Cells Flashcards
1
Q
What can cause urethritis?
A
Chlamydia trachomatiso
Neisseria gonorrhoeae
Non-specific urethritis: Mycoplasma, Ureaplasma, no organism found
2
Q
What might be symptoms of vaginal discharge?
A
Vulval itching and soreness
Creamy discharge
3
Q
What can cause vaginal discharge?
A
Gonorrhoea
Chlamydia
Trichomonas
Candidiasis (thrush), Bacterial vaginosis
Both caused by disruption of normal microbiota, not usually considered STI
4
Q
What might be symptoms of genital herpes?
A
Painful sores on vulva/ thighs Blisters which burst Very painful dysuria Headache Myalgia
5
Q
What might be symptoms of primary syphilis?
A
Painless swelling
Genital ulcers
Systemically well
6
Q
What can be causes of painful genital ulcers?
A
Herpes simplex (HSV) 2 and 1 Lymphogranuloma venereum Chlamydia trachomatis Chancroid (rare UK) Non-STI e.g Behçet’s, Stevens-Johnson
7
Q
What can be causes of painless genital ulcers?
A
Syphilis Lymphogranuloma venereum Granuloma inguinale Donovanosis- rare UK; Calymmatobacterium Non-STI e.g carcinoma
8
Q
What are symptoms of pelvic inflammatory disease?
A
History grumbling lower abdo pain Severe dyspareunia Mild dysuria Fever Discharge Bleeding
9
Q
What is pelvic inflammatory disease?
A
Infection upper genital tract
Most commonly STI, but also associated with IUCD (coil), peritonitis
10
Q
What are signs of pelvic inflammatory disease?
A
Tenderness incl RUQ, cervical excitation, endocervical pus
11
Q
What do you need to rule out first before diagnosing pelvic inflammatory disease?
A
Ectopic pregnancy as may present in same way
12
Q
What can be complications of pelvic inflammatory disease?
A
Chronic pelvic pain, tubal infertility, ectopic pregnancy
13
Q
What may be symptoms of Epididymo-orchitis?
A
Painful enlarged scrotum
Fever 39C
Ultrasound: no torsion
14
Q
What are causes of Epididymo-orchitis?
A
UTI: E. coli commonest
STI: Gonorrhoea, Chlamydia
Viral: mumps
Rare: TB, Brucella
15
Q
How do you diagnose epididymo-orchitis?
A
Depends on history Urine for microscopy, culture and sensitivity Urine for STI screen Urethral swab Viral serology
16
Q
What can be complications of epididymo-orchitis?
A
Scrotal abscess
Infertility
17
Q
What can cause genital lumps and bumps?
A
Genital warts
Molluscum contagiosum
18
Q
Give some examples of Disseminated manifestations of genital infections
A
Gonorrheal bacteraemia/ arthritis PID, perihepatitis Secondary and tertiary syphilis Reiter’s syndrome: reactive arthritis secondary to infection Herpes meningitis, encephalitis
19
Q
Give examples of Systemic disease without genital manifestations
A
HIV
Hepatitis viruses: A, B, C, (D)
20
Q
How do you make a microbial diagnosis?
A
See it (microscopy) Grow it (culture) Kill it (sensitivity)
Detect pathogen: Protein (antigen), Nucleic acid (DNA/RNA)
Detect response to pathogen: Antibody (serology)
21
Q
What do gonorrhoea look like?
A
Gram negative diplococci
22
Q
What technique other than microscopy can be used to diagnose gonorrhoea?
A
NAAT: nucleic acid amplification test 24-48h to result High sensitivity and specificity Combine with Chlamydia test No antimicrobial susceptibility Requires non-inhibitory specimen (body fluids, including urine may inhibit PCR), not suitable for normal swabs
23
Q
How can microscopy be used to diagnose gonorrhoea?
