Confused about the Doctor in Nepal? We help you to find best doctor according to your disease.Don't just wait .Contact us.
Matrika Eye Center
Dr Dinesh Upreti - General Physician At Rajbiraj,Nepal
Dr. Manu Basnet-One of the leading Gastroenterologist in Nepal
Dr.Manu Basnet is one of the leading Gastroenterologist in Nepal.Gastroenterologist is a doctor who is trained to find and treat disease of the gastro-intestinal tract.It includes disease of from mouth to colon including liver,gall bladder and pancreas.You may need to visit a gastroenterologist when you have problem with swallowing,chest burn,chronic diarrhoea,abdominal pain.
Dr.Manu Basnet Completed MBBS from BPKIHS, Dharan in 2000.He worked as house officer in ICU/CCU of TUTH, Maharajganj, Kathmandu for one year.He served in PHC Lete,Mustang and PHC Syringa,Gulmi under government of Nepal for one and half year.After 3 year of his service,he joined Internal Medicine Residency at TUTH,IOM,Maharajganj and got his post-graduate degree of Internal medicine in 2006.He then worked for improving the health quality of the country.He started working in Butwal Hospital Private Limited,Butwal.He then got a chance to be lecturer at Lumbini Medical College,Tansen and ignite the flame of knowledge in young minds.Without further ado,he joined Lumbini Medical College.
Dr Manu went to Hyderabad,India in 2011 and got training on endoscopy and Colonoscopy.He then started doing endoscopy and colonoscopy in Nepal.After returning from AIG,Institute Hyderabad,He worked as gastroenterologist in Norvic International Hospital from 2014 to 2021.
Dr Manu Basnet is the first doctor in Nepal to do enteroscopy in 2017.He is the one of the best doctor for Endoscopic ultrasound,ERCP and other endoscopic diagnostic and therapeutic procedure in Nepal.He is currently practicing at Star hospital,Sanepa with the best endoscopic equipment and suite.With years of trainning,he has expertise in treating :
1.Hepatitis
2.Pancreatitis
3.Peptic ulcer
4.Crohn's disease
5.Ulcerative Colitis
He says “People do not need to go India or other country for treatment. At the star hospital,we provide the best digestive disease service.” He has treated and cured thousands of patients with digestive disease.People are glad that they visited him for treatment.
Best Psychiatrist in Kathmandu-Nepal
We know it is frustrating when you can not focus in study or work, When your mind is overthinking each and every event.We understand that you are in search of good psychiatrist in Nepal and you will find them with Medicosguide.
Mental health is an important aspect of our health.There are so many mental health problems that can be treated with medicine and therapy but only under psychiatrist supervision.Mental health is as important as physical health.There are so many misconception regarding mental health problems.It is not true that you will need medicine for your entire life.Before going into any conclusion of mental diseases you should discuss your problem with a good psychiatrist which we have listed here under "Best Psychiatrist in Kathmandu,Nepal".What can be some of the symptoms of mental health problems?
Best Gastroenterologist in Nepal
1. Dr. Kamal Raj Subedi
Dr. Kamal Raj is a consultant gastroenterologist and interventional Gastrointestinal endoscopist at HAMS hospital and Grande International Hospital.He has worked in Dhulikhel Hospital, Kathmandu from 2018 to 2019.He was then actively involved in ERCP(Endoscopic Retrograde Cholangiopancreatography).He is also working at Kist Medical College and Teaching Hospital,Nepal as a consultant gastroenterologist.He has done Fellowship in Gastroenterology and Digestive Endoscopy from University of the East Ramon Magsaysay Memorial Medical Center,Philippines.
Contact: Dr. Kamal Raj Subedi – Welcome to HAMS Hospital
2. Dr. Nandu Silwal Poudyal
SHAPU (Seasonal Hyperacute Pan-uveitis) EYE DISEASE in Nepal
Around 34 patients of SHAPU(Seasonal hyper-acute panuveitis) has been reported in pokhara since one month.SHAPU has not been reported outside Nepal until now.The prevalence of disease is highest in Pokhara , from where the disease has originated in 1975.Most of the cases are reported in end of monsoon season (August-September).Only timely treatment can prevent blindless.
SHAPU is a rare entity occurring in odd years since 1975 in Nepal.It is increasing at an alarming rate in Gandaki province since beginning of this september.It mostly affects child of 5 to 15 years of age.It can rapidly cause destructive intra-ocular inflammation.It can progress to blindness if not treated.The etiology of SHAPU is not clear yet but it has strong associations with Gazalina moth.The dust on scale of the moth when comes in contact with eyes can cause damage to retina and pupil.Studies are being done to find out if SHAPU is due to auto-immune response to the moth antigens or by pathogens delivered by moth. Characteristics features of SHAPU are red eye,leukocoria,fibrinous exudates in anterior chamber and inability to dilate pupil with little or no pain.No standard treatment protocol has been developed against SHAPU till now.So to cover both infectious and immunological aspects,broad spectrum antibiotics and steroids are used for its treatment.Vitrectomy has been considered a useful procedure for treatment of SHAPU.
The fact that it commonly affects children is not well understood.The blame can be given to their low immunity than adult but no proof of state of immunocompromised has been found till date.
Nipah Virus-Recent death in Kerala,India.
A 12 year old boy of kerala,India died of Nipah virus on September 5,2021.It is after 3 years that kerala reported a case of Nipah virus after the outbreak was contained in 2018.
Nipah virus is a zoonotic virus that means the transmission occurs between animals and human.Bats are the natural reservoir of Nipah virus.The virus is known to infect pigs and human.It can cause from mild illness to encephalitis and ultimately death.In 1999,an outbreak of the disease in malaysia and singapore caused 300 human cases and more than 100 deaths.About one million pigs were killed to control the virus.It is now a disease of concern because man to man transmission are seen in caregivers of infected people in Bangladesh and India.
