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Z Phase 1 Others > Week 8 > Flashcards

Week 8 Flashcards

1
Q

How are the sections of the eat well plate divided?

A

Fruit & veg and Carbs/starchy foods take up two tirds and the final third is made up of protein, dairy and a very small amount of fat

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2
Q

Who does the eat well guide apply to?

A

Most people but those with dietary requirements should check with a medical professional about how they can adapt the guide

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3
Q

How does the guide apply to children?

A

Doesn’t apply to children below the age of 2, between 2 and 5 children should start to eat the same as their families

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4
Q

Should infants have fat in their diet?

A

None

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5
Q

What nutrients may you be deficient in if you don’t eat enough protein?

A

B vitamins,Vitamin E, iron, zinc and magnesium

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6
Q

What may happen if you are deficient in vitamin B12?

A

It affects the bodies ability to make red blood cells so can result in tiredness/weakness as the body has an impacted ability to transport oxygen

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7
Q

What may happen if you are deficient in Vitamin E?

A

Uncommon but can cause nerve and muscle damage that results in loss of feeling in limbs, loss of body movement control, weakness and vision problems. can also cause a weakened immune system

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8
Q

What may happen if you are deficient in iron?

A

Anaemia symptoms include general fatugue and weakness, pale skin, shortness of breath and diziness

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9
Q

What may happen if you are deficient in zinc?

A

Affects many different body systems so there is no distince set of symptoms. common symptoms include poor sense of smell and taste, poor wound healing, hair loss and deformed nails

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10
Q

What may happen if you are deficient in magnesium?

A

Can result in tremors, poor coordination, muscle spasms and appetite loss

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11
Q

What nutrients may you be deficient in if you don’t eat enough starchy foods?

A

Fiber, Calcium, iron and b vitamins

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12
Q

What may happen if you are deficient in fiber?

A

Increased risk of weight gain and heart disease. Symptoms include constipation, nausea, tiredness and in diabetics, blood sugar fluctuations

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13
Q

What may happen if you are deficient in calcium?

A

If not enough calcium is obtained through the diet the body starts taking it from the bones. This can lead to osteoparosis. Symptoms of calcium deficiency include muscle cramps, aches and spasms.

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14
Q

What nutrients may you be deficient in if you don’t eat enough dairy?

A

Vitamin A, Riboflavin, Niacin and calcium

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15
Q

What may happen if you are deficient in Vitamin A?

A

Impairs immunity and hematopoiesis and can cause rashes and vision issues like xerophthalmia

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16
Q

What is xerophthalmia?

A

Issues seeing in low light. Can lead to blindness if left untreated.

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17
Q

What may happen if you are deficient in riboflavin?

A

Essential for metabolic energy production. Long term deficiency causes anaemia. Symptoms include spre throat, lesions and conjunctivitis

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18
Q

What may happen if you are deficient in niacin?

A

Sever deficiency is known as pellagra. symptoms include rash when exposed to sunlight, swollen mouth, bright red tongue, and v&d

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19
Q

What nutrients may you be deficient in if you don’t eat enough fruit and veg?

A

potassium, vitamin C, folic acid and many more

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20
Q

What may happen if you are deficient in potassium?

A

Hypokalemia can make muscles feel weak,cramp,twitch or even become paralysed.

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21
Q

What may happen if you are deficient in vitamin C?

A

Can result in scurvy. Common symptoms include fatigue, depression and connective tissue defects

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22
Q

What may happen if you are deficient in folic acid?

A

can lead to anaemia

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23
Q

What are the key symptoms of bulimia nervosa?

A
  • recurrent episodes of overeating (eg once a week or more for at least a month) accompanied by compensatory behaviours
  • The individual is obsessed with their body image
  • they may have severe tooth decay, weakened muscles and in the long term, potential heart problems
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24
Q

How is Bulimia managed in adults?

A
  • bullimia focused guided self help
  • if this is unacceptable, CBT-ED
  • should be up to 20 sessions over 20 weeks focusing on normal eating behaviours
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25
Q

How is bulimia managed in children?

A

-Bulimia nervosa focused family therapy (FT-BN)
- should be 18-20 sessions over 6 months
- if this is unacceptable consider CBT-ED

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26
Q

What is CBT?

A

Cognitive behavioural therapy.
It aims to change the moods/feelings towards a certain situation or trigger

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27
Q

What are the key symptoms of binge eating disorder?

A

Frequent episodes of binge eating (eg once a week or more) without compensatory behaviours

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28
Q

How is binge eating charecterised?

A

-eating more quickly than normal
-eating until uncomforatbly full
-eating a lot when not hungry
eating alone out of embarassment
-feeling bad/guilty after eating

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29
Q

How is binge eating disorder managed?

A

-Binge eating disorder focused self help
-CBT self help
Adherance is especially important
-if self help is unsuccesful offer group CBT-ED

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30
Q

What are the key symptoms of Anorexia nervosa?

