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The nervous system is the master controlling and communicating system of the body.
Every thought, action, and emotion reflects its activity. It is a signaling device, or means of
communicating with body cells, is electrical impulses, which are rapid and specific and cause
The structural classification, which includes all nervous system organs, has two
subdivisions- the central and peripheral nervous system. The central nervous system (CNS),
consists of the brain and spinal cord. They interpret incoming sensory information and issue
instruction based on the past experience and current conditions. The peripheral nervous system
(PNS), the part of the nervous system outside of the central nervous system, consist of mainly
nerves that extend from the brain to the spinal cord. Spinal nerves carry impulses to and from the
spinal cord. Cranial nerves carry impulses to and from the brain. These nerves serve as
communication line. They link all parts of the body by carrying impulses from the sensory
receptors to the central nervous system and from the central nervous system to the appropriate
glands or muscles.
During embryonic development, the central nervous system first appears as a simple tube,
the neural tube, which extends down the dorsal median plane of the developing embryo’s body.
By the fourth week, the anterior end of the neural tube begins to expand, and brain formation
begins. The central canal of the neural tube, which continuous between the brain and the spinal
cord, becomes enlarged in four regions of the brain to form chambers called ventricles.
The adult’s brain’s unimpressive appearance gives few hints of its remarkable abilities. It
is about two good fistfuls of pinkish gray tissue, wrinkled like a walnut, and with the texture of
cold oatmeal. It weighs a little over three pounds. Because the brain is the largest and most
complex mass of nervous tissue in the body, it is commonly discussed in terms of its four major
The paired cerebral hemispheres are the most superior part of the brain and together are a
good deal larger that the other three brain regions combined. In fact, the cerebral hemispheres
enclose and obscure most of the brain stem, so many brain stem structures cannot normally be
The entire surface of the cerebral hemispheres exhibits elevated ridges of tissue called
gyri, separated by shallow grooves called sulci. Less numerous are the deeper grooves called
fissures, which separate large regions of the brain. Many of the fissures and gyri are important
anatomical land marks. The cerebral hemispheres are separated by a single deep fissure, the
longtitudinal fissure. Other fissures or sulci divide each cerebral hemisphere into a number of
lobes, named for the cranial bones that lie over them. S[eech, memory, logical and emotional
response, as well as consciousness, interpretation of sensation, and voluntary movement, are all
functions of cerebral cortex neurons, and many of the functional areas of the cerebral
hemispheres have been identified. The somatic sensory are is located in the parietal lobe
posterior to the central sulcus. Impulses traveling from the body’s sensory receptors (except for
the special senses) are localized and interpreted in this area of the brain. The somatic sensory
area allows you to recognize pain, coldness, or a light touch. The body is represented in an
upside-down manner in the sensory area. Body regions with the most sensory receptors – the lips
and the fingertips- send impulses to neurons that make up a large part of the sensory cortex.
Furthermore, the sensory pathways are crossed pathways- meaning that the left side of the
sensory cortex receives impulses from the right side of the body, and vice versa.
Impulses from the special sense organs are interpreted in other cortical areas. For
example, the visual area is located in the posterior part of the occipital lobe, the auditory area is
in the temporal love bordering the lateral sulcus, and the olfactory area is found deep inside the
temporal lobe.
The primary motor area that allows us to consciously move our skeletal muscles is
anterior to the central sulcus in the frontal lobe. The axons of these motor neurons from the
major voluntary motor tract- the pyramidal, or corticospinal, tract, which descends to the cord.
As in the comatic sensory cortex, the body is represented upside-down and the pathways are
crossed. Most of the neurons in the primary motor area control body areas having the finest
motor control; that is, the face, mouth, and the hands. A specialized area that is very involved in
our ability to speak, Broca’s area, is found at the base of the precentral gyrus. Damage to this are,
which is located in only one cerebral hemisphere (usually left), causes inability to say words
properly. You know what you want to say but you can’t vocalize the words.
Areas involved in higher intellectual reasoning are believed to be in the anterior part of
the frontal lobes. Complex memories appear to be stored in the temporal and frontal lobes. The
speech area is located at the junction of the temporal, parietal, and occipital lobes. The speech
area allows one to sound out words. This area (like Broca’s area) is usually in only one cerebral
hemisphere. The frontal lobes house areas involved with language comprehension (word
meanings).
The cell bodies of neurons involved in the cerebral hemisphere functions named above
are found only in the outermost gray matter of the cerebrum, the cerebral cortex. As noted
earlier, the cortical region is highly ridged and convoluted, providing more room for the
Most of the remaining cerebral hemisphere tissue- the deeper cerebral white matter- is
composed of fiber tracts (bundles of nerve fibers) carrying impulses to or from the cortex. One
very large fiber tract, the corpus callosum connects the cerebral hemispheres. The corpus
callosum arches above the structures of the brain stem and allows the cerebral hemispheres to
communicate with one another. This is important because, as already noted, some of the cortical
functional areas are in only one hemisphere. Although most of the gray matter is in the cerebral
cortex, there are several “islands” of gray matter, called basal nuclei, buried deep within the
white matter of the cerebral hemispheres. The basal nuclei help regulate voluntary motor
activities by modifying instructions sent to the skeletal muscles by the primary motor cortex.
The diencephalon, or interbrain, sits atop the brain stem and is enclosed by the cerebral
hemispheres. The major structures of the diencephalon are the thalamus, hypothalamus, and
epithalamus, The thalamus, which encloses the shallow third ventricle of the brain, is a relay
station for sensory impulses passing upward to the sensory cortex. As impulses surge through the
thalamus, we have a crude recognition of whether the sensation we are about to have is pleasure
or unpleasant. The actual localization and interpretation of the sensation is done by neurons of
nervous system center because it plays a role in the regulation of body temperature, water
balance, and metabolism. The hypothalamus is also the center for many drives and emotions, and
are the pineal body (part of the endocrine system) and the choroid plexus of the third ventricle.
The choroid plexus, knots of capillaries within each ventricle, from the cerebrospinal fluid.
The brain stem is about the size of a thumb in diameter and approximately 3 inches long.
Midbrain is a relatively small part of the brain stem. It extends from the mammillary
bodies to the pons inferiorly. The cerebral aqueduct is a tiny canal that travels through the
midbrain and connects the third ventricle of the diencephalon to the fourth ventricle below.
Anteriorly, the midbrain is composed primarily of two bulging fober tracts, the cerebral
peduncles (little feet of cerebrum), which convey ascending and descending impulses. Dorsally
Pons is the round structure that protrudes just below the midbrain. Pons means “bridge”,
and this area of the brain stem is mostly fiber tracts. However, it does have important nuclei
Medulla oblongata is the most inferior part of the brain stem. It merges into the spinal
cord below without any obvious change in structure. Like the pons, the medulla is an important
fiber tract area. The medulla also contains many nuclei that regulate vital visceral activities. It
contains centers that control heart rate, blood pressure, breathing, swallowing, and vomiting,
among others. The fourth ventricle lies posterior to the pons and medulla and anterior to the
cerebellum.
Cerebellum, the large cauliflowerlike projects dorsally from under the occipital lobe of
the cerebrum. Like the cerebrum it has two hemispheres and a convoluted surface. The
cerebellum also has an outer cortex made up of gray matter and an inner region of white matter.
The cerebellum provides the precise timing for skeletal muscle activity and controls our balance
and equilibrium. Fibers reach the cerebellum from the equilibrium apparatus of the inner ear, the
eye, the proprioceptors of the skeletal muscles and tendons, and many other areas. The
“intentions” with actual body performance by monitoring body position and amount of tension in
Nervous tissue is very soft and delicate, and the irreplaceable neurons are injured by even
slightest pressure. Nature has tried to protect the brain and spinal cord by enclosing them within
bone, membranes, and watery cushion. Protection from harmful substances on the blood is
The three connective tissue membranes covering and protecting the central nervous
system structures are meninges. The outermost layer the leathery durame mater, meaning “tough
or hard mother,” is a double-layered membrane where it surrounds the brain. One of its layers is
attached to the inner surface of the skull, forming the periosteum. The other called the meningeal
layer, forms the outermost covering of the brain and continues as dura mater of the spinal cord.
The dural layers are fused together except in three areas where they separate to enclose dural
sinuses that collect venous blood. In several places, the inner dural membrane extends inward to
The middle meningeal layer is the weblike arachnoid mater. Its threadlike extensions
span the subarachnoid space to attach it to the innermost membrane, the pia mater. The delicate
pia mater clings tightly to the surface of the brain and spinal cord, following every fold. The
subarachnoid space is filled with cerebrospinal fluid. Specialized projections of the arachnoid
membrane, arachnoud villi, protrude through the dura mater. The cerebrospinal fluid is absorbed
into the venous blood in the dural sinuses through the arachnoid villi.
Cerebrospinal fluid (CSF), is a watery “broth: similar in its make up to blood plasma,
from which it forms. However, it contains less protein, more vitamin C, and its ion composition
is different. It continually formed from blood by choroid plexus. Choroid plexus are clusters of
capillaries hanging from the “roof” in each of the brain ventricles. The cerebrospinal fluid in and
around the brain and cord forms a watery cushion that protects the fragile nervous tissue from
The cerebrospinal fluid is continually moving. It circulates from the two lateral ventricles
( in the cerebral hemispheres) into the third ventricle (in the diencephalon), and then through the
cerebral aqueduct of the midbrain into the fourth ventricle dorsal to the pons and medulla
oblongata. Some of the fluid reaching the fourth ventricle continues down the central canal of the
spinal cord, but most of it circulates into the subarachnoid space through three openings in the
walls of the fourth ventricle. The fluid returns to the blood in the dural sinuses through the
arachnoid villi. Ordinarily, cerebrospinal fluid forms and drains at a constant rate so that its
normal pressure and volume (150ml) are maintained. Any significant changes in cerebrospinal
Marieb, E. N. (2008). Essentials of human anatomy & physiology (9. ed.). San Francisco,
The brain and the rest of the nervous system are composed of many different types of cells, but
the primary functional unit is a cell called the neuron. All sensations, movements, thoughts,
memories, and feelings are the result of signals that pass through neurons.
The cell body contains the nucleus, where most of the molecules that the neuron needs to survive
and function are manufactured. Dendrites extend out from the cell body like the branches of a
tree and receive messages from other nerve cells. Signals then pass from the dendrites through
the cell body and may travel away from the cell body down an axon to another neuron, a muscle
The neuron is usually surrounded by many support cells. Some types of cells wrap around the
axon to form an insulating sheath. This sheath can include a fatty molecule called myelin, which
provides insulation for the axon and helps nerve signals travel faster and farther. Axons may be
very short, such as those that carry signals from one cell in the cortex to another cell less than a
hair's width away. Or axons may be very long, such as those that carry messages from the brain
all the way down the spinal cord. Scientists have learned a great deal about neurons by studying
the synapse, the place where a signal passes from the neuron to another cell. When the signal
reaches the end of the axon it stimulates tiny sacs. These sacs release chemicals known as
neurotransmitters into the synapse. The neurotransmitters cross the synapse and attach to
receptors on the neighboring cell. These receptors can change the properties of the receiving cell.
If the receiving cell is also a neuron, the signal can continue the transmission to the next cell.
Some Key Neurotransmitters at Work
excitable. It governs muscle contractions and causes glands to secrete hormones. Alzheimer's
disease, which initially affects memory formation, is associated with a shortage of acetylcholine.
make cells less excitable. It helps control muscle activity and is an important part of the visual
system. Drugs that increase GABA levels in the brain are used to treat epileptic seizures and
Serotonin is an inhibitory neurotransmitter that constricts blood vessels and brings on sleep. It is
mood and the control of complex movements. The loss of dopamine activity in some portions of
the brain leads to the muscular rigidity of Parkinson's disease. Many medications used to treat
Neurological Disorders
When the brain is healthy it functions quickly and automatically. But when problems occur, the
results can be devastating. Some 50 million people in this country - one in five - suffer from
damage to the nervous system. The NINDS supports research on more than 600 neurological
diseases. Some of the major types of disorders include: neurogenetic diseases (such as
Huntington's disease and muscular dystrophy), developmental disorders (such as cerebral palsy),
degenerative diseases of adult life (such as Parkinson's disease and Alzheimer's disease),
metabolic diseases (such as Gaucher's disease), cerebrovascular diseases (such as stroke and
vascular dementia), trauma (such as spinal cord and head injury), convulsive disorders (such as
Source: Antonios N., Silliman S., 2005, Diabetes Mellitus and Stroke, from
http://www.dcmsonline.org/jax-medicine/2005journals/Diabetes/diab05g-stroke.pdf
CARDIOVASCULAR SYSTEM
The cardiovascular system can be thought of as the transport system of the body. This
system has three main components: the heart, the blood vessel and the blood itself. The heart is
the system's pump and the blood vessels are like the delivery routes. Blood can be thought of as a
fluid which contains the oxygen and nutrients the body needs and carries the wastes which need
to be removed. The following information describes the structure and function of the heart and
The heart's job is to pump blood around the body. The heart is located in between the two
lungs. It lies left of the middle of the chest. It is a muscle about the size of a fist, and is roughly
cone-shaped. It is about 12cm long, 9cm across the broadest point and about 6cm thick.
The pericardium is a fibrous covering which wraps around the whole heart. It holds the heart in
place but allows it to move as it beats. The wall of the heart itself is made up of a special type of
The heart has two sides, the right side and the left side. The heart has four chambers. The left and
right side each have two chambers, a top chamber and a bottom chamber. The two top chambers
are known as the left and right atria(singular: atrium). The atria receive blood from different
sources. The left atrium receives blood from the lungs and the right atrium receives blood from
the rest of the body. The bottom two chambers are known as the left and right ventricles.
The ventricles pump blood out to different parts of the body. The right ventricle pumps blood to
the lungs while the left ventricle pumps out blood to the rest of the body. The ventricles have
much thicker walls than the atria which allows them to perform more work by pumping out
Blood Vessels
Blood Vessels are tubes which carry blood. Veins are blood vessels which carry blood from the
body back to the heart.Arteries are blood vessels which carry blood from the heart to the body.
There are also microscopic blood vessels which connect arteries and veins together
called capillaries. There are a few main blood vessels which connect to different chambers of the
heart. The aorta is the largest artery in our body. The left ventricle pumps blood into the aorta
which then carries it to the rest of the body through smaller arteries. The pulmonary trunk is the
large artery which the right ventricle pumps into. It splits into pulmonary arteries which take the
blood to the lungs. The pulmonary veins take blood from the lungs to the left atrium. All the
other veins in our body drain into the inferior vena cava (IVC) or thesuperior vena cava (SVC).
These two large veins then take the blood from the rest of the body into the right atrium.
Valves
Valves are fibrous flaps of tissue found between the heart chambers and in the blood vessels.
They are rather like gates which prevent blood from flowing in the wrong direction. They are
found in a number of places. Valves between the atria and ventricles are known as the right and
left atrioventricular valves, otherwise known as the tricuspid and mitral valves respectively.
