NURS 6501 Week 9: Discuss Concepts of Psychological Disorders

Sample Answer for  NURS 6501 Week 9: Discuss Concepts of Psychological Disorders Included After Question
In this exercise, you will complete a 5-essay type question Knowledge Check to gauge your understanding of this module’s content.
Possible topics covered in this Knowledge Check include:

Generalized anxiety disorder
Depression
Bipolar disorders
Schizophrenia
Delirium and dementia
Obsessive compulsive disease

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WEEKLY RESOURCES
BY DAY 7 OF WEEK 9
Complete the Knowledge Check by Day 7 of Week 9.
A Sample Answer For the Assignment:  NURS 6501 Week 9: Discuss Concepts of Psychological Disorders
Title:  NURS 6501 Week 9: Discuss Concepts of Psychological Disorders

Question 1  

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A ten-year-old boy is brought to clinic by his mother who states that the boy has been listless and not eating. She also notes that he has been easily bruising without trauma as he says he is too tired to go out and play. He says his bones hurt sometimes. Mother states the child has had intermittent fevers that respond to acetaminophen. Maternal history negative for pre, intra, or post-partum problems. Child’s past medical history negative and he easily reached developmental milestones. Physical exam reveals a thin, very pale child who has bruises on his arms and legs in no particular pattern. The APRN orders complete blood count (CBC), and complete metabolic profile (CMP). The CBC revealed Hemoglobin of 6.9/dl, hematocrit of 19%, and platelet count of 80,000/mm3. The CMP demonstrated a blood urea nitrogen (BUN) of 34m g/dl and creatinine of 2.9 mg/dl. The APRN recognizes that the patient appears to have acute leukemia and renal failure and immediately refers the patient to the Emergency Room where a pediatric hematologist has been consulted and is waiting for the boy and his mother. The diagnosis of acute lymphoblastic leukemia (ALL) was made after extensive testing.   
 
Question 1 of 2: 
 
What is ALL?   

Selected Answer:  
ALL is a malignant bone marrow disease where there is a proliferation of early lymphoid precursors that replace the normal bone marrow hematopoietic cells. It is the most common type of leukemia in the US and cancer in children. The malignant cells (lymphoblasts) get arrested in the early development stages, which is caused by abnormal gene expression following abnormalities in the number of chromosomes or   translocations of chromosomes. When the lymphoblasts proliferate, the number of normal elements in the bone marrow which produce other lines of blood cells decrease.  This explains why most patients usually present with thrombocytopenia, anemia, and neutropenia. In other instances, the lymphoblasts can also infiltrate the beyond the bone marrow, to the lymph nodes, liver, and spleen, causing enlargement.  

Correct Answer:  
 
Acute lymphoblastic leukemia (ALL) is a malignant (clonal) disease of the bone marrow in which early lymphoid precursors proliferate and replace the normal hematopoietic cells of the marrow. ALL is the most common type of cancer and leukemia in children in the United States. 
The malignant cells of acute lymphoblastic leukemia (ALL) are lymphoid precursor cells (ie, lymphoblasts) that are arrested in an early stage of development. This arrest is caused by an abnormal expression of genes, often as a result of chromosomal translocations or abnormalities of chromosome number. 
These aberrant lymphoblasts proliferate, reducing the number of the normal marrow elements that produce other blood cell lines (red blood cells, platelets, and neutrophils). Consequently, anemia, thrombocytopenia, and neutropenia occur, although typically to a lesser degree than is seen in acute myeloid leukemia. Lymphoblasts can also infiltrate outside the marrow, particularly in the liver, spleen, and lymph nodes, resulting in enlargement of the latter organs. 

