1.6: Outline of the Book
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Having formulated the theme and methodological framework for the conference in late 2008 / early 2009, we were astounded by the scale and range of the responses we received to the call for papers — a testament to the interest and need to bridge the gap between philologically and archaeologically oriented studies of writing. Twenty-five papers in total were presented at the annual conference of the Institute of Archaeology, University College London, held in May 2009. These were delivered by staff and graduate students from a range of museums and universities across the UK and from around the world, including the US, Europe and Australia.
A selection of these papers appear in this volume, exploring writing practices from the ancient past to more recent contexts, although there is a particular concentration on writing from the ancient Mediterranean region, and the Aegean in particular. This concentration reflects the responses to the original conference invitation and subsequent choices by both contributors and editors; interest in the materiality of writing is more developed in some fields than others. The diversity and asymmetry of temporal contexts and cultural areas represented may seem unconventional compared with conferences or publications for the traditional subject areas of textual or material cultural studies. Nevertheless, when mapping out a new research landscape differential engagement is to be expected — as methodological intersections between writing and material culture are identified and explored and new configurations which encourage fuller theorisation and sustained critical discourse are developed. Under these circumstances, which can be defined as a phase of ongoing epistemological reassessment, we feel that breadth should precede depth.
Fifteen 2 case studies set writing and related symbolic modes in relation to material practice including writing production, consumption and related performance and sensory experience. These studies critically explore traditional definitions and treatments of ‘writing’ to develop new perspectives and approaches that offer more holistic understandings of this evidence type. The volume also includes this Introduction and an Epilogue.
In spite of our emphasis on new perspectives and approaches, we have nevertheless organised the chapters in a somewhat conventional manner, generally following a geographical ordering with exceptions to allow for the treatment of subject matter according to chronological sequence. Starting with South and Meso-America, case studies shift to the Near Eastern heartland of writing and then return westwards to the Mediterranean, and on to Great Britain. We end with a methodological paper relating to the conservation of writing. This collection is not necessarily intended to be read in order, but rather dipped into at points of relevance, concern, and curiosity — hopefully prompting the reader to engage with less familiar evidence, and provoking consideration of analytical methods and interpretive frameworks that might be fruitfully adopted, adapted, or otherwise used to broaden the reader’s perspective.
Indeed, over the decades, explorations of the various facets of ‘written’ objects make clear that the question of what constitutes ‘writing’ in a given society must remain an open one if it is to be understood in the terms of its users, and need not be confined to notation systems that are related directly to spoken language. In his study of the khipus in Andean society, Frank Salomon looks at the functional implications of recording with fibre. He argues that khipus functioned not as fixed texts but as operational devices or simulators — visual models rather than verbal transcriptions. Whether this counts as writing is less important than recognising “graphical excellence” (Tufte 1983: 182) in one of its less familiar forms.
Sarah Jackson places similar emphasis on the importance of a context sensitive approach. Mayan image and text intersect and intertwine in profound ways and it is difficult if not ill-advised to attempt to separate them. In practice, writing may not be distinct from other symbolic modes, or may encompass multiple symbolic functions. Too rigid a definition may preclude identification of significant and meaningful relationships, hence the importance of taking account of this evidence type in terms of situated practice. Jackson interprets her examples of Mayan writing as an “orientational technology” that serves to locate people in culturally defined landscapes, especially socio-political landscapes that include both experiential and imagined aspects.
Roger Matthews discusses the earliest, and one of the longest-lasting, traditions of writing: the “cuneiform culture” of the ancient Near East. Initially developed as a system of writing on clay tablets and used mainly for accounting purposes, cuneiform also appears on many other media and was used for many different languages and a great variety of purposes. He shows how new research focussing on the materiality of cuneiform texts is addressing questions about the role(s) of writing in different Near Eastern societies.
Rachael Sparks considers how during the 2nd millennium bce the southern Levant became the meeting point for a number of different writing traditions, involving different languages and scripts, but also different materials, tools, and practices, as well as different contexts of use. She shows how this mixture of influences and practices allowed an unusual fluidity and experimentation with writing that led to the local development of alphabetic scripts.
Helène Whittaker investigates material practices associated with all the scripts of the Aegean Middle and Late Bronze Ages — Hieroglyphic, Linear A and Linear B (c.2000–1200 bce) in the context of palace bureaucracies. While concentrating on the materials employed and the techniques used for writing, in addition to script and language, she also demonstrates the relationships between context, text-content and the forms of material expression employed in constructing wider social meaning.
Sarah Finlayson also examines the three main writing systems of the Bronze Age Aegean in terms of the relationships between writing and its material supports. She adopts the basic hypothesis that the shape of objects which bear writing derives from the use to which they, object + writing, are put and the shape changes as this purpose changes. Focussing particularly on Linear A, which appears on a diverse range of writing supports, she assesses whether the different materials and objects relate in an organised way to the different uses they were put to, e.g. clay tablets to administrative purposes and ‘libation tables’ to ritual use.
Georgia Flouda focusses on Minoan writing (therefore excluding Linear B) and considers how different forms of expression worked, examining features such as material, shape, mode and direction of writing, as well as archaeological context. She demonstrates different trajectories for Hieroglyphic (seals, tablets, and other types) and Linear A respectively. She draws heavily on semiotic theory especially the work of Peirce, suggesting, for instance, that the isolated ‘pictographic’ signs first appearing on the seals were understood as semasiographic codes.
Helena Tomas also considers Aegean Bronze Age writing, but concentrates on one specific phenomenon: the practice of cutting clay tablets (with a special emphasis on Linear B). A detailed study of the location of the cuts and the way they were carried out suggests two different motivations. Whereas the page-shaped tablets were probably cut in order to remove unnecessary clay (probably to keep tablet size to a minimum), elongated tablets may have been cut for the purpose of rearranging the information (for instance, a reclassification according to the origin of the people registered).
With particular emphasis on Greek-speaking and -writing areas, Alan Johnston examines the influence of different surfaces and the use of brush, pen and chisel on the appearance of text in the early centuries (c.800 to 300 bce) of alphabetic writing. In addition to writerly issues, aids for the reader such as the boustrophedon system and use of interpuncts are also considered for the tensions they exhibit between aesthetic concerns and practicality.
Whereas writing is often understood to be a system developed by elite members of society to consolidate authority, and fix social meanings and relationships, Kathryn Piquette explores late 4 th and early 3 rd millennium BCE evidence from Egypt which reveals the dynamic unfolding and reformulation of early writing and related imagery. Focusing on funerary labels of bone, ivory and wood, stone vessels and a stele, Piquette considers the implications of practices of unmaking, re-making, and incompletion.
Stephen Kidd considers a single document, a 3 rd -century BCE Greco-Egyptian letter inscribed on papyrus: a bilingual letter, written in Greek and Demotic. The second language is used specifically to detail a dream which the author, Ptolemaios, claims has to be described in Egyptian. The change of language also involved a change in script, associated with very different material practices. So the shift was informed not only by the languages as they were processed in the author’s brain, but also by the scripts themselves as they were experienced in the motions of his hands, the movement of his eyes, and the material objects he used to interact with these scripts.
Elisa Perego considers ‘Situla Art’, an elaborate figurative decorative style found mainly on bronze objects during the 7 th to 3 rd centuries BCE around the head of the Adriatic Sea. She adopts the concept of iconic literacy — the skill of producing and interpreting images — to study situla art and compare it to traditional textual literacy, which develops at approximately the same time in parts of the region. She argues that both inscribed objects and the products of situla art were employed to negotiate and promote the social role of high-ranking individuals. However, because true writing and situla art rarely occur on the same objects, she suggests that they were seen as alternative systems of communication, and that situla art, which was not restricted to the users of a single spoken language, could be understood over a wider geographical area.
Ruth Whitehouse ’s chapter is also based on evidence from the north Italian Iron Age and looks specifically at tomb markers of different types and inscribed in two different languages, Etruscan and Venetic. In contrast to traditional studies concerned with languages and scripts, she concentrates on the different physical arrangements of the inscriptions on the stones and what these meant in terms of bodily movements and sensory engagements on the part of both the makers (‘writers’) and consumers (‘readers’) of the texts.
We then turn to Craig Cessford who examines 18 th and 19 th -century writing from the Grand Arcade site in Cambridge, England. He focusses on the ways in which material type, size, form and function of different kinds of artefact affect how writing was deployed. Cessford also considers why writing occurs incompletely or not at all on certain object types, highlighting a general yet critical issue for investigators of written culture — of accounting for absence alongside presence, and visibility as well as invisibility.
Elizabeth Pye draws our attention to the impact of the presence of writing, or the potential to reveal writing, on objects for decisions relating to conservation procedures and perceived values of objects. The common practice of prioritizing the revealing of writing may lead to adverse effects on the preservation of the writing supports — a problem that may be alleviated by modern techniques of digital imaging. However, digital imaging produces its own problems, as computer hardware and software themselves require conservation.
Finally, John Bennet brings the book to a close with an overview of writing and its ancient material expressions as covered in the chapters in this volume, while also reflecting on changing materialities and practices associated with modern emerging writing technologies.
2 In assembling these chapters from authors using both American and British spellings, we have decided to let each author follow either convention, while maintaining consistency within each chapter.


3: Creating Business Documents
In this unit, we discuss how to create and format two standard business documents, block-style business letters and memos. Word processing tools allow us to incorporate a variety of font styles to emphasize text. These techniques include creating text that is in bold type, in italics, and underlined. We can also use borders to create a visual break between sections of a document. Finally, we explore how you can add headers and footers to present a polished, professional, and organized business document.
Upon successful completion of this unit, you will be able to:
- outline the elements of a business letter and memo;
- format document margins and adjust spacing between headings and body text;
- add headers, footers, page numbers, and borders to a document;
- create a basic block-style business letter; and
- create a basic block-style business memo.


7.3.6A: The Productive Life Cycle of Animal Viruses
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- Ying Liu
- City College of San Francisco
Learning Objectives
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When given information about a virus in terms of how it penetrates the host cell, whether it has a DNA or RNA genome, and how it is released, describe how an enveloped virus accomplishes each of the steps of the productive life cycle listed below.
