Dyspepsia Flashcards
1
Q
What are the common causes of acute pancreatitis?
A
Gallstones, alcohol use, hypertriglyceridemia, idiopathic causes, trauma, steroid use, infections, autoimmune conditions, and certain medications.
Includes conditions like Hashimoto’s, IBD, and drugs such as tetracycline and furosemide.
2
Q
What are the autoimmune causes of acute pancreatitis?
A
- Autoimmune conditions like Hashimoto’s, IBD (ulcerative colitis) rheumatoid arthritis, Sjögren’s syndrome, sarcoidosis and primary biliary cholangitis.
3
Q
Which scorpion causes acute pancreatitis?
A
Tityus obscurus
Yellow scorpion
4
Q
What drugs cause acute pancreatitis?
A
- Drugs such as tetracycline, furosemide, thiazide, azathiioprine, valproic acid and
5
Q
What is the primary function of the pancreas?
A
Divided into exocrine (secreting pancreatic juice) and endocrine (secreting glucagon and insulin) functions. Pancreas is found in front of vertebrae L1 and L2, between the duodenum and spleen.
6
Q
What is the pathophysiology of pancreatitis?
A
Premature activation of trypsinogen in the duct increases duct pressure, causing tissue damage and inflammatory responses that causes micro vascular thrombosis and multi-organ dysfunction syndrome.
7
Q
What increases risk of pancreatitis?
A
smoking and bacterial infections like campylobacter jejuni, mycobacterium tuberculosis and mycobacterium Avium.
8
Q
What are the clinical presentations of acute pancreatitis?
A
Moderate to severe abdominal Epigastric pain, nausea, weight loss, and pain relief by sitting forward.
9
Q
How does biliary pancreatic pain present?
A
sharper pain radiating to back
10
Q
How does alcoholic/metabolic aetiology of pancreatitis present?
A
sluggish onset of dull and generalised epigastric pain
11
Q
What are the clinical findings for pancreatitis?
A
epigastric tenderness with decreased bowel sounds, rigidity and some guarding. Cullen’s sign, Grey-Turner’s
Fox’s sign
Type 3c diabetes may develop from pancreatitis, which is manageable with oral diabetes medications and insulin
Patient may have fever, tachycardia and hypotension. There may be signs of jaundice
12
Q
What does Cullen’s sign indicate?
A
Yellow/blue bruising around the bellybutton due to peritoneal hemorrhage.
13
Q
What is grey-turner sign?
A
Grey-Turner’s sign is ecchymosis in the flanks from intra-abdominal haemorrhage.
14
Q
What is Fox’s sign?
A
Fox’s sign is bruising over Inguinal ligament from retroperitoneal bleeding
15
Q
What are the three criteria for diagnosing acute pancreatitis?
A
1) Lipase/amylase level 3 times the normal upper limit. 2) Abdominal pain consistent with pancreatitis. 3) Abdominal imaging consistent with pancreatitis.
16
Q
What are the risk factors for pancreatitis?
A
Male gender, increasing age, obesity, and smoking.
17
Q
What is An indicator of pancreatic exocrine function?
A
faecal elastase enzyme
18
Q
What is an indicator for endocrine function?
A
glucose tolerance
19
Q
What are the investigations for acute pancreatitis?
A
ABG for prognostic scoring
Serum triglycerides, calcium, LFT
LDH and bone profile
CT with contrast for pancreas
Antibody testing for IgG4 which indicates biliary tract, pancreatic disease, liver and lung disease
ECG
Urinalysis
20
Q
What initial management is recommended for acute pancreatitis?
A
*Aggressive fluid resuscitation with crystalloid fluid 15-20ml/KGand monitoring of blood parameters.
*Nil-by-mouth until abdominal pain, vomiting, nausea, loss of appetite and ileum improve and nasojejunal feeding
*Monitoring of blood urea nitrogen and haematocrit
*Enteral nutrition within 72 hours of presentation
*Pain management with opioid analgesics starting with NSAID and progressing from low potent opioid to highly powerful opioid
21
Q
True or False: Type 3c diabetes can develop from pancreatitis.
A
True.
22
Q
What is the treatment of gallstones?
A
cholecystectomy or ERCP, which combines upper GI endoscopy and a tube to inject a dye into the biliary or pancreatic duct
Complications of acute pancreatitis
23
Q
What are the complications of acute pancreatitis in the first 4 weeks?