A

A significantly low BMI
Low weight with persistan pattern of behaviors to prevent weight gain
Central to the patients negative perception of themself

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31
Q

How is anorexia managed in adults?

A

CBT-Ed should consist of up to 40 sessions over 40 weeks
should aim to reduce risk to the patients health
trying to establish healthy eating

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32
Q

What is a cough?

A

An explosive expiration that provides a normal protective mechanism for clearing the tracheobronchial tree of secretions and foreign material

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33
Q

What may initiate the cough reflex?

A

excessive amounts of foreign matter or other causes of irritation

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34
Q

What forms the afferent limb of the cough reflex?

A

receptors within the sensory distribution of the trigeminal, glossopharyngeal, superior laryngeal and vagus nerves

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35
Q

What forms the efferent limb of the cough reflex?

A

the recurrent laryngeal nerve and the spinal nerve

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36
Q

Describe that caught reflex?

A

about 2.5 litres of air is inspired
epiglottis closes, vocal cords tightly shut to entrap the air within the lung
abdominal muscles contract forcefully, pushing against the diaphragm
internal intercostal muscles contract forcefully
pressure in lungs rises to 100mmHg or more
Markedly positive intrathoracic pressure causes narrowing of the trachea
vocal cords and epiglottis suddenly open widely
the large pressure difference between the airways and the atmosphere paired with tracheal narrowing produces rapid flow rates through the trachea

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37
Q

At what speed is air expelled from the lungs in a cough?

A

75-100mph

38
Q

What are some factors that contribute to asthma?

A

environmental alleges
viral respiratory tract infections
exercise, hyperventilation
gastro-oesophageal reflux disease
chronic sinusitis
aspirin or NSAID hypersensitivity
beta blockers
obesity
occupational exposure
emotional factors
exposure to tobacco smoke

39
Q

Describe the pathophysiology of asthma

A

It is complex and involves the following components;
airway inflammation
intermittent airflow obstruction
bronchial hypersensitivity

40
Q

Describe airway inflammation

A

varying degrees of mononuclear cell and eosinophil infiltration, mucous hyper secretion, desquamation of epithelium, smooth muscle hyperplasia and airway remodelling are present

41
Q

What are the main cells thought to be involved in airway inflammation?

A

mast cells
eosinophils
epithelial cells
macrophages
activated T lymphocytes

42
Q

What are the main cytokines thought to be involved in airway inflammation?

A

IL-4, IL5, IL-6, IL-9, IL-13

43
Q

What is the theory about TL1 and TL2 lymphocytes?

A

loss of balance between the cells types. In asthma TL2 is favoured - perhaps due to lack of infection exposure?

44
Q

What causes airflow obstruction in asthma?

A

acute bronchoconstriciton
airway oedema
chronic mucous plug formation
airway remodelling

45
Q

Describe the early asthmatic response

A

Response to aeroallergens
IgE dependent mediator release leads to acute bronchoconstriciton

46
Q

Describe the late asthmatic response

A

airway oedema 6-24 hours after allergen exposure

47
Q

What causes chronic mucous plug formation?

A

exudate of serum proteins and cell debris

48
Q

what causes airway remodelling?

A

long-standing inflammation - may reduce the reversibility of the obstruction

49
Q

What does airway obstruction cause?

A

Increased resistance to airflow and decreased expiratory flow rates
the changes lead to decreased ability to expel air and may result in hyperinflation

50
Q

What does bronchial hyper responsiveness lead to?

A

bronchospasm and typical asthmatic symptoms such as
wheezing, shortness of breath and coughing

51
Q

What can bronchospasm be a response to?

A

allergens
environmental irritants
viruses
cold air
exercise

52
Q

What are the non-pharmacological management options for asthma?

A

smoking cessation
weight loss
breathing exercises

53
Q

What are the pharmacological management options for asthma?

A

inhaled corticosteroids
long acting B2 agonist
short acting B2 agonist

54
Q

How is complete control of asthma defined?

A

no daytime symptoms
no night time awakening due to asthma
no need for rescue medication
mo asthma attacks
no limitations on activity
normal lung function
minimal side effects from medication

55
Q

What are the histological differences in asthma?

A

increase mucous production and increase goblet cells
increase eosinophils in mucous and cell tissue
thickened basement membrane
increased mast cells in lamina
increased neutrophils and T cells
smooth muscle hypertrophy

56
Q

What does IgE do?

A

it forms a complex with mast cells
The allergen binds to this and causes the release of histamine, prostaglandins and leukotrienes

57
Q

Describe intravenous administration

A

rapid onset
by-passes liver
permits titration
drawbacks - increased adverse effects, requires IV access, infection, pain

58
Q

Describe intramuscular admisnistration

A

absorption depending on blood flow
by-passes liver
rapid onset and shorter in duration
drawbacks - neuromuscular damage, bleeding, pain, infection, delayed absorption in shock

59
Q

Describe subcutaneous administration

A

absorption depending on blood flow
constant and slow absorption
prolonged effect
by-passes lover
drawbacks - pain, infection, delayed absorption in shock

60
Q

Describe oral or rectal administration

A

convenient
safest
cheapest
slowest onset, prolonged by less potent action
drug passes through liver
Drawbacks - absorption rate can be highly variable, absorption influenced by stomach contents, gastric acid can interfere with absorption, uncooperative patients may not take them.

