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133 Cards in this Set
- Front
- Back
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Describe what occurs in a Left to Right shunt in congenital heart disease.
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Atrial Septal Defect (ASD), Ventricular Septal Defect (VSD), AVSD and Patent Ductus Arteriosis (PDA) do not immediately cause cyanosis, but cause pulmonary hypertension, which can lead to pulmonary scarring and right ventricular hypertrophy compensation. Eventually if untreated, Eisenmenger's syndrome can develop and the shunt becomes a Right to Left shunt and cyanosis can develop.
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Describe what occurs in a Right to Left shunt in congenital heart disease.
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In Tetralogy of Fallot (TOF), Transposition of Great Vessels (TGA) and Eisenmenger's syndrome, blood bypasses the lungs, leading to immediate cyanosis, paradoxical embolism (venous clot), clubbing and polycythaemia.
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Give examples of obstructive congenital heart diseases.
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Coarctation of aorta, congenital aortic stenosis, pulmonary stenosis or atresia, tricuspid atresia.
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What are the 4 elements of the Tetralogy of Fallot?
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- Large, high, membranous VSD
- Pulmonary outflow tract stenosis - Aortic valve overlying the VSD - Right ventricular hypertrophy |
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When can you have a patent ductus arteriosis?
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Hypoxia delays closure in neonates, and sometimes patency is deliberately induced by administration of PGE2.
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What % of VSDs occur in isolation and in conjunction with other congenital cardiac abnormalities?
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30% of VSDs are isolated, and 70% occur in conjunction with other abnormalities.
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What is the most common cause of congenital cardiac anomaly at birth?
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Ventricular Septal Defects, ~1:200 live births and 40% of all congenital cardiac malformations.
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Describe patent ductus arteriosis in the context of the Tetralogy of Fallot.
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In this cyanotic heart disease it is common to get PDA, which is actually beneficial as it provides an alternative route for blood to get into the lungs to be oxygenated (usually the stenosed pulmonary valve decreases blood to the lung, reducing oxygenation).
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How does the heart appear in the CXR of someone with Tetralogy of fallot?
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Boot shaped - the right ventricular hypertrophy causes the Right Atrium to become more angular and prominent, the apex turns upward, and the atresia of the pulmonary trunk causes a decrease in the shadow of the upper left of the heart.
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What is a Blalock Taussig shunt?
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A procedure to palliate cyanotic heart defects in babies, such as in Tetralogy of Fallot. Temporarily directs blood to the lungs by separating the subclavian or carotid artery and connecting it to one of the pulmonary arteries. Mimics a PDA and temporarily eases cyanosis until corrective surgery is performed at age 1 year.
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Where do most coarctations of the aorta occur?
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Just distal to the left subclavian artery/ligamentum arteriosum.
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How often do coarctations of the aorta occur?
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1 in 2000 live births, 5% of all congenital cardiac malformations.
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Is the adult or juvenile form of coarctation of the aorta more common?
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Adult form, occurring distal to the ligamentum arteriosum.
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What does coarctation of the aorta lead to? (consider the different forms - juvenile and adult)
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In adults (distal to l. arteriosum) leads to left ventricualr hypertrophy, hypertensive atherosclerosis of the arch, upper limb and head vessels. Internal mammary arteries can serve as collaterals to move blood to the trunk and legs by anastomosing with arteries under ribs, which anastomose with the thoracic aorta distal to the coarctation.
In juvenile (coarctation is before the ductus arteriosis) you can often get PDA which allows the right ventricle to perfuse the trunk and lower limbs with de-oxygenated blood, leading to right ventricular hypertrophy and right sided heart failure |
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In coarctation of the aorta, what might you see in the CXR?
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Sawtooth notching of the ribs due to erosion by hypertrophied intercostal arteries, right or left ventricular hypertrophy (depending if juvenile or adult form)
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How often are people born with aortic stenosis?
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1 in 25 000 live births.
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How often does tricuspid atresia occur in a newborn?
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1 in 100 000 live births.
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What is a common complication of a high ventricular septal defect? Describe in details the mechanism of how this occurs.
