Upper And Lower gIT Diseases And Management Flashcards
What is stomatitis,
Where does stomatitis occur?
what are the types of stomatitis and explain the canker sores(what it is characterized by,it’s definition )and symptoms of stomatitis
I STOMATITIS
Definition
Stomatitis is a general term for an inflamed and sore mouth, can disrupt a person’s ability to eat, talk, and sleep.
-Stomatitis can occur anywhere in the mouth, including the inside of the cheeks, gums, tongue, lips, and palate.
Types of Stomatitis
- Canker sores/ aphthous stomatitis
- Cold sore/ Herpes stomatitis
Aphthous Stomatitis
Aphthous stomatitis is usually defined as canker sores that recur on a somewhat regular basis and is a fairly common condition.
- It is characterized by a single pale or yellow ulcer with a red outer ring or a cluster of such ulcers in the mouth: usually on the cheeks, tongue or inside the lip.
Symptoms of Stomatitis* Canker sores: √ It can be painful √ Usually last 5 to 10 days √Tend to recur √ Are generally not associated with fever
Cold sores:
√ Are usually painful
√ Usually go after 7 to 10 days.
√ Are usually associated with cold or flu-like symptoms.
What type of stomatitis result from a genetic predisposition and are considered autoimmune disease.
Stomatitis is the most common disease of the oral mucosa true or false
Canker sores are more common where?
Canker sores or aphthous stomatitis
True
Developed countries
What are cold sores?
Another name for cold sores is?
Where are they usually formed?
Where are they rarely formed?
Cold sores are usually associated with what before the actual sores occur?
State the difference between canker sores and cold sores
What causes cold sores specifically
-
Herpes stomatitis/ cold sores
-Also called fever blisters
They are fluid-filled sores that occur on or around the lips.
- They rarely form on the gums or the roof of the mouth.
-Cold sores later crust over with a scab and are usually associated with tingling, tenderness, or burning before the actual sores appear.
- Cold sores are caused by a virus called herpes simplex type 1.
Unlike canker sores, cold sores are contagious from the time the blisters ruptures to the time it has completely healed.
-
*
With cold sores, The initial infection often occurs before adulthood and may be confused with a cold or the flu.
- Once the person is infected with the virus, it stays in the body, becoming dormant and reactivated by such conditions as stress, fever, trauma, hormonal changes( such as menstruation) and exposure to sunlight.
- When sores reappear, they tend to form in the same location. In addition to spreading to other people, the virus can also spread to another body part of the affected person, such as the eyes or genitals.
True or false
True
State ten potential causes of stomatitis
Causes of stomatitis*
The main cause of stomatitis has not been established. However, there are many potential causes of stomatitis including:
1. Injury from surgery orthotics (such as braces or dentures) 2. Biting the tongue or cheek. 3. Burns from hot food or drinks. 4. Thrush 5. Chronic dry mouth 6.Tobacco use 7.sexually transmitted diseases. 8. Herpes viruses 9. Side effects of chemotherapy, radiation, or other medications 10.Chemical exposure 11. Certain allergies. 12. Stress or a weakened immune system. 13. Bacterial infections 14. Nutritional deficiencies. 15. Systemic diseases such as lupus
State the five stages of cold sores
There are five Stages of cold sores:
~ Tingling
~ Blistering
~ Weeping: Over 2-3 days, the blisters rupture and ooze fluid that is clear or slightly yellow. This is sometimes called the “weeping phase.”
~ Crusting and About 4-5 days after the cold sore appears, it crusts and scabs over. It might crack or bleed as it heals.
~ Healing
State five differences between cold sores and canker sores
Cold sores develop on the outside of the mouth usually along the edge of the lips while canker sores develop on the soft tissues inside the cheeks or the lips ,underneath the tongue or at the base of the gums
Cold sores are contagious until they crust over and heal completely while canker sores are not contagious
Cold sores appear as red blisters until they break ,ooze and form a crust while canker sores are round with a white or yellow center and a red border
Cold sores generally heal within ten days while canker sores generally heal within 1-2weeks
Cold sores are caused by herpes simplex virus while canker sores are caused by immune suppressing viruses ,autoimmune disorders and auto inflammatory disorders
Sunlight and stress can trigger a cold sore outbreak while an accidental cheek bite,food sensitivity,injury from dental work,hormonal changes ,bacteria and stress can trigger a canker sore outbreak
How is stomatitis diagnosed
*
Diagnosis
Many cases of stomatitis, especially canker sores or cold sores, can be diagnosed through a physical exam and a medical history including a history of symptoms and any medications that are being taken.
In other cases, blood work or allergy testing may be necessary. In more complicated cases, a biopsy or a skin scraping of the lesion is taken for testing to determine exactly what is causing the stomatitis.
State five differential diagnosis for stomatitis
Angular stomatitis can be jndicative of a particular disease why?
Stomatitis is self restrictive or self limiting if no other conditions causing it are present true or false
Oral candidiasis Gum inflammation Scurvy Gingivitis Oral Manifestations of drug induced diseases
We can get the differential diagnosis through the causes of stomatitis
- Nutritional deficiency eg kwashorkor
- SLE
Example is HIV coming w stomatitis
This occurs because
When one is immunocompromised, all these opportunistic diseases and infections are usually present
True
State the pharmacological,non pharmacological treatment of stomatitis and the complications of stomatitis
Pharmacological and Non-pharmacological Treatment
- Treatment Plan*
1. To control pain
2. To treat ulcers
3. To control stress
4. To prevent secondary infection.
Non-pharmacological
- Proper hygiene ( dental care)
- Relaxation
- Drink more water
- Rinse mouth with salt water.
Pharmacological
- Apply a topical anesthetic such as lidocaine or xylocaine to the ulcer.
- Topical corticosteroid preparation such as triamcinolone dental paste.
- Use pain relievers such as Ibuprofen.
For more severe sores, treatment may include;
- Lidex gel
- Aphthasol( an anti-inflammatory paste)
- Pendex mouthwash
Complications
Meningoencephalitis, recurrent skin and mouth infections, dissemination of the infection, and teeth loss are a few known complications of stomatitis. The prognosis for most types of stomatitis is good
Case study
A 17-year-old female reported with the chief complaint of pain, swelling and ulceration on her upper and lower lip for past one week. History of presenting illness revealed that patient developed small fluid filled boils on her lips following the use of a lip balm one week back. These blisters reportedly ruptured soon, followed by ulcerations and crusting on her lips. Patient also complained of stiffness and drying of her lips with occasional bleeding and fluid discharge. She further complained of inability to open her mouth and discomfort while chewing and swallowing of food. Patient had visited a dermatologist for the same problem one week back and was diagnosed with herpes labialis. She was prescribed antibiotics for 5 days which further aggravated the condition.
Gross examination of the patient was unremarkable. Patient denied any history of prodromal symptoms or similar episodes of dermatological lesions or allergic reactions in the past. Family history, personal history or systemic manifestations of the patient was non-contributory. Patient gave no known history of food or drug allergy.
Clinical examination revealed swelling and eversion of lower lip with extensive ulceration and sloughing. Presence of yellowish areas with crusting and few brownish areas were also noted. On palpation, the lip was tender, rough with slight bleeding, pus and fluid discharge. Upper lip also revealed less extensive, but similar lesion in its vermillion border with multiple fissures which was tender, rough and stiff on palpation.
Upper and lower lip showing swelling, extensive ulceration, crusting and sloughing on initial presentation
- What are the differential diagnosis?
- Why did the disease aggravate after taking the antibiotics?
Cold sores
Canker sores
Oral candidiasis
Final diagnosis is cold sores or herpes stomatitis
2.cuz the disease is caused by a virus and antibiotics don’t work on viruses
What is esophagitis?
State the types
According to epidemiology,which type of esophagitis is the most common?,which type is more common in immunocompromised patients,which type is more common in males in their second or third decade as well as is associated with atopic triad(eczema,food allergies and asthma),which type is a common complication of radiation?
Definition of Esophagitis
Esophagus + Inflammation
Basically, a condition involving the inflammation of the tissues of the esophagus, the muscular tube that delivers food( bolus) from the mouth to the stomach.
- common types of Esophagitis *
- Reflux/ Erosive Esophagitis
- Infective Esophagitis
- Pill induced Esophagitis
- Eosinophilic Esophagitis
- Radiation Esophagitis
Erosive esophagitis
Infective esophagitis
Eosinophilic esophagitis
Radiation esophagitis(depending on doses,lower doses or longer schedules are associated with lower rates of radiation esophagitis
With the anatomy of the esophagus ,what type of organ is the esophagus,what is it’s function with respect to the stomach,what is the wall of the esophagus composed of?
The esophagus runs posteriorly to which organs and anteriorly to which organ and passes through what?
Anatomically how many portions of the esophagus are there and state them
Anatomy
The esophagus is a tubular organ with approximately 18-26 cm length in adults, 8-10 cm at birth and 19cm at the age of 15 yrs.
It connects the pharynx to the stomach. The wall of the esophagus is composed of the mucosa, submucosa, muscularia propria and adventitia.
The esophagus runs posteriorly to the trachea or windpipe and the heart and anteriorly to the spine, passes through the diaphragm.
Anatomically there are three portions of the esophagus and they are the cervical, thoracic and the abdominal. With upper esophageal sphincter (UES), esophageal body itself and the Lower esophageal Sphincter (LES).
Physiologically,the esophagus is divided into 3 name em
Explain them and state how they help the functions of the esophagus
So the physiology aspect of the esophagus has been divided into secretory physiology, motor physiology and the sensory physiology
So the secretory physiology of the esophagus;
The primary role of the esophagus is to propel food or fluid into the stomach and most importantly to prevent or clear gastroesophageal reflux.
This role is made possible due to the esophageal glands secretions such as water, mucous, bicarbonate, mucins, epidermal growth factor and prostaglandins.
NB; most important secretion is the bicarbonate which plays a protective role during GERD.
Motor physiology,
The esophageal motor pattern is initiated by the act of swallowing called peristalsis, which moves the bolus through the UES into the esophageal body and proceeds distally along through to the LES and into the stomach.
Sensory:
The esophagus is inervated by the vagus nerve and cervical and thoracic sympathetic trunk.
Vagal afferents are sensitive to muscle stretch of the esophagus and some other stimuli like chemicals such as acid, temperature and the rest
What is the pathophysiology of erosive esophagitis?
- Erosive Esophagitis
This develops when the gastric contents are regurgitated into the esophagus. Reflux happens commonly; in most cases does not cause major harm, because the natural peristalsis movement of the esophagus clears the refluxate back to the stomach.
In other cases, where acid reflux of the stomach is persistent, the result is damage to the esophagus causing symptoms like heartburn associated with GERD and other macroscopic changes.
Gastric acid, pepsin and bile irritate the squamous epithelium of the esophagus leading to inflammation, erosion and ulceration of the esophageal mucosa.
What is the pathophysiology of infective esophagitis
And state the types
Infectious Esophagitis
This is commonly seen in immunocompromised hosts but also been seen in healthy adults and children.
This is as a result of abnormalities in the host defense( neutropenia, impaired chemotaxis and phagocytosis) which predispose them to opportunistic infections.
There are some 3 types under this and they are ;
- Fungal (candidal)
- Viral ( herpes)
- Tuberculosis Esophagitis
Pathophysiology of pill induced esophagitis
Name three drug classes that causes it
Name four factors that increases this condition
Pill induced Esophagitis
As the name suggests, this type of Esophagitis is induced by pills mostly when the pills gets stucked in the esophageal mucosa due to some factors.
Sometimes the pills gets trapped in the esophagus when there is a condition called Esophageal stricture leading to ulcerations.
Drugs classes like antibiotics, Potassium Chloride, NSAIDS, iron supplement, quinidine, bisphosphonates, etc accounts for 90% of the reported cases.
Some of the factors that increases this condition:
- Chemical nature of the drug
- Solubility of the drug
- Contact time with the mucosa
- Size, shape and pill coating
- Amount of water( too little to swallow pill)
- Preexisting esophageal pathology such as achalasia (rare disorder making it difficult for food and liquid to pass into the stomach.
Achalasia or cardiospasm results from damage to nerves in the food tube (oesophagus), preventing the oesophagus from squeezing food into the stomach. It may be caused by an abnormal immune system response. )and stricture.(abnormal narrowing of a bodily passage )
Pathophysiology of radiation esophagitis and eosinophilic esophagitis
Radiation Esophagitis
The radiation causes DNA damage and cell death of the esophageal mucosa. Depending on the the dose, eg, dose over 30cGy (centigray )to the mediastinum typically causes retrosternal burning and painful swallowing, which is usually mild and limited to the duration of the therapy.
