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3A > Things I need to learn > Flashcards

Things I need to learn Flashcards

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
Q

When are children screened for undescended testes?

A

NIPE- within72 hours of birth
At 6-8 weeks

Re-examined at 4-5 months if previously undescended

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26
Q

When should surgical repair of undescended testes take place?

A

6-18 months

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27
Q

when should referral to urologists for undescended testes occur?

A

by 6 months

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28
Q

what is the name of the surgery for undescended testes?

A

orchidoplexy

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29
Q

genetics of congenital adrenal hyperplasia

A

autosomal recessive

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30
Q

what is usually deficient in congenital adrenal hyperplasia?
What is an alternative form?

A

21- hydroxylase
11-beta hydroxylase

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31
Q

What does 21 hydroxylase do?

A

converts 17-hydroxyprogesterone into 11-deoxycortisol

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32
Q

pathophysiology of congenital adrenal hyperplasia

A

17-hydroxyprogesterone cannot be converted into cortisol or aldosterone
leads to excess being converted into testosterone

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33
Q

How does congenital adrenal hyperplasia present?

A

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

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34
Q

How is congenital adrenal hyperplasia diagnosed?

A

17-hydroxyprogesterone level - will be increased
ACTH supression test- will cause an abnormal increased in 17 hydroxyprogesterone

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35
Q

How is congenital adrenal hyperplasia treated

A

replace cortisol (glucocorticoids) and aldosterone (fludrocortisone)

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36
Q

How does he ACTH suppression test work in congenital adrenal hyperplasia?

A

it will cause an abnormal increase in 17- hydroxyprogesterone

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37
Q

what electrolyte abnormalities occur in salt wasting crisis?

A

hyponatraemia and hyperkalaemia

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38
Q

what skeletal abnormalities may be present in kallman syndrome?

A

short middle finger
scoliosis

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39
Q

When is the combined test done for downs syndrome screening?

A

between 11-13+6 weeks

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40
Q

When is the quadruple test done for downs syndrome

A

if the woman presents after 15 weeks (15-20 weeks)

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41
Q

What makes up the quadruple test and what results indicate down syndrome?

A

low AFP
low oestriol
high beta-hCG
high inhibin A

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42
Q

When would amniocentesis be done and when would chorionic villus sampling be done?

A

amniocentesis is done later in pregnancy, chorionic villus sampling can be done up to 15 weeks

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43
Q

what is an alternative to chorionic villus sampling and amniocentesis

A

non-invasive prenatal testing (NIPT)

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44
Q

Explain spastic cerebral palsy

A

damage to the upper motor neurones causing hypertonia.
Can be hemiplegic, diplegic or quadraplegic

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45
Q

explain dyskinetic cerebral palsy

A

damage to the basal ganglia and substantia nigra leading to athetoid movements and oromotor problems

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46
Q

explain ataxic cerebral palsy

A

damage to the cerebellum leading to problems with coordinated movement

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47
Q

How might cerebral palsy present?

A

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

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48
Q

why might surgery be done in cerebral palsy

A

to release contractures or lengthen tendons

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49
Q

What is rheumatic fever?

A

an immunological reaction to a recent infection with group A haemolytic strep- most commonly strep pyogenes causing tonsilitis

50
Q

what bacteria causes rheumatic fever?

A

group A haemolytic strep - most commonly streptococcus pyogenes

51
Q

Pathophysiology of rheumatic fever

A
  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
Q

What feature of strep. pyogenes causes molecular mimicry

A

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
Q

What is the diagnostic criteria of rheumatic fever and what is it made up of?

A

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
Q

How can evidence of a streptococcal infection be shown? (3)

A

anti-streptococcal antibody titres (ASOT)
increase in Dnase B titres
positive throat swab

55
Q

How does arthritis in rheumatic fever present?

A

migratory arthritis

56
Q

How does the rash in rheumatic fever present?

