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Year 5 😊✌🏼 > Path 4 > Flashcards

Path 4 Flashcards

1
Q

Common radiological findings in rickets

A
  • bowed femurs
  • epiphyseal plate widening
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2
Q

URTI vs LRTI examples

A

URTI
sinusitis
tonsilitis

LRTI
bronchitis
pneumonia
empyema
bronchiectasis
lung abscess

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3
Q

What is empyema?

A

pockets of pus that have collected inside a body cavity

Lungs: collection of pus in the pleural space.
Caused by an infection that spreads from the lung and leads to an accumulation of pus in the pleural space, the infected fluid can build up to a quantity of a pint or more, which puts pressure on the lungs, causing shortness of breath and pain.
Risk factors include recent lung conditions like bacterial pneumonia, lung abscess, thoracic surgery, trauma or injury to the chest.

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4
Q

Examples of compromises to respiratory defenses

A
  • poor swallow (CVA, muscle, alcohol)
  • abnormal ciliary function (smoking, viral infection, Kartagener’s)
  • abnormal mucous (CF)
  • dilated airways (bronchiectasis)
  • defects in host immunity (HIV, immunosuppression)
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5
Q

What is a collapsed lung lobe

A

Lobar collapse refers to the collapse of an entire lobe of the lung

As such it is a subtype of atelectasis

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6
Q

streptococcus on microscopy and sensitivity plates

A

gram +ve diplococci

alpha haemolytic on sensitivity plates

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7
Q

What % of CAP is b/c of strep pneumoniae?

A

30-50%

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8
Q

Presentation of strep pneumoniae pneumonia

A

acute onset
severe pneumonia
fever
rigors
lobar consolidation

almost always penicillin sensitive

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9
Q

How do you manage strep pneumoniae pneumonia

A

penicillin sensitive

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10
Q

What is pneumonia?

A

inflammation of the lung alveoli

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11
Q

mortality of pneumonia

A

5-10%

20-40% are admitted to hospital

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12
Q

Sx of penumonia

A

fever
cough
pleuritic chest pain
SOB

malasie, lethargy, n&v

abnormal CXR

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13
Q

Underlying factors to consider in pneumonia

A

pre-existing lung disease
immunocompromise
geography
seasons
epidemics
travel
exposure to animals

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14
Q

Main organisms causing CAP

A

in most cases, no microbiological ID made.

strep pneumoniae
haemophilus inluenzae
moraxella catarrhalis
staphylococcus aureus
klebsiella pneumoniae

so mainly g+ but can also be g-

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15
Q

Pneumonia pathogens in children and young people - common pathogens

A

0-1 mths- E.coli, GBS, Listeria

1-6mths- Chlamydia trachomatis, S aureus, RSV

6mths-5yrs- Mycolpasma, Influenza

16-30yrs- M pneumoniae, S pneumoniae

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16
Q

Typical and atypical causes of CAP

A

typical (85%)
- S. pneumonia
- H. influenza

Atypical (15%)
- Legionella
- mycoplasma (Epidemics 4-6 years)
- Coxiella burnetii (Q fever)-worldwide, farm animals, hepatitis
- Chlamydia psittaci (Psittacosis)-exposure to birds, splenomegaly, rash, haemolytic anaemia

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17
Q

Ix in ?pneumonia

A
  • FBC, U&E, CRP
  • blood culture
  • sputum MC&S
  • ABGs
  • CXR

Curb-65

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18
Q

CURB-65 score - clinical decision

A

score 2 = ?admit
score 2-5 = manage as severe

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19
Q

components of CURB-65

A

confusion
urea >7mmol/l
RR >30
BP <90 systolic or <50 diastolic
>65yo

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20
Q

What is bronchitis?

A

inflammation of medium sized airways

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21
Q

Main organisms causing bronchitis?

A
  • mainly viruses

S. penumoniae
H. influenza
M. catarrhalis

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22
Q

Physiotherapy in bronchitis

A
  • to remove the secretions
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23
Q

Haemophilus influenzae - microscopy morphology

A

gram -ve coccobacilli

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24
Q

What % of CAP is by H. influenzae

A

15-35%

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25
Q
A

H influenza is more common with pre-existing lung diseasse

may produce beta-lactamase

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26
Q

Legionella pneumophilia - route of transmission and key risk

A
  • inhalation of infected water droplets (aerosol exposure)
  • can result in MOF
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27
Q

What is atypical pneumonia?

