Gastroenterology Investigations

 ✓Broadly classified as

     1.Test of structure

     2.Test for infection

    3.Test of function

Imaging:

✓Plain Xary: important for diagnosis of intestinal obstruction, perforation,paralytic ileus.Calcified lymph node,Gall stones,renal stone can be detected.

✓Contrast studies:X-ray contrast usually done to assess anatomical abnormality and motility.It can detect filling defect such in tumors,structures,ulcer and motility disorders.

  Common contrast X-ray include

•Barium swallow/meal Xary to assess motility disorders (Achalashia,gastroparesis),For perforation or fistula(Non ionic contrast used)

Limitations of it:

           Risk of aspirations

           Poor mucosal detail

           Low sensitivity for early cancer

            Inability to perform Biopsy

•Barium follow-through:It can be done in Diarrhoea,abdominal pain of suspected small bowel origin,Suspected malabsorption, Assessment of Crohn's disease,Possible obstruction obstruction by stricture.

Limitations include:

         Time consuming

         Radiation exposure

         Relative insensitivity

•Barium Enema: Done in altered bowel habit, evaluation of stricture or diverticular disease,Megacolon,Chronic constipation.

Limitations are:

       Difficulty in frail or incontinent patient

       Low sensitivity for lesion less than 1 cm

✓Contrast Xary are not superior than Endoscopy,colonoscopy or CT,MRI etc.

✓Ultarsonogarm: Indication includes to detect Abdominal masses,Organomegaly, Ascites,Billiary tract dilatation,Guided biopsy of lesion,Also imaging of small bowel,Gall stones

Limitations are it is operator dependent,gas and obesity can obscure visualisation,Low sensitivity for samll lesion and gives little information about function.

✓Computed tomography:It is used for assessment of pancreatic disease, Hepatic tumor deposits,Tumor staging, Assessment of lesion vascularity,To see abscess and collection.

It has radiation exposure and cost is anothy limitation.

✓Magntic Resonance Imaging:Can be used for Hepatic tumor staging,MRCP,Pelvic or perianal mass,Crohn's fistula,Small bowel visualisation.

Limitations in claustrophobic patients,contraindicated in presence of metalic prostheses,cardiac pacemaker, cochlear implant.

✓CT-positron emission tomography (PET-CT)

Used to detect metastasis not seen in Ultrasound or CT images.

Limitations is signal detection detection of metabolic activity of tumor, but Al tumors are not metabolically active.

✓Endoscopy:It includes 

    1.Upper GIT Endoscopy

    2.Enfoscopic Ultrasound (EUS)

    3.Capsule Endoscopy

    4.Double ballin enteroscopy

    5.Sigmoidoscopy and Colonoscopy

    6.Magnetic Resonance cholangiopancreatography

    7.Endoscopic Retrograde cholangiopancreatogarpahy

✓Upper GIT Endoscopy:It is performed under light IV benzodiazepine sedation or lacal anesthesia as spray.Patient should be faster at least 4 hour.By this upto first part of Duodenum can be seen.

  Indications:

     a) Dyspepsia  inmore than 55 year age

     b) Dyspepsia less than 55 year age but having alarming symptoms such as weight loss,Anemia, vomiting,hematemesis and/or melena, Dysphagia,Palpable abdominal mass

    c) Atypical chest pain

    d)  patient with Dysphagia,vomiting,weight loss,Acute or chronic GIT bleeding

     e) Screening for oesopageal varices

     f) Abnormal city or barium meal

     g) Dudenal biopsy in malabsorption

     h) Therapeutic: treatment of bleeding lesion,banding/injection of varices, dilatation of stricture,insertion is stent, placement of percutaneous gastrostomies,ablation in Barret esophagus and reaction of high grade dysplastic lesions and early neoplasia in Upper GIT.

Contraindication of it:

   a) Severe shock

   b) Recent Myocardial Infarction,unstable angina,cardiac arrythmia (These are relative contraindication,can be performed by experienced hand safely)

  c) Severe respirator disease

  d) Atlantoaxial subluxation

  e)Possible visceral perforation

c,d also relative contradiction,can be performed in experienced hand.

