Monday, March 11, 2019
Restrictive vs Liberal approach to transfusion in Sepsis
Norepinephrine in ICU
Norepinephrine (noradrenaline) Levophed
8 to 12 mcg/minute (0.1 to 0.15 mcg/kg/minute)
A lower initial dose of 5 mcg/minute may be used, eg, in older adults 2 to 4 mcg/minute (0.025 to 0.05 mcg/kg/minute) 35 to 100 mcg/minute (0.5 to 0.75 mcg/kg/minute; up to 3.3 mcg/kg/minute has been needed rarely)
Initial vasopressor of choice in septic, cardiogenic, and hypovolemic shock.
Wide range of doses utilized clinically.
Must be diluted; eg, a usual concentration is 4 mg in 250 mL of D5W or NS (16 micrograms/mL).
Bhopalwala. H
Milrinone in ICU
Inotrope (nonadrenergic, PDE3 inhibitor)
Milrinone Primacor
Optional loading dose: 50 mcg/kg over 10 minutes (usually not given) 0.125 to 0.75 mcg/kg/minute
Alternative for short-term cardiac output augmentation to maintain organ perfusion in cardiogenic shock refractory to other agents.
Increases cardiac contractility and modestly increases heart rate at high doses; may cause peripheral vasodilation, hypotension, and/or ventricular arrhythmia.
Renally cleared; dose adjustment in renal impairment needed.
Must be diluted; eg, a usual concentration is 40 mg in 200 mL D5W (200 micrograms/mL); use of a commercially available pre-diluted solution is preferred.
Bhopalwala. H
Dobutamine in ICU
Dobutamine Dobutrex
0.5 to 1 mcg/kg/minute
(alternatively, 2.5 mcg/kg/minute in more severe cardiac decompensation) 2 to 20 mcg/kg/minute
20 to 40 mcg/kg/minute;
Doses >20 mcg/kg/minute are not recommended in heart failure and should be reserved for salvage therapy
Initial agent of choice in cardiogenic shock with low cardiac output and maintained blood pressure.
Add-on to norepinephrine for cardiac output augmentation in septic shock with myocardial dysfunction (eg, in elevated left ventricular filling pressures and adequate MAP) or ongoing hypoperfusion despite adequate intravascular volume and use of vasopressor agents.
Increases cardiac contractility and rate; may cause hypotension and tachyarrhythmias.
Must be diluted; a usual concentration is 250 mg in 500 mL D5W or NS (0.5 mg/mL); use of a commercially available pre-diluted solution is preferred.
Bhopalwala. H
Vasopressin in ICU
Vasopressin (arginine-vasopressin) Pitressin, Vasostrict
0.03 units per minute (alternatively 0.01 to 0.03 units/minute initially) 0.03 to 0.04 units per minute (not titrated)
0.04 to 0.07 units/minute;
Doses >0.04 units/minute can cause cardiac ischemia and should be reserved for salvage therapy
Add-on to norepinephrine to raise blood pressure to target MAP or decrease norepinephrine requirement. Not recommended as a replacement for a first-line vasopressor.
Pure vasoconstrictor; may decrease stroke volume and cardiac output in myocardial dysfunction or precipitate ischemia in coronary artery disease.
Must be diluted; eg, a usual concentration is 25 units in 250 mL D5W or NS (0.1 units/mL)
Bhopalwala. H
Sunday, March 10, 2019
LMR (Last minute revision) Stuff for obstetrics and gynecology drugs
In LMR sessions, I will share final year MBBS Viva things on drugs and specimen.You can add your list in the comments below.
Today I will share the Obstetric and gynaecology viva on drugs.
Lets get started.
1.Tranexamic acid and mefanemic acid combination
Tranexamic acid:
- anti-fibrinolytic
- Amino caproic acid derivative
- CONVERTS plasmin to plasminogen
- given during menstruation
- Adverse effect:- Intracranial thrombosis
Mefanemic Acid:
- COX inhibitor.
- Given during menstruation
- Adverse effect:- dyspepsia,gastric ulcer
- Ovulatory cycles of DUB
- Post IUCD bleeding
- Post sterilization mennorhagia
- Fibroid
Doxylamine is anti histaminics that has effects on acetylcholine and serotonin release. And you know their receptor is present on CTZ centers.
Vitamin B6 is pyridoxine.
In pregnancy and poor diet the amount decreases.
USE:- Emesis during pregnancy at bedtime (not more than 2 tablet in a day).
3.Dinoprostone gel
- Prostaglandin E2
- 500 micro gram into the cervical canal below the level of internal os
- Or 1-2 mg in the posterior fornix
- maximum 3 doses 6 hourly
- Applied in posterior fornix when membrane is ruptured
- applied in internal os when membrane is intact
- USE- Cervical ripening in IOL.
- Before and after CTG monitoring is must.
