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Phase 2a > Introductory Clinical Sciences > Flashcards

Introductory Clinical Sciences Flashcards

1
Q

What is the name of the main effector cell in acute inflammation?

A

Neutrophil Polymorph

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2
Q

Describe the function of neutrophil polymorphs

A

First on the scene of acute inflammation

  • Cytoplasmic granules full of enzymes that kill bacteria
  • Release chemicals that attract other inflammatory cells such as macrophages
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3
Q

Describe the role of endothelial cells in inflammation

A
  • Become sticky in areas of inflammation so inflammatory cells adhere to them
  • Become porous to allow inflammatory cells to pass into tissues
  • Grow into areas of damage to form new capillary vessels
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4
Q

Function of fibroblasts in inflammation

A

Form collagen in areas of chronic inflammation and repair

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5
Q

Which of the following is an example of acute inflammation?

a. Glandular fever
b. Leprosy
c. Appendicitis
d. Tuberculosis

A

Appendicitis

(glandular fever is an acute illness, but cells are lymphocytes & macrophages NOT neutrophils)

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6
Q

In which of the following does granulomatous inflammation occur?

a. Crohn’s disease
b. Acute appendicitis
c. Infectious mononucleosis
d. Lobar pneumonia

A

Crohn’s disease

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7
Q

What is another name for infectious mononucleosis?

A

Glandular fever

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8
Q

What is the specific name of calcification in diseased (as opposed to normal) tissues?

A

Dystrophic calcification

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9
Q

Which one of the following is a chronic inflammatory process from its start?

a. Appendicitis
b. Cholecystitis
c. Infectious mononucleosis
d. Lobar pneumonia

A

Infectious mononucleosis

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10
Q

What is the name of the cells which produce antibodies?

A

Plasma cells

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11
Q

What 4 questions is the coroner trying to answer?

A
  1. Who was the deceased?
  2. When did they die?
  3. Where did they die?
  4. How did they come about their death?
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12
Q

Who performs autopsies?

A

Doctors:

  • Histopathologists
  • Forensic pathologists
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13
Q

What is pus made up of?

A

Dead neutrophils

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14
Q

Why can an abrasion of the skin heal quickly?

A

Bottom layer of squamous cells is still present

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15
Q

What is the main difference between skin wounds healed by 1st vs 2nd intention?

A

In 1st intention, the edges are brought together immediately.

When a wound has to be healed by 2nd intention, there has been skin loss so the edges of the wound cannot be brought together straight away.

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16
Q

What cell produces collagen?

A

Fibroblasts

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17
Q

Where does gliosis occur?

A

The brain

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18
Q

What is the difference between fibrosis & gliosis?

A

Gliosis is more delicate

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19
Q

3 points on Virchow’s triangle?

A
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20
Q

What does Virchow’s triad show?

A

The 3 factors that can individually or combined contribute to thrombosis

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21
Q

How does aspirin reduce risk of thrombus formation?

A

Inhibits platelet aggregation

For a similar amount of endothelial cell injury, there won’t be a full thrombus formation

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22
Q

How is atherosclerotic plaque thought to form?

A

Any endothelial cell damage leads to a small amount of thrombus formation → plaques

Endothelial cells grow over thrombus formation → more endothelial cell damage → another thrombus etc etc

So the vessel becomes occluded more

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23
Q

Give an example of useful apoptosis in development

A

At some stage in development, we have webbed fingers

The cells in between our fingers must be killed

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24
Q

Define congenital

A

Present at birth

(doesn’t have to be genetic, can be acquired)

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25
Q

Give an example of a congenital disease & how it occurs

A

Club foot - thought to be due to a lack of amniotic fluid during development

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26
Q

Define acquired, in terms of disease

A

Caused by non-genetic environmental factors

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27
Q

Give an example of an acquired, congenital disease

A

Fetal alcohol syndrome (mother has drunk excess alcohol whilst pregnant)

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28
Q

What is adjuvant therapy?

