Paediatrics: Part 2 Flashcards
What structures produce ADH
Suproptic and paraventricular nuclei of the anterior pituitary gland -> stored in posterior.
Role of ADH
Causes re-absroption of water at the collecting ducts and vasoconstriction (i.e., vasopressin!)
What receptor does ADH bind o and what happens
V2, causes aquaporins to embed into the cell membrane, only allowing water to move back into the blood to improve blood osmolality
This makes urine more concentrated
What is Diabetes Insipidus
When too little water is re-absorbed from the urine. Leads to polyuria
Why do we get polydipsia in diabetes insipidus
Because of reduced osmolality in the blood, causing osmoreceptors to stimulate the thirst centre in the medulla.
Central Diabetes Insipidus vs Nephrogenic Diabetes
Lack of ADH -> Central Diabetes Insipidus
REDUCED ADH response by the kidneys -> Nephrogenic Diabetes
What structures contribute to central diabetes inspidus
Hypothalamus can’t produce ADH
Pituitary gland can’t store ADH
Causes of central diabetes insiipidus
- Pituitary Tumours
- Head Trauma
- Head Surgery
- Ischaemic Encephalopathy
What causes nephorgenic Diabetes Insipidus
More often than not, Hereditary Genetic defects in receptors.
Lithium - Reduces production of aquaporin proteins in collecting duct
Hypokalaemia
Hypercalcaemia
Demeclocycline (aquaporine receptor antagonist)
Symptoms of Diabetes Inspidius
- Polyuria (>3L of dilute urine/day)
- Polydipsia
Increase in plasma osmolality: Fatigue, nausea, poor concentration and confusion
How to diagnose DI
- Blood osmolality Test (>290)
- Urine specific Gravity <10006 (too dilute)
- Low Hyperosmotic volume concentration
- Water Deprivation Test to measure hourly measurements of urine volume (osmolality will stay dilute <300)
- Desmopressin test: Causes an increase in urine osmolality by 50% (central), if no change (nephrogenic)
Central vs nephrogenic
Low ADH vs Normal or High ADH
Treatment of central DI
Desmopressin and water
Treatment of nephrogenic DI
- Thiazide Diuretics to get rid of Na+
2. Or Amiloride (potassium sparing)
What is SIADH
The body makes too much ADH
What causes SIADH
- Ectopic ADH secretion from small cell lung carcinoma
- CNS surgeryy or head trauma that releases all stored ADH in pituitary gland.
- Pneumonia, COPD
- Cyclophosphamide (increases ADH receptors on principal cells)
Pathophysiology caused by SIADH
- Increase in ADH = Increased water reabsorption
ECF expands and water moves into ICF to correct but ECF still has a lot of extra cellular fluid = dilution hyponatraemia (Na+ amount is normal but in larger fluid) = euovolaemic hyponatraemia.
NO oedema as. Na+ is the same.
Impacts of SIADH on the body
- Increased blood volume and pressure
- More ANP or BNP to dilate BP and improve GFR to excrete water and Na+
- Reduced Renin release from kidneys = less aldosterone and angiotensin 2 to reduce sodium and water reabsorption
Cerebral oedema and Seizures = most important complication
Diagnosis of SIADH
- Hyponatraemia
- Reduced serum osmolality
- Increased urine osmolality
How to treat SIADH
- Tolvaptan which antagonises vasopressin receptors.
- FLuid Resus and IV hypertonic saline.
SLOWLY to prevent osmotic demyelination syndrome.
What food can cause red urine
Beetroot
What drug may cause red urine
Rifampicin
What is proteinuria in children
Over 0.15g/24hrs
What threshold defines a UTI
> 10 ^ 5 microorganisms
Clinical features of UTIs in infants
- VOmiting or diarrhoea
- Poor feeding/failure to thrive
- Prolongued Neonatal Jaundice
Upper vs lower UTI symptoms
- Fever, vomiting and loin pain vs dysuria, frequency, mild abode pain and enuresis.
Treatment of UTIs in children
Trimethoprim
What is the antiobiotic prophylaxis for recurrent UTIs
Trimethoprim oral
What is vesicoureteric reflux
- The retrograde flow of urine from the bladder into the upper urinary tract
What causes VUR
- Post surgery or congenital
What are the grades of vesicoureteric reflux
- Ureter
- Ureter, pelvis and calyces but no dilatation
- Mild dilation but no blunting of fornices
IV: obliteration of sharp angle of fornices
How to diagnose vesicoureteric reflux
- Micturarting cystourethrogram (urinary etherisation and radio contrast medium)
- Indirect Cystogram (scan)
Surgical treatment for VUR
STING, however they often spontaneously resolve.
Pre-Renal causes of AKIs
- Hypovolaemia (e.g., gastroeneritis, DKA or haemorrhage)
- Nephrotic syndrome
- Peripheral vasodilation (sepsis)
- Drugs (ACE inhibitors)
Renal causes of AKIs
- Acute tubular necrosis
- Interstitial nephritis
- Glomerulonephritis
- HUS
- Cortical necrosis
- Pyelonephritis
- Nephrotoxic drugs (NSAIDs)
- Tumour lysis syndrome
- Renal artery thrombosis
Post-renal causes of AKI
- Obstruction
- Calculi
- Tumours (rhabdomyosarcoma)
- Neurogenic bladder
- Post urethral valves
Investigations for AKIs
- Urinalysis with microscopy, cut,ture and protein:creatinine ratio
Myoglobin in urine (rhabdomyolysis)
Cultures: Stool E.Coli
Throat swab
Radiology: US Kidneys and bladder
Complications of AKIs
- Hyperkalaemia
- Metabolic Acidosis
- Hypertension
- Shock
- Fluid Overload
- Hypocalcaemia
- Hyponatraemia
How are fluids managed in AKIs
- Furosemide
Monitor Electrolytes at least 12-hourly until stable
Indications for Dialysis
- Severe Heyperkalaemia
- Urea > 40 mmol/L
- Rising urea and creatinine
- Encephalopathy.or seizures
- Untronctrolled Han
- Symptomatic fluid overload (cardiac failure)
What is the NICe criteria for detecting cute kidney injury
- Fall in urine outpiut to less than 0.5ml/hr for over 8 hours in children
- a 25% fall in children egfr over past 7 days
When should children be referred for renal replacement therapy
- Hyperkalaemia
- Metabolic acidosis
- Symptoms or complications of uraemia
- Fluid Overload
- Pulmonary Oedema
Haemodialysis vs peritoneal dialysis
- Blood is pumped out of body vs using the inside lining of your own belly as a filter.
