Lecture 23-24 Transient Ishemic Attack

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Michael Baker

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BCH210H © Lisa | Page 12 Lecture 23-24 Transient Ishemic Attack (Case Study – Nat)  Nat has a high-stress occupation  smoking is bad for tissues and vessels 2  BMI = mass[kg]/(height[m])  overweight is associated w hypertension  optimal BP 120/80  medications for hypertension:  water pills—reduce blood volume  β-blockers—control HR  aphasia—condition where the patient can move, see, and hear, but can’t talk  indication of a problem in the circulation to the brain  (dysphasia—can speak gibberish, or sound like they are drunk [makes sense to them])  trouble with writing during aphasia  problem with output of nervous sys  possibilities: block in blood flow (most common), or broken vessel in brain  stenosis—narrowing of blood vessel due to an occlusion  bruit—unusual vascular noise where there is a high-pitched noise (normally lower pitch blood flowing sound)  indicates stenosis—blood flowing through a narrower tube  obstruction in left side resulted in problem with right arm motor fx due to crossover of the hemispheres  3 major blood supplies to the brain (to supply glucose and O ) 2  left and right vertebral arteries ending in basilar artery  left internal carotid artery  right internal carotid artery  they come together to form circle of Willis in the brain (circle of arteriole blood flow)  occlusion is promoting formation of little clots bc of turbulence on platelets  jams a smaller arteriole when it gets to it  these emboli then flow into his brain and block blood supply to a specific area  the centre of controlling Nat’s speech  crescendo—worsening symptoms, which lead to a major event ex. a stroke  symptoms: aphasia, dysphasia, blindness, vertigo (dizziness), loss of spatial control momentarily  thrombus will form on the surface of the stenosis bump, and emboli will break off and clot an artery, resulting in an ischemic area blocking speech momentarily  transient ischemic attack (TIA)—can be forecasting something more serious like a stroke (loss of complete control in one brain hemisphere)  no O ,2no glucose, falling pH, loss of fx in that area  these problems usually occur at branch points in blood vessels under high pressure Risk Factors  preventable based on diet and lifestyle  parameters can be measured based on blood test  CAD—coronary artery disease  LDL is a major contributor to stenosis and plaque formation  LDL is an indicator for risk, normally <5mM, above is risk factor  HDL is good cholesterol—removes cholesterol and brings to liver for disposal BCH210H © Lisa | Page 22  LDL and HDL are lipoproteins  high in cholesterol  LPs are small particles that have a shell of phospholipids, cholesterol, and proteins, and a core interior made up of cholesterol esters and triglycerides  apoprotein—proteins that characterize LDLs imp in CVD  need LDL to carry lipids in small molecules so that lipids aren’t by itself and just glob together which would result in major clogging  triglycerides are the main storage of fat in the body  has long hydrophobic chains  free cholesterol has an –OH—found on shell of LDL  cholesterol ester has fatty acyl—found in core Making LPs  2 ways  when eat and digest fat in intestine, cells lining intestine will take up FFA and cholesterol, making TG, cholesterol esters proteins, and these cells in intestines will release LPs called chylomicrons (bigger than LDLs)  CM transport oil and fatty acids  CM have phospholipid, cholesterol shell, allowing them to flow  CM enter blood and supply tissues with FFA as fuel  good thing—circulates fuel to tissues  liver makes a diff LPs  is a good converter of CHO into fat  body converts CHO (starch) into fat  takes excess glucose, breaks it down, and converts to long FFA chains  liver assembles phospholipid, cholesterol, makes cholesterol esterase triglyceride, and packs it into VLDLs (very low density lipoproteins)  VLDLs are smaller than CM but are still effective transporters of cholesterol esterase triglycerides around body  thus, excess glucose will be converted to fat  VLDLs are smaller and heavier  they enter the blood  VLDLs an CMs are attacked by an enzyme in the capillaries (LPL—lipoprotein lipase)  LPL breaks down CM and VLDLs to smaller particles (hydrolyzes interior triglycerides)  FFA migrates to tissues to be used as fuel  CMs are minimized in size  VLDLs becomes IDL (intermediate size), but ultimately becomes LDL which is the smallest size  LDL is stripped of its TG but holds its cholesterol (rich in cholesterol)—high LDL = high cholesterol  LDL and CM should be absorbed at liver  problems with this can contribute to prolonged elevated LDLs in the blood  HDL picks up cholesterol and brings it back to the liver  made by liver  at the liver, cholesterol is engulfed and removed  liver has bile as a disposal system  bile flows from liver to intestine BCH210H © Lisa| Page 312  it modifies cholesterol into a bile acid and removes cholesterol through the intestine (no need for liver for removal)  but bile is not found in muscle How the LPL works  CM has proteins on outside recognized by LPL (active site rests on its stalk)  LPL binds to target protein on CM and starts digesting TAG to FFA and glycerol which than can diffuse out to the tissues nearby  tissues will make LDL which comes out into blood and sets up its post  CM or VLDL will from small LDL particles which Receptor-mediated endocytosis  normally LDL is rapidly taken up by an LDL receptor  LDL is taken into the cell and degraded  AAs are broken, cholesterol freed  cholesterol removal: cholesterol can be used and eliminated by the liver, sent out into the bile, changed to bile acids  vesicle formed which is digested by the lysosomal sys  active LDL uptake is good  when LDL receptor is impaired, it will promote elevation of LDL levels  results in familial hypercholesterolemia—elevated cholesterol in the blood  risk indicator for CVD  LDL can be modified by oxidation—problem is worse for smokers (elevated risk)  promotes LDL entry into arterial walls LDL Arterial Pathology  LDL can enter arterial walls and can’t get out (no bile system to eliminate cholesterol)  arterial walls aren’t supplied w a lot of blood (allow of blood flowing through), so it is hard to get rid of cholesterol (diffusion problems—accumulation of cholesterol)—no capillaries exiting walls bc of high pressure which would flatten the capillaries  results in enlarged cholesterol deposit
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