Nipah virus can be transmitted via
1.Direct contact with infected animals(pigs,bats)
2.Eating food products that are contaminated with body fluids of infected bats
3.Body fluids of an infected person(respiratory droplet,urine or blood)
Sign and symptoms of Nipah virus are very similar to Covid 19.It ranges from subclinical cases to acute respiratory infection to fatal encephalitis.Infected people usually develop symptoms after 4 to 14 days of exposure to the virus that means the incubation period of Nipah virus is 4-14 days.It initially presents with fever,headache,malaise,myalgia,sore throat and vomiting which progresses rapidly to dizziness,drowsiness,altered consciousness (neurological manifestations of encephalitis).Encephalitis and seizures occur in severe casses.The patient may progress to coma.The case fatality rate is 40-80 % that means death may occur in 40 - 80 % of cases. Persistent convulsions have been reported in survivors of Nipah virus.
The diagnosis of this virus is difficult due to its non-specific symptoms.The tests used to diagnose are real time polymerase chain reaction (RT-PCR) and ELISA.Early diagnosis helps in limiting the transmission of the Nipah virus.
There is no specific treatment or vaccine against Nipah virus.Management is supportive care with hydration,rest and symptomatic treatment as they occur.
Best Dermatologists in Nepal
1.Dr. Anil Kumar Bhatta,PhD
Speciality:Dermatologist, Venereologist and Aesthetician
Visit website here
Contact:01-5908320
2.Dr. Sabina Bhattarai,MD
Speciality:Venereologist and cosmetic Laser Surgeon
She has good practice of dermatology procedures like ablative lasers, photo therapy, cryotherapy, radiofrequency, electrocautery, ionotophoresis, skin biopsies, excision of moles, scar revision.
Visit Website here
Contact:9848841000
3.Dr. Vikash Paudel,MD
Speciality:Dermatologist, Venereologist.
He is one of the best pediatric dermatologist in Nepal.He also treats hair loss very well.
Visit Website here
Contact: 9849948600
4.Dr. Kamal Raj Dhital, MD
He is one of the best established dermatologist in Kathmandu,Nepal.He works in the field of dermatology, cosmetic surgery, Dermato-surgery and hair transplant surgery.He along with his team provide following services:
Hair transplant surgery in Kathmandu, Nepal
Hairloss treatment in Nepal
Non surgical hair restoration
PRP therapy for hair loss
Laser hair removal with US FDA approved triple wavelength laser
Tattoo removal , freckles removal
Melasma and pigmentation treatment
Fillers
Botox injections
Acne and acne scar treatment
Vitiligo Treatment
Visit Website here
Contact number:9815959413
5.Dr. Uma Keyal, PhD
Speciality: Dermatologist, Aesthetician & Laser Expert
She has good experience in diagnosing and managing the problems related to skin, hair, nails and sexually transmitted infections.In addition, she has good skill in botox injection, dermal fillers, and different types of laser.she has a good exposure to skin diseases and sexually transmitted infections.
Visit Website here
Contact number:9860999780
Scrub typhus in Nepal
Scrub typhus is a disease caused by Orienta tsutsugamushi.It is endemic in South east asia and some other places.More than one million cases are reported annually.This infection is transmitted to man through the bite of infected trombiculid mite larvae (chiggers).
The incubation period of scrub typhus is about 9 days.
How is diabetes diagnosed?
Diabetes is a disease condition when body is unable to produce or utilize produced insulin from pancreas.This lead to accumulation of glucose in blood called as hyperglycemia.Chronic hyperglycemia has deleterious effect on different tissue system including Cardiovascular system,renal,ocular and neurological tissues.
TYPES OF DIABETES
1.Type 1 Diabetes-It usually occurs at young age.It is due to auto-immune reaction which means that body itself starts destroying beta cells of pancreas.This lead to little or no production of insulin ultimately.
2.Type 2 Diabetes- It is usually diagnosed at
How can we prevent high blood pressure?
Hypertension or high blood pressure is a condition of raised blood pressure above normal.Normal blood pressure is considered to be 120/80 mm of Hg.Blood pressure is expressed in A/B form where A is systolic blood pressure and B is diastolic blood pressure.
How is Blood pressure regulated?
Milk-ejection reflex |Role of Oxytocin
Oxytocin that is responsible for this reflex. Now lets discuss about this reflex in detail oxytocin is secreted from hypothalamus via para-ventricular and supra-optic nucleus. Paraventricular nucleus is the major site for production of oxytocin where as supra-optic nucleus also produces it but in small quantity and from there it goes to posterior pituitary for storage via hypothalamus-hypophyseal tract system.Mammary gland has many touch receptors mainly around nipples. when the baby suckles the nipple, somatic afferent impulses are sent to spinal cord and via spinal cord,impulses are sent to hypothalamus to supra-optic nucleus and para-ventricular nucleus.From there the the impulse is sent to posterior pituitary via hypothalamus-hypophyseal tract.It stimulates release of oxytocin that is stored in posterior pituitary.The released oxytocin have its action on myo-epithelial cells of duct wall of mammary gland which leads to its contraction and eventually release of milk known as milk ejection reflex.
What is the cause of Jaundice?
In this article,we are going to talk about jaundice.lets get into our topic of jaundice. How can we define jaundice?
Jaundice is yellowish discoloration of skin,mucus membrane and sclera due to increased bilirubin in our blood that is hyperbilirubinemia. Normal serum level of bilirubin is upto 1 mg/dl .It can rise upto 1-2 mg/dl without clinical signs and symptoms called as latent jaundice.Overt jaundice is clinically detected jaundice which is when bilirubin is more than 2mg/dl.
Jaundice is classified into pre-hepatic,hepatic and post-hepatic Jaundice.Pre hepatic jaundice is when liver is not involved.Bilirubin comes from Red blood cell.
