BECOM 2 Exam #2 Flashcards
- Pseudostratified ciliated columnar epithelium
- Goblet cells
- Brush cells
- Small granule cells
- Basal cells
- filter and move foreign particles
- mucous production
- chemosensory receptors
- diffuse neuroendocrine system
- Mitotically active progenitor cells give rise to the above
Infant Respiration distress syndrome
leading cause of death for premature babies
-incomplete differentiation of type II alveolar cells leading to a deficiency in surfactant
Dust cells
alveolar macrophages
- Phagocytose erythrocytes and particulate matter that has gone all the way into the alveoli
- can get caught up in lungs (more in older ind. or people that work in saw mills, heat homes w wood, etc.)
- Found in alveoli and interalveolar septa
Emphysema
Dilation and permanent enlargement of bronchioles causing pulmonary acini and alveolar cell loss
Pulmonary hypertension
elevated pulmonary pressure resulting in pulmonary vessels thickening and narrowing airways
bronchial pneumonia
neutrophils infiltrate airway lumen
asthma
epithelial congestion, smooth muscle contraction, lumen constriction
pleuritis
inflammation of pleura
route to lungs (backwards for microciliary escalator)
nasal cavity, pharynx, larynx, trachea, bronchi, bronchioles, terminal bronchioles, {resp bronchioles, alveolar ducts, alveoli}
most likely lung cancer for non smoker and where it arises
adenocarcinoma
arise from bronchioles and alveoli epithelium
where does squamous cell carcinoma lung cancer arise
epithelium of bronchi
cystic fibrosis
dysfunction of micociliary escalator
transairway pressure formula
Pta = Paw (airway) - Ppl (pleural)
transpulmonary pressure formula
PL = PA (alveolar) - Ppl (pleural)
Force vital capacity (FVC) vs forced expiratory volume (FEV)
FVC: max inspiration to max expiration
FEV: the amount of volume produced from max inspiration to 1 sec
FEV1/FVC ratio
PEF
FEF25-75
75%-80%
peak expiratory flow
is the average FEF rate over the middle 50% of the FVC
oxygen hemoglobins content
1.36 ml/g hemoglobin
CO Hb shift?
anemia shift?
left and dec line
dec line not shift
Carbonic anhydrase
enzyme H2O + CO2 = H2CO3
pulmonary edema causes
- inc hydrostatic pressure (pulmonary hypertension)
- inc capillary permeability -> inc protein in interstitial space
- inc surface tension (dec alveoli)
- inc plasma oncotic pressure (e.g. hemodilution with saline infusion)
left vs right oxygen shift
left: higher affinity for oxygen
right: lower affinity to for oxygen
Functional residual capacity (FRC) during standing up and laying supine
FRC increases as one sits up because when laying down the diaphragm pushes on the lungs and when standing up the apex of the lungs pulls down increasing negative pressure pulling more air into the lungs
Residual volume during COPD
Increases bc during COPD an individuals lungs become less elastic meaning they can take in more air but can’t push that air out
Distensibility
describes the ease at which the lungs can be stretched/inflated
-dec inflation
Recoil
defines the ability of a stretched tissue to return to its resting volume
-inc inflation dec emptying bc dec recoil
Distensibility and effect if lost
describes the ease at which the lungs can be stretched/inflated
-dec inflation
Recoil and effect if lost
defines the ability of a stretched tissue to return to its resting volume
-inc inflation dec emptying bc dec recoil
FRC when one has loss of distensibility and recoil
distensibility: dec FRC
recoil: inc FRC
apex vs base compliance (CL) at FRC
apex has a lower compliance because more negative Ppl so higher volume.
apex vs base compliance at RV
apex more compliant because at RV the apex has a negative Ppl while the base has a positive Ppl which promotes collapse
apex vs base compliance (CL) at FRC and why is this good
apex has a lower compliance because more negative Ppl so higher volume.