What artery is used in haemodialysis
Femoral or jugular
What are the stages of CKD
- > 90 GFR and kidney damage with/without increased GFR
- 60-89
- 30-59
- 5-29
- <15
mL/min/1.73 m^2
Formula for GFR
40 * height (cm) / creatinine (mmol/l)
Congenital causes of CKD
- Renal dysplasia
- Obstructive uropathies
- Vesicoureteric reflux nephropathy
Hereditary causes of CKF
- PCKD
- Nephronophthisis
- Hereditary Nephritis
- Cystinosis
- Oxalosis
What are hypospadias
Where the meatus is on the bottom of the urethra.
Three types of hypospadias
- Glanular
- Midshaft
- Penoscrotal
Clinical presentation of hypospoadias
- Foreskin appears as a dorsal hood and not circumferential;;
- Chordee (penis has a hook shape)
- Inguinal hernia
- Crytptorchidism (absence of testes from the scrotum)
Painful urination, recurrent UTIs, sexual dysfunction and infertility.
Investigations for hypospadias
- Excretory Urogram (Rotation anomalies of kidneys, mental stenosis or vesicoureteral reflux)
- USS
- Endoscopy of the urethra to discard urethral anomalies
How are hypospadias treated
- Constructing a new urethra using shaft skin
- Hormone Therapy (mircopenis)
SHOULD NOT UNDERGO CIRCUMCISION
What are Epispadias
- Urethral opening is on the top of urethra
What causes epispadias
6th week of gestation: Genital Tubercle grows in a posterior direction (rectally than cranially)
Three types of epispadias
- Penopubic (most severe)
- Penile
- Glanular
Clinical presentation of epispadias
- Bladder Exstrophy (incomplete closure of abdomen, we can see th balder)
- Micropenis
- Displaced anus and incontinence
- Vesicoureteral reflux
Treatment of Epispadias
Urethroplasty
What causes gross haematuria
- UTIs
- Irritation of meatus and trauma
Nephrolithiasis, SCD, Postinfetcious glomerulonephritis
What causes microscopic haematuria
- Glomerulopathies
- Hypercalciuria
- Nutcracker syndrome
What is Nutcracker syndrome
Compression of the left renal vein
What can cause transient Haematuria
UTIs
Truma
Fever
Exercise
What would we consider as the underlying pathology if there was unilateral flank pain radiating to the groin
Obstruction
What would the underlying pathology be if a patient presented with flank pain, fever, dysuria and frequency or urgency
Pyelonephritis
Where is the haematuria organ if bleeding is happening at the same time as urination
Urethral bleeding
Where is the haematuria origin if bleeding is continuous
Bladder, ureter or kidneys
Where is the haematuria origin if the bleeding is at the end of urinagtion
Bladder Disease.
What is free haemoglobin in urinalysis indicative of
Rhambdomyolysis
What would show up on a urinalysis for glomerular bleeding
- Damaged RBCs
2. Protein excretion > 100 mg/m^3
What would show up on a urinalysis for an extraglomerular disease
- Urinary RBCs undamaged
If the urine culture is negative, what organism could cause UTIs
Adenovirus
GOLD standard for nephrolithiasis
Renal USS: Radiopaque stones
But misses out uric acid stones, small stones and obstructions
What blood test is used to check for post streptococcal glomerulonephritis
Serum C3 raised
Examination of congenital uteropelvic junction obstruction
CAUSES hydronephrosis:
Palpable abdo mass,
UTIs
Haematuria
Failure to thrive
Older children: Intermittent flank pain or abdominal pain
Nausea and Vomiting
Low Urine Output
What diagnostic scan is used to check for hydronephrosis
USS during Dietl’s crisis (pain) as dilated renal pelvis causes the abdo pain
Diuretic Renography
Voiding Cystourethrography
What would be seen in a USS for hydronephrosis
Dilated Renal Pelvis w/ collapsed proximal ureter.
What is the diruetic venography
Measures washout time, if it takes more than 20 mins = obstruction
Blood tests: CBC, Coagulation profile, electrolyte levels and BUN and serum creatinine
How to treat hydronephorsis
Pyeloplasty
What is an ectopic ureter
Abnormal posterior insertion o the ureter
Where can the ectopic ureter insert
Females:
Bladder neck, upper urethra, vaginal vestibule or vagina
Males:
Lower urinary bladder, posterior urethra, seminal vesicles, ductus deferent and ejaculatory duct
Presentation of ectopic ureter
- Epididymo-orchitis
- Sense of urgency
- Flank pain
- UTIs
Never present with inctoninence as ectopic ureter is proximal to the external urethral sphincter.
Female:
Urinary incontinence
UTIs
Urinary Obstruction
Diagnostic for ectopic ureter
- Renal USS, ureter dilated and abnormally low.
2. CT or MRI w/ contrast to pinpoint location of the ureter.
Diagnosis of Vesicocureteral reflux
Voiding Cystourethrogram
What causes vesicoureteral reflux
Usually intravesical ureter is tight by surrounding bladder muscles, stopping it from going back up into the kidneys
Congenital short intravesical ureter or abnormally high voiding pressure like posterior urethral valves stop this from happening.
Clinical Presentation of vesicoureteral Reflux
- Recurrent UTIs
- Urgency
- Burning sensation when urinating
- Decreased Urine Output
- Haematuria
What are posterior urethral valves
- Where the membranous folds within the lumen of the posterior urethra narrow the exit of urine = UTIs and Hydronephrosis
Clinical presentation of posterior urethral valves
MALES: Urgency Flank Pain Diffiiculty with Voiding Abdominal Distention Resp distress, nausea and vomiting UTIs
Diagnosis of posterior urethral valves
Voiding Cystourethrogram: Dilated and Elongated Posterior Urethra.
Cystoscopy for direct observation of the valves.
treatment of Posterior urethral Valves
- Temporary drainage using a catheter.
Most common cause of UTIs
E. coli
treatment of pyelonephritis or complicated UTI
- trimethoprim
What is the initial medical treatment of Nocturnal Diuresis
Desmopressin over 7 weeks
Indications for desmopressin
If rapid onset or an alarm is inappropriate
What is the first line management for nocturnal diuresis
Setting up an alarm as a reward system (wake up when the alarm goes off, go toilet and reset the alarm when your back)
What protein levels distinguish nephritic syndrome and nephrotic syndrome
Nephritic: 1-3.5 g/day
Nephrotic: >3,5 g/ day
Signs and symptoms of nephritic syndrome
- Peripheral Oedema
- Perioriibatal oedema
- HTN
- Oliguria.
