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BECOM 2 > BECOM 2 Exam #2 > Flashcards

BECOM 2 Exam #2 Flashcards

1
Q
  1. Pseudostratified ciliated columnar epithelium
  2. Goblet cells
  3. Brush cells
  4. Small granule cells
  5. Basal cells
A
  1. filter and move foreign particles
  2. mucous production
  3. chemosensory receptors
  4. diffuse neuroendocrine system
  5. Mitotically active progenitor cells give rise to the above
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2
Q

Infant Respiration distress syndrome

A

leading cause of death for premature babies

-incomplete differentiation of type II alveolar cells leading to a deficiency in surfactant

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3
Q

Dust cells

A

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
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4
Q

Emphysema

A

Dilation and permanent enlargement of bronchioles causing pulmonary acini and alveolar cell loss

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5
Q

Pulmonary hypertension

A

elevated pulmonary pressure resulting in pulmonary vessels thickening and narrowing airways

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6
Q

bronchial pneumonia

A

neutrophils infiltrate airway lumen

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7
Q

asthma

A

epithelial congestion, smooth muscle contraction, lumen constriction

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8
Q

pleuritis

A

inflammation of pleura

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9
Q

route to lungs (backwards for microciliary escalator)

A

nasal cavity, pharynx, larynx, trachea, bronchi, bronchioles, terminal bronchioles, {resp bronchioles, alveolar ducts, alveoli}

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10
Q

most likely lung cancer for non smoker and where it arises

A

adenocarcinoma

arise from bronchioles and alveoli epithelium

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11
Q

where does squamous cell carcinoma lung cancer arise

A

epithelium of bronchi

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12
Q

cystic fibrosis

A

dysfunction of micociliary escalator

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13
Q

transairway pressure formula

A

Pta = Paw (airway) - Ppl (pleural)

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14
Q

transpulmonary pressure formula

A

PL = PA (alveolar) - Ppl (pleural)

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15
Q

Force vital capacity (FVC) vs forced expiratory volume (FEV)

A

FVC: max inspiration to max expiration
FEV: the amount of volume produced from max inspiration to 1 sec

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16
Q

FEV1/FVC ratio
PEF
FEF25-75

A

75%-80%
peak expiratory flow
is the average FEF rate over the middle 50% of the FVC

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17
Q

oxygen hemoglobins content

A

1.36 ml/g hemoglobin

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18
Q

CO Hb shift?

anemia shift?

A

left and dec line

dec line not shift

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19
Q

Carbonic anhydrase

A

enzyme H2O + CO2 = H2CO3

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20
Q

pulmonary edema causes

A
  • 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)
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21
Q

left vs right oxygen shift

A

left: higher affinity for oxygen
right: lower affinity to for oxygen

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22
Q

Functional residual capacity (FRC) during standing up and laying supine

A

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

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23
Q

Residual volume during COPD

A

Increases bc during COPD an individuals lungs become less elastic meaning they can take in more air but can’t push that air out

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24
Q

Distensibility

A

describes the ease at which the lungs can be stretched/inflated
-dec inflation

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25
Q

Recoil

A

defines the ability of a stretched tissue to return to its resting volume
-inc inflation dec emptying bc dec recoil

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26
Q

Distensibility and effect if lost

A

describes the ease at which the lungs can be stretched/inflated
-dec inflation

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27
Q

Recoil and effect if lost

A

defines the ability of a stretched tissue to return to its resting volume
-inc inflation dec emptying bc dec recoil

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28
Q

FRC when one has loss of distensibility and recoil

A

distensibility: dec FRC
recoil: inc FRC

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29
Q

apex vs base compliance (CL) at FRC

A

apex has a lower compliance because more negative Ppl so higher volume.

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30
Q

apex vs base compliance at RV

A

apex more compliant because at RV the apex has a negative Ppl while the base has a positive Ppl which promotes collapse

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31
Q

apex vs base compliance (CL) at FRC and why is this good

A

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)

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32
Q

Why does absence of surfactant result in edema?

