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MBBS - Y1 > Week 8 - chronic diseases > Flashcards

Week 8 - chronic diseases Flashcards

1
Q

What are carbohydrates? (LO1)

A
  • The most abundant organic molecule.
  • Energy souce (glucose –> ATP).
  • Energy storage (glycogen).
  • Structural component.
  • Immune function.
  • Intracellular communication.
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2
Q

Describe the general classification and structure of carbohydrates. (LO1)

A
  • Carbo = carbon.
  • Hydrate = water.
  • General formula is (CH₂O)n
  • Monosaccharide = 1 sugar unit.
  • Disaccharide = 2 sugar units.
  • Oligosaccharide = 3-10 sugar units.
  • Polysaccharides = 11- >100 sugar units.
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3
Q

Describe the classification of carbohydrates by the number of carbon atoms. (LO1)

A
  • Triose = 3 carbons, e.g. glyceraldehyde.
  • Tetrose = 4 carbons, e.g. erythrose.
  • Pentose = 5 carbons, e.g. ribose.
  • Hexose = 6 carbons, e.g. glucose.
  • Heptose = 7 carbons, e.g. sedoheptulose.
  • Nonose = 9 carbons, e.g. neuraminic acid.
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4
Q

Describe the classification of carbohydrates by functional group. (LO1)

A

The most common functional groups are aldehydes (O=C-H) or ketones (C=O).

  • Monosaccharides + aldehyde function = aldoses (suffix -ose).
  • Monosaccharides + ketone function = ketoses (suffix -ulose).
  • Hexose + aldehyde function = ALDOHEXOSE.
  • Hexose + ketone function = KETOHEXOSE.

N.B. ketohexose is also known as fructose (it should be called fructulose but some idiot decided to make things confusing).

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5
Q

Describe the classification of carbohydrates by structure. (LO1)

A
  • Compounds that have the same chemical formula, but different structures are called isomers.
  • Carbohydrate isomers which only differ around one specific carbon atom are called epimers.
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6
Q

What are enantiomers? (LO1)

A
  • Pairs of structures that are mirror images of each other.

- Even if you rotate one mirror image, the molecules still do not superimpose on each other.

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7
Q

What is meant by L and D designations? (LO1)

A
  • These designations are based on the configuration of a single asymmetric carbon atom in glyceraldehyde.
  • Sugars with >1 chiral centre.
  • D and L refer to the farthest asymmetric carbon atom from the carbonyl group.
  • Most naturally occurring sugars are D isomers.
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8
Q

Describe the cyclisation of monosaccharides. (LO1)

A

> 99% of monosaccharides with >5 carbon atoms form a ring structure.

  • To form this, the aldehyde/ketone group reacts with the hydroxyl group of the same monosaccharide.
  • 5 carbon atoms + 1 oxygen atom = PYRANOSE RING.
  • 4 carbon atoms + 1 oxygen atom = FURANOSE RING.
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9
Q

How does cyclisation of monosaccharides change them? (LO1)

A
  • Creates a new stereogenic centre (also known as chiral centre).
  • The chiral centre becomes asymmetric.
  • In D-glucose, the newly generated hydroxyl group can be above or below the midplane of the cyclised molecule. Thus, the open chain monosaccharide yields two cyclic isomers: α-anomer and β-anomer.
  • In glucose, the full names of these molecules are α-D-glycopyranose and β-D-glucopyranose.
  • Both anomers of the sugar are in equilibrium in solution and can spontaneously interconvert.
  • This process is called mutarotation and can take hours.
  • In glucose, the ratio is 64:36 of β:α.
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10
Q

What is the chiral centre? (LO1)

A

The carbon atom bearing the carbonyl.

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11
Q

Give three examples of monosaccharides and their sources. (LO1)

A
  1. Glucose.
    - Primary energy source: preferred energy source for the brain, required energy source for cells with few/no mitochondria, essential in exercising muscles.
    - Source: diet, degradation of glycogen, gluconeogenesis.
  2. Fructose.
    - Sweeter than glucose.
    - Source: fruits, vegetables, honey.
  3. Galactose.
    - Less sweet than glucose.
    - Source: dairy products.
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12
Q

Give three examples of disaccharides. How are they made? (LO1)

A
  • Sucrose = glucose + fructose.
  • Maltose = glucose + glucose.
  • Lactose = glucose + galactose.
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13
Q

Describe the disaccharide bond between glucose and fructose in sucrose. (LO1)

A
  • Glycosidic bonds.
  • These bonds are named according to the numbers of the connected carbon atoms and the position of the anomeric hydroxyl groups involved in the bond.
  • E.g. if the hydroxyl group is in α-configuration, then it’s an α-bond.
  • In sucrose: α-(1–>2)-β-glycosidic bond.
  • This means that the hydroxyl group of carbon atom 1 in α-configuration has reacted with the hydroxyl group of carbon atom 2 in β-configuration.
  • This reaction leads to the elimination of one water molecule.
  • Scientific name of sucrose: α-D-glucopyranosyl-(1–>2)-β-D-fructofuranoside.
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14
Q

Describe the bond between the two glucose molecules in maltose. (LO1)

A
  • α-(1–>4)-glycosidic bond.
  • The hydroxyl group on carbon atom 1 on one glucose molecule in α-configuration reacts with the hydroxyl group on carbon atom 4 of another glucose molecule to form a bond between them by the elemination of one water molecule.
  • Scientific name of maltose: α-D-glucopyranosyl-(1–>4)-β-D-fructofuranoside.
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15
Q

Describe the bond between glucose and galactose in lactose. (LO1)

A
  • β-(1–>4)-glycosidic bond.
  • The hydroxyl group on carbon atom 1 of galactose in β-configuration reacts with the hydroxyl group on carbon atom 4 of glucose to form the bond between them by the elimination of one water molecule.
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16
Q

Give three examples of polysaccharides and their functions. (LO1)

A
  • Cellulose - structural.
  • Starch - storage (plants).
  • Glycogen - storage (animals).
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17
Q

What is cellulose? (LO1)

A
  • Polysaccharide consisting of a linear chain of 100,000s of β-glucose units.
  • Glucose molecules linked together by β-(1–>4)-glycosidic bonds.
  • Cellulose is an important component of dietary fibre which acts as a hydrophilic bulking agent for the faeces.
  • Major component of plant cell walls.
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18
Q

What is starch? (LO1)

A
  • Polysaccharide consisting of 100,00s of glucose units.
  • Glucose molecules linked together by α-(1–>4)-glycosidic bonds.
  • Found in all plant seeds and tubers.
  • Amylose and amylopectin are the 2 forms of starch.
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19
Q

What is amylose? (LO1)

A
  • Unbranched polymer.
  • A form of starch.
  • Linear polysaccharide just like cellulose.
  • Glucose molecules linked together by only α-(1–>4)-glycosidic bonds.
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20
Q

What is amylopectin? (LO1)

A
  • Branched polymer (every 20-30 carbon residues).
  • A form of starch.
  • Most glucose molecules linked by α-(1–>4)-glycosidic bonds.
  • Every 20-30 residues, the glucose molecules are also linked by α-(1–>6)-glycosidic bonds which form the branches.
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21
Q

What is glycogen? (LO1)

A
  • Branched polysaccharide consisting of 100,000s of glucose molecules.
  • More extensively branched and compact than amylopectin.
  • Similar structure to amylopectin with mainly α-(1–>4)-glycosidic bonds.
  • Every 8-10 residues, the glucose molecules are also linked by α-(1–>6)-glycosidic bonds.
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22
Q

Describe the the three areas where carbohydrates are digested and the enzymes involved. (LO1)

