Pathophysiology

 

 

 

 

 

 

 

 

 

 

 

 

 

Pathophysiology

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Pathophysiology

Question 1:  Pathogenesis of PCOS

PCOS (polycystic ovary syndrome) is a disorder in hormone levels in women. The polycystic ovaries get enlarged, thick, and smooth on both sides.  It is caused by women producing high amounts of male hormones like androgens (testosterone and androstenedione). Luteinizing hormone increases and follicle-stimulating hormone decreases; this increases the number of androgenic hormones and reduces estrogen leading to absent or irregular ovulation.  PCOS is correlated with body resistance to insulin. High insulin levels cause large amounts of testosterone by the ovaries, which alter follicle development necessary for ovulation. Ovulation is delayed or inhibited, leading to PCOS. Insulin resistance is amplified in obese or overweight women leading to severe PCOS. PCOS is an inherited or acquired hormonal imbalance in women causing them to produce more male hormones than female hormones.  Acquired PCOS is due to insulin resistance and hormone level disorder.

Question 2: How does PCOS affect a woman’s fertility or infertility?

Increased testosterone amounts cause ovary follicles not to mature, preventing ovulation. Lack of ovulation and menstruation prevents pregnancy. Hormone imbalance causes the uterine lining not to develop enough for implantation of the fertilized egg.

Question 3: What is the pathophysiology of PID?

PID (pelvic inflammatory disease) is a disorder that causes inflammation and infection of the upper part of the female genitalia (oviduct, uterus, and ovaries). Bacteria’s infection causes it in the cervix or vagina and its spread to the upper genitalia. The bacteria include Neisseria gonorrhea, streptococcus, and chlamydia trachomatis.

Question 4: Describe the 4 stages of syphilis.

A painless sore develops when the bacteria enters the body between days 10 and 90. The patient is very contagious at this stage. In men, the chancre appears on the genitals, while in women, it can appear in the inner part of the vagina or the outer genitals. Lymph nodes near the chancre may swell. The sore heals between the third and sixth weeks, leaving a scar. Secondary stage; a small, reddish-brown rash develops two to eight weeks after developing a sore (Nyatsanza & Tipple, 2016). Symptoms show that the infection has spread to the whole body like rashes on the hand palms and feet soles, sore throat, weight loss, fever,  and hair loss. Some moist sores which contain pus may develop on the mucous membrane. The skin rash heals within two months without scarring, followed by discoloration of the skin. Latent/hidden stage; it can last for one to twenty years, with no symptoms of syphilis. The person is still contagious. Tertiary /late-stage; occurs any time in a person’s life, and it is destructive. The complications include cardiovascular syphilis, neurosyphilis, and sores in the body called gummata.

Question: What is the pathophysiology of HSV-2?

HSV-2 (herpes simplex virus-2) is passed across through contact with seropositive individuals who are actively shedding the virus. The virus invades epithelial cells and replicates intracellularly.  Symptoms appear after ten to fourteen days after exposure. The virus is dormant in periaxonal sheath, and the immune system of the patient controls its replication. After reactivation of the virus occurs, it travels through the body’s sensory nerves to the mucocutaneous sites where it replicates.

Question: Discuss how bacteria in the urine cause epididymitis.

Due to straining or lifting, urine may flow back to the epididymis, the urine cause inflammation. The bacteria in the prostate or urinary tract spreads to the epididymis.

Question 7: Explain the differences between acute bacterial prostatitis and nonbacterial prostatitis.

Acute prostatitis is caused by bacterial infection of the prostate gland, which causes inflammation.  A tight muscle on the bladder neck leads to poor emptying by the bladder forming a stale urine pool in the bladder, which harbors bacteria (Holt et al., 2016). When the contaminated urine shoots to the prostate gland because of a turbulent flow, it may develop bacterial prostatitis if a bacterium is involved. If the infection on the prostate gland is caused by chemical inflammation and no bacteria is present, it is called nonbacterial prostatitis.

Question 8: Explain how endometriosis may affect female fertility

Endometriosis distorts the anatomy of the pelvis, scars the fallopian tubes, inflames pelvic structures, alters the ovum’s quality, changes the environment of the eggs, and impairs implantation for pregnancy.

Question 9: key concepts on platelets and their role in blood clotting

Platelets are blood cells that are tiny and help in forming clots to stop bleeding in the body. They are made in the bone marrow in levels of 150,000-450,000 platelets in a microliter of blood. Damaged blood vessels send signals to platelets, which rush to where the injury is and form a clot by adhering to one another using sticky tentacles to stop the bleeding. The platelets send chemical signals to attract more platelets, which pile on the clot through a process known as aggregation.

Question 10: Discuss iron deficiency anemia and how the patient’s menstrual bleeding contributed to the diagnosis.

Iron deficiency anemia is a type of anemia caused by a lack of enough iron to form red blood cells that are normal or due to chronic loss of blood but sometimes are a combination of both causes.  The menstrual blood loss that the patient had experienced in the past months was chronic, which meant the amount of red blood cells and hemoglobin in the body is meager.

Question 11: How does pernicious anemia develop?

An autoimmune response makes antibodies made by the body attack and destroys parietal cells in the stomach lining responsible for making intrinsic factor. The stomach can no longer make intrinsic factors; hence vitamin B12 cannot be absorbed from the stomach to the small intestines (Morawiec-Szymonik et al., 2020). Surgical removal of the stomach reduces parietal cells leading to a lack of intrinsic factor. Lack of intrinsic can also be caused by medicines, infections, and diet, leading to pernicious anemia.

