Hi friends,
Here's a quick way to remember the cause of Cleft lip and Cleft palate.
LMN
Cleft Lip - failure of fusion of Maxillary and median Nasal prominences!
PPP
Cleft Palate - failure of fusion of two Palatine Processes!
That's all!
-Rippie
Hi friends,
Here's a quick way to remember the cause of Cleft lip and Cleft palate.
LMN
Cleft Lip - failure of fusion of Maxillary and median Nasal prominences!
PPP
Cleft Palate - failure of fusion of two Palatine Processes!
That's all!
-Rippie
Here are some important things you should know about erythropoietin therapy.
It is used in patients on dialysis.
Resistance to erythropoietin is most commonly due to iron deficiency.
Adverse effects are associated with rapid rise in hematocrit and hemoglobin - Hypertension, Thrombosis.
Other side effects are: Headache, flu like symptoms, red cell aplasia.
Did you know?
Erythropoietin was the first human hematopoietic growth factor to be isolated.
Erythropoietin was originally purified from urine of patients with severe anemia.
It is banned by the International Olympics Committee.
That's all!
-IkaN
Hello lovely medical students!
Priapism is persistent, painful erection that develops without sexual simulation.
Here are a few causes of priapism:
Prazosin
(Mnemonic: PRazosin causes PRiapism)
Trazodone
(Mnemonic: Trazodone causes a boner - TrazoBone)
Perineal or genital trauma
Neurogenic lesions
Sickle cell disease and leukemia
Always check medications first, since it is often drug induced.
That's all!
-IkaN
Hello! In this post, I'll be talking about nephrotoxic antimicrobials.
Let's start with Aminoglycosides!
Aminoglycoside toxicity manifests in the form of tubular necrosis.
Did you know AKI due to Aminoglycosides manifest 5-7 days after therapy even after the drug has been discontinued? :O
Aminoglycosides accumulate in the renal cortex and cause non oliguric AKI. Hypomagnesemia is a common finding.
Amphotericin B also causes tubular necrosis. It binds to tubular membrane cholesterol and introduces pores. Clinical findings include polyuria, hypomagnesemia, hypocalcemia and NAGMA.
Mnemonic for nephrotoxic drugs: Drugs with A!
Aminoglycosides
Amphotericin B
Antivirals like acyclovir, tenofovir, cidofovir, foscarnet, pentamidine.
(Cause tubular toxicity)
Antibiotics like penicillin, cephalosporins, quinolones, sulfonamides, rifampin.
(Cause acute interstitial nephritis)
Remember, in acute interstitial nephritis, WBCs, WBC casts and urine eosinophils will be seen. However, in AKI, the urine sediment will show granular casts.
That's all!
The predominant feeling I have is that if gratitude (=
-IkaN
Good morning! =)
I was studying about radiolucent kidney stones and thought of sharing what I learnt with you all.
Mnemonic for radiolucent renal calculi: CATIX URL
Cysteine
Adenine (2,8-Dihydroxyadenine)
Triamterene
Indinavir
Uric acid
RadioLucent
Another mnemonic for medication stones: GUEST MIC
Guaifenesin stones (Radiolucent)
Ephedrine stones (Radiolucent)
Sulphonamides stones (Radiolucent)
Triamterene stones (Poorly radiopaque)
Magnesium trisilicate stones (Poorly radiopaque)
Indinavir stones (Radiolucent)
Cephalosporins stones (Radiolucent)
If you are asked to choose the radiolucent one between Orotic acid stones and cysteine stones, choose orotic acid. It is radiolucent, cystine is poorly radioopaque.
Magnesium ammonia phosphate (struvite) and Cystine calculi are less radiodense and are more difficult to visualize. Uric acid, orotic acid, xanthine, triamterene, dihydroxyadenine, and indinavir calculi are radiolucent and might not be seen on a plain radiograph.
(Source.)
Predisposing factors for uric acid stones:
1. Low urinary pH
2. High uric acid excretion
Treatment for uric acid stones:
1. Alkalinization of urine
(Sodium bicarbonate, potassium citrate)
2. Increase fruits, veggies. Decrease animal flesh.
3. XOI - Allopurinol, Febuxostat
Alkalinization of urine mnemonic: ABC.
Alkalinization. Bicarbonate. Citrate.
(Sodium bicarbonate and potassium citrate are used for alkalinization of urine)
That's all!
-IkaN
We were discussing a MCQ from pathologystudent.
Here's the question:
On a routine physical examination of an elderly male patient with no other medical problems, you note that his earlobes and fingertips are pale and slightly bluish. A CBC shows a hemoglobin of 10.6 g/dL (12 – 16) and an MCV of 88 (80 -100). Numerous red blood cell agglutinates are seen on the blood smear, made by smart technologists in your laboratory. Which of the following statements is true?
1. The antibody bound to the patient’s red blood cells in this disorder is probably IgG
2. Complement is probably bound to the patient’s red cells
3. The spleen is the main site of red cell destruction in this patient
4. 1 and 3
5. 1, 2, and 3
1 is not true. It's cold agglutinin disease. The main antibody is IgM here.
2 is correct since complement is involved.
The main site of destruction is liver macrophages (Kupffer cells). Therefore, 3 is incorrect.
Is there a specific reason for it?
Liver RECs have loads of C3 specific receptors. So most extravascular hemolysis that occurs in cold agglutinin disease is in the liver.
Another common mechanism of hemolysis in cold agglutinin disease is direct complement mediated intravascular hemolysis.
There's C3b on RBC and macrophage has CR3 (Complement receptor 3).
Liver macrophages lack the capacity of spleen to sequester cells. Hence, here the RBC destruction in liver occurs by phagocytosis predominantly.
Thanks, Divya, for explaining this.