Pathophysiology II Composite Exam Study Guide PDF

- What are some general causes of acidosis (blood pH \< 7.30)? - Excessive carbon dioxide accumulation in the blood - Decreased presence of bicarbonate in the blood - Increased presence of extra/inorganic acids in the blood - Respiratory Acidosis = increased CO2 retention,...

- What are some general causes of acidosis (blood pH \< 7.30)? - Excessive carbon dioxide accumulation in the blood - Decreased presence of bicarbonate in the blood - Increased presence of extra/inorganic acids in the blood - Respiratory Acidosis = increased CO2 retention, resulting in acidosis - What is considered the "central chemoreceptor"? - Medulla in response to increasing CO2 levels, forces expiration to remove CO2, decrease the acidity of the bloodstream - What are considered the "peripheral chemoreceptors"? - Peripheral chemoreceptors (located in aorta, carotid arteries)sense increasing CO2 levels AND/OR decreasing oxygen levels and send signals to the central chemoreceptors - How does the human body physiologically respond to a respiratory acidosis, in addition to increased expiration of CO2? - Increased reabsorption of bicarbonate in the kidneys - KEEP IN MIND Sodium and bicarbonate reabsorption are coupled! - What can the anion gap tell you clinically? - AG can indicate whether acidosis is due to pure loss of bicarbonate (normal AG metabolic acidosis) OR the presence of extra/inorganic acids (increased anion gap metabolic acidosis) - How do you calculate the anion gap? - AG = \[Na\] -- \[(Chloride) + (Bicarbonate)\] - AG greater than 12 = INCREASED anion gap metabolic acidosis - What are the causes of increased AG metabolic acidosis? - Remember the mnemonic "MUDPILES" - M Methanol - Extra Acid formic acid - What clinical phenotype can occur as a result of methanol toxicity? - BLINDNESS; due to optic nerve damage by formic acid - U Uremia - Extra Acid(s) phosphoric acid, sulfuric acid - Think RENAL FAILURE! - D Diabetic Ketoacidosis (and other causes of ketosis as well) - Extra Acid(s) KETONE BODIES! - What are the ketone bodies associated with DKA? - Beta-hydroxybutyrate - Acetoacetate - Acetone (responsible for fruity odor of breath) - P Propylene Glycol - Extra Acid Lactic Acid - Found in IV fluids (most common) - I Isoniazid, Iron supplements - Isoniazid Toxicity - Extra Acid Lactic Acid - Lactic acid is produced from GLUTAMATE - What vitamin is typically deficient as a result of isoniazid toxicity? What consequences does this have? - Pyridoxine (vitamin B6) important in the conversion of glutamate to GABA - Pyridoxine deficiency decreased conversion of glutamate to GABA; as a result, glutamate increases! - When glutamate accumulates glutamate can easily be converted to lactic acid! - What clinical phenotype is observed highly with isoniazid toxicity? - PERIPHERAL NEUROPATHY (numbness, tingling in the extremities) due to glutamate toxicity to peripheral nerves - L Lactic Acidosis - What are some causes of lactic acidosis? - Hypoxia - Hypovolemia/Hypotension - Increased inflammation/hyperinflammatory events (e.g., SEPSIS, SHOCK) - Sepsis systemic inflammatory response to an infection in the bloodstream; usually bacterial - Other conditions which increase anaerobic metabolism - E Ethylene Glycol - Typically found in antifreeze - Extra Acid(s) Glycolic Acid (causes the metabolic acidosis) and Oxalic Acid (causes calcium oxalate kidney stones) - REMEMBER: INCREASED AG METABOLIC ACIDOSIS + KIDNEY STONES = ETHYLENE GLYCOL TOXICITY! - S Salicylates - Most commonly, Aspirin (ASA) - Extra Acid(s) salicylic acid - What acid base conditions are