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Lecture 23-24 Transient Ishemic Attack.docx

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University of Toronto St. George
Michael Baker

BCH210H © Lisa| Page 112 LECTURE 23-24: TRANSIENT ISCHEMIC ATTACK CASE STUDY: NAT  59 year-old male  has a high-stress occupation  known to be very talkative  quit smoking 10 months ago  82 kg, 175 cm tall 2  BMI = mass[kg]/(height[m])  BMI = 26.8  he is overweight—associated w hypertension  recently began hypertension medication  before meds BP 145/90 (optimal BP 120/80)  w meds BP 125/80  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  in ER, Nat is able to talk again but has a tingling sensation in his right arm  CT head scan reveals no bleed or tumour in brain  neurologist listens to blood flow in carotid artery and detects an unusual noise over the left carotid artery  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  stenosis led to the formation of emboli (mini-clots) in the artery which then flowed into his brain and blocked the blood supply to the centre controlling speech  stenosis resulted in turbulence on platelets  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)  these problems usually occur at branch points in blood vessels under high pressure  crescendo—worsening symptoms, which lead to a major event ex. a stroke  symptoms: aphasia, dysphasia, blindness, vertigo (dizziness), loss of spatial control momentarily  no O 2 no glucose, falling pH, loss of fx in that area  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 BCH210H © Lisa| Page 212  right internal carotid artery  they come together to form circle of Willis in the brain (circle of arteriole blood flow)  bloodwork reveals  LDL cholesterol 6.2 mM  HDL cholesterol 1.05 mM  Nat’s age, past smoking history elevate his risk for vascular disease  25% risk LIPOPROTEINS  lipoproteins are small particles that have a shell of phospholipids, cholesterol, and proteins w a core-interior made up of cholesterol esters and triglycerides  free cholesterol has an –OH—found on shell of LDL  cholesterol ester has fatty acyl—found in core  triglycerides are fatty acid esters of glycerol  they are the major components of fat—are found in fat cells  also found in LPs circulating in the blood  has long hydrophobic FFA chains  LPs can be made in 2 major ways:  when you digest fat in your intestine, cells lining the intestine take up the fatty acids and cholesterol, make triglycerides, cholesterol esters, and proteins, and assemble large lipoproteins called chylomicrons  CM enter the blood and supply tissues w FFA from their TG as fuel  other tissues (mainly liver) can make LPs using TG, cholesterol, cholesterol esters, and proteins  liver readily converts excess dietary CHO (starch) into TG (fat)  liver breaks excess glucose down and converts it to long FFA chains  the liver LPs are VLDLs (very low-density lipoproteins)  VLDLs are smaller than CM but are still effective transporters of cholesterol esterase and TG around the body  VLDLs and CMs enter the blood and are attacked by an enzyme, lipoprotein lipase (LPL)  LPL recognize proteins on the surface of CM  LPL releases FFA from TG which diffuse out from the blood and enter nearby fat and muscle cells to be used as fuel  w the loss of TG, VLDL and CM decrease in size  the smaller CM remnants are readily taken up by liver and broken down  VLDL is converted into IDLs (intermediate size), but ultimately becomes smaller, denser LPs, LDLs (low-density lipoproteins) LDL (LOW-DENSITY LIPOPROTEINS)  LDLs are highly enriched in cholesterol and cholesterol esters (no TG)  are smaller and denser than VLDLs  can be removed from the blood by the liver  the liver has a surface protein, LDL receptor which binds LDL and allows uptake by the liver (receptor-mediated endocytosis)  AAs are broken, cholesterol is freed  cholesterol can be used and eliminated by the liver, sent out into the bile, changed to bile acids  forms vesicle which is digested by the lysosomal system and removed through the intestine  if LPL uptake is impaired, LDL levels remain elevated in the blood  results in hypercholesterolemia BCH210H © Lisa| Page 312  it is often inherited—familial hypercholesterolemia (FH)  risk indicator for CVD  LDL can be modified by oxidation rxns (increased risk for smokers) if they exist in the body for prolonged periods of time  these altered LDL particles are taken up by special scavenger LDL receptors in arteries  LDL entry into arterial walls (LDL arterial pathology)  LDL can enter arterial walls but can’t get out  cholesterol is difficult to degrade and accumulates  arterial walls aren’t supplied w a lot of blood (blood flows through artery), so it is hard to get rid of cholest
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