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Question 2  

A Sample Answer For the Assignment:  NURS 6501 Week 9: Discuss Concepts of Psychological Disorders
Title:  NURS 6501 Week 9: Discuss Concepts of Psychological Disorders

 
A ten-year-old boy is brought to clinic by his mother who states that the boy has been listless and not eating. She also notes that he has been easily bruising without trauma as he says he is too tired to go out and play. He says his bones hurt sometimes. Mother states the child has had intermittent fevers that respond to acetaminophen. Maternal history negative for pre, intra, or post-partum problems. Child’s past medical history negative and he easily reached developmental milestones. Physical exam reveals a thin, very pale child who has bruises on his arms and legs in no particular pattern. The APRN orders complete blood count (CBC), and complete metabolic profile (CMP). The CBC revealed Hemoglobin of 6.9/dl, hematocrit of 19%, and platelet count of 80,000/mm3. The CMP demonstrated a blood urea nitrogen (BUN) of 34m g/dl and creatinine of 2.9 mg/dl. The APRN recognizes that the patient appears to have acute leukemia and renal failure and immediately refers the patient to the Emergency Room where a pediatric hematologist has been consulted and is waiting for the boy and his mother. The diagnosis of acute lymphoblastic leukemia (ALL) was made after extensive testing.   
Question 2 of 2: 
 
How does renal failure occur in some patients with ALL?  
 
 
 
 

Selected Answer:  
In patients with ALL, renal failure occurs as a result of hyperuricemia and this can be at the point of diagnosis or active treatment. Cellular destruction during the metabolism of purine influences an increase in the levels of uric. Since major paths of excretion are through the kidneys, the urates can end up precipitating in the ureters or renal tubules resulting in symptoms of oliguria and subsequent acute renal failure.  
 

Correct Answer:  
 
Renal failure as a result of hyperuricemia can be associated with ALL, particularly at diagnosis or during active treatment. Uric levels rise as an end product of purine metabolism from cellular destruction. Because the major excretory pathway is through the kidneys, urates can precipitate in renal tubules or ureters and can lead to oliguria and acute renal failure. 

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Question 3  

A Sample Answer For the Assignment:  NURS 6501 Week 9: Discuss Concepts of Psychological Disorders
Title:  NURS 6501 Week 9: Discuss Concepts of Psychological Disorders

 
A 12-year-old female with known sickle cell disease (SCD) present to the Emergency Room in sickle cell crisis. The patient is crying with pain and states this is the third acute episode she has had in the last nine months. Both parents are present and appear very anxious and teary eyed. A diagnosis of acute sickle cell crisis was made. Appropriate therapeutic interventions were initiated by the APRN and the patient’s pain level decreased, and she was transferred to the pediatric intensive care unit (PICU) for observation and further management.   
 
Question 1 of 2: 
 
What is the pathophysiology of acute SCD crisis and why is pain the predominate feature of acute crises?   
 
 
 
 

Selected Answer:  
Vaso-occlusive crises occur in more than half of individuals who have homozygous HbS although frequency tends to vary. Potential triggers of crises may include; dehydration, hypoxemia, and potential changes in body temperature. Most people with HbSS have a chronic low level of pain in joint and bones.  RBCs with a sickle shape are stickier and have high amounts of adhesion molecules. During an inflammatory reaction, leukocytes release mediators which increase the adhesion of molecules to endothelial cells. These processes influence sickled erythrocytes to be arrested as they move into the microvascular compartment. The RBCs become stagnant and sluggish in inflamed vascular vessels increasing their likelihood to sickle, low oxygen tension, and obstruction. The lysed RBCs produce hemoglobin and the free hemoglobin can bind and inactivate nitric oxide, a vasodilator that also inhibits the aggregation of platelets. These processes influence a decrease in the Ph of blood which decreases the affinity of hemoglobin for oxygen increasing the amount of HbS that is deoxygenated in the tension of oxygen, and a predisposition to sickling. As the lungs receive less oxygen, there is a drop in PO2 which further influences sickling. The pain experienced   is caused by the lack of oxygen in major bones and organs and can result in  the death of vital organs  and ischemia.  
 