A
  • Salivary glands - alpha amylase.
  • Small intestine - pancreatic α-amylase.
  • Upper jejunum - dextrinase, glucoamylase (gamma amylase), isomaltase, maltase, sucrase, lactase.
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23
Q

How do the salivary glands aid the digestion of carbohydrates? (LO1)

A
  • Occurs in the mouth during chewing.
  • Saliva contains α-amylase which hydrolyses α-(1–>4) bonds.
  • E.g. starch –> maltose + dextrin.
  • Dextrin is a mixture of glucose polymers linked by α-(1–>4)-glycosidic bonds and α-(1–>6)-glycosidic bonds.
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24
Q

How does the small intestine aid the digestion of carbohydrates? (LO1)

A
  • Pancreatic alpha amylase creates more maltose and dextrin.
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25
Q

How does the mucosal lining of the upper jejunum aid the digestion of carbohydrates? (LO1)

A
  • Brush-border membrane-associated oligosaccharides and disaccharides hydrolyse the carbohydrates to yield glucose, fructose and galactose.
  • Dextrinase is a debranching enzyme. It hydrolyses α-(1–>6)-glycosidic bonds.
  • Glucoamylase (gamma amylase) hydrolyses α-(1–>6) and α-(1–>4)-glycosidic bonds, yielding glucose.
  • Finally, disaccharides are hydrolysed to monosaccharides.
  • Isomaltose is hydrolysed by isomaltase to yield two glucose molecules.
  • Maltose is hydrolysed by maltase to yield two glucose molecules.
  • Sucrose is hydrolysed by sucrase to yield glucose and fructose.
  • Lactose is hydrolysed by lactase to yield glucose and galactose.
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26
Q

Describe the absorption of monosaccharides. (LO1)

A
  • Monosaccharides are absorbed by intestinal mucosal cells.
  • Glucose and galactose are taken up by SGLT-1 (sodium-dependent glucose co-transporter 1).
  • Fructose is taken up by GLUT-5 (sodium-independent monosaccharide transporter).
  • All monosaccharides are transported from the intestinal wall into the portal circulation by GLUT-2.
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27
Q

How does the sodium-dependent glucose transporter 1 (SGLT-1) work to absorb carbohydrates? (LO1)

A
  • SGLT-1 (sodium-dependent glucose co-transporter 1) - take up glucose and galactose. This is an active transporter.
  • Glucose and galactose are taken up together with sodium ions.
  • This uptake is dependent on the existing sodium gradient.
  • The sodium gradient is achieved through the action of an ATP-dependent sodium-potassium pump which expels 3 sodium ions from the cell in exchange for 2 potassium ions entering the cell.
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28
Q

How do we manage sugar intolerance? (LO1)

A
  • Dietary avoidance of sugar.

- Enzyme replacement therapy.

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29
Q

What is galactosaemia? (LO1)

A
  • Genetic disorder - inability to metabolise galactose which leads to galactose accumulation.
  • Galactose is instead broken down and converted to toxic metabolism.
  • If any of the three enzymes involved in the metabolism of galactose to UDP-glucose are deficient/defective, then galactose accumulates.
  • The accumulated galactose is reduced to galactitol and oxidised to galactonate, which are both toxic metabolites.
  • The only treatment available for galactosaemia is the elimination of lactose and galactose from the diet.
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30
Q

Explain the normal physiological pathway of galactose metabolism. (LO1)

A
  • Galactose is converted to galactose-1-P.
  • Galactose-1-P is converted to UDP-glucose.
  • UDP-glucose is a substrate for the synthesis of glycogen (glycogenesis).
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31
Q

Describe glucose metabolism. (LO1)

A
  • After absorption from the intestinal tract, much of fructose and galactose are rapidly converted to glucose.
  • In the metabolic pathway of glycolysis, glucose is broken down to pyruvate. This pathway provides 2 ATP molecules and 2 NADH molecules. The 2 NADH molecules are equal to 6 ATP but as 2 ATP molecules have been used, the net ATP production is 4 molecules.
  • Glucose can be synthesised from pyruvate in the metabolic pathway of gluconeogenesis.
  • In anaerobic glycolysis, pyruvate is reduced to lactate so that glycolysis can continue.
  • Pyruvate is further broken down to acetyl-CoA, providing 2 NADH molecules which are equal to 6 ATP molecules.
  • Acetyl-CoA is completely oxidised to carbon dioxide in the Krebs cycle. This process provides 2 GTP molecules, 6 NADH molecules which are equal to 18 ATP molecules and 2 FADH molecules, which are equal to 4 ATP molecules.
  • In the pentose phosphate pathway, glucose is used to produce NADPH and ribulose-5-P.
  • Ribulose-5-P can be converted to ribose-5-P which is a precursor for RNA and DNA.
  • Finally, glucose can be stored in the form of glycogen.
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32
Q

How does the 2D diagram of the chemical formulae of carbohydrates indicate the 3D structure of the molecule? (LO1)

A
  • Carbon atoms are numbers by having the lowest number assigned to the carbon atom attached to the functional group (aldehyde/ketone). The rest are numbered consecutively down the chain.
  • The backbone of carbon atoms are shown to all lie along the same plane.
  • Solid, black wedges coming off the backbone indicate that atoms or groups are located above the plane of the carbon backbone.
  • Dotted wedges coming off the backbone indicate that atoms or groups are located below the plane of the carbon backbone.
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33
Q

Compare the structures of these monosaccharides: glucose, galactose, mannose and fructose. (LO1)

A
  • All of these monosaccharides have the same chemical formula of C₆H₁₂O₆ so they are isomers of each other.
  • The difference between glucose and fructose is obvious. It’s not so obvious between glucose, galactose and mannose.
  • Comparing the structures of glucose and galactose: the hydroxyl group on carbon atom 4 have different orientations - galactose and glucose are C-4 epimers.
  • Comparing the structures of glucose and mannose: the hydroxyl group on carbon atom 2 have different orientations - mannose and glucose are C-2 epimers.
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34
Q

Describe what happens with a deficiency of carbohydrate degradation. (LO1)

A
  • This is a hereditary deficiency of individual disaccharides.
  • Lactose intolerance (70-80%) of the world’s population is lactose intolerant.
  • Isomaltose/sucrose intolerance (10% of Greenland Inuits, 2% of North Americans of the trait).
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35
Q

What are the symptoms of carbohydate degradation deficiency? (LO1)

A
  • Undigested carbohydrates pass into large intestines leading to osmotic diarrhoea.
  • Bacterial fermentation of carb products produces large volumes of CO₂ and H₂ in the intestines leading to abdominal cramps, diarrhoea and flatulence.
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36
Q

What is the transtheoretical model? List the stages of this model (6). (LO2)

A
  1. Pre-contemplation.
  2. Contemplation.
  3. Preparation/determination.
  4. Action.
  5. Maintenance.
  6. Termination.
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37
Q

Describe what occurs in the pre-contemplation stage (1) of the transtheoretical model. (LO2)

A
  • People don’t intend to take action in the foreseeable future.
  • Underestimation of pros and emphasis of cons of changing behaviour.
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38
Q

Describe what occurs in the contemplation stage (2) of the transtheoretical model. (LO2)

A
  • People intending to start healthy behaviour in the foreseeable future.
  • Pros and cons of changing behaviour is contemplated.
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39
Q

Describe what occurs in the preparation/determination stage (3) of the transtheoretical model. (LO2)

A
  • Ready to take action within 30 days.

- People begin to take small steps towards behaviours and believe changing behaviour will lead to a healthier life.