A

erythema marginatum - pink rings of varying sizes on torso and proximal limbs

57
Q

What is sydenham’s chorea

A

irregular uncontrolled movements of the limbs, muscle weakness and emotional disturbance

58
Q

How is rheumatic fever treated?

A

Oral Pen V
NSAIDs

59
Q

How does carditis in rheumatic fever present?

A

bradycardia
murmurs (commonly due to mitral valve disease)
pericardial rub on auscultation
heart failure

60
Q

What bacteria most commonly causes infective endocarditis?

A

group A beta haemolytic strep (streptococcus viridans)

61
Q

How does infective endocarditis present?

A

fever
anaemia
splinter haemorrhages
changing cardiac sings (murmur)
roth spots
osler nodes
janeway lesions
splenomegaly

62
Q

What criteria is used for infective endocarditis?

A

DUKES criteria

63
Q

what makes up dukes criteria for infective endocarditis?

A

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
Q

How is infective endocarditis diagnosed?

A

blood cultures
echo

65
Q

How is infective endocarditis treated?

A

6 weeks IV antibiotics (if strep - penicillin )

66
Q

what tests might be used in the diagnosis of sickle cell anaemia

A

sickle solubility test
haemoglobin electophoresis
usually picked up on new born blood spot test

67
Q

what drug might be used in sickle cell anaemia and what is its action

A

hydroxycarbamide - works by increasing HbF

68
Q

overview of treatment of sickle cell disease

A

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
Q

how is pernicious anaemia treated?

A

IM hydroxycobalamin

70
Q

what causes pernicious anaemia ?

A

antibodies against parietal cells and intrinsic factor- these are needed for absorption of B12 in the terminal ileum

71
Q

what sign may be seen on x ray in patients with thalassaemia and why?

A

hair on end sign
extramedullary erythropoesis

72
Q

how does iron overload present?

A

fatigue
liver cirrhosis
infertility
arthritis
diabetes
osteoporosis

73
Q

what drug may be used as iron chelation?

A

desferrioxamine

74
Q

explain the pathophysiology of DKA

A

-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
Q

why does dehydration occur in ketoacidosis

A

the hyperglycaemia causes glucose to be lost in urine
This draws in water to the urine causing polyuria
this leads to dehydration

76
Q

what happens to potassium in DKA

A
  • insulin is needed to move potassium intracellularly
  • this means in DKA there will be high serum potassium but low total body potassium
77
Q

what happens to potassium in DKA when insulin is given

A
  • the serum potassium is rapidly moved intracellularly
  • this can lead to severe hypokalaemia and arrhythmias
78
Q

Why does GCS need to be monitored when treated DKA

A

as cerebral oedema can occur where the extracellular fluid moves intracellularly

79
Q

How does DKA present?

A

abdominal pain
polyuria
polydipsia
dehydration
kussmaul breathing
acetone smelling breath
reduced consciousness

80
Q

what will investigations show for DKA (3)

A

hyperglycaemia >11
ketones in blood >3
pH <7.3

81
Q

Management of DKA

A

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
Q

what two types of serological tests can be done for syphilis

A

treponemal and non-treponemal tests

83
Q

what two broad types of syphilis testing are there- describe each

A

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
Q

Give some examples of treponemal serological test for syphilis

A

T.pallidum enzyme immunoassay (TP-EIA) and TPHA

85
Q

give some examples of non-treponemal serological tests for syphilis and explain how they work

A

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
Q

what may cause false positives for syphilis, in particular with non-treponemal tests

A

pregnancy
SLE
TB
leprosy
malaria
HIV

87
Q

what does a Negative non-treponemal test + positive treponemal test suggest for syphilis

A

treated syphilis

88
Q

what does a positive non-treponemal test + positive treponemal test for syphilis suggest

A

active syphilis infection

89
Q

How is syphilis treated

A

IM benzathin penicillin

90
Q

what are some examples of AIDS defining illnesses

A

kaposi sarcoma
pneumonitis jjrovecii pneumonia
cytomegalovirus
oesophageal of brinchial candidiasis
lymphomas
TB
toxoplasmosis
encephalitis

91
Q

what is given as prophylaxis against pneumonitis jjroveccii pneumonia in HIV patients with a CD4 count less than 200

A

co-trimoxazole

92
Q

What two types of tests can be used to screen for HIV and what is the time window at which they can be used

A

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
Q

How is HIV treated?

