Amebic liver abscess and sympathetic pleural effusion

Approximately 20% to 35% of patients with an amebic liver abscess will have a sympathetic pleural effusion

Pleuro-pulmonary penetration of amoebic liver abscess occurs in 15%-20% cases. It develops when a right lobe abscess penetrates the diaphragm and produces an empyema or broncho-pleural fistula. Such involvement is associated with right lower chest pain, usually accompanied by persistant cough. When an abscess penetrates a bronchus, expectorated material has the characteristics of amoebic pus.

Examination of the pleural fluid from patients with subphrenic abscesses usually reveals an exudate with predominantly polymorphonuclear leukocytes.

Although the pleural fluid WBC may approach or even exceed 50,000/mm3, the pleural fluid pH and glucose level remain above 7.20 and 60 mg/dL, respectively. It is distinctly uncommon for the pleural
fluid to become infected (26). However, empyemas have resulted from contamination of the pleural space when the abscesses were drained percutaneously

Adrenal insufficiency

Drug induce secondary adrenal insufficiency recovery in 6-8 mth
cortisol must be measure (>10) to confirm recovery

Non toxic goiter treatment

Rx
1. Surgery most effective
2. I131 decrease size 40-50%
3. LT4 suppression lowest efficacy

Stop aspirin risk of recurrent ACS?

Acute coronary syndrome recurrent According to Aspirin Intake
Aspirin Withdrawal n = 51 No Aspirin Withdrawal n = 332
Non–ST-segment elevation coronary syndrome 31 (61%) 271 (82%)
ST-segment elevation coronary syndrome 20 (39%) 61 (18%)
Data are presented as n (%). p < 0.001.

Conclusions Individuals with a history of cardiovascular events who stop taking low dose aspirin are at increased risk of non-fatal myocardial infarction compared with those who continue treatment.

Aortic regurgitation

Aortic insufficiency (AI) is a condition in which the aortic valve fails to close completely at the end of systolic ejection, causing leakage of blood back through the valve during LV diastole.

The constant backflow of blood through the leaky aortic valve implies that there is no true phase of isovolumic relaxation. The LV volume is greatly increased due to the enhanced ventricular filling.

When the LV begins to contract and develop pressure, blood is still entering the LV from the aorta (since aortic pressure is higher than LV pressure), implying that there is no true isovolumic contraction. Once the LV pressure exceeds the aortic diastolic pressure, the LV begins to eject blood into the aorta.

The increased end-diastolic volume (increased preload) activates the Frank–Starling mechanism to increase the force of contraction, LV systolic pressure, and stroke volume.

ACC/AHA/ESC Guidelines for the Management of Patients With Supraventricular Arrhythmias 2003