Dental Problems:

• Deep, chronic inflammation of the gingiva

• Clinical Manifestations

- Bleeding, infection, gum recession and loosening of teeth

• Contributing factors

- Untreated gingivitis

- Inadequate dental hygiene

- Inadequate diet

Dental Problems:

• Inflammation and ulcers of the oral mucosa

• result from persistent damage to oral mucosal cells

• Damage is initially superficial, progress to ulceration and involvement of entire epithelium

Causes

• Viral infection

• Bacterial / fungal infection (e.g. Candida albicans)

Dental Problems:

• Manifestations

- Initial burning at site

- Clustered vesicular lesions on lip or oral mucosa

• Pathogenic organism: Herpes Simplex Virus

• Treatment

- Self limiting

- Antiviral agent, e.g. Acyclovir (Zoviarx)

- Avoid irritating foods

Dental Problems:

• Pathogenic organism: Candida albicans

• Manifestations

– Creamy white, curdlike patch

– Red, erythematous mucosa

• Treatment

– Topical antifungal agent,

e.g. Nystatin, fluconazole

– Mouth care

Dental Problems:

• Malignancy of the oral mucosa

• Most common site – lower lip, tongue and floor of the mouth

• Usually squamous cell carcinoma (SCC) that begins on the surface of the epithelium

• Cells begin to vary in size and shape

• Alterations in thickness of the lining of epithelium develop 🡪 result in atrophy

• Symptoms that warrant further assessment : a lesion that does not heal within 2 weeks or a lump or thickening in the cheek

Nursing responsibilities, Nystatin (Mycostatin) – Oral Suspension:

⮚ Shake suspension before measuring each dose

⮚ Instruct client to retain the drug on each side of the mouth as long as possible, then swallow

Nutritional management:

• Percutaneous endoscopic gastrostomy (PEG) before surgery / radiation to minimize malnutrition

• Parenteral fluids maybe given for the first 24-48 hours after surgery

Which are the risk factor of GERD?

1. Obesity

2. Drugs / chemicals that relax LES

3. Weakened or incompetent LES

4. Client with nasogastric tube

5. Hiatal hernia

6. Delayed gastric emptying

7. Positioning

Which are manifestations of GERD?

1. Heartburn

2. Regurgitation with bitter and sour liquid

3. Dysphagia

4. Chronic cough, hoarseness, laryngitis, pharyngitis

Manifestations of GERD, Heartburn:

Restrosternal sensation of burning or discomfort occurs (?) mins after eating

Complications of GERD:

- Local effect of gastric acid on esophageal mucosa

- Repeated oesophagitis may lead to scar tissue formation, stricture and dysphagia

Complications of GERD:

- Changes in cells lining of the oesophagus

- Risk of oesophageal cancer

Diagnostic tests of GERD and Hiatal Hernia:

- To evaluate the anatomical structure of oesophagus and stomach

Diagnostic tests of GERD and Hiatal Hernia:

- To have direct visualization of the oesophagus and stomach, to rule out any mucosal damage such as lower oesophagitis +/- ulcer

Nutrition and lifestyle management of GERD:

- Increase gastric acidity and interfere with gastric emptying

What is the intervention?

Nutrition and lifestyle management of GERD:

- Reduce pressure in the stomach and reduce oesophageal reflux

- Maintain ideal body weight to avoid obesity

What is the intervention?

Nutrition and lifestyle management of GERD:

- Prevent reflux with nighttime distress

What is the intervention?

Nutrition and lifestyle management of GERD:

- Prevent regurgitation of gastric content

What is the intervention?

Nutrition and lifestyle management of GERD:

- Gravity fosters oesophageal emptying

What is the intervention?

Nutrition and lifestyle management of GERD:

- Smoking increase gastric acidity, decrease LES pressure and interfere with healing

What is the intervention?

Nutrition and lifestyle management of GERD:

- Reduce intraabdominal pressure and oesophageal reflux

What is the intervention?

Which are the medical management of GERD?

1. Antacids

2. Mucosal protectant

3. Proton pump inhibitors

4. Histamine-2 receptor antagonists

Which are the risk factors of Hiatal Hernia?