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Bacterial endocarditis - the structural abnormality causes turbulence which damages the aortic valve and tricuspid valve and causes endothelial stretching, activating the surface for microthrombi formation. Transient bacteraemia, especially of biofilm forming bacteria (such as streptococci mutans which resides as part of dental flora) can then allow colonisation of this immune protected area. Division within the clot leads to vegetation formation.
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What are 3 systemic-pulmonary shunts present in foetal circulation?
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Ductus arteriosis (pulmonary trunk to aorta bypassing lungs)
Foramen ovale (Right atrium to Left bypassing lungs) Ductus venosus (50% from umbilical vein goes to IVC bypassing liver) |
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What is the normal foetal pO2 and why?
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30 - 40 mmHg as the foetus has less O2 demand and the foetal Hb has a greater affinity for oxygen.
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Describe foetal circulation.
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Placenta -> UV -> through ductus venosum to IVC -> RA (also receives from SVC) -> through foramen ovale to LA (also receives from PV) -> LV -> Aorta -> body
(some also goes RA -> RV -> PA -> 85% thru DA to Aorta, 15% to lungs) |
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Describe the qualities of foetal lungs.
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Fluid filled, excrete fluid, get 10 - 15% CO, high pressure in foetal pulmonary arteries due to fluid compression, low arterial PO2, local vasoconstrictors (PGF2A, TxA2, endothelin).
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How does the foetal CVS transition for birth while in utero?
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Foramen ovale reduces in size, ductus arteriosus becomes more muscular and less sensitive to PGL, catecholamines/cortisol/T4 elevated in interrupted blood supply during labour to prep the lungs (surfactant from type 2 cells, fluid excreting cells to absorbing), blood supply increased to heart and brain, fuels begin to be mobilised.
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What CVS changes occur early in the new-born baby?
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Lungs fill with air, fluid is expelled from lungs, O2 level rises, pulmonary vascular resistance decreases as NO and prostacyclin cause vasodilation, low resistance placenta removed from circulation causing an increase in systemic vascular resistance and pressure, 3 foetal systemic-pulmonary shunts close (DA - O2 and PGE2, FO - LA pressure increase, DV - reduced flow from umbilicus) allowing an increase in left sided heart blood pressure.
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What can cause a difficulties in a normal transition from foetal to new-born CVS in a premature delivery?
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Patent ductus arteriosis
Minimal lung surfactant |
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Under what circumstances will a normal transition from foetal to newborn CVS see difficulties?
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Congenital heart disease,
Premature delivery |
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What might you see in the presentation of an abnormal transition from foetal to postnatal circulation?
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cyanosis, repiratory distress, cardiac failure, shock
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If symptoms of an abnormal transition from foetal to post-natal circulation are present at birth, what is the most likely cause?
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Parenchymal lung disease.
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If symptoms of an abnormal transition from foetal to post-natal circulation are not present at birth but are seen within 4 hours, what is the most likely cause?
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May have lung disease.
If CHD, more likely to have inadequate pulmonary flow from hypoplasia of RH than inadequate systemic flow from hypoplasia of LH. |
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If symptoms of an abnormal transition from foetal to post-natal circulation are only present >4 hours after birth, what is the most likely cause?
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Parenchymal lung disease less likely.
If CHD, likely to be ductal dependent lesion. |
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How can you treat a newborn with a patent ductus arteriosis?
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prostaglandin synthetase inhibitors e.g. Ibruprofen.
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When would you ideally want CHD complicating normal transition to show symptoms?
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Within 4 hours with signs of cyanosis.
Shock with congestive heart failure from 4 - 24hrs. Shock without congestive heart failure from 1 - 14 days is worrying as the baby is usually sent home before treated. |
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Are women or men more likely to have hypertension?
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Men are more likely than women at age 30 ( 0.7:0.6) and at age 65 (1.2:1.1), possibly due to the beneficial effects of oestrogen.
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Describe RAAS.
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Low BP - JGA secretes renin - converts angiotensinogen to angiotensin I - ACE from lungs converts to angiotensin II - causes release of aldosterone from adrenal cortex - causes vasoconstriction and causes retention of Na and H20 = increased blood volume and pressure.
