ACEIs & ARBs<br><br>spironolactone (<b>diuretic)</b>CVS_pharm drugs that stop remodeling (B-blockers, ACEIs & ARBs, Spiro) are the only drugs to {{c1::reduce morbidity and mortality in CHF}}CVS_pharm ttt of chronic HF; what do we reduce?HF -<br><br>we need to relieve the heart; it cannot pump<br><br>- ↓ afterload<br><br>- ↓ preload<br><br>- ↓ remodelingCVS_pharm ttt of angina; what do we reduce?we need to increase O2 and decrease its consumption:<br><br>- ↓after load <br><br>- ↓ preload<br><br>- ↓ HR & contraction <br><br>(↓ O2 consumption)<br><br>- coronary VD<br><br>(increase O2)CVS_pharm clinical features of MI?Severe, crushing substernal chest pain (or pressure) that can radiate to the neck, jaw, epigastrium, or left arm.<br><br>Pain typically lasts several minutes to hours and is not relieved by nitroglycerin or rest.<br><br>Silent infarcts : 10% to 15% of MIs<br><br>Common in diabetes mellitus and elderly.<br><br>The pulse generally is rapid and weak, and patients are often diaphoretic (sweaty) and nauseous<br><br>With massive MIs (involving more than 40% of the left ventricle): cardiogenic shock developsCVS_pathology MI pain? character, duration <b>Severe</b>, <b>crushing</b> substernal chest pain (or pressure) that can <b>radiate</b> to the neck, jaw, epigastrium, or left arm.<br><br>Pain typically lasts <b>several minutes to hours</b> and is NOT relieved by <b>nitroglycerin or rest.</b>CVS_pathology % of silent infarcts10% to 15% of MIsCVS_pathology MI common in?diabetes mellitus and elderly, female<br>CVS_pathology when does cardiogenic shock accompany MI?with massive MIs involving 40%+ of LVCVS_pathology How to diagnose MI? x4"symptoms<br><br>ECG<br><br>Biochemical markers (troponin, serum creatine kinase, creatine kinase‐MB)<br><br>Coronary angiogram<br><br><img src=""paste-ce3ee31288507a5796017b0337054beac6c416ec.jpg"">"CVS_pathology outcome of MI (clinical)Death: 7% for in-hospital MI<br><br>Out of hospital is much worse.<br><br>STEMIs (transmural) --> 1/3 will die of arrhythmia (mainly VF) within an hour of symptom onset, before they reach the hospital<br><br>advanced age + female + DM + previous MI --> poor prognosis CVS_pathology A third of persons with (STEMIs) will die, usually of an {{c1::arrhythmia (mainly VF)}} within an hour of symptom onset, before they reach the hospitalCVS_pathology what does AMI (acute myocardial infarction) lead to? x41. electrical instability --> arrhythmias <br><br>2. impaired contractility --> exhausted heart, hypotension (including coronaries), more ischemia, CHF<br><br>3. pericardial inflammation<br><br>4. tissue necrosis <br>CVS_pathology what happens if there is necrosis in IVS?IVS -> venticular septal defect -> blood from right to left. -> deoxygenated + oxygenated mix<br><br>pressure (blood) from left to right --> more pressure in RV -> pulmonary hypertensionCVS_pathology "Cardiogenic shock means severe {{c1::""pump failure""}}"CVS_pathology Cardiogenetic shock occurs in {{c1::10-15}} % of pts after MICVS_pathology when does Cardio. shock occur?massive large infarcts --  >40% of LVCVS_pathology Cardio. shock accounts for nearly {{c1::70%}} mortality rateCVS_pathology Arrhythmias following sudden acute MI involve? (major) ventricular fibrillation (VF) & heart block (AV block)CVS_pathology less common arrhythmias following MI? x4<b>sinus bradycardia</b>, <br><b>tachycardia</b>, <br><b>ventricular premature contractions</b> <br><b>ventricular tachycardia<br></b><br>may occur.CVS_pathology Pericarditis: a fibrinous or hemorrhagic pericarditis usually develops within {{c1::2 to 3 days}} of a {{c2::<b>transmural</b> MI}}CVS_pathology Pericarditis following MI typically {{c1::spontaneously resolves}} with time.CVS_pathology Pericarditis cause following MI?Inflammatory response to the area of myocardial infarct.CVS_pathology Dressler syndrome is a {{c1::secondary form of pericarditis. }}CVS_pathology "Dressler syndrome's symptoms tend to occur {{c1::2–3 weeks}} after myocardial infarction."secondary Pericarditis, not acuteCVS_pathology Dressler syndrome is a secondary form of pericarditis. Cause?It is believed to result from an <b>autoimmune inflammatory reaction</b> to <b>myocardial