VESICOURETERIC REFLUX
International classification
-       1-  Partial filling of an undilated ureter
-       2-  Total filling of an undilated ureter
-       3 – Dilated calyces but fornices sharp
-       4 – Blunted fornices and degree of dilatation greater
-       5 - Massive hydronephrosis and tortuosity of the ureters
INDICATIONS FOR SURGERY IN VUR
-       1.  Break through infections
-       2.  Anatomic abnormalities at the junction
-       3.  4&5 reflux in lower pole of duplex system
-       4.  Persistent reflux in adolescence
-       5.  Grade 5 reflux
-       6.  Noncompliance with medical management
-       7.  Associated with ureteral obstruction
Hypospadias
-       Rx MAGPI
-       Duckett’s Chordee correction.
Cerebral Blood Flow & Its Regulation
-       Inhaled nitrous oxide (N2O) (Kety method). The average cerebral blood flow in young adults is 54 mL/100 g/min. The average adult brain weighs about 1400 g, so the flow for the whole brain is about 756 mL/min. In resting humans, the average blood flow in gray matter is 69 mL/100 g/min compared with 28 mL/ 100 g/min in white matter.
-       Because brain tissue and spinal fluid are essentially incompressible, the volume of blood, spinal fluid, and brain in the cranium at any time must be relatively constant (Monro–Kellie doctrine).
-       In the brain, auto regulation maintains a normal cerebral blood flow at arterial pressures of 65–140 mm Hg.
-       O2 consumption by the human brain (cerebral metabolic rate for O2, CMRO2) averages about 3.5 mL/ 100 g of brain/min (49 mL/min for the whole brain) in an adult. This figure represents approximately 20% of the total body resting O2 consumption.
-       Glucose enters the brain via GLUT 1 in cerebral capillaries.
-       Blood Flow in Various Parts of the Brain – Best is P.E.T (2 Deoxy Glucose).
-       CPP = MAP – CVP/ICP (whichever is higher), (Normal CPP 80-100 mmHg, ICP <10 mmHg).
-       Most important extrinsic influence on CPP is Arterial pCO2.
-       Cerebral Blood Flow changes by 5-7 % with 10C change of temperature.
The Renin–Angiotensin System
-       Renin is an aspartyl protease, contains 340 AA, t ½ < 80 min.
-       After Nephrectomy the prorenin levels may actually rise (from ovaries), but rennin falls to 0.
-       Angiotensinogen is found in the 2-globulin fraction.
-       Angiotensinogen -> AT-I (decapeptide) -> (ACE) AT-II (octapeptide) in Lungs. ACE  is a dipeptidyl carboxypeptidase that splits off histidyl - leucine from the physiologically inactive angiotensin I. AT II t ½ 1-2 minutes. The normal PRA in supine subjects eating a normal amount of sodium is approximately 1 ng of angiotensin I generated /mL/hr. The plasma angiotensin II concentration in such subjects is about 25 pg/mL (approximately 25 pmol/L).
-       Dry Cough in ACEI is d/t increased Bradykinin.
-       AT1 receptors are serpentine receptors coupled by a G protein (Gq).
-       1. JG cells (granular cells) - in the media of the afferent arterioles – intra renal pressure sensor, 2. Agranular lacis cells those are located in the junction between the afferent and efferent arterioles in the mesangium, 3. Macula densa (part of tubule – start of DCT, senses Na+) All 3 constitutes JGA.
-       GOLDBLATT Hypertension – Syn. Renal Hypertension –  decreased blood supply to one kidney -> increased renin.
Gilbert's syndrome - mutation in the UGT1A1 gene promoter- reduced UGT1A1- ADR with 1. Tranilast (in post CABG patients to prevent restenosis), 2.  Irinotecan, a prodrug, SN-38 active metabolite, potent Topoisomerase Inhibitor - Leucopenia, Neutropenia and Diarrhoea
Digenic inheritance - retinitis Pigmentosa. XLD – Incontinentia Pigmentosa – lethal to males.
Teratogenicity:      
-         1. Lithium – Ebstein’s Anomaly.
-         2. Pencillamine – Cutis Laxa.
-         3. Misoprostol – Mobius Sequence.
-         4. Warfarin – Chondrodysplasia
Free Water Clearance = CH2O = V x [1 – Uosm/Posm], V is Urine production in mL/min.          
Atrial Natriuretic peptide is degraded by Neutral Endopeptidase.
ORTHOPAEDICS
·         Radiological evidence of Callus formation: 3 weeks after the fracture.
·         ‘Creeping substitution’ is seen in healing of cancellous bone.
·         Hormones increasing Callus formation: Calcitonin and GH. (Cortisone decrease callus).
·         Thyroxine/PTH: increase remodeling.
·         Wolf”s Law – “Increased callus formation when there is increased stress”.
·         Healing time of a fracture can be predicted by using Perkin’s Time table
·         Low ultrasound inc. Ca2+ incorporation, results in stiffer, stronger callus, Accelerated enchondral ossification.
·         Member of TGF- family which stimulates mesenchymal cells into osteochondroblastic lineage - Bone Morphogenic Protein (Urist 1965). BMP 2,4 and 7 play a crucial role in bone healing.
·         Classification for ankle fractures –LAUGE HANSEN CLASSIFICATION, DANIS-WEBER CLASSIFICATION amplified by A.O (based on level of fracture in relation to syndesmosis).
·         Special X Ray taken for Ankle injuries: Internal Rotation of 15-200. MORTISE view.
·         MAISONNEUVE FRACTURE: special type of ankle, a spiral fracture around the neck of fibula above the level of syndesmosis -which need not be internally fixed.
·         Enchondroma, Osteochondroma ( Exostosis )