-this is good bc during TV the air prefers to be in the base which is where most of the blood is bc of gravity (inc perfusion rate)
Why does absence of surfactant result in edema?
the absence of surfactant will cause the alveoli to collapse resulting in an inc in interstitial fluid space decreases the interstitial fluid’s hydrostatic pressure resulting in an increase of water transfer from the capillaries to in interstitial fluid
forced expiration cycle
During forced expiration Ppl because positive pushing air out of the lungs. Alveolar pressure is high positive but decreases as it moves through the airways because of resistance. When Ppl and PA become equal (Pta = 0) the airway is at risk of collapsing. Generally this occurs where cartilage is located
Equal Point Pressure (EPP)
When Ppl and PA become equal (Pta = 0)
-airway can collapse if not reinforced by cartilage
forced expiration with emphysema
Emphysema causes the alveoli to have reduced elasticity (recoil) which causes a dec in PA. When forced expiration occurs and Ppl is positive this causes a EPP to occur earlier in the bronchiole tubes than normal (not near cartilage support) causing collapse of the bronchioles.
hysteresis
and what causes the most work for inflation
less work is required to deflate the lung than inflate, this difference in work is called hysteresis
-most work of inflation is countering surface area not so much so elasticity
most work and least to inflate the lungs is from …. to ……
RV to FRC
-TV
Obstructive pulmonary disease vs Restrictive lung disease
OPD: will cause a decrease in FEV1 but no change in FVC
-dec in FEV1 because airways are obstructed
-Forced Expiratory Flow will dec and graph will slouch
RLD: will have no change on FEV1 but a dec in FVC
-lungs cant take in normal amount of air bc lungs can’t expand normally
How is air trapping determine
test individuals slow vital capacity (SVC) and forced vital capacity (FVC)
-if air trapping RV will inc in FVC bc it is more likely for the airways to close during forced expiration than slow
alveolar dead space vs Total/physiological dead space
alveolar dead space: area in the lung where no gas exchange is occurring (no blood supply or no air)
Total/physiological dead space: alveolar dead space + anatomical dead space
tidal volume calculations
ml/min divided by breathes/min
how to calculate dead space (equation)
VD = VT (PACO2 - PECO2 / PACO2)
-PACO2 can be exchanged with PaCO2
alveolar oxygen (PAO2) equation
PAO2 = (PIO2 (barometric press - 47)) - ((1.2)PaCO2)
volume of gas diffusing per minute (Vgas) factors (inc and dec)
Inc Vgas: surface areas (As), diffusion coefficient (D), and partial pressure difference (delta P)
Dec Vgas: membrane thickness (T)
-DeltaP = PA - Pa
why does CO2 have a higher Vgas than O2 even though O2 has a higher partial pressure difference (delta P)?
CO2’s diffusion coefficient is 20x that of O2
-CO2 is more soluble in H2O
Diffusion Capacity definition, test (DLCO), what will cause it to inc/dec
- amount of gas moved across membrane / minute for 1 mmHg partial pressure gradient
- shows diffusion rate of CO if dec then we know there is a problem with diffusion of O2
- inc: exercise (inc blood flow and less oxygenated Hb pulling more oxygen), polycythemia (bc more Hb pulling more oxygen to blood)
- dec: pulmonary edema, reduced perfusion (blood flow) or loss of alveolar membrane (surface area)
Bohr effect
- right shift
- Hb has a tendency to travel from areas of high pH to areas of low pH which will cause a release of O2 (salt bridge formation)
- CO2 directly reacts with Hb decreasing Hb affinity for O2 (salt bridge formation)
CD56 is used to identify which cells by flow cytometry
NK cells
Nephelometry
-measures total immunoglobulin titers in serum
ELISA
ELISA-measures specific immunoglobulins or antigens in serum
Immunofluorescence
assesses presence of tissue antigens or serum immunoglobulins
Flow cytometry
assesses presence and phenotype of peripheral blood or tissue cells
CD80 & CD86
on APCs serve as co-stimulatory molecules for T cells and bind to CD 28 on T cells
common gamma chain (yc)
- receptor that bind cytokines IL-7 (T cells) and IL-15 (NK cells) resulting in proliferation
