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Medicine Sem 1 > Case 3 > Flashcards

Case 3 Flashcards

1
Q

What do different vitamin deficiencies cause?

A 
vitamin A - visual and skin changes
vitamin B12 - anaemia 
vitamin D - bone abnormalities 
vitamin E - neurological problems
vitamin K - blood clotting problems
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2
Q

How does Pseudomonas work?

A
  • It’s a real opportunist
  • A way in has been prepared
  • And it’s sadly not the end of the destructive process – paves the wave for more destruction
  • May follow in end stage lung disease
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3
Q

What does Pseudomonas do in the lower respiratory tract?

A
  • Behaves like a typical nasty Gram-Negative pathogen
  • Attaches and embeds (they have to hang on against the mucociliary elevator)
  • Destroys
  • Hides
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4
Q

Why is the lower respiratory tract ‘sterile’?

A
  • Mucociliary elevator
  • Constantly getting rid of potentially pathogenic organisms
  • Cilia line the primary bronchus to remove microbes and debris from the interior of the lungs
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5
Q

When does infection occur?

A
  • There is a breakdown of these innate defences
  • Or specifically VIRULENT pathogens can overcome the defences
    • infection of the alveolar tissue
    • consolidation of lung tissue i.e. no airspaces
    • as alveoli filled with inflammatory exudate
  • Combination
    • wrt Pseudomonas in CF
    • opportunistic pathogen – the mucociliary elevator stops working because mucus is to thick so uses this as an opportunity
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6
Q

How does Pseudomonas hide?

A

Biofilm – coats itself and then hides away – difficult for WBCs and antibiotics to get in

  • Produces alginates – biofilm formation – (antiphagocytic, anti-antibiotic)
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7
Q

How does Pseudomonas destroy tissue?

A

Produces many toxins that destroy tissue and provoke damaging inflammation
- ENDOTOXIN (endotoxic shock), elastases, proteases, phospholipases

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8
Q

What are biofilms? and how are they formed?

A

Biofilms are complex entities and they are everywhere

  • Their formation is intriguing and involves bacteria ‘talking to themselves’
  • Quorum sensing
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9
Q

What is propulsion?

A

The process by which the bolus is moved through the gastrointestinal tract, includes swallowing, peristalsis and mass movements

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10
Q

What is defecation?

A

The process by which undigested, non-absorbed foods, waste products and dead epithelial cells are excreted

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11
Q

What are the 2 distinct phases of growth from birth to adolescence?

A
  • Phase 1 (from birth to about age 1 to 2 yr): This phase is one of rapid growth, although the rate of growth decreases over that period.
  • Phase 2 (from about 2 yr to the onset of puberty): In this phase, growth occurs in relatively constant annual increments.
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12
Q

What’s the neonatal blood spot screening/blood test/heel prick test?

A

NHS Newborn Blood Spot (NBS) screening programme

  • Heel prick test, Guthrie test
  • Cheap
  • Acceptable test
  • Early intervention improves outcome
  • Performed 5-8 days after birth
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13
Q

What are chest x-rays often used to test for?

A

A radiograph is often taken where cystic fibrosis is suspected to confirm the presence of fluid, scarring which can confirm bronchiectasis

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14
Q

Explain the faeces analysis for cystic fibrosis?

A
  • Stool test for proteolytic enzymes produced in an inactive form in the pancreas before being activated in the small intestine to digest food proteins
  • Low levels suggest pancreatic insufficiency which is a common symptom of cystic fibrosis
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15
Q

How is the sweat test used to diagnose CF?

A
  • Both high IRT and a mutation in DNA does not allow for a diagnosis of CF – sometimes DNA has mutations but the person won’t have the disease
  • If baby has two high IRT tests and a genetic mutation then they then diagnose CF physiologically by using sweat test
  • Sweat (NaCl, water) moves from gland to duct, where sodium and chloride ions are reabsorbed to fine tune concentration
  • In CF, defective CFTR reduces chloride reabsorption from sweat
  • Sodium ions retained in sweat to maintain neutral charge
  • Therefore, sweat has unusually high sodium and chloride ion concentrations
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16
Q

How do you do the sweat test? and how do you reduce false positives?