Eosinophilic Esophagitis
Caused by chronic, autoimmune condition, antigen triggered infiltration by eosinophils into the esophageal mucosa
Mostly associated with the atopic triad (asthma, eczema and food allergies).
State five causes of esophagitis
Causes of Esophagitis
- GERD
- Medications/ Pills ( NSAIDS- ibuprofen, aspirin), Antibiotics ( tetracycline, doxycycline,clindamycin)
- Infections (HIV, Candida albicans, cytomegalovirus, Herpes Simplex Virus)
- Radiation
- Immune mediated allergic reactions
Another cause is corrosives in suicide attempt by a strong bleach or any harmful chemicals which is followed by painful burns of the mouth, the pharynx and through to the esophagus
What are the clinical presentations and physical examination techniques to be done in esophagitis
State some lab investigations used
- Chest pains
- Heartburn
- Dysphagia
- Odynosphagia
- Oral Thrush
- Esophageal Thrush
- Occasionally, haematemesis
- Nausea and vomiting
- Upper abdominal discomfort
- Some presents with coughing
The chest pain is retrosternal and epigastric pain
Physical exam:
- Rectal Examination to identify the presence of ocult bleeding.
- Examination of the oral cavity for thrush or ulcers.
- Search for signs immunosuppressive diseases and skin signs of systemic diseases.
Lab tests are usually unhelpful unless complications are present
1. Full Blood Count to check for neutropenia especially
2. Biopsy
3. ECG to rule out cardiac ischemia as it presents with chest pains similar to that of cardiac ischemia
4. CD4 Count: A lower CD4 counts indicates a weak immune system and hence susceptible to infections
And a higher CD4 counts indicates a strong immune system
5.endoscopy
State four differentials for esophagitis
State the pharmacological and non pharmacological treatments of esophagitis
Differential Diagnosis
- Esophageal Candidiasis
- Cardiac Ischemia
- Esophageal Cancer
- pericarditis
- Gastroesophageal Reflux disease
- Tonsillopharyngitis -which can also be tonsillitis or pharyngitis or both
Non Pharmacological Treatments
- Advise patients to drink plenty of water with medication
- Lying down just after taking pills/eating should be avoided. At least there should be 30 mins interval
- Encourage patients to loose weight
- Encourage patients to avoid alcohol and smoking
- Avoid certain medication that risks one for Esophagitis
Or liquid forms of some medications are preferred to avoid the Pill induced Esophagitis
Pharmacological:
Pharmacological Treatment
- Erosive Esophagitis: Proton pump Inhibitors such as Omeprazole, pantoprazole or lansoprazole ,mucosal strengthener like cytotec
- Infectious Esophagitis: when caused by;
- Candida Albicans- Fluconazole, itraconazole etc
- Herpes- Acyclovir, foscarnet ( resistant acyclovir)
- CMV - Ganciclovir or Valganciclovir
- HIV - antiretroviral therapy for HIV in conjunction with oral corticosteroid
- Radiation : amifostine, viscous lidocaine and sucralfate
- Eosinophilic ; PPIs or
Topical/systemic steroids.. fluticasone, budenoside.
Name four complications of esophagitis
Complications
- Barrett’s Esophagus (precancerous changes to the esophagus): Damage to the lower portion of the tube that connects the mouth and stomach (oesophagus).
Barrett’s oesophagus is usually the result of repeated exposure to stomach acid. It’s most often diagnosed in people with long-term gastro-oesophageal reflux disease (GERD). - Esophageal Stricture : An esophageal stricture is an abnormal tightening or narrowing of the esophagus.
- Bleeding
- Perforations with mediastinitis : Mediastinitis is swelling and irritation (inflammation) of the chest area between the lungs (mediastinum).
- Sinusitis
- Laryngitis
- In infants, apnea and failure to thrive
- Achalasia: A rare disorder making it difficult for food and liquid to pass into the stomach.
Achalasia or cardiospasm results from damage to nerves in the food tube (oesophagus), preventing the oesophagus from squeezing food into the stomach. It may be caused by an abnormal immune system response.
Case scenario:
Case Scenario
A 44 year old man with HIV presents with complaints of painful swallowing with both liquids and solids. He otherwise feels well. He takes no medications. He stopped taking antiretroviral medications 2 years ago after he moved to a new city, and has not yet established a new primary care. On exam, vitals are normal, oropharynx appear normal. Abdominal exam is unremarkable. Upper endoscopy findings are;
white, raised, thick plaques throughout the esophagus.
Which type of Esophagitis do we think the patient is suffering from?
What is the most likely diagnosis?
What is the most appropriate treatment?
Infectious Esophagitis.
Esophageal Candidiasis or Thrush caused by Candida albicans
The most appropriate treatment to this condition we’ve already talked about is Oral fluconazole
Chances of developing GERD increase after age?
GERD is a chronic condition true or false?
It is common in asthmatic patients true or false?
Define GERD
40
True
True
Gastro-oesophageal reflux disease develops when the oesophageal mucosa is exposed to gastroduodenal contents for prolonged periods of time, resulting in symptoms and, in a proportion of cases, oesophagitis.
State the types of GERD
EROSIVE
-PRESSENCE OF OESOPHAGEAL MUCOSAL BREAKS/ULCERS
•NON EROSIVE
-ABSENCE OF OESOPHAGEAL MUCOSAL BREAKS /ULCERS
According to the anatomy of the oesophagus,it is a muscular tube of 25cm length which begins at the level of the lower border of C6. True or false?
The oesophagus is divided into three parts name them
Name the three main areas of narrowing of the oesophagus which can be detected by barium swallow
State the two sphincters of the oesophagus and their functions and state the histology
True
Superior third:striated muscle only
Middle third:striated plus smooth
Inferior third:smooth muscle only
Areas of narrowing:
At the area of the cricopharyngeus muscle
Where the left mainstem bronchus and aortic arch cross
At the hiatus of the diaphragm(at the level of T10)
Upper oesophageal sphincter (formed by cricopharyngeus muscle):it prevents the passage of excess air into the stomach during breathing
Lower oesophageal sphincter:(physiological sphincter):prevents the reflux of gastric contents into the oesophagus
Histology:non-keratinized stratified squamous epithelium
At which vertebral level does the inferior vena cava,aorta and oesophagus transverse(being across : set crosswise,made at right angles to the long axis of the body) the diaphragm
Infertile vena cava:T8
Oesophagus:T10
Aorta:T12
Explain the physiology of the oesophagus
The lower oesophageal sphincter(LeS) is located 3cm above the junction between oesophagus and the stomach and remains contracted all the time except during the oesophageal stage of swallowing (physiology fo the oesophagus) true or false?
What is the pressure in the LeS?
Failure of LeS relaxation causes?
Failure of LeS contraction causes?
When intra-abdominal pressure is increased during coughing the lower part of the oesophagus is closed by a valve like action
True or false
When bolus enters the oesophagus,the upper sphincter relaxes when the larynx is lifted
Peristalsis begins
Circular fibers contract behind the bolus
Longitudinal fibers shorten the distance
Lower sphincter relaxes by receptive relaxation mechanism as food approaches
Travel time for solids is 4-8secs and liquids is 1second
True
30mmHg
Achalasia
Reflux of stomach content into the oesophagus causing reflux oesophagitis
True
What are the anti reflux mechanisms of physiological mechanism That protect the oesophagus against acid injury?
LES competence
- LES PRESSURE VERSUS INTRGASTRIC PRESSURE
- TRANSDIAPHRAGMATIC PRESSURE GRADIENT
•CRURAL FIBERS OF THE DIAPHRAGM
- contraction at LOS prevents reflux
- acts like an external sphincter
- large hiatus hernia can impair this mechanism
•UNIQUE ANATOMY OF THE STOMACH
-the angle of HIS
-mucosal rossete
- posterolaterial location of the fundus
•OESOPHAGEAL CLEARANCE
-by peristalsis
- by saliva
•Gastric emptying
State the pathophysiology of GERD
The pathogenesis of GERD involves an interplay of
1.Chemical mechanisms
2.Mechanical mechanisms
3.Psychologic mechanisms
4.Neurologic mechanisms
as such, GERD should be approached as a disorder beyond acid.
True or false
Reflux is normally followed by oesophageal peristaltic waves which efficiently clear the gullet, alkaline saliva neutralises residual acid, and symptoms do not occur
- gastroesophageal reflux is a normal physiologic phenomenon experienced intermittently by most people , particularly after a meal.
-Several factors are known to be involved in the development of gastro-oesophageal reflux disease.
-development is multifactorial
Factors involved:
•ABNORMALITIES OF THE OESOPHAGEL SPHINCTER
•DISRUPTION OF ANATOMICAL BARRIER
•DEFECTIVE OESOPHAGEL CLEARANCE
•DELAYED GASTRIC EMPTYING
•HYPERSECRETION OF ACID
•INCREASED INTRA-ABDOMINAL PPRESSURE
•DIETARY AND ENVIRONMENTAL FACTORS
True
Explain how the factors involved in causing GeRd in the previous card can cause GeRD
- ABNORMALITIES OF THE OESOPHAGEL SPHINCTER
- The lower oesophageal sphincter is tonically contracted under normal circumstances, relaxing only during swallowing.
- GERD occurs when the LES pressure is lower than the intragastric pressure(hypotensive LES)
- Some patients with gastro-oesophageal reflux disease have
- an ATONIC(REDUCED) LES
- transient increase in intra abdominal pressure
- spontaneous(frequent episodes) inappropriate LES relaxation
- The lower oesophageal sphincter is tonically contracted under normal circumstances, relaxing only during swallowing.
- DISRUPTION OF ANATOMICAL BARRIERS
- associated with hiatal hernia
- part of stomach pushes(bulges) into the chest cavity through an opening in the diaphragm where the oesophagus passes.
- Hiatus hernia causes reflux because the pressure gradient between the abdominal and thoracic cavities, which normally pinches the hiatus, is lost.
- the size of hiatal hernia is proportional to the frequency of LES relaxation - DEFECTIVE OESOPHAGEAL CLEARANCE
- oesophageal defense mechanisms can be broken down into two
- oesophageal clearance
- mucosal resistance
- oesopahgeal clearance functions to neutralize the acid reflux through the LES 1. Mechanical resistance is achieved by oesophageal peristalsis- chemical clearance is achieved with saliva
- causes of defective esophageal clearance
- chemical clearance is achieved with saliva
- infective peristalsis
- reduced salivary secreation
- reduced secretion from oesophageal submucosal glands
- Poor oesophageal clearance leads to increased acid exposure time.
- oesophageal defense mechanisms can be broken down into two
PATHOPHYSIOLOGY OF GERD
- DELAYED GASTRIC EMPTYING
- Gastric emptying is delayed in patients with gastro-oesophageal reflux disease.
- exact role remains to be clarified( reasons unknown)
- results in an increase in the volume of gastric contents available for reflux into the oesophagus.
- Gastric emptying is delayed in patients with gastro-oesophageal reflux disease.
PATHOPHYSIOLOGY OF GERD
- INCREASED INTRA-ABDOMINAL PPRESSURE
- conditions that increases intra-abdominal pressure can lead to GERD - OBESITY
- PREQNANCY
- BENDING
- STRAINING
- COUGHING
- TIGHT CLOTHES
6.DIETARY AND ENVIRONMENTAL FACTORS:
agents that lowers LES
1. DIET
-dietary fat
- chocolate
- alcohol
- coffee
coffee
- cigarettes
- Spicy foods
- orange and tomato juices
2. MEDICATIONS
- anticholinergics
- beta adrenergic agonists
- alpha adrenergic antagonists
- calcium channel blockers
- diazepam
- theophylline
- morphine
- NSAIDS
3.POSITION / ACTIVITY
- bending
- straining
- external pressure ( tight clothing, pregnancy)
State six risk factors for GeRd
GERD is more common in as the asthmatic patients and asthma is more common in patients w GeRd compared to controls true or false
Obesity
Hiatal hernia
Pregnancy
Connective tissues disorders example scleroderma
Delayed stomach emptying
Smoking
Eating large meals or eating late at night
Consuming acid reflux triggers(fatty or fried food)
Drinking certain drinsk(alcohol or coffee)
Taking certain medications(eg aspirin)
True
State ten signs of GeRd and six alarming signs seen in GErd,state some physical exam findings
State Three differentials diagnosis of GERd
SIGNS & SYMPTOMS
•Heartburn (pyrosis)
•Sensation of discomfort or burning behind the sternum rising up to the neck
•Occurs 1-2 hours after eating , often at night
-provoked by
1.Vigorous exercise
2.Bending forward
3.Straining
4.Lying down
- Relived by 5. Antiacids 6. Sitting upright
-Waterbrash
•production of excessive amounts of saliva which is due to reflex salivary gland stimulation as acid enters the gullet
•REGURGITATION
•Effortless return of gastric contents into the pharynx
•Bitter, acidic fluid in the mouth
•NOCTURNAL?
