Hey guys, Ikan posted a clinical vignette based on this differentiation. So I did a little digging.
Both Akathisia and RLS can be caused due to antipsychotics, Akathisia goes more with typical ones and RLS with atypical ones.
Besides RLS has some other characteristic features:
1. Associated with dysesthesia originating in legs whereas in case of akathisia patient feels like it's originating in the central core of the body.
2. RLS has evening-predominance, it disturbs sleep of the patient as the patient jerks his legs during sleep which might be noted by his gf or wife.
3. There is positive family history in RLS.
4. RLS can be induced by other centrally acting drugs like Diphenhydramine, Citalopram, Clonazepam etc if there is a positive family history.
Treatment:
First intervention should always be reduction of dose of antipsychotics.
While RLS responds well to dopamine agonists like Pramipexol and Ropinirole, Akathisia responds well to Mirtazapine, a tetracyclic antidepressant. Although withdrawing the causative drug works the best.
According to latest clinical trial reports, The first line treatment of akathisia is propranolol, second line is Benztropine and if these doesn't work we resort to benzodiazepines.
That's all! You never stop learning.
-VM
Hello everybody!
Let's learn a quick way to remember a few important X-linked Dominant Disorders.
The mnemonic goes like:
All Hypo Pigmented Rats Have Resistant Rickets.
All - Alport Syndrome.
Hypo - Familial Hypophosphatemia.
Pigmented - Incontinentia Pigmenti.
Rats - Rett Syndrome.
Resistant Rickets - Vit.D Resistant Rickets.
X linked dominant disorders are rare pattern of inheritance.
All affected males will transmit it to all their daughters and all affected females will transmit the disease to 50% of her sons/daughters.
If you have another mnemonic on the same do share.
Let's learn Together!
-Medha.
Did you know corticosteroid therapy can cause depression, mania, psychosis, and delirium?
Why?
The mechanism by which the corticosteroid induces symptoms such as mania, depression, and psychosis is not clear.
The administration of prednisone is associated with decreased levels of corticotrophin, norepinephrine, and beta-endorphin in the cerebrospinal fluid. Furthermore, corticosteroids induce an increased release of glutamate that induces neuronal toxicity due to accumulation effect.
-IkaN
Benzodiazepines frequently are administered to patients to induce sedation.
Paradoxical reactions to benzodiazepines, characterized by increased talkativeness, emotional release, excitement, and excessive movement, are relatively uncommon and occur in less than 1% of patients.
The exact mechanism of paradoxical reactions remains unclear.
It is important to be aware of this side effect because increasing the dose of benzodiazepine would worsen the condition.
Hello!
Let's learn about Acalculous cholecystitis today. These are my step 2 CK notes, made from UpToDate.
What is acalculous cholecystitis?
Acalculous cholecystitis is an acute necroinflammatory disease of the gallbladder with a multifactorial pathogenesis. It is typically seen in patients who are hospitalized and critically ill.
Clinical features:
In critically ill patients, the appearance of unexplained fever, leukocytosis, or vague abdominal discomfort may be the only sign of acalculous cholecystitis. Patients may also have jaundice or a right upper quadrant mass. Laboratory test abnormalities may include a leukocytosis or abnormal liver tests, but they are nonspecific.
Diagnosis: USG.
Why?
Advantages of ultrasonography are that it is noninvasive, can be done at the bedside, and has good sensitivity and specificity for diagnosing acalculous cholecystitis. In addition, ultrasonography may reveal alternative diagnoses (such as calculous cholecystitis). Thickening of the gallbladder wall is the most reliable feature seen in patients with acalculous cholecystitis.
Ultrasonographic features:
●Absence of gallstones or sludge
●Thickening of the gallbladder wall (>3 mm)
●Pericholecystic fluid
●Striated gallbladder
●A positive Murphy's sign induced by the ultrasound probe (may be absent in patients who are obtunded or sedated)
●Mucosal sloughing
●Gallbladder distension (>5 cm).