Valves between the ventricles and the great arteries are known as the semilunar valves. Theaortic
valve is found at the base of the aorta, while the pulmonary valve is found the base of the
pulmonary trunk. There are also many valves found in veins throughout the body. However,
there are no valves found in any of the other arteries besides the aorta and pulmonary trunk.
Cardiovascular System
The cardiovascular system refers to the heart, blood vessels and the blood. Blood contains
oxygen and other nutrients which your body needs to survive. The body takes these essential
nutrients from the blood. At the same time, the body dumps waste products like carbon dioxide,
back into the blood, so they can be removed. The main function of the cardiovascular system is
therefore to maintain blood flow to all parts of the body, to allow it to survive. Veins deliver used
blood from the body back to the heart. Blood in the veins is low in oxygen (as it has been taken
out by the body) and high in carbon dioxide (as the body has unloaded it back into the blood).
All the veins drain into the superior and inferior vena cava which then drain into the right atrium.
The right atrium pumps blood into the right ventricle. Then the right ventricle pumps blood to
the pulmonary trunk, through the pulmonary arteries and into the lungs. In the lungs the blood
picks up oxygen that we breathe in and gets rid of carbon dioxide, which we breathe out. The
blood is becomes rich in oxygen which the body can use. From the lungs, blood drains into the
left atrium and is then pumped into the left ventricle. The left ventricle then pumps this oxygen-
rich blood out into the aorta which then distributes it to the rest of the body through other
arteries. The main arteries which branch off the aorta and take blood to specific parts of the body
are:
• Hepatic artery, which takes blood to the liver with branches going to the stomach
The body is then able to use the oxygen in the blood to carry out its normal functions. This blood
will again return back to the heart through the veins and the cycle continues.
Cardiac Cycle
The cardiac cycle is the sequence of events that occurs in one complete beat of the heart. The
pumping phase of the cycle, also known as systole, occurs when heart muscle contracts. The
filling phase, which is known as diastole, occurs when heart muscle relaxes. At the beginning of
the cardiac cycle, both atria and ventricles are in diastole. During this time, all the chambers of
the heart are relaxed and receive blood. The atrioventricular valves are open. Atrial
systolefollows this phase. During atrial systole, the left and right atria contract at the same time
and push blood into the left and right ventricles, respectively. The next phase is ventricular
systole. During ventricular systole, the left and right ventricles contract at the same time and
pump blood into the aorta and pulmonary trunk, respectively. In ventricular systole, the atria are
relaxed and receive blood. The atrioventricular valves close immediately after ventricular systole
begins to stop blood going back into the atria. However, the semilunar valves are open during
this phase to allow the blood to flow into the aorta and pulmonary trunk. Following this
phase, the ventricles relax that is ventricular diastoleoccurs. The semilunar valves close to stop
the blood from flowing back into the ventricles from the aorta and pulmonary trunk. The atria
and ventricles once again are in diastole together and the cycle begins again.
The adult heart beats around 70 to 80 times a minute at rest. When you listen to your heart with a
stethoscope you can hear your heart beat. The sound is usually described as "lubb-dupp". The
"lubb" also known as the first heart sound, is caused by the closure of the atrioventricular valves.
The "dupp" sound is due to the closure of the semilunar valves when the ventricles relax (at the
beginning of ventricular diastole). Abnormal heart sounds are known as murmurs. Murmurs may
indicate a problem with the heart valves, but many types of murmur are no cause for concern.
The Electrocardiogram
The heart has an inbuilt rhythm of contraction and relaxation. A small group of heart muscle
cells called the pacemaker help achieve this. The pacemaker generates an electrical impulse
which spreads over the atria, making them contract. This impulse then spreads to the ventricles,
causing them to contract. The electrical changes that spread through the heart can be detected at
the surface of the body by an instrument called the electrocardiograph. Electrodes are placed in a
number of positions over the chest and the electrical changes are recorded on moving graph
As a part of the normal aging process a number of changes occur to the cardiovascular
system.
• Our heart rate slows down because the time between heartbeats increases as we age. This
is one of the main reasons why the heart is unable to pump out more blood during exercise when
we become old.
• The amount of blood the heart pumps each minute can change as we age. It decreases
slightly in older women. However, it does not change in healthy older men who have no heart
disease. The reason for the difference between the sexes is not fully understood.
• As we age, our blood pressure falls much more on standing from the sitting
position compared to when we are younger. This phenomenon is known as postural hypotension.
This explains why elderly people are more likely to feel dizzy or to fall when they stand up
http://www.virtualmedicalcentre.com/anatomy.asp?sid=16#C1
BLOOD FLOW
When the ventricles contract, they force blood into large, thick-walled elastic arteries that
expand as the blood is pushed into them. The high pressure in these arteries forces blood to
continually move into areas where the pressure is lower. The pressure is highest in the large
arteries and continues to drop throughout the pathway, reaching zero or negative pressure at the
venae cavae.
through the blood vessels. It is increased by many factors, but probably the most important is the
nervous system activity or atherosclerosis. Increased blood volume or blood viscosity (thickness)
also raise peripheral resistance. Any factor that increases either the cardiac output or peripheral
resistance causes an almost immediate reflex rise in blood pressure. Many factors can alter blood
pressure, such as: age, weight, time of day of, exercise, body position, emotional state and
autonomic nervous system has little or no effect on blood pressure, but sympathetic division is
important and is responsive to many different factors. The major action of sympathetic nerves on
the vascular system is to cause vasoconstriction, or narrowing of the blood vessels, which
increases blood pressure. The sympathetic center on the medulla of the brain is activated to cause
vasoconstriction in many different circumstances. When we stand up suddenly after lying down,
the effect of gravity causes the blood to pull in the vessels of the legs and feet and the blood
pressure drops. This activates pressoreceptors (called baroreceptors) in the large arteries of the
neck and chest. They send of warning signs that result in reflexive vasoconstriction, which
increases blood pressure back to homeostatic levels. When blood volume suddenly decreases, as
in hemorrhage, blood pressure drops, and the heart begins to beat more rapidly ( as it tries to
compensate). However, because venous return is reduced by blood loss. The heart also beats
weakly and inefficiently. In such cases, the sympathetic nervous system causes vasoconstriction
to increase the blood pressure so that venous return increase and circulation can continue.
The final example concerns sympathetic nervous system activity when we exercise vigorously or
are frightened and have to make a hasty escape. Under these conditions, there is a generalized
vasoconstriction except in the skeletal muscles to dilate to increase blood flow to the working
muscles. (It should be noted that the sympathetic nerves never cause vasoconstriction of blood
Marieb, E. N. (2008). Essentials of human anatomy & physiology (9. ed.). San Francisco, Calif.:
Benjamin Cummings
ENDOCRINE SYSTEM
Endocrine glands: Endocrine organs, called glands, secrete hormones into the bloodstream.
Hormones affect the activity of target sites that are often located far from the site of release.
Exocrine organs direct the function of their target sites by releasing their active.
Human endocrine system: The major endocrine organs include the hypothalamus and the
hypophysis, or pituitary gland. Other endocrine glands within the body include: thyroid,
pituitary gland. The hypothalamus receives input from other parts of the brain and from
peripheral nerves. This input affects neurosecretory cells within the hypothalamus.
• The pituitary gland: The anterior pituitary synthesizes its own hormones. Capillaries
within the anterior pituitary receive signals from the hypothalamus that tell the anterior
• The thyroid gland: The thyroid gland is a bilobed structure found at the trachea. It
1. thyroxine (T4),
3. calcitonin.
The parathyroids are four small glands embedded in the thyroid. They produce and
• The adrenal gland: The adrenal glands are located on top of the kidneys. Each gland is
• The pancreas: The pancreas is both an endocrine organ and an exocrine organ. The
exocrine portion of the pancreas secretes digestive enzymes into the pancreatic duct. The
endocrine portion of the pancreas secretes hormones, including insulin and glucagon.
• The testes: The testes are responsible for the synthesis and secretion of androgens, such
as testosterone. Interstitial cells, located between the seminiferous tubules of the testes,
produce androgens.
• The ovaries: The ovaries produce and secrete steroid hormones known as estrogens and
progesterone.
http://www.rapidlearningcenter.com/biology/anatomy-physiology/15-The-Endocrine-
System.html
Cerebral infarction is focal brain necrosis due to complete and prolonged ischemia that
The basic mechanisms of cell and tissue injury that were discussed under HIE apply also to
infarcts. One additional concept, the ischemic penumbra, is worth stressing. In every infarct,
there is a central core of total ischemia and necrosis which is irreversible. This area is surrounded
by a zone of borderline ischemic tissue, the ischemic penumbra. Ischemia, in the penumbra,
causes dysfunction due to ionic and metabolic dysfunction but is not severe enough to result in
agents may prevent structural damage in this area, thus limiting the neurological deficit.
Ischemic stroke is an emergency. The window of opportunity for salvaging the penumbra is very
short. If adequate blood supply is not restored within 3 hours, necrosis extends to the penumbra.
According to some authors, embolism is the most frequent cause of ischemic infarction.
Most emboli are fragments of blood clots that originate in the heart or major vessels. Conditions
causing cardiac emboli include myocardial infarcts, atrial fibrillation and other arrhythmias,
rheumatic heart disease, bacterial and non-bacterial endocarditis, prosthetic valves, mitral valve
prolapse, atrial myxoma, calcified mitral annulus, and cardiomyopathy. An embolus cannot be
to be embolic if it is hemorrhagic, there is a source of emboli, there are multiple infarcts of the
brain and other organs (kidney, spleen), and there is no atherosclerosis or other vascular disease.
Some emboli consist of atheromatous material that is detached from ulcerated atheromas of the
aorta or carotid arteries. Vascular manipulation (angiography, carotid endarterectomy) may cause
atheromatous embolism. Rarer causes of embolism are fat, air, and tumor emboli. Unlike
atherothrombotic infarcts, which may evolve within hours or days, embolic infarcts have
an abrupt onset.
Because the risk factors for these types of brain infarction are identical to the risks for coronary
artery disease and other blood vessel diseases, patients most at risk for ischemic stroke are often
the same patients who have heart disease or other peripheral vascular disease. Other causes of
ischemic stroke are less common. Blood clots from aneurysms, from heart conditions (such as
atrial fibrillation, septal defects or valve disease) and other sources are less common but do occur
in some patients.
Source: Agmanolis, D. , 2005, Cerebral Ischemia and Stroke, Retrieved June, 2010, from
http://www.neuropathologyweb.org/chapter2/chapter2bCerebralinfarcts.html
Essentials of Diagnosis
atherosclerosis.
General Considerations
In the USA, stroke remains the third leading cause of death, despite a general decline in the
incidence of stroke in the last 30 years. The precise reasons for this decline are uncertain, but
cardiac disease, AIDS, recreational drug abuse, heavy alcohol consumption, family history of
stroke) and improved prophylactic measures and surveillance of those at increased risk have
been contributory. A previous stroke makes individual patients more susceptible to further
strokes.
For years, strokes have been subdivided pathologically into infarcts (thrombotic or embolic)
and hemorrhages, and clinical criteria for distinguishing between these possibilities have been
emphasized. However, it is often difficult to determine on clinical grounds the pathological basis
for stroke.
1. LACUNAR INFARCTION
Lacunar infarcts are small lesions (usually < 5 mm in diameter) that occur in the
distribution of short penetrating arterioles in the basal ganglia, pons, cerebellum, anterior
limb of the internal capsule, and less commonly, the deep cerebral white matter. Lacunar
infarcts are associated with poorly controlled hypertension or diabetes and have been
found in several clinical syndromes, including contralateral pure motor or pure sensory
deficit, ipsilateral ataxia with crucal paresis, and dysathria with clumsiness of the hand.
The neurological deficit may progress over 24-36 hours before stabilizing.
areas, but in other patients no abnormality is seen. In some instances, patients with a
The prognosis for recovery from the deficit produced by a lacunar infarct is usually
good, with partial or complete resolution occurring over the following 4-6 weeks in many
instances.
2. CEREBRAL INFARCTION
Causes include the disorders predisposing to transient ischemic attacks (see above) and
atherosclerosis of cerebral arteries. The resulting deficit depends upon the particular
vessel involved and the extent of any collateral circulation. Cerebral ischemia leads to
release of excitatory and other neurons, thereby leading to cell death and increasing the
neurologic deficit.
Source: Tierney, L. M., McPhee, S. J., & Papadakis, M. A. (2006). Current medical diagnosis
In an ischemic brain attack, there is disruption of the cerebral blood flow due to obstruction of a
blood vessel. This disruption in blood flow initiates a complex series of cellular metabolic
The ischemic cascade begins when cerebral blood flow decreases less that 25 mL per 100 100g
of blood per minute. At this point, neurons are no longer able to maintain aerobic respiration.
The mitochondria must then switch to the anaerobic respiration, which generates large amounts
of lactic acid, causing a change in pH. This switch to the less efficient anaerobic respiration also
renders the neuron incapable of producing sufficient quatities of adenosine triphosphate (ATP)
to fuel the depolarization processes. The membrane pumps that maintain electrolyte balances
Early in the cascade, an area of low cerebral blood flow, referred to as the penumbra region,
exists around the area of infarction. The penumbra region is ischemic brain tissue that may be
slavaged with timely intervention. The ischemic cascade threatens cells in the penumbra
because memebrane depolarization of the cell wall leads to an increase in intracellular calcium
and the release of glutamate. The influx of calcium and the release of glutamate, if continued,
activate a number of damaging pathways that result in the destruction of the cell membrane, the
release of more calcium and glutamate, vasoconstriction, and the generation of free radicals.
These processes enlarge the area of infarction into the penumbra, extending the stroke. A person
experiencing a stroke typically loses 1.9 million neurons each minute that a stroke is not treated,
and the ischemic brain ages 3.6 years each hour without treatment.
Each steps in the ischemic cascade represents an opportunity for intervention to limit the extent
of secondary brain damage caused by stroke. The penumbra area may be revitalized by
administration of tissue plasminogen activator. Medications that protect the brain form
secondary injury are called neuroprotectants. A number of ongoing clinical trials focus on
Source: Brunner, L. S., & Smeltzer, S. C. (2010). Brunner & Suddarth's textbook of medical-
surgical nursing (12th ed.). Philadelphia: Wolters Kluwer Health/Lippincott Williams &
Wilkins.
