GI Flashcards
(129 cards)
1
Q
what is some anti reflux physiological mechanism
A
Lower oesophageal sphincter formed by the diaphragm
2
Q
what is oesophagitis
A
Inflammation of the oesophagus due to reflux
3
Q
Presentation of GORD
A
Heartburn, main feature
aggravated by lying down, bending
relieved by antacids
Burning pain
Other Dry cough chronic acid regurgitation water brash and increased production of saliva dysphagia bloating early satiety halitosis enamel erosion
4
Q
causes and factors associated with GORD,
lifestyle
drugs and diseases
A
LOS hypotension gastric acid hypersecretion slow gastric emptying loss of oesophageal peristaltic function Hiatus hernia family history pregnancy obesity large meals smoking eating fat chocolate, coffee alcohol drugs like CCB (relax LOS) antimuscarinic H Pylori
5
Q
diagnosis of GORD
A
usually a clinical diagnoses and sees its improved by PPI
6
Q
Investigations for GORD
A
first line is PPI trial, if symptoms persist past this time then further investigation
7
Q
Red flags for GORD, things that suggest further investigation is required
A
Over 55 YO Dysphagia vomiting weight loss GI Bleed hematemesis Persestat symptoms
8
Q
Further investigations for GORD
A
Barium swallow- if dysphagia
endoscopy, can show oesophagitis (erosive ulcers) or barrett’s oesophagus
ambulatory PH monitoring
9
Q
Management in GORD
conservative
A
50% of management is simple antacids
education: smoke less lose weight, reduce alcohol. raise head when sleeping
eat smaller meals, avoid over eating
education on diet of GORD
avoid certain drugs, CCB Nitrates anticholinergics, these slow oesophageal motility
avoid NSAIDs, Salts, these damage mucosa
10
Q
Triggers of GORD and foods to avoid
A
Caffeine, chocolate, spicy food, alcohol, citrus, fizzy drinks
11
Q
Drug treatment of GORD
A
can trial antacids
1st line PPI- omeprazole, lansoprazole
can use H2 antagonist if not responding to PPi Ranitidine
12
Q
surgical management of GORD
A
endoscopic nissen fundoplication, operation to treat Hiatus hernia
13
Q
complications of GORD
A
if prolonged can cause oesophagitis
Barrett’s oesophagus
oesophageal ulcers, perforation hemorrhage or strictures
14
Q
what is barrett’s oesophagus
A
pre malignant, epithelium of the oesophagus is usually squamous but after GORD squamous is replaced by columnar epithelium of the stomach since it can tolerate the acid
can become Oesophageal cancer
15
Q
how is GORD classified
A
Los angeles GORD classification
categories ulcerations and erosions as mucosal breaks. 1 to 4
16
Q
diagnoses of barrett’s oesophagus
A
Endoscopy with biopsy
17
Q
risk factors for barrett’s oesophagus
A
Age, white men
prolonged GORD
Smoker
18
Q
management of barrett’s oesophagus
A
PPI + surveillance
plus Radiofrequency ablations and endoscopic mucosal resection
Potential esophagectomy
19
Q
what is chronic idiopathic inflammatory bowel disease
A
life long long chronic inflammatory disease of bowel split into Ulcerative colitis and crohn’s disease
20
Q
where does crohn’s affect and where does it most commonly start
A
anywhere from mouth to anus. most commonly starts at terminal ileum
21
Q
where does UCs affect
A
only affects the colon unless ileocecal valve is incompetent or backwash ileitis
22
Q
epidemiology of crohn’s and UC
A
Crohn (0.1%) is more common in females. and affects people in 20s onset 15-40 years
UC usual onset is after 35
20-40 years
both get peaks after 60 Years
23
Q
describe crohn’s lesions
A
most commonly start in terminal ileum or ascending colon.
