Causes of elevated serum amylase mnemonic

Hi!

Causes of elevated serum amylase mnemonic:

RAISED-AM

Differential Diagnosis of Acute Pancreatitis mnemonic

Hi!

Differential Diagnosis of Acute pancreatitis mnemonic:

HI-PANC

D-lactic acidosis in short bowel syndrome

Hello everyone!

D-lactic acidosis is an unusual form of lactic acidosis.

Which patients develop D-lactic acidosis?
1. In patients with jejunoileal bypass, small bowel resection, or other causes of the short bowel syndrome.
2. Patient who receives or ingests a large amount of propylene glycol
3. Patients with diabetic ketoacidosis

In this post, I'm going to specifically talk about D-lactic acidosis in patients with small bowel syndrome.

How do patients with D-Lactic acidosis present?

Increased anion gap metabolic acidosis.
Neurologic findings of intermittent confusion, slurred speech, and ataxia.

Why does it happen in patients with small bowel syndrome?

Glucose and other carbohydrates are normally absorbed by the small bowel. If the small bowel is bypassed, removed, or diseased, then delivery of these substances to the colon increases.

Also, overgrowth of gram-positive anaerobes, such as Lactobacilli seen in small bowel syndrome contributes to lactic acidosis.

How is it metabolized?

D-lactate is not metabolized by L-lactate dehydrogenase, the enzyme that catalyzes the conversion of the physiologically occurring L-lactate into pyruvate. Thus, D-lactate is slowly metabolized in humans, accumulates in body fluids, and generates metabolic acidosis.

Diagnosis:
Laboratory studies show increased anion gap metabolic acidosis with normal plasma lactate levels, because the D-isomer is not measured by conventional laboratory assays for lactate. Diagnosis is confirmed by specifically measuring D-lactate.

Treatment:
Sodium bicarbonate if D-lactic acidosis and acidemia are severe.

Oral antimicrobial agents (such as metronidazole, neomycin, or vancomycin) can be used when D-lactic acidosis that decrease the number of D-lactate-producing organisms.
FYI: Although antimicrobials are sometimes helpful, they can occasionally precipitate D-lactic acidosis in susceptible subjects by causing an overgrowth of lactobacilli.

Low-carbohydrate diet (or the use of starch polymers rather than simple sugars) is also helpful because it diminishes carbohydrate delivery to the colon.

That's all!

-IkaN

Stones in Crohn's disease

Hello everyone, 

In this post, I'll be talking about the different types of stones seen in Crohn's disease. Let's learn why they form! 

CHOLESTEROL GALLSTONES: Either due to ileal involvement or ileostomy, in Crohn's, enterohepatic circulation of bile acids is perturbed resulting in supersaturation of bile with the cholesterol, altering the delicate composition of bile acids, phospholipids, and cholesterol of 10:3:1 in bile fluid.

CALCIUM BILIRUBINATE GALLSTONES: Due to alteration in colonic flora conjugated bilirubin is converted to unconjugated bilirubin, which along with seepage of excessive unabsorbed bile acids from the ileum, results in enhanced absorption of bilirubin from the colon causing increased concentration in bile.

CALCIUM OXALATE RENAL STONES:

Usually, calcium in the GI tract forms a complex with oxalate ions resulting in its excretion in stool but in Crohn's due to steatorrhea excessive unabsorbed negatively charged fatty acids bind with calcium, leaving unbound oxalate to be absorbed and subsequently excreted by urine causing nephrolithiasis.

URIC ACID RENAL STONES: Diarrhea in Crohn's causes metabolic acidosis due to decreased bicarbonate absorption or increased excretion from the colon which increases the acidity of tubular fluid. The increased acidity, simultaneous dehydration, hypocitraturia, and hypomagnesemia in such patients precipitate uric acid stones.

-Kirtan Patolia

True or False #8 Lower GI Bleed

1. Angiodysplasia is a high volume arterial bleed. T or F

2. Diverticulosis is a low volume arterial bleed. T or F

ANSWERS

1. FALSE

Angiodysplasia  more often than not involves low volume venous bleeding.

Angiodysplasias are composed of ectatic, dilated, thin-walled vessels that are lined by endothelium alone or endothelium along with small amounts of smooth muscle. Studies in which casts of angiodysplasias were made by injecting a silicone material demonstrated that the most prominent feature in angiodysplasias is the presence of dilated, tortuous submucosal veins.
Small arteriovenous communications are also present and are due to incompetence of the precapillary sphincter. Enlarged arteries may be seen in larger angiodysplasias and may be associated with arteriovenous fistulas, which explains why bleeding can be brisk in some patients.
Histologic confirmation is often difficult. When obtained, it shows dilated vessels in the mucosa and submucosa, sometimes covered by only a single layer of surface epithelium.