A

Pilocarpine – a non-selective, muscarinic receptor agonist in the parasympathetic nervous system – induces sweating
Iontophoresis – movement of ions in a weak electrical field; electrolyte solution carries pilocarpine through skin
<10 mins
Sweat collection – filter paper or plastic ‘condenser’ placed on skin
Sweat measured – chloride ion analysis in collected sweat
30 mins
>60mmol/L indicated CF
Repeat test over two days to reduce false positives
False positives:
Disease: Addison’s disease, Nephrogenic diabetes insipidus, hypothyroidism
Test: contamination, unknown technical error aka ‘one of those things’
How can we reduce these?
- Repeat test over two separate days

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17
Q

How do you screen for CF using immunoreactive trypsinogen?

A
  • Secretion of hormones e.g. insulin (endocrine, via capillary contact/bloodstream) and digestive enzymes e.g. trypsinogen (exocrine, via pancreatic duct)
  • In CF, mucus blocks pancreatic ducts and excess trypsinogen ‘leaks’ into bloodstream through capillaries that feed the pancreas
  • Babies with CF therefore have high circulating trypsinogen because it’s not going through their pancreas properly into their digestive system
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18
Q

How do you do the IRT test?

A

SCREENING FOR CF (1): IRT TEST

Blood spot eluted and trypsinogen detected via enzyme-linked immunosorbent assay (ELISA)

  1. Immobilised capture antibody binds trypsinogen
  2. Primary antibody binds to captured trypsinogen
  3. Secondary antibody carrying enzymatic activity binds to primary antibody
  4. Secondary antibody catalyses detectable colour reaction (colour intensity & IRT)
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19
Q

What’s positive predictive value? and how can you improve it?

A

The proportion of positive results that are true positives

- improve it by repeating the test

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20
Q

What could be the cause of the false positives?

A 
Disease:
Pancreatic disease or injury 
Stress (prematurity, other illnesses, distressing delivery)
Bowel problems 
Hypoglycemia 
Infection 
Hypoxia 
Test:
Contamination 
Unknown error
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21
Q

What is the second way for screening for CF?

A

Screening for CFTR mutations

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22
Q

How is screening for CFTR mutations done? and when?

A
  • If you get two IRT tests being positive for CF then you start looking at their DNA as likely have CF
  • > 1900 different mutations in CFTR gene that cause CF
  • Only 6 have frequency >1%
  • Most common mutation = deltaF508 – screen for this first
  • 3 bp deletion causing loss of phenylalanine at position 508
  • misfolded mutant protein retained/degraded in endoplasmic reticulum
  • First screen for the most common mutations
  • Blood spots from babies with high IRT are analysed for common CFTR mutations
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23
Q

What is cascade carrier screening?

A

Screening ‘cascaded’ to relatives (and partners) of proband (a person serving at the starting point for the genetic study of a family)

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24
Q

Describe how cascade carrier screening is done.

A

Phase 1: proband identified
Phase 2: 1st degree relatives offered screening
Phase 3: carriers identified
Phase 4: 1st degree relatives of carriers offered screening
Phase 5: carriers identified
Phase 6: other appropriate carrier screening

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25
Q

What is cascade screening of CF?

A
  • Untested carrier frequency 1/25 – risk of child with CF 1/2500
  • Risks increase after CF baby
  • Family members at higher risk than general population
  • E.g. unaffected sibling has carrier frequency of 2/3
  • Offered free to relatives of someone with CF or a known carrier
  • High uptake often observed, desire to plan families
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26
Q

Describe common point mutations.

