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BIO 176 LAB + LEC > The Respiratory System 3 > Flashcards

The Respiratory System 3 Flashcards

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1
Q

describe INTERNAL RESPIRATION

A
  • have CAPILLARY GAS EXCHANGE within the BODY’S TISSUES
  • our PARTIAL PRESSURES and DIFFUSION GRADIENTS—are now REVERSED compared to EXTERNAL RESPIRATION
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2
Q

describe OXYGEN TRANSPORT

A

OXYGEN + HEMOGLOBIN:

  • each Hb molecule has FOUR POLYPEPTIDE CHAINS—all containing a IRON-CONTAINING HEME GROUP
    • each HB can transport FOUR OXYGEN MOLECULES
  • OXYHEMOGLOBIN (HbO2):
    • HEMOGLOBIN-O2 COMBINATION
  • REDUCED HEMOGLOBIN (DEOXYHEMOGLOBIN) (HHb):
    • hemoglobin that has released OXYGEN
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3
Q

definition of the HEMOGLOBIN OXYGEN DISSOCIATION CURVE

A
  • DISSOCIATION CURVE:
    • the RATE OF LOADING and UNLOADING of OXYGEN is REGULATED to ENSURE ADEQUATE OXYGEN DELIVERY TO CELLS
    • the specific curve is S-SHAPED; the HEMOGLOBIN SATURATION PLOTTED AGAINST Po2 is NOT LINEAR
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4
Q

what are the VARIABLE FACTORS for the DISSOCATION CURVE?

A
  • VARIABLE FACTORS (shifts CURVE TO RIGHT);
    • Po2
    • TEMPERATURE (increase)
    • BLOOD pH (decrease)
    • Pco2 (increase)
    • DPG (increase)
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5
Q

describe the INFLUENCE of PO2 on HEMOGLOBIN SATURATION

A
  • IN ARTERIAL BLOOD:
    • Po2 - 100 mm Hg
    • contains around 20 ml OXYGEN per 100 ml blood (20% volume)
    • HEMOGLOBIN is 98% SATURATED
  • IN VENOUS BLOOD:
    • Po2 - 40 mm Hg
    • contains around 15% volume of oxygen
    • HEMOGLOBIN is 75% SATURATED
    • VENOUS RESERVE:
      • oxygen remaining in venous blood
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6
Q

what happens if our HEMOGLOBIN is LESS SATURATED?

A
  • known as the BOHR EFFECT; begins to ENHANCE OXYGEN UNLOADING to where it is needed the MOST
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7
Q

definition of HYPOXIA

A

the INADEQUATE OXYGEN DELIVERY to the TISSUES; also known as CYANOSIS

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8
Q

describe CARBON DIOXIDE TRANSPORT

A

*CO2 transported into BLOOD in THREE FORMS:

  1. DISSOLVED IN PLASMA as PCO2 (7-10%)
  2. BOUND TO GLOBIN (part of HEMOGLOBIN) (20%) – CARAMINOHEMOGLOBIN
  3. TRANSPORT OF BICARBONATE IONS HCO3 in PLASMA (70%)
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9
Q

describe the TRANSPORT and EXCHANGE of Co2 + O2 in SYSTEMIC CAPILLARIES

A
  • begins after HCO3 is created—begins to DIFFUSE from RBCS into PLASMA
  • process is balanced through the CHLORIDE SHIFT;
    • CL moves into RBCS from PLASMA as HCO3 OUTRUSHES
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10
Q

describe the TRANSPORT and EXCHANGE of CO2 + O2 in PULMONARY CAPILLARIES

A
  • opposite processes happen
  • HCO3 MOVES IN RBCS while CL MOVES OUT of RBCS back into the PLASMA
  • HCO3 binds with another HYDROGEN to create H2CO3
    • split by CARBONIC ANHYDRASE into CO2 and WATER
    • CO2 diffuses into the ALVEOLI
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11
Q

definition of HALDANE EFFECT

A
  • OXYGENATION of BLOOD WITHIN THE LUNGS — begins to DISPLACE CARBON DIOXIDE from HB (INCREASES REMOVAL OF CO2)
    • also reduces affinity for carbon dioxide in oxygenated blood
    • known as the BOHR EFFECT (oxygen dissociates from Hb due to more co2)
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12
Q

describe the CARBONIC-ACID-BICARBONATE BUFFER SYSTEM

A
  • helps blood RESIST CHANGES in PH
  • HCO3 acts as the ALKALINE RESERVE for the system
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13
Q

how can one ADJUST the CARBONIC-ACID-BICARBONATE BUFFER SYSTEM

A
  • CHANGES IN RESPIRATORY RATE + DEPTH can affect BLOOD ph:
    • SLOW SHALLOW BREATHING = INCREASE in CO2 in BLOOD = DROP in PH
    • RAPID DEEP BREATHING = DECREASE in CO2 in BLOOD = RISE in PH
  • CHANGES IN VENTILATION:
    • helps in adjusting pH due to issues with metabolism
    • BREATHING—super important for body’s ACID-BASE BALANCE
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14
Q

what are RESPIRATORY RHYTHMS regulated by (3)?

