Histology (Cardio) Flashcards

1
Q

Artery + veins + capilaries

A

Arteries = going away from the heart (to body or to lungs)

Veins = going towards the heart

Between the artery and the vein = capilary

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2
Q

What lines vascular sturctures

A

Endothelial cells line vacsular strutures

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3
Q

Artery

A

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)

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4
Q

Artery Structure

A
  1. Atery walls
    • Have thick multi layer strictires
    • Experince higehr blood pressures than otehr types of blood vessels
  2. Lumen (in middle) - inner pasage where blood flows
    • Small lumen to maintain high pressure
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5
Q

Layers of artery

A
  1. Interna (Intima)
  2. Media
  3. Externa
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6
Q

Intima

A

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

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7
Q

Media

A

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

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8
Q

Externa (Adventitia)

A

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

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9
Q

Elastic arteries

A

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

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10
Q

Musclar arteries

A

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

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11
Q

Elastic vs. musclar artery

A

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

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12
Q

Veins

A

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

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13
Q

Capilaries

A

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

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14
Q

Function of capilaries

A

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)

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15
Q

Continious capilaries

A

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

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16
Q

Fenestrated capilaries

A

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

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17
Q

Discontinous

A

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

18
Q

Endothelial cells

A

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

19
Q

Endothelial Cell function

A

Regulates the exchange between the blood stream and surrounding tissues (example exhnage gasses and nutrients)

  1. Regulates immune responses and inflamation
    • Protective barrier (ex. BBB)
    • Platlet adhesion
    • Lukeocyte acivtaion
  2. Angioghensis - forms new vessels and capilaries
  3. Role of vascular homeostasis - enables blood vessels to adapt diameter and wall thickness in reponse to blood pressure
    • Released endogenous vasodialtaors (Ex. NO)
20
Q

Histology of veins + artiers + capilaries

A

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

21
Q

Arthereioscerosis

A

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

22
Q

Artherosclesis Plaque

A

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

23
Q

Artherosclesis Plaque epidemeiology

A

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

24
Q

Risk factors of Atheroscelris Plaque

A
  1. high BP
  2. High cholestral (high LDL)
  3. Iriatants –> smoke (nictine + tobacco)
  4. Disease (Obesity + diabetes)
  5. Age (older people) - because arteroes harde = easier to get plaque
  6. Lack of physical acivity
25
Q

Treatment of Atheroscelris Plaque

A
  1. Lifestyle change (excersize + diet)
  2. Medicaltion (Lower BP or lower cholestral + lower surgar)
  3. can do surgery for advances stages
26
Q

Symptoms of Atheroscelris Plaque

A

Most symptoms do not show until a blockage occurs

  1. Chest pain or pressure (angina)
  2. Pain in legor arm (if the blood flow is blcoked to the ar or leg)
  3. Shortness of breath
  4. Fatigue
  5. Confusion or dimenta (if the blood flow is blocked to the brain)
  6. Muscle weakness
  7. High blood pressure or kidney failure (if blood flow is blocked to the kidney)
27
Q

Artherscelsosis developmnet

A

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

28
Q

Foam cells

A

Macrahes that atke up fat

29
Q

Image of Artherosclesis

A

Left image - right is noram and left has plaque

Right image - right side is normal vs with plaque

30
Q

Image #2 of arthersclerisis

A

H and E image - white is necrosis + surounde dby fiberous cap

31
Q

Angiogensis

A

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

32
Q

Angiogensis in Tumogenisis

A

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

33
Q

Histology of Angiogensis

A

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

34
Q

Myocardial infarction

A

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)

35
Q

Cardiomycyte cell division

A

cardiomyctes = don’t prolfertate = can’t regernate = get scarr

36
Q

Diagnose Heart attck

A

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

37
Q

Prognosis of heart attack

A

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

38
Q

Treatment of heart attack

A
  1. PCI (preffeed treatmnet) - put cataher with mesh and baloon –> inflate the baloon –> expand mesh –> mesh restores integrity of artery
  2. Fibrnysis = reduce clotting agents in blood
    • If after 120 minutes
39
Q

Histology of Heart #1

A

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

40
Q

Histoloy of heart attck

A

Image 2 - left is healthy ; right have ecresisis = have cell debri (nuclei) = have inflamation + scar tissue + see immune cels (macrophages)

41
Q

Look at own presnetaion

A