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40
Q

Describe what occurs in the action stage (4) of the transtheoretical model. (LO2)

A
  • People have recently changed their behaviour and intend to keep moving forward.
  • People exhibit modification of problem behaviour and adopting new healthy behaviours.
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41
Q

Describe what occurs in the maintenance stage (5) of the transtheoretical model. (LO2)

A
  • People have sustained the behaviour change for a while and intend to maintain the behaviour.
  • They work to prevent relapse of earlier stages.
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42
Q

Describe what occurs in the termination stage (6) of the transtheoretical model. (LO2)

A
  • People have no desire to return to their unhealthy behaviours so no relapse.
  • This is rarely achieved and people tend to stay in the maintenance stage.
  • This stage is often not even considered in health promotion programmes.
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43
Q

List the processes of change (10). (LO2)

A
  1. Consciousness raising: increasing awareness about healthy behaviour.
  2. Dramatic relief: emotional arousal about health behaviour, whether positive or negative.
  3. Self re-evaluation: self-reappraisal to realise healthy behaviour is part of what they want.
  4. Environmental re-evaluation: social reappraisal to realise how their unhealthy behaviour affects others.
  5. Social liberation: environmental opportunities that exist to show society is supportive of healthy behaviour.
  6. Self-liberation: commitment to change behaviour based on the belief that achievement of the healthy behaviour is possible.
  7. Helping relationships: finding supportive relationships that encourage desired change.
  8. Counter-conditioning: substituting healthy behaviours and thoughts for unhealthy behaviours and thoughts.
  9. Reinforcement management: rewarding the positive behaviour and reducing rewards coming from negative behaviour.
  10. Stimulus control: re-engineering the environment to have reminders and cues that support healthy behaviour and remove those supporting unhealthy behaviour.
    These processes result in strategies to maintain change.
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44
Q

What is the theory of planned behaviour? List the constructs of this theory (6). (LO2)

A
  1. Attitudes.
  2. Behavioural intention.
  3. Subjective norms.
  4. Social norms.
  5. Perceived power.
  6. Perceived behavioural control.
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45
Q

Describe the attitude construct (1) of the theory of planned behaviour. (LO2)

A
  • The degree to which a person has an favourable/unfavourable evaluation of a behaviour.
  • Consideration of the outcomes of performing the behaviour.
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46
Q

Describe the behavioural intention construct (2) of the theory of planned behaviour. (LO2)

A
  • Motivational factors that influence a given behaviour.

- The stronger the intention to perform the behaviour, the more likely it will be performed.

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47
Q

Describe the subjective norms construct (3) of the theory of planned behaviour. (LO2)

A
  • Refers to the beliefs about whether most people approve or not of the behaviour.
  • Relates to the person’s beliefs about whether peers and people of importance think they should engage in the behaviour.
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48
Q

Describe the social norms construct (4) of the theory of planned behaviour. (LO2)

A

These are considered normative or standard.

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49
Q

Describe the perceived power construct (5) of the theory of planned behaviour. (LO2)

A
  • Perceived presence of factors that facilitate or impede the performance of the behaviour.
  • Person’s perceived behavioural control over each of those factors.
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50
Q

Describe the perceived behavioural control construct (6) of the theory of planned behaviour. (LO2)

A

The level of ease or difficulty of performing the behaviour.

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51
Q

What is the health belief model? List the constructs of this model (6). (LO2)

A

This is a social psychological health behaviour change model developed to explain and predict health-related behaviours particularly in regard to the uptake of health services. There are 6 constructs to this model:

  1. Perceived susceptibility.
  2. Perceived severity.
  3. Perceived benefits.
  4. Perceived barriers.
  5. Cue to action.
  6. Self-efficacy.
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52
Q

Describe the perceived susceptibility construct (1) of the health belief model. (LO2)

A
  • Person’s subjective view of risk of acquiring illness or disease.
  • Wide variations in a person’s feelings of personal vulnerability.
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53
Q

Describe the perceived severity construct (2) of the health belief model. (LO2)

A
  • Person’s feelings on the seriousness of illness or disease.
  • Consideration of medical and social consequences.
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54
Q

Describe the perceived benefits construct (3) of the health belief model. (LO2)

A
  • Person’s perception of effectiveness of various actions available to reduce the threat of illness.
  • Person would accept the recommended health action if it was perceived as beneficial.
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55
Q

Describe the perceived barriers construct (4) of the health belief model. (LO2)

A
  • Person’s feelings on the obstacles to performing a recommended health action.
  • Wide variations in a person’s feelings of barriers which lead to cost/benefit analysis.
  • Weighs effectiveness with custom dangers, unpleasantness, time and inconvenience.
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56
Q

Describe the cue to action construct (5) of the health belief model. (LO2)

A
  • A stimulus is needed to trigger the decision-making process to accept a recommended health action.
  • Cues can be internal or external.
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57
Q

Describe the self-efficacy construct (6) of the health belief model. (LO2)

A

The level of a person’s confidence in their ability to successfully perform a behaviour.

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58
Q

What is the COM-B model? (LO2)

A

This model proposes that there are three components to any behaviour (B).
1. Capability (C).
2. Opportunity (O).
3. Motivation (M).
As each of these components interact, interventions must target one or more of these in order to deliver and maintain effective behaviour change.

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59
Q

Describe the capability component of the COM-B model. (LO2)

A

Attributes of a person that, together with opportunity, makes a behaviour possible or facilitates it. There are two types of capability:

  • Physical capability: capability that involves a person’s physique and musculoskeletal functioning.
  • Psychological capability: involves a person’s mental functioning.
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60
Q

Describe the opportunity component of the COM-B model. (LO2)

A

Attributes of an environmental system that, together with capability, makes a behaviour possible or facilitates it. There are two types of opportunity:

  • Physical opportunity: involves inanimate parts of the environmental system and time.
  • Social opportunity: involves other people and organisations.
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61
Q

Describe the motivation component of the COM-B model. (LO2)

A

Aggregates of mental processes that energise and direct behaviour. There are two types of motivation:

  • Reflective motivation: involves conscious thought process.
  • Automatic motivation: involves habitual, instinctive, drive-related and affective processes.
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62
Q

Describe the interactions between the three components of the COM-B model. (LO2)

A
  • Behaviour influences all three components.
  • All three components influence behaviour.
  • Capability and motivation influence each other.
  • Opportunity influences capability and motivation.
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63
Q

Define compliance with regard to treatment. (LO3)

A
  • The extent to which someone complies with advice provided by a doctor.
  • Compliance is a passive behaviour in which the patient is following a list of instructions.
  • Doctor-centred approach.
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64
Q

Define adherence with regard to treatment. (LO3)

A
  • The extent to which an individual adheres to agreed advice.
  • Adherence is a more proactive behaviour which results in a lifestyle change by the patient, who must follow a daily regimen.
  • Suggesting less of a doctor-centred view.
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65
Q

Define concordance with regard to treatment. (LO3)

A
  • Outcomes of a process whereby a doctor and patient come to a mutually agreeable route of action.
  • Much more patient-centred.
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66
Q

What counts as medical advice? (LO3)

A

Asking a patient to:

  • Change behaviours.
  • Complete physiotherapy exercises.
  • Take medications.
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67
Q

How can we assess adherence behaviours? (LO3)

A
  • Pill counts.
  • Self-report.
  • Clinical outcomes.
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68
Q

How can health professionals improve adherence? (LO3)

A
  • Adherence could be intentional or unintentional.
  • Good communication between the patient and doctor doubles adherence.
  • Medical adherence has been associated with: socio-economic status, healthcare system, condition therapy and patient-related factors.
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69
Q