(Tailor the life cycle to that virus.)
- viral attachment or adsorption to the host cell
- viral entry into the host cell
- viral movement to the site of replication within the host cell
- viral replication within the host cell
- viral assembly or maturation within the host cell
- viral release from the host cell
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When given information about a virus in terms of how it penetrates the host cell, whether it has a DNA or RNA genome, and how it is released, describe how a naked virus accomplishes each of the steps of the productive life cycle listed below. (Tailor the life cycle to that virus.)
- viral attachment or adsorption to the host cell
- viral entry into the host cell
- viral movement to the site of replication within the host cell
- viral replication within the host cell
- viral assembly or maturation within the host cell
- viral release from the host cell
For many animal viruses, the details of each step in their life cycle have not yet been fully characterized, and among the viruses that have been well studied there is great deal of variation. What follows is a generalized productive life cycle for animal viruses consisting of the following steps: adsorption, viral entry, viral movement to the site of replication and release of the viral genome from the remainder of the virus, viral replication, viral assembly, and viral release.
Viral Attachment or Adsorption to the Host Cell
Adsorption (Figures 1) involves the binding of attachment sites on the viral surface with receptor sites on the host cell cytoplasmic membrane.
For a virus to infect a host cell, that cell must have receptors for the virus on its surface and also be capable of supporting viral replication. These host cell receptors are normal surface molecules involved in routine cellular function, but since a portion of a molecule on the viral surface resembles the chemical shape of the body's molecule that would normally bind to the receptor, the virus is able to attach to the host cell's surface.
For example:
- Most human rhinoviruses that cause the common cold bind to intercellular adhesion molecules (ICAM-1) found on cells of the nasal epithelium. These ICAM-1 molecules are used normally for the recruitment of leukocytes into the respiratory tract.
- The human immunodeficiency viruses (HIV) adsorbs to first CD4 molecules and then chemokine receptors found on the surface of human T4-lymphocytes and macrophages . CD4 molecules are normally involved in immune recognition while chemokine receptors play a role in initiating inflammation and recruiting leukocytes.
- Human cytomegaloviruses (CMV) adsorb to MHC-I molecules . MHC-I molecules on human cells enable T8-lymphocytes to recognize antigens during adaptive immunity.
- The hepatitis B virus (HBV) adsorbs to IgA receptors on human cells. These receptors normally bind the antibody isotype IgA for transport across cells.
Viral Entry into the Host Cell
a. Enveloped viruses
Enveloped viruses enter the host cell in one of two ways:
1. In some cases, the viral envelope may fuse with the host cell cytoplasmic membrane and the nucleocapsid is released into the cytoplasm (see Figs. 2A , Figure \(\PageIndex{2}\)B and Figure \(\PageIndex{2}\)C) .
2. Usually they enter by endocytosis , whereby the host cell cytoplasmic membrane invaginates and pinches off, placing the virus in an endocytic vesicle (see Figure \(\PageIndex{3}\)A , Figure \(\PageIndex{3}\)B , Figure \(\PageIndex{3}\)C , and Figure \(\PageIndex{3}\)D) .
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3D animation illustrating adsorption and penetration of the dengue fever virus. Janet Iwasa, Gaël McGill (Digizyme) & Michael Astrachan (XVIVO). This animation takes some time to load. |
b. Naked viruses
Naked viruses enter the cell in one of two ways:
1. In some cases, interaction between the viral capsid and the host cell cytoplasmic membrane causes a rearrangement of capsid proteins allowing the viral nucleic acid to pass through the membrane into the cytoplasm (see Figure \(\PageIndex{4}\)A , Figure \(\PageIndex{4}\)B , Figure \(\PageIndex{4}\)C , and Figure \(\PageIndex{4}\)D ).
2. Most naked viruses enter by receptor-mediated endocytosis whereby the host cell cytoplasmic membrane invaginates and pinches off, placing the virus in an endocytic vesicle (see Figure \(\PageIndex{5}\)A , Figure \(\PageIndex{5}\)B , Figure \(\PageIndex{5}\)C , and Figure \(\PageIndex{5}\)D) .
3. Viral Movement to the Site of Replication within the Host Cell and Release of the Viral Genome from the Remainder of the Virus.
In the case of viruses that enter by endocytosis, the endocytic vesicles containing the virus move within the host cell. During this process the pH of the endocytic vesicle typically decreases and this enables the virus to leave the endocytic vesicle. Viruses exit the endocytic vesicle through a variety of mechanisms, including:
a. Fusion of the viral envelope with the membrane of the endocytic vesicle enabling the viral nucleocapsid to enter the cytoplasm of the host cell (see Figure \(\PageIndex{7}\)A , Figure \(\PageIndex{7}\)B , and Figure \(\PageIndex{7}\)C) .
b. Lysis of the endocytic vesicle releasing the viral nucleocapsid into the cytoplasm of the host cell (see Figure \(\PageIndex{7}\)D , and Figure \(\PageIndex{7}\)E) .
c. The viral capsid undergoing conformational changes that forms pores in the endocytic vesicle enabling the virial genome to enter the cytoplasm of the host cell (see Figure \(\PageIndex{9}\)A , Figure \(\PageIndex{9}\)B, and Figure \(\PageIndex{9}\)C).
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Flash animation showing viral capsid undergoing conformational changes that forms pores in the endocytic vesicle and enable the virial genome to enter the cytoplasm.
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html5 version of animation for iPad showing viral capsid undergoing conformational changes that forms pores in the endocytic vesicle and enable the virial genome to enter the cytoplasm.
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Before viruses can replicate within the infected host cell, the viral genome needs to released from the remainder of the virus. This process is sometimes referred to as uncoating.
In the case of most viruses with an RNA genome, the viral RNA genome is released from the capsid and enters the cytoplasm of the host cell (see Figure \(\PageIndex{8}\)A , and Figure \(\PageIndex{8}\)B) where replication generally occurs.
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Flash animation showing release of the viral genome from the capsid (uncoating).
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html5 version of animation for iPad showing release of the viral genome from the capsid (uncoating).
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In the case of most viruses with a DNA genome, the viral genome enters the nucleus of the host cell through one the mechanisms shown below. Most larger DNA viruses use either a or b to enter the nucleus. Method c is used by some very small DNA whose capsid is small enough to be carried through the nuclear pores.
a. The viral DNA genome is released from the capsid, enters the cytoplasm of the host cell, and subsequently enters the nucleus of the host cell through the pores in the nuclear membrane (see Figure \(\PageIndex{9}\)D and Figure \(\PageIndex{9}\)E).
b. The capsid of the viruses interacts with the nuclear membrane of the host cell enabling the viral DNA genome to enter the nucleus of the host cell via the pores in the nuclear membrane (see Figure \(\PageIndex{9}\)F and Figure \(\PageIndex{9}\)G) .
c. The nucleocapsid of a small DNA virus enters the nucleus of the host cell and the capsid is subsequently removed releasing the viral DNA genome into the nucleoplasm (see Figure \(\PageIndex{9}\)H and Figure \(\PageIndex{9}\)I) .
This uncoating begins the eclipse period , the period during which no intact virions can be detected within the cell. After uncoating and during the replication stage the virus is not infectious.
4. Viral Replication within the Host Cell
The viral genome directs the host cell's metabolic machinery (ribosomes, tRNA, nutrients, energy, enzymes, etc.) to synthesize viral enzymes and viral parts. The viral genome has to both replicate itself and become transcribed into viral mRNA molecules. The viral mRNA can then be translated by the host cell's ribosomes into viral structural components and enzymes need for replication and assembly of the virus.
As mentioned earlier under Viral Classification, viruses can store their genetic information in six different types of nucleic acid which are named based on how that nucleic acid eventually becomes transcribed to the viral mRNA:
a. (+/-) double-stranded DNA (see Figure \(\PageIndex{10}\)A). To replicate the viral genome, DNA-dependent DNA polymerase enzymes (usually provided by the cell) copy both the (+) and (-) DNA strands producing dsDNA viral genomes. To produce viral mRNA molecules, host cell-DNA-dependent RNA polymerase enzymes copy the (-) DNA strand into (+) viral mRNA. The (+) viral mRNA can then be translated into viral proteins by host cell ribosomes. Examples include most bacteriophages, Papovaviruses, Adenoviruses, and Herpesviruses.
b. (+) single-stranded DNA (see Figure \(\PageIndex{10}\)B). To replicate the viral genome, DNA-dependent DNA polymerase enzymes (usually provided by the cell) copy the (+) DNA strand of the genome producing a dsDNA intermediate. DNA-dependent DNA polymerase enzymes (again, usually provided by the cell) then copy the (-) DNA strand into ss (+) DNA genomes. To produce viral mRNA molecules, host cell-DNA-dependent RNA polymerase enzymes copy the (-) DNA strand into (+) viral mRNA. The (+) viral mRNA can then be translated into viral proteins by host cell ribosomes. Examples include Phage M13 and Parvoviruses.
c. (+/-) double-stranded RNA (see Figure \(\PageIndex{10}\)C) . To replicate the viral genome, viral RNA-dependent RNA polymerase enzymes (replicase) copy both the (+) RNA and (-) RNA strands of the genome producing a dsRNA genomes. To produce viral mRNA molecules, viral RNA-dependent RNA polymerase enzymes (transcriptase) copy the (-) RNA strand into (+) viral mRNA. The (+) viral mRNA can then be translated into viral proteins by host cell ribosomes. Reoviruses are an example.
d. (-) RNA (see Figure \(\PageIndex{10}\)D). To replicate the viral genome, viral RNA-dependent RNA polymerase enzymes (transcriptase) copy the (-) RNA genome producing ss (+) RNA. Transcriptase must be carried into the cell with the virion. Viral RNA-dependent RNA polymerase enzymes (replicase) then copy the (+) RNA strands producing ss (-) RNA viral genome. The (+) mRNA strands also function as viral mRNA and can then be translated into viral proteins by host cell ribosomes. Examples include Orthomyxoviruses, Paramyxoviruses, Rhabdoviruses.
e. (+) RNA (see Figure \(\PageIndex{10}\)E). To replicate the viral genome, viral RNA-dependent RNA polymerase enzymes (replicase) copy the (+) RNA genome producing ss (-) RNA. Viral RNA-dependent RNA polymerase enzymes (replicase) then copy the (-) RNA strands producing ss (+) RNA viral genome. To produce viral mRNA molecules. RNA-dependent RNA polymerase enzymes (replicase) copy the (-) RNA strand into (+) viral mRNA. The (+) viral mRNA can then be translated into viral proteins by host cell ribosomes. Examples include Picornaviruses, Togaviruses, and Coronaviruses.
f. (+) RNA Retroviruses (see Figure \(\PageIndex{10}\)F) . To replicate the viral genome, viral reverse transcriptase enzymes (RNA-dependent DNA polymerases) copy the (+) RNA genome producing ss (-) DNA strands. Viral reverse transcriptase can also function as a DNA-dependent DNA polymerase enzymes and will copy the (-) DNA strands to produce a dsDNA intermediate. Reverse transcriptase must be carried into the cell with the virion. The viral DNA will move to the nucleus where it integrates into the cell’s DNA using the viral enzyme integrase which also must be carried into the host cell with the virion. Once in the host cell’s DNA, host cell DNA-dependent RNA polymerase enzymes then copy the ds (-) DNA strands to produce ss (+) RNA genomes. To produce viral mRNA molecules, host cell DNA-dependent RNA polymerase enzymes copy the ds (-) DNA strand into (+) viral mRNA. The (+) viral mRNA can then be translated into viral proteins by host cell ribosomes. Retroviruses, such as HIV-1, HIV-2, and HTLV-1 are examples.