A
Peripancreatic fluid collection, pancreatic abscess, acute respiratory distress, and pancreatic necrosis.
24
Q
How is pancreatic necrosis treated?
A
treated with quinolone with metronidazole)
25
What are the complications of acute pancreatitis over 4 weeks?
pancreatic pseudocyst
Splenic thrombosis
Chronic pancreatitis
Pancreatic insufficiency
Acidosis
Abdominal compartment syndrome
26
What is a pancreatic pseudo cyst?
A fluid-filled sac of amylase rich fluid which can rupture with a fibrotic wall that lacks a true epithelial lining, arising after acute pancreatitis.
27
What is thescore used for assessing pancreatitis?
Glasgow Imrie score To assess severity of acute pancreatitis and predict mortality.
28
What are the aspects of Glasgow Imrie score?
on admission and 48 hours after admission with PANCREAS acronym:
*PaO2 less than 7.9
* Age over 55
* Neutrophil count high
* Calcium over 2.0
* Renal function lowered with high urea
* Enzyme LDH is high over 600 or AST over 200
* Albumin is high over 32
* Sugar is high over 10
29
What is used to assess pancreatitis at admission?
Ranson’s criteria such as:
High WBC
* Age over 55
* Glucose high
* AST over 250
* LDH over 350
30
What is assessed 48 hours after admission?
Drop in Hct
BUN
Ca over 8
Arterial pO2 less than 6kPa
Base deficit
Over 6 litres of fluid required in 48 hours
31
What are the clinical features of chronic pancreatitis?
Chronic epigastric pain, malabsorption, weight loss, diarrhea, and steatorrhoea.
32
What are the clinical features of chronic pancreatitis?
Clinical features of chronic pancreatitis is chronic epigastric pain radiating to the back, abuse and vomiting. There is impaired glucose regulation, malabsorption with weight loss, diarrhoea and steatorrhoea. There will be significant cachexia and tenderness in epigastric
33
What are the diagnostic findings for chronic pancreatitis?
On abdominal x-ray or CT abdomen, there will be calcification. Key bloods include faecal elastase which is an indicator of pancreatic exocrine function, where low levels are a sign of dysfunction
HbA1c
**Serum amylase and lipase are not typically raised in chronic pancreatitis.
34
What is the primary cause of pancreatic insufficiency?
Loss of over 90% of exocrine function due to conditions like chronic pancreatitis.
35
What is annular pancreas?
where the second part of duodenum is surrounded by a ring of pancreatic tissue which can block blood supply to rest intestines and lead to Pancras divisum
36
What is pancreas divisum?
Pancreas divisum is where the pancreatic duct remains as two distinct ducts which reduces the effieciny of draining and can lead to pancreatic draining.
Diagnosis of pancreatic duct is MRCP, endoscopic ultrasound, ERCP. Management of pancreas divisum is switching to low-fat, analgesics
37
What is necrotising pancreas?
Necrotising pancreatitis occurs due to ischaemia of pancreas should be managed with intravenous broad spectrum antibiotics because fo risk of systemic inflammation and MODs
38
Which type of calcium Imbalance occurs in pancreatitis?
Hypocalcaemia occurs in pancreatitis due to free fatty acids reacting with serum calcium to form salts, a process called saponification; this can cause tetany if severe
39
What is the management of chronic pancreatitis?
Abstinence from alcohol
Assessing serum hbA1c
Creon pancreatic enzyme replacement for lipase, amylase and enzymes
Replacement of vitamin A, D, E and K
ERCP for gall stone removal, stent placement or extra corporeal shock wave therapy
Surgical management with Frey’s procedure to remove the diseased part of the pancreatic head and forming a pancreaticojejunostomy
40
What is the surgical management of chronic pancreatitis?
Removal of pancreatic duct stones and strictures with extra corporeal shock wave therapy an endoscopic stone removal
Pancreaticojejunsotomy by joining the pancreas and jejunum for treating duct obstruction
Frey’s procedure for head of pancreas disease to improve drainage by removing sections
41
What is pancreatic insufficiency?
Pancreatic insufficiency is when over 90% of exocrine function of pancreas is lost, with clinical features of malabsorption like steatorrhoea, weight loss and abdominal bloating present.
42
What is the cause of pancreatic infussiciency?