1. Heavy lifting or bending over

2. Frequent coughing

3. Obesity

4. Ascites

5. Pregnancy

Type of Hiatal Hernia:

- The most common type (about 90%)

- The proximal portion of the stomach moves into the thoracic cavity through the oesophageal hiatus

- Gastroesophageal junction also slide upward through oesophageal hiatus

- Development of reflux is related to chronic exposure of LES to the lower pressure of thorax -> significantly decreased effectiveness of LES

Type of Hiatal Hernia:

- also known as paraesophageal hiatal hernia

- Junction between oesophagus and stomach remains inits normal position below the diaphragm

- Part of the stomach herniates through the oesophageal histus

- Reflux is usually not present because LES remains anchored below diaphragm

- Risks of volvulus, obstruction and strangulation are high

Manifestations of Hiatal Hernia:

1. Asymptomatic

2. Heartburn

3. Regurgitation

4. Dysphagia

5. Belching, indigestion

6. Ischaemia from hernia strangulation cause severe chest or epigastric pain, nausea, vomiting and GI bleeding

Complications of Hiatal Hernia:

1. Oesophagitis

2. Haemorrhage

3. Stenosis

4. Ulcerations

5. Strangulation

6. Regurgitation with tracheal aspiration

Manifestations of Oesophageal Foreign Body:

1. Dysphagia

2. Sore throat, neck pain, chest/abdominal pain

3. Dyspnoea

Diagnostic tests for Oesophageal Foreign Body:

1. X-rays

2. Laryngoscopy

3. Oesophago-gastro-duodenoscopy (OGD)

Complications of Oesophageal Varices:

• Bleeding oesophageal varices is an important consequence with high mortality rate.

Complications of Oesophageal Varices:

• Decrease cerebral, hepatic and renal perfusion

Complications of Oesophageal Varices:

• increased nitrogen load from bleeding into GI tract 🡪 Increase ammonia level in blood

Diagnostic tests for Oesophageal Varices:

1. Oesophago-gastro-duodenoscopy

2. Laboratory tests (blood tests)

Medical management of Variceal Bleeding:

1. Maintain patent airway

2. Restoration of haemodynamic stability

3. Correction of coagulopathy

4. Drug therapy

Drug therapy for Variceal Bleeding:

– To decrease blood flow from the internal organs to the portal vein so as to reduce the portal venous pressure.

– To induce splanchnic vasoconstriction so as to stop the variceal bleeding.

• Monitor intake and output, electrolyte level as hyponatraemia may develop and may have antidiuretic effect

• Drug examples: Sandostatin / Terlipressin

Drug therapy for Variceal Bleeding:

• Not used in the acute phase as it might further lower the existing low BP

• Prevent first bleeding episode in clients with known varices and to prevent rebleeding

• Action:

– To decrease high portal pressure and reduce risk for rupture

• Drug example: Propranolol (inderal)

Endoscopic therapy for Variceal Bleeding:

• place a rubber band around the base of varix, then the oesophageal vessels are occluded, causing necrosis, ulceration and eventual sloughing of the varix

Endoscopic therapy for Variceal Bleeding:

• A sclerosing agent (e.g. Tissue glue like N-butyl- cyanoacrylate) is injected directly into or adjacent to the bleeding oesophageal varices through endoscope to induce inflammation of the involved vein and eventual thrombosis

Balloon tamponade – SBT:

• Using syringe and a clamp, slowly inflate gastric balloon in (?)ml increments using either air or sterile water (with or without contrast) to the recommended volume (usually 300-400ml)

• Distress or unexpectedly high resistance to insufflation at this stage should raise suspicion of erroneous oesophageal placement of the gastric balloon warranting deflation and repositioning

• Double clamp the gastric balloon port to prevent leakage

Balloon tamponade – SBT:

• Gently apply traction until resistance is encountered indicating that the gastric balloon is abutting the gastroesophageal junction (usually 35 to 40cm)

• Withdraw the tube a further (?)cm to produce tamponade

• The tube must then be secured and a record made of the length inserted at the angle of the mouth to detect migration

Complications of Balloon tamponade – SBT:

1. Aspiration

2. Airway obstruction

3. Trauma to oesophagus

Nursing care of Balloon tamponade – SBT:

Deflate balloon for (?) min every 8 – 12 hours or according to hospital guideline to prevent tissue necrosis

Risk factors of Oesophageal Cancer:

1. Excess alcohol consumption

2. Cigarette smoking

3. Ingested carcinogens

4. Physical mucosal damage

5. Chronic achalasia

6. Congenital disorders

7. Chronic gastric reflux

8. Barrett’s oesophagus

Complications of Oesophageal Cancer:

1. Tracheoesophageal fistula

2. Tumour erode through oesophagus into aorta

3. Tumour enlargement

Oesophagectomy:

- GI tract integrity is maintained by anastomosing lower oesophagus to stomach

Oesophagectomy:

- Segment of colon may be used to maintain the oesophageal continuity

- or stomach can be elevated into the chest and proximal section of oesophagus anastomosed to stomach

Risk factors of ?