CLASSICALLY caused by aspirin toxicity? - Metabolic acidosis + RESPIRATORY ALKALOSIS! - Normal AG metabolic acidosis blood pH \< 7.3, BUT anion gap is WITHIN NORMAL RANGE! - What is the relationship between bicarbonate and chloride? - INVERSELY PROPORTIONAL; when bicarbonate levels DECREASE, chloride reabsorption INCREASES; in most situations, therefore, normal AG metabolic acidosis is associated with HYPERCHLOREMIA (increased chloride in the bloodstream) - Normal AG metabolic acidosis almost always due to direct bicarbonate loss - What are the causes of normal AG metabolic acidosis? - Remember the mnemonic "HA(A)RD-UPS" - H Hyperalimentation (THINK EXCESSIVE TOTAL PARENTERAL NUTRITION SUPPLEMENTATION) - TPN usually contains large amounts of chloride - Administration of excessive TPN increased chloride in the bloodstream - The increased Cl in the bloodstream body responds by increased EXCRETION OF BICARBONATE from the kidneys, resulting in hyperchloremic metabolic acidosis - A Acetazolamide (and other carbonic anhydrase inhibitors) - Inhibition of carbonic anhydrase in the kidneys DECREASED BICARBONATE uptake, increased excretion of bicarbonate; ALSO, LOSS OF SODIUM! - LOSS OF BICARBONATE increased reabsorption of chloride, increased retention of H+ hyperchloremic metabolic acidosis - A Adrenal Insufficiency - What are the three zones of the adrenal cortex? - Remember the mnemonic "GFR." - Zona Glomerulosa secretes aldosterone - Zona Fasciculata secretes cortisol - Zona Reticularis secretes secondary sex hormones - Primary Adrenal Insufficiency (due to infections, hyperinflammatory states such as exacerbations of chronic autoimmune diseases) ADDISON'S DISEASE - Destruction of the zona glomerulosa most common classically results in HYPERKALEMIA, HYPONATREMIA - Destruction of zona glomerulosa decreased aldosterone secretion INCREASED POTASSIUM RETENTION, DECREASED SODIUM EXCRETION - Secondary Adrenal Insufficiency caused by secondary conditions (usually pituitary issues such as cancer, sequelae of radiation therapy) - R Renal Tubular Acidosis (DO NOT LEARN) - D Diarrhea - Leads to a HYPOKALEMIC, HYPERCHLOREMIC METABOLIC ACIDOSIS. HOW? - Diarrhea (regardless of the cause) leads to a LOSS OF BICARBONATE AND POTASSIUM through the rectum results in HYPOKALEMIA, METABOLIC ACIDOSIS - Due to loss of bicarbonate, CHLORIDE REABSORPTION IS INCREASED - END RESULT: HYPOKALEMIC, HYPERCHLOREMIC METABOLIC ACIDOSIS - U Uretero-enteric fistula (i.e., an abnormal connection between the ureters and the GI tract, usually the colon; most commonly due to underlying IBD or surgical trauma) --DO NOT LEARN - P Pancreatic Fistula (usually due to pancreatic cancer) --DO NOT LEARN - S Spironolactone - Spironolactone = aldosterone ANTAGONIST; ideally, this results in SODIUM EXCRETION, POTASSIUM RETENTION (thus, potassium-sparing) - How does spironolactone lead to a metabolic acidosis? - Increased excretion of sodium increased excretion of bicarbonate in the PCT + increased retention of H+ metabolic acidosis - Keep in mind that potassium is also retained due to spironolactone. Therefore, the END RESULT IS... - HYPERKALEMIC METABOLIC ACIDOSIS - Vomiting/Emesis leads to HYPOKALEMIC, HYPOCHLOREMIC METABOLIC ALKALOSIS! How? - Vomiting/Emesis leads to a regurgitation of stomach contents + hydrochloric acid from the stomach to the oropharynx and, of course, to the outside of the body HYPOCHLOREMIA - Loss of chloride (through the vomitus) INCREASED REABSORPTION OF BICARBONATE + INCREASED EXCRETION OF H+ and K+ IN THE KIDNEYS METABOLIC ALKALOSIS + HYPOKALEMIA - END RESULT HYPOCHLOREMIC, HYPOKALEMIC METABOLIC ALKALOSIS!