unit 3 lymph, immune, resp syst

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main fxns of lymph syst

return interstitial fluid and leaked plasma proteins back to blood

assists in circulating body fluids (pick up extra fluid)

helps defend body against disease-causing agents

transport dietary lipids and lipid soluble vitamins (A,D,E,K, in GI-tract

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lymph

interstitial fluid once entered lymphatic vessels

24 L filtered out of vlood a day; 20.4 L returned to blood; 2.6 L back to lymph vessels

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mention fxn of lymph nodes

filtration - macrophages destroy microorganisms and debris

immune syst activation - monitor for antigens and mount an attack against them

*medulla- medullary chords extend from cortex and contain B, T, and plasma cells; macrophages reside on these fibers and phagocytize foreign matter

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fxn of thymus

fxns strictly in T lymphocyte maturation

does not directly fight antigens

produces hormones

secretes the hormones (thymopoietin and thymosins) that stim lymphocytes to become immunocompetent

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fxn of spleen

site of lymphocyte proliferation

immune surveillance and response

cleanses the blood - macrophages in sinuses remove debris and foreign matter

stores breakdown produces of RBCs for later reuse - spleen macrophages salvage and store iron for later use by bone marrow

site of fetal erythrocyte production (normally ceases after birth)

stores blood platelets

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______ are specialized lymphatic capillaries found in the small intestine that pick up digested fats/lipids + assist in transporting chyle (lipids + lymph mixed together) to the bloodstream

lacteals

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contrast blood capillaries w lymph capillaries

lymph: mini valves (loosely joined), start at tissue (endothelial); v permiable; withstand interstitial pressure + remain open (thanks to collagen filaments)

can absorb cell debris, pathogens, cancer cells, cells in LN cleanse + “examine” debris

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what makes up lymph

interstitial fluid + leaked proteins

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name the two lymph ducts and area of the body they drain

thoracic duct: rest of body, L side head, neck, chest and rest of body below diaphragm

R lymphatic duct: R arm, right side of head + neck, R chest

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between which veins is lymph drained

L subclavian (?), R internal jugular

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what makes thymus diff from all other lymph organs and tissues

prod homrones, no B cells present, fxns strictly in T lymphocyte maturation

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what is MALT? give examples of locations

mucosa associated lymphatic tissue: anywhere in mucosa - GI tract, resp syst, urinary,

masses of lymph tissue not surrounded by capsule; protects from foreign matter

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what tissues are involved in prod memory

MALT, peyer’s patches, tonsils, appendix, thymus (did i miss any)

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what are the two arms of the immune response

innate - 1st: epithelial barriers (skin, mucous mm), 2nd: protections against pathogens that break those external barriers

adaptive - 3rd: grp of mechanisms defeat pathogen + create “memory” for future encounters

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what distinguishes innate def from adaptive def syst?

innate - not specific, localized → if cut on arm, that’s where innate response

adaptive - specific, systemic, memory

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<p>explain 1st line defense weapon fxns</p>

explain 1st line defense weapon fxns

skin - wax, lysozyme, keratin, sebum + sweat (acid mantle), stomach → proteases, acid; enzymes break proteins

mucous mm - urine, mucous + cilia, tears, saliva

bacteria - your natural microbiome

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<p>explain 2nd line defense weapon fxns</p>

explain 2nd line defense weapon fxns

phagocytes - macrophages, neutrophils, eosinophils, mast cells, dendritic cells

antimicrobial proteins - interferon → inhibit virus replication; complement proteins → MAC: kill bacteria, inflamm

NKC inflamm - small disctinct grp of large granular lymphocytes; react nonspecifically and eliminate cancerous + virus-infected cells; kill targets by releasing perforins and other cytolytic chems; can lyse and kill cancer cells + virus-infected cells by puncturing their mm

fever

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<p>explain 3rd line defense weapon fxns</p>

explain 3rd line defense weapon fxns

humoral → antibody-mediated immunity; works mainly against extracellular stages of infectious microorgs; extracell viruses, bacteria, yeast, allergens, toxins, venoms. in event of mismatched blood transfusion, also destroys foreign erythrocytes - B cells prod antibodies to neutralize pathogens

cellular → T cells - directly kill infected/cancerous cells/help coordinate immune response

