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Unit 10 PBL cases > Bulimia > Flashcards

Bulimia Flashcards

1
Q

What is bulimia nervosa?

A

Eating disorder where people go through periods where they eat a lot of food in a short period of time (binge eating) and then purge as a compensatory behaviour to stop

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2
Q

What are methods of purging in bulimia nervosa?

A

Self-inducing vomiting
Using laxatives
Using diuretics
Fasting
Doing excessive excercise

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3
Q

What are the signs and symptoms of bulimia? (14)

A
  • Usually at or above normal body weight
  • Self-induced vomiting
  • Excessive exercise
  • Excessive fasting
  • Inappropriate use of laxatives or diuretics
  • Anxiety
  • Preoccupation with food/weight/body shape
  • Russell’s sign
  • Enlargement of parotid glands
  • Teeth discolouration
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4
Q

What Russell’s sign?

A

Calluses on the knuckles or the back of the hand due to repeated self-induced vomiting

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5
Q

What diagnostic tool can be used to diagnose eating disorders?

A

SCOFF questionaire

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6
Q

What is the SCOFF questtionaire?

A

S- Do you make yourself SICK because you feel uncomfortably full
C- Do you worry that you have lost CONTROL over how much you eat?
O- Have you recently lost more than ONE stone
F- Do you believe to be FAT when others say otherwise?
F- Would you say that FOOD dominates your life?

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7
Q

What should healthcare professionals be wary of when potentially diagnosing eating disorders?

A

SCOFF questionaire and other screening tools should not be the sole method to determine if someone has an eating disorder
People do not have to be underweight to have an eating disorder

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8
Q

What are the short term physical treatment for bulimia?

A

Oral rehydration solutions

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9
Q

What is ORT and how is it given?

A

Oral rehydration therapy
Mix of Na+, glucose, K+ and water which treats dehydration and and electrolyte imbalance
Taken by mouth but also nasogastric tube for continual administration

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10
Q

What effect does ORT have at the intestinal epithelium?

A
  • Na+ and glucose moves through Na+ glucose transport protein
  • Na+ moves into the epithelial cell by passive diffusion as there is lower conc of Na+ in the epithelium cells than the lumen
  • Glucose moves by active transport against conc gradient as lower conc gradient in epithelial cell than lumen
  • Energy created from passive movement of Na+ creates energy to transport glucose
  • Na+ pumped into blood via Na+/K+ ATPase pump
  • Glucose moves into blood by passive diffusion
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11
Q

Where may someone be taken if severely ill with bulimia nervosa?

A

Short stay unit
For patients requiring hospitalisation until their clinical needs are resolved

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12
Q

What does each part of the normal ECG show?

A

P wave: atrial depolarising beginning contraction of the atria
PR: atrial depolarisation completed
QRS: ventricular depolarisation begins, atria repolarisation
ST: ventricular depolarisation completing
T wave: ventricular wave
U wave: ventricular repolarisation

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13
Q

What is QT prolongation show?

A

Slow rate of repolarisation of ventricular myocytes
Hypokalaemia inhibits the conductance of the slow rectifier
K+ channel repsonsible for speeding up the repolarisation of the ventricular myocytes

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14
Q

What does prominent U waves show?

A

Hypokalaemia causes increase depolarisation of the heart which increases the repolarisation of the purkinje fibres

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15
Q

What is hypokalaemia?

A

Metabolic imbalance characterised by very low potassium levels in the blood. Can be due to disease or side effect of diuretic drugs

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16
Q

What is hyponatremia? causes?

A

Low sodium levels in the blood
Caused by hypovolaemia from fluid loss, diuretic use and vomiting
Low serum Na+ means Na+ will move by osmosis due to water potential gradient

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17
Q

What is hypochloremia? causes?

A

Low chlorine levels
Caused by loss of gastric juices - vomiting, diuretics, metabolic disease, metabolic alkalosis

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18
Q

What causes elevated serum urea?

A

misuse of diuretics and severe dehydration

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19
Q

Urinary potassium : creatinine ratio meaning if elevated?

A

Greater than 2.5 suggests renal potassium wasting =
- Too many loop diuretics/barters syndrome
> increased sodium excretion in the urine which stimulates aldosterone release from adrenal
> stimulates kidneys to excrete more potassium
> potassium wasting

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20
Q

Alkalosis vs acidosis

A

Alkalosis: pH greater than 7.45
Acidosis: pH less than 7.45

21
Q

What occurs during metabolic alkalosis? How does the body attempt to compensate?

A

Lower K+
> activation of H+/K ATPase in the nephron to pull more K+ out of cells into the blood
> H+ is pulled into the cells so it decreases acidity
Body attempts to compensate by respiratory compensation > lower resp rate > increases PaCO2 and decrease pH

22
Q

What is tested in arterial blood gases analysis?