Question 12: How does pernicious anemia cause the neurological manifestations that are often seen in PA patients?

Pernicious anemia causes degeneration of the patient’s spinal cord and damage to the myelin. Degenerated spinal leads to neurological manifestations and signs like ataxia, difficulty in walking and speaking, paresthesia, and memory loss.

 

Question 13: What is ACD, and how does it develop?

ACD (anemia of chronic disease) lacks enough red blood cells for carrying oxygen to the body from the lungs. It develops due to changes in the body due to chronic diseases like diabetes, arthritis, kidney disease, and cancer. The changes are the inability of bone marrow to make red blood cells, short-lived red blood cells, and the body’s iron’s inability to make red blood cells.

Question 14: Why do patients with chronic kidney disease (CKD) develop ACD?

When kidneys are diseased, they make insufficient EPO; hence the bone marrow makes fewer red blood cells leading to ACD; this deprives the body of oxygen. Blood loss during hemodialysis and reduced levels of folic acid, vitamin B12, and iron, which are needed by red blood cells to make hemoglobin lead to anemia in CKD patients.

Question 15: What is ITP, and why do you think this patient has acute, rather than chronic, ITP?

ITP (immune thrombocytopenic purpura) is a sickness where the immune system produces antiplatelet antibodies that attach themselves to platelet surfaces as if the platelets are invading viruses or bacteria. The infected platelets are recognized by the patient’s spleen as abnormal hence are removed from the body. It leads to a drop in platelets’ levels in the blood (Sugiura et al., 2018).  When the platelets are below the normal range, the person is diagnosed with thrombocytopenia. The patient experiences abnormal bleeding due to minor injuries like a bruise or small cut. Below 10,000 platelets, the patient may bleed even without injury. The patient has acute ITP because it has lasted less than three months, and the patient is fourteen years.

Question 16: What is the underlying pathophysiology of heparin induced thrombocytopenia?

The underlying mechanism behind heparin-induced thrombocytopenia is an immune response.  HIT thrombocytopenia is mainly because of the clearance of antibody-coated platelets and activated platelets.

Question 17: How does someone who is receiving heparin develop arterial and venous thrombosis?

Heparin has a high affinity towards PF4, which is found on cell surfaces and platelet granules. The heparin binds to PF4 depending on its molecular weight, sulfation degree, and chain length. After heparin binds to PF4, the PF4 conformation is changed, exposing neoepitopes, which are immunogens that generate heparin-PF4 antibodies. The Heparin-PF4 antibodies activate platelets leading to platelet consumption and release of platelet micro-particles that are thrombotically derived. The particles promote the generation of excess thrombin, which results in thrombosis.

Question 18: What is the pathophysiology of TTP?

TTP (thrombotic thrombocytopenic purpura) develops due to inhibition of the ADAMTS13 enzyme-mediated by auto-antibody. Metalloprotease cleaves large multimers of vWF (von Willebrand factor) to small groups. When the number of vWF multimers circulates increases, it increases the adhesion of platelets to endothelial injury areas leading to platelet clot formation (Sadler, 2015). As platelet clots to form thrombi, the number of circulating platelets decreases, causing bleeding, which is life-threatening. The red blood cells that pass through the clots undergo shear stress damaging their membranes, and the RBC ruptures in the blood vessels causing anemia and schistocyte formation. Blood clots present in the blood vessels reduce blood flow to the organs, causing cellular injury and organ damage.

Question 19: What is DIC, and how does it develop?

DIC (disseminated intravascular coagulation) is a condition causing blood clotting to occur abnormally in all the body’s blood vessels. It develops due to a disease or injury that causes an overreaction of the blood’s clotting process. The blood clots in the blood vessels reduce blood flow to the organ, leading to organ damage.  The clotting factors and platelets eventually get used up, leading to bleeding in the nose, mouth, inside the body, or beneath the skin.

Question 20: What factors contribute to the development of DIC?

• Infection caused by parasites or viruses causes the body’s immune response to cause inflammation.
• Major injury or damage of tissues and organs
• A lifestyle like a drug use
• Other medical conditions like cancer, heatstroke, and complicated pregnancy which cause clotting factors.

 

 

 

 

 

References

Holt, J. D., Garrett, W. A., McCurry, T. K., & Teichman, J. M. (2016). Common questions about chronic prostatitis. American family physician, 93(4), 290-296.

Morawiec-Szymonik, E., Foltyn, W., Marek, B., Głogowska-Szeląg, J., Kos-Kudła, B., & Kajdaniuk, D. (2020). Antibodies involved in the development of pernicious anemia and other autoimmune diseases. POLISH ARCHIVES OF INTERNAL MEDICINE-POLSKIE ARCHIWUM MEDYCYNY WEWNETRZNEJ, 130(1), 31-37.

Nyatsanza, F., & Tipple, C. (2016). Syphilis: presentations in general medicine. Clinical Medicine, 16(2), 184.

Sugiura, T., Yamamoto, K., Murakami, K., Horita, S., Matsusue, Y., Nakashima, C., & Kirita, T. (2018). Immune thrombocytopenic purpura detected with oral Hemorrhage: A case report—Journal of Dentistry, 19(2), 159.

Sadler, J. E. (2015). What’s new in the diagnosis and pathophysiology of thrombotic thrombocytopenic purpura. Hematology, 2015(1), 631-636.