Correct Answer:  
 
Approximately half the individuals with homozygous HbS disease experience vaso-occlusive crises. The frequency of crises is extremely variable. Some individuals have as many as 6 or more episodes annually, whereas others may have episodes only at great intervals or none at all. Each individual typically has a consistent pattern for crisis frequency. Triggers of vaso-occlusive crisis include the following: 

Hypoxemia: May be due to acute chest syndrome or respiratory complications 
Dehydration: Acidosis results in a shift of the oxygen dissociation curve 
Changes in body temperature (eg, an increase due to fever or a decrease due to environmental temperature change) 

Many individuals with HbSS experience chronic low-level pain, mainly in bones and joints. Intermittent vaso-occlusive crises may be superimposed, or chronic low-level pain may be the only expression of the disease. 
Sickle RBCs express higher than normal amounts of adhesion molecules and are sticky. During inflammatory reactions, leukocyte release of mediators increases the expression of adhesion molecules on endothelial cells. These reactions further promote sickled erythrocytes to be come arrested during movement through the microvascular. The sluggish and stagnant red cells within the inflamed vascular vessels result in extended exposure to low oxygen tension, sickling, and vascular obstruction. Lysed sickle erythrocytes release hemoglobin and free hemoglobin can bind and inactivate nitic oxide (NO), which is a powerful vasodilator and inhibitor of platelet aggregation. Decreased blood pH reduces hemoglobin affinity for oxygen leading to an increasing fraction of deoxygenated HbS at any oxygen tension and predisposition to sickling. As less oxygen is taken up by hemoglobin in the lungs, the PO2 drops promoting additional sickling. 
The intense pain of an acute crisis is due to lack of oxygen to major organs and bones. The lack of oxygen leads to ischemia and organ death. 

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Question 4  

Needs Grading 

 
A 12-year-old female with known sickle cell disease (SCD) present to the Emergency Room in sickle cell crisis. The patient is crying with pain and states this is the third acute episode she has had in the last nine months. Both parents are present and appear very anxious and teary eyed. A diagnosis of acute sickle cell crisis was made. Appropriate therapeutic interventions were initiated by the APRN and the patient’s pain level decreased, and she was transferred to the pediatric intensive care unit (PICU) for observation and further management.   
Question 2 of 2: 
 
Discuss the genetic basis for SCD. 
 
 
 
 

Selected Answer:  
SCD comprises of all genotypes that contain at least one sickle gene where the HbS comprises half of the present hemoglobin such as HbSS (sickle cell anemia), HbS/b+ thalassemia, HbS/ b-0 thalassemia, and HbSC disease. The heterozygous form (carriers) have up to 40% of HbS, no anemia, hematuria, and isosthenuria. SCD causes an illness but the trait does not. However, individuals who inherit two sickle hemoglobin genes from both parents can have SCD  
 

Correct Answer:  
 
SCD denotes all genotypes containing at least one sickle gene, in which HbS makes up at least half the hemoglobin present. Major sickle genotypes described so far include the following: 

HbSS disease or sickle cell anemia (the most common form) – Homozygote for the S globin with usually a severe or moderately severe phenotype and with the shortest survival 
HbS/b-0 thalassemia – Double heterozygote for HbS and b-0 thalassemia; clinically indistinguishable from sickle cell anemia (SCA) 
HbS/b+ thalassemia – Mild-to-moderate severity with variability in different ethnicities 
HbSC disease – Double heterozygote for HbS and HbC characterized by moderate clinical severity 
HbS/hereditary persistence of fetal Hb (S/HPHP) – Very mild or asymptomatic phenotype 

Sickle cell trait or the carrier state is the heterozygous form characterized by the presence of around 40% HbS, absence of anemia, inability to concentrate urine (isosthenuria), and hematuria. Under conditions leading to hypoxia, it may become a  pathologic risk factor. Sickle cell disease produces illness, while sickle cell trait usually does not. People who inherit two genes for sickle hemoglobin (one from each parent) have sickle cell disease. With a few exceptions, a child can inherit sickle cell disease only if both parents have one gene for sickle cell hemoglobin 

