Ano-Rectal anatomy: Above and below pectinate line

Here's an illustration I made :)

It shows the embryology, pathology, innervation, blood supply, venous drainage and lymphatic drainage on the rectum above and below pectinate line.

Step 2 CK: Manometric findings of achalasia and scleroderma

In achalasia:
Basal LES pressure - Increases / decreases?
Peristalsis - Increases / decreases?

In scleroderma:
Basal LES pressure - Increases / decreases?
Peristalsis - Increases / decreases?

This is high yield for CK!

Non lactose fermenters mnemonic

Shigella, Salmonella, Proteus, Yersinia - Motile or non motile? produces H2S or not?

Types of barium-contrast imaging.

Hello everybody!

Let's quickly revise the types of Barium investigations.

So to enlist the investigations are: Barium swallow, barium meal, barium follow-through, and barium enema.

The barium swallow, barium meal, and barium follow-through are together also called an upper gastrointestinal series (study), whereas the barium enema is called a lower gastrointestinal series (study).

Procedure:

In upper gastrointestinal series examinations, the barium sulfate is mixed with water and swallowed orally, whereas in the lower gastrointestinal series (barium enema), the barium contrast agent is administered as an enema through a small tube inserted into the rectum.

Let's review individual examinations breifly:

Barium swallow X-ray examinations are used to study the pharynx and esophagus.

Barium meal examinations are used to study the lower esophagus, stomach and duodenum.

Barium follow through examinations are used to study the small intestine.

Enteroclysis also called small bowel enema is a Barium X-ray examination used to display individual loops of the small intestine by intubating the jejunum with a small tube and administering Barium sulfate followed by methylcellulose or air.

Barium enema examinations are used to study the large intestine and rectum.

Hope this was useful!

Let's learn Together!

-Medha.

Pill induced esophagitis mnemonic

Pill induced esophagitis is caused by a pill! :D

Causes of pill induced esophagitis mnemonic: A PILL.

Aspirin
Alendronate
Antibiotics like tetracycline, clindamycin

Potassium chloride
Iron
Less water
Lying down immediately

Interesting anatomy correlation:
The most common sites of injury are the proximal esophagus near the compression from the aortic arch and the distal esophagus in patients with left atrial enlargement.

The typical endoscopic appearance of pill-induced esophageal injury is a discrete ulcer with relatively normal surrounding mucosa.

That's all!
-IkaN

“PILL” Esophagitis.

Hello!

Let's review a very common preventable condition of pill/drug induced esophagitis. 

It is occurs due to prolonged contact of the esophageal mucosa with a medication, which acts like the damaging agent.

Medications implicated in
“pill”esophagitis are :
Tetracycline
Potassium chloride
Ferrous sulfate
Nonsteroidal antiinflammatory drugs
Alendronate. 

Most often the offending tablet is ingested at bedtime with inadequate  water, this leads to prolonged contact  u of the drug with the esophageal mucosa leading to focal damage and esophagitis.

This causes acute discomfort followed  by progressive retrosternal pain,  odynophagia, and dysphagia.

Endoscopy reveals a focal lesion localized to one of the anatomic narrowed regions of the esophagus or an unsuspected pathologic narrowing. 

Treatment is supportive.
Antacids, topical anesthetics, bland or  liquid diets are often used.

Let's Learn Together!
-Medha.

Deglutition

Hello Everyone!

 Today lets discuss deglutition. Human's love this process :) .

1.What is Deglutition?

Process by which food  moves from mouth into stomach.

2.What are the different stages?

Oral

Pharyngeal

Oesophageal

3.Is it voluntary?

No, Only the Oral stage is voluntary.

4.What is the oral stage?

Bolus is pushed by the tongue into the Oropharynx.

What is the pharyngeal stage?

It is a involuntary stage. Here bolus moves from pharynx to oesophagus. Bolus has got 4 paths in pharynx

Back in mouth: This is prevented by position of tongue against soft palate.
Upward into nasopharynx: Prevented by elevation of soft palate.
Forward into larynx: Prevented as follows(Only if you don’t talk while swallowing food :P

• Approximation of vocal cords
• Forward and upward movement of vocal cords
• Backward movements of epiglottis to seal opening of larynx
• This causes Deglutition Apnea

Enters the Oesophagus:

• Pharyngoesophageal sphincter relaxes.
• Also upward movement of larynx stretches opening of oesophagus.

