Case Study Sildenafil

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Pages: 6

CC: Follow up on sildenafil HPI: Mr. TB is a 73 y/o Caucasian male with a past medical history of PAH, COPD, HTN, presents to clinic for a follow up regarding his new use of sildenafil. His medical conditions are managed with Albuterol, Furosemide, Oxygen, ProAir HFA, Sildenafil, Symbicort, Valsartan-hydrochlorothiazide. Patient c/o of increased ankle swelling that started about two weeks ago. The swelling is not associated with additional symptoms, and is generally worse in the morning. Patient denies coughing, SOB, orthopnea, and chest pain. PMH: HTN, PAH, COPD, previous Hepatitis A infection PSH: Cataract surgery Meds:
Albuterol 2.5 mg/3l q 4 hours
Astaxthin 12mg 1 per day
Coenzyme Q10 200mg
Furosamide 40 mg
Liver support
Multivitamins
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GU: denies incontinence, urinary frequency/urgency, nocturia or hesitancy
Extremities: denies recent new lumps, swollen glands, rashes, or changing moles
Psych: denies anhedonia, depressed mood, insomnia, or memory problems

Physical Exam
Wt: 227.1lbs Ht: 64 in BMI: 39
General: WDWN, NAD Vitals: BP: 118/64. Pulse: 78. Temp: 98.0F. Sat: 92. SuppO2: 8% HEENT: Normocephalic/Atramatic. PERRL, no conjunctival pallor, injection, or icterus, symmetrical eyelids. Atraumatic external nose and ears. Neck symmetric, trachea midline without thyromegaly or lymphadenopathy.

CVS: RRR, No M/R/G. Peripheral pulses 2+ and equal in all extremities. Cap refill < 2 seconds. No Carotid bruits. RESP: Unlabored respiratory effort. CTAB

GI: Not done

MSK: Extremities w/o deformity. 3+ edema present in lower limb. Skin: Warm, dry and intact. Erythema present in lower limb, bruises present on arm. Psych: AAO x 3. Appropriate mood and affect. Problem list
PAH
Edema
Chronic diastolic heart failure
COPD
HTN

Assessment and
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Genetics Home Reference. January 2016. Archived from the original on 28 July 2017. Retrieved 30 July 2017

Pulmonary arterial hypertension (PAH) is classically categorized into 4 different groups by WHO. WHO group 1 involves the narrowing or damage of the pulmonary blood vessels. WHO group 2 Pathogenesis in pulmonary hypertension due to left heart disease. WHO group 3 In pulmonary hypertension due to lung diseases and/or hypoxia. WHO group 4 is thought that the initial event is triggered by a blockage or narrowing of the pulmonary blood vessels with unresolved blood clots.

Our patient TB most likely has WHO group 2 PAH, but he may have a combination of WHO group 2 and 3 PAH. The specific pathology for group 2 pertains to left sided heart failure. This causes blood to pool in the lungs and causes back pressure in the pulmonary system, leading to pulmonary edema and pleural effusions. In WHO Group 3, the normal physiological reaction of pulmonary vasoconstriction under hypoxic can eventually lead to disease. In lung disease, alveolar hypoxia is widespread and prolonged, which triggers hypoxia-mediated vasoconstriction across an abnormally large portion of the pulmonary vascular bed, which causes an increase in pulmonary arterial pressure. This eventually causes thickening of the pulmonary vessel which contributes to the development of on-going pulmonary