Cause includes chronic pancreatitis, pancreatic resection and cystic fibrosis and Whipple’s procedure diagnosis is confirmed with the pancreatic function tests, with pancreatic faecal elastase indicating function imaging includes ERCP and MRCP.
43
What is the management of pancreatic insufficiency?
Management is with creon pancreatic enzyme supplements and treatment of osteoporosis.
44
What is pancreatic pseudo cyst?
Pancratic pseudo cyst is where there is localised fluid collection with a non epithelial wall, due to pancreatic duct disruption, such as from pancreatitis where i ill arise after 4 weeks. There may be biliary obstruction, portal vein Thrombosis and rupture. diagnosis is with trans abdominal ultrasound or contrast CT scan. Management is pancreatic rest with nasojejunal feeding
45
What is the criteria for 2week referral in dysphagia?
2 week referral criteria is indicated for dysphagia or those aged 55 years and over with weight loss and either upper abdominal pain, reflux or dyspepsia.
46
What are the mechanical causes of dysphagia?
benign strictures, malignancy and pharyngeal pouch
47
What are the motility causes of dysphagia?
achalasia, diffuse oesophageal spasm and systemic sclerosis
48
What are the neurological cauases of dysphagia?
cerebrovascualr disease, Parkinson’s disease, motor neurone disease and myasthenia gravis
49
What does odynophagia indicate?
infection, malignancy, ulcer or spasm
50
What is a common cause of benign oesophageal strictres?
*Corrosive substance ingesting, most common in children under 5 and adults which can cause necrosis of oesophagus
*Eosinophilia oesophagitis: WBC build up in oesophageal lining, with greater risk for those with environmental allergies
*Radiation therapy from head and neck or lung cancer treatment
*Post-endoscopy
*Anatomical stricture form early staged oesophageal cancer or from chemotherapy
*Infection with CMV, herpes, HIV and fungal infection with candidiasis, with odynopagia (painful swallowing) and tends to occur in immunocompromised atiens
51
Which drugs can cause benign oesophageal strictres?
Drug induced osopehagitis from NSAIDs, tetracycline antibiotics and potassium chloride
52
What is malignant strictre?
adenocarcinoma from Lower 1/3 of oesophagus and squamous cell carcinoma
53
What is the clinical presentation of oesophageal strictre?
Clinical presentation of oesophageal strictre is dysphagia, food impaction (medical emergency AKA choking) odynopahgia, chest pain and weight loss. Thee is progressive dysphagia from solid food to liquid food.
54
How does benign strictre present?
Benign strictres follows a slow and insidious course, while malignant stricture develops rapidly. Sometimes dysphagia is combined with pain in the presence of acute esophagitis. It should be assessed for associated symptoms like heartburn, vomiting, pain while swallowing and upper respiratory symptoms and water brash.
55
What is water brash?
Water brash may occur, where excessive amount of saliva mixes with stomach acids from acid reflux. Upper respiratory symptoms like chest tightness and shortness of breath should be assessed, morning soreness of throat and asthma-like wheezing.
56
What is achalasia?
An oesophageal motility disorder characterized by failure of the lower oesophageal sphincter to relax, from degeneration of myenteric plexus and vagus nerve fibres of lower sphincter, where Excitatory neurotransmitters for oesophageal contraction are acetylcholine and substance P are unopposed.
There is a loss of inhibitory neurons like nitric oxide synthase and vasoactive intestinal peptide which modulate lower oesophageal sphincter pressure and relaxation.
57
What are the clinical presentations of achalasia?
Dysphagia, regurgitation of undigested food, chest pain, and weight loss, nocturnal cough and risk of aspiration.
58
How can achalasia be diagnosed?
barium swallow, showing smooth tapering of lower oesophagus in a bird beak appearance, with dilation of proxima oesophagus.
Upper endoscopy to exclude lesions
Oesophageal manometers: gold standard to test for co-ordinated muscle movement of the oesophagus which will reveal lower oesophageal sphincter relaxation in response to swallowing
59
What are the treatment options for achalasia?
Endoscopic botulinum toxin injection
pneumatic dilatation (endoscopic balloon therapy)
Heller myotomy (muscles of cardiac are cut)
Surgical myotomy can be given for reducing pressure across the lower oesophageal sphincter. Complications include oesophageal perforation, recurrence, GERD, bloating and cancer.
60
What is the pharmacological treatment of achalasia?
administration of nitrate, calcium channel blockers and phosphodiesterase-5 inhibitors to reduce lower oesophageal sphincter pressure.