A
  • Missense mutation: results in an amino acid substitution
    - amino acid substitution
    - effects on structure / functionality
    - synonymous v. non-synonymous
  • Nonsense mutation: substitutes a stop codon for an amino acid
    - premature STOP codon (PTC)
    - inserted -> truncated protein
    - effects on structure / functionality
    - the earlier in the sequence, the more likely it is to be detrimental
  • Frameshift mutation: insertions or deletions of nucleotides may result in a shift in the reading frame or insertion of a stop codon
    - alters reading frame -> usually leads to a PTC
    - radically alters protein
    - sequence/structure/functionality
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27
Q

Describe DNA/single gene causes of genetic disorder. (inc. example, how common)

A
  • E.g. cystic fibrosis deltaF508 (3 base deletion)
  • 13 per 1000 live births
  • Monogenic
  • Mendelian inheritance
28
Q

Describe chromosomal abnormalities that cause genetic disorders. (inc. example, how common)

A
  • E.g. Down syndrome
  • 6 per 1000 live births
  • Aneuploidy
  • Structural abnormalities
29
Q

Describe the multifactorial causes of genetic disorder. (inc. example, how common)

A
  • E.g. neural tube defects (NTDs) e.g. spina bifida
  • Susceptibility genes
  • Environmental influences and lifestyle choices
30
Q

What are most ion channels like?

A
  • Most ion channels are gated – they open and close either spontaneously or in response to a specific stimulus, such as the binding of a small molecule to the channel protein or a change in voltage across the membrane
  • Most ion channels are selective, allowing only certain ions to pass through – some channels conduct only one type of ion (e.g. potassium), whereas other channels exhibit relative selectivity – for example, allowing positively charged cations to pass through while excluding negatively charged anions
  • Based on their structure, the majority of ion channels can be classified into six or seven superfamilies.
  • For potassium-selective channels, which are among the best-characterized ion channels, four homologous transmembrane subunits come together to create a tunnel, known as the conducting pore, that provides a polar pathway through the nonpolar lipid membrane.
  • Other channel types require either three or five homologous subunits to generate the central conducting pore.
31
Q

What is the important protein in terms of CF?

A

CFTR (cystic fibrosis transmembrane conductance regulator) protein

32
Q

What is CFTR? what does it function as? where’s it found?

A
  • CFTR is the protein encoded by the cftr gene (often write gene in lower case and italics)
  • It is a member of the ATP-binding cassette family of membrane proteins (ABC proteins) and has 1480 amino acid residues (quite large)
  • It functions as an ion channel (allowing Cl- ions to cross the cell membrane when a concentration gradient exists) – it’s found in epithelial cell membranes (usually on the apical side)
33
Q

What causes the destabilising and degradation of the CFTR protein?

A

F508del destabilises the protein and causes misfolding and its degradation by the cell’s quality control machinery

34
Q

Describe the structure of the CFTR protein.

A
  • ABC proteins have a modular structure, with 4 conserved domains (2 transmembrane domains and 2 ATP binding domains)
  • CFTR has an additional fifth domain called the Regulatory domain which regulates the activity of the protein – when it is phosphorylated, the channel can open – this also required the binding of ATP to the protein
35
Q

Describe the function of the CFTR protein. (focusing on bronchial epithelial cells)

A
  • The CFTR channel much be opened by phosphorylating the Regulatory Domain (protein kinase A does this at the end of signalling cascade) and by ATP binding to the ATP-binding domains
  • Chloride ions are more concentrated in the cell than in the extracellular fluid and so flow out of the cell via the CFTR channel
  • Na+ ions flow out of the cell via a separate channel in order to maintain electrical neutrality (otherwise Cl- ions would stop flowing out)
  • In order to maintain the osmotic potential, water diffuses out of the cell, following the Cl- and Na+ ions
  • The water maintains the volume of the extracellular fluid layer and keeps the external mucus layer hydrated and lowers its viscosity

The principle function of CFTR is to make sure that there is a homeostatic regulation of the water outside the cell
e.g. in the lungs, it’s important to maintain the right amount of liquid out of the epithelial cells as the ciliated are in the water and if there is too little water, the cilia can’t beat and waft fluid in the lungs properly (conveyer belt of cilia) – mucus layer sits on top of the liquid layer

36
Q

What happens when there’s CFTR dysfunction? (focusing on bronchial epithelial cells)

A
  • Mutations in CFTR either reduce the amount of CFTR in the membrane or prevent its channel activity (or sometimes both in combination)
  • Chloride ions cannot escape into the extracellular fluid and hence either can Na+ ions nor water
  • Hence, the extracellular liquid layer volume becomes reduced, the mucus becomes more concentration, and its viscosity increases
  • The mucus layer cannot be moved by the cilia and becomes static – it can obstruct airways and will become colonised by bacteria and fungi
  • Multiple rounds of infections trigger immune responses that slowly cause remodelling and fibrosis of the lung tissue (the lung function decreases from 100% to about 30% over many years)
37
Q

What is Mendelian inheritance?

