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Cardio Week 1 > ICL 1.2: Histology of Cardiovascular System > Flashcards

ICL 1.2: Histology of Cardiovascular System Flashcards

1
Q

what are the layers of the heart?

A
  1. pericardium
  2. epicardium
  3. myocardium
  4. endocardium
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2
Q

what is the epicardium?

A

outermost layer of heart wall

comprised of a mesothelium (simple squamous epithelia) that forms the visceral layer of pericardium and a subepicardial connective tissue layer with nerves, ganglia, coronary and adipose cells

the visceral layer of the serous pericardium IS the epicardium

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3
Q

what is the myocardium?

A

the thick middle layer of the heart

comprised of cardiomyocytes that are contractile, conducting or endocrine in function and that are arranged in muscle layers that insert onto a fibrous cardiac skeleton

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4
Q

what is the endocardium?

A

the innermost layer of the heart wall

comprised of endothelium (single layer of squamous cells that are continuous with intima of the large outflow vessels) and connective tissue with Purkinje cells and fibers. This endothelium covers all of the heart’s luminal structures.

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5
Q

what is pericarditis?

A

inflammation of the pericardium

usually caused by viral or bacterial infection, autoimmune diseases, kidney failure or injury

it can progress to cardiac effusion or arrhythmia

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6
Q

what are the symptoms of pericarditis?

A

chest pain, caused by the sac’s layers becoming inflamed, forming adhhesions and possibly rubbing against or constricting the heart.

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7
Q

which cells make up the myocardium?

A
  1. cardiomyocytes
  2. cardiac skeleton
  3. cardiac conduction system
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8
Q

how are cardiomyocytes of the myocardium connected?

A

myocytes are connected by gap junctions which allow for chemical communication between the cells to coordinate function like contraction

they also have intercalated discs and fasciae adherens which allow for structural support during contraction so that integrity is maintained

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9
Q

what are cardiomyopathies?

A

diseases that effect the cardiomyocytes and lead to heart dysfunction

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10
Q

what is dilated cardiomyopathy?

A

most common type of cardiomyopathy!

due to loss of myocytes, thinning/weakening of ventricular wall and dilation of lumen

this effects the hearts ability to pump blood and cardiac output is reduced because of systolic dysfunction

idiopathic or secondary causes such as toxins, medications, nutritional deficiencies, alcohol abuse, myocarditis (coxackie virus), pregnancy

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11
Q

what is hypertrophic cardiomyopathy?

A

thickening of ventricular or septal wall, cardiomyocyte hypertrophy and disarray, reduced ventricular filling or obstructed outflow

reduces the hearts ability to pump blood with reduced cardiac output due to diastolic dysfunction

usually caused by genetic mutations usually of sacromere myocyte proteins

can cause arrhythmias and sudden death

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12
Q

what is restrictive cardiomyopathy?

A

stiffening of ventricular wall doesn’t allow for complete filling of the ventricles = decreased compliance

reduced outflow due to excessive fibrosis of myocardium and deposition of extracellular proteins in some cases

causes are idiopathic or at times due to secondary amyloidosis

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13
Q

what is inflammatory cardiomyopathy?

A

T-lymphocyte infiltrates cause myocyte damage

usually occurs in viral, also Lyme Disease, toxoplasma or Chagas’ disease

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14
Q

what most commonly causes an MI?

A

coronary atherosclerosis with occluding thrombus

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15
Q

what histological changes do you see in someone who has had an MI?

A

coagulative necrosis –> neutrophil infiltrate –> granulation and scar

Within 1 hour there is intercellular edema and “wavy fibers” at the periphery of the infarct. These are noncontractile dead fibers, stretched by the adjacent viable contracting myocytes.

In 12 to 72 hours, there is infiltration of neutrophils with progressive coagulative necrosis of myocytes. Dead myocytes become hypereosinophilic with loss of nuclei.

Between 3 and 7 days, after onset, dead myocytes begin to disintegrate and are removed by macrophages. There is proliferation of fibroblasts with formation of granulation tissue, which progressively replaces necrotic tissue.

After 6 weeks, healing is complete by fibrosis

slide 9

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16
Q

what is the cardiac skeleton of the myocardium?

