Unit 10: Bulimia Nervosa - Rosie list Flashcards

1
Q

How does chronic vomiting cause cardiovascular complications?

A

Reduced electrolyte (particularly sodium absorption - hyponatermia)
Reduce water absorption
Causes dehydration leading to hypovolemia
Low plasma osmolarity
Can effect action potential

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2
Q

How does diuretuc abuse cause cardiovascular abnormalities?
Detailed and specific to bulimia

A

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.

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3
Q

How does chronic vomitting and diuretic use affect blood tests?

A

Hypokalemia
Hyponatermia

May also show hypochloremia and low glucose

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4
Q

How can chronic vomiting and diuretic use show on a urine test?

A

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)

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5
Q

How can chronic vomitting and diuretic use alter the arterial blood gas results?

A

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

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6
Q

Describe how chronic vomitting leads to hypokalemia?

A

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

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7
Q

Describe how diuretic abuse leads to hypokalemia?

A

Furosemide - inhibits NKCC2 in thick ascending loop of Henle, this inhibits K+ reabsorption in the nephron

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8
Q

What are the different ways metabolic alkalosis can present on an arterial blood gas analysis?

A
  1. Elevated HCO3- and elevated pH, normal CO2 - metabolic alkalosis with no respiratory compensation
  2. Elevated HCO3-, and elevated pH with elevated CO2 - metabolic alkalosis with respiratory compensation
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9
Q

What is the pharmacology of furosemide?

A

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

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10
Q

What are the clinical indications of loop diuretics?

A

Odematous states (cause edema) - heart failure, pulomary oedema, cirrhosis of liver
Hypertension
Hypercalcemia and hyperkalemia
Acute bromide/flouride/iodide intoxications

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11
Q

What are the contraindication of loop diuretics?

A

Dehydrated or hypovolemic patients
Sulfonamide allergy

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12
Q

What are the side effects of loop diuretics?

A

Indirect - metabolic alkalosis through increased HCO3- in the blood

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13
Q

How does hypokalcemia lead to metabolic alkalosis?

A

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.

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14
Q

In a bulimic individual describe the physiological events that underly emesis? (triggering in the vomiting centre)

A

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.

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15
Q

What is the mechanism underlying the propulsion of food in emesis?

A
  1. Retropulsion of food from the duodenum into the stomach, relaxation of duo, stomach and pyloric sphincter
  2. Relaxation of the UES
  3. Contraction and flattening of the diaphragm (causes forced inspiration), contraction of abdominal muscles - leads to increased intrabdominal pressure and decreases thoracic pressure
  4. 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
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16
Q

Explain the development of the Mallory-Weiss tear caused by vomiting damage

A

Repetivie chronic vomitting causing increased pressure in the oesophagus from rushing in of abdominal contents, typically near the LES results in longitudinal lacerations.
May be in the mucosa or also the submucosa
Common cause of upper GI bleeding.

17
Q

What are some of the physiological factors that affect food choice?

A
  1. Nutrient depletion - crave foods with these nutrients
  2. Endocrine and cytokine influence on taste receptor sensitivity
  3. Sodium appetite - regulated by aldosterone production - influence consumption of salty foods
18
Q

What are the key clinical signs of Bulimia nervosa?

A

Russels sign
Teeth discoloration
Enlargement of the parotid gland
Psuedobartter syndrome

19
Q

What is the mechanism behind Russel’s sign in Bulimia Nervosa?

A

Repeated contact of knuckles with incisors and stomach acid when used to induce vomiting.
Lead to open sores and callus (thickened skin as a protective measure) formation on the knuckles

20
Q

What is the mechanism behding teeth discoloration in Bulima Nervosa?

A

repeated stomach acid exposure erodes teeth enamel exposing the underlying dentin layer which has a slightly yellowish colour

21
Q

What is the mechanism behind enlargement of the parotid gland in Bulima Nervosa?

A

Increased saliva production to attempt to neutralise the acid present in the oral cavity after vomiting
Overproduction of salivary enzymes due to malabsorption, attempt of body to compensate for reduced digestion time

22
Q

What is the mechansim behind pseudo Bartters syndrome in Bulimia Nervosa?

