To all UW readers - let us help ourself .. - amith

[ArchivalUser]

Ca/Ph/PTH --------------CONUNDRUMS

1. Osteoprorosis
--nl PTH/Ca & Ph-- Dec osteoclast--->dec resorption, Bone loss but mineraliztion is normal

2. Pagets
--Nl PTH/Ca & PhInc ALP--defect in skeletal meneralization/incr bone turnover-incr resop & formation(Inc osteoclast And Inc Osteoblast---> thick sclerotic bone.)

3. Osteomalacia
--Vit D ineffective (not deficient)/low Ca & Ph/high PTH/ nl 1,25 Vit levels (aka calcitrol)
--Defect in mineralization/looser zoenes - pseudofractures/Blurring of Spine on X ray

4. Type II Vit D dependent Rickets
--Mutation of Vit D receptor thus nl Vit D levels (calcitrol) other Values same as osteomalacia
--defcet in mineraliztion of bone and cartilage (growth plate)

5. X linked Hypophophatemic Rickets
--isolated decr Ph / everything else normal/may nl to low Calcitrol

6. Milk Alki Syndrome
--incr Ca/decr PTH, alkalosis & renal failure

7. Osteogenis Imperfecta Type I
--Defect in Collagen Type I

8. Primary Hyperparathyroidsm
--incr PTH & Ca / decr Ph
--MCC = parathyroid adenoma

9. Secondary Hyperparathyroidsm
--incr PTH/ low Ca & Ph
--exp . Vit D def and Renal failure (incr PTH & Ph and decr Ca--?)

10. Pseudohypoparathyroidism
--incr PTH and Ph and decr Ca

11. CRF-- dec ca,incr phosphorous,inc PTH

[ArchivalUser]

The previous post was from Ben/star earlier discussion based on UW thx n from my collections

[ArchivalUser]

if routine antiepileptic mx does not break seizure, INTUBATION is the tt of choice
workup is done after the control of seizure

[ArchivalUser]

In a case of subarachmoid hge, the associated electrolyte imbalance os hyponatremia

Thsi is cerebral salt wasting syndrome, due to SIADH and increased vasopressin secretion

[ArchivalUser]

the drug PRIMIDONE mentioned before has S/e of acute intermmittent porphyria..to elaborate on its clinical presentation , the c/f of AIP will be
1.abdominal pain
2.psych
3.neurological abnormalities

[ArchivalUser]

Pulmonary embolism guys please dont get confused with this thread byfar this is the best discussion we ve had for PE MXN NSIMX----->I would take usmle20 and depa's conclusion as a review.....

http://www.usmleforum.com/forum/message.php?id=118928

[ArchivalUser]

the basic pathophysio underlying cataplexy is DISTURBED REM SLEEP REGULATION

Not a true syncope
d/d is through associated features:
no lossof conciousness
loss of muscular tone
assc with some emotion
coexistent with narcolepsy in 75% cases (daytime somnolece and hypnogogic hallucinations)

[ArchivalUser]

Best treatment: URGENT surgical decompression as it affects prognosis

[ArchivalUser]

ISOIMMUNISATION

fetus is at risk when
1.mother is ag -ve
2. father is ag +ve
3.atypical ag test is +ve
4.abs associated withhemolytic ds of newborn are +ve
5.>1:8ab titre fetus is at risk

is fetus anemic
what is to be done ?
1.Amniocentesis for af bil. Bil plotted on liley graph
2. PUBS
if fetal hematocrit is <25 anemic... nl is 40

is it the time to intervene? i.e is the anemia severe enough ?

on liley graph
zone1: no or mild anemia repeat amniocentesis
zone2: moderate repeat amniocentesis
zone3: high risk intervention required

intervention
if fetus<34wks --------------- intra uterine transfusion
if fetus>34wks --------------- deliver

Prevention
1. routinely to all rh-ve mothers at 28wks
2.within 72 hrs of cvs,amniocentesis,d&c to a rh-ve mother
3.within 72 hrs of delivery of rh+ve baby to a rh-ve mother
300micro gm of rhogam neutralises 15ml of fetal rbc i.e 30ml of fetal blood

TO REMEMBER

1.ABO incompatibility decreases risk of maternal isoimmunisation
2). Duffy ------------------>Dies
3) kell kills,lewis --------->lives
4.atypical abs test(att)------ INDIRECT COOMBS TEST
5.kleihauer-betke test----fetal cells in maternal blood both qualitative &quantitative

[ArchivalUser]

best tt: 100% O2
best med: nasal or subcutaneous SUMATRIPTAN