The illness started 2-1/2 years ago, when she started to experience occasional chest pain, lasting only for a few seconds especially during her aerobic exercise but does not incapacitate her. It did relieved by just resting. She did not bother to consult, thinking it was only the result of over-exercise. It did not affect her daily routine works. A year prior to consult, she noticed that her precordial had increased in intensity and last longer compared to those the previous ones. This manifestation of symptoms was experienced more after having an abortion but she was not D&C’d. A year ago, she has also an abortion and was D&C’d at AUFMC.
Consulted a physician to her pallor and was given Ferrous Sulfate attributing it to her abortion. Her condition improved and was asymptomatic until a week prior to consult when her chest pain recurred, precipitated by strenuous work and exercise. This time it took her about 30 minutes of rest to fell okay. She consulted to a physician and was found to be pregnant. She was advised to take easy on her work and refrain from further sex activity. An hour prior to consult, she just collapsed after complaining of moderate pre-cordial pain radiating to the back upon standing from seeing telenovela.
She was rushed to AUF emergency room and subsequently admitted. Review of Systems: Pale looking with fast heart rate and murmur over mitral area Abdomen – Ballotable mass 2 – 3 fb above s. pubis Past Personal History: Usual childhood diseases On and off URTI and given amoxicillin 500 mg Hyperacidity occasionally OB – GYNE HISTORY: Menarche at 14 years old, slight, lasting for 5 days, with no hypogastric pain, succeeding menses were regular lasting for 5 – 7 days, slight to moderate in amount with no accompanying pain, interrupted only by pregnancies.
LMP – October 17, 2013 Gr 1 – 2010 – Abortion, 10 weeks AOG, D&C’d at AUFMC Gr 2 – 2011 – Abortion, 8 weeks AOG, no D&C done because bleeding stopped after 5 days. Personal and Social History: Non – contributory Physical Examination: General Data: Conscious, coherent, ambulatory female patient Vital Signs: BP – 110/76 PR – 100/minute RR – 21/minute Temp – 37. 1C Weight – 125 lbs Ht – 63 cms Speculum Examination: No abnormalities noted Internal Examination: Cervix – Soft, non –tender, closed, thick Corpus – 2 – 3 finger breadths above s.pubis Adnexae – negative No discharge Extremities: Leg Edema (++) EPIDEMIOLOGY:
Recurrent episodes of ARF remain relatively common in adolescents and young adults. This pattern contrasts with the prevalence of RHD, which peaks between 25 and 40 years. There is no clear gender association for ARF, but RHD more commonly affects females, sometimes up to twice as frequently as males. RISK FACTORS: Organism Factors: ARF is exclusively caused by infection of the upper respiratory tract with group A streptococci.it is now thought that any strain of group A streptococcus has the potential to cause ARF.
Host Factors: Findings of familial clustering of cases and concordance in monozygotic twins—particularly for chorea—confirm that susceptibility to ARF is an inherited characteristic. Particular human leukocyte antigen (HLA) class II alleles appear to be strongly associated with susceptibility. Associations have also been described with high levels of circulating mannose-binding lectin and polymorphisms of transforming growth factor ? 1 gene and immunoglobulin genes.
High-level expression of a particular alloantigen present on B cells, D8-17, has been found in patients with a history of ARF in many populations, with intermediate-level expression in first-degree family members, suggesting that this may be a marker of inherited susceptibility. Environmental Factors: Overcrowding PATHOGENESIS: When a susceptible host encounters a group A streptococcus, an autoimmune reaction results, which leads to damage to human tissues as a result of cross-reactivity between epitopes on the organism and the host.
Cross-reactive epitopes are present in the streptococcal M protein and the N-acetylglucosamine of group A streptococcal carbohydrate and are immunologically similar to molecules in human myosin, tropomyosin, keratin, actin, laminin, vimentin, and N acetylglucosamine. It is currently thought that the initial damage is due to cross-reactive antibodies attaching at the cardiac valve endothelium, allowing the entry of primed CD4+ T cells, leading to subsequent T cellmediated inflammation.
Episodes of recurrent ARF will result to repeated or ongoing infections possibly driving the valvular inflammatory response ultimately resulting to rheumatic heart disease. CLINICAL MANIFESTATIONS: RHD does not always cause symptoms. When it does, symptoms may include: Chest pain Heart palpitations Breathlessness on exertion Breathing problems when lying down (orthopnea) Waking from sleep with the need to sit or stand up (paroxysmal nocturnal dyspnea) Swelling (edema) Fainting (syncope) Stroke Fever associated with infection of damaged heart valves. Reference: Harrison’s Principles of Internal Medicine, 18e.