NURS 6501 Knowledge Check Psychological Disorders

Sample Answer for NURS 6501 Knowledge Check 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

RESOURCES

Be sure to review the Learning Resources before completing this activity.
Click the weekly resources link to access the resources.

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 Knowledge Check Psychological Disorders

Title: NURS 6501 Knowledge Check Psychological Disorders

Question 1  

Needs Grading 

	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.  Response Feedback:   [None Given]

Question 2  

Needs Grading 

	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.  Response Feedback:   [None Given]

• Question 3  

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 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.  Response Feedback:   [None Given]

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  Response Feedback:   [None Given]

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.  Response Feedback:   [None Given]

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.  Response Feedback:   [None Given]

Question 7  

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 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.  Response Feedback:   [None Given]

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.  Response Feedback:   [None Given]

• Question 9  

Needs Grading 

	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.  Response Feedback:   [None Given]

• 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 vulnerable infant possessing intrinsic abnormalities in cardiorespiratory control  A critical period in the development of homeostatic control mechanisms  Exogenous extrinsic stressors (triggering factors)  Death occurs when vulnerable infants are subjected to stressors at times when normal defense mechanisms may be structurally, functionally, or developmentally deficient. Epidemiologic data suggest that genetic factors play a role, and many studies have attempted to identify SIDS-associated genes.  Response Feedback:   [None Given]

• Question 12  

Needs Grading 

	A 4-year-old female is brought to the pediatrician by her mother who states the child has been running a fever to 102.0 F, has “pink eye”, and that her tongue looks very bright red and swollen. The mother states the fever has been present for 5 days, noticed the child had developed a rash and that the child’s legs look “puffy”. No other symptoms noted. Past medical history noncontributory. All immunizations up to date. Physical exam remarkable for current fever of 102.8 F, bilateral conjunctivitis without purulent material, oral mucosa with bright red erythema, dry, with fissuring of the lips. Legs noted to have peripheral edema and are also erythematous. Palmar desquamation noted. There is fine maculopapular rash and + cervical adenopathy. The presumptive diagnosis currently (pending laboratory data) is Kawasaki Disease.     Question 1 of 2:    What is Kawasaki Disease and what is the pathophysiology?
	Selected Answer:   Also referred to as mucocutaneous lymph node syndrome, KD refers to an acute febrile illness that occurs in early childhood primarily characterized by vasculitis of medium-sized arteries. The laboratory findings for KD are consistent with leukocytosis, elevated ESR rate, hypoalbuminemia, hypoalbuminemia, elevated C-reactive protein (CRP), among other findings. It has four stages as follows;  Stage 1- edema of vascular media and endothelial cells.   Stage 2-occurs within 7-9 days after fever starts, there’s infiltration of neutrophils, and an inflammatory cascade which secret cytokines   Stage 3- replacement of inflammatory cells by  monocytes and fibroblasts, formation of fibrous connective tissue  in the blood vessel walls, proliferation and thickening of the intima. .  Stage 4- blood vessels scar, the intima thickens and  the coronary arteries calcify.     Correct Answer:     Kawasaki disease (KD), also known as mucocutaneous lymph node syndrome and Kawasaki syndrome, is an acute febrile illness of early childhood characterized by vasculitis of the medium-sized arteries. Laboratory findings include elevated erythrocyte sedimentation rate (ESR), elevated C-reactive protein (CRP), hypoalbuminemia, anemia, elevated alanine aminotransferase (ALT), thrombocytosis, leukocytosis, and pyuria.  The disease has 4 recognized stages:  Stage 1- endothelial cells and the vascular media become edematous, but the internal elastic lamina remains intact.  Stage 2-approximately 7-9 days after the onset of fever, an influx of neutrophils occurs, which is quickly followed inflammatory cells that secrete various cytokines that target the endothelial cells and result in a cascade of events that lead to fragmentation of the internal elastic lamina and vascular damage  Stage 3- the active inflammatory cells are replaced by fibroblasts and monocytes, and fibrous connective tissue begins to form within the vessel wall. The intima proliferates and thickens.  Stage 4- The vessel wall eventually develops scarring, intimal thickening, and calcification of coronary arteries.  Response Feedback:   [None Given]

• Question 13  

Needs Grading 

	A 4-year-old female is brought to the pediatrician by her mother who states the child has been running a fever to 102.0 F, has “pink eye”, and that her tongue looks very bright red and swollen. The mother states the fever has been present for 5 days, noticed the child had developed a rash and that the child’s legs look “puffy”. No other symptoms noted. Past medical history noncontributory. All immunizations up to date. Physical exam remarkable for current fever of 102.8 F, bilateral conjunctivitis without purulent material, oral mucosa with bright red erythema, dry, with fissuring of the lips. Legs noted to have peripheral edema and are also erythematous. Palmar desquamation noted. There is fine maculopapular rash and + cervical adenopathy. The presumptive diagnosis currently (pending laboratory data) is Kawasaki Disease.   Question 2 of 2:    How does Kawasaki Disease cause coronary aneurysms?
	Selected Answer:   The coronary arteries narrow and are occluded by a thrombus or stenosis. Cardiovascular death might be caused by an MI when a thrombus occludes the coronary aneurysm or when a large coronary aneurysm ruptures, Eventually, the walls of a blood vessels might narrow or be occluded by the thrombus or due to stenosis. There is an increase in the serum platelet count during the period of vascular damage, and this is the point where there is a high risk of death.     Correct Answer:     The coronary arteries become narrowed or occluded owing to stenosis or a thrombus. Cardiovascular death may occur from a myocardial infarction secondary to thrombosis of a coronary aneurysm or from rupture of a large coronary aneurysm. The vessel wall eventually becomes narrowed or occluded owing to stenosis or a thrombus. The period during of the greatest vascular damage is when a concomitant progressive increase in the serum platelet count occurs, and this is the point of the illness when the risk of death is most significant.  Response Feedback:   [None Given]