- mutation will cause no T cell or NK cells and B cells will have no function (SCID x linked disease)
B cell coreceptors
CD19, CD20, CD40 (bind CD40L on T cell)
Helper T cell
Cytotoxic T cell
Both
Helper T cell: CD4, CD40L
Cytotoxic T cell: CD8
Both: CD3, CD28 (binds to CD80/86 on APC)
-ONLY HAVE MHCI
cytokines that make more T cells and NK cells
T cells: IL7
NK cells: IL15
how does NK kill other cells
- perforin puts holes in the cell while granzyme degrades the host cell proteins and causes apoptosis
- Fas ligand: bind Fas on target cell -> apoptosis
interferon gamma (IFN-y)
- this cytokine releases from NK cells and maximizes MHC expression by normal cells and at the same time increases NK cell activity
- cytokine released from TH1 cells that stimulate B cells to produce more IgG
β 2 microglobulin
part of the MCHI structure and is the same across all MCHIs in a individual
-if this is mutated non functioning MCHI is the result
how are endogenous proteins processed
processed via proteasome, transported to the ER through TAP and presented in MCHI molecule
endogenous antigen processing
- bind CD8 cytotoxic T cells via MCHI
- are processed via proteasome into the ER by TAP and presented to MCHI molecules, where then the MCHI complex completes biosynthesis in the Golgi before moving to the membrane surface
- Immunoproteasome speeds up this process
exogenous antigen processing
- bind CD4 helper T cells via MCHII
- antigen is phagocytized by APC and used w a lysosome where it is degrades by proteases, MCHII are made in the ER and transferred to the Golgi where they release and are allowed to fuse with enosomal vesicles confining extracellular peptides
- invariant chain binds to MCHII molecule to keep it stable while awaiting peptide
- INF-y: unregulates MHC II and inc lysosomal activity
How does a super antigen work?
-T cell: stimulate large numbers of lymphocytes by binding to the vB domain of the TCR and MCHII outside of the normal binding site
- B cell: bind B cell Fab region
-
What do T cells do to recognize an antigen?
must have matching antigen and MHC molecule
-CD3 MHC complex
Where do naive T cells become activated / B cells mature?
T cells: paracortex, PALS spleen
B cells: germinal center of 2nd lymph organs (lymph nodes, spleen)
T cell clonal expansion process?
- naive T cells enter lymph node cortex via HEV -> paracortex
- APC enters paracortex form cortical sinus -> bind T cell
- T cell activated and proliferate and loose their ability to exit lymph node
- activated T cell become effector T cell and exit lymph node
- T cells can’t leave lymph node till activated, proliferate, and become effector cell
T cell recognition, coreceptors, and costimulation
CTC -Recognition: antigen, MHCI, CD3 -coreceptors: CD8 -costimulation: CD28 bind CD80/86 on APC HTC -Recognition: antigen, MCHII, CD3 -coreceptor: CD4 -costimulation: CD28 bind CD80/86 on APC
B cell recognition, coreceptors, and costimulation
recognition: antigen
coreceptors: CD19, CD20, CD81
costimulator: CD40 binds to CD40L on helper T cell
How does a lymphocyte not activate when it recognizes a non harmful antigen?
- when a lymphocyte encounters a non harmful antigen (don’t have CD80/86) the costimulator (CD24) will not bind and these T cells will be deleted
- this works when T cells bind to self MCH molecules of self tissue cells but will have no costimulation
Adjuvants
substances that enhance the immunogenicity of an antigen
- ex. aluminum salts
- put in vaccines so better response
Hyperpnea vs Tachypnea
- fast deep breaths
- fast shallow breaths
AIRE
enables the thymic medullary cells to express proteins normally only expressed in other organs
-if defective leads to autoimmune issues (ex. APECED)
IgG
- best opsonization
- most predominant
- transfer across placenta via brambell receptor (will protect child when initially born)
- passive immunizations
brambell receptor
allows IgG to transfer passively across placenta from mother to child
- As a result, a full-term infant will have the same antibodies as its mother. These antibodies will protect the infant from certain diseases for up to a year
- Transplacental IgG is the most important source of Ig in infancy.