1. Medication

2. Diet

3. Accidental ingestion of corrosive alkali / acid

4. Iatrogenic causes

5. Complication of other life threatening conditions

Risk factors of ?

1. Helicobacter pylori

2. Autoimmune

3. Pernicious anaemia

Manifestations of?

• Epigastric pain

• Dyspepsia

• Anorexia

• Hiccups

• Nausea and vomiting

• Haematemesis

• Melaena or haematochezia

Manifestations of?

• Asymptomatic until atrophy advanced to interfere with digestion and gastric emptying

• Vague epigastric discomfort relieved by eating

• Belching, early satiety

• Intolerance to spicy or fatty foods

• Nausea and vomiting

• Heartburn / Pyrosis

• Fatigue

• Anaemia

Which are the Investigations of Gastritis?

1. Urea breath test

2. Gastric analysis

3. OGD

4. Serum vitamin B12

5. Haemoglobin

Management of?

• Keep NPO to rest the GI tract

• Monitor for vital signs frequently

• If accompanied with severe nausea and vomiting, replace fluids and electrolytes as ordered

• Test vomitus for blood

• For gastritis result from ingestion of poisonous substance

- Gastric lavage to dilute and remove the substances immediately

• Actions:

– Act by neutralizing or reducing gastric acidity, thus increasing the pH of the stomach and relieving hyperacidity.

– containing magnesium have laxative effect and containing aluminium or calcium have

constipating effect.

• Uses:

– Treatment of hyperacidity

– Gastritis

– Gastric ulcer, duodenal ulcer

– Gastroesophageal reflux disease (GERD)/ heartburn

• Examples: – Triact

• Nursing Responsibility:

1. Instruct client to take 1-3 hours after meal and at bed time.

2. Tablets should be thoroughly chewed before swallowing and followed by a glass of water or milk.

3. Shake liquid suspensions thoroughly before pouring the drug.

4. Encourage fluid intake (2500 - 3000 ml/day)

5. Advise client to report persistent constipation or diarrhoea to the physician.

• Actions:

– Block the action of histamine on the histamine H2-receptors in the parietal cells of the gastric

mucosa, thus decreasing gastric acid secretion.

• Uses:

– Duodenal ulcer and gastric ulcers

– Gastritis

– Gastroesophageal reflux disease

– Zollinger-Ellison syndrome

• Examples: – Ranitidine (Zantac) / Famotidine (Pepcidine)

• Nursing responsibilities:

– Do not give an antacid within 1 hour before or after giving it

– avoid rapid intravenous injection as it may cause dysrhythmias and hypotension

• Actions:

– Suppress gastric acid secretion by binding irreversibly to hydrogen/potassium ATPase, the

enzyme that acts as a pump to release acid onto the surface of the GI mucosa

• Examples: – Omeprazole (Losec) / Pantoprazole (Pantoloc) / Esomeprazole (Nexium) / Lansoprazole (Takepron) / Rabeprozole (Pariet)

• Uses: – Gastroesophageal reflux disease / Peptic ulcers

• Nursing responsibilities:

– Administer 30 minutes before breakfast

– Do not crush, break or chew tablets

– Increase calcium intake or take calcium supplement as it can interfere with calcium absorption

– Instruct client to report if have black tarry stools, diarrhoea or abdominal pain

• Actions:

– Acts by protecting the gastric mucosa by increasing bicarbonate and mucous production

– May stimulate uterine contractions that may endanger pregnancy (i.e. contraindication).

• Uses:

– Prevention of aspirin and other NSAID induced gastric ulcers.

• Nursing responsibilities:

– Take with meals and at bedtime

– Use cautiously in clients with inflammatory bowel disease because it may worsen intestinal inflammation and cause diarrhoea

• Actions:

– It bounds to the ulcer base of damaged mucosa, thus creating a physical barrier that impairs

diffusion of hydrochloric acid in the gastrointestinal tract

– It absorbs pepsin and bile acids.

