Abdominal Disorders Flashcards
What is pyloric obstruction (stenosis)? What are the 2 types?
• blocking/narrowing of the stomach/duodenum opening
• 2 Types:
○ Congenital Defects: (early infancy; between 2 weeks and 4 months) sphincter muscle enlargement is poorly understood but may be due to stress-related factors in the mother, with increased gastrin secretion
○ Acquired:gastritis caused by ulcers or gastric carcinoma
What is congenital stenosis? What is the pathophysiology?
(early infancy; between 2 weeks and 4 months) sphincter muscle enlargement is poorly understood but may be due to stress-related factors in the mother, with increased gastrin secretion
Pathophysiology: pyloric muscle enlargement = hyperplasia and hypertrophy and the transforming growth factor alpha (TGFα) increase muscle mass = extra force to push the gastric contents
What are the clinical manifestations, diagnosis and tx of congenital stenosis?
Clinical Manifestations:
• Vomiting for 2-3 weeks after birth with no reason; vomiting becomes more forceful (projectile) over time; Infants are agitated/irritable and hungry; want food after vomiting
• Develop constipation (not much food reaches their intestines)
• Severe untreated cases (rare): fluid and electrolyte imbalances; chronic malnutrition and weight loss
Diagnosis:
• Based on a history of clinical manifestations
• Gastric peristalsis occasionally visible,
• Firm and small movable mass in RUQ
Treatment:
• Pyloromyotomy (separation of pyloric muscles). Medical and nutritional management need to be addressed
• Antispasmodic drugs (e.g. mebeverine) are used to block M3 receptors on GI smooth muscle and control intestinal spasms (diarrhoea)
What is acquired stenosis? What is the pathophysiology?
gastritis caused by ulcers or gastric carcinoma
Pathophysiology:
• Gastritis: inflammation of gastric mucosa - associated with drugs, alcohol and Helicobacter pylori (H. pylori) infection
• Ulcers: obstruction of pylorus; caused by inflammation, oedema, spasm and carcinoma
• Associated tumours near the pylorus grow to cause an obstruction
What are the clinical manifestations, diagnosis and tx of acquired stenosis?
Clinical Manifestations:
• Epigastric fullness, nausea and pain - disappear when chyme moves into the duodenum
• Severe obstructions: lack of muscle tone, loss of gastric motility, prolonged vomiting and weight loss
Diagnosis:
• Based on clinical manifestations, history of ulcers and confirmed with endoscopy (gastroscopy)
Treatment:
• If the obstructions are caused by ulcerations, then gastric drainage may be indicated to restore motility or pharmacology (e.g. esomeprazole, pantoprazole and omeprazole (PPIs); cimetidine) to reduce gastric secretions
• Fluids and electrolytes (IV) to rehydrate, IV nutrition for severely malnourished clients
• Surgery to treat gastric carcinoma
What do PPI and H2 antagonists do?
• PPIs inhibit formation of HCl = stop the supply of H+ that are produced by parietal cells (inactivates H+/K+ATPase enzyme)
○ Adverse effects commonly include headache, dry mouth and GI disturbances (nausea/vomiting, diarrhoea). Rarely, adverse effects may include altered liver function and skin rashes
• Cimetidine = histamine (H2) receptor antagonist - blocks HCl secretion via Histamine 2 receptor antagonism
○ Adverse effects include headache, dizziness, nausea/vomiting and diarrhoea/constipation
*High doses can cause anti-androgenic effects in men with decreased libido, sperm count and gynaecomastia
*Multiple drug-drug interactions (e.g. metformin, nifedipine, warfarin) can occur due to interference with – cytochrome p450s
What is nausea?
- Subjective experience associated with many conditions (visceral pain, motion, opioids)
- Conscious recognition of subconscious excitation in the medulla (emetic centre) associated with vomiting
- Can be caused by irritating stimuli in the gut itself, by impulses arising from the cortex or by impulses that originate in the lower brain linked to motion sickness
- Precedes vomiting
What is vomiting?
• Forceful emptying of gastric and intestinal contents (chyme) via the mouth
• Medulla initiates several motor responses: contraction of the diaphragm + simultaneous contraction of all abdominal wall muscles = increase intragastric pressure = forces opening of the oesophageal sphincter = chyme expelled *The cycle repeats until there is no more chyme in the stomach
• Chemoreceptor trigger zone (CTZ) – small area on the floor of the 4th ventricle in the brain
○ Can be activated by electrical stimulation and drugs - D2 agonists (levodopa, bromocriptine) and opioid agonists (codeine, morphine, oxycodone)
○ Stimulation of 5-HT, AChE (acetylcholinesterase), and substance P receptors in the CTZ = vomiting; 5-HT from the brainstem and enterochromaffin cells in the gut.