61
What are the investigations for oesophageal strictre?
Endoscopy with biopsy
Barium contrast swallow where endoscopes cannot pass through the strictre to provide radiographic image
Endoscopic ultrasound for assessing oesophageal wall
CXR for assessing foreign body imp action, diaphragmatic hernia and ruling out pulmonary conditions
62
What is the management of oesophageal strictre?
Management of strictre involves using endoscopi-guided balloon dilation to relieve dysphagia, stent placement for malignant/refractory benign strictres whic is ideally non-metal stents, surgical resection. Complications from stricture dilation is oesopageal perforation, bleeding, haemorrhage, aspiration pneumonia and displacement of the stent.
63
What is the staging score for clinical dysphagia?
0 - No dysphagia: able to eat a normal diet.
* 1 - Moderate passage: able to eat some solid foods.
* 2 - Poor passage: able to eat only semi-solid foods.
* 3 - Very poor passage: able to swallow only liquids only.
* 4 - No passage: unable to swallow anything.
64
What are the complications with oesophageal strictre?
food impaction, severe chest pain, asthma, oesophageal perforation and fistula formation.
65
What is Plummer-Vinson syndrome?
A condition characterized by dysphagia, iron-deficiency anemia, and glossitis, with a risk of squamous cell carcinoma. Endoscopy will show oesophageal webbing (indentations of intermittent dysphagia) which is more common in middle aged women.
66
What does Plummer-Vinson syndrome increase the risk of?
squamous cell carcinoma of the pharynx and proximal oesophagus.
67
Fill in the blank: The main tests for diagnosing pancreatic insufficiency include _______.
Pancreatic function tests and faecal elastase.
68
What is the management for chronic pancreatitis?
Abstinence from alcohol, dietary changes, and pancreatic enzyme replacement.
69
What causes hypocalcemia in pancreatitis?
Saponification due to free fatty acids reacting with serum calcium.
70
What is Plummer-Vinson syndrome characterized by?
Oesophageal webbing, dysphagia, and increased risk of squamous cell carcinoma of the pharynx and proximal oesophagus
## Footnote
More common in middle-aged women.
71
What are the causes of Plummer-Vinson syndrome?
Nutritional deficiencies, iron deficiencies, genetic predisposition, and autoimmunity
-> associated with coeliac and crohn disease, rheumatoid arthritis and thyorid disease
## Footnote
Associated with coeliac disease, Crohn disease, rheumatoid arthritis, and thyroid disease.
72
What is the pathophysiology of Plummer-Vinson syndrome?
The iron deficiency induces iron-dependent enzyme dysfunction causes oxidative stress damage and causes myasthenia changes in muscles responsible for swallowing, atrophy of oesopageal mucosa and formation of webs as epithelial complications. Oesophageal web is below the cricopharyngeal muscle and is asymmetrically
73
What are the clinical presentations of Plummer-Vinson syndrome?
Asymptomatic, koilonychia, glossitis, cheilosis, and dysphagia over time
## Footnote
Inflammation and crusting of the mouth with B2 deficiency.
74
How is Plummer-Vinson syndrome assessed?
Barium swallow and oesophagogastroduodenoscopy to confirm oesophageal webs with thin membranes which do not span the entire cirucumference of oesophagus.
## Footnote
To confirm oesophageal webs with thin membranes.
75
What is the treatment for Plummer-Vinson syndrome?
Iron supplementation and mechanical dilation with balloons guided by endoscopy. Patinets should be advised to eat slowly and chew thoroughly
## Footnote
Patients should eat slowly and chew thoroughly.
76
What pharmacological treatments are used for Plummer-Vinson syndrome?
Nitrate, calcium channel blockers, phosphodiesterase-5 inhibitors
## Footnote
To reduce lower oesophageal sphincter pressure.
77
What are the complications of Plummer-Vinson syndrome?
Oesophageal perforation, recurrence, GERD, bloating, and cancer
78
What investigations are performed for oesophageal stricture?
Endoscopy with biopsy, barium contrast swallow, endoscopic ultrasound, CXR, CT imaging
## Footnote
For assessing foreign body impaction, diaphragmatic hernia, and staging of malignant stricture.
79
What is the clinical dysphagia score?
0 - No dysphagia, 1 - Moderate passage, 2 - Poor passage, 3 - Very poor passage, 4 - No passage
80
What are the complications of oesophageal stricture?
