Question

 

What is the pathogenesis of polycystic ovarian syndrome (PCOS)?

How does PCOS affect a woman’s fertility or infertility?

What is the pathophysiology of pelvic inflammatory disease (PID).?

Describe the 4 stages of syphilis.

What is the pathophysiology of HSV-2?

Discuss how bacteria in the urine causes epididymitis.  

Explain the differences between acute bacterial prostatitis and nonbacterial prostatitis.

Explain how endometriosis may affect female fertility.

An APRN working in an anticoagulation clinic has been asked by the local college to present a lecture on platelets and their role in blood clotting to the graduate pathophysiology nursing students.  Question: What key concepts should the APRN include in the presentation?

Discuss iron deficiency anemia and how the patient’s menstrual bleeding contributed to the diagnosis.

How does pernicious anemia develop?

How does pernicious anemia cause the neurological manifestations that are often seen in patients with PA?

What is anemia of chronic disease (ACD) and how does it develop?

Why do patients with chronic kidney disease (CKD) develop anemia of chronic disease (ACD)?

What is immune thrombocytopenia purpura (ITP) and why do you think this patient has acute, rather than chronic, ITP?

What is underlying pathophysiology of heparin induced thrombocytopenia?

The APRN assesses the patient and notes there is a decreased right posterior tibial pulse with cyanosis of the entire foot. The APRN recognizes this probably represents arterial thrombus formation. How does someone who is receiving heparin develop arterial and venous thrombosis?

What is the pathophysiology of thrombotic thrombocytopenic purpura (TTP)?

What is disseminated intravascular coagulation (DIC) and how does it develop?

What factors contribute to the development of disseminated intravascular coagulation (DIC) ?  

Answer 1

 

Q)What is the pathogenesis of polycystic ovarian syndrome (PCOS)?

Ans -The pathogenesis of polycystic ovary syndrome (PCOS) is not precisely known. There are several mechanisms that have been suggested to play a role in the pathogenesis of PCOS, including hormonal imbalance, insulin resistance, and genetic inheritance. Polycystic ovaries are enlarged on both sides and have a smooth, thick, avascular capsule. Notably, hyperplasia of the cells surrounding the follicles can prevent the release of the egg and ovulation.

Q)How does PCOS affect a woman’s fertility or infertility?

Ans - PCOS is a complex hormonal condition which affects up to one in five women of reproductive age. Most women with PCOS have elevated levels of a type of hormone called luteinising hormone, which brings about ovulation, and reduced levels of a hormone called “follicle stimulating hormone”, which is essential for pubertal development and the function of women’s ovaries and men’s testes. Women with PCOS also have an underproduction of oestrogen (“female” hormones) and an overproduction of androgens (“male” hormones). This causes tiny cysts on the surface of the ovaries.Due to these hormonal imbalances, women with PCOS often have irregular menstrual cycles because they don’t ovulate or ovulate only occasionally. So women with PCOS are more likely to have trouble conceiving than other women. While most women who have PCOS become pregnant, they often take longer to fall pregnant and are more likely to need fertility treatment than women without PCOS.

Q) What is the pathophysiology of pelvic inflammatory disease (PID).?

Ans- Etiology. PID results from microorganisms ascending from the v_a_g_i_n_a and cervix into the endometrium and fallopian tubes. Neisseria gonorrhoeae and Chlamydia trachomatis are common causes of PID; they are transmitted sexually. Mycoplasma genitalium, which is also sexually transmitted, can also cause or contribute to PID.

Q) Describe the four stages of syphilis?

Ans -Basically this has been divided into 4 stages .In stage 1 the symptoms in the first two can be so mild that you might not notice them. One stage -- latent syphilis -- doesn’t have symptoms.

The other three phases have distinct symptoms. They develop as follows:

Primary

• Painless sores appear at the site of infection (mouth, anus, rectum, vagina, or penis). These are called chancres.
• The sores heal on their own after 3 to 6 weeks, but you can still spread syphilis.
• It’s easily treated and cured with medicine.

Secondary

• Rough red or reddish brown rash on palms of hands and soles of feet
• Swollen lymph nodes
• Fever
• Sore throat
• Patchy hair loss
• Headaches and body aches
• Extreme tiredness (fatigue)

These symptoms will go away, even if you don’t get treated. But if you’re not treated, your infection will get worse.

Latent

During this phase, the syphilis bacteria are still alive in your body, but you have no signs or symptoms of the infection. You’re not contagious during this stage, but syphilis may still affect your heart, brain, nerves, bones, and other parts of your body. This phase can last for years.

Q) What is the pathophysiology of HSV-2?

Ans- Acquisition of HSV-2 infection is usually the consequence of transmission by genital contact. Virus replicates in the genital, perigenital or anal skin sites with seeding of the sacral ganglia (Fig. 32.2). As is the case of HSV-1's ability to infect the genital tract, HSV-2 can infect the mouth.

Q)Discuss how bacteria in the urine causes epididymitis.  

Ans :Bacteria from a urinary tract or prostate infection might spread from the infected site to the epididymis. Also, viral infections, such as the mumps virus, can result in epididymitis. Urine in the epididymis (chemical epididymitis

Q)Explain the differences between acute bacterial prostatitis and nonbacterial prostatitis.