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Question 5  

Needs Grading 

 
The parents of a 9-month boy bring the infant to the pediatrician’s office for evaluation of a swollen right knee and excessive bruising. The parents have noticed that the baby began having bruising about a month ago but thought the bruising was due to the child’s attempts to crawl. They became concerned when the baby woke up with a swollen knee. Infant up to date on all immunizations, has not had any medical problems since birth and has met all developmental milestones. Pre-natal, intra-natal, and post-natal history of mother noncontributory. Family history negative for any history of bleeding disorders or other major genetic diseases. Physical exam within normal limits except for obvious bruising on the extremities and right knee. Knee is swollen but no warmth appreciated. Range of motion of knee limited due to the swelling. The pediatrician suspects the child has hemophilia and orders a full bleeding panel workup which confirms the diagnosis of hemophilia A.     
 
Question 1 of 2: 
 
Explain the genetics of hemophilia. 
 
 
 
 

Selected Answer:  
Deficiencies in factor XI, VIII, and IX   are linked with up to 90% of hemorrhagic bleeding disorders. The most common and widely known are type A and B m which are inherited and have an X-linked recessive pattern. This implies that, the genes associated with both types of hemophilia are located on the X chromosome. In males, only a single of the altered gene is adequate to cause hemophilia. Sons inherit from the mother but will have normal clotting, and a 50% likelihood of having hemophilia. Girls inherit the X chromosome with the dominant gene from fathers thus will not have hemophilia. 
 

Correct Answer:  
 
Deficiencies in factor VIII, IX, and XI are associated with 90% of hemorrhagic bleeding disorders. Hemophilia A and hemophilia B are inherited in an X-linked recessive pattern. The genes associated with these conditions are located on the X chromosome, which is one of the two sex chromosomes. In males (who have only one X chromosome), one altered copy of the gene in each cell is enough to cause the condition. A son inherits his mother’s other X chromosome, he will have normal blood clotting. A carrier’s son has a 50% chance of having hemophilia. A baby girl will inherit an X chromosome with a dominant gene for normal blood clotting from her father. Therefore, the daughter will not have hemophilia. 

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Question 6  

Needs Grading 

 
The parents of a 9-month boy bring the infant to the pediatrician’s office for evaluation of a swollen right knee and excessive bruising. The parents have noticed that the baby began having bruising about a month ago but thought the bruising was due to the child’s attempts to crawl. They became concerned when the baby woke up with a swollen knee. Infant up to date on all immunizations, has not had any medical problems since birth and has met all developmental milestones. Pre-natal, intra-natal, and post-natal history of mother noncontributory. Family history negative for any history of bleeding disorders or other major genetic diseases. Physical exam within normal limits except for obvious bruising on the extremities and right knee. Knee is swollen but no warmth appreciated. Range of motion of knee limited due to the swelling. The pediatrician suspects the child has hemophilia and orders a full bleeding panel workup which confirms the diagnosis of hemophilia A.     
Question 2 of 2: 
Briefly describe the pathophysiology of Hemophilia. 
 
 
 
 

Selected Answer:  
Hemophilia A results from an acquired or inherited genetic mutation   which occurs following the deficiency or dysfunction of factor VIII, or an acquired inhibitor which binds to factor VIII.  One third of genetic cases are caused by de novo mutations that lack in a mother’s X chromosome. When factor VIII is inadequate, there amount of thrombin generated by FIXa and FVIIIa complexes in the intrinsic pathway of coagulation is inadequate. These processes combined with   the effect of tissue-factor pathway inhibitor, causes impaired clotting in case of injury, particularly in individuals with spontaneous bleeding in hemophilia.  
 

