Showing posts with label Hepatobiliary system. Show all posts
Showing posts with label Hepatobiliary system. Show all posts

Wednesday, February 8, 2017

Alcohol and Drug Interactions: Disulfiram-like Reaction


Hey, guys...

So day before yesterday, there was my Forensic Medicine viva and the examiner asked me the causes of impotency. And I immediately started blabbing about Stress, Phimosis, Hypospadias, Peyronie's disease, I even mentioned Parkinson's disease. The examiner interjected me and asked the most common cause. I guessed heart disease and the related medications and he denied. Then he said it is excess consumption of alcohol and asked me not to underestimate alcohol and it's various interactions and correlations ever.
So here I am, trying to summarize the interactions of alcohol with the major classes of drugs.

Disulfiram-like Reaction


I am not going to go into the details of the mechanism. Just, in brief, Disulfiram-like reactions entails flushing(due to dilatation of blood vessels), nausea, vomiting, sweating, hypotension, so reflex tachycardia which can be deleterious to a patient of coronary artery disease(CAD).

Now let us try to use CAD as a mnemonic here while learning certain other things as well.

1. It starts with C, a lot of drugs starting with C have this reaction, like Cefamandole, Cefoperazone, Cefotetan, Chloramphenicol.

2. Patients with CAD have Pain, so let us now manage that some analgesics starting with P(for Pain), Phenylbutazone, Phenacetin.

3. Patients with CAD can have attacks of Angina, for which we give Nitrates, so let us take that. Drugs with Nitro group: Nitroglycerin, Isosorbide dinitrate, Nitrofurantoin, Metronidazole. Why leave Sulpha group behind?
Drugs with Sulpha group: Sulphamethoxazole, Sulfisoxazole.

4. CAD often co-exists with Diabetes Mellitus(DM). So let us manage that with some Sulfonylureas; Tolbutamide, Tolazamide, Chlorpropamide and even the 2nd gen drug Glyburide.

5. Patients with DM are immunosuppressed. Hence, they are predisposed to Mycoses and TB. Manage them with Griseofulvin and Isoniazid respectively.

That's all! :)
Do go through the other posts in this series, 2nd Part3rd Part, and 4th Part

-VM

Monday, January 9, 2017

The SAAG solution (Serum-Ascites Albumin Gradient simplified)

Yo people!

A good friend of mine asked me to review the concept of SAAG. So let's dive into a "Puddle" of ascitic fluid. :P

As you guys all know, SAAG stands for Serum-Ascites Albumin Gradient and it helps to differentiate the causes of ascites. What it means is pretty self explanatory, it is the difference (gradient) between the levels of albumin (a plasma protein) in two compartments i.e. Serum and Peritoneal fluid.

Sunday, January 1, 2017

Triad of Charcot

Hello

Charcot's triad in acute cholangitis: FOR
- Fever
- Obstructive jaundice
- Right upper quadrant pain

Chracot's triad in multiple sclerosis: SIN
- Scanning speech
- Intention tremors
- Nystagmus


Thats all
- Jaskunwar Singh

Monday, October 31, 2016

Fever : What questions to ask your patient and why

Fever
So we're familiar with the definition and measurement of fever. But while taking a case or interacting with a patient with this simple and most basic symptom , what all should we ask for to make sure we don't miss out on anything ?
Here's a list of things your Historytaking should elicit :
Ask for :

1. Onset and Duration.
When did the fever begin - and for how long has it lasted. (This would give a clue whether the person suffers from an Acute Febrile Illness - which can generally be attributed to Infectious Disease , or a rather Chronic form of fever which could be due to Granulomatous diseases or even Neoplastic and Autoimmune conditions )

2. Progression.
(Has it worsened or Become better since its onset. This gives a clue about the present status of the patient. )