• Question 14  

Needs Grading 

	A 9-year-old boy was brought to the Urgent Care Center by his parents who state that the child had a sudden onset of difficulty catching his breath, has a new cough and is making a “funny sound” when he breathes.  The parents state there is no prior history of this, and the child had not been ill prior to the start of the symptoms. Past medical history noncontributory. No family history of respiratory problems. No known allergies to drugs or food. Physical exam positive for respiratory rate of 26, use of accessory muscles, with suprasternal retractions, heart rate of 132 beats per minute, an audible inspiratory and expiratory wheeze noted, and the pulse oximetry is 89% on room air. After the APRN institutes appropriate urgent treatment, the child’s breathing slowly returned to normal, vital signs normalize, and the pulse oximetry increases to 97%. The APRN suspects the child has asthma and tells the parents that they need to bring the child to a pulmonologist for further evaluation and care.      Question:    What is the underlying pathophysiology of asthma?
	Selected Answer:   The inflammation of the airways is influenced by interactions between the environment, and this limits the flow of air resulting in structural and functional airway changes in the form of mucus plug formation, bronchospasms, and mucosal edema. Obstruction of the airways results in an increase in resistance to the flow of air and reduced expiratory flow rates. These changes can lead to hyperinflation with overdistension to maintain the patency of the airways hence increasing the expiratory flow rate and increasing the pulmonary mechanics of breathing.   Hyperinflation is a compensatory mechanism for obstructed airflow and the uneven changes that occur in   resistance of the airflow, uneven air distribution, and changes in   circulation caused by intra-alveolar pressure cause a mismatch in ventilation-perfusion.     Correct Answer:     Interactions between environmental and genetic factors result in airway inflammation, which limits airflow and leads to functional and structural changes in the airways in the form of bronchospasm, mucosal edema, and mucus plugs.  Airway obstruction causes increased resistance to airflow and decreased expiratory flow rates. These changes lead to a decreased ability to expel air and may result in hyperinflation. The resulting overdistention helps maintain airway patency, thereby improving expiratory flow; however, it also alters pulmonary mechanics and increases the work of breathing.  Hyperinflation compensates for the airflow obstruction, but this compensation is limited when the tidal volume approaches the volume of the pulmonary dead space; the result is alveolar hypoventilation. Uneven changes in airflow resistance, the resulting uneven distribution of air, and alterations in circulation from increased intra-alveolar pressure due to hyperinflation all lead to ventilation-perfusion mismatch.  Response Feedback:   [None Given]

• Question 15  

Needs Grading 

	A 24-year-old female with known cystic fibrosis (CF) has been admitted to the hospital for evaluation for possible lung transplant. She was diagnosed with CF when she was 9 months old and has had multiple hospitalizations for pneumonia, respiratory failure, and small bowel obstructions. She currently is oxygen dependent and has been told by her physicians that she has end stage pulmonary disease secondary to CF. The only recourse for her currently is lung transplant.      Question 1 of 2:    What is cystic fibrosis and discuss the pathophysiology.
	Selected Answer:   CF   is a disease of the exocrine gland function that involves multiple systems but primarily leads to insufficiency of pancreatic enzymes, chronic respiratory infections, and other related complications. In 90% of patients, the pulmonary system is involved and it can ultimately lead to death. It arises from defects of the cystic fibrosis gene, which codes transmembrane conductance regulator (CFTR). Mutations that occur in this gene can lead to abnormalities in the cAMP-regulated chloride transport across epithelial cells on mucosal surfaces. This can cause a decrease in the secretion of  of chloride and  increase  sodium reabsorption   across epithelial cells resulting in thicker and sticker mucus  that promotes inflammation and infection. Heavy mucus secretions in other organs such as the GI tract, pancreas, and sweat glands increases the difficulty to clear.   Correct Answer:     Cystic fibrosis (CF) is a disease of exocrine gland function that involves multiple organ systems but chiefly results in chronic respiratory infections, pancreatic enzyme insufficiency, and associated complications in untreated patients. Pulmonary involvement occurs in 90% of patients surviving the neonatal period. End-stage lung disease is the principal cause of death.  Cystic fibrosis is caused by defects in the cystic fibrosis gene, which codes for a protein transmembrane conductance regulator (CFTR) that functions as a chloride channel and is regulated by cyclic adenosine monophosphate (cAMP). Mutations in the CFTR gene result in abnormalities of cAMP-regulated chloride transport across epithelial cells on mucosal surfaces.  Defective CFTR results in decreased secretion of chloride and increased reabsorption of sodium and water across epithelial cells. The resultant reduced height of epithelial lining fluid and decreased hydration of mucus results in mucus that is stickier to bacteria, which promotes infection and inflammation. Secretions in the respiratory tract, pancreas, GI tract, sweat glands, and other exocrine tissues have increased viscosity, which makes them difficult to clear.  Most deaths associated with cystic fibrosis result from progressive and end-stage lung disease. In individuals with cystic fibrosis, the lungs are normal in utero, at birth, and after birth, before the onset of infection and inflammation (except possibly for the presence of dilated submucosal gland ducts in the airways). Shortly after birth, many persons with cystic fibrosis acquire a lung infection, which incites an inflammatory response. Infection becomes established with a distinctive bacterial flora. A repeating cycle of infection and neutrophilic inflammation develops.  Response Feedback:   [None Given]

• Question 16  

Needs Grading 

	A 24-year-old female with known cystic fibrosis (CF) has been admitted to the hospital for evaluation for possible lung transplant. She was diagnosed with CF when she was 9 months old and has had multiple hospitalizations for pneumonia, respiratory failure, and small bowel obstructions. She currently is oxygen dependent and has been told by her physicians that she has end stage pulmonary disease secondary to CF. The only recourse for her currently is lung transplant.    Question 2 of 2:    What is the reason people with CF are often malnourished?
	Selected Answer:   CFTR defects result in a decrease in the secretion of chloride water in the GI tract. During birth, this can cause a meconium ileus and later in life, can result in distal intestinal obstruction syndrome (DIOS). Insufficiency of the pancreas also reduces the absorption of  contents in the intestines and other mechanical problems such as  structures, scarring, and  inflammation  can increase the likelihood of contents in the intestines to sludge with subsequent obstruction, fecal impaction and intussusception.     Correct Answer:     Defects in CFTR lead to reduced chloride secretion with water following into the gut. This may result in meconium ileus at birth and in distal intestinal obstruction syndrome (DIOS) later in life. In addition, other pathologic disorders complicate the simple relationship between the apical chloride and water secretion and the disease. The pancreatic insufficiency decreases the absorption of intestinal contents. Mechanical problems associated with inflammation, scarring, and strictures may predispose the patient to sludging of intestinal contents, leading to intestinal obstruction by fecal impaction or to intussusception. Adhesions may form, leading to complete obstruction. A complete obstruction may require resection, leading to loss of absorptive epithelium of the distal ileum.  Other factors, such as reduced water content of secretions, precipitation of proteins, and plugging of ductules and acini, prevent the pancreatic enzymes from reaching the gut. Autodigestion of the pancreas occasionally leads to pancreatitis.  Most patients with cystic fibrosis (90-95%) have pancreatic enzyme insufficiency and present with digestive symptoms and/or failure to thrive early in life. Onset of pancreatic insufficiency varies, however, and may occur in patients older than 6 months. Some patients never develop pancreatic insufficiency.  Patients with pancreatic insufficiency typically present with poor weight gain in association with frequent stools that are malodorous, greasy, and associated with flatulence and colicky pain after feeding. The combination of increased energy intake demand at baseline, the added energy intake demand of chronic disease, difficulty sustaining energy uptake because of malabsorption, and anorexia associated with ongoing lung inflammation leads to poor weight gain.  Response Feedback:   [None Given]