A
Rapid: result in clinic
Less sensitive than NAAT
Requires skilled microscopist
Gives antimicrobial susceptibility result (but 2-3d after clinic visit)
Useful for individual patient treatment, also for epidemiological surveillance
24
Q
How can chlamydia be diagnosed?
A
Obligate intracellular bacterium
Will not grow in cell free culture (i.e on an agar plate)
Almost all diagnosis now via NAAT
90-95% sensitivity, >99% specificity
25
How can syphilis be diagnosed?
Microscopy: dark ground, specific but sensitivity low, Only available
primary syphilis, Skilled technician, Relies on good quality specimen Culture: Treponema pallidum unculturable, Antigen detection using fluorescent antibody, Highly specific if primary lesions present, Higher sensitivity than dark ground
Nucleic acid detection: PCR, High specificity in primary lesions, Not yet in routine clinical use
Serology (antibody detection): Venereal diseases research laboratory (VDRL) antigen, used to be 1st line, Now largely replaced with
simpler, automatable test, Allows diagnosis secondary syphilis
26
Describe primary syphilis
Single or multiple primary chancres
Usually painless; firm, round
Sore lasts 3-6 weeks with or without treatment
27
Describe secondary syphilis
Rashes, classically palms and soles
Multiple sores, mucous membranes
Fever, lymphadenopathy, fatigue
28
Describe latent Syphillis
if secondary untreated
Asymptomatic
Lasts 10-30 years, may progress to tertiary
29
Describe tertiary syphilis
Tabes dorsalis
GPI (general paralysis of the insane)
Dementia
Argyle Robertson pupils
30
What are the key points of syphilis diagnosis?
Most diagnoses by antibody detection
Serum: IgM indicates recent infection, IgG stays positive for months/ years/ life
If neurosyphilis suspected may need to test CSF, talk to microbiologist/ reference lab
31
What is the most commonly diagnosed STI?
Chlamydia
32
Which STIs increase transmission of blood borne virus STI?
STIs causing inflammation/ open lesions
33
How can STIs be transmitted?
Sexual contact: Not just genital, Rising incidence extra-genital gonorrhoea
Non-sexual contact: In utero syphilis, Peripartum gonorrhoea,
Chlamydia, Blood-borne BBVs, Other skin/ body fluid: e.g herpes simplex
34
What are the principles of controlling the spread of STIs?
Remove reservoirs & sources
Interrupt transmission
Increase host resistance
35
What are methods of primary prevention for STIs?
Safe sexual behaviours
Barrier contraceptive methods
Immunisation: currently only available for HPV (warts)
36
What are methods of secondary prevention for STIs?
Detect: screening, better access to GUM services, targeted information (16-25s)
If 1 STI, look for others
Prompt effective treatment, contact tracing
37
How can antibiotics develop resistance?
Efflux
Immunity and bypass
Target modification
Inactivating enzymes
38
Describe Antibiotic resistance in Neisseria gonorrhoeae
Altered target: resistance to quinolones (ciprofloxacin), resistance to beta-lactams (penicillin-binding proteins), resistance to macrolides (azithromycin)
Drug breakdown: resistance to penicillins
Drug efflux: multiple antibiotic resistance
39
How is antibiotic resistance spread between strains of gonorrhoeae?
Plasmid and chromosome mediated
| Rapid spread between strains
40
What are the Principles of antimicrobial therapy?
Right drug: For patient and organism. UK guideline on empiric treatment, because susceptibility not known at GUM clinic visit. Check for allergies, contraindications and interactions
Right dose: For patient (weight, liver and renal function), for bacteria (minimum inhibitory concentration)
Right time: Immediately!
Right duration: Single dose effective, increases concordance, minimises side-effects
41
What symptoms and signs might you get with urethritis? And what behaviours increase the risk of it?
```
Discharge from penis, staining in pants
Pain on passing urine
Multiple sexual partners
No regular sexual partner
No barrier protection
```
42
What is the Central dogma of molecular biology?