A

Therapy given after primary or initial treatment to maximise effectiveness

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29
Q

Name the 3 layers in a normal arterial wall from innermost to outermost

A

Tunica intima

Tunica media

Tunica adventitia

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30
Q

Main structural differences between arteries & veins

A

Arteries have:

  • smaller, rounder lumen
  • thicker elastic layer
  • thicker muscle layer
  • no valves
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31
Q

Summarise the 5 main stages in the formation of an atherosclerotic plaque.

A
  1. Endothelial dysfunction
  2. Formation of lipid layer or fatty streak within the intima
  3. Migration of leukocytes and smooth muscle cells into the vessel wall
  4. Foam cell formation
  5. Degradation of extracellular matrix
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32
Q

What is a foam cell?

A

A phagocytic macrophage that has absorbed lipoproteins

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33
Q

What problems can the formation of atherosclerotic plaque cause?

A

Causes ischaemia as it narrows blood vessels

When the plaque ruptures, a bit may break off and lead to infarction

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34
Q

Modifiable risk factors for atherosclerosis

A
  • Smoking
  • Obesity
  • Hypertension
  • Hyperlipidaemia
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35
Q

Non-modifiable risk factors for atherosclerosis

A
  • Age
  • Family history
  • Gender
  • Ethnicity
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36
Q

Primary preventative measures to take against atherosclerosis

A
  • Stop smoking
  • Become more active/weight loss
  • Reduce stress levels
  • Balanced diet with fewer saturated fats
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37
Q

Secondary preventative measures to take against atherosclerosis

A
  • Control diabetes
  • Aspirin
  • Statins
  • Calcium channel blockers
  • Regular checkups
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38
Q

Meaning of the term ‘co-benefits’ in relation to health and climate change. Give an example

A

The positive effects that a policy or measure aimed at one objective (climate change) might have on other objectives (health)

Increased walking & cycling rather than driving short distances = less fossil fuel emission & increase in activity for our patient.

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39
Q

Which of the following tumour never metastasises:

  • malignant melanoma
  • small cell carcinoma of the lung
  • basal cell carcinoma of skin
  • breast cancer
A

Basal cell carcinoma of skin

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40
Q

What is the name of a malignant tumour of striated muscle?

A

Rhabdomyosarcoma

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41
Q

Which of the follow tumours does not commonly metastasise to bone

  • Breast cancer
  • Lung cancer
  • Prostate cancer
  • Liposarcoma
A

Liposarcoma

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42
Q

As well as breast, lung and prostate cancer, name two cancers which commonly metastasise to bone

A

Renal cell & thyroid cancers

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43
Q

What term describes a cancer that has not invaded through the basement membrane?

A

Carcinoma in situ

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44
Q

What is the name of a benign tumour of glandular epithelium?

A

Adenoma

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45
Q

Which one of these tumours does not have a screening programme in the UK: breast, colorectal, cervical, lung?

A

Lung

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46
Q

Which one of the following is not known to be a carcinogen in humans:

  • Hep C virus
  • Ionising radiation
  • Aromatic amines
  • Aspergillus niger
A

Aspergillus niger (a fungus)

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47
Q

What is the name of a benign tumour of fat cells?

A

Lipoma

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48
Q

What is the name of a malignant tumour of glandular epithelium

A

Adenocarcinoma

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49
Q

Which one of the following is not a feature of malignant tumours:

  • vascular invasion
  • metastasis
  • increased cell division
  • growth related to overall body growth
A

Growth related to overall body growth

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50
Q

T or F: a transitional cell carcinoma of the bladder is a malignant tumour?

A

True

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51
Q

T or F: a leiomyoma is a benign tumour of smooth muscle?

A

True

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52
Q

T or F: radon gas is a cause of lung cancer

A

True

it is a radioactive gas

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53
Q

T or F: asbestos is a human carcinogen

A

True

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54
Q

T or F: ovarian cancer commonly spreads in the peritoneum

A

True

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55
Q

Where do all immune cells originate?

A

The bone marrow

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56
Q

Where do T cells mature?

A

The thymus

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57
Q

Where is a common place for B & T cells to accumulate?

A

Lymph nodes

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58
Q

What innate cell is involved in allergic reactions?

