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Things I need to learn Flashcards

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1
Q

Explain the pathophysiology of vesicoureteric reflux

A
  • the ureters are displaced to enter the bladder at less of an angle
  • this means they have a shorter intramural course
  • this means the vesicoureteric junction is less functional
  • urine therefore backflows from the bladder into the ureter and potentially the kidneys
  • this can cause recurrent infections and renal scarring
  • renal scarring can cause hypertension
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2
Q

Causes of vesicoureteric reflux (3)

A

genetic
bladder pathology
temporary during a UTI

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3
Q

How might vesicoureteric reflux present antenatally

A

hydronephrosis on USS

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4
Q

presentation of vesicoureteric reflux (3)

A
  • recurrent childhood UTIs
  • atypical UTIs
  • renal scarring causing hypertension
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5
Q

what is the gold standard investigation for vesicoureteric reflux

A

micturating cystourethrogram

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6
Q

what scan may be used to look for renal scarring in vesicoureteric reflux

A

DMSA scan - dimercaptosuccinic acid syntigraphy

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7
Q

how is vesicoureteric reflux treated

A

prophylactic Abx
may do surgery if scarring

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8
Q

most common causes of UTIs in children (3)

A

E.coli
proteus
pseudomonas

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9
Q

what are some predisposing factors for UTIs in children (3)

A

incomplete bladder emptying, may be due to:
- infrequent voiding
- hurried micturition
- constipation
- neuropathic bladder

Vesicoureteric reflux

Poo hygiene

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10
Q

What might cause incomplete bladder emptying in children? (4)

A

infrequent voiding
hurried micturition
constipation
neuropathic bladder

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11
Q

What are some features of atypical UTIs in children (6)

A

seriously ill or septic child
poor urine flow
abdominal or bladder mass
not caused by E.coli
not responsive to Abx in 48 hours
raised creatinine

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12
Q

What defines recurrent UTIs

A
  • two or more upper UTIs
  • one upper and one lower UTI
  • three lower UTIs
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13
Q

who should have an USS and when should it be done for UTIs (4)

A
  • during an infection for all children with an atypical UTI
  • 6 weeks after the infection if first- time UTI and below 6 months.
  • 6 weeks after the infection if over 6 months with recurrent UTI
  • during the infection if under 6 months with recurrent UTI
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14
Q

when should a DMSA scan be done in UTIs

A
  • for all children under 3 years with an atypical UTI
  • all children with recurrent UTIs

should be 4-6 months after an infection

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15
Q

How is a UTI in a child under 3 months treated

A

immediate paediatric referral

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16
Q

How is an upper UTI in child over 3 months treated

A

either admit for IV antibiotics or give oral co-amoxiclav or cephalosporins for 7-10 days

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17
Q

how is a lower UTI in a child over 3 months treated?

A

3 days of oral abx
either nitrouratoin, trimethoprim, coamoxiclav or cephalosporin

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18
Q

triad of haemolytic anaemia

A

microangiopathic haemolytic anaemia
thrombocytopenia
acute kidney injury

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19
Q

what is the most common cause of haemolytic uraemic syndrome and what toxin does it release

A

gastro infection caused by e.coli secreting shiga toxin

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20
Q

what is atypical haemolytic uraemic syndrome

A

a familial form of HUS that is caused by complement dysregulation

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21
Q

How investigations may be done for HUS and what will be seen (4)

A
  • FBC- haemolytic anaemia, thrombocytopenia
  • blood film- schistocytes and helmet cells
  • Uand E- AKI
  • stool culture- shows evidence of shiga toxin
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22
Q

How is haemolytic uraemic syndrome treated?

