BIOLOGY 03048 ANATOMY; WEEKS 4 AND 5: THE THORAX; CV AND PULMONARY HISTOLOGY

9/21/99 W. Crone (303 FTZ, 629-7439, cronewil@hvcc.edu, www.hvcc.edu/academ/faculty/crone/index.html)

Readings: Moore and Dalley, Ch. 1. Cormack, Chs. 3, 5, 6. van Wynsberghe and Cooley cases 8, 9, 10, 12, 18, 33.

possible web sites: http://www.med.unsw.edu.au/pathology/pathmus/m1007070.htm

(breast cancer specimen and discussion)

http://www-medlib.med.utah.edu/WebPath/TUTORIAL/MYOCARD/MYOCARD.html

(tutorial on myocardial infarction)

http://www.neosoft.com/~uthman/blood_cells.html (atlas of normal blood cells)

http://hms.medweb.harvard.edu/HS_Heme/AtlasTOC.htm (atlas of abnormal blood cells)

http://www.med.virginia.edu/medicine/clinical/pathology/educ/innes/text/nh/hema.html

(overall guide to hematology)

THE SECOND TEST COVERS THROUGH THIS MATERIAL

 

THE BONY THORAX: The bony thorax or rib cage protects the heart, lungs, and great vessels of the thoracic cavity. 7 true ribs articulate with the sternum via unossified costal cartilage; ribs 8, 9, 10 (false ribs) end in the costal cartilage of #7; and 11, 12 are floating. Disruption of cartilage (rib dislocation) or inflammation (costochondritis) is painful.5 The rib head includes facets for articulation to the vertebral bodies and the tubercle contains a facet for articulaton to a transverse process. The point of greatest curvature is the angle of the rib, hence, the most vulnerable to breakage. 5 Movements of the thoracic wall, particularly for ribs: during inspiration, increase in the dimensions of the thorax. The diaphragm is lowered by contraction (75% of inspiratory effort), the contraction of the intercostal muscles and the scalenes raises the ribs and expands the diameter of the thorax (25% of inspiratory effort), with expiration from muscular relaxation.

MUSCLES/BLOOD SUPPLY OF THE THORAX: The epaxial muscles are the deep muscles of the back and are innervated by the dorsal rami of those mixed spinal nerves, assisting in control over the spine. The hypaxial wall layers of muscle are best seen developed in the abdomen. In the thorax, they are broken up into the intercostal muscles between ribs. The external intercostal and internal intercostal muscles will make more sense when we describe their abdominal homologies (the tranverse muscle layer is mostly fascial in the rib region). Since these are hypaxial muscles, they are innervated by intercostal nerves. Along with these intercostal nerves are small arteries. In back, the posterior intercostal arteries arise from the descending aorta, and from the upper limbs' main supplier, the subclavian arteries, come the internal thoracic arteries along the sternum. These give off anterior intercostal arteries to each space, and the anterior/posterior intercostals anastomose. An intercostal nerve is sheltered by the overhang of the costal groove of a rib anteriorly but not posteriorly, as it lies inferior to an intercostal artery (VAN--don't forget the intercostal vein), so need to have consideration of needle placement for thoracentesis or regional anesthesia.5

THE BREAST: As with other placental mammals, we have a thickened mammary ridge of ectodermal material ventrally. The breast (mammary gland) develops as a branching ingrowth of ducts into the superficial fascia, and is supplied by intercostals and the internal thoracic arteries. A major clinical concern is breast cancer, and for that, the lymphatics of breast need to be considered. Central axillary nodes are the most frequently palpable, along the chest wall, midway between the anterior and posterior axillary folds. Overall, the breast mostly drains to axillary nodes, with the medial part of the breast draining to parasternal lymph nodes and the lower quadrants into abdominal nodes. 5 Retraction of skin from cancerous involvement of Cooper's ligaments; peau d' orange skin from interference with lymphatic drainage.3,4,5

Thoracic cavity: two pleural cavities and a pericardial cavity

The mediastinum is the midline space between and excluding the lungs; traditional divisions of the mediastinum into superior, anterior, middle, and posterior regions.

Visceral pleura reflects outward to line the inner surface of the chest wall (parietal pleura). The fluid between cuts down on friction and maintains capillary attraction between pleural surfaces (resisting pneumothorax).