A

pneumonia caused by organisms without a cell wall
(mycoplasma, legionella, chlamydia, coxiella)

-> cell wall active abx (e.g. penicillins do not work)

extra-pulmonary complications e.g. low sodium

flu-like prodrome before fever and pneumonia

20% of CAP

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28
Q

When to suspect atypical pneumonia?

A

extra pulmonary features

e.g. hepatitis, low sodium

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29
Q

Abx for atypical pneumonia

A

macrolides (clarithromycin, erythromycin)

tetracyclines (doxycycline)

-> antibiotics that are aimed at the cell wall (e.g. penicillins will not work)

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30
Q

legionella penumophilia

A

aerosol sperad
environmental outbreaks, can be associated with air conditioning
associated with confusion, abdo pain, diarrhoea
lymphopaenia, hyponatraemia
Dx by antigen in serum/urine
sensitive to macrolides

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31
Q

Coxiella burnelli (pneumonia)

A

common in domestic/farm animals
transmitted by aerosol or milk
dx by serology
sensitive to macrolides

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32
Q

Chlamydia psittaci (pneumonia)

A

Spread from birds by inhalation
Dx by serology
Sensitive to macrolides

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33
Q

classical CXR finding in TB

A

upper lobe cavitation

but can vary considerably, can be anything really

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34
Q

Test for TB

A

auramine stain and ziehl nielsen stain

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35
Q

Definition of HAP

A

> 48h in hospital

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36
Q

organisms causing HAP

A

often gram -ve

enterobacteriaciae 31%
staph aureus 19%
pseudomonas spp 17%
fungo (candida sp.) 7%
acinetobacter baumanii 6%

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37
Q

Pneumocystis jirovecii

A

protozoan
ubiquitous in environment, many will have been exposed
insidious onset
dry cough, weight loss, SOB, malaise
CXR ‘bat’s wing’
Dx immunofluorescence on BAL
Rx Septrin (co-trimoxazole)
prophylaxis septrin (e.g. in people with cancer)

test: measure sats at rest and after walking a few steps, they will desaturate

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38
Q

What medication do you treat PCP with?

A

septrin (co-trimoxazole)

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38
Q

What medication do you treat PCP with?

A

septrin (co-trimoxazole)

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39
Q

Different types of aspergillus fumigatus lung infection

A
  • allergic bronchopulmnary aspergillosis
  • aspergilloma
  • invasive aspergillosis
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40
Q

Aspergillus on microscopy

A

flowering spores

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41
Q

Immunosuppression and LRTI - what occurs with what?

A

HIV: PCP, TB, atypical mycobacteria

Neutropenia: fungi e.g. Aspergillus spp

BM transplant: CMV

splenectomy: encapsulated organisms (S. pneumonia, H. influenzae, one more) ?neiseria

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42
Q

microbio lab dx of LRTI

A

sputum/induced sputum *
blood cultures *

BAL
pleural fluid
Ag tests
Ab test
immunofluorescence
PCR

*send pre abx

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43
Q

urine antigen tests for pneumonia

A

S. pneumoniae
legionella pneumophillia

Send in severe community-acquired pneumonia

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44
Q

factors helping pick abx in treatment of RTI

A

community vs hospital
severity of illness
?ventilator

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45
Q

Mx of CAP

A

Follow local guidelines

Mild/moderate: Amoxicillin or erythromycin/clarithromycin

Moderate/severe: hospital admission
- augmentin (co-amoxiclav) and clarithromycin
- if allergic: cefuroxime and clarithromycin

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46
Q

Mx of HAP

A

1st line: Ceftazidime/Ciprofloxacin +/- vancomycin

2nd/ITU: Piperacillin/tazobactam AND vancomycin

Specific therapy:
MRSA: Vancomycin.
Pseudomonas: Piperacillin/tazobactam or Ciprofloxacin +/- gentamicin.