MCQS ON PEDIATRICS -DEVELOPMENTAL MILESTONE,INFECTIONS
1.Which of the following statements about ideal protocol and transport of the COVID-19 PCR samples in transport tubes is true? *
a. Specimens should be kept in room temperature (22°C) for storage and transported within 72 hours
b. Specimens should immediately be frozen and transported within 72 hours
c. Specimens should be stored at 12°C and transported on an ice pack within 72 hours
d. Specimens should be stored between 2°C and 8°Cand transported with a cold pack within 72 hours
2.Which of the following about development is NOT True: *
a. Pincer grasp at 4 months
b. Sitting at 6 months
c. Social smile at 3 months
d. Can use pleurals at 2 years
3.Newborn commonly has following except: *
a. Milia
b. Mongolian Spots
Clinical Scenario of Thermal injury for Medical students-The patient has blistering open burn wounds involving the circumference of his left arm and left leg, in addition to his entire back and buttock areas.
A 63-year-old man is extracted from fire in the house and brought to the hospital. According to the witness at the scene, the victim was unconscious in an upstairs bedroom of the house. His pulse rate is 110 beats/minute, blood pressure is 150/90 mm Hg, and respiratory rate is 28 breaths/minute. The pulse oximeter shows 91% oxygen saturation with oxygen by face mask. His face and the exposed portions of his body are covered with carbonaceous deposit. The patient has blistering open burn wounds involving the circumference of his left arm and left leg, in addition to his entire back and buttock areas.
Inference:The man presents with approximately a 45% TBSA burn(9+18+18) and inhalation injuries sustained in a house fire.
What should be first step for management of this thermal injury?
Definitive airway management by intubation is critical in this patient with likely inhalation injuries, carbon monoxide (CO) poisoning, and major burns.
FIRST-DEGREE BURN WOUNDS: Superficial burns that involve only the epidermis. These wounds appear red and are not blistered.
PARTIAL-THICKNESS BURN WOUNDS: (Formerly known as second-degree burns)
INTERNAL MEDICINE MCQS ON GI,HEPATOBILLIARY,CARDIOLOGY,HEMATOLOGY SYSTEM
1.Diagnosis
of Spontaneous bacterial peritonitis based on ascitic fluid PMN count *
a. ˃ 100/mm3
b. ˃ 150/mm3
c. ˃ 200/mm3
d. ˃ 250/mm3
2.The
normal portal venous pressure is: *
a. 3 – 5 mm hg
b. 5 – 10 mm hg
c. 10 – 15 mm hg
d. 15 – 20 mm hg
Clinical case scenario of DIABETES MELLITUS and DIABETIC KETOACIDOSIS
General Surgery-Surgery MCQS on Trauma Management,Blood transfusion,Shock,Hemorrhage,Wound healing,SIRS,Shock
1.Which one of the following is true about delayed primary suturing?
a. It is done immediately within 6 hours.
b. It is done on lacerated wounds.
c. Once infection subsides and healthy granulation tissue formed, delayed primary suturing is done.
d. Suturing the wound within 10 to 14 days later is delayed primary suturing.
2.Proliferative phase of wound healing includes except, *
a. Fibroblastic activity increases.
b. Growth of new blood vessels and capillary takes place.
c. Maturation of collagen takes place.
d. Re-epithelization of wound surface occurs.
What is normal level of sodium,potassium,calcium in the blood?
Sodium :The normal serum sodium level is 135–145 mmol/L.
Hypernatraemia:
This can be caused by hypovolaemia and dehydration as well as primary hyperaldosteronism, Cushing’s syndrome and excess salt intake. Patients present with lethargy, irritability, fever, nausea, vomiting and confusion. Management is with controlled hydration using 4% dextrose with 1/5 normal saline or 5% dextrose solution together with judicious diuretic therapy.
MEDICINE MCQS-KATHMANDU UNIVERSITY
1. Addison’s disease is characterized by all of the following except:
A) Hyperkalemia
Hyponatremia
Hypercalcemia
Hypotension
ANSWER= (C)
2. Pheochromocytoma predominantly secretes:
-
Epinephrine
LIVER FUNCTIONS TESTS-LIVER PANEL-LIVER DISEASE
LIVER FUNCTION TESTS
Aminotransferases (ALT/AST) :
This enzyme has two isoforms: alanine aminotransferase (ALT) and aspartate aminotransferase (AST).
Massive elevation of the serum levels of this enzyme is seen in severe viral hepatitis, hepatotoxic-induced liver injury and ischaemic liver injury.
Moderate elevations are characteristic of mild acute viral hepatitis, chronic active hepatitis, alcoholic hepatitis, cirrhosis and hepatic metastases.
Usually the ALT elevation parallels AST elevation, but in alcoholic liver disease AST elevation far exceeds that of ALT. The ratio of AST/ALT in this setting is > 2.
Alkaline phosphatase (ALP) :A striking elevation of this enzyme is seen in cholestatic disorders. Moderate and transient elevations are seen in all types of liver pathology, including hepatitis, metastatic disease and hepatic infiltrative conditions such as lymphomas, leukaemia and sarcoidosis.
Gammaglutamyl transpeptidase (GGT): The level of this enzyme correlates with that of ALP. Its level also goes up in alcoholism, diabetes mellitus, cardiac failure, pancreatic disease, fatty liver and renal failure. Elevation of the level of this enzyme is often non-specific.
Prothrombin time (PT) and international normalised ratio (INR): Elevation of the PT level and the INR is seen when hepatic synthetic function is impaired. All clotting factors except factor V are synthesised in the liver.
Serum albumin level: This marker also reflects the hepatic synthetic capacity, and hence it is low in significant liver disease.
