Disorders of appetite Flashcards

(50 cards)

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?

22
Q

Which amino acid is the precursor to serotonin?

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?

25
What are the BMI paramteris which each classification of anorexia?
* Mild >17 * Moderate 16-16.99 * Severe 15-15.99 * Extreme <15
26
What is the definition of obesity?
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
What BMI is linked with obesity?
• BMI > 30 or >25 + comorbidity or risk factor.
28
What physical parameters other than BMI are measured in the diagnosis of obesity?
• Abdominal girth – waist circumference is also measured.
29
What is the treatment for obesity?
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
What type of diet should be adhered to by obese patients?
* 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
What criteria makes a patient eligible for bariatric surgery?
A BMI of >40 or >35 with obesity related comorbidity
32
What are obesity related co-morbidities?
Hypertension, diabetes, sleep apnoea, GORD
33
How do surgical interventions work for obesity?
Surgery works by reducing hunger and increasing fullness
34
What are the common surgical interventions for the treatment of obesity?
Roux-en-Y gastric bypass & sleeve gastrectomy.
35
What is a sleeve gastrectomy?
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
Which cells produce GLP?
Intestinal epithelial endocrine L-cells
37
What stimulates the release of GLP-1?
Nutrient uptake
38
What does GLP-1 stimulate?
The release of insulin from beta-cells and inhibits glucagon secretion
39
What does GLP-I inhibit?
• GLP inhibits gastrointestinal motility and secretion  Ileal brake mechanism behaving as a physiological regulator of appetite and food intake.
40
Which enzyme degrades GLP?
dipeptidyl peptidase-4
41
Which cells produce Ghrelin?
P/D1 cells of the fundus or upper part of the stomach and in the pancreas
42
Which neurones does Ghrelin act upon?
NPY orexigenic neurones within the arcuate, promoting the sensation of hunger and appetite
43
What is the overall effect of Ghrelin?
Sensation of hunger and appetite
44
Which hormones are reduced in bariatric surgery?
Ghrelin
45
Which hormones are increased in bariatric surgery?
• GLP1, GLP2 & PYY
46
Which cells secretes peptide YY?
L cells residing within the mucosal layer of the terminal ileum, colon, and rectum
47
When is peptide YY released?
Post-prandially
48
Which types of neurones does Peptide YY interact with?
• Circulating peptide YY passes through the incomplete blood brain barrier and interacts with NPY/Agrp and POMC neurones within the arcuate nucleus.
49
Which neurones of the arcuate nucleus are activated by peptide YY?
POMC neurones
50
What type of effect is induced by Peptide YY?
a satiety inducing effect by releasing anorexigenic factors.