Complications:

   a) Cardiorespiratory depression due to sedation

    b)Aspiration pneumonia

    c) Perforation

✓Endoscopic Ultrasound: It combines with Endoscopy with intarluminal ultrasonography using high frequency transducer.It allows visualization of wall GIT and surrounding structure.It is useful to diagnose Pancreatic tumor,chronic pancreatitis, pancreatic cyst,cholangiocarcinoma,CBD stones, ampullary and submucosal tumors.Therapetic use of it in drainage of pancreatic fluid collections,Coeliac plexus block for pain management.Complication may be perforation,bleeding,cardiopulmonary events.

✓Capsule Endoscopy: Uses a capsule containing Ang imaging device, battery, transmitter and antenna.A battery powered recorded worn by the patient on a belt round the waist.Campsule transmit image and captured by the recorder.After about 8 hours capsule excreted.Images from the capsule analysed to localise the bowel segment where lesion seen then enteroscopy is usually require for confirmation and therapy.

  Indications includes obscure GIT bleeding,Samll bowel Crohn's disease, Assessment of Coeliac disease,Screening and surveillance for Familial polyposis syndromes

Suspected stricture,obstruction are contarindication as capsule retention can occur.

   

✓Double balloon Enteroscopy:It uses long endoscope with a flexible overtube.Sequential inflation and deflation done which allows the performer pushing and pulling along the whole length of the small intestine upto terminal ileum.

    

      

Gastroenterology Discussion Basic part 2

 ✓Water and electrolytes absorbed throughout the intestine by paracellular route passively and by transcellular route actively

✓ 100ml of water by faces passes by stool whear as total fluid enters into the GIT is 8 litre

✓Small intestine give protection by physical and immunological mechanism

✓ Physical defense mechanism exeryd by host bacteria,mucins and secreted antibacterial products including defendins and immunoglobulins.Also impermeable epithelial brush border,pattern recognition receptor on cell surface or intracellularly.

✓ Immunological defense mechanism:

       ∆MALT constitute 25% of total lymphatics which is the heart of adaptive immunity

     ∆ In the Peter's patches B lymphocytes differentiate into plasma cell following exposure to any Antigen and enters into the blood stream through mesenteric lymph node and then thoarcic duct.

    ∆ Plasma cell come back to lamina propria producing IgA which secreted in the limem

   ∆ T cell localise site of Antigen and macrophages phagocytose foreign materials and also sectte cytokines mediating inflammation

    ∆ Activation of mast cell causes release of IgE.

✓ Exocrine function of pancreas is crucial for digestion of carbohydrates,fat and protein.

✓Proenzymes secreted by from the acinar cell by stimulation of CCK,Secrtin,VIP, Ach,Bombesin, Substance P.

✓ Bicarbonate rich fluid secrted from ductilar cell by stimulation of Secrtin which maintains optimum pH for enzyme action.

✓ Colon act as storage organ also absorbs electrolytes and water having 2 movement Segmentation (mixing,ring contraction) and propulsive (peristaltic) 

✓Propulsive movement occurs several times a day causing passage of faeces to rectum.

✓All activities of colon stimulated after meals due to release of hormone such as 5-HT,Serotonin,motilin,CCK(Gastrocolic reflex)

✓During defecation there is contraction of abdominal muscles,increased intrabdominal pressure(Due to Valsalva monoevre)  and relaxation of anorectal muscle occur.

✓Human body contains 10^14 microbiota outnumbering the host cells

✓Genom of the microbiota 100 fold or more than host

✓Microbiotoa means the microorganism resides in particular area and microbiome means their genome

✓Metabolic capacity of microbiota is equivalent to liver

✓Example of microbiota phylum in different parts of the body include  Firmicutes,Bacteroids,Proteobacteria and Actinobacteria

✓There is degree of heredity but diet,drugs,physical activity,smoking,stress,natural aging has impact on microbiota

✓Intestinal microbiota acquired by the age of 2 years.

✓Dysbiosis between different components of microbiota asscoited with disease such as IBD, Colorectal cancer,liver disease including HCC,and also pathology outside GIT such as diabetes,asthma,obesity,CVS disease,psychiatric disorders such as depression.

✓Control of GOT function modulated by hormonal and neuronal factors

✓Centarl nervous system(CNS), Autonomic nervous system(ANS),Enteric nervous system(ENS) interact to regulate gut function.

✓ANS has parasympathetic pathway from vagal and sacral efferent causing increased smooth muscle tone,promoting sphicter relaxation(Cholinergic activity).And Sympathetic pathway releasing noradrenaline reduces smooth muscle tone and stimulate sphicter contraction.