The Approach to the Painful Joint
The approach to JOINT PAIN/STIFFNESS
In the clinical assessment it is important first to establish whether the presentation is that of a monarthritis or polyarthritis . Then check the distribution and the symmetry or asymmetry thereof. Other information that is useful includes:
1.Location and the exact joints involved
2.Onset, duration, diurnal pattern 3.Duration of pain and stiffness each day
4.Functional impairment
5.Precipitating and relieving factors and medications consumed so far
6.Progression over time and space
7.Associated other features, such as rash, weight loss, ocular symptoms, oral symptoms, genital symptoms
8.Muscle ache, headache, fever
Arthritis
Differential diagnoses that need to be considered include:
• rheumatoid arthritis
Septic Shock -Clinical presentation and Management
CLINICAL CASE SCENARIO OF SEPTIC SHOCK
A 44-year-old woman is admitted to the ICU after having undergone a 3-hour abdominal operation for the debridement of infected necrotizing pancreatitis (infected pancreas necrosis). The operation resulted in 800 mL of blood loss, and she received 3000 mL of crystalloid, 2 units of packed RBC, and 2 units of fresh frozen plasma during the operation. Prior to the surgery, she was receiving imipenem, itraconazole, and micafungin for Gram-negative bacteremia and fungemia. The patient’s skin appears warm and pink. She is intubated and mechanically ventilated. Her vital signs are pulse rate of 110 beats/minute, blood pressure of 94/60 mm Hg, and temperature of 39.1°C (102.4°F). Her breath sounds are present bilaterally and her abdomen is soft and distended. A chest radiograph reveals bibasilar atelectasis. A 12-lead ECG reveals sinus tachycardia. Complete blood count reveals WBC 24,000/mm3, hemoglobin 11 g/dL, and hematocrit 38%.
Likely causes of low blood pressure: Probably a combination of sepsis and blood loss.
Next steps in the management: Initial efforts should be to restore intravascular volume with crystalloid fluids and blood products. The addition of a vasoconstrictive medication should be considered if volume replacement does not normalize her blood pressure and improve end-organ perfusion.
Fever of unknown origin (FUO) -Causes of FUO
Fever of unknown origin (FUO)
refers to a prolonged febrile illness that persists without diagnosis after careful initial assessment. Although over 200 causes have been described, including rare diseases, most cases are due to familiar entities presenting in an atypical fashion.
(1) infections—including tuberculosis, endocarditis, abdominal and hepatobiliary infections and abscesses, complicated genitourinary tract infections, pleuropulmonary infections, bone and joint infections, salmonellosis, cytomegalovirus, Epstein-Barr virus and HIV;
(2) tumours—including lymphoma;
CLINICAL ANATOMY OF UPPER LIMBS-CLAVICLE,SCAPULA,RADIUS,ULNA
CLAVICLE
Peculiarities of the Clavicle
1 It is the only long bone that lies horizontally.
2 It is subcutaneous throughout.
3 It is the first bone to start ossifying.
4 It is the only long bone which ossifies in membrane.
5 It is the only long bone which has two primary centres of ossification.
6 There is no medullary cavity.
7 It is occasionally pierced by the middle supraclavicular nerve.
It receives weight of upper limb via lateral one-third through coracoclavicular ligament and transmits weight of upper limb to the axial skeleton via medial two-thirds part.
CLINICAL ANATOMY OF CLAVICLE
The clavicle is commonly fractured by falling on the outstretched hand (indirect violence). The most common site of fracture is the junction between the two curvatures of the bone, which is the weakest point. The lateral fragment is displaced downwards by the weight of the limb as trapezius muscle alone is unable to support the weight of upper limb
The clavicles may be congenitally absent, or imperfectly developed in a disease called cleidocranial dysostosis.
In this condition, the shoulders droop, and can be approximated anteriorly in front of the chest .
SCAPULA
CLINICAL ANATOMY OF SACPULA
Paralysis of the serratus anterior causes ‘winging’ of the scapula. The medial border of the bone becomes unduly prominent, and the arm cannot be abducted beyond 90° .
The scaphoid scapula is a developmental anomaly, in which the medial border is concave.
HUMERUS
CLINICAL ANATOMY OF HUMERUS
The common sites of fracture of humerus are the surgical neck, shaft and supracondylar region.
Supracondylar fracture is common in young age. It is produced by a fall on the outstretched hand. The lower fragment is mostly displaced backwards, so that the elbow is unduly prominent, as in dislocation of the elbow joint. This fracture may cause injury to the median nerve. It may also lead to Volkmann’s ischaemic contracture caused by occlusion of the brachial artery.
The humerus has a poor blood supply at the junction of its upper one-third and lower twothirds. Fractures at this site show delayed union or non-union.
The head of the humerus commonly dislocates inferiorly (subglenoid)
RADIUS
CLINICAL ANATOMY OF RADIUS
The radius commonly gets fractured about 2 cm above its lower end (Colles’ fracture). This fracture is caused by a fall on the outstretched hand . The distal fragment is displaced upwards and backwards, and the radial styloid process comes to lie proximal to the ulnar styloid process. (It normally lies distal to the ulnar styloid process.) If the distal fragment gets displaced anteriorly, it is called Smith’s fracture
A sudden powerful jerk on the hand of a child may dislodge the head of the radius from the grip of the annular ligament. This is known as subluxation of the head of the radius (pulled elbow) . The head can normally be felt in a hollow behind the lateral epicondyle of the humerus.
ULNA
CLINICAL ANATOMY OF ULNA
The ulna is the stabilising bone of the forearm, with its trochlear notch gripping the lower end of the humerus. On this foundation, the radius can pronate and supinate for efficient working of the upper limb.
The shaft of the ulna may fracture either alone or along with that of the radius. Cross-union between the radius and ulna must be prevented to preserve pronation and supination of the hand.
Dislocation of the elbow is produced by a fall on the outstretched hand with the elbow slightly flexed. The olecranon process shifts posteriorly and the elbow is fixed in slight flexion. Normally, in an extended elbow, the tip of the olecranon process lies in a horizontal line with the two epicondyles of the humerus; and in the flexed elbow, the three bony points form an equilateral triangle. These relations are disturbed in dislocation of the elbow.
Fracture of the olecranon process is common and is caused by a fall on the point of the elbow. Fracture of the coronoid process is uncommon, and usually accompanies dislocation of the elbow.
Madelung’s deformity is dorsal subluxation (displacement) of the lower end of the ulna, due to retarded growth of the lower end of the radius.
