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24 Cards in this Set

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Name the classes of beta-lactams
■Penicillins
■Cephalosporins
■Cephamycins
■Carbapenems
■Monobactams
■Beta-lactamase inhibitors
Beta-lactams mechanism of action
Inactivation of bacterial enzymes (penicilling-binding-proteins) that are involved in the 3rd stage of cell wall synthesis (peptidoglycan cross-linking)
This leads to activation of the autolytic system
Describe some mechanisms of resistance to beta-lactms
1. downregulation of porins through which beta lactams travel
2. beta-lactamases, which cleave beta-lactams
Describe the classification of penicillins
1. penicillin G
2. anti-staphylococcal penicillins e.g. nafcillin
3. broad spectrum penicillins (a) 2nd generation e.g. amoxicillin, ampicillin
(b) 3rd generation e.g. ticarcillin
(c) 4th generation e.g. piperacillin
Describe the range of action of penicillin G
gram positive cocci (non resistance)
gram negative cocci (e.g. Neisseria)
gram positive rods e.g. Listeria
most anaerobes
Describe the range of activity of antistaphylococcal penicillins
active against penicillinase producing organisms, but are ineffective against oxacillin-resistant organisms. in oxacillin sensitive organisms, a penicillin is preferred to vancomycin
what additional vaccines are required in a child found to have asplenia (or post splenectomy)
For pneumococcal, a further dose of 7-valent after one year of age, then 23-valent at 4 to 5 years, or two months after 7 valent. No further haemophilus is needed. One further meningococcal vaccine is needed.
what conditions are associated with functional asplenism?
sickle cell disease, thalassaemia major, coeliac disease, sarcoidosis, S.L.E., ulcerative colitis, amyloidosis
when should vaccination be undertaken in a patient having splenectomy?
for elective splenectomy, vaccination can commence at least 2 weeks prior to ensure optimal antibody response. For emergency splenectomy, immunisation should be delayed until at least two weeks after.
features of nephrotic syndrome
- Proteinuria >40 mg/m2/h
- Hypoalbuminemia.
- Edema.
- Hyperlipidemia.
- Lipiduria
is IgA nephropathy more common in males or females?
males
what is the usual presentation of IgA nephropathy?
- often benign
- gross haematuria, often 1-2 days within onset of an URTI or GI infection, may be assoc with loin pain
- can present with microscopic haematuria and/or proteinuria (usually mild proteinuria)
- acute nephritic syndrome, nephrotic syndrome or combined nephritic-nephrotic syndrome, can be assoc. with mild-mod hypertension
- NORMAL serum C3, helps to distinguish it from poststrep GN
in what percentage of patients with IgA will serum IgA be elevated?
15-50%
what is the usual outcome of IgA nephropathy in children?
- usually doesn't lead to significant kidney damage
- 20-30% will develop progressive disease over 20y i.e. in adulthood
what are the poor prognostic indicators at presentation with IgA nephropathy?
- diminished renal function
- persistent hypertension
- heavy/prolonged proteinuria
- histologic evidence of diffuse mesangial cell proliferation, crescent formation, glomerulosclerosis, tubulointerstitial changes incl. inflammation & fibrosis
what is the primary treatment of IgA nephropathy?
- BP control
- fish oil (omega-3 polyunsaturated fatty acids) decreases rate of disease progression
- immunosuppression with CTS +/- other Rx in some patients
- ACE/ARBs can reduce proteinuria and retard disease progression
- ??tonsillectomy (not proven)
- kidney transplantation - after which recurrence is frequent but usually the kidney survives
Common infections/conditions caused by S. pyogenes (GAS)
- Pharyngitis (Group A beta-haemolytic strep)
- Impetigo, pyoderma
- Scarlet fever
- Erysipelas
- Necrotizing fasciitis
- Perianal cellulitis, cellulitis
- Septicaemia, pneumonia, carditis, osteomyelitis, suppurative arthritis
- Toxic shock syndrome
- Rheumatic fever
- Glomerulonephritis
Describe S. pyogenes M types & association with pharyngitis, skin infections, rheumatic fever and glomerulonephritis
Those strains that cause pharyngitis are more likely to be associated with acute rheumatic fever
Those strains that cause skin infections, but also some pharyngeal strains (M type 12) are nephritogenic
What are the severe invasive GAS infections?
Septicaemia
Toxic shock syndrome
Necrotising fasciitis
Describe impetigo (streptococcal pyoderma)
Usually caused by colonisation of healthy skin which is disrupted e.g. by insect bite or abrasion. Can also pass skin to skin.
Describe virulence & antigens of S. pyogenes
- M protein which resists phagocytosis, there are many different types hence recurrence of strep infections - will never get complete immunity due to large number of types
- Pyrogenic exotoxins (types A, B, C), responsible for scarlet fever rash & for TSS
- streptolysin O is an antigen useful for measurement (ASOT)
- anti-DNAase can also be measured
Define failure to thrive
1. < 3-5th centile (excluding constitutional growth delay)
2. Growth dropping across 2 centiles
3. Low weight for height
Causes of FTT
1. Inadequate intake (psychosocial, anatomical e.g. cleft, neurological)
2. Inadequate appetite (systemic illness, hypotonia/weakness, CP, neuro, reflux)
3. Inadequate absorption (e.g. CP, vomiting, NEG, intestinal obstruction, diarrhoea), coeliac
4. Increased requirements (e.g. hyperthyroid, malignancy, chronic disease, heart disease)
Investigations for FTT
Bloods: FBC, EUC, ?CMP/B12/folate/Fe studies, TFTs
Bone age to confirm
Sweat test, coeliac screen