Histology: every practice question

The blood vascular system is the heart plus the closed loop of arteries, capillaries and veins. The lymphatic vascular system is a one-way set of blind-ended lymphatic capillaries and larger lymphatic vessels that collect excess tissue fluid and return it to the veins through the thoracic and right lymphatic ducts.

• Lymphoid organs (nodes, spleen, thymus) belong to the immune system; only the lymphatic vessels are part of the circulatory system in this course.
• Pulmonary + systemic circulation is how the blood vascular system itself is divided; it leaves out the lymphatic half altogether.

Both ventricles eject the same volume each beat, but the resistance they pump against differs. The systemic circuit (left ventricle → aorta → body) has a high resistance, so it needs a high pressure (about 120/80 mmHg). The pulmonary circuit (right ventricle → pulmonary trunk → lungs) has a low resistance and runs at roughly a sixth of that pressure.

• The reverse pairing swaps the two circuits.
• Same pressure: equal volume does not mean equal pressure; pressure depends on the resistance downstream.

This is why the left ventricular wall is about three times thicker than the right.

The terms describe the direction of flow relative to the structure being discussed. A vessel that carries blood or lymph towards an organ is afferent; one that carries it away is efferent.

• The swapped option reverses the definitions.
• Oxygenated vs oxygen-poor confuses direction with content: an afferent vessel can carry either kind of blood.

Hook from the slide: Afferent = Arriving, Efferent = Externalising.

The lecture's list of cardiovascular elements runs heart → arteries → capillaries → veins. The elastic arteries (aorta, pulmonary trunk) leave the heart; they branch into muscular arteries that distribute blood to organs, then into small arteries, and finally arterioles, the resistance vessels just before the capillaries. Veins run the other way: venules → small veins → medium-sized veins → large veins.

• Putting muscular before elastic reverses the first step: the aorta, right at the heart, is the elastic one.
• Putting small artery before muscular breaks the steady fall in size.

Endo- = inside, myo- = muscle, epi- = upon. The endocardium lines the chambers and faces the blood; the myocardium is the thick muscular middle; the epicardium covers the outer surface and faces the pericardial cavity.

• Epicardium → myocardium → endocardium is the right sequence read from outside in, not inside out.
• Endocardium → epicardium → myocardium puts the covering layer in the middle; the muscle always sits between the two thin layers.

The heart wall is a modified vessel wall: endocardium ≈ tunica intima, myocardium ≈ tunica media, epicardium ≈ tunica adventitia.

Both the endocardium and the tunica intima are an endothelium (simple squamous epithelium) on a thin layer of connective tissue, and they face the blood. Where the great vessels join the heart, one simply runs into the other, so the endothelium lining blood is one unbroken sheet from the heart to the capillaries.

• Tunica media is the vessel's muscular/elastic middle coat; its heart equivalent is the myocardium.
• Tunica adventitia is the outer connective-tissue coat; its heart equivalent is the epicardium.

The myocardium is the muscular wall of the heart: cardiac muscle cells arranged in spiral layers round the chambers, grouped into fascicles by connective-tissue septa that carry vessels and nerves. It does the pumping, as the smooth muscle of the tunica media does in an artery.

• The endocardium is a thin lining (endothelium plus connective tissue), not the bulk of the wall; it matches the intima.
• The adventitia is the outer connective-tissue coat; the epicardium, not the myocardium, corresponds to it.

The fibrous pericardium is a sac of dense collagenous connective tissue attached to the diaphragm and the roots of the great vessels. It holds the heart in place and stops it overfilling. Because collagen barely stretches, the sac cannot expand to make room for fluid that collects suddenly.

• Elastic and recoiling describes elastic tissue, not this collagen sac.
• Secreting fluid is the job of the serous pericardium's mesothelium, which lines the inside of the fibrous sac and covers the heart.

The pericardium has two parts. The fibrous pericardium is the outer sac. The serous pericardium is a closed double layer of mesothelium: its parietal layer lines the inside of the fibrous sac, then folds back at the great vessels to become the visceral layer, which sticks to the heart surface and is the epicardium. The thin pericardial cavity lies between the two serous layers.

• Putting the visceral layer first inverts the serous pair: the visceral layer is the one on the heart.
• Putting the parietal layer outside the fibrous sac is wrong: it lines the fibrous sac from the inside.

Picture a fist (the heart) pushed into a balloon: the layer touching the fist is visceral, the outer balloon wall is parietal.

Normally the cavity is only a slit holding a few tens of millilitres of serous fluid made by the mesothelium. The fluid lets the beating heart slide against the sac without friction.

• The fibrous pericardium and parietal layer are fused to each other; there is no space between them.
• The visceral layer and myocardium are joined by the loose subepicardial connective tissue (with fat and coronary vessels), not separated by a cavity.

Because both walls of the cavity are serous layers, any blood or fluid that collects there touches the epicardium directly.

The serous pericardium has two layers. The visceral one covers the heart and is called the epicardium; it is mesothelium on loose connective tissue that holds fat, coronary vessels and nerves. The parietal one lines the inside of the fibrous sac.

• The parietal layer faces the epicardium across the pericardial cavity but is part of the sac, not the heart wall.
• The fibrous pericardium is the outermost dense sac and has no mesothelium of its own.

Hook: visceral = on the viscus (the heart itself).

The epicardium's loose connective tissue holds variable amounts of fat, and the large coronary branches lie in this fat on the heart surface, for example the anterior interventricular artery in the fat of the anterior interventricular sulcus. Smaller branches then dive into the myocardium.

• The myocardium contains only the smaller penetrating branches and a dense capillary bed, not the main vessels.
• The endocardium is a thin lining nourished largely by diffusion from the chamber blood.

This is why a coronary bypass graft is sewn onto the surface of the heart.

On the slide the epicardium is the pale outer band of the heart wall. Its free surface is a single row of flat mesothelial cells. Beneath them is loose connective tissue (fibro-elastic) with fat cells, nerve bundles and branches of the coronary arteries and veins, and below that the cardiac muscle begins.

• Endothelium with Purkinje fibres describes the endocardium on the inner side of the wall.
• Dense fibrous tissue without a surface epithelium describes the fibrous pericardium, the outer sac.

Mesothelium is the simple squamous epithelium that lines the body's serous cavities. In the heart it covers the epicardium and lines the parietal pericardium, and it secretes a thin serous fluid into the pericardial cavity. The fluid lubricates the surfaces as the heart moves with each beat.

• Endothelium lines blood vessels and the heart chambers; it faces blood, not the pericardial cavity.
• The fibrous pericardium is dense connective tissue with no secretory epithelium, and the fluid does not feed the myocardium (the coronary vessels do).

The two are named by where they sit, not by their shape. In the heart wall, the mesothelium is the surface of the epicardium and of the parietal pericardium, facing the pericardial cavity. The endothelium is the surface of the endocardium, facing the blood in the chambers, and it continues into the intima of every vessel.

• The swapped option reverses where each one lies.
• Cuboidal is wrong for both: each is a single layer of flat cells.

The epithelium is always on the free surface, the side that faces the cavity. So the parietal pericardium has its mesothelium on the inside, supported by a thin areolar layer, with the tough dense fibrous layer on the outside. The epicardium mirrors this across the cavity: mesothelium facing the cavity, areolar tissue beneath, then myocardium.

• Putting mesothelium on the outside turns the sac inside out; the outside of the sac faces the mediastinum, not a serous cavity.
• Putting areolar tissue on the cavity side would leave the cavity without its lining epithelium.