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there are two important antimicrobial proteins:

complements and interferons

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what are complement proteins? how does it cause bacterial lysis? what are some of the compliment proteins

amplifies inflamm response, kills bact + destroys foreign substances, circulate in blood in inactive form

causes bact lysis by MAC (membrane attach complex) - MAC inserts into mm of cells and allows ions, water, other molecules to freely pass thru pores

some are C1, C2, C3 (a+b), C4, C5 (a+b), C6, C7, C8, C9

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what stims interferon prod, and how they protect uninfected cells

viral infection stims interferon prod (before specific immune syst)

interferons activate macrophages and mobilize NKs (to inhibit virus prod), so

protect by making other cells protect themselves - inter molecules leave infected cell and enter neighbor cells, then stims neighbor cells to activate genes for PKR (antiviral protein), which specifically blocks viral repro in neighboring cells

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know steps, fxns, and underlying mechanism of inflamm response

steps: mast cells detect injury to nearby cells + release histamine, initiating inflamm response; histamine increases blood flow to wound sites, bringing in phagocytes and other immune cells that neutralize pathogens. the blood influx causes the wound to swell, redden, and become warm and painful

fxns: prevent spread of damaging agents to nearby tissues, dispose of cell debris + pathogens, set stage for repair processes

mechanism: (? is this not the same as steps? kinda? idrk) stop pathogens from spreading, bring immune cells to location

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cardinal signs of inflamm

redness, swelling, pain, heat

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what is an antigen? compare and contrast complete and incomplete antigens (haptens)

antigens - illicit immune response; only certain parts of entire antigen are immunogenic (epitopes -specific part of antigen recognized by immune syst)

complete antigens - large (proteins, some lipids, nucleic acid), ultimate targets of immune response; B cells

incomplete antigens (haptens) - small molecules (peptides, nucleotides, many hormones); not immunogenic but reactive when attached to protein carriers (don’t illicit immune responded by themself. bind to protein to become complete and illicit immune response

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antigen-presenting cells did i give enough info?

do not respond to specific antigens; play essential auxiliary (supportive) roles in immunity

major role in immunity is to engulf foreign particles and present fragments of antigens on their own surfaces to be recognized by T cells

dendritic cells (usually in CT and epiderm) - major initiator of adaptive immunity; migrate to LN and 2ry lymphoid organs, and present antigens to T and B cells

macrophages - stay at site of infection; similar to dendritic, also secrete soluble proteins that activate T cells

lymphocytes, B cells

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<p>what does it mean when a T or B cell becomes immunicompetent</p>

what does it mean when a T or B cell becomes immunicompetent

means cells have receptor - can bind to other cells (display unique type of receptor that responds to distinct antigen)

B cells can prod antibodies by binding to antigens (substances that trigger immune response, prompting prod of antibodies)

B cells mature in bone marrow; T cells mature in thymus

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<p>what happens to B cells when activated for the first time? explain clonal selection</p>

what happens to B cells when activated for the first time? explain clonal selection

when b cell activated, clonal selection begins

a native immunocompetent B cells is activated when antigens bind to its surface receptors and T cell interactions; B cells quickly stimulated then multiply

result is army of cells (all exactly alike) bearing the same antigen-specific receptors; it is the antigen that does the selecting in clonal selection by “choosing” a lymphocyte with complementary receptors

(b cells witness crime (attack), show police sketch of criminal, tell others abt it)

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what determines our specificity towards a foreign substance

our genes

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why is the secondary response to an antigen so much faster than the primary response

because memory cells generated during the initial exposure to an antigen are ready to react much faster in later encounters

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compare and contrast humoral and cellular immunity. Make sure yk when each one is used

humoral: involves B cells + antibodies, deals w exogenous (originating from externals), relies on these to neutralize pathogens in bodily fluids (pleural+peritoneal cavities, after birth)

cellular: cytotoxic T cells fight specific antigen directly; bind to target cell and release perforins into its mm causing cell lysis by creating transmembrane pores, endogenous antigens; attakcs any of our cells infected w virus, parasite, cancer

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class II MHC proteins display what kind of antigens? what class of T cell recognizes antigens bound to class II MHC? what types of cells display these proteins?

bind complete antigens to exogenous antigens

CD4 (helper T cells [TH])

antigen-presenting cells (APCs)

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contrast active and passive immunity. be able to mention examples

active: make memory+plasma cells → natural - antibodies made after infection; artificial - ab after vaccine

passive: given, not prod by self; go away if given → natural - ab from mother’s milk; artificial - ab from serum shot of antibody itself (ex. IgG, snake venom)

