Why do lymph nodes become enlarged when we develop an infection?
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The B-lymphocyte proliferation in response to a
great deal of antigen (e.g., during infection) may result in lymph node
enlargement and tenderness (reactive lymph node)
,How long do platelets live in the circulation?
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Platelets circulate in the
bloodstream for about 8 to 10 days before losing their ability to carry out
thrombogenic activity. Senescent platelets are sequestered and destroyed
in the spleen by mononuclear cell
phagocytosis.
What is PKU?
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Phenylketonuria is an an inborn error in the metabolism of amino acids, an
autosomal recessive that is a mutation of the phenylalanie hydroxylase
gene (PAH). Loss of PAH activity reults in inability to convert the essential
amino acd phenylalanine to tyrosine, leading to accumulation of
phenylalanine in the serum causing damage to the CNS.
Why is the control of calcium important as it relates to the endocrine system?
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Hormone release is regulated by one or more of the following
mechanisms: (1) chemical factors (such as blood glucose or calcium levels).
In addition to being an important ion that participates in a multitude of
cellular actions, Ca++ is considered an important second messenger. For
cells that have calcium as their second messenger, an increase in
intracellular calcium concentration causes calcium to bind with calmodulin,
a regulatory protein. This step then initiates other intracellular
processes.Calcium signaling systems are crucial to
, healthy functioning of virtually every tissue system in the body including
heart, brain, bone, smooth muscle, and many others. The four parathyroid
glands are
located near the posterior side of the thyroid and function to control
serum calcium levels. Calcitonin, also called thyrocalcitonin, acts to lower
serum calcium levels by inhibition of bone-resorbing osteoclasts. The
overall effect of PTH secretion is to increase serum calcium concentration
and decrease serum phosphate level.
Parkinson's Disease
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Severe degen of basal ganglia (corpus stratum) involving the dopaminergic
nigrostriatal pathway
• loss of dopaminergic pigmented neurons in the substantial nigra
• S/S: rigidity, bradykinesia, akinesia, tremor, postural abnormalities,
autonomic-neuro endocrine symptoms, cognitive-affective symptoms of
dementia
• TX: Levodopa, anticholinergic drugs, antihistamines, Amantadine
Review the pathophysiology and signs and symptoms of Graves disease
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, Graves disease is the underlying cause of
50% to 80% of cases of hyperthyroidism. Although the cause of Graves
disease is not known, genetic factors interacting with environmental
triggers play an important role in the pathogenesis of this autoimmune
thyroid disease. Graves disease results from a form of type II
hypersensitivity in which there is stimulation of the thyroid by
autoantibodies directed against the TSH receptor. These autoantibodies,
called thyroidstimulating
immunoglobulins (TSIs; also called thyroidstimulating
antibodies [TSAbs] or thyroid receptor antibodies
[TRAbs]), override normal regulatory mechanisms. The TSI
stimulation of TSH receptors in the gland results in hyperplasia of the gland
(goiter) and increased synthesis of TH, especially of triiodothyronine (T3).
Increased levels of TH affect every physiologic system and result in the
classic signs and symptoms of hyperthyroidism. TSH production
by the pituitary is inhibited through the usual negative feedback loop. TSIs
also contribute to two major distinguishing clinical manifestations of Graves
disease: ophthalmopathy and pretibial myxedema (Graves dermopathy).
Graves ophthalmopathy affects more than half of individuals with Graves
disease. Increased secretion of hyaluronic acid, orbital fat accumulation,
inflammation, and edema of the orbital contents result in exophthalmos
(protrusion of the eyeball). Periorbital edema and extraocular muscle
weakness lead to diplopia (double vision). The individual may experience
irritation, pain, lacrimation, photophobia, blurred vision, decreased visual
acuity, papilledema, visual field impairment,
exposure keratosis, and corneal ulceration. A small number of individuals
with Graves disease and very high levels of TSI experience pretibial
myxedema (Graves dermopathy), characterized by subcutaneous swelling
on the anterior portions of the legs and by indurated and erythematous
skin
Review risk factors for cerebral vascular accident. What is the difference between
hemorrhagic and ischemic, Thrombotic, embolic, and lacunar.
Give this one a try later!
Give this one a try later!