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What is essential hypertension?
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No specific cause for the hypertension, it is idiopathic. >140/90 mm Hg
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What is malignant hypertension?
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Rapid increase over 1-2 years in blood pressure to >200/120 mmHg. Associated with severe headaches, chest pain, SOB, organ damage. Can be drug induced e.g. cocain, OC, Beta blocker withdrawal, alcohol.
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What are 5 main groupings for the causes of hypertension?
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Renal e.g. renal artery stenosis or glomerularnephritis causing RAAS activation
Endocrine e.g. menopause low Oe, OC, cushings, aldosteronism CVS e.g. coarctation of aorta Neurological e.g. acute stress (white coat syndrome - normally normal), sleep apnoea Idiopathic e.g. essential HT = 95% pts |
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What is renal artery fibromuscular dysplasia?
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Congenital predominantly female disease that can cause HT and kidney damage. Histologically appears bead-like due to segmental involvement, and can involve one or more layers e.g. media, adventitia
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List some endocrine causes for hypertension.
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Aldosteronism (adrenal excess of aldosterone)
Phaeochromocytoma (catecholamine secreting adrenal medulla tumour) Cushings Syndrome (pituitary tumour) Acromegaly (pituitary adenoma) Hyperthyroidism (excess stimulation) Hypothyroidism (decreased metabolism therefore decreased NO) |
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List some CVS causes of HT.
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Aortic coarctation
Polyarteritis nodosa (immue disorder against vessels) Other vasculitides Increased intravascular volume (thinning walls, fluid retention) |
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What are the effects on the left ventricle of chronic hypertension?
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Concentric left ventricular hypertrophy, where wall thickness exceeds 1cm and weight may be almost doubled to 500g, and diastolic volume is reduced, and may even obstruct the outflow tract. Myocytes are hypertrophied with large, irregular, angular hyperchromatic nuclei. Ischaemia and necrosis occurs as angiogenesis can not keep up with increase in cell thickness = fibrosis.
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How do you get Cor Pulmonale?
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Pulmonary disease or pulmonary vessel disease causing pulmonary hypertension, right ventricular hypertrophy and eventual failure.
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How does hypertension effect arterioles?
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Smooth muscle replaced with collagen and 'hyaline' in walls from extravasation of albumin from injured endothelium. Lumen is narrowed and proteinuria may occur as this especially effect arterioles of kidney.
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How does hypertension effect arteries?
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Constant pulsatile stress causes loss of elastin and smooth muscle in the media, which is replaced by fibrous tissue and causes arteriosclerosis, increasing risk for atherosclerosis. Endothelial is also activated to a small extent chronically.
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What are the effects of hypertension on the kidney?
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Afferent arteriole HT damage
Atherosclerosis Hypertensive nephrosclerosis RAAS ischaemia = loss of glomeruli bilateral finely granular contracted/fibrosed kidneys. |
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What can occur to the brain in hypertension?
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Cerebral infarction from atherosclerosis is a common stroke.
Increased risk of intracerebral harmorrhage Increased risk of rupture of berry aneurysms in circle of Willis = subarachnoid harmorrhage. |
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What can occur to the retina in hypertension?
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Retina
AV nipping (indentations in the bv), copper-wiring where thickened vessels reflect light better in the middle. Papilloedema of the optic cup (edge becomes obsure and the vessels appear hazy). Flame haemorrhage (ruptured bv tracks outward and in flame-like lines) Cotton wool exudate (pale patches from decreased perfusion) |
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What are the causes of death related to hypertension?
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Congestive cardiac failure = 60%
Strokes = 30% Aortic dissection Renal failure uncommon in benign HT Malignant HT. |
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What is the approximate risk of having a child with down syndrome with maternal ages of a)20 b)30 c)35 D)45?
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a) 20 years ~ 1:1400
b) 30 years ~ 1:950 c) 35 years ~ 1:350 d) 45 years ~ 1:32 (Learning topics are wrong, check the source that is referenced) |
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What is aneuploidy?
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Abnormal number of copies of a genomic region (absence or supernumerary).
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What 3 trisomies are able to be distinguished as syndromes?