✓ ENS senses contents and condtions in conjunction to ANS  and regulates motility,fluid exchange,secrtion,blood flow etc.

✓ENS makes two layers of neuronal networks along the length of gut intrinsic the gut wall called Menteric(Auerbach's) plexus having motor control in smooth muscle layer and Meissner's plexus in the submucosal layer having secrtory control on epithelium, enteroendocrine cells and blood vessels.

✓ENS can act autonomously by variety of transmitter such as Ach, noradrenaline,5-HT,nitric oxide, Substance P,calcitonin related peptide

✓Peristaltic movement of the gut triggered by wall distension can be influenced by innervation innervation but independently can occur.Basically electrical rytm originating from interstitial cells of Cajal in circular layer of smooth muscle which are stellate cells of mesenchymal origin calling 'pacemaker" of gut.

✓Migarating motor complexes are waves of contraction speeding from stomach to ileum occuring about 5 per minute every 90 minute or so between meals and fasting and inhibited by eating.

✓Gut hormone includes Gastrin,Somatostatin,CCK,Secrtin,Motilin,GIP,VIP,GLP-1,Ghrelin,Peptide YY.

✓Peptide YY secrted from ileum and colon,stimulated by feeding and Modulates satiety.

✓Ghrelin secrted from stomach(oxyntic cell),stimulated by fasting inhibited by eating,stmulates appetite,acid secretion and gastric emtying.

✓Vasoactive intestinal peptide or VIP released from nerve fibres throughout the GIT stimulation unknown has causes vasodilation,relaxes smooth muscle,stimulyaes water and electrolytes secretion.

✓Glucagon like Peptide or GLP-1 secrted from L cells of Ileum and colon, stimulated by carbohydrates, protein,fats.It causes stimulation of insulin release,inhibit acid secretion and gastric emtying.

✓Gastric inhibitory peptide or GIP comes from K cells of Duodenum and from Jejunum, stimulated by glucose and fat.It stimulated insulin release,inhibits gastric secretion but enhances satiety.

✓Motilin released from Duodenum,Jejunum & Colon(Mo cells) stimulated by fasting and dietary fat.It regulates Peristaltic activity including migrating motor complexes.

✓Secretin comes from duodenum and Jejunum (S cells) stimulated by Dudenal acids and fatty acids .It stimulates pancreatic fluid and bicarbonate secretion, Decreases acid secrtion,Reduces gastric emtying.

✓Cholecystokinin(CCK) secrted from Duodenum Ang Jejunum (I cells) also from ileal and colonic nerve ending stimulated by products of protein digestion,fat and fatty acids,Suppressed by trypsin.It stimulates pancreatic enzyme secrtion,stimulates gallbladder contraction,Relaxes sphicter of Oddi,Modulates satiety,Decrease gastric acid secrtion,Reduces gastric emptying,Regulates pancreating growth.

✓Somatostatin released from D cell throughout the gut stimulated by fat ingestion which inhibits Gastrin and insulin secretion, Decreases acid secretion, Decreases absorption,Inhibit pancreatic secretion.

✓Gastrin secreted from G cells of stomach stimulated by protein ingestion, suppressed by acid and Somatostatin.It stimulates gastric acid secrtion,stimulates growth of gastrointestinal mucosa. 

      

Gastrenterology Discussion Basic part 1

 

✓GIT is the most common site of cancer development

✓10% For indigestion and 1 in 14 come for GP consultation in UK

✓Functional bowel disease affects 10-15% and IBD 1in 250 population

✓Oesophagus 25 cm from cricoid cartilage to cariac orifice of stomach having ,2 construction upper and lower has perstaltinc activity which passages food to stomach.

✓Stomach act as hopper retains and grins food then propel to small intestine

✓From G cell of stomach secreted gastrin stimulate acid sevretion,somatostatin from D cell inhibit it's actionand Ghrelin from oxyntic cell increase appetite,gastric emtying and also acid secretion.

✓Protective factor from from ulcerative property of acid and pepsin are prostaglandins,mucin and trefoil factor family peptides

✓Small bowel starts from ligament if treitz to ileocal valve which has peristaltic activity in empty stomach every 1-2 hours during fasting which increase after eating.