12-23 rule
12 and 23 bp spacers connect during non homologous end joining during immunoglobin recombination
-RAG cuts at 23 and 12 bp segments between VDJ
absence of either Rag1 or Rag2
RAG1/2: initiate recombination event
-absence: B and T cell fail to develop but will still have NK cells
TdT–lymphocyte-specific DNA polymerase
TdT: expressed during the pro-B & T cell stage that randomly adds nucleotides (N regions) to the junctions between V, D, and J segments of the H chain and between all V region gene segments of the TCR
-marker for acute lymphocytic leukemia
TREC and KREC
TREC: marker for recently T cells
KREC: circular by product by product of BCR kappa gene rearrangement
allelic exclusion
- silencing of either the maternal or paternal allele in regards to BCRs and TCRs
- MHCs are codominant allelic expressed
where do Cytotoxic t cells become activated, proliferate, and effector function
paracortex of lymph node and PALS of spleen
effector function: periphery
how does t cell contraction work and what it involved?
Activated T cells express increased levels of CTLA-4, which has higher affinity for B7 molecules than CD28.
ADA
No NK, B cells, T cells
Positive selection
TCR are kept if they can bind to MHC self receptor/peptide moderately but will apoptosis if they bind to tightly or too loosely
Negative selection
TCR are apoptosed if they bind to MCH and self peptide with high affinity
-if def. AIRE then no expression of ectopic self antigen (APECED - autoimmune)
AIRE
enables the thymic MEDULLARY cells to express proteins normally only expressed in other organs
-if defective leads to autoimmune issues (ex. APECED)
PolyIg receptor
transfer J chain immunoglobulins across tissue
IgM
- show acute infection
- pentameric immunoglobulin connected by j chain
IgE
- mediates large parasite destruction and allergic reaction by crosslinking
- FcERs on mast cells, basophils, and eosinophils
- Degranulation
prostaglandin E production
resets core body temp higher
-shivering to increase body temp
NSAIDs vs Acetaminophen and what causes effect
NSAID: and anti-inflammatory activity
Acetaminophen: Anti-pyretic, analgesic
-Inhibit COX enzyme activity preventing prostaglandin synthesis
initial inc in HR is caused by
dec in parasympathetic innervation
CO = SV vs HR in hot conditions while exercise
SV will decrease because more blood is being shunted to skin to cool the body. CO stays the same though because HR will increase in this case
Valsalva Maneuver
- systolic pressure will increase with increase workload (inc treadmill elevation)
- diastolic will stay the same
Blood Pressure Response to Dynamic Exercise
Systolic: inc as workload inc bc inc HR
Diastolic: slightly dec bc dec TPR as a result of vasodilation of vessels to working muscles
Blood Pressure in Recovery
Blood pressure (systolic and diastolic) dec (hypotension) bc HR will dec after working out but still vasodilation of vessels to muscle
TPR whole body excercise vs upper body only
whole body: dec TPR because large muscle groups being used which will cause vasodilation
upper body: inc TPR because smaller muscle groups will vasodilate but the majority of the vessels will vasoconstrict
TPR during upper body isometric lift
smaller amount of muscles using large amount of oxygen but overall vasoconstriction in most of the body.
-high HR, vent rate,
DNApol μ & λ
fills 3’ overhang
TGF-B
cytokine that promotes IgA differentiation in mucosal associated lymph tissue (MALT)
TAP role
transports antigen into ER for MHC docking
CLIP
binds to MHCII antigen spot to stabilize the complex while awaiting a antigen peptide
Dendritic cells when encounter PAMP/DAMP
- process antigen (phagocytosis)
- migrate to lymph node (paracortex)
- inc MHC/antigen expression + costimulatores (CD80/86)
- release cytokines (IL-12 promotes Th1 immunity)
what is the role of coreceptors (CD3/4/8, CD19/20) ?
required for lymphocyte signaling
what is the BCR activation sequence for coreceptors?
CD19 -> CD81 -> ITAM becomes phosphorylated signaling between cell surface and cytoplasm
Class Switch Recombination
allows for different antibody isotopes
Class Switch Recombination
allows for different antibody isotypes but can only occur after a naive B cell (IgM IgD) comes in contact with an antigen and receives helper T cell help
Complement-dependent cell cytotoxicity (CDCC)
classical pathway of complement is activated by IgM (best) or IgG (IgG3 & IgG1»>IgG2, not IgG4). Complement cascade terminates with the membrane attack complex (MAC), which perforates (& kills) target.