A

Results in hypokalaemia, hypochloremia and metabolic alkalosis
1. Loss of Cl- from vomiting, replaced by HCO3- in blood as exchangeable in blood buffering = metabolic alkalosis and hypochloremia
2. Hyponateremia from vomiting, aldosterone production - reducing K+ reabsoprtion in the nephron results in hypokalemia

23
Q

How is the SCOFF questionnaire used in the diagnosis of Bulima Nervosa?

A

A score of 2 or above indicates increased likelihood of an eating disorder (screening not a diagnostic tool)
1. Make yourself sick because you feel uncomfortably full
2. Feel out od control of what you eat
3. Lost one pound or more in the last three months
4. Feel fat when others call you thin
5. Obsessive over food - dominates your life

24
Q

What is the purpose of postassium and rehydration solutions in Bulimia nervosa treatment?

A

Content high amounts of K+ and other electrolytes Na+ mainly
Taken orally - electrolytes are absorbed by GIT, increases the osmolarity of the blood, increasing water absorption from the GIT by osmosis
Leading to an increased blood volume and contributing to rebalancing the electrolyte levels

25
Q

What is the purpose of a short stay unit in the treatment of Bulima nervosa?

A

Patient expect to be in hospital for up to 72hours
Often admitted after a cardiac episode, given oral rehydration therapy, time to allow electrolyte levels to restabilise and ensure the patient is stable
Monitor for complications of treatment
Treatment that quickly resolves the medical problem, may also hold the patient whilst waiting on diagnostic test results

26
Q

What is the purpose of CBT in bulima nervosa therapy?

A

Adults with Bulimia nErvosa will recieve CBT alongside a self help program in treatment
If fails will receive CBT-ED
This aims to identify the thoughts underlying the patients behaviour, challenge these thoughts in order to change them, hence altering the patients behaviour.
Gives a holistic approach recognises that a persons thoughts and emotions can influence their behaviour

27
Q

What psychological factors can increase the risk of developing an eating disorder?

A

Low self esteem
Personality - perfectionist and neuroticism
Other mental health condition: anxiety, depression and OCD
Preoccupation with wanting to change appearance

More likely to develop maladaptive coping mechanisms associated with food as a method of control or pleasure

28
Q

What are some of the social risk factors for eating disorders?

A

Bullying or other form of discrimination
Lack of social support/relationship difficulties
Media - idealisation of the perfect body
Life transitions and stresses

29
Q

What are some biological risk factors for eating disorders?

A

Genetic - twin studies
Premature birth or birth complications - risk for binge
Brain changes - altered sensitivity for serotonin and dopamine, changes in reward processing (unsure if come before or after the eating disorder diagnosis)

30
Q

What are some psychosocial factors that are important in the treatment of eating disorders?

A

Good social support - strong relationships with others
Society that inspires body confidence and positive attitudes towards food
Support groups
Positive mindset and opinion of self - may be reinforced by CBT
Relationship with family is essential for children recovering from eating disorders

31
Q

How can the stages of change model by applied to recovering from an eating disorder?

A

Pre-contemplation: no want to change, educate on risk to health and life, encourage with restoring health not taking eating disorder away (scary thought for those who are ill)
Contemplation: scared but see benefits, offer support and encouragement, may refer to services, explore pros/cons of behaviour outcomes for same and change
Action: provide practical support and guidance - referral to ED services
Maintenance: acountability meetings, encouragement, method of motivation, anticipate and prevent relapse
Relapse: recognise release and how to prevent another in the future, encourage to go back to change, accept backwards step and move on

32
Q

How can the health belief model be applied to eating disorder recovery?

A

Percieved susceptibility - education on risk factors and statistics on symptoms and complication, many people with ED are in denial that they are ill
Percieved severity - educate on risk, go through and support to understand medical complications
Understand threat of ED

Percieved benefits - understanding reversible, what will gain from recovery
Percieved barriers - low self esteem don’t believe able to make a change
This encourages to evaluate behaviour

Cue to action - support from loved one, event in life, medical emergency
Self efficacy - require CBT to increase self confidence and esteem to complete change
Leads to behavioural change

33
Q

How should doctors approach discussing eating disorders with patients?

A

Doctors should follow MANTRA guidelines when treating a patient with an eating disorder.
Important to try to understand the reasoning behind the eating disorder and try to work this thought rather than directly tackling food
Avoid unconscious bias and discrimination against patients.
Build a rapport with patient.
Patient may feel uncomfortable being asked directly about ED habit with no warning - should work this into history or sign post - potentially sensitive questions but asked for patients presenting with these symptoms