Lab tests for nephritic syndrome
- Glomerular Haematuria
- Proteinuria
24-hr protein test: 1-3g a day
What is rapidly progressive Glomerularnephritis
A rapid decrease in the gFR rates over 3 months
Clinical Presentation of Rapidly progressive glomerulonephritis
- Fatigue
- Peripheral Oedema
- Gross Haematuria
- HTN
- Decreased Urine Output
Signs of nephrotic syndrome
- Peiprheral and periorbital oedema
- Ascites
- Pleural effusion
- HTN
Signs and symptoms of nephrotic syndrome
- Hypoalbuminaemia
- Hyperlipidaemia
- High LDLs and Triglycerides
- Lipiduria
What tests are done for Poststrep glomerulonephortis
- Antistreptolysin - O
- Anti-Hyaluronidase
- Anti-Streptokinase
- Anti-NAD
- Anti-DNASE B Antibodies
All raised apart from Antri streoptokinase
- C3 and C4 as these are low, these immune complexes deposit in the sub epithelial space causing inflammation
Signs of IGA Nephropathy (nephritic syndrome)
- Gross Haematuria
- Flank Pain
Accompanied with Acute Upper Respiratory Tract Infections
What can be seen on a Kidney Biopsy for IgA Nephorpathy
- Light Microscope: Mesangial Proliferation
2. Immunofluorescence and Electron Microscopy: IgA Deposits
Extraglomerular signs of IgA Nephropathy
- Symmetrical Rash
- Palpable Purpura
- Migratory Arthritis
- GI (nausea, vomiting and Abdominal Pain)
This is IgA vasculitis
What is Alport Sydnrome
Genetic Condition: Renal Failure + Hearing Loss
Symptoms of Alport Syndrome
Anterior Lenticonus (anterior part of the lens is conical)
Test for alport syndrome
- C3 - Normal
- C4 - Normal
- ANA Antibodies - Neg
If low, usually the following:
C3 glomerulopathy and Lupus Nephritis - need to be rules out
Then genetic testing
Treatment of Nephritic Syndrome
- ACE Inihbitors
- ARBs: Losartan
- Furosemide
Why is Nifedipine given in post strep glomerlonephritis instead of an ACE Inhibitor
As ACE Inhibitors can cause hyperkalaemia
Indications for harm-dialysis in Nephritic syndrome
Volume overload
Hyperkalaemia
Uremia
How is Post strep part of glomerulonephritis treated
Oral Penecillin
Treatment of IgA Nephropathy
Glucocorticoids in those with declining eGFR, proteinuria <1 g/ day even when on ACEi, Active disease (proliferative changes in the glomerulus)
IV Methylprednisolone 3 days or Oral Prednisolone (2 months and reduced)
Treatment of Rapidly Progressive Glomerulonephritis
- IV Methylprednisolone
2. Oral Prednisolone or Oral Cyclophophasmide
How is IgA Vasculitis treated
- Naproxen and bed rest
2. Oral Prednisolone if pain is persistent
If Proteinuria > 0.75 g / day, nephroyoc syndrome or rapidly progressive glomerulonephritis, what should be done
IV Methylprednisolone, Oral Prednisolone for 6 months
Treatment fo aport syndrome
ACEi or ARBs. for poretinuria
What diseases can cause nephrotic syndrome
- DM
- HIV
- Hep B
- Hep c
- SLE
- APL
What agent causes acute glomerulonephritis
Staph aureus and salmonella
What is the most common nephrotic syndrome seen in children
Minimal Change Disease
What is minimal change disease
The negative charges on the foot processes of podocytes stop immunoglobulins from getting through but allows albumin to be lost = minimal change disease as effacement to the membrane can’t be seen on light microscopy
What is minimal change disease associated with
Idiopathic but associated with Hodgkin’s lymphoma
Diagnosis of minimal change disease
Electron microscopy to see effacement of foot processes
Treatment of minimal change disease
Corticosteroids
What triggers haemolytic uraemia syndrome
An episode of bloody diarrhoea
What usually causes HUS
E.coli
Pathophysiology of HUS
- E coli attaches to intestinal wall and secretes shigella-like toxin
- Aborbes by intestinal blood vessels and picked up by eosinophils
- Taken.to the kidneys to be excreted
- Endothelial cells have Gb3 receptors with high affinity to shigella-like toxin
- Shigella-like toxins enters cell preventing aminoacyl-tRNA from binding to the ribosome = NO PROTEIN SYNTEHSIS and APOPTOSIS
- Then we get thrombotic Thrombocytopenia purpura:
Clots form inappropriately from vWF: ADAMTS13 is not active and does not cleave vWF, causing lots for no reason including the kdineys.
What is Atypical HUS
No initial diarrhoea, caused by endothelial cell damage or medications or autoimmune causes
Triad of findings in HUS
- Microangiopathic Haemolytic anaemia
- Thrombocytopenia
- Acute renal failure
What is microangiopathic haemolytic anaemia
Damage caused by platelets which act as boulders. RBCs move over the platelets and disintegrated and are haemolysed. This results in anaemia as there are reduced RBCs.