Two approaches are used to describe middle cerebral artery (MCA) anatomy. The
functional branching approach follows the MCA trunk from the source to the end branches. The
segmental approach analyzes branches of the MCA in relation to brain landmarks, dividing the
artery into 4 main segments. In the segmental approach, M1 is the portion most proximal to the
origin of the vessel, and M4 includes the terminal MCA branches at the brain surface. (Normal
The segmental approach is applied most often for angiographic purposes and relates
segments of the MCA to specific cerebral landmarks. The first of 4 segments, M1, describes the
artery from its origin to the limen insulae, most of which is the portion from which the
lenticulostriate arteries arise. The second portion of M1 describes the 3 branches that result from
the bifurcation of the MCA and enter the sylvian sulcus. M2 is the segment that runs along the
insula, and M3 follows the operculum superior to the insula. Finally, M4 describes branches of
the MCA that perfuse nearly the entire convex surface of the cerebral hemispheres, aside from
Using the functional branching approach to anatomy, the MCA generally arises as a
single trunk 18-26 mm long with a diameter of approximately 3 mm. The first branches consist
of 15-17 small lenticulostriate arteries that supply the putamen and pallidum or the lentiform
nucleus, internal capsule, and caudate nucleus of the basal ganglia. Occasionally, a few of the
smaller lenticulostriate arteries arise from the internal carotid arteries. After the lenticulostriate
branches, the MCA generally bifurcates, forming superior and inferior divisions. The superior
branch supplies the prefrontal and orbitofrontal cortex, and the inferior branch supplies the
Source: Slater D. MD, Middle Cerebral Artery Stroke, Updated Apr 12, 2010 from
http://emedicine.medscape.com/article/323120-overview
initial change of the affected area is a slight discoloration and softening with the gray matter
taking on a muddy color and the white matter losing is normal fine-grained appearance.
After 24-48 hours, infarction, necrosis, circumlesional swelling and mushy disintegration
Chipps, E. M., Clanin, N. J., & Campbell, V. G. (1992). Neurologic disorders . St. Louis: Mosby
Year Book.
A. Symptoms and Signs: Onset is usually abrupt, and there may then be very little
progression except that due to brain swelling. Clinical evaluation always includes
examination of the heart and auscultation over the subclavian and carotid vessels to
its junction with the anterior communicating artery causes weaknesses of the arm,
junction with the anterior communicating artery is generally well tolerated because of
loss, and homonymous hemianopia (ie, bilaterally symmetric loss of vision in half of
the visual fields), with the eyes deviated to the side of the lesion. If the dominant
distinguish this clinically from occlusion of the internal carotid artery. With occlusion
of either of these arteries, there may also be considerable swelling of the hemisphere,
branches of the middle cerebral artery cause more limited findings. For example,
dysphasia and to contralateral paralysis and loss of sensations in the arm, the face,
and to a lesser extent, the leg. Posterior branch occlusion produces a receptive
(Wernicke’s) aphasia and a homonymous visual field defect. With involvement of the
nondominant hemisphere, speech and comprehension are preserved, but there may be
lesion and the collateral circulation, the severity of these deficits may also occur,
including involuntary movements and alexia. Occlusion of the main artery beyond the
posterior inferior cerebellar arteries, may be clinically silent because the circulation is
basilar artery occlusion is seen unless there is good collateral circulation from the
When the small paramedian arteries arising from the vertebral artery are occluded,
cranial nerve palsy at the level of the lesion. An obstruction of the posterior inferior
cerebellar artery or an obstruction of the vertebral artery just before it branches to this
vessel leads ipsilaterally to spinothalamic sensory loss involving the face, ninth and
tenth cranial nerve lesions, limb ataxia and numbness, and Horner’s syndrome,
Occlusions of both vertebral arteries and the basilar artery lead to a coma with
pinpoint pupils, flaccid quadriplegia and sensory loss, and variable cranial nerve
abnormalities. With partial basilar artery occlusion, there may be diplopia, visual loss,
limbs, and discrete cranial nerve palsies. In patients with hemiplegia of pontine
origin, the eyes are often deviated to the paralyzed side, whereas in patients with a
hemispheric lesion, the eyes commonly deviate from the hemiplegic side.
spinothalamic loss also involves the face; with occlusion of the anterior inferior
cerebellar artery, there is ipsilateral spinothalamic sensory loss involving the face,
consciousness. For example, an infarct involving one cerebral hemisphere may lead
to such swelling that the function of the other hemisphere or the rostral brain stem is
disturbed and coma results. Similarly, coma occurs with bilateral brain stem
infarction when this involves the reticular formation, and it occurs with brain stem
the presence of a neoplasm would suggest that the neurologic deficit is due to metastasis
rather than stroke. A CT scan of the head (without contrast) is important in excluding
cerebral infarct and tumor. CT scanning is preferable to MRI in the acute stage because it
is quicker and because intracranial hemorrhage is not easily detected by MRI within the
C. Laboratory and Other Studies: Investigations should include a complete blood count,
sedimentation rate, blood glucose determination, and serologic tests for syphilis.
promote thrombosis and are associated with an increased incidence of stroke. Similarly,
elevated serum cholesterol and lipids may indicate an increased risk of thrombotic stroke.
Electrocardiography will help exclude a cardiac arrhythmia or recent myocardial
of the cerebrospinal fluid is not always necessary but may be helpful if there is diagnostic
Source: Tierney, L. M., McPhee, S. J., & Papadakis, M. A. (2006). Current medical diagnosis &
Patients with middle cerebral artery stroke syndrome (MCA stroke syndrome) may have some
Main trunk occlusion of either side yields contralateral hemiplegia, eye deviation toward the side
of the MCA infarct, contralateral hemianopia, and contralateral hemianesthesia. Eye and head
deviation toward the side of the lesion is probably due to damage of the lateral gaze center
(Brodmann area 8), or it can represent classic neglect, particularly when the right MCA is
involved.
Trunk occlusion involving the dominant hemisphere causes global aphasia, whereas involvement
from the stroke and more qualitative deficits of speech. Superior division infarcts lead to
contralateral deficits with significant involvement of the upper extremity and face and partial
extent of infarction. Right inferior branch infarcts also may lead to a left visual neglect. Finally,
resultant temporal lobe damage can lead to an agitated and confused state.
• Loss of consciousness - Initially this is rare after MCA stroke, but it occurs slightly more
often than in vertebrobasilar strokes (8.4% vs 5.7%). Loss of consciousness most often is
attributable to seizures, but it may result from secondary edema and subsequent
brainstem herniation.
MCA infarct has posed a significant challenge. The prognosis of such motor
deficit also has not completely been elucidated, with case reports of remarkable
o Partial hemiparesis patterns have been mapped more readily to certain MCA
Disorders and Stroke (NINCDS) data bank project gathered pilot data from 488
Equivalent weakness of the hip, foot, shoulder, and hand was the most
with weakness of the lower face, lower legs, toes, fingers, and forearm and
sparing of the forehead and proximal muscles of the upper and lower
and forearm. These deficits result from ischemic insult of the insula and
operculum.
• Visual deficits
o Hemianopia has long been known to accompany the syndrome following a large
MCA infarct; yet, only the superior portion of the optic radiation is supplied by
the MCA. The resultant hemianopia is probably due to a massive infarct with
• Neglect
o Neglect in classic form has been attributed to parietal insult, but data from
positron emission tomography (PET) scanning reveal that frontal lesions can
(eg, a patient who responds to a stimulus from the left by turning right and also
fails to blink upon threatening stimuli to the affected side) can aid in diagnosing
neglect. Patients with visual neglect often have difficulty naming objects
o Motor neglect with underuse of the side contralateral to the cerebral insult appears
encourage the patient to demonstrate strength and dexterity. Typically, the patient
has delayed withdrawal to noxious stimuli, fails to place the affected hand in the
lap when seated, and falls heavily to the affected side with no apparent effort to
minimize impact.
• Autonomic dysfunction
edema of the hand and foot arising within hours of the infarct and lasting up to 2
weeks. This edema is in contrast to the dependent edema that develops subacutely
Left-hemisphere (dominant) infarction - The left cerebral hemisphere is dominant for speech and
language in more than 95% of right-handed individuals. Defining cerebral dominance for left-
handed individuals is more difficult, but most left-handed patients also appear to have a
dominant left hemisphere. One study analyzing left-handed patients with aphasia showed that
60% had lesions confined to the left hemisphere. Other studies reveal bilateral speech
• Aphasia
o Ischemic injury to the sylvian fissure of the dominant hemisphere is the lesion
pathologies are categorized as fluent versus nonfluent. In this context, fluent does
not describe correct use of language or grammar but simply the ability to produce
o Surprisingly, studies have revealed patients with only mild speech deficits, despite
language. Such studies suggest a major role of deeper structures, particularly the
o Broca's aphasia, also termed expressive or motor aphasia, describes the ability to
The infarct responsible for Broca's aphasia encompasses the insula and
frontoparietal operculum.
does not use comprehension testing with simple questions. Initially, the
aphasia, and only later does a speech disturbance arise that is isolated to
communicate an idea.
often by occlusion of the lower division of the MCA bifurcation or one of its
structure, word substitution, and additional prefixes and suffixes. The speech is
occipital regions.
is missing key words and ideas and may be perseverative. The patients
pathways or of the arcuate fasciculus connecting the motor and sensory areas
concerned with speech. The clinical features of conductive aphasia are not
explained completely by this theory. Distinguishing a conductive aphasia is an
unfamiliar phrases and words and demonstrate much better auditory and
however, patients with conductive aphasia are more likely to recognize the
discovered tracts.
• Apraxia
o When referring to apraxia, Mohr states, "Motor engrams (programs) that guide
skilled acts have either been lost or cannot be accessed." Generally, the ability is
impaired rather than eliminated; thus, the term dyspraxia is more appropriate.
is thought to exist between the cortex containing plans for movement and the
precision. Aphasia and apraxia occur independently, and the cortex responsible
multistep tasks, such as obtaining a glass of water. Not all experts agree that
nondominant arm.
movements of the tongue and face upon command. Often these movements are
abnormalities. These behavioral deficits correlate much less to location and extent of the
infarction than do deficits following infarcts of the dominant hemisphere, and some are
stimuli on one side of the body, in the absence of any sensory or motor deficit severe
patients with right-sided brain damage versus 12% of patients with left-sided brain
damage among a stroke population studied by Battersby and coauthors. In severe cases,
the patient often ignores tactile, visual, and auditory stimuli on the left side and is turned
chronically to the right side. When asked to bisect lines, the patient often does this far to
the right of center. Unilateral spatial neglect is a subtler deficit, in which the patient may
fail to read words or recognize figures to the left of midline.More sizable infarcts lead to
anosognosia or imperception of field neglect and imply a much less favorable prognosis.
tasks; it is often accompanied with visuomotor and visuospatial deficits. This impairment
infarcts and is attributable to difficulty distinguishing right from left and up from down.
The patient is unable to dress without assistance despite having no apparent hemiplegia
• Topographic memory deficit - This term is used when individuals become lost in familiar
• General confusion and delirium - These findings often are more commonly appreciated in
patients with damage to the nondominant hemisphere. The central role the right
hemisphere plays in attention, vigilance, and distinguishing stimuli is probably
inability to recognize errors, disinhibition, and memory deficits. These deficits all are
common with damage to the nondominant hemisphere and to the frontal lobe.
type of apraxia can be appreciated by having affected patients copy designs or build 3-
dimensional models. This tendency is more common with right-sided lesions than with
studied by Piercy and colleagues. In this group, 25 had left-sided damage and 42 had
damage to the right hemisphere. The apraxia of the patients with a dominant-hemisphere
infarct often is described as decreased attention to detail. The apraxia with right-sides
damage is consistent with neglect, in which features to the left of midline are ignored.
• Allesthesia - This term describes sensory referral. For example, a patient touched on the
• Aprosody, lack of intonation in speech, and affective agnosia - These terms refer to the
Source: Slater D. MD, Middle Cerebral Artery Stroke, Updated Apr 12, 2010 from
http://emedicine.medscape.com/article/323120-overview
Infarction or ischemia affecting the carotid artery may cause a papillary abnormality
ptosis (eyelid drooping), visual deficit, pallor and petechiae of the conjunctiva.
The affected art of the brain is the right hemisphere in which cranial nerve III
(occulomotor nerve) lies. Due to the paralysis of the nerve, sinking of eyeballs, ptosis of the
upper eyelid, slight elevation of lower eyelid, papillary constriction and lack of tearing in the eye
(Horner’s syndrome) is manifested by the patient. The patient may lose her ability to blink.
Without a blink reflex, the cornea will dry and become abraded.
Causes
small and large vessels is still widely accepted as the primary etiology of strokes in general,
causing approximately 51% of all strokes in the anterior, middle, and posterior cerebral
vasculature combined; however, it is a relatively rare cause of middle cerebral artery strokes
(MCA strokes). Estimates suggest that 15-30% of all strokes are thought to be of embolic
etiology. The remaining cases have either an undetermined or a combined etiology or else are
caused by dissection.
• Embolism
o Most of the sources in the literature support embolism as the primary etiology of
total MCA strokes, 34% of deep MCA strokes, and 41% of cortical strokes in a
study by Moulin and coauthors. This same study, with a relatively large cohort,
more common role in posterior and anterior cerebral strokes than previously
thought. The study also revealed paroxysmal atrial fibrillation in 65% of all stroke
but its frequent occurrence certainly supports the need for cardiac monitoring and
differential diagnosis.
carotid disease. All of these data support widely accepted diagnostic studies,
telemetry to elucidate and treat pathology and prevent future embolic events.
o The location of MCA stroke depends largely on the size of the embolic mass.
Occlusion at the stem is rare and requires embolic matter of at least 3-5 mm.
Emboli can arise because of intravascular, rigid foreign matter (eg, shotgun
pellets, catheter tips, large thrombi combined with bacteria) or as a result of large
calcific plaques formed through direct internal carotid trauma or puncture. The
o Embolization occurs with equal frequency in the right and left MCA.
Angiography reveals that these occlusions are usually found in the first 24 hours,
but the vessels are generally patent within 48 hours. A persistent occlusion has a
less favorable prognosis. The size of the infarct also depends on the collateral
• Indirect ischemia
o Distal territories of the MCA are quite vulnerable to ischemia because of failure
o The prevalence of such strokes is uncertain, but they are not thought to be
uncommon, given the high correlation of carotid stenosis with distal territory
stroke.
• Atherosclerosis - Primary atherosclerosis of the MCA and branches accounts for only 7-
• Thrombosis - Approximately 2-7% of ischemic events in the MCA territory are due to
thrombotic occlusion. The diagnosis can be excluded using repeat angiography, but this is
of questionable utility.
• Amyloid angiopathy - This is a rare etiology for lobar cortical strokes in elderly patients.
• Other - Dissection and stenosis of the MCA are rarely documented as causes of MCA
stroke.
• Etiology based on age - Hemorrhagic stroke is the most common etiology in younger
persons (aged 18-45 y), with intracranial hemorrhage accounting for 41% and
subarachnoid hemorrhage accounting for 17% of strokes in persons in the younger age
group. The remaining 42% of strokes due to ischemia generally require a more
etiology.