-wakes patients up with coughing and choking
-provoked by lying down or bending over
-less relived by antiacids
-NON CARDIAC CHEST PAIN
•RETROSTERNAL
•EPIGASTRIC
•CAN MIMIC ANGINA
•MAY BE DUE TO REFLUX-INDUCED OESOPHAGEAL SPASMS
Alarming signs:
OTHER SIGNS & SYMPTOMS( ALARMING SIGNS )
•DYSPEPSIA
•DYSPHAGIA
- food sticks or hangs up
•ODYNOPHAGIA
- retrosternal pain with swallowing
•CHRONIC HOARNESS(DYSPHONIA)
•EARLY SATIETY
•COUGH
•WHEEZING
•VOMITING
•GI BLEEDING
•IRON DEFICIENCY ANEMIA
•WEIGHT LOSS
PHYSICAL EXAMINATION FINDINGS
•MAY BE NONE
•EPIGASTRIC TENDERNESS
•CHEST SIGNS( WHEEZING)
Differentials : GASTRITIS •PEPTIC ULCER •ESOPHAGITIS •ACHALASIA •CORONARY ARTERY DISEASE •ESOPHAGEAL MOTILITY DISORDERS •ESOPHAGEAL CANCER
State six investigations for GeRd
Young patients who present with typical symptoms of gastro-oesophageal reflux, without worrying features such as dysphagia, weight loss or anaemia, can be treated empirically without investigation.
-if the classic symptoms of heartburn and regurgitation exist in the absence of alarming symptoms ( other symptoms ), the diagnosis of GERD can be made clinically and treatment can be initiated
Ivestigations
•Upper gastro-intestinal tract endoscopy
-This is performed to exclude other upper gastrointestinal diseases that can mimic gastro-oesophageal reflux and to identify complications.
- allows direct visualization of the oesophageal mucosa and biopsy if need.
-checks for presence and severity of erosive oesophagitis
- detection of complications such as stricture or barret’s esophagus
Ivestigations
•AMBULATORY OESOPHAGEAL PH MONITIRING
- mostly used in cases that are difficult to download
•Twenty-four-hour pH monitoring is indicated if the diagnosis is unclear or surgical intervention is under consideration.
•Accepted standard for establishing or excluding presence of GERD for those patients who do no have mucosal changes
- This involves tethering a slim catheter with a terminal radiotelemetry pH- sensitive probe above the gastro-oesophageal junction. The intraluminal pH is recorded whilst the patient undergoes normal activities, and episodes of symptoms are noted and related to pH. A pH of less than 4 for more than 6–7% of the study time is diagnostic of reflux disease.
•checks the amount and timing of reflux
•Correlates the reflux and symptoms
• most useful in
• endoscopoy-negative patients
•Patients with chest pains
•Patients with pulmonary/upper respiratory symtoms
INVESTIGATIONS
•Chest X-ray
- to rule out other causes or diseases
• barium swallow with fluoroscopy
•Useful in children
•Patient swallows liquid barium while X-ray images are taken . The barium fills and coast the lining of the oesphagus so that it can diagnose anatomical abnormalities
•Can detect stricture( location , length)
•Mass( location , length)
•Hiatal hernia( size, type)
INVESTIGATIONS
•Lower Oesophageal sphicter manometry
-in cases that are difficult to diagnose
Other useful tests
- to rule out other diseases
How is GeRd treated and managed
Non pharmacological and pharmacological and surgical treatment
State four complications of GERd
Alleviate or eliminate the patient’s symptoms
•Decrease the frequency or recurrence and duration of gastro esophageal reflux.
•Promote healing of the injured mucosa
•Prevent development of complications
NON PHARMACOLOGICAL TREATMENT
- LIFESTYLE MODIFICATIONS
•Elevate head of bed by about 30degrees( 4-6 inches) or encourage patient to sleep on pillows
•Patient must avoid lying down 3-4 hours after a meal
•Patient must avoid over eating and large meals before bed time
•Patient must avoid medications an foods that potentiate or aggravate symptoms or disease
•CCB(Recent studies suggest that calcium channel blockers (CCBs), and particularly nifedipine, increase the risk of GERD by significantly reducing the tone of the LES, increasing esophageal exposure to gastric acid and reducing the amplitude and duration of esophageal peristalsis ), alpha agonists,NSAIDS,fats,alcohol, smoking , spicy foods ,fried food, carbonated beverages, onionsetc
•Encourage weight reduction in patients especially in overweight and obese patients.
•Avoid clothing that is tight around the waist.
PHARMACOLOGICAL TREATMENT
•ANTIACIDS
•PROTON PUMP INHIBITORS
•HISTAMINE H2 RECEPTOR ANTAGONISTS
- REFER TO STANDARD TREATMENT GUIDELINES FOR FUTHER INFORMATIONON PHARMACOLOGICAL TREATMENTS
SURGICAL TREATMENT( ANTI-REFLUX SURGERY)
-Failed medical treatment
•Patient preference
•GERD COMPLICATIONS
COMPLICATIONS
•EROSIVE ESOPHAGITIS
-A range of endoscopic findings, from mild redness to severe, bleeding ulceration with stricture formation, are recognized.
•BARRETE’S ESOPHAGUS
-Barrett’s oesophagus is a pre-malignant condition, in which the normal squamous lining of the lower oesophagus is replaced by columnar mucosa (columnar lined oesophagus; CLO) that may contain areas of intestinal metaplasia.
•Benign oesophageal stricture
-Fibrous strictures can develop as a consequence of longstanding oesophagitis, especially in the elderly and those with poor oesophageal peristaltic activity. The typical presentation is with dysphagia that is worse for solids than for liquids. Bolus obstruction following ingestion of meat causes absolute dysphagia
•Anemia
-Iron deficiency anaemia can occur as a consequence of occult blood loss from long-standing oesophagitis. Most patients have a large hiatus hernia and bleeding can stem from subtle erosions in the neck of the sac (‘Cameron lesions’).
More complications
-oesophageal stricture:result of healing of erosive oesophagitis
May need dilation
Case study
A 33-year-old male presents with a one-month history of episodes of mid-epigastric pain, a “burning” sensation in his chest, an associated dry cough, and occasional regurgitation. The pain worsens after eating and when he is lying flat. The patient has increasing postprandial fullness and early satiety. He also states waking up from the pain and burning, with a sore throat and hoarse voice. The patient reports associated mid-thoracic, bilateral back pain that occurs during the episodes. The symptoms are partially relieved by adjusting from a lying to a sitting position and with the use of over-the-counter (OTC) medications Mylanta® and Zantac.The patient has been a marketing manager for a mid-size company for eight years. He does not smoke, use any medication or drugs other than an occasional OTC, and is a social drinker only. He exercises regularly.
Case senior
•Physical Examination:
•Vital Signs:
•Eyes: Ears: Nares: P Throat :
•Temperature, 99.1° F; Blood Pressure, 132/78; Respiratory Rate, 18; Pulse, 80; Weight, 190 lbs.
•EYES: Pupils equally round and reactive to light.
•EARS: Tympanic membranes clear; canals clear bilaterally.
•NOSE: patient without nasal septal deviation; pharyngeal mucosa pink and moist. THROAT:Oropharynx pink and moist; no erythema, tonsillar enlargement, lesions, lingual erosion of teeth, lymphadenopathy, or nodulary; thyroid normal size.
•CARDIAC: Regular rate and rhythm; no murmurs, rubs, or gallops.
• LUNGS: Clear to auscultation bilaterally; no rales, rhonchi, or wheezing.
•ANDOMEN: Non-distended, soft, non-tender; normal active bowel sounds.
•Musculoskeletal: Muscle strength 5/5 upper and lower extremities, full range of motion,
•no tissue texture changes or asymmetry.
•Neuro: 2–12 intact; deep tendon reflexes intact bilaterally; sensation intact; 5/5 motor STRENGTH
State the: •DIFFERENTIAL DIAGNOSIS •IVESTIGATIONS •FINAL DIAGNOSIS •TREATMENT AND MANAGEMENT
1.GERD
PUD(gastric ulcer)
Hiatal hernia
2.upper GI endoscopy
FBC
Hb
3.GERD
4.patient should sleep with pillows and shouldn’t lie down straight but at an angle(I’ve forgotten the angle so check)
Patient shouldn’t eat large meals at night
Should stay away from spicy and acidy foods
Should lie down three to four hours after eating
Give PPI
Check
More on GERD management
In the US, H.pylori infection associated gastritis is more common in African Americans,then Hispanics and the elderly compared to whites
True or false?
Females are more affected w acute gastritis than males true or false
In H. Pylori infection associated gastritis,males are more commonly affected than females
True or false
True
True
True
What is the anatomy and physiology of the stomach
ANATOMY AND PHYSIOLOGY OF THE STOMACH
The stomach is divided into 4 major anatomic regions :
- The cardia*
- The fundus*
- The body* and
- The pyloric antrum*
The cardia is lined mainly by mucin secreting foveolar cell that form shallow glands that secrete mucus and bicarbonate
The antral glands are similar but also contain endocrine cells such as G cells that release gastrin to stimulate luminal acid secretion by the parietal cells within the gastric fundus and the body.
The well developed glands of the body and fundus contain chief cells that produce and secrete digestive enzymes such as pepsin.
Define gastritis
How is it diagnosed?
How is it treated?
Many cases are asymptomatic but dyspepsia and GI bleeding sometimes occur.
True or false
Definition of gastritis
Gastritis is the inflammation of the gastric mucosa caused by any several conditions including infection (H. pylori), Drugs (NSAIDs, alcohol), stress and autoimmune phenomena (atrophic gastritis).
Diagnosis is by endoscopy.
Treatment is directed at the cause but often includes acid suppression(a proton pump inhibitor or H2 blocker) and for H.pylori infection antibiotics.
In severe gastritis bleeding is managed with IV fluids and blood transfusion as needed
True
What is the pathology of gastritis
Pathology of Gastritis
The gastric lumen is strongly acidic and with a pH close to 1. It’s acidic environment contributes to digestion but also has the potential to damage the mucosa. Protective mechanisms of the stomach mucosa include:
- mucin secreted by the foveolar cells forms a thin layer of mucus that prevents large particles from directly touching the epithelium.
- layer of fluid covers the mucosa and has a neutral pH as a result of bicarbonate ion secretion by surface epithelial cells. Finally, the rich vascular supply to the gastric mucosa delivers oxygen, bicarbonate and nutrients while washing away acid that has back-diffused into the propria.
Acute or chronic gastritis can occur after disruption of any of the protective mechanisms of the stomach mucosa.
Reduced mucin synthesis in the elderly suggested to be one factor for increased susceptibility to gastritis.
NSAIDs interferes with production of prostaglandins and bicarbonate secretion.
Ingestion of harsh chemicals destroy the protective mechanisms of the stomach hence could cause gastritis.
H.Pylori infections is also a major cause of gastritis
State four adaptive features of H Pylori to the gastric mucosa
Continuation of pathology of gastritis
H. pylori infection is also a major cause of gastritis.
Below are the adaptive features of H. pylori to the gastric mucosa
- Flagella, which allow the bacteria to be motile in viscous mucus.
- Generates ammonia from endogenous urea, thereby elevating local gastric pH around the organism, protecting it from acidic pH of the stomach.
- H. pylori has adhesions that enhance bacterial adherence to the surface of foveolar cells.
- H. pylori produces toxin that may disrupt the stomach mucosa.
State the three major classification of gastritis
Classifications of gastritis
Gastritis can be classified based on this three major ways:
- Severity of mucosal injury as
a. Erosive gastritis
b. Nonerosive gastritis - Site of involvement
a. Cardia gastritis
b. Fundus gastritis
c. Body gastritis
d. Antrum gastritis - Histologically based on inflammatory cells
a. Acute gastritis
b. Chronic gastritis
Gastritis can also be classified based on uncommon syndromes such as
?
State five other classifications of gastritis’
*
- Menetrier’s diseases: Menetrier disease is a rare disorder characterized by massive overgrowth of mucous cells (foveola) in the mucous membrane lining the stomach, resulting in large gastric folds.