- C/I- Previous CS, Impending scar rupture,fetal distress,asthma,severe heart disease
4.L-Arginine+Folic acid+isothiocyanidin
- L-Arginine is precursor for Nitric oxide generation that will lead to vasodialtion
- USE: In IUGR, Severe oligohydroamnios, preventing pre-eclampsia
- PGE1
- ROUTE= sublingual,vaginal,rectal (never parentral)
- S/E:Fever,chills,shivering
- Teratogenic: Mobius syndrome (Category X drug)
- USES:-
- OBSTETRIC USES:
- Termination of pregnancy
- PPH prevention and treatment.
- Pe hysterectomy
- IUI
- Cervical pregnancy
- Treatment of peptic ulcer caused by NSAIDs.
- Loop diuretic.
- prior to blood transfusion in severe anemia
- congestive cardiac failure
- used in complications not as anti hypertensives
- PIH with massive edema
- USE: Mixed bacterial and fungal vaginosis
- USE: GERD, peptic ulcer
- Injectable Anti-coagulant
- In 1st trimester
- Antidote: Protamine sulfate
- USE: DVT, APLA, PE, recurrent abortion (Prophylaxis:ASPIRIN+HEPARIN)
- Prophylactic: 100mg elemental iron+500 micro gram folic acid daily from 2nd trimester throughout pregnancy +6 month postpartum
- Treatment: Oral iron 200 mg elemental iron daily
- Folic acid deficiency lead to abortions, abruptio, IUGR, NTD
- In folic acid deficiency dose is 4000mg
- IgG, intramuscular
- 300 micro gram=15 ml of D positive red cell/ 30 ml of fetal whole blood
- If ICT -VE at 28 weeks
- 2 doses 12 mg betamethasone i/m 24 hours apart
- 4 doses 6 mg dexamethasone 12 hours apart
- IV for Heart resuscitation, poor kidney function, Cocaine toxicity
- Poisoning cases
- Reviving newborn
- Preventing chemotherapy side effects
- Hyperkalemia
- metabolic acidosis
- Central Muscle relaxant and anti convulsant, Tranquilizer
- S/E:- Maternal (Hypotension) and Fetal (Respiratory depression, hypotonia)
- Direct arteriolar vasodilator
- Calcium channel blocker
- USE:Tocolytics
- A/E: Flushing, Hypotension, headache, Inhibition of labor
- Anti-hypertensive
- combined alpha and beta blocker
- orally 100mg tid to 2.4 g daily
- USE: Hypertension and hypertensive crisis
- S/E:tremor, headache, CCF.
- C/I: Hepatic disorder, asthma, CCF
- Anti-spasmodic (PDE-4 Inhibitor)
- Enhance cervical dilatation during childbirth
- USE: Acute renal colicky, augment labor.
Friday, March 8, 2019
Classification Criteria for Adult Still Disease
●Yamaguchi criteria – The Yamaguchi criteria require the presence of five features, with at least two being major diagnostic criteria . In addition, the presence of any infection, malignancy, or other rheumatic disorder known to mimic ASD in its clinical features precludes the diagnosis of ASD, at least for the purpose of research.
The four major Yamaguchi criteria are:
•Fever of at least 39ºC (102.2ºF) lasting at least one week
•Arthralgias or arthritis lasting two weeks or longer
•A nonpruritic macular or maculopapular skin rash that is salmon-colored in appearance and usually found over the trunk or extremities during febrile episodes
•Leukocytosis (10,000/microL or greater), with at least 80 percent granulocytes
The minor Yamaguchi criteria include:
•Sore throat
•Lymphadenopathy
•Hepatomegaly or splenomegaly
•Abnormal liver function studies, particularly elevations in aspartate and alanine aminotransferase and lactate dehydrogenase concentrations
•Negative tests for antinuclear antibody (ANA) and rheumatoid factor (RF)
Bhopalwala. H
Useful Pediatrics mobile apps
Wednesday, March 6, 2019
HAP and VAP
Pneumonia types — The 2016 Infectious Diseases Society of America (IDSA)/American Thoracic Society (ATS) guidelines distinguish the following types of pneumonia :
●Hospital-acquired (or nosocomial) pneumonia (HAP) is pneumonia that occurs 48 hours or more after admission and did not appear to be incubating at the time of admission.
●Ventilator-associated pneumonia (VAP) is a type of HAP that develops more than 48 hours after endotracheal intubation.
Bhopalwala. H
Saturday, March 2, 2019
qSOFA Score for Sepsis
The qSOFA (quick Sequential Organ Failure Assessment) score is easy to calculate since it only has three components, each of which are readily identifiable at the bedside and are allocated one point:
●Respiratory rate ≥22/minute
●Altered mentation
●Systolic blood pressure ≤100 mmHg
Bhopalwala. H
Thursday, February 28, 2019
Cogan's Syndrome
●Cogan's syndrome (CS) is a chronic inflammatory disorder that most commonly affects young adults. Clinical hallmarks are interstitial keratitis (IK) and vestibuloauditory dysfunction, and associations between CS and systemic vasculitis, as well as aortitis, also exist. There are a range of pathologic findings, most of which reflect immune-mediated injury of the affected tissues; however, despite an association with systemic vasculitis, eye and inner ear specimens of those with CS do not reveal any evidence of vasculitis. The underlying mechanisms responsible for the eye and inner ear disease in CS are unknown.