affect anywhere in GI tract, lesions tend to skip areas, so lesions are interspersed
the lesion affects transmurally and all the layer of bowel
if it affects the whole GI tract it is known as total collitis
24
Q
what is it known as when crohn’s affects the entirety of the GI tract
A
Total colitis
25
Describe UC lesions
start in rectum, once take cover full rectum (proctitis) it starts to spread up sigmoid and descending colon (Left colitis) and then spreads all the way to the Ileocecal valve (oan colitis)
stops at ileocaecal valve, unless there is backwash ileitis
Inflammation only covers the top layer of bowel (serosa) and is continuous, no interspaced lesion
26
Describe Crohns macroscopic appearance
small bowel is thickened and has ulcers and fissures that give rise to cobble stone appearance
27
Describe UC macroscopic appearance
mucosa appears reddened and inflamed
| Erythematous appearance
28
Describe Crohns Biposy result
```
Transmural inflammation
patchy inflammation
Granulomatous present in 50%
goblet cells present
Crypt abscess
```
29
Describe UC biopsy result
```
Affects only serosa
continuous inflammation
Goblet cell depletion
and crypt abscess
Granulomas are rare to see
```
30
Symptoms of Crohn's disease
Diarrhoea, abd pain and weight loss
Nausea and vomiting
malaise lethargy and anorexia
aphthous ulceration in mouth
Diarrhoea, very frequent, very malodorous
can be like 5-6 times in an hour so affects Q of L
31
Symptoms of UC
Diarrhoea with blood and mucous
abd discomfort
malaise lethargy anorexia
can have rectal bleeding
diarrhoea can be episodic or chronic, normal for a while then flares up
32
Biochemisty, bloods and serology in Crohns disease
Normocytic anemia, can have iron deficency
ESR CRP and WCC elevated
PANCA antibody -ve
ASCA +ve
33
Biochemistry Bloods and serology in UC
Iron deficeny anemia
ESR and CRP elevated
PANCA antibody present
ASCA -Ve
34
Investigations in Inflammatory Bowel disease
Bloods, FBC
Stool culture, do this with anyone presenting with diarrhoea - negative
ESR and CRP elevated
Gold standard: colonoscopy Plus Biopsy
can do CT MRI Barium Swallows and all sorts
35
Crohn's Management
| conservative and non disease modifying treatment
Symptomatic treatment, control diarrhoea (antidiarrhoeal agenst Imodium) control abd pain (analgesics)
stop smoking
36
Crohn's management
| Disease and pharmacological
Induce remission using prednisolone or (Hydrocortisone if severe)
then afterwards maintain remission using aminosalicylates, 5 ASA
Anti TNF Infliximab can also be used to induce and maintain remission
37
Crohn's management
| surgery option
resection of extremely inflamed areas
| treat complications like strictures of fissures
38
UC Management
All UC patients are treated with 5-ASA- Sulfasalazine
+ Fluids for dehydration and IV corticosteroids for flare ups
if very severe used Hydrocortisone to induce remission
anti TNF like Infliximab can be used
surgery for resection of terminal ileum or proctocolectomy, or in fissures, strictures, perforations, toxic dilations
39
what is a 5 ASA and method of action
anti inflammatory only in bowel, because it gets activated when in the lower PH of bowel
40
UC complications
```
Colon cancer
bowel perforation
toxic dilation
hemorrhage
ankylosing spondylitis (not a complication but can can occur concurrently)
```
41
CD Complications
```
stenosis strictures
fistulas
abscess forming
cancer in ileocaecal
malabsorption
perforation
obstruction
```
42
risk factors to inflammatory bowel disease
Family history age groups 20-40 and 60 plus
43
what is the gene associated with UC
HLA - B27
44
what is the prevalence of coeliac disease
1%
45
What is coeliac disease
Inflammation in the small intestine due to autoimmune response triggered by Gliadin in Gluten
46
Coeliac disease pathophysiology
Gliadin, a protein in Gluten is not broken down in the stomach, it is usually binds to IgG in the Intestines and is destroyed
But in coeliac that IgG Gliadin complex is transported across and is phagocytosis by macrophage and causes inflammation and damage to the small intestine
47
Presentation of coeliac disease
```
suspect in weight loss + diarrhoea
Abdominal distension - Bloating
Anemia - iron deficiency
Depression
Gas
failure to thrive in children
dermatitis herpetiformis
```
48
what is skin change associated with coeliac disease
dermatitis herpetiformis ( pretty much specific to Coeliac disease)
49
diseases associated with coeliac disease
Other autoimmune disorders
Type 1 DM
Thyroid disease
IBS
50
Complications of coeliac disease
```
Iron deficiency anemia
lactose intolerance
osteoporosis - since less mineral and ca absorption
T cell Lymphoma
Increased risk of malignancy
```
51
Investigations of Coeliac disease
Needs to be eating gluten for the past 6 weeks
