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BRS 2 > Disorders of appetite > Flashcards

Disorders of appetite Flashcards

1
Q

What is polydipsia?

A

Excessive sensation of thirst or abnormal behaviour of increased drinking

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2
Q

What is adipsia?

A

Adipsia is a decreased sensation or absent feeling of thirst – involves an increase in urine osmolarity which stimulates the secretion of ADH from the posterior pituitary gland to increase water reabsorption.
• Increased water retention
• Sensation of thirst decreased

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3
Q

What is anorexia?

A

Lack or loss of appetite for food

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4
Q

What is obesity?

A

Abnormal or excessive fat accumulation that presents a risk to health.

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5
Q

What is secondary polydipsia?

A

The most common pathological manifestation of secondary polydipsia that arises due to a disruption in osmoregulation or alterations in ADH release.

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6
Q

What happens to urine osmolarity when there is elevated plasma ADH?

A

Hyperosmolar and small volume of urine is excreted (anti-diuresis effect).

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7
Q

What type of effect is exhibited by low plasma ADH?

A

Hyposmolar and large volume of urine is excreted (water diuresis effect).

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8
Q

What are the chronic causes of secondary polydipsia?

A 
Diabetes insipidus & mellitus
Kidney failure
Conn’s Syndrome- hypokalaemia
Addison’s disease – low BP.
Sickle cell anaemia
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9
Q

What types of medications can induce secondary polydipsia?

A

Diuretics
Laxatives
Antidepressants

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10
Q

What are the main symptoms of diabetes mellitus?

A

• Osmotic symptoms: Polyuria, nocturia and polydipsia
• Blurred vision
• Fatigue
• Paraesthesia – extremities as a result of neuropathy in those with prolonged undiagnosed diabetes
• Infections: Candidal, UTI, and skin infections.
• Unintentional weight loss
• Acanthosis nigricans
Impaired clotting

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11
Q

How does Conn’s syndrome lead to polydipsia?

A

• Conn’s syndrome: Hypokalaemia can induce tubular damage and renal tubule ADH resistance – manifesting as polydipsia.

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12
Q

What are the main causes of primary polydipsia?

A
  • Mental illness – psychogenic polydipsia (or acquired)
  • Schizophrenia
  • Mood disorders- depression and anxiety
  • Anorexia
  • Drug use – Diuretics (For congestive heart failure or fluid overload).
  • Brain injuries and organic brain damage.
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13
Q

What problems are associated with polydipsia?

A
  • Kidney and bone damage
  • Headache
  • Nausea
  • Cramps
  • Slow reflexes
  • Slurred speech
  • Low energy
  • Confusion
  • Seizures
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14
Q

What are four main types of polydipsia?

A

Type A-D

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15
Q

What is Type A polydipsia?

A

Increased level in which solutes pass through cell membranes for vasopressin release and the activation of thirst

Change in AVP osmotic threshold - lower

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16
Q

What is type B polydipsia?

A

• Occurs when vasopressin responses are at a decreased level in the presence of osmotic stimuli – there is reduced secretion of AVP due to osmoreceptor deficits.

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17
Q

Which type of polydipsia is concerned with cranial diabetes inspidus?

A

Type C

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18
Q

What is Type C polydipsia?

A

• A complete elimination of osmoreceptors – no AVP release. This is found in patients with cranial diabetes insipidus.

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19
Q

What are the examples of eating disorders?

A

A mental disorder defined by abnormal eating habits includes:
• Binge eating disorder
• Anorexia nervosa
• Bulimia nervosa
• Pica
• Rumination syndrome
• Avoidant/restrictive food intake disorder

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20
Q

What are the signs of anorexia nervosa?

A
  • Low BMI
  • Continuous weight loss
  • Amenorrhoea
  • Halitosis
  • Mood swings
  • Dry hair, skin and hair thinning.
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21
Q

Which hormone is deficient in anorexia nervosa?

A

Serotonin

22
Q

Which amino acid is the precursor to serotonin?