Ans : In acute prostatitis, the patient will generally benefit from a course of antibiotics to clear the infection. Chronic prostatitis describes the recurrent, intermittent flare-up of pain due to inflammation of the prostate not relieved by a course of antibiotics.

Q)Explain how endometriosis may affect female fertility.

Ans : Endometriosis can influence fertility in several ways: distorted anatomy of the pelvis, adhesions, scarred fallopian tubes, inflammation of the pelvic structures, altered immune system functioning, changes in the hormonal environment of the eggs, impaired implantation of a pregnancy, and altered egg quality.

QUESTIONS--------

Q)What key concepts should the APRN include in the presentation?

Ans- Platelets are tiny blood cells that help your body form clots to stop bleeding. If one of your blood vessels gets damaged, it sends out signals to the platelets. The platelets then rush to the site of damage. they form a plug (clot) to fix the damage.The process of spreading across the surface of a damaged blood vessel to stop bleeding is called adhesion. This is because when platelets get to the site of the injury, they grow sticky tentacles that help them stick (adhere) to one another. They also send out chemical signals to attract more platelets. The additional platelets pile onto the clot in a process called aggregation.

Q) Discuss iron deficiency anemia and how the patient’s menstrual bleeding contributed to the diagnosis.

Ans -Iron deficiency is one of the most common causes of anemia, and blood loss is the most common cause of iron deficiency in adults. In men and postmenopausal women, iron deficiency usually indicates bleeding in the digestive tract. In premenopausal women, menstrual bleeding is the most common cause of iron deficiency.Excessive or prolonged menstrual bleeding can lead to other medical conditions, including: Anemia. Menorrhagia can cause blood loss anemia by reducing the number of circulating red blood cells.

Q)How does pernicious anemia develop?

Ans-There is also a juvenile form of the disease, but pernicious anemia typically does not appear before the age of 30. The onset of the disease is slow and may span decades. When the disease goes undiagnosed and untreated for a long period of time, it may lead to neurological complications.

Q) How does pernicious anemia cause the neurological manifestations that are often seen in patients with PA?

Ans - These neurologic symptoms are due to myelin degeneration and loss of nerve fibers in the dorsal and lateral columns of the spinal cord and cerebral cortex. Neurologic symptoms and findings may be present in the absence of anemia. This is more common in patients taking folic acid or on a high-folate diet.

Q)What is anemia of chronic disease (ACD) and how does it develop?

Ans- Anemia of chronic disease refers to having low levels of red blood cells as a result of autoimmune diseases (diseases in which the body's immune system attacks joints and/or body organs) or other chronic illnesses.

Q) Why do patients with chronic kidney disease (CKD) develop anemia of chronic disease (ACD)?

Ans- ACD, therefore, is caused by a complex interplay of proinflammatory cytokines which induce dysregulation in iron homeostasis, erythroid progenitor cell differentiation, erythropoietin synthesis and red cell longevity, all culminating in the pathogenesis of anemia.

Q)What is immune thrombocytopenia purpura (ITP) and why do you think this patient has acute, rather than chronic, ITP?

Ans- Idiopathic thrombocytopenic purpura is an immune disorder in which the blood doesn't clot normally. This condition is now more commonly referred to as immune thrombocytopenia (ITP). ITP can cause excessive bruising and bleeding. An unusually low level of platelets, or thrombocytes, in the blood results in ITP.

Q)What is underlying pathophysiology of heparin induced thrombocytopenia?

Ans-The pathophysiological basis of HIT results from the formation of an immunocomplex consisting of an auto-antibody against platelet factor 4 (PF4) - heparin complex, which binds to the surface of platelets and monocytes, provoking their activation by cross-linking FcgIIA receptors.

Q)What is the pathophysiology of thrombotic thrombocytopenic purpura (TTP)?

Ans- The pathophysiological basis of HIT results from the formation of an immunocomplex consisting of an auto-antibody against platelet factor 4 (PF4) - heparin complex, which binds to the surface of platelets and monocytes, provoking their activation by cross-linking FcgIIA receptors.

QUESTIONS-----

Q)How does someone who is receiving heparin develop arterial and venous thrombus Cytopenia and what is the Pathophysiology of TTP?

Ans-HIT predisposes to thrombosis (the abnormal formation of blood clots inside a blood vessel) because platelets release microparticles that activate thrombin, thereby leading to thrombosis. When thrombosis is identified the condition is called heparin-induced thrombocytopenia and thrombosis (HITT).

Pathophysiology --

The pathophysiological basis of HIT results from the formation of an immunocomplex consisting of an auto-antibody against platelet factor 4 (PF4) - heparin complex, which binds to the surface of platelets and monocytes, provoking their activation by cross-linking FcgIIA receptors.

Q)What is disseminated intravascular coagulation (DIC) and how does it develop?

Ans-Disseminated intravascular coagulation is a condition in which small blood clots develop throughout the bloodstream, blocking small blood vessels. The increased clotting depletes the platelets and clotting factors needed to control bleeding, causing excessive bleeding.

Q)What factors contribute to the development of disseminated intravascular coagulation (DIC) ?

Ans-Causes of DIC include: Inflammation in response to infection, injury, or an illness. Severe tissue damage, such as from burns or trauma. Clotting factors caused by some cancers or pregnancy complications