CHAPTER 048. ACIDOSIS AND ALKALOSIS (PART 5) PPS

Chapter 048. Acidosis and Alkalosis (Part 5) Metabolic Acidosis Metabolic acidosis can occur because of an increase in endogenous acid production (such as lactate and ketoacids), loss of bicarbonate (as in diarrhea), or accumulation of endogenous acids (as in renal failure). Metabolic[r]

Chapter 048. Acidosis and Alkalosis (Part 1) Harrison's Internal Medicine > Chapter 48. Acidosis and Alkalosis Normal Acid-Base Homeostasis Systemic arterial pH is maintained between 7.35 and 7.45 by extracellular and intracellular chemical buffering together with respiratory and rena[r]

Chapter 048. Acidosis and Alkalosis (Part 6) Lactic Acidosis An increase in plasma L-lactate may be secondary to poor tissue perfusion (type A)—circulatory insufficiency (shock, cardiac failure), severe anemia, mitochondrial enzyme defects, and inhibitors (carbon monoxide, cyanide)—or to aer[r]

Chapter 048. Acidosis and Alkalosis (Part 14) Chronic respiratory alkalosis is the most common acid-base disturbance in critically ill patients and, when severe, portends a poor prognosis. Many cardiopulmonary disorders manifest respiratory alkalosis in their early to intermediate stages, an[r]

Chapter 048. Acidosis and Alkalosis (Part 13) The clinical features vary according to the severity and duration of the respiratory acidosis, the underlying disease, and whether there is accompanying hypoxemia. A rapid increase in PaCO2 may cause anxiety, dyspnea, confusion, psychosis, and ha[r]

Chapter 048. Acidosis and Alkalosis (Part 12) Metabolic Alkalosis Associated with ECFV Expansion, Hypertension, and Hyperaldosteronism Increased aldosterone levels may be the result of autonomous primary adrenal overproduction or of secondary aldosterone release due to renal overproduction o[r]

Chapter 048. Acidosis and Alkalosis (Part 10) Differential Diagnosis To establish the cause of metabolic alkalosis (Table 48-6), it is necessary to assess the status of the extracellular fluid volume (ECFV), the recumbent and upright blood pressure, the serum [K+], and the renin-aldosterone[r]

Chapter 048. Acidosis and Alkalosis (Part 9) Approach to the Patient: Hyperchloremic Metabolic Acidoses In diarrhea, stools contain a higher [HCO3–] and decomposed HCO3– than plasma so that metabolic acidosis develops along with volume depletion. Instead of an acid urine pH (as anticipated w[r]

Chapter 048. Acidosis and Alkalosis (Part 8) Methanol (See also Chap. e34) The ingestion of methanol (wood alcohol) causes metabolic acidosis, and its metabolites formaldehyde and formic acid cause severe optic nerve and central nervous system damage. Lactic acid, ketoacids, and other uniden[r]

Chapter 048. Acidosis and Alkalosis (Part 7) Alcoholic Ketoacidosis: Treatment Extracellular fluid deficits almost always accompany AKA and should be repleted by IV administration of saline and glucose (5% dextrose in 0.9% NaCl). Hypophosphatemia, hypokalemia, and hypomagnesemia may coexist[r]

Chapter 048. Acidosis and Alkalosis (Part 11) Alkali Administration Chronic administration of alkali to individuals with normal renal function rarely, if ever, causes alkalosis. However, in patients with coexistent hemodynamic disturbances, alkalosis can develop because the normal capacity t[r]

Chapter 048. Acidosis and Alkalosis (Part 4) Approach to the Patient: Acid-Base Disorders A stepwise approach to the diagnosis of acid-base disorders follows (Table 48-3). Care should be taken when measuring blood gases to obtain the arterial blood sample without using excessive heparin. Blo[r]

Chapter 048. Acidosis and Alkalosis (Part 2) Table 48-1 Prediction of Compensatory Responses on Simple Acid-Base Disturbances and Pattern of Changes Range of Values Disorder Prediction of Compensation pH HCO3– PaCO2 Metabolic PaCO2= (1.5 x Low Low Low HCO3-) + 8 ± 2

shown by treating mucins with proteolytic enzymes and reducing agents that act onthese regions, and noting a resultant decrease in the size of mucin and gel formation(4–6). Intriguingly, more indirect evidence was found when database searches identi-fied a functionally unrelated protein, von Willebr[r]

3.1. Extraction and PurificationFor a detailed description, see Chapter 1.3.2. Rate-Zonal CentrifugationBecause of their extreme size, most gel chromatographic media are not useful forstudying size distribution of intact mucins. A useful alternative, however, is rate-zonalcentrifugation, which separ[r]

1. 6 M HCl.2. Redrying buffer: ethanol:triethylamine:water (2:2:1 [v/v/v]).3. Coupling buffer: ethanol:triethylamine:water:phenylisothiocyanate (PITC) (70:10:19:1[v/v/v/v]).4. 3µ ODS2 column (4.6 × 150 mm) (Phase Separations, Clwyd, UK).5. Buffer A: 12 mM sodium phosphate, pH 6.4.6. Buffer B:[r]

7. CarboPac MA-1 column (4 × 250 mm) (Dionex).8. CarboPac MA-1 guard (4 × 50 mm) (Dionex).9. 18 M Ω deionized water (Milli-Q Plus System, Millipore, Bedford, MA).10. NaOH 50% solution with less than 0.1% sodium carbonate (Baker, Deventer, The Netherlands).11. Anhydrous sodium acetate (Merck).12. Ace[r]

galactopyranoside (IPTG).Due to the large size of the mRNA of mucins (superior to 20 kb) described, it isnearly impossible to obtain a full-length cDNA by screening cDNA libraries. There-fore, methods have been developed to amplify DNA sequences from an mRNA tem-plate between a known internal site a[r]

brated and run in 10 mM of Tris-HCl, pH 8.0.20. Ultraturrax homogenizer (Jahnke and Kunkel, Stauffen, Germany).21. Ultracentrifuge routinely capable of 100,000g for up to 72 h.230 Corfield et al.3. Methods3.1. Metabolic Labeling3.1.1. Continuous Labeling of Mature Mucins (seeNotes 1 and 2)3.1.1.1. C[r]

3H]galactose.d. [35S]sulfate.3. Media (Gibco/BRL, Gaitersburg MD, USA) for metabolic pulse-labeling (15–60 min), asdescribed in detail in Chapter 19:a. Eagle’s minimal essential medium (EMEM) without L-methionine and L-cysteine.b. EMEM without L-threonine.c. EMEM with low D-glucose (50 µg/mL instead[r]