List the three factors affecting adherence. (LO3)

A
  • Information.
  • Motivation.
  • Strategy.
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70
Q

What is meant by information when talking about factors affecting adherence? (LO3)

A
  • Sometimes patients don’t understand what they need to do, maybe due to cognitive capacity, bad communication or an aspect of the illness.
  • To reduce this being an issue, test the patient’s understanding.
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71
Q

What is meant by motivation when talking about factors affecting adherence? (LO3)

A
  • Lack of motivation to follow advice stems from health benefits, treatment suggestions, coping strategies, comorbidities and mental well-being.
  • Cultural, peer and family beliefs are often taken into account by patients.
  • Patients are less likely to stay motivated if they think they can’t successfully achieve it.
  • To avoid this, boost their motivation.
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72
Q

What is meant by strategy when talking about factors affecting adherence? (LO3)

A
  • The treatment plan can’t always be just practical.
  • Low income and high cost of drugs means they’re difficult to afford.
  • This is the same issue with complicated drug regimens.
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73
Q

List the socio-economic factors affecting adherence to medical advice (6). (LO3)

A
  • Family support.
  • Other carer factors.
  • Social support.
  • Stigma.
  • Costs of treatment.
  • Prescription coverage.
  • Socio-economic status.
  • Employment status.
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74
Q

List the factors affecting adherence that could be related to the healthcare system (6). (LO3)

A
  • Barriers to healthcare, e.g. language.
  • Drug supply.
  • Prescription by specialist.
  • Information about drug administration.
  • Patient-health professional communication and relationship.
  • Follow-ups.
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75
Q

List the factors affecting adherence that could be related to the patient’s condition (6). (LO3)

A
  • Presence of symptoms.
  • Disease severity.
  • Clinical improvement.
  • Psychiatric condition.
  • Specific diagnosis/indications.
  • Disease duration.
76
Q

List the factors affecting adherence that could be related to the patient’s therapy (6). (LO3)

A
  • Adverse effects.
  • Patient-friendliness of regimen.
  • Drug effectiveness.
  • Duration of treatment.
  • Drug type.
  • Well-organised treatment.
77
Q

List the factors affecting adherence that could be related to patient demographics (6). (LO3)

A
  • Age.
  • Gender.
  • Marital status.
  • Education.
  • Ethnicity.
  • Housing.
  • Cognitive function.
  • Forgetfulness and reminders.
  • Knowledge.
  • Health beliefs.
  • Psychological profile.
  • Co-morbidities.
  • Alcohol or substance abuse.
  • Transportation difficulties.
78
Q

Describe pain as a homeostatic emotion. (LO4)

A
  • Pain signifies a threat to bodily integrity.
  • It’s more interoceptive than exteroceptive.
  • Pain is a specific emotion which reflects homeostatic behavioural drive.
  • Response to pain requires action - like bodily response to temperature, itch, hunger, thirst.
79
Q

Define interoceptive with regards to pain. (LO4)

A

Sensing bodily state.

80
Q

Define exteroceptive with regards to pain. (LO4)

A

Sensing external environment.

81
Q

What is the limbic system and what does it process? (LO4)

A

The limbic system is the “emotional brain”.

  • Reward.
  • Distress.
  • Motivation.
  • Anxiety.
  • Mood.
  • Pain - the unpleasantness component of pain.
82
Q

Explain the limbic pain pathway. (LO4)

A
  • Nociceptive input from tissue damaged is transmitted by Aδ and C fibres, enters the superficial dorsal horn and then forms a contralateral spinothalamic tract pathway.
  • Focus is more on projections associated with homeostasis and monitoring of bodily integrity which are in the parts of the brainstem.
83
Q

List the parts of the brain associated with assessing the bodily interoceptive state (5). (LO4)

A
  • Periaquaductal grey (PAG).
  • Parabrachial nucleus (PB).
  • Dorsal medial (MDvc) thalamus.
  • Cingulate cortex.
  • Insula cortex.
84
Q

Describe reward and motivation in pain and pain relief. (LO4)

A
  • The enhanced activation of the limbic system amplifying the negative threat.
  • The negative interoceptive state is probably a key factor that drives chronic pathological pain.
85
Q

What factors should be considered to determine whether pain should be considered as disease-related or pathological? (LO4)

A
  • Is pain related to nociceptive input?
  • Is pain a consequence of CNS/PNS pathology? - e.g. neuropathic pain.
  • Is pain protective? - e.g. if you have a broken leg, immobilisation due to pain is key as it allows for healing.
  • Is the behavioural response to pain appropriate or harmful?
86
Q

List the key considerations for the treatment of pain (3). (LO4)

A
  • Treat the underlying condition if it causes pain.
  • Consider the likely duration of symptoms and disease.
  • Consider the patient’s beliefs/understanding of symptoms.
87
Q

How does the limbic system amplify pain? (LO4)

A
  • The limbic system is amplified.
  • That is the key component maintaining pain and amplifying the amount of distress associated with it.
  • The emotional value that you associate with the pain and the relief of pain due to analgesia may drive this in a vicious cycle.
88
Q

Describe the psychological factors in pain. (LO4)

A
  • Prospective studies of pain from onset in community, workplace or post-surgical populations show that persistence of pain and disability are predicted by:
    1. Severity of pain at onset.
    2. Distress around the onset.
  • Psychological factors have a significant influence on pain and disability and are stronger determinants of outcome than biomedical factors.
  • Key psychological dimensions are:
    1. Attitudes and beliefs (cognitions).
    2. Pain behaviour and coping strategies.
    3. Emotions and distress.
89
Q

List some cognitions involved in the perception of pain (4). (LO4)

A
  • Unhelpful anxiety-provoking thoughts.
  • Catastrophising.
  • Rumination.
  • Expectations.
90
Q

Explain how unhelpful, anxiety-provoking thoughts can influence how we experience and respond to pain. (LO4)

A
  • Over-generalisation.
  • Using words like “always” and “never” - e.g. “the pain will never stop and only get worse.”
  • Jumping to conclusions (negative).
  • “should” thinking - e.g. “I should be able to do x and y.”
91
Q

Explain how catastrophising can influence how we experience and respond to pain. (LO4)

A
  • Extreme assumptions/amplifying of negative aspects.
  • Magnification - e.g. “I became afraid that the pain will get worse. I wonder whether something serious will happen.”
  • Helplessness - e.g. “I can’t go on. It’s terrible and won’t get better.”
92
Q

Explain how rumination can influence how we experience and respond to pain. (LO4)

A
  • E.g. “I keep thinking about how much it hurts.”
93
Q

Explain how expectations can influence how we experience and respond to pain. (LO4)

A
  • About course, management, recovery - e.g. “this should have recovered by now.”
  • Can be unrealistic.
  • These drive behaviour.
  • Impactful if expectations are not fulfilled.
94
Q

Describe the relationship between emotions and pain. (LO4)

A

Pain generates negative feelings of fear, anxiety, guilt, frustration, anger and depression:

  • Powerful driver of behaviours.
  • Linked to poorer outcomes, slower recovery, higher reporting of pain intensity, length of sick leave taken.

Significant emotions are fear and anxiety:

  • Anxiety - common persistent pain, e.g. about significance or meaning of their pain and the impact on their lives.
  • Fear - fight or flight - directly linked to cognitions and behaviours.