A
  1. HIGHER BRAIN RECEPTORS
  2. CHEMORECEPTORS
  3. OTHER REFLEXES
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15
Q

describe the NEURONAL MECHANISMS

A

control of respiration involving the NEURONS in the RETICULAR FORMATION of the MEDULLA + PONS

  • MEDULLA RESPIRATORY CENTER (within the MEDULLA OBLONGATA)
  • PRG (PONTINE RESPIRATORY GROUP) (within the PONS)
    • important for inhalation and exhalation while ACTIVE—ex. during exercise, sleeping, or talking
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16
Q

describe the MEDULLARY RESPIRATORY CENTERS

A

MRC:

  • CLUSTERED NEURONS in the MEDULLA
17
Q

describe the VENTRAL RESPIRATORY GROUP (VRG)

A
  • responsible for MOTOR CONTROL of INSPIRATORY and EXPIRATORY MUSCLES during exercise
  • has both inspiratory and expiratory neurons (excites the inspiratory and expiratory muscles — through the PHRENIC NERVE
    • ex. the diaphragm
    • controls around 12 - 16 breaths per minute
18
Q

describe the BOTZINGER COMPLEX

A
  • BOTZINGER COMPLEX:
    • cluster of neurons—helps with GENERATION OF RHYTHM OF BREATHING
19
Q

describe the DORSAL RESPIRATORY GROUP (DRG)

A
  • responsible for GENERATION OF INSPIRATION
    • network of neurons located near ROOT OF CRANIAL NERVE IX
20
Q

describe the PONTINE RESPIRATORY CENTERS

A
  • helps INFLUENCE and MODIFY ACTIVITY of VRG
    • helps SMOOTH OUT TRANSITION between INSPIRATION and EXPIRATION
  • helps TRANSMIT IMPULSES TO VRG—helps MODIFY and FINE-TUNE BREATHING RHYTHMS (VOCALIZATION, SLEEP, EXERCISE)
21
Q

what are the factors that INFLEUNCE BREATHING RATE and DEPTH ?

A
  • RESPIRATORY CENTERS:
    • CHEMICAL FACTORS
    • INFLUENCE OF HIGHER BRAIN CENTERS
    • PULMONARY IRRITANT REFLEXES
    • INFLATION REFLEX
22
Q

describe the CHEMICAL FACTORS

A
  • CHEMICAL FACTORS:
    • the MOST IMPORTANT for affecting depth and rate of INSPIRATION—the arterial pressure of carbon dioxide
    • changes the levels of PCO2, PO2, and pH
    • brain changes breathing depth in order to INCREASE OUR PH due to INCREASED ARTERIAL PCO2 (this has decreased our pH in our brain)—back to homeostatic balance
23
Q

where are the CHEMICAL and PERIPHERAL CHEMORECEPTORS FOUND?

A
  • CHEMICAL CHEMORECEPTORS
    • located throughout BRAIN STEM
  • PERIPHERAL CHEMORECEPTORS
    • aortic arch and carotid arteries
24
Q

what happens if we have a RISE OF BLOOD PCO2 LEVELS?

A
  • known as HYPERCAPNIA—carbon dioxide begins to accumulate and become CARBONIC ACID once joined with water
  • this begins to RELEASE HYDROGEN IONS—DROPPING OUR PH (INCREASED ACIDITY—known as ACIDEMIA)
    • this STIMLATES CENTRAL CHEMORECEPTORS (which works hand in hand with RESPIRATORY REG. CENTERS)
      • this INCREASES DEPTH and RATE OF BREATHING in order to get shit back to normal 🙉
25
Q

definition of HYPERVENTILATION

A
  • increased DEPTH and RATE of BREATHING that exceeds the BODY’S NEED TO REMOVE CO2
    • can be caused by anxiety attacks
    • leads to HYPOCAPNIA
      • can lead to CEREBRAL VASOCONSTRICTION + CEREBRAL ISCHEMIA
26
Q

describe the PULMONARY IRRITANT REFLEX

A
  • eceptors within BRONCHIOLES—responds to IRRITANTS
  • promotion of REFLEXIVE CONSTRICTION of AIR PASSAGES
    • communicates through vagal nerve fibers
27
Q

describe the INFLATION REFLEX

A
  • HERING-BREUER REFLEX;
    • stretch receptors in pleurae and airways—stimulated by LUNG INFLATION
28
Q

