Unit 10: Bulimia Nervosa - Rosie list Flashcards
How does chronic vomiting cause cardiovascular complications?
Reduced electrolyte (particularly sodium absorption - hyponatermia)
Reduce water absorption
Causes dehydration leading to hypovolemia
Low plasma osmolarity
Can effect action potential
How does diuretuc abuse cause cardiovascular abnormalities?
Detailed and specific to bulimia
Increased GFR and increased urine production - leads to less water absorption resulting in hypovolemia (hypotension)
Particularly increased excretion of K+ ions - hypokalemia (worsened by hyponatremia from vomiting increasing aldosterone production)
Results in QT prolongation and pronounced U waves, with a slow heart rate due to delayed ventricular repolarisation particular slow purkinje fibre repolarisation
In some cases may cause ventricular fibrillation as prolonged more positive membrane potential (from reduced K+ efflux) results in premature activation of L-type voltage gated Ca2+ channels, causing premature action potential hence contraction in ventricle myocytes independent of the SAN.
How does chronic vomitting and diuretic use affect blood tests?
Hypokalemia
Hyponatermia
May also show hypochloremia and low glucose
How can chronic vomiting and diuretic use show on a urine test?
Direct result:
Elevated potassium levels
High potassium:creatinine ratio
Result of weight loss:
Elevated urea from protein breakdown to produce energy
Elevated ketones from oxidation of fatty acids (important to rule of diabetic ketoacidosis)
How can chronic vomitting and diuretic use alter the arterial blood gas results?
Metabolic alkalosis - loss of Cl- in vomit leads to increased HCO3- as exchangeable in buffering blood
- loss of Na+ in vomit, leading to action of aldosterone, increases HCO3- rebasoprtion in the nephron worsening metabolic alkalosis
HCO3- increases and pH increases
CO2 may increases as attempt respiratory compensation
Describe how chronic vomitting leads to hypokalemia?
Loss of Na+ ions in vomit - hyponatremia
Low renal perfusion and low Na+ conc detected by macular densa cells, stimulates JG cells to release renin, activation of RAAS system leads to increased aldosterone production
Aldosterone increases Na+ reabsorption in the nephron, as a consequence increases K+ secretion
By increasing Na+K+ATPase activity, upregulating BK and ROMK channels and increases tubular flow rate
Describe how diuretic abuse leads to hypokalemia?
Furosemide - inhibits NKCC2 in thick ascending loop of Henle, this inhibits K+ reabsorption in the nephron
What are the different ways metabolic alkalosis can present on an arterial blood gas analysis?
- Elevated HCO3- and elevated pH, normal CO2 - metabolic alkalosis with no respiratory compensation
- Elevated HCO3-, and elevated pH with elevated CO2 - metabolic alkalosis with respiratory compensation
What is the pharmacology of furosemide?
Is a loop diuretic
Taken orally or IV - once in blood stream secreted from pertitubular capillaries to site of action
Inhibits the NKCC2 channel (specifically the Cl- binding site) on the luminal membrane of cells in the thick ascending loop of henle.
This inhibits Na+ K+ and Cl- reabsoption, so increases osmolarity of the renal lumen hence less water moves out of lumen by osmosis = less water reabsorption
This leads to an increase in the volume of urine produced
What are the clinical indications of loop diuretics?
Odematous states (cause edema) - heart failure, pulomary oedema, cirrhosis of liver
Hypertension
Hypercalcemia and hyperkalemia
Acute bromide/flouride/iodide intoxications
What are the contraindication of loop diuretics?
Dehydrated or hypovolemic patients
Sulfonamide allergy
What are the side effects of loop diuretics?
Indirect - metabolic alkalosis through increased HCO3- in the blood
How does hypokalcemia lead to metabolic alkalosis?
Type A intercalated cells in the collecting ducts will absorb K+ in severe hypokalemia
Reabsorbed from the luminal membrane through K+ H+ ATPase, the H+ for this pump is supplied by the reaction of CO2 and H2O to form HCO3- and H+
HCO3- is then recycled out the basolateral membrane in exchange for Cl-, hence HCO3- in the blood increases.
In a bulimic individual describe the physiological events that underly emesis? (triggering in the vomiting centre)
After a binge feel strong guilt and distress, detected by the higher cognitive and emotional areas in the brain, can activate the nucleus tractus solitarus (Psychogenic vomiting)
Mechanical irritation of the thraot/pharanyx from putting hand down throat causes release of seratonin that can be detected by 5-HT3 receptors on the vagus nerve, carries sensory information to the NTS
Distention of the stomach and other sensations after a binge episode is detected by stretch receptors on the stomach, carried on visceral afferent (splanchnic nerves or vagus) to the NTS
NTS activates the dorsal motor nucleus of vagus which causes vomiting.
What is the mechanism underlying the propulsion of food in emesis?
- Retropulsion of food from the duodenum into the stomach, relaxation of duo, stomach and pyloric sphincter
- Relaxation of the UES
- Contraction and flattening of the diaphragm (causes forced inspiration), contraction of abdominal muscles - leads to increased intrabdominal pressure and decreases thoracic pressure
- Propulsion of food from stomach to oesophagus to oral cavity, the LES must open for this to occur. The larynx will be forced forward and upwards
