NR507 Advanced Pathophysiology Quiz -Exam Questions and Answers

NR507 Advanced Pathophysiology Quiz -Exam Questions and Answers
NR507 Advanced Pathophysiology Quiz -Exam Questions and Answers
You are contacted by an attorney representing a client who has been charged with child abuse and whom faces loss of her child and 15 years in prison. The record indicated that the child was 4 years old and presented to the ER room with a broken arm and a broken leg. There also appeared to be multiple previous fractures. Now, you examine the child and find blue sclera, a sunken chest wall, severe scoliosis, and you observe a triangular face and prominent forehead. You confirm that there have been multiple previous fractures by evaluating the previous X-rays. This is a genetic disorder.

What is the most likely genetic disease that this presents and why?
What is the molecular basis of this disease?
Before, calling the police what should the initial clinician have done?

The presenting genetic disease is most likely osteogenesis imperfecta (OI), also known as brittle bone disease. OI consists of a diverse group of symptoms related to genetic mutations found in type 1 collagen biosynthesis (Golshani, Ludwig, Cohn, & Kruse, 2016). The Sillence classification system delineates OI based on the severity of the disease. Types II and III are the most severe, are characterized by autosomal recessive inheritance, can cause severe deformity in the neonate, stillbirth, and these patients have a short life expectancy (McCance, Huether, Brashers, & Rote, 2013). Types I and IV are considered less severe forms, are characterized by inherited autosomal dominant trait, and the onset varies in age from childhood to adulthood (McCance et al., 2013). The main characteristics of OI include low bone mass and elevated bone fragility that leads to fractures and deformities (Golshani et al., 2016). The classic manifestations associated with OI are osteoporosis like and include an increased incidence of fractures, triangular facies, possible bony deformations, poor dentition, possible blue sclera, and possible vascular weaknesses (McCance et al., 2013).
To fully understand the disease process, it is important to know what happens at the molecular level in regards to the biosynthesis of type 1 collagen. First, procollagen is created via rough endoplasmic reticulum as triple helix that form two collagen chains, a1(I) and a2(I), which are encoded by the COLIA1 and COILA2 genes (Golshani et al., 2016). Both chains have C and N terminal peptides (Golshani et al., 2016). These chains also have domains with repetitive amino acid sequence that contain glycine by every third amino acid, which permits the triple helix arrangement (Golshani et al., 2016). Once post-translational modifications and folding occurs, the procollagen molecule is carried to the extracellular matrix, cleavage of the terminal propeptides takes place, and the collagen molecule forms (Golshani et al., 2016). When the collagen molecule forms, it forms fibrils via covalent bonding inside and in the middle of triple helix molecules (Golshani et al., 2016). Additionally, the fibrils formed will accumulate and produce type 1 collagen fibers (Golshani et al., 2016).
Upon examination, medical professionals may find evidence of bone fractures in various stages of healing, including fractures of the skull, metaphysis bones, and ribs, leading to the suspicion of child abuse (Golshani et al., 2016). While OI is rare, it should still be included in ones differential diagnosis (Golshani et al., 2016). Evaluation and treatment of OI is established by the presence of clinical manifestations, therefore it is very important clinicians are able to recognize them (McCance et al., 2013). In all types of the disease process, serum alkaline phosphate levels will be elevated (McCance et al., 2013). Another way to evaluate OI is by culturing skin fibroblast collagen via electrophoresis; 95 percent of people tested who have OI show a decreased amount of collagen (McCance et al., 2013). The initial clinician should have questioned the child’s symptoms; diagnosis of OI is distinct when some key elements exist including blue sclera, scoliosis, wormian bones, and a family history (Golshani et al., 2016). Without these features, diagnosis can be difficult (Golshani et al., 2016).
Golshani, K.R., Ludwig, M.R., Cohn, P.L., & Kruse, R. (2016). Osteogenesis Imperfecta. Delaware Medical Journal, 88(6), 178-185.
McCance, K. L., Huether, S. E., Brashers, V. L., & Rote, N. S. (2013). Pathophysiology: The biologic basis for disease in adults and children (7th ed.). St. Louis, MO: Mosby.
Johnny is a 5-year-old Asian boy who is brought to a family practice office with a “runny” nose that started about 1 week ago but has not resolved.  He has been blowing his nose quite frequently and “sores” have developed around his nose.  His mother states, “The sores started as ‘big blisters’ that rupture; sometimes, a scab forms with a crust that looks like “dried maple syrup” but continues to seep and drain.”  She is worried because the lesions are now also on his forearm.  Johnny’s past medical and family histories are normal.  He has been febrile but is otherwise asymptomatic.  The physical examination was unremarkable except for moderate, purulent rhinorrhea and 0.5- to 1-cm diameter weeping lesions around the nose and mouth and on the radial surface of the right forearm.  There is no regional lymphadenopathy.