Source: Slater D. MD, Middle Cerebral Artery Stroke, Updated Apr 12, 2010 from
http://emedicine.medscape.com/article/323120-overview
DIAGNOSTIC EXAMINATIONS
Imaging Tests
Imaging tests can produce a detailed picture of the brain. These tests include computed
CT Scans
A CT scanner sends a series of X-rays through the head that are analyzed by a computer to create
a detailed picture of a "slice" of the area being studied. Each X-ray lasts a fraction of a second.
During a CT scan of the head, the head is positioned inside a CT scanner's cylinder. The entire
scanner can tilt, and the X-ray scanning cylinder within it can rotate to obtain the views needed.
For a head scan, 10 to 30 slices are usually taken. The results are highly-detailed images of the
head, including the brain, eyes, bones of the skull and sinuses within the bones around the nose.
This is often one of the first tests given to patients who may have had a stroke. These scans
provide important information about the cause of the stroke and the location and extent of brain
injury. CT scans are clearer pictures of the brain than regular X-rays.
Sometimes a special dye (contrast material) that contains iodine is injected into the blood during
a CT scan of the head. The dye makes blood vessels and certain structures inside the head more
MRI
An MRI produces a picture of the brain using a large magnetic field. It also can show the
location and extent of brain injury, but the image is sharper and more detailed. An MRI can
distinguish between the blockage of blood flow due to a clot, which causes transient ischemic
attack and ischemic stroke, and bleeding, which causes hemorrhagic stroke. This type of
diagnostic technique is often used to diagnose small, deep injuries. After the first 24 hours, MRI
can identify the exact size and location of the area affected by a stroke. This information may
help the doctor determine how well the person may recover from a stroke.
An MRI is more sensitive than a CT scan in identifying changes caused by lack of oxygen to
brain cells during the first 72 hours after a stroke. An MRI is more accurate than a CT scan of the
head in identifying multiple small strokes within the brain. An MRI is also better for detecting
strokes in the lower, back part of the brain (cerebellum) and the part of the brain that connects
with the spinal cord (brain stem). An MRI seems to be more accurate in detecting strokes caused
by clots (ischemic strokes) during the first 3 days after a stroke, but the test is less accurate if it is
Electrical activity tests record the electrical impulses of the brain. These tests include an
electroencephalogram (EEG) and evoked response tests. In an EEG, electrodes are put on a
person's scalp to pick up electrical impulses, which are printed out as brain waves. An evoked
response test measures how the brain handles different sensory information, using electrodes that
Blood flow tests can reveal problems in the flow of blood to the brain, normally through the use
of ultrasound technology. During these tests, a probe is placed over the artery in question -
usually the arteries of the neck or at the base of the skull - and the amount of blood flow is
measured. Such tests include B-mode imaging, Doppler testing and duplex scanning, which
Angiography
Angiography (also known as arteriography) is another type of blood flow test. In this, special
dyes are injected into the blood vessels and an X-ray is taken. This test evaluates the size and
location of blockages and can be especially valuable in diagnosing aneurysms and malformed
Carotid angiography is the best test available to identify and measure the blockage in the carotid
arteries of the neck. It is usually done after a carotid ultrasound has shown that there probably is
a blockage in the artery and if surgery (endarterectomy) is being considered to remove the
blockage and reopen the artery. In this test, a tiny tube (catheter) is inserted into an artery (often
in the arm) and threaded through other blood vessels to reach the carotid artery. A dye is then
injected through the tube and into the artery. The dye outlines the blood vessel and X-rays are
taken to evaluate the degree of narrowing and the condition of a plaque. If a plaque is rough,
clots are more likely to form in the blood vessel. When the dye is injected, some people feel a
burning sensation in the face and head, a brief headache, flushed on one side of the face or
nauseous. The test usually takes from one to three hours. The patient may be given a drug to help
Cerebral angiography uses the same technique to study the arteries of the brain. It is usually done
at the same time as carotid arteriography to evaluate blood flow through the brain. The results
will help decide whether surgery to reopen a blocked artery (carotid endarterectomy) is
appropriate. Angiography carries the risk that the procedure itself may cause a piece of plaque to
break away and travel through the blood to the brain, causing a stroke during the procedure.
Duplex Scans
Duplex scans are a sensitive form of ultrasound done of the neck when narrowing of the carotid
arteries due to plaque buildup is suspected. It is often the first test used when you are being
evaluated for surgery to reopen a blocked artery (carotid endarterectomy). In carotid artery
ultrasound scanning, high-pitched sound waves are bounced off the blood vessels and tissues of
the neck to create an image of the arteries. Duplex scanning, which is a newer technique than
traditional carotid artery ultrasound and now used more often, is able to measure blood flow at
many points in the blood vessel at one time. It is used more often than older carotid ultrasound
methods.
During duplex scanning, an instrument is moved over both sides of the neck. The resulting two-
dimensional picture shows clearly the amount of blockage in the artery. This method also shows
color pictures that indicate how fast blood is flowing in any point in the blood vessel. Although
carotid ultrasonography is quicker, safer, less painful and less expensive than carotid
arteriography, it may not always be as accurate in determining the amount of blockage of blood
flow as some other tests. However, carotid ultrasonography is often the first test used and can be
Magnetic resonance angiography (MRA) is a form of MRI that can measure blood flow through
blood vessels. The test uses a strong magnetic field and radio signals to create pictures of the
blood flow through blood vessels. With an MRA, both the blood flow inside of the vessel and the
condition of the blood vessel walls can be seen. An MRA takes pictures quickly that can be seen
• An MRA is often used to determine if narrowing of blood vessels (especially the carotid
• MRAs are relatively safe and easy to perform, and they cost less than some other tests.
People with pacemakers or certain metal implants cannot have an MRA done. Pregnant
• The pictures of the carotid arteries that are produced by an MRA are not as clear as those
expensive.
• MRAs do not produce clear pictures when the blood flow through the vessel is very rapid
• Holes (ulcerations) within plaque may not always be seen with an MRA.
Echocardiography
Echocardiography (ECHO) is a sophisticated type of blood flow test that uses high-pitched
sound waves to produce an image of the heart. The sound waves are sent through a device called
a transducer and are reflected off the various structures of the heart. These echoes are converted
into pictures of the heart that can be viewed on a monitor similar to a TV screen. An
echocardiogram is used to evaluate how well the heart chambers fill with blood and pump blood
to the rest of the body. ECHO can also be used to estimate the amount of blood pumped out of
the left ventricle with each heartbeat (called the ejection fraction).
An ECHO can help evaluate heart size and heart valve function, identifying areas of poor blood
flow in the heart, areas of heart muscle that are not contracting normally, previous injury to the
heart muscle caused by impaired blood flow or evidence of congestive heart failure, especially in
people with chest pain or a possible heart attack. In addition, ECHO can identify some heart
defects that have been present since birth (congenital heart defects).
• Transthoracic echocardiogram (TTE). This is the standard, most commonly used method
of echocardiography. Views of the heart are created by moving the transducer to different
instrument that emits sound waves (transducer) is passed down the esophagus instead of
being moved over the outside of the chest wall. A TEE may show clearer pictures of the
heart because the transducer is located closer to the heart and the lungs and bones of the
chest wall do not block the sound waves. A TEE requires a sedative and anesthetic
Other Tests
Another diagnostic test is the lumbar puncture (spinal tap), in which a needle is inserted into the
spinal canal to collect samples of the clear, fluid that surrounds the brain and spinal cord. The
pressure of this fluid is measured, and the samples are analyzed for color, blood cell counts,
protein, glucose and other substances. Some of the fluid may be placed under conditions that
promote the growth of infectious organisms (cultured), such as bacteria or fungi, to check for
infection.
and-Services/Stroke-Program/Stroke-Resources/Diagnostic-Testing.aspx
Duplex scanners
Duplex scanners display real-time grey-scale images which allow the operator to display the
speed of blood flowing in a selected part of the image. Figure 5 shows a duplex scan of a
The operator has placed a 'gate' in the image of the artery, and the blood velocity waveform is
displayed. In the common and superficial femoral arteries, the waveform normally has a forward
component followed by a reverse component and a second smaller forward component. This is
called a triphasic waveform because of the three phases. More distally in the superficial femoral
artery, the second forward component may be absent, giving a biphasic waveform with two
phases.
The duplex scanner detects the moving blood by using the Doppler effect. Ultrasonic echoes
returning to the probe from stationary structures come back with the same frequency. However,
if the target is moving towards or away from the probe, the echoes return with a higher or lower
frequency. The scanner detects any change in frequency, and can calculate the actual speed of
the target provided the angle between the direction of the ultrasonic beam and the direction of
movement is known. The operator therefore aligns a marker along the direction of flow in the
blood vessel and positions a cursor at the height of the peak systolic blood velocity. The scanner
The frequency shift caused by the Doppler effect depends on the frequency of the transmitted
ultrasound and the speed of the blood. It happens that the frequency shift is normally in the audio
range, so most duplex scanners send the signal to a pair of audio speakers, and this enables the
Colour Doppler scanners detect and display moving structures by superimposing colour onto the
grey-scale image. The operator positions a box on the image, and colour is superimposed
wherever the scanner detects a moving structure, usually blood. Figure 6 shows a colour Doppler
image of the popliteal artery behind the knee. The colour fills the lumen of the vessel, showing
that the blood is moving right up to the vessel wall.The hue of the colour shows the direction and
magnitude of the blood velocity. In this image, red and yellow indicate flow away from the
probe, with dark red representing low velocities and orange and yellow indicating higher
velocities. Flow towards the probe is indicated in blue and green, with green indicating higher
velocities. The hue can therefore be used to identify sites where the artery becomes narrower and
the blood has to move faster to achieve the same volume flow rate. When the blood velocity
exceeds the limit of the colour scale, aliasing occurs. The equipment interprets high velocity in
one direction as lower velocity in the other direction, and there is a sudden transition from
yellow to green or vice versa (Figure 4). This can be useful for identifying the raised velocities
Colour Doppler can also be used to display venous blood flow. The blood moves more slowly in
the veins so different settings are used. Most scanners come with a menu of recommended
settings for different applications, including peripheral arterial and peripheral venous studies.
Lunt/Doppler-Imaging.html
Carotid doppler ultrasound is a non-invasive test that uses sound waves to measure the flow of
blood through the large carotid arteries that supply blood to the brain. These arteries can become
narrowed due to arteriosclerosis or other causes, and this can lead to transient ischemic attack
(mini-stroke) or cerebral vascular accident (stroke). The carotid doppler test can help doctors
A carotid doppler test may be performed if you have had a stroke, or, if based on your doctor's
evaluation, you are considered to be at increased risk of having a stroke due to decreased blood
The ultrasound technician will apply a jelly-like substance to both sides of your neck, where the
carotid arteries are located. This helps lubricate the skin and allow the ultrasound sensor to move
more freely. The sensor is moved back and forth over the neck and generates sound waves that
bounce off the arteries. The echo that bounces back is measured, and the changes in frequency
can measure the flow of blood. The flow will be different in areas that are narrowed.
This test takes an average of 15 to 30 minutes for most people, though it can vary. Once the test
The completed test is recorded on a videotape by the ultrasound technician. The tape is reviewed
by a diagnostic radiologist who measures the blood flow and determines the amount and location
of any narrowing of the carotid arteries. The radiologist will send a report to your doctor. The
Your doctor will review the written report provided by the radiologist. Further treatment
recommendations will be based on the results of this test along with other factors as determined
endarterectomy. This surgical procedure is done to open up constricted arteries and increase
blood flow to the brain. There are other treatments that may also be recommended.
Source: (N.A.)(N.D.)Retrieved from
http://seniorhealth.about.com/od/stroke/p/carotid_doppler.htm
TREATMENT
If the neurologic deficit progresses over the following minutes or hours, heparinization
may be of value in limiting or arresting further deterioration. Since the signs of progressing
measreus. During the acute stage, there may be marked brain swelling and edema, with
cerebral edema. Prednisone (up to 100 md/d) or dexamethasone (16mg/d) has been used, but the
evidence that corticosteroids are of any benefit is conflicting. Dehydrating hyperosmolar agents
have also been prescribed in efforts to reduce brain swelling, but there is little evidence of any
lasting benefit. Likewise, clinical benefit from treatment with vasodilators such as parpavarine is
minimal. Neither hypercapnia nor hypocapnia has been shown to have any benefit. Barbiturates
are known to decrease neuronal metabolism and energy requirements and have been reported to
improve functional recovery in experimental stroke models; their use in humans, however is
experimental. Attempts to lower the blood pressure of hypertensive patients during the acute
phase has a stroke should be avoided, since there is loss of cerebral autoregulation and lowering
except when there is cardiac stroke, except when there is cardiac source of embolization.
Treatment is then started with intravenous heparin while warfarin is introduced. The target is an
international normalized ratio of 3:4 for the prothrombin time. If the CT scan shows no evidence
of hemorrhage and the cerebrospinal fluid is clear, anticoagulant treatment may be started
without delay. Some physicians prefer to wait for 2 to 3 days before intiating anticoagulant
treatment; the CT scan is then repeated and anticoagulant therapy is initiated if it again shows no
after onset (often difficult to determine) of stroke improves clinical outcome. Preliminary studies
suggest that calcium channel blocking drugs such as nimopidine (30mg orally every 6 hours for
four weeks) reduce deficit produced by cerebral ischemia and the morbidity and mortality rates
from stroke. Multicenter studies are now in progress to study further the effects of these agents in
calcium permeable channels, and studies in animals have shown that specific NMDA-receptor
antagonists reduce stroke size, deficits, and the percentage of severely ischemic neurons. The
Physical therapy has an important role in the management of patients with impaired
motor function. Passive movements at an early stage will help prevent contractures. As
cooperation increases and some recovery begins, active movements will improve strength and
coordination. In all cases, early mobilization and active rehabilitation are important.
Occupational therapy may improve morale and motor skills, while speech therapy may be
beneficial in patients with expressive dysphagia or dysarthia. When there is severe and persisting
motor deficit, a device such as a leg brace, toe spring, frame or cane may help the patient move
about, and the provision of other aids to daily living may improve the quality of life.
Source: Tierney, L. M., McPhee, S. J., & Papadakis, M. A. (2006). Current medical diagnosis &
Recent Studies
auditory sensory memory in patients who have suffered neural damage. Fifty-four patients in the
acute recovery phase following MCA stroke were divided into a music group, an audio book
group, and a control group. In order to index the patients' auditory sensory memory, magnetic
mismatch negativity (MMNm) responses to variations in the frequency and duration of sound
The authors found a significant increase in the frequency MMNm amplitude in the music
and audio book patients over that of the controls. Moreover, the audio book group showed a
greater increase in the duration MMNm amplitude than did the other 2 groups. Sarkamo et al
also found a correlation in the music group between frequency MMNm amplitude changes and
improvements in verbal memory and focused attention. The authors concluded that following
neural damage, patients can undergo long-term plastic changes in early sensory processing by
listening to music and speech. They suggested that such changes may help to restore higher
http://emedicine.medscape.com/article/323120-overview
UNITED STATES
The frequency of middle cerebral artery stroke (MCA stroke) is reported to be more than
80 cases per 100,000 people. According to Barnett and colleagues, most strokes occur in the
INTERNATIONAL
A systematic review of stroke incidence worldwide found that between 1970 and 2008,
stroke incidence decreased 42% in high-income countries and increased more than 100% in low-
to middle-income nations; between 2000 and 2008, the overall stroke incidence in low- to
middle-income countries was 20% higher than that in high-income countries. 3 This review did
not distinguish between middle cerebral artery strokes and other CVAs.