A

dense connective tissue

doesn’t conduct electricity so it acts as insulation which is important for the coordinated contraction of the ventricles and the heart

  1. annuli fibrosi
  2. left and right trigones
  3. septum membranacium
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17
Q

what are the important structures in the cardiac skeleton of the myocardium?

A
  1. annuli fibrosi
  2. left and right trigones
  3. septum membranacium
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18
Q

what is the function of the annuli fibrosi?

A

annuli fibrosi form the openings between the atria/ventricles and the outflow vessels

they also contribute to the valves that are at these openings

they provide structural support

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19
Q

what happens with calcification of the heart?

A

with aging calcium can accumulate in cardiomyocyte tissue and on cardiac skeleton

this accumulation can delay depolarisation wave in geriatric patients because the calcified tissue doesn’t conduct electricity well

calcified tissue can become ossified

slide 12

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20
Q

how does the cardiac conduction system of the myocardium work?

A

specificalized myocytes which generate and transmit electrical signals through the heart

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21
Q

how does the cardiac conduction system of the myocardium work?

A

SA node in the RA by the SVC is the pace maker composed of myocytes that send out signals to the AV node also in the RA which then relays the electrical signals through the Bundle of His in the interventricular septum

the bundle then splits into two branches which travel down the subendocardium into the ventricles and then branch out as Perkinje fibers

Perkinje fibers are conducting myocytes which transmit the electrical signals to the other myocytes

contraction starts at the apex of the heart and spreads upward towards the base to push blood towards the base of the heart where outflow tracts of the ventricles are located

slide 13

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22
Q

what do purkinje myocytes look like histologically?

A

they lack myofibrils which are present in the contractile myocytes

they have a dilated size and can be polynucleate

usually found in the connective tissue

they form gap junctions with the contractile myocytes which is how they transmit signals for contraction

slide 14

23
Q

what is cardiac conduction block?

A

a condition that interferes with the heart’s natural pacemaker due to some kind of obstruction in the electrical conduction system of the heart

heart block may cause no symptoms or cases where the heart’s ability to control and trigger heartbeats may be completely ineffective or unreliable, heart block can usually be treated by inserting an artificial pacemaker

24
Q

what are ventricular premature depolarizations?

A

this occurs often following MI and instead of having the normal pacing of heart contraction by the SA node, you get an enhanced electrical activity of the purkinje fibers which cause premature depolarizations and can disregulate the normal rhythm of the heart

they can trigger atrial fibrillation!!

A ventricular premature depolarizations (VPD) occurs when the heartbeat is initiated by Purkinje fibers in the ventricles rather than by the sinoatrial node. VPDs may cause no symptoms or may be perceived as a “skipped beat” or felt as palpitations in the chest. Single beat PVCs do not usually pose a danger but may also cause chest pain. More seriously, VPDs may be associated with underlying heart disease or sudden cardiac death.

Ventricular premature depolarizations (VPD) can trigger ventricular fibrillation and death. VPD often originates a site that is typically at the scar border and characterized by the presence of Purkinje potentials. The etiology of the enhanced electrical activity of the Purkinje network post myocardial infarction (MI) is unclear. One possible mechanism is related to its relative resistance to ischemia. Purkinje fibers within the scar are more likely to survive post MI and maintain their inherited automaticity due to its subendocardial location and exposure to cavitary blood.

25
Q

what is endocarditis?

A

an inflammation of the inner layer of the heart and is characterized by lesions, known as vegetations, a mass of platelets, fibrin, microcolonies of microorganisms, and some inflammatory cells

infective endocarditis is typically caused by a bacterial infection and less commonly a fungal infection and usually affects the valves.

symptoms may include fever, small areas of bleeding into the skin, heart murmur, feeling tired, and may include valvular insufficiency, heart failure, stroke, and kidney failure

the bacterial most commonly involved are streptococci or staphylococci

diagnosis is suspected based on symptoms and supported by blood cultures or ultrasound.

26
Q

what are the risk factors for endocarditis?

A
  1. valvular heart disease including rheumatic disease
  2. congenital heart disease
  3. artificial valves
  4. hemodialysis
  5. intravenous drug use
  6. electronic pacemaker
27
Q

what is an aortic dissection?