A

fluids- IV isotonic cystalloids
supportive

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23
Q

how is atypical/familial HUS treated

A

monoclonal Abx- eculizumab

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24
Q

what three key features may be seen with hypospadius

A

ventral opening of the urethral meatus
ventral curvature of the penis
dorsal hooded foreskin

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25
When are children screened for undescended testes?
NIPE- within72 hours of birth At 6-8 weeks Re-examined at 4-5 months if previously undescended
26
When should surgical repair of undescended testes take place?
6-18 months
27
when should referral to urologists for undescended testes occur?
by 6 months
28
what is the name of the surgery for undescended testes?
orchidoplexy
29
genetics of congenital adrenal hyperplasia
autosomal recessive
30
what is usually deficient in congenital adrenal hyperplasia? What is an alternative form?
21- hydroxylase 11-beta hydroxylase
31
What does 21 hydroxylase do?
converts 17-hydroxyprogesterone into 11-deoxycortisol
32
pathophysiology of congenital adrenal hyperplasia
17-hydroxyprogesterone cannot be converted into cortisol or aldosterone leads to excess being converted into testosterone
33
How does congenital adrenal hyperplasia present?
precocious puberty, infertility virilization of the female external genitalia with clitoral hypertrophy males may appear normal at birth salt wasting crisis - hypotension, dehydration and electrolyte disturbances
34
How is congenital adrenal hyperplasia diagnosed?
17-hydroxyprogesterone level - will be increased ACTH supression test- will cause an abnormal increased in 17 hydroxyprogesterone
35
How is congenital adrenal hyperplasia treated
replace cortisol (glucocorticoids) and aldosterone (fludrocortisone)
36
How does he ACTH suppression test work in congenital adrenal hyperplasia?
it will cause an abnormal increase in 17- hydroxyprogesterone
37
what electrolyte abnormalities occur in salt wasting crisis?
hyponatraemia and hyperkalaemia
38
what skeletal abnormalities may be present in kallman syndrome?
short middle finger scoliosis
39
When is the combined test done for downs syndrome screening?
between 11-13+6 weeks
40
When is the quadruple test done for downs syndrome
if the woman presents after 15 weeks (15-20 weeks)
41
What makes up the quadruple test and what results indicate down syndrome?
low AFP low oestriol high beta-hCG high inhibin A
42
When would amniocentesis be done and when would chorionic villus sampling be done?
amniocentesis is done later in pregnancy, chorionic villus sampling can be done up to 15 weeks
43
what is an alternative to chorionic villus sampling and amniocentesis
non-invasive prenatal testing (NIPT)
44
Explain spastic cerebral palsy
damage to the upper motor neurones causing hypertonia. Can be hemiplegic, diplegic or quadraplegic
45
explain dyskinetic cerebral palsy
damage to the basal ganglia and substantia nigra leading to athetoid movements and oromotor problems
46
explain ataxic cerebral palsy
damage to the cerebellum leading to problems with coordinated movement
47
How might cerebral palsy present?
failure to meet milestones increased or decreased tone hand preference before 18 months coordination problems speech problems hemoplegic gait (UMN) Other non-motor: - epilepsy - learning difficulties - squints - hearing impairemnts
48
why might surgery be done in cerebral palsy
to release contractures or lengthen tendons
49
What is rheumatic fever?
an immunological reaction to a recent infection with group A haemolytic strep- most commonly strep pyogenes causing tonsilitis
50
what bacteria causes rheumatic fever?
group A haemolytic strep - most commonly streptococcus pyogenes
51
Pathophysiology of rheumatic fever
1. Strep. pyogenes infection causes the immune system to produce IgG and IgM 2. A type 2 hypersensitivity reaction occurs in which the antibodies react with the cell wall of arteries in molecular mimicry
52
What feature of strep. pyogenes causes molecular mimicry
the cell wall of strep pyogenes has a virulence factor called M protein This is highly antigenic and antibodies against it cross-react with smooth muscle.
53
What is the diagnostic criteria of rheumatic fever and what is it made up of?
Jones criteria: Evidence of a recent streptococcal infection plus 2 major or one major+2 minor criteria Major criteria: JONES J- joint arthritis O- organ involvement (e.g. carditis) N- Nodules E- Erythema marginatum rash S - Syndenham chorea Minor criteria: - fever - ECG changes without carditis (prolonged PR interval) - arthralgia without arthritis - raised inflammatory markers (CRP and ESR)