Depression:

  • Reduced opportunity to engage in activities due to limitations caused by pain.
  • More frequent exposure to adverse events - e.g. treatment, hospital admission, etc.
  • Many failed interventions and chronic unresolved stress.
95
Q

Explain the persistent pain cycle (12 steps). (LO4)

A
  1. Persistent pain.
  2. Being less active.
  3. Loss of fitness, weak muscles, joint stiffness.
  4. Creation of “no-go” lists of things you cannot do.
  5. Sleep problems, tiredness and fatigue.
  6. Stress, fear, anxiety, anger and frustration.
  7. Medication side effects.
  8. Weight loss/gain.
  9. Negative thinking, fear of future.
  10. Depression and mood swings.
  11. Time off work, money worries, relationship concerns.
  12. Persistent pain.
96
Q

Describe the effect of anxiety in patients experiencing pain. (LO4)

A
  • Generalised anxiety disorder (GAD) is characterised by excessive anxiety and worry. For a diagnosis, this must have occurred on most days in the preceding 6 months - as specified by the DSM 5 criteria.
  • Associated with:
    1. Restlessness.
    2. Fatigue.
    3. Difficulty concentrating.
    4. Sleep disturbance.
    5. Marked muscle tension.
    6. The anxiety itself also causes distress and impairment.
97
Q

List some interventions for anxiety relating to pain (3). (LO4)

A
  • Education - to help understand that thoroughly investigated chronic pain does not indicate pathology.
  • Relaxation techniques: diaphragmatic breathing, guided imagery, progressive muscle relaxation (PMR) and a variety of other approaches.
  • CBT - working to challenge unhelpful or negative thoughts.
98
Q

List some interventions for depression relating to pain (4). (LO4)

A

Depression in pain is generally best tackled as an understandable psychological response. Clear diagnostic criteria as per the DSM 5.

  • CBT - working to challenge unhelpful or negative thoughts.
  • Education - helps understanding.
  • Realistic goal setting.
  • Graded and paced activity and exercise.
99
Q

What is cognitive behavioural therapy (CBT)? (LO5+LO10)

A
  • It was originally developed for depression and applied to other conditions, including chronic pain.
  • Does not work for everyone but can be effective.
  • Feeling stressed can lead to release of stress hormones. This can lead to increased body tension and heightened pain experience.
  • CBT helps assess beliefs: impact, cause, cure, prospects.
100
Q

What are some helpful cognitions? (LO5+LO10)

A
  • Address unhelpful patterns of thinking. Develop better coping strategies and tackle underlying beliefs. Talking therapies like CBT can do this.
  • Individualised therapy:
    1. Keep records of thoughts, identify unhelpful patterns of thinking, learning to challenge unhelpful thoughts.
    2. Building confidence through testing out thoughts such as, “I’m bound to fail”.
    3. Developing helpful cognitions such as, “I have got myself through tough days and I can help myself. Even though I may not be able to do everything, today I can do…”
101
Q

What is mindfulness based stress reduction (MBSR)? (LO5+LO10)

A
  • Medical culture is that pain and suffering can be fixed.
  • Mindfulness - pain and suffering are a part of life and we can learn how to deal with them and go on living.
  • Focus on increasing awareness of the moment-to-moment experiences.
  • Effects are comparable to CBT.
102
Q

What is acceptance and commitment therapy (ACT)? (LO5+LO10)

A
  • Uses acceptance and mindfulness skills to produce greater psychosocial flexibility and to help people live more meaningful lives.
  • Proposes that suffering is NORMAL.
  • Attempts to control and avoid internal negative experiences are the main problems leading to a vicious cycle.
  • Teaches psychological skills to deal with negative thoughts and feelings effectively.
  • Goal: refocus energy on what can be achieved despite pain - psychological flexibility.
103
Q

List the factors helping acceptance. (LO5+LO10)

A
  • Person understands:
    1. Reasons that pain persists.
    2. Limitations of existing treatments.
    3. Further treatments will not cure the pain.
    4. THEY CAN MAKE CHANGES which can improve the pain.
  • A sense of identity which is not tied to pain.
  • Support from healthcare professionals, family, friends, employers, etc.
104
Q

List some stress management and relaxation techniques to be used alongside CBT/ACT (5). (LO5+LO10)

A
  • Breathing techniques.
  • Exercise such as tai chi or yoga.
  • Attentional techniques to reduce tension in parts of the body - PMR.
  • Guided imagery exercises (relaxation CDs).
  • Listening to sounds from nature.
105
Q

List some non-pharmacological interventions aside from talking therapy. (LO5+LO10)

A
  • Hypnosis.
  • Biofeedback.
  • Exercise.
  • Acupuncture.
  • Osteopath/chiropractor.
  • Physical therapy:
    1. TENS (transcutaneous electrical nerve stimulation).
    2. Heat packs.
    3. Cold packs.
    4. Massage.
106
Q

What are two mentalities that could be barriers to psychological therapy for chronic pain? (LO5+LO10)

A
  • “If you are sending me to psych therapy, do you think I’m mad?”
  • “Are you saying it’s all in my head…that I’m making it up?”
107
Q

How would we respond to this statement: “If you are sending me to psych therapy, do you think I’m mad?” (LO5+LO10)

A
  1. No, you are not mad.
  2. Most people find that pain affects them both physically and mentally.
  3. Biopsychosocial symptoms, e.g. sleep disturbance, irritable, etc.
  4. Stress and low mood affect exercise tolerance.
  5. Psychologists can help overcome these.
108
Q

How would we respond to this statement: “Are you saying it’s all in my head…that I’m making it up?” (LO5+LO10)

A
  1. The pain is real.

2. These are methods to cope with the pain and fine tune existing coping mechanisms.

109
Q

What is the sick role? (LO6)

A
  • The sick role is a concept created to explain a form of social deviancy where an individual cannot fulfil the same duties as is accepted to be the ‘norm’ as a result of their illness.
  • Parson’s saw this role as a form of deviance because an ill person has different patterns of behaviour which are positively sanctioned - not punished, formally or informally.
  • E.g. absence from school is a deviance but if due to sickness, then it is accepted by teachers.
  • Involves two rights and two responsibilities.
110
Q

What is the function of the sick role and how is it regulated? (LO6)

A
  • The sick role is a temporary role into which all people can be admitted.
  • Doctors are considered to be the gatekeepers to the sick role as they decide whether or not the individuals have a disease.
  • The main function of the sick role is to control illness and reduce the disruptive effects on social systems by returning the ill to good health as quickly as possible.
111
Q

What are the two rights of the sick role? (LO6)

A
  1. The sick are not obliged to perform their normal social roles.
  2. The sick are not considered responsible for their own state.
112
Q

What are the two responsibilities of the sick role? (LO6)

A
  1. The sick are obliged to want to get well as soon as possible.
  2. The sick are obliged to consult and cooperate with medical experts.
113
Q

What is the result of failure to carry out the responsibilities of the sick role? (LO6)

A
  • The sick person forfeits their rights of the sick role.
  • Someone who appears not to want to get well is sometimes viewed as a malingerer or a hypochondriac.
  • Someone who does not cooperate with medical experts is seen as non-compliant and a non-compliant patient may be seen responsible for their illness in a way that other patients are not.
114
Q

What is the Marxist argument regarding the sick role in modern healthcare? (LO6)

A

They argue that in modern society, the actual treatments and hospital environment often make patients more ill and that there is an increasing medicalisation of life and it is becoming a more accepted norm to have medical issues.