- Eosinophilic gastritis
Other classifications* include:
- Gastritis caused by systemic disorder
- Gastritis caused by physical agents
- Infectious (septic) gastritis
- Autoimmune Metaplastic Atrophic Gastritis
- Post gastrectomy gastritis
Explain erosive and non erosive gastritis ,how they are diagnosed,how they manifest,how they are treated,state five causes of erosive gastritis
In erosive gastritis , Deep erosion, ulcers and sometimes perforation may occur in severe or untreated cases. Lesions typically occur in the body but the antrum may also be involved
True or false
EROSIVE GASTRITIS
It is a gastric mucosal erosion caused by damage to mucosal defenses.
It is typically acute, manifesting with bleeding, but may be subacute or chronic with few or no symptoms.
Diagnosis is by endoscopy.
Treatment is supportive, with removal of the inciting cause.
NONEROSIVE GASTRITIS
It refers to a variety of histologic abnormalities that are mainly the result of H.pylori infection. Most patients are asymptomatic.
Diagnosis is by endoscopy. Treatment is eradication of H.pylori and sometimes acid suppression.
Causes of erosive gastritis include NSAID, alcohol, stress, vascular injury and less commonly radiation, viral infection (eg. Cytomegalovirus), direct trauma(eg. nasogatric tubes)
True
For the cardia, fundus, body and antrum gastritis it’s simply the type of gastritis named after the part of the stomach it occurs
True or false
Explain acute gastritis
Explain chronic gastritis and state four causes of it
Acute gastritis lasts for 2-10days but if left untreated it may last from weeks to years
True
ACUTE GASTRITIS
It is a transient(less than three days ) mucosal inflammatory process that may be asymptomatic or cause variable degrees of epigastric pain, nausea and vomiting. In a more severe case may cause erosion, ulceration, hematemesis, melena or rarely, massive blood loss.
CHRONIC GASTRITIS
The symptoms and signs associated with chronic gastritis typically are less severe but more persistent than those of acute gastritis.
Nausea and abdominal discomfort may occur sometimes vomiting but hematemesis is uncommon.
Most common causes of chronic gastritis is infection with Helicopter pylori , autoimmune phenomena , radiation injury to the stomach mucosa and **chronic* bile reflux
Explain Mantriers disease ,symptoms,diagnosis,treatment
MANITRIER’S DISEASE
This is a rare idiopathic disorder that affects adults aged 30 to 60 and is more common among men. It manifests as a significant thinkening of the gastric folds of the gastric body but not the antrum. Gland atrophy and marked foveolar pit hyperplasia occur, often accompanied by mucus gland metaplasia and increased mucosal thickness with little inflammation . Hypoalbuminemia caused by GI protein loss may be present. As disease progresses the secretion of acid and pepsin decreases, causing hypochlorhydria.
Symptoms include: epigastric pain, nausea, weight loss, edema and diarrhea
Diagnosis is by endoscopy with deep mucosal biopsy or full thickness laparoscopic gastric biopsy
Treatment: anticholinergics, antisecretory drugs and corticosteroids. Partial or complete gastric resection may be necessary in cases of severe hypoalbuminemia.
Explain eosinophilic gastritis,symptoms,diagnosis,treatment
EOSINOPHILIC GASTRITIS
It is usually idiopathic but may result from nematode infestation . It involves extensive infiltration of the mucosa, submucosa and muscle layers with eosinophils often occurs in the antrum.
Symptoms: nausea, vomiting and early satiety
Diagnosis: endoscopic biopsy of involved areas.
Treatment: corticosteroids and surgery may be required for pyloric obstruction
State five systematic diseases that cause gastritis,
How do physical agents cause gastritis
Explain infectious or septic gastritis
GASTRITIS CAUSED SYSTEMATIC DISORDERS
Such as sarcoidoses(The growth of tiny collections of inflammatory cells in different parts of the body.) ,TB, amyloidiosesioses,and other granulomatous diseases can cause gastritis.
GASTRITIS CAUSED BY PHYSICAL AGENTS.
Radiation and ingestion of corrosives (especially acidic compounds) can cause gastritis. Exposure to>16 Gy of radiation causes marked deep gastritis, usually involving the antrum
more than corpus. Plyoric stenosis and perforation are possible complications of radiation-induced gastritis.
INFECTIOUS (SEPTIC) GASTRITIS.
Except for H. ployri infection, bacterial invasion of the stomach is rare and mainly occurs in ischemia , Debilitated or immunocompromised patients may devolop viral or fungal gastritis with cytomegalovirus,candida,histoplasmosis,or mucormycosis.
Explain autoimmune metaplastic strophic gastritis ,how it’s diagnosed and how it’s treated
What is Post gastrectomy gastritis
AUTOIMMUNE METAPLASTIC ATROPHIC GASTRITIS.
Autoimmune metaplastic atrophic gastritis (AMAG) is an inherited autoimmune disease that attacks parietal cells, resulting in hypochlorhydria( low acid secretion) and decreased production of intrinsic factor. Consequently leading to atrophic gastritis ( atrophy or disfunction of the gastric glands),B12 malabsorption and frequently, pernicious anaemia. Risk of gastric adenocarcinoma increases 3-fold. Diagnosis is by endoscopy. Treatment is with parenteral vitamin B12.
Post gastrectomy gastritis
Is a gastric atrophy developing after a partial or subtotal gastrectomy
State five differentials and five complications for gastritis
DIFFERENTIAL DIAGNOSIS
Peptic ulcer disease Gastric cancer GERD Gastroenteritis Crohn's disease Gastrinoma Gastric ulcers Peritonitis Enteric fever Food poisoning
Complications: Anemia Gastric perforations Sepsis Gastroparesis Gastrointestinal bleeding Peritonitis
Case study
Case scenario: A 21 year old male patient , presented with 7 days history of low grade fever with severe profuse vomiting; epigastric & lt hypochondriac pain which was < by touch, < after eating and drinking warm liquids; & generalized weakness, aversion to food, milk.
State some differentials and if it’s gastritis as the diagnosis then why was there Epi gastric pain
State four other organs in the Epi gastric region
A.PUD
Gastritis
Gastroenteritis
B.The stomach is located at the epigastric region . Organic pain is poorly localized. It radiates to the dermatome level, which receives visceral afferent from the organ concern.
The stomach is supplied by pain afferent that reach the T7 and T8 spinal sensory ganglia by the same sensory ganglia and spinal segment as the epigastric region.
Liver,spleen,duodenum,adrenal glands,pancreas
Note not the full thing tho but some parts of these organs can be found in the region
Define PUD,state and explain the types of PuD(where they occur,what the pain is characterized by)
Definition
PUD is a break in the inner lining of the stomach or duodenum OR is a sore in the lining of the stomach or duodenum.
There are common types of peptic ulcer:
- Gastric ulcer which is occurs in the stomach lining and is characterized by upper abdominal pain(epigastric pain) which worsens with eating and so people with gastric ulcers mostly tend to starve to avoid the pain
- Duodenal Ulcer* which occurs in the upper part of the small intestine, the duodenum and is also characterized by upper abdominal pain which occurs 3hrs after eating and it’s also relieved with eating.
In epidemiology,peptic ulcer disease caused by H pylori shows a decrease more so in developed countries because of the new drugs developed. H pylori is transmitted through ontaminated food and water and human saliva true or false
True
What are the signs and symptoms of PUD and what are the signs or symptoms specific to the types of ulcers
Signs and Symptoms
The signs and symptoms normally depend on the type of peptic ulcer. As said earlier, with gastric ulcers patients normally complain about pain with eating whilst with duodenal ulcer, patients normally complain about abdominal pain when they’re hungry and it’s relieved with eating but the common signs and symptoms patients present with are
- Upper abdominal pain mostly at the epigastric region of the abdomen
- Bloating: This means your tummy swells because your stomach is full of gas or air.
- Nausea and vomiting
- Loss of appetite and weight loss mostly with patients with gastric ulcers
What is the pathophysiology of PUD
Pathophysiology
Peptic ulcers are defects in the gastric or duodenal mucosa that extend through the muscularis mucosa. The epithelial cells of the stomach and duodenum secrete mucus in response to irritation of the epithelial lining and as a result of cholinergic stimulation. The superficial portion of the gastric and duodenal mucosa exists in the form of a gel layer, which is impermeable to acid and pepsin. Other gastric and duodenal cells secrete bicarbonate, which aids in buffering acid that lies near the mucosa. Prostaglandins of the E type (PGE) have an important protective role, because PGE increases the production of both bicarbonate and the mucous layer.
In the event of acid and pepsin entering the epithelial cells, additional mechanisms are in place to reduce injury. Within the epithelial cells, ion pumps in the basolateral cell membrane help to regulate intracellular pH by removing excess hydrogen ions. Through the process of restitution, healthy cells migrate to the site of injury. Mucosal blood flow removes acid that diffuses through the injured mucosa and provides bicarbonate to the surface epithelial cells.
Under normal conditions, a physiologic balance exists between gastric acid secretion and gastroduodenal mucosal defense. Mucosal injury and, thus, peptic ulcer occur when the balance between the aggressive factors and the defensive mechanisms is disrupted. Aggressive factors, such as nonsteroidal anti-inflammatory drugs (NSAIDs), H pylori infection, alcohol, bile salts, acid, and pepsin, can alter the mucosal defense by allowing the back diffusion of hydrogen ions and subsequent epithelial cell injury. The defensive mechanisms include tight intercellular junctions, mucus, bicarbonate, mucosal blood flow, cellular restitution, and epithelial renewal.
What are the causes of PUD
Causes
Some of the causes include
- A prolonged use of NSAID’s
- A bacteria called H. Pylori
- Tobacco Use
- Stress
- Dietary factors like eating a lot of spices
- And it can also be genetic
- Some medical conditions like Chron’s disease can also be a cause
State four causes of PUD
Causes
Some of the causes include
- A prolonged use of NSAID’s
- A bacteria called H. Pylori
- Tobacco Use
- Stress
- Dietary factors like eating a lot of spices
- And it can also be genetic
- Some medical conditions like Chron’s disease can also be a cause
State and explain four complications of PUD
- Complications*
- Bleeding: Bleeding can occur as slow blood loss that leads to anemia or as severe blood loss that may require hospitalization or a blood transfusion. Severe blood loss may cause black or bloody vomit or black or bloody stools.
- A hole (perforation) in your stomach wall: Peptic ulcers can eat a hole through (perforate) the wall of your stomach or small intestine, putting you at risk of serious infection of your abdominal cavity (peritonitis).
- Obstruction: Peptic ulcers can block passage of food through the digestive tract, causing you to become full easily, to vomit and to lose weight either through swelling from inflammation or through scarring.
- Gastric cancer: Studies have shown that people infected with H. pylori have an increased risk of gastric cancer.
How is PUD managed and treated and what are the aims in treating it
Management and Treatment
*Patients with peptic ulcer disease should be warned about known or potentially injurious drugs and agents. Some examples are as follows: NSAID Alcohol Aspirin Caffeine Tobacco
-
Aims
- To reduce gastric acid secretion
- To neutralize secreted gastric acid
- To increase mucosal resistance to acid pepsin attacks
- To eradicate H. Pylori
-
Drugs
- Proton pump inhibitors like Omeprazole, lansoprazole and esomeprasole
- Histamine Receptor antagonists like Cimetidine, Ranitidine and Famotidine
- Antacids like Aluminum hydroxide and magnesium hydroxide
- Mucosal strengtheners like misoprostol
- Bismuth compound such as bismuth subsalicyclate
- Alginates like Gaviscone
-
H. Pylori eradication regimen
- Dual therapy: Omeprazole + single antibiotic such as amoxicillin
- Triple therapy: Omeprazole + metronidazole + amoxicillin/clarithromycin for 1- 2 weeks
- Quadruple therapy: Triple therapy + bismuth compound for 3 days
What is gastroenteritis ?
The severity of gastroenteritis mainly depends on?
What does this imply?
DEFINITION
Gastroenteritis, also called stomach flu or bug is inflammation of the lining of the stomach and small and large intestines. The severity of gastroenteritis mainly depends on an individual’s immune system’s ability to fight the infection. This implies that, gastroenteritis is self limiting in non-immunocompromised individuals.
EPIDEMIOLOGY
It is responsible for significant morbidity and mortality worldwide with nearly 1.7 billion cases and at least 2million deaths per year many resulting from consumption of contaminated food and water.
Also, it affects 3 to 5 billion children worldwide and is responsible for 12% of deaths in children less than 5 years.
This condition is more common in developing countries where sanitation conditions are poor. However, Viruses are the most common cause of gastroenteritis in the US.