3. Chills , Rigors , Sweat .
(It's essential to include the presence or absence  of chills+Rigors + Sweat immediately in the fever description. Presence of Chills and Rigors indicate any infectious process in the body and can be found in Malaria and UTI's among other conditions. Sweating after feeling hot and then cold  is characteristically associated with Malaria)
(Important : Presence of the B Symptoms - which are Night Sweats ; Fever ; Weight loss. Seen with Lymphomas and TB)

4. Periodicity .
(It's of extreme value to understand the pattern of the fever.
If the fever is present throughout the day with a variation of not more than 1°C it is of the Continuous Type : As seen in Enteric Fever and even UTI's .
If the fever is present throughout the day but the variation is more than 1°C it is of the 'Remittent' variety. It may not be possible to distinguish between these 2 on history alone.
Intermittent is when the fever stays only for some duration during the day and the patient is afebrile during the remaining part )

5. Diurnal variation ?
(Night rise of fever could be suggestive of Tuberculosis)

6. Associated with Rash or any Spots ?
(Viral exanthems like Dengue , Chikungunya , Zika or even Rickettsial diseases commonly present with some form of rashes)
(Another possibility could be a primary Skin condition induced fever )

7. Arthralgia , Myalgia ?   
(Arboviruses like Dengue and Chikungunya are infamous for these. Arthralgia is especially debilitating in Chikungunya fever. Body ache is also common in both. Retro-orbital pain and Bifrontal headache are common with Dengue.)

8.  Icterus , High colored urine.
(Presence of these  - especially during the post monsoon season should raise suspicion of Leptospirosis or Acute Viral hepatitis. Enteric fever may be considered)

9. Cough , weight loss?
(Presence of these should raise query of TB or Pneumonia )

10. Dysuria, urgency , frequency?
( UTI is a common cause of AFI especially in Diabetics )

11. Altered sensorium, photophobia , vomiting ?
( Characteristic of Meningitis /Encephalitis)

12. Eating outside , GI disturbances ? (Enteric fever or Gastroenteritis should be suspected )


I hope this gave a crisp summary of how a fever case can be approached . Goodbye ! Happy-Treating !
A.P.Burkholderia

Tuesday, October 25, 2016

Study group discussion: Bradycardia

Name the causes of bradycardia!

Physiological bradycardia is seen during sleep and in athletes.

In typhoid fever, yellow fever and brucellosis, we see relative bradycardia.

Pathological bradycardia is seen in hypothermia, hypothyroidism, raised intracranial tension & inferior wall myocardial infarction, hypertension, bradyarrhythmia, etc.

What is relative bradycardia?

Thursday, September 29, 2016

SAAG mnemonic

Hello!

SAAG is serum albumin ascites gradient.

SAAG is >1.1 in portal HTN, CHF, HVT and constrictive pericarditis.

The mnemonic for this is SAAG is High in conditions with an H.

portal Hypertension
congestive Heart failure
Hepatic vein thrombosis
Heart constriction (Constrictive pericarditis)

For completion, SAAG < 1.1 is seen in nephrotic syndrome, cancer and infections (except SBP)

That's all!
Have an amazing day!
-IkaN

Sunday, September 18, 2016

Ceftriaxone and cefotaxime

Why is cefotaxime preferred over ceftriaxone in neonates and patient with liver disease?

Ceftriaxone-induced biliary sludge is a solubility problem that occurs in patients receiving high-dose treatment (greater than or equal to 2 g).

The risk of developing ceftriaxone-associated biliary "pseudolithiasis" increases with increasing ceftriaxone dose and in patients with impaired gallbladder emptying.

Cefotaxime has renal excretion and therefore preferred over ceftriaxone.

Sunday, August 28, 2016

Step 2 CK: Management of liver laceration

Hello!

Say you have a hemodynamically unstable patient with a gunshot wound or blunt trauma to the RUQ.
Why shouldn't you simply suture and close deep liver lacerations?

Because of the risk of hemobilia and abscess formation.

Here's what a surgeon must do:

Friday, July 15, 2016

Normal AST, ALT and ALP values mnemonic

Continuing the normal values mnemonic posts :D
Today's post is on liver enzymes!