A

Mendelian inheritance: The manner by which genes and traits are passed from parents to their children – the modes of Mendelian inheritance are autosomal dominant, autosomal recessive, X-linked dominant, X-linked recessive – also known as classical or simple genetics

  • Over 11000 traits or disorders in humans exhibit single gene Mendelian inheritance
  • However, characteristics such as height and many common familial disorders such as diabetes do not follow a simple pattern of Mendelian Inheritance
38
Q

What are Mendel’s laws?

A
  • Unit Inheritance – hereditary characters are determined by indivisible units of information
  • Principle of dominance – alleles occur in pairs in each individual, but effect of one allele may be masked by those of a dominant partner allele
  • Principle of segregation
  • Principle of independent assortment
39
Q

What are the flags that you are looking for with autosomal dominant disorders?

A
  • Males and females affected equally
  • Affected children with an affected parent
  • 50% recurrence in siblings
40
Q

What are the flags that you are looking for with autosomal recessive disorders?

A
  • Males and females affected equally
  • Affected children with unaffected parents
  • Consanguinity frequent (close genetic relationships producing offspring – same ancestor)
  • 25% recurrence in siblings
41
Q

What are the flags that you are looking for with X-linked disorders?

A
  • No male to male transmission
  • Excess of males with disease
  • Affected females will have affected father and sons
42
Q 
Pseudomonas aeruginosa:
what type of bacteria?
what does it do?
what are the symptoms?
where does it thrive?
A
  • Gram negative
  • Bacillus (rod) shaped
  • ‘opportunist pathogen’ – meaning that it exploits some break in the host defences to initiate an infection
  • Pseudomonas aeruginosa produces potent toxic proteins that enter and kill host cells, which not only cause extensive tissue damage, but also interfere with the human immune system’s defence mechanisms, leading to organ failure
  • It is resistant to many antibiotics
  • Symptoms: inflammation and sepsis
  • It thrives on most surface, this bacterium is also found on and in medical equipment, including catheters, causing cross-infections in hospitals and clinics
43
Q

What are the 4 main ways a bacterium can overcome antibiotics?

A
  1. It can stop the antibiotic getting in – gram negatives are very good at this as they have an extra outer membrane
  2. Can get in and then be ejected through efflux pumps along with cell waste
  3. The target for the antibiotic can be changed
  4. The organism can produce drug inactivating enzymes

(Pseudomonas can do all of the above)

44
Q

Why is Pseudomonas notoriously resistant?

A

Pseudomonas has a BIG genome and can do all 4 of the above: - notoriously resistant – no first-line antibiotics work

  • Extra impermeable cell wall
  • Multiple copies of drug targets (so can’t saturate all of them)
  • More antibiotic destroying enzymes
  • Many efflux mechanisms – pump out antibiotics with the waste

Therefore pseudomonas can survive and even flourish in the presence of many antibiotics/antiseptics

BIG problems in treatment – many strains are R to all available antibiotics

45
Q

What is population screening?

A

Screening is the process of identifying people who appear healthy but may be at increased risk of a disease or condition

  • Preventative medicine through early identification of at risk of affected individuals
  • Not intended to provide a diagnosis
  • ‘risk reduction’
  • Determining probabilities
46
Q

What is a classic model for population screening?

A

Population -> (screening test – not necessarily DNA based) -> high risk group -> (diagnostic test) -> individuals (deal with those that we think are at risk)

47
Q

What is the specific criteria for population screening?

