McNamara eating/personality disorders Flashcards
List the DSM 5 criteria for anorexia nervosa
(1) Restriction of energy intake relative to requirements leading to significantly low weight in context of age, sex, physical health.
(2) Intense fear of gaining weight or persistent behavior to avoid weight gain despite an already significantly low weight
(3) Disturbance in how body weight or shape is viewed, weight and body shape excessively influences self-worth/esteem, lacking recognition of seriousness of the low body weight.
DSM-5 criteria for bulimia
(1) Recurrent episodes of binge eating
-In a set period of time (e.g. 2 hours), patient eats definitely more than most individuals would eat in that time frame under similar circumstances.
-Lack of self control during binging
(2) Recurrent inappropriate compensatory responses
-Self induced vomitting, laxative, diuretic or other medication misuse, excessive exercise or fasting.
(3) Binging and compensation occurs on average >/= once a week for 3 months.
(4) Self-esteem excessively linked to body weight/shape
(5) Exclusion of anorexia nervosa
What are the main ECG findings in AN
(1) Bradycardia
(2) Prolonged QT
(3) Signs of hypokalemia
-> Increased P wave amplitude
-> PR prolonged
-> U waves in precordial leads
-> ST depression
-> T wave flattening/inversion
Hypokalemia may cause ventricular arrythmia or torsades de pointes.
Hypokalemia on ECG?
-> Increased P wave amplitude
-> PR prolonged
-> U waves in precordial leads
-> ST depression
-> T wave flattening/inversion
“P, Q, r, S, T, U”
Describe the electrolyte disturbances seen in someone with prolonged vomiting
(1) Loss of HCL from stomach -> less acid in the body
(2) Less H+ enters duodenum -> less bicarb released from pancreas to neutralise it and so HCO3- is retained in blood –> alkalosis
(3) Loss of chloride also cause HCO3- retention by kidneys to maintain anion charge
(4) Dehydration from vomiting reduces kidney perfusion –> RAAS
–> Sodium and bicarb reabsorption in PCT
–> Na+/H+ ATPase allows for sodium reabsorption but H+ secretion which worsens the alkalosis
–> Aldosterone increases K+ excretion causing hypokalemia
–> Hypokalemia causes intracellular K+ to shift extracellularly in exchange for H+ which moves intracellularly–> further reduces H+ levels and can increase HCO3 production in cells
–> ECF contraction from volume loss concentrates HCO3 in the blood further exacerbating the alkalosis
How do the kidneys respond to metabolic alkalosis
(1) Reduction in H+ secretion
(2) Decreased bicarb reabsorption
(3) Increased bicarb excretion
Define secondary amenorrhea and describe how it occurs in AN
Secondary amenorrhea is the absence of menses in a non-pregnant female for:
(i) 3 consecutive months if previously regular cycles
(ii)6 months if previously irregular cycles
Pathophysiology in AN
(i) Decreased GnRH production in the hypothamalus due to low body weight, low energy availability, leptin deficiency, increased cortisol and low thyroid hormones
(ii) Low GnRH = reduced secretion of LH and FSH from pituitary –> leads to anovulation and amenorrhea
Describe the neurohormonal control of hunger and satiety
Hunger
-Empty stomach, low glucose, low insulin or energy availability stimulates ghrelin release from the stomach’s enteroendocrine cells mostly, but also duodenum and pancreas.
-Ghrelin travels in blood stream and binds to its receptors in the arcuate nucleus of the hypothalamus/lateral hypothalamus, triggering AgRP neurons and neuropeptide Y producing neurons.
-These neurons inhibit pro-opiomelanocortin neurons which are normally responsible for inhibiting hunger
-This results in increased feelings of hunger, appetite and increases GI motility
Satiety
-High Insulin, cortisol or overnutrition results in leptin release from adipocytes.
-Leptin travels to arcuate nucleus/paraventricular nucleus in hypothalamus where it inhibits hunger via Pro-opiomelanocortin neurons which are appetite-supressors.
-Fats and proteins entering the duodenum triggers release of cholecystokinin from I cells (enterendocrine cells)
-CCK binds to receptors (CCK-A receptors) on the vagus nerve, which sends satiety signals to the brainstem (nucleus tractus solitarius).
–>It slows gastric emptying and promotes digestion by stimulating
bile release and pancreatic enzyme secretion.
–>These actions contribute to the sensation of fullness shortly after
a meal
List 4 possible clinical signs of anorexia nervosa
- Bradycardia
- Muscle weakness
- Lanugo body hair
- Hypotension
- Hypothermia
- dry skin
- Secondary amenorrhea
Russel’s sign (calluses) on knuckles, conjunctival hemorrhages, swollen parotids, yellowing of teeth (loss of enamel), esophagitis are signs of Bulimia and not AN
DSM-5 criteria for borderline personality disorder
at least 5 of the following
“I DESPAIRR”
I - Identity disturbance: Unstable self-image or sense of self.
D - Disordered relationships: Unstable, intense relationships with alternating idealization and devaluation.
E - Emptiness: Chronic feelings of emptiness.
S - Suicidal behavior: Recurrent suicidal gestures, threats, or self-mutilation.
P - Paranoia or dissociation: Transient, stress-related paranoia or dissociative symptoms.
A - Abandonment fears: Frantic efforts to avoid real or imagined abandonment.
I - Impulsivity: In at least two areas that are potentially self-damaging (e.g., spending, sex, substance abuse).
R - Rage: Inappropriate, intense anger or difficulty controlling anger.
R - Reactive mood: Affective instability due to a markedly reactive mood.
MOA of tricyclic anti-depressants
Tricyclic antidepressants (TCAs) work by blocking the reuptake of certain neurotransmitters, namely serotonin and norepinephrine, in the brain, thereby increasing their levels in the synaptic cleft
Amitryptaline, Trimipramine, Clomipramine
What BMI is considered malnutrition
<16kg/m2
Mechanism of GLP-1
*Released from L cells of the intestine following meal intake
*Promotes satiety by acting at the paraventricular and arcuate nuclei of the hypothalamus causing stimulation of POMC neurons and inhibiting AgRP and NPY neurons
*Causes insulin release from beta-cells of pancreas
*Inhibits glucagon release from alpha- cells of pancreas
*Slows gastric emptying through afferent vagal modification and increasing pyloric sphincter tone.