Serology testing Look for: anti TTG (transglutaminase) anti EMA (EndoMysial) IgA, and Alpha gliadin
Bloods- HB low Iron Low Ferritin low B12 low
genetic testing HLA testing
Duodenal biopsy is gold standard for investigations
52
what is the histology of coeliac disease show
this is shown by duodenal biopsy
villous atrophy and crypt hyperplasia
flattened villi and longer crypts
53
Management of coeliac disease
lifelong gluten free diet
involve a dietician to ensure they still get all essential nutrients from a gluten free diet
can prescribe gluten free flour bread pasta
carry on monitoring EMA testing to see effect
DEXA can to assess if any osteoporosis
54
what are commonest causes of malabsorption
Coeliac disease
chronic pancreatitis
Crohn's disease
55
other causes of malabsorption
Insufficient intake (Malnutrition)
Insufficient absorptive area: due to resection (crohns) coeliac
defective intraluminal digestion: pancreatitis, reduced Bile (due to Biliary obstruction or liver disease or ileal resection) bacterial overgrowth
Defective epithelial transport- genetic mutation
Lymphatic obstruction- lymphoma or TB
Lack of digestive enzymes: Disaccharidase deficiency (lactose intolerance)
56
Presentation of malabsorption
diarrhoea
weight loss
lethargy
steatorrhea
(anything from crohn's coeliac or infection, pain,
distention, anemia nausea and vomiting, malaise)
57
signs of malabsorption
anemia ( iron, B12, Folate)
bleeding disorder easy bruising ( vit K)
oedema (protein)
Osteoporosis (vit D and Ca)
58
tests for malabsorption
```
Bloods: FBC Ca B12 Folate INR
Coeliac test, anti TTG, EMA
AMA PBC, Liver failure investigations (ANA, Anti Trypsin copper and Iron)
Stool: check for overgrowth
ERCP: biliary stones or pancreatitis)
```
59
Common pathogen that lead to malabsorption and how is it treated
```
Giardia Lamblia (Extensive surface parisitation) diagnosed by biopsy
Treat with tetracycline
```
60
What is irritanble bowel syndrome
a group of abdominal syndromes where no other cause is found
61
main causes/RF of IBS
```
Depression and anxiety
psycological stress and trauma
GI infection
eating disorer
physical or sexual abuse
Female
```
62
IBS prevalence and age of onset
10-20%
| usually under 40 Y O
63
clinical features of IBS
pain or discomfort is alleviated by Defecation
Altered stool form or frequency (constipation and diarrhoea alternating)
Urgency
Incomplete evacuation
Abdominal bloating and distension
mucus PR
Symptoms worsen after food
symptoms exacerbated by stress, menstruation, Gastroenteritis
needs to be chronic (6 Months)
not attributable to other cause (coeliac, infection)
Other symptoms include backache, nausea, Bladder problems
64
Diagnostic criterias of IBS
6 month history of abdominal pain and discomfort
plus one of the following
symptoms relieved by defecation
alterations in stool form and frequency
```
Plus 2 of:
Urgency
frequency
Abdominal bloating
Mucus PR
```
65
further Investigations of IBS
```
Duodenal biopsy -ve
Stool cultures -ve
ESR and CRP -ve
endoscopy normal
colonoscopy normal
absence of EMA anti TTG IgA
ERCP etc
```
66
Management of IBS
Healthy diet
things that make it worst: Fiber, lactose, fructose, wheat, starch, caffeine, alcohol, fizzy drinks.
use of probiotics
potentially refer to psychologist for counseling if think of stress or depression. or to pain clinic, as can coexist
Psychological stress make symptoms worse, abuse
Symptomatic treatment:
Constipation:Bisacodyl
Diarrhoea: Loperamide
67
what is the differential for haematemesis
Upper GI Bleed. think peptic ulcer is commonest cause
GO Varices
mallory weiss tear
68
Natural defences of stomach against acid
Alkaline mucus
tight junctions
replacement of damaged cells
Feedback loops
69
Causes of peptic ulcers
NSAIDs, - inhibit prostaglandins which make mucus
Bile salts due to duodenal gastro reflux, Bile salts strip away mucus layer
H-Pylori
70
how does H pylori cause Peptic ulcers
secretes Urease, which becomes ammonia then ammonium which causes inflammation and destroys mucosal defence
H pylori is precursor for Gastritis and Peptic ulcers
71
Risk factors for peptic ulcers
```
H pylori infection
Smoking
NSAIDs
Duodenal reflux
Delayed gastric emptying
Stress
```
72
Presentation of peptic ulcers
Epigastric pain, relating to meals and hunger
Relived by antacids
can be in L and R UQ
Dyspepsia- Indigestion , feeling bloated
Heartburn and epigastric tenderness
73
Red Flags that for dyspepsia that make you think to exclude malignancy before thinking peptic ulcers
```
ALARM Symptoms
Anemia - iron deficient
Loss of weight
Anorexia
Recent onset
Malena / Haematemesis
Swallowing difficult
```
74
Differential diagnosis for dyspepsia
```
oesophagitis/ GORD
Duodenal or gastric ulcer
Gastric malignancy (ALARM signs)
Duodenitis