115
Q

What is the feminist argument regarding the sick role in modern healthcare? (LO6)

A
  • When women are ill, they are rarely exempt from their normal social role as mother or housekeeper.
  • This argument can be applied to other genders when looking at society’s attitudes towards people being ‘lazy’ if they do not perform the normal tasks such as cooking and cleaning and caring for others.
  • There is still a stigmatised view on those being ill and not performing these tasks. Therefore those in the sick role are not actually granted their rights.
116
Q

How has the doctor-centred approach changed in modern healthcare regarding the sick role. (LO6)

A
  • The sick role is a model based on doctor-centred care but in contemporary healthcare, patient-centred care is used much more broadly and has much better outcomes for the patient’s health.
  • This means the doctor does not have that level of power over a patient to cast them into the sick role.
  • The patient should be leading doctor-patient interactions and should not be put into a single role by the doctor.
117
Q

Explain the relevance of the sick role in modern healthcare. (LO6)

A
  • It can be used to explain how we treat those who are ill and how this can lead to illness behaviours.
  • Being treated as sick can help encourage an individual to go and seek medical treatment. This would allow them to get back to their normal roles sooner.
  • The ability to focus on getting better without having to work increases the chance of recovering quicker.
  • Helps us accept the deviance and reduce judgement/negative attitudes towards those who are unable to participate in certain aspects of society.
118
Q

Why might the sick role no longer be relevant? (LO6)

A
  • In modern society and modern healthcare, there are enough supportive measures that can be put in place to assist people to fulfil their expected duties, despite being ill.
  • Being given this support to fulfil their ‘normal’ roles in society will be more beneficial to society than them taking up the ‘sick role’.
119
Q

What are models of disability? (LO7)

A
  • 3 sociological models of disability created by sociologists to explain how impairment can be defined and how we understand what is actually meant by disability.
  • All these models are reductionist. They say that disability can only be explained by one aspect such as a biological impairments.
  • WHO combats this by integrating the three models to create the International Classification of Functioning, Disability and Health.
120
Q

List the models of disability (3). (LO7)

A
  • The medical model.
  • The social model.
  • The psychological model.
121
Q

What is the medical model of disability? (LO7)

A
  • The traditional model used to explain disability.
  • Explains disability as a direct consequence of underlying disease or disorder.
  • Looks at an individual’s impairment and focuses on how it is the root cause for an individual not being able to access goods/services or be able to participate fully in society.
  • Suggests the only way to reduce disability is to fix/treat the underlying pathology.
122
Q

What are the limitations of the medical model of disability? (LO7)

A
  • Pathology is a poor predictor of the impact of disability.

- The model does not take any other factors into account.

123
Q

What is the social model of disability? (LO7)

A
  • Emphasises the activity limitations and barrier to participation comes from social and environmental factors.
  • A person may be less disabled when the activity is supported better.
  • Even with an attempt in society to combat accessibility problems, there are still barriers created by stigma, e.g. language used by society reflects stigmatised attitudes towards disability.
124
Q

List some environmental factors acting as a barrier to participation in society for the disabled according to the social model of disability (3). (LO7)

A
  • Inaccessibility of buildings.
  • Lack of education.
  • Poor sound systems.
125
Q

What is the psychological model of disability? (LO7)

A
  • Explains that activities performed/not performed by someone with a health condition are influenced by the same psychological processes as those without.
  • Suggests that two people with identical biological conditions and social/environment factors may still have vastly different limitations as a result of different cognitions, emotions and coping strategies.
126
Q

Give an example of a situation involving the psychological model of disability. (LO7)

A

An individual tends to be motivated to do something if it results in something they like or because they hold the belief that those important to them would be happy if they did it.

127
Q

What is the international classification of functioning, disability and health (ICF)? (LO7)

A
  • More commonly known as ICF. It’s a classification of health and health-related conditions.
  • Identifies three components of disability.
  • Because functioning and disability of an individual occurs in a context, the ICF also includes environmental factors to provide a framework for measuring health and disability at individual and population levels.
  • This is the most appropriate model for the multi-disciplinary management of disability.
128
Q

What are the three components of disability identified by the international classification of functioning (ICF)? (LO7)

A
  • Impairments to body structure and functions.
  • Activity limitations.
  • Participation restrictions.
129
Q

Give an example of a situation involving the international classification of functioning (ICF). (LO7)

A

A stroke patient may require a team of different professionals, such as:

  • A neurologist to address underlying brain damage.
  • A physiotherapist to address activity limitations.
  • A psychologists to assist with cognitive function.
130
Q

What is the official (WHO) definition of public health surveillance? (LO8)

A

The ongoing, systematic collection, analysis and interpretation of health-related data essential to planning, implementation and evaluation of public health practice, closely integrated with the timely dissemination of these data to those responsible for prevention and control. - WHO.

131
Q

Define (simply) public health surveillance. (LO8)

A

It’s the collection and analysis of health-related data which is used to evaluate public health practice and sent to the appropriate people for prevention and control.

132
Q

What is public health surveillance used to monitor? (LO8)

A
  • Non-communicable diseases.
  • Injuries.
  • Health service uptake.
  • Vector distribution.
  • Environmental hazards.
  • Etc.
133
Q

What does public health surveillance allow us to do (8)? (LO8)

A
  • Describe the burden or potential for disease.
  • Detect sudden changes in disease occurrence and distribution.
  • Monitor change in disease prevalence over time.
  • Monitor changes in health behaviours.
  • Identify priorities.
  • Inform programmes and policies.
  • Evaluate prevention and control efforts.
  • Develop hypotheses and stimulate research.
134
Q

List the general principles of public health surveillance (5). (LO8)

A
  1. Detect health event - usually in a hospital or clinic.
  2. Code and store the data.
  3. Analyse the data and identify patterns.
  4. Disseminate data to appropriate people.
  5. Action to prevent these events from reoccurring.
135
Q

Define incidence (of a condition). (LO9)

A

Incidence is the rate of occurrence of new cases of a disease. Incidence conveys information about the risk of contracting the disease.

136
Q

Define prevalence (of a condition). (LO9)

A

Prevalence is the proportion of cases in the population at a given time. Prevalence indicates how widespread the disease is.

137
Q

Define mortality rate. (LO9)

A

Mortality rate is a measure of the frequency of occurrence of death in a defined population during a specified interval.

138
Q

Define case fatality rate. (LO9)

A

Case fatality rate is a measure of deaths assigned to a specific cause during a given time interval, relative to the total number of cases.

139
Q

There is a defined population of 1000 people and out of these, 100 people have heart disease. Out of these 100 people with heart disease, 10 people die. What is the mortality rate and what is the case fatality rate? (LO9)

A

The mortality rate is 10/1000.

The case fatality rate is 10/100.

140
Q

What are epidemic curves and how are they interpreted? (LO9)

A
  • They show progression of illness in an outbreak over time.
  • The x axis is the time (day, week or month).
  • The y axis is the number of people infected per time interval.
  • The curve is good at figuring out the method of transmission of a disease because different modes will allow the disease to spread at different rates.
141
Q

What are some things to consider before interpreting an epidemic curve? (LO9)

A
  • There is a delay between the date an illness starts and the date that the case is reported to public health authorities, e.g. 2-3 weeks for salmonella.
  • Some background cases of illnesses are likely to occur that would’ve happened even without an outbreak. Makes it difficult to identify the first case in an outbreak. This is why we usually identify the first cluster of cases than the first case.
  • Date of illness onset may not be known because it takes time before the sample of a disease enters the lab. So date of illness onset is estimated to be a few days before entering the lab.
  • Can be difficult to determine when cases will start to decline because there is a reporting delay. The full shape of the curve is only clear after the outbreak is over.
142
Q

Define frequency patterns. (LO9)

A
  • Frequency patterns are to do with the distribution of a disease. Epidemiology is concerned with the frequency and pattern of health events in a population.
  • Frequency refers not only to the number of cases but also the relationship of that number to the size of the population. This allows for comparisons of disease occurrence across different populations.
  • Patterns refers to the occurrence of health-related events by time, place and person. Characterising health events in this way is called descriptive epidemiology.
143
Q

What is meant by descriptive epidemiology? (LO9)

A

The characterising of health events by time, place and person patterns.

