Female, 21yo,50 kg, 159cm, Europe, medical student I was given a biomedical test results of a patient that has elevated levels of bilirubin and brown colour of urine. What are the possible diagnosis if all LFT's are within normal range? test results of patient
blood total protein 80 60-80 g/L albumin 45 35-50 g/L glucose 5 3.9-5.6 mM lakaline phosphatase 99 30-130 lU/L gamma-glutamyl transferase 40 10-55 lU/L alanine aminotransferase 35 5-50 lU/L Bilirubin 65. 0-20 uM urine colour brown yellow to amber pH 6 5.0-6.0 glucose negative. negative protein positive negative
Often in questions, it will say total bilirubin is 5 mg/dl and direct is 2.3 mg/dl is this a conjugated or unconjugated hyperbilirubinemia? This affects the thinking for my differential diagnosis
Before I read it was about 30%+ of the total, and some people have said 50%+, and I looked it up but couldn't find it either. So I was wondering if anyone knows the precise definition?
Use of D-Penicillamine in the Neonatal Hyperbilirubinemias
D-penicillamine (DPA) was first recognized as a potential benefit for neonatal hyperbilirubinemia (NHBI) caused by hemolytic diseases or immaturity of UDP-glucuronyltransferase enzyme. During this time there was a remarkedly low incidence of retinopathy of prematurity(ROP) in the infants treated with DPA. Later, our studies were replicated in other institutes in Hungary, Poland, U.S. A., India and Mexico. It is important to note that there was no intolerance or short- or long-term toxicity of the medication, in spite of the fact that in the newborn period DPA was used 10-20 times higher doses than those in adult. Juniper Publishers
For more Juniper Journals go through the below link
For more neurological disorders click on below link
I'd like to pose a question to reddit, and please know that doctors have already been consulted on this matter and treatment has already taken a path that they suggested. I would like to get a medical thought outside of that, as well, for the sake of scratching my own itch.
My son was born last Tuesday, and soon moved to the NICU with low blood sugar that could not be corrected by feeding. IV dextrose was administered and it quickly corrected, but shortly thereafter his bilirubin levels spiked, the highest blood serum reading being 17.8 mg/dl. He immediately went on to phototherapy, and was in the NICU for a week before being released with stable (not rising) levels around 13 mg/dl.
Skip to this afternoon. My wife has mastitis, and was prescribed Bactrim (Sulfamethoxazole/Trimethoprim) by her OB because she is allergic to several other antibiotics that are typically prescribed for this. She is nursing. He checked the book (I watched him do it) to make sure everything was fine with it. He noted that it did pass into breastmilk and is contraindicated due to that, but the medication wouldn't actually be harmful to the baby.
Well, I noticed on the bottle tonight a warning about direct sunlight exposure, so I decided to get online and find out why that is a problem. I'm not a Google Hypochondriacβ’ by any means, I was just curious. Well, what do I find but a thousand links that say this
> This drug passes into breast milk. While there have been no reports of harm to healthy infants, this drug may have undesirable effects on infants who are ill or premature or have certain disorders (jaundice, high blood levels of bilirubin, G6PD deficiency). Therefore, breast-feeding is not recommended for infants with these conditions. Consult your doctor before breast-feeding.
This morning (before the Bactrim), his level skin-tested at 16.8 at his pediatrician. He's going back to the hospital tomorrow for a blood test and some other things. The warning above, and others, claim that sulfonamides compete with bilirubin for binding to serum albumin, thus causing a rise in free unconjugated bilirubin. The 16.8 test this morning did not worry the doctors his because his age actually takes that level below what would be considered high risk. But it's close enough that I'm nervous about anything that could cause the bilirubin levels to rise. The Nurse Practitioner at the NICU we were at just told us over the phone that he would probably be okay for the night and to talk to t
... keep reading on reddit β‘Just got back from my doctors visit and found out I have a high bilirubin of 2.0. Doctor wasnβt too concerned and said it might be gilberts. I just remember my spleen being a little tender (1/10 on a pain scale). Doctor didnβt assess my spleen. Could this very well be due to a splenic issue?
Go post NSFW jokes somewhere else. If I can't tell my kids this joke, then it is not a DAD JOKE.
If you feel it's appropriate to share NSFW jokes with your kids, that's on you. But a real, true dad joke should work for anyone's kid.
Mods... If you exist... Please, stop this madness. Rule #6 should simply not allow NSFW or (wtf) NSFL tags. Also, remember that MINORS browse this subreddit too? Why put that in rule #6, then allow NSFW???