Write a differential of at least three (3) possible diagnoses and explain how each may be a possible answer to the clinical presentation above. Remember, to list the differential in the order of most likely to less likely.
Based upon what you have at the top of the differentials how would you treat this patient?

When would you allow the student back to school? Elaborate on your reasoning?

Impetigo is a bacterial skin infection seen in infants and children and is more commonly seen in mid to late summer, especially in climates that are hot and humid(McCance, Huether, Brashers, & Rote, 2013). Impetigo is prevalent in settings like daycare or in crowded areas with poor sanitary conditions (McCance et al., 2013). Impetigo pustules or vesicles may be seen anywhere however, the face and extremities are the more common sites (Allmon, Deane, & Martin, 2015). Predisposing factors for impetigo include anemia and malnutrition however, healthy children are also affected (McCance et al., 2013).
Bullous impetigo  – Bullous impetigo is a highly contagious bacterial infection caused by Staphylococcus aureus and is carried in the anterior nares, the fingernails, and the perineal area (McCance et al., 2013). The pathogen is transmitted via contact with an infected individual or by non-direct contact, such as equipment that is contaminated (McCance et al., 2013). A person becomes infected because the Staphylococcus aureus produces exfoliative toxins (ETs) that inoculate into the dermis and epidermis causing blisters to form (McCance et al., 2013). The blisters are usually located around the patient’s nose or mouth however, the hands and other exposed regions such as the extremities can also be affected (McCance et al., 2013). The blisters can amalgamate, forming superficial bullae that can be localized or spread over different areas of the skin (McCance et al., 2013). When the bullae break open, a honey colored crust will form around the area; this crust is a hallmark sign of impetigo (McCance et al., 2013). In bullous impetigo, regional lymphadenopathy is uncommon (McCance et al., 2013).
The treatment of choice for impetigo is antibiotics, either topical or systemic. Topical antibiotics, such as mupirocin or fusidic acid, are recommended for localized areas of impetigo (Watkins, 2013). Topical antibiotics need to be rubbed on the lesions and the skin area around the lesion 3 times a day for 7 to days or until the lesions are healed (Watkins, 2013). If a patient has an allergy to mupirocin or fusidic acid, an alternative antiseptic such as hydrogen peroxide, chlorhexidine, or iodine may be used (Watkins, 2013). If topical antibiotics are ineffective, the lesion should be swabbed to determine the causative pathogen and the pathogens sensitivity to antibiotics (Watkins, 2013). Systemic antibiotics may be needed for severe cases or for those that did not respond to topical antibiotics (Watkins, 2013). Systemic antibiotic options include flucloxacillin and clarithromycin, if the patient is allergic to penicillin (Watkins, 2013). Phenoxymethylpenicillin should be added to the treatment if erysipelas is present (Watkins, 2013). Patients with MRSA or glomerulonephritis need to be referred to a specialist for care (Watkins, 2013). Education should include proper hand hygiene and seclusion of the child’s items that could spread the infection such as wash cloths, linens, towels, clothes, and utensils and glasses used for eating and drinking (McCance et al., 2013). Children should not return to school or daycare until the lesions are completely crusted over and healed, or for at least 48 hours after beginning antibiotics because antibiotics reduce the infection period (Watkins, 2013).