What is Oesophageal Stage?

Food from oesophagus enters the stomach.Peristaltic waves aid in this process.Two types of Waves are seen:
Primary peristaltic contractions
Secondary peristaltic contractions

What is the role of lower oesophageal sphincter(LES)?

It undergoes Receptive Relaxation. i.e. it relaxes only upon entry of bolus. Otherwise it is constricted.We have 2 clinical conditions associated with it:

1.Achlasia cardia : Failure of sphincter to relax during swallowing. Causes accumulation of food in oesophagus.

2.Gastroesophageal Reflex disease(GERD): Due to incompetence of LES. Acidic content from stomach regurgitates back into pharynx.

That's all,
Thank you,
Chaitanya Inge

Paraneoplastic Dermatoses - Bazex Syndrome.

Hello everybody,

So to continue our series on cutaneous manifestations of internal malignancies
Let's quickly learn about Bazex Syndrome.

Bazex syndrome — acrokeratosis
paraneoplastica is a paraneoplastic phenomenon associated with squamous cell carcinoma of the upper digestive tract.

Presents more commonly in Males and over the age of 40.

Presentation: Erythematous to violaceous psoriasiform plaques predominantly located in acral areas (especially the fingers, toes, nose, and helices).

Nail dystrophy, palmoplantar keratoderma, and alopecia are common.

In most patients, manifestations of Bazex syndrome precede the diagnosis of malignancy or the malignancy is diagnosed concurrently.

The lesions of Bazex syndrome are usually resistant to targeted therapies, but treatment of the neoplasm usually leads to resolution of the cutaneous findings, although not always.

Let's learn together!
-Medha!

Paraneoplastic Dermatoses - Tripe Palm.

Hello everybody,

So from today onwards, I will cover a series of cutaneous manifestations of internal malignancies starting with the first one called Tripe Palm.

               (Image courtesy-Google)

(The palmar ridges are accentuated and resemble to the stomach mucosa of a ruminant-tripe.)

Tripe palm (also known as acanthosis palmaris and acquired pachydermatoglyphia) is a velvety thickening of the palms with a ridged or rugose appearance.

The term is derived from its resemblance to the stomach mucosa of ruminants (tripe).

It is associated with gastric or lung cancer.

In some cases, tripe palm is the initial presenting feature of the underlying malignancy.

Improvement of tripe palm occurrs in one-third of patients after beginning treatment for malignancy.

Hope it was helpful.

Let's learn Together!
-Medha.

Difference between Duodenal and Gastric Ulcer

Hello everyone, let’s talk about the ever confusing difference between Duodenal and Gastric Ulcer. Both the ulcers are a type of Peptic Ulcer which occurs due the action of acid resulting in the damage of alimentary mucosa. The main cause for both of them could be infection with H. pylori or intake of NSAIDs.

Watermelon stomach- GAVE!

Helloooo everybody....

So today's post is summer special ... A condition called as Watermelon stomach...

I am sharing here the most important points related to it... 

Do lemme know your thoughts on the same....And any important points that I may have missed...

Let's learn together!!

-Medha!

Fact of the day: Milk and acidity

Milk is commonly recommended as therapy for patients with peptic ulcer.

Percutaneous endoscopic gastrostomy.

Hello awesomites let's know about PEG .

PEG stands for Percutaneous Endoscopic Gastrostomy .We normally use PEG tube .
also known as Feeding tube,Esophagogastroduodenoscopy  tube.=P

In simple language PEG is method of placing a tube into the stomach percutaneously followed by endoscopy .
Tube is passed into a patient's stomach through abdominal wall .
It is preferred route of nutritional support in patients having dysphagia or in unconscious patients.
It offers superior exposure to GI systems.
Most of the PEG tube has mushroom shaped device at the end that holds it in the stomach and prevent it from falling .If it falls do not wait till next day the hole may heal and this may create complications.

Whereas PEG  is also contraindicated in:-
-Distal enteral obstruction.
-Hemodynamic instability.
-Severe ascites.
-Sepsis
-Severe Gastroparesisi.
-Thrombocytopenia.

H. pylori infection : Facts and Fallacies

Here are some interesting facts about cytotoxin- associated gene A (CagA)- positive strains of H. pylori and its role in esophageal and gastric carcinoma.