Please consider changing rule #6. I love this sub, but the recent influx of NSFW tagged posts that get all the upvotes, just seem wrong when there are good solid DAD jokes being overlooked because of them.
Thank you,
A Dad.
This case involves my daughter and granddaughter. This case is very complicated, so this will be an extensive post.
We found out that granddaughter had bilateral clubfoot during my daughters 2nd trimester scans. Within the next week we went to OU Childrenβs hospital for additional scans and consultation with a pediatric orthopedic surgeon to get the diagnosis confirmed. Which it was. We immediately went into research mode and started gathering as much information as possible, and we joined a support group. We started putting together a treatment plan with recommendations from our support group as well as information from the our Drβs.
Now, this is where everything gets complicated. My daughters OB called a couple of weeks later with some upsetting news. My daughter is Rh negative, which the OB knew about and this was her 2nd pregnancy, also something she knew, but she had failed to give her the rohgam shot, so she became sensitized. This condition obviously took precedence. We had to go weekly appointments to make sure baby wasnβt developing hydrops, which thankfully she did not. However, when she was born she developed hemolytic disease/hemolysis hyperbilirubinemia and she was admitted into the NICU for 3 weeks and had 5 blood transfusions. Her highest billi level was 23, but they held off on doing the blood tranfer/exchange because of the significant risk of brain damage that occurs with that procedure. However, we were informed of the damage already caused by her high billi levels as well as the damaged caused by the RH disease. This list included Cerebral Palsy. Of course this realization that there were going to be some cognitive and/or developmental disabilities was devastating news for all of us, but we did what we do and went into research mode.
Back to the clubfoot. Normally babies with clubfoot are evaluated and treated within the first few days of birth, but that wasnβt an option for us. She didnβt get her first evaluation until she was 6 weeks old. She was referred to Scottish Rite in Frisco TX. We took her there for her first 6 castings. We decided to seek a second opinion when the Dr wanted to do the tendonectomy and we just didnβt think her feet looked right. When then went to Shriners in Shreveport. One Dr at Shriners examined her feet and agreed that she was not ready for the tendonectomy and she needed more casting. Another Dr also evaluated her and wanted a neurological referral because she thought that her
... keep reading on reddit β‘Martin Freeman, and Andy Serkis.
They also play roles in Lord of the Rings.
I guess that makes them the Tolkien white guys.
She said apple-lutely
'Eye-do'
This is my first post pls don't kill me lol.
The people in the comment section is why I love this subreddit!!
Cred once again my sis wants credit lol
I heard parents named their children lance a lot.
First post please don't kill me
Edit: i went to sleep and now my inbox is dead, thank you kind strangers for the awards!
Well, toucan play at that game.
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Old Neeeeiiiiighvy
10+10 is twenty and 11+11 is twenty too
A buck-an-ear!
I Thank ye kind Matey for the booty! I be truly overwhelmed! Thank you!
Holy cow! Thank you everyone for the upvotes and awards! I wasnβt expecting this!
He should have a good vowel movement. His next diaper change could spell disaster though.
Making it all the way home and realizing that they forgot one of the containers:
Riceless
That was the punchline
From Siegenthaler's Differential Diagnosis in Internal Medicine:
Impaired Bilirubin Secretion
The secretion of bilirubin from liver cells into the bile canaliculi is the limiting step in bilirubin metabolism, while the glucuronidation of bilirubin is a relatively stable function with a high reserve capacity. Jaundice from hepatocellular damage in acute and chronic liver diseases is, therefore, characterized by a rise in conjugated bilirubin levels. The urine is dark brown second- ary to conjugated bilirubinuria. The stool color depends on the extent of hepatocyte damage, i. e., the greater the damage, the lighter the stool.
Intrahepatic and extrahepatic cholestasis also belong to this group. Biliary obstruction results in conjugated hyperbilirubinemia. In complete bile duct obstruction, the stool is acholic and urobilinogen cannot be detected in the urine.
^^If im understanding this correctly, it says that even hepatocellular damage from chronic liver diseases can cause stools to become lighter, by virtue of the fact that bilirubin cannot be excreted from within the cells to the bile canaliculi, regardless of any post-hepatic obstruction.
However, UpToDate does not list pale stools as a symptom anywhere in the cirrhosis page.
Harrison's doesnt seem to particularly rely on any aspect of the history to differentiate between hepatocellular and cholestatic jaundice, and i cannot find any specific information regarding the utility of pale stools there.
Could someone kindly shed some light on this? Thanks!