A

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

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33
Q

forced expiration cycle

A

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

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34
Q

Equal Point Pressure (EPP)

A

When Ppl and PA become equal (Pta = 0)

-airway can collapse if not reinforced by cartilage

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35
Q

forced expiration with emphysema

A

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.

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36
Q

hysteresis

and what causes the most work for inflation

A

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

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37
Q

most work and least to inflate the lungs is from …. to ……

A

RV to FRC

-TV

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38
Q

Obstructive pulmonary disease vs Restrictive lung disease

A

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

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39
Q

How is air trapping determine

A

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

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40
Q

alveolar dead space vs Total/physiological dead space

A

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

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41
Q

tidal volume calculations

A

ml/min divided by breathes/min

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42
Q

how to calculate dead space (equation)

A

VD = VT (PACO2 - PECO2 / PACO2)

-PACO2 can be exchanged with PaCO2

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43
Q

alveolar oxygen (PAO2) equation

A

PAO2 = (PIO2 (barometric press - 47)) - ((1.2)PaCO2)

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44
Q

volume of gas diffusing per minute (Vgas) factors (inc and dec)

A

Inc Vgas: surface areas (As), diffusion coefficient (D), and partial pressure difference (delta P)
Dec Vgas: membrane thickness (T)
-DeltaP = PA - Pa

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45
Q

why does CO2 have a higher Vgas than O2 even though O2 has a higher partial pressure difference (delta P)?

A

CO2’s diffusion coefficient is 20x that of O2

-CO2 is more soluble in H2O

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46
Q

Diffusion Capacity definition, test (DLCO), what will cause it to inc/dec

A
  • 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)
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47
Q

Bohr effect

A
  • 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)
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48
Q

CD56 is used to identify which cells by flow cytometry

A

NK cells

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49
Q

Nephelometry

A

-measures total immunoglobulin titers in serum

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50
Q

ELISA

A

ELISA-measures specific immunoglobulins or antigens in serum

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51
Q

Immunofluorescence

A

assesses presence of tissue antigens or serum immunoglobulins

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52
Q

Flow cytometry

A

assesses presence and phenotype of peripheral blood or tissue cells

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53
Q

CD80 & CD86

A

on APCs serve as co-stimulatory molecules for T cells and bind to CD 28 on T cells

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54
Q

common gamma chain (yc)

A
  • 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)
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55
Q

B cell coreceptors

A

CD19, CD20, CD40 (bind CD40L on T cell)

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56
Q

Helper T cell
Cytotoxic T cell
Both

A

Helper T cell: CD4, CD40L
Cytotoxic T cell: CD8
Both: CD3, CD28 (binds to CD80/86 on APC)
-ONLY HAVE MHCI

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57
Q

cytokines that make more T cells and NK cells

A

T cells: IL7

NK cells: IL15

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58
Q

how does NK kill other cells

A
  • perforin puts holes in the cell while granzyme degrades the host cell proteins and causes apoptosis
  • Fas ligand: bind Fas on target cell -> apoptosis
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59
Q

interferon gamma (IFN-y)

A
  • 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
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60
Q

β 2 microglobulin

A

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

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61
Q

how are endogenous proteins processed

A

processed via proteasome, transported to the ER through TAP and presented in MCHI molecule

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62
Q

endogenous antigen processing

A
  • 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
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63
Q

exogenous antigen processing

A
  • 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
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64
Q

How does a super antigen work?

A

-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
-

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65
Q

What do T cells do to recognize an antigen?

A

must have matching antigen and MHC molecule

-CD3 MHC complex

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66
Q

Where do naive T cells become activated / B cells mature?

A

T cells: paracortex, PALS spleen

B cells: germinal center of 2nd lymph organs (lymph nodes, spleen)

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67
Q

T cell clonal expansion process?