Gastritis
non ulcer dyspepsia
```
75
duodenal ulcers presentation
Epigastric pain before meals or night
relieved by eating or drinking milk
pain can be localised by finger
Epigastric tenderness
76
Investigations and management of dyspepsia
if they are Over 55 and show alarm symptoms carry out urgent upper GI endoscopy
Under 55 and no alarm symptoms:
Stop dyspepsia causing drugs,try antacids, and lifestyle changes like with GORD (alcohol, Caffeine, Fizzy drinks, Spicy foods)(sleep upright, don't overeat)
If symptoms don't improve carry out H Pylori Test
if -ve use PPI for 4 weeks before doing upper GI endoscope
77
Investigations for H. Pylori
Non Invasive C 13 Urea Breath test
78
Treatment for H. Pylori
Triple therapy
1 PPI- Lansoprazole, Omeprazole
2 antibiotics- Amoxicillin and clarithromycin
79
Complications of peptic ulcers
Hemorrhage and bleed
perforation
malignancy and gastric outlet obstruction (projectile vomiting)
80
What is H pylori
Gram -ve Curved bacteria present in around 50% f population but asymptomatic
81
What can H Pylori cause
Gastritis
Peptic ulcers, gastric or duodenal
Gastric cancer
82
what is zollinger ellison syndrome
Gastrin secreting tumour or hyperplasia in pancreatic islets causing recurrent peptic ulcers
83
what is gastritis
Inflammation of the gastric mucosa, essentially pre peptic ulcer stage
Describes the redness seen on endoscope
84
Causes of gastritis
injury to gastric mucosa
commonest cause is H pylori
Irritants, Bile Alcohol, NSAIDs
Autoimmune gastritis - autoimmune disease destroying parietal cells, leads to pernicious anemia
85
Treatment of gastritis
Treat Underlying disease,
| H pylori triple therapy
86
what are different types of intestinal obstruction
firstly small bowel (60^, commonest) or large bowel
can have Volvulus
Adhesions
Intussusception (Telescoping)
87
causes of small bowel Obstruction
Adhesions (commonest) often post surgery
Inguinal Hernia
Crohn's
malignancy
in Children
Appendicitis
volvulus
Intussusception
88
Pathophysiology of SBO and complications
obstruction causes proximal dilation.
less absorption and increased pressure can cause Perforation
increased secretions and sistension can cause anorexia and vomiting
SBO untreated will cause Ischemia necrosis or peroforation
89
what is adhesive obstruction
Extra luminal obstruction, usually post surgery, talc from gloves becomes silicon and binds parts of bowel together
90
what type of obstruction of crohn's disease
Intramural obstruction
91
What is a volvulus
Type of SBO extra luminal, occurs when bowel twists around itself in mesentery causing obstruction and can lead to ischemia
92
what are examples of Intramural obstructions
Crohn's or Diverticular disease
93
what is mechanical obstruction
obstructions in SBO
| volvulus, Hernia Adhesion
94
Presentation of small bowel obstruction
```
Colicky pain, nit localised
vomiting is early sign in SBO
Constipation is Late sign in SBO
distension
Projectile or feculent vomiting
```
shows signs of peritonitis if rupture,
95
Diagnosis of SBO
CT- Gold standard
`Abd X ray
FBC shows WBC elevated and electrolyte imbalance due to dehydration
Other is laparotomy Laparoscopy
96
Treatment of SBO
```
Analgesia + antiemetics
Antibiotics, ampicillin + Gentamicin
Bowel Decompression:
Fluid resuscitation
Surgery, Laparotomy to remove obstruction
```
97
causes of LBO
commonly malignancy 90%
volvulus
Benign structures ( diverticular disease, ischemia)
Hirschsprung disease
98
Indication of bowel perforation
Persistent tachycardia
Fever
Abdominal pain and tenderness, rebound tenderness and Guarding
99
pathophysiology of LBO
Obstruction causes proximal dilation. increased pressure.
This reduced mesenteric blood flow causing ischemia which will lead to dehydration and oedema in bowel.
This can progress to perforation
100
Presentation of LBO
```
Colicky pain
constipation, early
Obstipation no faeces or gas
Vomiting, late
sudden onset of pain= volvulus
weight loss
palpable mass in abdomen
palpable rectal mass
abnormal bowel sounds
Blood on DRE
rectal bleeding
fever
tenderness, rebound , guarding
```
101
Investigations in LBO
```
general: FBC:WCC
Electrolytes: Imbalance
renal function: elevated creatinine
serum amylase: can be elevated
prothrombin time Increased
```
```
Specific
Abdominal x ray, Shows dilation
CT scan
Flexible endoscopy + Biopsy
Contrast enema
```
102
Treatment of LBO
supportive measures: Antibiotics Gentamicin
IV fluids
potentially transfusion
Surgery emergency Laparotomy
103
What is Hirschsprung's disease
Balloon Man disease
congenital disease where no innervation of the colon so dilation and no peristalsis
this causes obstruction
104
What is diverticulitis
Intramural obstruction in Sigmoid colon (commonly)
Muscular layers has holes every once in awhile.