Symptoms of Anaemia
Thrombocytopenia purport can cause blood clots in brain (strokes, seizures and fever)
Diagnosis of HUS
- Schisocytes on blood smear (broken down cells from the boulder)
Treatment of TTP HUS
Plasmapharessis
Treatment of HUS
Supportive
Lymphadenopathy in lymphomas vs infections
Infections: Tender and mobile
Lymphomas are fixed and non tender
Diagnosis of lymphomas
Complete excision and microscopy of the lymph node
What cells differentiate between Hodgkin and non-hodgkin lymphomas
Reed-Sternberg cells
Properties of reed-sternberg cells
Bilobed nucleus with clear space surrounding it
What is the name of th staging system in lymphomas
Ann Arbour Staging System
Describe the Ann arbour staging system
1: 1 lymph node
2: Multiple lymph node regions on 1 side of the diaphragm
3: Multiple lymph nodes on both sides of the diaphragm
4: Metastasise to other organs
In what stages are Hodgkin’s lymphomas seen
Stage I or II
In what stages are non-hodgkin’s lymphomas seen
Stage III or IV
Where do Hodgkin’s lymphoma arise from
B-Cells in germinal center
Onset of Hodgkin’s lymphoma
2 peaks:
15-30
50+
What is classical vs non-classical Hodgkin’s lymphoma
Classical: Reed-Sternberg cells (CD15 and CD30)
Non-Classical: Popcorn cells (CD20 + CD45 positive)
What lymph nodes are primarily affected in Hodgkin’s lymphoma
- Cervical
- Axillary
- Mediastinal
Symptoms of Hodgkin’s lymphoma
- PEL EBSTEIN FEVERS
Mediastinal: Cough and SOB by pressing against airways
Hoarseness
Superior Vena Cava Syndrome
Pleural Effusion
MINIMAL CHANGE DISEASE
Treatment of stage I and II hodgkin’s
ABVD
Treatment of stage III and IV
BEACOPP
Treatment of popcorn cells
Rituximab
Difference between lymphadenopathy of Hodgkin’s and non Hodgkin’s lymphoma
Hodgkin’s: Cervical ,mediastinal and axillary
Non-hodgkin’s: Disseminated
Most common type of non-hodgkin’s lymphoma
Large B cell LYMPHOMA
Name four types of non Hodgkin’s lymphoma
- Large diffuse B cell lymphoma
- Follicular B cell lymphoma
- Burkitt Lymphoma
- Mantle cell lymphoma
- Marginal Zone Lymphoma
Which lymphoma can happen secondary to sjogre syndrome and H. pylori infection
Marginal Zone Lymphoma (non Hodgkin’s)
treatment of non-hodgkin’s lymphoma
R-CHOP
What cells form wills tumours
Metanephric blastemal cells
Role of metanephric blastemal cells
Used in kidney development
What gene is involved in films tumours
11p13 - code for WT1
Mostly idiopathic causes of mutations
What is WAGR syndrome
Sometimes in film’s tumour, deletion of WT1 causes neighbouring PAX6 gene to also be lost:
Wilm’s tumour
GU malformations
Aniridia (no iris)
mental Retardation
What is Denys-Drash Syndrome
Deletion of neighbouring genes in films’ tumour causes early onset nephrotic syndrome and male pseudohermaphroditism
What is Beckwith Widemann Syndrome
Deletion of WT1 causes neighbouring gene WT2 to be lost:
Wilm’s tumour
Macroglossia
Organomegaly
Hemihypertrophy
What do metanephric blastemic cells differentiate into
Stromal and epithelial cells
What structures are seen in a film’s tumour mass
Abortice structures of the nephron: tubules and glomerulus
What is a triphasic blastoma
Where blastemal, stroll and epithelial cells are all seen in the mass
Clinical presentation of films’ tumour
- HTN
- Flank mass that’s unilateral
- Haematuria
Treatment of film’s tumour
- Nephrectromy and Chemo
Clinical presentations of retinoblastomas
- LEUKOCORIA/ WHITE PUPILLARY REFLEX(abnormal white reflection from the eye)
- Strabismus (eyes pointing in different directions)
- Red Eye, tearing, corneal clouding, discolouration of the iris, and hyphema/glaucoma
RED FLAG SYMPTOMS
What ocular examinations would be done for a retinoblastoma
- Red Reflex Test (absent)
- Visual Acuity Tests (decreased)
- Slit Lamp Examination (ciliary injection or glaucoma)
- Fundoscopy of both eyes under anaesthesia
- Dilated fungus examination
- A and B scan USS for tumour height and thickness, retinal detachment and clarification
What would an A scan show
Variable reflectivity
What would a B scan show
Mass filling the globe with calcification
Why would MRI be needed in a retinobalstoma
Optic Nerve Involvement
2. Extraocular extension
Treatment of retinoblastoma
- Enucleation:
Systemic Chemotherapy with focal consolidation
Intraarterial chemotherapy
Cryopexy/ laser photocoagulation n
AVOID RADIOTHERAPY
What cells make up neuroblastomas
Neural Crest Cells
Role of neural crest cells
Development of the sympathetic nervous system
What is the most common cancer in infants (under 5)
Neuroblastoma
What do neural crest cells do in the 5th week of life
They migrate from the cranial end down the spine and start differentiating into the sympathetic ganglions.
Also differentiate into:
Adrenal Medulla
Where do neuroblastoma typically develop
In the adrenal medulla (but can happen anywhere along the sympathetic chain)
What cells are founding an undifferentiated neuroblastoma
Mostly Neural Crest Cells (Small Round Blue Cells, little cytoplasms and large nuclei)
What structures are specific to poorly differentiated neuroblastomas
Neuropils (bright red network of nerve fibres)
More cytoplasm
What structures are found specific to differentiating neuroblastomas
- LOTS OF CYTOPLASM
Shwann Stroma (Myelin ingredient)
Why do neuroblastomas metastasise so easily
Because they are highly sensitive to CXCL12 cytokines, and migrate to different organs when they sense them (lumph nodes, liver, bones and marrow)
Symptoms of neuroblastomas
- Fever
- Weight Loss
- Sweating
- Fatigue
from cytokine release
Location:
Thorax: grows into lungs - sob
Neck: presses on facial nerves (horners syndrome)
Spine: Muscle weakness, bowel and bladder problems
Adrenal Medulla: Painful abdo mass
Bone Marrow: Fatigue, easy bruising and infecions
Most common metastasis site for neuroblastoimas
Bones = fractures at the base of the skull!
Causes perirobital ecchymosis as fluid builds around the eyes.
Diagnosis of neurbolastoma
Serum HMA and VMA (breakdown products of noradrenaline and adrenaline)
CT for location and size
MRI
CBC: bone marrow metastasise
Treatment of neurbolastoma
- Surgery, chemo, medication
Which neurbolastoma type has the best prognosis
Differentiating neuroblastoma
Name two bone tumours that primarily affect young children
Osteosarcoma
Ewing’s Sarcoma
Presentation of osteosarcoma and Ewing’s Sarcoma
- Dull Pain that isn’t improved by NSAIDs
- Pain is worse at NIGHT
- Site is swollen and fractures after minor trauma
On what bone are osteosarcoma’s typically found
Femur and Tibia: The metaphysics
On what bone are Ewing’s sarcomas found
Diaphysis on the pelvis and femur
But may affect spine, chest wall and femur too
Where do osteosarcomas and Ewing’s sarcomas commonly metastasise to
Lungs (have a cough or dyspnoea)
What tissue do osteosarcomas derive from
Neuroectodermal Tissue
Investigation findings in osteosarcomas
X Ray:
Medullary and cortical destruction
Moth -eaten appearance
Soft tissue sunburst ossified
Codman’s triangle (new subperiosteal bone)
Lab Test results in osteosarcomas
- Increased Alkaline Phosphatase (high is poor outcome) and LDH
What lab test is checked to see is osteosarcoma therapy is effective
Declining Alkaline Phosphatase rates
Treatment of Osteosarcoma
MAP
Methotrexate
Doxorubicin
Cisplatin
Surgery
More MAP
Characteristic radiograph finding in Ewing’s Sarcoma
Osteolytic lesions (onion appearance)
sharpens fibers (hair on end appearance)
Codman’s triangle
What is Syndeham Chorea
A neurological presentation of rheumatic fever (rapid involuntary movements)
What is PANDAS
An Obsessive Compulsive Tic Disorder
What infection usually causes PANDAS
Strep A infections (alongside Syndeham chorea, rheumatic fever and glomerulonephritis)
What organism usually causes infections in kids from Cats
Bartonella Henselae
What is the first line test that should be done in neonatal jaundice and why
Coombs test:
If positive, indicates that Rh incompatibility which may be causing haemolytic (antibodies against erythrocytes)
If negative: Shows twin to twin transfusion or mother/feotus transfusion (physiological jaundice)
What a febrile seizures
These happen between 6 months to five years following a febrile illness (e.g., respiratory tract infection). These are single epsiodes that subside very quickly.