What is the pathophysiologoy of gastroenteritis
What are the causes of gastroenteritis categorised into?
PATHOPHYSIOLOGY
Adequate fluid balance in humans depends on the secretion and reabsorption of fluid and electrolytes in the intestinal tract; diarrhea occurs when intestinal fluid output overwhelms the absorptive capacity of the gastrointestinal tract. The 2 primary mechanisms responsible for acute gastroenteritis are (1) damage to the villous brush border of the intestine, causing malabsorption of intestinal contents and leading to an osmotic diarrhea, and (2) the release of toxins that bind to specific enterocyte receptors and cause the release of chloride ions into the intestinal lumen, leading to secretory diarrhea.
ETIOLOGY
This could be infectious or non-infectious.
What are the symptoms of gastroenteritis
How is it diagnosed ?(investigations included)
People may experience :
Pain areas: in the abdomen
Gastrointestinal: diarrhoea, stomach cramps, belching, gagging, indigestion, nausea, vomiting, or flatulence
Whole body: chills, dehydration, fatigue, fever, lethargy, light-headedness, or loss of appetite
Also common: fast heart rate, headache, low urine output, weakness, or weight loss
Diagnosis:
A doctor will diagnose gastroenteritis by first taking a complete history of your symptoms. Often, lab test are not needed to diagnose this condition.
• However, if you have persistent fever, blood in your stool or diarrhea , stool study tests for clostridium difficile, rotavirus and norovirus.
• Serum electrolytes, blood urea nitrogen (BUN), and creatinine should be obtained to evaluate hydration and acid-base status in patients who appear seriously ill.
• Complete blood count (CBC) is nonspecific, although eosinophilia may indicate parasitic infection.
• Renal function tests and CBC should be done about a week after the start of symptoms in patients with E. coli O157:H7 to detect early-onset hemolytic-uremic syndrome. It is unclear whether this testing is necessary in patients with non–E. coli O157:H7 Shiga toxin infection.
• Microscopy for confirming the presence of parasites, ova and cyst may be helpful.
In summary: Investigations
•Laboratory investigations are usually not necessary in patients with non-bloody diarrhea and no evidence of systemic toxicity
i.e. gastroenteritis is usually diagnosed by symptoms that is produced , primarily diarrhea.
•Selection of appropriate test is based on the history and physical examination findings
-copious watery diarrhea
-ingestion of potentially contaminated food
-recent travel
-known GI irritant
-contact with similarly ill people
-use of antibiotic and other drugs
•In terms of sever or persistent cases , stool testing for culture and sensitivity and microscopic examination is ordered
-if rectal examination shows occult blood
-if watery diarrhea persists for > 48 hours
•Other blood tests like FBC, BUN, serum electrolytes may be necessary
-eosinophilia in FBC may indicate parasitic infections
Investigations •Viral -stool electron microscopy -PCR to determine viral genome -ELISA to detect viral antigens in stools -e.t.c •Bacterial -microscopy -stool culture -serological typing -e.t.c
Name five complications of gastroenteritis and how gastroenteritis is treated
How is it prevented?
Complications of gastroenteritis include the following:
• Dehydration
• Malabsorption
• Transient lactose intolerance
• Chronic diarrhea
• Systemic infection (meningitis, arthritis, pneumonia) especially with Salmonella infections
• Sepsis (Salmonella, Yersinia, Campylobacter organisms)
• Hemolytic-uremic syndrome (much more common in children, especially with E coli O157:H7)
• Toxic megacolon
• Reactive arthritides (Salmonella, Shigella, Yersinia, Campylobacter, Giardia organisms)
• Persistent diarrhea
• Thrombotic thrombocytopenic purpura or TTP (E coli O157:H7)
• Guillain-Barré syndrome (Campylobacter
-weight loss
-Metabolic acidosis
-systemic infections like aspiration pneumonia
-electrolyte imabalance
TREATMENT
Gastroenteritis is usually an acute and self-limiting disease which does not require medication. Rest and rehydration are the mainstays of treatment.
If your child has viral gastroenteritis, you should give your child an oral rehydration solution—such as Pedialyte, Naturalyte, Infalyte, and CeraLyte—as directed to replace lost fluids and electrolytes. Oral rehydration solutions are liquids that contain glucose and electrolytes.
IV therapy can bring much-needed relief when you’re suffering from the symptoms of a stomach virus. When you use IV fluids for the stomach flu, you are replenishing your body when it’s dehydrated. The fluids contain high-quality vitamins, minerals, and electrolytes, which can help your body as you recover.
However, If you are seeking relief from nausea or diarrhea, there are some prescription medications that can ease your symptoms. Antiemetic such as promethazine, prochlorperazine, metoclopramide, or ondansetron may be prescribed to stop the nausea and vomiting.
You can also try an over-the-counter antidiarrheal medication, such as loperamide hydrochloride (Imodium) or bismuth subsalicylate (Pepto-Bismol).
Antibiotics can be given only if the cause is bacterial and not viral or parasitic.
NB: Do not use Pepto-Bismol in children
Pharmacological treatment
•Treatment depends on the cause
-antibioctics
-antiemetics
-antidiarrheal agents
-antispasmodics
-vaccines
Refer the pharmacology flashcards in the treatment of diarrhea in gastroenteritis
PREVENTION
* washing vegetables, fruits, and salads thoroughly before eating them. * avoiding close contact with people who have gastroenteritis. * drinking bottled water when traveling, especially in developing countries. * avoiding eating raw meat and fish. * Wash your hands with soap and running water * Swimmers should avoid swallowing water when they swim.
Why shouldn’t pepto bismol be used in kids
Regular Pepto-Bismol and Kaopectate, containing bismuth subsalicylate, are approved for kids 12 and older. Pepto-Bismol and Kaopectate contain aspirin-like ingredients and should not be used in children with chicken pox or flu-like symptoms because of the risk of Reye’s syndrome, a rare but serious illness.
Pepto-Bismol should only be used by adolescents and adults age 12 and older.
A children’s version of Pepto-Bismol is available for children age 2 and older, or you might try a natural method to address their symptoms.
Regular Pepto-Bismol is a concern for children because its main ingredient is bismuth subsalicylate, a derivative of aspirin (acetylsalicylic acid or ASA).
Medications containing ASA are associated with Reye’s syndrome, a rapidly progressing brain disorder that isn’t fully understood. The condition typically develops in people recovering from a viral infection. Most of the cases seen in children involved the use of aspirin to treat common illnesses such as influenza and chickenpox
Explain some causes of gastroenteritis (how they cause gastroenteritis)under infectious and non infectious causes of gastroenteritis
What is the infections transmission in gastroenteritis?
What are the four categories of virus that cause most gastroenteritis
Which bacteria and parasites are most commonly implicated in gastroenteritis?
Which type of infectious gastroenteritis is more common
Which type of infectious gastroenteritis causes inflammatory diarrhea due to mucosal invasion cuz if there’s no mucosal invasion then the diarrhea will be watery
How is parasitic infectious cause of gastroenteritis acquires?
Cryptosporidium parvum causes watery diarrhea associated with what symptoms?
INFECTIOUS GASTROENTERITIS
• Viral gastroenteritis : They infect enterocytes in the villous epithelium of the small bowel. The result is transudation of fluid and electrolytes into the intestinal lumen; sometimes, malabsorption of carbohydrates worsens symptoms by causing osmotic diarrhea. Diarrhea is watery. Inflammatory diarrhea (dysentery), with fecal white blood cells (WBCs) and red blood cells (RBCs) or gross blood, is uncommon. Four categories of viruses cause most gastroenteritis: norovirus and rotavirus cause the majority of viral gastroenteritis, followed by astrovirus and enteric adenovirus. * Bacterial gastroenteritis: The bacteria most commonly implicated are Salmonella, Campylobacter, Shigella, Escherichia coli (especially serotype O157:H7), Clostridium difficile. Bacterial gastroenteritis is less common than viral. Bacteria cause gastroenteritis by several mechanisms like producing enterotoxins that adhere to intestinal mucosa without invading. These toxins impair intestinal absorption and cause secretion of electrolytes and water by stimulating adenylate cyclase, resulting in watery diarrhea. Also, Mucosal invasion occurs with other bacteria (eg, Shigella , Salmonella , Campylobacter , C. difficile , some Escherichia coli subtypes) that invade the mucosa of the small bowel or colon and cause microscopic ulceration, bleeding, exudation of protein-rich fluid, and secretion of electrolytes and water. The invasive process and its results can occur whether or not the organism produces an enterotoxin. The resulting diarrhea contains WBCs and RBCs and sometimes gross blood. * Parasitic gastroenteritis: The parasites most commonly implicated are Giardia lamblia and Cryptosporidium. Certain intestinal parasites, notably Giardia intestinalis (G. lamblia), adhere to or invade the intestinal mucosa, causing nausea, vomiting, diarrhea, and general malaise. It is usually acquired via person-to-person transmission (often in day care centers) or from contaminated water. Cryptosporidium parvum causes watery diarrhea sometimes accompanied by abdominal cramps, nausea, and vomiting. In healthy people, the illness is self-limited, lasting about 2 weeks. In immunocompromised patients, illness may be severe and prolonged, causing substantial electrolyte and fluid loss. Cryptosporidium is usually acquired through contaminated water.
NB: infection transmission is fecal-oral.
NON-INFECTIOUS GASTROENTERITIS
This may occur from food sensitivity, inflammation of yourgastrointestinal tract, medicines, stress, or other causes not related to infection.Your symptoms willusuallylast from 1 to 3 days, but can last longer.Antibiotics are not effective, but simple home treatment will be helpful.
Name six physical examination findings in gastroenteritis(in the skin ,eyes,vitals,head,mucous membranes,abdomen,) and six differentials of gastroenteritis
Physical examination findings of Gastroenteritis
-most useful findings will come from vital signs and assessing dehydration status
- Vital signs= hypotension or tachycardia or fever may be present
- Skin=reduced skin turgor, skin discoloration
- Head = sunken fontanelles( in babies)
- Eyes = sunken eye balls and darkened eye circles
- Mucous membranes= dry
- Abdomen= mild diffuse tenderness
DIFFERENTIAL DIAGNOSIS
People with the following disorders may present with similar symptoms as gastroenteritis
⁃ Irritable bowel syndrome ⁃ Ulcerative Colitis ⁃ Inflammatory bowel disease ⁃ Appendicitis ⁃ Intussusception: condition in which part of the intestine telescopes into itself. Intussusception is a medical emergency involving obstruction of the intestine. It can be fatal if not treated. It occurs most often in children. ⁃ Increased intracranial pressure (vomiting) ⁃ Cholecystitis
Name four bacteria that cause gastroenteritis ,four virus and parasites that cause it
Bacteria
-vibrio cholerae
-Escherichia coli
-salmonella
-shigella
-campylobacter jejuni
-etc
•Virus
-rotavirus
-norovirus
-astrovirus
-enteric adenovirus
-etc
•Parasites
-giardia lamblia
-entamoeba hystolytica
-cryptosporidium
-etc
•Chemicals
-lead poisoning
-etc
•Drugs
-antibiotics
-etc
Mainly caused by microbes
Classification of Gastroenteritis •BACTERIAL GASTROENTERITIS •VIRAL GASTROENTERITIS •PROTOZOAL GASTROENTERITIS/ AMEBIC DYSENTERY True or false
diarrhea.
•May be acute or chronic
-ACUTE= lasts fewer than 14 days
-duration depends on the cause
- some within 1- 3 days
•HIGHLY CONTAGIOUS
True or false
True
True
What is IBD and state and explain (where they occur and what characterizes the types)the types of inflammatory bowel disease
Inflammatory bowel disease (IBD) is a relapsing and remitting condition characterized by chronic inflammation at various sites in the GI tract, which results in diarrhea and abdominal pain.
There are two major types of IBD. They are:
CROHN’S DISEASE (CD)
Crohn’s disease is a chronic transmural inflammatory disease that usually affects the distal ileum and colon but may occur in any part of the GI tract.
Symptoms include diarrhea and abdominal pain. Abscesses, internal and external fistulas, and bowel obstruction may arise.
Ulcerative colitis (UC) is a chronic inflammatory and ulcerative disease arising in the colonic mucosa, characterized most often by bloody diarrhea. UC is a mucosal disease that usually involves the rectum and extends proximally to involve all or part of the colon. Long-term risk of colon cancer is high.
In epidemiology of IBD,Appendectomy is protective against UC but is associated with an increased risk of CD
True or false?