A
  1. naive T cells enter lymph node cortex via HEV -> paracortex
  2. APC enters paracortex form cortical sinus -> bind T cell
  3. T cell activated and proliferate and loose their ability to exit lymph node
  4. 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
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68
Q

T cell recognition, coreceptors, and costimulation

A 
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
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69
Q

B cell recognition, coreceptors, and costimulation

A

recognition: antigen
coreceptors: CD19, CD20, CD81
costimulator: CD40 binds to CD40L on helper T cell

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70
Q

How does a lymphocyte not activate when it recognizes a non harmful antigen?

A
  • 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
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71
Q

Adjuvants

A

substances that enhance the immunogenicity of an antigen

  • ex. aluminum salts
  • put in vaccines so better response
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72
Q

Hyperpnea vs Tachypnea

A
  • fast deep breaths

- fast shallow breaths

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73
Q

AIRE

A

enables the thymic medullary cells to express proteins normally only expressed in other organs
-if defective leads to autoimmune issues (ex. APECED)

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74
Q

IgG

A
  • best opsonization
  • most predominant
  • transfer across placenta via brambell receptor (will protect child when initially born)
  • passive immunizations
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75
Q

brambell receptor

A

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.
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76
Q

12-23 rule

A

12 and 23 bp spacers connect during non homologous end joining during immunoglobin recombination
-RAG cuts at 23 and 12 bp segments between VDJ

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77
Q

absence of either Rag1 or Rag2

A

RAG1/2: initiate recombination event

-absence: B and T cell fail to develop but will still have NK cells

78
Q

TdT–lymphocyte-specific DNA polymerase

A

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

79
Q

TREC and KREC

A

TREC: marker for recently T cells
KREC: circular by product by product of BCR kappa gene rearrangement

80
Q

allelic exclusion

A
  • silencing of either the maternal or paternal allele in regards to BCRs and TCRs
  • MHCs are codominant allelic expressed
81
Q

where do Cytotoxic t cells become activated, proliferate, and effector function

A

paracortex of lymph node and PALS of spleen

effector function: periphery

82
Q

how does t cell contraction work and what it involved?

A

Activated T cells express increased levels of CTLA-4, which has higher affinity for B7 molecules than CD28.

83
Q

ADA

A

No NK, B cells, T cells

84
Q

Positive selection

A

TCR are kept if they can bind to MHC self receptor/peptide moderately but will apoptosis if they bind to tightly or too loosely

85
Q

Negative selection

A

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)

86
Q

AIRE

A

enables the thymic MEDULLARY cells to express proteins normally only expressed in other organs
-if defective leads to autoimmune issues (ex. APECED)

87
Q

PolyIg receptor

A

transfer J chain immunoglobulins across tissue

88
Q

IgM

A
  • show acute infection

- pentameric immunoglobulin connected by j chain

89
Q

IgE

A
  • mediates large parasite destruction and allergic reaction by crosslinking
  • FcERs on mast cells, basophils, and eosinophils
  • Degranulation
90
Q

prostaglandin E production

A

resets core body temp higher

-shivering to increase body temp

91
Q

NSAIDs vs Acetaminophen and what causes effect

A

NSAID: and anti-inflammatory activity
Acetaminophen: Anti-pyretic, analgesic
-Inhibit COX enzyme activity preventing prostaglandin synthesis

92
Q

initial inc in HR is caused by

A

dec in parasympathetic innervation

93
Q

CO = SV vs HR in hot conditions while exercise

A

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

94
Q

Valsalva Maneuver

A
  • systolic pressure will increase with increase workload (inc treadmill elevation)
  • diastolic will stay the same
95
Q

Blood Pressure Response to Dynamic Exercise

A

Systolic: inc as workload inc bc inc HR
Diastolic: slightly dec bc dec TPR as a result of vasodilation of vessels to working muscles

96
Q

Blood Pressure in Recovery

A

Blood pressure (systolic and diastolic) dec (hypotension) bc HR will dec after working out but still vasodilation of vessels to muscle