A case of Ulcerative colitis-A 28-year-old man comes with 2 days of abdominal pain
CLINICAL CASE SCENARIO OF COLITIS
A 28-year-old man comes to the emergency room complaining of 2 days of abdominal pain and diarrhea. He describes his stools as frequent, with 10 to 12 per day, small volume, sometimes with visible blood and mucus, and preceded by a sudden urge to defecate. The abdominal pain is crampy, diffuse, and moderately severe, and it is not relieved with defecation. In the past 6 to 8 months, he has experienced similar episodes of abdominal pain and loose mucoid stools, but the episodes were milder and resolved within 24 to 48 hours. He has no other medical history and takes no medications. He has no recent travel history nor had contact with anyone with similar symptoms. He works as an accountant and does not smoke or drink alcohol. No member of his family has gastrointestinal (GI) problems. On examination, his temperature is 99°F, heart rate 98 bpm, and blood pressure 118/74 mm Hg. He appears uncomfortable, is diaphoretic, and is lying still on the stretcher. His sclerae are anicteric, and his oral mucosa is pink and clear without ulceration. His chest is clear, and his heart rhythm is regular, without murmurs.
His abdomen is soft and mildly distended, with hypoactive bowel sounds and minimal diffuse tenderness but no guarding or rebound tenderness. Laboratory studies are significant for a white blood cell (WBC) count of 15,800/mm3 with 82% polymorphonuclear leukocytes, hemoglobin 10.3 g/dL, and platelet count 754,000/mm3. The HIV (human immunodeficiency virus) assay is negative. Renal function and liver function tests are normal. A plain film radiograph of the abdomen shows a mildly dilated air-filled colon with a 4.5-cm diameter and no pneumoperitoneum or air/fluid levels.
Most likely diagnosis: Colitis, probably ulcerative colitis.
Next step: Admit to the hospital, obtain stool samples to exclude infection, and begin therapy with corticosteroids.
The differential diagnosis for colitis includes ischemic colitis, infectious colitis (C difficile, E coli, Salmonella, Shigella, Campylobacter), radiation colitis, and IBD (Crohn disease vs ulcerative colitis).
The treatment of ulcerative colitis can be complex because the pathophysiology of the disease is incompletely understood. Management is aimed at reducing the inflammation. Most commonly, sulfasalazine and other 5-aminosalicylic acid (ASA) compounds such as mesalamine are used and are available in oral and rectal preparations.
They are used in mid to moderate active disease and to induce remission, and in the maintenance of disease to reduce the frequency of flare-ups. Corticosteroids may be used (po, PR, or IV) to treat patients with moderate to severe disease. Once remission is achieved, the steroids should be tapered over 6 to 8 weeks and then discontinued if possible to minimize their side effects. Immune modulators are used for more severe, refractory disease. Such medications include 6-mercaptopurine, azathioprine, methotrexate, and the tumor necrosis factor (TNF) antibody infliximab. Anti-TNF therapy, such as infliximab, has been an important treatment of patients with Crohn disease who are refractory to steroids, and more recently has shown efficacy in ulcerative colitis. Patients receiving the potent immunomodulator infliximab are at increased risk of infection, including reactivation of latent tuberculosis. Surgery is indicated for complications of ulcerative colitis. Total colectomy is performed in patients with carcinoma, toxic megacolon, perforation, and uncontrollable bleeding. Surgery is curative for ulcerative colitis if symptoms persist despite medical therapy.
It usually is accompanied by fever, leukocytosis, tachycardia, and evidence of serious toxicity, such as hypotension or altered mental status. Therapy is designed to reduce the chance of perforation and includes IV fluids, nasogastric tube placed to suction, and placing the patient npo (nothing by mouth). Additionally, IV antibiotics are given in anticipation of possible perforation, and IV steroids are given to reduce inflammation. The most severe consequence of toxic megacolon is colonic perforation complicated by peritonitis or hemorrhage. Patients with ulcerative colitis have a marked increase in the incidence of colon cancer compared to the general population. The risk of cancer increases over time and is related to disease duration and extent. It is seen both in patients with active disease and in patients whose disease has been in remission. Annual or biennial colonoscopy is advised in patients with ulcerative colitis, beginning 8 years after diagnosis of pancolitis, and random biopsies should be sent for evaluation. If colon cancer or dysplasia is found, a colectomy should be performed
Best Website and online lectures for MBBS students
Let us begin:
1.Medscape- Not less than any textbook when it comes to authentication.Medscape consists of Medical articles,Drugs,Diseases and a lot more .Everything for medical student is here.From overview of a disease to its complications ,everything is mentioned in a systematic manner.I strongly suggest you to use Medscape.
2.MSD Manual - MSD Manual is very similar to Medscape but in a very concise form.You will love to look MSD every day for your daily queries during Clinical Postings in the wards.
3.Pubmed - Everything and everything at one place when you want a deep vision into some approaches.
4.TeachmeAnatomy-Bored of your textbooks and having difficulties understanding relations.Just visit TeachmeAnatomy and enjoy Anatomy.You will be glad that you visited this site.
5.PhysiologyGuru-In my journey of physiology,this app helped me a lot.Dr Vivek is tutor here.He really has amazing concepts that these textbooks fail to convey This one is link to download this app in android.For ios,download here IOSAPP
Lets talk about some good youtube channels that medical students must subscribe.
1.Dr. Najeeb lectures-When he teaches a topic ,there is a magic .You understand everything.Everything means everything plus his lectures become funny sometimes with his jokes.
2.MEDCRAM-When you are bored of studying ,this channel will help to utilise that time by its videos on different topics.
3.OneMinuteMedicalSchool- This channel is a wonder beacuse of its one minute videos that makes impact not less than hour of lectures.Just one minute and you know the stuffs.Is not it great?
A case of ACL tear-A 25-year-old man has been hurt during football match by his opponent player
CLINICAL CASE SCENARIO KNEE INJURY-ANTERIOR CRUCIATE LIGAMENT TEAR
A 25-year-old man has been hurt during football match by his opponent player.He falls and twists his right leg.On examination, the right knee is swollen and tender. With the patient sitting on the stretcher with his knee flexed, the lower leg seems to have several centimeters of excess anterior mobility.