• Question 17  

Needs Grading 

	A 14-year old girl who was trying out for cheerleading underwent a physical examination by the APRN who notices that the girl had uneven hip height, asymmetry of the shoulder height, shoulder and scapular prominence and rib prominence. The rest of the physical exam was normal and the APRN referred the girl to an orthopaedist for evaluation for possible scoliosis. Radiographs in the orthopaedic office confirms the diagnosis of idiopathic scoliosis. The spinal curve was measured at 26 degrees and it was recommended that the girl be fit for a low-profile back brace.      Question:    What is thought to be the pathophysiology of idiopathic scoliosis?
	Selected Answer:   Patients with IS have a posterior column lesion within the central nervous system. This dysfunction often manifests as a decrease in proprioception and vibratory sensation. On the concave side of the curve, muscles, ligaments, and other soft tissues become shortened and when asymmetric forces are applied to the epiphyseal center of the ossification by shortened and tight soft tissue, the vertebral is deformed. This curve increases at times of peak skeletal growth and involve torso twisting, and bending.     Correct Answer:     It has been suggested that a posterior column lesion within the central nervous system might be present in patients who have idiopathic scoliosis. Such central nervous system (CNS) dysfunction was hypothesized to be manifested as decreased vibratory sensation and proprioception. The earliest pathologic changes occur in the soft tissues. The muscles, ligaments, and other soft tissues become shortened on the concave side of the curve. Vertebral deformity occurs as asymmetric forces are applied to the epiphyseal center of the ossification by shortened and tight soft tissue © 2020 Walden University 13 o the concave side of the curve. True curves involve not only bending but also twisting of the torso, leading to a rib hump seen when the child leans forward.  The curve increases most rapidly during periods of rapid skeletal growth. If the curve is less than 40 degrees at skeletal maturity, the risk of progression is small. In curves greater than 50 degrees, the spine is biomechanically unstable, and the curve usually progresses. For curves in the thoracic region over 80 degrees, there is marked cardiopulmonary compromise.  Response Feedback:   [None Given]

• Question 18  

Needs Grading 

	A 2-year-old boy was brought to Urgent Care by his parents who state the boy has been having large amounts of diarrhea, been very irritable and very pale. The parents noticed there was blood in the diarrhea and when the boy’s legs became swollen, they sought care. Past medical history noncontributory and all immunizations up to date.  Social history noncontributory and the child is in day care 5 days a week. No known exposure to other sick children and the only new event the parents could think of is the day care workers took the children to a local petting zoo about a week ago. Physical exam revealed a pale, ill appearing child with swollen legs, tender abdomen, and petechia on the legs and abdomen. The APRN suspects the child may have been exposed to a bacterium at the petting zoo and arranges for the patient to be transferred to the Emergency Room. There the child was found to be in renal failure, have hypertension and was diagnosed with hemolytic uremic syndrome (HUS).      Question:    What is the pathophysiology of HUS?
	Selected Answer:   The pathology of HUS   is often preceded by an ES (Escherichia Coli) producing Shiga toxin that causes colitis. Colon inflammation   promotes the systemic absorption of lipopolysaccharide and the toxin from the gut. This toxin bins to polymorphonuclear leukocytes and  reaches the kidney to cause a cascade of events  such as glomerular capillary lysis, separating endothelial cells from the glomerular basement, platelet aggregation and  activation,  and activating the coagulation cascade. The arterioles in the glomerular swell and occlude with clots of fibrin and platelets, the glomerular filtration reduces and the glomerular membrane is damaged. This causes proteinuria and hematuria. Since the blood vessels are narrowed, they injure passing erythrocytes which are removed by the spleen, causing acute hemolytic anemia and subsequent thrombocytopenia.     Correct Answer:     STEC-HUS is usually preceded by a colitis caused by Shiga toxin– producing Escherichia coli (STEC). Subsequent inflammation of the colon facilitates systemic absorption of the shiga toxin and lipopolysaccharide from the GI tract. The toxin binds to polymorphonuclear leukocytes in the gut and is transported to the kidney, causing a cascade of effects, including lysis of glomerular capillary endothelial cells, separation of endothelial cells from the basement membrane, activation and aggregation of platelets and the activation of the coagulation cascade. The glomerular arterioles become swollen and occluded with platelets and fibrin clots. There is decreased glomerular filtration and the damaged glomerular membrane results in hematuria and proteinuria. Narrow vessels injure passing erythrocytes. The damaged erythrocytes are removed by the spleen, causing acute hemolytic anemia. Severe thrombocytopenia ensues.  Response Feedback:   [None Given]

• Question 19  

Needs Grading 

	The parents of a 3-year-old boy bring the child to the pediatrician with concerns that their child seems “small for his age”. The parents state that the boy has always been small but did not worry until the child went to day care and they noticed other children of the same age were much bigger. They also note that his teeth were very late in coming in. Normal prenatal, perinatal and postnatal history and no medical history on either side of family regarding issues with growth and development. Physical exam is normal except for short limbs and small teeth. The pediatrician suspects the child has pituitary dwarfism. A complete laboratory and radiographic work up confirmed the diagnosis.    Question:    What is the pathophysiology of pituitary dwarfism?
	Selected Answer:   Individuals with pituitary dwarfism have a delayed dentition, short stature and delayed skeletal maturation. The secretion of pituitary GH (growth hormone) is stimulated by growth hormone–releasing hormone (GHRH) in the hypothalamus. However, a deficiency in the GH  can disrupt the GH axis in the pituitary, brain or hypothalamus.     Correct Answer:     Pituitary dwarfism is characterized by short stature, delayed dentition, and delayed skeletal maturation. Most cases of sporadic or isolated growth hormone deficiency have a normal-appearing pituitary gland on MRI, although a small adenohypophysis may be observed, particularly in cases of panhypopituitarism.  Pituitary growth hormone secretion is stimulated by growth hormone–releasing hormone (GHRH) from the hypothalamus and possibly by another signal, which may be stimulated by certain growth hormone–releasing peptides (GHRPs). Receptors for the GHRPs have been identified, and the natural ligand for these receptors has been determined to be ghrelin. Somatostatin secreted by the hypothalamus inhibits growth hormone secretion.  Growth hormone deficiency may result from disruption of the growth hormone axis in the higher brain, hypothalamus, or pituitary. This dysfunction can be congenital or acquired.  Response Feedback:   [None Given]