The two walls of the pericardial cavity are the two serous layers. The inner wall is the epicardium, whose mesothelium covers the heart; the outer wall is the parietal serous layer lining the fibrous sac. Blood that escapes into the cavity (haemopericardium) therefore bathes the epicardial surface.

• The fibrous pericardium is outside the parietal serous layer, so the blood is separated from it by that mesothelial lining.
• The myocardium lies beneath the epicardium and is not exposed to the cavity unless the wall has ruptured.

The pericardial cavity normally holds only a thin film of fluid. When blood or fluid collects quickly, the fibrous pericardium cannot expand, so the pressure in the sac rises and compresses the heart, first the thin-walled right atrium and ventricle. Less filling means a smaller stroke volume, falling blood pressure and, without drainage, death.

• If the sac stretched, there would be room for the fluid and no compression; it is the failure to stretch that matters.
• Scarring and thickening with no fluid is constrictive pericarditis, a different disease that also limits filling.

An effusion can be small and harmless, or large but slow enough for the sac to adapt. It becomes tamponade once the pressure in the sac stops the chambers filling, shown on the slide as a moderate effusion progressing to ventricular collapse.

• The swapped option reverses the two terms: tamponade is the severe, compressive end of an effusion.
• Fluid in the myocardium is myocardial oedema; an effusion is by definition in the pericardial cavity.

After a myocardial infarction the dead muscle is soft while it is being removed and before the scar is strong, typically in the first one to two weeks. A free-wall rupture lets ventricular blood under high pressure flood the pericardial cavity. The inextensible fibrous pericardium cannot expand, so the heart cannot fill: low blood pressure, fast pulse and sudden death.

• Pulmonary oedema comes from left heart failure raising pulmonary venous pressure; it does not follow from a hole that empties the ventricle into the sac.
• Pulmonary thromboembolism starts from deep vein thrombi in the legs, not from a ruptured ventricle.

Chronic inflammation of the pericardium (for example after tuberculosis) replaces it with dense scar tissue, sometimes calcified. The rigid shell stops the heart expanding in diastole, so blood backs up in the veins; the heart looks 'quiet' because it barely moves. The problem is filling, not pumping.

• Fluid-filled and stretched describes an effusion, and the problem in tamponade is also filling, not outflow.
• Scarred myocardium is a disease of the muscle; constrictive pericarditis spares the muscle.

The disease is a thick scarred sac, so the cure is to remove it. The lab's moving images show the same patient's heart barely moving before surgery and beating normally after pericardiectomy.

• Pericardiocentesis (needle drainage) treats tamponade, where the problem is fluid; there is no fluid to drain in constriction.
• Bypass grafting treats blocked coronary arteries, which are not the problem here.

Three clues point to the epicardium: a mesothelium on the surface, adipocytes (empty round spaces) and a nerve in the loose connective tissue, and cardiac muscle directly underneath. Coronary branches also run here.

• The endocardium also has flat surface cells (endothelium), but its connective tissue holds no fat or nerve bundles; it may hold pale Purkinje fibres, and it faces a chamber full of blood.
• The parietal pericardium has mesothelium too, but under it lies dense fibrous tissue, not cardiac muscle.

The cells themselves look the same: one layer of flattened cells with flat nuclei. What gives them away is the company they keep. Endothelium lines the endocardium, faces the lumen of a chamber and sits on thin connective tissue that runs into the subendocardium, where pale Purkinje fibres may appear. Mesothelium covers the epicardium, faces the pericardial cavity and sits on loose tissue with fat lobules, nerves and coronary vessels.

• Facing the pericardial cavity with fat and nerves below is the description of mesothelium.
• Cuboidal is wrong: both are simple squamous epithelia.

The spiral arrangement wrings blood out of the ventricles: when the layers contract, the chamber shortens and twists, squeezing blood toward the outflow valves. Between the fascicles, thin connective-tissue septa carry the rich capillary network and autonomic nerves that the working muscle needs. Ventricular fascicles are larger than atrial ones.

• Elastic laminae without vessels is wrong twice: the septa are ordinary connective tissue, and they carry the vessels and nerves.
• Straight longitudinal sheets would only shorten the chamber, not wring it; the slide shows spiral bands.

Wall thickness follows the pressure a chamber must produce. The left ventricle ejects into the aorta against the high systemic resistance; the right ventricle ejects the same volume into the low-resistance pulmonary circuit. In cross-section the left ventricle is a thick ring and the right a thin crescent wrapped against the interventricular septum.

• The pulmonary circulation is the right ventricle's target, and it is low pressure.
• Both ventricles hold and eject the same volume; otherwise blood would pile up in one circuit.

The slide also shows epicardial fat in the anterior interventricular sulcus, where the anterior interventricular artery runs.

The ventricles do most of the pumping, so their cells are wider and packed into bigger bundles. Atrial myocytes are thinner, and they have a second job: they carry small secretory granules of atrial natriuretic factor.

• The atrial-thicker option reverses the sizes.
• Thinner ventricular cells contradicts the lab manual: ventricular cells are the thicker ones.

When the atria are stretched by a high blood volume, the cells release ANF (also called atrial natriuretic peptide). The granules are tiny and are seen with the electron microscope rather than on routine H&E.

• Renin is made by the juxtaglomerular cells of the kidney, not by heart muscle.
• ADH is made by hypothalamic neurons and released from the posterior pituitary.

'Natriuretic' means causing sodium loss in the urine. ANF increases the glomerular filtration rate and blocks sodium reabsorption, and it also relaxes vascular smooth muscle. All its effects lower blood volume and pressure, the opposite of the renin–angiotensin–aldosterone system.

• Retaining sodium and water is what aldosterone and ADH do.
• Constricting arterioles is the action of angiotensin II and sympathetic stimulation; ANF dilates.

In longitudinal section, cardiac muscle shows fine cross-striations, oval nuclei sitting in the middle of each cell (often with a pale zone at each pole), branching cells, and dark, irregular, step-like intercalated discs crossing the fibres at intervals.

• Non-striated with central nuclei describes smooth muscle (which has no intercalated discs).
• Peripheral nuclei describes skeletal muscle, whose long multinucleated fibres push their nuclei under the cell membrane.

A skeletal muscle fibre forms by fusion of many myoblasts, so it is multinucleated and its nuclei lie just under the sarcolemma. A cardiac 'fibre' is a chain of separate cells joined end to end, each with its own one or two nuclei in the centre, surrounded by myofibrils.

• Cardiac peripheral / skeletal central puts both nuclei in the wrong place.
• Cardiac many / skeletal one swaps the whole pattern.

The branching lets cardiac cells form a three-dimensional meshwork that contracts as a unit, which suits emptying a chamber. A skeletal muscle fibre is one long cylindrical cell running much of the muscle's length.

• The swapped option gives each tissue the other's shape.
• Side-to-side, unbranched cardiac cells and branching skeletal fibres are both wrong: cardiac cells branch and meet end to end at intercalated discs.

The end-to-end junctions are the intercalated discs, the dark step-like lines crossing cardiac fibres. Skeletal muscle has nothing like them because each fibre is one continuous cell.

• Cross-striations are present in both cardiac and skeletal muscle, so they cannot tell them apart.
• Sarcomeres between Z lines is the structure of every striated muscle, cardiac and skeletal alike.

Exam tip: when an option is true of both tissues, it cannot be the distinguishing feature.

Each disc marks the boundary between two cardiac cells, so the discs occur at irregular intervals of one cell length, much farther apart than the closely spaced, regular striations. They stain darkly because the junctions are dense with protein.