97
Q

TPR whole body excercise vs upper body only

A

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

98
Q

TPR during upper body isometric lift

A

smaller amount of muscles using large amount of oxygen but overall vasoconstriction in most of the body.
-high HR, vent rate,

99
Q

DNApol μ & λ

A

fills 3’ overhang

100
Q

TGF-B

A

cytokine that promotes IgA differentiation in mucosal associated lymph tissue (MALT)

101
Q

TAP role

A

transports antigen into ER for MHC docking

102
Q

CLIP

A

binds to MHCII antigen spot to stabilize the complex while awaiting a antigen peptide

103
Q

Dendritic cells when encounter PAMP/DAMP

A
  1. process antigen (phagocytosis)
  2. migrate to lymph node (paracortex)
  3. inc MHC/antigen expression + costimulatores (CD80/86)
  4. release cytokines (IL-12 promotes Th1 immunity)
104
Q

what is the role of coreceptors (CD3/4/8, CD19/20) ?

A

required for lymphocyte signaling

105
Q

what is the BCR activation sequence for coreceptors?

A

CD19 -> CD81 -> ITAM becomes phosphorylated signaling between cell surface and cytoplasm

106
Q

Class Switch Recombination

A

allows for different antibody isotopes

107
Q

Class Switch Recombination

A

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

108
Q

Complement-dependent cell cytotoxicity (CDCC)

A

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.

109
Q

Antibody-dependent cell cytotoxicity (ADCC)

A

activating receptors on NK cells include FcRγIII. When NK cells bind IgG Fcr via FcRγIII, NK cells induce apoptosis of target cell (perforin & granzyme).

110
Q

Central tolerance

A

mechanisms within the primary lymphoid organs that promote tolerance to self (i.e. limit autoimmunity)

111
Q

Naïve T cells come in contact with MHC in the

A

paracortex of the lymph nodes or PALS of the spleen

112
Q

Def. CD4 ligand hyper

A

IgM antibodies

113
Q

TH1 secrete IL-2 in order to

A

CTLs require IL-2 for clonal expansion. IL-2 is also known as T cell growth factor

114
Q

TH1 secrete IL-2 in order to

A

cytotoxic T cells require IL-2 for clonal expansion.

115
Q

location of recognition, differentiation/proliferation, and effector function of T cells

A

recognition: paracortex of lymph node, PALS of spleen
differentiation/proliferation: paracortex of lymph node, PALS of spleen
effector: peripheral tissue

116
Q

CTLA-4

A
  • Activated T cells express increased levels of CTLA-4, which has higher affinity for B7 molecules than CD28
  • Tregs also express CTLA-4
117
Q

surrogate light chain purpose and proteins

A
  • 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
118
Q

Membrane versus Secreted Ig

A
  • Mediated by alternative splicing or processing of the RNA.

- Isotype does not change

119
Q

Somatic hypermutation (SHM)

A
  • 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.
120
Q

AID-deficiency

A
  • 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
121
Q

κ:λ ratio

A

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
122
Q

Low PaO2 vs Low PAO2

A

Low PaO2: diffusion problem

Low PAO2: ventilation problem

123
Q

why is oxygen diffusion slower than other gases?

A

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

124
Q

PaO2 during anemia and edema?

A

anemia: PaO2 dec but O2 sat stays the same
edema: PaO2 will decreases because dec diffusion rate causing hypoxia

125
Q

what all causes right shift?