Food impaction, severe chest pain, asthma, oesophageal perforation, fistula formation
81
What are peptic ulcers?
Peptic ulcer is open sores with duodenal and stomach ulcers, typically from H.pylori infection and NSAID use.
82
What are gastric ulcers typically caused by?
H.pylori infection and NSAID use
83
What are the common symptoms of gastric ulcers?
Epigastric pain 1-2 hours after eating, haematemesis, melena, heartburn, chest discomfort, early satiety, Zellinger-Ellison syndrome, Crohn disease and gastric outlet obstruction.
## Footnote
Common cause is gastric carcinoma.
84
What is the risk of H.pylor infection?
Risk of H.pylori infection is pan-gastritis, chronic inflammation of the entire stomach lining which prevents somatostatin release for gastrin secretion.
85
What is the treatment for gastric ulcers?
PPIs and H2 receptor antagonists
86
What is the primary cause of duodenal ulcers?
Recurrent NSAID use or H.pylori infection. Treated with PPI and H2 receptor antagonists.
87
What are the clinical presentations of duodenal ulcers?
Epigastric pain 2-5 hours after eating, melena, haematemesis, haematochezia with pain awakening the patient during the night. elevated BUN, anaemia.
It commonly occurs in patients aged 20 to 45 and more common in men, with epigastric tenderness and signs of anaemia like pale skin and positive faecal occult blood test. Complications include bleeding, perforation and obstructions
## Footnote
More common in patients aged 20 to 45.
88
What is the testing for H.pylori infection?
Urea breath test and stool antigen test. 24 hour pH test is the gold standard for diagnosing acid reflux, where a probe is placed 5cm above the gastro-oesophageal junction to measure the amount of acid passing in the region. It is quantified b
89
What is the gold standard for diagnosing acid reflux?
24-hour pH test
90
What causes GERD?
Impaired lower oesophageal sphincter function, transient lower-oesophageal relaxation Not triggered by swallowing, causing intragastric pressure exceeding lower oesophageal pressure.
Hiatal hernia increases the risk.
91
What are the clinical presentations of GERD?
Heartburn (retrosternal burning sensation), regurgitation, dysphagia, odynophagia, epigastric pain, nausea
## Footnote
Atypical symptoms include chest pain, chronic cough, asthma, laryngitis, dental erosions.
92
What is Barrett's oesophagus?
Change from squamous to columnar epithelia due to chronic acid exposure visible endosocpically 1cm above the gastrointestinal-oesophageal junction and confirmed with biospy. It typically affects males over 50 and those with longstanding GORD, smoking, hiatus hernia and age of 50-70. Signs and symptoms are identical to GORD with retrosternal chest pain, heart burn, acid taste in the mouth and bloating.
## Footnote
Occurs in patients with long-standing GERD.
93
What is the management of Barrett’s oesophagus?
Management is repeat surveillance via oesphagealgastroduodenoscopy every 2-3 years as there is risk of oesophageal adenocarcinoma
94
What is a hiatal hernia?
Hiatal hernia is a condition caused by abnormal protrusion of stomach or internal organs through diaphragm hiatus, which can compromise the lower oesophageal sphincter and cause gastrointestinal-oesophageal reflux disease
95
What is the cause of hiatal hernia?
It is caused by muscle weakness from age0related weakness prominent in older people, elevated intrabdominal pressure from chronic constipation and COPD. The hernia may prevent the upper part of the stomach returning to below the diaphragm during swallowing.
96
What is the presentation of hiatal hernia?
It can present with heartburn, regurgitation and difficulty swallowing And chronic cough like asthma.
97
What are the four types of hiatal hernia?
* Type I: Sliding type
* Type II: Paraesophageal hernia
* Type III: Combination of sliding and paraesophageal
* Type IV: Stomach and additional organ herniation
98
What is the most common type of hiatal hernia?
The sliding type, representing more than 95% of hiatal hernias. This type occurs when the GEJ is displaced toward the hiatus and slides up into the chest with similar treatment to GERD.
99
What is a type 2 hernia?
A paraesophageal hiatal hernia, which occurs when part of the stomach migrates into the mediastinum parallel to the esophagus. This can result in a gastric volvulus and reccomendations include surgical repair.
100
What is a type 3 hernia?