• Skeletal muscle has no intercalated discs; its fibres are single cells with no end-to-end boundaries.
• Pale longitudinal lines run the wrong way: the discs cross the fibre.

Do not confuse them with contraction bands in infarcted muscle: those are many dense bands within a single cell.

In the electron microscope the disc runs like a staircase. Its transverse parts (the 'treads') carry the fasciae adherentes, where actin filaments anchor, and the desmosomes, which bind the cells against the pull of contraction. Its lateral parts (the 'risers') carry the gap junctions, which pass ions from cell to cell.

• Tight junctions seal epithelia; there are none in the intercalated disc.
• Hemidesmosomes fix a cell to its basement membrane, not to a neighbouring cell.

Each contraction pulls hard on the ends of every cardiac cell. The fascia adherens is where the actin of the last sarcomere attaches to the cell membrane, passing the force to the next cell; desmosomes act as spot welds anchored to intermediate filaments.

• Passing the electrical signal is the job of the gap junctions in the same disc.
• Anchoring to the basement membrane is done by hemidesmosomes, which are not part of the disc.

A gap junction is a cluster of connexon channels that join the cytoplasm of two neighbouring cells. Current flows through them easily, so depolarisation spreads quickly through the myocardium and the cells contract together as a functional syncytium.

• Fasciae adherentes anchor actin filaments; they hold, they do not conduct.
• Desmosomes (maculae adherentes) are spot welds for mechanical strength.

Each junction of the intercalated disc has its own adhesion proteins. Desmosomes bind neighbouring cells with the cadherin-family proteins desmoglein and desmocollin, held inside by desmoplakin. The fascia adherens uses N-cadherin linked to actin. Gap junctions are built from connexins.

• Collagen VII is an extracellular matrix protein that anchors the basal lamina of skin to the dermis; it plays no part in cell-to-cell junctions.
• The other two options are genuine disc proteins.

Likewise, hemidesmosomes are never part of an intercalated disc.

Cardiac myocytes live for the whole lifetime and do not divide, so the leftovers of years of lysosomal digestion accumulate as golden-brown lipofuscin granules in the pale zone at each pole of the nucleus.

• Glycogen washes out in routine processing and leaves pale, clear sarcoplasm, not brown granules (it is plentiful in Purkinje fibres).
• ANF granules lie in atrial cells but are tiny, colourless and visible only by electron microscopy.

The myocardium is almost entirely cardiac muscle: striated, branched cells with one or two central nuclei, intercalated discs, and a rich capillary network in the thin connective tissue between fascicles.

• The endocardium is a thin layer of endothelium and connective tissue on the luminal side; its only muscle-like cells are the pale Purkinje fibres.
• The epicardium is mesothelium over loose tissue with fat, nerves and coronary vessels on the outer surface.

The inner lining of the heart has three parts: a simple squamous endothelium facing the blood; a middle myoelastic layer of connective tissue with scattered smooth muscle cells; and the subendocardial layer, loose connective tissue continuous with the myocardium's connective tissue. The subendocardium of the ventricles carries the Purkinje fibres.

• Mesothelium with fat describes the epicardium on the outside of the heart.
• Endothelium directly on muscle leaves out the connective-tissue layers in which the Purkinje fibres run.

The subendocardium is loose connective tissue between the endothelium-covered lining and the cardiac muscle. In the ventricles it carries the network of Purkinje fibres that spreads the impulse; from there the fibres contact the contractile muscle. The lecture slide calls it the 'subendothelial layer', meaning the same place.

• The myocardium is the contractile muscle the Purkinje fibres feed into, not the layer they run in.
• The epicardium carries coronary vessels, fat and nerves on the outer surface.

Read the section from the lumen: endothelium (En), then the subendocardium (SEn) with Purkinje fibres (P), then the myocardium (M). Purkinje fibres are wider than the contractile cells and pale because their glycogen dissolves during processing.

• Subepicardium with adipocytes is on the other side of the wall, under a mesothelium; fat cells are empty rings with flattened peripheral nuclei, not fibres with central nuclei.
• The myoelastic layer lies just under the endothelium; its smooth muscle cells are thin and spindle-shaped, not large and pale.

Purkinje fibres are modified cardiac muscle cells built for conduction, not force. Much of their cytoplasm is glycogen instead of myofibrils, so in H&E they look swollen and pale beside the dense pink working muscle; in a trichrome stain they are pale lavender above the deep-red myocardium.

• Smaller and darker with more myofibrils describes the contractile cells, not the conducting ones.
• Myoglobin and extra myofibrils would make them darker; their pallor comes from glycogen.

Giveaway: big pale cells just under the endocardium = Purkinje fibres.

The glycogen occupies the middle of the cell. When it is removed by routine fixation and staining, empty-looking sarcoplasm is left around the centrally placed nucleus, and the few myofibrils sit mainly near the cell edge.

• Lipid is not what fills them, and their nucleus stays central.
• Glycogen does not stain with H&E; it shows up only with a special stain such as PAS, where it turns magenta.

The glycogen that washes out in routine H&E, leaving Purkinje fibres pale, is kept and coloured by PAS. So the same fibres that look empty in H&E turn deep magenta in PAS, which confirms both their identity and their location in the endocardium.

• Lipid is dissolved by routine processing and is shown with fat stains on frozen sections, not PAS.
• Collagen is blue in trichrome; PAS colours it only faintly. The fibres here are muscle cells, not connective tissue.

The fascia adherens anchors actin of the contractile apparatus; Purkinje fibres have few myofibrils and do little contracting, so they need little of it. They do need gap junctions, because conducting the impulse quickly is their whole job.

• No gap junctions would stop them conducting.
• Tight junctions are not found in intercalated discs of any kind.

The SA and AV nodes are small masses of specialised myocardial tissue in the right atrial wall; the AV bundle, bundle branches and Purkinje fibres are conducting muscle cells joined by gap junctions. They contain few myofibrils.

• Neurons: the heart beats without its nerves; autonomic nerves only speed or slow the rate set by the SA node. 'Purkinje cells' of the cerebellum are neurons, but Purkinje fibres of the heart are muscle.
• Smooth muscle occurs in the endocardium's myoelastic layer and in vessel walls, but it does not conduct the heartbeat.

The impulse starts in the SA node in the right atrial wall and spreads over both atria. It is funnelled into the AV node, which delays it, then into the AV bundle (of His), the only path through the insulating cardiac skeleton. The bundle splits into right and left branches in the interventricular septum; about halfway down these become the subendocardial Purkinje network that reaches all of both ventricles.

• Putting the bundle of His before the AV node skips the delay: the AV node feeds the bundle, not the other way round.
• Starting at the AV node makes it the pacemaker; the SA node fires first because it is the fastest.

The SA node's impulse spreads cell to cell through the atrial muscle (through gap junctions), so the atria contract first. The wave converges on the AV node in the floor of the right atrium, which passes it on after a delay.

• The ventricular myocardium is the last to depolarise, after the Purkinje fibres.
• The bundle of His comes after the AV node, carrying the impulse through the cardiac skeleton.

The SA node is a small mass of specialised cardiac muscle under the epicardium at the junction of the superior vena cava with the right atrium. Its cells depolarise spontaneously faster than any other part of the conduction system, so each beat starts there. When it fails, an artificial pacemaker can take over.

• The left atrium has no node; both nodes are on the right side.
• The interventricular septum carries the AV bundle and its branches, not the pacemaker.