DNA makes heterogenous nuclear RNA, making messenger RNA, which makes polypeptides, which makes proteins
43
What determines our phenotype?
Genotype x Environment x Time
44
Describe classification of genetic disease
Monogentic: Single gene abnormal, Molecular genetic test
Chromosomal: Abnormality of structure or number, Cytogenetics
Multifactorial: Multiple genes and environmental influences, Can perform molecular genetic test to assess risk
45
What is an allele?
Variant versions of the same genes
46
What is a Common or wild type allele?
Common in population and NOT associated with a given disease
47
What is a polymorphism?
Genetic variants that occur commonly in the population with no significant association with disease e.g. blood groups
48
What are Mendel’s laws of inheritance?
Unit inheritance: Hereditary characters are determined by genes. An allele is one version of a gene
Dominance: Alleles occur in pairs in each indvidual, but effects of one allele may be masked by those of a dominant partner allele Segregation: During formaton of gametes, members of each pair of alleles separate so each gamete carries only one allele of each pair. Allele pairs are restored at fertilisation
Independent assortment: Different genes control different phenotypic characters and alleles of different genes re-assort independently of one another
49
What are exceptions to Mendels laws?
Sex-related effects: abnormalities inherited on X or Y chromosome
Mitochondrial inheritance: mitochondrial DNA always from mother
Genetic linkage: combinations of some alleles of different genes tend to be inherited together
Polygenic conditions: phenotype reflects actions of multiple genes and
environment, characteristics represent a continuim e.g. height
Overdominance: homozygotes for a given disease allele are distinguishable from heterozygotes, often homozygosity incompatible with life
Incomplete dominance: allele is only dominent in a certain situation Codominance: both alleles expressed in individual e.g. blood group
Variable expressivity: expression of genes modified by other genes and
enviroment so there may be different severities of disease
Incomplete penetrance: dominant allele not phenotypically expressed, due to negation from another factor
Genomic imprinting: mutant alleles confer different phenotypes depending on parent of origin
Dynamic mutation: genetic diseases present with increasing severity in
consecutive generations, due to expansion of a three-base repeat in their DNA
50
What are Principles of autosomal dominant (AD) inheritance?
Dominant alleles are expressed when present as single copies
Gain of function in protein coded for by mutant allele
Males and females express allele and can transmit it to all offspring Vertical pattern of inheritance (affected person has affected parent)
Parents unaffected, all children unaffected (unless new mutation)
Dominant alleles occur at low frequency as carriers less healthy than genetically normal homozygotes
Significant gene product usually NOT enzymic i.e. structural or a signalling molecule
51
Give examples of diseases inherited autosomal dominant
```
Familial hypercholesterolaemia
Adult polycystic kidney disease (APCKD)
Hereditary spherocytosis
Familial adenomatous polyposis coli
Huntington disease
Achondroplasia
```
52
Describe types of familial hypercholesterolaemia
```
No LDLR is produced
LDLR synthesis impaired before it reached PM
LDLR cannot bind LDL
LDLR do not move to coated pits
LDLR cannt release bound LDL
```
53
What can be Complications to the AD picture of inheritance?
Codominance: neither allele is dominant over the other and both are expressed in heterozygotes e.g. ABO blood grouping
54
What are principles of autosomal recessive inheritance?
Alleles are expressed when both are mutated
Carriers are heterozygote for mutant allele but phenotypically normal
AR diseases associated with loss of function of proteins
AR conditions common as carriers (heterozygotes), tend to be healthy
Autosomal so male and females are affected
Pattern of expression is horizontal (siblings), with breaks in pedigree
Affected children are often born to unaffected parents
If both parents are affected then ALL of the offspring MUST be affected
55
What Types of mating can produce recessive homozygotes with an autosomal recessive condition?
Two heterozygotes
Recessive homozygote and heterozygote
Two recessive homozygotes
56
What is consanguinity?