However, under 18 months do a lumbar puncture to exclude meningitis
What is galactosemia (breast milk jaundice)
A deficiency in GLP, which stops the conversion of galactose to glucose.
Milk contains galactose so causes an abidance of these and results in jaundice, failure to thrive, hepatomegaly
What is distinctive about breast milk jaundice
Infantile Cataracts
What infection is likely to be obtained from plants
Rhus dermatitis, fluid-filled vesicles (type of contact dermatitis from poison ivy, poison sumac and poison oak).
A common side effect of the MMR vaccine
A measles-like rash 10-14 days after vaccination, it’s non infectious and harmless.
E.coli and Cholera vs Shigella
Shigella infection also arises from hand-to hand routes unlike the others which are facet-oral.
E.coli causes water diarrhoea while shigella and salmonella cause bloody diarrhoea.
What is a complication of HUS
DIC, it is known to complicate HUS.
What is Dandy-Walker Syndrome
A congenital brain malformation in which the cerebellar vermis is missing and there is cystic dilation of the fourth ventricle .
Causes increased head circumference, bulging fontanelle and problems with nerves controlling the eyes, face and neck.
What is fifth disease (erythema infectious)
TWO Presentations:
Slapped Cheek Appearance on the face
OR
Lacy, macular truncal rash
the rash does not bother the patient
And B symptoms
What causes fifth disease
Parvovirus B19
Where does fifth disease commonly spread
In daycare (nurseries)
What is ITP
It is a transient condition that follows a viral illness/
What characterises ITP
THROMBOCYTOPENIA with or without cutaneous bleeding in an otherwise well patient.
What is Sturge-Weber SYndrome
A seizure in a child with a unilateral facial birthmark
N gonorrhoea infection vs c trachematis infections in children
Gonnorheoa symptoms show up in the first three days vs 5-14 days in chlamidyia.
What is the most common cause of acute scrotal swelling in children
Torsion of testicular appendage (mimics epidiymitis as the appendage is above the testes and swells).
Where are intracranial germinomas predominantly found
The pineal region or third ventricle (midline of the brain)
What is the most common type of pinealoma
Intracranial germinomas
Symptoms of a pinealoma
Obstructive hydrocephalus
Parinaud Syndrome
What is Parinaud Syndrome
Vertical Gaze and Convergence sight disabilities
What CSF levels are elevated in intracranial germinomas
AFP and B-HCG
What is Focal Segmental Glomerulosclerosis
Only some glomeruli are affected, and just some of them are diseased = Nephrotic syndrome.
What is Leukaemia
Cancer of Bone Marrow Progenitor Cells that spreads into the blood stream
How does Leukaemia affect WBC
> 11 x 10^9 cells/Litre
Four cells arising from myeloid progenitor cells
- Basophils
- Eosinophils
- Neutrophils
- Mast Cells
Three cells arising from Lymphoid cells
- T Cells
- B Cells
- NK Cells.
Role of Basophils
Release histamines during an allergic or asthmatic reaction
Role of eosinophils
Recognition cells of PAMPs
Role of Mast Cells
First line defence against antigens
What is the difference between acute and chronic lleukaemias
ACUTE: Blocking myeloblasts or lymphoblastic progenitor cells from differentiating at all -> immature blast cells
Chronic: Blocking differentiating blast cells into basophils, eosinophils etc -> mature blast cells
Immature are less likely to be good at their job, so we get more B symptoms. Chronic is often asymptomatic and comes up on routine FBCs as mature blast cells can work well.
If in a FBC, the majority of cells are neutrophils, what leukaemia should be suspected
AML or CML
If in a FBC, the majority of cells are lymphocytes, what leukaemia should be suspected
CLL or ALL
Onset for CML
Found in the elderly
What are the phases of CML
THREE (haematopoietic stem cells become more difficult to treat):
- Chronic Phase: Aymptomatic
Symptoms: Fatigue
Abdominal Fullness or Early Satiety from Splenomegaly.
Frequent infections + Bleeding (WBC and Platelet disfunction)
But this is not from neutropenia or thrombocytopenia. It’s form LOTS of mature blast cells that can only semi do their work.
- Accelerated Phase (cellular proliferation accelerates)
- Blast Phase: Where proliferation of mature blast cells continue -> Acute Leukaemia
AML
Sometimes even ALL from gene mutation that causes myeloid blast cells to differentiate into lymphoid tissue.
CML vs Leukemoid Reaction
Leukemoid is the normal over reaction to Infections or Stressors, causing an increase in WBC that is transient
Leukemoid cells take up Leucocyte Alkaline Phosphatase (LAP) but not by CML cells
Diagnosis of CML
- Bone Marrow Biopsy
Increased Ratio of Myeloid: Erythroid cells(can increase in infections as well)
Chronic:
<10% blast cells
Accelerated: 10-20%
Blast Phase: >20%
FISH Analysis for Chromosomal Translocations
What karyotype can lead to CML
- PHILADELPHIA CHROMSOME (9:22 translocation)
ABL Tyrosine Kinase (9) switches with BCR gene (22)
THIS IS NECESSARY FOR DIAGNOSING CML.