As the host cell's ribosomes attach to the viral mRNA molecules, the mRNAs are translated into viral structural proteins and viral enzymes. During the early phase of replication, proteins needed for the replication of the viral genome are made and the genome makes thousands of replicas of itself. During the late phase of replication, viral structural proteins (capsid and matrix proteins, envelope glycoproteins, etc.) and the enzymes involved in maturation are produced.
Some viral mRNAs are monocistronic, that is, they contain genetic material to translate only a single protein or polypeptide. Other viral mRNAs are polycistronic. They contain transcripts of several genes and are translated into one or more large polyproteins. These polyproteins are subsequently cut into individual functional proteins by viral enzymes called proteases.
In the case of most RNA viruses, replication and assembly occurs in the host cell's cytoplasm. With DNA viruses, most replication and assembly occurs in the nucleus of the host cell. The viral genome enters the nucleus of the host cell and here is transcribed into viral mRNA. The viral mRNA molecules then leave the nucleus through the pores in the nuclear membrane and are translated into viral proteins by the host cell's ribosomes in the cytoplasm. Most of these viral proteins then re-enter the nucleus where the virus assembles around the replicated genomes.
- Transmission electron micrograph of Herpes simplex viruses in the nucleus of an infected host cell ; courtesy of CDC.
Also during replication, viral envelope proteins and glycoproteins coded by the viral genome are incorporated into the host cell's cytoplasmic membrane (see Figure \(\PageIndex{11}\)A and Figure \(\PageIndex{11}\)B) or nuclear membrane.
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Flash animation showing viral replication.
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Whether a virus has an RNA or a DNA genome is significant when it comes to developing antiviral agents to control viruses. In the case of RNA viruses, all of the enzymes used in genome replication and transcription are viral encoded enzymes different from those of the host cell so these enzymes can potentially be targeted. On the other hand, DNA viruses use the host cell's RNA transcription machinery and DNA replication machinery so these enzymes, shared by the virus and the host cell, cannot be targeted without killing the host cell. Since all viruses use the host cell's translation machinery regardless of genome type, translation can not be targeted in any viruses.
5. Viral Assembly or Maturation within the Host Cell
During maturation, the capsid is assembled around the viral genome .
- Maturation of an enveloped virus: see Figure \(\PageIndex{12}\)A .
- Maturation of a naked virus: see Figure \(\PageIndex{12}\)B .
Viral Release from the Host Cell
a. Naked viruses
Naked viruses are predominantly released by host cell lysis (see Figure \(\PageIndex{13}\) C) . While some viruses are cytolytic and lyse the host cell more or less directly, in many cases it is the body's immune defenses that lyse the infected cell.
b. Enveloped viruses
With enveloped viruses, the host cell may or may not be lysed. The viruses obtain their envelopes from host cell membranes by budding. As mentioned above, prior to budding, viral proteins and glycoproteins are incorporated into the host cell's membranes. During budding the host cell membrane with incorporated viral proteins and glycoproteins evaginates and pinches off to form the viral envelope. Budding occurs either at the outer cytoplasmic membrane, the nuclear membrane, or at the membranes of the Golgi apparatus .
1. Viruses obtaining their envelope from the cytoplasmic membrane are released during the budding process (see Figure \(\PageIndex{14}\)A and Figure \(\PageIndex{14}\)B) .
- Transmission electron micrograph of Rubella viruses budding from an infected host cell ; courtesy of CDC.
2. Viruses obtaining their envelopes from the membranes of the nucleus, the endoplasmic reticulum, or the Golgi apparatus are then released by exocytosis via transport vesicles (see Figure \(\PageIndex{15}\)A and Figure \(\PageIndex{15}\)B) .
- Transmission electron micrograph of Coronaviruses in the endoplasmic reticulum of an infected host cell ; courtesy of CDC.
Some viruses, capable of causing cell fusion, may be transported from one cell to adjacent cells without being released, that is, they are transmitted by cell-to-cell contact whereby an infected cell fuses with an uninfected cell (see Figure \(\PageIndex{16}\)A , Figure \(\PageIndex{16}\)B , and Figure \(\PageIndex{16}\)C ).
Reinfection
As many as 10,000 to 50,000 animal viruses may be produced by a single infected host cell.
- Transmission electron micrograph showing envelope and glycoprotein spikes Coronaviruses ; courtesy of CDC.
Exercise: Think-Pair-Share Questions
- Animal viruses adsorb to receptors on the cytoplasmic membrane of host cells.
Why would our cells possess receptors that viruses could adsorb too?
- When we vaccinate against viral infections such as measles, mumps, rubella, poliomyelitis, and chickenpox, we inject an attenuated or inactivated form of the virus. The body responds by making antibodies that coat the surface of that virus by binding to its surface proteins or glycoproteins.
Briefly describe two ways this may prevent future infections with this virus.
| Flash Animation showing a summary animation of the life cycle of an enveloped virus. |
| Flash Animation showing a summary animation of the life cycle of a naked virus. |
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Flash Animation Showing All Viral Life Cycle Animations
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Nice Animation with Simplistic Explanation of the Replication of Influenza Viruses. created for NPR by medical animator, David Bolinsky |
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The dengue virus is an RNA virus that enters by endocytosis, gets its envelope by budding into the endoplasmic reticulum, and is packaged by the Golgi apparatus and released by exocytosis. Dengue fever is a mosquito-borne viral infection found mainly in tropical areas. Often asymptomatic and self-limiting but when symptoms do appear, they can include joint and muscle pain, headache, and a rash that may become hemorrhagic. The virus replicates in macrophages. Courtesy of HHMI's Biointeractive . |
Summary
- For a virus to infect a host cell, that cell must have receptors for the virus on its surface and also be capable of supporting viral replication.
- Adsorption involves the binding of attachment sites on the viral surface with receptor sites on the host cell cytoplasmic membrane.
- Once adsorbed, many viruses enter the host cell by endocytosis, whereby the host cell cytoplasmic membrane invaginates and pinches off, placing the virus in an endocytic vesicle. Some viruses enter by a fusion process whereby part of the virus fuses with the host cell enabling the remainder of the virus to enter the host cell’s cytoplasm.
- Following entry, the virus moves to the site of replication within the host cell. Most RNA viruses replicate in the host cell’s cytoplasm; most DNA viruses replicate in the host cell’s nucleus.
- During replication, the viral genome directs the host cell's metabolic machinery (ribosomes, tRNA, nutrients, energy, enzymes, etc.) to synthesize viral enzymes and viral parts. The viral genome has to both replicate itself and become transcribed into viral mRNA molecules. The viral mRNA can then be transcribed by the host cell into viral structural components and enzymes need for replication and assembly of the virus.
- During maturation, the capsid is assembled around the viral genome.
- Prior to or during release, enveloped viruses obtain their envelopes from host cell membranes by budding. Budding occurs either at the outer cytoplasmic membrane, the nuclear membrane, or at the membranes of the Golgi apparatus.
- Viruses obtaining their envelopes from the membranes of the nucleus, the endoplasmic reticulum, or the Golgi apparatus are then released by exocytosis via transport vesicles; viruses obtaining their envelope from the cytoplasmic membrane are released during the budding process.
- Naked viruses are predominantly released by host cell lysis.
- As many as 10,000 to 50,000 animal viruses may be produced by a single infected host cell.
Questions
Study the material in this section and then write out the answers to these questions. Do not just click on the answers and write them out. This will not test your understanding of this tutorial.
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An enveloped virus enters by fusion, has an RNA genome, and is released by budding. Describe how it accomplishes each of the following steps during its productive life cycle.
- viral attachment or adsorption to the host cell (ans)
- viral entry into the host cell (ans)
- viral movement to the site of replication within the host cell (ans)
- viral replication within the host cell (ans)
- viral assembly or maturation within the host cell (ans)
- viral release from the host cell (ans)
- When a virus infects the body, the body responds by producing antibodies that coat the virion. Discuss briefly how this might offer protection to the body. (ans)
- Why are viruses generally very specific as to the types of hosts, tissues, and cells they are able to infect? (ans)
- Multiple Choice (ans)


23.2: Bacterial Infections of the Urinary System
- Identify the most common bacterial pathogens that can cause urinary tract infections
- Compare the major characteristics of specific bacterial diseases affecting the urinary tract
Urinary tract infections (UTIs) include infections of the urethra, bladder, and kidneys, and are common causes of urethritis, cystitis, pyelonephritis, and glomerulonephritis. Bacteria are the most common causes of UTIs, especially in the urethra and bladder.
Cystitis
Cystitis is most often caused by a bacterial infection of the bladder, but it can also occur as a reaction to certain treatments or irritants such as radiation treatment, hygiene sprays, or spermicides. Common symptoms of cystitis include dysuria (urination accompanied by burning, discomfort, or pain), pyuria (pus in the urine), hematuria (blood in the urine), and bladder pain.