Correct Answer:  
 
Hemophilia A is caused by an inherited or acquired genetic mutation that results in dysfunction or deficiency of factor VIII, or by an acquired inhibitor that binds factor VIII. Of genetic cases, up to approximately one third are the result of de novo mutations not present in the mother’s X chromosome. 
Inadequate factor VIII results in the insufficient generation of thrombin by the FIXa and FVIIIa complex by means of the intrinsic pathway of the coagulation cascade. This mechanism, in combination with the effect of the tissue-factor pathway inhibitor, creates an extraordinary tendency for impaired clotting in response to trauma and, especially in persons with severe hemophilia, with spontaneous bleeding. 

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Question 7  

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During a routine 16-week pre-natal ultrasound, spina bifida with myelomeningocele was detected in the fetus. The parents continued the pregnancy and labor was induced at 38 weeks with the birth of a female infant with an obvious defect at Lumbar Level 2. The Apgar Score was 7 and 9. The infant was otherwise healthy. The sac was leaking cerebral spinal fluid and the child was immediately taken to the operating room for coverage of the open sac. The infant remained in the neonatal intensive care unit (NICU) for several weeks then discharged home with the parents after a prescribed treatment plan was developed and the parents were educated on how to care for this infant.   
 
Question 1 of 2: 
 
What is the underlying pathophysiology of myelomeningocele?  
 
 
 
 

Selected Answer:  
Defects of the neural tube are caused by teratogenic processes which result in abnormal differentiation and failed closure of the embryonic neural tube. They particularly occur between the 17th -30th day of gestation, at a time when a mother may fail to know if she is pregnant and the size of the fetus corresponds to that of a grain of rice. The most common neural tube defects are myelomeningocele and anencephaly. The latter occurs when the rostral end of the neural tube fails to close and there is an incomplete skull and brain formation. The former is caused by failure of the caudal end of the neural tube to close, leading to an open sac or lesion that contains a dysplastic spinal cord, skin, nerve roots, and meninges. In most cases, there’s always a direct correlation between the anatomic level of a myelomeningocele sac and a patients, sensory, motor, and neurologic deficits.    
 

Correct Answer:  
 
Neural tube defects are the result of a teratogenic process that causes failed closure and abnormal differentiation of the embryonic neural tube. Neural tube defects occur between the 17th and 30th day of gestation, at a time when the mother may not be aware that she is pregnant, and the fetus is estimated to be about the size of a grain of rice. 
The most common neural tube defects are anencephaly and myelomeningocele. Anencephaly results from failed closure of the rostral end of the neural tube, resulting in incomplete formation of the brain and skull. 
Myelomeningocele results from failed closure of the caudal end of the neural tube, resulting in an open lesion or sac that contains dysplastic spinal cord, nerve roots, meninges, vertebral bodies, and skin. The anatomic level of the myelomeningocele sac roughly correlates with the patient’s neurologic, motor, and sensory deficits. 

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Question 8  

Needs Grading 

 
During a routine 16-week pre-natal ultrasound, spina bifida with myelomeningocele was detected in the fetus. The parents continued the pregnancy and labor was induced at 38 weeks with the birth of a female infant with an obvious defect at Lumbar Level 2. The Apgar Score was 7 and 9. The infant was otherwise healthy. The sac was leaking cerebral spinal fluid and the child was immediately taken to the operating room for coverage of the open sac. The infant remained in the neonatal intensive care unit (NICU) for several weeks then discharged home with the parents after a prescribed treatment plan was developed and the parents were educated on how to care for this infant.   
Question 2 of 2: 
 
Describe the pathophysiology of hydrocephalus in infants with myelomeningocele.  
 