Johnny fits the presentation for impetigo, most likely bullous impetigo, based on his clinical manifestations, especially the lack of lymphadenopathy. However, a diagnosis of nonbullous is also conceivable. I  would start Johnny on topical antibiotics and advise his mother to keep him home until the lesions have healed or for at least 48 hours after starting the antibiotic treatment. I would also educate her on hygiene precautions so the infection does not spread to others. Also, she must thoroughly bathe him with soap and water, carefully removing any crust around the lesions (Watkins, 2013).
Nonbullous impetigo – Nonbullous impetigo, the more common of the types, is also a highly contagious bacterial infection caused by Staphylococcus aureus or group A Streptococcus pyogenes. A person can become infected with either pathogen via direct physical contact or via insect bites (McCance et al., 2013). Nonbullous impetigo forms superficial, acute, vesicles with honey like serum; when the vesicle ruptures, yellow to white-brown crust will form (McCance et al., 2013). These lesions can look similar to herpes simplex lesions and therefore a distinction should be made (McCance et al., 2013). Unlike bullous impetigo, it is common to see regional lymphadenopathy in nonbullous (McCance et al., 2013). Treatment and education are the same for both types of impetigo (McCance et al., 2013).
Even though nonbullous is the more common of the two types, based on clinical manifestations, nonbullous does not completely fit the presentation. However, the presentation between the two types is so similar it cannot be fully ruled out.
Herpes simplex virus – Herpes simplex virus (HSV) are usually caused by two different strains of the virus, HSV 1 and HSV 2 and can occur all over the body (McCance et al., 2013). The only way to distinguish between the two is laboratory testing. HSV type 1 is transmitted via infected saliva (McCance et al., 2013). The first infection is referred to as the primary infection where the virus travels to the dorsal ganglion root and remains latent (McCance et al., 2013). In the secondary phase, reactivation of the virus occurs and the virus travels via peripheral nerves to the original site of infection, where it sheds (McCance et al., 2013). Reactivation of the virus can occur related to stress, skin irritation, fatigue, ultraviolet light, and fever (McCance et al., 2013). HSV-1 lesions present as inflamed, painful vesicles in rash like patterns or clusters and in children are typically located on the lips, in and/or around the nose, on the tongue, and within the mouth (McCance et al., 2013). When the vesicle ruptures, a crust will form over the area (McCance et al., 2013). Lesions can last up to 6 weeks if left untreated (McCance et al., 2013). Generally, topical antivirals can help resolve the lesions in 2 weeks (McCance et al., 2013). Additionally, oral antivirals can be given for acute infections or for daily use as a suppressive therapy (McCance et al., 2013).
Impetigo can be mistaken for herpes simplex virus because their lesions can look similar. However, HSV does not fit the presentation. I do not believe Johnny has HSV.
Allmon, A., Deane, K., & Martin, K.L. (2015). Common skin rashes in children. American Family Physician, 92(3), 211-216.
McCance, K. L., Huether, S. E., Brashers, V. L., & Rote, N. S. (2013). Pathophysiology: The biologic basis for disease in adults and children (7th ed.). St. Louis, MO: Mosby.
Watkins, J. (2013). Bullous and non-bullous impetigo. Practice Nursing, 24(2), 95-96.
Keisha, a 13-year-old female, has come into your urgent care center. She has red conjunctiva, a cough and a fever of about 104 F, She also has a rash on her face a possibly the beginning of a rash on her arms. About 10 days ago she was around another student who had similar symptoms. 