Treatment of CML caused by the Philadelphia Chromosome
Tyrosine Kinase Inhibitors: Imatinib
What is a problem when treating the Philadelphia chromosome
Can get resistant to Imatinib and result in a blast crisis
How do we treat a treatment resistant blast cell crisis to imatinib
Allogeneic Haematopoieticc Stem Cell Transplantation
Onset of CLL
Adults and Elderly
Symptoms of CLL
Usually Asymptomatic but can cause lymphadenopathy or hepatosplenomegaly
Richter Syndrome
FBC findings in CLL
- Anaemia
2. Thrombocytopenia
What causes anaemia and thrombocytopenia in CLL
- CLL cells infiltrate the bone marrow
2. CLL cells make auto antibodies against RBCs (AIHA) or Platlets (ITP)
How to diagnose AIHA
Positive Direct Coombs Test
What is Hypogammaglobulinaemiai n CLL
- Lots of abnormal Lymphocytes can sometimes make antibodies that attack our OWN cells.
What is Richter Syndrome
Transformation of CLL into Diffuse Large B-Cell Lymphoma.
Diagnosis of CLL
- Peripheral Blood Smear: Raised lymphocyte count
- Smudge Cells (fragile CLL cells that smush easily)
- Flow Cytometry TO CONFIRM: CD5, CD19, CD23
No Bone Marrow Biopsy needed.
Treatment of CLL
RAI System:
0 - Absolute Lymphocytosis 1 - Lymphadenopathy 2- Hepatosplenomegaly 3 - Anaemia (due to infiltration) 4- Thrombocytopenia (due to infiltration)
0-3 = Watchful management as it doesn’t usually cause death
3-4 or young: Chemotherapy
How to treat AIHA or ITP
Prednisolone
What is Hariy Cell Laeukamia
- Similar to CLL except that it’s very symptomatic
B-Cell lymphoid neoplasm
Pancytopenia: Fatigue, Bleeding and Infections
MASSIVE Splenomegaly: Early Satiety and Abdominal Fullness
Can rupture
Peripheral Blood Smear shows Leukaemia cells with Hair-Like Projections
Usually Affects Men
Onset of AML
Elderly
Environmental RF for AML
- Exposure to Radiation
- Chemotherapy
- Benzene
- Smoking
What Bone Marrow Disorders can lead to AML
- CML
What Inherited Condition can lead to AML
- Down syndrome
How many subtypes of AML are tehre
9
Blood and Clinical Findings in AML
- Immature blast cells infiltrate bone marrow and destroy good cells:
Thrombocytopenia + Bleeding
Anaemia + Fatigue
Neutropenia + Multiple Infections
Leukostasis (SO MANY Leukaemia cells they block blood vessels): Local Hypoxia in tissues (dyspnoea, headaches, priapism)
Lab findings in AML
Auer Rods
In what subtype is leukostaiss most common
M5 Acute Monocytic Laeukemia form (because monocytes are huge)
Treatment of leukostaiss
Leukapharesis
Symptoms of Acute Monocytic Laeukmia
- Lymphadenopathy
- Hepatosplenomegaly
- Gingival Hyperplasia
What is the M3 subtype called
Acute Promyelocytic Leukaemia
What is the main consequence found in Acute Ppromyelocytic Leukaemia
DIC:
Petiechiae
Ecchymoses
Bleeding Sites
What Gene mutation causes Acute Promyelocytic Leukaemia
15:17 translocation
Retinoic Acid Receptor Gene and Promyelocytic Leukaemia Gene.
Treatment of AML
- Chemotherapy and then a Stem Cell Transplant
Treatment of Acute Promyelocytic Leukaemia
All-Trans-Retinoic-Acid (ATRA)
Major Complication of Chemotherapy
Tumour Lysis Syndrome
What is tumour lysis ysndrome
Large tumours are broken down all at once:
- Hyperkalaemia
- Hyperphosphataemia
- Hyperuriciaemia
- Hypocalcaemia
Treatment of tumour lysis syndrome
Rasburicase: Breaks down uric acid into allantoin to be excreted
Onset of ALL
CHILDREN (most common form of cancer in children overall)
Two types of ALL
Pre-B-Cell
Pre-T-Cell
Symptoms of Pre-B-Cell ALL
Similar to AML:
- Marrow failure: Fatigue, infections and bleeding
- Leukostasis
- Hepatosplenomegaly
- Lymphadenopathy
CNS: Headaches, meningitis, CN palsies
Symptoms of Pre-T-Cell ALL
- Anterior Mediastinal mass
Superior Vena Cava Syndrome (facial swelling)
- SOB
- Venous distention in neck and upper chest
Peripheral Blood Smear results in ALL
- Anaemia
- Neutropenia
- Thrombocytopenia
- Lymphoblasts
What is the purpose of low cytometry in ALL
To differentiate between B (CD19) and T cells (CD2,3,5,7)
What are the phases to ALL chemotherapy called
Three phases:
Induction, Consolidation, Maintenance.
What classes of drugs are used to treat ALL
- Anthracyclines
- Steroids
- Cyclophosphamides
Treatment of ALL
- CHEMO
- CNS Prophylaxis as children do not initially present with CNS but 80% do in relapses: Intrathecal Methotrexate
- Treat Phildelphia Chromosome (Imatinib)
Ultimately a Stem Cell Transplant is needed.
Role of glial cells
Support brain homeostasis and neuronal functions
Name two types of glial cells
Astrocytes (maintain the BBB, and nourishing neurones)
Ependymal Cells (Columnar, ciliated cells that line the ventricles and canals)
Role of Ependymal cells
Regulate the circulation of CSF
What tumour subtype make up most paediatric brain tumours
Infratentorial
What is the most common malignant brain tumour
Medulloblastoma
Where do medullablastomas originate from
In or around the cerebellum, next to the fourth ventricle
What cells do medullablastomas arise from
Embryonic Stem Cells
How do medullablastomas metastasise
Through the CSF (drop metastasis) to the base of the spine
What is the typical grade of medullablastomas
4
What are homer-wright rosettes
The appearance of medulloblastomas: Dense tangles of neurones and neuroglia cells
What is the most common benign brain tumour
- Juvenile Pilocytic Astrocytoma
Site of JPA
Mostly in the cerebellum or near the brainstem
Grade of JPAs
Grade 1 (generally benign)
Histological findings of JPA
- Cysts
2. Rosenthal Fibres (Worm shaped clumps of neurofibres)
Where are ependymal cells found
INFRATENTORIAL (at the cerebellum), as that’s where ependymal cells are found
Where do ependymomas form
At the fourth ventricle.
Grades of ependymomas
1->3
What are the appearance of classic ependymomas (grade II)
- Tumour cells have a round/oval nucleus.