In women, bladder infections are more common because the urethra is short and located in close proximity to the anus, which can result in infections of the urinary tract by fecal bacteria. Bladder infections are also more common in the elderly because the bladder may not empty fully, causing urine to pool; the elderly may also have weaker immune systems that make them more vulnerable to infection. Conditions such as prostatitis in men or kidney stones in both men and women can impact proper drainage of urine and increase risk of bladder infections. Catheterization can also increase the risk of bladder infection (see Case in Point: Cystitis in the Elderly ).
Gram-negative bacteria such as Escherichia coli (most commonly), Proteus vulgaris , Pseudomonas aeruginosa , and Klebsiella pneumoniae cause most bladder infections. Gram-positive pathogens associated with cystitis include the coagulase-negative Staphylococcus saprophyticus , Enterococcus faecalis , and Streptococcus agalactiae . Routine manual urinalysis using a urine dipstick or test strip can be used for rapid screening of infection. These test strips (Figure \(\PageIndex{1}\)) are either held in a urine stream or dipped in a sample of urine to test for the presence of nitrites, leukocyte esterase, protein, or blood that can indicate an active bacterial infection. The presence of nitrite may indicate the presence of E. coli or K. pneumonia; these bacteria produce nitrate reductase, which converts nitrate to nitrite. The leukocyte esterase (LE) test detects the presence of neutrophils as an indication of active infection.
Low specificity, sensitivity, or both, associated with these rapid screening tests require that care be taken in interpretation of results and in their use in diagnosis of urinary tract infections. Therefore, positive LE or nitrite results are followed by a urine culture to confirm a bladder infection. Urine culture is generally accomplished using blood agar and MacConkey agar, and it is important to culture a clean catch of urine to minimize contamination with normal microbiota of the penis and vagina.  The patient then releases a small amount of urine into the toilet bowl before stopping the flow of urine. Finally, the patient resumes urination, this time filling the container used to collect the specimen.
Bacterial cystitis is commonly treated with fluoroquinolones, nitrofurantoin, cephalosporins, or a combination of trimethoprim and sulfamethoxazole. Pain medications may provide relief for patients with dysuria. Treatment is more difficult in elderly patients, who experience a higher rate of complications such as sepsis and kidney infections.
Robert, an 81-year-old widower with early onset Alzheimer’s, was recently moved to a nursing home because he was having difficulty living on his own. Within a few weeks of his arrival, he developed a fever and began to experience pain associated with urination. He also began having episodes of confusion and delirium. The doctor assigned to examine Robert read his file and noticed that Robert was treated for prostatitis several years earlier. When he asked Robert how often he had been urinating, Robert explained that he had been trying not to drink too much so that he didn’t have to walk to the restroom.
All of this evidence suggests that Robert likely has a urinary tract infection. Robert’s age means that his immune system has probably begun to weaken, and his previous prostate condition may be making it difficult for him to empty his bladder. In addition, Robert’s avoidance of fluids has led to dehydration and infrequent urination, which may have allowed an infection to establish itself in his urinary tract. The fever and dysuria are common signs of a UTI in patients of all ages, and UTIs in elderly patients are often accompanied by a notable decline in mental function.
Physical challenges often discourage elderly individuals from urinating as frequently as they would otherwise. In addition, neurological conditions that disproportionately affect the elderly (e.g., Alzheimer’s and Parkinson’s disease) may also reduce their ability to empty their bladders. Robert’s doctor noted that he was having difficulty navigating his new home and recommended that he be given more assistance and that his fluid intake be monitored. The doctor also took a urine sample and ordered a laboratory culture to confirm the identity of the causative agent.
- Why is it important to identify the causative agent in a UTI?
- Should the doctor prescribe a broad-spectrum or narrow-spectrum antibiotic to treat Robert’s UTI? Why?
Kidney Infections (Pyelonephritis and Glomerulonephritis)
Pyelonephritis, an inflammation of the kidney, can be caused by bacteria that have spread from other parts of the urinary tract (such as the bladder). In addition, pyelonephritis can develop from bacteria that travel through the bloodstream to the kidney. When the infection spreads from the lower urinary tract, the causative agents are typically fecal bacteria such as E. coli . Common signs and symptoms include back pain (due to the location of the kidneys), fever, and nausea or vomiting. Gross hematuria (visible blood in the urine) occurs in 30–40% of women but is rare in men. 1 The infection can become serious, potentially leading to bacteremia and systemic effects that can become life-threatening. Scarring of the kidney can occur and persist after the infection has cleared, which may lead to dysfunction.
Diagnosis of pyelonephritis is made using microscopic examination of urine, culture of urine, testing for leukocyte esterase and nitrite levels, and examination of the urine for blood or protein. It is also important to use blood cultures to evaluate the spread of the pathogen into the bloodstream. Imaging of the kidneys may be performed in high-risk patients with diabetes or immunosuppression, the elderly, patients with previous renal damage, or to rule out an obstruction in the kidney. Pyelonephritis can be treated with either oral or intravenous antibiotics, including penicillins, cephalosporins, vancomycin, fluoroquinolones, carbapenems, and aminoglycosides.
Glomerulonephritis occurs when the glomeruli of the nephrons are damaged from inflammation. Whereas pyelonephritis is usually acute, glomerulonephritis may be acute or chronic. The most well-characterized mechanism of glomerulonephritis is the post-streptococcal sequelae associated with Streptococcus pyogenes throat and skin infections. Although S. pyogenes does not directly infect the glomeruli of the kidney, immune complexes that form in blood between S. pyogenes antigens and antibodies lodge in the capillary endothelial cell junctions of the glomeruli and trigger a damaging inflammatory response. Glomerulonephritis can also occur in patients with bacterial endocarditis(infection and inflammation of heart tissue); however, it is currently unknown whether glomerulonephritis associated with endocarditis is also immune-mediated.
Leptospirosis
Leptospira are generally harmless spirochetes that are commonly found in the soil. However, some pathogenic species can cause an infection called leptospirosis in the kidneys and other organs (Figure \(\PageIndex{2}\)). Leptospirosis can produce fever, headache, chills, vomiting, diarrhea, and rash with severe muscular pain. If the disease continues to progress, infection of the kidney, meninges, or liver may occur and may lead to organ failure or meningitis. When the kidney and liver become seriously infected, it is called Weil’s disease. Pulmonary hemorrhagic syndrome can also develop in the lungs, and jaundice may occur.
Leptospira spp. are found widely in animals such as dogs, horses, cattle, pigs, and rodents, and are excreted in their urine. Humans generally become infected by coming in contact with contaminated soil or water, often while swimming or during flooding; infection can also occur through contact with body fluids containing the bacteria. The bacteria may enter the body through mucous membranes, skin injuries, or by ingestion. The mechanism of pathogenicity is not well understood.
Leptospirosis is extremely rare in the United States, although it is endemic in Hawaii; 50% of all cases in the United States come from Hawaii. 2 It is more common in tropical than in temperate climates, and individuals who work with animals or animal products are most at risk. The bacteria can also be cultivated in specialized media, with growth observed in broth in a few days to four weeks; however, diagnosis of leptospirosis is generally made using faster methods, such as detection of antibodies to Leptospira spp. in patient samples using serologic testing. Polymerase chain reaction (PCR), enzyme-linked immunosorbent assay (ELISA), slide agglutination, and indirect immunofluorescence tests may all be used for diagnosis. Treatment for leptospirosis involves broad-spectrum antibiotics such as penicillin and doxycycline. For more serious cases of leptospirosis, antibiotics may be given intravenously.
- What is the most common cause of a kidney infection?
- What are the most common symptoms of a kidney infection?
Nongonococcal Urethritis (NGU)
There are two main categories of bacterial urethritis: gonorrheal and nongonococcal. Gonorrheal urethritis is caused by Neisseria gonorrhoeae and is associated with gonorrhea, a common STI. This cause of urethritis will be discussed in Bacterial Infections of the Reproductive System . The term nongonococcal urethritis (NGU) refers to inflammation of the urethra that is unrelated to N. gonorrhoeae . In women, NGU is often asymptomatic. In men, NGU is typically a mild disease, but can lead to purulent discharge and dysuria. Because the symptoms are often mild or nonexistent, most infected individuals do not know that they are infected, yet they are carriers of the disease. Asymptomatic patients also have no reason to seek treatment, and although not common, untreated NGU can spread to the reproductive organs, causing pelvic inflammatory disease and salpingitis in women and epididymitis and prostatitis in men. Important bacterial pathogens that cause nongonococcal urethritis include Chlamydia trachomatis , Mycoplasma genitalium , Ureaplasma urealyticum , and Mycoplasma hominis .
C. trachomatis is a difficult-to-stain, gram-negative bacterium with an ovoid shape. An intracellular pathogen, C . trachomatis causes the most frequently reported STI in the United States, chlamydia. Although most persons infected with C. trachomatis are asymptomatic, some patients can present with NGU. C. trachomatis can also cause non-urogenital infections such as the ocular disease trachoma (see Bacterial Infections of the Skin and Eyes ). The life cycle of C. trachomatis is illustrated in Figure 4.2.2 .
C. trachomatis has multiple possible virulence factors that are currently being studied to evaluate their roles in causing disease. These include polymorphic outer-membrane autotransporter proteins, stress response proteins, and type III secretion effectors. The type III secretion effectors have been identified in gram-negative pathogens, including C. trachomatis. This virulence factor is an assembly of more than 20 proteins that form what is called an injectisome for the transfer of other effector proteins that target the infected host cells. The outer-membrane autotransporter proteins are also an effective mechanism of delivering virulence factors involved in colonization, disease progression, and immune system evasion.
Other species associated with NGU include Mycoplasma genitalium, Ureaplasma urealyticum , and Mycoplasma hominis . These bacteria are commonly found in the normal microbiota of healthy individuals, who may acquire them during birth or through sexual contact, but they can sometimes cause infections leading to urethritis (in males and females) or vaginitis and cervicitis (in females).