Most likely diagnosis: Anterior cruciate ligament (ACL) tear
Mechanism of injury: Excessive rotational force strains or ruptures the ligament
CLINICAL CORRELATION
Injuries to the knee are very common because it bears weight, combines mobility in flexion and extension, and allows some rotation. The stability of the knee depends entirely on its ligaments and muscles. Sports injuries to the knee are most commonly caused by high-speed and rotational forces applied to the leg through the knee joint. In addition, certain ligaments are anatomically related to the menisci, on which the distal femur articulates. This 25-year-old man was involved in a football match, a common setting for ACL injury. The ACL passes from the posterior aspect of the distal femur to the intercondylar region of the anterior aspect of the proximal tibia; it limits anterior movement of the tibia in relation to the femur. Thus, on examination, this patient exhibits the “anterior drawer sign,” or excessive anterior mobility of the tibia with the knee flexed. This injury will usually require surgical repair.
Case of Wrist fracture-Clinical Anatomy
A 23-year-old male reports that during a game of basketball, he tripped while driving the ball to the basket, and fell on his outstretched right hand with the palm down. Two days later, he phoned his anatomist father and related that his right wrist was painful. Later that day, he visited his father, who noted that the wrist was slightly swollen and tender but without deformity. He instructed his son to extend the right thumb, thereby accentuating the anatomical “snuffbox,” which is extremely tender to deep palpation. His father advised him to get his hand and wrist x-rayed.
Discussion:
Most likely diagnosis: Wrist fracture
Most likely anatomical defect: Fracture of the narrow middle portion of the scaphoid carpal bone
CLINICAL CORRELATION
This young man tripped while playing basketball and stretched out his right hand to protect himself. His hand, with the palm down and probably deviated to the side of the radius, took the brunt of the fall, resulting in significant impact force to the wrist. This resulted in pain and swelling of the wrist, especially on the radial side, with point tenderness deep in the anatomical snuffbox. This is the common mechanism for a fracture of the scaphoid carpal bone, the most commonly fractured carpal bone. Point tenderness over a bone or bony process is a hallmark of a fracture at that site. Radiologic confirmation of a fracture is important. The scaphoid bone has a unique blood supply, and proper reduction and alignment of the segments is necessary to decrease the risk of avascular necrosis. A fall on an outstretched hand such that it produces hyperextension of the wrist may result in dislocation of the lunate bone. The lunate is usually displaced anteriorly into the carpal tunnel and may impinge on the median nerve. The lunate is the most commonly dislocated carpal bone. A fall on an outstretched palm may also result in a transverse fracture of the distal radius or a Colles fracture, which produces a dorsal displacement of the distal fragment, resulting in the characteristic “dinner fork” (also termed “bayonet”) deformity. A Smith fracture of the radius in the same region of younger individuals is less common. In a Smith fracture, there is trauma to the dorsal aspect of a flexed wrist, and the wrist is deformed with the distal radial fragment displaced ventrally in a “spade” deformity.
Everything about brachial plexus-Anatomy,Clinical Importance.
The brachial plexus arises from the inferior portion of the cervical spinal cord enlargement. It is formed by the ventral primary rami of spinal nerves C5 through C8 and most of T1. The network of nerves that form the brachial plexus is divided anatomically from proximal (medial) to distal (lateral) into roots, trunks, divisions, cords, and terminal branches (mnemonic: “R. Travis drinks cold Texas beer”). The roots unite to form superior, middle, and inferior trunks. The suprascapular nerve and the nerve to the subclavius muscle arise from the superior trunk. Each trunk is divided into anterior and posterior divisions, which will innervate musculature of the anterior and posterior compartments, respectively. The anterior divisions of the superior and middle trunks unite to form the lateral cord, which branches off to the lateral pectoral nerve. The anterior division of the inferior trunk continues distally as the medial cord, whose branches are the medial pectoral, medial brachial cutaneous, and medial antebrachial cutaneous nerves. The posterior divisions of all three trunks unite to form the posterior cord, and its branches are the upper and lower subscapular and thoracodorsal nerves. The three cords are named according to their relation to the axillary artery, which passes through the plexus at this level. The terminal branches of the brachial plexus are the axillary, musculocutaneous, median, ulnar, and radial nerves. The axillary nerve (C5 and C6) arises from the posterior cord and courses posteriorly around the surgical neck of the humerus, where it is at risk for injury. The posterior circumflex humeral artery accompanies the nerve in this course. The axillary nerve supplies the deltoid and teres minor muscles, is sensory to the skin over the lower portion of the deltoid, and is optimally tested on the “shoulder patch” portion of the upper arm. Axillary nerve injury, such as that due to fracture at the surgical neck of the humerus, results in an inability to abduct the arm at the shoulder to a horizontal position and in sensory loss in the shoulder patch area . The musculocutaneous nerve (C5–C7) is the continuation of the lateral cord. It courses distally through the coracobrachialis muscle to innervate it in addition to the biceps brachii and brachialis muscles. The lateral antebrachial cutaneous nerve to the skin of the lateral forearm represents the terminal continuation of this nerve. Damage to the musculocutaneous nerve causes weakness in supination and flexion of the shoulder and elbow. The upper portion of the brachial plexus arises from spinal cord segments C5 and C6; forms the superior trunk; and makes major contributions to the axillary, musculocutaneous, lateral pectoral, and suprascapular nerves and the nerve to the subclavius muscle. Injury to the upper plexus typically occurs with an increase in the angle between the shoulder and the neck. This can occur in a newborn during an obstetrical delivery or in adults as the result of a fall on the shoulder and side of the head and neck, which produces a widened angle. The resultant muscle paralysis due to such an injury may be understood more easily in an adult with such an injury. The upper extremity hangs limp by the side because the deltoid and supraspinatus (abductors of the arm) are paralyzed as a result of injury of the axillary and suprascapular nerves, respectively. In addition, the anterior deltoid, biceps brachii, and coracobrachialis (flexors of the arm) are paralyzed due to injury of the axillary and musculocutaneous nerves. The elbow is extended and the hand is pronated because of paralysis of the biceps brachii and brachialis muscles, both of which are innervated by the musculocutaneous nerve. The extremity is medially rotated because of paralysis of the teres minor and infraspinatus muscles (lateral rotators of the arm) and injury to the axillary and suprascapular nerves. The palm of the hand is turned posteriorly in the “waiter’s tip” sign. There is loss of sensation along the lateral aspect of the upper extremity, which corresponds to the dermatome at C5 and C6.