• Uses: – Active duodenal ulcer, gastric ulcer

• Nursing Responsibility:

1. Instruct client to take 1 hr before meals (empty stomach).

2. Avoid use of antacids within 30 mins of a dose.

• Actions:

– It has 3 main ingredients:

• sodium alginate which forms a gel-like layer on top of the acid in the stomach thatprotects the stomach lining;

• calcium carbonate and sodium bicarbonate are both antacids that neutralize excess acid in stomach.

• Actions:

– It is an antiemetic and antipsychotic.

– It blocks the dopamine receptors in the chemoreceptor trigger zone (CTZ) so stops the CTZ from sending the messages to the vomiting centre in the brain.

• Uses:

– Vertigo

– Nausea, vomiting

– Psychotic disorders

• Actions:

– It is an antiemetic and cholinergic.

– It blocks the dopamine receptors (dopamine D2 receptor antagonist) in the chemoreceptor

trigger zone (CTZ) so stops the CTZ from sending the messages to the vomiting centre in the brain.

• Uses: – Prevention of nausea, vomiting

• ulcers of the stomach.

• Site: Most often found on the lesser curvature and area immediately proximal to pylorus (antrum), adjacent to acid-secreting mucosa of the body

• Frequently caused by helicobacter pylori

• Gastric secretion maybe normal or less than normal, there maybe a decreased mass of parietal cells

• ulcers of the duodenum.

• May be associated with altered mucosal defense, rapid gastric emptying, elevated serum gastrin levels or acid production stimulated by smoking

• Site: Proximal portion of duodenum

• Lesions: sharply demarcated and usually less than 1cm in diameter

• Acute form of peptic ulcer that occurs after major physiologic stressor, such as:

- trauma or surgery, severe burns, shock, renal failure

• Usually multiple sites of ulceration are distributed within stomach or duodenum

Which are the Aetiology of peptic ulcer?

1. Helicobacter Infection

2. Severe physiological stress

3. Genetic predisposition

4. Drugs

5. Excessive use of alcohol

6. Smoking

7. Ingestion of corrosive substances

Manifestations of peptic ulcer

1. Epigastric pain

• exacerbated by food intake in ?

Manifestations of peptic ulcer

1. Epigastric pain

• relieved by taking of food or antacid in ?

Which are the Complications of peptic ulcer?

1. Haemorrhage

2. Gastric outlet obstruction

3. Perforation

Which are the Diagnostic tests for Peptic ulcer disease?

1. Oesophago-gastro-duodenoscopy

2. Chest X-ray (erect) to check for any free gas under diaphragm which may indicate perforation (PPU).

3. Urea breath test

Surgical management for Peptic ulcer disease:

• Severing the vagus nerve. Decrease gastric acid by diminishing cholinergic stimulation to parietal cells, making it less responsive to gastrin

Surgical management for Peptic ulcer disease:

• Longitudinal incision is made in pylorus and transversely sutured closed to enlarge the outlet and relax the muscle

• Usually accompanies truncal and selective vagotomies

Surgical management for Peptic ulcer disease:

• Removal of lower portion of antrum of stomach (which contains cells that secrete gastrin) as well as small portion of duodenum and pylorus

• The remnant of the stomach anastomosed with the duodenum

Surgical management for Peptic ulcer disease:

• Removal of lower portion (antrum) of the stomach with anastomosis to the jejunum

• A duodenal stump remains and is oversewn

Which are the Risk factors of Pyloric Stenosis?

1. Unknown aetiology

2. Congenital disorder

3. Hypergastrinaemia

4. Higher incidence for infants who received oral erythromycin before 2 weeks of age

Which are the Clinical manifestations of Pyloric Stenosis?

1. Infant appears well or regurgitates slightly after feedings

2. Projectile vomiting if obstruction progresses

3. Vomitus contains nonbilious +/- blood tinged due to repeated irritation to oesophagus

4. Feeding hungry after vomiting

5. Dehydration

6. Metabolic alkalosis 🡪 the loss of chloride in vomitus

Activated charcoal:

• Activated charcoal alone is becoming the primary choice for emergency management of poisoned clients

• Given orally or via large bore orogastric lavage tube

• It is recommended to give within (?) hour of ingestion of potentially toxic amount of xenobiotics

Procedure of Gastric lavage:

• The lavage should continue until (?) litres of clear return are obtained

Which are the Complications of Gastric lavage?