Normal SGOT, SGPT and ALP values!

Tuesday, June 14, 2016

Study group discussion: White jaundice

Can anyone explain about what is white jaundice?

I think it refers to cholestasis syndrome (obstruction of bile outflow)

Jaundice (Increased conjugated bilirubin)
Acholia (Pale stools, thus "white jaundice")
Choluria (Dark urine)
May have generalized pruritus (Due to cholesterol)

Here's what someone else wrote:

White Jaundice is not a separate disease, it is a very old term for jaundice.

Jaundice is a condition in which bilirubin, which is a yellow coloured pigment, accumulates in the body and causes the skin to turn bright yellow. In severe cases, the skin can appear brown.

To confirm that someone is jaundiced, and not just dark-skinned, the whites of the eyes are examined, yellow colouration here is a clear sign of jaundice, hence the old expression "white jaundice".

Tuesday, May 17, 2016

Viral hepatitis - A histologic clue to the causative virus

Viral hepatitis is predominantly caused by hepatotropic viruses, although others like EBV, CMV are also implicated in the causation. Though serological markers serve as a gold standard for diagnosis, the following histologic clues help a pathologist to suspect the causative virus.

HAV - The portal tracts show a large amount of plasma cell infiltrates.

HBV - Presence of Ground Glass cytoplasm

HCV- Lymphoid aggregates in the portal tracts with macrovesicular steatosis of hepatocytes (most marked with Type 3)
Steatosis in zone 1 is mainly due to HCV while steatosis in zone 3 is mainly due to metabolic causes or alcohol.
EBV - Beads on a string pattern of sinusoidal infiltrates of Atypical lymphocytes.

CMV- Formation of microabscesses with intracytoplasmic and intranuclear inclusions.

Herpes virus- Nonzonal punched out necrosis with nuclear ground glass (Cowdry A) inclusions.

Thus, a good pathological suspicion would add to the confirmatory serological reports.

Wednesday, September 16, 2015

Cirrhosis of liver: Concepts, mechanism and pathophysiology

Hello everyone! 

In this really long post, I'll be discussing the pathophysiology of some of the signs, symptoms and conditions seen in chronic liver failure / alcoholic liver disease. We are going to focus on the WHY.

Let's get started ^__^

Why is gynecomastia, testicular atrophy and female pubic hair distribution seen in males with chronic liver failure?
Physiology:
- Liver metabolizes estrogens.
Pathology:
- In cirrosis, estrogen degradation is decreased, so estrogen concentration are elevated causing testicular atrophy, gynecomastia & changes in pubic hair.
- Estrogen also induces SHBG production and this further reduces the free testosterone levels.

Stigmata of diseases

What does stigmata mean?

Stigmata means some lesion, mostly skin, which is visible, showing the patient is suffering from that particular disease.
In some diseases, like leprosy and tuberculosis, the patient may not want to reveal the condition because of the stigmata associated with the disease in society. But due to certain signs, the disease gets revealed. (These diseases were considered a disgrace in earlier days.)

Examples - 

Thursday, February 12, 2015

Study group discussion: Alcohol and liver enzymes

Which is the most sensitive enzyme for alcohol abuse?

Gamma glutamyl transaminase (GGT). 

What is the ALT:AST ratio specific for alcoholic hepatitis? 

1:2

2:1 is AST ALT. That was the catch if you got it wrong! Scotch and tonic is the mnemonic!

Which is more specific for liver disease.. ALT or AST?

ALT.

Why? 

ALT is more specific for liver disease than AST because AST is found in more types of cell (e.g. heart, intestine, muscle).

Wednesday, March 21, 2012

Exudate & Transudate

Hello everyone!

Whenever you find fluid in the body which is out of the circulatory system you need to differentiate whether this fluid is an exudate or a transudate (Only if it is in pathologically significant amounts!)

I'll let you know why this is important in a while.. Keep reading.