✓Function of small bowel include digestion of food,absorption of mineral,electrolytes,water,protection from toxins and immune regulation

✓Fat digestion include several phases that include

      1.Luminal phages: where secretion of CCK from dudenum acting on GB causing contraction and relaxing Sphincter of Oddi ultimately secretion of bile.CCK also causes secretion of enzymes like amylase,protease,collipase from pancreas

     2.Fat solubilization: Mixed micelle formation combining dietery fat containing cholesterol,phospholipids,fat suble vitamins and bike acid and salts.

     3.Digestion: By pancreatic lipase and cofactor collipase triglycerides to monoglyceride and fatty acid

     4. Absorption: When micerle comes to the brush border of enterocyte fat soluble vitamins, cholesterol,phospholipids,short chain fatty acids absorbed directly where as long chain fatty acid binds with protein and absorbed.Bile salts remain in the lumen and enter into enterohepatic circulation

5.Re estirification and chylomicrons formation:In the enterocyte fatty acid resterified to form triglycerides.Triglycerides,other fats,appoproteins together form chylomicrons.

6.Transport:By exocytosis chylomicrons leaves the enterocytes,enters into the mesenteric lymphatics,then to thoracic duct and ultimately to systemic circulation

 

✓Carbohyrate starch by pancreatic to and salivary hydrolyzed forming alfadextrin,maltose,maltotriose.Disaccharides by microvillus membrane enzyme converted to form monosaccharides,galactose,fructose and glucose.Fructose enters the cell by simple diffusion but glucose and galactose enter by engery requiring processs.

✓Protein digestion starts by gastric pepsin though minor contribution but it stimulate CCK secretion which stimulate pancreases to sevrtete protease enzyme such as trypsinogen,  chymotrypsinogen,  pro-elastases and  procarboxypeptidases.Trypsinogen in the small intestine by enterokinase converted to Trypsin which further activate other enzymes.Action these enzymes form peptides,amino acid Peptde in the cell by peptidase enzyme converted to amino acid and amino acid finally actively transported to portal circulation through basal border of enterocytes.

✓Control  of  acid  secretion:  Gastrin  released  from  antral  G  cells in  response  to  food  (protein)  binds  to  cholecystokinin  receptors  (CCK-2R) on  the  surface  of  enterochromaffin-like  (ECL)  cells,  which  in  turn  release histamine.  The  histamine  binds  to  H2  receptors  on  parietal  cells  and  this leads  to  secretion  of  hydrogen  ions  in  exchange  for  potassium  ions  at  the apical  membrane.  Parietal  cells  also  express  CCK-2R  and  it  is  thought  that activation  of  these  receptors  by  gastrin  is  involved  in  regulatory  proliferation of  parietal  cells.  Cholinergic  (vagal)  activity  and  gastric  distension  also stimulate  acid  secretion;  somatostatin,  vasoactive  intestinal  polypeptide (VIP)  and  gastric  inhibitory  polypeptide  (GIP)  may  inhibi it.

 

Reference:

 El-Oar E, McLeam MH..Gastroenterology.In.Ralston SH,Penman ID,Strachen MW, Hobson RP.Davidson's principles & practice of medicine.23rd edition.Elsevier.Elssevier Ltd.2018.p.764-769

Amnesia

 Amnesia is disturbance in the memory may due to disease, drugs

Transient memory loss may be occur in due to infections,post-ictal stage,r due to Transient global amnesia.

         Transient global amnesia

Affects middle-aged persons

An abrupt discrete loss of anterograde memory lasting few hours

Patient unable to reecord new memories

Repetitive questioning is the hallmark of this condition 

Consciousness preserved

During the attack which lasts or 4-6 hours maybe retrograde amnesia of he past days,weeks or years.

Recur around 10-20-% cases

Has no physical signs so history taking from witness important

A vascular etiology is unlikely

                   Persistent Amnesia 

 Serious neurological disease must be excluded

Symptoms shoul be corroborated wit relatives colleagues. 

Mood disorders likely if poor concentration

Episodic memory may be lost in Korsakoff syndrome or Tepomoral lobe damage

Progressive deterioraton may be due to underlying dementia

Important to identify and treat dementia

Reference:

Leach JP,Daveenport RJ.Neurology.In.Ralston SH,Penman ID,Strachen MW, Hobson RP.Davidson's principles & practice of medicine.23rd edition.Elsevier.Elssevier Ltd.2018.p.1081

 

 

Rhabdomyolysis

Also known as "Crush Syndrome" is a clinical syndrome caused by release of cellular contents after significant injury to striated muscle.[1]

A key feature is large quantities of fluid can be accumulated in inflammed muscle causing significant hypovolemia. So volume replacement is important and can prevent from acute kidney injury.[1]

Released intra-cellular component  special myoglobin is toxic to kidney producing AKI.[1]

Causes:

Trauma(crush injury)

Prolongeed imobility

Compartment syndrome

DSckle cell disease

Drug: Statin,Fibrates,Antimalrials,Zidovudine etc

Toxin:Alcohol,Heroin,Amphetamine etc.