A 
-less affinity for O2 (need high PO2 for Hb sat)
2,3 BPG
inc CO2
inc temp
inc H+ (dec pH)
sickle cell anemia
126
Q

causes of respiratory acidosis

A
  • inc CO2 dec pH
  • hypoventilation
  • Inc dead space (snorkel, blood/bronchiole clot)
  • mismatch ventialtion-perfuison
127
Q

Response to acidosis/hypercapnia

A
  • Inc PaCO2 will cause Hb to release O2

- pulmonary vasoconstriction known as hypoxic pulmonary vasoconstriction

128
Q
  1. dorsal respiratory group

2. ventral respiratory group

A
  1. inhalation

2. expiration

129
Q

Pre-Bötzinger complex

A

establish respiratory rhythm

130
Q

pontine group

A

smooth resp. rhythm

131
Q

Barbiturates

A

inhibit resp center and can die of hypoxia by inc GABA

132
Q

opioids

A

cough suppressants that work

133
Q

Failure of the PRG

A

apneusis (abnormal pattern of breathing characterized by deep, gasping inspiration with a pause at full inspiration followed by a brief, insufficient release)

134
Q

Cortical regulation of respiration

A

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
135
Q

Primary respiratory hypoventilation syndrome

A

is a respiratory disorder that results in respiratory arrest during sleep
-Characterized by defect in the automated respiratory mechanism (primarily conscious control)

136
Q

Paintal’s juxta-pulmonary capillary receptors (J receptors)

A
  • 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
137
Q

Hering-Breuer reflex

A

stretch receptors that are activated when over stretched

-fire “off switch” neurons to inspiratory center

138
Q

Peripheral chemoreceptors location

A

carotid and aortic body

139
Q

Peripheral chemoreceptors

A

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
140
Q

peripheral and central responses to hypercapnia?

A

20% peripheral (more rapid) 80% central (stronger)

141
Q

removal of carotid body?

A

no response to oxygen and immediate effect to hypercapnia

142
Q

ventilatory response to CO2 is reduced by

A

SLEEP
inc age
genetics

143
Q

pulmonary vs systemic circulation

A

pulmonary:
-low resistance
-more compliant
systemic:
-high resistance
-less compliant

144
Q

what happens to pulmonary BP with inc CO?

A

decreases

  • bc pulmonary capillaries are more compliant so they will distend and more capillaries will be recruited
  • good bc reduces edema
145
Q

intra and extra alveolar capillaries during inspiration and expiration
what does this mean

A 
Intra:
-inspiration: compress
-expiration: dilate
Extra:
-inspiration: dilate
-expiration: compress
*time of lease resistance of blood flow is TV
146
Q

shunt vs dead space

A

Dead space gets air but no blood

Shunt get blood but no air

147
Q

NO usage

A

used to dilation the vessels of the lungs during PHT

148
Q

What happens in salt water drawing?

A

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

149
Q

what happens in fresh water drowning?

A

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

150
Q

oxygen debt

A

still breathing hard after workout because still have inc lactic acid, inc temp, and inc catabolic hormones

151
Q

function on Bowman’s glands?

A

produce mucus to moisten the olfactory epithelium and bathe the olfactory neurons and help conduct odorants to them

152
Q

Club (Clara) Cells location and function

A

-terminal bronchioles
-Secrete many substances – protect bronchiolar epithelium
Cytochrome P450 enzymes
Lysozymes
IgA antibodies
Tryptase

153
Q

Thyroxin

A

TRH from hypothalamus increases cellular metabolism and heat production

154
Q

The Acute Cardiorespiratory Response to Exercise

A
  • 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
155
Q

anticipation to exercise

A

CO will increase because SNS will cause higher contractility -> inc SV and inc HR before starting exercise

156
Q

Oxygen consumption

A

the rate of oxygen delivery and utilization by the tissues during incremental exercise; oxygen required to drive energy production for sustained activity

157
Q

Factors Affecting the a-vO2 Difference

A
  • 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
158
Q

Functional hypertrophy

A

increased heart mass, increased capillarization proportionate to mass, normal cardiac function

159
Q

Concentric hypertrophy

A

afterload driven; thickening of left ventricle wall with minimal increase in left ventricle chamber diameter -> can be seen in weightlifters

160
Q

Eccentric hypertrophy

A

preload driven; elongation of myocytes which leads to proportionate increases in LV wall thickness  can be seen in endurance athletes