neo-antigens </b>formed as a result of the MI.CVS_pathology Myocardial rupture complicates {{c1::1% to 5%}} of MI patientsCVS_pathology Myocardial Rupture includes? x3 and its complication"1. rupture of the<span style=""background-color: rgb(255, 255, 255);""><b> ventricular free wall</b></span>, with fatal <u>hemopericardium</u> & <u>cardiac tamponade</u> <br><br> 2. rupture of the <b>infarcted IVS</b>, leading to a new <u>VSD & left-to-right shunt </u><br><br>3. rupture of<b> infarcted papillary muscle</b>, resulting in <u>severe mitral regurgitation</u>"CVS_pathology Rupture can occur at almost any time after MI but is most common {{c1::3 to 7 days}} after infarction; <br><br>when granulation tissue has not deposited sufficient collagenous matrix to repair the wall.CVS_pathology Dysfunction of a papillary muscle after MI causes {{c1::mitral regurgitation}}CVS_pathology Papillary muscle <b>dysfunction</b> can result from?I. <b>Ischemia</b> of papillary muscle & the underlying myocardium <br><br>II. Or rarely <b>rupture</b> of the infarcted papillary muscle CVS_pathology Mural thrombus cause?infarction expanding --> weakining of necrotic muscle --> stasis of blood (sludging) --> mural thrombus + systemic thrombo<b>embolism</b>CVS_pathology Ventricular aneurysm is a {{c1::late}} complication of MICVS_pathology aneurysms of the ventricular wall most commonly result from a {{c1::large transmural MI}}CVS_pathology aneurysms of the ventricular wall most commonly result from a large transmural MI that heals with the {{c1::formation of thin scar tissue}}CVS_pathology Complications of ventricular aneurysms include {{c1::mural thrombus}}, {{c1::arrhythmias}} & {{c1::heart failure}}CVS_pathology Chronic Ischemic Heart Disease is also called {{c1::ischemic cardiomyopathy}}CVS_pathology Chronic Ischemic Heart Disease is ?➢<b>Progressive</b> heart failure secondary to ischemic myocardial damage.CVS_pathology when does Chronic Ischemic Heart Disease appear?when the compensatory mechanisms (e.g., hypertrophy) of residual viable myocardium begin to <b>fail</b>.CVS_pathology Chronic Ischemic Heart Disease features?Left ventricular dilation and hypertrophy, <br><br>often with discrete areas of gray-white scarring from <b>previous</b> healed infarctsCVS_pathology "Major cardiac complications of hypertension, result from<span style=""background-color: rgb(255, 255, 255);""><b> </b></span>{{c1::pressure overload}}"CVS_pathology {{c1::➢Myocyte hypertrophy}} is an adaptive response of HTNCVS_pathology Persistent hypertension eventually can culminate in <br><br>{{c1::dysfunction}}, {{c1::cardiac dilation}}, {{c1::CHF}}, and even {{c1::sudden death.}}CVS_pathology Systemic hypertension: affects the {{c1::left side}} of the heart <br><br>Pulmonary hypertension: can cause {{c2::right-sided hypertensive changes}} called {{c2::cor pulmonale}}CVS_pathology Lipoprotein (a), or lp(a), is a particle that when present in large quantities in the plasma, is associated with {{c1::an increased risk of coronary heart disease.}}CVS_biochemistry Lipoprotein (a) is nearly {{c1::identical}} in structure structure to an LDL particle.<br><br>Its distinguishing feature is the presence of an additional apolipoprotein molecule, apo (a), that is covalently linked at a single site to apo B 100.CVS_biochemistry difference in structure between LDL and lipoprotein A?"ts distinguishing feature is the<b> presence of an additional apolipoprotein molecule, apo (a)</b>, that is covalently linked at a single site to <b>apo B 100.<br><br></b><img src=""paste-102c0054c15c902fe1beadd94660d181cc59f81c.jpg""><b><br></b>"CVS_biochemistry LP (a) plasma levels are determined by {{c1::genetics}} {{c1:: trans fat acids rich diet}} <br><br>{{c1::estrogen}} decreases LP(a) levelsCVS_biochemistry Apo (a) of the LP(a) is highly homologous (binding) to {{c1::plaminogen}} which is the precursor of {{c1::plasmin}} which causes {{c1:: fibrinolysis}}<br><br>therefore; Lp(a) lowers:<br><br>{{c2::fibrinolysis and blood-clots-breakdown}}CVS_biochemistry what does Lp(a) slow down? why?elevated LP (a) slows the <b>breakdown of blood clots</b> that trigger heart attacks<br><br>Apo A similar to plasminogen<br><br>--> Apo A competes w/ plasminogen for activators<br><br>plasminogen activator accidently binds to Apo A<br><br>Plasminogen cant intiate fibrinolysis (hasnt been activated) <br><br>CVS_biochemistry HDL formed by {{c1::liver cells}} and {{c1::small intestine}}CVS_biochemistry HDL is first formed as {{c1::discoidal HDL}} and is formed of <br><br>{{c1::PL bilayer}}, {{c1::free C}}, and {{c1::apolipoproteins (A,C,D,E)}}CVS_biochemistry discoidal HDL later on:<br><br>1.