A

antiretroviral therapy

94
Q

what classes of drugs make up antiretroviral therapy

A

nucleoside reverse transcriptase inhibitors (tenofovir and emtricitabine)

protease inhibitors (ritonavir)

Non-nucleoside reverse transcriptase inhibitors

95
Q

What are some side effects of antiretroviral therapy

A

renal impairment
peripheral neuropathy
bone disease (osteoporosis)

96
Q

what should be given during caesarens in women with HIV

A

zidovudine infusion

97
Q

What is the name of the lung lesions and lymph nodes that make up primary TB

A

Ghon complex

98
Q

what type of hypersensitivity reaction occurs in TB

A

type 4 hypersensitivity

99
Q

what is disseminated TB called ?

A

miliary TB

100
Q

where might TB spread to in secondary TB?

A

vertrebra (potts disease)
CNS
cervical lymph nodes
kidneys
GI tract

101
Q

what test is used in the screening of TB?

A

the mantoux skin test or interferon gamma release assay

102
Q

what investigations might be done if someone is suspected of having active TB

A

cultures and chest x ray

103
Q

what stain is used for TB?

A

ziehl - neelsen acid fast stain

104
Q

what may be seen on chest x ray of someone with active TB?

A

upper lobe cavitation if reactivated
patchy infiltrations if primary
perihilar lymphadenopathy

105
Q

what might be seen on x ray of someone with milliary TB?

A

millet seeds appearance

106
Q

how can a culture for TB be collected (3)

A

-deep cough
-sputum induction with nebulised saline
-bronchoscopy and bronchoalveolar lavage

107
Q

How is active TB managed ?

A

4 months of quadruple therapy with RIPE
2 months of just RI

108
Q

What are the 4 key drugs that might be used in TB treatment?

A

rifampicin
isoniazid
Pyrazinamide
ethambutol

109
Q

How is latent TB treated?

A

3 months of rifampicin and isonizid
or
6 months of just isoniazid

pyroxidine is given alongside isoniazid to prevent peripheral neuropathy

110
Q

side effects of rifampicin

A

orange secretions
hepatitis
induction of cytochrome p450

111
Q

side effects of isoniazid

A

peripheral neuropathy

112
Q

side effect of pyrazinamide

A

hyperuricaemia causing gout
and kidney stones

113
Q

side effect of ethambutol

A

optic neuritis- colour blindness and reduced visual acuity

114
Q

what are some risk factors for VTE in pregnancy ?

A

smoking
parity >3
age >35
BMI>30
reduced mobility
pre-eclampsia
multiple pregnancy
gross varicose veins
family history of VTE
thrombophilia
IVF

115
Q

management of meningitis below 3 months:

A

IV cefotaxime + IV amoxicillin

116
Q

management of meningitis over 3 months

A

IV cefotaxime or ceftriaxone

117
Q

what is the most common complication of termination of pregnancy?

A

infection

118
Q

how does ovarian hyperstimulation syndrome present?

A

GI side effects - nausea, vomiting, abdominal pain, bloating and diarrhoea
shortness of breath
fever
oliguira
peripheral oedema

119
Q

in premature ovarian insufficiency how long should hormone replacement be offered?

A

until the age of 51

120
Q

what two features in child with bornchiolitis might suggest pneumonia?

A

high fever (>39) and persitently focal crackles

121
Q
A

3A (42 decks)

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