Write three (3) differential diagnoses?
What are some of the complications of this disease, assume that the top of your differential is the definitive?
Assume that the second item you place on your differential is the definitive diagnosis. What are some complications of that disease?

Rubeola – Rubeola is an acute, viral disease seen in children that is very contagious (McCance, Huether, Brashers, & Rote, 2013). A specific RNA virus containing the paramyxovirus causes rubeola, it is transmitted via droplets from individuals already infected with the virus (McCance et al., 2013). This means Rubeola can be spread via sneezing, breathing, and coughing (Grif Alspach, 2015). The virus can remain on surfaces and in the air for up to 2 hours (Grif Alspach, 2015). Rubeola has an incubation period that lasts 7 to 12 days; during this time, the infected person will not have any symptoms (McCance et al., 2013). The virus is introduced via the respiratory tract where it latches onto alveolar macrophages and dendritic cells, the virus increases in size in the lymphatic tissue, and then advances to systemic disease (McCance et al., 2013). Early symptoms include high fevers (up to 105 degrees), skin rash, koplik spots, conjunctivitis, cough, malaise, and coryza (Grif Alspach, 2015). Approximately 1 to 4 days after being exposed to the virus, a maculopapular rash will appear, it begins on the forehead and spreads to the trunk, extremities, hands, feet and even the palms and soles of the hands and feet (Grif Alspach, 2015). It is important to know that patients are contagious 4 days prior to the development of the rash and 4 days after it begins (Grif Alspach, 2015). Immunocompromised patients may not develop a rash so providers should be able to recognize symptoms without the rash development (Grif Alspach, 2015). The rash will gradually begin to fade, beginning from the head down, and will typically resolve on it’s own within 7 to 10 days (Grif Alspach, 2015). One way to distinguish Rubeola from Rubella is conjunctivitis is present in Rubeola but not in Rubella (Grif Alspach, 2015). Confirmation via lab work can be achieved by serum or swabbing of nasal cavity or oropharyngeal cavity (Grif Alspach, 2015).  Even though most people will resolve the disease on their own, some people can have serious complications such as encephalitis and pneumonia (Grif Alspach, 2015). The best way to prevent Rubeola is through the MMR vaccine (Grif Alspach, 2015). Additionally, hand hygiene is essential in helping to decrease the spread of disease.
Rubella – Rubella is a communicable disease seen in children and young adults, it is caused by an RNA virus that enters via the respiratory tract and invades the bloodstream (McCance et al., 2013). Rubella is contracted via droplets, maternal-fetus transmission, or contact with nasopharyngeal secretions (Chan, MacFadden, & Leis, 2016). The virus has an incubation period of 14 to 23 days; patients are thought to be contagious one week prior to the onset of the rash and 4 days after the rash begins (Chan et al., 2016). Early symptoms include a low grade fever (which usually presents 1 to 5 days before the rash), possible enlarged postauricular and cervical lymph nodes, sore throat, headaches, cough, and runny nose (McCance et al., 2013). Other clinical manifestations may include arthritis, arthralgias, and cold symptoms (Chan et al., 2016). When the rash develops, it is characterized by pinpoint pink macules; the rash will begin on the head and spread down to the trunk and extremities in 24 hours (Chan et al., 2016). The rash with Rubella is absent on the palms and soles on the hands and feet (McCance et al., 2013). Once someone contracts the disease, a lifelong immunity develops against the disease (McCance et al., 2013). The diagnosis is typically made via lab work (Chan et al., 2016). Preventative treatment for Rubella is vaccination (Chan et al., 2016). Treatment for Rubella is supportive and includes using a vaporizer, fluids, and rest (McCance et al., 2013). Some patients may develop mild encephalitis or peripheral neuritis (McCance et al., 2013). Significant mortality occurs in people who do not vaccinate against Rubella with encephalitis, pneumonia, and croup causing the largest number of deaths related to the disease (McCance et al., 2013).