• Cerebral excitation (odors, psychological factors (e.g. fear)) may send impulses directly into the emetic centre not involving the CTZ
• Motion sickness (changing direction or rhythm of motion) stimulates receptors in the inner ear which via CN VIII initiate vomiting
What is the tx of nausea and vomiting?
• Tx by opioid agonists/analgesics can increase the production of endogenous opioids (endorphins, enkephalins) and decrease pain message within the CNS = inhibit release of substance P
○ Adverse effects: nausea, vomiting, physical dependence (withdrawal), constipation, respiratory depression, suppression of cough reflex and histamine release (neck flushing)
• Antiemetic medications - D2 antagonists (e.g. metoclopramide, prochlorperazine) - used if adverse effects include extrapyramidal side effects, drowsiness and headache
• Ondansetron: 5-HT3 antagonistic; effective treatment for nausea/vomiting
Adverse effects: rare transient visual disturbances (blurred) *older people more sensitive to adverse effects
What is constipation? What can it be caused by? What are the tx?
Constipation: slow movement of faeces through the large intestine = difficult or infrequent defecation (dry and hard faeces) *Normal bowel habits range from 2-3/day to 1/week
• Acute or chronic
• Not a significant issue until it causes health problems and affects the quality of life (bowel fullness, discomfort)
• Can be caused by any pathology of the intestines (e.g. tumours, adhesions) obstructing the movement of the contents
* Neurogenic disorders: alter neurotransmission or absence/degeneration of neural pathways = delay transit time through colon = constipation * Congenital megacolon/ Hirschsprung disease: lack of ganglion cells in the myenteric plexus of the large intestine = loss of propulsive movements * Sedentary lifestyle, diet low in fibre, medications with anticholinergic action (opioids, antidepressants)
Treatment: exercise, increased fluid and fibre intake, and dietary supplements (e.g. metamucil)
What is Diarrhoea ? What are the tx?
Diarrhoea: increase in frequency of defecation due to rapid movement of faecal matter through the large intestine (>3 loose stools/day is considered abnormal)
• Can cause dehydration, electrolyte disturbances, metabolic acidosis and weight loss
• Acute: bacterial/viral infection (enteritis) in which the mucosa is irritated and increased rate of absorption, watery stool, fever and possible cramping pain
• Chronic: inflammatory bowel disease
Treatment: restore fluid and electrolytes, treat cause and manage distressing symptoms
• Medications (e.g. loperamide) can activate opioid receptors in the gut wall = decrease fluid loss and diarrhoea
What is intestinal obstruction? What are the common causes?
Intestinal Obstruction: blockage of chyme flow or failure of normal intestinal motility
*Common causes include herniation, torsion (volvulus), fibrous adhesions, tumour, and diverticular disease
What are the 2 types of intestinal obstruction?
- Mechanical:
· Can be a simple obstruction = no alteration in blood flow (adhesions)
· Strangulated form = impairment of BF and necrosis = increased risk of perforation, peritonitis and sepsis- Functional Obstruction (paralytic ileus):
· Paralysis of intestinal motility = trauma or electrolyte imbalances
· Can occur in inflammatory conditions of abdomen and intestinal ischemia due to MI
- Functional Obstruction (paralytic ileus):
What is the pathophysiology of intestinal obstruction?
• Accumulation of gas and fluid inside the lumen: gas/air is swallowed; fluid: impaired electrolyte and H2O absorption
• With 8 litres of fluid (saliva, gastric juice, bile) produced within a 24 h period, distention occurs almost immediately - decrease in electrolytes and H2O absorption and an increase in their net secretions into the lumen
• Deepening of the location of the obstruction, alkalosis or acidosis can occur = severe pressure = occludes arterial circulation worsening metabolic acidosis (lactic acid accumulation) = ischemia, necrosis and perforation
*This may compound to develop bacterial proliferation and translocation leading to peritonitis and sepsis
*Prolonged strangulation can cause acidosis
What are the clinical manifestations, diagnosis and tx of intestinal obstruction ?
Clinical Manifestations: depends on degree of obstruction and duration will depend on which signs are evident. Cardinal signs and symptoms include:
• Complete obstruction – abdomen pain and distention, absolute constipation and vomiting
• Partial obstruction – can cause diarrhoea
• Mechanical Obstruction - severe and colicky pain
• Strangulation: constant pain
• Paralytic ileus - continuous pain and silent abdomen
These all have sweating, nausea and hypotension, decreased lung volume in severe distention and fever and leucocytosis (increase in WBC count)
Diagnosis:
• Clinical manifestations
• X-ray, US and/or CT scan
Treatment:
• Decompression of lumen/ bowel with nasogastric suction and replacement of fluid and electrolytes
• Immediate surgical intervention may be indicated with complete obstruction and strangulation
What is appendicitis and what is the pathophysiology?