A

a mechanical tear that disrupts the innermost layer of a vessel, the tunica intima

then you get blood pooling into the vessel wall between the tunica intima and tunica media which destabilizes the integrity of the vessel

28
Q

what are the layers of an arterial wall?

A
  1. tunica intima (inner)
  2. tunica media
  3. tunica adventitia
29
Q

what is the tunica intima?

A

the innermost layer of the arterial wall comprised of
squamous endothelium, basal lamina, subendothelium of loose connective tissue (collagen II, IV & V) and a few longitudinally arranged scattered smooth muscle cells

composed of squamous endothelial cells with gap junctions

form a nice thick surface for blood to flow past

an internal fenestrated elastic lamina separates the intima from media

30
Q

what is the tunica media?

A

a middle layer of the arterial wall that is smooth muscle

smooth muscle cells are helically arranged and prominent in muscular arteries

also contains elastic fibers, type III collagen & proteoglycans

an external elastic lamina in large muscular arteries separates t. media from t.adventitia

31
Q

what is the tunica adventitia?

A

the outer layer of arterial wall comprised of
longitudinally arranged elastic fibers, fibroblasts, type I collagen, blood vessels, nerves, muscle (in veins) and vasa vasorum-blood supply to vessels

32
Q

what are elastic arteries? what do they look like histologically?

A
  1. large flattened lumen
  2. thickened subendothelium
  3. internal elastic lamina that is difficult to discern
  4. prominent vaso vasorum in adventitia (blood supply)

typically 40-70 elastic lamellae in t. media of adults

the elastin allows for passive contraction

slide 21

33
Q

what are muscular arteries? what do they look like histologically?

A

muscular arteries have a round lumen and an attenuated subendothelium with a prominent, scalloped internal elastic lamina

these arteries have a thick t. media typically comprised of 5-20 smooth muscle cell layers and a thin t. adventitia often containing vaso vasorum in larger distributing vessels

these are called distributing arteries because the myocytes can contract and regulate flow through the arteries

slide 21

34
Q

what are arterioles? what do they look like histologically?

A

arterioles have a diameter < 0.1mm and a t. intima that contains an internal elastic lamina only in large arterioles

the t. media has 1-3 layers of smooth muscle and NO external elastic lamina

the t. adventitia is highly attenuated

the smallest arterioles are called metarterioles and have a discontinuous layer of smooth muscle cells that controls blood flow to capillary beds

35
Q

what is atherosclerosis? what does it look like histologically?

A

an inflammatory remodeling of the tunica intima

you get accumulation of fatty plaques and cholesterol and macrophages try to clear that material from the damaged vessel walls but sometimes they become residents and can induce changes in the structure of the tunica intima

you can an increase of smooth muscle cells and fibroblasts and you get a thickening of the t. intima to the point that you occlude blood flow – you can even get calcification if the plaques get really bad

slide 22

36
Q

what is Marfan syndrome?

A

caused by mutations in fibrillin-1, an esential glycoprotein component of the extracellular matrix, including the biogenesis and maintenance of elastic fibers

elastic fibers are found throughout the body, but are particularly abundant in the aorta

these patients are predisposed to developing aneurysms due to weakening of vessel walls!

37
Q

what is Ehlers-Danlos syndrome?

A

a group of genetic connective tissue disorders

mutations in these genes usually alter the structure, production, or processing of collagen or proteins that interact with collagen

collagen provides structure and strength to connective tissue

a defect in collagen can weaken connective tissue in blood vessels potentially resulting in aortic dissection

these patients are predisposed to developing aneurysms due to weakening of vessel walls!

38
Q

what is the function of a metaarteriole?

A

doesn’t have a standard tunica media but it does have scattered smooth muscle cells that act as capillary sphincters and can alter flow of blood into the capillary beds

blood flow through capillary networks is highly controlled!

39
Q

what is an arteriovenous anastomosis?

A

AV shunt is when blood flows from an arteriole to venule directly and totally bypassing the capillary bed

usually this is invoked in response to trying to conserve heat so it doesn’t dissipate in the capillary bed

ex. Reynaud’s syndrome

40
Q

what is Reynaud’s syndrome?