Chickenpox – Chickenpox affects most patients in the first decade of their life (McCance et al., 2013). It is spread via airborne droplets and contact with an infected person (McCance et al., 2013). Patients are contagious at least one day prior to the development of lesions and about 5 to 6 days after the lesions appear (McCance et al., 2013). Prodromal symptoms include itching, then vesicles will begin to appear (McCance et al., 2013). Fever may be present, up to 104 degrees and typically lasts 2 to 3 days (McCance et al., 2013). The vesicles usually appear on the face, scalp, or trunk first then will spread to the extremities later (McCance et al., 2013). In chickenpox, the lesions will characteristically heal in various stages therefore macules, papules, and vesicles can all be seen; there can be anywhere from 100 to 300 lesions present and all in different stages of development and healing (McCance et al., 2013). On occasion, vesicles may appear in the mouth, on the palms of hands, soles of feet, pharynx, and conjunctiva (McCance et al., 2013). Complications are unusual in children and more common in adults, complications can include epistaxis, hematuria, varicella pneumonia, and laryngeal edema (McCance et al., 2013). Once someone contracts the virus, immunity is developed (McCance et al., 2013). There is a vaccine to help prevent chickenpox (McCance et al., 2013). For uncomplicated cases, supportive care includes wet dressings, baths, and oral antihistamines (McCance et al., 2013). Oral antiviral medications can be given to reduce symptoms, especially in immunocompromised patients (McCance et al., 2013).
Chan, T., MacFadden, D.R., & Leis, J.A. (2016). Rubella in a returned traveller. CMAJ: Canadian Medical Association Journal = Journal De L’association Medicale Canadienne, 188(5), 363-366. doi: 10.1503/cmaj.150574
Grif Alspach, J. (2015). Measles: Eliminated but not eradicated. Critical Care Nurse, 35(4), 9-13. doi: 10.4037/ccn2015629.
McCance, K. L., Huether, S. E., Brashers, V. L., & Rote, N. S. (2013). Pathophysiology: The biologic basis for disease in adults and children (7th ed.). St. Louis, MO: Mosby
Thank you for your discussion.  The good (maybe) thing about this condition is that as the child grown, the fractures tend to decrease in severity.  Why might a thorough hearing examination be helpful in its diagnosis?
Dr. Winters7382
Hi Dr. Winters,
Thank you! One of my article does address the auditory issues that can arise, as well as our text, and I completely missed it! Per Swinnen, De Leenheer, Goemaere, Cremers, Coucke, and Dhooge (2012), skeletal conditions related to OI can improve when the patient enters into adulthood, unfortunately about 50 percent of these patients develop hearing loss sometime during adulthood. Hearing impairment is related to disease of the soft tissue in the ear as well as the middle ear bone (Golshani, Ludwig, Cohn, & Kruse, 2016). Hearing exams should begin in the teen years and continue regularly into adulthood (Golshani et al., 2016). Hearing impairment is usually related to a conductive hearing problem at first and typically advances to mixed hearing loss later; some patients may develop pure sensorineural hearing loss (SNHL) (Swinnen et al., 2012). Conductive hearing loss is usually related to otosclerosis-like lesions, which produce a fixed and thickened stapes footplate (Swinnen et al., 2012). Additionally, conductive hearing loss can also be related to ossicular discontinuity, particularly by atrophied or fractured stapes crura and replaced with fibrous threads (Swinnen et al., 2012). If or when the disease advances to a mixed hearing loss, a CT scan will show pericochlear demineralization (Swinnen et al., 2012). A thorough hearing exam could show middle ear abnormalities and/or conductive hearing loss, which could help lead to the diagnosis of OI.
Golshani, K.R., Ludwig, M.R., Cohn, P.L., & Kruse, R. (2016). Osteogenesis Imperfecta. Delaware Medical Journal, 88(6), 178-185.
Swinnen, F.R., De Leenheer, E.R., Goemaere, S., Cremers, C.J., Coucke, P.J., & Dhooge, I.M. (2012). Association between bone mineral density and hearing loss in osteogenesis imperfecta. The Laryngoscope, 122(2), 401-408.
Hi Amber,
Thank you for your post! I also had a hard time distinguishing between bullous and non-bullous impetigo. Ultimately, I went with bullous because the patient did not show any regional lymphadenopathy. However, the clinical manifestations are so similar I was not 100 percent sure I chose the correct type. According to Lewis (2016), bullous is less contagious than nonbullous and its lesions are more likely to affect the face, extremities, the trunk, axillae, and perianal areas. Bullous differs from nonbullous in two ways, bullous can affect buccal mucous membranes but rarely causes regional lymphadenopathy (Lewis, 2016). In the clinical setting, a bacterial culture may be obtained from fresh exudate (found under the scab) or a gram stain and culture of blister fluid may be performed (Lewis, 2016). The gram stain will show gram-positive cocci in clusters for Staphylococcus aureus and gram-positive cocci in chains for Streptococcus pyogenes (Lewis, 2016). The good news, per McCance, Huether, Brashers, and Rote (2013), is that the treatment for both is the same. Therefore, antibiotic therapies chosen have to provide coverage against Staphylococcus aureus and Streptococcus pyogenes (Lewis, 2016).
Lewis, L. (2016). Impetigo. Medscape. Retrieved from
McCance, K. L., Huether, S. E., Brashers, V. L., & Rote, N. S. (2013). Pathophysiology: The biologic basis for disease in adults and children (7th ed.). St. Louis, MO: Mosby.