Smoking is asssociated with a twofold increase risk of CD while the risk of UC in smokers is 40% that of non-smokers
True or false
NSAIDS may exacerbate IBD especially in CD true or false
Familial tendency is much higher in Crohn’s disease than in UC
Both sexes are equally affected
Most present aged 15–30yrs
The incidence is increasing among blacks and Latin Americans living in North America.
True or false
All true
The main causes of IBD are grouped into three. State them and causes under the three
ENVIRONMENTAL •Diet •Smoking •Antibiotics •Latitude •Psychological stress
GENETIC AND IMMUNOLOGAL •Early onset IBD •Turner’s syndrome •Glycogen storage disease •Immuno-dysregulation •Impaired epithelial barrier
MICROBIOLOGICAL •Salmonella spp. •Shigella spp. •Campylobacter spp. •Clostridium difficile
What is the structure of the bowel
The bowels are the intestines
The large intestine comes before the smaller one
Appendix is on the right side and from there you move up to the large intestine
You can refer to the slide on IBD
What is the pathophysiology of IBD and the pathophysiology of the types of IBD
Genetic factors mediate risk for IBD
In an IBD patient the normal flora is likely perceived inappropriately as if it were a pathogen due to defective immune regulation
Amplification of immune responses and release of inflammatory cytokines such as IL-1 and IL-2,TNF
Mucous breakdown due to fibrinogenesis,collagen production,activation of tissue metalloproteinase and the production of other inflammatory mediators
Inflammation
In ulcerative colitis : there is inflammation of the colonic mucosa that usually involves the rectum and extends proximallynto involve all or part of the colon
Mucosa becomes erythematous- edema occurs-hemorrhage-ulcers
Pseudopolyps grow ,cryptitis(, Cryptitis is a term used in histopathology to describe inflammation of the intestinal crypts. The crypts are glands found in the lining of the intestines. They are sometimes called the crypts of Lieberkühn. Crypts of Lieberkuhn are pits between villi as pointed out by the green arrow in the figure below. The crypts of Lieberkuhn (often referred to simply as crypts) are similar to the gastric pits in the stomach. )toxic colitis or mégacôlon may occur- the bowel wall may become thin causing perforation
Crohns: transmural spread of inflammation which leads to lymphedema
Extensive inflammation may result in hypertrophy of the muscularis mucosae,fibrosis, and stricture formation (thickening bowel wall),which can lead to bowel obstruction
Abscesses occur
Fistulas often penetrate into the adjoining structures including other loops of bowel ,the bladder,psoas muscle,skin or anterior abdomen
Cobblestones-lumen looks like a paved road
What are the clinical manifestations of UC and CD
The major symptoms of UC are diarrhea, rectal bleeding, tenesmus (Tenesmus is the feeling that you need to pass stools, even though your bowels are already empty. ), passage of mucus, and crampy abdominal pain.
•The severity of symptoms correlates with the extent of disease.
•Some cases develop after an infection (e.g., amebiasis, bacillary dysentery)
•For rectosigmoid (The rectosigmoid is that portion of the large intestine in which the narrow sigmoid colon undergoes a gradual enlargement before joining the rectum. )ulceration,the stool may be normal or hard and dry, but rectal discharges of mucus loaded with RBCs and WBCs.
•If ulceration extends proximally, stools become looser and the patient may have > 10 bowel movements per day, often with severe cramps and distressing rectal tenesmus, without respite at night. The stools may be watery or contain mucus and frequently consist almost entirely of blood and pus.
•Diarrhea is often nocturnal and/or postprandial.(occurring or done after a meal.)
•Extraintestinal manifestations include peripheral arthritis, episcleritis(Episcleritis is an inflammatory condition affecting the episcleral tissue between the conjunctiva (the clear mucous membrane lining the inner eyelids and sclera) and the sclera (the white part of the eye) that occurs in the absence of an infection ),aphthous stomatitis, erythema nodosum, and pyoderma gangrenosum (a rare condition that causes large, painful sores (ulcers) to develop on your skin, most often on your legs. )
CD:
•The most common initial manifestation is chronic diarrhea with abdominal pain, fever, anorexia, and weight loss.
•The abdomen is tender, and a mass or fullness may be palpable.
•Gross rectal bleeding is unusual except in isolated colonic disease.
•Patients with severe abscess are likely to have marked tenderness, guarding, rebound, and a general toxic appearance.
•Stenotic (narrowing or constriction of the diameter of a bodily passage or orifice )segments may cause bowel obstruction, with colicky pain(sharp, localized gastrointestinal or urinary pain that can arise abruptly, and tends to come and go in spasmlike waves ),distention, obstipation and vomiting.
•Abscess formation (abdominal, pelvic or ischiorectal(These abscesses form when suppuration transverses the external anal sphincter into the ischiorectal space. The ischiorectal fossa is the space that exists between the internal surface of the perineal skin and the plane of the plate of the levator ani muscle. It is perceived as descending during inhalation and rising during exhalation.)
•Fistulae (An abnormal connection between organs. )e.g. colovesical (bladder), colovaginal, perianal(the skin and the anus),enterocutaneous(an abnormal connection that develops between the intestinal tract or stomach and the skin. As a result, contents of the stomach or intestines leak through to the skin. Most ECFs occur after bowel surgery.),. An entero-vesical fistula may produce air bubbles in the urine (pneumaturia)
•Perforation.
•Beyond the gut: clubbing, skin, joint & eye problems
How is IBD diagnosed and state investigations used
Diagnosis of IBD is based on clinical, laboratory, endoscopic and radiographic features.
Laboratory tests include:
◂Full Blood Count (FBC)
◂Erythrocyte Sedimentation Rate (ESR) and C-reactive proteins - ↑(C-reactive protein is an annular pentameric protein found in blood plasma, whose circulating concentrations rise in response to inflammation. It is an acute-phase protein of hepatic origin that increases following interleukin-6 secretion by macrophages and T cells. An ESR test measures how quickly red blood cells settle to the bottle of a test tube. Inflammation or infection can lead to extra proteins in the blood, which can make the red blood cells settle faster. When this happens, the ESR is higher.)
◂Serum ferritin - ↑ (indicates absorption problems) As ferritin is a positive acute phase reactant, a possible early inflammation in cases later developing IBD would result in increased ferritin concentrations. Despite this, low ferritin was associated with increased risk for IBD
◂Retro-screening
◂Hep B, C screening
◂Stool examination and cultures to rule out infectious cause of the diarrhea e.g., Clostridium difficile
Name six differentials each for UC and CD
Remember these ddx is for both of them: NSAIDS enteropathy IBS Intestinal tuberculosis Colon cancer
UC:
Amebic colitis Schistosomiasis CD Colon cancer Irritable bowel syndrome (IBS) Intestinal tuberculosis NSAIDS enteropathy Infectious colitis Colitis complicated by HIV Radiation colitis
CD:
Celiac disease Behcet’s disease UC Colon cancer Irritable bowel syndrome (IBS) Intestinal tuberculosis NSAIDS enteropathy Eosinophilic enteritis Microscopic colitis Diverticulitis
What are the four aims in treating IBD
How is IBD treated and managed
(Name nine classes of drugs used and example of each)
The aim of treatment is to:
◂Improve and maintain patient’s wellbeing
◂Eliminate symptoms and reduce intestinal inflammation
◂Prevent hospitalization, complications and surgery
◂Maintain good nutritional status
These aims depend on the severity and location of the disease; side effects of medications; comorbidities among others.
Amino salicylates – most effective in mild to moderate UC e.g. mesalazine, sulfasalazine etc. Aminosalicylates work by limiting the inflammation in the lining of the gastrointestinal tract.
◂Immune modifiers e.g. mercaptopurine, cyclosporine, methotrexate etc.
◂Antibiotics – most effective in CD e.g. metronidazole, ciprofloxacin
◂Corticosteroids e.g. prednisone, budesonide, hydrocortisone etc.
◂Biologics e.g. infliximab, adalimumab (anti-TNF agents)
◂Antidiarrheals e.g. loperamide etc.
◂Analgesics e.g. acetaminophen, codeine etc
◂Vitamin B12, vitamin D, calcium, multivitamin supplementation
◂Parenteral iron, for chronic iron deficiency anemia
Mucus and Gross blood in stool is seen in? And occasionally in?
Systemic symptoms and Pain are seen occasionally in? And frequently in?
Abdominal mass is seen in which type of IBD and seen rarely in which type ?
Significant perineal disease and fistulas are not seen in ? But the first one is frequently seen in which and the fistulas are seen in which?
Seen in UC and occasionally in CD
Occasionally in UC and frequently in CD
Seen in CD and rarely in UC
Not seen in UC but frequent in CD and fistulas are seen in CD
For
More info on clinical interpretations from lab investigations check the slides given
Case study: Ted Lasso, a 24-year-old man is admitted to the hospital with a 1-year history of severe abdominal pain and chronic diarrhea, which has been bloody for the past 2 months. He reports a 20-lb weight loss, frequent fevers frequent fevers, and night sweats. He denies vomiting. His abdominal pain is crampy and primarily involves his right lower quadrant. He is otherwise healthy. Examination is concerning for an acute abdomen with rebound and guarding present. (Rebound tenderness, also called Blumberg’s sign . To check for rebound tenderness, a doctor applies pressure to an area of your abdomen using their hands. They quickly remove their hands and ask if you feel any pain when the skin and tissue that was pushed down moves back into place.
If you do feel pain or discomfort, you have rebound tenderness. And it helps to rule in or out peritonitis. Guarding vs. rigidity test. Guarding involves voluntarily flexing your abdominal muscles, making your abdomen feel firm to the tough. Rigidity is abdominal firmness that’s not related to flexing muscles. Your doctor can tell the difference by gently touching your abdomen and seeing if firmness decreases when you relax. ) CT shows free air in the peritoneum. He is urgently taken to the operating room for surgical exploration, where he is found to have multiple strictures and a perforation of his bowel in the terminal ileum. The rectum was spared and a fissure from the duodenum to the jejunum is found. The perforated area is resected and adhesions lysed.
- List five differential diagnosis in this scenario.
- What is the most likely diagnosis for this patient?
- What are some of the possible pathologies for the disease above?
- Outline the investigations needed to confirm the diagnosis above
- How will you manage this patient based on the diagnosis given.
For the diagnosis of the UC or CD ,check the slides on IBD there’s a table there
1.Crohns disease
Ulcerative Colitis (UC)
Irritable Bowel Syndrome (IBS)(IBS is a disorder of the gastrointestinal (GI) tract. IBD is inflammation or destruction of the bowel wall, which can lead to sores and narrowing of the intestines. )
Celiac Disease.
NSAIDS enteropathy
Behçet’s disease
Diverticulitis
Colon Cancer.
Vasculitis.
Intestinal tuberculosis
2.Crohns disease
3. it is transmural, involving all layers of the bowel, not just the mucosa and the submucosa, which is characteristic of ulcerative colitis. Furthermore, Crohn disease is discontinuous, with skip areas interspersed between two or more involved areas.
4.colonoscopy or sigmoidoscopy
FBC
ESR and C reactive proteins(if increased confirms it)
Serum ferritin if increased indicates absorption problems
Stool c/s to rule out infectious cause of the diarrhea
Retro screening
5. Corticosteroids e.g. prednisone, budesonide, hydrocortisone etc.
◂Biologics e.g. infliximab, adalimumab (anti-TNF agents)
◂Antidiarrheals e.g. loperamide etc.
◂Analgesics e.g. acetaminophen, codeine etc
◂Vitamin B12, vitamin D, calcium, multivitamin supplementation
◂Parenteral iron, for chronic iron deficiency anemia
Antibiotics – most effective in CD e.g. metronidazole, ciprofloxacin
What is proctitis?
UC is a mucosal disease that usually involves the rectum and extends proximally to involve all or part of the colon.
Proctitis can be viewed as an ulcerative colitis that is isolated at the rectum and has not extended to the proximal parts of the large bowels.
True or false
DEFINITION OF PROCTITIS
Proctitis is inflammation of the lining of the rectum. The rectum is a muscular tube that is connect to the end of your colon. Stool passes through the rectum on its way out of the body.
True
According to the structure of the rectum,it is the most distal segment of the large intestine and is the temporary store of faeces true or false
The rectum is continuous proximally with the? And terminâtes into the?
The rectum is approximately how many cm or inches long?
The rectum’s anatomical relations are different in men and women.
True or false
Where is the rectum located and it is the most posterior of the what viscera?
What structures are anterior to the rectum in the male and in the female and what a structures are posterior to the rectum in the male and female?
What is the function of the rectum
True
It is continuous proximally with the sigmoid colon, and terminates into the anal canal. The rectum is approximately 15 cm (6 inches) long.