 
 
 

Selected Answer:  
The development of a myelomeningocele is linked to an abnormal development of the cranial neural tube. The most significant is the Chiari type II malformation which is primarily characterized by hypoplasia of the cerebellar and different degrees of caudal displacement of the lower brainstem through the foramen magnum to the upper cervical canal. This abnormality impedes the absorption and flow of CSF   resulting in hydrocephalus, that commonly occurs in most infants who have myelomeningocele  
 

Correct Answer:  
 
Myelomeningocele is associated with abnormal development of the cranial neural tube, which results in several characteristic CNS anomalies. The Chiari type II malformation is characterized by cerebellar hypoplasia and varying degrees of caudal displacement of the lower brainstem into the upper cervical canal through the foramen magnum. This deformity impedes the flow and absorption of cerebrospinal fluid (CSF) and causes hydrocephalus, which occurs in more than 90% of infants with myelomeningocele. 

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Question 9  

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A preterm infant was delivered at 32 weeks gestation and was taken to the NICU for critical care management. Physical assessment of the chest and heart remarkable for a continuous-machinery type murmur best heard at the left upper sternal border through systole and diastole. The infant had bounding pulses, an active precordium, and a palpable thrill. The infant was diagnosed with a patent ductus arteriosus (PDA).   
 
Question: 
 
Discuss the hemodynamic consequences of a PDA.  
 
 
 
 

Selected Answer:  
Normally, the ductus arteriosus is patent during the life of a fetus. This is vital for its development as it plays a major role in blood flow to other structures and organs of a fetus. Starting from the 6th week forward the ductus plays a significant role in outflow of the right ventricle and contributes to 60% of the total cardiac output in the entire life of a fetus. Only 5%-10% of the outflow goes through the lungs. Continuous production of prostaglandin E2 (PGE2) helps to maintain its patency, and closure before birth can result in right heart failure. This can be influenced by the use of NSAIDs by a mother leading to a PDA (left to right shunt) where blood goes from the systemic to the pulmonary circulation causing excess of pulmonary blood flow. This gradually reduces pulmonary compliance and engorgement.  
 

Correct Answer:  
 
The ductus arteriosus is normally patent during fetal life; it is an important structure in fetal development as it contributes to the flow of blood to the rest of the fetal organs and structure. From the 6th week of fetal life onwards, the ductus is responsible for most of the right ventricular outflow, and it contributes to 60% of the total cardiac output throughout the fetal life. Only about 5-10% of its outflow passes through the lungs. 
This patency is promoted by continual production of prostaglandin E2 (PGE2) by the ductus. Closure of the ductus before birth may lead to right heart failure. Prostaglandin antagonism, such as maternal use of nonsteroidal anti-inflammatory medications (NSAIDs), can cause fetal closure of the ductus arteriosus. 
Thus, a patent ductus arteriosus (PDA) produces a left-to-right shunt. In other words, it allows blood to go from the systemic circulation to the pulmonary circulation. Therefore, pulmonary blood flow is excessive (see the image below). Pulmonary engorgement results with decreased pulmonary compliance. The reaction of the pulmonary vasculature to the increased blood flow is unpredictable. 
Prematurity or immaturity of the infant at the time of delivery contributes to the patency of the ductus. Several factors are involved, including immaturity of the smooth muscle within the structure or the inability of the immature lungs to clear the circulating prostaglandins that remain from gestation. These mechanisms are not fully understood. Conditions that contribute to low oxygen tension in the blood, such as immature lungs, coexisting congenital heart defects, and high altitude, are associated with persistent patency of the ductus. 

