HCP 6

Question 1

Patient with CF. Mechanism of constant productive cough

Answer 1

thick, desiccated hypoxic mucus -> stimulates c-fiber receptors -> c-fiber receptor release neurotransmitter signal via afferent CN X -> signal reaches cough center of medulla (NTS) -> efferent CN X contracts glottis, phrenic contracts diaphragm, spinal nerves contract external intercostals -> increase in pleural and intrapulmonary pressure behind closed glottis -> sudden opening of glottis ->expulsion of air and irritants from the mouth -> clearance of mucosal irritant

Question 2

Zone 1

Answer 2

Higher pressure in alveoli than arteriole therefore arterioles collapse Lowest blood flow

Question 3

Zone 3

Answer 3

Highest ventilation and perfusion

Question 4

Normal V/Q

Answer 4

0.8

Question 5

Pulmonary embolus (dead space)

Answer 5

causes obstruction in vessel -> unable to perfuse blood -> V/Q= infinity

Question 6

Shunt (airway obstruction)

Answer 6

mucus plug -> unable to ventilate alveoli -> V/Q= 0

Question 7

parasympathetic nervous system

Answer 7

pre-ganglionic Ach signal -> to nicotinic N2 receptors in ganglia -> release post ganglionic Ach signal -> muscarinic receptors on target organ ->

Question 8

Hardy-weinberg

Answer 8

p + q = 1 p2 + 2pq + q2 = 1

Question 9

bronchiectasis

Answer 9

chronic infection/inflammatory response d/t thick mucus stasis caused by defective mucociliary action in cystic fibrosis -> leads to recruitment of neutrophils, T lymphocytes, and monocyte derived cytokines -> neutrophils secrete elastase -> elastase cleaves elastic tissue in walls of bronchi and bronchioles -> destruction of supporting smooth muscle and elastic tissue -> decreased elasticity impairs exhalation, permanent dilation of bronchi and bronchioles -> progressive obliteration of smaller bronchioles due to fibrosis -> further accumulation of mucus, increased airway resistance and decreased airflow into and out of lungs -> hypoxia, vicious cycle of infection

Question 10

pseudomonas aeruginosa

Answer 10

break in first line defenses (wound or tracheal tube) -> attachment via pili, flagella, and alginate to host receptors of silica acid and N-acetylglucosamine on glycolipids (favors cell loss of surface fibronectin) -> Elastase -> secreted outside of host cell -> cleaves elastic fibers of lung and blood vessels -> hemorrhagic destruction Exo S -> transported into host cell by type III secretion system (inject via syringe apparatus) -> acts on regulatory G proteins -> affect cytoskeleton and signaling pathways -> trigger apoptosis of host cell Bacterial population reaches lactone/quinolone threshold (quorum-sensing) -> signals direct cytotoxic gene expression -> transcription of Exo A -> Exo A ADP-ribosylation inactivates ribosomal protein EF-2 -> DNA translation arrest -> inhibits protein synthesis -> host cell death pyocyanin -> reduces cAMP and ATP levels -> decreases ciliary beat frequency -> impairs mucociliary apparatus secretes alginate -> forms biofilm -> protects bacteria by inaccessibility of immune system and antimicrobial agents

Question 11

cilia dynein

Answer 11

molecular motor to power ciliary motions, ATPase that coverts energy released through ATP hydrolysis

Question 12

cilia nexin

Answer 12

restrict extent at which neighboring outer tubules can move with respect to each other

Question 13

ciliary beat frequency

Answer 13

600-900 beats a minute