The SA node lies along the crista terminalis where the superior vena cava enters the right atrium. Because its cells reach threshold fastest, every normal beat begins there.

• The AV node lies lower, in the floor of the right atrium at the atrioventricular junction; it fires spontaneously only if the SA node fails, and more slowly.
• The bundle of His is in the interventricular septum and only conducts what the AV node passes to it.

The lecture places the AV node at the junction between atria and ventricles; the textbook puts it more precisely in the floor of the right atrium. It collects the atrial impulse and passes it into the AV bundle, which pierces the cardiac skeleton.

• The left atrium has no nodal tissue.
• The upper interventricular septum below the skeleton is where the AV bundle runs and divides, after it has left the node.

The atria contract first and top up the ventricles at the end of their filling. If the impulse reached the ventricles at once, they would contract while the atria were still emptying, and the AV valves would close on incomplete filling.

• Ventricles emptying before the atria contract reverses the sequence: atrial contraction comes first.
• Ventricles contracting before the atria fill has nothing to do with the delay; the atria fill throughout ventricular contraction.

The bundle is the only muscular link between atria and ventricles. After piercing the fibrous skeleton it runs along the top of the muscular interventricular septum and bifurcates. About halfway down the septum the branches break up into the subendocardial Purkinje network.

• It cannot go around the skeleton: the skeleton insulates the atria from the ventricles all the way round, and the bundle runs in the septum, not the atrial wall.
• It does not enter the left ventricular free wall; it divides in the septum first, and both ventricles are reached through their own branch.

Purkinje fibres are the terminal branches of the right and left bundle branches, running in the subendocardium of both ventricles. They conduct faster than ordinary myocardium and end on the contractile cells, triggering contraction throughout both ventricles almost at once.

• The atria are reached directly from the SA node through atrial muscle, not through Purkinje fibres.
• Both bundle branches carry Purkinje fibres, so both ventricles are activated together.

Every free surface of the heart has a simple squamous epithelium: endothelium on the endocardium and both faces of every valve, mesothelium on the epicardium, and endothelium continuing into the aorta's intima. The SA node is a buried mass of specialised muscle at the superior vena cava–right atrium junction, under the epicardium, so it has no free surface of its own.

• The mitral valve is a fold of endocardium; endothelium covers both its surfaces.
• The epicardium is covered by mesothelium, which is also simple squamous.

As the impulse spreads through the myocardium, it creates voltage differences that reach the body surface. Electrodes at different points record them. The tracing shows heart rate, rhythm, conduction times through each part of the conduction system, effects of electrolytes and drugs, and the location of damaged muscle.

• Valve sounds are heard with a stethoscope or recorded by phonocardiography.
• Coronary flow is studied by angiography or perfusion scans, not by the ECG.

The skeleton must resist pull from every direction, as valves snap shut and muscle contracts on all sides, so its collagen bundles are woven in many directions, like the dermis. It lies mainly in the endocardium at the junction of atria and ventricles.

• Dense regular tissue has parallel bundles that resist pull in one direction only, as in tendons.
• Elastic tissue stretches and recoils, as in the aortic wall; the skeleton has to stay rigid to hold the valve openings in shape.

Seen from above with the atria removed, the skeleton is a flat plate between atria and ventricles: rings around the tricuspid, mitral, aortic and pulmonary openings, joined in the middle by the right and left fibrous trigones. The membranous part of the interventricular septum hangs down from it. The AV bundle passes through the right fibrous trigone.

• Cartilage: the human cardiac skeleton is fibrous connective tissue, not cartilage.
• Papillary muscles are muscular projections inside the ventricles; they pull on the chordae and are not part of the skeleton.

The dense connective tissue core of each valve leaflet is continuous with the fibrous ring it hangs from, and the chordae tendineae are cords of the same collagen. The small upper, membranous part of the interventricular septum is skeleton too.

• Papillary muscles and the muscular septum are cardiac muscle, not connective tissue.
• Purkinje fibres are modified muscle cells in the subendocardium; only the AV bundle passes through the skeleton.

In a four-chamber slice, nearly all of the interventricular septum is thick muscle. Only a small, thin patch at its top, just below the aortic root, is fibrous. This membranous septum is part of the cardiac skeleton; the AV bundle runs along its lower edge as it reaches the muscular septum.

• The muscular part is cardiac muscle, not skeleton.
• The membranous part is small and high, not the large lower portion.

The fibrous rings keep each valve opening the right shape so the cusps meet. The atrial and ventricular muscle bundles insert on the skeleton. Because connective tissue has no gap junctions, the skeleton blocks the atrial impulse everywhere except at the AV bundle.

• Pacemaking and coupling are done by the SA node and the AV node/bundle; the skeleton does the opposite of coupling.
• The skeleton does not conduct; and the coronary arteries are anchored in the epicardium, not by the skeleton.

This arrangement makes the AV node the gatekeeper. It delays the impulse so the atria can empty, and it limits how fast the ventricles can be driven if the atria beat abnormally fast. If the skeleton did not insulate, impulses could cross anywhere and the ventricles would contract out of step with the atria.

• Purkinje fibres are downstream, in the ventricular subendocardium; they do not cross the skeleton.
• Connective tissue has no gap junctions; that is exactly why it insulates.

There are two types of heart valve. The two AV valves (tricuspid on the right, mitral on the left) stop blood going back into the atria when the ventricles contract. The two semilunar valves (pulmonary and aortic) stop blood falling back into the ventricles when they relax.

• The swapped option reverses the two types.
• The cardiac skeleton surrounds the AV openings but does not close them; the AV valves hang from it.

The right AV valve has three cusps, the left two. The mitral valve is named for its resemblance to a bishop's mitre.

• Mitral on the right swaps the sides.
• Pulmonary and aortic are the semilunar valves at the exits of the ventricles.

Hook: 'Tricuspid on the Right'; the Left has the mitraL.

Each semilunar valve sits at the root of the great artery leaving a ventricle. The right ventricle feeds the lungs through the pulmonary trunk; the left feeds the body through the aorta.

• The first wrong option swaps which ventricle each valve serves.
• The second swaps which artery each valve opens into.

The mitral valve is an AV valve, never a semilunar one.

The collagen core (blue in trichrome) is continuous with the fibrous ring of the cardiac skeleton. It has no blood vessels: the thin leaflet is nourished by diffusion from the blood on both sides. Valves contain no muscle and open and close only with the pressure difference across them.

• Vascular loose tissue would be too weak and would bleed; the core is dense and avascular.
• Cardiac muscle stays in the myocardium and papillary muscles; the leaflet itself does not contract.

Because they are avascular, infected valves are hard for white cells and antibiotics to reach.

At the atrioventricular junction the skeleton lies mainly within the endocardium, and each leaflet grows out of it: its dense collagen core continues from the fibrous ring, and its endothelial covering continues from the endocardium of the atrium and ventricle.

• The myocardium stops at the base of the valve; the papillary muscles attach to the chordae, not to the leaflet core.
• The epicardium covers the outside of the heart and never reaches the valve openings.

The lecture lists the two forces: 'blood pressure closes valve' and 'papillary muscles tense chordae tendineae'. The pressure gradient does the closing; the papillary muscles, contracting with the rest of the ventricle, only keep the closed cusps from being blown back into the atrium.

• Papillary muscles pull the cusps toward the ventricle through the chordae; they brace the closed valve rather than shutting it.
• The cusps contain no muscle: they are dense connective tissue covered by endothelium.