And so many other causes

Clinical Features:

Myalgia

Weaknes

Dark urine upto 50%

 

Investigations:

 

Dipstick test

Urine routine examination

S.electrolytes:Shows hyperglycemia

Creatine kinase: Elevated,Also increased ASL,ALT, LDH

Calcium: Markedly decreased due to sequestration in injured muscle 

Consider:Toxicology screening, Thyroid function if cause is not clear

Management:

 

1.Vigorous fluid resuscitation to attain euvolemia. As much 12L/day may required.

2.Aim urine output more than 150l/hour

3.Urinary alkalization

4.Do not attempt to correct Ca unless symptomatic such as tetany.

5.Dialysis if not improved,severe hyperkalemia

6.Physiotherapy for debilitated patient

Reference:

1) Steddon S, Asman N, Chesser A Cunningham J.Oxford handbook of nephrology and hypertension.Oxford university press.Oxford.2nd edition.pp 152-154

কোন‌টির কামড় ‌বে‌শি বিষাক্ত:বাচ্চা না‌কি প্রাপ্তবয়স্ক সাপ ::

 ::কোন‌টির কামড় ‌বে‌শি বিষাক্ত:বাচ্চা না‌কি প্রাপ্তবয়স্ক সাপ ::

∆∆  এক‌টি কথা প্রচলন আ‌ছে যে,বাচ্চা সা‌পের তেজ বে‌শি,বে‌শি বিষাক্ত।এর কারণ হি‌সে‌বে বলা হয় বাচ্চা সাপ যখন কামড় দেয় তখন তার ম‌ধ্যে থাকা সমস্ত বিষ ঢে‌লে দেয় কারণ সে প্রাপ্ত বয়স্ক সা‌পের মত জা‌নে না যে কতটুকু বিষ প্র‌য়োগ কর‌লে তার শত্রু ঘা‌য়েল হ‌বে।অপর‌দি‌কে প্রাপ্ত বয়স্ক সাপ যখন কামড়াঢ তখন সে তা  বিষ প্র‌য়ো‌গের প‌রিমাণ নিয়ন্ত্রণ কর‌তে পা‌রে।‌সে জা‌নে তার অস্র বিষ তার নি‌জের জন‌্য একটা দামী জি‌নি‌স। সুতরাং অযথা বিষ প্রাপ্ত বয়স্ক সাপ নষ্ট কর‌তে চায় না।

✓✓ কিন্তু এক‌টি প্রাপ্ত বয়স্ক সাপ বাচ্চা সা‌পের চায়‌তে প্রায় ২০ হ‌তে ৫০ গুণ বা তার বে‌শি বিষ সংরক্ষণ ক‌রে বা কাউ‌কে কামড় দি‌লে  এ প‌রিমাণ বিষ  তার শরী‌রে ঢুক‌তে পা‌রে।

✓✓ আস‌লে মূলত সা‌পের বিষ‌ক্রিয়া নির্ভর ক‌রে বি‌ষের উপাদান,এবং সা‌পের কাম‌ড়ে বিষ কতটুকু ঢু‌কে‌ছে বা আদো বিষ ঢু‌কে‌ছে কি না।

✓✓ সুতরাং সহ‌জে বলা যায় বাচ্চা সাপের কামড় যে বে‌শি বিষাক্ত এ কথার তেমন কোন ভি‌ত্তি নেই।

∆∆ প‌রি‌শে‌ষে বলা যায় সাপ থে‌কে দু‌রে থাকাই উত্তম তা ছোট হোক আর বড় হোক।

•Reference

1.Hayes WK. Venom metering by juvenile prairie rattle- snakes (Crotalus v. viridis): effects of prey size and experience. Anim Behav. 1995;50:33–40.

2.https://www.google.com/amp/s/wsed.org/baby-snake-venom-myth/amp/

3.https://livingalongsidewildlife.com/?p=5057#:~:text=The%20legend%20goes%20that%20young,among%20laypeople%20and%20biologists%20alike.