A

Basophils

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59
Q

What innate cell is involved in parasitic infections?

A

Eosinophils

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60
Q

What are the two types of immune response in humans?

A

Innate & Acquired

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61
Q

What cell type is described below?

‘These are the most abundant white blood cell in humans and are characterised by the multi-lobed shape of their nucleus’

A

Neutrophil

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62
Q

Which antigen presenting cell is considered a professional at activating lymphocytes?

A

Dendritic cell

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63
Q

Which of the following is not a component of innate immune mechanisms?

  • Antimicrobial peptides
  • Mucosa
  • Inflammatory mechanisms
  • Antibody production
  • Skin
A

Antibody production

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64
Q

Antigen presenting cells process and present antigens for recognition by

  • Neutrophils
  • Red blood cells
  • Eosinophils
  • T cells
A

T cells

65
Q

Which of the following are features of the adaptive immune response

  • Does not require prior contact with the pathogen
  • It works with B and T lymphocytes
  • Lacks specificity
  • Distinguishes “self” from “non-self”
  • Enhanced by complement
A

It works with B and T lymphocytes

66
Q

Complements are the proteins that are involved in the clearance of antigen/bacteria.

Which of the following is not part of the Elimination phase of complement activation?

  • Opsonisation
  • Production of interferons
  • Target cell lysis
  • Chemoattraction of leukocytes
  • Phagocytosis
A

Production of interferon

67
Q

Which of the following are administered as a live attenuated vaccine in the UK:

  • Hep A
  • Tetanus
  • MMR
  • Flu
  • BCG (TB)
A

MMR & BCG (TB)

68
Q

Polysaccharide vaccines are composed of long chains of sugar molecules that make up the surface capsule of certain bacteria. These vaccines are available for the treatment of which of the following diseases?

  • Pneumococcal disease
  • Influenza type b
  • Rabies
  • Salmonella Typhi
  • Meningococcal disease
A

Pneumococcal disease, Salmonella Typhi, Meningococcal disease

69
Q

Influenza vaccine is targeted towards ‘at risk’ groups in the UK.

Which of the following are classified as ‘at risk’?

  • Asthmatics
  • 16 years old
  • Diabetics
  • The obese of any age
  • 6 months of age and over
A

6 months of age and over

70
Q

Which of the following is not an organ-specific auto-immune disease?

  • Type 1 diabetes mellitus
  • Graves disease
  • Ulcerative colitis
  • Hashimoto’s thyroiditis
  • Sjogren’s syndrome
A

Ulcerative colitis

71
Q

Which of the following are classical PAMPs?

  • Flagellin, a protein found in bacterial flagella
  • Lipopolysaccharide (LPS) from the outer membrane of gram-negative bacteria
  • Peptidoglycan, found in bacterial cell walls
  • Lipoarabinomannan of mycobacteria
  • Interleukin 12
A
  • Flagellin, a protein found in bacterial flagella
  • Lipopolysaccharide (LPS) from the outer membrane of gram-negative bacteria
  • Peptidoglycan, found in bacterial cell walls
  • Lipoarabinomannan of mycobacteria
72
Q

What is transudate?

A

Transudate is an ultrafiltrate of plasma that contains few, if any, cells and does not contain large plasma proteins, such as fibrinogen.

73
Q

When does transudate build up?

A

“Transudate” is fluid buildup caused by systemic conditions that alter the pressure in blood vessels, causing fluid to leave the vascular system.

74
Q

What is hypercoagulability?

A

Hypercoagulability can be defined as the tendency to have thrombosis as a result of certain inherited and/or acquired molecular defects.

75
Q

What is stasis?

A

Phenomena of interrupted blood flow

76
Q

What is the function of NOD2?

A

Activates inflammatory signalling pathways

77
Q

What is NOD2?