• Question 20  

Needs Grading 

	A 4-year-old boy was brought to the Emergency Room by his parents with a suspected femur fracture. The parents state the child was playing on the couch when he rolled off and cried out in pain. There were no other injuries noted. Review of the child’s chart revealed this was the 4th Emergency Room visit in the last 15 months for fractures after low impact injury. The parents were suspected of child abuse and Child and Protective Services were consulted. The APRN assessing the child noted that the child had unusually thin and translucent skin, poor dentition, and blue sclera. The APRN suspects the child may have osteogenesis imperfecta (OI). Laboratory results revealed an elevated serum alkaline phosphatase and the diagnosis OI was made based on the clinical picture and elevated alkaline phosphatase.      Question:    What is the pathophysiology of OI?
	Selected Answer:   OI is a fragile bone deformity caused by mutations in genes that encode type I procollagen. In other instances, it may result from increased levels of thyroxine.     Correct Answer:     Osteogenesis imperfecta (OI) is a disorder of bone fragility chiefly caused by mutations in the genes that encode type I procollagen. Severity ranges from mild forms to lethal forms in the perinatal period. Additional genes have been discovered in which mutations can also cause brittle bones.  Other metabolic abnormalities are associated with OI. Some individuals have increased serum thyroxine levels that suggest hyperthyroidism, which is consistent with reports of excessive sweating, heat intolerance, resting tachycardia and tachypnea.  Response Feedback:   [None Given]

Friday, May 28, 2021 6:48:25 AM EDT 

 

Week 9: Concepts of Psychological Disorders Knowledge Check: Psychological Disorders

Scenario 1: Schizophrenia

1. What are the known characteristics of schizophrenia and relate those to this patient?

Schizophrenia is a chronic mental disorder displayed in patients who interpreted reality abnormally just like the 22-year-old patient in the provided case study. It can lead to a combination of delusion. Hallucination and extremely disordered behaviour and thinking impair the patient normal functioning (Correll et al., 2019). The patient in the provided case study reported signs of auditory and visual hallucination, unexpected rage and crying, and delusion. Additional symptoms include disorganized speech and thinking as demonstrated by the results of the mental status examination. The patient also displayed negative symptoms such as inability to make eye contact and being socially withdrawn which are significant indications of schizophrenia disorder.

2. Genetics are sometimes attached to schizophrenia explains this.

Pre-molecular and molecular genetic studies have reported that genetics play a significant role in the development of schizophrenia.  Consequently, the inheritance pattern of the disease demonstrates increased risk among first relatives. At the molecular level, several positional and functional genes associated with the development of schizophrenia have been identified, such as neuregulin (NRG-1, 8p12–21), proline dehydrogenase (PRODH-2, 22q11.21), dysbindin, (DTNBP1,6p22.3), catechol-O-methyltransferase (COMT, 22q11.21), G72 (13q34) / D-amino acid oxidase (DAAO,12q24),5HT2A and dopamine D3 receptor (DRD3) and regulator of G protein signaling (RGS-4) (Cleynen et al., 2021). Recent studies support schizophrenia candidate regions on chromosomes 1q, 2q, 5q, 6p, 8p, 10p, 13q,15q and 22q. Additional studies are however required to provide a precise association with the above-mentioned genetic factors concerning how they lead to the development of schizophrenia.

3. What roles do neurotransmitters play in the development of schizophrenia?

Neurotransmitters are chemicals responsible for conveying messages between brain cells. Studies illustrate an association between changes in the levels of neurotransmitters in the brain to the development of schizophrenia. This is evident by the mechanism of antipsychotics in relieving symptoms of schizophrenia through altering the levels of certain neurotransmitters in the brain. Recent studies have reported several biochemical alterations in schizophrenia, concerningneurotransmitter dysfunction in different systems, with the most prominent being γ‎-aminobutyric acid (GABA), serotonin, glutamate, and dopamine (Müller, 2018). For instance, alterations in the signaling of dopamine and hyperactivity of the D2 receptor in the limbic and subcortical region of the brain have been associated with some of the schizophrenia symptoms including delusion and hallucination. Consequently, hypodopaminergic activity in the mesocortical system is also associated with negative symptoms of schizophrenia such as flattening, lack of pleasure, withdrawal, and inability to follow through.

4. Explain what structural abnormalities are seen in people with schizophrenia.

Through imaging studies, several complex patterns of structural abnormalities have been reported among patients diagnosed with schizophrenia, in addition to those who are at high risk of the disorder (Zhao et al., 2018). For example, MRI studies have reported a reduced volume of grey matter in the prefrontal, superior temporal, and medial temporal areas of the brain. These regions of the brain are involved in several functions such as short-term memory/decision making, processing of auditory information, and episodic memory respectively. Postmortem studies on the other hand report that a reduction in the cortical grey matter does not indicate loss of cell bodies but instead, reflects a reduction in synaptic density and dendritic complexity which may impair intraneuronal integration and communication leading to cognitive changes among other associated symptoms. Disruptions in the integrity of the white matter have also been implicated in schizophrenia, given that it forms the structural connections between different regions of the brain.

Scenario 2: Bipolar Disorder

5. How does genetics play in the development of bipolar 2 disorders?  

Bipolar disorder (BD) is characterized by extreme shifts in the patient’s mood, behaviour, and energy levels. The patient in the provided case study is however diagnosed with bipolar 2 disorder, which is characterized by hypomanic and depressive episodes. The inheritance pattern of bipolar 2 disorder is quite unclear. Studies however report greater risks among first-degree relatives, with genetic factors accounting for approximately 80% of the causes of this mental disorder (Gordovez& McMahon, 2020). Genome-wide association studies (GWASs) have associated increased risk of bipolar 2 disorder with several genetic factors such as alpha-1 subunit of the L-type voltage-gated calcium channel (CACNA1C), teneurin transmembrane protein 4 (ODZ4), ankyrin G node of Ranvier (ANK3), nesprin-1 (SYNE1) and diacylglycerol kinase eta (DGKH).For instance, the DGKH is involved in diacylglycerol (DAG) phosphorylation in the phosphoinositol pathway sensitive to lithium, which contributes to the development of the bipolar disorder.