Treatment:
In patients with acalculous cholecystitis, we recommend the initiation of broad spectrum antibiotics as soon as blood cultures have been drawn.
Infection with enteric pathogens, including E. coli, E. faecalis, Klebsiella, Pseudomonas, Proteus species, and Bacteroides is common.
Preferred surgery: Cholecystostomy rather than cholecystectomy.
Why?
Cholecystostomy is effective and is less invasive than cholecystectomy. (especially in critically ill patients.)
However, cholecystectomy should be performed if there are findings suggesting gallbladder necrosis, emphysematous cholecystitis, or perforation. Cholecystectomy is also a reasonable alternative in patients who are good surgical candidates.
That's all!
-IkaN
Hello
Women who have had breast biopsies in the recent past, that showed atypical hyperplasia, are at increased risk of breast cancer in the future. This is because of the changes in the breast that prompted the biopsies and not the biopsy itself, according to the Gail model of breast cancer risk assessment.
Moreover, high breast density (due to high fat diet and obesity) - individualised and as a modifiable risk factor itself, in combination with proliferative benign breast disease, increase the risk of cancer, but is relatively uncommon.
Source: http://jnci.oxfordjournals.org/content/105/14/1043.full.pdf
Thats all
- Jaskunwar Singh
Why does pertussis cause lymphocytosis even though it is a bacteria?
Pertussis toxin (PT), from Bordetella pertussis, causes lymphocytosis.
Lymphocytosis is because of impaired entry of lymphocytes into lymph nodes.
Here are my notes for Step 2 CK exam!
DVT treatment: Anticoagulation.
Duration: Minimum 3 months.
DVT with high risk of bleeding: IVC filter.
DVT in pregnancy, malignancy: LMW heparin.
Massive DVT: Thrombolysis / clot removal with anticoagulation.
DVT due to HIT: Stop heparin containing products. Start non heparin anticoagulation.
When should you hospitalize: Patients with massive DVT (eg, iliofemoral DVT, phlegmasia cerulea dolens), concurrent pulmonary embolism, a high risk of bleeding on anticoagulant therapy, comorbid conditions, or other factors that warrant in-hospital care.
Notes from UpToDate:
Anticoagulation is the mainstay of therapy for patients with acute lower extremity deep vein thrombosis (DVT).
In patients with asymptomatic proximal DVT, we suggest anticoagulation identical to that for patients with symptomatic DVT.
Options include subcutaneous low molecular weight (LMW) heparin, subcutaneous fondaparinux, the oral factor Xa inhibitors rivaroxaban or apixaban, or unfractionated heparin (UFH).
Although there is agreement on the minimum length of time a patient with a first episode of DVT should be treated (ie, three months), the optimal length of time is not known.
Outpatient anticoagulation rather than inpatient therapy can be considered when patients are hemodynamically stable, have a low risk of bleeding, do not have renal insufficiency, and have a practical system in place at home for the administration and surveillance of anticoagulant therapy. It is not appropriate in patients with massive DVT (eg, iliofemoral DVT, phlegmasia cerulea dolens), concurrent pulmonary embolism, a high risk of bleeding on anticoagulant therapy, comorbid conditions, or other factors that warrant in-hospital care.
For patients in whom anticoagulation is contraindicated or in whom the risk of bleeding is estimated to outweigh the risk of recurrent thromboembolism, we suggest the insertion of an IVC filter rather than no therapy.
For patients with active malignancy and pregnant women, we suggest that LMW heparin be selected as the initial and long-term anticoagulant of choice rather than other agents.
For patients with massive iliofemoral DVT or phlegmasia cerulea dolens with symptoms for <14 days and good functional status, we suggest systemic or catheter-directed thrombolytic therapy, and/or clot removal (eg, catheter extraction, catheter fragmentation, surgical thrombectomy) rather than anticoagulation alone.