A

It is an NLR

78
Q

4 aims of a perfect vaccine

A
  • Achieve long term protection (from a small number of immunisations)
  • Stimulate both B & T cells
  • To induce memory B & T cells
  • To stimulate protective high affinity IgG production
79
Q

4 categories of different types of vaccine

A
  • Whole organism
  • Subunit
  • DNA vaccines
  • Engineered virus
80
Q

2 types of whole organism vaccine

A
  • Live attenuated pathogen
  • Killed, inactivated pathogen
81
Q

4 advantages of live attenuated pathogen

A
  • Sets up a transient infection
  • Activates a full natural immune response
  • Stimulation of a memory response in T & B cell compartments
  • Often only a single immunisation required
82
Q

3 disadvantages of a live attenuated pathogen

A
  • Immunocompromised patients may become infected as a result of immunisation
  • In live measles vaccine, attenuated organism can revert to its virulent form
  • Typically needs refrigeration for stable storage
83
Q

Advantages of a killed, inactivated pathogen in a vaccine

A
  • No risk of infection
  • Storage is less critical
84
Q

Disadvantages of a killed, inactivated pathogen as a vaccine

A
  • Tends to just activate humoral response (not cell mediated)
  • Lack of T cell involvement
  • Immune response can be weak
  • Repeated booster vaccines required
85
Q

3 major types of subunit vaccines

A

Inactivated exotoxins (toxoids)

Antigenic extracts

Recombinant proteins

86
Q

What is an exotoxin?

A

A toxin secreted by bacteria

87
Q

Advantages of a subunit vaccine

A
  • Theoretically safer than handling live or inactivated pathogens
  • No risk of infection
  • Easier to store and preserve
88
Q

Disadvantages of a subunit vaccine

A
  • Immune response is less powerful than live attenuated vaccines
  • Repeat vaccines required & adjuvants
89
Q

Advantages of DNA vaccines

A
  • Do not require complex storage
  • Delivery can be simple & adaptable to widespread programs
90
Q

Disadvantages of DNA vaccines

A
  • As with ‘killed’ and subunit vaccines, no transient infection
  • DNA vaccination is likely to produce a mild immune response
  • Subsequent boosting required
91
Q

Advantages of recombinant vector vaccines?

A
  • Produce immunological memory
  • Safe - relative to live attenuated pathogen
92
Q

Disadvantages of recombinant vector vaccines?

A
  • Requires refrigeration for transport
  • Immune response to virus in subject can negate effectiveness
93
Q

3 main protein ports in cell membranes?

A

Uniporters

Symporters

Antiporters

94
Q

Define pharmacology

A

The study of the effects of drugs

95
Q

Define pharmacokinetics

A

How the body affects the drug (ADME)

  • Absorption
  • Distribution
  • Metabolism
  • Excretion
96
Q

Define pharmacodynamics

A

How the drug affects the body

97
Q

Define potency

A

Measure of how well a drug works

98
Q

Define agonist

A

A compound that binds to a receptor & activates it

99
Q

Define antagonist

A

A compound that reduces the effect of an agonist

100
Q

Define affinity

A

Describes how well a ligand binds to the receptor

101
Q

Define efficacy

A

Describes how well a ligand activates the receptor

102
Q

Define bioavailability

A

Amount of drug taken up as a proportion of the amount administered

103
Q

Define partial agonist

A

Binds to and activates the receptor, but only has partial efficacy when compared to a full agonist

104
Q

Define pro-drug

A

A drug that must be activated in the liver before it can work

105
Q

In terms of using opioids, what is the benefit of using a partial agonist instead of a full agonist?

A

With a partial agonist, there is a lower risk of the patient going into respiratory arrest

106
Q

What is the difference between dose of oral morphine compared with s/c (subcutaenous), IM, IV

A

50% of oral morphine is metabolised by first pass metabolism.

So double the dose is given compared to other routes

107
Q

Define tolerance in terms of pharmacology

A

Down regulation of receptors with prolonged use of a drug

So you need a higher dose to achieve the same effect

108
Q

What is the goal of opioids?

A

Block pain

109
Q

How do opioids work?

A

Inhibit the release of pain transmitters at the spinal cord and midbrain

Modulate pain perception in higher centres - changes the emotional perception of pain

110
Q

Side effects of opioids given systemically

A
  • Respiratory depression
  • Sedation
  • Nausea & vomiting
  • Constipation
  • Itching
  • Immune suppression
  • Endocrine effects
111
Q

If a patient goes into opioid induced respiratory depression, what steps should you take?