Antibody-dependent cell cytotoxicity (ADCC)
activating receptors on NK cells include FcRγIII. When NK cells bind IgG Fcr via FcRγIII, NK cells induce apoptosis of target cell (perforin & granzyme).
Central tolerance
mechanisms within the primary lymphoid organs that promote tolerance to self (i.e. limit autoimmunity)
Naïve T cells come in contact with MHC in the
paracortex of the lymph nodes or PALS of the spleen
Def. CD4 ligand hyper
IgM antibodies
TH1 secrete IL-2 in order to
CTLs require IL-2 for clonal expansion. IL-2 is also known as T cell growth factor
TH1 secrete IL-2 in order to
cytotoxic T cells require IL-2 for clonal expansion.
location of recognition, differentiation/proliferation, and effector function of T cells
recognition: paracortex of lymph node, PALS of spleen
differentiation/proliferation: paracortex of lymph node, PALS of spleen
effector: peripheral tissue
CTLA-4
- Activated T cells express increased levels of CTLA-4, which has higher affinity for B7 molecules than CD28
- Tregs also express CTLA-4
surrogate light chain purpose and proteins
- chain that associates with a successfully rearranged μ H chain—forming a pre-BCR—to permit surface expression prior to availability of κ or λ L chains
- λ5 & VpreB
Membrane versus Secreted Ig
- Mediated by alternative splicing or processing of the RNA.
- Isotype does not change
Somatic hypermutation (SHM)
- Activation-induced deaminase (AID) inserts cytosine to uracil mutations in germinal center B cells.
- Mutations occur predominantly in the CDR regions.
- Is not antigen specific, but the process is designed to achieve antibodies with higher affinity for specific antigen. AKA affinity maturation. B cell w/new BCR needs co-stim (activation) again.
AID-deficiency
- causes autosomal recessive hyper-IgM syndrome
- absence of Ig CSR
- lack of Ig SHM (& affinity maturation)
- lymph node hyperplasia due to giant [unproductive] germinal centers
κ:λ ratio
Ratios higher than 1.65 indicate excess κ FLC; ratios lower than 0.26 indicate excess λ FLC
- there are two different light chain loci Kappa and lambda
- generally B cell contain more kappa loci then lambda
- multiple myeloma
Low PaO2 vs Low PAO2
Low PaO2: diffusion problem
Low PAO2: ventilation problem
why is oxygen diffusion slower than other gases?
O2 concentration in blood is hidden bc is bind to hemoglobin so cannot be dissolved in blood and work toward equilibrium until Hb is saturated
PaO2 during anemia and edema?
anemia: PaO2 dec but O2 sat stays the same
edema: PaO2 will decreases because dec diffusion rate causing hypoxia
what all causes right shift?
-less affinity for O2 (need high PO2 for Hb sat) 2,3 BPG inc CO2 inc temp inc H+ (dec pH) sickle cell anemia
causes of respiratory acidosis
- inc CO2 dec pH
- hypoventilation
- Inc dead space (snorkel, blood/bronchiole clot)
- mismatch ventialtion-perfuison
Response to acidosis/hypercapnia
- Inc PaCO2 will cause Hb to release O2
- pulmonary vasoconstriction known as hypoxic pulmonary vasoconstriction
- dorsal respiratory group
2. ventral respiratory group
- inhalation
2. expiration
Pre-Bötzinger complex
establish respiratory rhythm
pontine group
smooth resp. rhythm
Barbiturates
inhibit resp center and can die of hypoxia by inc GABA
opioids
cough suppressants that work
Failure of the PRG
apneusis (abnormal pattern of breathing characterized by deep, gasping inspiration with a pause at full inspiration followed by a brief, insufficient release)
Cortical regulation of respiration
responsible for the neurons involved in the override completely bypass the respiratory center
- Suprapontine reflexes include sneezing, coughing and swallowing.