NURS 6501 Knowledge Check Psychological Disorders References

Cleynen, I., Engchuan, W., Hestand, M. S., Heung, T., Holleman, A. M., Johnston, H. R., … & Bassett, A. S. (2021). Genetic contributors to the risk of schizophrenia in the presence of a 22q11. 2 deletion. Molecular psychiatry, 26(8), 4496-4510. https://doi.org/10.1038/s41380-020-0654-3

Correll, C. U., Brevig, T., & Brain, C. (2019). Patient characteristics, burden, and pharmacotherapy of treatment-resistant schizophrenia: results from a survey of 204 US psychiatrists. BMC psychiatry, 19(1), 1-12. https://doi.org/10.1186/s12888-019-2318-x

Gordovez, F. J. A., & McMahon, F. J. (2020). The genetics of bipolar disorder. Molecular psychiatry, 25(3), 544-559.https://doi.org/10.1038/s41380-019-0634-7

Müller, N. (2018). Inflammation in schizophrenia: pathogenetic aspects and therapeutic considerations. Schizophrenia bulletin, 44(5), 973-982. https://doi.org/10.1093/schbul/sby024

Zhao, C., Zhu, J., Liu, X., Pu, C., Lai, Y., Chen, L., … & Hong, N. (2018). Structural and functional brain abnormalities in schizophrenia: a cross-sectional study at different stages of the disease. Progress in Neuro-Psychopharmacology and Biological Psychiatry, 83, 27-32. https://doi.org/10.1016/j.pnpbp.2017.12.017.

Week 9: Concepts of Psychological Disorders

Among the many risk factors for mental disorders are genetics and other pathophysiological factors. While other factors, such as environmental factors or substance abuse, can also have an impact, it is important to recognize the connections between biological factors and psychological disorders.

Ranging from anxiety to schizophrenia, psychological disorders offer unique challenges in diagnosis and treatment. Clearly, the presence of these disorders can be life-altering for patients, but they can also significantly impact families and other loved ones.

Click here to ORDER an A++ paper from our MASTERS and DOCTORATE WRITERS ON NURS 6501 Knowledge Check Psychological Disorders

This week, you examine fundamental concepts of psychological disorders. You explore common psychological disorders, and you apply the key terms and concepts that help communicate the pathophysiological nature of these issues to patients.
Learning Objectives

Students will:

Analyze concepts and principles of pathophysiology across the lifespan

Learning Resources

Required Readings (click to expand/reduce)

McCance, K. L. & Huether, S. E. (2019). Pathophysiology: The biologic basis for disease in adults and children (8th ed.). St. Louis, MO: Mosby/Elsevier.

Chapter 19: Neurobiology of Schizophrenia, Mood Disorders, Anxiety Disorders, and Obsessive-Compulsive Disorder, including Summary Review

Locke, A. B., Kirst, N., & Shultz, C. G. (2015). Diagnosis and management of generalized anxiety disorder and panic disorder in adults. American Family Physician, 91(9), 617–624. Retrieved from https://www.aafp.org/afp/2015/0501/p617.html

Credit Line: Diagnosis and management of generalized anxiety disorder and panic disorder in adults by Locke, A. B., Kirst, N., & Shultz, C., in American Family Physician, Vol. 91/Issue 9. Copyright 2015 by American Academy of Family Physicians. Reprinted by permission of American Academy of Family Physicians via the Copyright Clearance Center.

McIntyre, R. S. & Calabrese, J. R. (2019). Bipolar depression: The clinical characteristics and unmet needs of a complex disorder. Current Medical Research and Opinion, 1–14. doi:10.1080/03007995.2019.1636017. Retrieved from https://www.tandfonline.com/doi/full/10.1080/03007995.2019.1636017

Credit Line: Bipolar depression: The clinical characteristics and unmet needs of a complex disorder by McIntyre, R. S. & Calabrese, J. R., in Current Medical Research and Opinion. Copyright 2019 by Librapharm Ltd. Reprinted by permission of Librapharm Ltd via the Copyright Clearance Center.

Required Media (click to expand/reduce)

Module 6 Overview with Dr. Tara Harris

Dr. Tara Harris reviews the structure of Module 6 as well as the expectations for the module. Consider how you will manage your time as you review your media and Learning Resources throughout the module to prepare for your Knowledge Check. (1m)

Concepts of Psychological Disorders – Week 9 (12m)

Generalized Anxiety Syndrome

Osmosis.org. (2016, February 29). Generalized anxiety disorder (GAD) – causes, symptoms, & treatment [Video file]. Retrieved from https://www.youtube.com/watch?v=9mPwQTiMSj8

Note: The approximate length of the media program is 5 minutes.

Knowledge Check: Psychological Disorders

In this exercise, you will complete a 10- to 20-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

Photo Credit: agsandrew – stock.adobe.com

Complete the Knowledge Check By Day 7 of Week 9

To complete this Knowledge Check:

Module 6 Knowledge Check

What’s Coming Up in Module 7?

Photo Credit: [BrianAJackson]/[iStock / Getty Images Plus]/Getty Images

In Module 7, you will analyze processes related to women’s and men’s health, infections, and hematologic disorders through case study analysis. To do this, you will analyze alterations in the relevant systems and the resultant disease processes. You will also consider patient characteristics, including racial and ethnic variables, which may impact physiological functioning and altered physiology.

Week 10 Knowledge Check: Women’s and Men’s Health, Infections, and Hematologic Disorders

In the Week 10 Knowledge Check, you will demonstrate your understanding of the topics covered during Module 7. This Knowledge Check will be composed of a series of questions related to specific scenarios provided. It is highly recommended that you review the Learning Resources in their entirety prior to taking the Knowledge Check, since the resources cover the topics addressed. Plan your time accordingly.

Next Module

To go to the next module:

Module 7

Results Displayed All Answers, Submitted Answers, Correct Answers, Feedback, Incorrectly Answered Questions

Question 1

1.25 out of 1.25 points

Correct

Which of the following are positive clinical manifestations of schizophrenia?