The rectum is located within the pelvic cavity and is the most posterior of the pelvic viscera.
True
Male: anterior: rectovesical pouch,sigmoid colon,ileum,bladder,prostate,seminal vesicles
Female:anterior:rectouterine pouch,sigmoid colon,ileum,vagina,cervix
Both:posterior:
Saccrum and coccyx,piriformis,coccygeus,levator ani,sacral plexus
Function
The rectum’s job is to receive stool from the colon, let you know that there is stool to be evacuated and to hold the stool until evacuation happens.
Proctitis causes are classified into infectious and other causes
State five infectious causes and four other causes
Proctitis can be secondary to other diseases name four such diseases
Proctitis may happen secondary to ulcerative colitis (UC), Chronic Radioation proctitis(Radiation proctitis is inflammation of the rectum that occurs as a result of damage to the rectum sustained from pelvic radiation given to treat a cancer such as prostate or cervical cancer. ) , Proctopathy (CRP)-Radiation proctitis or radiation proctopathy is condition characterized by damage to the rectum after exposure to x-rays or other ionizing radiation as a part of radiation therapy. or Diversion Proctitis (DP)-Diversion colitis or diversion proctitis is a nonspecific inflammatory disorder that occurs in segments of the colon and rectum that are diverted from the fecal stream by surgery (eg, creation of a loop colostomy/ileostomy or an end colostomy/ileostomy with closure of the distal colon segment
- Infectious causes include
Clostridium difficile
Enteric infections: (Campylobacter, Shigella, Escherichia coli, Salmonella and amebiasis)
STI’s: (Gonorrhea, Chlamydia, Syphilis, Human Simplex Virus-“HSV”, Lymphogranuloma venereum-“LGV”, chancroid, Cytomegalovirus-“CMV”, Human Papillomavirus-“HPV”)
- Other causes include Ischemia Vasculitis Toxins as hydrogen peroxide enemas Medication side effect like antibiotics.
Gonococcal and chlamydia Proctitis are most frequently found in which groups of people? Incidence of these kind of proctitis is more in which gender than the other?
an observational study, investigators analyzed data from 26 patients with acute proctitis symptoms, lymphogranuloma venereum (LGV) serovar L2 was confirmed in all patients, all of whome were men who have sex with men (MSM) and 24 of who were HIV-positive.
Note that LGV is caused by the Chlamydia species.
True or false
Which group of people are at a higher risk of developing proctitis?
in women and homosexual men who practice anal-receptive intercourse,predominantly in young adults
Moreover, patients with inflammatory bowel diseases are at higher risk of developing proctitis
Incidence is more in males than females. Probably due to the rise of men sleeping with men.
True
Explain the pathology of proctitis
PATHOLOGY BEHIND PROCTITIS
The main pathology behind proctitis is simply inflammation. All the causes of inflammation can be applied here.
Inflammation is the response of vascularized living tissue to injury. It may be evoked by microbial infections, physical agents (notably radiation and trauma), chemicals, necrotic tissue, or immune reactions (for example in Inflammatory bowel diseases).
Proctitis is associated with many conditions and for that reason, the underlying cause can used to derive the type of proctitis.
For example, proctitis as a result of antibiotic may be said as antibiotic-induced proctitis, same for gonorrheal proctitis, herpetic proctitis, radiation proctitis, ulcerative proctitis, diversion proctitis and so on.
Explain the types of proctitis
Radiation proctitis occurs secondary to what changes due to radiation therapy?
Name three STIs that cause proctitis
Ulcerative proctitis
Ulcerative proctitis is simply ulcerative colitis that is isolated at the rectum. I hope we are well informed about what ulcerative colitis is. If not, kindly revisit yesterday’s presentation on Inflammatory Bowel disease.
Radiation proctitis
Occurs secondary to ischemic and fibrotic changes due to radiation therapy. Radiation injury occurs with doses 8 Gy (Gray (Gy) isthe unit used to measure the total amount of radiation that the patient is exposed to. )or higher causing damage to intestinal cell DNA with helical breaks and inability to replicated and undergo normal cellular repair.
Diversion proctitis:
Proximal fecal or Bowel diversion surgery allows stool to safely leave the body when—because of disease or injury—the large intestine is removed or needs time to heal.
Proximal fecal diversion causes increased nitrate-reducing bacteria and decreased obligate anaerobes resulting in short-chain fatty acids deficiency.
Diversion colitis may also be due to a reduction in nutrients delivered to the cells that live in the defunctioned colon after fecal matter has stopped passing through.
Proctitis due to STI’s
The aforementioned sexually transmitted microorganisms can cause proctitis.
STI’s (Gonorrhea, Chlamydia, Syphilis, Herpes Simplex Virus - HSV, Lymphogranuloma venereum-LGV, chancroid, CMV-Cytomegalovirus, HPV-Human Papillomavirus)
State the signs and symptoms of proctitis
Some signs and symptoms are often related to certain conditions.
For example,
Ulcerative proctitis secondary to ulcerative colitis presents with courses of remissions and relapses.
I.e. (It can diminish at one point in time and resurface just like ulcerative colitis)
True or false
What is tenesmus
SIGNS AND SYMPTOMS OF PROCTITIS
Inflammation of the rectal lining results in these general symptoms seen in proctitis.
- Feeling of rectal fullness
- Anal and rectal pain
- Diarrhea, usually frequent, small amounts
- Frequent or continuous urge to have a bowel movement (tenesmus)
- Pain in the lower left abdomen
- Passing mucus through the rectum
- Rectal bleeding
True
KEY TERM:
Rectal Tenesmus – a clinical symptom, where there is a feeling of constaltly needing to pass stools, despite an empty colon.
When the word “tenesmus” is used by itself, it usually means rectal tenesmus.
That said, there is another type relating to the urinary bladder called “vesical tenesmus”
Name some other likely symptoms of proctitis
Name some physical examination findings in proctitis
Other likely symptoms
Proctitis usually runs a mild, intermittent course over many years.
Occasionally there is neurological involvement with urinary bladder dysfunction, weakness and burning of the lower limbs (parasthesias) and pain in the thighs.
Men may have difficulty maintaining penile erections
This is because the rectal area is closely related to the above structures… as we can see from our structure highlight.
PHYSICAL EXAMINATION FINDINGS
When perform an examination such as proctosigmoidoscopy or proctoscopy it will reveal the following about the rectal lining:
- Pallor or erythema
- Loss of usual vascularity of mucosa
- Prominent telangiectasis
- Friability
- Bleeding
- Ulcerations
- Edema
- Scattered areas of scarring
- Vesicles/pustules
- Strictures
Some of these examination findings are key to certain types of proctitis. For instance, individuals with ulcerative proctitis show ulcers in the rectum.
Ulcerations are usually accompanied by rectal bleeding, straining of rectal muscles (tenesmus) and an anal discharge of bloody mucus.
How is proctitis diagnosed
(State the what you’re expected to see in someone w proctitis after doing the proctosigmoidoscopy)
We are looking at it from the perspective that, proctitis affects the rectum and not the remainder of the colon.
It does not mean that proctitis can not present with other inflammatory disease of the gut such as Inflammatory Bowel disease.
True or false?
Name some lab investigations used to diagnose it
INVESTIGATIONS
Diagnosis of proctitis is made when proctosigmoidoscopy (internal examination of the lower large bowel or colon reveals inflammation of the mucus lining of the rectum with a clearly demarcated upper border above which the lining is normal. The remainder of the colon and small intestine is found to be normal.
This finding is supported with some lab investigations.
LABORATORY INVESTIGATIONS
FBC: performed to evaluate leukocytosis, if an infections etiology or severity of anemia due to blood loss
C-reactive protein level: It is elevated in patients with extensive pancolitis (Pancolitis is an inflammation of the entire colon. The most common cause is ulcerative colitis (UC). Pancolitis can also be caused by infections like C. difficile, or can be associated with inflammatory disorders like rheumatoid arthritis (RA) ) but is frequently normal in patients with only distal disease (I.e. proctitis)
Cultures of rectal swab help diagnose gonorrhea or chlamydia
Cultures of vesicular fluid (Vesicles are small fluid-filled sacs or blisters that can appear on your skin. The fluid inside these sacs may be clear, white, yellow, or mixed with blood. Vesicles are fluid-filled lesions less than 5 mm (1/2 cm). If the fluid-filled lesion is greater than 0.5 mm, it’s called a bulla. ) or cytologic scrapings aid in the diagnosis of HSV
Serum Veneral Disease Research Laboratory (VDRL) test and dark field examination of scraping from the base of the chancre reveals spirochetes and confirms the diagnosis of syphilis
Stool specimen for C. difficile toxin
What is the aim in the treatment or management of proctitis
Treatment/Management
Aim
The goal of proctitis treatment are to reduce inflammation, control pain, and treat the underlying cause.
Specific treatments depend on the cause of proctitis.
Managing underlying conditions helps to relieve symptoms.
Name the three ways proctitis treated non pharmacologically and four ways it’s pharamacologically treatment and for the pharma treatment,state the class of drugs used,examples under each class,side effects,route,contraindications)
NON-PHARMACOLOGICAL
Aim for providing comfort during the examination.
Lifestyle adjustments to relieve proctitis:
- Take in diet that may reduce proctitis pain. Avoid spicy, acidic, or fatty foods during bouts of diarrhea.
- Rehydrate: Drink plenty of fluids, but avoid drinking caffeinated sodas, coffees, and teas. Caffeine, however, can irritate the digestive system. Drinking prevents dehydration from frequent loose stools and eases the passage of stool.
PHARMACOLOGICAL
Drug therapy consists of antibiotics, antivirals, corticosteroids and GI agents.
ANTIBIOTICS
These agents are active against most microbes that cause proctitis. Microbes such as anaerobic bacteria C. difficle, N.gonorrhoeae, mycoplasma, chlamydia, and rickettsia species.
Examples include: Metronidazole, Vancomycin, Ciprofloxacin, Ceftriaxone, Doxycycline, Penicilin G, Tetracycline
RECTAL ANTI-INFLAMMATORY AGENTS
These agents decrease inflammation associated with proctitis.
Examples include: sulfasalazine and mesalamine
ANTIVIRAL
These agents are used for the treatment of viral or Herpes-related proctitis. For example, acyclovir
CORTICOSTEROIDS
These agents have anti-inflammatory properties.
Dexamethasone, prednisolone, prednisone
Name five complications of proctitis
COMPLICATIONS
Complications of proctitis may include the following
Chronic ulcerative colitis
Fistula formation
Abscess
Treatment failure
Perforation
Anemia
Rectal prolapse
CASE PRESENTATION
A 20-year-old man presented with anorectal pain and blood rectal discharge for 2 months. He had neither a notable medical nor family history. He had not travelled anywhere recently. He was not taking medication including antibiotics. HE did not complain of other gastrointestinal symptoms, such as diarrhea and vomiting. He did not have systemic symptoms, such as general weekness, fever, or weight loss. He did not have a history of radiation therapy. On physical examination, his abdomen was soft, and there were no palpable lymph nodes in the inguinal area. Neither anal fissure nor hemorrhoids were observed on the rectal examination.
What other question will you ask this patient concerning the history?
2.
At this point, what are some of the differential diagnosis?
3. 3. At this point, what laboratory investigations can you request for?
4.Treatment recommendations
5.what advice will you give to the partner
- I’ll enquire about his sexual history, especially if he had experience of engaging homosexual practice.
2.rectal prolapse
Anusitis
POSSIBLE ANSWERS
All differentials diagnosis relating to proctitis caused by sexually transmitted microbes. (Gonorrhea, Chlamydia, Syphilis, HSV, Lymphogranuloma venereum, chancroid, CMV, HPV).
Therefore, we could have gonorrheal proctitic, syphilitic proctitis
3. POSSIBLE ANSWERS
Just like mentioned earlier, we could investigate the following.
FBC: performed to evaluate leukocytosis, if an infections etiology or severity of anemia due to blood loss
Cultures of rectal swab help diagnose gonorrhea or chlamydia
Cultures of vesicular fluid or cytologic scrapings aid in the diagnosis of HSV
Serum Veneral Disease Research Laboratory (VDRL) test and dark field examination of scraping from the base of the chancre reveals spirochetes and confirms the diagnosis of syphilis
Stool specimen (stool R/E) for C. difficile toxin
Besides confirming the presence of an infection… he reported with blood rectal discharge so having a good look at his HB is important.
- POSSIBLE ANSWERS
Antibiotics, antiviral, anti-inflammatory agents to treat bacterial infections, viral infections and inflammations respectively.
Based on laboratory investigations confirmation of the underlying infection.
