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IPAP Biochem Thompson > Respiratory > Flashcards

Respiratory Flashcards

1
Q

Pulmonary compliance?

A

Ability of pulmonary surfactant to greatly reduce surface tension, allowing easier expansion/stretching and shrinking of alveoli during respiration and the resulting changes in pressure.

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2
Q

What is COPD ?

A

EMpysema (narrowing of small airways) + Chronic bronchitis (inflammatory condition)

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3
Q

REstrictive lung diseases?

A

Loss or restriction of complete lung expansion.

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4
Q

Panacinar emphysema?

A

A-1-antitrypsin deficiency.

Inhibits neutrophil elastase and matrix metalloproteases -> limits damage to respiratory structures.

Neutrophil elastase destroys harmful stuff for the lungs

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5
Q

What is the rate limiting step of O2 saturation in the lungs?

A

Perfusion limited.

NOT DIFFUSION LIMITED.

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6
Q

What are pulmonary surfactants made of?

A
  • Lecithin+myelin
  • 90% are half DPPC (Dipalmitoylphosphatidylcholine) with smaller amounts of phosphatidylglycerol.

They are amphiphilic.
Reduce surface tension.

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7
Q

Pulmonary compliance?

A

THe ability of pulmonary surfactant to greatly reduce surface tension, allowing easier expansion/stretching and shrinking of alveoli during respiration and the resulting changes in pressure.

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8
Q

IRDS? Infant Respirtory Distress syndrome?

A

-Preemies (<32wks) are in trouble.

-Respiratory system develops only partially during pregnancy and becomes fully functional only after birth. Only partially formed pulmonary surfactants.
Steroids prompt surfactant production.

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9
Q

What does Carbonic Anhydrase do for CO2 transport?

A

Increases the rate of reaction about a million fold.

Most of the CO2 carried back to the lungs is as Bi-carbs.

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10
Q

What is the normal blood pH?

A

7.35-7.45

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11
Q

WHat is responsible for maintaining the acid base balance?

A

Lungs, kidneys, blood, and even the pancreas, are responsible for maintaining proper levels of H+

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12
Q

What is the henderson hasselbach equation?

A

Ph= pka+logbase/acid.

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13
Q

What is the HH equation in english?

A

Buffers are mixtures of weak acids and their conjugate bases.

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14
Q

If the levels of acid and base are the same then what is the ph?

A

Since log of 1 is 0 then ph=pka

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15
Q

Acute Respiratory acidosis?

A

Short-term decrease in respiratory function

HYPOVENTILATION

Less CO2 exhaled build up of pCO2 which is a build up of bicarb and H which makes a build up ACID!

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16
Q

Chronic Respiratory Acidosis

A

Caused by chronic respiratory problems such as chronic obstructive pulmonary disease (COPD), interstitial lung diseases, respiratory muscle fatigue

Longer term hypoventilation increases blood pCO2 leads to higher H.

17
Q

Respiratory Alkalosis ?

A

Acute or chronic increases in exhalation of CO2 hyperventilation/hypernea -> removes bicard and H from tissues lowers H.

Can result from

  • pneumonia and fever with increased rate of breathing.
  • Psychiatric
  • Neuro
  • Prego
  • Liver
  • Overusing aspiring/caffeine
  • altitude.
18
Q

Acid/Base compensation?

A
  • Our body can compensate.
  • TIssues take or release bicarb.

BAND 3 anion exchanger protein exchanges of chlodie for bicarb.

19
Q

Obstructive lung diseases?

A

Airflow is impaired

20
Q

Centroacinar emphysema?

A

Affects at end of bronchioles.

-effect of nicotine on neutrophils and neutrophil elastase enzyme.

21
Q

Acute bronchitis?

A

-Temporary irritant.

From infective agent such as virus (90%) or bacteria or environmental irritants

-cough w/ excessive mucus resolves when irritant is eliminated

22
Q

Chronic bronchitis?

A

Long-standing disorder diagnosed for cough productive of sputum that lasts for three months or longer per year for at least 2 years

  • can lead to bronchospasms
  • Smoking/environmental/occupational irritants are predominant cause of this medical condition.
23
Q

Asthma?

A
  • Chronic inflammatory condition of the bronchi.
  • Intermittent and partly reversible constriction of bronchi known as bronchospasm and airway obstruction.

Inflammatory cytokines, iGe.

Eosinophils, mast cells, and cd4 cells represent predominant cell types in the inflammatory process.

LARGLY REVERSIBLE UNLIKE COPD.

24
Q

Effect of Basophil Degranulation?

A

Blocks Beta2 receptors on bronchi smooth muscle cells.

Dilation of blood vessels in the lung and smooth muscle contraction.

Parasympathetic nerves are also stimulated which release acetylcholine.

25
Q

Bronchodilators?

A

Mainstay of asthma treatment.

Include short and long acting Beta agonists that activate adenyl cyclase AC and by muscarninic

26
Q

Short acting Beta 2 agonists?

A

Albuterol.
-Counteracts the inhibitory effect on the Beta 2 adrenergic receptor resulting in relaxation of bronchial smooth muscle and dilation of bronchial passages.

Lasts 4-6 hrs.

27
Q

Long acting Beta 2 agonists?

A

Salmeterol.
Same mechanism as short.

Lasts for approx 12 hrs.

28
Q

Anticholinergics/muscarinic antagonists ?

A

Blocks the action of acetylcholine leading to relaxation of bronchial smooth muscle and dilation of bronchial passages.

-USED FOR COPD

29
Q

HMA medications?

A

Leukotriene antagonists.

Blockage of leukotrience-associated bronchoconstriction.

30
Q

Corticosteroids?

Actions.

A

Binds to nuclear glucocorticoid receptors.

31
Q

What is the point of target for Leukotriene antagonists and corticosteroids?

A

They block LOX and stop arachidonic acid from becoming leukotrieneces.

Corticosteroids promote the inhibition of phospolipase A2 and the arachidonic acid pathway.

32
Q

ARDS?

A

Acute respiratory distress syndrome ARDS

High rate of fatality 30%

Inflamation of lung tissue.

33
Q

Restrictive diseases?

A

Continued exposure to occupational or environmental irritants.

Pneumoconisosis- any restrictive lung disease caused by the chronic exposure and inhalation of particules small enough to bypass the defense mechanism of the upper airway.

34
Q

Cystic fibrosis?

A

Deletion of AA 508 of CYSTIC FIBROSIS TRANSMEMBRANSE CONDUCTANCE REGULATOR CFTR

Chloride ion transport channel,

Inhibits production of sodium cholride in sweat.

35
Q

Bordetella pertussis?

A

Pertussis toxin adds ADP molecules to alpha subunits of G proteins, blocking normal binding to G-protein associated receptors.
Gi proteins are among those affected and being inhibited by the ADP ribosylation, are unable to stop adenyl cyclase produciton of CAMP

36
Q

Aspergillosis?

A

Fungal infections represented in a spectrum of diseases.

Bronchoconstriction and increased vascular permeability

37
Q

TB?

A

Mycobacterium species.

DENDRITES UNDER ATTACK#@#@

38
Q

Pneumoconiosis?

A

Any restrictive lung disease causedby the chronic exposure and inhalation of particles small enough to bypass the defense mechanism ofthe upper airway.

IPAP Biochem Thompson (4 decks)

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