A

pH
PaCO2
PaO2
Bicarbonate
Oxygen saturation
Oxygen content
Base excess

23
Q

What are the symptoms of alkalosis?

A
  • Confusion - due to low O2 conc
  • Nausea and vomiting, diarrhoea
  • Tremors, muscle cramps and tingling of peripheries
  • Hypokalaemia
  • Restlessness followed by lethergy
  • Tachycardia
24
Q

What causes metabolic alkalosis?

A

Gastric juices have high HCl content. Gastric juice loss leads to increased alkalinity of the blood
- Diuretics can cause increased urinary acid secretion > make blood more alkaline
- Potassium deficiency > H+ normally in ECF move into cells > Absence of H+ makes ECF and blood more alkaline

25
Q

What are the normal potassium levels in the blood?

A

3.5-5.3 mmol/L

26
Q

What is renal excretion determined by?

A

Sum of three:
- Rate of K+ filtration (GFR x plasma K+ conc)
- Rate of K+ reabsorption by the tubules
- Rate of K+ secretion by tubules

27
Q

How is Potassium regulated in the kidneys?

A

GLOMERULUS: Freely filtered
PCT:
- Na+/K+ ATPase pumps Na+ out of cell and K+ into cell = osmotic + electrochemical gradient - water and Cl- moves out of PCT
- 2/3 K+ reabsorbed passively and follows Cl- into blood
THICK ASCENDING LOH:
- Na+/K+ ATPase on basolat. memb pump K+ into limb - keeps Na+ conc in cell low = gradient
- NKCC2 on apical memb pumps Na+, K+ and 2Cl- into cell. Intracellular K+ enter bloodstream
- K+ moves through ROMK channels into lumen > positive voltage in lumen > driving passive reabsorption for K+
DCT and CCT:
- Apical H+/K+ ATPase mediates H+ movement into lumen, driving K+ into cell
- Basolateral K+ channel allows passive reabsorption into blood
Secretion from DCT and CCT:
- Na+/K+ ATPase in basolat memb of principle cells pumps Na+ into blood which drives K+ into cell
> High intracellular K+ and low Na+ creates a chemical gradient with luminal conc.
> Na+ moves into lumen through ENaC - electrochemical gradient > K+ secretion via K+ channels on apical membrane

28
Q

What occurs in severe K+ depletion?

A

K+ secretion is stopped, net reabsorption occurs in late distal via type A intercalated cells, and collecting tubule
H+/K+ ATPase transport mechanism in luminal membrane contributes

29
Q

How is hypokalemia caused in purging individuals?

A

Not directly from vomiting
Blood volume depletion activates the RAAS system
- Renin released from kidneys converts angiotensinogen from liver to angiotensin I
- Angiotensin I converted to Angiotensin II by ACE from lungs
- Stimulates aldosterone secretion > increases K+ excretion through increasing K+ channels and Na+/K+ ATPase in principle cells of CT > increased urinary K+ loss

30
Q

How does hypokalaemia affect the heart?

A

Neurones to cardiac muscle have high selective permeability to K+ ions in the heart for negative resting potential
Low potassium > affects conduction of APs > promote arrhythmias > QT prolongation

31
Q

What are the three phases of vomiting?

A

Nausea: feeling of wanting to vomit, excess salivation, paleness to skin, antiperistalsis
Retching: forceful involuntary contractions of diaphragm and abdominal muscles
Vomiting: rapid inspiration , closure of epiglottis and elevation of soft palette - prevent entry into lungs and nasal cavity.
Compression of stomach , increases intra-abdominal pressure > expulsion of gastric contents

32
Q

What is the CTZ?

A

Chemoreceptor trigger zone
In the dorsal surface of the medulla oblongata, on lateral wall of fourth ventricle
Outside the BBB
Detects emetic agents - toxins - in the blood and relays to vomiting centre to induce vomiting reflex

33
Q

What is the vomiting reflex?

A
  • A deep breath
  • Easing of the hyoid bone and larynx to pull UOS open
  • Closing of the glottis to prevent the entry of vomit into lungs
  • Elevation of soft palette to prevent the entry of vomit into nasopharynx
  • Strong contraction of diaphragm and abdominal wall muscles
  • LOS relaxes
  • Expulsion of vomitus up oesophagus
  • During emesis, may experience sweating, tachycardia and increased salivation
34
Q

What may stimulate the vomiting reflex?

A

Mechanical stimuli to pharynx:
- Sensation to posterior pharyngeal wall, tonsillar pillars, or base of tongue detected by sensory receptors
- Impulses transmitted to vomiting centre through vagus and sympathetic afferent fibres
- Motor impulses to cause act of vomiting
Motion sickness:
- Motion stimulates receptors in the vestibular labyrinth of inner ear, impulses sent through vestibulocochlear nerve > vestibular nuclei in pons > cerebellum, then CTZ > vomiting centre
Pregnancy: changes in intra-abdominal pressure/hormonal/metabolic changes

35
Q

What are the vertebral levels of features of the oesophagus and stomach?