A

Tryptophan

23
Q

Why does serotonin decrease in anorexia nervosa?

A

Tryptophan is the precursor molecule of serotonin – available in diet. Therefore, excessive diet restriction and malnutrition decreases the store of serotonin, as the precursor is less available to the rate liming enzyme of 5-HT synthesis.

24
Q

Mild anorexia is defined as a BMI of?

A

• Mild >17

25
Q

What are the BMI paramteris which each classification of anorexia?

A
  • Mild >17
  • Moderate 16-16.99
  • Severe 15-15.99
  • Extreme <15
26
Q

What is the definition of obesity?

A

Obesity is defined as a chronic adverse condition due to an excess amount of body fat – Body mass index is the most widely used method to determine obesity.

27
Q

What BMI is linked with obesity?

A

• BMI > 30 or >25 + comorbidity or risk factor.

28
Q

What physical parameters other than BMI are measured in the diagnosis of obesity?

A

• Abdominal girth – waist circumference is also measured.

29
Q

What is the treatment for obesity?

A

Dietary and physical activity modifications are effective ways to elicit weight loss in individuals with obesity.
• Ensure a diet with a caloric deficit
• The low carbohydrate/high-protein diet has been found to produce greater weight loss than the low-fat diet.
• Adherence to the diet and the reliability of patient reporting of caloric intake is limitation of this treatment option.

30
Q

What type of diet should be adhered to by obese patients?

A
  • Ensure a diet with a caloric deficit

* The low carbohydrate/high-protein diet has been found to produce greater weight loss than the low-fat diet

31
Q

What criteria makes a patient eligible for bariatric surgery?

A

A BMI of >40 or >35 with obesity related comorbidity

32
Q

What are obesity related co-morbidities?

A

Hypertension, diabetes, sleep apnoea, GORD

33
Q

How do surgical interventions work for obesity?

A

Surgery works by reducing hunger and increasing fullness

34
Q

What are the common surgical interventions for the treatment of obesity?

A

Roux-en-Y gastric bypass & sleeve gastrectomy.

35
Q

What is a sleeve gastrectomy?

A

A surgical weight-loss procedure in which the size of the stomach is reduced to 15% of its original size through the removal of a substantial portion of the stomach along the greater curvature.

36
Q

Which cells produce GLP?

A

Intestinal epithelial endocrine L-cells

37
Q

What stimulates the release of GLP-1?

A

Nutrient uptake

38
Q

What does GLP-1 stimulate?

A

The release of insulin from beta-cells and inhibits glucagon secretion

39
Q

What does GLP-I inhibit?

A

• GLP inhibits gastrointestinal motility and secretion  Ileal brake mechanism behaving as a physiological regulator of appetite and food intake.

40
Q

Which enzyme degrades GLP?

A

dipeptidyl peptidase-4

41
Q

Which cells produce Ghrelin?

A

P/D1 cells of the fundus or upper part of the stomach and in the pancreas

42
Q

Which neurones does Ghrelin act upon?

A

NPY orexigenic neurones within the arcuate, promoting the sensation of hunger and appetite

43
Q

What is the overall effect of Ghrelin?

A

Sensation of hunger and appetite

44
Q

Which hormones are reduced in bariatric surgery?

A

Ghrelin

45
Q

Which hormones are increased in bariatric surgery?

A

• GLP1, GLP2 & PYY

46
Q

Which cells secretes peptide YY?

A

L cells residing within the mucosal layer of the terminal ileum, colon, and rectum

47
Q

When is peptide YY released?

A

Post-prandially

48
Q

Which types of neurones does Peptide YY interact with?

A

• Circulating peptide YY passes through the incomplete blood brain barrier and interacts with NPY/Agrp and POMC neurones within the arcuate nucleus.

49
Q

Which neurones of the arcuate nucleus are activated by peptide YY?

A

POMC neurones

50
Q

What type of effect is induced by Peptide YY?

A

a satiety inducing effect by releasing anorexigenic factors.

BRS 2 (62 decks)

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