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21 = down syndrome
18 = edward's syndrome 13 = patau syndrome |
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What % of trisomy 21 result in spontaneous pregnancy loss?
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80%
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What is the most common trisomy of the human chromosome?
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Chromosome 21, HSA21, overall being 1 in 750 live births.
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Describe mosaicism, referring to down syndrome.
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When not every cell in the body has the same DNA, can occur by chance during early embryonic development (the later, the less cells effected). Well reported in down syndrome and can account for individuals with mild forms. If germline mosaic, it is only present in the sperm/eggs, not the body, but will be passed on to offspring.
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What errors in cell division lead to trisomy 21? Clarify % of instances which are found in each gender and type of division.
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Maternal 95%, paternal 5%.
Meiosis 95%, Mitosis 5%. Meiosis I non disjunction (75% of maternal, 25% of paternal), Meiosis II non-disjunction (75% of paternal, 25% of maternal). |
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What is a robertsonian translocation?
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Fusion between the centromeres of a pair of the acrocentric (centromere not central) chromosomes = 13, 14, 15, 21, 22.
If balanced, no excess/deficit of genes results, if not can get trisomies in offspring. |
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How do you screen for Trisomy 21 prenatally?
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Amniotic fluid from amniocentesis and chorionic villus cells can be tested using karyotyping, FISH, Chromosome Micro Array. Also nuchal translucency ultrasound at 11-12 weeks, maternal serum paramaters.
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What are the common phenotypic features seen at birth of someone with trisomy 21?
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Craniofacial = skin folds at neck back, flattened face, small mid face, epicanthic folds, upslanting palpebral fissures, protruding tongue; Hypotonia and joint laxity; Wide spaced toes, single transverse palmar crease, curving of little finger.
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What is a possible explanation for early onset alzheimer's in down syndrome patients?
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triplication of the amyloid precursor protein gene (APP).
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Why does having an extra gene copy matter?
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Some genes are dose sensitive.
Some genes regulate other genes. Dosage of conserved functional non-genic sequences. |
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What genes are responsible for causing some post-genomic changes in trisomy 21?
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DYRKIA an DSCR1, both which regulate the phosphorylation of NFAT, which when dephosphorylated activates genes downstream. When either are switched on/off at the wrong time, can effect development.
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Why do down syndrome patients have an increased chance of leukaemia?
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Mutations in GATA1 which plays a role in myeloid lineage commitment, particularly in acute megakaryoblastic leukaemia (AMKL).
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Are all triplicated genes overexpressed in down syndrome?
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No, genes can be overexpressed, normally expressed or underexpressed, depending on different regulatory functions etc.
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What is an intellectual disability?
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Limitations in intellectual function 2 or more below SD of population mean (IQ <70) and limitations in 2 areas of adaptive functioning, and onset in development period before adulthood.
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What is the prevalence of intellectual disability?
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Ranges from 1-3% (mild often underdiagnosed)
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How often is the aetiology of an intellectual disability able to be identified?
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50-60% time
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What was to median survival for people with down syndrome in 2003?
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57.8 for Women, 61.1 for Men
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What congenital malformations are seen in people with down syndrome?
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Congenital heart disease (50%) = AVD, VSD, PDA, TOF = therefore must screen with echo in neonate.
GIT malformations (10%) = duodenal atresia, blockages |
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What vision disorders are commonly seen in people with down syndrome, and how often should the be screened for?
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60% prevalence so check annually in childhood and 5-yearly in adulthood.
Include strabismus, refractive errors, cataracts, keratoconus (thin conical cornea), blepharoconjunctivitis. |
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What hearing impairments are seen in people with down syndrome and how often should you check hearing?
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Childhood - conductive loss from serous otitis media (50-70%). Adults -sensorimotor loss more common Can further impair language, attention span, and behaviour.
Check annually in childhood, 3 -yearly in adults. |
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What are the clinical signs of hypothyroidism?
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dry hair/skin, constipation, bradycardia, delayed reflexes, slowing of motor and mental activities, exacerbated growth/cognitive delay in children.
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How often should you monitor hypothyroidism in a person with down syndrome and what do you look for?
