Question

Mr J 78yrs in clinic with complain of fever, chillc and cough. Also reports dyspnea. Histoy of right side CVA, COPD, Dyslipidemia, and HTN. He reports use of albuterol inhaler, lisinoril, atorvastatin 40mg and salmerol. VS temp 101.8, pulse 108, resp 21. Pa02 in room air 86% on O2 4l nasal canula 94%. CMP WNL., WBC 18.4. physical exam reveals thin anxious gentle man with mild hemiparesis on left side due to diminished gag reflex, uneven elevation of uvula, resp coarse throught lung fileds . chest xray revels consolidation in right lower lob. He was diagnosed with community acquired pneumonia.

Question: patient was hypoxic as evidenced by the low PaO2. Explain the pathologic processes that caused these patients hypoxemia.

Please the answers should be 2-4 sentences NOT paragraphs.please provide intext citations used.

Answer 1

Ans) After an hypoxic-ischemic (HI) insult, a multi-faceted complex cascade of events occurs that ultimately causes cell death and neurological damage to the central nervous system.

- The various cascades include, amongst others: immunological changes, such as the activation of the complement system and the generation of antibodies; increased inflammation through the actions of pro-inflammatory cytokines and chemokines; the production of reactive oxygen species leading to oxidative stress; and diminished mitochondrial function leading to the activation of apoptotic pathways and subsequent alteration in the function of neurons within the contralateral hemisphere.

- It addresses the immunological aspects following HI, the role of various cytokines (both pro-inflammatory and anti-inflammatory) and chemokines after the induction of HI. In addition, the role of free radicals in producing HI-induced neurodegeneration and the contribution that mitochondrial dysfunction has in neuronal apoptotic cell deathñ

- It covers the changes that the previously assumed "internal control", the contralateral hemisphere, undergoes due to HI and describes the difficulties associated with therapy intended to prevent neuronal injury associated with HI.