A paraesophageal hernia combined with a sliding hernia, where both the GEJ and a portion of the stomach have migrated into the mediastinum
101
What is a type 4 hernia?
The stomach and an additional organ, such as the colon, small intestine, or spleen, herniate into the chest which has a risk of volvulus so requires urgent treatment that can cause ischaemia and necrosis.
102
What risk factors are associated with hiatal hernia?
Obesity, prior hiatal surgery, increased intra-abdominal pressure, chronic cough
## Footnote
Symptoms include heartburn, regurgitation, dysphagia, and chronic cough.
103
How is hiatal hernia diagnosed?
Endoscopy
barium enema
oesophageal manometer to exclude other differentials
24 hour pH test is the gold standard which measures the amount of time esophageal pH is below 4, the number of reflux episodes, the duration of the longest reflux episode, and the total number of reflux episodes lasting longer than 5 minutes. A score of 14.7 or above indicates significant gastroesophageal reflux.
104
What is the treatment of hiatal hernia?
double dose PPI
Conservative management includes weight loss, avoiding heavy lifting and practising good posture
105
What is Zenker's diverticulum?
False diverticulum forming a pouch at C5 to C6 vertebra due to cricopharyngeus muscle overtightening. food can catch in the pouch and salivary secretions, t is most typically seen in the elderly and more common in men
106
What are the symptoms of Zenker's diverticulum?
Difficulty swallowing, bad breath, chronic cough, sensation of lump in the throat.
## Footnote
Regurgitation hours after a meal.
107
What is the primary investigation for Zenker’s diverticulum?
barium swallow which shows a pool of residual contrast in the pouch. Endoscopy should be avoided due to risk of lesion perforation
108
What is the treatment of Zenker’s diverticulum?
Treatment involves use of botulinum toxin to relieve symptoms of dysphagia where it is associated with achalasia. Typically large or symptomatic pouches require suRgical removal.
109
What is appendicitis?
Inflammation of the veriform appendix where the 3 taenia coli meet and has a peak incidence between 10-20 years old, leading cause of abdominal surgery in children. Obstruction of the blind opening of the appendix can cause necrosis and gangrene with rupture of the appendix resulting in peritonitis.
110
What is the cause of appendicitis?
*Faecalith: faecalith matter hardened blocking opening of appendicitis, causing an increase in back pressure and risk of bacterial colonisation which is more common in adults
*Lymph node hyperplasia narrowing the opening of the appendix, increasing back pressure and bacterial colonisation, more common in children, increasing the risk of perforation
*Neoplasm such as caecal adenocarcinoma or appendices neuroendocrine tumour blocking opening to the pelvis, more common in over 50s
111
Which pathogens have the greatest risk of infection in appendicitis?
Risk of infection is highest from E.Coli,pseudomonas and bacteriodes.
112
What are the common symptoms of appendicitis?
Dull central periumbilical pain moving to right iliac fossa, loss of appetite, nausea, vomiting, low-grade fever
## Footnote
Positive signs include Rovsing’s sign and Dunphy sign.
113
What are the clinical features of appendicitis?
guarding, rebound tenderness in right iliac fossa
Percussion tenderness
Tenderness in McBurney’s point
Rovsing’s sign
Dunphy sign
Psoas sign
Obturator sign
114
What is McBurney’s point?
Maximal Tenderness in the lower right quadrant
115
What is Rovsing’s sign?
palpation of left iliac fossa causing pain in the right iliac fossa.
116
What is Dunphy sign?
coughing or activity that increases Intraductal-abdominal pressure increases pain
117
What is the psoas sign?
extending/flexing the R hip causes R iliac fossa pain due to a retrocaecal appendix pressing against psoas muscle
118
What is the obturator sign?
flex the hip with resistance causes R iliac fossa pain, indicates retrocecal appendix when inflamed appendix brushes against obturator internus muscle
119
What is the appendices mass?
Appendices mass is the inflammed appendix with an adherent covering of the omentum and small bowel and omentum, causing a palpable mass in the right lower abdomen and mesenteric adenitis .
120
What is the gold standard for diagnosing appendicitis?
Laparoscopic appendectomy which allows indirect visualisation of other organs. Appendix should be sent to histopatholohy once removed to assess for underlying malignancy
121
Which diagnostic tests should be ruled out for appendicitis?
Appendicitis may be mistaken for, Ectopic pregnancy so rule out with serum/urine HCG, Ovarian cysts, Meckel’s diverticulum
122
What are the diagnostic findings for appendicitis?