2. Perivascular Pseudorosette (cells surround a single blood vessel).
Most common type of supretentorial tumour
Craniopharygnioma
Where do craniopharyngiomas usually dveleop
Near the pituitary gland from remnants of rathe’s pouch
Outline the embryological process of the pituitary glands
1 Formed by cells of the brain (posterior) and oropharynx (anterior)
- Cells from oropharynx form the rathe’s pouch -> Anterior pituitary gland.
Grade of cranipharyngiomas
1
Histological findings of crnaiopharyngiomas
- Cysts
- Cells that stratify (arranged in layers)
- A wet keratin appearance.
Symptoms of Brain tumours
- Headaches
- Nausea
- Vomiting
- Seizures
Pinealoma: Raised B-HCG and AFP (early onset puberty)
Infratentorial tumours can compress the ventricles, blocking CSF -> Hydrocephalus (bulging fontanelles)
Diagnosis of Brian tumors
- Histologic of biopsy
MRI brain
What genetic disorders can give rise to brain tumours
- Neurofibromatosis Type 1
- Neurofibromatosis type 2
- Tuberous Sclerosis
What tumours are seen in NF type 1
Optic Nerve Gliomas
Schwannomas
What tumours are seen in NF Type 2
Bilateral Schwannomas
What tumours are seen in tuberous sclerosis
Subependymal Giant Cell Astrocytomas
What tumours are seen in Von-Hippel-Lindau
- Renal tumours, phaeochromocytomas, cerebellar and retina hemanioblastomas
Charcters of a Brian tumour headache
- Worsens in the morning, change in position, coughing, sneezing
Symptoms of vestibular Schwannomas
Compresses the 8th cranial nerve: Hearing Loss and Tinnitus
What is the triad of symptoms seen in increased ICP
CUSHING’s
HTN
Bradycardia
Irregular Breathing Patterns.
Most common form of glioma
Gliblastoma Multiforme
CT findings in glioblastomas
- Rim of Enhancement as centre is necrotic but peripheral is live
- Cerebral Metastasis and Lymphoma
Crosses the corpus callous (butterfly appearance of the tumour)
Low grade gliomas do not usually enhance
Symptoms of hemangioblastomas
Secrete erythropoietin -> polycythaemia
What are the three structures involved to cause developmental dysplasia of the hip
- Abnormal development of the acetabulum and proximal femur
2. Mechanical instability of th ships joint
What usually causes developmental dysplasia of the hip
- Ligament laxity
2. In Utero positioning
Risk Factors for DDH
- FH
- Female
- Breech > 34 weeks
- Tight Lower Extremity Swaddling
Physical examination for DDH
- Limited Range of Motion
- Assymetry in limbs
- Asymmetric Skin Creases in Thigh and Groin
Up to 6 months of age, what tests can be done to check for DDH
- Barlow
2. Ortolani
What is the Barlow test
- Flex the legs in neutral position and adduct. Put pressure on the knee posteriorly
What does a positive Barlow test indicate
A clunk noise, indicating that the head of the femur is moving out the acetabulum
What is the Ortolani test
- The knee is moved away from the midline
Pressure put non the trochanter
What is a positive ortolans test
Clunk, indicating that the femoral head is dislodging from the acetabulum and relocating in the cavity
After 6 months, what examination is done to check for DDH
- Hip Abduction test
What is a positive hip abduction test in DDH
- Usually abduces to 70 degrees but the ligament laxity involved in DDH causes this abduction to be less than 45 degrees.
What should be done following the ortolans or Barlow test
Imaging Study
USS scan findings in DDH (<6 months)
Subluxation: abnormal relationship between the femoral head and acetabulum
Measures % femoral epiphysis covered by acetabulum
What scan is used over 6 months
X Ray:
Lateral and Superior positioning of the femoral head and neck
Delayed ossification of the femoral head
Treatment of DDH
Under 4 weeks:
Abduction Splint
Over 6 months: Open or Closed Reduction surgery with a Spica Cast
Over 6 years: Salvage Osteotomies.
Onset of Legg-Calve-Perthies
6 Years
What is Legg-Calve-Perthes
Idiopathic Avascular Necrosis of the epiphyses on the proximal femur.
Follows with re-vascularisation.
Risk Factor for Legg-Calve-Perthies
- Male
- Maternal smoking during pregnancy
- FH of skeletal dysplasias
Symptoms of Legg-Calve-Perthies
- Shorter
- Hyperactive
- Quadricepts and Gluteal muscle atrophy
- Insidious Antalgic Gait
What is an antalgic gain
Limp that happens secondary to pain
What test can be done to check for Legg-Calve-Perthes
Trendelenburg’s test
What is Trendelenburg’s test
Stand on one leg for 30 seconds without falling
What is a positive trendelenburg’s test
- Negative: Level hip
Positive: Pelvis DROPs towards unsupported side
X-Ray findings in Perthies
- Joint Space Widening
- Subchondral Fracture
- Sclerosis
- Fragmentation
- Subchondral collapse of ossification centre.
GOLD STANDARD DIAGNOSTIC FOR PERTHIES
MRI for osteonecrosis and revascularisation signs
When are lab studies indicated for perthies
Only if there is evidence of pain, to exclude other diagnoses.
Lab results for perthies
CBC is normal, ESR and CRP is raised
Treatment of Perthies
Under 5:
- Physical therapy to restore ROM
- NSAIDs
Under 7:
Epiphyseal involvement <50%
^ same treatment as above
Epiphyseal involvement > 50%: pelvic or femoral osteotomies
Salvage procedures.
Onset of Slipped Capital Femoral Epiphyses
13-15
What is Slipped Capital Femoral Epiphyses
Where the Epiphyses slips down from the metaphyses
What causes Slipped Capital Femoral Eiphyses
Obesity
Growth Surges
Endocrine Disorders: Hypothyroidism, growth hormone deficiency
Two types of slipped capital femoral epiphyses
- Stable and Unstable (can they walk without support?)
Symptoms of Slipped Capital Femoral Pelvis
Pain in the hip, thigh, groin or knee
Inability to bear weight
Physical exam findings in slipped capital femoral pelvis
Reduce internal rotation, abduction and flexion of the hip
What is obligatory external rotation
Passively flexed leg, the thigh automatically abducts and externally rotates.