1. Mucosal injury

2. Perforation of stomach or oesophagus

3. Inadvertent placement of tube in trachea

4. Pulmonary aspiration of gastric content or lavage fluid

5. Fluid and electrolyte imbalance

6. Hypothermia

7. Hypoxaemia

8. Cardiac arrhythmia

Gastrostomy Feeding Procedure, Assess gastric residual volume (GRV):

Initial Checking

Frequency during first 48 hours of enteral feeding

Gastrostomy Feeding Procedure, Assess gastric residual volume (GRV):

Ongoing Monitoring

Frequency after 48 hours if tolerating feeds

Gastrostomy Feeding Procedure, Assess gastric residual volume (GRV):

How much previous feeding perform checking in an adult client, need to notify doctor?

Gastrostomy Feeding Procedure, Flush Tube Prior to Feeding:

Using (?)mL of water as prescribed or according to department guideline

To flush the tube to confirm patency

Which are the Common PEG Complications?

1. Tube Blockage

2. Leakage

3. Early or late Tube Dislodgement

4. Stoma Infection

5. Buried Bumper syndrome

6. Granulation Tissue around exit site

Prevention Methods for Buried Bumper Syndrome:

1. Rotate tube (?)

2. Push in about a thumb’s length into the stomach slightly

3. Pull back to original position daily

4. Secure the tube

Late Tube Dislodgement:

Matured tract (~ (?) weeks post-insertion)

Clinical Manifestations of Stomach Cancer:

• Early satiety

• Anorexia

• Dyspepsia (indigestion)

• Nausea & vomiting

• Ulcer-like pain, unrelieved by antacids, occurring after meals

Clinical Manifestations of Stomach Cancer:

• Weight loss

• Cachexia

• Palpable abdominal mass

• Occult blood maybe present in stool

• Haematemesis

Which are the Diagnostic studies for Stomach Cancer?

1. Barium swallow

2. Abdominal ultrasound

3. Oesophagogastroduodenoscopy

4. Abdominal computed tomography

Stomach Cancer, Postoperative complications – dumping syndrome:

• Self limiting, lasting for around (?) months after surgery

Stomach Cancer, Early dumping syndrome:

• Occur within (?) mins after eating

Definition: When epithelium of the anal canal over the internal sphincter become abraded

Causes:

• Irritating diarrhoeal stools

• Tightening of anal canal with increased sphincter tension

• Childbirth trauma

• Habitual cathartic use

• Laceration by a foreign body

• Anal intercourse

Definition

• One opening in the anal canal with the other usually found in perianal skin

Causes

• Crohn’s disease

• After anorectal abscess drainage

Which are the Clinical Manifestations of Appendicitis?

1. Begin with dull periumbilical pain, followed by anorexia, nausea and vomiting

2. Pain intensifies and localizes in right lower quadrant of abdomen, aggravated by moving, walking or coughing

3. On palpation, rebound tenderness are noted at McBurney’s point

4. Extension or internal rotation of the right hip increases the pain

5. Low grade fever

Which are the Causes of Peritonitis?

1. Perforated peptic ulcer

2. Perforated bowel

3. Perforated diverticulum

4. Ruptured appendix/urinary bladder

5. Ruptured gallbladder/spleen

manifestations of Peritonitis:

• Diffuse or localized pain

• Board-like rigidity

• Diminished/absent bowel sounds

• Abdominal distention

• Nausea and vomiting due to pooling of gastrointestinal secretions

manifestations of Peritonitis:

• Fever

• Malaise

• Tachycardia

• Tachypnoea

• Confusion

• Oliguria

Which are the Manifestations of Colorectal Cancer?

1. Symptoms are vague until the disease is advanced

2. Change in bowel habits

3. Blood mixed with stool (diarrhoea or constipation)

4. Tenesmus (feeling that the bowel does not empty completely)

5. Narrow calibre stool

6. Pain, anorexia and weight loss in advanced disease

7. Palpable abdominal or rectal mass may be present

8. Fatigue and malaise

Which are the Complications of Colorectal Cancer?