The upper brachial plexus injury is known as Erb’s or Duchenne-Erb palsy. The ulnar nerve (C8 and T1) is a continuation of the medial cord, which enters the posterior compartment through the medial intermuscular septum and passes distally to enter the forearm by curving posteriorly to the medial epicondyle. Here it is superficial and at risk for injury. It enters the anterior compartment of the forearm, where it innervates the flexor carpi ulnaris and the bellies of the flexor digitorum profundus to the ring and little fingers. The ulnar nerve enters the hand through a canal (Guyon canal) superficial to the flexor retinaculum. The nerve supplies all the intrinsic muscles of the hand except for the three thenar muscles and the lumbricals of the index and middle fingers. It is sensory to the medial border of the hand, the little finger, and the medial aspect of the ring finger. Damage to the ulnar nerve in the upper forearm causes lateral (radial) deviation of the hand, with weakness in flexion and adduction of the hand at the wrist and loss of flexion at the distal interphalangeal joint of the ring and little fingers. Damage to the ulnar nerve in the upper forearm or at the wrist also results in loss of abduction and adduction of the index, middle, ring, and little fingers due to paralysis of the interossei muscles.
A “claw hand” deformity results, and with longstanding damage, atrophy of the interosseous muscles occurs. Injury to the lower brachial plexus, known as Klumpke palsy, occurs by a similar mechanism, that is, an abnormal widening of the angle between the upper extremity and the thorax. This may occur at obstetrical delivery by traction on the fetal head or when an individual reaches out to interrupt a fall. The roots from C8 and T1 and/or the inferior trunk are stretched or torn. Spinal cord segments C8 and T1 form the ulnar nerve and a significant portion of the median nerve. Most of the muscles of the anterior forearm are innervated by the median nerve and will display weakness. Most of the muscles of the hand are innervated by the ulnar nerve. There will be loss of sensation along the median aspect of the arm, forearm, hypothenar eminence, and little finger (C8 and T1 dermatome).
Clinical case scenario-Schizophrenia
S is a 32-year-old moderately obese man brought into the ED by the police after attempting to cut himself with a piece of glass from his bathroom mirror. He said he had to cut himself in order to "let the evil out!"· In the examination room, S looked suspiciously at the interviewer and was muttering to himself.
His Past Medical History is significant for chronic schizophrenia. HTN, hyperlipidemia, and major depressive disorder. Medications include thioridazine, benztropine. paroxetine, atorvastatin, and metoprolol, although he states he discontinued all his medications 3 weeks ago for fear he was being poisoned.
PE: On physical examination, he has noticeable cuts on his hands. During the interview, he demonstrated noticeable facial grimacing and lip smacking, a stooped posture, and sluggish gait.
Case Conclusion S's symptoms are consistent with the diagnosis of uncontrolled chronic schizophrenia (paranoid type). Because S is experiencing positive and negative symptoms and has evidence of(EPS) Extra Pyramidal Symptoms. he should be switched to an atypical antipsychotic agent Olanzapine is traditionally reserved for treatment-resistant patients and is not a first line agent due to the risk of agranulocytosis. Olanzapine and quetiapine can be problematic due to weight gain and potential insulin resistance (if the patient has family history of diabetes mellitus type 2). Risperidone is also associated with a higher incidence of EPS symptoms compared with other atypical agents. In addition, He is also taking paroxetine that can significantly elevate levels of risperidone. Therefore, ziprasidone would be the best choice for this patient
DISCUSSION
Atypical antipsychotic agents or "newer" agents alleviate both positive and negative symptoms. The atypical antipsychotics also improve cognitive deficits associated with schizophrenia. Although these agents are much safer, they have added cost and have been associated with their own class of adverse effects.
Extrapyramidal symptoms are common adverse effects of traditional neuroleptics, although they may still occur with atypical agents. Pseudoparkinsonism, akathisia, and acute dystonic reactions are the three early-onset types of EPS. Atypical agents have a low risk for inducing EPS.The management of early-onset EPS symptoms includes drug discontinuation, dosage reduction of the antipsychotic agent, or switching to an agent with less risk for inducing EPS. Anticholinergic agents (diphenhydramine, benztropine) can be used to treat acute dystonic reactions, parkinsonism, and akathisia.
Management of Myocardial infarction
In any acute myocardial infarction the first priority is to assess the patient’s clinical stability and assess the requirement for, and urgency associated with, coronary revascularisation.
Remember: patients presenting with an infarction could present with acute pulmonary oedema, cardiogenic shock, malignant ventricular tachyarrhythmias or severe bradycardia. Once the patient’s haemodynamic stability and cardiac rhythm stability are established, perform an urgent ECG to confirm the diagnosis and identify the nature of the infarction—whether it is an ST segment elevation infarction (STEMI) or a non-ST segment elevation infarction (non-STEMI).
STEMI
If the infarction is a STEMI, urgent reperfusion therapy is needed. Acute reperfusion therapy could be primary percutaneous transluminal coronary angioplasty (primary PTCA) with insertion of a stent or thrombolysis. If the centre offers a primary angioplasty service and the patient fulfils the criteria (see below), urgent transfer to the cardiac catheterisation laboratory should take place. Patients presenting in the first 4–6 hours of onset of chest pain are considered suitable for primary PTCA. Previous coronary artery bypass grafts, peripheral vascular disease, untreatable terminal illness and dementia are exclusion criteria for this procedure. If primary PTCA is not an option, the patient should be thrombolysed with the relevant thrombolytic agent. If the patient presents within the first hour after the onset of chest pain, thrombolysis would be a preferred option (the ‘golden hour’ phenomenon). Usually a recombinant tissue plasminogen activator (rTPA) or an analogue is given to the patient immediately. Streptokinase is an alternative for patients over the age of 65 or those with evidence of an inferior myocardial infarction presenting after 4 hours of the onset of chest pain. Those who have been treated with streptokinase previously should not be given streptokinase again, due to the heightened risk of an allergic reaction. The ECG criteria for primary PTCA and thrombolysis are similar (see below), but thrombolysis may be useful up to 12 hours or even 24 hours after the onset of chest pain.
