pathophysiolgy exam 2
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8/6/2019 Pathophysiolgy Exam 2
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1. A 25-year-old female is admitted to the hospital after suffering a seizure. She has no
personal history of seizures in the past. On admission, an MRI scan demonstrates that the
patient has multiple sclerosis.
a. When the nurse meets the patient, the patient asks him if he can explain what multiple
sclerosis is. Can you simply explain the pathophysiology of this disease. (6 points)
b. What clinical features (signs and symptoms) should the nurse expect to see in a
patient with this disease? (6 points)
Because MS can affect any area of the brain, optic nerve, or spinal cord, MS can cause almost
any neurologic symptom. Typical relapses of MS involve episodes of numbness, weakness, or dyscoordination affecting an arm, a leg, or both. Disease localized to the spinal cord can cause
sensory or motor changes involving one side of the body or below a certain spinal cord level(i.e., hemiparesis or paraparesis). Brainstem involvement can manifest as diplopia, alteredsensation in the face, or ataxia. Inflammation of the optic nerve (optic neuritis) usually manifests
as blurry vision with painful eye movements.
Of all the lesions in MS, cerebral lesions are most common, but they cause the fewest symptoms.
Very large cerebral lesions can manifest with weakness or numbness and rarely cause aphasia or other cortical dysfunction. Most cerebral lesions are not in eloquent regions and so are clinically
silent and identified only by brain MRI. Lhermitte's sign is a nonspecific sign, whereby flexion
of the neck causes an electric shock–like shooting sensation extending into the arms or down the back. Lhermitte's sign is believed to arise from partially demyelinated tissue, whereby
mechanical stimulation leads to axonal activation.
Other common symptoms of MS include bladder and bowel dysfunction, decreased memory,
fatigue, and affective disorders such as depression. Although these symptoms are not uncommonat the diagnosis of MS, they are also nonspecific and can be seen in a multitude of disorders.
c. Your text states “MS is a disease of the CNS neurons.” In your own words, explain
the four clinical courses (pathways) that may occur in this condition. (6 points)
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2. A patient was admitted to the emergency room after being in a car accident. He hit his
forehead on the windshield and had a short loss of consciousness. The admittingdiagnosis is a contusion of the frontal lobe.
a. Review the functions of the frontal lobe and describe what type of clinicalmanifestations (signs and symptoms) the nurse might expect to find in this patient.
(6 points)
The frontal lobe involved in higher mental function. The function of the frontal lobes
involves the ability to recognize future consequences resulting from current actions,
override and suppress unacceptable social responses, and determine similarities and
differences between things or events. Additionally, the frontal lobe plays an important part
in retaining longer term memories which are not task-based. These are often memories
associated with emotions derived from input from the brain's limbic system. The frontal
lobe modifies those emotions to generally fit socially acceptable norms .The frontal lobes
are considered our emotional control center and home to our personality. The frontal lobesare involved in motor function, speech, movement problem solving, spontaneity, memory,
language, initiation, planning, judgment, reasoning, impulse control, and social and sexual
behavior. There are important asymmetrical differences in the frontal lobes. The left
frontal lobe is involved in controlling language related movement, whereas the right frontal
lobe plays a role in non-verbal abilities.
Contusions are characterized by loss of consciousness associated with stupor and
confusion. Other characteristics can include tissue alteration and neurologic deficit without
hematoma formation, alteration in consciousness without localizing signs, and hemorrhage
into the tissue that varies in size and is surrounded by edema. The effects of injury
(hemorrhage and edema) peak after about 18 to 36 hours. Patient outcome depends on thearea and severity of the injury.
Some clinical manifestations the nurse should expect to find include:
• Paralysis: Disturbance of motor function is typically characterized by loss of fine
movements and strength of the arms, hands and fingers.
• Broca's Aphasia or difficulty in speaking or inability to express language.
• Difficulty in interpreting feedback from the environment: Perseverating on a
response, risk taking, and non-compliance with rules, and impaired associated
learning (using external cues to help guide behavior) are a few examples of this type
of deficit.• Inability to plan a sequence of complex movements needed to complete multi-
stepped tasks, such as making coffee
• Loss of spontaneity in interacting with others.
• Loss of flexibility in thinking.
• Attending which is an inability to focus on task
• Mood changes
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• Changes in personality. A person's personality can undergo significant changes
after an injury to the frontal lobes, especially when both lobes are involved. There
are some differences in the left versus right frontal lobes in this area. Left frontal
damage usually manifests as pseudo depression and right frontal damage as pseudo
psychopathic.
•Difficulty with problem solving.