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47
Q

Diabetes definition

A

Fasting plasma glucose over 7.0mM

HbA1c >6.5% (48mmol/mol)

OGTT of > 11.0mM

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48
Q

causes of metabolicc alkalosis

A

H+ loss e.g. vomiting
hypokalaemia
ingestion of bicarbonate

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49
Q

Formula for osmolality

A

2 (Na+K) + urea + glucose

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50
Q

Anion gap formula

A

Na + K - Cl - bicarb

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51
Q

Causes of hypokalaemia

A
  1. intestinal loss (diarrhoea, vomiting, fistula)
  2. renal loss (mineralocorticoid excess, diuretics, renal tubular disease)
  3. redistribution (insulin, alkalosis)
  4. decreased intake (rare!!)
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52
Q

Cushing’s with severe hypokalaemia

A

ectopic ACTH production likely

there are no RCTs proving this but Karim Meeran said this

How? high levels of glucocorticoid bind to aldosterone receptor causing hypokalaemia

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53
Q

Causes of ectopic ACTH

A

lung cancer
other cancers

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54
Q

How do you manage ATN?

A

dialysis for 3 weeks

the patient should then recover

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55
Q

What % of population have kidney disease?

A

11%

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56
Q

main barrier in transplantation

A

HLA/MHC

minor histocompatibility complex and ABO blood groups are less important

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57
Q

Chromosome of HLA genes

A

6

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58
Q

HLA class 1 and class 2 letters

A

1: A, B, C

2: DP, DQ, DR

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59
Q
A

peptide binding groove present to T-cells

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60
Q

are HLA antigens highly polymorphic?

A

yes, there are many variants one might have

61
Q

Most antigenic HLAs

A

A B and DR

Over the last years we have also learned that DQ mismatches are also quite antigenic

62
Q

What do HLA mismatches refer to? e.g. 0:0:0 or 1:1:0

A

HLA-A
HLA-B
HLA-DR

63
Q

probability of HLA matching with sibling

A

6 MM - 25%
3 MM - 50%
0 MM - 25%

64
Q

tissue typing - what is it?

A

determining the donor and recipient HLA type

via PCR based DNA sequence analysis for HLA alleles to determine the individuals genotype

65
Q

How does HLA disparity cause rejection?

A

T-cell mediated rejection
- phase 1: presentation of donor HLA by APC in the context of recipient HLA
- phase 2: T-cell activation, IL-2 and IL-15 production, help for Ab production by B-cells
- phase 3: effecter phase: graft damage by immune cells (cytotoxic T-cells, monocytes/macrophages)

66
Q

Biopsy of immune T-cell mediated rejection

A

Lymphocytes and macrophages infiltration ( in tubules in renal transplant, this makes the kidneys not filter as well as they should and this makes their creatinine rise; when the patient comes for check ups and Cr is raised you do a real biopsy and may find T-cell rejection)

67
Q
A

T-cell rejection can occur in any solid organ transplant

pancreas - acini
heart - interstitial infiltration in between myocytes

68
Q

Drugs used in T-cell mediated transplant rejection

A
  • calcineurin inhibitors (e.g. tacrolimus)
  • MTOR inhibitors
  • anti proliferative drug like azothiaprine, myciophenolate motefil
  • corticosteroids
    etc.
69
Q

Ab- mediated transplant rejection

A

Phase 1: B-cells recognise foreign HLA
Phase 2: proliferation and maturation of B-cells with anti-HLA Ab production
Phase 3: effector phase; antibodies bind to graft endothelium

70
Q

antibodies in infection - box divided in whether they need complement activation or not

A

complement dependant and complement independent damage to the graft
???

71
Q

microscope of Ab mediated rejection

A
  • capillaries filled with inflammatory cells
  • swollen endothelial cells

in T-cells it is in the interstituum and tubules; in Ab mediated

72
Q

What is worse, T-cell or Ab mediated rejection?

A

acutely they both present the same
T-cell mediated responds well to treatment
Ab mediated is very difficult to treat.

73
Q

are anti-HLA antibodies naturally occurring?

A

No

pre-foremed: transplantation, pregnancy, transfision
post-formed: arise after transplantation

other

74
Q

ABOq

A

glycoproteins on

75
Q

screening for HLA antibodies

A

before transplant

at time of transplant

post transplant

76
Q

types of assay for anti-HLA antibodies

A

cytotoxicity assay (does the recipient serum kill the donor’s lymphocytes in the presence of complement

Flow cytometry: does recipient serum bind to donor lymphocytes

Solid phase assay (more recent): synthetic beads coated with different HLA epitope; if recipient has antibodies they will stick to the bead. Then your run this through flow cytometry

77
Q

Treatment of antibody mediated rejection

A

plasma exchange to remove antibodies

rituximab to deplete B-cells

proteasome inhibition (Velcade)

complement inhibitors (e.f. eculizumab)

IVIg to reduce the production of immunoglobulins globally

78
Q

How do we prevent organ rejection?