describe HYPOTHALAMIC CONTROLS

A
  • acts through LIMBIC SYSTEM to change RATE and DEPTH of breathing
  • ex. holding one’s breath causes pain
29
Q

defintiion of ACCLIMINATIZATION

A
  • respiratory and hematopoietic adjustments to LONG-TERM MOVE to HIGH ALTITUDE
    • more RESPONSIVE CHEMORECEPTORS
    • any SUBSTANTIAL DECLINE in PO2—stimulation of PERIPHERAL CHEMORECEPTORS
    • results;
      • more VENTILATION PER MINUTE—begins to stabilize after a couple of days
30
Q

definition of ACUTE MOUNTAIN SICKNESS

A
  • ACUTE MOUNTAIN SICKNESS:
    • traveling of altitudes above 2400 meters (8000 feet)
    • have LOWER ATM PRESSURE and OXYGEN
    • show signs of HEADACHES, shortness of breath, dizziness—even LETHAL CEREBRAL + PULMONARY EDEMA
31
Q

describe CHRONIC OBSTRUCTIVE PULMONARY DISEASE

A
  • CHRONIC OBSTRUCTIVE PULMONARY DISEASE:
    • from CHRONIC BRONCHITIS and EMPHYSEMA
    • the IRREVERSIBLE DECREASE in the ability to FORCE AIR OUT OF LUNGS
  • FEATURES:
    • seen in over 80% of SMOKING PATIENTS
    • DYSPNEA
    • coughing and pulmonary infections
    • RESPIRATORY FAILURE—HYPOVENTILATION
32
Q

describe EMPHYSEMA

A
  • the PERMANENT ENLARGEMENT OF ALVEOLI—the DESTRUCTION OF ALVEOLAR WALLS + DECREASED LUNG ELASTICITY
  • can lead to HYPER INFLATION — FLATTENED DIAPHRAGM — REDUCED VENTILATION EFFICIENCY
    • cause of “BARREL CHEST”
  • DAMAGED PULMONARY CAPILLARIES can lead to an ENLARGED RIGHT VENTRICLE
    • cause of “TEARDROP HEART”
33
Q

describe CHRONIC BRONCHITIS

A
  • CHRONIC BRONCHITIS:
    • INHALED IRRITANTS
      • leading to CHRONIC EXCESSIVE MUCUS
        • which begins to INFLAME and FIBROSE LOWER RESPIRATORY PASSAGEWAYS
    • we now have OBSTRUCTED AIRWAYS
      • and begins to IMPAIR LUNG VENTILATION and GAS EXCHANGE
      • can cause frequent pulmonary infections
34
Q

describe ASTHMA

A
  • known as REVERSIBLE COPD
  • known for its COUGHING, DYSPNEA, WHEEZING, or CHEST TIGHTNESS
    • often due to ACTIVE INFLAMMATION OF AIRWAYS
      • often due to release of INTERLEUKINS, IgE, and INFLAMMATORY CELLS—acts as an IMMUNE RESPONSE
35
Q

describe TUBERCULOSIS

A
  • TUBERCULOSIS (TB):
    • caused by MYCOBACTERIUM TUBERCULOSIS
    • SYMPTOMS:
      • night sweats
      • weight loss
      • coughing
  • TREATMENT:
    • 12 month course of antibiotics
36
Q

what are the COMMON TYPES OF LUNG CANCER?

A
  • the LEADING CAUSE of cancer deaths in USA
  • over 90% results of SMOKING
  • COMMON TYPES:
    • ADENOCARCINOMA (40%)
      • seen in PERIPHERAL LUNG AREAS—bronchial glands , alveolar cells
    • SQUAMOUS CELL CARCINOMA (20-40%)
      • seen in BRONCHIAL EPITHELIUM
    • SMALL CELL CARCINOMA (20%)
      • seen in PRIMARY BRONCHI
      • have LYMPHOCYTE-LIKE CELLS
37
Q

definition of CYSTIC FIBROSIS

A
  • the MOST COMMON LETHAL GENETIC DISEASE
  • have ABNORMAL VISCOUS MUCUS CLOGS—can lead to BACTERIAL INFECTIONS
    • can affect out LUNGS, PANCREATIC + REPRODUCTIVE DUCTS
  • often due to an ABNORMAL GENE within CL MEMBRANE CHANNEL
38
Q

where was the DEVELOPMENT of the RESPIRATORY SYSTEM?

A
  • MESODERM:
    • connective tissue
    • cartilage
    • smooth muscle
  • ENDODERM:
    • epithelium and glands of trachea
    • bronchi
    • alveoli

BIO 176 LAB + LEC (20 decks)

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