Genetic load: hidden detrimental component of genome i.e. lethal pre-natal mutations and harmful recessive disorders for which we are carriers
Sharing of blood means that partners share at least one ancestor back to great-grandparent level i.e. second cousins
Children born to consanguinous relationships have 2x higher risk of
autsomal recessive disease
57
What are presenting features of cystic fibrosis?
Meconium ileus: mucus plug blocks intestine when newborn
Hepatopancreatobiliary system: blockage of ducts leads to build up of mucus
Pancreas: blocked enzymes autodigest the pancreas leading to pancreatic insufficiency, malabsorption (inc fat soluble vitamins), failure to thrive and eventually possibly diabetes
Congenital bilateral absence of the vas deferens in males
Blockage of airways: build up of mucus, secondary infections manifesting as a COPD and bronchiectasis
58
What type of inheritance is cystic fibrosis?
Autosomal recessive
59
What is the genetic basis of cystic fibrosis?
Mutation in CF transmembrane conductance regulator (CFTR)
When activated CFTR protein normally: cAMP regulated Chloride channels (Cl- moves out), Adjacent Na+ channels close (Na+ not able to move in)
Defective ion transport creating salt imbalance and water depletion
60
What is Phenylkenonuria (PKU) ?
Children are blond with blue eyes
Convulsions, intellectual impairment (reduction in IQ of 1-2 points per week of untreated disease)
Deficiency in pheylalanine hydroxylase (PAH) so struggle to convert PA into tyrosine and PA levels in the blood become elevated
61
What are the most common sex linked inherited disorders?
Recessive x linked that manifest in males
62
What is mosaicism?
At a cellular level, gene expression in much of one of the X chromosomes is inactivated in every female body cell line
63
Give examples of sex linked recessive inherited conditions
Red and green colour blindness (rhodopsin)
Duchene muscular dystrophy
Fragile X syndrome
Hemophilia A
64
Describe duchenne muscular dystrophy
Presents before five years
Clinical features: clumsiness, muscle weakness, pseudo-hypertrophy of the calfs (fatty replacement of muscle)
Mortality by 18 is usual
X linked recessive
65
What is fragile X syndrome?
Triplet expansion of CGG
Features: Learning difficulties, autism, hyperactivity
High forehead and prominent lower jaw
Males: macroorchidism
66
How do we depict pertinent information relating to risk of disease?
When assessing risk of disease a full history needs to be taken from
the consultand
Family pedigree needs to be generated
Issues that need to be considered: Consanguinity, OB and Gynae history: miscarriages, terminations of pregnancy, still births
Neonatal or infant deaths
Disability especially in children
For each individual depicted on pedigree include: full name, date of birth, date and cause of death and any specific medical conditions
67
What is the value of a pedigree diagram?
Provide information on: Mode and risk of inheritance
Genetic counselling is often sought: In process of family planning, assess risk to pregnancy, assess recurrence risk in future pregnancy, assess risk of a disease in offspring of close relatives, assess risk of late onset disease
68
How are chromosomes formed?
```
Base pairs forming
DNA double helix wrapping around
Nucleosomes, giving beads on a string, coiling
Solenoid
Looped solenoid on a central scaffold
Compacted chromosomes
```
69
Describe typical chromosome structure
Telomere: Specialised end of the chromosome
Centromere: Non-duplicated DNA present during early mitosis, Connects two identical sister chromatids, Forms focus of kinetochore for mitotic spindle formation
Arms: p= the petite or short arm, q= the long arm
70
What is the unit of length of DNA?
Base pair, nucleotides
71
What makes up a nucleotide?
Sugar
Phosphate group
Nitrogenous base
72
DNA must be transcribed into RNA in order to produce a protein, the steps involved are:
hnRNA- heterogenous nuclear RNA production
mRNA- messenger RNA production
Translation into a polypeptide
Post translational modification and processing
73
What is a codon?