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Question 10  

Needs Grading 

 
A 7-year-old male was referred to the school psychologist for disruptive behavior in the classroom. The parents told the psychologist that the boy has been difficult to manage at home as well. His scholastic work has gotten worse over the last 6 months and he is not meeting educational benchmarks. His parents are also worried that he isn’t growing like the other kids in the neighborhood. He has been bullied by other children which is contributing to his behaviors. The psychologist suggests that the parents have some blood work done to check for any abnormalities. The complete blood count (CBC) revealed a hypochromic microcytic anemia. Further testing revealed the child had a venous lead level of 21 mcg/dl (normal is < 10 mcg/dl). The child was diagnosed with lead poisoning and it was discovered he lived in public housing that had not finished stripping lead paint from the walls and woodwork.      Question:    How does lead poisoning account for the child’s symptoms?           Selected Answer:   The most vulnerable system to lead toxicity is the CNS system where children are more likely to develop toxicity and in adults, the peripheral nervous system is more prone to toxicity. Lead is a major inhibitor of sulfhydryl enzymes that increase the permeability of membranes increasing cerebral edema, ICP, and ischemia of tissues. This is followed by tissue atrophy and irreversible necrosis with subsequent changes in behavior, convulsions, reduced 1Q, coma and eventually death. The main manifestations in children include irritability, a decrease in activity, hyperactivity, temperamental lability and changes in behavior. In other instances, children may have symptoms similar to those of DHD and lower IQ. In very severe cases, children tend to present 3with convulsions, delirium, and encephalopathy. Anemia is caused by impaired heme synthesis, RBCs hemolysis and shortened survival of RBCs as well as it impairs the uptake and utilization of iron. The child’s skeletal system is affected since there is tertiary accumulation of calcium and lead phosphate which interferes with the growth of bones longitudinally   in long bone metastases that decreases the rate of growth  Correct Answer:     The neurological system is most vulnerable to lead toxicity.  Children are more likely to develop central nervous system toxicity while the peripheral nervous system is more often affected in adults. Lead inhibits sulfhydryl enzymes, which causes increase membrane permeability which causes increased intracranial pressure (ICP) and cerebral edema, tissue ischemia followed by irreversible necrosis and tissue atrophy with the final outcome of behavioral changes, decreased IQ, convulsions and eventually coma and death.  The manifestations in children include temperamental lability, irritability, behavioral changes, hyperactivity or decreased activity, loss of developmental milestones and language delay. Lower IQ and ADHD like symptoms may be present. Severe toxicity can cause delirium, convulsions and encephalopathy. Depression and anxiety are more common in patients. Lead causes demyelination of the peripheral nervous system and the abnormalities mostly affect the extensor motor nerves and may result in hand and foot drop.  Anemia may develop with lead poisoning due to impaired synthesis of heme, hemolysis of red cells and shortened red cell survival. Lead impairs uptake and utilization of iron.  The skeletal system is affected as lead is accumulated as tertiary lead phosphate and calcium. This interferes with longitudinal bone growth in the metaphases in long bones which decreased growth rate.  Response Feedback:   [None Given]           Question 11   Needs Grading        Emergency Medical Services (EMS) was dispatched to a home to evaluate the report of an unresponsive 3-month-old infant. Upon arrival, the EMS found a frantic attempt by the presumed father to resuscitate an infant. The EMS took over and attempted CPR but was unable to restore pulse or respiration. The infant was transported to the Emergency Room where the physician pronounced the child dead of Sudden Infant Death Syndrome (SIDS). The distraught parents were questioned as to the events surrounding the discovery of the baby. Parents state the child was in good health, had taken a full 6-ounce bottle of formula prior to being put down for the evening. The child had been sleeping through the night prior to this. Parents stated the baby had had some “sniffles” a few days before and was taken to the pediatrician who diagnosed the child with a mild upper respiratory tract viral syndrome. No other pertinent history.     Question:    What is thought to be the underlying pathophysiology of SIDS?           Selected Answer:   There are multiple hypotheses that describe the pathophysiology of SIDS. The most commonly known is the triple-risk model which suggests   that SIDS is a representation of   factors that intersect such as, a highly vulnerable infant   with intrinsic abnormalities in cardiorespiratory control, extrinsic trigger factors and a crucial period in the development   of homeostatic control mechanisms. Death happens when   the infant  is exposed t triggers and the  normal  defense mechanisms  may be developmentally, structurally, or functionally deficient.        Correct Answer:     Although multiple hypotheses have been proposed as the pathophysiologic mechanisms responsible for SIDS, none have been proven. A triple-risk model suggests that SIDS represents an intersection of factors, including the following:  A vulnerabl