Criteria for primary PTCA or thrombolysis
• ST segment elevation of more than 1 mm in more than two contiguous limb leads
or
• ST segment elevation of more than 2 mm in more than two contiguous precordial leads
or
• new left bundle branch block.
Clinical case of Diabetic nephropathy for MBBS-Which drug to use?
M is 64-year-old Asian man who presents to the clinic for an HTN foIlow up examination after starting hydrochlorothiazide 6 months ago. He denies chest pain. shortness of breath, dizziness or Headache. His past medical history is significant for diabetes and HTN. He Is currently only receiving hydrochlorothiazide.
On examination
Vital signs are T -37.5degree C, BP 154/92 mm Hg. HR 82/ min. and RR 16 breaths/min. His 8P remains elevated above goal ( 130/85 mm Hg).
labs: K+ 4.3 mEq/l. BUN 26mg/dl,Cr 1.4 mg/dL.
UrinaIysis(UA): 3+ protein
Case Conclusion :
A 24-hour urine collection is performed, which reveals 780 mg of protein and a creatinine clearance rate of 58 mL/min. Thus. this patient has chronic renal disease. most likely diabetic nephropathy. Therefore, an ACE-Inhibitor would be a good choice for this patient
Discussion
ACE -I are particularly useful in treating patients with diabetic nephropathy. In these patients, ACE-I can decrease proteinuria and stabilize renal function independent of their antihypertensive effects. The benefits are attributed to their effects on renal hemodynamics. Angiotensin II may adversely affect the kidney by increasing the glomerular efferent arteriole resistance. Hence, the decrease in production of angiotensin II results in vasodilatation of the efferent arteriole and lowering intra-glomerular capillary pressure.
ACE-I blocks the conversion of angiotensin I to angiotensin II, which causes vasoconstriction and stimulates the production of aldosterone synthesis. Thus, ACE-I promote vasodilatation and decrease sodium retention, consequently lowering blood pressure.
ANATOMY MCQS-ABDOMEN-The right suprarenal gland is related to the
1.The right suprarenal gland is related to the
Explain:-
2. The celiac nodes receive lymphatic drainage from the
Explain:-
3.Buck’s fascia is related to
Explain:-
4. The least dilatable part of the Urethra is
Explain:-
5.Normal portal venour pressure is- (JIPMER 87)
Explain:-
6. In portal hypertension the sites of portosystemic anastomosis includes -
Explain:-
Clinical case of Myasthenia Gravis for MBBS
#Mr X is a 25-year-old businessman . Over the last 6 months, he experienced "strange" symptoms. He had severe eyestrain when he read for longer than 15 minutes. He became tired when he chewed food, brushed teeth, he had extreme fatigue on the work. He does not like people not doing work on time but he himself is unable to do works at time due to fatigue. Serum was sent for Anti-AChR ab(antibody).
DISCUSSION:
Neuromuscular transmission is the process whereby an action potential in a motor neuron produces an action potential in the muscle fibers that it innervates. The steps in neuromuscular transmission, are as follows:
(1) An action potential is propagated down the motor neuron until the presynaptic terminal is depolarized.
(2) Depolarization of the presynaptic terminal causes voltage-gated Ca2+ channels to open, and Ca 2+ flows into the nerve terminal.
(3) Uptake of Ca2+ into the nerve terminal causes exocytosis of stored acetylcholine (ACh) into the synaptic cleft.
(4) ACh diffuses across the synaptic cleft to the muscle end plate, where it binds to nicotinic ACh receptors (AChR).
(5) The nicotinic AChR is also an ion channel for Na+ and K+, WhenACh binds to the receptor, the channel opens.
(6) Opening of the channel causes both Na+ and K+ to flow down their respective electrochemical gradients, As a result, depolarization occurs.
(7) This depolarization, called the end plate potential, spreads to neighboring regions of the muscle fiber.
(8) Finally, the muscle fibers are depolarized to threshold and fire action potentials, Through this elaborate sequence of events, an action potential in the motor neuron causes an action potential in the muscle fibers that it innervates.
In myasthenia gravis, abnormal antibodies to AChR (AChR-ab) are produced, circulate in the blood, and bind to nicotinic receptors on the muscle end plates. When antibodies are bound to AChR, the receptors are not available to be activated by ACh that is released physiologically from motor neurons. Thus, while normal action potentials occur in the motor neurons and ACh is released normally, the ACh cannot cause depolarization of muscle end plates. Without depolarization of muscle end plates, there can be no action potentials or contraction in the muscle.
After ACh binds to and activates AChR on the muscle end plate, it is degraded by acetylcholinesterase, an enzyme that is also present on the muscle end plate. This degradative step, whose byproducts are choline and acetate, terminates the action of ACh on muscle.
Pyridostigmine is an acetylcholinesterase inhibitor that binds to acetylcholinesterase and thereby prevents binding and degradation of ACh at the muscle end plate. In the treatment of myasthenia gravis, pyridostigmine prevents degradation ofACh, increases its synaptic concentration, and prolongs its action. The longer the muscle end plate is exposed to high concentrations of ACh, the greater the likelihood that action potentials and contraction in the muscle will occur.
He was given pyridostigmine.Mr X immediately felt better while taking the drug; his strength returned to almost normal.
May be interested in
-
We know it is frustrating when you can not focus in study or work, When your mind is overthinking each and every event.We understand that yo...
-
1. Dr. Kamal Raj Subedi Dr. Kamal Raj is a consultant gastroenterologist and interventional Gastrointestinal endoscopist at HAMS hospital an...