For patients with a DVT and a diagnosis of heparin-induced thrombocytopenia (HIT), all forms of heparin should be discontinued and immediate anticoagulation with a non-heparin anticoagulant started.
Extra: For select patients with isolated distal DVT (eg, those at high risk of bleeding, negative D-dimer level, asymptomatic or minor symptoms, without risk factors for extension, and/or minor thrombosis of the muscular veins), we suggest surveillance with serial ultrasound over a two-week period rather than anticoagulation. Those who exhibit signs of thrombus extension should be anticoagulated.
That's all!
-IkaN
This one will help you in having a fair idea about the linking of Trypanosoma species with the diseases caused and the vectors associated.
1. T. cruzi- American Chaga's disease.
Americans have big fat freeways on which they love to cruise in their cars. Also,if you are into automobiles, you can remember the car 'Cruze'
from Chevrolet, the American carmaker.
The vector is reduviid(kissing) bug. Do I need to say more?!
2. T.brucei- This one is full of the phonetic 'sa' in it- T. brucei causes sleeping sickness with the vector being the tsetse fly!
That's all!
-Sushrut Dongargaonkar
The tubes used for serological diagnosis of typhoid are frequently asked and it takes many bungling to get the answer right. Here's a mnemonic which may come handy-
1. Felix tube- Short round bottomed which detects the 'O' antigen.
Remember the round bottom and round shape of the letter 'O'.
2. Dreyer's tube- Narrow, conical bottomed one which detects the 'H' antigen
Deserts are 'dry' and pyramids, which resemble cones are in the deserts of Egypt. Hence, conical bottomed Dreyer's tube. The letter 'H' is not round, so, it is this antigen which this tube detects.
Revise this mnemonic more than once so you get it clearly what's what.
-Sushrut Dongargaonkar
Hi everyone.
Posted in Ob-Gyn now. Let's just say it's not a lot of fun looking at diseased hoo-hoo's.
Just kidding.
Here's a Mnemonic for the absolute indications of Episiotomy.
Remember : PPPP
1. Perineum is rigid
2. Perineum has been operated on. (For Prolapse, stress urinary incontinence , etc)
3. Procedures are to be used. (Like Ventouse or Forceps)
4. Position / Presentation are abnormal. (Like Breech , face to pubis, shoulder dystocia , macrosomia)
The other indications which are non-absolute include :
- Maternal exhaustion
- Preterm/ post mature baby
- Trial of labour.
So I hope this didn't tear you up. (Pun intended).
Happy studying !
Stay awesome.
~ A.P.Burkholderia
An anterior shoulder dislocation is usually caused by a blow to the abducted, externally rotated, and extended arm (eg, blocking a basketball shot).
Violent muscle contractions following a seizure or electrocution represent the most common causes of posterior shoulder dislocation.
Hey guys, there are multiple causes of acute kidney injury in a cancer patient, namely sepsis, metastasis, tumor lysis syndrome, etc. But there is another reason which we often overlook, which is drug-induced.
1. Thrombotic microangiopathy: Associated with agents targeting vascular endothelial growth factor(VEGF), eg., Ranibizumab, Bevacizumab. These drugs also block the angiogenesis in the glomerular vasculature, such that the injured endothelium isn't replaced, leading to multiple foci of platelet aggregations just like in TTP and HUS.
2. Focal segmental glomerulosclerosis: Associated with tyrosine kinase inhibitors are the most common and are frequently associated with acute kidney injury.
3. Acute Interstitial Nephritis:
The checkpoint inhibitors ipilimumab, nivolumab, and pembrolizumab activate host T cells to enhance tumor killing by preventing tumor ligand binding to cytotoxic T-lymphocyte antigen 4 and programmed death 1 receptors, which deactivate T cells. However, this effect causes loss of self-tolerance (and perhaps tolerance to other drugs), leading to various forms of autoimmune injury, including acute interstitial nephritis, which is associated with moderate-to-advanced-stage acute kidney injury.
That's all!
-VM