What physical exam should be done to check for slipped capital femoral epiphysis
Trenelenburg test positive: Pelvic tilt as unaffected hip is lower
There should be obligatory external rotation and a positive trendelenburg test -> Radiography
X-Ray findings in Slipped Capital Femoral Epiphyses
- Klein’s Line does not intersect the femoral head (usually should do)
- Positive Bloomburg’s sign (blurred physis)
- Blanch Sign of Steel
GOLD STANDARD for slipped
MRI
Other tests for slipped capital
BLOOD TESTS as endocrine involvement
Treatment of slipped capital femoral epiphysis
Surgical stabilisation (Placing a screw through the metaphyses and epiphyses to secure them in place).
What is transient synovitis
Inflammation of the hip without a clear cause
RF for Transient Synovitis
- Recent Upper Respiratory Infection
Physical exam findings in transient synovitis
- Limited abduction and internal rotation of the hip
- Tender hip on palpation
- Can’t bear weight
GOLD STANDARD for transient synovitis
LOG ROLL: The leg is rolled side to side.
What is the positive test in a log roll
Involuntary muscle guarding in the leg.
X-Ray findings in transient synovitis
- Slight demineralisation of the bone in the proximal femur
- Joint Space Widening
- Capsular Distention
Transient Synovitis vs Septic Arthritis (4)
- Fever
- Limp but can bear weight
- ESR <40 mm/hr
- Serum WBC <12,000 cells/mm^3
Treatment of transient synovitis
NSAIDs
Onset of Osteochondrosis (osgood-schlatter)
13-15
What is Osgood-Schlatter Disease
Inflammation of tibial tubercle.
What causes osgood-schlatter disease
Growth Spurts
Physical Activity
Symptoms of Osgood-Schlatter Disease
- Unilateral Anterior Knee Pain that gets WORSE over time
- The pain gets worse on movement
- causes a limp
- Pain might limit quadriceps flexibility.
RF for osgood-schlatter disease
- Athletic
2. Male
When is imaging done for osgood-schlatter disease
Usually done based on symptoms and RF alone:
UNLESS:
- Atypical presentation
- Unilateral
- Severe
- Persistent
What is seen on physical examination of the knee in osgood-schlatter disease
- soft tissue swelling ANTERIOR to the tibial tuberosity
2. Increased density of the tubercle
Treatment of osgood-schlatter disease
Activity Modification
NSAIDs and Physiotherapy
Drilling the tibial tubercle or resection of the tubercle
When in gestation, do we give rise to scoliosis
4-6 weeks
Onset of scoliosis
No problems until adolescence
Symptoms of scoliosis
- back pain
2. SOB
What is the physical exam special test we need to do in scoliosis
Adam’s Forward test
What is the Adam’s Forward test
Bends forward, while we check for abnormalities
What is a positive Adam’s Forward test
Tilted shoulders blades
Prominence of ribs on one side
Uneven waist line
Diagnostic tests for scoliosis
- Scoliometer (to measure difference in shoulder prominence). Significant if over 5 degree difference
- Radiograph if over 10 degrees: Cobb’s Angle
Only over 10 degrees as Cobb’s Angle is not accurate
What is Cobb’s Angle
This is the degree measured between the superior vertebra and inferior vertebra.
Needs to be at least 10 degrees for a positive scoliosis diagnosis
What is the most common soft tissue sarcoma in childhood
Rhabdomyosarcoma: usually causes mass, pain and obstruction of the bladder, pelvis, nasopharynx, orbits
What is the main cause a=of limping in 0-5 years
DDH, Transient Synovitis, Septic Argritis, Osteomyelitis,
What is the main cause of limping 5-10 years
- Tranisnet synovitis, Perthes, Septic arthritis
Osteomyelitis
What is the main cause of limping from 10-15
- Slipped femoral, septic, osteomyelitis, osgood-schlatter disease, osetochrondritis, chondromalacia patella
Tumours: Ewing;s and osteosarcomas, neuroblastomas
Osteoid Osteoma
Role of the synovial membrane
- Remove Debris
2. Produce Synovial Fluid
Inflammatory vs Non-inflammatory arthritis
Pain is symmetrical vs asymmetric pain
Pain gets better with use vs pain gets worse with use
Prolongued morning stiffness (1+ hours) vs morning stiffness (<1 hr).
No extraarticular symptoms.
four types of deformities seen in RA
- Swan-neck (flexion of DIJ, hyperextension of proximal)
- Bobutonniere (flexion of proximal and extension of DIJ)
- Ulnar Drift (fingers lean away from the thumb and towards the pinkie from weakened ligaments)
- Z-deformity (thumbs up)
Name a major CNS symptoms from RA
Carpal Tunnel Syndrome
What is Caplan’s Syndrome
Pneumoconiosis and RA
Onset of Juvenile Idiopathic Arthritis
<16
RF for Juvenile Idiopathic Arthritis
HLA-B27 and Infections
Autoimmune
Cytokines move to different parts of the body and cause tissue injury
Presentation of Juvenile Idiopathic Arhritis
- Symmetrical Involvement of the LARGE joints (e.g., the knees or ankles)
- Worse in the morning or with rest
Most common form of juvenile Idiopathic Arthritis
Oligoarticular Arthritis (< 4 Joints)
The other form is Polyarticular Arthritis (5+ Joints).
Systemic Juvenile Idiopathic Arthritis
Symptoms of Systemic Juvenile Idiopathic Arthritis
Salmon Pink Macular Rash w/ Fever
Symptoms of Oligoarticular Arthritis
Uveitis Enthesitis Daily Spiking Fever Splenomegaly Generalised Adenopathy Pericarditis or Pleuritis.
IMPORTANT: Joint involvement can occur weeks or Months after systemic symptoms
Diagnosis of Juvenile Idiopathic Arthritis
Blood: Leukocytosis Thrombocytosis Anaemia Raised ESR and CRP RF, ANA, Anti-CCP
Genetic Testing: HLA-B21
Treatment of JIA
Methotrexate
What is a menisci
Crescent-Shaped Fibrocartilage Cushions, absorb compressive force
Name the two joints in the knee
Femoropatellar Joint Tibiofemoral Joint (formed by junction between the condyles)
What are the main ligaments that are involved in a meniscus tear
- ACL
- MCL
- Lateral Meniscus
What test is done to check for meniscus tear
McMurray Test
What hormones stimulate babies to start breathing
Adrenaline and Cortisol
What causes the closure of the foramen Ovale
The baby’s first breath expands the alveoli, decreasing pulmonary vascular resistance. This reduces the pressure in the right atrium, stopping shunting (becomes lower than LA)
What molecule keeps the ductus arteriosus open
Prostaglandins. Increase in oxygenated blood reduces prostaglandin levels and the ductus closes
What is the lifelong consequence of hypoxia
Hypoxic ischaemia leads to cerebral palsy
