Histology (Cardio) Flashcards
Artery + veins + capilaries
Arteries = going away from the heart (to body or to lungs)
Veins = going towards the heart
Between the artery and the vein = capilary
What lines vascular sturctures
Endothelial cells line vacsular strutures
Artery
Overall - carries blood away from the heart
Used in:
1. Systemic system - prvides oxygenated blood to the tissues
2. Pulminary system - carries dexogentaed blood to the lungs (to have has exchange)
Artery Structure
- Atery walls
- Have thick multi layer strictires
- Experince higehr blood pressures than otehr types of blood vessels
- Lumen (in middle) - inner pasage where blood flows
- Small lumen to maintain high pressure
Layers of artery
- Interna (Intima)
- Media
- Externa
Intima
Has simply squamous endothelial cell lining - appear to be wave due to constriction of smooth muscles
- Has internal elastic memebrane made of thick elastic fibers in larger arteries (provides stucture while allowing the artery to stretch)
- Can streatch and recoil
- Has basement membrane - provides strength and flexbility + bidns the endothelium to connective tissue
Composed of epithelial and connective tissue
Media
Thickest layer in arteries
- Consists of layers of smooth muscle + connective tissues arrenged in circular sheets
Has smooth muscles and elastic fibers
- Propertions of these vary depending on distance from heart
Has external elastic membrane in large vessels
Function - responsible for constriction and dilation which leads to chnages in blood flow
- As constrcite the lumen gets smaller = flow increase = lower BP increases
- Dilation = lumen increases = lower BP
Externa (Adventitia)
Normally thinner than media (EXCEPT in the largest arteries)
Sheath of connective tissue (mostly collegen)
Has collegenous fibers - structural and connective tissues + suport for blood vesels
- Edges are interlaced wit surounding tissuve - miantains arteries in the same relative position
Elastic arteries
Closest to the heart + Thickest walls + Veseels larger than 10 mm
Has the largest percent of collegen + elastic fiers –> they can stretch and recoil with each heart beat
- Elastic recoil eklps miantain the ressure greaduent that drives the blood throughout the body
- Amount of elastic fibers decreases the further form the heart
Musclar arteries
Fartehr from the heart
Function - disrtibute oxygen to organs + regulate blood flow through vasodilation and constriction
- Does vasodilation + constrictoion
There is a higer percent of muscle and less elastic in the media –> helps in blood flow regulation
Run parallel to veins - allows the arteyes pulsations to help blood move through the veins
Elastic vs. musclar artery
Elastic - closer to heart + more elastin + maintain blood flow by absorbing pressure from heary contraction
Musckar - farther form the heart + can regulate blood flow through constriction
There is no clear line of demarcation where elastic becomes musclar
Veins
Same layers of the arteries BUT lack the elastic maina and have a thinner media + larger lumens + sooth muscle more loosley arraged
Conatins one-way valvles (outfoldsing of the tunica intima)
- Venus system is at low prssure —> have one way valves that prevent backflow + mucle contarction in leg ai blood flow from lower extremities
Function - retrun blood to the heart
Capilaries
One layer of endothelial cells + epithelia cells form a protextive layer (layer is the basal lamina)
Have three types:
1. Continous
2. Fenestrated
3. Dscontinous
Function of capilaries
Overall - exchnages material between blood and tissue
- Provides nutrients and oxytegn to tissue + remices CO2 and wate from tissue
Mechanism of exchnage:
1. Simple diffusion
2. Membrane trabsport carriers
3. Transcytosis - used fro large mileculares (uses endo/exocytosis)
Continious capilaries
Most common type
Endothlial cells are join by a tight junction –> forms a continous tube
Less permable (only small molecules can pass through)
- Has barreier function (Example - form the BBB)
EM image - see tight junction being pointed out
Image 2 - see basal lamina + endthelium (thciket layer) _ see tight junction
Fenestrated capilaries
Endothelia wall contains pores (called fenetra) - covered by a thin layer of diaphram
- basal lamina is continous
More permable –> fenetrate allows larger molecules to pass through (exmaple proteins can pass)
- Facilitates absorption
Image 1 - lumen surface is green + see black pores
Discontinous
Aka Sinusoidal
Endotheliam has large opening which lack diaphrams
Basal lamina is thin and discontinous over opening
Most permable - large protains and cells can pass openings
- Allows trafficking of blood cells
- Site of contraction
Endothelial cells
Single layer of cells that line the entire vascular system
Component of intima
Selectivley permeable
Phenotypically heterogenous depening on localization (example - diffrent location have different permabiblity)
Left - lume ends and the endotjlial cells line
Right - vascular lumen where vesslesare + see RBCs passing + see endothlial covering outter layer of the lumen
Endothelial Cell function
Regulates the exchange between the blood stream and surrounding tissues (example exhnage gasses and nutrients)
- Regulates immune responses and inflamation
- Protective barrier (ex. BBB)
- Platlet adhesion
- Lukeocyte acivtaion
- Angioghensis - forms new vessels and capilaries
- Role of vascular homeostasis - enables blood vessels to adapt diameter and wall thickness in reponse to blood pressure
- Released endogenous vasodialtaors (Ex. NO)
Histology of veins + artiers + capilaries