A

Disease

  • Important health problem (serious, fairly common)
  • Acceptable, effective intervention
  • Recognisable asymptomatic period
  • Well-defined natural history

System

  • Facilities for diagnosis and treatment
  • Agreed policy on whom to treat
  • Cost-benefit ratio
  • Continuous screening
  • Good communication of results
  • Autonomy, confidentiality, informed choice

Test

  • Suitable test (specific, sensitive)
  • Acceptable test (ethically and socially)
48
Q

What is sensitivity?

A

The ability to detect affected people.

49
Q

What is specificity?

A

The ability to exclude unaffected people - not telling people that aren’t going to develop the disease that they might do

50
Q

What is the process of protein synthesis?

A

Transcription:

  • Uracil replaces thymine on RNA
  • For each gene only one strand of the DNA acts as the template and this varies throughout the genome
  • The transcripted strand is known as the sense strand and the template as the antisense strand.
    1. The enzyme RNA polymerase catalyses transcription of DNA
    2. RNA polymerase binds to the promoter region (special sequence of nucleotide bases) on the DNA - this is where transcription starts
    3. Transcription of the DNA strands ends at another special nucleotide sequence called the terminator region
    4. Regions within a gene called introns do not code for parts of the proteins
    5. They are located between regions called exons that do code for segments of a protein
    6. Immediately after transcription, the transcript includes information from both introns and exons and this is called pre-mRNA
    7. The introns are removed from the pre-mRNA by small nuclear ribonucleoproteins (snRNPs) - the snRNPs are enzymes that cut out the introns and splice together the exons
    8. The resulting product is a functional mRNA molecule that passes through a nuclear pore.

Before the mRNA molecule leaves the nucleus it undergoes a number of modifications:
1. mRNA splicing
2. 5’ capping – shortly after transcription the mRNA is modified by the addition of a nucleotide to the 5’ end of the molecule, the so called 5’ cap – it’s thought that it facilitates transport and attachment to the ribosomes, as well as to protect the RNA transcript from degradation
Translation:
1. mRNA becomes associated with ribosomes and protein synthesis initiates
2. In the cytoplasm is transfer RNA (tRNA)
3. Amino acids are covalently bound to tRNA
4. An mRNA molecule binds to the small ribosomal subunit at the mRNA binding side
5. A special tRNA, called initiator tRNA, binds to the start codon on mRNA, where translation begins
6. The tRNA anticodon attaches to the mRNA by pairing between the complementary bases.
7. The initiator tRNA, with its amino acid, fits into the P site of the ribosome
8. The anticodon of another tRNA with its attached amino acid pairs with the second mRNA codon at the A site of the ribosome
9. Peptide bonds form between the tRNA at the P site and the tRNA at the A site
10. After peptide bond formation, the empty tRNA at the P site detaches from the ribosome, and the ribosome shifts the mRNA strand by one codon
11. The tRNA in the A side bearing the two-peptide protein shifts into the P side, allowing another tRNA with its amino acid to bind to a newly exposed codon at the A site
12. Protein synthesis ends when the ribosome reaches a stop codon at the A site, which causes the completed protein to detach from the final tRNA.
DNA Proofreading:
- Wherever inappropriate DNA nucleotides have been matched up with the nucleotides of the original template strand, special enzymes cut out the defective areas and replace these with appropriate complementary nucleotides
- This is achieved by the same DNA polymerases and DNA ligases that are used in replication
- Because of repair and proofreading, the transcription process rarely makes a mistake

51
Q

What is PICO?

A

P: patient/problem – describe/summarise relevant patient characteristics and/or the target disorder of interest – the P can also stand for population if you have a broader query relation to population health
I: intervention – what you want to do with this patient or group of patients – the main intervention that you are considering (could be a drug treatment, clinical therapy, exposure, a diagnostic test, lifestyle behaviour change, or screening for a disease in the case of Population Health)
C: comparison (or control) – the alternative management strategy (perhaps surgery, or a different drug), or maybe an alternative diagnostic test – can be ‘none’ if interested in what treatment would compared to doing nothing
O: outcome of interest to you – cure, diagnosis, cost, quality of life, side effects, morbidity, complications etc.

52
Q

What is primary literature? when is and isn’t it useful?