MORTALITY/MORBIDITY
A significant number of patients (15-30%) die from acute stroke within the first 30 days
after the event. Survival after hemorrhagic stroke is less common, with only a 20% survival rate.
Death in the first week after stroke is directly due to the stroke in 90% of cases. Pulmonary
embolism is the most common cause of death within 2-4 weeks of stroke. Pneumonia is the most
common cause of mortality within 2-3 months after the event. Thereafter, cardiac disease is the
higher risk for ischemic stroke. One study revealed the total prevalence to be 191 strokes per
100,000 people surveyed in the black population, 149 strokes per 100,000 people surveyed in the
Hispanic population, and 88 strokes per 100,000 people surveyed in the white population.
SEX
Males are affected by middle cerebral artery strokes more often than are females, with a male-to-
AGE
Risk of middle cerebral artery stroke (MCA stroke) increases with age. The highest incidence of
MCA strokes is in the seventh and eighth decades of life. Stroke in younger persons (aged 18-45
y) is far less common than in elderly persons. Hemorrhagic stroke is the most common etiology,
with intracranial hemorrhage accounting for 41% and subarachnoid hemorrhage accounting for
17% of strokes in persons in the younger age group. Studies reveal that dissection is an
underrecognized cause of stroke in younger populations. Still, even with advances in diagnostic
HYPERTENSION
When the ventricles contract, they force blood into large, thick-walled elastic arteries that
expand as the blood is pushed into them. The high pressure in these arteries forces blood to
continually move into areas where the pressure is lower. The pressure is highest in the large
arteries and continues to drop throughout the pathway, reaching zero or negative pressure at the
venae cavae.
through the blood vessels. It is increased by many factors, but probably the most important is the
also raise peripheral resistance. Any factor that increases either the cardiac output or peripheral
resistance causes an almost immediate reflex rise in blood pressure. Many factors can alter blood
pressure, such as: age, weight, time of day of, exercise, body position, emotional state and
autonomic nervous system has little or no effect on blood pressure, but sympathetic division is
important and is responsive to many different factors. The major action of sympathetic nerves on
the vascular system is to cause vasoconstriction, or narrowing of the blood vessels, which
increases blood pressure. The sympathetic center on the medulla of the brain is activated to cause
vasoconstriction in many different circumstances. When we stand up suddenly after lying down,
the effect of gravity causes the blood to pull in the vessels of the legs and feet and the blood
pressure drops. This activates pressoreceptors (called baroreceptors) in the large arteries of the
neck and chest. They send of warning signs that result in reflexive vasoconstriction, which
increases blood pressure back to homeostatic levels. When blood volume suddenly decreases, as
in hemorrhage, blood pressure drops, and the heart begins to beat more rapidly ( as it tries to
compensate). However, because venous return is reduced by blood loss. The heart also beats
weakly and inefficiently. In such cases, the sympathetic nervous system causes vasoconstriction
to increase the blood pressure so that venous return increase and circulation can continue.
Marieb, E. N. (2008). Essentials of human anatomy & physiology (9. ed.). San Francisco, Calif.:
Benjamin Cummings ;.
MANILA, Philippines—High blood pressure has been established as a major risk factor for
stroke and the unfortunate thing about it is that most hypertensive patients have no symptoms.
• Less than half of hypertensive patients are aware that they have high blood pressure.
• Only about 10 percent, or even less, have adequately controlled high blood pressure.
Trivialize hypertension
What is quite tragic is that many hypertensive patients are aware that they have high blood
pressure, but since they have no symptoms, they trivialize their hypertension. Sadly, many of
these potential victims of the “silent killer” see no need and no strong motivation to take their
medicines religiously to make sure that their blood pressures are controlled to optimal levels.
Not until they develop a serious stroke or a heart attack do they realize what their wanton
disregard for their hypertension has cost them. And by then, it’s too late already.
The effective strategy therefore is quite obvious. If we can only make the 90 percent with
untreated or uncontrolled hypertension aware of the risk they are unduly exposed to, we can
significantly reduce the incidence of stroke and other cardiovascular complications in our
country.
Increase awareness
Hopefully, the I-Stroke campaign, spearheaded by Dr. Joey Navarro and Otsuka, and the
Therapharma, will significantly increase awareness on hypertension and stroke among Filipinos
and stem the tide of what could produce a population with many disabled stroke victims.
According to the World Health Organization, 15 million people worldwide will suffer from
stroke this year. Five million will die and another five million will be permanently disabled. In
the Philippines, stroke affects 486 out of 100,000 Filipinos or roughly half a million Filipinos,
according to Dr. Navarro in his study published in The Philippine Journal of Neurology.
many Filipinos at risk for stroke and its life-threatening complications,” explains Dr. Johnny
Once an individual develops signs and symptoms of stroke or brain attack, he should not delay
going to the hospital ER because time is of the essence to prevent more severe complications.
The symptoms of stroke are sudden weakness of the facial muscles, arm or leg, usually on one
One may also feel sudden numbness on one side of the body, confusion, difficulty in speaking or
understanding speech, blurring of vision in one or both eyes, difficulty in walking, dizziness, loss
The PNA and SSP are encouraging the establishment of specialized acute stroke units in all
tertiary hospitals to make sure that stroke patients are promptly and adequately treated with
medications and interventions that can prevent more severe, irreversible damage to the brain.
Currently, there are about 16 of these acute stroke units nationwide. Hopefully, most medical
centers will have such facility which will be a big boost in treating stroke patients and preventing
its complications.
104135/Stroke_prevention_campaigns
MYOCARDIAL INFARCTION AND ATHEROSCLEROSIS
Myocardial infarction (heart attack) is a serious result of coronary artery disease. Coronary
artery disease occurs from atherosclerosis, when arteries become narrow or hardened due to
cholesterol plaque build-up. Further narrowing may occur from thrombi (blood clots) that form
on the surfaces of plaques. Myocardial infarction occurs when a coronary artery is so severely
blocked that there is a significant reduction or break in the blood supply, causing damage or
death to a portion of the myocardium (heart muscle). Depending on the extent of the heart
muscle damage, the patient may experience significant disability or die as a result of myocardial
infarction.
spasm of a coronary artery. When this occurs, the artery narrows and the blood flow from the
artery is significantly reduced or stopped. Though the cause of coronary artery spasm is still
unknown, the condition can occur in both normal blood vessels and those partially blocked by
plaques.
http://www.imaginis.com/heart-disease/heart-disease-myocardial-infarction-heart-attack-1
Coronary artery bypass graft surgery involves the bypass of a blockage in one or more of
the coronary arteries using the saphenous veins, mammary artery, or radial artery as conduits or
replacement vessels. Before surgery, coronary angiography precisely locates lesions and points
During traditional CABG surgery, a median sternotomy incision is made so that the heart
and aorta can be seen. The client is placed on cardiopulmonary bypass (CPB) and the heart is
stopped (cardioplegia) using a solution of iced saline containing potassium. After the bypasses
have been performed, the client is taken off of the machine, and the heart takes over again. Three
different types of “less invasive” CABG surgery are also performed: (1) off-bypass CABG
performed through a median sternotomy with a smaller incision; (2) minimally invasive direct
bypass; and port-access CABG with femoral-to-femoral bypass and cardioplegia with a limited
incision. Many institutions are performing MIDCABG surgery. In off-bypass CABG, the surgery
is performed on a beating heart after a reduction in cardiac motion with several different
medications and devices. The benefit of this type of CABG surgery is the avoidance of the use of
Saphenous veins can be used as the new coronary artery. The distal end of the vein is
saturated to the aorta, and the proximal end is swen to the coronary vessel distal to the blockage.
The veins are reversed so that their valves do not interfere with blood flow. The internal
mammary artery (IMA) can also be grafted to a coronary artery. It is more routinely used to
revascularize the portion of the myocardium supplied by the left anterior descending (LAD)
artery. The disadvantage of the IMA is that more time is required to remove it and the mammary
artery is shorter. An advantage is that IMA grafts have greater chance of remaining patent.
Radial arteries have also been used in repeat CABG and when radiation therapy to the chest
makes it impossible to use the IMA. The radial artery has had excellent patency rates.
For clients who need revascularization of the anterior coronary arteries, MIDCABG is a
less invasive approach. The IMAs are used as conduits, and the client does not need to be placed
on CPB. MIDCABG surgery is less costly than traditional CABG surgery and is associated with
invasive bypass procedures found that fewer cardiac and pulmonary complications were reported
VALVE REPLACEMENT
When valvuloplasty is not a viable alternative (eg, when the annulus or leaflets of the
valve are immobilized by calcifications, severe fibrosis or fusion of the chordate tendinea,
papillary muscles, and leaflets below the valve), vavle replacement is performed. General
anesthesia and cardiopulmonary bypass are used for valve replacement s. Most procedures are
performed through a median sternotomy, although the mitral valve may be approached through a
right thoracotomy incision. Mitral, and more rarely aortic ,valve replacement can be performed
with minimally invasive techniques thatv do not involve cutting through the sternum.
Instead,incisions are only made in the upper or lower half part of the sternum or between ribs;
these incisions are 2 to 4 inches long. Some of these minimally invasive procedures are robot
assisted and the surgeon, watching a video display, uses a joystick to control the robot and
surgical instruments. With these procedures,patients have less bleeding,pain,risk for infection
and scarring. Hospital stays average3 days and recovery may be as short as 3 weeks.
After the valve replacement is visualized, the leaflets of the aortic or pulmonic valve are
removed, but some or all the mitral valve structures ( leaflets, chordae, and papillary muscles.)
are left in place to help maintain the shape and function of the left ventricle after the mitral valve
replacement. Sutures are placed around the annulus and then through the valve prosthesis. The
replacement valve is slid down the suture into position and tied into place. The incision is closed
and the surgeon evaluates the function of the heart and the quality of the prosthetic repair. The
patient is weaned from cardiopulmonary bypass, the surgical repair is often assessed in color
Before the surgery, the heart gradually adjusts to the pathology but the surgery abruptly
“corrects” the way blood flows through the heart. Complications unique to valve replacement are
related to sudden changes in intracardiac blood pressures. All prosthetic valve replacement create
a degree of stenosis when they are implanted in the heart. Usually the stenosis is mild and does
not affect heart function. If valve replacement was for a stenotic valve blood flow through the
heart is often improved. The signs and symtoms of the backward heart failure resolve in a few
hours or days. If valve replacement was for a regurgitant valve into which blood had been
regurgitating to achieve it’s optimal postoperative function. The signs and symptoms of of heart
failure resolve gradually as the heart function improves. Patients are at risk for may
surgical nursing (12th ed.). Philadelphia: Wolters Kluwer Health/Lippincott Williams &
Wilkins.
ATRIAL FIBRILLATION
Atrial fibrillation (A Fib) is the most common supraventricular dysrythmias encountered in the
Atriall fibrillation is characterized by rapid chaotic atrial depolarization from reentrant pathway.
Ectopic atrial foci produce impulses between 350 and 600 beats/min. at extremely rapid rates,
however, the entire atrium may not be able to recover from one depolarization wave before next
begins, resulting in mechanical and electrical disorganization of the atria without effective atrial
contraction. Small irregular baseline undulations that vary in the size and shape, called f waves,
are identified which differ from the formed “saw-toothed” waves atrial flutter. Similar to atrial
flutter, the AV node is bombarded with more impulses than it can conduct so a rapid ventricular
response comparable to the atrial rate cannot occur. Most if these impulses are blocked; however,
as a result of the erratic atrial impulses, the ventricular rhythm is very irregular. The ventricular
Examination of the ECG reveals erratic unidentifiable P waves and underlying ventricular
rhythm that reveals to be irregular. Because of atrial disorganization “atrial kick” is lost, thereby
decreasing cardiac outputby as much as 30%. With increasing ventricular rates allowing less
filling time, cardiac output declines even further and may result in dyspnea, angina pectoris,
heart failure and shock. The clinet may have a pulse deficit between apical and radical pulses.
Atrial fibrillation most commonly occurs because of the following:
Coronary artery disease, congestive heart failure, valvular heart disease (particularly mitral and
During atrial fibrillation, blood pools in the ‘quivering” atria because of lack of adequate
contraction of atrial appendages. Pooling blood is prone to clot, forming a mural thrombus, ,
which increases the risk of cerebral and peripheral vascular emboli. Most clients with sudden
onset of atrial fibrillation are given anticoagulant to reduce risk of thrombus formation and
embolic events. Approximately 20% to 25% OF CEREBRAL vascular accidents are due to
cardiogenic emboli.
Type 2 diabetes affects approximately 90% to 95% of people with the disease. It occurs
commonly among people who are older than 30 years of age and obese and Kidney Diseases,
although its incidence is rapidly increasing in younger people because of the growing epidemic
of obesity in children, adolescents, and young adults. The two main problems related to insulin in
type 2 diabetes are insulin resistance and impaired insulin secretion. Insulin resistance refers to a
decreased tissue sensitivity to insulin. Normally, insulin binds to special receptors on cell
surfaces and initiates a series of reaction involved in glucose metabolism. In type 2 diabetes,
these intracellular reactions are diminished, making insulin less effective at stimulating glucose
uptake by the tissues and at regulating glucose release by the liver. The exact mechanism that
lead to insulin resistance and impaired insulin secretion in type 2 diabetes are unknown, although
To overcome insulin resistance and to prevent the buildup of glucose in the blood,
incease amounts of insulin must be secreted to maintain the glucose level at a normal or slightly
hypercholesterolemia, and abdominal obesity. However of the beta cells cannot keep up with the
increased demand for insulin, the glucose level rises and type 2 diabetes develops.
Despite the impaired insulin secretion that is characteristic to type 2 diabetes, there is enough
insulin present to prevent the breakdown of fat and the accompanying production of ketone
bodies. Therefore, DKA does not typically occur in type 2 diabetes. However, uncontrolled type
syndrome. Because type 2 diabetes associated with a slow, progressive glucose intolerance, its
onset may go undetected for many years. If the patient experiences symptoms, they are
frequently mild and may include fatigue, irritability, polyuria, polydipsia, poorly healing skin
For most patient (approximately 75%), type 2 diabetes is detected incidentally (eg, when routine
diabetes is that long-term diabetes complications (eg, eye disease, peripheral neuropathy,
peripheral vascular disease) may have developed before the actual diagnosis of diabetes is made,
signifying that the blood glucose has been elevated for a time before diagnosis.