Selected Answer:
Correct

Hallucinations, delusions, and incoherent speech
Answers:

Social withdraw, blunted affect, and failure to respond to simple questions

Correct

Hallucinations, delusions, and incoherent speech

Hallucinations, blunted affect, and social withdraw

Delusions, hallucinations, and failure to respond to simple questions
Question 2

1.25 out of 1.25 points

Correct

A patient with schizophrenia will have alterations in their dorsolateral prefrontal cortex. The APRN would expect it to be described as:
Selected Answer:
Correct

hypoactive
Answers:

stimulated

absent

hyperactive

Correct

hypoactive
Question 3

0 out of 1.25 points

Incorrect

The neurobiology of depression is believed to be related to the atrophy of neurons in the:
Selected Answer:
Incorrect

amygdala
Answers:

hypothalmus

Correct

hippocampus

thalmus

amygdala
Question 4

1.25 out of 1.25 points

Correct

The APRN is assessing a patient that is talking to his mother in the corner of the room even although you are the only other person in the room. This is an example of:
Selected Answer:
Correct

Hallucination
Answers:

Delusion

Correct

Hallucination

Anhedonia

Pressured speech
Question 5

0 out of 1.25 points

Incorrect

The APRN is treating a patient with bipolar II disorder. The major focus of treatment is on:
Selected Answer:
Incorrect

mania
Answers:

mania

Correct

depression

anxiety

panic attacks
Question 6

1.25 out of 1.25 points

Correct

Monoamine neurotransmission is hypothesized to be _______________ during mania.
Selected Answer:
Correct

increased
Answers:
Correct

increased

decreased

absent

suspended
Question 7

1.25 out of 1.25 points

Correct

Abnormalities in brain development related to schizophrenia are thought to develop when?

Selected Answer:
Correct

Prenatal
Answers:
Correct

Prenatal

Infancy

Early Childhood

Adolescent
Question 8

1.25 out of 1.25 points

Correct

Obsessive compulsive disorder is characterized by what types of thoughts and behaviors?
Selected Answer:
Correct

repetitive irrational thoughts and ritualized behavior
Answers:

disorganized irrational thoughts and disorganized behavior

constant irrational thoughts and constant behavior

Correct

repetitive irrational thoughts and ritualized behavior

repetitive irrational thoughts and disorganized behavior
Question 9

1.25 out of 1.25 points

Correct

Monoamine neurotransmission is hypothesized to be _______________ during depression.
Selected Answer:
Correct

decreased
Answers:

increased

Correct

decreased

absent

stimulated
Question 10

1.25 out of 1.25 points

Correct

What type of thoughts are characteristic of post traumatic stress disorder?
Selected Answer:
Correct

intrusive
Answers:

disorganized

Correct

intrusive

anxious

disturbing
Question 11

0 out of 1.25 points

Incorrect

The APRN would expect to find elevated blood levels of which of the following markers for patients with a diagnosis of depression?
Selected Answer:
Incorrect

Calcium and Cortisol
Answers:

Proinflammatory cytokines and pH

Calcium and Cortisol

Calcium and pH

Correct

Proinflammatory cytokines and cortisol
Question 12

1.25 out of 1.25 points

Correct

The APRN is treating a patient with bipolar 1 disorder. The major focus of treatment is on:
Selected Answer:
Correct

mania
Answers:
Correct

mania

depression

anxiety

panic attacks
Question 13

0 out of 1.25 points

Incorrect

Which of the following are negative clinical manifestations of schizophrenia?

Selected Answer:
Incorrect

Hallucinations, delusions, and incoherent speech
Answers:
Correct

Social withdraw, blunted affect, and failure to respond to simple questions

Hallucinations, delusions, and incoherent speech

Hallucinations, blunted affect, and social withdraw

Delusions, hallucinations, and failure to respond to simple questions
Question 14

1.25 out of 1.25 points

Correct

The APRN is assessing a patient that is talking so rapidly and urgently that it is difficult to understand. This is an example of:
Selected Answer:
Correct

Pressured speech
Answers:

Delusion

Hallucination

Anhedonia

Correct

Pressured speech
Question 15

1.25 out of 1.25 points

Correct

The APRN is assessing a patient that states that Napoleon Bonaparte is the King of France even thought he has a book that says he is dead. This is an example of:
Selected Answer:
Correct

Delusion
Answers:
Correct

Delusion

Hallucination

Anhedonia

Pressured speech
Question 16

1.25 out of 1.25 points

Correct

The APRN is assessing a patient that has monotone speech and unchanged facial expressions even though he states he is happy and excited about his life. This is an example of:
Selected Answer:
Correct

Anhedonia
Answers:

Delusion

Hallucination

Correct

Anhedonia

Pressured speechLiterature, cinema, and other cultural references have long examined differences between women and
men. These observations extend well beyond obvious and even inconspicuous traits to include cultural,
behavioral, and biological differences that can impact pathophysiological process and, ultimately,
health.
Understanding these differences in traits and their impact on pathophysiology can better equip acute
care nurses to communicate to patients of both sexes. Furthermore, APRNs who are able to
communicate these differences can better guide care to patients, whatever their gender.

	Scenario 2: Bipolar Disorder A 44-year-old female  came to the clinic today brought in by her husband. He notes that she has been with various states of depression and irritability over the past 3 months with extreme fatigue, has lost 20 pounds and has insomnia. He has come home from work to find his wife sitting in front of the TV and not moving for hours. In the past few days, she suddenly has become very hyperactive, has been talking incessantly, has been easily distracted and seems to “flit from one thing to another.”. She hasn’t slept in 3 days. The wife went on an excessive shopping spree for new clothes that resulted in their credit card being denied for exceeding the line of credit. The wife is unable to sit in the exam room and is currently pacing the hallway muttering to herself and is reluctant to talk with or be examined the ARNP. Physical observation shows agitated movements, rapid fire speech, and hyperactivity. DIAGNOSIS: bipolar type 2 disorder. Question 1.     How does genetics play in the development of bipolar 2 disorders?
	Selected Answer: The pathophysiology of bipolar disorder, or manic-depressive illness (MDI), has not been fully identified, and there are no objective biologic markers that correspond definitively with the disease state. Twin, family, and adoption studies indicate that bipolar disorder has a significant genetic component. First-degree relatives of a person with bipolar disorder are approximately seven times more likely to develop bipolar disorder than the rest. The heritability of bipolar I disorder (BPI) has recently been estimated at 0.73. Bipolar individuals, who may exhibit psychotic behavior, have deficits in reelin expression linked to genetic loci located on chromosome 22, which confers susceptibility to schizophrenia. Given that, large variations in clinical symptoms still suggest that developmental and environmental factors are as important as genetic factors in contributing to the etiology of mood disorders. Correct Answer: The pathophysiology of bipolar disorder, or manic-depressive illness (MDI), has not been fully identified, and there are no objective biologic markers that correspond definitively with the disease state. Twin, family, and adoption studies all indicate that bipolar disorder has a significant genetic component. Firstdegree relatives of a person with bipolar disorder are approximately 7 times more likely to develop bipolar disorder than the rest of the population, and the heritability of bipolar I disorder (BPI) has recently been estimated at 0.73. Bipolar individuals, who may exhibit psychotic behavior, have deficits in reelin expression linked to genetic loci located on the chromosome 22, which confers susceptibility to schizophrenia. Given that, there still are large variations in clinical symptoms suggests that developmental and environmental factors are as important as genetic factors in contributing to the etiology of mood disorders. Response Feedback: [None Given]