3 bases, which code for an amino acid
74
Describe the structure of genes
Upstream controlling DNA sequences - enhancers, silencers
Non-coding sequences within the coding section - introns
Exons - coding DNA
75
What does the transcription unit contain?
Introns- non-coding DNA (spliced from RNA)
| Exons- coding DNA
76
What are mutations?
Permanent alterations in the base sequence of DNA
77
Describe substitution mutations
Replacement of a base pair with another
Silent: new codon codes for the same amino acid
Missense: new codon codes for a different amino acid, Conservative- no alteration in the chemical properties of the protein produced, Non-conservative- deleterious effect on the protein produced
Premature termination or non-sense mutation: new codon is a STOP codon
78
Describe deletion/ insertion mutations
Single base pair or two base pairs then FRAMESHIFT mutation
translational reading frame is disrupted
Erroneous protein downstream of the deletion/insertion
79
What are different types of genetic alterations?
```
Substitution
Deletion
Insertion
Duplication
Copy number variation
Transcriptional control
Splicing mutations
```
80
Describe duplication or deletion of genes
Duplications of whole genes- increase the ‘dose’ of the protein can have deleterious effects
81
What is copy number variation?
Large deletions or insertions of various lengths created by unequal crossing over between misaligned DNA segments
82
How can transcriptional control result in a mutation?
Mutations in enhancer and silencer regions can have quantitative effects on the amount of product produced e.g. haemophilia B
83
How can splicing mutations cause deleterious effects?
Affects the RNA produced e.g. Beta thalassaemia
84
What is genomic imprinting?
Occurs during gametogenesis, methylation of segments of DNA
Only one of inherited alleles is expressed i.e. paternal or maternal in certain tissues
Genetic diseases arising in imprinted genes vary with the parent of origin of abnormal gene
85
Give an example where genomic imprinting results in different phenotypic expression of disease
Microdeletion of 15q
Maternal deletion: Angelman syndrome, Jerky movements, Epilepsy, Developmental delay
Paternal deletion: Prader-Willi syndrome, Obesity, V shaped upper lips, Small hands, Learning difficulties
86
What is a dynamic mutation?
Expansion of triplet or trinucleotide repeats
Diseases typically show anticipation in successive generations i.e.:
occurs earlier in successive generations and is more severe
Aggregation of toxic protein in transcription region e.g. Huntingtons Disease
Blockage of transcription if in the silencer/enhancer/promoter regions
e.g. Fragile X
87
What is Pleiotropy?
One gene being responsible for diverse phenotypic effects
| Eg collagen mutation will affect multiple systems
88
What is Locus heterogeneity?
Two or more genetic loci creating similar phenotypic effects
| Eg blindness can have multiple separate genetic causes
89
Describe different types of chromosomes
Metacentric: Centromere in the middle
Sub-metacentric: Centromere sub median
Acrocentric: Centromere near one end 13, 14, 15, 21, 22, Y
Telecentric: Centromere at the end
90
What is Cytogenetics?
Study of the number and structure of chromosomes usually to give a karyotype
91
Give some indications for chromosomal analysis
Suspected chromosomal abnormality
Multiple congenital abnormalities and or developmental delays
Disorders of sexual function
Intellectual impairment of unknown cause
Certain malignancies
Infertility or multiple miscarriages
Stillbirth or neonatal death
92
Describe chromosome staining
Compact tightly coiled chromatin stains dark (G-bands)
Loosely coiled chromatin stain lightly ( R-bands)
R-bands contain majority of the structural genes
93
Describe karyotype formulae
```
Number of chromosomes
Sex chromosomes present
Any abnormalities: Number, substructure
Genetically normal female- 46, XX
Genetically normal male- 46, XY
```
94
What are Abnormalities of number of chromosomes?
```
Euploidy= number of chromosomes is an integral multiple of the haploid number (23)
Aneuploidy= number of chromosomes is NOT an integral multiple of haploid number, Occurs due to abnormal separation of chromosomes during meiosis 1 or 2, Trisomy= three copies of one chromosome, Monosomy= single copy of a chromosome, autosomal monosomies are nearly always incompatible with life
```
95
Which are the only autosomal trisomies compatible with life?
