Albuterol 2.5 mg/3l q 4 hours
Astaxthin 12mg 1 per day
Coenzyme Q10 200mg
Furosamide 40 mg
Liver support
Multivitamins …show more content…
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 …show more content…
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