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what are the general functions of antibodies

ammunition of humoral imm; capable of binding specifically w certain antigen

“tie up prisoner” until help arrives

Neutralization, Agglutination, Precipitation, Complement, Opsonization (foreign patho coated w opsonins, making susceptible to phagcyto by imm cells), NK cells

a NAP can help you CONcentrate

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specific fxn IgM

main antibody of primary responses (first secreted in response to new antigen), best at fixing complement; monomer form of IgM serves as B cell receptor

doesn’t cross placenta

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specific fxn IgG

main blood antibody of 2ry responses, neutralizes toxins, opsonization

crosses placenta

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specific fxn IgA

secreted into mucus, tears, saliva, colostrum

doesn’t cross placenta

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specific fxn IgE

antibody of allergy (histamine) and antiparasitic activity

doesn’t cross placenta

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specific fxn IgD

B cell receptor

doesn’t cross placenta

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which class of antibody is most abundant in blood? which is secreted first in a primary immune response? which is most abundant in secretion?

IgG, IgM, IgA

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what makes up the respiratory and conductive zones of the resp syst

resp: resp bronchi, alveolar ducts, alveoli

conductive: nose, nasal cavity, nasopharynx, larynx, trachea, bronchi, bronchioles

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know all fxns of resp syst

exchange CO2 + O2, speech and other vocalizations, sense of smell, influences pH of body fluids by eliminating CO2 (acid-base balance)

BP reg by helping synthesis of angiotensin II (→vasoconstrictor→ADH+aldosterone→inc BP), blood+lymph flow, lungs filter small clots (blood filtration), expulsion of abdominal contents: breath-holding assists in urination, defecation, childbirth (valsalva maneuver)

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<p>contrast internal resp, external resp, pulmo ventilation. what is the goal of all 3?</p>

contrast internal resp, external resp, pulmo ventilation. what is the goal of all 3?

internal - systematic gas exchange (between blood + cells)

external - alveolar gas exchange do i just need to know whats in pictures?

pulmo vent - breathing, quiet breathing (at rest, rhythmic); inspiration+expiration; change in vol causes gas pressure changes in thoracic cavity. change in vol causes gas pressure changes in thoracic cavity (do we need to know these details)

<p>internal - systematic gas exchange (between blood + cells)</p><p>external - alveolar gas exchange <mark data-color="red" style="background-color: red; color: inherit">do i just need to know whats in pictures?</mark></p><p>pulmo vent - breathing, quiet breathing (at rest, rhythmic); inspiration+expiration; <mark data-color="red" style="background-color: red; color: inherit">change in vol causes gas pressure changes in thoracic cavity. change in vol causes gas pressure changes in thoracic cavity (do we need to know these details)</mark></p>
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be able to answer questions on anat and/or fxns (including types of cells, structure, such as cartilage/smooth musc presence) of all resp structures (from nasal cavity to alveoli)

table in canvas

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why pseudostratified ciliated columnar epithelium is common in many resp structures?

has goblet cells that prod mucus to catch bacteria, dust, etc

cilia remove intrusions (idk lol)

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which resp structure provides the greatest surface area for gas exchange?

alveolus(i)

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what cells would you find in an alveoli and what is the fxn for each cell?

type I - simp squam epi - gas exchange

type II - secrete surfactant (dec surface tension of water in alveoli, keeps open w o collapse)

macrophages - eat bact

simp squam epi - gas exchange

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discuss relationship of pleurae to the lungs and thoracic wall, and their fxnal importance

pleurae surround lungs, w visceral layer touching lungs and parietal layer touching thoracic wall

fxnal importance - keep lungs inflated bc pressure

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how does alveoli’s surfactant prevent the collapsing of alveoli?

dec surface tension of water

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know what steps, muscs, events (such as pressure differences) are involved in breathing:

define intrapulmonary and intrapleural pressure

intrapulmonary - pressure in lungs (alveoli)

intrapleural - pressure between visceral and parietal pleura (pressure around lungs)

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know what steps, muscs, events (such as pressure differences) are involved in breathing:

the contraction of the diaphragm and the external intercostals begins inspiration. which nerves are involved in the contraction of these muscles? explain what happens in terms of volume and pressure changes in the lungs when these muscs contract. make sure to include movement of air and pressure diffs inside lungs and pleural pressure. then explain what happens during expiration

diaphragm nerve - phrenic (diaphragm down/flat)

external intercostal nerve - intercostals nerve

volume - 500mL air - tidal volume; vol up, pressure down

pressure - pressure in lungs less than pressure in atmosphere (760mmHg)

movement of air - air in alveoli

pressure diffs in lungs + pleural pressure - intrapulm(in alveoli) begins 760, interpleural is 756. when diaphragm and ext intcosts contract, vol inc intrapulm pressure down to 759 and intrapleural down 754.