54
How can evidence of a streptococcal infection be shown? (3)
anti-streptococcal antibody titres (ASOT) increase in Dnase B titres positive throat swab
55
How does arthritis in rheumatic fever present?
migratory arthritis
56
How does the rash in rheumatic fever present?
erythema marginatum - pink rings of varying sizes on torso and proximal limbs
57
What is sydenham's chorea
irregular uncontrolled movements of the limbs, muscle weakness and emotional disturbance
58
How is rheumatic fever treated?
Oral Pen V NSAIDs
59
How does carditis in rheumatic fever present?
bradycardia murmurs (commonly due to mitral valve disease) pericardial rub on auscultation heart failure
60
What bacteria most commonly causes infective endocarditis?
group A beta haemolytic strep (streptococcus viridans)
61
How does infective endocarditis present?
fever anaemia splinter haemorrhages changing cardiac sings (murmur) roth spots osler nodes janeway lesions splenomegaly
62
What criteria is used for infective endocarditis?
DUKES criteria
63
what makes up dukes criteria for infective endocarditis?
2 major criteria 1 major and 3 minor criteria or 5 minor criteria Major: - positive blood cultures suggestive of an organism know to cause infective endocarditis - evidence of endocardial involvement on echo minor: - predisposing heart condition or IV drug use - fever - vascular phenomenon (e.g. janeway lesions, conjunctival haemorrhages) - immunologic phenomenon- osler nodes, roth spots - positive blood cultures that don't meat the criteria
64
How is infective endocarditis diagnosed?
blood cultures echo
65
How is infective endocarditis treated?
6 weeks IV antibiotics (if strep - penicillin )
66
what tests might be used in the diagnosis of sickle cell anaemia
sickle solubility test haemoglobin electophoresis usually picked up on new born blood spot test
67
what drug might be used in sickle cell anaemia and what is its action
hydroxycarbamide - works by increasing HbF
68
overview of treatment of sickle cell disease
avoid triggers vaccines prophylactic antibiotics hydroxycarbamide blood transfusions bone marrow transplant New- crizanlizumab (monoclonal antibody that targets P-selectin and prevents RBC adhering to walls of vessels)
69
how is pernicious anaemia treated?
IM hydroxycobalamin
70
what causes pernicious anaemia ?
antibodies against parietal cells and intrinsic factor- these are needed for absorption of B12 in the terminal ileum
71
what sign may be seen on x ray in patients with thalassaemia and why?
hair on end sign extramedullary erythropoesis
72
how does iron overload present?
fatigue liver cirrhosis infertility arthritis diabetes osteoporosis
73
what drug may be used as iron chelation?
desferrioxamine
74
explain the pathophysiology of DKA
-when then there is no insulin the body cannot -utilise glucose -This causes the body to start undergoing ketogenesis to use fatty acids as energy -This produces ketones, which along with hyperglycaemia cause ketoacidosis
75
why does dehydration occur in ketoacidosis
the hyperglycaemia causes glucose to be lost in urine This draws in water to the urine causing polyuria this leads to dehydration
76
what happens to potassium in DKA
- insulin is needed to move potassium intracellularly - this means in DKA there will be high serum potassium but low total body potassium
77
what happens to potassium in DKA when insulin is given
- the serum potassium is rapidly moved intracellularly - this can lead to severe hypokalaemia and arrhythmias
78
Why does GCS need to be monitored when treated DKA
as cerebral oedema can occur where the extracellular fluid moves intracellularly
79
How does DKA present?
abdominal pain polyuria polydipsia dehydration kussmaul breathing acetone smelling breath reduced consciousness
80
what will investigations show for DKA (3)
hyperglycaemia >11 ketones in blood >3 pH <7.3
81
Management of DKA
1st line: - fluid replacement over 48 hours - insulin infusion other key points: -once blood glucose is at 14mmol/l 10% dextrose should be initiated - potassium may be needed to add to fluids
82
what two types of serological tests can be done for syphilis
treponemal and non-treponemal tests
83
what two broad types of syphilis testing are there- describe each
direct tests- look for the presence of treponema pallidum from swab, by either dark-field microscopy or PCR serological tests: test the quantity of antibodies produced by the body to syphilis. Includes treponemal and non-treponemal tests