Trisomy 21 (Down syndrome)
T18 (Edwards syndrome)
T13 (Patau syndrome)
96
What types of trisomy can there be?
Complete trisomy: severe clinical phenotype
| Partial trisomy: translocation of part of the chromosome often with milder clinical manifestations
97
What are features of Down's syndrome?
```
Flat facial profile
Epicanthal fold
Single transverse palmar crease
General hypotonia
Large sandal gap between 1st and 2nd toes
Life expectancy- 50-60 years
Commonly associated with cardiac defects
```
98
Which is the only Monosomy compatible with life?
X chromosome monosomy: Turner syndrome
Karyotype- 45 X
Clinical features: Low hairline, webbed neck, widely spaced nipples, primary ovarian failure, short stature, coarctation of the aorta
99
What is Klinefelter syndrome?
Karyotype: 47 XXY, 48 XXXY, 49 XXXXY etc
Body type is male with the following features
Gynaecomastia, Elongated forearms and lower legs, Small testis and azoospermia, Variable learning differences
100
What chromosomal structural abnormalities can occur?
Translocations
Deletions
Inversions
Ring chromosomes
101
Describe chromosomal translocation
Transpositions of chromosome material between chromosomes
Centric or Robertsonian: Break at or near centromere followed by fusion, Typically with deletion/loss of the non-fused segments
Reciprocal: Interchromosomal exchange, Carrier normally healthy but can effect future generations
Insertional: Insertion of deleted segment interstitially at another location
102
In childhood vulnerable groups include:
Babies born prematurely (7% of babies in UK)
Babies with developmental problems e.g. cerebral palsy (6% of children in UK are disabled)
Children with chronic illnesses e.g. asthma, epilepsy, TIDM, CF
Small babies in general
103
What is fever in children and what can cause it?
Temperature >37.5°C
Most causes of temperature in childhood are due to benign, self
limiting viral illnesses
104
Give examples of causes of temperature in children
```
Post immunisation
Upper respiratory tract infections
Otitis media
Lower respiratory tract infections
Pneumonia
Gastroenteritis
Urinary tract infection
Septicaemia
Meningitis
Osteomyelitis
```
105
How do you assess the severity of a temperature in children?
History: Age of child- serious infection more common in babies 5 days, Other symptoms – rash, breathing difficulties, posture
Examination: ABC, general examination
Investigations: Bloods, FBC: raised white cell count, U+E: used as baseline for IV fluids, CRP: raised, Blood cultures: culture of pathogen
Radiology, CSF: raised white cells, low CSF glucose, high protein, Urine: raised white cells, culture of pathogen
106
What are febrile convulsions?
Commonest type of seizure in childhood affecting 1:20 children
Occurs in children age 6 months to 6 years
Simple convulsion:
107
What can be infectious causes of vomiting and diarrhoea in children?
```
Viral
Bacterial
Urinary tract infection
Pneumonia
Sepsis
Meningitis
```
108
What problems can arise from excessive vomiting and diarrhoea in children?
Dehydration
| Hypoglycaemia (babies have limited glycogen stores)
109
What could be the cause of a vesicular rash in children?
Chicken pox
Herpes
impetigo
110
What could be causes of a papular rash in children?
Urticaria
| Insect bites
111
What could be causes of a red and scaly rash in children?
Eczema (will have epidermal breakage)
| Psoriasis
112
What could be causes of a red but not scaly rash in children?
```
Cellulitis
Viral exanthema (measles, rubella)
```
113
What could be causes of a purpuric rash in children?