2. FALSE

Diverticular bleeding involves high volume arterial bleed

Diverticular bleeding — As a diverticulum herniates, the penetrating vessel responsible for the wall weakness at that point becomes draped over the dome of the diverticulum, separated from the bowel lumen only by mucosa. Over time, the vasa recta is exposed to injury along its luminal aspect, leading to eccentric intimal thickening and thinning of the media. These changes may result in segmental weakness of the artery, predisposing to rupture into the lumen. Diverticular bleeding typically occurs in the absence of diverticulitis

Adverse reactions of Digitalis mnemonic

Hey guys
I am back :D

My first blog post of the year - Adverse effects of Digitalis ( Digitalis toxicity ) mnemonics

Though the ADRs are divided into extra-cardiac and cardiac symptoms, I will present a more systematic mnemonification ;p

Moderate Ascites : An approach to management

Hi everyone ! This is just a general proforma on how to manage Moderate ascites occuring due to Liver Cirrhosis.
Hope you find this helpful.

Moderate Ascites

Ix :

- Complete hemogram
- LFT : complete ; look for Liver dysfunction. Important parameters for Alcoholic liver disease : AST / ALT ratio > 2 and GGT levels raised.
- Creatinine BUN : for Pre renal AKI / Hepatorenal Syndrome
- Electrolytes : Sodium , Potassium , Calcium.
- Urine Routine and Microscopy

Ascitic fluid analysis -
∆ Biochem : SAAG ( Serum Ascites Albumin Gradient) , Ascitic fluid Proteins , ADA.
∆ Path :  Cell count. ( > 250 per micro litte suggests Spontaneous Bacterial Peritonitis).
∆ Micro : Microscopy and Culture.

USG
AFP (Alpha feto protein) for HCC screen.

Rx : 
- Bed rest and admit the patient
- Salt reduced to < 2g/day
- Fluid restricted - less than 1 L per day
- Spironolactone 100 mg per day +/- Frusemide 40 mg. ( Gen Frusemide added on day 4)
- Monitor output , input , girth , weight
- Ideal Weight loss - 0.5 - 1 kg/day
- If not - amp up doses of diuretics by day 3/4
- Max doses = Spironolactone 400 mg
Lasix = 160 mg
- Therapeutic Paracentesis indicated if - Tense Ascites , Child B Cirrhosis , creatinine < 3.
5-10 L in an hour can be removed  + IV albumin 6-8 gm/L

If failure to respond to Max dose of diuretics - that is 400 mg Spironolactone and 160 mg Frusemide , it is termed as Refractory Ascites and needs further evaluation and Paracentesis.

_________________________________________
Basis for using Spironolactone as preferred drug in Cirrhotic Ascites : Ascites occurs in these patients  Largely due to lack of degradation of Steroids by liver, and activation of Renin Angiotensin Aldosterone system.

Basis for SAAG ratio :
Difference between Serum and Ascitic fluid Albumin.
i.e. SAAG = Serum protein - Ascitic fluid protein
If the difference is more than 1.1 it indicates the Ascitic fluid was not very proteinaceous and in fact had low protein compared to serum , i.e. , it's a Transudative Ascites. Most important of which is Liver Cirrhosis (Where the Serum proteins are low themselves as well, so is the total Ascitic fluid protein.)

If the difference is less than 1.1 it indicates the Ascitic fluid was highly protein rich and it's an Exudative Ascites.

Let me know if you'd like anything clarified.
Hope this helps !
Happy Studying!
Stay awesome :)

~ A.P. Burkholderia

Hepatic encephalopathy

Hello Awesomites! :D

Long time.

Today we will be discussing the Treatment of Hepatic Encephalopathy.

I like this topic because of its integration with biochemistry.

-After stable: Identify and treat trigger of Encephalopathy.

-Nasogastric aspiration (in case of bleeding) and protection of airway with a endotracheal tube. Always prefer to give prophylaxis for SBP with Amoxiclav / Cephalosporin if GI bleed is the trigger.

-Avoid constipation and favour bowel emptying by bowel wash, enema or by lactulose (15-30ml 3 to 4 times daily) or lactitol.  

-Bowel sterilisation by neomycin 1 gm qid or ampicillin. Neomycin helps in decreasing ammonia production or its absorption from the bowel. 

-Avoid drugs, especially sedatives and diuretics. 

-Protein is restricted and vegetable based protein may be given. 

-IV mannitol as a fast drip for reducing cerebral oedema.