A
  1. Call for help
  2. ABC
  3. Naloxone
    1. IV is fastest route
    2. Titrate to effect
112
Q

Define adrenergic

A

Relating to adrenaline, noradrenaline & their receptors

113
Q

Define cholinergic

A

Relating to ACh and its receptor

114
Q

3 main differences between somatic and autonomic divisions of the efferent NS

A

Somatic:

  • Single neuron between CNS & skeletal muscle
  • Innervates skeletal muscle
  • Leads to muscle excitation (not inhibition)

Autonomic

  • 2 neuron chain
  • Smooth muscle, cardiac muscle, glands (GI neurones)
  • Leads to excitation or inhibition
115
Q

2 major neurotransmitters involved in the autonomic division of the efferent NS

A

ACh & noradrenaline (NAd)

116
Q

In the autonomic NS, what neurotransmitter acts on the preganglionic neurone?

A

ACh

117
Q

In the autonomic NS, what type of receptor is found on the preganglionic neurone?

A

Nicotinic

118
Q

In the autonomic NS, what neurotransmitter acts on the postganglionic neurone?

A

Parasympathetic: Muscarinic

Sympathetic: α & ß receptors

119
Q

In the autonomic NS, what neurotransmitter acts on the postganglionic neurone?

A

Parasympathetic: ACh acts on muscarinic receptors

Sympathetic: noradrenaline acts on α & ß receptors

120
Q

What activates muscarinic receptors?

A

Muscarine

121
Q

How many types of muscarinic (M) receptors are there?

A

5 (M1-M5)

122
Q

Where is each type of M receptor present?

A

M1: brain

M2: heart

M3: all organs with parasympathetic innervation

M4: mainly CNS

M5: mainly CNS

123
Q

When the M2 receptor at the SAN is activated, what happens?

A

HR decreases

124
Q

When the M2 receptor at the AVN is activated, what happens?

A

Decreases conduction velocity

Increases AV node block (increases PR interval)

125
Q

When the M3 receptor in the resp system is activated, what happens?

A

Produces mucus

Increased smooth muscle contraction

126
Q

When the M3 receptor in the GI tract is activated, what happens?

A

Increased saliva production

Increased gut motility

Stimulates biliary secretion

127
Q

When the M3 receptor in the skin is activated, what happens?

A

(only place where sympathetic releases ACh)

Causes sweating

128
Q

When the M3 receptor in the urinary system is activated, what happens?

A

Contracts detrusor muscle

Relaxation of internal urethral sphincter

(allows urine to pass out of the bladder into the urethra)

129
Q

When the M3 receptor in the eye is activated, what happens?

A

Causes myosis

Increases drainage of aqueous humour

Secretion of tears

130
Q

2 muscarinic antagonists

A

Atropine - M2 antagonist

Hyoscine - M3 antagonist

131
Q

In terms of receptors, what happens in myasethenia gravis

A

Blockage of nicotinic ACh receptors

leads to skeletal muscle weakness, particularly on repeated attempts at movement

132
Q

What can myaesthenia gravis be treated with?

A

Anti-cholinesterase to increase ACh availability at a neuromuscular junction

133
Q

Effect of agonist binding to α1 receptor?

A

Increases intracellular Ca2+

Contracts smooth muscle (pupil, blood vessels)

134
Q

Which agonist is favoured at an α1 receptor?

A

NAd>Ad

135
Q

Effect of agonist binding to α2 receptor?

A

Gi signalling, inhibition of cAMP generation

Mixed effects on smooth muscle

136
Q

Which agonist is favoured at an α2 receptor?

A

NAd = Ad (no preference)

137
Q

Agonism of ß1 receptors leads to…

A

Tachycardia

Increased SV

Renin release → increased vascular tone

Lipolysis & hyperglycaemia

138
Q

Beta 1 blockers will…

A

Reduce HR

Reduce SV

Reduce myocardial O2 demand & help remodelling the heart in heart failure & post MI

139
Q

Example of an agonist drug to ß2 receptor

A

Salbutamol

140
Q

Effect of an agonist binding to a ß2 receptor?