Meningococcal sepsis
| Low platelet count (idiopathic thrombocytopenic purpura, leukaemia)
114
Describe prevalence and associated factors of eczema
5-10% of infants get eczema
50% resolve by 5 years, 30% more by teenage
Associated with atopy – may develop asthma or hay fever when older
Causes itching, scratching, misery, prone to skin infections
Source of huge anxiety and stress to families
115
What can be causes of cough in childhood?
Upper respiratory: URTI, Croup (Parainfluenza), Allergy, Pertussis
Lower respiratory: Pneumonia, Asthma, Bronchiolitis (Viral illness often due to respiratory syncytial virus)
116
What is pertussis? And how would you recognise it?
```
Whooping cough
Paroxysmal, violent rapid cough. All air expelled followed by an
inspiratory whoop
Cyanotic episodes
Apnoea in babies
```
117
What clinical signs might be seen in a child with a cough?
Upper respiratory: No chest signs unless severe obstruction
Lower respiratory: Tachypnoea, Recession, Abnormal breath sounds, Added sounds, Abnormalities in percussion
118
What can be causes of a wheeze in children?
Upper Respiratory Tract Infection: Toddlers and pre-school children
Bronchiolitis: Infants
Asthma: Reversible airways obstruction due to smooth muscle spasm and inflammation, Rarely diagnosed before 2 years old
119
What clinical features increase the probability of asthma?
Wheeze, cough, difficulty breathing, chest tightness, worse at night/morning, triggered by cold, exercise, pets, emotions, damp
Personal history of atopic disorder
Family history of atopic disorder/ asthma
Widespread wheeze on auscultation
Improvement in condition with bronchodilators
120
What clinical features lower the probability of asthma?
Symptoms with colds only
Isolated cough in absence of wheeze or dyspnoea
History of moist cough
Dizziness, light headedness, peripheral tingling
Normal examination of chest when symptomatic
Normal PEF or spirometry when symptomatic
No response to asthma therapy
Clinical features of alternative diagnosis
121
What clinical investigations could be performed to assess a cough in children ?
Chest X ray: exclude other causes of recurrent cough
| Peak flow: Difficult in children younger than 6 years
122
How would you define acute severe asthma in a child over 2?
Sats 125 for over 5s, >140 for 2-5 yrs
| Resp rate >30 for over 5s, >40 for 2-5 yrs
123
How would you describe life threatening asthma in a child over 2?
Sats
124
How do you manage acute asthma in children?
ABC
History: Severity and management of previous episodes
Examination: Respiratory examination
Investigation: U+E – salbutamol causes hypokalaemia
CXR if severe, not responding or possibility of pneumothorax
125
Breast alveoli become capable of milk production during:
Pregnancy
126
What limits lactation until after parturition?
High levels of oestrogen and progesterone
127
What turns on milk secretion?
Changing ratio between oestrogen and progesterone which leads to alveolar cells becoming sensitive to Prolactin
Prolactin is made in the anterior pituitary, under tonic inhibition from the hypothalamus
Suckling produces a neuro endocrine response which reduces dopamine levels and allows prolactin to rise and stimulate milk production
128
What causes ejection of the milk?
Oxytocin, from posterior pituitary is released by a neuroendocrine response. The myoepithelial cells in the breast then contract to eject the milk
129
What reflex is triggered in some women by hearing their baby cry?
Milk let down reflex
130
Why might some women experience uterine cramps during breast feeding?
Oxytocin
131
Why is regular breast feeding more likely to be successful than sporadic?
Suckling promotes prolactin production
132
How would a dopamine like drug affect lactation?
Suppress it
133
Name 4 advantages of breast feeding for women
Increased skin to skin contact with baby, Promotion of attachment, Involution of uterus, Lower risk of breast and ovarian cancer, Lower risk of hip fractures, Prevention of rheumatoid arthritis
134
Breastfed babies may have better:
Neurological development
135
Difficulties with breast feeding can include?
Inverted nipples, nipples too big for baby’s mouth (as in some premature babies who will need to be tube fed), Sore/Cracked nipples, breast engorgement, mastitis