{{c1:: accept free C from extrahepatic tissues<br>}}<br>2. {{c1::this C is esterified by LCAT}}CVS_biochemistry LCAT is secreted by {{c1::the liver}} and binds to {{c1::HDL}} and is activated by {{c1::apo A-1 present in HDL}}CVS_biochemistry LCAT catalyzes the transfer of {{c1::acyl group}} from {{c1::position 2 of lecithin}} to C to form <b>CE</b> and <b>lysolecithin</b>CVS_biochemistry what is discoidal HDL made of?mainly formed of PL bilayer, free C, and apolipoproteins (A,C,D,E)CVS_biochemistry what happens to Discoidal HDL for it to become HDL<sub>3</sub>?needs to accept <b>free C</b> from tissue<br><br>then <b>esterified </b>by <b>LCAT</b> <br><br>esterified C<b> (CE) </b>then forms a central hydrophobic core <br><br>that pushes the PL bilayer apart and <br><b><br>converts the discoidal HDL into the spherical HDL<sub>3</sub></b>CVS_biochemistry "what happens to HDL<sub>3</sub> for it to become HDL<span style=""font-size: 16.6667px;""><sub>2 </sub></span>?"HDL<sub>3</sub> receives excess surface lipids, <b>C, PL from CM and VLDL</b> when broken by LPL enzyme.<br><br> HDL3 now becomes HDL<sub>2</sub>CVS_biochemistry what enzyme turns HDL<sub>2 </sub>back into HDL<sub>3</sub>?<b>Hepatic lipase</b> hydrolyzes and removes part of the TAG, CE, PL from HDL2 reforming HDL3CVS_biochemistry HDL act as reservoir for different {{c1::apoproteins (C,E)}}, which are important for metabolism of {{c2::CM and VLDL.}}CVS_biochemistry HDL by the mean of {{c1::CETP (apo D)}} provide CE to CM remnants, VLDL and LDL in exchange with TAG.CVS_biochemistry HDL are endocytosed by {{c2::liver cells}}, where CE are hydrolyzed. <br><br>The free C released is either {{c1::repacked into lipoproteins}} or {{c1::converted to bile acids to be secreted in bile}}CVS_biochemistry HDL are important important for removal of C from {{c1::tissues}} to {{c1::the liver}} (reverse C transport)CVS_biochemistry what components of the Lipid Profile are <b>not</b> impacted by food?Total Cholesterol and HDL CholesterolCVS_biochemistry what lipids are particularly impacted by food?triglyceride level (and thus LDL)CVS_biochemistry The LDL cholesterol cholesterol is a value often obtained obtained by a calculated method that relies on the accurate {{c1::measurement of triglycerides}}CVS_biochemistry a non-fasting sample can raise <b>triglycerides</b> and yield an inaccurate <b>LDL cholesterol calculation</b>TAGs give us LDL %CVS_biochemistry VLDL cholesterol is usually estimated as a {{c1::percentage of your triglyceride value}}CVS_biochemistry LDL % equation<br><br>• LDL cholesterol (mg/dL) = total cholesterol – HDL cholesterol – (triglycerides/5)CVS_biochemistry "• LDL cholesterol (mg/dL) = total cholesterol – HDL cholesterol – (triglycerides/5)<br><br><br>""triglycerides/5"" represents?"VLDL-CCVS_biochemistry Non-HDL cholesterol, does not {{c1::rely on triglycerides}}, and can be done as a {{c1::non-fasting}} sample.<br><br>LDL and VLDL depend on TAGs and need to be done while fastingCVS_biochemistry Your non-HDL cholesterol result refers to your {{c1::total cholesterol value minus your HDL cholesterol.}}CVS_biochemistry if we have a non-fasting patient we use?HDL and non-HDL (this is enough to see CVS problems)CVS_biochemistry if one desires an accurate triglyceride and LDL cholesterol level, it is ideal to {{c1::fast for 8-12 hours prior to the test}}CVS_biochemistry LDL composition varies in the blood from {{c1::large and fluffy}} to {{c1::small and dense}}CVS_biochemistry Diuretics basic function Drugs which ↑urine volume (water & salts).CVS_pharm Diuretics are drugs which ↑urine volume (water & salts).<br><br>what is the mechanism that follows this?lower Na+ in arterioles: <br><br>1. ↓basal tone of vascular smooth muscles & ↓vessel stiffness. <br><br>2. ↓response to NE & angiotensin II. <br><br>3.