- Prolonged conversation overrides the pontine regulation
Primary respiratory hypoventilation syndrome
is a respiratory disorder that results in respiratory arrest during sleep
-Characterized by defect in the automated respiratory mechanism (primarily conscious control)
Paintal’s juxta-pulmonary capillary receptors (J receptors)
- are stimulated by reactive O2 species, tissue damage, accumulation of interstitial fluid and release of inflammatory mediators
- Activation -> increase ventilation rate
- pulmonary embolism, pulmonary vascular congestion and ventilator response to exercise
Hering-Breuer reflex
stretch receptors that are activated when over stretched
-fire “off switch” neurons to inspiratory center
Peripheral chemoreceptors location
carotid and aortic body
Peripheral chemoreceptors
Respond to ↓in PaO2, pH and ↑ in PaCO2
- first to respond but not the strongest
- only one to respond to hypoxia
- if body removed will not immediate effect
peripheral and central responses to hypercapnia?
20% peripheral (more rapid) 80% central (stronger)
removal of carotid body?
no response to oxygen and immediate effect to hypercapnia
ventilatory response to CO2 is reduced by
SLEEP
inc age
genetics
pulmonary vs systemic circulation
pulmonary:
-low resistance
-more compliant
systemic:
-high resistance
-less compliant
what happens to pulmonary BP with inc CO?
decreases
- bc pulmonary capillaries are more compliant so they will distend and more capillaries will be recruited
- good bc reduces edema
intra and extra alveolar capillaries during inspiration and expiration
what does this mean
Intra: -inspiration: compress -expiration: dilate Extra: -inspiration: dilate -expiration: compress *time of lease resistance of blood flow is TV
shunt vs dead space
Dead space gets air but no blood
Shunt get blood but no air
NO usage
used to dilation the vessels of the lungs during PHT
What happens in salt water drawing?
Will swallow salt water and NaCl will enter interstitial fluid.
This will cause a osmotic effect pulling water from the capillaries to the interstitial fluid
what happens in fresh water drowning?
Swallowed water will enter lung increasing hydrostatic pressure favoring water to enter the capillaries. High uptake of water into the blood will cause RBC to lyse releasing K+ -> acute hyperkalemia -> ventricle fibrillation
oxygen debt
still breathing hard after workout because still have inc lactic acid, inc temp, and inc catabolic hormones
function on Bowman’s glands?
produce mucus to moisten the olfactory epithelium and bathe the olfactory neurons and help conduct odorants to them
Club (Clara) Cells location and function
-terminal bronchioles
-Secrete many substances – protect bronchiolar epithelium
Cytochrome P450 enzymes
Lysozymes
IgA antibodies
Tryptase
Thyroxin
TRH from hypothalamus increases cellular metabolism and heat production
The Acute Cardiorespiratory Response to Exercise
- Inc CO
- Ince MAP
- Redistribution of blood flow
- Increase a-v O2 diff
- Increase in tidal volume – light to moderate
- Increase in respiratory/ventilatory rate (ventilatory threshold) – moderate to intense
anticipation to exercise
CO will increase because SNS will cause higher contractility -> inc SV and inc HR before starting exercise
Oxygen consumption
the rate of oxygen delivery and utilization by the tissues during incremental exercise; oxygen required to drive energy production for sustained activity
Factors Affecting the a-vO2 Difference
- Redistribution of flow to active tissues during exercise
- Increased capillary density due to training increases surface area and O2 extraction
- Increased number and size of mitochondria
- Increased oxidative enzymes
- Vascular and metabolic improvements
Functional hypertrophy
increased heart mass, increased capillarization proportionate to mass, normal cardiac function
Concentric hypertrophy
afterload driven; thickening of left ventricle wall with minimal increase in left ventricle chamber diameter -> can be seen in weightlifters
Eccentric hypertrophy
preload driven; elongation of myocytes which leads to proportionate increases in LV wall thickness can be seen in endurance athletes
max VO2 equation
= Q (CO) x a-vO2 difference
Insulin Suppression During Exercise