Increased pressure in lumen (often due to poor fiber diet) causes mucosa to pass though these gaps.
Diverticulitis occurs when fecal matter get stuck in thee gaps and becomes inflamed can become Perforated
105
Presentation of diverticulitis
Severe pain in Left iliac fossa
Constipation and fever
Abdominal tenderness and potentially a mass
106
Investigations and management of diverticular disease
Ultrasound or CT of abdomen will show diverticular disease
Fluid and antibiotics amoxicillin or metronidazole
Surgery if perforated
107
appendicitis pathophysiology and causes
Inflammation of the appendix often due to faecolith, poop stone gets stuck.
this causes localized peritonitis and if left untreated and ruptures will gangrene and rupture causing generalised peritonitis or abscess
108
Clinical features of Appendicitis
Vague abdominal Pain that will develop into localized severe R Iliac fossa pain
Tenderness, rebound
guarding
Nausea vomiting diarrhoea anorexia
109
Investigations of Appendicitis
WCC ESR and CRP all elevated
Ultrasound is diagnostic
Can do CT if unclear
110
Management of appendicitis
Laparoscopic surgery to do appendectomy
| IV antibiotics, Cefoxitin
111
Differential diagnosis of Appendicitis
```
Gynaecological causes Ectopic or Ovarian Torsion
Testicular Torsion
Colic, Renal Or biliary
Crohn's
Intussusception
```
112
Causes of localised peritonitis
Any inflammation, Appendicitis, Cholecystitis
113
causes of Generalised Peritonitis
Infection or perforated
appendix, gallbladder gangrene and perforation and Bowel perforation
Perforated Ulcer
114
Features of localised peritonitis
Secondary to inflammation
| Slower onset and symptoms are that of underlying condition. tenderness, rebound tenderness guarding
115
Features of generalised Peritonitis
```
Sudden Onset
Acute severe abdominal pain
collapse and shock
can lead to septicemia
rebound tenderness and guarding
pain made worse by moving
```
116
Investigations for peritonitis
CXR, checks for air under diaphragm Serum Amylase- check acute pancreatitis
Ultrasound CT - Diagnostic
117
Management of peritonitis
surgically treated
NG tube
Iv Fluid
antibiotics- Metronidazole
118
What is spontaneous bacterial peritonitis
when there is an infection in ascites: often e coli, kelbestia or enterococci
119
causes of bowel ischemia
most commonly, Thrombosis or thromboemboli
other occlusive causes is volvulus, tumour, intussusception, herno
and hypovolemic causes like spesis or reduced Co after MI
120
where is ischemic colitis most likely to occur
Always in large bowel
| commonly in Splenic flexure or L colon
121
Where is mesenteric colitis likely to occur
Small bowel
122
Mesenteric colitis presentation
Severe abdominal pain, Central and around right iliac fossa
no peritonitis signs but can develop onto hypovolemia, shock, tachycardia hypotension, weak pulse, confusion, reduced urine output
123
Ischemic colitis presentation
```
Sudden onset of abdominal pain, round hypochondriac, splenic, o L Iliac fossa, L colon
Passage or bright red blood from rectum
diarrhea
Distended +tender abdomen (peritonitis
signs of shock
```
124
Investigations of Ischemic colitis
Ultrasound or CT to exclude perforation
AXR
later can do Barium enema
colonoscopy + Biopsy
125
Investigations of mesenteric colitis
```
Bloods, Look for loss of plasma = increased HB
Increased WCC, metabolic acidosis
AXR- rule out other causes
Laparotomy- diagnostic
CT,MRI angiography also diagnostic
```
126
what is gold standard to exclude perforation
CT
127
Management of ischemic colitis
fluids and antibiotics
metronidazole and gentamicin
ultrasound or CT to Monitor for gangrene
Stricture formation is common so use Barium enema
if IC plus gangrene , perforation, shock, peritonitis= surgery
128
how to identify stricture formations
Barium enema
129
Management of Mesenteric colitis
fluid plus antibiotics
gentamicin plus metronidazole
IV heparin
Surgery to remove necrotic bowel
monitor for signs of sepsis