A
79
Q

How ado we treat graft rejection?

A
80
Q

What must we balance when treating organ transplant rejection/prphylaxis?

A

need for immunosuppression

vs

risk of infection/malignancy/drug toxicity

81
Q

Tx of post transplant lymphoproliferative disease

A

malignant transformation f B-cells
associated with EBV infection

reduce IS drugs
sometimes give chemotherapy

82
Q

Which cells cause damage in T-cell mediated rejection effector phase?

A

T-cells and macrophages/monocytes

83
Q

What does TRH stimulate?

A

TSH and prolactin

84
Q
A

If PRL is >6000 and the patient is not pregnant it is always a prolactinoma

85
Q

DA agonists

A

cabergoline and bromocriptine

86
Q

dynamic test for acromegaly

A

OGTT

87
Q

best treatment for acromegaly

A

surgery

if suitable for the patient, surgery is 1st line

radiotherapy, cabergoline and octreotide are also options

88
Q

What is the mechanism for spherocyte production in autoimmune haemolytic anaemia?

A

partial membrane loss due to spleen taking bits off?? relsiten to this part or read

89
Q

What is the mechanism for spherocyte production in hereditary spherocytosis?

A

inability to assemble membrane correctly due to genetic mutation

90
Q

In what conditions do you get DAT+ve acquired haemolytic anaemia?

A

CLL
lymphoma
SLE
rheumatoid

myeloid d/o don’t have association with acquired haemolytic anaemic; not all because the patient would be dead from sepsis or on treatment before this could develop

patients with any disease of the immune system, e.g. malignant (CLL, Lymphoma) or non-malignant e.g. SLE or rheumatoid

91
Q

causes of mediastinal masss

A

teratoma
thymoma
terrible lymphoma

3 Ts

occasionally B cell lymphomas

92
Q

why do teratomas cause widening of the mediastinum?

A

?

93
Q

What are the major pathogens in surgical site infections?

A

MSSA
MRSA
E coli
Pseudomonas aeruginosa

94
Q

What type of bacteria is pseudomonas?

A

gram -ve gammaproteobacteria
rod shaped
polar flagellated

it is a MDR organism

95
Q

what dose of bacteria in surgical site increases risk of SSI?

A

If surgical site is contaminated with
> 10^5 microorganisms per gram of tissue, risk of SSI is increased.

dose of bacteria needed is much lower if there is foreign material present (e.g. silk suture)

96
Q

Levels of SSI

A

Superficial incisional- affect skin and subcutaneous tissue

Deep incisional- affect fascial and muscle layers

Organ/space infection- any part of anatomy other than incision

97
Q

Neisseria meningitidis - what type of bacteria

A

gram -ve meningococcus

98
Q

RFs for SSI

A

older age (>75)
obesity
underlying illness (ASA >=3; diabetes;l malnutrition; low serum albumin; radiotherapy; steroid use; rheumatoid arthritis;
Smoking

99
Q

Why is smoking associated with an increased risk of SSI?

A
  • Nicotine delays primary wound healing
  • Peripheral vascular disease
  • Vasocontrictive effect of reduced oxygen-carrying capacity of blood

-> Encourage tobacco cessation
-> Smoking duration and number of cigarettes smoked relevant

100
Q

RA - how to manage DMARDs to reduce the risk of SSI

A

Stop disease modifying agents for 4 weeks before and 8 weeks post-op.

101
Q

How much does diabetes increase risk of SSI? How should you control glucose?

A

2-3x increased risk

Association with post-op hyperglycaemia

-> Control blood glucose. HbA1C < 7

102
Q

measures to decrease risk of post op infections

A
  • pre-surgery skin decontamination - no difference if chlorhexidine or soap/bar is used; shower the day of or before surgery
  • hair removal - do not shave because micro-abrasions can increase risk of infection; DO NOT remove hair unless it will interfere with surgery
  • nasal decontamination (important RF for SSI following cardiothoracic surgery)
  • prophylactic antibiotics
103
Q

ABx prophylaxis in surgery - when should bactericidal concentration be achieved?