• One of the most common effects of frontal damage can be a dramatic change in
social behavior.
a. If this patient had sustained an injury to the back of his head and his hindbrain, what
body functions could be affected? List at least 3 body functions. (6 points)
The hind brain consists of the cerebellum the medulla oblongata and the Pons. The
cerebellum, located at the base of the skull, controls balance and equilibrium coordination
of voluntary motor movement and muscle tone. The medulla lies next to the spinal cord.
The medulla contains part of the reticular formation, including nuclei that control vital
functions such as regulation of the cardiovascular system, respiration, and skeletal muscle
tonus. The Pons is an integral part of the brain’s pathways. It is an important sensory relay
system that provides information to the cerebellum, cerebrum, and spinal cord. It playsimportant role in arousal, sleep, relaying sensory information between cerebrum and
cerebellum and assisting control of autonomic functions. The Pons also functions as a
motor relay center.
Damage to the hind brain can affect body functions various body functions which includes
Loss of ability to walk, inability to reach out and grab objects, tremors, dizziness (Vertigo),
slurred speech (Scanning Speech) and inability to make rapid movements. Specifically,
damage to the medulla oblongata can affect autonomic functions such as respiration and
heart rate and damage to the cerebellum impairs fine motor skills, such as writing typing
or playing a musical instrument
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e. What are the effects of hypercapnia on the central nervous system? (6 points)
Hypercapnia refers to a state of increased carbon dioxide in the blood. Carbon dioxide is much
more easily diffused than oxygen; therefore, hypercapnia presents only in cases of severe
alveolar hypoventilation and subsequent hypoxia. Conditions that inhibit ventilation or promote
trapping of air in the alveoli contribute to the development of hypercapnia. The major effect isrespiratory acidosis caused by CO2 retention. This can lead to electrolyte disturbances, which can
alter cardiac conduction and brain function, resulting in an ineffective heart rhythm, coma, and
death. The determination of the level of hypercapnia requires measurement of arterial bloodgases.
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4. T.J. is a 6-year-old boy who was rushed to the emergency room disoriented. His parents
report that he has been really thirsty over the past few weeks; he has been waking up two
to three times per night asking for water. He has also started wetting his bed again,something he has not done for more than a year. Additionally, he has been really tired
although he has been eating a lot. However, the waist of his pants has become very loose.
At the hospital, his blood sugar level was 423mg/dL. His urine was positive for ketones.He was then diagnosed with diabetes mellitus.
a. What type of diabetes does T.J. most likely have? T.J has Type 1 diabetes which is
also known as Juvenile onset diabetes and insulin dependent diabetes.
Please explain why you chose this answer. (6 points)
I chose Type 1diabetes mellitus based on the information given: the age of the child, the
clinical manifestations, the tests done and the knowledge acquired about diabetes.
Diabetes mellitus is a chronic metabolic disorder caused by an absolute or relative
deficiency of insulin. Insulin is produced by the beta cells of the islets of Langerhans
located in the pancreas, and the absence, destruction, or other loss of these cells results in
type 1 diabetes (previously known as insulin-dependent diabetes mellitus (IDDM) or
juvenile-onset diabetes)). Most children with diabetes have type 1 diabetes mellitus and a
lifetime dependence on exogenous insulin.
The case study states T.J is six years old. Type 1 diabetes tends to occur in young, lean
individuals, usually before 30 years of age, however, older patients do present with this
form of diabetes on occasion. Type 2 diabetes is more common in persons over the age of 30
and in the obese.
The clinical manifestations of type 1 diabetes mellitus are related to severe hyperglycemia
and hyperketonemia, as well as to inadequate energy and nutrient metabolism. The clinical
manifestations most commonly associated with type 1 diabetes include: polydipsia
(excessive thirst), Polyuria (excessive urination), Polyphagia (excessive hunger).Other
symptoms include nocturia (urination at night), fatigue, lethargy, weight loss, and blurred
vision.
From the information given, this child has been having most of the symptoms mentioned
above: he has been experiencing polydipsia, polyuria, polyphagia, nocturia, weightloss and
lethargy.
The diagnosis of type 1 diabetes mellitus is based on a thorough patient history and
physical examination, including specific laboratory and diagnostic tests. The presence of
polyuria, polydipsia, polyphagia, weight loss, and fatigue, along with an elevation in the
fasting blood glucose above 126 mg/dL or the random blood glucose level above 200 mg/dl,
is usually sufficient for diagnosis. Checking urine for ketones can also provide information
on the presence of hyperketonemia; urine ketone levels are proportional to blood ketone
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levels. Noting well that urine should be free of protein, glucose, ketones, nitrite, leukocyte
esterase, crystals, and stones.