The chordae tendineae are collagen cords running from the free edges of the AV cusps to the papillary muscles on the ventricular wall. As ventricular pressure rises, the papillary muscles shorten in step and keep the cords taut, so the cusps meet but cannot evert (prolapse) into the atria. If a papillary muscle ruptures after an infarct, the valve flips back and blood regurgitates into the atrium.

• Slack chordae would let the cusps blow back.
• Bracing like a tripod is how the semilunar valves stay shut; they have no chordae or papillary muscles.

When the ventricle relaxes, blood in the aorta or pulmonary trunk falls back toward it, fills the pocket-shaped cusps and pushes them together at the centre. The three cusps meet along their thick edges, with the nodules sealing the middle, and hold one another up.

• Chordae and papillary muscles belong to the AV valves only.
• Smooth muscle is not present in the cusps; valve movement is passive.

Exam point: 'three cusps, no muscular support' = semilunar.

The two ventricles work together, so valves of the same type always do the same thing on both sides. When the ventricles contract, their pressure rises above atrial pressure (closing the tricuspid and mitral valves) and above arterial pressure (opening the aortic and pulmonary valves). When they relax, the AV valves open to let them fill and the semilunar valves close.

• AV open, semilunar closed is the picture of relaxed, filling ventricles.
• Mitral and aortic open together mixes the two states; a valve and its partner on the other side always move together.

When the valve closes, the lunules of neighbouring cusps press against each other and the three nodules meet in the centre to seal the gap. Behind each cusp the vessel wall bulges out as a sinus; blood fills the sinuses during diastole and keeps the cusps from sticking to the wall.

• Swapping nodule and lunule reverses them: the nodule is the single thickening in the middle.
• Chordae tendineae belong to the AV valves; nothing tethers a semilunar cusp.

The aortic valve has right, left and posterior cusps, each with a sinus behind it. The coronary ostia sit in the right and left aortic sinuses, just above the valve. The pulmonary valve's cusps are named left, anterior and right, and it has no coronary openings.

• The posterior sinus is the non-coronary one, so it cannot be one of the two.
• Anterior is a pulmonary cusp name; the aortic valve has no anterior cusp.

Trichrome stains collagen blue and muscle red/purple. A leaflet whose dense connective-tissue core (C) is continuous at its base with the fibrous skeleton in the endocardium (En), between atrium (A) and ventricle (V), with cords (CT) attached, is an atrioventricular valve. The chordae are the cords tying its free edge to the papillary muscles.

• A semilunar cusp has no chordae tendineae, and it hangs from the root of the aorta or pulmonary trunk, not between atrium and ventricle.
• A papillary muscle would stain red like the myocardium; only its chordae are blue.

Mouth bacteria (often viridans streptococci) can enter the blood during dental work and settle on the valves, which are covered by endothelium and have an avascular connective-tissue core. Clumps of bacteria, platelets and fibrin grow there as vegetations and can damage the valve.

• Myocardium: infection of the muscle is myocarditis, not lesions on the valves.
• Epicardium: infection of the outer surface is pericarditis; the epicardium never covers a valve.

The aortic sinuses are the three bulges of the aortic root behind the valve cusps. The right coronary artery leaves the right sinus and the left coronary artery the left sinus, so the heart muscle is the first tissue supplied with freshly ejected blood.

• The aortic arch is farther along and gives off the vessels to the head and arms.
• Nothing arises below the valve: that is still inside the ventricle.

During ejection the aorta stretches and stores energy in its elastic wall. When the ventricle relaxes and the aortic valve closes, the wall recoils and keeps the aortic pressure high, pushing blood into the coronary arteries from the aortic sinuses. During contraction, the squeezing myocardium compresses its own vessels, so flow, especially to the left ventricle, falls.

• The ventricular squeeze squashes the intramural coronary vessels rather than filling them.
• The pulmonary trunk does not give rise to the coronary arteries.

A fast heart rate shortens diastole and so shortens the time for coronary filling.

The anterior interventricular artery runs down the anterior interventricular sulcus, in epicardial fat, supplying the front of both ventricles and most of the septum. The circumflex runs round the left side in the coronary (atrioventricular) groove.

• The right marginal artery is a branch of the right coronary artery.
• The posterior interventricular artery usually comes from the right coronary artery.

The right coronary artery runs in the right coronary groove, gives the right marginal artery along the lower border of the heart, and usually continues as the posterior interventricular artery in the posterior interventricular sulcus (a 'right-dominant' heart).

• The anterior interventricular and circumflex arteries are the two branches of the left coronary artery.
• A left marginal artery arises from the circumflex, a left coronary branch.

A clot that blocks a coronary artery (coronary thrombosis) cuts off oxygen to the muscle it supplies. After about 20–30 minutes of severe ischaemia the cells start to die. The slides show a coronary artery whose lumen is filled by a thrombus and the infarcted muscle.

• Spasm without cell death describes angina-type ischaemia, which is reversible.
• Pericardial scarring is constrictive pericarditis, a different disease.

After macrophages clear the dead muscle, granulation tissue grows in and fibroblasts lay down collagen. By about a month the infarct is largely fibrous tissue, which matures into a dense, pale collagen scar over the following weeks (complete by about two months). Because the scar cannot contract, the heart pumps less well, and a large scar can lead to heart failure.

• Myocyte division (hyperplasia) does not happen in the adult heart to any useful degree; the muscle is a permanent tissue.
• Myocytes do not turn into smooth muscle.

A raised afterload makes the left ventricle work harder. It responds by thickening its wall: each muscle cell makes more sarcomeres and becomes larger, while the number of cells stays about the same.

• Hyperplasia needs cells that can divide; adult cardiac muscle cells, like neurons, essentially cannot.
• Fatty change makes cells pale and vacuolated but does not double the weight of the heart.

When dying cardiac muscle is flooded with calcium (for example when blood flow returns), its myofibrils hypercontract into thick, dense, eosinophilic bands crowded together across the cell. Healthy muscle shows only one intercalated disc at each end of a cell.

• Intercalated discs are thin, step-like lines at the cell borders, roughly one cell length apart.
• Lipofuscin is golden-brown granules at the nuclear poles, not bands across the cell.

A tunic is a concentric coat of the vessel wall. The intima lines the lumen (endothelium plus a thin subendothelial layer); the media is the middle coat of smooth muscle and elastic tissue; the adventitia (tunica externa) is the outer connective-tissue coat that blends with the surrounding tissue.

• Media first is impossible: the endothelium always faces the blood, and it belongs to the intima.
• Adventitia first reverses the order; adventitia means the coat that comes from outside.

Almost every vessel-identification question is really asking which of these three coats dominates. Hook: I-M-A, from inside out.

The endothelium is a single layer of flat cells resting on a basal lamina. Beneath it lies the subendothelial layer, a thin band of loose connective tissue (in large arteries it also holds a few smooth muscle cells). In arteries the internal elastic lamina marks the outer edge of the intima.

• A thick layer of circular smooth muscle is the tunica media, the next coat out.
• Loose connective tissue with nerves and vasa vasorum describes the adventitia.

The lecture describes the capillary wall as intima: endothelium only; media: "none" (pericytes); adventitia: none. So the one coat every vessel shares is the intima, whose essential part is the endothelium lining the lumen.

• Tunica media (smooth muscle) is missing from capillaries and from postcapillary venules; scattered pericytes are the closest a capillary comes to a media.
• Tunica adventitia is also absent from capillaries; it is very thin even in arterioles.