A

at incision

give abx at induction of anaesthesia

104
Q

What to do intra-op to reduce the risk of SSI?

A
  • keep number of people in theatre to a minimum
  • ventilation
  • sterilisation of surgical instruments
  • antiseptic skin prep
  • asepsis and surgical technique
  • normothermia
  • oxygenation
105
Q

SA stats

A

Incidence is 2-10 cases per 100,000
In patients with RA incidence is 28-38 per 100,000 population.
Mortality is 7-15%
Morbidity is 50%

106
Q

RFs for SA

A

Rheumatoid arthritis , osteoarthritis, crystal induced arthritis
Joint prosthesis
Intravenous drug abuse
Diabetes, chronic renal disease, chronic liver disease
Immunosuppression- steroids
Trauma- intra-articular injection, penetrating injury

107
Q

SA pathophys

A

Organisms adhere to the synovial membrane, bacterial proliferation in the synovial fluid with generation of host inflammatory response.

Joint damage leads to exposure of host derived proteins such as fibronectin to which bacteria adhere

108
Q

Bacterial factors in SA

A

S.aureus has receptors such as fibronectin binding protein that recognise selected host proteins.
Kingella kingae synovial adherence is via bacterial pili

Some strains produce the cytotoxin PVL ( Panton-Valentine Leucocidin) which have been associated with fulminant infections.

109
Q

Host factors in SA

A

Leucocyte derived proteases and cytokines can lead to cartilage degradation and bone loss.
Raised intra-articular pressure can hamper capillary blood flow and lead to cartilage and bone ischaemia and necrosis.

Genetic variation in expression of cytokines may lead to differential susceptibility to septic arthritis.

110
Q

Causative organisms in SA

A

Staph. aureus 46%
- Coagulase negative staphylococci 4%
Streptococci 22%
Streptococcus pyogenes
Streptococcus pneumoniae
Streptococcus agalactiae
Gram negative organisms
-E.coli
- Haemophilus influezae
- Neisseria gonorrhoeae
- Salmonella
Rare- Lyme, brucellosis, mycobacteria, fungi

111
Q

Ix for SA

A

Blood culture before antibiotics are given

Synovial fluid aspiration for microscopy and culture
ESR,CRP
-Traditionally a synovial count> 50,000 cells/mm3 used to suggest septic arthritis
(Negative culture result does not exclude septic arthritis)

112
Q

Imaging in SA

A

US- confirm effusion and guide needle aspiration

MRI- joint effusion, articular cartilage destruction, abscess, contiguous osteomyelitis

113
Q

locaalisation of vertebral osteomyelitis

A

cervical- 10.6%
cervico-thoraco- 0.4%
lumbar 43.1%

114
Q

Sx of vertebral osteomylitis

A

Back pain- 86%
Fever- 60%
Neurological impairment 34%

115
Q

Commonest causative organisms in vertebral osteomyelitis

A

S.aureus- 48.3%
CNS- 6.7%
GNR- 23.1%
Strep- 43.1%

116
Q

How can you get vertebral osteomyelitis?

A

Acute haematogenous

Exogenous
- after disc surgery
- implant associated

117
Q

Ix for vertebral osteomyelitis

A

MRI: 90% sensitive
Blood cultures
CT/ open biopsy

118
Q

Mx of vertebral osteomyelitis

A
  • Six weeks treatment
  • Longer treatment if undrained abscesses/implant associated
  • Surgery if there is spinal cord compression
119
Q

chronic osteomyelitis Sx

A

Pain
Brodies abscess
Sinus tract

120
Q

Ix for chronic osteomyeltitis

A

MRI
Bone biopsy for culture and histology

121
Q

Masquelet technique

A

used for chronic osteomyelitis

Radical sequestrectomy
Removal of foreign bodies; filling the defect with antibiotic loaded cement spacer and external fixation

In 6-8 weeks , remove the cement spacer, and fill the defect with autologous bone graft

122
Q

Sx of prosthetic joint infection

A

Pain
Patient complains that the joint was ‘never right’
Early failure
Sinus tract

123
Q

Causative organisms of prosthetic joint failure

A

Gram positive cocci
-coagulase negative staphylococci
-staphylococus aureus
Streptococci sp
Enterococci sp

Aerobic gram negative bacilli
Enterobacteriaceae
Pseudomonas aeruginosa

Anaerobes
Polymicrobial
Culture negative
Fungi

124
Q

Traffic light system for risk of Prosthetic joint infection

A

Fig 1

https://online.boneandjoint.org.uk/doi/full/10.1302/0301-620X.103B1.BJJ-2020-1381.R1#F1

  1. PJI unlikely
  2. Infection likely
  3. PJI confirmed
125
Q

Intraoperative Microbiological sampling

A

Tissue specimens from at least 5 sites around the implant

Histopathology – infection defined as >5 neutrophils per high power field.