- Chronic Helicobacter pylori infection results in lower gastric acid secretion by inducing atrophic gastritis, thus hinting to have an inverse association with EC.
- H. pylori infection reduces ghrelin synthesis due to loss of P/D1 cells in the fundus and body of stomach which decreases gastrointestinal motility and induces delay in gastric emptying, thus increasing the risk of GERD.
- Also the CagA positive strains induce fluctuations in the levels of somatostatin, gastrin, dopamine and other essential hormones, which might cause increased reflux symptoms and metaplastic changes in chronic cases.
- Upregulation of proinflammatory cytokines and impaired TNF-alpha levels might play a role in pathogenesis of esophageal and gastric carcinoma. Extragastric diseases such as Colorectal polyps, nonalcoholic fatty liver disease, dental caries, coronary heart disease, the parkinson's disease, and iron deficiency anemia are also associated with H pylori infection through multiple signaling pathways.

Inspite of much evidence, there have been arguments and debates on the underlying mechanisms in causing esophageal carcinoma. A meta- analytic study, on the other hand has recently concluded that CagA- positive strains of H. pylori have a protective role in EAC while there is no such clear association with ESCC.

Thats all
- Jaskunwar Singh

The basics : Constipation

Today I am gonna give some brief review about how to treat constipation .So let's start with basics

Why constipation occurs ?
-Water serves as a transporter of stools ,decrease in concentration of water in intestine can lead to constipation ,it may be either due to increase absorption from the extracellular space or decrease water content in body.
-Decrease bowel moment

How to treat constipation?
-As now we know cause of the constipation ,we can treat constipation either by :-increasing water content or decrease loss of water from intestinal lumen
And also by increasing bowel moments so less water or salts are absorbed (Yet some drugs uses another mechanism.)

Drugs used :-
1)We can use Dietary fibers which will just form a bulk in intestine and will increase water content of faeces ,also due to bacterial degradation some osmotic active substances are produces which further increases water content Hey but there is one drawback ,it may causes gas :D.
2)Stool softeners:
-They permit water and lipid to penetrate stool .
-They are either given orally or rectally!
(Yes a drug acting on intestine can also given rectally)
-Again there is one drawback ,prolong use can cause impair  absorption of fat soluble vitamins ( A,D,E,K)

3)Osmotic laxatives (Laxative is term used for drugs for treatment of constipation)
-Colon can neither concentrate /dilute fecal fluid  so fecal fluid is isotonic throughout the colon
-Generally we use non-absorable sugars /salts eg:-Magnesium citrate & sodium phosphate.
-Osmotic laxatives are commonly used but should not be used in patient with renal insufficiency.
-But patient using sodium phosphate must take adequate water to compensate fluid loss due to it
,It may causes hyperphosphatemia,hyper natremia , hypocalcemia,hypokalemia.
-So should not be used in cardiac patients

4)Stimulant laxatives
    a) Anthraquinones:It after hydrolysis produces bowel moment in 6-12hrs if given orally or within 2 hrs if given rectally.!
   -It may causes melanosis coli.
   b)Diphenylmethane derivatives : It increases  bowel moments in 6-10hrs when given orally and in 30-60mins when given rectally.
-It has minimum systemic absorption

5) Opioid receptor antagonism
-Now this is  an interesting type of drug mechanism rather than increasing motility it "decreases" motility .

Confused ?!!

Still it is used in prevention of constipation ?!

Yes ,by decreasing motility it prolonges the transient time required for absorption of water and salts from surrounding
Eg:-Methylnaltrexone & alvimopan.

~Ojas

The basics: Peptic ulcer

Peptic ulcer is excoriated area of stomach  or intestinal mucosa caused by  excessive gastric acid secretion or upper intestinal tract secretion .A type of peptic ulcer called as marginal peptic ulcer is caused during surgical process whenever there is opening made in between stomach and jejunum of small intestine like gastrojejunostomy.

Common site of peptic ulcer ?
Mostly on lesser curvature of antral end  of stomach and rarely on lower end of stomach.

Causes of peptic ulcer ?
1)Increase in acid secretion and peptic content in stomach .
2) Irritation to mucosa.
3)Poor blood supply .
4)Poor secretion of mucus.
5)Infection by H.pylori.