Tension pneumothorax:"one-way" valve action that traps air in pleural space, squeezing mediastinum and contralateral lung.5 Flail chest with paradoxical wall movement.5 With expiration and relaxation of diaphragm, recesses of the pleural cavity form, and could be the sites of possible pleural effusions with various disease processes. Inflammation of pleura: pleurisy.

LUNGS: Trachea is 10 cm long and is anterior to esophagus, extending from larynx. The trachea bifurcates into the right and left main bronchi, posterior to the great vessels, at the anterior landmark of the sternal angle. Foreign bodies will tend to fall into the right bronchus, as vs. the left. The carina (ridge at the bifurcation) can be widened in mediastinal illnesses, e.g., lung cancer.5

Lungs are paired, cone-shaped organs that fill the pleural cavities from the neck to the diaphragm. Each primary bronchus enters the lung at the hilus or indentation. Bronchi and pulmonary blood vessels connected by connective tissues together make the root of the lung. The base of the lung rests on the diaphragm, and the apex projects 2-4 cm above the inner 1/3 of the clavicle (so potentially vulnerable to stabbings in that area). The lungs are divided by pleura-lined fissures into lobes: 3 on right, 2 on left. Furthermore, lungs are divided into triangular, resectable units called bronchopulmonary segments, each served by a segmental bronchus, artery, and drained by segmental veins and lymphatics.

Lung circulation for oxygenation of blood: The right ventricle narrows into a conus arteriosus, leading to the pulmonary trunk, which bifurcates into the right and left pulmonary arteries, and the pulmonary arteries divide into lobar arteries, and increasingly small branches from there, which would lead to the risk of pulmonary thromboembolism from deep veins of the lower extremities. Pulmonary capillaries drain into venules that join with pulmonary veins (2 on each side, superior and inferior). Pulmonary veins then drain into the left atrium.

DIAPHRAGM: the thoracic diaphragm is a broad, thin muscle, with origin including ribs 6-12, and inserting to a central tendon, innervated by the phrenic nerve. The phrenic nerve is the sole motor innervation of the diaphragm, and arises from C3-C5 nerves. Developmentally, the muscle of the diaphragm is hypaxial muscle derived from cervical body segments (think of the expanding lungs"pushing" them inferiorly).2 The diaphragm is dome-shaped, with the pericardium sitting on the dome (so that the heart rides up and down during respiration). Pleuropericardial folds prominent in development"catch" the phrenic nerves so that they are near the fibrous pericardium.2

Fetal circulation differs from the adult in that without use of the lungs, it is appropriate to send right atrial blood to the systemic circulation. Two mechanisms seen in the thorax:

1) leaving the VI aortic arch connected to the dorsal aorta (ductus arteriosus, adult remnant known as ligamentum arteriosum)

2) making a hole in the heart's median septum between the atria (foramen ovale, adult remnant known as fossa ovalis)

 

The ligamentum arteriosum is the site near which the left recurrent laryngeal nerve loops, so that mediastinal disease can lead to hoarseness.

HEART: The heart is a fist-sized, muscular organ that is positioned slightly left midline in the mediastinum, between the 2nd and 5th intercostal spaces. On external examination, most of anterior cardiac surface is right ventricle, because of rotation during development. With the pulmonary artery, the right ventricle makes a wedge to the left of the sternum. The inferior border of the heart is at the level of the sternum and xiphoid junction. The left ventricle makes up the left border of the heart and puts the"apical impulse" in left 5th ICS.

Heart and surrounding structures with the following parts, working from superficial to deep:

pericardium, the sac that covers the heart, consists of two parts: outer fibrous pericardium, inelastic and protective; inner serous parietal pericardium

pericardial space (cavity), with lubricant serous fluid. Additional fluid, e.g., blood, trapped in here may lead to cardiac tamponade.

heart wall itself with three layers: outer epicardium or the visceral pericardium; myocardium making up the bulk of the heart; endocardium, with endothelial tissue

 

The heart has four chambers, right and left atria, right and left ventricles.

The right and left atria are separated by the interatrial septum. Atrial septal defect (ASD): large ones create a"left to right" shunt.

The right and left ventricles, separated by the interventricular septum, are very thick walled, with the left ventricle more thick walled than the right. Ventricular septal defects (VSD) can be at the membranous septal portions.

Normally, atria receive blood returning to heart and pump it to the inferior ventricles through the right AV tricuspid valve and the left AV bicuspid or mitral valve. The cusps of the AV valves are secured by chordae tendinae blending into the papillary muscles, which contract with the ventricular muscles tensing the cords and preventing systolic backflow.