161
Q

max VO2 equation

A

= Q (CO) x a-vO2 difference

162
Q

Insulin Suppression During Exercise

A

Mechanism: SNS -> NE -> alpha adrenergic inhibition of beta cells of pancreas

163
Q

what increase and decreases when working out at hot temps

A

Inc: HR
Dec: blood volume and SV

164
Q

trained vs untrained

A 
At rest trained: 
-Lower HR higher SV same CO
Exercise trained: 
-same HR much higher SV higher CO
-inc lactate threshold
165
Q

Purpose of myoglobin

A

to take up oxygen for tissue and store it

-higher affinity of oxygen the hemoglobin

166
Q

Germinal centers of secondary lymph nodes

A

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

167
Q

conjugated vaccines protect against

A

Haemophilus influenzae type b (Hib), Neisseria meningitidis, and Streptococcus pneumoniae

168
Q

role of Immunoproteasome stimulated by INF y

A

Faster peptide generation
Longer peptide antigens
Preferred MHC I binding

169
Q

Cross-presentation

A 
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
170
Q

IFN-γ for MHCII

A

Upregulated transcription of MHC II

Increased lysosomal activity (cathepsin) improve antigen digestion

171
Q

IgA

A

Neutralization
Found in mucosal associated tissue (produced by TGF-B)
Transferred through secretions (ex. Breast milk)
Dimer (j chain polyIgreceptor)

172
Q

FOXP3

A

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

173
Q

combinatorial vs junctional

A
  • 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
174
Q

Deficiencies of MAC lead to a higher risk for infection of

A

Neisseria species

175
Q

allotype

A

expression of an allotype is genetically determined

176
Q

expression difference between TCR/BCR and MHC

A

TCR/BCR: Monoallelic expression (allelic exclusion)

MHC: co-dominant allelic expression

177
Q

Hemolytic Uremic syndrome (HUS):

A

deficiency in complement inhibitors
o Complements continuously binding (autoimmune)
o Increase in thrombosis

178
Q

Systemic Lupus Erythematosus (SLE):

A

deficiency in early complements (C1-C4)

o Most likely to have increase in sinus and respiratory infections

179
Q

Late compliment deficiency

A

deficiency in late complements (C5-C9), no MAC

o Deficiency in MAC lead to a higher risk for infection of Neisseria species

180
Q

Hereditary Angioedema (HAE)q

A

deficiency in C1 protease inhibitor
o Over activation of classical pathway
o Upregulate C2a and bradykinin (inflammation)
o Swollen face

181
Q

FRC definition

A

amount of air in lungs when PA = 0

182
Q

increase in surfactant

A

inc vent
inc in alveolar size from deep breathes
endocrine stimulation

183
Q

Why do bronchioles have less resistance than bronchi?

A

more surface area

184
Q

Oxygen hemoglobin content

A

1.36 mL/g hemoglobin

185
Q

Irritant pulmonary receptors

A
  • 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.
186
Q

black diving

A
  • 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
187
Q

heat acclamation

A

acclimated people will have

  • greater sweat rate
  • more dilute sweat
  • lower HR
188
Q

Upper body isometric (TRP dramatic increase!) WHY?

A

Valsalva Maneuver

-isometric: resisting weight but not moving muscle

189
Q

Antidiuretic Hormone

Aldosterone

A

Antidiuretic Hormone: H2O Reabsorption & Retention
-increases during exercise
Aldosterone: Na+ Reabsorption & Retention
-Generally only increases during recovery

190
Q

Older/compromised Patients exercise in a hot, humid climate requires electrolyte replacement (Na+, Cl-, K+) beverage

A

Prolonged >1 hr

191
Q

Young/health Patients exercise in a hot, humid climate requires electrolyte replacement (Na+, Cl-, K+) beverage which may help protect against SIADH

A

Prolonged (>4 hr)

BECOM 2 (7 decks)

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