Left - artery and vein
- Difffernces = smooth muscle in artery is thicj and thin the vein
Right - capilary size (9-12 microns) - see endothelian layer + RBCs inside
Arthereioscerosis
Blood vessels that carry oxygen and nutrients from the hart to other parts of the body become thick and stiff –> resticts blood flow to rogans and tissues (lose elasticty)
- Because artery walls can harden
Artherosclesis Plaque
Plaque = a subtype of artheresclesis
Caised by a buildup of fats + cholestral in the arteries and walls
- Buildup = plaques
- Caused by formation
Plauqe narrows the arteries + blocks the blood flow + can burst + can cause blood clots
Preventable and treatable
Artherosclesis Plaque epidemeiology
Less preventlant in central south merica and afria asia
More prevelant in US and Japan
US - corany artery disease casies 1 out of 6 deaths
Accounts for 400,000 deaths each year
Risk factors of Atheroscelris Plaque
- high BP
- High cholestral (high LDL)
- Iriatants –> smoke (nictine + tobacco)
- Disease (Obesity + diabetes)
- Age (older people) - because arteroes harde = easier to get plaque
- Lack of physical acivity
Treatment of Atheroscelris Plaque
- Lifestyle change (excersize + diet)
- Medicaltion (Lower BP or lower cholestral + lower surgar)
- can do surgery for advances stages
Symptoms of Atheroscelris Plaque
Most symptoms do not show until a blockage occurs
- Chest pain or pressure (angina)
- Pain in legor arm (if the blood flow is blcoked to the ar or leg)
- Shortness of breath
- Fatigue
- Confusion or dimenta (if the blood flow is blocked to the brain)
- Muscle weakness
- High blood pressure or kidney failure (if blood flow is blocked to the kidney)
Artherscelsosis developmnet
Have high LDL in the blood –> LDL is oxidized into a proinflamatory particle –> get endothelia (intima) dmage –> damage causes an immune reponse (endoltheliam secretes adherion + smoother msucle will casie immune response ad secrete kemokines) –> Immune cdells come (monocytes become macrophages - macrophages take up LDL and become foam cells) –> macrophages accumilate –> get fatty streak fomration (causes necrosis) –> steam becomes he plaque (Plaque formation and growth) –> Fiberous cap formation –> plaque rupture or erosion
- Fiberous cap = protext the plauqe from breaking up
- Cap can rupture and cause blood clot (cause heart attck or stroke
Foam cells
Macrahes that atke up fat
Image of Artherosclesis
Left image - right is noram and left has plaque
Right image - right side is normal vs with plaque
Image #2 of arthersclerisis
H and E image - white is necrosis + surounde dby fiberous cap
Angiogensis
Formation of new blood vessels from pre-exiting ones
- Induced by angiogensis fcators (Ex. VEGF)
Proccess - Endothelial cells differentiate –> divide –> migrate withing the lining of blood vessels
- factor sguide drection to make new blood vessels
- If vessels are inactived = can regress over time
Occurs during embryonic development + post natal growth + wound repair
Angiogensis in Tumogenisis
When normal cells become cancerous (due to oncogenic mutaions and clonal expansion) = get rapid cel division
Intially the cancer cells form solid tumors - solid timors utilize nutrients in surround tissue –> over time tumor will become hypoxic = needs more nuterinets –> cells expressed VEGF to grow vessels = get nuertients
- Intial tumores are avasculate and get oxugen and nuertients from surrounding tissie
Histology of Angiogensis
Left - normal (uniform + organized)
Right = cancerous (see abnormal vascular surroundig cancer + have soace and blood vesels (cancer cells can gointo blood vessels)
- Lining of vessel wall is thin = get nurteints + oxygen
Myocardial infarction
Myocardial infacation = heart attack
Have decreased/cesstion of blood flow to the mayocardium (coronal arteries) - results in ischemia and death (get cel death of cariomycytes)
- Ischemia intially presents as retrosternal chest (under sternum)/upper extremity pain (can be quick or gradual)
- causes Ischemia = loss of blood flow = dangerous (starve cardiomyctes = get cell detah = heart can’t function)
- Heart attcks can happen over several days or sudden
Often teh result of plaque buildup/rupture (plaque comes off lining and blocks coronary artery) or artery occulasion pr blood clot –> causes decreased blood flow
Can cause necrosis (issue because cardiomycyes are non proliferative)
Cardiomycyte cell division
cardiomyctes = don’t prolfertate = can’t regernate = get scarr
Diagnose Heart attck
Diagnose with EKG or image or syrum
Usually you have low levels of troponin in the serum –> see increase in tropinin = diagnose acute or chronic versions of heart attcks
- Look at cardiac toprnin T and cardiac Tropinin I
- can dfferentate chromic or acute
Prognosis of heart attack
Acute and chromic –> 5-30% mortality rate
- First year mortality rate –> 5-12%
Biggest danger = after –> pateint has damage heart that causes heart defects and heart disease
Treatment of heart attack
- PCI (preffeed treatmnet) - put cataher with mesh and baloon –> inflate the baloon –> expand mesh –> mesh restores integrity of artery
- Fibrnysis = reduce clotting agents in blood
- If after 120 minutes
Histology of Heart #1
Image 1 - Shows tiisue after heart attack – white arrow shows scar tissue
- D - see scar tissue + have blood clots (thrombi) –> long term damae that casies hear failure
Histoloy of heart attck
Image 2 - left is healthy ; right have ecresisis = have cell debri (nuclei) = have inflamation + scar tissue + see immune cels (macrophages)
Look at own presnetaion