Source: Brunner, L. S., & Smeltzer, S. C. (2010). Brunner & Suddarth's textbook of medical-
surgical nursing (12th ed.). Philadelphia: Wolters Kluwer Health/Lippincott Williams &
Wilkins.
The pathogenesis of type 2 diabetes mellitus differs significantly from that of type 1. A limited
beta-cell response to hyperglycemia appears to be a major factor in its development. Beta cells
chronically exposed to high blood levels of glucose becoming progressively less efficient when
by normalizing glucose levels. The ratio of proinsulin (a precursor to insulin) to insulin secreted
also increases.
biologic activity of insulin in both the liver and peripheral tissues. The state is known as insulin
resistance, People with type 2 diabetes mellitus have a decreased sensitivity to glucose which
results in continued hepatic glucose production even with high blood glucose levels. This is
coupled with an inability of muscle and fat tissues to increase glucose uptake. The mechanism
causing peripheral insulin resistance is not clear; however it appears to occur after insulin binds
problems occur: (1) decreased glucose utilization, (2) increased fat mobilization, and (3)
require for fuel. Nerve tissues, erythrocytes, and the cells of the intestines, liver, and kidney
tubules do not require insulin for glucose transport. However, adipose tissues, along with skeletal
and cardiac muscle requires insulin for glucose transport. Without adequate amounts of insulin,
With inadequate amounts of insulin, blood glucose levels rise. The elevation continues because
the liver cannot store glucose as glycogen without sufficient insulin levels. In an attempt to
restore balance and return blood glucose levels to normal, the kidney excretes the excess glucose.
Glucose appears in the urine (glycosuria), acts as an osmotic diuretic and causes excretion of
In type 1 diabetes mellitus and occasionally with severe stress in type 2 diabetes mellitus, the
body turs to fat stores for energy production when glucose is unavailable. Fat metabolism causes
breakdown in products called ketones to form. Ketones accumulate in the blood and are excreted
through the kidneys and lungs. Ketone levels can be measured in the blood and urine; high levels
Ketones interfere with the body’s acid-base balance by producing hydrogen ions. The pH
can decrease, and metabolic acidosis can develop. In addition, when ketones are excreted,
sodium is also eliminated, sodium is also eliminated, resulting in sodium depletion and further
acidosis. The excretion of ketones also increases osmotic pressure, leading to increase fluid loss.
Also, when fats are the primary source of energy, body lipid levels can increase to five times
Lack of insulin leads to protein wasting. In healthy people, proteins are constantly being broken
down and rebuilt. In people with type 1 diabetes mellitus, without insulin to stimulate protein
synthesis, the balance is altered, which leads to increased catabolism (destruction). Amino acids
are converted to glucose in the liver, further elevating glucose levels. If this condition goes
untreated, clients with type 1 diabetes mellitus appear emaciated. The pathophysilogic processes
Clinical Manefistations
An elevated blood glucose level, called hyperglycemia, leads to common clinical manifestations
associated with diabetes mellitus. In type 1 diabetes mellitus, the onset of clinical manifestations
may be subtle with the possibility of life-threatening situations likely to happen (i.e., diabetic
ketoacidosis). In type 2 diabetes mellitus, the onset of clinical manifestations may develop so
gradually that clients may notice few or no clinical manifestations for a number of years.
(polyuria), increased thirst or fluid intake (polydipsia), and, as the disease progresses, weight loss
Physical examination, medical history, and laboratory tests are employed to evaluate clients with
diabetes mellitus. Clinical manifestations suggest the presence of diabetes mellitus, but
A fasting blood glucose sample is drawn when the client has not ingested any nutrients other that
water for at least 8 hours. This blood sample generally reflects glucose level from hepatic
production. If the client is receiving a dextrose intravenous solution, results of the test must be
analyzed with that variable in the mind. In clients who are known to have diabetes mellitus, food
and insulin are withheld until after the specimen is obtained. The diagnosis of diabetes mellitus is
made when a client’s fasting blood glucose level is greater than 126 mg/dl. Values between 110
and 125mg/dl indicate an IFG. The fasting blood glucose measurement provides the best
mellitus.
Clients may also be diagnoses with diabetes mellitus based on clinical manifestations and a
casual (random) blood glucose level greater than 200mg/dl. A casual blood glucose sample can
be drawn any time of the day without regard to fasting. Elevated blood glucose levels may occur
after meals, after stressful events, in sample drawn from an IV site, or in cases of diabetes
mellitus.
A postload or postprandial (after a meal) glucose level can also be drawn and used to diagnose
diabetes mellitus. Postload blood glucose samples are drawn every 2 hours after a standard meal
and reflect the efficiency of insulin-mediated glucose uptake by peripheral tissues. Normally,
blood glucose level should return to fasting levels within 2 hours. A 2-hour postload glucose
level greater than 200mg/dl during oral glucose tolerance test (OGTT) is confirmation for a
In older adults, postload levels are higher, typically increasing by 5 to 10 mg/dl decade
after age 50 years because of the normal decline in glucose tolerance associated with aging.
Smoking and drinking coffee can lead to falsely elevated values at 2 hours, whereas strenuous
Glucose normally attaches itself to the haemoglobin molecule on a red blood cell. Once
attatched, it cannot dissociate. Therefore the higher the blood glucose levels, the higher the levels
of glycosylated haemoglobin (HbA1c). The term HbA1c is referred to as an A1C. The A1C is an
average blood glucose level measured over the previous 3 months. It is stated as a percentage
The ADA recommends that A1C testing be done routinely on all people with diabetes
mellitus. The A1C test should be done semiannually in client’s who have met the primary target
goal for glycemic control (<7%) and quarterly in clients who have not met the primary glucose
for goal for glycemic control. Conditions that increases erythrocyte turnover, such as bleeding,
pregnancy, or asplenia (absence of spleen as after splenectomy), lead to falsely low A1C
concentrations. High aspirin does, alcohol ingestion, uremia, elevated haemoglobin levels, and
Glucose also attaches to proteins, primarily albumin. The concentration of glycosylated albumin
(fructosamine) represents the average blood glucose level over the previous 7 to 10 days. This
measurement is useful when short-term determinations of average blood glucose level are
When the proinsulin produced by pancreatic beta-cells is broken apart by an enzyme, two
products are formed, insulin and connecting peptide, commonly called C-Peptide. Because C-
peptide and insulin are formed in equal amounts, this test indicates the amount of endogenous
insulin production. Clients with type 1 diabetes mellitus usually have no or low concentration of
C-peptide. Clients with type 2 diabetes mellitus tend to have normal or elevated levels of C-
peptide.
Ketonuria
Urine levels of ketones can be tested by clients’ use of dip-strips or tablets. The presence of
ketones in the urine (a condition called ketonuria) indicates that the body is using fat as a major
source of energy, which may result in ketoacidosis. Test results are indicated by the presence of
All clients with diabetes mellitus should test their urine for ketones during acute illness or stress,
when blood glucose levels are elevated (>240mg/dl), and when they are pregnant or have
Some testing strips detect ketones as well as glucose. Although urine testing is important for
checking ketones, urine testing for glucose is not a reliable method for monitoring.
Proteinuria
disease. Testing the urine for microalbuminuria shows early neurophaty, long before it would be
evidenton routine urinalysis. The ADA recommends that all clients with diabetes mellitus be
tested for microalbuminuria annually. Some clients, however, require more frequent testing to
detect progression of kidney disease related to adverse effects of certain medications on the
kidneys.
They key to managing diabetes mellitus to keep the blood glucose level as close to normal as
possible or within a target range that is agreed upon between the client and healthcare provider.
Self-monitoring blood glucose (SMBG) provides immediate feedback and data on blood glucose
levels. SMBG is recommended for all clients with diabetes mellitus, regardless whether they are
type 1, type 2, or gestational diabetes. SMBG is a way to know how the body responds to food,
The frequency and timing of SMBG depend on the needs and goals of each individual client. For
most clients with type 1 diabetes mellitus and pregnant women taking insulin, SMBG is
recommended three or more times daily. Testing should be done before each meal, before
bedtime, and possibly in the middle of the night. For clients with type 2 diabetes mellitus, the
frequency and timing of SMBG are mutually agreed upon by the client and health care provider.
If the client with type 2 diabetes are taking oral medications, they usually do not have to monitor
as often as someone with type 2 diabetes mellitus taking insulin. Extra times to SMBG level
• When starting an over-the-counter medication that affects the blood glucose levels (e.g.
steroid)
• When you think your glucose level is too high or too low
• When there is a change in your medication dose, eating plan, or physical activity.
Health promotion action for type 2 diabetes mellitus include the following:
• Exercising regularly
• Screening high risk individuals (i.e., people with family history of diabetes mellitus in the
than age 45 with any other risk factors, people with hypertension or hyperlipidemia;
clients with previous impaired flucose tolerance, women with previous gestational
diabetes mellitus or those who have had a baby weighing more than 9 pounds , and
glycemic control.
treating coexisting risk factors such as smoking, hypertension, hyperlipidemia, and use of
nephrotoxic drugs.
• Follow-up visits to assess for complications of diabetes mellitus and reinforce learning
needs
betalipoproteins as well as progressive azotemia. In contrast to all other renal disorders, the
proteinuria associated with diabetic nephropathy does not diminish with progressive renal failure
(patients continue to excrete 10-11 g daily as creatinine clearance diminishes). As renal failure
Hypertension develops wit progressive renal involvement, and coronary and cerebral
have hypertension. Once diabetic nephropathy has progressed to the stage of hypertension,
proteinuria, or early renal failure, glycemic control is not beneficial in influencing it course. In
dietary protein to 0.6 g/kg body weight per day are recommended. ACE inhibitors have been
shown to protect against deterioration in renal function in IDDM patients with clinical
that cannot be explained only by the antihypertensive action of these drugs. One long term study
using captopril (25 mg three times daily) showed a 50% reduction in the risk of the combined
end points of death, dialysis and transplantation in IDDM subjects with diabetic nephropathy and
clinical proteinuria. During initiation of ACE inhibitor therapy, the rare occurrence of persistent
serum createnine reaches 5 mg/dL, consultation with personnel at a center where renal
Dialysis has been of limited value in the treatment of renal failure due to diabetic
more promising and is the treatment of choice in cases where there are no contraindications such
• Stroke
blood supply to a part of the brain. Ischemic stroke is caused by a thrombotic or embolic
blockage of blood flow to the brain. Bleeding into the brain tissue or the subarachnoid space
causes a hemorrhagic stroke. Ischemic strokes account for about 83% of all strokes. The
remaining 17% of strokes are hemorrhagic. Cerebrovascular disorders are the third leading cause
of death in the United States and account for about 150,000 mortalities annually. An estimated
550,000 people experience a stroke each year. When second strokes are considered in the
estimates, the incidence increases to 700,000 per year in the United States alone. Stroke is a
leading cause of adult disability and a leading primary diagnosis in long-term care. More than 4
million stroke survivors are living with varying degrees of disability in the Unites States. Along
with a high death rate, strokes produce significant morbidity in people who survive them. Of
stroke survivors, 31% require assistance with self-care, 20% require assistance with ambulation,
71% have some impairment in vocational ability up to 7 years following the stroke, and 16% are
institutionalized.
Blood flow to the brain can be decreased in several ways. Ischemia occurs when the
blood supply to a part of the brain is interrupted or totally occluded. Ultimate survival or
ischemic brain tissue depends on the length of time it is deprived plus the degree of altered brain
metabolism. Ischemia is commonly due to thrombosis or embolism. Thrombotic strokes are more
Risk factors:
The incidence of stroke and stroke mortalities has gradually declined in many
risk factors. Modifiable risk factors can be reduced or eliminated through lifestyle changes.
Hypertension is the most important modifiable risk factors for both ischemic and hemorrhagic
stroke. Adequate blood pressure control is associated with a 38% reduction in stroke incidence.
Cardiovascular disease and atrial defibrillation are also associated with an increased risk
of stroke. Diabetes Mellitus increases the risk of stroke and morbidity and mortality after stroke.
• Diabetes Mellitus
There are 18.2 million people in the United States who have diabetes mellitus (DM). The
prevalence of this medical disorder increases with age. Half of all cases occur in people over the
age of 55, and it is estimated that 18% of the United States population over the age of 60 have
DM.Patients with DM are more prone to develop vascular diseases, including strokes. In addition
to being a deadly disorder in diabetics, stroke is a disabling disorder. Most stroke survivors are
left with some physical and/or cognitive deficits. Stroke is the leading cause of permanent
disability in the United States and it is the second leading cause of cognitive decline. Thus
healthcare providers who care for patients with DM should be knowledgeable about the
interrelationship between DM and stroke, as well as interventions that can minimize their
patients’ risk of primary and secondary stroke. In this article we will discuss epidemiologic
relationships between DM and stroke, effects of DM on outcome from stroke, and stroke
based epidemiologic studies conducted in the United States and Europe suggest that
An initial diagnosis of DM is often made at the time of acute hospitalization for stroke. For
example, in the Copenhagen Stroke Study, 75% of the diabetics had known DM prior to their
stroke, whereas DM was diagnosed in the remaining 25% of patients during hospitalization for
their stroke.
pathway. Risk factors may, or may not, be related to the etiology of the disease. Case control
studies of stroke patients and prospective epidemiologic studies have confirmed an independent
effect of diabetes on ischemic stroke in both men and women, with an increased relative risk in
that DM is a risk factor that plays an essential role in producing the vascular pathology
atherosclerosis, it is very likely that DM is a risk factor that plays an essential role in producing
the vascular pathology underlying ischemic stroke. Other established independent risk factors for
ischemic stroke include cigarette smoking, chronic hypertension, hyperlipidemia, and atrial
fibrillation. A substantial number of strokes are attributable to these risk factors. The population-
attributable risk is an estimate of the percentage of excess stroke in a population that is
attributable to a given risk factor. The population-attributable risk takes into account both the
prevalence and potency of a risk factor. In the United States chronic hypertension has the highest
to have a population-attributable risk of approximately 35%. This figure for DM is greater than
the estimates of the population-attributable risk for cigarette smoking (12.3%) and atrial
fibrillation (9.4%). Intracerebral hemorrhage (ICH) accounts for approximately 15% of strokes
in the United States. Most casecontrol studies examining the relationship between DM and ICH
have not concluded that DM is an independent risk factor for ICH. A cohort study, however,
conducted on over 20,000 middle-aged male cigarette smokers found that the presence of DM
A meta-analysis that combined this cohort study with 9 case-control studies suggested that DM
is a risk factor for ICH (RR=1.30; 95% CI, 1.02 to 1.67) DM is not, however, as potent a risk
factor for ICH as chronic hypertension since epidemiologic studies have consistently shown a
accounts for 5% of strokes in the western hemisphere. DM has not been found to be
The cerebrovascular system is comprised of large and small caliber arteries. The components of
the large arterial circulation are the extracranial and intracranial segments of the carotid and
vertebral arteries, and the other arteries that comprise the Circle of Willis (basilar artery, middle
cerebral arteries, anterior cerebral arteries, and the posterior cerebral arteries). Infarction
occurring in the distribution of these arteries is usually of thrombo-embolic origin. Small caliber
arteries comprise the microcirculation. These arteries are 100µm-400µm in diameter and they
supply blood to the white matter of the cerebral and cerebellar hemispheres, the thalami, the
basal ganglia, and brainstem parenchyma. Occlusion of a small artery is thought to be produced
by degenerative arterial pathology within the vessel wall. These arteriopathies include
occluded small artery is commonly called a lacunar infarction. DM has been independently
associated with two forms of large artery disease and with small artery infarctions detected by
a population-based cohort study of 1192 men and women examined at a 5-year interval,
progression of intima-media thickness on ultrasound studies of the common carotid artery (CCA)
and internal carotid artery (ICA) was approximately twice the rate in diabetics compared with
non-diabetics. Progression rate in the ICA was greater in patients with undiagnosed diabetes
Intracranial large artery atherosclerotic disease produces stenotic lesions within the
arteries that comprise the Circle of Willis. This arteriopathy is responsible for approximately
10% of all ischemic strokes. DM was found to be an independent risk factor for intracranial large
vessel occlusive disease in a hospital-based study of 166 patients with a first ischemic stroke or
In addition, the diabetic patients were more likely than non-diabetic patients to have had
a larger number of diseased vessels than non-diabetics. The greatest extent of intracranial large
vessel occlusive disease was seen in diabetics with high lipoprotein (a) levels, suggesting a
synergistic interaction between these two factors. DM is a well established risk factor for small
artery occlusive disease affecting the retina, kidneys, and cranial nerves. The role of DM in
cerebral small vessel occlusive disease is less well characterized. Autopsy studies have yielded
conflicting results, some of them suggesting a relationship between diabetes and lacunes, and
examine whether or not DM is an independent risk factor for stroke due to small vessel
occlusion.