The internal elastic lamina is a sheet of elastin with small holes (fenestrae) that let nutrients diffuse to the media. After death or fixation the artery contracts, so the lamina buckles into a crisp wavy line, dark in an elastic stain. It is most prominent in muscular arteries; most veins lack one.

• The external elastic lamina sits at the other side of the media, between media and adventitia.
• The basal lamina lies directly under the endothelial cells; it is an electron-microscope structure, not the wavy line seen in the light microscope.

The media is built of circumferentially arranged smooth muscle cells with elastic fibres and lamellae (and some collagen) between them. The smooth muscle cells themselves secrete this matrix. In elastic arteries the elastic lamellae dominate; in muscular arteries the smooth muscle does; in veins the media is thin.

• Skeletal muscle is never part of a vessel wall; it is voluntary muscle.
• Loose connective tissue with vasa vasorum and nerves is the adventitia.

Vasoconstriction and vasodilation are changes in lumen diameter produced by contraction or relaxation of the circular smooth muscle of the media. That is how muscular arteries distribute blood and arterioles set resistance.

• The intima (endothelium) releases signals such as nitric oxide and endothelin-1 that act on the media, but it does not itself contract.
• The adventitia is connective tissue that anchors the vessel; its smooth muscle bundles appear only in large veins, and it does not set lumen size.

Arteries are bounded on both sides of the media by elastic sheets: the internal elastic lamina between intima and media, and the thinner, less distinct external elastic lamina between media and adventitia. It is clearest in large muscular arteries in an elastic stain and is often hard to see in H&E. Having both laminae is a feature of arteries; veins usually have neither, or only a thin internal one in the largest veins.

• Internal elastic lamina is the inner border, under the intima.
• Basal lamina underlies the endothelium (and surrounds smooth muscle cells); it is not a tunic border.

The tunica adventitia (tunica externa) is mostly type I collagen and elastic fibres with fibroblasts. It blends into the surrounding connective tissue, holding the vessel in place, and it carries the vessel's own nerves and, in large vessels, the vasa vasorum. It is thin in arteries and is the thickest coat of veins.

• The inner coat that lines the lumen is the intima with its subendothelial layer.
• The smooth-muscle coat that sets diameter is the media.

An artery must withstand and smooth out high, pulsatile pressure (elastic arteries) or actively change diameter (muscular arteries and arterioles). Both jobs belong to the media, so it is the thickest tunic, and the artery's wall is thick compared with its lumen.

• The intima is thin in every healthy vessel; a thick intima suggests disease such as atherosclerosis.
• The adventitia is the thickest tunic of veins, not arteries.

Rule for slides: thickest layer media → artery; thickest layer adventitia → vein.

Veins carry blood at low pressure and do not need a strong muscular media. Their wall is mainly a thick adventitia of collagen and elastic fibres, which gets thicker as veins get larger; in the largest veins (venae cavae) it also contains longitudinal bundles of smooth muscle.

• The media is the most prominent layer of arteries; in veins it is only a few layers of smooth muscle.
• The intima of veins is well developed enough to fold into valves, but it is still thin.

The vasa vasorum are a microvasculature (arterioles, capillaries and venules) running in the adventitia of large arteries and veins and sending branches into the outer part of the media. They are larger and more numerous in veins than in arteries, because venous blood in the lumen carries less oxygen.

• Lacteals are the lymphatic capillaries of intestinal villi, not part of a vessel wall.
• The tunica media is the middle coat, not something carried inside the adventitia.

Diffusion works only over short distances. Small vessels are fed entirely from their lumen, but the outer media and adventitia of large vessels lie too far away, so they are supplied by vasa vasorum in the adventitia. They do for the wall of a large vessel what the coronary arteries do for the heart wall.

• Too little oxygen in the lumen is false for the aorta, which carries fully oxygenated blood and still needs vasa vasorum (lower venous oxygen only explains why veins have more of them).
• Impermeable endothelium is false: the inner wall is fed by diffusion across the endothelium.

In this scanning micrograph the three tunics are labelled by their initials: TI/EC (tunica intima with endothelial cells facing the lumen), TM (tunica media, the compact smooth-muscle ring, thrown into folds because the artery contracted when fixed) and TA (tunica adventitia, the loose connective-tissue fibres outside).

• The tunica intima is the thin lining of endothelial cells (EC) at the lumen surface.
• The tunica adventitia is the loose fibrous meshwork (TA) at the periphery.

The lab aorta slide shows the vasa vasorum as small clear spaces lined by simple squamous endothelium in the adventitia and outer media. They are arterioles, capillaries and venules, so they hold red blood cells.

• Lymphatic capillaries also have thin walls but never contain red blood cells.
• Nerve bundles (nervi vasorum) also run in the adventitia, but they are solid with no lumen.

The endothelium lines the heart, every blood vessel and the lymphatics. Its cells are elongated and very thin, aligned with the direction of flow, and rest on a basal lamina; junctional complexes (tight junctions and adherens junctions) hold them together. Being so thin, it lets substances pass quickly between blood and tissue.

• Columnar cells are tall; endothelial cells are flat (squamous).
• Several layers of cuboidal cells describes a stratified cuboidal epithelium (e.g. sweat-gland ducts), not a vessel lining.

Every molecule or cell moving between blood and tissue must cross the endothelium, so it acts as a selective barrier. It is also an active organ: it keeps four pairs of opposing signals in balance (dilatation vs constriction, growth inhibition vs growth promotion, antithrombosis vs prothrombosis, anti-inflammation vs proinflammation).

• Passive lining ignores all of these functions.
• Tensile strength comes from collagen in the adventitia and media, not from a single layer of thin cells.

This is the dilatation vs constriction pair on the lecture's balance. Endothelial cells make nitric oxide (NO), which diffuses into the smooth muscle of the media and relaxes it, and prostacyclin (PGI₂), which also relaxes muscle and inhibits platelets. Endothelin-1 is a peptide that strongly contracts vascular smooth muscle.

• The two wrong options each put endothelin-1 among the dilators or nitric oxide among the constrictors; NO is the classic endothelium-derived relaxing factor.

The molecules come from the textbook; the slide shows the pair as dilatation vs constriction.

The slide pictures normal endothelial function as a balance between two sets of four:

• Growth promotion (stimulating smooth-muscle proliferation, e.g. by growth factors) is on the opposing side.
• Prothrombosis is also on the opposing side, paired against antithrombosis.

Antithrombosis means preventing clots. The intact endothelium separates blood from the thrombogenic subendothelial collagen; its surface carries heparin-like molecules (heparan sulfate) that act with antithrombin to inactivate thrombin; it secretes tissue plasminogen activator (tPA), which turns plasminogen into fibrin-dissolving plasmin; and its NO and prostacyclin inhibit platelets.

• von Willebrand factor is prothrombotic: it tethers platelets to exposed collagen.
• Exposed collagen and plasminogen activator inhibitor both favour clotting.

von Willebrand factor (vWF) is a large glycoprotein made by endothelial cells and stored in rod-shaped Weibel–Palade bodies. When the vessel is injured it bridges platelet receptors to exposed subendothelial collagen, the first step of the platelet plug. It sits on the prothrombosis side of the endothelial balance.

• Tissue plasminogen activator breaks clots down (fibrinolysis), so it is antithrombotic.
• Prostacyclin inhibits platelet aggregation and dilates vessels, so it is antithrombotic too.

In infection or tissue damage, signals such as histamine and cytokines activate the endothelium. It becomes leakier and displays adhesion molecules (selectins, then integrin ligands) on its luminal surface; leukocytes roll, adhere and squeeze between the endothelial cells into the tissue. The postcapillary venule is the main site.