If 3 or more specimens yield identical organisms, this is highly predictive of infection (sensitivity 65%, specificity 99%)

126
Q

Single Stage Revision (surgery)

A

Remove all foreign material and dead bone

Change gloves, drapes etc

Re-implant new prosthesis with antibiotic impregnated cement and give iv antibiotics .

127
Q

Endo Klinik single stage revision

A

Aspirate joint to identify pathogen
Excision of infected tissue , synovectomy
Add antibiotics to bone cement according to culture results
Implantation of a cemented hip or knee prosthesis using antibiotic loaded cement
Give 7-10 days of iv antibiotics
Culture drain tips
Success rate is 89% in 2002

128
Q

Two stage revision (surgery)

A

for prosthetic joint infection

Remove prosthesis
Take samples for microbiology and histology
Period of iv antibiotics (6weeks). Stop antibiotics for 2 weeks
Re-debride and sample at second stage
Re-implantation with antibiotic impregnated cement
No further antibiotics if samples clear
OPAT

129
Q

DAIR (surgery)

A

( debridement, antibiotics and implant retention)

for prosthetic joint infection

Within 3 weeks of operation
Tissue sampling
Radical debridement
Exchange of modular components
Antibiotics

130
Q

Causes of abnormal colliery function?

A

smoking
viral infection
Kartagener’s syndrome

131
Q

Kartageners syndrome

A
  • rare
  • autosomal recessive
  • triad of: situs inversus, chronic sinusitis, bronchiectasis
  • larger group of ciliary motility disorders called primary ciliary dyskinesias
132
Q

Mx of Bronchitis

A

bronchodilation
physiotherapy
+/- abx

133
Q

features of H influenza pneumonia

A

15-35% of CAP
more common in pre-existing lung disease
may produce beta-lactamase
more commonly presents as bronchopneumonia

134
Q

Moraxella catarrhalis gram stain

A

g-

135
Q

klebsiella pneumoniae gram stain

A

g-

136
Q

What is the difference between bronchopneumonia and segmental pneumonia

A

?

137
Q

How do you culture legionella pneumophilia?

A

buffered charcoal yeast extract

138
Q

What causes bat wing on CXR?

A

Pneumocystis jirovecii

139
Q

Pneumocystis jirovecii CXR finding

A

bat wing

140
Q

Mx of Pneumocystis jirovecii pneumonia

A

Rx Septrin (Co-trimoxazole)

prophylaxis: septrin

141
Q

Management of invasive aspergillosis

A

Amphotericin B

142
Q

Who gets invasive aspergillosis?

A

immunocompromised poeple

143
Q

Sx of Allergic bronchopulmonary aspergillosis

A

Chronic wheeze, eosinophilia
Bronchiectasis

144
Q

Sx of Allergic bronchopulmonary aspergillosis

A

Chronic wheeze, eosinophilia
Bronchiectasis

145
Q

Aspergilloma

A

Fungal ball often in pre-existing cavity
May cause haemoptysis

146
Q

abx for MRSA HAP

A

Vancomycin.

147
Q

abx for pseudomonas HAP

A

Piperacillin/tazobactam or Ciprofloxacin +/- gentamicin.

148
Q

Ab tests in pneumonia

A

Only useful on paired serum samples

Usually collected on presentation and 10-14 days later

Look for rise in antibody level over time

Most useful for organisms that are difficult to culture eg:
- Chlamydia
- Legionella

149
Q

Which pathogen (causing pneumonia) can immunofluorescence be used for dx?

A
  • PCP – Pneumocystis carinii (now renamed P. jiroveci) immunofluorescence is the only common IF test used in microbiology laboratories
  • Antibody labelled with fluorescent dye
  • Technique often used in Virology
  • May also be detected by Silver stain in cytology lab

Year 5 😊✌🏼 (53 decks)

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