DM not only significantly increases the risk of stroke, but also is a predictor of reduced survival
following stroke. Higher mortality rates from stroke have been reported in diabetics, compared to
non-diabetics in most 3,14-17 but not all studies. These studies demonstrate that the higher
mortality rate is present throughout the entire post-stroke time period. Mortality rates are higher
in diabetics during acute hospitalization for stroke, one year, and one decade after the stroke. DM
may affect the rate of recovery of neurologic function following a stroke. Lithner et al. reported
that four days after hospital admission, more stroke patients with DM than without DM were still
confined to bed. In the Copenhagen Stroke Study, patients with DM recovered more slowly than
non-diabetic patients; however the amount of neurological deficit at hospital discharge was
Prevention of stroke is divided into primary and secondary prevention. Primary prevention refers
interventions to prevent primary and secondary strokes in these patients, some of which are
outlined below.
Treatment of hyperglycemia
Glycemic control may have a protective effect in primary stroke prevention. The UKPDS-35
study was a prospective study of 3642 patients with a median follow-up of 10.4 years for all
cause mortality. The study investigators found stroke risk was decreased by 12% for every 1%
reduction in hemoglobin A1C, although this was not statistically significant (p=.035).
In this study, the hemoglobin A1C was reduced from a median of 7.9% to 7.0%. It is
possible that the impact on stroke risk would have been more profound if patients with worse
In the Veterans Administration feasibility trial, there was no benefit found on stroke
Despite the findings of these two studies, and the remaining uncertainty as to whether
tight diabetic control can significantly reduce risk of a first stroke, tight control has been shown
to prevent other vascular complications in the diabetic, and it may be inferred that stroke risk
may be reduced. In addition, improved diabetic control may reduce the progression of large
vessel atherosclerotic disease in the diabetic. The Atherosclerosis Risk in Communities Study
Investigators (ARIC) found that patients with previously undiagnosed DM were found to have an
even greater rate of progression of carotid atherosclerosis than known diabetics, suggesting that
early diagnosis and treatment of DM may help to prevent progression of large vessel disease. No
clinical trial assessing the utility of aggressive control of hyperglycemia in diabetic stroke
patients, with secondary stroke as an outcome, has been conducted. Thus we do not know
Source: Antonios N., Silliman S., 2005, Diabetes Mellitus and Stroke, from
http://www.dcmsonline.org/jax-medicine/2005journals/Diabetes/diab05g-stroke.pdf
GOUTY ARTHRITIS
Gout
Gout is a heterogeneous group or conditions related to a genetic defect or purine metabolism that
results in hyperuricemia. Over secretion of uric acid, or a combination of both, occurs. The
prevalence of gout is reported to be less than 1% to 15.3%, and it appears to be on the rise. The
incidence increases with age and body mass index. It occurs more commonly in males than in
appear to be consequences of faulty uric acid metabolism. Primary hyperuricemia may be caused
by severe dieting or starvation, excessive intake of foods that are high in purines (shellfish, organ
number genetic or acquired processes, including conditions in which there is an increase in cell
turnover (leukemia, multiple myeloma, some types of anemias, psoriasis) and an increase in cell
breakdown. Altered renal tubular function, either as a major action or as an unintended side
effect of certain pharmacologic agents (eg, diuretics such as thiazides and furosemide), low-dose
Pathophysiology
Hyperuricemia (serum concentration greater than 7mg/dl) can but does not always cause
monosodium urate crystal deposition (Becker & Jolly, 2005). However, as uric acid levels
increase, the risk becomes greater. Attacks of gout appear to be related to sudden increase or
decreases of serum uric acid levels. When the urate crystals precipitate within a joint, an
inflammatory response occurs, and an attack of gout begins. With repeated attacks,
accumulations of sodium urate crystals, called tophi, are deposited in peripheral areas of the
body, such as the great toe, the hands, and the ear. Renal urate lithiasis (kidney stones), with
The finding of urate crystals in the synovial fluid of asymptomatic joints suggests that factors
other than crystals may be related to the inflammatory reaction. Recovered monosodium urate
crystals are coated with immunoglobulins that are mainly IgG. IgG enhances crystal
Clinical Manifestations
Manifestations of the gout syndrome include acute gouty arthritis (recurrent attacks of severe
tissue, osseous tissue, soft tissue, and cartilage), gouty nephropathy (renal impairment), and uric
acid urinary calculi. Four stages of gout can be identified: asymptomatic hyperuricemia, acute
gouty arthritis, intercritical gout, and chronic tophaceous gout. The subsequent development of
gouty is directly related to the duration and magnitude of the hyperuricemia. Therefore, the
commitment to lifelong pharmacologic treatment of hyperuricemia is deferred until there is an
Medical Management
synovial fluid of the involved joint. Uric acid crystals are seen within the polymorphonuclear
tophi, joint destruction, and renal disorders is usually initiated after the acute inflammatory
process has subsided. Uricosuric agents, such as probenecid (Benemid), correct hyperuricemia,
and dissolve deposited urate. When reduction of serum urate level is indicated, uricosuric agents
are the medications of choice. If the patient has, or is at risk for, renal insufficiency or renal
calculi (kidney stones), allopurinol, a xanthine oxidase inhibitor, is also effective (Wortmann &
Kelley, 2005). Corticosteroids may be used in patients who have no response to other therapy. If
the patient experiences several acute episodes or there is evidence of tophi formation,
prophylactic treatment is considered. Specific treatment is based on the serum uric acid level.
Nursing Management
Although severe dietary restriction is not necessary, the nurse should encourage the patient to
restrict consumption of foods high in purines, especially organ meats, and to limit alcohol intake.
Maintenance of normal body weight should be encouraged. In an acute episode of gouty arthritis,
pain management with prescribed medications is essential, along with avoidance of factors that
increase pain and inflammation, such as trauma, stress, and alcohol. During the intercritical
period, the patient feels well and may abandon preventive behaviours, which may result in an
acute attack. Acute attacks are most effectively treated if therapy is begun early in the course.
Brunner, L. S., & Smeltzer, S. C. (2010). Brunner & Suddarth's textbook of medical-surgical
nursing (12th ed.). Philadelphia: Wolters Kluwer Health/Lippincott Williams & Wilkins.
PARKINSON’S DISEASE
Parkinson’s disease is a slowly progressing neurologic movement disorder that eventually leads
to disability. It is the fourth most common neurodegenerative disease, and 50,000 new cases are
reported each year in the United States (Chen and Fernandez, 2007; Thomure, 2006). The
disease affects men more often than women. Symptoms usually first appear in the fifth decade of
The degenerative or idiopathic form of Parkinson’s disease is the most common; there is
also a secondary form with a known or suspected cause. Although the cause of most cases is
excessive accumulation of oxygen free radicals, viral infection, head trauma, chronic use of
Pathophysiology
neuronal cells in the substantia nigra in the basal ganglia region of the brain. Fibers or neuronal
pathways project from the substantia nigra to the corpus striatum, where neurotransmitters are
(excitatory) and dopamine (inhibitory), striatal neurons relay messages to higher motor centers
that control and refine motor movements. The loss of dopamine stores in this area of the brain
Clinical symptoms do not appear until 60% of the pigmented neurons are lost and the
striatal dopamine level is decreased by 80%. Cellular degeneration impairs the extrapyramidal
tracts that control the semiautomatic functions and coordinated movements; motor cells of the
motor cortex and extrapyramidal tracts are not affected. Researchers are working on uncovering
the exact mechanisms of neurodegeneration; current theories suggest that it results from
oxidative stress in a portion of the neuron known as Lewy bodies, protein aggregation, or a
Clinical Manifestations
Parkinson’s disease has a gradual onset, and symptoms progress slowly over a chronic,
prolonged course. The cardinal signs are tremor, rigidity, bradykinesia (abnormally slow
Tremor
Although symptoms are variable, a slow, unilateral resting tremor is present in the majority of
patients at the time of diagnosis. Resting tremor characteristically disappears with purposeful
movement but is evident with the extremities are motionless. The tremor may manifest as a
rhythmic, slow turning motion (pronation-supination) of the forearm and the hand and a motion
of the thumb against the fingers as if rolling a pill between the fingers. Tremor is present while
the patient is at rest; it increases when the patient is walking, concentrating, or feeling anxious.
Rigidity
extremity may cause the limb to move in jerky increments, referred to as lead-pipe or cog-wheel
movements. Involuntary stiffness of the passive extremity increases when another extremity is
engaged in voluntary active movement. Stiffness of the arms, legs, face, and posture are
common. Early in the disease, the patient may complain of shoulder pain due to rigidity.
Bradykinesia
One of the most common features of Parkinson’s disease is bradykinesia, which refers to the
overall slowing of active movement. Patients may also take longer to complete activities and
have difficulty initiating movement, such as rising from a sitting position or turning in bed.
Postural instability
The patient commonly develops postural and gait problems. A loss of postural reflexes occurs,
and the patient stands with the head bent forward and walks with a propulsive gait. The posture
is caused by the forward flexion of the neck, hips, knees, and elbows. The patient may walk
faster and faster, trying to move the feet forward under the body’s center of gravity (shuffling
gait). Difficulty in pivoting causes loss of balance (either forward or backward). Gait impairment
and postural instability place the patient at increased risk for falls.
Brunner, L. S., & Smeltzer, S. C. (2010). Brunner & Suddarth's textbook of medical-surgical
nursing (12th ed.). Philadelphia: Wolters Kluwer Health/Lippincott Williams & Wilkins.
COPING OF PATIENTS WITH STROKE
Following a stroke, almost two-thirds of people turn to religion on a regular basis and
about 12 percent frequently use humor to cope with the stress that results from having a stroke.
who also found that about two-thirds of stroke patients use acceptance as a way to move forward
Results of the study, which showed that certain coping strategies enable people to adjust
better to life after a stroke, were presented at the American Heart Association's 27th International
The study evaluated the coping style and psychological adjustment of 56 stroke survivors
treated at the University of Maryland Medical Center (34 women and 22 men) one year after
their stroke. The most common strategies among the patients were turning to religion,
acceptance, and positive reinterpretation and growth, which means that they tried to find
something positive from their experience, shifted their priorities, and gained new appreciation for
their family and friends. Almost half of the patients studied used positive reinterpretation and
While many patients use a variety of coping strategies, the researchers looked at the most
and positive a year after their stroke," says the study's lead author, Lynn Grattan, Ph.D., an
"Turning to religion can also help patients cope effectively following a stroke, especially
if they are using it to seek strength to deal with the challenges they face," says Dr. Grattan.
The researchers also found that stroke patients who avoided addressing the issues related
to their stroke had higher levels of depression one year after the stroke. These individuals used
"behavioral disengagement" as a coping strategy, acting as though their stroke didn't happen and
diverting their attention away from activities that would help them with rehabilitation and
recovery. For example, they may have skipped follow-up doctor or physical therapy
prevent a future stroke. Behavioral disengagement was used frequently by seven percent of
avoiding the emotional and behavioral aspects of what they went through, Dr. Grattan says
patients who disengage are not dealing with natural feelings of loss and are not allowing
"We believe these findings are important to keep in mind as we work with patients early
"Two people with the same stroke-related disabilities can have very different outcomes.
One person may return to work and social activities, while the other may end up on permanent
disability. We believe pre-stroke personality and coping strategies play a major role in how well
Dr. Grattan says health care providers should first assess the patient's dominant coping
style and tailor therapy to that individual. "Through counseling, stroke support groups and other
methods, we can encourage patients to use the most effective coping strategies, especially during
the year following a stroke, to maximize their adjustment and recovery," she says.
In a related study, Dr. Grattan and her colleagues found that patients who had adjusted
most successfully one year after their stroke had received support from family and friends. The
most useful types of support included driving them to doctor appointments, picking up
prescriptions, and empathic listening, which means listening with sensitivity to the person's
Stroke is the leading cause of serious disability among adults. About 600,000 people
Dr. Grattan on the study: Natasha Kabitski, Marjan Ghahramanlou, Christopher Vaughan,
Source: Levitt, E.B.February 7,2002.University of Maryland study finds certain coping strategies
http://www.umm.edu/news/releases/stroke_recovery.htm
Coping Mechanism of Stroke Patients
Recovery from a stroke is easier if you make simple changes that help you cope better. You can
stay independent and productive by taking control of your health and daily life. All that is needed
Patients need to keep their movements strong and lively. You also need to keep blood pressure
and cholesterol under control to prevent complications or another stroke. Both practices help a
patient cope with the condition of restricted blood flow and circulation, and the weakening of
muscles from inactivity. Regular walking strengthens muscles and the cardiovascular system.
Weight lifting or tai chi can make you stronger and raise your conditioning so you can have a
Diet
Liveliness in daily activities depends upon a controlled weight and low blood pressure and
cholesterol. Eat a healthful diet low in salt, fat and sugars. Vegetables, fiber-rich whole grain
breads and chicken or fish are good for controlling your weight and cardiovascular system.