Appendicitis: inflammation of the appendix
*Most common surgical emergency of the abdomen seen in the 5-30 year-old age group, however, it can occur at any age
Pathophysiology:
• Appendix becomes swollen, gangrenous = perforates
• If not managed causes peritonitis and sepsis
• A common theory is that obstruction by a hard piece of stool or twisting or other foreign bodies causes an obstruction to the lumen = increase intraluminal pressure = bacterial infection, inflammation and ischemia
What are the clinical manifestations, diagnosis and tx of appendicitis?
Clinical Manifestations:
• Abrupt onset; pain referred to the epigastric or periumbilical region. Pain increases over time (2-12 hours) and becomes colicky with nausea, vomiting and diarrhoea in children
• When the inflammatory process extends to the serosal layer, peritoneum pain becomes localised to the RLQ with fever and elevated WBC
Diagnosis:
• Based on physical assessment findings, lab tests (high WBC); X-ray, CT and US is used to confirm the diagnosis
Treatment: appendectomy (surgical removal of the appendix) and antibiotics are used to treat a possible infection
What are 2 main disorders of the gall bladder?
- Obstruction: cholelithiasis/ gallstones (can remain in the gallbladder or be ejected); caused by cholesterol and pigmented gallstones
Risk factors of cholesterol stones include obesity, age/family history and gender (females more likely to have them)- Cholecystitis: inflammation of the gall bladder
• Secondary to obstruction (most cases) of the gallbladder outlet, i.e. lodging of a gallstone in the cystic duct
• In other cases, it can be from sepsis, severe trauma and infection
- Cholecystitis: inflammation of the gall bladder
What is the pathophysiology of cholelithiasis?
Pathophysiology:
· Cholesterol gallstones: bile supersaturated with cholesterol or micro-stones leading to macro-stones
· Super-saturation of bile could be linked to an enzymatic defect = increase cholesterol synthesis
· Decrease in the secretion of bile acids and decreased reabsorption of bile salts from the ileum leads to decreased motility of gallbladder smooth muscle
· Pigmented gallstones (dark brown/black): combination of bilirubin in bile and Ca2+/other salts
What are the clinical manifestations, diagnosis and tx of cholelithiasis?
Clinical Manifestations: Many individuals with gallstones have no symptoms
· Symptoms occur when bile flow is obstructed
· Biliary colic pain in the RUQ radiating to the upper back, right shoulder, or mid-scapular region. Pain is abrupt in onset, increases steadily in intensity (persists for 2-8 hours) and followed by soreness in the RUQ
· Small stones <8 mm can pass into the common bile duct producing indigestion and biliary colic
· Larger stones obstruct flow and cause jaundice with epigastric pain and intolerance to fatty foods, flatulence
Diagnosis: patient history, imaging and laboratory studies including liver function test (LFT) – ALP (alkaline phosphatase)
Treatment:
· Surgery is the preferred treatment option; laparoscopic approach - cholecystectomy
· Drugs that dissolve the stones may be considered, such as bile acid chenodeoxycholic acid (CDCA) or ursodeoxycholic acid (UDCA)
What is the pathophysiology of cholecystitis?
- Obstruction in cystic duct = release of phospholipase from the epithelium of the gallbladder = enzyme breaks down lecithin and releases a membrane-active toxin = disrupt protective lining = damages mucosal cells = inflammation
- Inflammatory response and distention = decrease in blood flow, ischemia, necrosis and perforation
What is acute cholecystitis?
rapidly progresses to gangrene and perforation
• Acute onset of RUQ or epigastric pain
• Fever, nausea, vomiting, and leucocytosis, increase in bilirubin and alkaline phosphatase level
What is chronic cholecystitis?
Chronic cholecystitis: repeated episodes of acute cholecystitis or chronic irritation of the gallbladder by stones
• More difficult to detect with an intolerance to fatty foods, abdominal discomfort and colicky pain
What are the diagnoses and tx to cholecystitis?
Diagnosis:
• US: detect gallstones and wall thickening = indicates inflammation
• CT scan: useful to detect thickening of the gallbladder wall
• Nuclear Scanning: enhance visualisation enables the liver to extract a rapidly injected radionuclide that is excreted into the bile duct
Treatment:
• Analgesics and antibiotics (e.g. gentamicin) to control pain and infection
• To prevent complications, a cholecystectomy may be indicated
*Complications may include pancreatitis and pancreatic abscesses associated with the procedure