M. genitalium is a more common cause of urethritis in most settings than N. gonorrhoeae , although it is less common than C. trachomatis . It is responsible for approximately 30% of recurrent or persistent infections, 20–25% of nonchlamydial NGU cases, and 15%–20% of NGU cases. M. genitalium attaches to epithelial cells and has substantial antigenic variation that helps it evade host immune responses. It has lipid-associated membrane proteins that are involved in causing inflammation.
Several possible virulence factors have been implicated in the pathogenesis of U. urealyticum (Figure \(\PageIndex{3}\)). These include the ureaplasma proteins phospholipase A, phospholipase C, multiple banded antigen (MBA), urease, and immunoglobulin α protease. The phospholipases are virulence factors that damage the cytoplasmic membrane of target cells. The immunoglobulin α protease is an important defense against antibodies. It can generate hydrogen peroxide, which may adversely affect host cell membranes through the production of reactive oxygen species.
Treatments differ for gonorrheal and nongonococcal urethritis. However, N. gonorrhoeae and C. trachomatis are often simultaneously present, which is an important consideration for treatment. NGU is most commonly treated using tetracyclines (such as doxycycline) and azithromycin; erythromycin is an alternative option. Tetracyclines and fluoroquinolones are most commonly used to treat U. urealyticum , but resistance to tetracyclines is becoming an increasing problem. 3 While tetracyclines have been the treatment of choice for M. hominis , increasing resistance means that other options must be used. Clindamycin and fluoroquinolones are alternatives. M. genitalium is generally susceptible to doxycycline, azithromycin, and moxifloxacin. Like other mycoplasma, M. genitalium does not have a cell wall and therefore β-lactams (including penicillins and cephalosporins) are not effective treatments.
- What are the three most common causes of urethritis?
- What three members of the normal microbiota can cause urethritis?
Urinary tract infections can cause inflammation of the urethra (urethritis), bladder (cystitis), and kidneys (pyelonephritis), and can sometimes spread to other body systems through the bloodstream. Figure \(\PageIndex{4}\) captures the most important features of various types of UTIs.
Key Concepts and Summary
- Bacterial cystitis is commonly caused by fecal bacteria such as E. coli.
- Pyelonephritis is a serious kidney infection that is often caused by bacteria that travel from infections elsewhere in the urinary tract and may cause systemic complications.
- Leptospirosis is a bacterial infection of the kidney that can be transmitted by exposure to infected animal urine, especially in contaminated water. It is more common in tropical than in temperate climates.
- Nongonococcal urethritis (NGU) is commonly caused by C. trachomatis, M. genitalium, Ureaplasma urealyticum, and M. hominis.
- Diagnosis and treatment for bacterial urinary tract infections varies. Urinalysis (e.g., for leukocyte esterase levels, nitrite levels, microscopic evaluation, and culture of urine) is an important component in most cases. Broad-spectrum antibiotics are typically used.
Footnotes
- 1 Tibor Fulop. “Acute Pyelonephritis” Medscape , 2015. http://emedicine.medscape.com/article/245559-overview .
- 2 Centers for Disease Control and Prevention. “Leptospirosis.” 2015. http://www.cdc.gov/leptospirosis/health_care_workers .
- 3 Ken B Waites. “Ureaplasma Infection Medication.” Medscape , 2015. emedicine.medscape.com/articl...470-medication.


1.12: Respiratory System
Learning Objectives
- Examine the anatomy of the respiratory system
- Determine the main functions of the respiratory system
- Differentiate respiratory system medical terms and common abbreviations
- Recognize the medical specialties associated with the respiratory system
- Discover common diseases, disorders, and procedures related to the respiratory system
Respiratory System Word Parts
Click on prefixes, combining forms, and suffixes to reveal a list of word parts to memorize for the Respiratory System.
Introduction to the Respiratory System
How long you can hold your breath as you continue reading… How long can you do it? Chances are you are feeling uncomfortable already.  Although oxygen is critical for cells, it is the accumulation of carbon dioxide that primarily drives your need to breathe.
The major structures of the respiratory system function primarily to provide oxygen to body tissues for cellular respiration, remove the waste product carbon dioxide, and help to maintain acid-base balance. Portions of the respiratory system are also used for non-vital functions, such as sensing odors, speech production, and for straining, such as coughing.
Did you know?

Watch this video:
Media 12.1. Respiratory System, Part 1: Crash Course A&P #31 [Online video]. Copyright 2015 by CrashCourse .
Practice Medical Terms Related to the Respiratory System
Anatomy (Structures) of the Respiratory System
The Nose and its Adjacent Structures
The major entrance and exit for the respiratory system is through the nose . When discussing the nose, it is helpful to divide it into two major sections:
- external nose
- internal nose
The nares open into the nasal cavity, which is separated into left and right sections by the nasal septum ( Figure 12.2 ). The nasal septum is formed anteriorly by a portion of the septal cartilage and posteriorly by the perpendicular plate of the ethmoid bone and the thin vomer bones.
Each lateral wall of the nasal cavity has three bony projections: t he inferior conchae are separate bones, and t he superior and middle conchae are portions of the ethmoid bone. Conchae increase the surface area of the nasal cavity, disrupting the flow of air as it enters the nose and causing air to bounce along the epithelium, where it is cleaned and warmed. The conchae and meatuses trap water during exhalation preventing dehydration.
The floor of the nasal cavity is composed of the hard palate and the soft palate . Air exits the nasal cavities via the internal nares and moves into the pharynx.
Paranasal sinuses serve to warm and humidify incoming air and are lined with a mucosa which produces mucus. Paranasal sinuses are named for their associated bone:
- frontal sinus
- maxillary sinus
- sphenoidal sinus
- ethmoidal sinus
The nares and anterior portion of the nasal cavities are lined with mucous membranes, containing sebaceous glands and hair follicles that serve to prevent the passage of large debris, such as dirt, through the nasal cavity. An olfactory epithelium used to detect odors is found deeper in the nasal cavity.
The conchae, meatuses, and paranasal sinuses are lined by respiratory epithelium composed of pseudostratified ciliated columnar epithelium ( Figure 12.3 ). The epithelium contains specialized epithelial cells that produce mucus to trap debris. The cilia of the respiratory epithelium help to remove mucus and debris with a constant beating motion, sweeping materials towards the throat to be swallowed.
This moist epithelium functions to warm and humidify incoming air. Capillaries located just beneath the nasal epithelium warm the air by convection. Serous and mucus-producing cells also secrete defensins , or immune cells that patrol the connective tissue providing additional protection.
Did you know?
Cold air slows the movement of cilia that may result in the accumulation of mucus, leading to rhinorrhea during cold weather.
Pharynx
The pharynx is divided into three major regions: the nasopharynx , the oropharynx , and the laryngopharynx (see Figure 12.4 ).
At the top of the nasopharynx are the pharyngeal tonsils. The function of the pharyngeal tonsil is not well understood, but it contains a rich supply of lymphocytes and is covered with ciliated epithelium that traps and destroys invading pathogens that enter during inhalation. The pharyngeal tonsils are large in children but tend to regress with age and may even disappear. The uvula and soft palate move like a pendulum during swallowing, swinging upward to close off the nasopharynx to prevent ingested materials from entering the nasal cavity. Auditory (Eustachian) tubes that connect to each middle ear cavity open into the nasopharynx. This connection is why colds often lead to ear infections.
The oropharynx is bordered superiorly by the nasopharynx and anteriorly by the oral cavity. The oropharynx contains two distinct sets of tonsils:
-
The palatine tonsils.
- A palatine tonsil is one of a pair of structures located laterally in the oropharynx in the area of the fauces .
-
The lingual tonsils.
- The lingual tonsil is located at the base of the tongue.
Similar to the pharyngeal tonsil, the palatine and lingual tonsils are composed of lymphoid tissue, and trap and destroy pathogens entering the body through the oral or nasal cavities.
The laryngopharynx is inferior to the oropharynx and posterior to the larynx. It continues the route for ingested material and air until its inferior end, where the digestive and respiratory systems diverge. The stratified squamous epithelium of the oropharynx is continuous with the laryngopharynx. Anteriorly, the laryngopharynx opens into the larynx, whereas posteriorly , it enters the esophagus.
Larynx
The structure of the larynx is formed by several pieces of cartilage. Three large cartilage pieces form the major structure of the larynx.
-
Thyroid cartilage (anterior):
- The thyroid cartilage is the largest piece of cartilage that makes up the larynx. The thyroid cartilage consists of the laryngeal prominence, or “Adam’s apple,” which tends to be more prominent in males.
-
Epiglottis (superior):
- Three smaller, paired cartilages—the arytenoids, corniculates, and cuneiforms—attach to the epiglottis and the vocal cords and muscle that help move the vocal cords to produce speech.
-
Cricoid cartilage (inferior):
- The thick cricoid cartilage forms a ring, with a wide posterior region and a thinner anterior region.
When the epiglottis is in the “closed” position, the unattached end of the epiglottis rests on the glottis . A vestibular fold, or false vocal cord, is one of a pair of folded sections of mucous membrane. A true vocal cord is one of the white, membranous folds attached by muscle to the thyroid and arytenoid cartilages of the larynx on their outer edges. The inner edges of the true vocal cords are free, allowing oscillation to produce sound.
The act of swallowing causes the pharynx and larynx to lift upward, allowing the pharynx to expand and the epiglottis of the larynx to swing downward, closing the opening to the trachea. These movements produce a larger area for food to pass through, while preventing food and beverages from entering the trachea.
Similar to the nasal cavity and nasopharynx, this specialized epithelium produces mucus to trap debris and pathogens as they enter the trachea. The cilia beat the mucus upward towards the laryngopharynx, where it can be swallowed down the esophagus.
Did you know?
Folds of the true vocal cords differ between individuals resulting in voices with different pitches.
Trachea
The trachea is formed by 16 to 20 stacked, C-shaped pieces of hyaline cartilage that are connected by dense connective tissue. The trachealis muscle and elastic connective tissue together form the fibroelastic membrane . The fibroelastic membrane allows the trachea to stretch and expand slightly during inhalation and exhalation, whereas the rings of cartilage provide structural support and prevent the trachea from collapsing. The trachealis muscle can be contracted to force air through the trachea during exhalation. The trachea is lined with pseudostratified ciliated columnar epithelium, which is continuous with the larynx. The esophagus borders the trachea posteriorly.