144
Q

What is meant by time patterns when referring to frequency patterns? (LO9)

A
  • Annual.
  • Seasonal.
  • Weekly.
  • Daily.
  • Hourly.
  • Weekday vs weekend.
  • Any other breakdown of time that can influence disease occurrence.
145
Q

What is meant by place patterns when referring to frequency patterns? (LO9)

A
  • Geographical variation.
  • Urban vs rural.
  • Location of work sites or schools.
146
Q

What is meant by personal patterns when referring to frequency patterns? (LO9)

A
  • Age.
  • Sex.
  • Marital status.
  • Socioeconomic status.
  • Behaviour.
  • Environmental exposures.
147
Q

What is chronic fatigue syndrome (CFS)? (LO11)

A
  • Also known as myalgic encephalomyelitis (ME).
  • Characterised by debilitating fatigue for more than 6 months.
  • WHO classifies CFS as a neurological illness.
  • There are no objective diagnostic tests, verified biomarkers, curative medications or treatments.
  • Main aims are to improve functionality.
  • The fatigue is not related to other medical or psychiatric conditions.
148
Q

Describe the epidemiology of chronic fatigue syndrome. (LO11)

A
  • Rates vary between 0.11-2.6% in the UK.
  • 2 to 3 times more likely in women than men.
  • Peak ages of onset were during adolescence and between 30-50 years of age.
  • 0.003-0.5% of adolescents.
  • Prevalence amongst Pakistani descent was 3.5% compared to 0.8% in white people.
149
Q

Describe the presentation of chronic fatigue syndrome. (LO11)

A
  • Persistent disabling fatigue - not alleviated by sleep, rest or activity restriction.
  • Post-exertional malaise/fatigue (PEM), exertional exhaustion.
  • Short-term memory and/or concentration impairment.
  • Sore throat.
  • Generalised arthralgia without inflammation.
  • Headache/migraine with onset after the fatigue.
  • Unrefreshing sleep.
  • Orthostatic intolerance.
  • Diffuse muscular, tendon, fascial and other pain.
150
Q

List the investigations for chronic fatigue syndrome. (LO11)

A
  • DePaul symptom questionnaire.
  • FBC with WBC differential - to exclude infection, not diagnostic.
  • ESR - to exclude inflammation, not diagnostic.
  • CRP - to exclude inflammation, not diagnostic.
  • Comprehensive metabolic panel - to exclude renal/liver dysfunction, acute infection or malignancy, diabetes.
  • Thyroid-stimulating hormone - to exclude hypothyroidism.
  • Antinuclear antibody (ANA), rheumatoid factor - high titre means SLE.
  • HIV antibody test - to exclude HIV infection.
151
Q

List the findings of the first line investigations for chronic fatigue syndrome. (LO11)

A
  • FBC with WBC differential is normal.
  • ESR is normal to low.
  • CRP is normal.
  • Comprehensive metabolic panel is normal.
  • Thyroid-stimulating hormone is normal.
  • Antinuclear antibody has been frequently stated to be positive in chronic fatigue syndrome so it’s important to determine whether there is a high titre suggestive of SLE or a low titre.
  • HIV antibody test is normal.
152
Q

What is the DePaul symptom questionnaire? (LO11)

A
  • A validated screening tool for ME/CFS.
  • Both frequency and severity of the symptoms are assessed.
  • The checklist of 54 items provides a thorough evaluation and grading of patient complaints.
153
Q

Describe the management for chronic fatigue syndrome. (LO11)

A
  • No curative medications or treatments.
  • Main goals are to manage symptoms and improve functional capacity.
    1. Counselling and supportive care - energy envelope refers to the amount of energy the patient has available to perform all of their daily activities.
    2. Individualised exercise programme - low intensity as per the patient.
    3. Multidisciplinary rehabilitation treatment - includes body awareness therapy, mindfulness, sleep hygiene, occupational therapy, orthostatic tolerance.
    4. CBT.
154
Q

Describe the prognosis of chronic fatigue syndrome. (LO11)

A
  • 17-64% of patients improve with treatment.
  • However, less than 10% of patients meet the criteria for full recovery.
  • Up to 20% of patients may worsen with time.
155
Q

What is fibromyalgia? (LO12)

A

Chronic pain syndrome diagnosed by the presence of widespread body pain.

156
Q

Describe the epidemiology of fibromyalgia. (LO12)

A
  • Common condition worldwide in all ethnic and socio-economic groups.
  • Prevalence in general population: 0.5-5%.
  • Age of onset is typically between 20 and 60 years of age. Average age of onset: 35 years old.
  • More prevalent in females than men.
  • Can also present in childhood in some cases.
157
Q

Why are women more likely to be diagnosed with fibromyalgia? (LO12)

A
  • 1990 fibromyalgia criteria required a certain number of tender points. Women are inherently more tender than men so many more will meet this criteria.
  • Subsequent criteria do not have such a strong female predominance.
158
Q

List the risk factors for fibromyalgia (5). (LO12)

A
  • Family history of fibromyalgia - first-degree relatives of people with fibromyalgia are 8 times more likely to develop it.
  • Rheumatological conditions.
  • Aged 20-60.
  • Female sex.
  • Presence of associated condition (weak) - IBS, tension headache, CFS, temporomadibular joint disorder and interstitial cystitis.
159
Q

List the presentations of fibromyalgia (10). (LO12)

A 
Key symptoms:
- Chronic pain.
- Diffuse tenderness on examination.
Other symptoms:
- Fatigue unrelieved by rest.
- Sleep disturbance.
- Mood disturbance.
- Cognitive dysfunction.
- Headaches.
- Numbness/tingling sensations.
- Stiffness.
- Sensitivity to sensory stimuli such as bright light, odours, noises.
160
Q

Describe the investigations for fibromyalgia. (LO12)

A
  • There is no x-ray or lab testing for fibromyalgia, only tests to rule out other diseases.
  • The diagnosis is strictly clinical.
  • If the patient does not meet the clinical criteria for a diagnosis of fibromyalgia, then some further tests may help explain the patient’s musculoskeletal pain or fatigue.
161
Q

Describe the management of fibromyalgia. (LO12)

A
  • Tricyclic antidepressants (TCA) - e.g. amitriptyline, cyclobenzaprine.
  • Serotonin-noradrenaline re-uptake inhibitors (SNRI) - e.g. duloxetine, milnacipran.
  • Gabapentinoids - e.g. pregabalin, gabapentin.
  • Some patients benefit from two or three drug classes together. Others respond to just one.
  • All patients should be tried on one or two TCAs first because these are expensive but they do work. They often improve sleep and visceral motility as well as pain.
  • SNRIs should be used as first line when the patient suffers from comorbid depression or fatigue.
  • Gabapentinoids used when patient suffers from comorbid sleep issues.
  • Once the patient improves, advocate for non-pharmacological therapies.
162
Q

Describe the prognosis for fibromyalgia. (LO12)

A
  • Fibromyalgia is chronic illness and patients should expect exacerbation and remissions to vary over time.
  • With good adherence to exercise, sleep, CBT, most patients will improve with time.
  • The goal of treatment is to decrease physical and mental symptoms and to increase functioning, not to cure.
163
Q

What is the recommended intake of protein for males and females? (LO13)

A
  • Males: 55g/day.

- Females: 45g/day.