Mechanism: SNS -> NE -> alpha adrenergic inhibition of beta cells of pancreas
what increase and decreases when working out at hot temps
Inc: HR
Dec: blood volume and SV
trained vs untrained
At rest trained: -Lower HR higher SV same CO Exercise trained: -same HR much higher SV higher CO -inc lactate threshold
Purpose of myoglobin
to take up oxygen for tissue and store it
-higher affinity of oxygen the hemoglobin
Germinal centers of secondary lymph nodes
ph nodes and the spleen where mature B cells proliferate, differentiate, and mutate their antibody genes (through somatic hypermutation aimed at achieving higher affinity), and switch the class of their antibodies
conjugated vaccines protect against
Haemophilus influenzae type b (Hib), Neisseria meningitidis, and Streptococcus pneumoniae
role of Immunoproteasome stimulated by INF y
Faster peptide generation
Longer peptide antigens
Preferred MHC I binding
Cross-presentation
is the ability of certain antigen-presenting cells to take up, process and present extracellular antigens with MHC class I molecules to CD8 T cells (cytotoxic T cells). -APCs take up dead cell that are virally infected and present the virus on MHCI complex
IFN-γ for MHCII
Upregulated transcription of MHC II
Increased lysosomal activity (cathepsin) improve antigen digestion
IgA
Neutralization
Found in mucosal associated tissue (produced by TGF-B)
Transferred through secretions (ex. Breast milk)
Dimer (j chain polyIgreceptor)
FOXP3
trans factor that codes CD4 cell to T reg cells
-T reg cells express CTLA which has a higher affinity fo B7 (CD80/86) than CD28. Controlling immune response
combinatorial vs junctional
- Combinatorial: the different combinations of D, J combinations then DJ, V combinations
- Beta chains: VDJ
- Alpha cahins: VJ (Kappa or Lambda)
- Junctional: DNA polymerases make diverse junctional gene segments
Deficiencies of MAC lead to a higher risk for infection of
Neisseria species
allotype
expression of an allotype is genetically determined
expression difference between TCR/BCR and MHC
TCR/BCR: Monoallelic expression (allelic exclusion)
MHC: co-dominant allelic expression
Hemolytic Uremic syndrome (HUS):
deficiency in complement inhibitors
o Complements continuously binding (autoimmune)
o Increase in thrombosis
Systemic Lupus Erythematosus (SLE):
deficiency in early complements (C1-C4)
o Most likely to have increase in sinus and respiratory infections
Late compliment deficiency
deficiency in late complements (C5-C9), no MAC
o Deficiency in MAC lead to a higher risk for infection of Neisseria species
Hereditary Angioedema (HAE)q
deficiency in C1 protease inhibitor
o Over activation of classical pathway
o Upregulate C2a and bradykinin (inflammation)
o Swollen face
FRC definition
amount of air in lungs when PA = 0
increase in surfactant
inc vent
inc in alveolar size from deep breathes
endocrine stimulation
Why do bronchioles have less resistance than bronchi?
more surface area
Oxygen hemoglobin content
1.36 mL/g hemoglobin
Irritant pulmonary receptors
- These are thought to lie between airway epithelial cells, and they are stimulated by noxious gases, cigarette smoke, inhaled dusts, and cold air.
- The impulses travel up the vagus in myelinated fibers, and the reflex effects include bronchoconstriction and hyperpnea.
black diving
- CO2 triggers urgent breathing
- O2 level will trigger blackout
- hyperventilate will decrease CO2 levels but O2 levels will remain the same
- CO2 doesn’t reach urgent breath point before O2 levels trigger blackout
heat acclamation
acclimated people will have
- greater sweat rate
- more dilute sweat
- lower HR
Upper body isometric (TRP dramatic increase!) WHY?
Valsalva Maneuver
-isometric: resisting weight but not moving muscle
Antidiuretic Hormone
Aldosterone
Antidiuretic Hormone: H2O Reabsorption & Retention
-increases during exercise
Aldosterone: Na+ Reabsorption & Retention
-Generally only increases during recovery
Older/compromised Patients exercise in a hot, humid climate requires electrolyte replacement (Na+, Cl-, K+) beverage
Prolonged >1 hr
Young/health Patients exercise in a hot, humid climate requires electrolyte replacement (Na+, Cl-, K+) beverage which may help protect against SIADH
Prolonged (>4 hr)