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Clinical signs (can be subtle), thyroid function tests (serum TSH T3, T4). This should be monitored annually throughout life.
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What is a serious consequence of the joint laxity seen in people with down syndrome?
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Atlanto-axial intability leading to compression of the spinal cord = neck pain and limited mobility, gait abnormality, spasticity, hyperreflexia, weakness, urinary incontinence.
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What causes the increased risk of developing obstructive sleep apnoea in people with down syndrome?
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large tongue, narrow orophyarynx, obesity, hypotonia
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What cancers are increased in people with down syndrome?
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Acute leukaemia within the first 5 years of life, and a 5 fold increase in testicular cancer, possibly related to undescended testes.
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How many people with down syndrome have a mental health condition?
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23%, approx 1 in 4
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What is the most common mental health condition found in people with down syndrome and why is this thought to be so?
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Depression - withdrawal, deterioration of skills, insomnia, possible aggression, can be misinterpreted as dementia onset.
Physical pain, adverse physical and social environments and life experiences, limited social networks, limited cognitive and communication skills, delayed social maturity, decreased resilience and limited coping skills increase risk. |
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What are the differential diagnoses for down syndrome patients suspected of having Alzheimer's disease?
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depression****, hypothyroidism, sensory impairments, B12 defiiciency.
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How will a person with down syndrome usually be educated?
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Mainstream class with aids/resources, or a support class of all intellectually impaired students with specific programs in a mainstream school, or a special school if mainstreaming isn't suitable. Younger can be mainstreamed better, as get older focus is on survival skills and independent living.
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When won't it be suitable to place someone with a disability in mainstream schooling?
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If not toilet trained or if they would not be safe around others in a maintstream setting.
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What are forms of family support to the families of people with down syndrome?
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genetic counselling, down syndrome association, respite care, financial support
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What QRS axis will you find in the normal ECG of newborns and why?
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~120 degrees due to right ventricular dominance causing right axis deviation (I = negative, AvF = +)
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What is the normal QRS axis in the ECG of a 1 year old?
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~90 degrees, as Left Ventricle takes dominance.
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How will the P wave appear in the ECG of a patient with Right atrial enlargement?
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abnormally peaked and a high value
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How will the P wave appear in the ECG of a patient with left atrial enlargement?
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longer width/duration to the P wave
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What is the duration of a P wave in lead II of a perosn a) <3 years b) >3 years?
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a) 0.03 - 0.09 sec
b) 0.05 - 0.1 sec |
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What is the normal QRS complex duration for someone a) <7 years b) >7 years?
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a) <0.08 sec
b) <0.09 sec |
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What direction will the T wave be in lead V1 of the ECGs of people < 5 days old and also in adults?
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upright in V1
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What is the QTc?
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QT interval (start QRS to end of T) corrected for heart rate by bazett's formula, to bring back to a standard of comparison at 60 bpm.
= QT/ squareroot RR >0.46 sec = prolonged |
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What are some risk factors for developing a congenital heart defect?
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maternal prenatal rubella (PDA, P and A stenosis), maternal alcohol abuse (septal defect), maternal drug treatment and radiation, genetic abnormalities, chromosomal abnormalities (down syndrome, Turner's syndrome).
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What are the malformations and features seen in the newborn with down syndrome?
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Cardiac malformations (40%) AVD, VSD, TOF, ASD. Gastrointestinal anomalies (10-18%) duodenal atresia, Hirschsprung disease. Undescended testes. Hypotonia, excessive skin folds at the back of neck, maxillary hypoplasia, curving of little finger, sandal gap in toes, epicanthic fold, single transverse palmar crease
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What are features of down syndrome commonly seen in childhood?
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Delayed psychomotor development, intellectual disability, prominence of tongue, short stature, burshfield spots, joint hypermobility, atlanto-occiptiial instability, visual and hearing issues, leukaemia, hypothyroidism
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What are features of down syndrome commonly seen in adults?
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Intellectual disability, premature aging, presenile dementia early onset dementia (Alzheimers), depression.
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What is the septum primum?