61
Q

What is bioavailability?

A

fraction of the administered drug dose that reaches the systemic circulation
expressed as F

62
Q

What factors may affect bioavailability?

A

drug factors - molecular weight, ionisation
absorption - gastric pH / health of GI tract
first pass metabolism (hepatic)

63
Q

When does F=1?

A

for IV drugs

64
Q

What is the volume of distribution?

A

apparent volume into which a known amount of drug must be dispersed to give the measured plasma concentration

65
Q

What does volume of distribution depend on?

A

plasma protein and tissue binding
molecular weight
lipid solubility

66
Q

What is volume distribution used to determine?

A

loading dose amount
elimination half-life, dosage interval

67
Q

What is the loading dose?

A

target concentration X volume

68
Q

What is clearance?

A

theoretical volume of plasma “cleared” of drug per unit time

69
Q

What is half-life?

A

the time required for serum plasma concentrations to decrease by half

70
Q

What is half life determined by?

A

clearance and volume of distribution
proportional to VD/CL

71
Q

How many half-lives does it take to clear a drug?

A

4-5

72
Q

When is a loading dose required?

A

drugs with a long half-life

73
Q

What is meant by steady state?

A

the amount of drug administered is equal to the amount of drug eliminated within one dosing interval

74
Q

How long does it take to reach steady state?

A

4-5 half lives

75
Q

Describe type I hypersensitivity

A

immediate
IgE, mast cells - release of histamine and other inflammatory factors

76
Q

What is type II hypersensitivity?

A

antibody-mediated

77
Q

What is type III hypersensitivity?

A

immune complex -mediated

78
Q

What is type IV hypersensitivity?

A

T cell - mediated

79
Q

Describe transplant rejection

A

T cells activated against donor transplantation antigens
stimulation in peripheral lymphoid tissues
Both CD4+ and CD8+ T cells
also macrophages, neutrophils, B cells, NK cells
Antigen production, compliment activation

80
Q

Describe public health

A

responds to societal health concerns
informed by a worldview prevailing at the time - science, ethics, aesthetic
led in different eras by different types of leaders and organisational forms

81
Q

Describe the first wave of health improvement in the UK

A

1830-1900
classical public health interventions (water and sanitation), emerging civil and social order
social reformers
municipal authorites

82
Q

Describe the second wave of health improvements in the UK

A

1890-1950
science rationalism provides breakthroughs in many fields

83
Q

Describe the third wave of health improvements in the UK

A

1940-1980
the welfare state and post-war consensus saw the emergence of the NHS, social security, social housing and universal education

84
Q

Describe the forth wave of health improvements in the UK

A

1960-2000
effective health care interventions prolong life.
Risk factors and lifestyle become a central concern in public health

85
Q

Name some health concerns we face today

A

health inequalities
obesity
population growth and ageing demographic
Human impacts of planet’s life support system
climate change

86
Q

describe ion-channel linked receptors

A

also called transmitter-gate ion channels
hydrophilic pores
mediate passive transport
show selectivity

87
Q

Describe the mechanism of ion channel linked receptors

A

ligand (e.g. ACh) binds to multimeric receptor
opens channel
ions diffuse according to concentration gradient
terminated by removal of ligand

88
Q

Explain signal transduction via RTKs

A

RTK monomers are single-pass transmembrane molecules
cytoplasmic domain has tyrosine kinase activity
extracellular ligand induces dimerisation of RTK monomers
Dimer undergoes autophosphorylation
creates phosphotyrosine residues on cytoplasmic domain
“docking sites” for intracellular proteins - scaffolds and substrates
Simultaneous activation of downstream pathways
RTK signalling often culminates in activation of enzyme or transcription factor

89
Q

Give an example of an RTK pathway

A

mitogen activated protein kinase (MAPK) - features ras, a monomeric g protein

90
Q

Describe G proteins

A

can bind to GTP
G proteins are GTPases- can hydrolyse GTP to GDP
G proteins may be monomeric or trimeric
Ras is a monomeric G proteins (in RTK pathway)
For G protein receptor coupled signalling must be trimeric G proteins

91
Q

Describe the mechanism of G protein coupled receptors

A

also called serpentine receptors
no intrinsic enzymatic activity
binding of ligand causes the receptor to undergo a conformational change
This lets a G protein bind to it
The binding of the receptor to the G protein phosphorylates the bound GDP to GTP
Alpha subunit with bound GTP activates effector enzyme
G protein then hydrolyses GTP back to GDP and protein is no longer needed so diffuses away

Z Phase 1 Others (11 decks)

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