Bronchial Tree
The trachea branches into the right and left primary bronchi at the carina . These bronchi are also lined by pseudostratified ciliated columnar epithelium containing mucus-producing goblet cells ( Figure 12.7b ). The carina is a raised structure that contains specialized nervous tissue that induces violent coughing if a foreign body, such as food, is present. Rings of cartilage, similar to those of the trachea, support the structure of the bronchi and prevent their collapse. The primary bronchi enter the lungs at the hilum . The bronchi continue to branch into a bronchial tree. A bronchial tree (or respiratory tree) is the collective term used for these multiple-branched bronchi. The main function of the bronchi, like other conducting zone structures, is to provide a passageway for air to move into and out of each lung. The mucous membrane traps debris and pathogens.
A bronchiole branches from the tertiary bronchi. Bronchioles, which are about 1 mm in diameter, further branch until they become the tiny terminal bronchioles, which lead to the structures of gas exchange. There are more than 1,000 terminal bronchioles in each lung. The muscular walls of the bronchioles do not contain cartilage like those of the bronchi. This muscular wall can change the size of the tubing to increase or decrease airflow through the tube.
Respiratory Zone
In contrast to the conducting zone , the respiratory zone includes structures that are directly involved in gas exchange. The respiratory zone begins where the terminal bronchioles join a respiratory bronchiole, the smallest type of bronchiole (see Figure 12.8 ), which then leads to an alveolar duct, opening into a cluster of alveoli.
Alveoli
An alveolar duct opens into a cluster of alveoli. An alveolus is one of the many small, grape-like sacs that are attached to the alveolar ducts. An alveolar sac is a cluster of many individual alveoli that are responsible for gas exchange. An alveolus is approximately 200 μm in diameter with elastic walls that allow the alveolus to stretch during air intake, which greatly increases the surface area available for gas exchange. Alveoli are connected to their neighbors by alveolar pores, which help maintain equal air pressure throughout the alveoli and lung (see Figure 12.9 ).
Concept Check
- What are the components of the bronchial tree?
- What is the purpose of cilia?
- Where does gas exchange take place?
Gross Anatomy of the Lungs
The lungs are pyramid-shaped, paired organs that are connected to the trachea by the right and left bronchi; on the inferior surface, the lungs are bordered by the diaphragm . The lungs are enclosed by the pleurae, which are attached to the mediastinum. The right lung is shorter and wider than the left lung, and the left lung occupies a smaller volume than the right. The cardiac notch allows space for the heart (see Figure 12.10 ). The apex of the lung is the superior region, whereas the base is the opposite region near the diaphragm. The costal surface of the lung borders the ribs. The mediastinal surface faces the midline.
Each lung is composed of smaller units called lobes. Fissures separate these lobes from each other. The right lung consists of three lobes: the superior, middle, and inferior lobes. The left lung consists of two lobes: the superior and inferior lobes. A pulmonary lobule is a subdivision formed as the bronchi branch into bronchioles. Each lobule receives its own large bronchiole that has multiple branches. An interlobular septum is a wall, composed of connective tissue, which separates lobules from one another.
Can you correctly label the respiratory system structures?
Physiology (Function) of the Respiratory System
Blood Supply
The major function of the lungs is to perform gas exchange, which requires blood from the pulmonary circulation.
- This blood supply contains deoxygenated blood and travels to the lungs where erythrocytes pick up oxygen to be transported to tissues throughout the body.
- The pulmonary artery carries deoxygenated, arterial blood to the alveoli.
- The pulmonary artery branches multiple times as it follows the bronchi, and each branch becomes progressively smaller in diameter.
- One arteriole and an accompanying venule supply and drain one pulmonary lobule. As they near the alveoli, the pulmonary arteries become the pulmonary capillary network.
- The pulmonary capillary network consists of tiny vessels with very thin walls that lack smooth muscle fibers.
- The capillaries branch and follow the bronchioles and structure of the alveoli. It is at this point that the capillary wall meets the alveolar wall, creating the respiratory membrane.
- Once the blood is oxygenated, it drains from the alveoli by way of multiple pulmonary veins, which exit the lungs through the hilum .
Nervous Innervation
The blood supply of the lungs plays an important role in gas exchange and serves as a transport system for gases throughout the body. Innervation by both the parasympathetic and sympathetic nervous systems provides an important level of control through dilation and constriction of the airway.
- The parasympathetic system causes bronchoconstriction.
- The sympathetic nervous system stimulates bronchodilation.
Reflexes such as coughing, and the ability of the lungs to regulate oxygen and carbon dioxide levels, also result from autonomic nervous system control. Sensory nerve fibers arise from the vagus nerve, and from the second to fifth thoracic ganglia. The pulmonary plexus is a region on the lung root formed by the entrance of the nerves at the hilum. The nerves then follow the bronchi in the lungs and branch to innervate muscle fibers, glands, and blood vessel s.
Pleura of the Lungs
Each lung is enclosed within a cavity that is surrounded by the pleura. The pleura (plural = pleurae) is a serous membrane that surrounds the lung. The right and left pleurae, which enclose the right and left lungs, respectively, are separated by the mediastinum.
The pleurae consist of two layers:
- The visceral pleura is the layer that is superficial to the lungs and extends into and lines the lung fissures (see Figure 12.11 ).
- The parietal pleura is the outer layer that connects to the thoracic wall, the mediastinum, and the diaphragm.
The visceral and parietal pleurae connect to each other at the hilum . The pleural cavity is the space between the visceral and parietal layers.
The pleurae perform two major functions:
- Produce pleural fluid that lubricates surfaces, reduces friction to prevent trauma during breathing, and creates surface tension that helps maintain the position of the lungs against the thoracic wall. This adhesive characteristic of the pleural fluid causes the lungs to enlarge when the thoracic wall expands during ventilation, allowing the lungs to fill with air.
- The pleurae also create a division between major organs that prevents interference due to the movement of the organs, while preventing the spread of infection.
Pulmonary Ventilation
The difference in pressures drives pulmonary ventilation because air flows down a pressure gradient, that is, air flows from an area of higher pressure to an area of lower pressure.
- Air flows into the lungs largely due to a difference in pressure; atmospheric pressure is greater than intra-alveolar pressure, and intra-alveolar pressure is greater than intrapleural pressure.
- Air flows out of the lungs during expiration based on the same principle; pressure within the lungs becomes greater than the atmospheric pressure.
Pulmonary ventilation comprises two major steps: inspiration and expiration. Inspiration is the process of having air enter the lungs and expiration is the process of expelling air from the lungs ( Figure 12.12 ). A respiratory cycle is one sequence of inspiration and expiration.
Two muscle groups are used during normal inspiration : t he diaphragm and the external intercostal muscles. Additional muscles can be used if a bigger breath is required.
- The diaphragm contracts, it moves inferiorly toward the abdominal cavity, creating a larger thoracic cavity and more space for the lungs.
- The external intercostal muscles contract and move the ribs upward and outward, causing the rib cage to expand, which increases the volume of the thoracic cavity.
Due to the adhesive force of the pleural fluid, the expansion of the thoracic cavity forces the lungs to stretch and expand as well. This increase in volume leads to a decrease in intra-alveolar pressure, creating a pressure lower than atmospheric pressure. As a result, a pressure gradient is created that drives air into the lungs.
The process of normal expiration is passive, meaning that energy is not required to push air out of the lungs.
- The elasticity of the lung tissue causes the lung to recoil, as the diaphragm and intercostal muscles relax following inspiration.
- The thoracic cavity and lungs decrease in volume, causing an increase in intrapulmonary pressure. The intrapulmonary pressure rises above atmospheric pressure, creating a pressure gradient that causes air to leave the lungs.
There are different types, or modes, of breathing that require a slightly different process to allow inspiration and expiration:
- Quiet breathing , also known as eupnea , is a mode of breathing that occurs at rest and does not require the cognitive thought of the individual. During quiet breathing, the diaphragm and external intercostals must contract.
- Diaphragmatic breathing , also known as deep breathing, requires the diaphragm to contract. As the diaphragm relaxes, air passively leaves the lungs.
- Costal breathing , also known as a shallow breath, requires contraction of the intercostal muscles. As the intercostal muscles relax, air passively leaves the lungs.
-
Forced breathing
, also known as
hyperpnea
, is a mode of breathing that can occur during exercise or actions that require the active manipulation of breathing, such as singing.
-
During forced breathing, inspiration and expiration both occur due to muscle contractions. In addition to the contraction of the diaphragm and intercostal muscles, other accessory muscles must also contract.
- During forced inspiration , muscles of the neck contract and lift the thoracic wall, increasing lung volume.
- During forced expiration , accessory muscles of the abdomen contract, forcing abdominal organs upward against the diaphragm. This helps to push the diaphragm further into the thorax, pushing more air out. In addition, accessory muscles help to compress the rib cage, which also reduces the volume of the thoracic cavity.
-
During forced breathing, inspiration and expiration both occur due to muscle contractions. In addition to the contraction of the diaphragm and intercostal muscles, other accessory muscles must also contract.
Concept Check
-
Breathing normally, place your hand on your stomach and take in one full respiratory cycle.
- What type of breathing are you doing?
-
Keeping your hand on your stomach, take in one large breath and exhale.
- What type of breathing are you doing?
-
Complete 10 jumping jacks. Once completed, place your hand on your stomach and take in one full respiratory cycle.
- What type of breathing are you doing?
Respiratory Rate and Control of Ventilation
Breathing usually occurs without thought, although at times you can consciously control it, such as when you swim under water, sing a song, or blow bubbles. The respiratory rate is the total number of breaths that occur each minute. Respiratory rate can be an important indicator of disease, as the rate may increase or decrease during an illness or in a disease condition. The respiratory rate is controlled by the respiratory center located within the medulla oblongata in the brain, which responds primarily to changes in carbon dioxide, oxygen, and pH levels in the blood.
The normal respiratory rate of a child decreases from birth to adolescence:
- A child under 1 year of age has a normal respiratory rate between 30 and 60 breaths per minute.