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the membrane which grows downward towards the endocardial cushion in the developing foetal heart, forming the wall between the left and right atrium.
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What is the ostium primum?
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The gap which is slowly closed as the septum primum grows down forming the intra-atrial wall in a developing foetus' heart.
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What is the ostium secundum?
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The perforations that appear and join in the superior part of the septum primum in a developing foetal heart.
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What is the septum secundum?
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A membranous wall which grows down next to the right of the septum primum and ostium secundum, in foetal cardiac development.This decreases the flow through the ostium secundum, forming the foramen ovale. At birth, the increased pressure in the left atrium forces the septum primum and secundum together, eventually causing their fusion and the closing iof the foramen ovale. This creates the fossa ovalis depression in the atrial wall.
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What are some of the clinical features in a newborn with an ASD?
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Majority are asymptomatic, may have RV heave at lower left sternum, loud S2 with widened fixed splitting, systolic murmor in pulmonary area due to increased flow, mid diastolic mumur in tricuspid area due to increased flow.
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What are some of the clinical features in a patient with VSD?
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Small = asymptomatic. tachypnoea, poor feeding, failure to thrive, if reverses cyanosis and dyspnoea, bacterial endocarditis, harsh holosystolic murmur at left sternal border, systolic thrill, mid diastolic rumble at apex.
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What are some of the clinical features found in a patient with a PDA?
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Children generally asymptomatic. tachycardia, poor feeding, slow growth, fatigue, dyspnoea, palpiations, AF due to LA dilation, turbulent flow causing endarteritis, continuous machine like murmur in left subclavian area, murmur in shorter diastolic component if pulmonary vasculature effected, eisenmenger may deveop witth lower extremity cyanosis and clubbing.
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Describe an AVSD?
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Can be partial, where a primum ASD and a cleft anterior mitral leaflet causes mitral insufficiency, or it can be a complete AVSD, where a combined AV septal defect leads to essentailly a hole in the centre of the heart which allows all 4 chambers to freely communicate, inducing volume hypertrophy of all. 1/3 of those with AVSD have down syndrome.
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What are the 2 types of coartations of the aorta?
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1) Pre-ductal (2%), where the narrowing is proximal to the ductus arteriosum and this leads to decreased blood flow and hypoplastic aorta development.
2) Post ductal (98%), muscular ductus arteriosum tissue extends into the aorta during foetal life, when DA constricts after birth, ectopic tissue in aorta constricts = obstruction. |
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What are the clinical features used to help diagnose coarctation of the aorta?
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Preductal = heart failure symptoms after birth, cyanosis
Postductal = HT in upper extremeties, weak/delayed pulses in lower extremities (claudication, cold etc). Adults may get collateral development, leading to increased size of mammary and intercostal arteries and notchings on a CXR, a midsystolic ejection murmur may be present. thrill may be present, LV hypertrophy, may have murmurs over chest due to prominence of collaterals. |
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What are the clinical features of a TOF?
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Dyspneoa,irritability, cyanosis, hyperventilation, syncope, convulsions after exertion, alleviated by squatting which increases systemic vascular resistance. Moderate stenosis evident as mild cyanosis of lips, mucous membranes and digits, chonic hypoxaemia leading to clubbing, RV heave from hypertrophy. S2 not split, soft S2, systolic ejection murmur in the pulmonary area due to stenosis.
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What are the clinical features of a patient with TGA?
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Cyanosis, loud S2 over aortic valve, RV impulse at lower sternal border.
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To be considered developing normal, what fine movement skills should an infant have by...4 months? 6 months? 9 months? 12 months? 3 years?
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4 months = reaches, feet and hands in midline
6 months = plays with feet, transfers 9 months = pincer grip, evolution of grasp 12 months = picks up 2 cubes 3 years = picks up ten cubes |
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What age should a child turn head to a soft sound at ear level? and when 40cm away?
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3 months, 9 months
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What age should smiling socially start?
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4-6 weeks
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What age should a child begin to show pleasure in familiar experiences?
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3 months
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What age should a child laugh?
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4 months
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What age will an infant start to show stranger anxiety?
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6 months
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What age will a child develop a concept of permanence for things they can't see?