The B-lymphocyte proliferation in response to a
great deal of antigen (e.g., during infection) may result in lymph node
enlargement and tenderness (reactive lymph node)
,How long do platelets live in the circulation?
Give this one a try later!
Platelets circulate in the
bloodstream for about 8 to 10 days before losing their ability to carry out
thrombogenic activity. Senescent platelets are sequestered and destroyed
in the spleen by mononuclear cell
phagocytosis.
What is PKU?
Give this one a try later!
Phenylketonuria is an an inborn error in the metabolism of amino acids, an
autosomal recessive that is a mutation of the phenylalanie hydroxylase
gene (PAH). Loss of PAH activity reults in inability to convert the essential
amino acd phenylalanine to tyrosine, leading to accumulation of
phenylalanine in the serum causing damage to the CNS.
Why is the control of calcium important as it relates to the endocrine system?
Give this one a try later!
Hormone release is regulated by one or more of the following
mechanisms: (1) chemical factors (such as blood glucose or calcium levels).
In addition to being an important ion that participates in a multitude of
cellular actions, Ca++ is considered an important second messenger. For
cells that have calcium as their second messenger, an increase in
intracellular calcium concentration causes calcium to bind with calmodulin,
a regulatory protein. This step then initiates other intracellular
processes.Calcium signaling systems are crucial to
, healthy functioning of virtually every tissue system in the body including
heart, brain, bone, smooth muscle, and many others. The four parathyroid
glands are
located near the posterior side of the thyroid and function to control
serum calcium levels. Calcitonin, also called thyrocalcitonin, acts to lower
serum calcium levels by inhibition of bone-resorbing osteoclasts. The
overall effect of PTH secretion is to increase serum calcium concentration
and decrease serum phosphate level.
Parkinson's Disease
Give this one a try later!
Severe degen of basal ganglia (corpus stratum) involving the dopaminergic
nigrostriatal pathway
• loss of dopaminergic pigmented neurons in the substantial nigra
• S/S: rigidity, bradykinesia, akinesia, tremor, postural abnormalities,
autonomic-neuro endocrine symptoms, cognitive-affective symptoms of
dementia
• TX: Levodopa, anticholinergic drugs, antihistamines, Amantadine
Review the pathophysiology and signs and symptoms of Graves disease
Give this one a try later!
, Graves disease is the underlying cause of
50% to 80% of cases of hyperthyroidism. Although the cause of Graves
disease is not known, genetic factors interacting with environmental
triggers play an important role in the pathogenesis of this autoimmune
thyroid disease. Graves disease results from a form of type II
hypersensitivity in which there is stimulation of the thyroid by
autoantibodies directed against the TSH receptor. These autoantibodies,
called thyroidstimulating
immunoglobulins (TSIs; also called thyroidstimulating
antibodies [TSAbs] or thyroid receptor antibodies
[TRAbs]), override normal regulatory mechanisms. The TSI
stimulation of TSH receptors in the gland results in hyperplasia of the gland
(goiter) and increased synthesis of TH, especially of triiodothyronine (T3).
Increased levels of TH affect every physiologic system and result in the
classic signs and symptoms of hyperthyroidism. TSH production
by the pituitary is inhibited through the usual negative feedback loop. TSIs
also contribute to two major distinguishing clinical manifestations of Graves
disease: ophthalmopathy and pretibial myxedema (Graves dermopathy).
Graves ophthalmopathy affects more than half of individuals with Graves
disease. Increased secretion of hyaluronic acid, orbital fat accumulation,
inflammation, and edema of the orbital contents result in exophthalmos
(protrusion of the eyeball). Periorbital edema and extraocular muscle
weakness lead to diplopia (double vision). The individual may experience
irritation, pain, lacrimation, photophobia, blurred vision, decreased visual
acuity, papilledema, visual field impairment,
exposure keratosis, and corneal ulceration. A small number of individuals
with Graves disease and very high levels of TSI experience pretibial
myxedema (Graves dermopathy), characterized by subcutaneous swelling
on the anterior portions of the legs and by indurated and erythematous
skin
Review risk factors for cerebral vascular accident. What is the difference between
hemorrhagic and ischemic, Thrombotic, embolic, and lacunar.
Give this one a try later!