-Newer/ Experimental modalities:

Bromocriptine

Flumezanil (BDZ antagonist)

*LACTULOSE OR LACTILOL

-It creates an acidic intestinal environment to prevent NH3 absorption.

-Promote growth of glycolytic bacteria rather than proteolytic bacteria.

-Increase GI motility.

* L-ornithine-L-aspartate (LOLA)

-Provide a urea cycle alternative substrate.

* Rifaximin

-The recommended dose is one 550 mg tablet taken orally two times a day. Poorly absorbed Antibiotic to alter GI microbes.

*Correct Hyponatremia,Hypoglycemia and Hypovolemia.

*Branched chain Amino acids in diet. (Leucine and isoleucine)

-When no response to standard treatment, portosystemic shunting is considered.

Liver transplant allocation can be determined by using the MELD and sodium level (MELD-NA) score.

MELD score consist of:-

-Bilirubin (Means how well my liver take up byproduct from blood)

-INR (Means synthesis function of liver)

-Creatinine (Hepatorenal syndrome)

I hope it helped.

I want to thank Antariksh for edits in this post. :))

-Upasana Y. :)

USMLE Step 3: CCS Inflammatory bowel disease checklist

These are just my notes / checklist from the UW case 3. This post will not make sense to you if you are not preparing for CCS.

How to remember Sulfasalazine is associated with low sperm count

Hello!

I keep forgetting that sulfasalzine is the IBD drug associated with oligospermia... Sooo mnemonic.

Cushing Vs Curling Ulcer

Hello!

Its time to differentiate between two confusing ulcers - Cushing and Curling.

What is Cushing Reflex?
It is a triad of Bradycardia, Hypertension and altered respiration following Head injury.

What is Cushing Ulcer?
Stress Ulcer following Head injury.
Most common site - Acid producing area of Stomach.

What is Curling Ulcer?
Stress Ulcer following Burn.
Thomas Blizzard Curling.
Reduced plasma volume leads to ischemia and cell necrosis of the mucosa.
Most common site - 1st part of Duodenum.
cURling = bURn

This may help you to remember the difference between these two.

Thanks

MD Mobarak Hussain (Maahii)

Post operative ileus ( mechanical obstruction vs paralytic )

Hey Awesomites

Under normal circumstances, bowel movements usually do not appear till 72 hours after a certain abdominal or non - abdominal surgery, with a characteristic pattern of initiation of small bowel movements within 24 hours, stomach within 48 and colonic ( proximal to distal ) within 72 hours after surgery.

The assessment of gastrointestinal recovery is done with consideration to certain factors like the time taken to ingestion of first solid food, and time to either bowel movements or the first flatus passed, whichever occurs later.

Prolonged post operative paralytic ileus means:
- No return of bowel movements ( on auscultation ) after 72 hours
- Absence of flatus or stool on day 6 after surgery
- Feeling of discomfort, nausea or vomiting on oral intake, thus requiring i.v. support, NG tube placement by PO day 5.
- Partial return of bowel movements after PO day 5.

On the other hand, post operative ileus due to mechanical obstruction, inspite of sharing many signs and symptoms, is an important differential to exclude. Most of the patients with PO mechanical obstruction in the bowel ( due to herniation, adhesions, stomas, masses, etc. ) have an initial return of bowel function that may be partial/ complete, and oral intake, after a physiological period of 72 hours post operatively. 

It is then followed by intermittent episodes of nausea, feculent vomiting abdominal intense cramping pain and distension, that is often paroxysmal and rapidly progressing..

Also, patient with mechanical bowel obstruction after surgery may have other signs suggestive of ischemia of bowel loop distal to the obstruction, such as localised tenderness, fever, tachycardia, and peritoneal signs, which would mean immediate surgical intervention so as to prevent further complications !!
( Refer to UpToDate)

Thats all
Hope this helps :)

- Jaskunwar Singh

Factors increasing iron absorption in the intestine mnemonic

Hello! Long time, no see!

Did you know a number of dietary factors influence iron absorption?

Ascorbate (vitamin C) and citrate increase iron uptake in part by acting as weak chelators to help solubilize it in the duodenum.

Cushing Ulcers : An overview

Hi Everyone ! Here's a short post on Cushing and Curling ulcers.

For Cushing Ulcers you need to remember these key points :

C
U - Ulcerating - can even perforate.
S - Stomach
H - Head injury induced Stress Ulcer
I   - lNcreased
N - INcreased
G - Gastric Acid secretion.