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9 months
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What age will a child turn to and know their own name?
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12 months
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What is the IQ of someone with an Intellectual Disability?
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<68 (85 normal)
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What milestones should a child have reached at 6 weeks?
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holds chin up, turns head, watches people, follows a moving object, begins to smile
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What milestones should a child have reached at 8 weeks?
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holds chin up, turns head, watches people, follows a moving object through 180 degrees, smiles on social contact, listens to voice
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What milestones should a child have reached at 6 months?
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turns head to music/talking/cooing, pushes chest off, sits unsupported, rolls, can take cube from a table, drink from a cup
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What are some of the alert signs for developmental delay in an infant at 6 months?
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doesn't roll over, impossible to comfort, does not smile on their own, cannot sit with help, does not laugh or squeal, does not actively reach for objects, stiff/tight or floppy/ragdoll muscles, flopping head when pulled to sit, reaches with only one hand, refuses cuddles, shows no affection for carer, no enjoyment around people, eye/s turn in/out, does not respond to sounds, has difficulty getting objects to mouth, does not follow object with both eyes, does not bear weight on legs, does not try to attract attention through actions, does not babble, shows n interest in games, regression of skills
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What milestones should a child have reached at 12 months?
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3 words, walks around pen, holds pencil, finger feeds, object permanence, laughter
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What are some of the alert signs for developmental delay in an infant at 2 years?
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Cannot walk or walks only on toes (18 months), speaks <15 words, does not use 2 word sentences, no knowledge of household object function, does not imitate actions/words, does not follow simple instructions, cannot push a wheeled toy, regression of skills
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What milestones should a child have reached at 3 years?
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3 word phrases, naming colours, knows 2 adjectives, jump, throw ball, balance on each foot, tower 8 cubes, name friend, brush teeth, start to dress
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What milestones should a child have reached at 5 years?
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correct grammar, jokes, riddles, abstract words, hops, skips, walks along line, copies square, draw a man, dresses self, washes hands, uses knife and fork, knows age, birthday, 6-10 colours, count to 20, point to 4-6 objects
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What are some of the alert signs for developmental delay in an infant at 5 years?
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fearful, aggressive, unable to separate from parents, easily distracted, little interest in other people, limited fantasy/play, unhappy, disengaged, limited emotions, trouble eating sleeping or using toilet, inability to distinguish fantasy and reality, passive, cannot understand 2 part commands, can't give full name, doesn't use plurals/tense properly, doesn't talk about daily experiences, cant build 6 block tower, can't easily hold crayon, trouble dressing and brushing teath and washing/drying hands, regression of skills
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What is cyanosis?
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dusky blue discolouration of skin/mucous membrane due to higher than normal concentrations of deozygenated haemoglobin in the tissue cappillaries
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What are the 2 basic mechanisms which cause cyanosis?
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1) arterial blood entering these capillaries is less saturated than normal
2) circulation slowed so more O2 is extracted |
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What must PaO2 fall to for the SaO2 to fall to 90%?
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60mmHg (respiratory distress)
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What concentration of deoxyHb is present to be able to detect central cyanosis ?
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<50 gm?L
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What carries 50% of the foetal CO to the placenta?
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2 large umbillical arteries that leave the iliac artery
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What carries oxygenated blood back from the placenta?
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the umbilican vein, that joins the IVC bypassing the liver
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What % of the blood returning to the right atrium in foetal circulation crosses the foramen ovale?
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50%, to go into the Left atrium
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What % of the blood that enters the pulmonary artery in foetal circulation bypasses the lung by entering the ductus arteriosus?
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50%, this reaches the aorta to reach systemic cirulation
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t/f... foetal pulmonary pressure is low, while systemic is high
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false, foetal pulmonary pressure is high, while the placenta makes foetal systemic pressure low
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What are the 3 main changes to foetal circulation at birth?
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Peripheral resistance doubles as placenta is removed, increasing L heart pressure. First breath decreases pulmonary resistance, decreasing R heart pressure. Flow slowly stops through the ductus arteriosis as the smooth muscle contracts, and through the foramen ovale as the pressure changes close it.
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