*Diagnosis is based on examination and raised inflammatory markers. *Imaging includes CT scan to confirm diagnosis which will show enlarge appendix, thickening of appendices wall or ultrasound for female patients to rule out gynaecolical pathology.
*Abdominal X ray may be performed to assess for penumoperitonem.
* Urinalysis should be performed to exclude ureteric stones or UTI neutrophil and CRP may be raised.
123
What are the complications of appendicitis?
Perforation Due to increase in intraluminal pressure and reduction in arterial blood supply and lymphatic compression of the area of appendix causes wall erosion peritonitis
abscess formation
124
What is the treatment for complicated appendicitis?
Complicated appendicitis indicates perforation- Antibiotics (cephalosporin, ceftriazone and betalactam anibiotics) and emergency appendectomy with laparoscopic surgery
125
What are risk factors for mortality with appendicitis?
Age > 80, immunosuppression, severe cardiovascular disease, presence of other comorbidities
126
What are the presentations of retrocaecal appendix?
Right loin pain and tenderness, positive psoas test There will be no muscular rigidity and tenderness on deep palpation because of protection from the overlying caecum.
127
What are the presentations of subcaecal and pelvic appendix?
Suprapubic pain, urinary frequency, diarrhoea, tenesmus but rectal or vaginal tenderness may be present on the right side; microscopic haematuria and leucocytes may be present on urine dipstick testing.
## Footnote
Rectal or vaginal tenderness may be present.
128
What is gastric Volvos?
the stomach twists on itself by 180 degrees, leading to obstruction of the gastric passage and tissue necrosis, and requires prompt surgical intervention.
129
How does a gastric Volvulus present?
Clinically, this can present with Borchardt’s triad: (1) sudden severe epigastric pain (2) retching without vomiting (3) inability to pass a nasogastric tube.
An urgent CT scan is required and often needing emergency surgery
130
What is gastroparesis?
Delayed gastric emptying over 3 months in absence of mechanical obstruction resulting in nausea, vomiting, bloating, early satiety and abdominal pain.
## Footnote
Reduced contraction of the antrum and pyloric relaxation may arise from neuropathy of the vagus nerve.
131
What are the common symptoms of gastroparesis?
Nausea, vomiting, bloating, early satiety, abdominal pain.
## Footnote
These symptoms can lead to a risk of malnutrition.
132
What is the most common cause of gastroparesis?
Idiopathic.
## Footnote
It is strongly associated with diabetes mellitus due to autonomic and enteric neuropathy.
133
Which type of diabetes is less commonly associated with gastroparesis?
Type 1 diabetes.
## Footnote
Gastroparesis is more commonly seen in Type 2 diabetes.
134
Name some other conditions that put patients at risk for gastroparesis.
* Parkinson’s disease
* Multiple sclerosis
## Footnote
These conditions may contribute to the development of gastroparesis.
135
Why are women more likely to have gastroparesis?
Due to links to autoimmune conditions.
## Footnote
Women may benefit from antibody plasmapheresis.
136
What surgical procedures can cause gastroparesis?
* Gastrectomy
* Pancreatic cancer cryoablation
* Pancreatoduodenectomy
* Fundoplication
## Footnote
These procedures may disrupt normal gastric function.
137
What might a clinical examination of a patient with gastroparesis reveal?
Epigastric distention or tenderness in absence of guarding or rigidity.
## Footnote
This can help differentiate gastroparesis from other conditions.
138
What is the gold standard for diagnosing gastroparesis?
Scintigraphic solid meal gastric emptying study with a radioisotope meal.
## Footnote
This test visualizes retention of contents and rates emptying to grade gastroparesis from mild to severe.
139
What is the first-line management for gastroparesis?
Metoclopramide administered 15 minutes before meals.
## Footnote
This antiemetic helps improve gastric emptying.
140
What are two additional medications used in the management of gastroparesis?
* Domperidone (dopamine blocker)
* Erythromycin (antibiotic)
## Footnote
Domperidone speeds up gastrointestinal peristalsis while erythromycin stimulates gastric emptying.
141
How can gastroparesis affect glucose management in diabetes?
It can cause poor glucose management.
## Footnote
Delayed gastric emptying may lead to unpredictable blood sugar levels.
142
What is first line for gastroparesis?
Metacolopromide and domperiodne