A

Oesophagus starts at C6
Oesophageal hiatus at T10, to stomach through oesophageal hiatus at T11
Cardia surrounding opening at T11

36
Q

What are the layers of the oesophageal wall?

A
  • Mucosa: non-keratinised stratified squamous into simple columnar in stomach
  • Submucosa
  • Muscle: 3 layers. Superior third - voluntary striated. Middle third - voluntary striated. Inferior third - smooth muscle
  • Adventitia: outer layer of CT. Distal and peritoneal portion covered in serosa
37
Q

What is a Mallory-Weiss tear and how does it occur?

A

Laceration in mucous membrane, involves mucosa and submucosa
Severe vomiting > sudden increase in intra-abdominal pressure > partial thickness laceration below gastroesophageal junction > mucosal bleeding

38
Q

What are the causes and symptoms of a Mallory weiss tear?

A

Causes:
- Vomiting
- Straining
- Coughing
- Blunt abdominal injury
- NG tube
- Gastroscopy
Signs:
- Haematemesis
- Melena
- Epigastric/back pain
- Haemodynamic instability

39
Q

How are mallory weiss tears treated?

A

Should heal in 24-48 hours, but if persistent, collagen deposition and fibrosis can occur > long term damage
- PPI - acid suppression
- Antiemetics
- Surgery - cauterisation, haemoclips with adrenaline

40
Q

How do loop diuretics work?

A

Reduce NaCl reabsorption in the thick ascending limb of the LoH:
- Binds reversibly to the Na-K-2Cl carrier protein > reduces entry of luminal Na and Cl into cell
- Less Na reabsorbed into bloodstream , increases Na concentration in nephron
- Prevents passive reabsorption of water in the descending limb of LoH
- Increased urine production
Can also cause excretion of Cl- and K+ ions > hypokalaemia, hypochloraemia

41
Q

What is the appetite control centre?

A

Arcuate nucleus in the hypothalamus

42
Q

How is appetite controlled in the CNS?

A

Signals sent via vagus nerve afferent pathway
Primary neurones will process external nutritional, hormonal and neuronal signals. Will be excitatory or inhibitory
Excitatory will release NT: neuropeptide Y (NPY), agouti-related peptide (AgRP) = promote hunger
Inhibitory neurones will release NT: CART and POMC = suppress hunger
Secondary neurones will coordinate the inputs

43
Q

What hormonal signals stimulate hunger? Where do they come from, how do they work?

A

Ghrelin:
Peptide hormone produced by P/D1 cells in stomach , also in pancreas, SI and brain. Released when stomach is empty. Stimulates excitatory primary neurones > stimulate appetite
Prepares gut for food: gastric acid production and gut motility
Increases hunger, increases hepatic glucose secretion due to starved state
Decreases insulin secretion, decreases thermogenesis to decrease energy use

44
Q

What hormone signals suppresses hunger?

A

PYY:
Released from L cells in ileum and colon after eating fats and protein. Bile, gastric acid, CCK, vasoactive intestinal polypeptide stimulates PYY release. Rises after 15 of eating, plateaus at 90 minutes, lasts 6 hours
Leptin:
Released from adipocytes in white adipose tissue. Level in blood DP to amount of adipose tissue. Neuronal, pancreatic, hepatic, cardiac leptin receptors
Insulin:
Released from beta cells in islet of langerhans in pancreas.
THESE ALL stimulate inhibitory neurones, inhibit stimulatory neurones in arcuate nucleus, cause release of CART and POMC from primary neurones. Suppresses appetite and gut motility.

45
Q

What receptors in the gut can affect appetite?

A

Mechanoreceptors/stretch receptors detect if organs are distended (fed state) - can stimulate/inhibit inhibitory/stimulatory neurons
Chemoreceptors detect blood glucose levels, amino acid and fat levels and can detect if the body is in a fed state.

46
Q

What psychological factors influence developing an eating disorder?

A

Body image dissatisfaction
Low self esteem
Peer and social infleunce
Family dynamics
Trauma and stress
Perfectionism
Social media
Psychological distress

47
Q

What is the stages of change model?

A

Pre-contemplation
Contemplation
Determination
Action
Relapse
Maintenance
Then possibly back again

48
Q

What is the health belief model?

A

Demographic variables and psychological characteristics lead into
- Perceived susceptibility
- Perceived severity
- Health motivation
- Perceived benefits
- Perceived barriers
Which all lead into action

49
Q

What are the stages in CBT for eating disorders?

A

Stage 1: getting to know the patient, setting goals
Stage 2: review progress, set a plan
Stage 3: tackling things that maintain difficulties with eating
Stage 4: reflection, changes the patient has made, how to deal with setbacks

Unit 10 PBL cases (6 decks)

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