Internally, muscular ridges (trabeculae carneae) stretch across the ventricular cavity, attached at their ends (the trabeculation enhances chamber emptying). Blood is pumped out the right ventricle through the pulmonary (a semilunar) valve, and out the left through the aortic (a semilunar) valve. These pocket-like pulmonary and aortic semilunar valves fill up and prevent reflux during systole. Hence, disruption of valve function can have a great effect on hemodynamics, e.g., stenosis and insufficiency. Example of: aortic stenosis: left ventricular hypertrophy (LVH).

A conduction system controls the heartbeat, consisting of specialized cardiac muscle cells that conduct electrical impulses. The sinuatrial (SA) node in the wall of the right atrium, just below the entrance of the superior vena cava, serves as the heart's pacemaker, and initiates the depolarization waves that sets the pace of cardiac contraction or sinus rhythm. The SA node is innervated by both the parasympathetic and sympathetic nervous system. The atrioventricular node (AV) node is in the inferior portion of the interatrial septum. The AV node acts as an electrical bridge between the atria and ventricles, receiving and passing on impulses from the SA node. Slowness in AV node conduction: heart block. From the AV node, depolarization waves pass rapidly to the AV bundle (bundle of His), left and right bundle branches, and Purkinje fibers (a network of muscle fibers through the ventricular myocardium for coordinated ventricular depolarization).

Blood supply to heart: in general, coronary arteries form an upside-down"crown" around the heart, with the coronary arteries lying in grooves or sulci. Both left and right coronary arteries arise from small opening (aortic sinuses) just above the semilunar valve cusps.

The right coronary artery: runs in coronary groove between right auricle (part of atrium), with marginal branch. Also, posterior interventricular (descending) branch. The RCA supplies (60% of population) SA node and (90% of population) AV node.5

The left coronary artery: anterior interventricular (left anterior descending) branch, and circumflex branch, with marginal branch off of that. Supplies most of left ventricle.

Anastomoses of cardiac veins throughout the myocardium, with most named veins feeding into the coronary sinus elaboration of the great cardiac vein.

Coronary artery disease: common sites for occlusion are the LAD, right main, and left circumflex coronary arteries.1

Referred pain in angina pectoris: pain stimulation travels back with sympathetic fibers to their spinal nerve source (T1-T5) and the corresponding dorsal root ganglia.

Dermatome patterns then explain the referred pain (contrast visceral pain to localizable parietal pain).1

THORACIC VESSELS, ARTERIES: The ascending aorta forms an aortic arch with 3 vessels coming off it: a) brachiocephalic (innominate) artery branches to the right, while to the left branch the b) left common carotid artery and c) left subclavian artery. The descending aorta becomes the thoracic aorta.

Coarctation of the aorta can lead to a visibly increased collateral circulation.5

THORACIC VESSELS, VEINS: Superior vena cava with three tributaries of R and L brachiocephalic veins draining the head, neck, and upper limbs, and (right-sided) azygos vein assisting to drain the intercostal and lumbar regions.

The azygos system also provides a means of returning blood to the heart from the lower limb and trunk in case of inferior vena cava obstruction.6

THORACIC VESSELS, LYMPHATICS: Lymphatic vessels carry interstitial tissue fluids back to the bloodstream. Lymph drains in increasingly larger vessels until it reaches the right lymphatic duct or the thoracic duct. The right lymphatic duct drains only the R side of the head, thorax, and RUE, while the thoracic duct drains the rest. The thoracic duct, a continuation of the abdominal cisterna chyli, joins the venous circulation at the junction of the left internal jugular and subclavian veins and the lymphatic duct does the same on the right.

ESOPHAGUS: a collapsible muscular tube, conducting food from the laryngopharynx to the stomach by peristaltic contractions. 3 possible stricture sites with physiologic narrowing: a) pharyngeal junction at C6; b) when L main bronchus crosses over at T5; c) at diaphragm at T10 (hiatal hernia). Hiatal hernias may either be sliding or paraesophageal. These correspond to common sites of damage from swallowing caustic materials or cancer.1

THYMUS: with two lobes, is in superior and anterior mediastinum, receiving uncommitted lymphocytes from bone marrow. Thymus actively engaged in T cell proliferation and differentiation during embryonic, fetal, and early life, but begins to involute after puberty.