Stress ulcers are typically non ulcerative superficial erosions  of the gastric mucosa.
They occur when a person is subjected to physical stress in the form of Trauma, Sepsis, Burns, Hemorrhage among many others.
Psychological stress doesn't cause 'Stress ulcers' , although it does pre dispose to getting Peptic Ulcer Disease on its own accord. All the same, it doesn't cause 'Stress ulcer'.

Cushing ulcers are type of stress ulcers occuring secondary to Head injury. They occur in the stomach  commonly , and  are associated with increased Gastric acid secretion. They are typically erosive and ulcerative , more likely to perforate than other stress ulcers.

Another named stress ulcer is Curling Ulcer occuring secondary to Burns. They occur in the 1st part of duodenum  commonly , and  are NOT associated with increased Gastric acid secretion.

Presentation :
Painless upper GI bleeding within 1-2 days of traumatic event.
Usually slow and intermittent bleeding.

Diagnosis :
Endoscopy.
(More to rule out other causes of GI bleed rather than ruling this in).

Treatment :

- Treat underlying causes.
- Fluids
-  Gastric pH to be maintained > 5  (using PPI like Pantoprazole)
- If lot of bleeding - Ligation of vessel at base of ulcer.

That's all!
Happy studying !
Stay awesome !

~ A.P.Burkholderia

Image based question on gallstone

Hello awesomites!

Yesterday, we posted an Image based MCQ on Facebook, Instagram, Tumblr and Twitter - And as promised, here is the answer!

Q. What type of stone is this?
Hint - This is the most common stone worldwide.

Options:
A. Cholesterol
B. Mixed
C. Black
D. Brown 

The correct answer is B. Mixed gallstone.

The given pathological specimen shows a Gall Bladder removed after cholecystectomy and multiple faceted stones found inside it.

Stones are multiple in number, the cut section shows the central brown core which is pigmented surrounded by whitish/pale layer of cholesterol making it a mixed stone.

Hope you enjoyed this question and we will be back with another one soon!

-MD Mobarak Hussain (Maahii)

Emphysematous Cholecystitis

Hello guys! Here's a brief description about Emphysematous Cholecystitis.

What are the risk factors for Emphysematous Cholecystitis?

1. Diabetes Mellitus (Most Important)
2. Immunosuppresion
3. Vascular compromise (Obstruction & stenosis of Cystic artery).

Emphysematous Cholecystitis is a life-threatening form of Acute cholecystitis & caused due to infection of the gall bladder wall with Gas forming bacteria like: Clostridium welchi.
Gas forms in gall bladder wall with occasional detection of crepitation (that's why called Emphysematous).

Development of gangrene & perforation is common.

It is managed by Emergency cholecystectomy with broad spectrum antibiotics.

Thank you

MD Mobarak Hussain (Maahii)

Oxalate stones in Crohn's Disease

A tricky Concept based question often asked in Medicine/Pathology MBBS Professional Exam-

Why Crohn's Disease patient often develop Kidney/Renal STONES, particularly OXALATE stones?

Brain to gut: Lets talk

Hey Awesomites

The brain and gut chat and share neurohumoral and immunologic messages with each other most of the times. That is why our emotions affect our stomach and intestines and vice versa. This healthy communication is disturbed when we are stressed out, anxious, or depressed.



Stress (more of psychological type) influences the type of bacteria inhabiting the gut, making a loss of our bowel flora diversification and increasing the concentration of harmful pathogens in the gut, thus leading to certain inflammatory and infectious processes.

Chronic flare - ups of inflammatory bowel disease result in deviation of the mood towards negative side by upto 60 percent by a process of rewiring the neuronal circuitary, called neuroplasticity. This inturn worsens the condition of gut on long-term basis.
Recent studies suggest that talk therapy - particularly cognitive behavioral therapy, and anti- depressants may be supportive in such cases to reduce the flaring up of inflammatory bowel syndrome.

In case of irritable bowel syndrome, that is a functional disorder ( without any actual organic cause ), the CBT and use of anti- depressants improve the symptoms in upto 60 percent patients. But which patients are likely to benefit still needs further research. Till then, we know that a referral for talk therapy in the patients of IBS is a must.


Thats all
- Jaskunwar Singh

Ultrasonography in Acute Appendicitis

Hey Awesomites

Ultrasonography ( graded compression technique ) is the investigation of choice in cases of acute appendicitis.

Step 2 CK: Differentiating ileus from SBO

Hello! Short post.

SBO: Small bowel obstruction.

Both: Nausea, vomiting, abdominal distension

Ileus: Hypoactive bowel sounds
Dull and constant pain
Dilated bowel but no air fluid levels

SBO: Initially hyperactive, later hypoactive
Colicky abdominal pain
Air fluid levels seen

That's all!
Back to studying.
-IkaN