 

NURS 6501 Knowledge Check Psychological Disorders Grading Rubric Guidelines DQ

Performance Category	10	9	8	4	0
Scholarliness Demonstrates achievement of scholarly inquiry for professional and academic decisions.	Provides relevant evidence of scholarly inquiry clearly stating how the evidence informed or changed professional or academic decisions Evaluates literature resources to develop a comprehensive analysis or synthesis. Uses valid, relevant, and reliable outside sources to contribute to the threaded discussion	Provides relevant evidence of scholarly inquiry but does not clearly state how the evidence informed or changed professional or academic decisions. Evaluates information from source(s) to develop a coherent analysis or synthesis. Uses some valid, relevant, reliable outside sources to contribute to the threaded discussion.	Discusses using scholarly inquiry but does not state how scholarly inquiry informed or changed professional or academic decisions. Information is taken from source(s) with some interpretation/evaluation, but not enough to develop a coherent analysis or synthesis. Little valid, relevant, or reliable outside sources are used to contribute to the threaded discussion. Demonstrates little or no understanding of the topic.	Discusses using scholarly inquiry but does not state how scholarly inquiry informed or changed professional or academic decisions. Information is taken from source(s) without any interpretation/evaluation. The posting uses information that is not valid, relevant, or reliable	No evidence of the use of scholarly inquiry to inform or change professional or academic decisions. Information is not valid, relevant, or reliable
Performance Category	10	9	8	4	0
Application of Course Knowledge – Demonstrate the ability to analyze, synthesize, and/or apply principles and concepts learned in the course lesson and outside readings and relate them to real-life professional situations	Posts make direct reference to concepts discussed in the lesson or drawn from relevant outside sources; Applies concepts to personal experience in the professional setting and or relevant application to real life.	Posts make direct reference to concepts discussed in the lesson or drawn from relevant outside sources. Applies concepts to personal experience in their professional setting and or relevant application to real life Interactions with classmates are relevant to the discussion topic but do not make direct reference to lesson content	Posts are generally on topic but do not build knowledge by incorporating concepts and principles from the lesson. Does not attempt to apply lesson concepts to personal experience in their professional setting and or relevant application to real life Does not demonstrate a solid understanding of the principles and concepts presented in the lesson	Posts do not adequately address the question posed either by the discussion prompt or the instructor’s launch post. Posts are superficial and do not reflect an understanding of the lesson content Does not attempt to apply lesson concepts to personal experience in their professional setting and or relevant application to real life	Posts are not related to the topics provided by the discussion prompt or by the instructor; attempts by the instructor to redirect the student are ignored No discussion of lesson concepts to personal experience in the professional setting and or relevant application to real life
Performance Category	5	4	3	2	0
Interactive Dialogue Replies to each graded thread topic posted by the course instructor, by Wednesday, 11:59 p.m. MT, of each week, and posts a minimum of two times in each graded thread, on separate days. (5 points possible per graded thread)	Exceeds minimum post requirements Replies to each graded thread topic posted by the course instructor, by Wednesday, 11:59 p.m. MT, of each week, and posts three or more times in each graded thread, over three separate days. Replies to a post posed by faculty and to a peer Summarizes what was learned from the lesson, readings, and other student posts for the week.	Replies to each graded thread topic posted by the course instructor, by Wednesday, 11:59 p.m. MT, of each week, and posts a minimum of two times in each graded thread, on separate days Replies to a question posed by a peer Summarizes what was learned from the lesson, readings, and other student posts for the week.	Meets expectations of 2 posts on 2 different days. The main post is not made by the Wednesday deadline Does not reply to a question posed by a peer or faculty	Has only one post for the week Discussion posts contain few, if any, new ideas or applications; often are a rehashing or summary of other students’ comments	Does not post to the thread No connections are made to the topic
	Minus 1 Point	Minus 2 Point	Minus 3 Point	Minus 4 Point	Minus 5 Point
Grammar, Syntax, APA Note: if there are only a few errors in these criteria, please note this for the student in as an area for improvement. If the student does not make the needed corrections in upcoming weeks, then points should be deducted. Points deducted for improper grammar, syntax and APA style of writing. The source of information is the APA Manual 6th Edition	2-3 errors in APA format. Written responses have 2-3 grammatical, spelling, and punctuation errors. Writing style is generally clear, focused, and facilitates communication.	4-5 errors in APA format. Writing responses have 4-5 grammatical, spelling and punctuation errors. Writing style is somewhat focused.	6-7 errors in APA format. Writing responses have 6-7 grammatical, spelling and punctuation errors. Writing style is slightly focused making discussion difficult to understand.	8-10 errors in APA format. Writing responses have 8-10 grammatical, spelling and punctuation errors. Writing style is not focused, making discussion difficult to understand.	Post contains greater than 10 errors in APA format. Written responses have more than 10 grammatical, spelling and punctuation errors. Writing style does not facilitate communication. The student continues to make repeated mistakes in any of the above areas after written correction by the instructor
	0 points lost				-5 points lost
Total Participation Requirements per discussion thread	The student answers the threaded discussion question or topic on one day and posts a second response on another day.				The student does not meet the minimum requirement of two postings on two different days
Early Participation Requirement per discussion thread	The student must provide a substantive answer to the graded discussion question(s) or topic(s), posted by the course instructor (not a response to a peer), by Wednesday, 11:59 p.m. MT of each week.				The student does not meet the requirement of a substantive response to the stated question or topic by Wednesday at 11:59 pm MT.