1. Bowel obstruction

2. haemorrhage

3. Perforation

4. Direct extension

Screening for Colorectal Cancer:

• Flexible sigmoidoscopy (FS) and Annual FOBT plus FS every (?) years

Screening for Colorectal Cancer:

• Colonoscopy every (?) years

• A common temporary colostomy procedure

• Surgical resection of diseased part of rectosigmoid colon

• End colostomy (a connection between the bowel and an opening of the abdominal wall) is formed

• Closure of the rectal stump and kept intraperitoneally (common practice)

- Allow bowel rest or healing

• After about 3 – 6 months, the colostomy is closed and the colon is reconnected

• It is an operation to remove part or all the rectum

• Parts of the rectum and sigmoid colon with Iymph nodes / blood vessels are removed

• Anastomosis is made between the remaining colon and the rest of the rectum

• Lower risks of local recurrence with compared with anterior resection of rectum

• Excision of rectum and mesorectum (fatty tissue directly adjacent to the rectum with blood vessels and lymph nodes)

• Use transanal excision / transanal endoscopic microsurgery and remove the area up to 20cm from anal verge

• Anastomosis is made between the remaining colon & the rest of anal canal

• Surgical resection of :

- The sigmoid colon

- Rectum

- Anal sphincter complex

• Both anterior abdominal & perineal incisions

• A permanent colostomy is formed

Diverticular Disease:

- Asymptomatic diverticular disease

- Mucosal layer of the colon herniates through the muscularis layer

- Usually multiple diverticula are present

Diverticular Disease:

- Inflammation of the diverticula which may cause obstruction, perforation, abscess, fistula formation and haemorrhage

Complications of?

1. Haemorrhage

2. Diverticulitis

Complications of?

1. Perforation leading to peritonitis

2. Abscess formation

3. Bowel obstruction

4. Fistula formation

5. Haemorrhage

Haemorrhoid:

• Appears above the internal anal sphincter and above the dentate line/pectinate line (mucocutaneous junction of anus)

• Cannot be seen on inspection of the perineal area

Haemorrhoid:

• Appears outside the external sphincter

• Below the dentate line/ mucocutaneous junction

• Extremely painful because of the presence of somatic nerve supply the skin and mucosa below the dentate line

• Prolapsed haemorrhoid can become thrombosed or inflamed, or they can bleed

Classification of Haemorrhoid:

do not prolapse & protrude into anal canal

Classification of Haemorrhoid:

protrude on defaecation but reduce spontaneously

Classification of Haemorrhoid:

protrude and require manual reduction

Classification of Haemorrhoid:

prolapsed to the extent that they may not be reduced

Clinical Manifestations of Haemorrhoid:

• Usually asymptomatic

• Report of pain if constricted

• Bleeding (bright red), unmixed with stool, vary in quantity from streaks on toilet tissue to enough to colour the water in toilet

• Mucous discharge

• Tenesmus/Feeling of incomplete evacuation of stool

• Chronic, dull, aching discomfort when the haemorrhoids have prolapsed

Clinical Manifestations of Haemorrhoid:

• Asymptomatic

• Reddish blue appearance for the thrombosed external haemorrhoid

• Pain on palpation especially prolapsed / thrombosed haemorrhoid

• Itching & burning sensation

• Bleeding is rare

• Anal irritation

• Feeling of pressure after bowel movement

• Difficulty in cleansing the anal region

Management of Haemorrhoid:

• Injection of sclerosing agent into tissues surrounding the haemorrhoids to induce inflammation and eventual fibrosis and scarring

• It is used to treat recurrent bleeding and early prolapse of internal haemorrhoids

Management of Haemorrhoid:

• Haemorrhoids are necrosed by freezing with a cryoprobe; infrared photocoagulation; or electrocoagulation

Management of Haemorrhoid:

• For Enlarged or prolapsing haemorrhoids

• A small rubber band is placed snugly around haemorrhoidal plexus and surrounding mucosa

• Tissue distal to the rubber band becomes necrotic after several days and sloughs off within 7 – 10 days

Management of Haemorrhoid:

• Resection of the haemorrhoid

• Indicated for the permanent prolapse, chronic bleeding and anaemia or painful thrombosed haemorrhoids

• Surgical removal is done by cautery, clamps or excision

• After removing the haemorrhoids, the tissue is either sutured and the wound heals by primary intention or the area is left open and healing takes place by secondary intention

• Indicated when there is marked prolapse, excessive pain or bleeding, or large or multiple thrombosed haemorrhoids

Sitz Bath with Diluted KMnO4:

• Prescribed in diluted form ?