I can safely say that this child has diabetes mellitus type 1 based on the clinical
manifestations , his age as mentioned before and his laboratory and diagnostic tests. His
blood glucose levels were above 200mg/dl , it was 423mg/dl, and his urine containedketones.
b. What is the probable cause of this condition? (6 points)
The etiology of type 1 diabetes is multifactorial and includes both genetic and
environmental influences leading to autoimmune destruction of beta cells. Exposure to a
trigger in the environment, such as a virus or toxin, then stimulates cell-mediated
destruction and a process of autoimmunity that promotes destruction of the beta cells.
c. List 3 ways used to treat this condition. (6 points)
Three ways to treat this condition includes:
• Diet (Carbohydrate (food) intake)
• Exercise
• Insulin replacement therapy
The goal of treatment is to stabilize blood glucose levels within the expected range (70 to
120 mg/dL). Blood glucose levels are measured frequently using self-blood glucose
monitoring systems in T.J’s case, T.J’s parents will need to make sure his glucose levels
stay within a safe range by monitoring them as directed by the physical.
The aim of dietary management is to balance the child's food intake with insulin dose and
activity and to keep blood glucose concentrations as close as possible to reference ranges,
avoiding extremes of hyperglycemia and hypoglycemia. Food intake increases blood
glucose levels. Eating appropriate foods is for management of blood sugar level. Therefore,
food intake must equal the available insulin and metabolic needs of the body. The diet
should include complex carbohydrates, protein, and unsaturated fat sources while limiting
simple sugars, cholesterol, and saturated fats. Typically, the carbohydrate to insulin ratio
needed is around 10 to 15 grams of carbohydrate to 1 unit of rapid-acting insulin.
Exercise decreases blood glucose levels through increased glucose usage by muscle tissue.
Increases in exercise must be matched with reductions in insulin or increases in food
intake. hildren and their caretakers must be able to recognize and treat symptoms of
hypoglycemia. Hypoglycemia following exercise is most likely after prolonged exercise
involving the legs, such as walking, running or cycling. It may occur many hours after
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exercise has finished and even affect insulin requirements the following day. A large
presleep snack is advisable following intensive exercise.
Insulin replacement therapy is integral to the treatment plan for type 1 diabetes. Insulin is
destroyed in the gastrointestinal tract if taken orally, so it must be injected subcutaneously
via intermittent injections or with an insulin infusion pump. T.J’s parents are responsiblefor administering the right dosage of insulin as directed by the physician.
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People who have excess body fat — especially if a lot of it is at the waist — are
more likely to develop heart disease. Excess weight increases the heart's work. It
also raises blood pressure and blood cholesterol and triglyceride levels, and
lowers HDL ("good") cholesterol levels.
(6 points)
b. How would exercise have a positive effect on her cholesterol levels? (6 points)
Exercise burns calories, which helps to control cholesterol levels. Regular, moderate
physical activity increases HDL levels and reduces triglyceride levels, decreasing the
incidence of coronary events and reducing overall mortality risk. The goal for most people
is a total of 30 minutes of moderate exercise (such as brisk walking) on most days.
Atherosclerosis is thought to be an inflammatory disorder. Outline the role of macrophages in the formation of atherosclerotic plaques. (10 points)
Atherosclerosis is thought to begin as fatty streaks of lipids that are deposited in the intima
of the arterial wall. These lesions commonly begin early in life. Not all fatty streaks later
develop into advanced lesions. Genetics and environmental factors are involved in the
progression of these lesions. The development of atherosclerosis over many years involves
an inflammatory response, which begins with injury to the vascular endothelium. The
injury may be initiated by smoking, hypertension, and other factors. The presence of
inflammation has multiple effects on the arterial wall, including the attraction of
inflammatory cells, such as monocytes (macrophages). The macrophages ingest lipids,
becoming “foam cells” that transport the lipids into the arterial wall. Activatedmacrophages also release biochemical substances that can further damage the
endothelium, attracting platelets and initiating clotting .
Smooth muscle cells within the vessel wall subsequently proliferate and form a fibrous cap
over a core filled with lipid and inflammatory infiltrate. These deposits, called atheromas
or plaques, protrude into the lumen of the vessel, narrowing it and obstructing blood
flow .Plaque may be stable or unstable, depending on the degree of inflammation and
thickness of the fibrous cap. If the fibrous cap over the plaque is thick and the lipid pool
remains relatively stable, it can resist the stress of blood flow and vessel movement. If the
cap is thin and inflammation is ongoing, the lesion becomes what is called vulnerable
plaque. At this point, the lipid core may grow, causing it to rupture and hemorrhage into
the plaque.
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