Treatment of peptic ulcer.
We give anti-ulcer therapy for peptic ulcer treatment
Following are goals of anti-ulcer therapy
a) Relief of pain.
b)Ulcer healing.
c)Prevention of complications.(like bleeding ,perforation)
d)Prevention of relapse.

Approach of  treatment of peptic ulcer :
(I have made some lame tricks for memorising drugs name:D ,if you have some mnemonics please comment !)
1) Decrease acid secretion :It includes total 4 categories ,they are described below .

a) H2 Anti-histamine (They all end with -tidine)
-Cimetidine .     
-Famotidine.
-Ranitidine.
-Roxatidine.

b)Proton -pump inhibitor.(ends with -prazole)
-Omeprazole.
-Esomeprazole.(Read it as Es-omeprazole)
-Lansoprazole.
-Pantoprazole.
-Rabeprazole.
-Dexrabeprazole
(Read it as Dex-rabeprazole!)

c)Anti-cholinergic drugs:
-Pirenzepine .
-Propantheline.
(Read it as Propan-the-line).
-Oxyphenonium .

d) Prostaglandin analogue:Misoprostol !

2)Neutralization of gastric acid secretion
    (Antacids) .It includes 2 categories
a) Systemic:
-Sodium bicarbonate .
-Sodium citrate.

b)Non-systemic:
-Magnesium hydroxide .
-Magnesium trisilicate.
-Aluminium hydroxide.
-Calcuim carbonates.

c)Ulcer protective:
-Sucralfate.
-CBS (Colloidal bismuth subcitrate!).

d)Anti-H pylori drugs:
-Amoxicillin.
-Tetracyclin.
-Clarithromycin.
-Tinidazole.
-Metronidazole.

~Ojas
 

Complicated vs. Non complicated appendicitis

• Complicated appendicitis has a perforated or gangrenous appendix.
• Non complicated appendicitis has a non-perforated appendix.

The treatment plans are different too!

• Non complicated appendicitis needs an immediate appendectomy
• Complicated appendicitis need to go through an antibiotic course before going to an appendectomy.

Reference : Schwartz Principles of Surgery 10E

Jay :)

Causes of Acute Pancreatitis

Hi guys,

I have an exam soon and I was struggling with this, so, I made this up!

To remember causes of Acute Pancreatitis, you need to think of none other than your nursery school days! :P

So, here we go- ABCDEFGHI, (oh wait did I just say "HI" :P)

Now going a little off track, but, when I was small I used to do a lot of gardening, so I remember rest of the causes as Me POT.

Alcohol ingestion  (acute or chronic)
Biliary calculus
Connective tissue diseases- SLE, TTP,  PAN
Drugs- diuretics- frusemide, thiazide. (Others are anti retroviral drugs, sulphomamides, tetracycline, tamoxifen, etc)
Endoscopic procedures
Familial/ Genetic
Hereditary Pancreatitis/ Hyperparathyroidism/ hypercalcemia/ Hypertrigylceridemia
Infections- viral

Metabolic conditions - renal failure,
Penetrating Peptic Ulcer
OPC poisoning
Trauma to abdomen

Phew, a long list. Isn't it?

Hope it helps!!
That's it!

-Rippie

Duodenal atresia notes and mnemonic

Duodenal atresia

Hey!

In this post, I wanted to emphasize duodenal atresia is associated with double bubble sign.

It's common in Downs syndrome and polyhydramnios maybe seen in utero.

Bilious vomiting is seen because the obstruction is after the ampulla of Vater.

Because the child is vomiting, abdominal distension is not seen.

That's all!
I need sleep right now.
-IkaN

Enteric nervous system (ENS)

Recently, while studying pharmacology, I came to know about the third system of ANS - Enteric nervous system, apart from sympathetic and parasympathetic systems .

Here is some information of ENS:

It consists of highly organized neurons situated in the wall of GI tract.

It mainly includes Auerbach's plexus and Meissner's plexus.

The most interesting point about ENS is this network receives preganglionic fibers from the parasympathetic system and from postganglionic sympathetic neurons.

ENS controls GI motility, secretions, mucosal blood flow.

ENS causes relaxation or stimulation of smooth muscles.

Non-cholinergic excitatory transmitters such as substance - P plays a modulatory role in controlling ENS!

~Ojas