↓NE release. <br><br>4.↓fluid retention & blood volume.CVS_pharm Diuretics are more potent in {{c1::blacks}}, {{c1::older & obese}} pts. and pts. with {{c1::↑plasma volume or ↓renin}}. <br><br>More effective in {{c2::systolic hypertension}}CVS_pharm Thiazides are the most effective {{c1::antihypertensive}} diuretics.<br>NOT diuretics CVS_pharm mechanism of Thiazides as diuretic 1. ↓ renal tubular reabsorption of Na + in<b> early part of DCT (minor)</b> → ↑loss of (10% filtered) Na+ , CI- and H2O in urine. <br><br>2↑ renal PG release (mild).CVS_pharm mechanism of Thiazides as hypotensive first of all it made you piss out Na+ more, meaning:<br><br>1.↓Na+ in arterioles →..... <br><br>2.↓ fluid retention & blood volume (initial hypotensive mechanism only).<br><br>but a special thing about this drug<br><br>3. direct <b>opening of K+ channels </b>--> hyperpolar --> less Ca++ (plateu) --> VDCVS_pharm uses of thiazides1. Essential hypertension.<br>In mild to moderate types with <b>normal</b> renal function. <br><br>2. CHF. <br><br>3. Renal edema and nephrotic syndrome. <br><br>4. Renal Ca ++ calculi and idiopathic hypercalcuria. Also reduces osteoporosis & hip fracture in old hypertensives. thiazides for which hypertensive patient?mild to moderate essential HTN, with <b>normal renal function</b>CVS_pharm causes of Myocarditis?- idiopathic (most common)<br><br>-viral (most common cause)<br><br>- bacteria<br><br>-SLE CVS_micro symptoms of Myocarditis? x5-viral illness present in some cases <br>– various degrees of CHF <br>– chest pain <br>– arrhythmias, heart block <br>– sudden deathCVS_micro ttt of myocarditisself-limited <br>• Supportive: rest, sleep with elevated head of bed, O2<br><br>Medication: <br>Antibiotic (if non viral), <br><br>anti-inflammatory drugs: NSAIDs or steroids – Aspirin, Ibuprofen, Naproxen, Celecoxib<br><br>Antihypertensive treatment (b –blockers, diuretics)CVS_micro prognosis of myocarditis (early vs prolonged)early resolution <2 weeks --> complete recovery <br><br>prolonged (>2weeks - months) --> <br><b>dilated cardiomyopathy</b>, <br>worsening heart failure, <br>death (or cardiac transplantation)CVS_micro Viruses associated with acute myocarditis? (most common x1 vs others x5)Most common: – <br><b>enteroviruses</b> (particularly <b>coxsackie B</b>) <br><br>Others <br>– <b>adenoviruses</b> <br>– <b>herpesviruses</b> • CMV • EBV • HHV-6<br>– <b>parvovirus</b> B19 <br>– <b>HIV</b> <br>--<b>influenza</b>CVS_micro coxsackie B is a {{c1::single strand of ribonucleic acid (RNA)}} (structure)CVS_micro bacteria that causes Acute pericarditisbacteria (S. pneumoniae, S. aureus).CVS_micro patient with bacterial pericarditis is {{c1::much more ill}}, with {{c1::shaking chills and high fever}}CVS_micro infectious causes of Acute pericarditis?- enteroviruses (coxsackievirus, echovirus) <br>– HIV<br>– bacteria (S. pneumoniae, S. aureus)<br>– <b>tuberculosis</b> <br>– <b>rheumatic fever (rare)</b>CVS_micro non infectious causes of Acute pericarditis x8post-MI.<br>Post-pericardiotomy.<br>trauma, uremia.<br>radiation therapy.<br>lupus, <br>drugs (<b>procainamide</b>, <b>hydralazine</b>), <br>neoplasmCVS_micro drugs that cause Acute pericarditis?<b>procainamide</b>, <b>hydralazine</b>CVS_micro we monitor Acute infectious pericarditis pts for?Monitor for development of pericardial effusion or tamponade.CVS_micro (myocarditis) Bacterial infection requires specific antibiotic therapy and usually requires {{c1::drainage of pericardial fluid}}CVS_micro Infective Endocarditis is {{c1::A <b>microbial</b> infection of the endothelial surface of the heart or valves}}CVS_micro Infective Endocarditis is usually near {{c1::congenital or acquired cardiac defects}}CVS_micro Infective Endocarditis is usually {{c1::Bacterial}}CVS_micro Infective Endocarditis involved bacteria? x2• Hemolytic (viridans) streptococci (50 - 60%): attacks deformed valves<br><br>Staphylococcus aureus (10 - 20%): attacks healthy or deformed valves ,and major cause of intravenous drug abusers.CVS_micro

CVS

Add this document to collection(s)

Add this document to saved

Suggest us how to improve StudyLib