 

As we begin this session, I would like to take this opportunity to clarify my expectations for this course:

Please note that GCU Online weeks run from Thursday (Day 1) through Wednesday (Day 7).

 

Course Room Etiquette:

• It is my expectation that all learners will respect the thoughts and ideas presented in the discussions.
• All postings should be presented in a respectful, professional manner. Remember – different points of view add richness and depth to the course!

 

Office Hours:

• My office hours vary so feel free to shoot me an email at [email protected] or my office phone is 602.639.6517 and I will get back to you within one business day or as soon as possible.
• Phone appointments can be scheduled as well. Send me an email and the best time to call you, along with your phone number to make an appointment.
• I welcome all inquiries and questions as we spend this term together. My preference is that everyone utilizes the Questions to Instructor forum. In the event your question is of a personal nature, please feel free to post in the Individual Questions for Instructor forumI will respond to all posts or emails within 24 or sooner.

 

Late Policy and Grading Policy

Discussion questions:

• I do not mark off for late DQ’s.
• I would rather you take the time to read the materials and respond to the DQ’s in a scholarly way, demonstrating your understanding of the materials.
• I will not accept any DQ submissions after day 7, 11:59 PM (AZ Time) of the week.
• Individual written assignments – due by 11:59 PM AZ Time Zone on the due dates indicated for each class deliverable.

Assignments:

• Assignments turned in after their specified due dates are subject to a late penalty of -10%, each day late, of the available credit. Please refer to the student academic handbook and GCU policy.
• Any activity or assignment submitted after the due date will be subject to GCU’s late policy
• Extenuating circumstances may justify exceptions, which are at my sole discretion. If an extenuating circumstance should arise, please contact me privately as soon as possible.
• No assignments can be accepted for grading after midnight on the final day of class.
• All assignments will be graded in accordance with the Assignment Grading Rubrics

Participation

• Participation in each week’s Discussion Board forum accounts for a large percentage of your final grade in this course.
• Please review the Course Syllabus for a comprehensive overview of course deliverables and the value associated with each.
• It is my expectation that each of you will substantially contribute to the course discussion forums and respond to the posts of at least three other learners.
• A substantive post should be at least 200 words. Responses such as “great posts” or “I agree” do notmeet the active engagement expectation.
• Please feel free to draw on personal examples as you develop your responses to the Discussion Questions but you do need to demonstrate your understanding of the materials.
• I do expect outside sources as well as class materials to formulate your post.
• APA format is not necessary for DQ responses, but I do expect a proper citation for references.
• Please use peer-related journals found through the GCU library and/or class materials to formulate your answers. Do not try to “Google” DQ’s as I am looking for class materials and examples from the weekly materials.
• I will not accept responses that are from Wikipedia, Business com, or other popular business websites. You will not receive credit for generic web searches – this does not demonstrate graduate-level research.
• Stay away from the use of personal pronouns when writing.As a graduate student, you are expected to write based on research and gathering of facts. Demonstrating your understanding of the materials is what you will be graded on. You will be marked down for lack of evidence to support your ideas.

Plagiarism

• Plagiarism is the act of claiming credit for another’s work, accomplishments, or ideas without appropriate acknowledgment of the source of the information by including in-text citations and references.
• This course requires the utilization of APA format for all course deliverables as noted in the course syllabus.
• Whether this happens deliberately or inadvertently, whenever plagiarism has occurred, you have committed a Code of Conduct violation.
• Please review your LopesWrite report prior to final submission.
• Every act of plagiarism, no matter the severity, must be reported to the GCU administration (this includes your DQ’s, posts to your peers, and your papers).

Plagiarism includes:

• Representing the ideas, expressions, or materials of another without due credit.
• Paraphrasing or condensing ideas from another person’s work without proper citation and referencing.
• Failing to document direct quotations without proper citation and referencing.
• Depending upon the amount, severity, and frequency of the plagiarism that is committed, students may receive in-class penalties that range from coaching (for a minor omission), -20% grade penalties for resubmission, or zero credit for a specific assignment. University-level penalties may also occur, including suspension or even expulsion from the University.
• If you are at all uncertain about what constitutes plagiarism, you should review the resources available in the Student Success Center. Also, please review the University’s policies about plagiarism which are covered in more detail in the GCU Catalog and the Student Handbook.
• We will be utilizing the GCU APA Style Guide 7th edition located in the Student Success Center > The Writing Center for all course deliverables.

LopesWrite

• All course assignments must be uploaded to the specific Module Assignment Drop Box, and also submitted to LopesWrite every week.
• Please ensure that your assignment is uploaded to both locations under the Assignments DropBox. Detailed instructions for using LopesWrite are located in the Student Success Center.

Assignment Submissions

• Please note that Microsoft Office is the software requirement at GCU.
• I can open Word files or any file that is saved with a .rtf (Rich Text Format) extension. I am unable to open .wps files.
• If you are using a “.wps” word processor, please save your files using the .rtf extension that is available from the drop-down box before uploading your files to the Assignment Drop Box.

Grade of Incomplete

• The final grade of Incomplete is granted at the discretion of the instructor; however, students must meet certain specific criteria before this grade accommodation is even possible to consider.
• The grade of Incomplete is reserved for times when students experience a serious extenuating circumstance or a crisis during the last week of class which prevents the completion of course requirements before the close of the grading period. Students also must pass the course at the time the request is made.
• Please contact me personally if you are having difficulties in meeting course requirements or class deadlines during our time together. In addition, if you are experiencing personal challenges or difficulties, it is best to contact the Academic Counselor so that you can discuss the options that might be available to you, as well as each option’s academic and financial repercussions.

Grade Disputes

• If you have any questions about a grade you have earned on an individual assignment or activity, please get in touch with mepersonally for further clarification.
• While I have made every attempt to grade you fairly, on occasion a misunderstanding may occur, so please allow me the opportunity to learn your perspective if you believe this has occurred. Together, we should be able to resolve grading issues on individual assignments.
• However, after we have discussed individual assignments’ point scores, if you still believe that the final grade you have earned at the end of the course is not commensurate with the quality of work you produced for this class, there is a formal Grade Grievance procedurewhich is outlined in the GCU Catalog and Student Handbook.