A
  • Background questions can often be answered by going to a textbook
  • But, complex foreground questions are best answered by consulting the primary literature
  • Primary literature comprises original reports of research studies (e.g. clinical trials) published in peer-reviewed medical or scientific journals
  • In these articles, rigorous methods have been used for collecting and analysing data which are then presented in an unambiguous interpretable style
53
Q

What are bibliographic databases? and why are they useful?

A
  • Use to quickly and effectively search the primary literature for the most relevant evidence to answer foreground questions
  • An electronic database containing an index of articles published in many different journals, which you can search to create a list of references relevant to you
    Medline
  • The largest and most commonly used biomedical database
  • It refers to articles published in over 3000 different journals
54
Q

What are secondary sources of evidence?

A
  • A secondary source is where evidence regarding a particular question has already been searched for and appraised
  • Cochrane Library – a database of systematic reviews (summaries of all of the high-quality research around a particular question)
  • Clinical Evidence, BestBETs, Essential Evidence Plus
  • There are also secondary journals
55
Q

Give an overview of the stage theory by Jean Piaget.

A
  • Cognitive development associated with biological processes – maturation
  • Not simply about learning more (quantity)
  • Age linked with different characteristic types of thought processes (quality)
  • Active interaction with environment
56
Q

What are Piaget’s stages of development?

A
  • Sensory-motor stage (0-2 yrs) – acquiring skills and cognitive tools – object permanence
  • Pre-operational stage (2-7 yrs) – characteristic styles of thought (e.g. egocentric)
  • Concrete operational (7-11 yrs) – can undertake adult style operations but need concrete examples (largely physical) – increasing ability to recognise alternative viewpoints of others
  • Formal operational (11+ yrs) – capable of more abstract thought – increasing ability to draw conclusions from hypothetical examples – use of logic – embarrassment levels
57
Q

What is object permanence?

A
  • At beginning if an object is covered by something, to the child, that object no longer exists
  • However, over first two years, object permanence is developed
58
Q

What are the sensorimotor substages?

A

3 months – recognition of familiar faces
7-8 months – stranger anxiety, missing carer (link to object permanence)
12 months – first words (understanding occurs earlier)
18 months – short sentences ‘more milk’

59
Q

What show babies haves social awareness?

A
  • Babies can tease
  • Can be embarrassed
  • Empathise – what makes others laugh and cry
60
Q

What are the characteristic styles of thought during the pre-operational stage?

A
  • Predicting consequences
  • Immediate versus long-term perspectives
  • Egocentrism
  • Some but limited appreciation of alternative viewpoints
  • Sophisticated mimicry
  • Start to comprehend symbols as representations
61
Q

What it Theory of Mind?

A
  • Idea that other people have independent perspectives – different beliefs
  • Understanding false beliefs (believing something that isn’t true but understanding that they’re not lying) and intentions
62
Q

Why is theory of mind important?

A
  • Awareness that others have perspectives
  • Allows children to PREDICT other people’s responses
  • Important feature of social interaction and relationships
  • Key deficit in some developmental disorders (e.g. some autism)
63
Q

What’s conservation of number?

A
  • If a row of sweets is longer they think that there is more even if the sweets are just more spread out – development of understanding this develops fairly soon
  • Conservation of volume – taller doesn’t mean bigger volume
  • Conservation of weight – idea that something that’s small and dense can be as heavy as something bigger and less dense
64
Q

What is the role of play in development? and why is ti crucial?

A

Curiosity:
- Child led play/activity leads to wider changes to neural networks
Children need opportunities for both structured and unstructured (they can make choices) play

Why crucial?

  • Opportunity to interact with the world and to manipulate objects
  • exploration and experimentation
  • volitional
  • active
  • Opportunity for cognitive restructuring, meta-representations, social rules
65
Q

Describe the formal operational stage.

A
  • Capable of more abstract thought
  • Increasing ability to draw conclusions from hypothetical examples
  • Use of logic
    (Easier to use examples in a clinical setting)
  • Make social decisions in different ways to adults
  • Use different strategies
  • Still find it harder to recognise viewpoints of others (even adolescents)
  • Embarrassment levels
  • Impulse control

Medicine Sem 1 (8 decks)

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