●The predominant ocular feature of CS is IK, which typically causes eye redness, pain, photophobia, and blurred vision. Slit-lamp examination commonly demonstrates a patchy, deep, granular corneal infiltrate. IK is not essential for the diagnosis; ocular inflammation may involve other parts of the eye and may lead to iridocyclitis, conjunctivitis, episcleritis, anterior or posterior scleritis, or retinal vasculitis.
●The inner ear manifestations of CS are Ménière-like attacks consisting of vertigo, ataxia, nausea, vomiting, tinnitus, and hearing loss. Vestibular dysfunction may also cause oscillopsia, and caloric testing often reveals absent vestibular function. Recurrent episodes of inner ear disease frequently result in profound sensorineural hearing loss. Noninflammatory down-fluctuations in hearing may be difficult to distinguish from those of inflammatory origin. If hearing loss is associated with eye inflammation or other features of active CS or does not resolve within three to five days, an inflammatory origin is more likely.
●When present, the systemic vasculitis associated with CS is a large- or medium- to small-sized vessel vasculitis or an aortitis. The pattern of vessel involvement may be overlapping. Other systemic manifestations of CS include fever, fatigue, weight loss, lymphadenopathy, hepatomegaly, hepatitis, splenomegaly, pulmonary nodules, pericarditis, abdominal pain, arthralgia, arthritis, myalgia, and urticaria. An association with inflammatory bowel disease has also been observed.
●Evaluation of the patient with possible CS requires ophthalmologic examination to establish the presence of IK, scleritis, or episcleritis and to exclude other diseases and ocular pathology; neurologic and otologic examination to establish the presence of vestibuloauditory abnormalities; and rheumatologic examination to seek evidence of systemic vasculitis. We diagnose CS based upon the presence of characteristic inflammatory eye disease and vestibuloauditory dysfunction. The eye and inner ear are nearly equally likely to be the cause of presenting symptoms, while less than 5 percent of patients initially present with systemic manifestations
Bhopalwala. H
Wednesday, February 27, 2019
GPA vs MPA Flares
The distinction between GPA ( Granulomatosis with Polyangiitis) and MPA (Microscopic Polyangiitis) is important chiefly because of differential tendencies to flare. Although both diseases may flare after the achievement of remission, GPA is substantially more likely to relapse.
That's all.
Bhopalwala. H
ANCA titers and Disease flare.
Does a rise in ANCA titers predict a disease flare? — This has been a controversial area in the literature almost since ANCA were first identified in the 1980s. However, several rigorous studies have demonstrated that elevations in the titers of ANCA do not predict disease flares in a timely manner . The largest of these studies was performed on a clinical trial cohort of 180 patients (Wegener's Granulomatosis Etanercept Trial [WGET] Research Group, 2005), with serum samples drawn at three-month intervals and ANCA assays performed at the Mayo Clinic . The following findings were observed:
●Among patients who were PR3-ANCA positive compared with negative at baseline, there were no differences in the median time to relapse, disease activity score , or organ involved at relapse. Decreases in PR3-ANCA levels were not associated with a shorter time to remission, and increases were not associated with relapse.
●Relapses occurred among 46 of 101 patients (46 percent) who were mature-PR3-ANCA positive at baseline and achieved remissions of at least six months' duration. However, the proportion of patients who experienced a disease flare within one year of an elevation in ANCA titer was only 40 percent.
Other studies have come to slightly different conclusions, indicating that persistently high or rising titers of ANCA are associated with an increased risk of disease relapse . However, even in those studies, the temporal relationship between a rise in ANCA titer and the occurrence of a disease flare was poor. As an example, in a prospective study of 100 ANCA-positive patients observed over a two-year period, relapse did not occur in 43 and 29 percent of those with a rise in ANCA titers by immunofluorescence and in PR3-ANCA titers by ELISA, respectively .
In addition, a meta-analysis of 18 studies found that neither a rise in ANCA titer nor a persistently elevated ANCA titer were strong predictors of a subsequent disease flare . Therapies for relapsed ANCA-associated vasculitis (often, high doses of glucocorticoids and cytotoxic agents) carry substantial risk, including severe infections, cystitis, bladder cancer, lung fibrosis (rarely), and death. Treating all patients with increases in ANCA titers would result in unnecessary risks of toxicity in a substantial percentage of patients, nearly 30 percent in the study mentioned above. Because of these concerns, using a rise in ANCA titer as the sole parameter to justify altering immunosuppressive therapy cannot be endorsed.
A reasonable recommendation is to closely follow patients with rising ANCA titers but not to alter their therapy unless there are clear clinical signs of active disease.
Bhopalwala. H