- By the time a child is about 10 years old, the normal rate is closer to 18 to 30.
- By adolescence, the normal respiratory rate is similar to that of adults, 12 to 18 breaths per minute.
Did you know?
Respiratory rate is the total number of breaths that occur each minute
Watch this video:
Media 12.1. Respiratory System, Part 2: Crash Course A&P #32 [Online video]. Copyright 2015 by CrashCourse .
Practice Terms Related to the Respiratory System
Common Abbreviations for the Respiratory System
Many terms and phrases related to the respiratory system are abbreviated. Learn these common abbreviations by expanding the list below.
Diseases and Disorders of the Respiratory System
A variety of diseases can affect the respiratory system, such as asthma, emphysema, chronic obstructive pulmonary disorder (COPD), and lung cancer. All of these conditions affect the gas exchange process and result in labored breathing and other difficulties.
The Effects of Second-Hand Tobacco Smoke
The burning of a tobacco cigarette creates multiple chemical compounds that are released through mainstream smoke, which is inhaled by the smoker, and through sidestream smoke, which is the smoke that is given off by the burning cigarette. Second-hand smoke , which is a combination of sidestream smoke and the mainstream smoke that is exhaled by the smoker, has been demonstrated by numerous scientific studies to cause disease. At least 40 chemicals in sidestream smoke have been identified that negatively impact human health, leading to the development of cancer or other conditions, such as immune system dysfunction, liver toxicity, cardiac arrhythmias , pulmonary edema , and neurological dysfunction. Tobacco and second-hand smoke are considered to be carcinogenic . Exposure to second-hand smoke can cause lung cancer in individuals who are not tobacco users themselves.
- It is estimated that the risk of developing lung cancer is increased by up to 30% in nonsmokers who live with an individual who smokes in the house, as compared to nonsmokers who are not regularly exposed to second-hand smoke.
- Children who live with an individual who smokes inside the home have a larger number of lower respiratory infections, which are associated with hospitalizations, and higher risk of sudden infant death syndrome (SIDS). Second-hand smoke in the home has also been linked to a greater number of ear infections in children, as well as worsening symptoms of asthma.
Chronic Obstructive Pulmonary Disease (COPD)
COPD is a term used to represent a number of respiratory diseases, including chronic bronchitis and emphysema. COPD is a chronic condition with most symptoms appearing in middle-aged or older adults. Signs and symptoms include shortness of breath, cough, and sputum production. There is no cure for COPD. Shortness of breath may be controlled with bronchodilators. The best plan is to avoid triggers and getting sick. Clients with COPD are advised to avoid people who are sick, get vaccinated against influenza and pneumococcal pneumonia, and reduce their exposure to pollution and cigarette smoke. While there are several risk factors, as many as 75% of cases are associated with cigarette smoking (National Heart, Lung, and Blood Institute, n.d.). To learn more about COPD, visit the National Heart, Lung, and Blood Institute’s web page .
Asthma
Asthma is a chronic disease characterized by inflammation, edema of the airway, and bronchospasms which can inhibit air from entering the lungs. Bronchospasms can lead to an “asthma attack.” An attack may be triggered by environmental factors such as dust, pollen, pet hair, or dander, changes in the weather, mold, tobacco smoke, and respiratory infections, or by exercise and stress.
Signs and symptoms of an asthma attack involve coughing, shortness of breath, wheezing, and tightness of the chest. Symptoms of a severe asthma attack require immediate medical attention and may include dyspnea that results in cyanotic lips or face, confusion, drowsiness, a rapid pulse, sweating, and severe anxiety. The severity of the condition, frequency of attacks, and identified triggers influence the type of medication that an individual may require. Longer-term treatments are used for those with more severe asthma. Short-term, fast-acting drugs that are used to treat an asthma attack are typically administered via an inhaler. For young children or individuals who have difficulty using an inhaler, asthma medications can be administered via a nebulizer.
Lung Cancer
Lung cancer is a leading cause of cancer death among men and women. Smoking is the most significant risk factor for lung cancer, with 90% of cases in men and 80% of cases in women attributed to tobacco smoking. Signs and symptoms may include shortness of breath, wheezing, blood in the mucus, hoarseness, and trouble swallowing (MedlinePlus, n.d.).
 Both cancers occur when malignant cells form in the tissues of the lung. If metastasis occurs, lung cancer cells spread to other parts of the body. Treatment will depend on the type of lung cancer and the stage at diagnosis. Treatments may include surgery, chemotherapy, targeted therapy, immunotherapy, and radiation therapy (National Cancer Institute, 2021a, 2021b).
Sleep Apnea
Sleep apnea is a chronic disorder that occurs in children and adults. It is characterized by the cessation of breathing during sleep. These episodes may last for several seconds or several minutes, and may differ in the frequency with which they are experienced. Sleep apnea leads to poor sleep. Signs and symptoms include fatigue, evening napping, irritability, memory problems, morning headaches, and excessive snoring. A diagnosis of sleep apnea is usually done during a sleep study, where the patient is monitored in a sleep laboratory for several nights. Treatment of sleep apnea commonly includes the use of a device called a continuous positive airway pressure (CPAP) machine during sleep. The CPAP machine has a mask that covers the nose, or the nose and mouth, and forces air into the airway at regular intervals. This pressurized air can help to gently force the airway to remain open, allowing more normal ventilation to occur.
Medical Terms in Context
Medical Specialties and Procedures Related to the Respiratory System
Respiratory Therapists (RTs)
Respiratory therapists (RTs) are healthcare professionals that monitor, assess, and treat people who are having problems breathing. RTs must have at least a two-year degree. RTs measure lung capacity, test oxygen and carbon dioxide levels, perform chest physiotherapy to remove mucus from patients’ lungs, and operate ventilator equipment (Bureau of Labor Statistics, 2021). For more information, visit the American Association for Respiratory Care web page .
Thoracic Surgeon
A thoracic surgeon refers to a surgeon who has specialized in either thoracic (chest) surgery or cardiothoracic (heart and chest) surgery (National Cancer Institute, n.d.). To learn about the career path, read this PDF from The Society of Thoracic Surgeons.
Spirometry Testing
Spirometry testing is used to find out how well lungs are working by measuring air volume.
- Respiratory volume describes the amount of air in a given space within the lungs, or which can be moved by the lung, and is dependent on a variety of factors.
- Tidal volume refers to the amount of air that enters the lungs during quiet breathing, whereas inspiratory reserve volume is the amount of air that enters the lungs when a person inhales past the tidal volume.
- Expiratory reserve volume is the extra amount of air that can leave with forceful expiration, following tidal expiration.
- Residual volume is the amount of air that is left in the lungs after expelling the expiratory reserve volume.
- Respiratory capacity is the combination of two or more volumes.
- Anatomical dead space refers to the air within the respiratory structures that never participates in gas exchange, because it does not reach functional alveoli.
- Respiratory rate is the number of breaths taken per minute, which may change during certain diseases or conditions.
Both respiratory rate and depth are controlled by the respiratory centers of the brain, which are stimulated by factors such as chemical and pH changes in the blood. These changes are sensed by central chemoreceptors, which are located in the brain, and peripheral chemoreceptors, which are located in the aortic arch and carotid arteries. A rise in carbon dioxide or a decline in oxygen levels in the blood stimulates an increase in respiratory rate and depth.
Watch this video:
Media 12.3. Peak Flow and Spirometry – Lung Function Tests [Online video]. Copyright 2012 by Oxford Medical Education .
Respiratory System Vocabulary
Adenoidectomy: Excision of the adenoids.
Alveolar duct: Small tube that leads from the terminal bronchiole to the respiratory bronchiole and is the point of attachment for alveoli.
Alveolitis: Inflammation of the alveoli.
Aphonia: Condition of the absence of one’s voice.
Apnea: A temporary absence of respiration.
Asphyxia: Condition caused by a lack of oxygen that leads to impending or actual death.
Aspirate: To withdraw fluid, tissue, or other substances from a body cavity, cyst, or tumor.
Atelectasis: Failure of the lung to expand (inflate) completely.
Autonomic: Involuntary or unconscious.
Benign: Non-cancerous.
Bronchiectasis: Dilation of the bronchi.
Bronchitis: Inflammation of the bronchus.
Bronchodilators: A type of drug that causes small airways in the lungs to open up.
Bronchogenic carcinoma: Cancer that begins in the tissue that lines or covers the airways of the lungs, including small cell and non-small cell lung cancer.
Bronchopneumonia: Inflammation of the lung, particularly the bronchioles and alveoli, that is associated with bronchitis.
Bronchoscope: A thin, tube-like instrument used to examine the inside of the trachea, bronchi, and lungs.
Bronchoscopy: A procedure involving a bronchoscope to examine the inside of the trachea, bronchi, and lungs.
Bronchospasm: Spasmodic contraction of the smooth muscle of the bronchi.
Carcinogen: Any substance that causes cancer.
Cardiac notch: An indentation on the surface of the left lung.
Carina: A ridge at the base of the trachea (windpipe) that separates the openings of the right and left main bronchi (the large air passages that lead from the trachea to the lungs).
Chronic: A condition that lasts a long time with periods of remission and exacerbation.
Computerized tomography (CT): A noninvasive imaging technique that uses computers to analyze several cross-sectional X-rays in order to reveal minute details about structures in the body.
Conducting zone: The major functions of the conducting zone are to provide a route for incoming and outgoing air, remove debris and pathogens from the incoming air, and warm and humidify the incoming air.
Cyanotic: Pertaining to abnormal color of blue (bluish color, lips and nail beds) caused by deoxygenation.
Defensins: The lysozyme enzyme and proteins which have antibacterial properties.
Diaphragm: A sheet of skeletal muscle separating the thoracic and abdominal cavities that has to contract and relax for you to breathe.
Dysphonia: Condition of difficult speaking, including hoarseness and change in pitch or quality of the voice.
Dyspnea: Difficulty breathing.
Epiglottitis: Inflammation of the epiglottis.
Endoscope: A thin, tube-like instrument used to look at tissues inside the body.
Endoscopy: A procedure that uses an endoscope to examine the inside of the body.
Epiglottis: Leaf-shaped piece of elastic cartilage that is a portion of the larynx that swings to close the trachea during swallowing.