CARDIAC AND PULMONARY HISTOLOGY

HISTOLOGICAL ASPECTS OF THE CARDIOVASCULAR SYSTEM:

arterial walls with three layers:

inner: tunica intima; endothelium

middle: tunica media; smooth muscle

outer: tunica adventitia; connective tissue, nerve fibers

Veins also have 3 layers, with more irregular lumens, and a comparatively thicker adventitia within an overall thinner wall.

Lymphatic vessels: large lumens and valves, with thin walls of endothelium in the lymphatic capillaries.

ATHEROSCLEROSIS / ARTERIAL SCLEROSIS

An atheroma is more of an intimal disease with fibroblast proliferation, and arteriosclerosis is more of a medial disease with replacement of medial smooth muscle with fibrous tissue, but they often occur together.4

HISTOLOGICAL ASPECTS OF THE RESPIRATORY SYSTEM

TRACHEA

Note support from C-rings of hyaline cartilage and a tracheal epithelium made of ciliated pseudostratified columnar cells with goblet cells. The cilia remove small inhaled particles, and the goblet cells produce mucus that is also regularly moved by the cilia. Note muliple glands in a submucosa.

LUNG

Depending on the slide, one should be able to see differences among bronchioles (with smooth muscle)  respiratory bronchioles (cuboidal epithelium)  alveolar ducts, sacs  alveoli (should appear"lacy" with simple squamous epithelial lining). Capillaries are interspersed in the interalveolar septa. Type I alveolar cells are the squamous pulmonary epithelial cells. Type II alveolar cells (surfactant-producing) are septal cells that bulge slightly into the alveolus.

EMPHYSEMA

Enlarged alveoli and collapsed airways from destructive changes in their walls.

PNEUMONIA

Pneumonia: inflammation of the lungs. Bacterial pneumonias induce intra-alveolar exudates and consolidation of pulmonary parenchyma. If the consolidation is massive: lobar pneumonia. If the consolidation is patchy: bronchopneumonia.1 Try to detect the lung tissue"underneath" the disease pattern.

OVERVIEW OF NORMAL HEMATOLOGY

How to examine a blood smear: (courtesy of J. O'Leary, HVCC Biology)

Generally, be systematic, so you won't miss major abnormalities.

1. Examine at low power (10X) to check that the smear is adequate--look for large abnormalities, e.g., many large blast cells or rbc clumpings.

2. Where red cells are slightly overlapping, go to oil immersion (100X) for wbc differential. A"typical" range for wbc differential: 60% neutrophils [<10% immature neutrophils], 30% lymphocytes, 6% monocytes, 3% eosinophils, 1% basophils. Also, check for platelet number and rbc morphology. At 100X, the # of platelets in 20 fields x 100 should give the platelet count per mm3. Where the red cells are close but not touching should be a good spot to look for red cell morphology. Variations are ranked 1+ to 4+ depending on severity.

NORMAL APPEARANCE OF CELLS3

erythrocytes: biconcave disc, 7  m across

neutrophils: granulocytes with segmented nuclei; phagocytotic

"bands:" immature neutrophils

lymphocytes: specific immunity

monocytes: large, give rise to macrophages

eosinophils: red granules, asssociated with allergies and parasites

basophils: very dark granules, associated with inflammatory mediators

Hematopoesis occurs in the bone marrow, with stem cells that differentiate among different cell lines to blast cells and then mature cells. Erythropoietin (from kidneys) stimulates rbc production by stimulating erythroblast production. From there, normoblasts to reticulocytes (without nucleus, but with staining polyribosomes) to mature anucleate erythrocytes. Blast series exist for wbcs as well--can be seen in the periphery in acute leukemia.3

  1. DR Cahill, Lachman's Case Studies in Anatomy, 4th ed. (Oxford U Press, 1997), pp. 153-165
  2. M Cartmill et al., Human Structure (Harvard U Press, Cambridge, MA, 1987), pp. 91-103, 119-127
  3. DH Cormack, Clinically Integrated Histology (Lippincott-Raven, Philadelphia, 1998), pp. 39, 42, 43.
  4. ADT Govan et al., Pathology Illustrated, 4th ed. (Churchill Livingstone, Edinburgh, 1995), p. 208.
  5. KL Moore, AF Dalley, Clinically Oriented Anatomy (Lippincott Williams & Wilkins, Philadelphia, 1999), pp. 64, 72, 77, 78, 87, 104, 135, 147-148.

 


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