Sitz Bath with Diluted KMnO4:

• Do sitz bath for (?) minutes and use towel to dry up

Risk factors of Hernia:

1. Obesity

2. Ascites

3. Tumours

4. Pregnancy

5. Heavy lifting

6. Smoking

7. Chronic straining for urination or defaecation

8. Chronic cough e.g. COPD

Types of Abdominal Hernia:

 Acquired defects that result from weakness of the posterior inguinal wall

Types of Abdominal Hernia:

 Occurs at previous surgical incision with inadequate healing / following abdominal muscle tears

 Noted when pulls to a sitting position from a lying position

Surgical management of Hernia:

 Reinforcement of the weakened area with wire or mesh

• Diffuse inflammation beginning in rectum and may spread up to the entire colon in a continuous pattern, stopping at ileocaecal junction

• Most severe in the recto-sigmoid area

• Inflammation and ulcerations occur in mucosa and submucosa

• An idiopathic inflammatory disorder that affects any part of the GI tract from the mouth to the anus

• The distal small intestine and proximal large colon are most commonly affected

• Inflammatory process involves the entire bowel wall (Transmural) with segmental pattern (skip lesion)

Classification of IO, Onset:

• Sudden onset

• e.g. torsion, intussusception, herniation

Classification of IO, Onset:

• Protracted onset

• e.g. tumour growth, progressive formation of strictures

Classification of IO, Extent of obstruction:

• Incomplete obstruction of intestinal lumen

Classification of IO, Extent of obstruction:

• Complete obstruction of intestinal lumen

Classification of IO, Location of obstructing lesion:

• Obstruction develop within lumen

• e.g. foreign bodies, gallstones, tumours

Classification of IO, Location of obstructing lesion:

• Obstruction originates outside the intestine

• e.g. tumours, torsion, fibrosis, hernia

Classification of IO, Effects on intestinal wall:

• Luminal obstruction without impairment of blood supply

Classification of IO, Effects on intestinal wall:

• Luminal obstruction with occlusion of blood supply

Classification of IO, Effects on intestinal wall:

• Obstruction at each end of a segment of the intestine

Classification of IO, Causal factors:

• Blockage of the intestinal lumen by intrinsic or extrinsic lesions

• Usually treated surgically

Classification of IO, Causal factors:

• Paralysis of intestinal musculature as a result of accidental or surgical trauma , peritonitis, electrolyte imbalance

• Usually treated medically

Classification of Stoma:

• Constructed by dividing the bowel and bringing out the proximal end as a single stoma  Colostomy or ileostomy

• Distal portion of GI tract is either surgically removed (stoma will be permanent) or distal segment is oversewn and left in abdominal cavity with its mesentery intact (creation of Hartmann’s pouch)

• For Hartmann’s pouch, the bowel can be reanastomosed and the stoma closed

Classification of Stoma:

• Constructed by bringing a loop of bowel to abdominal surface and then opening the anterior wall of bowel to provide faecal diversion

• Result in one stoma with proximal opening for faeces and distal opening for mucous drainage from distal bowel

• An intact posterior wall separates two openings

• Plastic rod holds the loop of bowel in place for 7 – 10 days postoperatively to prevent slipping back into the abdominal cavity

Which are the Risk factors of Cholelithiasis?

1. Obesity

2. Rapid weight loss in obese individuals

3. Use of oral contraceptives

4. Low HDL cholesterol level

5. Hypertriglyceridemia

Risk Factors of?

1. Alcoholism

2. Obstructive biliary tract disease

3. Peptic ulcers

4. Abdominal trauma

5. Infection

6. Hyperlipidemia

7. Medications

8. Genetic factors

Risk Factors of?

1. Recurrent pancreatitis

2. Obstruction from gallstones

3. Autoimmune chronic pancreatitis usually occurs in association with autoimmune disease

4. Gene mutations

5. Smoking

6. Heavy alcohol abuse

Classification of Liver cirrhosis:

• Caused by toxic effects of alcohol metabolism on the liver, triglyceride and fatty acid synthesis increase, and formation and release of lipoproteins decrease, lead to fatty infiltration of hepatocytes

• With alcohol abuse continue, inflammatory cell infiltrate liver, cause necrosis, fibrosis and destruction of functional liver tissue

• Malnutrition commonly occur

Classification of Liver cirrhosis:

- Chronic hepatitis B or C

- Autoimmune hepatitis

- Nonalcoholic fatty liver disease

• Liver is shrunken and nodular, with extensive liver cell loss and fibrosis

Classification of Liver cirrhosis:

• Scarring occurs in the liver around the bile ducts

• Usually results from chronic biliary obstruction may caused by gallstones, tumours, fibrotic strictures or chronic pancreatitis and infection (cholangitis)