- It’s better for the partner too should be screened for any STI and treated if any.
They should use protection
Seek counseling on homosexuality
Define pruritis ani
Anal itch is a symptom, not an illness, and it can have many different causes. In many cases, a person with anal itch does not have a disease of the rectum rather a symptom of a different disease.
pruritus ani is a dermatological condition characterized by itching in the anal area. The itching may become worse at night or after a bowel movement. Scratching the area results in further irritation and makes the itching worse instead of relieving it. Scratching with the fingernails may result in skin damage or an infection. If the itch-scratch cycle persists, it can lead to extreme discomfort, soreness, and burning.
True or false
State and define the types of it
Definition
📍 Pruritis Ani* is also called *anal itch , is an irritating, itching sensation around the anus ( the opening through which stool passes out of the body).
What are the types of pruritus ani?
There are two main types of pruritus ani, namely: primary* and *secondary.
📍 Primary ( idiopathic (relating to or denoting any disease or condition which arises spontaneously or for which the cause is unknown.)
pruritus ani :This condition has no identifiable underlying cause. This is the most common type of pruritus ani.
📍 Secondary pruritus* *ani :This condition may be due to many different underlying causes. They may include infections, contact dermatitis or other dermatological conditions, systemic diseases, and other factors.
Pruritis ani is four times more common in which gender than in which gender?
What type of ani is common than the other?
What group of people does pruritis ani affect more?
Which age group is it most common in?
It is estimated that 1-5% of the population is affected. Pruritus ani is about 4 times more likely to occur in men than in women. Primary or idiopathic pruritus ani accounts for the majority (about 50-90%) of cases.Pruritis ani most commonly affects adults, affecting from 1% to 5% of people in the general population. The condition is most common in people age 40s to 60s. There are many causes of pruritis ani, and an accurate diagnosis is important in order to treat the specific cause.
What is the hypothesized pathophysiology of ani
Pathophysiology of* *PRURITIS ANI
📍The pathophysiology of pruritus ani has not been elucidated yet. It has been hypothesized that when sensory nerves in the perianal area are stimulated, skin irritation and subsequent pruritis is induced; consequently, the skin is excessively scratched, which causes skin injury.
Explain the cases of pruritis ani
Etiology
What causes pruritus ani (anal itching)?
📍 Pruritis ani is usually not caused by poor hygiene. Rather, the overuse of soaps and other topical products to clean the anal region or vigorous scrubbing with a washcloth or rough toilet paper can cause irritation.
📍 A hypersensitivity reaction may occur if perfumed powders, lotions, creams, ointments, or other products are applied in the anal region.
📍 Excess perspiration or moisture may become trapped in the anal area if constricting or tight-fitting underwear is worn. Some foods and beverages, such as carbonated drinks, caffeinated beverages (coffee, tea, colas) and spicy or acidic foods (tomatoes, citrus fruits) have been linked to the condition. Having frequent bowel movements (diarrhea) or infrequent ones (constipation) may also play a role.
Other causes of pruritus ani include:
📍 Infections : Some types of bacteria, fungi (yeast), or parasites can cause itching. Staphylococcus aureus or Streptococcus pyogenes (types of bacteria), Candida albicans (a yeast), pinworms (mainly inchildren), and Sarcoptes scabiei (scabies mites) are some organisms that result in itching and irritation.
📍 Dermatological* *conditions: Psoriasis, contact dermatitis (inflammation due to allergens or other irritants), or atopic dermatitis (a chronic condition found in patients with allergies) may cause a rash in the perianal region.
📍 Inflammatory bowel disease (Crohn’s disease)
📍 Psychological factors such as stress or anxiety.
📍 Systemic diseases: These include diabetes mellitus, leukemia, lymphoma, thyroid disease, renal disease, and liver disorders (obstructive jaundice).
📍 Colorectal and anal* *disorders: Rectal prolapse, internal or external hemorrhoids, anal fissures (ulcers), or fistulas (abnormal tube-like passages) are associated with pruritus ani. Residual amounts of feces may be difficult to remove with large external hemorrhoids. Internal hemorrhoids may cause bleeding, fecal soiling, or drainage.
📍 Systemic or topical* *medications: Use of drugs such as quinine, colchicine, and mineral oil has been linked to pruritus ani.
📍 Fecal or urinary* *incontinence : Children and the elderly are more likely to experience incontinence of the bowel or bladder.
What’s re the predisposing factors of ani
Other causes( Predisposing factors) of pruritus ani include;
📍Chronic anorectal disease,
📍HIV-related infections,
📍Diabetes-remember diabetes can cause skin infections and illnesses and these can cause itching
📍Cancer
📍Illnesses that produce hyperbilirubinemia.-It is thought that bile salts that deposit into the skin are responsible for the pruritus (itching)
State the signs and symptoms of pruritis ani
Symptoms
Anal itching may be associated with;
📍Redness
📍Burning
📍Soreness.
The itching and irritation may be temporary or more persistent, depending on the cause.
Signs;
Anal itching is severe or persistent if
📍You have anal bleeding or stool leakage
How is ani diagnosed?
DIAGNOSIS AND TESTS
How is pruritus ani (anal itching) diagnosed?
📍The doctor will obtain a full medical history and perform a physical examination to identify possible underlying causes, such as dermatological conditions and other illnesses. He or she will visually inspect the area to look for changes in skin color or texture, rashes, or lesions .
📍The doctor will ask about any medications that you take and the type and frequency of bowel movements.
📍The doctor may obtain skin specimens and perform tests to screen for bacterial or other infections.
📍Parents of children who may have pinworms can place a small piece of surgical tape, or scotch tape, near the child’s anus before bedtime. The worms are more likely to emerge at night . In the morning, when the child awakens, the tape can be removed to see if the worms or their eggs are present. This is called the scotch* *tape test.
What are nine physical findings in ani?
Physical Examination findings
📍Physical examination focuses on the anal region, particularly looking for perianal skin changes, signs of fecal staining or soilage (suggesting inadequate hygiene), and hemorrhoids.
📍External inspection should also note the integrity of the perianal skin, whether it appears dull or thickened (suggesting chronicity), and the presence of any cutaneous lesions, fistulas, excoriations(the act of abrading or wearing off the skin chafing and excoriation of the skin. 2 : a raw irritated lesion (as of the skin or a mucosal surface) )or signs of local infection. Sphincter tone is assessed by having the patient contract the sphincter during digital rectal examination. The patient should then be asked to bear down as if for a bowel movement, which may show prolapsing internal hemorrhoids. Anoscopy may be necessary to further evaluate the anorectum for hemorrhoids.
Name four lab investigations performed in the diagnosis of ani
The following screening laboratory tests are recommended:
CBC count with differential: People with iron deficiency of any kind may develop pruritus, which is the medical term for itchy skin
This test assists in uncovering polycythemia vera, in which the hemoglobin level, hematocrit value, WBC count (including absolute neutrophil count; see the Absolute Neutrophil Count calculator), and platelet count are elevated. Abnormalities are also seen in persons with hematologic malignancies. Patients with iron deficiency may have microcytosis and low hemoglobin levels. However, those with pruritus and iron deficiency may not be anemic; tests of and serum iron, ferritin, and total iron-binding capacity may be ordered to confirm or exclude the diagnosis.
Serum creatinine and blood urea nitrogen values: Persons with chronic renal failure have elevated levels. When the kidneys fail, the build-up of waste in your blood can cause severe itching.
Serum alkaline phosphatase and bilirubin, direct and indirect: Elevated levels may suggest cholestasis. If elevated, antimitochondrial antibody and serum anti–hepatitis C tests may be ordered to confirm primary biliary cirrhosis and hepatitis C, respectively, if these are suspected. Other tests may be needed to confirm other causes of cholestasis. A positive antimitochondrial antibody finding has 98% specificity for primary biliary cirrhosis.
Bile Salts- Those with liver disease may have higher levels of bile salt building up under the skin, which may cause itching. Normally, bilirubin is made in the liver and removed from the body in digestive fluid called bile, but people with liver or gallbladder problems may end up with too much bilirubin that accumulates in their blood and skin. One side effect of jaundice is intense and uncontrollable itching. Cholestasis is Any condition in which the flow of bile from the liver stops or slows.
Thyrotropin and thyroxine: The results assist in ruling out hypothyroidism and hyperthyroidism.
Fasting glucose value, if prompted by signs or symptoms
Stool for occult blood in patients aged 40 years or older: A positive result suggests possible malignancy in the GI tract. Although persistent rectal itching (pruritus ani) can be a sign of rectal cancer, it is not the most common cause.
HIV antibody test, if risk factors are present
Skin biopsy for routine pathology and immunofluorescence to exclude subacute occult autoimmune conditions such as pemphigoid and dermatitis herpetiformis
What is the management and treatment of ani
MANAGEMENT /TREATMENT.
How is pruritus ani (anal itching) treated?* *(Pharmacological)
📍 Usually, treatment focuses on establishing and maintaining a routine for proper anal hygiene. If a secondary or underlying cause is found, the treatment will depend on the specific condition.
📍 Topical medications: Topical steroids, such as creams or ointments containing 1% hydrocortisone, may help to relieve itching and irritation. The cream or ointment may be applied two or three times to the affected area each day.
📍 Topical capsaicin has been studied as an alternative to steroids for patients with chronic pruritus ani.
📍 Oral medications: Antibiotic or antifungal medications may be prescribed if an infection is present.
📍 Methylene blue injection (anal tattooing): This technique may be used to treat more advanced cases that do not respond to topical medications. Methylene blue (a dye) is injected under the skin in the perianal region thought that the methylene blue relieves pain and itching by deadening the nerve ending dye is injected.
Again..depending depending on the extent of itching one can add an anti-histamine agent to it…like Cetirizine to bring down the itching
What are some tips for self-care?* *(Non- pharmacological )
📍 Resist the urge to scratch. The itching might seem worse at night, so people might unconsciously scratch the anal area with their fingernails during sleep.
📍 Wear clean, soft cotton gloves at bedtime to prevent irritation and infection.
📍 Keep the perianal area clean and dry. Use clear water instead of soap or moistened toilet paper to clean the perianal region after a bowel movement.
📍 A shower head be used to gently clean the perianal area. Use a hair dryer on a low setting to dry the area. If using toilet paper or a towel, gently pat or blot the area until it is dry.
📍 Apply a small amount of cornstarch or piece of cotton to the area to keep it dry during the day. A
small cotton gauze pad can be used instead.
📍 Do not use soap when cleansing the anal area or scrub vigorously with toilet paper or a washcloth.
📍 Avoid using perfumed creams, lotions, bubble baths, powders, or other products that may cause irritation to the area.
📍 Eat foods high in fiber. A healthy diet can help prevent diarrhea or constipation and ensure regular bowel movements.
📍 Avoid any foods that might go promote itching, such spicy or acidic foods or caffeinated beverages.
📍 Avoid wearing tig constricting underwear. Cotton underwear can helpV to absorb moisture better than synthetic fabrics.
📍 Make sure underwear Can fits properly and change it frequently. Wash clothing with fragrance-free detergents.
📍 Use topical medications as directed. Apply the cream or ointment sparingly and discontinue use if the itching does not subside or gets worse.
Common topical agent used is Anusol gel
You can also encourage sit baths…where you put warm (not hot) water in bucket and add salt to it..then patient sits on it twice daily for about a week.
patient can do savlon baths as well…adding savlon to the water for bathing
savlon alone to the water…patient adds soap to it for bathing
State some complications of ani
Complications
📍Rectal cancer(11 percent),
📍Anal cancer (6 percent),
📍Adenomatous polyps (4 percent),
📍Colon cancer (2 percent).
📍Hemorrhoids (20 percent) and anal fissures (12 percent) were the most common pruritus-related anorectal diseases.
State five differentials for ani
What four things can cause itching and dryness in the anal area?
Differential diagnosis
📍Dermatological conditions:
📍Psoriasis, : skin disease marked by red, itchy, scaly patches.
📍contact dermatitis (inflammation due to allergens or other irritants), or atopic dermatitis (a chronic condition found in patients with allergies) may cause a rash in the perianal region.
📍Inflammatory bowel disease (Crohn’s disease)
📍Psychological factors such as stress or anxiety.
Conclusion
What can cause dryness and irritation in the anal area?
The anal area may become dry and irritated due to the use of harsh soaps, sanitary wipes, or rough toilet paper to clean the area after a bowel movement. A hypersensitivity reaction may occur if perfumed powders, lotions, creams, ointments, or other products are applied in the anal region. Excess perspiration or small amounts of fecal matter can cause irritation and itching.