Considering the pathophysiology of osteoporosis, which cytokines and hormones decrease receptor activator of RANKL expression?(Points : 2)

IL-4 and transforming growth factor-beta (TGF-ß)

IL-1 and tumor necrosis factor-alpha (TNF-)

IL-11 and glucocorticoids

IL-17 and parathyroid hormone (PTH)

Rhabdomyolysis is characterized by (Points : 2)

paralysis of skeletal muscles resulting from impaired nerve supply.

smooth muscle degeneration resulting from ischemia.

lysis of skeletal muscle cells through the initiation of the complement cascade.

release of myoglobin from damaged striated muscle cells.

Which type of osteoporosis would a person develop after having the left leg in a cast for 8 weeks to treat a compound displaced fracture of the tibia and fibula? (Points : 2)





Considering the pathophysiology of osteoporosis, what are the effects of extracellular signal regulated kinases (ERKs) and receptor activator of RANKL on osteoblasts and osteoclasts? (Points : 2)

ERKs increase the life span of osteoclasts and RANKL decreases the life span of osteoblasts.

ERKs and RANKL increase the life span of osteoclasts and decrease the life span of osteoblasts.

ERKs and RANKL increase the life span of osteoblasts and decrease the life span of osteoclasts.

ERKs increase the life span of osteoblasts and RANKL decreases the life span of osteoclasts.

What is the diagnosis of a person who has tennis elbow characterized by tissue degeneration or irritation of the extensor carpi brevis tendon? (Points : 2)

Lateral epicondylitis

Medial tendinitis


Lateral tendinitis

Which statement is false about giant cell tumors? (Points : 2)

They are an overexpression of genes including osteoprotegerin ligand (OPGL).

They are malignant, solitary, irregularly shaped tumors.

They are typically located in the epiphysis in the femur, tibia, radius, and humerus.

They are slow-growing tumors that extend over the articular cartilage.

What pattern of bone destruction is described as not well defined and not easily separated from normal bone? (Points : 2)





The pain experienced in Legg-Calvé-Perthes disease is referred to as involving (Points : 2)

elbows and upper and lower arms that is aggravated by activity and relieved by rest.

knees, inner thighs, and groin and is described as a continuous ache and relieved by anti-inflammatory drugs.

knees, inner thighs, and groin that is aggravated by activity and relieved by rest.

elbows and upper and lower arms and is described as a continuous ache and relieved by anti-inflammatory drugs.

In osteomyelitis, bacteria gain access to the subperiosteal space in the metaphysis, which is considered the “path of least resistance.” What factor makes this route for bacteria the path of least resistance? (Points : 2)

Cortex of the bone in this area is porous or maze-like.

Blood supply to the metaphysis is easily compromised.

Macrophages and lymphocytes have limited access to the subperiosteal space.

Bacteria usually spread down the medullary cavity of the bone.

Molecular analysis has demonstrated that osteosarcoma is associated with (Points : 2)





Ewing sarcoma arises from (Points : 2)

bone marrow.

bone-producing mesenchymal cells.

metadiaphysis of long bones.

embryonal osteocytes.

Which serum laboratory test is elevated in all forms of osteogenesis imperfecta? (Points : 2)



Alkaline phosphatase

Total protein

The _____ is cartilage that retains the ability to form and calcify new cartilage and deposit bone until the skeleton matures. (Points : 2)

epiphyseal line


epiphyseal cartilage

metaphyseal plate

Osteochondrosis is caused by a(n) (Points : 2)

imbalance between calcitonin and parathyroid hormone.

nutritional deficiency of calcium and phosphorus.

bacterial infection of the bone.

vascular impairment and trauma to bone.

An insufficient dietary intake of vitamin _____ can lead to rickets in children. (Points : 2)





In latex allergies, which immunoglobulin is associated with an immediate reaction? (Points : 2)





Chickenpox may be followed years later by (Points : 2)



warts (verrucae).

herpes zoster.

Cutaneous vasculitis develops from the deposit of _____ in small blood vessels as a toxic response allergen. (Points : 2)

immune complexes



T lymphocytes

Which malignancy is characterized by slow-growing lesions that usually have depressed centers and rolled borders and are frequently located on the face and neck? (Points : 2)

Squamous cell carcinoma

Kaposi sarcoma

Malignant melanoma

Basal cell carcinoma

Scleroderma is more common in women and is associated with a(n) (Points : 2)

X-linked recessive gene.

X-linked dominant gene.



Thrush is a superficial infection that commonly occurs in children and is caused by (Points : 2)




Candida albicans

What is the cause of chickenpox? (Points : 2)


Varicella-zoster virus (VZV)


Human papillomavirus

Which vascular anomaly is a congenital malformation of dermal capillaries that does not fade with age? (Points : 2)

Cutaneous hemangioma

Port-wine (nevus flammeus) stain

Strawberry hemangioma

Cavernous hemangioma

What is a common source of tinea corporis? (Points : 2)





Which contagious disease creates a primary skin lesion that is a pinpointed macule, papule, or wheal with hemorrhagic puncture site?(Points : 2)


Tinea capitis



NR507 Advanced Pathophysiology Quiz -Exam Questions and Answers


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