84
Give some examples of treponemal serological test for syphilis
T.pallidum enzyme immunoassay (TP-EIA) and TPHA
85
give some examples of non-treponemal serological tests for syphilis and explain how they work
they are based upon the reactivity of serum from infected patients to a cardiolipin-cholesterol-lecithin antigen examples include: - rapid plasma reagin (RPR) - - Venereal Disease Research Laboratory (VDRL)
86
what may cause false positives for syphilis, in particular with non-treponemal tests
pregnancy SLE TB leprosy malaria HIV
87
what does a Negative non-treponemal test + positive treponemal test suggest for syphilis
treated syphilis
88
what does a positive non-treponemal test + positive treponemal test for syphilis suggest
active syphilis infection
89
How is syphilis treated
IM benzathin penicillin
90
what are some examples of AIDS defining illnesses
kaposi sarcoma pneumonitis jjrovecii pneumonia cytomegalovirus oesophageal of brinchial candidiasis lymphomas TB toxoplasmosis encephalitis
91
what is given as prophylaxis against pneumonitis jjroveccii pneumonia in HIV patients with a CD4 count less than 200
co-trimoxazole
92
What two types of tests can be used to screen for HIV and what is the time window at which they can be used
fourth generation laboratory combined tests- test for antibodies to HIV and the P24 antigen. Can be used after 45 days since exposure point of care tests - can be used from 90 days after exposure
93
How is HIV treated?
antiretroviral therapy
94
what classes of drugs make up antiretroviral therapy
nucleoside reverse transcriptase inhibitors (tenofovir and emtricitabine) protease inhibitors (ritonavir) Non-nucleoside reverse transcriptase inhibitors
95
What are some side effects of antiretroviral therapy
renal impairment peripheral neuropathy bone disease (osteoporosis)
96
what should be given during caesarens in women with HIV
zidovudine infusion
97
What is the name of the lung lesions and lymph nodes that make up primary TB
Ghon complex
98
what type of hypersensitivity reaction occurs in TB
type 4 hypersensitivity
99
what is disseminated TB called ?
miliary TB
100
where might TB spread to in secondary TB?
vertrebra (potts disease) CNS cervical lymph nodes kidneys GI tract
101
what test is used in the screening of TB?
the mantoux skin test or interferon gamma release assay
102
what investigations might be done if someone is suspected of having active TB
cultures and chest x ray
103
what stain is used for TB?
ziehl - neelsen acid fast stain
104
what may be seen on chest x ray of someone with active TB?
upper lobe cavitation if reactivated patchy infiltrations if primary perihilar lymphadenopathy
105
what might be seen on x ray of someone with milliary TB?
millet seeds appearance
106
how can a culture for TB be collected (3)
-deep cough -sputum induction with nebulised saline -bronchoscopy and bronchoalveolar lavage
107
How is active TB managed ?
4 months of quadruple therapy with RIPE 2 months of just RI
108
What are the 4 key drugs that might be used in TB treatment?
rifampicin isoniazid Pyrazinamide ethambutol
109
How is latent TB treated?
3 months of rifampicin and isonizid or 6 months of just isoniazid pyroxidine is given alongside isoniazid to prevent peripheral neuropathy
110
side effects of rifampicin
orange secretions hepatitis induction of cytochrome p450
111
side effects of isoniazid
peripheral neuropathy
112
side effect of pyrazinamide
hyperuricaemia causing gout and kidney stones
113
side effect of ethambutol
optic neuritis- colour blindness and reduced visual acuity
114
what are some risk factors for VTE in pregnancy ?
smoking parity >3 age >35 BMI>30 reduced mobility pre-eclampsia multiple pregnancy gross varicose veins family history of VTE thrombophilia IVF
115
management of meningitis below 3 months:
IV cefotaxime + IV amoxicillin
116
management of meningitis over 3 months
IV cefotaxime or ceftriaxone
117
what is the most common complication of termination of pregnancy?
infection
118
how does ovarian hyperstimulation syndrome present?
GI side effects - nausea, vomiting, abdominal pain, bloating and diarrhoea shortness of breath fever oliguira peripheral oedema
119
in premature ovarian insufficiency how long should hormone replacement be offered?
until the age of 51
120
what two features in child with bornchiolitis might suggest pneumonia?
high fever (>39) and persitently focal crackles
121
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