Elizabeth Holland

EXSC 224, Section 5

Lab Quiz 3

1.
a) Emphysema is a type of COPD characterized by a permanent enlargement of the alveoli
and destruction of the alveolar walls, which results in the loss of elasticity in the lungs
(Marieb, 871). One of the consequences of Emphysema is that the bronchioles open
during inspiration but collapse during expiration and trap huge volumes of air in the
alveoli (Marie, 871). The trapped air causes a reduction in the flow of air out of the
lungs. Chronic Bronchitis is a type of COPD caused by inhaled irritants. The irritants
lead to chronic excessive mucus production by the mucosa of the lower respiratory
passageways and to inflammation and fibrosis of the mucosa (Marieb, 871). This
response to irritants obstructs the airways and severely impairs lung ventilation and gas
exchange thereby reducing the flow of air out of the lungs (Marieb, 871).
b) The equation for flow (F=deltaP/R) can be used to explain the decreased air flow in
individuals with COPD. This formula is the relationship between gas flow (F), pressure
(P) and resistance (R) (Marieb, 849). Inhaled irritants activate a parasympathetic reflex
that causes an increase in resistance and a decrease in flow (Marieb, 850). The
accumulation of mucus, infectious material or solid tumors are common with COPD and
all increase resistance and decrease flow (Marieb, 850). Symptoms of COPD mainly
decrease the flow of air by increasing resistance.
c) FVC, which stands for forced vital capacity, is the amount of gas expelled when a deep
breath is taken and then forcefully exhaled as rapidly as possible (Marieb, 853). FEV1,
which stands for forced expiratory volume, is the amount of air expelled during the first
second of the FVC test (Marieb, 853). This ratio can evaluate loss in pulmonary function
by distinguishing between obstructive pulmonary disorders and restrictive pulmonary
disorders (Marieb, 853). Healthy individuals can expel around 80% of FVC in one
second (Marieb, 853). Someone with an obstructive pulmonary disease expels much less
than 80% of their FVC in one minute while individuals with restrictive disease can still
expel 80% or more but their FVC is greatly reduced (Marieb, 853). COPD is obstructive
and causes a decreased FEV1/FVC ratio.
d) In obstructive disorders the FEV1, or the amount of air expelled in one second, is the part
of the ratio most affected. A key feature of COPD is the decrease in ability to force air
out of the lungs, which would significantly decrease FEV1 (Marieb, 871).

2. Normal inspiration involves the diaphragm and the intercostal muscles. The diaphragm
descends and the intercostal muscles contract which causes an increase in the volume of the
thoracic cavity by lifting the rib cage. This stretches the lungs and increases intrapulmonary
volume, which causes a drop in intrapulmonary pressure. The drop in intrapulmonary pressure
causes air flow into the lungs down its pressure gradient (Marieb, 848). Normal expiration is
typically a passive process, unless an individual has some sort of health problem (Marieb, 849).
The diaphragm and intercostal muscles relax, the rib cage returns to its resting position and the
lungs recoil (Marieb, 849). The relaxing decreases the thoracic and intrapulmonary volume,
which raises the pulmonary pressure and causes a pressure gradient that forces air out of the
lungs (Marieb, 849). Normal inspiration and expiration occur during normal, day to day, life for
healthy individuals when no extenuating circumstances are present.
Forced inspiration is a type of inspiration that would occur during vigorous exercise and
in some individuals with COPD. Forced inspiration requires the further increase of thoracic
volume through activity of the accessory muscles (Marieb, 849). The scalenes and
sternocleomastoid muscles in the neck and the pectoralis minor of the chest raise the ribs more
than in normal inspiration to bring in more air (Marieb, 849). Forced Expiration is an active
process, unlike the passive normal expiration. Forced expiration is produced by contraction of
the muscles of the abdominal wall, most specifically the oblique and transverse muscles (Marieb,
849). The contraction of the abdominal wall muscles increases the intra-abdominal pressure and
depresses the rib cage to decrease thoracic volume to control the flow of air from the lungs
(Marieb, 849). For example, a trained vocalist holds and releases a musical note through the
coordinated activity of many of the muscles of forced expiration (Marieb, 849).

3.
a) GFR can be controlled intrinsically and extrinsically with the goal of maintaining a stable
GFR as well as a constant blood volume. Intrinsic controls are local within the kidney to
maintain GFR while the extrinsic controls involve the nervous and endocrine system to maintain
blood pressure and volume (Marieb, 1008). During times with a normal volume of extracellular
fluid and an inactive sympathetic nervous system the renal autoregulation mechanisms prevail
(Marieb, 1010). During stress or emergency situations neural controls can overcome renal
autoregulatory mechanisms (Marieb, 1010). Sympathetic nerve fibers release norepinephrine
and the adrenal medulla releases epinephrine. These neurotransmitters are taken up by the
adrenergic receptors on vascular smooth muscle which constricts afferent arterioles and therefore
inhibits filtrate formation (Marieb, 1010). Increase in sympathetic nervous system activity
increases systemic blood pressure which decreases the GFR.
b) The sympathetic nervous system is involved with the renin-angiotensin system. Sympathetic
nerve fibers release norepinephrine, which is taken up by the alpha adrenergic receptors on
vascular smooth muscle, which constricts the afferent arterioles (Marieb, 1010). The
constriction of the arterioles inhibits filtrate formation, which stimulates the macula densa cells
and therefore indirectly trips the renin-angiotensin mechanism (Marieb, 1010). Renin release by
the granular cells is also stimulated by the sympathetic nervous system (Marieb, 1010). The
renin-angiotensin system has stabilizing effects on the systemic blood pressure and extracellular
fluid volume (Marieb, 1010). Renin converts angiotensin to angiotensin I and then angiotensin
converting enzyme converts from angiotensin I to angiotensin II. Angiotensin II is able to raise
MAP through vasoconstriction, stimulate the reabsorption of sodium, stimulate the release of
ADH, increase fluid reabsorption and target glomerular mesangial cells causing them to contract
and reduce GFR by decreasing the surface area available for filtration (Marieb 1010). All five of
these actions allow the renin-angiotensin system to regulate GFR.
c) Chronic stress will stimulate the sympathetic nervous system. Stimulation of the sympathetic
nervous system will shift blood flow away from the kidneys, decreasing the blood volume in this
area, which will decrease GFR. This will also cause the production of corticosteroids which will
inhibit immune system function and tissue repair (Marieb, 1010).

Works Cited
Marieb, Elaine N., and Katja Hoehn. Human Anatomy & Physiology. 7th ed.
Menlo Park, CA: Pearson Benjamin Cummings, 2007. Print.