Epistaxis: Nosebleed.
Erythrocytes: Red blood cells.
Eupnea: A mode of breathing that occurs at rest and does not require the cognitive thought of the individual; also known as quiet breathing.
Expiration: Exhalation, or the process of causing air to leave the lungs.
External nose: The surface and skeletal structures that result in the outward appearance of the nose and contribute to its numerous functions.
Fauces: The opening of the oral cavity into the pharynx.
Fibroelastic membrane: A flexible membrane that closes the posterior surface of the trachea, connecting the C-shaped cartilages.
Glottis: Composed of the vestibular folds, the true vocal cords, and the space between these folds.
Hard palate: Located at the anterior region of the nasal cavity and is composed of bone.
Hemothorax: Hemorrhage within the pleural cavity.
Hematologist: A doctor who has special training in diagnosing and treating blood disorders.
Hematology: The study of blood and blood-forming issues.
Hilum of the lung: A concave region where blood vessels, lymphatic vessels, and nerves also enter the lungs.
Hypercapnia: Abnormally elevated blood levels of CO2 (carbon dioxide).
Hyperpnea: Forced breathing or breathing that is excessive.
Hypocapnia: Abnormally low blood levels of CO2 (carbon dioxide).
Hypoxemia: Below-normal level of oxygen saturation of blood (typically <95 percent).
Hypoxia: Lack of oxygen supply to the tissues.
Inferior: A position below or lower than another part of the body proper.
Influenza (flu): An acute viral infection involving the respiratory tract.
Inspiration: Inhalation, or process of breathing air into the lungs.
Laryngeal: Pertaining to the larynx.
Laryngitis: Inflammation of the larynx.
Laryngopharynx: One of the three regions of the pharynx; inferior to the oropharynx and posterior to the larynx.
Laryngoplasty: Surgical repair of the larynx.
Laryngoscope: A thin, tube-like instrument used to examine the larynx.
Laryngoscopy: Examination of the larynx with a mirror or laryngoscope.
Larynx: A cartilaginous structure inferior to the laryngopharynx that connects the pharynx to the trachea and helps regulate the volume of air that enters and leaves the lungs; also known as the voice box.
Lobectomy: Excision of the lobe(s) of an organ.
Lymphocytes: The second most common type of leukocyte and are essential for the immune response.
Malignant: Cancerous.
Mucus: A thick, slippery fluid made by the membranes that line certain organs of the body.
Nasopharyngitis: Inflammation of the nose and pharynx.
Nasopharynx: The upper part of the throat behind the nose. An opening on each side of the nasopharynx leads into the ear.
Nebulizer: A device used to turn liquid into a fine spray.
Nosocomial infection: Infection acquired in hospital.
Oropharynx: A passageway for both air and food; borders the nasopharynx and the oral cavity.
Oximeter: Instrument used to measure the oxygenation of tissues.
Pharyngeal tonsil: The tonsil located at the back of the throat; also known as the adenoid when swollen.
Pharyngitis: Inflammation of the pharynx.
Pharynx: A tube formed by skeletal muscle and lined by mucous membrane that is continuous with that of the nasal cavities; also known as the throat.
Pleural effusion: An abnormal collection of fluid between the thin layers of tissue (pleura) lining the lung and the wall of the chest cavity.
Pleurisy: Inflammation of the pleura.
Pneumoconiosis: A condition caused by the inhalation of dust.
Pneumonectomy: Excision of the lung.
Pneumonia: A severe inflammation of the lungs in which the alveoli (tiny air sacs) are filled with fluid.
Pneumothorax: An abnormal collection of air in the space between the thin layer of tissue that covers the lungs and the chest cavity that can cause all or part of the lung to collapse.
Polysomnography (PSG): Simultaneous and continuous monitoring of several parameters during sleep to study normal and abnormal sleep.
Posterior: Describes the back or direction toward the back of the body.
Pulmonary artery: Artery that arises from the pulmonary trunk.
Pulmonary edema: Fluid accumulation in alveoli and bronchioles (related to heart failure).
Pulmonary embolism: A blood clot within the lung.
Radiologist: A doctor who has special training in creating and interpreting pictures of areas inside the body.
Radiography: A procedure that uses x-rays to take pictures of areas inside the body.
Radiology: The use of radiation or other imaging technologies to diagnose or treat disease.
Respiratory zone: The respiratory zone includes structures that are directly involved in gas exchange.
Rhinitis: Inflammation of the mucous membranes of the nose.
Rhinoplasty: A plastic surgical operation on the nose, either reconstructive, restorative, or cosmetic.
Rhinorrhea: Excess nasal drainage; also called a “runny nose.”
Septal cartilage: The flexible hyaline cartilage connected to the nasal bone.
Sinusitis: Inflammation of the sinuses.
Soft palate: Located at the posterior portion of the nasal cavity and consists of muscle tissue.
Sonogram: A computer picture of areas inside the body created by high-energy sound waves.
Spirometry: The measurement of volume of air inhaled or exhaled by the lung.
Sputum: Mucus and other matter brought up from the lungs by coughing.
Stethoscope: An instrument is used to hear sounds produced by the heart, lungs, or other parts of the body.
Sympathetic nervous system (SNS): The division of the nervous system involved in our fight-or-flight responses. It continuously monitors body temperature and initiates appropriate motor responses.
Tachypnea: Rapid breathing.
Thoracalgia: Pain in the chest.
Thoracentesis: Removal of fluid from the pleural cavity through a needle inserted between the ribs.
Thoracic: Pertaining to the chest.
Thoracoscope: A thin tube-like instrument used to examine the inside of the chest.
Thoracoscopy: Examination of the inside of the chest, using a thoracoscope.
Thoracotomy: An operation to open the chest.
Tonsillectomy: Excision of the tonsils.
Tonsillitis: Inflammation of the tonsils.
Tracheitis: Inflammation of the trachea.
Tracheostomy: Surgery to create an opening into the trachea.
Tracheotomy: Surgical incision of the trachea.
Trachea: The windpipe.
Upper respiratory infection: Infection of the nasal cavity, pharynx and larynx cause by a virus.
Uvula: A small bulbous, teardrop-shaped structure located at the apex of the soft palate.
Ventilator: A machine used to help a patient breathe.
Test Yourself
References
Bureau of Labor Statistics. (2021). Respiratory therapists. In Occupational outlook handbook . U.S. Department of Labor. https://www.bls.gov/ooh/healthcare/respiratory-therapists.htm
CrashCourse. (2015, August 24). Respiratory system, part 1: crash course A&P #31 [Video]. YouTube. https://youtu.be/bHZsvBdUC2I
CrashCourse. (2015, August 31). Respiratory system, part 2: crash course A&P #32 [Video]. YouTube. https://youtu.be/Cqt4LjHnMEA
National Cancer Institute. (n.d.). Thoracic surgeon definition . National Institutes of Health, U.S. Department of Health. https://www.cancer.gov/publications/dictionaries/cancer-terms/def/thoracic-surgeon
National Cancer Institute. (2021a). Non-small cell lung cancer treatment (PDQ®)-Patient version . National Institutes of Health, U.S. Department of Health. https://www.cancer.gov/types/lung/patient/non-small-cell-lung-treatment-pdq
National Cancer Institute. (2021b). Small cell cancer treatment (PDQ®)-Patient version . National Institutes of Health, U.S. Department of Health. https://www.cancer.gov/types/lung/patient/small-cell-lung-treatment-pdq
National Heart, Lung, and Blood Institute. (n.d.). COPD. National Institutes of Health, U.S. Department of Health. https://www.nhlbi.nih.gov/health-topics/copd
Oxford Medical Education. (2012, May 13). Peak flow and spirometry – Lung function tests [Video]. YouTube. https://www.youtube.com/watch?v=M4C8EInOMOI
Image Descriptions
Figure 12.1 image description: This figure shows the upper half of the human body. The major organs in the respiratory system are labeled. [Return to Figure 12.1].
Figure 12.2 image description: This figure shows a cross section view of the nose and throat. The major parts are labeled. [Return to Figure 12.2].
Figure 12.3 image description: This figure shows a micrograph of pseudostratified epithelium. [Return to Figure 12.3].
Figure 12.4 image description: This figure shows the side view of the face. The different parts of the pharynx are color-coded and labeled (from the top): nasal cavity, hard palate, soft palate, tongue, epiglottis, larynx, esophagus, trachea. [Return to Figure 12.4].
Figure 12.5 image description: The top panel of this figure shows the anterior view of the larynx, and the bottom panel shows the right lateral view of the larynx. [Return to Figure 12.5].
Figure 12.6 image description: This diagram shows the cross-section of the larynx. The different types of cartilages are labeled (clockwise from top): pyriform fossa, true vocal cord, epiglottis, tongue, glottis, vestibular fold, trachea, esophagus. [Return to Figure 12.6].
Figure 12.7 image description: The top panel of this figure shows the trachea and its organs. The major parts including the larynx, trachea, bronchi, and lungs are labeled. [Return to Figure 12.7].
Figure 12.8 image description: This image shows the bronchioles and alveolar sacs in the lungs and depicts the exchange of oxygenated and deoxygenated blood in the pulmonary blood vessels. [Return to Figure 12.8].
Figure 12.9 image description: This figure shows the detailed structure of the alveolus. The top panel shows the alveolar sacs and the bronchioles. The middle panel shows a magnified view of the alveolus, and the bottom panel shows a micrograph of the cross section of a bronchiole. [Return to Figure 12.9].
Figure 12.10 image description: Diagram of the lungs with the major parts labelled (from top, clockwise): trachea, superior lobe, main bronchus, lobar bronchus, segmental bronchus, inferior lobe, inferior lobe, middle lobe, superior lobe of the left lung. [Return to Figure 12.10].
Figure 12.11 image description: This figure shows the lungs and the chest wall, which protects the lungs, in the left panel. In the right panel, a magnified image shows the pleural cavity and a pleural sac. [Return to Figure 12.11].
Figure 12.12 image description: The left panel of this image shows a person inhaling air and the location of the chest muscles. The right panel shows the person exhaling air and the contraction of the thoracic cavity. [Return to Figure 12.12].