164
Q

What is dietary fat? (LO13)

A
  • Saturated fats = no double bonds.
  • Monosaturated fatty acids (MUFA) = one double bonds.
  • Polysaturated fatty acids (PUFA) = >1 double bond.
  • We eat fats in oil blends.
  • Saturated fats are found in not very lean meats, butter and oil.
165
Q

What is the recommended intake of dietary fats? What are the sources of fat? (LO13)

A

In the UK, the recommended intake is:

  • > 450mg EPA + DHA per day.
  • Total fats should make up <35% of food energy.
  • Saturated fats should make up <11% of food energy.
  • Linoleic and linolenic acids should make up >1% and 0.2% of food energy.

Sources:

  • Fish oils - herring, mackerel, salmon.
  • Cod liver oil.
  • Chicken.
166
Q

What are dietary carbohydrates? (LO13)

A
  • They can be simple or complex.
  • Simple: monosaccharides (e.g. glucose, fructose, galactose) and disaccharides (e.g. maltose, lactose, sucrose).
  • Complex: polysaccharides (e.g. starch, glycogen, fibres).
167
Q

What is the recommended intake of carbohydrates (not free sugars). (LO13)

A

Carbohydrates should make up >50% of food energy.

168
Q

What is the recommended intake of free sugar (simple sugars apart from lactose)? (LO13)

A
  • Used to be 10% of food energy but has been halved to 5% or less.
  • It is now 30g per day in adults.
  • 1 teaspoon of sugar = 4g.
  • 1 can of coke = 30g.
169
Q

What is the average intake of free sugar for different age groups? (LO13)

A
  • 4-10y - 13.5% of energy.
  • 11-18y - 14.2% of energy.
  • Adults - 11.6% of energy.
  • Note, for adults, the recommended is 5% so the average sugar consumption is too high.
170
Q

Why is the recommended intake of free sugar so low? (LO13)

A
  • Blood glucose levels peak rapidly after consuming white sugar, white bread, potatoes, etc.
  • The peak is slower with whole grain products which is preferable.
  • PUFA and wholegrain carbs show reduced risk of coronary heart disease compared with saturated fatty acids and white grains.
171
Q

How much excess energy needs to be consumed to become overweight or obese? (LO13)

A
  • Only 1-2% excess of energy intake daily is required to become overweight/obese.
  • Eating 25-70kcal extra per day leads to a 1kg gain in weight per year.
172
Q

Describe the management for obesity. (LO13)

A
  • Lifestyle changes:
    1. Reduced calorie intake.
    2. Increased physical activity.
  • Diet:
    1. Low fat, <30% energy, high carb, (fat is the most energy dense macronutrient).
    2. Low carb, <40% energy from carbs - depletes liver glycogen and increases circulating ketones which may suppress appetite.
    3. Portion control.
    4. Regimes used by slimming world, weight watchers, etc.
    5. High protein, high fat (Atkin’s diet) - can induce ketosis and rapid weight loss.
    6. Very low-calorie diet (VLCD).
  • Pharmacotherapy, e.g. Oristat (lipase inhibitor).
  • Bariatric surgery.
173
Q

What is the role of protein in weight loss and the maintenance of weight loss. (LO13)

A
  • Modest satiety effect - greater perceived fullness and elevated satiety hormones.
  • Protein supplements - enhances the effect of resistance exercise leading to muscle hypertrophy and weight loss.
  • Greater weight loss, fat mass loss and preservation of lean mass.
174
Q

List some government actions against obesity (7). (LO13)

A
  • Online ads for sugary foods banned before 9pm.
  • BOGOF restricted and not allowed on sugary items.
  • More discounts on fruit and veg.
  • Restaurants with >250 employees must label their food with calorific values.
  • Alcohol calorie labelling.
  • Front of pack “traffic-light” labelling.
  • Expansion of the NHS weight management services:
    1. Self-care apps + online tools.
    2. Incentives for GPs to support obese patients to lose weight.
    3. Prescriptions for exercise and social exercise.
    4. Acceleration of NHS diabetes prevention programme.
175
Q

Why is the malnutrition universal screening tool used? (LO13)

A
  • Malnutrition affects more than 10% of adults.

- Malnutrition also includes obesity.

176
Q

What are the criteria for dietary approaches to stop hypertension (DASH)? (LO13)

A
  • Diets which restrict salt intake to 3g of sodium per day.

- Best results are achieved with an 8 week course of fruit and veg diet with low fat dairy.

177
Q

Describe the Mediterranean diet. (LO13)

A
  • Very low use of salt.
  • Mainly use herbs and spices for flavouring.
  • PREDIMED study: recruited 55-60 year olds with no heart disease and either diabetes or all three risk factors for heart disease.
  • They were split into two groups. One control and one Mediterranean diet group. Those in the diet group were less likely to have acute cardiac events.
178
Q

Bonus question: what are the three main risk factors for heart disease? (LO13)

A
  • High blood pressure.
  • High cholesterol.
  • Smoking.
179
Q

List the risk factors for chronic pain (4). (LO14)

A
  • Trauma/surgery.
  • Cancer.
  • Age.
  • Obesity.
180
Q

What are the two classifications for chronic pain? (LO14)

A
  • Nociceptive.

- Neuropathic.

181
Q

Describe what is meant by nociceptive pain. (LO14)

A
  • Pain arising from the activation of nociceptors following tissue injury - Ad and C-fibre terminals.
  • There is a pathological reason for the pain, e.g. injury.
182
Q

Describe what is meant by neuropathic pain. (LO14)

A
  • Pain arising from diseases or damage to the nervous system which is frequently long-lasting and the pain is not proportional to tissue injury.
  • Chronic pain is usually neuropathic for this reason but could be nociceptive pain.
183
Q

Describe the mechanism of chronic pain. (LO14)

A
  • The precise mechanism depends on the type of disease or the actual pain.
  • Enhanced activation of the limbic system amplifying the negative threat or negative interoceptive state is probably a key factor driving chronic pathological pain.
  • The mechanism may not even involve any underpinning pathological process.
  • There’s more room for research for mechanisms of chronic pain as it’s not just neurological factors but also psychological factors.
  • For now, we conclude that chronic pain is not just acute pain that persists. Chronic pain can be a disease in itself and what initiates the pain may not be the mechanism underlying its persistence.
184
Q

Describe the epidemiology of chronic pain. (LO15)

A
  • Around 43% of the UK population report uncontrolled pain while 15% chronic widespread pain.
  • Fibromyalgia:
    1. Women to men, 3:1.
    2. Rises with age to a maximum in people around 60 years of age.
    3. 1-10% in the whole population have fibromyalgia.
185
Q

List the investigations for chronic pain. (LO15)

A

Investigations are usually used to rule out nociceptive pain. They may not even be used for some cases.

  • Mainly history taking based.
  • Research uses brain scanning showing areas for pain stimulation and emotion - showing the nociceptive stimulation.
  • X-rays, CT scans, PET scans, MRIs and blood scans do not show pain.
186
Q

Describe the management of chronic pain. (LO15)

A
  • Biopsychosocial pain management - useful model for the treatment of chronic pain.
  • This model involves sensory (nociception), cognitive (pain), affective (suffering), illness (pain behaviour) and social/cultural factors.
  • There is no certain treatment for chronic pain.
  • Doctor-patient discussions on planning management and trying different methods.
187
Q

Describe the prognosis of chronic pain. (LO15)

A
  • Chronic pain is a long-term condition, possibly life-long.
  • Patients can try to manage their pain and learn to cope with the chronic pain.
  • Younger patients with lower pain scores have a better outcome - higher possibility of daily life being least affected by chronic pain.

MBBS - Y1 (14 decks)

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