Tuesday, November 12, 2019
Differential Diagnosis of Acute Pancreatitis mnemonic
Sunday, July 28, 2019
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
Thursday, November 22, 2018
Stones in Crohn's disease
Saturday, November 17, 2018
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
Monday, March 12, 2018
Adverse reactions of Digitalis mnemonic
I am back :D
Thursday, January 25, 2018
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
Tuesday, January 23, 2018
Hepatic encephalopathy
Tuesday, October 10, 2017
USMLE Step 3: CCS Inflammatory bowel disease checklist
How to remember Sulfasalazine is associated with low sperm count
I keep forgetting that sulfasalzine is the IBD drug associated with oligospermia... Sooo mnemonic.
Monday, August 21, 2017
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)
Thursday, August 17, 2017
Post operative ileus ( mechanical obstruction vs paralytic )
- 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.
( Refer to UpToDate)
Hope this helps :)
Thursday, August 10, 2017
Factors increasing iron absorption in the intestine mnemonic
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
Tuesday, July 25, 2017
Image based question on gallstone
Hint - This is the most common stone worldwide.
A. Cholesterol
B. Mixed
C. Black
D. Brown
Monday, July 24, 2017
Emphysematous Cholecystitis
2. Immunosuppresion
3. Vascular compromise (Obstruction & stenosis of Cystic artery).
Gas forms in gall bladder wall with occasional detection of crepitation (that's why called Emphysematous).
Thursday, July 20, 2017
Oxalate stones in Crohn's Disease
Monday, July 17, 2017
Brain to gut: Lets talk
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
Monday, July 3, 2017
Ultrasonography in Acute Appendicitis
Ultrasonography ( graded compression technique ) is the investigation of choice in cases of acute appendicitis.
Friday, June 9, 2017
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