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<p>explain what happens during expiration. explain what happens in terms of volume and pressure changes in the lungs when diaphragm and external intercostal muscs contract. make sure to include movement of air and pressure diffs inside lungs and pleural pressure. </p>

explain what happens during expiration. explain what happens in terms of volume and pressure changes in the lungs when diaphragm and external intercostal muscs contract. make sure to include movement of air and pressure diffs inside lungs and pleural pressure.

volume - 500mL

pressure - vol down, pressure up

movement of air - air moves our alveoli

pressure diffs in lungs + pleural pressure - intrapulm pressure beginning at 760 and interpleural at 754. diaphragm + ect intcosts relax, vol dec intrapulm pressure inc to 761 and intrapleural back to 756

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know what steps, muscs, events (such as pressure differences) are involved in breathing:

on the other hand, if you have to force your breathing in what muscs would be involved?

sternocleidomastoid - elevate sternum

scalene - elevating 2 upper ribs

pectoral minor - elevate 3-5 ribs

serratus posterior - ribs 2-5

erector spinae - straighten vertebral column

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know what steps, muscs, events (such as pressure differences) are involved in breathing:

on the other hand, if you have to force your breathing out what muscs would be involved?

internal intercostals - depress the ribs

abdominal wall muscles - move abdominal content upward to push diaphragm upward

transversus thoracis - ribs 2-6

serratus posterior inferior - ribs 9-12

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<p>during external resp, where are oxy and CO2 concentrations higher? what drives O2 and CO2 to move from one region to another? dont forget abt mmHg for CO2 and O2</p>

during external resp, where are oxy and CO2 concentrations higher? what drives O2 and CO2 to move from one region to another? dont forget abt mmHg for CO2 and O2

PO2 higher in alveolus until bv pass alveolus, PCO2 higher in bvs until pass alveolus

partial pressure gradient (?) drives O2 and CO2 to move from one region to another

part 1 [deoxy from arteries]: pulmo caps - PO2 = 40mmHg, PCO2 = 45mmHg

part 2: alveolus - PO2 = 104mmHg, PCO2 = 40mmHg → pulmo caps- PO2 = 104mmHg, PCO2 = 40mmHg

part 3 [reoxy in veins]: (bronchial circulation) pulmo caps- PO2 = 100mmHg, PCO2 = 40mmHg

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during internal resp, where are oxy and CO2 concentrations higher? what drives O2 and CO2 to move from one region to another? dont forget abt mmHg for CO2 and O2

PO2 higher in bv until pass to cells, PCO2 higher in cells until passed to bvs

pt 1: systemic caps - PO2 = 100mmHg, PCO2 = 40mmHg

pt 2: cells (maybe? i think?) - PO2 = 40mmHg, PCO2 = 45mmHg

pt 3: systemic caps - PO2 = 40mmHg, PCO2 = 45mmHg

<p>P<sub>O2</sub> higher in bv until pass to cells, P<sub>CO2</sub> higher in cells until passed to bvs</p><p>pt 1: systemic caps - P<sub>O2</sub>  = 100mmHg, P<sub>CO2</sub>  = 40mmHg</p><p>pt 2: cells (maybe? i think?) - P<sub>O2</sub>  = 40mmHg, P<sub>CO2</sub>  = 45mmHg</p><p>pt 3: systemic caps - P<sub>O2</sub>  = 40mmHg, P<sub>CO2</sub>  = 45mmHg</p>
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know everything abt O2 and CO2 transport. include: where in blood they are transported

hemoglobin

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know everything abt O2 and CO2 transport. include: how its transport is affected by factors such as temp, acidity and BPG, etc…

saturation - the higher the PO2 difference, the higher the oxygen dissociation

temp - the higher it is, the higher the oxy dissociation

pH (high H+) - the lower it is, the higher the oxygen dissociation (exercise = lactic acid = lower pH = higher O2 dissociation

PCO2 - inc CO2, inc O2 unloading

BPG - higher BPG, higher oxy dissociation

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know diff resp ctrls (resp ctrl center [VRG and DRG] and PRG)

medullary resp centers:

ventral respiratory grp (VRG) - ctrls auto resp; primary generator of resp rhythm; generates gasping during extremely low oxy

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mention diff reasons that could change our breathing pattern and their effect on breathing depth/rate