Solutions.
What 2 OMM techniques can be used to thin mucous secretions in a pt with
Asthma?
Asthma is the most common chronic disease in childhood and asthma symptoms
include wheezing, shortness of breath, chest tightness and cough. Asthma
involves hypersensitivity of the bronchi and lower airways to allergens, cold or
other irritants. This results in inflammation, bronchospasm and mucous
plugging. β-2-agonists help dilate the bronchioles but do not directly affect the
sympathetic nerves which regulate secretions. Persistent asthma can drive the
upper thoracic (particularly T1-T4) sympathetic nerves into a chronically active
state. One particularly significant physiologic response of this is proliferation of
goblet cells. These cells in the bronchial mucosa produce thick, tenacious
secretions which are difficult to clear. Rib raising is one method of normalizing (in
this case, decreasing) sympathetic tone to thin the secretions. Another useful
method is the thoracic pump, which can be particularly helpful in normalizing
lymphatic flow out of congested tissues.
Sympathetic Vicerosomatics
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,Isolated Tricuspid Stenosis MC from?
The most common causes are due to carcinoid heart disease and right atrial
myxoma.
What is the MOA of an Aspirin Overdose?
It causes the uncoupling of oxidative phosphorylation and thereby reduces the
amount of ATP produced. Aspirin transports protons generated by the electron
transport chain back into the mitochondrial matrix. This decreases the amount of
protons available for ATP synthase to use for formation of ATP. As a result, there is
an accumulation of carbon dioxide in the body. Which leads to a respiratory
alkolosis which is then followed by a Metabolic acidosis to recompensate (Mixed)
What is the Antidote for Cyanide Poisoning?
Amyl nitrite. Cyanide inhibits cytochrome oxidase enzyme in the electron
transport chain within mitochondria. This causes depletion of ATP. Patients with
cyanide poisoning present with elevated heart rates, drowsiness, and eventual
coma and death.
Alkpatonuria
An AR disorder that results from deficient activity of the enzyme homogentisic
oxidase. It results in elevated levels of homogentisic acid which forms a pigment
that is deposited in connective tissue and joints throughout the body. It typically
presents in the 3rd decade of life, with initial pigmentation occurring in the ear
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, cartilage and sclera of the eyes. A dark pigment is also deposited in the large joints
and the lumbosacral spine. This leads to early onset arthritis and can result in joint
replacements at a younger age. The disorder is characterized by urine that is of a
normal color initially, but turns a dark black color if left standing due to oxidation
of the homogentisic acid. The diagnosis is confirmed by measurement of
homogentisic acid in the urine. No effective therapy is available for alkaptonuria.
Metachromatic Leukodystrophy
An AR lysosomal storage disease that causes progressive demyelination of the
central and peripheral nervous system. It is due to a deficiency in Arylsulfatase A.
Common manifestations include regression of motor skills, gait abnormalities,
ataxia, hypotonia, upper motor neuron signs, and peripheral neuropathy. The
diagnosis is established by demonstrating deficient arylsulfatase A activity in
leukocytes or elevated sulfatides
McArdle Disease
An AR glycogen storage disease due to a deficiency in the
enzyme myophosphorylase. Myophosphorylase is involved in the breakdown
of glycogen to glucose in the muscles. McArdle disease usually presents
in adolescence or early adulthood with fatigue, myalgias, muscle cramps,
weakness, exercise intolerance, and myoglobinuria. These symptoms are brought
on by exercise. An ischemic muscle forearm test would reveal a failure of the
lactate levels to rise in venous blood after ischemic exercise.
Some AD diseases
Tuberous Sclerosis
achondroplasia
Huntington disease
Marfan syndrome
neurofibromatosis.
Some AR diseases
cystic fibrosis
sickle cell anemia
hemochromatosis
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