Daily Living
Daily living can be difficult after a stroke if you do not make changes to your home. With less
control, balance and vision on one side of your body, walking through the home can be
obstructed by a narrow doorway or end in slips or falls. A patient needs clear access to each part
of the house. If necessary, paths are wide enough for walking with a walker or cane, or moving
in a wheelchair. Reorganizing the furniture so all pathways are clear is a wise choice. Danger can
be avoided by removing throw rugs. Modifications also might be a good choice. Instead of
leaning on furniture or fixtures, you can install grab bars for walking stairs or entering the
Communications
When a patient has had a stroke in the left side of the brain, a disruption of communications
occurs due to loss of blood flow to the language center in the brain. This condition is called
aphasia. A patient with aphasia has difficulty forming words to speak or write, or can not
understand when others talk to them. Telling family and friends about the condition that is in the
way of communicating helps you cope with the difficulties in relating. Regular speech practice
Patients can be depressed or upset by living with the effects of a stroke. Life is made more vital
by staying engaged with family and friends, and staying active, to keep the emotions stable.
Encourage friends and family to check in with you and do social activities with you. Join a
support group with stroke patients who understand your condition. For vitality and pleasant
satisfaction, live a physically active life and do the things you enjoy.
http://www.ehow.com/about_5479458_coping-mechanism-stroke-patients.html
COPING OF FAMILIES WITH STROKE PATIENT
The victims of stroke are not the only ones who must deal with the devastating
consequences of this condition; their families also do as well. Sometimes families have to deal
with the shock of seeing a once capable individual suddenly deteriorate and need help for the
simplest things. Other times they may blame themselves for not spotting the vague signs of
stroke in the very short window of time that could have prevented further brain damage. Since
many stroke victims need to be convinced to go to the hospital if they are still conscious, a
family member may feel guilt over not being more convincing sooner. Many family members
have to alter their own plans such as employment or education to compensate for the family need
to care for the stroke victim. The families themselves are often overlooked when they have to
take a stroke victim to rehabilitation and doctors appointments, plus care for all the duties of the
household.
Relationships can be disrupted as family members may have to take on unfamiliar roles. Perhaps
the stroke victim supported the family or cared for another relative, and this upsets the balance of
the household when the rest of the family often have to pick up the victim's responsibilities and
learn how to be a caretaker at the same time. A large part of how your family works and interacts
with each other - whether as caretaker, breadwinner, cook, or emotional support, is altered
quickly and replaced with tremendous responsibility. Some issues that families must deal with
include knowing how to handle the stroke victims employment, especially if they are self
employed and it is unclear if the person will be able to return to work in that capacity.
Should the family sell the business? Hire a new person to help out? How long do they hold on to
the family business if it is losing money? Does the victims insurance issue from the business, and
will it be affected if the business is sold or closed? Can you afford to keep the business and the
home if the business is not generating money? It is not much easier to decide about a job either,
perhaps they will rehabilitate to a reasonable degree, but what if it takes a few years? This sort of
problem makes long term financial decisions very difficult, such as what is to be done about the
children's' education if the school of choice may not be an option if adequate income may not
exist, yet the child cannot necessarily plan on scholarships due to financial need if this cannot be
Since many stroke victims may feel frustration and perhaps an altered personality, they may be
very short tempered with those who care for them. While the victim themselves is reliant upon
the family often for basic things such as being driven somewhere or caring for financial tasks or
tasks that require coordination, it is hard to feel and act grateful for help doing something they
likely feel they should be able to do themselves. This makes caring for a stroke victim very
stressful, especially since the responsibility doesn't let up for the family members. This can
severely affect the family by affecting their own health as they are often too busy to care for their
own needs and they never get a day off. It is also difficult dealing with a stroke altered
personality that you may not necessarily like. A formerly kind and patient person may have their
higher cortical functions altered enough to just not act like the person you know, and often, the
complete opposite - impulsive, emotional, harsh, and anxious.
However, the same stroke victim may be able to carry on short conversations with others in a
pleasant manner, such as a phone call, a visit, or dealing with a stranger for a short period of
time. Because of this, personality changes may not be recognized by non-family members who
do not see the person as altered. Doctors may be greeted pleasantly and treated well by the stroke
victim and therefore not take caretakers concerns seriously when they state that the stroke victim
acts differently at home. Such isolation is often burdensome to caretakers who feel like the stroke
victim has only changed their behavior towards them. Not recognizing that polite chit chat and
manner towards others and coping with day to day needs and emotions are not the same,
caretakers are left confused about the emotions they see and often feel little can be done to fix
things.
If you have a friend or family member who cares for a stroke victim, often they can use a day or
afternoon off, even if just to take a nap. You may not be a professional caretaker, but when
store or drive them somewhere. Even coming over with a few favorite movies of the stroke
victim or some favorite music to listen to will give the caretaker a bit of a break, often help cheer
up the stroke victim and will not require you to make too much conversation with the stroke
victim themselves if you do not know them very well or do not know what to say. While difficult
to do in practice, try not to take any remarks the stroke victim makes to you too seriously if they
seem altered.
It is also important for family members to try to take turns so that all the burdens do not fall on
one person. While you may be taking more than your share, if you are not dealing with the care
of the person each day like the main caretaker is, then you are not dealing with the same
emotional burdens that the main caretaker does. Even having a another person in the house
alleviates some of the burden so that the caretaker can concentrate on other duties without being
overly concerned about the whereabouts of a stroke victim if some else just comes by to visit or
NOM, Yahoo! Contributor Network (2007). Suffering a Stroke: Family Members are Victims of
http://www.associatedcontent.com/article/221766/suffering_a_stroke_family_members_are_pg
3.html?cat=5
hypothyroidism, silent myocardial infarction, TIA’s and dehydration and those who smoke are
among the high risk candidates for cerebrovascular accident, the third leading cause of death in
this age group. Although a ruptured blood vessel can be responsible for this problem, most
CVAs in elderly are caused by partial or complete cerebral thrombosis. Light headedness,
dizziness, headache, drop attack (feeling of being strongly and suddenly pulled to the ground),
and memory and behavioural changes are some of the warning signs of CVA. A drop attack is a
fall caused by a complete muscular flaccidity in the legs but with no alteration in consciousness.
Eliopoulos C. (2001), Gerontologiccal Nursing (5th ed.), Lippincontt Williams and Wilkins 530
OTHER DIAGNOSTICS
MCHC
Mean corpuscular hemoglobin (MCH) is the average amount of hemoglobin per red blood cell
in a blood sample. MCH is used to help diagnose the type (cause) and severity of anemia. When
MCH is low, this can mean a person has iron-deficiency anemia. This type of anemia can be
caused by insufficient iron in the diet or by blood loss. Blood loss, such as what might occur with
tumors in the colon and other parts of gastrointestinal tract, can cause low iron levels and a low
MCHC.
High MCH levels may indicate the presence of macrocytic anemia and can have a variety of
causes, including liver disease, and deficiencies of vitamin B12 and folic acid (folate). MCH is
http://coloncancer.about.com/od/glossary/g/MCH.htm
RDW
Red cell distribution width (abbreviated as RDW) is a measurement of the amount that
red blood cells vary in size. A cell is the smallest, most basic unit of life, that is capable of
existing by itself. Red blood cells help carry oxygen in the blood.
Electronic instruments are capable of analyzing the blood sample and detecting the pulses
that are produced by red blood cells. The stronger the pulses are, the greater the red blood cells
are in size. Likewise, the weaker the pulses are, the smaller the red blood cells are in size.
The normal RDW level is 10.2 to 14.5%. It is important to keep in mind that the ranges
mentioned above will be different depending on the machine used to do the blood test. Always
use the normal range printed on the lab report to decide what range is normal.
A high RDW (over 14.5%) means that the red blood cells vary a lot in size. There are
many possible reasons why the RDW level can be too high. To determine what the possible
cause of a high RDW level is, a comparison is made to the mean corpuscular
volume (abbreviated MCV). The MCV is the average amount of space occupied by each red
blood cell.
If both the RDW and MCV levels are increased, there are several possible causes. One
possible cause is liver disease. The liver is the largest organ in the body and is responsible for
filtering (removing) harmful chemical substances, producing important chemicals for the body,
and other important functions. Another cause of high RDW & MCV levels is hemolytic anemia.
Hemolytic anemia is a condition in which the red blood cells are destroyed earlier than they
should be.
The RDW and MCV levels can both be increased if there is too little vitamin B12 or folic
acid (a type of vitamin) in the body. A vitamin is one of a group of substances made up partly of
carbon (an element) that are essential in small amounts for normal bodily functioning and
Another scenario is that the RDW level can be high, but the MCV level can be low. This
can happen because of iron deficiency anemia. Iron deficiency anemia is a decrease in
hemoglobin in the blood that is caused by an inadequate supply of iron. Hemoglobin is substance
present in red blood cells that help carry oxygen to cells in the body. Iron is needed to make
hemoglobin.
Another cause of a high RDW level and a low MCV level is thalessemia intermedia.
Thalessemia intermedia is another type of blood disorder in which there is impaired production
of one or more of the elements that make up hemoglobin. If the red blood cells are fragmented
(broken) into smaller parts, this can cause the RDW to be high and the MCV to be low. In this
situation, the red blood cells vary in size when they are broke up (which is why the RDW level is
high) but the cells do not take up much space (which is why the MCV level is low).
A final possibility is that the RDW level is increased and the MCV level is normal. This can
be caused by the beginning stages of a decrease in vitamin B12 or folic acid (a type of vitamin)
in the body. It can also be caused by the beginning stages of iron deficiency anemia, which was
reason for a low RDW level is macrocytic anemia. Macrocytic anemia is a blood disorder in
which not enough red blood cells are produced, but the ones that are present are large. Another
cause of a low RDW level is microcytic anemia. Microcytic anemia is a condition in which
abnormally small red blood cells are present. In these two disorders the red blood cells do not
vary much in size because they are either all small or all large. This is what causes the RDW
level to be low.
http://www.medfriendly.com/redcelldistributionwidth.html
HbA1c
In the blood stream are the red blood cells, which are made of a molecule, haemoglobin. Glucose
A1C or HbA1C. The more glucose in the blood, the more haemoglobin A1C or HbA1C will be
Red cells live for 8 -12 weeks before they are replaced. By measuring the HbA1C it can tell you
how high your blood glucose has been on average over the last 8-12 weeks. A normal non-
The HbA1C test is currently one of the best ways to check diabetes is under control; it is the
blood test that gets sent to the laboratory, and it is done on the spot in some hospital clinics.
If your diabetes is controlled (basically an HbA1C lower than 7%), every 3-6 months.
But if the last reading is above 7% and you are in reasonable health, you will need to achieve a
lower level if possible, and the next reading should be sooner. This assumes you will make
changes to improve your control. There is no point in having your HbA1c measured if you are
not trying to achieve good control of your diabetes, although the level does predict the likelihood
Glucose levels fluctuate from minute to minute, hour to hour, and day to day. Thus for hour to
The HbA1C level changes slowly, over 10 weeks, so it can be used as a 'quality control' test.
In diabetes glucose tend to rise more than usual, dropping with exercise, rising after food, rising
a lot more after sweet food, and can make it hard to control.
• >6.5% = diabetes
http://medweb.bham.ac.uk/easdec/prevention/what_is_the_hba1c.htm
Lilian Anekwe (2010). Diabetes work to soar under HbA1c switch. Retrieved from Pulse Today:
http://www.pulsetoday.co.uk/story.asp?storycode=4125181
The urinary tract is comprised of the kidneys, ureters, bladder, and urethra A urinary
bacteria, fungi, or parasites) in any of the structures that comprise the urinary tract.
However, this is the broad definition of urinary tract infections; many authors
prefer to use more specific terms that localize the urinary tract infection to the
infection).
Other structures that eventually connect to or share close anatomic proximity to the
urinary tract (for example, prostate, epididymis, and vagina) are sometimes
included in the discussion of UTIs because they may either cause or be caused by
UTIs. UTIs are common, more common in women than men, leading to
Although some infections go unnoticed, UTIs can cause problems that range from dysuria
(pain and/or burning when urinating) to organ damage and even death.
The kidneys are the active organs that, during their average production of about 1.5 quarts
of urine per day, function to help keep electrolytes and fluids (for example,
potassium, sodium, water) in balance, assist removal of waste products (urea), and
produce a hormone that aids to form red blood cells. If kidneys are injured or
The most common causes of UTI infections (about 80%) are Escherichia coli bacterial
strains that usually inhabit the colon. However, many other bacteria can
Proteus, Staphylococcus, Mycoplasma, Chlamydia, Serratia and Neisseria spp) but are
far less frequent causes than E. coli. In addition, fungi (Candida and Cryptococcus)
Schistosoma causes other problems, with bladder infections as only a part of its
There are many risk factors for UTIs. In general, any interruption or impedance of the usual flow
of urine (about 50 cc per hour in normal adults) is a risk factor for a UTI. For example, kidney
stones, urethral strictures or any anatomical abnormalities in the urinary tract increases infection
risk. This is due in part to the flushing or wash-out effect of flowing urine; in effect the
pathogens have to "go against flow" because the majority of pathogens enter through the urethra
and have to go retrograde (against a barrier, urine flow) to reach the bladder, ureters, and
eventually the kidneys. Many investigators suggest that women are far more susceptible than
men to UTIs because their urethra is short and its exit (or entry for pathogens) is close to the
People who require catheters have an increased risk (about 30% of patients with indwelling
catheters get UTIs) as the catheter has none of the protective immune systems to eliminate
The caregiver should obtain a detailed history from the patient, and if a UTI is suspected, a urine
sample is usually obtained. The best sample is a midstream sample of urine placed in a sterile
cup because it usually contains only the pathogenic organisms instead of the transient organisms
that may be washed from adjacent surfaces when the urine stream begins. Male patients with
foreskin should retract the foreskin before providing a midstream urine sample. In some patients
who cannot provide a midstream sample, a sample can be obtained by a catheter. The urine
Most UTIs cause no complications if they spontaneously resolve quickly (a few days) or if
treated early in the infection with appropriate medications. However, there are a number of
complications that can occur if the UTI becomes chronic or rapidly advances. Chronic infections
may result in urinary strictures, abscesses, fistulas, and kidney damage. Rapid advancement of
A good prognosis is usual for spontaneously resolved and quickly treated UTIs. The prognosis
begins to decline if the UTI is not quickly recognized or treated. Elderly and immunodepressed
patients may not have the UTI recognized early; their prognosis may range from fair to poor,
depending on how much damage is done to the urinary tract or if complications like sepsis occur.
Like adults, most adequately treated children will have a good prognosis. Children and adults
with recurrent UTIs may develop complications and a worse prognosis; recurrent UTIs may be a
Many methods have been suggested to reduce or prevent UTIs. Some of these are considered
home remedies and have been discussed (see above home remedies section). There are other
suggestions that may help prevent UTIs. Good hygiene for males and females is useful; for
females, wiping from front to back helps keep pathogens that may reside or pass through the anal
Incomplete bladder emptying and resisting the normal urge to urinate can allow pathogens to