• Nitric oxide release is the dilatation function.
• Tissue plasminogen activator is part of the antithrombotic function.

Injury from high blood pressure, high LDL, smoking or hyperglycaemia removes the protective signals (NO, prostacyclin, tPA). The four functions then all tip to the same side:

• The second option describes the healthy side, not damage.
• The third mixes the two sides; damage tips all four the same way.

Chronic endothelial injury (hypertension, high LDL, smoking, diabetes) makes the endothelium more permeable. LDL enters the subendothelial intima and is oxidised; monocytes follow, become macrophages, and engulf oxidised LDL to become lipid-laden foam cells (a fatty streak). Smooth muscle cells migrate into the intima and lay down collagen, forming the fibrous cap of an atheroma that narrows the lumen.

• The second sequence puts endothelial injury after LDL entry; injury comes first and lets LDL in.
• The third places the lesion in the media and adventitia; atheromas are intimal lesions.

The atheroma grows in the intima, between the endothelium and the internal elastic lamina, which is why it bulges into and narrows the lumen. It contains pools of lipid and cholesterol, foam cells, lymphocytes, and smooth muscle cells that have migrated from the media and secrete the collagen of the fibrous cap.

• Media is wrong: the media under a large plaque may thin, but the plaque itself is intimal.
• Adventitial inflammation around obliterated vasa vasorum is syphilitic aortitis, which weakens the media and causes aneurysm, not an atheroma.

The lecture's functional names: elastic arteries = conducting (low-resistance pathway); muscular arteries = distributing; arterioles = resistance; capillaries = exchange. The elastic arteries are the largest arteries, closest to the heart: the aorta, the large arteries leaving its arch (brachiocephalic, common carotid, subclavian), the common iliacs, and the pulmonary trunk and arteries.

• Resistance vessels are the arterioles; the wide aorta offers little resistance.
• Femoral and radial arteries are muscular (distributing) arteries.

In the adult aorta the media contains dozens (about 50) of elastic lamellae: sheets of elastin with holes (fenestrae) that let nutrients diffuse. Between them lie smooth muscle cells (which secrete the elastin and collagen), collagen and a few fibroblasts. In an elastic stain (Verhoeff or Weigert) the lamellae are dark wavy lines filling the whole media; in H&E they are pink and refractile.

• Many smooth-muscle layers with little elastic material is the media of a muscular artery.
• Loose connective tissue with vasa vasorum is the adventitia.

During systole the aorta takes the full force of each ejection; its elastic lamellae stretch and absorb part of the stroke volume. During diastole they recoil, pushing that stored blood onward and keeping arterial pressure up (to about 80 mmHg rather than zero). This damps the pressure swings and keeps flow continuous. Elastic recoil also drives coronary filling in diastole.

• Rhythmic contraction is wrong: the recoil is passive and elastic, not muscular pumping.
• Rigid wall, pressure falling to zero is the opposite; a stiff aorta (as in old age) gives a higher systolic and lower diastolic pressure.

The aorta's three tunics in an elastic stain: a pale, narrow intima (endothelium and subendothelium); a very thick media crowded with concentric, wavy, black-staining fenestrated elastic membranes; and a relatively thin adventitia of collagen with vasa vasorum.

• The intima is the thin, lighter strip next to the lumen; it has no stack of lamellae.
• The adventitia is the thickest layer of the vena cava, not the aorta.

Fibrillin-1 forms the microfibrils on which elastin is laid down. In Marfan syndrome the elastic fibres are defective (and excess TGF-β activity degrades them further). The structure richest in elastic tissue is the media of elastic arteries, especially the ascending aorta. Its weakened lamellae let the wall bulge (aneurysm) or split within the media (dissection), presenting as tearing chest pain radiating to the back.

• The intima is the site of atherosclerosis, not of the Marfan defect.
• The adventitia is mostly collagen; damage to its vasa vasorum is the mechanism of syphilitic aneurysm.

The vasa vasorum feed the adventitia and outer media of the aorta. In syphilitic aortitis an obliterative endarteritis of these small vessels starves the outer media; patches of smooth muscle and elastic lamellae die and are replaced by scar. The weakened wall stretches under arterial pressure, typically forming an aneurysm of the ascending aorta. This shows why thick walls need their own blood supply.

• Intimal lipid and atheroma is atherosclerosis, which begins with endothelial injury.
• Medial thickening and hypertension is the wrong direction: loss of the vasa vasorum destroys media; it does not add muscle.

Most named arteries (radial, femoral, coronary, renal, splenic) are muscular arteries. The lecture says they are distributing vessels that respond to stimulus and regulate blood pressure: sympathetic nerves and local signals change the tone of their thick smooth-muscle media.

• Conducting vessels are the elastic arteries (aorta, pulmonary trunk).
• Exchange vessels are the capillaries.

Moving away from the heart, arteries gradually lose elastin and gain smooth muscle. A muscular artery's media is several to about 40 layers of circular smooth muscle cells, with a few elastic fibres between them, and is bounded by a prominent internal and a thinner external elastic lamina. Contraction of this muscle lets the vessel regulate flow to its organ.

• Many elastic lamellae with little muscle is the elastic artery.
• One to three smooth-muscle layers is an arteriole.

The lecture lists "prominent internal elastic lamina" in the intima of muscular arteries; the lab notes it is visible even in H&E. Behind it lies a thick media of smooth muscle. Smooth muscle alone is not distinctive (every artery has some), and vasa vasorum are only sometimes present.

• The external elastic lamina lies at the outer edge of the media (not the adventitia) and is thinner and less obvious.
• Many lamellae through the whole media identifies an elastic artery.

Both have three tunics and a thick media; what differs is what the media is made of, and it follows from the job. The elastic artery must recoil, so its media is a stack of elastic lamellae (it looks like a patch of curly ramen). The muscular artery must change diameter, so its media is smooth muscle, bordered by a prominent internal elastic lamina.

• The swapped option reverses the two.
• No elastic lamina at all is wrong for a muscular artery; its internal elastic lamina is its best clue (arterioles may lack one).

The lecture calls arterioles "resistance vessels, the primary site of vascular resistance". The largest drop in blood pressure occurs across them, and the tone of their smooth muscle sets both systemic vascular resistance and how much blood enters each capillary bed.

• Exchange vessels are the capillaries.
• Capacitance vessels are the veins, which hold most of the blood volume at low pressure.

The lecture's arteriole: intima endothelium, no connective tissue or smooth muscle; media 1–3 layers of smooth muscle; adventitia very thin connective tissue. On a slide its lumen is narrow, roughly as wide as its wall is thick, and an internal elastic lamina is usually absent (at most a thin one in the largest arterioles). A small artery has more muscle layers.

• No smooth muscle, scattered pericytes describes a capillary or postcapillary venule.
• Prominent internal elastic lamina and many muscle layers describes a muscular artery.

Arterioles are numerous, narrow and sit just upstream of the capillary beds. Because resistance rises with the inverse fourth power of the radius, a small contraction of their thin muscle coat changes resistance, and therefore flow, a great deal. That is why they are the main site of vascular resistance and the main way blood is redistributed between organs.

• Direct proportion to radius understates the effect and gets the direction wrong: a wider vessel has less resistance.
• Viscosity depends mainly on haematocrit; the vessel wall does not regulate it.