A

Bronchi → Bronchodilation

Bladder wall → Inhibits micturation

Uterus → Initiation of labour

Skeletal muscle → Increased contraction speed

Pancreas → Insulin & glucagon secretion

141
Q

A patient with COPD becomes progressively breathless.

He has heard about some medicines which may help

Which drugs do these use & which receptors do they affect?

A

Salbutamol.

Beta 2 receptors: role in bronchi is bronchodilation

142
Q

A patient complains of dry mouth on days when he uses his inhaler too much & he gets palpitations

Why is this?

Which drugs are responsible?

A

His inhaler contains salbutamol which is is a beta 2 agonist. Side effects of this include tacchyarrythmia

Dry mouth - due to the antimuscarinic. When M3 receptors are stimulated in resp system, saliva production is increased. (so when this is blocked saliva production will decrease)

143
Q

Upon which receptor does the muscle relaxant suxamethonium work?

A

Works by mimicing ACh at the neuromuscular junction - muscarinic receptors

144
Q

A patient suffers a heart attack following an operation & develops atrial fibrillation. He is commenced on bisoprolol.

Upon which receptor does bisprolol predominantly work? What positive effects will it have?

A

Acts on beta 1 receptor as an antagonist

This will:

  • Slow HR
  • Reduce myocardial O2 demand
  • Help cardiac remodelling post MI
145
Q

Define anaphylaxis

A

Anaphylaxis is an acute, potentially life-threatening hypersensitivity reaction, involving the release of mediators from mast cells, basophils and recruited inflammatory cells

146
Q

Possible anaphylaxis trigger agents that may be encountered in a hospital environment?

A

Penicillin

Latex gloves

Antibiotics

NSAIDs

General anaesthetic

IV contrast used in some imaging

147
Q

Why may a second dose of adrenaline be required following anaphylactic shock?

A

Adrenaline has a short half-life (in plasma about 2-3 minutes)

148
Q

Effect of adrenaline following anaphylaxis?

A

Stimulates ß1 adrenoreceptors

Positive ionotropic effect = increases heart contraction

Positive chronotropic effect = increases HR

Increases vasodilation

149
Q

What blood test can be done to confirm anaphylaxis?

A

A timed blood test for mast cell tryptase

Histamine is released from mast cells during anaphylaxis.

Mast cell tryptase breaks down mast cells. If levels of this are increased this shows an increase in the number of mast cells (shown in anaphylaxis)

150
Q

Symptoms & signs of anaphylaxis?

A

Respiratory distress

Abdominal issues/pain

Skin redness/urticaria

Hypotension

151
Q

How do protein kinase inhibitors work?

A

Targeted to specific mutations

Modifies specific parts of a pathway by recognising specific mutations that occur

152
Q

What is the goal of gene therapy?

A

To use genes to treat or prevent disease

153
Q

3 ways gene therapy can work?

A
  • Replace mutated gene with healthy copy
  • Inactivating a mutated gene that is functioning improperly
  • Introducing a new gene into the body to help fight a disease
154
Q

Give an example of a disease that can be treated with gene therapy

A

Spinal muscular atrophy

(a rare genetic disease that affects motor nerve cells in the spinal cord)

155
Q

What is drug repurposing?

A

A technique whereby existing drugs are used to treat emerging and challenging diseases

156
Q

Define ‘adverse drug reaction’

A

Unwanted or harmful reaction following administration of a drug or combination of drugs under normal conditions of use and is suspected to be related to the drug

  • Has to be noxious (unpleasant) & unintended
157
Q

Define ‘side effect’

A

An unintended effect of a drug related to its pharmacological properties and can include unexpected benefits of treatment

158
Q

Define ‘idiosyncrasy’

A

An inherent abnormal response to a drug

159
Q

Which disease are covered in a 6-in-1 vaccine given to 8 week old babies?

A
  • Diptheria
  • Hep B
  • Haemophilus influenza type B (Hib)
  • Polio
  • Tetanus
  • Whooping cough

Phase 2a (12 decks)

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