A

Raynaud’s Disease most commonly manifests after exposure to cold and occurs because of spasm of smooth muscle of small arteries and arterioles that feed some peripheral capillary beds

spasms of terminal arterioles would reduce or shunt blood flow away from the peripheral capillary beds

the cause of Raynaud’s phenomenon is unknown, although abnormal sympathetic nerve control of blood-vessel diameter and nerve sensitivity to cold are suspected of being involved

secondary Reynaud’s can result in ulceration of the tissues

41
Q

what is the structure of a capillary?

A

capillaries have a single layer squamous endothelial cells oriented with blood flow with marginal folds overlap on upstream edge of cell, a basal lamina, some areola CT and no T.media

vessels are 5-10 µm in diameter and cells are joined by occludens (tight) junctions

vessels may be encapsulated by myoepithelial pericytes that form gap junctions with endothelium and contract to aid in controlling blood flow

42
Q

what are the functions of the capillaries?

A
  1. transport and exchange of materials between blood & parenchyma
  2. deposition of adhesion molecules
  3. maintenance of vascular tone
  4. produce and exocytoticly release clotting factors such as von Willebrand factor (VWF)
43
Q

what are the different types of capillaries?

A
  1. continuous
  2. fenestrated
  3. discontinuous/sinusoids
44
Q

what are continuous capillaries? where are they found in the body?

A

no pores or fenestrations, cont. basal lamina

present in muscle, nerve, c.t.

tight junctions (zonula occludens)

45
Q

what are fenestrated capillaries? where are they found in the body?

A

fenestrae of 60-80 nm with diaphragm

found in pancreas, intestines, endocrine glands

renal glomerulus has no diaphragms

46
Q

what are sinusoidal capillaries? where are they found in the body?

A

they have an incomplete basal lamina and large intracellular clefts

these are designed to allow large molecules and cells to pass back and forth!

found in the liver, spleen, lymph nodes, marrow

47
Q

what is systemic capillary leak syndrome?

A

systemic capillary leak syndrome (SCLS) is a rare acquired disorder characterized by acute and severe recurrent attacks associated with a rapid fall in blood pressure

repeated flares of massive leakage of plasma from blood vessels into neighboring body cavities and muscles

attacks often last several days and require emergency care

the underlying cause of SCLS is not known but is thought to be autoimmune

48
Q

what are the 3 types of veins?

A
  1. large veins
  2. medium sized vein (*have valves)
  3. venule
49
Q

what do medium veins look like histologically?

A
  • poorly defined IEL
  • few circularly oriented SMCs
  • no EEL
  • thick tunica adventitia
  • valves!

slide 32

50
Q

what do large veins look like histologically?

A

return blood to heart

  1. thin wall compared to diameter
  2. no IEL
  3. thick subendothelial c.t.
  4. modest tunica media (except legs)
  5. prominent tunica adventitia with longitudinal smooth muscle
  6. deep vaso vasorum because they’re transporting a lot of blood with low oxygen

slide 35

51
Q

what are the major histological differences between arteries and veins?

A

arteries have a much thicker tunica media = more smooth muscle

arteries have an internal elastic lamina; veins don’t

slide 36

52
Q

what is the lymphatic vascular system?

A

the right lymphatic duct drains the upper right part of the body

the thoracic duct drains the rest of the body

interstitial fluid gets taken up into lymphatic capillaries which can be distinguished because unlike veins, don’t have RBCs in the lumen, instead they’ll have WBCs

53
Q

what is lymphedema?

A

swelling in one or more extremities that results from impaired flow of the lymphatic system

lymphedema most often affects a single arm or leg, but in uncommon situations both limbs are affected

primary lymphedema is the result of an anatomical abnormality of the lymph vessels and is a rare, inherited condition

secondary lymphedema results from an identifiable damage to or obstruction of normally-functioning lymph vessels and nodes

usually this occurs with parasites that block lymph flow but in the US it’s most related to breast cancer surgery where lymph nodes are removed which can lead to bad drainage

Cardio Week 1 (15 decks)

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