The tone of arteriolar smooth muscle resists blood flow, helps set systemic blood pressure and controls flow into the capillaries. In exercising muscle, local metabolites relax these arterioles, so the muscle's share of cardiac output rises while arterioles elsewhere (gut, kidney) constrict.

• The aorta is a low-resistance conducting vessel; it cannot steer blood to one organ.
• Muscular arteries distribute blood to whole organs and adjust somewhat, but the fine control of flow into capillary beds is at the arterioles, the main site of resistance.

The common end point of all forms of primary hypertension is increased peripheral vascular resistance, set by small arteries and arterioles. Under chronic high pressure their smooth muscle hypertrophies and multiplies and the intima thickens, so the wall gets thicker and the lumen smaller, and resistance rises further.

• Thinner walls and wider lumens would lower resistance and blood pressure, the opposite.
• Fragmented elastic lamellae and aneurysm is a lesion of large elastic arteries (Marfan, dissection), not of arterioles.

The lecture's microvasculature diagram shows three arrangements: the simple pathway (artery → arteriole → capillary bed → venule → vein), the arteriovenous shunt (arteriole joined directly to venule, bypassing capillaries), and the portal system (two capillary beds in series joined by a portal vein).

• Venule → capillaries → arteriole runs backwards; blood flows from the arterial to the venous side.
• Arteriole → venule → capillaries puts the capillaries after the venule.

Capillaries arise either directly from arterioles or from metarterioles, short vessels with scattered smooth muscle cells. Each true capillary leaving a metarteriole is guarded by a small ring of smooth muscle, the precapillary sphincter, which controls whether blood enters it. The metarteriole continues as a thoroughfare channel that drains into a postcapillary venule.

• The thoroughfare channel is the distal, muscle-free continuation of the metarteriole; there are no elastic valves.
• A muscular artery is far larger and never feeds capillaries directly.

Precapillary sphincters work like switches at the entrance of each true capillary. When tissue activity rises (more CO₂, H⁺, adenosine, less O₂), they relax and blood spreads through the network for exchange.

• No flow through the metarteriole is wrong: the metarteriole stays open whatever the sphincters do.
• Routing through the thoroughfare channel is what happens when the sphincters contract.

With the sphincters shut, only the central metarteriole-to-thoroughfare-channel route stays open, so most of the bed receives little flow. This lets a resting tissue limit its perfusion while blood still passes on to the venous side.

• Spreading through all capillaries is the relaxed state.
• Diversion into a portal vein describes a portal system, a fixed anatomical arrangement, not a sphincter response.

Arteriovenous shunts are muscular channels connecting arterioles straight to venules. When they open, blood bypasses the capillary bed; when they constrict, blood is forced through the capillaries. They are common in the skin of the fingertips, nose and ears, where coiled shunts wrapped in a capsule form glomus bodies, and they help the body conserve or shed heat.

• The liver receives gut blood through a portal system, two capillary beds in series, not a shunt.
• Fat absorption in the gut goes into lacteals; no arteriole drains into a lymphatic.

Normally blood passes through one capillary bed between artery and vein. In a portal system the pathway is artery → capillary bed → portal vein → second capillary bed → vein. The hepatic portal vein carries absorbed nutrients from the intestine to the liver sinusoids; the hypophyseal portal veins carry hypothalamic releasing hormones to the anterior pituitary.

• The spleen and posterior pituitary are not portal systems (the posterior pituitary is supplied directly by the inferior hypophyseal arteries).
• Parallel beds fed by one arteriole are just an ordinary capillary network; "portal" means beds in series.

The capillary wall is a single thin endothelial cell, the shortest possible diffusion distance, and capillaries have the largest total cross-sectional area and the slowest flow of any vessel, giving time for exchange.

• Conducting vessels are the elastic arteries.
• Resistance vessels are the arterioles.

A capillary is a tube of one to three endothelial cells rolled around a lumen just wide enough for a red cell (about 5–10 µm). The endothelium rests on a basal lamina, and here and there a pericyte wraps around it. There is no smooth-muscle layer and no connective-tissue coat.

• A thin smooth-muscle media first appears in arterioles (and muscular venules).
• An internal elastic lamina belongs to arteries; capillaries have none.

Structure follows function: capillaries exist for exchange, and the rate of diffusion falls steeply with distance. A single attenuated endothelial cell (often less than 1 µm thick away from the nucleus) on a basal lamina keeps the barrier as thin as possible.

• Withstanding higher pressure needs a thicker wall (law of Laplace); capillaries cope only because their radius is tiny.
• Keeping red cells in depends on the endothelium being continuous, not on how thin it is; sinusoids are thin and do let cells through.

The lecture defines pericytes as small cells that surround the endothelial cells; they are the capillary's only cells outside the endothelium ("media: none, pericytes"). On a slide their nucleus sits on the outside of the endothelium, and scanning micrographs show their processes clasping the capillary. Postcapillary venules have them too ("intima: endothelium, pericytes").

• A continuous smooth-muscle coat is a media, which capillaries lack; pericytes are scattered.
• Arterioles and muscular arteries have a true smooth-muscle media instead.

In a transmission electron micrograph of a capillary (labels E, P, L, BL) the pericyte's processes lie against the outer surface of the endothelium, and both cells are wrapped in basal lamina. The pericyte has its own basal lamina, which often merges with the endothelial one, so the pericyte appears enclosed within it.

• Bare is wrong: the basal lamina is always present around both cells.
• The internal elastic lamina is an arterial structure; capillaries have none.

Pericytes have contractile proteins like smooth muscle cells. By contracting they can narrow a capillary, which is why the lecture lists them where the media would be. They also stabilise the capillary wall; their loss in diabetes contributes to retinal microaneurysms.

• Fenestrae are pores in the endothelial cells of fenestrated capillaries.
• Phagocytosis is the job of macrophages (such as the macrophages lining liver sinusoids), not pericytes.

Pericytes are mesenchymal cells that keep stem-cell potential. When a vessel is injured or new vessels form, they proliferate and become smooth muscle cells of the new vessel wall or fibroblasts, so they take part in vessel repair and in building the media of new venules and arterioles. On a micrograph, the cell hugging the outside of a capillary is the pericyte, an adult stem cell.

• Terminally differentiated is the opposite of what textbooks describe.
• Macrophages come from monocytes and are phagocytic; pericytes are not.

Position gives it away. Endothelial cells form the tube itself, and their nuclei protrude into the lumen. Pericytes hug the outside of the tube, so their nuclei sit outward, on the far side of the endothelium, inside the basal lamina. In the classic transmission micrograph the endothelial cell (E) faces the lumen (L) and the pericyte (P) lies outside it, with basal lamina (BL) around both.

• The swapped option reverses inner and outer.
• Capillaries have no internal elastic lamina.

The lab manual notes that capillaries in all tissues look very similar in the light microscope but differ markedly in the electron microscope. The types are defined by whether the endothelium has pores (fenestrae) or gaps, and whether the basement membrane is continuous. Each type occurs where its leakiness suits the organ.

• Capillaries have no smooth-muscle layer, so it cannot be used.
• Pericyte number varies but does not define the type.

The lecture: most common type; uninterrupted endothelium; continuous basement membrane. The lab table adds tight junctions with adjacent cells plus marginal folds (flaps of cytoplasm projecting into the lumen at the cell junctions), no fenestrae, and the smallest diameter. Substances cross by diffusion, through intercellular clefts or in pinocytotic vesicles (caveolae) that shuttle across the cell.

• Pores closed by diaphragms define the fenestrated capillary.
• A discontinuous basement membrane belongs to sinusoids only.